FAD Quiz 3

What is the most commonly seen form of Rabies?

Furious Form (animal is aggressive and attacks without being provoked)

What do you do with an animal that has signs of Rabies but it may be a similarly presenting disease?

Strict quarantine for 6 months

What are CS of Rabies?

-Behavioral changes
-Tenesmus
-Salivation (mouth foaming)
-Progressive lameness
-Ataxia
-Posterior paresis

What is the causative agent of Tetanus?

Clostridium tetani (anaerobic gram positive bacteria)

What types of situations with ruminants are Tetanus outbreaks seen in?

-Castration
-Shearing
-Docking
-Vaccinations or injections
-Wounds
-Postpartum metritis

What is the common name of Tetanus?

Lock Jaw

What are CS of Tetanus?

-Change in gait (First CS is a stiff gait)
-Bloat
-Rigid limb extension
-Raised tail head
-Tetany of facial muscles (trismus)
-Locked jaw
-Prolapsed third eyelid

How is Tetanus diagnosed?

-CS (muscular spasms, erect head, 3rd eyelid flashing)
-Presence of a wound, history of a recent surgery, or calving
-Direct smears from wound or spleen help with confirmation (gram positive rods with terminal spores)

How can Tetanus be treated?

-place the animal is a dark, quiet environment
-Eliminate: doses of penicillin and wound cleaning
-Neutralize: antitoxin (3-5 days)
-relieve muscle spasms (acepromazine, diazepam, or guaifenesin)
-Good nursing (fluids and nutrition)

How can Tetanus be prevented?

-large ruminant farms should vaccinate if there are multiple incidences
-vaccination recommended in small ruminants

What is the causative agent of Botulism?

Clostridium botulinum

When is botulism seen?

-after feeding solage stored in plastic bags (most common cause)
-consumption of carrion

What are CS of Botulism?

-Weak tongue tone
-Dysphagia
-Drooling
-Generalized muscle weakness
-Tremors
-Recumbency
-Dilated pupils / poor PLR
*FLACCID PARALYSIS*

How is Botulism diagnosed?

-CS ad exclusion of other diseases
-ID of spore in feed, feces, or GI contents
(there are usually no pathologic lesions)

How can Botulism be treated?

-Nutritional support (flaccid paralysis may make eating difficult/impossible)
-Nursing a recumbent patient (turn every 4-6 hours)
-Bovine origin antitoxin is available

How can Botulism be prevented?

-Toxoid is commercially available
-Remove any decaying or spoiled silage
-Proper carcass disposal

What are signs that a Botulism infection will have a poor prognosis?

-when an animal goes down, the prognosis decreases
-if the animal goes down in less than 24 hours post exposure
-Dyspnea (death comes next)

What diseases are similar in appearance to Botulism?

Rabies, BSE, Milk fever, listeria

What is the causative agent for Listeriosis?

Listeria monocytogenes (gram positive rod found in soil, silage, and feces)

What does Listeriosis cause?

microabscesses in the brain

When is Listeria more likely to be seen?

in older animals, and cases are more frequent in the winter

What are CS of Listeriosis?

-Fever, anorexia
-Knuckling, weakness, paralysis
-Lips droop, unable to blink
-Head tilt\***
-Circling/ataxia
-Dysphagia
-Abortions (late gestation)
-Septicemia

How is Listeriosis diagnosed?

-History and CS (presumptive)
-Necropsy (definitive)

How can you treat Listeriosis?

-Antibiotics (penicillin, ampicillin, amoxicillin, aminoglycosides, macrolides
NSAIDs (pain relief)
-Supportive care (fluids, nutrition)

How can Listeriosis be prevented?

Adequate silage preparation

What causes Polioencephalomalacia?

A deficiency in Thiamine (Vitamin B1)

What animals are most at risk for Polioencephalomalacia?

calves from 2-12 months of age (still getting their rumen microbial activity established)

What are some situations where Thiamine production could decrease or thiamine destruction could increase?

-Grain overload
-Sudden diet change

Why is Thiamine important?

it is needed for CHO metabolism to glucose
(decrease in glucose metabolism in the brain leads to cerebral edema and necrosis)

What are CS of Polioencephalomalacia?

-Anorexia
-Ataxia
-Head-pressing
-Dorso-medial strabismus ("star gazing")
-Recumbency
-Opisthotonus (back tilting of the head and neck)
-Convulsions
Death within a few days

How is Polioencephalomalacia diagnosed?

-CS and response to treatment (presumptive)
-Postmortem (definitive)

How can Polioencephalomalacia be treated?

-Thiamine (response w/in 2-12 hours)
-Corticosteroids and mannitol (cerebral edema)
-Diazepam (convulsions)
-Transfaunation

What is Hypomagnesemia also know as?

