Zuku Sample Questions Flashcards

Question

**Which canine parasite can cause cutaneous larva migrans in people?** A - Habronema spP. B - Trichostrongylus spp. C - Ancylostoma spp. D - Spirocerca sp. E - Trichuris spp.

Answer 1

Answer: **Ancylostoma** Hookworms (Ancylostoma spp.) may cause cutaneous larva migrans in people. Note that roundworms (Toxocara spp., Toxasacaris spp., Baylisascaris spp.) are also zoonotic, causing visceral and ocular larva migrans in people. In dogs, whipworms, Trichuris spp. are associated with a hypoadrenocorticism-like syndrome (hyponatremia, hyperkalemia, azotemia, metabolic acidosis). Whipworm infection has been suggested as one cause of cecocolic intussusception. Habronema spp. in horses can cause tumorlike stomach nodules and sometimes cutaneous lesions. Trichostrongylus spp. cause parasitic gastritis and enteritis in sheep, goats, and cattle. **Hookworms in Small Animals - Comprehensive Veterinary Information** Definitions and Terminology: • Hookworms: Intestinal nematodes, primarily affecting dogs and cats, leading to significant health issues. Causative Agents: • Species: • Ancylostoma caninum (dogs) • Ancylostoma tubaeforme (cats) • Ancylostoma braziliense (dogs and cats) • Ancylostoma ceylanicum (dogs and cats) • Uncinaria stenocephala (dogs and cats in cooler regions) Physiopathology: • Life Cycle: Eggs pass in feces, hatch in soil, and larvae infect hosts through ingestion, skin penetration, or transmammary routes. • Larval Migration: Skin penetration, blood to lungs, coughed up, swallowed, mature in intestines. Arrested larvae in tissues can reactivate. Clinical Findings: • Acute Anemia: Normocytic, normochromic progressing to hypochromic, microcytic in puppies. • Chronic Infections: Anemia, melena, hypoproteinemia, weakness, diarrhea. • Lesions: Hemorrhagic enteritis, pneumonia in pups, dermatitis (interdigital spaces). Diagnosis: • Fecal Flotation: Detects thin-shelled, oval eggs. • Antigen Tests: For hookworm detection. • Postmortem: Examination of intestines for adult worms. Treatment: • Anthelmintics: • Fenbendazole • Moxidectin • Pyrantel pamoate • Milbemycin • Nitroscanate • Supportive Care: Blood transfusions, iron supplements, high-protein diet for severe anemia. • Drug Resistance: Monitor efficacy post-treatment, especially in A. caninum cases. Control and Prevention: • Regular Deworming: Based on age and risk factors. • Sanitation: Dispose of feces promptly, maintain clean environments. • Preventive Measures: Treat pregnant bitches, routine fecal checks. Key Points: • Zoonotic Potential: A. braziliense and A. ceylanicum can infect humans. • Drug Resistance: Emerging problem, particularly in the southeastern US. [Merck Manual](https://www.merckvetmanual.com/digestive-system/gastrointestinal-parasites-of-small-animals/roundworms-in-small-animals) [Zuku Question](https://zukureview.com/zuku-qod/navle/1699?chosen=27%2BrMcuytoyi7l9pz3P%2BT2EQjV1w9o05nPa77jLkjhc%3D&utm_source=Zukureview+Subscribers&utm_campaign=6ea6a9efb9-EMAIL_CAMPAIGN_2024_04_16_01_52&utm_medium=email&utm_term=0_1c9568dbdc-6ea6a9efb9-%5BLIST_EMAIL_ID%5D)

Answer 2

Answer: **Both mother and baby are safe** Both mother and baby are safe. The toxoplasmosis organism causes birth defects in a developing fetus if a mother is infected for the first time in her life while pregnant (ie: IgM positive while pregnant). Toxoplasmosis is not generally dangerous to immune-competent people and a positive IgG result suggests a previous infection. There are challenges to toxoplasmosis testing in pregnant women (false positives). If a pregnant woman is IgM positive, confirmatory tests must be done. **Comprehensive Summary on Toxoplasmosis in Animals** Definition and Etiology Toxoplasmosis is a zoonotic infection caused by Toxoplasma gondii, an apicomplexan protozoan. It infects all warm-blooded animals, including humans. Cats are the only definitive hosts, shedding oocysts in their feces. Transmission: • Ingestion: of sporulated oocysts from contaminated environment or tissue cysts in undercooked meat. • Vertical Transmission: Transplacental transfer from mother to fetus. Pathophysiology: • Stages of Infection: • Tachyzoites: Rapidly multiplying form causing tissue damage. • Bradyzoites: Slow division form in tissue cysts. • Sporozoites: Infectious form in mature oocysts. • Replication: After ingestion, the parasite invades intestinal epithelium, replicates, and disseminates via blood and lymph, causing tissue necrosis. Clinical Findings: • General Signs: Often asymptomatic in immunocompetent hosts. • Acute Infection: Fever, diarrhea, cough, dyspnea, icterus, seizures, and death in young or immunocompromised animals. • Reproductive Issues: Abortion, stillbirth in sheep, goats, and pigs. • Chronic Infection: Subclinical with bradyzoites in tissue cysts. Diagnosis • Serologic Testing: Indirect hemagglutination, ELISA, and other serological assays to detect IgM and IgG antibodies. • Histology and PCR: Identification of tachyzoites or bradyzoites in tissues; PCR for definitive diagnosis. Treatment • Anticoccidial Drugs: Sulfadiazine (15–25 mg/kg PO every 12 hours) and pyrimethamine (0.44 mg/kg PO every 12 hours) for 4 weeks. • Combination Therapy: Trimethoprim-sulfamethoxazole (15 mg/kg PO every 12 hours) for 4 weeks. • Clindamycin: Preferred treatment for dogs and cats (10–12.5 mg/kg PO for dogs, 25–50 mg/kg PO for cats every 12 hours for 3-4 weeks). • Other Options: Diaminodiphenylsulfone, atovaquone, spiramycin, toltrazuril, ponazuril, and diclazuril for acute infections and to reduce oocyst shedding in cats. Prevention and Zoonotic Risk • Hygiene: Wash hands thoroughly after handling raw meat or contaminated objects. Clean and disinfect surfaces. • Food Safety: Cook meat to 67°C (152.6°F), avoid raw or undercooked meat, and ensure good kitchen hygiene. • Pet Care: Feed cats commercially prepared food, clean litter boxes daily, and avoid exposure of pregnant women to cat feces. [Zuku](https://zukureview.com/zuku-qod/navle/1693?chosen=880IhrDfWfwmivh/GPpo3Q9kdgXg86Zr7ZxFWq4pUeE%3D&utm_source=Zukureview+Subscribers&utm_campaign=b41fc05a7a-EMAIL_CAMPAIGN_2024_04_15_01_52&utm_medium=email&utm_term=0_1c9568dbdc-b41fc05a7a-%5BLIST_EMAIL_ID%5D)

Answer 3

Answer: **Immune-mediated thrombocytopenia** This is *immune-mediated thrombocytopenia*, the most common cause of spontaneous bleeding in dogs. It may be primary (idiopathic, most common) or secondary to infection, neoplasia, or certain drugs. Most common in middle-aged females; cockers, poodles, and old English sheepdogs predisposed. Dogs with disseminated intravascular coagulation (DIC) have thrombocytopenia with a prolonged PT and aPTT. Follow this link to see a table of the four most important [coagulation disorder patterns](https://zukureview.com/node/100828) **Immune-Mediated Thrombocytopenia (ITP) in Animals** Definition: • ITP: Immune-mediated destruction of platelets or marrow megakaryocytes. • Also Known As: Idiopathic thrombocytopenic purpura. Causes and Risk Factors: • Idiopathic: No identifiable underlying cause. • Risk Factors: Middle-aged, spayed female dogs, especially Cocker Spaniels. Pathophysiology: • Mechanism: Immune system targets and destroys platelets or megakaryocytes. • Autoantibodies: Directed against platelet surface antigens. Clinical Signs: • Bleeding: Petechiae, ecchymoses, melena, epistaxis. • Severe Thrombocytopenia: Platelet counts <30,000/μL, often <10,000/μL. Diagnosis: • Exclusion: Rule out other causes of thrombocytopenia. • Tests: Bone marrow aspirate (rarely needed), platelet count, clinical signs. Treatment: • Corticosteroids: High-dose initial treatment, tapered gradually. • Vincristine: 0.01-0.02 mg/kg IV, shortens recovery time. • Transfusion: Fresh whole blood for severe anemia. • Splenectomy: For recurrent cases. • Monitoring: Regular platelet count checks during steroid tapering. • Avoid: Drugs interfering with coagulation. **Disseminated Intravascular Coagulation (DIC) in Animals - Comprehensive Study Guide** Definition: • Disseminated Intravascular Coagulation (DIC): A secondary condition characterized by systemic activation of blood coagulation, leading to widespread clotting, bleeding, and organ damage. Causative Agents: • Primary Diseases: Bacterial, viral, rickettsial, protozoal, parasitic infections, heat stroke, burns, neoplasia, and severe trauma. Pathophysiology: • Mechanism: Systemic inflammatory response activates coagulation, leading to widespread clot formation. This results in consumption of coagulation factors and platelets, causing bleeding and organ failure due to microvascular thrombosis. Symptoms: • Clinical Signs: Variable, ranging from no overt signs to severe bleeding, organ failure, and microvascular thrombosis. Diagnosis: • Laboratory Tests: Prolonged APTT, PT, elevated D-dimer, reduced fibrinogen, and platelet count. Thromboelastography can help differentiate stages. Treatment: • Underlying Cause: Identify and treat the primary disease. • Medications: Heparin in hypercoagulable stages; fresh frozen plasma in hypocoagulable stages. • Supportive Care: Fluids, plasma expanders to maintain effective circulating volume.

Answer 4

Answer: **Type II - Antibody binds cell antigen and activates complement.** Pemphigus foliaceus, pemphigus vulgaris, and bullous pemphigoid are generally considered type lI reactions. Antibody binds antigen on a cell, then the antibody-antigen complex activates complement, causing cell lysis. In general, think of rare, autoimmune skin diseases characterized by varying presentations of ulceration, crusting, pustules, vesicles. FYI: "Delayed hypersensitivity" is the same as a type IV reaction. **Hypersensitivity Diseases in Animals** Definitions and Terminology: • Hypersensitivity: An exaggerated or inappropriate immune response to an antigen, causing tissue damage. • Types of Hypersensitivity: • Type I (Immediate): IgE-mediated reaction causing mast cell degranulation (e.g., anaphylaxis, atopy). • Type II (Cytotoxic): Antibody-mediated destruction of cells (e.g., autoimmune hemolytic anemia). • Type III (Immune Complex): Immune complex deposition in tissues (e.g., glomerulonephritis). • Type IV (Delayed-Type): T-cell-mediated response causing tissue damage (e.g., contact dermatitis). Pathophysiology: 1. Type I (Immediate Hypersensitivity): • Sensitization Phase: Initial exposure to an allergen causes IgE production. • Effector Phase: Re-exposure to the allergen leads to IgE binding on mast cells, causing degranulation and release of histamine and other mediators. • Clinical Manifestations: Anaphylaxis, urticaria, atopic dermatitis. 2. Type II (Cytotoxic Hypersensitivity): • Mechanism: IgG or IgM antibodies bind to antigens on cell surfaces, leading to complement activation or antibody-dependent cell-mediated cytotoxicity (ADCC). • Clinical Manifestations: Autoimmune hemolytic anemia, immune-mediated thrombocytopenia. 3. Type III (Immune Complex Hypersensitivity): • Mechanism: Immune complexes formed in the bloodstream are deposited in tissues, causing complement activation and inflammation. • Clinical Manifestations: Systemic lupus erythematosus (SLE), glomerulonephritis. 4. Type IV (Delayed-Type Hypersensitivity): • Mechanism: Sensitized T cells release cytokines upon antigen re-exposure, attracting macrophages and causing tissue damage. • Clinical Manifestations: Contact dermatitis, tuberculosis skin test reaction. Clinical Changes and Symptoms: • Type I: • Anaphylaxis: Rapid onset, difficulty breathing, collapse, hives, swelling. • Atopic Dermatitis: Pruritus, erythema, chronic skin infections. • Type II: • Autoimmune Hemolytic Anemia: Pale mucous membranes, jaundice, tachycardia, weakness. • Immune-Mediated Thrombocytopenia: Petechiae, ecchymoses, bleeding tendencies. • Type III: • Systemic Lupus Erythematosus: Polyarthritis, skin lesions, renal disease. • Glomerulonephritis: Proteinuria, edema, hypertension. • Type IV: • Contact Dermatitis: Red, itchy, and inflamed skin at the site of contact. • Tuberculosis Skin Test Reaction: Local swelling and induration at the test site. Diagnosis: 1. Clinical Examination: • History: Detailed history of clinical signs, potential allergens, and previous reactions. • Physical Examination: Identifying characteristic signs based on the type of hypersensitivity. 2. Laboratory Tests: • CBC and Serum Biochemistry: Assessing overall health, anemia, thrombocytopenia, renal function. • Allergy Testing: Intradermal skin tests or serum IgE testing for Type I hypersensitivity. • Coombs Test: Detects antibodies against red blood cells for Type II hypersensitivity. • Immunofluorescence: Identifies immune complexes in tissues for Type III hypersensitivity. • Patch Testing: Identifies contact allergens for Type IV hypersensitivity. 3. Imaging Studies: • Radiography and Ultrasound: Assessing organ involvement in systemic hypersensitivity reactions. Management Strategies: 1. Type I (Immediate Hypersensitivity): • Anaphylaxis: Immediate administration of epinephrine, antihistamines, and corticosteroids. Supportive care includes oxygen therapy and IV fluids. • Atopic Dermatitis: Allergen avoidance, antihistamines, corticosteroids, immunotherapy (allergen-specific desensitization), and anti-inflammatory medications. 2. Type II (Cytotoxic Hypersensitivity): • Autoimmune Hemolytic Anemia: Immunosuppressive therapy (corticosteroids, azathioprine), blood transfusions if needed. • Immune-Mediated Thrombocytopenia: Immunosuppressive therapy, platelet transfusions in severe cases. 3. Type III (Immune Complex Hypersensitivity): • Systemic Lupus Erythematosus: Immunosuppressive therapy, NSAIDs for pain and inflammation, supportive care for organ involvement. • Glomerulonephritis: Immunosuppressive therapy, management of hypertension and proteinuria, renal support. 4. Type IV (Delayed-Type Hypersensitivity): • Contact Dermatitis: Allergen avoidance, topical corticosteroids, and systemic corticosteroids for severe reactions. • Tuberculosis Skin Test Reaction: Monitoring and management based on underlying TB infection. Medications: • Antihistamines: • Diphenhydramine: 1-2 mg/kg orally or intramuscularly every 8-12 hours. • Corticosteroids: • Prednisolone: 0.5-2 mg/kg orally or intravenously once daily for immunosuppression. • Epinephrine: • Anaphylaxis: 0.01 mg/kg intramuscularly or intravenously, repeat as needed. • Immunosuppressive Drugs: • Azathioprine: 2 mg/kg orally once daily. • Cyclosporine: 5-10 mg/kg orally once daily for atopic dermatitis. • NSAIDs: • Carprofen: 2.2 mg/kg orally once daily for inflammation and pain. Prognosis: • Type I Hypersensitivity: Good with prompt treatment, but recurrent exposure to allergens can cause repeated reactions. • Type II Hypersensitivity: Variable; early and aggressive treatment improves outcomes. • Type III Hypersensitivity: Dependent on the extent of organ involvement and response to immunosuppressive therapy. • Type IV Hypersensitivity: Good with allergen avoidance and appropriate treatment.

Answer 5

Answer: 7% Saline 7% saline is a hypertonic solution. Use it for fluid resuscitation in patients with shock. Hypertonic saline solution (HSS) contains 1283 mEq/L of sodium and chloride compared to 154 mEq/L in normal saline (0.9%). The osmolality of HSS is 2567 milliosmoles/L, compared to 300 mOsm/L of plasma. HSS is effective at small doses, typically 1-4 ml/kg over 15-20 mins. This is 1-20 mL for a 10 lb cat, 23-92 mL for a 50 lb dog and 1-2 L for a 1100 lb horse. Fluid Resuscitation Plan in Animals 1. Concepts: • Fluid Resuscitation: Restoring blood volume and correcting electrolyte imbalances in animals. • Physiological/Anatomical Considerations: Fluid compartments (intravascular, interstitial, intracellular) and maintaining perfusion. 2. Steps of Resuscitation: • Assess Perfusion Parameters: Heart rate, capillary refill time, mucous membrane color. • Calculate Deficits: Estimate dehydration percentage, calculate fluid deficits. • Fluid Administration: Bolus or continuous rate infusion depending on severity. • Reassessment: Continuous monitoring of clinical parameters. 3. Determining Deficits: • Physical Examination: Skin turgor, mucous membrane moisture, body weight changes. • Laboratory Tests: Packed cell volume (PCV), total protein, serum electrolytes. 4. Selecting Solutions: • Crystalloids: • Isotonic: 0.9% saline, Lactated Ringer’s Solution (LRS) for general fluid replacement. • Hypotonic: 5% dextrose in water (D5W) for free water replacement. • Hypertonic: 7% NaCl for rapid intravascular volume expansion. • Colloids: • Synthetic: Hydroxyethyl starch (HES), Dextrans for maintaining intravascular volume. • Natural: Plasma, albumin for volume expansion and protein replacement. 5. Characteristics of Solutions: • Crystalloids: Rapidly distribute across extracellular space, short-term volume expansion. • Colloids: Stay within intravascular space longer, provide longer-term volume support. 6. Electrolytes: • Sodium (Na+): Essential for osmolality and volume status, monitor to prevent hypernatremia or hyponatremia. • Potassium (K+): Vital for cellular function, supplement cautiously to avoid hyperkalemia. 7. Types of Colloids: • Synthetic Colloids: HES, dextrans used for hypoproteinemia, shock. • Natural Colloids: Plasma, albumin for hypoproteinemia, coagulopathies. 8. Fluid Selection Criteria: • Patient Condition: Dehydration, hypovolemia, shock. • Electrolyte Imbalance: Specific deficits or excesses. 9. Determining End Points: • Clinical Signs: Normalization of heart rate, blood pressure, urine output, mucous membrane color. • Laboratory Values: Normalization of PCV, total protein, serum electrolytes. 10. Calculating Resuscitation: • Dehydration Calculation: Body weight (kg) x % dehydration = liters of deficit. • Shock Doses: Dogs: 90 ml/kg, Cats: 60 ml/kg (initial bolus of 20-30 ml/kg). • Maintenance Fluids: 40-60 ml/kg/day.

Answer 6

Answer: Horse. The horse is the only domestic species to sweat as a primary method of heat dissipation. Higher primates (i.e., monkeys, apes, and humans) also cool off by sweating. The other species do not sweat and use different methods to cool down. Pigs wallow in mud to cool by evaporation. Cats and dogs sweat a small amount through their paws, but dogs predominantly pant to cool off. Cattle and sheep do not sweat efficiently and rely on respiration to cool themselves.

Answer 7

Answer: Vitamin A deficiency This is an aural abscess, which can occur secondary to vitamin A deficiency. Captive terrestrial box turtles are most at risk, usually due to diets containing little vitamin A. Other presentations of hypovitaminosis A include froth from the nose (a sign of respiratory disease) and renal disease. For information on wild turtle conservation (and stunning photography), have a look at the Turtle Conservancy. https://www.turtleconservancy.org/news/ Bacterial Diseases of Reptiles Definitions and Causative Agents • Septicemia: Often caused by Aeromonas and Pseudomonas spp.. Common in reptiles, leading to systemic infections. • SCUD: Septicemic Cutaneous Ulcerative Disease primarily affects aquatic turtles, often caused by Citrobacter freundii. • Ulcerative Dermatitis: Also known as scale rot, common in snakes and lizards. • Abscesses: Frequently caused by traumatic injuries and can involve various bacteria. • Infectious Stomatitis: “Mouth rot” seen in snakes, lizards, and turtles. • Pneumonia: Respiratory infections, often involving mixed bacterial populations. • Mycoplasmosis: Notably affects chelonians and crocodilians. • Otitis: Ear infections, particularly common in turtles. • Cloacitis: Infection of the cloaca, often traumatic. • Spinal Osteopathy/Osteomyelitis: Chronic bacterial osteomyelitis in reptiles, especially snakes. • Mycobacteriosis: Chronic infections with mycobacterial species. • Salmonella enterica Infection: Common in reptiles, often asymptomatic carriers. Pathophysiology and Transmission • Septicemia: Bacteria enter the bloodstream, leading to widespread infection. • SCUD: Bacteria invade through the skin or shell lesions, leading to systemic spread. • Ulcerative Dermatitis: Infections often start with minor skin lesions, exacerbated by poor environmental conditions. • Abscesses: Localized infections that can spread systemically if not treated. • Infectious Stomatitis: Starts with oral lesions, can progress to systemic infection. • Pneumonia: Often linked to poor husbandry conditions, including temperature and humidity imbalances. • Mycoplasmosis: Chronic respiratory disease in reptiles, often leading to systemic infection. • Otitis: Inflammation and infection of the ear, often related to vitamin deficiencies. • Cloacitis: Infections in the cloacal area, often related to trauma or parasites. • Spinal Osteopathy: Chronic infection leading to bone deformities. • Mycobacteriosis: Chronic granulomatous disease affecting various organs. • Salmonella: Common commensal organism, zoonotic potential. Clinical Signs • Septicemia: Respiratory distress, lethargy, petechiae. • SCUD: Pitted scutes, anorexia, lethargy, liver necrosis. • Ulcerative Dermatitis: Erythema, necrosis, ulceration. • Abscesses: Nodules or swellings, often on the face or limbs. • Infectious Stomatitis: Oral petechiae, caseous material along dental arcades. • Pneumonia: Open-mouth breathing, nasal discharge, dyspnea. • Mycoplasmosis: Rhinitis, upper respiratory tract disease. • Otitis: Swelling at the tympanic membrane, caseous material. • Cloacitis: Edema, hemopurulent discharge. • Spinal Osteopathy: Progressive spinal lesions. • Mycobacteriosis: Granulomas, often with chronic wasting. • Salmonella: Often asymptomatic but can cause enteritis. Diagnosis • Septicemia: Blood culture, cytology, and histopathology. • SCUD: Culture from lesions, biopsy. • Ulcerative Dermatitis: Clinical signs, culture, and sensitivity tests. • Abscesses: Fine needle aspiration, culture. • Infectious Stomatitis: Clinical examination, culture. • Pneumonia: Radiographs, culture from respiratory secretions. • Mycoplasmosis: PCR, serology. • Otitis: Clinical examination, culture. • Cloacitis: Radiographs, culture, and sensitivity tests. • Spinal Osteopathy: Biopsy, radiographs. • Mycobacteriosis: Culture, histopathology. • Salmonella: Fecal culture. Treatment • Septicemia: Systemic antibiotics, supportive care. • SCUD: Systemic antibiotics, wound debridement, sanitation. • Ulcerative Dermatitis: Systemic and topical antibiotics, debridement. • Abscesses: Surgical excision, local treatment. • Infectious Stomatitis: Surgical debridement, systemic antibiotics. • Pneumonia: Antibiotics, supportive care, nebulization. • Mycoplasmosis: Tetracyclines, macrolides. • Otitis: Surgical drainage, antiseptic lavage. • Cloacitis: Surgical debridement, systemic antibiotics. • Spinal Osteopathy: Long-term antibiotics, supportive care. • Mycobacteriosis: Often euthanasia due to poor prognosis. • Salmonella: Management of zoonotic risk, often asymptomatic. Prevention and Management • Husbandry: Optimal environmental conditions, proper nutrition. • Sanitation: Clean and disinfect habitats regularly. • Isolation: Separate infected individuals to prevent the spread. • Biosecurity: Prevent introduction of new pathogens. • Public Health: Manage zoonotic risks, particularly with Salmonella.

Answer 8

Answer: Mycoplasma hyopneumoniae This is the smoldering low-level illness and cranioventral consolidation of Mycoplasma hyopneumoniae, also called "enzootic pneumonia." Follow this link to see lung tip atelectasis (dark, collapsed areas on tips - you can't breathe with lungs like that). M. hyopneumoniae causes mild endemic respiratory disease in pigs characterized by a dry cough and reduced weight gain. Stressors (parasites, other infections, even the weather) can result in severe pneumonia. Swine influenza A virus varies in severity, and is characterized by rapid onset in whole herd of fever, depression, anorexia, coughing, followed by almost-as-sudden recovery. Mannheimia hemolytica is more a sheep/goat/cow pneumonia (think shipping fever complex), but is often thought of in same risk category as Pasteurellae. Glaesserella (formerly Haemophilus) parasuis is the cause of Glasser's disease, seen mostly in piglets 6-8 wk old. Characterized by short course, sudden death. Clinical signs include high fever, severe coughing, abdominal breathing, swollen joints, CNS signs like lateral decubitus, paddling, trembling. In addition to respiratory illness, look for reproductive problems (abortions, stillbirths) in sows with porcine reproductive and respiratory syndrome (PRRS). https://zukureview.com/zuku-qod/navle/529?chosen=fFr%2BwWbNIceoDyfGzlks%2BoGUOau0yfY/9E8gmELOw/4%3D&utm_source=Zukureview+Subscribers&utm_campaign=308b54fb2d-EMAIL_CAMPAIGN_2022_12_01_02_50&utm_medium=email&utm_term=0_1c9568dbdc-308b54fb2d-%5BLIST_EMAIL_ID%5D Mycoplasmal Pneumonia in Pigs - Comprehensive Information for BCSE Test Definitions and Causative Agents: • Mycoplasmal Pneumonia: Chronic respiratory disease caused by Mycoplasma hyopneumoniae. • Causative Agents: Mycoplasma hyopneumoniae, often complicated by other mycoplasmas, bacteria, and viruses. Epidemiology: • Transmission: Aerosol, direct contact, from dam to piglets. • Age Susceptibility: Pigs of all ages, highest prevalence in pigs 3-5 months old. Clinical Findings: • Signs: Persistent dry cough, reduced growth rate, sporadic severe pneumonia. • Lesions: Gray or purple, consolidated lung areas, primarily in apical and cardiac lobes, histological lymphoid hyperplasia. Diagnosis: • Methods: Clinical signs, histopathology, PCR, serologic tests. • Samples: Tracheal, laryngeal, bronchial swabs, lung tissue. Treatment: • Antibiotics: Effective against Mycoplasma spp (e.g., tetracyclines, macrolides). • Supportive Care: Improved ventilation, reduced stress. Control: • Vaccination: Reduces clinical signs, does not prevent infection. • Management: All-in/all-out practices, gilt acclimation.

Answer 9

Answer: Treat newborns piglets at birth with type C antitoxin In acute outbreak of Clostridium perfringens type C, prophylactic type C antitoxin and/or antibiotic is protective if given to piglets within 2 hours of birth. The necropsy identified hemorrhagic intestines characteristic of the disease. Affects piglets up to 3 weeks old with a severe hemorrhagic necrotizing diarrhea and high mortality. Treatment of sick piglets is rarely efficacious. Best prevention in newborns is to vaccinate the pregnant dam in last third of pregnancy with the appropriate toxoid. Important to assure newborn gets sufficient colostrum. Clostridium perfringens Type C Enteritis in Pigs - Comprehensive Veterinary Information Definitions and Terminology: • Clostridium perfringens Type C Enteritis: A highly fatal necrohemorrhagic enteritis in piglets. Causative Agent: • Pathogen: Clostridium perfringens type C. Physiopathology: • Transmission: Fecal-oral route; spores ingested from contaminated environment. • Pathogenesis: Beta toxin causes necrosis of intestinal villi, leading to hemorrhage and necrosis of the mucosa. Clinical Findings: • Symptoms: Sudden onset of hemorrhagic diarrhea, collapse, and death in piglets 1-3 days old. Brownish liquid feces, pasty-gray diarrhea, progressive emaciation in subacute cases. • Lesions: Dark red, hemorrhagic intestines, necrotic membrane in chronic cases. Diagnosis: • Clinical Signs: Hemorrhagic diarrhea, sudden death. • Lab Tests: Detection of beta toxin in feces, culture, genotyping. • Postmortem Examination: Histopathology shows segmental hemorrhagic necrosis and presence of large gram-positive rods. Treatment and Control: • Treatment: Limited value after onset; prophylactic antitoxin or antimicrobials if given early. • Prevention: Vaccination of sows with type C bacterin-toxoid during gestation.

Answer 10

Answer: Chorioptic mange This is chorioptic mange - the most common mite in horses. Chorioptes equi is characterized by long legs and short pedicles. Most commonly it is found on the lower limbs (esp. the hind legs), where it causes pruritus. Chorioptes infestation is often seen as a component of pastern dermatitis, a multi-factorial disease that is very common in draft horses, especially those breeds with heavy feathering. In non-feathered breeds, it can occur elsewhere on the body. It is also called scratches, greasy heel, and dermatitis verrucosa. It is a surface mite and causes extreme pruritus. It is very contagious horse-to-horse (occasionally on fomites) so if one in a herd has it, the others probably do as well. Tx: Ideal to remove the feathers (clients rarely allow this) then use some combination of topical permethrin or coumaphos, systemic or topical ivermectin/moxidectin, selenium sulphide shampoos, or topical products w/ fpronil (usually used in small animal). Here's a great review of chorioptic mange, with images, from the University of Liverpool. https://www.liverpool.ac.uk/media/livacuk/equine/equinepractice/Chorioptic,Mites.pdf Chorioptic Mange in Horses Chorioptic mange is caused by infestation with Chorioptes bovis (formerly (equi) and is the most common form of mange in horses. Draft horses are commonly infested, although all breeds are susceptible. Lesions caused by C bovis start as a pruritic dermatitis affecting the distal limbs around the foot and fetlock. Papules are evident first, followed by alopecia, crusting, and thickening of the skin. A moist dermatitis of the fetlock develops in chronic cases. Infested horses may stamp their feet or rub one foot against the opposite leg or object. Chorioptic mange is a differential diagnosis for "greasy heel" in draft horses. Clinical signs subside in summer but recur with the return of cold weather. The disease course is usually chronic without treatment; however, the prognosis is favorable when treated. Topical and oral treatments recommended for other types of mange are effective. Hot lime sulfur is labeled for use against Chorioptes in horses. Treatment should be repeated every 12 days if needed, following the species-specific dilution on the label. Treatment is aided by clipping long hair from infested areas. Although not labeled for treatment of mange in horses, oral ivermectin at 200 mcg/kg administered for two doses 14 days apart (field studies), or a single treatment with oral moxidectin at 400 mcg/kg, has effectively treated psoroptic, chorioptic, and sarcoptic mange in horses.

Answer 11

Answer: Bovine Viral Diarrhea Virus [Bovine viral diarrhea virus (BVD).](https://www.merckvetmanual.com/nervous-system/congenital-and-inherited-anomalies-of-the-nervous-system/congenital-and-inherited-cerebellar-disorders-in-animals?redirectid=30646) In utero infection with BVD is a common cause of cerebellar hypoplasia in cattle. Other causes are bluetongue, Akabane, or Wesselsbron viruses. Caudal occipital malformation syndrome is a disorder seen mainly in Cavalier King Charles Spaniels. The malformed occipital bone causes crowding at the caudal fossa and cerebellar herniation at the foramen magnum. *Bovine Viral Diarrhea (BVD) is a significant viral disease in cattle caused by the Bovine Viral Diarrhea Virus (BVDV), a pestivirus. It has two biotypes: noncytopathic (NCP) and cytopathic (CP). BVD can lead to a wide range of symptoms from mild to severe, including diarrhea, respiratory issues, reproductive failure, immunosuppression, and mucosal disease. Persistent infection can occur if a fetus is infected before the immune system matures. Control measures include vaccination, biosecurity, and managing persistently infected animals.*

Answer 12

Answer: Buy only vaccinated chicks Buy only chicks vaccinated against Marek disease. This chicken has ocular evidence of Marek disease. There is no treatment, but the problem is preventable when chicks are vaccinated at hatching or before 2 weeks of age. Diffuse infiltration of mononuclear cells can turn the irises of affected chickens from a normal yellow color to a pale tan to gray color (a.k.a. "gray eye"). Cellular infiltration can also occur in many other tissues (skin, nerves, viscera), and there may be palpable tumors in the muscle and skin. ' Marek disease is common in commercial poultry. Dx usually based on enlarged nerves and lymphoid tumors in the viscera. Lymphoid leukosis is a key differential. Absence of bursal tumors helps distinguish Marek disease from leukosis. But if you find bursal tumors, Marek disease is still on the DDX list pending other tests, like immunochemistry. Chicks as young as 3 weeks can show Marek disease, but lymphoid leukosis is typically seen in chickens more than 14 weeks old. Marek’s Disease is a highly contagious viral disease affecting chickens, caused by an alphaherpesvirus. It primarily targets the nervous system and can cause tumors in various organs. Clinical signs include paralysis, weight loss, and immunosuppression, which predisposes birds to secondary infections. The disease is often fatal, especially in young birds. Diagnosis is typically based on clinical signs and post-mortem examination. Control measures include vaccination, which is effective in preventing disease but does not prevent infection or virus shedding.

