chapter_23_GI Tract - Summer 2020.pdf

Chapter 23 Infectious Diseases Affecting the Gastrointestinal Tract 1 Gastrointestinal tract • • • • • • • • Mouth Pharynx Esophagus Stomach Small intestine Large intestine Rectum Anus 2 Figure 23.1 Major structures of the digestive system Uvula Tongue Teeth Salivary glands Pharynx Mouth Eso...

Chapter 23 Infectious Diseases Affecting the Gastrointestinal Tract 1 Gastrointestinal tract • • • • • • • • Mouth Pharynx Esophagus Stomach Small intestine Large intestine Rectum Anus 2 Figure 23.1 Major structures of the digestive system Uvula Tongue Teeth Salivary glands Pharynx Mouth Esophagus Liver Stomach Pancreas Gallbladder Duodenum Small Jejunum intestine Ileum Transverse colon Ascending Large colon intestine Descending colon Sigmoid colon Rectum Anus 3 Protection • • • • • • • • Intestinal surfaces - layer of mucus Secretory IgA Muscular walls (peristalsis) Saliva Stomach acid Bile Gut-associated lymphoid tissue (GALT) Commensal or normal flora 4 Normal flora • Numerous species present – Bacteria – Fungi – Protozoa • Oral cavity – more than 550 species of bacteria • Stomach and small intestine – sparsely populated • Large intestine – more than 1011 per gram of contents 5 Diseases • • • • • • • • • • • Tooth and gum infections Mumps Gastritis and ulcers Acute Infectious Diarrhea Acute diarrhea with vomiting Chronic diarrhea Hepatitis Helminthic intestinal infections Liver and intestinal disease Muscle and Neurological Symptoms Liver disease 6 Tooth and gum infections • Dental caries • Periodontal diseases 7 Dental caries • Bacterial infection • Most common infection • Dissolution of solid tooth surface – Carbohydrates are fermented by bacteria and produce acids 8 Dental Caries/Trench mouth • Streptococcus mutans • The most common communicable disease. • Sucrose fermentation is the culprit. • Prevention = good dental hygiene. • Trench mouth – acute necrotizing ulcerative gingivitis • Treponema vincenti • Necrosis, pain chewing , foul odor, fever. 9 The different stages of plaque development, and the degrees of cariogenesis. 10 Fig. 22.3 stages in plaque development and cariogenesis. Vegetable dye staining tablets enables macroscopic detection of plaque, while microscopic detection by SEM reveals a mixed bacterial aggregate. Fig. 22.4 The macroscopic and microscopic appearance of plaque. 11 Features of dental caries. 12 Checkpoint 22.1 Dental caries Periodontal diseases • Periodontitis • Necrotizing ulcerative gingivitis and periodontitis 13 Periodontitis • Communities of different bacterial species • Gingivitus – early infection • Periodontitis – late or more serious infection • Plaque • Caculus 14 Necrotizing ulcerative gingivitis and periodontitis • • • • Community of different bacterial species Severe condition Synergistic At risk - poor hygiene, AIDS patients, diabetes, smoking 15 The stages involved in the formation of periodontitis. Fig. 22.5 Stages in soft-tissue infection, gingivitis, and Peroidontitis. 16 A radiograph of teeth showing calculus, caries, and bone destruction. 17 Fig. 22.6 The nature of calculus. Features of periodontal diseases. 18 Checkpoint 22.2 Periodontal diseases Oral Candidiasis “thrush” • Candida albicans (opportunistic normal flora) • Symptoms: white growths that when scraped off reveal angry red tissue underneath. • Circumstances reduced immunity, antibiotics, pregnancy • Treatment over the counter treatment and prescriptions. 19 Mumps • • • • • • • Viral infection Classic gopherlike swelling of the cheeks Humans are exclusive natural host Parotitis Syncytium Vaccine Complications 20 Mumps • Mumps virus • Respiratory droplets • Symptoms- swelling of parotids and other salivary glands, fever, mild pain. Brain and testes can be involved. • MMR vaccination • 40 years ago, very common, now usually rare 21 The classic swelling of the cheeks or parotitis. Fig. 22.7 The external appearance of swollen parotid glands in Mumps. 