AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

After malaria, schistosomiasis is the second most prevalent tropical disease in the world. In some parts of the world, it also is known as bilharzia in honor of Theodore Bilharz, who first identified the etiological agent for Schistosoma hematobium in Egypt in 1851.

The pathophysiology of schistosomiasis involves the immune response against the schistosome eggs. The clinical manifestations depend on the species of parasite, intensity of worm burden, and immunity of the person to the parasite. Recent World Health Organization (WHO) reports estimate that 500-600 million people in 74 tropical and subtropical countries are at risk for schistosomiasis. More than 200 million people in these countries are infected. Of these, 120 million are symptomatic, with 20 million having severe clinical disease.

Persons at risk include those who live or travel in areas where schistosomiasis occurs and who come into contact with fresh water that contains the appropriate type of snail intermediate host. The main forms of human schistosomiasis are caused by 5 species of flatworm in the genus Schistosoma, within the class Trematode. The 5 species are as follows: S hematobium, Schistosoma mansoni, Schistosoma japonicum, Schistosoma intercalatum, and Schistosoma mekongi. The worms also are called blood flukes because they live in the vascular system of humans and other vertebrates.

The life cycle of the flatworms that cause human schistosomiasis involves a sexual stage in the human and an asexual stage in the freshwater snail host. The adult worms are small, 12-26 mm long and 0.3-0.6 mm wide, and vary with the different species. S hematobium lives in the venous plexus near the urinary bladder and ureters, S mansoni lives in the inferior mesenteric vein, and S japonicum lives in the superior mesenteric vein of both the large and small intestines.

Adult worms mate and lay eggs. The eggs are nonoperculate, possess a spine, and contain a miracidium. The microscopic appearance of the egg allows diagnostic differentiation of the 5 species. An adult S hematobium produces 20-200 round, terminally spined eggs per day; S mansoni produces 100-300 ovoid, laterally spined eggs per day; and S japonicum produces 500-3500 round, small, laterally spined eggs per day. The eggs of S intercalatum have prominent terminal spines, and S mekongi have small lateral spines.

When the ova reach the fresh water, the miracidia are released and penetrate the snail. Within 3-5 weeks, they asexually multiply into hundreds of fork-tailed cercariae. The cercariae leave the snail and swim to a human or nonhuman animal, where they penetrate the skin. Once inside, cercariae travel to the heart, to the lungs, and through the systemic circulation to reach the portal veins, where they develop into adult worms. The time between cercariae penetration and the first ova production is 4-6 weeks.

Humans are estimated to excrete approximately 50% of the eggs. The rest are trapped in various parts of the body. Occasionally, the worm can be in ectopic positions, such as in the spinal cord, where it produces unusual clinical manifestations.

Pathophysiology

The pathophysiology of infection correlates with the life cycle of the parasite, as follows:

• Cercariae: Skin penetration of cercariae produces an allergic dermatitis at the site of entry. With prior sensitization, a pruritic papular rash develops. This also is observed with nonhuman avian schistosomes.
• Schistosomula: These are tailless cercariae that are transported through blood or lymphatics to the right side of the heart and lungs. Heavy infection can cause symptoms such as cough and fever. Eosinophilia may be observed.
• Adult worm: Adult worms do not multiply inside the human body. In the venous blood, adult male and female worms mate, and the female lays eggs 4-6 weeks after cercarial penetration. Adult worms are rarely pathogenic. The female adult worm lives for approximately 3-8 years and lays eggs throughout her life span.
• Eggs: They cause Katayama fever and schistosomiasis.
• • Katayama fever: The exact pathophysiology is not known. It occurs 4-6 weeks after infection, at the time of the initial egg release. It is reported most commonly with S japonicum but also has been reported with S mansoni. Katayama fever is believed to be due to the high worm and egg antigen stimuli that result from immune complex formation and lead to a serum sickness–like illness. This syndrome is not due to granuloma formation.
  • Schistosomiasis: It is due to immunological reactions to Schistosoma eggs trapped in tissues. Antigens released from the egg stimulate a granulomatous reaction comprised of T cells, macrophages, and eosinophils that results in clinical disease. Symptoms and signs depend on the number and location of eggs trapped in the tissues. Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease, the pathology is associated with collagen deposition and fibrosis, resulting in organ damage that may be only partially reversible.

