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Virology > Parvoviridae > Flashcards

Parvoviridae Flashcards

1
Q

Family Parvoviridae

A

Viruses are v stable

Disinfection of contaminated premises is difficult

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2
Q

Family Parvoviridae: replication

A

Replication occurs in the nucleus of dividing cells

Infection leads to large intranuclear inclusion bodies

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3
Q

Genus Parvovirus

A

Virus replication occurs only in cells that pass through mitotic S phase (actively dividing cells)
Cannot replicate in stationary cells, as rely on enzymes of actively dividing cells (mitosis)

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4
Q

Human Parvovirus B19

A

Different from the parvovirus seen in dogs and cats. No evidence of transmission of B19 to humans from dogs or cats or vice versa

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5
Q

Feline Panleukopenia

A

Feline distemper, feline infectious enteritis

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6
Q

Feline Panleukopenia: etiology

A

Feline parvovirus

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7
Q

Feline Panleukopenia: host

A

Highly contagious, often fatal disease of cats

Severe in kittens

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8
Q

Feline Panleukopenia: epidemiology

A

The virus is ubiquitous because of its contagious nature and capacity for persistence in the environment
Virtually all cats are exposed and infected within 1st year of life
Unvaccinated kittens that acquire maternal antibodies are protected up to 3 months of age
Most infections are subclinical, as much as 75% of unvaccinated healthy cats have demonstrable antibody titers by 1 year of age
Cats can shed the virus in their urine or feces for a max of 6 weeks after recovery
FPV is maintained in population by environmental persistence rather than by prolonged viral shedding
Owners losing a kitten to feline panleukopenia should not introduce a new kitten into household without having it vaccinated

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9
Q

Feline Panleukopenia: Transmission

A

Cats are infected oro-nasally by exposure to infected animals, their feces, secretions, or contaminated fomites
In-utero transmission occurs
Mechanical transmission by flies

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10
Q

Feline Panleukopenia: Hallmark of disease

A

Panleukopenia
The more severe the leukopenia, the poorer the prognosis
Profound leukopenia involved destruction of all white blood cell elements, including lymphocytes, neutrophils, monocytes, and platelets
Thrombocytopenia (due to damage to bone marrow) may accompany leukopenia

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11
Q

Feline Panleukopenia: pathogenesis

A

Enteritis- virus selectively damages replicating cells deep in the crypts of the intestinal mucosa
During FPV infection, loss of cells from tip of villus continues as a normal process, however since virus replicates and destroys cells of crypts, there is no replacement of the lost absorptive cells at tips of villi with cells from the crypts
This results in shortening of intestinal villi, marked villus blunting and fusion, malabsorption and diarrhea

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12
Q

Feline Panleukopenia: in-utero infection- early

A

Early fetal death and resorption with infertility
Abortions
Birth of mummified fetuses

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13
Q

Feline Panleukopenia: in utero infection- end

A

Birth of live kittens with varying degree of damage to the late-developing neural tissues
Variable effects on kittens from the same litter

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14
Q

Feline Panleukopenia: CNS Infection

A

The CNS, optic nerve, and retina are susceptible to damage by FPV during prenatal or early neonatal development
Of neurological lesions, cerebellar damage has been most commonly reported
Cerebellar hypoplasia is usually observed in fetuses infected during last 2 weeks of pregnancy and first 2 weeks of life

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15
Q

Feline Panleukopenia: cerebellar hypoplasia

A

Lysis of mitotic cells of the external germinal layer
Impaired cerebellar development
Kitten with marked ataxia

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16
Q

Feline Panleukopenia: DIC

A

Kittens with FPV infection are also susceptible to secondary bacterial infection
G- endotoxemia, with or without bacteremia, is a common sequelae of systemic FPV infection
Endotoxin (LPS) induces expression of tissue factor (factor III) on endothelial cells
Tissue factor is a potent activator of coagulation, resulting in DIC followed by hemorrhages

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17
Q

Feline Panleukopenia: Clinical signs

A

Most common in kittens
Affected cells, consequences, clinical manifestation:
-Intestinal crypt epithelium, Villous collapse/enteritis, diarrhea
-Lymph node/Thymus, Germinal center depletion/apoptosis of lymphocytes/thymic atrophy, lymphopenia
-Bone marrow, Stem cell depletion, neutropenia (later also thrombocytopenia and anemia)
-All cells in foetus, Fetal death, loss of pregnancy
-Developing cerebellum, cerebellar hypoplasia, cerebellar ataxia

Fever, depression, anorexia, rough coat, repeated vomiting, profuse persistent and freq bloody diarrhea
Severe dehydration, hypothermia, sudden death from complications with secondary bacterial infections, dehydration and DIC
Queens infected or vaccinated during pregnancy may show infertility or abortion of dead or mummified fetuses
Cerebellar hypoplasia: kittens are ataxic, usually not apparent until kitten walks at 3-4 wks
Retinal degeneration in infected kittens

