Schistosomiasis (Bilharzia) and Swimmer's Itch

Schistosomiasis or bilharzia is a disease affecting many people in developing countries. In the form of 'acute' schistosomiasis it is sometimes referred to as snail fever and cutaneous schistosomiasis. A similar condition causes swimmer's itch in North America but is a distinctly different condition. Although it has a low mortality rate, schistosomiasis can be very debilitating. Bilharzia, or bilharziosis, is named after Theodor Bilharz, who first described the cause of urinary schistosomiasis in 1851.

There are five species of flatworms that cause schistosomiasis. Each causes different symptoms. Schistosomiasis may travel to different parts of the body, and its localization determines the person's symptoms.

Schistosoma mansoni and Schistosoma intercalatum cause intestinal schistosomiasis.

Schistosoma haematobium causes urinary schistosomiasis.

Schistosoma japonicum and Schistosoma mekongi cause Asian intestinal schistosomiasis .

Geographical distribution and epidemiology

The disease is found in Africa, the Caribbean Eastern South America, East Asia and in the Middle East.

•  Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East.

•  S. haematobium in Africa and the Middle East.

•  S. japonicum in the Far East.

•  S. mekongi and S. intercalatum are found focally in Southeast Asia and central West Africa, respectively .

Schistosomiasis map Source: CDC

Worldwide 207 million people have the disease with 120 million being symptomatic. Urbanization, pollution, and/or consequent destruction of snail habitat has reduced exposure, with a subsequent decrease in new infections. The most common way of getting schistosomiasis in developing countries is by wading or swimming in lakes, ponds and other bodies of water which are infested with the snails (usually of the Biomphalaria Bulinus, or Oncomelania genus) that are the natural reservoirs of the Schistosoma pathogen .

Schistosomiasis life cycle. Source: CDC

Schistosomes have a trematode vertebrate-invertebrate lifecycle (infecting both a vertebrate and invertebrate), with humans being the definitive host. The life cycles of all human schistosomes are similar: parasite eggs are released into the environment from infected individuals. The eggs hatch on contact with fresh water to release the free-swimming miracidium.

Miracidia infect fresh-water snails by penetrating the snail's foot. After infection, close to the site of penetration the miracidium transforms into a primary (mother) sporocyst.

Germ cells within the primary sporocyst will then begin dividing to produce secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas. Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide again, this time producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals.

Cercariae emerge daily from the snail host in a circadian rhythm, dependent on ambient temperature and light. Young cercariae are highly motile, alternating between vigorous upward movement and sinking to maintain their position in the water. Cercarial activity is particularly stimulated by water turbulence, shadows and human skin chemicals. Penetration of the human skin occurs after the cercaria have attached to and explored the skin. The parasite secretes enzymes that break down the skin's protein to enable penetration of the cercarial head through the skin. As the cercaria penetrates skin it transforms into the schistosomulum stage.

Schistosomulum may remain in the skin for 1-2 days before going to a post-capillary venule and then travelling to the lungs where it undergoes changes for subsequent migration to the liver. Eight to ten days after penetration of the skin, the parasite migrates to the liver sinusoids.

S. japonicum migrates more quickly than S. mansoni, and usually reaches the liver within 6-8 days of penetration.

Juvenile S. mansoni and S. japonicum worms develop an oral sucker after arriving at the liver, and the parasite begins to feed on red blood cells. The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the male.

Adult worms are about 10 mm long. Snail vector

Worm pairs of S. mansoni and S. japonicum relocate to the mesenteric or rectal veins. S. haematobium schistosomula ultimately migrate from the liver to the perivesical venous plexus of the bladder, ureters and kidneys through the hemorrhoidal plexus.

Egg producing stage

Parasites reach maturity in 6-8 weeks, at which time they begin to produce eggs. Adult S. mansoni pairs residing in the mesenteric vessels may produce up to 300 eggs per day during their reproductive lives.

S. japonicum may produce up to 3000 eggs per day. Many of the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be passed out of the body in faeces.

S. haematobium eggs pass through the ureteral or bladder wall and into the urine. Only mature eggs are capable of crossing into the digestive tract, possibly through the release of proteolytic enzymes, but also as a function of host immune response, which fosters local tissue ulceration. Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged. Worm pairs can live in the body for an average of four to five years, but may persist up to 20 years.

Trapped eggs mature normally, secreting antigens that elicit a vigorous immune response. The eggs themselves do not damage the body. Rather, it is the cellular infiltration resultant from the immune response that causes the pathology classically associated with schistosomiasis.

Pathology

Above all, schistosomiasis is a chronic disease. Pathology of S. mansoni and S. japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers' pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in the brain or spinal cord. Pathology of S. haematobium schistosomiasis includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in the brain or spinal cord. Bladder Cancer diagnosis and mortality are generally elevated in affected areas.

