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Large Animal Medicine > Viral & Bacterial Neurologic Diseases of Ruminants > Flashcards

Viral & Bacterial Neurologic Diseases of Ruminants Flashcards

1
Q

What are the 3 most common signs of BSE? What else is seen?

A

slowly progressive (insidious) onset of apprehension, increated tactile and auditory hyperesthesia, and mild incoordination

  • kicking
  • aggression
  • TERMINAL = falling, recumbency
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2
Q

What is the etiologic agent of BSE? Where is it found?

A

prion proteins - medulla oblongata at the obex

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3
Q

Is treatment available for BSE? How does it compare to rabies?

A

none - die between 2 weeks to 6 months after signs

if rabies, bovine would die within 10 days after signs begin

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4
Q

What age is most commonly affected by BSE?

A

> 20 months —> 4-5 years most common

  • incubation period is months to years
  • incubation period is inversely related to dose
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5
Q

What resulting in a significant drop in cases of BSE in the US?

A

close surveying of imported cattle from the UK and banning of feeding meat and bone meal to herds (commonly contain neuro tissue in the mix)

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6
Q

What are the main red flags associated with rabies? What other signs are seen?

A

constant straining to the point of having a rectal prolapse + yawning

  • hindlimb ataxia, weakness, or paralysis
  • salivation
  • bellowing
  • aggressiveness
  • self-mutilation
  • unlikely to find bite wounds
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7
Q

What are the 3 forms of rabies? Where in the CNS do they originate? What signs are seen with each?

A
  1. FURIOUS - cerebral; aggression, photophobia, hyperesthesia, straining, convulsions
  2. DUMB - brainstem; depression, dementia, ataxia, drooling, pharyngeal paralysis
  3. PARALYTIC - spinal cord; progressive ascending paralysis
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8
Q

How is rabies diagnosed? When is this not seen? When do cows die?

A

send brain into the lab —> viral isolation, Negri body formation

only spinal cord disease (paralytic)

death within 10 days of clinical signs (if case gets better it’s NOT rabies)

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9
Q

What ages of ruminants are most susceptible to rabies? How long in the incubation period?

A

all ages!

few weeks to 6 months depending on site of inoculation –> must pass along neurons within the nervous system

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10
Q

What treatments are used to prolong rabies development? How is it controlled?

A

anti-inflammatories and coma induction —> slows neuron death

vaccination in endemic areas and valuable animals (not as economic due to costing ~ $6.50 per dose

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11
Q

How does rabies transmission in cattle compare to dogs?

A
  • dogs - shed in saliva about 10 days prior to clinical signs
  • cows - rare to have saliva and mammary samples positive, shed in low levels in mild +/- transplacental transfer
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12
Q

A distinguishing characteristic of BSE that differentiates it from rabies is:

a. proprioception deficits
b. lack of aggression
c. insidious onset with prolonged disease course
d. intense pruritis

A

C

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13
Q

What is pseudorabies?

A

Mad Itch, Aujeszky’s disease —> acute herpesvirus encephalitis of ruminants primarily characterized by severe pruritus at area of infection

  • pigs typically act as carries and are primary hosts, but young can undergo seizures
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13
Q

If a mother cow has rabies, could a calf get rabies from dinking her milk? When do rabid cows shed the virus?

A

its a possibility, but it’s considered rare

don’t tend to shed until clinical signs are evident

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13
Q

What clinical signs are associated with pseudorabies?

A
  • multiple animals in a herd with severe pruritus
  • dermal abrasions, swelling, and alopecia at viral inoculation site
  • fever, bellowing, bloat
  • stamping feet, salivation
  • tongue chewing
  • sudden death without signs possible

(die sooner compared to rabies)

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14
Q

How is pseudorabies diagnosed?

A

submit areas of intense pruritis (especially neural tissue) for gross necropsy and histopath

  • call state vet, reportable
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15
Q

What affects the likelihood of ruminants developing pseudorabies? How does disease progress? What animals are resistant?

A

proximity of housing to pigs/feral swine

incubation for 4-7 days with duration of illness for 8-72 hours

horses

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16
Q

Where is pseudorabies in swine most commonly seen?

