Review%20from%20last%20time:%20Mycobacterium%20tuberculosis

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Review from last timeMycobacterium tuberculosis

• Microbiology of M. tuberculosis
• History and Epidemiology
• Immunobiology and Disease
• Testing and Vaccination
• Therapy chemoprophylaxis and treatment
• Drug Resistance
• Host susceptibility

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Some after-thoughts on TB

• Why treat latent TB?
• Why do the skin test or vaccine NOT cause
  disease?

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Skin Wound infections

• Denise Kirschner, Ph.D.
• Dept. of Micro/Immuno
• MICRO 532 Nov 28, 2001
• Chapters

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Outline

• Skin Infections
• Contrasting Staph aureus with Strep pyogenes
• Folliculitis, boils and carbuncles
• Rocky mountain spotted fever (R. rickettsii)
• Lyme disease (B. burgdorferi)
• Anthrax (Bacillus anthracis)
• Bacterial infections of Wounds
• Tetanus (C. tetani)
• Gangrene (C. perfringens)
• Burn infections (P. auerginosa)
• Actinomycosis (A. israelii)

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SKIN- anatomy and physiology

• Large complex organ covering the external body
  surface
• Protective layer offers resistance to infection-
  acidic, dry, unstable, toxic
• Important role in vitamin D synthesis
  (bones/teeth)

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Produce sebum
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Hair follicle
Skin surface
Propionibacteria
INDIGENOUS MICROFLORA 3 groups 1)Propionibacteriu
m acnes (Corynebacterium genera)- G,
non-motile 2)Staphylococci (S. epidermis is the
primary) Colonization resistance 3)Malassezia
(yeast)
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Outline

• Skin Infections
• Contrasting Staph aureus with Strep pyogenes
• Folliculitis, boils and carbuncles
• Rocky mountain spotted fever (R. rickettsii)
• Lyme disease (B. burgdorferi)
• Anthrax (Bacillus anthracis)

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Folliculitis, boils and carbuncles- most caused
by S. aureus

• Infection of the hair follicle
• Folliculitis red bump, remove hair and resolves
• Boil- if infection extends into local tissues
  causing inflammation (rubor, dolor, tumor, color)
• pus drainage
• Carbuncles-large area of inflammation with
  several sites of draining pus- usually develop in
  areas of skin that are thick (accompanied by
  fever plus other signs of serious infection)
• Other skin infections caused by b-hemolytic,
  group A Streptococci- Flesh eating bacteria and
  most skin infections as well

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S. aureus infects a hair follicle (a)
(b)infection spreads Deeper into the tissue Where
abscess develops
c) An abscess forms below the skin with necrotic
plug
AbscessLocalized collection of pus
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Staphylococcus aureus

• Facultative anaerobe, G coccus
• Virulence Factors
• Capsule (inhibit phagocytosis)
• Protein A (binds Fc portion of Ab, inhibiting
  phagocytosis)
• TSST (toxin that causes rash, diarrhea, shock)
• Coagulase (impedes leukocyte recruitment)
• Epidermolytic toxin (separates layers of skin
  causing scalded skin syndrome) newborns, elderly
  etc
• Can be part of IM in almost all persons (nose)

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S. aureus
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Pyoderma

• Skin infection characterized by pus production
• Results from infection of an insect bite, burn or
  other wound
• Impetigo- the most common type
• Superficial skin infection
• Isolated pustules that weep become crusted and
  rupture
• Caused by both S. pyogenes gtgt S. aureus
• Reminder S. pyogenes (b-hemolytic group A)
• Treatment penicillin or other anti-staph
  antibiotic

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Streptococcus pyogenes
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Impetigo. This type of pyoderma is often caused
by Streptococcus pyogenes and may result in
glomerulonephritis.
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Outline

• Skin Infections
• Contrasting Staph aureus with Strep pyogenes
• Folliculitis, boils and carbuncles
• Rocky mountain spotted fever (R. rickettsii)
• Lyme disease (B. burgdorferi)
• Anthrax (Bacillus anthracis)

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Rocky Mountain Spotted Fever

