Nematodes/roundworms of man

Pinworms, Ascaris, Toxocara, Anisakis, hookworms, filariae, Anisakis, Trichinella, guinea worm



Nematodes cause some of the most important parasitic diseases of humans world-wide. Billions of people are infected with some species, many are killed. There is probably no person who has not had at least one nematode species at one stage of her/his life, such as pinworms, Ascaris or hookworms. Several species of filariae are important agents of tropical disease leading to serious symptoms and even death.

An outline is given of the morphology, life cycles, modes of infection, symptoms caused and treatment of the various species.


General background

Nematoda, roundworms is one of the most common and diverse animal groups, including many free-living and many parasitic species infecting plants and animals. They are of very great medical and economic importance. For example, nematodes cause huge losses to agriculture and to the livestock industry, and they also include many species  responsible for serious human diseases. Nematodes are important components of ecosystems in the marine, freshwater and terrestrial environments. It is highly likely that the majority of species has not yet been described. Thus, they form one of the largest groups of invertebrates on the deep sea floor and in the meiofauna of beaches, but  very few studies have been made. They range in size from a few mm to about 1m, and have – with few exceptions – separate sexes. In spite of their great species diversity, their structure is surprisingly uniform. Worms are round in cross-section and elongate, with a simple digestive tract consisting of a mouth followed by a muscular pharynx and intestine which opens near the posterior end. The body is covered by a cuticle. The gonopore of females is located somewhere in the middle of the body, the male gonopore is located posteriorly. Males possess copulatory sclerites which are introduced into the vagina during copulation, and in some groups the posterior end of the male is modified to a copulatory bursa which can embrace the female. Some organs consist of a constant number of cells. The typical life cycle involves four moults, i.e., four larval stages and one adult stage. Parasitic species have either direct (without intermediate hosts) or indirect life cycles (with intermediate hosts).[1]

Enterobius vermicularis – enterobiasis. 

The human pin- or threadworm is highly host specific, infecting humans and only occasionally a few species of monkeys and apes. It is cosmopolitan, although less common in tropical latitudes. Infection is particularly common when people (children in particular) are in close proximity. It is likely that hundreds of millions of people become infected every year. Female worms are about 8-13 mm long, males about 2-5 mm. Females creep out of the anus and lay thin-shelled eggs on the skin around the anus which contain well developed larvae. Itching produced by the worms leads to scratching and adhesion of infective eggs to the fingers. Children in particular become infected when swallowing eggs on dirty fingers. But infection may also occur by the very small and light eggs widely spread in dust, on linen etc.. It has also been claimed that infection can occur by retrofection, i.e. migration of larvae through the anus into the intestine, although this is unlikely. – Larvae hatch from swallowed eggs in the small intestine, moult several times to become adults in the caecum. After copulation females creep to the rectum and out of the anus to lay eggs.


Life cycle of Enterobius vermicularis. Public domain


Symptoms are usually mild including itching around the anus, but worms that have migrated into the appendix can cause appendicitis. Other symptoms include abdominal pain and fever, and rarely granulomas in the intestinal wall, the greater omentum and subcutaneous tissue. In women, worms can invade the urethra, vagina and abdominal cavity. Very rare are epileptic fits and even insanity.

Diagnosis is by applying sticky transparent tape to the anal region and examining it under the microscope for eggs. Various anthelminthics are used for treatment.

Further information here, here, here.


Ascaris lumbricoides – ascariasis.

This infection is caused by the large roundworm of humans Ascaris lumbricoides, although the very similar A. suum (now usually considered a separate species) is found in pigs. A. lumbricoides can also infect domestic and wild pigs, apes, etc.. The species is widely spread, including the tropics and cold environments. Female worms reach a length of about 20-35 cm, males of 15-30 cm. Males can be distinguished by the coiled posterior end. 

Female Ascaris lumbricoides. Public domain.

