Malathion intermediate syndrome

Sudakin DL, Mullins ME, Horowitz BZ, Abshier V, and Letzig L (2000) Intermediate syndrome after malathion ingestion despite continuous infusion of pralidoxime. Clinical Toxicology 38 47-50. 

After acute effects subside, OPs produce a condition called the intermediate syndrome mediated through the enzyme neurotoxic esterase (Annau 1992). Symptoms consist of muscle weakness developing days after initial symptoms. Organophosphate-induced delayed neurotoxicity, a second delayed OP effect, develops weeks after exposure (Davis and Richardson 1980 Ecobichon 1996 Willems et al. 1984). Another condition described as wasting away results from toxic by-products generated during synthesis of OP insecticides, especially malathion (Chambers 1992). 

OP insecticide-induced intermediate syndrome (IMS) was reported for the first time in human patients in Sri Lanka in 1987 (Senanayake and Karalliede, 1987). Since then, this syndrome has been diagnosed in OP-poisoned patients in South Africa (1989), Turkey (1990), Belgium (1992), the United States (1992), Venezuela (1998), France (2000), and elsewhere. IMS is usually observed in individuals who have ingested a massive dose of an OP insecticide either accidentally or in a suicide attempt. IMS is clearly a separate clinical entity from acute toxicity and delayed neuropathy. A similar syndrome has also been observed in dogs and cats poisoned maliciously or accidentally with massive dosc.s of certain OPs. OPs that are known to cause IMS include bromophos, chlorpyrifos, diazinon, dicrotophos, dimethoatc, fenthion, malathion, merphos, methamidophos, methyl parathion, monocrotophos, omethoate, parathion, phosmet, and trichlorfon. These compounds and IMS are discussed further in Chapter 26. 

Benslama et al. (2004) have reported two unnsnal cases of malathion poisoning with a rare-type of complication from intermediate syndrome arising 2 to 4 days after the onset of cholinergic effects. The symptoms were respiratory paresis with difficulties of weaning from assisted respiratory, deficit of proximal limbs, neck flexors and cranial nerves. The authors attributed this syndrome to prolonged inhibition of acetyl-cholinesterases and not to any mnscnlar fiber s necrosis. 

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