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ACVIM General copy > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

What breeds (dog and cat) are predisposed to Mycobacterium avium?

A
  1. Bassetts

2. Siamese

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2
Q

Where does the life cycle of Pneumocystis carinii occur?

A

The entire life cycle occurs within the alveolar spaces (trophozoites and cysts)

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3
Q

Clinical disease with Pneumocystis carinii occurs in what scenarios?

A
  1. Immunosuppression
  2. Crowding
  3. Distemper patients
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4
Q

What is the pathophysiology behind Pneumocystis carinii?

A
  1. Inhaled but rarely multiply in IMMUNOCOMPETENT host
  2. If IMMUNOSUPPRESSED → Multiply → alveolocapillary blockage and decreased gas exchange → thickened alveolar septa
    * Organisms rarely invade the parenchyma and are rarely found in alveolar macrophages
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5
Q

Which breeds are predisposed to Pneumocystis carinii?

A
  1. Mini (long-haired red) daschunds <1 year → can have a common variable immunodeficiency → absence of B cell + dysfunctional T cells
  2. Cavalier King Charles
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6
Q

How is Pneumocystis carinii definitely diagnosed?

A
  1. Lung biopsy or BAL

* Low globulins may also be present on bloodwork if common variable immunodeficiency is present

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7
Q

How is Pneumocystis carinii treated?

A

TMS
- more effective and less toxic than pentamidine
AZOLES ARE NOT EFFECTIVE

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8
Q

If a patient is diagnosed with Pneumocystis carinii what else should you look for?

A

Immunodysfunction

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9
Q

Where are pythium and lagenidium located geographically?

A

SE US

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10
Q

What is the infective form of pythiosis?

A

Motile biflagellate zoospore

*Encysts in damaged skin or GI mucosa

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11
Q

Pythiosis affects which layers of the GI tract?

A

Submucosal or muscular

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12
Q

How are oomycetes different from true fungi?

A
  • Pythiosis and Lagenidiosis
    1. Produce motile, flagellate zoospores
    2. Have cell walls that lack chitin
    3. Cell membranes LACK ergosterol
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13
Q

What segments of the GI tract are most commonly affected by pythium?

A
  1. Gastric outflow region
  2. Proximal duodenum
  3. Iliocecocolic junction
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14
Q

Cytology and histopathology of pythium and lagenidium often reveal what kind of inflammation?

A

Eosinophilic and pyogranulomatous inflammation

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15
Q

What are the best diagnostic tools for pythium?

A
  1. ELISA for serum antibodies → indicates active infection, high Sens and spec
    - Can be used to monitor response to treatment
  2. Culture → most successful from biopsy specimen
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16
Q

How can response to treatment be monitored in pythium patients?

A

ELISA for serum antibodies

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17
Q

What are the most common clinical signs associated with lagenidium?

A

Progressive cutaneous and subcutaneous lesions → typically ulcerated and edematous

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18
Q

(Pythium/Lagenidium) can cause rupture of the great vessels

A

Lagenidium

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19
Q

Serology for lagenidium will cross react with which other disease process?

A

Pythium

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20
Q

(Pythium/Lagenidium/Both) can be observed with a GMS stain

A

Both

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21
Q

(Pythium/Lagenidium/Both) can be observed on an H&E stain

A

Lagenidium

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22
Q

What is the preferred treatments for lagenidium and pythium?

A
  1. Aggressive surgical resection

2. Itraconazole and terbinafine post-op to help prevent recurrence

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23
Q

In pythiosis, complete resection should result in what % drop in ELISA?

A

50% in 3 months

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24
Q

Salmonella: Gram (+/-)

A

Gram -

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25
Q

What % of dogs with salmonella are asymptomatic carriers? Cats?

A
  1. 30%

2. 18%

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26
Q

When does clinically significant disease with salmonella occur?

A

Young, parasitized, immunocompromised animals

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27
Q

What are the possible outcomes after salmonella infection?

A
  1. Asymptomatic carriage
  2. Gastroenteritis
  3. Bacteremia/Septicemia
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28
Q

When should salmonella infections be treated?

A

When clinical signs appear. Should not be treated if healthy.

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29
Q

What is a good starting choice for antibiotics for salmonella?

A

Fluoroquinolones

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30
Q

What is the most globally widespread zoonotic disease?

A

Leptospirosis

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31
Q

What is the most prominent leptospirosis serovar in the US today?

A
  1. Grippotyphosa

- Icterohemorrhagic and canicola were most prominent prior to 1960

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32
Q

Where are the following leptospirosis serovars located geographically?

  1. Grippotyphosa
  2. Pomona
A
  1. East of the Mississippi

2. Northeast

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33
Q

Which leptospirosis serovars commonly cause

  1. Liver signs
  2. Renal failure
A
  1. Icterohemorrhagica and grippotyphosa

2. Grippotyphosa and pomona

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34
Q

What is the most common means of leptospirosis spread?

A

Water contact

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35
Q

What is the maintenance host for leptospirosis?

A

Burrowing rodents

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36
Q

Which dog breed is at higher risk for leptospirosis?

A

German shepherd

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37
Q

Acute renal failure is recognized in what % of leptospirosis cases?

A

90%

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38
Q

How does leptospirosis cause acute renal failure?

A

Acute decrease in GFR due to swelling that impairs renal perfusion

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39
Q

Concurrent hepatic failure along with acute renal failure is observed in what % of leptospirosis cases?

A

10-20%

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40
Q

Why might PU/PD in the absence of azotemia occur in a dog with leptospirosis

A

Nephrogenic diabetes insipidus secondary to lepto antigen

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41
Q

When do vaccinal titers for leptospirosis start to wane?

A

3-4 months after vaccination

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42
Q

As antibody concentrations increase, leptospirosis is cleared from most tissues except ____

A

Kidneys

*This is why the host can shed from kidneys for months to years after clinical recovery

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43
Q

What is the most common test for leptospirosis antibodies?

A

Microscopic agglutination test

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44
Q

MAT titers of ___ are supportive of a leptospirosis diagnosis but _____ is preferred.

A
  1. 1:800

2. Fourfold rise in titer over a 2-4 week interval

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45
Q

Which immunoglobulin increases first in leptospirosis infection?

A

IgM → rises in the first week (before MAT titers) and peaks in 14 days
- IgG becomes positive in 2-3 weeks after infection and peaks at 1 month

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46
Q

A single IgG/IgM test is suitable to distinguish between natural vs vaccine for leptospirosis because vaccinated dogs should have high ____ and low ___

A
  1. IgG

2. IgM

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47
Q

Which can identify the infective serovar for leptospirosis - MAT or PCR?

A

MAT

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48
Q

PCR for leptospirosis is (sensitive/specific) so you should only trust the (positive/negatives)

A
  1. Specific

2. Positives

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49
Q

Which antibiotic should be used to treat ill leptospirosis patients?

A

Ampicillin

*Eliminates the leptospiremic phase but does NOT eliminate the organism from the renal tubules

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50
Q

Once patients with leptospirosis are taking oral drugs or have recovered from ARF - which antibiotic should be used?

A
  1. Streptomycin - eliminate the leptospiruric phase
    OR
  2. Doxycycline - eliminates both the leptospiremic and leptospiruric phases
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51
Q

When should ciprofloxacin be used in the treatment of leptospirosis? Why?

A
  1. When meningitis or uveitis is observed

2. It crosses the blood brain barrier

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52
Q

What are negative prognostic factors for leptospirosis?

A
  1. German shepherd

2. Pomona serovar

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53
Q

What is the prognosis for leptospirosis?

A

50-80% survival

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54
Q

True/False: Giardia is zoonotic

A

True

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55
Q

How does giardia infect the host?

A

Ingested oocytes excyst in the upper SI and trophozoites attach to the intestinal mucosa from the duodenum to the ileum

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56
Q

Most giardia infections are (clinical/non-clinical)

A

Non-clinical

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57
Q

What are the options for diagnosing giardia?

