Pus-Causing Bacteria and Spore-Forming Organisms

a pus-causing chain-coccus ; whereas the staphylococcus pyogenes is a pus-causing cluster-coccus. ‘There may be several kinds of staphylococcus or streptococcus, each of which has a distinctive adjective added to its name. Thus we have the white pus-causing grape-coccus and one of a golden color. which has a similar pathogenic action. Pa 1 =, OE > av VE x A‘- a, Bacillus subtilis with spores. b. suction anthracis with spores. ¢. ciosttaom form with spores d. Bacillus of tetanus with end spores. (ABBOTT. ) In multiplying, the schizomycetes, or fission fungi, to which has been given the name bacteria, divide so as to form two or more indi- vidual cells. Some of them, however, multiply by the formation of spores, round or oval bodies, which grow within the cells, and subse- quently become separate individuals. Some of these micro-organisms have the power of motion and are called, therefore, motile forms. The various forms differ from each other in the character of food which they require; though carbon, hy- drogen, nitrogen, phosphorus, sulphur, magnesium and potassium are needed, probably, by all. The presence of water is necessary for the development of fungi; therefore, thorough drying prevents multipli- cation of fungi, and, in some cases, kills them, Some require oxygen, which others can do without ; hence they are called aérobic and anaér- obic. The temperature to which they are exposed has also an impor- tant bearing on the life and development of nearly all forms. They are killed by boiling, or by a degree of heat very little above the boiling- point, provided that moist heat is used. Dry heat does not destroy them until it reaches a point considerably above the boiling-point. The bacillus of malignant pustule is of all pathogenic micro-organisms the most difficult to destroy by heat. Spores will resist a higher de- gree of heat and more changes of condition without loss of vitality than will fully developed fungi. 24 INFLAMMATION. Bacteria are found in the air, in the water, in the earth, and upon the external surface of the human body. These organisms in large numbers, both pathogenic and non-pathogenic, are found under the nails and in the various folds of the skin, such as the axilla. They are also numerous upon the mucous membranes which come in contact with the air, such as the bronchial and intestinal mucous membranes and those of the mouth and cwsophagus. In many instances they do no harm, even if pathogenic, because of the resistance of the tissues to their action, which is great when the vitality of the tissues is unim- paired ; or because of the comparatively small number which gain ac- cess to the tissues. Under favorable circumstances, however, multi- plication is very rapid, and one individual may develop into many millions in twenty-four hours. The epidermis on the outside of the animal and the epithelium cov- ering the mucous membranes constitute an armor-like protection against infection of the system by the entrance of bacteria. The se- cretions on the mucous membranes may also protect from bacterial in- vasion by exerting a germicidal influence, or by washing the germs away. A wound in the epidermis or epithelium is usually the atrium or portal of entry for the micro-organisms. Sometimes the wound may be so insignificant as to be overlooked; or it may have healed before symptoms of infection have shown themselves. Fresh wounds absorb bacteria and their toxines, or products, rapidly ; but granulating wounds and those in which the vessels are closed with co- agula, absorb them slowly. There may be no lesion exhibited at the portal of entrance, but the symptoms of infection may appear else- where. When organisms enter the blood a “septicemia” is said to be present. Surgeons often employ the word “septicemia” for a special form of infection. It has previously been stated that the mere presence of pathogenic organisms in the blood current is not sufficient to give rise to disease. This, according to present pathological views, can only occur when the circumstances are favorable to their development within the body, and the resisting power of the tissue to their injurious action is imperfect. The antagonism of the tissues to microbic invasion tends to prevent disease, unless the number or dose of infecting germs is too large to be successfully repelled. The leucocytes may form a wall or barrier around the bacteria, and, thus hemming them in, prevent their dissem- ination through the body ; or they may be taken into the interior of the phagocytes and their vitality be destroyed. The blood serum is also antagonistic. Some animals are immune to certain infections and particularly sus- ceptible to others ; and some individuals of a given variety of animals have immunity, either acquired or inherited, against certain infections. Erysipelas of the face, for example, is liable to recur, while a man who has once had typhoid fever is not likely to have it again, because he has acquired immunity. The formation of antitoxic substances in the body capable of neutralizing the poisonous products of the infecting bacteria is not yet well understood. VARIETIES, 25 Varieties.