The central market in Bangalore, India. Food safety standards barely exist in most of the developing world.
A street vendor goes with his instinct to know when his kabobs are ready to eat in Bangalore, India.
Mushrooms come from Canada, peppers from the Netherlands, squash from California. A global harvest supplies Seattle’s Pike Place Market. Raw products are responsible for an increasing percentage of foodborne diseases.
To combat Salmonella, Arkansas graduate student sprays “healthfull” bacteria onto chicks to determine if they can out-compete harmfull bacteria in their intestinal tracts.
Production Processing Distribution Preparation
Escherichia coli SALMONELLA SHIGELLA YERSINIA Yersinia pestis (urban plaque, sylvatic plaque) Yersinia enterocolitica ENTEROBACTERIACEAE
Klebsiella pneumoniae Proteus mirabilis Enterobacter, Citrobacter, Serratia, Providencia Helicobacter pylori ENTEROBACTERIACEAE(cont.)
Escherichia coli Septicemia Urinary Tract Infections Neonatal Meningitis Gastroenteritis SALMONELLA Enterocolitis Septicemia Enteric Fever Asymptomatic (chronic) carriage SHIGELLA Dysentery
YERSINIA Yersinia pestis (urban plaque, sylvatic plaque) Yersinia enterocolitica Klebsiella pneumoniae Proteus mirabilis Enterobacter, Citrobacter, Serratia, Providencia Helicobacter pylori
Enterobacteria • The largest, most heterogeneous collection of pathogenic Gram-negative bacilli. • Normal flora of the GIT of humans and animals. • Present worldwide in soil, water and vegetation - excretion from the GIT. • Responsible for 30-35% of all septicemias, over 70% of urinary tract infections, and many intestinal infections.
Shigella, Salmonella and Yersinia pestis • Always associated with disease. • NOT found as normal flora in the human. E. coli, Klebsiella pneumoniae and Proteus mirabilis • Commensals that can cause opportunistic infections.
Enterobacteria infections can originate from: • Animal reservoir (most Salmonellainfections) • Human carrier (Shigellaand Salmonella typhi) • Endogenous spread (Escherichia coli)
EnterobacteriaPhysiology and Structure • Gram-negative bacilli, motile or non-motile, do not form spores. • Aerobes and facultative anaerobes. • Simple nutritional requirements, ferment glucose, reduce nitrate. • Catalase-positive and oxidase-negative. • Some members of the family have prominent capsules (e.g., Klebsiella).
EnterobacteriaSerological Classification • The O antigen - the outer polysacharide portion of lipopolysaccharides (LPS) • The K antigen - capsular polysaccharide (Vi in Salmonella typhi) • The H antigen - on the flagellar proteins
EnterobacteriaVirulence Factors • Endotoxin (LPS) • Capsule • Antigenic Phase Variation - to evade antibody response - alternative expression of capsular [K] and flagellar [H] antigens • Exotoxin production
EnterobacteriaVirulence Factors(cont.) • Expression of Adhesion Factors (fimbriae) • Intracellular Survival and Multiplication (invasion, replication and spread in the colonic epithelium) • Sequestration of Growth Factors/Iron (siderophores and hemolysins) • Resistance to Serum Killing • Antimicrobial Resistance
A shadow-cast electron micrograph of E. coli showing flagella.
Scanning electron micrograph showing E. coli interacting with human mast cell
E. coli-Clinical Syndromes • Septicemia • Urinary Tract Infections • Neonatal Meningitis • Gastroenteritis (five groups)
E. coli - Clinical Syndromes(cont.) • Septicemia - originates from infections in the urinary tract or the GIT. • Neonatal meningitis - E. coli and group B streptococci(S. agalacatiae) - the most common cause of neonatal meningitis.
E. coli - Clinical Syndromes(cont.) • Urinary Tract Infections - over 80% of community-acquired urinary tract infections and the majority of hospital-acquired infections (urinary catheters). Ascending infections - originate from the GIT, attach to urethra epithelium, ascend into the bladder, and may migrate to the kidney or prostate. These strains produce adhesins, which bind to cells lining the bladder and upper urinary tract.
