CNS BACTERIAL INFECTIONS (DR. NEELY)

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davis.tiff
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CNS BACTERIAL INFECTIONS (DR. NEELY)
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2012-09-15 15:53:04
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MICROBIOLOGY INFECTIOUS DISEASES
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MICRO/ID EXAM IV
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  1. Central nervous system
    General characteristics.
    • CNS should be sterile
    • Blood vessels and nerves that traverse the skull and vertebral column are main routes of infections
    • Blood-borne invasion is the most common route of infection
    • Abscesses - suppurative infection of the brain tissue
    • Encephalomyelitis - inflammation of the spinal cord
    • Blood-borne invasion involves blood-brain-barrier or blood-CSF-barrier
    • Blood-brain-barrier - tightly joined endothelial cells surrounded by glial processes
    • Blood-CSF-barrier - endothelium with fenestrations and tightly joined choroid plexus epithelial cells
  2. What are 3 ways in which microbes can cross the blood-brain-brarrier and the blood-CSF-barrier?
    • infect cells that make up the barriers
    • passive transport via intracellular vacuoles
    • carried across via WBCs
  3. 10 steps involved in the mechanism of CNS bacterial infection:
    • 1. mucosal colonization
    • 2. invasion of bloodstream (survival and multiplication)
    • 3. crossing blood-brain-barrier
    • 4. survival and multiplication in the meninges/brain parenchyma
    • 5. bacterial products (pro-inflammatory) cause edema and increased pressure
    • 6. bacterial products recruit WBCs and there is a release of pro-inflammatory cytokines
    • 7. cytokines recruit more WBCs which causes edema and increased intracranial pressure > increased permeability
    • 8. infiltration of neutrophils and lymphocytes into CNS
    • 9. WBCs produce even more cytokines which affects neuronal cells > neuronal injury
    • 10. neuronal injury and edema > neuronal death
  4. Which pathogens have a relatively high percentage (>25%) of carriage rates in the CNS? (remember: S.H.I.N.E.S.!)
    • S. agalactiae (Group B strep)
    • H. influenzae
    • I.gnore
    • N. meningitidis
    • E. coli K1
    • S. pneumoniae
  5. How many WBCs (per microliter of CSF) are indicative of an acute bacterial infection?
    >1,000 (neutrophils)
  6. What % of PMNs in CSF is indicative of an acute bacterial infection?
    >50
  7. How many RBCs (per microliter of CSF) are indicative of an acute bacterial infection?
    0-10
  8. How much glucose (per mg/dl of CSF) is indicative of an acute bacterial infection?
    <30
  9. How much protein (per mg/dl of CSF) is indicative of an acute bacterial infection?
    >100
  10. What are some causes of acute meningitis?
    • viral or bacterial meningeal infection
    • diseases that cause inflammation (without infection)
  11. What are the main symptoms of acute bacterial meningitis?
    • high fever
    • severe and persistent headache
    • stiff neck
    • N/V
    • confusion
    • sleepiness
    • difficulty waking up
    • In infants: irritability/tiredness, poor feeding and fever
  12. What are the virulence factors involved in acute post-neonatal S. pneumoniae bacterial meningitis?
    • adhesins - binds to choline (CHO) on cell surfaces
    • IgA protease (Iga)
    • pneumolysin - cytotoxin released when bacteria is lysed; inhibit Ab binding to bacteria
    • autolysin - causes release of pneumolysin
    • capsule - >90 serotypes
    • peptidoglycan and teichoic acid - proinflammatory > tissue damage
  13. What pathogen causes the most common acute post-neonatal bacterial meningitis?
    S. pneumoniae
  14. What are the etiology/pathogenesis factors involved in acute post-neonatal S. pneumoniae bacterial meningitis infection?
