Migration of Schistosomes in the Human Body

Infection ! schistosomula penetrate subcutaneous tissues ! find venous capillaries or lymph vessels ! migrate through the venous circulatory system into the right ventricle of the heart and the lungs ! travel hematogenously into the intrahepatic portal vein branches where development into adult worms takes place as wells as male-female pairing just prior to sexual maturity ! retrograde migration of pairs into mesenteric veins or to the vesical plexus (Table 10.2).

Depending on the Schistosoma species involved, the prepatent period lasts about four to 10 weeks. Schistosomes remain in the definitive host for an average of two to five years, but in some cases for as long as 20-40 years.

Epidemiology. Schistosomosis occurs as an autochthonous infection in tropical and subtropical regions. Aquatic freshwater snails that prefer standing or slow-moving bodies of water are the intermediate hosts for S. hematobium,

S. mansoni, S. intercalatum, and S. mekongi (Table 10.2). The intermediate hosts of S. japonicum are amphibious snails also found on moist ground and plants, e.g., in rice paddies.

Although the cycles of all Schistosoma species can include animals as hosts, humans are the most important parasite reservoirs (Table 10.2). However, animals contribute significantly to the dissemination of the eggs of S. japonicum and S. mekongi. Travelers to endemic tropical areas can acquire the infection by a single instance of contact with water containing cercariae.

Pathogenesis and clinical manifestations. The infection can be divided into the following phases:

■ Penetration phase: penetration of cercariae into the skin, either without reaction or—especially in cases of repeated exposure—with itching and skin lesions (erythema, papules), which disappear within a few days.

■ In the acute phase, about two to 10 weeks after a severe initial infection, the symptoms may include fever, headache, limb pains, urticaria, bronchitis, upper abdominal pain, swelling of the liver, spleen and lymph nodes, intestinal disturbances, and eosinophilia (= Katayama syndrome). Due to release of Schistosoma antigens, the serum antibody levels (IgM, IgG, IgA) rise rapidly and immune complexes are formed that can cause renal glomerulopathies. These symptoms persist for several days to several weeks. Normally, Schistosoma eggs are not yet excreted at the beginning of this phase (see prepatent periods). In low-level infections this phase is usually inapparent or subclinical.

■ Chronic phase: the most significant phase in pathogenic terms begins after an incubation period of about two months with oviposition by the Schis-

— Schistosoma granuloma in the Liver

— Schistosoma granuloma in the Liver

Urinary Bilharzioma

tosoma females. A large proportion (up to 50%) of the eggs laid remain in human body tissues, not only near the worms (urinary bladder, intestine), but also in more distant localizations due to hematogenous spreading (mainly to the liver and lungs, more rarely to the CNS, the skin, and other organs), where they lodge in small vessels.

The miracidia, which remain viable for about three weeks, produce antigens (proteins, glycoproteins), which are secreted through the eggshell into the tissue and are still present in the egg after the ciliated larva has died off. After antigenic stimulation of T lymphocytes secreted cytokines contribute to produce granulomatous reaction foci (so-called "pseudotubercles"): above all macrophages, neutrophilic and eosinophilic granulocytes, as well as fibro-blasts, aggregate around single eggs or a number of centrally located eggs (Fig. 10.5). These foci may merge and form a starting point for larger, granulomatous proliferations that protrude into the lumen of the urinary bladder or intestine. The eggs in the tissues die off within about three weeks and are either broken down or they calcify. The granulomas are replaced by connective tissue, producing more and more fibrous changes and scarring.

The main forms of schistosomosis are differentiated according to the localization of the lesions:

■ Urinary schistosomosis (urinary bilharziosis). Causative agent: S. hema-tobium. Incubation 10-12 weeks or longer, morbidity rate as high as 50-70%. Hematuria (mainly in the final portion of urine), micturition discomfort, hyperemia, increasing fibrosis, 1-2 mm nodules, necroses, ulcers and calcification of the bladder wall, pyelonephrosis and hydronephrosis, urethral strictures, lesions in the sexual organs. In some endemic areas, an increased incidence of urinary bladder cancer has been associated with the S. hemato-bium infection.

