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DURATION OF PROTECTION ACCORDED BY LIVE ORAL POLIOVIRUS VACCINE
831
Letters to the Editor
mortality, in part, on interval since delivery should consider the advantage of investigating deaths occurring within 90 days after delivery. When possible, they should compare mortality rates from maternal and non-maternal
CHANGING THE DEFINITION OF MATERNAL MORTALITY: A NEW LOOK AT THE POSTPARTUM INTERVAL often been studied in detail because of varied definitions and incomplete reporting.The World Health Organisation currently defines maternal mortality as deaths occurring during pregnancy or within 42 days of the end of pregnancy.2 We have used data from Georgia to show that increasing the interval to 90 days would increase the detection of maternal deaths without including an excessive number of non-maternal deaths, and that maternal mortality declines exponentially during the postpartum period while non-maternal mortality does not
SIR,-Maternal mortality has
not
change. To determine the risk of death from maternal causes after delivery of a live infant, we compared information on 159 233 live births to Georgia women for 1975and 1976 with the information on the 3190 deaths of Georgia women in 1975, 1976, and the first 2 months of 1977. Thus, women were observed for 2-14 months after delivery. Based on medical records, we classified the causes of death as maternal and non-maternal. We identified 36 deaths from maternal causes and 42 from non-maternal causes. Details of these cases will be published elsewhere. 3 We used life table methodology to estimate mortality risks after delivery and assumed that the number of women observed decreased linearly between months 2 and 14. Mortality from maternal causes during the first year after delivery was 38 per 100 000 woman-years of observation and 44 from nonmaternal causes. Mortality from maternal causes was 433 per 100 000 woman-years during the first 9 days after delivery and declined to 4 per 100 000 woman-years in the last interval (see table). Moreover, maternal factors caused more deaths than did nonmaternal factors for each interval during the first 2 postpartum months and for 2 of 6 deaths during the third postpartum month. The 42-day limit excludes 6/36 (17%) deaths from maternal causes, and ignores the 43-90 day period when 4/9 (44%) of the deaths were from maternal causes. The causes of these deaths were thrombotic thrombocytopenia, renal failure, pulmonary embolism following a caesarean section delivery, and heart failure. Investigating all deaths in the first 3 months compared with the first 42 days postpartum increased the number of deaths from 39 to 46. During the first 42 days postpartum, 8% of all deaths were from maternal causes, while 74% of deaths in the first 90 days were from maternal causes. Extending the investigation to all deaths during the first year postpartum would result in a decrease to 46%. We conclude that those who base their definition of maternal
causes.
Family Planning Evalulation Division, Center for Health Promotion and Centers for Disease Control, Atlanta, Georgia 30333, U.S.A.
Education,
ROGER W. ROCHAT GEORGE L. RUBIN RICHARD SELIK BENJAMIN P. SACHS CARL W. TYLER
DURATION OF PROTECTION ACCORDED BY LIVE ORAL POLIOVIRUS VACCINE
SIR,-Concern has been expressed about the duration of protecprovided by live oral poliovirus vaccine, since antibody levels
tion
seem to
fall with time.
20 years ago, when I
was 38, my poliovirus antibodies were I had been for study because I had few antibodies selected reported. against type I poliovirus and no antibodies against types II and III, had never received a killed poliovirus (Salk) vaccine, and had shown immunological responsiveness in 1958 to an experimental modified live virus (chick embryo origin) anti-rabies vaccine. Three experimental capsules were administered orally one each week for a 3 week period. Each capsule contained approximately 100 000 TCD50 (median tissue culture infecting dose) of type I, II, or III live, attenuated poliovirus vaccine (Lederle). This procedure failed to produce an immune response other than a minimal increase in type I titre (an increase in antibody titre to >1:4 was used to indicate an adequate immunological response to oral poliovirus vaccine). The subsequent oral administration of a 0’ 5 ml dose of a new, experimental, liquid, trivalent, live, attenuated poliovirus vaccine (Lederle) containing about (300 000 TCDso of each poliovirus type, also failed to prompt a serological response.
