Bacteria Causing Neurological Disease

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Histophilus somni (description)

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Gram - facultative anaerobe, gram (-) bacillus

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Histophilus somni (reservoir)

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persists at mucosal sites in diseased and subclinical animals, transmission by inhalation

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Histophilus somni (disease)

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respiratory disease and can cause TME thrombotic meningoencephalitis, usually seen in feedlot cattle, usually affects cattle 6-12 months of age, stress contributes to disease, neurological signs are usually preceded for 1-2 weeks by dyspnea and a dry harsh cough

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Histophilus somni (signs)

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recumbency, ataxia, fever, weakness, knuckling, crossing over, eyes are partially or fully closed, rapidly fatal in 8-12 hours

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Histophilus somni (pathogenesis)

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multiplies inside mac’s, virulence attributes include transferrin iron binding protein, Ig binding proteins, varying the lipooligosaccharide (LOS) induces apoptosis in endothelial cells, leading to collagen exposure, thrombus formation and vasculitis, leads to multifocal hemorrhage necrosis in the brain, vasculitis

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Histophilus somni (diagnosis)

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gram - , typically at necropsy, grows on blood agar and chocolate agar (10% CO2), small yellowish dewdrop colonies appear in 24-48 hours

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Histophilus somni (prevention and treatment)

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Bacterin of Histophilus somni is available, IV tetracycline, once one is diagnosed, often administer prophylactic to rest of herd

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Listeria monocytogenes (description)

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bacilli, gram positive, facultative anaerobe

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Listeria monocytogenes (reservoir)

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widespread in nature, acquired by ingestion, more common in the winter, called silage disease, found in silage not acidic enough, commonly called circling disease, causes encephalitis, lesions on the brain stem typically on one side, see unilateral neurological signs such as facial droop, circling, zoonotic via ingestion, seen in pregnant women (abortion) and immunocompromised individuals. see perivascular cuffing

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Listeria monocytogenes (virulence factors)

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1. internalin: used to induce uptake phagocytosis,
2. listeriolysin: pore forming toxin, allows escape from the vacuole into the cytoplasm
3. ActA: cell surface protein that activates actin, used for mobilization in cells and between cells, once in the cell never need to be extracellular again, can move from Macs to neurons, cause damage by replicating in the cell, can be killed by cell mediated immunity (activated macs)

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Listeria monocytogenes (diagnosis)

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identification of gram + rods in infected brain tissue. Growth on Blood agar 10% CO, 35 C, subject to cold enrichment, refrigerate brain samples then culture on blood agar (beta hemolytic)

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Listeria monocytogenes (prevention and treatment)

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prevent access to poor quality silage

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Streptococcus suis (description)

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non spore forming gram positive cocci in chains, encapsulated, Type 2 capsule associated with meningitis

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Streptococcus suis (reservoir)

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natural inhabitant of URT, transmission by inhalation and fomites, found in post weaning piglets associated with stress, zoonotic can cause meningitis in humans (sick pigs or raw pork)

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Streptococcus suis (disease)

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see symptoms a few weeks after weaning, disease associated with stress, earliest sign is an increased rectal temperature, fever, anorexia, depression, incoordination, recumbency, paddling, spasms, opisthotonus (arching) and convulsions

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Streptococcus suis (virulence attributes)

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replicates inside macrophages, enters CSF in association with migrating monocytes through the choroid plexus: 1. Adhesions: essential for respiratory tract colonization
2. Suilysin: membrane damaging toxin to brain microvascular endothelial cells

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Streptococcus suis (diagnosis)

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Gram + cocci (in chains) upon meningeal swabbing, alpha hemolytic colonies on blood agar

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Streptococcus suis (treatment and prevention)

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mass medication of animals during an outbreak, resistance to penicillins is common, best method is to reduce stress, there is a bacterin vaccine that sucks

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Clostridium tetani (description)

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gram positive, spore forming bacillus (tennis racket), obligate anaerobe, terminal spores (autoclaving will destroy)

