Allergic Lobar Pneumonia

Abstract

Lobar or fibrinous pneumonia is caused in most instances by the Diplococcus lanceolatus (pneumococcus) and rarely by the Diplococcus mucosus, the staphylococcus, or the streptococcus. The infection is effected as a rule through inhalation of the pathogenic microorganism by way of the upper respiratory tract. It is stated that the diplococcus reaches primarily the lymph nodes at the hilum of the lungs, wherefrom it spreads toward the pulmonary parenchyma. However, this opinion is contradicted on the following ground: Since the hilum, one argues, is the point of convergence of the lungs with the lymph flowing thereto from the periphery, the spread of the microorganism should be then a retrograde one, which is thought to be unlikely.The clinical and pathological aspects of the disease are likewise matters for debate. Thus it is not understood why the pneumococcus will cause in instances a bilateral, patchy, or lobular bronchopneumonia with its gradual onset, while in the pneumonia the object for discussion in the present report, the onset is sudden and the lesion is lobar and unilateral.The brusqueness in the development and the rapid spread of the inflammatory processes in one lung in cases of lobar (genuine) pneumonia has led to the suggestion that the disease is probably an expression of an altered sensitiveness of the lung toward the Pneumococcus pneumoniae, or that one is dealing in this condition with an allergic phenomenon.

Acute Immunologic Pulmonary Alveolitis

“…Another approach to the study of immunologic lung diseases has involved active sensitization of animals, followed by administration of antigen via intrapulmonary (transbronchial) passage or intravenous challange. With actively sensitized animals it becomes very difficult to discern the immunological mechanism of tissue injury, but it has been assumed that in most cases immune complexes are involved (6)(7)(8)(9)(10)(11)(12). In several of these studies massive amounts of antigen, much of it in crude form, have been introduced intrabronchially, making the results difficult to interpret.…”

Experimental Hypersensitivity Pneumonitis1,2

“…Opie (13) injected horse serum through the thoracic wall into the lung of a sensitized rabbit and found that it caused a localized consolidation with leukocytes and edema surrounding a central focus of necrosis. Primary vascular lesions in the lungs of rabbits sensitized by foreign proteins intratracheally and intranasally were observed by Fried (14) and by Cannon and associates (15), respectively. Gregory and Rich (16) produced anaphylactic pulmonary lesions, characterized by damage to the alveolar capillaries, by repeated intravenous injection of foreign proteins into rabbits.…”

Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT)

“…In rabbits immunized to ovalbumin, Cannon and Walsh 40 describe alveolitis and bronchitis featuring vasculitis, but the histologic findings are not described. Fried 39 observed an influx of “granulocytes” 12 to 15 hours after intratracheal injection of horse serum into immunized rabbits. Eosinophils were also seen, but “on rare occasions”.…”