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Invisible InvadersInvisible InvadersInvisible InvadersInvisible InvadersAmazing AlliesAmazing AlliesAmazing AlliesAmazing Allies

Chapter 25 Microbial Diseases of the Digestive System

• Microbial diseases are transmitted via the fecal-oral cycle– disease results from ingesting food or water

contaminated with pathogens– Pathogens enter food or water via fecal matterPathogens enter food or water via fecal matter

• Sanitation disrupts this cycle• Need for new tests that reliably detect pathogens in

food• CDC estimates – 76 million cases of foodborne

disease resulting in 5000 deaths annually in the USdisease resulting in 5000 deaths annually in the US• As more of our fruits and vegetables are grown in

countries where sanitation is poor, an increase in foodborne disease is expected.

Structure and Function of the Digestive System

Learning Objective

Name the structures of the digestive system that contact food.

Structure and Function of the Digestive System

• Gastrointestinal (GI) tract or alimentary canal

M th– Mouth– Pharynx (throat)– Esophagus– Stomach– Small and large intestine

• Accessory structuresy– Teeth and tongue– Salivary glands– Liver– Gallbladder– Pancreas

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Parotid (salivary)gland Pharynx

Oral cavityTongueTeeth

The human digestive system

Esophagus

LiverGallbladder StomachDuodenumPancreas Small intestine

Large intestine

AnusRectum

Structure and Function of the Digestive System

• Main function: breakdown of food into small molecules that are taken up

• Absorption of foods– 25 tons of food pass through the GI tract in a lifetime– Intestinal gas: swallowed N2 and microbial produced H2,

CO2, and CH4

• 80% of the immune system is located in the i t sti l t tintestinal tract

– Gut-associated lymphoid tissue (GALT)• Lymph nodes• Peyer's patches

Normal Microbiota of the Digestive System

Learning Objective

Identify parts of the gastrointestinal tract that normally have microbiota.

Normal Microbiota of the Digestive System• Millions of bacteria per ml of saliva• Few microorganisms in the stomach

– Due to HCl production

• Small intestine also has few bacteria– Rapid movement of food– Paneth cells

• Granule-filled phagocytic cells• Produce defensins and lysozyme

• Large numbers of bacteria in the large intestine– Anaerobes and facultative anaerobes– Assist in enzymatic breakdown of food

• 100 billion (1011) bacteria per gram of feces

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Bacterial Diseases of the Mouth

Learning Objective

Describe the events that lead to dental caries and periodontal disease.

A healthy human tooth

CrownEnamelDentinPulp cavity

Neck

Root

Gingival creviceGum (gingiva)Periodontal ligament

BoneCementumRoot canal

Blood vessels and nerves in pulpcavity

Dental Caries (Tooth Decay)• Dental plaque

– Biofilms involved in the formation of dental caries

• 700 species of bacteria in the oral cavity– Streptococcus mutans is the most important

cariogenic organism• Gram-positive coccus; falcultative anaerobe• Converts sucrose to lactic acid which attacks the tooth

enamelenamel• Produces dextran, a polysaccharide that forms plaque

• Plaques attract other cariogenic bacteria– Mainly, Streptococci; filamentous Actinomyces– But may harbor over 400 bacterial species

Streptococcus mutans

Glucose broth Sucrose broth

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Dental Caries (Tooth Decay)• Caries penetrate from enamel into the

dentin– Caused by gram-positive rods and filamentous – Caused by gram-positive rods and filamentous

bacteria

• Decay can reach pulp, which contains the blood supply and nerve cells– May advance to the soft tissues, leading to

abscessesa c

• Introduction of table sugar in the diet is correlated with the level of dental caries

The stages of tooth decay

EnamelDentinP l

Plaque DecayRoot canal therapy

Healthy tooth withplaque

Decay in enamel

Advanced decay

Decay in dentin

Decay in pulp

PulpBoneRoot

plaque

• Plaque is not permeable to saliva and lactic acid produced is not diluted or neutralized.

