Chapter 25 Digestive System Infections Introduction Who determined that the cholera outbreak in 1850s London was due to contaminated water from the Broad Street pump and approached the problem by removing the pump handle at the contaminated site Local residents had to go to a different pump for their water o John Snow o Lack of water sanitation was the culprit different species on teeth cheek tongue host limits population size of bacteria on oral mucous membranes by constantly shedding cells teeth don t shed so bacteria can colonize to high density plaque The Digestive System Digestive system alimentary tract gastrointestinal tract o lone of the body s main boundaries with the environment o major route of microbial invasion o divided into upper and lower tracts o upper mouth salivary glands esophagus stomach o lower intestines pancreas and liver Most of the normal flora of digestive tract is in the oral cavity and intestines o Esophagus has very little flora o Stomach contains no microorganisms killed by stomach acid o Mouth is colonized by relatively few species mainly various streptococci Gram chain forming Normal Microbiota Intestines o Upper small intestine small population numbers continually flushed away aerobic and facultative Gram bacilli and some streptococci o Large intestine very high numbers 1011 bacteria per gram of feces 100 billion bacteria due to abundance of nutrients in feces Escherichia coli and other enterobacteria predominate important source of opportunistic infections especially urinary tract Normal intestinal flora prevents colonization of large intestine by pathogens Bacterial Disease of the Upper Digestive Tract human diseases occur in the mouth The most common o dental caries o peridontal gum disease Complications o Oral flora can enter bloodstream during dental procedures and cause sub acute bacterial endocarditis a chronic infection of heart lining and valves Dental Caries o Causative Agent mixture of microbes but mainly Streptococcus mutans colonizes teeth grows well at low pH sucrose glucose fructose produces lactic acid from fructose metabolism recall fermentation produce insoluble extracellular sticky polymer glucans from glucose o Pathogenesis bacteria adhere to specific receptors on pellicle protein coat from saliva or on other bacteria glucans bind organisms together and to tooth dental plaque dietary sugar Fig 25 4 experiment with glucose rinse drop in pH acidity calcium phosphate in enamel dissolves pits and cracks for colonization o Prevention o Treatment restrict dietary sucrose and other sugars most important fluoride hardens tooth enamel more resistant to dissolving in acid added to public drinking water in many communities young more susceptible pits and fissures wear down with age mechanical removal of plaque tooth brushing and flossing disrupt the biofilm strongly reduces incidence of caries application of sealants prevents decay in pits and fissures drill out decay cavity and fill with amalgam Periodontal Disease o Symptoms most cases are asymptomatic common symptoms bleeding gums gum inflammation sensitivity bad breath teeth become loose discolored receding gums o Cause o Pathogenesis dental plaque forms at junction of gums and teeth Plaque tartar forms on teeth at gum line extends into gingival crevice inflammation gingivitis membranes and bone soften tooth may be lost o Epidemiology mainly disease of individuals 35 years most 65 have some disease immuno deficient often have severe disease o Prevention and treatment careful flossing and brushing combined with semi annual polishing and cleaning cleaning to clear inflamed gingival crevice and removing plaque advanced cases usually require surgery to expose root of teeth for cleaning Trench Mouth progresses as pathogen s make collagenase and hyaluronidase enzymes that weaken gingival tissue gingival crevice wider and deeper Gram microbes multiply and release endotoxins and exotoxins which attack host tissue o also known as Vincent s disease or acute necrotizing ulcerative gingivitis ANUG o distinct o disease rampant during World War I from other forms of periodontitis Soldiers in trenches unable to maintain oral hygiene Oral spirochete Treponema genus probably working with other anaerobic bacteria of mouth leads to necrosis and ulceration of gums between teeth o Caustive Agent o Symptoms abrupt onset fever bleeding and painful gums foul odor nutritional deficiency Helicobacter pylori Gastritis o Symptoms Most are asymptomatic o Complications ulcers abdominal pain tenderness bleeding stomach and upper duodenal cancer o Causative Agent discovered in early 1980 s Helicobacter pylori short spiral Gram negative microaerophile multiple polar knobbed flagella o Pathogenesis H pylori survives extreme acidity of the stomach neutralizes its environment by making ammonia from urea with powerful urease uses flagella to corkscrew through mucosal lining and multiply inflammatory response begins Infection persists for many years often for life Inflammation drop in mucus production stomach lining exposed to acidic environment and pepsin ulcer 10 20 infected ulcers most ulcer patients are infected very small cancer 90 stomach cancer patients are infected with H pylori o Epidemiology infections tend to cluster in families most likely fecal oral transmission increases with age o Prevention and Treatment No known prevention measures Infection can usually be eradicated with triple antibiotic therapy plus bismuth bismuth Pepto bismol inhibits production of stomach acid Lower Digestive Disease Cholera o 7 cholera pandemics since the early 1800s 1832 1836 200 000 died in the US 2nd and 4th most recent 1991 Lima Peru probably due to freighter contaminated bilgewater dumped in the harbor 700 00 cases and 6 000 deaths o Symptoms classic example of severe diarrhea up to loss of 20 liters of fluid per day rice water stools due to appearance vomiting common muscles cramps common due to severe loss of fluids and electrolytes o Causative Agent Vibrio cholerae Gram negative curved bacillus salt tolerant tolerates high pH o Pathogenesis large infective dose needed due to killing by low stomach pH in small intestine organisms adhere to epithelial lining and multiply Cholera Toxin an enterotoxin causes symptoms A B toxin acts on intestinal epithelial cells o B fragment binds toxin to intestinal microvilli o A fragment toxin enters epithelial cells excess secretion of fluids and electrolytes chloride followed by