SIMULTANEOUS BACTERIAL AND VIRAL MENINGITIS

SIMULTANEOUS BACTERIAL AND VIRAL MENINGITIS

984 reduced dose were compared with those after intramuscular vaccination with a regular dose (table). Anti-HBs (geometric mean) decreased at a simila...

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984 reduced dose were compared with those after intramuscular vaccination with a regular dose (table). Anti-HBs (geometric mean) decreased at a similar rate in both groups, and after 19-21 months reached a level about one-tenth that obtained after the third injection (month 7). Thus, the proportional decrease of anti-HBs is similar after vaccination by the two routes. A comparable decrease of anti-HBs after intramuscular vaccination was also observed in a larger group of vaccinees. 4,5 In group 1 (intradermal) of our study anti-HBs in the sera of two vaccinees with low levels after the third injection (<100 IU/1) were below the recommended protective threshold of 10 IU/1 at 19-21 months. A further three vaccinees in group 1 had anti-HBs levels below 100 IU/1, whereas in group 2 none had an anti-HBs level below 10 IU/1, and two had levels below 100 IU/1 at 19-21 months. Our results suggest that after intradermal vaccination with a reduced dose anti-HBs titres should be checked 18 months after the last injection, and those vaccinees with levels below 10 IU/1 should be revaccinated. GERT ZOULEK Max von Pettenkofer Institute for Hygiene and Medical Microbiology,

University of Munich, D-8000 Munich, West Germany

BERND LORBEER WOLFGANG JILG FRIEDRICH DEINHARDT

1. Miller KD, Gibbs RD, Mulligan MM, Nutman TB, Francis DP. Intradermal hepatitis B virus vaccine: Immunogenicity and side effects in adults. Lancet 1983; ii: 1454-56. 2. Redfield RR, Jnnis BL, Cannon HG, Scott RM, Bancroft WH Immunogenicity and reactogenicity of low dose intradermally administered Heptavax-B-vaccine in man. In: Vyas GN, Dienstag JL, Hoofnagle JH, eds. Viral hepatitis and liver disease. Orlando, Florida: Grune and Stratton, 1984: 694. 3. Zoulek G, Lorbeer B, Jilg W, Deinhardt F. Evaluation ofa reduced dose of hepatitis B vaccine administered intradermally. J Med Virol 1984; 14: 27-32. 4. Jilg W, Schmidt M, Zachoval R, Deinhardt F. Persistenz von Antikörpern gegen Hepatitis B Oberflächenantigen nach Impfung gegen Hepatitis B. Dtsch Med Wochenschr (in press). 5. Jilg W, Schmidt M, Deinhardt F, Zachoval R. Hepatitis B vaccination: How long does protection last? Lancet 1984; ii: 458.

CHRONIC LEUKAEMIA IN SIBLINGS

SIR,-The letter by Dr Lillicrap and Dr Sterndale (Sept 22, p 699) familial chronic myeloid leukaemia (CML) prompted us to report two siblings with Ph*-positive CML. The first patient was 28 years old when he was incidentally found to have leucocytosis after blood donation in December, 1967. Hb was 12-8 gldl, total WCC was 36 x 109/1, and platelets 465 x 109/1. Differential white cell count was typical of chronic phase CML. Cytochemical and cytogenetic studies confirmed PhI-positive CML. He has been treated intermittently with busulphan since diagnosis, and in 1978 had acute staphylococcal endocarditis; his aortic valve was replaced successfully. He remains well and in chronic phase. His sister, at the age of 40, presented in August, 1977, with a history of malaise and weight loss. She had 10 cm splenomegaly and a WCC of 276 x 109/1. Platelets were 178 x 109/1. Leucocyte alkaline on

score was 9 (normal range 40-100) and cytogenetic studies of unstimulated peripheral blood demonstrated the Ph’J chromosome in nearly all dividing cells. She was treated with busulphan and remained in chronic phase for 6 years until October,1983, when she became pancytopenic. In January, 1984, the WCC rose to with 88% blasts. Morphological, cytochemical, and immunological markers demonstrated a "lymphoid" blastic transformation and she was treated with vincristine and prednisone, with a return to chronic phase for 7 months. A relapse in August was followed by a further short vincristine-prednisone induced remission to chronic phase. She has now relapsed again with lymphoid blast crisis and probable CNS disease. A further feature of interest in these patients is the prolonged course of the disease, the chronic phase having lasted 17 years and 6 years, respectively. This contrasts with the more usual course, such as that described by Lillicrap and Sterndale, where blast cell transformation occurs within 3 years.

