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Clinical Sciences Exam 4 > Livestock D+: Older Animals Part 2 > Flashcards

Livestock D+: Older Animals Part 2 Flashcards

1
Q

winter dysentery

A
  • lactating heifers and adult dairy cattle
  • coronavirus!
  • fall, winter, confined barns
  • rapidly spreading outbreak of D+
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2
Q

when does winter dysentery strike?

A

when dairy cattle are confined indoors during cold snaps in fall and winter

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3
Q

hallmark of winter dysentery

A

rapid spread of explosive D+ with or without blood (small amt to large clots = dysentery) and mucus WITH an abrupt drop in milk production

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3
Q

winter dysentery basics

A
  • acute, contagious diarrheal dz of cattle
  • epizootic fashion within DAIRY herds
  • cold months of year in CONFINED INDOOR dairies
  • great lakes states and northeast dairies
  • not seen in outdoor CO or western states
  • usually cattle maintained in free stall barns or corrals
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4
Q

cause of winter dysentery

A

coronavirus: related to enteric coronas of calfhood
RNA: very able to mutate, may be antigenically different from calfood enteric coronas

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5
Q

clinical signs of winter dysentery

A
  • diarrhea +/- blood
  • afebrile
  • rapid drop in milk reduction
  • self-limiting, recovery in 1-2 weeks
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6
Q

presence of blood in winter dysentery indicates what

A

strains of corona can infect small intestine and large intestine = red blood

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6
Q

T/F: winter dysentery often presents with a mild fever

A

false- fever is uncommon. affected cows may show transient loss of appetite

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7
Q

when are outbreaks of winter dysentery seen

A

fall and early winter, northern states and canada

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7
Q

T/F: winter dysentery animals do not need fluids or electrolyes

A

true- dehydration may occur if D+ persists, but most animals are ok and fluids and electrolytes not necessary

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8
Q

how does wintery dysentery affect infected cells

A

lyses them like neonatal coronas

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9
Q

how is milk affected by winter dysentery

A

production drops dramatically for several days and then recovers = $$ loss

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10
Q

how common is death from winter dysentery

A

extremely rare

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11
Q

differentials for winter dysentery

A

BVDV, salmonellosis, grain overload, parasitism

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12
Q

clinical pathology of winter dysentery

A

unremarkable but CBC may have inflammatory response for a few days

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13
Q

treatment of winter dysentery

A

specific treatment not usually needed bc most animals recover spontaneously

D+ for 2-4 days in entire herd and blows through a tapers. treat symptomatically with feed/water, salt, rest
herd will be resistant for next several years

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14
Q

who brings winter dysentery onto farm

A

vets, milk machine repair, visitors
could be rodents and birds
dont be fomite! biosecurity! cleanliness!

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15
Q

what age of cattle does johne’s disease affect

A

disease seen in the ADULT, but infection established in the NEONATE

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16
Q

pathogenesis of Johne’s

A
  • slow infection of ileum
  • slow spread to regional lymph nodes
  • gradual increase of S and L intestine
  • infection starts at/near the ileocecal junction and spreads orad and aborad from there
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16
Q

cause of johne’s

A

mycobacterium avium ssp paratuberculosis
causes chronic, granulomatous enterocolitis (MAP)

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17
Q

johne’s results in what impact on the GIT

A

chronic granulomatous enteritis
protein exudation thru inflamed bowel leads to PLE

