  Probably the most universally known fact respecting bacteria is that they are related in some way to the production of disease. Yet we have seen that it was not as disease-producing agents that they were first studied. Indeed, it is only within comparatively the latest period of the two centuries during which they have been more or less under observation that our knowledge of them as causes of disease has assumed any exactitude or general recognition. Nor is this surprising, for although an intimate relationship between fermentation and disease had been hinted at in the middle of the seventeenth century, it was not till the time of Pasteur that the bacterial cause of fermentation was experimentally and finally established. In the middle of the seventeenth century men learned, through the eyes of Leeuwenhoek, that drops of water contained "moving animalcules." A hundred years later Spallanzani demonstrated the fact that putrefaction and fermentation were set up in boiled vegetable infusions when outside air was admitted, but when it was withheld from these boiled infusions no such change occurred. Almost a hundred years more passed before the epoch-making work of Tyndall and Pasteur, who separated these putrefactive germs from the air. Quickly following in their footsteps came Davaine and Pollender, who found in the blood of animals suffering from anthrax the now well-known specific But we must look less cursorily at the growth of the idea of bacteria causing disease. More than two hundred years ago Robert Boyle (1627–91), the philosopher, who did so much towards the foundation of the present Royal Society, wrote a learned treatise on The Pathological Part of Physic. He was one of the earliest scientists to declare that a relationship existed between fermentation and disease. When more accurate knowledge was attained respecting fermentation, great advance was consequently made in the etiology of disease. The preliminary discoveries of Fuchs and others between 1840 and 1850 had relation to the existence in diseased tissues of a large number of bacteria. But this was no proof that such germs caused such diseases. It was not till Davaine had inoculated healthy animals with bacilli from the blood of an anthrax carcass, and had thus produced the disease, that reliance could be placed upon that bacillus as the vera causa of anthrax. Too much emphasis cannot be laid upon this idea, that unless a certain organism produces in healthy tissues the disease in question, it cannot be considered as proven that the particular organism is related to (a) The organism must be demonstrated in the circulation or tissues of the diseased animal. (b) The organism thus demonstrated must be cultivated in artificial media outside the body, and successive generations of a pure culture of that organism must be obtained. (c) Such pure cultures must, when introduced into a healthy and susceptible animal, produce the specific disease. (d) The organism must be found and isolated from the circulation or tissues of the inoculated animal. It is evident that there are some diseases—for example, cholera, leprosy, and typhoid—which are not communicable to lower animals, and therefore their virus cannot be made to fulfil postulate (c). In such cases there is no choice. They cannot be classified along with tubercle and anthrax. Bacteriologists have little doubt that Hansen's bacillus of leprosy is the cause of that disease, yet it has not fulfilled postulates (b) and (c). Nor has the generally accepted bacillus of typhoid fulfilled postulate (c), yet by the majority it is provisionally accepted as the agent in producing typhoid. Hence it will be seen that, though there is an academical classification of causal pathogenic bacteria according as they respond to Koch's postulates, yet nevertheless, there are a number of pathogenic bacteria which are looked upon as causes of disease provisionally. Anthrax and tubercle, with perhaps the organisms of suppuration, tetanus, plague, and actinomycosis, stand in the first order of pathogenic germs. Then comes a group awaiting further confirmation. It includes the organisms related to typhoid, cholera, malaria, leprosy, diarrhoea,and pneumonia. In the production of bacterial disease there are two factors. First, there is the body tissue of the individual; secondly, there is the specific organism. Whatever may be said hereinafter with regard to the power of micro-organisms to cause disease, we must understand one cardinal point, namely, that bacteria are never more than causes, for the nature of disease depends upon the behaviour of the organs or tissues with which the bacteria or their products meet (Virchow). Fortunately for a clear conception of what "organs and tissues" mean, these have been reduced to a common denominator, the cell. Every living organism, of whatever size or kind, and every organ and tissue in that living organism, contains and consists of cells. Further, these cells are composed of organic chemical substances which are not themselves alive, but the mechanical arrangement of which determines the direction and power of their organic activity and of their resistance to the specific agents of disease. With these facts clearly before us, we may hope to gain some insight into the reasons for departure from health. The normal living tissues have an inimical effect upon bacteria. Saprophytic bacteria of various kinds are normally present on exposed surfaces of skin or mucous membrane. Tissues also which are dead or depressed in vitality from injury or previous disease, but which are still in contact with the tissues, afford an excellent nidus for the growth of bacteria. Still these have not the power, unless specific, to thrive in the normal living tissue. It has been definitely All the foregoing points in one direction, namely, that if the tissues are maintained in sound health, they form a very resistant barrier against bacteria. But we know from experience that a full measure of health is not often the happy condition of human tissues; we have, in short, a variety of circumstances which, as we say, predispose the individual to disease. One of the commonest forms of predisposition is that due to heredity. Probably it is true that what are known as hereditary diseases are due far more to a hereditary predisposition than to any transmission of the virus itself in any form. Antecedent disease predisposes the tissues to form a nidus for bacteria; conditions of environment or personal habits frequently act in the same way. Damp soils must be held responsible for many disasters to health, not directly, but indirectly, by predisposition; dusty trades and injurious occupations have a similar effect. Any one of these three different influences may in a variety of ways affect the tissues and increase their susceptibility to disease. Not infrequently we may get them combined. For example, the The channels of infection by which organisms gain the vantage-ground afforded by the depressed tissues are various, and next to the maintenance of resistant tissues they call for most attention from the physician and surgeon. It is in this field of preventive medicine—that is to say, preventing infective matter from ever entering the tissues at all—that science has triumphed in recent years. It is, in short, applied bacteriology, and therefore claims consideration in this place. 1. Pure Heredity. By this term may be understood the actual transmission from the mother to the unborn child of the specific virus of the disease. That such a conveyance may occur is generally admitted by pathologists, but it is impossible to enter fully into the matter in such a book as the present. Summarily we may say that, though this sort of transmission is possible, it is not frequent, nor is disease appreciably spread through such a channel. Sixty per cent. of consumptives, it has been estimated, have tuberculous progenitors, and this is the highest figure. Many would be justified from experience in placing it at half that number. 2. Inoculation, or inserting virus through a broken surface of skin, is itself a sufficiently obvious mode of infection to call for little comment. Yet it is under this heading that From time to time examples occur of bacterial disease being directly inoculated in wounds made with polluted instruments, or in cuts made by contaminated broken glass, or in gunshot wounds. Tetanus is, of course, one of the most marked examples. 3. Contagion is a term which has suffered from the many ways in which it has been used. Defined shortly and most simply, we should say a disease is contagious when it can be "caught" by contact, through the unbroken surfaces, between diseased and healthy persons. Ringworm is an example, and there are many others. 4. The Alimentary Canal: Food. The recent Royal Commission on Tuberculosis has collected a large mass of evidence in support of the view that tubercle may be spread by articles of food. Milk and meat from tuberculous animals naturally come in for the largest amount of condemnation. To these matters we refer elsewhere. 