phosphatase

124 x 109/1

Department of Haematology, Queen’s University of Belfast, Institute of Pathology, Belfast BT12 6BL

ZUREENA R. DESAI M. BRIDGES

JOHN

SIMULTANEOUS BACTERIAL AND VIRAL MENINGITIS

SiR,-A 3-year-old girl was referred by her general practitioner a 24 h history of vomiting, fever, and irritability, followed by increasing drowsiness and a grand mal convulsion lasting 10 mm. On arrival at hospital she was semiconscious, poorly perfused,

with

febrile (37-7°C), with severe neck stiffness and opisthotomc posture, but no focal neurological signs. The cerebrospinal fluid (CSF) contained 3812 leucocytes/1 (95% polymorphs), 916 red blood cells/1, protein 0-95 mg/ml, glucose 0 - 2 pmol/ml, and lactate 8-35 mol/ml (upper limit of normal 2-87). A stained smear revealed numerous pleomorphic gram-negative rods. The patient was treated with intravenous chloramphenicol 100 mg/kg daily by 6-hourly injections. Haemophilus influenzae type b, beta-lactamase negative, was isolated from blood cultures and CSF within 24 h. The fever settled within 13 h of the child’s admission, but she remained irritable with persistent opisthotonus, neck stiffness, and intermittent drowsiness for over 48 h. In view of the poor clinical response to treatment, lumbar puncture was repeated 48 h after admission. The CSF contained 10 600 leucocytes/pl (90% polymorphs), 1200 red cells/1, protein 0-98 mg/ml, and glucose 21 jmol/ml. A gram-stained smear showed no organisms and culture for bacteria was negative. However, this specimen yielded echovirus type 25 in tissue culture. There was a recurrence of fever to 38 - 4° C on day 3 and this persisted for 48 h. After this the fever settled and the patient improved clinically. Chloramphenicol was continued for 12 days and the patient made an uneventful recovery. Wright et all described the first case of concurrent viral and bacterial meningitis (H znfluenzae type b and echovirus type 9). Two cases of simultaneous meningococcal and enteroviral infection of the CSF have subsequently been reported.2,3 Although viral culture of the first CSF specimen from our patient was not attempted, isolation of a virus from a second specimen taken just 48 h later strongly implies that this was a further case of simultaneous bacterial and viral meningitis. Prospective studies of the aetiology of meningitis suggest that such dual infections are very rare.l,3 Nevertheless, secondary fever during the course of treated bacterial meningitis is common and its aetiology often remains uncertain.4 In this child, persisting drowsiness prompted re-examination of the CSF, an investigation which provided an unexpected but rewarding explanation for the patient’s clinical course. ’

Department of Microbiology and Public Health Laboratory, John Radcliffe Hospital, Oxford OX3 9DU

R. P. EGLIN R. A. SWANN

University Department of Paediatrics, John Radcliffe Hospital, Oxford

D. ISAACS E. R. MOXON

Wright HT, McAllister RM, Ward R. "Mixed" meningitis: Reports of a case with isolation of Haemophilus influenzae type b and echovirus type 9 from the cerebrospinal fluid. N Engl J Med 1962; 267: 142-44. 2. Dickinson RJ, Murdoch JMcC, Edmond E. Simultaneous infection of the meninges by Coxsackie B virus and Neisseria meningitidis in an elderly female Lancet 1976; ii 1

1412. 3. Hutchinson

DN, Hesling AG, Darling WM Simultaneous bacterial and viral of meninges. Lancet 1977; i: 371. Balagtas RC, Levin S, Nelson KE, Gotoff SP. Secondary and prolonged fevers in bacterial meningitis. J Pediatr 1970; 77: 957-64. infections

4.

HTLV-I-POSITIVE T-CELL LYMPHOMA/LEUKAEMIA IN AN AFRICAN RESIDENT IN UK

SIR,-Adult T-cell lymphoma/leukaemia (ATLL) is

a

disease

closely associated with the presence, in the genome of the neoplastic cells, of human T-cell leukaemia virus (HTLV-1).1 Although the two main clusters of the disease are Japan2 and the Caribbean basin3,4 HTLV-I may have originated from Africa,’ where it is enzootic in certain species of monkey.5 It is not clear, however, whether ATLL is also prevalent in Africa. Two Nigerian patients with lymphoid neoplasia, seropositive for HTLV, one of them with ATLL, have been reported.We have recently seen an African patient with ATLL with antibodies to HTLV-1 and whose lymphocytes expressed, after culture, the major structural proteins p 19 and p241 of the retrovirus. A 29-year-old Black man, born in Sierra Leone and resident in the UK for the previous 7 years, presented with a 6-week history of