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Test 2- Parvoviridae Flashcards

1
Q

Family Parvoviridae

 General Properties:

A

 General Properties:
 Nonenveloped icosahedral virion, small size, 18-25 nm in diameter.
 Virion capsid is composed of 60 protein subunits, T=1
 Single- stranded DNA genomes which are linear, approximately 4–6 kb in size  Most viruses hemagglutinate red blood cells

Viruses are very stable, resisting 60°C for 60 minutes and pH 3 to pH 9. Disinfection of contaminated premises is difficult.

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2
Q

Family Parvoviridae

 Replication:

A

 Replication:
 Replication occurs in the nucleus of rapidly dividing cells.
 Infection leads to large intranuclear inclusion bodies.

primary in nucleus with inclusion bodies

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3
Q

Family Parvoviridae

 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).

 Feline panleukopenia

 Canine parvovirus
 Porcine parvovirus

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4
Q

Family Parvoviridae

 Genus: Erythrovirus (Fifth Disease, Slap Cheek Rash):

A

 Genus: Erythrovirus (Fifth Disease, Slap Cheek Rash):

 Replicate autonomously.
 Includes human parvovirus B19.

 In children, B19 causes:

 Mild rash illness, also called erythema infectiosum.  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 or cats, or vice versa (source: CDC)

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5
Q
A

Family Parvoviridae  Genus: Erythrovirus (Fifth Disease, Slap Cheek Rash):

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6
Q

Family Parvoviridae

 Genus: Dependovirus

A

 Viruses are themselves replication defective and do not cause disease as they are unable to replicate except in the presence of a helper virus, usually an adenovirus.

 Includes goose and duck parvoviruses and, provisionally, bovine parvovirus 2.

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7
Q

 Genus: Bocavirus

A

 Bocaviruses are unique among parvoviruses, as they contain a third ORF (Open Reading Frame) between non-structural and structural coding regions

 These viruses generally infect the gastrointestinal and respiratory tracts.

 Found in human, dogs, cattle.

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8
Q
A

Human bocavirus

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9
Q

Family Parvoviridae

A

Family Parvoviridae Feline parvovirus

Disease: Feline panleukopenia (FPV)

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10
Q

Feline panleukopenia

Etiology, Host, distribution

A 
Feline panleukopenia (FPV)
 Synonyms: Feline distemper; feline infectious enteritis

 Etiology: Feline parvovirus. Antigenically related to canine parvovirus 2 and mink parvovirus

 Host:
 All members of the family Felidae are probably susceptible to infection.
Highly contagious, often fatal disease of cats. Severe in kittens.

 Also in related families, such as raccoon, mink, etc.

 Distribution: Worldwide

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11
Q

Feline panleukopenia (FPV)

 Epidemiology:

A

 Epidemiology:

 The virus is ubiquitous because of its contagious nature and capacity for persistence in the environment.

Virtually all cats are exposed and infected within first 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 maximum 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 the household without having it vaccinated.

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12
Q

Feline panleukopenia

Transmission:

A

 Transmission:

 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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13
Q

Feline panleukopenia Pathogenesis

A
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14
Q

Feline panleukopenia Pathogenesis

A

 After virus entry in the oropharynx, initial virus replication occurs in pharyngeal lymphoid tissue.

 Cell-associated viremia(virus in blood) to other organs and tissues via the blood stream.

 Cells that have appropriate receptors and are in the S phase of the cell cycle are infected and killed or prevented from entering mitosis.

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15
Q

Feline panleukopenia Pathogenesis

 Panleukopenia:

A

 Hallmark of the disease- The more severe the leukopenia, the poorer the prognosis

 The characteristic profound leukopenia involves destruction of all white blood cell elements, including lymphocytes, neutrophils, monocytes, and platelets.

Cells present in the circulation [consequence of virus adsorption and cytotoxic lysis] as well as those in lymphoid organs, including the thymus, bone marrow, lymph nodes, spleen, and Peyer’s patches are destroyed.

 Thrombocytopenia (due to damage to bone marrow) may accompany leukopenia.

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16
Q
A

Feline hemorrhagic ileocecal lymph node

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17
Q

Panleukopenia

WBC counts

A

• TotalWBCcountsof five cats infected with feline parvovirus

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18
Q

Feline panleukopenia Pathogenesis

 Enteritis:

A

 Virus selectively damages replicating cells deep in the crypts of the intestinal mucosa.

