Life history of Ascaris & it's control
Adult female Ascaris lumbricoides .EPIDEMIOLOGY — It is estimated that more than 1.4 billion people are infected with A. lumbricoides, representing 25 percent of the world population. A number of features account for its high prevalence including a ubiquitous distribution, the durability of eggs under a variety of environmental conditions, the high number of eggs produced per parasite, and poor socioeconomic conditions that facilitate its spread. Transmission is enhanced by the fact that individuals can be asymptomatically infected and can continue to shed eggs for years, yet prior infection does not confer protective immunity.
Although ascariasis occurs at all ages, it is most common in children 2 to 10 years old, and prevalence decreases over the age of 15 years. .
Transmission — Transmission occurs mainly via ingestion of water or food (raw vegetables or fruit in particular) contaminated with A. lumbricoides eggs and occasionally via inhalation of contaminated dust. Children playing in contaminated soil may acquire the parasite from their hands. Transplacental migration of larvae has also occasionally been reported. Coinfection with other parasitic diseases occurs with some regularity because of similar predisposing factors for transmission.
Adult worms inhabit the lumen of the small intestine, usually in the jejunum or ileum. They have a life span of 10 months to 2 years and then are passed in the stool. When both female and male worms are present in the intestine, each female worm produces approximately 200,000 fertilized ova per day. When infections with only female worms occurs, infertile eggs that do not develop into the infectious stage are produced. With male-only worm infections, no eggs are formed.
The ova are oval, have a thick shell, a mamillated outer coat, and measure 45 to 70 µm by 35 to 50 µm. The ova are passed out in the feces, and embryos develop into infective second-stage larvae in the environment in two to four weeks (depending upon environmental conditions). When ingested by humans, the ova hatch in the small intestine and release larvae, which penetrate the intestinal wall and migrate hematogenously or via lymphatics to the heart and lungs. Occasionally, larvae migrate to sites other than the lungs, including to the kidney or brain.
Larvae usually reach the lungs by four days after ingestion of eggs. Within the alveoli of the lungs, the larvae mature over a period of approximately 10 days, then pass up via bronchi and the trachea, and are subsequently swallowed. Once back in the intestine, they mature into adult worms. Although the majority of worms are found in the jejunum, they may be found anywhere from the esophagus to the rectum. After approximately two to three months, gravid females will begin to produce ova which, when excreted, complete the cycle.
Adult worms do not multiply in the human host, so the number of adult worms per infected person relates to the degree of continued exposure to infectious eggs over time. Worm burdens of several hundred per individual are not uncommon in highly endemic areas, and case reports of more than 2,000 worms in individual children exist. However the number of eggs produced per female worm tends to decrease as the worm burden increases. It has been estimated that 9 x 10 eggs contaminate the soil per day worldwide.
Life Cycle Figure – Adult worms (1) live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces .(2) unfertilized eggs may be ingested but are not infective. (3) Fertile eggs embryonate and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil).(4) After infective eggs are swallowed, the larvae hatch(5) , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the (6)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(7). 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.
CLINICAL FEATURES — The majority of infections with A. lumbricoides are asymptomatic. However, the burden of symptomatic disease worldwide is still relatively high because of the high prevalence of disease. Clinical disease is largely restricted to individuals with a high worm load. When symptoms do occur, they relate either to the larval migration stage or to the adult worm intestinal stage. Pathophysiologic mechanisms include
- Direct tissue damage
- The immunologic response of the host to infection with larvae, eggs or adult worms
- Obstruction of an orifice or the lumen of the gastrointestinal tract by an aggregation of worms
- Nutritional sequelae of infection
The symptoms and complications of infection can be classified into the following:
1. Pulmonary and hypersensitivity manifestations — Transient respiratory symptoms can occur in sensitized hosts during the stage of larval migration through the lungs.
2. Intestinal symptoms — Heavy infections with Ascaris are frequently believed to result in abdominal discomfort, anorexia, nausea and diarrhea. However, it has not been confirmed whether or not these non-specific symptoms can truly be attributed to ascariasis.
3. Intestinal obstruction — A mass of worms can obstruct the bowel lumen in heavy Ascaris infection, leading to acute intestinal obstruction. The obstruction occurs most commonly at the ileocecal valve. Symptoms include colicky abdominal pain, vomiting and constipation.
4. Hepatobiliary and pancreatic symptoms — Symptoms related to the migration of adult worms into the biliary tree can cause abdominal pain, biliary colic, acalculous cholecystitis, ascending cholangitis, obstructive jaundice, or bile duct perforation with peritonitis.
Ascaris lumbricoides in small intestine – Intestinal obstruction occurs when large masses of Ascaris accumulate.
DIAGNOSIS — The diagnosis of ascariasis is usually made via stool microscopy Other forms of diagnosis are through eosinophilia, imaging, ultrasound or serology examination..
:Microscopy — Characteristic eggs may be seen on direct examination of feces or following concentration techniques. However, eggs do not appear in the stool for at least 40 days after infection; thus, the main drawback of relying upon eggs in feces as the sole diagnostic marker for Ascaris infection is that an early diagnosis cannot be made, including during the phase of respiratory symptoms. In addition, no eggs will be present in stool if the infection is due to male worms only. Sometimes an adult worm is passed, usually per rectum. If an Ascaris worm is found in the feces, a stool specimen can be checked for eggs to document whether or not additional worms are present prior to instituting therapy.
Ascaris lumbricoides in stool – Wet mount of stool (x400) showing the ovum of ascaris lumbricoides.
Treatment consists of choosing the right to drugs, therapy, follow-up and supportive care for patients.
