On the other hand, numerous pathogenic germs are found to be the cause of empyema, the pneumococcus being most predominant. Netter found in one-half to one-fourth of the cases pneurnococci in pure culture, besides pneumococci associated with strepto- and staphylococci, tubercle bacilli, then streptococci in pure culture in 13-16 per cent. of cases, less frequently ssith staphylococci and tubercle bacilli. Tubercle bacilLi were found in 5-7 per cent. of the eases, mostly as a mixed infection; furthermore, staphylococci and coil bacteria, but only in isolated numbers in pure culture; and lastly septic bacteria in putrid empyerna.
In contrast to the adult, Netter found a remarkable difference in the participation of the various micro-organisms, Viz : Pneumoeocei Streptocoeei Tubercle bacilli Adults (154 cases) ....... 24.9% 41.2% 17.6% Children (90 SI eases).. e0.7-65.4%. 13.3-19.7%T 5.5-7.4% Accordingly, in infantile empyema the pneurnococcus is most pre dominant; whereas on the other hand the streptococcus is the most frequent cause of empyema in the adult. The investigations of other observers verify the predominant position of the pneumococci in ernpy ema of children. Koplik (72 cases) found the pneumococcus in pure culture in GO per cent., streptococcus in 15 per cent., staphylococcus in 9 per cent. of cases. At the highest 7 per cent. were tuberculous. Beck found pneumococci in 75 per cent.; Blaker 91 per cent. of cases of infantile empyenia. Whenever the pus of an ernpyema appears bac teriologically sterile, it inclicates a tuberculous nature. From what has been stated the preponderance of purulent pleurisy in the infant in con trast to the adult is clearly established. It depends partly on the fact of the great tendency to suppuration of the pneumococcus pleurisy- of infancy. On the other hand, tuberculous pleurisy in any form is not frequent in children, whereas in adults it embraces one-fiftla of the cases of empy-ema and fully- one-half of serous pleurisy.
The character of the empyerna may be assumed with considerable certainty from the very beginning. In primary cases and following croupous pneumonia it is commonly a pneumococcus empy-ema, as also often in bronchopneumonia and grippe. In the acute infectious diseases streptococci preponderate, more rarely staphylococci, e.specially in scarlet fever, diphtheria, measles; and in addition the bacteria of the underlying di.sease (typhoid, tubercle bacilli, coli bacteria) may be found.
Most commonly the micro-organisms penetrate the pleural cavity di rectly from the lungs, or from some other disease focus in the vicinity; and frequently from the peritoneum or tonsils through the blood and lymph channels.
Pathological loss of lustre and adhesions of the pleural reflections are found in many cases on post-mortem examination, in which no definite symptom.s were ever present (luring life. In the mildest form, the dry or fibrinous pleurisy is a frequent accompaniment of various pulmonary diseases, often without any clinical manifestations. There is a lack of lustre and injection of pleural surface to a varying extent. The surface is rough and covered by a felt-like layer of fibrin. in pleurisy with effusion the pleural cavity is filled with a serous fluid, mostly of a yellowish color, seldom bloody, at tinies clear, sometimes cloudy, containing shreds of fibrin which are also found on the pleural surface as a felt-like covering. If the lymph-cells found in addition to the endothelial cells in the effusion are very numerous, a seropurulent or a complete purulent exudate will be formed, which occasionally though rarely is putrid in character. In slight effusions the exudate becomes fibrinopurulent in character from deposits of thick vinous fibrin (see Plate 55.) The pleural layers are often very much thickened.
Complete restitution ad integrum may take place from absorption of the inflammatory exudate. After the termination of a pleurisy, however, either card-like or extensive adhesions of the surfaces of the costal and pulmonary pleura often remain; and often extensive thick ening of the connective tissue (pleuritic thickening) wldch may be from 1-2 cm. in thickness, going hand in hand with retraction of the affected half of the chest, shrinkage of the lung, and bronchiectasis. Large, purulent effusions do not become absorbed, but when untreated often lead to a fatal termination from eachexia or pytemia, or they may rupture through the bronchi or chest wall (empyema necessitatis). Regarding the bacterial content see above.
General the physical finding, the symptoms of pleurisy are often varied and changeable according to the form of the disease met with, whether acute or chronic, serofibrinous or purulent, primary or secondary, so that it is scarcely possible to give an adequate clinical picture. We shall therefore be content to point out several of the most salient features.