 Differentiating adsorptive cells on the surface of the villi are non-dividing and are not affected.

 Normally, the epithelial cells at the tips of the intestinal villi are continuously lost into lumen of the gut.

 These are replaced by dividing cells from the crypts.

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19
Q

Feline panleukopenia Pathogenesis

 Enteritis:

A
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20
Q

Feline panleukopenia Pathogenesis

 During FPV infection

A

 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 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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21
Q
A

Feline panleukopenia

Enteritis

Hemorrhagic Spleen, Intestines and Mesenteric Lymph Node

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22
Q
A

Feline panleukopenia

Dark , Hemorrhagic Jejunum and a Ileum

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23
Q
A

Feline panleukopenia

Enteritis

Intestine opened to Show Fibrinous Cast

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24
Q
A

Feline panleukopenia

Enteritis

Basophilic Intranuclear Inclusion Bodies [Arrows]

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25
Q
A

Feline panleukopenia ENTERITIS

Feline small intestine dilatation

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26
Q
A

Feline panleukopenia ENTERITIS

Feline small intestine epithelial necrosis, hypereplasia

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27
Q
A

Feline panleukopenia ENTERITIS

Feline ileocecal junction necrotic enteritis

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28
Q
A

Feline panleukopenia ENTERITIS

Feline GI tract dilated, congested jejunum

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29
Q

Feline panleukopenia

 In-Utero infection

A

 Early in-utero infection in pregnant queen can result in :

 Early fetal death and resorption with infertility of the queen

 Abortions

 Birth of mummified fetuses.

 Infection closer to end of gestation:

 Birth of live kittens with varying degree of damage to the late-developing neural tissues.- You will see ataxia in the kittens

 Variable effects on kittens from the same litter.

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30
Q

Feline panleukopenia

 Central Nervous System infection:

A

 Central Nervous System infection:

 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 the last 2 weeks of pregnancy and the first two weeks of life.

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31
Q
A

Dark foci in retina from a kitten with optic nerve hypoplasia as a result of in-utero FPV infection

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32
Q

Feline panleukopenia

A

Fetal cerebellum consists of external germinal layer, cells of which undergo rapid cell division and migrate to form internal germinal and Purkinje cell layers.

Normal postnatal cerebellar cortex, outer germinal layer with stellate cells; middle Purkinje cell layer and a deeper granular layer.

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33
Q
A

Feline panleukopenia

Cerebellar Hypoplasia

 Lysis of mitotic cells of the external germinal layer

 Impaired cerebellar development

DESTROY GERMINAL LAYER- which causes no developement of the cerebellum

34
Q
A

Feline panleukopenia

Cerebellar Hypoplasia

35
Q
A

Feline panleukopenia

Cerebellar Hypoplasia

Normal Cerebellum [Right] and
Cerebellar Hypoplasia [Left]

36
Q
A

Feline panleukopenia

Kitten with Marked Ataxia

37
Q
A

Feline panleukopenia

Hydranencephaly- no development of brain and fluid in the brain because a part has not developed

38
Q

Feline panleukopenia

 Disseminated Intravascular Coagulation

A

 Disseminated Intravascular Coagulation

 Kittens with FPV infection are also susceptible to secondary bacterial infection.

 Gram-negative 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.

39
Q

Feline panleukopenia

 Clinical signs:

A

 Most common in kittens 3 to 5 months of age.

 Incubation period ranges from 2-10 days [5 days]

 Fever, depression, anorexia, rough coat, repeated vomiting, profuse, persistent and frequently 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 begins to walk at 3-4 weeks of age.

 Retinal degeneration in infected kittens.

40
Q
A

Feline panleukopenia in a young kitten

41
Q
A

A moribund kitten infected by FPV

42
Q

Feline panleukopenia

Diagnosis

 Clinical signs, postmortem findings.

A

 Hematology:
Leukopenia_, neutropenia_ more consistent than lymphopenia.
Total WBC counts <2,000 cells/μL are associated with a poorer prognosis.

Virus isolation in cell culture: Swabs from pharynx or rectum, spleen, ileum, or mesenteric lymph nodes.

Fecal viral antigen testing using immunochromatographic test kit or ELISA. Results may remain positive up to 2 weeks following MLV vaccination.