• Acid production results in softening of the enamel, which is low in fluoride and is more susceptible to the acid

Periodontal Disease• Gingivitis

– Inflammation and infection of the gums– Half of the adult population has experienced this– Appears in a few weeks if brushing is stopped– Caused by streptococci, actinomycetes, and anaerobic

gram-negative bacteria

• Periodontitis– Bone and tissue supporting the

teeth are destroyedteeth are destroyed– Caused by Porphyromonas

• Acute necrotizing ulcerative gingivitis (trench mouth)– Caused by Prevotella intermedia

The stages of periodontal disease

PlaqueToothGum(gingiva)BoneCementumPeriodontalligament Healthy Gingivitis Periodontal Periodontitis

q

ligament Healthy gingivae

Gingivitis Periodontal pockets

Periodontitis

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Bacterial Diseases of the Lower Digestive System

Learning Objective

List the causative agents, suspect foods, signs and symptoms, and treatments for staphylococcal food poisoning, shigellosis, salmonellosis, typhoid fever, h l st t itis d ti cholera, gastroenteritis, and peptic

ulcer disease.

• Disease of the digestive system are of 2 types– infection– intoxication

• Infection occurs when a pathogen enters the GI d l i litract and multiplies

– grow in the mucosa or penetrate to other organs– GI disturbance is delayed while bacteria multiply; fever

usually occurs• Intoxication is due to ingestion of a toxin

– sudden appearance; no feverpp ; f

• Both types are associated with abdominal cramps, nausea, diarrhea, and vomiting

• Diarrhea and vomiting are designed to rid the body of the harmful substance.

• Dysentery – diarrhea accompanied with blood or mucus

• Gastroenteritis – inflammation of the stomach and intestinal mucosa

• In developing countries, diarrhea is a major factor in infant mortality (1 out of 4 children die)4 children die)

• Disease of the digestive system are often related to food ingestion.

Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis)

• Enterotoxin produced by Staphylococcus aureus– Serological type A

C l t bl d l• Coagulates blood plasma– Toxin is not killed by boiling

• S. aureus inhabits nasal passages• Toxins produced when the organism

is allowed to incubate in food (temperature ( pabuse)– S. aureus outgrows most bacteria in high osmotic

pressure and high temperature (600C for 30 mins)

• Phage typing traces sources of contamination

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Sequence of events in a typical outbreak of staphylococcal food

poisoning

Refrigeration is best preventive methodsmethods

Shigellosis (Bacillary Dysentery)• Infection caused by the genus Shigella

– Facultatively anaerobic; gram-negative; four species– Up to 20 bowel movements in one day– 12 h to 2 weeks incubation time

• Only spread from person to person; no animal reservoir

• Produces the Shiga toxin (inhibits protein synthesis)• Small infectious dose

A h M ll i d d d h ll– Attaches to M cells, invades, and spreads to other cells• Damage to the intestinal wall• Can invade the bloodstream

• CDC estimates 450,000 cases annually; no vaccine yet• Treated with fluoroquinolones and oral rehydration

ShigellosisShigellaM cellEpithelial celllining intestinal tractMembrane ruffle

Shigella enters an epithelial cell.g p

Shigella multiplies inside the cell.

Shigella invades neighboring epithelial g g g pcells, thus avoiding immune defenses.

An abscess forms as epithelial cells arekilled by the infection. The bacteria rarely spread in the bloodstream.

Mucosal abscess

Salmonellosis (SalmonellaGastroenteritis)

• Salmonella enterica– Gram-negative, facultative anaerobe, g , ,

nonendospore-forming rods– Normal inhabitant of the human intestinal tract– 2000 serotypes

• Invades intestinal mucosa and multipliesPasses through M cells and enters the lymphatics– Passes through M cells and enters the lymphatics

– Replicates in macrophages

• Incubation of 12 to 36 hours; fever, nausea, pain and cramps, diarrhea

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SalmonellosisSalmonella

Epithelial cell lining the intestinal tract

M cell

Membrane ruffle

Salmonella enters an epithelial cellSalmonella enters an epithelial cell.

Salmonella multiplies within a vesicleinside the cell.

Salmonella multiplies in mucosal cells;h h fl l there the inflammatory response results in

diarrhea. Occasionally, the bacteria cross the epithelial cell membrane and enter the lymphatic system and bloodstream.

