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Taylor Viro Final > paramyxo > Flashcards

paramyxo Flashcards

1
Q

What are some general properties of paramyxoviriae

A

-pleomorphic (filamentous and spherical forms)-virions are enveloped-diameter of about 150nm-covered w glycoprotein spikes-herringbone shaped helically symmetrical nucleocapsid-single strand of linear, negative sense, ssRNA, 13-19kb

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2
Q

what are 5 important viral proteins of paramyxoviridae?

A

F- fusion proteinHN- hemagluttinin neuraminidaseM-matrix proteinP- phosphoproteinN - nucleoproteinL- polymerase

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3
Q

What is the role of attachment spike protein in paramyxoviridae?

A

attachment of viruses to host cellelicit neutralizing antibodies, induce protective immunity

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4
Q

t/f - the attachment protein varies b/w genera of paramyxoviridae

A

true

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5
Q

which genera of paramyxoviridae have hemagglutinin-neuraminidase as their attachment protein? what does HN do?

A

Genera: Respirovirus, Avulavirus, Rubulavirus-cause hemagglutination-has neuraminidase; virion release, destruction of mucin inhibitors

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6
Q

which genera of paramyxoviridae have hemagglutinin as their attachment protein? what does it do?

A

genus morbillivirus-hemagglutination, but NO NEURAMINIDASE

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7
Q

which genera of paramyxoviridae have G-protein as their attachment protein? what does it do?

A

henipavirus, pneumovirus, metapneumovirus-no hemagglutination-no neuraminidase

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8
Q

describe paramyxoviridae membrane fusion.

A

fusion protein, present in all genera, mediates the fusion of the viral envelop with the plasma membrane of the host cell. Virus penetration by this process is not dependent on a low pH environment.Cell-to-cell spread of viruses occurs this way, big part of presistent infection (immune response evasion)cause syncytium formation, elicits neutralizing antibodies

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9
Q

t/f Matrix (M) protein is important for virion stability

A

true

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10
Q

what does Nucleoprotein (N or NP) do?

A

bind to RNA, protection of genomic RNA

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11
Q

what is transcriptase complex made of?

A

Large(L) proteinphosphoprotein(P)cysteine-rich protein (V)

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12
Q

t/f - paramyxoviruses replicate in the nucleus

A

false - replicate in cytoplasm of cells

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13
Q

what are some major histological features of paramyxoviridae infections? how about the genus morbillivirus specifically?

A

acidophilic cytoplasmic inclusions, made of ribonucleoproteinsformations of syncytiamorbillivirus specifically: characteristic acidophilic intranuclear inclusions

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14
Q

what are the five main genera of subfamily paramyxovirinae?

A

-Respirovirus-Avulavirus-rubulavirus-morbillivirus-henipavirus

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15
Q

what are the two main genera of the subfamily pneumovirinae?

A

-pneumovirus-metapneumovirus

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16
Q

what condition is caused by respirovirus?

A

bovine parainfluenza virus-3 respiratory disease

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17
Q

what is the host and the transmission of BPV3 Respiratory disease?

A

host is cattle and sheeptransmission is primarily aerosol, but also occurs by ingestion of contaminated fomites (nasal discharge)

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18
Q

what is the pathogenesis of BPV3 respiratory dz?

A

epithelial cells of respiratory tract targetedinfection results in necrosis and inflammation in small airways in the lungs - bronchitis and bronchiolitispredispose animal to bacterial invasion/pneumonia

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19
Q

clinical signs of BPV3 respiratory disease

A

uncomplicated cases result in mild respiratory dz-calves and lambs: fever, lacrimation, serous nasal discharge, dyspnea, and coughing. recovery in 3-4 days-bovine pneumonia: role in initiating so-called shipping fever aka bovine respiratory dz complex. w/ other viruses or as sole pathogen, predisposes animals to secondary bact infection(especially Mannheimia haemolytica)–> bact bronchopneumonia

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20
Q

how do you diagnose BPV3 respiratory dz?

A

-virus isolation from nasal discharge-id in nasal discharge and resp tissues by FAT and ELISA-paired sera(acute/convalescent):antibodies quantitated by VN test, HI test, ELISA-RT-PCR

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21
Q

how do you control BPV3 respiratory dz?

A

inactivated or live modified(attenuated) vaccines, usually combo with other pathogens. intranasal or parenteral

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22
Q

is newcastle dz reportable?

A

YES

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23
Q

what causes newcastle dz?

A

Avulavirus: avian paramyxovirus serotype 1

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24
Q

what are the differences b/w low and high virulence strains of avian paramyxovirus serotype 1?

