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64 Cards in this Set
- Front
- Back
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What are the most common causative viruses for viral meningitis?
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Coxsackie B
Echovirus Coxsackie A |
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When do most cases of viral meningitis occur?
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Summer/autumn months
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T or F: Viral meningitis is more severe than bacterial meningitis.
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False
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What does the CSF profile look like for a patient with viral meningitis?
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CSF is turbid
WBCs increased No bacteria present Elevated protein Pressure and glucose are normal |
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What are the most common causative viruses for viral encephalitis?
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HSV-1 and 2
Arboviruses (EEEV, WEEV, SLEV, WNV) |
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What are neuroinvasiveness and neurovirulence?
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Neuroinvasiveness: ability of virus to cross BBB
Neurovirulence: ability of virus to cause CNS disease once inside |
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What are the symptoms of viral meningitis?
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Fever
Stiff neck Headache Vomiting Nausea Photophobia *Lack of neurological signs/symptoms |
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Describe enteroviruses.
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Small virus
+ssRNA Non-enveloped Picornaviridae family Includes coxsackie B and echovirus |
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What is the mode of transmission, diagnosis, and control of enteroviruses?
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Transmission: fecal oral route
Diagnosis: virus isolation, PCR from feces Control: sanitation, hygiene |
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What are the symptoms of viral encephalitis?
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Headache
Fever Irritability Confusion *Patient has notable behavioral/neurological changes |
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Describe herpesviruses.
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Enveloped
Linear dsDNA *Latent viruses |
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What is the mode of transmission for HSV-1 and where is latent?
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Direct skin-skin contact usually in childhood
Latency in trigeminal ganglion |
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What is the most common cause of fatal, sporadic encephalitis?
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HSV-1
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How does HSV-1 cause encephalitis?
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Ascends olfactory, trigeminal nerve to the brain (temporal lobe)
Acts as *cytolytic virus: causes direct cell death in parenchyma |
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What are the symtoms of HSV-1 encephalitis?
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Fever
Headache Altered mental state Acute onset (less than a week) |
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How is HSV-1 encephalitis diagnosed and treated?
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Diagnosis: PCR of CSF
Treatment: DNA polymerase inhibitors |
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What is HSV-2 more associated with and how is it transmitted and diagnosed in neonates?
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Closely associated with genital herpes
~75% neonatal herpes due to HSV-2 Transmitted during birth Diagnosed by isolated virus from CSF |
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T or F: HSV can cause eye infections as well.
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True
HSV-1: keratitis and conjunctivitis HSV-2: typically only in neonates |
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Describe HIV.
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Enveloped
+ssRNA "Retrovirus" - uses reverse transcriptase to generate DNA copy of RNA genome |
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How does HIV affect the body?
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Infects and kills CD4 T cells
Causes AIDS - profound immunosuppression that predisposes patients to opportunistic infection DIRECTLY causes meningitis, neuropathy, and myelopathy |
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How does HIV enter the CNS and cause neurological damage?
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Enters CNS via monocytes
Replicates in macrophages and microglia of brain Monocytes act as reservoir for HIV in brain Secretion of cytokines lead to neuronal death |
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What are neuropathy and myelopathy?
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Neuropathy: numbness, pain, tingling
Myelopathy: gait imbalance, leg weakness, incontinence, secretion of neuron damaging signals |
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Describe the JC virus.
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Endemic worldwide
Present in 70-80% of adult population Latent infection Papovaviridae family dsDNA Non-enveloped |
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What group of people is most susceptible to latent virus reactivations and what does it cause?
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Immunocompromised patients, specifically AIDS
Causes progressive multifocal leukoencephalopathy (PML) |
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How do JC virus and PML cause neurological damage and how is it treated?
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Kill oligodendrocytes and astrocytes
Causes demyelination Treatment: Cessation of immunosuppressive therapy if possible |
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Describe HTLV-1
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Human T-Lymphotrophic Virus 1
Enveloped ssRNA retrovirus |
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What does HTLV-1 cause and what are the symptoms of it?
