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Microbial Diseases of the Digestive system:
Chapter 25 Microbial Diseases of the Digestive system:
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The Digestive System Learning Objective 25-1 Name the structures of the digestive system that contact food.
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Figure 25.1 The human digestive system.
Oral Cavity Tongue Parotid (salivary) gland Teeth Pharynx Esophagus Insert Fig 25.1 Liver Stomach Gallbladder Duodenum Small intestine Pancreas Large intestine Rectum Anus
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Normal Microbiota of the Digestive System
Learning Objective 25-2 Identify parts of the gastrointestinal tract that normally have microbiota.
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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
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Your defenses Stomach Paneth cells Immune system surveillance
Sense bacteria and secrete antimicrobial proteins called “defensins” Immune system surveillance
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Vaishnava S et al. PNAS 2008;105:20858-20863
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Bacterial Diseases of the Mouth
Learning Objective 25-3 Describe the events that lead to dental caries and periodontal disease.
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Insert Fig 25.4 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
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Dental caries
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Insert Fig 25.5 Figure 25.5 The stages of periodontal disease. Plaque
Tooth Gum (gingiva) Bone Insert Fig 25.5 Cementum Periodontal ligament Healthy gingivae Gingivitis Periodontal pockets Periodontitis
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Periodontal disease
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Prevention Brushing Flossing Mouthwash Fluoride
Removal of food particles Removal of bacteria Neutralizing acid Flossing Mouthwash Fluoride Hardens enamel
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Bacterial Diseases of the Mouth
Pathogen Dental caries Initially S. mutans, then Gram positive rods and filamentous bacteria Periodontal disease Porphyromonas spp. Acute necrotizing gingivitis Prevotella intermedia
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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.
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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
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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
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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
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Staphylococcal Food Poisoning
Pathogen Staphylococcus aureus Symptoms Nausea, vomiting, and diarrhea Intoxication/Infection Intoxication Enterotoxin (superantigen) Treatment None
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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 enough to form and release toxins. (Reheating will eliminate staphylococci but not the toxins.) Insert Fig 25.6 Food containing toxins is eaten. In 1–6 hours, staphylococcal intoxication occurs.
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Figure 25.7 Invasion of intestinal wall by Shigella bacterium.
M cell on epithelia wall Shigella bacterium Insert Fig 25.7
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Figure 25.8 Shigellosis. Insert Fig 25.8 Shigella M cell
Epithelial cell lining intestinal tract Membrane ruffle (see Figure 25.7) Shigella enters an epithelial cell. Shigella multiplies inside the cell. Insert Fig 25.8 Shigella invades neighboring epithelial cells, thus avoiding immune defenses. An abscess forms as epithelial cells are killed by the infection. The bacteria rarely spread in the bloodstream. Mucosal abscess
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Shigellosis (Bacillary Dysentery)
Pathogen Shigella spp. Symptoms 20 BM/day, diarrhea is often bloody, cramps, fever Intoxication/Infection Infection Endotoxin and Shiga exotoxin Diagnosis Isolation of bacteria Treatment Oral rehydration, Fluoroquinolones
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Figure 1 Risk of shigellosis per 100
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
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Figure 25.9 Salmonellosis. Insert Fig 25.9 Salmonella M cell
Epithelial cell lining intestinal tract Membrane ruffle Salmonella enters an epithelial cell. Salmonella multiplies within vesicle inside the cell. Insert Fig 25.9 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
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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
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Mary Mallon (aka Typhoid Mary)
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Disease Salmonellosis Typhoid Fever Pathogen Salmonella enterica S. typhi Symptoms Nausea and diarrhea High fever, headache, significant mortality Intoxication/ Infection Infection Endotoxin Diagnosis Isolation of bacteria; serotyping Treatment Oral rehydration Quinolones; cephalosporins
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Salmonellosis vs. typhiod fever
Insert Fig 25.10 Typhoid fever Salmonellosis Year Reported cases per 100,000 population 30 25 20 10 5 15 ’34 ’ ’ ’ ’ ’ ’ ’ ’ ’ ’ ’ ’06
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Vibrios Cholera Noncholera vibrios
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
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Vibrio cholerae Insert Fig 25.11
Figure Vibrio cholerae, the cause of cholera. Vibrio cholerae Insert Fig 25.11