— All forms of inflammation are either acute or chronic. The acute is rapid in course or severe in symptoms, the chronic slow in progress or less severe in symptoms. It will thus be seen that the terms acute and chronic each contain, perhaps improperly, two ideas— one referring to time, the other to severity. The word subacute is used to express an intermediate severity between acute and chronic, but has no reference to time. Hence inflammation, as to time, is termed either acute or chronic; as to severity,it is expressed as acute, sub- acute, or chronic. Although inflammation is essentially the same in whatever tissue it may occur, the character of the exudate varies in accordance with the resistance of the tissue, the intensity of the injurious causative influ- ence, and the time of action of that influence. These variations in the exudate may often be found in the same inflammation by examining different areas of inflamed structure. Srrovs InrLaMMaTIoN.—In serous inflammation the exudate is characterized by a small amount of albumin and few lencocytes, being, indeed, very slightly different from the normal transudate of healthy tissues. This fluid does not coagulate. Instances of serous inflam- mation are seen in pleuritis with effusion, arthritis, hydrocele, and in inflammatory cedema of connective tissue. This form of exudate may be expected after slight or momentary injuries, in the early stages of more severe inflammations, and in cases where the blood is impov- erished. Fisrtvovs InFLAMMaTIoN.—Fibrinous inflammation gives rise to an exudate containing larger quantities of albumin and more leucocytes than that of serous inflammation, and hence is more coagulable. It forms, upon free surfaces and in the substances of organs, that which is clinically denominated “lymph.” Lymph, then, is an inflammatory product consisting of fibrin and entangled leucocytes. It is sometimes called plastic lymph, to show that it is entirely different from the fluid called lymph which circulates in the lymphatic vessels. The best examples of this form of inflammation are seen in the serous membranes, such as the peritoneum and pleura, and in the long continued or chronic inflammations of slight intensity in connective tissue. At times occurs a grade of inflammation intermediate between these forms, which may be termed sero-fibrinous inflammation. These varieties of the inflammatory process may end by absorption of the exudate, which is accomplished by the leucocytes returning into the circulation by entering the lymphatic vessels, and by the fibrin and some of the leucocytes undergoing fatty degeneration previous to such absorption by the lymphatic system. The veins also take part in the absorption of the exudate. Suppurative IxrLamMation.—In this very common form of in- flammation the exudate contains the same elements as in the fibrinous, but does not coagulate. No lymph, therefore, is deposited, or, if any lymph has been deposited by the previous form of inflammation, it is destroyed by the accession of the suppurative stage. It is thus seen 26 INFLAMMATION. that the so-called varieties of inflammation are rather stages, or de- grees, of the process, Suppurative inflammation is the result of a more irritative or longer continued cause than the serous or fibrinous forms. It is due practically always to pus-producing bacteria. Acute suppuration is another term signifying the same process. If the suppuration is circumscribed in an abnormal cavity, the resulting condition is called abscess ; if diffused in the tissues, purulent infiltra- tion. Pus contained in a normal cavity, such as the pleural sac or knee-joint, is called a purulent effusion. If suppuration occurs upon a free surface of mucous membrane the condition is called purulent catarrh, provided the epithelium of the mucous surfaces is not de- stroyed ; while it is called ulceration if the epithelium and subjacent tissues are destroyed. Suppuration attacking a cutaneous surface gives rise to what is also called ulceration. Propuctive INFLAMMATION.—When the exudate of a serous or fibrinous inflammation becomes converted into new connective tissue, the inflammation is termed productive, because of the formation of this new structure. The healing of a wound is a good illustration of pro- ductive inflammation. This process is accomplished by the fibrin dis- appearing and numerous leucocytes coming into the lymph, after which vascular loops from the capillary vessels of the inflamed structures penetrate the lymph and become surrounded by young cells. This new tissue, consisting of capillary loops and young cells, which have developed within the substance of the lymph, is called granulation tissue. The new tissue is produced most probably by proliferation of the native cells of the tissue rather than by proliferation of the leucocytes. Granulation tissue may be converted into connective tis- sue, often called scar tissue; it may degenerate into typical tubercles ; it may become material looking like pus, but which is not true pus ; or finally, it may actually break down into pus, the inflammation as- suming the character of suppurative inflammation, which it then is. The third transformation of granulation tissue gives rise to what is variously called “chronic” or “cold” abscess, and to chronic sup- puration in bone. The tubercle bacillus is practically always the cause of the second and third alteration. Modes of Extension.