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HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) aka chronic progressive myelopathy
Symptoms: slow progressive weakness and spasticity of extremities, hyperreflexia, urinary/fecal incontinence, mild loss of peripheral sensation. Avg age 40, women more common |
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How is HTLV-1 diagnosed, transmitted, and prevented?
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Diagnosis: demonstration of HTLV-1 antibodies in CSF
Transmission: blood products, breast milk Prevention: screening transfusion blood and mothers for Abs |
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Describe West Nile Virus.
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Flaviviridae family (an arbovirus)
+ssRNA virus Vector: mosquitoes |
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What are arboviruses?
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Arthropod borne viruses (broad classification)
Reservoir: natural vertebrate host (birds, mice, squirrel) Focus of infection: geographic location Dead end host: horses and humans *leading cause of viral encephalitis worldwide |
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How does WNV present?
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Majority of cases are asymptomatic (80%)
Symptomatic cases (20%): fever, headache, fatigue, rash on trunk, swollen lymph glands, eye pain |
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How does WNV cross the BBB?
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Increased cell permeability (TNF alpha)
Breakdown of cell tight junctions "Trojan horse" - infection of immune cells, transport across BBB |
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As a CNS disease, WNV infects/kills neurons where?
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Brain stem, cortex, cerebellum
Spinal cord, hippocampus |
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How does WNV present as a CNS disease?
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<1% of infected pts present with severe disease
West Nile meningitis/encephalitis Ataxia and extrapyramidal signs, optic neuritis Seizures, weakness, changed mental status, myelitis Flaccid paralysis sometimes seen |
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What are the risk groups for WNV?
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Seasonality: late summer/fall (mosquitos, outdoors, weather, etc)
Age: chance of severe neurological symptoms and fatality increase with age |
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What is St. Louis Encephalitis virus (SLEV)? What is the reservoir and vector?
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Flaviviridae
Used to be most common US arbovirus Reservoir: birds, humans dead-end host Vector: many species of mosquito Asymptomatic to fulminant encephalitis |
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Where is SLEV seen?
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Prevalent over entire US, urban and rural
Low income eastern urban areas: standing water Rural areas in west: ditches, standing water, etc Elderly and low income persons |
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What are EEEV and WEEV and what is the reservoir?
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Togaviridae (enveloped (+)ssRNA viruses)
Reservoir: birds, humans dead-end host Virus replication at bite site followed by viremia and involvement of brain (encephalitis) Both are rare viral infections in US, EEEV more serious |
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What is La Crosse virus? What is the reservoir and vector?
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Bunyavirus
California encephalitis virus Vector: Aedes triceriatus Reservoir: small mammals Eastern and upper midwest US Rarely fatal, neurological damage can persist in ~10% of population contracting encephalitis |
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What is the diagnosis, treatment and prevention of Arbovirus infection?
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Hemagglutination inhibition, ELISA for IgMs, agglutination assays (RT-PCR from CSF for WNV)
Treatment: supportive care only Vaccines for some arboviruses - horse vaccine for WNV Prevention: mosquito control |
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What is rabies?
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Rhabdoviridae
Lyssavirus: (-)ssRNA, enveloped, "bullet-shaped" Zoonotic infection Local paraesthesia is only reasonable prodromal symptom |
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Which animals can carry rabies virus?
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Raccoons, skunks, *bats
Susceptible domestics: *dogs, cats, cattle, horses, sheep, goats, pigs |
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What are the two forms of rabies?
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1. Furious rabies - aggressive behavior, agitation, confusion, excessive salivation, hydrophobia
2. Dumb (paralytic) rabies - weakness, inability to swallow, excessive salivation, choking behavior |
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What is the incubation period for rabies?
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Ranges from 10 days to months
Depends on proximity of bite to CNS, severity of wound, degree of innervation at bite site, amount of virus inoculated |
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How is a rabies diagnosis made premortem and postmortem?
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Pre: bite history, RT-PCR for viral RNA from saliva (skin biopsies at bite site; base of neck), CSF for Abs, no single test sufficient
Post: Ag detection in barin, presence of Negri bodies (hippocampus and cerebellum), neurological symptoms of rabies Direct Fluorescent Antibody Test - antibody directed against viral nucleoprotein; requires euthanasia of animal, brain biopsies By the time symptoms and antibodies appear, too late to intervene |
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What is the treatment for rabies?