5. The Respiratory Tract: Air. The air may become infected with germs of disease from dusty trades, dried sputum, etc. If such infected air be inhaled, pathogenic These, then, are the five possible ways in which germs gain access to the body tissues. The question now arises, How do bacteria, having obtained entrance, set up the process of disease? For a long time pathologists looked upon the action of these microscopic parasites in the body as similar to, if not identical with, the larger parasites sometimes infesting the human body. Their work was viewed as a devouring of the tissues of the body. Now, it is well known that, however much or little of this may be done, the specific action of pathogenic bacteria is of a different nature. It is twofold. We have the action of the bacteria themselves, and also of their products or toxins. In particular diseases, now one and now the other property comes to the front. In bacterial diseases affecting or being transmitted mostly by the blood, it is the toxins which act chiefly. The convenient term infection is applied to those conditions in which there has been a multiplication of living organisms after they have entered the body, the word intoxication indicating a condition of poisoning brought about by their products. It will be apparent at once that we may have both these conditions present, the former before the latter, and the latter following as a direct effect of the former. Until intoxication occurs there may be few or no symptoms, but directly enough bacteria are present to produce in the body certain poisons in sufficient amount to result in more or less marked tissue change, then the symptoms of that tissue change appear. This period of latency between infection and the appearance of the disease is known as the incubation period. Take typhoid, for example. A man drinks a typhoid-polluted water. For about fourteen days the bacilli are making headway in his body without his being aware of it. But at the end of that incubation Speaking generally, we may note that pathogenic bacteria divide themselves into two groups: those which, on entering the body, pass at once, by the lymph or blood stream, to all parts of the body, and become more and more diffused throughout the blood and tissues, although in some cases they settle down in some spot remote from the point of entrance, and produce their chief lesions there. Tubercle and anthrax would be types of this group. On the other hand, there is a second group, which remain almost absolutely local, producing only little reaction around them, never passing through the body generally, and yet influencing the whole body eventually by means of their ferments or toxins. Of such the best representatives are tetanus and diphtheria. The local site of the bacteria is, in this case, the local manufactory of the disease. Whilst the mere bodily presence of bacteria may have mechanical influence injurious to the tissues (as in the small peripheral capillaries in anthrax), or may in some way act as a foreign body and be a focus of inflammation (as in tubercle), the real disease-producing action of pathogenic bacteria depends upon the chemical poisons (toxins) formed directly or indirectly by them. Though within recent years a great deal of knowledge has been acquired about the formation of these bodies, their exact nature is not known. They are allied to albuminous bodies and proteoses, and are frequently described as tox-albumens. It may be found, after all, that they are not of a proteid nature. Sidney Martin has pointed out that there is much that is analogous between the production of toxins and the production of the bodies of digestion. Just as ferments are necessary in the intestine to bring about a change in the food by which Lastly, we may turn to consider the action of the toxins on the individual in whose body-fluids they are formed. It is hardly necessary to say that any action which bacteria or toxins may have will depend upon their virulence, in some measure upon their number, and not a little upon the channel of infection by which they have gained entrance. It could not be otherwise. If the virulence is attenuated, or if the invasion is very limited in numbers, it stands to reason that the pathogenic effects will be correspondingly small or absent. The influence of the toxins is twofold. In the first place (i.) they act locally upon the tissues at the site of their formation, or at distant points by absorption. There is inflammation with marked cell-proliferation, and this is, more or less rapidly, followed by a specific cell-poisoning. The former change may be accompanied by exudation, and simulate the early stages of abscess formation; the latter is the specific effect, and results, as in leprosy and tubercle, in infective nodules. The site in some diseases, like typhoid (intestinal ulceration, splenic and mesenteric change) or diphtheria (membrane in the throat), may be definite and always the same. But, on the other hand, the site may We may now consider briefly some of the more important types of disease produced by bacteria: 1. Tuberculosis. In 1834 Laennec described all caseous deposits as "tubercles," insisting upon four varieties: (1) Miliary, which were about the size of millet seeds, and in groups; (2) Crude, miliary tubercles in yellow masses; (3) Granular, similar to the last, but scattered; (4) Encysted, a hard mass of crude tubercle with a fibrous or semi-cartilaginous capsule. The tubercle possesses in many cases a special structure, and certain cell-forms frequently occur in it and give it a characteristic appearance. The central part of the tubercle It was not till 1865 that the specific nature of tuberculosis was asserted by Villemin. Burdon Sanderson (1868–69) in England confirmed his work, and it was extended by Connheim, who a few years later laid down the principle that all is tubercular which by transference to properly constituted animals is capable of inducing tuberculosis, and nothing is tubercular unless it has this capability. Klebs (1877) and Max Schiller (1880) described masses of living cells or micrococci in many tuberculous nodules in the diseased synovial membrane and in lupus skin. In 1881 Toussaint declared he had cultivated from the blood of tubercular animals and from tubercles an organism which was evidently a micrococcus, and in the same year Aufrecht stated that the centre of a tubercle contained small micrococci, diplococci, and some rods. But it was not till the following year, 1882, that Koch discovered and demonstrated beyond question the specific Bacillus tuberculosis. It is now held to be absolutely proved that the introduction of the bacillus, or its spores or products, is the one and only essential agent in the production of tuberculosis. Its recognised manifestations are as follows:
The disease may occur generally throughout the body or locally in the suprarenal capsules, prostate, intestine, larynx, membranes of the heart, bones, ovaries, pleura, kidneys, spleen, testicles, Fallopian tubes, uterus, etc. We may summarise the history of the pathology of tubercle thus: 1794. Baillie drew attention to grey miliary nodules occurring in tuberculosis, and called them "tubercles." 1834. Laennec described four varieties: miliary; crude; granular; encysted. 1843. Klencke produced tuberculosis by intravenous injection of tubercular giant cells. 1865. Villemin demonstrated infectivity of tubercular matter by inoculation of discharges; Connheim, Armanni, Burdon Sanderson, Wilson Fox, and others showed that nothing but tubercular matter could produce tuberculosis. 1877. Living cells were found in tubercles, "micrococci" (Klebs, Toussaint, Schiller). 1882. Koch isolated and described the specific bacillus, and obtained pure cultivations (1884). The Bacillus of Koch, 1882. Delicate cylindrical rods, measuring 1.5–4 micromillimetres in length and about .2 µ in breadth; non-motile. Many are straight with rounded ends; others are slightly curved. They are usually solitary, but may occur in pairs, lying side by side or in small masses. They are chiefly found in fresh tubercles, more sparingly in older ones. Some lie within the giant cells; others lie outside; shorter in tissue sections of bovine tuberculosis, but longer in the milk (Crookshank). When stained they appear to be composed of irregular cubical or spherical granules within a faintly stained sheath. In recent lesions the protoplasm appears more homogeneous, and takes on the segmented or beaded character only in old lesions, pus, or sputum. Morphological differences are found under different circumstances, and within limits variation occurs according to the environment. Cultivation on Various Media. Koch inoculated solid blood serum with tubercular matter from an infected lymphatic gland of a guinea-pig, and noticed the first signs of growth in ten or twelve days in the form of whitish, scaly patches. These enlarged and coalesced with neighbouring patches, forming white, roughened, irregular masses. Nocard and Roux showed that by adding 5/8 per cent. of glycerine to the media commonly used in the laboratory, such as nutrient agar or broth, the best growth is obtained. On glycerine broth or glycerine agar abundant growth appears at the end of seven or eight days. By continuous sub-culture on glycerine agar the virulence of the bacillus is diminished. But in fifteen days after inoculation of the medium the culture equals in extent a culture of several weeks' age on blood serum. Sub-cultures from glycerined media will grow in ordinary broth without glycerine (Nocard, Roux, Crookshank). In alkaline broth to which a piece of boiled white of egg was added Klein obtained copious growths, and found that continued sub-culturing upon this medium also lessens the virulence. Description of Cultivations:—On glycerine agar minute white colonies appear in about six days, raised and isolated, and coalescing as time advances, forming a white lichenous growth, fully developed in about two months. On glycerine broth a copious film appears on the surface of the liquid, which if disturbed falls to the bottom of the flask as a deposit. Spore Formation. In very old cultivations spore-like bodies can be observed both in stained and unstained preparations, but neither the irregular granules within the capsule nor the unstained spaces between the granules are 1. That tubercular sputum, when thoroughly dried, maintains its virulent character (Koch, Schill, Fischer, etc.). No sporeless bacillus is known which can survive through drying. 