Trematodes (Schistosomes and Liver, Intestinal, and Lung Flukes)

The trematode flatworms that infect humans include the schistosomes, which live in venules of the gastrointestinal (GI) or genitourinary tract, and other flukes, which inhabit the bile ducts, intestines, or lungs. The geographic distribution of each species of trematode parallels the distribution of the specific freshwater snail that serves as its intermediate host ( Table 288.1 ). Six species of schistosomes infect more than 230 million persons, and more than 100 species of other trematodes infect at least 65 million persons.

TABLE 288.1

Features of Schistosomes and Other Important Trematodes

PARASITE	SNAIL INTERMEDIATE HOST (GENUS)	SECOND INTERMEDIATE HOST	GEOGRAPHIC DISTRIBUTION	LOCATION OF ADULT WORMS	TREATMENT
Schistosomes ^a
Schistosoma mansoni	Biomphalaria	None	Brazil, Venezuela, Suriname, Sub-Saharan Africa, Caribbean, Middle East	Mesenteric venules	Praziquantel, 40 mg/kg/day in 1 or 2 doses × 1 day Oxamniquine ^b
Schistosoma japonicum	Onchomelania	None	China, Philippines, Indonesia	Mesenteric venules	Praziquantel, 60 mg/kg/day in 3 doses × 1 day
Schistosoma mekongi	Neotricula	None	Cambodia, Laos	Mesenteric venules	Praziquantel, 60 mg/kg/day in 3 doses × 1 day
Schistosoma intercalatum, Schistosoma guineensis	Bulinus	None	Central and West Africa	Mesenteric venules	Praziquantel, 40 mg/kg/day in 1 or 2 doses × 1 day
Schistosoma haematobium	Bulinus	None	Africa, Middle East, Corsica (France)	Venules of lower urinary tract	Praziquantel, 40 mg/kg/day in 1 or 2 doses × 1 day Metriphonate ^b
Liver Flukes
Clonorchis sinensis	Bithynia, Parafossarulus	Freshwater fish	China, Taiwan, Korea, Japan, Vietnam	Bile, pancreatic ducts	Praziquantel, 75 mg/kg/day in 3 doses × 1–2 days Albendazole, ^c 10 mg/kg/day × 10 days
Opisthorchis viverrini	Bithynia	Freshwater fish	Thailand, Laos, Cambodia	Bile, pancreatic ducts	Praziquantel, 75 mg/kg/day in 3 doses × 1–2 days Albendazole, ^c 10 mg/kg/day × 10 days
Opisthorchis felineus	Bithynia	Freshwater fish	Eastern Europe, former Soviet Union	Bile, pancreatic ducts	Praziquantel, 75 mg/kg/day in 3 doses × 1–2 days Albendazole, ^c 10 mg/kg/day × 10 days
Fasciola hepatica	Lymnaea	Watercress, other aquatic plants	Americas, Europe, Asia, western Pacific, North Africa	Bile ducts	Triclabendazole, ^d × 10 mg/kg × 1 day Nitazoxanide ^e
Intestinal Flukes
Fasciolopsis buski	Segmentina	Aquatic plants	Far East, India	Small intestine	Praziquantel, 25 mg/kg/day × 1 day Niclosamide, ^c 1 g × 1 day Triclabendazole ^e
Heterophyes heterophyes	Pirenella, Cerithidea	Freshwater fish	Far East, Egypt, Middle East, southern Europe	Small intestine	Praziquantel, 25 mg/kg/day × 1 day Triclabendazole ^e
Metagonimus yokogawai	Semisulcospira	Freshwater fish	Far East, Russia, southern Europe	Small intestine	Praziquantel, 25 mg/kg/day × 1 day Triclabendazole ^e
Lung Flukes
Paragonimus westermani; other species	Semisulcospira, Onchomelania, Thiara	Freshwater crabs, crayfish	Far East, South Asia, Philippines, West Africa, South and Central America, USA	Lungs	Praziquantel, 75 mg/kg/day in 3 doses × 2 days Triclabendazole, ^c 10 mg/kg day × 3 days

a Some experts recommend higher doses (e.g., praziquantel 60 mg/kg/day in divided doses for all species), multiple doses (e.g., for 2 or 3 days), or a repeated dose at 4 to 6 weeks to achieve higher rates of cure in persons not exposed to reinfection.

