Review from last time: Sexually transmitted diseases

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Review from last timeSexually transmitted
diseases

• Epidemiological principles of STDs
• UTI/Bladder infections
• Infections of mucosal surfaces
• Neisseria gonorrhea and Chlamydia trachomatis
• Ulcerative Infections
• Syphilis (T. pallidium) and Chancroid (H. ducreyi)

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Alimentary Tract Infections

• Denise Kirschner, PhD
• Dept of Micro/Immuno
• MICRO 532 Dec 3,2001

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Outline

• Physiology and IM
• Upper Alimentary Tract (UAT) Infections
• Dental pathogens
• H. pylori
• Lower Alimentary Tract (LAT) Infections
• Cholera (V. cholerae)
• Dysentery or Shigellosis (Shigella sp.)
• Gastroenteritis, food poisoning and salmonellosis
• Salmonella (S. cholerasuis and S. typhumurium)
• Travelers Disease (E. coli)
• Typhoid fever (Salmonella typhi)
• Diarrhea (Campylobacter jejuni)
• Non-Salmonella food poisoning

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Anatomy and Physiology of UAT

• Breakdown of food teeth and saliva (amylase)
  cooperate and esophagus tranfers food to stomach
  via peristalsis for digestion
• Pits and crevices in teeth are ideal places for
  anaerobic bacteria growth
• HCL and pepsin breakdown food in stomach
• IM-esophagus and stomach have none

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Indigenous Microflora of MouthMOST oral
infections caused by IM

• Attachment to cell surfaces in mouth (cheeks,
  gingiva, teeth, etc)
• All that flow through, only a few colonize
• Not uniform, most prominent Streptococci
• S. salivarius upper part of tongue
• S. sanguis-teeth, S. mitis- cheeks
• Dental plaqueMasses of bacteria (100bil/gm of
  plaque)
• Mouth is anaerobic(!) and gingiva is VERY
  anaerobic

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Dental caries

• Most common infectious disease in humans
• 20 bil/yr in cost
• Bacteria produce glucan (from sugars) which helps
  attach
• Bacteria store polysaccharides that are later
  metabolized to lactic acid
• Acid dissolves enamel of teeth, thus plaque acts
  like a sponge layer filled with acid soaking
  teeth
• Main characters Actinomyces(G),
  Lactobacillus(G), Neisseria(G-), Rothia(G),
  Streptococci(G), Veillonella(G-)
• Each are preferred anaerobes and do fermentation
  and/or lactic acid production

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Prevention of dental caries

• Flouride makes teeth more resistant to the
  action of acid (important to give to children
  when teeth are developing- in water supply)
• Teeth-brushing and flossing to remove bacteria
• Receding gums should be checked
• Restrict sugar in diet

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SEM of dental plaque. Note the hetergeneous
Population and the attachment To tooth and each
other
SEM of Streptococci adhering To oral mucosa
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Periodontal Disease

• Bacterial infection of the gums
• Plaque and calculus (calcified plaque) are
  involved (not known exactly how)
• Infection produced gingivitis (inflammation in
  the space between teeth and gums)
• Epidemiology most common in older people who do
  not practice good dental hygiene (chief cause of
  tooth loss)
• Penicillin can work, but better to brush, floss,
  remove plaque and calculus.
• Vaccine is presently under development

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Extreme outcomes of acute caries

• Trenchmouth-(ANUG- acute necrotizing ulcerative
  givngivitis) is an acute form of gingivitis with
  bacterial invasion into tissues
• Marked overgrowth of of plaque (Treponema
  denticula)
• Associated with poor oral hygiene
• Bacterial endocarditis
• Bacteremia usually follows dental procedures
  (usually cleared)
• In people with abnormal heart valves, bacteria
  can colonize the valves
• Treat with penicillin in patients suspected with
  problems for a few days before (and after) to
  reduce oral bacteria (drug-resistant strains
  grow-up quickly)

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The stomach antral and corpal regions
Corpus
Antrum
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The glands of the stomach
Taken from H.F. Helander (1992)
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H. Pylori (identified in 1982)

• Gram negative, spiral-shaped, motile bacteria.
• Strict human pathogen- colonizes the stomach
• Different disease trajectories
• Colonization/persistence superficial gastritis
  (most common outcome)- acts like IM
• Peptic ulcer disease (75 correlated)
• Duodenal ulcers (95 correlated)
• Dyspepsia
• Lymphomas/ carcinomas
• pH- dependent growth, virulence is adherence and
  motility
• Some countries 100 infected, USA- 50 prevalence
• Treatment antibiotics for 6 weeks
• How does this pathogen survive in the hostile
  environment of the stomach?
• pH, shedding of mucus, sloughing of cells,
  peristalsis

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• Lower Alimentary Tract (LAT) Infections
• Cholera (V. cholerae)
• Dysentery or Shigellosis (Shigella sp.)
• Gastroenteritis, food poisoning and salmonellosis
• Salmonella (S. cholerasuis and S. typhumurium)
• Travelers Disease (E. coli)
• Typhoid fever (Salmonella typhi)
• Diarrhea (Campylobacter jejuni)
• Non-Salmonella food poisoning

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Liver
Stomach
Gall bladder
Pancreas
Large intestine (colon)
Upper small Intestine (duodenum)
Small intestine
8-9 ft./ 30sq ft of surface area due to microvilli
Appendix
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Peyers patches the lymph nodes of the gut
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Anatomy and Physiology and LAT