Lymph nodeBloodstream

Salmonellosis (Salmonella Gastroenteritis)• 1.4 million cases; shed from feces for 6 months• 400 deaths annually• Associated with commercial chicken and egg • Associated with commercial chicken and egg

production– Hens are susceptible to infection– Bacteria survive in the albumin, which contains

antibacterials such as lysozyme and lactoferrin– Caution for raw egg consumptiongg p– 1 in 20,000 eggs are contaminated

• Bacterial source: intestines of many animals• Diagnosed directly from the stool or by PCR• Treatment with oral rehydration therapy

Typhoid Fever• Caused by Salmonella typhi

– Most virulent serotype of Salmonella– Spread only by human feces

R i th U it d St t t d d t it ti– Rare in the United States today due to sanitation– Globally, 21 million cases annually leading to tens of thousands

of deaths

• Bacteria spread throughout the body in phagocytes– Releases organism into the bloodstream (spleen and liver)

Hi h f h d h i t ti l ll l ti• High fever, headache, intestinal wall ulceration• 1–3% of patients become chronic carriers

– Harbor the organism in the gallbladder (Typhoid Mary)

• Treated with chloramphenicol, quinolones, or cephalosporins

The incidence of salmonellosis and typhoid fever

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Cholera• Caused by Vibrio cholerae

– Slightly curved, gram-negativerod with single polar flagellum

– Associated with salty waters– Produces the cholera toxin

• Toxin causes the host cells to secrete electrolytes and water

• Lysogenic bacteriophage carries the toxin• Causes "rice water stools“ (mucus-epithelial cells)Causes rice water stools (mucus epithelial cells)

• Can lose 12 to 20 liters of fluid per day– Causes shock, collapse, organ failure, and death

• Treatment includes IV fluid replacement

Cholera after Natural Disasters

• Cholera increases when sanitation and sewage disposal systems are g p y mcompromised

• Outbreak in Haiti after earthquake due to deficient septic system at the Nepalese base– Nepalese soldiers were part of the United

Nations peacekeeping force

Cholera after Natural Disasters

• Strategies for disaster preparednessO l h d l– Oral rehydration solutions

• Salt, sugar, and water– Stockpiling vaccines

• The ultimate solutionProper sanitation water storage – Proper sanitation, water storage, handwashing

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Noncholera Vibrios

• 11 other Vibrio species cause disease in humanshumans

• Mostly adapted to salty coastal waters– Vibrio parahaemolyticus

• Found in saltwater estuaries• Common cause of gastroenteritis• Raw oysters and crustaceans are associated with y

outbreaks• Require early antibiotic therapy as these

infections may be life-threatening

Escherichia coli Gastroenteritis• Enteropathogenic E. coli (EPEC)

– Diarrhea in developing countries– Secret effector proteins that are Secret effector proteins that are

translocated into host cells– Causes the host cells to form

pedestals where the bacteria attach• Enteroinvasive E. coli (EIEC)

– Causes Shigella-like dysenterySame pathogenic mechanism as Shigella– Same pathogenic mechanism as Shigella

• Enteroaggregative E. coli (EAEC)– Only in humans– Produce an enterotoxin causing watery diarrhea

• Enterohemorrhagic E. coli (EHEC)– Produces Shiga-like toxin

• Released upon the cell's lysis

– Most outbreaks are due to serotype O157:H7– Cattle are the main reservoir and unaffected– Ingested food and petting zoos– Infective dose is fewer than 100 bacteria– Causes hemorrhagic colitis (inflammation of the

colon with bleeding) and hemolytic uremic syndrome (blood in the urine)syndrome (blood in the urine)

– 5% mortality in children; kidney transplants may be needed

– Diagnosed by the inability to ferment sorbitol and pulsed-field gel electrophoresis

• Enterotoxigenic E. coli (ETEC)– Secretes enterotoxins that cause diarrhea– Often fatal for children under 5– One toxin resembles cholera toxin in

function

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Traveler's Diarrhea

• Most common cause is ETEC• Second most common cause is EAEC• Can also be caused by Salmonella,

Shigella, and Campylobacter• Oral rehydration therapy and bismuth-

containing preparationscontaining preparations

Campylobacter Gastroenteritis• Caused by Campylobacter jejuni

– Gram-negative, microaerophilic, spirally curved

• Leading cause of foodborne illness in US– Common in the intestines of poultry– Contaminates almost all chicken– 60% of cattle excrete organism in feces

and milk– Do not replicate in food

• Fever cramping abdominal pain diarrhea Fever, cramping, abdominal pain, diarrhea, dysentery

• 2 million cases annually in the US• 1 in 1000 cases leads to a neurological disorder

Guillain-Barré syndrome, a temporary paralysis

Helicobacter Peptic Ulcer Disease• Caused by Helicobacter pylori

– Infects 30–50% of the population in the developed worldp

– Grows in the stomach acid by producing urease• Converts urea to alkaline ammonia