b Not available or limited availability.

c Alternative drug.

d In the United States it is available from the Centers for Disease Control and Prevention Drug Service after approval by the US Food and Drug Administration.

e Limited data.

Trematodes vary in length from 1 mm to more than 10 cm, are flattened dorsoventrally, and have an anterior and ventral sucker and a blind bifurcate intestinal tract. Schistosomes differ from other trematodes in several ways: The sexes of adult worms are separate, transmission is through penetration of skin by larvae, and there is only a single intermediate host, whereas other trematodes are hermaphroditic and are transmitted through ingestion of infected fish, crustaceans, or aquatic plants that serve as second intermediate hosts. Unusually, free-swimming larvae of nonschistosomal trematodes directly invade the human conjunctiva or anterior chamber and cause ocular granulomata, as in the case of Procerovum varium , a parasite of fish-eating birds in Asia and the western Pacific. Only a small proportion of persons with trematode infections harbor large numbers of worms and are at risk for severe disease; most are asymptomatic or experience subtle morbidity, such as fatigue and cognitive or physical impairment.

Schistosomes

Of more than 230 million persons infected with schistosomes in 78 countries and territories, about 120 million have symptoms, 20 million have severe disease, and as many as 200,000 or more die each year. Although control programs and socioeconomic development have eliminated or nearly eliminated transmission of schistosomiasis in more than a dozen countries, progress has been slow elsewhere, especially in sub-Saharan Africa, where greater than 90% of cases occur. Moreover, water resource development projects and population movements continue to spread the disease into regions where it was not previously endemic. Three main species, namely, Schistosoma mansoni, Schistosoma japonicum, and Schistosoma haematobium, and three species with narrow geographic distribution, namely, Schistosoma mekongi, Schistosoma intercalatum, and Schistosoma guineensis, cause human schistosomiasis or bilharziasis, named after Theodor Bilharz who first identified the parasite in 1852. A dozen or more other species of animal schistosomes can cause human infection, including schistosomes of birds and small mammals that cannot mature in the human host but die in the skin, where they cause a dermatitis. Hybrid schistosomes infective for human beings result from crossbreeding of different species of human schistosomes or human and zoonotic schistosomes.

Life Cycle

Adult worms, measuring 1 to 2 cm in length and 0.3 to 0.6 mm in width live, mate, and feed on blood in the portal and mesenteric vessels ( S. japonicum, S. mekongi, S. mansoni, S. intercalatum, and S. guineensis ) or vesical plexus (S. haematobium). The male worm folds around and encloses the female in its gynecophoral canal. Egg production varies from about 300 eggs per day for female S. mansoni and S. haematobium and 3000 eggs daily for S. japonicum ( Fig. 288.1 ). Eggs, measuring 145 × 55 µm for S. mansoni and S. haematobium and 85 × 60 µm for S. japonicum ( Fig. 288.2 ), are deposited in the venules and make their way into the urine or feces and hatch in fresh water, where the miracidium, a 0.1-mm ciliated larva, emerges. The miracidium penetrates the body of the appropriate snail intermediate host and multiplies asexually. Within 4 to 6 weeks, thousands of motile, forked-tail cercariae, 0.1 to 0.2 mm long, emerge. On encountering human skin, the cercariae penetrate with the help of their glandular secretions, and within minutes they lose their tails and change into schistosomula. This transformation from a freshwater environment to parasitic existence in the human host is associated with the unique formation of a heptalaminate membrane and other dramatic changes in morphology, metabolism, and physiology. The schistosomula migrate to the lungs and liver and, in about 6 weeks, they mature to adult worms and descend through the venous system to their final habitat. Eggs appear in the feces or urine 4 to 6 weeks after cercariae penetrate the skin. Adult schistosomes live an average of 3 to 5 years but can survive for 30 years or more.

