BENEFITS OF HIV ANTIBODY TESTING IN SYMPTOM-FREE RISK GROUPS

512 within 3-8 weeks and one within 6 months.6 CSF contained 50-1140 white cells1 with 57-97% polymorphs. Neither toxoplasma nor HIV-1 infection of the nervous system accounted for this man’s clinical course. Despite the absence of histological proof, he very probably had the CMV-associated cauda equina syndrome described above. Administration of ganciclovir has been advised in such cases and our patient is, to our knowledge, the first whose symptoms regressed. Cauda equina syndrome in a seropositive patient is an indication for treatment by ganciclovir. Departments of Neurology and Internal Medicine, CMC Foch, 92151 Suresnes, France

PH. GRAVELEAU R. PEROL A. CHAPMAN

exceeds that of its Caribbean neighbours, then permanent quarantine is not a viable containment strategy. It is understandable that many countries find it difficult to be entirely candid about the extent of the epidemic. It is nevertheless critical that reliable information be transmitted to the World Health Organisation so that the true magnitude of the problem can be appreciated and the necessary resources mobilised. St Elizabeth’s

Hospital,

WILLIAM H. ANDERSON

Boston, Massachusetts 02135, USA 1 Bayer R, Healton C. Conrolling AIDS 2 DeMedina M, Fletcher NA, Valledor

Cuba N Engl JMed 1989; 320: 1022-24 MD, Ashman M, Gordon AM, Schiff ER. Serological evidence for HIV infection in Cuban immigrants in 1980. Lancet 1987; m

ii 166. 1. Behar

R, Wiley C, McCutchan JA. Cytomegalovirus polyradiculoneuropathy in acquired immune deficiency syndrome. Neurology 1987; 327: 557-61. 2. Bishopric G, Bruner J, Butler J. Guillam-Barré syndrome with cytomegalovirus infection of peripheral nerves Arch Pathol Lab Med 1985; 109: 1106-08. 3. Eidelberg D, Sotrel A, Vogel H, Walker P, Kleefield J, Crumpacker CS Progressive polyradiculopathy in acquired immune deficiency syndrome Neurology 1986; 36: 912-16. 4.

5.

Jeantils V, Lemaitre M-O, Robert J, Gaudouen Y, Knvitzky A, Delzant G. Subacute polyneuropathy with encephalopathy in AIDS with human cytomegalovirus pathogenicity. Lancet 1986; ii: 1039. Mahieux F, Gray F, Fenelon G, et al. Acute myeloradiculitis due to cytomegalovirus as the initial manifestation of AIDS. J Neurol Neurosurg Psychiatry 1989; 52:

270-74. 6. Moskowitz LB,

7.

Gregones JB, Hensley GT, Berger JR. Cytomegalovirus-induced demyelination associated with acquired immune deficiency syndrome. Arch Pathol Lab Med 1984; 108: 873-77. Singh BM, Levine S, Yarrish RL, Hyland MJ, Jeanty D, Wormser GP. Spinal cord syndrome in the acquired immune deficiency syndrome. Acta Neurol Scand 1986; 73: 590-98.

AIDS IN CUBA AIDS control is unique, with universal of adults and testing quarantine of seropositive individuals. Draconian measures such as these suggest a major public health problem-yet Cuba claims to have a very low level of HIV seroprevalence. Bayer and Healton’ have recently reported that testing of almost 3 million Cubans gave a seropositivity rate of 89 per million, one of the lowest levels in the world. This is not plausible, given previous reports and making reasonable demographic inferences. This suggests unreliability of the Cuban programme of testing and casts doubt on the rationale for quarantine. An earlier study of confirmed seropositivity in Cuban refugees with samples taken in 1980 showed a 45-fold greater prevalence than Bayer and Healton report 8 years later. Although refugees are seldom entirely representative of the base population, it must be remembered that in 1980 HIV was much less common everywhere. Thus it would be difficult to explain this large difference by selection bias alone. The Caribbean is an intense focus of AIDS. Rates of AIDS by mid-1987 ranged from 1200 per million in Bermuda to 10 per million in Guyana.3 It seemslikely that this large range stems from reporting differences as well as genuine rates of infection.

