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!

I. BACTERIAL DISEASES ACQUIRED THROUGH THE DIGESTIVE SYSTEM

Streptococcus mutans

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)

Bacteroides gingivalis

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.

Shigellosis (Bacillary Dysentery)

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

Typhoid Fever

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)

Salmonellosis

Important: classified as a food poisoning, but is a true infection caused by bacteria multiplying in the bowel – not a foodborne intoxication.

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.

E. coli

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.

Cholera

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.

Campylobacteriosis

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).

Peptic ulcers

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!!!!!

Botulism (a food-borne intoxication)

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

Infant Botulism (not a food-borne intoxication – bacteria produce toxin while multiplying inside body)

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.

Pseudomembranous colitis – C. diff Diarrhea

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.

Listeriosis

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.

II. VIRAL DISEASES ACQUIRED THROUGH THE DIGESTIVE SYSTEM

Rotavirus

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.

Norwalk Agents

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.