Frequency

United States

Frequency is estimated at more than 400,000 infected persons. The appropriate snail intermediate host for endemic schistosomiasis is not endemic to the United States. All cases are imported, except for the rare laboratory accident. The diagnosis should be considered in a person from an endemic area or a traveler who had contact with fresh water in an endemic area.

International

Intestinal schistosomiasis caused by S mansoni occurs in 52 countries, including Caribbean countries (ie, Saint Lucia, Antigua, Montserrat, Martinique, Guadeloupe, Dominican Republic, Puerto Rico), eastern Mediterranean countries, South American countries (ie, Brazil, Venezuela, Surinam), and most countries in Africa. Other Schistosoma species that can cause intestinal symptoms and diseases include S intercalatum, S japonicum, and S mekongi. S intercalatum is found in 10 countries within the rain forests of central Africa. S japonicum is endemic in 4 countries in the western Pacific region (ie, China, Philippines, Indonesia, Thailand). S mekongi infection occurs in the Mekong River area of Southeast Asia (ie, Kampuchea, Laos, Thailand). Urinary schistosomiasis caused by S hematobium affects 54 countries in Africa and the eastern Mediterranean.

According to the WHO, the global distribution of schistosomiasis has changed in recent years. It has been eradicated from Japan and the Lesser Antilles islands; transmission has been stopped in Tunisia; and transmission is very low in Morocco, Saudi Arabia, Venezuela, and Puerto Rico.

Mortality/Morbidity

• Acute schistosomiasis: Although most clinical manifestations are benign, some are severe and may require hospitalization. If acute schistosomiasis is not suspected clinically and treated appropriately, it can result in severe morbidity or death.
• Chronic schistosomiasis: Most patients are asymptomatic or mildly symptomatic and do not require medical attention. Only a small proportion of the endemic population harbors a heavy worm burden that later leads to clinical complications.
• • Gastrointestinal schistosomiasis: The most common complication is periportal fibrosis, also termed Symmers clay pipestem fibrosis. This leads to portal hypertension and gastrointestinal hemorrhage. Liver failure is uncommon except for in persons with concomitant chronic hepatitis or cirrhosis. Recently, people co-infected with either hepatitis B or C and S mansoni have been shown to have rapid progression of liver disease.
  • Urinary tract schistosomiasis: This can lead to renal failure due to obstructive uropathy, pyelonephritis, or bladder carcinoma (occurring usually 10-20 y after the initial infection). In addition, immune complexes that contain worm antigens may deposit in the glomeruli, leading to glomerulonephritis and amyloidosis.
  • Female genital schistosomiasis (FGS): S haematobium causes lesions in the female lower genital tract (ie, cervix, valva, vagina). FGS has been identified as a major social and medical problem that may facilitate the spread of some sexually transmitted diseases such as HIV and human papillomavirus (HPV).¹
  • Schistosomal cor pulmonale: This is an important complication that develops in about 5% of patients with hepatosplenic S mansoni.
  • CNS schistosomiasis: Most cases of cerebral schistosomiasis are observed with S japonicum, constituting 2-4% of all S japonicum infections. However, CNS schistosomiasis can also occur with other species. Spinal schistosomiasis usually presents as transverse myelitis and is primarily due to S mansoni infection.
  • Schistosomiasis in pregnancy: This has been associated with anemia and low birth weight.²

Race

No racial predilection exists.

Sex

Schistosomiasis is more common in males, most likely because of increased exposure to infected water via bathing, swimming, and agricultural activities.

