- Email: [email protected]
Emergence of novel strain of Vibrio cholerae with epidemic potential in southern and eastern India
703
THE LANCET
3. Achtman M, Pluschke G. Clonal analysis of descent and virulence among selected Escherichia coli Ann Rev Microbiol 1986; 40: 185-210. 4. Namavar F, van Steenbergen TJM, Verweij-van Vught AMJJ, MacLaren DM. Restriction endonuclease DNA analysis of Bacteroides fragilis. Microb Ecol Health Dis 1991; 4: 113-16. 5. Thomas JE, Gibson GR, Darboe MK, Dale A, Weaver LT. Isolation of Helicobacter pylori from human faeces. Lancet 1992; 340: 1194-95.
SIR,-Helicobacter pylori
are
bacteria that have been
highly
correlated with duodenal ulcer disease and histological gastritis in apparently normal persons in the past decade.1 Professor Lee
investigation of various host factors as they relate to infection. Other workers2,3 have also suggested that pylori emotional states such as depression and anxiety might be related to immune system functioning. Our team has conducted three investigations of the relation between H pylori and self-reported depression (with the Zung depression scale) and trait anxiety (Spielberger state-trait anxiety inventory). Study A was of 24 community medical centre outpatients, study B 90 Veterans Administration (VA) medical centre inpatients and outpatients, and study C 55 VA nurses, physicians, and physician assistants. Presence of H pylori in studies A and B was established by silver stain from antral biopsy specimens obtained within 3 cm of the pylorus. H pylori measurements in study C was by a commercially available ELISA. Depression and anxiety scores in all three studies did not differ between individuals with and without H pylori: encourages
H
L.
Use
4S
1U4
55 -i
Any direct association seems unlikely between self-reported and trait anxiety scores and the presence of H pylori infection. However, these studies do not preclude the association of other psychological variables (eg, subjectively perceived life stress, internalised anger) or other factors (eg, increased amount of pepsinogen, ABO blood type) as being possibly meaningful in determining the importance of psychological variables in the aetiology of infection. In addition, methodological issues (such as particular assessment techniques used, varying times between H pylori determination and assessment) may limit generalisations
depression
from these studies.
(hours)
course.
————=mean blood pressure (mm Hg), urine output (mL per h), and E-0 =enalapril at (ng/mL)
urine output of 20 mL over the previous 4 h. Investigations revealed normal electrolytes with urea 91 mmol/L (normal 2-5-7-5) and creatinine 231 !llloljL (30-120). Previous measurement had revealed normal renal function. In view of the pharmacological effect of angiotensin-converting enzyme (ACE) inhibitors, profound lack of distal glomerular arteriolar tone due to overdose was conjectured to be the cause of the oliguria. Conventional management had been ineffective and an angiotensin infusion was started at 1410 h at 3 ug per min, increasing to 18 ug per min for the first 3 h, then to 5Rg per min over the final 2 h. Urine output dramatically increased with an associated improvement in blood pressure and a conversion from junctional to sinus rhythm (figure). After the end of the infusion, these variables remained stable despite drug estimations suggesting that profound ACE inhibition continued. Concentration of enalapril over 10 ng/mL are equivalent to more than 90% ACE inhibition, and the enalapril concentration remained at 260 ng/mL 12 h after the angiotensin infusion was discontinued at 1900 h. Intensive Care Unit,
We thank Dr James B. Farnum and Dr Flora B. Shoaf for assistance in H pylori determinations in studies A and B and to Mr Ed Jones and Mr Gary Thomas for scoring assessments.
JOSEPH K. NEUMANN Psychology/Gastroenterology Services, Veterans Affairs Medical Center, Mountain Home, Tennessee 37684, USA
MATTHEW A. ROHRBACH SCOTT WILHOITE EAPEN THOMAS
1. Dooley CP, Cohen H, Fitzgibbons
PL, et al. Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989; 321: 1562-66. 2. Kiecolt-Glaser JK, Dura JR, Speicher CE, et al. Spousal caregivers of dementia victims: longitudinal changes in immunity and health. Psychosom Med 1991; 53: 345-62. 3.
