1. Ch 25
Microbial Diseases of the Digestive System

2. SLOs
List examples of normal microbiota for each part of the gastrointestinal tract
Describe the events that lead to dental caries and periodontal disease
List the causative agents, suspect foods, signs and symptoms, and treatments for staphylococcal food poisoning, shigellosis, salmonellosis, typhoid fever, cholera, gastroenteritis, and peptic ulcer disease
Differentiate between hepatitis A, hepatitis B, hepatitis C
List the causative agents, mode of transmission, and symptoms of viral gastroenteritis
List the causative agent, modes of transmission, symptoms, and treatment for giardiasis
List the causative agents, modes of transmission, symptoms, and treatments for tapeworms, pinworm, and ascariasis

3. Intro and Normal Microbiota
Diseases of the digestive system are the 2nd most common illnesses in the US.
Diseases of the digestive system usually result from the ingestion of microorganisms or their toxins in food and water
Fecal–oral transmission can be interrupted by
proper disposal of sewage
disinfection of drinking water
proper food preparation and storage
>700 bacterial species in mouth
Stomach and small intestine have few resident microbes
Up to 40% of fecal mass is microbial cells
Bacteria in large intestine assist in degrading food and synthesizing vitamins. They also competitively inhibit pathogens, chemically alter medications, and produce carcinogens

4. Dental Caries (Tooth Decay)
S. mutans is 1 causative agent
Cariogenic plaque binds to receptors on tooth pellicle
Sucrose  glucose + fructose
Glucose polymerization  dextran
Fructose fermentation  lactic acid  cavity formation
Starch, mannitol, xylitol, etc. are not used by cariogenic bacteria
Dental Calculus or Tartar  old calcified plaque
Control: fluoride and restricting dietary sucrose
Dietary sucrose changes both the thickness and the chemical nature of plaque. Mutans streptococci and some other plaque bacteria use the monosaccharide components (glucose and fructose) and the energy of the disaccharide bond of sucrose to assemble extracellular polysaccharides. These increase the thickness of plaque substantially, and also change the chemical nature of its extracellular space from liquid to gel. The gel limits movement of some ions. Thick gel-plaque allows the development of an acid environment against the tooth surface, protected from salivary buffering. Plaque which has not had contact with sucrose is both thinner and better buffered. A diet with a high proportion of sucrose therefore increases caries risk. Thicker plaque occurs in pits and fissures (which is why Site 1 lesions begin there), just beneath the contact area (Site 2) and, in patients with poor oral hygiene, near the gingival margin (Site 3).

5. Mutans streptococci participate in the formation of biofilms on tooth surfaces. These biofilms are known as dental plaque(s). Sucrose is required for the accumulation of mutans streptococci. Also required for this accumulation are the enzymes glucosyltransferases (GTFs), which are constitutively synthesized by all mutans streptococci. a | Initial attachment of mutans streptococci to tooth surfaces. This attachment is thought to be the first event in the formation of dental plaque. The mutans streptococcal adhesin (known as antigen I/II) interacts with -galactosides in the saliva-derived glycoprotein constituents of the tooth pellicle. Other moieties at the surface of mutans streptococci include glucan-binding protein (GBP), serotype carbohydrate and GTFs. b | Accumulation of mutans streptococci on tooth surfaces in the presence of sucrose. In the presence of sucrose, GTFs synthesize extracellular glucans from glucose (after the breakdown of sucrose into glucose and fructose), and this is thought to be the second event in the formation of dental plaque. The mutans streptococcal protein GBP is a receptor-like protein that is distinct from GTFs, and it specifically binds glucans. GTFs themselves also have a glucan-binding domain and can therefore also function as receptors for glucans. So, mutans streptococci bind pre-formed glucans through GBP and GTFs, and this gives rise to aggregates of mutans streptococci. c | Acid production by mutans streptococci. The metabolism of various saccharides (including glucose and fructose) by the accumulated bacterial biofilm results in the production and secretion of considerable amounts of the metabolic end-product lactic acid, which can cause demineralization of the tooth structure when present in sufficient amounts in close proximity to the tooth surface. This is thought to be the third event in the formation of dental plaque, and it eventually results in a carious lesion (that is, in dental caries).

6. Periodontal Disease
Ginigivitis: Inflammation of gums. Due to inflammatory response to a variety of bacteria growing on gums
Gingivitis can progress to periodontitis
Chronic periodontitis can cause bone destruction and tooth loss in older people
Acute necrotizing ulcerative gingivitis (ANUG) – Trench mouth

7. The Stages of Tooth Decay
Fig 25.4
The Stages of Periodontal Disease
Fig 25.5

8. Bacterial Diseases of the Lower Digestive System
Infection is caused by the growth of a pathogen in the intestines.
Incubation times range from 12 hours to 2 weeks. Symptoms of infection generally include a fever.
Intoxication due to ingestion of preformed bacterial toxins.
Symptoms appear 1–48 hours after ingestion of the toxin. Fever is not usually a symptom of intoxication.
Infections and intoxications cause diarrhea and dysentery (some gastroenteritis)
Usually treated with fluid and electrolyte replacement.
Dysentery: diarrhea containing mucus and blood in the feces.

