Lecture 10 Microbial Diseases of the Digestive System PDF

7/15/2024 Lecture 10 Microbial Diseases of the Digestive System General Microbiology MW 211 2023-2024 Instructor: Dr. Roba Bdeir Dr. Roba Bdeir 1...

7/15/2024 Lecture 10 Microbial Diseases of the Digestive System General Microbiology MW 211 2023-2024 Instructor: Dr. Roba Bdeir Dr. Roba Bdeir 1 Dr. Roba Bdeir 2 1  7/15/2024 Normal Flora M.o entering the mouth are washed down into the GIT by the flow of saliva. About 8 x 1010 microbes are swallowed every day. Patterns of salivary flow vary from person to person; some are highly efficient at rinsing food and microbes away, while others are inefficient, accordingly tooth decay is greatly affected by the degree of efficiency. More than 400 species of m.o live in oral cavity. Esophagus does not have permanent normal microflora. The stomach’s acid pH usually prevents colonization by microbes. It and the first two thirds of the small intestine contain very few microbes, mainly lactobacilli and streptococci that are merely passing through. Dr. Roba Bdeir 3 In the last third of the small intestine, motility of contents is slower, and some microbes are able to colonize its surfaces. These are mainly Gram-negative, facultatively anaerobic bacteria, Enterobacteriaceae (e.g., Escherichia coli), plus obligate anaerobes (e.g., Bacteroides and Clostridium). large intestine, food may remain as long as 60 hours, allowing m.o to colonize & replicate Feces are composed about 50% by weight and volume of bacteria. Most of these are species of Bacteroides. The adult human gut holds hundreds to thousands of species and more than 100 trillion (100 x 1012) individual bacteria. Dr. Roba Bdeir 4 2  7/15/2024 Bacterial diseases of oral cavity Dental plaque Is a continuous formed coating of m.o & organic matter on tooth surfaces, it is the 1st step in tooth decay & gum disease It is not removed by home cleaning methods, it is removed by professional cleaning (at dentists) but starts to build up few minutes after cleaning. Plaque starts when proteins in saliva attach to enamel & form a film. Normal flora (~30 different genera) attach to the film. M.o change sucrose to fructose & glucose & glucose polymers (dextran) that act as bridge to hold cells in plaques. If not removed regularly → Strep, lactobacilli, other acid producing bacteria accumulate → produce acids from fructose → eats away tooth enamel. Plaques also offer protection to bacteria growing in the gingival cervices (between teeth & gum), with time will change into anaerobic pockets full of bacteria that irritate gums & destroy the bone. In some people, plaque mineralizes into calculus (tartar) that causes inflammation & bleeding Dr. Roba Bdeir 5 Dr. Roba Bdeir 6 3  7/15/2024 Dental caries Is the dissolution of enamel & deeper parts of teeth. If not treated may go deep & form abscess in the bone that supports the tooth. It is caused by acids & protein digesting enzymes produced by bacteria. Sugar alcohol (sorbitol, xylitol) can not be metabolized by bact so don’t contribute to tooth decay. Treatment: removing decay & filling the cavity with resins (plastic material) or amalgum (mix of silver & other metal). Prevention or decrease incidence: limit intake of sugary & sticky food, brushing regularly with plaque removing tooth paste & flossing between teeth. Use of fluoride is most significant in reducing tooth decay, it inhibits demineralization of tooth enamel & enhance remineralization. Fluoride: added to drinking water, toothpaste, mouth wash Dr. Roba Bdeir 7 Periodontal disease A combination of gum inflammation & erosion of periodontal ligament & the bone that supports teeth, occurs as a result of bacteria entrapment in gingival cavities which produce endotoxins & acids →inflammation initiated by plaque formation. its mildest form is gingivitis (affects only gums) which responds to Antibiotics. Advanced periodontal dis. Doesn’t respond to AB & leads to chronic periodontitis → affects bone & tissues that support the teeth & gums. Causative agent: various bact most important Porphyromonas gingivalis (G-ve anaerobe). Treatment of chronic Po: Antimicrobial mouth rinse, surgery to eliminate pockets & AB. Prevention: daily thorough cleaning & frequent professional removal of plaque from the pockets Recent study: chronic Po dis activates immune system leading to cardiovascular autoimmune disease. Po bacteria can also invade CVS from open wounds in the gums to cause heart abnormalities in animals & platelet clumping