SCHISTOSOMIASIS

SCHISTOSOMIASIS

Schistosomiases (bilharziases, schistosomoses) are severe systemic parasitic diseases, caused by flat worms - bilharziases and schistosomoses - that are separate-sex hematophag trematodes that live in the vascular system.

Five species of Schisostoma are pathogenic in human beings: S. Haematobium, the etiologic agent of urogenital schistosomiasis; S. masoni, responsible for intestinal and, sometimes, hepatosplenic schistosomiasis; S. japonicum and S. mekongi causes a redoubtable intestinal schistosomiasis, with arterial and venial complications; S. intercalatum causes a rectal schistosomiasis, with genital complications.

Schistosomiasis is the most wide-spread helmintiasis in the tropical and subtropical areas. It affects 200-300 million people worldwide, its prevalence being on the rise. In the majority of the agricultural developed areas in Africa, Middle East, South America, South-East Asia and the Caribbean, the infection with Schistosoma is endemic. Paradoxically, the fight against underdevelopment in various geographical areas, through agricultural development programs and vast irrigation works in the tropical areas, increases the risk of spreading of this parasitosis through the creation of supplementary gasteropodes aquatic 'nests', which are intermediary hosts for schistosomes. The more the special problems posed by an increase in the 353c23d prevalence of this parasitosis are justified, the more expensive and random the prophylactic measures proved to be.

Schistosomiases represent a major public health problem because of its serious consequences on the human communities due to their being wide spread, the long duration of the disease, the chronic evolution, with numerous severe complications which, in untreated cases, lead to disablement or death.

HAEMATOBIUM SCHISTOSOMA SCHISTOSOMIASIS

S. haematobium schistosomiasis (urogenital schistosomiasis) is a systemic disease caused by the settling of adult S. haematobium worms in perivesical and perirectal venial plexi, affecting mostly the urinary bladder, which leads to the emergence of hematuria.

ETIOLOGY

S. haematobium is a flat worm of class Trematoda, family Schistosomidae, genus Schistosoma.

Morphology. The body of the male adult worm is covered with a thick cuticle (with numerous thorns or tubercles), of cylindrical shape in the anterior third and flattened in the rest, having a foliaceous aspect, with closely set lateral extremities forming a cylindrical canal - gynecophoric canal - that hosts the females with which they form inseparable couples. The male measures 10-15/0.75-1 mm.

The body of the female adult is cylindrical, filiform and longer than the male: 20-26/0.2 mm.

The inseparable schistosome couples, once formed, remain in the circulatory system for a long time (10-15 or even 30-40 years).

The eggs are oval shaped and measure 83-187/60-70 microns. The eggshell (smooth, thick and transparent) surrounds a ciliar and mobile embryo called miracidium. The embryo develops in the egg in approximately 16 days. The embryonated eggs, expelled in the environment, die after 21 days if they cannot find an intermediary host in whose body to continue their development. The eggs have, at one of the poles, a characteristic polar spur.

The biologic cycle. The miracidium (a ciliar larvae) secretes lytic enzymes that allow the egg to cross the capillary endothelium, then the urinary bladder or rectum wall, to reach the lumen of these organs, from where they are expelled with the excretions (urine, stool). The development of the eggs takes place only in an aquatic environment (fresh water), if it has the proper conditions (temperature of 25-30 C, neutral pH and sufficient light). Under these conditions, the egg ecloses in 2-3 days and sets the ciliar larvae (150 microns) free. This actively swims in the water and keeps its infectiousness in the intermediary hosts for 8-12 hours (though it cannot survive in the water for more than 48 hours). Miracidium continues its development only in the body of a compulsory intermediary host, represented by the gasteropode molluscs, genus Bulinus and Planorbis. Miracidium, in contact with the body surface of a snail, actively crosses the tegument and penetrates the soft tissues of the snail where it develops, becoming a primary sporocyst. If the snail is not a potential intermediary host, the larvae is destroyed through the phagocitary action of the host organism. In 96 hours, the primary sporocyst is mature. The primary sporocyst develops and there will appear numerous secondary sporocysts that migrate in other parts of the body of the snail (lax conjunctive tissue, hepatopancreas). There takes place another larval stage; from every secondary sporocyst there will appear numerous furcocercariae (with a length of 1 mm). Finally, from one single miracidium there will develop thousands of furcocercariae, all of the same gender, which represent the infective form of the parasite for the definitive host. The duration of the development cycle in the body of the snail is 4-5 weeks. A snail can spread some 500-3000 cercariae in the water daily, in the warm hours of the day (between 10-16 in the tropical areas) and live freely in the water for 36-48 hours, after which they die if they cannot find the definitive host (man) where to continue their development.