A

Southern US —> California, Texas, Oklahoma, Louisiana, Georgia, Florida, South Carolina

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17
Q

What is Listeriosis? What initial signs are seen?

A

acute meningoencephalitis of ruminants characterized by circling and UNILATERAL cranial nerve (V-XII) deficits

anorexia, depression, salivation —> can’t swallow (XII)

(AKA Circling Disease)

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18
Q

What clinical signs are associated with Listeriosis?

A
  • proprioceptive deficits
  • head pressing and tilt
  • depressed consciousness - not aggressive!
  • constant or sporadic walking/circling
  • dropped jaw, facial anesthesia
  • ptosis, loss of menace, absent palpebral reflex
  • drooped ears, loss of levator nasolabialis musculature
  • decreased lip tone
  • stertorous breathing, dysphagia, paresis of tongue = protrusion on just one side
  • without treatment, signs progress to coma, convulsions, and death

all to the side of the lesion! —> inner ear infection a common differential

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19
Q

Listeriosis:

A
  • cloudy eyes
  • drooling —> fluids an important part of tx!
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20
Q

What is absent when diagnosing Listeriosis? What way of diagnosis is preferred?

A

inflammatory leukogram

CSF —> mononuclear pleocytosis with mild elevation in proteins; can also culture

+/- IHC of microabscesses in brainstem

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21
Q

Which anti-microbial would be illegal to use for Listeriosis?

a. Draxxin
b. Penicillin
c. Tetracycline
d. Baytril
e. Zactram
f. Nuflor
g. Micotil
h. sulfas
i. Ceftiofur

A

D —> not indicated for uses other than respiratory disease

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22
Q

What 3 aspects to treatment is especially important for overcoming Listeriosis? How long?

A
  1. alkalizing fluids - losing saliva that is necessary for buffering ruminal contents
  2. antibiotics - OTC, PPG, KPen
  3. TLC - good footing and environment
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23
Q

What causes Listeriosis in cattle? What are 4 sources?

A

Listeria monocytogenes - common, sporadic, occasional outbreaks with hematogenous ascension toward CN V

  1. spoiled silage - aerobic silage with a pH >5.4 (proper ensilage = anaerobic and more acidic)
  2. shed in feces
  3. rotting vegetation
  4. soil survival
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24
Q

What causes outbreaks of Listeriosis? How do most properly and timely treated ruminants respond?

A

high environmental contamination associated with spoiled silage

commonly survive, may have permanent neurological deficits

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25
Q

Once BSE affected cattle demonstrate clinical signs, they usually die within…

a. <10 days
b. 1-6 months
c. 6 months to a year

A

B

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26
Q

The ruminant waste product that is still legal to feed to cattle is…

a. blood meal
b. bone meal
c. meat meal
d. none of the above

A

A

27
Q

A 2 y/o Long Island cow with neurologic issues would most likely have…

a. BSE
b. rabies
c. Listeriosis

A

C

BSE and rabies are uncommon on LI

28
Q

Which species is resistant to pseudorabies?

a. canine
b. equine
c. ovine

A

B

all ruminants susceptible!

29
Q

In regard to clinical signs, affected nerves, treatment options, and case management of Listeriosis, choose all that apply.

a. affected cattle are often blind
b. cranial nerves are usually affected unilaterally
c. treatment is seldom effective and immediate slaughter should be considered

A

B

29
Q

A CSF tap of a Listeriosis case would most likely present as…

a. mostly mononuclear cells
b. mostly neutrophils
c. normal

A

A

30
Q

What cattle are most commonly affected by thromboembolic meningoencephalitis (TEME)? What clinical signs are characteristic? What causes it?

A

feedlot cattle in winter months

blindness, somnolence, and death

Histophilus somni

31
Q

What clinical signs are associated with TEME? What other forms are seen?

A
  • acute onset of anorexia, staggering, fever, and depression
  • BLINDNESS
  • paralysis, tonic-clonic seizures, opisthotonos
  • cranial nerve paralysis
  • proprioceptive deficits with knuckling and crossing over

pneumonia and polyarthritis

32
Q

What are 3 ways of diagnosing TEME?

