1071
primary responses in those given a second vaccination,8 and results such as these, explain the reasoning behind the recent decision not to recommend vaccination for those in the UK working with cowpox and vaccinia viruses. Department of Medical Microbiology, Department of Veterinary Clinical Science, University of Liverpool, Liverpool L69 3BX, UK
DERRICK BAXBY MALCOLM BENNETT
1. Baxby D, Shackleton WB, Wheeler J, Turner A.
Comparison of cowpox-like viruses isolated from European zoos. Arch Virol 1979; 61: 337-40. 2. Fenner F, Wittek R, Dumbell KR. The orthopoxviruses. Orlando, Florida: Academic Press, 1989. 3. Thomsett LR, Baxby D, Denham EM. Cowpox in the domestic cat. Vet Rec 1978; 108: 567. 4. Bennett M, Gaskell CJ, Baxby D, et al. Feline cowpox virus infection. J Small Animal Pract 1990; 31: 167-73. 5 Editorial What’s new pussycat? Cowpox. Lancet 1987; ii: 668. 6. Baxby D. Is cowpox misnamed? A review of 10 human cases. Br Med J 1977; i: 1379-81. 7 Dixon C. Smallpox. London: Churchill, 1962. 8. Symposium. Clinical and serological study of four smallpox vaccines, comparing variation of dose and route of administration. J Infect Dis 1977; 135: 131-86.
Dengue-2 virus
in
Kenya
SIR,—The first isolation of dengue type 2 virus in East Africa was in 1982, after an epidemic of febrile illness in the Coastal Province.At the same time the prevalence of dengue-2 antibody in outpatients attending Kilifi and Malindi district hospitals in Coastal Province rose from 7% in June, 1982, to 52% by October of that year.2 A small follow-up survey at Kilifi in April, 1983, revealed a 57% (55/96) prevalence rate, which suggests a decline in transmission since the prevalence of dengue-2 antibody had not increased (Johnson BK, et al, unpublished). Environmental conditions suitable for the endemic transmission of dengue viruses in coastal Kenya and the confirmation of dengue type 2 transmission in Somalia and Sudan suggested that the virus might be an annual cause of morbidity in East Africa .3,4 In September, 1987, 1059 sera were obtained from outpatients attending Kilifi and Malindi hospitals and tested for dengue type 2 antibody by indirect fluorescence with antigen produced in VERO cells (clone E6 cells and spotted on slides). Only 1 -3% (14/1059) had antibody detectable at a minimum serum screening dilution of 1 in 20. No titres exceeded 80 and only 1 of 227 individuals under the age of 10 years (mean age 3-7) was positive. In endemic areas, the prevalence of antibody to dengue viruses in adults usually exceeds 50%,s so the low prevalence of dengue type 2 antibody in residents of coastal Kenya does not support endemic transmission. Furthermore, the low titres in positive individuals suggests a natural waning of antibody, with no indication of booster inoculations by infected mosquitoes. Our results suggest that dengue-2 virus is not endemic in coastal Kenya but occurs as irregular epidemics, as suggested by previous unconfirmed outbreaks and serological data. Whether the virus is reintroduced by infected people or by spillover from a wild primate reservoir is yet to be determined.6
Hyams KC, Oldfield EC, Scott RM, et al. Evaluation of febrile patients in Port Sudan, Sudan: isolation of dengue virus. Am J Trop Med Hyg 1986; 35: 860-65. 5. Smith CEG. The distribution of antibodies to Japanese encephalitis, dengue, and yellow fever viruses in five rural communities in Malaya. Trans R Soc Trop Med Hyg 1958; 51: 241-50. 6. Saluzzo JF, Comet M, Adam C, Eyraud M, Digoutte JP. Dengue 2 au Senégal oriental: enquête serologique dans les populations simiennes et humaines 1974-1985. Bull Soc Path Exp 1986; 79: 313-22.
4.
