Ascaris Lumbricoides is the largest of the parasitic round worms found in the human intestinal track which causes a disease known as Ascariasis. It is the third most frequent helminth infection (Adeoye, 2007). Ascaris Lumbricoides is a common nematode infecting human worldwide with increased prevalence in tropical and subtropical area of less developed countries especially in places with poor sanitations and where untreated human faeces are used as fertilizers. It is spread by faecal pollution of the environment.
Ascaris Lumbricoides, worms that are matured lives freely in intestine. Fertilized female worms produce many eggs per day which remain viable in the soil for several years. Ascaris Lumbricoides can mostly be found among children of 3-8 years. Large heavily infected, when fingers become contaminated while playing on an open ground. The infection occurs in all ages but mostly prevalence in the 5-9 years old children, who are frequently exposed to contaminated soil than adults (Franklin and Harold, 2005).
The distribution of Asaris Lumbricoides in Africa were assessed, it is estimated that about 54 million are children less than 15 years old. Infection with this round worm is extremely common, it is also estimated that one quarter of the world‘s population is infected, of 1500 million cases per year. Ascaris live in people’s body, and the adult round worm is found in the lumen of the small intestine of humans. They do well living in people’s body because they are 200,000 new ones born per day for a year. They can live for 3 years in the human body (Garrett, 2008).
Ascaris Lumbricoides endangers children’s health in a subtle and debilitating way; chronic infections compromise healthy growth, cognitive development, physical fitness, iron status and affect immune response of infected children.
Ascaris Lumbricoides, a morphologically indistinguishable species Ascaris suum is found in pig, other related general include parascaris in equines and toxascaris in a variety of domesticated animals. The round worm’s eggs are “sticky” and may be carried to the mouth by hands or other body parts, or food. Ascaris Lumbricoides produces a pepsin inhibitor so we cannot digest it and it also uses muscular activity that prevents it from being excreted.
A large population of people especially children carrying this worm remains undetected for years until they develop some symptoms such as abdominal pains, vomiting, etc. Due to a large group of asymptomatic individuals with intestinal ascariasis, these worms are occasionally and unexpectedly identified during routine endoscopic procedures (Khuroo, 2006) and with the aid of simple microscope.
Ascaris Lumbricoides is the giant round worm of humans, growing to a length of up to 35 cm (Aaron, 2008). An ascaris nematode of the phylum Nematode, it is the largest of the most common parasite worm in humans responsible for the disease ascariasis, a type of helminthiasis. One – sixth of the human population is estimated to be infected by A. Lumbricoides or another round worm (Harhay, 2010). Ascariasis is prevalent worldwide, especially in tropical and sub-tropical countries.
According to Williams (2004) infection are usually asymptomatic especially of the number of worms of are small; they may however be accompanied by inflammation, fever, diarrhoea, and serious problem may develop, if the worms migrate to other part of the body, perhaps as many as one quarter of the world’s people are infected.
An estimated 807 – 1,221 million people in the world are infected with Ascaris lumbricoides (sometimes called just “Ascaris”). Ascaris, hookworm and whip worm are known as soil- transmitted helminths. (Parasitic worms) together, they account for a major burden of disease worldwide. Ascariasis is now uncommon in United States. Ascariasis occurs in rural areas of the south eastern United States. In the United State ascariasis is the third most frequent helmith infection, exceeded only by hook worm and trichurus trihuria (Whip Worm) (Khuroo, 2006).
Ascaris Lumbricoides is the largest intestinal nematode of man. The females’ worms are larger than that of the males and can measure 20-40 cm in length and 6 mm in diameter. They are white or pink and are tapered at both ends. The parasite, it infects only humans although ascaris worms are found in people of all ages, children are mostly likely to be heavily infected, if only few worms are present. They may be on symptoms initially, but during the migrating phase, the larvae may penetrate in the tissue and circulate around the body through the blood and lymphatic systems, commonly to the lungs. In the lungs the larvae penetrate the pulmonary capillaries to enter the alveoli, from which ascend into throat and descend back into the gut where they may grow as large as length (Dold, 2011). Adult worms generally eat the food of their hosts, but heavy infection causes tangles of worms which can obstruct the gut. Clinical infections are typically found in young individuals although older individual may serve as source of infection.