FIG. 288.2, Life cycle of important parasitic flukes.

Epidemiology

Transmission of schistosomiasis requires an appropriate snail intermediate host; fecal or urinary contamination of warm, slowly moving fresh water; and human entry into the snail-infested water. The snail host is specific for each species and strain of schistosome, which have a specific geographic distribution ( Table 288.1 ). S. mansoni occurs in three South American countries, several Caribbean islands, and, along with S. haematobium, in Africa and the Middle East, often in areas where the two species overlap. S. intercalatum and S. guineensis also can overlap with S. haematobium in parts of West and Central Africa but are less common. S. japonicum is found in China, the Philippines, and Indonesia; and S. mekongi is found in Cambodia and Laos. Cattle, water buffaloes, pigs, dogs, and other mammals are naturally infected with S. japonicum and S. mekongi and act as reservoir hosts, with a major role in transmission. Infections of rodents, sheep, primates, and other animals occur with S. mansoni and, rarely, S. haematobium; although they seem to contribute little to maintenance of the life cycle, they may jeopardize public health efforts to eliminate transmission and lead to the emergence of zoonotic parasitic hybrids infective to humans.

Transmission is focal in endemic countries and most intense in poor rural areas with inadequate sanitation and water supplies. The distribution of schistosomiasis is changing in many areas. The risk for infection is now nonexistent or negligible in previously highly endemic countries, including Japan, Morocco, Tunisia, Algeria, Oman, Jordan, Turkey, Iran, Mauritius, and the Caribbean countries. Control programs have significantly reduced the incidence of infection and morbidity in Brazil, Venezuela, China, Saudi Arabia, Egypt, Cambodia, and the Philippines. Since 2000 strategies to reduce morbidity from schistosomiasis have been successfully implemented in several African countries, but in most of sub-Saharan Africa, high levels of endemicity persist, including in areas where dams and irrigation projects have led to major increases in the prevalence and extension of transmission to new areas. An outbreak of urogenital schistosomiasis, likely related to arrival of infected individuals from endemic regions of Africa, was detected in Corsica, France, which marked the first instance of European transmission since the 1960s. New foci of schistosomiasis have been identified in Myanmar. Urban transmission occurs in some large cities of Brazil and Africa, and global climate change is predicted to increase transmission in many areas.

In endemic communities the distribution of the infection fits a negative binomial curve, with most infected persons harboring low worm burdens and only a small proportion, usually children ages 8 to 12 years, having heavy infections. Aggregation of the worm burden in a small proportion of infected individuals probably reflects a combination of factors, including the amount of water exposure, partial acquired immunity, age, and genetic susceptibility. Typically, the intensity of infection declines after the early teenage years as partial immunity to new infections builds up, older worms die, and contact with fresh water decreases. Because worms do not multiply in the host, the intensity of the infection depends on the number of cercariae encountered. Persons with heavy infections are at most risk for developing severe disease.

In the United States and other temperate areas, infection cannot be transmitted because of the absence of the appropriate snail intermediate host. Schistosomiasis is seen among immigrants from endemic areas and returning travelers, and sometimes it appears in small epidemics among travelers engaging in adventure and nature tourism.

Pathogenesis

The disease associated with schistosomiasis is largely due to the host's immune response to the larvae and eggs. Mature adult worms evade the host's immune defenses by binding host antigens to their tegument and regenerating their tegument, along with other mechanisms, thus contributing little to the immunopathology of the disease. Different mechanisms are responsible for tissue injury during the stage of larval penetration, the acute stage, and the chronic infection.

