Infectious Diseases Flashcards

(1072 cards)

1
Q

What is a major risk factor for infectious diseases in young animals?

A

Increased risk due to lack of immunity

An example is parvovirus in puppies.

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2
Q

What is a major risk factor for infectious diseases in older animals?

A

Increased risk due to cumulative pathogen exposure

An example is heartworm disease.

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3
Q

What is a key consideration in the context of infectious disease diagnosis in cats?

A

FeLV and FIV status

These statuses are critical to document.

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4
Q

What causes lymphocytosis in dogs?

A
  • Vector-borne diseases
  • Chronic antigenic stimulation
  • Some acute infections
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5
Q

What is a common cause of eosinophilia?

A

Parasitic infections

Eosinophilia is also reported with certain fungal and protozoal infections.

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6
Q

What does hypoalbuminemia suggest?

A
  • Loss via GI tract or kidneys
  • Reduced hepatic production due to severe inflammation
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7
Q

What pattern clusters suggest infectious disease?

A
  • Lymphocytosis + Hyperglobulinemia + Proteinuria
  • Hyperglobulinemia + Hypercalcemia
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8
Q

What are some infections associated with hypercalcemia?

A
  • Fungal infections (e.g., Aspergillosis)
  • Bacterial infections (e.g., Mycobacterium spp.)
  • Parasitic infections (e.g., Heterobilharzia americana)
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9
Q

What laboratory findings should prompt consideration of fungal infections?

A

Hyperglobulinemia + Hypercalcemia

These findings can indicate potential infections including schistosomiasis.

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10
Q

What tests are included in autoimmune panels that may return positive results in infectious diseases?

A
  • Antinuclear antibodies (ANA)
  • Rheumatoid factor (RF)
  • Perinuclear antineutrophil cytoplasmic antibodies (pANCA)

These tests have limited value unless infectious diseases are ruled out.

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11
Q

What are the two main types of diagnostic testing for infections?

A
  • Direct Testing (Detects Organism)
  • Indirect Testing (Detects Immune Response)

Direct tests confirm the presence of the organism while indirect tests reflect exposure.

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12
Q

What are examples of direct testing methods?

A
  • Culture
  • Cytology
  • PCR
  • Antigen tests (e.g., ELISA, IFA)

A positive direct test generally confirms the presence of the organism.

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13
Q

What do positive antibody tests typically indicate?

A

Exposure, not necessarily active infection

Antibody tests may not confirm current infection status.

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14
Q

What can cause false positives in diagnostic tests?

A
  • Cross-reactivity
  • Prior exposure
  • Vaccination

These factors can affect the accuracy of serologic tests.

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15
Q

What does seroconversion indicate in terms of infection?

A

A fourfold increase in titers from acute to convalescent samples

This is considered the best evidence for active infection.

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16
Q

What are key signs of hypercalcemia associated with infections?

A
  • Aspergillosis
  • Coccidioidomycosis
  • Histoplasmosis
  • Blastomycosis
  • Pythiosis
  • Mycobacterium spp.
  • Nocardiosis

These infections can lead to elevated serum calcium concentrations.

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17
Q

What should be done if diagnostic tests yield negative results but suspicion of infection remains high?

A
  • Repeat testing
  • Consider alternative sample types
  • Empirical treatment

Clinical reasoning is critical in interpreting test results.

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18
Q

What is the primary purpose of diagnosing infectious diseases in veterinary medicine?

A

To integrate clinical findings with laboratory and diagnostic test results for accurate treatment and population management.

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19
Q

What are the key intents of diagnostic testing?

A
  • Diagnosis (ruling in a disease)
  • Screening (ruling out infection)
  • Risk evaluation
  • Prognostication
  • Guiding treatment decisions
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20
Q

What is the purpose of confirmatory testing following a non-negative screening test?

A

To ensure the accuracy of the diagnosis with more specific tests.

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21
Q

What are the key performance characteristics of diagnostic tests?

A
  • Diagnostic Accuracy
  • Analytic Sensitivity
  • Analytic Specificity
  • Diagnostic Sensitivity
  • Diagnostic Specificity
  • Positive Predictive Value (PPV)
  • Negative Predictive Value (NPV)
  • Reproducibility (Precision)
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22
Q

Fill in the blank: High _______ is desired when early detection is critical and false negatives carry risk.

A

sensitivity

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23
Q

What types of methods are included in modern veterinary clinical microbiology?

A
  • Traditional methods (staining, culture, serology)
  • Advanced tools (proteomics, molecular diagnostics)
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24
Q

What is the preferred method for diagnosing acute infections?

A

Organism detection methods.

