E. vermicularis ova
Pinworm findings in archaeological material outside the New World have been scarce for unknown reasons, and it is hypothesized that this parasite did not originate in the Americas, but rather arrived via land route through the Beringia. Pinworm is one of the few helminths that could have possibly arrived through this route, as most helminths require a particular soil temperature to progress to the infective stage, a stage pinworms do not require and would not have been possible to attain through migration in the cold northern territories.The worms are small, white, and threadlike, with the larger females ranging between 8-13 mm x 0.3-0.5 mm and the smaller males ranging between 2-5 mm x 0.1-0.2 mm. Females also possess a long, pin-shaped posterior end from which the parasite's name is derived. They dwell primarily in the cecum of the large intestine, from where the gravid females migrate at night to lay up to 15,000 eggs on the perineum.

Pinworm eggs are flattened asymmetrically on one side, ovoid, approximately 55 mm x 25 mm in size, and embryonate in six hours. These eggs can remain viable for about twenty days in a moist environment, and viable eggs and larvae were even found in the sludge of sewage treatment plants in Czechoslovakia in 1992.

Pinworm is a cosmopolitan parasite with particularly high prevalence in countries with a temperate climate. It has the widest distribution of any parasitic helminth, and it is estimated that approximately 200 million people are infected internationally. The most common helminth infection in the USA and Western Europe, it has become the most common intestinal parasite seen in a primary care setting, regardless of factors such as race, socioeconomic status, and culture. As such, pinworm serves as an exception to the general rule that intestinal parasites are uncommon in affluent societies.

In the United States alone, prevalence is estimated to be between 20-40 million, and a CDC surveillance study conducted in 1992 in 35 states found that 11.4% of 9597 tests for pinworm infection were positive. While it is mainly seen in children, pinworm cases have been documented in adults, especially in households where infected children transmit the infection to the rest of the family. Prevalence in children in certain communities has been found to be as high as 61% in India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark.

It has also been recently speculated that pinworms themselves may serve as an intermediate host toDientamoeba fragilis, a relatively mysterious protozoa that is still struggling to gain recognition as a human pathogen in certain countries. However, an increasing number of studies are incriminating it as a legitimate enteric pathogen, and it has been associated with clinical syndromes such as abdominal pain, diarrhea, nausea, vomiting, and fatigue. However, much about this pathogen, including its transmission, is still being investigated. Most intestinal protozoa are transmitted fecal-orally via a cyst form, but D. fragilisis generally accepted as not having a cyst form. Therefore, researchers have turned to its proposed nearest relative,Histomonas meleagridis, for comparison. H. meleagridis possesses several characteristics comparable to those of D. fragilis, and it is interesting to note that it is transmitted via the eggs of the nematode Heterakis gallinae. Burrows and Swerldlow proposed in 1956 that D. fragilis is transmitted via pinworm eggs based on the analysis of 22 appendices in which D. fragilis was isolated: There was a 20-fold greater incidence of pinworm infection than calculated, and small ameboid bodies bearing great resemblance to the nuclei of D. fragilis were observed in the pinworm eggs. However, it is still worth bearing in mind that D. fragilis has been associated with other intestinal parasites (such as Ascaris lumbricoides), and that the lack of a cyst stage yet to be conclusively proven, as D. fragilis has been found to have a high rate of coinfection with organisms which are transmitted fecal-orally.

Humans are the only natural host of pinworms, and there currently is no confirmed pinworm reservoir. However, in 2004, Chan et. aldocumented the existence of pinworm and Trichinella in cockroaches from hospitals and grade schools in Hawaii. While cockroaches are known carriers of bacteria and fungi that produce disease in humans, the link between cockroaches and pathogenic helminths has not yet been elucidated, and this was the first report of pinworm infestation in naturally occurring cockroaches.

In 2005, Tatfeng et. al isolated pinworm ova from cockroaches (Diploptera punctata), as well as the ova, cysts, oocysts, and mature parasites of several other parasites. This team trapped 234 cockroaches from areas in and around households in Ekpoma, Africa. The cockroaches were placed in containers of formol saline, which were then shaken vigorously to detach the parasites from the insects. The fluid was then spun and examined under a microscope.

