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The mortality from pneumonia in childhood has always been greatest in infancy. In the infant ward at Cook County Hospital many patients with pneumonia are treated, and the mortality has always been high. In 1937 and 1938, before chemotherapy was used, the mortality rates were 32 per cent and 31 per cent respectively. The infants, all under 1 year of age, were drawn from essentially the same group and were treated by the same medical personnel and with the same therapeutic measures other than specific chemotherapy as the 1940 series which is the subject of this paper. While it is true that the incidence and mortality of pneumonia vary somewhat from season to season, these figures at least serve as a base line from which some conclusions can be drawn with regard to a human experiment in which adequate control is practically impossible.With the advent of specific therapy, particularly specific chemotherapy, there was a distinct change in the outlook for babies with pneumonia. Serum therapy never was of outstanding value for this age group because of the difficulties encountered in obtaining and typing organisms. The administration of sulfapyridine (2-[paraaminobenzenesulfonamidoj-pyridine), however, could be initiated quickly, without the necessity of knowing the exact organism present in a given case. This report consists of an analysis of the results obtained for a series of 289 infants observed from March 1939 to July 1940, to whom sulfapyridine was given.In the past few years a considerable amount of literature has accumulated relating to the use of sulfapyridine or related compounds in the therapy of pneumonia. In general, the results have shown a Read at a meeting of the Chicago Pediatric Society, Jan. 21, 1941.

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In the present state of our knowledge it must be concluded that the outstanding anatomic changes directly attributable to acute iron poisoning are in the gastrointestinal tract and the liver. Both seem to be due to the direct action of iron upon living cells. In the stomach and small bowel the changes appear to be due to the corrosive effect of the iron salt whether in solution or in tablet form. And the anion may indeed play the predominant role as demonstrated by the observation of the severe corrosive changes observed when accumulations of ferrous sulfate tablets occur in areas of the stomach or small bowel. That the mucosal barrier to iron is broken down seems incontrovertible. And it is no longer tenable to assume that the severe complications of iron poisoning are due to the local necroses in the gastrointestinal tract. The liver, being the first parenchymal organ encountered by absorbed iron, is involved to a varying degree. The anatomic changes can progress to frank necrosis in severe cases. And even in those where overt histologic damage is not demonstrable, alterations in biochemical function occur. Anatomic changes in other parenchymal organs are probably largely secondary to dehydration, shock, hemorrhage, and infection. But the possibility of disordered enzyme systems here as well must be borne in mind though so far not demonstrated. In severe cases where hemorrhages play so large a role, albeit infrequently, the specific action of iron in interference with coagulation mechanisms is of the utmost importance. The role of therapy with deferoxamine in production of shock is discussed below. In this connection breakdown of the mucosal barrier with release of apoferritin and ferritin as a hypotensive mechanism has also been suggested by Smith.

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