9. Staphylococcal Food Poisoning
Staphylococcus aureus – inoculated into foods during preparation
2nd most reported food borne disease
Heat resistant exotoxin acts as enterotoxin – boiling for 30 mins not sufficient to denature the exotoxin!
Incubation period 1 – 6 hours; rapid recovery
Contaminated meats (ham!), fish, potato salad, custards, etc.
Mode of transmission: Human reservoir (nose); skin abscesses

10. Events in Staphylococcal Food Poisoning
Fig 25.6

11. Bacterial Infections
Longer incubation periods than intoxication (2 days to 2 weeks)
Shigellosis (Bacillary Dysentery)
Toxin. Severe diarrhea or dysentery; 20,000 – 30,000 cases /year in US
Salmonellosis (Salmonella enterica) - Gastroenteritis
Most reported of foodborne diseases in US
Typhoid Fever (Salmonella typhi)
Only in humans (carriers); enteroinvasive  blood; Symptoms last 2–3 weeks, antibiotics
Cholera (Vibrio cholerae)
Primarily third world problem. Toxin. Severe diarrhea (rice water stool), extreme dehydration  Antibiotics plus ORS or iv fluids

12. Oral (ORS) or i.v. rehydration reduces mortality rate from ~70% to < 1%
(additional: tetracycline)
ORS - Oral Rehydration Salts : The most effective, least expensive way to manage diarrhoeal dehydration.
Cholera:  Even though cholera is still endemic in many countries of Africa, Asia and Latin America, its death toll has been reduced dramatically over the past 50 years. Through inexpensive, effective case management, WHO has made it possible to decrease the global cholera case fatality rate to the current 1.8% from more than 50% in the early 1950s. The disease remains a public health problem and requires constant attention both at national and international levels.

13. Escherichia coli Gastroenteritis
Traveler’s diarrhea may be caused by
Enterotoxigenic strains (ETEC)  present like mild form of cholera
Enteroinvasive strains (EIEC)  Shigella like dysentery
Generally self-limiting, ORS but no chemotherapy.
Enterohemorrhagic strains produce Shiga toxins (STEC) that cause inflammation and bleeding of the colon, including hemorrhagic colitis and hemolytic uremic syndrome (HUS). E.g.: E. coli O157:H7

14. Clostridium difficile–associated diarrhea
C. difficile growth following antibiotic therapy
Exotoxin production
From mild diarrhea to life threatening colitis
Millions of cases per year
Nosocomial disease, associated with hospitalized patients and nursing home residents

15. Helicobacter pylori Gastritis
Inflammatory response to bacteria  Peptic ulcer disease (gastric and duodenal ulcers)
% of people in US infected – only ~ 15% develop ulcers. (Blood type O more susceptible)
Bacteria produces urease (urea  ammonia) – neutralizes stomach acid
Antibiotic treatment is effective

16. Fig 25.13

17. VIRAL DISEASES OF THE DIGESTIVE SYSTEM: Hepatitis
Trans-mission
Causative agent
Chronic liver disease?
Vaccine?
Hepatitis A
Fecal-oral
Picornaviridae No
Inactivated virus
Hepatitis B
Parenteral, STD
Hepadnaviridae
Yes
Recombinant
Hepatitis C
Parenteral
Filoviridae
Hepatitis D
Pareteral, HBV coinfection
Deltaviridae
HBV vaccine
Hepatitis E
Caliciviridae

18. Viral Gastroenteritis
Rotavirus:
3 million cases annually
Main diarrheal illness of infants and children
1-2 day incubation; 1 week illness
Norovirus:
50% of U.S. adults have antibodies
1-2 day incubation; 1-3 day illness
Treated with rehydration

19. Protozoan GI Diseases Giardiasis – caused by Giardia lamblia
Drinking feces contami- nated water (camping, swimming)
Type of traveler’s diarrhea
Symptoms: malaise, nausea, flatulence, weakness, and abdominal cramps that persist for weeks.
Diagnosis is based on identification of the protozoa in the small intestine.
 7% of population healthy carriers

20. HELMINTHIC DISEASES OF THE DIGESTIVE SYSTEM

21. Tapeworms
contracted by consumption of undercooked beef, pork, or fish containing encysted larvae
Scolex attaches to the intestinal mucosa of humans (definitive host)  matures into adult tapeworm
Eggs shed in feces and must be ingested by an intermediate host
Adult tapeworms may be undiagnosed in a human
Diagnosis based on observation of proglottids and eggs in feces.
Dipylidium caninum vs. Echinococcus granulosus (hydatid disease)
Fig 12.27

22. THE COMMON TAPEWORM (Dipylidium caninum)
Tapeworm segment breaks, releasing eggs
Tapeworm segments and flea dirt are found together in Rover’s dog bed.
Rover licks himself and swallows fleas
Eggs eaten by grazing flea larvae
Tapeworm segments break releasing eggs
Flea larvae pupate

23. Pinworm Disease / Enterobiasis
Enterobius vermicularis, up to 10 mm long
Most common worm infection in US (30% of children, 16% of adults infected)
Live in human rectum. While infected person sleeps, female pinworms leave intestines through anus and deposit eggs on surrounding skin.
Diagnosis with cellophane tape (scotch-tape test) first thing in the morning.
Self limiting, but treatment of all family members recommended.

24. Diagnosing Pinworm Disease
pinworm paddle
Do test immediately after waking up. Several samples might need to be examined.
Since scratching of the anal area is common, samples taken from under the fingernails may also contain eggs.
Fig 17.9

25. ova
Pinworm (Enterobius vermicularis) in sigmoid colon

26. Ascariasis Ascaris lumbricoides up to 20 cm long
Lives in human intestines
After pinworm 2nd most common worm infection in US. (Most prevalent in tropics and subtropics)
~85% infections are asymptomatic, however “general failure to thrive” as in many intestinal parasites.
Transmitted by ingesting Ascaris eggs
Figure 25.25

27. The End