Widespread dissemination of cysticerci throughout the human body was reported as early as 1912 by British Army medical officers stationed in India [3]. Priest, in 1926, described probably the first case of extensive somatic dissemination of C. cellulosae in a British soldier who had swelling of his muscles, epileptic seizures, mental dullness and widespread subcutaneous nodules [4]. Subsequent studies failed to highlight this form of clinical presentation, because of its relative rarity [4]. An extensive search of the the English literature on PubMed has yielded 22 cases reported by Wadia et al. [4] and an additional 16 cases reported up until 2006.
Human cysticercosis is caused by the dissemination of embryos of T. solium from the intestine via the hepatoportal system to the tissues and organs of the body. The organs most commonly affected are subcutaneous tissues, skeletal muscles, the lungs, the brain, eyes, the liver and occasionally the heart. Widespread dissemination of the cysticerci can result in the involvement of almost any organ of the body.
The main features of DCC include intractable epilepsy, dementia, enlargement of muscles, subcutaneous and lingual nodules and a relative absence of focal neurological signs or obviously raised intracranial pressure, at least until late in the disease [1, 3]. Absence of calcification in soft tissues and the head on radiological examination and the presence of living cysticerci at biopsy or autopsy are important findings, although the latter has not been sufficiently observed. Pseudohypertrophy of the muscles is the most common presentation of DCC, followed by palpable nodules and seizures [4]. Our patient presented with epilepsy, subcutaneous nodules and nodules in the thyroid gland and did not have pseudohypertrophy.
Computed tomography (CT) scans and MRI are useful in anatomical localization of the cysts and in documentation of the natural history. MRI is more sensitive than CT as it identifies scolex and live cysts in cisternal spaces and ventricles and identifies the response to treatment [5, 6]. Unenhanced CT scans of muscles can show innumerable cysts standing out clearly against the background of the muscle mass in which they are embedded, the CT image appearing like a honeycomb or leopard spots [5]. In our patient the CT scan had a characteristic 'starry sky' appearance but did not reveal any calcified foci in muscles.
In addition to having subcutaneous nodules our patient also had cysticerci in the thyroid gland, as evidenced by ultrasound examination of the neck. Involvement of the thyroid gland has not previously been described in the literature. We could not demonstrate definitive histopathology, as biopsy from the thyroid gland could not be performed.
In addition, the symptoms of fever and arthralgia have not been previously described and are unique to our case. Our patient had fever, arthralgia and proteinuria, and was positive for non-specific RA factor and antinuclear antibodies, suggesting a type III hypersensitivity reaction which has not been reported in other cases.
Management of DCC includes symptomatic treatment of central nervous system lesions using steroids and antiepileptics. In patients with raised intracranial tension, surgical removal of cysts and ventriculoperitoneal shunting can alleviate symptoms.
Pharmacological management with the cysticidal drugs praziquantel and albendazole is indicated as they help by reducing the parasite burden [7]. These drugs hasten the death of the cysts, which may occur even in the absence of such treatment. Pharmacological treatment may be associated with severe reactions, which may result from enlargement of cysts, massive release of antigens causing local tissue swelling and generalized anaphylactic reaction [1]. Priming with corticosteroids before starting the cysticidal drug [1, 4] decreases the incidence of such complications.
