Chapter 25: Digestive System InfectionsIntroduction- 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 Snowo Lack of water sanitation was the culpritThe Digestive System- Digestive system/ alimentary tract/ gastrointestinal tracto lone of the body’s main boundaries with the environmento major route of microbial invasiono divided into upper and lower tractso upper = mouth, salivary glands, esophagus, stomacho lower = intestines, pancreas and liver- Most of the normal flora of digestive tract is in the oral cavity and intestineso Esophagus has very little florao Stomach contains no microorganisms - killed by stomach acido Mouth is colonized by relatively few species- mainly various streptococci- Gram+, chain-forming 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 => plaqueNormal Microbiota- Intestineso Upper small intestine: small population numbers continually flushed away aerobic and facultative Gram- bacilli and some streptococcio 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 pathogensBacterial Disease of the Upper Digestive Tract- The most common human diseases occur in the mouth!o dental carieso peridontal gum disease- Complicationso Oral flora can enter bloodstream during dental procedures and cause sub-acute bacterial endocarditis - a chronic infection of heart lining and valves- Dental Carieso 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 glucoseo 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 colonizationo Prevention 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 ageo Treatment 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 Diseaseo Symptoms most cases are asymptomatic common symptoms - bleeding gums- gum inflammation, sensitivity- bad breath- teeth become loose, discolored- receding gumso Cause dental plaque forms at junction of gums and teetho Pathogenesis Plaque (‘tartar’) forms on teeth at gum line extends into gingival crevice- => inflammation = gingivitis  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- membranes and bone soften- tooth may be losto Epidemiology mainly disease of individuals >35 years most >65 have some disease immuno-deficient often have severe diseaseo 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 Moutho also known as Vincent’s disease or acute necrotizing ulcerative gingivitis (ANUG)o distinct from other forms of periodontitiso disease rampant during World War I Soldiers in trenches unable to maintain oral hygieneo Caustive Agent Oral spirochete Treponema genus probably working with other anaerobic bacteria of mouth leads to necrosis and ulceration of gums between teetho Symptoms abrupt onset fever bleeding and painful gums foul odor nutritional deficiency - Helicobacter pylori Gastritiso Symptoms Most are asymptomatico 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 flagellao 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. pylorio Epidemiology infections tend to cluster in families most likely fecal-oral transmission increases with ageo 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 acidLower Digestive Disease- Cholerao 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 deathso 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 electrolyteso Causative Agent Vibrio cholerae- Gram-negative- curved bacillus- salt tolerant- tolerates high pHo Pathogenesis large