Ascaris Lumbricoides, a round worm, infect human when an ingested fertilized egg become a larvae. Worm that penetrates the wall of the duodenum and enters the blood streams from there, it is carried to the liver and heart, and enters pulmonary circulation to break free in the alveoli, where it grows and molts in three weeks, the larvae pass from the respiratory system to be coughed up, swallowed and thus returned to the small intestine, where they mature to adult male or female worms. Fertilization can now occur and the female produces as many as 200,000 eggs per day for a year. These fertilized eggs become infections after two weeks in soil; they can persist in soil for 10 years or more (Murray and Patrick, 2005). The eggs have a lipid layer which makes them resistances to the effects of acids and alkalis as well as other chemicals. This resilience helps to explain this nematode in such ubiquitous parasite (Piper, 2007).
Species: A. Lumbricoides
Epidemiology / prevalence
It is estimated that more than 1.4 billion people are infected with A. lumbricoides representing 25% of the world’s population. A number of features account for its high prevalence including a ubiquitous distribution, the durability of egg under a variety of environmental conditions, the high number of eggs produced per parasite and poor socio economic 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 (Seitzer, 2005). Roughly 1.5 billion individuals are infected with these worms primarily in Africa and Asia (Crompton, 2004)
According to Silva (2004), prevalence of ascariasis is the highest in western pacific region (705 millions) followed by South – East Asia (237 millions) and Africa (173 millions) ascaris is endemic with high prevalence due to their temperate climate. In another study cited in Agwu and Salako (2007), the rate of intestinal parasitism among Almajiris as 80.9% include Ascaris lumbricoides this prevalence in the South – South Nigeria (67.2%) South Eastern Nigeria (55.2%) and South – West Nigeria (28%) and this was due to some factors like low socio economic conditions characterized by inadequate water supply and poor sanitary disposal of faeces.
Damen, et al (2011), stated that in Kenduga Borno State Nigeria, a prevalence of 19.16 was obtained. The study also stated that age group 6-8 years had the highest prevalence of 85.76 child age group of 13-16 years has the least prevalence of 77.7%. The predisposing factors where because of indiscriminative disposal of human waste and unhygienic way of life, lack of potable water, proper system of refuse and human waste disposed also contributed. The predominant prevalence of Ascaris in the study is also similar to those of Eneaya, and Anikwe (2005), who stated that Ascaris is dominant among children between the ages of 6-10 years older.
The report of Uneke, et al (2006), showed a prevalence of 10.86. It also stated that males were more infected than females (18.3% vs 15.5%) and the age group of 4-6 years had more Ascaris lumbricoides. This is because of poor local level of environmental sanitation and personal hygiene.
The report of Houmosou, et al (2009) showed the prevalence of Ascaris Lumbricoides to be 16.1%. This parasite was found in all the age groups and in both sexes equally. However, the ascaris lumbricoides was more prevalent within the ages of 4-10 years as compared to 11-20 years. This is because the ages less 10 years play more outdoors and more in contact with sand and eat indiscriminately with unwashed hands. The study of Ikon and Useh (2009) showed that the distribution of parasite among sex groups showed that more males are affected than females during an epidemiological study of gastrointestinal parasite away urban and sub-urban communities.
However another study showed that school children in Igbo – Eze South Local Government Area, Enugu State, Nigeria were studied in 2005 the ages of 4-15 years examined for intestinal helminths. And ascaris lumbricoides had the highest prevalence of (9.3%). Hook worm (6.0%) and trichuris trichuria (2.3%). (Ekpenyong and Eyo, 2008).
Also in central school, Ovoko community primary school, Ikeakpa- Awka had a prevalence of ascaris lumbricoides (7.0% ) between the age of 4-6 years and between the sexes female having comparatively more of Ascaris lumbricoides than the males (Ekpenyong and Eyo, 2008).
History of ascaris lumbricoides
The anatomy of A. Lumbricoides was first described by Edward Tyson in 1683. However at this time it was known as Lumbricus teres not A. Lumbricoides. It was actually Linnaeus, who renamed Ascaris and gave it its current name. Linnaeus named the round worm Ascaris Lumbricoides because it showed very similary morphology as that of the earth worm, Lumbricus terrestrials. Then in 1917, Brayton Ranson and Winthrop foster were able to document the actual life cycle of Ascaris afterward in 1922, Simesu Koino experimented on himself and his younger brother in order to describe the clinical disease produced by Ascaris. Koino worked with both A. Lumbricoides and A. Suum. He swallowed 2000. A Lumbricoides eggs, and he made his younger brother swallowed 500. A. Suum larvae. Koino became very ill for the experiment but luckily no lasting damage occurred and his brother did not suffer from as severe a disease specifically, in this daring self experiment, Koino showed that pneumonia like syndrome can develop during early infection with Ascaris. He also discovered that this syndrome was caused by migration of larvae through the lungs to the stomach (Cromptom, 2004).
