Introduction Diseases of the digestive system are the second most common illnesses in the United States.
Microbial Diseases of the Digestive System Transmitted in food and water Fecal-oral cycle can be broken by Proper sewage disposal Disinfection of drinking water Proper food preparation and storage
The Digestive System Figure 25.1
Structure and Function of the Digestive System The gastrointestinal (GI) tract, or alimentary canal, consists of the mouth, pharynx, esophagus, stomach, small intestine, and large intestine. In the GI tract, with mechanical and chemical help from the accessory structures, large food molecules are broken down into smaller molecules that can be transported by blood or lymph to cells. Feces, the solids resulting from digestion, are eliminated through the anus.
Normal Microbiota >700 species in mouth Large numbers in large intestine, including Bacteroides E. coli Enterobacter Klebsiella Lactobacillus Proteus
Normal Microbiota of the Digestive System Large numbers of bacteria colonize the mouth. The stomach and small intestine have few resident microorganisms. Bacteria in the large intestine assist in degrading food and synthesizing vitamins. Up to 40% of fecal mass is microbial cells.
protective Waldeyer’s ring Mucus lining and high acid (stomach) Paneth cells (small intestine) Phagocyte Release defensin and lysozymes Normal miocrobiota (large intestine)
Dental Caries Figure 25.3
Dental Caries (Tooth Decay) Dental caries begin when tooth enamel and dentin are eroded and the pulp is exposed to bacterial infection. Streptococcus mutans-uses sucrose to form dextran from glucose and lactic acid from fructose. Bacteria adhere to teeth and produce sticky dextran, forming dental plaque. Acid produced during carbohydrate fermentation destroys tooth enamel at the site of the plaque.
Dental Caries (Tooth Decay) Gram-positive rods and filamentous bacteria ( Actinomycosis ) can penetrate into dentin and pulp. Carbohydrates such as starch, mannitol, sorbitol, and xylitol are not used by cariogenic bacteria to produce dextran and do not promote tooth decay. Caries are prevented by restricting the ingestion of sucrose and by the physical removal of plaque.
Periodontal Disease Caries of the cementum and gingivitis are caused by streptococci, actinomycetes, and anaerobic gram-negative bacteria. Chronic gum disease (periodontitis) can cause bone destruction and tooth loss; periodontitis is due to an inflammatory response to a variety of bacteria growing on the gums. Acute necrotizing ulcerative gingivitis is often caused by Prevotellaintermedia.
Periodontal Disease Figure 25.5
Bacterial Diseases of the Lower Digestive System A gastrointestinal infection is caused by the growth of a pathogen in the intestines. Incubation times range from 12 hours to 2 weeks. Symptoms of infection generally include a fever.
Bacterial Diseases of the Lower Digestive System A bacterial intoxication results from the ingestion of preformed bacterial toxins. Symptoms appear 1–48 hours after ingestion of the toxin. Fever is not usually a symptom of intoxication. Infections and intoxications cause diarrhea, dysentery, or gastroenteritis. These conditions are usually treated with fluid and electrolyte replacement.
Staphylococcal Food Poisoning Staphylococcus aureusenterotoxin is a superantigen. Figure 25.6
Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis) ingestion of an enterotoxin (improperly stored foods) bacteria grow and produce enterotoxin (room temperature) Heat stable, 30 minutes of boiling Temperature abuse Foods with high osmotic pressure and those not cooked immediately before consumption (most common often source)
Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis) Higher osmotic pressure/ low moisture food (cream pies, custard and hams). Refrigeration is important (prevention)
Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis) 1million bacteria/gram of food Diagnosis is based on symptoms. Nausea, vomiting, and diarrhea begin 1–6 hours after eating and last about 24 hours. Laboratory identification of S. aureus isolated from foods is used to trace the source of contamination. Serological tests are available to detect toxins in foods.
Shigellosis (Bacillary Dysentery) Shigellosis is caused by any of four species of Shigella. Shigellasonnei- most cpommon in US, mild dysentery, traveller’s diarrhea Symptoms severe dysentery and prostation blood and mucus in stools, abdominal cramps, and fever. Infections by S. dysenteriae result in ulceration of the intestinal mucosa. With “Shiga toxin) Shigellosis is diagnosed by isolating and identifying the bacteria from rectal swabs.
