Microbial Diseases of the Digestive System

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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
y y y

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
y y y y y y

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)
y y

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.

DENTAL CARIES (TOOTH DECAY)
lactic acid Saliva(lysozyme) Crevicular fluid

TOOTH DECAY

Figure 25.4

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 Prevotella intermedia.

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 aureus enterotoxin 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
Shigella spp. Gram negative facultative bacilli producing Shiga toxin Shiga toxin causes inflammation and bleeding. Families, daycare facilities

Figures 25.7, 25.8

SHIGELLOSIS (BACILLARY DYSENTERY)
Shigellosis is caused by any of four species of Shigella. Shigella sonnei- 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 ³Shiga toxin)

Shigellosis is diagnosed by isolating and identifying the bacteria from rectal swabs.

Rex Karl S. Teoxon, R.N, M.D

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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

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SIGNS AND SYMPTOMS
Fever abdominal pain diarrhea is watery to bloody with pus tenesmus

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DIAGNOSIS

stool culture

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MANAGEMENT
Oresol Ampicillin Trimethoprim-Sulfamethoxazole, Chloramphenicol, Tetracycline, Ciprofloxacin Flouroquinolones

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SALMONELLOSIS
Salmonella enterica serovars 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 enterica serovars. Symptoms include nausea, abdominal pain, and diarrhea and begin 12±36 hours after eating large numbers of Salmonella.
y

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
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SIGNS AND SYMPTOMS

Rose spot (abdominal rashes), Step ladder fever 40-41 deg, headache, abdominal pain, constipation (adults), mild diarrhea (children)

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Rex Karl S. Teoxon, R.N, M.D

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PATHOPHYSIOLOGY
Oral ingestion Bloodstream Reticuloendothelial system (lymph node, spleen, liver) Bloodstream Gallbladder Peyer¶s patches of SI ulceration necrosis and
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TYPHOID FEVER

1st week
y

step ladder fever (BLOOD) rose spot and fastidial typhoid psychosis (URINE & STOOL) (complications) intestinal bleeding, perforation, peritonitis, encephalitis, (lysis) decreasing S/SX (convalescent)
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2nd week
y y

3rd week
y

4th week
y

5th week
y

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

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CHOLERA
Vibrio cholerae 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 lostshock, collapse and death

Figure 25.11

CHOLERA
Brackish (salty) waterscopepods, algae, aquatic plants and plankton Sensitive to stomach acid Epidemic : y serotype O:1 y Serotype O:1 Eltor/ El Tor y Serotype O:139 y None serotype O:1/ O:139

100 million of bactreia per gram of stool Tx. doxycycline

Figure 25.11

CHOLERA

Vibrio cholerae 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..

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

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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

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MANAGEMENT

IV fluids, Tetracycline, Doxycycline, Erythromycin, Quinolones, Furazolidone and Sulfonamides (children)

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NONCHOLERA VIBRIOS

Usually from contaminated crustaceans or mollusks
y y y

V. cholerae serotypes other than O:1, O:139, and eltor V. parahaemolyticus V. vulnificus

NONCHOLERA VIBRIOS
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.
y y

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

Enterohemorrhagic E. coli, such as E. coli O157:H7
y

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
y

Grow in intestinal tract, producing exotoxin Grow following antibiotic therapy Associated with hospitalized patients and nursing home residents

Clostridium difficile±associated diarrhea
y y

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
A CONDITION EYES THIRST Well, alert normal Drinks N Not thirsty Goes back quickly No signs of dehydration B Restless, irritable sunken Thirsty Drinks eagerly Goes back slowly C Lethargic, unconcsious sunken Drinks poorly Not able to drink Goes back very slowly

SKIN PINCH DECIDE

If pt. has 2 or If pt. has 2 or more signs B (C) more signs C Some Dehydration Severe Dehydration Tx plan B Tx plan C

TREAT

Tx plan A

MUMPSvirus Mumps
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.

MUMPS
RNA, Mumps virus Mumps vaccine - > 1yo MMR ± 15 mos Lifetime Immunity

IP: 12-16 days MOT: Droplet, saliva, fomites
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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

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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.

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

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HEPATITIS
Transmission Causative agent Chronic liver disease? No Yes Yes Yes No Vaccine?

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Fecal-oral Parenteral, STD Parenteral Pareteral, HBV coinfection Fecal-oral

Picornaviridae Hepadnaviridae Filoviridae Deltaviridae Caliciviridae

Inactivated virus Recombinant No HBV vaccine No

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
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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

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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

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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)

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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)

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HBV
Active Immunity (hepavax-B) Passive Immunity (HBIg) Carrier state

IP: 2-5 months MOT: Blood and other body fluids route, percutaneous, perinatal, sexual

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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 tremors or asterixis Stage IV recovery (lifetime carrier) or death
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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

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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

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Rex Karl S. Teoxon, R.N, M.D

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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

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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

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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)
y

Hepatitis D virus (HDV) has a circular strand of RNA and uses HBsAg as a coat.

Hepatitis E
y

Hepatitis E virus (HEV) is spread by the fecal±oral route.

Other Types of Hepatitis
y

There is evidence of the existence of hepatitis types F and G.

VIRAL GASTROENTERITIS

Rotavirus:
y y

3 million cases annually 1-2 day incubation; 1 week illness

Norovirus:
y y

50% of U.S. adults have antibodies 1-2 day incubation; 1-3 day illness

Treated with rehydration

Figure 25.17

MYCOTOXINS produced by some fungi Mycotoxins are
y

Claviceps purpurea

Grows on grains Produces ergot

Toxin restricts blood flow to limbs; causes hallucination

y

Aspergillus flavus

Grows on grains Produces aflatoxin

Toxin causes liver damage; liver cancer

GIARDIASIS
Giardia lamblia 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

ECHINOCOCCUS GRANULOSUS

Figure 12.28

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

Trichinella spiralis 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.

TRICHINOSIS

Figure 25.26

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