GEOGRAPHICAL RANGE SCIENTIFIC CLASSIFICATION. Super Family Ascaridoidea

Transcription

1 SCIENTIFIC CLASSIFICATION Kingdom Phylum Class Animalia Nematoda Secernentea Subclass Order Rhabditida Ascaridida Super Family Ascaridoidea Family Genus Ascarididae Ascaris Species lumbricoides GEOGRAPHICAL RANGE Ascaris lumbricoides infections have been reported in more than 150 countries across the globe, particularly in tropic, subtropic and temperate regions. Approximately 1.4 billion people worldwide are infected, 4 million of whom live in the United States. As an obligate internal parasite of humans, Ascaris lumbricoides can theoretically be found wherever humans are present. The highly durable eggs can remain dormant in the soil for upto 10 yrs and are resistant to many adverse conditions(chong, 2003; Dora-Laskey et al. 2009; Khuroo,1996) HABITAT The roundworm, Ascaris lumbricoides is an obligate internal parasite and adults usually reside in the small intestine of humans, specifically the jejunum.

2 The life cycle involves no free-living stages or intermediate hosts, although fertilized eggs require up to 3 weeks of embryonation in soil before becoming infective and can survive for up to 10 years in soil under warm, moist conditions. As part of the life cycle, larva briefly migrate via the circulatory and lymphatic systems through the liver, heart and lungs. MORPHOLOGY Ascaris lumbricoides is characterized by its great size. Males are 2-4mm in diameter and 15-31cm long. The males posterior end is curved ventrally and has a bluntly pointed tail with a pair of spicule. Females are 3-6mm wide and cm long. In both sexes, the mouth is surrounded by one dorsal and two ventrolateral lips. The posterior end of the female is straight. The didelphic female reproductive system is located in the posterior third of the body length with the vulva located in the anterior end and accounts for about a third of its body length. EGG OF ASCARIS LUMBRICOIDES Fertilized eggs are oval to round in shape and are µm long and µm wide with a thick oter shell. Unfertilized eggs measure 88-94µm long and 44µm wide (Roberts Larry S, Janovy and John Jr,2009) The female lay eggs in the duodenum which are evacuated with faeces. Both unfertilized and fertilized eggs are passed in stool. Often only female worms are recovered from the intestine. Fertilized eggs passed in stool become infective within 2 weeks in warm, moist soil, where they can remain viable for months or even years. The total absence of fertilized eggs means that only female worms are present in the intestine. SOURCE OF INFECTION FOR HUMAN & TRANSMISSSION The source of transmission is from soil and vegetation on which faecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human

3 faeces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves bt a different type of roundworm can cause infection with that type of worm (Toxocaracanis, etc.) As occasionally occurs with groomers. Transmission also comes through municipal recycling of wastewater into crop fields. This is quite common in emerging industrial economies, and poses serious risks for not only local crop sales but also exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable wxports ( Pawlowski ZS, Schultzberg K, 1986) LIFE CYCLE 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 occur, infertile eggs that do not develop into the infectious stage are produced. With male-only worm infections, no eggs are formed. 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, incluing 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

4 endemic areas, and case reports of more than 2,000 worms in individual children exist (Reeder MM, 1998) CLINICAL SPECTRUM 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 (Khuroo MS, 1996). When symptoms do occur, they relate either to the larval migration stage or to the adult worm intestinal stage. Symptoms and pathogenesis attributed to 1. The host immune response 2. Effects of larval migration 3. Mechanical deficiencies caused by the presence of adult worms. The first symptoms produced are respiratory, due to passage of larvae through the lungs leading to benign pneumonitis- Loeffler s syndrome. Main symptoms in children are abdominal pain, loss of appetite and failure to thrive. LOEFFLER S PNEUMONIA: Initial passage of larva through liver and lung generally produces no symptoms, pneumonitis occurs with very large number of larvae. Subsequent larval migrations lead to intense tissue reactions even with a smaller number of larvae. Pronounced tissue reactions around the larvae in liver and lungs, with infiltration of eosinophils, macrophages and epitheloid cells leads to ascaris pneumonitis, which is accompanied by allergic dyspnoea, dry or productive cough, wheeze, fever. Sputum contains eosinophils, Charcot-Leyden crystals, and sometimes may even contain larvae. If needed gastric washings are more helpful in detection of larvae. Asthma and urticaria may continue during the intestinal phase of ascariasis. Allergic manifestations (asthma, hives, peripheral eosinophilia) begin with the 10-day pulmonary phase but continue into the intestinal phase. INTESTINAL MANIFESTATIONS: The main symptoms in children are abdominal pain, anorexia and failure to thrive. Heavy infestations may lead to the protrusion of abdomen. EOSINOPHILIC GASTROENTERITIS: Signifies the inflammatory disease characterized by eosinophilic infiltration of the gastrointestinal tract accompanied by varying abdominal symptoms and usually by peripheral eosinophilia.

