Medical Helminthology Medical Helminthology

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

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

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

GGeneral characteristic of Flatworms (Phylum Plathelminthes)eneral characteristic of Flatworms (Phylum Plathelminthes) The flatworms consists of 12, 200 species, including classes

of parasitic worms: Trematoda, Cestoda

All flatworms are acoelomate, triploblastic, bilaterally symmetrical; flattened dorsoventrally

They have a definite head at the anterior end

Their bodies are solid: the only internal space consists of the digestive cavity. They have no anus; a single opening to the digestive system serves as both mouth and anus

Wastes probably move out of flatworms mostly by diffusing across the general body surface

The most of flatworm species are hermaphrodites.

General characteristic of Class Trematoda General characteristic of Class Trematoda

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: 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 FLUKESBLOOD FLUKES - - genus genus

SCHISTOSOMASCHISTOSOMA Distribution: Africa, Asia, Middle East, Latin

America. Schistosoma mansoni and Schistosoma

japonicum cause Hepatosplenic Schistosomiasis.

Schistosoma haematobium causes Urinary Schistosomiasis.

Localization: venous vessels of bowel, liver, and bladder.

Morphology: atypical trematodes which the adult female nesting within a specialized groove in the body of the larger male.

BLOOD FLUKESBLOOD FLUKES Infective stage for

human: cercariae.

Definitive host: man.

Intermediate host: snail.

Mode of transmission: penetration of skin by cercarie.

BLOOD FLUKESBLOOD FLUKESClinical manifestations of Hepatosplenic

Shistosomiasis: eosinophilia, polyps in colon, fever, anorexia, weight loss, anemia, portal hypertension; cirrhosis of liver; pruritic 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.

BLOOD FLUKESBLOOD FLUKES

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.

LLUNGUNG FLUKE FLUKE: : PARAGONIMUS PARAGONIMUS

WESTERMANI - an agent of paragonimiasisWESTERMANI - an agent of paragonimiasis

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

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

LLUNGUNG FLUKE FLUKE

Mode of transmission: ingestion of metacercaria 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, dyspnoa, pleuritic chest pain, and pneumonia.

Laboratory diagnosis: eggs in sputum or feces.

Prevention: cooking crabs and crayfish properly.

LLUNGUNG FLUKE FLUKE

BILIARY (LIVER) BILIARY (LIVER) FLUKESFLUKES

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

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

Localization: bile ducts, gallbladder, and pancreas.

CLONORCHIS SINENSISCLONORCHIS SINENSIS

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

CLONORCHIS SINENSISCLONORCHIS SINENSIS Transmission: fecal-oral (ingestion

of contaminated raw, frozen, dried, pickled, and salted fish).

Infective stage: metacercariae. Final hosts: carnivorous mammals

and humans. Intermediate hosts: 1- snail (miracidium, sporocyst,

rediae, cercariae), 2 - fish Cyprinidae genus- the

family that includes carp and goldfish (metacercariae).

CLONORCHIS SINENSISCLONORCHIS SINENSIS 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.

Laboratory diagnosis: immature eggs in feces

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

FASCIOLA HEPATICAFASCIOLA HEPATICA an agent of fascioliasis.

Distribution: endemic in Far East.

Localization: bile ducts, gallbladder, and pancreas.

Morphology: large size (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.

FASCIOLA HEPATICAFASCIOLA HEPATICA Life-cycle: Final host - herbivorous

mammals (horses) and humans.

Intermediate host — the snail Limnea truncatula.

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.

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.

FASCIOLA HEPATICAFASCIOLA HEPATICA

OPISTHORCHIS FELINEUSOPISTHORCHIS FELINEUS small biliary fluke, causing Opisthorchiasis. Distribution: Siberia. 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 roseolla-like testis in the back of the uterus - a diagnostic sign of this worm.

OPISTHORCHIS FELINEUSOPISTHORCHIS FELINEUS Life-cycle: Final host -

carnivorous mammals and humans.

Intermediate hosts: 1) snail Bithynia leachi genus;

2) fish. Transmission: ingestion of

contaminated raw, frozen, dried, pickled, and salted fish, which contains metacercariae.Invasive stage: metacercariae in fish muscles.

Localization: bile ducts, gallbladder, liver.

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.

