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VIROLOGY FINAL > Reoviridae > Flashcards

Reoviridae Flashcards

1
Q

what is the structure of a reovirus?

A

non-enveloped, nearly spherical in outline.

3 concentric layers - outer, middle and inner capsule

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2
Q

what is the genome of a reovirus like?

A

segmented dsRNA, ranging from 10-12 segments, depending on genus

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3
Q

where does reovirus replication occur?

A

in the cytoplasm

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4
Q

t/f reovirus genetic reassortment occurs b/w viruses w/in a genus or a serogroup

A

true - can even have RNA segments mixed from human and animal viruses

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5
Q

what are two major diseases from the genus orbivirus?

A

african horse sickness virus

bluetongue virus

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6
Q

what is a reovirus that is important to humans?

A

colorado tick fever virus, genus coltivirus

also small mammals, zoonotic

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7
Q

what does genus orthoreovirus cause in birds?

A

Avian reovirus - multiple serotypes
chickens, turkey, geese, ducks
arthritis, enteritis, respiratory dz, myocarditis, nephrosis, etc

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8
Q

what is bluetongue?

A

an infectious, non-contagious, insect-borne dz of domestic and wild ruminants caused by the bluetongue virus (BTV), a member of the genus orbivirus

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9
Q

what are the most susceptible hosts to BTV?

A

sheep (especially fine wool and mutton breeds that are common in europe) and white-tailed deer

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10
Q

what host has inapparent infection with BTV?

A

cattle, goats, and some wild ruminants

Cattle are the primary reservoir and amplifying host

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11
Q

t/f - bluetongue is a “List A” dz of the Office of International Epizootics

A

true; big deal

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12
Q

describe bluetongue’s etiology, and the genome of the virus

A

BTV (ovine orbivirus) belongs to genus Orbivirus, in the family Reoviridae
the BTV genome consists of ten segments of dsRNA

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13
Q

how is BTV transmitted?

A
  • biologically by Culicoides spp (biting midge)
  • USA, mostly Culicoides variipennis var sonorensis
  • except southeast US, where it is C. insignis

less significant: also occasional transplacental and venereal

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14
Q

which BTV serotypes are found in the USA?

A

10, 11, 13, and 17

2 as well, mainly in the southeast US

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15
Q

What is the pathology of BTV in sheep?

A
  • damage to vascular endothelium
  • intravascular coagulation
  • necrosis of tissues and organs supplied by damaged capillaries
  • edema
  • hemorrhage
  • congestion
  • abortion(abortive form of BTV in enzootic areas)
  • CNS malformations
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16
Q

What are some clinical findings of BTV in sheep?

A
  • profuse salivation, edema of muzzle, reddening of the nasal mucosae
  • mucopurulent nasal discharge, often blood-stained. crust formation on nostrils and lips
  • cyanosis, necrotic ulceration of tongue
  • erosion of dental pad, necrosis, hyperemia and ulceration in oral cavity
  • coronitis, laminitis –> lameness
  • facial swelling
  • aborted, macerated fetuses
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17
Q

what are the major tools for diagnosing BTV?

A
  • detection of antigen: immunohistochemical tests, such as immunofluorescence, immunoperoxidase tests
  • detection of nucleic acid: PCR
  • detection of antibody: agar gel immunodiffusion test (AGID), competitive ELISA
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18
Q

what is key to preventing BTV?

A

vector control

19
Q

what is african horse sickness?

A

AHS is an infectious, non-contagious, arthropod borne dz of horses, donkeys, and mules

20
Q

t/f- Dogs can contract AHS

A

true; sometimes they contract a highly fatal form of AHS, resulting from the ingestion of infected carcass material from horses that have died from AHS

21
Q

how does the OIE classify african horse sickness?

A

List A infectious dz

enzootic in sub-saharan africa, although occasional outbreaks reported in northern africa, middle east, and europe.

22
Q

what is the etiology of african horse sickness?

