Hexachlorophene toxicosis in a litter of Doberman pinschers.

A litter of 5-week-old Doberman Pinschers with pustular dermatitis was treated dermally with a hexachlorophene-containing emulsion. Shortly after a second treatment, all of the puppies developed neurologic signs consisting of muscle tremors, ataxia, and apparent muscle weakness. The clinical history and signs, histologic lesions within the central nervous system, and measurement of hexachlorophene in liver and kidney tissue confirmed a diagnosis of hexachlorophene toxicosis.

Neurotoxicosis associated with the use of hexachlorophene in a cat.

Two weeks after daily topical application of hexachlorophene, a 4-week-old female kitten developed cardiovascular collapse, corneal ulcers, trembling, lethargy, and weakness. The kitten was euthanatized. At necropsy, the tissues appeared macroscopically normal; however, microscopic examination of tissue specimens indicated status spongiosis, astrocytosis, and microgliosis of the cerebral and cerebellar white matter and corticospinal tracts. Neuronal cell bodies forming the affected white matter were intact, indicating that demyelination may have been the cause of the lesions. The neurologic lesions were considered compatible with those of hexachlorophene-induced toxicosis.

Protection with butylated hydroxytoluene and other compounds against intoxication and mortality caused by hexachlorophene.

The antioxidants butylated hydroxytoluene (BHT) and ethoxyquin protected rats against intoxication and mortality normally produced by hexachlorophene (HCP, 100 mg/kg). BHT also prevented the elevation of cerebrospinal fluid pressure, a central nervous system effect of HCP poisoning. In addition, both phenobarbital and SKF-525A protected against HCP poisoning, with the barbiturate also offering significant protection against triethyltin. L-Ascorbic acid, vitamin E, N,N-diphenyl-p-phenylenediamine and reduced and oxidized glutathione over a range of doses were ineffective in preventing HCP lethality. The protective effect of phenobarbital against HCP and triethyltin intoxication further supports existing evidence of a common or similar mechanism of toxic action for these two structurally dissimilar compounds.

[Caustic diaper dermatitis and encephalitis secondary to the application of talcum contaminated with hexachlorophene]. / Dermite caustique du siège et encéphalite secondaires à l'application de talc contaminé par l'hexachlorophène.

Five observations of infants with transcutaneous intoxication by 6,3 p. 100 hexachlorophene contaminated talcum powder are reported. The diaper dermatitis is particular because of its topography (red pants shape), of its sudden occurring, of its papyraceous aspect evoking caustic origin, and of its association with severe encephalopathy. The neurological signs start with epileptic fits leading rapidly to coma. Prognosis is serious leading either to death or to paraplegia. Enquiry on that epidemic shows that mortality raised up to 18 p. 100. The neurological signs with oedematous degeneration of myelin are characteristic of hexachlorophene toxicity. Plasma levels of toxics range up to 15,94 mg/ml i.e. 30 times more than the rates observed by Curley in a premature washed with a commercial solution containing 3 p. 100 hexachlorophene. During a toxic neurological syndrome, the existence of diaper dermatitis with red plants shape must lead to an aetiological diagnosis of the possibility of transcutaneous intoxication even if the product seems as harmless as talcum powder.

Hexachlorophene retinopathy in suckling rats. A light- and electron-microscopic study of short-term and long-term effect of hexachlorophene intoxication on the retina of young rats.

Hexachlorophene (HCP) in very large doses has a toxic effect on the retina of adult rats. The present study examined the sensitivity of the developing retina to smaller doses and its ability to recover from neurotoxic damage. Suckling rats were intoxicated with HCP added to the mothers' diet. The retinae of the pups were examined by light and electron microscopy for early and late effects. All dose levels above 100 ppm caused vacuolar degeneration of the outer segments of photoreceptor cells within 14 days of intoxication, followed by degeneration of the inner segments after 28 days. The cell bodies of photoreceptor cells and all other retinal layers remained normal. Suckling intoxicated with HCP (100 - 500 ppm) added to the mothers' diet for 28 days and then withdrawn, showed no recovery of the outer or inner segments o photoreceptors when examined up to 150 days later. In addition, extensive degeneration and loss of photoreceptor cell occurred after withdrawal of HCP and the degenerative process extended to involve the inner nuclear layer. The rate of appearance of pathological changes was proportional to the total amount of ingested HCP. This study showed that photoreceptor cells in newborn rats are highly sensitive to HCP. The retinal lesions were irreversibly an continued to progress by continued trans-synaptic degeneration after withdrawal of the toxic agents.

New aspects of the origin of hepatocellular vacuoles. An ultrastructural study on rat and mice liver after different intoxications.

The stages of vacuolar formations in liver parenchymal cells of rats and mice following application of phalloidine, amanitine, o-phenylphenol, hexachlorophene and p-chloro-m-cresol were demonstrated by electron microscopic investigations. After treatment the intercellular spaces are markedly widened and in restricted regions exhibit large sacculi penetrating into the cytoplasm of adjacent hepatocytes. In cross-sections these invaginations frequently appear as intracellular vacuoles. Our present investigations, however, clearly demonstrate that these vacuoles are still in direct connection with the intercellular space. The vacuolar formation is more pronounced in older animals and it is suggested that an increased patho-physiological portal hypertension leads to the swelling of the intercellular space.

Accidental percutaneous hexachlorophane intoxication in children.

Eighteen children with normal skin were accidentally intoxicated by a talc powder containing 6% hexachlorophane. Four died and two remained paraplegic. The clinical picture was intracranial hypertension, eight patients developing signs of spinal cord damage. The condition seemed to result from massive intramyelinic oedema. In the spinal cord vascular disturbances may occur as mechanical complications of oedema, giving rise to permanent sequelae.