-Caveat Lector-
Subject:
[MCS-CI] Interesting article in British Medical Journal
BMJ 1998;317:268-269 ( 25 July )
Clinical review
Lesson of the week
A foodborne outbreak of organophosphate poisoning
Indiscriminate use of organophosphates without public education on safety
increases the potential threat of foodborne outbreaks of poisoning
Rama Chaudhry, additional professor, a Shyam Bala Lall, additional
professor, b Baijayantimala Mishra, senior resident, a Benu Dhawan, senior
research associate (pool scheme). at
a Department of Microbiology, All India Institute of Medical Sciences, New
Delhi-110 029, India, b Department of Pharmacology, All India Institute of
Medical Sciences
Correspondence to: Dr Chaudhry [EMAIL PROTECTED]
Foodborne diseases have a major impact on public health. Early and correct
identification of the cause of an outbreak of food poisoning enables
specific treatment to be started as soon as possible, and this can be life
saving. We 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 syndromemainly because they
developed the symptoms earlymost 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 their
series of patients with organophosphate poisoning who developed
intermediate
syndrome.3 The refference 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 ingestedcase 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 monocrotophosbut 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 :
1.Flanagan RJ, Braithwaite RA, Brown SS, Widdop B, de Wolff FA. Basic
analytical toxicology. London: MacMillan, 1995:187-189.
2.Jeyaratnam J. Acute pesticide poisoning: a major global health problem.
World Health Stat Q 1990; 43: 139-144[Medline].
3.Senanayake N, Karalliedde L. Neurotoxic effects of organophosphate
insecticides: an intermediate syndrome. N Engl J Med 1987; 316:
761-763[Medline].
4.De Bleecker JL. The intermediate syndrome in organophosphate poisoning:
an
overview of experimental and clinical observations. Clin Toxicol 1995; 33:
683-686.
(Accepted 5 May 1998)
© British Medical Journal 1998
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