■ Intestinal schistosomosis (intestinal bilharziosis). Causative agents: mainly S. mansoni and S. japonicum, also S. mekongi (rare: rectal lesions caused by S. hematobium). Incubation four to 13 weeks (acute phase), months to years (chronic phase). The course of an initial infection is only rarely symptomatic (see above: Katayama syndrome), inapparent and subclinical courses being the rule. Manifestations in the chronic phase are restricted almost entirely to large intestine with hyperemia, granulomatous nodules, papillomas ("bilharziomas"), ulcerations, hemorrhages, and increasing fibrosis, abdominal pain and bloody diarrhea.

■ Other forms: the causative agents of the hepatosplenic form are mainly S. japonicum, less frequently S. mansoni. This fibrotic form is caused by eggs deposited around the branches of the portal vein in the liver ("pipestem" fibrosis according to Symmers) and results in circulatory anomalies, portal hypertension, splenomegaly, ascites, hemorrhages in the digestive tract, and other symptoms. Pulmonary schistosomosis is observed mainly in severe S. mansoni infections, more rarely in infections with other species (including S. hematobium). Cerebral schistosomosis is relatively frequent in S. japoni-cum infections (2-4%).

■ Cercarial dermatitis. Cutaneous lesions (itching, erythema, urticaria, papules) in humans, caused by (repeated) skin penetration of schistosomatid cercariae parasitizing birds (e.g., Bilharziella, Trichobilharzia) or mammals (e.g., Schistosoma spindale). The infection occurs worldwide in freshwater or brackish water and is known as "swimmer's itch." The symptoms generally abate after a few days. The cercariae of schistosomes from humans can cause similar, although usually milder, symptoms.

Immunity. The prevalence and intensity of Schistosoma infections rise in endemic regions in children until the age of about 14, followed by a decline usually also accompanied by reduced egg excretion. This acquired immune status, known as "concomitant immunity," is characterized by total or partial protection against cercarial infection. However, the schistosomes already established in the body are not eliminated and may persist for years or even decades.

The immune defense is directed against schistosomula that have penetrated the skin, are a few hours old, and present their own antigens on their surface. Young schistosomula can be killed mainly by eosinophils and macrophages assisted by specific antibodies to these antigens and/or by complement. By the time the schistosomula reach the lungs they are resistant to such cytotoxic attacks. The explanation for this phenomenon is that the older schistosomula are able to acquire host antigens (e.g., blood group or histo-compatibility antigens) and to synthesize hostlike macromolecules, thus "masking" their surfaces (= molecular mimicry) to circumvent the immune

response (= immunoevasion). Additional immunoevasive mechanisms have also been described, e.g., shedding part of the tegument and secretion of im-munosuppressive substances.

The current immune status of persons infected with Schistosoma is apparently also determined by the balance of those antibodies which enhance the above-mentioned immune response (IgE and perhaps IgA) and others that inhibit it (IgM, IgG2, or IgG4).

Diagnosis. Following the prepatent period, i.e., four to 10 weeks p.i. at the earliest, the eggs can be detected in stool specimens or in urine sediment (Fig. 10.1, p. 545, Table 10.2, p. 547). The eggs can also be found in intestinal or urinary bladder wall biopsies. Immunodiagnostic methods (Table 11.5, p. 625) are particularly useful for detecting infections before egg excretion begins (important for travelers returning from tropical regions!). Detection of microhematuria with test strips is an important diagnostic tool in bladder schistosomosis. Clinical examination with portable ultrasonic imaging equipment has proved to be a highly sensitive method of detecting lesions in the liver and urogenital tract in epidemiological studies.

Therapy. The drug of choice for treatment of schistosomosis is praziquantel, which is highly effective against all Schistosoma species and is well tolerated. Oxamniquine is effective against S. mansoni.

Control and prevention. Current schistosomosis control strategies are based mainly on regular drug therapy of specific population groups. Morbidity, mortality, and egg excretion rates are clearly reduced by such programs. Hygienic and organizational measures (construction of latrines, improvement of water supply quality, etc.) aim to reduce Schistosoma egg dissemination and contact with contaminated bodies of water. Individual preventive measures in Schis-tosoma-contaminated areas include avoidance of skin contact with natural or artificial bodies of water (freshwater). Drinking water that could be contaminated with cercariae must be decontaminated before use by boiling, chlori-nation, or filtration.

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