5 NUTRITIONAL COMPLICATIONS: in the under-five child heavy burden of worms may lead to severe nutritional impairment. Studies have shown increased loss of faecal fat and nitrogen and impaired carbohydrate absorption, which correspond to worm load. Lactose malabsorption is common and deficiency of vitamin A and vitamin C also occurs. The long-term effect of impaired nutrition is growth retardation of growth and development. EDUCATIONAL ACHIEVEMENT: An association between helminthic infection and educational achievement has long been recognized. Antihelminthic treatment has resulted in improvement in test scores, learning ability, concentration and eye-hand coordination in the affected children. Ascariasis has been shown to be associated with lower test scores in language, social-, gross motor-, and fine motor- skills. Malnutrition associated with intestinal helminthiasis is an important contributory factor for increased prevalence of developmental disabilities in the developing world. WANDERING WORM: Ascaris has a propensity to migrate from its usual habitat, duodenum to other areas. Worm migration is stimulated by fever, general anaesthesia, other abnormal conditions, or the need fo the female worm to copulate or postmortem state of the worm. They may enter the stomach and lead to vomiting or traumatic bleeding. Worms may enter a nasogastric tube and block it. Worms may ascend the oesophagus and reach epiglottis and hence to upper repiratory tract leading to respiratory difficulty (stridor, cyanosis, dyspnoea ). It has even caused cardiac arrest. Worms have come out of the nose or lachrymal duct. They may enter the Eustachian tube and lead to perforation of the lymphatic membrane, and exit through the ear. Worms have strayed into paranasal sinuses. Migration into lower intestine is the most frequent and most important complication. A tangled mass of worms moves from the duodenum to lodge in the ileocaecal valc\ve, especially in the under-fives. This leads to vomiting, abdominal pain and distension, constipation and partil or total obstruction on plain x-ray abdomen. They may enter the appendix or Meckel s diverticulum and lead to obstruction, symptoms and signs of appendicitis, sometimes with perforation and peritonitis. Intestinal obstruction is the single most common complication accounting for 38-88% of all complication. The complication is commoner in young children. Case fatality ranges widely, and may exceed 8%. Pancreatic duct is easily accessed, leading to pancreatitis with severe, acute abdominal pain, tenderness and raised serum amylase levels. Pancreatic strictures may occur. Worms can enter the bile duct, the gall bladder and the intrahepatic biliary tree. They may cause biliary lithiasis, acute cholecystitis or acute cholangitis. They may reach the liver parenchyma and cause hepatic ascariasis. They may carry various pathogens on

6 their surface which may prove disastrous in immuno-compromised host. Liver abscesses may perforate into the pleural cavity, the lungs and the pericardium. In one case, 60 adult worms were surgically removed from the liver of a patient suffering from acute obstructive cholangitis. In endemic areas, ascariasis should be considered in any child with hepatobiliary symptoms. The worm may move to the peritoneal cavity through intestinal ulcerations. Rarely the worm may itself perforate the intestine. The female worm lays eggs which prouce a granulomatous inflammation and itself dies leading to a large abscess. Clinically it presents as a tumour like mass anywhere in the abdomen. Peritonitis is often fatal since there is secondary bacterial infection. Post- surgery the may wander into the peritoneal cavity or come out of the sutures of the skin wound. Unusual migrations: Worms may enter any tube or opening. They have entered nasogastric tubes, T-tubes, fistulas between intestine and the ureter, sinus tracts in the gluteal region, fistula of ulcerated inguinal hernia etc. They may pass out from the mouth, nose, ear, or even eye. They have been found to pass into the placenta and even recovered from the intestine of the delivered baby. Postmortem migrations: After its death the worm can go to any place it could visit during life. However, absence of inflammatory changes in the visited organ exclude premortem migration. Inside the intestine, adult worms when scant usually cause no difficulty. However, because of the tendency of the adult worm to migrate, even a single worm can cause serious sequelae. Wandering worms may move to any organ of the gastrointestinal system (including liver, biliary tract, gall bladder, pancreatic duct, appendix) or to the peritoneal cavity. they may come out of the anus, mouth, nose. Unexpected body sites as kidney or pleural cavity have been involved (Bashir Gaash, ) THE COMPLICATIONS OF INFECTION CAN BE CLASSIFIED INTO THE FOLLOWING: 1. Pulmonary and hypersensitivity manifestations 2. Intestinal symptoms 3. Intestinal obstruction 4. Hepatobiliary and pancreatic symptoms 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