in humans Dr. Roba Bdeir 8 4  7/15/2024 Mumps Viral disease, humans are only host for it. Disease occurs mostly in children. Transmitted by saliva or aerosol droplets, enters thru respiratory tract or oral cavity Virus replicates in oropharynx & travels to salivary glands & sometimes to other glands like testes & meninges. Symptoms: up to 40% of cases asymptomatic, swelling of parotid glands. Complication: if disease occurs in postpubertal males, 20-30% develop orchitis (inflammation of testes) causing sterility but rarely do so. Other complications regardless of age or sex: meningioencephalitis, eye & ear infection, inflammation of ovaries & pancreas (cause juvenile diabetes?) Vaccine: weakened viruses as part of MMR. Thrush Oral infection by Candida albicans Treatment: drops, lozenges, gels of antifungal drugs (nystatin, miconazole) Dr. Roba Bdeir 9 Bacterial diseases of GI Food poisoning Clostridium perfringens Enterotoxin released during sporulation under anaerobic conditions like undercooked meat & gravy when kept warm Symptoms: diarrhea, self limiting. Prevented by sanitary food handling Clostridium botulinum Release potent neurotoxin, botulinum toxin in food which is fatal. Dr. Roba Bdeir 10 5  7/15/2024 Staphylococcus enterotoxicosis S. aureus → enterotoxins (exotoxins) → Inflame intestinal lining & inhibiting water absorption (diarrhea) & cause neural stimulation of the vomiting center in brain (vomiting). The time required for symptoms to appear depends on how long it takes for absorption of a sufficient quantity of toxin to produce them (~1-6hr). These toxins are heat stable & withstand boiling for 30min. Source: food contaminated with m.o from food handlers or environment. Nearly any food can be contaminated with S. aureus, but those with a starch or cream base are most likely candidates. Contamination is difficult to detect as appearance, odor, taste are not changed. In healthy adults no treatment is required (self limiting), recovery does not confer immunity as no sufficient Ig produced. Dr. Roba Bdeir 11 Bacterial enteritis & enteric fevers An intestinal infection (not intoxication) that causes inflammation of the intestines. The causative bacteria invade & damage intestinal mucosa or deeper tissues. Enteritis that affects mainly small intestines causes diarrhea If the large intestine is affected → dysentery which is severe diarrhea often contains large quantities of mucus & sometimes blood & pus. Some pathogens spread thru the body from intestines & cause systemic condition called enteric fever E.g: salmonellosis, typhoid fever, shigellosis, cholera, traveler's diarrhea Dr. Roba Bdeir 12 6  7/15/2024 Salmonellosis Enteritis Caused by some sp. of Salmonella. Transmission: Salmonella sp (except S. typhi) is present in GIT of many animals including poultry, eggs, wild birds & turtles. Transmission often by contaminated food, meat, dairy product & uncooked eggs, also by contaminated water or food contaminated by carriers. Signs & symptoms: abdominal pain, fever, diarrhea with blood & mucus. They are associated with the organisms’ invading the mucosa of both the small and large intestines. Fever probably is caused by endotoxins, toxins that are released from bacterium only when it is lysed. Disease self limiting. Antibiotics usually not given to healthy patients as they tend to induce carrier state & resistant strains. Dr. Roba Bdeir 13 Typhoid fever One of the most serious enteric infections, caused by Salmonella typhi. Humans are the only reservoir for it Transmission: food or drink contaminated with feces or sewage having the m.o. Disease: m.o invade mucosa of small intestine →lymphoid tissue →m.o phagocytized →m.o multiply inside phagocytes. Bacteremia & septicemia occur. M.o invade many tissues including intestinal mucosa & excreted in stool, it can multiply in bile & from gall bladder reinfect intestinal mucosa & lymphoid tissue Symptoms: fever (40C), headache, malaise →abdominal distention, ‘rose spots’ on the trunk & abdomen appear& enlargement of the spleen (no diarrhea), low WBC. some patients suffer from complications like internal hemorrhage & perforation of bowels & pneumonia This disease provides cell mediated immunity against future infections Treatment: fluoroquinolones, broad spectrum cephalosporins, chloramphenicol. Vaccination: live attenuated oral typhoid vaccine (+boosters every 3yrs) Prevention: good sanitation & good sewage systems Dr. Roba Bdeir 14 7  7/15/2024 Shigellosis, or bacillary dysentery caused by