PCR for detection of viral DNA in tissues

Direct hemagglutination of pig or rhesus RBCs.

43
Q

Feline panleukopenia

 Diagnosis:

 Serologic testing:

A

 Serologic testing:

 Single sample antibody titers do not distinguish between active infection or past

exposure to virulent or vaccine strains.

 Paired serum samples, the 1st one as soon as possible during illness, and second one 2 weeks after.

A fourfold rise in titer is considered indicative of acute infection.

 Virus neutralization test is commonly used.

 Also, Complement fixation, hemagglutination, hemagglutination inhibition.

44
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 antibiotics to prevent secondary bacterial infection.

45
Q

Feline panleukopenia

Control

A

Control:

 Large catteries: strict hygiene and quarantine of incoming cats.
 Disinfection: Inactivated by bleach [6% sodium hypochlorite], 4% formaldehyde and 1% glutaraldehyde in 10 minutes at room temperature.

46
Q

Feline panleukopenia

Vaccination

A

 Attenuated (modified) live vaccines (MLV)

 Inactivated vaccines

47
Q

 MLV should not be administered to:

A

 Pregnant cats
 Immunosuppressed cats
 Sick cats

 Kittens less than 4 weeks old.

48
Q

Feline panleukopenia

 Time of Vaccination:

A

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

49
Q

Canine Parvovirus (CPV)

A

Considered a canine-specific variant of the feline panleukopenia virus that emerged in 1978 as a consequence of an interspecies jump from other carnivores to dogs.

 Canine parvovirus 1 (CPV-1):
Mild to inapparent illness (diarrhea) in dogs, especially in young pups less than 8 weeks old.
Not important.

 Canine parvovirus 2 (CPV-2):
One of most common infectious diseases of dogs.
 Three antigenic variants: CPV-2a, CPV-2b and CPV-2c.

50
Q

Canine parvovirus 2(CPV-2)

Host, Distribution, Transmission, Epidemiology

A

 Host: Domestic and wild Canidae. Self limiting-infection in experimentally infected cats.

 Distribution: Worldwide. In north America, CPV-2b and CPV-2c are more common.

 Epidemiology:
 Virus is highly contagious and very stable in the environment.
 Resistant to many common detergents and disinfectants.
 Infectious CPV can persist indoors at room temperature for at least 2 months.

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

51
Q

Pathogenesis & Clinical Findings:

A

Pathogenesis & Clinical Findings: Similar to FPV

 Enteritis
 Myocarditis
 Panleukopenia

 Neurologic disease:
 Cerebellar hypoplasia
 Hemorrhage in CNS, DIC, Hypoglycemia

 Cutaneous Disease: Ulceration, vesicles

Clinically, three age –related syndromes have been recognized:

 2-12 days: Generalized neonatal disease. Uncommon.
 3-8 weeks: Myocarditis.
 2-4 months: Enteritis & Panleukopenia. Most common.

52
Q

Canine parvovirus 2(CPV-2)

 Enteritis:

A

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

53
Q
A

Immunoperoxidase Stain

CPV antigens in crypt epithelium

CPV-2 Enteritis

54
Q
A

CPV-2 Enteritis

Crypt Necrosis

55
Q
A

Dog with severe bloody diarrhea

CPV-2 Enteritis

56
Q
A

Three month old dog infected with CVP-2, exhibiting watery stool.

CPV-2 Enteritis

57
Q
A

Hemorrhagic Enteritis

Enteritis

58
Q
A

Acute Parvovirus Infection

Enteritis

59
Q
A

Collapse and Necrosis of Intestinal Villi

Enterisitis

60
Q
A

Canine Parvovirus Infection (Courtesy: Dr. Richard Miller)

Hemorrhagic Intestine Ballooned Small Intestine

61
Q
A

Canine Parvovirus Infection

Ingesta visible through Small
Intestinal Wall

62
Q

Canine Parvovirus 2 (CPV-2)

 Myocarditis:

A

Develops from infection in-utero or from pups < 6 weeks of age.
Myocardial necrosis with acute cardiopulmonary failure.
 Sudden death, or die after short period of clinical signs (dyspnea, crying & retching).