After copulation, females lay about 200 000 very thick-shelled eggs per day which escape in the stool and develop outside a host. After two moults the larva reaches the infective stage within the egg. When ingested, the larva hatches, penetrates through the intestinal wall into the portal vein, is carried to the liver (or it reaches the liver on its own), penetrates into a vein, is carried to the lungs (or reaches the lungs on its own), and enters the alveoli. After about 10 days in the lungs they creep up the bronchus and trachea, and down through the oesophagus into the intestine. After two more moults they mature and copulate.

Symptoms are caused by migrating larvae and the adults in the gut. The former cause liver disorders and pneumonitis (and even death). Adults can cause appendicitis, ileus, perforation of the gut, and they may migrate into the bile duct and liver, and pancreas. Worms have even been observed to come out through the mouth or ear. Allergic reactions to the worms include fever, nausea and epileptic fits, among others. – Infection intensity can be very high.
Diagnosis is by demonstrating eggs in the stool, treatment by various anthelminthics.
Further information here, here, here.

Toxocara canis – toxocariasis

Adult worms infect dogs and other Canidae (dog family) [2]. They resemble small Ascaris lumbricoides but are much shorter (female 8-13 cm, male 5-8 cm). Their life cycle is simlilar to that of Ascaris, the main difference being (apart from the hosts) that larvae in the lungs of adult dogs do not get into alveoli but are disseminated all over the body in the blood stream (“somatic migration”); pups may also become infected by larvae penetrating through the placenta or mammary gland of the mother. The species is medically important because children who have swallowed eggs suffer symptoms due to somatic migration: eosinophilic granulomata in various organs, and organ lesions by larvae migrating freely in soft tissues (“visceral larva migrans”). The eyes are not rarely affected (over 2 000 cases reported in man world-wide). Symptoms include enlargement of the liver, infiltration of the lungs, loss of vision, neuropathy, etc., beside fever. As in many parasitic infections, the number of eosinophilic leukocytes is very high (“eosinophilia”: up to 90% of all white blood cells may be eosinophils).

Diagnosis is by biopsy (examination of tissue for larvae), which – however – is often not possible. Eye diseases and high eosinophilia and close contact with dogs are indicative of the infection. Treatment is difficult.

Less common in humans than T. canis is Toxocara cati, adults of which infect cats and related species. Humans become infected by swallowing eggs or third-stage larvae, which cause larva migrans symptoms as in T. canis. Toxascasis leonina occurs world-wide in species of the cat and dog families. It is possible but not certain that larvae of the species may infect humans.

Further information here.

Anisakis simplex, Pseudoterranova decipiens – anisakiasis.

Species of the family Anisakidae cause the syndrome (= complex of symptoms) of anisakiasis [3][4][5]. The species most frequently encountered in man is Anisakis simplex, less common is Pseudoterranova decipiens , and very rare are Anisakis physeteris, Contracaecum osculatum and Hysterothylacium aduncum. Adult Anisakis simplex infect dolphins and other toothed whales,  Pseudoterranova decipiens (seal worm) live in the intestine of seals. We discuss the life cycle of the latter species. Eggs are shed in the faeces and sink to the seafloor. The third, “sheathed” larval stage (0.2 mm long) leaves the egg, it attaches itself with its tail end to the substratum and is ingested by various small crustaceans (copepods, juvenile amphipods and mysids). Larvae break through the sheath and penetrate into the haemocoel of the host. Copepods are eaten by larger invertebrates (adult amphipods, mysids, polychaetes), in which larvae can reach a length of more than 8 mm. Small fish become infected by eating infected invertebrates. Large fish, in turn, become infected by eating invertebrates or small fish. Larvae (still in the third stage) penetrate through the intestinal wall of fish and grow in their musculature to a length of about 3-6 cm. Finally, seals become infected by eating infected fish or invertebrates. The last two moults occur in the intestine of seals. Humans are not necessary for the completion of the life cycle; they play the role of transport (paratenic) hosts for the third larva. Infection of man is by eating insufficiently cooked fish and invertebrates (cephalopods).

