Medical Micro Exam 3

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Medical Micro Exam 3
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  1. Pseudomonas
    • Oxidative gram-negative bacilli
    • Produce acid from glucose or other carbohydrates
    • Pseudomonas aeruginosa oxidizes but does not ferment glucose
  2. Pseudomonas aeruginosa
    • Non-fermentive
    • Obligately aerobic
    • Motile
    • Straight or slightly curved rod
    • Oxidase and Catalse +
    • Pigments- Pyocynin (blue), fluorescein (yellow), pyorubin (red)
    • Oppertunistic pathogen
  3. Pseudomonas aeruginosa
    Virulence Factors
    • Capsule
    • LPS
    • Pyocyanin
    • Toxins
  4. Pseudomonas aeruginosa
    Epidemiology
    • Ubiquitous
    • Simple nutritional requirements – grow where other bacteria cannot
    • Colonize respiratory and GI tract of patients
  5. Pseudomonas aeruginosa
    Clinical Disease
    • Pulmonary infect
    • Skin infec
    • Folliculitis/Nail
    • UTI
    • Ear
    • Eye
    • Bacteremia
    • Endocarditis
  6. Pseudomonas aeruginosa
    Clinical Diseases
    Pulmonary infections
    • Risk factors
    • -Cystic fibrosis
    • -Use of broad spectrum Abx
    • -Prior use of respiratory therapy equipment
  7. Pseudomonas aeruginosa
    Clinical Diseases
    Skin infection
    • Burn infection – localized vascular damage, tissue necrosis, bacteremia
    • Burns have moist surface and lack neutrophils
  8. Pseudomonas aeruginosa
    Clinical Diseases
    Folliculitis/Nail infections
    Results from immersion in contaminated water
  9. Pseudomonas aeruginosa
    Clinical Diseases
    Ear & Eye Infections
    • Ear:
    • Mild irritation of external ear
    • More severe form can destroy cranial bones
    • Eye:
    • caused by trauma & contaminated water
  10. Pseudomonas aeruginosa
    Laboratory Diagnosis
    • Culture:
    • Simple nutritional requirements
    • Identification:
    • colonial morphology - (Flat colonies with spreading border)
    • hemolytic activity - (beta hemolysis)
    • pigmentation - (green)
    • odor - (grape-like odor)
    • biochem test - (oxi +)
  11. Pseudomonas aeruginosa
    Treatment
    • Antibiotic resistance is common
    • Usually use combination therapy
  12. Pseudomonas aeruginosa
    Prevention/Control
    • Hard to eliminate from hospital environments
    • Concentrate on preventing contamination of sterile equipment
  13. Haemophilus
    • Gram-negative bacilli liking blood
    • Small, pleomorphic, aerobic and fastidious
    • Requires hemin (X-factor) and NAD (V-factor) for growth
    • Intact blood has V-factor inhibitor
  14. Haemophilus influenzae
    Virulence Factors
    • Capsule –6 Sterotypes (A to F)
    • Non encapsulated strains-spread from upper respiratory tract (URT) to ear, sinuses, LRT
    • Encapsulated strains – URT to bloodstream, systemic spread
    • Type B (Hib) is invasive – resists complement, antiphagocytic
  15. Haemophilus
    Epidemiology
    • Asymptomatic carriers
    • Hib generally not part of normal flora
    • Risk factor- absence of Ab against capsule – children under 1 yr
    • Crowding increases rate of disease by encapsulated strains
    • Conjugated vaccine introduced in 1987
  16. Haemophilus influenzae
    Clinical Disease
    Meningitis
    • CSF 50-95% culture +
    • Blood 50-95% culture +
  17. Haemophilus influenzae
    Clinical Disease

    Epiglottitis
    • Blocked airway
    • Pharyngitis, fever, trouble breathing
    • Blood 90-95% culture +
  18. Haemophilus ducreyi
    Clinical Disease
    Chancroid
    • STD
    • Characterized by tender papule with and erthematous base
    • Progresses to painful ulceration
    • Lesions similar to herpes and syphilis
  19. Haemophilus influenzae
    Laboratory Diagnosis
    • Microscopy of CSF –
    • gram neg rods ranging in size from small coccobacilli to large
    • pleomorphic filaments
    • Culture –
    • use chocolate agar (has factor X and V)
    • Antigen detection – detects PRP of Hib
  20. Haemophilus influenzae
    Treatment
