incidence - About 76 million people are sickened
annually by food-borne bacteria, with 325,000 hospitalized and
500 deaths; was ~150 deaths per 100,000 people in US in the
year 1900
epidemiology:
Streptococcus mutans - other acidogenic normal
microbiota, including S. sanguis, S. mitis and
S. salivarius
pathogenesis: Streptococci adhere to tooth surface
via glucans and levans produced from carbohydrates such as
sucrose (develops into plaque as salts are incorporated);
caries (cavities) generated as lactic acid (produced during
sugar catabolism) dissolves tooth enamel
treatment: physical removal of brownish-black
"rotted" material, then "filling" with dental amalgam (problem:
amalgam contains mercury)
prevention: tooth brushing and flossing; fluoride
treatment (toothpaste, drinking
water, dentist's office); reduction of simple sugar content
of diet
epidemiology: Bacteriodes forsythus, Leptotrichia
buccalis, Pophyromonas gingivalis, Treponema vincentii and
Eikenella spp. (normal bacterial microbiota)gingival
(gum) tissue (spreads to soft palate, tonsilar areas) leads to
decay of gingiva (foul odor, vile taste), which causes
loosening and loss of teeth
pathogenesis:
dental plaque accumulation leads to punched-out ulcers in
gingival (gum) tissue (spreads to soft palate, tonsilar areas)
leads to decay of gingiva (foul odor, vile taste), which causes
loosening and loss of teeth
treatment: surgery, antibiotic treatment
prevention:
reduce plaque accumulation by brushing and flossing teeth as
well as by reducing dietary sugar content
~40,000 of them are hospitalized due to this condition
~6,000 people die of complications of ulcers, which include
bleeding, perforation of the organ walls, and narrowing and
obstruction of digestive tract passages
pathogenesis:
bacterium lives in gastric mucus, moves toward gastric epithelial
cells using its flagella, adheres to these cells by binding
proteins or glycoproteins (especially Lewisb antigens
on type O cells), produces urease (neutralizes stomach
acid; induces inflammation) and vacuolating cytotoxin (damages
gastric cells); infiltrating phagocytes secrete cytokines that
augment and prolong inflammation, leading to formation of ulcers,
which generate a gnawing or burning pain in the abdomen ...
from the navel upwards to the breastbone; less common signs
and symptoms include: belching, nausea, vomiting, poor appetite,
weight loss, feeling tired and weak; complications include perforated
ulcers and an up to 12-fold increased rate of gastric adenocarcinoma
(a form of cancer) ... more
on cancer; possible link with sudden infant death syndrome
(SIDS)
treatment:
two combination drug therapy approaches are:
Two-week, triple therapy - 90% effective in curing ulcers,
but hard for patients to accomplish and causes a number
of unpleasant side-effects (yeast infection in women,
stomach upset, nausea, vomiting, bad taste, loose or dark
bowel movements, and dizziness):
Metronidazole (or clarithromycin) 4 times/day
Tetracycline (or amoxicillin) 4 times/day
Bismuth subsalicylate (active ingredient in PeptoBismol)
4 times/day
Rantidine (Zantac)
may also be used to block acid production (optional)
Two-week, dual therapy - 80% effective in curing ulcers,
and is simpler for patients with fewer side-effects:
Omeprazole (Prilosec) 2 times/day to block acid
production
prevention: avoidance of contact with feces or vomitus
(which may contain H. pylori);diminished smoking, caffeine
intake, use of nonsteroidal anti-inflammatory drugs (NSAIDs)
and stress may also help, because these all seem to be cofactors
in prolonging or worsening ulcers
Food Intoxication
epidemiology:botulism
is caused by ingestion
of botulin produced by Clostridium botulinum in
foods contaminated with spores and improperly canned (~20 cases
per year in US; Did ya know ... infant
botulism is an infectious disease transmitted by infants
eating nonpasteurized honey,
which contains Clostridium botulinum spores?));
staphylococcal
Intoxication is caused by ingestion of enterotoxin produced
by Staphylococcus aureus in contaminated foods (millions
of cases each year in the US); one form of mycotoxicosis
is caused by ingestion of aflatoxin produced by Aspergillus
flavus, a fungus that grows on food stored in moist places
... another is caused by Aminita, Clitocybe, and
Psilocybes (fungi) which are poisonous
mushrooms due to their production of one or more of these
toxins
... phalloidina, amatoxin, ibotenic acid,
muscimol, muscarine, psilocybin
pathogenesis:botulin causes flaccid
paralysis of neck and chest (kills up to 70% of untreated cases
and ~5% of treated cases by cardiac and/or respiratory
failure); staphylococcal enterotoxin causes vomiting and
diarrhea, but is rarely fatal; mycotoxicosis due to
aflatoxin ingestion damages intestines and liver (can lead to
liver cancer)
treatment:botulism - antitoxin;
staphylococcal intoxication - TLC, self-limiting disease
(antibiotics generally not necessary...nor recommended);
mycotoxicosis - TLC (liver transplant in severe mushroom
poisoning cases)
prevention: avoid ingestion of contaminated foods
via better food washing and handling techniques
(sanitation)
Enteritis
epidemiology:
Bacteria - Salmonella
enteritidis (ingested with milk, poultry, eggs; ~40,000
cases per year), Shigella
(water; ~20,000 cases per year), Escherichia
coli (food, water; millions of cases per year ...
