European Journal of Epidemiology 15: 379±381, 1999. Ó 1999 Kluwer Academic Publishers. Printed in the Netherlands.
Faecal excretion of Vibrio cholerae during convalescence of cholera patients in Calabar, Nigeria S.J. Utsalo1, F.O. Eko1,2, F. Umoh1 & A.A. Asindi3 1
Department of Medical Microbiology & Parasitology, College of Medical Sciences, University of Calabar, Calabar, Nigeria; Present address: Institute of Microbiology and Genetics, University of Vienna, Vienna, Austria; 3Department of Paediatrics, College of Medicine, King Saud University, Abha, Saudi Arabia
2
Accepted in revised form 1 December 1998
Abstract. The pattern of faecal excretion of Vibrio cholerae was studied over a duration of eight months among 13 cholera convalescents by twoweekly surveillance cultures. Stools and rectal swabs were cultured on Thiosulphate citrate bile salts sucrose (TCBS) agar for the recovery of vibrio pathogens. Clinical phase and convalescent phase V. cholerae strains were compared for antibiogram pro®les. The population of vibrios recovered from faecal inocula was usually scanty (7 months ClPsa CoPsb
+ + + +
+ + + +
+ +
ClPs: clinical phase strains. CoPs: convalescent phase strains. c Tetracycline-resistant variants. b
+ +
+ + +
+ + + + + +
+ + + +
+ +
0.5±4
0.5±4
0.5 1.0 1.0 4.0 2.0 0.5 1.0 4.0 4.0 0.5 2.0 1.0 0.5
0.5 2.0 4.0 0.5 4.0 4.0 1.0 5.0 0.5 1.0
HIV Ab
64±128c
128.0 64.0 128.0
) ) ) ) ) ) ) ) ) ) ) + +
381 sewage facilities. Both factors are strongly associated with stabilization of cholera endemicity [5]. Vibrio diarrhoea patients were usually discharged after two days of tetracycline regimen (30 mg/kg/day), intended to abolish enteric colonization or reduce the duration of excretion. Our study suggests that the adoption of negative cultures as evidence of bacteriological cure at the point of patients' discharge is at best presumptive. The antecedents of convalescent strains that were concordant with clinical phase strains recovered during this surveillance study remain a puzzle. First, we speculate that enteric colonization by the causative strains may account for these excretions. The fact that 10 pairs (76.9%) of the strains studied had identical antibiogram pro®les appears consistent with this impression. Presumably, the brief tetracycline therapy during hospitalisation might have suppressed faecal loads to levels not readily detectable in thickening stools from the time of discharge to early convalescence. On the other hand, our opinion is strong in favour of asymptomatic re-infections with the circulating endemic strains during convalescence, at least with respect to the children who excreted tetracycline-resistant variants. For instance in one child, excretion was detected only once; at one month after discharge. We suspect that break-through re-infections could readily occur among the immunologically naive children in whom clinical episodes may induce ®nite quantities of immune factors that can be overwhelmed by reasonable infectious doses [10]. Perhaps other than these three cases, neither antibiogram nor any other assays of strain identity correlations would be informative if excretions were derived from re-infections with the common strains in circulation. We interpret with caution the ®nding that two patients who tested positive for HIV infections also had consistently the longest duration of excretions. This is because of the small number of these patients which makes it dicult for the relevance of HIV status to be evaluated meaningfully. A more extensive study of a large cohort of HIV-infected excretors may provide the insight into this relationship. Our ®ndings have established that cholera convalescents may shed low numbers of vibrios in faeces sporadically and over variable periods. Although the antecedents of these convalescent strains were not de®nitely established in this study, we recognise the bene®t of our surveillance model in identifying the
excretion status of persons who may serve as agents of contamination of this estuarine environment and an important stabilizing factor in cholera endemicity in this focus.
References 1. Eko FO, Nansel A, Bunka S, Lubitz W. Immunogenicity of Vibrio cholerae ghost cells following intraperitoneal immunization of mice. Vaccine 1994; 12: 1330±1334. 2. Mulder GD, Ries TM, Beaver TR. Non-toxigenic Vibrio cholerae wound infection after exposure to contaminated lake water. J Infect Dis 1989; 159: 809±810. 3. Glass RI, Svennerholm A-M, Khan K, Hudas S, Huq MI, Holmgren J. Sero-epidemiological studies of E1 Tor cholera in Bangladesh; Association of serum antibody level with protection. J Infect Dis 1985; 151: 236± 242. 4. Utsalo SJ, Eko FO, Antia-Obong OE. Features of cholera and Vibrio parahaemolyticus diarrhoea endemicity in Calabar, Nigeria. Eur J Epidemiol 1992; 8: 856±860 5. Eko FO, Udo SM, Antia-Obong OE. Epidemiology and spectrum of vibrio diarrhoeas in the lower Cross River Basin of Nigeria. Eur J Publ Hlth 1994; 2: 37±41. 6. Utsalo SJ, Mboto CI, Gemade EII, Nwangwa MA. Halophilic Vibrio spp. associated with hard clams (Mercenaria spp.) from the Calabar River estuary. Trans Roy Soc Trop Med Hyg 1988; 82: 327±329. 7. Colwell RR, Spira WM. The ecology of Vibrio cholerae. In: Barua D, Greenough WB III (eds), Cholera. New York: Plenum Medical Book Co., 1992: 107±127. 8. Kelly MT, Hickman-Brenner FW, Farmer JJ. Vibrio. In: Balows A, Hausler WJ, Herrmann KL, Isenberg HD, Shadomy HJ (eds.), Manual of Clinical Microbiology. Washington, DC: American Society for Microbiology, 1991: 384±395. 9. Black RE. Epidemiology of diarrhoeal disease; Implication for control by vaccines. Vaccine 1993; 11: 100± 106. 10. DA, Freij L, Holmgren J. Prospects for public health bene®ts in developing countries from new vaccines against enteric infections. J Infect Dis 1991; 163: 503± 506.
Address for correspondence: S.J. Utsalo, Department of Medical Microbiology & Parasitology, College of Medical Sciences, University of Calabar, Calabar, Nigeria E-mail:
[email protected]
