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POD > 3.7 RNA viruses 3 > Flashcards

3.7 RNA viruses 3 Flashcards

1
Q

what are the structural and genomic characteristics of Family Orthomyxoviridae? where does it replicate?

A
  • Genome is negative sense single stranded
    RNA organized into 6-8 segments
  • Helical symmetry
  • Enveloped virus
  • RNA replication: in the nucleus**
  • Viral protein synthesis in the cytoplasm
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2
Q

how are Family Orthomyxoviridae pathogens classified?

A
  • Classified into subtypes based on
    surface antigens:

Hemagglutinin: virus attachment and envelope fusion
- variation: 18 sub-types (H1-H16);
(H17-H18 bats)

Neuraminidase: release of virus from infected cells
- variation: 11 sub-types (N1-N9); (N10&N11 bats)

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3
Q

what genera of Family Orthomyxoviridae are there? which affects the most species? which effects cattle and sheep? which only effects pigs and humans

A

Genera: Influenza A, B, C, D
A: effects many species, excludes cattle, sheep, camels, goats
B: seals, pigs, humans
C: pigs, humans
D: cattle, camel, sheep, goat, horse

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4
Q

what important genus influenza A viruses are there? which are reportable?

A

Genus Influenza A virus:
* Avian influenza (many) OIE list 2020
* Equine influenza (H3N8 and H7N7) OIE list 2020
* Swine influenza (H1N1 and H3N2)
* Canine influenza (H3N8 and H3N2)

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5
Q

what important reportable Genus Isavirus is in family orthomyoxoviridae?

A

Genus Isavirus
* Infectious salmon anaemia virus OIE list 2020

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6
Q

mechanisms for variability of influenza virus and their characteristics?

A

antigenic shift: major antigenic variation, re-assortment, leads to epidemics and pandemics, Influenza A only

antigenic drift: minor antigenic variation, point mutations over period of time, seasonal outbreaks (inter pandmeic), influenza A or B

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7
Q

what are re-assortments in terms of antigenic shift for influenza virus?

A

New combinations of H and N can occur by reassortments of the RNA segments coding for H and N proteins when cells are coinfected with 2 different subtype viruses

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8
Q

what is avian influenza virus? what are its characteristics? what are its H/N characteristics? Can it be transmitted to humans, and how? which strain is highly pathogenic and present in asia?

A
  • Common, economically important and notifiable disease (H5 and H7 avian influenza viruses) in Canada.
  • Highly pathogenic H5N1 virus present in Asia, rarely causes disease in humans.
  • Transmission to humans has occurred through close contact with infected birds or heavily contaminated environments.

-subtypes are H1-16, N1-9
-zoonotic!

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9
Q

which subtypes of avian influenza are low pathogenic (LPAI)? where do we find it and what are its effects?

A

all HA subtypes 1-16
-common in wild birds, but causes no disease in wild birds
-occasional, mild disease in poultry

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10
Q

which subtypes of avian influenza are high pathogenic (HPAI)? what are their characteristics and where do we find it?

A

-“bird flu”
-only H5, 7 subtypes
-causes outbreaks in poultry
-associated with disease and death in poultry and wild birds
-uncommon in wold birds

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11
Q

what must happen for avian influenza for the virus to infect a cell?

A

Hemagglutinin (HA) must be cleaved post-translationally for the virus to fuse with the cell membrane so the genome is released to the cytoplasm to travel to the nucleus and become infectious!

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12
Q

in low pathogenic avian influenza (LPAI), how does the HA cleavage process occur? where?

A

Low pathogenic avian influenza (LPAI) - produced in a non- infectious form and cleavage of HA occurs extracellularly
* Only a single amino acid (arginine) at the hemagglutinin cleavage site
* proteases cleaving the HA are restricted to the GI and respiratory tracts

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13
Q

in high pathogenic avian influenza (HPAI), how does the HA cleavage process occur? where?