A
  1. Trophozoites in duodenal juice or fresh fecal smear
  2. Oocysts on ZINC SULFATE float → shedding is intermittent
  3. Giardia antigen by fecal ELISA
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58
Q

How is giardia treated?

A
  1. Metronidazole for 5 days

2. Albendazole or Fenbendazole are also options (fenbendazole preferred because albendazole can cause BM suppression)

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59
Q

What compounds can help clean the environment of giardia?

A
  1. Steam

2. Quaternary ammonium compounds

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60
Q

Actinomyces vs Nocardia:

- Partial acid fast staining

A

Nocardia

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61
Q

Actinomyces vs Nocardia

- Hard to culture

A

Actinomyces

- Nocardia is easy to culture

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62
Q

Actinomyces vs Nocardia:

- Long filamentous in DENSE mats

A

Actinomyces

- Nocardia is in LOOSE mats or individual

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63
Q

Actinomyces vs Nocardia:

- Present in adult hunting dogs

A

Actinomyces

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64
Q

Actinomyces vs Nocardia:

- Present in young dogs (<2 years)

A

Nocardia

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65
Q

Actinomyces vs Nocardia:

- Spread directly (typically plant foreign bodies)

A

Actinomyces

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66
Q

Actinomyces vs Nocardia:

- Spread hematogenously

A

Nocardia

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67
Q

Actinomyces vs Nocardia:

- High mortality

A

Nocardia

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68
Q

Actinomyces vs Nocardia

- Sulfur granules present

A

Actinomyces

- Sulfur granules variable for nocardia

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69
Q

Actinomyces vs Nocardia:

- Treat with penicillin

A

Actinomyces

- Nocardia has variable susceptibility to sulfonamides, tetracyclines, or aminoglycosides

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70
Q

Aflotoxicosis is caused by ___. Which is generated by metabolism by ____ and then conjugated with ____ by ____.

A
  1. 8,9 epoxide
  2. Cytochrome p450 enzymes
  3. Glutathione
  4. Phase II enzymes
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71
Q

8,9 epoxide is (highly/minimally) lipophilic and is absorbed completely in the duodenum

A
  1. Highly
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72
Q

What is the mechanism of pathogenesis for 8,9 epoxide?

A
  1. Binds to other molecules in the cell leading to DNA adducts.
  2. Causes renal tubular and hepatic necrosis
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73
Q

What is another possible differential for aflotoxicosis?

A

Leptospirosis

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74
Q

What are the consequences of aflotoxicosis for patients that survive?

A

Fibrosis

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75
Q

How is aflotoxicosis treated?

A
  1. Various liver protectants

2. Oltipraz → inhibits phase I enzymes (CYP1A2) and induces phase I enzymes including glutathione

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76
Q

What is the causative agent of feline infectious peritonitis?

A

Feline corona virus → enveloped ssRNA virus

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77
Q

The majority of cats infected with feline corona virus (will/will not) develop FIP

A

Will not

- Only 1/10 will develop FIP

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78
Q

How soon is feline coronavirus shed in feces following infection?

A

2 days

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79
Q

When do most cats clear feline coronavirus infections?

A

After 2-3 months of fecal shedding

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80
Q

The following may associated with what disease process?

  1. Rising FeCoV titers
  2. Polyclonal gammopathy
  3. a1-acid glycoprotein
A

Feline infectious peritonitis

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81
Q

How is FIP definitively diagnosed?

A

IHC to demonstrate presence of FCoV virus in lesions (pyogranuloma, area of vasculitis)

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82
Q

Leptospirosis PCR has (high/low) Sens and spec?

A

Sens: Low
Spec: High

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83
Q

Feline infectious peritonitis: Effusive vs Non-effusive forms

  1. Antibody mediated immunity vs Cell mediated immunity
  2. Immune reaction type
A

Effusive: Strong AMI, Weak CMI, Type III

Non-Effuse: Strong AMI, Adequate CMI, Type IV

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84
Q

FIP ascites is caused by what?

A

Infected monocytes producing VEGF

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85
Q

What is antibody enhanced disease in the context of FIP?

A

If a FCoV + cat is vaccinated, it is more likely to have the effusive form of the disease and die from the disease - does not make a difference in a FCoV - cat

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86
Q

What is the gold standard for FCoV testing?

A

IFAT

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87
Q

What precautions should be taken if a cat has FCoV antibodies?

A

DO NOT STRESS THEM

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88
Q

How is pythium infection acquired?

A

Skin inoculation

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89
Q

Cryptosporidium vs Giardia

Site of infection: Primarily jejunum

A

Cryptosporidium

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90
Q

Cryptosporidium vs Giardia

Site of infection: Primarily small intestine

A

Giardia

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91
Q

Cryptosporidium vs Giardia

Trophozoites attach to brush border of GI epithelium

A

Giardia

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92
Q

Cryptosporidium vs Giardia

Type II merozoites attach to GI epithelium

A

Cryptosporidium

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93
Q

Cryptosporidium vs Giardia

Very small, require oil immersion microscopy for diagnosis

A

Cryptosporidium

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94
Q

What is required for 95% sensitivity in testing for giardia on zinc sulfate floats?

A

Need to perform at least 3 floats

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95
Q

What is the preferred method of giardia diagnosis?

A

Fecal ELISA - detects antigen

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96
Q

Cryptosporidium vs Giardia

Treated with paromyocin or nitazoxanide

A

Cryptosporidium

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97
Q

Cryptosporidium vs Giardia

Treated with metronidazole or fenbendazole

A

Giardia

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98
Q

Cryptosporidium vs Giardia

Oocysts can survive in the environment for months

A

Cryptosporidium

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99
Q

Cryptosporidium vs Giardia

Can be removed from the environment with quaternary ammonium compounds

A

Giardia

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100
Q

Cryptosporidium vs Giardia

Which is enteroinvasive?

A

NEITHER!

- They are found on the surface of the enterocytes and pathogenesis is not likely due to direct cellular damage.

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101
Q

Cryptococcus can be identified by which stain?

A

India ink stain

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102
Q

What test is preferred for cryptococcus diagnosis? What does it detect?

A

Latex agglutination test → detects capsular antigen

- Antibody titers are not useful due to the thick capsule keeping the body from producing a strong humoral response

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103
Q

What are sequelae that may result from canine distemper virus infection?

A
  1. Hyperkeratosis → paw pads and nasal planum
  2. Acute encephalomyelitis → occurs not long after infection
  3. Chronic distemper encephalitis → neurologic signs in older dogs that do not have a history of distemper infection
  4. Thymic atrophy → post-mortem finding in puppies
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104
Q

Where is canine distemper virus antigen found in dogs with hyperkeratosis?

A

Stratum spinosum and stratum granulosum

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105
Q

What should be ruled out before a diagnosis of distemper can be made in dogs with hyperkeratosis?

A
  1. Familial footpad keratosis → Irish terriers and Dogue de Bourdeaux
  2. Zinc responsive dermatitis → Huskies and Alaskan malamute
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106
Q

Dogs with chronic distemper encephalitis are (infectious/non-infectious)

A

Non-infectious

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107
Q

What is a post-mortem finding that can be found in puppies that had distemper virus?

A

Thymic atrophy

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108
Q

What is the organism?

  1. Zoonotic
  2. Found in 50% of puppies and 100% of kennels
  3. Causes voluminous watery diarrhea
  4. Zinc sulfate float often needed for diagnosis
  5. Treated with metronidazole
A

Giardia

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109
Q

What is the organism?

  1. Causes yellow, watery diarrhea
  2. Difficult to diagnose
  3. Zoonotic: Kills ~10% of AIDS patients
  4. Treatment is primarily supportive therapy
A

Cryptosporidium sp.

