Phylum Platyhelminthes. Class Trematoda. Class Cestoda

Phylum Nemathelmithes. Class Nematoda.

 

Phylum Platyhelminthes. Class Trematoda.

1.     General characteristic of class Trematoda.

2.     Blood Flukes: Schistosoma haematobium, Schistosoma mansoni, Schistosoma japonicum.

3.     Lung Fluke: Paragonimus westermani.

4.     Biliary Flukes: Clonorchis sinensis, Fasciola hepatica, Opisthorchis felineus, Dicrocoelium lanceatum.

According to the way of development parasites are classificated into biohelminthes and geohelminthes.

Geohelminthes develop without intermediate hosts. Soil is the best environment for their egg's development. Humans are infected through dirty fruits and vegetables which contain geohelminthe's eggs (for example, Ascaris lumbricoideus).

Biohelminthes have complete life cycle with intermediate hosts. There are trophycal connections between definitive and intermediate hosts (for example, Taenia solium).

General characteristic of Flatworms (Phylum Plathelminthes).

The flatwotms (phylum Platyhelminthes) consists of some 12, 200 species. These ribbon-shaped, soft-bodied animals are also called because they are flattened dorsoventrally, from top to bottom. Flatworms are among the simplest of bilaterally symmetrical animals, but they have a definite head at the anterior end. Their bodies are solid: the only internal space consists of the digestive cavity. Flatworms are acoelomates. The acoelomates are some bilaterally symmetrical animals that have no body cavity at all other than the digestive system.

Phylum Plathelminthes includes two classes: 1) Class Trematoda; 2) Class Cestoda.

General characteristic of Class Trematoda (Flukes):

1)    Flattened dorsoventrally (leaf-like).

2)    Unsegmented.

3)    Body is covered by cuticle.

4)    Organs of fixation: oral sucker, ventral sucker.

5)    Organs and systems of Flatworms: digestive system, excretory system, nervous system, genital system: Trematodes are hermaphrodites except genus Schistosoma.

6)    The life cycle is passed in two hosts (alternation of hosts) and has sexual and asexual stages.

BLOOD FLUKES: genus SCHISTOSOMA (S.haematobium, S.mansoni, S.japonicum), which are affect population of Asia, Africa, Latin America, and the Middle East. Three species of the Schictosoma cause the disease called schistosomiasis.

Localization:  venous vessels of bowel, liver, bladder.

Schistosoma mansoni causes Hepatosplenic Schistosomiasis.

Schistosoma japonicum  causes Hepatosplenic Shistosomiasis.

Schistosoma haematobium  causes Urinary Schistosomiasis.

Transmission: infection through skin of larvae (cercariae) from snail hosts.

Infective stage: cercariae.

Definitive host: man.

Intermediate host: snail.

Mode of transmission: penetration of skin by cercarie.

Clinical manifestations of Hepatosplenic Shistosomiasis: eosinophilia, granulomatous polyps in colon, fever, anorexia, weight loss, anemia, portal hypertension; dysentery and cirrhosis of liver; prurit skin rash. Eggs go back through portal circulation to liver, causing hepatomegaly, liver tenderness.

Clinical manifestations of Urinary Schistosomiasis: eosinophilia, hematuria, terminal dysuria (pain, difficulty at the end of urination); obstructed urine flow.

Laboratory diagnostics of Hepatosplenic Schistosomiasis: eggs with lateral spine in feces.

Laboratory diagnostics of Urinary Schistosomiasis: eggs with  terminal  spine in urine

Prevention: involves proper disposal of human waste and eradication of the snail host when possible. Swimming in endemic areas should be avoided.

LUNG FLUKE: PARAGONIMUS WESTERMANI – an agent of paragonimiasis.

Distribution: Far East, Central America, Africa, India.

Morphology: an egg-like form of the body, from 7,5 to 16 mm.

Mode of transmission: ingestion of metacercarial cysts in crabs or crayfish.

Final hosts: carnivoirous mammals, pigs, humans.

Intermediate hosts: 1) snail (sporocyst, redia, cercaria); 2) crabs or crayfish (metacercaria).

