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Canine Distemper has already been recognized from a clinical point of view as an infectious disease before the era of bacteriology by Youatt (1830), Renner & Karle (1844), Weiss (1852), Hertwig (1853), Camille Leblanc (1857), Röll (1867), Venuta (1873) and others. Numerous records on its etiology have hitherto been reported.
It was Semmer who, in 1875, first demonstrated a bacterium as the causal agent of the disease. An organism similar to the above was also isolated by Friedberger in 1881. Since that time, many other strains of bacteria have been found in local lesions. Krajewski (1883) isolated diplococci from the tissues and the blood of an infected animal, Laoson (1882) bacilli and diplococci, Rabe (1883) diplococci and streptococci from the pustules, tears and nasal discharge, Mathis (1887) diplococci from the body fluid, pustules, tears and nasal discharge, Marcone and Meloni (1888) micrococci, Millais (1890) a bacillus as the primary and a micrococcus as the secondary causal agent from the lung lesions, Legrain and Jacquot (1890) a motile micrococcus from the pustules, Galli- Valerio an ovoid bacillus from the brain, spinal cord and lungs, Babes and Barzanesco (1895) a motile, Gram-negative, non-sporebearing bacillus from the blood, liver and lungs, Jensen (1896) a streptococcus, Babes and Starcovici (1897) a bacillus resembling the Bacillus typhosus, Taty and Jacquin (1898) a diplococcus from the central nervous system, Jess (1899) a small bipolar bacillus, 1.8-2.3μ in length, 0.6μ in breadth, from the tears, nasal discharge, blood, abdominal fluid and internal organs, Petropawski (1899) a bacillus, Monkton Copeman and Mallais (1900) a Gram-negative coccobacillus, Lignières and Phisalix (1900) a bacillus, Pasteurella canis, from the cardiac blood, and Wunsch heim (1905) a coccobacillus, Bacillus canicidus.
Contrary to those findings above mentioned, Carré (1905-1906) declared that the cause of the disease is an ultramicroscopic virus which passes through bacterial filters, and this opinion has been supported by Vallée, Bosc and McFadyean.
Kregenow, however, was of opinion different from Carré, and later Ferry (1910), McGowan (1910) and Leitch reported that they have proved independently a small, motile Gram-negative, non-sporebearing bacillus, 0.5-2.3μ in length, 0.4-0.5μ in breadth, as the primary causative agent, to which Ferry gave the name Bacillus bronchicanis, subsequently changing this Bacillus bronchisepticus.
Wunschheim, in 1913, described in his report that the disease is caused by the Bacillus paratyphosus B.
As will be seen from the facts referred to above, the cause of the disease is not yet determined. So it will be of interest to study the etiological significance of organisms isolated from various organs, especially from the lungs of the infected animal. For this purpose I have made, in the first place, some experiments upon the transmission of the virus into normal dogs and then upon the isolation of organisms from the lungs and other organs of the infected animal.
The results of these investigations are summarized as follows:
1) The disease could be transmitted into dogs by inoculating an emulsion prepared from the lungs of an infected dog. It is, however, highly probable that some other unknown factors should be required to produce the disease in experimental animals, for the artificial infection showed no constant transmission of this disease.
2) No evidence of infection was found in dogs which were inoculated with filtrate of the emulsion prepared from the affected lungs.
3) In 46 cases or about 85% of 54 affected lungs, a Br. type bacillus, similar to the Bacillus bronchisepticus, was found.
In 50% of these numbers, the bacillus was isolated in pure culture, while in 35% it was found in mixed culture with other organisms-streptococci in 19% and staphylococci in 11%.

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[in Japanese]

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[in Japanese]

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In the veterinary circles carbon disulphide (CS₂) has long been known as an anthelminticum, chiefly used in the treatment of stomach disorders in the horse caused by the larvae of Gastrophilus equi, and of late it is highly recommended by many authors to employ this medicament as a specific for this parasitary disease.
In spite of having an effective anthelmintic property. the toxic action of CS₂ has not yet thoroughly been studied and in connection with this only a few experiments have hitherto been made.
In the books of toxicology by Kobert, Kunkel, Jaksch, etc., we find some descriptions about a number of cases of CS₂intoxication in men, most of them, however, being related to chronic intoxications occurred among workmen in match or rubber factories. Acute cases, in which men have taken CS₂ mistaking it for a drink, are also quoted in those books.
In the case of acute intoxication, according to the results obtained from the experiments with animals, paralysis of the respiratory system first appears, then that of the heart and finally general paralysis followed by coma. If it is the case of a slight intoxication, in which the animal is exposed to the CS2 gas for a short time, then it will easily be recovered under the supply of fresh air, but if exposed for a long time, the animal may die in one or two days, though once recovered. They report that an inhalation of air containing 5 volume % CS₂ gas is enough to kill experimental animals in a few minutes.
As to the subjective and objective symptoms which appear in men in the case of acute or chronic intoxication, they declare that the CS₂ content below 0.8mg in 1 litre of air is not dangerous.
I have made some CS₂ intoxication experiments with mice, guinea-pigs, and rabbits, etc.; from the results obtained I come to the following conclusions.
1) 1.5 volume per cent. CS₂ in the air can be considered as the minimal lethal dose, causing an acute intoxication in an experimental animal, and 3 volume per cent. CS₂ is enough to kill the animal within ten minutes; Thus the result of my experiments is coincident with that of the authors above mentioned, who stated that the air containing 5 volume per cent. CS₂ kills the animal within a few minutes. As already mentioned, if the CS₂ content in 1 litre of air is below 0.8mg, no disturbance will be recognized in the physiological functions of workers in a factory, though the air is stinking. 0.8mg in 1 litre is equal to 0.125 volume per cent. at 15°C and 760mm Hg, so this volume per cent. is less than 1/120 of the minimal lethal dose (1.5 vol. per cent.) obtained in the animal experiments.
2) The phrenic nerves of a rabbit which is in a state of apnoea, intoxicated by inhalation of a certain dose of CS₂, still react to an electric irritation in the same degree as before intoxication. This fact proves that the cause of intoxication death is the paralysis of the respiratory centre. The simultaneous disappearance of the movements of the alae of the nose and the accessory respiratory muscles, and of the movement of the diaphragma also proves that the inhalated CS₂ has given rise to the paralysis of the respiratory centre.
3) The respiration of an animal which breathes the air containing CS₂ at first accelerates, then becomes slow and finally stops. The blood pressure rises with the acceleration of respiration but it suddenly falls down at the stage of apnoea and a few minutes later palpitation of the heart stops.

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