Josh's Medicine Questions Flashcards
What are the aetiological agents for cat flu syndrome? 4
Major = Feline calicivirus (85%), feline herpesvirus (10%); Minor = Bordatella bronchiseptica, Chylamidophila felis. Secondary = Mycoplasma, streptococci, reoviruses, cowpox.
Describe the pathogenesis of feline herpes virus. 4
Cat - (virus introduced) Acute infection - Chronic Damage
Acute infection can also - clinical recovery - true recovery
Clinical recovery can result in carrier status (80-90%) with a latent virus and reactivation leads to shedding and sometimes clinical signs.
What are the clinical signs of FHV? 3
Anorexia, pyrexia, depression, marked nasal and ocular discharges.
Ocular signs common - acute and chronic conjunctivitis and ulcerative keratitis.
What are the similarities and differences between FHV and FCV? 6
FHV - One serotype, highly virulent, labile (<1d), incubation 2-17dd, disease course 2-4wk.
Sneezing, oculo-nasal discharge, karatitis, chronic rhinitis. 90% Latent carriers, intermittent excretion.
FCV - Many serotypes, variable virulence, can survive upto 7d, incubation 2-10dd, disease course 1-2wk.
Sneezing, oculo-nasal discharge, stomatitis, gingivitis. less than 50% carriers, continual excretion.
How do you diagnose and treat Chlamydophila felis? 4
Conjunctival swab for PCR (1st), bacterial isolation (die in transit), serology.
Treatment - Tetracyclines for 4 weeks, treat all cats in the household, topical 1% chlortetracycline ointment may be useful. Clearance may not occur.
What are the clinical signs of Bordatella bronchiseptica in cats? 3
Sneexing, nasal discharge, coughing uncommon, submandibular LN enlargement, pyrexia, bronchopneumonia/sudden death in kittens.
Describe a general treatment protocol for cat flu. 5
TLC (warm and quiet), consider appetite stimulants, prophylactic antibiotics, decongestants. With severe stomatitis test for FeLV and FIV, Corneal ulcerswith acyclovir, oral L-lysine suggested for FHV.
When would you use a killed/inactivated vaccine in cats? 3
Pregnant cats, immuno-suppressed cats (FIV), closed colonies of large cats in close contact with each other.
Describe the clinical signs associated with the various forms of FPV (feline panleukopaenia). 3
Per-acute - Severe depression, subnormal temps and rapid death <24hrs
Acute - Pyrexia, anorexia, depression, and marked abdominal pain. Vomiting and diarrhoea develop 24-72hrs after initial signs and may be haemorrhagic.
Infection in utero - First trimester results in fetal death and resorption; middle third results in cerebellar hypoplasia.
Why can the FPV vaccine fail? 1
Kittens are protected in the first few weeks of life by maternally derived antibodies and this can extend up to 12 weeks.
What is the pathogenesis of FIP? 4
Ingestion - Replication in pharyngeal, respiratory or intestinal epithelium. Two options
1 - Strong CMI/low virulence - asymptomatic or mild diarrhoea, virus eliminated.
2 - Viraemia, mutation of FCov allowing target cell infection (macrophage):
i) Weak CMI - Effusive FIP - many blood vessels involved resulting in increased vascular permeability and leakage of protein rich exudates.
ii) Moderate CMI - Non-effusive FIP - Fewer blood vessels affected, discrete pyogranulomas form throughout the body.
What factors determine whether a cat exposed to FCoV develops FIP? 4
Strain (different strains have different virulence)
Dose (higher dose more likely get FIP)
Stress (history 3-6weeks before FIP development)
Genetic Susceptibility
What are the clinical signs with wet and dry FIP? 3
Wet - Ascites, pleural effusion (dyspnoea), BAR or dull, weight loss.
Dry - Weight loss and inappetence, ocular lesions (keratitis, uveitis, hypopyon), CNS signs (nystagmus, paresis, head tilt, seizures), hepatic, splenic or renal enlargement.
