Flashcards: Neurology

What is the causative agent of Rabies?

Lyssavirus, family Rhabdoviridae

Describe the pathogenesis of Rabies.

Replicates at the site of inoculation, Travels via peripheral nerves to the spinal cord and cranial nerves, Ascends to the brain → Descends to salivary glands and other organs

What are the primary reservoirs of Rabies?

30 known species, including terrestrial carnivores and bats; Most important: Dogs (globally), Cats (most reported domestic cases in the U.S.)

How is Rabies transmitted?

Virus-laden saliva through bite wounds; Aerosol transmission unlikely (except in densely populated bat caves)

What are the clinical signs of Rabies?

Suggestive signs: Acute behavioral changes, aggression, progressive paralysis, altered phonation; 3 Phases: Prodromal (1-3 days): Nonspecific signs, Acute Excitative ("furious" form): Hyperexcitability, aggression, Paralytic/End Stage: Death from paralysis

How is Rabies diagnosed?

Clinical signs are suggestive, but lab confirmation is required; Gold Standard: Direct immunofluorescence (IFA) on fresh brain tissue; PCR assay may also be used

What are the key prevention and control measures for Rabies?

Vaccination: Inactivated, recombinant (MLV not available in the U.S.); Post-exposure prophylaxis (PEP): Wound care + Rabies immune globulin + Vaccination; Stray population management, public education, oral wildlife vaccines

What are the regulatory aspects of Rabies?

Reportable disease; Unvaccinated animals exposed to Rabies: Unclaimed: Euthanize immediately; Owned: Immediate vaccination + 4-6 months strict isolation; Vaccinated animals: Immediate revaccination + 45-day observation

What is the causative agent of Pseudorabies (Aujeszky’s Disease)?

DNA Herpesvirus

How is Pseudorabies transmitted?

Direct contact, fecal-oral, aerosol

What are the clinical signs of Pseudorabies?

Young pigs: CNS disease, tremors, high mortality; Weaned pigs: Respiratory disease, lower mortality; Other species: Intense pruritus, sudden death

How is Pseudorabies diagnosed?

Clinical signs + Serology/PCR/Virus isolation

What are the key prevention and control measures for Pseudorabies?

Vaccination (MLV); Quarterly vaccines for breeding herds; U.S. commercial swine industry is free of Pseudorabies

What are the causes of Polioencephalomalacia (PEM)?

High-concentrate diets, High sulfur intake, Thiamine deficiency

What are the clinical signs of Polioencephalomalacia (PEM)?

Acute form: Blindness, ataxia, recumbency, seizures, coma; Subacute form: Anorexia, isolation, head-pressing, stargazing

How is Polioencephalomalacia (PEM) diagnosed?

Presumptive: Response to thiamine treatment; Definitive: Necropsy

How is Polioencephalomalacia (PEM) treated?

Thiamine administration, Supportive care, Dietary modification for prevention

What are examples of Prion Diseases?

Bovine Spongiform Encephalopathy (BSE), Scrapie, Chronic Wasting Disease

How are Prion Diseases transmitted?

BSE: Foodborne (meat & bone meal contamination); Scrapie: Oral/environmental contamination

What are the clinical signs of Prion Diseases?

BSE: Progressive nervous system decline, ataxia, aggression, weight loss; Scrapie: Pruritus, ataxia, gait abnormalities, weight loss

How are Prion Diseases diagnosed?

Postmortem tests: ELISA, Western blot, IHC

What are the key control measures for Prion Diseases?

BSE: Ban on meat & bone meal, removal of specified risk materials (SRMs); Scrapie: Genetic selection, depopulation, import restrictions

What is the causative agent of Equine Protozoal Myeloencephalitis (EPM)?

Sarcocystis neurona

How is Equine Protozoal Myeloencephalitis (EPM) transmitted?

Opossum feces contaminate feed/water

What are the clinical signs of Equine Protozoal Myeloencephalitis (EPM)?

Asymmetric ataxia, muscle atrophy, cranial nerve abnormalities

How is Equine Protozoal Myeloencephalitis (EPM) diagnosed?

CSF-to-serum antibody ratio

How is Equine Protozoal Myeloencephalitis (EPM) treated?

Antiprotozoal drugs, supportive care.