Means of transmission
Transmission occurs mainly through ingestion of water food (raw vegetables or fruit in particular) contaminated with A. Lumbricoides eggs and occasionally through inhalation of contaminated dust. Children playing in contaminated soil may acquire the parasite from their hands. Transplancetal migration of larvae has also occasionally been reported (Chu, 2004).
Co-infection with other parasitic disease occurs with some regularity because of similar predisposing factors for transmission (Tietze, 2006). Ascaris infection fact sheet stated that transmission from human to human by direct contact is impossible. Pawlowski and Schuctzbeny (2005) stated that transmission also come through municipal recycling of waste water in crops fields. This is quite common in emerging industrial economics and poses serious risks for not only local crop sales but also export of contaminated vegetables. In 1986, outbreak of ascariasis in Italy was traced to irresponsible waste water recycling used to grow ball can vegetable exploits.
Morphology of ascaris lumbricoides
Adult worms: Ascaris Lumbricoides worm are pink or yellow – white in colour. The female is larger (20 – 35 x 0.3 – 0.6 cm) than the male (15 – 30 x 0.2 – 0.4 cm) the tail of the male is curved and has two rodluce projections (spicules) A small mouth is surrounded by three lips.
Fertilized egg: it is round oval measuring 60 x 40 um, yellow – brown in colour and is covered by an outer coarsely mamillated thick aluminous covering. The egg contains a mass of unsegmented embryo densely impregnated with lecithin granules. Sometimes the albuminous coast of the egg may be absent and it may appear pale yellow with a smooth shell. It is described as ‘decorticated’.
Unfertilized egg: it is thinner shell with an irregular coating of albumin and is completely filled with an amorphous mass of protoplasm with large retractile granules (Adeoye, 2007).
Adult worms inhabit the lumen of the small intestine, usually in the jejumum or ileum. They have a life of 10 months – 2 years and then passed in the stool. When both female and male worms are present in the intestine, each female worm produce 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 oval, have a thick shell animillated outer coat and measured 45 to 70 um by 35 to 50 um. The ova are passed out in the faeces and embryo 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 hematogenousely or through lymphatics to the heart and lungs. Occasionally, larvae migrate to sites other than the lungs including the kidney or brain.
Larvae usually reach the lungs by four days after ingestion of eggs within the alveoli of the lungs, the larvae matures over a period of approximately 10 days, then pass up through 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 oesophagus to the rectum after approximately two to three mouth, 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 egg over time. Worm burden of several hundred per individual are not uncommon in highly endemic areas and case report of more than 2,000 worms in individuals children exist (Reeder, 2004).
Swartzman (2006) indicated that the number of eggs produces per female worm tends to decrease as the worm burden increases. It has been estimated that 9 x10 (14) eggs contaminated the soil per day worldwide.
Ascaris Lumbricoides Life Cycle, Nematode (Roundworm)
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, 2006).
When symptoms do occur, they relate either to the larval migration stage or to the adult worm intestinal stage path physiological mechanisms includes:
- Direct tissue damage
- The immunologic response of the host to infection of larvae, eggs, or adult worm (Seltzer, 2005).
- Nutritional sequelae of infection.
The symptoms and complications of infection can be classified into the following:
- Pulmonary and hypersensitivity manifestations
- Intestinal symptoms
- Intestinal obstruction
- Hepatobiliary and pancreatic symptoms
Pulmonary and hyper sensitivity manifestations:
Transcent respiratory symptoms can occur in sensitized hosts during the stage of larval migration through the lungs. Symptoms associated with the pneumonitis, which are known as coffler’s syndrome, tend to occur one to two weeks after ingestion of the eggs. The severity of symptoms tends to correlate with larval burden, but pulmonary symptoms are also less common in countries transmission of A. Lumbricoides. Urticaria and other symptoms related to hypersensitivity usually occur towards the end of the period of migration through the lungs.
Heavy infections with Ascaris Lumbricoides are frequently believed to result in abdominal discomfort, anorexia, nausea, and diarrhoea. However, it has not been confirmed whether or not these non specific symptoms can truly be attributed to ascariasis.
With relatively heavy infections impaired absorption of dietary proteins, lactose and vitamin A. has been noted and steatorrhea may occur one review concluded that ascaris free or treated children showed better nutritional status in terms of growth, lactose, tolerance, vitamin A and C and albumin levels than Ascaris infected children based upon almost 20 years of published cross sectional and interpretation studies from Africa, Asia and South American (Hlaing, 2005).