In previously exposed persons a protective response consisting primarily of specific immunoglobulin E (IgE) antibodies, eosinophils, and macrophages is directed against the schistosomula after cercarial penetration of the skin. As a result, some organisms die in the skin and are surrounded by edema and cellular infiltrates in the dermis and epidermis that can give rise to a papular dermatitis.

The syndrome of acute schistosomiasis occurs 2 to 12 weeks after a heavy first exposure to larvae during worm maturation and the initiation of egg deposition. A febrile illness with features of serum sickness results from formation of circulating immune complexes in response to larval and egg antigens and production of high levels of proinflammatory cytokines. Acute disease develops primarily in previously unexposed persons and less commonly in heavy reinfections, usually due to S. japonicum. Symptomatic acute infections are rarely reported among persons who grow up in an endemic area, perhaps because of sensitization in utero as a result of maternal infection.

Disease during the chronic stage of infection is due to the presence of eggs in host tissues and the immune response directed against the egg antigens. Miracidia in the eggs secrete antigenic glycoproteins through pores in the eggshell that induce an inflammatory response that facilitates passage of the eggs through blood vessel walls and tissues en route to the lumen of the intestinal or urinary tract. One-third to one-half of eggs reach the environment, with the remainder trapped in tissues or embolized to a distant site. The host response to toxic egg antigens and eggs retained in the tissues includes acute eosinophilic inflammation, followed by granuloma formation, initially consisting of neutrophils, eosinophils, and mononuclear cells and, later, mostly lymphocytes, macrophages, multinucleated giant cells, and fibroblasts. In S. mansoni and S. haematobium infections the granulomatous response has been shown to be orchestrated by CD4 ⁺ T lymphocytes and is tightly regulated by various immunologic mechanisms. They involve balanced helper T cell type 1 and 2 responses and the production of cytokines locally in the granulomas and systemically; these responses in turn are regulated by numerous other mediators and mechanisms. In addition to destroying eggs, granulomas may mediate their passage into the lumen of the bowel or urinary tract. This hypothesis is supported by the finding of reduced egg output in persons with advanced human immunodeficiency virus (HIV) disease.

Granulomas initiate tissue injury first through the inflammatory infiltrate and replacement of normal tissue and later through extensive collagen deposition and scarring. Large granulomas and fibrosis cause the major pathologic lesions in chronic schistosomiasis. In the case of schistosomes that inhabit the mesenteric vessels, the pathologic process is greatest in the intestines and the liver, the major site of egg embolism. With S. haematobium infection, the main system involved is the urinary tract. The result is inflammatory lesions and ulcerations of the mucosa; fibrotic scarring of the bowel, bladder, and lower ureteral walls; and obstruction of portal blood flow in the liver and urine flow through the ureters and bladder. During the early stages of schistosome infection, the granulomatous response is exuberant. Later, modulation of granulomatous hypersensitivity results in smaller granulomas and less fibrosis, which in turn probably play a significant role in limiting progression of the disease. Treatment of children during the early stage can completely resolve the granulomatous inflammation. A subset of untreated persons immunoregulate their response to egg antigens poorly and develop extensive fibrosis and severe disease.

The severity of disease in schistosomiasis is determined in part by the duration and intensity of the infection. This relationship is not exact, however, and other variables, such as genetic susceptibility to disease, parasite strain, and coinfections with malaria, hepatitis viruses, HIV, and other infectious agents, may be important. Chronic schistosomiasis appears to be associated with a partial degree of resistance to reinfection directed against invading immature worms and mediated by IgE antibodies, eosinophils, and cytokines, such as interleukin-4 (IL-4) and IL-5.

Clinical Syndromes

Infections with human schistosomes are frequently asymptomatic. Illness, when present, is strongly influenced by location in endemic versus nonendemic sites and related to factors such as prevalence of immunity and intensity of infection. Acute symptomatology is more frequent in previously uninfected individuals, and chronic illness, which is associated with a higher burden of infection, occurs most often in endemic areas.