A
  • virus belonging to genus orbivirus
  • at least 9 antigenic serotypes of AHS virus, based on variations in outer capsid protein VP2 and to a lesser extent VP5 proteins
23
Q

describe transmission and pathogenesis of AHS

A
  • transmitted by culicoides; at least the following two species - imicola and bolitinos
  • zebras, inapparently infected reservoirs. culicoides bites, then passes to horse. pathogenesis identical to bluetongue in sheep
24
Q

clinical findings in acute(pulmonary) horse sickness (Dunkopf)

A
  • profuse nasal discharge of serous fluid and froth
  • frothy discharge becomes blood stained
  • lung exhibits severe interlobular edema, petechiae on the pulmonary pleura
  • pulmonary edema w hemorrhage
  • frothy fluid in lungs
25
Q

clinical findings in subacute (cardiac) horse sickness (Dikkop)?

A
  • edema of supraorbital fossae and neck
  • edema of eyelids
  • hydropericardium
  • edema of muscles
  • serosal petechiae on the apex of the cecum
  • hydroperitoneum
  • numerous petechiae in the serosa of the large intestine
26
Q

how do you prevent/control african horse sickness?

A
  • vaccination in enzootic areas
  • control of vector
  • reduce exposure to biting insects
  • slaughter sick or viremic animals
27
Q

Rotaviruses are one of the major causes of severe viral ______ in the young of
mammals and birds

A

diarrhea

28
Q

This virus had a characteristic wheel like appearance, and eventually came to be
known as _______

A

rotavirus

rota means wheel

29
Q

describe the structure and classification of rotaviruses

A
  • 11 segments of dsRNA
  • VP6 protein middle layer
  • based on differences in VP6 protein and gene, rotaviruses are classified into at least 8 groups/species, designated as RVA-RVH
  • RVAs (group A rotaviruses) are the most common cause of viral diarrhea in the young of humans and wide variety of animal species and birds
30
Q

describe the classification of RVA strains

A

rotavirus group A:

  • G-genotypes are based on variations in VP7 (glycoprotein)
  • P-genotypes and P-serotypes are based on VP4 (protease-sensitive protein)

example RVA strain Wa: G1P1A[8]

  • G1 = G1 is G geno/serotype
  • P1A = 1A is P serotype
  • [8] = 8 is P genotype
31
Q

rotavirus: Infected stool contains _______ number of viruses

A

large

32
Q

rotavirus: _________ transmission is the most likely route of rotavirus spread

A

fecal-oral

33
Q

rotavirus: The main site of viral multiplication is the mature __________ on the villi of __________

A

enterocytes; upper small intestine

34
Q

describe rotavirus pathogenesis

A
  • infection of mature enterocytes in intestinal villi
  • intestinal villus cells damaged during virus replication and release (stunted villi)
  • diarrhea

*remember NSP4 - nonstructural protein 4 - acts as enterotoxin

35
Q

signs of rotavirus?

A
  • severe diarrhea in young animals
  • profuse diarrhea, anorexia, dehydration, occasionally mild fever
  • feces are watery to pasty in consistency, often pale yellow, sometimes with mucous and blood flecks
36
Q

best tool to diagnose rotavirus?

A

polyacrylamide gel electrophoresis (PAGE)

37
Q

etiology of avian reovirus? describe the genome.

A

genus orthoreovirus

10 segments of dsRNA

38
Q

what is avian reovirus?

A

involved in a variety of dz conditions in domestic poultry, of which the most important is viral arthritis/tenosynovitis in chickens

39
Q

what are the hosts of avian reovirus?

A
  • viral arthritis/tenosynovitis predominantly dz of meat-type chickens (broilers) and is an important cause of leg weakness.
  • reoviruses have also been isolated from turkeys with tenosynovitis. In muscovy ducks, reoviruses cause high moribidity and mortality, with necrotic foci in the liver, spleen and kidneys.
40
Q

major routes of avian reovirus transmission?

A

Fecal-oral!!!
transovarial
inhalation

41
Q

pathogenesis of avian reovirus?

A

pathogenic viruses localize in the hock joint, where the cause arthritis

42
Q

clinical findings of avian reovirus?

A
  • lameness, viral arthritis/tenosynovitis
  • swollen, inflamed hock joints, with clear synovial fluid and inflamed synovial membranes
  • ruptured gastrocnemius tendons
43
Q

prevention of avian reovirus?

A
  • live and killed vaccines available
  • since chicks are most susceptible to avian reovirus infection immediately after hatching, protocols aim at offering passive immunity to chicks from maternal antibody following vaccination of the breeder hens, or by active immunity after early vaccination with a live vaccine.

VIROLOGY FINAL (18 decks)

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