Cercarial dermatitis, more commonly known as swimmer's itch, is an itchy
inflammatory reaction to non-human Schistosoma parasites that enter the skin.
Generally, skin exposure to infected water in ponds, lakes or other water
bodies causes the infection. This disease is also known by the names of clam
digger's itch and sedge pool itch.
Cercarial dermatitis generally occurs in the warm, late summer weather.
It is a common skin ailment. This is mainly because a large number of
people have the regular habit of swimming in lakes and rivers. It is more
common among children, who are obviously more avid swimmers.
Diagnosis and differential diagnosis
The standard diagnostic practice in cercarial dermatitis involves a detailed
inspection of the monomorphic (presenting a single discrete unchanging
form) maculopapular eruptions in parts of the human skin that comes in
contact with the infecting water. This apart, it must also involve a record
of the patient’s updated clinical history.
The differential diagnosis of cercarial dermatitis must exclude the following:
- Insect bites
- Human schistosomiasis (particularly in Africa, Asia
and South America)
- Contact dermatitis from poison ivy
- Sea bather’s eruption
These syndromes can be differentiated from cercarial dermatitis if any
of the following conditions occur:
- Rashes in the skin locations that are covered by swimming costumes
- Skin rashes after bathing in the salty sea water
- Presence of
larval forms of crustaceans
- Presence of pieces of jelly fish tentacles
Some of the clinical examinations that can help identify the disease
and its causative factors are:
- Tests conducted with the infected patient’s serum. The serum
is examined by means of various different serological procedures.
- The cercarial fluorescent antibody test (antigen Schistosoma mansoni)
is also relevant.
Clinical features and pathology
Cercarial dermatitis displays the following clinical traits:
- Itchy monomorphic (occurring in a single form) inflammation triggered
by an immunological response to the infiltration of cercariae into
- Scattered eruptions, mainly in the bare areas of the skin
reddened papules and papulopustules
Histological (microscopic tissue study) features include:
- An enlarged epithelium
- Subepidermal oedema
- Perivascular lymphohistiocytic penetration
- Presence of cercariae
within the stratum corneum of the epidermal layer of the skin
The cercariae, which enters our skin and triggers cercarial dermatitis,
is the larvae of trematodes belonging to species of Schistosoma and Trichobilharzia.
The species T. ocellata is particularly widespread in central Europe.
The usual habitat of trematodes includes:
- Fresh water bodies such as lakes, ponds, streams, irrigation canals,
rice paddies etc.
- All salt water bodies, besides Antarctica
The average cercariae life cycle has the following pattern:
Stage 1: Primary carriers such as water birds (ducks) pass parasite eggs
in their feces.
Stage 2: The completely formed larvae (miracidiae) hatch from the eggs
in the water and enter water snails, which act as transitional carriers.
Stage 3: Miracidiae reside in the digestive gland of the snail where
they develop into sporocysts (a protective covering created by sporozoans
in which sporozoites grow) in two months time.
Stage 4: When there is suitable light available in the upper 5 cm of
the water and suitable temperature that should be greater than or equal
to 17°C, the snails discharge innumerable cercariae.
Stage 5: These cercariae once again infect water birds. They cling to
the carrier’s skin with the help of thermotactile stimulation and
non-selective chemoattractants such as ceramide and cholesterol.
Stage 6: They enter their main target hosts - human beings - through
the stratum corneum of the skin with the help of the production of proteolytic
(that can breakdown proteins or peptides into less complex molecules)
enzymes. They however die in the epidermis after a few hours.
Stage 7: The enzymes of the cercariae are immunogenic (creating immunity
or an immune response) and cause allergic reaction only after two weeks
after the initial exposure. Thereafter successive contact causes inflammation
within a few hours. In certain patients, there has been no history of
earlier skin rashes on exposure to cercariae. Often there have been only
some skin lesions on certain body locations. The lesions progressed after
the peak period of exposure.
Therapy involves both prevention and symptomatic medications. Antihistamines
and topical corticosteroids generally help check itching. After 1 to 2
weeks, the rashes reduce automatically. The best way to prevent the attack
is to avoid long-term contact with shallow, stagnant, sluggish water in
the hot summer weather.