Anisakidae larvae. Public domain

Symptoms of anisakiasis depend on which organs or tissues are infected (“stomach, intestinal and
extraintestinal anisakiasis”). An acute and chronic form an also be distinguished. The former is mainly characterised by fast developing (two to seven hours after infection) abdominal pains, often with nausea and vomiting. In the mild chronic stomach anisakiasis pains are often weaker and can last for more than two years (if parasites are not removed by surgery). Almost all cases of intestinal anisakiasis are acute, usually with strong abdominal pains, nausea, congestion and diarrhea. In most extra- intestinal cases symptoms are localized and mild. Infections can be prevented by cooking of hosts, or by freezing at -20o C for one to several days. The probability of acquiring an infection can be reduced by removal of viscera of fish a short time after capture, which prevents migration of larvae from the intestine into the tissues, although some larvae are already in the tissues. The effectiveness of control measures is evidenced by the fact that no new cases of human infections occurred after the Netherlands government had introduced a law that made it compulsory to freeze fish before sale as “green herring”. However, in many countries fresh fish are preferred over frozen ones.

Further information here.


Ancylostoma spp., Necator americanus – ancylostomiasis.

Human hookworms are widespread, especially in warm countries, but also in warm localities at high latitudes, such as mines [2]. Ancylostoma duodenale  is common in the eastern hemisphere, but also in parts of South America, Necator americanus is common in Africa, many parts of Asia, southern North America, and Central and South America. Other species of Ancylostoma (A. caninum, A. braziliense, A. ceylanicum) also infect humans, but only in their larval stage, causing creeping eruption, an inflammation of the skin. Ancylostoma differs from Necator in the structure of its oral cutting plates, they possess hooks in the former and cutting edges in the latter. – Female Ancylostoma duodenale is about 10-13 mm long, the male about 8-11 mm. Necator is slightly smaller, the female about 9-11 and the male about 7-9 mm long. Females have a pointed posterior end, males a posterior copulatory bursa used to clasp the female during copulation. The main host is man, although some other mammals can also occasionally be infected. A female of A. duodenale lays about 10 000 – 20 000 eggs per day, a female Necator americanus about 5 000 – 10 000. Cleavage begins in the egg while it is still in the host, and continues after it has been passed out. The first larval stage, the rhabditiform larva (characterized by a short pharynx containing a strong constriction) develops by a first moult to the filariform larva (pharynx longer and less constricted), and by a second moult to the next larval stage which is still contained withing the cuticle of the previous stage and therefore called a sheathed larva. This stage is passed in the stool. It is highly resistant to environmental effects and can survive in the top layers of soil for up to nine weeks in the tropics and half a year at higher latitudes. It survives in the soil but creeps up on vegetation responding to heat from humans. It infects humans either by ingestion or penetration through the skin. Ancylostoma duodenale prefers the oral route, Necator americanus the percutaneous one. In the host, larvae shed their sheath and penetrate into the wall of the small intestine, where they stay for a few days and moult for the third time to the next larval stage, which returns to the intestinal lumen, moulting a fourth time to the adult. – Some larvae in the intestinal wall do not stay there but get into the blood vessels and lungs; they move up the trachea, down the oesophagus, stomach and intestine. – In Necator americanus, larvae stay for a few days in the skin after infection, move to the lungs in blood or lymph vessels, and then through the oesophagus and stomach to the intestine.

Life cycle of human hookworms. Public domain.

Symptoms caused by Ancylostoma and Necator are more or less the same. First, cutaneous infection results in a dermatitis, and oral infection causes “wakana” or “young green” disease, with nausea, vomiting and asthma-like symptoms. Second, adults in the small intestine suck blood and lead to considerable blood loss (much stronger in A. duodenale than in N. americanus), causing anaemia and sometimes hypertrophy and dysfunction of liver and heart. Children are frequently infected and may show retardation of growth and mental development. Symptoms are not always present and depend on the number of worms and the health condition of the host.

Diagnosis is by demonstrating eggs in the stool. Concentration of eggs by flotation or other methods may be advisable. Treatment is by anthelminthics; treatment of aenemia may be important.

Some hookworms infect humans only in their larval stage, causing dermatitis when larvae attempt to penetrate into a host. Species include Ancylostoma caninum (dogs common hosts for the adult), A. braziliense (dogs and cats) and A. ceylanicum.

Further information here, here, here.