Answer 13

Answer: C - Need orthogonal radiographic view An orthogonal view is necessary to determine the next best step because it is not possible to determine if this hip luxation is dorsal or ventral with only the VD. Conservatively treat craniodorsal coxofemoral (hip) luxations (most common) with closed reduction and an Ehmer sling. Typically presents as a non-weight-bearing lameness, usually after blunt force trauma, (e.g., being hit by a car). Occasionally ventral luxations occur and an Ehmer sling predisposes these to re-luxation, as it positions the limb in an abducted, externally rotated position. Instead, use hobbles to prevent abduction and re-luxation. In this case closed reduction is appropriate as the injury is recent (less than 24-48 hr since it occurred). Additionally, the hip anatomy is normal, with no signs of avulsion fragments, hip dysplasia, or osteoarthritis. Closed reduction is associated with a re-luxation rate of ~50%, treated with open reduction and stabilization: e.g., toggle pinning, iliofemoral suture, capsulorrhaphy, trochanteric transposition, and prosthetic joint capsule. Risk of re-luxation after closed reduction is higher with chronic injuries or dysplastic hips, and these patients are at risk of progressive arthritis. Consider salvage options such as femoral head osteotomy or total hip replacement. Ehmer slings have a high risk of bandage complications. Carefully monitor post-reduction for sling-related injuries and instruct owners on how to monitor. https://pubmed.ncbi.nlm.nih.gov/31149876/ Here is some useful information from the University of Illinois about closed reduction of hip luxations, and here is more helpful information from the American College of Veterinary Surgeons. https://vetmed.illinois.edu/2021/04/13/coxofemoral-luxation-tips-for-closed-reductions/ https://www.acvs.org/small-animal/hip-luxation/ Hip Luxation Traumatic dislocation of the hip is most frequently a craniodorsal displacement of the femoral head relative to the acetabulum. Clinical signs include lameness, pain during manipulation of the hip joint, and a shortened limb due to dorsal displacement of the femur. Radiography is useful in confirming the luxation and delineating the presence of other fractures in the femoral head or acetabulum. Treatment involves either closed manipulation and postoperative slings to maintain the reduction or open surgical stabilization using sutures or toggle pins. Femoral head and neck resection or total hip replacement can be performed after failed reductions. Prognosis for recovery is usually excellent.

Answer 14

Answer: T13, L1and L2 The spinal nerves, T13, L1, and L2 must be blocked to completely desensitize the flank of a cow. The paravertebral (PV) nerve block targets these nerves. It can be performed via two techniques â?? the proximal or distal PV block. https://www.merckvetmanual.com/management-and-nutrition/pain-assessment-and-management/local-and-regional-analgesic-techniques-in-animals?autoredirectid=20983 The proximal block places local anesthetic in the space just caudal to the transverse processes of the vertebrae - T13, L1, and L2. The distal block is placed at the ends of the transverse processes of the vertebrae â?? L1, L2, and L4 as the nerves gradually course caudally after they exit the spinal foramen. Proper placement of the anesthetic results in warming of the skin from vasodilation, anesthesia of the skin and body wall, and a curvature of the spine in some cows. The latter is caused by relaxation of the epaxial musculature on the affected side; the spine curves in a convex manner. Click here for a useful review of Local Anesthesia and Analgesia by Lyon Lee DVM, PhD. pp. 12-14. https://www.westernu.edu/mediafiles/veterinary/vet-anesthesia-analgesia/local-anesthesia-analgesia.pdf

Answer 15

Answer: **Choanal atresia** Choanal atresia is one of the most common congenital problems of South American camelids. Choanal atresia occurs when the caudal nares (choanae) fail to open during embryologic development. Can be unilateral or bilateral and may cause complete or partial blockage. [Merck](https://www.merckvetmanual.com/exotic-and-laboratory-animals/llamas-and-alpacas/diseases-of-llamas-and-alpacas)

Answer 16

Answer: Antibodies against P2-myelin protein. Antibodies against P2-myelin protein. The top differential for this horse with cauda equina signs PLUS cranial nerve signs is polyneuritis equi. Horses with this condition can have circulating antibodies against P2-myelin protein, but many false positives. Other diseases to rule out in this case would be equine herpesvirus-1 and equine protozoal encephalomyelitis. Unfortunately there is no definitive Tx and prognosis is poor for functional recovery. Polyneuritis Equi Neuritis of the cauda equina (polyneuritis equi) is characterized by inflammation of the sacrocaudal nerves and occasionally other nerves. It is seen in adult horses of all breeds in Europe and North America. The cause is unknown, although an immunologic reaction incited by a viral infection is possible. Affected horses have circulating antibodies against P2 myelin protein. The most consistent clinical signs reflect involvement of the sacrocaudal nerves and include urinary and fecal incontinence, tail paralysis, perineal paresthesia or analgesia, atrophy of the gluteal muscles, mild pelvic limb ataxia, and, in male horses, penile paralysis. Affected horses may rub the tail. The thoracic limbs and cranial nerves may also be affected. Diagnosis can usually be based on clinical findings. CSF may be xanthochromic, with increased protein content and mononuclear pleocytosis. Sacral fracture should be excluded by rectal examination and radiography. There is no treatment, and the prognosis for recovery is poor. Histopathologically, there is granulomatous inflammation primarily affecting the extradural portions of the sacrocaudal nerves. https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-horses/equine-herpesvirus-infection https://www.merckvetmanual.com/horse-owners/brain,-spinal-cord,-and-nerve-disorders-of-horses/equine-protozoal-myeloencephalitis

Answer 17

Answer: Supportive therapy Supportive care is the first and best treatment for severe coliform mastitis (i.e., E.coli, Klebsiella, Enterobacter spp.). Lipopolysaccharide (LPS) endotoxins released from the bacteria trigger immune-related sepsis. Treat with IV fluids and oral calcium. NSAIDs administered early in the course of disease can decrease the severity of clinical signs and improve treatment outcomes. The subsequent use of antimicrobial therapy in severe coliform mastitis cases is controversial, but about half of endotoxic cases will also be bacteremic. Some studies suggest improved patient outcomes with IV oxytetracycline or IM cephalosporins. Both are extra-label drug use and require Food and Drug Avoidance Residue Databank (FARAD) approved drug withdrawal times in the US. Pirlimycin is a lincosamide that targets gram-positive Staph spp. and Strep spp. and would not be indicated in this case. Prevent new cases of environmental mastitis pathogens with antiseptic teat dip before each milking, good bedding management, and fly control. Vaccinate dry cows with bacterin toxoid to aid in prevention of coliform mastitis and endotoxemia. Expect 1-2 cases of clinical mastitis per 100 cows/month on well managed herds. Coliform Mastitis in Cattle: Comprehensive Veterinary Guide Definition: Coliform mastitis is a form of mastitis in dairy cattle caused by gram-negative, lactose-fermenting bacteria, primarily Escherichia coli, Klebsiella spp., and Enterobacter spp. Pathophysiology: • Invasion: Bacteria enter through the teat canal, proliferate in the mammary gland, and release endotoxins. • Immune Response: Endotoxins trigger an acute inflammatory response, characterized by neutrophil influx and cytokine release. • Systemic Effects: Severe cases can lead to systemic toxemia, including fever, shock, and even death. Causes: • Environmental Factors: Contaminated bedding, water, and equipment; poor milking hygiene; and trauma to the teats. • Specific Pathogens: E. coli and Klebsiella are common environmental pathogens associated with coliform mastitis. Symptoms: • Local: Swollen, firm udder, with watery, bloody, or pus-laden milk. • Systemic: Fever, anorexia, dehydration, and in severe cases, shock. Clinical Changes: • Milk Changes: Reduced milk yield, abnormal milk appearance (watery or containing clots). • Udder Changes: Swelling, heat, and pain in the affected quarter(s). Assessment: • Clinical Signs: Observation of milk and udder condition, systemic symptoms. • Laboratory Tests: Somatic cell count (SCC) in milk, bacterial culture to identify the causative agent. Treatment: • Antibiotics: Systemic and intramammary antibiotics, ideally chosen based on sensitivity testing. • Cephalosporins: Commonly used due to efficacy against gram-negative bacteria. • Aminoglycosides and Fluoroquinolones: Used for severe cases but require careful monitoring for residues in milk. • Supportive Care: Fluid therapy to manage dehydration and shock, anti-inflammatory drugs to reduce fever and pain. Prevention: • Hygiene: Proper milking procedures, clean and dry bedding, regular equipment maintenance. • Teat Care: Use of post-milking teat dips to reduce bacterial colonization. • Vaccination: Some vaccines are available for prevention against E. coli and Klebsiella spp. Prognosis: • Severity: Varies based on the extent of infection and timeliness of treatment. • Outcomes: Potential for chronic infections, reduced milk production, and, in severe cases, death or culling. Epidemiology: • Incidence: Higher in herds with poor environmental management; outbreaks can occur in warmer climates or with improper bedding materials. • Zoonotic Risk: Although rare, some coliform bacteria can be zoonotic, posing a risk to humans. Key Points: • Early Detection: Critical for effective treatment; regular monitoring of SCC and milk quality is essential. • Veterinary Involvement: Regular herd health assessments and consultations for mastitis management and antibiotic stewardship.

Answer 18

Answer: **Multilobular osteochondrosarcoma, osteosarcoma, chondrosarcoma** The top differential diagnoses of this skull tumor are osteosarcoma (OSA), chondrosarcoma (CSA), and multilobular osteochondrosarcoma (MLO). [Skull Tumors](https://vsso.org/skull-tumors) [OSA](https://vsso.org/bone-axial-osa#general_considerations) [Bone CSA](https://vsso.org/bone-csa) [Bone MLO](https://vsso.org/bone-mlo) OSA is the most common primary bone tumor of dogs and skull OSA accounts for < 3% of all OSA. Axial OSA carries a more favorable prognosis than appendicular OSA, and Tx consists of radiation and chemotherapy. [Merck Osteopathies](https://www.merckvetmanual.com/musculoskeletal-system/osteopathies-in-small-animals/osteomyelitis-in-dogs-and-cats) [Merck Masticatory Myositis](https://www.merckvetmanual.com/musculoskeletal-system/myopathies-in-small-animals/masticatory-myositis-in-dogs-and-cats) Chondrosarcoma is a malignant, cartilage-producing tumor, and the second-most common primary bone tumor. Unlike OSA, CSA is more common in the axial skeleton than appendicular skeleton. Surgery is the Tx of choice for CSA, with radiation therapy recommended for unresectable tumors. MLO presents as a firm, fixed mass arising from the periosteum. Clinical signs are referable to location. Tx is surgical with unknown effects of chemotherapy and radiation. Osteomyelitis is infection and inflammation of bone. Masticatory myositis is immune-mediated inflammation of the muscles of mastication. Hypertrophic osteodystrophy is a developmental disorder of the metaphysis of long bones of young, growing dogs. Craniomandibular osteopathy is a proliferative bone disorder of growing terrier dogs that affects the mandible and tympanic bullae. Multiple cartilaginous exocytosis affects young dogs and cats: see multiple ossified protuberances arising from the surfaces of long bones. Hemangiosarcoma is a tumor arising from endothelial cells. Meningioma is a benign, space-occupying tumor arising from the dura of the brain or spinal cord. Squamous cell carcinoma is a skin tumor that can result in firm, nodular, +/- erosive mass lesions. Rhabdomyosarcoma is a malignant primary muscle tumor. Hypertrophic osteopathy is a paraneoplastic proliferation of long bones secondary to intrathoracic or intraabdominal tumors. [Zuku Question](https://zukureview.com/zuku-qod/navle/1842?chosen=LTO%2B3G5b006tyuXbvHfv6qpJDK%2BxzqnHE/QJZklazLvQzTfHyOpaSo/%2B3JL1ldoF2FIzgMvubO8NTjBG29T1eA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=d2456ebbe6-EMAIL_CAMPAIGN_2024_06_20_01_54&utm_medium=email&utm_term=0_1c9568dbdc-d2456ebbe6-%5BLIST_EMAIL_ID%5D)

Answer 19

Answer: Amblyoma spp ticks. Amblyomma spp. are vectors for Ehrlichia ruminatium (formerly Cowdria ruminatium), the causative agent of heartwater disease in ruminants. The clinical progression of this case and the pericardial effusion seen on necropsy (as identified by the blue arrow) are classical for acute heartwater disease. Animals may just be found dead with peracute disease. Definitive diagnosis typically requires necropsy with microscopic evaluation of stained brain tissue. This disease is endemic in parts of Africa and the Caribbean but is considered a foreign animal disease in the mainland Americas. Dermacentor spp. are vectors for Babesia caballi in horses, Anaplasma marginale in cattle, Rickettsia rickettsii (Rocky Mountain spotted fever), Powassan virus, as well as the agents of Q fever and tularemia, among other infectious diseases throughout the world. Face flies (Musca autumnalis) are an important vector for eyeworm (Thelazia spp.) and Mycoplasma bovis, one agent of infectious bovine keratoconjunctivitis of ruminants. Horseflies (Tabanid spp.) can be vectors for bovine leukosis virus, the cause of enzootic bovine leukosis and lymphosarcoma. https://zukureview.com/zuku-qod/navle/1836?chosen=0Ztdg77cp3gaVcyt47SqX1vdoRLmclo74iC42jx4KRY%3D&utm_source=Zukureview+Subscribers&utm_campaign=72802b1fd8-EMAIL_CAMPAIGN_2024_06_18_01_55&utm_medium=email&utm_term=0_1c9568dbdc-72802b1fd8-%5BLIST_EMAIL_ID%5D

Answer 20

Answer: Left cranial lung lobe has alveolar infiltrates. This dog has pneumonia of the left cranial lung lobe. There are diffuse alveolar infiltrates within the left cranial lung lobe with air bronchograms. You should cancel the anesthetized procedure and wake up the patient because she is oxygenating poorly. Recheck radiographs are recommended once she is awake to rule out any component of atelectasis due to recumbency and sedation. There is an incidental gastric foreign body (rounded metal opacity within the stomach that is in close association with additional irregular metal opacity). The dog does have spondylosis deformans, which is a very common and incidental radiographic finding in older dogs. https://www.merckvetmanual.com/nervous-system/diseases-of-the-spinal-column-and-cord/degenerative-diseases-of-the-spinal-column-and-cord-in-animals?autoredirectid=16745 Although these changes are present, they are not the most clinically important findings on these radiographs. Click here to see normal canine thoracic radiographs. Radiographic interpretation and images courtesy, Dr A. Zwingenberger and Veterinary Radiology. Normal radiograph links courtesy, Imaging Anatomy, Univ. of Illinois Vet Med. Pneumonia in Dogs and Cats Concepts Pneumonia is an inflammation of the pulmonary parenchyma (small airways, interstitium, and alveoli) caused by various infectious agents, including bacteria, viruses, fungi, and protozoa, or by aspiration of foreign materials. Etiology • Bacterial: Common pathogens include Streptococcus, Staphylococcus, E. coli, and Bordetella bronchiseptica. • Viral: Canine distemper virus, adenovirus types 1 and 2, parainfluenza virus, and feline calicivirus. • Fungal: Cryptococcus, Aspergillus, and Blastomyces. • Parasitic: Filaroides, Aelurostrongylus, and Paragonimus spp. • Protozoal: Toxoplasma gondii and Pneumocystis jiroveci. • Aspiration: Gastric contents, medications, or food. Symptoms • General: Lethargy, anorexia, cough (dry or productive), fever, leukocytosis, respiratory distress, hypoxia. • Auscultation: Crackles or dull areas indicating lung consolidation. • Species Differences: • Dogs: More prone to mycotic granulomatous pneumonia and tuberculous pneumonia. • Cats: Cryptococcal pneumonia is more common. Pathogenesis • Inflammatory Response: Infiltration of inflammatory cells, cytokine release, increased mucus production, and consolidation of lung tissue. • Aspiration Pneumonia: Secondary bacterial infection following inhalation of foreign material, leading to severe inflammatory response. Diagnostic Methods • History and Clinical Findings: Recent anesthesia, severe vomiting, or persistent cough. • Thoracic Radiography: Interstitial and/or alveolar changes, increased lung density. • Cytologic Examination: Neutrophilia, presence of bacteria. • Bacterial Culture and Sensitivity: To guide antibiotic therapy. • Bronchoalveolar Lavage: For cytology and culture. Treatment • Supportive Care: Oxygen therapy (40%-60%), pulmonary physiotherapy, bronchodilators. • Antimicrobial Therapy: Empirical broad-spectrum antibiotics, adjusted based on culture results. • Monitoring: Frequent reexaminations, repeat chest radiographs every 2 weeks to monitor progress. Pathological Findings • Bacterial Pneumonia: Neutrophilic infiltration, bacterial colonies. • Viral Pneumonia: Interstitial infiltrates, viral inclusions. • Fungal Pneumonia: Granulomatous inflammation, fungal hyphae or yeast. • Parasitic Pneumonia: Eosinophilic infiltration, larvae or adult parasites. • Protozoal Pneumonia: Infiltration by protozoa, associated with immune suppression.

Answer 21

Answer: Vitamin A deficiency This is an aural abscess, which can occur secondary to vitamin A deficiency. Captive terrestrial box turtles are most at risk, usually due to diets containing little vitamin A. Other presentations of hypovitaminosis A include froth from the nose (a sign of respiratory disease) and renal disease. For information on wild turtle conservation (and stunning photography), have a look at the Turtle Conservancy. [Merck](https://www.merckvetmanual.com/exotic-and-laboratory-animals/reptiles/bacterial-diseases-of-reptiles) [Merck](https://www.merckvetmanual.com/exotic-and-laboratory-animals/reptiles/management-and-husbandry-of-reptiles?redirectid=31134) [Link](https://www.turtleconservancy.org/news/)

Answer 22

Answer: **Bronchoscopy.** Bronchoscopy is the next best step. The radiographs show an alveolar pulmonary pattern; tracheal narrowing and intraluminal opacity that may indicate edema, mucus, or foreign material; and a dilated pharynx and aerophagia that support an upper airway obstruction. In more detail: there is an alveolar pulmonary pattern in the left cranial and right middle lung lobes, consistent with aspiration pneumonia, and patchy increased opacity in the remaining lobes (seen best on the left), most consistent w/ non-cardiogenic pulmonary edema. The trachea is narrowed at the thoracic inlet, with an apparent linear intraluminal opacity. There is dilation of the pharynx with air, and gas within the esophagus and gastrointestinal tract - a common finding in patients w/ respiratory distress from upper airway obstruction. The dog received a diagnosis of bronchopneumonia, and a seven-inch tracheal foreign body. Click here to see normal canine thoracic radiographs. Radiographic interpretation and images courtesy, Dr A. Zwingenberger and Veterinary Radiology. Normal radiograph links courtesy, Imaging Anatomy Univ. of Illinois Vet Med. [Merck](https://www.merckvetmanual.com/respiratory-system/aspiration-pneumonia-in-large-animals/aspiration-pneumonia-in-large-animals) [Thorax](https://vetmed.illinois.edu/imaging_anatomy/canine/thorax/ex02/thorax02.html) [Radiology](http://mirc.veterinaryradiology.net/storage/ss1/docs/9999.120659355827952154282177226211514216670/MIRCdocument.xml)

Answer 23

Answer: Ultrasonography Use ultrasonography to identify testicular torsion in dogs with acute onset testicular swelling and pain. Other Ddx: scrotal hernia and epididymitis (usually bilateral). Doppler ultrasonography of a torsed testicle will show reduced or absent perfusion, testicular enlargement, decreased parenchymal echogenicity, and enlargement of the epididymis and spermatic cord. Clinical signs with testicular torsion are very suggestive. The contralateral testis is normal in size and shape, which differs from testicular tumors that often alter secretion of sex hormones, causing atrophy of the unaffected testicle. Additionally, dogs with testicular torsion are in severe pain; often the patient needs very deep sedation for palpation and ultrasonography. Give appropriate doses of opioids and/or ketamine early if suspect testicular torsion. Tx with castration to remove the affected testicle. This post-op image shows a hemorrhagic and infarcted right testicle (compared to normal left, consistent with torsion. https://www.merckvetmanual.com/reproductive-system/reproductive-diseases-of-the-male-small-animal/orchitis-and-epididymitis-in-dogs-and-cats https://zukureview.com/zuku-qod/navle/1821?chosen=Ir2r4R%2BtdyJJoCr7Hb1Ygw%3D%3D

Answer 24

Answer: **Pour-on moxidectin** These are the larvae of [Hypoderma bovis](https://www.merckvetmanual.com/integumentary-system/cattle-grubs/hypoderma-spp) or H. lineatum (the common and northern cattle grub, respectively) and pour-on moxidectin or eprinomectin are approved for use in both lactating dairy and beef cattle. Other products are approved for non-lactating and beef cattle. Withdrawal times must be followed. Organophosphates are not approved for this use in cattle in the United States. While the grubs can be manually expulsed/squeezed out, care must be taken to prevent rupture of the grubs. Crushed larvae release antigens leading to a systemic anaphylactic reaction in cattle. These pests are less common now since macrocyclic lactones gained widespread use in the last few decades. The adult flies (gad flies or heel flies) lay eggs on the lower limbs of cattle over the summer. The larvae penetrate the skin and migrate to their respective preferred locations. By early winter, the larvae arrive in the subcutaneous tissues of the back and make breathing pores. This cyst/warble stages lasts four to eight weeks, culminating in 3rd-stage larvae dropping to the ground and completing the life cycle. Clinical presentation of the larval infections range from localized tissue trauma around the warbles/cysts to periostitis, osteomyelitis, and neurological dysfunction. Death of 1st-stage larvae in the esophagus or spinal canal can lead to location-specific clinical signs. Cattle bothered by adult flies in summer show gadding behavior stamping and running with tails in the air. Dx: Identify 3rd stage larvae. **Key Information on Hypoderma spp. (Cattle Grubs)** Etiology and Life Cycle: • Causative Agents: Hypoderma bovis and Hypoderma lineatum. • Hosts: Cattle, occasionally horses, sheep, goats, and humans. • Lifecycle Stages: Egg deposition on hair, larval penetration, migration to resting sites (esophagus for H. lineatum, spinal canal for H. bovis), subcutaneous warbles on back. Clinical Findings and Pathogenesis: • Signs: Warbles, reduced productivity, carcass trimming, hide depreciation, gadding behavior. • Complications: Dysphagia, bloat, paralysis if larvae die in resting sites. Diagnosis: • Methods: Clinical examination for warbles, serologic testing for antibodies. Treatment and Control: • Medications: Macrocyclic lactones (e.g., ivermectin). • Management: Treat at the end of fly season, avoid mechanical removal of larvae.

Answer 25

Answer: High ringbone This is an example of high ringbone (i.e., degenerative joint disease [DJD] of the proximal interphalangeal joint). Very common in horses. Can be due to chronic wear and tear, overuse, or secondary to a traumatic episode. See a radiograph of arthrodesis of the proximal interphalangeal joint to resolve DJD. Osselets are traumatic arthritides of the metacarpophalangeal joints. Pedal osteitis is demineralization of the solar margin of the distal phalanx, usually due to inflammation. Bone spavin is osteoarthritis of the distal intertarsal, tarsometarsal, and less commonly, the proximal intertarsal joints. Osteoarthritis of the Proximal Interphalangeal Joint in Horses Definitions: • Osteoarthritis (OA): Degenerative joint disease affecting the proximal interphalangeal (pastern) joint, commonly referred to as “high ringbone.” Causative Agents: • Primary Causes: Trauma, wear and tear, overuse. • Secondary Causes: Infection, developmental orthopedic disease. Physiopathology: • Cartilage Degeneration: Loss of cartilage, new bone formation around the joint. • Chronic Changes: Subchondral bone sclerosis, joint space narrowing. Symptoms: • Subtle lameness progressing to more noticeable lameness as disease advances. Clinical Changes: • Radiographic Findings: New bone formation, subchondral lysis, joint space loss. Assessment: • Diagnostic Analgesia: Localizes lameness. • Flexion Tests: May reveal pain. Treatment: • Medical: Anti-inflammatories (NSAIDs, corticosteroids), intra-articular injections (e.g., ethanol). • Surgical: Arthrodesis using plates and screws for severe cases. Medications: • NSAIDs: Reduce inflammation and pain. • Corticosteroids: Potent anti-inflammatory effects. • Biologic Therapies: Platelet-rich plasma, stem-cell therapy. [Zuku](https://zukureview.com/zuku-qod/navle/1777?chosen=gU3O87sa%2Buyqgo7azsEKAw%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=f9eddcc10e-EMAIL_CAMPAIGN_2024_05_24_01_50&utm_medium=email&utm_term=0_1c9568dbdc-f9eddcc10e-%5BLIST_EMAIL_ID%5D)

Answer 26

Answer: Antigen - antibody complex Type III In type Ill reactions such as purpura hemorrhagica, antigen-antibody complexes are deposited on the endothelium, stimulating complement and a neutrophilic inflammatory response and vascular damage. The petechiae and distal limb edema in this horse are consistent with vasculitis. Classic type III diseases include: Glomerulonephritis Hypersensitivity pneumonitis (think moldy hay) Purpura hemorrhagica (think post-strangles infection, but possible with other infections as well) Anterior uveitis https://zukureview.com/zuku-qod/navle/1776?chosen=2WC76OIttc0kQZcE0uORIhb1thKz4G47KGSX%2BemM0vArrJLRwspYIto6oaP1OtC8&utm_source=Zukureview+Subscribers&utm_campaign=94fba8eb06-EMAIL_CAMPAIGN_2024_05_23_01_50&utm_medium=email&utm_term=0_1c9568dbdc-94fba8eb06-%5BLIST_EMAIL_ID%5D

Answer 27

Answer: Avian tuberculosis. This is classic avian tuberculosis (usually caused by Mycobacterium avium subsp. avium), which can affect all types of birds. It is a chronic, granulomatous bacterial infection that is slow to spread and is characterized by gradual weight loss. M. avium is prevalent worldwide and is spread by infective feces. It is ZOONOTIC in immune-compromised people. Dx: difficult. Positive wattle or skin tuberculin test confirms exposure but negative does not rule out disease. Suspicion can be based on seeing lots of acid-fast bacteria on smears from lesions. Rx: none. Prevent by careful purchasing and/or quarantine (at least 6 months!) of new birds. Improved sanitation and rapid flock turnover in commercial flocks has mostly eliminated this infection from these groups. Candidiasis is an intestinal mycotic disease typically characterized by thickened mucosa and white, raised pseudomembranes lesions in the crop and esophagus. Colibacillosis (Escherichia coli) is common in chickens and can cause subacute pericarditis, airsacculitis, salpingitis, peritonitis, and acute fatal septicemia. It can occasionally cause granulomas in the liver and spleen (but not the intestine, bone marrow like in this chicken). Lameness would also be less common in the history for colibacillosis. Infectous coryza is a respiratory disease of chickens that acutely causes nasal discharge, sneezing, and facial swelling. Ulcerative enteritis (Clostridium colinum) causes depression, anorexia, and diarrhea. https://zukureview.com/zuku-qod/navle/1775?chosen=PAlciwsYYapQcMDF/4yizGuaAFFmbpAogokKFm9EIn4%3D&utm_source=Zukureview+Subscribers&utm_campaign=1e46ba7409-EMAIL_CAMPAIGN_2024_05_22_01_50&utm_medium=email&utm_term=0_1c9568dbdc-1e46ba7409-%5BLIST_EMAIL_ID%5D

Answer 28

Answer: **Fever, petechiations, hemolytic anemia** Fever, petechiations, hemolytic anemia. This cytology shows *Babesia caballi*, one of the causative agents of **equine piroplasmosis** (the other is Theileria equi - looks like a maltese cross under the microscope) and acute disease is characterized by fever, petechiations, and signs consistent with hemolytic anemia. Piroplasmosis is characterized by hemolytic anemia and is spread primarily by ixodid ticks or blood contamination. It is endemic in tropical, subtropical, and some temperate regions. It is REPORTABLE in the USA. Clinical infection can be acute, chronic, or inapparent, depending on strain, the horse's health, and geographic region. Acute clinical signs include those described here along with lethargy, anorexia, pale or icteric mucous membranes, and with worsening disease - tachycardia, tachypnea, weakness, and hemoglobinuria. Weight loss, poor performance, and partial anorexia can be seen along with mild anemia in horses with chronic piroplasmosis. Dx: Demonstrate intra-erythrocytic organisms on blood smear and/or serology. Rx: Imidocarb dipropionate and supportive care. There is a different duration of Tx depending on whether in endemic or nonendemic region (because trying to treat clinical signs in endemic region vs. clear disease in nonendemic region). Limb edema, ventricular arrhythmias, and ataxia (the latter two uncommonly) can be seen with Anaplasma phagocytophila infections in horses, along with fever, petechiations, icterus, and depression. [Zuku](https://zukureview.com/zuku-qod/navle/1761?chosen=9XS83s9tyJMi%2BCsyDIqqJzjVjqCaNOTKRr/0H1RLMBBhEI1dcPaNOZz2u%2B4y5I4X&utm_source=Zukureview+Subscribers&utm_campaign=c0ab8357b6-EMAIL_CAMPAIGN_2024_05_16_01_51&utm_medium=email&utm_term=0_1c9568dbdc-c0ab8357b6-%5BLIST_EMAIL_ID%5D)

Answer 29

Answer: **Lavender Foal Syndrome** This presentation is consistent with lavender foal syndrome (LFS), an inherited lethal neurologic disorder that affects Arabian foals with a dilute coat color. LFS is a recessive genetic disorder and newborn foals present as in this case. Affected foals are typically euthanized within days of birth. There is no treatment. A genetic test is available and affected animals should not be bred. Botulism in foals less than ~1 month old (i.e., shaker foal syndrome) is characterized by progressive symmetric motor paralysis with muscular tremors. Affected foals cannot stand for more than a few minutes at a time. Overo lethal white syndrome is characterized by colic and meconium impaction due to ileocolonic agangliosis. It occurs in Paint foals with blue eyes that are the result breeding two Overos (a type of coat pattern in Paint horses). Myasthenia gravis is not reported in horses. Neurologic signs seen with hyperammonemia associated with portosystemic vascular anomalies (PSVAs, also referred to as portosystemic shunts) are not seen until affected foals are 2-3 months old and eating more grain and forage.