2. That tubercular matter and cultures survive temperature up to 100°C. Non-spore-bearing bacilli and micrococci are killed by being exposed for five minutes to a temperature of 65–70°C., whereas spores of other bacilli withstand much higher temperatures. 3. Tubercular sputum distributed in salt solution does not lose its virulence by being kept at 100°C. for one or two minutes; sporeless bacilli certainly would (Klein). 4. A solution of per-chloride of mercury does not kill the tubercle bacilli, as it does sporeless bacilli (Lingard and Klein). Koch and many bacteriologists have declared the bacillus to be a "true parasite." Koch based this view upon the belief which he entertained that the bacillus can grow only between 30°C. and 41°C., and therefore in temperate zones is limited to the animal body and can originate only in an animal organism. "They are," he said, "true parasites, which cannot live without their hosts. They pass through the whole cycle of their existence in the body." But at length Koch and others overcame the difficulties and grew the bacillus as a saprophyte. Schottelius It has now been abundantly proved that the bacillus of tuberculosis is capable of accommodating itself to circumstances much less favourable than had been supposed, especially as regards temperature. Temperature of Growth of Bacillus. 30–41°C. have been laid down by Koch as the limits of temperature at which the bacillus will grow in culture medium outside the body. The generally accepted temperatures as most favourable to the growth of the bacillus are between 36°C. and 38°C. Sir Hugh Beevor, however, was able to grow the bacillus upon glycerine agar at 28°C. (82°F.), obtaining an ample culture which developed somewhat more slowly than on blood serum, and to a less extent than at 37°C. In both Beevor succeeded in growing the bacillus at a lower temperature even than on agar, viz., at a temperature rarely above 60°F. Sheridan DelÉpine and others have also been successful in obtaining growths at room temperature both in summer and winter. Although, speaking generally, there is an actual cessation of growth at low temperature, the bacillus may be exposed to very low temperatures for a considerable time without losing its power of again becoming active when returned to a favourable environment (Woodhead). The Relation of the Bacillus to the Disease. All four of Koch's postulates have been fulfilled in the case of Bacillus tuberculosis. Hence we are dealing with the specific cause of the disease. Yet, whilst this is so, we may usefully ask ourselves: How does the bacillus set up the changes in normal tissues which result in tubercular nodules? In arriving at a solution of this problem we are materially aided if we bear in mind the fact that such an organism in healthy tissues has a double effect. First, there is an ordinary inflammatory irritation, and secondly, there is a specific change
The exact period of giant-cell formation depends on the rapidity of the formative processes. Thus different conditions occur. Inside the giant cells the bacilli are arranged in relation to the nuclei in one of three ways: (a) polar, (b) zonal, or (c) mixed. The breaking down of the nodule is partly due to the cell-poisons, and partly because the nodule is non-vascular, owing to the fact that new capillaries cannot grow into the dense nodule, and the old ones are all occluded by the growth of the nodule. From the local foci of disease the tubercle process spreads chiefly by three channels: (a) By the lymphatics, affecting particularly the glands. Thus we get tuberculosis set up in the bronchial, tracheal, mediastinal, and mesenteric glands, and it is so frequently present as to be a characteristic of the disease. This is the common method of dissemination in the body. (b) By the blood-vessels, by means of which bacilli may be carried to distant organs. (c) By continuity of tissues, infective giant-cell systems encroaching upon neighbouring tissues, or discharge from lungs or bronchial glands obtaining entrance to the gullet and thus setting up intestinal disease also. It has been abundantly proved that the respiratory and digestive systems are principally affected by Koch's bacillus. Wherever the bacilli are arrested, they excite formation of granulations or miliary tubercular nodules, which increase and eventually coalesce. The lymphatic glands which collect the lymph from the affected region are the earliest affected, always the nearest first, and then the disease appears to be appreciably stopped on its invading march. Each lymphatic gland acts as a temporary barrier to progress until the disease has broken its structure down. It remains local, in spite of increase in number and importance of the foci of disease, as long as the bacilli have not gained access to the blood stream. Toxins and Tuberculin. Koch, Crookshank, and Herroun, Hunter, and others have isolated products from pure cultures of the tubercle bacillus. These have comprised chiefly albumoses, alkaloids, and various extractives. Koch's observations led him to suppose that in pure cultures of tubercle a substance appeared having healing action on tuberculosis, Flask used in the Preparation of Tuberculin Flask used in the Preparation of Tuberculin The announcements in 1890 and 1891 to the effect that a "cure" had been discovered for consumption will be remembered. The hopes thus raised were unfortunately not to be realised. Koch advocated injections of this tuberculin in cases of skin tubercle (lupus) and consumptive cases. In many of these benefit was apparently derived, but its general application was not founded upon any substantial basis. Dead tissue, full of bacilli, could not thus be got rid of; nor could the career of the isolated bacilli distributed through the body be thus checked. Tuberculin has, however, found a remarkable sphere of usefulness in causing reaction in animals suffering from tuberculosis. Indeed, tuberculin is the most valuable means of diagnosis that we possess (MacFadyen). When injected (dose, 30–40 centigrammes) it causes a rise of one and a half to three degrees. The fever begins between the twelfth and fifteenth hour after injection, and lasts several hours. The duration and intensity of the reaction have no relation to the number and gravity of the lesions, but the same dose injected into healthy cattle causes no appreciable febrile reaction. The tuberculous calf reacts just as well as the Tuberculosis of Animals. Cattle come first amongst animals liable to tubercle. Horses may be infected, but it is comparatively rare, and among small ruminants the disease is rarer still. Dogs, cats, and kittens may be easily infected. Amongst birds, fowls, pigeons, turkeys, and pheasants, the disease assumes almost an epidemic character. Especially do animals in confinement die of tubercle, as is illustrated in zoÖlogical gardens. Respecting the lesions of bovine tuberculosis, it will be sufficient to say that nothing is more variable than the localisation or form of its attacks. The lungs and lymphatic glands come first in order of frequency, next the serous membranes, then the liver and intestines, and lastly the spleen, joints, and udder (Nocard). The anatomical changes in bovine tubercle are mostly found in the lungs and their membranes, the pleurÆ. It also affects the internal membrane lining, the abdomen and its chief organs, the peritoneum, and the lymphatic glands. In both these localities a characteristic condition is set up by small grey nodules appearing, which increase in size, giving an appearance of "grapes." Hence the condition is called grape disease, or Perlsucht. The organs, as we have said, are equally affected, and when we add the lymphatic glands we have a fairly complete summary of the form of the disease as it occurs in cattle. As has been clearly pointed out by Martin, Woodhead, and others in their evidence before the Royal Commission, the organs, glands, and membranes are the sites for tubercle, not the muscles (or "meat"). This latter is most liable to convey infection when the butcher smears it with the knife which he has used to remove tubercular organs. As regards the udder in its relation to milk infection, it The general anatomical characteristics of the disease are similar to those occurring in man. The percentage of cattle suffering from tubercle varies. In Germany it appears to vary from 2 to 8 per cent. of all cattle, in Saxony 17 to 30 per cent., in England 22 per cent. approximately (in London 40 per cent.), in France 25 per cent. Lowland breeds are much more infected than mountain breeds, which possess stronger constitutions. Tuberculosis of the pig is less common than that of cattle, but not so rare as that of the calf (Nocard). In nine out of ten cases the pig is infected by ingestion, particularly when fed on the refuse from dairies and cheese factories. The disease follows the same course as in cattle. The finding