Trichostrongylus spp. – trichostrongyliasis

10 species are known to infect humans [2]. Important in Japan, China and Korea is T. orientalis. Females are 5-7, males 4-5 mm long. The life cycle is similar to that of hookworms. Oral infection is most common, but infection can also occur through the skin. Worms mature in the small intestine and are also found in the stomach. Symptoms are usually absent but may include abdominal pain, diarrhea, headache etc. Diagnosis is by demonstrating eggs in the stool, using a floating method for concentrating the eggs; treatment is with anthelminthics.

Further information here.

Angiostrongylus cantonensis – angiostrongyliasis

Normal final hosts of the rat-lungworm Angiostrongylus cantonensis are various rodents, among others rats [6] Humans are abnormal hosts who contain the third larval stage. The worms do not mature in humans. Adult worms live in the lung arteries of rodents (at high infection intensities also in the right ventricle). They produce eggs, from which larvae hatch in the lung arteries and capillaries. They migrate up the trachea, are swallowed and shed in the faeces. Terrestrial and freshwater molluscs (intermediate hosts) eat the larvae or are infected by external penetration of the larvae. The larvae develop within a few weeks to the third stage, which is infective to rodents. In the rodents, the larvae reach the surface of the brain via the blood or nervous system. After a few weeks they migrate into the lung arteries. – Various brackish water and marine fish as well as invertebrates including marine shrimps, oysters and mussels could be experimentally infected and must therefore be considered to be potential intermediate hosts..

The syndrome caused by the worms is eosinophilic meningoencephalitis (or eosinophilic meningitis), an inflammation of the cerebral membranes with an accumulation of eosinophilic white blood cells. Very strong headaches, paralysis, vomiting and fever are only some of the possible symptoms. In extreme cases mental disturbances and death may result.  Larvae can be killed by freezing and heating. Diagnosis is by demonstrating eosinophilia in the peripheral blood and cerebrospinal fluid, and by finding worms in the eyes or cerebrospinal fluid.

Beside A. cantonensis, A. costaricensis is an agent of the disease, known from North, Central and South America (a similar species is known from Asia). Its main host is the cotton rat, but many other rodents are infected as well. Intermediate hosts are slugs. Worms can mature in humans. Symptoms include abdominal pains, fever, vomiting and eosinophilia. Diagnosis is by immunological tests and clinical symptoms, and by demonstrating worms, usually in the appendix.

Further information here, here, here.

Strongyloides stercoralis, S . fuelleborni – strongyloidiasis

All male adults of this species are free living (so-called R-form males because of the rhabditiform pharynx with a distinct constriction), whereas females have free-living and parasitic generations [2]. Female parasitic forms, about 2 mm long, are referred to as filariform female adult (=F-form female) because of their elongate pharynx lacking a constriction. They produce eggs by parthenogenesis (i.e., from egg cells without fertilization). Free living females, about 1-1.7 mm long, are called R-form females (because of the short rhabditiform with a distinct constriction). They produce eggs from fertilized egg cells. Both female generations produce rhabditiform larvae (R-from larva)  which hatch from the egg. It develops to the next larval stage, the filariform larva (F-form larva) by two moults, the infective stage. It can survive for over a month in soil. Humans, cats and dogs are hosts. Important is the occurrence of autoinfection. Female R-forms larvae which are passed out of a host become infective F-forms after two moults (the so-called “direct development”), when environmental conditions are unfavourable. However, in constipated hosts or hosts with immune deficiency, female R-forms can directly develop to F-form larvae in the gut and invade the intestinal wall. Also, female R-forms excreted through the anus may transform to infective F-form larvae while attached to the region around the anus, and infect the same host through the skin (“autoreinfection”). – F-form larvae that have infected a host percutaneously or through the mucosa get into the blood system, reach the lung and alveoli, and go from there through the trachea, oesophagus and stomach into the small intestine. They become F-form female adults after two moults. But larvae can also reach the intestinal walls in the blood circulation.