Infective stage: metacercariae

Clinical disease: a chronic cough with bloody sputum, dyspnea, pleuritic chest pain, pneumonia.

Laboratory diagnosis: eggs in sputum or feces.

Prevention: cooking crabs and crayfish properly.

BILIARY (LIVER) FLUKES:

CLONORCHIS SINENSIS – oriental small biliary (liver) fluke, causes Clonorchiasis.

Distribution: endemic in Far East, China, Japan, Vietnam.

Localization: bile ducts, gallbladder, pancreas.

Morphology: the adult worms are 1 to 2 cm; the eggs are small, brownish.

Transmission: fecal-oral (ingestion of contaminated raw, frozen, dried, pickled, and salted fish, which contain metacercariae).

Infective stage: metacercariae.

Clinical disease: cholecystitis and cholelithiasis, hepatic colic, associated with profound weight loss and diarrhea. An individual fluke may live for 15-30 years in the liver. In humans a heavy infestation of liver flukes may cause cirrhosis of the liver and death. They can lead to adenomatous hyperplasia, which increases the risk for cholangiocarcinoma (carcinoma of bile ductal epithelia).

Final hosts: carnivorous mammals and humans.

Intermediate hosts: First - the snail (miracidium, sporocyst, rediae, cercariae), second - fish Cyprinidae genus- the family that includes carp and goldfish (metacercariae).

Laboratory diagnosis: immature eggs in feces, in fluid from biliary drainage, or duodenal aspirate.

Prevention: adequate cooking of fish and proper disposal of human waste.

FASCIOLA HEPATICA – an agent of fascioliasis. It is a biliary (liver) fluke. Relatively common large fluke.

Distribution: endemic in Far East.

Localization: bile ducts, gallbladder, pancreas.

Morphology: large sizes (3-5 cm) and conical form of the body; possess sucking disks (oral and abdominal) that provide them motion. Multibranched uterus is situated under the abdominal sucking disk. Testis are branched too and situated in the middle part of the body;

Transmission: fecal-oral (ingestion of water, some non-water plants and vegetables, which contain adolescariae).

Invasive stage: adolescariae.

Clinical disease: Parasites obstruct bile ducts and lay eggs within them, leading to cholelithiasis (gallstones). Biliary obstruction can occur, sometimes causing biliary cirrhosis.

Life-cycle: Final host - herbivorous mammals (horses, pigs) and humans. Intermediate host — the snail Limnea truncatula. Eggs are excreted in feces of infected host. Egg hatches and forms a miracidium in water. It penetrates a snail host. In snail, after such stages as sporocyst and redia, free-swimming cercariaes are released to water. Cercariaes lose their tails and are covered by thick membrane and transform into adolescariae. They collect on watercress plants. Adolescariae are ingested by humans (final host), where they transform into juvenile and then — adult fluke.

Diagnosis: immature eggs in feces. An egg has large sizes, thin membrane, yellow color and small cover in one pole.

Prevention: involves not eating wild aquatic vegetables.

OPISTHORCHIS FELINEUS – small biliary fluke, causing Opisthorchiasis.

Distribution: Siberia.

Localization: bile ducts, gallbladder, liver.

Morphology: flat, the length of the body 4-13 mm. In the middle part of the body there is a branched uterus. Behind it there is a round ovary. There is a rosella-like testis in the back of the uterus - a diagnostic sign of the Opisthochis felineus.

Transmission: ingestion of contaminated raw, frozen, dried, pickled, and salted fish, which contains metacercariae.

Invasive stage: metacercariae cysts in fish muscles.

Clinical disease: cholecystitis and cholelithiasis, hepatic colic, cirhosis. Clinical picture is very similar to Clonorhis infection. Infection can lay dormant for several years before presenting clinically.

Life-cycle: Final host - carnivorous mammals and humans. First intermediate host - the snail Bithynia leachi genus, second - fish. Life cycle of Opisthochis felineus is the same as of Clonorshis sinensis.

Diagnosis: immature eggs in feces, in fluid from biliary drainage, or duodenal aspirate. Eggs are 15-30 mcm in sizes, have oval form and yellow color. The outer membrane is thick, and there is a cover in the front of the egg. The internal structure of the egg is microgranular.

