incidence - About 76 million people are sickened
annually by food-borne bacteria, with 325,000 hospitalized and
500 deaths
Gastrointestinal
Diseases
Dental Caries
epidemiology:
Streptococcus mutans - other acidogenic normal
microbiota, including S. sanguis, S. mitis and
S. salivarius (bacteria)
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
pathogenesis:
dental plaque accumulation leads to punched-out ulcers in
gingival (gum) tissue (spreads to soft palate, tonsilar areas)
which leads to decay of gingiva (foul odor, vile taste) which
causes loosening and loss of teeth as a result of bone
resorption
treatment: surgery, antimicrobial agent
treatment
prevention:
reduce plaque accumulation by brushing and flossing teeth as
well as by reducing dietary sugar content
Oral Herpes and Herpes
Labialis
epidemiology: Herpes Simplex Virus 1
(HSV-1)
is transmitted by direct oral contact and most people are infected as children;
as many as 90% of US adults have anti-HSV1 antibodies; more
herpes information
epidemiology: Mumps Virus is
transmitted via respiratory secretions or saliva before symptoms appear; ~6500 cases of mumps
reported in the US each year (most age 5-10); ~one-third asymptomatic;
the name comes from the English word "mump" (to sulk, to be sullen)
pathogenesis: parotid salivary gland infection causes fever,
accumulation of saliva (parotid swelling, tenderness) after
16-18 days; complications - infection of ovaries, testes, thyroid,
pancreas, CNS (meningitis, encephalitis, deafness)
treatment: TLC
prevention: MMR vaccine (down
from 152,000 cases in 1968), avoid contact with respiratory
secretions or saliva of infected persons
epidemiology:
Helicobacter pylori
(bacterium)
is transmitted, probably by oral or fecal/oral contact, early
in life; 80% of people in developing countries (40% in
developed countries) are infected; relationship
between H. pylori and ulcers first discovered in 1982 by Marshall
and Warren;
ulcers affect ~25 million people in the US during their
lifetime; each year:
~4 million people in the US develop ulcers
~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); 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
epidemiology:
Clostridium botulinum (bacterium)
- foods contaminated with spores (from soil) and improperly canned; 32
cases of foodborne botulism in US during 2007
pathogenesis: after 12-36 hour incubation period,
exotoxin (botulin) causes flaccid paralysis of neck and chest,
which can cause death (up to 70% of untreated cases; ~5% of
treated cases) due to cardiac and/or respiratory failure (Did
ya know ... infant
botulism is an infectious disease transmitted by infants
eating nonpasteurized honey,
which contains Clostridium botulinum spores?; 85 cases in US during
2007)
treatment: antitoxin (available from CDC)
prevention: avoid ingestion of contaminated foods
via better food washing and canning techniques
(sanitation)
Staphylococcal
Intoxication
epidemiology: ingestion of enterotoxin produced by
Staphylococcus aureus (bacterium)
in foods contaminated with it by food handlers with lesions, then "incubated" before
serving; millions of cases each year in the US (Did ya know . . . food
poisoning costs more than $22 billion per year in treatment and
lost productivity in the US?)
pathogenesis: 2-6 hours after ingestion, enterotoxin
causes emesis (vomiting) and accumulation of water in small
intestine, which causes abdominal cramps and hypermotility,
that results in diarrhea
treatment: TLC; self-limiting disease (antimicrobial
agents generally not necessary . . . nor recommended)
prevention: avoid ingestion of contaminated foods
(sanitation, hygiene)
Mycotoxicosis
epidemiology:
Aspergillus flavus (fungus) grows on food
(especially peanuts) stored in moist places and produces
aflatoxin
Aminita, Clitocybe, and Psilocybes (fungi)
are poisonous
mushrooms due to their production of one or more of
these toxins ... phalloidina, amatoxin,
ibotenic acid, muscimol, muscarine,
psilocybin
pathogenesis:
ingestion of aflatoxin along with food damages
intestines and liver; complications - liver cancer
ingestion
of various toxins when one eats poisonous
mushrooms can cause damage to certain portions of the body
amanitin (amatoxin) causes kidney and liver
toxicity followed by violent vomiting, bloody diarrhea,
and severe abdominal cramps, and can cause death if the
dose is high enough
ibotenic acid and muscimol cause nausea
and vomiting, together with CNS effects including
confusion, visual distortion, a feeling of greater
strength, delusions, convulsions and drowsiness (may fall
asleep and cannot be roused)
muscarine causes excessive salivation,
sweating, tears, lactation (in pregnant women), plus
severe vomiting and diarrhea
psilocybin causes hallucinations
treatment: TLC, supportive therapy aimed at
eliminating toxins, possible liver transplant for
amanitin poisoning
prevention:
avoid eating aflatoxin by preventing fungal
contamination of foods that will be ingested (low-moisture
storage conditions for peanuts, etc.)
