Bio216 Digestive System Infections PDF

CHAPTER 15 – DIGESTIVE SYSTEM INFECTIONS BIO216 – Introduction to Microbiology Dr. Abdel-Samad 15-Digestive System Infections 1 Learning outcomes Describe the func...

CHAPTER 15 – DIGESTIVE SYSTEM INFECTIONS BIO216 – Introduction to Microbiology Dr. Abdel-Samad 15-Digestive System Infections 1 Learning outcomes Describe the functions of the main components of the upper and lower digestive tract. Compare and contrast dental caries, periodontal disease, and acute necrotizing ulcerative gingivitis. Describe Helicobacter pylori gastritis and how it relates to gastric ulcers and stomach cancer. Compare and contrast herpes simplex (cold sores) and mumps. Compare and contrast cholera, shigellosis, E. coli gastroenteritis, and Clostridium difficile infection. Recognize the characteristics of diseases caused by rotaviruses and noroviruses. Understand the transmission and characteristic of the protozoan disease giardiasis. 15-Digestive System Infections 2  Introduction – Digestive System Anatomy and Function Main function: convert food inro a form that the body’s cells can use as a source of energy and raw materials for growth. Two general components: Digestive tract Accessory organs Like the respiratory system, it is one of the body’s major boundaries with environment. But distinct in that it provides plentiful sources for microbial growth. Most microbes live in harmony with host, but this balance is delicate. 15-Digestive System Infections 3 Infectious Diseases of the Upper Digestive System Bacterial diseases Mouth: Dental caries Periodontal disease Acute necrotizing ulcerative gingivitis Stomach: Helicobacter pylori gastritis Viral diseases of the mouth Oral herpes Mumps 15-Digestive System Infections 4 Infectious Diseases of the Lower Digestive System Bacterial diseases of LDS Cholera Shigellosis Escherichia coli gastroenteritis Clostridium difficile infection Salmonella gastroenteritis Enteric fever (typhoid and paratyphoid) Viral diseases of LDS Rotavirus Norovirus Hepatitis Protozoan disease of LDS 15-Digestive System Infections 5 Dental caries Dental caries is a chronic biofilm-mediated disease that damages tooth enamel, often resulting in the development of holes called dental cavities. [Non-communicable] Causative agent: Streptococcus mutans (or related species): live only on teeth (not in mouth) Pathogenicity: They attach to the surface of the tooth and start producing polymer => biofilm Bacteria ferment dietary sugar and produce acid that causes tooth decay Treatment and prevention: Restoration: drilling out cavity then filling defect with resin Control: restrict dietary sucrose and other refined carbohydrates Symptoms: Usually appear after disease (tooth decay) becomes very advanced. Can start as tooth sensitivity or discoloration Severe, throbbing pain of toothache. 15-Digestive System Infections 6 Periodontal disease (1) The periodontal disease is a bacterial disease of the gum. Pathogenicity: Results from plaque accumulation near the gum margin => bacterial products in plaque trigger inflammation => tissue damage Signs and symptoms: tender gums that bleed easily => resolved when plaque removed chronic periodontitis characterized by bad breath, red gums bleeding easily, bone loss (loosened teeth) 15-Digestive System Infections 7 Periodontal disease (2) Causative agent: Typically anaerobic bacteria (different from plaques associated with dental caries) Epidemiology: Can begin in childhood. After 65, 70% of people have it to some degree. Treatment and prevention: Cleaning out inflamed gums, removal of plaque. In advanced cases, minor surgery can be required to expose and clean the roots of the teeth. Careful toothbrushing, flossing, regular polishing or removal of tartar reduce the incidence of periodontal disease. 15-Digestive System Infections 8 Acute necrotizing ulcerative gingivitis (ANUG) ANUG is a more severe bacterial infection of the gum. Pathogenicity: Spirochetes (and other anaerobes) invade tissue and cause necrosis and ulcerations. Epidemiology: First called “trench mouth” (common among WW1 soldiers). Since 2005, dramatic increase in cases associated with methamphetamine use => “meth mouth”. Signs and symptoms: bleeding, painful gums often ulcerated, and sometimes necrotic lesions. Some patients also have extremely bad breath and report an unpleasant metallic taste. Fever, malaise, and swollen lymph nodes may be present. Causative agent: Polymicrobial infections (like periodontal disease). Associated with heavy growth of anaerobes at the gum line. Treatment and prevention: Mouthwash of hydrogen peroxide (because most bacteria are anaerobes), pain medication, debridement of necrotic tissue. Antibiotic with systemic symptoms. Daily brushing, flossing, regular professional cleaning. 15-Digestive System Infections 9 Summary: important infections of teeth and gums 15-Digestive System Infections 10 Helicobacter pylori gastritis Causative agent: 15m91armiger Helicobacter pylori is a short, curved, Gram-negative, microaerophilic bacterium with multiple polar flagella. Epidemiology: H. pylori is present in many people, but can cause gastritis (inflammation of the stomach) 35% of adults in the US are infected; up to 80% incidence in people over age 75. In some cases it leads to peptic ulcers (lesions in the lining of the stomach or duodenum) Chronic gastritis leads to stomach cancer in a small number of people. Symptoms: Typically asymptomatic, but can cause belching (burping), bloating, loss of appetite, nausea, vomiting. In case of peptic ulcers => abdominal pain, tenderness, bleeding (detected in stool) Treatment: x Helicobacter pylori infections can be treated with a combination of antibiotics and a medication that inhibits stomach acid production => clearing of gastritis and healing of ulcers. No proven preventive measure. 