Clinical features

Many infections are subclinically symptomatic, with mild anemia and malnutrition being common in endemic areas. Symptoms depend on where the eggs are:

Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include:

Colonic polyposis with bloody diarrhea ( Schistosoma mansoni mostly);

Portal hypertension with hematemesis and splenomegaly ( S. mansoni , S. japonicum ;

Cystitis and ureteritis ( S. haematobium ) with hematuria, which can progress to bladder cancer;

Pulmonary hypertension ( S. mansoni , S. japonicum , more rarely S. haematobium );

Glomerulonephritis; and central nervous system lesions.

Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia.

Laboratory diagnosis

Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. The stool exam is the more common of the two. For the measurement of eggs in the feces of presenting patients the scientific unit used is epg or eggs per gram. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected.

Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures.

Eggs can be found in the urine (recommended time for collection: between noon and 3 PM) and with S. japonicum na S. intercalatum. Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a Nucleopore® membrane of a standard volume of urine followed by egg counts on the membrane.

Investigation of S. haematobium should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.

Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium ) may demonstrate eggs when stool or urine examinations are negative.

The eggs of S. haematobium are ellipsoidal with a terminal spine, S. mansoni eggs are also ellipsoidal but with a lateral spine, S. japonicum eggs are spheroidal with a small knob .

Antibody detection can be useful in both clinical management (e.g., recent infections) and for epidemiologic surveys.

Treatment

Schistosomiasis is readily treated using a single oral dose of the drug Praziquantel . While Praziquantel is safe and highly effective in curing an infected patient, it does not prevent re-infection by cercariae and is thus not an optimum treatment for people living in endemic areas. As with other major parasitic diseases, there is ongoing and extensive research into developing a vaccine that will prevent the parasite from completing its life cycle in humans.

Antimony has been used in the past to treat the disease. In low doses this toxic metalloid bonds to sulfur atoms in enzymes used by the parasite and kills it without harming the host. This treatment is not referred to in present-day peer-review scholarship; Praziquantel is universally used.

Mirazid is a new Egyptian oral drug for treatment, with a promising efficacy .

Experiments have shown medicinal Castor oil as an oral anti-penetration agent to prevent Schistosomiasis and have shown that praziquantel's effectiveness depended upon the vehicle used to administer the drug (e.g., Cremophor / Castor oil)

Prevention through good design

The main focus of prevention is eliminating the water-borne snails which are natural reservoirs for the disease. This is usually done by identifying bodies of water, such as lakes, ponds, etc., which are infested, forbidding or warning against swimming and adding niclosamide, acrolein, copper sulfate, etc., to the water in order to kill the snails.

Unfortunately for many years from the 1950's onwards, despite the efforts of some clinicians to get civil engineers to take it into account in their designs, civil engineeers were busy building vast dam and irrigation schemes oblivious that this would cause a massive rise in water borne infections from schistosomiasis.

Irrigations schemes can be designed to make it hard for the snails to colonize the water, and to reduce the contact with the local population .

Prevention for travelers

The main focus of prevention is eliminating the water-borne snails which are natural reservoirs for the disease. This is usually done by identifying bodies of water, such as lakes, ponds, etc., which are infested, forbidding or warning against swimming and adding niclosamide, acrolein, copper sulfate, etc., to the water in order to kill the snails.

Recent studies have indicated the possibility of biocontrol of the parasite. Introducing or adding to existing populations of crayfish in the ponds and rivers where the parasite is prevalent would keep host snail populations down, thus significantly reducing the parasite population .

Travelers should know not to swim or bathe in freshwater in endemic countries. Anedotally travellers have been counselled to give a vigourous scrub with a towel after inadvertant immersion in possibly contaminated freshwater although this is not verifiable

Swimmers's Itch "clam digger's itch"

In Asian countries it is often named in reference to the rice paddies where it is contracted, producing names which translate to "rice paddy itch".In Japan it is called "kubure" or "kobanyo", in Malaysia, "sawah", and in Thailand, "hoi con".

Swimmer's itch, duck itch, or cercarial dermatitis, is a short-term, immune reaction occurring in the skin of people that have been infected by water-borne trematode parasites.

Symptoms, which include itchy, raised papules, commonly occur within hours of infection and do not generally last more than a week.

The trematodes that cause swimmer's itch are parasitic schistosomes that use both snails and vertebrates as hosts in their life cycles.

Most cases are caused by parasites that use waterfowl as the vertebrate host.

These avian schistosomes cannot complete their life cycles in mammals, but accidentally infect humans, giving rise to mildly itchy spots on the skin.

Within hours, these spots become raised papules that are more intensely itchy.

The papules are caused by localized inflammatory immune reactions, each corresponding to the penetration site of a single parasite, which dies in the skin within hours.

Two schistosome genera that infect waterfowl and are associated with swimmer's itch are Trichobilharzia and Gigantobilharzia .

