Viral Pathogens of the Nervous System Flashcards
describe signalment and transmission of rabies
transmission:
-bite from infected animal
-direct contact of infective material to mucous membranes, open wound, spreads to CNS tissue, saliva, and salivary glands
signalment: any age, any warm blooded animal
describe pathophysiology of rabies
- virus enters peripheral nerves or replicates locally in tissue
-can also enter at NMJ and neurotendinal spindles
-at this stage: pruritis, licking, biting at inoculation site - migrates up to central nervous system, ipsilateral neuron
-retrograde axoplasmic flow
-approximately 100mm/day (10-400) - once in CNS, spreads to contralateral neurons and ascends rapidly
-actively replicating in the CNS
-neurologic signs can vary based on site of inoculation, time interval in disease progression - virus moves outward to other body tissues via nerves
-rides cranial nerves to salivary glands - death secondary to cardiopulmonary dysfunction, seizures
-brainstem and cerebellum required for fluorescent antibody testing!
define quarantine, strict isolation, and observation period as relates to rabies
quarantine: 10-day period of confinement for observation of health status for a domestic animal (dog, cat, or ferret only) which has bitten a person, no matter if the animal is currently vaccinated or not
strict isolation: the confinement of an animal exposed or potentially exposed to rabies in a manner that prevents direct contact with other animals or persons. In most cases, this term applies to an unvaccinated domestic animal exposed to a rabid wild or domestic animal; the duration of strict isolation should be four months for dogs and cats and six months for large animals and ferrets
observation period: In animal (domestic) to animal (potential rabid wild or domestic animal) encounters involving currently vaccinated animals (or dogs/cats with documentation of one previous vaccine who receive a booster immediately after exposure), the observation period is a 45-day period in which the animal is kept under the owner’s control to monitor for
the development of clinical signs of rabies
exposure:
bite
non-bite
what do you do at the first sign of illness? small animal rabies
euthanize and test (should for all, BUT)
unvaccinated animals:
-euthanasia and test or
-strict isolation: 3 months for dogs and cats, 6 months for ferrets
overdue booster (dogs, cats):
-revaccinate, observation for 45 days
without documentation (dogs, cats): treat like unvaccinated animal
currently vaccinated (dog, cat, ferret): treat like overdue booster
what do you do at the first sign of illness? livestock and horses
should euthanize and test BUT
unvaccinated (livestock, horses):
-euthanasia and test or
-strict isolation for 6 months
vaccinated animals (livestock, horses):
-revaccinate, observation for 45 days
other animals: euthanasia and test
what do you do following an animal bite? rabies
first sign of illness: euthanize and test
owned dogs, cats, and ferrets:
-quarantine for 10 days
-REGARDLESS OF VX STATUS
stray or unwanted dogs, cats, ferrets: euthanize and test
wildlife: talk to wildlife officials for euthanasia
-wild carnivores: euth and test
-rodents and lagomorphs: contact GPH lab
-bats: euth and test
describe signalment and transmission of canine distemper
transmission: oronasal contact with secretions, excretions, aerosols
-mucus, saliva, vomit, feces, urine, env fomites
signalment:
-primarily young animals but ALL ages are susceptible
-dogs, ferret, raccoons > cats
describe pathophysiology of canine distemper
- aerosol droplets with virus contact upper resp tract epithelium
- virus infects, multiplies in resident tissue macrophages
- macrophages migrate to tonsils, bronchial lymphnodes
- replication in lymphocytes, macrophages
-virus-mediated cell death associated with lymphopenia
-immunosupression leads to secondary dsease - hematogenous, lymphatic dissemination
-lymphoid organs
-visceral organs - neuroinvasion, disseminated disease occurs if dog has insufficient cell mediated immune response
-free virus or lymphocyte-associated virus infects brain via directly crossing BBB OR through CSF via the choroid plexus
-the type of lesion and course of disease depends on numerous factors (age, immunocompetence, virus properties) but can include seizures, myoclonus ataxia, paraparesis, or paraplegia
what causes pathology in canine distemper virus?
- due to direct and indirect consequences of viral infection
- direct: virus-mediated cell death
-oligodendrocytes: degeneration, demyelination
-neurons: necrosis - indirect: inflammation due to immune response
-astrocytes: recruit dendritic cells
-microglia: enhanced secretion of reactive oxygen radials
-result in destruction of oligodendrocytes and myelin
describe signalment and transmission of feline infectious peritonitis
transmission:
-fecal-oral transmission of feline enteric coronavirus (FECV)
-mutation of FECV to feline infectious peritonitis virus
-1 in 100 FIPV mutations lead to disease
signalment:
-primarily young cats (<7 years); mostly between 16 weeks to 1.5 years old
describe pathophysiology of feline infectious peritonitis
exact still unclear
- FECV infects mature epithelium at the tips of intestinal villi
- mutation from FECV to FIPV: loses tropism for enterocytes and gains tropism for monocytes, macrophages
- replication in tissue macrophages
- hematogenous, lymphatic dissemination
describe the disease caused by feline infectious peritonitis
- likely due to host’s inefficient immune response (both forms)
- type III hypersensitivity reaction (effusive)
-antibodies bind to virus, form antigen-antibody complexes which are deposited in blood vessels
-complement binds to antigen-antibody complexes: attracts and activates neutrophils, facilitates uptake by and activates macrophages
-pro-inflammatory cytokine release results in vasculitis
-increased vascular permeability due to vasoactive amines, and vasculitis leads to fibrin leakage
can also be
- type IV hypersensitivity response (non-effusive)
-Th1 lymphocytes secrete cytokines to activate macrophages and cytotoxic T cells
-activated cells secrete pro-inflammatory cytokines resulting in inflammation - effusive and non-effusive disease can overlap and clinical signs are highly variable; diagnosis is challenging and mostly based on clinical signs, presentation, signalment
describe clinical signs of FIP in the brain and in the eys
brain:
1. spontaneous muscle twitches, atypical limb extension and swallowing motions, staring
2. ataxia, nystagmus, depression, seizures, head tilt, nystagmus
eyes:
1. uveitis: iris color change, aqueous flare, keratic precipitates
2. retinitis
describe signalment and transmission of feline leukemia virus
transmission:
1. vertical: transplacental, close contact
2. horizontal: oronasal contact with secretions, excretions, fomites
-saliva, mucus, milk, urine, feces, blood, transfusion, contaminated instruments (dental)
-friendly, social contact
signalment:
-primarily young cats (1-6 years)
-young, immunosuppressed cats at higher risk of developing progressive disease
describe pathophysiology of feline leukemia virus
- disease and progression due to host’s inefficient immune response
- virus infects lymphocytes and monocytes in oropharyngeal lymphoid tissues
- retrovirus, so integrates into host genome
- hematogenous, lymphatic dissemination to lymphoid organs, salivary and mammary glands
- 4 types of infection, based on host immune response
-abortive infection: prevents replication and manifests as lethargy, fever, lymphadenomegaly
-regressive infection: immune response prevents or contains infection of the bone marrow; may not be able to detect on SNAP test
-progressive infection: associated with extensive virus replication secondary diseases
-focal infection can also occur in some tissue; not technical FIV in samples collected
