1248 A girl delivered vaginally at 35 weeks of gestation was admitted to neonatal intensive care with severe respiratory distress. Nasopharyngeal secretions and bronchial aspirate yielded L monocytogenes. Treatment with ampicillin led to complete recovery within 10 days. L monocytogenes was not isolated from vaginal swabs from the mother who had had a mild influenza-like illness in the previous 4 months. The second patient was a boy delivered at a gestational age of 37 weeks with symptoms of severe hypoxia. He had been admitted to the same neonatal intensive care unit 2 days after the first baby and had been placed in an adjacent room. The clinical picture rapidly evolved into septicaemia and respiratory distress, and L monocytogenes was isolated from blood, gastric aspirate, and nasopharyngeal swabs. The baby responded well to ampicillin, recovering completely within 2 weeks. L monocytogenes was not isolated from the mother’s vagina and there was no history consistent with a maternal infection during gestation. The L monocytogenes strains isolated from the 2 babies were sensitive to several antibiotics. Both were assigned to serogroup 1 using commercial antisera. They were sent to Dr J. Rocourt (Pasteur Institute, Paris) for phage typing, and both were found to be non-typable. Given the inadequacy of these typing methods in establishing the epidemiological relation between the two strains, we decided to use restriction endonuclease analysis of chromosomal DNA, a technique now receiving increasing consideration in clinical microbiology and epidemiology.9 With three endonucleases (BamHI, EcoRI, and Hindlll), identical DNA fingerprints were obtained for the two strains after agarose gel electrophoresis of respective enzyme digests. Moreover, plasmid analysis showed that both isolates carried a single plasmid of identical size (about 40
MD). In conclusion, chromosomal DNA fingerprinting and plasmid analysis (neither previously applied to epidemiological investigations of listeriosis) showed that the L monocytogenes strains were indistinguishable, supporting the hypothesis of a baby-tobaby cross-infection within the neonatal unit which could not be established by the more conventional typing methods. Chromosomal DNA fingerprinting in particular appears to warrant more extensive investigation as an alternative method for typing L monocytogenes isolates. Plasmid analysis, on the contrary, is less likely to be of general value since most L monocytogenes strains carry no
plasrnids.10
Institute of Microbiology, University of Ancona Medical School,
Ancona, Italy
B. FACINELLI P. E. VARALDO
Institute of Microbiology, Medical School, University of Modena
C. CASOLARI U. FABIO
J, Saunders NA, Ridley AM, Taylor AG. Listenosis and food-borne transmission. Lancet 1988; i: 177-78. 2. Gilbert RJ, Pini PN. Listeriosis and food-borne transmission Lancet 1988; i. 472-73. 3. Sizmur K, Walker CW. Listeria in prepacked salads. Lancet 1988; i: 1167. 4. Kerr K, Dealler SF, Lacey RW. Listeria m cook-chill food. Lancet 1988; ii: 37-38 5. Hall SM, Crofts N, Gilbert RJ, Pini PN, Taylor AG, McLauchlin J. Epidemiology of listeriosis, England and Wales. Lancet 1988; ii: 502-03. 1. McLauchlin
CA, Broome CV, et al. Association of sporadic listeriosis with consumption of uncooked hot dogs and undercooked chicken. Lancet 1988; ii: 779-82. 7. McLatichlin J. Listeria monocytogenes, recent advances in the taxonomy and epidemiology of listeriosis in humans. J Appl Bacteriol 1987; 63: 1-11 8. Bibb WF, Kuffner TA, Weaver RE. Typing of Listeria monocytogenes by isoenzyme analysis. Annual meeting of the American Society for Microbiology (1986): abstr 393 9. Wachsmuth K Molecular epidemiology of bacterial infections examples of methodology and of investigations of outbreaks. Rev Infect Dis 1986; 5: 682-92. 10. Pérez-Diaz JC, Vicente MF, Baquero F Plasmids in Listeria Plasmid 1982, 8: 112-18 6. Schwartz B, Ciesielski
HIV IN SALIVA
SIR,-Dr Rozenbaum and colleagues (June 18, p 1395) report possible transmission of HIV by oral sexual activity. We and others’have rarely found infectious HIV in saliva samples. In our studies, whole saliva from 55 subjects was tested; from 16, parotid gland specimens were also obtained by cannulation of Stensen’s duct. Virus detection was by inoculation onto mitogen-stimulated