Answer 30

Answer: **Coagulopathy** Coagulopathies are common in association with crotalid (e.g., rattlesnake) envenomation. Additional concerns include thrombocytopenia, neurotoxicity, and cardiovascular toxicity. Temporary tracheostomy should be performed immediately in a horse in severe respiratory distress due to upper airway obstruction. The physical examination and further supportive care can be delayed until after an airway is obtained. Additional diagnostics include CBC/blood smear/serum biochemistry/coagulation profile. See hypofbrinogenemia, thrombocytopenia, prolonged prothrombin time, and increased FDPs. Might see echinocytes in heparin or citrate samples, and severity of echinocytosis is associated with severity of envenomation. Rx: IV fluids for hypotension, NSAIDs for analgesia, steroids are controversial (1 dose early may be beneficial), tetanus prophylaxis, antimicrobial prophylaxis, antivenin if owner can afford it/it is available, and occasional blood transfusion. If you look closely at the picture of this horse, you can see he is receiving a blood transfusion. **Snakebites in Animals** Overview Snakebites in animals can result in a variety of clinical signs and outcomes depending on the species of snake, the amount of venom injected, and the location of the bite. Prompt recognition and appropriate treatment are crucial for improving the prognosis. Types of Venomous Snakes 1. Pit Vipers (Crotalinae): • Examples: Rattlesnakes, copperheads, cottonmouths (water moccasins). • Venom: Hemotoxic, causing tissue destruction, coagulopathy, and systemic effects. 2. Elapids: • Examples: Coral snakes, cobras, kraits. • Venom: Neurotoxic, causing paralysis and respiratory failure. Pathophysiology • Venom Composition: Contains enzymes, proteins, and peptides causing local and systemic effects. • Hemotoxic Venom: • Local Effects: Pain, swelling, hemorrhage, tissue necrosis. • Systemic Effects: Coagulopathy, hypotension, shock. • Neurotoxic Venom: • Local Effects: Minimal, often no significant swelling or pain. • Systemic Effects: Neuromuscular blockade, respiratory paralysis, cardiovascular collapse. Clinical Changes and Symptoms 1. Local Signs: • Pain and Swelling: Rapid onset, progressing over several hours. • Ecchymosis and Hemorrhage: Bruising and bleeding at the bite site. • Necrosis: Tissue death, potentially leading to severe infection. 2. Systemic Signs: • Weakness and Collapse: Often early signs in severe envenomation. • Hypotension and Shock: Decreased blood pressure, tachycardia. • Coagulopathy: Prolonged bleeding, petechiae, hematuria. • Respiratory Distress: Particularly in neurotoxic envenomation. • Neurologic Signs: Paralysis, ataxia, altered mental status. Diagnosis 1. Clinical Examination: • History: Details of the bite incident, snake identification if possible. • Physical Examination: Assessing the bite site, systemic signs, and vital parameters. 2. Laboratory Tests: • CBC: Leukocytosis, thrombocytopenia. • Coagulation Profile: Prolonged clotting times, decreased fibrinogen. • Serum Biochemistry: Elevated creatine kinase, renal function tests for myoglobinuria. • Urinalysis: Hematuria, myoglobinuria. 3. Imaging: • Radiography/Ultrasound: Assessing for tissue damage and complications such as compartment syndrome. Management Strategies 1. Immediate Care: • Immobilization: Keep the animal calm and immobilize the affected limb to slow venom spread. • Avoid Tourniquets and Incisions: These can cause more harm than benefit. 2. Supportive Care: • Intravenous Fluids: To maintain blood pressure and hydration. • Pain Management: Opioids (e.g., morphine), avoiding NSAIDs due to potential coagulopathy. • Antihistamines: To manage allergic reactions if needed. 3. Antivenom Therapy: • Indications: Moderate to severe envenomation with systemic signs. • Types: Species-specific or polyvalent antivenoms. • Administration: Intravenous infusion, monitoring for allergic reactions. 4. Additional Therapies: • Antibiotics: For secondary bacterial infections, particularly in necrotic wounds. • Corticosteroids: Use is controversial; may be considered in severe cases with significant inflammation. • Tetanus Prophylaxis: Recommended for animals with unknown vaccination status. 5. Monitoring and Aftercare: • Frequent Monitoring: Vital signs, coagulation status, renal function. • Wound Care: Cleaning, debridement, and dressing changes for necrotic tissue. • Rehabilitation: Physical therapy for long-term recovery if needed. Prognosis • Variable: Depends on the species of snake, the amount of venom injected, the location of the bite, and the timeliness of treatment. • Early and Appropriate Treatment: Significantly improves outcomes, reducing mortality and long-term complications. Summary for Veterinary Professionals • Snakebites can cause severe local and systemic effects, with pit vipers and elapids being the primary venomous snakes of concern. • Clinical signs vary with the type of venom and include pain, swelling, coagulopathy, respiratory distress, and neurologic deficits. • Diagnosis involves clinical examination, laboratory tests, and imaging to assess the extent of envenomation and complications. • Management includes immobilization, supportive care, antivenom therapy, pain management, and wound care. • Prognosis is variable but can be improved with early and appropriate treatment.

Answer 31

Answer: **Basophil** This is a basophil, typically associated with allergy or parasite infestation. Basophils (BSO), eosinophils (EOS), and neutrophils (PMNs) are the three types of granulocytic white blood cells. [Phagocytosis](https://www.merckvetmanual.com/circulatory-system/hematopoietic-system-introduction/white-blood-cells-in-animals#Phagocytes_v3256829) is an important function of EOS and PMNs but this is not a primary role of BSOs. Granulocytic phagocytes have segmented nuclei and cytoplasmic granules - orange/pink in EOS; purple/dark blue in BSOs; pale pink in PMNs. The granules of basophils contain many mediators of inflammation and large amounts of histamine. They commonly respond to allergic conditions and parasite infestation, similar to eosinophils. For more info and images, see the Cornell Clin Path website: [Hematology Atlas](https://eclinpath.com/atlas/hematology/), and [Equine blood cells](https://eclinpath.com/atlas/hematology/equine-blood/). **White blood cells (WBCs) in animals, relevant for your NAVLE preparation:** Phagocytes: • Mononuclear Phagocytes: Arise from marrow, circulate as monocytes, and become macrophages in tissues. They play a role in antigen presentation and produce substances like interleukin-1. • Granulocytes: Include neutrophils, eosinophils, and basophils. Neutrophils are short-lived and move from blood to tissues. Eosinophils respond to histamine and are involved in parasite defense and inflammation modulation. Basophils contain histamine and other inflammation mediators. Lymphocytes: • T Lymphocytes: Differentiated into “helper” T4 cells (involved in humoral antibody production) and “cytotoxic” T8 cells (responsible for immune responses against specific antigens). These cells are crucial for cellular immunity. • B Lymphocytes: Responsible for humoral immunity through antibody production. B cells differentiate into plasma cells that produce immunoglobulins (IgA, IgM, IgG, IgE), each with specific functions (e.g., IgE in allergic reactions). • Natural Killer Cells: Destroy foreign cells like neoplastic cells without prior sensitization. Immune Responses: • Appropriate Response: Activation of the immune system during infections or vaccinations. • Inappropriate Response: Immune-mediated diseases (e.g., immune-mediated hemolytic anemia) and allergies, which involve the immune system attacking host tissues or reacting to allergens (e.g., anaphylaxis). Diseases and Conditions: • Neutropenia: Caused by marrow failure, infections, or immune-mediated destruction, leading to increased risk of bacterial infections. • Lymphocytosis: Can occur due to epinephrine release or chronic infections, while lymphopenia is often a response to glucocorticoid secretion. • Lymphoproliferative Disorders: Include lymphomas, and leukemias, often manifesting as abnormal proliferation of lymphocytes. Medications: • Glucocorticoids: Used to manage inappropriate immune responses by reducing inflammation and suppressing the immune system. Diagnostic and Treatment Approaches: • Assessment: Blood tests, bone marrow analysis, and histopathology to assess WBC counts, morphology, and function. • Treatment: Tailored to underlying causes, including immunosuppressants, antibiotics for secondary infections, and supportive care. [Veterinary Merck Manual](https://www.merckvetmanual.com/circulatory-system/hematopoietic-system-introduction/white-blood-cells-in-animals)

Answer 32

Answer: ** E - Cannot tell if either kid is truly CAE positive or negative** You cannot tell if either kid is truly CAE positive or negative yet. Should probably retest both after 90 days, or at next semiannual herd testing. A positive ELISA test for caprine arthritis encephalitis (CAE) in a kid less than 90 days old may reflect maternal antibody or a false positive. A negative test in a kid less than 90 days old does not rule out CAE (though most kids infected at birth from colostrum develop a measurable antibody response by 4-10 weeks after infection). Note lots of qualifiers about CAE testing: A positive test in an adult goat implies infection, but does not confirm that clinical signs were caused by CAE virus. Negative tests do NOT rule out CAE infection. DEFINITIVE Dx is to find characteristic lesions by biopsy/necropsy. Virus isolation can substantiate Dx, but may not be practical on herd basis. **Caprine Arthritis and Encephalitis (CAE) in Goats** Concepts CAE is a persistent viral infection caused by the Caprine Arthritis Encephalitis Virus (CAEV), a lentivirus affecting goats. It manifests in various forms, including arthritis, leukoencephalomyelitis, mastitis, and interstitial pneumonia. Etiology • Infectious Agent: CAEV, an enveloped, single-stranded RNA lentivirus in the Retroviridae family. • Transmission: Primarily through ingestion of infected colostrum or milk by kids. Horizontal transmission occurs via direct contact, fomites, and contaminated equipment. Pathogenesis • Virus Spread: Infected macrophages in colostrum and milk are absorbed, spreading the virus systemically via mononuclear cells. Periodic replication induces characteristic lymphoproliferative lesions in target tissues like the lungs, synovium, choroid plexus, and udder. • Immune Response: The infection elicits strong humoral and cell-mediated immune responses, but these are not protective. Symptoms • Polysynovitis-Arthritis: Most common in adult goats, leading to joint swelling, lameness, weight loss, and poor hair coats. • Leukoencephalomyelitis: Mainly in kids aged 2-6 months, causing weakness, ataxia, proprioceptive deficits, progressing to paralysis. • Interstitial Pneumonia: Chronic, leading to progressive dyspnea in adult goats. • Indurative Mastitis: “Hard udder” syndrome, causing firm, swollen mammary glands with low milk production. Diagnostic Methods • Clinical Signs: Based on observable symptoms. • Serologic Testing: Agar gel immunodiffusion and ELISA tests to determine herd CAEV status. • Histopathology: Definitive diagnosis through characteristic lesions in biopsy or post-mortem samples. • Differential Diagnoses: Includes infectious arthritis (Mycoplasma spp.), traumatic arthritis, enzootic ataxia, spinal cord abscesses, cerebrospinal nematodiasis, polioencephalomalacia, listeriosis, and rabies. Treatment and Control • No Vaccine or Specific Treatment: Supportive care includes regular foot trimming, additional bedding, NSAIDs for arthritis, and good nursing care for encephalomyelitis. • Management Practices: Isolation of kids at birth, feeding heat-treated colostrum and pasteurized milk, semi-annual serologic testing, segregation, and culling of seropositive goats. • Supportive Care: High-quality, readily digestible feed, antibiotics for secondary infections. https://www.merckvetmanual.com/generalized-conditions/caprine-arthritis-and-encephalitis/caprine-arthritis-and-encephalitis

Answer 33

Answer: **Inability to close the mouth** Idiopathic trigeminal neuritis, due to inflammation of cranial nerve 5 (CN 5), is characterized by acute onset of flaccid jaw paralysis. Affected animals cannot close their mouth and have difficulty eating and drinking. Seen occasionally in dogs, rare in cats. Idiopathic facial nerve paralysis, affecting cranial nerve 7 (CN 7), results in the inability to move the eyelid, lip, or ear and dryness of the eyes and mouth. Masticatory myositis is characterized by pain on opening the mouth and swelling of the muscles of mastication (acute) or atrophy of the temporalis and masseter muscles with the inability to open the mouth due to fibrosis (chronic). Dysphagia, dsyphonia, and stridor are most often associated with dysfunction of the vagus nerve, cranial nerve 10 (CN 10). Circling and head tilt toward the side of the lesion with no other signs is a common presentation of vestibulocochlear nerve, cranial nerve 8 (CN 8) lesions. Concurrent CN 7 paralysis and Horner syndrome (ptosis, miosis, enophthalmos) may be present with middle- and inner-ear infections. *Acquired Myasthenia Gravis:* • Etiology: Autoimmune destruction of acetylcholine receptors at the neuromuscular junction. • Clinical Forms: Generalized (exercise-induced weakness), focal (facial, pharyngeal weakness), fulminant (acute paralysis). • Diagnosis: Edrophonium chloride test, serum antibody detection. • Treatment: Pyridostigmine (1-3 mg/kg, PO, 2-3 times/day), immunosuppressive therapy, management of complications like megaesophagus. Acute Idiopathic Polyradiculoneuritis: • Etiology: Immune-mediated, often triggered by raccoon bites or vaccination. • Clinical Signs: Flaccid tetraparesis, respiratory paralysis, normal pain perception. • Diagnosis: CSF analysis, electromyography. • Treatment: Supportive care, recovery within 2-6 months. Chronic Inflammatory Demyelinating Polyneuropathy: • Etiology: Unknown, immune-mediated suspected. • Clinical Signs: Tetraparesis, cranial nerve dysfunction. • Diagnosis: Nerve biopsy, slowed conduction on electromyography. • Treatment: Corticosteroids, with potential relapses.

Answer 34

Answer: **Edema disease** Edema disease is caused by shiga toxin-producing E. coli (STEC). Look for severe acute illness ranging from peracute death with no signs to CNS involvement with ataxia, paralysis, and recumbency in healthiest pigs one to two weeks after weaning. Streptococcus suis could cause sudden death but would not cause diarrhea and would see polyserositis on necropsy. Clostridium perfringens type C enteritis, also called enterotoxemia in other animals, is characterized by a HEMORRHAGIC diarrhea in one-to three-day-old piglets. Porcine proliferative enteritis is principally a diarrheal disease of growing finishing (40- to 80-lb) pigs and young breeding pigs. Epidemic transmissible gastroenteritis (TGE) in non-immune pig herds characterized by HIGH MORBIDITY and HIGH MORTALITY in piglets less than one week old. ** Edema Disease in Pigs - Comprehensive Study Guide** Definition: • Edema Disease: Peracute vasculitis causing facial swelling, enteritis, and sometimes focal encephalomalacia in post-weaning pigs. Causative Agent: • Escherichia coli (E. coli): Specifically hemolytic strains producing F18 fimbriae and Shiga toxin 2e (Stx2e). Pathophysiology: • Transmission: Fecal-oral route from contaminated environments or infected pigs. • Infection Mechanism: Colonization of the intestine followed by toxin production. Toxin binds to specific receptors on vascular endothelium, leading to cell death and vascular damage. Clinical Signs: • Peracute Death: Often with no prior signs. • CNS Signs: Ataxia, paralysis, recumbency. • Visible Edema: Especially in the face, eyelids, and larynx. • Other Signs: Anorexia, dyspnea, submandibular swelling. Lesions: • Gross Lesions: Subcutaneous edema, stomach submucosa edema, mesocolon edema. • Microscopic Lesions: Degenerative angiopathy, necrosis of arterial smooth muscle cells, focal encephalomalacia in the brainstem. Diagnosis: • Clinical Signs: Characteristic facial edema and sudden death. • Necropsy: Edema in characteristic sites. • Laboratory Confirmation: Isolation and PCR identification of Stx2e and F18-positive E. coli. Treatment and Control: • Treatment: Often ineffective for affected pigs due to rapid disease progression. Oral antimicrobials for unaffected pigs in infected herds based on sensitivity testing. • Control Measures: • Feed Management: High-fiber, low-protein diets. • Vaccination: Various commercial vaccines targeting different aspects of the E. coli strain. • Passive Immunity: Systemic immunization or oral immunization with anti-F18 antibodies. **St reptococcus suis Infection in Pigs: NAVLE Study Guide** Definitions and Causative Agents: • Streptococcus suis (S. suis): A gram-positive, facultatively anaerobic coccus causing septicemia, meningitis, arthritis, and endocarditis in pigs, particularly post-weaned piglets. • Serotypes: 29 serotypes recognized, with serotype 2 being most common in Europe and Asia. Pathogenesis: • Transmission: Colonization occurs at birth from vaginal secretions and nursing. Spread via direct contact, fomites, and possibly through the intestinal route. • Virulence Factors: Capsular polysaccharide, muramidase-released protein, extracellular factor, and hemolysin (suilysin). Clinical Findings: • Acute Signs: Fever, septicemia, meningitis (opisthotonos, convulsions, paddling), arthritis, endocarditis, and sudden death. • Lesions: Neutrophilic meningitis, polyserositis, fibrinopurulent exudates, endocarditis, and splenomegaly. Diagnosis: • Methods: Based on clinical signs, bacterial culture, serotyping, PCR assays, and histopathology. • Differential Diagnoses: Include polyserositis, meningitis from other pathogens, endocarditis, septicemia, and polyarthritis from other bacteria. Treatment and Prevention: • Antibiotics: Beta-lactams (penicillin, ampicillin, amoxicillin). Resistance may vary. • Anti-inflammatories: To reduce tissue inflammation. • Vaccination: Autogenous vaccines with varying effectiveness. • Management: Early detection, environmental control (overcrowding, ventilation), and prompt treatment. Zoonotic Risk: • Human Infection: Can cause septicemia, meningitis, endocarditis, and arthritis. Transmission through contact with infected pigs or consumption of raw pork products. Higher risk in Southeast Asia. [Zuku question](https://zukureview.com/zuku-qod/navle/1963?chosen=MNS4vGCLeUF0Fos0r4TrHXpAgmG221Bs%2BLmK7gsUi9UxWK%2Bb/qHdMuk793PQQTDn&utm_source=Zukureview+Subscribers&utm_campaign=dce840d132-EMAIL_CAMPAIGN_2024_08_15_01_52&utm_medium=email&utm_term=0_1c9568dbdc-dce840d132-%5BLIST_EMAIL_ID%5D)

Answer 35

Answer: **Palmar digital** The palmar digital nerve block (also called a PD or heel block) would anesthetize at least the palmar third of the foot, including the navicular bone. [Diagnostic Anesthesia for Lameness Localization in Horses](https://www.merckvetmanual.com/musculoskeletal-system/diagnostic-anesthesia-for-lameness-localization-in-horses/diagnostic-anesthesia-for-lameness-localization-in-horses?mredirectid=3462) Historically, the PD block was considered to anesthetize the palmar/plantar 1/3 of the foot and sole. However, it has been shown that it desensitizes 70-80% of the foot in most horses. All of the other nerve blocks can desensitize the navicular bone too, but would not be as specific as a palmar digital nerve block because they also desensitize a larger region. The abaxial sesamoidean nerve block (ASNB, also called a pastern or foot block) would anesthetize the entire foot and much of the pastern. Sometimes an ASNB is needed to completely eliminate or diagnose navicular lameness, but it is less specific than the PD block. A low four-point nerve block (also called low palmar or volar block) would desensitize the fetlock and areas distal to it. The median and ulnar nerve block would anesthetize the carpus and areas distal to it. The tibial and peroneal nerve block would anesthetize the tarsus and areas distal to it. **Regional Anesthesia in Equine Lameness** Palmar (or Plantar) Digital Nerve Block: • Usage: Localizes lameness in the heel or sole. • Pathology: Navicular disease, heel pain. • Localization: Medial and lateral palmar digital nerves at the pastern level. • Medication: Mepivacaine HCl (2%). • Dose: 1-2 mL per site. • Technique: Injection proximal to the collateral cartilage. • Advantages: High specificity. • Complications: Rare, but include infection or nerve damage. Abaxial Sesamoid Nerve Block: • Usage: Localizes lameness in the pastern or foot. • Pathology: Pastern osteoarthritis, ringbone. • Localization: Abaxial to the proximal sesamoid bones. • Medication: Mepivacaine HCl (2%). • Dose: 1-2 mL per site. • Technique: Injection at the base of the proximal sesamoid bones. • Advantages: Effective for pastern lameness. • Complications: Infection, inadvertent tendon sheath puncture. Low Palmar (or Plantar) Nerve Block (Low Four-Point Block): • Usage: Localizes lameness in the fetlock or below. • Pathology: Fetlock arthritis, flexor tendon injuries. • Localization: Medial and lateral palmar nerves and palmar metacarpal nerves. • Medication: Mepivacaine HCl (2%). • Dose: 2-3 mL per site. • Technique: Injection at the level of the distal ends of the splint bones. • Advantages: Broad area of desensitization. • Complications: Rare, but include hematoma. High Palmar (or Plantar) Nerve Block (High Four-Point Block): • Usage: Localizes lameness in the metacarpal or metatarsal region. • Pathology: Suspensory ligament injuries. • Localization: Medial and lateral palmar nerves and palmar metacarpal nerves. • Medication: Mepivacaine HCl (2%). • Dose: 3-5 mL per site. • Technique: Injection just below the carpus or hock. • Advantages: Effective for high suspensory issues. • Complications: Hematoma, inadvertent nerve damage. Median and Ulnar Nerve Block: • Usage: Localizes lameness in the carpal region or below. • Pathology: Carpal arthritis, severe tendon injuries. • Localization: Median nerve (medial aspect of the radius), ulnar nerve (distal to the accessory carpal bone). • Medication: Mepivacaine HCl (2%). • Dose: 10-15 mL per site. • Technique: Separate injections for median and ulnar nerves. • Advantages: Provides complete desensitization of the lower limb. • Complications: Risk of hitting blood vessels, hematoma. Deep Branch of the Lateral Plantar Nerve Block: • Usage: Localizes lameness in the proximal suspensory ligament. • Pathology: Proximal suspensory desmitis. • Localization: Deep branch of the lateral plantar nerve at the level of the hock. • Medication: Mepivacaine HCl (2%). • Dose: 5-10 mL. • Technique: Injection near the origin of the suspensory ligament. • Advantages: Specific for suspensory ligament issues. • Complications: Difficult to perform, risk of damaging surrounding structures. Tibial and Peroneal Nerve Block: • Usage: Localizes lameness in the tarsal region or below. • Pathology: Tarsal arthritis, severe lower limb injuries. • Localization: Tibial nerve (medial aspect of the hock), peroneal nerve (lateral aspect of the hock). • Medication: Mepivacaine HCl (2%). • Dose: 10-15 mL per site. • Technique: Separate injections for tibial and peroneal nerves. • Advantages: Provides extensive desensitization. • Complications: Hematoma, inadvertent vascular puncture. Intra-Articular Blocks: • Usage: Directly desensitize specific joints. • Pathology: Joint arthritis, synovitis. • Localization: Specific joints (e.g., carpal, fetlock, hock). • Medication: Mepivacaine HCl (2%), sometimes combined with steroids. • Dose: Varies by joint size. • Technique: Sterile injection directly into the joint capsule. • Advantages: Highly specific. • Complications: Infection, joint flare. Epidural Anesthesia: • Usage: Provides hindlimb analgesia. • Pathology: Severe hindlimb pain, dystocia. • Localization: Epidural space, typically at the first coccygeal interspace. • Medication: Mepivacaine HCl (2%), sometimes combined with opioids. • Dose: 10-20 mL. • Technique: Injection into the epidural space. • Advantages: Effective for hindlimb analgesia. • Complications: Infection, ataxia, urinary retention. [Zuku](https://zukureview.com/zuku-qod/navle/1962?chosen=kV2JYGNMqa9Ox8TRt1AFOdVAmy8Je4pmL7CKypvRHHM%3D&utm_source=Zukureview+Subscribers&utm_campaign=4125963086-EMAIL_CAMPAIGN_2024_08_14_01_52&utm_medium=email&utm_term=0_1c9568dbdc-4125963086-%5BLIST_EMAIL_ID%5D)

Answer 36

Answer: **Hypothyroidism** Tail alopecia and tragic facial expression are a classic signs of hypothyroidism in dogs. Other areas of bilateral alopecia that are common in hypothyroidism are the ventral and lateral trunk, caudal thighs, ventral neck and dorsum of the nose. Hyperadrenocorticism commonly has truncal alopecia and also presents with obesity. It is more common in toy dog breeds. ** Comprehensive NAVLE Preparation: Hypothyroidism in Dogs** Definitions & Etiology: • Hypothyroidism: A common endocrine disorder in dogs, primarily due to the destruction of the thyroid gland (primary hypothyroidism) via autoimmune lymphocytic thyroiditis or idiopathic atrophy. Secondary and tertiary hypothyroidism, caused by pituitary or hypothalamic dysfunction, are rare. • Primary Hypothyroidism: Accounts for most cases and is often linked to immune-mediated processes or idiopathic thyroid atrophy. Autoantibodies to thyroglobulin (TgAA) are markers of autoimmune thyroiditis. Pathophysiology: • Destruction of thyroid tissue leads to decreased production of thyroid hormones (T4 and T3). This causes a reduction in metabolic rate, affecting various body systems, including the cardiovascular, nervous, reproductive, and dermatologic systems. Signalment: • Most commonly affects middle-aged dogs (average age ~7 years), with certain breeds, like Golden Retrievers, Doberman Pinschers, and Beagles, showing increased susceptibility. Gender predisposition is minimal, and congenital hypothyroidism is rare. Clinical Signs: • General Signs: Weight gain, lethargy, exercise intolerance, and cold intolerance. These signs are often subtle and gradual in onset. • Dermatologic Signs: Alopecia (often bilaterally symmetrical), seborrhea, hyperpigmentation, pyoderma, and myxedema (leading to a “tragic” facial expression). • Neurological Signs: Peripheral neuropathy (generalized weakness, ataxia, proprioceptive deficits) and, less commonly, central nervous system involvement (nystagmus, paresis). • Cardiovascular Signs: Bradycardia, weak pulses, decreased myocardial contractility, and rare cases of reversible congestive heart failure. • Reproductive Signs: Infertility in females, prolonged parturition, and poor neonatal outcomes. Males are less affected. Diagnostic Tests: • Laboratory Findings: Common findings include hypercholesterolemia, hypertriglyceridemia, mild nonregenerative anemia, and occasionally elevated creatine kinase. • Thyroid Function Tests: • Total T4: Often the initial test; decreased in >90% of hypothyroid dogs. Not reliable in dogs with nonthyroidal illness or on certain medications. • Free T4 (fT4): More accurate than total T4, especially using equilibrium dialysis, less affected by nonthyroidal illness or medications. • TSH (Thyroid-Stimulating Hormone): Elevated in 65-75% of cases. Combining TSH with T4 or fT4 improves diagnostic accuracy. • Thyroid Autoantibodies: TgAA indicates autoimmune thyroiditis and is useful when thyroid function tests are equivocal. Differential Diagnoses: • Conditions that mimic hypothyroidism include hyperadrenocorticism, alopecia X, metabolic and neurologic disorders, primary cardiac disease, and other endocrine disorders. Treatment: • Levothyroxine: The treatment of choice, administered at 0.02 mg/kg once daily. Dosage adjustments are based on therapeutic monitoring of clinical response and serum T4 levels. Dogs with concurrent diseases (e.g., diabetes, renal failure) may require lower starting doses. • Therapeutic Monitoring: Clinical improvement is the primary measure, with follow-up thyroid function tests (T4 levels) performed after 6-8 weeks of treatment. Prognosis: • Excellent for Most Dogs: With proper treatment, most dogs show complete recovery. Dogs with congenital hypothyroidism may have long-term complications like mental retardation or skeletal abnormalities. The prognosis is guarded for dogs with myxedema coma. https://zukureview.com/zuku-qod/navle/1951?chosen=j9rMj3DK0cdgoRQ8lU2ryg%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=4ec80037ca-EMAIL_CAMPAIGN_2024_08_13_01_52&utm_medium=email&utm_term=0_1c9568dbdc-4ec80037ca-%5BLIST_EMAIL_ID%5D

Answer 37

Answer: **Stomach** The stomach is markedly enlarged and filled with fluid and gas. There is mineral opacity material with a sharp edge in the body and pylorus. There are small mineral opacities (gravel sign) in the dependent portion of the stomach. The enlarged stomach is causing a mass effect and displacing the other organs caudally, however peritoneal detail is good. The radiographs show evidence of pyloric outflow obstruction such as a mass, stricture, polyp, or granuloma. [Link](https://vetmed.illinois.edu/imaging_anatomy/canine/ab/ex03/ab03.html) [Zuku](https://zukureview.com/zuku-qod/navle/1950?chosen=egOLPEU36gVtqFMf04Kf6A%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=bf327a26fb-EMAIL_CAMPAIGN_2024_08_12_01_52&utm_medium=email&utm_term=0_1c9568dbdc-bf327a26fb-%5BLIST_EMAIL_ID%5D)

Answer 38

Answer: **Did you use chlorine or other chemicals near the tank/ equipment or do a recent water change with tap water?** Ask: Did you use chlorine or other chemicals near the tank/equipment or do a recent water change with tap water? Chlorine is commonly used to disinfect tanks and equipment but is highly toxic to fish. This is a common problem because both chlorine and chloramine (type of chlorine stabilized by amination) are frequently found in municipal water sources. Chronic and subacute chlorine exposure result in signs as described here: cloudy eyes, inflammation and necrosis of the gills, excess mucus covering gills, and lethargy. Acute chlorine toxicosis can cause sudden death. There is a colorimetric test readily available from pool supply stores that measures chlorine (free and total); levels should be nondetectable when tested on site. If the sample of water needs to be transported for testing, use a sealed glass bottle with no air space (it may dissipate); false negatives are possible. Need to measure both free and total to get the most accurate results. Tx with dechlorination products (often containing sodium thiosulfate) available at pet stores and then recheck free and total chlorine levels. Increase aeration because of gill compromise. Addition of 1-3 ppt salt may also help with osmoregulatory issues. Check out this article on "Emergency Care of A Tancho Koi (Cyprinus carpio) Suffering From Acute Chlorine Toxicity" by Bakal et al. from North Carolina State University. https://www.merckvetmanual.com/exotic-and-laboratory-animals/aquatic-systems/environmental-diseases-of-aquatic-animals-in-aquatic-systems?autoredirectid=21586 https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11114&catId=29070&id=3981363

Answer 39

Answer: **Papillomatosis** These are warts, or papillomas, which is related to infection with equine papilloma virus. Equine papillomatosis occurs most frequently in young horses and are most commonly found on the inner surfaces of the pinna, muzzle, distal limbs, and genitalia. They are contagious, and since they usually resolve spontaneously, treatment is rarely pursued. These differ from equine aural plaques, which are papillomas of the inner ear associated with fly bites that do not typically self-resolve. https://www.merckvetmanual.com/integumentary-system/tumors-of-the-skin-and-soft-tissues/epidermal-and-hair-follicle-tumors-in-animals https://zukureview.com/zuku-qod/navle/1750?chosen=umoM3v1aLC9sEzeqnYPe0w%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=9057429c8c-EMAIL_CAMPAIGN_2024_05_13_01_51&utm_medium=email&utm_term=0_1c9568dbdc-9057429c8c-%5BLIST_EMAIL_ID%5D

