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Small Animal Medicine > Viral Diseases > Flashcards

Viral Diseases Flashcards

1
Q

What animals can be infected by canine distemper virus? Where is it frequently seen?

A

carnivores —> dogs are reservoirs

breeding and shelter environments

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2
Q

How is CDV transmitted? How long are hosts contagious?

A

oronasal exposure to virus-contaminated respiratory secretions, vomit, feces, urine, and environmental fomites

up to 3 months

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3
Q

What is the initial step to the pathogenesis of CDV? What happens next? What happens when the host recovers?

A
  • infects macrophages and monocytes in the upper respiratory tract and spreads to the stomach, bowels, spleen, liver, BM, lymphatics, and eventually the eyes, skin, and CNS where it persists
  • infects epithelial tissues throughout the body and shed from everywhere until the resolution of respiratory signs

no longer spreads, even if neurologic signs develop

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4
Q

What does the effect of CDV depend on?

A

immune response

  • good response = do not get ill, clears infection
  • mild response = will get clinical disease and likely get better, can persist and develop CNS signs
  • no response = severe disease and death likely

can cause immunosuppression —> concurrent infections common

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5
Q

What dogs are likely to suffer from severe illness from CDV?

A

puppies

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6
Q

What is the first week of CDV illness like?

A

hard to differentiate from other infectious upper respiratory disease

  • vomiting, severe diarrhea
  • fever, dehydration
  • lymphopenia
  • lethargy, anorexia
  • conjunctivitis
  • respiratory signs, viral pneumonia nad secondary bacterial pneumonia
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7
Q

What is the most common symptom of clinically ill patients with CDV? Where does it most commonly progress to? What does this result in?

A

respiratory signs

  • ocular epithelium: photophobia, anterior uveitis, chorioretinitis, permanent hyperreflective retinal lesions
  • renal and bladder epithelium
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8
Q

How is the skin most commonly affected by CDV?

A
  • pustular rashes
  • hyperkeratosis and hardening of the paw pads
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9
Q

How are teeth affected by CDV?

A

permanent denal enamel hypoplasia of adult teeth prior to eruption in puppies

  • gives a clue of previous infection
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10
Q

What additional sign is can be seen in young large breed dogs infected with CDV?

A

metaphyseal osteosclerosis of long bone, not usually associated with lameness

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11
Q

When can CNS signs appear in patients infected by CDV?

A

any point in their life —> progressive, affects prognosis

  • during infection
  • 1-3 weeks after recovery
  • can develop in dogs that never had symptoms
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12
Q

What CNS sign is strongly suggestive of CDV? What other signs are seen?

A

myoclonus - spastic twitching of temporal or appendicular muscles

  • seizures
  • ataxia
  • hypermetria
  • paraparesis or tetraparesis
  • severe cervial pain
  • puppies infected in utero or as neonates can develop CNS signs within the first 4-6 weeks of life
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13
Q

How is CDV diagnosed? What is able to be seen within 1-2 weeks of infection? Why is it difficult?

A
  • clinical signs
  • known poor vaccination history
  • lymphopenia, thrombocytopenia, hypoalbuminemia, hypoglobulinemia
  • radiographs show pneumonia

intranuclear and intracytoplasmic viral inclusions in monocytes, lymphocytes, neutrophils, or erythrocytes

neurologic disease seen can be difficult to narrow down to CDV without history or evidence of systemic signs

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14
Q

What are the 3 major ways to diagnose CDV?

A
  1. serology - not helpful at the peracute stage, 4x increase in serum IgG titer over 2-3 week period or IgM levels indicative of a current infection
  2. cytology - IN and IC inclusion bodies found in cells on stained peripheral blood smears or conjunctival swabs/scrapings
  3. PCR - any fluid or tissue, may not differentiate vaccine vs actual infection
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15
Q

What is treatment for distemper like?

A

SUPPORTIVE

  • fluids
  • antibiotics if there is secondary bacterial bronchopneumonia —> broad-spectrum for several weeks
  • seizure control

myoclonus has no known effective treatment, prognosis with neurologic disease is guarded to poor

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16
Q

How is CDV prevented?

A

VACCINATION

  • at least 3 vaccines every 3-4 weeks between the ages of 6-16 weeks of age with the last booster given at 16 weeks
  • an extra administration of a dose at 18-20 weeks recommended if dogs are in high-risk environments
  • next dose given in a year, then q 3 weeks
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17
Q

How is CDV prevented?

A
  • susceptible to most routine hospital disinfectants
  • isolate dogs with GI or respiratory signs to avoid aerosolization
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18
Q

CDV manifestations:

A
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19
Q

How is canine parvovirus transmitted? Why is it so easily spread?