A
  1. CBC - inflammatory leukogram, not specific, but r/o Listeriosis
  2. CSF - neutrophilic, high RBCs and proteins, xanthochromia
  3. culture brain and kidney - H. somni dies rapidly on swabs and should be plated rapidly (samples from CSF and joint fluid are difficult to culture)
33
Q

What post-mortem signs are indicative of TEME? What are 3 other differentials?

A

CNS vasculitis, infarction, and abscess formation into shotgun lesions

polioencephalopathy, lead poisoning, water intoxication —> BLINDNESS

34
Q

What treatment is indicated for TEME? When is prognosis fair to good?

A
  • antibiotics - OTC
  • fluids and electrolytes
  • anticonvulsants as needed

if still ambulatory —> downer = poor

35
Q

What risk factors are associated with TEME? What is the pathophysiology?

A

winter + feedlot + shipping fever (stress!!)

  • enter via the respiratory system and causes bacteremia
  • bacteria travels to brain and causes thrombosis in smaller vessels, which exposes subendothelial collagen
  • this initiates blood-clotting cascade
36
Q

Is vaccinated feedlot cattle against TEME worthwhile?

A

(H. somni) —> YES, ~ $1 per dose, higher morbidity in feedlots now + a very effective vaccine!

37
Q

What ruminant is most commonly affected by meningitis? What signs are seen?

A

passive failure calves

  • hyperesthesia - slight tactile stimulation = sudden extension of the limbs and opisthotonus(like BSE in older cows!)
  • seizures, blindness
  • depression, fever, diarrhea, sinusitis, otitis
  • normal to hyperesthetic spinal reflexes
38
Q

What is the best test for diagnosing meningitis? What 5 findings are indicative?

A

CSF tap +/- C&S and CBC

  1. neutrophilic pleocytosis
  2. increased proteins
  3. turbid to white fluid that can be foamy or clot
  4. Gram stain reveals bacteria
  5. negative for glucose (usually 40-90)- bacteria use up glucose for energy
39
Q

What 4 treatments are recommended for meningitis?

A
  1. broad (to negative) spectrum antibiotics - 4-6 weeks, damaged BBB allows most to reach brain, Ceftiofur recommended (tetracyclines and penicillins have poorer penetration)
  2. anti-inflammatories
  3. fluids - plasma, ringers, electrolytes, glucose
  4. anticonvulsants - Diazepam
40
Q

How do most ruminants develop meningitis?

A
  • hematogenous
  • direct inoculation due to skull fractures, otitis, sinusitis, or dehorning injuries
41
Q

How is meningitis development controlled? What is prognosis like?

A

ensure adequate colostral intake

fair to poor - case fatality high, early recognition and treatment necessary

42
Q

What is the minimum amount of beef cow colostrum necessary to ensure adequate passive transfer to calves? Dairy cows?

A

2 quarts

1 gallon —> colostrum is more dilute

43
Q

What ruminant is most commonly affected by meningitis from dehorning injuries?

A

goat kids —> loose bone and hair fall into the sinus

44
Q

When do calves develop dehorning injuries that can lead to meningitis?

A

if the hot iron is too small —> need to be kept on the horn longer, leading to direct damage to the skull

= heat meningitis

45
Q

You are presented with a 10 m/o Holstein heifer with acute onset of head pressing, depression, anorexia, and occasional circling. What is the most likely disease?

a. BSE
b. Listeriosis
c. TEME
d. IBR

A

B

  • dairy cattle = TEME less likely
  • circling!
  • good chance of recovery when caught and treated early —> bicarbonate fluids (drooling + can’t swallow saliva), antibiotics (OTC, Penicillins), NSAIDs
  • will have mononuclear CSF
46
Q

What is the prognosis of brain abscesses like?

A

poor without surgical drainage and long-term antibiotics

  • no economical solutions
  • neurological signs depend on location
47
Q

What signs are indicative of brain abscesses? How is it diagnosed?

A

normal vital signs with slow onset of asymmetric neurological signs

CSF/CBC = inflammatory

48
Q

What treatments are necessary for brain abscesses? What are some risk factors for development?

A

antimicrobial therapy and surgical drainage —> walled out abscess and BBB do not allow antibiotic therapy to work alone, will response and relapse after treatment stops without drainage

  • dehorning
  • sinusitis
  • inner ear infection
  • nasal FB
49
Q

What is the most common etiologic agent of brain abscesses? What causes signs?