However, swimmer's itch can also be caused by schistosome parasites of non-avian vertebrates, such as Schistosomatium douthitti , which infects snails and rodents.

The schistosomes that give rise to swimmer's itch should not to be confused with those of the genus Schistosoma , which infect humans and cause the serious human disease schistosomiasis, or with larval stages of thimble jellyfish ( Linuche unguiculata ), which give rise to seabather's eruption.

Life cycles of non-human schistosomes

The non-human schistosomes use two hosts in their life cycles.

One is a snail, the other, a vertebrate such as a mammal, bird or, in Australia, crocodile. Sexual reproduction takes place in the vertebrate host. In genera that infect birds, adult worms occur in tissues of the host's gastrointestinal tract, where they produce eggs that are shed into water with host feces.

Once a schistosome egg is immersed in water, a short-lived, non-feeding, free-living stage known as the miracidium emerges.

The miracidium uses cilia to follow chemical and physical cues thought to increase its chances of finding the first host in its life cycle, a snail.

After infecting a snail, it develops into a mother sporocyst , which in turn undergoes asexual reproduction, yielding large numbers of daughter sporocysts, which asexually produce another short-lived, free-living stage, the cercaria.

Cercariae use a tail-like appendage to swim to the surface of the water, as well as other physical and chemical cues, in order to locate the next and final host in the life cycle, a bird.

After infecting a bird, the parasite develops into a schistosomulum and migrates through the host's circulatory system (or nervous system in case of T. regenti ) to the final location within the host body where it matures and, if it encounters a mate, sheds eggs to begin the cycle anew.

Risk factors

Humans usually become infected with avian schistosomes after swimming in lakes or other bodies of slow-moving fresh water.

Snails shed cercariae most intensely in the morning and on sunny days, and exposure to water in these conditions may therefore increase risk.

Duration of swimming is positively correlated with increased risk of infection in Europe and North America, and shallow inshore waters -- snail habitat -- undoubtedly harbour higher densities of cercariae than open waters offshore.

Onshore winds are thought to cause cercariae to accumulate along shorelines. Studies of infested lakes and outbreaks in Europe and North America have found cases where infection risk appears to be evenly distributed around the margins of water bodies as well as instances where risk increases in endemic swimmer's itch "hotspots ".

Children may become infected more frequently and more intensely than adults but this probably reflects their tendency to swim for longer periods inshore, where cercariae also concentrate.

Stimuli for cercarial penetration into host skin include unsaturated fatty acids, such as linoleic and linolenic acids. These substances occur naturally in human skin and are found in sun lotions and creams based on plant oils

Control measures

Various strategies, targeting either the mollusc or avian hosts of schistosomes, has also been used by lakeside residents in recreational areas of North America to deal with outbreaks of swimmer's itch.

Copper sulphate has been used as a molluscicide to reduce snail host populations and thereby the incidence of swimmer's itch.

Another method targeting the snail host, mechanical disturbance of snail habitat, has been also tried in some areas of North America and Lake Anecy in France, with promising results.

Some work in Michigan suggests that administering praziquantel to hatchling waterfowl can reduce local swimmer's itch rates in humans.

Work on schistosomiasis showed that water-resistant topical applications of the common insect repellent DEET prevented schistosomes from penetrating the skin of mice.

Public education regarding risk factors, a good alternative to the above mentioned interventionist strategies, can also reduce human exposure to cercariae.

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References

Wikipedia Schistosomiasis and swimmer's Itch

Blankespoor, HD and RL Reimink (1991) The control of swimmer's itch in Michigan: Past, present, and future. Michigan Academician 24: 7 – 23

Blankespoor, CL, RL Reimink and HD Blankespoor (2001) Efficacy of Praziquantel in treating natural schistosome infections in common mergansers. Journal of Parasitology 87: 424 – 426

Chamot, E, L Toscani and A Rougement (1998) Public health importance and risk factors for cercarial dermatitis associated with swimming in Lake Leman at Geneva, Switzerland. Epidemiology and Infection 120: 305 – 314

The Manitoba Water Quality Handbook

Linking Swimmer's Itch Awareness with Schistosomiasis Prevention

Although both diseases are quite distinct they do share the same mode of contagion- tremadode infested water.

In North America swimmer's itch is a nuisance and occasionally gets in the news.

Abroad Balharzia is infrequent in travelers but is not as well known to take precautions against.

Explaining the risks of swimmer's itch to our out going travelers may make them more familiar with the concept of clean bathing waters since they are more likely to have heard of Swiller's itch. Explaining to them that schistosomiasis is a more dangerous diseases that is prevented in the same ways may lead to a greater acceptance and understanding of preventative measures.

Many provinces have started lake water awareness programs and the following is from Manitoba to educate summer recreational water users about swimmer's itch.