A

fecal-oral and fomites

  • shed in huge amounts in stool for 2 weeks after initial exposure
  • resistant to many disinfectants, allowing for long persistence in the environment

(recovered dogs don’t transmit infection)

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20
Q

What breeds are more susceptible to developing parvovirus? When can they begin to become infected?

A

BLACK AND TAN - Rottweilers, Pit Bulls, Dobermans, English Springer Spaniel, German Shepherds

12-14 weeks, once maternal antibodies wane

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21
Q

What do puppies infected in utero with CPV typically develop? Why is this rarely seen?

A

myocarditis

  • most bitches are vaccinated and confer maternal antibodies to their pups
  • pups with myocarditis will rarely survive long enough to see signs of it
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22
Q

What is an especially rare manifestation of CPV?

A

erythematous cutaneous lesions (erythema multiforme)

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23
Q

What cells does CPV-2 target? What can exacerbate signs?

A

rapidly dividing cells - thymus, bone marrow, spleen, crypt cells of the gut epithelium

STRESS: weaning, concurrent infections, GI parasites, overcrowding, poor nutrition, age

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24
Q

What is the pathogenesis of CPV? How do most patients initially present?

A

viral destruction of intestinal crypt cells cause villus collapse, diarrhea, vomiting, intestinal bleeding, and bacterial invasion

depression, hyporexia, vomiting typically without diarrhea at first

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25
Q

What is characteristic of CPV infection? What secondary effect is common?

A
  • severe hemorrhagic diarrhea with fetid odor developing 24-48 hours following initial infection
  • vomiting prominent enough to mimic FB obstruction or cause esophagitis

intestinal protein loss = hypoproteinemia

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26
Q

How can CPV affect the bone marrow?

A

damages BM progenitor cells or BM necrosis —> transient or prolonged neutropenia = increased susceptibility to serious infections, especially with GIT translocation

(neutropenia also caused by demand for neutrophils in the GIT)

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27
Q

What is indicative of serious GIT translocation seen with CPV? What most commonly causes death?

A
  • hypoglycemic due to endotoxic shock from G - bacteria
  • skin necrosis
  • polyarthritis, diskospondylitits
  • intussusception

septicemia, endotoxemia, and shock

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28
Q

What CBC signs are seen with CPV? What are some positive prognostic factors?

A

neutropenia and overall low WBCs

  • development of a left shift
  • increases in lymphocytes, monocytes, and eosinophils following their decrease
29
Q

What are the 2 major diagnostics used for CPV?

A
  1. PCR - sensitive and specific, but must be sent out
  2. fecal point of care testing*
30
Q

What in-house diagnostic is available for CPV? How is it used? What should be done if a patient has the clinical signs, but the test comes back negative?

A

fecal ELISA SNAP detects parvoviral antigens 2-4 days after onset

aids in diagnostics, still look at a blood smear

false negatives possible with bloody stool or if it is performed too soon —> repeat test within a few days

31
Q

What fluids are preferred for CPV patients?

A

Normosol R with KCl and 2.5% dextrose added

32
Q

What practices are especially important for the health and comfort of CPV patients?

A
  • nasogastric feeding tube - syringe feeding not ideal due to vomiting or nausea, can use proparacaine on nose —> feeding is protective to enterocytes
  • antinauseants - Cerenia, Onsansetron
  • vitamin B12 for intestinal cell growth
  • pain management - Buprenorphine, Ketamine
  • Entyce
33
Q

What broad-spectrum antibiotics are recommended for CPV patients?

A
  • Ampicillin-Sulbactam
  • Cefazolin
  • Ampicillin
  • Metronidazole - controversial, stop after 2 days if diarrhea persists
34
Q

What treatments are avoided in CPV cases? What treatments have mixed results?

A

corticosteroids, NSAIDs

  • granulocyte colony-stimulating factor
  • recombinant feline IFN omega
  • blood/plasma transfusion
  • antivirals
35
Q

What promising treatment is available for CPV infections?

A

canine parvovirus monoclonal antibody —> mimics natural antibodies and binds to and neutralizes the virus before it can enter cells

36
Q

How is CPV infection prevented?

A
  • vaccination
  • dilute bleach 1:30/32 with contact time of at least 10 mins
  • TrifectantTM
37
Q

How long does feline panleukopenia virus (parvo) last in the environment?

A

more than 1 year —> highly stable

  • VERY CONTAGIOUS
38
Q

How is feline panluekopenia virus (parvo) transmitted?

