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Taylor Viro Final > orthomyxo > Flashcards

orthomyxo Flashcards

1
Q

what 3 general types of orthomyxoviridae are seen?

A

pleomorphicsphericalfilamentous

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2
Q

which two envelope spikes are present in influenza A and B viruses?

A

-rod shaped, consisting of homotrimers of the hemagglutinin glycoprotein-mushroom shaped, consisting of homotetramers of the neuraminidase protein

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3
Q

influenza C viruses lack ______.

A

neuraminidase

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4
Q

influenza C viruses have what glycoprotein spike?

A

only one type: made of multifunctional hemagglutinin-esterase molecules

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5
Q

what is hemagglutinin responsible for?

A

virus attachment to host cell is mediated by HAHA binds to sialic acid containing receptors on the plasma membrane of host cells

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6
Q

antibodies against _______ neutralize the infectivity of the virus, by preventing attachment of the virus to the ______

A

hemagglutinin (HA)host cell

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7
Q

what is the function of neuraminidase?

A

NA cleaves receptors in mucin and on host cells.-after budding, HA of progeny influenza virions are still bound to sialic acid containing receptors on the host cell surface.-NA cleaves those receptors, and releases the HA. this frees the virus from the infected host cell.**critical for cell-to-cell spread of influenzaantibodies targeting NA would restrict cell to cell spread, but would not neutralize virus

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8
Q

Describe the genomes of orthomyxoviridae

A

-linear, negative-sense ssRNA, divided into six-eight segments-eight segments; influenzavirus A and B-seven segments; influenzavirus C-gene segments are associated with a helically symmetrical nucleocapsid

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9
Q

describe the replication of orthomyxoviridae

A

-HA mediated attachment, then adsorption and penetration by endocytosis-low pH within the endosome –> conformational change in the HA, resulting in fusion of viral envelope with endosomal membrane-protons enter virion through M2 channel, resulting in dissociation of M1 protein from ribonucleoprotein(RNP). the RNP then enter the nucleus-transcription and RNA replication occur in the nucleus-virus snatches the 5’-methylguanosine cap plus 10-15 nucleotides from host cell mRNA. This is used as a primer for transcription by virus RNApol-budding takes place on the plasma membrane

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10
Q

there are five genera of orthomyxoviridae, what are the three important ones?

A

-Influenzavirus A; humans, horses, swine, dogs, fowl, mink, seals, whales-influenza B; human-influenza C; pathogens of humans and swine, viruses rarely cause dz

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11
Q

what is the basis for classification of influenzavirus

A

each of the three genera are identified by antigenic differences in their nucleoprotein and matrix protein

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12
Q

What are the Influenza A virus subtypes based on? how many are there?

A

-influenza A subtypes are based on variations in the envelope proteins, HA and NA-there are 18 known HA subtypes, and 11 known NA subtypes

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13
Q

t/f - There is cross-protection b/w different HA or NA influenza A subtypes

A

falsethere is usually little or none

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14
Q

What are the major subtypes of influenza A for Avian species?

A

16 HA types: HA1 thru HA169 NA types: NA1-NA9

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15
Q

what are the major subtypes of influenza A for horses?

A

H7N7H3N8

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16
Q

What are the major influenza A subtypes for swine?

A

H1N1, H1N2, and H3N2

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17
Q

When the process of genetic reassortment involves the gene segments encoding the HA and/or NA genes it has been termed ___________.

A

antigenic shift; there are major changes in the HA and/or NA proteins

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18
Q

Mutations that change amino acids in the antigenic portions of the surface glycoproteins HA and NA is known as _________.

A

antigenic drift; may allow virus to evade pre-existing immunityminor changes in HA/NA proteins

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19
Q

what is the etiology of equine influenza?

A

A/H7N7 (last outbreak 1979) or A/H3N8 (identified in all recent outbreaks)

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20
Q

where is equine influenza found?

A

virtually everywhere, except island countries, such as iceland and new zealand

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21
Q

how is equine influenza transmitted?

A

-highyl contagious-spread rapidly in stables by aerosolized exudates-close contact between horses facilitates rapid transmission

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22
Q

equine influenza viruses replicate in ________

A

epithelial cells of the upper and lower respiratory tract

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23
Q

t/f - equine influenza causes destruction of the ciliated epithelial lining

A

true

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24
Q

common equine influenza lesions?