The findings from both studies have great public health implications. Cockroaches are ubiquitous, and both studies detected pinworm in cockroaches taken from human-occupied settings. If they are indeed reservoirs for pinworms, control of cockroach populations and limiting contact with cockroaches could possibly greatly minimize not only the spread of pinworm infection, but of many other infectious diseases as well.

As with many other GI nematodes, pinworms do not need to rely on a vector for transmission. Pinworm infection usually occurs via ingestion of infectious eggs by direct anus-to-mouth transfer by fingers. This is facilitated by the perianal itch (pruritis ani) induced by the presence of pinworm eggs in the perianal folds, and commonly occurs as a result of nail biting, poor hygiene, or inadequate hand-washing.
Retroinfection is also possible, where some of the pinworm larvae which hatch on the anus return to the gastrointestinal tract of the original host, leading to a very high parasitic load as well as ensuring continued infestation.
However, the transfer can also occur by touching contaminated surfaces, such as clothing, bed linen, and bathroom fixtures followed by ingestion, or even through inhalation or ingestion of aerosolized eggs from the aforementioned surfaces. As such, pinworm infections are easily spread among young children with the habits of nail biting and or poor hygiene, and infected children can easily spread the infection to other family members through the mechanisms listed above.

Eggs are deposited at night by the gravid females.

Eggs are ingested via person-to-person transmission through the handling of contaminated surfaces (such as clothing, linen, curtains, and carpeting), or airbourne eggs may be inhaled and swallowed. Self-infection may also occur if eggs are transferred from to the mouth by fingers that have scratched the perianal area.

After ingestion, larvae hatch from the eggs in the small intestine. The adults then migrate to the colon. The life span of the adults is about two months. Adults mate in the colon, and the males die after mating.

Gravid females migrate nocturnally to the anus and ovideposit eggs in the perianal area. The females die after laying their eggs. The time period from ingestion of infective eggs to the ovideposition of eggs by females is approximately one month.

The larvae develop and the eggs become infection within 4-6 hours. Newly hatched larvae may also migrate back into the anus, and this is known as retroinfection.

C.philippinensis ova

Capillraia philippinensis is a parasitic nematode which causes intestinal capillariasis. This sometimes fatal disease was first discovered in Northern Luzon, Philippines in 1964. Cases have also been reported from China, Egypt, Indonesia, Iran, Japan, Korea, Lao PDR, Taiwan and Thailand. Cases diagnosed in Italy and Spain were believed to be acquired abroad, with one case possibly contracted in Colombia. The natural life cycle of C. philippinensis is believed to involve fish as intermediate hosts, and fish-eating birds as definitive hosts. Humans acquireC. philippinensis by eating small species of infested fish whole and raw.

The complete life cycle of C. philippinensis has been demonstrated in experimental studies, and may be either indirect (involving an intermediate host) or direct (complete in one host).

Indirect life cycle. Fish-eating birds which harbor adult C. philippinensis in their intestines, shed embryonated eggs in their feces. When these eggs are fed to uninfected fish, C. philippinensis larvae are recovered from the intestines of fish. If the fish are fed to uninfested birds, the larvae develop into adults in the intestinal tract of the birds. Larvae recovered from the fish also developed into adults when fed to gerbils or monkeys, with eggs shed in the feces of these mammalian hosts. Naturally infested fish (Hypseleotris bipartita and Apagonsp.) and birds (Ixobrychus sp.) have also been found. Humans become infested when they eat raw or undercooked fish, probably small fish eaten whole, which have the infective larvae in their intestinal tract. Raw fish are commonly eaten by several of the Asian cultures in which C. philippinensis infestations have been found.

