Exam 2 - Family: Parvoviridae Flashcards Preview

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Flashcards in Exam 2 - Family: Parvoviridae Deck (46):
1

Family: Parvoviridae - Properties

Nonenveloped, small size (18-25 nm), virion capsid (60 subunits, T=1), Single-stranded DNA genome which are linear, very stable, replicates in the nucleus of dividing cells

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Subfamily: Parvovirinae

Five genera that infect vertebrates:

1. Parvovirus
2. Dependovirus
3. Amdovirus
4. Erythrovirus
5. Bocavirus

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Genus: Erythrovirus

Fifth disease, slap cheek rash

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Genus: Erythrovirus - Properties

- Replicate autonmously
- Include human parvovirus B19
- Causes mild rash illness, also called infectiosum in children
- Aplastic anemia in children
- Painful joints
- Different from the parvovirus seen in dogs and cats. No evidence of transmission of B19 to humans from dogs and cats, or vice versa

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Genus: Dependovirus

- Unable to replicate except in the presence of a helper virus, usually an adenovirus

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Genus: Bocavirus

Contain a third ORF (Open Reading Frame) between non-structural and structural coding region

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Genus: Parvovirus - Properties

Diseases include:
1. Feline parvovirus
2. Canine parvovirus 1
3. Canine parvovirus 2
4. Porcine parvovirus
5. Mink enteritis virus

Cannot replicating in stationary cells. Occurs in cells that pass through mitotic S phase.

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Feline parvovirus

Feline Panleukopenia (FPV)

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FPV - Synonyms

Feline distemper, feline infectious enteritis

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FPV - Host

Highly contagious, often fatal disease of cats, severe in kittens

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FPV - Transmission

Are infected oro-nasally by exposure to infected animals, their feces, secretions, or contaminated fomites. In-utero transmission, mechanical transmission by flies.

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FPV - Pathogenesis

Replicates in pharyngeal lymphoid tissues. Cell-associated viremia to other organs and tissues via blood stream.

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FPV - Panleukopenia

- Hallmark of the disease
- More severe the leukopenia, the poorer the prognosis
- Destruction of all white blood cell elements
- Cells present in the circulation (consequence of virus absorption and cytotoxic lysis) as well as those in lymphoid organs are destroyed

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FPV - Enteritis

Loss of cells from tip of villus continues as a normal process. However, since virus replication and destroys cells of crypts, there is no replacement of the lost absorptive cells at tips of the 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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FPV - Early in-utero infection

Results in early fetal death and resorption with infertility, abortion, birth of mummified fetuses

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FPV - Infection closer to end of gestation

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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FPV - CNS Infection

Damage to optic nerve, retina, and cerebellar

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FPV - Cerebellar hypoplasia

Usually observed in fetuses infected during the last 2 weeks of pregnancy and the first two weeks of life. Lysis of mitotic cells of the external germinal layer. Impaired cerebellar development.

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FPV - DIC

Kittens with FPV infection are also susceptible to secondary gram negative bacterial infection.

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FPV - Clinical signs

- 3 to 5 months
- Incubation period ranges from 2-10 days
- Fever, depression, anorexia, rough coat, repeated vomiting, profuse, persistent and frequently blood diarrhea

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FPV - Diagnosis - Hematology

- Leukopenia, neutropenia more consistent than lymphopenia
- Virus isolation in cell culture
- Fecal viral antigen testing using immunochromatographic test kit or ELISA
- PCR for detection of viral DNA in tissues
- Direct hemagglutination

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FPV - Treatment

-Nursing care, fluid therapy, withholding in early stages to less vomition and slow down mitotic activity of cells.
- Broad spectrum antibiotics to prevent secondary bacterial infection

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FPV - Vaccination

MLV and inactivated vaccines

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FPV MLV should NOT be administered to

Pregnant queens, immunosuppressed cats, sick cats, and kittens less than 4 weeks old

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FPV - Time of Vaccination

- Kittens receive two or three modified live vaccine doses SC, 3-4 weeks apart
- The first vaccination is usually give 6-9 weeks of age
- The last dose of the initial vaccination series should not be administered before the kitten is 16 weeks old, to ensure that interfering maternal antibodies do not activate the modified live virus.

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Canine Parvovirus-1 (CPV-1)

Not important. Mild to inapparent illness in dogs.

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Canine Parvovirus-2 (CPV-2)

One of the most common infectious diseases of dogs. Three antigenic variants

1. CPV-2a
2. CPV-2b
3. CPV-2c

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Canine Parvovirus - Distribution

North America, CPV-2b and CPV-2c

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Canine Parvovirus - Transmission

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

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Canine Parvovirus - Diagnosis

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

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Canine Parvovirus - Vaccination

- Vaccination with a MLV is recommended at 6-8, 10-12 and 14-16 weeks of age, followed by a booster administration 1 year later and then every 3 years
- Because of potential damage by CPV to myocardial or cerebellar cells, inactivated rather than MLV are indicated in pregnancy dogs or colostrum-deprived puppies vaccinated before 6-8 weeks of age.

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Canine Parvovirus - Use of Oseltamivir (Tamiflu)

- Treatment of canine parvoviral enteritis
- Neuraminidase is an important enzyme used by pathogenic bacteria invading through the protective mucous barrier of the GIT and by this process indirectly facilitate CPV infection. Tamiflu may act on these bacterial neuraminidase.

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Canine Parvovirus-2 (CPV-2) - Clinical findings

- Hemorrhagic enteritis
- Myocarditis
- Panleukopenia
- Neurologic disease
- Cutaneous disease

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CPV-2 Clinically three age related syndromes

1. 2-12 days: generalized neonatal disease. uncommon.
2. 3-7 weeks: myocarditis
3. 2-4 months: enteritis and panleukopenia. most common.

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CPV-2 - Enteritis

Infects germinal epithelium of the intestinal crypts, causing destruction and collapse of the epithelium. No replacement of cells loss from tips of villus. Villi shortened.

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CPV-2 Myocarditis

Myocardial necrosis with acute cardiopulmonary failure. Sudden death, or die after short period of clinical signs

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Porcine Parvovirus (PPV)

Disease is an infectious cause of reproductive failure in swine throughout the world

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SMEDI

Stillbirth
Mummification
Embyronic Death
Infertility

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PPV - Transmission

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

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PPV - Pathogenesis

Oronasal infection of the non-immune pregnant dam followed by viremia. It takes about 15 days after maternal infection for the virus to reach the fetus.

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PPV - Transplacental infection

Not all embryos or fetus are infected at the same time due to separate placenta. Death at different stages of pregnancy is typically of PPV infections

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PPV - Sites of Viral Replication

Predilection for mitotically active cells in fetal tissues. Extensive endothelial cell damage may be reflected in damage to many organs.

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PPV - Clinical signs

The increase in mummified fetuses after a normal gestation period is the hallmark of PPV. Abortions are uncommon.

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PPV - Diagnosis

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

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PPV - Immunity

Some gilts can become seronegative at time of conceiving and are susceptible to infection. Unlike most parvoviruses, PPV can cause PI with periodical shedding of virus.

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PPV - Vaccination

Vaccinate all susceptible breeding stock twice, 2 weeks apart, several weeks before breeding.