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110
Q

What is the organism?

  1. Occasional cause of diarrhea and death via colitis/enteritis
  2. Treatment is TMS and supportive care (albon also approved)
A

Coccidiosis

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111
Q

Toxoplasma gondii is excreted in the feces as a (sporulated/unsporulated) oocyst

A

Unsporulated

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112
Q

How long does it take for unsporulated Toxoplasma oocysts to sporulate?

A

Sporulated in 1-5 days but can survive in the environment for over 1 year

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113
Q 
Toxoplasma gondii
(Tachyzoites/Bradyzoites) replicate in intestinal walls
A

Tachyzoites

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114
Q

Toxoplasma gondii

(Tachyzoites/Bradyzoites) encyst in tissue

A

Bradyzoites

*Will encyst in tissue for the life of the host

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115
Q

Toxoplasma gondii
(Tachyzoites/Bradyzoites) can be the cause of reactivated infection such as after immunosuppression or can be a cause of chronic uveitis in cats

A

Bradyzoites

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116
Q

What is a unique feature for cats in the context of toxoplasma gondii?

A

They are the only species that can complete the life cycle and pass RESISTANT oocytes in feces

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117
Q

What is a consequence of immunocomprised cats being infected with toxoplasma gondii?

A
  1. They can have FATAL DISSEMINATION and intracellular replication of tachyzoites
  2. They can have transmammary infection as well
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118
Q

What tissues are most commonly affected in cats with disseminated toxoplasma gondii?

A
  1. Hepatic
  2. Pulmonary
  3. CNS
  4. Pancreatic
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119
Q

How does toxoplasma gondii infection occur?

A
  1. Ingestion of sporozoites, tachyzoites, or bradyzoites in most warm blooded vertebrates
  2. Transplacental is possible in most species → tachyzoites to fetus
  3. Transmammary is possible in cats
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120
Q

Which cats develop the worst clinical signs from toxoplasma gondii?

A

Kittens that were infected transplacentally or transmammary

- Generally die of hepatic disease or pulmonary disease

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121
Q

What is one of the most common causes of feline infectious uveitis?

A

Toxoplasma gondii

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122
Q

Toxoplasma gondii is (commonly/rarely) associated with clinical disease in the dog

A

Rarely

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123
Q

What is the duration that most cats and dogs will be Ab + with toxoplasma gondii infection?

A

For life → no point in repeated serum Ab titers after disease manifestations have resolved

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124
Q

Toxoplasma gondii

90% of cats with clinical toxoplasmosis have an elevated ___

A

IgM

- Greater than 1:64 is positive

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125
Q

Toxoplasma gondii: IgG vs IgM

___ has a higher predictive value than ___

A
  1. IgM

2. IgG

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126
Q

Toxoplasma gondii:

Serology for IgM is indicative of what kind of infection?

A

Either early infection or recurrent infection

- Detectable 2-4 weeks after infection and resolves in 16 weeks

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127
Q

Toxoplasma gondii

Serology for IgG is indicative of what?

A

Indicates past exposure to toxoplasma

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128
Q

What % of cats with clinical toxoplasmosis will have an increased IgG

A

60%

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129
Q

Toxoplasma gondii is now correlated to what human diseases?

A
  1. Schizophrenia

2. Learning disabilities

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130
Q

What precautions should be taken by households with pregnant women and cats?

A
  1. Clean the litter box every 24 hours → will not allow toxoplasma gondii oocysts time to sporulate
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131
Q

When do cats shed toxoplasma gondii oocysts?

A

Days to weeks following their PRIMARY INFECTION → repeat shedding rarely occurs even if the cat relapses with immunosuppression

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132
Q

Most seropositive cats with toxoplasmosis (are/are not) shedding oocysts

A

Are not

- Those shedding oocysts are usually not seropositive yet

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133
Q

What is the treatment for toxoplasmosis?

A

Clindamycin or TMS

- Will not totally clear the body of the organism → recurrent disease is common

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134
Q

What is the definitive host of neospora?

A

The dog

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135
Q

What are the intermediate hosts for neospora?

A
  1. Cow
  2. Dog
  3. Sheep
  4. Goat
  5. Horse
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136
Q

How is neospora transmitted?

A
  1. Aborted fetus/placenta/raw meat ingested from intermediate host
  2. Encystment in muscle and shedding of oocysts in feces
  3. Intermediate host ingests feces
    * Dogs and cows can also do transplacental or transmammary
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137
Q

What are the clinical signs of neospora in:

  1. Puppies <6 mo
  2. Dogs >6 mo
A
  1. Ascending LMN paralysis

2. LMN flaccid paralysis with meningitis, encephalomyelitis, and cerellaritis

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138
Q

What is the definitive diagnostic tool for neospora? What are other options?

A
  1. ID of tissue cysts is definitive

2. Serology best, fecal unrewarding

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139
Q

What is the treatment for neospora?

A

Clindamycin for 4-6 weeks

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140
Q

What is the organism?

  1. Found in almost all puppies
  2. Zoonotic - visceral larval migrans
  3. Treated with Fenbendazole
A

Toxocara canis

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141
Q

How is toxocara canis treated?

A

Fenbendazole

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142
Q

What is the organism?

  1. Causes cerebrospinal nematodiasis
  2. Affects dogs
A

Baylisascaris

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143
Q

What is the organism?

  1. Zoonotic - creeping eruption cutaneous larval migrans
  2. Clinical effects due to blood loss (anemia, melena)
  3. Treated with fenbendazole
A

Hookworms

Ancylostoma, Uncinaria spp

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144
Q

How are hookworms (ancylostoma, uncinaria) treated?

A

Fenbendazole

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145
Q

What is the organism?

  1. Difficult to diagnose due to few eggs and intermittent shedding
  2. Bloody diarrhea, tenesmus
  3. Diagnose based on response to treatment
  4. Treated with fenbendazole
A

Whipworms

Trichuris vulpis

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146
Q

How are whipworms (trichuris vulpis) treated?

A

Fenbendazole

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147
Q

Where do dirofilaria immitis live in teh body?

A

Right ventricle and pulmonary arteries

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148
Q

Which rickettsial organism is part of the disease process for dirofilaria immitis?

A

Wolbachia

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149
Q

How are dipylidium spp transmitted? Are they zoonotic?

A
  1. Flea ingestion

2. yes

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150
Q

How are dipylidium spp treated?

A

Tapeworms

Droncit (praziquantel)

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151
Q

How are Taenia spp treated?

A

Tapeworms

Droncit (praziquantel)

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152
Q

Are Taenia spp zoonotic?

A

Yes

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153
Q

What are the results of intermediate host and definitive host infection of Taenia spp. in humans?

A

IH: Neural cystocercosis can lead to epilepsy
DH: Intestinal tapeworm from uncooked pork

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154
Q

What does the larval form of echinococcus granulosus cause?

A

Hydatid cysts in the brain, anaphylaxis

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155
Q

Which is more severe Echinococcus granulosos or Echinococcus multilocularis infection?

A

Multilocularis

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156
Q

What is Echinococcus multilocularis infection often thought to be?

A

Metastatic cancer → can cause multiloculated, thin walled, invasive cysts

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157
Q

What is the treatment for echinococcus spp?

A

Droncit (praziquantel)

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158
Q

How is rabies definitively diagnosed?

A

Direct immunoflourescence in brain tissue

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159
Q

What kind of virus is rabies?

A

Single stranded RNA lyssavirus

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160
Q

E. coli: Gram (+/-)

A

-

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161
Q

E. coli: anaerobic or aerobic

A

Facultative anaerobe

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162
Q

Salmonella: anaerobic or aerobic

A

Facultative anaerobe

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163
Q

What are the pathogenic forms of E. coli?