    • —Broad spectrum Abx - Cephalosporins, Fluoroquinolones
    • —Ampicillin resistance on the rise
  21. Haemophilus influenzae
    Prevention/Control
    • —Conjugated PRP vaccine against Hib
    • 3 doses before the age of 6 months
  22. Bordetella
    • Small
    • gram -
    • aerobic
    • coccobacillus
    • Fastidious
    • Nonfermentative
    • Oxidize amino acids
  23. Bordetella
    Types
    • Bordetella pertussis = Whooping Cough
    • Bordetella parapertussis = milder form of whooping cough
    • Bordetella bronchiseptica = respiratory disease in animals (kennel cough)
  24. Bordetella pertussis
    Virulence Factors
    • Adhesins
    • Toxins
  25. Bordetella pertussis
    Epidemiology
    • Human is only host
    • Highly communicable (aerosols)
    • Worldwide distribution
    • Children under 1 year at greatest risk- shifting to older children and adults
    • Greatest risk in non-vaccinated or inadequately vaccinated
  26. Bordetella pertussis
    Pathogenesis
    • Mainly toxin-mediated
    • Inhalation of infected droplets
    • Colonization of respiratory tract – attach to ciliated epithelial cells
    • Localized multiplication with localized tissue damage
    • —Inflammation interferes with clearance of pulmonary secretions
    • Systemic toxicity – CNS effects, leukocytosis
  27. Bordetella pertussis
    Clinical Disease
    • 7-10 days: none
    • 1-2 wks: Rhinorrhea, malaise, fever, sneezing, anorexia
    • 2-4 wks: Repetitive cough w/ whoops, vomiting, leukocytosis
    • 3-4+ wks: less cough, pneumonia
  28. Bordetella pertussis
    Laboratory Diagnosis
    • Extremely sensitive to drying
    • DFA useful but not specific
    • Culture on selective media (Bordet-Gengou medium)
    • -Requires nicotinamide and charcoal, starch, blood, or albumin to absorb toxic substances
    • Fastidious and slow-growing
    • PCR most sensitive
  29. Bordetella pertussis
    Treatment
    • Macrolides- reduce length of infectious stage
    • -—Illness not recognized during peak contagiousness
  30. Bordetella pertussis
    Prevention/Control
    • Killed whole cell vaccine part of DTP
    • Acellular vaccine now available (DTaP)
    • -Use various subunits – filamentous hemagglutinin, pertactin fimbriae, etc)
  31. Legionella Discovery
    • Discovered in 1976
    • Outbreak of severe pneumonia that caused many deaths in American Legion members attending a convention
    • A previously unknown gram-neg rod was isolated
    • It was spread through the air conditioning ducts
    • Named Legionella after the group
  32. Legionella
    • Gram-negative rod
    • Tissue- short coccobacilli
    • Stains poorly w/ dyes
    • Fastidous obligate aerobe
    • Non-fermentative, metabolize amino acids
    • Ubiquitous aquatic saprophyte
    • L. pneumophila causes 85% of Legionella infections
  33. Legionella
    Pathogenesis
    • Respiratory disease spread by aerosol droplets
    • Facultative intracellular parasites
    • Multiply in macrophages, monocytes, and free-living amoebas
    • Complement initiates phagocytosis
    • Phagolysosome fusion is inhibited
    • Cells replicate and lyse cell
  34. Legionella
    Epidemiology
    • Worldwide distribution
    • Lives in natural bodies of water, air conditioning cooling towers, condensers, water system (showers, hot tubs)
    • Survives in moist environments at high temps and disinfectant
    • Parasitize amoebas and replicate in protected environment
    • Disease is difficult to document – incidence is unknown
  35. Legionella
    Clinical Disease
    2 forms
    • Pontiac fever
    • -Influenza-like illness
    • Legionnaire’s Disease
    • -Severe form of pneumonia
  36. Pontiac Fever
    • Named after an epidemic in Pontiac, Michigan in 1968
    • Self-limiting with symptoms of fever, chills, muscle pain, general body weakness and lethargy(malaise), headache, flu-like
    • No evidence of pneumonia
    • Symptoms develop over a 12 hour period and then stick around for 2 to 5 days, then spontaneously disappears without antibiotic treatment.