• Caustive agent Rickettsia rickettsii
• Obligate, intracellular, G-, non-motile
• Induces endocytosis by host cells (small blood
  vessel-lining cells)
• Very hard to diagnose
• Zoonotic transmission- mammalian tick is carrier
  (Dermacentor species) dog/tick
• Requires 4-10 hour feed to transmit
• Symptoms headaches, sore joints, rash
• Treatment with antibiotics works if given early
  enough. W/o treatment- 20 death rate, (higher in
  elderly)

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1990
Rocky Mountain spotted fever
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Lyme Disease

• Isolated in 1982 in Lyme, Connecticut
• Causative agent Borrelia Burgdorferi a
  spirochete (not G/G-)
• Deer/mouse/tick zoonosis
• Disease stages and some mimic others (i.e.
  flu-like)
• Stage 1 (incubation) hallmark bullseye rash
  erythema chronicum migrans (after stage 1,
  difficult to isolate bacteria)
• Stage 2 2-8 weeks -heart and CNS impairments
  leading to paralysis and fatigue
• Stage 3 6 months after rash- arthritis and joint
  swelling (can last for years)
• Most common vector borne disease in USA
• Treatment preventionprotection, antibiotics if
  early

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Outline

• Skin Infections
• Contrasting Staph aureus with Strep pyogenes
• Folliculitis, boils and carbuncles
• Rocky mountain spotted fever (R. rickettsii)
• Lyme disease (B. burgdorferi)
• Anthrax (Bacillus anthracis)

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Bacillus anthracis

• G, soil organism that mainly infects cattle,
  sheep, goats and horses
• No human-human transmission
• Has a spore form (very stable!)
• Cutaneous anthrax If spore enters skin abraision
  a pimple develops that later becomes a blister
  with a swollen black scab. Usually curable.
• Spores can enter through inhalation (or
  ingestion)- almost 100 fatal in a few days (high
  bacteremia)
• Virulence capsule and toxin
• Since 1970 groups of military immunized
• No real incidence /prevalence in human pops

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Pathogenesis

• Endospores introduced into the body are
  phagocytized by macrophages and then germinate to
  vegetative bacteria.
• Intracellular stages take several hours.
• Mf take up all spores types rapid efficient.
• Anthrax spores have Mf-specific germination
  systems signals.
• Newly germinated bacilli escape the phagolysosome
  can grow in cytoplasm (membrane active toxins).
• Vegetative bacilli are released from host Mf into
  the blood. (108 /ml of blood)

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TOXINS- A-B type

• Lethal toxin lethal factor (LF) protective
  antigen (PA)
• Stimulates Mf to release TNF-a and IL-1- both
  leads to shock and sudden death in systemic
• Edema toxin edema factor (EF) PA
• Edema in cutaneous anthrax due to cyclic AMP
  homeostasis upset
• PA is the binding moeity (like the B in A-B)

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1-2 mm
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Outline

• Bacterial infections of Wounds
• Tetanus (C. tetani)
• Gangrene (C. perfringens)
• Burn infections (P. auerginosa)
• Actinomycosis (A. israelii)

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Tetanus

• Clostridium tetani
• Anerobic, motile G rod, spore forming
• Pathogenesis release of exotoxin that is
  extremely potent when taken up by nerve cells
  lockjaw
• Ubiquitous in soil /dust
• Prevention and treatment antitoxin together with
  TIG (tetanus immunoglobulin). Immunization with
  DPT. Toxoid. NEED boosters.

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C. tetani- tennis racket appearance
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Tetanus Incidence
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Gas Gangrene

• Caused by Clostridium perfringens
• Grows easily in dead or poorly oxygenated tissues
• Releases toxin
• A complication of dirty or neglected wounds

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Burn infections

• Pseudomonas aeruginosa
• Ubiquitous organism found in soil, water, etc
• Prevents healing
• Produces tissue damage
• Promotes septic shock
• Toxin similar to diptheria toxin
• Treatment- highly resistant, but some antibiotics
  work at high doses

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Actinomycosis can develop following dental surgery

• A slow progressive infection characterized by
  painful swelling under the skin that eventually
  opens and drains pus chronically (head/neck)
• Actinomyces israelii G, anaerobic bacterium
  (mistakenly named as a fungus)
• lumpy jaw
• Infection has cycles of abscess formation,
  scarring and pus tracts.
• Introduced (from IM) into wounds along with other
  bacteria (dental procedures)
• Seems to heal only to return days or weeks later

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