This review also found significant improvement in weight or height following therapy for Ascariasis but this is not in line with other studies, and the true effect of ascariasis on nutrition is still widely debated, especially as additional nutritional deficiency common co-exist in infected children (Ahpta, 2008).
It has also been proposed that heavy infectious may be associated with impaired cognitive development in children (Hadidjaja, 2008).
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 value. Symptom include: coliday, abdominal pain, vomiting and constipation. Vomits may contain worms. Approximately 85 percent of obstructions occur in children between the ages of one and five years. Sometimes on abdominal mass that changes in size and location on serial examination may be appreciated (Tietze, 2006). Complications including volvulus, ileocecal intussceptions gangrene, and intestinal perforation occasionally result.
The overall incidence of obstruction is approximately in 500 children. In endemic areas, it has been shown that between five and 35 percent of all cases of bowel obstruction are due to ascariaris (Khuroo, 2006).
In a recent metaonalysis of morbility and mortality related to Ascariasis, intestinal obstruction accounted for a mean of 72 percent of complication of the infection (Silva, 2004). Ascariasis is said to be the most common cause of acute abdominal surgical emergencies in certain countries include South America (Reeder, 2004).
Hepatobiliary and pancreatic symptoms
Symptoms related to the migration of adult worms into the biliary tree can cause abdominal pains, biliary colic, acalculous cholecystitis, ascending cholangitis, and obstructive jaundice, or bile duct perforation with peritonitis. Structures of the biliary tree may occur (Ahearaivi, 2006).
Hepatic abscesses can also result. Retained worm fragments can serve as a nidus for recurrent pyogenic cholangitis. The pancreatitis, and the appendix resulting in appendicitis. Occasionally, migrating adult worms emerge from the mouth, nose lacrimal duct, umbilicus or inguinal canal. High fever, diarrhoea, spicy foods, anaesthesia and other stresses have all been associated with an increased likelihood of worm migration (Tietze, 2006)
In endemic countries such as India, ascariasis has been found to cause up to one – third of biliary and pancreatic disease (Rhuroo, 2004).
Complications associated with A. lumbricoides infections are fatal in up to five percent of cases. It is estimated that 20,000 deaths from Ascaricisis occur annually, primarily as a consequence of intestinal obstruction (Pawlowski, 2009).
The diagnosis of ascariasis is usually made through stool microscopy. Other forms of diagnosis are through eosinophillia, Imaging, Ultrasound, or serology examination
Characteristic eggs may be seen on direct examination of faeces 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 faeces as the sole diagnostic marker for Ascaris infection is that on 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 worms is found in faeces a stool specimen can be checked for eggs present prior to instituting therapy (Teitze, 2006).
Peripheral eosinophillia can be found particularly during the phase of larval migration through the lungs but also sometimes at other stages of Ascaris infection (Weller, 2007). Eosinophil levels are usually in the range of 5 to 12 percent but can be as high as 30 to 50 percent. Serum levels of IgG and IgE are also often elevated during early infection.
In heavily infested individuals, particularly children, large collections of worms may be detectable on plain film of the abdomen. High mass of worms contrasts against the gas in the bowel, typically producing a “whirl pool” effect. Radiological detection of adult worms is sometimes made by detecting elongated filling defects following barium meal examinations of the small bowel. The worms also sometimes highest barium, in which case the alimentary canal appear as a white thread bisecting the length of the worm’s body. Radiographs will also show when there is associated intestinal obstruction (Reeder, 2004)
Ultra sound examinations can help to diagnose hepatobilary or pancreatic ascariasis. Single worm bundles of worms, or a pseudotumor – like appearance may be seen. Individual body segments of worms may be visible, and on prolonged scanning, the worms will show curling movements.
Computed tomographic (CT) scanning or magnetic resonance imaging (MRI) may also be used to identify worm in the liver or bile ducts, but this is not usually necessary. Imaging the worm in cross – section gives a “bull’s eye” appearance (Sandouk, 2007).
Infected individuals make antibodies to A. lumbricoides which can be detected. However, serology is generally reserved for epidemiologic studies rather than in the diagnosis (seltzer, 2005). IgG, antibodies are not protective against infection (McSnarry, 2006). Antibodies to ascents also often cross react with antigens from other helminthes.
- Avoid contacting soil that may be contaminated with human faeces.
- Do not defecate out doors
- Dispose of diapers properly
- Wash hands with soap and water before handling food.
- When travelling to countries where sanitation and hygiene are poor, avoid water or food that may be contaminated.
- Wash, peel or cook all raw vegetables and fruit before eating.