A
  1. ETEC → adheres and produces toxins (but doesn’t invade)
  2. EIEC → invades, replicates, and destroys epithelial cells
  3. EPEC → (not invasive or toxigenic) but attach and efface the brush border of enterocytes
  4. EHEC → produces verocytdtoxins that induce hemorrhagic ileitis and colitis
  5. EAEC → induce enterocyte pathology
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164
Q

Is salmonella enteroinvasive?

A

Yes

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165
Q

Where does rotavirus infect?

A

The villous tip in the intestine and causes sloughing and villous atrophy

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166
Q

Giardia, Crypto, Toxo: Large or small bowel diarrhea

A

Small

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167
Q

E. histolitica, T. foutus: Large or small bowel diarrhea

A

Large

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168
Q

What kind of virus is feline panleukopenia virus?

A

Small NONENVELOPED single stranded DNA virus

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169
Q

Feline panleukopenia is characterized by ___ and ___ with a (high/low) mortality

A
  1. Enteritis and panleukopenia

2. High

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170
Q

Feline panleukopenia virus has an affinity for what kind of cell?

A

Rapidly dividing (lymphoid, bone marrow, and crypt epithelium)

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171
Q

Feline panleukopenia is more sever in what kind of cat?

A

Young kittens

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172
Q

Feline panleukopenia virus - what is the consequence of infection at the following points in pregnancy?

  1. Early
  2. Middle 3rd to immediately post-natally
A
  1. Fetal death and resorption

2. Cerebellar hypoplasia

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173
Q

What has a good sensitivity for feline panleukopenia virus diagnosis?

A

Fecal viral DNA PCR

*Antibody titers may be useful to aid diagnosis

174
Q

What kind of lesions are seen on necropsy for feline panleukopenia virus?

A

Intranuclear inclusions in crypt epithelium

175
Q

What is the prognosis for feline panleukopenia virus?

A

50-90% mortality

176
Q

Why should modified live vaccines for feline panleukopenia virus not be used in pregnant queens or kittens <4 weeks old?

A

Risk of cerebellar hypoplasia

177
Q

Feline panleukopenia virus environmental cleaning methods

A
  • Very stable in the environment

- Need bleach or glutaraldehyde

178
Q

In utero or neonatal feline panleukopenia virus may result in what type of state?

A

Carrier state - but carriers play a minor role in spreading the disease

179
Q

What kind of virus is feline herpesvirus

A

Double stranded DNA, ENVELOPED

180
Q

What is the disease course for feline herpesvirus?

A

Initial infection is respiratory → recrudescent infections usually ocular/conjunctival

181
Q

Where does the typical α herpes virus replicate? Where does it establish a latent infection?

A
  1. Replicates in epithelial tissue during infection

2. Establishes latency in the trigeminal ganglia

182
Q

During stress, how does feline herpesvirus spread?

A

Down sensory axon

183
Q

What kind of keratitis occurs with feline herpesvirus?

A

STROMAL keratitis → CD4 inflammatory response to virus

184
Q

What is the best form of PCR for feline herpesvirus? Why?

A

Tissue (Conjunctival/oral swabs) → serum is bad because the majority of cats have been exposed

185
Q

What does PCR for feline herpesvirus detect?

A

A short sequence in the thymidine kinase gene of the virus

186
Q

What is the effect of L-lysine for feline herpesvirus?

A

Inhibits replication by competitively inhibiting the incorporation of arginine into the virus

187
Q

What can be used for treatment of acute feline herpesvirus infections?

A

Topical antibiotics used for Chlamydia psittici (tetracycline, chloramphenicol, or erythromycin)
*Systemic abx should not be used unless resp infection noted

188
Q

What is produced by feline herpesvirus vaccination (humoral vs CM)? What is the result of vaccination?

A
  1. Produces a humoral response to feline herpesvirus.

2. Will lessen the SEVERITY of the disease

189
Q

What is the mechanism of imiquamod for treatment of feline herpesvirus?

A

Activation of TLR7

190
Q

What is the incubation period for feline calicivirus?

A

2-10 days

191
Q

What are the clinical signs associated with feline calicivirus?

A
  1. Ocular discharge
  2. Nasal discharge
  3. Oral ulceration
  4. Conjunctivitis
    * May also have lameness from polyarthritis
192
Q

What is the most reliable diagnostic method for feline calicivirus?

A

Virus isolation from nasal, conjunctiva, or oral swabs

- >90% sensitivity in virulent systemic disease cases

193
Q

What is feline calicivirus associated virulent systemic disease?

A

A more severe/hemorrhagic form of feline calicivirus

194
Q

Are adults or kittens at higher risk of more severe feline calicivirus infection?

A

Adults

195
Q

What pathologic finding is seen with feline calicvirius virulent systemic disease?

A

Centrilobular hepatocellular necrosis

196
Q

How is feline calicivirus inactivated?

A

Bleach

- NOT inactivated by chlorhex or quaternary ammonium compounds

197
Q

Cutaneous horns can be seen with what diseases?

A
  1. FeLV
  2. SCC
  3. Viral papillomas
    - 8% of Bowen’s cases (SCC in situ) are feline papilloma virus +
198
Q

Is feline orthopox virus (feline cowpox) zoonotic?

A

Yes

199
Q

How does infection of feline orthopox virus occur

A

Ingestion of rodents (reservoir host)

200
Q

What is the primary lesion in feline orthopox virus?

A

Dermatologic lesions (ulcerating macule or plaque)

201
Q

What kind of virus is canine parvovirus/panleukopenia virus (CPV-2)

A

Small ENVELOPED single strand DNA virus

202
Q

Canine parvovirus/panleukopenia virus (CPV-2) has an affinity for what kind of cell?

A

Rapidly dividing cells → results in apoptotic cell death

203
Q

CPV-1 is only pathogenic in what kind of dog?

A

Neonates

- Can be isolated from healthy dogs

204
Q

What is important about dogs <6 weeks of age in context of canine parvovirus/panleukopenia virus (CPV-2)

A

They are protected by maternal Abs

205
Q

Which dogs are most at risk for canine parvovirus/panleukopenia virus (CPV-2) infection

A
  1. > 6 mo MALES are more often affected
  2. More severe in black/tan dogs (Rotts, Dobs)
  3. More severe in Pitts and English Springer Spaniels
206
Q

What occurs 4-7 days after canine parvovirus/panleukopenia virus (CPV-2) infection?

A

Severe diarrhea

207
Q

What is a possible sequelae to the severe diarrhea caused by canine parvovirus/panleukopenia virus (CPV-2) infection?

A

Intussusception → due to hypermotility

208
Q

When does myocarditis occur with canine parvovirus/panleukopenia virus (CPV-2) infection?

A

If infected in utero or shortly after birth if maternal Ab is absent

209
Q

How is canine parvovirus/panleukopenia virus (CPV-2) diagnosed?

A

Fecal ELISA (for viral antigen) is most sensitive in first 7-10 days

210
Q

What is a common biochemical findings with canine parvovirus/panleukopenia virus (CPV-2)

A

Leukopenia in 85% of cases

- Neutropenia due to consumption in GI tract plus destruction of progenitor cells

211
Q

What are canine intracytoplasmic inclusion bodies diagnostic for?

A

Distemper

*Intracytoplasmic EOSINOPHILIC inclusions (negri bodies) have been reported in rabies as well

212
Q

What are canine intranuclear inclusion bodies diagnostic for?

A
  1. Distemper

2. Rabies

213
Q

What are feline intracytoplasmic inclusion bodies diagnostic for?

A
  1. Chlamydia felis

2. Feline cowpox

214
Q

What are feline intranuclear inclusion bodies diagnostic for?

A
  1. Feline panleukopenia

2. Feline herpesvirus

215
Q

What is the most common disease syndrome in chronic FIV cats? What % have this disease syndrome?

A

Chronic stomatitis - 50%

216
Q

Which is more pathogenic FeLV or FIV?