    • There have been no deaths reported
  37. Legionnaires' disease
    • More severe causes morbidity and death unless treated properly
    • Incubates for 2 to 10 days followed by symptoms of fever, chills, dry nonproductive cough, headache
    • Often present is multiorgan disease, including the GI tract, CNS, liver, and kidneys.
    • Pneumonia is the primary manifestation
    • Pulmonary function deteriorates in patients with no treatment
    • Mortality rate is 15-20%
  38. Legionella
    Lab Diagnosis
    • Direct microscopy
    • Clinical specimens stain poorly with Gram stain
    • Use Dieterle’s silver or Ginenez’s stains
    • Direct Fluorescent Antibody (DFA) more sensitive
  39. Legionella
    Lab Diagnosis
    • Culture on buffered charcoal yeast extract (BCYE)
    • Contains L-cysteine and iron salt
    • Antigen test sensitive for L. pneumophilia serogroup1 but poor for others
    • PCR is sensitive and specific
  40. Legionella
    Treatment
    • Some antibiotics are incapable of penetrating macrophages
    • Macrolides and fluroquinolones
    • Specific treatment for pontiac fever is not necessary as it is self limiting
  41. Legionella
    Prevention/Control
    • Identification of the environmental source and elimination of it
    • Hyperchlorination of the water supply
    • Maintenance of elevated water temperatures
    • Elimination of the organism is difficult
    • Hospitals -monitor their water supply
  42. Clostridium
    • Clostridium historically classified on four properties
    • Produce endospores
    • Strict anaerobes
    • Cannot reduce sulfate
    • Gram positive cell
    • Reorganization underway
  43. Clostridium
    Histotoxic group
    • Tissue infec
    • cellulilitis
    • myonecrosis
    • gas gangrene
    • fasciitis
  44. Clostridium
    Enterotoxigenic group
    gastrointestinal disease
  45. Clostridium perfingens
    • Large Gram+ bacilli
    • Spores rarely seen in ivtro or in clinical specimens
    • Non-motile but has rapid spreading growth on media – similar to motile organisms
    • Major agent of clostridial myonecrosis – gas gangrene
    • Black muscle tissue – decaying tissue
    • 5 types – based on production of toxins
    • —Type A
    • – human infections
    • —Types B-E
    • – animal infections
  46. Clostridium perfingens
    Virulence Factors
    • Multiple Toxins –
    • α, β, ε, ι,
    • Collagenase
    • DNase
    • Hyaluronidase
    • All involved in necrosis
  47. Clostridium perfingens
    Epidemiology
    • Ubiquitous
    • Widely distributed in soil & water
    • Commonly inhabits intestinal tract of humans and animals
    • Endogenous or exogenous spread
  48. Clostridium perfingens
    Pathogenesis
    Tissue infections
    • Tissue trauma
    • Inoculation
    • Decreased oxygen tension
    • Multiplication
    • Toxin production and subsequent gas production
    • Spread along muscle plains
    • Kills all cells in path – creates more necrosis
    • If untreated – bacteremia & death
  49. Clostridium perfingens
    Clinical Diseases
    Soft Tissue Infections
    • Cellulitis– localized edema and erythema with gas formation in soft tissue
    • Suppurative myositis – accumulation of pus in muscle with no necrosis
    • Myonecrosis (gas gangrene) – painful rapid destruction of muscle tissue
    • High mortality – death within 2 days of onset
  50. Clostridium perfingens
    Clinical Diseases
    • Gastroenteritis
    • Food poisoning – intoxication
    • Rapid onset of symptoms – abdominal cramps, diarrhea
    • No fever, nausea or vomiting
    • Last 1-2 days
    • Necrotizing Enteritis
    • Necrosis of jejunum – toxin mediated
    • Symptoms include abdominal pain, vomiting, bloody diarrhea and peritonitis
    • Mortality-50%
  51. Clostridium perfingens
    Laboratory Diagnosis
    • Laboratory diagnosis is confirmatory – therapy must be initiated right away
    • Direct microscopy of clinical specimens – large gram + rectangular rods
    • Double zone of hemolysis on blood agar
    • Small beta hemolysis zone
    • Large alpha hemolysis zone
    • Grow on egg-yolk agar
    • —α-toxin hydrolyzes phospholipids producing opaque precipitate
  52. Clostridium perfingens
    Treatment