While the natural host range is not known, experimental infestations of several fishes, including Cyprinus carpio, Puntius gonionotus,Rasbora borapetensis, Eleotris melanosoma, Ambassis commersoni and Apagon sp., with C. philippinensis eggs yielded infective larvae. Experimental infestations of several birds, including Amaurornis phoenicurus, Ardeola bacchus, Nycticorax nycticorax, Bubulcus ibis, Ixobrychus sinensis, Gallinula chloropus, and Rostratula benghalensis, with larvae yielded mature adults.

Direct life cycle. Researchers also found that feeding just a few dozen larvae from the intestines of fish to Mongolian gerbils (Meriones unguiculatus) or monkeys (Macaca sp.) led to infestations with thousands of adult worms through "autoinfection." Autoinfection is when the offspring produced by adults can reinfest the same host, allowing the infestation to multiply within a single host animal. Bothoviparous (egg-laying) and larviparous (giving birth to active larvae) adult female C. philippinensis were found in Mongolian gerbils and some birds. The experimentally infested monkeys never developed any clinical symptoms, even during prolonged, active infestations. Of several rodents tested, only Mongolian gerbils developed severe symptoms due to infestation and died.

strongyloides stercoralis

strongyloides stercoralis

Strongyloides stercoralis is one of the smallest nematodes of man. It is very common in the tropics and subtropics. Its distribution is similar to that of hookworms. Adult worms live in the host’s intestinal mucosa in the upper part of the intestine, although they may be found anywhere from the duodenum to the rectum.

Among the domestic animals, dogs are readily susceptible to S. stercoralis and probably contribute to human infections through their faecal contamination of the environment. Cats can become infected but the infection appears to be transitory, the parasites dying after a few months. Other species of Strongyloides occur in monkeys, rodents, sheep and pigs.

Life cycle

Female worms that are extremely slender, measuring about 2 to 2.5 mm long by 40 to 50 µ in diameter, produce eggs parthenogenetically. Each female worm lays slightly less than 50 eggs per day that are deposited in the intestinal mucosa where they undergo development and after hatching the larvae make their way into the intestinal lumen to be expelled with host faeces.

The larvae are rhabditiform, resembling hookworm larvae, only distinguishable by having a very small mouth cavity. Larval development may take either a direct course or an indirect course. Under the direct mode of development, the rhabditiform larvae, after undergoing two moults, transform into infective ensheathed filariform larvae, which then infect the host through skin penetration.

Under the indirect course of development, the rhabditiform larvae deposited with faeces, feed, grow, and after four moults become adult free-living males and females. The females then produce eggs that hatch into rhabditiform larvae, which develop into infective filariform larvae after two moults. These ensheathed filariform larvae appear about 2 days and by day 5 or 6, are numerous in the soil. These larvae infect a new host by skin penetration. There may be more than one free-living generation but this seldom occurs.

Under rare cases, the whole life cycle may take place within the host. Under this so-called hyperinfective mode of development, the rhabditiform larvae produced by parasitic females transform into filariform larvae in the intestinal lumen after undergoing two moults. These then penetrate the host intestinal mucosa, where they develop into adult worms and produce eggs.

The filariform larvae from direct or indirect mode of development that penetrate the skin appear in the lungs three days later and spend sometime there undergoing further growth. They then travel to the small intestine via the tracheopharyngeal route and on arriving in the small intestine, enter the epithelium of the glands. The larvae continue their growth and after moulting twice attain maturity with new larvae appearing in the faeces three weeks post-infection.

Following skin penetration by the larvae, there may be a transient period of cutaneous larval migrans, in which the larvae wander within the subcutaneous tissues before they find their way to the lungs. This causes mechanical damage, intense itching and pain. The passage of the larvae through the lungs causes little reaction in light infections, but in heavy infections, there may be alveolar haemorrhage, oedema, pneumonitis, eosinophilia and coughing.

The presence of adult worms in the small intestine causes little reaction except when large numbers are involved. There is usually moderate leukocyte infiltration and other inflammatory cells. Heavy infections may be accompanied by severe erosion of the intestinal mucosa, which increasingly becomes non-functional, with intense infiltration of inflammatory cells into the submucosa, atrophy of the villi and destruction of large areas of the mucosa. The destructive effect of the infection on the intestinal wall leads to malabsorption and emaciation. Strongyloides stercoralis rarely causes death.