Age

• Exposure to infection can start shortly after birth.
• People aged 10-14 years are at the maximum risk of exposure.
• The lower prevalence in adults is possibly due to partial immunity and decreased exposure to infected water.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Acute manifestations
• • Cercarial dermatitis: Individuals who have been exposed to fresh or salt water may develop a pruritic rash due to cercarial dermatitis (also called swimmer's itch). This has been described in North America due to nonhuman avian schistosomes.
  • Katayama syndrome: Fever, lethargy, and myalgia are the most common symptoms. Less common symptoms include cough, headache, anorexia, and rash. These symptoms mimic any acute viral, bacterial, or malarial illness. Consequently, acute illness is often missed unless schistosomiasis is suspected. A travel history that includes exposure to fresh water in an endemic area is an important part of the medical history.
• Chronic manifestations
• • Symptoms depend on the species of schistosome causing infection, the duration and severity of infestation, and the immune response to the eggs.
  • Typically, onset is insidious.
  • S mansoni, S mekongi, S intercalatum, and S japonicum cause intestinal tract and liver disease.
  • S hematobium only rarely causes intestinal or liver disease but characteristically causes urinary tract disease.
  • Hepatic schistosomiasis: In the early stage, dyspepsia, flatulence, and pain are present in the left hypochondrium due to spleen enlargement. Anemia or cor pulmonale may cause generalized pain, weakness, and shortness of breath. In the later stages, abdominal distention, lower limb edema, hematemesis, and melena can occur. Symptoms of liver failure are rare unless other infectious, toxic, or malignant causes of hepatitis are present.
  • Intestinal schistosomiasis: Fatigue, abdominal pain, diarrhea, and dysentery occur.
  • Urinary schistosomiasis: Dysuria, urinary frequency, and terminal hematuria occur.
  • Cardiopulmonary schistosomiasis may cause larval pneumonitis with a cough, mild wheezing, and a low-grade fever.
  • In schistosomal cor pulmonale, easy fatigability, palpitations, dyspnea on exertion, and hemoptysis are present.
  • CNS schistosomiasis involves focal and generalized seizures; headache; and myeloradiculopathy with lower limb and back pain, bladder dysfunction, paresthesia, and lower limb weakness.
  • Female genital schistosomiasis (FGS): The history includes postcoital bleeding, genital ulceration, irregular menstruation, and pelvic pain.

Physical

• Acute schistosomiasis
• • Generalized lymphadenopathy
  • Hepatosplenomegaly
  • Rash
  • Fever
• Chronic schistosomiasis
• • Portal hypertension with abdominal distention, hepatosplenomegaly, pedal edema, pallor, distended abdominal veins, and ascites
  • Intestinal polyposis with heme-positive stool, pallor, and signs of malnutrition
  • CNS symptoms, including focal neurological findings, seizures, and spinal cord lesions
  • Renal failure with anemia and hypertension
  • Cor pulmonale with signs of right heart failure
  • Genital lesions including ulcer or nodular lesions of the cervix, valva, or vagina or vesicovaginal fistula

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Acute nephritis
Acute viral syndrome (including HIV)
Cancer of the urogenital tract
Drug reactions
Epilepsy
Helminthic parasitic diseases
Pancreatitis
Renal tuberculosis
Space-occupying lesion
Tropical splenomegaly
Visceral leishmaniasis

WORKUP

Section 5 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Stool or urine analysis
• • Identify and speciate the eggs in the stool or urine.
  • Urinary excretion of eggs is not uniform. The urine is most likely to be positive for S hematobium from 10 am until 2 pm.
  • Quantification of the egg excretion is calculated by collecting 24-hour urine or stool, homogenizing the sample, and counting the eggs in a measured sample.
  • Urine or stool egg count in a 24-hour collection quantitates the severity of the infection.
  • Fewer than 100 eggs per gram indicates a light infection, 100-400 eggs per gram indicates a moderate infection, and more than 400 eggs per gram indicates a heavy infection.
• Egg viability test
• • This test is important for assessing the effectiveness of treatment.
  • It requires mixing the stools or urine with room-temperature distilled water and observing for hatching miracidia.
  • An active infection produces viable eggs, while treated or past infection results in nonviable eggs and an absence of miracidia.
• Acute illness is often associated with eosinophilia in the blood and tissues.
• With chronic illness, peripheral eosinophilia may be minimal or absent while tissue eosinophilia persists.
• Urinary schistosomiasis (occurs with chronic disease)
• • Urine syringe filtration techniques provide a quantitative estimate of eggs in the urine.
  • Urine analysis and culture for hematuria, proteinuria, leukocyturia, and associated urinary infections
  • A Salmonella urinary tract infection should always lead to suspicion of schistosomiasis.
  • Blood chemistries, including renal function tests
  • Blood cultures for salmonella bacteremia
  • CBC count for anemia and eosinophilia
• Intestinal and liver schistosomiasis (chronic disease)
• • Direct stool examination is not a sensitive test.
  • Concentration techniques such as a Kato-Katz thick smear are needed. This demonstrates the number of eggs excreted per day.
  • Blood in the stool should be ruled out.
  • CBC for anemia and eosinophilia
  • Additional testing for HIV and HPV should be considered in female genital schistosomiasis (FGS).
  • Liver function test results usually are within the reference range until the end stage of disease. An exception may include a mild elevation of alkaline phosphatase levels. If liver function test results are abnormal, look for other co-infections or diseases.
  • Diagnostic tests for hepatitis B and C should be considered in liver schistosomiasis.
• Serology
• • The antibody test is a useful epidemiological tool but cannot be used to differentiate active and past illness.
  • It does not allow quantification of egg burden.
  • Serology findings can be used to reach a diagnosis in a patient from a nonendemic area because a negative antibody test result would be expected.
  • Detecting antibodies specific to S mansoni, S hematobium, and S japonicum adult worm microsomal antigens (ie, Mansoni adult worm microsomal antigen [MAMA], hematobium adult worm microsomal antigen [HAMA], japonicum adult worm microsomal antigen [JAMA]) have been reported to be highly specific for all 3 species when used in the Falcon assay screening test (FAST), enzyme-linked immunoassay (ELISA), and immunoblot assays.³