Symptoms include a dermatitis due to penetrating larvae, coughing when larvae are in the lungs and trachea, rarely a bronchitis when F-form larvae abnormally mature in the mucosa of the bronchi, lesions in the gut, as well as in the bile and pancreatic ducts, abdominal pain, diarrhea and fever. Autoinfection makes these symptoms worse, leading to bloody diarrhea, anemia, edema, ascites etc. Diagnosis is by  demonstrating larvae in the stool. Treatment is difficult, but anthelminthis can be used.

A related species, S. fuelleborni, infects African and Asian apes and monkeys for example in Japan, and humans. Human infections are common in parts of Africa. Structure and life cycle are similar to those of S. stercoralis. However, eggs appear in fresh stool instead of larvae.

Further information here, here.

Thelazia callipaeda, T. californiensis – thelasiasis

Two species of this genus infect humans and cause “eyeworm disease” [2]. T. callipaeda infects dogs, cats and humans in eastern and southern Asia, but also other mammals. Females are 15 mm long, males 10 mm. Intermediate hosts are insects, in Japan several species of Drosopholidae. Adults live in the conjunctival sac, continually producing larvae. Final hosts become infected when infective insects lick tears in their eyes. Symptoms include conjunctivitis, treatment is by removing the worms. T. californiensis infects many mammals in America, including humans.

Further information here, here.

Gnathostoma spp. – gnathostomiasis

More than 20 species of Gnathostoma are known from a variety of mammals, and a few occasionally infect humans [2]. They possess a characteristic head bulb with patterns of spines that are used for species differentiation. G. spinigerum uses species of the dog and cat families (Canidae, Felidae) as final hosts, infecting their gastric walls producing tumors. Females are about 1.5-3.3 cm long, males 1.2-3 cm. Copepods are first and various crustaceans, fish, amphibians, reptiles, birds and mammals (except for Felidae and Canidae) are second intermediate and paratenic hosts. Final hosts become infected by swallowing infected vertebrates or occasionally copepods, humans become infected by eating raw meat, usually fish such  as mullet. Larvae penetrate the gastric or intestinal wall, get into the liver and then into the muscles and subcutaneous tissue in any part of the body. In humans, worms migrating in the muscles may be adults, but adults were not found in the human gastric wall. Symptoms include anorexia, vomiting, abdominal pain, fever, skin lesions and liver damage. Diagnosis is by biopsy or immunological diagnosis, and demonstration of eosinophilia, as well as observation of symptoms. Treatment is by removing the worms, when possible. Other species found (but rarely) in man are G. hispidum (normal hosts pigs), G.nipponicum (normal host weasel), and G. doloresi (normal hosts pigs).

Further information here, here.

Wuchereria bancrofti, Brugia spp., Dirofilaria spp., Onchocerca volvulus, Loa loa, Mansonella spp. – filariasis

Human filariae are common in  warm and humid countries. They have indirect life cycles, using insects as intermediate hosts (in filariae of cotton rats, for example, mites serve as intermediate hosts). A number of species are involved [2].

Wuchereria bancrofti

The parasite is found in temperate to tropical parts of SE Asia, Oceania, Pacific islands, Africa and America. Females reach a length of about 10, males of about 4.5 cm. Humans are the only known naturally infected final hosts, although various monkeys can be experimentally infected. Mosquitoes are intermediate hosts, mainly of the genera Culex and Aedes. Worms are usually found in the lymph system. Females lay so-called microfilariae into the lymph, from where they get into the blood system. In most regions, microfilariae invade the peripheral blood system only during the night  (“nocturnal periodicity”), an adaptation to the habits of mosquito species transmitting them: they suck blood at night. An exception is the Pacific islands (Polynesia, New Caledonia), where they are found in the peripheral blood system during the daytime as well: mosquitoes are active also during the day. – Symptoms are often absent over many years, although microfilariae are present in the blood. Fever may be a first symptom, and bacterial infections may spread in infected tissues. Elephantiasis, usually of the lower extremities, scrotum, penis, labia, forearm and breast may develop, sometimes leading to very large swellings. Diagnosis is by observing disease symptoms and demonstration of microfilariae in the blood (blood taken at night in most areas, see above). Treatment is by anthelminthics, specific to larvae and adults, respectively.

Life cycle of Wuchereria bancrofti. Public Domain.