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25
In which situations might antibody detection methods be more appropriate?
* Chronic or persistent infections * Situations with measurable immune response * Acute infections with rapid antibody rise detectable through paired serologic testing
26
What is the significance of cytologic evaluation in clinical microbiology?
It provides rapid presumptive diagnoses of pathogens through examination of specimens.
27
What is the Gram stain performance discrepancy rate found in a multicenter study?
5% of Gram stain results were discrepant with culture.
28
How long does it typically take for aerobic bacteria to grow in culture?
18–24 hours (some up to 48 hours).
29
What type of environment do anaerobes like Clostridium and Bacteroides require?
Oxygen-free environment
30
What is the typical turnaround time for anaerobes?
48 hours to 5–7 days
31
What are facultative anaerobes?
Organisms that grow with or without oxygen
32
What is a defining characteristic of fastidious organisms like Campylobacter jejuni?
Require enriched media, specific O₂/CO₂ levels, and higher temperatures (42°C)
33
What is the gold standard for bacterial identification and susceptibility testing?
Culture
34
What is MALDI-TOF-MS?
Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry, a method for rapid identification of bacteria and yeast
35
How quickly can MALDI-TOF-MS identify organisms?
In minutes
36
What is one advantage of using MALDI-TOF-MS in clinical microbiology?
Reduces time to diagnosis and improves clinical outcomes
37
What are the common methods for Antimicrobial Susceptibility Testing (AST)?
* Broth microdilution (standard method) * Kirby-Bauer disk diffusion * Antibiotic gradient strips (e.g., Etest)
38
What is the role of chromogenic agar in microbiology?
Useful for detecting specific pathogens
39
What is the mortality rate of sepsis in humans?
30–50%
40
What is the correlation between blood volume and culture positivity?
For every 1 mL increase in blood volume, there is a 1% increase in culture positivity
41
What are the advantages of automated blood culture systems?
* Faster detection * Continuous monitoring
42
What is the function of Next-Generation Sequencing (NGS) in diagnostics?
Allows direct sequencing of DNA from clinical specimens
43
What does Whole Genome Sequencing (WGS) provide?
* Organism identification * Strain typing * Prediction of antimicrobial resistance genes * Detection of virulence factors
44
What is a challenge of using NGS in veterinary medicine?
Complex test validation
45
What are the key components of diagnostic stewardship?
* Selecting the right test * For the right patient * To generate clinically actionable results ## Footnote A multidisciplinary approach enhances the effectiveness of diagnostic stewardship.
46
What does next-generation sequencing (NGS) offer in veterinary diagnostics?
The ability to identify novel, rare, or co-infecting pathogens and predict resistance profiles directly from complex specimens ## Footnote NGS represents a significant advancement in the capabilities of diagnostic testing.
47
What are Modified Live Vaccines (MLVs)?
* Contain live, attenuated organisms * Induce robust, long-lasting immunity * Generate humoral and cell-mediated immune responses * Can provide lifelong immunity ## Footnote MLVs typically require fewer doses than inactivated vaccines.
48
What are Inactivated (Killed) Vaccines?
* Contain antigenic but non-replicating organisms * Less immunogenic than MLVs * Usually require multiple doses and adjuvants * Induce shorter duration of immunity ## Footnote The rabies vaccine is an exception, being highly immunogenic despite being inactivated.
49
When should puppy core vaccinations begin?
At 6–8 weeks of age ## Footnote Vaccinations should be administered every 2–4 weeks until at least 16 weeks.
50
What is the purpose of the 12-month booster for puppies?
To catch any non-responders to the primary vaccination series ## Footnote WSAVA recommends this booster ideally closer to 26 weeks.
51
What are widely used non-core vaccines for dogs?
* Bordetella bronchiseptica * Canine parainfluenza virus (CPIV) * Leptospira species ## Footnote Leptospira is increasingly considered core in endemic areas.
52
What is the main purpose of vaccines against respiratory pathogens?
To reduce disease severity, not necessarily to prevent infection ## Footnote Common targets include CPIV and Bordetella bronchiseptica.
53
What are core vaccines for cats?
* Feline panleukopenia virus (FPV) * Feline herpesvirus-1 (FHV-1) * Feline calicivirus (FCV) * Rabies (in endemic areas) ## Footnote These vaccines are often provided in combination formulations.
54
When should kitten vaccinations start?
At 6–8 weeks of age ## Footnote Kitten vaccinations are given every 2–4 weeks until at least 16 weeks.
55
What vaccines are not recommended for dogs?
* Canine Enteric Coronavirus * Giardia duodenalis * Dermatophytosis (Ringworm) ## Footnote These vaccines have limited efficacy or are ineffective at preventing infections.
56
What is the controversy surrounding Borrelia burgdorferi vaccines?
Protection is incomplete, and no vaccine has proven protection against Lyme nephritis ## Footnote Vaccines available include monovalent, bivalent, and trivalent formulations.
57
What are the types of formulations available for FeLV vaccines?
* Inactivated whole-virus (adjuvanted) * Subunit vaccines * Recombinant canarypox vector (non-adjuvanted) ## Footnote FeLV stands for Feline Leukemia Virus.
58
What is the vaccination schedule for FeLV in kittens?
Start ≥8 weeks, 2 doses 3–4 weeks apart. ## Footnote FeLV testing is recommended before vaccinating.
59
True or False: FIV vaccines have variable efficacy and may interfere with diagnostic testing.
True. ## Footnote This can lead to false positives in diagnostic tests.
60
What are the adverse events following vaccination in cats?
* Transient fever * Lethargy * Anorexia * Lymphadenopathy * Type I hypersensitivity reactions * Immune-mediated diseases * Feline injection site sarcoma (FISS) ## Footnote Most reactions are mild and transient.
61
What is the incidence of adverse events following vaccination?
0.3–0.5% incidence (~30–50 per 10,000 vaccinations). ## Footnote Most reactions are mild and transient.
62
Fill in the blank: Feline Infectious Peritonitis (FIP) vaccine has __________ evidence of clinical efficacy.
insufficient ## Footnote The vaccine is not recommended for general use.
63
What is the recommendation for senior animals regarding serologic testing?
Testing is done annually to monitor immunosenescence.
64
What is the estimated prevalence of HAIs among hospitalized patients in the U.S.?
Approximately 1 in 31 hospitalized patients ## Footnote This statistic highlights the commonality of HAIs in hospital settings.
65
What percentage of unexpected in-hospital deaths are attributed to HAIs?
Up to one-third ## Footnote This underscores the severe impact of HAIs on patient outcomes.
66
How do HAIs in veterinary medicine differ from those in human medicine?
Veterinary patients are generally less immunocompromised, have shorter hospital stays, and are treated in smaller facilities ## Footnote Despite these differences, HAIs remain a concern in veterinary practice.
67
Name two types of pathogens reported in veterinary HAIs.
* Methicillin-resistant Staphylococcus spp. (MRSP, MRSA) * Salmonella ## Footnote These pathogens represent significant risks in veterinary hospitals.
68
What are common HAI syndromes in veterinary patients?
* Surgical site infections * Infections associated with invasive devices * Respiratory diseases * Diarrhea * Opportunistic infections in immunocompromised patients ## Footnote These syndromes illustrate the variety of infection risks in veterinary settings.
69
What percentage of veterinary teaching hospitals reported at least one outbreak in the previous five years?
82% ## Footnote This statistic indicates the prevalence of outbreaks in veterinary settings.
70
What percentage of HAIs in human hospitals are estimated to be preventable?
20–70% ## Footnote This statistic suggests a similar potential for preventability in veterinary medicine.
71
What is Lyme disease also known as?
Borreliosis ## Footnote It is the most common tick-borne disease in humans in North America.
72
Which species causes Lyme disease?
Borrelia burgdorferi ## Footnote Many dogs and cats are exposed but only a small subset develops clinical illness.
73
How many recognized Borrelia species exist?
52 species ## Footnote They are divided into the Lyme disease group and the Tick-borne relapsing fever group.
74
What are the two main groups of Borrelia species?
* Lyme disease group (21 species)* * Tick-borne relapsing fever (29 species)
75
What is the primary vector for Borrelia burgdorferi?
Ixodes spp. ticks ## Footnote These ticks have co-evolved with Borrelia for millennia.
76
What is the typical life cycle of Ixodes ticks?
* Eggs hatch in summer* * Larvae feed on birds and rodents* * Larvae molt into nymphs* * Nymphs feed in spring* * Nymphs molt into adults* * Adults feed in autumn
77
When does B. burgdorferi transmission typically occur?
≥53 hours after tick attachment ## Footnote This is the time it takes for OspA to be downregulated.
78
In which U.S. states are most human Lyme disease cases reported?
* Maine* * Vermont* * Pennsylvania* * New Hampshire* * Rhode Island* * Delaware* * Massachusetts* * New Jersey* * Connecticut* * New York* * Wisconsin* * Minnesota* * Maryland* * Virginia* * West Virginia
79
What is the prevalence of Lyme disease in dogs in Minnesota?
76% ## Footnote This is a significant prevalence rate before widespread tick prevention.
80
What are some other pathogens transmitted by Ixodes ticks?
* Borrelia mayonii* * B. bissettiae* * Anaplasma phagocytophilum* * Ehrlichia muris* * Babesia microti* * Bartonella spp. * Powassan virus
81
What is a key characteristic of pathogenic Borrelia?
Spiral-shaped, motile, Gram-negative spirochetes
82
How can Borrelia burgdorferi evade host immunity?
* Antigenic variation* * Persistence as peptidoglycan remnants* * Dormant cystic forms
83
How is TBRF (Tick-borne relapsing fever) diagnosed?
* PCR* * Culture using Barbour-Stoenner-Kelly (BSK) medium
84
What is a common finding in canine Lyme disease after tick exposure?
Self-limiting febrile illness after 2–5 months ## Footnote Symptoms include fever, hyperesthesia, and lameness.
85
What is the estimated prevalence of true Lyme arthritis among seropositive dogs?
<3% ## Footnote Despite high seroprevalence, clinical disease is rare.
86
What does the SNAP® 4Dx Plus test detect?
Antibodies to: * B. burgdorferi C6 peptide * Ehrlichia canis * Anaplasma phagocytophilum * Heartworm antigen
87
What is the significance of the C6 peptide in serologic testing?
Derived from the conserved VlsE antigen expressed only during natural infection
88
What does the titer magnitude not correlate with in asymptomatic, non-proteinuric dogs?
Clinical illness or need for treatment ## Footnote Titer magnitude is not a reliable indicator of disease severity in these cases.
89
What happens to levels after treatment in dogs with Lyme disease?
Levels typically decrease, but qualitative SNAP test often remains positive for years ## Footnote This indicates that past infections may still show positive test results long after treatment.
90
What is OspA and where is it found?
Present in all Lyme vaccines and occasionally in natural infection
91
When does OspC rise post-infection and when does it decline?
Rises 2–3 weeks post-infection, declines in 3–5 months without re-exposure
92
What is the clinical significance of OspF?
Rises 6–8 weeks post-infection and has longer persistence
93
What percentage of naturally infected dogs have P39 antibodies compared to vaccinated dogs?
88% of naturally infected dogs vs 47% of vaccinated dogs
94
What is the sensitivity comparison between VETSCAN and SNAP 4Dx Plus?
VETSCAN: 41%, SNAP 4Dx Plus: 96%
95
What do OspC and OspF titers suggest?
Natural exposure to the pathogen
96
What is the recommendation for seropositive, asymptomatic, non-proteinuric dogs?
No treatment; monitor urine for PLN several times annually
97
List some co-infections to assess for in seropositive dogs.
* Anaplasma spp. * Babesia spp. * Bartonella spp. * Ehrlichia spp. * Rickettsia rickettsii * Leptospira * Other Borrelia spp. (e.g., B. miyamotoi)
98
What is the expected response time for clinical signs after starting doxycycline for Lyme arthritis?
1–2 days
99
What type of vaccine induces OspA antibodies?
Recombinant OspA subunit (non-adjuvanted)
100
What is a limitation of Lyme vaccination?
Duration of immunity is a concern; up to 50% of vaccinated dogs may be unprotected at 15 months
101
True or False: Vaccines prevent Lyme nephritis.
False
102
What are mycobacteria?
Aerobic, acid-fast, non-spore-forming, non-motile bacilli ## Footnote Typically intracellular and can be primary or opportunistic pathogens
103
What factors contribute to the underreporting of mycobacterial infections in dogs and cats?
Nonspecific clinical signs, low index of clinical suspicion, diagnostic challenges ## Footnote These factors lead to an underestimated prevalence
104
Which mycobacteria are classified as rapidly growing?
M. fortuitum, M. abscessus, M. smegmatis, M. chelonae ## Footnote Typically environmental organisms and opportunistic pathogens
105
What are the etiologic agents of tuberculosis in companion animals?
Mycobacterium bovis, Mycobacterium tuberculosis, Mycobacterium microti ## Footnote M. bovis is zoonotic and primarily associated with cattle
106
Which species are more commonly affected by tuberculosis, dogs or cats?
Cats ## Footnote Transmission routes include ingestion of infected prey and close contact with infected animals
107
What clinical signs are associated with actinomycosis?
Localized abscesses, draining tracts ## Footnote Often associated with penetrating injuries
108
What are Nocardia spp.?
Aerobic, partially acid-fast, branching filamentous gram-positive bacteria ## Footnote Typically opportunistic pathogens in immunocompromised animals
109
What are common clinical manifestations of nocardiosis?
Cutaneous-subcutaneous infections, pulmonary nocardiosis, disseminated/systemic infections ## Footnote Rarely occurs in immunocompetent animals
110
What is the most commonly implicated slow-growing mycobacteria in systemic infections in dogs and cats?
Mycobacterium avium complex (MAC) ## Footnote Primarily affects young or immunosuppressed individuals
111
What is the genetic mutation associated with increased susceptibility to MAC infections in Miniature Schnauzers?
CARD9 gene mutation ## Footnote Essential for innate immune signaling against mycobacteria
112
What toxin is produced by Mycobacterium ulcerans?
Mycolactone ## Footnote Responsible for Buruli ulcers
113
Which species is primarily responsible for feline leprosy?
Mycobacterium lepraemurium ## Footnote Common in young, male cats with rodent exposure
114
What is the traditional diagnostic gold standard for mycobacterial infections?
Culture ## Footnote Can take 4–12 weeks for slow-growing species
115
What is the prognosis for dogs with systemic slow-growing mycobacterial infections?
Grave prognosis ## Footnote Often euthanized shortly after diagnosis
116
What treatment is recommended for feline infections caused by slow-growing mycobacteria?
Prolonged dual or triple antibiotic therapy ## Footnote Includes rifampin, fluoroquinolone, and macrolide
117
True or False: Most North American mycobacterial infections are zoonotic.
False ## Footnote The risk is higher in Europe and Great Britain
118
What is the prognosis for systemic slow-growing mycobacterial infections?
Grave prognosis ## Footnote Often leads to euthanasia shortly after diagnosis
119
What is a notable feature of Canine Leproid Granuloma Syndrome (CLGS)?
Often undergoes spontaneous remission ## Footnote Treatment is only indicated for refractory or disfiguring lesions
120
What are the treatment components for Canine Leproid Granuloma Syndrome (CLGS)?
* Surgical resection * Dual antimicrobial therapy ## Footnote Excellent prognosis in most cases
121
What is the most common manifestation of rapidly growing mycobacteria in cats?
Paniculitis ## Footnote Prognosis varies by species and geography
122
What is the etiology of Actinomycosis?
Actinomyces spp.: facultative anaerobic or microaerophilic, gram-positive, branching filamentous bacteria ## Footnote Non-spore forming, non-acid-fast, non-motile
123
What common conditions can lead to Actinomycosis infections?
* Foreign body migration * Periodontal disease * Bite wounds * Plant material injuries * Aspiration pneumonia
124
In which animals is Actinomycosis most commonly found?
Typically affects immunocompetent animals, but can occur with concomitant immunosuppressive disease or neoplasia ## Footnote Young male large-breed outdoor dogs are overrepresented
125
What are the common clinical signs of Actinomycosis in dogs?
* Periodontal disease * Subcutaneous or soft tissue abscesses * Pleuritis and pneumonia ## Footnote Other manifestations include CNS infections and ocular infections
126
What is the preferred diagnostic method for Actinomycosis?
16S rRNA gene sequencing ## Footnote Offers species-level identification and improved accuracy
127
What is the mainstay treatment for Actinomycosis in dogs?
Combination of surgical and antimicrobial therapy ## Footnote Superior to antibiotics alone
128
What are common antimicrobial therapies for mycobacteria in dogs?
* Rifampin: 10–15 mg/kg PO q24h * Enrofloxacin: 10 mg/kg IV/IM/PO q24h * Clarithromycin: 5–10 mg/kg PO q12h * Azithromycin: 5–15 mg/kg PO q24h * Pyrazinamide: 15–40 mg/kg PO q24h * Isoniazid: 10–15 mg/kg PO q24h
129
What are common adverse effects associated with Rifampin in dogs?
Hepatotoxicity, GI upset ## Footnote Max dose is 60 mg/day
130
Fill in the blank: The most successful treatment for rapidly growing mycobacteria in cats involves _______.
Pre- and perioperative antibiotics, radical surgical excision, targeted antimicrobial therapy
131
What is the main treatment for Nocardia spp. infections in dogs?
Trimethoprim-Sulfonamide (TMS): 50 mg/kg PO q12h ## Footnote Adverse effects include bone marrow suppression, hepatitis, KCS
132
What are the common clinical signs of Nocardiosis in animals?
* Superficial abscesses * Indurated nodular masses * Pyothorax * Granulomatous pneumonia
133
What is a significant difference between Actinomyces and Nocardia?
Actinomyces are mucosal commensals, while Nocardia are saprophytic soil organisms ## Footnote Nocardia are found ubiquitously in the environment
134
What is the prognosis for disseminated Nocardiosis in dogs and cats?
Grave prognosis ## Footnote Many animals are euthanized due to deterioration or treatment failure
135
What type of bacteria is Brucella spp.?
Intracellular, host-adapted gram-negative aerobic coccobacilli
136
Name the host-adapted strains of Brucella.
* Brucella abortus: Cattle * Brucella melitensis: Small ruminants * Brucella suis: Swine * Brucella canis: Dogs
137
What distinguishes rough strains from smooth strains of Brucella?
Rough strains lack the mucoid O-polysaccharide side chain on their LPS, while smooth strains have it
138
Which Brucella strains pose the greatest zoonotic concern?
* Brucella abortus * Brucella melitensis * Brucella suis
139
What regions are considered endemic for brucellosis?
* Middle East * Africa * Asia * Latin America
140
What are the main routes of transmission for Brucella?
* Mucosal (oral, nasal, venereal) * Transplacental * Perinatal (milk, discharge contact)
141
List some reproductive signs of canine brucellosis.
* Abortion * Infertility * Orchitis * Epididymitis
142
What are the common diagnostic modalities for canine brucellosis?
* Direct Detection (PCR, Culture) * Serologic Testing (RSAT, 2-ME RSAT, TAT, LFIA, AGID, ELISA)
143
What is the gold standard for diagnosing Brucella?
Culture
144
What is the recommended treatment protocol for B. canis?
* Triple therapy: Doxycycline + Gentamicin + Rifampin for 3 months * Monotherapy: Enrofloxacin
145
What should be done with positive dogs in a kennel situation?
* Isolate * Euthanize if outbreak risk
146
What is the sensitivity of the LFIA test for detecting antibodies to B. canis?
98.6%
147
What are the key prevention strategies for brucellosis in dogs?
* Pre-entry screening * Routine testing * Quarantine newly introduced dogs * Public education
148
What are common seroprevalence estimates for B. canis in Brazil?
High (>20%)
149
What is the duration of bacteremia in dogs infected with B. canis?
May last 6–64 months
150
What is the risk associated with untreated canine brucellosis?
High recrudescence rate and zoonotic risk
151
What is the significance of the study on intact versus neutered dogs regarding B. canis serology?
Positive serology more frequent in neutered animals
152
What is the typical test timing consideration after suspected exposure to B. canis?
Re-test 8–12 weeks later if initial test is negative
153
What are the potential clinical manifestations of canine brucellosis?
* Lymphadenomegaly * Discospondylitis * Osteomyelitis * Polyarthritis
154
What are the causative agents of tetanus and botulism?
Tetanus: Clostridium tetani Botulism: Clostridium botulinum ## Footnote Both are gram-positive, anaerobic, spore-forming bacilli.
155
What type of paralysis does tetanus toxin cause?
Spastic paralysis ## Footnote Tetanus toxin inhibits neurotransmitter release, leading to muscle contraction.
156
What type of paralysis does botulinum toxin cause?
Flaccid paralysis ## Footnote Botulinum toxin prevents neurotransmitter release, leading to muscle relaxation.
157
What is the mechanism of action of tetanospasmin?
Inhibits release of glycine and GABA by cleaving synaptobrevin ## Footnote This leads to disinhibition of α-motor neurons.
158
What are the clinical signs of generalized tetanus?
Stiff gait, sawhorse stance, elevated tail, hypertonia, lockjaw, dysphagia, facial spasms ## Footnote Additional signs include third eyelid protrusion and respiratory paralysis.
