A 34-year-old AIDS patient in stage C3 clinical disease (1993 Centers for Disease Control and Prevention classification), developed a traumatic haematoma on the left arm in November 1994, after a fall in the countryside. One month later, the swelling appeared to spread to the left pectoral region and there was a crunching sensation when this region was fingered. Laboratory tests showed the following: white blood count 4.1 × 109/l, 78% neutrophils, haemoglobin 10 g/dl, haematocrit 30%, platelets 252 × 109/l, CD4 lymphocytes 7 × 106/l, prothrombin time test 89%. Muscle enzymes and liver function tests were normal. Echography and magnetic resonance imaging showed a dissociation of muscular fibres. In January 1995, an incision on the left arm produced a fluid that contained many transparent, spherical masses, 1–3 mm in diameter. Hydatidosis and cysticercosis serology was negative. Microscopic examination revealed parasites to have single or multiple external buds at the opposite side of the scolex invagination (sometimes evagination), which were compatible with larvae of Taenia crassiceps (Fig. 1). Ocular examination, brain computed tomography, and heart and abdominal echographies were normal. Tredemine test was negative for the patient and his two dogs.
Praziquantel (50 mg/kg daily) was started and a second operation was performed in February 1995, which showed small subcutaneous cavities with moving larvae. The dose of praziquantel was increased to 100 mg/kg daily, and albendazole was introduced at 800 mg daily. The therapy was well tolerated, and after 6 months of therapy he was considered to be in clinical remission. Administration of albendazole and praziquantel was stopped in August and September 1995, respectively. In April 1996, recurrence of T. crassiceps infection in the left arm was treated using the same drugs. One month later he was in clinical remission. In June 1996, after treatment with foscarnet for cytomegalovirus retinitis, the patient developed acute toxic renal insufficiency and hepatitis. All drugs were stopped, but 2 weeks later he developed another parasite infection, which was again treated effectively with praziquantel and albendazole at the same dosages. The patient died in December 1996 due to renal insufficiency.
T. crassiceps is a cestode parasite (tapeworm) [1–3], with a mean length of 7–14 cm. The head, called the scolex, is spherical and comprises four oval suction pads, 20 μm in diameter, and an anterior excrescence that is armed with 30–34 hooks arranged in a double crown. The body comprises 78–86 coils. The larvae of T. crassiceps are transparent, ovoid vesicles of 4–5 mm. At one of the poles, a single scolex is invaginated or sometimes evaginated. The scolex is armed with 16–17 hooks and four suction pads. The buds are situated at the opposite pole of the scolex and produce the strings of vesicles.
Rodents, the principal intermediate hosts, are infested by ingesting the eggs eliminated in the faeces of foxes, the definitive habitual host. The fox is infested after ingesting the infected rodents.
Unlike Taenia solium and Echinococcus multilocularis, T. crassiceps rarely occurs in humans, and only four human cases have been reported [4–7]. The diagnosis of intraocular infection of T. crassiceps was made in a 17-year-old girl in 1973 . Since then, two other intraocular larval forms have been reported, without association to HIV infection [5,6]. The fourth case involved a 33-year-old AIDS patient in Germany  who developed haematoma in the paravertebral area where T. crassiceps larvae were found. This was associated with a deficiency of clotting factor V. He was given praziquantel (15 mg/kg daily) with mebendazole (6 mg daily) for 2 weeks, and was only given praziquantel after a successful surgical intervention. A break in therapy was responsible for recurrence 2 months later. Two months after this, he died due to a cardiac problem and no autopsy was performed.
Our patient had no factor V deficiency. Treatment with praziquantel and albendazole was empirical and based on the drugs' efficiency in canine cases . Surgery did not seem to be sufficient to achieve a complete elimination of the parasites, but it was useful to identify the specific aetiological agent. Treatment duration for this infection has not been defined, but we suggest that it should be longer than 6 months because of the possibility of relapse.
Ingestion of taeniid eggs eliminated by foxes or dogs appears to be the mode of infection in the current case. There was no cutaneous wound for possible penetration. The development of haematoma in our present case and that in the German case seems to suggest that its presence may act as a reservoir in which the parasites mature. In our case, the two recurrences of infection occurred without trauma or haematoma.
The authors thank Natasha Curran (Royal University Hospital, Liverpool, UK) for her technical help.
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