1 5 4 Jou rna l o f Travel Medicine, Volume 4, Number 3

First Case O n the day after having taken the fourth dose of

me5oquine as chemoprophylaxis, a 19-year-old woman complained of the sudden nocturnal onset of retroster- nal and precordial pain. She had not previously experi- enced angina-like pain.The pain did not radiate, and was so severe that it kept her awake the rest of the night.The pain was constricting, not relieved by changing position, and not aggravated by deep breathing or coughing. She denied dyspnea, nausea, vomiting and sweating.The pain lasted for about 10 minutes followed by mild relief for a few minutes. Cycles of paidrelief presented through- out the night.

Her past history as well as family, social, and occu- pational history were unrevealing. The physical exami- nation revealed bradycardia (heart rate = 54 per minute), and occasional episodes of inappropriate smiling and laughing. Electrocardiogram was normal except for sinus bradycardia. Parenteral pethidine gave her mild relief for a few hours. Her symptoms resolved after 48 hours. She did not take me5oquine again, and for the rest of her 2-month stay in Uganda she never again experienced chest pain, bradycardia or psychiatric symptoms.

Second Case Two days after taking the third weekly dose of

mefloquine as chemoprophylaxis, a 70-year-old man complained of retrosternal and precordial pain.Ten years earlier he had been diagnosed with partial right bundle branch block. Physical examination was unremarkable except for bradycardia (heart rate = 56 per minute). Electrocarhogram 1 hour after onset of pain showed only partial right bundle branch block and sinus bradycardia. Parenteral pethidine gave him mild relief for a few hours. The pain resolved after 12 hours.

Such adverse events should remind us all that the decision to recommend chemoprophylaxis against malaria should always take into account the relative risk of acquiring malaria as well as the morbidity and mortal- ity of the dlsease compared to potential adverse drug reac- tions, regardless of which prophylaxis regimen is chosen.

Maurizio Ravera Hoima Hospital, Hoima, Uganda

References

1, Kofi Ekue JM. A double blind comparative clinical trial of mefloquine and chloroquine in syniptomatic falciparuni malaria. Bull World Health Organ 1983;61:713-718. HarinasutaT. Mefloquine, sulfadoxine, and pyrimethamine in the treatment of symptomatic falciparum malaria: a double blind trial for determining the most effective dose. Bull World Health Organ 1987;65:363-367. Rouveix B. Mefloquine and an acute brain syndrome. Ann Intern Med 1989;110:577-578.

2.

3.

4. 5.

Stuiver PAcute psychosis after mefloquine. Lancet 1989;2:282. Prophylactic and therapeutic use of mefloquine. Wkly Epi- demiol Rec 1989;64:247-248.

Trans-Pacific Delusional Parasitosis: The Suitcase Sign

To the Editor: Delusions of parasitosis may occur in a wide vari-

ety of organic and psychiatric disorders, but can also affect apparently well adjusted and intelligent members of society.’ A reliable feature is the “matchbox sign,”’ a variant of which recently caught me off guard.

In mid 1993, a fax arrived from a 33-year old North American computer programmer who believed he was infected with canine hookworms. Disillusioned by local clinicians, he was seeking help from doctors experi- enced with the disease. His descriptions of recurrent abdominal pains, blood counts showing eosinophilia, and a convincing history of exposure, were consistent with Ancylostoma caninum-induced eosinophilic enteritis, which he knew was my research in t e re~ t .~ By coincidence, his infection might have originated not in the United States, but in North Queensland, where he had developed a skin rash while gardening on holiday!

Numerous subsequent faxes revealed a more com- plex story: he had been consulting infectious diseases physicians throughout the United States, and predomi- nant among his symptoms were lower back pain, with leg weakness and numbness. He searched the literature diligently, faxing me copies of key papers (obtained from various university libraries), as well as reports of his clin- ical progress, test results and comments from various doctors. He also informed me that a CT scan showed enlargement and calcification of his right psoas muscle, prompting my reassurance that hookworm larvae could not be responsible. His rejoinder (with supporting ref- erences) was that these larvae were known to invade skele- tal muscle fibers, and calcification was likely to follow, as it did with other helminthiases.

Pichinella and cysticercosis serology, both done upon my advice, proved to be negative, but his serum reacted positive in our early canine hookworm ELISA (later, the more specific Western blot would test negative).This was the trigger: would I, or a close colleague, take over his management, in return for using him as a “guinea pig” in our research? After all, here was the first ever case of muscle calcification resulting from encysted hookworm larvae! He could not be dissuaded from returning to Aus- tralia to receive proper diagnosis and treatment from the “real experts in this disease.” Having just completed an intensive course of mebendazole (1 77 tablets, worth USSSOO), and spent over US$50,0OO on air fares, medical

C o r r e s p o n d e n c e 155

consultations and investigations, he was also desperate to try albendazole (then unavailable in the USA) “to erad- icate the hypobiotic larvae in my muscles.”

O n arriving in Brisbane (August 1993), he impressed me as a pleasant, respectful and thoughtful young man, albeit obsessive and introspective. He brought a small suit- case, packed with medical reports and letters, test results, x-rays, C T and MR scans, reprints of published exper- imental studies and case reports, copies of chapters from surgical and anatomical text books, and extensive per- sonal summaries and critiques of his symptoms, medical history and laboratory results.

The critical evidence of “muscle calcification” was at long last revealed-a pelvic CT scan showing a sin- gle, dense opacity which, to me (and the radiologist as well, according to the enclosed report) looked suspiciously like contrast medium in the right ureter! The psoas mus- cles appeared normal, although asynimetrical fascia1 conipartmentalization and the oblique plane of the scan could suggest to a lay observer that the right muscle was enlarged.This one flawed premise laid the foundation for an elaborately constructed edifice of internally consis- tent delusions. The past history of lumbar spine surgery for pain and disk disease, of which I had been totally unaware, then surfaced. Rather than relieve his back pain, it led to neurological complications in the right leg, which he attributed to nerve entrapment by the “enlarged” and “calcified” psoas.

Clearly, this misguided patient needed only an expla- nation, in simple terms, of his symptoms, and the biol-

ogy of hookworms, to reassure him once and for all that albendazole treatment would be futile. After I spent well into the afternoon providing just that, he apologized for using my time, thanked me profusely and, carrying his suitcase out the door, expressed disappointment at my obtuseness and waste of this opportunity to extend our research. His quest would continue for albendazole, the only solution to all his problems.When contacted in late 1995, he had completed an 18-day course of albenda- zole 800 mg b.d. (purchased in Mexico), and had com- menced an exercise program; his musculoskeletal symptoms had markedly improved.

Delusional parasitosis can assume an interesting array of forms, and travel medicine physicians should be aware of the less conventional manifestations of this fas- cinating but usually refractory problem.

Paul Pro& M B BS, PhD, FRACC FRCPA, FAFPHM, FACTM Associate Professor in Medical Parasitology, Department o f Parasitology 7 k e University of Queensland, Australia

References

1.

2. 3.

Wykoff RE Delusions of parasitosis: a review. Rev Infect Dis

Editorial.The matchbox sign. Lancet 1983;2:261. Loukas A, Croese J, Opdebeeck J, Prociv P. Immunologic incrimination of Ancylusfuma caninurn as a human enteric pathogen. Am JTrop Med Hyg 1994;50:69-77.

1987;9:433-437.

Submitted by Alan M. Spira, M.D.