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Virology > Canine & Feline Parvo > Flashcards

Canine & Feline Parvo Flashcards

1
Q

What is the structure of viruses in the family Parvoviridae?

A
  • 5kb ssDNA
  • Noneveloped
    *
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2
Q

How stable are parvo viruses?

A
  • Highly resistant to disinfection/temperature/pH
  • Infectious for months to years
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3
Q

How do parvo viruses replicate in the host?

A
  • Occurs in cells with high mitotic rates
    • No viral DNA polymerase
    • Requires host nucleoprotein synthesis (DNA replication)
  • Primary sitesL
    • tissues undergoing organogenesis in fetal or neonatal development
    • Enteric epithelial crypt cells, hematopoietic and lymphoid tissues
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4
Q

What is Canine Parvovirus (CPV-2)?

A
  • 1978 - now present worldwide
  • Infects dogs, coyotes, wolves, foxes, raccoons, sknks
  • 3 main variants ( 2a, 2b, 2c)
    • similar virulence
    • 2b - most commonly associated with illness
    • 2c - most recent emergence
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5
Q

How is CPV-2 transmitted?

A
  • Direct: oronasal contact with infectious feces
  • Indirect: oronasal contact with contaminated fomites
    • environment, personnel, equipment
    • D
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6
Q

When do infected dogs start shedding the CPV-2 virus?

A
  • 4-5 dpi
    • can occur prior to clinical onset of disease
  • continues up to 10 days after clinical resolution
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7
Q

What happens during phase 1 of CPV-2 infection?

A
  • Initial replication in oropharyngeal lymphoid tissue
  • Subsequent replication in Peyer’s patches and GI lymphoid tissue
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8
Q

What happens during phase 2 of CPV-2 infection?

A
  • Virus spreads by blood and lymphatics to secondary sites of replication
  • Targets rapidly dividing cells:
    • SI crypt epithelium
    • Bone marrow
    • Primary and secondary lymphopoietic tissue
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9
Q

What is the pathogenesis of CPV-2 in the lymphopoietic/hematopoietic cells/tissues, intestinal crypt epithelium, or in utero infection?

A
  • Lymphopoietic/hematopoietic cells/tissues:
    • Leukopenia (lymphopenia, neutropenia
    • Immunosuppression
  • Intestinal crypt epithelium:
    • epithelial necrosis and villus atrophy
    • Impaired absorptive capacity
    • Disrupted gut barrier - bacterial translocation
  • In utero / < 8 week sw/out maternal antibodies:
    • Myocarditis
    • Myocardial necrosis
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10
Q

What are the 2 disease syndromes of CPV-2?

A
  • Myocarditis
  • acute enteritis
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11
Q

What happens with CPV-2 associated myocarditis?

A
  • Infection in utero or < 8 weeks
  • Clinical presentation:
    • acute cardiopulmonary failure or delayed, progressive cardiac failure
      • +/- enteritis
  • Less common
    • maternal antibodies from vaccination or exposure are protectie
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12
Q

What happens with CPV-2 associated acute enteritis ?

A
  • Most common
  • Young puppies (6wk - 6 mo)
    • waning maternal antibodies
    • unvaccinated or incomplete vaccination
    • Breed susceptibility: Dobermans, rottweilers, labs, pit bulls
  • Co-morbidities affect disease severity
    • Elevated stress, poor nutrition, GI parasites, others
  • Intussusception can occur
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13
Q

What is the clinical presentation of CPV-2 enteritis?

A
  • Clinical signs develop w/in 5-7 dpi and last between 2-14 days
  • Early signs can be nonspecific - lethargy, decreased appetite
  • Progresses to vomiting and small-bowel diarrhea (often hemorrhagic) w/in 24-48 hrs
  • Depression, pyrexia, dehydration, abdominal pain, dilated and fluid-filled intestinal loops
  • Septic shock: weak femoral pulse, prolonged CRT, tachycardia, hypothermia, collapse
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14
Q

What are the results of a CBC on a CPV-2 infected dog?

A
  • Moderate to severe leukopenia characterized by lymphopenia and neutropenia
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15
Q

What are the serum chemistry results associated with CPV-2?

A
  • Prerenal azotemia, hypoalbuminemia (protein loss through GI tract) hyponatremia, hypokalemia, hypochloremia, hypoglycemia, increased liver enzymes
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16
Q

What gross necropsy lesions are associated with CPV-2?

A
  • Thickened and discolored intestinal wall
  • Watery, mucoid, or hemorrhagic intestinal contents
  • Edema and congestion of lymph nodes
  • Thymic atrophy
17
Q

What histopathologic lesions are associated with CPV-2?

A
  • Multifocal necrosis of intestinal crypt epithelium
  • Intestinal villus blunting and sloughing
  • Lymphoid depletion
  • Bone Marrow hypoplasia
18
Q

Hos is CPV-2 diagnosed?

A
  • High index of suspicion at presentation:
    • young, incomplete or no vaccination, compatible clinical signs
    • may be newly acquired - incomplete medical history
  • SNAP test - ELISA for CPV-2 capsid antigen in feces
    • Widely available, easy to use, rapid results
    • Detects all subtypes, minimal reactivity with MLVs
    • Good specificity; sensitivity depends on virus shedding
      • Test at presentation/onset of clinical illness
      • Negative w/ high index of suspicion should be re-tested in 1-2 days
  • Detection of virus/antigen in feces
    • PCR, EM, VI
  • Detection of CPV-2 antibodies
    • 4x increase in IgG titer over 14 day period
    • IgM antibody without recent vaccination (>4wks)
19
Q

What is the treatment for CPV-2?