SIR,-Cuba’s policy

on

Seropositivity may reasonably be estimated at ten to twenty times figures. By September, 1986, Cuba had reported 1 case of clinical AIDS.’4 Bayer and Healton did not give an updated figure, but their reported seropositivity would place Cuba at the extreme lower end of the scale for the region. Cuba has a population of 10million, of whom 60% are under age 30. More than 12% of the men under 30, according to Bayer and Healton, have served for extensive periods of military and diplomatic duty in central Africa. There has also been an increasing incidence of syphilis and gonorrhoea. Cuban personnel have been concentrated in Angola, for which no seroprevalence reports exist. A reasonable assumption is that Angola shares the high risk of its contiguous neighbours. Duty stations have been urban centres, and especially the oil-producing province of Cabinda, at the mouth of the Zaire river and a major focus for AIDS. Combat casualties in the south have required the use of unscreened local blood donors until recently. Thus it seems likely that Cuba will have a larger problem than Bayer and Healton report. If HIV prevalence in Cuba equals or these

3 4.

Fleming AF, et al, eds. The global impact of AIDS. New York Alan R Liss, 1988: 27 Lange WR, Jaffe JH. Aids in Haiti. N Engl J Med 1987; 316: 1409-10.

BENEFITS OF HIV ANTIBODY TESTING IN SYMPTOM-FREE RISK GROUPS

SIR,-Any attempt to broaden the scope of voluntary HIV testing to include large numbers of symptom-free individuals who may have placed themselves at risk has been countered by arguments about the problems associated with a positive test result and the absence of specific therapy. Over the past two years, evidence of the potential benefits to the individual of knowing about a positive test result early has been accumulating.1-3 Although some of the difficulties remain, these benefits deserve re-examination since they seem not to be fully appreciated either by those at risk or, often, those involved in counselling and support. There is evidence that patients with AIDS and the AID S-related complex benefit from, and experience less toxicity with, the early introduction of zidovudine. It may seem logical to extend the use of this drug to those with symptomless infection but this temptation must be resisted until placebo-controlled trials have proved a benefit to symptomless individuals and defmed the best disease stage for intervention. Since opportunistic infections progressively affect patients with low and falling CD4 T-lymphocyte counts, all symptom-free HIV-infected individuals should be clinically assessed every 3-6 months, with monitoring of CD4 counts. This approach would allow patients to benefit from any advances in therapy and from the current treatment options of zidovudine and Pneumocystis carinii prophylaxis at the earliest opportunity. The timing of intervention should ideally be resolved by controlled trials. However, the decision of the Centers for Disease Control to recommend that P carinii prophylaxis should be offered to any symptomless HIV-infected person whose CD4 count falls below 200/il or 20% of total lymphocytes’ is an indication of pressure to intervene before clinical features of immunodeficiency appear. Thus, HIV testing followed by CD4 monitoring conveys an advantage for survival. In the United States, influenza and pneumococcal polysaccharide immunisation are recommended for all HIVinfected individuals,’*before antibody responses are compromised by immunodeficiency. Haemophilus influenzae infectionand tuberculosis are risks faced by HIV-infected individuals, who might benefit from immunisation and treatment, respectively. HIV counselling and testing has been suggested for all new cases of tuberculosis and, in the United States, isoniazid prophylaxis is being recommended. (The widespread use of BCG in the UK may be protective but would make chemoprophylaxis difficult because of the difficulty in interpreting tuberculin tests.) For a seropositive female testing permits reasoned decisions about contraception and pregnancy, and may be an indication for frequent cervical screening." Those who learn that they are HIV-positive are more likely to reduce high-risk sexual behaviours than those who tested negative or who did not take an HIV test.9,10 However, some still engage in high-risk activities and specific counselling, ideally with their regular partners, may be required. Targeting of health education at this group is essential if the spread of HIV infection is to be controlled. In public health, it is not HIV testing per se around which policy should be organised, but the opportunity for counselling and the information that accompany the test.