Describe the difficulties with diagnosing FIP. What are the advantages and disadvantages of the various tests? 8
Biochemistry - Hyperglobulinaemia, low albumin:globulin ratio (35g/l, Alb:glob <5000/ml (neuts and macrophges)
Serology for FCoV - INTERPRET WITH CARE - high prevalence or seropositivity in general cat population, esp multicat households. Suggested more are killed through misinterpretation of serology than by FIP.
RT-PCR - In blood not conclusive as other conditions can still have positive RT-PCR, negative result does not rule it out. Effusion likely to be FIP but not diagnostic.
Histopathology - Only certain way.
What are the possible outcomes following FeLV infection? 6
1) Transient infection then recovery - most cases, only 10-20% persistently viraemic if exposed >6mths
2) Persistent viraemia and development of FeLV-related disease - no recovery from infection - time course variable.
3) Latent infection - Virus not detected in blood but still in bone marrow, controlled by neutralising antibodies. Most eventually eliminate infection but stress/IMS can resstart.
What diseases are associated with FeLV? 6
Malignant Diseases:
1) Lymphomas - Mediastinal, Multicentric, Alimentary, Extra-nodal.
2) Leukaemias - Lymphoid, myeloid and erythroid.
Non-Malignant
1) Anaemia - non-regenrative (pure red cell aplasia, myelofibrosis, myelopthesis).
- regenerative (co-infection with Mycoplasma haemofelis, IMTP/IMHA)
2) Immunosuppression
3) Others (Uveitis, Infertility, Glomerulonephritis, neuro, polyarthrisis).
Describe the different tests used for diagnosing FeLV. 5
How should you interpret these tests? 5
ELISA - p27 antigen - possible false positives but easy to use.
RIM assays - p27 antigen - as ELISA
Virus Isolation - Serum - Gold standard 7-10dd
Immunofluorescence - FeLV antigen in neuts and platelets - Gold Standard - smear important
PCR - Mat be too sensitive.
After ELISA/RIM - re-test in 12 weeks as may be transient, confirm with VI or IFA, test 12 weeks after exposure to known positive cat, false negatives rare.
What are the pros and cons of pre-vaccination blood testing with FeLV? 6
Pros - Infected cats identified and potentially treated; Vaccinating cats that already have it will have no benefit; Identification of viraemia likely to reflect subclinical infection, not vaccine failure.
Cons - Costs more; Prevalence in healthy cat population is low; in house kits not 100%; vaccination unlikely to do any harm to FeLV positive cat anyway.
What is the pathogenesis of FIV? 5
Inoculation via bite wound leading to an initial viraemia. Viraemia subsides then variable time course and then get future depletion of T and B cells. Immunodeficiency and FIV-related diseases ensue.
What are the difficulties in diagnosing FIV? 4
What are the gold standard tests? 3
No clinical signs are pathognomic, 10-15% with FIV have no detectable antibody due to early infection, terminal immune collapse, lack of antibody, failure of test to detect antibody.
IFA or Western Blotting. PCR now possible.
How should you manage FIV positive cats? 4
Try to stop them spreading the disease, keep stress free and treat infections early and aggressively. Use killed vaccines and keep up to date. FIV status is not an indication for euthanasia.
Compare FIV and FeLV. 9
FeLV: Retrovirus; Young cats (<4); 20x increased risk of neoplasia; anaemia is common and severe; most eliminate the virus; diagnose by detecting viral antigen/whole virus; prevent with vaccine; 80% die in 3yrs.
FIV: Lentivirus; middle aged to older roamers; 5x increase in neoplaisa; usually mild anaemia in 15-20%; no recovery from infection; diagnose by detecting viral antibody; no vaccine; may live for years.
What are the three pathogens involved in FIA in the UK? 3
Mycoplasma haemofelis; Candidatus M haemominutum; Candidatus M turicensis.
Describe the pathogensis and epidemiology of FIA. 3
Pathogenesis - Cycles of parisatamia at regular intervals with 6 dd between episodes. PCV falls, oraganism cleared quickly, PCV rises over next few days.
Epidemiology - Spread by fleas? Most asymptomatic.