A
  • Fluid therapy
    • lactated ringers or 0.9% saline
    • SQ fluids for mild dehydration (<5%)
    • IV fluids for moderate to sever dehydration
      • +/- dextrose and KCl supplementation
      • +/- colloid for sever hypoproteinemia
  • Antibiotics
    • prevent secondary infection
    • broad-spec w/ good gram negative coverage (enterics)
      • ampicillin-sulbactam IV - inpatient
      • Cefovecin - outpatient
  • Antiemetics - prolonged/intractable vomiting
  • Nutritional support
    • small amounts of bland flood when vomiting resolved
20
Q

What is the prognosis of CPV-2?

A
  • W/out treatment:
    • death can occur w/in 1-3 days of clinical onset
    • mortality can be >90%
  • W/ supportive treatment:
    • 70-90% of dogs with enteritis survive
    • most pups that survive the first 3-4 days will recover
21
Q

What biosecurity measures should be taken with CPV-2?

A
  • Limit environment contamination and spread
  • Isolate positive patients - separate housing and equipment
    • consider moving suspect animals out of the waiting room
  • Proper PPE
  • Frequent cleaning/disinfection:
    • Bleach (1:30), Virkon-S, accelerated hydrogen peroxide
22
Q

What is the CPV-2 vaccine?

A
  • AAHA Core vaccine
  • Modified-live vaccine
    • initial 6-8wks, 10-12 wks, 14-16 wks
    • Booster 1 year later, then every 3 yrs
  • Inactivated vaccine
    • pregnant dogs or colostrum deprived pups
  • Protective against different subtypes
23
Q

What is Feline Panleukopenia Virus (FPV)?

A
  • “Feline distemper”
  • Before 1900
  • Worldwide distribution - infrequent due to vaccination
  • Causes disease in felids, raccoons, foxes and mink
24
Q

How is FPV transmitted?

A
  • Oronasal exposure - direct or indirect
    • virus is abundant in all secretions/excretions during acute phase of illness
  • Shedding typically occurs over a short period (1-2 days) but up to 6 wks has been reporterd
25
Q

What is the pathogenesis of FPV in pregnant queens?

A
  • Virus may spread transplacentally
  • Embryonic resorption, fetal mummification, abortion/stillbirth
26
Q

What is the pathogenesis of FPV in Perinatal kittens?

A
  • Virus infects the germinal epithelium of the cerebellum (dividing neuroblasts)
  • Cerebellar hypoplasia:
    • ataxia, tremors, blindness, hypermetric movements
  • Syndrome has become rare due to passive maternal antibody transfer
27
Q

What is phase one of FPV infection?

A
  • Initial replication in oropharyngeal lymphoid tissue
  • subsequent replication in Peyer’s patches and GI lymphoid tissues
28
Q

What is phase two of FPV infetion?

A
  • Hematogenous spread (viremia) to secondary sites of replication
  • Targets rapidly dividing cells:
    • SI crypt epithelium
    • Bone Marrow
    • Primary and secondary lymphopoietic tissue
  • Viremia usually resolves within 5-7 days due to induction of neutralizing antibodies
29
Q

What is the clinical presentation of FPV?

A
  • Most infections are subclinical
  • Clinical disease most common in cats 3-5 months of age
  • Disease more common with rescues and groups of unvaccinated cats
  • Peracute cases - may die suddenly
  • Acute:
    • Clinical signs appear within 2-7 dpi, last approx 4-7 days
    • Pyrexia, decreased appetite, depression, +/- transient diarrhea, vomiting, dehydration, +/- abdominal pain, thickened intestinal loops, enlarged mesenteric lymph nodes
    • CBC/chem: similar to CPV-2
    • Septic shock: hypothermia, DIC
30
Q

What are the lesions associated with FPV?

A
  • Dilated intestinal loops with thickened and hyperemic walls
  • Petechiae on intestinal serosal surfaces
  • Dilated intestinal crypts
  • Necrotic intestinal epithelial cells
  • Villus blunting and fusion
31
Q

How is FPV diagnosed?

A
  • Presumptive: hx, vaccination status, clinical signs, leukopenia
  • Fecal antigen/virus detection
    • Rapid ELISA antigen test: false negative possible = short duration of virus shedding
    • PCR - more sensitive
  • FPV antibody tests - mainly for retrospective use
32
Q

What is the treatment for FPV?

A
  • Fluid therapy and parental broad-spectrum antibiotics
33
Q

What is the prognosis for cats with FPV?

A
  • Better for cats receiving adequate supportive therapy
    • mortality highest in kitten s< 5 month
    • prognosis is poorer with low total WBC (<2,000/uL)
  • Cats will be briefly immunosuppressed following FPV infection
34
Q

What is the FPV vaccine?

A
  • AAFP Core Vaccine
  • Modified live virus
    • begin at 6-9 wks
    • boost every 3-4 weeks until 16-20 wks of ag
    • Booster at 6 months, 1 year, and then every 3 years
  • Inactivated vaccines:
    • safer for pregnant, immunosuppressed, FIV or FeLV + cats

Virology (37 decks)

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