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CAT-SCRATCH FEVER has become a newly recognized clinical entity, separable from other regional adenopathies by means of a specific skin test. This entity has also been termed nonbacterial regional lymphadenitis1 and, more recently, benign inoculation lymphoreticulosis.2 It was first reported in this country by Greer and Keefer 3 and since then, many hundreds of cases have been recorded (references 4-6 among others). These reports have outlined well the usual clinical course and some have even associated chronic lymphadenitis with cat-scratch syndrome.1,5,7 Rarely a lymph node may remain enlarged for one to two years.4,5The case presented below is that of a recurrence over two years after the initial lesion. Report of a CaseBD, a 13-year-old white female, presented herself on Dec 5, 1961, with the chief complaint of a tender swelling in the right femoral triangle, of one month's duration. She was accompanied by her 17-year-old sister, (RD), who gave a similar complaint involving the left inguinal area. Neither patient had had any systemic :ompIaints or fever during their illnesses. Each had received a course of tetracycline and BD had also received a sulfonamide in spite of which the bubos :ontinued to increase in size. Abnormal physical findings in both patients were limited to the areas of local lymphadenopathy, where tX4 cm, firm, slightly tender, swellings were palpated. These nodes were fixed to the overlying skin which ¡vas slightly red.A complete blood count was normal. Urinalysis was lormal. Tuberculin tests were negative. Both patients reacted to an intradermal injection of a properly jrepared and standardized cat-scratch antigen; BD îad a 1X1 cm area of induration surrounded by 5X4 cm area of erythema, and RD had a 0.6X0.6 cm irea of induration surrounded by 3X3 cm area of erythema. One week later, a vaccinia-type reaction

Five additional cases of galactosemia are added to the steadily increasing number of reports in the literature. A follow-up note is included regarding a sixth case in a patient now 18 years of age, previously reported from this hospital. Two of these cases developed cirrhosis of the liver in a manner suggesting that galactosemia per se was the cause. Histologic examination of the liver in both cases confirmed the anatomic diagnosis. A 10 year follow-up on Mason and Turner's reported Case 7 demonstrates that the illness is chronic but that with advancing years, demonstrable evidence of somatic damage is lacking. Mental retardation is a common complication of the disorder in the present investigators' experience. Cirrhosis of the liver accompanying galactosemia appears to be reversible, so far as can be determined.