7 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 infections does not confer protective immunity (Seltzer E, 1999) 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. Infections tend to cluster in families, and worm burden correlates with the number of people living in a home. (Haswell-Elkins M, Elkins D and Anderson RM. 1989) The highest prevalence of ascariasis occurs in tropical countries where warm, wet climates provide environmental conditions that favour year-round transmission of infection. This contrasts to the situation in dry areas where transmission is seasonal, occurring predominantly during the rainy months (Warren KS and Mahmoud AA, 1977) The prevalence is also greatest in areas where suboptimal sanitation practices lead to increased contamination of soil and water. The majority of people with ascariasis live in Asia (73 percent), Africa (12 percent) and South America (8 percent), where some populations have infection rates as high as 95 percent (Sarinas PS and Chitkara RK, 1997, Reeder MM, 1998) In the United States the prevalence of infection decreased dramatically after the introduction of modern sanitation and waste treatment in the early 1900s (Jones JE, 1983) It is estimated that the current prevalence of A.lumbricoides in stool samples is approximately two percent in the United States, but it may be more than 30 percent in children between the ages of one to five years, particularly in rural areas of the South (Tietze PE and Tietze PH, 1991; Jones JE, 1981). It is also seen th travelers from endemic areas (Sarinas PS and Chitkara RK, 1997) The eggs are resistant to usual methods of chemical water purification but are removed by filtration or by boiling. Developing larvae will be destroyed by sunlight and dessication. There is no significant animal reservoir, but A. suum, which infects pigs, is morphologically similar to A. lumbricoides, and the larval forms can occasionally infect humans. WHO estimated that more than 1.4 billion people are infected with Ascaris Lumbricoides representing about 25% of the world population.

8 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 faces or following concentration techniques. However, eggs do not appear in the stool for at least 40 days after infection, thus the main deawback of relying upon eggs in faces as the sole diagnostic marker for Ascaris infection is that an early diagnosis cannot be made, including during the phase of respiratory symptoms. EOSINOPHILIA : peripheral eosinophilia can be found, particularly during the phase of larval migration through the lungs but also sometimes at other stages of Ascaris infection (Weller PF, 1992). Eosinophil levels ar usually in the range of 5 to 12 percent but can be as high as 30 to 50 percent. Serum levels of lgg and lge are also often elevated during early infection. IMAGING : in heavily infested individuals, particularly children, large collections of worms may be detectable on plain film of the abdomen. The mass of worms contrasts against the gas in the bowel, typically producing a whirlpool effect (Reeder MM, 1998) Radiologic detection of adult worms is sometimes made by detecting elongated filling defects following barium meal examinations of the small bowel. The worms also sometimes ingest barium, in which case the alimentary canal appears as a white thread bisecting the length of the worm s body (Reeder MM, 1998), Radiographs will also show when there is associated intestinal obstruction. ULTRASOUND : ultrasound examinations can help to diagnose hepatobiliary or pancreatic ascariasis.single worms, bundles of worms, or a pseudotumor-like appearance may be seen (Scjulman A, 1998) Individual body segments of worms may be visible, and on prolonged scanning, the worms will show curling movements (Makde HM and Chadha D, 1993) Computed tomographic (CT) scanning or magnetic resonance imaging (MRI) may also be used to identify worm(s) in the liver or bile ducts, but this is not usually necessary. SEROLOGY : infected individuals make antibodies to A. lumbricoides which can be detected. However, serology is generally reserved for epidemiologic studies rather than in the diagnosis

9 in a particular individual (Seltzer E, 1999) lgg antibodies are not protective against infection (Mc Sharry C, Xia Y, Holland CV and Kennedy MW, 1999). Antibodies to Ascaris also often cross react with antigens from other helminthes. TREATMENT Treatment consists of choosing the right drugs, therapy, follow-up, and supportive care for each patient. 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. PYRANTEL PAMOATE : Pyrantel pamoate (11 mg/kg to a maximum 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 (Warren KS and Mahmoud AA, 1977) MEBENDAZOLE : mebendazole (100 mg BDI for 3 days or 500 mg as a single dose) is an alternative. Adverse effects include transient GI discomfort, headache, and rarely leucopenia. 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 (Norhayati M, Oothuman P, Azizi O and Fatmah MS, 1997). 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 ibstruction since this drug paralyzes worm to aid expulsion. LEVAMISOLE : levamisole (150 mg for adults and 5mg/kg for children) is safe and is effective in 77 to 96 percent of cased of ascariasis.

10 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 rendomixed 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 the 97 percent (Albonilo M, Smith PG & Hall A et al. 1994). Similar results with both drugs and good tolerability have also been observed in other studies. (Jongsuksuntigul P et. Al. 1993; Bartoloni A et. Al. 1993, Maipanich W et. Al. 1997) 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 (Warren KS and Mahmoud AA, 1977) closely associated with those geohelminths that inhabit the small intestines namely Ascaris lunbricoides (1,4), Hookworm(5) and strongyloides stercoralis(5) of which A.lumbricoides is the most prevalent (6) P(1)