A

Highly pathogenic avian influenza (HPAI) - produced in a non- infectious form BUT cleavage of HA occurs in the infected cell by abundantly expressed proteases
* Several basic amino acids at the cleavage site of HA protein
* Cleavage can be done by ubiquitously expressed endopeptidase furins in many different tissues

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14
Q

how is Highly pathogenic avian influenza (HPAI) virus transmitted?

A

Transmitted by fecal-oral route, and migrating birds carry viruses between winter and summer habitats

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15
Q

what are the clinical signs of highly pathogenic avian influenza (HPAI) virus?

A

Non-specific systemic clinical signs
– Depression, anorexia, drop in egg production, conjunctivitis, respiratory signs, swollen and cyanotic combs, and neurological signs
*Most birds in affected flocks die suddenly

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16
Q

how can we diagnose avian influenza? what to do if we find HPAI?

A
  1. Clinical signs are not specific
  2. PCR, if positive, test for specific H5 and H7 genes
  3. If PCR positive, sequencing to determine properties of cleavage site
  4. If several basic amino acids are detected: HPAI

What to do?
Report, biosecurity, surveillance, and depopulation
In 2022 alone we had several outbreaks of HPAI in Ontario

Other diagnostic tests you can use…
Virus isolation: eggs or cell culture
Serology: ELISA and Hemagglutination Inhibition

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17
Q

how can we control and prevent avian influenza?

A
  • Surveillance of H5 and H7 LPAI in domestic poultry, that could lead to HPAI.
  • Reliant on biosecurity, surveillance, and depopulation if HPAI are detected
  • Education of workers, biosecurity practices, quarantine, surveillance, rapid depopulation when indicated.
  • Segregate domestic and wild birds (e.g. live poultry markets)
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18
Q

Which of the following statement(s) is NOT CORRECT about Orthomyxoviruses:
a. Orthomyxoviruses have segmented RNA genome
b. Hemagglutinin is responsible for virus attachment and fusion of the virus to the host cell
c. Neuraminidase cleaves host cell receptors (sialic acid) and promote release of virions
d. Low pathogenic avian influenza viruses have viral hemagglutinin protein with multiple cleavage sites in their fusion protein domain

A

d. Low pathogenic avian influenza viruses have viral hemagglutinin protein with multiple cleavage sites in their fusion protein domain

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19
Q

Which of the following statement(s) is CORRECT about control and prevention of highly pathogenic avian influenza (HPAI) virus:
a. HPAI are highly stable in the environment due to their envelope
b. Surveillance of HPAI is recommended to prevent or control outbreaks
c. Irrespective of test status all the migratory wild birds should be eradicated to prevent potential disease in farmed birds
d. Humans show clinical disease after eating poultry products from H5N1 infected farm

A

b. Surveillance of HPAI is recommended to prevent or control outbreaks

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20
Q

what are the structural and genetic characteristics of Family Paramyxoviridae? what kind of illness can they cause?

A
  • Non-segmented, negative-sense single-stranded RNA genome
    -Enveloped virus
    -Size: ~120-240 nm
    -Can cause respiratory or systemic illnesses
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21
Q

in the Family Paramyxoviridae what diseases are important for us to know in Genus Morbilivirus and Genus Avulavirus? which are reportable?

A

Genus Morbilivirus
* Canine distemper virus (CDV)
* Rinderpest virus OIE list

Genus Avulavirus
* Avian Paramyxovirus 1 (Newcastle Disease) OIE list

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22
Q

what is newcastle disease virus? what does it infect? what are the signs of infection?

A
  • There are 9 serotypes of Avian Paramyxovirus (APMV-1 to APMV-9)
    > Newcastle disease is caused by Avian Paramyxovirus 1
  • All avian species have demonstrated some level of susceptibility
  • In avian hosts characteristic disease involves respiratory, circulatory, gastrointestinal, and nervous signs
  • Humans: conjunctivitis (zoonosis)
23
Q

how many pathotypes of NDV are there? what are they and what do they do?