A

Trueperella pyogenes

compression > inflammation

50
Q

What is the most common cause of pituitary abscesses in ruminants? How does most commonly get to the pituitary>

A

Trueperella pyogenes > Corynebacterium, Actinobacillus, Arcanobacterium

nasal FB causes itchy allergic rhinitis and invasion into rete mirabila (vasculature around the pituitary) = hematogenous spread

51
Q

What signs are seen with pituitary abscesses?

A

acute and progression over 7-10 days

  • ataxia
  • head and neck extension
  • inappetence, depression, bradycardia
  • wide-based stance, head-pressing
  • asymmetric CN deficits with dysphagia, blindness, anisocoria, lack of PLR, mydriasis, lack of tongue tone, nystagmus, facial paralysis, ventrolateral strabismus, head tilt
  • recumbency, coma, death
52
Q

Pituitary abscess:

A
53
Q

What is tetanus? What signs are associated?

A

progressive muscular rigidity due to Clostridium tetani neurotoxin

  • saw horse stance, airplane ears —> limbs resistant to passive flexion
  • head and neck extension
  • retracted lips, trismus (lockjaw)
  • lateral recumbency becomes worse with auditory, ocular, or tactile stimuli
  • respiratory paralysis = death
54
Q

What history is associated with tetanus development? Why is diagnosis difficult without considering signs?

A
  • castration
  • parturition
  • tail docking

no reliable clinicopathological tests, no characteristic lesions on necropsy —> can culture suspected site of entry, but it may be unknown by the time of diagnosis

55
Q

Tetanus, cytology:

A

tennis rackets

56
Q

Tetanus:

A
  • rigid flexion —> sawhorse, opisthotonos
  • sheep more susceptible
57
Q

How is tetanus treated? What are 4 ways this is done?

A

eliminate toxin

  1. debride affected area
  2. infuse KPen or PPG around wound margins or IV
  3. tetanus antitoxin - only binds free toxins, need 50000-100000 IU once
  4. tetanus toxoid - natural exposure for immune response given at a more distant site compared to antitoxin
58
Q

What supportive treatments are used for tetanus?

A
  • antibiotics - also protects against aspiration pneumonia
  • muscular relaxation - place in a quiet and dark area, pack ears with cotton, tranquilize as needed
  • TLC - good footing, fluids, nutrition
  • rumenostomy - bloat, easy feeding and hydration
59
Q

Where is Clostridium tetani most commonly found?

A

soil and feces —> commonly enters via the uterus

  • sporadic / epidemic with elastrators
  • incubation period of 2 weeks to a month
60
Q

What is responsible for clinical signs of tetanus?

A

tetanospasmin - binds to nerves and is transported into the CNS

  • crosses synaptic clefts to presynaptic inhibitory interneurons in the spinal cord
  • inhibits release of glycine and GABA from Renshaw cells
  • results in disinhibition of gamma motor neurons and hypertonia/muscular spasms
61
Q

What promotes the spread of tetanus?

A

tetanolysin —> increases local tissue necrosis

62
Q

How is tetanus controlled?

A

vaccine —> not routine in cattle (but is in sheep and goats!)

  • good for problem herds or situations with risk factors —> vaccinate mothers 1 month before calving/lambing
  • treatment = $$$$
63
Q

What is botulism? How is it diagnosed?

A

progressive muscular hypotonia from rear to front with no effect on peripheral sensory nerves and CNS, caused by Clostridium botulinum

ID toxin in serum, GI, or food —> present for 6 days!

64
Q

How is botulism treated?

A

(equine origin polyvalent) antitoxin —> effective early with TLC

65
Q

How is botulism transmitted? In what ruminants is this rarely seen? What vaccine is available?

A

preformed toxin in animal carcasses (C), spoiled silage (B) or in the environment (D, caused by pica) is ingested by adult cattle

sheep, goats

type B vaccine for horses

66
Q

What is the most common sign of botulism? What else is seen?

A

flaccid tongue —> NOT weak and unlikely to become a downer (unlike Listeriosis)

other cranial nerve defects (no palpebral reflex)

Large Animal Medicine (34 decks)

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