Answer 40

Answer: **A - Treat affected cows with 2 classes of dewormer** The correct action is to treat affected cattle with 2 classes of dewormer. An abomasum with a cobblestone or "Moroccan leather" appearance in the fall in the southern U.S. is pathognomonic for Type I| ostertagiasis caused by Ostertagia ostertagi. This finding in a herd with routine deworming suggests anthelmintic resistance. Current recommendations are to deworm with two different classes of dewormer concurrently combined with a refugia program. By deworming only the affected animals (targeted treatment), the other animals serve as a source of refugia. [Merck Manual](https://www.merckvetmanual.com/digestive-system/gastrointestinal-parasites-of-ruminants/overview-of-gastrointestinal-parasites-of-ruminants) [Link](https://www.fda.gov/media/85805/download) **Ostertagia ostertagii**, commonly known as the brown stomach worm, is a parasitic nematode that primarily infects the abomasum of cattle, leading to a condition known as ostertagiosis. This parasite is of significant economic importance in the cattle industry due to its impact on animal health and productivity. Also Known As: • Brown stomach worm Affected Species: • Primarily cattle (Bos taurus and Bos indicus) • Occasionally reported in sheep, goats, wild ruminants, and horses Type of Agent: • Nematode (roundworm) Classification of the Agent: • Phylum: Nematoda • Class: Secernentea • Order: Strongylida • Family: Trichostrongylidae • Genus: Ostertagia • Species: Ostertagia ostertagi Clinical History: • Ostertagiosis is prevalent in cattle populations worldwide, especially in temperate climates. Infections are commonly observed in young cattle during their first grazing season, with clinical disease typically occurring in late summer and autumn. Older cattle may develop immunity over successive grazing seasons. Transmission of the Disease: • Direct Transmission: • Ingestion of infective third-stage larvae (L3) from contaminated pasture during grazing. • Environmental Factors: • Larval development and survival are influenced by temperature and humidity, with optimal conditions promoting higher infection rates. Affected Age or Stage: • Primarily affects young cattle during their first grazing season. • Older cattle may harbor infections but often develop partial immunity, reducing clinical manifestations. Clinical Presentation: • Type I Ostertagiosis (Summer Ostertagiosis): • Occurs in calves during their first grazing season, typically in late summer and autumn. • Clinical signs include: • Profuse watery diarrhea • Weight loss • Reduced appetite (inappetence) • Submandibular edema (“bottle jaw”) in severe cases • Type II Ostertagiosis (Winter Ostertagiosis): • Occurs in yearlings and older cattle due to the synchronous emergence of hypobiotic larvae from the gastric glands, typically in late winter or early spring. • Clinical signs are similar to Type I but may be more severe: • Intermittent diarrhea • Weight loss • Anorexia • Submandibular edema • Possible mortality if untreated Changes in Clinical Pathology Tests: • Elevated plasma pepsinogen levels due to abomasal mucosal damage. • Hypoalbuminemia resulting from protein loss into the abomasum. • Mild anemia may be observed in severe cases. Differentials: • Coccidiosis • Salmonellosis • Bovine viral diarrhea (BVD) • Johne’s disease • Nutritional diarrhea Diagnostic Tests to Confirm: • Fecal Egg Counts (FEC): • Detection of nematode eggs in feces; however, egg counts may not correlate directly with worm burden due to prepatent infections or hypobiotic larvae. • Plasma Pepsinogen Assay: • Elevated levels indicate abomasal damage consistent with ostertagiosis. • Post-mortem Examination: • Visualization of characteristic “morocco leather” appearance of the abomasal mucosa with nodular lesions. Possible Treatments (Medications, Routes, and Doses): • Anthelmintic Therapy: • Benzimidazoles (e.g., fenbendazole): 5 mg/kg orally. • Macrocyclic lactones (e.g., ivermectin): 0.2 mg/kg subcutaneously or orally. • Imidazothiazoles (e.g., levamisole): 7.5 mg/kg orally or subcutaneously. • Supportive Care: • Ensure adequate nutrition and hydration. • Manage secondary bacterial infections if present. Zoonotic Risk: • Ostertagia ostertagi is not zoonotic; there is no risk of transmission to humans. Reportability: • Ostertagiosis is not a reportable disease; however, it has significant economic implications for the cattle industry. Control Measures: • Pasture Management: • Implement rotational grazing to reduce larval contamination. • Avoid overstocking pastures to minimize

Answer 41

Answer: **D - Chronic external blood loss** Chronic external blood loss (i.e., gastrointestinal hemorrhage) is the most common cause of iron-deficiency anemia. Dietary iron or copper deficiency or excessive zinc may also cause iron deficiency anemia. Look for microcytic, hypochromic anemia which may be regenerative or non-regenerative. Also look for evidence of red blood cell (RBC) fragmentation - i.e., acanthocytes, schistocytes, and keratocytes. The heme group of hemoglobin contains iron and therefore deficiency causes decreased hemoglobin production. The most common cause of iron deficiency anemia is chronic external blood loss (e.g., chronic gastrointestinal bleeding). [Vet Merck Manual](https://www.merckvetmanual.com/circulatory-system/anemia/nonregenerative-anemias-in-animals?mredirectid=2750) [Causes of Anemia](https://eclinpath.com/hematology/anemia/causes-of-anemia/)

Answer 42

Answer: **Lavender Foal Syndrome ** This presentation is consistent with lavender foal syndrome (LFS), an inherited lethal neurologic disorder that affects Arabian foals with a dilute coat color. LFS is a recessive genetic disorder and newborn foals present as in this case. Affected foals are typically euthanized within days of birth. There is no treatment. A genetic test is available and affected animals should not be bred. Botulism in foals less than ~1 month old (i.e., â? ?shaker foal syndromeâ??) is characterized by progressive symmetric motor paralysis with muscular tremors. Affected foals cannot stand for more than a few minutes at a time. Overo lethal white syndrome is characterized by colic and meconium impaction due to ileocolonic agangliosis. It occurs in Paint foals with blue eyes that are the result breeding two Overos (a type of coat pattern in Paint horses). Myasthenia gravis is not reported in horses. Neurologic signs seen with hyperammonemia associated with portosystemic vascular anomalies (PSVAs, also referred to as portosystemic shunts) are not seen until affected foals are 2â??3 months old and eating more grain and forage. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855325/?tool=pubmed **Botulism in Animals - Detailed Veterinary Summary** Etiology and Pathogenesis • Causative Agent: Clostridium botulinum types A-G • Transmission: Ingestion of toxin in decaying carcasses or spoiled plant material; sometimes via wounds • Affected Species: Horses, cattle, birds, and others; variable susceptibility among species Clinical Findings • Symptoms: Flaccid paralysis, progressive motor paralysis, disturbed vision, difficulty chewing/swallowing, paresis, respiratory failure • Lesions: No characteristic gross/histologic lesions; general paralytic action on muscles Diagnosis • Tests: • Mouse Inoculation Test: Traditional but not always reliable • ELISA: Detects toxin in samples • Clinical Signs: Suggestive but not confirmatory • Differential Diagnosis: Rule out other motor paralysis causes Treatment and Control • Supportive Care: Hydration, electrolyte correction, respiratory support • Medications: • Botulinum Antitoxin: Varies by type and species, e.g., 30,000 IU type B for foals • Prevention: High-quality feed, remove decaying materials, vaccination (types C and D toxoid) Key Points • Botulism often results from toxin ingestion rather than infection • Diagnosis is challenging; primarily via clinical signs and ruling out other conditions • Effective treatment includes antitoxin administration and supportive care • Prevention focuses on feed quality and environmental management https://www.merckvetmanual.com/generalized-conditions/clostridial-diseases/botulism-in-animals?mredirectid=916 https://www.merckvetmanual.com/digestive-system/congenital-and-inherited-anomalies-involving-the-digestive-system/congenital-and-inherited-anomalies-of-the-small-and-large-intestines-in-animals?autoredirectid=20437 https://www.merckvetmanual.com/digestive-system/hepatic-disease-in-large-animals/miscellaneous-hepatic-disorders-in-large-animals

Answer 43

Answer: ** D - Old, small-breed dogs; cavalier King Charles Spaniel** This is endocardiosis (a.k.a. myxomatous degeneration) of the mitral valve and older, small breed dogs are predisposed. It is an inherited disease in the cavalier King Charles spaniel and dachshund. Note the nodular thickening of the valve margins which results in ineffective closure of the valve and resultant regurgitation of blood from the ventricle into the atrium. Degenerative valve disease accounts for 75% of all canine cardiac disease. Approx. 60% of cases involve only the mitral valve, 30% have mitral and tricuspid lesions, and < 10% only have tricuspid involvement. Think of myxomatous mitral valve disease in older, small-breed dogs with a heart murmur. It is an inherited disease in cavalier King Charles spaniels and dachshunds. Don't confuse endocardiosis with infective endocarditis which is due to bacterial infection of the cardiac valves (typically the atrioventricular or aortic valve) and endocardial muscle. https://www.merckvetmanual.com/circulatory-system/various-heart-diseases-in-dogs-and-cats/myxomatous-atrioventricular-valve-degeneration-in-dogs-and-cats https://www.merckvetmanual.com/circulatory-system/various-heart-diseases-in-dogs-and-cats/infectious-endocarditis-in-dogs-and-cats

Answer 44

Answer: ** B - Dysphagia, dysphonia and stridor** Idiopathic trigeminal neuritis, due to inflammation of cranial nerve 5 (CN 5), is characterized by acute onset of flaccid jaw paralysis. Affected animals cannot close their mouth and have difficulty eating and drinking. Seen occasionally in dogs, rare in cats. Idiopathic facial nerve paralysis, affecting cranial nerve 7 (CN 7), results in the inability to move the eyelid, lip, or ear and dryness of the eyes and mouth. Masticatory myositis is characterized by pain on opening the mouth and swelling of the muscles of mastication (acute) or atrophy of the temporalis and masseter muscles with the inability to open the mouth due to fibrosis (chronic). Dysphagia, dsyphonia, and stridor are most often associated with dysfunction of the vagus nerve, cranial nerve 10 (CN 10). Circling and head tilt toward the side of the lesion with no other signs is a common presentation of vestibulocochlear nerve, cranial nerve 8 (CN 8) lesions. Concurrent CN 7 paralysis and Horner syndrome (ptosis, miosis, enophthalmos) may be present with middle- and inner-ear infections. ** Trigeminal Neuritis in Dogs and Cats** Idiopathic trigeminal neuropathy is common in dogs and uncommon in cats. It is characterized by acute onset of flaccid jaw paralysis. Affected animals cannot close the mouth and have difficulty eating and drinking. Horner syndrome, facial paresis, and decreased facial sensation are also possible. The cause is unknown. Histopathologically, there is bilateral nonsuppurative inflammation and demyelination in the motor branches of the trigeminal nerve. Affected animals usually recover spontaneously within 3-4 weeks. Fluid therapy and nutritional support may be necessary. https://www.merckvetmanual.com/nervous-system/diseases-of-the-peripheral-nerves-and-neuromuscular-junction/inflammatory-disorders-of-the-peripheral-nerves-and-neuromuscular-junction-in-animals#Sensory-Ganglioneuritis_v26304956 ** Facial Paralysis in Animals** 1. Definitions and Causative Agents: • Facial Paralysis: Involves paralysis of muscles of facial expression due to lesions of the facial nerve (cranial nerve VII). • Causes: Trauma, otitis media, guttural pouch infections, hypothyroidism, neoplasia, idiopathic. 2. Physiopathology: • Lesions affecting the facial nerve or its nucleus in the brainstem cause dysfunction in facial muscle movement, tear and saliva production. 3. Symptoms and Clinical Changes: • Inability to blink, drooping lips, ear droop, reduced tear production, deviation of the nose, drooling, food accumulation in the mouth. 4. Diagnosis: • Based on clinical signs, neurologic examination, otoscopic examination, thyroid testing, imaging (CT/MRI), and possibly CSF analysis for infections. 5. Treatment and Medications: • Underlying Cause: Address primary condition (e.g., antibiotics for infections, surgery for neoplasia). • Supportive Care: Artificial tears, manage corneal ulcers, corrective surgery for nostril collapse. • Medications: Antibiotics for infections (based on culture), thyroid supplements for hypothyroidism, corticosteroids for inflammation. 6. Prognosis: • Variable, depending on etiology. Early treatment increases recovery chances. Idiopathic cases may partially recover. https://www.merckvetmanual.com/nervous-system/facial-paralysis/facial-paralysis-in-animals?autoredirectid=14324 https://www.merckvetmanual.com/musculoskeletal-system/myopathies-in-small-animals/masticatory-myositis-in-dogs-and-cats

Answer 45

Answer: **B - Did you use chlorine or other chemicals near the tank/ equipment or do a recent water change with tap water?** Ask: Did you use chlorine or other chemicals near the tank/equipment or do a recent water change with tap water? Chlorine is commonly used to disinfect tanks and equipment but is highly toxic to fish. This is a common problem because both chlorine and chloramine (type of chlorine stabilized by amination) are frequently found in municipal water sources. Chronic and subacute chlorine exposure result in signs as described here: cloudy eyes, inflammation and necrosis of the gills, excess mucus covering gills, and lethargy. Acute chlorine toxicosis can cause sudden death. There is a colorimetric test readily available from pool supply stores that measures chlorine (free and total); levels should be nondetectable when tested on site. If the sample of water needs to be transported for testing, use a sealed glass bottle with no air space (it may dissipate); false negatives are possible. Need to measure both free and total to get the most accurate results. Tx with dechlorination products (often containing sodium thiosulfate) available at pet stores and then recheck free and total chlorine levels. Increase aeration because of gill compromise. Addition of 1-3 ppt salt may also help with osmoregulatory issues. Check out this article on "Emergency Care of A Tancho Koi (Cyprinus carpio) Suffering From Acute Chlorine Toxicity" by Bakal et al. from North Carolina State University. [Link](https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11114&catId=29070&id=3981363)

Answer 46

Answer: **Bovine Viral Diarrhea Virus** Bovine viral diarrhea virus (BVD). In utero infection with BVD is a common cause of cerebellar hypoplasia in cattle. Other causes are bluetongue, Akabane, or Wesselsbron viruses. Caudal occipital malformation syndrome is a disorder seen mainly in Cavalier King Charles Spaniels. The malformed occipital bone causes crowding at the caudal fossa and cerebellar herniation at the foramen magnum. **Comprehensive Information on Bovine Viral Diarrhea (BVD) for NAVLE Preparation** Definition & Etiology: • Bovine Viral Diarrhea (BVD): A disease caused by Bovine viral diarrhea virus (BVDV), a Pestivirus in the Flaviviridae family. • Transmission: Mainly through direct contact with infected animals or contaminated fomites. Vertical transmission can lead to persistently infected (PI) calves. Pathophysiology: • BVDV can cause immunosuppression, leading to secondary infections. • Cerebellar Hypoplasia: In utero infection during mid-gestation can result in cerebellar hypoplasia in calves, characterized by ataxia, tremors, and inability to stand properly. Clinical Signs: • Diarrhea, fever, nasal discharge, immunosuppression, and mucosal disease in PI animals. • Neurological signs in calves with cerebellar hypoplasia include ataxia, intention tremors, and hypermetric gait. Diagnosis: • PCR and virus isolation are used to detect BVDV. • Serology to identify antibodies in the dam or calf. Prevention: • Vaccination: Prophylactic vaccination of breeding animals is essential to prevent vertical transmission and cerebellar hypoplasia in calves. Treatment: • No specific antiviral treatment; focus on supportive care and prevention of secondary infections. https://www.merckvetmanual.com/nervous-system/congenital-and-inherited-anomalies-of-the-nervous-system/congenital-and-inherited-cerebellar-disorders-in-animals?redirectid=30646

Answer 47

Answer: **Buy only vaccinated chicks** Buy only chicks vaccinated against *Marek disease*. This chicken has ocular evidence of Marek disease. There is no treatment, but the problem is preventable when chicks are vaccinated at hatching or before 2 weeks of age. Diffuse infiltration of mononuclear cells can turn the irises of affected chickens from a normal yellow color to a pale tan to gray color (a.k.a. "gray eye"). Cellular infiltration can also occur in many other tissues (skin, nerves, viscera), and there may be palpable tumors in the muscle and skin. Marek disease is common in commercial poultry. Dx usually based on enlarged nerves and lymphoid tumors in the viscera. Lymphoid leukosis is a key differential. Absence of bursal tumors helps distinguish Marek disease from leukosis. But if you find bursal tumors, Marek disease is still on the DDX list pending other tests, like immunochemistry. Chicks as young as 3 weeks can show Marek disease, but lymphoid leukosis is typically seen in chickens more than 14 weeks old. **Comprehensive Information on Marek’s Disease for NAVLE Preparation** Definition & Etiology: • Marek’s Disease (MD): A highly contagious viral disease in chickens caused by an alphaherpesvirus known as Marek’s disease virus (MDV). It leads to the formation of tumors and affects the nervous system. Pathophysiology: • MDV infects lymphocytes, leading to the development of T-cell lymphomas. The virus causes immunosuppression and can also result in neurological damage, leading to paralysis. Clinical Signs: • Progressive paralysis, especially of the legs and wings. • Ocular form causes irregularly shaped pupils and blindness. • Cutaneous form manifests as skin nodules. Diagnosis: • Based on clinical signs, postmortem findings of enlarged nerves, and histopathology showing lymphocytic infiltration. Prevention: • Vaccination: Administered in ovo or at hatch, providing lifelong immunity. Biosecurity measures are also critical to prevent the spread of MDV. [Common Infectious Diseases](https://www.merckvetmanual.com/exotic-and-laboratory-animals/backyard-poultry/common-infectious-diseases-in-backyard-poultry) [Marek](https://www.merckvetmanual.com/poultry/neoplasms-in-poultry/marek-s-disease-in-poultry?autoredirectid=23789&autoredirectid=23789&autoredirectid=16879#Control_v3342456) [Leukosis in Poultry](https://www.merckvetmanual.com/poultry/neoplasms-in-poultry/avian-leukosis-in-poultry?autoredirectid=23791) [Zuku](https://zukureview.com/zuku-qod/navle/1984?chosen=hO3J/VsV5gKHka9efFXLsuWBtiF2Wy48rVT5xmlvUyFpZB4rAyfp8KPbuHyEbpZN4zWd27P7/%2BJ5bEl0B4w9yg%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=b3c53e896a-EMAIL_CAMPAIGN_2024_08_28_01_51&utm_medium=email&utm_term=0_1c9568dbdc-b3c53e896a-%5BLIST_EMAIL_ID%5D)

Answer 48

Answer: **Blue tongue** Swollen, sore muzzles with mucous membrane erosions, high fevers, and lameness suggests infection with *bluetongue virus*. Signs are worse in young lambs (up to 30% mortality). Remember infection of pregnant dams produces fetuses with hydrancephaly or porencephaly causing ataxic and blind lambs. Bluetongue is almost exclusively seen in sheep, though white-tailed deer, pronghorn antelope, and desert bighorn sheep in North America can be severely affected. Rare in cows. REPORTABLE. There are at least 24 serotypes of the bluetongue virus (genus Orbivirus in the family Reoviridae). Worldwide distribution mimics its vector's (Culicoides biting midges) distribution. Dx: serology (ELISA or AGID), virus isolation from blood of febrile animals, and PCR to identify the specific isolate. Treatment is supportive care. Prevention relies on controlling vectors and vaccination, the latter of which is used in endemic regions (but no cross-protection between different serotypes) or during outbreaks in non-endemic regions. Bluetongue is clinically indistinguishable from foot and mouth disease (FMD), so that is a good second choice. But FMD is unlikely in the scenario above because FMD mainly affects pigs and cattle. Ovine progressive pneumonia (OPP is a chronic disease of wasting and dyspnea in sheep and goats, caused by a lentivirus (retrovirus family). OPP is most common in animals older than four years and rarely occurs in sheep and goats under two years of age. **Bluetongue in Ruminants - Comprehensive Study Guide** Definition: • Bluetongue: A viral disease of ruminants caused by Bluetongue virus (BTV), affecting sheep, cattle, and other ruminants. Causative Agents: • Bluetongue Virus (BTV): An Orbivirus in the family Reoviridae, with at least 29 serotypes worldwide. Pathophysiology: • Transmission: Primarily by Culicoides biting midges. The virus infects endothelial cells, causing vascular damage, hemorrhage, and edema. • Lifecycle: Virus spreads through local lymph nodes, leading to viremia and systemic spread. Symptoms: • Sheep: Fever, edema of lips, tongue, face, nasal discharge, oral ulcers, lameness, and death in severe cases. • Cattle: Generally mild signs, fever, oral vesicles, and ulcers, increased respiratory rate, and stiffness. • Other Ruminants: Similar signs as in sheep and cattle, with occasional severe hemorrhagic disease. Diagnosis: • Clinical Signs: Edema, hemorrhages, and necrosis in characteristic locations. • Laboratory Tests: Virus isolation, PCR, serologic tests (AGID, competitive ELISA). Treatment: • Supportive Care: Rest, soft food, good husbandry, and treatment of secondary infections. • Control: Vaccination in endemic areas, vector control using insecticides, and management practices to reduce exposure to midges. Prevention: • Vaccination: Attenuated and inactivated vaccines available, use during non-vector seasons to avoid transmission of vaccine strains. • Vector Control: Reducing midge bites through insecticides and protective measures. [Blue Tongue](https://www.merckvetmanual.com/generalized-conditions/bluetongue/bluetongue-in-ruminants?autoredirectid=17866) [FMD](https://www.merckvetmanual.com/generalized-conditions/foot-and-mouth-disease/foot-and-mouth-disease-in-animals) [Zuku](https://zukureview.com/zuku-qod/navle/1983?chosen=9LEARvvRrESZW%2Bls3Vkge%2BbCBdMnHYlcXw2nRw6pT60%3D&utm_source=Zukureview+Subscribers&utm_campaign=e11519ea73-EMAIL_CAMPAIGN_2024_08_27_01_51&utm_medium=email&utm_term=0_1c9568dbdc-e11519ea73-%5BLIST_EMAIL_ID%5D)

Answer 49

Answer: **Bacterial infection** Bacterial infection. There are both intracellular and extracellular bacteria present in this cytology. The abscess should be drained and the animal placed on appropriate antibiotics. Mast cell tumors are round cell tumors with basophilic granules that are smaller than bacteria. [Merck Vet Manual](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/wound-management-in-small-animals/drains-in-wound-management-of-small-animals?mredirectid=821) [Merck Vet Manual](https://www.merckvetmanual.com/integumentary-system/tumors-of-the-skin-and-soft-tissues/lymphocytic-histiocytic-and-related-cutaneous-tumors-in-animals)

Answer 50

Answer: **Thoracocentesis and chest tube** This puppy has a pneumothorax and needs immediate thoracocentesis and chest tube placement. The left hemithorax appears gas distended with marked rightward mediastinal shift. A large, loculated area of subcutaneous emphysema is seen over the caudal dorsolateral thorax; however, a communication with the thoracic cavity or the external body wall cannot be identified. A triangular wedge of soft tissue opacity is seen in the mid left thorax and is consistent with collapsed left lung. A smaller, poorly demarcated area of increased soft tissue opacity is also seen superimposed over the 10th left rib adjacent to the body wall at the level of the most severe subcutaneous emphysema. There is mild pleural effusion in the right hemithorax. The right pulmonary parenchyma is difficult to evaluate, but appears to be within normal limits. The musculoskeletal structures appear within normal limits. This is severe left sided tension pneumothorax with collapse of the left lung lobes. Click here to see normal canine thoracic radiographs Radiographic interpretation and images courtesy, Dr A. Zwingenberger and Veterinary Radiology. Normal radiograph links courtesy, Imaging Anatomy Univ. of Illinois Vet Med. **Trauma in Emergency Medicine in Small Animals - Comprehensive Veterinary Information** **Definitions and Terminology:** - **Trauma:** Physical injuries caused by external forces. - **Blunt Trauma:** Associated with bleeding, organ rupture, fractures, and neurologic injuries. - **Penetrating Trauma:** Localized injuries from objects. **Causes:** - **Blunt Trauma:** Car accidents, falls. - **Penetrating Trauma:** Bites, sharp objects. **Clinical Findings:** - **Thoracic Trauma:** Pulmonary contusions, pneumothorax, rib fractures, diaphragmatic hernia. - **Abdominal Trauma:** Hemorrhage, organ rupture, herniation. - **Neurologic Injuries:** Spinal fractures, head trauma. **Physiopathology:** - **Initial Response:** Airway, breathing, circulation assessment; control hemorrhage, pain relief. - **Secondary Survey:** Evaluate nervous system, thorax, abdomen, integument, musculoskeletal systems. **Assessment:** - **Physical Examination:** Palpation for pain, fluid, hernias; auscultation for lung sounds. - **Diagnostic Imaging:** Radiographs, ultrasound, CT for internal injuries. **Treatment:** - **Fluid Resuscitation:** Isotonic crystalloids, blood products. - **Analgesia:** Pain management. - **Surgical Intervention:** Indications include ongoing hemorrhage, organ rupture. **Monitoring:** - **Vital Signs:** Temperature, pulse, respiration, blood pressure. - **Laboratory Tests:** PCV, total solids, blood gases, electrolytes, lactate. **Medications:** - **Antibiotics:** For penetrating wounds. - **Antiarrhythmics:** Lidocaine for cardiac arrhythmias. **Prognosis:** - **Severity Dependent:** Based on initial injury severity, timely intervention, and ongoing monitoring. For more detailed information, visit the [Merck Veterinary Manual](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/specific-diagnostics-and-therapy/trauma-in-emergency-medicine-in-small-animals?autoredirectid=20423). [Vet Illinois](https://vetmed.illinois.edu/imaging_anatomy/canine/thorax/ex02/thorax02.html)

Answer 51

Answer: **Thoracocentesis and chest tube** This puppy has a pneumothorax and needs immediate thoracocentesis and chest tube placement. The left hemithorax appears gas distended with marked rightward mediastinal shift. A large, loculated area of subcutaneous emphysema is seen over the caudal dorsolateral thorax; however, a communication with the thoracic cavity or the external body wall cannot be identified. A triangular wedge of soft tissue opacity is seen in the mid left thorax and is consistent with collapsed left lung. A smaller, poorly demarcated area of increased soft tissue opacity is also seen superimposed over the 10th left rib adjacent to the body wall at the level of the most severe subcutaneous emphysema. There is mild pleural effusion in the right hemithorax. The right pulmonary parenchyma is difficult to evaluate, but appears to be within normal limits. The musculoskeletal structures appear within normal limits. This is severe left sided tension pneumothorax with collapse of the left lung lobes. Click here to see normal canine thoracic radiographs Radiographic interpretation and images courtesy, Dr A. Zwingenberger and Veterinary Radiology. Normal radiograph links courtesy, Imaging Anatomy Univ. of Illinois Vet Med. **Trauma in Emergency Medicine in Small Animals - Comprehensive Veterinary Information** **Definitions and Terminology:** - **Trauma:** Physical injuries caused by external forces. - **Blunt Trauma:** Associated with bleeding, organ rupture, fractures, and neurologic injuries. - **Penetrating Trauma:** Localized injuries from objects. **Causes:** - **Blunt Trauma:** Car accidents, falls. - **Penetrating Trauma:** Bites, sharp objects. **Clinical Findings:** - **Thoracic Trauma:** Pulmonary contusions, pneumothorax, rib fractures, diaphragmatic hernia. - **Abdominal Trauma:** Hemorrhage, organ rupture, herniation. - **Neurologic Injuries:** Spinal fractures, head trauma. **Physiopathology:** - **Initial Response:** Airway, breathing, circulation assessment; control hemorrhage, pain relief. - **Secondary Survey:** Evaluate nervous system, thorax, abdomen, integument, musculoskeletal systems. **Assessment:** - **Physical Examination:** Palpation for pain, fluid, hernias; auscultation for lung sounds. - **Diagnostic Imaging:** Radiographs, ultrasound, CT for internal injuries. **Treatment:** - **Fluid Resuscitation:** Isotonic crystalloids, blood products. - **Analgesia:** Pain management. - **Surgical Intervention:** Indications include ongoing hemorrhage, organ rupture. **Monitoring:** - **Vital Signs:** Temperature, pulse, respiration, blood pressure. - **Laboratory Tests:** PCV, total solids, blood gases, electrolytes, lactate. **Medications:** - **Antibiotics:** For penetrating wounds. - **Antiarrhythmics:** Lidocaine for cardiac arrhythmias. **Prognosis:** - **Severity Dependent:** Based on initial injury severity, timely intervention, and ongoing monitoring. For more detailed information, visit the [Merck Veterinary Manual](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/specific-diagnostics-and-therapy/trauma-in-emergency-medicine-in-small-animals?autoredirectid=20423). https://vetmed.illinois.edu/imaging_anatomy/canine/thorax/ex02/thorax02.html

Answer 52

Answer: ** B - Did you use chlorine or other chemicals near the tank/ equipment or do a recent water change with tap water?** Ask: Did you use chlorine or other chemicals near the tank/equipment or do a recent water change with tap water? Chlorine is commonly used to disinfect tanks and equipment but is highly toxic to fish. This is a common problem because both chlorine and chloramine (type of chlorine stabilized by amination) are frequently found in municipal water sources. Chronic and subacute chlorine exposure result in signs as described here: cloudy eyes, inflammation and necrosis of the gills, excess mucus covering gills, and lethargy. Acute chlorine toxicosis can cause sudden death. There is a colorimetric test readily available from pool supply stores that measures chlorine (free and total); levels should be nondetectable when tested on site. If the sample of water needs to be transported for testing, use a sealed glass bottle with no air space (it may dissipate); false negatives are possible. Need to measure both free and total to get the most accurate results. Tx with dechlorination products (often containing sodium thiosulfate) available at pet stores and then recheck free and total chlorine levels. Increase aeration because of gill compromise. Addition of 1-3 ppt salt may also help with osmoregulatory issues. Check out this article on "Emergency Care of A Tancho Koi (Cyprinus carpio) Suffering From Acute Chlorine Toxicity" by Bakal et al. from North Carolina State University. https://zukureview.com/zuku-qod/navle/1949?chosen=5cewrhrCdz9kJT3k0XUM18K/llgpQxfC/Z1kpaEv%2BJy5gFTklxnnQ6%2BpLCwAfM2YNFskNWyZEvvmyGttECXtd5qtDguS/rmYiTtp2eiYHPs%3D&utm_source=Zukureview+Subscribers&utm_campaign=43bbd5ca1c-EMAIL_CAMPAIGN_2024_08_09_01_52&utm_medium=email&utm_term=0_1c9568dbdc-43bbd5ca1c-%5BLIST_EMAIL_ID%5D

Answer 53

Answer: **Low dietary copper** *Low dietary copper levels (Cu)* causes bones of growing animals to be brittle because they do not develop the normal trabecular structure. Higher fracture rates are seen in Cu deficient than in Cu replete animals. Pathologic fractures are more common during periods of exertion, such as the morning round up. Rough handling exacerbates the number of fractures. Treatment of Cu deficiency includes copper glycinate injections, and feeding of mineral mixes with Cu. Copper boluses can also be given. In areas with high levels of molybdenum (Mb) in the soil, Cu levels are often low. Mb interferes with absorption of Cu, hence Mb excess results in Cu deficiency. [Merck Nutrients Requirements](https://www.merckvetmanual.com/management-and-nutrition/nutrition-beef-cattle/nutrient-requirements-of-beef-cattle?autoredirectid=22126) [Merck](https://www.merckvetmanual.com/management-and-nutrition/nutrition-beef-cattle/nutrient-requirements-of-beef-cattle?autoredirectid=22126) [Zuku Question](https://zukureview.com/zuku-qod/navle/1948?chosen=bvwW297qRVQpH4PHNu64IUKmTXfRGirgYkxSdB%2BxUx4%3D&utm_source=Zukureview+Subscribers&utm_campaign=9eaee92738-EMAIL_CAMPAIGN_2024_08_08_01_52&utm_medium=email&utm_term=0_1c9568dbdc-9eaee92738-%5BLIST_EMAIL_ID%5D)

Answer 54

Answer: **Low dietary copper** *Low dietary copper levels (Cu)* causes bones of growing animals to be brittle because they do not develop the normal trabecular structure. Higher fracture rates are seen in Cu deficient than in Cu replete animals. Pathologic fractures are more common during periods of exertion, such as the morning round up. Rough handling exacerbates the number of fractures. Treatment of Cu deficiency includes copper glycinate injections, and feeding of mineral mixes with Cu. Copper boluses can also be given. In areas with high levels of molybdenum (Mb) in the soil, Cu levels are often low. Mb interferes with absorption of Cu, hence Mb excess results in Cu deficiency. https://www.merckvetmanual.com/management-and-nutrition/nutrition-beef-cattle/nutrient-requirements-of-beef-cattle?autoredirectid=22126 https://www.merckvetmanual.com/management-and-nutrition/nutrition-beef-cattle/nutrient-requirements-of-beef-cattle?autoredirectid=22126 https://zukureview.com/zuku-qod/navle/1948?chosen=bvwW297qRVQpH4PHNu64IUKmTXfRGirgYkxSdB%2BxUx4%3D&utm_source=Zukureview+Subscribers&utm_campaign=9eaee92738-EMAIL_CAMPAIGN_2024_08_08_01_52&utm_medium=email&utm_term=0_1c9568dbdc-9eaee92738-%5BLIST_EMAIL_ID%5D

Answer 55

Answer: **Classical swine fever** Hemorrhages on the kidneys and other organs are characteristic of both *classical swine fever* (CSF, also called "hog cholera") and African swine fever (ASF). African swine fever cannot be differentiated from classical swine fever based on clinical and postmortem signs alone. Confirmation is based on either PCR or ELISA antigen testing. Both are reportable diseases. Classical swine fever was last reported in North America in the 1970s. Click here to see more images of CSF. Erysipelas is characterized by fever, painful joints, and sometimes, urticarial diamond-shaped skin lesions. Glaesserella parasuis (formerly Haemophilus parasuis; cause of Glasser's disease) occurs mainly in young piglets. Pigs with postweaning multisystemic wasting syndrome (PMWS) typically have enlarged, pale lymph nodes, growth retardation, wasting, and dyspnea. Mycoplasma hyopneumoniae is a common cause of pneumonia in adults pigs; present with a barking cough and slow growth. Ref: Jackson and Cockcroft, Handbook of Pig Medicine, pp. 182-84 and Zimmerman et al., Diseases of Swine, 11th ed. [Zuku Question](https://zukureview.com/zuku-qod/navle/1947?chosen=%2BJeZ2rEjQ1PM4SJWhaNqQuiQGe/i2YbcgwM8J5MckNZHee9yrwsZj1FkO2D0/GQM&utm_source=Zukureview+Subscribers&utm_campaign=7bd7bc98ab-EMAIL_CAMPAIGN_2024_08_07_01_52&utm_medium=email&utm_term=0_1c9568dbdc-7bd7bc98ab-%5BLIST_EMAIL_ID%5D) **Classical Swine Fever (CSF) Comprehensive Overview** Etiology and Pathogenesis • Causative Agent: Classical swine fever virus (CSFV), an enveloped RNA virus in the genus Pestivirus, family Flaviviridae. • Pathogenesis: • Infects pigs via direct contact, contaminated feed, or fomites. • Virus replicates in tonsils and lymph nodes, spreading through the bloodstream. • Causes vasculitis leading to hemorrhages and necrosis. Epidemiology • Distribution: Endemic in Central and South America, the Caribbean, and parts of Asia. Free in Australia, New Zealand, Canada, the US, and some European countries. • Transmission: • Direct contact with infected pigs or pork products. • Wild boars and Suidae family members are reservoirs. • Can survive in pork products for extended periods, especially when frozen. Clinical Signs and Lesions • Acute Form: • Incubation: 3-7 days. • Symptoms: High fever (>41°C), hemorrhages, lethargy, diarrhea, vomiting, purple skin discoloration. • Lesions: Petechial hemorrhages, splenic infarction, “button” ulcers in the intestine. • Chronic Form: • Symptoms: Prolonged fever, weight loss, diarrhea, skin discoloration. • Lesions: Atrophy of the thymus, depletion of lymphoid follicles. • Subclinical Form: Poor reproductive performance, congenital tremors in piglets. Diagnosis • RT-PCR and RT-qPCR: Detect viral RNA in tissues, blood, serum, or oronasal fluids. • Antigen Detection: Immunofluorescence on tissue sections, ELISA for herd screening. • Serological Tests: ELISA, virus neutralization assays for detecting antibodies. • Virus Isolation: In cell cultures using tissue suspensions or fluids from suspected cases. Differential Diagnosis • Similar Diseases: African swine fever (ASF), other hemorrhagic diseases, systemic infections. Control and Prevention • No Treatment Available. • Vaccination: • Live, attenuated vaccines (LAVs) provide rapid immunity. • Oral vaccines for wild boars. • New marker vaccines allow differentiation of infected from vaccinated animals (DIVA). • Biosecurity Measures: Prohibit swill feeding, stringent farm hygiene, and control of animal movements. • Outbreak Response: Quarantine and culling of exposed herds, emergency vaccination in ring around outbreaks. Key Points for Veterinary Professionals • CSF is a highly infectious, often fatal viral disease of swine. • Early diagnosis, biosecurity, and vaccination are critical for control. • Differentiation from similar diseases is necessary for accurate diagnosis. ** African Swine Fever (ASF), comprehensive overview:** Etiology and Pathogenesis • Causative Agent: ASF virus (ASFV), a large DNA virus in the Asfarviridae family. • Pathogenesis: Infection through contact, ingestion, or tick bites. It replicates in macrophages and causes systemic infection, leading to hemorrhagic fever. Clinical Signs and Lesions • Acute Form: High fever, cyanosis, hemorrhages, vomiting, diarrhea, and sudden death. • Chronic Form: Weight loss, respiratory issues, joint swelling. Diagnosis • Laboratory Tests: PCR, ELISA, virus isolation from blood, spleen, or lymph nodes. • Necropsy Findings: Hemorrhages in organs, enlarged spleen, and lymph nodes. Treatment and Control • No treatment; focus on biosecurity, quarantine, and culling. • Prevention: Strict biosecurity measures, including movement control, cleaning, and disinfection.

