Parasitologi Pdf
No notes for slide. Cysts are the parasite stage responsible for transmission of balantidiasis. The host most often acquires the cyst through ingestion of contaminated food or water. Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine. The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur. Trophozoites undergo encystation to produce infective cysts.
Some trophozoites invade the wall of the colon and multiply. Some return to lumen and disintegrate. Mature cysts are passed with feces. Geographic Distribution: Worldwide.
Because pigs are an animal reservoir, human infections occur more frequently in areas where pigs are raised. Other potential animal reservoirs include rodents and nonhuman primates. Cysts are the parasite stage responsible for transmission of balantidiasis. The host most often acquires the cyst through ingestion of contaminated food or water. Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine.
The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur. Trophozoites undergo encystation to produce infective cysts. Some trophozoites invade the wall of the colon and multiply. Some return to lumen and disintegrate. Mature cysts are passed with feces. Geographic Distribution: Worldwide.
Because pigs are an animal reservoir, human infections occur more frequently in areas where pigs are raised. Other potential animal reservoirs include rodents and nonhuman primates. Cysts are the parasite stage responsible for transmission of balantidiasis. The host most often acquires the cyst through ingestion of contaminated food or water.
Parasitology Pdf
Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine. The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur.
Trophozoites undergo encystation to produce infective cysts. Some trophozoites invade the wall of the colon and multiply. Some return to lumen and disintegrate. Mature cysts are passed with feces. Geographic Distribution: Worldwide. Because pigs are an animal reservoir, human infections occur more frequently in areas where pigs are raised. Other potential animal reservoirs include rodents and nonhuman primates.
Cysts are passed in feces. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts, which are passed in the feces. Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. (Trophozoites can also be passed in diarrheal stools, but are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.) In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa (: intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations.
It has been established that the invasive and noninvasive forms represent two separate species, respectively E. Histolytica and E. Dispar, however not all persons infected with E. Histolytica will have invasive disease. These two species are morphologically indistinguishable.
Transmission can also occur through fecal exposure during sexual contact (in which case not only cysts, but also trophozoites could prove infective). Geographic Distribution: Worldwide, with higher incidence of amebiasis in developing countries. In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages). The cysts are hardy, can survive several months in cold water.
Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites). In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites).
Trophozoites multiply by longitudinal binary fission remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk. Encystation occurs as the parasites transit toward the colon.
The cyst is the stage found most commonly in non-diarrheal feces. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear. Geographic Distribution: Worldwide, more prevalent in warm climates, and in children. Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, promastigotes, during blood meals. Promastigotes that reach the puncture wound are phagocytized by macrophages and transform into amastigotes.
Amastigotes multiply in infected cells and affect different tissues, depending in part on the Leishmania species. This originates the clinical manifestations of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes (, ). In the sandfly's midgut, the parasites differentiate into promastigotes, which multiply and migrate to the proboscis. Geographic Distribution: Leishmaniasis is found in parts of about 88 countries. Approximately 350 million people live in these areas.
Most of the affected countries are in the tropics and subtropics. The settings in which leishmaniasis is found range from rain forests in Central and South America to deserts in West Asia. More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil. Leishmaniasis is found in Mexico, Central America, and South America - from northern Argentina to southern Texas (not in Uruguay, Chile, or Canada), southern Europe (leishmaniasis is not common in travelers to southern Europe), Asia (not Southeast Asia), the Middle East, and Africa (particularly East and North Africa, with some cases elsewhere). Causal Agents: The term microsporidia is also used as a general nomenclature for the obligate intracellular protozoan parasites belonging to the phylum Microsporidia. To date, more than 1,200 species belonging to 143 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. Microsporidia, are characterized by the production of resistant spores that vary in size, depending on the species.