Rex Karl S. Teoxon, R.N, M.D 24
25 BACILLARY DYSENTERY/SHIGELLOSIS Shiga bacillus: dysenteriae (fatal), flexneri (Philippines), boydii, sonnei; gram (-) Shiga toxin destroys intestinal mucosa Humans are the only hosts Not part of normal intestinal flora IP: 1-7 days MOT : oral fecal route
26 SIGNS AND SYMPTOMS Fever abdominal pain diarrhea is watery to bloody with pus tenesmus
Salmonellosis Salmonella entericaserovars such as S. typhimurium Mortality (<1%) due to septic shock caused by endotoxin Figure 25.9
Salmonellosis (Salmonella Gastroenteritis) Salmonellosis, or Salmonella gastroenteritis, is caused by many Salmonella entericaserovars. Symptoms include nausea, abdominal pain, and diarrhea and begin 12–36 hours after eating large numbers of Salmonella. Septic shock can occur in infants and in the elderly. Fever might be caused by endotoxin.
Salmonellosis (Salmonella Gastroenteritis) Mortality is lower than 1%, and recovery can result in a carrier state. Cooking food will usually kill Salmonella. Laboratory diagnosis is based on isolating and identifying Salmonella from feces and foods.
Salmonellosis and Typhoid Fever Incidence Figure 25.10
Typhoid Fever Salmonella typhi Frequent cause of death in the world with poor sanitation Bacteria is spread throughout body in phagocytes. Lysed and released to the bloodstream incubation period of 2-3 weeks High grade fever 40C and headache Diarrhea and fever decline 2nd or 3rd week Severe cases fatal ulceration and perforation of intestine
Typhoid Fever 1-3% becomes Chronic carrier (gallbladder) 1 to 3% recovered patients become carriers, harboring Salmonella in their gallbladder.
Typhoid Fever Salmonella typhi causes typhoid fever; the bacteria are transmitted by contact with human feces. Fever and malaise occur after a 2-week incubation period. Symptoms last 2–3 weeks. S. typhi is harbored in the gallbladder of carriers. Typhoid fever is treated with quinolones and cephalosporins; vaccines are available for high-risk people.
TYPHOID FEVER Salmonella typhii, gram (-) Carried only by humans Enteric Fever Active Immunization Carrier state – harbor in gallbladders IP: 1-3 weeks MOT: oral fecal route 39
47 DIAGNOSIS Blood culture (typhi dot) 1st week Stool and urine culture 2nd week Widal test (Ab to O and H Ag) - nonspecific Mgmt: Chloramphenicol, Amoxicillin, Sulfonamides, Ciprofloxacin, Ceftriaxone
Cholera Vibriocholerae serotypes that produce cholera toxin. Toxin causes host cells to secrete Cl–, HCO–, and water. SEVERE diarrhea and violent vomiting with severe dehydration, no fever 12-20 liters (3-5gallons) fluid lost- shock, collapse and death Figure 25.11
Cholera Brackish (salty) waters- copepods, algae, aquatic plants and plankton Sensitive to stomach acid Epidemic : serotype O:1 Serotype O:1 Eltor/ El Tor Serotype O:139 None serotype O:1/ O:139 100 million of bactreia per gram of stool Tx. doxycycline `` Figure 25.11
Cholera Vibriocholerae O:1 and O:139 produce an exotoxin that alters the membrane permeability of the intestinal mucosa; the resulting vomiting and diarrhea cause a loss of body fluids. The symptoms last for a few days. Untreated cholera has a 50% mortality rate. Fluid and electrolyte replacement provide effective treatment..