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 DICROCOELIUM LANCEATUM – – causes Dicrocoeliasiscauses Dicrocoeliasis

Distribution: worldwide. Localization: bile ducts,

gallbladder and liver of mammals (cattle, horses). Very rare in humans.

Morphology: the worms are 1 cm 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 this worm.

DICROCOELIUM LANCEATUMDICROCOELIUM LANCEATUM Life-cycle: Final host - herbivorous mammals

(cattle, horses). Intermediate hosts: 1) the snail of

Zebrina and Helicela genus, 2) ants Fornica genus.

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

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.

Tapeworms (Cestoda)Tapeworms (Cestoda) consist of a rounded head, called

a scolex, and long strobila or chain of proglottids (multiple segments) of varying stages of maturity.

They have no digestive tract of its own at any point in its life cycle.

The scolex has specialized means of attaching to the intestinal wall, namely suckers, hooks, or sucking grooves.

All cestodes have stage of larva and stage of oncosphere in the life cycle.

Taenia soliumTaenia solium The adult form of T. solium causes

taeniasis solium. T. solium larvae cause cysticercosis.

Distribution 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.

Taenia soliumTaenia solium Life cycle Transmittion: fecal-oral Definitive hosts – humans Intermediate hosts - pigs Humans can be infected

by eating raw or undercooked pork containing the larvae cysticercus.

In the small intestine, the larvae attach to the gut wall and take about 3 months to grow into adult worm.

The gravid terminal proglottids detach daily, are passed in the feces.

Taenia saginata causes taeniasis saginata.

Distribution: 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 without hooklets. Its gravid proglottids have 17-35 primary uterine branches. Larva of T.saginata called cysticercus.

Transmittion: fecal-oral Invasive stage: cysticerci

Taenia saginata Life cycle Definitive hosts: humans Intermediate hosts: cattle Humans can be infected by eating raw or undercooked

beef containing larvae. In the small intestine, the larvae attach to the gut wall.

The gravid terminal proglottids detach, are passed in the feces, and are eaten by cattle.

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.

Clinical manifestation of teniasis soleum and teniasis saginata: abdominal pain, nausea, diarrhea, weight loss, infection may by asymptomatic

Diphyllobothrium latum, the fish tapeworm, causes diphyllobothriasis

Distribution: Scandinavia, northern Russia, Japan, Canada, USA.

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 worm is the longest of the tapeworms, measuring up to 13 m.

Larva called plerocercoid.

Diphyllobothrium latum Definitive hosts: humans Intermediate hosts: 1)copepod crustacea 2) freshwater fish Humans infected by eating raw or undercooked

fish containing plerocercoids In the small intestine, the larvae attach to the gut

wall and develop into adult worms. Gravid proglottids release fertilized eggs. The immature eggs must be deposited in fresh water for the life cycle to continue.

Transmittion: fecal-oral Invasive stage: plerocercoid

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 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).

Invasive stage:egg.

Hymenolepis nana

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

Diagnosis can be proved by observing eggs in stool. Prevention consists of good personal hygiene and avoidance of fecal contamination of food and water.

Echinococcus granulosus (dog tapeworm)

is found primarily in shepherds 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 Invasive stage:egg Life cycle. Definitive hosts: dogs. Intermediate hosts: sheep,

humans. 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 to the liver also to the lungs, bones, and brain. The embryos develop into large fluid-filled hydatid cysts

The life cycle is completed when the entails of slaughtered sheep are eaten by dogs.

Diagnosis: made by Clinical manifestations. 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.

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, the USA. 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 faeces.

The disease occurs primarily in hunters and trappers. Within the human liver, the larvae form multiloculated cysts with few protoscoleces. 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.

Parasite:Parasite: Ascaris lumbricoidesDisease:Disease: ascariasisGeographical distribution:Geographical distribution: cosmopolitanMorphology:Morphology: Adult wormsAdult worms are creamy or pink, spindle-shaped, covered by striated cuticle. Adult male about 20 cm in length, posterior end curved ventrally, adult female about 25-40 cm in length, posterior end straight. Eggs are brown, oval, covered by membranes. An external membrane is tuberous.Host: manMode of transmission:Mode of transmission: faecal-oral (alimentary).Infective stage:Infective stage: eggs. Localisation:Localisation: small intestine (adult), liver, lungs, heart (larvae).