What are the mechanisms behind the anaemia? 4
Sequestration in the spleen; Anti-body mediated haemolysis; Erythrophagia by splenic macrophages; decreased RBC lifespan.
What are the four types of Mycobacterium infections in cats? 4
1) Tuberculosis mycobacterium
2) Feline Leprosy
3) Non-tuberculosis mycobacterium
4) Opportunistic mycobacterium
What are the factors that influence the severity of CPV-2 infections? 5
Maternally-derived antibodies are protective upto 18 weeks but can go in 8 weeks with some puppies.
Vaccination status; Stress factors; Presence of other enteric pathogens; Viral load.
What are the blood results with a PCV-2 infection? 2
Panleukopaenia, normal or reduced PCV (HGE - increased, helps to differentiate).
How do you treat parvo? 6
Aggressive IVFT and correct electrolytes.
Anti-emetics
Antibiotics
Analgesia
Recombinent interferon
Supportive nursing and nutritional support.
What are the clinical signs of classical canine distemper? 5
Conjunctivitis, Dry cough that can progress to a wet, productive cough (bronchopneumonia), mucopurulent ocular and nasal discharges develop, pyrexia (>40), anorexia. Gastroenteritis signs or opportunistics may follow respiratory signs.
What are the “chronic” signs of canine distemper? 3
Hyperkeratosis of the nose and footpads 3-6wks after infection.
Enamel hypoplasia can suggest previous CDV infection
Neurological signs - seizures, ataxia, paresis/paralysis - 1-3 weeks after recovery from systemic illness.
What are the serovars and which are vaccinated for in canine leptospirosis? 5
icterohaemmorhagica, canicola, grryptotyphosa, pomona, bratislava. Ictero and canicola vaccinated against.
What is the pathogenesis of leptospirosis? 3
Direct contact with urine, penetrates mucosal surfaces and damaged skin, replicate in bloodstream and spread to renal and hepatic tissue and replicate further.
How can you diagnose leptospirosis? 5
Historical clues, blood tests can show leucocytosis and thrombocytopaenia, increased liver enzymes, bile acids and bilirubin, increased urea/creatinine, coagulopathies (DIC).
Dark-field microscopy.
Serology - Microscopic agglutination test - 4x increase over 4 weeks.
What are the clinical signs associated with leptospirosis? 6
Peracute - Pyrexia, muscle pain, shock, DIC and death coagulation.
What should you do to treat and prevent leptospirosis? 6
Penicillin effective at terminating leptospiraemia.
Move on to doxycycline for two weeks after penacillin to remove carrier state.
Supportive - IVFT, anti-emetics; treat renal failure.
Prevention - Killed vaccines, protect disease but subclinical infection can still occur and other serovars present, duration of immunity can be less than a year as well.
What is the cause and what are the clinical signs of infectious canine hepatitis? 5
Lethargy, depression, anorexia, reluctance to move.
Abd pain, hepatomegaly and jaundice (40%).
Pale mucous membranes, occ petechial haemorrhages.
Corneal oedema blue eye approx 7dd post infection (20%).
How can you prevent canine infectious hepatitis? 2
Vaccinate with CAV-2 as CAV-1 associated with side-effects (blue-eye). CAV-2 cross protective.
What are the most prevalent infectious agents associated with canine infectious tracheobronchitis? 5
Bordatella bronchiseptica, Parainfluenza; Canine adenovirus 1 and 2; CDV; (CHV, reoviruses, mycoplasmas, canine influenza virus).
How do you treat kennel cough? 4
Tetracyclines, amoxyclav and fluroquinolones work against Bordatella. Cough suppressants (not conseidered helpful); Expectorants and mucolytics; Bronchodilators.
What is the life cycle of Angiostrongylus vasorum? 4
Infective L3 ingested from intermediate host; Larvae develop and migrate through the alimentary tract, abd LNs, venous system and right heart into the pulmonary artery. Mature and lay eggs that go to alveoli, L1 in capillaries, hatch and move to alveolus and out and coughed up and swallowed. L1 eaten by intermediate.
