Lecture 45-48
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| CNS vulnerability | show 🗑
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| show | encephalitis is viral, acute meningitis is viral or bacterial, chronic meningitis is tubercle bacteria or fungi, brain abscesses are polymicrobial
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| show | meningitis, (bacterial, fungal, viral, non-infectious), encephalitis (viral), myelitis (rabies/polio), brain abscesses (aerobic and anaerobic, fungal, parasites)
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| Clues about etiology | show 🗑
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| show | infection of meninges, worldwide more than 1 million cases/year , over 50% are viral, bacterial are more serious (higher mortalitly)
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| show | Common viral: enteroviruses (most), arboviruses, HSV-2. Uncommon viral: mumps, CMV, HIV, HHV-8. Common bacteria: borrelia burgdorferi, partially treated bacterial meningitis. Uncommon bacterial: M. tuberculosis, Leptospira, M. pneumoniae
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| Septic meningitis | show 🗑
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| show | Early: fever, malaise, aches and pains, nausea, vomitig, headache. Late: photophobia, neck stiffness, drowsiness, fits, inconsolable crying (babies), vasculitic rash
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| Encephalitis | show 🗑
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| show | acute inflammation of the spinal cord, can be acute flaccid paralysis, headache, fever, signs of meningeal irritation, weakness of one or more extremities. Caused by polio previously, now WNV mostly
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| show | localized pyogenic infection of the brain parenchyma and subdural or epidural meningeal spaces. symptoms reflective of space occupying lesion: headache, changes in mental status, seizure. Triad: headache, low grade fever, focal deficit
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| show | 25%, sinuses, teeth, middle ear/mastoid enable access to brain. Aerobic/anaerobic streptococci, Bacteroides, Enterobacteriaeae, Pseudomonas, Fusobacterium, Prevotella, Peptococcus. Normal flora of region or common opportunistic pathogens
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| Hematogenous spread | show 🗑
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| penetrating head wound/neurosurgery | show 🗑
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| show | encephalitis: mosquitoes or ticks. May be non human vertebrate host that are intermediary to transmission. Arboviruses: humans are usually dead end hosts
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| routes of entry: hematogenous | show 🗑
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| Neural entry | show 🗑
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| Direct inoculation by surgery or trauma | show 🗑
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| show | leukocytes 0-6, neutrophils 0%, RBC 0-2, glucose 40-80, protein 20-50
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| CSF acute bacterial meningitis | show 🗑
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| show | leukocytes 100-500, neutrophils <10%, RBC 0-2, glucose <40, protein 50-100 fungal, >100 bacterial
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| show | leukocytes <300, neutrophils predominate first 24 hr then <50%, RBC 0-2, glucose 40-80, protein 50-100
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| show | leukocytes 10-500, neutrophils predominate first 24 hours then <50%, RBC 10-500, glucose 40-80, protein 50-100
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| CSF brain abscess | show 🗑
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| neuroimaging | show 🗑
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| CSF PCR | show 🗑
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| Culture | show 🗑
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| Neisseria meningitidis | show 🗑
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| show | A: large scale epidemics B:epidemics and outbreaks C:local outbreaks W135:pilgrimage to Mecca in 2001-2002 Y: occasional cases
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| show | susceptible individuals, high level of transmissibility, virulent encapsulated strain
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| N. meningitidis pathogenicity | show 🗑
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| show | iron acquisition capability, LOS: causes most clinical manifestations, IgA1 protease, Pili: antigenetically variable (phase variation), capsule: production regulated according to disease (down regulated in initial attachment, upregulated intracellular)
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| show | temperate and cold climates, peaks in winter, more irregular in tropical countries, meningitis belt of Africa: epidemics in dry season every 5-10 years, outbreaks last 2-3 years
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| N. meningitidis culture | show 🗑
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| N. meningitidis prevention | show 🗑
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| show | meningitis, brain abscesses. divided into 7 main groups based on 16srRNA: 1.pyogenic 2.anginosus 3.mitis (pneumoniae, mitis) 4.salivarium 5.bovis 6.mutans 7.unclustered
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| hemolysis patterns Streptococci | show 🗑
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| S. pneumoniae | show 🗑
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| show | 1. pneumolysin: pore forming toxin, potent neurotoxin, can trigger apoptosis. 2. hydrogen peroxide: contributes to apoptosis, large amounts produced in growth due to lack of catalase. 3. May have retrograde axonal transport: teichoic/lipoteichoic acid