Symptoms

Coughing and pneumonitis follow the migration of the worms through the pulmonary tissue. In rare cases, the filariform infective larvae develop to the adult stage within the lungs causing acute inflammatory reaction. Examination of the sputum reveals the presence of adult worms, filariform, rhabditiform larvae and eggs.

In the intestine, light infections lead to abdominal pain and diarrhoea. The blood picture is characterised by leucocytosis with a moderate to high eosinophilia. Mild to moderate chronic infections elicit symptoms of abdominal pain, nausea, vomiting, and diarrhoea. In severe cases, there may be uncontrollable diarrhoea with blood and undigested food in the stools. The loss of blood and continued fluid drain from the body results in severe emaciation.

Ectopic infections caused by filariform larvae migrating subcutaneously are common with S. stercoralis and are characterised by urticarial creeping eruption of the skin of the buttocks, abdomen and thighs.

Epidemiology

In S. stercoralis infections, rhabditoid larvae rather than eggs are passed in the faeces, and these can mature rapidly in 24 to 36 hours to the infective filariform stage by direct development in faeces, soil or water. Under suitable conditions, indirect development through the free-living adult generation may occur instead and since the progeny of each free-living female is about 30 to 50, this leads to considerable pollution of the soil with larvae.

Strongyloides seems to parallel hookworm in some geographical areas, occurring mainly in warm, humid river basins and coastal areas, and related to poor sanitation. It generally has a lower prevalence than hookworm infection but in some tropical areas such as Brazil andColombia, it appears to be more prevalent and serious than hookworms. It is usually common in institutions like mental hospitals, prisons and homes for retarded children.

Dogs are readily susceptible to human strains of S. stercoralis and probably do play a role in the transmission of the parasite to humans.

Diagnosis

Eggs of S. stercoralis are difficult to find in the stool although adult worms can be detected in fresh stool. Detection of active rhabditoid larvae in the fresh stool confirms presence of strongyloidiasis. Filariform larvae may be found in old faeces that have stayed for a day or more.

Control

Proper disposal of human faeces are a sure way of preventing strongyloidiasis. The same steps required to control hookworm and other intestinal parasites apply to S. stercoralis.

Treatment

Both thiabendazole and albendazole are effective drugs for the treatment of strongyloidiasis.

Hookworm infections

Hookworms are present in most of the countries of the world. Two species of hookworms are parasites of man. These areAncylostoma duodenale and Necator americanus. They differ slightly in structure but have identical life cycles. They also somehow differ in distribution although very often this overlaps. A. duodenale is found mainly in the northern regions -Europe, North Africa, Asia, China and Japan. N. americanus is dominant in the southern United States, Mexico, Central America, the West Indies, South America, East Africa, Central and southern Africa. Nevertheless, the two seem to coexist in much of the continent of Africa. In East Africa, N. americanus is more predominant than A. duodenale.

Hookworms are among the most important parasites of man accounting for thousands of deaths each year. In 1949, the global prevalence of hookworm infection was estimated at 457 million but in 1962, the figure was revised to 600 million. The current estimate puts the number of people infected with hookworms at between 800 million – 1500 million with about 60000 deaths per year.

A. duodenale females measure 12 mm and the males 9 mm long. N. Americanus, on the other hand, is smaller and more slender than A. duodenale with the females being about 10 to 11 mm long. Its vulva, which is anterior to the middle of the body, lacks a spine.

http://histologyatlasforstudent.blogspot.com/The male has a longer and narrower bursa than that of A. duodenale. The buccal capsule of N. americanus is provided with cutting plates unlike that of A. duodenale, which consists of paired tooth-like processes. In both species, the adult worms live in the small intestine attached to the intestinal mucosa by their armed teeth. They feed on blood and other nutrients present in the small intestine. The female N. americanus produces between 5000 to 10000 eggs daily while A. duodenaleproduces about 30000 eggs per day.