    • Rapid treatment critical for severe infections
    • Debridement – surgical removal of dead tissue and debris from wound
    • Clean to healthy, bleeding tissue
    • High dose penicilin
    • Anti-α-toxin and hyperbaric oxygen chamber no longer used – ineffective
    • Symptomatic treatmentfor food poisoning
  53. Clostridium perfingens
    Prevention/Control
    Proper wound care and prophylactic Abx
  54. Clostridium tetani
    • Causative agent of tetanus
    • Gram positive
    • obligate anaerobe with prominent terminal spore (drumstick appearance)
    • Vegetative cell extremely sensitive to oxygen
    • Spores enables long-term survival
  55. Clostridium tetani
    Virulence Factors
    • Tetanospasmin – neurotoxin
    • Plasmid encoded
    • Intracellular toxin released by cellular autolysis during stationary phase
    • Heat labile (can be killed by heat)
    • A-B toxin
    • A subunit binds to sialic acid receptors on motor neurons
    • B-subunit inhibits proteins that regulate release of inhibitory neurotransmitters
    • Results in spastic paralysis – uncontrolled contraction
  56. Clostridium tetani
    Epidemiology
    • Ubiquitous
    • Spores found in soil
    • Exposure to spores is common
    • Disease is uncommon in U.S. - < 40 cases annually
    • Proper medical care and vaccine available
    • More than 1 million cases worldwide
    • Mortality- 30-50 %
  57. Clostridium tetani
    Pathogenesis
    • Puncture wound
    • Contaminated with spores
    • Germinate in anaerobic environment
    • Multiply at site – do not invade
    • Release toxins
    • Toxins spreads
    • Blocks neurotransmitted
    • Spastic paralysis
  58. Clostridium tetani
    Clinical Disease
    • Generalized tetanus most common form
    • Involvement of masseter muscles – resulting in lockjaw
    • Risus sardonicus – sardonic smile resulting from sustained contraction
    • Other signs include drooling, sweating and persistent back spasms
    • Localized tetanus confined to site in primary infection
    • Cephalic tetanus –confined to the head
    • Neonatal tetanus –initial infection of the umbilical stump
    • High mortality – 90%
  59. Clostridium tetani
    Laboratory Diagnosis
    • Diagnosis made on the basis of clinical signs
    • Very hard to isolate organism from patient
    • Microscopy and culture have low sensitivity – 30%
    • Neither toxin or anti-toxin antibodies are present in serum
  60. Clostridium tetani
    Treatment
    • Debridement ofinfected area
    • Antibiotic of choice– metronidazole
    • Passive immunization with anti-toxin antibodies
  61. Clostridium tetani
    Prevention/Control
    • DTP
    • 3 doses of tetanus toxoid with booster every 10 years
  62. Clostridium botulinum
    Structure and Virulence Factors
    • Gram positive
    • spore forming bacillus
    • Obligate anaerobe – very sensitive to oxygen
    • Fastidious
    • 8 distinct toxins (A-G)
    • A, B, E and F associated with human disease
    • Similar to tetanus toxin
    • Prevents release of acetylecholine at myoneural junction (where neuron meets muscle)
    • Results in flaccid paralysis
  63. Clostridium botulinum
    Epidemiology
    Ubiquitous
  64. Clostridium botulinum
    Clinical Disease
    Infant botulism
    • C. botulimun colonized intestinal tract of infants
    • Cannot colonize adults
    • Initially nonspecific symptoms – constipation, weak cry, “failure to thrive”
    • Progress to flaccid paralysis and respiratory arrest
  65. Clostridium botulinum
    Clinical Disease
    Foodborne Botulism
    • mostly associated with home canned foods
    • Blurred vision, dry mouth, constipation and abdominal pain
    • ->flaccid paralysis and bilateral descending weakness of
    • peripheral muscles
  66. Clostridium botulinum
    Clinical Disease
    Wound botulism
    • Clinical presentation the same as foodborne botulism
    • Less GI symptoms
  67. Clostridium botulinum
    Clinical Disease
    Inhalation botulism
    Bioterrism
  68. Clostridium botulinum
    Laboratory Diagnosis
    • Adult cases harder to diagnose - no single test has greate than 60% specificity
    • Culture organism from feces of patient or from suspected food.
