Ascaris lumbricoides I. Morphology The most common intestinal nematode of man is Ascaris lumbricoides or the giant worm which occurs most frequently in tropics. It is stated that more than 1 billion individuals are affected; 70% of which are from Asia. The specific name of A. lumbricoides is a tribute to its resemblance to the common earthworm which is called lumbricoides. A. lumbricoides is a worm belongs to the so-called “polymyarian type” of somatic muscle arrangement wherein the cells are numerous and project well into the body cavity. The white or pink worm is identified by (1) large size, with males 10 to 31cm and females 22 to 35 cm, (2) smooth, finely striated cuticle, (3) conical anterior and posterior extremities, (4) ventrally curved papillated posterior extremity of male with two spicules, (5) terminal mouth with three oval lips with sensory papillae, and (6) paired reproductive organs in posterior two thirds of female, and a single long tortuous tubule in male. Larvae stimulate the morphology of the adult. The fertilized eggs measure 45 to 70 μ by 35 to 50 μ. There is an outer, coarsely mammillated, albuminous covering that serves as an auxiliary barrier top permeability but may be absent or lost in “decorticated eggs”. The egg proper has a thick, transparent, hyaline shell with a relatively thick outer layer that acts as a supporting structure, and a delicate vitelline, lipoidal, inner membrane that is highly impermeable. At oviposition the shell contains an ovoid mass of unsegmented protoplasm densely impregnated with lecithin granules. The typical infertile eggs, 88 to 94 μ, are longer and narrower than fertile eggs, have a thinner shell with an irregular coating of albumin, and are completely filled with an amorphous mass of protoplasm, with refractile granules. Bizarrely shaped eggs without albuminous coating or with abnormally extensive and irregular coating are also found. The infertile eggs are difficult to identify and may be missed by the unwary and untutored. They are found not only in the absence of males but in about two fifths of all infections, since repeated copulations are necessary for the continuous production of fertile eggs. II. Life Cycle The adult worms normally live in the lumen of the small intestine. They obtain their nourishment from the semidigested food of the host. Male or female worms are found alone in very lightly infected persons. A female worm has a productive capacity of 26 million eggs and an average daily output of 200, 000. The eggs are unsegmented when they leave the host in the feces. Under favorable environmental conditions in the soil, infective second-stage larvae, after the first molt, are formed within the egg shell in about 3 weeks. The optimal temperature for development is about 25°C, ranging from 21°to30°C. Lower temperature retard development but favor survival. At 37°C they develop only to the eight-cell stage. Since eggs require oxygen, their development in putrefactive material is retarded. The infective egg, when ingested by humans, hatches in the upper small intestine, freeing its rhabditiform larva (200 to 300 μ by 14 μ in size), which penetrates the intestinal wall to reach the venules or lymphatics. In the portal circulation larvae pass to the liver and thence to the heart and lungs. The larvae may reach the lungs 1 to 7 days after infection. Since they are 0.02 mm in diameter and the pulmonary capillaries only 0.01 mm in diameter, they break out of the capillaries into the alveoli. Occasionally some reach the left heart by the pulmonary veins and are distributed as emboli to various organs of the body. In the lungs the larvae undergo their second and third molts. They migrate or are carried by the bronchioles to the bronchi, ascend the trachea to the glottis, and pass down to the esophagus to the small intestine. During the pulmonary cycle the larvae increase fivefold, to 1.5mm in length. On arrival in the intestine they undergo a fourth molt. Ovipositing females develop about 2 to ½ months after infection, and they live from 12 to 18 months. Figure 1. Life Cycle of Ascaris Lumbricoides III. Epidemiology Ascaris lumbricoides has a cosmopolitan distribution. Over one billion people globally are estimated to have Ascaris, and at least 20,000 die annually, mostly children. The risk of infection exists whether fecal disposal is adequate. The disease remains endemic in many countries of South Asia, Africa, Central and South America. A. lumbricoides is a prominent parasite in both temperate and tropical zone, but is more common in warm countries and more prevalent were the sanitation is poor. In many countries, Philippines included, the prevalence may reach 80%. Ascaris occurs at all ages, but it is most prevalent in the 5- to 9-year-old group of preschool and young school children, who are more frequently exposed to contaminated soil than are adults. The incidence is approximately the same for both sexes. The poorer urban and the rural classes, because of heavy soil pollution and unsatisfactory hygiene, are most afflicted. Infection is a household affair, the family being the unit of dissemination. Infected small children provide the chief source of soil contamination by their promiscuous defecation in dooryards and earthen-floored