18
Q

susceptible animals to johne’s

A

cattle, sheep, goats, camelids, rabbits, deer, antelope, yaks

19
Q

johne’s doesnt occur in what species

20
Q

how do you test for MAP

21
how do cows get johne's
- transplacental transmission possible; 20-40% calves born to infected symptomatic cows are infected in utero - majority in neonate via colostrum or milk or contaminated environment - more common in dairies from concentrated management methods (large areas of feces)
22
at what age does it become difficult to establish a johne's infection in a dairy cow?
after a year of age majority of clinical cases infected as young stock from birth to a year or so
23
incubation of johne's
2-10 years clinical signs seen between 2-6 years old clinical disease rarely seen in animals as young as 13 months; likely from overwhelming infections
24
timeline of johne's infection
1. infx established when animal in calfhood - TRUE FOR ALL SUSCEPTIBLE SPECIES: NEONATES AND JUVENILES UP TO A YEAR OF AGE 2. usually came in contact with adult animal feces 3. entry route: M cells of ileum: uptake MAP up to year of life 4. MAP spreads slowly thru wall of ileum and colon 5. macrophages called in = chronic granulomatous inflammation 6. intestinal wall thickens from inflammatory cell influx 7. problem: inflamm cells can't clear if infx started in neonate/juvenile!
25
classic clinical signs of johne's tells you that what part of the infection has set in?
protein loss (edema) and intestinal dysfunction from slow progressive inflammation (diarrhea and weight loss)
26
when do Johne's patients start to show signs of disease?
infected animal typically shows NO SIGNS early in course of infxx, and may appear healthy otherwise WELL INTO ADULTHOOD but immune response cannot clear infx, and MAP slowly invades to new lengths of S and L intestine. even when in adulthood will heave protein leakage = malabsorption = organism into gut wall = body condition starts to decline = D+ in cattle
27
johne's disease is a _____________ of the _______________ that begins with ____________
DISEASE of the ADULT ANIMAL that begins with INFECTION AS A NEONATE
28
titers of jone's
development is slow and gradual, once adult showing clinical signs of weight loss and D+, serologic tests are typically positive
29
clinical signs of johne's
- gradual weight loss despite NORMAL APPETITE - afebrile - pipestream D+ develops slowly, recurs during stress. normal looking D+ - over time cattle become emaciated - serious: lethargy, weakness, apathy, cachexia in terminal stages die of sheer weakness or opportunistic infx tha occur
30
why might a johne's cow have edema?
- albumin loss in feces exceeds liver's capacity to synthesize new albumin - loss of oncotic pressure + hypoalbuminemia = edema - intermandibular space shows it really well = bottle jaw loss of globulin can also occur, creating a panhypoproteinemia
31
clinpath of johne's
- CBC often just reflects protein loss (decreased TP) - reflects that inflammatory lesions expand very slow - classic leukocyte changes we associate with inflamm response typically not present - exceptions would be animals that develop co-morbidities
32
most common sign of johne's in sheep, goats, camelids
wasting disease: ill thrift, thin body condition diarrhea less common and often a terminal event
33
what sign of johne's in cattle is not seen in sheep, goats, and camelids?
chronic D+ just see weight loss despite a good appetite feces may appear normal or soft piles if D+ occurs is a terminal thing
34
how do you diagnose johne's
1. serologic testing 2. fecal culture or PCR 3. necropsy (histopath)
35
serologic testing of johne's (AGID or ELISA)- detect antibody to the agent
seroconversion happens late in the course of the infection - immune response slowly builds from slow infx - subclinical- can't detect - clinical cases are seropositive may not detect infected animals prior to their shedding of the agent in feces
36
T/F: serologic testing is reliable for latent or preclinical cases of johne's
false- not reliable because of low antibody production during this phase of disease
37
how fast are serologic test results of johne's
rapid turnaround
38
pros vs cons of fecal culture or PCR for johne's
- takes time (3-6 months) - not sensitive in early course of dz bc not shedding much - GOLD STANDARD TEST IN CATTLE - culture not sensitive in early disease bc of low and intermittent shedding
39
slowest growing bacterial pathogen in human and veterinary medicine
MAP
40
what is the gold standard test in cattle for johnes
fecal culture
41
what happens if a non-infected johne's adult ingests feces contaminated with MAP
adults are resistant to developing infection, MAP will simply pass thru gut of this animal BUT PCR or culture could detect it in the feces
42
what is a pass through fecal positive Johnes test
a noninfected adult ingests johnes infected feces- adult herdmate is NOT actively infected and not truly diseased, MAP not infected gut wall and replicating, just passing thru via the contaminated feed
43
how do you rule out the pass through positive pass through johnes test
- expect that some of these cases will exist esp if contamination of feed or they feed off ground - rigorous feed and water hygiene! get D+ away from feed - remove clinically infected shedding cases away from population (CULL) - allow 2-4 months to pass, letting "innocent" cows pass the MAP from GIT - next do more fecal testing- will be clean
44
necropsy of johne's
classic bovine lesion: thickened ileum terminal small intestine, cecum and proximal colon thickened and corregated - mesenteric and ileocecal lymph nodes enlarged and edematous
45
what do you see on johnes histpathology
clumps of acid fast bacilli within macrophages
46
what site do you sample for histopath of johnes
infection starts near ileocecal junction- that piece of bowel with several cm of ileum also can do ileocecal lymph nodes within ileocecal fold! infected macrophages migrate there: leaves a "histologic fingerprint" and can be cultured fromthose sittes too
47
control of johnes disease
1. not good treatment options: euthanize bad cases 2. id and cull infected animals- or isolate, repeat serology - test in parallel: fecal culture or PCR and serology simultaneous, cull if EITHER test is positive 3. isolate neonates !! 4. feed neonates pasteurized colostrum/milk from seronegative dams 5. improve measures to separate feces and feed
48
testing in parallel
submit 2 diagnostic tests for disease simultaneously and consider animal to be positive if either of those tests come back positive. intended to MAXIMIZE sensitivity = maximize chances of finding truly diseased animals

Clinical Sciences Exam 4 (9 decks)

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