53 CHOLERA Vibrio coma (inaba, ogawa, hikojima), vibrio cholerae, vibrio el tor; gram (-) Choleragen toxin induces active secretion of NaCl Active Immunization IP: few hours to 5 days MOT: oral fecal route
54 SIGNS AND SYMPTOMS Rice watery stool with flecks of mucus (mucus and epithelial cells) s/sx of severe dehydration i.e. Washerwoman’s skin, poor skin turgor Dx: stool culture
55 MANAGEMENT IV fluids, Tetracycline, Doxycycline, Erythromycin, Quinolones, Furazolidone and Sulfonamides (children)
Noncholera Vibrios Usually from contaminated crustaceans or mollusks V. cholerae serotypes other than O:1, O:139, and eltor V. parahaemolyticus V. vulnificus
NoncholeraVibrios Ingestion of other V. cholerae serotypes can result in mild diarrhea. Vibrio gastroenteritis can be caused by V. parahaemolyticus and V. vulnificus. These diseases are contracted by eating contaminated crustaceans or contaminated mollusks.
Escherichia coli Gastroenteritis Occurs as traveler's diarrhea and epidemic diarrhea in nurseries. 50% of feedlot cattle may have enterohemorrhagic strains in their intestines. Enterohemorrhagic strains such as E. coli O157:H7 produce Shiga toxin. O = cell wall antigen H = flagellar antigen
Escherichia coli Gastroenteritis Traveler’s diarrhea may be caused by enterotoxigenic or enteroinvasive strains of E. coli. The disease is usually self-limiting and does not require chemotherapy.
Escherichia coli Gastroenteritis EnterohemorrhagicE. coli, such as E. coli O157:H7 produces Shiga toxins that cause inflammation and bleeding of the colon, including hemorrhagic colitis and hemolytic uremic syndrome. Shiga toxins can affect the kidneys to cause hemolytic uremic syndrome.
Campylobacter Gastroenteritis Campylobacter jejuni Campylobacter is the second most common cause of diarrhea in the United States. Usually transmitted in cow's milk
Helicobacter Peptic Ulcer Disease Treated with antibiotics H. pylori causes stomach cancer Figure 11.12
Helicobacter Peptic Ulcer Disease Helicobacter pylori produces ammonia, which neutralizes stomach acid; the bacteria colonize the stomach mucosa and cause peptic ulcer disease. Bismuth and several antibiotics may be useful in treating peptic ulcer disease.
Helicobacter Peptic Ulcer Disease Figure 25.14
Yersinia Gastroenteritis Y. enterocolitica and Y. pseudotuberculosis Can reproduce at 4°C Usually transmitted in meat and milk
Clostridium Infections Clostridium perfringens Gastroenteritis Grow in intestinal tract, producing exotoxin Clostridium difficile–associated diarrhea Grow following antibiotic therapy Associated with hospitalized patients and nursing home residents
Clostridium Perfringens Gastroenteritis C. perfringens causes a self-limiting gastroenteritis. Endospores survive heating and germinate when foods (usually meats) are stored at room temperature. Exotoxin produced when the bacteria grow in the intestines is responsible for the symptoms. Diagnosis is based on isolation and identification of the bacteria in stool samples.
Clostridium Difficile–Associated Diarrhea Growth of C. difficile following antibiotic therapy can result in mild diarrhea or colitis. The condition is usually associated with hospitalized patients and nursing home residents.
Bacillus cereus Gastroenteritis Ingesting food contaminated with the soil saprophyte Bacillus cereus can result in diarrhea, nausea, and vomiting. Ingestion of bacterial exotoxin produces mild symptoms.
ASSESMENT OF DIARRHOEA
Mumps Mumps virus Enters through respiratory tract Infects parotid glands Prevented with MMR vaccine Figure 25.15
Mumps Mumps virus enters and exits the body through the respiratory tract. About 16–18 days after exposure, the virus causes inflammation of the parotid glands, fever, and pain during swallowing. About 4–7 days later, orchitis may occur.
Mumps After onset of the symptoms, the virus is found in the blood, saliva, and urine. A measles, mumps, rubella (MMR) vaccine is available. Diagnosis is based on symptoms or an ELISA test is performed on viruses cultured in embryonated eggs or cell culture.
94 SIGNS AND SYMPTOMS Unilateral or bilateral parotitis Orchitis - sterility if bilateral Oophoritis Stimulating food cause severe pain aseptic meningitis Dx: serologic testing, ELISA Mgmt: supportive
Hepatitis Inflammation of the liver. Inflammation of the liver is called hepatitis. Symptoms include loss of appetite, malaise, fever, and jaundice Hepatitis may result from drug or chemical toxicity, EB virus, CMV, or the hepatitis viruses.