TIME
Patient’s
Halley FM. Self-regulation of the immune system through biobehavioral strategies. Biofeedback Self Regul 1991; 16: 55-74.
Enalapril overdose treated with angiotensin infusion SIR,-A 44-year-old man with history of hypertension presented after overdose of enalapril (30 x 20 mg), verapamil (30 x 240 mg slow-release), and temazepam (10 x 10 mg). He was conscious and alert with heart rate of 40 per min, sinus rhythm, and blood pressure 75/40 mm Hg. Initial management consisted of intravenous fluids and parenteral administration of calcium gluconate, ephedrine, and atropine." Charcoal suspension was given only. These measures failed to increase blood pressure or heart rate significantly and urine output remained below 10 mL per h. After admission to the intensive care unit at 0600 h, central venous monitoring was initiated and dopamine (3 Ilgjkg per min) and adrenaline (002 Ilgjkg per min) infusions were started. At this time, heart rate was 40 per min in junctional rhythm, blood pressure 80/50 mm Hg, central venous pressure of + 20 cm H2O, with a
TREVOR JACKSON CHARLES CORKE JOHN AGAR
Geelong Hospital, Geelong, Victoria 3220, Australia
1. Barr CS, Payne R, Newton RW. Profound prolonged hypotension following captopril
overdose.
Postgrad Med J 1991; 792: 953-54. GV, Mirchandani HG. Suicide by captopril overdose. J Toxicol Clin
2. Park H, Purnel
Toxicol 1990; 28: 379-82.
Anonymous. Captopril overdose and hypotension. JAMA 1988; 260: 2508. 4. Augenstein WL, Kulig KW, Rumack BH. Captopril overdose resulting hypotension. JAMA 1988; 259: 3302-05. 3.
in
Emergence of novel strain of Vibrio cholerae with epidemic potential in southern and eastern India
SIR,-Vibrio cholerae serotype 01 is responsible for epidemic cholera. The non-01 group is associated with sporadic cases of gastroenteritis and extraintestinal infections1 but does not have epidemic potential. In November, 1992,48 representative strains of V cholerae isolated from a typical cholera-like outbreak that started on October 19, 1992, and continued until the end of November, 1992, in Madras, Tamilnadu state, were sent to the National Institute of Cholera and Enteric Diseases, Calcutta, for confirmation. In January, 1993, an additional 28 and 48 strains of V cholerae isolated from cases of acute secretory diarrhoea in the cities of Madurai and Vellore, respectively, in Tamilnadu arrived for confirmation. Serological characterisation of the 124 strains revealed that they did not agglutinate with 01 antiserum nor with any of the monoclonal antibodies raised in our laboratory against factors A, B, and C of V cholerae 01. They were, therefore, identified as V cholerae non-01. Except for 1, all the other strains from the Madras outbreak were untypable in the panel of 138 antisera developed for V cholerae non-O1at the National Institute
704
THE LANCET
of Health, Japan, indicating that these strains belonged to a hitherto undescribed new serotype. In Calcutta (eastern India), although there was no increase in the number of cases of cholera admitted to the Infectious Diseases Hospital (IDH), there was an unusual increase in the rate of isolation of V cholerae non-01 compared with that of 01 starting in November, 1992. By the end of December, non-O 1s predominated ( > 95 %) in isolates from choleric diarrhoeal patients screened at IDH, and this trend continues. Like the Tamilnadu isolates, the strains of V cholerae from Calcutta were untypable. All 48 strains from Madras hybridised with DNA probes specific for the cholera toxin gene and the newly recognised zonula occludens toxin gene, but did not hybridise with the DNA probe specific for the heat-stable enterotoxin of V cholerae non-O1 (NAG-ST). Production of cholera toxin by these strains was confirmed by a highly sensitive enzyme-linked immunosorbent assay.2 The amount of toxin produced by the Madras strains ranged from 10.4 to 80 or more ng/mL, which corresponds to that normally produced by clinical strains of V cholerae 01.3 Cholera toxin produced by these strains was completely neutralised by 10 µg IgG antibody to the toxin. 96% and 86% of the other strains from Tamilnadu and from Calcutta, respectively, produced cholera toxin. Most of the strains were resistant to co-trimoxazole (98%), streptomycin (92%), and furazolidone (86%), but sensitive to other commonly used antibiotics including tetracycline. The ability of most V cholerae non-O strains to produce cholera toxin is an unusual trait which differentiates these strains from other non-01 strains associated with sporadic cases of gastroenteritis. The similarity in the biochemical, serological, and toxigenic status of the strains of V cholerae non-01, the association with an outbreak in Madras, and the isolation of similar strains from widely separated regions within India confers an epidemic potential to these isolates and indicates the clonal spread of a novel non-O1 serotype, which is being carefully monitored. The strains of V cholerae from Tamilnadu
were
sent
by Dr P.