A

FeLV

217
Q

What are the important antigens in FeLV infections? Why?

A
  1. p27 → in plasma of infected cats → this is what IFA and ELISA test for
  2. Envelope (env) → gp70 → most important for inducing immunity → vaccines are made with this
  3. p15E (envelope) → causes immunosuppression
218
Q

FeLV or FIV?

  • Macrocytic normochromic anemia
  • Erythroid and granulocyte hypoplasia
A

FeLV

219
Q

FeLV or FIV

- Erythroid and granulocyte hyperplasia

A

FIV

220
Q

What is the effect on CD4+ T cells in FeLV and FIV?

A

They are decreased

221
Q

What are the potential outcomes before BM involvement in cats infected with FeLV?

A
  1. Immune response eliminates the virus
  2. Virus may be sequestered in a latent form
  3. Persistent viremia
222
Q

How is FeLV transmitted?

A

Close intimate contact → licking, biting, and transplacental/transmammary

223
Q

How is FIV transmitted?

A

Fighting

224
Q

FeLV or FIV

- Diagnostics directed toward antigen?

A

FeLV

225
Q

FeLV or FIV

- Diagnostics directed toward antibody

A

FIV

226
Q

What is the primary diagnostic for FeLV infection? What is it testing for? What is the confirmatory test? What does it detect?

A
  1. ELISA
  2. p27/p30 in plasma
  3. IFA
  4. Detection of p27 in neutrophils and platelets
227
Q

What are the issues with diagnostic testing for FIV?

A
  • FIV Ag in the blood is too low to be detected → must rely on Ab testing
  • ELISA has a risk of false + → must confirm with western blot or IFA
228
Q

What is the additional risk of LSA in cats diagnosed with FeLV? FIV?

A
  1. 62 x more likely → usually get T cell

2. 5 x more likely → usually get B cell

229
Q

Can you differentiate between vaccinated and infected cats with FeLV?

A
  1. Yes, test is for Ag so it can differentiated
230
Q

What are the recommended management strategies for cats with FeLV? FIV?

A
  1. Keep cats indoors and separate positive vs negative cats

2. Keep cats indoors but no need to separate

231
Q

What % of FeLV cats are infected with the following and what is associated with each?

  1. FeLV-A
  2. FeLV-B
  3. FeLV-C
A
  1. All FeLV infected cats → Immunosuppression
  2. 50% of FeLV infected cats → Neoplastic disease is more common than in cats with FeLV-A alone
  3. 1% → Severe anemia
232
Q

What is the most common cause of thrombocytopenia and neutropenia in cats?

A

FeLV infection

233
Q

What does a macrocytic anemia in the absence of polychromasia strongly indicate in cats?

A

Strong predictor of FeLV infection

234
Q

Tick paralysis is a (infectious/non-infectious) disease process that is associated with ____ tick species?

A
  1. Non-infectious

2. Dermacentor

235
Q

What is the vector for Ehrlichia canis?

A

Rhipicephalus sanguineus

236
Q

What life stage does Rhipicephalus acquire ehrlichia and what life stage does it transmit ehrlichia to the dog?

A
  1. Feeding on an infected dog in either the larva or nymph form
  2. Transmits either in the nymph or adult form
237
Q

What is the incubating period of Ehrlichia canis?

A

8-20 days

238
Q

How long is the acute phase of infection in Ehrlichia canis? What is happening during this phase?

A
  1. 2-4 weeks
  2. The organism is multiplying within circulating mononuclear cells → cells are phagocytized in the liver, spleen, and lymph nodes
239
Q

Where do cells infected with Ehrlichia canis adhere? What does this cause?

A
  1. Adhere to the vascular endothelium and induce a vasculitis and subendothelial tissue infection
  2. Leads to platelet consumption, sequestration, and destruction → seen as a thrombocytopenia during the acute phase of infection
240
Q

What is the most consistent hematologic abnormality seen in both the acute and chronic phases of any ehrlichiosis?

A

Thrombocytopenia

241
Q

How long does it take for dogs to become serum IFA positive in ehrlichiosis?

A

7-28 day

242
Q

What is the treatment for Ehrlichia canis?

A
  1. Doxycycline
  2. Chloramphenicol
  3. Imidocarb
243
Q

Can dogs be reinfected with Ehrlichia canis?

A

Yes

244
Q

Why do dogs with Ehrlichia canis have a hyperglobulinemia?

A

They can mount a humoral response but it is ineffective

245
Q

What is the reservoir host for Ehrlichia canis?

A

Wild and domestic canids

246
Q

Where geographically does Neorickettsia helmintheca occur?

A

NW coastal US

247
Q

How is Neorickettsia helmintheca transmitted to the dog?

A

Trematodes (nanophytes salmincola) harbor the rickettsia → eaten by snail → fish eats snail → dog eat fish → fluke eggs passed through dog feces but rickettsia stays in the dog

248
Q

When do clinical signs appear after being infected with neorickettsia helminthecia?

A
  1. 1-2 weeks after eating raw fish
249
Q

What clinical signs are associated with neorickettsia helmintheca?

A
  1. Fever
  2. V/D
  3. Lymphadenomegaly
  4. Thrombocytopenia
250
Q

How long does it take for serology to become positive for neorickettsia helmintheca?

A

2 weeks

251
Q

What is the treatment for neorickettsia helmintheca?

A

Doxycycline and praziquantel

252
Q

What is the end result of neorickettsia helmintheca infection?

A
  1. FATAL if not treated in 7-10 days
253
Q

What is another name for infection with neorickettsia helmintheca?

A

Salmon poisoning disease

254
Q

What is the reservoir host for Ehrlichia ewingii?

A
  1. White tailed deer
255
Q

What is the vector for Ehrlichia ewingii?

A

Amblyomma americanum (Lone star tick)

256
Q

What are unique clinical signs associated with E. ewingii?

A
  1. Joint swelling
  2. CNS signs
    * Has other clinical signs that are similar to E. canis
257
Q

How is E. eweingii treated?

A

Doxycycline

258
Q

What is the reservoir host for Anaplasma phagocytophilum?

A

Deer and mouse

259
Q

What is the vector for Anaplasma phagocytophilum? What is important about this vector/host relationship?

A
  1. Ixodes scapulars
  2. Needs to feed for 24 hours to infect!
    * Often co-infected with Lyme disease since it is the same vector
260
Q

What are the clinical signs associated with Anaplasma phagocytophilum?

A
  1. VAGUE illness
  2. Arthropathy
  3. Thrombocytopenia
261
Q

What is the most common Clin path finding for both A. phagocytophilum and A. platys?

A

Thrombocytopenia

262
Q

E. canis vs A. phagocytophilum

- More likely to see morale in neutrophils

A

A. phagocytophilum

263
Q

What is the treatment of Anaplasma phagocytophilum?

A

Doxycycline

264
Q

What cells are infected by Anaplasma phagocytophilum? A. platys?

A
  1. Neutrophils and eosinophils

2. Platelets

265
Q

Dogs infected with Anaplasma platys are (likely/not likely) to have clinical signs?

A

Not likely

266
Q

Co-infection with A. platys and what other tick borne disease is common?

A

E. canis → same vector

267
Q

What is the vector for A. platys?

A

Rhipicephalus sanguineous

268
Q

What is the treatment for A. platys?

A

Doxycycline

269
Q

What is the vector for Leishmaniasis?

A

Sandfly → dont know if this is in the US

270
Q

What is the transmission cycle for Leishmaniasis?

A

Sandfly injects flagellated promastigotes into host during feeding → promastigotes enter macrophages and disseminate → 1 month - 7 years later, amastigotes (non-flagellates) form and cutaneous lesions develop

271
Q

What cells are infected by Leishmaniasis?

A

Macrophages and lymphocytes

272
Q

What cells are infected by FIV during active infection?