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Treatment of site of infection - wound care
Injection of human rabies immunoglobulin (HRIG) Vaccination with human diploid cell vaccine (HDCV) - chemically inactivated viral vaccine, not live virus Post-exposure prophylaxis/vaccination: Day 0 - administer HRIG at bite site Day 0, 3, 7, 14 - administer vaccine (IM) |
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How is rabies prevented?
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Post-exposure therapy
Stray animal control Vaccination of dogs and cats |
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What is polio virus?
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Picornaviridae, Enterovirus
3 serotypes of polio cause human disease (1, 2, 3) Non-enveloped (+)ssRNA virus Acute viral infection of meninges and motor nerves of spinal cord, brainstem No cases of wild type poliomyelitis in US since 1979 |
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How is polio diagnosed?
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PCR from CSF is gold standard
PCR/virus detection from feces is also used Serology is slower |
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What is the Salk vaccine against polio?
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IPV (inactivated) - injected
Prevents disease but not infection - requires booster for long immunity (4 inoculations over 1-2 years) Inexpensive, stable No risk of vaccine related disease US recommendation: IPV, not OPV |
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What is the Sabin vaccine against polio?
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OPV (live-attenuated) - oral, easy to administer
Prevents infection and disease - life-long immunity, induces secretory Ig response similar to natural infection Herd immunity More expensive, less stable May result in vaccine-related paralytic disease Risk of polio in immunocompromised |
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What is post-polio syndrome?
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30-40 years later, after "recovery"
New weakening in muscles that were previously affected by polio infection, and in muscles that seemingly were unaffected |
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What is prions disease?
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Transmissible spongiform encephalopathies (TSEs)
Fatal neurological degeneration, deposition of fibrils in brain, and loss of brain matter Large vacuoles form in brain - characteristic spongy appearance |
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What is the incubation period for prions?
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Prolonged incubation period - months to years
No detectable immune or inflammatory response - it is a "self" antigen |
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What is a prion?
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Proteinaceous infections agents
Composed of single prion protein (PrP) - no nucleic acid component has been demonstrated All mammals contain normal PrP gene (normal PrP protein) |
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What are the two stable tertiary structures of PrP?
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1. Normal: alpha-helical, called PrPc (cellular PrP)
2. Disease form: beta-sheets, called PrPSc (disease, or scrapie PrP) |
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How does a prion undergo replication?
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Abnormal prion protein (PrPSc) binds to normal cellular protein (PrPc)
Changes conformation of the normal protein to the diseased form |
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What is the pathogenesis of prions?
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Newly altered proteins (PrPSc) clump together, inhibiting function of neuronal cells, leading to disease
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What are the prion diseases?
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Animals: scrapie (sheep), *BSE (cattle)
Humans: *Creutxfeldt-Jakob disease (CJD), *variant CJD, *Kuru |
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What is CJD?
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Rare but fatal
3 forms: sporadic (unknown cause), familial (mutated PrP gene), iatrogenic (growth hormone derived from human tissue, improperly sterilized instruments) |
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What are the clinical manifestations of CJD?
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Rapidly progressive dementia, memory loss
Decreased cognition Myoclonia, ataxia Death in <1 year Most pts >60 yrs old |
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What is Kuru?
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Fore tribes of New Guinea
Ritualistic cannibalism of dead family members Cannibalism ceased in late 50's - no more cases Incubation period is 4-40 years Damage predominantly cerebellar Ataxia, tremors, inability to walk Duration of illness: 6-36 months, resulted in death |
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What is BSE?
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Bovine Spongiform Encephalopathy
Epidemic in cattle in Great Britain Theory of origin: feeding of scrapie-infected sheep to cattle Officially designated a zoonosis - potential for spread to humans |
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How did BSE spread to humans (vCJD)?
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Link between BSE and vCJD suspected
Transmission route - human consumption of contaminated beef |