A

-low: produce precursor F proteins cleaved only by a trypsin-like protease which have a restricted tissue distribution and are usually distributed extracellularly.-high: precursor F’s cleaved intracellularly by proteases present in cells lining mucous membranes. viruses replicate in more cell types

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25
Q

describe the five pathotypes of newcastle dz virus

A

1)asymptomatic enteric2)lentogenic - less virulentvND(virulent Newcastle dz)3)mesogenic - moderately virulent4/5)velogenic pathotype strains - highly virulent (viscerotropic and neurotropic)Exotic Newcastle Dz(END): US name for velogenic viscerotropicvelogenics aren’t present in usa, but are brought in via illegally imported game chickens and exotic birds

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26
Q

what are the hosts of newcastle dz

A

most avians-pigeons highly susceptible-canaries, finches pretty resistant-humans: conjunctivitis

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27
Q

transmission of newcastle dz occurs how?

A

 Respiratory secretions and feces contain high concentrations of virus. Virus is shed for up to 4 weeks in all secretions and excretions of birds that survive the infection. Major route of transmission: Inhalation of aerosols and dust particles Ingestion of contaminated feed and water Contaminated fomites. Mechanical spread between flocks is facilitated by the relative stability of the virus and its wide host range. Vertical transmission rare: reported for lentogenic virus strains

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28
Q

what’s the pathogenesis of Newcastle dz?

A

Initially it replicates in the mucosal epithelium of the URT and GIT, then one of two things can happen:1) no further dz spread for lentogenic and enteric strains2)vND: primary viremia –> spread to bone marrow and spleen –> secondary viremia –> infection of other target organs; lung, intestine, CNS

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29
Q

what are the clinical signs of visceroptropic velogenic newcastle dz?

A

respiratory, w/ depression, watery green diarrhea, and swelling of the head and neckhemorrhages and ulcer-like lesions are seen in the digestive tractmortaliy approaches 100% in all age groups

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30
Q

what are the clinical signs of neurotropic velogenic newcastle dz?

A

respiratory signs, followed by nervous signs of tremors, paralyzed wings and legs, twisted necks, circling, clonic spasms, and complete paralysiscns lesions are encephalomyelitis, with neuronal necrosishemorrhages absent from GI tractmortality approches 100% in all age groups

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31
Q

what are the clinical signs of mesogenic and lentogenic newcastle dz?

A

mesogenic: acute respiratory dz, reduced egg production, and uncommonly neuro signs; mortality aproaches 25% in young chickens, rare in adultslentogenic: respiratory signs of gasping, coughing sneezing and rales predominatethe dz in turkeys is similar but usually less severe than that in chickens; there are signs of respiratory and nervous involvement

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32
Q

t/f - severe depression with a reluctance to stand or move is associated with viscerotropic velogenic ND

A

true

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33
Q

t/f - abnormal perching reflex is associated with newcastle dz

A

true

34
Q

t/f - feather loss is associated w newcastle dz

A

false, ruffled feathers are associated

35
Q

t/f - mild conjunctivitis and dehydration are associated with newcastle dz

A

false; severe acute conjunctivitis and edema are associated with newcastle dz

36
Q

t/f - watery greenish diarrhea is associated with viscerotropic velogenic newcastle dz

A

true

37
Q

t/f periorbital, facial and neck edema are associated with viscerotropic, velogenic newcastle dz

A

true

38
Q

t/f - sometimes soiled vents with diarrhea are associated w/ viscerotropic velogenic newcastle dz

A

true

39
Q

what are the three main tools to diagnose newcastle dz?

A

virus isolation, RT-PCR, and serology

40
Q

What must be done to determine the virulence of newcastle dz?

A

intracerebral pathogenicity index in day old chickens (0.7 or more)presence of a specified amino acid motif at the cleavage site of the fusion protein(F) precursor(FO).

41
Q

what must be done to farms infected with newcastle dz?

A

quarantine and depopulation.Newcastle DZ is REPORTABLE

42
Q

what vaccinations are available for newcastle dz?

A

-live lentogenic vaccines, chiefly B1 and LaSota strains, are widely used and typically administered to poultry by mass application in drinking water of by spray-oil adjuvanted inactivated vaccines are also used after live vaccine in breeders and layers-fowlpox or turkey herpesvirus-vectored NDV vaccines are commercially available for chickens

43
Q

what does newcastle dz cause in humans?

A

ndv can produce a transitory conjunctivitis in humans, and occurs primarily in laboratory workers and in members of vaccination teams

44
Q

what major virus is from the rubulavirus genus?

A

canine parainfluenza virus-5

45
Q

what is the canine parainfluenza virus responsible for?

A

one of several pathogens that cause kennel cough

46
Q

how is CPiV-5 transmitted?

A

aerosolized microdroplet

47
Q

what is the pathogenesis of CPiV?