15-Digestive System Infections 11 Helicobacter pylori pathogenesis 1. Producing urease that neutralizes acidity in microenvironment 2. Burrowing within mucus lining of stomach 12 Summary: Helicobacter pylori gastritis 15-Digestive System Infections 13 Viral Diseases of the Upper Digestive Tract Oral Herpes (Cold Sores): caused by Herpes Mumps: caused by a member of the Simplex Viruses (HSVs) (mostly HSV-1) Paramyxoviruses family. The virus multiplies in the epithelium of the Fever, loss of appetite, headache, painful mouth or throat and destroys infected cells. swelling on one or both parotid glands. Some epithelial cells fuse, producing large, Enters the body when virus-containing multinucleated giant cells. droplets of saliva are inhaled, then spreads throughout the body in the bloodstream. The virus can become latent in sensory nerve. Tissues that can be No treatment, no vaccination infected are the parotid glands (salivary), meninges, pancreas, ovaries, or giantee testicles No treatment, but effective vaccine. 14  Bacterial diseases of the lower digestive system Cholera Shigellosis E. coli gastroenteritis Salmonella gastroenteritis Enteric fever (typhoid and paratyphoid) Campylobacteriosis Clostridium difficile infection Diarrheal diseases cause the death of thousands of children around the world each year. In the US and other developed countries, fatalities are much less common, but millions of cases still occur. Diarrheal diseases can be referred to as gastroenteritis. The pathogenesis of diarrheal disease varies according to causative agent. 15-Digestive System Infections 15 Cholera Cholera causes diarrhea so severe that it can be fatal within hours. Last cholera epidemic began in 1961 and continues to this day (in countries where poverty or war disrupt sanitation, water treatment, and access to health care) Causative agent: Vibrio cholera is a curved (name), Gram-negative rod, with a single flagellum. Signs and symptoms: Abrupt symptoms after 12-48 hours: severe watery diarrhea (20L a day!) Severe diarrhea leads to dehydration => shock => organ failure => death Vomiting and muscle cramps (caused by loss of fluid and electrolytes) usually also occur Epidemiology: Most common source of infection is fecally contaminated water. U.S. cases involve international travel. Treatment and prevention: Rapid replacement of fluid and electrolytes. Control requires adequate sanitation and safe water supply. 15-Digestive System Infections 16 Cholera pathogenesis Pathogenesis: Vibrio cholera cells are killed by acid, so a large number needs to be ingested before enough survive passage through stomach. Once in small intestine, surviving bacteria adhere to epithelium, and multiply without causing visible damage. Bacteria produce a diarrhea-inducing enterotoxin called cholera toxin. Cholera toxin is an A-B toxin: B subunit attaches to receptors on epithelial cells, the A subunit continually activate adenylate cyclase, and accumulated cAMP causes the cell to continually secrete chloride, followed by other electrolytes, then by water => severe diarrhea. water Electrolytes leaving 15-Digestive System Infections 17 Cholera summary 15-Digestive System Infections 18 Shigellosis Causative agent: Shigellosis can be caused by four species of Shigella: S. dysenteriae, S. flexneri, S. boydii, S. sonnei. S. dysenteriae (in developing countries) is the most virulent, S. sonnei (US) is the least virulent. Shigella species are Gram-negative rods. Signs and symptoms: Dysentery: bloody, mucoid diarrhea (some species cause watery stool) Other symptoms include headache, vomiting, fever, stiff neck, convulsions, and joint pain. Epidemiology: Human disease, transmitted by fecal-oral route (rapid spread in overcrowded populations). Infectious dose is very small, 10 to 200 cells (unlike cholera, shigella cells are not killed by acid). Treatment and prevention: Clears on its own, but antimicrobial medication useful in severe cases. But many strains have R plasmids that encode resistance to a variety of medications. Controlled by sanitary measures that reduce fecal contamination of food and water supplies. 15-Digestive System Infections 19 Shigella pathogenesis Shigella species invade cells, leading to a strong inflammatory response. To initiate invasion, the bacteria take advantage of M cells, which deliver microbes from the intestinal lumen to macrophages on the other side of the epithelium. Once inside macrophages, Shigella cells escape from the phagosome, multiply in the cytoplasm, and then induce apoptosis (death) in host cell. receptors This releases the bacterial cells, which then attach to specific receptors on the base of intestinal epithelial cells and induce those to take them by endocytosis. Shigella cells produces an “actin tail” that propels them within the cell and sometimes into neighboring cells. Death and sloughing off of patches of epithelium => intense inflammation, patches covered with pus and blood => dysentery. 