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Virology > Parvoviridae > Flashcards

Parvoviridae Flashcards

1
Q

Describe the general characteristics and replication of Parvoviridae.

A

GC:
-stable virus
>disinf of contam premises difficult
Replication:
-in nucleus of dividing cells
-inf -> lg intranuclear inclusion bodies

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2
Q

Describe genus parvovirus.

A

-virus rep in cells that pass thru mitotic S phase (actively dividing)
-cant rep in stationary cells bc rely on enzymes of actively dividing cells (mitosis)

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3
Q

Describe how the human parvovirus B19 is different than the parvovirus seen in dogs or cats.

A

-no evidence of transmission of B19 from dogs or cats

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4
Q

Describe the general characteristics of feline panleukopenia.

A

‘Feline distemper, feline inf enteritis’
1. Etiology: feline parvovirus
2. Host: contagious, fatal, severe in kittens
3. Transmission:
-oro-nasal, feces, secretions, contam fomites
-in utero
-mechanical transmission by flies

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5
Q

Describe the epidemiology of FPV.

A

-virus is ubiquitous bc its contagious & can persist in environment
-all cats exposed & inf in first yr of life
-unvaccinated kittens acquire maternal Ab protected for 3mo
>75% unvaccinated healthy cats have Ab titer by 1yr
-most inf subclinical
-cats shed virus in urine & feces max of 6wk after recovery
>maintained in pop by environmental persistence than shedding
-owners who lost a kitten to FPV shouldn’t intro a new kitten in house w/o having it vacc

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6
Q

Describe the pathogenesis of feline panleukopenia.

A
  1. hallmark of dz: panleukopenia
    >more severe leukopenia = poorer prognosis
    >destruction of all WBC elements (lymphocytes, neutrophils, monocytes, platelets)
  2. thrombocytopenia (damage to BM)
  3. enteritis = virus damage rep cells in crypt of intestinal mucosa
    >loss of cells from tip of villus cont as a normal process w no replacement = lose absorptive cells -> shortened intestinal villi w blunting & fusion -> malabsorption & diarrhea
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7
Q

Describe FPV in utero infection.

A
  1. Inf early in preg
    -early fetal death & reabsorption w infertility
    -abortion
    -birth of mummified fetus
  2. Inf closer to gestation
    -birth of live kitten w varying damage to late developing neural tissue
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8
Q

Describe CNS infection of FPV.

A

-CNS, optic n, retina = sus to damage during prenatal or early neonatal development
-neuro lesions = cerebellar damage most common
-cerebellar hypoplasia in fetus inf during last 2wk of preg & first 2 wk of life
>lysis of mitotic cells of ext germinal layer = impaired development
>ataxia

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9
Q

Describe FPV DIC.

A

-kittens sus to 2ndary bacterial inf
-gram neg endotoxemia, w/ or w/o bacteremia = systemic inf
-endotoxin (LPS) = express tissue factor III on endothelial cells
>activator of coagulation -> DIC -> hemorrhage

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10
Q

Describe FPV clinical signs.

A

common in kittens
-fever, depression, anorexia, rough coat, vomiting, diarrhea w blood, dehydration, hypothermia, sudden death w complication w secondary bacterial inf, DIC
-queens inf or vacc during preg = infertility or abortion of dead/mummified fetus
-cerebellar hypoplasia = ataxic (3-4wk old)
-retinal degen

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11
Q

Describe the diagnosis of FPV.

A
  1. hematology: leukopenia & neutropenia more consistent than lymphopenia
    >total WBC count <2000 cells/uL = poor prognosis
  2. fecal viral antigen test using immunochromatographic test kit or ELISA
    >results remain pos for 2wk after MLV vacc
  3. Serological testing
    -single sample Ab titer dont distinguish active inf or past exposure
    -paired serum sample -> 1st ASAP during illness & 2nd 2wk after
    -4fold rise in titer = acute inf
    -virus neutralization test
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12
Q

Describe the treatment, control, & vaccine of FPV.