different species of shigella. It spreads rapidly in overcrowded conditions with poor sanitation. Humans, chimpanzees and gorillas are the only reservoirs of infection, but the organisms can persist in foods for up to a month. The pathogens spread by contaminated food, fingers, flies, feces, and fomites. Playing, bathing, and washing clothes in contaminated water play significant roles in transmitting Shigella. The ingestion of just 10 organisms is sufficient to cause infection. Signs & symptoms: abdominal cramps, fever, and profuse diarrhea with blood and mucus suddenly appear. In the most serious cases, diarrhea can cause dangerous protein deficiencies and vitamin B12 deficiencies, which, together with loss of electrolytes, can result in neurological damage Dr. Roba Bdeir 15 Shigellosis, or bacillary dysentery continue…. Signs & symptoms: Shigella cause fever due to endotoxins, some species produce Shiga toxin. Some strains release neurotoxin that causes coma & convulsions resulting in high fatality rate. Shigella cause ulceration and bleeding of the intestinal lining and sometimes deeper intestinal layers. The disease is usually self-limiting, but can cause severe dehydration and fluid and electrolyte imbalance. Treatment is necessary in children and debilitated patients. Restoring fluid and electrolytes is essential Fluoroquinolones or trimethoprim/ sulfamethoxazole are used for treatment Dr. Roba Bdeir 16 8  7/15/2024 (Asiatic) Cholera Causative agent: Vibrio cholerae, causes epidemics mainly in Asia. It releases enterotoxin choleragen. Intestinal lining is shredded causing numerous small white flecks like rice grains to be passed in feces. Symptoms: severe nausea, vomiting, abd.pain, diarrhea, stool rapidly becomes clear, containing mucus plugs (rice-water stools), ~22L of fluids & electrolyte lost/day →severe dehydration →death Treatment: fluid & electrolyte replacement. Doxycycline or tetracycline reduces duration but does not eliminate m.o or toxin. Recovery confers temporary immunity, many recovered patients remain in carrier state & can infect others Dr. Roba Bdeir 17 Traveler’s diarrhea A self limiting mild to severe diarrhea affecting travelers (symptoms: nausea, vomiting & diarrhea). Treatment: antidiarrheal agent. Causative agent: most common is pathogenic strains of E. coli, which differ with geographic location so travelers are likely to be exposed to new strains & cause enteritis. Finding E. coli in water indicates that any pathogens found in feces might also be present, because it is always present in water contaminated with fecal material & is more numerous than other organisms and is easier to isolate. Enterohemorrhagic strains of E. coli O157:H7 have caused deadly outbreaks of bloody diarrhea, massive recalls of food & changed the way of cooking (no pink or rare meat) It releases toxins, present in intestines of cattle, but can contaminate fruits & vegetables (manure soil) Onset begins with abdominal cramping, non-bloody diarrhea, which usually becomes bloody on the second or third day; plus vomiting ~6% of patients mainly children & elderly develop hemorrhagic uremic syndrome (HUS) that leads to acute renal failure Dr. Roba Bdeir 18 9  7/15/2024 Peptic ulcer & chronic gastritis Peptic ulcer: lesions of mucous membrane lining esophagus, stomach, duodenum caused by sloughing of dead inflammatory tissue & exposure to acids Chronic gastritis: stomach inflammation can be mild (no signs & symptoms) or produce pain & indigestion. Severe gastritis may lead to ulceration Helicobacter pylori known to cause peptic ulcer, chronic gastritis & a cofactor of stomach cancer. It is isolated from 95% of duodenal ulcers & 70% of gastric ulcers It colonizes gastric mucosa & produces ammonia to neutralize acidity around its cells Portal of entry & exit: unknown?? Treatment: omeprazole + one or 2 AB (metronidazole, amoxicillin, clarithromycin) + Bismuth Dr. Roba Bdeir 19 Viral diseases of GI Viral enteritis Rotavirus: major cause of viral enteritis in infants & young children, has high morbidity & mortality rate. Also can be caused by some species of enterovirus Transmission: oral-fecal route Treatment: restoring fluids & electrolytes. Hepatitis Inflammation of the liver usually caused by viruses, can also be caused by amoeba & toxic chemicals. Dr. Roba Bdeir 20 10  7/15/2024 Hepatitis A most common viral hepatitis, caused by HAV, can occur in epidemics due to contaminated water or food. There are no animal reservoirs. Virus replicates in GIT →blood →liver, spleen, kidneys. Signs& symptoms: jaundice (yellow skin) due to accumulation of bilirubin (product of Hb breakdown in liver) due to impaired liver function, malaise, nausea, diarrhea, abdominal pain, lack of appetite. 