peripheral blood mononuclear cells.3 The results were:
In the 4 samples in which the virus was detected, the level was extremely low. Judging from the length of time needed to recover the HIV in culture (over two months of passage), we estimate that there is less than one infectious particle per ml. Based on the amount
of saliva that would have been involved in the sexual activities described, it is highly unlikely that transmission occurred via oral/gential contact. We cannot rule out the possible transfer of HIV by this sexual route. However, the frequency of this transmission would be so low that further information on individuals giving this risk as the sole source of virus infection should be obtained. Department of Medicine and of Stomatology, University of California School of Medicine, San Francisco, California 94143, USA
JAY A. LEVY DEBORAH GREENSPAN
Levy JA, Kaminsky LS, Morrow WJW, et al. Infection by the retrovirus associated with the acquired immunodeficiency syndrome. Ann Intern Med 1985; 103: 694. 2. Ho DD, Byington RE, Schooley RT, et al. Infrequency of isolation of HTLV-III virus from saliva in AIDS. N Engl J Med 1985; 313: 1606. 3. Levy JA, Shimabukuro J, Hollander H, Mills J, Kaminsky LS. Isolation of AIDS-associated retroviruses from cerebrospinal fluid and brains of patients with neurological symptoms. Lancet 1985; ii: 586-88. 1
TRANSMISSION OF HIV BY BLOOD FROM SERONEGATIVE DONORS
SiR,—Current screening methods will not detect recently infected blood donors who have not yet developed antibodies to HIV.’ To evaluate the importance of this "window" in terms of blood-borne transmission we evaluated the status of recipients of blood components derived from the negative donation that immediately preceded the one found to be HIV positive. We looked at 740 211 donations since July, 1985, and examined records of 53 repeat donors who had proved seronegative and were later found to be seropositive. 9 donations were via plasmapheresis. HIV antibodies were tested for by enzyme immunoassay (EIA) and western blotting. HIV antigen p24 was tested for by EIA (Diagnostics Pasteur) and positive results were confirmed by neutralisation. We tested for antibody to hepatitis B core antigen (anti-HBc) in samples from the anti-HIV positive donations. 50 recipients could be identified. 23 had died from their underlying disease and 15 were lost to follow-up, so the study was on the 12 surviving recipients transfused with blood components from 12 donors. The recipients (8 men and 4 women aged 19-75) had been transfused in haematology, gastroenterology, nephrology, and surgical wards. The interval between transfusion and testing ranged from 4 to 36 months. 3 of the 12 recipients were anti-HIV positive. None admitted any other risk factor. Of the 12 donors (10 men and 2 women aged 20-45) 9 were interviewed. 5 men admitted homosexual activity, 1 woman had a bisexual partner, and 1 woman had a heterosexual partner who had been infected by transfusion; the interview was inconclusive for 2 men. The lapse of time between the positive non-transfused and the negative transfused donations was 14, 17, and 25 weeks for the anti-HIV positive recipients and 12-49 weeks for the 9 anti-HIV
negative recipients In 5 further cases, previous seronegative plasma donations, which had not been used for transfusion or fractionation, were available for retesting. 2 donations proved positive for p24 antigen (table). 21 (40%) out of the 53 seroconverting donors tested positive for anti-HBc, including 2 of the 3 donors known to have transmitted HIV infection. The prevalence of anti-HBc carriage among anti-HIV positive donors in our institution is 60%. We can thus confirm the possibility of HIV transmission by seronegative blood donors in the serologically silent "window" period.’.2 However, the data from the 9 seronegative cases indicate short latency periods, since donations as close as 12 weeks to the anti-HIV positive donation have apparently failed to infect recipients. These findings are in keeping with the 6-8 week latency documented in patients with accurately dated contaminations. 3-55