Fatal Encephalopathy Research Articles

Hexachlorophene Storage in a Burn Patient Associated With Encephalopathy

Hexachlorophene (HCP), a chlorinated phenolic hydrocarbon with bacteriostatic properties against Staphylococcus, is used in a number of topical products. Absorption through normal and damaged human skin has been appreciated and neurologic changes have been described in experimental animals, but instances of human toxicity have been reported infrequently. A 10-year-old boy who sustained a 25% burn did well initially but died in the second week of convalescence with hyperthermia, lower-extremity weakness, and cerebral edema. His treatment had included frequent applications of HCP. Analysis of post-mortem tissue revealed the presence of toxic levels of HCP in the blood (2.2 mug/gm) and brain (2.2 mug/gm), with storage in skin (25 mug/gm), liver (4.4 mug/gm), and fat (6.0 mug/gm). This case suggests that topical applications of HCP in man may result in an extensive absorption with fat storage and may cause fatal encephalopathy.

Transmission of Creutzfeldt-Jakob Disease from Man to the Guinea Pig

Intracerebral and intraperitoneal inoculation of two guinea pigs with biopsy material from a patient with Creutzfeldt-Jakob disease produced a similar fatal encephalopathy characterized by status spongiosus 422 and 512 days after inoculation. Serial transmission of this disease from guinea pig to guinea pig was achieved in subsequent passages.

Tropism of Mycoplasma gallisepticum for arterial walls.

The fatal encephalopathy associated with M. gallisepticum strain S6 in turkey poults was completely curable by treatment with tylosin or pleuromutilin. The lesions of cerebral polyarteritis disappeared after therapy. Polyarthritis developed in some birds after recovery from encephalitis. Immunofluorescent studies revealed that intravenously injected organisms became localized as microcolonies within the walls of cerebral and periarticular arteries, and in the glomeruli. Turkey IgG deposition was demonstrated on the glomerular basement membranes, but not in the arterial lesions. The results suggest that the pathologic changes caused by this microorganism are due to selective localization and growth in arteries.

Transmissible mink encephalopathy: experimental transmission to the squirrel monkey.

A progressive, fatal spongiform encephalopathy developed in three squirrel monkeys 11 months after inoculation with primate-passaged transmissible mink encephalopathy agent. The clinical symptoms and histopathologic and electron microscopic findings suggest that this naturally occurring disease of mink has been transmitted experimentally to squirrel monkeys.

Infection as the etiology of spongiform encephalopathy (Creutzfeldt-Jakob disease).

Fatal spongiform encephalopathy occurred in four chimpanzees 12 to 14 months after inoculation with suspensions of brain from four patients, respectively. Chimpanzee to chimpanzee transmission was effected without reduction in incubation period. Retransmission of the disease to a second chimpanzee occurred when an inoculum that had been stored at -70 degrees C for over 2 years was used.

Creutzfeldt-Jakob disease (spongiform encephalopathy): transmission to the chimpanzee.

Biopsy material taken from the brain of a patient with CreutzfeldtJakob disease with status spongiosus induced a similar fatal encephalopathy in a chimpanzee 13 months after inoculation.

Encephalopathy With Hepatorenal Alterations

To the Editor:— Jabbour et al and Winograd (194:1245, 1247, 1965), report cases of fatal encephalopathy in children, with degenerative changes in liver and kidneys, similar in character, and resembling others reported in recent years from Australia. In 1946 entirely similar cases were seen in Connecticut and New York following rectal suppository administration of the diallylacetic acid salt of bismuth (135:28, 1947). There were three deaths and one survival. The compound was withdrawn from the market at that time, and could not be responsible for the recent cases. However, the past experience may furnish a lead. It demonstrated a class of chemical compounds capable of causing toxic encephalopathy and fatty change of the liver and kidneys in very small doses, namely the allyl compounds.

Encephalopathy in Salmonella infections.

Different neurological complications of typhoid are known to occur. A bacterial invasion of the meninges, a true bacterial meningitis, is rare and occurs mainly below 2 years of age. 14 Peripheral neuritis, radiculitis, and radiculomyelitis, occasionally from the ascending type, 7,8 and finally cases of brain involvement have been described. 1,4,11,12 Some authors speak of encephalitis, others of encephalopathy; the latter is probably more correct. However, all these complications are rare. It is the purpose of this paper to present five cases of encephalopathy in Salmonella infections observed at the American University Hospital in Beirut. During this period of time about 150 cases of uncomplicated salmonellosis were admitted to this institution. However, these two figures do not permit a conclusion as to incidence of Salmonella encephalopathy, since many milder and even some of the severe cases are not hospitalized. Case1.— Fatal Encephalopathy Due to Paratyphoid B with Coma, Electrolyte

FATAL TOXIC ENCEPHALOPATHY APPARENTLY CAUSED BY STREPTOMYCIN

Few fatal complications of streptomycin therapy have been reported in the medical literature.¹However, it is well recognized that streptomycin produces dysfunction of the eighth cranial nerve in man²and that its administration is sometimes followed by symptoms which are best explained by the assumption that temporary damage to nervous or vascular tissue has occurred. Thus, paresthesias of the hands, the tongue and the circumoral region are not uncommon.³Furthermore, there is on record at least one report of convulsions having occurred during the administration of streptomycin intravenously.⁴We have recently witnessed a case of fatal encephalopathy which we believe was caused by streptomycin. The observations may throw some