Life cycle

The two species of hookworms produce thin-shelled, transparent and ovoid eggs that are indistinguishable. In fresh stool, the eggs are usually in a four–celled stage of development. Under warm, wet temperatures, embryonation proceeds faster and hatching takes place in 24 to 48 hrs. Optimal conditions include good aeration, moisture, shade and a temperature of around 36 ^oC. The emerging tiny rhabditiform larvae feed on bacteria and organic debris, while undergoing growth and after shedding the cuticle, continue to feed and grow bigger. After a period of 5 to 8 days, they cease feeding, shed their cuticles and become third stage infective filariform larvae. The filariform larvae are slender with a closed mouth, an elongated oesophagus and a sharply pointed tail.

Under favourable conditions, the larvae move from the lower parts of the faeces to the surface and to the surrounding vegetation. However, if the sun is too hot, they retreat to the lower parts of the faeces to avoid desiccation. The larvae can remain in the soil for several days, even weeks, depending on the environmental conditions.

Human infection occurs when the infective larva is in contact with any part of the skin. Often it is the hands and feet that are in contact with soil contaminated with human faeces.

The larvae enter the body by penetrating the skin where they remain dormant for 1 to 2 days. The larvae reach the lungs via the blood and enter the air sacs. From the lungs, the larvae migrate to the throat where they are swallowed.

On reaching the small intestine, the larvae, now much larger and in their fourth stage of development, invade the spaces between the villi and moult one more time into sexually mature males and females. Mating ensues and about 6 weeks post-infection, the females start passing out eggs in the faeces. Adult hookworms can live in the human intestine for up to 6 to 5 years, depending on the strain of the parasite and the nutritional status of the host.

Pathogenesis

The penetration of the skin by the larvae is followed by itching and pain at the entry site. The migrating larvae damage the tissues through which they pass, especially the alveolar sacs of the lungs. On reaching the intestine, the worms attach themselves to the mucosal surface of the small intestine by their buccal cavities, puncturing the local blood and lymph vessels in the process. Hookworms feed on blood; the amount of blood lost by the host is dependent on the number of worms present. It has been estimated that each adult worm drinks approximately 1 ml of blood daily.

The important damage produced by hookworms is haemorrhage from the intestinal wall. This is usually proportional to the number of worms present. Counts of less than 50 eggs per gm of faeces are not associated with serious haemorrhage and rarely evoke any clinical symptoms. However, people with more than 200 eggs per gm of faeces, lose a lot of blood and develop anaemia. Hookworm anaemia is typically of microcytic and hypochromic nature.

http://histologyatlasforstudent.blogspot.com/

N.americanus compared with A.duodenale

Useful substances like food nutrients, mineral salts and immunoglobulins are lost through leakage. The picture may further be complicated by a secondary bacterial infection. In addition to loss of blood and other nutrients, a heavy infection impairs the intestinal mucosa causing malabsorption and aggravating the nutritional status in persons who do not have enough to eat and are already malnourished.

The diet is important in influencing the severity of infection. In light and moderately heavy infections, the blood loss can be compensated for by an adequate, well-balanced diet that is rich in minerals, including iron, animal proteins and vitamin A. In severe hookworm disease, however, even with a highly balanced diet, the body is unable to produce new supplies of normal red blood cells as rapidly as they are lost. Moreover, the perennial protein deficiency in the diet of inhabitants of the developing world, does contribute greatly to the anaemia of hookworm patients, whose ordinary diet is predominantly carbohydrate.

In endemic areas infection is acquired in childhood and by the time the individual reaches maturity he will have been exposed to the hookworm infection repeatedly a number of times. For that reason, a large section of the population will have developed some protective immunity. Immune individuals carry fewer worms and do not experience serious symptoms.