    • Heat to 80C for 10 mins to kill contaminating microbes
    • grow on egg-yolk agar
    • mouse bioassay to test for pre sence of toxin
    • Infant botulism more likely to culture from feces and detect toxin in blood
  69. Clostridium botulinum
    Treatment
    • Metronidazole- elimination of bacteria from GI tract
    • Trivalent antitoxin
    • —Ventilator support
  70. Clostridium botulinum
    Prevention and Control
    • —Destroying spores in food – very hard for practical reasons
    • —Prevent spore germination – acid pH, high sugar concentration or spore at 4C
    • —Destroy preformed toxin by proper cooking – at least 60C for 10 min
    • —Infant botulism associated with consumption of spore contaminated honey – no honey to children yuonger than 1 yr
  71. Clostridium difficile
    Structure and Virulence Factors
    • Gram +
    • spore forming rod
    • obligate anaerobe
    • Produce two toxins
    • enterotoxin
    • —cytotoxin
  72. Clostridium difficile
    Epidemiology
    • Ubiquitous
    • Colonizes GI tract of small percentage of healthy individuals (5%)
    • Broad spectrum Abx leads to overgrowth of C. difficile
    • Spores are shed in infected people
    • Detected in hospital rooms – leads to exogenous spread
  73. Clostridium difficile
    Clinical Disease
    • Antibiotic associated diarrhea
    • Acute diarrhea develops 5-10 days post initiation of Abx treatment
    • Ampicillin, clindamycin
    • Usually brief and self-limiting
    • Pseudomembranous colitis
    • -More severe
    • -False membrane of fibrin, mucus and inflammatory cells line intestinal mucosa
    • -White plaques
    • -Profuse diarrhea, abdominal cramps and fever
  74. Clostridium difficile
    Laboratory Diagnosis
    • Detect toxin in feces
    • Commercial immunoassays
    • Isolation of bacteria in feces confirms colonization but not disease
  75. Clostridium difficile
    Treatment
    • Discontinue suspected Abx in mild disease
    • —Metronidazole or vancomycin for severe disease
    • Kills vegetative cells not spores – relapse common
  76. Clostridium difficile
    Prevention and Control
    Thorough cleaning of hospital room of infected patient after discharge
  77. Mycoplasma
    • Smallest free-living bacteria – non-intracellular parasites
    • Form pleomorphicfilaments
    • Have “fried egg appearance”
    • Lack cell wall
    • Incorporate sterols into plasma membrane
    • Resistant to Penicillin, Cephalosporins
    • Originally thought to be a virus
  78. Mycoplasma
    Bacteria like
    • Divide by binary fission
    • Most facultatively anaerobic
    • Contain both RNA and DNA
    • Grow on cell-free media
  79. Mycoplasma
    Virus like
    • No cell wall
    • Filterable
    • Stain poorly
  80. Mycoplasma pneumoniae
    Pathogenesis
    • Extracellular pathogen
    • Infection by inhalation
    • Adheres to respiratory epithelium by protein attachment factor