Imaging Studies

• With acute schistosomiasis, a chest radiograph sometimes demonstrates a generalized increase in vascular and interstitial marking and mild lymphadenopathy.
• Urinary schistosomiasis (occurs with chronic disease)
• • Plain abdominal radiographs may demonstrate bladder and ureteral calcifications.
  • On a sonogram, hydronephrosis, hydroureters, and bladder wall irregularities may be visible.
  • Urography may demonstrate abnormalities in the ureter and bladder wall.
• Liver and intestinal schistosomiasis (chronic disease)
• • Ultrasonography of liver and spleen is used to reach an early and accurate diagnosis of periportal fibrosis and a diagnosis of hepatosplenomegaly and ascites.
  • On CT scan of the liver, calcified capsules and septa are visible.
  • Mucosal irregularities are revealed by contrast studies of the intestine.
• Lung schistosomiasis (chronic disease)
• • CT scan of the lungs may demonstrate early interstitial fibrosis.
  • Findings on echocardiogram reflect pulmonary hypertension due to egg emboli to pulmonary vasculature.
• CNS schistosomiasis also occurs with chronic disease, and a CT scan and MRI scan of the brain and spinal cord may show lesions.

Other Tests

• Detecting circulating antigen
• • Because these tests measure parasite antigen as opposed to host antibody response, they reflect active infection. The tests are still investigational.
  • With effective treatment, a reduction in antigenemia is expected.
  • The 2 proteoglycan gut-associated antigens that appear most promising are circulating anodic antigen (CAA) and circulating cathodic antigen (CCA). These antigens can be found in urine or serum.
  • Studies are underway to evaluate the sensitivity and specificity of these investigational antigen tests.

Procedures

• Rectal biopsy or bladder mucosal biopsy
• • Mucosal biopsy is effective for visualizing eggs.
  • Biopsy is helpful when stool sample findings are negative or in light infection.
  • Obtain multiple biopsy samples and crush them between slides (to increase egg-detecting sensitivity).
• Sigmoidoscopy/proctoscopy
• • To obtain mucosal biopsies (including rectal)
  • For diagnosis and to identify complications such as pedunculated and sessile polyps
• Upper endoscopy
• • Assess for esophageal varices.
  • Treat upper intestinal bleeding with endoscopic sclerotherapy.
• Cystoscopy
• • To obtain mucosal biopsy for diagnosis
  • To assess complications such as bladder cancer
• Surgical biopsy findings may be used to diagnose ectopic schistosomiasis.

TREATMENT

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Medical Care

• Prehospital care should include treating acute complications, such as acute intestinal bleeding.
• Emergency department care
• • Stabilize patients who have acute complications.
  • If appropriate, include schistosomiasis as one of the differential diagnoses.
  • Send urine or stool sample to the parasitology laboratory with a special request to look for eggs indicative of schistosomiasis.

