Bacterial Gastroenteritis Dr. Maitham F. Jalal M.B.CH.B- F.I.C.M.S( neurology )

3 groups of gram negative bacteria account for most bacterial intestinal infections: Vibrio cholerae (Cholera) Enterics (Salmonella, Shigella, E. coli) Campylobacter jejuni

Cholera Causative agent: Vibrio cholerae High infectious dose Bacteria sensitive to stomach acid Adheres to small intestine and multiply Bacteria don’t enter cells

Cholera toxin Potent exotoxin Causes intestinal cells to rapidly pump out electrolytes Passive osmotic H2O loss follows Metabolic acidosis Shock

Untreated cases potentially fatal Heavy loss of fluid “rice-water stool” Up to 20L of fluids lost per day May discharge 1 million bacteria per ml of feces Untreated cases potentially fatal Fluid/electrolyte replacement Tetracycline reduces toxin production

Shigellosis Causative Agent: Shigella sp. Low infecting dose S. dysenteriae, S. flexneri, S. boydii, S. sonnei Low infecting dose Bacteria not sensitive to stomach acid Characterized by fever and dysentery

Infects cells of large intestine and initiates intense inflammatory response Dead cells slough off Produces areas covered with pus and blood

All species produce enterotoxin and type III secretion systems S. dysenteriae produces powerful endotoxin shiga-toxin Ciprofloxacin, rifampin or azithromycin may reduce duration and infectivity

Traveler’s Diarrhea Causative Agent: Escherichia coli Multiple antigenic strains (O, H, K) Virulent strains have fimbriae, adhesions and multiple toxins Enterotoxigenic E. coli Enterotoxins Type III secretion system Typically self limiting

Enterohemorrhagic E. coli Produce potent Shiga-like toxins and type III secretion systems Antimicrobials cause increase in toxin production

Salmonellosis and Typhoid Fever Causative agent: Salmonella enterica 2000 strains (serotypes) Typhimurium and Enteritidis commonly cause Salmonellosis Typhi and Paratyphi cause Typhoid Fever

Common intestinal flora of many animals Contaminated animal products are reservoir Reptiles, eggs and undercooked poultry

Virulent strains tolerate stomach acid and pass to intestines Toxin induces phagocytosis in intestinal cells Pathogen reproduces inside phagosome killing host cell Bacteria (Typhi) may pass through intestinal cells into bloodstream

Typhoid fever is an enteric fever Macrophages carry bacteria to liver, spleen, bone marrow and gallbladder Treated with ciprofloxacin or ampicillin Surgical removal of gallbladder

Campylobacteriosis Causative agent: Campylobacter jejuni Leading cause of bacterial diarrhea in United States Estimated 1million cases annually with ~100 deaths Associated with poultry Low infecting dose

Virulent strains possess adhesions, cytotoxins and endotoxin Induce endocytosis in cells of intestine and initiate inflammation and bleeding lesions Non-motile mutants are avirulent Severe cases treated with ciprofloxacin or azithromycin

Guillain-Barré Syndrome Tingling of the feet leads to progressive paralysis of the legs, arms and rest of the body 40% of cases preceded by campylobacteriosis May be associated with autoimmune response 80% recover completely; 5% mortality with treatment

Bacterial Food Intoxication Staphylococcus aureus Halotolerent; grows well in foods at room temp Associated with cafeterias and social functions

5 heat stable enterotoxins: 1000 for up to 30 min Stimulate muscle contractions, nausea and intense vomiting, diarrhea and cramping Acute and self limiting symptoms begin 4-6 hrs after consumption and end within 24 hrs

Botulism Causative agent: Clostridium botulinum Obligate anaerobic, Gram +, spore forming bacillus Produce 7 different neurotoxins One of most deadly toxins known

Signs & Symptoms Dizziness, dry mouth, blurred vision Abdominal symptoms include pain, nausea, vomiting and diarrhea or constipation Progressive paralysis Paralysis of respiratory muscles most common cause of death

3 forms of botulism: Food-borne botulism – progressive paralysis of all voluntary muscles due to toxin production Wound botulism – similar symptoms Infant botulism – bacteria grow in the intestines, producing non-specific symptoms “floppy baby syndrome”

Epidemiology Food borne botulism Wound botulism Infant botulism Commercial sterilization Toxin destroyed by heating foods Wound botulism deep crushing wounds Infant botulism Inhalation or ingestion of spores Commonly associated with honey or juices

Prevention Treatment Proper sterilization and sealing of canned food No honey or unpasteurized juices for infants!! Treatment Antitoxin Gastric washing and surgical removal of tissues Artificial respiration may be required Anti-microbials given to kill bacteria in infant and wound botulism