63
Q
A

Necrotizing Myocarditis

Necrotizing Myocarditis with Eosinophilic Inclusions

64
Q

Canine Parvovirus

 Diagnosis:

A

 Clinical signs- Primary

 Fecal viral antigen testing using immunochromatographic test kit or ELISA.

 Nucleic acid detection using PCR

 Virus isolation

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

65
Q

Canine Parvovirus

 Control:

A

Same as FPV

66
Q

 Vaccination:

Canine Parvovirus

A

Vaccination with a modified-live vaccine is recommended at 6–8, 10–12, and 14–16 wk of age, followed by a booster administered 1 yr later and then every 3 yr.

 Because of potential damage by CPV to myocardial or cerebellar cells, inactivated rather than modified-live vaccines are indicated in pregnant dogs or colostrum- deprived puppies vaccinated before 6–8 wk of age.

67
Q

Canine Parvovirus
Use of oseltamivir (Tamiflu) in the treatment of canine parvoviral enteritis

A

MOA (Mechanism of Action) not clear, as parvovirus 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.

STUDIES HAVE SHOWN THAT IT HELPS WITH A BACTERIA

68
Q

Porcine Parvovirus

General + Transmission

A

Porcine parvovirus disease is an infectious cause of reproductive failure in swine throughout the world.

 Some manifestations of the disease are described by the acronym, SMEDI (stillbirth, mummification, embryonic death, infertility).

 In most herds, a large proportion of gilts are infected naturally before they conceive, and hence are immune.

 Transmission:

 Oronasal in the non-immune pregnant Sow followed by transplacental transmission.

 Venereal transmission is possible, as Boars shed virus in semen for protracted periods.

69
Q

Porcine Parvovirus

 Pathogenesis:

A

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

70
Q

Porcine Parvovirus

 Transplacental infection:

A

 Transplacental infection:

 Each fetus or embryo has a separate placenta. Therefore, not all embryos or fetuses are infected at same time.

 However, infection of a fetus or embryo is followed by virus spread through the uterus and infection of some or all remaining fetuses or embryos.

 Hence, death at different stages of pregnancy is typical of PPV infections

71
Q

 Sites of Viral replication:

Porcine Parvovirus

A

 Predilection for mitotically active cells in fetal tissues.

 Virus replicates in blood lymphocytes , monocytes , macrophages, lymph nodes,

tonsils, thymus, spleen, lungs, salivary glands, and other organs.

Extensive endothelial cell damage may be reflected in damage to many organs.

72
Q

Porcine Parvovirus

 Clinical signs:

A

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

 Abortions are uncommon.

73
Q

 Time of infection of Porcine Parvovirus is critical:

A

Embryo/Fetus (<30 days): Dies and reabsorbed. Dams may return to estrus.

Early fetus (30-70 days): Fetuses die and become relatively dehydrated (mummified)-expelled at the end of normal gestation period

Late fetus (>70 days to term): Frequently develop lesions, but also mount an immune response and usually survival in-utero.

74
Q

Immunotolerant pigs

A

 Immunotolerant pigs: some piglets are born immunotolerant and can shed the virus continuously or intermittently.

 Boars, Sows and Gilts( THUS IN ADULTS): Mostly inapparent or subclinical infection.

75
Q

Porcine Parvovirus

• Major cause of

A

• Major cause of SMEDI Stillbirth, mummification, embryonic death, and infertility • Less common

Respiratory tract infections; vesicular diseases; and systemic neonatal disease

• Long-term infection in swine herds

76
Q
A

PPV-SMEDI

Mummies and Stillborn

77
Q

Porcine Parvovirus

 Diagnosis:

A

 FA staining of frozen sections of fetal tissues.

 PCR for nucleic acid detection in fetus

 ELISA, HA, or HI.

Serologic tests are of limited value, because the virus is so widespread in

swine, and vaccination may interfere.

78
Q

Porcine Parvovirus

 Immunity:

A

 Passively acquired maternal antibody can persist for up to 6 months.

 Some gilts can become seronegative at time of conceiving and are susceptible to

infection.

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

79
Q

Parvo in pigs- vaccination/immunization

A

 Vaccination/Immunization:

 A number of inactivated and live vaccines are available to prevent PPV infection.

Best way: Vaccinate all susceptible breeding stock twice, 2 weeks 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 the virus.

80
Q
A

Viro (14 decks)

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