of the bacillus is difficult, and the only safe test is inoculation (Woodhead). Sheep are very rarely tuberculous by nature, though there is evidence to believe that very long cohabitation with Tuberculosis in the horse is relatively very rare. It attacks the organs of the abdominal cavity, especially the glands; it affects the lung secondarily as a rule. The cases are generally isolated ones, even though the animal belongs to a stud. Nocard holds that the bacillus obtained from the pulmonary variety is like the human type, whilst the abdominal variety is more like the avian bacillus. Nocard says "If the dog can become tuberculous from contact with man, the converse is equally true. Infection is at any rate possible when a house-dog scatters on the floor, carpet, or bed, during its fit of coughing, virulent material, which is rendered extremely dangerous by drying, especially for children, its habitual playmates. The most elementary prudence would recommend the banishment from a room of every dog which coughs frequently, even though it only seems to be suffering from some common affection of the bronchi or lung." Tuberculosis is a common disease among the birds of the poultry-yard: poultry, pigeons, turkeys, pea-fowl, guinea-fowl, etc. They are infected almost exclusively through the digestive tract, generally by devouring infected secretions of previous tubercular fowls. Whatever the position or form of avian tuberculosis, the bacilli are present in enormous numbers, and are often much shorter and sometimes much longer than those met with in tuberculous mammalia, and grow outside the body at a higher temperature (43°C.). They are also said to be more resistant and of quicker growth. The species is probably identical with Koch's bacillus, though there are differences. In the nodule, which is larger than in human tuberculosis, there are few or no giant cells, and it does not so readily break down. Nocard and others have demonstrated the fact that the Bacillus tuberculosis of Koch is the common denominator in all tubercular disease, whatever and wherever its manifestations, in all animals. The bacillus, they hold, may, however, experience profound modifications by means of successive passages through the bodies of divers species of animals. But if the modifications which it undergoes as a result of transmissions through birds, for example, are profound enough to make the bacillus of avian tubercle a peculiar variety of Koch's bacillus, they are not enough, it is generally believed, to make these bacilli two distinct species. We may, therefore, take it for granted that tuberculosis is one and the same disease, with various manifestations, common to man and animals, intercommunicable, and having but one vera causa: the Bacillus tuberculosis of Koch. The Prevention of Tuberculosis. At the present time much attention is being directed to the administrative personal control of tuberculosis. How greatly this is needed in so preventable a disease is evident from a perusal of the following quotation from the Registrar-General's reports. (See opposite page.) These figures show a marked decline in the three worst forms of the disease. But this decline is apparently less marked in tabes than in phthisis or tubercular meningitis, i. e., less in the kind of tubercle due to the ingestion of infected milk. Fortunately the State is beginning to realise its duty in regard to preventive measures. The abolition of private slaughter-houses, the protection of meat and milk supplies, the seizure of tuberculous milch cows, and such like measures fall obviously within the jurisdiction of the State rather than the individual, and claim the earnest and urgent attention of the public health departments of states. ENGLISH DEATH-RATES FROM ALL TUBERCULAR DISEASES THE FOLLOWING IS A TABLE OF DEATH-RATES TO A MILLION LIVING (ENGLAND), 1877–1897 (Reg.-Gen. Annual Reports):—
Tabes mesenterica is tuberculosis of the alimentary canal and mesenteric lymph glands. Tubercular meningitis is the name of the same disease as it affects the membranes of the brain (acute hydrocephalus). Phthisis is the term applied to "consumption," or tubercle in the lungs. But personal hygiene and the prevention of the transmission of the disease depend very largely indeed upon the mass of the population. Hence we hail with satisfaction the recent endeavours to educate public opinion. In order to make this matter very simple indeed, we have placed in a footnote a series of statements embodying some of the chief facts which every individual in our crowded communities should know. Bacillus of Diphtheria Bacillus of Diphtheria Diphtheria (Klebs-LÖffler Bacillus, 1882–1884). Diphtheria is an infective disease characterised by a variety of clinical symptoms, but commonly by a severe inflammation followed by a fibrous infiltration (constituting a membrane) of certain parts. The membrane ultimately breaks down. The Bacillus diphtheriÆ was isolated from the many bacteria found in the membrane by LÖffler. Klebs had previously identified the bacillus as the cause of the disease. It retains its vitality in cultures and sometimes in the throat for months. Three or four weeks is the average length of time for its existence in the membrane, but, owing to the difficulty of killing it in situ, it may live on for as long as a year. All the conditions in the throat—mucous membrane, blood-heat, moisture, air—are extremely favourable to the bacillus; but it is very materially modified in virulence. It is secured for diagnostic purposes by one of two methods: (a) Either a piece of the membrane is detached, and after washing carefully examined by culture as well as the microscope; or (b) a "swab" is made from the infected throat and cultured on serum, and incubated at 37°C. for eighteen hours and then microscopically examined. Both methods—and there is no further choice—present some difficulties owing to the large number of bacteria found in the throat. Hence a negative result must be accepted with reserve. We have already referred at some length to the question of toxins in diphtheria, and need not dwell further upon that matter. Still a word or two may be said here summarising the general action of the bacillus. Locally it produces inflammatory change with fibrinous exudation and some cellular necrosis. In the membrane a ferment is probably produced which, unlike the localised bacilli, passes throughout the body and by digestion of the proteids produces albumoses and an organic acid which have the toxic influence. The toxins act on the blood-vessels, and nerves, and muscle fibres of the heart, and many of the more highly specialised cells of the body. Thus we get degenerative changes in the kidney, in cells of the central nervous system, in the peripheral nerves (post-diphtheritic paralysis), and elsewhere, these pathological conditions setting up, in addition to the membrane, the signs of the disease. The bacil The influence of drainage, milk, and schools must not be forgotten by sanitary authorities any more than the essential importance of adequate isolation hospital accommodation. Mr. Shattock's experiments on the effect of sewer air upon attenuated Klebs-LÖffler bacilli have been mentioned (see p. 105). Nevertheless there can be no doubt that emanations from defective drains have a materially predisposing effect, not, it is true, upon the bacilli, but upon the tissues. Sore throats thus acquired are par excellence the site for the development of diphtheria. The influence of school attendance has claimed the recent attention of the Medical Officer of the London School Board and the Medical Officer of the administrative County of London. In London since 1881 there has been a marked increase of diphtheria, which has occurred, though in a much less degree, throughout England and Wales. The Registrar-General has only classified diphtheria as a separate disease since 1855, when the death-rate per 1,000,000 in England and Wales was stated as 20. The following are the figures for four decades up to 1895: AVERAGE DEATH-RATE PER MILLION OF THE POPULATION FROM DIPHTHERIA IN ENGLAND AND WALES AND IN LONDON (IN DECADES 1856–95)