159
What is the incubation period for tetanus?
5–12 days (range up to 3 weeks) ## Footnote This varies based on the severity of the infection.
160
What is a key pathophysiologic concept of tetanus?
Tetanospasmin targets inhibitory interneurons, disrupting glycine and GABA release ## Footnote This leads to loss of control over α-motor neurons.
161
What is the primary treatment for botulism?
Supportive care ## Footnote This includes ventilation, fluids, and nutrition.
162
What are the routes of exposure for botulism?
Foodborne, wound botulism, toxicoinfectious, iatrogenic ## Footnote Foodborne is the most common route due to pre-formed toxin ingestion.
163
What is the hallmark clinical sign of botulism?
Ascending symmetric flaccid paralysis ## Footnote This pattern typically starts in the pelvic limbs and progresses to respiratory failure.
164
What is the mechanism of action of botulinum neurotoxins (BoNTs)?
Cleaves SNARE proteins, preventing ACh release at neuromuscular junctions ## Footnote This leads to flaccid paralysis.
165
What is the prognosis for tetanus in dogs with severe cases?
Up to 50% mortality ## Footnote Prognosis worsens with increasing classification of severity.
166
What is the role of antitoxin in the treatment of tetanus?
Neutralizes unbound tetanospasmin ## Footnote Ineffective once bound to neurons.
167
What is the preferred antibiotic for treating Clostridium tetani?
Metronidazole ## Footnote It is superior to penicillin for achieving therapeutic anaerobic concentrations.
168
What is the typical onset time for clinical signs of botulism after exposure?
12 hours to 6 days ## Footnote Timing can vary based on the route of exposure.
169
What supportive treatments are used for severe cases of tetanus?
Mechanical ventilation, sedation, muscle relaxants ## Footnote Intensive nursing care is critical for survival.
170
What is the significance of sympathetic overactivity in tetanus?
Causes tachycardia, hypertension, and autonomic instability ## Footnote This is due to loss of central inhibitory control.
171
Fill in the blank: Tetanospasmin leads to the disinhibition of _______ neurons.
α-motor ## Footnote This results in sustained muscle contraction.
172
What is a common post-recovery sequelae in dogs recovering from tetanus?
Residual motor deficits ## Footnote Abnormal REM sleep behaviors may also occur.
173
What is the mechanism of magnesium sulfate therapy in tetanus treatment?
Inhibits neuromuscular transmission and reduces autonomic dysregulation ## Footnote It serves as an adjuvant therapy.
174
What happens to botulinum spores in the small intestine?
Spores germinate and produce the inactive progenitor toxin complex ## Footnote This process is crucial for the activation of the toxin.
175
How is the botulinum toxin activated?
Within the alkaline environment of the small intestine ## Footnote The conditions of the small intestine facilitate the activation of the toxin.
176
What process allows the botulinum toxin to enter the body?
Endocytosis into intestinal epithelium, then entering lymphatic and vascular systems ## Footnote This is how the toxin spreads throughout the body.
177
What does the heavy chain of botulinum toxin bind to?
Presynaptic peripheral cholinergic nerve terminals with high affinity ## Footnote This binding is essential for the toxin's mechanism of action.
178
What is the result of the light chain cleaving SNARE proteins?
Inhibition of acetylcholine (ACh) release at the neuromuscular junction ## Footnote This leads to muscle paralysis.
179
What is required for recovery from botulism?
Regeneration of axon terminals and reformation of neuromuscular junctions ## Footnote This process contributes to the prolonged disease course.
180
What is the typical onset time for symptoms after toxin ingestion?
Within 12 hours ## Footnote Early onset of symptoms is a key feature of botulism.
181
What cranial nerve involvements are seen in botulism?
Facial nerve paralysis, decreased jaw tone, decreased gag reflex, reduced vocalization, megaesophagus ## Footnote These signs indicate cranial nerve dysfunction.
182
What autonomic signs may be present in botulism cases?
Altered heart rate, mydriasis with depressed PLR, keratoconjunctivitis sicca, urinary retention, constipation ## Footnote Autonomic dysfunction can complicate the clinical picture.
183
What respiratory involvement may occur in severe cases of botulism?
Diaphragmatic breathing with increased abdominal effort ## Footnote The diaphragm's resistance suggests advanced disease.
184
What complications can lead to death in botulism cases?
Respiratory failure, aspiration pneumonia, prolonged recumbency complications ## Footnote These complications highlight the severity of the disease.
185
What is the gold standard for definitive diagnosis of botulism?
Detection of botulinum toxin in serum, feces, or gastric contents ## Footnote This method is most sensitive early in the disease.
186
What is the role of mouse bioassay in diagnosing botulism?
Gold standard for toxin detection ## Footnote If available, this assay is the most reliable test.
187
What may be observed in electrodiagnostics for botulism?
Reduced compound muscle action potential (CMAP) amplitude ## Footnote Normal conduction velocity and no temporal dispersion are also noted.
188
What is important in bladder care for botulism patients?
Manual expression, catheterization, or medications may be needed ## Footnote Urinary retention is a common issue in affected animals.
189
When is antitoxin effective in botulism treatment?
If administered early, before toxin binds nerve terminals ## Footnote It does not reverse established neuromuscular blockade.
190
What precautions should be taken when administering type C antitoxin?
Use with caution due to risk of anaphylaxis ## Footnote A test dose and emergency medications should be prepared.
191
What is the prognosis for dogs with botulism with early supportive care?
Favorable, with full recovery expected in most cases within 2–3 weeks ## Footnote Some may experience residual weakness for up to a year.
192
What factors can worsen the prognosis of botulism?
Delayed diagnosis, severe cranial nerve or respiratory involvement, development of aspiration pneumonia ## Footnote These factors can complicate recovery.
193
What are Bartonella spp.?
Gram-negative, hemotropic, facultative intracellular bacteria transmitted by blood-sucking arthropods
194
Which animals are the natural reservoirs for Bartonella henselae?
Cats
195
What is the primary reservoir for Bartonella vinsonii subsp. berkhoffii?
Dogs
196
Which vector is the most relevant for the transmission of B. henselae?
Ctenocephalides felis (cat flea)
197
What is the prevalence of Bartonella in cats?
5% to 40%
198
What percentage of asymptomatic dogs are infected with B. henselae or B. vinsonii subsp. berkhoffii?
~18–20%
199
What is the primary target of Bartonella in the body?
Endothelial cells
200
How long can cats maintain relapsing bacteremia with B. henselae?
Up to 454 days
201
What percentage of canine infective endocarditis cases does Bartonella account for?
19–28%
202
What are common clinical findings in dogs with Bartonella endocarditis?
* Heart murmur: 89% * Lameness: 43% * Respiratory signs: 28%
203
What is the gold standard for diagnosing Bartonella?
Solid media culture
204
Fill in the blank: Cats infected with B. vinsonii subsp. berkhoffii have documented _______.
Osteomyelitis
205
What are some of the proposed pathogenetic mechanisms associated with Bartonella infection?
* Intravascular infection * Immune-mediated response * Lymphatic infection * Pyogranulomatous lesions * Abnormal vascular proliferation
206
What imaging technique is high sensitivity for detecting vegetative lesions in Bartonella cases?
Echocardiography
207
What is the recommended treatment for symptomatic dogs with Bartonellosis?
Combination therapy targeting both intracellular and extracellular compartments
208
What is a key principle of treating canine Bartonellosis?
Only treat symptomatic dogs or those with confirmed serious disease
209
What is the recommended treatment protocol for general Bartonellosis in dogs?
Doxycycline 5 mg/kg PO q12h or 10 mg/kg PO q24h + Enrofloxacin 5–10 mg/kg PO q12h for 6 weeks ## Footnote This protocol is aimed at treating general Bartonellosis.
210
What is the alternative CNS protocol for treating Canine Bartonellosis?
Azithromycin 10 mg/kg PO q24h x7 days, then q48h + Rifampin 5 mg/kg PO q12h for 4–6 weeks ## Footnote This is for cases involving CNS involvement.
211
What should be done if systemic inflammatory signs develop during treatment for Canine Bartonellosis?
Treat with short-term glucocorticoids ## Footnote Prednisone in dogs: 0.5–1 mg/kg PO once daily; Prednisolone in cats: 1–2 mg/kg PO once daily.
212
What is the minimum duration of treatment for Canine Bartonellosis?
4–6 weeks ## Footnote Ideally, continue therapy for 2 weeks beyond resolution of clinical signs.
213
Why is treatment not recommended for healthy bacteremic cats with Feline Bartonellosis?
Due to the risk of antimicrobial resistance and lack of proven benefit ## Footnote There is no current justification for screening or treating healthy cats for Bartonella.
214
What is the preferred antibiotic for long-term home therapy in cats with bacteremia?
Doxycycline + Pradofloxacin ## Footnote Doxycycline dosage: 5 mg/kg PO q12h or 10 mg/kg PO q24h; Pradofloxacin: 10 mg/kg PO q24h.
215
What are the recommended antibiotic combinations for endocarditis in cats?
Marbofloxacin + Azithromycin ## Footnote Marbofloxacin: 5.5 mg/kg PO q24h; Azithromycin: 10 mg/kg PO q24h x 7 days, then q48h.
216
What is the primary method of preventing Bartonellosis?
Vector control ## Footnote Year-round ectoparasite prevention is essential for both dogs and cats.
217
What precautions should veterinary professionals take to reduce occupational risk for Bartonellosis?
Use of personal protective equipment (PPE) when handling flea-infested animals or specimens ## Footnote Avoiding needle stick injuries, bites, and scratches.
218
True or False: Direct dog-to-human transmission of Bartonella has been documented.
False ## Footnote However, Bartonella DNA has been found in dog saliva.
219
What are the characteristics of Leptospira?
Thin, elongated, highly motile, helical organisms with distinctive hooked ends.
220
How does Leptospira stain?
Exhibit Gram-negative staining but possess features of both Gram-positive and Gram-negative bacteria.
221
What is the basis for serologic typing of Leptospira?
Differences in the carbohydrate component of lipopolysaccharide (LPS).
222
Which animals are significant reservoirs for Leptospira?
Small rodents, dogs, cats, and humans.
223
What are the common clinical signs of acute leptospirosis in dogs?
* Anorexia * Vomiting * Lethargy * Abdominal pain * Diarrhea * Jaundice * Dehydration * Fever or hypothermia.
224
What is Leptospiral Pulmonary Hemorrhagic Syndrome (LPHS)?
A major cause of mortality characterized by intra-alveolar hemorrhage with minimal inflammatory infiltration.
225
What are the predominant lesions in renal pathology due to leptospirosis?
Acute interstitial nephritis with tubular cell necrosis, apoptosis, and regeneration.
226
What is the correlation between hyperbilirubinemia and hepatocellular necrosis in leptospirosis?
Hyperbilirubinemia is not correlated with hepatocellular necrosis.
227
What is the gold standard for diagnosing leptospirosis?
Serology – Microscopic Agglutination Test (MAT).
228
What limitations does the Microscopic Agglutination Test (MAT) have?
* False negatives may occur * Single titers are difficult to interpret.
229
What is the purpose of PCR testing in leptospirosis diagnosis?
Detects leptospiral DNA in blood or urine, useful in the acute phase or concern for vaccination causing elevated titers
230
What are the limitations of point-of-care ELISA and lateral flow assays?
* False negatives may occur in early infection * False positives may occur due to previous vaccination.
231
What are the common findings on abdominal ultrasound in leptospirosis?
* Renal cortical hyperechogenicity * Renomegaly * Pyelectasia.
232
What findings may indicate hepatic involvement in chronic leptospirosis?
Chronic granulomatous hepatitis has been suggested, although less defined.
233
What is the recommended diagnostic technique for liver tissue in leptospirosis?
* Silver staining * Immunohistochemistry * Immunofluorescence.
234
What is the role of chronic leptospiral infection in chronic kidney disease (CKD)?
Remains incompletely understood but may progress to renal fibrosis.
235
What are the limitations of serologic testing for leptospirosis?
* False negatives may occur in early infection due to lack of seroconversion * False positives may occur due to previous vaccination
236
When is blood PCR typically positive in experimentally infected dogs?
During the first week of infection
237
What are common PCR targets for leptospirosis testing?
* LipL32 gene (specific for pathogenic leptospires) * 23S rDNA
238
What are the two molecular typing methods available for leptospirosis?
* Multiple Locus Sequence Typing (MLST) * Multiple Locus Variable Number Tandem Repeat Analysis (MLVA)
239
What should be done if doxycycline is not tolerated in leptospirosis treatment?
Start with an IV penicillin-class drug: Penicillin G, ampicillin, or amoxicillin
240
What is the management approach for Leptospiral Pulmonary Hemorrhagic Syndrome (LPHS)?
Supportive management including thoracic radiographs and avoiding stress, overhydration, and systemic hypertension
241
What percentage of dogs may have persistent renal impairment after leptospirosis recovery?
Approximately 50%
242
What is recommended for dogs in contact with leptospirosis-infected dogs?
Prophylactic treatment with doxycycline (5–10 mg/kg PO q12–24h for 14 days)
243
What is the most consistent histopathological lesion in cats infected with leptospirosis?
Interstitial nephritis
244
What type of vaccines are available for leptospirosis prevention?
* Bivalent vaccines (Canicola, Icterohaemorrhagiae) * Quadrivalent vaccines (Canicola, Icterohaemorrhagiae, Grippotyphosa, Pomona)
245
What significant finding was associated with quadrivalent vaccination in a Swiss case-control study?
Significantly reduced odds of developing leptospirosis
246
What is the main family of the order Rickettsiales that includes Ehrlichia?
Anaplasmataceae
247
What disease is caused by Ehrlichia canis in dogs?
Canine monocytic ehrlichiosis (CME)
248
What is the vector for Ehrlichia canis?
Rhipicephalus sanguineus (brown dog tick)
249
What are the common clinical signs in the acute phase of Canine Monocytic Ehrlichiosis?
* Fever * Lethargy * Anorexia * Weight loss * Lymphadenopathy * Splenomegaly
250
What hematologic finding is most consistent in Canine Monocytic Ehrlichiosis?
Thrombocytopenia
251
What is a potential chronic complication of Canine Monocytic Ehrlichiosis?
* Bleeding diathesis * Nonregenerative anemia * Pancytopenia * Neurologic signs * Protein-losing nephropathy
252
What is the standard method for serology diagnosis of Canine Ehrlichiosis?
Indirect fluorescent antibody (IFA) and ELISA assays
253
True or False: E. chaffeensis is zoonotic and less common in dogs.
True
254
What are the vectors for Anaplasma phagocytophilum?
* Ixodes scapularis * Ixodes pacificus * Ixodes ricinus * Ixodes persulcatus
255
What disease does Anaplasma platys cause?
Canine cyclic thrombocytopenia
256
What are the clinical signs of Canine Granulocytic Anaplasmosis?
* Fever * Lethargy * Inappetence * Stiffness * Lameness
257
What is the sensitivity of the SNAP 4Dx Plus test for detecting E. canis?
97.8%
258
Fill in the blank: Ehrlichia ewingii is transmitted by the _______.
Amblyomma americanum (Lone Star tick)
259
What is the primary host for Ehrlichia chaffeensis?
Humans
260
What is the hallmark finding in blood for Anaplasma phagocytophilum?
Morulae in neutrophils
261
What is the treatment duration for Anaplasma phagocytophilum?
14 days
262
What is a rare but potential route of transmission for tick-borne diseases?
Blood transfusion
263
What are the common breeds affected by Anaplasma phagocytophilum?
* Labrador Retrievers * Golden Retrievers
264
What diagnostic method is the gold standard for confirming Anaplasma phagocytophilum infection?
PCR
265
What is the suspected vector for A. platys?
Rhipicephalus sanguineus ## Footnote Vector transmission not confirmed
266
What are the typical clinical signs of A. platys?
Usually subclinical or mild May cause: * Thrombocytopenia * Rarely fever, splenomegaly, bleeding
267
What diagnostic methods are used for A. platys?
* Cytology: Morulae in platelets or megakaryocytes * Serology: Cross-reacts with A. phagocytophilum * PCR: Required for definitive diagnosis
268
What is the causative agent of Salmon Poisoning Disease?
Neorickettsia helminthoeca
269
What is the primary vector for Neorickettsia helminthoeca?
Nanophyetus salmincola
270
What is the life cycle of Neorickettsia helminthoeca?
Fluke eggs shed in dog feces → become miracidia → infect aquatic snail → develop into cercariae → penetrate salmonid fish → encyst as metacercariae in fish tissue
271
What species are overrepresented in the susceptibility to Neorickettsiosis?
Male Labrador Retrievers Other susceptible species include: * Foxes * Coyotes * Bears
272
What are the early clinical signs of Salmon Poisoning Disease?
* High fever (up to 42°C / 107.6°F) * Anorexia
273
What laboratory abnormalities are observed in Salmon Poisoning Disease?
* Thrombocytopenia * Neutrophilia ± left shift * Lymphopenia * Monocytosis * Hyponatremia * Hypokalemia * ↑ ALT, ALP * Hypoalbuminemia
274
How is Salmon Poisoning Disease diagnosed?
* Fecal flotation & sedimentation * Lymph node cytology * PCR testing
275
What is the primary host for Neorickettsia risticii?
Horses
276
What is the mechanism of transmission for Potomac Horse Fever?
Ingestion of infected aquatic insects containing trematode metacercariae
277
What are the vectors for Rocky Mountain Spotted Fever?
* Dermacentor variabilis (American dog tick) * Dermacentor andersoni (Rocky Mountain wood tick) * Rhipicephalus sanguineus
278
What cells are primarily targeted in Rocky Mountain Spotted Fever?
Vascular endothelial cells
279
What are the common clinical signs of Rocky Mountain Spotted Fever in dogs?
* Fever * Lethargy * Petechiae * Neurologic signs * Thrombocytopenia
280
What is the incubation period for Rocky Mountain Spotted Fever?
2–14 days (mean: 7 days)
281
What are the prevention methods for Rocky Mountain Spotted Fever?
Tick control is the primary preventive strategy No vaccine available
282
What is the significance of dogs in relation to Rocky Mountain Spotted Fever?
Dogs are sentinels for human risk of RMSF
283
What is the etiologic agent of feline monocytic ehrlichiosis?
Ehrlichia canis-like organisms
284
What are the common clinical signs of feline monocytic ehrlichiosis?
* Fever * Lethargy * Anorexia * Pallor * Splenomegaly
285
What laboratory abnormalities are seen in feline monocytic ehrlichiosis?
* Non-regenerative anemia * Hyperglobulinemia
286
What is the etiologic agent of feline granulocytic anaplasmosis?
Anaplasma phagocytophilum
287
What are the clinical signs of feline granulocytic anaplasmosis?
* Lethargy * Anorexia * Fever * Pallor * Thrombocytopenia
288
What is the common sign of Ehrlichia canis-like infection?
Fever, pallor, anemia, arthritis ## Footnote These signs can overlap with other infectious or inflammatory diseases in cats.
289
What is the common sign of Anaplasma phagocytophilum infection?
Fever, lethargy, lameness, thrombocytopenia ## Footnote Signs may vary and can be nonspecific.
290
What type of cells does Ehrlichia canis-like infection target?
Mononuclear cells
291
What type of cells does Anaplasma phagocytophilum infection target?
Granulocytes
292
What are the consistent lab abnormalities for Ehrlichia canis-like infection?
Non-regenerative anemia, hyperglobulinemia
293
What are the consistent lab abnormalities for Anaplasma phagocytophilum infection?
Thrombocytopenia, possibly anemia
294
What diagnostic tools are used for Ehrlichia canis-like infection?
PCR, cytology, (limited serology)
295
What diagnostic tools are used for Anaplasma phagocytophilum infection?
Cytology, PCR, (limited serology)
296
What are hemotropic mycoplasmas?
Small (0.3–1.0 µm), wall-less bacteria that attach to the surface of erythrocytes. ## Footnote Historically classified as Haemobartonella, they have been reclassified under the genus Mycoplasma.
297
What distinguishes hemoplasmas from typical Mycoplasma spp.?
Hemoplasmas differ from typical Mycoplasma spp. as they infect erythrocytes rather than colonizing mucosal surfaces.
298
What is the prevalence range of Mycoplasma haemofelis in cats?
0.4% – 27%
299
What is the median prevalence of 'Candidatus Mycoplasma haemominutum' in cats?
15.5%
300
What are common risk factors for hemoplasma infections in cats?
* Male, outdoor, non-pedigreed cats * Older age * Positive FeLV or FIV status * Feral or free-roaming lifestyle
301
What clinical signs are associated with Mycoplasma haemofelis in cats?
* Acute hemolytic anemia * Regenerative response (reticulocytosis) * Clinical signs appear ~2–34 days post-infection
302
What is the diagnostic gold standard for hemoplasma infections?
PCR
303
What is a characteristic of the carrier state in cats infected with hemoplasmas?
Long-term subclinical carriers exist, especially for 'Ca. M. haemominutum'.
304
Fill in the blank: Hemoplasma DNA has been found in ______, ticks, and mosquitoes.
fleas
305
What treatment is indicated for hemoplasmosis?
Positive PCR for a pathogenic hemoplasma with clinical signs and supportive clinicopathologic findings.
306
What is the role of quantitative PCR (qPCR) in hemoplasma infections?
Allows monitoring of blood organism load and assessment of treatment efficacy.
307
What are common laboratory findings in hemoplasma infections?