    • spread from person to person via aerosols or direct contact with secretions
    • ubiquitous
    • risk factors involved: immunosuppresion, distant foci of infection, low-levels of circulating Abs to capsular polysaccharide
  15. What is the clinical ID S. pneumoniae?
    • gram+ lancet-shaped diplococci
    • catalase-
    • alpha-hemolytic
    • optochin sensitive
    • bile sensitive
    • Quellung reaction - swelling of the capsule
  16. What are the vaccines that are available for acute post-neonatal S. pneumoniae bacterial meningitis infection?
    • 23-valent - 23 serotypes of polysaccharide capsule that is responsible for 90% of infections
    • 7-valent - 7 serotypes of polysaccharide capsule that are most prevalent in children, immunocompromised and elderly
  17. What pathogen is the second leading cause in acute post-neonatal bacterial meningitis in the U.S.?
    N. meningitis
  18. What are the virulence factors involved in acute post-neonatal N. meningitidis bacterial infection?
    • IgA protease
    • Pili - adherence
    • LOS - toxic, proinflammatory
    • Capsule - most common type is serogroup B
  19. What are the etiology/pathogenesis factors involved in acute post-neonatal N. meningitidis bacterial meningitis infection?
    • Spread from person to person or direct contact with oral secretions
    • Ubiquitous
    • risk factors: close contact with infected people, areas of outbreak
  20. What are some symptoms of acute post-neonatal N. meningitidis bacterial meningitis infection?
    hemorrhagic rash with petechiae - can have complications due to disseminated intravascular coagulation, endotoxemia and shock, and renal failure
  21. What is the clinical ID N. meningitidis?
    • gram- cocci, diplococci
    • fastidious - grows on CAP
    • oxidase+
    • lactose+
  22. What are the virulence factors involved in acute post-neonatal H. influenzae B bacterial infection?
    • IgA protease
    • LPS
    • Capsule - 6 serotypes
    • serotype B - most common causative agent
  23. What are the etiology/pathogenesis factors involved in acute post-neonatal H. influenzae B bacterial meningitis infection?
    • spread from person to person by aerosols or direct contact with oral secretions
    • Ubiquitous
    • Risk factors: close contact with infected people, areas of outbreak
  24. What is the clinical ID H. influenzae B?
    • gram- pleomorphic coccobacilli
    • faculative anaerobe
    • encapsulated or nonencapsulated
    • fastidious growth - grows on CAP, factor V
  25. What are the vaccines that are available for acute post-neonatal H. influenzae B bacterial meningitis infection?
    • Hib vaccine
    • protective immunity response by age 5
  26. What are the risk factors involved in college students acquiring acute bacterial meningitis?
    • poor eating habits
    • alcohol use
    • smoking
    • pulmonary infections
  27. Which pathogen involved in acute bacterial meningitis lacks pili and endotoxin?
    S. pneumoniae
  28. Neonatal infection of acute bacterial meningitis can lead to permanent sequelae that includes:
    • cerebral palsy
    • epilepsy
    • mental retardation
    • hydrocephalus
  29. What is the clinical diagnosis of acute neonatal bacterial meningitis?
    • fever
    • poor feeding
    • V/D
    • respiratory distress
  30. What pathogens are involved in acute neonatal bacterial meningitis infections? (remember: L.E.S.T.!)
    • L. monocytogenes
    • E. coli K1
    • S. agalactiae (Group B strep)
    • T. gondii
  31. What are the virulence factors involved in chronic M. tuberculosis bacterial meningitis?
    • droplet inhalation - infect lung macrophages
    • disseminate to blood via lymphatics
    • bacteremia > dissemination to CNS
  32. What are the etiology/pathogenesis factors involved in chronic M. tuberculosis bacterial meningitis?
    • spread from person to person by aerosols
    • reactivation of latent disease
    • prevalence in urban and endemic areas
    • risk factors: previous TB infection, immunosuppresion, travel to endemic areas
  33. What are the causes of encephalitis?
    • viral infection
    • fungal infection of the brain
    • dissemination of bacterial infection
  34. What are the symptoms of bacterial encephalitis?
    • sudden fever
    • headache
    • vomiting
    • sensitivity to light
    • stiff neck and back
    • Need immediate attention if:
    • confusion
    • drowsiness
    • clumsiness
    • unsteady gait
    • irritability
    • loss of consciousness
    • poor responsiveness
    • seizures
    • muscle weakness
    • sudden severe dementia
    • memory loss
    • withdrawal from social interaction
    • impaired judgement
  35. What 2 pathogens are the most common causitive agents of bacterial encephalitis?
    • B. burgdorferi (lyme disease)
    • T. pallidum (tertiary Syphilis)
  36. What are the virulence factors involved in B. burgdorferi (Lyme disease) bacterial encephalitis?
    • dissemination leads to inflammatory response and skin lesion at site of insect bite
    • spread hematogenously > inflammatory response
    • localize in brain tissue
    • usually aseptic due to inflammatory response
  37. What are the etiology/pathogenesis factors involved in B. burgdorferi (Lyme disease) bacterial encephalitis?
    • acquired from tick bite
    • most common in NE U.S., and now in Midwest
    • risk factors: residence in or travel to endemic areas
  38. What are some symptoms of B. burgdorferi (Lyme disease) bacterial encephalitis?
    • skin lesion
    • arthritis
    • neurological problems
  39. What is the clinical ID of B. burgdorferi?
    • difficult to gram stain and culture
    • requires special medium
    • spirochete,microaerophilic
    • serological tests with variable reliability
  40. What are the virulence factors involved in T. pallidum (tertiary Syphilis) bacterial encephalitis?
    • primary: multiplication of bacteria at site of entry
    • secondary: dissemination of bacteria to other tissues (like CNS)
    • tertiary: may occur after 20-30 years
  41. What are the etiology/pathogenesis factors involved in T. pallidum (tertiary Syphilis) bacterial encephalitis?
    STD
  42. What are some symptoms of T. pallidum (tertiary Syphilis)?
    • genital chancre sore
    • skin rash
    • difficulty coordinating muscle movements
    • paralysis
    • numbness
    • gradual blindness
    • dementia
  43. What is the clinical ID of T. pallidum (tertiary Syphilis)?
    • gram- spirochete
    • immunological tests available
  44. What pathogen is responsible for CNS post-infectious syndrome related to bacterial meningitis (i.e. Gullian Barre Syndrome)?
    C. jejuni
  45. What are the virulence factors involved in CNS post-infectious syndrome caused by C. Jejuni (Gullain Barre Syndrome)?
    • ingestion of 800 organisms
    • chemotaxis, motility, and flagella - attachment and colonization of gut epithelium
    • iron acquisition
    • host cell invasion
    • toxin production
    • epithelial disruption
  46. What are the etiology/pathogenesis factors involved in CNS post-infectious syndrome caused by C. Jejuni (Gullain Barre Syndrome)?
    acquired from eating contaminated food
  47. What are the symptoms of CNS post-infectious syndrome caused by C. Jejuni (Gullain Barre Syndrome)?
    • food poisoning
    • acute paralysis
  48. What is Gullain Barre Syndrome?
    demyelinating disorder characterized by immunological attack upon peripheral nerve myelin due to cross-reactivity between microbial ganglioside-like epitopes in LPS that cross-react with neural antigens
  49. What is the clinical ID of C. jejuni (Gullain Barre Syndrome)?
    • gram- curved rod
    • microaerophilic
    • motile
  50. What is a polymicrobial abscess?
    localized suppurative infection in brain; often leads to a space occupying lesion which compressing brain structures
  51. What are the symptoms of a polymicrobial abscess?
    • headache
    • drowsiness
    • confusion
    • hemiparesis
    • seizures
    • speech difficulties
    • fever
    • no stiff neck
  52. How does one go about diagnosing a polymicrobial abscess of the CNS?
    • CT scan
    • 4-5 days abscess is surrounded with fibrous capsule > "ring enhancing appearence" on CT with contrast
  53. What are the etiology/pathogenesis factors involved in polymicrobial abscess of the CNS?
    • 50% are caused by anaerobes
    • most common organisms involved:
    • gram+:
    • streptococcus spp., bacteroides spp., peptostreptococcus spp., nocardia spp., actinomyces spp.
    • gram-:
    • prevotella spp. fusobacterium spp. E. coli, C. koseri, P. mirabilis
    • acquired from normal microbiota, including GI tract
    • risk factors: immunocompromised. distal infections (like sinusitis)
  54. What is the most common Streptococcus organism recovered from culture that is involved in polymicrobial abscesses in the U.S.?
