see Chp 5 for parasitic/fungal/helminthic infections
Parts
of the digestive system: oral
cavity, esophagus, stomach, small intestine, large intestine (colon), associated
structures (salivary glands, liver, pancreas)
Clinical
syndromes:
¨ Gastro = stomach; entero = small intestine; col = colon or large intestine
¨ Gastritis
– inflammation of the stomach; causes pain and occasional bleeding
¨ Gastroenteritis
– diarrhea, nausea, vomiting, crampy abdominal pain; can be caused by viruses or
bacterial enterotoxins; also caused by intoxications (toxins produced outside of the body
in food and are then ingested)
¨ Colitis
– involves colon; involves significant cellular damage (unlike gastroenteritis);
diarrhea contains blood and mucous; called enterocolitis (dysentery) if it involves both
coon and some of lower small intestine.
¨ Dental
caries – cavities or tooth decay
¨ Periodontal
disease or periodontis – destruction of gum and bone tissue
¨ Parotitis
– infected parotid salivary glands (over jaw, below ear)
¨ Hepatitis
– liver damage; symptom is jaundice (the liver filter bilirubin out of the blood and
secretes it into bile that is dumped into the small intestine; if the liver is not
functioning, then bilirubin remains in the blood stream; bilirubin is a yellow pigment
that comes from the breakdown of hemoglobin, the pigment in red blood cells responsible
for the transport of oxygen in the blood.)
¨ Food-borne
intoxication – toxin is produced in food and is then ingested; disease is not caused
by bacteria multiplying inside the body; antibiotics are useless!
Disease – dental caries
Mechanism
of pathogenesis; What makes this strep cariogenic? Bacteria possess adhesins on its pili that allow it to cling firmly to tooth
enamel; it produces a glucan mesh from sucrose (mesh + bacteria + debris = dental plaque);
it also produces lactic acid which damages dental enamel.
Susceptibility – determined by consumption of sugar, genetic factors, fluoride (makes enamel stronger)
Prevention
– future vaccine; introduce antibodies (passive immunization); modify mouth’s
normal flora (introduce a species to compete with S.
mutans)
Disease
– gingivitis & periodontal disease; leading cause of tooth loss in adults;
dkamages tissue that surround and support teeth; most infections affect the gingiva and
then spread to periodontal structures.
Etiologic agent – Shigella (G- rod;
nonlactose fermenter; does not produce H2S)
Clinical
Signs – fever; enterocolitis (stools are streaked with blood and contain strings of
mucous composed of many neutrophils); toxin may also contribute to watery diarrhea; toxin
may affect other organs in body; causes convulsions in children; can be life threatening
due to dehydration.
Mechanism
of pathogenesis/invasiveness – adhesin proteins on pili bind to human colon cells;
colon cells phagocytize the bacteria; they are taken into the cytoplasm where they
multiply and inhibit protein synthesis; bacteria then cause lysis of the host cells;
produce patchy areas of destruction and inflammation called microabscesses; shiga toxin
causes damage to blood vessels in intestinal wall and intense inflammation.
Epidemiology
Transmission – fecal –oral route (flies, food, water, fomites are
vehicles)
Who? Children are more affected than adults; used to be known as asylum dysentery due to massive outbreaks in mental institutions.
Treatment – fluid therapy; antimicrobial therapy
Etiologic
agent – Salmonella typhi (G- rod;
nonlactose fermenter; produce H2S)
Clinical
Signs – high fever (>104) continues for days or weeks; some develop rose spots
(faint rash); majority recover (about 10% die); some develop a chronic gallbladder
infection that makes them persistent carriers (may not work around children or food).
Mechanism
of pathogenesis/invasiveness – invasive (unlike Shigella); produce an endotoxin (accounts for
high fevers)
Treatment – antibiotics (chloramphenicol is drug of choice, but has toxic side
effects)
Etiologic
agent – Salmonella enteritidis & Salmonella
cholerasuis (G- rod; nonlactose fermenter; produce H2S)
Clinical
Signs – diarrhea (from enterotoxin), abdominal cramps, fever, nausea, vomiting, can
develop into severe dehydration or systemic bloodborne infection; onset of illness is
usually 1-2 days.
Epidemiology
Transmission
– contaminated food (poultry, unpasteurized milk, eggs); estimated that about 1 in 4
chickens are contaminated; major health concern.
Prevention
– using nonporous cutting boards; disinfecting cutting boards and cooking utensils;
thoroughly cooking foods; washing hands.
Treatment
– antibiotic treatment of uncomplicated salmonellosis is medically inadvisable
(treatment may cause them to become chronic carriers); growing drug resistance among
strains due t widespread use of antibiotics in animal feed.
