Infectious Diseases Flashcards

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
True or False: Giardia trophozoites significantly contribute to transmission.
False ## Footnote Trophozoites are fragile in the environment.
390
What are the potential treatments for cryptosporidiosis?
* Nitazoxanide * Azithromycin * Paramomycin * Auranofin
391
What combination therapy has shown promise in human medicine?
Azithromycin + Paramomycin
392
What is the FDA-approved drug for Cystoisosporiasis?
Sulfadimethoxine
393
Which drug is considered safe and highly effective for Cystoisosporiasis in kittens and puppies?
Ponazuril
394
What is the drug of choice for Tritrichomonas fetus in cats?
Ronidazole
395
What is the typical duration of Ronidazole treatment?
14 days
396
What are the considerations for Ronidazole treatment failure?
* Inadequate dose or duration * Reinfection from a subclinical carrier * Drug resistance
397
What essential testing is needed for evaluating response in T. fetus?
PCR testing
398
What should not be used to assess treatment efficacy for Giardia?
ELISA for Giardia antigen
399
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
400
Name three key potentially zoonotic protozoa in companion animals.
* Giardia duodenalis * Cryptosporidium spp. * Toxoplasma gondii
401
What genetic assemblages of Giardia duodenalis are zoonotic?
A1, A2, B3, B4
402
What is the primary host for C. hominis?
Humans
403
What is the zoonotic potential of C. parvum?
Yes
404
How does Toxoplasma gondii typically infect humans?
* Ingestion of sporulated oocysts from contaminated soil, water, or vegetables * Consumption of undercooked meat containing tissue cysts
405
What is the zoonotic risk from Entamoeba histolytica?
Minimal
406
Which animal is the primary reservoir for Balantidium coli?
Pigs
407
What zoonotic assemblages of Giardia duodenalis occur in both pets and humans?
A and B
408
What is the risk level of zoonotic transmission from pets, according to CAPC and CDC?
Low but not negligible
409
What is the genus of the intraerythrocytic protozoan parasites that infect mammals?
Babesia ## Footnote Babesia is part of the phylum Apicomplexa.
410
What are the two phases of Babesia's life cycle?
Sexual reproduction in the definitive host and asexual reproduction in the intermediate mammalian host.
411
What is the primary route of transmission for Babesia?
Tick bite inoculation.
412
List the common clinical manifestations of Babesia infection.
* Fever * Lethargy * Pallor * Tachycardia * Tachypnea * Hypotensive shock * Splenomegaly * Icterus * Petechiae * Neurologic signs * Rhabdomyolysis * Acute kidney injury
413
What laboratory finding is associated with Babesia infections 2-3 weeks post-infection?
Regenerative anemia.
414
What is the most sensitive diagnostic method for Babesia?
PCR.
415
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.
416
True or False: Relapses are common in Babesia infections.
True.
417
What are the two phases of the lifecycle of Cytauxzoon felis?
* Schizogonous (tissue phase) * Erythrocytic (piroplasm) phase.
418
What is the mortality rate of untreated domestic cats infected with Cytauxzoon felis?
~90%.
419
What are the common clinical signs of Cytauxzoonosis?
* Lethargy * Anorexia * Fever * Icterus * Dehydration.
420
What is the first-line treatment for Cytauxzoon felis?
Atovaquone and Azithromycin.
421
What is the causative agent of leishmaniasis in dogs?
Leishmania species.
422
What form of leishmaniasis is most common in dogs?
Visceral leishmaniasis.
423
What are the two forms of Leishmania?
* Promastigotes * Amastigotes.
424
What is the primary vector for Leishmania transmission?
Sandflies.
425
What is a key characteristic of the immune response in leishmaniasis?
A strong T-cell (Th1) response can control or clear the infection.
426
What are the common laboratory abnormalities in Cytauxzoonosis?
* Pancytopenia * Hyperbilirubinemia * Elevated liver enzymes * Hyperglycemia.