What are the main signs of European Heartworm? 3
Coughing (47%); Dyspnoea (42%); Haemorrhagic diatheses (29%); Collapse (22%); Exercise intolerance (20%); GI signs (20%); lethargy (18%).
How can you diagnoses Angiostrongylus vasorum infection? 5
L1 in faeces by Baermann sedimentation (intermittent excretion, 3 samples over 7 days)
L1 in BAL samples; FNA of lungs; Coagulation (Prolonged APTT and OSPT, elevated D-dimers and FDPs, occ decreased vWF) plus other non-specific findings such as anaemia, thrombocytopaenia, eosinophilia etc.
What is the pathogenesis of tetanus? 4
Spores of Clostridium tetani enter wounds, usually a penetrating wound. The spores germinate, toxins are released and travel in the bloodstream and then enter the peripheral nerves. Two exotoxins produced, bind to neuronal cell bodies of inhibitory interneurones, preventing GABA and glycine release reulting in spastic paralysis.
Describe the more common clinical signs of tetanus in the cat. 3
Increased stiffness of a muscle or entire limb in close proximity to affected site. Stiffness can spread to opposite extremity. Process eventually involves all of the CNS.
How do you treat tetanus? 4
1) Antitoxin - neutralise unbound or toxin yet to be formed. More effective if given intrathecally. Beware anaphylaxis.
2) Antibiotics - Kill vegetative bacteria in wound to prevent further toxin production. Penicillin G best.
3) Sedatives - Control excitability and spasticity.
4) Nursing - essential, beware aspiration pneumonia and pressure sores.
What are the clinical signs of Borrelia burgdoferi infection? 4
Experimentally infected dogs the clinical signs occurred in 2-5 months after tick exposure.
Systemic - Fever, lymphadenopathy, anorexia and general malaise.
Arthritis - Polyarthritis.
What are the clinical signs of the furious form and dumb form of rabies? 3,3
Furious - Hyperexcitability, pyrexia, pica and aggression.
Dumb - Timid, affectionate, dysphonia, drooling and dysphagia. (can still be aggressive)
Both result in paralysis and death.
Describe the pathogenesis of leishmaniasis.
Non-flagellated forms multiply in cells of mononuclear phagocyte system and infected macrophages are transferred to mouthparts of sandfly. In vector, parasite multiplies and develops into flagellated form, transferred back to skin or bloodstream which are phagocytosed by macrophages, revert to previous form and multiply and invade local tissues.
What are the clinical signs of leishmaniasis? 6
Waxing and waning; lethargy, anorexia and pyrexia.
Dermatological changes such as exfoliative dermatitis, hyperkeratosis of the footpads, excessive claw growth, periorbital alopecia.
Spread to visceral organs results in visceral leishmaniasis
Generalised mild lymphadenopathy, Splenomegaly, pallor, panophthalamitis, immune-mediated nephropathy.
How do you diagnose and treat Leishmaniasis? 6
Diagnosis: 1) Demonstrate parasite in impression smears; 2) Serology; 3) PCR testing; 4) Clinicopathological - sigf hyperglobulinaemia, leucocytosis, thrombocytopaenia, non-regen anaemia, severe proteinuria.
Treatment - Cure unlikely and can only suppress clinical signs - It is zoonotic so consider euthanasia.
What are the signs associated with acute and chronic forms of babesiosis? 3,3
Acute - Haemolytic anaemia, icterus, haematuria, hepatoslenomegaly, collapse, shock DIC and death.
Chronic - Pyrexia, weight loss, atypical signs such as joint pain, swellings and GI signs.
What are the clinical signs associated with monocytic ehrlichiosis (E.canis) and granulocytic ehrlichiosis (A. phagocytophilum)? 3,3
Monocytic - Depressin, weight loss, bleeding tendencies, ophthalmic signs, neuro signs, hepatosplenomegaly and lymphadenopathy, bone marrow suppression, hyperglubulinaemia.
Granulocytic - Fever, depression, anorexia, reluctance to move, lameness of one or more limb, joint swelling, limb oedema, meningitis.
