stance clusters of cocci (usually Staphylococcus pyogenes aureus), whilst the underlying portion of mucous membrane is in a state of smallcelled infiltration (Fig. 133). Whether true typhoid ulcers (ie., ulcers caused by typhoid bacilli) also occur is somewhat doubtful. Regarding the efflorescences which sometimes form also in the larynx in variola, see p. 224. 4. Infective Granulomata and New-formations.-Tuberculosis of the larynx and trachea, which usually occurs in the course of pulmonary tuberculosis in consequence of penetration of tubercle bacilli into the mucous membrane from the sputum, is localised most frequently on the processus vocales and vocal chords in the larynx, and in the trachea on the posterior wall in the neighbourhood of the ducts of mucous glands. There first form beneath the epithelium either FIG. 134.-ULCERATING GUMMA OF THE TRACHEAL MUCOUS MEMBRANE. X 77. small-celled foci and giant-celled tubercles, or else more diffuse cellular infiltrations (granulation tissue), which caseate and ulcerate. Later it is not uncommon also to meet with round- or epithelioidcelled tubercles lying scattered in the submucosa or in still deeper strata. Leprosy causes affections in the laryngeal mucous membrane similar to those which are found in the skin; glanders and rhinoscleroma changes analogous to those in the nasal cavity. In syphilis there form either erosions of the mucous membrane or BRONCHIAL CATARRH 271 gummata. The latter usually develop in the submucosa, and may either subside again or protrude the mucous membrane continually more and more as their growth advances, until, the centre of the gumma having first undergone caseation, the membrane also falls victim to necrosis (Fig. 134). In this manner ulcers are formed which extend to variable depths and are followed later by cicatrisation and narrowing of the laryngeal or tracheal lumen. The most frequent new-formations are papillomata, which develop in inflammatory conditions, but also apart from such, and are commonly situated on the true vocal chords. They consist as elsewhere of branched or less often simple papilla, rich in blood-vessels and in cells, and covered with a thick stratified squamous epithelium. chondromata and osteomata are also observed. En Carcinoma may occur primarily in the larynx, and is then a flatcelled epithelioma.1 III. THE BRONCHI. 5. Inflammation. In acute catarrh the character of the secretion and the alterations in the mucous membrane are in general identical with those in the same class of inflammation affecting the upper part of the air-passages. When the catarrh persists longer the process spreads to the ducts of the mucous glands also, which then become distended with desquamated epithelial cells in a state of mucous degeneration, as well as with leucocytes. In chronic catarrh the cellular infiltration of the mucosa shows a tendency to pass deeper, and hence when the inflammation is protracted the exterior strata of the bronchial wall and even the peribronchial connective tissue are also found to be infiltrated with cells. The proliferative processes in the mucous membrane may lead to the formation of ridged or papilliform elevations of the surface (Fig. 135, a), and even the muscular bundles of the bronchi may take part in the hypertrophy. Later, however, when the glands, muscle, and even cartilage are destroyed by the pressure of the cellular infiltration, and the bronchial wall is thus rendered very yielding, dilatations of the bronchi may result which are known as bronchiectases (p. 272). When the bronchial secretion stagnates, a putrid decomposition is sometimes set up in it by the action of putrefactive bacteria (putrid bronchitis). In rare cases the tissue of the thyroid gland may force its way into the larynx and trachea in consequence of adhesion of the gland to these organs. It enters the lateral wall between the cartilages, and then forms small nodes underneath the mucous membrane. Croupous inflammation may be caused either by descent of the same process from the trachea, or by extension of the croupous exudation in a pneumonic lung to the smaller bronchi. There is also a chronic form of bronchial croup in which tubular croupous membranes are formed extending throughout the whole of the bronchial system or the greater part of it, and hence showing a branching arborescent figure (plastic bronchitis). Peribronchitis. As has already been partially explained, when a bronchitis is of longer duration the cellular infiltration and the newformation of connective tissue arising from it may not only involve the entire thickness of the bronchial wall, but may also spread to the peribronchial connective tissue (Fig. 135, e) and adjoining FIG. 135.