Choice of Drugs — A number of drugs can be used in the treatment of ascariasis. These include: pyrantel pamoate, mebendazole, albendazole, ivermectin, piperazine citrate, and levamizole.
Ascaris lumbricoides expelled following effective drug treatment.
* Pyrantel pamoate — Pyrantel pamoate (11 mg/kg up to a maximum of 1 g) is administered as a single dose. Adverse effects include gastrointestinal (GI) disturbances, headaches, rash, and fever. Parasite immobilization and death occur, although this happens slowly and complete clearance of the worm from the GI tract may take up to three days. Efficacy varies with worm load, but single dose therapy is approximately 90 percent effective in eradicating adult worms [6].
* Mebendazole — Mebendazole (100 mg BID for 3 days or 500 mg as a single dose) is an alternative. Adverse effects include transient GI discomfort, headache, and rarely leukopenia. The three-day regimen is approximately 95 percent effective, and the single dose seems to have similar results.
* Albendazole — A single dose of albendazole (400 mg) is effective in almost 100 percent of cases, although reinfection commonly occurs [39]. Albendazole causes the same adverse effects as mebendazole.
* Ivermectin — Ivermectin causes paralysis of adult worms and is approximately as effective as other available therapies but is not generally used.
* Piperazine citrate — Piperazine citrate (50 to 75 mg/kg QD up to a maximum of 3.5 g for 2 days) was a frequent treatment regimen, but it is now being withdrawn from the market in many developed countries because the other alternatives are less toxic and more efficacious. However, it may still be recommended when there is suspected intestinal or biliary obstruction since this drug paralyzes worms to aid expulsion.
* Levamisole — Levamisole (150 mg for adults and 5 mg/kg for children) is safe and is effective in 77 to 96 percent of cases of ascariasis.
Choice of therapy — The mainstays of treatment currently are the benzimidazoles, mebendazole and albendazole. However, they should not be given during pregnancy because of possible teratogenic effects. Thus, pyrantel pamoate should be used in pregnancy. In a randomized study conducted among 2,294 children aged 6 to 12 years in Zanzibar, single dose mebendazole and albendazole were both found to have efficacies greater than 97 percent . Similar results with both drugs and good tolerability have also been observed in other studies.
Follow-up — All of these therapies act against the adult worm but not the larvae. Following therapy, patients should be reevaluated at two to three months to ensure that no eggs are detectable, either because of inadequate elimination of adult worms or because of reinfection. Reinfection occurs frequently; more than 80 percent of individuals in some endemic areas become reinfected within six months. Evaluation of other family members should be entertained whenever the diagnosis is made because of the propensity of the infection to cluster in families
Supportive care — In addition to specific anthelminthic therapy, supportive therapy for complications of ascariasis may be required, including potential surgical intervention for intraabdominal complications. In biliary infections, conservative therapy with anthelminthics, often combined with antispasmodics, is often successful. However, surgical or endoscopic interventions may be required.
Since pulmonary ascariasis is a self-limited disease, symptomatic alleviation of wheeze and cough with inhaled bronchodilators can be instituted. Occasionally, systemic corticosteroids may be required for symptoms. Following symptomatic therapy, standard therapy for intestinal ascariasis can be given after the worms have developed to maturity in the small intestine [6]. Anthelminth therapy is not usually given at the time of pulmonary symptoms because dying larvae may do more harm than migrating ones.
Biliary ascariasis – An adult Ascaris lumbricoides worm protruding from the major papilla is grasped with forceps during endoscopic retrograde cholangiopancreatography.
Prevention and control of reinfection poses a substantial problem since Ascaris parasites are abundant in soil. Good sanitation to prevent fecal contamination of soil is required. An education program advising against the use of human feces as a fertilizer is also needed in some areas. Soil treatments have been attempted but are generally not practical.
Mass treatments with single dose mebendazole or albendazole for all school-age children every three to four months has been used in some communities. This serves the dual function of treating the children and reducing the overall worm burden in the community. Indeed, mass community therapy has been shown to reduce Ascaris burden and transmission, although it has a greater effect on the intensity of infection than on the overall prevalence. This approach has been shown to be cost-effective. Because reinfections occur so frequently, shorter intervals between treatments have been found to be preferable. Targeted treatment helps control the morbidity of infection but does not have a substantial effect on transmission. In a large randomized trial of school-based deworming performed in Zanzibar, for example, single dose mebendazole, given either twice or three times a year, decreased intensity of A. lumbricoides infection by 63 and 97 percent, respectively, compared to control children who received no mebendazole.
- Khuroo, MS. Ascariasis. Gastroenterol Clin North Am 1996; 25:550
- Seltzer, E. Ascariasis. In: Tropical Infectious Diseases: Principles, Pathogens and Practice. 1st ed, Guerrant, RL, Weller, PF (Eds), Philadelphia: Churchill Livingstone; 1999
- Sarinas, PS, Chitkara, RK. Ascariasis and hookworm. Semin Respir Infect 1997; 12:130
- Reeder, MM. The radiological and ultrasound evaluation of ascariasis of the gastrointestinal, biliary, and respiratory tracts. Semin Roentgenol 1998; 33:57.
- Jones, JE. Parasites in Kentucky: the past seven decades. J Ky Med Assoc 1983; 81:621.
- Tietze, PE, Tietze, PH. The roundworm, Ascaris lumbricoides. Prim Care 1991; 18:25
- Jones, JE. The royal roundworm: Ascaris lumbricoides [11, 80]
- Chu, WG, Chen, PM, Huang, CC, Hsu, CT. Neonatal ascariasis. J Pediatr 1972; 81:783.
Comments
Post a Comment