1. Cox
HR, Cabasso VJ, Markham FS, Moses MJ, Moyer AW, Roca-Garcia M, Ruegsegger JM. Immunological response to trivalent oral poliomyelitis vaccine. Bri Med J 1959; II: 591-97.
ANTIBODY PATTERN OF AN ADULT AFTER THE ADMINISTRATION OF DIFFERENT DOSAGES OF
LIVE ATTENUATED ORAL POLIOVIRUS VACCINE
1 Rochat RW Maternal and perinatal mortality statistics. In: Silvio A, ed. Obstetrical practice. St Louis CV Mosby, 1980. 2 World Health Organisation. Manual of the international statistical classification of diseases, injuries, and causes of death. 1975: Vol. I. Geneva: WHO, 1977. 3 Rubin G, McCarthy BJ, Shelton J, Rochat RW, Terry J. The risk of childbearing reevaluated Am J Publ Health (in press).
MORTALITY DUE TO MATERNAL AND NON-MATERNAL CAUSES, BY INTERVAL AFTER DELIVERY, GEORGIA, 1975-76
Entries in italic type refer to post feeding samples. * No. 7-1238-801 contained equal volumes of type I (no. 7-1231-115), type II (no.F 7-1232-217), and type II (no. 7-1233-319) vaccines, Lederle. tNo. 7-1238-801 Lederle. * Concentrations of approximately 800 000 type I, 100 000 type 2, and 500 000 type 3 (Sabin) Onmune Lederle. § NDC 0005-2084-07 (Sabm) Onmune Lederle. Before this date, titres were measured by the macroscale; from Dec. 19, 1974, on, the titres were measured on microscale. ** During the summer of 1977, additional testing of the sera obtained on Oct. 12, 1976, and March 8, 1977, revealed the same type of fluctuation on the repeated type I assays.
-
832 I was given a 2-00 ml dose containing approximately 1200 000 TCDso of each of the three poliovirus strains. Titration of a serum sample a month later showed a good response: antibody titres were 1: 1024 for type I, 1: 512 for type II, and 1: 32 for type III. This antibody conversion strongly influenced the final choice of dosage strength for commercial preparations. Since 1959, I have been tested periodically and have had two additional booster doses-one in 1970 and the other in 1976-of ’Orimune’ poliovirus vaccine live, attenuated, oral, trivalent, Sabin strains, type 1, 2, and 3. These doses consisted of poliovirus concentrations which had been adjusted so that the predominant type (type 2) might not inhibit the action of the others (types 1 and 3). These concentrations and the booster response antibody patterns they induced are shown in the accompanying table, which also contains data from previous vaccine administrations. A gradual decline in poliovirus antibody levels has been reported in children at 1;21, 2, and 3;3 5;4 8;5 and 106 years after immunisation. Based on the response of the adult individual reported here, it appears that although antibody titres may decline in level, they rise promptly in response to booster doses. Presumably, low antibody titres in proven vaccine-responsive individual would also respond to exposure to live wild viruses; thus protection would be afforded under those circumstances.
IF TITRES TO KHF VIRUS IN SEVEN SERA FROM GREEKS
Finally, ’
P.O. Box 338, San Anselmo, California 94960, U.S.A.
ALEXANDER THOMSON
been higher than the values shown in the table because the sera were not frozen and spent 2 weeks in transit from Greece to Korea. The results point to the spread of KHF virus in northern Greece. The next step is to attempt KHF virus isolation from patients in Greece with syndromes resembling Korean haemorrhagic fever. This work was partly supported by NATO research grant RG 12380, and partly by grant DAMD-17-80-G-9468 of the U.S. Army Medical Research and Developmental Command, Washington, D.C. W.H.O.