Serological evidence of reinfection among vaccinees during rubella outbreak SIR,-In Italy rubella immunisation is recommended for all girls aged 11-13, but is not widely practised. We report the main findings of a rubella vaccine field trial’2 with the live attenuated strain RA 27/3, which began in 1984. 596 seronegative girls were immunised. Data from all scheduled serum samples over a 5-year follow-up (1984-89) were available for 102 vaccinees who had seroconverted following immunisation. None of these subjects had evidence of reinfection, as shown by a four-fold or higher rise in titres of haemagglutination inhibiting (HAI) rubella antibodies, between 1 and 2 years after vaccination. 10 vaccinees (9-8%) were reinfected during the 5th year after vaccination, a year in which there was a rubella epidemic. None of 153 naturally infected subjects matched by age, geographical area, and antibody titres (1984) similar to those elicited by vaccination showed evidence of reinfection between 1984 and 1989. In the 10 vaccinees who had evidence of reinfection the geometric mean antibody titre (GMT) fell significantly faster in the 4 years after immunisation than in vaccinees without evidence of reinfection after the epidemic:
In all reinfected subjects the HAI titre at year 4 was 128 or lower. Of the 92 subjects without reinfection, only 32-6% had such a low HAI titre. These data suggest that a substantial number of vaccinees are reinfected by circulating wild rubella virus, even within a few years of vaccination. This risk seems more pronounced for those in whom vaccine-induced antibodies decrease rapidly after immunisation. Institute of Microbiology, University of Siena, 53100 Siena, Italy
M. G. CUSI G. M. ROSSOLINI P. E. VALENSIN
Institute of Infectious Diseases, University of Siena
C. CELLESI A. ZANCHI
C, Bianchi Bandinelli ML, Cusi MG, Di Cairano ML, Valensin PE, Rossolini A. Rubella in teenagers: epidemiology and prophylaxis in Siena, Italy. J Biol Stand
1. Cellesi
1985; 13: 283-93. PE, Rossolini GM, Cusi MG, Zanchi A, Cellesi C, Rossolini A. Specific antibody patterns over a two-year period after rubella immunization with RA 27/3 live attenuated vaccine. Vaccine 1987; 5: 289-93.
2. Valensin
Supported by NMRDC, Bethesda, Maryland, work unit no 3M161l02BSIO.AI.430. We thank Dr Atef K. Soliman and J. Gonzales for technical assitance and Dr Douglas M. Watts for his critical review of the manuscript.
Kenya Virus Research Institute, Virus Research Centre, Nairobi, Kenya
B. K. JOHNSON F. OKOTH P. M. TUKEI M. MUGAMBI
Cairo, Egypt,
J. N. WOODY J. C. MORRILL
FP0 09527, NY USA
K. C. HYAMS
US Naval Medical Research Unit No 3,
1
Johnson BK, Musoke M, Ocheng D, Gighogo A, Rees PH. Dengue-2 virus in Kenya. Lancet 1982, ii: 208-09. 2. Johnson BK, Ocheng D, Gichogo A, et al. Epidemic dengue fever caused by dengue type 2 m Kenya: preliminary results of human urological and serological studies E Afr Med J 1982; 59: 781-84. 3. Saleh EH, Hassan A, Scott RM, et al. Dengue in north-east Africa. Lancet 1985; ii: 211-12
Right-to-left shunt and neurological decompression sickness in divers SIR,-Dr Cross and colleagues (Sept 1, p 568) have misquoted our results.1 We found a 24% prevalence of right-to-left shunts in our control group, not 32 %. Also the statement that their findings are at variance with our observations (and, by implication, the findings of Moon et aP) does not stand up to scrutiny. We used predetermined criteria to divide our subjects with neurological decompression sickness (DCS) into two subgroups, which had significantly different prevalences of shunts (17% and 66%). It is invalid for Cross and colleagues to compare the prevalence in their pooled group (32%) with one of our subgroups. We are not supplied with enough information for us to subgroup their patients and compare the findings with our subgroups. We
primary responses in those given a second vaccination,8 and results such as these, explain the reasoning behind the recent decision not to recommend vaccination for those in the UK working with cowpox and vaccinia viruses. Department of Medical Microbiology, Department of Veterinary Clinical Science, University of Liverpool, Liverpool L69 3BX, UK
