A Case of Reye’s-Like Syndrome in a 68-Day-Old Infant: Water-Damaged Home, Mold, Bacteria and Aflatoxins
Reye’s Syndrome is characterized by acute encephalopathy, hepatic injury accompanied with elevated serum ammonia, serum fatty acids, amino acids and triglycerides; hypoglycemia, prolonged prothrombin time, fatty infiltration of the liver, and mitochondrial pathology. We present an infant that died at 68 days of age with Reye ’s syndrome. The infant and parents were exposed to airborne fungi, bacteria and toxic bioaerosols resulting from water intrusion in the home. The purpose of this study was to investigate and, if possible, to determine the cause of death of the infant with respect to the fungi, bacteria and their toxins present in the families water-damaged home.
Materials and Methods
Health and genetic history was done on the family (father, mother and two siblings). Environmental evaluation was carried out to identify airborne fungi and bacteria in the home. Clinical testing of the baby while in the hospital provided data on blood chemistry and EEG results. Mitochondrial studies on skin fibroblasts and skeletal muscle were carried out testing for functions of Complexes I-IV and mitochondrial DNA mutations. Light and E.M. microscopy were done on liver biopsy material. Immunoaffinity column and fluorometry were used to detect aflatoxins (B1, B2, G1 and G2) in liver autopsy material. The mother’s breast milk and urine was tested for mycotoxins: trichothecenes, aflatoxins and ochratoxin.
Medical and genetic history were negative for familial diseases similar to Reye’s syndrome and for mitochondrial DNA mutations. Aortic and pulmonic valve abnormalities were observed. Environmental testing revealed the presence of elevated levels of several species of fungi and bacteria in the infant’s bedroom and other rooms of the home. Clinical diagnostic tests of the infant revealed metabolic acidosis, elevated serum ammonia, triglycerides, pyruvic and lactic acids, serum alanine, and beta-hydroxybutyrate. Mitochondrial studies showed decreased function of complexes I-IV and the absence of known mutations associated with mitochondrial diseases. Microscopy (light and E.M.) of biopsies demonstrated the accumulation of glycogen in muscle and fatty droplets in the liver. Aflatoxins were detected in the infant’s liver (2.1 ppb), and the mother’s breast milk (15 ppb), while maternal urine was positive for trichothecenes (4.76 ppb) and ochratoxin (3.4 ppb).
After a review of the peer reviewed literature, we conclude that the infant died of a Reye’s-Like Syndrome at the age of 68 days (all 22 cited criteria were met). Clinical and autopsy findings were consistent with this disease process. The valvular abnormalities found are associated with actinomycetes exposure. The medical and genetic histories were negative for any familial diseases of a similar nature. The infant had mitochondrial dysfunction of complexes I-IV, suggesting mitochondrial disease consistent with alflatoxin toxicity. The presence of aflatoxins in the liver supports the causal role of this mycotoxin in the illness of this infant. We have discussed the role of other factors in the indoor environment that may also lead to similar conditions.
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