Collaborating Centre for the Study of Korean Haemorrhagic Fever,
Institute for Viral Diseases, Korea University Medical College, Seoul, Korea
Ho WANG LEE
Department of Microbiology,
SEROLOGICAL EVIDENCE FOR KOREAN HAEMORRHAGIC FEVER IN GREECE
SIR,-The aetiological agent of Korean haemorrhagic fever (KHF) is a virus carried by the rodent Apodemus agrarius coreae in the rural endemic areas of Korea. Epidemic haemorrhagic fever with an associated renal syndrome attracted attention during the Korean war and very similar syndromes have been reported in the U.S.S.R., China, Scandinavia, Eastern Europe, and Japan. The isolation of the aetiological agent of KHF7,has permitted the establishment, by indirect fluorescent (IF) antibody technique, of the close relation of KHF with haemorrhagic fever with an associated renal syndrome seen outside Korea. We have looked for serological evidence of KHF virus people in northern Greece, using the indirect IF technique. KHF antigens were derived from KHF viral passage in A. agrarius.2 445 sera from healthy people living in Greek towns or villages close to the Bulgarian and Yugoslavian borders and 97 sera from patients with glomerular disease of unknown origin (kindly provided by Prof. P. Metaxas, University of Thessaloniki) were posted without dry ice to Korea for antibody testing. 4 of the 445 healthy people and 3 of the 97 sera from patients with glomerular disease were positive for KHF antibody (see table). The frequence ofseropositivity in healthy Greeks is similar to that of Korean people living in non-endemic areas, whereas the frequency in the patients with glomerular disease is similar to that of Korean people living in hyperendemic areas.8 The mean titres of IF antibodies in Korea were much higher, perhaps because of some 9 antigenic difference between KHF and the agent in Greece. However, our true IF antibody titres against KHF virus may have
among
2. 3 4.
5.
6. 7.
8. 9.
W. Response of infants to trivalent poliovirus vaccine (Sabm strains). Paediatrics 1967; 40: 980-85. Cabasso VJ, Nozell H, Ruegsegger JM, Cox HR. Poliovirus antibody three years after oral trivalent vaccine (Sabin strains). Pediat 1966; 68: 199-203. J Krugman RD, Hardy GE Jr, Sellers C, Parkman PD, Witte JJ, Meyer BC, Meyer HM Jr. Antibody persistence after primary immunization with trivalent oral poliovirus vaccíne. Pediatrics 1977; 60: 80-82. Rousseau WE, Noble GR, Tegtmeier GE, Jordan MC, Chin TDY. Persistence of poliovirus neutralizing antibodies eight years after immunization with live, attentuated-virus vaccine. N Engl J Med 1973; 289: 1357-59 Sanders DY, Cramblett HG. Antibody titers to polioviruses in patients ten years after immunization with Sabin Vaccine. J Pediat 1974: 406-08 Lee HW, Lee PW. Korean haemorrhagic fever I Demonstration of causing antigen and antibodies. Korean J Int Med 1976; 19: 371-83. Lee HW, Lee PW, Johnson KM. Isolation of the etiological agent of Korean hemorrhagic fever. J Infect Dis 1978; 137: 298-308. Svedmyr A, lee PW, Gajdusek DC, Gibbs CJ, Nystrom K. Antigenic differentiation of the viruses causing Korean haemorrhagic fever and epidemic (endemic) nephropathy of Scandinavia. Lancet 1980; ii: 315-16.