• Indigenous microflora colon contasins a large
  no. of species (gt 300). Bacteriodes (major one,
  bulk of bacteria), E. coli, Enterobacter,
  Klebsiella, Proteus
• Bacteria can be 1/3 of fecal weight (1011
  bacteria/ gm of feces)
• Small intestines digestive enzymesabsorption
• Large recycle intestinal water and absorption

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Disease in the LAT

• Infectious diarrhea is widespread and 5 mil/yr
  die (80 lt 1 yr of age)
• Two main mechanisms
• Toxin production
• Invasion of epithelium
• 3 characteristics of all gut pathogens
• All cause diarrhea (watery or bloody)
• All have adhesins (fimbriae, pili, capsules)
• Fecal-oral transmission
• Treatment with ORT
• Oral rehydration therapy water, glucose and
  electrolytes
• (UNICEFs main goal)

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http//www.cdc.gov/foodnet/annual/98/pdf/FN_98_fin
al_report.pdf
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Cholera Vibrio cholerae

• Second isolated pathogen by R. Koch
• Extracellular, G-, motile with pilus and toxin
• Once colonized intestine, releases toxin that
  causes watery diahhrea by induces cells to
  excrete ions and water (up to 20 liters/day)
• A-B toxin encoded by a phage
• Epid several pandemics of cholera- most recently
  in 1992, ¾ mil people infected (V. cholera O139)
• Treatment ORT disease eventually subsides. Keep
  water supply clean (oral vaccine available, 50
  effective for 6 months killed celltoxin B)

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VibrVVibrio cholerae
Scanning EM
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Dysentery (Shigellosis) Shigella

• G-, rod, intracellular, facultative anaerobe
• Destroys colon cells, bloody, pus diarrhea
• Moves through cells like a comet using actin
  filaments and grows beneath cell layer
• Lysteria monocytogenes has a smiliar lifestyle
• Virulence low ID50, and produces toxin (A-B)
• Shiga toxin (similar to cholera toxin), but main
  affect is not toxin mediated like V. cholerae
• Prevalent under low sanitary conditions, US gt
  20,000 cases/yr
• Treatment sanitary measures, antibiotics can
  limit duration (or sulfur). There are drug
  resistant strains

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Actin filaments
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Salmonellosis (food poisoning)

• Diarrheal diseases caused by Salmonella sp.
• G- rods, anaerobes, intracellular pathogens by
  penetrating epithelium
• S. cholerasuis and S. typhumurium
• Causes inflammation leading to fluid secretion
  (watery diarrhea)
• Treatment adequate cooking of food, checking
  meat sources, normally self-limiting
• Proper surveillance of an outbreak can contain it

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Travelers disease E. coli

• Part of IM, thought to be non-pathogenic, but
  some species cause diarrhea (G-)
• Virulent strains have aquired factors 4 main
  groups
• ETEC enterotoxogenic (toxin similar to
  cholera)- travelers and infant diarrhea. These
  also have adhesins for epithelium
• EPEC enteropathogenic (hospital nurseries and
  chronic diarrhea in children). Causes loss of
  microvilli and thickening of cells at attachment
  site
• EIEC enteroinvasive (similar to Shigellosis)
• EHEC enterohemorrhagic
• EHEC- (1982). Causes bloody diarrhea via toxin.
  Outbreak in Washington hamburgers fatal in
  infants and elderly (predominant serotype E.
  coli O157H7)
• TreatmentPrevention adequate food cooking, ORT,
  bismuth some antibotic treatment

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Escherichia coli - urine smear
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Typhoid Fever Salmonella typhi

• Intracellular, G-, strict human pathogen
• Destroys epithelium leading to bloody diarrhea
• Gets through to phagocytes in the gut (in the
  peyers patches and near M cells) to grow
• Virulence factors Cell wall (O antigen), Capsule
  (Vi antigen), Flagella (H antigen), Low ID50
• Has a high asymptomatic carriage (excreting 10
  billion bacteria/gm of feces). In these people,
  gall bladder has become infected.
• Typhoid Mary caused 53 cases over 15 years
• TreatPrev surveillance, sanitation,vaccine
  available, long antibotic regimens, carriers-
  removal of gall bladder

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Campylobacter jejuni

• Gram-negative bacteria
• spiral-shaped, small
• Motile, intracelluar
• Usually microaerophilic
• Tissue-like O2-5, CO2-10
• Similar to Shigella (bloody diarrhea)
• Associated with humans and animals
• ID50 is 500 or less
• Pentrates epithelium of small or large intestines
• Multiplies within and beneath cells
• Self-limiting (10 days), but erythromycin works
  in severe cases

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Sources of C. jejuni infection

• commercial poultry
• asymptomatic colonization of chickens
• found in 67-98 of processed meats (Chicken)
• MOST COMMON FOOD BORNE PATHOGEN
• in USA
• unpasteurized milk
• contaminated water

Virulence and colonization factors of C. jejuni

• ID50 lt 500 bacteria
• Unipolar flagellum
• Motile
• Cellular invasion
• Adherence
• Cytolethal distending toxin

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Other food poisonings

• Caused by bacterial PRODUCTS (exotoxins) not
  bacteria
• Staphylococcal S. aureus exotoxin (very heat
  stable)
• Clostridium perfringens (IM), Bacillus cereus
  (rice, 2-6 hr incubation) and Clostridium
  botulinum (A-B nuerotoxin)
• All toxin producing
• Cooking food destroys toxin (heat labile)
• For C. botulinum (botulism) ¼ of patients die
• Only a few drops are needed to cause disease