Abstract
TWO ETIOLOGIC agents for rat bite fever have been described1— Spirillum minus and Streptobacillus moniliformis. The clinical picture can be caused not only by the bites of rats and other animals2but by the ingestion of infectious material. The Haverhill outbreak of 1926 illustrates the latter mode of infection. In 86 cases reported by Place, Sutton and Willner3the disease was traced to the ingestion of unpasteurized milk and ice cream from a single source Parker and Hudson4isolated Str. moniliformis from the blood in 11 of these cases. In their review, Brown and Nunemaker1dfurther stressed the frequency of Str. moniliformis as the etiologic agent in rat bite fever. Treatment of this disease, until recent years, was limited to the use of arsenicals, gold salts and sulfonamide compounds. The last two have been of no value. The use of neoarsphenamine and oxophenarsine hydrochloride has given apparently
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