Microbes Bacterial making history and in the news

1
Microbes (Bacterial) making history and in the
news

• Bubonic plague (Yersinia pestis)
• Anthrax (Bacillus anthracis)
• E. coli and Salmonella
• H. pylori

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Plague (Yersinia pestis)

• Claimed gt 200 million deaths thru history
• Bubonic form 50-75 mortality (flea)
• Pneumonic form gt 90 mortality and highly
  contagious (person to person)
• 2003 -- still exists, gt2000 cases worldwide (97
  in US since 1990)
• Currently antibiotics successfully treat 90 of
  reported cases, but R plasmids now foundin some
  infections

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Plague (Yersinia pestis) pix

• www.insecta-inspecta.com
• www.raschart.com/images/YersiniaPestis

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Bubonic plague

• Y. pestis causative agent -- G- rod, obligate
  parasite 26-280 vs. 370
• 2 stages of infection (intra- and
  extra-cellular), 3 plasmids encode virulence
  factors
• Y. pestis are engulfed by macrophages but can
  grow inside, travel to and spread within lymph
  nodes first, later encapsulated bacteria are
  released into blood and travel throughout the
  body
• Capsule (F1 protein) only produced at 370,
  prevents phagocytosis by both PMNs and M? is
  adhesin for IL-1R
• Type III secretion system (includes V antigen)
  injects 6 prots (apoptotic)
• pla (plasminogen activator) is a protease that
  inactivates compliment proteins
• Siderophores transport iron
• Exotoxins, endotoxins contribute to septicemia

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Anthrax -- Bacillus anthracis

• Ubiquitous facultative anaerobe, Gram rod
  found in soil
• Soil forms have endospores, but lack capsules, M?
  take up spores
• Pathogenic strains multiply within M?s, develop
  capsules and lyse cells
• Encapsulated strains resist further phagocytosis,
  release toxins
• Pulmonary anthrax (spore inhalation) mortality
  rates nearly 100 if not treated immediately
  after exposure

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Bacillus anthracis (Fig. 22.1)

• Anthrax toxin comprised of 3 plasmid-encoded gene
  products (PA, LF and EF)
• LF kills WBCs as well as many other kinds of
  cells -- protease that inhibits major signaling
  pathways
• EF elevates cAMP (adenylate cyclase)
• PA acts to get LF and EF toxins into cell
• Endothelial cells become leaky, causing shock and
  death

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Anthrax as a weapon

• Refers to small size particles of endospores
• No person-person spread
• Antibiotics readily available
• In 1979 1 g spores were released causing 77
  cases with 66 deaths (Russia)
• In 2001 there were 22 cases, 5/11 pulmonary cases
  fatal in US

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Pathogenic Enteric bacteria

• Approximately 10-20 of all bacteria are
  pathogenic, but are limited by competition
• Disease often associated with the ability to
  colonize epithelial lining and then cause disease
  via a multitude of virulence factors
• Pathogens often transfer virulence genes to other
  strains (found on plasmids, phage and often on
  transposable elements)

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Pathogenic E. coli

• Usually E. coli strains are enteric commensals
• There are 200 known pathogenic strains that cause
  diarrheal diseases or UTIs
• Enterhemorrhagic EC (EHEC, e.g., O157H7) produce
  verotoxins(Shiga-like) that cause bloody diarrhea
  and kidney failure (70,000cases/60 deaths/yr in
  US) (Phage-encoded)
• Enterotoxigenic strains cause watery (ETEC,
  Travelers) diarrhea via 1 or 2 enterotoxins
  (plasmid-encoded)
• Enteropathogenic (EPEC) strains produce no toxins
• Enteroinvasive (EIEC) escape phagocytosis after
  being taken up, grow in phagocytes, then escape
  and invade cells of colon

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E. coli O157H7

• O157H7 most prevalent pathogenic E. coli in
  developed countries (ingest 10 bacteria and get
  sick)
• Has type III secretion system that injects
  intestinal cells with adhesins, causing further
  binding of the pathogen
• Produces Shiga-like toxins called verotoxins
  (kills cells by stopping protein synthesis) that
  cause kidney failure and bloody diarrhea spreads
  by binding to PMNs
• staff.vbi.vt.edu/www.freewebs.com

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Salmonella sp.

• Over 2000 strains of S. enterica known, 1/3 of
  all chicken eggs contaminated
• Reptile pets frequently carriers
• S.typhi causes typhoid fever --gt bacteria pass
  through intestinal wall, are phagocytosed but not
  killed in blood, are carried to liver, spleen,
  gall bladder
• Carriers (Typhoid Mary) often maintain bacteria
  in gall bladder

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Ulcers -- the H. pylori connection

• Helicobacter pylori is responsible for most
  peptic ulcers
• Very common -20-50 of people have it, but
  usually doesnt make ulcers
• It secretes enzymes (urease) that neutralize acid
  and high levels of SOD and catalase help to
  inhibit phagocytic death
• Disruption of mucoid covering and inflammation
  cause stomach acid to erode stomach lining,
  allowing the bacteria to invade deep into tissues
• Treatment antibiotics