513

false-positive result can have serious consequences, so screening tests must be confirmed. However, false-positive tests can A

almost be eliminated with confirmation in reference laboratories. A true-positive test usually causes anxiety and depression-natural reactions that to some extent can be countered by more commitment from health-care workers and counsellors. Confidentiality is essential to avoid discrimination." We are not suggesting mass screening of the low-risk population, but the growing list of benefits to the individual who has been tested positive should prompt physicians to encourage at-risk individuals to present for voluntary and informed testing. Physicians will also have to campaign to ensure that discrimination and inequalities of care are removed from population groups at risk of infection so that the benefits of HIV testing continue to outweigh the disadvantages. Infectious Diseases Unit,

City Hospital, Edinburgh EH10 5SB

C. L. S. LEEN R. P. BRETTLE A. G. BIRD

1. Rhame FS, Maki DG. The case for wider use of testing for HIV infection. N Engl J Med 1989; 320: 1248-54. 2. Lo B, Steinbrook RL, Cooke M, Coates TJ, Walters EJ, Hulley SB. Voluntary screening for human immunodeficiency virus (HIV) infection. Ann Intern Med 1989; 110: 727-33. 3. Drotman PD. Earlier diagnosis of human immunodeficiency virus (HIV) infection and more counselling. Ann Intern Med 1989; 110: 680-81. 4. CDC. Guidelines for prophylaxis against Pneumocystis cannii pneumonia in persons with human immunodeficiency virus. MMWR, June 15, 1989. 5. CDC. Prevention and control of influenza. MMWR 1988; 37: 361-64. 6. CDC. Pneumococcal polysaccharide vaccine. MMWR 1989; 38: 64-68, 73-76. 7. Rolston KV, Uribe-Botero G, Mansell PW. Bactenal infections in adult patients with the acquired immune deficiency syndrome (AIDS) and AIDS-related complex. Am J Med 1987; 83: 604-05. 8. Sillman F, Stanek A, Sedlis A, et al. The relationship between human papillomavirus and lower genital intraepithelial neoplasia in immunosuppressed women. Am J Obstet Gynecol 1984; 150: 300-08. 9. Stall RD, Coates TJ, Hoff C. Behavioural risk reduction for HIV infection among gay and bisexual men; a review of results in the United States. Am Psychol 1988; 43: 878-85. 10. Cates W Jr, Handsfield HH. HIV counselling and testing: does it work? Am J Publ Health 1988; 78: 1533-34. 11. Osbom JE. AIDS: politics and science. N Engl J Med 1988; 318: 444-47.

PREVALENCE OF AND MORTALITY FROM HIV TYPE 2 IN GUINEA BISSAU, WEST AFRICA

SIR,-Dr Poulsen and colleagues (April 15, p 827) conclude from their investigation of HIV-2 infection prevalence and mortality in Guinea Bissau that perinatal transmission of HIV-2 may be "rare or absent". We believe that such conclusions should be drawn with caution pending results of prospective studies. We report a family cluster of HIV-2 infection. A 20-month-old male child was admitted for malnutrition. He had been breast-fed until age 19 months, and had no clinically significant medical history. He was uncircumcised and had not received ritual scarification. He had a 2-week history of acute diarrhoea, appeared malnourished, and had abnormally straight and fragile hair and generalised lymphadenopathy. Enzyme-linked immunosorbent assay (ELISA) and western blot were positive for HIV-2 and negative for HIV-1antibodies. His mother, aged 31 years, had amenorrhoea and unquantified weight loss. She had never travelled outside the Ivory Coast. Physical examination showed generalised lymphadenopathy. ELISA and western blot were positive for HIV-2 and negative for HIV-1 antibodies. A 7-year-old daughter, also with generalised lymphadenopathy, showed serological evidence of HIV-2 infection. Two healthy siblings, aged 13 and 10 years, were HIV-negative. The mother has been separated from her husband for about 1 year. Serological testing of the husband, who was not examined, showed antibodies to HIV-1 and HIV-2 on ELISA, western blot, and synthetic peptide ELISA. The latter two tests sometimes allow serological distribution between HIV-1 and HIV-2 infection on crossreacting samples.1 Dual serological reactivity to HIV-1 and HIV-2 may indicate, but does not prove, dual infection.1-s This family cluster supports earlier reports that HIV-2 may be transmitted from mother to child.6 It also suggests that HIV-2 infection has been present in the Ivory Coast for at least 7 years.