A

1) Asymptomatic: no disease

2) Lentogenic: subclinical to mild respiratory disease in chicks => Virulent ND (vND)

3) Mesogenic: moderately virulent- respiratory or neurological disease

4) velogenic: most pathogenic - generalized disease in all ages
4.1 Velogenic neurotropic: respiratory and neurological
4.2 Velogenic viscerotropic: hemorrhagic intestinal

24
Q

what is a major contributor to strain differences in NDV virulence and ability to spread rapidly?

A

A major contributor to strains differences in NDV virulence depends on the cleavability of the fusion (F) protein which is synthesized as inactive precursor protein.
* In turn the cleavability in different tissues influences the tropism of the viral strain and the capacity of the strain to spread rapidly.

25
Q

how do avirulent and virulent strains of NDV differ in their cleavability?

A
  • Avirulent strains have a single amino acid basic amino acid within the cleavage site- only activated by extracellular proteases of ONLY epithelial cells of the respiratory and gastrointestinal tract.
  • In the virulent strains F precursors have multiple basic amino acids within the cleavage site and can be cleaved by ubiquitous cellular proteases in many types of infected cells.
26
Q

what disease is clinically indistinguishable from Avian Influenza

A

virulent ND

27
Q

what are the clinical signs of virulent ND

A

Clinically indistinguishable from Avian Influenza
Clinical signs are not specific:
* Drop in egg production
* Numerous deaths within 24 to 48 hours
* Deaths continue for 7 to 10 days
* Respiratory signs
* Surviving birds may have neurological damage
* Edema of head, especially around eyes
* Greenish, dark watery diarrhea

28
Q

Post-mortem findings of virulent Newcastle disease

A
  • Edema of head and neck
  • Edema, hemorrhage, necrosis or ulceration of lymphoid tissues
  • Hemorrhagic lesions
    – Tracheal mucosa
    – Proventriculus
    – Intestinal mucosa
29
Q

what is Rinderpest virus? where is it found and what have its consequences been? how does it infect?

A

(Cattle plague), Paramyxoviridae family
* In regions where there was outbreak it destroyed the entire cattle populations and caused famines
* Cattle, wild ruminants, sheep, goats…
* No disease in humans
* Morbilliviruses use receptors on immune cells (lymphocytes, macrophages and dendritic cells) and epithelial cells

30
Q

what are the clinical signs of Rinderpest virus (Cattle plague)

A
  • Fever, depression, anorexia, hemorrhagic diarrhea
  • Serous to mucopurulent nasal/ocular discharge
  • Necrosis and erosion of the oral mucosa
  • Enlarged lymph nodes
  • Death in 6-12 days
31
Q

what is canine distemper virus? what is the main host and what are other hosts? how is it shed? what cells does it infect? what is its mortality rate?

A
  • Dogs of 2-6 months age are the main host
  • Infects other species: Canidae (fox, coyote, wolf), ferrets, minks, skunks, raccoons, panda, and Felidae (lions, tigers)
  • Virus shedding: nasal and ocular secretions, urine (6-22 days), feces
  • Disease of the immune system: infects leukocytes (immunosuppression)
  • Most infections are subclinical; mortality rate between 30-80%
32
Q

what group experiences the highest mortalities from canine distemper disease?

A
  • Highest mortality in puppies; immune status complications
33
Q

what are common clinical signs of canine distemper disease??

A
  • It is a generalized disease with a variety of clinical signs: neurologic, pneumonia, enteritis

eg. Bilateral purulent conjunctivitis and rhinitis (respiratory – pus in the trachea and bronchi)

34
Q

what forms of canine distemper disease are there?

A

peracute, acute, subacute neurological, late

35
Q

what are the signs of the peracute form of canine distemper disease?

A

Rare and characterized by sudden onset of
fever and sudden death.

36
Q

what are the signs of the acute form of canine distemper disease?

A

This form is characterized by biphasic fever, severe leukopenia, anorexia, catarrh, conjunctivitis, depression, respiratory and gastrointestinal signs. Central nervous system (CNS) signs may also develop.

37
Q

what are the signs of the subacute neurological form of canine distemper disease?