Describe the life cycle of Dirofilaria immitis and the diseases it causes. 3,4
Adult worms in pulmonary artery, microfilaria in blood, ingested by mosquito, larvae develop, incubated in dog.
Disease - Pulmonary end-arteritis, eosinophilic peumonia, pulmonary hypertension and RSHF.
How do you treat Dirofilaria immitis? 4
Manage consequences of infestation
Adulticide therapy (preds maybe should be given prior)
Microfilaricide treatment - Milbemycin three to four weeks later.
Prophylaxis - Monthly milbemycin and ivermectin one month before exposure.
What fungi affect dogs and cats? 4
Aspergillus and penicillium in dogs.
Cryptoccoccus neoformans or maduromycosis in cats.
How can you diagnose fungal rhinitis? 4
1) Fungal organism is not always present in material taken for culture for positive cases and may be in 40% clinically normal dogs.
2) Serological agar gel double diffusion test and ELISA tests are of value.
3) Radiological signs - Loss of trabecular pattern due to turbinate destruction, especially rostral portion leading to radiolucency. Mixed pattern or truncate lucencies.
4) Endoscopy, maybe with biopsies.
What intranasal tumours are seen in the cat and dog? 4
Dogs - adenocarcinoma most common, fibrosarcoma, chondrosarcoma, osteosarcoma and SCC seen.
Cats - Lymphosarcoma most commonl, but others seen.
What adventitious sounds are present in respiratory disease? 4
Crackles - intermittent, non-musical explosive sounds.
Wheezes - continuous musical or whistling sounds.
Pleural friction rub - Combination of continuous and discontinuous sounds produced by inflamed pleura rubbing together.
Silent lung - Pneumothorax, pleural effusion, diaphragmatic hernia, SOL, consolidated lung, obesity, shallow breathing.
What are the differential diagnoses with acute coughing? 3
Infectious tracheobronchitis; Airway irritation; Bronchopneumonia; Allergic lung disease; Inhaled FB; Pulmonary oedema/haemorrhage; Airway trauma.
Explain some causes of bronchopneumonia. 5
Infectious - Secondary to kennel cough, chronic bronchitis, bronchiectasis, ciliary dyskenesia; FB inhalation; 1’ neoplaisa; immunocompromised.
Aspiration - Secondary to megaoesophagus, swallowing disorders or laryngeal paralysis, aspiration of liquid paraffin; smoke or allergen inhalation; broncho-oesophageal fistula; chronic rhinitis.
How do you treat bronchpneumonia? 9
1) Ensure patient airway
2) Oxygen therapy if in severe distress
3) Keep environment warm and moist - do not stress
4) IVFT, nebulisation, do not over-hydrate.
5) Antibiotics - early high dosages.
6) Bronchodilators if bronchospasm
7) Expectorants may help
8) Physiotherapy - coupage and mild exercise
9) Surgery if limited to one lobe.
What are the causes for chronic or persistent coughing? 5
Chronic bronchitis; Bronchopneumonia; Allergic lung disease; Bronchiectasis; LSHF; Oslerus osleri; Auerulostrongylus abstrusus; Angiostrongylus vasorum; FB; 1’ or 2’ neoplasia; 1’ abscess/granuloma; Airway pressure; Tracheal collapse.
Describe the aetiology of chronic bronchitis. 4
Associated with excessive mucous production, hyperplasia and infiltration of the bronchial mucosa, loss of cliliated epithelial cells and failure of mucociliary carpet. Associated with 1’ ciliary dyskenesia in young dogs.
What is the aetiology of feline asthma and how do you treat it? 8
Thought to be allergic but putative agents unknown, smoke, aerosol sprays, feathers and cat litter maybe?
Sudden onset paroxysmal dry coughing, dyspnoea and wheezing, often with marked expiratory dyspnoea and end-expiratory effort.
Treatment - Control obesity, control 2’ bacterial infection, GCC therapy may be dramatic; bronchdilators; nebulisation; supplemental oxygen in severe attack.