* Regenerative macrocytic hypochromic anemia * Reticulocytosis * Positive Coombs test
308
What should be monitored to assess treatment response in hemoplasma infections?
Recheck CBC to assess response (e.g., improved PCV, regenerative indices)
309
What is the typical pathogenicity of 'Candidatus M. haemominutum'?
Mild to non-pathogenic alone; anemia generally occurs only with concurrent diseases.
310
True or False: Hemoplasma infections are commonly diagnosed by cytology.
False (organism load must be high to find in smear and can be mistaken for Heinz bodies)
311
List the conditions that may be differential diagnoses for hemoplasma infections.
* Primary or secondary IMHA * Hemotropic parasites * Retroviral infections * Hypophosphatemia * Toxin-induced hemolysis
312
What therapy is usually sufficient for treating hemoplasma-associated anemia?
Antibiotic therapy and supportive care
313
Under what condition should glucocorticoid therapy be initiated for hemoplasma-associated anemia?
Strong evidence of concurrent primary IMHA unresponsive to antibiotics
314
What should be used for ectoparasite prevention?
Year-round flea and tick preventives
315
What are some risk factors for hemoplasma infection?
* Outdoor exposure * Shelter environments * Dog fighting
316
What is mandatory for blood donor screening?
PCR screening for hemoplasma infection
317
What must be considered before restricting outdoor access for cats?
Behavioral and welfare needs of cats used to outdoor access
318
Is vertical transmission definitively proven for feline hemoplasmas?
No, it is suggested but not definitively proven
319
What is a key recommendation regarding glucocorticoids?
Not routinely indicated; may cause reactivation
320
What is strongly recommended for all at-risk animals?
Ectoparasite control
321
What are common clinical signs of bacterial enteritis?
Mild to moderate diarrhea (watery, mucoid, or bloody), tenesmus, lethargy, dehydration, anorexia, vomiting, fever, abdominal pain ## Footnote Extra-GI signs may include cholangiohepatitis, cholecystitis, reproductive issues, and neurologic abnormalities.
322
What are the characteristics of Campylobacter species?
Gram-negative rods (0.2–0.8 µm wide by 0.5–5 µm long), occurring singly, in pairs, or in chains
323
How are Campylobacter organisms transmitted?
Via the fecal-oral route, either directly or indirectly
324
What species of Campylobacter are commonly isolated from dogs?
* C. upsaliensis * C. jejuni * C. helveticus
325
What is the significance of co-infections in Campylobacter cases?
Common co-infections include parvovirus, coronavirus, circovirus, endoparasites, and Clostridium spp.
326
What factors contribute to the pathogenicity of Campylobacter?
* Bacterial motility * Adhesiveness * Invasiveness * Toxin production * Multidrug resistance * Stress-response genes
327
How can Campylobacter adherence to intestinal cells occur?
Through flagella and adhesins
328
What methods can confirm a Campylobacter diagnosis?
Isolating the organism from feces or other specimens via microaerophilic culture
329
What is a common method for identifying Campylobacter species?
MALDI-TOF mass spectrometry
330
What are the treatment options for Campylobacter infections?
* Erythromycin: 10–15 mg/kg PO q8h * Tylosin: 6–16 mg/kg PO q12h * Azithromycin: 5–10 mg/kg PO q24h * Enrofloxacin: 5 mg/kg PO q24h
331
What is the prognosis for uncomplicated bacterial enteritis, including Campylobacteriosis?
Generally excellent with appropriate supportive care
332
What is the zoonotic potential of Campylobacter?
It is one of the most common causes of foodborne illness in humans
333
What increases the risk of Campylobacter infection in humans?
Contact with immature or diarrheic pets, especially for children, pregnant women, the elderly, and immunocompromised individuals
334
What dietary practices are significant risk factors for Campylobacter infection in pets?
Feeding pets a raw meat or bones diet
335
What is essential for client education regarding Campylobacter?
Hygiene education, especially for high-risk households
336
What is a major challenge in diagnosing bacterial enteritis in dogs and cats?
High prevalence of asymptomatic carriage ## Footnote This complicates the identification of symptomatic infections.
337
What is the recommended culture medium for isolating Campylobacter spp.?
Modified charcoal cefoperazone deoxycholate agar (mCCDA) ## Footnote This medium supports the growth of microaerophilic bacteria like Campylobacter.
338
What is the significance of the CDT toxin in Campylobacter infections?
Causes mucosal cell cycle arrest and damage ## Footnote This contributes to the pathogenicity of the bacteria.
339
What is the zoonotic potential of Campylobacter jejuni?
Major concern, especially from undercooked poultry ## Footnote Identical strains can be found in pets and humans.
340
What are the common clinical signs of Salmonella infection in animals?
* Asymptomatic in most * Acute gastroenteritis * Diarrhea (watery, mucoid, hemorrhagic) * Anorexia * Fever * Vomiting * Abdominal pain
341
What is the key method for diagnosing Salmonella infections?
Culture from feces or other tissues, requiring selective enrichment ## Footnote Media such as MacConkey or XLD agar are used.
342
What is Clostridioides difficile and its transmission route?
Gram-positive, anaerobic, spore-forming bacillus; transmitted via fecal-oral route ## Footnote It can survive in contaminated environments for long periods.
343
What are the primary toxins produced by Clostridioides difficile?
* TcdA (enterotoxin A) * TcdB (cytotoxin B) * Binary toxin CDT
344
What is the zoonotic risk associated with Clostridioides difficile?
Considered low, but community-acquired human CDI could involve pets ## Footnote Hygiene and handling precautions are recommended.
345
What are the notable features of Salmonella enterica?
* MDR common * Systemic spread possible * Primary pathogen in mammals
346
What is the prevalence of Salmonella in healthy dogs and cats?
* Dogs: 0–3.6% * Cats: 0–4%
347
What is the significance of raw meat-based diets (RMBD) in relation to Salmonella?
Significant risk factor for transmission ## Footnote RMBDs can harbor Salmonella and other pathogens.
348
What are the clinical signs of Clostridioides difficile infection when present?
* Small or large bowel diarrhea * Vomiting * Lethargy * Anorexia
349
What is Clostridioides difficile?
Anaerobic, gram-positive, spore-forming bacillus ## Footnote Spores are highly resistant to environmental conditions and disinfectants.
350
How is Clostridioides difficile transmitted?
Fecal–oral route, often from contaminated environments ## Footnote Found in the intestinal tracts of humans and animals.
351
What is the prevalence of Clostridioides difficile in healthy dogs and cats?
Healthy dogs: up to 58%; Healthy cats: up to 21% ## Footnote Higher prevalence in juveniles and hospitalized animals.
352
What is required for the pathogenesis of Clostridioides difficile disease?
Disruption of normal flora and overgrowth of toxigenic strains ## Footnote Toxins include TcdA (enterotoxin A) and TcdB (cytotoxin B).
353
What are the clinical signs of Clostridioides difficile infection?
Small or large bowel diarrhea, vomiting, anorexia, lethargy ## Footnote Hospital outbreaks in dogs and cats have occurred.
354
What is the preferred method for diagnosing Clostridioides difficile?
PCR (preferred) for detecting TcdA and TcdB genes ## Footnote Anaerobic fecal culture and antigen testing are also used.
355
What are the treatment options for Clostridioides difficile infection?
Discontinue unnecessary antibiotics, supportive care, probiotics, dietary changes, Fecal Microbiota Transplant (FMT) ## Footnote FMT shown to be superior to metronidazole in dogs.
356
What is Clostridium perfringens?
Anaerobic, gram-positive, spore-forming bacillus ## Footnote Seven toxotypes (A–G) based on toxin production.
357
What is the prevalence of Clostridium perfringens in dogs?
Up to 84% in healthy dogs; up to 91% in diarrheic dogs ## Footnote Type A, enterotoxigenic strains most commonly implicated in food poisoning in humans.
358
What triggers disease caused by Clostridium perfringens?
Sporulation of toxigenic strains leading to enterotoxin (CPE) release ## Footnote Inciting factors include diet change, antimicrobials, co-infections.
359
What are the diagnostic methods for Clostridium perfringens?
Direct fecal PCR for toxin genes and CPE ELISA ## Footnote Diagnosis requires detection of toxigenic strain and clinical correlation.
360
What are the treatment options for Clostridium perfringens infections?
Supportive care, probiotics, antibiotics only for severe cases ## Footnote Metronidazole, Tylosin, and Ampicillin are options.
361
What is Escherichia coli (E. coli)?
Facultative anaerobic, gram-negative, pleomorphic rods ## Footnote Classified by surface antigens: O, H, and K.
362
What are the pathotypes of concern for E. coli?
EPEC, ETEC, EHEC (including VTEC and NTEC), EIEC, EAEC, AIEC ## Footnote Most strains are commensals but can become pathogenic.
363
What are the clinical signs of AIEC granulomatous colitis?
Chronic large bowel diarrhea, hematochezia, weight loss ## Footnote Histopathology shows ulceration and PAS-positive macrophages in mucosa.
364
What is Yersinia enterocolitica?
Gram-negative, motile, facultative anaerobe ## Footnote Member of the family Enterobacteriaceae.
365
What are the clinical signs of Yersinia enterocolitica infection?
Most infections are subclinical; may present with enteritis or extra-GI infections ## Footnote Rare cases may exhibit myocarditis or hepatitis.
366
What is the treatment for Yersinia enterocolitica infections?
Most cases are self-limiting; antibiotics based on susceptibility testing if required ## Footnote Ingestion of contaminated pork or other meats is suspected as the primary route.
367
What is Clostridium piliforme (Tyzzer’s Disease)?
Obligate intracellular gram-negative spore-forming bacillus ## Footnote Transmission occurs via ingestion of spores from wild rodents or rabbit feces.
368
What are the clinical signs of Clostridium piliforme infection?
Acute, often fatal; affects liver, GI tract, myocardium ## Footnote Diagnosis is through histopathology and PCR.
369
What are the general guidelines for infection control in hospital settings?
Animals with suspected bacterial enteritis should be housed in isolation wards ## Footnote Managed with barrier precautions and walked in designated separate areas.
370
What is the primary route of transmission for enteric protozoa?
Fecal-oral transmission. ## Footnote Except for Cystoisospora satanus, whose transmission pathway is unknown in dogs and cats.
371
What are the life cycles of coccidian parasites like Cystoisospora and Toxoplasma gondii?
Direct life cycles ## Footnote Infection occurs via ingestion of sporulated oocysts from the environment.
372
How do Cryptosporidium spp. infect hosts?
Immediately infectious upon excretion as sporulated oocysts ## Footnote Capable of autoinfection and highly environmentally resistant.
373
What is the infectious stage of Giardia spp.?
Cysts ## Footnote Cysts are environmentally resistant and transmitted via ingestion from contaminated sources.
374
What distinguishes Trichomonads from other protozoa in terms of transmission?
No cyst form; transmission occurs by ingestion of trophozoites.
375
What are paratenic hosts in the context of enteric protozoan transmission?
Invertebrate hosts like flies, cockroaches, and dung beetles that can transmit Giardia and Cystoisospora.
376
Which parasites are commonly found in dogs?
* Giardia duodenalis * Cryptosporidium spp. * Cystoisospora spp. * Neospora caninum
377
What is the prevalence of E. histolytica in dogs as per a Pakistani study?
9% ## Footnote Detected via microscopy.
378
What are the general mechanisms of pathogenesis for enteric protozoa?
Replication in intestinal epithelial cells, especially villus enterocytes or lamina propria.
379
What are the clinical signs associated with Cystoisospora spp. infections?
* Diarrhea * Weight loss * Dehydration * Severe cases: anorexia, vomiting, depression, death.
380
What is the prepatent period for Cryptosporidium parvum in dogs?
2–14 days.
381
What diagnostic methods are used for enteric protozoan detection?
* Direct fecal smear * Fecal flotation via centrifugation * ELISA * PCR * Culture
382
What is the purpose of using zinc sulfate in fecal flotation?
Preferred medium for Giardia to minimize cyst distortion.
383
What is the first-line therapy for giardiasis?
* Metronidazole (monotherapy) * Metronidazole + Fenbendazole * Fenbendazole (monotherapy) * Sulfadimethoxine
384
What is a common challenge in treating cryptosporidiosis?
Often self-limiting in immunocompetent animals.
385
What is a significant risk factor for E. histolytica infection in dogs?
Co-infection with certain colonic bacteria.
386
What type of diarrhea is associated with Tritrichomonas fetus?
Large bowel diarrhea with semi-formed feces, mucus, and fresh blood.
387
What is the survival time of T. fetus trophozoites in moist feces?
7 days at 23–24°C.
388
What is the expected patent period for Giardia spp. in dogs?
Weeks to months.
389
What are the potential treatments for cryptosporidiosis?
* Nitazoxanide * Azithromycin * Paramomycin * Auranofin
390
What is the FDA-approved drug for Cystoisosporiasis?
Sulfadimethoxine
391
Which drug is considered safe and highly effective for Cystoisosporiasis in kittens and puppies?
Ponazuril
392
What is the drug of choice for Tritrichomonas fetus in cats?
Ronidazole
393
What are the considerations for Ronidazole treatment failure?
* Inadequate dose or duration * Reinfection from a subclinical carrier * Drug resistance
394
What essential testing is needed for evaluating response in T. fetus?
PCR testing
395
What should not be used to assess treatment efficacy for Giardia?
ELISA for Giardia antigen
396
What is a significant finding regarding Giardia cyst shedding in puppies?
90% reduction seen with 2 doses of secnidazole (30 mg/kg) 2 weeks apart
397
Name three key potentially zoonotic protozoa in companion animals.
* Giardia duodenalis * Cryptosporidium spp. * Toxoplasma gondii
398
What genetic assemblages of Giardia duodenalis are zoonotic?
A1, A2, B3, B4
399
What is the primary host for C. hominis?
Humans
400
How does Toxoplasma gondii typically infect humans?
* Ingestion of sporulated oocysts from contaminated soil, water, or vegetables * Consumption of undercooked meat containing tissue cysts
401
What is the zoonotic risk from Entamoeba histolytica?
Minimal
402
Which animal is the primary reservoir for Balantidium coli?
Pigs
403
What zoonotic assemblages of Giardia duodenalis occur in both pets and humans?
A and B
404
What is the risk level of zoonotic transmission from pets for Giardia, according to CAPC and CDC?
Low but not negligible
405
What is the genus of the intraerythrocytic protozoan parasites that infect mammals?
Babesia ## Footnote Babesia is part of the phylum Apicomplexa.
406
What are the two phases of Babesia's life cycle?
Sexual reproduction in the definitive host and asexual reproduction in the intermediate mammalian host.
407
What is the primary route of transmission for Babesia?
Tick bite inoculation.
408
List the common clinical manifestations of Babesia infection.
* Fever * Lethargy * Pallor * Tachycardia * Tachypnea * Hypotensive shock * Splenomegaly * Icterus * Petechiae * Neurologic signs * Rhabdomyolysis * Acute kidney injury
409
What laboratory finding is associated with Babesia infections 2-3 weeks post-infection?
Regenerative anemia.
410
What is the most sensitive diagnostic method for Babesia?
PCR.
411
What treatment protocol is used for B. gibsoni, B. conradae, and B. vulpes?
Azithromycin 10 mg/kg PO q24h + Atovaquone 13.3 mg/kg PO q8h for 10 days.
412
True or False: Relapses are common in Babesia infections.
True.
413
What are the two phases of the lifecycle of Cytauxzoon felis?
* Schizogonous (tissue phase) * Erythrocytic (piroplasm) phase.
414
What is the mortality rate of untreated domestic cats infected with Cytauxzoon felis?
~90%.
415
What are the common clinical signs of Cytauxzoonosis?
* Lethargy * Anorexia * Fever * Icterus * Dehydration.
416
What is the first-line treatment for Cytauxzoon felis?
Atovaquone and Azithromycin.
417
What form of leishmaniasis is most common in dogs?
Visceral leishmaniasis.
418
What are the two forms of Leishmania?
* Promastigotes * Amastigotes.
419
What is the primary vector for Leishmania transmission?
Sandflies.
420
What is a key characteristic of the immune response in leishmaniasis?
A strong T-cell (Th1) response can control or clear the infection.
421
What are the common laboratory abnormalities in Cytauxzoonosis?
* Pancytopenia * Hyperbilirubinemia * Elevated liver enzymes * Hyperglycemia.
422
Fill in the blank: The primary vector for Cytauxzoon felis is _______.
Amblyomma americanum.
423
What is the geographical distribution of Cytauxzoon felis in the United States?
Midwest, Southeast, and Mid-Atlantic regions.
424
What is the role of bobcats in the epidemiology of Cytauxzoon felis?
Typically subclinical carriers.
425
How is Leishmania transmitted?
Sandflies, blood transfusion, vertical transmission ## Footnote Old World vector is Phlebotomus spp. and New World vector is Lutzomyia spp.
426
What are early clinical manifestations of Leishmaniasis?
Alopecia, papules, nodules, scaling ## Footnote These cutaneous lesions can precede systemic signs.
427
What are systemic signs of Leishmaniasis?
Weight loss, muscle wasting, fever, splenomegaly, lymphadenopathy, anterior uveitis, polyarthritis, glomerulonephritis, renal failure ## Footnote Hematologic abnormalities include non-regenerative anemia and lymphopenia.
428
What is the preferred method for definitive diagnosis of Leishmaniasis?
PCR ## Footnote PCR is preferred due to high sensitivity.
429
What is the goal of treatment for Leishmaniasis?
Clinical remission—not curative ## Footnote Relapse and reinfection are common in endemic areas.
430
What is the first-line therapy for Leishmaniasis in dogs?
Allopurinol and Meglumine antimoniate ## Footnote Meglumine antimoniate is not available in the U.S.
431
What are the two causative species of Hepatozoonosis in dogs?
Hepatozoon canis and Hepatozoon americanum ## Footnote H. canis is endemic in Europe, Asia, Africa, and South America, while H. americanum is found in the southeastern U.S.
432
How is Hepatozoonosis transmitted?
Ingestion of infected ticks or prey ## Footnote Infection does not occur via tick bite.
433
What are common clinical signs of Hepatozoonosis?
Fever, lethargy, muscle pain or lameness, mucopurulent ocular discharge, stiff gait, myalgia, muscle atrophy ## Footnote These signs can vary in severity.
434
What laboratory findings are associated with Hepatozoonosis?
Non-regenerative anemia, marked leukocytosis, hypoglycemia, hypoalbuminemia, elevated ALP ## Footnote Radiographs may show periosteal proliferation.
435
What is the most sensitive and specific method for diagnosing Hepatozoonosis?
PCR ## Footnote PCR differentiates between H. americanum and H. canis.
436
What is the triple therapy for Hepatozoonosis?
Potentiated sulfonamide + clindamycin + pyrimethamine ## Footnote This treatment is not curative and relapses are common.
437
What is the definitive host of Toxoplasma gondii?
Domestic cats ## Footnote Sexual reproduction occurs in the feline GI tract.
438
What are the life stages of Toxoplasma gondii?
Oocysts, Tachyzoites, Bradyzoites ## Footnote Oocysts are infectious after sporulation, tachyzoites are rapidly dividing, and bradyzoites are slow-dividing in tissue cysts.
439
What are common clinical signs of Toxoplasmosis in cats?
Fever, lethargy, icterus, dyspnea, seizures, uveitis, chorioretinitis ## Footnote Signs can vary in severity and may also affect other organs.
440
What is the treatment for Toxoplasmosis?
Clindamycin, Trimethoprim-sulfonamide combinations, Azithromycin ## Footnote Treatment duration is a minimum of 4 weeks.
441
What is the greatest zoonotic risk associated with Toxoplasmosis?
Ingestion of undercooked meat or contaminated food/water ## Footnote Direct contact with cats is not a significant risk.
442
What is the definitive host of Neospora caninum?
Dogs ## Footnote Oocyst shedding occurs in the feces of dogs.
443
What are the clinical signs of Neosporosis in congenitally infected puppies?
Ascending paralysis, hyperextension of pelvic limbs, muscle atrophy ## Footnote Severe signs can lead to death in neonates.
444
What laboratory findings are associated with Neosporosis?
Elevated CK and AST, non-regenerative anemia, increased protein in CSF ## Footnote Imaging may show multifocal CNS lesions.
445
What differentiates Neospora caninum from Toxoplasma gondii?
Electron microscopy, immunohistochemistry, or PCR ## Footnote N. caninum tissue cysts have thicker walls than T. gondii.
446
What are the treatment options for Neosporosis?
Clindamycin, Trimethoprim-sulfonamides + pyrimethamine ## Footnote Cyclosporine may also be used.
447
What is the cross-reactivity of IFA of Neosporia with T. gondii?
Low cross-reactivity ## Footnote This means that the test is specific and does not produce false positives for T. gondii.
448
What is a key morphological difference between N. caninum and T. gondii tissue cysts?
N. caninum tissue cysts have thicker walls (>1 µm) than T. gondii (<1 µm) ## Footnote This structural difference aids in the identification of the parasites.
449
What is one of the primary treatments for N. caninum?
Clindamycin ## Footnote Clindamycin is commonly used in treating infections caused by N. caninum.
450
Which combination of medications can be used for treatment?
Trimethoprim-sulfonamides + pyrimethamine ## Footnote This combination is effective in managing N. caninum infections.
451
What new drugs show promise against N. caninum in vitro?
Artemisinin derivatives ## Footnote These drugs are being researched for their potential effectiveness against the parasite.
452