Murphy
School of Medicine, Aristotelian University of Thessaloniki, Thessaloniki, Greece
A. ANTONIADIS
LAGOS BAT VIRUS IN SOUTH AFRICA
SIR,-In June, 1980, a virus indistinguishable from that of rabies
by the fluorescent antibody-test was isolated from the brain of an unidentified bat found sick iti a garden in Pinetown, a borough adjoining Durban, Natal. During the next three months five more made and in these cases the bats were identified as being Epomophorus wahlbergi, the common epauletted fruit bat. Additional cases have occurred since,’’ also in Epomophorus, and it is probable that the index case was also of this species. This virus has been identified by Dr G. H. Tignor of the Yale Arbovirus Research Unit, Yale University School of Medicine, and by Dr J. Crick of the Animal Virus Research Institute, Pirbright, U.K. as Lagos bat virus, a member of the rabies serogroup, originally isolated by Boulger and Porterfield’ from Eidolon helvum fruit bats on Lagos island, Nigeria. This third reported’isoiation appears to be of particular public health importance because Epomophorus bats are common garden residents in the subtropical towns of Natal and the virus apparently causesa fatal rabies-like disease in these Megachiroptera while virtually nothing is known of its pathogenicity, if any, for man. In the only known possible human exposure associated with the Natal outbreak, a motorcyclist was pursued and attacked, sustaining bite wounds in the region of the eye, by an unidentified bat which subsequently escaped. He was treated with human rabies immune globulin and human diploid cell vaccine (Merieux) and has remained healthy for more than 150 days. E. helvum is widely distributed in Africa and breeds in a broad belt .spanning the equatorial region. Its migratory range is much greater covering most of sub-Saharan Africa and including the whole of the southern half of the continent. Although uncommon in South When the Africa its range certainly overlaps that of Natal bats became infected with Lagos bat virus’is impossible to assess since, without the public awareness of rabies which arose from a concurrent canine epizootic in this same area, the bat cases mentioned here would probably have passed unnoticed or at least isolations
were
Epomophorus.
uninvestigated. The isolation of Duvenhage, a rabies-related virus, from a fatal human case reportedly bitten by an unidentified Microchiropteran bat in 19702 indicated that more attention should be paid to the 1. 2.
a from Nigerian fruit bats. Trans Roy Soc Boulger LR, Porterfield JS. Isolation of virus Trop Med Hyg 1958; 52: 421-24. Meredith CD, Rossouw AP, van Praag Koch H. An unusual case of human rabies thought to be of Chiropteran origin. S Afr Med J 1971, 45: 767-69
Letters to the Editor
mortality, in part, on interval since delivery should consider the advantage of investigating deaths occurring within 90 days after delivery. When possible, they should compare mortality rates from maternal and non-maternal
CHANGING THE DEFINITION OF MATERNAL MORTALITY: A NEW LOOK AT THE POSTPARTUM INTERVAL often been studied in detail because of varied definitions and incomplete reporting.The World Health Organisation currently defines maternal mortality as deaths occurring during pregnancy or within 42 days of the end of pregnancy.2 We have used data from Georgia to show that increasing the interval to 90 days would increase the detection of maternal deaths without including an excessive number of non-maternal deaths, and that maternal mortality declines exponentially during the postpartum period while non-maternal mortality does not
SIR,-Maternal mortality has
not
change. To determine the risk of death from maternal causes after delivery of a live infant, we compared information on 159 233 live births to Georgia women for 1975and 1976 with the information on the 3190 deaths of Georgia women in 1975, 1976, and the first 2 months of 1977. Thus, women were observed for 2-14 months after delivery. Based on medical records, we classified the causes of death as maternal and non-maternal. We identified 36 deaths from maternal causes and 42 from non-maternal causes. Details of these cases will be published elsewhere. 3 We used life table methodology to estimate mortality risks after delivery and assumed that the number of women observed decreased linearly between months 2 and 14. Mortality from maternal causes during the first year after delivery was 38 per 100 000 woman-years of observation and 44 from nonmaternal causes. Mortality from maternal causes was 433 per 100 000 woman-years during the first 9 days after delivery and declined to 4 per 100 000 woman-years in the last interval (see table). Moreover, maternal factors caused more deaths than did nonmaternal factors for each interval during the first 2 postpartum months and for 2 of 6 deaths during the third postpartum month. The 42-day limit excludes 6/36 (17%) deaths from maternal causes, and ignores the 43-90 day period when 4/9 (44%) of the deaths were from maternal causes. The causes of these deaths were thrombotic thrombocytopenia, renal failure, pulmonary embolism following a caesarean section delivery, and heart failure. Investigating all deaths in the first 3 months compared with the first 42 days postpartum increased the number of deaths from 39 to 46. During the first 42 days postpartum, 8% of all deaths were from maternal causes, while 74% of deaths in the first 90 days were from maternal causes. Extending the investigation to all deaths during the first year postpartum would result in a decrease to 46%. We conclude that those who base their definition of maternal
causes.
