Читать книгу The Fundamentals of Bacteriology - Charles Bradfield Morrey - Страница 6

The transmission of disease from person to person was recognized by the ancients of European and Asiatic countries. Inoculation of smallpox was practiced in China and India probably several thousand years ago and was introduced by Lady Mary Wortley Montague into England in 1721, from Constantinople. These beliefs and practices do not seem to have been associated with any speculations or theories as to the cause of the disease.

Apparently the first writer on this subject was Varo, about B.C. 70, who suggested that fevers in swampy places were due to invisible organisms. The treatment of wounds during the thirteenth and fourteenth centuries by hot wine fomentations and by the application of plasters was based on the theory that the air brought about conditions in the wounds which led to suppuration. These practices were indeed primitive antisepsis, yet were not based on a germ theory of the conditions which were partially prevented. Fracastorius (1484–1553), in a work published in 1546, elaborated a theory of “disease germs” and “direct and indirect contagion” very similar to modern views, though based on no direct pathological knowledge. Nevertheless Kircher (mentioned already) is usually given undeserved credit for the “contagium vivum” theory. In 1657 by the use of simple lenses he observed “worms” in decaying substances, in blood and in the pus from bubonic plague patients (probably rouleaux of corpuscles in the blood, certainly not bacteria in any case). Based on these observations and possibly also on reading the work of Fracastorius, his theory of a “living cause” for various diseases was published in 1671, but received little support.

The discoveries of Leeuwenhoek which proved the existence of microscopic organisms soon revived the “contagium vivum” idea of Kircher. Nicolas Andry in a work published in 1701 upheld this view. Lancisi in 1718 advanced the idea that “animalcules” were responsible for malaria, a view not proved until Laveran discovered the malarial parasite in 1880.1 Physicians ascribed the plague which visited Southern France in 1721 to the same cause, and many even went so far as to attribute all disease to animalcules, which brought the theory into ridicule. Nevertheless the “contagium vivum” theory survived, and even Linnaeus in his Systema Naturæ (1753–6) recognized it by placing the organisms of Leeuwenhoek, the contagia of diseases and the causes of putrefaction and fermentation in one class called “Chaos.”

Plenciz, a prominent physician and professor in the Vienna Medical School, published in 1762 a work in which he gave strong arguments for the “living cause” theory for transmissable diseases. He taught that the agent is evidently transmitted through the air and that there is a certain period of incubation pointing to a multiplication within the body. He also believed that there was a specific agent for each disease. His writings attracted little attention at the time and the “contagium vivum” theory seems to have been almost lost sight of for more than fifty years. Indeed, Oznam, in 1820, said it was no use to waste time in refuting hypotheses as to the animal nature of contagium.

Isolated observers, were, however, keeping the idea alive, each in his own locality. In 1787 Wollstein, of Vienna, showed that the pus from horses with glanders could infect other horses if inoculated into the skin. Abilgaard, of Copenhagen, made similar experiments at about the same time. In 1797 Eric Viborg, a pupil of Abilgaard’s, published experiments in which he showed the infectious nature not only of the pus but also of the nasal discharges, saliva, urine, etc., of glandered horses. Jenner in 1795–98 introduced vaccination as a method of preventing smallpox. This epoch-making discovery attracted world wide attention and led to the overcoming of this scourge which had devastated Europe for centuries, but contributed little or nothing to the question of the causation of disease. Prevost’s discovery of the cause of grain rust (Puccinia graminis) in 1807 was the first instance of an infectious disease of plants shown to be due to a microscopic plant organism, though not a bacterium in this case.

Doubtless one reason why the work on glanders and grain rust attracted little attention among the practitioners of human medicine was owing to the prevalent belief in man’s complete separation from all lower forms of life. The evolutionists had not yet paved the way for experimental medicine.