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Clostridium tetani (reservoir)

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widely found in the environment, entry through deep puncture wounds (no O2), remain localized at the site of infection, produce a neurotoxin causing spastic paralysis, spores may remain dormant

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Clostridium tetani (disease)

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spastic paralysis, prolapse of 3rd eye, increased muscle stiffness, muscle tremor, lockjaw, sawhorse posture, remain conscious, death from respiratory arrest

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Clostridium tetani (virulence factors)

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1. Tetanus toxin: horses most susceptible, than cows and sheep then dogs than poultry and cats (who are essentially resistant), travels up peripheral nerves retrograde transport into the CNS and taken up into inhibitory neurons causing decrease release of inhibitory neurotransmitters.
2. Tetanolysin: membrane damaging toxin

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Clostridium tetani (diagnosis)

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smears at wound site, gram positive with terminal spores

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Clostridium tetani (prevention and treatment)

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antibiotic administration, antitoxin and muscle relaxants, Vaccine using tetanus toxoid, make sure to disinfect instruments

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Clostridium botulinum (description)

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gram positive, spore forming bacillus (tennis racket), obligate anaerobe, terminal spores (autoclaving will destroy)

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Clostridium botulinum (reservoir)

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natural in soils and some aquatic sediments, grows on decomposing plant and animal matter, common inhabitant of the alimentary tract of herbivores, acquired usually by ingestion, rarely by wound infections (toxicoinfectious botulism)

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Clostridium botulinum (disease)

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causes flaccid paralysis, incoordination leading to recumbency, in Shaker foal syndrome (C. botulinum serotype B) foals ingest bacteria, in intestine pathogen produces toxin, see animal get up, then drop, muscle tremors cycling, 72 hrs die from respiratory arrest, wound botulism is very rare

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Clostridium botulinum (virulence factors)

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1. C1: botulinum toxin, 7 different antigenic types, some are encoded in a bacteriophage, same type of resistance listed above
2. C2: toxin is dermonecrotic
3. C3: toxin is cytotoxic

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Clostridium botulinum (diagnosis)

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detection of toxin in plasma, detection of toxin in feed

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Clostridium botulinum (prevention and treatment)

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Purgatives to remove toxin from GI tract, antitoxins, in shaker foal syndrome or wound botulism debride wounds treat with anti toxins (before debridement) and antibiotics, vaccine are toxoids need to know prevailing type in area, prevention of Type D by counteracting P or protein deficiences (animals eat carcases)

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Cryptococcus neoformans

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2 variants, always found as a yeast

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Cryptococcus neoformans (reservoir)

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(C. neoformans var. neoformans found in bird droppings), (C. neoformans var gatti found in association with flower buds on eucalyptus trees) yeast found in bird droppings, last for years in droppings, very good N source, other variant found in flower buds of eucalyptus, acquired by inhalation (yeasts and spores), spread to CNS

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Cryptococcus neoformans (Disease)

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localize in the CNS following dissemination from the lungs signs include depression, seizures, circling, head pressing, ataxia, loss of smell, in dogs see eye involvement, dogs most likely to develop signs, sometimes seen in cats, in cats and dogs also see ulcerative lesions in the mouth and in the head

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Cryptococcus neoformans (virulence factors)

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1. polysaccharide capsule inhibits respiratory burst, and phagocytosis
2. melanin (uses Dopa as a precursor) and mannitol scavenge free radicals, protects them in the phagolysosome

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Cryptococcus neoformans (Diagnosis)

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tain CSF exudates with India Ink (looking for capsule), encapsulated yeast with narrow base, capsular polysaccharide antigen can be detected, culture on blood agar (37 C) and Sabouraud's agar (RT) see colonies in a week

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Cryptococcus neoformans (treatment and prevention)

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decontaminate with lime, treat with fluconazole

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Encephalitozoon cuniculi

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microsporidia, obligate intracellular, unicellular “fungi”, ingestion, see in rabbits and puppies (4-10 weeks old), cause encephalitis and nephritis, zoonotic