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ZUKU NAVLE PREP > Cross Species Top 10 Reportable Diseases - Part 2 > Flashcards

Cross Species Top 10 Reportable Diseases - Part 2 Flashcards

1
Q

what diseases are involved in equine arboviral encephalomyelitis?

A

west nile virus, eastern equine encephalomyelitis, western equine encephalomyelitis, & venezuelan equine encephalitis

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2
Q

what is the classic case presentation of west nile virus in horses?

A

through out the USA & canada - fever, fasciculations of the face/neck, hyperesthesia, & colic

altered mentation, cranial nerve abnormalities, ataxia/paresis/paralysis

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3
Q

what is the classic case presentation of eastern equine encephalomyelitis?

A

east of the mississippi river & eastern canada - forebrain signs including head pressing/circling/seizures

highly pathogenic in horses with a mortality of 50-90%

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4
Q

what is the classic case presentation of western equine encephalomyelitis?

A

west of the mississippi river & western canada - characteristic head droop, less pathogenic/less active than the others

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5
Q

what is the classic case presentation of venezuelan equine encephalomyelitis?

A

altered mentation, cranial nerve abnormalities, ataxia/paresis/paralysis

highly pathogenic in horses - mortality of 50-90%

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6
Q

how are equine arboviral encephalomyelitis diseases diagnosed?

A

CSF fluid analysis

IgM capture ELISA for WNV

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7
Q

how are equine arboviral encephalomyelitis diseases treated?

A

supportive care - prevention includes vaccination & minimizing mosquito exposure

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8
Q

which of the equine arboviral encephalomyelitis diseases is the horse not a dead end host?

A

VEE - horses are viremic

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9
Q

T/F: equine arboviral encephalomyelitis diseases are pathogenic to humans

A

true

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10
Q

T/F: if a horse is recumbent due to an equine arboviral encephalomyelitis disease, it makes for a poor prognosis

A

true

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11
Q

how are equine arboviral encephalomyelitis diseases spread?

A

primarily spread by mosquitos during the summer transition season or the mosquito to bird to rodent cycle

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12
Q

what are the main differentials you should consider for equine arboviral encephalomyelitis diseases?

A

rabies

equine protozoal myeloencephalitis

neuroborreliosis

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13
Q

the stance & head droop this horse is displaying is typical for what equine arboviral encephalomyelitis disease?

A

WEE

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14
Q

what clinical signs are seen with rabies that make you consider it as a differential for equine arboviral encephalomyelitis diseases?

A

behavioral changes, progressive flaccid paralysis, distress/agitation, rolling (mistaken for colic), & self-inflicted wounds

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15
Q

what clinical signs are seen with EPM that make you consider it as a differential for equine arboviral encephalomyelitis diseases? what is the definitive host?

A

sarcocystis neurona, in north, south, & central america - ataxia, cranial nerve deficits, asymmetric muscle atrophy especially in the gluteal muscles

host - opossum, horses are infected orally from feed contaminated with opossum feces

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16
Q

what clinical signs are seen with neuroborreliosis that make you consider it as a differential for equine arboviral encephalomyelitis diseases? how is it treated?

A

borrelia burgdorferi from an infected tick that is most common in the northeast & upper midwest - neck stiffness, ataxia, vestibular deficits

treated with tetracyclines

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17
Q

what is another name for ornithosis?

A

chlamydiosis

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18
Q

what is the classic case presentation of chlamydiosis?

A

any parrot species, most frequent in cockatiels & budgies (possible in any species of bird, especially pigeons/doves) at any age - causes depression, anorexia, green/yellow diarrhea/urates, & sometimes conjunctivitis & upper respiratory signs in cockatiels

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19
Q

what is the etiology of chlamydiosis?

A

chlamydia psittaci

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20
Q

how is chlamydiosis diagnosed from a dead bird?

A

histopathology with the machiavello stain to demonstrate elementary bodies in hepatocytes or other cells

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21
Q

how is chlamydiosis diagnosed from a live bird?

A

blood, choanal/cloacal swab for serology/PCR

elevated WBC count, +/- elevated liver enzymes

radiographs - splenomegaly +/- hepatomegaly

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22
Q

how is chlamydiosis transmitted?

A

directly - aerosol or fecal/oral

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23
Q

why is chlamydiosis reportable?

A

zoonotic disease that causes flu-like symptoms in humans (parrot fever or psittacosis)

24
Q

what is the prognosis of chlamydiosis?

A

good if caught early

25
Q

how is chlamydiosis treated?

A

doxycycline (or tetracyclines, chloramphenicol) for 6 weeks & supportive care

26
Q

what is the classic case presentation of avian newcastle disease?

A

affects ALL avian species - acute, highly contagious disease causing respiratory & neurologic signs (sometimes diarrhea) with virulence varying

high mortality with virulent forms - if confirmed in your country, trade restrictions are in place

27
Q

what is the classic case presentation of highly pathogenic avian influenza/fowl plague?

