Hepatobiliary symptoms have been reported in patients with Ascariasis and are due to the migration of adult worms into the biliary tree. Aff ected individuals can experience biliary colic, jaundice, ascending cholangitis, acalculous cholecys- titis and perforation of the bile duct. Pancreatitis may develop as a result of an obstruction of the pancreatic duct. Hepatic abscesses have also been reported. Sandouk et al studied 300 patients in Syria who had biliary or pancreatic involve- ment. Ninety-eight percent of the patients presented with abdominal pain, 16% developed ascending cholangitis, 4% developed pancreatitis and 1% developed obstructive jaundice. Both ultrasonography, as well as endoscopic retrograde cholangiopancreatography (ERCP) have been used as diagnostic tools for biliary or pancreatic ascariasis. In Sandouk’s study extraction of the worms endoscopi- cally resulted in resolution of symptoms.
Diagnosis
Th e diagnosis of ascariasis is made through microscopic examination of stool specimens. Ascaris eggs are easily recognized, although if very few eggs are present the diagnosis may be easily missed (Fig. 3.3). Techniques for concentrating the stool
3
specimen will increase the yield of diagnosis through microscopy. Occasionally an adult worm is passed via rectum. Eosinophilia may be present, especially during the larval migration through the lungs. In very heavily infected individuals a plain X-ray of the abdomen may sometimes reveal a mass of worms.
Treatment
Both albendazole and mebendazole are effective therapies for ascariasis. Mebendazole can be prescribed as 100 mg BID for 3 days or 500 mg as a single dose. Th e adverse eff ects of the drug include gastrointestinal symptoms, headache and rarely leukopenia. Albendazole is prescribed as a single dose of 400 mg. Albendazole’s side eff ect profi le is similar to mebendazole.
Th e drug piperazine citrate is an alternative therapeutic option, but it is not widely available and has been withdrawn from the market in some developed countries as other less toxic and more eff ective therapy is available. However, in cases of intestinal or biliary obstruction it can be quite useful as it paralyses the worms, allowing them to be expelled by peristalsis. It is dosed as 50-75 mg/kg QD, up to a maximum of 3.5 g for 2 days. It can be administered as piperazine syrup via a naso-gastric tube.
Finally, pyrantel pamoate can be used at a single dose of 11 mg/kg, up to a maxi- mum dose of 1 g. Th is drug can be used in pregnancy. Th e side eff ects of pyrantel pamoate include headache, fever, rash and gastrointestinal symptoms. It has been reported to be up to 90% eff ective in treating the infection.
Th ese medications are all active against the adult worm and are not active against larval stage. Th us, reevaluation of infected individuals is recommended following therapy. Family members should also be screened as infection is common among other members of a household. Treatment does not protect against reinfection.
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Ascariasis
3
Prevention
Given the high prevalence of infection with Ascaris lumbricoides and the potential health and educational benefi ts of treating the infection in children, the World Health Organization (WHO) has recommended global deworming measures aimed at school children. Th e goal of recent helminth control programs has been to recommend periodic mass treatment where the prevalence of infection in school aged children is greater than 50%. Th e current goal is to treat infected individual 2 to 3 times a year with either mebendazole or albendazole. Integrated control programs combining medical treatment with improvements in sanitation and health education are needed for eff ective long-term control.
Suggested Reading
1. Ali M, Khan AN. Sonography of hepatobiliary ascariasis. J Clin Ultrasound 1996; 24:235-41.
2. Anderson TJ. Ascaris infections in human from North America: Molecular evidence for cross infection. Parasitology 1995; 110:215-29.
3. Bean WJ. Recognition of ascariasis by routine chest or abdomen roentgenograms. Am J Roentgenol Rad Th er Nucl Med 1965; 94:379.
4. Blumenthal DS, Schultz AG. Incidence of intestinal obstruction in children infected by Ascaris lumbricoides. Am J Trop Med Hyg 1974; 24:801.