In 1822 Gaspard showed the poisonous nature of material from infected wounds by injecting it into animals and causing their death. Tiedemann (1822), Peacock (1828) described “little bodies” in the muscles of human cadavers which Hilton (1832) considered to be parasitic in nature. Paget (1835) showed that these bodies were round worms and Owen (1835) described them more accurately and gave the name Trichina spiralis to them. Leidy (1846) found organisms in the muscles of hogs which he considered to be the same as Owen’s Trichina and paved the way for the work of Zenker (1860) in showing the pathological relation between the Trichina of pork and human Trichinosis. Bearing on the “contagium vivum” theory was the rediscovery of the “itch mite” (Sarcoptes scabiei) by Renucci (1834), an Italian medical student. This had been declared several hundred years before but had been lost sight of. Chevreuil and Pasteur, in 1836, showed that putrefaction did not occur in meat protected from contamination, and suggested that wound infection probably resulted from entrance of germs from without. Bassi, investigating a disease of silkworms in Italy, demonstrated that a certain mold-like fungus (Botrytis bassiana) was the cause in 1837. This was the first instance of a microscopic vegetable organism proved to be capable of causing disease in an animal.

Boehm, in 1838, observed minute organisms in the stools of cholera patients and conjectured that they might have a causal connection with the disease. Dubini of Milan in 1838 discovered the Ankylostoma duodenale which later was further described by Omodei in 1843 and shown to be the cause of Egyptian chlorosis by Griesinger (1851). The fungous nature of favus, a scalp disease, was recognized by Schönlein in 1839, and the organism was afterward called “Achorion schoenleinii.” Berg, in 1839–41, showed that thrush is likewise due to a fungus, “Oidium albicans.”

These discoveries led Henle, in 1840, to publish a work in which he maintained that all contagious diseases must be due to living organisms, and to propound certain postulates (afterward restated by Koch and now known as “Koch’s postulates” p. 233) which must be demonstrated before one can be sure that a given organism is the specific cause of a given disease. The methods then in vogue and the instruments of that period did not enable Henle to prove his claims, but he must be given the credit for establishing the “contagium vivum” theory on a good basis and pointing the way for men better equipped to prove its soundness in after years.

PLATE II

SIR JOSEPH LISTER

In 1842–43 Gruby showed that Herpes tonsurans, a form of ringworm, is due to the fungus Trichophyton tonsurans. Klencke, in 1843, produced generalized tuberculosis in a rabbit by injecting tuberculous material into a vein in the ear, but did not carry his researches further. In 1843, Doctor Oliver Wendell Holmes wrote a paper in which he contended that puerperal fever was contagious. Liebert identified the Peronospora infestans as the cause of one type of potato rot in 1845. The skin disease Pityriasis (tinea) versicolor was shown to be due to the Microsporon furfur by Eichstedt in 1846. In 1847 Semmelweiss of Vienna recommended disinfection of the hands with chloride of lime by obstetricians because he believed with Holmes in the transmissibility of puerperal fever through poisons carried in this way from the dissecting room but his theories were ridiculed.