22 Paramyxoviruses infect host cells, cause multinucleated cells or syncytia, which enable viruses to pass from an infected cell to noninfected cells. 23 Fig. 22.8 The effects of paramyxoviruses. Features of mumps. 24 Checkpoint 22.3 mumps Gastritis and gastric ulcers • Bacterial infection (Caused by Helicobacter pylori) • Pain and lesions (peptic ulcers) in the abdomen • Common for blood type O individuals • Bacteria neutralizes stomach acid environment • Immune response damages epithelium • Possibly zoonotic 25 Stomach Ulcers - gastritis • Inflammation of the gastric lining. • Survives the acidity with urease changes urea into ammonia to neutralize the acid. • Flagella enable burrowing through stomach lining • Adhesins facilitate attachment to gastric cells • Pain, gastric bleeding. • Rx – antibiotics, possibly an acid blocker (Pepcid, Zantac, Tagamet) 26 An endoscope is used to visualize the lesions caused by Helicobacter pylori, causative agent of peptic ulcers. 27 Fig. 22.9 endoscopy Acute infectious diarrhea • • • • Bacterial infection Common nonbacterial infection HKO antigens Common among population – particular day care centers • Developing countries – serious health effects, fatal • In the U.S., 1/3 due to contaminated food 28 HKO antigens • • • • H = flagellar antigen K= capsular antigen O= cell wall antigen Ex. E. coli O157:H7 29 Bacterial • • • • • • • • Salmonella Shigella Shiga-toxin producing Escherichia coli Non-shiga-toxin E. coli Campylobacter Yersinia Clostridium difficile Vibrio cholerae 30 Salmonella • • • • Contaminated animal products Salmonellosis - mild Typhoid fever – severe Normal flora in animals 31 Shigella • • • • • • Primarily a human parasite Infects the large intestine No perforation of intestine Dysentery Exotoxin (shiga-toxin) Enterotoxin 32 Shigellosis (dysentery) • Shigella species (dysenteriae) Shiga toxins. Goes into intestinal epithelial tissue by phagocytosis, then produces toxins • Fecal to Oral route transmission (only 200 cells needed for infection) • Fever abdominal pain, possible seizures, extreme fluid loss, extreme dehydration resulting in decreased blood pressure and shock. 33 • Poor sanitation, cleanliness, lack of clean drinking water are to blame • Antibiotics/re-hydration therapy 34 Shiga-toxin (E. coli) • O157:H7 • Enterohemorrhagic E. coli (EHEC) • Serious manifestations – hemolytic uremic syndrome, neurologic symptoms • Shiga-toxin gene present on bacteriophage genome • Type III secretion system 35 Non-shiga-toxin (E. coli) • • • • Enterotoxigenic – traveler’s diarrhea Enteroinvasive – no exotoxin Enteropathogenic – similar to EHEC Enteroaggregative – chronic diarrhea 36 Campylobacter • Most common bacterial cause of diarrhea • Related to Guillain-Barre syndrome (GBS) – paralysis 37 Campylobacter jejuni has a unique S-shaped and spiral morphology, and is closely related to H. pylori. Fig. 22.13 Scanning micrograph of Campylobacter jejuni, Showing comma, S, and spiral forms. 38 Yersinia • • • • High degree of abdominal pain Mistaken for appendicitis Infects the small intestine Some can affect the lymphatic system (intracellular) 39 Clostridium difficile • Pseudomembranous colitis or antibiotic associated colitis • Capable of superinfecting the large intestine due to drug treatments • Enterotoxins 40 A mild and more severe case of antibiotic-associated colitis. 41 Fig. 22.14 Antibiotic-associated colitis. Figure 23.9 Pseudomembranous colitis Lesions 42 Vibrio cholerae • • • • • • Cholera Unique O and H antigens Cholera toxin (CT) – A-B toxin Bacteria never enter host cells Heavy lost of fluid “rice-water stool” Untreated cases can be fatal 43 Vibrio cholerae has a unique curved shaped and single polar flagellum. 