The extremely virulent parasite, which kills its host, will die with the host unless it has effected a means of exit before its death and escapes into a new host. For this reason Pasteur failed to exterminate the rabbits of Australia. He believed that with races of the bacillus of rabbit septicemia, which were very virulent, and which destroyed life very quickly, all that would be necessary was to start the disease among the rabbits of Australia and that it would tend to spread and would kill off all of the rabbits. But the parasite killed the animals before it had perfected for itself a means of escape from the body and thereupon died.
“From the biologic standpoint which I have endeavored to present, we may conceive of all highly pathogenic bacteria as incompletely adapted parasites, or parasites which have escaped from their customary environment into another in which they are struggling to adapt themselves, and to establish some equilibrium between themselves and their host. The less complete the adaptation, the more virulent the disease produced. The final outcome is a harmless parasitism or some well-established disease of little or no fatality, unless other parasites complicate the invasion. The logical inference to be drawn from the theory of a slowly progressive parasitism would be that in the long run mortality from infectious diseases would be greatly reduced through the operation of natural causes. But morbidity would not be diminished, possibly greatly increased by the wider and wider diffusion of these parasites, or potential disease producers. The few still highly mortal plagues would eventually settle down to sporadic infections or else disappear wholly because of adverse conditions to which they cannot adapt themselves.
“In this mutual adaptation of microorganism to host, there is, however, nothing to hinder a rise in virulence in place of the gradual decline if proper conditions exist. In fact, it is not very difficult to furnish adequate explanations for the recrudescence and activities of many diseases today, though the natural tendencies are toward a decline in virulence. In the more or less rapid changes in our environment due to industrial and social movements the natural equilibrium between host and parasite established for a given climate, locality, and race or nationality is often seriously disturbed and epidemics of hitherto sporadic diseases result.
“These illustrations indicate that so-called natural law does not stand in the way of our having highly virulent types of disease, if we are ignorant enough to cultivate them. The microorganism is sufficiently plastic to shape itself for an upward as well as a downward movement. Among the most formidable of the obstacles toward a steady decline of mortality is the continual movement of individuals and masses from one part of the world to another, whereby the partly adapted parasites become planted as it were into new soil and the original equilibrium destroyed. These various races of disease germs become widely disseminated by so-called germ carriers, and epidemics here and there light up their unseen paths.”
An example of increasing virulence from changing environmental conditions, is the experience in the United States Army camps in 1917 and 1918 with the streptococcus. This microorganism, which at first was but a secondary invader, particularly to measles, became so exalted in virulence that it soon became the cause of primary disease. This is likewise true of the various secondary invaders of the influenza epidemics. They become so highly virulent that they dominate the picture in the later stages. The organisms included in this group are particularly the streptococcus, the various pneumococci, and the meningococcus. Probably the tubercle bacillus should be added to this list.
It requires a certain amount of time for such organisms to attain increased virulence. The earliest cases in any epidemic are comparatively very mild. Thus Major Billings, epidemiologist at Camp Custer, says that for the first five days of the autumn influenza epidemic in that camp the cases admitted to the hospital were very mild in character and were recorded as simple bronchitis and pharyngitis, of no great severity, the majority soon recovering. Five days after the first case was admitted, however, the entire symptom complex seemed to change, and the cases admitted to the hospital from then on were a very different and much more severe type. Major Billings, after going over the records, feels that both types of cases were the same disease, the second being a more severe form. Woolley reports essentially the same condition from Camp Devens.
The same phenomena were found in 1889. During the 1889 epidemic Prudden examined by current bacteriologic methods seven cases of influenza and six cases of influenza-pneumonia. In them he found staphylococcus pyogenes aureus, streptococcus pyogenes, diplococcus pneumoniae, and in other cases he found a streptococcus. He concludes that the use of culture methods and media commonly employed has brought to light no living germ which there is reason to believe has anything to do with causing the disease. He emphasizes the probable importance of streptococcus pyogenes in particular in inducing the various complications.
At this point we should include for the sake of completeness reference to a recent theory propounded by Sahli explaining influenza epidemics, a theory to which we do not subscribe. He believes that the pneumococcus, the streptococcus, the influenza bacillus, and possibly other organisms, form a complex group, an obligate complex, a symbiosis, a higher unit, which infects the organism as a unit. It is all of these organisms acting together which produce the influenza. After infection has occurred one or the other member of the group may develop preferentially. In favor of this he says that in one of his cases the sputum was swarming with influenza bacilli on one day, and that the next day the sputum was a thick pure culture of the pneumococcus. He says that if an ultramicroscopic germ should yet be discovered this would not invalidate the theory, but would merely add another member to the group forming the obligate complex virus unit.
Meteorologic conditions.—Formerly attempts were made to demonstrate etiologic relationships between the occurrence of influenza and unusual conditions of the atmosphere. In most cases no relationship has been discovered. Nevertheless it is conceivable that the changes in the atmosphere, particularly seasonal variations, might influence the virulence of the organism. It has been found that nearly all of the many epidemics apparently originating in Russia took their origin there either in the late autumn or in the winter months. The spread of influenza appears to be uninfluenced by atmospheric conditions, but the severity of the disease is definitely increased in the winter months, and Leichtenstern believes that the development of a primary spread from its point of origin is also influenced by the season. Hirsch found that out of 175 correlated pandemics or epidemics, 50 occurred in the winter between December and February, 85 in the spring from March to May, 16 in the summer from June to August and 24 in the autumn.
The soil plays no part in the spread of the disease. It prevails on every soil or geologic formation; on the mountain top, in the low malarial swamps, in the tropics and within the arctic circle. Volcanic eruptions, fogs, electrical conditions, ozone, direction of the wind, have all been considered in previous epidemics and successively eliminated as etiologic factors.