Microfilaria of Wuchereria bancrofti in blood smear. Also note a few leukocytes. Public domain:

Further information here, here.

Brugia malayi, B. pahangi, B. timori

Brugia malayi is found in coastal areas of eastern Asia, southeastern Asia and the Pacific islands. The structure and biology of the species resemble Wuchereria bancroft in many respects, but it is smaller. Final hosts are humans, experimental hosts cats and apes. Intermediate hosts are mosquitoes of the genera Mansonia and to a lesser degree Anopheles and Aedes. Microfilariae show a nocturnal periodicity. Symptoms are similar to those cause by Wuchereria, but are usually mild, with a mild elephantiasis. – Brugia pahangi is known from Malaysia and infects the lymphatic system of many mammals including man. Vectors are mosquitoes of the genera Anopheles and Mansonia. – B. timori has been recorded from Indonesia, it infects the lymphatic system of cats, the pangolin and humans. Vectors are mosquitoes of the genus Anopheles.

Further information here.

Dirofilaria immitis, D. repens, D. tenuis

Dirofilaria immitis infects the heart and pulmonary artery of dogs and many other mammals including man, females are up to about 3, and males 2 cm long. Mosquitoes (Aedes, Culex) are intermediate hosts. In dogs, adult females produce microfilariae, but in humans microfilariae have not been found in the blood, although worms may mature. Embolism of the pulmonary artery has been demonstrated, and symptoms may include cough, chest pain, fever, bloody sputum etc. – D. repens is a parasite of dogs, cats etc. including humans in Eurasia and Africa and infects the subcutaneous tissue. Vectors are Anopheles, Aedes and Mansonia mosquitoes. – D. tenuis is know from the subcutaneous tissue of the racoon and man in North America, vectors are Aedes and Anopheles mosquitoes.

Further information here.

Onchocerca volvulus

Onchocerca is the causative agent of “river blindness”, referring to the fact that infections are found along rivers in Africa and Central and South Americ, and lead to eye damage. Worms are entangled with each other forming lumps (“onchocercomas”) in the subcutaneous tissue. Females reach a length of half a meter, males of 4.5 cm. Humans, apes and monkeys may be naturally infected. Intermediate hosts are species of Simuliidae (midges, black flies, black gnats, coffee flies). Insects become infected by taking up microfilariae while sucking blood. Larvae infective to man get into his subcutaneous tissue where they mature and survive for up to 15 years. Most damage is done by the microfilariae which cause strong itching leading to dermatitis. When onchocercomas are close to an eye, microfilariae may cause serious damage to it, leading to atrophy of the eye nerve and blindness. Diagnosis is by biopsy of the onchocercoma or demonstration of microfilariae in the skin, eyes or urine, as well as by immunological methods. Drugs for treatment are available, and excision of the onchocercomas is effective treatment.

Further information here.

Loa loa

Loa loa or eye worm is known from tropical Africa. In some areas 50- 90% infection rates have been recorded. Females are 5-7, males 3-3.5 cm long. Final hosts are humans, apes and monkeys, intermediate hosts are flies of the genus Chrysops. Adults live usually under the skin, and microfilariae have a diurnal periodicity, appearing in the peripheral blood during the day. Adult worms cause inflammation and allergic reactions  leading to oedemas (“Calabar swellings”). The eye is frequently involved. Diagnosis is by observation of symptoms and microfilariae and eosinophilia in the blood. Removal of worms is the preferred treatment. Drugs for treatment are also available.

Further information here, here, here.

Mansonella perstans, M. ozzardi, M. streptocerca

Mansonella perstans occurs in South America, southern Central America and Africa. Humans and apes are infected, and the infection is transmitted by flies of the genus Culicoides. Adults live in the abdominal and less frequently the chest and pericardial cavities. Microfilariae are found in the peripheral blood at day and night. Symptoms include abdominal pain and itching. Diagnosis is by demonstrating microfilariae and eosinophilia. Treatment by drugs is possible. – M. ozzardi occurs in Central and South America including the West Indies. Humans and apes are hosts, their body cavities are infected. Gnats of the genera Culicoides and Simulium are intermediate hosts. – M. streptocerca infects the subcutaneous tissue of apes and humans in Africa, Culicoides gnats transmit the infection.

