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Schistosomiasis Paul R. Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolás, NL 66451, Mexico Paul R. Earl.

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Presentation on theme: "Schistosomiasis Paul R. Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolás, NL 66451, Mexico Paul R. Earl."— Presentation transcript:

1 Schistosomiasis Paul R. Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolás, NL 66451, Mexico Paul R. Earl

2 Schistosomiasis has sometimes been termed silent, partly because disease manifestations are slow to appear after infection by cercidias (infective swimmimg stage from the snail intermediate host) in freshwater. It can be eradicated cheaply by treatment of infected children and secondly adults, although monkeys like baboons serve as reservoir hosts. Intestinal schistosomiasis caused by Schistosoma mansoni occurs in 53 countries in Africa, the Eastern Mediterranean, the Caribbean and South America.

3 Endemic countries like Brazil, China, the Philippines and Egypt have sustained control program for a prolonged period, while others such as Puerto Rico, Venezuela, Saudi Arabia, Tunisia and Morocco are nearing eradication or have already achieved this goal. In spite of these results, and of the fact that cost-effective control tools are now available, schistosomiasis is far from eradication, because it has a low priority. Like malaria and other tropical diseases, Public Health (PH) does not have or does not spend the money that is obviously required for eradication, aside from poor results due to embezzlement.

4 The World Health Organization (WHO) suggests a) make praziquantel, the drug of choice available at an affordable price at all levels of health care, b) obtain proper case management, c) integrate schistosomiasis control in school health programs, and d) give simple but effective health education. Fortunately, praziquantel will also eliminate filariasis.

5 Classification. Phylum Platyhelminthes: II. Class Trematoda II-2. Subclass Digenea Order Strigeatoida Superfamily Schistosomatoidea Family Schistosomatoidae Schistosoma japonicum S. mansoni S. haematobium

6 Life cycle. The egg contains a miracidium (a larval form) that secretes enzymes that allow the egg to pass through the blood vessel and into the lumen of the bowel or bladder, from which it is then expelled. On reaching fresh standing water, the egg hatches, releasing the miracidium. First, the miracidium finds and penetrates one of the specific snails like Linus globosus that serve as intermediate hosts; then each miracidium undergoes extensive growth to become a cercaria (final stage larva) that is produced within the snail.

7 Linus globosus, snail intermediate host

8

9 Views of continuous copulation with the female inside the male worm.

10 Mircidium

11 Life cycle (cont) 1 / Eggs are laid within the wall of small and large intestines. Females discharge 500-3,500 eggs/day. Eggs penetrate the intestinal wall to destroy the tissue and blood vessels so patients often have intestinal bleeding. Eggs sometimes flow into the liver and even the brain. Eggs develop in a week. They derive nutrition for development from the intestinal wall. The first larva, the miracidium is within the egg. 2/ Miracidia hatch immediately allowing the miracidia to escape into the water to contact an appropriate snail.

12 Stunted 11-year old boy of 22 kg with schistosomiasis.

13 Clinical manifestations. When the cercarias contact the skin and begin their penetration, a transient burning pruritus (like swimmer’s itch) may develop. Over the next 3 days, a punctate hemorrhagic component followed by crusting develops. After several weeks, the eruption resolves, leaving postinflammatory hyperpigmentation. In humans, this cercarial dermatitis is known as schistosomal dermatitis, is less severe than that produced by nonhuman schistosomes, and may be more severe in individuals who have been sensitized by previous exposure. The cercarias of swimmer’s itch likely belong to ducks or another host.

14 An acute syndrome that begins suddenly occurs in infected individuals can be related to either migration of the worm or the initial release of eggs by the mature worm. The acute syndrome, known as Katayama fever, occurs 2-6 weeks after penetration by cercarias and may last 1-2 months. That is a Japanese term; note that Schistostoma japanicum was eradicated from Japan in Manifestations include spiking afternoon fevers, chills, bronchitis, pneumonitis, headache, lymphadenopathy, hepatosplenomegaly, joint pain, diarrhea, urticaria, eosinophilia, leukocytosis and an elevated erythrocyte sedimentation rate.

15 Chronic schistosomiasis is due to a granulomatous response to egg deposition in target tissues like the bladder. Localized in the venous plexus of the host’s bladder, S haematobium releases its eggs, resulting in a characteristic urogenital syndrome in which hematuria, obstructive uropathy, and bladder cancer figure prominently. The other schistosomes that cause disease in humans are found in the venous plexus of the bowel: S japonicum in the superior mesenteric plexus and S mansoni in the inferior mesenteric plexus.

16 Diagnosis. It is systemic illness rather than cutaneous disease that leads the patient to seek treatment. The diagnosis of Katayama fever is considered when patients who recently have been in an endemic area present with fever, headache, fatigue, diarrhea or eosinophilia. Chronic illness due to complications of egg granulomas is suspected more readily when patients are in endemic areas. Difficulties may arise though, when such patients present in nonendemic areas to physicians who may be less familiar with the disease. Finding ova in the feces or urine is the standard method of diagnosis: S haematobium is an oval egg.

17 Immunological notes. Schistosoma mansoni egg-induced pulmonary granuloma formation is a cell- mediated inflammatory response associated with dominant Th2-type cytokine expression, tissue eosinophilia, and high levels of serum IgE. Reinfection after cure can result in a twofold smaller granuloma size at 6-9 weeks after infection. During primary infection schistosome-soluble egg antigen (SEA)- induced cytokine production correlates with granulomatous inflammation.


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