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Abstract
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An outbreak of central nervous system illness involving 14 cases, with 8 deaths at the time of the first roport, occurred in the western highlands of Guatemala in the region around Quetzaltenango in the summer of 1965. The cases had developed during the period July to September 1965 in Indian families of a predominantly farming population living in scattered groups in a remote mountainous area. The crops grown include wheat, corn and potatoes, while livestock consists of chickens, pigs and a few horses and cattle. Corn is the main and pre- ferred staple. Water comes from unprotected wells or from shallow streams and there are virtually no sanitary facilities. The illness was at first thought to be an arthropod-borne encephalitis and, early in September, assistance was sought from the Pan American Health Organization by the Guatemalan Ministry of Health. PAHO arranged for three investigators to visit the area affected.
During the investigation, interviews with local health officials, physicians, affected families and their neighbors and a review of hospital records brought to light an additional 31 cases with 12 deaths making a total of 45 cases of CNS illness causing 20 deaths for the whole outbreak. All had a strikingly similar clinical picture.
The illness began with weakness in the legs which sometimes progressed to spastic paralysis with hyper-flexion and a positive Babinski; in some instances the arms were also involved. The lesions were symmetrical without loss of sensory or sphincter function. Neither fever nor malaise was a prominent symptom unless a pulmonary complication developed. The involvement of the legs was almost invariably followed in 4 to 7 days by impairment of vision, usually progressing to total blindness. Once established, there was no regression in either the paralyses or the visual impairment. In fatal cases there was a period of impaired consciousness merging into coma before death.
All patients were of poor nutritional status. The sexes were equally affected and the age distribution ranged from 2 to 55 years with over half the cases being under 10 years of age. The duration of illness varied and most cases had difficulty in walking and impaired vision for 1 to 4 weeks before coming to the hospital; patients who died had remained in the hospital for periods ranging from 1 week to 1 year before death.
The weeks of onset of 43 of the 45 cases occurring in 1965, or of their admission to the hospital, ranged from July 11 to September 19, 1965. There had been four cases in 1964 and one in 1963, all of which occurred during the same season of the year as the 1965 cases. Thirty-eight of the 45 cases occurred in three villages in the wheat-growing area; there was a high incidence within given families, frequently affecting children under 10 but never those who were breast feeding (Table 1). Both the clinical and epidemiological evidence suggested a toxic rather than an infectious origin.
Inquiry revealed that the families concerned participated in a wheat co-operative whereby they received each year, in May, a certain quantity of wheat seed which was treated with the fungicide methyl mercury dicyandiamide("Panogen 15"). The farmers were expected to return, to the co-operative organization at the end of the harvest, an amount of wheat equal to the quantity of treated seed given to them the previous spring. They had been warned not to eat the treated seed.
Several farmers' families had not heeded this warning and had ground the panogen-treated wheat to make tortillas. The distribution of illness among the members of the families who admitted eating the treated wheat was uneven. In one instance the first sign of illness in a family using the wheat appeared one week after it was eaten; in another it was 3 weeks later that the first symptoms appeared. Certain other families who had eaten the treated wheat suffered no symptoms at all, presumably due to dilution of the meal from the treated wheat with corn meal, or with wheat flour made from untreated wheat.
Specimens of kidney, liver, spleen and brain obtained from fatal cases of the illness in Guatemala have been examined in the CDC Toxicology Laboratory and have yielded amounts of alkyl mercury (9 to 20 ppm of Hg) consistent with fatal mercury poisoning. Table 2 compares the Guatemala findings with those of episodes of fatal mercury poisoning in other countries. Examination of a specimen of the treated seed contained 17 ppm expressed in metallic mercury. |