Consultations

Appropriate consultations depend on the suspected complications but may include an infectious disease physician, urologist, or gastroenterologist.

MEDICATION

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The aim of chemotherapy is 2-fold. The first goal is to cure the disease or at least minimize morbidity. The second goal is to control transmission of the parasite in the endemic areas. Praziquantel and oxamniquine (no longer available in the United States) are used commonly, but praziquantel is the treatment of choice for all species of schistosomiasis. Clinical studies show that artemether, which is used as antimalarial treatment, is also active against all 3 major schistosome parasites (mainly schistosomula).⁴ In addition, trials that involve the combination of artemether and praziquantel show beneficial effect.⁵

The following drugs and doses are based on recommendations in the August 2004 publication in The Medical Letter, "Drugs for Parasitic Infections."

Drug Category: Anthelmintics

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

FOLLOW-UP

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Further Inpatient Care

• Patients with severe complications, such as GI bleeding, GI obstruction, renal failure, cardiac failure, bacteremia due to Salmonella, and CNS complications, need inpatient care.

Further Outpatient Care

• Response to treatment is evaluated by counting the amount of decrease in egg excretion.
• • In the initial 2 weeks after treatment, the egg count may not decrease because eggs laid before the treatment require 2 weeks to be shed.
  • Viable eggs can be excreted for 6-8 weeks after treatment.
• When measured 5-10 days after treatment, newer tests that measure antigens may help assess therapeutic response.
• Persistent circulating antigen and the excretion of eggs indicate residual infection. These patients should be retreated with praziquantel.

Deterrence/Prevention

• No vaccine or prophylactic chemotherapy is currently available.
• Clinical trials involving human volunteers are underway to develop an effective vaccine against schistosomiasis.
• Clinical studies show artemether may be used as a prophylactic agent if given once every 2-4 weeks.⁴
• Travelers to endemic areas should avoid contact with fresh water.
• Suspect acute schistosomiasis in a setting of recent contact with fresh water and treat early if diagnostic test results are positive or clinical suspicion is high.
• Controlling schistosomiasis in an endemic area should include the following:
• • Population-based preventive chemotherapy: The WHO has recommended preventive chemotherapy for at-risk populations in endemic areas⁶
  • Providing a safe water supply
  • Health education that includes improving water sanitation and avoiding schistosome-contaminated urine or stool
  • Snail control

Complications

• GI bleeding
• GI obstruction
• Malnutrition
• Schistosomal nephropathy
• Renal failure
• Pyelonephritis
• Bladder cancer
• Sepsis (Salmonella)
• Pulmonary hypertension
• Cor pulmonale
• Neuroschistosomiasis

Prognosis

• Early disease usually improves with treatment.
• Hepatic, renal, and intestinal pathology improves with treatment.
• Hepatosplenic schistosomiasis carries a relatively good prognosis because hepatic function is preserved until the end of the disease (unless variceal bleeding occurs).
• Cor pulmonale usually does not improve significantly with treatment.
• Depending on location and size, brain lesions usually improve with treatment.
• Spinal cord schistosomiasis carries a guarded prognosis. Praziquantel should be administered as soon as possible.

MISCELLANEOUS

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• Follow-up
• Miscellaneous
• Multimedia
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Medical/Legal Pitfalls

• Failure to record travel and residence history in the appropriate clinical setting
• Delayed diagnosis and failure to institute early, aggressive treatment of spinal cord schistosomiasis
• Failure to provide advice in a traveler's clinic (eg, to avoid exposure to fresh water in endemic areas)

Special Concerns

• The following manifestations of schistosomiasis may also indicate other disorders:
• • Acute schistosomiasis
  • • Acute viral syndrome (including HIV)
    • Typhoid fever
    • Malaria
    • Hepatitis
  • Fever and rash with eosinophilia: These could be due to other helminthic parasitic diseases or drug reactions.
  • Hematuria
  • • Renal tuberculosis
    • Urogenital tract cancer
    • Acute nephritis
  • Intestinal and liver symptoms
  • • Peptic ulcer disease
    • Pancreatitis
    • Visceral leishmaniasis
    • Myeloproliferative syndromes
    • Tropical splenomegaly
  • Seizures and focal neurological symptoms
  • • Any space-occupying lesion
    • Epilepsy