The infestation takes place at contact with infected water (bathing, some professions: ricers, fishermen etc.). The cercariae become attached to the tegument (even indemn) and penetrate the human organism transcutaneously. Exceptionally, the cercariae, swallowed with the water, can enter the human organism crossing the buccal mucosa. After penetration they lose their caudal extremity and turn into schistosomule (another larval stage), which penetrate the epidermis, then the subcutaneous cellular tissue and, from here on, they enter the peripheral lymphatic system or the venal circulation (venules). Passively, the schistosomules reach the lung, where they continue their development, and then the left heart where, through the systemic circulation, they enter the capillaries of the hepatic portal venous system. This migration of the schistosomules lasts for 10-12 days. In the portal intrahepatic venules, they continue their development, becoming adult worms that form inseparable couples (after 26 days).

The adult worm couples travel, against the blood flow, toward the pontal places, respectively the perivesical (mainly) and pelvic venous plexi. After 3-4 months (in average 30-40 days) from the infection, the females expel the embryonated eggs in the capillary venules. Most of the eggs remain in the vessels near the vesical and intestinal lumen. Some though can penetrate the vascular wall and either stay in the tissues of the host organs (the urinary bladder wall or the intestinal wall) or penetrate their mucosa, reaching the lumen of the cavitary organs (urinary bladder, intestine), where they are excreted with the urine or faeces. Other eggs from the capillary bed are embolised in the portal ramifications in the liver, pulmonary arterioles and many other organs (central nervous system, genital tract etc.). The eggs stay alive for approximately 25 days and cause tissular reactions of the host tissues.

EPIDEMIOLOGY

Geographical spread - prevalence. Infection with Schistosoma is endemic in 74 countries in Africa, Middle East, South-East Asia, South America and Caribbean. It is estimated that there are 200-300 million people infected and that 600 million - up to a billion people worldwide are at risk to be infected with it.

S. haematobium schistosomiasis affects approximately 100 million people and is endemic in 52 countries. The main endemic areas are the Nile Valley, intertropical Africa, especially West and South Africa. Small foci are to be found in southern Tunisia, Algeria, Morocco, eastern coast of Madagascar and Mauritius. There are limited foci in Yemen, Middle East, West Asia and the Indian Ocean islands. The endemic areas are dispersed, depending on the presence and spread of gasteropodes, which are compulsory intermediary hosts for schistosomes.

The infection reservoir and the definitive host for S. haematobium is only human.

Ways of transmission. Infection is transcutaneous, the cercariae penetrating the tegument or, very rarely, the buccal mucosa through massively contaminated water consumption.

Receptivity to the disease is universal but the maximum incidence is in the childhood and teenage years, between 10-20 years. After this age, the intensity of the infection significantly decreases, a massive infection being rare in over 30-year-old people.

Immunity. The primary infection from childhood is followed by numerous reinfections in the following years but the prevalence of the disease decreases with the age (especially in over 30-year-old people). Many of the adults in the endemic areas, who have been primarily infected in their childhood years, develop a partial immunity that protects them from reinfections or, if the infection has triggered the disease, this evolves in a mild form, with a discreet clinical symptomatology.

DIAGNOSIS

A positive diagnosis is ensured by corroborating the epidemiological data (patient from an endemic area), clinical data (terminal, and then permanent, hematuria and other characteristic clinical symptoms and signs) and lab exams:

Hypereosinophilia - very high (15-50%) in the toxemic stage, then lower (2-15%);

Proof of presence of characteristic eggs in the urine and faeces, rectal biopsy material (eggs with terminal spur acid-alcohol resistant to Ziehl-Nielsen stain, thus colouring in green);

Proof of presence of specific seric antibodies through the following techniques: indirect immunofluorescence, ELISA, RIA, immune electrophoresis (specific 4-precipitin arc), RFC;

Proof of presence of antibodies against the peri-cercarian membrane through Vogel-Minning peri-cercaria reaction;

Proof of presence of live eggs through Oliver-Gonzales circumoval reaction;

Paraclinical examinations: simple abdominal radiography (shows vesical and ureteral calcifications), urography, cystoscopy;

Urine exam and Addis test (proteinuria, hematuria);

Functional renal exploration (urea, seric creatinine, electrolytes);

Uroculture (shows the germs that cause bacterial suprainfections).

The differential diagnosis

In the invasion stage, the differential diagnosis is made with dermatitis and various urticarial eruptions, syphilides, scab, plain lichen, pholiculitis, etc.

In the toxemic stage, the schistosomiasis must be differentiated from other febrile diseases: malaria, typhoid fever, leptospirosis, septicaemia, tuberculosis, brucellosis, Dengue fever, arbovirosis and influenza.

In the stage period, the differential diagnosis is made with other urogenital, liver, intestinal, cardio-pulmonary and nervous affections.