The dissemination of B. influenzæ in patients with measles was not controlled by segregation of “carriers” and “noncarriers” of this organism as identified by throat cultures in separate wards.

CHAPTER VI
THE PATHOLOGY AND BACTERIOLOGY OF PNEUMONIA FOLLOWING MEASLES

Eugene L. Opie, M.D.; Francis G. Blake, M.D.; James C. Small, M.D.; and Thomas M. Rivers, M.D.

Among 18 autopsies upon men who have died with pneumonia following measles there are pulmonary lesions representing almost every type of pneumonia which has been found in association with influenza. In most instances pneumonia made its appearance during the second week of measles and death occurred during the third week. Of 16 instances in which the record is definite, pneumonia had its onset during the first week of measles in 4 instances, during the second week in 11 instances, and in one instance (Autopsy 390) perhaps not referable to measles in the fifth week. The duration of pneumonia varied from three to thirty-two days; in 10 instances it did not exceed one week, in 5 instances it was between one and two weeks and in one instance, thirty-two days. When the duration of pneumonia exceeded ten days some evidence of chronic pulmonary disease was found at autopsy.

The same lack of correspondence between clinical diagnosis and pulmonary lesions noted with influenza was found following measles. In accordance with the prevailing opinion concerning the character of pneumonia following measles, the diagnosis of bronchopneumonia was made in 13 instances and in all of these cases bronchopneumonia was found at autopsy. The diagnosis of lobar pneumonia was made 5 times and was correct only once. Nevertheless, lobar pneumonia was present 4 times, but was recognized only once (Autopsy 486.) Failure to recognize lobar pneumonia, was doubtless due in part at least to its association with purulent bronchitis and peribronchiolar pneumonia (Table LXXI).

Table LXXI
NO. OF AUTOPSYRACELENGTH OF MILITARY SERVICEDURATION OF ILLNESSDURATION OF PNEUMONIACLINICAL DIAGNOSISPURULENT BRONCHITISLOBAR PNEUMONIAPERIBRONCHIOLAR CONSOLIDATIONHEMORRHAGIC PERIBRONCHIOLAR CONSOL.LOBULAR CONSOLIDATIONPERIBRONCHIAL CONSOLIDATIONABSCESSINTERSTITIAL SUPPURATIVE PNEUMONIAMULTIPLE ABSCESSES IN CLUSTERSEMPYEMABRONCHIECTASISUNRESOLVED BRONCHOPNEUMONIAORGANIZING BRONCHITISBACTERIA IN SPUTUMBACTERIA IN BRONCHUSBACTERIA IN LUNGBACTERIA IN BLOOD OF HEART
390W1m.356L M + No S. Hem. Pneum. II a
438W2m.2212?BP + + + E + B. inf.S. hem., B. inf.Pneum. II, S. vir.,0
B. inf., S. hem.
439W10d.1411?BP M++ + +No S. hem.B. coliPneum. IIa, S. aur.0
441W1m.1611BP +++M + B. inf., S. aur.B. inf., S. aur.0
442W1m.172+LP M + N+ E No S. hem.B. inf., S. hem. S. hem.
443W21d.2314BP + M ++ No S. hem.B. inf., B. coli.B. coli.0
444W1m.93BP M++ B. inf.Pneum. IIa, B. inf.Pneum. IIa, B.inf.Pneum. II a.
450W29d.195B +M B.inf., No. S. hem.B. inf., Staph.B. inf.Pneum. IV.
453W36d.136BP + +M + Pneum. I, B. Inf.Pneum. I.Pneum. I.
481W54d.4+3?BP + + ++ No S. hem.B. inf., Pneum. IIa, S.hem.B. inf.0
484W42d.207BP + +M ++ Pneum. IV, B. inf.B. inf., Diploids 0
486C6d.178LP+ No S. hem.B. inf., Pneum. IIa, S. hem., Staph.B. inf.0
491W2m.195B + + E S. hem.B. inf., B. coli.S. hem., B. coli.S. hem.
492W49d.20?11?LP M++M+ E++ S. hem., B. inf. S.hem., Pneum. IV, B. coli., B. inf.S. hem.
496W1m.4332LP + + +++B. inf., no S. hem.B. inf.00
505C4m.166BP+ No S. hem.Pneum. II a., S. hem.Pneum. II a.Pneum. II a.
507C5m.143B N+ E S. hem.S. hem., B. inf., S. aur.S. hem., S. aur.S. hem.
508C2m.165B +M M S. hem.Pneum. IIa, B. inf., S. hem.Pneum. II a.Pneum. II a.

Changes in Bronchi.—The changes in the bronchi do not differ in character from those associated with pneumonia following influenza. Purulent bronchitis recognized at autopsy by the presence of mucopurulent material in the small bronchi was found in a much larger proportion of instances in this group of autopsies occurring in 13 of 18 instances (72.2 per cent), whereas it was present in only 55.6 per cent of autopsies on individuals with pneumonia following influenza. There was peribronchial hemorrhage recognizable on gross examination in 3 autopsies and microscopically in 3 additional instances.

Bronchiectasis was present in a considerable proportion of these autopsies, dilatation of bronchi being noted in 7, but it was usually moderately advanced and at times limited to the bases of the lungs. The short duration of respiratory disease perhaps explains the infrequency of advanced bronchiectasis. The incidence of the lesion is greater with measles (43.7 per cent) than with influenza (22.4 per cent).

Microscopic changes in the bronchi do not differ from those found after influenza. Evidence of acute inflammation, often hemorrhagic in character, is found within the lumen of the bronchus and in the tissues immediately in contact with the lumen. Not infrequently the epithelium is lost; there is superficial necrosis and deposition of fibrin upon the surface and within the tissue. In the deeper tissues of the bronchial wall there is infiltration with lymphoid and plasma cells, which in the larger bronchi is particularly advanced about the mucous glands of which the acini exhibit degenerative changes. With the onset of chronic changes new formation of fibrous tissue occurs in the wall of the bronchus and in the contiguous interalveolar walls. The lining epithelium often loses its columnar cells and assumes a squamous type.

Changes in the bronchi with bronchiectasis have been similar to those following influenza. Weakening of the wall permitting dilatation is brought about by necrosis extending outward from the lumen a varying distance into the bronchial wall and permitting the formation tears which diminish resistance to intrabronchial pressure.