St. Louis encephalitis and dengue fever in the Caribbean area: evidence of possible cross-protection.

160 NOTES St Louis Encephalitis and Dengue Fever in the Caribbean Area: Evidence of Possible Cross-protection * by JAMES 0. BOND, Director, Epidemiology Research Center, Florida State Board of Health, Tampa, Fla., USA Although St Louis encephalitis (SLE) virus was first identified 600 miles (or some 1000 km) inland from the Gulf of Mexico,a most of the significant human illness related to this virus has been limited to those southern States of the United States of America which border upon this body of water. Exceptions to this observation have been the epidemics which occurred in California in 1952, in the high plains of northern Texas and Colorado in 1956, and in New Jersey in 1964. In the Lower Rio Grande Valley, which separates Texas from Mexico, major SLE epidemics occurred in 1954 in Hidalgo County and in 1957 in Cameron County.b c The Tampa Bay area, on the west coast of the Florida peninsula, experienced 3 SLE epidemics in 1959, 1961, and 1962.d, e, f Subsequently, Texas had a large outbreak in Houston in 1964, followed by similar urban out- breaks in Dallas and Corpus Christi in 1966. g, h Each of the latter Florida and Texas epidemics occurred either on the coastal plains or immediately adjacent to the Gulf of Mexico (Fig. 1). The epidemics were quite similar. Each occurred in the late summer or early fall. Elderly individuals were primarily affected, with case-fatality rates * Paper read at the Eighth International Congresses on Tropical Medicine and Malaria, Teheran, September 1968. a Leake, J. P. (1933) J. Amer. med. Ass., 101, 928-929. b Kunin, C. M. & Chin, T. D. Y. (1957) Publ. Hlth Rep. (Wash.), 72, 519-525. c Brody, J. A. & Browning, G. (1960) Amer. J. trop. Med. Hyg., 9, 436-443. d Bond, J. O., Ballard, W. C., Markush, R. E. & Alexan- der, R. R. (1963) The 1959 outbreak of St Louis encephalitis in Florida. In: Tampa Bay area arbovirus investigations, 1959-1961, pp. 2-18 (Florida State Board of Health: Mono- graph Series, No. 5). e Waters, C. M., Quick, D. T., Oard, H. C. & Allen, F. K. (1963) The 1961 outbreak of St Louis encephalitis in Pinellas, Manatee, and Sarasota counties. In: Tampa Bay area arbovirus investigations, 1959-1961, pp. 19-29 (Florida State Board of Health: Monograph Series, No. 5). f Bond, J. O., Quick, D. T., Witte, J. J. & Oard, H. C. (1965) Amer. J. Epidenm., 81, 392-404. g Luby, J. P., Miller, G. P., Gardner, P., Pigford, C. A., Henderson, B. E. & Eddins, D. (1967) Amner. J. Epidem., 86, 584-597. h Peavey, J. E., Dewlett, H. J., Metzger, W. R. & Bagby, J. (1967) Amer. J. publ. Hlth, 57, 2111-2116. varying from 5% to 20%. The mosquito vectors included Culex nigripalpus, Culex pipiens fatigans (= C. quinquefasciatus) or Culex tarsalis. Sporadic clinical cases of human SLE occurred in both Florida and Texas over the period 1954-66. In 1958, a cluster of 5 cases was identified in Miami, Fla., and these were thought to be related to 5 others which occurred in Trinidad, Jamaica, and Panama that same year.i From one of the 1958 Trinidad cases, the SLE virus was recovered from the blood, although the child did not have symptoms or signs suggesting encephalitis.j In Surinam, 2 cases of encephalitis in 1952 were attributed to SLE virus on the basis of the results of serological tests and histo- pathology.k Contrasting with the epidemic pattern, sporadic cases have been scattered throughout the year and have occasionally involved those of younger ages. Endemic or enzootic SLE activity is present over a large portion of the tropical and subtropical areas of North, Central, and South America and the Caribbean Islands. Serological surveys or viral isolations have confirmed such activity in Panama,' Mexico, Jamaica,m Trinidad,n Surinam,° French Guiana,P Florida,q Texas,r and Brazil.s Arthropods i Ehrenkranz, N. J., Pond, W. L., Pennington, R. M. & Carter, M. J. (1963) Amer. J. Med., 35, 673-681. J Spence, L., Downs, W. G. & Boyd, C. (1959) W. Indian med. J., 8, 195-198. k Collier, W. A., Winckel, W. E. F. & Blom, F. A. E. (1963) Docum. Med. geogr. trop. (Amst.), 5, 225-234. t Galindo, P., Peralta, P. H., Mackenzie, R. B. & Beye. H. K. (1964) Amer. J. trop. Med. Hyg., 13, 455. m Ventura, A. K. (1965) A,ner. J. trop. Med. Hyg., 14, 297-303. n Aitken, T. H. G., Downs, W. G., Spence, L. & Jonkers, A. H. (1964) Amer. J. trop. Med. Hyg., 13, 450-451. 