50% are asymptomatic. most cases recover completely with life long immunity Treatment: only to alleviate symptoms Vaccine: available. For temporary immunity, gammaglobulin is given Dr. Roba Bdeir 21 Hepatitis B Caused by HBV Transmission: IV or percutaneous injections, blood, semen, breast milk. Virus replicates in liver cells, lymphoid tissue, it can persist in blood for years → carrier state. 40% of carriers die of liver cancer. Virus can insert its DNA into liver cell DNA leading to liver cell carcinoma. Chronic active hepatitis can destroy liver cells (not like HAV) causing cirrhosis Treatment: relieves symptoms but doesn’t cure Vaccine: safe vaccine made by recombinant DNA. Hepatitis C (non A, non B) Characterized by high blood conc of alanine transferase (liver enzyme). Disease: from mild or inapparent to severe disease in compromised individuals. 20% cases progress to cirrhosis & liver cancer Leading reason for liver transplant No vaccine available & immunity doesn’t follow infection Transmission: blood Treatment: antiviral (Ribavirin) and interferon. Cure is probably in the near future Dr. Roba Bdeir 22 11  7/15/2024 Hepatitis B Caused by HDV. Transmitted by IV drug abuse. Alone it fails to cause disease because it requires HBV antigen for replication, so it occurs as coinfection or superinfection with HBV, HBV +HDV together has higher mortality rate than other (due to liver cirrhosis or cancer). Vaccination against HBV will prevent infection with HDV Hepatitis E Transmitted thru fecally contaminated water supplies, more common in adults than children. Chronic cases do not occur. High mortality among pregnant women No vaccine & no immunity after infection. Recently 3 more viruses are linked to hepatitis like disease, if confirmed will be called F, G, H Dr. Roba Bdeir 23 Protozoan diseases of GI Amoebic dysentery & chronic amebiasis Caused by Entamoeba histolytica, a pathogenic amoeba Transmission: fecally contaminated water or food Amoebiasis can be severe acute disease called amoebic dysentery or chronic amebiasis (invade intestinal mucosa & live indefinitely) which can suddenly revert to acute stage The parasites may invade liver and lung tissue, & cause abscesses Symptoms: severe diarrhea (30 times/day) contain mucus & blood, causes dehydration from excessive fluid loss. Treatment: metronidazole, tinidazole + fluid intake Dr. Roba Bdeir 24 12  7/15/2024 Helminth diseases of GI Tape worm infestation Transmission: eating poorly cooked contaminated beef, fish, pork Caused by Taenia saginata (beef) 5-25m, T. solium (pork) 2-7m. larvae → enter body → intestines → develop to worm →absorbs large quantities of nutrients → malnutrition. Long warm → tangles into large mass & blocks intestines Body segments may carry 60,000 eggs Ingested eggs or autoinfection by worm eggs→can invade blood & spread to body sites → most serious CNS (convulsions & paralysis) Treatment: niclosamide cysts in brain Dr. Roba Bdeir 25 Ascariasis Caused by Ascaris lumbricoides (round worms)25-35cm Transmission: food or water contaminated by eggs ,when larvae invade tissue they cause immunological rxns larvae invade many tissues mainly respiratory tract → pharynx → swallowed → s. intestines where they mature & produce eggs May cause Pneumonitis: hemorrhage, edema, blockage of alveoli from worms & if 2ndary bacterial infection appeared →fatal Malnutrition: as worms feed on intestinal contents, if numerous amounts → blockage & perforation to intestines Toxic wastes →allergy Abscess in liver Treatment: piperazine, mebenadazole Dr. Roba Bdeir 26 13  7/15/2024 Pinworm (Enterobius vermicularis) 8-13mm a type of round worm, called also seat worm Transmission: eggs transmitted by bedclothes, by debris under fingernails of people who scratch the itchy area around anus, also by inhalation of airborne eggs Worm eggs are found around the anus when the patient is sleeping or after he awakens Causes discomfort & inadequate rest & malnutrition mainly in children Treatment: piperazine, mebendazole. If one member of a family has pinworm, all family members are presumed infected & should be treated. Bed linens, clothing & towels should be washed (boiled) & the house hold cleaned thoroughly. Reinfection is very likely It is non fatal disease Dr. Roba Bdeir 27 14