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| S. agalactiae | show 🗑
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| E. coli | show 🗑
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| show | gram+, motile, intracellular rod, reservoir: soil, water, decaying vegetation, animals, asymptomatic humans (5-10%). Acquired by ingestion, meningitis in immunocompromised, crosses placenta
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| show | Literiolysin O: pore forming cytotoxin (hemolysi) enables escape from phagosome into cytosol, Internalins: trigger entry, Actin based motility: use host cell actin to move within and between host cells
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| viruses | show 🗑
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| show | HSVE, meningitis, myelitis. linear, dsDNA, enveloped. 1/1000000, most important treatable cause of encephalitis in US (90% HSV1, rest 2:immunocompromised, neonates)
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| show | primary: genital accompanied by meningitis in 30% women and 11% men. Reactivation of latent. Re-infection. No specific seasonal pattern, most frequent in 50-70 year olds
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| HSV pathogenesis | show 🗑
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| show | >90% of viral meningitis, some encephalitis and myelitis. ss+RNA, non-enveloped, isocahedralm include polio, coxsackie, echovirus, enterovirus. humans are main reservoir, worldwide distribution, asymptomatic infection common.
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| show | acute flaccid paralysis, infection of anterior horns cells of gray matter, signs common to meningeal irritation with weakness in one or more extremities.
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| show | May be asymptomatic, non-paralytic, or paralytic (<2%): invasion of CNS from blood, spread by peripheral nerves, viral replication causes damage or destruction of nerves causing asymmetrical paralysis. 85% cases due to poliovirus type 1
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| polio pathogenesis | show 🗑
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| show | attaches by poliovirus receptor CD155, triggers conformational change in virion, viral RNA released into cell cytosol &binds to ribosomes, translated into polyprotein, cleaved by proteinases, new viral RNA synthesized, released via host cell lysis: 5-10hr
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| polio prevention | show 🗑
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| Arboviruses | show 🗑
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| show | ss+RNA, enveloped, no symptoms in 80%, WN fever: 20%, mild flu like, duration 1-2 wks. Neuroinvasive: <1%, 10% hospitalized patients developed acute flaccid paralysis
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| WNV pathogenesis | show 🗑
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| show | E=enveloped glycoprotein, elicits neutralizing Ab, structural domains:I antigenic II fusion of E II binds to host cells. prM=premembrane protein, block premature viral fusion
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| WNV non-structural proteins | show 🗑
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| show | S. europe, Africa, central and S Asia. Vector:mosquitoes, many avian host species
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| WNV diagnosis | show 🗑
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| St. Louis encephalitis | show 🗑
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| show | fatal meningoencephalitis, initial prodrome of non-specific symptoms then symptoms relating to wound site, then encephalitis (2/3 of people) then paralytic illness. Mortality 100% with symptoms. incubation 20-90d, depends on bit proximity to brain
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| Rabies viral characteristics | show 🗑
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| Rabies epidemiology | show 🗑
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| Rabies pathogenesis | show 🗑
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| show | Ag by immunofluorescence, virus isolation, histological changes, ELISA of CSF, DNA amplification (most sensitive), latex agglutination
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| Rabies treatment/prevention | show 🗑
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| Crytococcus neoformans | show 🗑
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| C. neoformans symptoms | show 🗑
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| show | inhalation results in colonization: asymptomatic colonization, symptomatic pneumonitis, asymptomatic of lungs and lymph nodes. cellular immune response-->granulomatous inflammation-->yeasts killed or dormant-->defects allow replication and spread
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| C. neoformans virulence | show 🗑
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| Prions | show 🗑
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| Prions unique characteristics | show 🗑
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| show | sporadic (85%) or inherited, classic and variant forms. BSE: human exposure when eating contaminated meat (vCJD form). vCJD: early onset (29yr), slow progression (14mo), longer course of illness
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| Subacute sclerosing panencephalitis | show 🗑
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| SSPE pathogenesis | show 🗑
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Created by:
kamarsh
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