avoid eating wild (noncommercial) mushrooms
Enteritis
epidemiology: Bacteria - Salmonella
enteritidis (ingested with milk, poultry, eggs; 47,995
cases in US during 2007), Enterotoxic Escherichia
coli (ETEC;
food, water; millions of cases per year);
Bacillus cereus (rice, potatoes; hundreds of cases per
year); Clostridium perfringens (meat; hundreds of cases
per year); Campylobacter
jejuni (food and water; 5-11% of diarrheal disease;
more
about Campylobacter);
Viruses - Rotavirus (~870,000
cases per year ... ~50,000 hospitalized), Coxsackie virus and
Echovirus (water; millions of cases per year)
pathogenesis: enterotoxin or LPS (bacteria) or viral
cell damage lead 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 (4847
cases in US during 2007) 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
epidemiology: Giardia
lamblia (protozoan)
- fecal/oral transmission via contaminated water; 19,417 cases in US during
2007 ... most commonly detected protozoan disease in US
pathogenesis: cyst survives stomach, develops into
trophozoite in the intestines where it adheres and proliferates
rapidly, causing maladsorption and tissue damage leading to
nausea, abdominal cramps, flatulence, foul-smelling watery
diarrhea; complications - chronic disease; carrier state
treatment: furazolidone or metronidazole
(due to side-effects of these drugs, physicians sometimes
prefer to let disease run its course without treatment)
epidemiology:
Cryptosporidium parvum (protozoan)
grows in GI tract of calves, pigs, chickens and other poultry;
transmitted to humans via improperly treated drinking water;
disease first recognized in US in 1976; 11,170 cases in US during 2007;
~one-third of all surface waters contain Cryptosporidium cysts
pathogenesis:
protozoal damage causes headache, low-grade fever, sweating,
nausea, anorexia, vomiting, severe abdominal cramping and
diarrhea of short duration in normal, healthy humans; but
causes chronic severe (sometimes uncontrollable) diarrhea in
immunosuppressed people and may cause death in addition to
wasting syndrome
treatment: TLC, replace lost fluids and
electrolytes; effective antiparasitic drugs have not been
discovered yet
epidemiology: Shigella dysenteriae, Shigella boydii, Shigella
flexneri, Shigella
sonnei (bacteria);
transmitted via fecally-contaminated drinking water or food; 19,758
cases of Shigellosis in US during 2007; ~165 million cases of severe
dysentery and ~1 million deaths worldwide (mostly in developing
countries) each year
pathogenesis: Shigella damages epithelial cells of intestine, causing nausea,
abdominal cramping, diarrhea (leads to dehydration and electrolyte loss), mucosal ulceration,
rectal bleeding, blood and "sheets" of PMNs in stools (S. dysenteriae may produce
a neurotoxin that causes vomiting and/or Shiga toxin that can lead to hemolytic uremic syndrome);
may last 3-6 weeks; complications - death (10-15%) due to circulatory collapse in severe cases
treatment: replace water and salts; trimethoprim-sulfamethoxazole, norfloxacin, ciprofloxacin,
or furazolidone if patient is very young or very old and at risk of death
epidemiology: Entamoeba histolytica (protozoan)
transmitted via cysts ingested with food or water contaminated with human fecal material;
~10% of world (including ~5% of US) population are carriers; afflicts millions of people and
accounts for ~100,000 deaths per year worldwide
pathogenesis: cysts develops into trophozoites in small intestine, then penetrate
the colon, causing ulcerations, sharp abdominal pain, colitis, diarrhea, dysentery; complications -
recurrent attacks, carrier state; invades bloodstream, causes fatal brain, liver and/or lung
abscesses
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
epidemiology: Salmonella typhi (bacterium);
transmitted via fecally contaminated food or water; ~400 cases
per year in the US
pathogenesis: invades via intestinal epithelium,
multiplies in lymph nodes, spreads systemically (bacteremia;
rose spots); proliferates in (and damages) liver, then
reinfects small intestine (via bile secreted by gall bladder);
results in fever (104 degrees F), lethargy and delirium;
complications include carrier state (10-15%) and death (severe
cases)
epidemiology: Polio
Virus (virus) is transmitted via water
(summer); fewer than 10 cases per year in the US; ~270,000 cases (~25,000 deaths) per
year, worldwide;
polio costs ~$1.5 billion per year ($230 million in the
US)
pathogenesis: intestinal infection leads to