Answer 56

Answer: ** E - Mannheimia haemolytica** *Mannheimia haemolytica* pneumonia typically has a cranioventral distribution - as demonstrated by the hepatized lung (dark red, liver-like) seen in the bottom half of this image. M. haemolytica and Pasteurella multocida are commensals in the upper airway of sheep. Mannheimia haemolytica of sheep and goats is a different strain (type A2) from that in cattle (type A1). Infection is more likely if there is a primary viral (e.g., parainfluenza-3) or bacterial (e.g., Mycoplasma ovipneumoniae) infection. Pneumonia with these pathogens is most common after recent stress or comingling with new animals. Prevention involves decreasing stress and exposure. There are currently no vaccines available for respiratory disease in sheep and goats and cattle vaccines have not been shown to be effective. Ovine progressive pneumonia causes chronic wasting with respiratory distress and occasional indurative mastitis. Necropsy findings include lungs with mottled gray and brown areas of consolidation and very enlarged mediastinal and tracheobronchial lymph nodes. Corynebacterium pseudotuberculosis causes caseous lymphadenitis in sheep and goats. Multifocal abscesses would be seen on necropsy. Click here to see C. pseudotuberculosis hepatic abscesses. Dictyocaulus filaria can cause bronchitis or pneumonia in sheep and infection is characterized by tachypnea and coughing. Hepatization of the lungs would be an uncommon finding at necropsy. Perilla frutescens causes acute bovine pulmonary emphysema and edema in cattle. https://zukureview.com/zuku-qod/navle/1935?chosen=qL5FVi9IipslWn/VS9F0poViWRjrmzFawdvQPBWmzHQ%3D&utm_source=Zukureview+Subscribers&utm_campaign=c9b48097ca-EMAIL_CAMPAIGN_2024_08_06_01_53&utm_medium=email&utm_term=0_1c9568dbdc-c9b48097ca-%5BLIST_EMAIL_ID%5D

Answer 57

Answer: **Bovine Tuberculosis** These are the classic granulomas and abscesses of bovine tuberculosis. Most commonly caused by Mycobacterium bovis or Mycobacterium tuberculosis in cattle. TB is reportable. Look for cows with chronic debilitation, emaciation, but without the telltale watery diarrhea of Johne's disease. It is transmitted via aerosol route. Here is an excellent image set of TB lesions in 3 animals. Actinobacillosis causes wooden tongue in cows. **Overview of Tuberculosis in Animals** Definitions and Terminology • Tuberculosis (TB): A chronic, infectious disease caused by various species of the genus Mycobacterium. • Mycobacterium bovis (M. bovis): The primary causative agent of bovine tuberculosis. • Mycobacterium tuberculosis (M. tuberculosis): Causes tuberculosis in humans but can also infect animals. • Mycobacterium avium complex (MAC): Includes species causing tuberculosis-like diseases in birds and occasionally in other animals. Causative Agents and Characteristics • Mycobacterium bovis: Acid-fast, rod-shaped bacterium, part of the Mycobacterium tuberculosis complex. • Transmission: Primarily through inhalation of aerosols from infected animals, ingestion of contaminated feed or water, or direct contact with lesions. Pathophysiology • Infection Process: • Inhalation or ingestion leads to initial infection in the lungs or alimentary tract. • Macrophages engulf bacteria, but Mycobacterium species resist destruction, leading to granuloma formation. • Granulomas, or tubercles, are composed of macrophages, lymphocytes, and fibrous tissue, often with a necrotic center. • Dissemination: Bacteria can spread through lymphatic or hematogenous routes to other organs, leading to generalized tuberculosis. Clinical Changes and Symptoms • Cattle: • Early Stages: Often asymptomatic. • Progressive Disease: Coughing, dyspnea, weight loss, decreased milk production, lymph node enlargement. • Other Species: • Similar respiratory and systemic signs; species-specific variations in symptom presentation. Diagnosis • Tuberculin Skin Test (TST): Intradermal injection of purified protein derivative (PPD) tuberculin; swelling at the injection site indicates a positive reaction. • Interferon-Gamma Release Assay (IGRA): Measures the release of interferon-gamma by T-cells in response to Mycobacterium antigens. • Culture and PCR: Definitive diagnosis through isolation and identification of Mycobacterium species from tissue samples. • Radiography and Ultrasound: Imaging to detect granulomas in the lungs or other organs. Management Strategies 1. Cattle: • Test-and-Slaughter Programs: Regular testing and culling of positive animals to control and eradicate tuberculosis. • Biosecurity Measures: Preventing introduction of infected animals, controlling wildlife reservoirs, and ensuring proper sanitation. 2. Wildlife: • Management Practices: Controlling wildlife populations, vaccination programs in some regions, and reducing interactions between wildlife and livestock. 3. Pets (Dogs and Cats): • Diagnosis and Treatment: Similar diagnostic methods; long-term antibiotic therapy (e.g., combination of isoniazid, rifampin, and pyrazinamide) may be attempted but is often impractical. Medications • Antibiotics: • Isoniazid: Inhibits mycolic acid synthesis, crucial for mycobacterial cell wall. • Rifampin: Inhibits RNA synthesis. • Pyrazinamide: Disrupts mycobacterial cell membrane metabolism. • Ethambutol: Inhibits arabinosyl transferases involved in cell wall synthesis. • Doses: Vary by species and specific case, often requiring combination therapy for extended periods (6-12 months or more). Prevention • Vaccination: Limited use in animals due to variable efficacy and interference with diagnostic tests. Bacille Calmette-Guérin (BCG) vaccine is used in some wildlife management programs. • Biosecurity Measures: Quarantine and testing of new animals, minimizing contact between livestock and wildlife, maintaining hygiene and sanitation. Summary for Veterinary Professionals • Tuberculosis is a significant zoonotic disease requiring vigilant control measures. • Diagnosis relies on skin tests, blood assays, culture, and molecular techniques. • Management includes test-and-slaughter programs, biosecurity, and, in some cases, antibiotic therapy. • Prevention focuses on vaccination in wildlife, biosecurity in livestock, and proper management practices. https://zukureview.com/zuku-qod/navle/1987?chosen=dt9WMq21kThLlgTrycVgcA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=59bc1682c4-EMAIL_CAMPAIGN_2024_09_02_01_51&utm_medium=email&utm_term=0_1c9568dbdc-59bc1682c4-%5BLIST_EMAIL_ID%5D

Answer 58

Answer: ** B - H1 histamine receptor antagonist; corticosteroids** This is a well-differentiated **mast cell tumor (MCT)**, which should be treated with an H1 histamine receptor anatagonist (a.k.a. blocker - e.g., diphenhydramine) and a corticosteroid (e.g., prednisone) prior to surgery. De before surgical excision: CBC, serum chemistry panel, urinalysis, and regional lymph node aspiration (regardless of node size). CBC changes can include eosinophilia, basophilia, and regenerative or nonregenerative anemia. If there is lymph node metastasis, tumor recurrence, or peritumoral edema/bruising also consider abdominal ultrasound +/- hepatic and splenic aspirates and bone marrow cytology. Complete excision requires at least two-cm lateral margins and one fascial plane. Mast cell tumors can occur in any age or breed. Predisposed breeds include Boston terrier, pug, Shar-pei, Staffordshire bull terrier, golden and Labrador retrievers, and Jack Russell terriers. Treat pre-surgically to shrink the tumor, minimize degranulation, and block the effects of histamine and other vasoactive mediators. Risk of histamine-induced gastric ulceration can be decreased with proton pump inhibitors (e.g., omeprazole) +/- H2 histamine blockers (e.g., famotidine). 1. Lymphoid Tumors of the Skin: Includes extramedullary plasmacytomas and cutaneous lymphosarcoma, found mainly on the head and extremities, affecting primarily middle-aged to senior dogs. Treatments involve surgical excision, radiation, and chemotherapy. 2. Cutaneous Mast Cell Tumors: Common in dogs, appearing as raised, nodular masses often on limbs, abdomen, and thorax. Diagnostic tools include fine-needle aspirates and biopsy. Treatments range from surgical excision with wide margins to chemotherapy and radiation, depending on the tumor grade. 3. Tumors with Histiocytic Differentiation: Covers diseases like histiocytoma and malignant histiocytosis, mainly affecting younger dogs. These tumors often require surgical removal, with chemotherapy used for more aggressive forms. 4. Transmissible Venereal Tumors: Contagious tumors primarily affecting the external genitalia of dogs and transmitted by contact. Treatment typically involves chemotherapy. 5. Cutaneous Lymphoma: Occurs less frequently but is notable for its two forms, epitheliotropic (involving skin cells directly) and nonepitheliotropic. Treatment options vary widely from topical therapies to systemic chemotherapy. For a more comprehensive understanding, ensure to review the detailed descriptions, symptoms, diagnostic criteria, and therapeutic approaches provided on the Merck Veterinary Manual website. This will be essential for your BCSE test preparation.

Answer 59

Answer: **E - Diazepam, lidocaine drip** Treat the ventricular tachycardia with a lidocaine drip and address hyperactivity/seizures with diazepam (Valium ®) or methocarbamol. If response to diazepam inadequate, consider barbiturates like phenobarbital (given slowly). This is a classic presentation of severe chocolate toxicity, due to toxic methylxanthine alkaloids (e.g., theobromine, theophylline, caffeine). Common around Halloween, Christmas, and Valentine's Day holidays, see excitement, seizures, and arrhythmias. This dog's ECG shows ventricular tachycardia (V-tach). Most chocolate toxicities are milder - hyperactivity, vomiting, urinating, diarrhea. Decontamination with emesis (induced with apomorphine) can be helpful up to eight hours after exposure in asymptomatic dogs. If animal is sedated because of seizures, consider gastric lavage. If vomiting is controlled, give activated charcoal (AC) only if the dog ate a lethal dose. Chocolate will increase the risk of hypernatremia from AC, so the benefit must outweigh the risk. If AC is given, monitor for hypernatremia and associated signs (tremor, ataxia, seizures). Tx arrhythmias depending on type - usually a tachycardia; give LIDOCAINE for V-tach or BETA-BLOCKERS (propranolol/esmolol) for supraventricular tachycardias. Chocolate toxicity from most toxic to least toxic: cacao beans and baking chocolate are worse than semisweet chocolate which is worse than milk chocolate. 49 grams of baking chocolate (one 2-oz bar) can kill a 7-kg dog. It would take 420 grams of milk chocolate (about eight 2-oz bars) bars to kill a 7-kg dog. [Zuku question](https://zukureview.com/zuku-qod/navle/1763?chosen=BLwcgF0L/VtuOP3VJnlEx7arFJLD6Zpt7mCgrVuDH0lbZIADKgpUVq2Twv2KGS6p&utm_source=Zukureview+Subscribers&utm_campaign=751612a1fe-EMAIL_CAMPAIGN_2024_05_20_01_51&utm_medium=email&utm_term=0_1c9568dbdc-751612a1fe-%5BLIST_EMAIL_ID%5D)

Answer 60

Answer: ** D - Sarcoptes scabei** This is Sarcoptes scabei, a highly contagious mite. A positive pinnal-pedal reflex (scratching action with the dog's hind limb when the examiner firmly rubs the edge of the dog's pinna between thumb and forefinger) is seen in 82% of dogs with sarcoptic mange but observed in only 7% of dogs with pruritus caused by other diseases. Cheyletiellosis (walking dandruff) is another highly contagious mite. Unlike Sarcoptes, they have very prominent mouthparts. Image courtesy, Dr Kalumet. https://zukureview.com/zuku-qod/navle/1759?chosen=UeXGnk5Xz9YqakYaok3orEv8lAWqVzfppkd6r2Doan4%3D&utm_source=Zukureview+Subscribers&utm_campaign=5c0ddd5c3a-EMAIL_CAMPAIGN_2024_05_14_01_51&utm_medium=email&utm_term=0_1c9568dbdc-5c0ddd5c3a-%5BLIST_EMAIL_ID%5D

Answer 61

Answer: **C - Clarithromycin and rifampin** Start this filly on clarithromycin and rifampin. In this case, a chest radiograph with consolidated nodular lung lesions and mediastinal lymphadenopathy is highly suggestive of Rhodococcus equi in a foal under five months of age. Polyarthritis, polysynovitis, and diarrhea can also be seen in affected foals Combination treatment of rifampin combined with either erythromycin, clarithromycin, or azithromycin is appropriate to treat R. equi pneumonia. However, in one retrospective study, the combination of clarithromycin and rifampin was shown to be the most effective of the three. Tilmicosin, while a macrolide, is not very active against R. equi and swelling can occur at injection sites in foals; it is not recommended for treatment of R. equi pneumonia. Click here to see an ultrasound video from Merck of a three-month-old foal with [rhodococcal pneumonia.](https://zukureview.com/zuku-qod/navle/1747?chosen=5XIg2ba95xnJGKRtSCb2n5mID4UOUaFGSi9qpaeTY9axFPrpBhXhbMPtRy3e28K4&utm_source=Zukureview+Subscribers&utm_campaign=5cd7044d13-EMAIL_CAMPAIGN_2024_05_08_01_51&utm_medium=email&utm_term=0_1c9568dbdc-5cd7044d13-%5BLIST_EMAIL_ID%5D)

Answer 62

Answer: **Camelids** Camelids (llamas, camels, alpacas) normally have ellipsoid red blood cells (RBCs, erythrocytes), which lack central pallor. Birds and reptiles have nucleated, elliptical RBCs. It is important to know what normal looks like for the main veterinary species. https://zukureview.com/zuku-qod/navle/1744?chosen=USjLsVBVjd2i7MmRvQPNWA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=5db7dbd7a6-EMAIL_CAMPAIGN_2024_05_07_01_51&utm_medium=email&utm_term=0_1c9568dbdc-5db7dbd7a6-%5BLIST_EMAIL_ID%5D

Answer 63

Answer: ** A - PVP decreases as prevalence decreases** Don't overthink this: As prevalence of a disease goes DOWN, PVP of your serologic test also goes DOWN. That is, as your disease becomes more and more rare, the predictive value of your same old test gets WORSE. That is all you need to know. Read more only if you want to see the math (but you don't need it). Let's say prevalence of pedunculated giblet disease is 30% in 1000 turtles (that's 300 infected, 700 disease-free, then). A test with 90% sensitivity would correctly Dx 270 (cell "a") with the disease (true pos) and correctly say 30 were negative (cell "c"). A test with 90% specificity would correctly Dx 630 (cell "d") as disease-free (true negs) and correctly say 70 were positive (cell "b"): PVP=a/(a+b)=270/(270+70)= 79%. Follow this link to See a PVP Diagram. Now, do the same math on 1000 turtles, but assume prevalence is now only ~1% after your vaccination program. You will see PVP goes down to ~ 1%. https://zukureview.com/zuku-qod/navle/1733?chosen=vECc2%2B8mvtDqTQSX81WWldWFRQc9vPaSbibsNibwe%2B51KzrHLEXGIHGD8T45ZyW3&utm_source=Zukureview+Subscribers&utm_campaign=40cb2d9fbc-EMAIL_CAMPAIGN_2024_05_06_01_51&utm_medium=email&utm_term=0_1c9568dbdc-40cb2d9fbc-%5BLIST_EMAIL_ID%5D

Answer 64

Answer: **C - Rare disease; early diagnosis improves prognosis** You need a very sensitive test if: 1. Disease is rare (e.g.: BSE) 2. Early Dx improves prognosis (e.g.: HIV in people) 3. The disease is highly lethal or consequences of missing a case are severe (e.g.: rabies, brucellosis, BSE, screw-worm, FMD, EIA) Remember that a HIGHLY SENSITIVE test will have very FEW false negatives. That means if a test is highly sensitive, you can TRUST a NEGATIVE TEST. This sounds contradictory, but it makes more sense if you review this sensitivity diagram. Sensitivity=a/(a+c). "a" are true positives. "c" are false negatives. If sensitivity is HIGH then "c" (FALSE negs) must be small. Therefore, high sensitivity means you can really trust a NEGATIVE result to be correct. https://zukureview.com/zuku-qod/navle/1732?chosen=Pp0VYwRosYKkjqbIcmTrJXvPwWTnxLwypeuHF6dIYeUnxxg6Roe8EzXOBdleIRD5&utm_source=Zukureview+Subscribers&utm_campaign=4c5b321d0f-EMAIL_CAMPAIGN_2024_05_03_01_51&utm_medium=email&utm_term=0_1c9568dbdc-4c5b321d0f-%5BLIST_EMAIL_ID%5D

Answer 65

Answer: **E - Septic arthritis** The duck has septic arthritis. There is diffuse soft tissue swelling of the left pelvic limb. There also appears to be intracapsular soft tissue swelling of the left tibiotarsal joint causing the joint space to widen asymmetrically. An osseous fragment is noted at the medial aspect of the joint. The articular margins of the tibiotarsus and the tarsometatarsus appear lytic and irregular. Egg-binding signs are nonspecific but lameness is not a key finding typically. Sometimes the bird will adopt a penguin-like posture. Egg-binding is more often seen during the spring and summer. [Merck Infectious Skeletal Disorders](https://www.merckvetmanual.com/poultry/disorders-of-the-skeletal-system-in-poultry/infectious-skeletal-disorders-in-poultry#v14343876) [Zuku Question](https://zukureview.com/zuku-qod/navle/2004?chosen=UVZCTJY8E3tIZbVbiOBdsA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=6589dba74f-EMAIL_CAMPAIGN_2024_09_03_01_51&utm_medium=email&utm_term=0_1c9568dbdc-6589dba74f-%5BLIST_EMAIL_ID%5D)

Answer 66

Answer: **Acinar cell atrophy** This dog has exocrine pancreatic insufficiency (EPI) due to pancreatic acinar atrophy (PAA). PAA is the most common cause of EPl in German shepherd dogs and is considered hereditary. It is also seen in rough-coated Collies and Eurasians. In cats and older dogs EPl is most commonly caused by chronic pancreatitis. Serum TLI is the best test for EPI in dogs and cats. A significantly low (<2.5 mg/L) fasting TLI is diagnostic for EPI. In EPI there is impaired synthesis and release of digestive enzymes by pancreatic acinar cells, resulting in maldigestion, weight loss/failure to gain weight, diarrhea, and polyphagia. Concurrent small intestinal dysbiosis and cobalamin deficiency are common. Treat with oral enzyme replacement and cobalamin supplementation if deficient. Patients with EPI require life-long enzyme replacement. Prognosis is good with appropriate treatment. [Link](https://vetmed.tamu.edu/gilab/service/assays/tli/) [Zuku question](https://zukureview.com/zuku-qod/navle/1731?chosen=8Z9%2BxwvLaX1TNXtc4whNRK4pdGe1VTXJ9z/9duXMj6w%3D&utm_source=Zukureview+Subscribers&utm_campaign=f9ddd25514-EMAIL_CAMPAIGN_2024_05_02_01_51&utm_medium=email&utm_term=0_1c9568dbdc-f9ddd25514-%5BLIST_EMAIL_ID%5D)

Answer 67

Answer: **Laminitis** In horses, retained placenta and septic metritis can lead to acute laminitis. There are four main types of laminitis: - sepsis/SIRS-related (following septic metritis, pleuropneumonia, colitis, grain overload, etc.; in research they induce this with black walnut (Juglans nigra) or carbohydrate overload) - endocrinopathic (horses with insulin dysregulation/equine metabolic syndrome or equine Cushing's disease; also associated with lush spring grasses) - traumatic (a.k.a. "road founder") - support-limb (e.g., severe lameness on one limb requiring over-dependency on opposite leg, which then develops laminitis) **Parturition in Horses** Overview Parturition, or foaling, in horses is a critical process that requires careful monitoring and management to ensure the health and safety of both the mare and the foal. Understanding the stages of labor, recognizing signs of impending foaling, and being prepared to assist if complications arise are essential for successful outcomes. Stages of Parturition 1. Stage I: Preparation • Duration: 1-4 hours. • Signs: • Restlessness, sweating, frequent urination or defecation. • Mild colic-like symptoms, getting up and down frequently. • Tail switching and kicking at the abdomen. • Physiological Changes: • Cervical dilation. • Uterine contractions begin to position the foal for delivery. • End of Stage I: Rupture of the allantochorion (“water breaking”), releasing allantoic fluid. 2. Stage II: Delivery of the Foal • Duration: 15-30 minutes (can be up to 60 minutes). • Signs: • Strong, forceful abdominal contractions. • Appearance of the amniotic sac at the vulva. • The foal’s forelimbs should be visible within the amniotic sac, followed by the head. • Normal Presentation: Front legs extended with one slightly ahead of the other, head resting on the forelimbs. • Progression: • Delivery of the shoulders, then the rest of the body. • End of Stage II: Complete expulsion of the foal. 3. Stage III: Expulsion of the Placenta • Duration: 1-3 hours. • Signs: • Mild uterine contractions to expel the placenta. • Mare may show mild discomfort. • Normal Outcome: Entire placenta should be expelled intact. • Importance: Retained placenta can lead to serious complications, such as metritis or laminitis. Monitoring and Assistance 1. Pre-Foaling Preparation: • Environment: Clean, quiet, and safe foaling area. • Supplies: Clean towels, antiseptic solution, gloves, umbilical cord clamps, and emergency veterinary contact information. 2. Observation: • Mare Behavior: Monitor for signs of impending foaling (waxing teats, relaxed pelvic ligaments, changes in behavior). • Stage I and II Monitoring: Continuous observation, especially as labor progresses to ensure timely intervention if necessary. 3. Assistance During Foaling: • Intervention Indications: Prolonged labor, malpresentation, mare exhaustion, or signs of distress in the mare or foal. • Actions: Gently assist the foal’s passage if necessary, ensuring proper presentation and avoiding excessive force. • Emergency Situations: Contact a veterinarian immediately for dystocia (difficult birth), incorrect foal positioning, or failure of the foal to progress through the birth canal. Post-Partum Care 1. Mare: • Observation: Monitor for signs of complications such as retained placenta, hemorrhage, or colic. • Placenta Examination: Ensure the entire placenta is expelled and inspect for completeness. • Vital Signs: Check the mare’s temperature, heart rate, and respiratory rate. 2. Foal: • Immediate Care: Clear the foal’s airways, dry the foal, and encourage bonding and nursing. • Vital Signs: Monitor for normal breathing, heart rate, and activity levels. • Umbilical Care: Disinfect the umbilical stump with antiseptic. • Colostrum Intake: Ensure the foal nurses within the first 1-2 hours to receive colostrum for passive immunity. Common Complications 1. Dystocia: • Definition: Difficult or abnormal labor due to malpresentation, oversized foal, or uterine inertia. • Management: Veterinary intervention for repositioning the foal or performing an emergency cesarean section. 2. Retained Placenta: • Definition: Failure to expel the placenta within 3 hours post-foaling. • Management: Administration of oxytocin to stimulate uterine contractions, manual removal by a veterinarian if necessary, and antibiotic therapy to prevent infection. 3. Post-Partum Hemorrhage: • Definition: Excessive bleeding following delivery. • Management: Immediate veterinary care to control bleeding and stabilize the mare. Summary for Veterinary Professionals • Parturition in horses consists of three stages: preparation, delivery of the foal, and expulsion of the placenta. • Close monitoring of the mare during foaling is crucial for timely intervention if complications arise. • Post-partum care includes monitoring the mare for complications, ensuring the foal receives colostrum, and inspecting the placenta for completeness. • Common complications include dystocia, retained placenta, and post-partum hemorrhage, requiring prompt veterinary attention. [Zuku question](https://zukureview.com/zuku-qod/navle/1730?chosen=uTXBjaj2v89zO7U56tbwVXlUdpnkqGiHdjRr4/MT4d0%3D&utm_source=Zukureview+Subscribers&utm_campaign=613dee4e88-EMAIL_CAMPAIGN_2024_05_01_01_51&utm_medium=email&utm_term=0_1c9568dbdc-613dee4e88-%5BLIST_EMAIL_ID%5D)

Answer 68

Answer: **Histomoniasis** This is histomoniasis; the combination of characteristic "bull's-eye" lesions on liver and cecal changes are pathognomonic. [Histomoniasis in Poultry](https://www.merckvetmanual.com/poultry/histomoniasis/histomoniasis-in-poultry) [Necrotic Enteritis](https://www.merckvetmanual.com/poultry/necrotic-enteritis/necrotic-enteritis-in-poultry?autoredirectid=21096) Caused by the protozoa Histomonas meleagridis, and transmitted in eggs of cecal nematode Heterakis gallinarum. Expect a presentation of depression/diarrhea. [Hemorrhagic enteritis](https://www.merckvetmanual.com/poultry/hemorrhagic-enteritis-marble-spleen-disease/hemorrhagic-enteritis-marble-spleen-disease-in-poultry?autoredirectid=14418&redirectid=25520) [Hemorrhagic enteritis](https://www.merckvetmanual.com/multimedia/image/hemorrhagic-enteritis-intestinal-hemorrhaging-turkey) Expect to see more sudden death with necrotic enteritis caused by Clostridium perfringens. Follow this link to see the so-called ["Turkish towel" intestinal pseudomembrane of necrotic enteritis.](https://www.merckvetmanual.com/multimedia/image/necrotic-enteritis-small-intestine-chicken) Signs of avian spirochetosis are highly variable, may be absent: see listlessness, shivering, increased thirst, green/yellow diarrhea with increased urates early on. Caused by a tick-borne Borrelia. Look for characteristic enlarged, mottled spleen with petechial hemorrhages, similar to Marble spleen disease of pheasants. Expect depression, bloody droppings, substantial mortality with [hemorrhagic enteritis of turkeys.](https://www.merckvetmanual.com/multimedia/image/hemorrhagic-enteritis-enlarged-spleen-turkey) Expect diarrheal presentation with coronaviral enteritis of turkeys but NOT the characteristic cecal/liver lesions described on necropsy above. [Link](https://www.merckvetmanual.com/poultry/viral-enteritis-in-poultry/coronaviral-enteritis-of-turkeys?autoredirectid=25426) [Link](https://www.merckvetmanual.com/multimedia/image/hemorrhagic-enteritis-enlarged-spleen-turkey) [Zuku](https://zukureview.com/zuku-qod/navle/1729?chosen=Vq0o2/cB/zYhqJvz4kUDcjUJIyzUCQF7SPfNyEehyUc%3D&utm_source=Zukureview+Subscribers&utm_campaign=1654ef6ff1-EMAIL_CAMPAIGN_2024_04_30_01_51&utm_medium=email&utm_term=0_1c9568dbdc-1654ef6ff1-%5BLIST_EMAIL_ID%5D) [Cornell University](https://partnersah.vet.cornell.edu/avian-atlas/#/)

Answer 69

Answer: **A - Clostridioides difficile (formerly Clostridium difficile).** A history of recent antimicrobial therapy is common in cases of Clostridioides difficile (formerly Clostridium difficile associated diarrhea. [Clostridial enterocolitis](https://www.merckvetmanual.com/digestive-system/infectious-diarrheal-diseases-in-horses/clostridial-enterocolitis-in-horses?autoredirectid=19930) Adult horses exposed to erythromycin are particularly at risk for C. difficile enterocolitis. Mares are very close with their foals and thus, if the foal is receiving a medication, the mare is likely ingesting some as well. Clostridium novyi is the cause of infectious necrotic hepatitis, which is primarily seen in sheep but can also be seen in cattle, hogs, and horses. [Infectious Necrotic Hepatitis in Animals](https://www.merckvetmanual.com/infectious-diseases/clostridial-diseases/infectious-necrotic-hepatitis-in-animals?mredirectid=3471&mredirectid=920) [Lawsonia intracellularis](https://www.merckvetmanual.com/digestive-system/diarrheal-diseases-in-foals/bacterial-diarrhea-in-foals?mredirectid=1138) is the cause of proliferative enteropathy, resulting in diarrhea and hypoproteinemia in foals and swine. [Rhodococcus equi](https://www.merckvetmanual.com/digestive-system/diarrheal-diseases-in-foals/bacterial-diarrhea-in-foals?mredirectid=1138) is a notable cause of pneumonia in older foals characterized by pulmonary abscessation as well as some extrapulmonary manifestations. [Escherichia coli](https://www.merckvetmanual.com/digestive-system/diarrheal-diseases-in-foals/foal-heat-diarrhea?mredirectid=1139) can be a cause of septicemia and diarrhea in foals and calves. [Zuku](https://zukureview.com/zuku-qod/navle/1718?chosen=iwXtlldTbc98CQrBM563LpYyy9ovLECYXQaGqFI4dpQentT61eAr%2BI/vVAPVJKcKhIWMof8hW3iiV8NiFV7QLA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=d80584f334-EMAIL_CAMPAIGN_2024_04_29_01_51&utm_medium=email&utm_term=0_1c9568dbdc-d80584f334-%5BLIST_EMAIL_ID%5D)