PLATE III

ROBERT KOCH

Pollender, in 1849, and Davaine and Rayer, in 1850, independently observed small rod-like bodies in the blood of sheep and cattle which had died of splenic fever (anthrax). That Egyptian chlorosis, afterward identified with Old World “hookworm disease,” is caused by the Ankylostoma duodenale was shown by Greisinger in 1851. In the same year the Schistosomum hematobium was shown to be the cause of the “Bilharzia disease” by Bilharz. Küchenmeister discovered the tapeworm, Tænia solium, in 1852, Cohn, an infectious disease of flies due to a parasitic fungus (Empusa muscæ) in 1855, and Zenker showed the connection between trichinosis of pork (“measly pork”) and human trichinosis (1860) as indicated above. The organisms just mentioned are, of course, not bacteria, but these discoveries proved conclusively that living things of one kind or another, some large, most of them microscopic, could cause disease in other organisms and stimulated the search for other “living contagiums.” In 1863 Davaine, already mentioned, showed that anthrax could be transmitted from animal to animal by inoculation of blood, but only if the blood contained the minute rods which he believed to be the cause. Davaine later abandoned this belief because he transmitted the disease with old blood in which he could find no rods. It is now known that this was because the bacilli were in the “spore” form which Davaine did not recognize. He thus missed the definite proof of the bacterial nature of anthrax because he was not familiar with the life history of the organism which was worked out by Koch thirteen years later. In 1865 Villemin repeatedly caused tuberculosis in rabbits by subcutaneous injection of tuberculous material and showed that this disease must be infectious also. In the same year Lord Lister introduced antiseptic methods in surgery. He believed that wound infections were due to microörganisms getting in from the air, the surgeon’s fingers, etc., and without proving this, he used carbolic acid to kill these germs and prevent the infection. His pioneer experiments made modern surgery possible. In this year also, Pasteur was sent to investigate a disease, Pebrine, which was destroying the silkworms in Southern France. He showed the cause to be a protozoan which had been seen previously by Cornalia and described by Nägeli under the name Nosema bombycis and devised preventive measures. This was the first infectious disease shown to be due to a protozoan. In 1866 Rindfleisch observed small pin-point-like bodies in the heart muscle of persons who had died of wound infection. Klebs, in 1870–71, published descriptions and names of organisms he had found in the material from similar wounds, though he did not establish their causal relation. Bollinger, in 1872, discovered the spores of anthrax and explained the persistence of the disease in certain districts as due to the resistant spores. In 1873 Obermeier observed in the blood of patients suffering from recurrent fever long, flexible spiral organisms which have been named Spirochæta obermeieri. Lösch ascribed tropical dysentery to an ameba, named by him Amœba coli, in 1875. Finally, Koch, in 1876, isolated the anthrax bacillus, worked out the life history of the organism and reproduced the disease by the injection of pure cultures and recovered the organism from the inoculated animals, thus establishing beyond reasonable doubt its causal relationship to the disease. This was the first instance of a bacterium proved to be the cause of a disease in animals. Pasteur, working on the disease at the same time, confirmed all of Koch’s findings, though his results were published the next year, 1877. Bollinger determined that the Actinomyces bovis (Streptothrix bovis) is the cause of actinomycosis in cattle in 1877. Woronin in the same year discovered a protozoan (Plasmodiophora brassicæ) to be the cause of a disease in cabbage, the first proved instance of a unicellular animal causing a disease in a plant. In 1878 Koch published his researches on wound infection in which he showed beyond question that microörganisms are the cause of this condition, though Pasteur in 1837, had suggested the same thing and Lister had acted on the theory in preventing infection.

These discoveries, especially those of Koch, immediately attracted world-wide attention and stimulated a host of workers, so that within the next ten years most of the bacteria which produce disease in men and animals were isolated and described. It is well to remember that the first specific disease of man proved to be caused by a bacterium was tuberculosis, by Koch in 1882.

Progress was greatly assisted by the introduction of anilin dyes as suitable stains for organisms by Weigert in 1877, by Koch’s application of special technic and gelatin cultures for isolation and study, 1881, and the great improvements in the microscope by Prof. Abbé, of Jena.

Laveran’s discovery of the malarial parasite in 1880 turned attention to protozoa as the causes of disease and led to the discovery of the various piroplasmoses and trypanosomiases in man and the lower animals.

Pasteur’s protective inoculations in chicken cholera and anthrax directed attention to the possibility of using bacteria or their products as a specific protective or curative means against particular diseases. This finally led to the discovery of diphtheria antitoxin by Behring, and independently by Roux, in 1890, a discovery which opened up the wide field of immunity which is so persistently cultivated at the present time.

PLATE IV

LOUIS PASTEUR

While the causation of disease by bacteria has probably attracted most attention, especially in the popular mind, it should not be forgotten that this is but one of the numerous ways in which these organisms manifest their activities, and in a sense it is one of their least-important ways, since other kinds are essential in many industries (dairying, agriculture) and processes (sewage purification) and are even indispensable for the very existence of all green plants and hence of animals, including man himself.