—Inflammation cannot spread unless its cause extends before it; hence, inflammations due to mechanical and chem- ical irritants do not spread beyond the point at which the irritation was first exerted. All those inflammations which tend to spread from the original site are probably due to microbic causes. Such inflammations spread in three ways—by continuity of tissue, by the lymph current, and by the blood current. When inflammation spreads by continuity of tissue, the bacteria which have settled there are spread into the surrounding tissues by be- ing carried thither by leucocytes and by the lymph channels. This mode of extension of an inflammatory process is comparatively limited in its action. When mycotic inflammation spreads by the lymphatic vascular sys- PATHOLOGY. 27 tem the bacteria are carried along by the current in the lymphatic vessels until they reach the first gland, where they are filtered out by the ramifications which the current makes in passing through the in- terstices of the gland. After being arrested thus they multiply and act as an exciting cause of inflammation, producing in the gland a secondary inflammation which is located at a considerable distance from the primary disease. This is quite different from the method of ex- tension just described, where the fungi travel a short distance only in the lymph current, or are carried short distances by the white blood cells, choosing, as they do, the paths of least resistance. The blood current may carry bacteria to all parts of the body, but they are in- nocuous, as a rule, until they are arrested by extravasation, by clotting of the blood, or embolic plugging of the vessels, Under these circum- stances, secondary or metastatic inflammation occurs. Pyemia is a good example of such metastatic inflammation. The inflammation of mumps being carried to the breast and testicle is a similar example of metastatic inflammation. It is difficult to explain all cases of so-called sympathetic inflammation. It may be that the process is due to the infective agent being localized in certain organs ; or to the absorption of the chemical products of inflammation in one organ being absorbed and having a special pathogenic influence on some other particular or- gan only. PATHOLOGY, SYMPTOMS, AND TERMINATIONS OF INFLAMMATION. Pathology.—The study of the pathological or essential nature of in- flammation must be divided into a consideration of the rdles played by (1) the nerves, (2) the small blood vessels, (3) the blood, and (4) the tissues. The changes occurring in each of these, though in the main synchronous, must be investigated separately. 1, Nerves.—The agency of nerves is really unknown. It is not a vaso-motor influence. Researches show pretty conclusively that in- flammatory phenomena depend on a direct injurious influence upon, and a vital alteration of, the walls of the blood vessels, without the neces- sity of any direct nervous agency. 2. Bioop Vesseis.—As has been previously stated, the essential factor or lesion of inflammation is perhaps the change that occurs in the walls of the small blood vessels, by which the friction between the wall and the blood current is increased and the wall is made more porous. It is possible that the increase of blood in the inflamed region is the result of an alteration in the attraction between the blood and the tissues. It is denied by some writers that the essential feature of inflammation is the change in the vessel wall. In inflammation of non-vascular tissues, such as the cornea and cartilage, the same vascu- lar alterations take place in the vessels which surround these struc- tures, and upon which their nutrition depends. The vascular phe- nomena of inflammation are dilatation of the arteries, capillaries, and 28 INFLAMMATION. veins and abnormal permeability of the vessel walls ; followed by ac- celeration, with subsequent abnormal retardation, of the blood current. Mere acceleration of blood flow not followed by abnormal retardation and abnormal permeability does not constitute inflammation, though it may lead to it. The dilatation of the vessels and the abnormal re- tardation of the current must be permanent, A preliminary contraction of the capillaries is at times seen, but it is not an essential factor. While vascular dilatation and blood retardation are being established, the white corpuscles accumulate, especially in the venules, and the red corpuscles generally in the capillaries, until stagnation or stasis of the current occurs. This stage of absolute cessation of motion is preceded by one in which is seen a mere oscillation of the vessel contents syn- low of Intlammatory changes in a small vein: @, normal circulation, showing d, miccessive changes, showing dilatation, accumulation of leucocytes, and emigra- chronous with the cardiac pulsations, Synchronous with these vascular changes there occur permeation of the blood elements through the vessel walls and inereased absorption by the lymphatic vessels. 