houses, where the resistant eggs remain viable for long periods. The infective eggs are chiefly transmitted hand-to-mouth by children who have come in contact with contaminated soil directly, through playthings or through dirt eating. In districts of Europe and in the Far East, where night soil is extensively used for the fertilization of market gardens, human infection in all ages is also derived from vegetables. Drinking water is rarely a source of infection. Ascaris eggs are susceptible to desiccation, although they are more resistant than are Trichuris eggs. A moisty, loose soil with moderate shade provides a suitable environment. Dryness is unfavorable for survival. The eggs are destroyed by direct sunlight within 15 hours and are killed at temperatures above 40°C, perishing within an hour at 50°C. Exposure to -8°C to -12°C, although fatal to Trichuris eggs, has no effect on Ascaris eggs, which, in the soil, can survive the ordinary freezing temperatures of winter. Eggs are resistant to chemical disinfectants and can withstand temporary immersion in strong chemicals. They survive for months in sewage or night soil, fecal matter, or even in the 10% formalin solution used for preservation. IV. Pathology and Symptomatology The usual infection, consisting of 5 to 10 worms, often goes unnoticed by the host and is discovered only on a routine stool examination or by the discovery of an adult worm passed spontaneously in the stool. The most frequent complaint of patients infected with Ascaris is vague abdominal pain. An eosinophilia is present during the larval migration, but patients harboring the adult worms may exhibit little or no eosinophilia. During the lung migration, the larvae may produce host sensitization that result in allergic manifestations, such as pulmonary infiltration, asthmatic attacks, and edema of the lips. Some instances of Loeffler’s syndrome and tropical eosinophilia have been attributed to migrating Ascaris larvae. Koino ingested 2000 embryonated Ascaris eggs of human source at one time and thereby demonstrated that large numbers of larvae simultaneously migrating through the lungs may cause a serious hemorrhagic pneumonia. In Nigeria, Fiske attributes the high bronchopneumonia rate in children of over 5 months of age to the migration of Ascaris larvae. Serious and sometimes fatal effects of ascariasis are due to the migrations of the adult worms. They may be regurgitated and vomited, escape through the external nares, or, rarely, be inhaled into a bronchus. Many instances of invasion of the bile ducts, gall bladder, liver, and appendix have been reported. They may occlude the ampulla of Vater and cause acute hemorrhagic pancreatitis. The worms may carry intestinal bacteria to these sites and stimulate the production of abscesses. The worms may penetrate the intestinal wall, migrate into the peritoneal cavity, and produce peritonitis. Continuing their migration, they may come out through the body wall, usually at the umbilicus in children and the inguinal region in adults. Intestinal volvulus, intussusception, and obstruction may also result from Ascaris infection. Fever and certain drugs are two of the causative factors of Ascaris migration.Even when the worms cause little or no traumatic damage, the byproducts of living or dead worms may rarely produce marked toxic manifestations in sensitized persons, such as edema of the face and giant urticarial, accompanied by insomnia and loss of appetite and weight.Young pigs infected with Ascaris do not gain weight normally, and it is likely that the human Ascaris may affect undernourished children similarly. This action may be due to the food actually consumed by the worms, or production of substances that interfere with the digestive process, or simply by reducing the appetite of the host. V. Diagnosis Clinical diagnosis of the Ascariasis is rather inaccurate because the signs and symptoms are quite vague and are indistinguishable from those of other intestinal nematode infections or from non-parasitic infections. Hence, the clinical diagnosis of Ascariasis should be confirmed or established by microscopic examination of a stool sample. The disease should be highly suspected in children who reportedly past out the worm in their feces. In laboratory, the usual techniques used to diagnose ascariasis consist of the finding eggs in the feces using the following techniques: 1) Direct Fecal Smear (DFS) – wherein about 2 mg feces is emulsified in a drop of NSS on a glass slide. A cover slip is placed and it is examined under a microscope using a low power microscopic lens. 2) Kato-technique or cellophane thick smear method- where the amount of the fecal sample used is from 20 to 60 mg. This Kato-technique is purely a qualitative method and is recommended for the mass examination of the feces for Ascaris infection diagnosis. 