E. coliGastroenteritis - five groups: 1. Enterotoxigenic E. coli (ETEC) - "travelers' diarrhea" 2. Enteroinvasive E. coli (EIEC) 3. Enteropathogenic E. coli (EPEC) 4. Enterohemorrhagic E. coli (EHEC) - E. coli strain O157:H7 5. Enteroaggregative E. coli (EAggEC)
E. coli 1. Enterotoxigenic E. coli (ETEC) - enterotoxins stimulate secretion and fluid loss. Secretory diarrhea follows 1-2 day incubation period and persists for 3-4 days (mild symptoms, cramps, nausea, vomiting, watery diarrhea;"travelers' diarrhea". 2. Enteroinvasive E. coli (EIEC) - invade and destroy the colonic epithelium. 3. Enteropathogenic E. coli (EPEC) - enteroadherent E. coli (pediatric diarrhea in impoverished countries).
Drug Therapies Used to Treat Moderate to Severe Traveler's Diarrhea in Adults Ciprofloxacin (Cipro), 500 mg twice daily for one to three days, or one 750-mg dose (if diarrhea resolves) Norfloxacin (Noroxin), 400 mg twice daily for one to three days Ofloxacin (Floxin), 300 mg twice daily for one to three days Trimethoprim-sulfamethoxazole (Bactrim DS), 160 mg/800 mg twice daily for three days Doxycycline (Vibramycin), 100 mg twice a day for three days ------------------------------------------------------------------------ NOTE: In the absence of dysentery, loperamide (Imodium A-D), two 2-mg tablets at the start of diarrhea, followed by one 2-mg tablet after each loose stool (maximum daily dosage: 8 mg), can be used with any of the antibiotic therapies.
E. coli 4. EnterohemorrhagicE. coli (EHEC) - produces verotoxin. The most common strains producing disease in developed countries. • The CDC estimates 20,000 cases/year in the U.S.; 200 people die; 2-7% of infected individuals develop hemolytic uremic syndrome (HUS), and of those 3-5% die, with 33% left with lingering kidney problems. • Symptomes: from mild diarrhea to hemorrhagic colitis with severe abdominal pain, bloody diarrhea (dysyntery), no fever; HUS (acute renal failure, thrombocytopenia, hemolytic anemia).
E. coli 4. EnterohemorrhagicE. coli (EHEC) - produces verotoxin. E. coli O157:H7 is NOT a problem if food is thoroughly cooked, BUT ~62,000 (Science, May, 2001) or ~73,000 (National Geographic, May, 2002) people are infected each year in the U.S., and 60 – most of them children - die. E. coli O157:H7 can survive the gentle heating of rare hamburgers.
Enterohemorrhagic E. coli (EHEC) Outbreaks of infection by E. coli strain O157:H7: • The first cases - 1982 and 1983 - undercooked hamburgers. • 1991 - cider pressed from apples that had fallen into manure and were not washed. • 1999 - the cow manure-water chain outbreaks of infection at the county fairs. 5. Enteroaggregative E. coli (EAggEC) - persistent watery diarrhea with vomiting and dehydration in infants in developing countries.
SALMONELLA • Salmonella are found in virtually all animals (poultry, livestock, rodents, domestic animals, birds) and humans. • Salmonella typhi (capsule) and Salmonella paratyphiare highly adapted to man and do NOT cause disease in non-human hosts. • Other Salmonella strains are adapted to animals and when they infect humans, can cause severe human disease (Salmonella choleraesuis). • Many strains cause disease in both humans and animals.
SALMONELLAThe source of most infection: • Contaminated water or food products(poultry, eggs, dairy products) • Direct fecal-oral spread in children(pet turtles in the U.S.) • Salmonella typhi- ingestion of food and water contaminated by infected food handlers (foreign travel) (no animal reservoir).
SALMONELLA - Clinical Syndromes • Enterocolitis - the most common form of salmonellosis, symptoms 6 to 48 hours after consumption of the contaminated food or water (nausea, vomiting, non-bloody diarrhea, fever, abdominal cramps, myalgia, headache). • Septicemia
SALMONELLA - Clinical Syndromes • Enteric Fever - Typhoid Fever(S. typhi) • Paratyphoid Fever- (S. paratyphi A) Incubation period 10-14 days; increasing remittent fever (headache, myalgias, malaise, anorexia) then gastrointestinal symptoms. This cycle corresponds to an initial bacteremic phase followed by reinfection of the intestines.