0 Jonkers, A. H., Downs, W. G., Aitken, T. H. G. & Spence, L. (1964) Trop. geogr. Med., 16, 135-145. P C. Sdri6, Institut Pasteur, Cayenne, French Guiana; personal communication. q Bond, J. O., Quick, D. T., Lewis, A. L., Hammon, W. M. & Sather, G. E. (1966) Amer. J. Epidem., 83, 564-570. r Hammon, W. M., Reeves. W. C. & Irons, J. V. (1944) Tex. Rep. Biol. Med., 2, 366-375. 8 Causey, 0. R., Shope, R. E. & Theiler, M. (1964) Amer. J. trop. Med. Hyg., 13, 449. 2285c ST LOUIS ENCEPHALITIS AND DENGUE FEVER IN THE CARIBBEAN AREA 161 FIG I LOCATION OF MAJOR EPIDEMICS AND SPORADIC CASES OF ST LOUIS ENCEPHALITIS OALLAS IS- TEXAS LOUNSIANA MISS. 0 SLE EPIDEMICS 0 ----.* \ *A SPORADIC CASES *CAMCONI 1957 0ORLN DOCOUNTY AREA195 io.AL i9540-CoQPUS CHRISTI I96r\COUNTY *.*o" OrAfMXICo fTMYEA MIAMI IS5s MEXICO CA--R/ZA6A SEA b S TRINIDAD 1198 VENHEZUeLA WHO 9004 C yielding SLE virus have included the following genera: Culex, Psorophora, Aedes, Sabethes, Tricho- prosopon, Wyeomyia, and Gigantolaelaps. A wide variety of avian and mammalian species have also manifested evidence of infection with SLE virus. Two other group B arboviruses, dengue and liheus, are commonly found in the Caribbean area and bear close serological relationships to SLE virus. This produces an immunological overlap in sero- logical testing, which obscures the interpretation of serological surveys of both man and animals. Both dengue and Ilheus virus have been considered endemic in all of the islands of the Greater and Lesser Antilles, along the coastal regions of most of the countries of northern South America, in Central America, and in Mexico t (Fig. 2). Ilheus virus has never been identified in the southern USA. However, dengue viruses have produced repeated epidemics throughout the entire GulfCoast area ofthe southern USA. The last known dengue epidemic in the United States of America occurred in Brownsville, t Taylor, R. M. (1968) Catalogue of arthropod-borne viruses of the world, Washington, D.C., US Government Printing Office (Public Health Service Publication No. 1760). Texas, in 1941. The most recent dengue fever activity in the Caribbean involved Jamaica and Puerto Rico in 1963." In Florida, epidemic dengue was last identified in 1934. Epidemiological and serological studies conducted during and after the 1962 SLE epidemic in the Tampa Bay area demonstrated significantly lower clinical attack rates of SLE in that portion of the population with serological evidence of prior infec- tion with dengue-2 virus. In members of the white population over the age of 28 years, who had lived in the Tampa Bay area since before 1934, the clinical SLE age-adjusted attack rates were estimated to be 5.2 per 100 000 for persons with dengue immunity and 22.5 for those without dengue antibodies. The comparable rates in non-whites were 0 and 6.5, respectively.v In. laboratory experiments at the Florida State Board of Health, mice immunized with live dengue-2 u Neff, J. M., Morris, L., Gonzalez-Alcover, R., Cole- man, P. H., Lyss, S. B. & Negron, H. (1967) Amer. J. Epidem., 86, 162-183. v J. 0. Bond & W. M. Hammon-manuscript to be published. 12 162 NOTES FIG. 2 AREAS OF ENDEMIC DENGUE FEVER AND MAIN EPIDEMICS G AROUND THE CARIBBEAN AND THE GULF OF MEXICO IN THE 20TH CENTURY .~~ MEXICO /,aM,/A @5 vA~~~~~O- *'5 I A ,ASICAN SE *, aThemalnepGdemics a jreindicated by the year of outbreak and th lace name. WHO 9O~4*t £ The maIn epidemics are Indicated by the year of outbreak and the place name. virus vaccine showed reduced mortality of 46% when challenged with doses of SLE virus as compared with unimmunized controls w (Fig. 3). At the University of Pittsburgh, 4 of 10 monkeys with naturally acquired group B antibodies, assumed to be dengue, did not develop detectable viraemia, when challenged with SLE virus. In further experiments with ham- sters at the University of Pittsburgh, the protection afforded against West Nile virus by dengue-2 virus proved highly significant, especially when the chal- lenge dose of West Nile virus was heavy.x In an historical and geographical review,Y we have observed that no Murray Valley encephalitis (MVE), Japanese encephalitis (JE), West Nile (WN), or Ilheus fever epidemics have ever been reported in endemic dengue fever areas of the world, which may w J. 0. Bond et al.