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Chapter 25 Microbial Diseases of the Digestive system: The Digestive System Learning Objective 25-1 Name the structures of the digestive system that contact food. Figure 25.1 The human digestive system. Oral Cavity Parotid (salivary) gland Tongue Pharynx Teeth Esophagus Insert Fig 25.1 Liver Gallbladder Stomach Duodenum Small intestine Pancreas Large intestine Rectum Anus Normal Microbiota of the Digestive System Learning Objective 25-2 Identify parts of the gastrointestinal tract that normally have microbiota. Your normal flora Millions of bacteria per mL of saliva Mouth, pharynx, and esophagus Stomach has few resident microbes Small and large intestine ◦ 100 trillion bacteria in the intestines (most in the large intestine) ◦ 60% of the dry weight of feces is bacteria Your defenses Stomach Paneth cells ◦ Sense bacteria and secrete antimicrobial proteins called “defensins” Immune system surveillance Vaishnava S et al. PNAS 2008;105:20858-20863 Bacterial Diseases of the Mouth Learning Objective 25-3 Describe the events that lead to dental caries and periodontal disease. Figure 25.4 The stages of tooth decay. Plaque Decay Enamel Dentin Pulp Insert Fig 25.4 Bone Root Healthy tooth with plaque Decay in enamel Advanced decay Decay in dentin Decay in pulp Dental caries Figure 25.5 The stages of periodontal disease. Plaque Tooth Gum (gingiva) Insert Fig 25.5 Bone Cementum Periodontal ligament Healthy gingivae Gingivitis Periodontal pockets Periodontitis Periodontal disease Prevention Brushing ◦ Removal of food particles ◦ Removal of bacteria ◦ Neutralizing acid Flossing Mouthwash Fluoride ◦ Hardens enamel Bacterial Diseases of the Mouth Disease Dental caries Periodontal disease Acute necrotizing gingivitis Pathogen Initially S. mutans, then Gram positive rods and filamentous bacteria Porphyromonas spp. Prevotella intermedia Diseases of Lower Digestive System Learning Objective 25-4 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. Diseases of Lower Digestive System Infection: growth of a pathogen ◦ Incubation is from 12 hours to 2 weeks ◦ Fever Intoxication: ingestion of toxin ◦ Symptoms appear 1 to 48 hours after ingestion Gastroenteritis: diarrhea, dysentery Treatment: oral rehydration therapy Diarrheal disease Bacterial, viral, protozoan, parasitic Defined as passing three or more loose or liquid stools per day Three varieties ◦ acute watery diarrhea – lasts several hours or days, and includes cholera ◦ acute bloody diarrhea – also called dysentery; and ◦ persistent diarrhea – lasts 14 days or longer Diarrheal disease Second leading cause of death in children under 5 Kills 1.5 million children per year 2 billion cases per year Dehydration and electrolyte imbalance Staphylococcal Food Poisoning Pathogen Symptoms Staphylococcus aureus Nausea, vomiting, and diarrhea Intoxication/Infection Intoxication Enterotoxin (superantigen) None Treatment Figure 25.6 The sequence of events in a typical outbreak of staphylococcal food poisoning. Food containing protein is cooked (bacteria usually killed). Then food is contaminated by worker with staphylococci on hands (competing bacteria have been eliminated). Food is left at room temperature. Organisms incubate in food (temperature abuse) long Insert Figenough 25.6 to form and release toxins. (Reheating will eliminate staphylococci but not the toxins.) Food containing toxins is eaten. In 1–6 hours, staphylococcal intoxication occurs. Figure 25.7 Invasion of intestinal wall by Shigella bacterium. M cell on epithelia wall Shigella bacterium Insert Fig 25.7 Figure 25.8 Shigellosis. Shigella M cell Epithelial cell lining intestinal tract Membrane ruffle (see Figure 25.7) Shigella enters an epithelial cell. Insert Fig 25.8 Shigella multiplies inside the cell. Shigella invades neighboring epithelial cells, thus avoiding immune defenses. Mucosal abscess An abscess forms as epithelial cells are killed by the