Published Date: 2002-12-13 23:50:00
Subject: PRO/EDR> Undiagnosed febrile illness, children - India (UP)(07)
Archive Number: 20021213.6056

UNDIAGNOSED FEBRILE ILLNESS, CHILDREN - INDIA (UP) (07)
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Date: Fri 13 Dec 2002
From: A-Lan Banks <A-Lan.Banks@derwent.co.uk>
Source: Times of India online, Fri 13 Dec 2002 [edited]
<http://timesofindia.indiatimes.com/cms.dll/html/uncomp/articleshow?artid=31098388>


Organophosphate Pesticides Now Suspected as Cause of Mystery Disease
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The confusion surrounding the 'mystery disease' that has claimed many
lives in western Uttar Pradesh in the past week is close to being
solved. And the villains of this tragedy may well turn out to be
'organophosphate compounds' -- the most commonly used form of
pesticides in the country.

Scientists, who have been struggling to identify the cause of the
deaths, [are now focusing on a single] probable cause; namely,
pesticide poisoning. They are now racing towards identifying the
vector/mode of transmission, spread and dilution pattern, symptoms,
and line of treatment for the disease.

Both scientists at the Industrial Toxicology Research Centre (ITCR)
and doctors at the Directorate of Health, Uttar Pradesh, [discount
the epidemic theory]. Senior scientists at ITRC pointed out that air
and water can be almost be ruled out as the mode of transmission. The
Director-general (health), Dr Gayatri Sharma, said: "Viral diseases
are common in the Terai region, hence we tested _Culex vishnoi_
mosquitoes from the region to see whether they were vectors." (_Culex
vishnoi_ mosquitoes are vectors of Japanese encephalitis virus.)
"However, the mosquitoes turned out to be negative," she said. "These
facts indicate that the disease is possibly being transmitted through
eatables such as fruits, vegetables, agricultural produce and meat,"
said a senior ITRC scientist.

Saharanpur has a concentration of orchards, fertile agricultural
land, and a sizable presence of animal husbandry. There are 2 reasons
for the ITRC scientists to zero in on organophosphate-based
pesticides as the cause of the disease. The first being that it is
not only young children who are falling prey to the disease, but also
young cattle. The second reason is symptomatic. The key lies in the
manner in which, such pesticides work: by attacking and breaking down
the central nervous system (CNS).

Organophosphate-based pesticides easily dissolve in water and hence
their effect is immediate and they attack the synapse between nerve
cells in the CNS. More specifically, they are cholinesterase
inhibitors. This attack on the CNS by such pesticides is acute and
causes convulsions and tremors, apart from watering of eyes and nose.
These were the symptoms that were observed in children suffering from
the disease.

--
A-Lan Banks
<A-Lan.Banks@derwent.co.uk>

[This theory is more acceptable than the earlier suggestion of an
outbreak of "atypical measles". The report indicates, however, that
the accuracy of the pesticide exposure explanation has still to be
established; nonetheless presumptive remedial measures can be put in
place immediately. Final confirmation of the diagnosis is awaited
with interest. - Mod.CP]

[Organophosphates irreversibly bind to cholinesterase, causing the
phosphorylation and deactivation of AChE. The clinical effects are
secondary to acetlycholine (ACh) excess at cholinergic junctions
(muscarinic effects), in the CNS, at skeletal nerve-muscle junctions,
and at autonomic ganglia (nicotinic effects).

The clinical picture after poisoning depends on the rate at which the
pesticide is absorbed. There is also significant variability in the
affinity of various organophosphates for AChE. Some organophosphates
such as diazinon and parathion have significant lipid solubility
allowing fat storage with delayed toxicity due to late release. Some
need to be metabolized to a more active form to produce toxicity.
Members of the phosphorothiotate group (e.g. chlorpyrifos,
parathion)need to be activated by oxidation of the P=S bond to the
phosphate form before producing toxicity.

All signs and symptoms of acute organophosphate poisoning are
cholinergic in nature and effect nicotinic, muscarinic, and central
nervous system receptors. These effects develop within minutes to
hours, depending on the type of exposure. The quickest symptoms occur
with inhalation, followed by GI absorption and dermal exposure, with
respiratory symptoms being the most critical.

The nicotinic (sympathomimetic) effects from ACh excess at motor end
plates cause persistent depolarization of skeletal muscles, resulting
in fasciculations, muscle weakness, hypertension, and tachycardia.
Also, mydriasis can be present.

Muscarinic effects from postganglionic parasympathetic activity of
smooth muscles may cause smooth muscle contractions in all organs
(eg. lung, gastrointestinal, eye, bladder, secretory glands). These
include bronchospasm, GI upset, miosis and urination. Effects also
include reduction of sinus node and AV conduction, causing brady- or
ventricular dysrhythmias.

CNS effects may cause excessive stimulation (seizures), CNS
depression and/or coma. Patients may present in a coma with or
without seizure activity, or the patient may rapidly progress to a
severely depressed mental status. Actual signs/symptoms depend on the
balance of muscarinic and nicotinic receptor stimulation.

CNS effects may cause excessive stimulation (seizures), CNS
depression and/or coma. Patients may present in a coma with or
without seizure activity, or the patient may rapidly progress to a
severely depressed mental status. Actual signs/symptoms depend on the
balance of muscarinic and nicotinic receptor stimulation.

The patient can have wheezing, chest tightness, and productive cough.
The bronchorrhea can be significant with frothy and/or bloody sputum
and severe pulmonary edema. The primary cause of death in acute
poisoning is usually respiratory failure with a contributing
cardiovascular component. Toxic myocardiopathy has been noted in some
severe poisonings. Bradycardia is the usual cardiac sign, but there
can be tachycardia and hypertension from nicotinic, sympathetic
stimulation.

Headache, dizziness, and the SLUDGE syndrome of salivation,
lacrimation, urination, defecation, GI upset and emesis are some of
the common early symptoms reported. Sweating and rhinorrhea also
frequently are present. Weakness, fasciculations, incoordination, and
GI distress all are markers of a worsening poisoned condition. Blurry
or darkened vision can be present with miosis. Confusion, anxiety,
restlessness and toxic psychosis can occur and there have been
reports of memory loss and depression.

Signs and symptoms in children are often different than in adults.
Less common are sweating, lacrimation, bradycardia and
fasciculations. Mental status changes including lethargy and coma
(54%-96%) and seizures (25%) are more common. Seizures are an
infrequent presentation in adults. - Mod.TG]

See Also

Undiagnosed febrile illness, children - India (UP) 20021201.5942
Undiagnosed febrile illness, children - India (UP)(02) 20021203.5960
Undiagnosed febrile illness, children - India (UP)(04) 20021206.5978
Undiagnosed febrile illness, children - India (UP)(05) 20021207.6001
Undiagnosed febrile illness, children - India (UP)(06) 20021208.6006
1999
----
Organophosphate pesticide poisoning - USA (California): 1998 19990313.0374
Organophosphate pesticide poisoning - India: 1997 19990307.0329
....................cp/pg/tg/lm

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