96 HEPATITIS Hepa A – fecal oral route Hepa B – body fluids Hepa C – non A non B, BT, body fluids Hepa D – hypodermic, body fluids Hepa E – fecal oral route, fatal and common among pregnant women Hepa G – BT, parenteral
Hepatitis A Hepatitis A virus (HAV) causes hepatitis A; at least 50% of all cases are subclinical. HAV is ingested in contaminated food or water, grows in the cells of the intestinal mucosa, and spreads to the liver, kidneys, and spleen in the blood. The virus is eliminated with feces..
Hepatitis A The incubation period is 2–6 weeks; the period of disease is 2–21 days, and recovery is complete in 4–6 weeks. Diagnosis is based on tests for IgM antibodies. A vaccine is available; passive immunization can provide temporary protection.
HEPATITIS A RNA, Hepa A virus Infectious hepa Poor sanitation Worldwide distribution Mortality 1%, with full recovery IP: 3 - 5 weeks MOT: Fecal oral route, food handlers 101
102 SIGNS AND SYMPTOMS Flu like symptoms Diarrhea, fatigue and abdominal pain Loss of appetite Nausea, diarrhea and fever Jaundice and dark colored urine Pale stools Young children are asymptomtic
103 PATHOGENESIS Enters and infects the liver, interlobular infiltration with mononuclear cells Necrosis and hyperplasia of kuffer cells PERIOD OF COMMUNICABILITY – a week before and after the appearance of symptoms
104 DIAGNOSIS Anti HAV IgM – active infection Anti HAV IgG – old infection; no active disease Liver function test Mgmt: supportive Active Immunity (Havrix) Passive Immunity (HAIg)
Hepatitis B ( Hepatitis B virus (HBV) causes hepatitis B, which is frequently serious. HBV is transmitted by blood transfusions, contaminated syringes, saliva, sweat, breast milk, and semen. Blood is tested for HBsAg before being used in transfusions. The average incubation period is 3 months; recovery is usually complete, but some patients develop a chronic infection or become carriers. A vaccine against HBsAg is available.
Hepatitis B Virus Figure 25.16
Hepatitis B ( Hepatitis B virus (HBV) causes hepatitis B, which is frequently serious. HBV is transmitted by blood transfusions, contaminated syringes, saliva, sweat, breast milk, and semen. Blood is tested for HBsAg before being used in transfusions.
HEPATITIS B DNA, Hepa B virus Serum hepa Worldwide distribution Main cause of liver cirrhosis and liver cancer Blood recipients, hemodialysis, IV drug users, sexually active homosexual, tattoing and health care workers (high risk) 109
110 HBV Active Immunity (hepavax-B) Passive Immunity (HBIg) Carrier state IP: 2-5 months MOT: Blood and other body fluids route, percutaneous, perinatal, sexual
111 MANIFESTATIONS Stage I pre-icteric for 1-21 days Anorexia, nausea and vomiting, LBM, weight loss RUQ pain, fatty food intolerance, fever, chills and headache Stage II icteric for 2-6 weeks Jaundice, pruritus, weight gain, ascites, dark-tea colored urine (urobilirubin), S/sx of ADEK deficiency Stage III pre coma NH3 level increases with decreasing LOC, Flapping tremorsor asterixis Stage IV recovery (lifetime carrier) or death
112 DIAGNOSIS Elevated AST or SGPT (specific) and ALT or SGOT Increased IgM during acute phase (+) or REACTIVE HBsAg = INFECTED, may be acute, chronic or carrier (+) HBeAg = highly infectious HBcAg = found only in the liver cells
113 DIAGNOSIS (+) Anti-HBc = acute infection (+) Anti-HBe = reduced infectiousness (+) Anti-HBs = with antibodies (from vaccine or disease) Blood Chem Liver biopsy (to detect progression to CA)
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Rex Karl S. Teoxon, R.N, M.D 115
118 MANAGEMENT Prevention of spread – Immunization and Health Education Enteric and Universal precautions Assess LOC Bed rest ADEK deficiency intervention High CHO, Moderate CHON, Low fat
119 COMPLICATION 1. Fulminant Hepatitis – s/sx of encephalopathy 2. Chronic Hepatitis - lack of complete resolution of clinical sx and persistence of hepatomegaly 3. HBsAg carrier
Hepatitis C Hepatitis C virus (HCV) is transmitted via blood. The incubation period is 2–22 weeks; the disease is usually mild, but some patients develop chronic hepatitis. Blood is tested for HCV antibodies before being used in transfusions.