A
  1. T cells
  2. B cells
  3. Macrophages
273
Q

What % of dogs with Leishmaniasis are clinically affected?

A

~10% → Dogs are usually not clinical for disease

274
Q

If dogs with Leishmaniasis have cutaneous disease, what other kind of disease can you assume they have?

A
  1. Visceral
275
Q

What diagnostic test is used for diagnosing Leishmania in dogs?

A
  1. IgG titers → increase 14-28 days after infection → correlated highly with infection since prevalence in US is so low → decline 45-80 days after infection
  2. rk39 ELISA → amastigote antigen → does NOT cross react with T. cruzi
276
Q

How is Leishmania treated?

A
  1. Leishmania CANNOT be cleared from the body

2. Treatment with allopurinol and antimony may help prevent recurrent infections

277
Q

What is the vector for Trypanosoma cruzi?

A

Kissing bug (reduvid bug)

278
Q

What are the cellular targets for Trypanosoma cruzi?

A
  1. Macrphages

2. Myocytes

279
Q

What is the transmission cycle for Trypanosoma cruzi?

A

Reduvid bug defecates during feeding → EPIMASTIGOTES enter macrophages or myocytes → divide until rupture → release → TRYPOMASTIGOTE picked up by bug during blood meal

280
Q

What is caused by Trypanosoma cruzi?

A
  1. Cardiomyopathy → parasite damage to myocardial cells or immune mediated reaction
  2. Increased creatinine kinase
281
Q

How is Trypanosoma cruzi diagnosed?

A
  1. Serology → positive tests correlate with infection in America
282
Q

What is the treatment for Trypanosoma cruzi?

A

Nifurtimox for 2-5 months

283
Q

B. gibsoni vs B canis

- Occurs singly in RBCs

A

B. gibsoni

284
Q

B. gibsoni vs B canis

- Occurs in pairs in RBCs

A

B. canis

285
Q

What is the vector for B. gibsoni? What is unique about tick transmission for B. gibsoni?

A
  1. Haemophysalis spp

2. Transovarial tick transmission can occur

286
Q

What is the vector for B. canis

A

Rhipicephalus sanguineous

287
Q

What are common findings in dogs infected with B. gibsoni?

A
  1. Regenerative anemia
  2. Thrombocytopenia
  3. Fever
  4. Hyperglobulinemia
  5. Some can have a positive Coombs test → 85% in one study
  6. Splenomegaly
288
Q

What are common findings in dogs infected with B. canis?

A
  1. Usually mild disease

2. Anemia, thrombocytopenia, splenomegaly

289
Q

Observing B. canis or B. gibsoni on RBCs has a (high/low) sensitivity

A

Low

290
Q

What diagnostic test can be used to differentiate Babesia spp?

A

PCR

291
Q

How is B. gibsoni treated?

A
  1. Atovaquone and azithromycin → will clear the infection
  2. Imidocarb → will just induce remission
    * Splenectomy makes the disease worse
292
Q

How is B. canis treated?

A

Imidocarb

*Splenectomy makes the disease worse

293
Q

How are Theileria and Babesia species differentiated?

A

Theileria spp first infect LEUKOCYTES before erythrocytes

294
Q

Mycoplasma haemofelis and haemocanis attach to what?

A

The outside of RBCs

295
Q

What increases the risk of M. haemofelis infection?

A
  1. FeLV infection
  2. Lack of vaccine
  3. Young
  4. Cat bite
  5. Outdoors
296
Q

What kind of hemolysis occurs with M. haemofelis?

A

Primarily extravascular but intravascular can occur

297
Q

What % of M. haemofelis cats are FeLV +

A

50%

298
Q

How can you differentiate M. haemofelis from Heinz bodies or reticulocytes?

A

New methylene blue staining

299
Q

How is M. haemofelis diagnosed?

A
  1. Visualize on blood smears (<50% of cases)

2. PCR readily available and can distinguish species

300
Q

What does M. haemofelis cause in the cat?

A

Hemolytic anemia

301
Q

How is M. haemofelis treated?

A

Doxycycline or flouroquinolone

302
Q

When does clinical M. haemocanis infection typically occur?

A

Splenectomized dogs

*Can also reactivate an infection post splenectomy

303
Q

What kind of anemia is seen in dogs infected with M. haemocanis?

A

Macrocytic hypochromic anemia

304
Q

How is M. haemocanis treated?

A

Doxycycline or fluoroquinolones

305
Q

Where is Bartonella henselae found in the body?

A
  1. Intra-RBCs
306
Q

What is the vector of Bartonella henselae?

A

Fleas and flea dirt

307
Q

Is Bartonella henselae zoonotic?

A

Yes, cat scratch disease

308
Q

What are the clinical signs associated with Bartonella henselae infection?

A
  1. Found in clinically healthy cats
    - Can infect stem cell progenitors
  2. Can also infect dogs
309
Q

How is Bartonella henselae diagnosed?

A
  • Use culture or PCR to diagnose in cats but it does not tell you if it is the cause of their clinical signs
  • Diagnosis is difficult because up to 50% of all HEALTHY cats can have serologic titers and 40% are bacteremic
310
Q

What is the treatment for Bartonella henselae?

A

Azithromycin

- 2nd choice is doxycycline

311
Q

Are dogs or cats infected by Bartonella visonii berkhoffi?

A

Dogs

312
Q

What disease is associated with Bartonella visonii berkhoffi in dogs?

A

Endocarditis → especially aortic valves

313
Q

What is the organism?

  • Canine with subaortic stenosis
  • Endocarditis present
  • Culture negative
A

Bartonella visonii berkhoffi

314
Q

Is serologic testing useful in the diagnosis of Bartonella visonii berkhoffi in dogs?

A

Yes, more useful than serologic testing in cats.

- If antibodies are detected in a sick dog, it is safe to assume that it is the cause of the clinical signs

315
Q

What is the treatment for Bartonella visonii berkhoffi?

A

Azithromycin

316
Q

Where is Cytauxzoan felis found geographically?

A

Midwest and SE

317
Q

What does Cytauxzoan felis infect?

A
  1. Monocytes

2. RBC

318
Q

What life cycle stage of Cytauxzoon felis plays a role in the tissue phase of the disease?

A

Schizont

319
Q

What life cycle stage of Cytauxzoon felis plays a role in the RBC phase of the disease?

A

Piroplasm

320
Q

What is a distinguishing factor between Cytauxzoon and Babesia life cycle stages?

A

Babesia does NOT have a tissue phase

321
Q

What is the vector for Cytauxzoon felis?

A

Dermacentor variabilis

322
Q

What is the natural host of Cytauxzoon felis?

A

Bobcat

*Only Felidae are susceptible

323
Q

When do clinical signs develop after cytauxzoon felis infection? What is the end result of the disease?

A
  1. 13-16 days after infection

2. FATAL 5 days after clinical signs develop

324
Q

What Clin path abnormalities are assoc. with Cytauxzoon felis?

A
  1. Non-regenerative anemia → because it is so acute
  2. Leukocytosis
  3. THrombocytopenia
  4. Hyperbilirubinemai → way more icteric than for the level of anemia
325
Q

What is the underlying mechanism for illness in Cytauxzoon felis?

A

Macrophages infected → schizogeny (asexual) to form schizonts → occlude venous channels in many organs

326
Q

What happens to cats that are exposed to only the piroplasm form of Cytauxzoon felis?

A

They develop protective immunity

327
Q

How is Cytauxzoon felis diagnosed?

A
  1. Schizonts within macrophages in tissue or LN/BM aspirate
  2. Signet rings in RBCs → cats may die from schizonts before this stage occurs (piroplasm stage is in the RBC)
  3. PCR is good but not commercially available
328
Q

How is Cytauxzoon felis treated?

A
  1. Atoviquone

2. Azithromycin

329
Q

What is the causative agent of Rocky Mountain Spotted Fever?