Kuganantham, Communicable Diseases Hospital, Madras, and Prof Mary V. Jesudason, Christian Medical College and Hospital, Vellore, and Institute of Microbiology, Madurai.
National Institute of Cholera and Enteric Diseases, PO Box 177, Calcutta 700 010, India
T. RAMAMURTHY SURABHI GARG RAKHI SHARMA S. K. BHATTACHARYA G. BALAKRISH NAIR
National Institute of Health,
Tokyo, Japan
TOSHIO SHIMADA
National Children’s Medical Research Centre,
Tokyo, Japan
TAE TAKEDA
Department of Microbiology, Faculty of Medicine, Kyoto University, Kyoto, Japan
TADAHIRO KARASAWA HISAO KURAZANO AMIT PAL YOSHIFUMI TAKEDA
1. Morris JG. Non-O group 1 Vibrio cholerae: a look at the epidemiology of an occasional pathogen. Epidemiol Rev 1990; 12: 179-91. 2. Ramamurthy T, Pal A, Nair GB, et al. Experience with toxin bead ELISA in cholera outbreak. Lancet 1990; 336: 375-76. 3. Ramamurthy T, Pal A, Bhattacharya MK, et al. Serovar, biotype, phagetype, toxigenicity and antibiotic susceptibility patterns of Vibrio cholerae isolated during two consecutive cholera seasons (1989-90) in Calcutta. India J Med Res 1992; 95: 125-29.
Large outbreak of clinical cholera due to Vibrio cholerae non-O1 in Bangladesh SIR,--Vibrio cholerae serotype 01 can cause large epidemics of cholera. Non-01 serotypes are mostly associated with sporadic cases of diarrhoea and extraintestinal infections.1 In mid-January, 1993, an outbreak of acute watery diarrhoea resembling cholera occurred in southern Bangladesh mostly affecting adults. Through to the middle of February about 10 000 people have been affected with an estimated 500 deaths and new cases still occur. Since the third week of January, an unusually large number of adult diarrhoeal cases clinically resembling cholera have also been seen at our treatment centre in Dhaka. Of the 27 rectal swabs cultured from the field outbreak, 18 (67%) yielded V cholerae non-Ol, and none
V cholerae 01. Of the 53 rectal swabs cultured from admitted
patients, 37 (70%) yielded V cholerae non-O1 and 1 V cholerae O1. The bacterium responsible for the outbreak resembled V cholerae 01 by colony morphology on Monsur’s medium2 and biochemically but did not agglutinate with V cholerae 0’ antisera. All 55 strains were tested for reactivity with a monoclonal antibody specific for the A factor of V cholerae 01by an indirect fluorescent antibody technique3 and all were non-reactive. Therefore we refer to the strain associated with the outbreak as V cholerae non-01.1 Serotyping remains to be done. All the 55 strains were positive for cholera toxin production by Yl adrenal cell assay and the toxin could be neutralised by rabbit polyclonal antiserum to cholera toxin.’ Primers specific for the cholera strain operon from V cholerae 01 amplified sequences corresponding to toxin in these strains in the polymerase chain reaction.’ A selected subsample of strains induced fluid accumulation in the adult rabbit ileal loop assay’ and induced profuse watery diarrhoea in the reversible-ileal-tie adult rabbit models similar to that due to V cholera 01. All 55 strains were susceptible to tetracycline, ampicillin, chloramphenicol, erythromycin, and ciprofloxacin, but were resistant to co-trimoxazole and the vibriostatic compound 2,4diamino-6,7-disopropylpteridine (O/129). This result contrasts with the antibiotic susceptibility of currently prevalent strains of V cholerae 01 in Bangladesh, about 70% of which are resistant to tetracycline. All strains were resistant to Mukherjee’s phages specific for both biotypes of V cholerae O1. These data also suggest that the strains are not V cholerae 01.1 To our knowledge, V cholerae non-Olhas never been associated with such a large outbreak of diarrhoea. V cholerae non-0I produce cholera toxin at a very low frequency,’ unlike in the present outbreak in which all tested strains produced the toxin. The higher attack rate of diarrhoea in adults is reminiscent of cholera epidemics in virgin populations.6 The data suggest that the present large cholera-like outbreak in Bangladesh is due to a V cholerae non-01. We presume that the cholera-like outbreaks in India (see previous letter) are due to the same clone of V cholerae non-O1 as the one in Bangladesh. The pandemic potential of this "new" strain of V cholerae seems real and it should be monitored by public health authorities in the Indian subcontinent and adjacent regions. M. JOHN ALBERT A. K. SIDDIQUE M. S. ISLAM A. S. G. FARUQUE International Centre for Diarrhoeal Disease M. ANSARUZZAMAN Research, Bangladesh, S. M. FARUQUE GPO Box 128, Dhaka 1000, Bangladesh R. BRADLEY SACK 1 Janda JM, Powers C, Bryant RG, Abbott SL. Current perspective on the epidemiology and pathogenesis of clinically significant Vibrio spp. Clin Microbiol Rev 1988; 1: 245-67. 2. Monsur KA. A highly selective gelatin-taurocholate tellurite medium for the isolation of Vibrio cholerae. Trans R Soc Trop Med Hyg 1961; 55: 440-42. 3. Brayton PR, Tamplin ML, Hug A, Colwell RR. Enumeration of Vibrio cholerae O1 in Bangladesh waters by fluorescent-antibody direct viable count. Appl Environ Microbiol 1987; 53: 2862-65. 4. Shirai H, Nishibuchi M, Ramamurthy T, Bhattacharya SK, Pal SC, Takeda Y. Polymerase chain reaction for detection of the cholera enterotoxin operon of Vibrio cholerae. J Clin Microbiol 1991; 29: 2517-21. 5. Spira WM, Sack RB, Froehlich JL. Simple adult rabbit model for Vibrio cholerae and enterotoxigenic Escherichia coli diarrhea. Infect Immun 1981; 32: 739-47. 6. Gil A, Gabilondon A, Molina ME, Burton B, Lanata CF, Bravo N. Isolation of Vibrio cholerae O1 biotype E1 Tor from children under three years of age in an epidemic of cholera in pen-urban Lima, Peru. Proceedings of the 27th joint conference on cholera and related diarrhoeal disease. Charlottesville: The US-Japan Co-operative Medical Science Program, 1991: 14-16.
CORRECTIONS Acquired resistance to clarithromycin as combined therapy in Mycobacterium avium intracellulare infection.-In this letter by Dr S. De Wit and colleagues (Jan 2, p 53), the second author’s name should have been Maurizio D’Abbraccio.
Use of non-prescription decongestant to abort anaphylaxis-In this letter by Dr K. T. Kun and colleagues (Feb 13, p 439), the concentration of oxymetazoline hydrochloride should have been 0-05%.