Prevention involves not eating undercooked or contaminated raw, frozen, dried, pickled, and salted fish; eradication of snail hosts when possible.

DICROCOELIUM LANCEATUM – causes Dicrocoeliasis.

Distribution: worldwide.

Localization: bile ducts, gallbladder and liver of herbivorous mammals (cattle, horses). Very rare in humans.

Morphology: the worms are 1 centimeter long with lanceolate form of the body;

the intestine (gut) has two nonbranched channels which are situated in the lateral sides of the body. Two round testis are situated in the front of the body - the diagnostic sign of the Dicrocoelium lanceatum.

Transmission: ingestion of plants with the ants, which contain metacercariae.

Invasive stage: metacercariae.

Clinical disease: is similar to fascioliasis.

Life-cycle: Final host - herbivorous mammals (cattle, horses). First intermediate host — the snail of Zebrina and Helicela genus, second intermediate host — ants Fornica genus.

Diagnosis: immature eggs in feces. An egg have oval form, smooth membrane, brown color, a cover is present in the front end.

Prophylactics: eradication of the snails, ants when possible; dehelmithization of cattle.

 

 Phylum Plathelminthes. Class Cestoda (Tapeworms).

1.General characteristics of class Cestoda.

2. Medical importance of cestodes.

Tapeworms (Cestoda) consist of a rounded head, called a scolex, and long strobila or chain of proglottids  (multiple segments) of varying stages of maturity. The scolex has specialized means of attaching to the intestinal wall, namely suckers, hooks, or sucking grooves. The worm grows by adding new proglottids from its germinal center next to the scolex. The oldest proglottids at the distal end are gravid and produce many eggs, which are excreted in the feces and transmitted to various intermediate hosts. Humans usually acquire the infection when undercooked flesh containing the larvae is ingested. In certain instances, eg, cysticercosis and hydatid disease, the eggs are ingested and the resulting larvae cause the disease. All cestodes have stage of larva and stage of oncosphere in the life cycle.

Taenia solium. The adult form of T. solium causes taeniasis solium. T. solium larvae cause cysticercosis. Teniasis and cysticercosis occur worldwide but is endemic in areas of Asia, South America, and eastern Europe.

Morphology. T. solium can be indentified by its scolex with  4 suckers and circle of hooks and by its gravid proglottids, which have 7-12 primary uterine branches. Larva of T.solium called cysticercus. A cysticercus consist of a pea-sized fluid-filled bladder with an invaginated scolex.

T. solium cysticercus.

 

 

 

 

T. solium scolex

Life cycle. Humans are infected by eating raw or undercooked pork containing the larvae (fecal-oral way of transmittion). In the small intestine, the larvae attach to the gut wall and take about 3 months to grow into adult worms measuring up to 5 m. The gravid terminal proglottids detach daily, are passed in the feces, and are accidentally eaten by pigs. A 6-hooked embryo (oncosphere) emerges from each egg in the pig’s intestine. The embryos burrow into a blood vessel and are carried to skeletal muscle. They develop into cysticerci in the muscle, where they remain until eaten by a human. Humans are the definitive hosts, and pigs are the intermediate hosts.

A different and far more dangerous sequence occurs when a person ingests the eggs in food or water that has been fecally contaminated or ingestion of T. solium eggs after  vomiting (in patient with taeniasis). The cysticerci can become large in eye, subcutaneous tissue, brain, lung, heart, and muscle. In the brain, they manifest as a space-occupying lesion. Living cysticerci do not cause inflammation, but when they die they can release substansis that provoke an inflammatory response.

Clinical manifestation of teaniasis solium: abdominal pain, nausea, diarrhea, weight loss, infection may by asymptomatic.

Clinical manifestation of cysticercosis in the brain: headache, meningoencephalitis, vomiting, and seizures; in the eyes: uveitis, retinitis.

Diagnosis of teaniasis solium: gravid proglottids (with 7 - 12 uterine branches) may be found in the stools.

Diagnosis of cysticercosis depends on demonstrating the presence of the larvae of T.solium in tissue by x-ray, or computed tomography scan.