Schistosome Dermatitis (“Swimmer's Itch”)

During penetration of cercariae, some previously exposed and unexposed persons experience a prickling sensation and may note urticaria, followed by a macular rash several hours later. In persons exposed for the first time, this rash disappears quickly, but in previously sensitized persons, it may persist and progress to a pruritic maculopapular rash that lasts for days. The rash is most severe in persons infected with schistosomes of birds or aquatic mammals, which die in the skin. This “swimmer's itch” is common in the Great Lakes region, New England, and other parts of the United States, Canada, Europe, and elsewhere in the world (see Chapter 290 ).

Acute Schistosomiasis (Katayama Fever)

Previously uninfected persons from nonendemic areas may have no symptoms after first exposure or may develop symptoms of acute schistosomiasis (Katayama syndrome) 2 to 12 weeks after exposure, particularly to S. japonicum or S. mansoni . The Katayama fever syndrome is unusual with S. haematobium and most severe with heavy infections, especially with S. japonicum. It may occur in persons previously infected with S. japonicum. Onset of fever is often acute and accompanied by chills, fatigue, headache, myalgia, abdominal pain, diarrhea, and occasionally bloody stools. As many as 70% of patients develop nonproductive cough, dyspnea, chest pain, and diffuse and nodular infiltrates seen on chest radiography. In a few cases in which lung nodules were biopsied, granulomas around eggs were seen. The liver, spleen, and lymph nodes are often enlarged. Urticaria is common, and eosinophilia occurs in nearly all cases, but eggs may not be seen in the stools until late in the illness. Symptoms and signs usually disappear after 2 to 10 weeks, but persistent and more serious disease and even death may occur with heavy infections. Lesions of the central nervous system (CNS), genital tract, and skin are due to aberrant migration of adult worms and ectopic deposition of eggs, which occurs in a small number of cases of acute infection, including in persons without systemic manifestations. In some cases eosinophil-mediated toxicity leading to vasculitis and small vessel thrombosis may be responsible for neurologic disease during acute infection. Patients with acute schistosomal encephalopathy present with headache, altered mental status, and often seizures and focal deficits. Computed tomography (CT) and magnetic resonance imaging (MRI) show edema and multifocal enhancing lesions and occasionally border zone infarctions.

Chronic Schistosomiasis

Symptoms may be absent or mild in many patients who have light or moderate worm burdens. However, careful analysis of clinical and epidemiologic data has demonstrated subtle but important morbidity in persons with even light infections. Chronic granulomatous inflammation and elevated levels of proinflammatory cytokines are believed to contribute to poor caloric intake, undernutrition, anemia of chronic inflammation, stunting, and impairment of work capacity and cognitive development in persons with chronic schistosomiasis. Similar mechanisms, along with placental infection and inflammation, may be responsible for decreased birth weight and poor birth outcomes in infants born to mothers with chronic schistosomiasis. When these previously underappreciated sequelae of infection have been taken into account, estimates of the disability associated with schistosomiasis suggest a burden of disease as much as 50 times greater than previously reported. Regardless of symptoms, eosinophilia is often present in persons with chronic schistosomiasis.

Intestinal and Hepatosplenic Schistosomiasis

Patients with light infections caused by the intestinal schistosomes S. mansoni, S. japonicum, and S. mekongi may complain of fatigue, intermittent abdominal pain, and diarrhea. In heavy infections blood loss from ulcerations or dysentery may lead to a moderate degree of anemia. Intestinal polyps have been observed, most commonly in Egypt, and strictures or large inflammatory masses may cause obstruction or mimic carcinoma. An association between intestinal schistosomiasis and cancer of the bowel has been suggested but not yet confirmed.