THE LANCET
3. Achtman M, Pluschke G. Clonal analysis of descent and virulence among selected Escherichia coli Ann Rev Microbiol 1986; 40: 185-210. 4. Namavar F, van Steenbergen TJM, Verweij-van Vught AMJJ, MacLaren DM. Restriction endonuclease DNA analysis of Bacteroides fragilis. Microb Ecol Health Dis 1991; 4: 113-16. 5. Thomas JE, Gibson GR, Darboe MK, Dale A, Weaver LT. Isolation of Helicobacter pylori from human faeces. Lancet 1992; 340: 1194-95.
SIR,-Helicobacter pylori
are
bacteria that have been
highly
correlated with duodenal ulcer disease and histological gastritis in apparently normal persons in the past decade.1 Professor Lee
investigation of various host factors as they relate to infection. Other workers2,3 have also suggested that pylori emotional states such as depression and anxiety might be related to immune system functioning. Our team has conducted three investigations of the relation between H pylori and self-reported depression (with the Zung depression scale) and trait anxiety (Spielberger state-trait anxiety inventory). Study A was of 24 community medical centre outpatients, study B 90 Veterans Administration (VA) medical centre inpatients and outpatients, and study C 55 VA nurses, physicians, and physician assistants. Presence of H pylori in studies A and B was established by silver stain from antral biopsy specimens obtained within 3 cm of the pylorus. H pylori measurements in study C was by a commercially available ELISA. Depression and anxiety scores in all three studies did not differ between individuals with and without H pylori: encourages
H
L.
Use
4S
1U4
55 -i
Any direct association seems unlikely between self-reported and trait anxiety scores and the presence of H pylori infection. However, these studies do not preclude the association of other psychological variables (eg, subjectively perceived life stress, internalised anger) or other factors (eg, increased amount of pepsinogen, ABO blood type) as being possibly meaningful in determining the importance of psychological variables in the aetiology of infection. In addition, methodological issues (such as particular assessment techniques used, varying times between H pylori determination and assessment) may limit generalisations
depression
from these studies.
(hours)
course.
————=mean blood pressure (mm Hg), urine output (mL per h), and E-0 =enalapril at (ng/mL)
urine output of 20 mL over the previous 4 h. Investigations revealed normal electrolytes with urea 91 mmol/L (normal 2-5-7-5) and creatinine 231 !llloljL (30-120). Previous measurement had revealed normal renal function. In view of the pharmacological effect of angiotensin-converting enzyme (ACE) inhibitors, profound lack of distal glomerular arteriolar tone due to overdose was conjectured to be the cause of the oliguria. Conventional management had been ineffective and an angiotensin infusion was started at 1410 h at 3 ug per min, increasing to 18 ug per min for the first 3 h, then to 5Rg per min over the final 2 h. Urine output dramatically increased with an associated improvement in blood pressure and a conversion from junctional to sinus rhythm (figure). After the end of the infusion, these variables remained stable despite drug estimations suggesting that profound ACE inhibition continued. Concentration of enalapril over 10 ng/mL are equivalent to more than 90% ACE inhibition, and the enalapril concentration remained at 260 ng/mL 12 h after the angiotensin infusion was discontinued at 1900 h. Intensive Care Unit,
We thank Dr James B. Farnum and Dr Flora B. Shoaf for assistance in H pylori determinations in studies A and B and to Mr Ed Jones and Mr Gary Thomas for scoring assessments.
JOSEPH K. NEUMANN Psychology/Gastroenterology Services, Veterans Affairs Medical Center, Mountain Home, Tennessee 37684, USA
MATTHEW A. ROHRBACH SCOTT WILHOITE EAPEN THOMAS
1. Dooley CP, Cohen H, Fitzgibbons
PL, et al. Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989; 321: 1562-66. 2. Kiecolt-Glaser JK, Dura JR, Speicher CE, et al. Spousal caregivers of dementia victims: longitudinal changes in immunity and health. Psychosom Med 1991; 53: 345-62. 3.