Answer 70

Answer: **C - Liver and muscle** In dogs and cats, damage to liver and muscle cells may cause increases in serum alanine aminotransferase (ALT). [Clinical biochemistry](https://www.merckvetmanual.com/clinical-pathology-and-procedures/diagnostic-procedures-for-the-private-practice-laboratory/clinical-biochemistry) ALT is a "leakage" enzyme meaning that the enzyme is intracellular. It leaks out of cells and ultimately into the circulation following damage to the cell membrane. In other species (e.g., horses, ruminants, pigs, and birds), ALT is less useful because there are not high intracellular levels. Aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), and glutamate dehydrogenase (GLDH) are the predominant leakage enzyme in these animals (availability is lab-dependent). The magnitude of increase of leakage enzymes may be deceiving. Severe damage to a healthy liver may result in very high levels, while low levels may be seen when significant atrophy or fibrosis of the liver is present and few cells are left. Differentiate ALT from muscle vs. liver by evaluation of the clinical picture and other serum biochemistry results. Other muscle enzymes include creatine phosphokinase (CK) and AST; and other liver enzymes are AST, SDH, GLDH, gamma glutamyl transferase (GGT), and alkaline phosphatase (ALP). Leakage enzymes do NOT provide an estimate of liver function. This is evaluated by measurement of substances dependent on the efficacy of liver function such as bile acids, blood urea nitrogen, albumin, and glucose. [Zuku](https://zukureview.com/zuku-qod/navle/1717?chosen=HdsMGv9Um0JThs9LcshD1hdiuELqCe6sDDeU1e4t5%2B0%3D&utm_source=Zukureview+Subscribers&utm_campaign=1b87d1b03e-EMAIL_CAMPAIGN_2024_04_26_01_51&utm_medium=email&utm_term=0_1c9568dbdc-1b87d1b03e-%5BLIST_EMAIL_ID%5D)

Answer 71

Answer: **A - Cervicothoracic: C6-T2** Weak, hypotonic (i.e., lower motor neuron a.k.a. "LMN") forelimbs and spastic paresis (i.e., upper motor neuron a.k.a. "UMN") hindlimbs are signs of a cervicothoracic (C6-T2) lesion. May see worse signs in forelimbs than hindlimbs. NOTE: This is the OPPOSITE presentation as Schiff-Sherrington syndrome - i.e., SEVERE acute spinal cord trauma in the region of T3-L3 and, when in lateral recumbency, the thoracic limbs are rigid and extended and the pelvic limbs appear flaccid in comparison. However, pelvic limb reflexes are normal to increased, as would be expected with an upper motor neuron lesion. Can localize T3-L3 lesions by checking cutaneous trunci reflex - the lesion is usually 1-2 vertebrae cranial to where the reflex disappears. With C1-C5 would expect UMN signs in all four limbs, usually worse in hinds. With a T3-L3, would see UMN hind limb signs and normal forelimbs. [Zuku Question](https://zukureview.com/zuku-qod/navle/1716?chosen=vYs5tF55m5fsVtjvqgWMctlbI/Gnw5M7IvUr2UDu86k%3D&utm_source=Zukureview+Subscribers&utm_campaign=ea8cc60593-EMAIL_CAMPAIGN_2024_04_25_01_52&utm_medium=email&utm_term=0_1c9568dbdc-ea8cc60593-%5BLIST_EMAIL_ID%5D)

Answer 72

Answer: **C - Closure of atrioventricular valves, opening of semilunar valves** The first heart sound (S1 or the "lub" in "lub-dub") is caused by closure of the atrioventricular valves (AV valves, mitral and tricuspid) and opening of the pulmonic and aortic valves (semilunar valves). This is the end of diastole and start of systole. The second sound (S2) is the closure of the aortic and pulmonic valves and opening of the AV valves. This is the end of systole and start of diastole. A third sound (S3) is the end of rapid ventricular filling and a fourth sound (S4) is atrial systole (atrial contraction). You can often hear all 4 sounds in horses, but typically hear only S1 and S2 in cattle and small animals. [Zuku question](https://zukureview.com/zuku-qod/navle/1715?chosen=8H%2BIQzgOqJ3Ok9K%2BKKhg/lA6Koa9E3ze9cihxcE7hIM6ALll9XmAdiG/kSORx6Cai9U7LH4P%2B3uUlAaK4R/to2WF%2BK9A1ic3hu%2BOyvEfqPM%3D&utm_source=Zukureview+Subscribers&utm_campaign=4ad426cd19-EMAIL_CAMPAIGN_2024_04_24_01_52&utm_medium=email&utm_term=0_1c9568dbdc-4ad426cd19-%5BLIST_EMAIL_ID%5D)

Answer 73

Answer: **Facial Nerve** Think of facial nerve paralysis (C7) with a unilaterally droopy face. Remember the facial nerve is motor to the muscles of facial expression (causing drooped ear, lip, and eyelid) and innervates the lacrimal and salivary glands. Loss of lacrimal innervation can lead to dry eye and exposure keratitis if dog loses ability to close eyelid from damage to facial nerve innervation of the orbicularis oculi muscle. Idiopathic in 75% of canine cases (25% of cats). Can also see these signs with middle ear damage (from otitis media), facial nerve trauma (ear surgery in dogs, or pressure from halter buckles in anesthetized horse), or neoplasia. Follow this link to see a horse with facial nerve damage: note the nose pulled to horse's left. (means facial nerve damaged on right). Think more of a dropped jaw with trigeminal neuropathy (CN 5-dogs, horses). https://zukureview.com/zuku-qod/navle/1714?chosen=%2BDjN/AlCLNJhEzHhEYZL8g%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=f65c309e3b-EMAIL_CAMPAIGN_2024_04_23_01_52&utm_medium=email&utm_term=0_1c9568dbdc-f65c309e3b-%5BLIST_EMAIL_ID%5D

Answer 74

Answer: **Panosteitis** This is panosteitis, an acute-onset shifting leg lameness with long bone pain most commonly seen in young (5-18 mos) medium to large breed dogs. German Shepherds are at the highest risk of developing panosteitis. Hypertrophic osteodystrophy (HOD) is a an uncommon developmental orthopedic disease of young (2-8 mos), growing dogs. Large and giant breeds, in particular the great Dane, are predisposed. It is characterized by symmetrical distal metaphyseal pain and swelling of long bones (most commonly the ulna and tibia), fever, anorexia, and depression. https://zukureview.com/zuku-qod/navle/1709?chosen=LTO%2B3G5b006tyuXbvHfv6u7vQy19G12tP3nnjyivWaM%3D&utm_source=Zukureview+Subscribers&utm_campaign=1338f90fa8-EMAIL_CAMPAIGN_2024_04_22_01_52&utm_medium=email&utm_term=0_1c9568dbdc-1338f90fa8-%5BLIST_EMAIL_ID%5D

Answer 75

Answer: **B - Actinobacillus pleuropneumoniae** This is a classic scenario of an outbreak of pleuropneumonia, caused by Actinobacillus pleuropneumoniae. [Pleuropneumonia in Pigs](https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-pigs/pleuropneumonia-in-pigs) Primarily a growing pig disease, although adults can be affected as well, and sows can abort. Mortality is high if untreated. Survivors may experience lowered growth rates and have a persistent cough. Image courtesy of Meghann Pierdon, VMD, DACAW. [Zuku](https://zukureview.com/zuku-qod/navle/1708?chosen=RavNZiX4hv9VzibSd1ZIykb3fklGd3Tr5TgJbzMKX4w%3D&utm_source=Zukureview+Subscribers&utm_campaign=b0fbb1a3e0-EMAIL_CAMPAIGN_2024_04_19_01_52&utm_medium=email&utm_term=0_1c9568dbdc-b0fbb1a3e0-%5BLIST_EMAIL_ID%5D)

Answer 76

Answer: **Myxomatous mitral valve disease** Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs. It is the most common cause of a heart murmur in adult small-to medium-sized dogs, especially Cavalier King Charles spaniels, dachshunds, Yorkies, Chihuahuas, and mini poodles. Myxomatous degeneration of the tricuspid valve can also occur. Stage dogs with MMVD to determine the need for intervention - use thoracic radiographs, +/- echocardiogram, +/- ECG. Asymptomatic dogs with a heart murmur and normal thoracic radiographs are considered class B1. Do not treat class B1 dogs, but monitor for progression. Progression can be slow to negligible. There is no Tx that slows or reverses MMVD; however, dogs with cardiomegaly (i.e., class B2) benefit from Tx with pimobendan to slow progression to congestive heart failure (CHF). If CHF is present, Tx to alleviate clinical signs and improve quality of life. More invasive procedures, such as mitral valve annuloplasty, transcatheter edge-to-edge repair, and chordae tendineae replacement, have been undertaken in research settings and some client-owned dogs at a few facilities around the world. The use of these procedures in veterinary medicine is still in its infancy, and as such, medical management of MVD remains the standard of care at this time. Read the useful and informative American College of Veterinary Internal Medicine consensus guidelines for the diagnosis and treatment of mitral valve disease. https://zukureview.com/zuku-qod/navle/1705?chosen=VILFHxx2QTtX0HGjmFFjUA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=5b79cbf829-EMAIL_CAMPAIGN_2024_04_18_01_52&utm_medium=email&utm_term=0_1c9568dbdc-5b79cbf829-%5BLIST_EMAIL_ID%5D

Answer 77

Answer: **Myxomatous mitral valve disease** Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs. It is the most common cause of a heart murmur in adult small-to medium-sized dogs, especially Cavalier King Charles spaniels, dachshunds, Yorkies, Chihuahuas, and mini poodles. Myxomatous degeneration of the tricuspid valve can also occur. Stage dogs with MMVD to determine the need for intervention - use thoracic radiographs, +/- echocardiogram, +/- ECG. Asymptomatic dogs with a heart murmur and normal thoracic radiographs are considered class B1. Do not treat class B1 dogs, but monitor for progression. Progression can be slow to negligible. There is no Tx that slows or reverses MMVD; however, dogs with cardiomegaly (i.e., class B2) benefit from Tx with pimobendan to slow progression to congestive heart failure (CHF). If CHF is present, Tx to alleviate clinical signs and improve quality of life. More invasive procedures, such as mitral valve annuloplasty, transcatheter edge-to-edge repair, and chordae tendineae replacement, have been undertaken in research settings and some client-owned dogs at a few facilities around the world. The use of these procedures in veterinary medicine is still in its infancy, and as such, medical management of MVD remains the standard of care at this time. Read the useful and informative American College of Veterinary Internal Medicine consensus guidelines for the diagnosis and treatment of [mitral valve disease.](https://pmc.ncbi.nlm.nih.gov/articles/PMC6524084/) [Zuku](https://zukureview.com/zuku-qod/navle/1705?chosen=VILFHxx2QTtX0HGjmFFjUA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=5b79cbf829-EMAIL_CAMPAIGN_2024_04_18_01_52&utm_medium=email&utm_term=0_1c9568dbdc-5b79cbf829-%5BLIST_EMAIL_ID%5D)

Answer 78

Answer: **Munge** This is the clinical picture of munge (idiopathic nasal/perioral hyperkeratotic dermatosis). Some affected animals have lesions on the bridge of the nose and around the eyes and ears. Average age of onset is six months to two years old. Tx - address secondary bacterial infections (e.g., daily 10% povidone iodine scrubs and apply 7% tincture of iodine). If minimal response, include a topical glucocorticoid or intralesional triamcinolone acetonide. If still no response, evaluate immune function. Dorsal nasal alopecia is characterized by alopecia over the bridge of the nose with normal to variably scaly, hyperpigmented, and thickened skin. It is more common in dark-haired animals. It can be secondary to fly bites or rubbing the nose. Click here to see a llama with dorsal nasal alopecia. Animals with idiopathic hyperkeratosis (zinc-responsive dermatosis) present with thickened, nonpruritic papules with tightly adherent crusts in the less densely haired areas of the perineum, ventral abdomen, inguinal region, medial thighs, and axilla. Signs can begin at any age. [Zuku Quesion](https://zukureview.com/zuku-qod/navle/1702?chosen=wfOStFmgW9nO59xqKEV1833%2BR3qrkJdSjEMjbOtnJfc%3D&utm_source=Zukureview+Subscribers&utm_campaign=43456d44da-EMAIL_CAMPAIGN_2024_04_17_01_52&utm_medium=email&utm_term=0_1c9568dbdc-43456d44da-%5BLIST_EMAIL_ID%5D)

Answer 79

Answer: **Both mother and baby are safe** Both mother and baby are safe. The toxoplasmosis organism causes birth defects in a developing fetus if a mother is infected for the first time in her life while pregnant (ie: IgM positive while pregnant). [Toxoplasmosis in Animals](https://www.merckvetmanual.com/generalized-conditions/toxoplasmosis/toxoplasmosis-in-animals?autoredirectid=14229) Toxoplasmosis is not generally dangerous to immune-competent people and a positive IgG result suggests a previous infection. There are challenges to toxoplasmosis testing in pregnant women (false positives). [Symptoms of Toxoplasmosis](https://www.cdc.gov/toxoplasmosis/symptoms/?CDC_AAref_Val=https://www.cdc.gov/parasites/toxoplasmosis/diagnosis.html) If a pregnant woman is IgM positive, confirmatory tests must be done. [CDC](https://www.cdc.gov/dpdx/toxoplasmosis/index.html) Click here for more on pregnancy and [toxoplasmosis](https://www.cdc.gov/toxoplasmosis/about/index.html?CDC_AAref_Val=https://www.cdc.gov/parasites/toxoplasmosis/gen_info/pregnant.html#cdc_disease_basics_testing_screening-diagnosis) [CAPC Toxoplasma gondii](https://capcvet.org/guidelines/toxoplasma-gondii/) [Zuku](https://zukureview.com/zuku-qod/navle/1693?chosen=880IhrDfWfwmivh/GPpo3Q9kdgXg86Zr7ZxFWq4pUeE%3D&utm_source=Zukureview+Subscribers&utm_campaign=b41fc05a7a-EMAIL_CAMPAIGN_2024_04_15_01_52&utm_medium=email&utm_term=0_1c9568dbdc-b41fc05a7a-%5BLIST_EMAIL_ID%5D)

Answer 80

Answer: **Normal Finding** Normal male crias are born with adhesions between the free end of the penis and the prepuce. As they sexually mature these adhesions gradually detach, so puberty can be seen clinically when the penis can be completely exteriorized. Castration prior to puberty may result in continued adhesions. In Peru, males are not generally used for breeding until 3 years of age. Male llamas reach puberty at approximately 21 months (range 9-31 months). Alpacas mature earlier, around 12 months of age.

Answer 81

Answer: **Due to colostrum absorption** Very high GGT levels are seen with colostrum absorption. In newborn calves, lambs, and pups, an increase in [GGT](https://www.merckvetmanual.com/digestive-system/laboratory-analyses-and-imaging-in-hepatic-disease-in-small-animals/enzyme-activity-in-hepatic-disease-in-small-animals?mredirectid=1181#v3267944) up to a 1000 times is normal when they receive high levels of [colostrum](https://www.merckvetmanual.com/digestive-system/hepatic-disease-in-large-animals/overview-of-hepatic-disease-in-large-animals#Diagnosis_v3265327) from the dam. In calves it takes four to six weeks for these GGT levels to return to the normal adult reference range. High levels of GGT are produced in the mammary epithelium during lactation. When evaluating bloodwork, make sure to utilize reference ranges specific for the age of the patient. [Zuku](https://zukureview.com/zuku-qod/navle/1691?chosen=E5Q3%2BkptaJSR197I6v7Og7ObNqCo94K8KQL5ikadElCKk6VWaKjvM7w8HQjpEL2l&utm_source=Zukureview+Subscribers&utm_campaign=c8ffc18539-EMAIL_CAMPAIGN_2024_04_11_01_52&utm_medium=email&utm_term=0_1c9568dbdc-c8ffc18539-%5BLIST_EMAIL_ID%5D)

Answer 82

Answer: **Mare will need episiotomy before foaling** The mare will need an episiotomy (a surgically planned incision on the perineum and the posterior vaginal wall) prior to foaling. Sometimes an episiotomy may be needed prior to breeding by stallion if the remaining vulvar cleft is too small to permit intromission. A Caslick operation (vulvoplasty, a superficial form of the episioplasty) is used to treat pneumovagina in horses to prevent genital infections and infertility. [Link](https://www.merckvetmanual.com/management-and-nutrition/management-of-reproduction-horses/breeding-soundness-examination-of-the-mare) Click here to see a horse that has had a [Caslick operation](https://www.merckvetmanual.com/management-and-nutrition/management-of-reproduction-horses/breeding-soundness-examination-of-the-mare)

Answer 83

Answer: **1 hour** Dystocia in the sow is present when one hour or more has passed between piglets. [Link](https://www.merckvetmanual.com/management-and-nutrition/management-of-reproduction-pigs/breeding-management-of-pigs?autoredirectid=16798) Intervention should be swift to prevent death of piglets from anoxia. In sows, dystocia is often due to uterine inertia, similar to other animals that produce multiple offspring. Other causes include fetal malposition, fetopelvic disproportion, obstruction of the pelvic canal, deviation of the uterus, and excitement in the dam. Medical therapy can be given with oxytocin and/or calcium only when an obstructive dystocia is not present. [Link](https://www.merckvetmanual.com/management-and-nutrition/management-of-reproduction-pigs/breeding-management-of-pigs?autoredirectid=16798)

Answer 84

Answer: **Exploratory Laparotomy** Exploratory laparotomy is the most appropriate next step for this linear foreign body. On the lateral radiographs, there is an area of the small intestine with very small gas bubbles where the walls of the small intestine appear undulating. In this case, the linear foreign body was a bikini string. A linear foreign body is a surgical emergency due to potential intestinal perforation and septic peritonitis. In severe cases, the "sawing action" of the linear foreign body against the intestinal mucosa can cause extensive damage requiring extensive resection and anastomosis. Occasionally, the intestinal damage is too extensive and euthanasia is the best course. If a definitive Dx is not evident on radiographs, consider abdominal ultrasound to further evaluate the gastrointestinal tract. Click here to see normal feline https://zukureview.com/zuku-qod/navle/1672?chosen=nipbTi8rwOSqEhFTF2at/jmuPF9pm%2Bgy9P6ZJnvYP/g300lrUwJMiJsZjxcJ6Xla&utm_source=Zukureview+Subscribers&utm_campaign=e8a9336018-EMAIL_CAMPAIGN_2024_04_08_01_52&utm_medium=email&utm_term=0_1c9568dbdc-e8a9336018-%5BLIST_EMAIL_ID%5D

Answer 85

Answer: **D - Grain overload, ethylene glycol toxicity, renal failure** Think of an increased anion gap (AG) with renal failure, ethylene glycol toxicity, lactic acidosis from grain overload or strenuous exercise, and diabetic ketoacidosis. The AG is an assessment of acid-base status and evaluates unmeasured anions such as ketones, lactate, uremic metabolites, and toxins (e.g., ethylene glycol). Anion gap = (Na* + K*) - (HCO3 + CI) If venous blood gas analysis is unavailable substitute TCO2 for HCO3 Here is more information from Cornell's eClinPath website about measurement of the anion gap. [Zuku Question](https://zukureview.com/zuku-qod/navle/1671?chosen=6T7pBWa3KzDoHUQmKskaeA8lytdDvhL%2BGEu7ycecGMLn7sj/%2BySuxcDXMrhsXNNFZm1xjC63PHDSjXYFjSHHJOnLsVbSKbX9In2IL8yOIY0%3D&utm_source=Zukureview+Subscribers&utm_campaign=6b810ea075-EMAIL_CAMPAIGN_2024_04_05_01_52&utm_medium=email&utm_term=0_1c9568dbdc-6b810ea075-%5BLIST_EMAIL_ID%5D)

Answer 86

Answer: **120-150 days** An experienced practitioner can reliably feel fremitus (vibration in uterine artery of the gravid uterine horn) between 120 and 150 days. Remember that fremitus in the uterine artery is a supportive sign of pregnancy but NOT conclusive evidence of pregnancy. An experienced practitioner can reliably feel the membrane slip of chorioallantoic membranes rectally at 30-35 days and can feel placentomes at around 70-75 days. Placentomes and membrane slip ARE cardinal signs of pregnancy. One way to remember these is that the EARLIEST occurs in REVERSE alphabetical order ie: Slip 30-35 days Placentomes 70-75 days Fremitus 120-150 days https://zukureview.com/zuku-qod/navle/1670?chosen=Li8MEfMvRsyfP%2BKVqXOwqw%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=d2c0e8204d-EMAIL_CAMPAIGN_2024_04_04_01_52&utm_medium=email&utm_term=0_1c9568dbdc-d2c0e8204d-%5BLIST_EMAIL_ID%5D

Answer 87

Answer: **Common opening of the pancreatic and common bile ducts into duodenum** In cats, there is a common opening of the pancreatic and common bile ducts into the duodenum. It is thought that this may predispose them to ascending cholangitis and pancreatitis after vomiting associated with inflammatory bowel disease, resulting in extrahepatic biliary obstruction. [Merck](https://www.merckvetmanual.com/digestive-system/hepatic-diseases-of-small-animals/extrahepatic-bile-duct-obstruction-in-small-animals?mredirectid=1156) Other possible etiologies of EHBO include neoplasia, biliary stricture, duodenal obstruction, diaphragmatic hernia, and parasitic infection. In all cases, there is a lack of bile entry into the intestinal tract, leading to decreased absorption of fat and fat soluble vitamins such as vitamin K, potentially resulting in coagulopathies. Except in transient cases that are related to acute pancreatitis, need surgical intervention to relieve the obstruction as well as appropriate supportive care, antimicrobial treatment, and vitamin K administration. Click here to see a good summary of extrahepatic biliary obstruction with images, courtesy of the American College of Veterinary Surgeons (ACVS). [Extrabiliary Obstruction](https://www.acvs.org/small-animal/extrahepatic-biliary-tract-obstruction/) [Zuku question](https://zukureview.com/zuku-qod/navle/1669?chosen=ESTUa%2BWkWQ9q/8R8E0RfErvQLpoWv/dhNAj/tuLFaEKKcrzGBvBF0FtaJL9443gzkXe8rVZAlO6dkJ0tZYelBw%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=179365ae71-EMAIL_CAMPAIGN_2024_04_03_01_52&utm_medium=email&utm_term=0_1c9568dbdc-179365ae71-%5BLIST_EMAIL_ID%5D)

Answer 88

Answer: **A. Normal age-related change** These are normal age related changes. Rats normally live two to three years, though some may live to five years of age. With age, the hair coat of white rats normally develop yellowing fur. They may also show a brownish, granular sebaceous secretion at the base of affected hair shafts which an owner may mistake for a skin parasite.

Answer 89

Answer: **C - Thoracic radiographs to evaluate for congestive heart failure** This is a classic presentation for dilated cardiomyopathy (DCM); perform thoracic radiographs to evaluate for congestive heart failure. Perform electrocardiogram to better assess the cardiac rythm. Use echocardiography to confirm the diagnosis. Consider veterinary point of care ultrasound (POCUS) to assess for pleural effusion and alveolar infiltrates. Tx to control arrhythmia and diminish clinical signs. Therapy may include diuretics (e.g., furosemide), positive inotropes (e.g., pimobendan), angiotensin converting enzyme inhibitors (e.g., enalapril) and antiarrhythmics (e.g., diltiazem, sotalol). Px is guarded, especially for Dobermans - with Tx may live six months to two years. Large and giant breeds are at increased risk, including Irish wolfhounds and great Danes. Boxers can develop arrhythmogenic right ventricular cardiomyopathy, distinct from DCM. Dobermans have two genetic mutations that can lead to development of DCM: PDK4 and DCM2. Each mutation independently can lead to DCM: dogs affected with both are 30 times more likely to develop DCM than a normal dog. https://zukureview.com/zuku-qod/navle/1657?chosen=/aAohEOm/tj%2B8SkQ1bBK5W9gNbdZaeYSwy41OnRhFP4UfpWSdHkndGIAlthdIunFDGkMponqYgx1zyDmVy54y3t20nfLm%2BsTZcM6hD%2Bp%2BtkY7EoupLMie%2BJZWclPMT8bykHR80CLl3iF2VukGAzUXA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=dd8bdf9f66-EMAIL_CAMPAIGN_2024_04_01_01_52&utm_medium=email&utm_term=0_1c9568dbdc-dd8bdf9f66-%5BLIST_EMAIL_ID%5D

Answer 90

Answer: **Flehmen** This is flehmen. This is a behavior seen in the following circumstances: normal stallion response to pheromones, normal response of all horses to new smells (even foals do it!), sign of colic, or associated with granulosa cell tumors in mares. Many other animals also show this response, for example here is a cat doing flehmen. Image courtesy, Waugsberg. [Zuku question](https://zukureview.com/zuku-qod/navle/1656?chosen=R8MeipsSyLTwETdstETZYA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=53142829a3-EMAIL_CAMPAIGN_2024_03_29_01_53&utm_medium=email&utm_term=0_1c9568dbdc-53142829a3-%5BLIST_EMAIL_ID%5D)

Answer 91

Answer: **Flehmen** This is flehmen. This is a behavior seen in the following circumstances: normal stallion response to pheromones, normal response of all horses to new smells (even foals do it!), sign of colic, or associated with granulosa cell tumors in mares. Many other animals also show this response, for example here is a cat doing flehmen. Image courtesy, Waugsberg. https://zukureview.com/zuku-qod/navle/1656?chosen=R8MeipsSyLTwETdstETZYA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=53142829a3-EMAIL_CAMPAIGN_2024_03_29_01_53&utm_medium=email&utm_term=0_1c9568dbdc-53142829a3-%5BLIST_EMAIL_ID%5D

Answer 92

Answer: **Exploratory_laparotomy** Exploratory laparotomy is the most appropriate next step for this linear foreign body. On the lateral radiographs, there is an area of the small intestine with very small gas bubbles where the walls of the small intestine appear undulating. In this case, the linear foreign body was a bikini string. A linear foreign body is a surgical emergency due to potential intestinal perforation and septic peritonitis. In severe cases, the "sawing action" of the linear foreign body against the intestinal mucosa can cause extensive damage requiring extensive resection and anastomosis. Occasionally, the intestinal damage is too extensive and euthanasia is the best course. If a definitive Dx is not evident on radiographs, consider abdominal ultrasound to further evaluate the gastrointestinal tract.

Answer 93

Answer: **Grain overload, ethylene glycol toxicity, renal failure** Think of an increased anion gap (AG) with renal failure, ethylene glycol toxicity, lactic acidosis from grain overload or strenuous exercise, and diabetic ketoacidosis. The AG is an assessment of acid-base status and evaluates unmeasured anions such as ketones, lactate, uremic metabolites, and toxins (e.g., ethylene glycol). Anion gap = (Nat + K*) - (HCOz- + CI) If venous blood gas analysis is unavailable substitute TCO2 for HCO3 Here is more information from Cornell's eClin Path website about measurement of the anion gap. https://eclinpath.com/chemistry/acid-base/chemistry-tests/anion-gap/

Answer 94

Answer: **Cervicothoracic C6-T2** Weak, hypotonic (i.e., lower motor neuron a.k.a. "LMN") forelimbs and spastic paresis (i.e., upper motor neuron a.k.a. "UMN") hindlimbs are signs of a cervicothoracic (C6-T2) lesion. May see worse signs in forelimbs than hindlimbs. NOTE: This is the OPPOSITE presentation as Schiff-Sherrington syndrome - i.e., SEVERE acute spinal cord trauma in the region of T3-L3 and, when in lateral recumbency, the thoracic limbs are rigid and extended and the pelvic limbs appear flaccid in comparison. However, pelvic limb reflexes are normal to increased, as would be expected with an upper motor neuron lesion. Can localize T3-L3 lesions by checking cutaneous trunci reflex - the lesion is usually 1-2 vertebrae cranial to where the reflex disappears. With C1-C5 would expect UMN signs in all four limbs, usually worse in hinds. With a T3-L3, would see UMN hind limb signs and normal forelimbs. https://zukureview.com/zuku-qod/navle/2204?chosen=vYs5tF55m5fsVtjvqgWMctlbI/Gnw5M7IvUr2UDu86k%3D&utm_source=Zukureview+Subscribers&utm_campaign=0ba8259863-EMAIL_CAMPAIGN_2024_12_02_02_50&utm_medium=email&utm_term=0_1c9568dbdc-0ba8259863-7334655

Answer 95

Answer: **Closure of atrioventricular valves, opening of semilunar valves** The first heart sound (S1 or the "lub" in "lub-dub") is caused by closure of the atrioventricular valves (AV valves, mitral and tricuspid) and opening of the pulmonic and aortic valves (semilunar valves). This is the end of diastole and start of systole. [Heart sounds in animals](https://www.merckvetmanual.com/circulatory-system/diagnosis-of-heart-disease/diagnosis-of-heart-disease-in-animals?mredirectid=1107#Heart-Sounds_v3259374) The second sound (S2) is the closure of the aortic and pulmonic valves and opening of the AV valves. This is the end of systole and start of diastole. A third sound (S3) is the end of rapid ventricular filling and a fourth sound (S4) is atrial systole (atrial contraction). You can often hear all 4 sounds in horses, but typically hear only S1 and S2 in cattle and small animals. [Zuku question](https://zukureview.com/zuku-qod/navle/2196?chosen=7RzBxpIRSVxlcCzoaA2OC4OMj5DlS3pf/%2BKXMgjkwz7C3xs%2BEvAzxy2sc3dzWgENpkKhFM5mY4n3VjtaWrUEOg%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=c72ebe5f45-EMAIL_CAMPAIGN_2024_11_28_02_50&utm_medium=email&utm_term=0_1c9568dbdc-c72ebe5f45-7334655)

Answer 96

Answer: **Facial nerve** Think of facial nerve paralysis (CN 7) with a unilaterally droopy face. Remember the facial nerve is motor to the muscles of facial expression (causing drooped ear, lip, and eyelid) and innervates the lacrimal and salivary glands. Loss of lacrimal innervation can lead to dry eye and exposure keratitis if dog loses ability to close eyelid from damage to facial nerve innervation of the orbicularis oculi muscle. Idiopathic in 75% of canine cases (25% of cats). Can also see these signs with middle ear damage (from otitis media), facial nerve trauma (ear surgery in dogs, or pressure from halter buckles in anesthetized horse), or neoplasia. Follow this link to see a horse with facial nerve damage: note the nose pulled to horse's left. (means facial nerve damaged on right). Think more of a dropped jaw with trigeminal neuropathy (CN 5-dogs, horses). https://zukureview.com/zuku-qod/navle/2195?chosen=%2BDjN/AlCLNJhEzHhEYZL8g%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=e5edd9c98f-EMAIL_CAMPAIGN_2024_11_27_02_50&utm_medium=email&utm_term=0_1c9568dbdc-e5edd9c98f-7334655

Answer 97

Answer: **Panosteitis** This is panosteitis, an acute-onset shifting leg lameness with long bone pain most commonly seen in young (5-18 mos) medium to large breed dogs. German Shepherds are at the highest risk of developing panosteitis. Hypertrophic osteodystrophy (HOD) is a an uncommon developmental orthopedic disease of young (2-8 mos), growing dogs. Large and giant breeds, in particular the great Dane, are predisposed. It is characterized by symmetrical distal metaphyseal pain and swelling of long bones (most commonly the ulna and tibia), fever, anorexia, and depression. Hypertrophic osteopathy is a diffuse periosteal proliferative disease of long bones in dogs secondary to a neoplastic mass or other disease (e.g., heartworm Dz) in the thoracic or abdominal cavity. Multiple cartilaginous exostoses is a rare benign proliferation of bone/cartilage that can affect the metaphyseal cortical surfaces of long bones, vertebrae, and ribs in young dogs and cats. Animals may have no signs at all. Click here to see a CT image of cartilaginous exostoses of the vertebral body. Osteosarcoma is unlikely in a young dog and does not cause shifting leg lameness. https://zukureview.com/zuku-qod/navle/2193?chosen=9gnvCWj/neyRbufocBxwuQ%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=c54009a9b8-EMAIL_CAMPAIGN_2024_11_26_02_50&utm_medium=email&utm_term=0_1c9568dbdc-c54009a9b8-7334655

Answer 98

Answer: **Normal finding** Normal male crias are born with adhesions between the free end of the penis and the prepuce. As they sexually mature these adhesions gradually detach, so puberty can be seen clinically when the penis can be completely exteriorized. Castration prior to puberty may result in continued adhesions. In Peru, males are not generally used for breeding until 3 years of age. Male llamas reach puberty at approximately 21 months (range 9-31 months). Alpacas mature earlier, around 12 months of age.