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Vibrio cholerae O:1 and O:139 V. vulnificus
Disease Cholera Noncholera Vibrios Pathogen Vibrio cholerae O:1 and O:139 V. parahaemolyticus V. vulnificus Symptoms Diarrhea with large water loss Cholera-like diarrhea, but generally milder Rapidly spreading tissue destruction Intoxication/Infection Cholera toxin (exotoxin) Infection, enterotoxin Infection, siderophores Diagnosis Isolation of bacteria Treatment Rehydration; doxycycline Rehydration; antibiotics Antibiotics
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Figure 25. 12 Pedestal formation by Enterohemorrhagic E
Figure Pedestal formation by Enterohemorrhagic E. coli (EHEC) O157:H7. Insert Fig 25.12
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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
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Escherichia coli Gastroenteritis
Intoxication/Infection: infection; endotoxin Diagnosis: PFGE of sorbitol-negative E. coli Treatment: oral rehydration
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Campylobacter Gastroenteritis
Pathogen Campylobacter jejuni Symptoms Fever, abdominal pain, diarrhea Intoxication/Infection Infection Diagnosis Isolation of bacteria Reservoir Chickens, cows
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Traveler’s Diarrhea ETEC EAEC Salmonella Shigella Campylobacter
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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) Insert Fig 25.13 Hydrochloric acid Mucus-secreting epithelial cells lining stomach Blood capillary (cross section) Connective tissue Lymphocyte Neutrophil Plasma cell Submucosal cell
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Helicobacter Peptic Ulcer Disease
Pathogen Helicobacter pylori Symptoms Peptic ulcers Intoxication/Infection Infection Diagnosis Urea breath, bacterial culture Treatment Antimicrobial drugs
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Yersinia Gastroenteritis
Pathogen Y. enterocolitica, Y. pseudotuberculosis Symptoms Abdominal pain and diarrhea, usually mild; may be confused with appendicitis Intoxication/Infection Infection Endotoxin Diagnosis Bacterial culture; serotyping Transmitted Meat, milk
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Clostridium and Bacillus Gastroenteritis
Pathogen C. perfringens C. difficile B. cereus Symptoms Diarrhea Diarrhea to colitis Nausea and vomiting; diarrhea Intoxication/Infection Infection Exotoxin Intoxication Diagnosis Isolation of bacteria Cytotoxin assay
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Clostridium and Bacillus Gastroenteritis
Pathogen C. perfringens C. difficile B. cereus Treatment Oral rehydration Metronidazole; discontinue other antibiotic therapy None Source of Infection Meats Elimination of normal microbiota Rice dishes
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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
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Viral Diseases of the Digestive System
Mumps Pathogen Mumps virus Symptoms Swollen parotid glands Incubation 16–18 days Diagnosis Treatment Preventive vaccine
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Figure A case of mumps. Insert Fig 25.14
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Hepatitis An inflammation of the liver
May result from drug or chemical toxicity, EB virus, CMV, or the hepatitis viruses
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Insert healthy liver photo from Diseases in Focus 25.3, p. 731.
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
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Insert damaged liver photo from Diseases in Focus 25.3, p. 731.
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
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Hepatitis Viruses Disease Transmission Pathogen Chronic Liver Disease?
Vaccine? Hepatitis A Fecal-oral Picornaviridae No Inactivated virus Hepatitis B Parenteral, STI Hepadnaviridae Yes Recombinant Hepatitis C Parenteral Filoviridae None Hepatitis D Parenteral, HBV coinfection Deltaviridae HBV vaccine Hepatitis E Caliciviridae HAV vaccine
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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
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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
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Figure Rotavirus. Insert Fig 25.16
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Diseases in Focus 25.4 Viral Diseases of the Digestive System
Insert photo from Diseases in Focus 25.4, p If possible on this slide, include title: Norovirus Norovirus
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Mark left by ventral sucker
Figure The trophozoite form of Giardia lamblia, the flagellated protozoan that causes giardiasis. Insert Fig 25.17 Mark left by ventral sucker
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Giardiasis Pathogen Giardia lamblia Symptoms
Protozoan adheres to intestinal wall, leading to diarrhea Reservoir Water or mammals Diagnosis FA test Treatment Metronidazole; quinacrine
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Intestinal mucosa Oocyst Insert Fig 25.18
Figure Cryptosporidiosis. Intestinal mucosa Oocyst Insert Fig 25.18
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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
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Number of reported cases
Chapter 12, unnumbered figure B, page 357. Insert Figure B from Clinical Focus on p If possible on this slide, include title: Cryptosporidium hominis in the U.S. [Note C. hominis must be italicized] Number of reported cases Year Cryptosporidium hominis in the U.S.