From these figures the extraordinary increase during the last few years is clearly demonstrated. Sir Richard Thorne Thorne, in 1891, drew attention to the influence of damp soils and schools upon diphtheria. In 1894 Mr. Shirley Murphy, Medical Officer to the London County Council, reported that there had been an increase in diphtheria mortality in London at school ages (three to ten) as compared with other ages since the Elementary Education Act became operative in 1871; that the increased mortality from diphtheria in populous districts, as compared with rural districts, since 1871, might be due to the greater effect of the Education Act in the former; and that there was a diminution of diphtheria in London during the summer holidays at the schools in 1893, but that 1892 did not show any marked changes for August. In 1896 Professor W. R. Smith, the Medical Officer to the London School Board, furnished a report Although it is said that "statistics can be made to prove anything," there can be little doubt that both of these reports contain a great deal of truth; nor are these truths incompatible with each other. They both emphasise age as a great factor in the incidence of the disease, and whatever affects the health of the child population, like schools, must play, directly or indirectly, a not unimportant part in the transmission of the disease. The Pseudo-diphtheria Bacillus. 1. The pseudo-bacillus is thicker in the middle than at the poles, and not so variable as the Bacillus diphtheriÆ. Polar staining is absent. 2. Its growth on potato reveals cream-coloured colonies visible in a couple of days; the real bacillus is invisible. 3. The pseudo-bacillus will not grow at all anaËrobically in hydrogen, but the Bacillus diphtheriÆ is able to do so. 4. There is the great difference in virulence. Suppuration. This term is used to designate that general breaking down of cells which follows acute inflammation. An "abscess" or "gathering" is a collection, greater or smaller, of the products of suppuration. The word pus is generally used to describe this matter. We may have such an advanced inflammatory condition in any locality of the body, and it will assume different characters according to its site. Hence there are connected with suppuration, as causal agents, a variety of bacteria. Pus is not matter containing a pure culture of any specific species, but, on the contrary, is generally filled with a large number of different species. The most important are as follows: 1. Staphylococcus pyogenes aureus. These are micrococci arranged in groups, which have been likened to bunches of grapes. They are the common organisms found in pus, and were with other auxiliary bacteria first distinguished as such by Professor Ogston, of Aberdeen. There are several forms of the same species, differing from each other in colour. Thus we have the S. pyogenes aureus (golden yellow), albus (white), citreus (lemon), and others. They occur commonly in nature, in air, soil, water, on the surface of the skin, and in all suppurative conditions. The aureus is the only one credited with much virulence. It occurs in the blood in blood-poisoning (septicÆmia, pyÆmia), and is present in all ulcerative conditions, including ulcerative disease of the valves of the heart. The Staphylococcus cereus albus and S. cereus flavus are slightly modified forms of the S. pyogenes aureus, and are differentiated from it by being non-liquefying. They produce a wax-like growth on gelatine. Staphylococcus pyogenes aureus, the type of the family, is grown in all ordinary media at room temperature, though more rapidly at 37°C. Liquefaction sets in at a comparatively early date, and subsequently we have in the gelatine test-tube cultures a flocculent deposit of a bright yellow amorphous mass, and in gelatine plates small depressions of liquefaction with a yellow deposit. It renders all media acid, and coagulates milk. Its thermal death-point in gelatine is 58°C. for ten minutes, but when dry considerably higher. It is a non-motile and a facultative anaËrobe; but the presence of oxygen is necessary for a bright colour. Its virulence readily declines. 2. Streptococcus pyogenes. In this species of micrococcus the elements are arranged in chains. Most of the streptococci in pus, from different sources, are one species, having approximately the same morphological and biological characters. Their different effects are due to different degrees of toxic virulence; they are always more virulent when associated with other bacteria, for example, the Proteus family. The chains vary in length, consisting of more elements when cultured in fluid media. They multiply by direct division of the individual elements, and in old cultures it has been observed that the cocci vary in form and size. Types of Streptococcus Types of Streptococcus In culture upon the ordinary media streptococcus is comparatively slow-growing, producing minute white colonies on or about the sixth day. It does not liquefy gelatine, and remains strictly localised to the track of the inoculating needle. Like the staphylococcus, it readily loses virulence. The thermal death-point is, however, lower: 54°C. for ten minutes. Marmorek has devised a method by which the virulence may be greatly increased, and he holds that it depends upon the degree of virulence possessed by any particular streptococcus as to what effects it will produce. By the Streptococcus pyogenes has been isolated from the membrane of diphtheria, and from small-pox, scarlet fever, vaccinia, and other diseases. In such cases it is not the causal agent, but merely associated with the complications of these diseases. Suppuration and erysipelas are the only pathological conditions in which the causal agency of streptococcus has been sufficiently established. 3. The Bacillus pyocyaneus occurs in green pus, and is the cause of that colouration. Gessard was the first to prove its significance, and he describes two varieties. Micrococcus Tetragonus Micrococcus Tetragonus It is a minute, actively motile, non-sporulating bacillus, which occasionally complicates suppuration and produces green pus. Oxygen is necessary for pigmentation, which is due to two substances: pyocyanin, a greenish-blue product extracted with chloroform, and pyoxanthose, a brown substance derived from the oxidation of the former pigment. Both these colours are produced in cultivation outside the body. On gelatine the colour is green, passing on to olive. There is liquefaction. On potato we generally obtain a brown growth (compare Bacillus coli, B. mallei, and others). The organism grows rapidly on all the ordinary media, which it has a tendency to colour throughout. It will be remembered that when speaking of the antagonism of organisms, we referred to the inimical action of Bacillus pyocyaneus upon anthrax. 4. Micrococcus Tetragonus. This species occurs in phthisi 5. Bacillus coli communis and many putrefactive germs commonly occur in suppurative conditions, but they are not restricted to such disorders (see p. 64). Diplococcus of Neisser Diplococcus of Neisser 6. Micrococcus gonorrhoeÆ (Neisser, 1879). This organism is more frequently spoken of as a diplococcus. It occurs at the acute stage of the disease, but is not readily differentiated from other similar diplococci except by technical laboratory methods. Each element presents a straight or concave surface to its fellow. A very marked concavity indicates commencing fission. The position which these diplococci take up in pus is intracellular, and arranged more or less definitely around the nucleus. Difficulty has often been found in cultivating this organism in artificial media outside the body. Wertheim and others have suggested special formulÆ for the preparation of suitable media, but it is a very simple matter to secure cultures on agar plates smeared with human blood from a pricked finger. The plate is incubated at 37°C. At the end of twenty-four hours small raised grey colonies appear, which at the end of Anthrax. This disease was one of the first in which the causal agency of bacteria was proved. In 1849 Pollender found an innumerable number of small rods in the blood of animals suffering from anthrax. In 1863 Davaine described these, and attributed the disease to them. But it was not till 1876 that Koch finally settled the matter by isolating the bacilli in pure culture and describing their biological characters. It is owing in part to its interesting bacterial history, which opened up so much new ground in this comparatively new science, that anthrax has assumed such an important place in pathology. But for other reasons, too, it claims attention. It appears to have been known in the time of Moses, and was perhaps the disease described by Homer in the First Book of the Iliad. Rome was visited by it in 740 B.C. Anthrax is an acute disease, affecting sheep, cattle, horses, goats, deer, and man. Cats, white rats, and Algerian sheep are immune. Swine become infected by feeding on the offal of diseased cattle (Crookshank). The post-mortem signs are mainly three: The spleen is greatly enlarged and congested, is friable to the touch, and contains enormous numbers of bacilli; the skin may show exudations forming dark gelatinous tumours; and the blood
Clinically there is rise of temperature and rapid loss of muscular power. The bacilli of anthrax are square-ended rods 1 µ broad and 4–5 µ long. In the tissues of the body they follow the lines of the capillaries, and are irregularly situated. In places they are so densely packed as to form obstructions to the onward flow of blood. In cultures they are in chains end to end, having as a rule equal interbacillary spaces. In cultures long filaments and threads occur. The exact shape of the bacillus depends, however, upon two things: the staining and spore formation. Both these factors may very materially modify the normal shape. The spores of anthrax are oval endospores, produced only in the presence of free oxygen, and at any temperature between 18 and 41°C. On account of requiring free oxygen, they are formed only outside the body. The homogeneous pro The bacillus is aËrobic, non-motile, and liquefying. Broth cultures become turbid in thirty-six hours, with nebulous masses of threads matted together. The pellicle which forms on the surface affords an ideal place for spore formation. Cultures in the depth of gelatine show a most characteristic growth. From the line of inoculation delicate threads and fibrillÆ extend outwards horizontally into the medium. Liquefaction commences at the top, and eventually extends throughout the tube. On gelatine plates small colonies appear in thirty-six hours, and on the second or third day they look, under a low power of the microscope, like matted hair. The colonies after a time sink in the gelatine, owing to liquefaction. On potato, agar, and blood serum anthrax grows well. Channels of Infection. 