What is the prognosis for dogs with severe neurologic involvement with Neospora?
Guarded ## Footnote This indicates a poor outlook for recovery in such cases.
453
What is a limitation of clindamycin in treating N. caninum?
May not clear infection ## Footnote Clindamycin may help manage symptoms but not fully eradicate the parasite.
454
Have N. caninum antibodies been detected in humans?
Yes, including AIDS patients ## Footnote This indicates potential exposure but does not confirm infection.
455
What is the status of confirmed human infections with N. caninum?
No confirmed human infections ## Footnote Despite antibody detection, there have been no documented cases of human disease.
456
What preventive measures should be taken to reduce zoonotic risk for Neospora?
Avoid dog feces contamination of livestock feed, prevent ingestion of bovine placenta or venison by dogs, spay bitches producing affected litters ## Footnote These measures help control the spread of N. caninum.
457
What are Brucella spp.?
Intracellular, host-adapted gram-negative aerobic coccobacilli ## Footnote Highly transmissible within their natural host species but capable of cross-species infection, including zoonosis in humans.
458
Which Brucella species are host-adapted to dogs?
Brucella canis
459
What is the difference between rough and smooth Brucella strains?
Rough strains lack the mucoid O-polysaccharide side chain on their LPS ## Footnote Smooth strains contribute to immunogenicity and form the basis for serologic screening tests.
460
Which Brucella strains pose the greatest zoonotic concern?
B. abortus, B. melitensis, B. suis
461
What symptoms are associated with B. canis in humans?
Nonspecific, flu-like symptoms
462
Who are considered high-risk populations for brucellosis?
Children, elderly, pregnant women, immunocompromised
463
In which regions is brucellosis endemic?
Middle East, Africa, Asia, Latin America
464
What is a key prevention strategy for brucellosis?
Animal control
465
What is the primary route of transmission for Brucella spp.?
Mucosal (oral, nasal, venereal)
466
What is the infectious dose for oral transmission of Brucella?
10⁶ CFU
467
What are common reproductive signs of brucellosis in bitches?
Abortion and infertility
468
What is the gold standard for diagnosing canine brucellosis?
Culture
469
What does PCR detect in brucellosis diagnosis?
Brucella DNA (viable or non-viable organisms)
470
What is the sensitivity of the LFIA test for brucellosis?
98.6%
471
What is a common challenge in diagnosing canine brucellosis?
Variable clinical presentation and subclinical carriers
472
What treatment is often recommended for B. canis infections?
Euthanasia
473
What is the treatment protocol for canine brucellosis that has reported success?
Triple therapy: Doxycycline + Gentamicin + Rifampin for 3 months
474
What should be done with Brucella positive dogs in a kennel?
Isolate and euthanize if outbreak risk
475
What is the timing consideration for post-exposure serologic testing of Brucella?
Re-test 8–12 weeks later if initial test is negative
476
What are the causative agents of Tetanus and Botulism?
Tetanus: Clostridium tetani Botulism: Clostridium botulinum ## Footnote Both are gram-positive, anaerobic, spore-forming bacilli.
477
What type of paralysis does Tetanus toxin cause?
Spastic paralysis ## Footnote Tetanus toxin inhibits the release of neurotransmitters leading to sustained muscle contraction.
478
What type of paralysis does Botulinum toxin cause?
Flaccid paralysis ## Footnote Botulinum toxin inhibits acetylcholine release at the neuromuscular junction.
479
What is the mechanism of action of Tetanospasmin?
Inhibits release of glycine and GABA by cleaving synaptobrevin ## Footnote This leads to disinhibition of α-motor neurons and sustained muscle contraction.
480
What are the clinical signs of generalized Tetanus in dogs?
Stiff gait, sawhorse stance, elevated tail, hypertonia of all limbs, lockjaw, dysphagia ## Footnote May progress to respiratory paralysis and central respiratory arrest.
481
What is the incubation period for Tetanus?
5–12 days, up to 3 weeks ## Footnote This can vary based on the severity of the exposure.
482
What are the four classes of Tetanus severity in dogs?
I: Facial signs only II: Generalized rigidity or dysphagia III: Class I or II signs + recumbency or seizures IV: Class I–III + autonomic dysfunction ## Footnote Prognosis worsens with increasing class.
483
What is the gold standard for diagnosing Botulism?
Mouse bioassay ## Footnote This test detects botulinum neurotoxins in serum, feces, or food.
484
What is the primary treatment for Tetanus?
Supportive care, antitoxin, and antimicrobial therapy ## Footnote Intensive nursing is critical for survival.
485
What is the preferred antibiotic for treating Tetanus?
Metronidazole ## Footnote It is shown to achieve superior therapeutic anaerobic concentrations.
486
What are the common species affected by Tetanus?
Dogs > Cats (rare); horses also susceptible ## Footnote Dogs, especially young large breeds, are the most commonly affected.
487
Fill in the blank: Toxin binding in Tetanus is ______.
irreversible ## Footnote Recovery requires new axonal growth.
488
What are the major signs of Botulism in small animals?
Decreased jaw tone, hypoventilation, megaesophagus, aspiration pneumonia ## Footnote Mentation remains normal despite the effects.
489
What is a key difference in the mechanism of spread between Tetanus and Botulism?
Tetanus spreads via retrograde axonal transport to CNS; Botulism remains peripheral ## Footnote Botulism does not involve CNS ascension.
490
What are the potential post-recovery sequelae of Tetanus?
Residual motor deficits, abnormal REM sleep behaviors ## Footnote Up to 50% of recovering dogs may exhibit dream enactment behaviors.
491
What is the prognosis for severe Tetanus in dogs?
Mortality rate up to 50% ## Footnote Poor prognostic indicators include autonomic dysfunction and recumbency.
492
What are the types of botulinum neurotoxins that affect humans?
Types A, B, E, and F ## Footnote Types C and D are most common in animals.
493
What is the role of magnesium sulfate in Tetanus treatment?
Inhibits neuromuscular transmission and reduces autonomic dysregulation ## Footnote It is used as an adjuvant therapy.
494
True or False: Autonomic dysfunction is a major feature of Botulism.
False ## Footnote Autonomic dysfunction is not a major feature compared to Tetanus.
495
What is the main route of exposure for Botulism in dogs?
Ingestion of pre-formed toxin in carrion or spoiled food ## Footnote Other routes like toxicoinfectious botulism are rare in dogs.
496
What is a rare mechanism of botulism in dogs and cats?
Toxicoinfectious botulism ## Footnote This type of botulism is less commonly seen compared to others.
497
What activates the botulinum toxin in the small intestine?
Alkaline environment ## Footnote The toxin is initially inactive until it reaches this specific environment.
498
What does the heavy chain of botulinum toxin bind to?
Presynaptic peripheral cholinergic nerve terminals ## Footnote This binding is essential for the toxin's effects on the nervous system.
499
What is the result of the light chain of botulinum toxin cleaving SNARE proteins?
Inhibition of acetylcholine (ACh) release at the neuromuscular junction ## Footnote This leads to flaccid paralysis.
500
What is the clinical presentation onset time for botulism after ingestion?
Within 12 hours ## Footnote This rapid onset is characteristic of the condition.
501
What type of paralysis is associated with botulism?
Afebrile, acute-onset flaccid paralysis ## Footnote This paralysis typically starts in the pelvic limbs.
502
What are some signs of cranial nerve involvement in botulism?
* Facial nerve paralysis * Decreased jaw tone * Decreased gag reflex * Reduced vocalization * Megaesophagus ## Footnote These symptoms indicate neurological effects of the toxin.
503
What autonomic signs may be present in a botulism case?
* Altered heart rate (bradycardia or tachycardia) * Mydriasis with depressed PLR * Keratoconjunctivitis sicca (KCS) * Urinary retention * Constipation ## Footnote These signs reflect the toxin's impact on autonomic regulation.
504
What is a potential cause of death in severe botulism cases?
* Respiratory failure * Aspiration pneumonia * Prolonged recumbency complications ## Footnote These complications highlight the severe impact of botulism on the body.
505
What is a presumptive diagnosis for botulism based on?
Clinical signs and dietary history ## Footnote Exposure to carrion is a key factor in diagnosis.
506
What is the mainstay of treatment for botulism?
Supportive care ## Footnote This includes management of recumbency and bladder care.
507
What is the role of antitoxin in botulism treatment?
Effective only if administered early ## Footnote It cannot reverse established neuromuscular blockade.
508
What factors worsen the prognosis of botulism?
* Delayed diagnosis * Severe cranial nerve or respiratory involvement * Development of aspiration pneumonia ## Footnote These factors can lead to a more challenging recovery.
509
What is the expected recovery time for most dogs with botulism?
2–3 weeks ## Footnote However, some may experience residual weakness for up to a year.
510
What are Bartonella spp.?
Gram-negative, hemotropic, facultative intracellular bacteria transmitted by blood-sucking arthropods.
511
Which animals are the natural reservoirs for Bartonella henselae, B. clarridgeiae, and B. koehlerae?
Cats.
512
Which animals are the primary reservoirs for Bartonella vinsonii subsp. berkhoffii and B. rochalimae?
Dogs.
513
What is the most commonly diagnosed condition associated with Bartonella in dogs and cats?
Infective endocarditis.
514
What is the primary vector for B. henselae?
Ctenocephalides felis (cat flea).
515
What role do ticks play in Bartonella transmission?
Suspected vectors based on epidemiologic and in vitro evidence, though not definitively confirmed.
516
What are some risk factors for dogs regarding Bartonella infection?
* Rural living * Multi-dog households * Outdoor access * Proximity to cats or rodents
517
What percentage of clinically healthy dogs and cats are bacteremic?
~18–20% of asymptomatic dogs.
518
What is the primary tropism of Bartonella?
Endothelial cells.
519
What are the four distinct genotypes of B. vinsonii subsp. berkhoffii?
Types I–IV.
520
What percentage of canine infective endocarditis cases does Bartonella account for?
19–28%.
521
List some clinical findings associated with canine Bartonellosis.
* Heart murmur: 89% * Lameness: 43% * Respiratory signs: 28% * Weakness/collapse: 17%
522
What are the commonly reported clinical signs in cats associated with Bartonella infection?
* Fever * Lymphadenopathy * Lethargy * Uveitis * Myocarditis * Neurologic signs
523
What are some laboratory abnormalities often found in dogs with Bartonella infection?
* Proteinuria: 40% * Anemia: 38% * Leukocytosis: 36% * Thrombocytopenia: 34%
524
What is the gold standard for Bartonella diagnosis?
Solid media culture.
525
What is the recommended antibiotic protocol for general Bartonellosis in dogs?
Doxycycline and Enrofloxacin.
526
True or False: Serology is a reliable indicator of active Bartonella infection.
False.
527
How does genetic diversity of Bartonella species affect immunity?
Leads to poor cross-protective immunity.
528
What is a key point regarding infection rates in cats compared to dogs?
Cats often have higher bacteremia levels than dogs.
529
What is the significance of maternal antibodies in kittens regarding Bartonella?
Do not protect against heterologous strains.
530
Fill in the blank: Bartonella may also be transmitted via _______ from cats to dogs and humans.
bites or scratches.
531
What is the role of PCR in Bartonella diagnosis?
High specificity and sensitivity; allows species and strain identification. Likely positive if causing endocarditis
532
What are some common clinical manifestations associated with intravascular infection from Bartonella?
* Endocarditis * FUO * Thromboembolic disease * Polyarthritis
533
What is the treatment protocol for symptomatic dogs with canine bartonellosis?
Treat symptomatic dogs or those with confirmed serious disease like endocarditis, myocarditis, or CNS disease. ## Footnote Asymptomatic, PCR-positive dogs should be monitored, not treated empirically.
534
What is the alternative CNS protocol for treating canine bartonellosis?
Azithromycin 10 mg/kg PO q24h for 7 days, then q48h + Rifampin 5 mg/kg PO q12h for 4–6 weeks ## Footnote This is for dogs with CNS involvement.
535
What is the recommended treatment for endocarditis in dogs with canine bartonellosis?
Doxycycline + Amikacin 20–30 mg/kg IV/IM/SQ q24h during hospitalization ## Footnote Start second antibiotic 5–7 days after initiating therapy.
536
How should Herxheimer reactions be managed in dogs undergoing treatment for bartonellosis?
Do not discontinue antibiotics; treat with short-term glucocorticoids such as Prednisone 0.5–1 mg/kg PO once daily ## Footnote For cats, use Prednisolone 1–2 mg/kg PO once daily.
537
What is the minimum duration of treatment for canine bartonellosis?
4–6 weeks, ideally continuing therapy for 2 weeks beyond resolution of clinical signs ## Footnote Some cases may require several months.
538
What should be monitored during treatment for canine bartonellosis?
Clinical response, CBC/chem panel abnormalities, repeat serology, and BAPGM ePCR at 2 and 6 weeks post-treatment ## Footnote This is to evaluate for microbial clearance.
539
Why is it not recommended to treat healthy bacteremic cats for Bartonella?
Due to the risk of antimicrobial resistance and lack of proven benefit ## Footnote There is no justification for screening or treating healthy cats.
540
What are the preferred antibiotic options for treating sick cats suspected of Bartonellosis?
* Pradofloxacin * Doxycycline * Azithromycin ## Footnote Dual antimicrobial therapy with different mechanisms of action is recommended.
541
What is the recommended antibiotic combination for bacteremia in cats?
Doxycycline + Pradofloxacin for a minimum duration of 4–6 weeks ## Footnote Doxycycline: 5 mg/kg PO q12h or 10 mg/kg PO q24h; Pradofloxacin: 10 mg/kg PO q24h.
542
What is the minimum treatment duration for endocarditis in cats?
6 weeks ## Footnote This involves Marbofloxacin + Azithromycin.
543
What is the primary method of preventing Bartonella infection?
Vector control, including year-round ectoparasite prevention ## Footnote This reduces the risk of infection from Bartonella and other vector-borne diseases.
544
What precautions should veterinary professionals take regarding Bartonellosis?
* Use personal protective equipment (PPE) * Avoid needle stick injuries, bites, and scratches * Use feline-friendly handling practices ## Footnote This is to reduce occupational risk.
545
Is there documented direct dog-to-human transmission of Bartonella?
No documented direct dog-to-human transmission via bite or scratch ## Footnote However, Bartonella DNA has been found in dog saliva.
546
What type of staining do Leptospira exhibit?
Gram-negative staining ## Footnote They possess phenotypic features of both Gram-positive and Gram-negative bacteria.
547
What are the four subclades of the genus Leptospira?
* P1: Pathogenic * P2: Intermediate * S1 & S2: Saprophytic
548
What are the primary reservoir hosts for Leptospira?
Small rodents ## Footnote A broad range of species, including dogs, cats, and humans, can also serve as reservoirs.
549
What is the most common renal finding in acute leptospirosis?
Acute interstitial nephritis with tubular cell necrosis ## Footnote This is associated with apoptosis and regeneration.
550
What are the histologic lesions associated with hepatic pathology in leptospirosis?
* Cholestatic hepatitis * Hepatocellular necrosis * Periportal edema with inflammatory infiltrates * Kupffer cell proliferation
551
What is Leptospiral Pulmonary Hemorrhagic Syndrome (LPHS)?
A syndrome characterized by intra-alveolar hemorrhage with minimal inflammatory infiltration ## Footnote LPHS is a major cause of mortality in dogs and humans.
552
What diagnostic tool remains the gold standard for diagnosing leptospirosis?
Microscopic Agglutination Test (MAT) ## Footnote MAT detects serum antibodies that agglutinate live leptospiral serovars.
553
What are the proposed mechanisms for LPHS?
* Coagulopathies * Systemic inflammation * Immune-mediated tissue destruction * Direct toxin-mediated injury
554
What are the limitations of serologic testing in leptospirosis?
* False negatives may occur in early infection * False positives may occur due to previous vaccination
555
What is a common finding on abdominal ultrasound in dogs with leptospirosis?
Renal cortical hyperechogenicity ## Footnote Other findings may include renomegaly and pyelectasia.
556
What serovar is associated with chronic kidney disease in dogs?
Serovar Canicola ## Footnote Progression from tubulointerstitial nephritis to tubular atrophy and renal fibrosis has been observed.
557
What is a key characteristic of leptospiral outer membrane components?
Induce cell damage and inflammation in renal tubular epithelium in vitro
558
What is the purpose of serologic testing in leptospirosis?
Detection of anti-leptospiral IgM and/or IgG antibodies using ELISAs or lateral flow tests can support early clinical decision-making.
559
What are the limitations of point-of-care ELISA and lateral flow assays?
* False negatives may occur in early infection due to lack of seroconversion. * False positives may occur due to previous vaccination.
560
What is the recommendation for using serologic tests?
Use these tests in conjunction with MAT (ideally paired titers) and retest initially negative dogs within a few days if clinical suspicion remains high.
561
When is blood PCR positive in experimentally infected dogs with leptospirosis?
Blood PCR is positive during the first week of infection.
562
When does urine PCR become positive in experimentally infected dogs with lepto?
Urine PCR becomes positive later (after blood), as organisms localize to the kidneys.
563
What are common PCR targets for leptospirosis detection?
* LipL32 gene (specific for pathogenic leptospires) * 23S rDNA
564
What are the two molecular typing methods available for leptospirosis?
* Multiple Locus Sequence Typing (MLST) * Multiple Locus Variable Number Tandem Repeat Analysis (MLVA)
565
What should be done if doxycycline is not tolerated?
Start with an IV penicillin-class drug: Penicillin G, ampicillin, or amoxicillin, then transition to doxycycline once tolerated.
566
What is the management approach for Leptospiral Pulmonary Hemorrhagic Syndrome (LPHS)?
Management is supportive, including performing thoracic radiographs and avoiding stress, overhydration, and systemic hypertension.
567
What are the potential treatments explored for LPHS in humans?
* Methylprednisolone * Dexamethasone * Desmopressin * Plasmapheresis
568
What is the renal recovery timeline post-acute leptospirosis?
Renal recovery may take months, and ~50% of dogs had persistent renal impairment over 1 year post-discharge.
569
What is the clinical significance of leptospirosis in cats?
Cats can be infected and shed leptospires in urine, but clinical illness is rare.
570
What is the most consistent histopathological lesion in cats infected with leptospirosis?
Interstitial nephritis.
571
What types of vaccines are available for leptospirosis prevention?
* Bivalent vaccines (Canicola, Icterohaemorrhagiae) * Quadrivalent vaccines (Canicola, Icterohaemorrhagiae, Grippotyphosa, Pomona)
572
What was the association found in a Swiss case-control study regarding quadrivalent vaccines?
Vaccination with a quadrivalent vaccine was associated with significantly reduced odds of developing leptospirosis.
573
What order includes the families Anaplasmataceae and Rickettsiaceae?
Rickettsiales
574
Name one species of Ehrlichia that causes canine monocytic ehrlichiosis.
Ehrlichia canis
575
What is the vector for Ehrlichia canis?
Rhipicephalus sanguineus (brown dog tick)
576
What is the geographic distribution of Ehrlichia canis?
Southern U.S., Central & South America, Africa, Asia, Europe
577
What is the most consistent hematologic finding in Canine Monocytic Ehrlichiosis?
Thrombocytopenia
578
What is a common diagnostic method for Canine Ehrlichiosis?
Serology
579
What is the disease caused by Anaplasma phagocytophilum in dogs?
Canine Granulocytic Anaplasmosis (CGA)
580
Fill in the blank: Ehrlichia ewingii is transmitted by _______.
Amblyomma americanum (Lone Star tick)
581
What is the primary host of Ehrlichia chaffeensis?
Humans
582
What is the vector for Rocky Mountain Spotted Fever?
Rickettsia rickettsii
583
True or False: E. canis can be transmitted through blood transfusion.
True
584
What laboratory finding is most common in cases of Anaplasmosis?
Thrombocytopenia
585
What type of bacteria is Ehrlichia canis?
Intracellular Gram-negative bacterium
586
What is a key clinical takeaway regarding chronic Canine Monocytic Ehrlichiosis?
Subclinical carriers can develop chronic disease later
587
Fill in the blank: The most common chronic complication of Canine Monocytic Ehrlichiosis is _______.
Bleeding diathesis
588
What is the expected outcome of treatment for Canine Monocytic Ehrlichiosis?
Clinical improvement within 24–48 hours
589
What is the disease associated with Anaplasma platys?
Canine Cyclic Thrombocytopenia
590
What is the vector suspected for Anaplasma platys?
Rhipicephalus sanguineus
591
What are the clinical signs of Ehrlichia ewingii infection in dogs?
* Fever * Anorexia * Lethargy
592
What is the significance of high antibody titers in serology for Ehrlichia?
May persist for months and do not confirm active infection
593
What is Neorickettsia helminthoeca associated with?
Salmon Poisoning Disease (SPD)
594
What is the primary vector for Neorickettsia helminthoeca?
Nanophyetus salmincola
595
What is the incubation period for Neorickettsia helminthoeca after ingestion of infected fish?