They possess a unique organelle, the polar tubule or polar filament, which is coiled inside the spore as demonstrated by its ultrastructure. The microsporidia spores of species associated with human infection measure from 1 to 4µm and that is a useful diagnostic feature. There are at least 14 microsporidian species that have been identified as human pathogens: Enterocytozoon bieneusi, Encephalitozoon intestinalis, Encephalitozoon hellem, Encephalitozoon cuniculi, Pleistophora sp., Trachipleistophora hominis, T. Anthropophthera, Nosema ocularum, N. Algerae, Vittaforma corneae, Microsporidium ceylonensis, M. Africanum, Brachiola vesicularum, B. Encephalitozoon intestinalis was previously named Septata intestinalis, but it was reclassified as Encephalitozoon intestinalis based on its similarity at the morphologic, antigenic, and molecular levels to other species of this genus.
Based on recent data it is now known that some domestic and wild animals may be naturally infected with the following microsporidian species: E. Intestinalis, E. Causal Agents: The term microsporidia is also used as a general nomenclature for the obligate intracellular protozoan parasites belonging to the phylum Microsporidia. To date, more than 1,200 species belonging to 143 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. Microsporidia, are characterized by the production of resistant spores that vary in size, depending on the species.
They possess a unique organelle, the polar tubule or polar filament, which is coiled inside the spore as demonstrated by its ultrastructure. The microsporidia spores of species associated with human infection measure from 1 to 4µm and that is a useful diagnostic feature. There are at least 14 microsporidian species that have been identified as human pathogens: Enterocytozoon bieneusi, Encephalitozoon intestinalis, Encephalitozoon hellem, Encephalitozoon cuniculi, Pleistophora sp., Trachipleistophora hominis, T. Anthropophthera, Nosema ocularum, N. Algerae, Vittaforma corneae, Microsporidium ceylonensis, M. Africanum, Brachiola vesicularum, B. Encephalitozoon intestinalis was previously named Septata intestinalis, but it was reclassified as Encephalitozoon intestinalis based on its similarity at the morphologic, antigenic, and molecular levels to other species of this genus.
Based on recent data it is now known that some domestic and wild animals may be naturally infected with the following microsporidian species: E. Intestinalis, E. Life Cycle: The infective form of microsporidia is the resistant spore and it can survive for a long time in the environment. The spore extrudes its polar tubule and infects the host cell.
The spore injects the infective sporoplasm into the eukaryotic host cell through the polar tubule. Inside the cell, the sporoplasm undergoes extensive multiplication either by merogony (binary fission) or schizogony (multiple fission).
This development can occur either in direct contact with the host cell cytoplasm (e.g., E. Bieneusi ) or inside a vacuole termed parasitophorous vacuole (e.g., E. Intestinalis ). Either free in the cytoplasm or inside a parasitophorous vacuole, microsporidia develop by sporogony to mature spores. During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is disrupted and releases the spores to the surroundings.
These free mature spores can infect new cells thus continuing the cycle. Geographic Distribution: Microsporidia are being increasingly recognized as opportunistic infectious agents worldwide. Cases of microsporidiosis have been reported. in developed as well as in developing countries, including: Argentina, Australia, Botswana, Brazil, Canada, Czech Republic, France, Germany, India, Italy, Japan, The Netherlands, New Zealand, Spain, Sri Lanka, Sweden, Switzerland, Thailand, Uganda, United Kingdom, United States of America, and Zambia. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host.
Sporozoites infect liver cells and mature into schizonts, which rupture and release merozoites. (Of note, in P. Ovale a dormant stage hypnozoites can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ).
Merozoites infect red blood cells. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites. Some parasites differentiate into sexual erythrocytic stages (gametocytes). Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal. The parasites’ multiplication in the mosquito is known as the sporogonic cycle.
While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes. The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts. The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. Members of the cat family (Felidae) are the only known definitive hosts for the sexual stages of T. Gondii and thus are the main reservoirs of infection. Cats become infected with T.
Gondii by carnivorism. After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are then excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become infective).
Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes. Human infection may be acquired in several ways: A) ingestion of undercooked infected meat containing Toxoplasma cysts; B) ingestion of the oocyst from fecally contaminated hands or food; C) organ transplantation or blood transfusion; D) transplacental transmission; E) accidental inoculation of tachyzoites. The parasites form tissue cysts, most commonly in skeletal muscle, myocardium, and brain; these cysts may remain throughout the life of the host. Geographic Distribution: Serologic prevalence data indicate that toxoplasmosis is one of the most common of humans infections throughout the world.
Infection is more common in warm climates and at lower altitudes than in cold climates and mountainous regions. High prevalence of infection in France (85%) has been related to a preference for eating raw or undercooked meat, while high prevalence in Central America has been related to the frequency of stray cats in a climate favoring survival of oocysts. The overall seroprevalence in the United States as determined with specimens collected by the third National Health and Nutritional Assessment Survey (NHANES III) between 1988 and 1994 was found to be 22%, with seroprevalence among women of childbearing age (15 to 45 years) of 10% to 15%. Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate, where it replicates by binary fission. The parasite does not appear to have a cyst form, and does not survive well in the external environment.
Trichomonas vaginalis is transmitted among humans, its only known host, primarily by sexual intercourse. Geographic Distribution: Worldwide.
Higher prevalence among persons with multiple sexual partners or other venereal diseases. During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina ) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream. Inside the host, they transform into bloodstream trypomastigotes, are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission. The entire life cycle of African Trypanosomes is represented by extracellular stages.
The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host (, ). In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes. The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission. The cycle in the fly takes approximately 3 weeks.
Humans are the main reservoir for Trypanosoma brucei gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T. Geographic Distribution: T.
Gambiense is found in foci in large areas of West and Central Africa. The distribution of T. Rhodesiense is much more limited, with the species found in East and Southeast Africa. Chagas Disease: An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva. Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodinius, and Panstrongylus.
Inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes.
Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites.
The ingested trypomastigotes transform into epimastigotes in the vector’s midgut. The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. Geographic Distribution: The Americas from the southern United States to southern Argentina. Mostly in poor, rural areas of Central and South America. Chronic Chagas disease is a major health problem in many Latin American countries.
With increased population movements, the possibility of transmission by blood transfusion has become more substantial in the United States. Sordaria macrospora is a filamentous ascomycete which is closely related to Neurospora crassa. But in contrast to Neurospora, Sordaria is homothallic, which means that a single strain produces fruiting bodies without the need for a partner of opposite mating type.
The life cycle of S. Macrospora is shown in the picture. It starts with an ascospore which germinates and produces a mycelium. Within a week, fruiting bodies develop in which asci are produced that contain eight ascospores each. The ascospores are ejected from the fruiting body and the cycle starts again.
Eggs are passed in the stool, and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil, and after 5 to 10 days (and two molts) they become become filariform (third-stage) larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions.
On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed.
The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host. Most adult worms are eliminated in 1 to 2 years, but longevity records can reach several years. Duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle).
In addition, infection by A. Duodenale may probably also occur by the oral and transmammary route.
Americanus, however, requires a transpulmonary migration phase. Geographic Distribution: The second most common human helminthic infection (after ascariasis). Worldwide distribution, mostly in areas with moist, warm climate. Americanus and A. Duodenale are found in Africa, Asia and the Americas. Necator americanus predominates in the Americas and Australia, while only A.
Duodenale is found in the Middle East, North Africa and southern Europe. Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces. Unfertilized eggs may be ingested but are not infective.
Fertile eggs embryonate and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed.
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Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years. Geographic Distribution: The most common human helminthic infection. Worldwide distribution. Highest prevalence in tropical and subtropical regions, and areas with inadequate sanitation.
Occurs in rural areas of the southeastern United States. Guinea Worm Disease: Humans become infected by drinking unfiltered water containing copepods (small crustaceans) which are infected with larvae of D. Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space. After maturation into adults and copulation, the male worms die and the females (length: 70 to 120 cm) migrate in the subcutaneous tissues towards the skin surface. Approximately one year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures.