A

Rickettsia rickettsii

330
Q

Where is Rickettsia rickettsii located geographically

A
  1. SE or South Central US
331
Q

What is the cellular target of Rickettsia rickettsii?

A

Vascular endothelium

332
Q

What is the vector for Rickettsia rickettsii

A

Dermacentor variabilis

333
Q

What clinical signs are associated with Rickettsia rickettsii?

A

Rocky Mountain Spotted Fever

  1. Fever
  2. Depression
  3. Lymphadenopathy
  4. Vestibular Signs
  5. Vasculitis
    * Animals either get better or they die
334
Q

What would be observed on a tissue biopsy of a dog infected with Rickettsia rickettsii?

A

Necrotizing vasculitis

335
Q

Rocky Mountain Spotted Fever is a(n) (acute/chronic) disease?

A

Acute

- It is never chronic!

336
Q

How is Rocky Mountain Spotted Fever diagnosed?

A
  1. 4x increase on IFA titer → will cross react with non-pathogenic spotted fever rickettsia group
  2. DFA on skin biopsy → will also see necrotizing vasculitis
337
Q

What is not a sensitive method for Rickettsia rickettsii diagnosis?

A

PCR

338
Q

How is Rickettsia rickettsii treated?

A
  1. Doxycycline
  2. Chloramphenicol
  3. Enrofloxacin
    * Dogs that survive will develop long lasting immunity
    * Treat BEFORE confirming diagnosis
339
Q

Do dogs become chronic carriers for Rickettsia rickettsii?

A

No! They either get better or die

340
Q

What is the causative agent for Lyme disease?

A

Borrelia burgdorferi

341
Q

What is the cellular target of Borellia burgdorferi?

A

They are an extracellular pathogen

342
Q

What is the vector of Lyme disease?

A

Ixodes spp

343
Q

What are the clinical signs associated with Lyme disease?

A
  1. Most dogs remain asymptomatic
  2. Intermittent lameness, fever, lethargy, anorexia
  3. Lyme nephritis (uncommon) → occurs without lameness and most dogs die despite therapy
    * Causes a RASH in people
344
Q

What is a good test for Lyme disease? What is it testing for specifically?

A
  1. 4DX SNAP test

2. C6 peptide → good because it is not found in the vaccine

345
Q

What is the treatment for Lyme disease?

A
  1. Doxycycline

2. Ampicillin

346
Q

What protein does the lyme vaccine contain?

A

OspA

347
Q

What is the cellular target of Hepatozoon?

A
  1. Muscle

2. Inflammatory cells

348
Q

What is the vector for Hepatozoon?

A

Amblyomma maculatum (gulf coast tick)

349
Q

How is Hepatozoon transmitted?

A
  1. Dogs must INGEST the tick containing oocysts

2. Vertical transmission is also possible

350
Q

What life cycle stage of hepatozoon is responsible for severe pyogranulomatous inflammation?

A

Merozoites being released from skeletal muscle

351
Q

What is the organism?

- Onion skin cysts found in skeletal muscle

A

Hepatozoon americanum

352
Q

What life cycle stage of H. americanum infects inflammatory cells?

A

Gamonts

*When gamonts infect inflammatory cells they can then infect ticks

353
Q

How is H. americanum diagnosed?

A
  1. Muscle biopsy

2. Serum antibodies → 93% sens and 96% spec

354
Q

What clinical signs are associated with H. americanum?

A
  1. Pyogranulomatous vasculitis and periostitis
  2. Myositis/Pain
  3. Extreme neutrophilic leukocytosis
  4. Periosteal reaction of long bones
  5. Liver signs → decreased albumin, glucose, and BUN, but bile acids are normal → does not indicate liver failure
355
Q

How is H. americanum treated?

A
  1. TMS
  2. Clindamycin
  3. Pyrimethamine
  4. Decoquinate
356
Q

What is the benefit of adding decoquinate to H. americanum therapy?

A

Prolongs MST from 10-12 months to 6 years!

357
Q

What is the causative agent for Q fever?

A

Coxiella burnetti

358
Q

Is Coxiella burnetti zoonotic?

A

Yes

359
Q

What is the target of Coxiella burnetti infection?

A

Urogenital tract

360
Q

What species are most commonly affected by Coxiella burnetti (Q fever)?

A
  1. Cattle, sheep, and goats

2. Cats can be infected but are usually subclinical → can have abortions

361
Q

For the 4DX SNAP test - Which portions are antigen tests vs antibody tests?

  1. Dirofilaria immitis
  2. Ehrlichia canis
  3. Anaplasma phagocytophilum
  4. Borrelia burgdorferi
A
  1. Antigen
  2. Antibody
  3. Antibody
  4. Antibody
362
Q

The IFA test for Ehrlichia canis will cross react with what other diseases?

A
  1. E. chafensis
  2. E. ewingii
  3. N. helminthoeca
363
Q

The IFA test for E. chafensis will cross react with what other diseases?

A
  1. E. canis

2. E. ewingii

364
Q

The IFA test for Anaplasma phagocytophilum will cross react with what other diseases?

A
  1. E. canis
  2. E. ewingii
  3. A. platys
365
Q

The IFA test for Neorickettsia riticci will cross react with what other diseases?

A
  1. E. canis

2. H. heminthoeca

366
Q

The IFA test for Neorickettsia helminthoeca will cross react with what other diseases?

A
  1. E. canis

2. N. risicii

367
Q

What are the two forms of feline coronavirus? What do they infect?

A
  1. Feline enteric coronavirus → enterocytes

2. Feline infectious peritonitis virus → macrophages

368
Q

What percentage of cats seropositive for feline coronavirus are shedding in feces?

A

1/3

- Seropositivity does not correlate with shedding

369
Q

Cats with feline coronavirus that (do/do not) mount a humoral immune response do not develop FIP

A

Do not

370
Q

What is the general underlying mechanism for pathogenesis in feline coronavirus infection?

A

Immune mediated disease

*Complement fixation leads to a release of vasoactive amines → vasculitis

371
Q

The effusive form of FIP is the (acute/chronic) form of the disease. The non-effusive form is the (acute/chroni) form.

A
  1. Acute

2. Chronic

372
Q

What other clinical signs are common with the non-effusive form of FIP?

A
  1. Ocular

2. Neurologic (usually ataxia, but hydrocephalus is highly suggestive of FIP)

373
Q

FeLV is (stable/unstable) in the environment

A

Unstable

-Inactivated in seconds

374
Q

FeLV PCR has (good/bad) sensitivity and (good/bad) specificity

A
  1. Bad → false negatives can happen from processing, mutant strains, proviral DNA fragility
  2. Good → a positive is a positive
375
Q

Fading kitten syndrome is associated with what infectious disease process?

A

FeLV

376
Q

The deleterious effects of bacteria from the gut may be secondary to (systemic endotoxin/systemic bacterial infection)

A
  1. Systemic endotoxin

2. GALT may fight off bacteria → in the process LPS is released

377
Q

What is an important amino acid for enterocytes and maintaining a mucosal barrier?

A

Glutamine

378
Q

What are the mechanisms for acquired bacterial resistance to antibiotics?

A
  1. Synthesis of enzymes that alter the antibiotic
  2. Alter antibiotic target
  3. Decreased entry of antibiotic into the organism
379
Q

What is the innate antibiotic resistance associated with Pseudomonas spp.?

A

Very small porin channels

380
Q

Enterococcus spp have innate resistance to what kinds of antibiotics?

A
  1. Cephalosporins

2. Fluoroquinolones

381
Q

What is the best test for FIV?

A

Antibody ELISA → should be confirmed by western blot

382
Q

When should kittens be tested for FIV?

A

After 6 months → can be false positive due to maternal Antibodies
*If mom is positive, isolate kittens for 6 months until they can be tested

383
Q

Cats with FIV have been shown to have a (higher/lower) prevalence of azotemia and proteinuria compared to an age-matched control group

A

Higher

384
Q

Cats with neurologic disease secondary to FIV have responded well to what medication?

