Page:EB1911 - Volume 21.djvu/902

 metals are found, but often a much larger quantity of minerals such as calcite, barytes, fluorspar, quartz and tourmaline which serve as a matrix or gangue, and have been deposited by the same agencies, and often at the same time as the valuable minerals.

In their passage upwards and outwards through the rocks of the earth’s crust, these gases and liquids not only deposit minerals in the fissures along which they ascend, but attack the surrounding rocks and alter them in many ways. The granite or other plutonic mass from which the vapours are derived is especially liable to these transformations, probably because it is at a high temperature, not having yet completely cooled down. Around the tin-bearing veins in granite there is extensive replacement of felspar and biotite by quartz, tourmaline and white micas (the last-named often rich in lithia). in this way certain types of altered granite are produced. such as (q.v.) and schorl rock (see ). In the slates adjacent to the tin veins tourmalinization also goes on, convening them into schorl-schists. The alteration of felspar into kaolin or china clay is also a pneumatolytic process. and is often found along with tin veins or other types of mineral deposit; probably both fluorine and carbonic acid operated in this instance along with water. Equally common and important is the silicification of rocks near mineral veins which carry gold, copper, lead and other metals. Granites and felsites may be converted into hard cherty masses of silica. Limestones undergo this transformation very readily; at the same time they are regarded as rocks very favorable to the deposition of ores. Probably the great frequency with which they undergo silicification and other types of meta somatic replacement is one of the main causes of the abundance of valuable deposits in them. The process known as “propylitization,” which has extensively affected the andesites of the Hungarian goldfields, is believed to be also a consequence of the action of pneumatolytic gases. The andesites change to dull, soft, greenish masses, and their original minerals are to a large extent replaced by quartz, epidote, chlorite, sericite and kaolin. Around granites intrusive into serpentine and other rocks containing much magnesia, there is often extensive “steatisation,” or the deposit of talc and steatite in place of the original minerals of the rock. Some of the apatite veins of Canada and Norway accompany basic rocks of the gabbro group; it has been argued that the apatite (which contains phosphorus and chlorine) was laid down by vapours or solutions containing those gases, which may play a similar part in the basic rocks to that taken by fluorine and boron in the pneumatolytic veins around granites. In the country rock around the veins (q.v.), a lime alumina silicate, containing chlorine, often is substituted for lime-felspar.

These extensive changes attending the formation of mineral veins are by no means common phenomena, but in many plutonic masses pneumatolytic action has contributed to the formation of s (q.v.).

 PNEUMONIA (Gr. , lung), a term used for inflammation of the lung substance. Formerly the disease was divided into three varieties: (1) Acute Croupous or lobar pneumonia; (2) Catarrhal or Broncho-pneumonia; (3) Interstitial or Chronic pneumonia.

1. Acute Croupous or Lobar Pneumonia (Pneumonic Fever) is now classed as an acute infective disease of the lung, characterized by fever and toxaemia, running a definite course and being the direct result of a specific micro-organism or micro-organisms. The micrococcus lanceolatus (pneumococcus, or diplococcus pneumonia) of Fränkel and Weichselbaum is present in a large number of cases in the bronchial secretions, in the affected lung and in the blood. This organism is also present in many other infective processes which may complicate or terminate lobar pneumonia, such as pericarditis, endocarditis, peritonitis and empyema. The bacillus pneumonia of Friedländer is also present in a proportion of cases, but is probably not the cause of true lobar pneumonia. Various other organisms may be associated with these, but they are to be regarded as in the nature of a secondary invasion. Lobar pneumonia may be considered as an acute endemic disease of temperate climates, though epidemic forms have been described. It has a distinct seasonal incidence, being most frequent in the winter and spring. Osler strongly supports the view that it is an infectious disease, quoting the outbreaks reported by W. L. Rodman of Frankfort, Kentucky, where in a prison of 735 inhabitants there were 118 cases in one year; but direct contagion does not seem to be well proved, and it is undoubted that the pneumococcus is present in the fauces of numbers of healthy persons and seems to require a lowered power of resistance or other favouring condition for the production of an attack.

