Chapter 12 of 61 · 813 words · ~4 min read

CHAPTER VII

RAT BITE FEVER

DEFINITION

Rat bite fever is a relapsing type of fever following the bite of rats infected with _Leptospira morsus-muris_, which brings about the infection of man with this spirochaete. Following the healing of the wound we have developing in the cicatrix inflammatory signs with lymphangitis and swelling of the tributary lymphatic glands. The onset is sudden with rigors and fever, which latter continues for several days to then fall to normal and after an apyrexial period to be followed by relapse. Numerous relapses follow during the following weeks, months or even years of the disease. In Japan the disease is known by the name of Sodoku.

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.

[Illustration: 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.)]

[Illustration: 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.

SYMPTOMATOLOGY

Following a rather long incubation period of from six to eight weeks, although cases have been reported where not more than two weeks had elapsed from the time of injury, during which time the wound of the rat bite heals, we have a rather sudden onset with headache, nausea and marked weakness. The cicatrix now becomes inflamed and the surrounding tissues show oedema and at times vesicle formation. Leading from the inflamed areas is a line of tender lymphatics which extend to a group of swollen lymphatic glands.

The onset is often characterized by chills and malaise. A rapid pulse and prostration are present during the pyrexial period.

The fever rises rapidly to 101°F. or 102°F. and within two or three days has reached about 104°F. and remains high for two or three more days. About this time it falls rapidly to normal, attended with profuse sweating. The temperature remains normal for a few days, during which time the local swelling and inflammation subside. An eruption of purplish spots may accompany the fever, appearing chiefly on chest and arms. There may be urticarial lesions. Joint pains, together with motor and sensory disturbances, may be noted.

Symptoms of nephritis may appear.

After the critical fall of temperature there is usually an apyrexial period of several days during which time the local manifestations about wound and glands subside. The fever again comes on, to later disappear and reappear.

The successive paroxysms are usually of less severity.

The fever is suggestive of the relapsing fevers. The pulse is rapid and weak. There may be as many as twelve of these febrile accessions and the course of the disease may extend over several months. There is an eosinophilia and during the febrile paroxysm a leucocytosis of about 15,000. The spirochaetes should be looked for in the blood during the early febrile periods. The dark-field illumination is the best method for their demonstration.

TREATMENT

Treatment is entirely symptomatic. Some success seems to have followed the administration of salvarsan.

Strychnine for the heart weakness and tonics during convalescence are recommended.

Aspirin is often necessary to relieve the headache and joint pains.

As prophylactic measures the same precaution should be taken as to cauterization of the wound as one would observe in rabies.

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