Helminth Infections in Neonates and Young Children

Andrea J. Lack, MD; Jill E. Weatherhead, MD; Laila Woc-Colburn, MD, DTM&H


June 25, 2014

The Outcomes of Childhood Helminth Infections

All of the choices in the preceding question represent potential long-term outcomes of childhood helminth infections. The remainder of this article will address these devastating consequences, their burden on society, and efforts to reduce this burden.

Lymphatic Filariasis

Lymphatic filariasis is arguably the most stigmatizing of all helminth infections. Three species of nematodes can cause the disease. W bancrofti is found in sub-Saharan Africa, India, Southeast Asia, parts of the Caribbean, and Latin America. Brugia malayi is endemic to India, China, and Southeast Asia, whereas Brugia timori occurs in Indonesia. Larvae are transmitted by mosquitos, which migrate through the lymphatic system, where they mature into adults.

Lymphatic obstruction can progress to massive hydrocele and disfiguring lymphedema, particularly of the extremities and breasts. As a result, victims may become ostracized, unemployable, and utterly dependent on family or community members. Globally, an estimated 120 million people are infected, resulting in the loss of 5.8 million DALYs. Another 1.6 billion people are at risk of acquiring the disease.[2]

Historically, lymphatic filariasis was considered a disease of adolescents and adults. However, more recent data indicate that first acquisition often occurs in childhood and is positively correlated with subsequent disease in adulthood. The prevalence of infection in children younger than 10 years of age is approximately one third the prevalence in adults. This increases to two thirds the prevalence in adults during adolescence.[29] A study in northeast Tanzania found a 30% prevalence of W bancrofti antigen in children younger than 5 years.[30] In utero exposure from maternal lymphatic filariasis infection has been linked to higher rates of subsequent infection, as well as reduced responsiveness to childhood vaccines.

The treatment of choice for lymphatic filariasis is diethylcarbamazine, except in patients coinfected with onchocerciasis or a high burden of loiasis. (Loiasis, also known as African eye worm, is caused by the parasitic worm Loa loa.) In those cases, rapid microfilariae killing can result in adverse outcomes. Treatment of onchocerciasis or an alternative therapy is indicated in these patients.


In light of the "hygiene hypothesis" (which postulates that increases in autoimmune and allergic diseases in western countries are due to decreases in infections and parasitic exposures), it may seem counterintuitive that a parasitic infection could cause symptoms of atopy and asthma. Yet, Toxocara may do just that.

Toxocara canis and Toxocara cati are zoonotic nematodes carried by dogs and cats, respectively. Transmission occurs by ingestion of eggs from dirt contaminated with dog or cat feces. As with ascariasis and trichuriasis, young children who play in contaminated soil are at higher risk for exposure.

Classically, infection presents as visceral or ocular larva migrans. Although these overt manifestations are rare, more subtle presentations with wheezing, pulmonary infiltrates, bronchial reactivity, and eosinophilia occur much more commonly.[31] Toxocara infection has been associated with asthma, allergic symptoms, and significantly reduced FEV1 on spirometry.[32,33,34,35] A study also recorded improvement or resolution of atopy and asthma symptoms after antihelminthic therapy.[36]

Of note, toxocariasis is not limited to low-income countries. In the United States, Toxocara seroprevalence appears to be highest in non-Hispanic black persons and in those living in poverty,[36,37] and overlaps populations with the highest rates of severe asthma. As a result, Toxocara may represent the most common neglected disease of the poor in the United States.[31]


Schistosomiasis is caused by trematodes (flukes), a member of Platyhelminthes. All species are carried by snail vectors. Cercariae, the larval stage, enter human skin during contact with infected water. The adult worms of Schistosoma mansoni (in sub-Saharan Africa and parts of Latin America) and Schistosoma japonicum (in Asia) live in mesenteric venules, where they release eggs to be shed through the intestines.

Unfortunately, eggs often lodge in intestinal or liver tissue, where they induce inflammation, granulomas, and fibrosis. Acute infection can induce a systemic hypersensitivity syndrome called "Katayama fever." Chronic infection can produce portal hypertension with hepatosplenomegaly, ascites, and variceal bleeding.

S haematobium is found predominately in Africa and the Middle East. Adult worms reside in the venous plexus of the urinary tract. From there, they release eggs that can become lodged in the ureters, bladder, or genital tract tissue, inciting an inflammatory response that can produce hematuria, urinary obstruction, hydronephrosis, chronic renal disease, and bladder cancer. In women, genital tract lesions can result in dyspareunia, increased transmission of HIV, and infertility.[38]

Combined, these 3 species of Schistosoma infect an estimated 207 million people. Although Schistosoma was once thought to affect mainly school-aged children and adolescents, more recent studies demonstrate substantial prevalence in younger children.[25,39] Current WHO chemoprophylaxis guidelines recommend praziquantel starting at age 4 years, but others have advocated for earlier therapy to close the "praziquantel treatment gap."[24,40]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.