Ascaris lumbricoides

Female

Male

Ascaris lumbricoides

Egg

LLife cycle of LLife cycle of Ascaris lumbricoidesAscaris lumbricoides

 1. Immature eggs pass in the feces (200,000 eggs/day).  2. Under favourable environmental conditions (temperature 20-25 C, oxygen, humidity 70-90%) larvae develop inside the eggs in the soil within 24 days (infective stage).  3. Eggs may be ingested through contaminated, water or raw vegetables, hands.  4. Eggs hatch in the small intestine.  5. 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. 6. Within the small intestine, larvae become adult worms. Eggs appear in feces about 2 months after infection.

Clinical manifestation: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 infection are asymptomatic. Laboratory diagnosis:Laboratory diagnosis: microscopic examination of feces (availability of eggs); larvae may be found in sputum. Prophylaxis: washing hands before meals; proper washing of vegetables eaten raw; treatment of patients; health education.

Ascaris lumbricoides

Parasite:Parasite: Enterobius vermicularis Disease:Disease: enterobiasis Geographical distribution:Geographical distribution: cosmopolitan Morphology: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. Host:Host: man. Mode of transmission:Mode of transmission: faecal-oral (alimentary). Infective stage:Infective stage: eggs. Localisation:Localisation: large intestine (caecum).

Enterobius vermicularis

Male

Female

Life cycle of Enterobius vermicularis:Life cycle of Enterobius vermicularis:

1.  The adult pinworms live in the colon approximately 30 days. 2.  After fertilisation female worm migrates from the anus and releases thousands of fertilized eggs on perianal skin. 3. Within 6 hours, eggs develop into larvae and become infectious. 4. 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. Perianal pruritus (itching) is most common symptom. Laboratory diagnosis: the eggs are recovered from perianal skin by using the “Scotch tape” technique and can be microscopically. Prophylaxis: keep sanitary condition, dehelminthization of the population.

Parasite:Parasite: Trichuris trichiura Disease: Disease: trichocephaliasis (whipworm infection) Geographical distribution:Geographical distribution: cosmopolitan Morphology:Morphology: Adult female worms are up to 5,5 cm in length, and male are up to 4 cm. The front end of the body is thread-like extend. The eggs are brown, barrel-shaped with a plug at each end, 20-50 micro;m in size. Host:Host: man. Mode of transmission:Mode of transmission: faecal-oral (alimentary). Infective stage:Infective stage: eggs. Localisation:Localisation: caecum, appendix, first 1/3 part of large intestine.

Trichuris trichiura

EggEgg

Life cycle of Trichuris trichiura:Life cycle of Trichuris trichiura:1. Immature eggs pass in the faeces (2,000 eggs/day).2. Under favourable environmental conditions (temperature 26-28 C, oxygen, humidity 80-90%) larvae develop inside the eggs in the soil within 4 weeks (infective stage).3.Embryonated eggs may be ingested through contaminated, water, raw vegetables and hands.4. Eggs hatch in the small intestine; larvae become adults in few days, then migrate to the large intestine.5. Eggs appear in faeces about 2 months after infection. 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 faeces (availability of eggs). Prophylaxis: washing hands before meals; proper washing of vegetables eaten raw; treatment of patients; health education.

Parasites:Parasites: Ancylostoma duodenale, Necator americanus Disease:Disease: ancylostomiasis Morphology: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. Host:Host: man. Mode of transmission:Mode of transmission: penetration of skin by filariform larva Infective stage:Infective stage: filariform larva.

Buccal capsule of Ancylostoma duodenale

Life cycle of Ancylostoma and Necator:Life cycle of Ancylostoma and Necator:

1. Filariform larvae penetrate the skin, usually of feet or legs in moist soil. 2. They are carried by the blood to the lungs, migrate into the alveoli and up the bronchi and trachea, and then are swallowed. 3. They develop into adults in the small intestine, attaching to the wall with either cutting plates (Necator) or teeth (Ancylostoma). They feed blood. 4. Immature eggs pass in the faeces about 2 months after infection. 5. Under favourable environmental conditions in the soil eggs develop into rhabditiform larva and then into filariform larvae. (infective stage). Clinical manifestation: 1) invasion stage: dermatitis and itching (“ground itch”); 2) migration stage: pneumonia, eosinophilia; 3) intestinal stage: anemia, diarrhea, abdominal pain, nausea. Laboratory diagnosis: microscopic examination of feces (availability of eggs). Blood in the stool is frequent. Prophylaxis: disposing of sewage properly and wearing shoes.