A

laryngitis, tracheitis, bronchitis, bronchointerstitial pneumonia, accompanied by pulmonary congestion and alveolar edema

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25
Q

describe systemic effect of equine influenza

A

attributed to cytokine response to infectionhowever, vasculitis, myositis, and myocarditis are seen infrequently.

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26
Q

what are the clinical signs of equine influenza?

A

-sudden onset, rapid spread, high fever, conjunctivitis, reddening of nasal mucosa, serous followed by mucopurulent nasal discharge-characteristic harsh, dry, paroxysmal cough-prolonged fever in pregnant mares may lead to abortion-mortality is rare in uncomplicated cases-predispose to secondary bact inf

27
Q

diagnosis of equine influenza?

A

-RT-PCR; nasal or oropharyngeal swabs taken early in infection-antigen-capture ELISA tests-influenza A antigen detection (patient-side kit)[Directigen-Flu-A test]-virus isolation in embryonated eggs (allantoic or amniotic)

28
Q

control of equine influenza?

A

-stables, racing facilities quarantined if outbreak occurs… cleaning/disinfecting after all horses recovered-most vaccines are inactivated, adjuvanted vaccines containing two different lineages of A/equine(H3N8) viruses-H7N7 equine influenza virus has been eliminated from most reformulated vaccines since 2000

29
Q

etiology of canine influenza?

A

-disease of dogs only not humans-comes from an A/H3N8 virus which was originally equine-believed that the virus jumped species and has mutated to cause illness in dogs, and spread among kennels/shelters/dogs in a home.-Now considered dog-specific lineage of H3N8-Other viruses also can affect dogs (H3N2, H5N1, H1N1)

30
Q

transmission of canine influenza?

A

direct contactthrough the airaerosolized respiratory secretions

31
Q

pathogenesis of canine influenza?

A

-destroys ciliated epithelial cells of resp tract-rhinitis, tracheitis, bronchitis, bronchiolitis-preisposes to secondar bact inf-greyhounds especially susceptible

32
Q

clinical signs of canine influenza?

A

-indistinguishable from kennel cough (canine respiratory dz complex)-Mild form: most dogs show this form of dz-severe form: high fever, increased respiratory rate with dyspnea, consolidation of lung lobes, other indications of pneumonia

33
Q

diagnosis of dog flu?

A

-difficult to differentiate from kennel cough-antibody determination in paired serum collected in acute and convalescent phase of disease. four-fold increase in titer indicates active infection-virus isolation, RT-PCR from nasal and pharyngeal swabs

34
Q

control of dog flu?

A

-licensed vaccine for H3N8 canine influenza virus is commercially available in US

35
Q

swine flu etiology?

A

most common: H1N1, H1N2, H3N2

36
Q

hosts of swine flu?

A

swine, humans, turkeys.-pigs considered mixing vessel for influenza virus because of their ability to become co-infected with both avian and human strains of influenza virus.

37
Q

main method of transmission of swine flu?

A

aerosolization and pig to pig contact

38
Q

sources of swine flu virus?

A

-infected (clinical or asymptomatic) pigs. carriers may harbor virus up to 3 months-infected humans in contact w pigs-other species, such as birds.

39
Q

describe pathogenesis of the classic acute form of swine flu.

A

-focal necrosis of the bronchial epithelium, focal atelectasis, and gross hyperemia of the lungs.-pneumonic areas are clearly demarcated, collapsed, and purplish red.-there may be severe pulmonary edema and emphysema

40
Q

in uncomplicated swine flu infections, lesions are usually confined to ________

A

the thoracic cavity

41
Q

larvae of __________ can exacerbate swine flue and endemic pneumonia.

A

the large roundworm, Ascaris suum

42
Q

clinical signs of swine flu?

A

-outbreaks mostly in late fall/winter-acute upper respiratory: fever, lethargy, anorexia, weight loss, labored breathing. coughing, sneezing, nasal discharge-abortions, as seen w/ some H3 reassortant viruses-secondary bact inf, or other viral inf-secondary potentially fatal bronchopneumonia is occasionally seen

43
Q

diagnosis of swine flu?

A

-often confused with other infectious dz, ie actinobacillus, mycoplasma; the gross lung lesions strongly resemble M. hyopneumoniae-for routine dx, RT-PCR and quant. RT-PCR have replaced virus isolation-ID of the virus genotype is by hemagglutinin and neuraminidase specific genotypic RT-PCR tests

44
Q

Turkeys infected with swine influenza viruses may develop _______, ______, or ______.