TIME
Patient’s
Halley FM. Self-regulation of the immune system through biobehavioral strategies. Biofeedback Self Regul 1991; 16: 55-74.
Enalapril overdose treated with angiotensin infusion SIR,-A 44-year-old man with history of hypertension presented after overdose of enalapril (30 x 20 mg), verapamil (30 x 240 mg slow-release), and temazepam (10 x 10 mg). He was conscious and alert with heart rate of 40 per min, sinus rhythm, and blood pressure 75/40 mm Hg. Initial management consisted of intravenous fluids and parenteral administration of calcium gluconate, ephedrine, and atropine." Charcoal suspension was given only. These measures failed to increase blood pressure or heart rate significantly and urine output remained below 10 mL per h. After admission to the intensive care unit at 0600 h, central venous monitoring was initiated and dopamine (3 Ilgjkg per min) and adrenaline (002 Ilgjkg per min) infusions were started. At this time, heart rate was 40 per min in junctional rhythm, blood pressure 80/50 mm Hg, central venous pressure of + 20 cm H2O, with a
TREVOR JACKSON CHARLES CORKE JOHN AGAR
Geelong Hospital, Geelong, Victoria 3220, Australia
1. Barr CS, Payne R, Newton RW. Profound prolonged hypotension following captopril
overdose.
Postgrad Med J 1991; 792: 953-54. GV, Mirchandani HG. Suicide by captopril overdose. J Toxicol Clin
2. Park H, Purnel
Toxicol 1990; 28: 379-82.
Anonymous. Captopril overdose and hypotension. JAMA 1988; 260: 2508. 4. Augenstein WL, Kulig KW, Rumack BH. Captopril overdose resulting hypotension. JAMA 1988; 259: 3302-05. 3.
in
Emergence of novel strain of Vibrio cholerae with epidemic potential in southern and eastern India
SIR,-Vibrio cholerae serotype 01 is responsible for epidemic cholera. The non-01 group is associated with sporadic cases of gastroenteritis and extraintestinal infections1 but does not have epidemic potential. In November, 1992,48 representative strains of V cholerae isolated from a typical cholera-like outbreak that started on October 19, 1992, and continued until the end of November, 1992, in Madras, Tamilnadu state, were sent to the National Institute of Cholera and Enteric Diseases, Calcutta, for confirmation. In January, 1993, an additional 28 and 48 strains of V cholerae isolated from cases of acute secretory diarrhoea in the cities of Madurai and Vellore, respectively, in Tamilnadu arrived for confirmation. Serological characterisation of the 124 strains revealed that they did not agglutinate with 01 antiserum nor with any of the monoclonal antibodies raised in our laboratory against factors A, B, and C of V cholerae 01. They were, therefore, identified as V cholerae non-01. Except for 1, all the other strains from the Madras outbreak were untypable in the panel of 138 antisera developed for V cholerae non-O1at the National Institute
704
THE LANCET
of Health, Japan, indicating that these strains belonged to a hitherto undescribed new serotype. In Calcutta (eastern India), although there was no increase in the number of cases of cholera admitted to the Infectious Diseases Hospital (IDH), there was an unusual increase in the rate of isolation of V cholerae non-01 compared with that of 01 starting in November, 1992. By the end of December, non-O 1s predominated ( > 95 %) in isolates from choleric diarrhoeal patients screened at IDH, and this trend continues. Like the Tamilnadu isolates, the strains of V cholerae from Calcutta were untypable. All 48 strains from Madras hybridised with DNA probes specific for the cholera toxin gene and the newly recognised zonula occludens toxin gene, but did not hybridise with the DNA probe specific for the heat-stable enterotoxin of V cholerae non-O1 (NAG-ST). Production of cholera toxin by these strains was confirmed by a highly sensitive enzyme-linked immunosorbent assay.2 The amount of toxin produced by the Madras strains ranged from 10.4 to 80 or more ng/mL, which corresponds to that normally produced by clinical strains of V cholerae 01.3 Cholera toxin produced by these strains was completely neutralised by 10 µg IgG antibody to the toxin. 96% and 86% of the other strains from Tamilnadu and from Calcutta, respectively, produced cholera toxin. Most of the strains were resistant to co-trimoxazole (98%), streptomycin (92%), and furazolidone (86%), but sensitive to other commonly used antibiotics including tetracycline. The ability of most V cholerae non-O strains to produce cholera toxin is an unusual trait which differentiates these strains from other non-01 strains associated with sporadic cases of gastroenteritis. The similarity in the biochemical, serological, and toxigenic status of the strains of V cholerae non-01, the association with an outbreak in Madras, and the isolation of similar strains from widely separated regions within India confers an epidemic potential to these isolates and indicates the clonal spread of a novel non-O1 serotype, which is being carefully monitored. The strains of V cholerae from Tamilnadu
were
sent
by Dr P.
