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produce detectable amounts of the thermostable direct haemolysin as judged by a modified Elek test.’ They were also negative for the thermostable direct haemolysin gene when examined by DNA colony hybridisation.’ Moreover, the serovars of the Kanagawa negative strains were all 03:K6. The Kanagawa negative isolates induced intestinal fluid accumulation in rabbit ileal loops. We conclude that there was an outbreak of gastroenteritis due to Kanagawa negative V parahaemolyticus in the Maldives in 1985. The clinical symptoms were indistinguishable from those seen in typical Kanagawa positive V parahaemolyticus infection. Thus Kanagawa negative as well as positive V parahaemolyticus can cause gastroenteritis, and the thermostable direct haemolysin (at least an ordinary one) may not be the sole virulence factor of V parahaemolyticus. We also think that this is the first reported episode of V parahaemolyticus infection in the Maldives.

Airport Quarantine Station, 3-555, Hotarugaike Nishi-machi, Toyonaka, Osaka, Japan

SHUN-ICHI HONDA IKUO GOTO ICHIROU MINEMATSU NAGASHIGE IKEDA NOBUO ASANO

Osaka Prefectural Institute of Public Health

MASANORI ISHIBASHI YOSHIO KINOSHITA

Research Institute for Microbial Diseases, Osaka University

MITSUAKI NISHIBUCHI TAKESHI HONDA TOSHIO MIWATANI

Osaka

1. Takeda Y. Thermostable direct

probe. X-ray screening can also be used to check probe positioning, and have found good correlation with the manometric sphincter.

we

The probe position is almost invariably found to be 3 cm below the hilum of the lung on lateral screening. This was so in 84 % of cases, and in the remainder it was within 2 cm of this area. There was no correlation with either vertebral level or distance above the diaphragm. In centres where manometry is not available, we would suggest that X-ray screening, using the hilum of the lung as a landmark, is the most satisfactory way of placing the pH electrode. We also forbid coffee drinking and smoking during the tests; also, and in common with other centres, we limit the diet during testing to foods with a pH above 5. This excludes almost all fruitcontaining foods and drinks which, because of their acidity, can mimic an acid reflux when swallowed. We agree that 24 h pH testing is a valuable tool in district general hospitals. Standardisation of the method would improve the quality of the test and allow valid comparison of results between centres. Department of Gastroenterology, Royal Naval Hospital, Haslar, Gosport, Hampshire PO12 2AA

D. L. STOKER J. G. WILLIAMS

1. Dodds WJ. Instrumentation and methods for intraluminal oesophageal manometry Arch Intern Med 1976; 136: 515-23. 2. Dehn TCB. 24 hour ambulatory pH recording in gastro-oesophageal reflux GI Futures 1986, 1: 10-12.

hemolysin of Vibrio parahaemolyticus. Pharmac Ther

1983; 123-46 Colwell RR, Kaper JB. Vibrio parahaemolyticus and related halophilic vibrios. CRC Crit Rev Microbiol 1983; 10: 77-124. 3. Sakazaki R, Tamura K, Kato T, Obara Y, Yamai S, Hobo K Studies on the enteropathogenic, facultatively halophilic bacteria, Vibrio parahaemolyticus III: Enteropathogenicity. Jpn J Med Sci Biol 1968, 21: 325-31. 4. Honda T, Chearskul S, Takeda Y, Miwatani T Immunological method for detection of Kanagawa phenomenon of Vibrio parahaemolyticus. J Clin Microbiol 1980; 11: 600-03. 5. Nishibuchi M, Ishibashi M, Takeda Y, Kaper JB. Detection of the thermostable direct hemolysin gene and related DNA sequences in Vibrio parahaemolyticus and other vibrio species by the DNA colony hybridization test. Infect Immun 1986; 49: 481-86

2.