Prevention. Prevention of taeniasis involves cooking pork adequately and preventing pigs from ingesting human feces by disposing of waste properly. Prevention of cysticercosis consists of treatment of patients to prevent autoinfection plus observation of proper hygiene, including hand washing, to prevent contamination of food with the eggs.

Taenia saginata causes taeniasis saginata. Taeniasis saginata occur worldwide but is endemic in areas of Asia, South America, and eastern Europe.

Morphology. T. saginata can be indentified by its scolex with 4 suckers but in contrast to T.solium, no hooklets. Its gravid proglottids have 17-35 primary uterine branches. Larva of T.saginata called cysticercus.

Life cycle. Humans are infected by eating raw or undercooked beef containing larvae (fecal-oral way of transmittion). In the small intestine, the larvae attach to the gut wall and take about 3 months to grow into adult worms measuring up to 10 m. The gravid terminal proglottids detach, are passed in the feces, and are eaten by cattle.  Embryos (oncospheres) emerge from the eggs in the cow’s intestine and burrow into a blood vessel, where they are carried to skeletal muscle. They develop into cysticerci in the muscle. The cycle is completed when the cysticerci are ingested. Humans are the definitive hosts, and cattle the intermediate hosts.

Clinical manifestation of teniasis saginata: abdominal pain, nausea, diarrhea, weight loss, infection may by asymptomatic. In some, proglottids appear in the stools and may even protrude from the anus.

Laboratory diagnosis: gravid proglottids (with 17-35 uterine branches) may be found in the stools.

Prevention. Prevention of taeniasis saginata involves cooking beef adequately and preventing cattle from ingesting human feces by disposing of waste properly.

Diphyllobothrium latum, the fish tapeworm, causes diphyllobothriasis.

The disease is found worldwide but is endemic in areas where eating raw fish is the custon, such as Scandinavia, northern Russia, Japan, Canada, USA (northern Michigan, Minnesota).

Morphology. Diphyllobothrium latum can be indentified by its scolex with 2 elongated sucking grooves by which the worm attaches to the intestinal wall.

The proglottids are wider than they are long, and the gravid uterus is in the form of a rosette.

Adult D.latum is the longest of the tapeworms, measuring up to 13 m. Larva of  D.latum called plerocercoid.

Life cycle. Humans are infected by eating raw or undercooked fish containing larvae (fecal-oral way of transmittion). In the small intestine, the larvae attach to the gut wall and develop into adult worms. Gravid proglottids release fertilized eggs, and the eggs are then passed in the stools. The immature eggs must be deposited in fresh water for the life cycle to continue. The embryos emerge from the eggs and are eaten by tiny copepod crustacea (first intermediate hosts). There, the embryos differentiate and form  procercoid  larvae in the body cavity. When the copepod is eaten by freshwater fish, eg, pike, trout, and perch, the larvae differentiate into plerocercoids in the muscle of the fish (second intermediate host). The cycle is compelled when raw or undercooked fish is eaten by humans (definitive hosts).

Clinical disease: infection by D.latum causes little damage in the small intestine. In some individuals, megaloblastic anemia occurs as a result of vitamin B₁₂ deficiency caused by preferential uptake of the vitamin by the worm. Most patients are asymptomatic, but abdominal discomfort and diarrhea can occur.

Diagnosis depends on finding the typical eggs, oval, yellow-brown eggs with an operculum (lidlike opening) at one end, in the stools.

Prevention. Prevention involves adequate cooking of fish and proper disposal of human feces.

Hymenolepis nana (dwarf tapeworm) is found worldwide, commonly in the tropics.

Morphology. It is only 2-3 cm in length. Scolex has round form and contain suckers and hooks. A neck is very long and thick. Strobila has 200 proglottides. The uterus has an excretory ostium . Eggs are released from it into the feces.

Transmission: fecal-oral (by the ingestion of eggs from contaminated food or water).

Life cycle. H.nana is different from other tapeworms, because its eggs are directly infectious for humans; ie, ingested eggs can develop into adult worms without an intermediate host. Within the duodenum, the eggs hatch and differentiate into cysticercoid larvae and then into adult worms. Gravid proglottids detach, disintegrate, and release fertilized eggs. The eggs either pass in the stool or can reinfect the small intestine (autoinfection). In contrast to infection by other tapeworms, where only one adult worm is present, many H.nana worms (sometimes hundreds) are found.

