Etiology and Epidemiology
Etiology.—In a study of this disease Futaki and others discovered a spirochaete in the tissues of the bite area and the adjacent lymphatic glands (1915). These spirochaetes were about 10 microns long. In the blood of man and infected animals shorter and thicker spirochaetes are found (3 to 6 microns). When cultivated in the media used for other Leptospira we have longer forms up to about 20 microns. The shorter forms are considered as young organisms.
Leptospira morsus-muris is found in the blood of infected mice, rats or guinea pigs during the first two weeks and then becomes distributed in the connective tissues especially that of the lips, bridge of nose and tongue. They are not secreted in the saliva but the transfer seems to occur by a break in the spirochaete-containing tissues and thus inoculated into the bite wound. The organism may possibly be excreted in the urine.
Epidemiology.—It has been found that about 3% of house-rats in Japan are carriers of the disease. It is less frequent in other countries although reported from various European countries, America and especially China. The disease has also been reported from Australia. It seems probable that the construction of the Japanese houses gives greater opportunity for the occurrence of bites of rats than elsewhere.
Fig. 51.—Spirochaeta (morsus) muris in lung of mouse inoculated with blood from human rat bite fever. Silver impregnation. × 1500. (From MacNeal. After Futaki, Takaki, Taniguchi and Osumi.)
Fig. 52.—Spirochaeta (morsus) muris in blood of guinea pig with experimental-rat-bite fever. Giemsa’s stain. × 1250. (From MacNeal. After Futaki and associates.)
Pathology
In infected guinea pigs there is swelling of the lymphatic glands and the spleen with the presence of spirochaetes. The liver is congested and may show a few spirochaetes. In human autopsies there are degenerative changes in the liver and kidneys. The infection is rarely fatal in experimental animals although it causes about a 10% mortality in man.