A
  • fecal-oral transmission from all secretions of a sick patient
  • fomites (anesthesia masks!)
39
Q

What cells does feline panleukopenia affect? What lesions are most prominent? What do in utero infections cause?

A

rapidly developing cells

bone marrow > intestinal crypts

CNS signs - cerebellar development continues during the first 2 weeks after birth —> cerebellar hypoplasia

40
Q

What happens 2-7 days following infection of feline panleukopenia?

A

viremia

lymphoid necrosis —> proliferation

41
Q

How is the GIT affected by feline panleukopenia? What does this cause?

A

intestinal crypt cells develop shortened intestinal villi, causing increased permeability and malabsorption (jejunum, ileum > colon)

endotoxemia with G - bacteria via translocation of intestinal microbes through damaged walls

42
Q

What are the 4 major results of feline panleukopenia?

A
  1. abortion if early
  2. CNS effects if late in pregnancy - kitten born with cerebellar hypoplasia (seen by 10-14 days)
  3. thymic atrophy
  4. retinal dysplasia/blindness
43
Q

What signalment is most commonly associated with feline panleukopenia?

A
  • kittens > adults for developing clinical disease
  • no gender or breed disposition
44
Q

What is associated with feline panleukopenia? What clinical signs are most commonly seen?

A

fading kitten syndrome - neonatal death before weaning

ACUTE DISEASE MOST COMMON - lethargy, depression, anorexia, vomiting, diarrhea (less common), recurring infections

45
Q

What is seen on physical exam in patients with feline panleukopenia? CBC/Chem?

A
  • dehydration, fever
  • abdominal discomfort - ropey, fluid-like intestines
  • signs of DIC

CBC = (pan)leukopenia with neutropenia first, thrombocytopenia, anemia with GI bleeding

Chem = prerenal azotemia, hepatic changes

46
Q

What is the best diagnostic available for feline panleukopenia? What should be done if this comes back negative?

A

canine SNAP fecal ELISA —> only detectable in feces for 24-48 hrs post-infection, can be positive up to 2 weeks following vaccination

PCR of blood/feces

47
Q

Why is the use of antibiotics especially important for feline panleukopenia? Which 3 groups are used?

A

GI translocation + neutropenia = DEATH due to the enteric bacteria (G-, anerobes)

  1. ANAEROBES - Penicillin, Cephalosporins, Clindamycin, Metronidazole
  2. GRAM NEG - Aminoglycosides, Fluoroquinolones
  3. BROAD-SPECTRUM - Ceftazidime (3rd gen)
48
Q

What treatment is recommended for feline panleukopenia? What is prognosis associated with?

A
  • aggressive fluid resuscitation
  • broad-spectrum antibiotics
  • feed the gut early with NG tubes —> glucose and glutmine
  • antiemetics - Ondansetron, Cerenia
  • gastroprotectants - Sucralfate

age, wallet size

49
Q

How is feline panleukopenia prevented? What is the immunity gap?

A

vaccines —> ML has faster protection, maternal antibodies interfere until around 12 weeks

kitten age of around 8-12 weeks where maternal antibodies are present to interfere with vaccination, but not high enough to protect from the virus

  • recommend to start vaccinations at 8 weeks and repeat ever 2-3/3-4 weeks until 16 weeks old
50
Q

How can feline panleukopenia be avoided?

A
  • 1:32 bleach - not “splash-less”
  • accelerated hydrogen peroxide (Rescue)
  • quaternary ammoniums not as effective despite label claims
51
Q

What serotypes of feline coronavirus are commonly seen? How is it transmitted?

A

I = most common
II = less common, recombinant form
BOTH CAN CAUSE FIP
(5-10% of cats exposed to FeCoV develop FIP)

highly infections via fecal-oral route from litter pans

52
Q

What is the most common effect of FeCoV? How can it cause FIP?

A

subclinical or transient, mild GI illness in kittens - diarrhea most common

mutations of FeCoV occur (thought to be the 3c gene), forming the virulent FIPV, which replicates in monocytes and macrophages —> minimal shedding in feces (at this point, don’t need to separate cats)

53
Q

What is thought to cause the signs associated with FIPV? What is seen in early infections?

A

abnormal immune response where FIPV attracts antibodies, macrophages, and neutrophils, which leads to complement fixation —> effusions

infects monocytes and macrophages = dissemination and systemic inflammation

54
Q

What does the course of FIPV disease depend on?

A

cell-mediated immunity

  • strong immunity = viral elimination or latency
  • course shorter in younger cats, most commonly effusive
  • course longer in older cats, most commonly non-effusive
55
Q

What is the principle lesion of wet/effusive FIP? What are clinical signs associated with?