Hepatitis D (Delta Hepatitis) Hepatitis D virus (HDV) has a circular strand of RNA and uses HBsAg as a coat. Hepatitis E Hepatitis E virus (HEV) is spread by the fecal–oral route. Other Types of Hepatitis There is evidence of the existence of hepatitis types F and G.
Figure 25.17 Viral Gastroenteritis Rotavirus: 3 million cases annually 1-2 day incubation; 1 week illness Norovirus: 50% of U.S. adults have antibodies 1-2 day incubation; 1-3 day illness Treated with rehydration
Mycotoxins Mycotoxins are produced by some fungi Claviceps purpurea Grows on grains Produces ergot Toxin restricts blood flow to limbs; causes hallucination Aspergillus flavus Grows on grains Produces aflatoxin Toxin causes liver damage; liver cancer
Giardiasis Giardialamblia Transmitted by contaminated water Symptoms of giardiasis are malaise, nausea, flatulence, weakness, and abdominal cramps that persist for weeks Diagnosed by microscopic examination of stool for ova and trophozoite Treated with metronidazole Figure 25.18
Cryptosporidiosis Cryptosporidium hominis Transmitted by oocysts in contaminated water Diagnosed by acid-fast staining of stool or presence of antibodies by FA or ELISA Treated with oral rehydration Figure 25.19
Cyclospora Diarrheal Infection Cyclospora cayetanensis Transmitted by oocysts in contaminated water Diagnosed by microscopic examination for oocysts Treated with trimethoprim and sulfamethoxazole
Amoebic Dysentery Entamoeba histolytica Amoeba feeds on RBCs and GI tract tissues Diagnosis by observing trophozoites in feces Treated with metronidazole Figure 12.18b
Helminthic Diseases of the Digestive System Figure 25.21
Tapeworms Taenia spp. Transmitted as cysticerci in undercooked meat Cysticerci may develop in humans Diagnosed by observing proglottids and eggs in feces Treatment with praziquantel Neurocysticercosis may require surgery Figure 12.27
Tapeworms Tapeworms are contracted by the consumption of undercooked beef, pork, or fish containing encysted larvae (cysticerci). The scolex attaches to the intestinal mucosa of humans (the definitive host) and matures into an adult tapeworm. Eggs are shed in the feces and must be ingested by an intermediate host. Adult tapeworms can be undiagnosed in a human.
Tapeworms Figure 25.22
Hydatid Disease Echinococcus granulosus Definitive host: Dogs, wolves Intermediate host: Sheep and other herbivores; humans Transmitted by ingesting E. granulosis eggs Treatment is surgical Figure 25.23
Figure 12.28 Echinococcus granulosus
Pinworms Enterobius vermicularis Definitive host: Humans Transmitted by ingesting Enterobius eggs Treatment with pyrantel pamoate or mebendazole
Pinworms Figure 12.29
Hookworms Larvae in soil hatched from eggs shed in feces Larvae bore through skin; migrate to intestine Treated with mebendazole Figure 12.30
Hookworms Figure 25.24
Ascariasis Ascaris lumbricoides Lives in human intestines Transmitted by ingesting Ascaris eggs Treated with mebendazole Figure 25.25
Trichinosis Trichinella spiralis Larvae encyst in muscles of humans and other mammals Transmitted by ingesting larvae in undercooked meat Treated with mebendazole to kill adults worms Figure 25.26a–b
Trichinellosis Trichinellaspiralis larvae encyst in muscles of humans and other mammals to cause trichinellosis. The roundworm is contracted by ingesting undercooked meat containing larvae. Adult females mature in the intestine and lay eggs; the new larvae migrate to invade muscles.
Trichinellosis Symptoms include fever, swelling around the eyes, and gastrointestinal upset. Biopsy specimens and serological tests are used for diagnosis.