Answer 99

Answer: **Chronic external blood loss** Chronic external blood loss (i.e., gastrointestinal hemorrhage) is the most common cause of iron-deficiency anemia. Dietary iron or copper deficiency or excessive zinc may also cause iron deficiency anemia. Look for microcytic, hypochromic anemia which may be regenerative or non-regenerative. Also look for evidence of red blood cell (RBC) fragmentation - i.e., acanthocytes, schistocytes, and keratocytes. The heme group of hemoglobin contains iron and therefore deficiency causes decreased hemoglobin production. The most common cause of iron deficiency anemia is chronic external blood loss (e.g., chronic gastrointestinal bleeding). [Causes of anemia:](https://eclinpath.com/hematology/anemia/causes-of-anemia/) [Zuku](https://zukureview.com/zuku-qod/navle/2223?chosen=5bMPhiDlq4lLGoi703zbmLV5BG8oCF6MEwLocvy7%2Bmw%3D&utm_source=Zukureview+Subscribers&utm_campaign=9228c2d4e1-EMAIL_CAMPAIGN_2024_12_13_02_51&utm_medium=email&utm_term=0_1c9568dbdc-9228c2d4e1-7334655)

Answer 100

Answer: **Normal finding** Normal male crias are born with adhesions between the free end of the penis and the prepuce. As they sexually mature these adhesions gradually detach, so puberty can be seen clinically when the penis can be completely exteriorized. Castration prior to puberty may result in continued adhesions. In Peru, males are not generally used for breeding until 3 years of age. Male llamas reach puberty at approximately 21 months (range 9-31 months). Alpacas mature earlier, around 12 months of age.

Answer 101

Answer: **Camelids** Camelids (Ilamas, camels, alpacas) normally have ellipsoid red blood cells (RBCs, erythrocytes), which lack central pallor. Birds and reptiles have nucleated, elliptical RBCs. It is important to know what normal looks like for the main veterinary species.

Answer 102

Answer: **Rare disease; early diagnosis improves prognosis** You need a very sensitive test if: 1. Disease is rare (e.g.: BSE) 2. Early Dx improves prognosis (e.g.: HIV in people) 3. The disease is highly lethal or consequences of missing a case are severe (e.g.: rabies, brucellosis, BSE, screw-worm, FMD, EIA) Remember that a HIGHLY SENSITIVE test will have very FEW false negatives. That means if a test is highly sensitive, you can TRUST a NEGATIVE TEST. This sounds contradictory, but it makes more sense if you review this sensitivity diagram. Sensitivity=a/(a+c). "a" are true positives. "c" are false negatives. If sensitivity is HIGH then "c" (FALSE negs) must be small. Therefore, high sensitivity means you can really trust a NEGATIVE result to be correct.

Answer 103

Answer: **Liver and muscle** In dogs and cats, damage to liver and muscle cells may cause increases in serum alanine aminotransferase (ALT). ALT is a "leakage" enzyme meaning that the enzyme is intracellular. It leaks out of cells and ultimately into the circulation following damage to the cell membrane. In other species (e.g., horses, ruminants, pigs, and birds), ALT is less useful because there are not high intracellular levels. Aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH), and glutamate dehydrogenase (GLDH) are the predominant leakage enzyme in these animals (availability is lab-dependent). The magnitude of increase of leakage enzymes may be deceiving. Severe damage to a healthy liver may result in very high levels, while low levels may be seen when significant atrophy or fibrosis of the liver is present and few cells are left. Differentiate ALT from muscle vs. liver by evaluation of the clinical picture and other serum biochemistry results. Other muscle enzymes include creatine phosphokinase (CK) and AST; and other liver enzymes are AST, SDH, GLDH, gamma glutamy! transferase (GGT), and alkaline phosphatase (ALP). Leakage enzymes do NOT provide an estimate of liver function. This is evaluated by measurement of substances dependent on the efficacy of liver function such as bile acids, blood urea nitrogen, albumin, and glucose. Enzyme activity in Hepatic Disease: https://www.merckvetmanual.com/digestive-system/laboratory-analyses-and-imaging-in-hepatic-disease-in-small-animals/enzyme-activity-in-hepatic-disease-in-small-animals?mredirectid=1181

Answer 104

Answer: **Panosteitis** This is panosteitis, an acute-onset shifting leg lameness with long bone pain most commonly seen in young (5-18 mos) medium to large breed dogs. German Shepherds are at the highest risk of developing panosteitis. Hypertrophic osteodystrophy (HOD) is a an uncommon developmental orthopedic disease of young (2-8 mos), growing dogs. Large and giant breeds, in particular the great Dane, are predisposed. It is characterized by symmetrical distal metaphyseal pain and swelling of long bones (most commonly the ulna and tibia), fever, anorexia, and depression. Hypertrophic osteopathy is a diffuse periosteal proliferative disease of long bones in dogs secondary to a neoplastic mass or other disease (e.g., heartworm Dz) in the thoracic or abdominal cavity. Multiple cartilaginous exostoses is a rare benign proliferation of bone/cartilage that can affect the metaphyseal cortical surfaces of long bones, vertebrae, and ribs in young dogs and cats. Animals may have no signs at all. Osteosarcoma is unlikely in a young dog and does not cause shifting leg lameness. {Developmental Osteopathies in Dogs and Cats} [https://www.merckvetmanual.com/musculoskeletal-system/osteopathies-in-small-animals/developmental-osteopathies-in-dogs-and-cats] https://zukureview.com/zuku-qod/navle/2193?chosen=9gnvCWj/neyRbufocBxwuQ%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=c54009a9b8-EMAIL_CAMPAIGN_2024_11_26_02_50&utm_medium=email&utm_term=0_1c9568dbdc-c54009a9b8-7334655

Answer 105

Answer: **Interruption of inhibitory neuron input from lumbar spinal cord** Schiff-Sherrington posture occurs due to interruption of inhibitory neuron input from the lumbar spinal cord. The posture is characterized by rigid forelimb extension with normal function, with concurrent hindlimb paresis and paralysis. Trauma to the spinal cord between T3-L3 results in inhibitory pathway interruption. Neurons caudal to the cervical intumescence are "released," causing excessive extensor tone in the forelimbs. This posture is not associated with prognosis of the underlying disease. Think of Schiff-Sherrington posture when you see a combination of forelimb extensor rigidity and hind limb flaccid paralysis in an animal with spinal trauma, like being hit by a car or acute intervertebral disc disease.

Answer 106

Answer: **Good prognosis for survival with surgery** This dog has a gastric dilation/volvulus (GDV) and, based on the lactate level, he has a good prognosis for survival with surgery. Plasma lactate concentration is the most important prognostic indicator in dogs with GDV. Dogs with a lactate < 6 mmol/L on presentation have a 99% survival rate with surgery. A lactate > 7.4 mmol/L at presentation predicts gastric necrosis and decreasing prognosis with high accuracy. However, comparing pre- and post-treatment lactate levels may be more predictive of survival than an initial one-time lactate measurement. A 50% or greater reduction in lactate within 12 hours of presentation carries an improved prognosis. GDV is an acute enlargement and rotation of the stomach, mostly seen in large- and giant-breed dogs. The enlarged stomach compresses the caudal vena cava, leading to hypovolemia; pushes on the diaphragm, causing respiratory dysfunction; and puts pressure on Gl contents, leading to bacterial translocation and endotoxemia. Lactate increases secondary to systemic hypotension, inflammation, and tissue necrosis. Diagnosis relies on clinical findings plus abdominal radiographs, in which the gas-filled pylorus cranial and dorsal to the fundus of the stomach creates the classic "double bubble" sign. Click here to see a good summary on GDV with images, courtesy of the American College of Veterinary Surgeons (ACVS). https://www.merckvetmanual.com/digestive-system/diseases-of-the-stomach-and-intestines-in-small-animals/gastric-dilation-and-volvulus-in-small-animals https://www.acvs.org/small-animal/gastric-dilatation-volvulus/

Answer 107

Answer: **Sarcoptes scabei** This is Sarcoptes scabei, a highly contagious mite. A positive pinnal-pedal reflex (scratching action with the dog's hind limb when the examiner firmly rubs the edge of the dog's pinna between thumb and forefinger) is seen in 82% of dogs with sarcoptic mange but observed in only 7% of dogs with pruritus caused by other diseases. Cheyletiellosis (walking dandruff) is another highly contagious mite. Unlike Sarcoptes, they have very prominent mouthparts. https://www.merckvetmanual.com/integumentary-system/mange/mange-in-dogs-and-cats?redirectid=24977

Answer 108

Answer: **Fever, petechiations, hemolytic anemia** Fever, petechiations, hemolytic anemia This cytology shows Babesia caballi, one of the causative agents of equine piroplasmosis (the other is Theileria equi - looks like a maltese cross under the microscope) and acute disease is characterized by fever, petechiations, and signs consistent with hemolytic anemia. Piroplasmosis is characterized by hemolytic anemia and is spread primarily by ixodid ticks or blood contamination. It is endemic in tropical, subtropical, and some temperate regions. It is REPORTABLE in the USA. Clinical infection can be acute, chronic, or inapparent, depending on strain, the horse's health, and geographic region. Acute clinical signs include those described here along with lethargy, anorexia, pale or icteric mucous membranes, and with worsening disease - tachycardia, tachypnea, weakness, and hemoglobinuria. Weight loss, poor performance, and partial anorexia can be seen along with mild anemia in horses with chronic piroplasmosis. Dx: Demonstrate intra-erythrocytic organisms on blood smear and/or serology. Rx: Imidocarb dipropionate and supportive care. There is a different duration of Tx depending on whether in endemic or nonendemic region (because trying to treat clinical signs in endemic region vs. clear disease in nonendemic region). Limb edema, ventricular arrhythmias, and ataxia (the latter two uncommonly) can be seen with Anaplasma phagocytophila infections in horses, along with fever, petechiations, icterus, and depression. Image courtesy of Alan R. Walker. ChGPT: Equine Granulocytic Anaplasmosis (EGA) https://www.merckvetmanual.com/generalized-conditions/equine-granulocytic-anaplasmosis/equine-granulocytic-anaplasmosis?redirectid=31747

Answer 109

Answer: **Fever, petechiations, hemolytic anemia** Fever, petechiations, hemolytic anemia This cytology shows Babesia caballi, one of the causative agents of equine piroplasmosis (the other is Theileria equi - looks like a maltese cross under the microscope) and acute disease is characterized by fever, petechiations, and signs consistent with hemolytic anemia. Piroplasmosis is characterized by hemolytic anemia and is spread primarily by ixodid ticks or blood contamination. It is endemic in tropical, subtropical, and some temperate regions. It is REPORTABLE in the USA. Clinical infection can be acute, chronic, or inapparent, depending on strain, the horse's health, and geographic region. Acute clinical signs include those described here along with lethargy, anorexia, pale or icteric mucous membranes, and with worsening disease - tachycardia, tachypnea, weakness, and hemoglobinuria. Weight loss, poor performance, and partial anorexia can be seen along with mild anemia in horses with chronic piroplasmosis. Dx: Demonstrate intra-erythrocytic organisms on blood smear and/or serology. Rx: Imidocarb dipropionate and supportive care. There is a different duration of Tx depending on whether in endemic or nonendemic region (because trying to treat clinical signs in endemic region vs. clear disease in nonendemic region). Limb edema, ventricular arrhythmias, and ataxia (the latter two uncommonly) can be seen with Anaplasma phagocytophila infections in horses, along with fever, petechiations, icterus, and depression. Image courtesy of Alan R. Walker. ChGPT: Equine Granulocytic Anaplasmosis (EGA) https://www.merckvetmanual.com/generalized-conditions/equine-granulocytic-anaplasmosis/equine-granulocytic-anaplasmosis?redirectid=31747

Answer 110

Answer: **Need orthogonal radiographic view** An orthogonal view is necessary to determine the next best step because it is not possible to determine if this hip luxation is dorsal or ventral with only the VD. Conservatively treat craniodorsal coxofemoral (hip) luxations (most common) with closed reduction and an Ehmer sling. Typically presents as a non-weight-bearing lameness, usually after blunt force trauma, (e.g., being hit by a car). Occasionally ventral luxations occur and an Ehmer sling predisposes these to re-luxation, as it positions the limb in an abducted, externally rotated position. Instead, use hobbles to prevent abduction and re-luxation. In this case closed reduction is appropriate as the injury is recent (less than 24-48 hr since it occurred). Additionally, the hip anatomy is normal, with no signs of avulsion fragments, hip dysplasia, or osteoarthritis. Closed reduction is associated with a re-luxation rate of ~50%, treated with open reduction and stabilization: e.g., toggle pinning, iliofemoral suture, capsulorrhaphy, trochanteric transposition, and prosthetic joint capsule. Risk of re-luxation after closed reduction is higher with chronic injuries or dysplastic hips, and these patients are at risk of progressive arthritis. Consider salvage options such as femoral head osteotomy or total hip replacement. Ehmer slings have a high risk of bandage complications. Carefully monitor post-reduction for sling-related injuries and instruct owners on how to monitor. Here is some useful information from the University of Illinois about closed reduction of hip luxations, and here is more helpful information from the American College of Veterinary Surgeons. https://www.merckvetmanual.com/musculoskeletal-system/arthropathies-and-related-disorders-in-small-animals/joint-trauma-in-dogs-and-cats

Answer 111

Answer: **Cerebellar hypoplasia** This is cerebellar hypoplasia, although cerebellar abiotrophy is also possible. This is a congenital, irreversible condition. Think of kittens with cerebellar hypoplasia due to in utero feline panleukopenia infection. [Merck Manual](https://www.merckvetmanual.com/generalized-conditions/feline-panleukopenia/feline-panleukopenia) MRI interpretation: Representative T1 and T2 weighted MRI images. The cerebellum is small with a resulting large collection of CSF in the vicinity. There are no other abnormalities of signal intensity. Follow this link and click additional images to see another example of [cerebellar hypoplasia in a dog.](http://mirc.veterinaryradiology.net/storage/ss1/docs/20090116144645942/MIRCdocument.xml) Radiographic interpretation and images courtesy, Dr A. Zwingenberger and Veterinary Radiology. [Cerebellar hypoplasia](https://www.merckvetmanual.com/nervous-system/congenital-and-inherited-anomalies-of-the-nervous-system/congenital-and-inherited-cerebellar-disorders-in-animals) **Cerebellar hypoplasia** is seen in kittens after in utero infection with feline panleukopenia virus. The condition is nonprogressive, and affected cats may make suitable pets. Diagnosis can be obtained antemortem using MRI. Concomitant hydrocephalus or hydranencephaly may also be seen. Cerebellar hypoplasia has also been reported in Chow Chows and is seen in association with lissencephaly in Irish Setters and Wirehaired Fox Terriers. A selective hypoplasia of the cerebellar vermis is also seen in dogs, and when combined with hydrocephalus and cyst-like dilatation of the fourth ventricle, the condition has been termed the Dandy-Walker syndrome, which may have a familial basis. An autosomal recessive deletion mutation in the very low density lipoprotein receptor (VLDLR) gene in Eurasier dogs has been identified. The cerebellar vermis may be partially or completely absent. Clinical signs are typical of a cerebellar disorder and include tremors, ataxia, and hypermetria. Occasionally, signs of head tilt and circling may also be present. Toy Fox Terrier dogs are predisposed to the Dandy-Walker form.

Answer 112

Answer: **Spirocerca lupi** A disease of dogs in the Southern U.S. and tropical climates, Spirocerca lupi (esophageal worms) make reactive granulomas of variable size in the esophageal, gastric or aortic walls. Spirocercosis may also lead to aneurysm in the thoracic aorta or an ossifying spondylitis of the posterior thoracic vertebrae. Typically asymptomatic, but large granulomas can cause esophageal obstruction. Large granulomas may become neoplastic (osteosarcoma, fibrosarcoma). Some dogs develop spondylitis or enlargement of the extremities characteristic of hypertrophic osteopathy. All of the other choices are gastric parasites. Ollulanus tricuspis is an uncommon gastric parasite of cats. Physaloptera spp. is a stomach worm that may cause vomiting, anorexia, dark feces in dogs and cats. Haemonchus spp., Ostertagia spp. and Trichostrongylus spp. are found in the abomasum of ruminants. Gasterophilus spp. are the larvae of horse bot flies, found in the stomach of horses. ChGPT: **Spirocerca lupi** https://www.merckvetmanual.com/digestive-system/gastrointestinal-parasites-of-small-animals/spirocerca-lupi-in-small-animals ChGPT: **Hypertrophic osteopathy (HO)** https://www.merckvetmanual.com/musculoskeletal-system/osteopathies-in-small-animals/hypertrophic-osteopathy-in-dogs [Zuku full question](https://zukureview.com/zuku-qod/navle/1399?chosen=kMtTkDVBpgMaAPwEkgJewA%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=d6168c1852-EMAIL_CAMPAIGN_2023_11_29_02_50&utm_medium=email&utm_term=0_1c9568dbdc-d6168c1852-%5BLIST_EMAIL_ID%5D)

Answer 113

Answer: **Chorioptic mange** This is chorioptic mange - the most common mite in horses. Chorioptes equi is characterized by long legs and short pedicles. Most commonly it is found on the lower limbs (esp. the hind legs), where it causes pruritus. Chorioptes infestation is often seen as a component of pastern dermatitis, a multi-factorial disease that is very common in draft horses, especially those breeds with heavy feathering. In non-feathered breeds, it can occur elsewhere on the body. It is also called scratches, greasy heel, and dermatitis verrucosa. It is a surface mite and causes extreme pruritus. It is very contagious horse-to-horse (occasionally on fomites) so if one in a herd has it, the others probably do as well. Tx: Ideal to remove the feathers (clients rarely allow this) then use some combination of topical permethrin or coumaphos, systemic or topical ivermectin/moxidectin, selenium sulphide shampoos, or topical products w/ fipronil (usually used in small animal). Here's a great review of chorioptic mange, with images, from the University of Liverpool. [Mange in Horses](https://www.merckvetmanual.com/integumentary-system/mange/mange-in-horses) ChGPT: **Mange in horses, also known as acariasis**

Answer 114

Answer: **Common opening of the pancreatic and common bile ducts into duodenum** In cats, there is a common opening of the pancreatic and common bile ducts into the duodenum. It is thought that this may predispose them to ascending cholangitis and pancreatitis after vomiting associated with inflammatory bowel disease, resulting in extrahepatic biliary obstruction. Other possible etiologies of EHBO include neoplasia, biliary stricture, duodenal obstruction, diaphragmatic hernia, and parasitic infection. In all cases, there is a lack of bile entry into the intestinal tract, leading to decreased absorption of fat and fat soluble vitamins such as vitamin K, potentially resulting in coagulopathies. Except in transient cases that are related to acute pancreatitis, need surgical intervention to relieve the obstruction as well as appropriate supportive care, antimicrobial treatment, and vitamin K administration. Click here to see a good summary of extrahepatic biliary obstruction with images, courtesy of the American College of Veterinary Surgeons (ACVS). [Extrahepatic Bile Duct Obstruction in Small Animals](https://www.merckvetmanual.com/digestive-system/hepatic-diseases-of-small-animals/extrahepatic-bile-duct-obstruction-in-small-animals?mredirectid=1156) ChGPT: **Extrahepatic bile duct obstruction (EHBDO) in small animals**

Answer 115

Answer: **Thoracic radiographs to evaluate for congestive heart failure** This is a classic presentation for dilated cardiomyopathy (DCM); perform thoracic radiographs to evaluate for congestive heart failure. Perform electrocardiogram to better assess the cardiac rythm. Use echocardiography to confirm the diagnosis. Consider veterinary point of care ultrasound (POCUS) to assess for pleural effusion and alveolar infiltrates. Tx to control arrhythmia and diminish clinical signs. Therapy may include diuretics (e.g., furosemide), positive inotropes (e.g., pimobendan), angiotensin converting enzyme inhibitors (e.g., enalapril) and antiarrhythmics (e.g., diltiazem, sotalol). Px is guarded, especially for Dobermans - with Tx may live six months to two years. Large and giant breeds are at increased risk, including Irish wolfhounds and great Danes. Boxers can develop arrhythmogenic right ventricular cardiomyopathy, distinct from DCM. Dobermans have two genetic mutations that can lead to development of DCM: PDK4 and DCM2. Each mutation independently can lead to DCM: dogs affected with both are 30 times more likely to develop DCM than a normal dog. [Dilated Cadiomyopathy in Dogs and Cats](https://www.merckvetmanual.com/circulatory-system/cardiomyopathy-in-dogs-and-cats/dilated-cardiomyopathy-in-dogs-and-cats) ChGPT: **Dilated cardiomyopathy (DCM)**

Answer 116

Answer: **Diabetic remission** This cat is in diabetic remission, which may be achieved in up to 30% of cats; characterized by resolution of clinical signs weeks to months after beginning insulin and diet treatment. Clinical diabetes mellitus may or may not recur in the future. One factor associated with diabetes remission in cats is feeding a low-carbohydrate diet. Persistent fasting hyperglycemia and glucosuria are consistent with a diagnosis of diabetes mellitus. [Diabetes Melitus in Dogs and Cats](https://www.merckvetmanual.com/endocrine-system/the-pancreas/diabetes-mellitus-in-dogs-and-cats) ChGPT: **Comprehensive NAVLE Preparation: Diabetes Mellitus in Dogs and Cats** PDF: **Managing Feline Diabetes current perspectives**

Answer 117

Answer: **Acinar cell atrophy** This dog has exocrine pancreatic insufficiency (EPI) due to pancreatic acinar atrophy (PAA). PAA is the most common cause of EPI in German shepherd dogs and is considered hereditary. It is also seen in rough-coated Collies and Eurasians. In cats and older dogs EPI is most commonly caused by chronic pancreatitis. Serum TLI is the best test for EPI in dogs and cats. A significantly low (< 2.5 ug/L) fasting TLI is diagnostic for EPI. In EPI there is impaired synthesis and release of digestive enzymes by pancreatic acinar cells, resulting in maldigestion, weight loss/failure to gain weight, diarrhea, and polyphagia. Concurrent small intestinal dysbiosis and cobalamin deficiency are common. Treat with oral enzyme replacement and cobalamin supplementation if deficient. Patients with EPI require life-long enzyme replacement. Prognosis is good with appropriate treatment. [Exocrine Pancreatic Insufficiency in Dogs and Cats](https://www.merckvetmanual.com/digestive-system/the-exocrine-pancreas/exocrine-pancreatic-insufficiency-in-dogs-and-cats?query=exocrine%20pancreatic%20insufficiency) ChGPT: **Exocrine pancreatic insufficiency (EPI)** [Serum Trypsine-like Immunoreactivitylaboratory](https://vetmed.tamu.edu/gilab/service/assays/tli/)

Answer 118

Answer: **Hyperphosphatemia, non-regenerative anemia** This is chronic kidney disease; look for hyperphosphatemia and non-regenerative anemia in addition to renal azotemia. Chronic kidney disease is a common cause of polyuria, polydipsia, anorexia, and weight loss in older cats. Stage chronic kidney disease in dogs and cats based on the International Renal Interest Society (IRIS) guidelines. Staging is based on degree of azotemia and presence of hypertension and proteinuria. This cat has IRIS stage 3 chronic kidney disease. Perform blood pressure measurement and urine protein quantification to further substage the disease. [Renal Dysfunction in Small Animals](https://www.merckvetmanual.com/urinary-system/noninfectious-diseases-of-the-urinary-system-in-small-animals/renal-dysfunction-in-small-animals?ruleredirectid=463) ChGPT: **Renal dysfunction in small animals** [IRIS Staging of CKD](http://www.iris-kidney.com/guidelines/staging.html)

Answer 119

Answer: **Strict hypoallergenic diet trial** Recommend a strict hypoallergenic diet trial to definitively diagnose cutaneous adverse food hypersensitivity/reaction (CAFR). Intradermal skin or serum allergen testing is not reliable for diagnosis of CAFR. Clinical signs of food-induced and non-food-induced hypersensitivities (i.e., atopic dermatitis) are clinically indistinguishable so perform the hypoallergenic food trial before considering allergy testing otherwise it is difficult to interpret the results. A positive response (i.e., improvement in signs) to an appropriate 8-week elimination diet using either a commercial hydrolyzed protein diet or a true novel diet with strict compliance plus a positive challenge trial (refeeding previous diet) at the end confirms the Dx of CAFR. If there's no change with a proper elimination diet, proceed to allergy testing for non-food-induced atopic dermatitis. The only Tx for CAFR is elimination of the food(s) causing the reaction. Also check for, and Tx, any secondary conditions such as skin infections (bacterial and/or fungal) or parasites (such as sarcoptic mange). Also often need to use antipruritic measures (oral antihistamines, bathing). In very severely affected and uncomfortable patients, add a 1-to 2-week (max) course of corticosteroids. [Cutaneous Food Allergy in Animals](https://www.merckvetmanual.com/integumentary-system/food-allergy/cutaneous-food-allergy-in-animals) ChGPT: **Cutaneous food allergies**

Answer 120

Answer: **Ureteroliths** This patient most likely has ureterolithiasis with a condition known as "big kidney, little kidney," which has caused acute renal failure. In this condition, ureteral obstruction occurs at an earlier time on one side resulting in permanent renal damage and scarring. Then subsequent obstruction of the contralateral kidney results in acute renal failure due to the diminished function of the previously damaged kidney. The most common composition of nephroliths/ureteroliths in cats is calcium oxalate. Ureteral obstruction is most commonly unilateral and may be found incidentally. Bilateral ureteral obstruction is a cause of acute renal failure. [Urolithiasis in Small Animals](https://www.merckvetmanual.com/urinary-system/noninfectious-diseases-of-the-urinary-system-in-small-animals/urolithiasis-in-small-animals) ChGPT: **Urolithiasis**

Answer 121

Answer: **Megaesophagus** This is megaesophagus, as highlighted by yellow arrows on the image above. Megaesophagus can be idiopathic or secondary to other disorders such as myasthenia gravis, heavy metal toxicity, or Addison disease. Other causes of megaesophagus include esophagitis and esophageal stricture or diverticulum. To further evaluate for a primary etiology perform a complete neurologic examination and complete bloodwork including adrenal testing. The history in this case is consistent with regurgitation, even though the owner describes "vomiting." Always closely question an owner to distinguish between vomiting and regurgitation as often owners will describe both problems in the same way. A work-up for vomiting in a dog with regurgitation is likely to be low-yield and will likely fail to identify the primary problem. [Dilatation of the Esophagus in Small Animals](https://www.merckvetmanual.com/digestive-system/diseases-of-the-esophagus-in-small-animals/dilatation-of-the-esophagus-in-small-animals?qt=megaesophagus&alt=sh) ChGPT: **Esophageal dilatation**

Answer 122

Answer: **Paired plasma and effusion potassium and creatinine** This cat has a traumatic urinary bladder rupture (uroabdomen/-peritoneum) best diagnosed with paired serum and effusion potassium and creatinine measurements. Uroperitoneum is a surgical emergency. In cats, a fluid to blood creatinine ratio of 2:1 (same in dogs, foals) and fluid to blood potassium ratio of 1.9:1 (1.4:1 in dogs; not done in foals) is diagnostic for uroabdomen. BUN measurement is often not helpful because it readily equilibrates across the peritoneum. High rise syndrome is a common polytrauma in cats, characterized by a triad of thoracic, craniofacial, and limb injuries. Stabilize life-threatening thoracic trauma such as pneumothorax, pulmonary contusions, and diaphragmatic hernia before surgical treatment of orthopedic trauma. Uroperitoneum also occurs in newborn foals (more common in males, often associated with birth or prolonged recumbency in the NICU). Affected foals typically present within a couple days of birth with abdominal straining and distention, tachypnea, and decreased nursing with depression. Labs: hyponatremia, hypochloremia, hyperkalemia, and azotemia. Click here to see a classic ruptured bladder on ultrasound. [Trauma in Emergency Medicine in Small Animals](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/specific-diagnostics-and-therapy/trauma-in-emergency-medicine-in-small-animals?autoredirectid=20423) [Uroperitoneum in Foals](https://www.merckvetmanual.com/urinary-system/noninfectious-diseases-of-the-urinary-system-in-large-animals/uroperitoneum-in-foals)

Answer 123

Answer: **Mediastinum** This cat has a cranial mediastinal mass. There is a small volume pleural effusion causing widened fissure lines and retraction of the lung lobes. There is focal widening of the cranial mediastinum on the ventrodorsal projection, which is apparent as a soft tissue opacity flattening the margin of the cranial lung lobe on the lateral projection. The trachea is mildly elevated and narrowed in this area. The most common causes of a cranial mediastinal mass in cats are thymoma and thymic lymphoma. This cat was diagnosed with lymphoma. Rule out FeLV in cats with this condition. [Feline Leukemia Virus Disease](https://www.merckvetmanual.com/generalized-conditions/feline-leukemia-virus/feline-leukemia-virus-disease?autoredirectid=17869) Click here to see [normal feline thoracic radiographs](https://vetmed.illinois.edu/imaging_anatomy/feline/thorax/ex03/thor03-f%20.html) Radiographic interpretation and images courtesy, Dr A. Zwingenberger and [Veterinary Radiology](http://mirc.veterinaryradiology.net/storage/ss1/docs/20101123184336307/1/MIRCdocument.xml) Normal radiograph links courtesy, Imaging Anatomy Univ. of Illinois Vet Med. **Feline Leukemia Virus (FeLV) Disease: NAVLE Study Guide** Definitions and Causative Agents • Feline Leukemia Virus (FeLV): A retrovirus causing immunosuppression, anemia, and neoplasia in cats. • Classification: Retrovirus, Oncovirinae family. • Genome: Enveloped virus with a positive-sense single-stranded RNA genome, requiring a double-stranded DNA intermediate (provirus stage) for replication. Pathogenesis • Virus Subgroups: • FeLV-A: Archetypal form, primary infection. • FeLV-B: Increases neoplastic diseases. • FeLV-C: Associated with severe anemia. • FeLV-T: Infects T lymphocytes, leading to immunodeficiency. • Lifecycle: Oronasal replication in lymphoid tissue, primary viremia phase, systemic spread to spleen, lymph nodes, bone marrow, and other tissues. Secondary viremia involves bone marrow transmission with leukocytes and platelets in peripheral blood. • Infection Outcomes: Abortive, regressive, or progressive. Clinical Findings • Symptoms: • Acute Stage: Mild fever, malaise, lymphadenopathy, cytopenia. • Chronic Stage: Immunosuppression, anemia, lymphomas, reproductive issues, secondary infections. • Disease Associations: Chronic gingivostomatitis, systemic vasculitis, glomerulonephritis, polyarthritis, anemia, leukemia, neurologic disorders, FeLV-associated enteritis. Diagnosis • Testing: • Point-of-Care (POC) ELISA/RIM: Detects FeLV antigen. • Confirmatory Tests: Microplate ELISA, PCR assay for proviral DNA, immunofluorescent antibody (IFA) testing. • Quantitative PCR: Distinguishes between regressive and progressive infections. • Neoplasia Diagnosis: Cytologic examination, bone marrow analysis, biopsy with histologic examination. Treatment and Prognosis • Supportive Care: High-quality nutrition, regular preventive healthcare. • Antiretroviral Drugs: Limited evidence; zidovudine may reduce viral loads but has side effects. • Interferons: Mixed results; some benefit from parenteral feline interferon omega. • Management: Strict indoor environment, routine vaccinations, parasite prevention, early treatment of secondary infections. Prevention and Control • Vaccination: Effective but does not prevent FeLV in already infected cats. • Testing: Regular testing for at-risk cats, new acquisitions, and before blood donation. • Management: Prevent contact with infected cats, good husbandry practices, and stress minimization. Key Points • Infection Management: Early identification, supportive care, and prevention of secondary infections are crucial. • Life Expectancy: Varies; average survival time post-diagnosis is 2.4 years, with high mortality within 3 years. For further detailed information, please refer to the Merck Veterinary Manual article on FeLV.