SALMONELLA Asymptomatic (chronic) carriage - after typhoid and paratyphoid fever, 1-5% patients, gall bladder - reservoir. Typhoid vaccine - Two typhoid vaccines are currently available for use in the U. S.: 1. An oral, live, attenuated vaccine (Vivotif Berna vaccine, manufactured from the Ty21a strain of S. typhi by the Swiss Serum and Vaccine Institute). 2. A Vi capsular polysaccharide vaccine (ViCPS) (Typhim Vi, manufactured by Aventis Pasteur) for intramuscular use. Both vaccines - protect 50%–80% of recipients.
SHIGELLA • Four species (non-capsulated): S. dysenteriae, S. flexneri, S. boydii, S. sonnei. • Shigellosis (bacterial dysentery) is primarily a pediatric disease. • Endemic disease in adults (contact with infected children). • Epidemic outbreaks - day-care centers, nurseries, etc.
SHIGELLA • Shigellosis- thefecal-oral route, contaminated hands ("disease of dirty hands"), less commonly in water or food. • In contrast to Salmonella infections, food-borne disease is uncommon. • The only reservoir is the human intestine. • Epidemic outbreaks - between soldiers during wars, in concentration camps; contemporary wars - refugee camps.
SHIGELLA - Pathogenesis and Immunity • Shigella remain localized in the ileum and colon. • Produce exotoxins - cytotoxic, enterotoxic and neurotoxic (cell death and necrosis). • Invade the intestinal epithelium - the intense inflammatory response characterized by bloody, mucopurulent diarrhea (dysentery).
SHIGELLA - Clinical Syndromes • Abdominal cramps, diarrhea, fever and bloody stools. • Symptoms - 1 to 3 days after the bacilli are ingested. • Colonize the small intestine and begin to multiply within the first 12 hours. • The initial sign - profuse water diarrhea is mediated by an enterotoxin.
SHIGELLA - Clinical Syndromes • Abdominal cramps and tenesmus, pus and blood in the stool (invasion of the colonic mucosa, destruction of superficial mucosal layer and production of mucosal ulceration). • Bacteremia is uncommon. • Infection is usually self-limited - antibiotic treatment is recommended to reduce the risk of secondary spread (family members).
YERSINIA • Yersinia pestis • Y. pseudotuberculosis • Y. enterocolitica • All Yersinia infections are zoonotic, with human as the accidental hosts.
Yersinia pestis • XIV century, epidemic plaque [the "Black Death"] - claimed 25 million people. • Urban plaque - spread between rats or from rats to humans by infected fleas. • With effective control of rats and better hygiene, urban plaque has been eliminated from most communities. • Sylvatic plaque - persists today in many countries, including the U.S. (prairie dogs, mice, rabbits, rats and flea vectors are widespread).
Yersinia enterocolitica • Enterocolitis - diarrhea, fever, abdominal pain (children, pseudoappendicitis). • Transmission from animal sources is usually by contaminated food or water.
Klebsiella pneumoniae • Isolated from the oropharynx and the GIT of ~5% of healthy people. • Community acquired primary lobar pneumonia. • Wound and soft tissue infections. • Urinary tract infections (nosocomial). • Otitis and sinusitis. • Large capsule protects against phagocytosis.
Proteus mirabilis • Common infection of the urinary tract. • Highly mobile, producing urease. • Urease - hydrolysis of urea into CO2 and NH3, this raises the urine pH and facilitates the formation of kidney stones.
Enterobacter, Citrobacter,Serratia, Providencia • Associated with hospital-acquired infections in patients with a compromised immune system.
Helicobacter pylori • Gram-negative pathogen colonizes the human stomach (1982). • Infection is acquired during childhood, persists lifelong if not eradicated (50% of the world's human population is chronically infected). • Chronic gastritis, and an increased risk of peptic ulcer disease and gastric cancer. • Highly motile (flagella; corkscrew motility). • A neutral pH-optimum urease enables gastric colonization.