infection.The bacteria rarely spread in the bloodstream. Shigellosis (Bacillary Dysentery) Pathogen Symptoms Shigella spp. 20 BM/day, diarrhea is often bloody, cramps, fever Intoxication/Infection Infection Endotoxin and Shiga exotoxin Isolation of bacteria Oral rehydration, Fluoroquinolones Diagnosis Treatment Figure 1 Risk of shigellosis per 100?000 travelers to different regions of the world. Karl Ekdahl , Yvonne Andersson The epidemiology of travel-associated shigellosis?regional risks, seasonality and serogroups Journal of Infection Volume 51, Issue 3 2005 222 - 229 http://dx.doi.org/10.1016/j.jinf.2005.02.002 Figure 25.9 Salmonellosis. Salmonella M cell Epithelial cell lining intestinal tract Membrane ruffle Salmonella enters an epithelial cell. Insert Fig 25.9 Salmonella multiplies within vesicle inside the cell. Salmonella multiplies in mucosal cells; there the inflammatory response results in diarrhea. Occasionally, the bacteria cross the epithelial cell membrane and enter the lymphatic system and bloodstream. Lymph node Bloodstream Typhoid Fever Caused by Salmonella typhi No animal reservoir Bacteria spread throughout body in phagocytes 1–3% of recovered patients become chronic carriers 5-20 liters of liquid stool passed daily Mary Mallon (aka Typhoid Mary) Disease Salmonellosis Typhoid Fever Pathogen Salmonella enterica Nausea and diarrhea S. typhi Symptoms Intoxication/ Infection Infection Endotoxin High fever, headache, significant mortality Infection Endotoxin Diagnosis Isolation of bacteria; serotyping Isolation of bacteria; serotyping Treatment Oral rehydration Quinolones; cephalosporins Salmonellosis vs. typhiod fever 30 25 Reported cases per 100,000 population Salmonellosis 20 Typhoid fever 15 Insert Fig 25.10 10 5 0 ’34 ’40 ’46 ’52 ’58 ’64 ’70 Year ’76 ’82 ’88 ’94 ’00 ’06 Vibrios Cholera ◦ Vibrio cholerae serotypes that produce cholera toxin ◦ Toxin causes host cells to secrete Cl−, HCO−, and water Noncholera vibrios ◦ ◦ ◦ ◦ Usually from contaminated crustaceans or mollusks V. cholerae serotypes other than O:1, O:139, El Tor V. parahaemolyticus V. vulnificus Figure 25.11 Vibrio cholerae, the cause of cholera. Vibrio cholerae Insert Fig 25.11 Disease Pathogen Symptoms Cholera Vibrio cholerae O:1 and O:139 Diarrhea with large water loss Noncholera Vibrios V. parahaemolyticus V. vulnificus Cholera-like diarrhea, but generally milder Intoxication/ Cholera Infection toxin (exotoxin) Infection, enterotoxin Rapidly spreading tissue destruction Infection, siderophores Diagnosis Isolation of bacteria Isolation of bacteria Isolation of bacteria Treatment Rehydration; Rehydration; doxycycline antibiotics Antibiotics Figure 25.12 Pedestal formation by Enterohemorrhagic E. coli (EHEC) O157:H7. Insert Fig 25.12 Escherichia coli Gastroenteritis EPEC Stimulate host-cell actin to form pedestals beneath attachment site EIEC Access intestinal submucosa through M cells EAEC Not invasive; enterotoxin causing a watery diarrhea EHEC (STEC) Phage-encoded Shiga toxin Escherichia coli Gastroenteritis Intoxication/Infection: infection; endotoxin Diagnosis: PFGE of sorbitol-negative E. coli Treatment: oral rehydration Campylobacter Gastroenteritis Pathogen Symptoms Intoxication/Infection Diagnosis Reservoir Campylobacter jejuni Fever, abdominal pain, diarrhea Infection Isolation of bacteria Chickens, cows Traveler’s Diarrhea ETEC EAEC Salmonella Shigella Campylobacter Figure 25.13 Helicobacter pylori infection, leading to ulceration of the stomach wall. Mucus layer protects stomach from activity of gastric acids (HCl) Helicobacter pylori Mucus layer Urease, a bacterial enzyme, produces highly alkaline ammonia by activity on urea. The ammonia neutralizes hydrochloric acids of stomach. (NH3 + HCl NH4Cl) Hydrochloric acid Insert Fig 25.13 Mucus-secreting epithelial cells lining stomach Connective tissue Submucosal cell Blood capillary Lymphocyte (cross section) Neutrophil Plasma cell Helicobacter Peptic Ulcer