Clinical disease:  asymptomatic, but diarrhea and abdominal cramps may be present.

Diagnosis can be proved by observing eggs in stool. The characteristic feature of H.nana eggs is the 8-10 polar filaments lying between the membrane of the 6-hooked larva and the outer shell.

Prevention consists of good personal hygiene and avoidance of fecal contamination of food and water.

Echinococcus granulosus (dog tapeworm) is found primarily in shepcherds living in the Mediterranean region, the Middle East, and Australian, USA (western states).

Morphology. Worm is up to 3-5 mm. Scolex has suckers and hooks. A neck is short. Strobila has 3-5 proglottides. Posterior segment (mature) is the largest and contains uterus with the haustrums, genital pore situated in the back of the proglottid.

Transmission: fecal-oral (by the ingestion of eggs from contaminated food or water).

Life cycle. Dogs are the most important definitive hosts. The intermediate hosts are usually sheep. Humans are almost always dead-end intermediate hosts. Worms in the dog’s intestine liberate thousands of eggs, which are ingested by sheep (or humans). The oncosphere embryos emerge in the small intestine and migrate primarily to the liver but also to the lungs, bones, and brain. The embryos develop into large fluid-filled hydatid cysts, the inner germinal layer of which generates many protoscoleces within “brood capsules”. The outer layer of the cyst is thick, fibrous tissue produced by the host. The life cycle is completed when the entails (eg, liver containing hydatid cysts) of slaughtered sheep are eaten by dogs.

 

Clinical manifestations. Many individuals with hydatic cysts are asymptomatic, but liver cysts may cause hepatic dysfunction. Cysts in the lungs can erode into a bronchus, causing bloody sputum, end cerebral cysts can cause headache and focal neurologic sings. If the cysts ruptures spontaneously or during trauma or surgical removal, life-threatening anaphylaxis can occur (the cyst fluid contains parasite antigens, which can sensitize the host).

Diagnosis: made by routine X-ray, observation of eosinophilia, serologic tests.

Prevention of human disease involves not feeding the entrails of slaughtered sheep to dogs.

Echinococcus multilocularis is found in northern Europe, Siberia, Canada (western provinces), the USA (North and South Dakota, Minnesota, and Alaska).

Many of the features of this organism are the same as those of E. granulosus, but the definitive hosts are mainly foxes and the intermediate hosts are various rodents. Humans are infected by accidental ingestion of food contaminated with fox feces. The disease occurs primarily in hunters and trappers. Within the human liver, the larvae form multiloculated cysts with few protoscoleces. No outer fibrous capsule forms, so the cysts continue to proliferate, producing a honeycomb effect of hundreds of small vesicles (without fluid).

The clinical picture usually involves jaundice and weight loss. The prognosis is poor. Surgical removal may be feasible.

         Nematodes (also known as Nemathelmintes) are roundworms with a cylindrical body and a complete digestive tract including mouth and anus. They are unsegmented, pseudocoelomate worms. The body is covered with a noncellular, highly resistant coating called a cuticle, which is molted as they grow.  Nematodes have separate sexes; the female is usually larger than the male. The male typically has a coiled tail. The medically important nematodes can be divided into 2 categories according to their primary location in the human body, namely intestinal and tissue nematodes. 

        Ascaris lumbricoides causes ascariasis. It is distributed worldwide. Morphology: Adult worms are creamy or pink, spindle-shaped, covered by striated cuticle. Adult male about 20 cm in length, posterior end is curved ventrally; adult female about 25-40 cm in length, posterior end is straight. Eggs are brown, oval, covered by membranes. An external membrane is tuberous.

       Mode of transmission: fecal-oral (alimentary). Humans are infected by eating eggs in soil contaminated with human feces. Eggs hatch in the small intestine, and the larvae migrate through the gut wall into the bloodstream and then to the liver, heart, lungs. They enter the alveoli, pass up the bronchi and trachea, and are swallowed. Within the small intestine, larvae become adult worms. Thousands of eggs are laid daily, are passed in the feces, and form embryos in warm, moist soil.