An early sign of chronic schistosomiasis caused by S. mansoni, S. japonica, or S. mekongi is hepatomegaly from granulomas around embolized eggs that become trapped in small portal venules. Such inflammatory hepatomegaly is common during childhood and diminishes or resolves with time; it should be distinguished from hepatomegaly due to periportal, or Symmers “pipestem,” fibrosis that is seen after years of infection in up to 5% to 10% of infected young and middle-aged adults. Granulomas and fibrosis cause a presinusoidal block to portal blood flow and eventually portal hypertension, splenomegaly, hypersplenism, and development of portosystemic collateral blood vessels. In most cases of hepatosplenic schistosomiasis, liver cell perfusion is not reduced, hepatic function is preserved, and levels of hepatic aminotransferases remain normal. Persons with coexisting alcoholic cirrhosis, chronic hepatitis B, or hepatitis C may develop jaundice and ascites. Natural progression of schistosomal disease occurs more rapidly in persons with schistosomiasis from S. japonicum than from S. mansoni and occasionally leads to decompensated liver disease as well. Repeated episodes of hematemesis from bleeding esophageal varices occur, which usually are associated with low mortality in persons with compensated disease but may lead to hepatic failure and death in persons with decompensated disease. Persons with both schistosomiasis mansoni and chronic hepatitis B or C are at higher risk for cirrhosis and perhaps hepatocellular carcinoma than persons infected with hepatitis viruses alone.

Infections with S. intercalatum and S. guineensis tend to be lighter and produce less pathology than infections due to S. mansoni or S. japonicum. Egg deposition occurs primarily in the colon, and patients may present with blood and mucus in the stool; in these cases endoscopy shows polyps and inflamed rectal mucosa. More severe disease can be seen in persons with S. mekongi infections, with advanced hepatosplenic disease similar to that seen in S. mansoni and S. japonicum infections.

Genitourinary Schistosomiasis

In infection with S. haematobium, hematuria and dysuria from inflammation and small ulcerations in the bladder mucosa may appear within 3 to 4 months of infection. In endemic areas most children have microhematuria by age 10 years, and gross hematuria is common as well. Later, polyps, hypertrophic nodules, and “sandy patches” around egg deposits may be visible on cystoscopy. Granulomas, fibrosis, and, ultimately, calcification of the bladder wall cause reflux and obstruction of urine flow, with hydroureter, hydronephrosis, chronic bacteriuria, bladder cancer, and, in a small percentage of cases, renal failure. Deposition of S. haematobium eggs in the genital tract occurs in up to 75% of women and causes sandy patches with mucosal bleeding, abnormal blood vessels, and occasionally ulcerative, nodular, or papillomatous lesions of the vulva, perineum, and cervix. These lesions, which are illustrated in WHO's pocket atlas for health care professionals (available at https://www.who.int/schistosomiasis/genital_schistosomiasis ), increase the patient's susceptibility to HIV infection and other sexually transmitted diseases, and lesions of internal pelvic organs may cause bleeding and infertility. Antischistosomal treatment of infected girls can cause regression of lesions before they become irreversible. Hematospermia results from involvement of the prostate and seminal vesicles with schistosomiasis haematobia, which has been implicated in male infertility as well. Associations have been demonstrated between S. haematobium infection and squamous cell carcinoma of the bladder; the latter has especially affected young and middle-aged men in Egypt.

Pulmonary Hypertension and Glomerulopathy

With infection with S. mansoni and S. japonica, eggs may bypass the liver through portosystemic collateral vessels and cause pulmonary disease; in infection with S. haematobium, eggs escape the vesical plexus and reach the lungs directly. Pulmonary hypertension develops in 10% to 20% of persons with hepatosplenic schistosomiasis, but only in the most severe cases does obstruction to pulmonary blood flow due to granulomatous inflammation and arteritis of small pulmonary arteries lead to cor pulmonale. Subclinical glomerulonephritis is not uncommon in persons with chronic schistosomiasis; kidney biopsy has shown deposits of immune complexes containing schistosomal antigens in the glomerular basement membrane. Clinically important glomerulopathy occurs most commonly in persons with hepatosplenic disease; its prevalence has decreased in areas where cases of severe schistosomiasis have become uncommon.