A

AZT (zidovudine) → blocks reverse transcriptase

385
Q

What changes to the lymphocyte population have been seen experimentally with Bartonella infection in dogs?

A
  1. Decreased number of CD8 T lymphocytes

2. Increase in CD4 lymphocytes but with altered surface phenotypes

386
Q

What general type of disease is associated with Bartonella infection in dogs?

A
  1. Granulomatous disease
    - 2 dogs with granulomatous lymphadenitis reported
  2. Endocarditis also possible
387
Q

Ehrlichia: Gram (+/-)

A

Gram -

388
Q

What is the gold standard diagnostic test for E. canis?

A

IFA

- ELSIA is also good (96% Sens, 100% spec)

389
Q

What is unique about the thrombocytopenia associated with Anaplasma platys?

A
  1. It is typically severe (A. phagocytophilum is usually mild)
  2. Chronic, cyclical thrombocytopenia can be seen following the initial event every 7-14 days
390
Q

How long does it take for infection to occur during a tick bite for Rocky Mountain spotted fever?

A

<24 hours

391
Q

True/False

- Dermacentor ticks can pass infection of R. rickets to their offspring (transovarial)

A

True

392
Q

What is the only gram - intracellular bacteria that is transmitted by trematodes (flukes)

A

Neorickettsia helminthoeca

393
Q

How is Nanophyteus salmincola (trematode in salmon poisoning disease) diagnosed?

A

Fecal flotation and sedimentation for ova

394
Q

What % mortality occurs with treatment for Rickettsia ricketsii infection?

A

15-30%

395
Q

What is the causative agent of tetanus? What kind of organism is it? Where is it located?

A
  1. Clostridium tetani
  2. Gram + anaerobic spore forming bacilli
  3. Soil
396
Q

Clinical signs of clostridium tetani develop secondary to what?

A
  1. Secondary to active infection of a penetrating wound with tetanus
397
Q

What is the cause of the neurologic signs seen with clostridium tetani? Why?

A
  1. Develop due to toxin tetanospasmin
  2. Attaches to the presynaptic nerve terminal of LMN and is taken up by phagocytosis → moves by retrograde axonal transport → cleaves docking protein (synaptobrevin) needed for exocytosis of the inhibitory neurotransmitter GABA
398
Q

What is important about the docking protein cleaved by Clostridium tetani?

A

Synaptobrevin

- Part of the SNARE complex needed for exocytosis of GABA

399
Q

Clinical signs of tetanus develop how long after infection?

A

3 days to 3 weeks

400
Q

How is Clostridium tetani diagnosed?

A

ELISA toxin assay available

401
Q

What are the clinical signs associated with Clostridium tetani?

A
  1. Hyperthermic

2. Spastic paralysis → may be localized near the wound but can become generalized

402
Q

How is tetanus treated?

A
  1. One dose of tetanus antitoxin

2. Metronidazole

403
Q

What is the prognosis for tetanus?

  1. Mild
  2. Severe
A
  1. 100% survival

2. 60% survival

404
Q

What is the causative agent for botulism? What kind of organism is it?

A
  1. Clostridium botulinum

2. Gram + anaerobic spore forming bacillus

405
Q

Clinical signs of Clostridium botulinum occur secondary to what?

A

Secondary to ingestion of botulinum toxin produced within infected carrion
*ACTIVE INFECTION DOES NOT OCCUR

406
Q

What is the cause of the neurologic signs seen with Clostridium botulinum? Why?

A
  1. Develop due to ingestion of botulinum toxin C
  2. Attaches to the presynaptic nerve terminal of peripheral CHOLINERGIC synapses (neuromuscular junction and autonomic nervous system) → taken up by phagocytosis → cleaves docking proteins (synaptotaxin and syntaxin) needed for exocytosis of ACh
407
Q

What are the clinical signs associated with botulism? How quickly do they develop?

A
  1. LMN signs including loss of tone and reflexes
    - Death is common secondary to aspiration pneumonia or diaphragmatic paralysis
  2. Within 12-72 hours after ingestion
408
Q

How is botulism diagnosed?

A

ELISA toxin assay available

409
Q

How is botulism treated?

A

Supportive care

410
Q

What is important about the following stages of the heart worm life cycle?

  1. L1
  2. L3
  3. L5
A
  1. Microfilaria - produced by the adult heart worms in the pulmonary artery
  2. L3 larvae can infect dogs → live in the tissue for 2-3 months and when they have matured to L5 they will invade the vasculature
  3. Immature adult → takes 4-5 months to fully mature
411
Q

What is the total time from infection to adult heart worms?

A

6-9 months

412
Q

Where and how long do adult heart worms live?

A

Pulmonary artery for 5-7 years

413
Q

The pulmonary effects seen in heart worm disease are secondary to what?

A
  1. Eosinophilic pneumonia

2. Pulmonary thromboembolism

414
Q

The cardiac effects seen in heartworm disease are secondary to what?

A
  1. Fibrosis of the vasculature leading to severe pulmonary fibrosis
  2. Right sided heart failure secondary to pulmonary hypertension
415
Q

Canine heartworm testing is an (antigen/antibody) test? What is detected in this test?

A
  1. Antigen

2. Only detects antigen from adult female worms

416
Q

What is the mechanism behind prophylactic heartworm therapy?

A

Macrocyclic lactones
1. Cause irreversible opening of glutamate gated chloride channels leading to neuronal depolarization → parasitic paralysis

417
Q

What is adulticideal therapy for heartworm disease?

A
  1. Should only progress after clearing circulating microfilaria for 1-3 months
  2. Melarsomine is an organoarsenic and is the most effective adultacide
418
Q

What are risks associated with melarsomine therapy?

A
  1. Thromboembolic disease

- Occurs in 30% of dogs treated

419
Q

The following organism is a vector for what diseases?

- Rhipicephalus

A
  • Tick
    1. Hepatauxzoon canis (ingestion)
    2. Babesia canis
    3. Ehrlichia canis
    4. Anaplasma platys
    5. Rickettsia rickettsii
420
Q

The following organism is a vector for what diseases?

- Dermacentor

A
  • Tick
    1. Cytauxzoon
    2. Rickettsia rickettsii
421
Q

The following organism is a vector for what diseases?

- Amblyomma

A
  • Tick
    1. Rickettsia rickettsii
    2. E. ewingii
    3. E. chaffensis
    4. Cytauxzoon
    5. Hepatauxzoon americanum (ingestion)
422
Q

The following organism is a vector for what diseases?

- Ixodes

A
  • Tick
    1. Borellia burgdorferi
    2. Anaplasma phagocytophilum
423
Q

The following organism is a vector for what diseases?

- Reduviid

A
  1. Trypanosoma
424
Q

The following organism is a vector for what diseases?

- Sand Fly

A
  1. Leishmania
425
Q

The following organism is a vector for what diseases?

- Mosquito

A
  1. Dirofilaria immitis
426
Q

The following organism is a vector for what diseases?

- Fleas

A
  1. Mycplasma hemophelis
  2. Bartonella hensilae
  3. Diplidium caninum
427
Q

What is the most common form of canine influenza? Where did it come from?

A
  1. H3N8

2. Jumped species from equine to dogs without genetic reassortment

428
Q

What is a zoonotic pathogen present in both dogs and horses?

A
  1. Staph aureus → clinical infections in vet med uncommon

* H3N8 has not been shown to transmit to humans

429
Q

When is antibody testing used for heartworm disease?

A
  1. In cats
  2. May be helpful if an antigen test is negative due to a low worm burden
  3. Specific but not sensitive
430
Q

Rectal scraping is helpful in diagnosing which organism in dogs?

A

Histoplasmosis

ACVIM General copy (15 decks)

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