Causes. The disease is transmitted by contagion and almost exclusively in the act of coition. Hayne has seen the affection in geldings, and Haxthausen in mares that had never been served. Schneider, Buffard, Nocard, Blaise and others have transmitted it freely by inoculation of blood and nervous matter, so that the possibility of infection through other channels than the generative organs must be admitted. But such irregular means of casual infection are so rare, and the probability of transmission of the virus from a non-breeding animal is so remote that in the practical measures of sanitary police, the breeding horses alone need be taken into account.
The extra vascularity of the male and female generative organs at the period of coition undoubtedly favors infection, as a latent or apparently recovered case will relapse under its frequent repetition. The abrasion of the epithelial surface also forms infection atria and favors new multiple points of infection.
The disease has occurred congenitally (Rodolff, Jessen). It has been claimed that the higher bred horses with lighter frames are the more susceptible (Fischer), but this is probably a delusion, the disease having been often introduced by the Barb and Arabian and propagated among their grade descendants. The heavy Percheron shows a very ready susceptibility and a virulent and fatal form of the affection.
Microbiology. That the affection was due to a microbe was clearly shown by its absence from every part of the world into which infected horses had not been brought. The secluded countries, Belgium, England, Scandinavia, that breed their own horses, the distant Australia, New Zealand and South America remained free in face of the constant presence of the infection in different parts of Central and Southern Europe, in Africa and Asia. The horses of America and South Africa showed a ready susceptibility to the virus brought by infected horses, and rigorous sanitary police control speedily cleared a district of the trouble.
Thanhoffer found in the blood, vaginal mucous, testicle, semen, spinal fluid, myelon, and roots of the dorsal and lumbar nerves cocci, especially streptococci and less constantly bacilli, to which he attributed the malady. More recently Schneider and Buffard have apparently demonstrated that an infusorian, the trypanosoma of dourine, is the essential pathogenic agent.
The Trypanosoma Equiperdum varies greatly in form at different stages of its growth or in different media. In the exudate of the slight early tumefaction, without as yet other symptoms, it is found as minute granules in groups, as larger spherical very refrangent bodies like very large cocci, each having a strongly staining nucleus, and as larger bodies in which a delicate membranous covering encloses one, two or three masses of chromatin and extends to form one or more points (club-shaped or fusiform). Each chromatin mass has a nucleolus on its outer surface or slightly apart from it. Twenty-four hours later there may be added: First, short, thick chromatin bodies, with two slightly undulating, pointed, membranous prolongations. Second, more delicate, fusiform bodies, each with one chromatin nucleus, a detached nucleolus, and the membrane prolonged into two actively moving flagella. Third, larger pyriform bodies with chromatin nuclei and nucleoli and the membrane prolonged into one or several flagella. Fourth, fusiform bodies, thick or delicate, each having a chromatin nucleus and nucleolus, and arranged singly or in groups of two, four, six or more, united together at one end and diverging at the other to form a stellate mass. These last, 20 to 30μ long by 1.5 to 2μ broad, may perhaps be the adult form of the parasite from which the small granular or spore forms found in the most recent lesions are derived. The fusiform outline, the deep staining central mass, with its adjacent nucleolus, and the pointed or flagellate membranous prolongations, more or less motile or undulating, are characteristic features.
In its morphology and evolutionary forms the trypanosoma of dourine has not been shown to differ from that of surra, nor the nagana or Tsétsé disease, the granule form, the spherical, the club-shaped or pyriform, the fusiform with more or less stellate grouping, are characteristic of all (Lydia Rabinowitsch, Kemper, Schneider, Buffard). The distinction is found in the pathogenesis of the two diseases.
With active cutaneous or mucous lesions, the parasite is usually found abundantly in the blood, sperm, milk, vaginal secretions, and the erosions of the vaginal mucosa or penis. During intermissions, however, and in the absence of local lesions, examination of the blood may fail to detect it, yet its inoculation on a dog will usually produce the affection. It disappears from the blood and tissues with great rapidity after death, so that, to prove successful, inoculations should be made before death or immediately after. They are ineffective after 48 hours.
Schneider and Buffard, Nocard and others found the trypanosoma in the blood and exudates of horses, asses and dogs, suffering from dourine, and failed to find it, in the same localities, in animals of the same species which were free from dourine. The infected blood, preserved for 24 hours in sealed glass tubes, and then inoculated on two dogs produced characteristic dourine, with the extensive production of trypanosoma in the blood, the destruction of blood globules, and the pathognomonic local lesions. Inoculation of two other dogs, with the same material, at the end of 48 hours produced a slight transient hyperthermia only, without local lesions or propagation of the parasite in the blood. The same blood inoculated after 15 days produced neither local lesion nor fever.
Lesions. Horse. In the early stages are found a phlegmonous or œdematous swelling of the sheath, scrotum, penis and inguinal glands and a yellowish liquid effusion into the scrotal cavity. The skin covering these parts may show a papular or vesicular eruption or if this has passed, a mottling with white spots shows where the lesions have been. Later still the inguinal glands are shrunken and have undergone fibroid degeneration and induration and the testicles, swollen or shrunken, contain centres of caseation. The connective tissue of the epididymus and cord is the seat of a gelatinoid exudation. The walls of the scrotum may be greatly thickened and the seat of abscess or of caseous degenerated hyperplasia. In advanced cases the testicles are usually abnormally small even if the scrotal mass is enormously distended. The sheath and penis may be the seat of more or less numerous ulcers, and swellings, contractions and distortions of the latter organ are not uncommon. The penis may, however, retain its normal dimensions. The walls of the lymphatics in the inguinal region may be the seat of hyperplasia, the thickening causing them to stand out like cords as in glanders. In the advanced stages the muscles, especially those of the hind limbs, become pale and atrophied.