MULTIMEDIA

Section 10 of 11  

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• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Egg of Schistosoma hematobium, with its typical terminal spine.
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Media type:  Photo

Media file 2:  Granuloma in the liver due to Schistosoma mansoni. The S mansoni egg is at the center of the granuloma.
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Media type:  Photo

REFERENCES

Section 11 of 11

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• References

1. Mosunjac MB, Tadros T, Beach R, et al. Cervical schistosomiasis, human papilloma virus (HPV), and human immunodeficiency virus (HIV): a dangerous coexistence or coincidence?. Gynecol Oncol. Jul 2003;90(1):211-4. [Medline].
2. Friedman JF, Mital P, Kanzaria HK, Olds GR, Kurtis JD. Schistosomiasis and pregnancy. Trends Parasitol. Apr 2007;23(4):159-64. [Medline].
3. Al-Sherbiny MM, Osman AM, Hancock K, et al. Application of immunodiagnostic assays: detection of antibodies and circulating antigens in human schistosomiasis and correlation with clinical findings. Am J Trop Med Hyg. Jun 1999;60(6):960-6. [Medline]. [Full Text].
4. N'Goran EK, Utzinger J, Gnaka HN, et al. Randomized, double-blind, placebo-controlled trial of oral artemether for the prevention of patent Schistosoma haematobium infections. Am J Trop Med Hyg. Jan 2003;68(1):24-32. [Medline]. [Full Text].
5. Utzinger J, Keiser J, Shuhua X, et al. Combination chemotherapy of schistosomiasis in laboratory studies and clinical trials. Antimicrob Agents Chemother. May 2003;47(5):1487-95. [Medline]. [Full Text].
6. World Health Organization. Preventive chemotherapy in human helminthiasis. Geneva: World Health Organization; November, 2006. [Full Text].
7. Barsoum RS. Schistosomiasis and the kidney. Semin Nephrol. Jan 2003;23(1):34-41. [Medline].
8. Bergquist NR, Leonardo LR, Mitchell GF. Vaccine-linked chemotherapy: can schistosomiasis control benefit from an integrated approach?. Trends Parasitol. Mar 2005;21(3):112-7. [Medline].
9. Brown M, Mawa PA, Joseph S, et al. Treatment of Schistosoma mansoni infection increases helminth-specific type 2 cytokine responses and HIV-1 loads in coinfected Ugandan adults. J Infect Dis. May 15 2005;191(10):1648-57. [Medline].
10. Corachan M. Schistosomiasis and international travel. Clin Infect Dis. Aug 15 2002;35(4):446-50. [Medline].
11. Cunha BA. Antibiotic Essentials. Royal Oak, Mich: Physicians Press; 2005.
12. King CH, Mahmoud AAF. Schistosomiasis. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases: Principals, Pathogen, & Practice. Vol 2. ed. Philadelphia, Pa: Churchill Livingstone; 1999:1031-8.
13. Lucey DR, Maguire JH. Schistosomiasis. Infect Dis Clin North Am. Sep 1993;7(3):635-53. [Medline].
14. MMWR. Acute schistosomiasis with transverse myelitis in American students returning from Kenya. MMWR Morb Mortal Wkly Rep. Aug 10 1984;33(31):445-7. [Medline].
15. Pearce EJ. Progress towards a vaccine for schistosomiasis. Acta Trop. May 2003;86(2-3):309-13. [Medline].
16. Ross AG, Bartley PB, Sleigh AC, et al. Schistosomiasis. N Engl J Med. Apr 18 2002;346(16):1212-20. [Medline].
17. Shoff WH, Chen EH, Shepherd SM. Shistosomiasis (part I and II). Infect Dis Pract. 2005;29:419-36.
18. Vennervald BJ, Dunne DW. Morbidity in schistosomiasis: an update. Curr Opin Infect Dis. Oct 2004;17(5):439-47. [Medline].
19. WHO Expert Committee. Prevention and control of schistosomiasis and soil-transmitted helminthiasis. World Health Organ Tech Rep Ser. 2002;912:i-vi, 1-57, back cover. [Medline].

Article Last Updated: Nov 26, 2007