427
Fill in the blank: The primary vector for Cytauxzoon felis is _______.
Amblyomma americanum.
428
What is the geographical distribution of Cytauxzoon felis in the United States?
Midwest, Southeast, and Mid-Atlantic regions.
429
What is the role of bobcats in the epidemiology of Cytauxzoon felis?
Typically subclinical carriers.
430
What is the prognosis for treated Cytauxzoonosis?
Guarded.
431
What is the treatment duration for Cytauxzoon felis?
Typically 10 days.
432
How is Leishmania transmitted?
Sandflies, blood transfusion, vertical transmission ## Footnote Old World vector is Phlebotomus spp. and New World vector is Lutzomyia spp.
433
What are early clinical manifestations of Leishmaniasis?
Alopecia, papules, nodules, scaling ## Footnote These cutaneous lesions can precede systemic signs.
434
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.
435
What is the preferred method for definitive diagnosis of Leishmaniasis?
PCR ## Footnote PCR is preferred due to high sensitivity.
436
What is the goal of treatment for Leishmaniasis?
Clinical remission—not curative ## Footnote Relapse and reinfection are common in endemic areas.
437
What is the first-line therapy for Leishmaniasis in dogs?
Allopurinol and Meglumine antimoniate ## Footnote Meglumine antimoniate is not available in the U.S.
438
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.
439
How is Hepatozoonosis transmitted?
Ingestion of infected ticks or prey ## Footnote Infection does not occur via tick bite.
440
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.
441
What laboratory findings are associated with Hepatozoonosis?
Non-regenerative anemia, marked leukocytosis, hypoglycemia, hypoalbuminemia, elevated ALP ## Footnote Radiographs may show periosteal proliferation.
442
What is the most sensitive and specific method for diagnosing Hepatozoonosis?
PCR ## Footnote PCR differentiates between H. americanum and H. canis.
443
What is the triple therapy for Hepatozoonosis?
Potentiated sulfonamide + clindamycin + pyrimethamine ## Footnote This treatment is not curative and relapses are common.
444
What is the definitive host of Toxoplasma gondii?
Domestic cats ## Footnote Sexual reproduction occurs in the feline GI tract.
445
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.
446
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.
447
What is the treatment for Toxoplasmosis?
Clindamycin, Trimethoprim-sulfonamide combinations, Azithromycin ## Footnote Treatment duration is a minimum of 4 weeks.
448
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.
449
What is the definitive host of Neospora caninum?
Dogs ## Footnote Oocyst shedding occurs in the feces of dogs.
450
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.
451
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.
452
What differentiates Neospora caninum from Toxoplasma gondii?
Electron microscopy, immunohistochemistry, or PCR ## Footnote N. caninum tissue cysts have thicker walls than T. gondii.
453
What are the treatment options for Neosporosis?
Clindamycin, Trimethoprim-sulfonamides + pyrimethamine ## Footnote Cyclosporine may also be used.
454
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.
455
What methods can differentiate N. caninum from T. gondii?
Electron microscopy, immunohistochemistry, or PCR ## Footnote These techniques help in identifying the specific organism and its characteristics.
456
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.
457
What is one of the primary treatments for N. caninum?
Clindamycin ## Footnote Clindamycin is commonly used in treating infections caused by N. caninum.
458
Which combination of medications can be used for treatment?
Trimethoprim-sulfonamides + pyrimethamine ## Footnote This combination is effective in managing N. caninum infections.
459
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.
460
What is the prognosis for dogs with severe neurologic involvement with Neospora?
Guarded ## Footnote This indicates a poor outlook for recovery in such cases.
461
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.
462
Have N. caninum antibodies been detected in humans?
Yes, including AIDS patients ## Footnote This indicates potential exposure but does not confirm infection.
463
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.
464
What preventive measures should be taken to reduce zoonotic risk?
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.