Ectopic Egg Deposition and Central Nervous System Schistosomiasis

Ectopic egg deposition from aberrant migration of adult worms and embolization of eggs from distant sites are common with all species of schistosomes and can involve almost any organ. In most cases the resulting lesions do not produce symptoms, but involvement of the CNS can cause serious cerebral and spinal cord disease. CNS schistosomiasis is most common with S. japonicum infection, occurring in as many as 2% to 5% of infections and accounting for high rates of epilepsy in endemic areas. The brain is the usual site of CNS disease with S. japonicum infection, only occasionally with S. mansoni infection, and virtually never with S. haematobium infection. Patients present with focal or generalized seizures, focal neurologic deficits, signs of increased intracranial pressure due to the mass effect, and diffuse encephalitis. CT and MRI of the head show nodular and ring-enhancing lesions with surrounding edema. With S. haematobium and S. mansoni infections, eggs reach the lower spinal cord through the Batson plexus and produce either transverse myelitis with back pain and paraplegia or myeloradiculopathy from granulomatous lesions of the conus medullaris and cauda equina.

Coinfections

Concurrent infection with other organisms may affect the clinical course of schistosomiasis. Prolonged bacteremia with Salmonella typhi and other Salmonella species has been reported in persons chronically infected with S. mansoni, S. japonicum, S. intercalatum, and S. haematobium. Unlike typhoid fever, the illness is indolent, with persistent fever, weight loss, and continuous bacteremia, and it can last months. Treatment of the bacterial infection without treating the schistosomiasis may result in relapse of bacteremia and symptoms. Salmonella can attach to the tegument and gut of schistosomes, and there is evidence that schistosomes and Salmonella share antigens that elicit immunologic tolerance to the bacterial infection. Chronic Salmonella bacteriuria can complicate infection with S. haematobium. Salmonella bacteremia and bacteriuria have been associated with glomerulonephritis and nephrotic syndrome in persons infected with either S. haematobium or S. mansoni.

Chronic coinfection with hepatitis B or C worsens the prognosis of persons with hepatosplenic schistosomiasis, as already described. The high rate of hepatitis C coinfection noted in Egypt probably reflects widespread transmission associated with parenteral antischistosomal treatment that was practiced until the 1980s. HIV coinfection has been associated with decreased egg excretion in persons with S. mansoni and S. haematobium infections and decreased hematuria with S. haematobium infections because of impaired granuloma formation and increased trapping of eggs in tissue. Schistosomiasis appears to increase susceptibility to HIV infection by as much as threefold to fourfold in women with genital lesions. Infection with schistosomes may increase HIV viral load, accelerate progression of HIV disease, and increase HIV transmission by the vertical and horizontal routes. Treatment of schistosomiasis in persons with HIV coinfection has led to a decrease in HIV viral load, an increase in CD4 ⁺ T-cell counts, and a decrease in schistosomal fecundity and egg excretion but poor killing of adult worms. An immune reconstitution syndrome after initiation of antiretroviral therapy among persons previously treated for schistosomiasis may present with worsening manifestations of schistosomiasis, such as new or increasing bloody diarrhea or hematuria, increasing hepatomegaly or splenomegaly, rash, or constitutional symptoms.

Diagnosis

Schistosomiasis should be suspected in persons who have a history of freshwater exposure in endemic areas even in the absence of suggestive clinical findings or eosinophilia. Hematuria is common with S. haematobium infections, and screening children for blood in their urine by using dipsticks has provided reliable estimates of the prevalence of infection in areas of high endemicity. Commonly used diagnostic tests for schistosomiasis include serologic tests and microscopic examination of stool, urine, or tissue for eggs.

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