8. Bioob.—The white corpuscles are relatively increased in in- flammatory blood (leucocytosis) and show a tendency to keep near the walls of the v x. ‘They are less heavy than the red corpuscles, and hence are thrown to the margin of the blood stream. Inflammatory blood when drawn shows more fibrin than non-inflammatory blood. r PATHOLOGY. 29 This condition of hyperinosis and the buffy coat, formerly considered diagnostic of inflammation, have no diagnostic or therapeutic value. During inflammation white cells migrate through the walls of the venules, and red cells are pressed, as it were, through the walls of the Fic. 3. e process of emigration, otserved under high power. The blood is supposed toflom on the left of Phe tissue is on the right. x 1000. (After THOMA.) The the line in the direction indicated by the arrow. capillaries into the surrounding tissues. This escape occurs through small openings (stomata) resulting probably from the contractile power of the endothelial cells composing the walls of the dilated vessels. There is no emigration from the vessels in which absolute stagnation has taken place, nor from the arterioles. The escape of the white corpuscles usually greatly exceeds that of the red, and the vessels soon become surrounded and obscured by the crowd of extra-vascular leuco- cytes. In intense inflammations in very vascular tissues the red escape in greater numbers than the white corpuscles, and a resulting hemor- thagic spot is visible to the naked eye. The number of migrating cells is increased in the later stages of the inflammatory process. It is possible for the emigrated leucocytes—(1) to be transformed into tissue cells ; (2) to reénter the blood vessels ; (3) to enter the lymphatic vessels ; (4) to become pus-cells. There also occurs an escape or exudation of fluid derived from the blood liquor and similar to it ; which, when associated with the escaped white and red blood corpuscles and the proliferating cells of the in- flamed tissues, constitutes the inflammatory exudate, or, as it has been termed by some writers, inflammatory lymph or fibrin. The escaping fluid differs from the simple serous or dropsical effusion, that occurs in congestion or mechanical hyperemia, in that it contains more white corpuscles, more albumin, and is more prone to spontaneous coagulation. It differs from blood liquor, or liquor sanguinis, in hav- 30 INFLAMMATION. ing less albumin and less coagulability. This inflammatory fluid is well termed an exudation of lymph or simply an exudate ; and the escape arising from venous distention a transudation of serum, or simply a transudate. This exudate or inflammatory lymph is of paramount importance to the surgeon, for, by its organization and transformation into tissue analogous to that at the seat of injury or disease, hemorrhage is pre- vented, wounds united, abscesses circumscribed and limited, plastic surgery made possible, and other reparative surgical processes accom- plished. At times, however, it produces morbid conditions, such as strictures and adhesions, alters structure by interstitial deposit, and is exceeding destructive to functional integrity. It is well to apply the term exudate, or lymph, to effusions occur- ring from inflammation, even when they closely resemble the serous transudate of mechanical venous obstruction. The milder forms of inflammation give rise to a fluid containing so little albumin and having so little tendency to coagulation that it is impossible to dis- tinguish it from the fluid of a non-inflammatory dropsy. On mucous or serous surfaces the exudate is readily seen during the progress of inflammation ; in some tissues it is exhibited as swelling ; in the cornea and other non-vascular structures it is found surround- ing the part, because it is the adjacent vessels which present the in- flammatory alterations. The blood phenomena of inflammation, then, are increase of white cells, retardation of current, migration, and exu- dation. 4, Tissues.—The tissues are swollen and infiltrated with the escap- ing blood elements, and the proper cells of the tissue involved show disordered nutrition, such as coagulation-necrosis and fatty degenera- tion. The impairment of nutrition may result in the formation of in- ferior tissue, suppuration, or gangrene. The peptonizing action of micro-organisms