44 Fig. 22.15 Vibrio cholerae Common nonbacterial • Cryptosporidium • Rotavirus 45 Cryptosporidium • • • • • • Protozoan infection Zoonotic Oocysts Intracellular AIDS patients are at risk Associated with fresh water outbreaks 46 Acid-fast staining enables oocysts to be identified, as they stain red or purple. 47 Fig. 22.17 Acid-fast stain in Cryptosporidium A SEM of Cryptosporidium shows attachment to the intestinal epithelium, prior to intracellular invasion. 48 Fig. 22.16 Scanning electron micrograph of Cryptosporidium Rotavirus • Responsible for most morbidity and mortality from diarrhea • Babies lacking maternal antibodies are at risk • Unique morphological appearance 49 Figure 23.14 Deaths from rotaviral diarrhea are most common in developing countries = 1000 deaths 50 Viral gastroenteritis, Rotavirus Characterized by watery diarrhea, fever, vomiting. Fecal to oral route. Best prevention handwashing. Common in school age children. 51 A feces sample containing Rotavirus, which has a unique “spoked-wheel” appearance. Fig. 22.18 Rotavirus visible in a sample of feces from A child with gastroenteritis. 52 Features of acute diarrhea. 53 Checkpoint 22.5 Acute diarrhea Acute diarrhea with vomiting • Food poisoning - toxin – Staphylococcus aureus – Bacillus cereus – Clostridium perfringens 54 Features of acute diarrhea with vomiting. 55 Checkpoint 22.6 Acute diarrhea with vomiting Chronic diarrhea • • • • Enteroaggregative (EAEC) E. coli Cyclospora cayetanensis Giardia lamblia Entamoeba histolytica 56 The protozoan Giardia is typically transmitted by its cysts, which eventually germinates into the trophozoite and damages the jejunum. Fig. 22.21 The “face” of a Giardia lamblia trophozoite. 57 Giardiasis • Giardia lamblia • Fecal to oral route, 2 weeks after infection severe cramping, explosive diarrhea, foul smelling gas. • Resistant to chlorine, Day care centers, camping • Metronidazole and quinacrine 58 Features of chronic diarrhea. 59 Checkpoint 22.7 Chronic diarrhea. Hepatitis • Viral infection – Hepatitis A – Hepatitis B – Hepatitis C • Inflammation of the liver • Jaundice • Noninfectious conditions can cause hepatitis 60 Hepatitis A virus • • • • • • Low virulence Poor hygiene – fecal-oral Developed countries – adult Developing countries- child Vaccine Similar to Hepatitis E – pregnant women are at risk 61 Hepatitis B virus • • • • • • • High virulence Serum hepatitis Cirrhosis Dane particle S antigen Chronic infection – particularly children Associated with hepatocellular carcinoma 62 Hepatitis C virus • “Silent epidemic” – symptoms not seen for years • Blood contact • Chronic • No vaccine • Liver transplants • Associated with cancer 63 Hepatitis Hepatitis A – Fecal to oral route. Jaundice, fatigue, loss of appetite, vomiting. Body recovers. 2 vaccines. Hepatitis B – Blood and sexual contact. Like A but can cause cancer and liver failure, 6% chronic infection. Vaccine is now routine. Hepatitis C – mostly blood rather than sexual contact. 75-85% of patients will develop chronic liver disease, symptoms appear about 6 months after infection. 64 Helminthic intestinal infections • Various parasites – Small roundworms to large tapeworms • Eosinophilia • Four major life cycles – Definitive host – Intermediate host • Antihelminthic therapy • Intestinal distress • Intestinal distress with migratory symptoms 65 Examples of four basic helminth life and transmission cycles. 66 Fig. 22.26 Four basic helminth life and transmission cycles. Pinworms Enterobius vermicularis – (pin worms) most common worm, 30% of kids and 16 % of adults are infected. Lives in the rectum and exits the anus to deposit eggs. • mebendazole, pyrantel pamoate • Anal itching, (scotch tape) 67 Figure 23.18 Features of tapeworm morphology-overview 68 An example of the unique morphology of tapeworms, which includes a sucker and hooklets, and the extensive length. 