DERRICK BAXBY MALCOLM BENNETT
1. Baxby D, Shackleton WB, Wheeler J, Turner A.
Comparison of cowpox-like viruses isolated from European zoos. Arch Virol 1979; 61: 337-40. 2. Fenner F, Wittek R, Dumbell KR. The orthopoxviruses. Orlando, Florida: Academic Press, 1989. 3. Thomsett LR, Baxby D, Denham EM. Cowpox in the domestic cat. Vet Rec 1978; 108: 567. 4. Bennett M, Gaskell CJ, Baxby D, et al. Feline cowpox virus infection. J Small Animal Pract 1990; 31: 167-73. 5 Editorial What’s new pussycat? Cowpox. Lancet 1987; ii: 668. 6. Baxby D. Is cowpox misnamed? A review of 10 human cases. Br Med J 1977; i: 1379-81. 7 Dixon C. Smallpox. London: Churchill, 1962. 8. Symposium. Clinical and serological study of four smallpox vaccines, comparing variation of dose and route of administration. J Infect Dis 1977; 135: 131-86.
Dengue-2 virus
in
Kenya
SIR,—The first isolation of dengue type 2 virus in East Africa was in 1982, after an epidemic of febrile illness in the Coastal Province.At the same time the prevalence of dengue-2 antibody in outpatients attending Kilifi and Malindi district hospitals in Coastal Province rose from 7% in June, 1982, to 52% by October of that year.2 A small follow-up survey at Kilifi in April, 1983, revealed a 57% (55/96) prevalence rate, which suggests a decline in transmission since the prevalence of dengue-2 antibody had not increased (Johnson BK, et al, unpublished). Environmental conditions suitable for the endemic transmission of dengue viruses in coastal Kenya and the confirmation of dengue type 2 transmission in Somalia and Sudan suggested that the virus might be an annual cause of morbidity in East Africa .3,4 In September, 1987, 1059 sera were obtained from outpatients attending Kilifi and Malindi hospitals and tested for dengue type 2 antibody by indirect fluorescence with antigen produced in VERO cells (clone E6 cells and spotted on slides). Only 1 -3% (14/1059) had antibody detectable at a minimum serum screening dilution of 1 in 20. No titres exceeded 80 and only 1 of 227 individuals under the age of 10 years (mean age 3-7) was positive. In endemic areas, the prevalence of antibody to dengue viruses in adults usually exceeds 50%,s so the low prevalence of dengue type 2 antibody in residents of coastal Kenya does not support endemic transmission. Furthermore, the low titres in positive individuals suggests a natural waning of antibody, with no indication of booster inoculations by infected mosquitoes. Our results suggest that dengue-2 virus is not endemic in coastal Kenya but occurs as irregular epidemics, as suggested by previous unconfirmed outbreaks and serological data. Whether the virus is reintroduced by infected people or by spillover from a wild primate reservoir is yet to be determined.6
Hyams KC, Oldfield EC, Scott RM, et al. Evaluation of febrile patients in Port Sudan, Sudan: isolation of dengue virus. Am J Trop Med Hyg 1986; 35: 860-65. 5. Smith CEG. The distribution of antibodies to Japanese encephalitis, dengue, and yellow fever viruses in five rural communities in Malaya. Trans R Soc Trop Med Hyg 1958; 51: 241-50. 6. Saluzzo JF, Comet M, Adam C, Eyraud M, Digoutte JP. Dengue 2 au Senégal oriental: enquête serologique dans les populations simiennes et humaines 1974-1985. Bull Soc Path Exp 1986; 79: 313-22.
4.
