Lecture 12: Bacterial and Other Causes of Neurologic Disease

brain abscess prognosis

very poor without surgical drainage and long term antibiotics

brain abscess clinical signs

• vital signs normal, slow onset, asymmetric

• CSF/CBC: inflammatory to normal

• antimicrobial therapy and surgical drainage for success

• adults to young adults

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

• trueperella pyogenes

• signs due to compression rather than due to inflammation

pituitary abscess

defined as a relatively rare abscess of the pituitary often caused by trueperella pyogenes in ruminants

pituitary abscess clinical signs

• acute and progress rapidly over a 7-10 day period

• general signs include ataxia, head and neck extension, inappetence, depression, and bradycardia

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

• eventually recumbency, coma, and death

pituitary abscess EEP

• pyogenic infection of the head may predispose → vegetative foreign material

• agent reaches pituitary via hematogenous spread

what is this?

pituitary abscess

plant foreign bodies

• remnants of 5-inch thorny stick was removed from the right nasal passage and along with the heat, was determined to be the cause of the open mouth breathing → allergic rhinitis, rete mirabilia

• also consider fox tails and plant awns

tetanus

progressive muscular rigidity due to a clostridium tetani neurotoxin → gram + rod

tetanus clinical signs

• initially stiff, airplane ears, sawhorse stance, hypertonia, retracted lips, trismus (lockjaw)

• lateral recumbency and muscular rigidity that becomes worse with auditory, ocular, or tactile stimuli → eventual respiratory paralysis and death

tetanus diagnosis

• limbs and head resistant to passive flexion

• history → castration, parturition, tail docking

• no reliable clinicopathological tests

• no characteristic lesions on necropsy

• culture suspected at site of entry

tetanus treatment

• eliminate toxin → remove existing and future toxin

• tetanus antitoxin → binds free tetanus toxin only → 50,000 to 100,000 once

• tetanus toxoid

• antibiotics

• muscular relaxation

• TLC

• consider rumenostomy

cannulation for rumen fluid collection and enteral feeding

• sources → cannulated cow, animal at slaughter, oral collection

• use → ASAP, can be started short term

tetanus EEP

• soil and feces

• sporadic but epidemics reported

• incubation period is 2 weeks and 1 month

• entry via the uterus → common in dairy cattle

tetanospasmin

• toxin responsible for clinical signs

• 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 indisinhibition of gamma motor neurons

• results in hypertonia and muscular spasms

tetanolysin

promotes spread of tetanus by increasing local tissue necrosis

tetanus vaccine

not routine in cattle (should be routine in sheep and goats)

tetanus mortality is

up to 80%

botulism

• progressive muscular hypotonia → rear to front, no effect on peripheral sensory nerves and CNS

• clostridium botulinum

• ID toxin in serum, GI, or food

• antitoxin is effective early, TLC

botulism incubation period is

1-7 days

botulism performed toxin

• animal carcasses (type C)

• spoiled silage (type B)

• pica (type D)

botulism snare protein

• SNAp REceptor → aids in fusion of vesicles of neurotransmitters

• botulinum toxin → cleaves snare proteins and prevents fusion of vesicle

botulism treatment

• EQ → antitoxin and toxoids

• healing is based on the decay of bound botulism toxin at the nerve

• supportive care

otitis media

• commonly due to infections by mycoplasma bovis

• can see concurrent infections with respiratory disease and arthritis

• source is thought to be contaminated milk/colostrum

otitis media radiographs

may show opacification of the tympanic bulla (normally air filled)

what is this?

otitis media with opacification of tympanic bulla

otitis media therapy

• appropriate antimicrobial

• ± myringotomy

• ± TBO

• full recovery 60%

lead poisoning

• a diffuse cerebral disease

• aggression, convulsions, central blindness, wandering, head pressing, opisthotonos, odontoprisis, bellowing, and eventual death

• CBC → basophilic stippling and nucleated RBCs

what is this?

lead poisoning histology

lead poisoning therapy

• urinary lead extraction following Ca EDTA, D-penicillamine or succine treatment

• treat with thiamine as well

• magnesium sulfate laxatives help form insoluble lead sulfides

sources of lead poisoning

lead paint, linoleum, caulking compounds, batteries (auto), old machinery oil or grease, etc

lead poisoning control

• minimize contact

• other mineral deficiencies can enhance lead absorption

lead poisoning prognosis

fair with aggressive and early treatment

locoweed

• species of oxytropis and astragalus

• toxin is swainsonine

• at altitudes it can lead to heart failure

swainsonine

• leads to a storage disease similar to mannosides

• inhibits alpha-mannosidase

• quick removal of the toxin can be reversible

• chronic exposure is irreversible

organophosphate

• OP vary considerably in potency → inhibit the recycling of inhibitory acetylcholinesterase

• differential for rear end weakness and flaccid paralysis

• treatment often unsuccessful → atropine, cholinesterase reactivators, emetics, cathartics, etc

salt poisoning

• overload of salt or lack of water intake

• aggressiveness then recumbency to coma

• diagnostic history → distance to water or frozen water or lack of water

• serum and CSF Na markedly elevated

• histopath → brain edema and cortical lesions

salt poisoning treatment

• slowly decrease sodium levels

• quick/fast administration of significantly less osmolar substances will lead to water intake into nervous tissue and cell bursts

• infrequent PO offering of water

• calculating and IV administration of slightly less osmolar fluids

vitamin A deficiency

• characterized by central blindness due to vitamin A deficiency

• occurs primarily when stock does not have access to succulent plants

• abnormal bone development constricts optic nerve

• calves born with normal levels may require supplementation

• prominent blindness not reversible

what is this?

calf born with micropthalmia from vitamin A deficiency

clinical signs of vitamin A deficiency

• reduced feed intake and growth

• rough hair coat

• blindness

• night blindness

• edema

• diarrhea

• seizures

• decreased repro growth and growth performances