    • Interacts with sialated glycoprotein receptors at the base of cilia
    • Ciliostasis followed by destruction of superficial epithelial cells
    • Disrupts normal clearance of upper respiratory system
    • M. pneumoniae acts as superantigen
    • —Contributes to both clearance of cells and observed disease
  81. Mycoplasma pneumoniae
    Epidemiology
    • Worldwide cause of pneumoniae
    • No consistent increase in seasonal occurrence
    • Epidemics every 4 to 8 yrs
    • Most common in school-aged kids and young adults
    • True incidenceunknown – not reportable, no reliable diagnostic test
    • Spread by nasal secretions – close contact required
  82. Mycoplasma pneumoniae
    Clinical disease
    • Pneumonia – walking pneumonia or typical pneumonia or atypical
    • Starts out as mild fever, malaise, headache
    • 2-4 days later – nonproductive cause
    • May progress to tracheobronchitis – bronchial inflammation
    • Develop pneumonia – patchy bronchopneumonia
    • Secondary complications include otitis media, erythema multiforme, myocarditis, pericaditis and CNS involvement
    • Erythema multiforme – allergic reaction of skin and mucus membranes
  83. Mycoplasma pneumoniae
    laboratory Diagnosis
    • Microscopy – not useful due to poor staining
    • Culture – slow (2-6 weeks)
    • PCR – excellent sensitivity but undefined specificity (may detect non-pathogenic strains)
    • Serology – detect antibodies against M. pneumoniae via complement fixation or enzyme agglutination
  84. Mycoplasma pneumoniae
    Treatment
    • —Erythromycin, tetracycline or fluoroquinolones
    • Tetracylcine fluoroquinolones – adults only
  85. Mycoplasma pneumoniae
    Prevention/Control
    • Spread byclose contact – isolation of infected individuals
    • —Impractical since patients are infectious for long periods of time
    • —Experimental vaccines have not conferred protective immunity
  86. Rickettsia
    • Small pleomorphic coccobacilli
    • Obligate intracellular parasite – grow only in cytoplasm or eukaryotic
    • Stain poorly
    • Most are transmitted by vectors
    • Also first thought to be a virus
  87. Rickettsia
    Bacteria like
    • DNA and RNA
    • Gram negative cell wall
    • Binary fission
    • Has ribosomes, makes enzymes for Krebs
    • Inhibited by Abx
  88. Rickettsia
    Virus like
    • Small
    • Obligate intracellular parasite
    • Poor Gram stain
  89. Rickettsia
    Pathogenesis
    • Transmitted by arthropod bite
    • Penetrates endothelial cells lining small blood vessels
    • Multiplication in endothelial cells
    • Cell rupture
    • Leakage thrombosis and vasculitis
    • Results in rash– blood in skin
    • Role of endotoxin is minimal
  90. Rickettsia rickettsii
    Epidemiology
    • Etiological agent of Rocky Mountain Spotted Fever
    • 500-1000 casesannually in U.S.
