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. Tongue. Parotid (salivary) gland. Teeth. Pharynx. Esophagus.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
Chapter 25 Microbial Diseases of the Digestive system:
The Digestive System Learning Objective 25-1Name the structures of the digestive system that contact food.
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
Normal Microbiota of the Digestive System Learning Objective 25-2Identify 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
Bacterial Diseases of the Mouth • 25-3 Describe the events that lead to dental caries and periodontal disease. Learning Objective
Figure 25.4 The stages of tooth decay. Decay Plaque Enamel Dentin Pulp Insert Fig 25.4 Bone Root Healthy tooth with plaque Decay in enamel Decay in dentin Decay in pulp Advanced decay
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
Prevention • Brushing • Removal of food particles • Removal of bacteria • Neutralizing acid • Flossing • Mouthwash • Fluoride • Hardens enamel
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
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.
Figure 25.7 Invasion of intestinal wall by Shigella bacterium. M cell on epithelia wall Shigellabacterium 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. 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
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. 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
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
Salmonellosis vs. typhiod fever Reported cases per 100,000 population 30 25 Salmonellosis 20 Typhoid fever 15 Insert Fig 25.10 10 5 0 ’34 ’40 ’46 ’52 ’58 ’64 ’70 ’76 ’82 ’88 ’94 ’00 ’06 Year
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
Figure 25.12 Pedestal formation by EnterohemorrhagicE. coli (EHEC) O157:H7. Insert Fig 25.12
Escherichia coli Gastroenteritis • Intoxication/Infection: infection; endotoxin • Diagnosis: PFGE of sorbitol-negative E. coli • Treatment: oral rehydration
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) Insert Fig 25.13 Hydrochloric acid Mucus-secreting epithelial cells lining stomach Blood capillary (cross section) Lymphocyte Connective tissue Neutrophil Plasma cell Submucosal cell
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
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 fromDiseases 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 fromDiseases in Focus 25.3, p. 731. If possible on this slide, include title: Viral Hepatitis