    S. anginosus
  55. What are the most common organisms that are involved in polymicrobial abscesses in HIV/AIDS population?
    • Toxoplasma
    • Cryptococcus
  56. Where would the primary lesion of a middle ear infection abscess be located?
    Middle and posterior cranial fossae
  57. Where would the abscess of a congenital heart disease be located?
    middle cerebral artery
  58. Where would the primary lesion (abscess) of a sinus infection be located?
    subdural sinus
  59. What are the virulence factors involved in chronic meningoencephalitis caused by C. neoformans fungal infection?
    • usually asymptomatic
    • reactivation of latent infection, can disseminate to CNS or remain in lungs
    • capsule - evades microphages, Ab, and complement
    • melanin - protects against oxidative defenses of macrophages
    • phospholipase B
  60. What are the etiology/pathogenesis factors involved in chronic meningoencephalitis caused by C. neoformans fungal infection?
    • acquired through inhalation
    • found in pigeon excreta and rotting wood
    • risk factors: immunosuppressed patients (i.e. HIV patients)
  61. What is the clinical ID of C. neoformans?
    • gram+ yeast
    • India ink+ (negative stain for capsule)
    • Calcofluor White+ (fungal stain)
    • urease+
    • capsular antigen in CSF or serum
  62. What is the most ubiquitous virulence factor found amongst the majority of CNS pathogens?
    capsule
  63. What are the virulence factors involved in chronic meningoencephalitis caused by C. imitis (Valley fever) fungal infection?
    • once in the lungs > arthroconidia transform into spherical cells (spherules)
    • acute respiratory infection occurs 7-21 days after exposure (usually resolves immediately, but can result chronic pulmonary condition or disseminate to CNS
  64. What % of patients who have disseminated C. imitis (Valley fever) infection also have meningitis?
    25%
  65. What are the etiology/pathogenesis factors involved in chronic meningoencephalitis caused by C. imitis (Valley fever) fungal infection?
    • acquired through inhalation, no person to person spread
    • endemic to SW U.S.
    • risk factors: ourbreaks occur during dust storms, earthquakes and earth excavations
  66. What are the symptoms of chronic meningoencephalitis caused by C. imitis (Valley fever) fungal infection?
    initial flu-like symptoms, can spread to CNS leading to meningitis (fatal unless treated)
  67. What are the virulence factors involved in chronic meningoencephalitis caused by H. capsulatum (North American Histoplasmosis) fungal infection?
    • acquired through inhalation of macroconidia in soil
    • prevalence in Southern U.S.
    • risk factors: immunosuppressed patients (disseminated diseased seen), children <2, elderly, exposure to large inoculum
    • dissemination results in chronic meningitis or encephalitis
  68. What are the etiology/pathogenesis factors involved in chronic meningoencephalitis caused by T. cruzi (Chagas disease) parasitic infection?
    • acquired from Triatome bug
    • found in southern U.S. to southern Argentina
    • risk fatctors: infants: travel to endemic areas
  69. What are the symptoms of chronic meningoencephalitis caused by T. cruzi (Chagas disease) parasitic infection?
    • sore develops at site of bite
    • fever and acute encephalitis
    • chronis disease develops over the course of a few years > affects heart, colon, CNS
  70. What are the etiology/pathogenesis factors involved in chronic meningoencephalitis caused by P. falciparum (Malaria) parasitic infection?
    • aquired from bite of mosquito
    • infects liver and RBCs
    • risk factors: age <10, exposure to a malaria-endemic area
  71. What are the symptoms of chronic meningoencephalitis caused by P. falciparum (Malaria) parasitic infection?
    • malarial fever
    • can travel to CNS if untreated > brain lesions and coma
  72. What is the life cycle of P. falciparum?
    sporozoites released from mosquito and infect human > sporozoites travel to liver > liver cells lyse and release merozoites which infect RBCs > asexual cycle occurs in RBCs > RBCs lyse and release gametocytes into blood stream > sexual cycle occurs in female mosquito > sporozoites > cycle begins anew

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