A

the virus causes destruction of the ciliated epithelial cells of the respiratory tract, predisposing to secondary infections

48
Q

What are the three main things which characterize rinderpest?

A

the 3 D’s: discharge, diarrhea, and death

49
Q

what is the etiology of canine distemper?

A

canine morbillivirus

50
Q

how many strains of canine morbillivirus are there? how are they classified?

A

there are at least ten strains, based on differences in the hemagglutinin gene.

51
Q

what 3 strains of canine morbillivirus are regarded as highly virulent and neurotropic?

A

snyder hillA75/17R252

52
Q

How does canine morbillivirus (distemper) persist in different temperatures?

A

in warm climates, the virus will not persist in kennels after infected dogs have been removedin near freezing temperatures (0-4 C) the virus survives in the environment for weeks

53
Q

how resilient is canine morbillivirus in the face of most disinfectants?

A

ordinary disinfectants can inactivate the virus

54
Q

what are the hosts of canine morbillivirus (distemper)

A

domestic and wild dogsraccoon, panda, ferret, mink, bears, etcCNS infections in exotic felidae

55
Q

how is canine morbillivirus transmitted?

A

inhalation of infected dropletstransplacental infections can occur from viremic dams

56
Q

what cell types does canine morbillivirus replicate in?

A

macrophagest and b lymphocytesepithelial cellsnervous tissue

57
Q

what is the pathogenesis of canine morbillivirus?

A

1) the virus replicates in the macrophages in URT tissues, then spreads to tonsils and regional lnn.2)after multiplication in the lymph nodes, the virus enters the bloodstream, circulating in b and t lymphocytes.3)virus spreads to lymphoid tissues in body; GALT, mesenteric lymph nodes, kupffer’s cells of the liver4) virions formed in these sites are then carried by blood mononuclear cells during secondary viremia5) further spread of CDV to epithlial and CNS tissues on day 8-9 PI occurs hematogenously, and depends on the dog’s cell-mediated and humoral immune response

58
Q

How does the cell mediated and humoral response influence the outcome of infection?

A

in dogs with >1:100 antibody titers, on day 8 or 9, there is no more spread of virus, and it is cleared from lymphoid tissues. the infection remains subclinical.In dogs with low antibody titers and poor cell-mediated immune response by day 14 post-infection: virus spreads to many tissues including the epithelium of the GI tract, respiratory tract and genitourinary tract.

59
Q

t/f - In canine morbillivirus, invasion of CNS occurs when the viremia is of sufficient magnitude.

A

true - details to know:Infection of the central nervous system occurs relatively late in the course of infection.Dogs producing anti-envelope antibodies appear to prevent persistent infection of CNS.

60
Q

describe acute canine distemper virus encephalitis

A

occurs in young and immunosuppressed animals, and is characterized by direct viral replication and injury to CNS.  Acute noninflammatory demyelination in microglial and astroglial cells

61
Q

describe subacute to chronic CDV encephalitis

A

characterized by reduced expression of CDV antigen and a strong upregulation of inflammatory response.  The immune reaction rather than virus replication causes demyelination at this stage.  Chronic perivascular cuffing with demyelination

62
Q

what are the late complications of CDV?

A

Observed in old dogs. These may also be seen in dogs with no history of earlier acute or subacute disease. Hardpad disease: Hyperkeratosis of foot pads and the nose due to virus multiplication in the skin. Old Dog Encephalitis:  Extremely rare, chronic , progressive inflammatory disease of gray matter of cerebral hemispheres and brainstem of CNS. Occurs in immunocompetent animals with persistent virus in their neurons in a replication defective form.  Often marked by ataxia, compulsive movements such as head pressing.

63
Q

what are the signs of canine distemper in an old dog?

A

 Clinical signs:1) Transient fever usually occurs 3–6 days after infection with leukopenia (especially lymphopenia). 2) A second febrile response indicates serious phase of the infection, accompanied by profound leukopenia. 3) Serous or mucopurulent nasal discharge, conjunctivitis, and depression.4) Some dogs show primarily respiratory signs, whereas others develop gastrointestinal signs: Respiratory signs reflect inflammation and injury to the upper respiratory tract and large airways. Productive cough; bronchitis and interstitial pneumonia may follow. Gastrointestinal involvement: vomiting and watery diarrhea. Both respiratory and GI signs may be complicated by secondary bacterial infection.5) Dogs surviving the acute phase may have hyperkeratosis of the footpads and epithelium of the nasal planum. Hyperkeratosis of the nose and footpads is often found in dogs with neurologic manifestations

64
Q

what is the greatest diagnostic tool for CDV?