acid/alkali junction found to be above the LOS at insertion of the

Joseph SW,

24-HOUR MONITORING OF OESOPHAGEAL OUTPATIENTS

pH IN

SIR,-We read with interest the paper by Dr Donald and colleagues (Jan 10, p 89) on 24 h pH monitoring in a district general hospital. We have made 53 recordings over the past nine months, on 8 healthy volunteers and 45 patients with atypical chest pain or clinically severe oesophageal reflux. Our figures for positive diagnostic yield are similar to those of Donald et al, but our technique differs in some important respects, with we feel improvement in the quality of the test. We use a Novo Memolog 600 system with glass electrode, which has shown itself to be reliable, with an equipment failure rate of 6%; only two patients have been unable to tolerate the catheter. One healthy volunteer was withdrawn, having been found to be achlorhydric with the pH electrode. We are fortunate to have manometry equipment which is used to map the position of the lower oesophageal sphincter (LOS)l and gives valuable information on oesophageal motility. This enables us to place the pH electrode very accurately 5 cm above the upper end of the LOS. In the absence of this equipment, however, we do not think that a peroral measurement of gastro-oesophageal mucosal junction using the endoscope is reliable, since its position in relation to the LOS can vary (as in Barrett’s oesophagus) and the nasopharyngeal distance may vary between patients. We have measured the acid/alkali junction by withdrawing the pH electrode from the stomach back into the oesophagus,2 and found this to be a very variable and unpredictable point. In 53% the junction was 1 cm or more (mean 4 . 1 cm, range 1-13) below the lower edge of the LOS high-pressure zone. In the remaining 47% the junction lay within the limits of the sphincter zone. In no patient was the

PARKINSONISM AND INDUSTRIAL CHEMICALS

SIR,—Dr Bocchetta and Professor Corsini (Nov 15, p 1163) reported irreversible parkinsonism in a farmer who applied pesticides and a worker who manufactured pesticides. We agree that the relation between pesticides and parkinsonism requires study. We would also call attention to other reports--eg, in a 48-year-old cropduster who worked with organophosphate pesticides for 13 years.’We have reported grainstorage workers who had incipient or manifest parkinsonism associated with the use of liquid-solvent fumigants and pesticides, mainly a carbon disulfide/carbon tetrachloride insecticide mixtureCarbon disulfide, especially in the viscose rayon industry,3 has long been associated with parkinsonism. One case-report linked carbon tetrachloride to parkinsonism in a 40-year-old chemist chronically exposed to leaks.’ We have also noted parkinsonism after inadvertent ingestion of seed-com treated with the fungicide hexachlorobenzene. The early signs of extrapyramidal disorder included cogwheeling, increased muscle tone, and reduced associated movements. The findings of the Corsini-Bocchetta group that the enhances diethyldithiocarbamate neurotoxicity of methylphenyltetrahydropyridine in mice6 (MPTP) may be significant for grainworkers exposed to carbon disulfide-based fumigants plus other neurotoxic compounds in that industry. Dithiocarbamates are a metabolic breakdown product of carbon disulfide reactions with aminogroups.7 Other findings with MPTP have indicated greater susceptibility to chemically-induced parkinsonism with age, reminiscent of the age-related incidence rates for MPTP-induced parkinsonism in mice.8 We have noted a similar relation between parkinsonism severity and age in the small groups of occupational exposures that we have studied. Several neurotoxic industrial chemicals, in addition to those in pesticides, have been linked to parkinsonism and to neurological disorders such as peripheral neuropathy, encephalopathy, encephalomyelitis, multiple sclerosis, and amyotrophic lateral sclerosis.9 Of the 588 compounds of known toxicological significance that are most frequently encountered in industry, 25% have documented neurotoxic effects whereas less than 10% have been linked to cancers and fewer than 5% to cardiovascular toxicity." The study of neurotoxic disorders is outside the mainstream of medicine. As a result, the physician is often disadvantaged in the diagnosis of chemically induced diseases. Greater attention must be paid to diagnoses of neurological diseases as sentinel indicators of