Grass Tetany

What is the caused of Hypomagnesemia?

Magnesium deficiency

When can Hypomagnesemia be seen?

-reduction in food intake in weather
-transport
-when cows graze pasture low in Mg (lush, immature pasture)
-Calves raised indoors on milk

What are the CS of Hypomagnesemia?

-Anorexia
-Isolation
-Hyperexcitable
-Tetanic muscle spasms
-Ataxia
-Violent convulsions
-Death

How is Hypomagnesemia diagnosed?

-CS and history
-Response to therapy

How is Hypomagnesemia treated?

-IV admin of Calcium borogluconate and Magnesium hypophosphate
(don't stimulate animals to rise for 30 mins after treatment)

How soon will cattle get up following treatment for Hypomagnesemia?

within 1 hour of treatment

Why is calcium administered for Hypomagnesemia?

it goes with the magnesium because straight magnesium can lead to heart failure

What is the most common metabolic disease in dairy cattle?

Hypocalcemia (Milk Fever)

What percentage of cases of Hypocalcemia occur within 24 hours of calving?

75%

What is Hypocalcemia caused by?

a sudden loss of calcium due to the initiation of lactation

What are the CS for Hypocalcemia?

-Stage 1 (mild excitement, tetany without recumbency, weak rumen contractions, tachycardia, hyperthermia)
-Stage 2 (sternal recumbency, flaccid paralysis, fine muscle tremors, cold extremeties, mild bloat, loss of anal reflex, constipation, pupil dilation)
-Stage 3 (lateral recumbency, progressively lose consciousness, severe bloat, compromised CO)

How is Hypocalcemia diagnosed?

-Response to treatment
-Low serum calcium levels

How is Hypocalcemia treated?

-Stage 1 \= oral calcium or IV calcium gluconate
-Stage 2 or 3 \= immediate treatment with IV calcium gluconate (not oral admin)

How is Hypocalcemia prevented?

historically, we lowered Ca intake during dry period (at least 10 days before calving)

What is the causative agent of Cerebrospinal Nematodiasis in cattle?

Hypoderma bovis

How does Hypoderma bovis cause Cerebrospinal Nematodiasis?

-larvae burrow into skin , into the spinal canal, and lie dormant in epidural fat unless killed (release proteins that cause edema and inflammation at death)

When is it most common to see Cerebrospinal Nematodiasis caused by Hypoderma bovis?

between July and October

What are CS of Cerebrospinal Nematodiasis caused by Hypoderma bovis?

Usually seen 24/72 hours after anthelmintic admin:
-Ataxia
-weakness
-Proprioceptive deficits
-altered limb reflexes
(Hind limbs usually more commonly affected\---larva prefer the lumbosacral region)

How is Cerebrospinal Nematodiasis caused by Hypoderma bovis diagnosed?

-CS, history of parasite treatment
(definitive diagnosis only at necropsy)

How is Cerebrospinal Nematodiasis caused by Hypoderma bovis treated?

-symptomatic (steroids and nosteroidal anti-inflammatories)
-Euthanasia for animals with severe damage to spinal cord and remain recumbent

How can Cerebrospinal Nematodiasis caused by Hypoderma bovis be prevented?

Appropriate timing of systemic anthelmintic treatments

What is the causative agent of Cerebrospinal Nematodiasis in small ruminants?

Parelaphostrongylus tenuis

What is the most common species affected by Cerebrospinal Nematodiasis caused by Parelaphostrongylus tenuis?

White-tailed deer

What are CS of Cerebrospinal Nematodiasis caused by Parelaphostrongylus tenuis?

In normal sites (usually BAR):
-Paraplegia/ paraparesis/ tetrapalegia/ tetraparesis
-Posterior ataxia that progresses to recumbency
When in aberrant site and causes Brain Stem Disease:
-depressed sensorium
-conscious proprioceptive deficits
-Cranial nerve deficts

How is Cerebrospinal Nematodiasis caused by Parelaphostrongylus tenuis diagnosed?

-CS and CSF evaluation (presumptive)
-Necropsy (definitive)

How is Cerebrospinal Nematodiasis caused by Parelaphostrongylus tenuis treated?

-multiple high doses of anthelmintics (IVERMECTIN, fenbendazole, moxidectin)
-NSAIDs and dexamethasone
-Supportive care

How can Cerebrospinal Nematodiasis caused by Parelaphostrongylus tenuis be prevented?

-Frequent deworming
-reduce exposure to white-tailed deer

What is the causative agent for Neosporosis?

Neospora caninum

How is Neospora caninum passed to ruminants?

Dogs pass oocysts in feces that contaminates food/water for cattle, and tachyzoites can be passed through the placenta and infect the fetus

How are CS of Neosporosis?