Serological evidence of reinfection among vaccinees during rubella outbreak SIR,-In Italy rubella immunisation is recommended for all girls aged 11-13, but is not widely practised. We report the main findings of a rubella vaccine field trial’2 with the live attenuated strain RA 27/3, which began in 1984. 596 seronegative girls were immunised. Data from all scheduled serum samples over a 5-year follow-up (1984-89) were available for 102 vaccinees who had seroconverted following immunisation. None of these subjects had evidence of reinfection, as shown by a four-fold or higher rise in titres of haemagglutination inhibiting (HAI) rubella antibodies, between 1 and 2 years after vaccination. 10 vaccinees (9-8%) were reinfected during the 5th year after vaccination, a year in which there was a rubella epidemic. None of 153 naturally infected subjects matched by age, geographical area, and antibody titres (1984) similar to those elicited by vaccination showed evidence of reinfection between 1984 and 1989. In the 10 vaccinees who had evidence of reinfection the geometric mean antibody titre (GMT) fell significantly faster in the 4 years after immunisation than in vaccinees without evidence of reinfection after the epidemic:
In all reinfected subjects the HAI titre at year 4 was 128 or lower. Of the 92 subjects without reinfection, only 32-6% had such a low HAI titre. These data suggest that a substantial number of vaccinees are reinfected by circulating wild rubella virus, even within a few years of vaccination. This risk seems more pronounced for those in whom vaccine-induced antibodies decrease rapidly after immunisation. Institute of Microbiology, University of Siena, 53100 Siena, Italy
M. G. CUSI G. M. ROSSOLINI P. E. VALENSIN
Institute of Infectious Diseases, University of Siena
C. CELLESI A. ZANCHI
C, Bianchi Bandinelli ML, Cusi MG, Di Cairano ML, Valensin PE, Rossolini A. Rubella in teenagers: epidemiology and prophylaxis in Siena, Italy. J Biol Stand
1. Cellesi
1985; 13: 283-93. PE, Rossolini GM, Cusi MG, Zanchi A, Cellesi C, Rossolini A. Specific antibody patterns over a two-year period after rubella immunization with RA 27/3 live attenuated vaccine. Vaccine 1987; 5: 289-93.
2. Valensin
Supported by NMRDC, Bethesda, Maryland, work unit no 3M161l02BSIO.AI.430. We thank Dr Atef K. Soliman and J. Gonzales for technical assitance and Dr Douglas M. Watts for his critical review of the manuscript.
Kenya Virus Research Institute, Virus Research Centre, Nairobi, Kenya
B. K. JOHNSON F. OKOTH P. M. TUKEI M. MUGAMBI
Cairo, Egypt,
J. N. WOODY J. C. MORRILL
FP0 09527, NY USA
K. C. HYAMS
US Naval Medical Research Unit No 3,
1
Johnson BK, Musoke M, Ocheng D, Gighogo A, Rees PH. Dengue-2 virus in Kenya. Lancet 1982, ii: 208-09. 2. Johnson BK, Ocheng D, Gichogo A, et al. Epidemic dengue fever caused by dengue type 2 m Kenya: preliminary results of human urological and serological studies E Afr Med J 1982; 59: 781-84. 3. Saleh EH, Hassan A, Scott RM, et al. Dengue in north-east Africa. Lancet 1985; ii: 211-12
Right-to-left shunt and neurological decompression sickness in divers SIR,-Dr Cross and colleagues (Sept 1, p 568) have misquoted our results.1 We found a 24% prevalence of right-to-left shunts in our control group, not 32 %. Also the statement that their findings are at variance with our observations (and, by implication, the findings of Moon et aP) does not stand up to scrutiny. We used predetermined criteria to divide our subjects with neurological decompression sickness (DCS) into two subgroups, which had significantly different prevalences of shunts (17% and 66%). It is invalid for Cross and colleagues to compare the prevalence in their pooled group (32%) with one of our subgroups. We are not supplied with enough information for us to subgroup their patients and compare the findings with our subgroups. We