1. The Alimentary Canal. This is the usual mode of infection in animals grazing on infected pasture land. A soil suitable for the propagation of anthrax is one containing abundance of air and proteid material. Feeding on bacilli alone would probably not produce the disease, owing to the germicidal effect of the gastric juice. But spores can readily pass uninjured through the stomach and produce anthrax in the blood. Infected water as well as fodder may convey the disease. Water becomes infected by bodies of animals dead of anthrax, or, as was the case once at least in the south-west of England, by a stream passing through the washing-yard of an infected tannery. Manure on fields, litter in stalls, and infected earth may all contribute to the transmission of the disease. Darwin pointed out the services which are performed in superficial soils by earthworms bringing up casts; Pasteur was of opinion that in this way earthworms were responsible for continually bringing up the spores of anthrax from buried corpses to the surface, where they would reinfect cattle. Koch disputed this, but more recently Bollinger has demonstrated the correctness of Pasteur's views by isolating anthrax contagium from five per cent. of the worms sent him from an anthrax pasture. Bollinger also maintains that flies and other insects may convey the disease from discharges or carcasses round which they congregate. Alimentary infection in man is a rare form, and it reveals itself in a primary diseased state known as mycosis intestinalis, an inflamed condition of the intestine and mesenteric lymph glands. 2. Through the Skin. Cutaneous anthrax goes by the name of malignant pustule, and is caused by infective anthrax matter gaining entrance through abrasions or ulcers in the skin. This local form is obviously most contracted by those whose occupation leads them to handle hides or other anthrax material (butchers and cleaners of hides). 3. Respiratory Tract. In man this is the commonest form of all, and is well known under the term "wool-sorters' disease," or pulmonary anthrax. This mode of infection occurs when dried spores are inhaled in processes of skin-cleaning. It frequently commences as a local lesion affecting the mucous membrane of the trachea or bronchi, but it rapidly spreads, affecting the neighbouring glands, which become greatly enlarged, and extending to the pleura and lung itself. Such cases, as a rule, rapidly end fatally. From what has been said, it will be clear that anthrax carcasses are better not opened and exposed to free oxygen. An extended post-mortem examination is not necessary. Burning the entire carcass in a crematorium would be the ideal treatment. As such is not generally feasible the next best thing is to bury the carcass deeply with lime below and above it, and rail in the area to prevent other animals grazing off it. A very small prick will extract enough blood to examine for the anthrax bacilli which are driven by the force of the blood-current to the small surface capillaries. This occurs, of course, only when the disease has become quite general, for in the early stage the healthy blood limits the bacilli to the internal organs. In such cases examination of the blood of the spleen is necessary. Anthrax covers a wide geographical area all over the world, and no country seems altogether exempt. In Germany as many as 3700 animals have been lost in a single year. About 900 animals were attacked in 1897 in Great Britain. Plague. This disease, like anthrax and leprosy, has a long historical record behind it. As the Black Death it decimated the population of England in the fourteenth century, and visited the country again in epidemic form in the middle of the seventeenth century, when it was called the Great Plague. Now, it is highly probable that these two scourges and the recent epidemic in the East are all forms of one and the same disease. As a matter of fact, it is difficult to be sure what was the exact pathology of a number of the grievous ailments which troubled our country in the Middle Ages, but from all accounts bubonic plague and true leprosy were amongst them. The former came and went spasmodically, as is its habit; the latter dragged through the length of several centuries. Bacillus of Plague Bacillus of Plague The distribution of plague at the present time is fortunately a somewhat limited one, namely, a definite area in Asia known as the "Plague Belt." From Mesopotamia, as a sort of focus, the disease spreads northwards to the Caspian Sea, westwards to the Red Sea, southwards as far as Central India, and eastwards as far as the China Sea. This constitutes the "belt," but the disease may take an epidemic form, and is readily, though very slowly, conveyed by infection or contagion. It appears to be infectious by means of infective dust, and contagious by prolonged and intimate contact with the plague-stricken. Rats have been accused of conveying the disease from port to port, and The bacteriology of plague is almost the latest addition to the science. Kitasato, of Tokio, demonstrated the cause of plague to be a bacillus during the Hong Kong epidemic in 1894. This was immediately confirmed by Yersin, and further proved by the isolation in artificial media of a pure culture of a bacillus able to cause the specific disease of bubonic plague. The bacillus was first detected in the blood of patients suffering from the disease. It takes the form of a small, round-ended, oval cell, with marked polar staining, and hence having an appearance not unlike a diplococcus. In the middle there is a clear interspace, and the whole is surrounded with a thick capsule, stained only with difficulty. The organisms are often linked together in pairs or even chains, and exhibit involution forms. In culture the bacillus is even more coccal in form than in the body. The plague bacillus grows readily on the ordinary media at blood-heat, producing circular cream-coloured colonies with a wavy outline, which eventually coalesce to form a greyish film. The following negative characters help to distinguish it: No growth occurs on potato, milk is not coagulated, and gelatine is not liquefied; Gram's method does not stain the bacillus, and there are no spores; the bacillus is readily killed by heat and by desiccation over sulphuric acid at 30°C. Both in cultures and outside the body the bacillus loses virulence. To this may be attributed possibly the variety of forms of the plague bacillus which differ in virulence. On gaining entrance to the human body Haffkine has prepared a vaccine to be used as a prophylactic. He grows a pure culture of Kitasato's bacillus in broth upon the surface of which some globules of fat ("ghee") have been placed. The bacillus grows upon this fat in copious stalactite form. From time to time this growth is shaken down, until after five or six weeks the shaken broth appears milky. The contained bacilli are killed by heating the fluid to 70°C. for one hour. The resultant is the vaccine, of which the dose is 3 cc. Haffkine believes that inoculated persons in India have suffered twenty times less than non-inoculated living under the same conditions. Plague is essentially a "filth disease," and it is frequently preceded by famine. Temperature and overcrowding exert an influence upon it. The areas affected by the disease in the Middle Ages, in the seventeenth century, and in 1894–96 are alike in being characterised by filth and overcrowding. There is little fear, speaking generally, of the plague ever flourishing under Western civilisation, where the conditions are such that even when it appears there is little to encourage or favour its development. Leprosy. This ancient disease is said to have existed in Egypt 3500 B.C., and was comparatively common in India, China, and even in parts of Europe 500 B.C. We know it has existed in many parts of the world in the past, in which regions it is now extinct. Some of the earliest notices we At one time or another there were as many as two hundred institutions in the British Isles for the more or less exclusive use of lepers. Many of these establishments were of an ecclesiastical or municipal character, and probably the exact diagnosis of diseases was a somewhat lax matter. Bury St. Edmunds, Bristol, Canterbury, London, Lynn, Norwich, Thetford, and York were centres for lepers. Burton Lazars and Sherburn, in Durham, were two of the more famous leper institutions. At the present time the distribution of the disease is mostly Asiatic. Norway contains about 1200 lepers, Spain approximately the same number. Scattered through Europe are perhaps another 600 or 700, in India 100,000, and a large number in Japan. The Cape possesses a famous leper hospital on Robben Island, with a number of patients. The disease is also endemic in the Sandwich Islands. Descriptions of the pathological varieties of leprosy have been very diverse. The classification now generally adopted includes three forms: the tuberculated, the anÆsthetic (or maculo-anÆsthetic), and the mixed. Lepra tuberculosa is that form of the disease affecting chiefly the skin, and resulting in nodular tuberculated growth or a diffuse infil The Bacillus leprÆ was discovered by Hansen in 1874. He found it in the lepra cells in the skin, lymph glands, liver, spleen, and thickened parts of the nerves. It is common in the discharges from the wounds of lepers. It is conveyed in the body by the lymph stream, and has rarely been isolated from the blood (KÖbner).
