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Microbial Diseases of the Digestive System

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.

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 “Shiga toxin)

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

Rex Karl S. Teoxon, R.N, M.D 24

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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

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. 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.

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TYPHOID FEVER Salmonella typhii, gram (-) Carried only by humans Enteric Fever Active Immunization Carrier state – harbor in gallbladders

IP: 1-3 weeksMOT: 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)

Rex Karl S. Teoxon, R.N, M.D 41

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PATHOPHYSIOLOGY

Oral ingestion

Bloodstream

Reticuloendothelial system (lymph node, spleen, liver)

Bloodstream

Gallbladder

Peyer’s patches of SI necrosis and ulceration

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TYPHOID FEVER

1st week step ladder fever (BLOOD)

2nd week rose spot and fastidial typhoid psychosis (URINE & STOOL)

3rd week (complications) intestinal bleeding, perforation,

peritonitis, encephalitis, 4th week

(lysis) decreasing S/SX 5th week

(convalescent)

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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

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 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

 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..

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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 daysMOT: 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)

NONCHOLERA VIBRIOS

Usually from contaminated crustaceans or mollusks 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. 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 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 DIARRHOEAA B C

CONDITION Well, alert Restless, irritable

Lethargic, unconcsious

EYES normal sunken sunken

THIRST Drinks NNot thirsty

ThirstyDrinks eagerly

Drinks poorlyNot able to drink

SKIN PINCH Goes back quickly

Goes back slowly

Goes back very slowly

DECIDE No signs of dehydration

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

If pt. has 2 or more signs CSevere Dehydration

TREAT Tx plan A Tx plan B Tx plan C

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.

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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 bilateralOophoritisStimulating food cause severe painaseptic meningitis

Dx: serologic testing, ELISAMgmt: 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.

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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

Transmission Causative agent Chronic liver disease?

Vaccine?

Hepatitis A Fecal-oral Picornaviridae No Inactivated virus

Hepatitis B Parenteral, STD

Hepadnaviridae Yes Recombinant

Hepatitis C Parenteral Filoviridae Yes No

Hepatitis D Pareteral, HBV coinfection

Deltaviridae Yes HBV vaccine

Hepatitis E Fecal-oral Caliciviridae No No

HEPATITIS

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.

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HEPATITIS A RNA, Hepa A virus Infectious hepa Poor sanitation Worldwide distribution Mortality 1%, with full recovery

IP: 3 - 5 weeksMOT: 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 infectionAnti HAV IgG – old infection; no active diseaseLiver 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.

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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 daysAnorexia, nausea and vomiting, LBM, weight loss RUQ pain, fatty food intolerance, fever, chills and headache

Stage II icteric for 2-6 weeksJaundice, pruritus, weight gain, ascites, dark-tea colored urine (urobilirubin), S/sx of ADEK deficiency

Stage III pre comaNH3 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)

Rex Karl S. Teoxon, R.N, M.D 114

Rex Karl S. Teoxon, R.N, M.D 115

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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 encephalopathy2. 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 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 surgeryFigure 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 

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