    • First described in Idaho and Montana
    • Primarily seen in southern Atlantic state
    • Principle vector– wood tick
    • Seasonal occurrence– 90% of cases between April and October
  91. Rickettsia rickettsii
    Clinical Disease
    • Rocky mountain spotted fever
    • Symptoms develop 2-14 days after tick bite
    • High fever, chills, headache, followed by rash – small petichial lesions
    • Rash usually seen in extremities then spread to trunk – can involve palms and soles (differentiate from measles)
    • Complications include GI symptoms, encephalitis and respiratory and/or renal failure
  92. Rickettsia rickettsii
    Laboratory Diagnosis
    • Culture – tissue culture of chicken embryos
    • —More for research/reference labs
    • Microscopy – DFA, MIF
    • —Microimmunofluorence (MIF) – detects specific outermembrane proteins
    • —Useful to detect genus, Western blot to confirm species
    • PCR – also genus specific
  93. Rickettsia rickettsii
    Treatment
    • 20% mortality if untreated
    • Doxycycline drug of choice
    • —Fluoroquinolones as alternative
  94. Rickettsia rickettsii
    Prevention/Control
    • No vaccine
    • Avoid ticks, wear protective clothing, insecticides
  95. Rickettsia prowazekii
    Epidemiology
    • Etiological agent of epidemic typhus (aka louse-borne typhus)
    • Primary reservoir– human
    • Spread by human head/body louse
    • Crowding, unsanitary conditions favor spread
    • Incidence in U.S. unknown (pretty low) – not reported
    • More common in Central and South America and Africa
  96. Rickettsia prowazekii
    Clinical Disease
    • Initial symptoms of high fever, severe headache, chills, myalgias (muscle pain), arthralgia (joint pain) – nonspecific symptoms
    • About 40% develop petechial rash
    • Complications include myocarditis and CNS disorders
    • Mortality rate up to 66%
  97. Rickettsia prowazekii
    Lab Diagnosis
    MIF
  98. Rickettsia prowazekii
    Treatment
    tetracycline or chloramphenicol
  99. Rickettsia prowazekii
    Prevention
    inactivated vaccine available for at risk populations
  100. Spirochetes
    • Thin, helical, gram negitive bacteria
    • Order: Spirochaetales
    • —Family: Spirochaetaceae
    • Genus: Treponema
    • Borrelia
    • —Family: Leptospiraceae
    • Genus: Leptospira
  101. Treponema pallidum ssp pallidum
    Characteristics
    • Thin, tightly coiled spirochetes with tapered ends
    • Causitive agent of syphilis
    • Motile by periplasmic flagella
    • Cannot be grown on artificial cultures
    • Does not survive well outside of host
    • Does not stain well
    • Need to visualize with dark field or fluorescent microscopy
  102. Treponema pallidum ssp pallidum
    Virulence Factors
    • Adherence– outermembrane proteins
    • Ability to penetrate epithelial cells
    • Coating of fibronectin – antiphagocytic
  103. Treponema pallidum ssp pallidum
    Epidemiology
    • ¢Found
    • Worldwide
    • 3rd most common STD in U.S.
    • Transmitted from direct sexual contact or from mother to fetus
    • Not highly contagious - ~30% chance of acquiring disease after single exposure to infected partner
    • Transmission rate dependent upon stage of disease
    • Long incubation period during which time host is non-infectious
    • Prostitution for drugs or for money to purchase drugs remains central epidemiologic aspect of transmission
  104. Treponema pallidum ssp pallidum
    Pathogenesis
    • Tissue destruction and lesions primarily a result of an autoimmune response
    • Syphilis is a disease of blood vessels and of the perivascular areas
    • Host produces a vigorous immune response but the organisms are capable of persisting for decades
    • Infection is neither fully controlled nor eradicated
    • In early stages, there is an inhibition of cell-mediated immunity
    • Inhibition of CMI abates in late stages of disease, hence late lesions tend to be localized
  105. Treponema pallidum ssp pallidum
    Clinical diseases
    • Syphilis
    • Primarily a STD
    • Can be transferred congenitally
    • Occurs in phases
  106. Treponema pallidum ssp pallidum
    Clinical Diseases
    Primary syphilis
    • Invasion of mucus membranes, rapid multiplication & wide dissemination in lymphatics and systemic circulation
    • Prior to primary lesion
    • Papule develops at the site of inoculation
    • Erodes to become a painless ulcer with raised borders (Chancre)
    • Chancre changes from hard to ulcerative with profuse shedding of spirochetes – very contagious
    • Regresses in two months
  107. Treponema pallidum ssp pallidum
    Clinical Diseases
    Secondary Syphilis
    • Secondary disease 2-10 weeks after primary lesion
    • Flu-like symptoms appear then skin rash
    • Secondary lesions of the skin and mucus membranes are highly contagious
    • Resolves slowly over a period of weeks to months
  108. Treponema pallidum ssp pallidum
    Clinical Diseases
    Latent Syphilis
    • Following secondary disease, host enters latent period
    • First 4 years = early latent
    • Subsequent period = late latent
    • About 40% of late latent patients progress to late tertiary syphilitic disease
  109. Treponema pallidum ssp pallidum
    Clinical Diseases
    Tertiary Syphilis
    • Diffuse, chronic inflammation can cause destruction to any tissue/organ
    • Often localized granulomatous dermal lesions in which few organisms are present
    • Granulomas reflect containment by the immunologic reaction of the host to chronic infection
    • —CNS involvement – dementia, seizures, etc.