Disease Pathogen Symptoms Helicobacter pylori Peptic ulcers Intoxication/Infection Diagnosis Infection Urea breath, bacterial culture Antimicrobial drugs Treatment Yersinia Gastroenteritis Pathogen Symptoms Intoxication/Infection Diagnosis Transmitted Y. enterocolitica, Y. pseudotuberculosis Abdominal pain and diarrhea, usually mild; may be confused with appendicitis Infection Endotoxin Bacterial culture; serotyping Meat, milk Clostridium and Bacillus Gastroenteritis Pathogen Symptoms C. perfringens C. difficile Diarrhea Diarrhea to colitis B. cereus Nausea and vomiting; diarrhea Intoxication/ Infection Infection Exotoxin Infection Exotoxin Intoxication Diagnosis Cytotoxin assay Isolation of bacteria Isolation of bacteria Clostridium and Bacillus Gastroenteritis Pathogen Treatment C. perfringens C. difficile B. cereus Oral Metronidazole; None rehydration discontinue other antibiotic therapy Source of Infection Meats Elimination of normal microbiota Rice dishes Clostridium dificile (C dif.) Growing threat in hospitals Common following a long course of antibiotics Uncommon in people who haven’t been on antibiotics Treatments: ◦ Antibiotics ◦ Surgery ◦ Fecal transplantation Viral Diseases of the Digestive System Disease Mumps Pathogen Mumps virus Symptoms Swollen parotid glands Incubation 16–18 days Diagnosis Symptoms Treatment Preventive vaccine Figure 25.14 A case of mumps. Insert Fig 25.14 Hepatitis An inflammation of the liver May result from drug or chemical toxicity, EB virus, CMV, or the hepatitis viruses Diseases in Focus 25.3 Characteristics of Viral Hepatitis Insert healthy liver photo from Diseases in Focus 25.3, p. 731. If possible on this slide, include title: Viral Hepatitis Diseases in Focus 25.3 Characteristics of Viral Hepatitis Insert damaged liver photo from Diseases in Focus 25.3, p. 731. If possible on this slide, include title: Viral Hepatitis Hepatitis Viruses Disease Transmission Pathogen Chronic Liver Vaccine? Disease? Hepatitis A Fecal-oral Picornaviridae No Hepatitis B Parenteral, STI Hepadnaviridae Yes Recombinant Hepatitis C Parenteral Filoviridae Yes None Hepatitis D Parenteral, HBV coinfection Deltaviridae Yes HBV vaccine Hepatitis E Fecal-oral Caliciviridae No HAV vaccine Inactivated virus Applications of Microbiology: A Safe Blood Supply Nucleic acid testing (NAT) is used to test donated blood and plasma: ◦ HCV ◦ HIV ◦ West Nile virus Virus inactivation is used on plasma Viral Gastroenteritis Pathogen Rotavirus Norovirus Symptoms Vomiting, diarrhea; 1 week Vomiting, diarrhea; 2–3 days Incubation period 1–3 days 18–48 hours Diagnostic test EIA PCR Treatment Oral rehydration Figure 25.16 Rotavirus. Insert Fig 25.16 Diseases in Focus 25.4 Viral Diseases of the Digestive System Insert photo from Diseases in Focus 25.4, p. 736. If possible on this slide, include title: Norovirus Norovirus Figure 25.17 The trophozoite form of Giardia lamblia, the flagellated protozoan that causes giardiasis. Insert Fig 25.17 Mark left by ventral sucker Giardiasis Pathogen Giardia lamblia Symptoms Protozoan adheres to intestinal wall, leading to diarrhea Reservoir Water or mammals Diagnosis FA test Treatment Metronidazole; quinacrine Figure 25.18 Cryptosporidiosis. Intestinal mucosa Oocyst Insert Fig 25.18 Cryptosporidiosis Pathogen Cryptosporidium hominis Symptoms Self-limiting diarrhea; may be life-threatening in immunosuppressed people Reservoir Cattle; water Diagnosis Acid-fast stain; FA; ELISA Treatment Oral rehydration Number of reported cases Chapter 12, unnumbered figure B, page 357. Insert Figure B from Clinical Focus on p. 357. If possible on this slide, include title: Cryptosporidium hominis in the U.S. [Note C. hominis must be italicized] Year Cryptosporidium hominis in the U.S. Figure 12.19b Amebae. Red blood cells Insert Fig 12.19(b) Nucleus Entamoeba histolytica Figure 25.19 Section of intestinal wall showing a typical flask-shaped ulcer caused by Entamoeba histolytica. Normal