-manuscript to be published. x Sather, G. E. & Hammon, W. M. (1968) Bact. Proc. (Abstracts of 68th Annual Meeting of the American Society for Microbiology, Detroit, Mich., 5-10 May 1968). Y Bond, J. 0. (1967) Cross-protection between dengue and St Louis encephalitis arboviruses, Thesis, University of Pitts- burgh, Graduate School of Public Health, Pittsburgh, Pa. FIG. 3 MORTALITY RATIOS IN LABORATORY MICE IMMUNIZED WITH DENGUE-2 VIRUS AND CHALLENGED INTRAPERITONEALLY WITH SLE VIRUS Dengue-2 Immunization Group Ratio O Dose 34/46 1 Dose 18127 3 Doses 26/57 20 40 60 80 100 PERCENTAGE MORTALITY IV be defined as lying between the 30th parallels %.a latitude. The Guam epidemic ofJE was a possible excepti*2, to this observation; however, it occurred in an are' where dengue had recently been eradicated and; tf-- cases were restricted almost entirely to the age-groul: ST LOUIS ENCEPHALMS AND DENGUE FEVER IN THE CARIBBEAN AREA 163 never exposed to dengue.z The SLE epidemics in Florida and Texas occurred 28-40 years after the last dengue fever outbreaks and primarily affected the most recent immigrants into the areas. Our findings suggest significant cross-protection between dengue fever virus (particularly dengue-2) and SLE. We would encourage similar studies with dengue and MVE, JE, or WN viruses. If our hypothesis on Z Hammon, W. M., Tigertt, W. D., Sather, G. E., Berge, T. 0. & Meiklejohn, G. (1958) Amer. J. trop. Med. Hyg., 7, 441-467. cross-protection is correct, it may be necessary to administer attenuated dengue virus vaccines to large groups in the tropics and subtropics to restore the ecological balance after the eradication of Aedes aegypti mosquitos. * These studies were supported in part by the NIH Grant AI-05504 from the National Institute of Allergy and Infectious Diseases to the Florida State Board of Health. Non-Agglutinable Vibrios Isolated in the 1966 Epidemic of Cholera in Iraq by N. EL-SHAWI, Professor of Bacteriology and A. J. THEWAINI, Assistant Professor of Bacteriology, Depart- ment of Microbiology, College of Medicine, University of Baghdad, Iraq During the 1966 epidemic of cholera in Iraq, many organisms biochemically identical to Vibrio cholerae were isolated but they did not agglutinate with cholera 0 group 1 antiserum. Some of these orga- nisms were isolated from patients with clinically diagnosed cholera or from individuals suspected of being carriers. Others were isolated from water or from sewage during routine examinations for the presence of cholera organisms. The question of the pathogenicity and origin of these non-agglutinable (NAG) organisms has been the subject of many «ports in the literature. Many consider that they re non-pathogenic and are to be found free-living in vater or sewage. Others are of the opinion that these irganisms were originally agglutinable forms which ave lost their agglutinability owing to loss of anti- en. Bhattacharji & Bose a claimed that they could -hieve transformation of Vibrio cholerae into NAG brios and vice versa. In this communication we report a study of those inisms isolated during the 1966 epidemic of Iraq i were described as NAG vibrios, and an ipt to repeat Bhattacharji & Bose's experiments. Bhattacharji, L. M. & Bose, B. (1964) J. med. Res., 1;41771. Materials and methods Isolation of the organisms. Stool or sewage speci- mens were inoculated on alkaline peptone water for 6 hours. Water specimens were filtered through a Millipore filter and the filter was put in alkaline peptone water for the same length of time. Sub- cultures were made on TCBS plates and subcultures from suspicious colonies were inoculated on Kligler iron-agar (both stab and streak inoculations). Tubes which showed an acid butt and an alkaline slant, with no gas, were regarded as suspicious and subcultures were made from these, on peptone water to test for the production of indole, on semi-solid mannitol to test for acid production and motility and on agar slants for agglutination tests. Cultures which were indole-positive, motile and mannitol-positive but which gave a negative agglutination reaction with polyvalent cholera antisera, were provisionally described as NAG vibrios; further tests were carried out before the organism was definitely classified. Maintenance of cultures. Strains of NAG vibrios, as well as El Tor vibrios, were maintained by stab cultures on semi-solid nutrient agar (0.5% agar). The cultures were kept at room temperature (200C- 28°C). Cultures were transferred on to semi-solid i5D