Viral Pathogens CNS & Encephalopathy
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Created by:
reindeersp on March 13, 2010
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22 terms
Terms | Definitions |
|---|---|
 Encephalitis Causes | Herpes simplex, Rabies, Enteroviruses, EBV, HIV, West Nile Virus (WNV) |
| Encephailitis Px | Drowsiness, Confusion, Behavioural disturbance, [focal] seizures |
| Paralysis Causes | Enteroviruses esp Polio, Mumps, WNV, HSV |
| Paralyis Px | Flaccid paralysis (lower motor neurone +/- meningitis) |
| Post-infectious encephalitis C & Px | Measles, Rubella, Varicella. Px after acute illness w/signs encephalitis |
| Viral Infections- ASK | History Travel Animal exposure -- Unusual but worth getting Sexual history where appropriate eg. HSV 2, HIV Contact with other infected individuals eg. hand, foot and mouth Caused by one of the Coxsackie viruses |
| Viral Meningitis | Lymphocytic response in CSF and normal glucose concentration Causative viruses Mumps, Echo, Coxsackie, non-polio enteroviruses -- most common; Herpes viruses (HSV-2) Occasionally HIV, WNV After primary multiplication in other sites the virus may reach the CSF : Along nerve pathways Through the olfactory mucosa Via the bloodstream (the usual route) |
| Dx Viral Meningitis | o Lumbar puncture Before check CT brain to check raised ICP o CSF under pressure but typically clear Check pressuse- you attach a pressure monitor to it o Elevated white cell count and protein but normal glucose o PCR and viral culture o Serology may occasionally be helpful eg. acute and convalescent sera for mumps |
| Tx Viral Meningitis | Usually Mild, Self Limiting o Acyclovir if HSV meningitis suspected --> With pure meningitis only if herpes- has nothing on the enteroviruses |
| Herpes Simplex Encephalitis | • Most common causative agent of encephalitis in Northern Europe • Due to HSV 1 or 2 (most often HSV 1) • Human-only infection. Spread from sites of latent infection in cranial nerve ganglia to the frontal or temporal lobes of the brain. The mechanism of reactivation of the latent virus is not understood • 2 forms: o Neonatal -- Global involvement, brain is almost liquefied. -- Mortality rate approaches 100%. o Focal disease -- Temporal lobe-- Children and adults. -- Many of these arise from reactivation of virus. --Mortality rate is high (70%) without treatment. |
| Prognosis | MAKE IT EARLY + High dose Acyclovir IV. W/O tx high mortality and morbidity rate. |
| HSE Clinical Features | Acute neurological syndrome characterised by -- Behavioural disturbance -- Hemiparesis -- Aphasia, focal seizures |
| Tick Borne encephalitis | • Arthropod borne encephalitis • Significant problem throughout world • Spread from animal to animal via infected arthropod usually: mosquito or tick -- North America: o West Nile Virus o St.Louis Encephalitis o La Crosse Encephalitis Virus -- Asia: o Japanese encephalitis • Tropics: o Dengue |
| WNV | West Nile Virus Mosquito-borne flavivirus with birds as the main reservoir First documented case (USA) in NYC, 1999 Infects many vertebrates - highest mortality in horses, at 30% Diagnosed by detection of specific IgM antibody in blood or CSF •Epidemiology --1 in 5 get mild febrile illness with malaise, myalgia, headache, etc -- 1 in 150 patients get meningo-encephalitis or meningitis -- 1 in 3 patients with CNS involvement get seizures and -- 1 in 8 cases hospitalised die, almost 1 in 3 if > 70 years • No antiviral treatment that has been proven to be effective |
| Polio Virus | 3 immunologically distinct serotypes of Poliovirus: 1, 2 and 3. o Type 1 is the type most likely to cause paralysis o Paralysis in infected -- 1 in 1000 -- Human-only infection -- Source of infection GI tract from excretion -- Chronic gastrointestinal tract (or respiratory) carriage does not occur -- 12 weeks infectiousness |
| CNS manifestations of polio | o Meningism or Meningitis o Paralysis of muscles innervated by efferent nerves from infected anterior horn cells (asymmetric flaccid paralysis with no sensory loss) o Bulbar poliomyelitis due to replication in motor nuclei of lower cranial nerves |
| Lab Dx Polio | o Isolation of the virus -- Specimens • Throat swab • Faeces • CSF (if meningitis) --Inoculate in Tissue culture : Monkey Kidney or Human Embryo lung cells (because only in animals/primates) • CPE within 48hrs • Neutralisation tests for different type |
| Polio Vaccine | 1. Inactivated Poliovirus "IPV" (Salk) • Contains the three viruses and produces immunity (antibody) to each; produces little secretory IgA; • Three doses must be given in primary course 2. Live attenuated poliovirus (Sabin) OPV • Administered orally induces secretory IgA in addition to humoral immunity • Oral - simpler to administer • Cheaper to produce than IPV • Three doses must be given in primary course |
| Coxsackie Viruses | Divided into group A & B. Recovered from blood in early stages as well as throat for up to 6 weeks. FO and Inhalation spread. Group A: herpangina; hand, foot, and mouth disease & acute hemorrhagic conjunctivitis. Group B: myocarditis, pericarditis, and meningoencephalitis. Dx tissue culture, serology, PCR |
| PML | Progressive multifocal leucoencephalopathy o Uncommon opportunistic infection caused by reactivation of papova virus (JC virus) resulting in demyelination o Diagnosis : imaging, molecular [PCR]; serology is not useful o No treatment - reduce immunosuppression |
| Transmissible spongiform encephalopathy | "prions" --> abnormal isoforms of a cell surface glycoprotein (PrP) o PrPSc interacts with normal PrP resulting in its conversion to PrPSc o Gradual accumulation of abnormal results in neurodegenerative disease Classification o Sporadic CJD o Inherited e.g. Gerstmann-Straussler-Scheinker o Acquired --> Kuru, Iatrogenic, Variant CJD [vCJD] • All TSEs share the following, o An incubation period of months to years o Gradual increase in severity leading to death o None evoke an immune response o A common non-pathologic process restricted to CNS • Features o Iatrogenic-- Intracerebral inoculation for e.g. via contaminated EEG electrodes or cornea transplant -- Human growth hormone recipients o Variant CJD - Florid amyloid-like plaques in brain which are quite distinct from those of sporadic CJD; Duration longer, psychiatric symptoms ^^, EEG findings not found; ? ingestion of contaminated beef |
| Dx, Tx of TSE | DX: Conclusively by histological examination at post-mortem Spongiform changes in brain, Neuronal loss, Astrocytosis, Amyloid plaques rich in prion isoforms Newer techniques (for vCJD) involve tonsillar biopsy, EEG, CT and MRI exclude other disease, Marker protein 14-3-3 in CSF in sporadic CJD TX: No proven effective agents • Prevention is focused on o Blood supply screening, identify sources, e.g. meat (community) o Measures to protect staff from inoculation injuries (hospitals) o Appropriate autoclaving & decontamination (healthcare facilities) •Surgical instruments o Destroyed by incineration, if used on brain, spinal cord, posterior eye o Other surgical procedures o After thorough cleaning, autoclave • Heat sensitive equipment should not be use |
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