Virology

Question 1

Organism ID w/out lesions

Answer 1

infection

Question 2

Organism ID w/ lesions

Answer 2

disease (clinical or subclinical)

Question 3

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

Answer 3

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

Question 4

Organism ID w/ lesions + clinical signs

Answer 4

clinical disease

Question 5

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

Answer 5

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.

Question 6

What viruses do you see cerebellar hypoplasia & hypomyeligenesis?

Answer 6

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

All = trans-placental infections!

Question 7

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

Answer 7

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

Question 8

Where are seizures localized to? Ataxia?

Answer 8

Forebrain; cerebellum

Question 9

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

Answer 9

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].

Question 10

Canine Distemper clinical signs:

Answer 10

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

Question 11

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

Answer 11

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

image: cerebellum

Question 12

How is canine distemper dx?

Answer 12

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

Question 13

Why is rabies so endemic on almost all continents?

Answer 13

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

Question 14

What determines the incubation period for rabies?

Answer 14

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

Question 15

Describe the pathogenesis of rabies

Answer 15

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

Question 16

What inclusion is this / what virus?

Answer 16

Purkinje cells - negri bodies **Rabies

Purkinje cells = specialized cells that release GABA

Question 17

What differential is made with rabies in cats?

Answer 17

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)

Question 18

Where does feline coronavirus (FCoV) replicate?

Answer 18

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

Question 19

Why is FIP difficult to dx?

Answer 19

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

Question 20

Signalement of FIP-infected cats? Transmission?

Answer 20

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

Question 21

Type of inflammation seen on histo for FIP dry form

Answer 21

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

Question 22

Histo of FIP wet form

Answer 22

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

Question 23

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

Answer 23

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

Question 24

Pathogenesis of FIV and clinical signs

Answer 24

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

Question 25

What is unique about lentiviruses like FIV?

Answer 25

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

Question 26

DDx?

Answer 26

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

Question 27

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

Answer 27

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?

Question 28

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

Answer 28

• 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

Question 29

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

Answer 29

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

ALL ZOONOTIC // MOSQUITO-BORNE

Question 30

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

Answer 30

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

Question 31

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

Answer 31

IgM ELISA on serum + PCR or IHC on CNS tissue

Prevented via standard-of-care vaccines