Lecture 12: Continuation of Bacterial & Intro to "Other" Causes of Neurological Disease in Ruminants

What is the prognosis of a brain abscess?

very poor without surgical drainiage and long term antibiotics

What are the clinical signs of a brain abscess?

• Vital signs normal, slow onset, asymmetric

• CSF/CBC: inflammatory to normal

• Adults to young adults; other pyogenic process

• Dehorning/sinusitis/inner ear infections, nasal foreign bodies are risk factors

• Trueperella pyogenes

• Signs due to compression rather than due to inflammation

What is the common etiologic agent of pituitary abscesses in ruminants?

Trueperella pyogenes

What are the clinical signs of pituitary abscesses?

• acute signs progress rapidly over 7-10 day period

• general: ataxia, head and neck extension, inappetence, depression, bradycardia

• neurologic: base-wide stance, ataxia, head-pressing, asymmetric CN deficits with dysphagia, blindness, anisocoria, lack of papillary light reflexes, mydriasis, lack of tongue tone, nystagmus, facial paralysis, ventrolateral strabismus, and head tilt

• eventually recumbency, coma, and death

What might predispose an animal to a pituitary abscess?

plant foreign bodies

What are the clinical signs of tetanus?

• Initially stiff, “airplane ears”, sawhorse stance, hypertonia, retracted lips, trismus (“lockjaw”)

• Lateral recumbency & muscular rigidity that becomes worse with auditory, ocular, or tactile stimuli

• Eventual respiratory paralysis and death

How is tetanus diagnosed?

• Limbs & head resistant to passive flexion

• History...castration, parturition, tail docking

• No reliable clinicopathological tests

• Necropsy: no characteristic lesions

• Culture suspected site of entry

What is the treatment for tetanus?

• eliminate toxin - remove existing and future toxin → debride the affected area and infuse penicillin around wound margins

• tetanus antitoxin: binds free tetanus toxin only

• tetanus toxoid: no natural exposure immune response, give at a distant site to the tetanus antitoxin

• Muscle relaxation, antibiotics, TLC, and consider rumenostomy (temporary)

How is tetanus spread?

• sporadically in the soil and feces

• incubation period is 2 week and 1 month

• entry via the uterus is common in dairy cattle

What is the toxin responsible for tetanus and what is its pathogenesis?

tetanospasmin: binds to nerves and transported to CNS → at spinal cord, crosses synaptic cleft to presynaptic inhibitory interneurons → inhibits release of glycine and GABA from Renshaw cell → results in disinhibition of gamma motor neurons and hypertonia and muscular spasms

What does tetanolysin do?

promotes spread by increasing local tissue necrosis

What organism causes progressive muscular hypotonia from the rear to the front, but has no effect on peripheral sensory nerves and CNS?

clostridium botulinum

What is the treatment for botulism?

• antitoxin effective early + TLC

• healing is based on the decay of bound botulism toxin at the nerve → can take weeks to months to form new synapses

What are common signs of botulism in cattle?

flaccid tongue and other cranial nerve deficits (no blink)

Explain the relationship between botulinum toxin and SNARE protein?

• SNAp REceptor: Aids in fusion of vesicles of neurotransmitters

• Botulinum toxin: Cleaves SNARE proteins and prevents fusion of vesicle

Cannot release neurotransmitter

What organism commonly causes otitis media and how is it spread?

mycoplasma bovis

source is thought to be contaminated milk/colostrum

What is the treatment of otitis media?

• Appropriate antimicrobial: Florfenicol, tulathromycin; Consider mycoplasma coverage

• +/- Myringotomy

• +/- TBO

What diffuse cerebral disease causes aggression, convulsions, central blindness, wandering, head pressing, opisthotonos, odontoprisis, bellowing, and eventual death?

lead poisoning

What clinical pathologic sign is characteristic of lead poisoning?

CBC: basophilic stippling and nucleated RBCs

What is the therapy for lead poisoning?

• Urinary lead excretion following Ca EDTA, D-Penicillamine, or succime treatment

• Treat with thiamine as well

• Magnesium sulfate laxatives help form insoluble lead sulfides

What toxin is contained in locoweed and what effect does it have?

• toxin is swainsonine

• Leads to a storage disease similar to mannosidosis

• Swainsonine inhibits alpha- mannosidase → Accumulation of materials and vacuolation of the neurons

• Quick removal of the toxin can be reversible

• However, chronic exposure is irreversible

What can locoweed ingestion cause at high altitudes?

congestive heart failure

What is the pathogenesis of organophosphates?

inhibit the recycling of inhibitory acetylcholinesterase

You are called to examine a neurologic and recumbent pig in January. You notice the water source is frozen. What is your top differential

salt poisoning (overload of salt or lack of water intake)

What is the treatment for salt poisoning?

• Slowly!!! Decrease the sodium levels → Quick/fast administration of significantly less osmolar substances will lead to water intake into nervous tissue → Cells burst

• Infrequent PO offering of water

• Calculating and IV administration of slightly less osmolar fluids

What are the clinical signs of vitamin A deficiency?

• Reduced feed intake and growth

• Rough hair coat

• Blindness
• Night blindness

• Edema

• Diarrhea
• Seizures
• Decreased reproductive and growth performances

What neurologic effect does vitamin A deficiency have?

central blindness: abnormal bone development constricts optic nerve (prominent blindness not reversible)