Symptoms

Nausea, headache and an irritating cough are the usual symptoms of an acute early infection. The symptoms are mainly caused by larvae migrating through the tissues and lung air sacs. Between 4 and 6 weeks post-infection, the patient experiences severe colicky pains, flatulence, diarrhoea, and loss of weight, dyspnoea, dizziness, and marked paleness. During this period, a significant leucocytosis may persist at a significant level for months.

In severe cases, the haemoglobin may be reduced to 30% or less, with 200 000 or less corpuscles. The most noticeable symptoms are a severe pallor, tiredness, indifference and withdrawal from participating in social activities, enlarged and palpating heart, irregular weak pulse, oedema making the face puffy and pot-bellied abdomen. Children suffer physical and mental retardation, stupidity and backwardness in school.

Epidemiology

Hookworm infection is one of the commonest parasitic diseases in the tropics. It thrives well under warm, moist temperatures and ample rainfall that are needed for the survival of the eggs and development of the larval stages in the soil. Human infection is caused by two species of hookworm - N. americanus and A. duodenale. Wherever these parasites are endemic, they result from unsanitary disposal of human faeces.

The continued propagation of hookworm disease depends largely on the frequency of contact with contaminated soil. People working in fields that have recently been fertilised with human faeces are at risk of being infected whenever the hands or feet touch the soil, while miners in unsanitary underground tunnels may become infected on practically any area of the skin.

Diagnosis

Diagnosis is based on the detection of eggs in faeces. The presence of more than 200 eggs /gm of faeces indicates a severe infection in both Necator americanus and A. duodenale. In general, the latter is more prolific than the latter, usually producing twice as many eggs as the former and causing more damage.

Treatment

A light infection may be treated directly with drugs without prescribing any supportive diet. There may, however, be need to prescribe a diet rich in protein if the patient’s haemoglobin level is low, and iron to replace that lost through haemorrhage caused by the worms. The most effective drugs for treatment of hookworms are mebendazole and pyrantel pamoate.

Control

Proper disposal of human faeces are mandatory to a successful control of hookworm infection. The use of toilets and pit latrines is essential part of the strategy to control transmission of hookworms in order to prevent soil pollution. Where the pollution of the soils with eggs and larvae is deemed high, it might be necessary to use chemicals to disinfect them.

Infected individuals should be treated to clear the infection and allow the damaged intestinal tissue to heal. If the infection is rampant in the population, mass treatment of the entire community should be undertaken at regular intervals. This helps to reduce each individual’s worm load and concentration of eggs in the soil.

In severe hookworm disease, infected persons should be given dietary supplements rich in animal minerals, proteins and vitamin A to reinforce the iron and other minerals lost. As the infection is acquired through the contact of the infective larvae with the skin, particularly the foot, the wearing of shoes reduces the contact with the larvae. It is quite helpful to encourage people, especially children to wear shoes regularly.

Acylostomacraniumfemale -

Trichuris trichura

Trichuris trichura or whipworm derives its name from its whip-like structure, in which the posterior end is thick and the anterior end is thin like a thread. The thick posterior end contains the reproductive organs of the organism. The oesophagus occupies the whole of the anterior end. The male worm measures 30 to 40 mm in length while the female measures between 35 and 60 mm long.

The natural location of Trichuris trichura is the caecum and the lower part of the large intestine.

Trichuris is also found in dogs, pigs and apes. The worm has a cosmopolitan distribution and thrives well under wet, warm conditions. Its distribution is, for the most part, similar to that of Ascaris lumbricoides.

Like all other intestinal nematodes, T. trichura is associated with poverty and ignorance. It is therefore common where the level of poor personal hygiene is low and the general sanitation is poor.

Life cycle

The female worm produces 4000 to 7000 eggs daily. Each spear-like egg is brown with a plug on each end. Under warm wet conditions, the embryonated eggs take about 3 to 6 weeks to become infective. Infection is acquired through drinking water or eating raw vegetables that have been contaminated with the embryonated eggs. Under normal atmospheric conditions, the eggs can remain viable for one to two months, or even longer. Children are particularly vulnerable to infection because of their habits of picking soiled objects and getting their hands dirtied.