Family Planning Evalulation Division, Center for Health Promotion and Centers for Disease Control, Atlanta, Georgia 30333, U.S.A.
Education,
ROGER W. ROCHAT GEORGE L. RUBIN RICHARD SELIK BENJAMIN P. SACHS CARL W. TYLER
DURATION OF PROTECTION ACCORDED BY LIVE ORAL POLIOVIRUS VACCINE
SIR,-Concern has been expressed about the duration of protecprovided by live oral poliovirus vaccine, since antibody levels
tion
seem to
fall with time.
20 years ago, when I
was 38, my poliovirus antibodies were I had been for study because I had few antibodies selected reported. against type I poliovirus and no antibodies against types II and III, had never received a killed poliovirus (Salk) vaccine, and had shown immunological responsiveness in 1958 to an experimental modified live virus (chick embryo origin) anti-rabies vaccine. Three experimental capsules were administered orally one each week for a 3 week period. Each capsule contained approximately 100 000 TCD50 (median tissue culture infecting dose) of type I, II, or III live, attenuated poliovirus vaccine (Lederle). This procedure failed to produce an immune response other than a minimal increase in type I titre (an increase in antibody titre to >1:4 was used to indicate an adequate immunological response to oral poliovirus vaccine). The subsequent oral administration of a 0’ 5 ml dose of a new, experimental, liquid, trivalent, live, attenuated poliovirus vaccine (Lederle) containing about (300 000 TCDso of each poliovirus type, also failed to prompt a serological response.
1. Cox
HR, Cabasso VJ, Markham FS, Moses MJ, Moyer AW, Roca-Garcia M, Ruegsegger JM. Immunological response to trivalent oral poliomyelitis vaccine. Bri Med J 1959; II: 591-97.
ANTIBODY PATTERN OF AN ADULT AFTER THE ADMINISTRATION OF DIFFERENT DOSAGES OF
LIVE ATTENUATED ORAL POLIOVIRUS VACCINE
1 Rochat RW Maternal and perinatal mortality statistics. In: Silvio A, ed. Obstetrical practice. St Louis CV Mosby, 1980. 2 World Health Organisation. Manual of the international statistical classification of diseases, injuries, and causes of death. 1975: Vol. I. Geneva: WHO, 1977. 3 Rubin G, McCarthy BJ, Shelton J, Rochat RW, Terry J. The risk of childbearing reevaluated Am J Publ Health (in press).
MORTALITY DUE TO MATERNAL AND NON-MATERNAL CAUSES, BY INTERVAL AFTER DELIVERY, GEORGIA, 1975-76
Entries in italic type refer to post feeding samples. * No. 7-1238-801 contained equal volumes of type I (no. 7-1231-115), type II (no.F 7-1232-217), and type II (no. 7-1233-319) vaccines, Lederle. tNo. 7-1238-801 Lederle. * Concentrations of approximately 800 000 type I, 100 000 type 2, and 500 000 type 3 (Sabin) Onmune Lederle. § NDC 0005-2084-07 (Sabm) Onmune Lederle. Before this date, titres were measured by the macroscale; from Dec. 19, 1974, on, the titres were measured on microscale. ** During the summer of 1977, additional testing of the sera obtained on Oct. 12, 1976, and March 8, 1977, revealed the same type of fluctuation on the repeated type I assays.