Adeoye, A. (2009): A text book for medical laboratory practice, (1st ed), Edoson. Lag; Nig. Pp 53 – 86.
AlKarawi, M., Sanai, F. M., Yasawy, M. l. (2006): Structures and cholangitis secondary to ascariasis, endoscopic management. Gastrointest endosc; 50:695-706.
Chu, W.G., Chen, P. M., Huang, C .E, (2004): Neonatal ascariasis. J. Pediatric. 81- 765-783.
Crompton, D. W. (2004): Ascariasis and children malnutrition. Trans R Soc Trop Med Hyp; 86: 577-86.
Damen, J., Luka, E., Biwan, I,.(2011): prevalence of intestine parasites among pupils in Rural North Eastern Nigeria. Niger Med. J. 52(1) 4-6.
Desilva, N. R., Guyatt, H. L., Bundy, D.A. (2004): Morbidity and mortality due to Ascaris-Induced intestinal Obstruction. Trans R Soc Trop Med Hyg. 91:31-46.
Dold, C., Holland, C.V. (2010): Ascaris and Ascariasis microbas infect, Trans R Soc Trop Med Hyg 13(7): 671-86.
Eneanya, C., Anikawe, C. (2005): A school based intestinal helminthiasis programme in Nigeria. Nig .J. of parasitol 25:55 – 60.
Harhay, M. O., Horton, J., Olliaro, P.l. (2010): Epidemiology and control of human gastrointestinal parasite children. Expert review of Anti-infective therapy 8(2): 219-34.
Hadidjaja, P., Bonangi, E., Suyardi, M. A. (2008): The effect of intervention methods on nutritional status and cognitive function of primary school children infected with Ascaris lumbricoides. Am J. Trop med Hyp 59:79 -91.
Hlaing, T. (2005): Ascariasis and children word malnutrition. Parasitology. 107 suppl: s125.
Hournosu, R., Arnuta, E. & Oyusi, T. (2009): Prevalence of intestinal parasites among primary school children in Makurdi Benue Nigeria. Int J. infect. dis. 8(1): 12 – 16.
Ikon, G. & Useh, M. (2009): Epidemiology of gastrointestinal helminthes among pupils in urban and sub-urban communities in Nigeria Med. Lab. Sci. 8: 1-6.
Khuroo, M.S. (2006): Ascariasis Gastrol Clin North Am. 25:553-562.
Lindo, J.F., Dubon, J.M., Ager, A.L. (2008): intestinal practice infections in human immunodeficiency virus (HIV) positive and Hiv Negative individuals in san Pedro Sula, Hondiesas. Am J Trop Med Hyg. 58:481-498.
Mesharry, C., Xia, Y., Holland, C. V., Kennedy, M. I. (2006): Natural immunity to Ascaris lumbricoides associated with immunoglobin to antibody to ABO. Allergen and inflammation indicators in children infect immune 67: 484 – 493.
Murray, P., Rosenthal, R. (2005): Medical microbiology 5th edition, United States: Elsevier Mosby 54-9.
Pawlowski, W.T. (2009): Morbidity and Mortality in Ascariasis and its Prevention and Control; Am J Trop Med Hyg. 45: 67-73.
Piper, R. (2007): Extraordinary Animals: An Encyclopaedia of curious and usual Animals. Green Wood Press. 219-34.
Reeder, M. M. (2004): The Radiological and ultra sound evaluation of Ascariasis of the Gastrointestinal, Biliary and Respiratory tracks. Semin Roentgenol 13: 49-57.
Rousham, E.K., Mascie, T. (2008): An 18-month study of the effect of periodic antihelminthic treatment states of pre-school children in Bangladesh. Ann Hum Biol 21:315-323.
Sarinas, P. S., Chitkara, R. T. (2005): Ascariasis and Hookworm. Semin Regar Infection 12:130-146.
Sandonk, F., Haffar, S., Zads, M. M. (2007): Pancreatic biliary ascariasis, experience of 300 cases, Am. J Gastroenterol, G2:22 – 64.
Seitzer,E. (2005): Ascariasis in Tropical infections, disease, principle, pathogens and practice (1st Ed.) Phladelphia: Churchill Living Stone; 553.
Tietze, P. E., Tietze, P. H. (2006): The round worm, Ascaris lumbricoides. Prim care; 18:25-34.
Uneke, C., Eze, P., Oyibo, N. (2006): Soil transmitted helminthes infection in school children in South East Nigeria. Int. J. of 3rd world med. 4(1): 6-8.
Weller, P.F. (2007): Eosinophillia in travelers. Med Clin. North Am; 76:141-3.