G- rod,
lactose fermenter; Most abundant facultative anaerobe in large intestine of humans –
part of normal flora; most strains are harmless; also important pathogen of urinary tract.
Diseases - Traveler’s Diarrhea, Dysentery, Epidemic Diarrhea in Nurseries, Hemolytic-uremic syndrome
Clinical
signs – may involve nausea, vomiting, diarrhea, bloating, malaise and abdominal pain;
a typical case of t.d. causes 4-5 loose stools per day for 3-4 days; the toxin causes
excessive water and electrolyte secretion; can invade intestinal epithelium and cause
dysentery; deadly outbreaks of strain 157:H7 have been attributed to undercooked
hamburgers – several cases involved the kidneys and resulted in the condition known
as hemolytic-uremic syndrome.
Mechanism
of pathogenesis – causes a dysentery syndrome almost identical to shigellosis;
produce proteins that allow bacteria to invade human cells; it’s ”Shiga-like
toxins” inhibit protein synthesis; not as virulent as Shigella.
Prevention
of t.d. – some travelers take antibiotics prophylactically – not recommended
(not effective and contributes to development of mutant strains); a better practice is to
keep an antidiarrhea medicine available and us it only after symptoms appear.
Etiologic agent – Vibrio cholerae(short,
curved G- rod; flagellated)
Pandemics
in the 18OO’s led to the adoption of modern systems of sewage disposal and public
sanitation; The current pandemic is caused by the El Tor strain. It began in Indonesia in 1958 and is still
rampant in parts of Africa (remember the thousands of Rwandan refugees that contracted
it?), South America, and Asia. There was a
small outbreak in Alabama (Dauphin island) in 1991 – officials had to close an oyster
reef – they prevented an epidemic.
Clinical
Signs – dehydration from diarrhea (lose as much as a liter an hour); characteristic
rice water stools (water flecked with small particles of mucous); dehydration is sudden
and dramatic; a person can die in a day.
Mechanism
of pathogenesis – cholera exotoxin causes epithelial cells to secrete large
quantities of chloride into intestine, causing water, sodium and other electrolytes to
follow and leave body as diarrhea.
Epidemiology
Transmission – fecal-oral (contaminated water, infected shellfish, fish)
Prevention – sanitation; current vaccine is not effective.
Treatment
– replacing lost fluid; administer water & electrolytes intravenously;
tetracycline.
Etiologic
agent – Campylobacter jejuni (slightly
curved G- rod); not recognized until the 1970’s because they are so difficult to
cultivate in the lab.
Clinical
Signs – frequent episodes of bloody diarrhea, abdominal pain, fever; major cause of
diarrheal illness and dysentery; causes over 2 million illnesses in the U.S. each year
(more than Salmonella or Shigella).
Mechanism
of pathogenesis/invasiveness – destroys epithelial lining; produce a toxin and invade
cells.
Epidemiology
Transmission
– grows in intestinal tract of cattle, sheep, poultry, dogs, cats; human infection
probably occurs from ingesting contaminated meat or
milk; direct person-to-person transmission may occur.
Treatment
– usually non-life threatening and self-limiting (lasts about a week).
Etiologic
agent – Helicobacter pylori(G- rod); has
only been associated with ulcers since 1993!
How
do the bacteria survive the HCL in stomach? Produces an enzyme that converts urea to
ammonia, raising the pH in its vicinity.
Treatment – antibiotics!!!!!
Etiologic
agent – Clostridium botulinum (G+ rod,
spore-former, anaerobic); toxin production depends on a prophage; bo-tox is the most
poisonous natural substance known (as little as .000005 micrograms can kill a mouse –
one oz. would kill the entire US. Population!)
Clinical
Signs – flacid paralysis; muscle paralysis starts with the eye muscles; no fever;
usual cause of death is respiratory paralysis
Mechanism of pathogenesis – produces a neurotoxin that affects the nervous
system.
Epidemiology
Transmission – usually from improperly home-canned nonacid foods
Treatment
- antitoxin
Etiologic
agent - Clostridium botulinum (G+ rod,
spore-former, anaerobic); disease first recognized in 1976.
Clinical
Signs – infant becomes lethargic and loses the ability to suck and swallow (disease
is sometimes called “floppy baby” syndrome); may be cause of some infant deaths
attributed to SIDS.
Epidemiology
Transmission
– associated with feeding honey to infants (10% of honey contains botulism
endospores; endospores germinate and grow in the immature digestive tract of infants)
Prevention – do not give honey to a child under the age of 12 months.