A

Immunofluorescent assay or reverse transcriptase (RT) PCR

65
Q

describe canine distemper control and vaccination

A

 Control: Control of canine distemper virus infection is based on adequate diagnosis, quarantine, sanitation, and vaccination.  The virus is very fragile, and susceptible to standard disinfectants. Vaccination: Successful immunization of pups with canine distemper modified live virus (MLV) vaccines depends on the lack of interference by maternal antibodyAlternatively, measles virus vaccine induces immunity to canine distemper virus in the presence of relatively greater levels of maternal distemper antibody.  Remember:  MLV vaccines should not be used in late-pregnant or early-lactation bitches.  MLV vaccines can produce postvaccinal illness in some immunosuppressed dogs.

66
Q

what does morbillivirus cause in ruminants?

A

Peste des petits ruminants (PPR)aka Goat Plague

67
Q

t/f - PPR aka Goat Plague is a reportable dz

A

True

68
Q

describe the lineage of PPR viruses

A

Peste des petits ruminants virus has been grouped into four distinct lineages based on the sequence of the F protein. Lineages 1 and 2 occur in West Africa Lineage 3 in East Africa, the Middle East, and southern India Lineage 4 extends from the Middle East to Tibet

69
Q

what is the host of PPR?

A

Host: Goats and Sheep.  More severe in goats than in sheep.

70
Q

how is PPR transmitted?

A

 Infection is primarily by inhalation There is no carrier state in goats and sheep

71
Q

describe the pathogenesis of ppr

A

Inhalation–> Retropharyngeal mucosa–> Viremia–> damage to alimentary, respiratory and lymphoid systems. Infected cells undergo necrosis, resulting in mucosal erosions and lymphopenia. Death may occur from severe diarrhea and dehydration, before respiratory lesions become severe

72
Q

what are the clinical signs of PPR?

A

 The acute form of the disease is seen in goats and similar to rinderpest, except that severe respiratory distress is a common feature of PPR. Early, the nasal discharge is serous; later, it becomes mucopurulent and gives a putrid odor to the breath. Extensive erosions and necrosis in the mucosal lining of the oral cavity, and also in esophagus, abomasum, and small intestine (necropsy) Profuse catarrhal conjunctivitis, high fever, necrotic stomatitis Diarrhea may be profuse Bronchopneumonia Pregnant animals may abort

73
Q

how do you diagnose PPR?

A

 Clinical signs: Necrotic lesions in mouth, profuse diarrhea Necropsy: Streaks of congestion with “zebra-striped” appearance in large intestine. Field conditions: Agar-gel immuno-diffusion test and the PPR penside test ELISA RT-PCR

74
Q

describe how to control PPR

A

 Local and federal authorities should be notified when PPR is suspected. Eradication is recommended when the disease appears in previously PPR-free countries. Attenuated vaccine has been prepared in Vero cell culture

75
Q

what is the etiology of Bovine Respiratory Syncytial Dz?

A

genus pneumovirustwo antigenic subtypes based on differences of the G protein.

76
Q

describe the hosts and transmission of BRSV

A

cattle of all ages, but mostly <6 months of age Bovine respiratory syncytial virus (BSRV) infection occurs most often during the winter months, when are housed in confined conditions. Virus spreads rapidly, probably through aerosols or droplets of respiratory tract excretions.

77
Q

describe the pathogenesis of BRSV

A

 Pathogenesis: BSRV causes rhinitis, tracheitis, bronchitis, bronchiolitis & mild interstitial pneumonia. The pathogenesis of fatal pneumonia due to BSRV may be associated with an immune mediated mechanism (hypersensitivity reaction mediated by IgE).  The severe highly fatal form of the disease, known as “malignant form” or “the Paroxystic Respiratory Distress Syndrome (PRDS) , has been associated with extensive pulmonary mast cell degranulation.  Gross lesions include a diffuse interstitial pneumonia with subpleural and interstitial emphysema along with interstitial edema

78
Q

what will you see in BRSV infections on histological samples?

A

 Syncytial cells in bronchiolar epithelium and lung parenchyma. Intracytoplasmic inclusion bodies. Edema, and hyaline membrane formation

79
Q

what are the clinical signs of BRSD?

A

 Fever (104–108°F [40–42°C]), depression, decreased feed intake, increased respiratory rate, cough, and nasal and lacrimal discharge are common. Dyspnea, possibly with open-mouthed breathing, later stages of disease. Secondary bacterial pneumonia is a frequent occurrence

80
Q

describe diagnosis and control of BRSD

A

 Diagnosis: Clinical signs Necropsy: Dramatic distension of lungs by edema, alveolar hyperinflation, emphysema. Histopathology Virus isolation: Transtracheal aspirate. Difficult as virus is fragile. Specimens should not be frozen.  FAT test or immunohistochemical staining RT-PCR VN test on paired sera (convalescent and acute samples)  Control: Immunity is incomplete and transient following natural BRSV infection of calves

Taylor Viro Final (12 decks)

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