69 Fig. 22.27 Tapeworm characteristics. Helminthic Infestations of the Intestinal Tract • Tapeworm Infestations – Signs and symptoms • Usually asymptomatic • Nausea, abdominal pain, weight loss, and diarrhea may occur – Pathogens • Taenia saginata – beef tapeworm • Taenia solium – pork tapeworm • Life cycle divided between a primary and intermediate host 70 © 2012 Pearson Education Inc. Ascariasis • Fecal oral route • Asymptomatic, coughing, bile duct or intestinal obstruction • Good hygiene, mebendazole pyrantel pamoate • Wash fruits and vegetables well!! Contaminated soil • Weird life cycle 71 Migration of some helminths is due to their hook or oral cutting plates which anchors it to the host intestinal villi. 72 Fig. 22.28 Cutting teeth on the mouths Hookworm Necator (hookworm) • Very small worms, continually take blood meals, causing chronic bleeding, anemia, bloody stool, nausea, vomiting, weakness, fatigue • Hookworms are acquired through the feet (skin). • Animals carry hookworm, can transmit, but with good sanitation usually do not. 73 An example of the migratory nature of Strongyloides. Fig. 22.29 A patient with disseminated Strongyloides infection. 74 Examples of some antihelminthic therapeutic agents and their effects. 75 Table 22.1 Antihelminthic therapeutic agents and their effects. Features of intestinal distress. 76 Checkpoint 22.9 Intestinal distress. Features of intestinal distress plus migratory symptoms. 77 Checkpoint 22.10 Intestinal distress plus migratory symptoms. Liver and intestinal disease • Helminth infection • Begins in the intestine and migrates to the liver • Liver flukes • Definitive and intermediate host 78 An example of the sheep live fluke Fasciola hepatica. 79 Fig. 22.30 Fasciola heepatica, the sheep liver fluke Features of liver and intestinal diseases. 80 Checkpoint 22.11 Liver and intestinal disease. Muscle and neurological disease • • • • Protozoan infection Trichinosis Life spent entirely in mammal host Common to the U.S. and Europe – Pork, bear meat 81 Trichinosis Trichenella – (trichina worm) found in pigs, rats, and bears. Acquired through undercooked meat. • The larvae travel through the bloodstream and deposit into any muscle tissue. • Fever, muscle pain, malaise • Autopsies reveal 15% of people have some amount of trichinosis. • Can be severe if many larvae are ingested 82 Features of muscle and neurological symptoms. 83 Checkpoint 22.12 Muscle and neurological symptoms Liver disease • • • • Helminth infection Schistosomiasis Blood flukes Evades host immune system by coating itself with proteins from the host bloodstream • Endemic 84 The life of Schistosoma is complex. 85 Fig. 22.31 Stages in the life cycle of Schistosoma. Features of liver disease caused by blood flukes. 86 Checkpoint 22.13 Liver disease Summary of the diseases in the gastrointestinal tract. Taxomonic organization of microorganisms causing Disease in the GI tract. 87 Infectious Diseases Affecting the Gastrointestinal Tract. 88 Fig. 22.p730 89 A cross section of a tooth showing all the major structures associated with the crown and root. 90 Fig. 22.2 The anatomy of a tooth. Cases of typhoid fever and salmonelloses. Fig. 22.10 Data on the prevalence of typhoid fever and other salmonelloses 91 Infection of the large intestine by Shigella dysenteriae. Fig. 22.11 The appearance of the large intestional mucosa In Shigella dysentery. 92 EAEC E. coli can be identified by its ability to adhere to human cells in aggregates. 93 Fig. 22.19 Enteroaggregative E. coli adhering to epithelial cells. The protozoan Cyclospora can be identified by the acidfast stain, in which large cysts stain pink to red and have a wrinkled outer wall. Fig. 22.20 An acid-fast stain of Cyclospora in a human Fecal sample. 94 Entamoeba histolytica have different cellular forms, which includes a trophozoite that contains a karyosome and hosts cells (rbc) and bacteria, and a mature cyst which undergoes excystment. 95 Fig. 22.22 Cellular forms of Entamoeba hystolytic