SUMMARY Asthmatic children with presumptive isolated bacterial allergy were selected for a placebo controlled study of the effect of treatment with bacterial vaccines. Of more than 400 children studied only 25 satisfying the criteria for the diagnosis “isolated bacterial allergy” were found. During the investigation period of 12–24 months repeated testings were performed and specific allergies were demonstrated in an additional 10 children out of the 25. At the start of the period active infectious rhinosinusitis was found in 16 of the 25 patients. Elimination of the infections resulted in marked improvement of the allergic symptoms in all but two children. There was no significant difference between the results in the vaccine and placebo groups. The side effects were also equally distributed between the two groups.
SUMMARY A fatal case of generalized BCG infection following vaccination is reported. The patient, a girl BCG‐vaccinated at the age of six weeks, developed septic fever and leucocytosis at 5 1/2 months of age and died at 7 months of age in a poor condition with extensive edemas, icterus and severe attacks of general convulsions. Autopsy revealed disseminated tuberculosis. The histological picture showed little tendency to tuberculoid structure, marked caseous necrosis and myriads of acid‐fast bacilli in the affected areas. By bacteriological examination the acid‐fast bacilli were indistinguishable from BCG. Increased virulence or other changes in the BCG vaccine which might explain the fatal complication has not been found. Two of the patient's three siblings had previously shown definite signs of reduced resistance to infection, and both died at an early age from infections. Adding this to the patient's case history, one feels justified in concluding that a familial resistance impairment to infection is present. The cause of this deficiency is discussed. There are at present five known cases of fatal BCG infection following vaccination in Scandinavia, and the number of persons vaccinated is estimated to be between 6 and 7 millions. The probable incidence of fatal complications can thus be put at less than one case per million vaccinated. As the protective effect of BCG vaccination is beyond doubt and the serious complications extremely rare, there seems to be no ground at present for objecting to continued BCG vaccination.
This study is based upon investigations concerned with 360 children suffering from epilepsy, made over a five-year period from 1950-1955. 200 were inpatients and 160 out-patients, and they ranged in age from 0-14 years. 188 were boys and 172 girls. Succesful pneumo-encephalographic (PEG) investigation was carried out on 165 in-patients. Summary and Conclusions:1. Of probable etiologic importance were following data: Seizures had occured in the families of 28.7 % of the 360 patients. 24% had a birthweight over 4000 gr.against 14% in the normal Norwegian population. Prematurity occured in 9.5% and pathologic birth and perinatal complications in 15.5 %.2. 60 % of the 165 pneumo-encephalographically examined patients suffering from epilepsy had pathological changes in their brains varying from slight t o extremely severe. 3. The earlier in life the seizures started, the more frequent and severe were the pathological PEG findings. Thus 80% of the children where seizures started before 2 years of age (in all 88 patients) had abnormal PEG findings.4. There is no clear correlation between the severity and extent of the epilepsy and the demonstrated brain injuries. Extensive pathological brain changes can be followed by a mild form of epilepsy and vice versa. 5.There is a similar lack of correlation between the PEG and the electroencephalographic findings in these epileptic children.6. In 40% of our patients where the PEG was pathologic, no etiologic factor causing brain injuries was found. I t is reasonable t o suspect that the damage in many cases had occured during intrauterine life, as the symptoms were noticeable soon after birth.The conclusion drawn from our investigation is that when epilepsy starts early in childhood a surprising number show organic brain injuries. DISCUSSION P . Plum, Denmark. -(Questions Dr. Eek.) (1) What is the PEG like in hereditary conditions?(2) What is the PEG like in petit mal? (3) Is it possible to indicate a correlation between the PEG and the course of the disease?
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