– Disrupts stomach mucosa, causing inflammation

• Treated with antimicrobial drugs and bismuth subsalicylatebismuth subsalicylate

• Diagnostic test requires a biopsy, culture, antigen detection in stools, and urea breath test

Helicobacter pylori leads to ulcers in the stomach wall

Mucus l r pr t cts

Helicobacter pylori

Urease produces alkaline ammonia from urea. The ammonia neutralizes hydrochloric acid of stomach. (NH3 + HCl ➝ NH4Cl)

Mucus layer protects stomach from activity of gastric acid (HCl). Mucus

layer

Hydrochloric acidMucus-secretingpith li l ll

Plasma cell

Lymphocyte

NeutrophilBlood capillary(cross section)

Submucosal cells

Connective tissue

epithelial cellslining stomach

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Yersinia Gastroenteritis• Caused by Yersinia enterocolitica and

Yersinia pseudotuberculosis– Gram-negativeGram negative– Inhabits animals; transmitted in meat and

milk– Grows at 4C

• Diarrhea, fever, headache, abdominal painpain– Often misdiagnosed as appendicitis

• Treatment with antibiotics and oral rehydration

Clostridium perfringens Gastroenteritis

• Gram-positive, endospore-forming, obligately anaerobic rodanaerobic rod

• Also causes gas gangrene• Associated with foods containing animal intestinal

contents– Creates low oxygen level when cooked– Endospore germinates and bacterium grows

• Produces an exotoxin• Symptoms are usually mild

– Occur 8 to 12 hours after ingestion

Clostridium difficile–Associated Diarrhea

• Gram-positive, endospore-forming anaerobeI h l f h l h d l• In the stools of many healthy adults

• Causes more deaths than all other intestinal infections combined– Mostly in health care settings

• Life-threatening colitisg– Ulceration and perforation of the intestinal wall

• Precipitated by the extended use of antibiotics– Eliminates competing intestinal bacteria

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Bacillus cereus Gastroenteritis

• Large, gram-positive, endospore forming– Common in soil and vegetation

• Foodborne disease• Spores survive heating

– Germinate and produce toxinsp• Different toxins cause different symptoms

Viral Diseases of the Digestive System

Learning Objectives

List the causative agents, modes of transmission, sites of infection, and symptoms for mumps.

Differentiate hepatitis A, hepatitis B, hepatitis C, hepatitis D, and hepatitis E.

List the causative agents, mode of transmission, and symptoms of viral gastroenteritis.

Mumps

• Virus targets the parotid glands of the digestive system

P i f l lli 16 t 18 d ft – Painful swelling 16 to 18 days after exposure• Transmitted in the saliva and respiratory

secretions– Multiplies in respiratory tract and reaches the

salivary glands via the bloodstream– Portal of entry is the respiratory tracty p y

• May cause orchitis (swelling of testes), meningitis, ovary inflammation, and pancreatitis

• Prevented with the MMR (measles, mumps, rubella) vaccine

A case of mumps

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Hepatitis

• Inflammation of the liver• At least 5 viruses cause hepatitis• May result from drug or chemical

toxicity, Epstein-Barr virus (EBV), cytomegalovirus (CMV), or the hepatitis viruses

Hepatitis A• Hepatitis A virus (HAV)

– Single-stranded RNA; lacks an envelope

• Entry via the oral route; multiplies in • Entry via the oral route; multiplies in the epithelial lining of the intestinal tract– Spreads to the liver, kidneys, and spleen

• Anorexia, malaise, nausea, diarrhea, fever, chills– Later, jaundice and dark urine

Symptoms last 2 to 21 days; low mortality– Symptoms last 2 to 21 days; low mortality

• Detected via IgM anti-HAV• Treated with immune globulin• Inactivated vaccine for prevention

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Hepatitis B• Hepatitis B virus (HBV)

– Double-stranded DNA; enveloped• Transmitted via the blood and bodily fluids• Transmitted via the blood and bodily fluids

– Up to 1 billion viruses per ml of blood– Complete virions (Dane particle)– Spherical particles and filamentous particles

• Lack DNAC t i h titi B f ti (HB A )• Contain hepatitis B surface antigen (HBsAg)

• Health-care workers are at risk• Prevented by a vaccine• Treated with hepatitis B immune globulin (HBIG)

Hepatitis B virus (HBV)