A

This form may follow the acute disease or subclinical infection. Encephalitis with convulsions and seizures are seen. Most of the surviving dogs have permanent CNS sequelae such as involuntary leg movements.

38
Q

what are the signs of the late form of canine distemper disease?

A

Old dog encephalitis is a slowly progressive loss of neurological functions, and hard pad disease, in which hyperkeratosis of footpads and nose may be seen.

39
Q

Which of the following is NOT CORRECT about Paramyxoviruses:
a) Can cause necrosis and erosion of the oral mucosa
b) Avian influenza and Newcastle disease are clinically distinguishable
c) Strains of NDV differ in their virulence depending on the cleavability of the fusion protein.
d) Canine distemper disease in dogs can present with generalized symptoms involving the digestive, respiratory system along with neurological signs

A

b) Avian influenza and Newcastle disease are clinically distinguishable

40
Q

what are the structural and genetic characteristics of Family Rhabdoviridae

A
  • Segmented negative sense RNA
  • Helical symmetry
  • “Bullet shape” enveloped virus
41
Q

what are the 2 reportable viruses in Family Rhabdoviridae

A

OIE list 2020
* Rabies virus
* Vesicular stomatitis virus

42
Q

what species does Vesicular stomatitis virus infect? what are the symptoms and how fast is the recovery?

A

Affects horses, cattle, swine, camelids, humans
* Fever and vesicles that resemble FMD
* Humans: flu-like symptoms
* Recovery in ~2 weeks

43
Q

how is Vesicular stomatitis virus transmitted?

A
  • Vectors (sandflies, blackflies)
  • Direct contact with infected animals or surfaces
44
Q

when was vesicular stomatitis last reported in canada?

A

Last reported in Canada in 1949!

45
Q

what symptoms do all vesicular diseases produce?

A

All vesicular diseases produce a fever with vesicles that progress to erosions in the mouth, nares, muzzle, teats, and feet

46
Q

what are the characteristics of rabies? what animals can get infected? what is the incubation period?

A
  • Fatal disease of the central nervous system
  • All mammals can theoretically get rabies
  • Incubation period: 2 weeks - 6 months (axonal transport of the virus can take time!)
47
Q

what is the course of rabies in dogs? what clinical signs will we see?

A
  • Course of rabies in dogs (3-8 days)
  • early phase: behaviour change
  • advanced stage: furious form and paralytic stage

Clinical signs: Neurological signs including
* Nervousness, aggression,
* Difficulty swallowing leading to salivation,
* Convulsions, paralysis, complete incoordination,
* Coma, death

48
Q

how is rabies transmitted?

A
  • Saliva (bite or very close contact)
  • Rarely: by inhalation of aerosol particles containing the virus (as in a bat infested cave)
49
Q

where is rabies maintained and what is it also called?

A

Rabies virus is maintained in wildlife reservoirs and is called SYLVATIC RABIES

50
Q

what part of the body does rabies effect? what is the pathogenesis?

A

Affects hippocampus (limbic system)
-rabies virus in the bite site enters a motor neuron endplate
-moves to spinal cord where it multiplies rapidly in spinal cord neurons
-rabies virus moves up spinal cord neuron to the brain

51
Q

how can we diagnose rabies?

A
  • There are no reliable ante-mortem diagnostic methods

Post-mortem:
* Fluorescent antibody test on brain smears, RT-PCR
* Negri bodies may be present in the neurons (histology)

52
Q

what will we see histologically in a rabies case?

A

using an H&E stain: Rabies virions (small dark-grey rod-like particles) and Negri bodies: eosinophilic, sharply outlined, pathognomonic inclusion bodies found in the cytoplasm of nerve cells infected with rabies virus.

53
Q

Which statement is NOT CORRECT about rhabdoviruses?
a. Rabies virus is maintained in wildlife reservoirs
b. Negri bodies are pathognomonic of rabies diagnosis
c. Vesicular stomatitis virus causes erosive oral lesions like Foot and mouth disease
d. Rabies virus causes fatal encephalitis in mammals including dogs, humans, cattle and bats

A

all are correct apparently?

POD (21 decks)

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