When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae. The larvae are ingested by a copepod and after two weeks (and two molts) have developed into infective larvae. Ingestion of the copepods closes the cycle. Geographic Distribution: An ongoing eradication campaign has dramatically reduced the incidence of dracunculiasis, which is now restricted to rural, isolated areas in a narrow belt of African countries and Yemen.
Eggs are deposited on perianal folds. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g., curtains, carpeting). Some small number of eggs may become airborne and inhaled.
These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon. The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. The life span of the adults is about two months.
Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions. Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown. Geographic Distribution: Worldwide, with infections more frequent in school- or preschool- children and in crowded conditions. Enterobiasis appears to be more common in temperate than tropical countries.
The most common helminthic infection in the United States (an estimated 40 million persons infected). Eggs are eliminated with feces or urine. Under optimal conditions the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and shed their forked tail, becoming schistosomulae. The schistosomulae migrate through several tissues and stages to their residence in the veins (, ).
Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species. For instance, S. Japonicum is more frequently found in the superior mesenteric veins draining the small intestine, and S. Mansoni occurs more often in the superior mesenteric veins draining the large intestine. However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location.
Haematobium most often occurs in the venous plexus of bladder, but it can also be found in the rectal venules. The females (size 7 to 20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine ( S. Mansoni and S. Japonicum ) and of the bladder and ureters ( S. Haematobium ), and are eliminated with feces or urine, respectively.
Pathology of S. Mansoni and S. Japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S.
Haematobium schistosomiasis includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes.
Various animals, such as dogs, cats, rodents, pigs, hourse and goats, serve as reservoirs for S. Japonicum, and dogs for S. Geographic Distribution: Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East; S.
Haematobium in Africa and the Middle East; and S. Japonicum in the Far East. Schistosoma mekongi and S. Intercalatum are found focally in Southeast Asia and central West Africa, respectively. Life cycle of Taenia saginata and Taenia solium Humans are the only definitive hosts for Taenia saginata and Taenia solium. Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the environment. Saginata ) and pigs ( T.
Solium ) become infected by ingesting vegetation contaminated with eggs or gravid proglottids. In the animal's intestine, the oncospheres hatch, invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine.
Length of adult worms is usually 5 m or less for T. Saginata (however it may reach up to 25 m) and 2 to 7 m for T.
The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). Saginata adults usually have 1,000 to 2,000 proglottids, while T. Solium adults have an average of 1,000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. Saginata may produce up to 100,000 and T.
Solium may produce 50,000 eggs per proglottid respectively. Geographic Distribution: Both species are worldwide in distribution. Taenia solium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork, and in very rare in Muslim countries. Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella.
After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms (female 2.2 mm in length, males 1.2 mm; life span in the small bowel: 4 weeks). After 1 week, the females release larvae that migrate to the striated muscles where they encyst. Trichinella pseudospiralis, however, does not encyst. Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable for several years. Ingestion of the encysted larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining the endemicity of this infection.
Carnivorous/omnivorous animals, such as pigs or bears, feed on infected rodents or meat from other animals. Different animal hosts are implicated in the life cycle of the different species of Trichinella. Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat). Geographic Distribution: Worldwide. Most common in parts of Europe and the United States. Different species of the following genera of mosquitoes are vectors of W. Bancrofti filariasis depending on geographical distribution.
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Among them are: Culex ( C. Annulirostris, C. Bitaeniorhynchus, C. Quinquefasciatus, and C.
Pipiens ); Anopheles ( A. Arabinensis, A. Bancroftii, A. Koliensis, A. Punctulatus and A. Wellcomei ); Aedes ( A.
Aquasalis, A. Polynesiensis, A. Pseudoscutellaris, A.
Scapularis, and A. Vigilax ); Mansonia ( M. Pseudotitillans, M. Uniformis ); Coquillettidia ( C. Juxtamansonia ). During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound.
They develop in adults that commonly reside in the lymphatics. The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by.1 mm. Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity.
The microfilariae migrate into lymph and blood channels moving actively through lymph and blood. A mosquito ingests the microfilariae during a blood meal. After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles.
There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae. The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis and can infect another human when the mosquito takes a blood meal.
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