5–33 days
596
What are the early clinical signs of Neorickettsia helminthoeca infection?
* High fever (up to 42°C / 107.6°F) * Anorexia
597
What laboratory abnormalities are associated with Neorickettsia helminthoeca?
* Thrombocytopenia * Neutrophilia ± left shift * Lymphopenia * Monocytosis * Hyponatremia * Hypokalemia * ↑ ALT, ALP * Hypoalbuminemia
598
What is the treatment for Neorickettsia helminthoeca?
* Doxycycline 10 mg/kg PO q24h for ≥7–10 days * Supportive care including fluids and antiemetics * Praziquantel for fluke treatment
599
What is the primary host for Neorickettsia risticii?
Horses
600
What is the causative agent of Rocky Mountain Spotted Fever?
Rickettsia rickettsii
601
What are common vectors for Rickettsia rickettsii?
* Dermacentor variabilis * Dermacentor andersoni * Rhipicephalus sanguineus
602
What is the expected mortality rate for humans infected with Rickettsia rickettsii?
2–10%
603
What are the laboratory findings associated with Rickettsia rickettsii infection?
* Leukocytosis ± left shift * Thrombocytopenia * Anemia * ↑ ALT/ALP * Electrolyte imbalances
604
What is the primary etiological agent for Feline Monocytic Ehrlichiosis?
Ehrlichia canis-like organisms
605
What are common clinical signs of Feline Granulocytic Anaplasmosis?
* Lethargy * Anorexia * Fever * Pallor * Epistaxis * Hyperesthesia
606
What are common signs of Anaplasma phagocytophilum Infection?
* Fever * Lethargy * Lameness * Thrombocytopenia ## Footnote These signs can also indicate other conditions.
607
What cell types are targeted in Ehrlichia canis-like Infection?
Mononuclear cells ## Footnote This is a key aspect of the infection's pathology.
608
What cell types are targeted in Anaplasma phagocytophilum Infection?
Granulocytes ## Footnote Understanding the target cells is crucial for diagnosis.
609
What are the consistent lab abnormalities seen in Ehrlichia canis-like Infection?
* Non-regenerative anemia * Hyperglobulinemia ## Footnote These lab findings are important for diagnostic considerations.
610
What are the consistent lab abnormalities seen in Anaplasma phagocytophilum Infection?
* Thrombocytopenia * Possibly anemia ## Footnote These findings can indicate the severity of the infection.
611
What diagnostic tools are used for Ehrlichia canis-like Infection?
* PCR * Cytology * Limited serology ## Footnote These tools help confirm the diagnosis.
612
What diagnostic tools are used for Anaplasma phagocytophilum Infection?
* Cytology * PCR * Limited serology ## Footnote Similar to Ehrlichia canis-like, these tools assist in diagnosis.
613
How does the response to treatment for Anaplasma phagocytophilum Infection typically present?
Rapid and complete ## Footnote A favorable response suggests successful management of the infection.
614
What are hemotropic mycoplasmas?
Small, wall-less bacteria that attach to the surface of erythrocytes.
615
Are zoonotic infections possible with hemoplasmas?
Yes, human cases have been reported.
616
What is the median prevalence of Mycoplasma haemofelis in cats?
5.1%.
617
What is the pathogenicity of ‘Candidatus Mycoplasma haemominutum’?
Mild pathogenicity; may cause anemia in immunocompromised cats.
618
What are common risk factors for hemoplasma infection in cats?
* Male * Outdoor lifestyle * Older age * Positive FeLV or FIV status * Feral or free-roaming lifestyle
619
Which species is the most pathogenic hemoplasma in cats?
Mycoplasma haemofelis.
620
What is the diagnostic gold standard for hemoplasma infections?
PCR.
621
What is the primary clinical sign of Mycoplasma haemofelis infection?
Acute hemolytic anemia.
622
Which species is associated with hemolytic anemia in splenectomized dogs?
Mycoplasma haemocanis.
623
Fill in the blank: Hemoplasmas may cause _______ anemia in immunocompromised dogs.
hemolytic.
624
What are common clinical signs of hemoplasma infection?
* Lethargy * Pallor * Weakness * Weight loss * Intermittent fever
625
What is a potential complication of using enrofloxacin in cats?
Retinal toxicity/blindness.
626
List the diagnostic methods for hemoplasma infections.
* Cytology * PCR * Serology
627
What is the significance of a positive PCR result in hemoplasma infections?
Does not confirm causality; subclinical carriers exist.
628
What is a common laboratory finding in hemoplasma infections?
Regenerative macrocytic hypochromic anemia.
629
What is the risk factor associated with splenectomy in dogs?
Increased risk for hemoplasmosis due to Mycoplasma haemocanis.
630
What is the typical pathogenicity of ‘Candidatus M. turicensis’?
Mild; usually subclinical.
631
What is the significance of antigenic variation in Mycoplasma haemofelis?
Contributes to immune evasion.
632
Are glucocorticoids recommended for treatment of suspected IMHA in hemoplasma-infected patients?
Generally not recommended ## Footnote Antibiotic therapy and supportive care are usually sufficient. Risks include infection reactivation.
633
What is a documented case regarding glucocorticoids and IMHA?
PCR for M. haemocanis became negative only after stopping prednisolone ## Footnote This was after prednisolone was started for presumed IMHA.
634
When should glucocorticoid therapy be initiated for hemoplasma-associated anemia?
Only with strong evidence of concurrent primary IMHA unresponsive to antibiotics or if hemoplasma infection has been ruled out via PCR ## Footnote This caution is due to the risk of infection reactivation.
635
What is mandatory for blood donor screening in canines and felines?
PCR screening for hemoplasma infection ## Footnote Subclinical carriers may appear healthy but can transmit infection via transfusion.
636
What is recommended regarding ectoparasite control?
Strongly recommended in all at-risk animals ## Footnote This is vital for preventing hemoplasma infection.
637
Is there a vaccine available for hemoplasma infection?
No vaccine available ## Footnote Currently, there is no vaccine to prevent hemoplasma infections.
638
What are the challenges in diagnosing and managing bacterial enteritis in dogs and cats?
Complex due to: * High prevalence of asymptomatic carriage * Co-infections with viruses, parasites, and other bacteria * Most infections being self-limiting
639
What are the important exceptions to the self-limiting nature of enteric bacterial infections?
Animals with: * Severe systemic signs * Sepsis * Extra-GI infection * Immunocompromised status
640
What are the non-specific clinical signs of enteric bacterial diseases?
Signs include: * Diarrhea (acute or chronic) * Anorexia * Lethargy * Tenesmus * Vomiting * Abdominal pain
641
What findings might be present in a minimum database for enteric bacterial diseases?
CBC may show: * Neutrophilia (with/without left shift) * Regenerative anemia * Neutropenia in sepsis Chemistry may show: * Electrolyte derangements * Azotemia * Mild liver enzyme elevation * Hyperbilirubinemia
642
What imaging techniques are used in the diagnostic approach to enteric bacterial diseases?
Imaging is used to rule out: * Obstruction * Peritonitis * Neoplasia Ultrasound may show: * Mucosal thickening * Abnormal layering * Lymphadenopathy
643
What are the testing options for diagnosing enteric bacterial diseases?
Options include: * Fecal PCR panels * Culture (requires microaerophilic conditions) * Identification by MALDI-TOF MS * Antimicrobial susceptibility testing
644
What are the characteristics of Campylobacter species?
Characteristics include: * Gram-negative, spiral rods * 30 species, many are commensals * Prevalence in fecal samples: Dogs 0–87%, Cats 0–75%
645
What are the common species of Campylobacter found in dogs and cats?
Common species include: * Dogs: C. upsaliensis, C. jejuni, C. helveticus * Cats: C. helveticus, C. upsaliensis, C. jejuni
646
How is Campylobacter transmitted?
Transmission is fecal–oral, direct or indirect, and it survives weeks in feces.
647
What are the virulence factors of Campylobacter?
Virulence factors include: * Flagella * Adhesins * Invasins * CDT toxin
648
What are the typical clinical manifestations of Campylobacter infections?
Signs include: * Often subclinical * Diarrhea (watery, mucous, or bloody) * Tenesmus * Lethargy * Dehydration * Anorexia
649
What are the challenges in diagnosing Campylobacteriosis?
Challenges include: * High asymptomatic carriage * Co-infections complicating clinical significance
650
When is antimicrobial therapy recommended for Campylobacter infections?
Recommended for: * Severe clinical signs * Immunocompromised patients * Extraintestinal disease
651
What antibiotics are recommended for Campylobacter treatment?
Recommended antibiotics include: * Erythromycin * Tylosin * Azithromycin * Enrofloxacin
652
What is the zoonotic potential of Campylobacter species?
Major concern with: * Campylobacter jejuni * C. coli Most common human source: undercooked poultry
653
What are the key features of Salmonella species?
Features include: * Gram-negative rods * Facultative anaerobic * Motile * Serotyped by O, K, H antigens
654
How is Salmonella transmitted?
Transmission occurs via: * Fecal-oral route * Contaminated food or water * Fomites
655
What are the clinical signs of Salmonella infection?
Signs include: * Asymptomatic in most * Acute gastroenteritis * Diarrhea * Anorexia * Fever * Vomiting
656
What are the virulence factors of Salmonella?
Virulence factors include: * Adhesins * Invasion * Toxin production
657
What is the treatment approach for Salmonella infections?
Supportive care is primary; antibiotics are avoided unless necessary due to resistance concerns.
658
What is Clostridioides difficile's microbiological classification?
It is a Gram-positive, anaerobic, spore-forming bacillus.
659
What are the common clinical signs of Clostridioides difficile infection?
Signs include: * Small or large bowel diarrhea * Vomiting * Lethargy * Anorexia
660
What are the treatment options for Clostridioides difficile infections?
Treatment includes: * Discontinuation of current antibiotics * Supportive care * Probiotics * Fecal Microbiota Transplant (FMT)
661
What zoonotic considerations are associated with Clostridioides difficile?
Toxigenic ribotypes found in humans also identified in pets; zoonotic risk is considered low.
662
What are the notable features of Salmonella enterica?
Notable features include: * High prevalence in pets * Multidrug resistance common * Systemic spread possible
663
What are the notable features of Clostridioides difficile?
Notable features include: * Toxins A/B * FMT effective * ELISA not validated in dogs/cats
664
What type of bacterium is Clostridioides difficile?
Anaerobic, gram-positive, spore-forming bacillus
665
How are Clostridioides difficile spores characterized?
Highly resistant to environmental conditions and disinfectants
666
What is the primary transmission route for Clostridioides difficile?
Fecal–oral route, often from contaminated environments
667
What is the prevalence of Clostridioides difficile in healthy dogs?
Up to 58%
668
What is the prevalence of Clostridioides difficile in healthy cats?
Up to 21%
669
What triggers disease caused by Clostridioides difficile?
Disruption of normal flora and overgrowth of toxigenic strains
670
What are the key toxins produced by Clostridioides difficile?
* TcdA (enterotoxin A) * TcdB (cytotoxin B) * Some strains produce binary toxin CDT
671
What are common clinical signs of Clostridioides difficile infection?
* Small or large bowel diarrhea, sometimes hemorrhagic * Vomiting * Anorexia * Lethargy
672
What is the preferred diagnostic method for Clostridioides difficile?
PCR (preferred): Detects TcdA and TcdB genes
673
What is the treatment approach for Clostridioides difficile infections?
* Discontinue unnecessary antibiotics * Supportive care * Probiotics * Dietary changes * Fecal Microbiota Transplant (FMT)
674
What is the zoonotic risk associated with Clostridioides difficile?
Minimal but possible risk of community-acquired CDI from pets
675
What type of bacterium is Clostridium perfringens?
Anaerobic, gram-positive, spore-forming bacillus
676
How many toxotypes does Clostridium perfringens have?
Seven toxotypes (A–G) based on toxin production
677
What are the major toxins produced by Clostridium perfringens?
* Alpha * Beta * Epsilon * Iota * CPE * NetB
678
What is the prevalence of Clostridium perfringens in healthy dogs?
Up to 84%
679
What is the prevalence of Clostridium perfringens in diarrheic dogs?
Up to 91%
680
What triggers disease caused by Clostridium perfringens?
Sporulation of toxigenic strains leading to enterotoxin (CPE) release
681
What are the diagnostic methods for Clostridium perfringens?
* Direct fecal PCR for toxin genes * CPE ELISA
682
What is the cornerstone of treatment for Clostridium perfringens infections?
Supportive care
683
What is the microbiological classification of Escherichia coli?
Facultative anaerobic, gram-negative, pleomorphic rods
684
What are the pathotypes of concern for Escherichia coli?
* Enteropathogenic (EPEC) * Enterotoxigenic (ETEC) * Enterohemorrhagic (EHEC) * Enteroinvasive (EIEC) * Enteroaggregative (EAEC) * Adherent-Invasive (AIEC)
685
What is the prevalence of Escherichia coli in shelter kittens?
60 of 61 positive for E. coli
686
What zoonotic risk is associated with Escherichia coli?
Moderate, especially ESBL-producing strains
687
What is the microbiological classification of Yersinia enterocolitica?
Gram-negative, motile, facultative anaerobe
688
What is the primary transmission route for Yersinia enterocolitica?
Ingestion of contaminated pork or other meats
689
What are the clinical signs of Yersinia enterocolitica infections?
* Enteritis (diarrhea, vomiting, abdominal pain) * Extra-GI infections (e.g., myocarditis or hepatitis)
690
What is the treatment approach for Yersinia enterocolitica infections?
Most cases are self-limiting; antibiotics based on susceptibility testing if required
691
What is the zoonotic risk associated with Yersinia enterocolitica?
Significant foodborne pathogen in humans
692
What is the etiology of Clostridium piliforme?
Obligate intracellular gram-negative spore-forming bacillus
693
What is the prognosis for Clostridium piliforme infections?
Poor, due to rapid clinical course
694
What is the recommended method for environmental cleaning in outbreak situations?
Use 1:10 bleach dilution, surfaces should be pre-cleaned and scrubbed for 10 minutes
695
What is the primary route of transmission for enteric protozoa?
Fecal-oral transmission ## Footnote Except for Cystoisospora satanus, whose transmission pathway remains unknown in dogs and cats.
696
How do coccidian parasites such as Cystoisospora and Toxoplasma gondii typically infect hosts?
Ingestion of sporulated oocysts from the environment ## Footnote They have direct life cycles and undergo asexual and sexual replication in host enterocytes.
697
What is unique about Cryptosporidium spp. regarding its infectious stage?
Immediately infectious upon excretion as sporulated oocysts ## Footnote Capable of autoinfection and highly environmentally resistant.
698
How are Giardia spp. transmitted?
Ingestion of cysts from contaminated feces, food, or water ## Footnote Cysts are the infectious and environmentally resistant stage.
699
What are the primary habitats of Giardia trophozoites in dogs and cats?
Dogs: duodenum to ileum; Cats: jejunum to ileum ## Footnote Trophozoites do not significantly contribute to transmission.
700
True or False: Trichomonads have a cyst form.
False ## Footnote Transmission occurs by ingestion of trophozoites.
701
What is the infectious form of Entamoeba histolytica and Balantidium coli?
Cyst ## Footnote Cysts are ingested and excyst in the small intestine.
702
What type of hosts can transmit Giardia and Cystoisospora?
Invertebrate paratenic hosts (e.g., flies, cockroaches) ## Footnote Ingestion of infected prey may also transmit other protozoa.
703
What are common enteric protozoan parasites in dogs?
* Giardia duodenalis * Cryptosporidium spp. * Cystoisospora spp. * Neospora caninum ## Footnote Common parasites differ from those found in cats.
704
What is the general mechanism of pathogenesis for enteric protozoa?
Replication in intestinal epithelial cells ## Footnote Many infections are asymptomatic in immunocompetent hosts.
705
What clinical signs are associated with Cystoisospora spp. infections?
* Diarrhea * Weight loss * Dehydration ## Footnote Severe cases may lead to anorexia and vomiting.
706
What diagnostic methods can be used for detecting Giardia?
* Direct fecal smear * Fecal flotation via centrifugation * ELISA for antigen detection ## Footnote PCR is also used for higher sensitivity.
707
What is the first-line therapy for giardiasis?
* Metronidazole * Metronidazole + Fenbendazole * Fenbendazole ## Footnote Treatment is recommended only for symptomatic animals.
708
What is a major challenge in treating cryptosporidiosis?
Often self-limiting in immunocompetent animals ## Footnote More severe in immunosuppressed hosts; no drug is fully curative.
709
What is the typical prepatent period for Cryptosporidium parvum in dogs?
2–14 days ## Footnote Patent period ranges from 3 to 33 days.
710
What are clinical signs of Tritrichomonas fetus infections?
* Large bowel diarrhea * Semi-formed feces * Mucus and fresh blood ## Footnote Often presents with waxing and waning signs.
711
Fill in the blank: E. histolytica may cause _______ in dogs.
ulcerative colitis ## Footnote Typically subclinical but can lead to severe signs.
712
What is the infective form of Balantidium coli?
Cyst ## Footnote Shed in feces and can either be a commensal or invasive parasite.
713
What is the significance of the 9% prevalence of E. histolytica found in a Pakistani study?
Indicates potential public health concern ## Footnote Suggests the need for awareness and monitoring in dog populations.
714
What is the FDA-approved drug for Cystoisosporiasis?
Sulfadimethoxine
715
What is the dosage for Sulfadimethoxine?
55 mg/kg PO once, then 27.5 mg/kg PO SID
716
Which drug is considered safe and highly effective for Cystoisosporiasis in kittens and puppies?
Ponazuril
717
What is the dosage for Ponazuril?
50 mg/kg PO × 1–3 days
718
What is the drug of choice for Tritrichomonas fetus in cats?
Ronidazole
719
What is the dosage and duration for Ronidazole treatment?
30 mg/kg PO SID for 14 days
720
What should be assessed 2–4 weeks post-treatment with Ronidazole?
Efficacy assessed by PCR
721
What are potential reasons for Ronidazole treatment failure?
* Inadequate dose or duration * Reinfection from a subclinical carrier * Drug resistance
722
What is essential for evaluating response in T. fetus treatment?
PCR testing
723
Why should treatment efficacy not be assessed based on ELISA for Giardia antigen?
Due to prolonged antigen shedding post-resolution
724
What is the observed reduction in Giardia cyst shedding with secnidazole in puppies?
90% reduction with 2 doses of 30 mg/kg
725
What led to clinical and parasitological cure in dogs within 5–10 days?
Auranofin
726
What is a common issue with NTZ treatment?
Frequently induces vomiting
727
What are the key potentially zoonotic protozoa in companion animals?
* Giardia duodenalis * Cryptosporidium spp. * Toxoplasma gondii * Entamoeba histolytica * Balantidium coli
728
What determines the zoonotic potential of Giardia duodenalis?
Genetic assemblage
729
What assemblages of Giardia duodenalis are zoonotic?
* A1 * A2 * B3 * B4
730
Which assemblages of Giardia duodenalis are host-specific?
* C * D * F * E * G * H
731
What are the primary hosts for Cryptosporidium spp.?
* C. hominis: Humans * C. parvum: Ruminants, humans * C. canis: Dogs * C. felis: Cats
732
How is Toxoplasma gondii primarily transmitted to humans?
* Ingestion of sporulated oocysts from contaminated sources * Consumption of undercooked meat containing tissue cysts
733
What is the zoonotic risk associated with Entamoeba histolytica?
Minimal; primarily a human pathogen
734
What is the primary reservoir for Balantidium coli in humans?
Pigs
735
What routine hygiene practices are recommended for pet owners?
* Wash hands after handling feces * Avoid exposure to pet feces * Disinfect contaminated surfaces
736
What should high-risk populations avoid concerning pet feces?
* Handling pet feces * Contact with litterboxes * Cleaning up diarrhea
737
What is the zoonotic risk from pets according to CAPC and CDC?
Low but not negligible, especially in immunosuppressed individuals
738
What is the genus of intraerythrocytic protozoan parasites that infect mammals?
Babesia ## Footnote Babesia spp. are part of the phylum Apicomplexa.
739
What are the two types of reproduction in the life cycle of Babesia?
* Sexual reproduction in the definitive host (ticks) * Asexual reproduction in the intermediate mammalian host
740
What is the primary route of transmission for Babesia?
Tick bite inoculation
741
Name the two classifications of Babesia based on size.
* Large Babesia * Small Babesia
742
Which species of large Babesia is considered the least pathogenic?
Babesia vogeli
743
What are common clinical findings in cases of Babesia infection?
* Fever * Lethargy * Pallor * Tachycardia * Tachypnea * Hypotensive shock
744
What diagnostic method is most sensitive and specific for Babesia?
PCR
745
What is the first-line treatment for large Babesia species?
Imidocarb dipropionate
746
What is the causative agent of Cytauxzoonosis?
Cytauxzoon felis
747
What is the primary vector for Cytauxzoon felis?
Amblyomma americanum (lone star tick)
748
What are the two phases of the lifecycle of Cytauxzoon felis in cats?
* Schizogonous (tissue phase) * Erythrocytic (piroplasm) phase
749
What is the mortality rate of untreated domestic cats with Cytauxzoonosis?
~90%
750
What are common lab abnormalities in cats infected with Cytauxzoon felis?
* Pancytopenia * Hyperbilirubinemia * Elevated liver enzymes
751
What is the preferred treatment for Cytauxzoon felis?
* Atovaquone * Azithromycin
752
What is the primary causative agent of leishmaniasis in dogs?
>30 species of Leishmania, primarily Leishmania infantum
753