15-Digestive System Infections 20 tail Shigellosis summary co producedbyecoli 15-Digestive System Infections 21  F coli gramnegative willbePinkRods Escherichia coli gastroenteritis Sepi grampostin purplecircus E. coli strains are intestinal residents of almost all humans and a number of other animals. Most are harmless, but certain strains produce virulence factors to cause intestinal disease. Other strains with different virulence factors cause urinary tract infections, sepsis, meningitis. tract ecolicauseurinary Causative agent: Escherichia coli is a Gram-negative rod (closely related to Shigella species). Signs and symptoms: Depending on infecting strain, watery diarrhea or dysentery. diarreanwith andindicates Epidemiology: watery Also depends on strain, but mostly foodborne: contaminated beef, unpasteurized milk,... Treatment and prevention: Fluid replacement (typically without antibacterial medication because most cases are self-limiting). Prevention measures include handwashing, pasteurizing juices, cooking food thoroughly. causes fluidloss dangerous severe anydiseasethat 15-Digestive System Infections 22 Escherichia coli pathogenesis different mechanisms of pathogenicity that different E coli mayhave Depending on the strain: Alterations in the host cell villi Toxin production myp Enterotoxins Cytotoxins ateimnetht eu Cell invasion diarreah perasing microvillidisappear pedestal hidefromtheimmunesystem 15-Digestive System Infections 23 damage tocellsexplainswhysee bloodismucous Escherichia coli gastroenteritis summary 15-Digestive System Infections 24 Viral diseases of the lower digestive tract Intestinal tract: Rotavirus gastroenteritis: incubation period of 24 to 48 hours, vomiting and slight fever, followed by profuse, watery diarrhea. Symptoms gone in a week but fluids must be replaced (fatal dehydration). Norovirus gastroenteritis: abrupt onset of nausea, vomiting, watery diarrhea => dehydration. Liver: Different viruses cause different types of hepatitis diseases (A, B, C, D, E) Viruses unrelated but they all damage the liver and cause similar signs and symptoms during acute infections Most noticeable sign is jaundice (yellowing of the skin and the whites ofso the eyes). Patients with any form of hepatitis should avoid alcohol, acetaminophen, and any other chemicals known to damage the liver. 15-Digestive System Infections 25 Protozoan diseases of the lower digestive system Giardiasis Cryptosporidiosis (“Crypto”) Cyclosporiasis Amebiasis 15-Digestive System Infections 26 Giardiasis Many have fecal-oral transmission by contaminated food or water, or for some species by person-to-person contact if poor sanitation. A common infectious protozoan is Giardia lamblia. Signs and symptoms: About 2/3 of exposed individuals develop symptoms. telal oral or not washing hands Symptoms range from mild (indigestion, “gas”, nausea) to severe (vomiting, explosive diarrhea, abdominal cramps, fatigue, and weight loss). Causative agent: severeweightloss Giardia lamblia is a flagellated protozoan shaped liked a pear. PTTaped The parasite exists in two forms: a feeding trophozoite and a dormant cyst. Epidemiology: mina nigidggigooanTm Transmitted by fecal-oral route. Spreads easily because of low.E infectious dose (10 cysts) Treatment and prevention: Treatment not necessary if mid symptoms. Effective antiprotozoan available of required. Filtered water (because not killed by the level of chlorine); or boiling water. to 15-Digestive System Infections 27  Giardiasis pathogenesis slow itthey Cysts are infectious because they are resistant to stomach acid (unlike trophozoites). Once in upper part of intestine, trophozoites emerge from cysts. They use their flagella to move freely in intestinal mucus. Trophozoites interfere with intestine’s ability to absorb nutrients and secrete digestive enzymes. __ The result is bulky feces containing fat, intestinal gas from bacterial fermentation of unabsorbed nutrients, and malnutrition. Trophozoites detach from epithelium. And if transit time long enough, they develop into cysts. Thus, a person who has formed stools is more likely to eliminate cysts in feces, whereas a person with diarrhea is more likely to eliminate trophozoites in feces. Why is an infected person with diarrhea less likely to transmit giardiasis than one who has formed stool? 28 Giardiasis summary 15-Digestive System Infections 29 Review questions Name the body parts that constitutes the upper digestive system and those that constitute the lower digestive system. How do dental caries develop? Compare the periodontal disease to the acute necrotizing ulcerative gingivitis. Describe the pathogenesis of Helicobacter pylori and how it leads to the typical symptoms. By comparing symptoms, how can you differentiate between the disease caused by Herpes Simplex Viruses and that caused by Paramyxoviruses. Describe symptoms and transmission of cholera, and explain the causative agent’s pathogenesis. Compare the pathogenesis of the intestinal pathogens Escherichia coli and Shigella species. Explain how Clostridium difficile infection occurs in patients. Name one protozoan disease and explain its cycle of transmission. 15-Digestive System Infections 30