T. Bergstrom et al. Scand J Infect Dis 30204

infection most probably had occurred months earlier asjudged by the intracerebral calcifications found in the child.Such a long duration of T. gondii infection was earlierreported in 1 case, where a preconceptual infection resultedin congenital transmission (15). Whether this is an excep-tion or the rule might be answered by a PCR-based studyof the parasitaemia in mothers of congenitally infectedneonates.

REFERENCES

1. Desmonts G, Couvreur J. Congenital Toxoplasmosis: aprospective study of 378 pregnancies. N Engl J Med 1974; 290:1110–6.

2. Hohlfeld P, Daffos F, Costa JM, Thulliez P, Forestier F,Vidaud M. Prenatal diagnosis of congenital toxoplasmosiswith a polymerase-chain-reaction test on amniotic fluid. NEngl J Med 1994; 331: 695–9.

3. Thulliez P, Daffos F, Forestier F. Diagnosis of toxoplasmainfection in the pregnant woman and the unborn child: currentproblems. Scand J Infect Dis 1992; 24 Suppl 84: 18–22.

4. Gross U, Muller J, Roos T, Schrod L, Heesemann J. Possiblereasons for failure of conventional tests for diagnosis of fatalcongenital toxoplasmosis: report of a case diagnosed by PCRand immunoblot. Infection 1992; 20: 149–52.

5. Grover CM, Thulliez P, Remington JS, Boothroyd JC. Rapidprenatal diagnosis of congenital Toxoplasma infection by us-ing polymerase chain reaction and amniotic fluid. J ClinMicrobiol 1990; 28: 2297–301.

6. van de Ven E, Melchers W, Galama J, Camps W, MeuwissenJ. Identification of toxoplasma gondii infections by B1 geneamplification. J Clin Microbiol 1991; 29: 2120–4.

7. Li S, Ding Z, Liang Y. A preliminary study on the antenatal

diagnosis and prevention of the fetus toxoplasmosis infection.Chung Hua Fu Chan Ko Tsa Chih 1995; 30: 200–2.

8. Fuentes I, Rodriguez M, Domingo CJ, del C, Juncosa T, AlvarJ. Urine sample used for congenital toxoplasmosis diagnosis byPCR. J Clin Microbiol 1996; 34: 2368–71.

9. Remington JS. The present status of IgM fluorescent antibodytechnique in the diagnosis of congenital toxoplasmosis. J Pedi-atr USA 1969; 75: 1116–24.

10. Voller A, Bidwell DE, Barlett A, Fleck DG, Perkins M,Oladehin B. A microplate enzyme-immunoassay for toxo-plasma antibody. J Clin Pathol 1976; 29: 150–3.

11. Landgren M, Kyllerman M, Bergstrom T, Dotevall L,Ljungstrom L, Ricksten A. Diagnosis of Epstein–Barr virus-induced encephalitis by DNA amplification from cerebrospinalfluid. Ann Neurol 1994; 35: 631–5.

12. Weiss LM, Udem SA, Salgo M, Tanowitz HB, Wittner M.Sensitive and specific detection of toxoplasma DNA in anexperimental murine model: use of Toxoplasma gondii-specificcDNA and the polymerase chain reaction. J Infect Dis 1991;163: 180–6.

13. Burg JL, Perelman D, Kasper LH, Ware PL, Boothroyd JC.Molecular analysis of the gene encoding the major surfaceantigen of Toxoplasma gondii. J Immunol 1988; 141: 3584–91.

14. Cornelissen AWCA, Overdulve JP, Van der Ploeg M. Determi-nation of nuclear DNA of five Eucoccidian parasites, Isospora(Toxoplasma) gondii, Sarcosystis cruzi, Eimeria tenella, E.acervulina and Plasmodium berghei with special reference togamotetogenesis and meiosis in I. (T) gondii. Parasitology1984; 88: 531–53.

15. Vogel N, Kirisits M, Michael E, Bach H, Hostetter M, BoyerK, et al. Congenital toxoplasmosis transmitted from an im-munologically competent mother infected before conception.Clin Infect Dis 1996; 1055–1060.

Submitted No6ember 20, 1997; accepted March 10, 1998

Scand J Infect Dis 30: 204–205, 1998 CASE REPORT

Thrombosis of the Ulnar Veins—an UnusualManifestation of Loa loa filariasis

SØREN PETERSEN1, JENS RØNNE-RASMUSSEN2 and PETER BASSE1

From the 1Department of Orthopaedic Surgery, Næst6ed Hospital and 2Clinic for Tropical Diseases, Copenhagen,Denmark

A 49-y-old male, who had travelled in Central Africa, was admitted to hospital with oedema of the right forearm. He wasdiagnosed as having thrombosis of the ulnar veins. Subsequently eosinophilia and positive serology for filariae established theaetiologic agent as Loa loa. The patient received antithrombotic and antiparasitic therapy. This is, to our knowledge, the firstreported case of thrombosis of the ulnar veins associated with Loa loa.

