LESSON OF THE WEEK: A FOODBORNE OUTBREAK OF ORGANOPHOSPHATE POISONING
July 25/98
British Medical Journal 317:268-269
Researchers from the Department of Microbiology and Department of Pharmacology at the India Institute of Medical Sciences, New Delhi report an outbreak of fatal food poisoning caused by the pesticide malathion.
Case reports On 6 July 1997, 60 men aged 20-30 years attended a communal lunch at which they ate chapatti, cooked vegetables, pulses, and halva. They all developed nausea, vomiting, and abdominal pain over the next three hours. The men were taken to a local primary healthcare centre where they received treatment for their symptoms. Fifty six responded to the treatment and were discharged home the same day. However, the condition of the remaining four patients deteriorated. Their level of consciousness fell, and they developed respiratory distress and generalised muscular weakness. The next day they were moved to an urban emergency hospital.
Case 1
A 20 year old man presented with miosis, sweating, impaired consciousness, and hypotension. The muscle power in his arms and legs was graded as 3/5. Reflexes in the arms and legs were reduced, but he did not have sensory impairment. He had noticeable weakness of neck flexion, to the extent that he could not raise his head off the pillow. Initial treatment included intravenous fluids, antiemetics, and antibiotics. On the second day after admission to the urban emergency hospital, he developed respiratory insufficiency. Because he needed endotracheal intubation and intermittent positive pressure ventilation, he was transported immediately to a tertiary care hospital. Over the next 24 hours he developed type II respiratory failure with paralysis of thoracic, neck, and diaphragmatic muscles. He underwent tracheostomy and was ventilated mechanically for the next few days. He was treated with atropine and pralidoxime (1 g intravenously), but his neurological status did not improve appreciably, nor did his muscle strength improve much over the nine days after admission to hospital. On day 10 he had a cardiac arrest and could not be revived.
Cases 2, 3, and 4
Three patients developed mild generalised muscle weakness and respiratory distress, and their level of consciousness was reduced. They were admitted to the urban emergency hospital for further management, responded to treatment for their symptoms, and were discharged home a week later.
Investigations and assays
The 60 men who succumbed to food poisoning had eaten a lunch cooked in the community kitchen. Detailed questioning of those working in the kitchen showed that on the morning of the outbreak the kitchen had been sprayed with pesticide containing malathion, an organophosphate. The raw materials for cooking were stored in open jute bags. All 60 people who had eaten the meal developed signs and symptoms, but the severity of illness was greatest in case 1. He had eaten at least eight chapatti while the others had eaten three or four. Before treatment at the tertiary care hospital was started, samples of serum and gastric fluid were obtained from case 1 for Clostridium botulinum toxin mouse assay. Samples of the wheat flour, chapatti, spices, and oil used in the meal and samples of faeces and gastric fluid from case 1 were cultured anaerobically for C botulinum. The results of toxin bioassay and culture for C botulinum were negative. The neurological features of the patients and the history of insecticide spraying prompted the collection of gastric aspirate from case 1 for toxin and chemical analysis. The gastric aspirate was positive for organophosphate.1 This positive test result was achieved seven days after case 1 had been admitted to the tertiary care hospital. Food samples from the shared lunch, including leftover chapatti, wheat flour, spices, and oil, were also sent to the toxicology laboratory for analysis. Culture and toxin assay of the sample of chapatti and wheat flour were negative for C botulinum, but an organophosphate compound was detected. The remaining foods were negative for toxins and chemicals.
Discussion
In developing countries, the widespread use of organophosphates has been accompanied by an appreciable increase in the incidence of poisoning with these agents. This is a result of their easy availability, indiscriminate handling and storage, and the lack of knowledge about the serious consequences of poisoning. Latest estimates from the World Health Organisation indicate that each year one million serious accidental poisonings and two million suicide attempts involving pesticides occur worldwide.2 In the incident we describe, the severity of the illness in case 1 raised the possibility of botulism, and C botulinium was sought by microbiological investigation. However, when subsequent investigation showed that the kitchen had been sprayed with insecticide, a complete toxicological examination was carried out. In fact, the presenting features of case 1 were more consistent with organophosphate poisoning than botulism. These included rapid onset of the illness (within three hours of the meal), excessive sweating, depressed level of consciousness, miosis, and hypotension. The rapid clinical improvement seen in most patients (except case 1) over 24 hours was also more consistent with organophosphate poisoning than botulism.
All 60 patients had a well defined cholinergic phase. Cases 1 to 4 subsequently developed symptoms of the intermediate syndrome. The intermediate syndrome set in nearly 24 hours after the exposure to organophosphate, well before the patients had recovered from the initial cholinergic crisis. It is characterised by weakness of the proximal limb muscles, neck flexor muscles, motor cranial nerves, and respiratory muscles; it generally occurs 24-96 hours after poisoning and after the resolution of a well defined cholinergic phase. The respiratory insufficiency in all four cases drew attention to the onset of this syndrome. Even though they did not meet fully the criteria for the intermediate syndrome[---]mainly because they developed the symptoms early[---]most of their symptoms and signs agreed with this phase. On the basis of these observations, a diagnosis of early intermediate syndrome was made in these four patients.
A similar observation has been made by Senanayake and Karalliedde in theirseries of patients with organophosphate poisoning who developed intermediate syndrome.3 The difference in the severity of the neuropathy and the clinical course observed in our four cases can be attributed to differences in the amount of organophosphate ingested[---]case 1 ate eight chapatti. Delay in making a correct diagnosis, evaluation, and management of organophosphate poisoning meant that case 1 did not receive appropriate treatment early enough. Furthermore, the development of the intermediate syndrome before its expected onset has been described previously with organophosphates such as dimethoate, fenthion, methamidophos, and monocrotophos[---]but never with malathion.4 The increasing and indiscriminate use of organophosphates as agricultural and household insecticides without any accompanying public education about their storage and safe use increases the potential for more outbreaks of food poisoning. This report is a reminder to epidemiologists, toxicologists, and microbiologists that organophosphate food poisoning is a continuing hazard, especially in developing countries. Health professionals should be familiar with the acute illness syndromes associated with organophosphate poisoning so that they can differentiate between these and the neurological symptoms caused by other forms of poisoning. Skilled and prompt treatment can provide a good outcome for a potentially lethal condition.
Acknowledgments
Contributors: RC initiated and coordinated the investigation, participated in data analysis and interpretation, and edited the paper. SBL carried out the toxicological study and helped write the paper. BM participated in the microbiological investigations. BD participated in the design, investigations, and in collecting and interpreting the data, and had a major part in writing the paper. SBL is guarantor of this paper. Funding: The study was supported by grants for routine diagnostic services provided by All India Institute of Medical Sciences.
Conflict of interest: None.
References
Peter Ormesher's comments on this issue:
"Pesticide poisoning is a growing concern everywhere in the developing world. A combination of low literacy rates and lack of training on the proper use of these products mean that Hedley's products will be in significant demand by governments and health organizations everywhere."