Etiologic
agent – Clostridium difficile –
produces a type of iatrogenic (antibiotic induced) diarrhea; antibiotics kill off normal
flora, but C. difficile is resistant; can be
life-threatening; often occurs in hospitals (nosocomial).
Epidemiology
Treatment - vancomycin
Clostridium
perfringens food poisoning (food-borne intoxication)
Clinical
Signs – mild gastroenteritis; diarrhea; illness lasts less than a day; seldom
reported; noticeable illness occurs only if high numbers of spores are ingested.
Epidemiology
Transmission
– lives in the g.i. tract of animals, humans, & is common in feces-rich soil;
spores usually contaminate meat; ; when food is left unrefrigerated after cooking, spores
germinate and new cells produce toxin which is then ingested.
Staph. aureus food poisoning
(foodborne intoxication)
Grapelike clusters of G+ cocci; can survive in foods with a high sugar or salt
content.
Clinical
Signs – vomiting, diarrhea, crampy abdominal pain; onset of illness is rapid (2-6
hours).
Mechanism
of pathogenesis – produce a heat stable enterotoxin; toxin cannot be destroyed by
refrigeration or cooking.
Epidemiology
Transmission
– most frequently reported food poisoning in the U.S. – occurs in large
outbreaks at picnics or social gathering; most occur because of lapses in food prep or
storage; usually introduced into food from body of person preparing it (remember that path
Staph are found in many healthy people).
Treatment – illness is usually brief and self-limiting; fluid replacement may
be necessary.
Bacillus
cereus food poisoning (foodborne
intoxication)
G+
anaerobe; produces endospores.
Clinical
Signs – gastroenteritis is usually mild and brief; there are 2 forms of illness
associated with 2 enterotoxins; one form causes vomiting, the other causes diarrhea.
Epidemiology
Transmission
– present in soil, water, g.i. tract of humans and animal, so often found in food;
when food is left unrefrigerated after cooking, spores germinate and new cells produce
enterotoxins which are then ingested.
Etiologic agent – Listeria monocytogenes;
G+ rod; psychrophilic
Now
a leading cause of infection in kidney transplant patients.
Can cross the placenta and cause miscarriage and stillbirth; responsible for many
cases of fetal damage.
Epidemiology
Transmission
– by improperly processed milk, cheese, meat (hotdogs, lunch meat), and vegetables.
Major
cause of viral enteritis (water diarrhea) among infants and young children; number of
cases rises during winter months in U.S. (helps to distinguish it from bacterial
diarrheas; transmission is fecal-oral; viral capsids resemble little wheels.
Virus
is named for a 1968 outbreak in Norwalk, Ohio; responsible for nearly half of all U.S.
outbreaks of acute infectious nonbacterial enteritis; affects older children and adults
more often than infants or preschoolers; outbreaks occur throughout the year;
characterized by 1-2 days of diarrhea, vomiting, or both; immunity does not follow an
attack.
Poliomyelitis
Caused
by 3 strains of polioviruses that have an affinity for motor neurons of the spinal cord
and brain.
Clinical
signs
High
fever, back pain, and muscle spasms can occur. Most
infections are inapparent, or mild and nonparylitic.
In less than 1% of cases, partial or complete paralysis of muscles can occur;
nature and degree of paralysis depends on which neurons in the spinal cord and brain are
damaged. Any paralysis remaining after
several months is permanent.
Epidemiology
Transmission
– fecal-oral route and from pharyngeal secretions; danger of fecally contaminated
swimming pools
Vaccines:
1.) Salk
vaccine – injectable, inactivated (killed) with formalin; became available in 1955;
may not produce immunity in all recipients (may require boosters); has to be refrigerated
(unlike oral)
2.) Sabin
vaccine – oral, attenuated (live); provides longer-lasting immunity, but in a small
number of cases (about 6 each year in the US), viruses have mutated into virulent viruses;
cannot be administered to immunocompromised patients.
Absence
of animal reservoirs plus availability of effective vaccines have made health authorities
choose polio as the next disease to eradicate from the planet.
Hepatitis
A Virus (HAV)
Transmission
is fecal-oral; occurs most often in children and young adults; shellfish can be
contaminated; outbreaks due to contaminated food in fast-food restaurants have been on the
rise; symptoms include malaise, nausea, diarrhea, abdominal pain, and jaundice; jaundice
is caused by impaired liver function (the liver normally filters out hemoglobin from worn
out red blood cells and breaks it down into the yellow pigment bilirubin; bilirubin is
normally deposited in bile and is eliminated from the body in feces; if liver function is
impaired, bilirubin builds up in the blood stream); disease
is usually self-limiting; chronic infections are rare; no treatment except for alleviating
symptoms; vaccine is now available.