A

low pathogenic - respiratory signs

high pathogenic - sudden death forms

HPAI: cyanosis, head edema, hemorrhages, greenish diarrhea, & high mortality!!!

ZOONOTIC!!

28
Q

what is the mortality of salmonella pullorum?

A

nearly 100% mortality in young chickens & turkeys (2-3 weeks old) - in adult chickens, can see high mortality but no clinical signs

29
Q

T/F: salmonella pullorum has been mostly eliminated from commercial flocks in north america

A

true

30
Q

what is the classic case presentation of bovine johne’s disease?

A

alert with no fever, chronic intermittent diarrhea that is loose then pea soup like then watery, appetite starts off fine, milk production decreases with protein levels

weight loss, debilitation, emaciation, & submandibular & ventral edema

31
Q

what is the number one sign of johne’s disease in sheep/goats?

A

weight loss

32
Q

what is the classic case presentation of johne’s disease in sheep/goats?

A

weight loss, weakness, diarrhea isn’t common, wool break (sheds easily), submandibular edema without ventral edema, & decreased milk production

33
Q

what is the etiology of johne’s disease?

A

mycobacterium avium subspecies paratuberculosis

34
Q

what is seen on necropsy of a cow with johne’s?

A

thickened, corrugated intestines especially in the terminal ileum

enlarged edematous lymph nodes

35
Q

what is seen on necropsy of sheep/goats with johne’s?

A

foci of caseation with calcification of the intestinal wall & lymph nodes

enlarged distal mesenteric lymph nodes

36
Q

how is johne’s disease diagnosed?

A

culture is done for m. paratuberculosis from feces or a post mortem specimen - culture takes weeks & need to use a USDA approved lab

herd testing isn’t useful - wastes resources unless management is good

37
Q

what treatment is used for johne’s disease?

A

no treatment - cull clinically affected animals

38
Q

how is johne’s disease transmitted?

A

mostly fecal/oral - also colostrum, milk, intrauterine

39
Q

when does shedding of johne’s disease begin?

A

begins prior to the onset of clinical signs

40
Q

what is the number one mode of transmission of johne’s disease?

A

silent shedder cows

41
Q

why is johne’s hard to deal with?

A

survives over a year in soil & even longer in water - isn’t killed by pasteurization either

42
Q

T/F: johne’s disease is reportable in sheep & goats in all US states & reportable for cattle in some of them

A

true

43
Q

what are the 3 forms of rabies?

A
  1. cerebral - furious
  2. brainstem - dumb
  3. paralytic - subset of dumb
44
Q

what is the classic case presentation of the cerebral/furious form of rabies?

A

aggression, restlessness, howling, bellowing in cattle, excessive salivation, seizures, & tenesmus

45
Q

what is the classic case presentation of the brainstem/dumb form of rabies?

A

somnolence, stupor, ataxia, opisthotonus, dropped jaw, dysphagia, excessive drooling, facial paralysis, & hypalgesia (decreased sensitivity to pain)

46
Q

what is the classic case presentation of the paralytic form of rabies?

A

subset of the dumb form - ascending flaccid paralysis, monoparesis/plegia, truncal, limb, & perineal hyporeflexia/hypalgesia, priapism, urinary incontinence, self-mutilation, & profuse salivation

47
Q

what is the etiology of rabies?

A

genus lyssavirus, family rhabdoviridae

48
Q

how is rabies diagnosed?

A

direct/indirect fluorescent antibody stain of the brainstem & cerebellum shipped COLD!!

histopathology - variable, mononuclear infiltration, perivascular cuffing, lymphocytic foci, babes nodules (tight groups of glial cells), & negri bodies (intracytoplasmic inclusions - NOT PATHOGNOMONIC)

immunohistochemistry is more sensitive than histopathology

49
Q

what does worldwide rabies prevention focus on?

A

focuses on controlling rabies in dogs - dog registration, stray control, reduction of contact between susceptible dogs through leash laws, dog movement control, & quarantine, mass immunization, & notification of suspected cases & euthanasia of dogs with clinical signs or dogs bitten by a rapid animal

50
Q

what prevention of rabies is used in north america?

A

pet vaccination to limit virus circulation to wild reservoirs such as raccoons, bats, skunks, & foxes

1950’s pet vaccination laws resulted in a huge decrease in human rabies deaths from 100s to 1-2/year

minimizing pet-wildlife contact - not leaving pet food outside at night

51
Q

how is rabies transmitted?

A

usually through saliva - bite wound

virus passes through neurons in a retrograde fashion causing initial hyperactivity of neurons with hyperesthesia/tremors & later neuronal death with flaccid paresis/hypalgesia

52
Q

what animals are most commonly affected by rabies in canada?

A

raccoons, foxes, skunks, & bats

53
Q

when is world rabies day?

A

september 28th lol

54
Q

what is the SINGLE BEST REFERENCE on rabies for veterinarians?

A

compendium for rabies prevention and control, 2016

55
Q

T/F: rabid dogs, mostly in africa, asia, & latin america, cause 99% of human rabies deaths worldwide

A

true

ZUKU NAVLE PREP (178 decks)

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