18
Q

Feline Panleukopenia: diagnosis

A

Hematology: leukopenia, neutropenia more consistent than lymphopenia- total WBC counts <2k cells/ul are associated with poorer prognosis
Fecal viral antigen testing using immunochromatographic test kit/ELISA- results may remain positive up to 2 wks following vaccination

19
Q

Feline Panleukopenia: diagnosis- serological testing

A

Single sample antibody titers do not distinguish between active infection or past exposure to virulent or vaccine strains
Paired serum samples, the 1st ASAP during illness, and second 2 wks later
Fourfold rise in titer=acute infection
Virus neutralization test is commonly used

20
Q

Feline Panleukopenia: treatment

A

good nursing care, fluid therapy, withholding in early stages to lessen vomition and slow down mitotic activity of cells
Broad spectrum AB to prevent secondary bacterial infection

21
Q

Feline Panleukopenia: control

A

Large catteries: strict hygiene and quarantine of incoming cats
Disinfection: inactivated by bleach, 4% formaldehyde, adn 1% glutaraldehyde in 10 min at room temp

22
Q

Feline Panleukopenia: vaccination

A

Attenuated (modified) live vaccines
Inactivated vaccines
MLC should not be given to: pregnant cats, immunosuppressed cats, sick cats, kittens less than 4 wks old

23
Q

Canine parvovirus 1

A

Mild to inapparent illness (diarrhea) in dogs, esp in young pups less than 9 wks old
Not important

24
Q

Canine parvovirus 2

A

One of most common infectious diseases of dogs
Three antigenic variants a, b, and c
b and c more common in north america

25
Q

Canine parvovirus 2: epidemiology

A

Virus is highly contagious and very stable in environment
Resistant to many common detergents and disinfectants
Infectious CPV can persist indoors at room temp for 2 months

26
Q

Canine parvovirus 2: transmission

A

Oro-nasal exposure to contaminated feces
In-utero infection
Contact with virus-contaminated fomites (environment, personnel, equipment)

27
Q

Canine parvovirus 2: pathogenesis and CF

A

similar to FPV
Enteritis,
Myocarditis
Panleukopenia

28
Q

Canine parvovirus 2: enteritis

A

CPV-2 infects the germinal epithelum of the intestinal crypts, causing destruction and collapse of the epithelium
No replacement of cells lost from tip of villus. Villi shortened
Hemorrhagic diarrhea
Ballooned small intestine

29
Q

Canine parvovirus 2: Myocarditis

A

Develops from infection in utero or from pups < 6 wks of age
Myocardial necrosis with acute cardiopulmonary failure
Sudden death, or die after short period of clinical signs (dyspnea, crying and retching)
Necrotizing myocarditis

30
Q

Canine parvovirus 2: Diagnosis

A

Serology (antibody detection) is not best method to test CPV, because most dogs are vaccinated or have been previously exposed
SNAP parvo test

31
Q

Canine parvovirus 2: vaccination

A

Because of potential damage by CPV to myocardial or cerebellar cells, inactivated rather than MLV are indicated in pregnant dogs or colostrum-deprived puppies vaccinated before 6-8 wks

32
Q

Canine parvovirus 2: Tamiflu

A

For enteritis
MOA not clear, as parvo does not use neuraminidase in its replication
Speculation is that neuraminidase is an important enzyme used by pathogenic bacteria invading through the protective mucous barrier of the GI tract, and by this process indirectly facilitate CPV infection
Tamiflu may act on these bacterial neuraminidase

33
Q

Porcine Parvovirus

A

infectious cause of reproductive failure in swine throughout world
Some manifestations of the disease are described by the acronym SMEDI
In most herds, large proportion of gilts are infected naturally before they conceive and hence are immune

34
Q

Porcine Parvovirus: transmission

A

Oronasal in the non immune pregnant sow followed by transplacental transmission
Venereal possible

35
Q

Porcine Parvovirus: pathogenesis

A

Oronasal infection of the nonimmune pregnant dam followed by viremia
After maternal infection of the virus to fetus

36
Q

Porcine Parvovirus: transplacental infection

A

Death at different stages of pregnancy is typical of PPV infections

37
Q

Porcine Parvovirus: clinical signs

A

The increase in mummified fetuses after normal gestation period=hallmark
Abortions uncommon
Embryo/fetus (<30 d): dies and reabsorbed. Dams may return to estrus
Early fetus (30-70d): fetuses die and become relatively dehydrated (mummified)
Late fetus (>70d to term): frequently develop lesions, but also mount an immune response and usually survival in utero
Boars, sows, gilts: mostly inapparent or subclinical infection

38
Q

Porcine Parvovirus: diagnosis

A

Serological tests of limited value- because virus is so widespread in swine and vaccination may interfere

39
Q

Porcine Parvovirus: immunity

A

Unlike most parvos, porcine can cause persistent infection with periodical shedding of virus

40
Q

Porcine Parvovirus: vaccination

A

A number of inactivated and live vaccines are available to prevent PPV infection
Best way: vaccinate all susceptible breeding stock twice, 2 wks apart, several weeks before breeding
Alternatively, gilts can be naturally infected several weeks before breeding, by mingling with older breeding stock that may be shedding

Virology (28 decks)

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