The bacillus is present in enormous numbers in the skin and tissues, and has a form very similar indeed to Bacillus tuberculosis. It is a straight rod, and showing with some staining methods marked beading, but with others no beading at all. It measures 4 µ long and 1 µ broad. Young leprosy bacilli are said to be motile, but old ones are not. Neisser has maintained that the bacillus possesses a capsule and spores. The latter have not been seen, but Neisser holds that this is the form in which the bacillus gains entrance to the body. There is a characteristic which fortunately aids us in the diagnosis of this disease in the tissues, and that is the arrangement of the bacilli, which are rarely scattered or isolated, but gathered together in clumps and colonies. Bordoni-Uffreduzzi and Campania claim to have isolated the bacillus and grown it on artificial media, the former aËrobically on peptone-glycerine-blood-serum, at 37°C., the latter anaËrobically. But no other worker has been able to do this. Hence we are not able to study the bacteriology of leprosy at all completely, nor have inoculation experiments proved successful. Nevertheless there is At the Leprosy Congress held in Berlin in 1897, Hansen again emphasised his belief that segregation was the cause of the decline of leprosy wherever it had occurred. But there appears to be some evidence to show that leprosy has We may fitly add here the conclusions arrived at by the English Leprosy Commission "1. Leprosy is a disease sui generis; it is not a form of syphilis or tuberculosis, but has striking etiological analogies with the latter. "2. Leprosy is not diffused by hereditary transmission, and, for this reason and the established amount of sterility among lepers, the disease has a natural tendency to die out. "3. Though in a scientific classification of diseases leprosy must be regarded as contagious, and also inoculable, yet the extent to which it is propagated by these means is exceedingly small. "4. Leprosy is not directly originated by the use of any particular article of food, nor by any climatic or telluric conditions, nor by insanitary surroundings, neither does it peculiarly affect any race or caste. "5. Leprosy is indirectly influenced by insanitary surroundings, such as poverty, bad food, or deficient drainage or ventilation, for these by causing a predisposition increase the susceptibility of the individual to the disease. "6. Leprosy, in the great majority of cases, originates de novo, that is, from a sequence or concurrence of causes and conditions dealt with in the Report, and which are related to each other in ways at present imperfectly known." The practical suggestions of the Commission for preventive treatment included voluntary isolation, prohibition of the sale of articles of food by lepers, leper farms, orphanages, and "improved sanitation and good dietetic conditions" generally. Serum-therapy has been attempted on behalf of the French Academy of Medicine, but without success. Many forms of treatment ameliorate the miserable condition of the leper, but up to the present no curative agent has been found. Diplococcus of Pneumonia Diplococcus of Pneumonia Pneumonia. Some of the difficulty which has surrounded the bacteriology of inflammation of the lungs is due to the confusion arising from supposing that attacks of the disease differed only in degree. Pneumonia, however, has various forms, arising now from one cause, now from another. The specific or croupous pneumonia is associated with two organisms: Fraenkel's diplococcus and FriedlÄnder's pneumo-bacillus. Several other bacteria have from time to time been held responsible for pneumonia, a streptococcus re The diplococcus of Fraenkel is a small, oval diplococcus found in the "rusty" sputum of croupous pneumonia. It is non-motile, non-liquefying, and aËrobic. When examined from cultures the diplococci are frequently seen in chains, not unlike a streptococcus, and there is some reason to suppose that this form gave rise to the belief that it was another species; when examined from the tissues it possesses a capsule, but in culture this is lost. It is difficult to cultivate, but grows on glycerine agar and blood serum at blood-heat. On ordinary gelatine at room temperature it does not grow, or, if so, very slightly. The ideal fluid is a slightly alkaline liquid medium, and in twenty-four hours a powdery growth will occur in such broth. On potato there is apparently no growth. It rapidly loses its virulence on solid media, and is said to be non-virulent after three or four sub-culturings. A temperature of 54–58°C. for a few minutes kills the bacteria, but not the toxin. This, however, is removed by filtration, and is therefore probably intracellular. It is attenuated by heating to 70°C. Fraenkel's diplococcus occurs, then, in the acute stage of pneumonia, in company with streptococci and staphylococci. It also occurs in the blood in certain suppurative conditions, in pleurisy and inflammation of the pericardium, and sometimes in diphtheria, and therefore it is not peculiar to pneumonia. There is one other point to which attention should be drawn. Fraenkel's organism is said to be frequently present in the saliva of healthy persons. Pneumonia depresses the resistant vitality of the tissues, and thus affords to the diplococcus present in the saliva an excellent nidus for its growth. FriedlÄnder's Pneumo-bacillus is a capsulated oval coccus, assuming the form of a small bacillus. It is inconstant in pneumonia, unequally distributed, and scarce; it is aËrobic, and facultatively anaËrobic; it occasionally occurs in long forms and filaments; it is non-motile, non-liquefying, and has no spores; it does not stain by Gram's method, which stain is therefore used for differential diagnosis; it will grow fairly well in ordinary gelatine at 20°C.; and it is a denitrifying organism, and also an actively fermentative one, even fermenting glycerine. It is not unlike Bacillus coli communis, and to distinguish it from that organism we may remember that the B. coli is motile, never has a capsule, produces indol, and does not ferment glycerine. Bacillus of Influenza Influenza. In 1892, during the pandemic of influenza, Pfeiffer discovered a bacillus in the bronchial mucus of patients suffering from the disease. It is one of the smallest bacilli known, and frequently occurs in chains not unlike a streptococcus. Carron obtained the same organism from the blood. In the bronchial expectoration it can retain its virulence for as long as a fortnight, but it is quickly destroyed by drying. The bacillus is aËrobic, non-motile, and up to the present spores have not been found. It grows somewhat feebly in artificial media, and readily dies out. Blood serum, glycerine agar, broth, and gelatine have all been used at blood-heat. It does not grow at room tem Yellow Fever. Sternberg and Havelburg have both isolated bacilli from cases of yellow fever; but the organism discovered by Sanarelli, the Bacillus icteroides, is now accepted as the causal agent of the disease. It is a small, short rod, with round ends, and generally united in pairs; it has various pleomorphic forms; it grows well on all the ordinary media; it is killed in sea-water at 60°C., and also by direct sunlight in a few hours. Diarrhoea of Infants. From time to time different organisms have been isolated in this diseased condition. Bacillus coli and B. enteriditis sporogenes (Klein) have been held responsible for it. W. D. Booker, of Johns Hopkins University, sums up an extended research into the question as follows: "No single micro-organism is found to be the specific exciter of the summer diarrhoea of infants, but the affection is generally to be attributed to the result of the activity of a number of varieties of bacteria, some of which belong to well-known species, and are of ordinary occurrence and wide distribution, the most important being the streptococcus and Proteus vulgaris. "The first step in the pathological process is probably an injury to the epithelium from abnormal or excessive fermentation, from toxic products of bacteria, or from other factors. "Bacteria exert a direct injury upon the tissues in some instances, whereas in others the damage is brought about indirectly through the production of soluble poisons." Actinomycosis. This disease affects both animals and man. As