Kuganantham, Communicable Diseases Hospital, Madras, and Prof Mary V. Jesudason, Christian Medical College and Hospital, Vellore, and Institute of Microbiology, Madurai.
National Institute of Cholera and Enteric Diseases, PO Box 177, Calcutta 700 010, India
T. RAMAMURTHY SURABHI GARG RAKHI SHARMA S. K. BHATTACHARYA G. BALAKRISH NAIR
National Institute of Health,
Tokyo, Japan
TOSHIO SHIMADA
National Children’s Medical Research Centre,
Tokyo, Japan
TAE TAKEDA
Department of Microbiology, Faculty of Medicine, Kyoto University, Kyoto, Japan
TADAHIRO KARASAWA HISAO KURAZANO AMIT PAL YOSHIFUMI TAKEDA
1. Morris JG. Non-O group 1 Vibrio cholerae: a look at the epidemiology of an occasional pathogen. Epidemiol Rev 1990; 12: 179-91. 2. Ramamurthy T, Pal A, Nair GB, et al. Experience with toxin bead ELISA in cholera outbreak. Lancet 1990; 336: 375-76. 3. Ramamurthy T, Pal A, Bhattacharya MK, et al. Serovar, biotype, phagetype, toxigenicity and antibiotic susceptibility patterns of Vibrio cholerae isolated during two consecutive cholera seasons (1989-90) in Calcutta. India J Med Res 1992; 95: 125-29.
Large outbreak of clinical cholera due to Vibrio cholerae non-O1 in Bangladesh SIR,--Vibrio cholerae serotype 01 can cause large epidemics of cholera. Non-01 serotypes are mostly associated with sporadic cases of diarrhoea and extraintestinal infections.1 In mid-January, 1993, an outbreak of acute watery diarrhoea resembling cholera occurred in southern Bangladesh mostly affecting adults. Through to the middle of February about 10 000 people have been affected with an estimated 500 deaths and new cases still occur. Since the third week of January, an unusually large number of adult diarrhoeal cases clinically resembling cholera have also been seen at our treatment centre in Dhaka. Of the 27 rectal swabs cultured from the field outbreak, 18 (67%) yielded V cholerae non-Ol, and none
V cholerae 01. Of the 53 rectal swabs cultured from admitted
patients, 37 (70%) yielded V cholerae non-O1 and 1 V cholerae O1. The bacterium responsible for the outbreak resembled V cholerae 01 by colony morphology on Monsur’s medium2 and biochemically but did not agglutinate with V cholerae 0’ antisera. All 55 strains were tested for reactivity with a monoclonal antibody specific for the A factor of V cholerae 01by an indirect fluorescent antibody technique3 and all were non-reactive. Therefore we refer to the strain associated with the outbreak as V cholerae non-01.1 Serotyping remains to be done. All the 55 strains were positive for cholera toxin production by Yl adrenal cell assay and the toxin could be neutralised by rabbit polyclonal antiserum to cholera toxin.’ Primers specific for the cholera strain operon from V cholerae 01 amplified sequences corresponding to toxin in these strains in the polymerase chain reaction.’ A selected subsample of strains induced fluid accumulation in the adult rabbit ileal loop assay’ and induced profuse watery diarrhoea in the reversible-ileal-tie adult rabbit models similar to that due to V cholera 01. All 55 strains were susceptible to tetracycline, ampicillin, chloramphenicol, erythromycin, and ciprofloxacin, but were resistant to co-trimoxazole and the vibriostatic compound 2,4diamino-6,7-disopropylpteridine (O/129). This result contrasts with the antibiotic susceptibility of currently prevalent strains of V cholerae 01 in Bangladesh, about 70% of which are resistant to tetracycline. All strains were resistant to Mukherjee’s phages specific for both biotypes of V cholerae O1. These data also suggest that the strains are not V cholerae 01.1 To our knowledge, V cholerae non-Olhas never been associated with such a large outbreak of diarrhoea. V cholerae non-0I produce cholera toxin at a very low frequency,’ unlike in the present outbreak in which all tested strains produced the toxin. The higher attack rate of diarrhoea in adults is reminiscent of cholera epidemics in virgin populations.6 The data suggest that the present large cholera-like outbreak in Bangladesh is due to a V cholerae non-01. We presume that the cholera-like outbreaks in India (see previous letter) are due to the same clone of V cholerae non-O1 as the one in Bangladesh. The pandemic potential of this "new" strain of V cholerae seems real and it should be monitored by public health authorities in the Indian subcontinent and adjacent regions. M. JOHN ALBERT A. K. SIDDIQUE M. S. ISLAM A. S. G. FARUQUE International Centre for Diarrhoeal Disease M. ANSARUZZAMAN Research, Bangladesh, S. M. FARUQUE GPO Box 128, Dhaka 1000, Bangladesh R. BRADLEY SACK 1 Janda JM, Powers C, Bryant RG, Abbott SL. Current perspective on the epidemiology and pathogenesis of clinically significant Vibrio spp. Clin Microbiol Rev 1988; 1: 245-67. 2. Monsur KA. A highly selective gelatin-taurocholate tellurite medium for the isolation of Vibrio cholerae. Trans R Soc Trop Med Hyg 1961; 55: 440-42. 3. Brayton PR, Tamplin ML, Hug A, Colwell RR. Enumeration of Vibrio cholerae O1 in Bangladesh waters by fluorescent-antibody direct viable count. Appl Environ Microbiol 1987; 53: 2862-65. 4. Shirai H, Nishibuchi M, Ramamurthy T, Bhattacharya SK, Pal SC, Takeda Y. Polymerase chain reaction for detection of the cholera enterotoxin operon of Vibrio cholerae. J Clin Microbiol 1991; 29: 2517-21. 5. Spira WM, Sack RB, Froehlich JL. Simple adult rabbit model for Vibrio cholerae and enterotoxigenic Escherichia coli diarrhea. Infect Immun 1981; 32: 739-47. 6. Gil A, Gabilondon A, Molina ME, Burton B, Lanata CF, Bravo N. Isolation of Vibrio cholerae O1 biotype E1 Tor from children under three years of age in an epidemic of cholera in pen-urban Lima, Peru. Proceedings of the 27th joint conference on cholera and related diarrhoeal disease. Charlottesville: The US-Japan Co-operative Medical Science Program, 1991: 14-16.
CORRECTIONS Acquired resistance to clarithromycin as combined therapy in Mycobacterium avium intracellulare infection.-In this letter by Dr S. De Wit and colleagues (Jan 2, p 53), the second author’s name should have been Maurizio D’Abbraccio.
Use of non-prescription decongestant to abort anaphylaxis-In this letter by Dr K. T. Kun and colleagues (Feb 13, p 439), the concentration of oxymetazoline hydrochloride should have been 0-05%.