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Insert Fig 12.19(b) Figure 12.19b Amebae. Red blood cells Nucleus
Entamoeba histolytica
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Figure Section of intestinal wall showing a typical flask-shaped ulcer caused by Entamoeba histolytica. Normal mucosa Ulcer Insert Fig 25.19
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Amebic Dysentery Pathogen Entamoeba histolytica Symptoms
Abscesses; significant mortality rate Reservoir Humans Diagnosis Microscopy; serology Treatment Metronidazole
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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.
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Figure 25.20 The woldwide prevalence of human infections with selected intestinal helminths.
Percentage of world population infected Trichinella 1.0% Flukes (liver, lung) 1.5% Tapeworms 3.0% Schistosomes 6.0% Insert Fig 25.20 Enterobius 10% Hookworms 21% Ascaris 30% Number of people infected (100 millions)
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Insert Fig 12.27 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
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Insert Fig 25.21 Figure 25.21 Ophthalmic cysticercosis.
Fluid-filled bladder Scolex Insert Fig 25.21
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Insert Fig 12.28 Sexual Asexual reproduction reproduction
Figure The life cycle of the tapeworm, Echinococcus, spp. Adult tapeworm releases eggs. 1 Intermediate host Scoleces from cyst attach to intestine and grow into adults. 6 2 Human intermediate host ingests eggs. Dead end. Egg (30–38 mm) Adult tapeworm Intermediate host Scolex Sexual reproduction Insert Fig 12.28 Asexual reproduction 2 Intermediate host ingests eggs. Definitive host Larva 5 Definitive host eats intermediate host, ingesting cysts. Eggs hatch, and larvae migrate to liver or lungs. 3 Hydatid cyst Brood capsule 4 Larvae develop into hydatid cysts. Scolex
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Figure 25.22 A hydatid cyst formed by Echinococcus granulosus.
Brain Insert Fig 25.22 Left orbit (eye socket)
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Tapeworms and Hydatid Disease
Pathogen Taenia saginata, T. solium, Diphyllobothrium latum Echinococcus granulosus Symptoms Neurocysticercosis Tissue damage Intermediate Host Cattle, pigs, fish Humans Definitive Host Dogs
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Tapeworms and Hydatid Disease
Diagnosis Microscopic exam of feces Praziquantel; albendazole Treatment Serology; X-ray exam Surgical removal; albendazole
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Insert Fig 12.29 Adult pinworm
Figure The pinworm Enterobius vermicularis. Mouth Intestine Mouth Ovary Genital pore Anus Intestine Insert Fig 12.29 Testis Genital pore Egg (55 μm long) Spicules Anus Larva Female (8–13 mm long) Male (2–5 mm long) Adult pinworm Pinworm egg
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Pinworms Pathogen Enterobius vermicularis Symptoms Itching around anus
Intermediate host Humans Definitive host Diagnosis Microscopy Treatment Pyrantel pamoate
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Figure 25.23 An Ancylostoma hookworm attached to intestinal mucosa.
Insert Fig 25.23 Intestinal mucosa
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Figure 25.24 Ascaris lumbricoides, the cause of ascariasis.
Insert Fig 25.24
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Ascaris lumbricoides
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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 Section of encysted T. spiralis 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
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Roundworms Disease Hookworm Ascariasis Whipworm Trichinellosis
Pathogen Necator americanus, Ancyclostoma duodenale Ascaris lumbricoides Trichuris trichiura Trichinella spiralis Symptoms Anemia Few Abdominal pain, diarrhea Intermediate Host Larvae in soil Humans Mammals Definitive Host
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Roundworms Disease Hookworm Ascariasis Whipworm Trichinellosis
Diagnosis Microscopy Biopsy; ELISA Treatment Mebendazole Mebendazole; corticosteroids
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