mucosa Ulcer Insert Fig 25.19 Amebic Dysentery Pathogen Entamoeba histolytica Symptoms Abscesses; significant mortality rate Reservoir Humans Diagnosis Microscopy; serology Treatment Metronidazole Helminthic Diseases of the Digestive System Learning Objective 25-10 List the causative agents, modes of transmission, symptoms, and treatments for tapeworms, hydatid disease, pinworms, hookworms, whipworms, ascariasis, and trichinellosis. Figure 25.20 The woldwide prevalence of human infections with selected intestinal helminths. Percentage of world population infected Trichinella Flukes (liver, lung) Tapeworms 1.0% 1.5% 3.0% Schistosomes 6.0% Enterobius Insert Fig 25.20 10% Hookworms 21% Ascaris 30% 1 2 3 4 5 6 7 8 Number of people infected (100 millions) 9 10 11 Figure 12.27 General anatomy of an adult tapeworm. Scolex Hooks Sucker Neck Insert Fig 12.27 Sucker Genital pore Ovary Mature proglottid will disintegrate and release eggs Figure 25.21 Ophthalmic cysticercosis. Fluid-filled bladder Scolex Insert Fig 25.21 Figure 12.28 The life cycle of the tapeworm, Echinococcus, spp. 1 6 Adult tapeworm releases eggs. Intermediate host Scoleces from cyst attach to intestine and grow into adults. 2 Human intermediate host ingests eggs. Dead end. Egg (30–38 mm) Adult tapeworm Intermediate host Scolex SexualInsert Fig 12.28 Asexual reproduction reproduction Definitive host 5 Definitive host eats intermediate host, ingesting cysts. 2 Larva 3 Hydatid cyst Brood capsule Scolex Intermediate host ingests eggs. 4 Larvae develop into hydatid cysts. Eggs hatch, and larvae migrate to liver or lungs. Figure 25.22 A hydatid cyst formed by Echinococcus granulosus. Cyst Brain Insert Fig 25.22Left orbit (eye socket) Tapeworms and Hydatid Disease Disease Tapeworm Hydatid Disease Pathogen Taenia saginata, T. solium, Diphyllobothrium latum Echinococcus granulosus Symptoms Neurocysticercosis Tissue damage Intermediate Host Cattle, pigs, fish Humans Definitive Host Humans Dogs Tapeworms and Hydatid Disease Disease Tapeworm Hydatid Disease Diagnosis Microscopic exam Praziquantel; of feces albendazole Treatment Serology; X-ray exam Surgical removal; albendazole Figure 12.29 The pinworm Enterobius vermicularis. Mouth Intestine Mouth Ovary Genital pore Anus Intestine Testis Insert Fig 12.29 Genital pore Spicules Anus Adult pinworm Female (8–13 mm long) Male (2–5 mm long) Egg (55 μm long) Larva Pinworm egg Pinworms Pathogen Enterobius vermicularis Symptoms Itching around anus Intermediate host Humans Definitive host Humans Diagnosis Microscopy Treatment Pyrantel pamoate Figure 25.23 An Ancylostoma hookworm attached to intestinal mucosa. Hookworm Insert Fig 25.23 Intestinal mucosa Figure 25.24 Ascaris lumbricoides, the cause of ascariasis. Insert Fig 25.24 Ascaris lumbricoides Figure 25.26 The life cycle of Trichinella spiralis, the causative agent of trichinellosis. Ingested cysts develop into Trichinella spiralis adults in the pig’s intestinal wall. Adult worms produce larvae that encyst in the pig’s muscles. Garbage, including undercooked or raw pork Capsule Meanwhile, other animals eat infected meat that has been dumped. Insert Fig 25.26 Human eats undercooked pork containing cysts that are infective to humans or animals that ingest it. Trichinellosis in humans; ingested cysts develop into T. spiralis adults. Adults produce larvae that encyst in muscles. T. spiralis adult Section of encysted T. spiralis Roundworms Disease Hookworm Pathogen Necator Ascaris americanus, lumbricoides Ancyclostoma duodenale Trichuris trichiura Trichinella spiralis Symptoms Anemia Few Abdominal pain, diarrhea Few Intermediate Larvae in soil Host Humans Humans Mammals Definitive Host Humans Humans Humans Humans Ascariasis Whipworm Trichinellosis Roundworms Disease Hookworm Ascariasis Whipworm Trichinellosis Diagnosis Microscopy Microscopy Microscopy Biopsy; ELISA Treatment Mebendazole Mebendazole Mebendazole; Mebendazole; corticosteroids corticosteroids