Another report described antibodies to HIV-2 in two serum samples collected in the Ivory Coast in 1966/ EMMANUEL GNAORE KEVIN M. DE COCK HELENE GAYLE ANNE PORTER Projet Retro-Ci, RAMATA COULIBALY 01 BP 1712 Abidjan, Ivory Coast; MARGUERITE TIMITE AIDS Program, JEROME ASSI-ADOU Centers for Disease Control, USA; and University of Abidjan, Ivory Coast WILLIAM L. HEYWARD 1. Porter A, Lee S, De Cock K, et al. Dual serologic reactivity for HIV-1 and HIV-2 in Abidjan. Fifth International Conference on AIDS, Montreal, June 4-9, 1989. 2. Rayfield M, De Cock KM, Heyward WL, et al. Mixed human immunodeficiency virus (HIV) infection in an individual: demonstration of both HIV type 1 and type 2 proviral sequences by using polymerase chain reaction. J Infect Dis 1988; 158: 1170-76. 3. Evans LA, Moreau J, Odehouri K, et al. Simultaneous isolation of HIV-1 and HIV-2 from an AIDS patient. Lancet 1988; ii; 1389-91. 4. Simon F, Peeters M, Delaporte E, et al. HIV-2 positive sera from Cape Verde Islands and Mali react differently on HIV-1 assays. Third International Conference on AIDS and Associated Cancers in Africa, Arusha, Sept 14-16, 1988. 5. Tedder RS, O’Connor T, Hughes A, N’jie H, Corrah T, Whittle H. Envelope cross-reactivity in western blot for HIV-1 and HIV-2 may not indicate dual infection. Lancet 1988; ii: 927-30. 6. Matheron S, Di Maria H, Dormont D, et al. HIV-2 infection in mother-infant couples. Third International Conference on AIDS and Associated Cancers m Africa, Arusha, Sept 14-16, 1988. 7. Kawamura M, Yamazaki S, Ishikawa K, Kwofie TB, Tsujimoto H, Hayami M. HIV-2 in West Africa in 1966. Lancet 1989; i: 385.

CRYPTOGENIC MENINGITIS AND UNEXPLAINED EPISODES OF COMA IN A YOUNG CHILD

SiR,—Ireport an exceptional case of neurological disorder in a child in whom the cause remains obscure. A previously healthy six-year-old boy, born in Saudi Arabia, came to England at age six weeks. Since then he has never been abroad and his parents are of Anglo-Scots origin. An uncle has biopsy-proven cutaneous lupus erythematosus. He presented in August, 1987, with an eight-day history of headaches, vomiting, drowsiness, abdominal pain, and a temperature up to 38°C. A computed tomographic brain scan was normal, and the cerebrospinal fluid (CSF) contained 23 x 106/1 white cells (90% mononuclear), and 0-2 g/1 protein. Viral encephalitis was tentatively diagnosed, and in case of herpes simplex infection intravenous acyclovir was given. Intermittent fever, abdominal pain, and increasing neck stiffness and a deteriorating conscious level led to unsuccessful blind therapy with intravenous ceftazidime 4-5 g daily and metronidazole 600 mg daily. By day 13, the CSF white-cell count had increased to 50 x 106/1 (70% mononuclear), and protein to 0,4 g/1. Tests for bacterial, fungal, parasitic, viral, and tuberculous infection were negative, as was bone marrow examination. Antituberculous therapy was begun with rifampicin, isoniazid, and pyrazinamide. The boy gradually lapsed into coma,

and we thought he would die. A repeat CT scan was normal, and on day 27 he was started on prednisolone 40 mg daily. Thereafter he slowly improved, and his motor and intellectual function returned to normal. In November, 1987, when the prednisolone dose was 2-5 mg daily, he had a partial seizure, and the dose was increased to 5 mg daily for a week. In December, 1987, while receiving prednisolone 2-5 mg daily, and following a three-day history of intermittent weakness of the right leg, he had a headache, was unable to speak or use his right arm, and became comatose. A CT scan showed three wedge shaped areas of low attenuation in the left temporal, left occipital, and right parietal lobes; the appearances suggested infarction, possibly due to vasculitis. Dexamethasone 16 mg daily was started immediately, and within two days he was able to walk; he had completely recovered within a few weeks. A repeat CT scan in March, 1988, showed near complete resolution of the low attenuation areas. Steroid treatment was withdrawn gradually and was stopped in October, 1988. Full antituberculous chemotherapy was given for 18 months, and stopped in March, 1989. In June, 1989, the patient suddenly became unresponsive and comatose, with a period of six hours of intermittent seizure activity which was poorly responsive to intravenous diazepam and phenytoin. A CT scan showed a large