A
  1. Treatment
    -nursing care & fluid therapy (withhold in early stage) to lessen vomit & slow down mitotic activity of cells
    -broad spec antibiotic to prevent secondary bacterial inf
  2. Control
    -lg catteries = hygiene & quarantine of new cats
    -disinf = inactivated by bleach (6% Na hypochlorite), 4% formaldehyde, 1% glutaraldehyde in 10 min @ room temp
  3. Vaccine
    -attenuated MLV
    >NOT GIVEN TO: preg, immunosuppressed, sick, kittens less than 4wk old
    -inactivated
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13
Q

Describe canine parvovirus 1 & 2.

A

CPV1:
-mild to inapparent illness (diarrhea) in dogs, esp young pups less than 8wk old
-not imp
CPV2:
-most common inf dz in dogs
-3 antigenic variants = CPV-2a, CPV-2B, CPV-2c

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14
Q

Describe CPV2 general characteristics.

A

north America CPV-2B & CPV-2c more common
1. Epidemiology
-virus contagious & stable in environ
-resistant to common detergents & disinf
-persist indoors at room temp for 2 mo
2. Transmission
-oro nasal exposure to contaminated feces
-in utero
-virus contam fomites

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15
Q

Describe the pathogenesis & clinical findings of CPV2.

A
  1. Enteritis
    -inf germinal epi of intestinal crypts = destroy & collapse (necrosis) epi -> no replacement of cells lost from tip of villi -> shortened -> hemorrhagic diarrhea
    -acute parvo inf
    -ballooned SI + ingesta visible thru wall
  2. Necrotizing Myocarditis
    -develop from inf in utero or from pups <6wk
    -myocardial necrosis w acute cardiopulmonary failure
    -sudden death or die after short period of CS (dyspnea, crying, retching)
  3. Panleukopenia
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16
Q

Describe the diagnosis and vaccination of canine parvovirus.

A

Diagnostics:
1. serology (Ab) not best method bc most dogs vacc or prev exposed
2. SNAP parvo test
Vaccine:
-bc damage to myocardial or cerebellar cells = inactivated rather than MLV vacc for preg dog or colostrum deprived pups vacc before 6-8wk old

17
Q

Describe the use of oseltamivir (Tamiflu) in the treatment of canine parvovirus enteritis.

A

-MOA not clear bc parvovirus doesnt use neuraminidase in rep
-neuraminidase imp enzyme used by pathogenic bacteria invading thru protective mucous barrier of GIT = indirectly facilitate CPV inf

18
Q

Describe porcine parvovirus general characteristics.

A

GC:
-cause of repro failure in swine worldwide
-SMEDI = stillbirth, mummification, embryonic death, infertility
-gilts inf naturally before conceive = immune
Transmission:
-oro nasal in non immune preg sow followed by transplacental transmission
-venereal
Pathogenesis:
-oro nasal inf of non immune preg dam followed by viremia after maternal inf -> reach fetus
-transplacental inf = death at diff stages of preg

19
Q

Describe the clinical signs of PPV.

A

-inc in mummified fetus after normal gestation period = hallmark
-abortion uncommon
-boars, sow, gilts = inapparent/subclin inf
TIME OF INF:
1. Embryo/fetus (<30d) = die & reabsorbed -> dam return to estrus
2. Early fetus (30-70d) = fetus die & become mummified
3. Late fetus (>70d-term) = lesions + IR = survive in utero

20
Q

Describe the diagnosis, immunity, & vaccine of PPV.

A
  1. Diagnosis
    -serologic test = limited value bc virus widespread in swine & vacc interfere
  2. Immunity
    -cause persistent inf w periodical shedding
  3. Vaccine
    -inactivated & live
    -best way: vacc all sus breeding stock 2x, 2 week apart, several wks before breeding
    -OR: gilts can be naturally inf several weeks before breeding by mingling w older breeding stock that are shedders

Virology (24 decks)

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