3) Kato-Katz Technique – This is a modified Kato-technique because of the feces to examined is measured hence it is used to quantify the number of eggs found in the fecal sample. It is therefore a quantitative technique and can be used to determine egg reduction rate after treatment and to enable one to make egg counts of the parasite per gram of feces. This technique can be used in determining the intensity of Ascaris infection. There is no doubt tat the DFS is less sensitive compare to Kato and Kato-Katz techniques. The last two methods are useful for both individual and mass screening in schools or in the community. Aside from being locally available, these two methods are low-cost and easy to maintain VI. Treatment Ideally all individuals found positive for Ascaris eggs in the stool should be treated to avoid serious allergic reactions and other life threatening complications. Individual infections are cured by a single dose if any of the broad spectrum anthelminthics such as: albenzole, mebendazole, pyrantel pamoate and Piperazine Citrate. Albendazole (Albenza, Zentel), a nitroimidazole that binds irreversibly to tubulin, blocking microtubule assembly and inhibiting glucose uptake by the worm, is now considered the drug of choice in treatment if Ascariasis and all of the intestinal roundworms with the exception of Strongliolydes, A single oral dose of 400 my (200 mg for children under 2 years of age) is highy effective. Side effects are minimal, consisting of diarrhea and abdominal pain. Hypersensitivity to albendazole has been reported, but is rare. Mebendazole (Vermox) has the same side effects and much the same spectrum of activity against intestinal roundworms as dose albenazole, but it must be administered at the rate of 100 mg orally twice daily for 3 days. Alternatively, pyrantel pamote (Antiminth), a pyrimidine, may be administered in a single dose of 11 mg/kg body weight (maximum dose 1g). It depolarizes the myoneutral junction in the worms, paralyzing them in a spastic condition. Occasional side effects of headache, dizziness, fever, nausea, and vomiting occurs; abdominal cramps and diarrhea may be seen. The drug is ineffective in Stronglyoidiasis and Trichuriasis. When Ascaris worms obstruct the sphincter of Oddi or migrate up the biliary tree, producing acute abdominal pain suggestive of the passage of the gallstone, pancreatitis or cholangitis may result, and surgical or endoscopic removal of the worms has been necessary. Biliary Ascariasis is a regular encountered complication in China, where traditional Chinese medicine, using nonoperative procedures including herbal prescriptions, is used in treatment. Ninety-five percent of 9192 diagnosed cases of biliary ascariasis were successfully treated by such noninvasive procedures (Zhou et al., 1999). Intestinal obstruction due to ascarids is treated by nasogastric suction until vomiting is controlled. One or 3 hours after suction is discontinued, an anthelmintic may be administered through the nasogastric tube, which is allowed to remain in place. Although albendazole, also available as oral suspension, would seem the logical choice for treatment of this complication, we have seen no publish reports of its use, and its proclivity to stimulate migartry activityon the part of the worms might be a reason to not ued it in a patient who is obstructed. The present recommendation is to treat with initial doze of Piperazine. Piperazine citrate is safe and very effective in ascariasis; a single dose will cure 75% to 85^ of the infections. A dose on 2 consecutive days will eliminate approximately 95% of the infections. Piperazine can be given at any time of day, since the presence of food in the digestive tract has little, if any, effect on its activity against Ascaris. Purgation is not required. The dosage schedule is a 2-day course of 75 mg per kg orally (max. of 3.5g) daily. Piperazine acts on the transmembrane potential of Ascaris muscle, temporarily relaxing it. The worm thereby loses its urge to move upstream and to press against the sides of its host’s intestine in order to maintain its position. Peristalsis carries the worm out while it is relaxed. Piperazine citrate syrup has been used successfully for the medical treatment of partial intestinal obstruction secondary to ascariasis, combined with abdominal decompression with a Levin tube and supportive therapy. If, in addition to Ascaris, hookworms are also present, mebendazole or pyrantelpamoatemay be used, since they are effective against both parasites. They are used in the same dosage as for hookworm; ie, 3 days at 100 mg b.i.d. daily for the former, and a single 11 mg per kg dose for the latter. VII. Prevention Since Ascariasis is essentially a household and dooryard infection and is intimately associated with family hygiene, prophylaxis depends upon the sanitary disposal of feces and upon health education. Anthelmintic treatment is ineffective because of repeated reinfection in endemic areas. Mass chemotherapy must done periodically, two to three times per year with children as target population. Studies show that treatment of children alone in the community has te same effect as treating everybody. The Prevention and Control is difficult because of ignorance, poverty, and inertia among the place most afflicted. The installation of a latrine, 4 to 6 feet deep, is ineffective unless accompanied by an educational campaign designed to promote its use, especially by children. This educational program calls for the concerted efforts of schools, civic organizations, home economics educators, and public health workers. Night soil should not be used as fertilizer unless treated by compost manuring or chemicals.