-
832 I was given a 2-00 ml dose containing approximately 1200 000 TCDso of each of the three poliovirus strains. Titration of a serum sample a month later showed a good response: antibody titres were 1: 1024 for type I, 1: 512 for type II, and 1: 32 for type III. This antibody conversion strongly influenced the final choice of dosage strength for commercial preparations. Since 1959, I have been tested periodically and have had two additional booster doses-one in 1970 and the other in 1976-of ’Orimune’ poliovirus vaccine live, attenuated, oral, trivalent, Sabin strains, type 1, 2, and 3. These doses consisted of poliovirus concentrations which had been adjusted so that the predominant type (type 2) might not inhibit the action of the others (types 1 and 3). These concentrations and the booster response antibody patterns they induced are shown in the accompanying table, which also contains data from previous vaccine administrations. A gradual decline in poliovirus antibody levels has been reported in children at 1;21, 2, and 3;3 5;4 8;5 and 106 years after immunisation. Based on the response of the adult individual reported here, it appears that although antibody titres may decline in level, they rise promptly in response to booster doses. Presumably, low antibody titres in proven vaccine-responsive individual would also respond to exposure to live wild viruses; thus protection would be afforded under those circumstances.
IF TITRES TO KHF VIRUS IN SEVEN SERA FROM GREEKS
Finally, ’
P.O. Box 338, San Anselmo, California 94960, U.S.A.
ALEXANDER THOMSON
been higher than the values shown in the table because the sera were not frozen and spent 2 weeks in transit from Greece to Korea. The results point to the spread of KHF virus in northern Greece. The next step is to attempt KHF virus isolation from patients in Greece with syndromes resembling Korean haemorrhagic fever. This work was partly supported by NATO research grant RG 12380, and partly by grant DAMD-17-80-G-9468 of the U.S. Army Medical Research and Developmental Command, Washington, D.C. W.H.O.
Collaborating Centre for the Study of Korean Haemorrhagic Fever,
Institute for Viral Diseases, Korea University Medical College, Seoul, Korea
Ho WANG LEE
Department of Microbiology,
SEROLOGICAL EVIDENCE FOR KOREAN HAEMORRHAGIC FEVER IN GREECE
SIR,-The aetiological agent of Korean haemorrhagic fever (KHF) is a virus carried by the rodent Apodemus agrarius coreae in the rural endemic areas of Korea. Epidemic haemorrhagic fever with an associated renal syndrome attracted attention during the Korean war and very similar syndromes have been reported in the U.S.S.R., China, Scandinavia, Eastern Europe, and Japan. The isolation of the aetiological agent of KHF7,has permitted the establishment, by indirect fluorescent (IF) antibody technique, of the close relation of KHF with haemorrhagic fever with an associated renal syndrome seen outside Korea. We have looked for serological evidence of KHF virus people in northern Greece, using the indirect IF technique. KHF antigens were derived from KHF viral passage in A. agrarius.2 445 sera from healthy people living in Greek towns or villages close to the Bulgarian and Yugoslavian borders and 97 sera from patients with glomerular disease of unknown origin (kindly provided by Prof. P. Metaxas, University of Thessaloniki) were posted without dry ice to Korea for antibody testing. 4 of the 445 healthy people and 3 of the 97 sera from patients with glomerular disease were positive for KHF antibody (see table). The frequence ofseropositivity in healthy Greeks is similar to that of Korean people living in non-endemic areas, whereas the frequency in the patients with glomerular disease is similar to that of Korean people living in hyperendemic areas.8 The mean titres of IF antibodies in Korea were much higher, perhaps because of some 9 antigenic difference between KHF and the agent in Greece. However, our true IF antibody titres against KHF virus may have
among
2. 3 4.
5.
6. 7.
8. 9.