-Recumbency
-Lethargy
-Difficulty rising
-Ataxia
-Opisthotonus
-Seizures
-Affected calves are usually smaller than normal

How is Neosporosis diagnosed?

-not much to go on antemortem
-definitive diagnosis at necropsy
-serological titers can be used

How can Neosporosis be treated?

No treatment (cattle are infected for life)

How can Neosporosis be prevented?

-prevent canine access to feed
-cull seropositive cows

What are the 3 categories of cerebellar disease?

-In utero or neonatal viral infection (CS at birth)
-Malformation of genetic or unknown cause
-Degenerative diseases (abiotrophies)

What are CS of Cerebellar Diseases?

-Hypermetria (over-exaggerated walking)
-Base-wide stance
-Truncal ataxia
-Intention tremor

What are diseases known to be able to cause cerebellar disease?

-BVDV (90-170 days of gestation)
-Border Disease Virus (mainly sheep, CS depend on age, no treatment, no vaccine)
-Bluetongue Virus (most common CNS defect is hydraencephaly, vaccine available in endemic areas)

What ages have CS of Cerebellar Disease caused by Border Disease Virus?

-Adults and newborn lambs are usually asymptomatic
-newborns infected 16-80 of gestation show CS that generally gradually disappear within 3-4 months

What causes cerebellar disease genetically?

An autosomal recessive trait

What is Cerebellar Abiotrophy?

-premature death of cerebellar tissue
-CS usually develop at 3-9 months of age

What breeds are most reported when it comes to cerebellar diseases with genetic or unknown causes?

-Hereford
-Shorthorn
-Aberdeen angus

What breeds are most reported when it comes to cerebellar diseases related to cerebellar abiotrophy?

-Holstein
-Charolais
-Limousine
-Angus

What happens with an Obturator Nerve Injury?

-occurs as a complication of dystocia (especially with first calving)
-using too much force to deliver an oversized, malpositioned fetus is a common cause

What is Calving Paralysis?

calving damages both the obturator and sciatic nerves
-loss of adductor function and knuckling of distal hind limb joints
-no loss of cutaneous sensation (pain)

What are CS of an Obturator nerve injury?

-Hopping gait
-Splay legged
-unable to rise in a "frog-like" position
-cows legs split on slippery surfaces

How is an Obturator nerve injury diagnosed?

CS and history

How is an Obturator nerve injury treated?

-Reduce Inflammation (Dexamethasone, Phenylbutazone)
-Pain relief (Banamine, Phenylbutazone)
-Stall rest
-Turn recumbent animals 6-8 times a day
-Hobbles (prevent splitting)

What does BSE stand for?

Bovine Spongiform Encephalopathy

What is BSE caused by?

an abnormal protein in brain tissue called a prion that can cause fatal disease when ingested (REPORTABLE)

How was BSE spread?

when cattle ingested contaminated "ruminant" meat and bone meal as a dietary supplement (Banned in 1997 in the US)

Where have 95% of cases of BSE been reported?

in the UK

What are CS of BSE?

-Hyperexcitability
-Anxious/Apprehensive
-Sensitive to sound and touch
-Aggression
-Ataxia
-Facial/ear twitching

How is BSE diagnosed?

History and CS or a histopath of the brain (obex)

How is BSE treated?

Euthanasia

What is Chronic Wasting Disease (CWD)?

a prion that affects deer, elk, reindeer, and moose found in some areas of North America (REPORTABLE)

What parts of the animal does CWD affect?

brain, spinal cord, and other tissues

Is CWD zoonotic?

Not proven, but there is no strong evidence of CWD occuring in humans

How is CWD transmitted?

direct contact or environmental contamination with infected animals body fluids

What are CS of CWD?

-Wasting
-Lack of coordination
-Aggression
-Fearlessness of humans
-Polyuria/polydipsia
-Drooling
-Listlessness
-Drooped ears

How is CWD diagnosed?

-CS are NOT diagnostic, only suggestive
-obex examination

How is CWD treated?

no treatment or vaccine available

What is the causative agent of Blackleg?

Clostridium chauvoei

What is blackleg associated with?

-ingestion of endospores
-animal does not need a wound to contract this
-generally affects animals 6 months to 2 years old
-Death comes in 12 to 48 hours
-Penicillin may help

What is the causative agent of Malignant Edema?

Clostridium septicum

What is Malignant Edema associated with?

-develops when an open wound gets infected
-causes edema
-death occurs quickly

What is the causative agent of Red Water?

Clostridium haemolyticum

What is Red Water associated with?

-spores lodge in the liver, reliant of liver flukes damaging the tissue enough to invade
-attacks RBCs
-Early treatment is essential

What is the causative agent of Black Disease?

Clostridium novyi type B