A

respiratory dz, decreased egg production, or produce abnormal eggs.

45
Q

ferrets and mink w/ swine flu show _________

A

respiratory signs of varying severity

46
Q

swine flu vaccination?

A

-commercially available killed vaccines-FluSure XP - two strains of H1N1, one strain of H1N2, one strain of H3N2-vaccines do not always prevent infection or shedding, but appropriately vaccinated pigs generally have milder dz

47
Q

how do we classify avian influenza for pathogenicity?

A

-LPNAI (low pathogenicity notifiable avian influenza)-HPNAI (high path…)-Based on the ability of the virus to cause severe dz in IV inoculated young chickens in the laboratory, or the possession of certain genetic features associated with HPAI virusesFully virulent HPAI viruses have always contained H5 or H7

48
Q

The vast majority of LPAI viruses are maintained in ______________.

A

asymptomatic wild birds, mainly waterfowl, in aquatic habitats.

49
Q

t/f - HPAI viruses are frequently found in wild birds.

A

falseHPAI are not normally found in wild birds, although some have been detected and caused outbreaks.

50
Q

viruses that have adapted to poultry ___________ in wild birds.

A

rarely re-establish

51
Q

what three things may occur when LPAI is transmitted from wild bird to domestic?

A

1) virus circulates inefficiently and dies out2) virus adapts to new host, continues to circulate as LPAI3) if LPAI contains H5 or H7, may mutate to HPAI virus

52
Q

geographic distribution of avian flu?

A

 LPAI viruses are cosmopolitan in wild birds. Different viral lineages circulate in North America and Eurasia. They may reassort between themselves. LPAI viruses are usually not endemic in commercial poultry in developed nations, but they may be present in other domesticated birds.  HPAI viruses are eradicated from all domesticated birds, whenever possible, and HPAI is usually not endemic in developed countries. Asian lineage H5N1 HPAI viruses are considered endemic in poultry in a few Asian or Middle Eastern countries

53
Q

avian influenza viruses are shed in _______.

A

feces and respiratory secretions

54
Q

avian flu transmission is mainly by _________

A

fecal-oral and aerosols

55
Q

avian flu is periodically introduced in to susceptible flocks by ___________

A

interspecies transmission involving wild migratory birds, espiecially ducks, and may also involve in-between intermediate domestic birds (ducks, sparrows, etc) and/or fomites

56
Q

t/f pathogenesis of avian flu is the same as pathogenesis in mammals

A

falsevirus replication occurs in the intestinal tract as well as the respiratory tract

57
Q

in infections with the most virulent HPAI strains, there is ________, which results in ________.

A

-viremia, multifocal lymphoid and visceral organ necrosis-pancreatitis, myocarditis, myositis, and encephalitis.

58
Q

birds that die from HPAI exhibit _______

A

petechial hemorrhages and serous exudates in respiratory, digestive, and cardiac tissues.

59
Q

clinical signs of LPAI?

A

-subclinical infections or mild illness-sneezing, coughing, decreased egg prod, anorexia, sinusitis, ocular and nasal discharges

60
Q

HPAI clinical signs?

A

-severe illness in chickens and turkeys-peracute cases: signs or gross lesions may be lacking before death-blood tinged oral and nasal discharge-greenish diarrhea-cyanosis/edema of head, comb, wattle-edema, red discoloration of the shanks and feet (sub-q ecchymotic hemorrhages)-petechial hemorrhages on visceral organs and in muscles-survivors of peracute inf may develop CNS involvement; torticollis, opisthotonos, incoordination, paralysis, drooping wings

61
Q

how to diagnose avian flu?

A

-viruses detected in oropharyngeal, tracheal, and/or cloacal swabs from live birds-detection of influenza A matrix or nucleoprotein antigens using AGID or other suitable immunoassays, like ELISA-RT-PCR method of choice for detecting viral RNA

62
Q

control of avian flu?

A

-dz reporting; anything with H5 or H7 must be reported to OIE-depopulation, quarantine, movement controls, and maybe vaccination during outbreaks-trade restrictions; H5N1 HPAI strain has been detected in commercial poultry in some countries-quarantine; all imported live birds must be quarantined for 30 days at USDA facility, and tested for virus before entering usa

63
Q

Avian flu vaccine?

A

-use requires approval by the state veterinarian-use of H5 and H7 AI vaccines requires USDA approval

Taylor Viro Final (12 decks)

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