~4500 cases caused by O157:H7 strain); Bacillus cereus
(rice, potatoes; hundreds of cases per year);; Clostridium
perfringens (meat; hundreds of cases per year); Campylobacter
(food and water; 5-11% of diarrheal disease); Viruses -
Rotavirus
(~870,000 cases per year ... ~50,000 hospitalized), Coxsackie
virus and Echovirus (water; millions of cases
per year); Protozoa
- Giardia
(improperly treated drinking water; giariasis is the most
commonly detected protozoan disease in the US) and
Cryptosporidium
(improperly treated drinking water; ~2500 cases of
Cryptosporidiosis per year; up to 1/3 of all surface waters
contain Cryptosporidium cysts)
pathogenesis: enterotoxin or LPS (bacteria) or cell
damage caused by viruses or protozoa
leads to accumulation of water in small intestine, which causes
abdominal cramps and hypermotility, resulting in diarrhea
(~accompanied by fever, nausea and vomiting); complications -
dehydration, electrolyte loss; death (rare) ... E. coli
O157:H7 causes more severe disease, often complicated by
hemolytic-uremic syndrome that leads to kidney damage
treatment: replace water and salts as needed;
antimicrobial agent therapy (sulfa drugs, ampicillin) is used
in life-threatening cases only; effective antiparasitic drugs
have not yet been discovered for cryptosporidiosis
epidemiology:
Vibrio cholerae (bacterium) - present in water
throughout world; ~10 cases per year in US; an epidemic that
began in 1991 in South America resulted in more than a million
cases and several thousand deaths; there were ~223,000 cases of
cholera worldwide in 1999, leading to ~8,500 deaths
pathogenesis: after 2-3 days' intestinal
colonization, these bacteria produce enough cholera
toxin to cause massive accumulation of water in small
intestine leading to "explosive" diarrhea (rice-water stools)
and vomiting, which leads to dehydration and electrolyte loss;
complications - coma (poor blood flow to brain) and death due
to shock (mortality rate is 60% in untreated cases, ~1% in
treated cases)
treatment: replace water and salts (i.v. and/or
oral); tetracycline
prevention: vaccines
(available only in other countries, and not recommended for
travelers by CDC); avoid ingestion of contaminated food or
water ... maintain adequate sewage
treatment and drinking
water purification
epidemiology: Hepatitis
Virus A; ~75,000 cases per year in US; transmitted via raw shellfish,
produce, other fecally-contaminated foods, especially in institutions
(hepatitis E, caused by Hepatitis Virus E is similar)
Links to recent outbreak info in the Cincinnati area:
pathogenesis:
intestinal infection (anorexia, nausea, vomiting, low-grade fever) systemic
distribution leads to liver damage (jaundice); complications - chronic
disease, relapses are common; ~100 deaths per year in US
epidemiology: as established by Prusiner, prions are
ingested by people eating beef from cattle stricken with Bovine Spongioform Encephalopathy
(BSE); this disease was discovered in Great Britain in the 1980s, and ~100 Brittons have
died of it so far, but BSE has yet to emerge in the US
pathogenesis: prions are taken up from the digestive tract and somehow get into
the brain, where they interact with cell receptors, changing
their conformation, which causes accumulation of prion molecules as the cells replace
the altered receptor molecules; this causes accumulation of fibrils of insoluble prion complexes
and results in slow degeneration of the central nervous system with obvious dysfunction,
progressive dementia, and vacuolar degeneration of the brain known as new variant Creutzfeldt-Jakob
disease (nvCJD) disease