Parasites:Parasites: Strongyloides stercoralis Disease:Disease: strongyloidiasis Geographical distribution:Geographical distribution: cosmopolitan Morphology:Morphology: 1) adults; 2) eggs; 3) rhabditiform larvae; 4) filariform larvae; 5) free-living female and male. Localisation:Localisation: small intestine. Host:Host: man. Mode of transmission:Mode of transmission: penetration of the skin by filariform larva. Infective stage:Infective stage: filariform larva.

Life cycle of Strongyloides stercoralisLife cycle of Strongyloides stercoralis

1.  Filariform larvae penetrate the skin, usually of feet or legs in moist soil. 2.  They migrate to the lungs, enter the alveoli, pass up the bronchi and trachea, and then are swallowed. 3.   Larvae develop into adults in the small intestine and produce eggs. 4.  The eggs form rhabditiform larvae that are passed in the faeces and appear in stool within 4 weeks of infection. 5.   Some rhabditiform larvae form filariform larvae, which penetrate the intestinal wall directly without leaving the host and migrate to the lungs (autoreinfection). 6.  In the soil, the rhabditiform larvae develop into filariform larvae (infective for man). 7.  The rhabditiform larvae molt into free-living males and females.  8.  Female worms lay eggs in the soil. 9. The eggs develop into rhabditiform larvae; rhabditiform larvae form filariform larvae (infective for man).

  7.  The rhabditiform larvae molt into free-living males and females.  8.  Female worms lay eggs in the soil. 9. The eggs develop into rhabditiform larvae; rhabditiform larvae form filariform larvae (infective for man).

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

Laboratory diagnosis: microscopic examination of faeces (availability of rhabditiform larvae).

Prophylaxis: disposing of sewage properly and wearing shoes.

Parasites:Parasites: Trichinella spiralis Disease:Disease: trichinosis Geographical distribution:Geographical distribution: especially Europe, west Africa Morphology:Morphology: 1) The adult female worms are up to 3-4 X 0.6 mm; the adult male worms are up to 1.5 0.04 mm; 2) the incysted larvae (1 mm) is enclosed in a fibrous cyst wall. Localisation:Localisation: small intestine (adult worms) and striated muscles (larvae). Hosts:Hosts: man, pig, rat, bear, fox. Infective stage:Infective stage: larva Mode of transmission:Mode of transmission: alimentary (eating raw or undercooked meat (usually pork), containing larvae.

Larva of Trichinella spiralisLarva of Trichinella spiralis

Life cycle of Trichinella spiralis:Life cycle of Trichinella spiralis:1. The larvae excyst and mature into adults within the small intestine of host.2. Male worms die after fertilization, female worms lay larvae. 3. Larvae are released and distributed via the bloodstream to striated muscles (diaphragm, tongue, m.deltoideus, m.pectoralis, m.intercostalis).4. Larvae encyst in the muscles within fibrous capcule and can remain viable for several years. Clinical manifestation: initially diarrhea, abdominal pain; by 1-2 weeks later – fever, muscle pain, periorbital edema, eosinophilia. 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.

Pork inspection in slaughter houses using a trichinoscope.

Species: Wuchereria bancroftiCommon Name of Disease: FilariasisEndemic Areas: Tropics primarily. 250 million persons are affected, mostly in South Asia and tropical sub-Saharal Africa. Mode of Transmission: bite of mosquitoClinical Findings: Obstruction of lymphatic vessels, causing edema of legs and genitalia (elephantiasis).Diagnosis: Blood smear (microfilariae can be demonstrated).

1.     During a blood meal, an infected female mosquito introduces filarial larvae (third-stage) onto the skin of the human host, where they penetrate into the bite wound. 2.     They develop in adults that reside in the lymphatics. The female measures between 8 and 10 cm in length and 0.2 to 0.3 mm in width, males about 4 cm. Adults produce microfilariae. 3.     The microfilaria has a body length of 250 to 300 m, a width of 7 to 9 |m. Microfilariae first appear in the peripheral blood in 6 months to 1 year after mosquito bite. 4. Microfilariae are taken up in the blood meal of mosquitoes, and within hours of arrival in the mid-gut of an appropriate host, these microfilariae cast their sheaths, penetrate the wall of the gut, and find their way to the muscles of the thorax. In the thorax, over a period of 10 to 14 days, the filariae develop into infective (third-stage) larvae.

