The patient is a 28-year-old male from Burma, who has been living in the United States for one year.  He presented with a 1.5 cm tender non-erythematous subcutaneous nodule on the right cheek.  The lesion is slightly mobile and has been present for the past three years.  The patient states that the lesion has gotten progressively larger over the past three years.  No other lesions were identified elsewhere on his body.  The clinical impression was a cystic lesion with concern for a parasitic infection versus a sebaceous cyst.  A local excision of the lesion was performed.

Fig 1. Dermal abscess and chronic inflammation with central irregular cavity.

Figure 1

Fig 2. Causative agent recovered from the cystic cavity showing an undulating membranous wall with thick tegument.

Figure 2

Figure 3

Figure 4

Diagnosis:

Cutaneous cysticercosis

Comment:

Abstract: Biopsy of a subcutaneous cyst of  the cheek from a 28-year-old man revealed cysticercosis. Such lesions primarily present as multiple, mobile, 1-2 cm nodules in the subcutaneous tissue.  They may be painless or mildly tender.  The overlying epidermal skin surface is usually normal and the nodular lesions are often clustered.  Most commonly, they are seen on the trunk, upper extremities, and face.  Definitive diagnosis of subcutaneous cysticercosis requires an excisional biopsy, which demonstrates the cysticercus.  For uncomplicated subcutaneous nodules, treatment requires surgical excision.  The primary significance of subcutaneous cysticercosis is that it may indicate involvement of the central nervous system (neurocysticercosis) that may need systemic anti-parasitic therapy.

Discussion: Cysticercosis affects approximately 50 million people worldwide, and is endemic in Mexico and South America, sub-Saharan Africa, India, and East Asia.  Approximately 1,000 new cases of cysticercosis are reported annually in the United States. It is a systemic illness due to dissemination of the larval form (Cysticercus cellulosae) of the pork tapeworm, Taenia solium [3]. The clinical syndromes caused by Taenia solium are categorized as either neurocysticercosis (NCC) or extra-neural cysticercosis. The most frequently reported locations are skin, skeletal muscle, heart, eye, and the central nervous system (CNS).

Subcutaneous cysticercosis primarily presents as multiple freely mobile nodules.  These nodules are 1-2 cm in size and are deep-seated in the subcutaneous tissue [6].  They may be painless or mildly tender.  The overlying skin surface is usually normal and the nodular lesions are often clustered [6].  Most commonly, they are seen on the trunk, upper extremities, and face.  Gross examination findings for subcutaneous cysticercosis may reveal a solitary cystic lesion with white-colored, solid nodules that are adhered to the cyst wall.  The differential diagnosis for subcutaneous cysticercosis includes: lipoma, neurofibroma, epidermoid cyst, sarcoidosis, scrofula, ganglion cyst, metastatic carcinoma, and lymphadenopathy.  Definitive diagnosis of subcutaneous cysticercosis requires histological examination of the biopsy sample showing the cystericercus, that appears as an undulating laminated membranous wall of a cysticercus (the larvae of a tapeworm), with associated marked inflammatory reaction.  The cyst is composed of a thick integument and an outer surface covered with microvilli. The tegumental cells may display degenerative changes in the inner layer of the cyst wall. The scolex may or may not be found in the specimen.  Additionally, stool examination for ova and parasites should be performed to assess for a concomitant intestinal parasite infection.  The primary significance of subcutaneous cysticercosis is that is a possible indicator of neurocysticercosis.

In order to assess the involvement of the CNS, a CT scan of the head (with and without contrast) should be done on all patients suspected with neurocysticercosis or confirmed cysticercosis at another body location.  Cases of neurocysticercosis will demonstrate multiple calcified cysts in the brain parenchyma on CT scan.   The serious pathologic findings of neurocysticercosis include: seizures, encephalopathy, obstructive hydrocephalus, meningoencephalitis, and vascular accidents [2].  Clinical expression of NCC depends primarily on the number and location of CNS cysticerci and degree of the host immune response and resultant peri-cystic inflammation [5].

The ingestion of encysted pork does not directly cause cysticercosis. Rather, it produces an intestinal infection of the adult T. solium tapeworm and man becomes a carrier for the T. solium eggs. T. solium worms may reach a length of several meters. The morphology of a T. solium adult worm consists of a scolex with four suckers, and a double crown of prominent hooks. When the adult tapeworm reaches the small intestine, the scolex attaches to the intestinal mucosa and a proglottid chain grows. The adult tapeworm releases three to six proglottids per day, which bear 30,000 to 70,000 eggs per proglottid into the small intestine [4]. Nearly 250,000 eggs are passed daily into the human feces and to the environment [4]. Infections with cysticercus larva occur after humans consume egg-contaminated food/water or through self-infection via the fecal-oral route [1].

Treatment depends on the location, number of cysts, and the patient’s clinical presentation. For uncomplicated subcutaneous nodules, surgical excision is sufficient.  However, for symptomatic neurocysticercosis, anti-parasitic therapy (albendazole or praziquantel) should be given in combination with corticosteroids and anticonvulsants to reduce the inflammation surrounding the cysts and lower the risk of seizures [5].  Asymptomatic cysts may never lead to symptomatic disease and in many cases do not require therapy [5].  Education of person hygiene practices and proper food handling techniques should be performed.

In our case, the patient was referred to an infectious disease specialist for further work-up; however the patient did not return for follow-up care and could not be reached.

 

References:

  • 1) Cysticercosis.  http://www.dpd.cdc.gov/dpdx/HTML/cysticercosis.htm.
  • 2) DeGiorgio CM, Medina MT, Durón R, Zee C, Escueta SP. Neurocysticercosis. Epilepsy Curr. 2004 May-Jun; 4(3):107-11. PubMed PMID: 16059465.
  • 3) García HH, Gonzalez AE, Evans CA, Gilman RH; Cysticercosis Working Group in Peru. Taenia solium cysticercosis. Lancet. 2003 Aug 16; 362(9383):547-56. PubMed PMID: 12932389.
  • 4) Davis, LE. “Neurocysticercosis” Emerging Neurological Infections edited by Power, C and Johnson RT. Taylor & Francis Group, 2005. pp 261-287.
  • 5) Riley T, White AC Jr. Management of neurocysticercosis. CNS Drugs.2003; 17(8):577-91. PubMed PMID: 12775194.
  • 6) Uthida-Tanaka AM, Sampaio MC, Velho PE, Damasceno BP, Cintra ML, de Moraes AM, Zanardi V. Subcutaneous and cerebral cysticercosis. J Am Acad Dermatol. 2004 Feb;50(2 Suppl):S14-7. PubMed PMID: 14726858.