What is the primary vector for Leishmania transmission?
Sandflies (Phlebotomus spp. in the Old World, Lutzomyia spp. in the New World)
754
What are common clinical signs of leishmaniasis in dogs?
* Weight loss * Fever * Lymphadenopathy * Splenomegaly
755
What is the first-line therapy for leishmaniasis in dogs?
Allopurinol
756
True or False: Cytauxzoon felis can cause acute kidney injury in cats.
True
757
Fill in the blank: The __________ phase of Cytauxzoon felis infection leads to hemolytic anemia.
Erythrocytic (Piroplasm)
758
What percentage of dogs infected with Leishmania may remain subclinical carriers?
Relapse common; subclinical carriers may later develop disease
759
What are the geographic regions where leishmaniasis is endemic?
* South America * Southern Europe * Middle East * North Africa
760
What are the main transmission routes for Leishmaniasis?
Transmission occurs via: * Sandfly bites * Blood transfusion * Vertical transmission ## Footnote Dogs serve as reservoirs for human infection.
761
What are the two morphological forms of Leishmania?
The two forms are: * Promastigotes: extracellular; infectious stage from sandfly to mammal * Amastigotes: intracellular; replicate in macrophages
762
What is the role of macrophages in the pathogenesis of Leishmaniasis?
Macrophages phagocytose promastigotes, transforming them into amastigotes which replicate intracellularly.
763
How does the immune response affect the outcome of Leishmaniasis?
A Th1 (cell-mediated) immunity leads to control or clearance, while a Th2 (humoral) or inadequate response results in chronic infection and disease.
764
List systemic signs associated with Leishmaniasis.
Systemic signs include: * Weight loss * Muscle wasting * Fever * Splenomegaly * Lymphadenopathy * Anterior uveitis * Polyarthritis * Glomerulonephritis * Renal failure
765
What laboratory findings are indicative of Leishmaniasis?
Hematologic abnormalities include: * Non-regenerative anemia * Lymphopenia * Polyclonal or monoclonal gammopathy
766
What are the definitive diagnostic methods for Leishmaniasis?
Definitive diagnosis can be made via: * Cytology/histology: ID of amastigotes in tissue * PCR: preferred due to high sensitivity
767
What is the first-line treatment for Leishmaniasis?
First-line therapy includes: * Allopurinol (10–20 mg/kg PO q12h) * Meglumine antimoniate (not available in U.S.)
768
What is the goal of treatment for Leishmaniasis?
The goal of treatment is clinical remission—not curative.
769
What are the key statistics regarding Cytauxzoonosis?
Key statistics include: * ~90% mortality untreated * ~60% survival with combination therapy
770
What are the two causative species of Hepatozoonosis in dogs?
The two species are: * Hepatozoon canis * Hepatozoon americanum
771
How is Hepatozoonosis transmitted?
Transmission occurs via ingestion of infected ticks or prey—not via tick bite.
772
What are the clinical signs of Hepatozoonosis?
Clinical signs include: * Fever * Lethargy * Muscle pain or lameness * Mucopurulent ocular discharge * Stiff gait, myalgia, or muscle atrophy
773
What laboratory findings are associated with Hepatozoonosis?
Laboratory findings include: * Non-regenerative anemia * Marked leukocytosis * Hypoglycemia * Hypoalbuminemia * Elevated ALP
774
What is the most sensitive diagnostic method for Hepatozoonosis?
PCR (whole blood or buffy coat) is the most sensitive and specific method.
775
What constitutes the treatment for Hepatozoonosis?
Treatment includes: * Triple therapy: potentiated sulfonamide + clindamycin + pyrimethamine * Decoquinate for long-term clinical remission
776
What are the transmission routes for Toxoplasma gondii?
Transmission routes include: * Ingestion of sporulated oocysts * Bradyzoites * Tachyzoites * Transplacental transmission
777
What are the life stages of Toxoplasma gondii?
The life stages include: * Oocysts * Tachyzoites * Bradyzoites
778
List the common clinical signs of Toxoplasmosis in cats.
Common signs in cats include: * Fever * Lethargy * Icterus * Dyspnea * Seizures * Uveitis * Chorioretinitis
779
What is the treatment for Toxoplasmosis?
Treatment options include: * Clindamycin * Trimethoprim-sulfonamide combinations * Azithromycin
780
What is the zoonotic risk associated with Toxoplasma gondii?
The greatest risk is ingestion of undercooked meat or contaminated food/water.
781
What are the clinical signs of Neosporosis in congenitally infected puppies?
Signs include: * Ascending paralysis * Hyperextension of pelvic limbs * Muscle atrophy * Dysphagia * Death common in neonates
782
What are the life stages of Neospora caninum?
The life stages include: * Oocysts * Tachyzoites * Bradyzoites
783
How is Neospora caninum transmitted?
Transmission occurs via: * Ingestion of oocysts or tissue cysts * Transplacental transmission
784
What are the diagnostic findings for Neosporosis?
Diagnostic findings include: * Elevated CK and AST * Non-regenerative anemia * CSF analysis showing increased protein
785
What is the treatment for Neosporosis?
Treatment options include: * Clindamycin * Trimethoprim-sulfonamides + pyrimethamine
786
What is the cross-reactivity level of IFA with T. gondii?
Low ## Footnote IFA stands for Immunofluorescent Antibody.
787
Where can antibodies be found besides serum?
CSF ## Footnote CSF stands for cerebrospinal fluid.
788
What methods can be used to differentiate N. caninum from T. gondii?
Electron microscopy, immunohistochemistry, or PCR ## Footnote PCR stands for polymerase chain reaction.
789
How thick are the tissue cyst walls of N. caninum compared to T. gondii?
N. caninum >1 µm, T. gondii <1 µm
790
What combination of drugs is used in the treatment of N. caninum?
Trimethoprim-sulfonamides + pyrimethamine
791
What may be required in the treatment of N. caninum?
Sequential therapy
792
Which new drugs show promise in vitro for treating N. caninum?
Artemisinin derivatives
793
What is the prognosis for dogs with severe neurologic involvement of Neospora?
Guarded
794
What may improve survival in N. caninum cases?
Early treatment
795
What is a possible outcome even after treatment with Clindamycin?
Relapse
796
What should be avoided to prevent zoonotic risk?
Dog feces contamination of livestock feed
797
What should be prevented to avoid dogs ingesting N. caninum?
Bovine placenta or venison
798
What is a preventive measure for bitches who produce clinically affected litters?
Spay
799
What is Feline Immunodeficiency Virus (FIV)?
A Lentivirus in the family Retroviridae that causes immunosuppression in domestic cats worldwide. ## Footnote Often compared to HIV due to some shared pathophysiologic mechanisms.
800
What is the primary route of transmission for FIV?
Deep bite wounds during aggressive encounters (saliva or blood). ## Footnote Uncommon routes include rare vertical transmission and cohabitation in stable households.
801
What are the five major subtypes of FIV?
* A * B * C * D * E ## Footnote Based on up to 26% sequence variation in the env gene.
802
What is the average age of diagnosis for FIV-positive cats?
5–6 years.
803
What are the three broad phases of FIV infection?
* Acute/primary phase * Subclinical phase * Terminal phase ## Footnote Unlike HIV, most FIV-infected cats do not develop a terminal AIDS-like syndrome.
804
What clinical signs are FIV-infected cats predisposed to?
* Immune dysfunction * Opportunistic infections * Chronic gingivostomatitis * Cytopenias * Neoplasia * Neurologic signs * Cachexia/Wasting syndrome
805
Who should be tested for FIV?
* Ill cats of unknown retroviral status * Cats with fight wounds or abscesses * Free-roaming cats, strays, or shelter intakes * Blood donors * Cats being adopted or rehomed * Kittens from FIV-positive queens * Cats prior to FIV vaccination
806
What is the most effective prevention method for FIV?
Confinement indoors.
807
What was the reason for the withdrawal of the FIV vaccine in the U.S.?
* Concerns about efficacy against heterologous subtypes * Interference with antibody-based testing
808
What is the sensitivity and specificity of ELISA tests for FIV in unvaccinated cats over 6 months of age?
High sensitivity (94–100%) and specificity (94–100%).
809
What is the increased risk of neoplasia in FIV-infected cats?
5–6× increased risk of lymphoma, especially high-grade extranodal B-cell lymphomas.
810
What should be done if a cat has a negative serologic result for FIV?
* No further action if low risk * Repeat test in 60 days if recent exposure possible * Consider false negative in high-risk cats
811
What are the common clinical syndromes in sick FIV-infected cats?
* Secondary infections * Cytopenias * Chronic inflammatory disease * Wasting and weight loss * Neoplasia
812
What is the recommendation for health maintenance of FIV-infected cats?
Biannual veterinary visits recommended.
813
What should be monitored in FIV-infected cats?
* Early signs of secondary infections * Neoplasia * Immune dysfunction
814
What is the role of glucocorticoids in treating FIV-infected cats?
May be justified for immune-mediated hemolytic anemia, inflammatory bowel disease, and chronic gingivostomatitis.
815
What is the impact of vaccination on FIV testing?
Vaccinated cats test antibody-positive on many point-of-care kits.
816
What are the adverse effects of Zidovudine (AZT) in FIV-infected cats?
* Anemia * Neutropenia * GI signs
817
What is the primary prevention strategy for FIV?
Confinement indoors to prevent transmission and physical trauma.
818
What is the recommendation regarding dental care for FIV-infected cats?
Emphasize dental care due to the association with gingivostomatitis.
819
What is the prognosis for FIV-infected cats?
Majority live normal life spans; prognosis is generally good, especially for indoor-only cats.
820
What is Feline Leukemia Virus (FeLV)?
A retrovirus that affects domestic cats globally, associated with neoplasia, bone marrow suppression, and immunodeficiency ## Footnote FeLV is particularly known for causing lymphoma and increasing susceptibility to secondary infections.
821
What is the global prevalence of FeLV in the United States?
2.3–3.3% ## Footnote Prevalence varies across regions, with Europe ranging from 0–15.6%, South America from 3–28.4%, and Asia/Australia/New Zealand from 0–24.5%.
822
What are the four possible outcomes of FeLV infection?
1. Progressive 2. Regressive 3. Abortive 4. Focal/Atypical ## Footnote Each outcome is influenced by immune response strength and viral load.
823
What characterizes a progressive FeLV infection?
Persistent viremia and antigenemia; high proviral load; clinical disease ## Footnote This outcome has the worst prognosis.
824
What defines a regressive FeLV infection?
Initial viremia, then aviremic; no antigenemia; proviral DNA may persist ## Footnote This outcome is less severe than progressive infections.
825
Fill in the blank: High levels of soluble p27 antigen are associated with _______.
shorter survival
826
What are common clinical signs associated with FeLV infection?
* Bone marrow disorders (especially anemia) * Neoplasia (particularly lymphoma) * Immunosuppression leading to increased secondary infections ## Footnote Many infected cats may remain clinically healthy for years.
827
Which factors increase the risk of FeLV prevalence?
* Male, intact, adult cats * Associated diseases (e.g., lymphoma, anemia) * Behavior (e.g., aggression, mutual grooming) * Lack of vaccination * Outdoor access * Living in multi-cat households ## Footnote Environmental and socioeconomic factors also play a significant role.
828
What is the primary route of FeLV transmission?
Horizontal transmission via saliva (e.g., grooming, shared food/water bowls) and aggression (bite wounds) ## Footnote Vertical transmission can also occur in utero or via milk.
829
What testing methods are used for diagnosing FeLV?
* Point-of-Care (POC) Testing * PCR Testing * Immunofluorescence Assay (IFA) * Antibody Testing ## Footnote Each method has specific indications and limitations.
830
What is the significance of the soluble p27 antigen in FeLV diagnosis?
It is used to detect progressive infection and indicates viral load ## Footnote High levels of p27 antigenemia at intake predict shorter survival.
831
What is the best-case scenario for FeLV infection outcomes?
Abortive infection ## Footnote This outcome is characterized by complete prevention of viral replication and no clinical signs.
832
What are the environmental control measures for preventing FeLV transmission?
Segregation and routine disinfection ## Footnote FeLV is easily inactivated by detergents, drying, and common disinfectants.
833
What is the most common tumor associated with FeLV infection?
Lymphoma ## Footnote Progressively infected cats are significantly more likely to develop lymphoma than FeLV-negative cats.
834
Fill in the blank: FeLV integrates near ________, triggering neoplastic transformation.
proto-oncogenes
835
What is a significant factor influencing the course of FeLV infection?
Inadequate immune response ## Footnote This may lead to progressive infection, especially in younger cats.
836
What are the common associated diseases with FeLV infection?
* Anemia * Respiratory infections * Lymphoma * Myeloproliferative disease * Stomatitis ## Footnote These conditions highlight the clinical burden of FeLV in affected cats.
837
What is the median survival for cats with progressive FeLV infection?
3.1 years (range 0.6–6.5 years) post-infection ## Footnote This is based on long-term experimental studies.
838
How can FeLV transmission be prevented in homes and clinics?
Through segregation and routine disinfection ## Footnote Transmission requires direct contact.
839
What types of vaccines are available for FeLV?
* Adjuvanted inactivated whole-virus vaccines * Recombinant antigen vaccines * Non-adjuvanted canarypox-vectored vaccines
840
Why are studies on FeLV vaccine efficacy difficult to compare?
* Varied methodologies * Differing formulations * Confounding by immunosuppressive drug use or parvovirus contamination
841
What is a potential advantage of non-adjuvanted FeLV vaccines?
Cause less local inflammation and potentially lower risk of injection site sarcomas ## Footnote They are less likely to cause adverse reactions.
842
What does vaccination against FeLV significantly reduce?
Progressive infection and disease risk ## Footnote However, it does not prevent proviral integration.
843
Who should receive FeLV vaccinations?
* Outdoor cats * Cats in high-prevalence regions * Multi-cat settings * All kittens in endemic regions
844
What is the recommended duration of immunity for FeLV vaccines?
At least 2 years ## Footnote A booster every 3 years is recommended after 2 years of age.
845
Why is pre-vaccination testing essential for FeLV?
Vaccinating FeLV-infected cats offers no benefit.
846
What should be the general management for FeLV-positive cats?
Keep indoors, prevent spread, and continue routine preventive care.
847
What is the ideal prevention strategy in multi-cat households for FeLV?
Full segregation of infected and uninfected cats.
848
What should be avoided in the treatment of symptomatic FeLV-positive cats?
Glucocorticoids, immunosuppressives, or myelosuppressive drugs unless clearly indicated.
849
What is the recommended treatment for lymphoma in FeLV-positive cats?
Chemotherapy (e.g., COP protocol: cyclophosphamide, vincristine, prednisone).
850
What is the prevalence of lymphoma in progressive FeLV-positive cats?
Up to 25%.
851
What is the risk increase for lymphoma in FeLV-positive cats?
~60-fold.
852
What is a common co-morbidity in shelters for FeLV-positive cats?
Upper respiratory infections (URI): 16% in FeLV+ vs 20% in FeLV−.
853
What is the antiviral use status in FeLV treatment?
Limited benefit; most studies show no efficacy.
854
What are the two biotypes of FCoV?
* Feline Enteric Coronavirus (FECV) * Feline Infectious Peritonitis Virus (FIPV)
855
What does FECV cause?
Subclinical to mild, self-limiting enteritis.
856
What is FIPV?
A mutated, immune-evasive form of FCoV that causes systemic, usually fatal, immune-mediated vasculitis.
857
How does FIPV arise?
From spontaneous mutations of FECV within individual hosts.
858
What are the two serotypes of Feline Coronavirus?
* FCoV Type 1: Unknown receptor, most common in nature * FCoV Type 2: Aminopeptidase N (APN) receptor, less common
859
What is the primary target of Feline Enteric Coronavirus (FECV)?
Intestinal epithelium.
860
What are the clinical signs of FECV?
* Often subclinical * May cause transient fever * Anorexia * Diarrhea
861
What environmental factors affect FECV survival?
* Survives 1–2 days on surfaces * Up to 7 weeks in dried feces in lab settings
862
What is the hallmark lesion of FIP?
Granulomatous phlebitis.
863
What type of immune response is seen in Wet FIP?
Weak CMI, strong Th2/Humoral.
864
What are the features of Dry (Non-effusive) FIP?
* Granulomatous lesions in CNS, eyes, kidneys, liver, lymph nodes * Slower clinical course
865
What cytokines are involved in the immunopathogenesis of FIP?
* TNF-α * IL-1β * IL-6 * VEGF * MMPs
866
What does a positive Rivalta Test indicate?
Supports FIP but is not definitive.
867
What are the characteristics of typical FIP effusion?
* High protein (>3.5 g/dL) * Low-to-moderate cellularity * Predominantly macrophages and non-degenerate neutrophils
868
What is the gold standard for definitive diagnosis of FIP?
Histopathology and Immunohistochemistry (IHC) for FCoV antigen.
869
What is GS-441524?
An investigational nucleoside analog inhibitor used for FIP treatment.
870
What is the primary mechanism of action of GS-441524?
Mimics adenosine; halts viral RNA synthesis.
871
What factors increase the risk of developing FIP?
* Impaired cellular immunity * Genetic susceptibility * Overcrowded housing
872
What is the significance of mutations in the S protein for FIP?
Critical for macrophage tropism required for FIP.
873
What is the internal mutation hypothesis regarding FIP emergence?
FIPV arises spontaneously via mutations in FECV within each individual cat.
874
What are the immune profiles of cats with dry FIP?
Mixed Th1-Th2 immune response.
875
What is the role of genetic susceptibility in FIP?
Pedigree cats, especially purebred males, are at higher risk.
876
What is Molnupiravir?
Alternate nucleoside analog with ambiguous base pairing mechanism
877
What are the safety concerns associated with Molnupiravir?
Potentially mutagenic; safety concerns under evaluation
878
What is Remdesivir?
Prodrug of GS-441524; expensive and off-label
879
What is the mechanism of action for GC-376?
Inhibits the 3C-like protease, required for viral protein processing
880
What was the initial response rate in the study of GC-376?
19/20 cats showed initial response
881
What does RT-PCR detect in relation to FIP?
Detects both FIPV and FECV
882
What does serology indicate regarding FIP?
Indicates exposure, not disease
883
What is the response rate of GS-441524 in antiviral therapy for FIP?
84% response rate
884
What is recommended for prophylactic use in multi-cat environments?
GS-441524-based oral antiviral
885
What is a concern regarding the vaccine for FCoV?
Not recommended by AAFP/AAHA due to limited efficacy
886
What is the transmission route for canine coronaviruses?
Typically fecal-oral or aerosol
887
What are the two biotypes of Enteric Canine Coronavirus (CCoV)?
* Classic CCoV * Pantropic CCoV
888
What does pantropic CCoV cause?
Systemic illness, even fatal disease, without co-infection
889
What is the gold standard for diagnosing canine coronaviruses?
Post-mortem immunofluorescence or immunostaining for viral antigen
890
What is the treatment for canine coronavirus infections?
Supportive care including fluid therapy and electrolyte replacement
891
What is the primary transmission method for Canine Respiratory Coronavirus (CRCoV)?
Spread via aerosols; highly contagious
892
What is a key finding regarding GS-441524 treatment for FIP?
84% recovery rate; ~8/196 cats relapsed
893
What receptor does SARS-CoV-2 use for cellular entry?
Angiotensin-converting enzyme 2 (ACE2)
894
What is the typical clinical presentation of SARS-CoV-2 in cats?
Mild respiratory signs or subclinical
895
What has been observed in infected cats regarding immunity?
Mount a robust neutralizing antibody response
896
What are the species susceptibility rankings for SARS-CoV-2?
Cats > Ferrets > Hamsters > Dogs
897
What potential cardiac involvement has been reported in pets during the Alpha variant surge?
Increased cases of myocarditis
898
What is a notable zoonotic concern regarding SARS-CoV-2?
Human-to-cat transmission confirmed; cat-to-human transmission extremely rare
899
What ongoing studies may help understand SARS-CoV-2 transmission in animals?
Studies on pathogenesis, transmission, and long-term immune consequences
900
What type of viruses are parvoviruses?
Small, non-enveloped, single-stranded DNA viruses (~5,000 bp genome)
901
What are the two main species of parvoviruses?
* Canine parvovirus (CPV) * Feline panleukopenia virus (FPV)
902
What disease does Canine parvovirus (CPV) cause?
Parvoviral enteritis in dogs
903
What disease does Feline panleukopenia virus (FPV) cause?
Panleukopenia in cats
904
What is the genetic similarity between CPV and FPV?
∼98% genetic similarity
905
How did CPV evolve?
CPV evolved from FPV and adapted to infect dogs
906
What determines host range and pathogenicity in parvoviruses?
Minor amino acid differences (<10) in capsid proteins affecting interaction with the transferrin receptor (TfR)
907
What is the role of TfR polymorphisms in parvovirus infections?
They affect host specificity
908
List the CPV-2 variants that have evolved.
* CPV-2a * CPV-2b * CPV-2c
909
Can CPV infect cats?
Yes, CPV-2a and CPV-2b can infect cats and cause disease indistinguishable from feline panleukopenia, though this is rare
910
What is the primary transmission route for CPV and FPV?
Fecal-oral route
911
How much virus can infected dogs shed?
Up to 10⁹ TCID₅₀/g of feces
912
When does virus shedding begin after infection?
Begins 3 days post-infection, peaks at days 3–4, and declines by day 7