infection of motor neurons, damage causes paralysis;
complications include muscle
atrophy, paralysis, death (postpolio
syndrome, which only affects
those who had polio earlier in their lives, and for which
there is some help)
treatment: TLC, supportive measures ... such as
braces,
wheelchairs
or iron
lungs
prevention:
sanitation ... adequate treatment of drinking
water and prevention of its contamination with sewage
epidemiology:
Hepatitis
A or Hepatitis
E virus; ~3500 cases
per year in US; transmitted via raw shellfish, produce, other fecally-contaminated foods, especially
in institutions
pathogenesis: intestinal infection with Hepatitis A or E virus leads to anorexia, nausea,
vomiting, low-grade fever; systemic distribution leads to liver damage, which causes jaundice;
some people are asymptomatic, however; complications - chronic disease, relapses
are common; ~100 deaths per year in US
epidemiology: Toxoplasma gondii (protozoan)
infection occurs via oocysts transmitted via cat
feces or tissue cysts transmitted by eating undercooked meat, especially pork, lamb or venison;
>20% of adults in US and >30% of world population have been infected
pathogenesis: cysts develop into tachyzoites in
intestines, invade the intestinal lining and multiply in the
intestinal cells, then spread throughout the body to multiply
in other cells, causing disseminated infection that leads to
chronic fatigue, fever, malaise, sore throat, headache, muscle
pain, swelling of spleen, liver, and lymph nodes; these signs and symptoms last several weeks,
then subside as the immune system controls (but does not eliminate) the infection; some people
are asymptomatic; complications include
chronic latent infection often with neurologic or retinal disease (retinochoroiditis); birth
defects if infected during third trimester of pregnancy;
this disease is a big problem in AIDS and other
immunocompromised patients
treatment: pyrimethamine and sulfadiazine, plus
folinic acid.
prevention: cook meat to safe temperatures; avoid
cat feces (pregnant women should not clean cat litter boxes)
Pinworm (Enterobiasis)
epidemiology:
Enterobius
vermicularis is a roundworm (a type of helminth)
that is transmitted by fecal/oral contact; pinworm infects
20-50 million people per year in the US ... 10-40% of children
under 12, and 16% of adults, have worms at some time in their
lives (most prevalent multicellular parasite in US)
pathogenesis:
worms proliferate in large intestine (takes 2-4 weeks), causing
damage that results in abdominal discomfort, diarrhea,
pruritus
treatment: mebendazole
prevention: avoid ingesting contaminated soil,
animal and human feces
epidemiology:
Trichinella
spiralis (roundworm ...a type of helminth)
is transmitted by ingestion of pork; ~one million cases in the US in 1950 ... currently ~15
cases reported each year; 4% of US population
infected
pathogenesis:
ingested cysts develop into worms, which mature in intestine
(in 2 days), release many larvae (after 5 days) causing nausea,
abdominal pain, vomiting, constipation; larvae enter
bloodstream (after 7-14 days) causing fever, then localize in
muscles and encyst (after 3 weeks) causing myalgia, facial
edema, damage throughout body (heart, muscles, CNS);
complications - incapacitation, death (~6% - depends on worm
burden)
treatment: thiabendazole or mebendazole are used in
addition to steroids, which reduce severe symptoms ... but no
known cure for this chronic disease
prevention: cook pork at 350 degrees F for 45
minutes per pound until internal temperature is 170 degrees F
(77 degrees C)
epidemiology: Taenia
saginata (in beef), Taenia solium (in pork),
Diphyllobothrium latum (in fish) - these flatworms
(helminths) are
transmitted by ingestion of cysts in poorly cooked meat or
fish
pathogenesis: tapeworm attaches to intestine via
scolex, absorbs nutrients directly through their external
surfaces (most infestations are asymptomatic, but some patients
experience nausea, abdominal cramps, hunger pains, anorexia,
weight loss); complications - intestinal obstruction (many
worms present); poor absorption of vitamin B12
treatment: niclosamide or praziquantel
prevention: avoid soil contamination with human
feces; avoid eating raw or poorly cooked beef or pork - cook
for 15 min at 131 degrees F (55 degrees C)
epidemiology: Prusiner
established that 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 ~200 people 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 shape or 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)