Further information here, here.

Dracunculus medinensis – dracunculiasis

Females reach a length of more than 1 m, males of about 4 cm. Various mammals, such as dogs, cats, horses etc. are hosts, but mainly humans [2]. The infection used to be widely spread in the African tropics, Middle East, parts of eastern Central Asia, India and Sri Lanka, and occasionally in southeastern Asia. When an infected host enters water, the female worm sticks its anterior end containing the uterine pore out and lays 100 000’s of larvae. Freshwater copepods serve as intermediate hosts, they become infected by ingesting larvae, which moult twice to the infective third stage larva. Infected copepods swallowed by the final host transmit the parasite. Female worms in tissues close to the body surface cause dizziness, nausea and vomiting, and intense itching and burning around the blister produced by the head end of the worm. Secondary infections by bacteria can lead to sepsis and tetanus. Diagnosis is by observing the outline of the worm under the skin and the blister produced by it, and finding larvae or the head end of the worm. Treatment is by removing the worm (surgery, or pulling out). One can avoid infection by filtering or boiling water.

Life cycle of Dracunculus medinensis. Public Domain.

Further information here.

Trichurus trichiura, T. vulpis – trichuriasis

Whipworms have a world-wide distribution, particularly in warm and humid countries [2]. The name is derived from the structure of the worms: their anterior end is very long and thin, whip-like. The female is about 3.4-4.5, the male 3-4.5 cm long. Humans  are main hosts, with apes and pigs occasionally infected. Worms in the intestine lay eggs which are passed out in the stool, and larvae develop within them. When ingested, larvae hatch and move down the intestine until they reach the caecum. The thin anterior end is inserted into the mucosa repeatedly during migration down the gut and once in the caecum. Appendix, large intestine and lower part of small intestine may also be infected. At low infection intensities symptoms are minor or absent altogether, at higher intensities symptoms may include abdominal pain, anaemia, bloody stool, among others. Diagnosis is by demonstrating eggs in the stool. Treatment is by anthelminthics.

A second species, T. vulpis, infects mainly dogs and other Canidae, but also humans.

Further information here, here.

Capillaria spp. – capillariasis

This disease is caused by species of the genus Capillaria, of which 100 species are known from mammals [2]. Capilaria hepatica infects the liver mainly of rodents but also of any other mammals including man. Female worms reach a length of about 8 cm, males of about 4 cm. The life cycle is direct, i.e., no intermediate host is required, although two final hosts are usually necessary for completion of the life cycle. Infection of man is by mature eggs contained in food or drink, or on dirty fingers. The liver is infected, leading to necrosis of the liver parenchyma and fibrosis. Symptoms at low infection intensities are absent or mild, at heavy infection intensities they include fever, enlargement of the liver and eosinophilia. Diagnosis is by liver biopsy. Treatment is difficult.

C. philippinensis infects the intestine of man. Intermediate hosts are freshwater fish. Infection of man occurs by eating raw fish or food or drinks contaminated with stool. Repeated autoinfection can lead to an increase in worm numbers and serious symptoms including  extensive damage to the intestinal mucosa leading to diarrhea and abdominal pain. Diagnosis is by finding eggs in the stool or by haemagglutination and intradermal tests. Treatment is by anthelminthics.

C. aerophila is common in foxes, but occurs also in many other mammals. Human cases are known. Infection sites are the mucosa of the trachea, bronchi and bronchioli, and occasionally the paranasal sinuses. Humans become infected by contaminated food, drinks or fingers. Symptoms of bronchitis, bronchiolitis or pneumonia occur including bloody sputum. Diagnosis is by demonstrating eggs in ths sputum or stool, and biopsy. Anthelminthics for treatment are available.

Further information here, here.