5. Blumenthal DS, Schultz MG. Eff ect of Ascaris infection on nutritional status in children. Am J Trop Med Hyg 1976; 25:682.
6. Chevarria AP, Schwartzwelder JC et al. Mebendazole, an eff ective broad spectrum anti-heminthic. Am J Trop Med Hyg 1973; 22:592-5.
7. Crampton DWT, Nesheim MC, Pawlowski ZS, eds. Ascariasis and Its Public Health Signifi cance. London: Taylor and Francis, 1985.
8. De Silva NR, Guyatt HL, Bundy DA. Morbidity and mortality due to Ascaris-induced intestinal obstruction. Trans R Soc Trop Med Hyg 1997; 91:31-6.
9. DeSilva NR, Chan MS, Bundy DA. Morbidity and mortality due to ascariasis: Re-estimation and sensitivity analysis of global numbers at risk. Trop Med Int Health 1997; 2:519-28.
10. Despommier DD, Gwadz RW, Hotez PJ et al, eds. Parasitic Diseases, 5th edition. New York: Apple Tree Productions, 2005:115-20.
11. Gelpi AP, Mustafa A. Seosonal pneumonitis with eosinophilia: A study of larval ascariasis in Saudi Arabia. Am J Trop Med Hyg 1967; 16:646.
12. Jones JE. Parasites in Kentucky: the past seven decades. J KY Med Assoc 1983; 81:621.
13. Khuroo MS. Ascariasis. Gastroenterol Clin North Am 1996; 25:553-77. 14. Khuroo MS. Hepato-biliary and pancreatic ascariasis. Indian J Gastroenterol 2001;
20:28.
15. Loeffl er W. Transient lung infi ltrations with blood eosinophilia. Int Arch Allergy Appl Immunol 1956; 8:54.
16. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practices of Infectious Disease, 5th edition. Philadelphia: Churchill Livingstone, 2000:2941.
17. Norhayati M, Oothuman P, Azizi O et al. Effi cacy of single dose albendazole on the prevalence and intensity of infection of soil-transmitted helminths in Orang Asli children in Malaysia. Southeast Asian J Trop Med Public Health 1997; 28:563. 18. O’Lorcain, Holland CU. Th e public health importance of Ascaris lumbricoides.
Parasitology 2000; 121:S51-71.
19. Phills JA, Harold AJ, Whiteman GV et al. Pulmonary infi ltrates, asthma, eosino- philia due to Ascaris suum infestation in man. N Engl J Med 1972; 286:965.
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20. Reeder MM. Th e radiographic and ultrasound evaluation of ascariasis of the gastrointestinal, biliary and respiratory tract. Semin Roentgenol 1998; 33:57. 21. Sandou F, Haff ar S, Zada M et al. Pancreatic-biliary ascariasis: Experience of 300
cases. Am J Gastroenterol 1997; 92:2264-7.
22. Sinniah B. Daily egg production of Ascaris lumbricoides: Th e distribution of eggs in the feces and the variability of egg counts. Parasitology 1982; 84:167. 23. Stephenson LS. Th e contribution of Ascaris lumbricoides to malnutrition in
children. Parasitolgy 1980; 81:221-33.
24. Warren KS, Mahmoud AA. Algorithems in the diagnosis and management of exotic diseases, xxii ascariasis and toxocariaisis. J Infec Dis 1977; 135:868. 25. WHO Health of school children: Treatment of intestinal helminths and schistoso-
miasis (WHO/Schisto/95.112; WHO/CDS/95.1). World Health Organisation 1995.
CHAPTER 4
Medical Parasitology, edited by Abhay R. Satoskar, Gary L. Simon, Peter J. Hotez
and Moriya Tsuji. ©2009 Landes Bioscience.