       Clinical manifestation: 1) Migrating larvae may lead to pneumonia, eosinophilia. 2) Adults in the intestine may cause intestinal obstruction, penetration of the intestinal wall, occlusion of the bile duct, the pancreatic duct or the appendix, toxic effects (nausea, vomiting). Most infections are asymptomatic.

      Laboratory diagnosis: microscopic examination of feces (eggs are oval with an irregular surface); larvae may be found in sputum.

      Prophylaxis: washing hands before meals; proper washing of vegetables eaten raw; treatment of patients; proper disposal of feces; health education.

Ancylostoma duodenale and Necator americanus (hookworms) cause ancylostomiasis (hookworm infection). Disease occurs primarily in children and construction workers who are exposed to infected soil.

    Morphology: 1) Adult worms about 1 cm in length; 2) Eggs are translucent, oval with blunt poles, 40-60 micro;m in size; 3) the rhabditiform larva is about 0.25-0.5 micro;m with rhabditiform oesophagus (1/3 body length), pointed tail end; 4) the filariform larva is about 0.6-0.7 micro;m with cylindrical oesophagus (1/4 body length), sharply pointed tail.

     Hosts: humans.

     Mode of transmission: penetration of skin by filariform larva

     Infective stage: filariform larva.

Filariform larvae penetrate the skin, usually of feet or legs after exposure to infected soil. They are carried by the blood to the lungs, migrate into the alveoli and up the bronchi and trachea, and then are swallowed. Larvae develop into adults in the small intestine, attach to the wall with either cutting plates (Necator) or teeth (Ancylostoma). They feed blood. Up to 0.1-0.3 ml per worm can be lost per day. Immature eggs pass in the feces about 2 months after infection. The eggs develop into rhabditiform larva and then into filariform larvae (infective stage) in warm, moist soil.

      Clinical manifestation: 1) invasion stage (the larvae penetrate the skin): dermatitis and itching (“ground itch”); 2) migration stage: pneumonia with eosinophilia; 3) intestinal stage: anemia, diarrhea, abdominal pain, nausea.     

      Laboratory diagnosis: eggs in the stool; blood in the feces is frequent finding.

      Prophylaxis: disposing of sewage properly and wearing shoes.

Strongyloides stercoralis causes strongyloidiasis. It occurs primarily in the tropics, especially in Southeast Asia.

Morphology: 1) adults; 2) eggs; 3) rhabditiform larvae; 4) filariform larvae; 5) free-living female and male.

        Localisation: small intestine.

        Hosts: humans.

        Mode of transmission: penetration of the skin by filariform larva.

        Infective stage: filariform larva.

S.stercoralis has 2 distinct life cycle, one within the human body and the other free-living in the soil. 

1) Within the human body:

Filariform larvae penetrate the skin, usually of feet or legs after exposure to infected soil. They migrate to the lungs, enter the alveoli, pass up the bronchi and trachea, and then are swallowed. Larvae develop into adults in the small intestine and produce eggs. The eggs form rhabditiform larvae that are passed in the feces and appear in stool within 4 weeks of infection. In the soil, the rhabditiform larvae develop into filariform larvae (infective for man). Some rhabditiform larvae form filariform larvae, which penetrate the intestinal wall directly without leaving the host and migrate to the lungs (autoreinfection).

2) Free-living in the soil:

If larvae are passed in the feces and enter warm, moist soil, the rhabditiform larvae moult into free-living males and females. Female worms lay eggs in the soil. The eggs develop into rhabditiform larvae; rhabditiform larvae form filariform larvae (infective for humans).

Clinical manifestation: 1) invasion stage: pruritis (ground itch) at the site of larval penetration of the skin; 2) migration stage: pneumonia with eosinophilia; 3) intestinal stage: diarrhea, abdominal pain.

Laboratory diagnosis:  rhabditiform larvae in the stool.

Prevention: disposing of sewage properly and wearing shoes.

 

 Phylum Nemathelmithes. Class Nematoda.

1.     Trichinella spiralis: morphological peculiarities, distribution, life cycle, transmission, pathogenic significance.

