Microbial Diseases of the Digestive System Ch 25 Microbial Diseases of the Digestive System

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

Dig Sys Intro and Normal Microbiota 2nd most common illnesses in US Usually result from 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 Fecal mass: Up to 40% microbial cells Bacteria in large intestine assist in degrading food and synthesizing vitamins. They also competitively inhibit pathogens, chemically alter medications, and produce carcinogens

Dental Caries (Tooth Decay) 1 causative agent: ___________ Bacteria bind to pellicle proteins  Cariogenic plaque Sucrose fermentation  _________ cavity formation Starch, mannitol, xylitol, etc. are not used by cariogenic bacteria Old calcified plaque  Dental Calculus or Tartar Control: fluoride and restricting dietary sucrose S. Mutans Acids (e.g: lactic acid) 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).

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).

Periodontal Disease Ginigivitis: Gum Inflammation. Due to inflammatory response to variety of bacteria grow ing 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

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

Bacterial Diseases of the Lower Digestive System Infection: caused by growth of a pathogen in intestines. Incubation times range from 12 hours to 2 weeks. Symptoms generally include fever. Intoxication: due to ingestion of preformed bacterial toxins. Symptoms appear 1– 48 hours after ingestion. Usually no fever. 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.

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

Events in Staphylococcal Food Poisoning Fig 25.6

Bacterial Infections Longer incubation periods than intoxication (12 hours 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. Exotoxin. Severe diarrhea (rice water stool), extreme dehydration  Antibiotics plus ORS or iv fluids

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.

Escherichia coli Gastroenteritis Many different strains. Some pathogenic. E.g.: Enterotoxigenic strains (ETEC)  present like mild form of cholera Enteroinvasive strains (EIEC)  Shigella like dysentery Generally self-limiting, ORS but no chemotherapy. Enterohemorrhagic strains (EHEC)  Shiga toxins cause inflammation and bleeding of the colon, including hemorrhagic colitis and hemolytic uremic syndrome (HUS). E.g.: E. coli O157:H7 Traveler’s diarrhea: E. coli and many others! “Traveling broadens mind and loosens bowel” Quote might be from Physician-author Abraham Verghese (born 1955) is Professor for the Theory and Practice of Medicine at Stanford University Medical School a

Campylobacter Gastroenteritis Campylobacter jejuni Microaerophilic  special culture conditions Almost all retail chicken contaminated Also in beef Low ID50 (~ 1000) 1in 1000 cases: Guillain-Barré syndrome

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

Helicobacter pylori Gastritis Inflammatory response to bacteria  Peptic ulcer disease (gastric and duodenal ulcers) 30 - 50 % 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

Fig 25.13

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/ subunit Hepatitis C Parenteral Filoviridae Hepatitis D Pareteral, HBV coinfection Deltaviridae HBV vaccine Hepatitis E Caliciviridae

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

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. Day care centers

Foodborne 2011 Illnesses Hospitalizations Deaths CDC estimates that each year roughly 1 in 6 Americans (or 48 million people) gets sick, 128,000 are hospitalized, and 3,000 die of foodborne diseases. 31 pathogens known to cause foodborne illness. Many of these pathogens are tracked by public health systems that track diseases and outbreaks. Deaths http://www.cdc.gov/foodborneburden/2011-foodborne-estimates.html

HELMINTHIC DISEASES OF THE DIGESTIVE SYSTEM Enterobius: most common in US Ascaris: second most common in US

The End