After the eggs have been ingested, the larvae hatch in the lower part of the small intestine and the large intestine, penetrate the mucosa of the colon and caecum and undergo development. About 3 months later, mature worms appear and egg production begins.

Pathogenesis

The severity of the infection depends very much on the intensity of the infection and the nutritional status of the individual. Light infections are usually without symptoms. Heavy infections provoke extensive irritation of the mucosa surface of the colon and the caecum, which show evidence of erosion, bleeding and the presence of large numbers of parasites. Observed symptoms are loss of appetite, nausea, diarrhoea, steaks of blood on stools, loss of weight, anaemia, eosinophilia, abdominal discomfort, emaciation and sometimes fever. Heavy infections may also be suggestive of a concomitant hookworm disease or infection with Entamoeba histolytica.

In chronic infections, mucosal irritation of both the colon and the rectum may eventually lead to the prolapse of the rectum.

Children aged 1 to 5 years are frequent victims of trichuriasis and quite often suffer from chronic diarrhoea or dysentery, rectal prolapse and loss of weight. They may also suffer from anaemia of the microcytic type because of lack of adequate nutrition and loss of blood from the affected intestinal mucosa.

Epidemiology

The unembryonated eggs of T. trichura require a shaded soil and warm, moist conditions to develop and after about 4 weeks, a coiled larva can be seen inside the eggshell. The eggs can be ingested with soil or via contaminated hands. The conditions that favour the transmission of A. lumbricoides are the same conditions that favour T. trichura, so that the two are usually found together. It is particularly common in children and, even in localities where the transmission is quite high in the whole population, the incidence and intensity of infection in children remain higher than in the general population.

Diagnosis

Diagnosis is accomplished by the demonstration of characteristic eggs in the faeces. Numerous adult and immature worms are usually attached the mucosal epithelium of a prolapsed rectum.

Control

Effective control measures involve maintenance of high personal standard of hygiene and use of toilets for disposal of human faeces. In addition to the above measures, children in endemic areas should be give regular treatment with mebendazole, which is quite effective and safe.

Ascaris

Ascaris lumbricoides is the largest roundworm of man and mammals. It is a common human parasite in the tropics and subtropics, with a high prevalence in children. It prefers warm, moist conditions and is normally present together with another roundworm, Trichuris trichura.

These are large elongated and cylindrical worms, tapering at the ends. The posterior end of the male is curved ventrally. The male measures 12 - 31 cm long by 3 mm in diameter and the female measures 20 - 35 cm in length by 3 – 6 mm in diameter. A closely related form, Ascaris suum, infects pigs and occasionally humans.

Life cycle

The female worm is highly prolific producing more than 200000 eggs daily. These relatively large and ovoid eggs have thick transparent shells with coarse rough appearance. They are covered by a cuticle that is quite resistant to desiccation and chemicals but shows less resistance to heat, freezing and direct light. If kept in a 10 % formalin solution, the eggs remain viable for weeks.

Favourable conditions for the survival and persistence of viable eggs are moist, well-aerated shady soils, especially loamy soils. In some parts of the world, coffee and banana plants, which are grown around the dwellings, provide ideal conditions for Ascaris and other intestinal parasites.

Unembryonated eggs are passed out in faeces. Embryonation occurs in moist environment and normally takes about two to three weeks. Under favourable conditions of temperature, moisture and air, the eggs develop active embryos, which do not become infective until they have moulted to the second larval stage.

Following the ingestion of the embryonated infective eggs, the larvae are liberated in the duodenum. The larvae penetrate the intestinal wall, enter mesenteric blood veins and lymphatic vessels and reach the lungs, where they spend at least a week. Around the 10th day since hatching, the larvae, which are now quite large, leave the lungs via the tracheal passages to the throat, where they will be swallowed and taken to the small intestine. The third moult takes place in either the lungs or intestine. A final moult that occurs in the small intestine produces mature worms. It has taken at least 8 to 12 weeks since ingestion of the eggs for the worms to become sexually mature and begin mating. Adult worms remain in the small intestine for 9 to 12 months. Quite often, however, they are expelled spontaneously before that.