Professor Crookshank points out, it has long been known in this country, Here we can only mention the most outstanding facts concerning the disease. It is caused by the "ray fungus," or Streptothrix actinomyces, which, growing on certain cereals, often gains entrance to the tissues of man and beast by lacerations of the mucous membrane of the mouth, by wounds, or by decayed teeth. Barley has been the cereal in question in some cases. The result of the introduction of the parasite is what is termed an "infective granuloma." This is, generally speaking, of the nature of an inflammatory tumour composed of round cells, epithelioid cells, giant cells, and fibrous tissue, forming nodules of varying sizes. In some cases they develop to large tumours, in others they soon break down. Actinomycosis in some ways closely resembles tuberculosis in its tissue characters. In the discharge or pus from human cases of the disease small sulphur-yellow bodies may be detected, and these are tufts of "_clubs_" which are the broken-down rays of the parasite; for in the tissues which are affected the parasite arranges itself in a radiate manner, growing and extending at its outer margin and degenerating behind. In cattle the centre of the old ray becomes caseated, like cheese, or even calcified, like a stone. In the human disease abundant "_threads_" are formed as a tangled mass in the middle of the colony. As clubs characterise the bovine actinomycosis, so threads are a feature of the human form of the disease. But in both there is a third element, namely, small round cells, called by some spores, by others simply cocci. Authorities are not yet agreed as to the precise significance and rÔle of these round cells. The life-history of the micro-organism may be summed up thus: "The spores sprout into excessively fine, straight or sinuous, and sometimes distinctly spirilliform threads, which branch irreg Possibly these clubs represent organs of fructification, and produce the spores. These latter are, it is believed, set free in the vicinity of the ray, and create fresh centres of disease. In man the disease manifests itself in various parts according to the locality of entrance. When occurring in the mouth it attacks the lower jaw most frequently. In one recorded case the disease was localised to the bronchi, and did not even extend into the lungs. It was probably contracted by inhalation of the parasite. The disease may spread to distant parts by means of the blood stream, and frequently the abscesses are apt to burrow in various directions. In the ox the disease remains much more localised, and frequently occurs in the lower jaw, palate, or tongue. In the last site it is known as "wooden tongue," owing to the hardness resulting. The skin and subcutaneous tissues are also a favourite seat of the disease, producing the so-called wens or clyers so commonly seen in the fen country (Crookshank). Actinomycosis in cattle is specially prevalent in river valleys, marshes, and on land reclaimed from the sea. The disease occurs at all seasons, but perhaps more commonly in autumn and winter. It is more frequently met with in young animals. The disease is probably not hereditary nor readily communicated from animal to animal. Actinomyces may be cultivated, like other parasitic diseases, outside the body. Gelatine, blood serum, agar, glycerine agar, and potato have been used for this purpose. After a few days on glycerine agar at the temperature of the blood little white shining colonies appear, which in Glanders in the horse and ass, and sometimes by communication in man also, is caused by a short, non-motile, aËrobic bacillus, named, after the old Roman nomenclature (malleus), Bacillus mallei. It was discovered in 1882 by LÖffler and SchÜtz. It is found in the nasal discharge of glandered animals. In appearance the bacillus is not unlike B. tuberculosis, except that it is shorter and thicker. The beading of the bacillus of glanders, like that in tubercle, does not denote spores. B. mallei can be cultivated on the usual media, especially on glycerine agar and potato. On the latter medium it forms a very characteristic honey-like growth, which later becomes reddish-brown. In the horse glanders particularly affects the nasal mucous membrane, forming nodules which degenerate and emit an offensive discharge. From the nose, or nasal septum, as a centre, the disease spreads to surrounding parts. It may also occur as nodules in and under the skin, when it is known as "farcy." Persons attending a glandered animal may contract the disease, often by direct inoculation. Mallein is a substance analogous to tuberculin, and is made by growing a pure culture of Bacillus mallei in glycerine-veal broth in flat flasks, with free access of calcined air. After a month's growth the culture is sterilised, filtered, concentrated, and mixed with an equal volume of a .5 per cent. solution of carbolic. The dose is 1 cc., and it is used, like tuberculin, for diagnostic purposes. If the suspected animal reacts to the injection, it is suffering from glanders. Swine fever, foot-and-mouth disease, chicken cholera, dysentery, rinderpest, and other diseases of animals have micro-organisms intimately related to them. There is a group of diseases due to the presence in the blood or tissues of hÆmatozoa, that is, protozoa which can live and perform their function in the blood. Amongst these are malaria, sleeping sickness, and other tropical diseases in man, and surra and various hÆmatozoa in horses, fish, frogs, or rats. Malaria. Although a Bacillus malariÆ has been described as the cause of this disease, it is now almost universally supposed that the true cause is a protozoan parasite. In 1880 Laveran first described this organism, and the discovery was confirmed by Marchiafava, Celli, and others. Laveran claimed that it occurred in four different forms during the progress of its life-history: (a) Spherical or Irregular Bodies attached to the blood corpuscle, or free in the blood plasma. They are a little smaller than the blood-cells, and may or may not contain pigment. They eventually invade the corpuscles, possess more pigment, and lose their amoeboid movement. Within the red blood corpuscles they increase in size until they reach the adult stage. (b) Segmentation Forms, often assuming a rosette shape, follow next. They are pigmented, are possibly a sporing stage, and are finally set free in the blood. (c) The Crescents, or Semilunar Bodies, are free in the blood, but motionless. They are colourless, have a distinct membrane, and generally show a little pigment about the middle; they taper towards the poles. They appear in the blood after the fever has existed for some time, occurring (d) The Flagellated Bodies apparently occur only in the blood outside the body. They are extracorpuscular bodies, and possess several long flagella, and are therefore actively motile. They are derived from the crescents or irregular intracorpuscular bodies. What is the precise significance of these various forms and modifications of them is not at present known. Possibly the semilune is a resting stage inside the body, and the flagellated body another similar stage outside. Attempts to cultivate the parasite outside the body have failed. There is a good deal of evidence to show that the mosquito is the host outside the human body. There may be different forms and varieties of parasite, if not actually different species, causing the diverse forms of clinical malaria. The above account of diseases caused by bacteria does not profess to be in any sense exhaustive. It is merely illustrative. It reveals some of the disease-producing powers of micro-organisms. There are a large number of other diseases in which bacteria have been found. They are not the causes, but only accidentally present or associated with "secondary infection." Variola (small-pox), scarlet fever, and measles are excellent examples. It is possible that the danger at the present time is rather in the direction of supposing that every disease will readily yield its secret to the bacteriologist. Such, of course, is not the case. Nevertheless, as in the past, so in the future, constant research and patient investigation is the only hope we have for the elucidation of truth in respect to the causes of disease. |
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