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S&S - Exam 2 > Virology > Flashcards

Virology Flashcards

1
Q

Organism ID w/out lesions

A

infection

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2
Q

Organism ID w/ lesions

A

disease (clinical or subclinical)

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3
Q

What does serology tell you? Can it inform you about clinical disease?

A

Did the animal contract virus / did its immune response respond? Antibodies also may be from passive transfer- not a clinical disease response!

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4
Q

Organism ID w/ lesions + clinical signs

A

clinical disease

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5
Q

what CNS disease manifests in puppies (< 6 weeks) with Canine herpes virus?

A

Encephalitis –

Canine Herpes Virus: Alpha herpes virus. Replicate in nuclei of epithelial (RT) or endothelial (placenta) cells via fusion entry. Shed in resp. secretions, vaginal secretions, latent in trigem ganglia. Only first litters are affected.

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6
Q

What viruses do you see cerebellar hypoplasia & hypomyeligenesis?

A
  1. Feline Panleukopenia Virus FPV
  2. Bovine Viral Diarrhea Virus BVDV
  3. Classical Swine Fever

All = trans-placental infections!

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7
Q

Feline Leukemia Virus pathogenesis, clinical signs (esp. neurological), prevention

A

Feline Leukemia Virus = RNA retrovirus & oncogenic. Close contact + bodily secretions -> virus infects/replicates tonsilary & pharyngeal lymphoid tissue -> LNs -> Viremia –> –> MYELITIS! (prog. ataxia, paraparesis-plegia)

Prevention = FeLV VACCINE

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8
Q

Where are seizures localized to? Ataxia?

A

Forebrain; cerebellum

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9
Q

Young puppy with no vax history, ataxia, occasional seizures: DDX

A

Rabies v Distemper

Canine Distemper: RNA paramyxo, replicate in cytoplasm, produce intracytoplasmic and intranuclear inclusion bodies. V+, d+ KC-like signs, (-) sense strand [have to be translated].

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10
Q

Canine Distemper clinical signs:

A

V+, d+, kennel-cough-like signs; hyperkeratosis, lethergy; Neuro: ANY CLINICAL MANIFESTATION OF CNS DZ

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11
Q

What histology findings are seen for canine distemper (3)?

A
  • intracytoplasmic and intranuclear inclusion bodies in the brain
  • demyelination of axons! (oligodendrocytes affected)***
  • lymphosplasmacytic perivascular cuffing (not pathognomic, just indicates viral infection)

image: cerebellum

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12
Q

How is canine distemper dx?

A

clinical signs (peracute polysystemic disease // clinical signs); postmortem: histopathology (intranuclear / intracytoplasmic inclusion bodies), PCR

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13
Q

Why is rabies so endemic on almost all continents?

A

It infects the CNS of all mammals (including humans, wildlife)

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14
Q

What determines the incubation period for rabies?

A

the location of the bite (further from CNS = longer incubation); no longer than 6 months

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15
Q

Describe the pathogenesis of rabies

A

Saliva inoculation –> virus travels to CNS via motor and neuron axon terminals

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16
Q

What inclusion is this / what virus?

A

Purkinje cells - negri bodies **Rabies

Purkinje cells = specialized cells that release GABA

17
Q

What differential is made with rabies in cats?

A

Feline infectious peritonitis (FIP)
- neurological signs, replicates in macrophage, fatal prognosis

  • feline parvo (panleuk) is not, unless the cat in question is a very young kitten (early weeks)
18
Q

Where does feline coronavirus (FCoV) replicate?

A

The epithelial cells of the intestinal tract –> mutated from (FIP) spread via FECES

19
Q

Why is FIP difficult to dx?

A

Because it emerges as a mutated form of FCoV ; dx typically post mortem

If lesions/areas outside the GIT are sampled and PCR(+), FIP can be diagnosed

20
Q

Signalement of FIP-infected cats? Transmission?

A

<1 year-old kittens; multi-cat households; spread via ingestion/inhalation of fecal matter

21
Q

Type of inflammation seen on histo for FIP dry form

A

pyogranulamatous (chronic inflammatory lesion, predom of macrophages and neutrophils)

22
Q

Histo of FIP wet form

A

fibrinous pleuritis, peritonitis, pericarditis
(fibrinous = mix of fibrin & neutrophils)

23
Q

What type of virus is feline immunodeficiency (FIV)? How is it transmitted/what is the usual signalement?

A

Retrovirus & lentivirus
Transmitted via bites (free-ranging male cats)

24
Q

Pathogenesis of FIV and clinical signs

A

bite wound -> dendritic cells (APCs) –> local lymph nodes -> infects and replicates in T-cells -> spreads to other LNs

Persistent fever, gingivitis, stomatitis, meningoencephalitis or encephalitis -> seizures or behavioral changes; fever, dullness, circling, depression, blindness

25
Q

What is unique about lentiviruses like FIV?

A

Causes chronic infections // infections for life (if antibodies appear on serology, you know the cat is 100% infected)

26
Q

DDx?

A

rabies v.
equine herpesvirus (stress-induced) v.
West nile virus v.
Equine Encephalitis virus (Western or Venezuelan)

27
Q

How do the D and N strains differ in equine encephalitis?

A

D strain = neurologic form
N strain = respiratory and reproductive (last few cases, however, have been neurologic!)

Does viral load determine neurologic form vs. strain type?

28
Q

Equine Herpes Myeloencephalopathy
- strain
- follows what series of events
- histo findings
- dx

A
  • D752
  • outbreak of respiratory dz farm
  • Vasculitis, necrosis, hemorrhage in CNS
  • DX:
    Antemortem = PCR (only D and N strains differentiates), Postmortem = IHC or PCR of CNS tissue
29
Q

What are the two arthropod-borne viruses in equines (Arboviruses)?

A

Flaviviruses (West Nile)
Togaviridae (Eastern, Western, and Venezuelan equine Encephalitis = EEE, WEE, VEE)

ALL ZOONOTIC // MOSQUITO-BORNE

30
Q

Which has a more severe disease manifestation- EEE or WEE?

A

EEE- death occurs 3-4 days after neurologic signs manifest

31
Q

How are togaviridae (equine encephalitides) dx? How are they prevented?

A

IgM ELISA on serum + PCR or IHC on CNS tissue

Prevented via standard-of-care vaccines

S&S - Exam 2 (16 decks)

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