Lobar Pneumonia begins by the setting up of an acute inflammatory process in the alveoli. The changes which take place in the lung are chiefly three. (1) Congestion, or engorgement, the blood-vessels being distended and the lung more voluminous and heavier than normal, and of dark red colour. Its air cells still contain air. (2) Red Hepatization, so called from its resemblance to liver tissue. In this stage there is poured into the air cells of the affected part an exudation consisting of amorphous fibrin together with epithelial cells and red and white blood corpuscles, the whole forming a viscid mass which occupies not only the cells but also the finer bronchi, and which speedily coagulates, causing the lung to become firmly consolidated. In this condition the cells are entirely emptied of air, their blood-vessels are pressed upon by the exudation, and the lung substance, rendered brittle, sinks in water. The appearance of a section of the lung in this stage has been likened to that of red granite. It is to the character of the exudation, consisting largely of coagulable fibrin, that the term croupous is due. (3) Grey Hepatization. In this stage the lung still retains its liver-like consistence, but its colour is now grey, not unlike the appearance of grey granite. This is due to the change taking place in the exudation, which undergoes resolution by a process of fatty degeneration, pus formation, liquefaction and ultimately absorption—so that in a comparatively short period the air vesicles get rid of their morbid contents and resume their normal function. During resolution the changes in the exudate take place by a process of autolysis or peptonization of the inflammatory products by unorganized ferments, absorption taking place into the lymphatics and circulation. The absorbed exudate is mainly excreted by the kidneys, excess of nitrogen being found in the urine during this period. This is happily the termination of the majority of cases of lobar pneumonia. One of the most remarkable phenomena is the rapidity with which the lung tissue clears up, and its freedom from alteration or from infiltration into the connective tissue as frequently takes place after broncho-pneumonia. When resolution does not take place, death may occur from extension of the disease and subsequent toxaemia, from circulatory failure, from the formation of one or more abscesses or more rarely from gangrene of the lung or from the complication mentioned below. Chronic interstitial pneumonia is infrequent, following on the acute variety. The most frequent seat of pneumonia is the base or lower lobes, but occasionally the apices are the only parts affected. The right lung is the most often attacked. Pneumonia may extend to the entire lung or it may affect both lungs. The death rate of acute lobar pneumonia in the chief London hospitals is 20%. With an organism so prevalent as the pneumococcus it follows that alcoholism, diabetes and other general diseases and intoxications must render the body liable to an attack. Males are more commonly attacked than females, and a previous attack seems to give a special liability to another. The incubation period of pneumonia is unknown; it is probably very short.

The symptoms are generally well marked from the beginning. The attack is usually ushered in by a rigor (or in children a convulsion), and the speedy development of the febrile condition, the temperature rising to a considerable degree—101° to 104° or more. The pulse is quickened, and there is a marked disturbance in the respiration, which is rapid, shallow and difficult, the rate being usually accelerated to some two or three times its normal amount. The lips are livid, and the face has a dusky flush. Pain in the side is felt, especially should any amount of pleurisy be present, as is often the case. Cough is an early symptom. It is at first frequent and hacking, and is accompanied with a little tough colourless expectoration. which soon, however, becomes more copious and of a rusty red colour, either tenacious or frothy and liquid. Microscopically this consists mainly of epithelium, casts of the air cells and fine bronchi, together with granular matter, blood and pus corpuscles and haematoidin crystal. The micro-organisms usually present are the pneumococcus, Friedländer’s bacillus, and sometimes the influenza bacillus. The following are the chief physical signs in the various stages of the disease. In the stage of congestion fine crackling or crepitation is heard over the affected area; sometimes there is very little change from the natural breathing. In the stage of red hepatization the affected side of the chest is seen to expand less freely than the opposite side; there is dullness on 