2.     Enterobius vermicularis (pinworm): morphological peculiarities, distribution, life cycle, transmission, pathogenic significance.

3.     Trichuris trichiura (whipworm): morphological peculiarities, distribution, life cycle, transmission, pathogenic significance.

4.     Laboratory diagnostic of ascariasis, enterobiasis, trichuriasis, trichinosis, ancylostomiasis.

5.     Prevention of ascariasis, enterobiasis, trichuriasis, trichinosis, ancylostomiasis.

   Trichinella spiralis causes trichinosis. It occurs worldwide, especially in eastern Europe and west Africa.

Morphology: 1) The adults female worms are up to 3-4 C 0.6 mm; the adult male worms are up to 1.5 C 0.04 mm; 2) the incysted larvae (1 mm) is enclosed in a fibrous cyst wall.

Localisation: small intestine (adult worms) and striated muscles (larvae).

Any mammal (rat, bear, fox) can be infected, but pigs are the most important reservoirs of human disease.

Infective stage for humans: larva.

Mode of transmission: alimentary (eating raw or undercooked meat, usually pork, containing larvae encysted in the muscle).

The larvae excyst and mature into adults within the small intestine of host. Male worms die after fertilization, female worms lay larvae. They are released and distributed via the bloodstream to striated muscles (diaphragm, tongue, m.deltoideus, m.pectoralis, m.intercostalis). Larvae encyst in the muscles within fibrous capsule and can remain viable for several years. Humans are end-stage hosts, because the infected flesh is not consumed by other animals.

      Clinical manifestation: initially diarrhea, abdominal pain followed by 1-2 weeks later by fever, muscle pain, periorbital edema, and eosinophilia. Death, which is rare, is usually due to congestive heart failure or respiratory paralysis.

      Laboratory diagnosis: muscle biopsy reveals larvae within striated muscle; serologic test (become positive 3 weeks after infection).

      Prophylaxis by properly cooking pork and by feeding pigs only cooked garbage; pork inspection in slaughter houses using a trichinoscope.

  Enterobius vermicularis causes enterobiasis. It is distributed worldwide. Morphology: Adult female worms are up to 10 mm in length, and male worms are up to 5 mm. Eggs are transparent and colourless, asymmetrical, with thin and smooth membrane, 40-60 micro;m.

Mode of transmission: fecal-oral (alimentary). Infective stage: eggs. The adult pinworms live in the large intestine approximately 30 days. After fertilization female worm migrates from the anus and releases thousands of fertilized eggs on perianal skin. Within 6 hours, eggs develop into larvae and become infectious. Reinfection can occur if they are carried to the mouth by fingers after scratching of the itching skin.

     Clinical manifestation: Infection is frequent among children under 12 years of age. Perianal pruritus (itching) is most common symptom.

      Laboratory diagnosis: the eggs are recovered from perianal skin by using the “Scotch tape” technigue and can be observed microscopically (eggs are not found in the stools). Seldom adult worms can be found in the stools.

      Prophylaxis: keep sanitary condition, treatment of patients.

Trichuris trichiuria causes trichocephaliasis (whipworm infection). It occurs worldwide, especially in the tropics. Morphology: Adult female worms are up to 5,5 cm in length, and male are up to 4 cm. The anterior end of the body is hairlike. The eggs are brown, barrel-shaped with a plug at each end, 20-50 micro;m in size.

       Mode of transmission: fecal-oral (alimentary). Infective stage: eggs. Eggs hatch in the small intestine; larvae become adults in few days, migrate to the large intestine. Adults mate, and produce thousands of eggs daily. Immature eggs pass in the feces, and form embryos in warm, moist soil.

 Embryonated eggs may be ingested through contaminated water, raw vegetables and hands.

       Pathogenesis and clinical manifestation: Adult worms burrow their hairlike anterior ends into the intestinal mucosa. They feed blood. Trichuris may cause diarrhea, abdominal pain, nausea, acute appendicitis. Most infections are asymptomatic.

       Laboratory diagnosis: microscopic examination of feces (finding the typical eggs).

       Prophylaxis: washing hands before meals; proper washing of vegetables eaten raw; treatment of patients; proper disposal of feces; health education.