Envelope (HBSAg)

Capsomere Spikes

Assembly of a complete virion is not efficient

Capsomere

DNA

Dane particle(complete HBV)

Spherical particle(envelope particle)

Filamentous particle(tubular envelope particle)

Hepatitis B• Acute hepatitis B

– Often subclinical, patient is unaware– Similar symptoms to hepatitis A; gradual recovery– Fulminant hepatitis in 1% of cases

• Sudden massive liver damage; fatal

• Chronic hepatitis B (HBeAg)– Involves 10% of infected patients, particularly

children– 350 million are chronic carriers– May lead to liver cirrhosis or liver cancer– Presence of HBeAg indicates a vigorously replicating

virus– Treated with interferons and nucleoside analogs

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Hepatitis C• Hepatitis C virus (HCV)

– Single-stranded RNA; enveloped– Often transfusion-transmitted

• Destroys the liver by using genetic variation to evade the immune response

• Kills more in the United States than AIDS• 85% of cases become chronic85% of cases become chronic

– 25% develop liver cirrhosis or cancer

• Treated with peginterferon and ribavirin• No vaccine

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Other Hepatitis Viruses

• Hepatitis D– Acute (coinfection) and chronic – Acute (coinfection) and chronic

(superinfection) forms– Linked to hepatitis B infection

• Hepatitis E (HEV)– Spread by fecal-oral transmission

• Similar to hepatitis A– Endemic in areas with poor sanitation

Hepatitis E

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Viral Gastroenteritis• 90% of acute viral gastroenteritis is caused by:

• Rotavirus– Common in children; low mortality– Fecal-oral transmission– 3 million cases with fewer than 100 deaths– 2 to 3 day incubation; low-grade fever,

diarrhea, vomiting– Prevented with a live oral vaccine

• Norovirus– Caliciviruses– Fecal-oral transmission– Low infectious dose– 18 to 48 hour incubation; diarrhea and vomiting– Detected with PCR and EIA tests

20 million Noravirus cases annually

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Fungal Diseases of the Digestive System

Learning Objective

Identify the causes of ergot poisoning and aflatoxin poisoning.

Fungal Diseases of the Digestive System

• Mycotoxins: toxins produced by fungi th t that cause:– Blood diseases– Nervous system disorders– Kidney damage– Liver damageLiver damage– Cancer

Ergot and Aflatoxin Poisoning

• Ergot poisoning– Mycotoxins produced by y p y

Claviceps purpurea• Occurs in grains• Restricts blood flow (gangrene) and causes

hallucinations

• Aflatoxin poisoningf p g– Mycotoxins produced by Aspergillus flavus

• Likely to be found on peanuts• Causes liver cirrhosis and liver cancer

Protozoan Diseases of the Digestive System

Learning Objective

List the causative agents, modes of transmission, symptoms, and treatments for giardiasis, cryptosporidiosis, and amebic dysentery.

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Giardiasis• Caused by Giardia intestinalis

– Flagellated protozoan– Forms cysts in feces and water;

t h it i th b dtrophozoites in the body– Attaches to the intestinal wall

• Transmitted by contaminated water supply• Prolonged diarrhea, malaise, weight loss, flatulence,

crampsHydrogen sulfide detected in the breath or stools– Hydrogen sulfide detected in the breath or stools

• 7% are healthy carriers in the US that shed cysts• Diagnosed with a string test, ELISA, or fluorescent

antibody test• Treated with metronidazole and nitazoxanide

Trophozoite form of Giardia intestinalis, the flagellated protozoan that causes giardiasis

Mark left byventral sucker

Cryptosporidiosis

• Caused by Cryptosporidium parvum and C. hominis

• Ingested oocysts release sporozoites • Ingested oocysts release sporozoites – Invade the intestinal epithelium

• Cholera-like diarrhea for 10 to 14 days• Transmitted through recreational and drinking

water; fecal-oral route– Resistant to chlorination

• Diagnosed with a fluorescent antibody test or immunoassay tests

• Treatment with nitazoxanide

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Figure 25.17 Cryptosporidiosis.