Life cycle of Wuchereria bancrofti

Pathogenesis and clinical findings.Pathogenesis and clinical findings. Adult Wuchereria bancrofti reside within lymphatic channels, frequently within dilated vessels of inguinal, epitrochlear, and axillary nodes; within major lymphatics distal to these nodes; and within the lymphatics of the testis, epididymis, and spermatic cord. They cause attack of adenolymphangitis (localized pain, tenderness, swelling, and erythema is the hallmark of lymphatic fillariasis). Adult worms in the lymph nodes cause obstruction of lymphatic vessels, causing edema of the legs and genitalia (elephantiasis). Laboratory diagnosis.Laboratory diagnosis. Blood smears taken from the patient at night reveal the microfilariae. PreventionPrevention involves mosquito control with insecticides and the use of protective clothing, mosquito netting, and repellents.

Wuchereria bancrofti causes elephantiasis

Wuchereria bancrofti causes edema of leg and genitalia

Species:Species: Onchocerca volvulus Common Name of Disease:Common Name of Disease: Onchocerciasis (river blindness)Endemic Areas:Endemic Areas: Africa, Central America. Infection rates are often over 80% in endemic areas. Mode of Transmission:Mode of Transmission: bite of blackfly (genus Simulinum)

Clinical Findings:Clinical Findings: Inflammation occurs in subcutaneous tissue, pruritic papules and nodules form; lesions of the eyes (blindness). DiagnosisDiagnosis:: Skin biopsy.

1.     During a blood meal, an infected female blackflies of the genus Simulinum introduces filarial larvae onto the skin of the human host, where they penetrate into the bite wound. All Simulium species vectors are day-biting insects that rarely enter houses. Their highest biting intensity is near their breeding sites along the rivers. 2.     The larvae migrate into the subcutaneous tissue, where they differentiate into adults, usually within dermal nodules. In Africa adult worms are predominantly found in the dermis and subcutaneous tissues around the pelvis. In heavy infections they are found over many other bony prominences and in deeper sites. In Guatemala and Mexico a greater proportion of adult worms are found in the upper part of the body, especially the head. 3.     After the male and female adult worms copulate, the gravid female produces millions of microfilariae, which tend to concentrate in skin, eyes, and lymph nodes. 4. The female measures between 23 and 50 cm in length and 250 to 450 m in width, males about 30 cm. Adults can live in the dermal nodules approximately 15 years. Humans are the only definitive hosts.

Life cycle of Onchocerca volvulusLife cycle of Onchocerca volvulus

Pathogenesis and clinical findings.Pathogenesis and clinical findings. Inflammation occurs in subcutaneous tissue, and pruritic papules and nodules are formed. Microfilariae migrate through subcutaneous tissue, ultimately concentrating in the eyes. There they cause lesions that can lead to blindness (“river blindness”).

Laboratory diagnosis.Laboratory diagnosis. Biopsy of the affected skin reveals microfilariae.

PreventionPrevention involves control of the blackfly with insecticides. Wear protective clothing. Long pants with socks and shoes are of value against the low-biting vectors in Africa and Venezuela; in Guatemala and Mexico a hat and veil will be necessary to protect against the vector. Insect repellents temporarily reduce fly exposure. The worm load in affected communities can be greatly reduced by providing alternative water supplies and locating houses and villages away from the rivers.

Species:Species: Loa loa Common Name of Disease:Common Name of Disease: Loiasis Endemic Areas:Endemic Areas: Central and West Africa, including Zaire (up to 25% prevalence of infection in the west and north), Northwest Angola, Congo, Gabon, Central African Republic, Cameroun, Nigeria, Chad, and Southwest Sudan; probably also in Equatorial Guinea and Bissau; and perhaps also in Ghana and Uganda.Mode of Transmission:Mode of Transmission: bite of deer fly (genus Chrysops)Clinical Findings:Clinical Findings: Transient, localized, nonerythematous, subcutaneous edema, most commonly in the region of the wrists and forearms and often following trauma (Calabar swellings); adult worm crawling across the conjuctiva of the eye. DiagnosisDiagnosis:: Blood smear taken during the day (microfilariae can be demonstrated).