Answer 124

Answer: **Fever, petechiations, hemolytic anemia** This cytology shows Babesia caballi, one of the causative agents of equine piroplasmosis (the other is Theileria equi - looks like a maltese cross under the microscope) and acute disease is characterized by fever, petechiations, and signs consistent with hemolytic anemia. Piroplasmosis is characterized by hemolytic anemia and is spread primarily by ixodid ticks or blood contamination. It is endemic in tropical, subtropical, and some temperate regions. It is REPORTABLE in the USA. Clinical infection can be acute, chronic, or inapparent, depending on strain, the horse's health, and geographic region. Acute clinical signs include those described here along with lethargy, anorexia, pale or icteric mucous membranes, and with worsening disease - tachycardia, tachypnea, weakness, and hemoglobinuria. Weight loss, poor performance, and partial anorexia can be seen along with mild anemia in horses with chronic piroplasmosis. Dx: Demonstrate intra-erythrocytic organisms on blood smear and/or serology. Rx: Imidocarb dipropionate and supportive care. There is a different duration of Tx depending on whether in endemic or nonendemic region (because trying to treat clinical signs in endemic region vs. clear disease in nonendemic region). Limb edema, ventricular arrhythmias, and ataxia (the latter two uncommonly) can be seen with Anaplasma phagocytophila infections in horses, along with fever, petechiations, icterus, and depression. [Equine Granulocytic Anaplasmosis](https://www.merckvetmanual.com/generalized-conditions/equine-granulocytic-anaplasmosis/equine-granulocytic-anaplasmosis?redirectid=31747) ChGPT: **Equine Granulocytic Anaplasmosis (EGA)** is an infectious, noncontagious, seasonal disease in horses caused by the tick-transmitted bacterium Anaplasma phagocytophilum. This pathogen infects neutrophils and occasionally eosinophils, leading to a range of clinical signs from mild fever to severe systemic illness. Etiology and Transmission: • Causative Agent: Anaplasma phagocytophilum, a rickettsial bacterium. • Vectors: Transmitted primarily by ticks of the Ixodes species, including I. pacificus (western black-legged tick), I. scapularis, I. ricinus, and I. persulcatus. • Hosts: Infects a wide range of hosts, including horses, burros, dogs, llamas, rodents, and humans (where the disease is known as human granulocytic anaplasmosis). • Seasonality: In regions like California, cases occur predominantly in late fall, winter, and spring, correlating with tick activity. Pathophysiology: After transmission through a tick bite, A. phagocytophilum enters neutrophils and forms intracytoplasmic inclusion bodies called morulae. The presence of the bacterium within neutrophils leads to systemic inflammation and clinical signs associated with EGA. Clinical Presentation: • Incubation Period: Approximately 1–3 weeks post-infection. • Clinical Signs: • Foals (<1 year): May exhibit only fever. • Yearlings (1–3 years): Fever, depression, mild limb edema, and ataxia. • Adults and Geriatric Horses: Fever (103°–104°F; can reach up to 107°–108°F), partial anorexia, depression, reluctance to move, limb edema, petechiation, and icterus. Fever typically peaks around day 5 and can persist for 6–12 days. • Hematologic Findings: Leukocytopenia or pancytopenia with moderate to severe thrombocytopenia. • Lesions: Gross petechiation, ecchymoses, and edema in the subcutis and fascia, predominantly affecting the legs. Diagnosis: • Clinical Evaluation: Consider EGA in horses from endemic areas presenting with acute fever and associated clinical signs, especially during peak tick activity seasons. • Laboratory Testing: • Blood Smear: Giemsa or Wright-Leishman stained smears may reveal morulae within neutrophils. • PCR Assay: Detection of A. phagocytophilum DNA in unclotted blood or buffy coat samples. • Serology: Indirect fluorescent antibody tests may be negative early in the disease; a four-fold rise in antibody titers over 2–4 weeks can retrospectively confirm the diagnosis. Treatment: • Antibiotic Therapy: Oxytetracycline is highly effective against A. phagocytophilum. Administer intravenously at 6.6 mg/kg once daily for 5–7 days. Dilution in saline can reduce gastrointestinal side effects. • Supportive Care: Ensure adequate hydration and monitor for secondary infections or complications. Prognosis: With prompt and appropriate treatment, the prognosis for EGA is generally favorable. Most horses respond rapidly to oxytetracycline therapy. However, if left untreated, the disease can lead to more severe complications, especially in older horses. Prevention: • Tick Control: Implement measures to reduce tick exposure, such as the use of acaricides, environmental management to decrease tick habitats, and regular inspection and removal of ticks from horses. • Monitoring: Be vigilant for clinical signs of EGA, especially during seasons of high tick activity, and in horses residing in or traveling to endemic areas. Understanding the detailed aspects of Equine Granulocytic Anaplasmosis, including its etiology, pathophysiology, clinical presentation, diagnostic methods, treatment protocols, and preventive measures, is crucial for veterinary professionals preparing for the NAVLE and for effective clinical practice.

Answer 125

Answer: **Pour-on eprinomectin** Treat this chorioptic mange (also called "leg mange") with pour-on eprinomectin or moxidectin (both approved for lactating dairy cattle). Pour-on doramectin and ivermectin as well as eprinomectin and moxidectin are approved for this use in beef cattle. Isolation is not practical because of the contagious nature of the disease. Assume all animals in the group are infested and treat accordingly. Classic chorioptic mange is seen in winter in the northeastern U.S. Cattle present with crusty, pruritic skin disease around the perineum and caudal upper thigh. On skin scrape, look for long legs and short unsegmented pedicles in chorioptes. In contrast to the short legs and long unsegmented pedicles of sarcoptes. **Chorioptic mange in Cattle** [Chorioptic Mange in Cattle](https://www.merckvetmanual.com/integumentary-system/mange/mange-in-cattle#Psoroptic-Mange_v3279754) Chorioptic mange in cattle is caused by infestation with Chorioptes bovis or C texanus. Species of Chorioptes are not host specific, and C bovis can be found on domestic ruminants and horses throughout the world. Chorioptic mange caused by infestation with C bovis is the most common type of mange in cattle in the US. C texanus has been reported on cattle from Brazil, China, Germany, Israel, Japan, Malaysia, South Korea, and the US. C bovis live on the skin surface and do not burrow. Transmission is by direct contact of infested and naive hosts. The mites can live off their host for up to 3 weeks and can be transmitted to cattle via contact with contaminated fomites and housing. C bovis likely feeds on sloughed skin cells and other surface debris. While feeding, C bovis irritates the host skin, causing abrasions that become contaminated with secretions and feces from the mites. Most cattle are subclinically infested with C bovis. However, the mites may cause an allergic, exudative, mildly pruritic, flaky dermatitis. Lesions include nodules, papules, crusts, and ulcers that typically begin at the pastern and spread up the legs to the udder, scrotum, tail, and perineum. Self-trauma and alopecia may be evident. Lesions and clinical signs appear in late winter and spontaneously regress during summer months. Chorioptic mange is less pathogenic than sarcoptic or psoroptic mange in cattle. In the US, the following treatments are approved for use against C bovis at the labeled dosages: • pour-on doramectin • eprinomectin (both pour-on and injectable formulations) • pour-on moxidectin Hot lime sulfur dips or sprays are labeled for use against chorioptic mites and may be used following the label directions for species-specific dilution. Lime sulfur treatment should be repeated at 12-day intervals if needed. Of these, the pour-on formulations of eprinomectin and moxidectin as well as hot lime sulfur are approved for use on dairy animals in the US. [Zuku question](https://zukureview.com/zuku-qod/navle/2252?chosen=2OnvvQLpJqXf8PSYloaLUw%3D%3D&utm_source=Zukureview+Subscribers&utm_campaign=8f5cce31be-EMAIL_CAMPAIGN_2024_12_25_02_51&utm_medium=email&utm_term=0_1c9568dbdc-8f5cce31be-7334655)

Answer 126

Answer: **Coelom** This owl has a coelomic mass. There is a large soft tissue opacity mass occupying the majority of the coelom. On survey radiographs, the right wing amputation is evident. The bird's body condition is thin. The heart appears mildly enlarged. The proventriculus is displaced ventrally, and the ventriculus is not clearly seen. The contrast radiograph reveal a ventrally displaced proventriculus, with the intestines wrapped peripherally around the mass. The brush border visible on the mucosal surface is normal. The intestinal tract appears to be patent with barium present in the cloaca at 30 min. Necropsy images from this case. [Miscellaneous Diseases of Pet Birds](https://www.merckvetmanual.com/exotic-and-laboratory-animals/pet-birds/miscellaneous-diseases-of-pet-birds) [Cecal impaction](http://mirc.veterinaryradiology.net/storage/ss1/docs/20090428155125053/MIRCdocument.xml)

Answer 127

Answer: **Coelom** This owl has a coelomic mass. There is a large soft tissue opacity mass occupying the majority of the coelom. On survey radiographs, the right wing amputation is evident. The bird's body condition is thin. The heart appears mildly enlarged. The proventriculus is displaced ventrally, and the ventriculus is not clearly seen. The contrast radiograph reveal a ventrally displaced proventriculus, with the intestines wrapped peripherally around the mass. The brush border visible on the mucosal surface is normal. The intestinal tract appears to be patent with barium present in the cloaca at 30 min. Necropsy images from this case. [Miscellaneous Diseases of Pet Birds](https://www.merckvetmanual.com/exotic-and-laboratory-animals/pet-birds/miscellaneous-diseases-of-pet-birds) [Cecal impaction](http://mirc.veterinaryradiology.net/storage/ss1/docs/20090428155125053/MIRCdocument.xml)

Answer 128

Answer: **Amblyomma spp ticks** *Amblyomma spp.* are vectors for *Ehrlichia ruminatium (formerly Cowdria ruminatium)*, the causative agent of heartwater disease in ruminants. The clinical progression of this case and the pericardial effusion seen on necropsy (as identified by the blue arrow) are classical for acute heartwater disease. Animals may just be found dead with peracute disease. [Amblyomma spp](https://www.merckvetmanual.com/integumentary-system/ticks/amblyomma-spp?query=amblyomma%20spp) [Heartwater](https://www.merckvetmanual.com/generalized-conditions/heartwater/heartwater?autoredirectid=24165) Definitive diagnosis typically requires necropsy with microscopic evaluation of stained brain tissue. This disease is endemic in parts of Africa and the Caribbean but is considered a foreign animal disease in the mainland Americas. Dermacentor spp. are vectors for Babesia caballi in horses, Anaplasma marginale in cattle, Rickettsia rickettsii (Rocky Mountain spotted fever), Powassan virus, as well as the agents of Q fever and tularemia, among other infectious diseases throughout the world. [Dermacentor](https://www.merckvetmanual.com/integumentary-system/ticks/dermacentor-spp) Face flies (Musca autumnalis) are an important vector for eyeworm (Thelazia spp.) and Mycoplasma bovis, one agent of infectious bovine keratoconjunctivitis of ruminants. [Eye worms of large animals](https://www.merckvetmanual.com/eye-diseases-and-disorders/eyeworm-disease/eyeworms-of-large-animals?redirectid=27601) [Infectious keratoconjunctivitis in Cattle and Small Ruminants](https://www.merckvetmanual.com/eye-diseases-and-disorders/infectious-keratoconjunctivitis/infectious-keratoconjunctivitis-in-cattle-and-small-ruminants?autoredirectid=23792&redirectid=28048&redirectid=27602) Horseflies (Tabanid spp.) can be vectors for bovine leukosis virus, the cause of enzootic bovine leukosis and lymphosarcoma. [Bovine leukosis](https://www.merckvetmanual.com/generalized-conditions/bovine-leukosis/bovine-leukosis?autoredirectid=20435) **Comprehensive List of Important Information on Heartwater** Etiology and Transmission 1. Causative Agent: • Ehrlichia ruminantium (formerly Cowdria ruminantium). • Transmitted by Amblyomma ticks through transstadial transmission. Pathogenesis 1. Infection Process: • Tick saliva introduces the pathogen. • Replicates in regional lymph nodes, then disseminates via the bloodstream to endothelial cells, especially in the brain. Clinical Findings 1. Symptoms: • Peracute: Sudden death, respiratory distress, convulsions. • Acute: Anorexia, depression, congested mucous membranes, nervous signs (e.g., hyperesthesia, high-stepping gait), terminal opisthotonus, convulsions. Diagnosis 1. Methods: • Clinical signs, “brain squash smear” stained with Giemsa. • PCR and immunoperoxidase staining. Treatment 1. Medications: • Oxytetracycline (10-20 mg/kg), doxycycline (2 mg/kg). • Supportive therapy: corticosteroids, diazepam. Prevention 1. Vaccination and Control: • Vaccination with infected sheep blood. • Tick control measures. • Chemoprophylaxis with oxytetracycline injections. For detailed information, refer to the original Merck Veterinary Manual article.

Answer 129

Answer: **Antigen-antibody complex type III** In type Ill reactions such as purpura hemorrhagica, antigen-antibody complexes are deposited on the endothelium, stimulating complement and a neutrophilic inflammatory response and vascular damage. The petechiae and distal limb edema in this horse are consistent with vasculitis. Classic type Ill diseases include: Glomerulonephritis Hypersensitivity pneumonitis (think moldy hay) Purpura hemorrhagica (think post-strangles infection, but possible with other infections as well) Anterior uveitis Image courtesy of Nora Grenager, VMD, DACVIM. **Type III Hypersensitivity Reactions** A type Ill hypersensitivity reaction is the deposition of antigen-antibody complexes (immune complexes) in tissues or small blood vessels, which activate complement in situ and cause acute inflammation. This activation results in the production of peptides (complements 3a and 5a [C3a and C5a]) that are chemotactic for neutrophils. The neutrophils are unable to ingest any complexes that are bound to the blood vessel walls, and they release their granule contents in the tissue. These granules contain enzymes and oxidants that cause severe tissue damage. The most frequently affected sites of immune complex deposition are the joints, skin, kidneys, lungs, and brain. A prerequisite for the development of immune complex disease is the persistent presence of soluble antigen and antibody. These form insoluble immune complexes that become trapped on the basement membrane of small blood vessels. These antigens may persist for a number of reasons, including chronic infections and certain cancers, especially lymphoreticular neoplasms. Chronic antigen exposure may also occur with inhaled antigens, and, in such cases, immune complexes can form in the alveolar walls. Lastly, some animals respond to self-antigens, which then act as a source of chronic antigenic exposure. In many cases, the origin of the antigen within these immune complexes cannot be determined. The location of the immune complexes is largely determined by the route through which antigen enters the body. Inhaled antigens give rise to a pneumonitis, antigens that enter through the skin cause local skin lesions, and antigens that access the bloodstream form immune complexes that are deposited in renal glomeruli or joints. Clinical signs are therefore variable but may include the following: • fever • cutaneous signs and vasculitis (such as erythema multiforme) • polyarthritis (shifting-leg lameness or painful, swollen joints) Other clinical signs may include ataxia; behavior changes; renal insufficiency (proteinuria, isosthenuria, polydipsia, polyuria), or nonspecific clinical signs such as vomiting, diarrhea, or abdominal pain. Diagnosis is based on the exclusion of more common causes of clinical signs. Supporting evidence to confirm the diagnosis may be gathered in several ways: • establishing a temporal relationship if a drug or infectious agent is suspected as the cause • identifying chronic infections or malignancies • performing histopathologic and immunohistochemical examinations of biopsies to identify immune-mediated vasculitides or nephritis Treatment should include supportive care, removal of the causative agent, or treatment of the underlying disorder, such as the following: • appropriate antimicrobial treatment for bacterial infections • surgical drainage of abscesses or infected tissue • treatment for heartworm disease • withdrawal of the offending drugs Immunosuppressive therapy may be needed to prevent the continued deposition of immune complexes. [Type III](https://www.merckvetmanual.com/immune-system/immunologic-diseases/hypersensitivity-diseases-in-animals#Bovine-Neonatal-Pancytopenia_v48829507)

Answer 130

Answer: **B - Review infectious bovine rhinotracheitis (IBR) vaccination protocols** Evaluation of the herd vaccination program is a top priority to prevent infectious bovine rhinotracheitis (IBR) with pustular vulvovaginitis from occurring again. Evaluating the herd biosecurity protocol is also important to prevent introduction of NEW cases. IBR is a common infection in cattle. Infected animals develop fibrinonecrotic plaques at the site of inoculation and, from there, the virus ascends to the regional ganglia and becomes latent. During stressful episodes, recrudescence and shedding of latent virus occurs, perpetuating infection in herds. There are many vaccine products and protocols to help prevent outbreaks. There are several different types BR virus with different tissue specificities. One type causes mucosal lesions and respiratory or vaginal infections. A second type primarily causes abortion, and a third causes fatal nonsuppurative encephalitis in calves. IBR is identifiable by the fibrinonecrotic plaques on the mucosal eithelium, and may be confirmed by collection of nasal or ocular swabs for virus isolation, ELISA, or fluorescent antibody testing. [Viral Infections Associated with Bovine Respiratory Disease Complex in Cattle](https://www.merckvetmanual.com/respiratory-system/bovine-respiratory-disease-complex/viral-infections-associated-with-bovine-respiratory-disease-complex-in-cattle?mredirectid=1755)

Answer 131

Answer: **B - Left side of the neck** Palpate and visualize (as it passes down) the nasogastric tube in the left side of the neck. The esophagus runs down the left side of the horse's neck. It is NOT possible to see or safely palpate it in the larynx or oropharynx. It is critical to confirm proper placement prior to administration of fluids or medications through the NG tube. Other methods to confirm that the NG tube is in the stomach: 1) Blow into the end and have an assistant auscult the stomach with a stethoscope. 2) Most patients cough if the tube is placed into the trachea; however, this is NOT fool-proof. Sedated or very sick patients, or those in which a very small diameter tube is used, may not cough. 3) Negative pressure upon aspiration is a sign of being in the stomach. However, can also get negative pressure if the tube is up against soft tissue (in the lung or esophagus) so is not definitive. Do NOT attempt to suck fluid out of the stomach - personnel can become very sick from the possible contents.

Answer 132

Answer: **Treat the entire group with an anthelmintic** Treat the entire group with an appropriate anthelmintic for this lungworm infection (verminous pneumonia) caused by Dictyocaulus viviparous. Seen mostly in yearlings on pasture in the summer and fall, the primary clinical sign is coughing. Those not showing clinical signs may still be subclinically infected and benefit from treatment. Products used to treat lungworms also impact Gl nematodes, so treating an entire group will impact gastrointestinal nematode refugia and anthelminitic resistance. This should be factored into your treatment decisions. Diagnosis is by finding larvae (not eggs) in feces or adult worms in the airways on necropsy. 4- Ipomeanol toxicity from moldy sweet potatoes or Perilla mint can present similarly but necropsy shows pulmonary edema and emphysema. [Treatment of Lungworm](https://www.merckvetmanual.com/respiratory-system/lungworm-infection/lungworm-infection-in-animals?autoredirectid=16768#Diagnosis_v3293039) [Lungworm infection in Animals](https://www.merckvetmanual.com/respiratory-system/lungworm-infection/lungworm-infection-in-animals?autoredirectid=16768) [Ipomeanol toxicity](https://www.merckvetmanual.com/respiratory-system/non-infectious-respiratory-system-diseases-in-cattle/4-ipomeanol-toxicosis-moldy-sweet-potato-and-perilla-ketone-toxicosis-purple-mint-toxicosis-in-cattle?mredirectid=1758)

Answer 133

Answer: **Upper left** You are looking at an iliac fracture in the UPPER LEFT quadrant. Click here to see the left ilial fracture indicated with an arrow. Generally, when you assess pelvic rads after trauma, you are looking for pelvic fractures, femoral fractures, (especially head-and-neck fractures) or hip dislocation/luxation (usually cranio-dorsal). [Fractured Limbs](https://www.acvs.org/small-animal/fractured-limbs/) [Hip Luxations](https://www.acvs.org/small-animal/hip-luxation/) [Click here to see a radiograph of hip dislocation in a dog](https://www.merckvetmanual.com/multimedia/image/hip-luxation) Sometimes, the priorities of triage require you to accept less-than-optimal radiograph positioning in the service of rapid assessment. [Emergengy Medicine in Animals](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/emergency-medicine-introduction/emergency-medicine-in-animals) The visible space evident at the sacroiliac junction on the upper right is not a subluxation, it is simply poor positioning: a common hazard when taking radiographs on an awake dog. Ref: The American College of Veterinary Surgeons, Small Animal Surgery Topics. Image courtesy of Dr. Scot Nachbar. [Small Animal Topics](https://www.acvs.org/topics/?_animal_type=small-animal)

Answer 134

Answer: **Salmonella typhimurium** Salmonella typhimurium is associated with rectal strictures in growing pigs. Caused by an ulcerative proctitis that damages rectal tissue. Can see large numbers of cases. Can see sporadic rectal strictures as a sequelae to rectal prolapse. Follow this link to see a Merck image of [rectal prolapse in a sheep.](https://www.merckvetmanual.com/multimedia/image/rectal-prolapse-sheep) [Intestinal spirochetosis](https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/intestinal-spirochetosis-in-pigs) is a post-weaning diarrhea seen in the ABSENCE of Brachyspira (Serpulina) hyodysenteriae (swine dysentery), but similar in presentation to it. This syndrome is being recognized more frequently worldwide. [Rectal Strictures in Pigs](https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/rectal-strictures-in-pigs) [Rectal Prolapse in Animals](https://www.merckvetmanual.com/digestive-system/diseases-of-the-rectum-and-anus/rectal-prolapse-in-animals?redirectid=31728) [Swine dysentery](https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/swine-dysentery)

Answer 135

Answer: **Multiple myeloma** This is multiple myeloma (MM), a malignancy of plasma cell origin. Malignant plasma cells arise from bone marrow and produce immunoglobulins (Ig), resulting in hyperglobulinemia. Hyperglobulinemia causes hyperviscosity and many of the clinical signs seen with MM. [Hypercalcemia in Dogs and Cats](https://www.merckvetmanual.com/endocrine-system/the-parathyroid-glands-and-disorders-of-calcium-regulation-in-dogs-and-cats/hypercalcemia-in-dogs-and-cats?autoredirectid=21712) Clinical signs include lethargy, weight loss, bone pain or fractures, CNS signs, capillary bleeding, visual disturbances (due to retinal hemorrhage), organomegaly, and heart murmurs (due to hyperviscosity). [Gammapathies in Animals](https://www.merckvetmanual.com/immune-system/immunologic-diseases/gammopathies-in-animals) De requires two or more of the following: - Monoclonal gammopathy on serum electrophoresis - Bence Jones proteinuria - Lytic bone lesions on radiographs - Plasma cell infiltration of the bone marrow Here is more useful info on immunoglobulins from [Cornell's eClinPath website.](https://eclinpath.com/chemistry/proteins/immunoglobulins/) Ref: Cote, Clinical Veterinary Advisor: Dogs and Cats, 4th ed., pp. 663-5. Image courtesy, Seth Chapman, DVM, MS, DACVP.

Answer 136

Answer: **Mediastinal lymphoma** On the lateral thoracic radiograph, there is a mass in the cranial mediastinum with mild dorsal displacement of the trachea. The most likely diagnosis for a mediastinal mass in a dog with hypercalcemia is lymphoma. [Hypercalcemia in Dogs and Cats](https://www.merckvetmanual.com/endocrine-system/the-parathyroid-glands-and-disorders-of-calcium-regulation-in-dogs-and-cats/hypercalcemia-in-dogs-and-cats?autoredirectid=21712) ChGPT: **Hypercalcemia in Dogs and Cats: Comprehensive Veterinary Guide** Radiographic interpretation: The cardiovascular structures are normal in size and shape. No abnormalities are seen within the pulmonary parenchyma. On the lateral projection there is a mass in the cranial mediastinum with mild dorsal displacement of the trachea. The mediastinum is widened on the /d projection, and is wider than the vertebral column. The pleural space and musculoskeletal structures are normal. Check out Zuku's [chart on calcium testing.](https://zukureview.com/node/100698) [Radiographic interpretation and images](http://mirc.veterinaryradiology.net/storage/ss1/docs/9999.63960389107404687681137565972027706955/MIRCdocument.xml) courtesy, Dr A. Zwingenberger and [Veterinary Radiology](https://www.veterinaryradiology.net)

Answer 137

Answer: **Classical swine fever** Classical swine fever (CSF, "hog cholera"). [Veterinary Merck Manual](https://www.merckvetmanual.com/generalized-conditions/classical-swine-fever/classical-swine-fever?redirectid=29630) Virology is required to confirm and differentiate from other causes of febrile hemorrhagic diseases. The best tissues to submit are tonsils, maxillary or submandibular lymph nodes, mesenteric lymph nodes, spleen, ileum, and kidney. [Glaesserella parasuis](https://vetmed.iastate.edu/vdpam/FSVD/swine/index-diseases/glasser-disease) (formerly Haemophilus parasuis)(Glasser’s disease), is an acute bacterial infection, characterized by different combinations of meningoencephalitis, polyserositis and polyarthritis and can contribute to bacterial pneumonia. Images courtesy, [The Pig Site](https://www.thepigsite.com/pighealth/article/447/classical-swine-fever-csf-hog-cholera-hc)

Answer 138

Answer: **Measure resting ACTH and insulin** Measure resting ACTH and insulin for pituitary pars intermedia dysfunction (PPID, a.k.a. equine Cushing's) and [equine metabolic syndrome](https://www.merckvetmanual.com/metabolic-disorders/equine-metabolic-syndrome/equine-metabolic-syndrome) (EMS), respectively. These hooves show evidence of chronic laminitis (see all those rings) and endocrinopathic laminitis is the most common cause. [Laminitis in Horses](https://www.merckvetmanual.com/musculoskeletal-system/disorders-of-the-foot-in-horses/laminitis-in-horses?mredirectid=2651) Equids can have EMS or PPID or both. If resting ACTH and insulin are normal, the next phase of testing (i.e., have increased sensitivity) for EMS and PPID are: the oral sugar test for EMS and thryrotropin-releasing hormone stimulation test for PPID. Grazing is typically contraindicated in horse with EMS because the fructans in fresh grass exacerbate the insulin response and laminitis. Steroids also worsen insulin dysregulation and should be avoided in horses with EMS. [Click here](https://static1.squarespace.com/static/65296d5988c69f3e85fa3653/t/667984057bceca614c913a83/1719239689544/2022-EMS-Recommendations.pdf) for the 2022 Guidelines on the Diagnosis and Management of EMS and [one on PPID](https://static1.squarespace.com/static/65296d5988c69f3e85fa3653/t/6596d092174c8f1c3ae122b2/1704382615558/2023+EEG+PPID+-+Digital+version+with+insert+-+12.22.2023.pdf), courtesy of the Equine Endocrinology Group. Photograph courtesy of Dr. Ines Pinto.

Answer 139

Answer: **Abdominal radiographs** There is an enterolith in the manure so abdominal radiographs should be recommended. There is often more than one, and abdominal radiographs are the least invasive way to evaluate for more (80% sensitivity). Exploratory laparotomy is the definitive method but is invasive, costly, and not warranted without radiographs and/or clinical signs. Click here to see an abdominal radiograph from a horse with an [enterolith](https://zukureview.com/sites/default/files/2022-09/entrad.png) Enteroliths are composed of magnesium, ammonium, and phosphate and typically form around a nidus of sand or foreign material. They are most common in Arabians that eat alfalfa hay in certain regions of the USA (CA, southwest, Texas, FL). While small stones can be passed, enteroliths more often become too large to pass per rectum. They cause recurrent colic or acute colic when they become lodged in narrow bowel (e.g., transverse colon, small colon). DefinitiveTx - ventral midline celiotomy to remove the stones via enterotomy. Prognosis is excellent. Images courtesy of Nora Grenager, VMD, DACVIM. **Enterolithiasis associated with colic in horses** [Merck](https://www.merckvetmanual.com/digestive-system/colic-in-horses/diseases-associated-with-colic-in-horses-by-anatomic-location?autoredirectid=16615#Enterolithiasis_v3262901) Enteroliths are concretions of magnesium ammonium phosphate crystals that form around a nidus (eg, wire, stone, nail). Enteroliths may occur singly or in groups and are commonly causes of colic in horses in certain parts of the US, including California, the southwest, Indiana, and Florida. Enterolithiasis commonly affects Arabian horses, but the popularity of these horses in the aforementioned areas confounds the question regarding breed association. Most horses with enteroliths are ~10 years old; enterolithiasis rarely occurs in horses < 4 years old. Although not all factors that contribute to the formation of enteroliths have been identified, results of clinical studies indicate that large-colon contents from horses with enteroliths have higher mineral (magnesium, calcium, and phosphorus) concentrations and pH than contents from horses with colic not due to enteroliths. A common factor associated with enterolithiasis is the consumption of alfalfa hay, which results in a higher pH and increased concentrations of calcium, magnesium, and sulfur in the large colon. Many horses with enterolithiasis have a history of recurring colic, presumably indicating that the enterolith(s) previously had caused partial or temporary obstruction of the colonic lumen. If the enterolith becomes lodged at the origin of the transverse colon, the colon proximal to the obstruction distends with gas and the pain is severe. Distention of the abdomen may be marked. Heart and respiratory rates are increased, and the mucous membranes may be pale or pink. Generally, colonic and cecal distention is evident on rectal examination; however, the mass rarely is palpable because the transverse colon is cranial to the cranial mesenteric artery. Analysis of the peritoneal fluid is usually within normal limits unless ischemia of the colonic wall has developed over the enterolith. In areas where the problem is endemic, radiography may be used to identify the enteroliths. Treatment involves surgery via a ventral midline celiotomy to decompress the colon and cecum and then to remove the stone(s). The left portion of the large colon is exteriorized and positioned on a sterile colon tray, the ingesta removed via an enterotomy, and then the enterolith(s) removed. If the stone has a flat side or a polyhedral shape, this is indicative of the presence of one or more additional enteroliths. Consequently, the rest of the large and small colons must be thoroughly checked for other stones. The prognosis is excellent, with practices in endemic areas reporting survival rates of 95%.

Answer 140

Answer: **3.5 to 4 years** The 4th incisors are actually canine teeth and they erupt at 3.5 to 4 years in cattle. Cattle age is not always given in a history and estimating age during physical exam helps narrow differentials. [Dental Anatomy of Ruminants](https://vivo.colostate.edu/hbooks/pathphys/digestion/pregastric/cowpage.html) References for times of eruption vary by about six months because the times of tooth eruption vary among individual animals and breeds. Full eruption of a new tooth may take another six months. Follow this link to a Merck Manual [tooth eruption table](https://www.merckvetmanual.com/digestive-system/dental-development-and-anatomy/estimation-of-age-by-examination-of-the-teeth-in-animals) REMEMBER ruminants don't have upper incisors but instead have a dental pad.