Chapter 23 Infectious Diseases Affecting the Gastrointestinal Tract

Gastrointestinal tract Mouth Pharynx Esophagus Stomach Small intestine Large intestine Rectum Anus

Figure 23.1 Major structures of the digestive system Uvula Tongue Teeth Salivary glands Pharynx Mouth Esophagus Liver Stomach Pancreas Gallbladder Transverse colon Duodenum Ascending colon Small intestine Large intestine Jejunum Descending colon Ileum Sigmoid colon Rectum Anus

Protection Intestinal surfaces - layer of mucus Secretory IgA Muscular walls (peristalsis) Saliva Stomach acid Bile Gut-associated lymphoid tissue (GALT) Commensal or normal flora

Normal flora Numerous species present Oral cavity 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

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

Tooth and gum infections Dental caries Periodontal diseases

Dental caries Bacterial infection Most common infection Dissolution of solid tooth surface Carbohydrates are fermented by bacteria and produce acids

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.

The different stages of plaque development, and the degrees of cariogenesis. 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.

Features of dental caries. Checkpoint 22.1 Dental caries

Periodontal diseases Periodontitis Necrotizing ulcerative gingivitis and periodontitis

Periodontitis Communities of different bacterial species Gingivitus – early infection Periodontitis – late or more serious infection Plaque Caculus

Necrotizing ulcerative gingivitis and periodontitis Community of different bacterial species Severe condition Synergistic At risk - poor hygiene, AIDS patients, diabetes, smoking

The stages involved in the formation of periodontitis. Fig. 22.5 Stages in soft-tissue infection, gingivitis, and Peroidontitis.

A radiograph of teeth showing calculus, caries, and bone destruction. Fig. 22.6 The nature of calculus.

Features of periodontal diseases. 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.

Mumps Viral infection Classic gopherlike swelling of the cheeks Humans are exclusive natural host Parotitis Syncytium Vaccine Complications

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

The classic swelling of the cheeks or parotitis. Fig. 22.7 The external appearance of swollen parotid glands in Mumps.

Paramyxoviruses infect host cells, cause multinucleated cells or syncytia, which enable viruses to pass from an infected cell to noninfected cells. Fig. 22.8 The effects of paramyxoviruses.

Features of mumps. 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

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)

An endoscope is used to visualize the lesions caused by Helicobacter pylori, causative agent of peptic ulcers. 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

HKO antigens H = flagellar antigen K= capsular antigen O= cell wall antigen Ex. E. coli O157:H7

Bacterial Salmonella Shigella Shiga-toxin producing Escherichia coli Non-shiga-toxin E. coli Campylobacter Yersinia Clostridium difficile Vibrio cholerae

Salmonella Contaminated animal products Salmonellosis - mild Typhoid fever – severe Normal flora in animals

Shigella Primarily a human parasite Infects the large intestine No perforation of intestine Dysentery Exotoxin (shiga-toxin) Enterotoxin

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.

Poor sanitation, cleanliness, lack of clean drinking water are to blame Antibiotics/re-hydration therapy

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

Non-shiga-toxin (E. coli) Enterotoxigenic – traveler’s diarrhea Enteroinvasive – no exotoxin Enteropathogenic – similar to EHEC Enteroaggregative – chronic diarrhea

Campylobacter Most common bacterial cause of diarrhea Related to Guillain-Barre syndrome (GBS) – paralysis

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.

Yersinia High degree of abdominal pain Mistaken for appendicitis Infects the small intestine Some can affect the lymphatic system (intracellular)

Clostridium difficile Pseudomembranous colitis or antibiotic associated colitis Capable of superinfecting the large intestine due to drug treatments Enterotoxins

A mild and more severe case of antibiotic-associated colitis. Fig. 22.14 Antibiotic-associated colitis.

Figure 23.9 Pseudomembranous colitis Lesions

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

Vibrio cholerae has a unique curved shaped and single polar flagellum. Fig. 22.15 Vibrio cholerae

Common nonbacterial Cryptosporidium Rotavirus

Cryptosporidium Protozoan infection Zoonotic Oocysts Intracellular AIDS patients are at risk Associated with fresh water outbreaks

Acid-fast staining enables oocysts to be identified, as they stain red or purple. Fig. 22.17 Acid-fast stain in Cryptosporidium

A SEM of Cryptosporidium shows attachment to the intestinal epithelium, prior to intracellular invasion. 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

Figure 23.14 Deaths from rotaviral diarrhea are most common in developing countries

Viral gastroenteritis, Rotavirus Characterized by watery diarrhea, fever, vomiting. Fecal to oral route. Best prevention handwashing. Common in school age children.

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.

Features of acute diarrhea. Checkpoint 22.5 Acute diarrhea

Acute diarrhea with vomiting Food poisoning - toxin Staphylococcus aureus Bacillus cereus Clostridium perfringens

Features of acute diarrhea with vomiting. Checkpoint 22.6 Acute diarrhea with vomiting

Chronic diarrhea Enteroaggregative (EAEC) E. coli Cyclospora cayetanensis Giardia lamblia Entamoeba histolytica

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.

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

Features of chronic diarrhea. Checkpoint 22.7 Chronic diarrhea.

Hepatitis Viral infection Inflammation of the liver Jaundice Hepatitis A Hepatitis B Hepatitis C Inflammation of the liver Jaundice Noninfectious conditions can cause hepatitis

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

Hepatitis B virus High virulence Serum hepatitis Cirrhosis Dane particle S antigen Chronic infection – particularly children Associated with hepatocellular carcinoma

Hepatitis C virus “Silent epidemic” – symptoms not seen for years Blood contact Chronic No vaccine Liver transplants Associated with cancer

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.

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

Examples of four basic helminth life and transmission cycles. 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)

Figure 23.18 Features of tapeworm morphology-overview

An example of the unique morphology of tapeworms, which includes a sucker and hooklets, and the extensive length. 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 © 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

Migration of some helminths is due to their hook or oral cutting plates which anchors it to the host intestinal villi. 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.

An example of the migratory nature of Strongyloides. Fig. 22.29 A patient with disseminated Strongyloides infection.

Examples of some antihelminthic therapeutic agents and their effects. Table 22.1 Antihelminthic therapeutic agents and their effects.

Features of intestinal distress. Checkpoint 22.9 Intestinal distress.

Features of intestinal distress plus migratory symptoms. 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

An example of the sheep live fluke Fasciola hepatica. Fig. 22.30 Fasciola heepatica, the sheep liver fluke

Features of liver and intestinal diseases. 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

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

Features of muscle and neurological symptoms. 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

The life of Schistosoma is complex. Fig. 22.31 Stages in the life cycle of Schistosoma.

Features of liver disease caused by blood flukes. Checkpoint 22.13 Liver disease

Summary of the diseases in the gastrointestinal tract. Taxomonic organization of microorganisms causing Disease in the GI tract.

Infectious Diseases Affecting the Gastrointestinal Tract. Fig. 22.p730

A cross section of a tooth showing all the major structures associated with the crown and root. 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

Infection of the large intestine by Shigella dysenteriae. Fig. 22.11 The appearance of the large intestional mucosa In Shigella dysentery.

EAEC E. coli can be identified by its ability to adhere to human cells in aggregates. Fig. 22.19 Enteroaggregative E. coli adhering to epithelial cells.

The protozoan Cyclospora can be identified by the acid-fast 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.

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. Fig. 22.22 Cellular forms of Entamoeba hystolytic