1.   The fly bites a host, larvae enter through the puncture wound, and males and females develop in the subcutaneous connective tissues. 2. Adult Loa in the subcutaneous connective tissues are thin, transparent worms; the females measure 50 to 70 x 0.5 mm, the males 30 to 35 x 0.3 to 0.4 mm. 3.   Fertilization occurs by 90 days. Microfilariae have been recovered from spinal fluids, urine and sputum, in blood (during day). They appear in the peripheral blood stream in 6 to 12 months. The adult worms are extremely long-lived, surviving for 4 to 17 years. 4. The day-biting female flies pick up the microfilariae of Loa in their blood meal. The ingested microfilariae lose their sheaths, penetrate the gut wall, and migrate to the cells of the fat body, where they molt twice. The infective filariform larvae develop in 10 to 12 days and move to the proboscis. Many larvae (up to 100) can develop in a single fly.

Life cycle of Loa loaLife cycle of Loa loa

Species:Species: Dracunculus medinensis Common Name of Disease:Common Name of Disease: DracunculiasisEndemic Areas:Endemic Areas: Tropical Africa and Asia Mode of Transmission:Mode of Transmission: Ingestion of copepods in water Clinical Findings:Clinical Findings: Inflammation, blistering, and ulceration of the skin; papule itches. DiagnosisDiagnosis:: Clinical (by finding the head of the worm in the skin ulcer).

Life cycle ofLife cycle of Dracunculus medinensisDracunculus medinensis 1.  Humans are infected when tiny crustaceans (copepods) containing infective larvae are swallowed in drinking water. 2. The larvae penetrate the small intestine and enter the abdominal cavity and retroperitoneal space.

3.  After maturation into adults and copulation, the male worms die and the female (meter-long) migrate in the subcutaneous tissues.

4. Approximately one year after infection, the females cause the skin to ulcerate, generally on the distal lower extremity and then release motile larvae into fresh water.

5. Copepods eat the larvae, which molt to form infective larvae. The cycle is completed when these are ingested in the water.

Dracunculus medinensis causes dracunculiasis

Species:Species: Toxocara canis Common Name of Disease:Common Name of Disease: Visceral larva migransEndemic Areas:Endemic Areas: Worldwide Mode of Transmission:Mode of Transmission: Ingestion of eggs Clinical Findings:Clinical Findings: Fever, hepatomegaly, blindness, eosinophilia. DiagnosisDiagnosis:: Clinical and serologic.

Life cycle ofLife cycle of Toxocara canisToxocara canis 1.  The definitive host for Toxocara canis is a dog. 2. The adult T.canis female in the dog’s intestine produces eggs that are passed in the feces and then into the soil. 3. Humans ingest soil containing the eggs, which hatch into larvae in the small intestine. 4.  The larvae migrate to many organs, especially the liver, brain, and eyes. The larvae eventually are encapsulated and die. 5. The life cycle is not completed in humans. Humans are therefore accidental, dead-end hosts.

Life cycle Life cycle of Toxocara of Toxocara caniscanis

SpeciesSpecies Common Common Name of Name of DiseaseDisease

Endemic Endemic AreasAreas

Mode of Mode of Trans-Trans-missionmission

Clinical FindingsClinical Findings DiagnosisDiagnosis

Wuchere-ria bancrofti

Filariasis Tropics primarily

Mosquito bite

Obstruction of lymphatic vessels, causing edema of legs and genitalia (elephantiasis).

Blood smear (microfilariae can be demonstrated)

Onchocer-ca volvulus

Onchocerciasis (river blindness)

Africa, Central America

Blackfly bite

Inflammation of subcutaneous tissue, pruritic papules and nodules form; lesions of the eyes (blindness).

Skin biopsy

Loa loa Loiasis Tropical Africa

Deer fly bite

Transient, localized, nonerythematous, subcutaneous edema (Calabar swellings); adult worm crawling across the conjuctiva of the eye.

Blood smear (microfilariae can be demonstrated)

Dracuncu-lus medinen-sis

Dracunculiasis

Tropical Africa and Asia

Ingestion of copepods in water

Inflammation, blistering, and ulceration of the skin; papule itches.

Clinical (by finding the head of the worm in the skin ulcer)

Toxocara canis

Visceral larva migrans

Woldwide Ingestion of eggs

Fever, hepatomegaly, blindness, eosinophilia.

Clinical and serologic

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