  110. Treponema pallidum ssp pallidum
    Clinical Diseases
    Congenital Syphilis
    • Congenital syphilis results from transplacental infection
    • Causes septicemia in the developing fetus with widespread dissemination
    • Abortion, neonatal mortality and late mental and physical problems
  111. Treponema pallidum ssp pallidum
    Laboratory Diagnosis
    • Microscopy– Dark field or DFA of exudate from skin lesions
    • —Must be done right away – do not survive long outside the body
    • Culture– none
  112. Treponema pallidum ssp pallidum
    Laboratory Diagnosis
    Serology
    • Treponemal tests
    • Fluorescent treponemal antibody-absorption (FTA-ABS)
    • Immobilized T. pallidum > patient serum > fluorescently tagged anti-human Ab.
    • —Treponema pallidum particle agglutination (TP-PA)
    • Particles with T. pallidum antigens mixed with patient serum
    • Nontreponemal test – measure Ig against lipids released from damaged
    • cells
    • Venereal Disease Research Laboratory test (VDRL)Rapid
    • Plasma Reagin Test
  113. Treponema pallidum ssp pallidum
    Treatment
    • Penicillin remains drug of choice
    • Alternatives– tetracycline, doxycycline
    • Only penicillin for neurosyphilis
    • 7-10 days continuously for early stage
    • At least 21 days continuously beyond the early stage
  114. Treponema pallidum ssp pallidum
    Prevention
    • Abstinence
    • Practice safe-sex
  115. HIV Transmission
    • Exposure to blood products
    • Transfusions
    • Hemophiliacs
    • Transplants
    • Needle sticks (health care workers)
    • Other –dentist, tattoos, etc
    • IV drug users – a major route of transmission of HIV in U.S.
    • Perinatal-
    • Before birth
    • During birth
    • —Through breast milk
  116. HIV Pathogenesis
    Sexual intercourse
    HIV infects and sticks to Langerhan and Dendritic cells, carried to lymph nodes
  117. HIV Pathogenesis
    Direct injection
    Infect Dendritic cells or monocytes/macrophages, carried to lymph nodes
  118. HIV Pathogenesis
    Immune system responds
    • Cell mediated and hemoral response
    • Viremia decreases, anti-HIV antibody titers increase
    • Body’s immune system clears viral particles from blood
    • HIV remains in lymphoid tissue in latent or proviral form
    • Incubation up to 10 years
    • MORE
  119. HIV Clinical Syndromes
    Asymptomatic period (acute phase)
    slide 17
  120. HIV Clinical Syndromes
    Early symptomatic
    Slide 18
  121. HIV Clinical Syndromes
    AIDS
    slide 19
  122. HIV Epidemiology
    homosexual men in U.S.-spread throughout world
  123. HIV Epidemiology
    2 types
    • HIV-1
    • HIV-2
  124. HIV-1
    • More virulent
    • —Responsible for worldwide epidemic
    • Severity of infection varies from person to person
  125. HIV-2
    • —Primarily found in western Africa
    • —Not transmitted as efficiently
    • Genome more closely related to SIVmm than HIV-1
  126. HIV Treatment
    • Anti-HIV drugs classified into 4 categories
    • —Fusion-penetration inhibitors
    • —Nucleoside analogue reverse transcriptase inhibitors
    • —Non-nucleoside analogue reverse transcriptase inhibitors
    • —Protease inhibitors

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