S. Petersen, MD, Kingos7ej 45, st. th. DK-2630 Taastrup, Denmark

CASE REPORT

The patient a 49-y-old Dane, had during the last decade, been onnumerous safaris to Africa. In 1994 he visited northern Cameroonand in April 1996 the rain forest in the southeastern parts ofCameroon. The patient was vaccinated and had taken malariaprophylaxis according to current recommendations. Three monthsafter his return to Denmark he became increasingly tired and

dizzy, and 4.5 months after the trip, the patient’s right forearmsuddenly became tender and swollen. As the swelling increasedduring the following week, he contacted his general practitionerwho started treatment with penicillin and antihistamine. After anadditional 10 d, the swelling extended to the right wrist, and thepatient was referred to the orthopaedic department.

On admission, the entire right forearm and back of the hand was.

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An unusual manifestation of Loa loa filariasisScand J Infect Dis 30 205

Fig. 1. Contrast venography of the deep veins of the right forearm,showing occlusion of the ulnar veins below the elbow.

adult worm. Calabar swellings are recurrent localized sub-cutaneous angioedemas within the same fascial plane, usu-ally lasting from hours to a few days. Thepathophysiological mechanism is still unclear (2–4). Thecourse is usually benign, although complications includenephropathy, endomyocardial fibrosis, retinopathy,arthritis, lymphangitis, peripheral neuropathy and en-cephalopathy (2–5).

The symptoms are more often pronounced in travellers,than in the local population, and, as in our case, areaccompanied by high titres of antibody towards filariae,hypereosinophilia and low probability of detecting microfi-lariae in the blood (6, 7). Diagnosis in travellers is thereforeoften clinical, based on the history of exposure, clinicalpresentation, serology and eosinophilia (8, 9). The currentdrug of choice for loiasis is DEC (3, 10).

This case is, to our knowledge, the first report of throm-bosis of the ulnar veins associated with loiasis. A possiblemechanism of thrombosis could be compression of theveins by the surrounding oedema. We therefore would findit interesting, if patients with prolonged swellings due toloiasis were examined for venous thrombosis, to establishwhether this complication occurs more frequently.

REFERENCES

1. Rapaport SI. Hemorrhagic disorders. In: Berkow R, FletcherAJ, eds. The Merck manual, 16th edn. Rahway, NJ: MerckResearch Laboratories, 1992: 1195–206.

2. Pinder M. Loa loa—a neglected filaria. Parasitol Today 1988;4: 279–84.

3. McMahon JE, Simonsen PE. Loa loa. In: Cook GC, ed.Mansons tropical diseases, 20th edn. London: W.B. Saunders,1996: 1351–4.

4. Ottensen EA. The filariases and tropical eosinophilia. In:Warren KS, Mahmoud AAF, eds. Tropical and geographicalmedicine, 2nd edn. New York: McGraw-Hill, 1990: 420–6.

5. Carme B, Boulesteix J, Boutes H, Puruehnce MF. Five cases ofencephalitis during treatment of loiasis with diethylcarba-mazine. Am J Trop Med Hyg 1991; 44: 684–90.

6. Klion AD, Massougbodji A, Sadeler B-C, Ottesenn EA, Nut-man TB. Loiasis in endemic and nonendemic populations:Immunologically mediated differences in clinical presentation.J Infect Dis 1991; 163: 1318–25.

7. Noireau F, Apembet JD, Nzoulani A, Carme B. Clinicalmanifestations of loiasis in an endemic area in the Congo.Trop Med Parasitol 1990; 41: 37–9.

8. Rakita RM, Clinton White Jr A, Kielhofner MA. Loa loainfection as a cause of migratory angioedema: Report of threecases from the Texas Medical Center. Clin Infect Dis 1993; 17:691–4.

9. Scott JAG, Davidson RN, Moody AH, Bryceson ADM. Diag-nosing multiple parasitic infections: Trypanosomiasis, Loiasisand Schistosomiasis in a single case. Scand J Infect Dis 1991;23: 777–80.

10. Moore TH, Nash TE. Tissue helminths. In: Schlossberg D, ed.Current therapy of infectious disease. St Louis, Mosby-YearBook. 1996: 552–3.

Submitted No6ember 4, 1997; accepted March 3, 1998

oedematous. The sensibility and mobility of the extremity wasnormal, and there was no discolouration. An ultrasound Dopplerscan showed normal venous flow from the cubital vein and cen-trally. Contrast venography was performed and showed occlusionof the ulnar veins (Fig. 1). As a thrombosis of the ulnar veins wassuspected, anticoagulation therapy with heparin and phenprocou-mon was started.

Blood biochemistry revealed normal values of haemoglobin,haematocrit, thrombocytes and coagulation parameters. However,plasma D-dimer was raised to 1.5 mg/l (0.0–0.5 mg/l), indicatingthat cross-linked fibrin had been present (1). Analysis af the WBCshowed hypereosinophilia [absolute eosinophil count 3.37×109/l(0.04–0.45×109/l)]. In the blood smear no malarial parasites ormicrofilariae were seen.

The patient was referred to a specialist in tropical medicine,who, after finding positive filarial antibodies and a p-IgE elevatedto 804 IU/ml (0–100 IU/ml), diagnosed the patient as havingloiasis, and instituted treatment with diethylcarbamazine (DEC)for 21 d. The anticoagulation therapy was discontinued after 2months, and 6 months later he was symptomless, with bloodsamples that were nearly normalized.

DISCUSSION

The filaria Loa loa is endemic in the forest areas in Centraland West Africa, and is transmitted by flies of the genusChrysops (2). The typical symptoms are fatigue, pruritus,Calabar swellings and subconjuntival migration of the

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