Hookworm
David J. Diemert
Introduction
Human hookworm infection is a soil-transmitted helminth infection caused primarily by the nematode parasites Necator americanus and Ancylostoma duo-
denale. It is one of the most important parasitic infections worldwide, ranking
second only to malaria in terms of its impact on child and maternal health. An estimated 576 million people are chronically infected with hookworm and an- other 3.2 billion are at risk, with the largest number of affl icted individuals living in impoverished rural areas of sub-Saharan Africa, southeast Asia and tropical re- gions of the Americas. N. americanus is the most widespread hookworm globally, whereas A. duodenale is more geographically restricted in distribution. Although hookworm infection does not directly account for substantial mortality, its greater health impact is in the form of chronic anemia and protein malnutrition as well as impaired physical and intellectual development in children.
Humans may also be incidentally infected by the zoonotic hookworms
Ancylostoma caninum, Ancylostoma braziliensis and Uncinaria stenocephala,
which can cause self-limited dermatological lesions in the form of cutaneous larva migrans. Additionally, Ancylostoma ceylanicum, normally a hookworm infecting cats, has been reported to cause hookworm disease in humans espe- cially in Asia, whereas A. caninum has been implicated as a cause of eosinophilic enteritis in Australia.
Life Cycle
Hookworm transmission occurs when third-stage infective fi lariform larvae come into contact with skin (Fig. 4.1). Hookworm larvae have the ability to actively penetrate the cutaneous tissues, most oft en those of the hands, feet, arms and legs due to exposure and usually through hair follicles or abraded skin. Following skin penetration, the larvae enter subcutaneous venules and lymphatics to gain access to the host’s aff erent circulation. Ultimately, they enter the pulmonary capillaries where they penetrate into the alveolar spaces, ascend the brachial tree to the trachea, traverse the epiglottis into the pharynx and are swallowed into the gastrointestinal tract. Larvae undergo two molts in the lumen of the intestine before developing into egg-laying adults approximately fi ve to nine weeks aft er skin penetration. Although generally one centimeter in length, adult worms exhibit considerable variation in size and female worms are usually larger than males (Fig. 4.2).
Adult Necator and Ancylostoma hookworms parasitize the proximal portion of the human small intestine where they can live for several years, although diff erences
4
exist between the life spans of the two species: A. duodenale survive for on average one year in the human intestine whereas N. americanus generally live for three to fi ve years (Fig. 4.3). Adult hookworms attach onto the mucosa of the small intestine by means of cutting teeth in the case of A. duodenale or a rounded cutting plate in the case of N. americanus. Aft er attachment, digestive enzymes are secreted that enable the parasite to burrow into the tissues of the submucosa where they derive nourishment from eating villous tissue and sucking blood into their digestive tracts. Hemoglobinases within the hookworm digestive canal enable digestion of human hemoglobin, which is a primary nutrient source of the parasite.
Figure 4.1. Life cycle of the hookworm, Necator americanus. Reproduced from: Nappi AJ, Vass E, eds. Parasites of Medical Importance. Austin: Landes Bioscience, 2002:80.
23
Hookworm
4
Humans are considered the only major defi nitive host for these two parasites and there are no intermediate or reservoir hosts; in addition, hookworms do not reproduce within the host. Aft er mating in the host intestinal tract, each female adult worm produces thousands of eggs per day which then exit the body in feces. A. duodenale female worms lay approximately 28,000 eggs daily, while the output from N. ameri-
canus worms is considerably less, averaging around 10,000 a day. N. americanus and A. duodenale hookworm eggs hatch in warm, moist soil, giving rise to rhabditiform
larvae that grow and develop, feeding on organic material and bacteria. Aft er about seven days, the larvae cease feeding and molt twice to become infective third-stage fi lariform larvae. Th ird-stage larvae are nonfeeding but motile organisms that seek out higher ground such as the tips of grass blades to increase the chance of contact with human skin and thereby complete the life cycle. Filariform larvae can survive for up to approximately two weeks if an appropriate host is not encountered.
A. duodenale larvae can also be orally infective and have been conjectured to
infect infants during breast feeding.