-INDURATIVE PERIBRONCHITIS, WITH BRONCHIECTASIS. x 80. (Hæma parenchyma of the lung. Vice versa, inflammatory processes may pass from the alveoli, or from the pleura and interlobular connective tissue, to the peribronchial tissue, alike whether they are of a purulent, indurative, or tubercular nature. 6. Bronchiectasis and Tuberculosis.-Bronchiectasis may occur after BRONCHIECTASIS 273 long-protracted bronchitis, when, as observed above, the powers of resistance of the bronchial wall have become reduced in consequence of the inflammation; or it may also be due to retraction of the newly-formed connective tissue in a peribronchitis, or to accumulation of secretion in the bronchi. The mucous membrane of the dilated bronchus may appear more or less atrophied, as may also the cartilage (which may be partially replaced by connective tissue); or, on the contrary, not only the mucous membrane (Fig. 135, a) but the submucosa (b) and peribronchial connective tissue (e) are thickened owing to cellular infiltration and great dilatation of the blood-vessels, and sometimes papillary growths may even be present on the mucous membrane (a). The epithelium may remain perfectly intact, or low cubical cells may now alone be visible instead of the columnar ciliated elements. A gangrenous inflammation of the bronchial wall and surrounding tissue of the lung is not uncommon in bronchiectases as a result of putrid decomposition of the stagnating secretion. There is also a congenital cystic form of bronchiectasis which occurs in consequence of faulty development of the proper pulmonary tissue. The malformed portion of lung may finally be composed of cysts of different sizes lined with ciliated epithelium, the fibrous wall of which may still include islets of cartilage, whilst between the cysts lies a non-pigmented but sometimes very vascular connective tissue. Such bronchiectases may also, of course, be attacked by inflammation. In tuberculosis of the bronchi the same products are formed as in the larynx and trachea, except that caseation of the secretion plugging the bronchioles may also result. IV. THE LUNGS. 7. Emphysema, Hæmorrhagic Infarction, Fat-Embolism, Edema, and Brown Induration.-Emphysema.—Acute vesicular emphysema merely consists in an abnormal distention of the alveoli and alveolar passages, whereas in chronic or substantial emphysema (Fig 136) an atrophy of the alveolar septa () is superadded, which again may be favoured by disturbances of nutrition or congenital weakness of the septa. The atrophy commences with an enlargement of the spaces between the capillaries, by which the elastic fibres of the septa are separated from one another and gradually destroyed, while the capillaries as well as the small arteries and veins become obliterated. Apertures then appear at the thinnest parts of the septa and gradually enlarge, thus causing coalescence of the alveoli and alveolar passages to form S cavities (b) which become progressively larger. The epithelium of the alveoli frequently shows fatty degeneration, whilst the muscular bundles at their entrance may even become hypertrophied C a b d FIG. 136.-CHRONIC EMPHYSEMA OF THE LUNG. X 77. (Hæmatoxylin and eosin.) a. Slightly dilated alveolus; b, Cavity formed by coalescence of several alveoli; the alveoli partially filled with serum; c, Thinned alveolar septa; d, Vestiges of ruptured septa. (compensatory hypertrophy). The emphysema which is due to old age is known as senile emphysema. In hæmorrhagic infarction, which occurs after embolism or thrombosis of pulmonary arteries, or from the formation of hyaline thrombi in the capillaries, the alveoli (Fig. 110, a) and bronchioles are found evenly filled with red corpuscles, with which are mixed usually only a few leucocytes and filaments of fibrin, whilst the septa of the alveoli are sometimes also found to be ruptured, so that the latter unite to form large cavities full of blood. The further changes are the same as in hæmorrhagic infarctions in other organs (see pp. 211-212). Should the embolus contain pyococci or putrefactive bacteria, or should the latter find their way into the infarction with the inspired air, the results will be respectively |