OocystIntestinalmucosa

Amebic Dysentery (Amebiasis)• Caused by Entamoeba histolytica

– Produces cysts that survive stomach acidTrophozoites produced from cysts in the – Trophozoites produced from cysts in the intestines

• Multiply in the wall of the large intestine

• Feces contain blood and mucus• Can perforate the intestinal wall, causing

abscessesabscesses– Organisms invade the liver

• Detection with latex agglutination and FA tests• Treatment with metronidazole plus iodoquinol

Section of intestinal wall showing a typical flaskshaped ulcer caused by Entamoeba histolytica

Normal mucosa Ulcer

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Helminthic Diseases of the Digestive System

Learning Objective

List the causative agents, modes of transmission, symptoms, and treatments for tapeworms, hydatid disease, pinworms, hookworms, and trichinellosis.

Worldwide prevalence of human infections with selected intestinal helminths

• 2 billion people are infected• Kill 500,000 worldwide yet no control on infection• Often have few symptoms, particulary with light infections• Neglected Tropical Diseases

Tapeworms• Beef tapeworm: Taenia saginata

- seldom causes significant symptoms• Pork tapeworm: Taenia solium; cisticercosis• Fish tapeworm: Diphyllobothrium latum

- CDC warns of infection from sushi- pike, trout, salmon, perch

• Taeniasis: adult tapeworm infects the intestine; benign but host expels eggs in feces

• Cysticercosis: infection in muscle or brain with the larval y fstage by ingesting eggs

• Ophthalmic cysticercosis: larvae lodge in the eye• Neurocysticercosis: larvae develop in the central nervous

system; symptoms similar to epilepsy

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Tapeworms• Three-stage life cycle

– Eggs are excreted in the feces and ingested by animalsanimals

– Eggs hatch into a larval cysticercus that lodges in the muscle

– Human ingests undercooked meat containing cysticerci, which develop into adult tapeworms in the intestine

• Diagnosis with eggs or segments in the • Diagnosis with eggs or segments in the feces

• Treatment with praziquantel and albendazole

Hydatid Disease• Caused by the tapeworm

Echinococcus granulosus• Eggs are ingested and migrate to the liver, lungs, or

b ibrain– Develops a hydatid cyst

• Can grow and hold up to 15 liters of fluid• May rupture, causing anaphylactic shock due to proteinaceous

content of the fluid

• Diagnosis with serological tests, X rays, CT, and MRI• Over 1 million infected globally• One of the most dangerous tapeworms• Affects people who raise sheep or hunt wild animals• Treatment with surgical removal (care must be taken

not to rupture the cyst) or albendazole

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A hydatid cyst formed by Echinococcus granulosus

Cyst

Brain

Left orbit(eye socket)

Pinworms• Enterobius vermicularis

– Tiny nematodeny n m

• Eggs are ingested• Eggs hatch in the duodenum and eventually

migrate to the colon• Mating occurs g• Lays eggs around the anus, causing local itching• Treatment with pyrantel pamoate and

mebendazole

The pinworm, Enterobius vermicularis

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Hookworms

• Caused by the nematodes Necator americanus and Ancylostoma duodenaleAncylostoma duodenale

• Attaches to the intestinal wall and feeds on blood and tissue

• Anemia, lethargic behavior, and craving for peculiar foods (pica) like laundry starch or s il ith t i t p f lsoil with a certain type of clay

• Transmitted from human feces in soil that contact bare skin

• Treatment with mebendazole

L3 is highly motile

Requires:- human feces

with eggs to t th ilenter the soil

- Bare skin- Decrease in

infection due to sanitation and shoes

Hookworm worldwide prevalence

Trichinellosis

• Caused by the roundworm Trichinella spiralis• Encysted larvae are ingested from undercooked

k d h pork and other meats– Digestion removes the cyst wall and the worm matures

into an adult– Adults produce larvae in the intestines that invade

tissues and form new cysts• Fever eye swelling gastrointestinal upset• Fever, eye swelling, gastrointestinal upset• Treatment with albendazole or mebendazole• Death is rare

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Trichinella spiralis larvae within the diaphragm muscle of a pig

Life cycle of Trichinella spiralis, the causative agent of trichinellosisIngested cysts develop into Trichinellaspiralis adults in the pig's intestinal wall.

Garbage, including undercooked or raw pork

Adult worms producelarvae that encyst in thepig's muscles.

Capsule

Section of

Meanwhile, other animals eat infected meat that has been dumped.

Section of encysted T. spiralis

Human eatsundercooked porkcontaining cysts that are infective to humans

T. spiralis adult

are infective to humans or animals that ingest it

Trichinellosis in humans; ingested cysts develop into T. spiralis adults. Adults produce larvae that encyst in muscles.