913
What factors contribute to parvovirus outbreaks?
* Unsanitary or crowded environments * High population turnover of unvaccinated or maternally unprotected puppies/kittens
914
What environmental factors correlate with CPV enteritis caseloads?
* Positively correlated with wind speed * Inversely correlated with humidity
915
Which dog breeds show increased susceptibility to CPV?
* Rottweilers * Doberman Pinschers * American Pit Bull Terriers * German Shepherd Dogs * English Springer Spaniels
916
What is the significance of maternally derived antibodies (MDA) in puppies?
90% acquired via colostrum; half-life ≈ 10 days; susceptibility increases at 12–14 weeks of age as MDA wanes
917
What is the pathogenesis of parvovirus infection?
Targets mitotically active cells, leading to atrophy and lymphoid depletion in lymphoid and thymic tissues
918
What are common complications in recovering puppies from CPV?
* Skin necrosis * Bacterial polyarthritis * Discospondylitis
919
What is the most common cause of death in acute CPV and FPV infections?
Septicemia
920
What diagnostic tests are used for CPV and FPV?
* Fecal ELISA antigen test * PCR
921
What is the most common electrolyte abnormality in severe parvovirus cases?
Hypokalemia
922
What nutritional support is recommended for parvovirus-infected animals?
Early enteral nutrition via nasogastric tube
923
True or False: Canine myocarditis is common in the early CPV-2 pandemic.
True
924
What are the clinical signs of feline cerebellar hypoplasia due to FPV?
* Mild cerebellar signs * Severe hydrocephalus
925
What is the significance of hypoglycemia in parvovirus infections?
Common and multifactorial, contributing to seizures in infected puppies
926
What is the prognosis for parvovirus-infected young animals?
High mortality rate without prompt supportive care
927
What is the role of recombinant interferons in treating diseases?
Shown to reduce disease severity and mortality, though not widely available ## Footnote Recombinant interferons are proteins that can enhance the immune response.
928
What is the effect of recombinant canine G-CSF?
Increased WBC counts, but unclear benefit on clinical outcomes ## Footnote G-CSF is used to stimulate the production of white blood cells.
929
What are the survival rates for untreated patients with CPV?
<10% if untreated ## Footnote This highlights the critical need for prompt and effective treatment.
930
What is the survival rate with aggressive supportive care with CPV?
>90% with aggressive supportive care ## Footnote Supportive care significantly improves prognosis.
931
What are some negative prognostic indicators of CPV?
* Leukopenia * Neutropenia * Lymphopenia * Monocytopenia * Systemic inflammatory response syndrome (SIRS) ## Footnote These indicators can suggest a poorer outcome for patients.
932
What does the composite model for outcome prediction incorporate for CPV?
* Plasma antithrombin * AST * Lipase * Monocyte and lymphocyte counts ## Footnote This model has high sensitivity and specificity for predicting outcomes.
933
At what age should puppy vaccinations start?
4–6 weeks of age ## Footnote Early vaccination is crucial to establish immunity.
934
What is the recommended frequency for puppy vaccinations until 16 weeks of age?
Every 3–4 weeks ## Footnote This schedule helps ensure adequate protection against diseases.
935
What is the risk associated with administering live vaccines to pregnant animals with CPV?
Fetal risks ## Footnote Live vaccines can pose a risk to developing fetuses.
936
When can vaccination begin in breeding facilities experiencing outbreaks?
As early as 4 weeks of age, using high-titer, modified-live virus (MLV) vaccines ## Footnote Early vaccination helps protect puppies with insufficient maternal antibodies.
937
What are effective disinfectants against non-enveloped viruses?
* 0.75% sodium hypochlorite (bleach) * Potassium peroxymonosulfate (e.g., Virkon®) ## Footnote These disinfectants are recommended for infection control.
938
What has increased in some regions despite a global decline in human rabies cases?
Wildlife rabies ## Footnote This increase is driven by better surveillance and real epizootic spread.
939
What is the agent responsible for rabies?
Rabies virus, Genus Lyssavirus, Family Rhabdoviridae
940
What is the structure of the rabies virus?
Enveloped, bullet-shaped virus with a single-stranded negative-sense RNA genome
941
How is rabies most commonly transmitted?
Through bite wounds from infected animals
942
Which species are considered reservoirs for rabies?
Bats and carnivores ## Footnote Specifically, Chiroptera (bats) and Carnivora (carnivores).
943
Which rabies variant is endemic from Florida through Maine?
Raccoon Rabies Virus Variant (RRVV)
944
True or False: Cats are diagnosed with rabies more often than dogs in the U.S.
True
945
What percentage of rabid dogs had prior rabies vaccination according to U.S. surveillance data?
4.9%
946
What does the incubation period of rabies typically last?
Several weeks to several months
947
What is the gold standard for diagnosing rabies?
Direct fluorescent antibody (DFA) test on fresh brain tissue
948
What should be avoided during initial testing for rabies to ensure timely diagnosis?
Formalin fixation
949
What are the early clinical signs of rabies?
Lethargy, anorexia, vomiting, diarrhea
950
What is the recommended action if a vaccinated animal is exposed to rabies?
Administer a rabies vaccine booster immediately
951
What unique behavior may rabies-infected animals exhibit?
Abnormal vocalizations that attract predators
952
What is a notable feature of rabies virus transmission in laboratory settings?
Accidental infection via aerosolized virus
953
What is the rabies exposure observation period for biting animals?
10 days
954
What alternative management is suggested for overdue but previously vaccinated pets?
Immediate wound cleansing and rabies booster vaccination
955
What factors influence the risk of developing clinical rabies?
Host species susceptibility, virus variant, virus dose, route of exposure
956
What is the rabies virus's behavior regarding shedding?
No shedding in urine or gastrointestinal secretions
957
What does Post-Exposure Prophylaxis (PEP) include?
* Wound cleaning * Human rabies immune globulin (HRIG) * Rabies vaccination series
958
What is the effectiveness rate of PEP in rabies-naive humans when initiated promptly?
Nearly 100% effective
959
What is the benefit of pre-exposure rabies vaccination?
* Provides immunologic priming * Simplifies post-exposure prophylaxis (PEP) * Reduces urgency and delays in treatment if exposed
960
How often should serum rabies virus neutralizing antibody (RVNA) titers be checked for 'frequent risk' groups?
Every 2 years
961
What is the protocol for previously vaccinated individuals after rabies exposure?
* No HRIG required * Booster vaccinations on days 0 and 3 only
962
What is the primary responsibility of public health agencies in rabies management?
* Rabies surveillance * Educational outreach * Diagnostic testing * Regulatory updates * Post-exposure human case management
963
What are the primary acute respiratory signs associated with CIRDC?
* Cough * Sneezing * Nasal discharge * Ocular discharge * Conjunctivitis
964
Which bacterial agent is commonly associated with CIRDC?
Bordetella bronchiseptica
965
Name two viral causes of CIRDC.
* Canine adenovirus type 2 (CAV-2) * Canine parainfluenza virus
966
What is the incubation period for CIRDC?
2–14 days
967
True or False: Vaccines for CIRDC completely prevent infection.
False
968
What is the recommended first-line antimicrobial for CIRDC?
Doxycycline
969
Fill in the blank: Most CIRDC cases are ______ and self-limiting.
viral
970
Which two canine influenza virus strains are primarily associated with CIRDC?
* H3N8 * H3N2
971
What type of vaccine is effective against B. bronchiseptica?
Intranasal modified live virus (MLV) vaccines
972
What is a common clinical sign observed in dogs with severe CIRDC?
Terminal retch or expectoration of foamy material
973
What is the role of PCR in diagnosing CIRDC?
Amplifies nucleic acids from CIRDC agents for testing
974
List two opportunistic bacteria that may cause inflammation in conjunction with viral infections.
* Pasteurella * Staphylococcus
975
What is the significance of co-infections in CIRDC?
They are common and may worsen clinical severity
976
True or False: Canine distemper virus is a viral cause of CIRDC.
True
977
What should be done when a dog with CIRDC shows poor response to treatment?
Consider pathogen-specific testing
978
What is the Canine distemper virus (CDV)?
An enveloped, single-stranded RNA virus of the Paramyxoviridae family, genus Morbillivirus.
979
Which species are most commonly affected by CDV?
* Domestic dogs * Ferrets * Raccoons * Skunks * Coyotes
980
Is CDV zoonotic?
No, there is no evidence supporting transmission to humans.
981
What is the typical incubation period for CDV?
Ranges from <1 week to 4 weeks.
982
List some early clinical signs of CDV.
* Fever * Lethargy * Ocular discharge * Conjunctivitis * Nasal discharge * Coughing
983
What are potential gastrointestinal signs of CDV?
* Vomiting * Diarrhea (may be bloody) * Anorexia * Muscle wasting
984
What neurologic signs can occur with CDV?
* Myoclonus * Chewing-gum fits * Seizures * Ataxia * Paralysis
985
What are population-level indicators of CDV in shelters?
* Increased respiratory illness frequency * Worsening respiratory illness severity * Emergence of neurologic signs * History of CDV in community * Delayed vaccination at intake
986
What is the primary transmission route of CDV?
Primarily aerosolized respiratory droplets.
987
What is the mortality rate of CDV in naïve, unvaccinated populations?
Can be >50%.
988
What factors influence susceptibility to CDV?
* Immune status * Infectious dose
989
What is the significance of modified-live virus (MLV) vaccines for CDV?
They provide high efficacy and protection against all circulating CDV strains.
990
What is the diagnostic gold standard for CDV?
RT-PCR (reverse transcriptase polymerase chain reaction).
991
What does RT-PCR positivity indicate?
Presence of viral RNA but does not confirm viable virus.
992
What are the common antemortem sample types for RT-PCR?
* Nasal swabs * Deep pharyngeal swabs * Blood
993
What is the role of antibiotics in CDV treatment?
Essential to combat secondary bacterial pneumonia.
994
What are some common bacterial pathogens associated with secondary infections in CDV?
* Bordetella bronchiseptica * Streptococcus spp. * E. coli
995
What is recommended for outbreak management of CDV in shelters?
* Prompt recognition and diagnostics * Risk assessment * Immediate vaccination on intake
996
What can CDV infection in unvaccinated pregnant dogs result in?
Loss of both dam and puppies.
997
What is the safest vaccine for pregnant dogs?
Canarypox-vectored recombinant CDV vaccine.
998
What role does RT-PCR play in managing CDV outbreaks?
Use RT-PCR and clinical signs to inform housing and isolation duration ## Footnote RT-PCR detects RNA but not viable virus; its limitations must be considered.
999
What is the significance of serology in risk assessment for CDV?
Serology helps identify protective antibody titers ## Footnote Antibody-positive, RT-PCR-negative dogs are considered non-infectious and protected.
1000
True or False: RT-PCR can distinguish between wild and vaccine virus of CDV.
False ## Footnote RT-PCR cannot differentiate between wild and vaccine strains.
1001
What is a key takeaway regarding outbreak management?
Defined isolation, vaccination, and flow control are essential ## Footnote These factors can transform chaotic outbreaks into manageable situations.
1002
What is the importance of flow management in disease prevention?
To prevent disease spread ## Footnote Effective flow management is critical in managing outbreaks.
1003
What does a high CT value in RT-PCR indicate?
Low viral load ## Footnote This must be interpreted with timing and clinical signs.
1004
What is Feline Upper Respiratory Infection (FURI)?
A multifactorial disease complex involving viral and/or bacterial pathogens affecting the nasal, ocular, and respiratory mucosa.
1005
What are the typical clinical signs of FURI?
Sneezing, nasal discharge, nasal congestion, ocular discharge, ulceration, systemic signs like inappetence and fever.
1006
What factors influence the severity of clinical signs in FURI?
* Pathogen(s) involved * Infectious dose * Number of co-infections * Host immune status * Environmental conditions * Nutritional status and stress levels
1007
Where is FURI endemic?
In most feline populations.
1008
What environments have higher prevalence of FURI?
Crowded, stressful, or unhygienic environments like shelters and catteries.
1009
How is FURI primarily transmitted?
Via direct contact with oral, nasal, or ocular secretions.
1010
What is the incubation period for FURI?
Typically 2–10 days.
1011
What are the primary viral pathogens associated with FURI?
* Feline Herpesvirus-1 (FHV-1) * Feline Calicivirus (FCV)
1012
What is the pathogenesis of Feline Herpesvirus-1 (FHV-1)?
Infects oral, nasal, conjunctival, and corneal epithelium, causing cytolysis and latency.
1013
What are the chronic sequelae of FHV-1?
* Permanent damage to nasal turbinates * Osteolysis * Immune-mediated chronic rhinitis
1014
What type of virus is Feline Calicivirus (FCV)?
Non-enveloped, single-stranded RNA virus.
1015
What is a significant characteristic of FCV regarding mutation?
High mutation rate due to lack of proofreading.
1016
Name a common bacterial pathogen associated with FURI.
Mycoplasma felis.
1017
What is the role of Chlamydia felis in FURI?
Infects conjunctival epithelium; ocular secretions are the main transmission route.
1018
What environmental factors contribute to the spread of FURI?
Poor hygiene, overcrowding, concurrent infection, and immunosuppression.
1019
What are common clinical signs specific to FHV-1?
* Sneezing * Nasal congestion * Mucopurulent nasal discharge * Conjunctivitis * Dendritic corneal ulcers
1020
What are common clinical signs specific to FCV?
* Oral ulceration * Sneezing * Nasal and ocular discharge * Acute lameness * Fever
1021
What diagnostic challenges are associated with FURI?
Clinical signs overlap significantly, co-infections are common, and healthy carriers may shed pathogens.
1022
What is the first-line antibiotic for treating bacterial complications in FURI?
Doxycycline.
1023
What supportive care measures are essential in treating FURI?
* Hydration * Nutrition * Stress reduction
1024
What is the importance of environmental management in FURI?
To reduce population density and stress in multi-cat settings.
1025
What antiviral therapy is used for severe FHV-1 infections?
Famciclovir.
1026
What are the key takeaways regarding the management of FURI?
* FURI is primarily viral in origin. * Supportive care and stress reduction are critical. * Antimicrobials should be used judiciously.
1027
Fill in the blank: The infectious period for FURI is usually _______.
<10 days.
1028
True or False: FHV-1 causes latent infections.
True.
1029
What are the environmental stability characteristics of FHV-1 and FCV?
* FHV-1: Fragile, inactivated by common disinfectants * FCV: Resilient, can survive days to weeks in the environment
1030
What is L-lysine historically used for?
FHV-1 ## Footnote Current evidence is inconclusive or does not support its benefit.
1031
What is the role of recombinant interferons in treating FURI?
May have benefit in some cases, but evidence remains mixed and inconsistent
1032
When is diagnostic testing valuable in FURI cases?
In outbreaks, unresolving illness, or severe cases
1033
What is the primary focus of treatment for FURI?
Supportive care and stress reduction
1034
What should antibiotics and antivirals be used based on?
Clinical signs and progression
1035
What are the key prevention strategies for FURI?
Environmental management, vaccination, and immune support
1036
How is FURI primarily transmitted?
Via direct contact
1037
Which pathogen can persist on fomites and requires environmental decontamination?
Feline Calicivirus (FCV)
1038
What is the first step in the general guidelines for disinfection?
Pre-cleaning: All surfaces contaminated with dirt, organic matter, or bodily fluids should be cleaned with a detergent.
1039
What is an effective disinfectant against FCV?
Bleach (5.25% sodium hypochlorite, diluted 1:32)
1040
What are the limitations of using bleach for disinfection?
* Inactivated by organic matter and sunlight * Corrosive and potentially harmful to respiratory mucosa
1041
What are the advantages of using accelerated hydrogen peroxide formulations for disinfection?
* Broad-spectrum efficacy (including FCV) * Short contact times * Stability in the presence of organic debris * Lower toxicity and corrosiveness
1042
What is the target air exchange rate in shelter settings?
Minimum 8–12 air exchanges per hour
1043
What is the carrier state in cats recovering from FURI?
Many become asymptomatic carriers, especially those infected with FHV-1 or FCV
1044
What characterizes the latency of FHV-1?
Lifelong latency in trigeminal ganglia with episodic reactivation
1045
What is the prognosis for uncomplicated FURI?
Excellent – Resolution within 7–14 days with supportive care
1046
What factors can lead to a guarded prognosis in FURI cases?
* Young, geriatric, or immunocompromised status * Involvement of highly pathogenic strains * Comorbidities, poor hygiene, overcrowding, or antibiotic resistance
1047
True or False: Carrier status in cats necessitates permanent isolation.
False ## Footnote Healthy carrier status does not necessitate permanent isolation if managed properly.
1048
What should disinfection protocols for FURI prioritize?
Inactivation of FCV, the most environmentally stable FURI pathogen
1049
What is typically true about the prognosis of most FURI cases?
Most cases resolve with supportive care, and prognosis is typically very good
1050
What is the focus of Chapter 206?
Emerging viral infections of cats ## Footnote This chapter discusses newly discovered or recently linked viruses that impact feline health.
1051
How many viral families have been identified as potential feline pathogens?
At least 15 viral families ## Footnote This includes emerging viruses whose impact on feline health is still being investigated.
1052
What methodology is commonly used to establish causality in viral infections?
Modified Koch’s postulates ## Footnote This method has been adapted for modern viral discovery.
1053
What are viromes?
Unique communities of viruses that colonize various body surfaces ## Footnote Virome analyses have revealed these communities in normal cats.
1054
What is the significance of some persistent infections in cats?
They may alter immune function or physiology ## Footnote Under certain conditions, these infections can lead to disease.
1055
When was Domestic Cat Hepadnavirus (DCH) first reported?
2018 in Australia ## Footnote DCH is a member of the Orthohepadnavirus genus.
1056
What is the prevalence range of DCH in cats?
6.5–12.4% ## Footnote Detected via PCR of whole blood or serum.
1057
What is DCH strongly associated with?
Liver disease in cats ## Footnote This includes chronic hepatitis and hepatocellular carcinoma.
1058
What is the proposed disease association of Feline Morbillivirus (FeMV)?
Tubulointerstitial nephritis (TIN) ## Footnote FeMV may be a major cause of feline chronic kidney disease (CKD).
1059
What complicates diagnostics for FeMV?
High genetic diversity and evidence of recombination among isolates ## Footnote This makes interpretation of findings challenging.
1060
What are the key takeaways regarding DCH and FeMV?
DCH linked to liver disease; FeMV's role in kidney disease is under investigation ## Footnote Ongoing research is crucial for both viruses.
1061
What is Felis catus Gammaherpesvirus 1 (FcaGHV1) associated with?
Increased risk of high-grade B-cell lymphoma in FIV-infected cats ## Footnote Similar to links between certain herpesviruses and lymphomas in humans.
1062
What is the prevalence range for FcaGHV1?
6–23% ## Footnote Based on PCR detection.
1063
Is FcaGHV1 known to infect humans?
No, it is not known or suspected to infect humans ## Footnote It is primarily associated with domestic cats.
1064
What is the clinical relevance of Bovine Herpesvirus 4 (BHV4) in cats?
Controversial; early studies suggested upper respiratory disease ## Footnote No consistent molecular evidence has been found in feline infections.
1065
What clinical syndrome is associated with Rustrial Virus (RusV)?
Staggering disease, a non-suppurative meningoencephalitis ## Footnote First reported in the 1970s.
1066
What percentage of clinically normal cats have serologic evidence of Borna Disease Virus (BDV) exposure?
Up to 20% ## Footnote BDV's role in staggering disease remains uncertain.
1067
What is the detection rate of Feline Bocavirus 1 (FBoV-1) in cats?
~7% ## Footnote Identified in blood, feces, respiratory, and urinary samples from healthy cats.
1068
What is a potential association of FBoV?
Diarrhea and respiratory disease (unproven) ## Footnote FBoV is often found alongside multiple other viruses.
1069
What is the classification of Feline Fomevirus?
Retrovirus in the Spumavirus genus ## Footnote It is extremely common with a seroprevalence exceeding 50% in many feline populations.
1070
What is the current understanding of Feline Chapparvovirus (FeChPV)?
Detected in less than 50% of samples from affected cats during an outbreak ## Footnote Prevalence and transmission patterns remain unknown.
1071
What is the role of Feline Astrovirus (FeAstV) in feline health?
May act as a co-pathogen exacerbating disease ## Footnote Its exact role in feline enteric disease needs further investigation.
1072
What is the significance of emerging feline viruses?
Complicated by high carrier rates and subclinical infections ## Footnote Multifactorial causation models are needed for understanding disease.