Trichinella spiralis, T. nativa – trichinelliasis

Trichinelliasis (trichinosis) is due to infection with Trichinella, which is widespread [7]. Encapsulated larvae of T. spiralis live in the striated muscles of mammals such as pigs and humans, and in many other carnivorous and omnivorous mammals (and even birds ?: a related species, T. pseudospiralis, uses birds as hosts). Humans become infected usually by eating insufficiently cooked pork. Larvae mature in the small intestine, adults copulate, males die soon but females survive and produce large numbers of larvae by ovoviviparity (i.e., not eggs but larvae are laid). Larvae get into the lymph and blood systems and are distributed throughout the body. Only those reaching striated muscle cells develop further to the  encapsulated stage infective to other animals (however, some genotypes do not encapsulate). Infections had plague-like proportions in many including European countries until effective measures were introduced (meat inspection, cooking pork properly). Note that freezing meat can kill infective larvae. Symptoms included an inflammation and diarrhea due to adult worms in the gut at high infection intensities, and various symptoms due to larvae, depending again on infection intensity. These symptoms include oedema of the face, fever, eosinophilia, muscle pain, fatigue and even death.

Marine mammals and humans living in Arctic regions can carry the species Trichinella nativa, which is tolerant to freezing. 60% of  polar bears and up to 60% of walrus are infected in some regions. Meat of walrus and polar bears is the most important source of human infection. Symptoms depend on infection intensity. Even freezing at  –20o C for four years did not kill all larvae (for details see here).

Further information here, here.

Dioctophyma renale – dioctophymiasis

The giant kidney worm (female over 1 m long, male 45 cm) infects the kidney and abdominal cavity of various carnivorous mammals [2]. Intermediate host is the earthworm Lumbricus variegatus, paratenic hosts are fish and frogs. Both intermediate and paratenic hosts transmit the infection to the final host, when eaten. Few human cases are known. Kidneys were damaged. Diagnosis is by demonstrating eggs or worms in the urine. Treatment consists of removing the worms.

Further information here.

Other parasitological knols

Aspidogastrea I:
Aspidogastrea II:
Aspidogastrea III:
Marine parasites of man:
Links to parasitology knols:

Further Reading

Bogitsh  B.J. & Cheng T.C. (1990). Human Parasitology. Saunders College Publishing, New York.

Odening K. (1969). Entwicklungswege der Schmarotzerwürmer. Akademische Verlagsgesellschaft Geest & Portig K.G., Leipzig.

Rohde, K. (2001). Parasitism. Encyclopedia of Biodiversity. Academic Press.

Schmidt G.D., Roberts L.S. & Janovy, J. (1995). Foundations of Parasitology 5th Edition. McGraw Hill, New York.

Urquhart, G.M. & Jennings, F.W. (1996). Veterinary Parasitology 2nd Edition. Iowa State University Press, Ames, Iowa.


  • McClelland, G. (2005). Nematoda (roundworms). In: K. Rohde (Ed.), Marine Parasitology. CSIRO Publishing Melbourne, und CABI Publishing, Wallingford, Oxon, S.104-115.
  • Miyazaki, I. (1991). An Illustrated Book of Helminthic Zoonoses. International Medical Foundation of Japan. Tokyo.
  • Forbes, L. B. (2005) Zoonotic aspects of trichinellosis. In: K. Rohde (Ed.), Marine Parasitology. CSIRO Publishing Melbourne, und CABI Publishing, Wallingford, Oxon, 436-439.
  • Nagasawa, K. (2005). Anisakiasis. In: K. Rohde (Ed.), Marine Parasitology. CSIRO Publishing Melbourne, und CABI Publishing, Wallingford, Oxon, S. 430-434.
  • Smith, J.W. and Wootten R. 1978. Anisakis and anisakiasis. Advances in Parasitology 16, 93-163
  • Overstreet, R.B. (2005). Infections by the rat lungworm, Angiostrongylus cantonensis. In: K. Rohde (Ed.), Marine Parasitology. CSIRO Publishing Melbourne, und CABI Publishing, Wallingford, Oxon, S.442-44
  • Forbes, L. B. (2005) Zoonotic aspects of trichinellosis. In: K. Rohde (Ed.), Marine Parasitology. CSIRO Publishing Melbourne, und CABI Publishing, Wallingford, Oxon, 436-439.

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