A

pyogramuloma

Arthus-type vasculitis causes pleural and peritoneal effusion due to leakage of serum protein and fluids into body cavities

(more acute and quickly developing)

56
Q

What is characteristic of dry/non-effusive FIP? What is thought to cause this? What are clinical signs caused by?

A

granulomas in parenchyma of tissues

partially successful, cell-mediated immune response, resulting from the slow replication

granuloma formation on organ systems

57
Q

What signalment is associated with FIP? What breed predilection is associated?

A
  • <3 y/o, >10 y/o = BIMODAL
  • M > F
  • predigree cats: Abyssinian, Bengal, Birman, Himalayan, Ragdoll, Rex
  • history of a recent stressor - rehoming, elective surgeries, concurrent illness, boarding
  • concurrent infection with FeLV
58
Q

What are the most common signs of effusive FIP? What else is seen?

A
  • nonspecific signs of inflammation - fever, weight loss
  • pleural/pericardial effusion - muffled heart sounds, dyspnea, tachypnea, cyanosis
  • ascites - abdominal distension

icterus, scrotal enlargement, lymphadenopathy, lameness, enlarged mesenteric LN, abdominal mass effect from adhesions, pale MM

59
Q

What are some signs of non-effusive FIP?

A

depends where pyogranulomas are

  • ocular lesions common - anterior uveitis, hyphema, miosis, keratic precipitates, iritis (color change to brown), perivascular cuffing, blindness, retinal edema/detachment
  • neuro lesions common - meningitis, pyogranulomas in spine, ataxia
  • anorexia, lethargy, ADR, weight loss
  • mesenteric lymphadenopathy
  • irregular viscera (kidneys)
  • dyspnea
  • focal GI granulomas = vomiting, diarrhea, obstipation
60
Q

How is FIP diagnosed on CBC, UA, and biochemistry?

A

CBC - nothing is pathognomonic, lymphopenia and anemia most common + neutrophilia, anemia, thrombocytopenia

UA - bilirubinemia in icteric cats, proteinuria with glomerulonephritis

CHEM - hyperproteinemia, polyclonal hyperglobulinemia (r/o neoplasia), low albumin

61
Q

What is diagnostic of wet FIP on effusion analysis?

A
  • modified transudate with viscous, straw-colored/golden yellow color
  • high protein (>3.5 g/dL) = froths when shaken
  • low to moderate cellularity typically nonseptic and nondegenerate neutrophils > macrophages, lymphocytes
62
Q

What 3 tests are performed on effusions in probable cases of wet FIP?

A
  1. A:G ratio
  2. Rivalta test - differentiated transudate from exudate based on the formation of a precipitate when the sample of an effusion is added to acetic acid
  3. quantitative rtPCR and immunostaining
63
Q

What is highly diagnostic of wet FIP?

A

fluid with….

  • A:G ratio <0.45
  • protein level of >3.5 g/dL
  • low cellularity with predominantly neutrophils and macrophages
  • positive Rivalta
64
Q

What antemortem diagnostics are available for FIP?

A
  • serologic measurement of FeCoV antibody titers often unhelpful —> not specific for FIPV
  • blood titers > 1:1600
  • CSF titer > 1:640

positive does not rule in FIP, negative does not rule out FIP

65
Q

What is used for definitive diagnosis of FIP? What is a hallmark sign? What differentials of pyogranulomatous disease need to be ruled out?

A

consistent histopathological changes in affected tissues + FCoV antigen immunostaining by IHC

perivascular pyogranulomatous inflammation

  • mycobacteria
  • Actinomyces
  • Nocardia
  • Rhodococcus
  • Barotnella
  • Pseudomonas
  • fungi
66
Q

What 2 direct tests are available for diagnosing FIP?

A
  1. quantitative reverse transcriptase PCR - performed on fluids, FNAs, and tissue, infected cats with have higher viral loads
  2. ICC/IHC - positive staining in macrophages
67
Q

What promising new treatments may eventually be available for FIP?

A

not licensed yet

antiviral GS-441524 or GD376 - nucleoside analogue

68
Q

How is FIP prevented?

A
  • avoid or minimize stress
  • antibody testing on incoming cats in catteries and shelters before adding them to groups
  • provide an adequate number of litter trays and perform daily cleaning to minimize contamination of the environment and spread
  • 1:32 bleach
69
Q

What FIP vaccine is available? Why is it not commonly used?

A

IN MLV able to be given to kittens > 16 weeks

NON-CORE - not effective in FeCoV antibody-positive cats and can make FIP worse

Small Animal Medicine (52 decks)

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