FIP & Canine Distemper Flashcards

1
Q

FIP vs FEC cell preference for replication

A

FIP- prefers to replicate inside monocytes and macrophages

FEC- replicates inside intestinal epithelial cells

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2
Q

FIP vs FEC- organ systems affected

A

FIP- can go systemically so it can infect various organs

FEC- intestines

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3
Q

Signalment of cats at risk for FIP vs FEC

A

FIP- cats 6mo to 3yrs

FEC- kittens less than 1yr

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4
Q

FIP vs FEC clinical signs

A

FIP- severe clinical signs with a fatal prognosis

FEC- mild diarrhea, good prognosis

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5
Q

When does Effusive FIP (wet) occur? (think in relation to the immune system) Why?

A

completely impaired cell-mediated immune response but function humoral response

Why?? Humoral arm uses antibodies that recognize and attach to the virus and present the virus to the macrophage. PROBLEM b/c the macrophage is where the virus can replicate and get transported all over the body. The antibody-virus complex can also congregate around blood vessels. If there’s no cell mediated arm to combat this, the complex (and the macrophages) can cause gaps to open in the blood vessel, increasing vascular permeability.

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6
Q

What happens when the blood vessels become more permeable in the case of effusive FIP?

A
  • effusion of protein rich fluid (into the pleura or peritoneum, pending on where the blood vessel permeability occurs)
  • neutrophils will also leak from the vessels
  • eventually the neutrophils will release lysozymes that increase inflammation and results in endothelial cell necrosis and more vessel permeability
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7
Q

When does Non-effusive FIP (dry) occur? (think in relation to the immune system) Why?

A

partial cell-mediated immune response is present

small amounts of virus are still replicated and accumulate in complex near blood vessels; vasculitis is present but not as bad as in effusive FIP; neutrophils are still able to get through the vessel wall and reach surrounding tissues

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8
Q

What happens when neutrophils get through the vessel wall in non-effusive FIP?

A

they form small nodules filled with neutrophils (pyogranulomas) to develop on the surface of many abdominal organs

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9
Q

Clinical signs associated with effusive FIP

A

nonspecific
weight loss
anorexia
depression

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10
Q

Clinical signs associated with non-effusive FIP

A

nonspecific

often related to affected organs

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11
Q

How does FIP alter a CBC?

A

neutrophilia as a result of increased neutrophil recruitment across the body

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12
Q

How does FIP alter a serum panel?

A

Hyperglobulinemia and decreased albumin:globulin ratio

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13
Q

How to test for FIP

A

If effusive, collect fluid from a body cavity and evaluate it for protein that leaks out due to the increased permeabilitty

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14
Q

Are antibody titer useful for FIP diagnoses?

A

No because FEC can also induce the body to produce antibodies, and we can’t tell the difference between FIP and FEC antibodies; many kittens have undiagnosed FEC so testing for the antibodies would be pointless

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15
Q

Nursing interventions for healthy FIP+ cat

A

not much can be done

avoid stressful situations

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16
Q

Nursing intervention for sick FIP+ cat

A

therapy is aimed at prolonging a good QoL
concentrate on supportive/palliative care
fluid and nutrition therapy often needed

17
Q

After onset of clinical signs for FIP, how long do cats usually live?

A

1wk to 6mo

18
Q

FIP prevention

A

keep positive cats in one cat households

quarantine screen new cats for FIP antibodies

19
Q

Define peritoneum vs pleura

A

Peritoneum- tissues that line abdominal wall and cover most abdominal organs

Pleura- tissue covering lungs & lines interior wall of chest cavity

20
Q

Describe the Canine Distemper Virus (CDV)

what’s its genome, can it survive outside the body

A

enveloped RNA virus
only lives about 20min in exudates outside host
destroyed easily by disinfectants, heat, drying

21
Q

Signalment for dogs at risk for acquiring CDV

A
  • unvax/immunocomp. animals
  • typically puppies 3-6mo old
  • usually have Hx of no vaccine series, poor husbandry/environment, unvaccinated dams, potential exposure to unvax animals
22
Q

How is CDV transmitted?

A

aerosolization of viral particles and inhalation into upper respiratory tract

23
Q

How is CDV primarily shed?

A

exudates and feces

24
Q

Where can CDV replicate?

A

lymphoid, nervous, and epithelial tissues

25
Q

What pathway does CDV take once it is inhaled?

A

virus phagocytized by the alevolar macrophage –> carried to bronchial LN –> virus disseminates through the body w/ a predisposition to infect respiratory tract, oculonasal, GI tract –> patient mounts antibody response and recovers; if it doesn’t mount an antibody response –> continued viral multiplication –> possibly gets into CNS –. demyelination and necrosis of nerves –> death

26
Q

What organ/body systems can CDV infect?

A

epithelial cells of conjunctiva, nasal, pharyngeal, and tracheal mucosa
epithelial cells of stomach and SI
CNS
Derm

27
Q

Clinical signs of CDV infection of conjunctiva, nasal, pharyngeal, and tracheal mucosa

A
ocular and nasal discharge (clear and colorless)
sneezing
occasional cough (nonproductive)
anterior uveitis
optic neuritis
retinochorditis
28
Q

Clinical signs of CDV infection of stomach and SI

A

anorexia
vomiting
diarrhea
dehydration and depression secondary to fluid loss and lack of nutrients

29
Q

Clinical sings of CDV infection of CNS

A

CS develop after original CS start to resolve
hyperesthesia
seizures (generalized or partial)
cerebellar signs
vestibular signs
(these CS typically get progressively worse)

30
Q

When are dermal signs of CDV usually seen, and what are they?

A
  • usually occur in pets who survive the infection
  • proliferation of cells that leads to hyperkeratosis of nose/footpads
  • pustular dermatitis
31
Q

What is “old dog encephalitis”? What are it’s clinical signs?

A
  • Describes CNS signs occurring in patients >6yr old who have survived CDV infection in the puppyhood
  • Chronic condition that is often progressive
  • Clinical Signs stem from the reaction of the immune system to the original CDV infection (depression circling, head pressing, visual defects)
32
Q

What are some things you can evaluate to possibly point toward a CDV diganosis?

A
  • nonspecific changes in leukogam (lymphopenia, thrombocytopenia)
  • development of inclusion bodies in RBC (first 2-9 days of infection)
  • buffy coat and bone marrow to ID viral inclusion bodies
  • antibodies to CDV in CSF may help support an active infection
33
Q

What is the prognosis for a CDV infection?

A

grave if CNS signs
favorable if pustular dermatitis
dependent on competency of pet’s immune system

34
Q

What nursing care can be offered to CDV patients?

A
Supportive;
fluids for GI signs
antiemetics for vomiting
anticonvulsants for seizures
antibiotics for assumed damage to mucosal lining of resp/GI tracts and to help prevent sepsis if normal GI bacteria translocates from mucosa into systemic circulation
35
Q

Prevention of CDV

A
  • vaccinate

- don’t expose immunocomp./unvaccinated animals to unvaccinated animals