Pathogenesis and symptomatology

Migrating larvae cause a lot of damage to the liver and the lungs. However, this depends on the numbers of larvae involved. A few larvae will usually provoke no response from the host, especially if it is an initial infection. However, subsequent migrations cause intense tissue reaction in the liver and lungs, even when relatively few larvae are involved.

Headache, muscular pain, pneumonitis consisting of a dyspnoea often of the asthmatic type, a productive cough, wheezing and fever are common symptoms associated with Ascaris infection. During the period of the productive cough, the sputum may contain many eosinophils and larvae. Lesions due to larvae are also found in the spinal cord, brain, and heart muscle.

Infection in children is usually associated with abdominal pain, loss of appetite, listlessness and at times nervous symptoms.

Adult worms in the small intestine frequently provoke no symptoms. However, susceptible individual and people lacking proper nutrition tend to carry heavy parasite burdens and may experience mild abdominal discomfort, lack of appetite, diarrhoea and constipation. A heavy ascarial infection is likely to interfere with the host’s protein nutrition, something of great concern in areas of the world where a protein-rich diet is rare.

Sometimes when disturbed by the drugs or other factors, adult worms tend to migrate forwards or backwards and become entangled with one another and cause obstruction of the intestine, resulting in gangrene and even death. Some of the worms may enter the bile and pancreatic ducts causing jaundice or pancreatic haemorrhage. Worms may enter the appendix and cause appendicitis. But should the worms penetrate the intestine and reach the heart or brain, they can cause death.

An aspect that is more of an embarrassment than injury is when a worm leaves the intestine, wanders up the alimentary canal and creeps out of the nostrils. On rare occasions, larvae have been seen coming out of the lachrymal duct.

Epidemiology

Ascaris is maintained by faecal contamination of the soil. In rural and in congested centres in the developing countries human faeces are usually deposited by small children (and older children during the hours of darkness) in and around the home and since the eggs are quite resistant to desiccation and can remain viable in the soil for months, or even years, the numbers build up in the soil to considerable levels as the time passes. With time, the compound, house floors and even the utensils may be heavily polluted with the eggs of Ascaris and, if the picture is the same in the whole village, the rate of transmission will be high and many people will be infected. With such a high rate of transmission, the intensity of infection in children and other vulnerable groups can be very high indeed.

Human infection is possible in a number of ways. Children can ingestion dirt contaminated with eggs or they may transfer eggs to the mouth via unclean hands. Furthermore, infection may be contracted through eating raw food especially vegetables that have not be cleaned sufficiently, or through drinking water contaminated with faecal matter.

Control Methods

The maintenance of proper sanitary conditions considerably reduces the transmission of infection. This involves the regular use of toilets to prevent soil contamination with human faeces and adhering to personal hygiene by washing hands before eating and eating food that has been properly cooked. Salads that are usually eaten raw should be washed thoroughly.

Mebendazole, pyrantel pamoate and piperazine are effective against ascariasis. All have a wide margin of safety.

Other Ascrids

Ascaris suum is a common pig roundworm that is similar to A. lumbricoides in many ways and is of great economic importance to pig-keepers all over the world. It causes stunting of growth in piglets.

Ascaris suum probably constitutes an occasional source of intestinal ascariasis in man. In some instances, it will develop to adult stage in man. Likewise, A. lumbricoides larvae have been shown to develop in pigs to adult stage.

Other important ascarids include Toxocara canis in dogs, Toxocara cati in cats and Parascaris equorum in horses. The latteris an important parasite of horses throughout the world that inflicts considerable mechanical damage through its migrating larvae on the tissues and lungs of horses, causing pneumonia and even introducing bacteria and viral infections. Like the human Ascaris, adult worms may perforate the intestinal wall, damage the liver and bile ducts and cause general toxaemia from metabolic waste products.