W. Response of infants to trivalent poliovirus vaccine (Sabm strains). Paediatrics 1967; 40: 980-85. Cabasso VJ, Nozell H, Ruegsegger JM, Cox HR. Poliovirus antibody three years after oral trivalent vaccine (Sabin strains). Pediat 1966; 68: 199-203. J Krugman RD, Hardy GE Jr, Sellers C, Parkman PD, Witte JJ, Meyer BC, Meyer HM Jr. Antibody persistence after primary immunization with trivalent oral poliovirus vaccíne. Pediatrics 1977; 60: 80-82. Rousseau WE, Noble GR, Tegtmeier GE, Jordan MC, Chin TDY. Persistence of poliovirus neutralizing antibodies eight years after immunization with live, attentuated-virus vaccine. N Engl J Med 1973; 289: 1357-59 Sanders DY, Cramblett HG. Antibody titers to polioviruses in patients ten years after immunization with Sabin Vaccine. J Pediat 1974: 406-08 Lee HW, Lee PW. Korean haemorrhagic fever I Demonstration of causing antigen and antibodies. Korean J Int Med 1976; 19: 371-83. Lee HW, Lee PW, Johnson KM. Isolation of the etiological agent of Korean hemorrhagic fever. J Infect Dis 1978; 137: 298-308. Svedmyr A, lee PW, Gajdusek DC, Gibbs CJ, Nystrom K. Antigenic differentiation of the viruses causing Korean haemorrhagic fever and epidemic (endemic) nephropathy of Scandinavia. Lancet 1980; ii: 315-16.
Murphy
School of Medicine, Aristotelian University of Thessaloniki, Thessaloniki, Greece
A. ANTONIADIS
LAGOS BAT VIRUS IN SOUTH AFRICA
SIR,-In June, 1980, a virus indistinguishable from that of rabies
by the fluorescent antibody-test was isolated from the brain of an unidentified bat found sick iti a garden in Pinetown, a borough adjoining Durban, Natal. During the next three months five more made and in these cases the bats were identified as being Epomophorus wahlbergi, the common epauletted fruit bat. Additional cases have occurred since,’’ also in Epomophorus, and it is probable that the index case was also of this species. This virus has been identified by Dr G. H. Tignor of the Yale Arbovirus Research Unit, Yale University School of Medicine, and by Dr J. Crick of the Animal Virus Research Institute, Pirbright, U.K. as Lagos bat virus, a member of the rabies serogroup, originally isolated by Boulger and Porterfield’ from Eidolon helvum fruit bats on Lagos island, Nigeria. This third reported’isoiation appears to be of particular public health importance because Epomophorus bats are common garden residents in the subtropical towns of Natal and the virus apparently causesa fatal rabies-like disease in these Megachiroptera while virtually nothing is known of its pathogenicity, if any, for man. In the only known possible human exposure associated with the Natal outbreak, a motorcyclist was pursued and attacked, sustaining bite wounds in the region of the eye, by an unidentified bat which subsequently escaped. He was treated with human rabies immune globulin and human diploid cell vaccine (Merieux) and has remained healthy for more than 150 days. E. helvum is widely distributed in Africa and breeds in a broad belt .spanning the equatorial region. Its migratory range is much greater covering most of sub-Saharan Africa and including the whole of the southern half of the continent. Although uncommon in South When the Africa its range certainly overlaps that of Natal bats became infected with Lagos bat virus’is impossible to assess since, without the public awareness of rabies which arose from a concurrent canine epizootic in this same area, the bat cases mentioned here would probably have passed unnoticed or at least isolations
were
Epomophorus.
uninvestigated. The isolation of Duvenhage, a rabies-related virus, from a fatal human case reportedly bitten by an unidentified Microchiropteran bat in 19702 indicated that more attention should be paid to the 1. 2.
a from Nigerian fruit bats. Trans Roy Soc Boulger LR, Porterfield JS. Isolation of virus Trop Med Hyg 1958; 52: 421-24. Meredith CD, Rossouw AP, van Praag Koch H. An unusual case of human rabies thought to be of Chiropteran origin. S Afr Med J 1971, 45: 767-69