The Leucocyte Count in Rheumatic Heart Disease in Childhood.

Cabot' stated that a leucocytosiQ cf about 14,000 per c.mm. was the rule in children suffering from acute rheumatism. Ewing2 considered that mild cases of rheumatism showed no leucocytosis, but that with fever and swelling of the joints a leucocytosis from 10,000 per c.mm. occurred. If the leucocytosis be greater than 20,000 per c.mm. it indicates the presence of some complication. The leucocytes return to normal in defervescence. Quoting Tuirk, he stated that with a total count of under 10,000 per c.mm. the differential count is not disturhed, but that with a greater leucocytosis than this the proportion of polymorphonuclears is increased, and this after defervescence, is followed by an cosinophilia. Macalister3 in 1909 fouind that 8 cases of chorea all showed an eosinophilia to a greater or lesser extent. This was not found to be the case in acute rheumatism, and he considered that this indicated different causes for the two conditions. Bose and Carrieu4, from an examination of 12 cases of acute rheumatism, concluded that this is usually associated with a leucocytosis. There is a relative mononucleosis with a greatly increased number of 'medium, large and very large mononuclears' and occasionally of lymphocytes. In convalescence the mononucleosis persists and is accompanied by an eosinophilia. Leorold5 in 1914 found in 20 cases of chorea an eosinophilia of from 1-16 per cent.; higher in second attacks than in the first. Berger" made a series of counts in 40 children with chorea aged from 7-14 years. He found that all but 5 of these showed an eosinophilia at some stage or other. The highest eosinophilia found was 26 per cent. of the total count, ind the lowest 0 per cent. The averago for the series was 7-6 per cent. The rise and fall of the eosinophilia was unconnected with any change in the clinical course of the illness. No other cause for an eosinophilia could be demonstrated. Swift, Miller and Boots7, by repeated white cell counts, found that cases with a single 'monocyclic' attack of polyarthritis showed a slightleucocytosis which rapidly fell with anti-rheumatic therapy, and showed a light temporary rise on its discontinuance. In cases with a relapsing arthritis the leucocytes tended to remain above normal for a longer period, and were less influenced by therapeutic measures. In cases with a pronounced cardiac lesion, half of whom showed nodules, there was a persistent leucocytosis with occasional falls to normal, followed later by a rise again, and almost entirely uninfluenced by drugs. They conclude that (1) Rheumatic fever is associated with a leucocytosis. (2) The leucocyte curve gives some idea of the severity and duration of the infection. (3) Patients with arthritis and exudative phenomena show a more marked leucocytosis than those with a proliferative reaction, such as myocarditis and nodules. (4) A leucocytosis depressed by anti-rheumatic drugs, indicates a mild infection of short duration. The persistence of the leucocytosis in spite of diugs, or its return on the discontinuance of the administration of the drug, indicates a more persistent infection. (5) Relapses are heralded by a rise in the leucocyte count. Gulland and Goodall8 reported in chorea a slight leucocytosis and, despite contrary reports, no evidence of the constant, or even usual, occurrence of an cosinophilia. In acute rheumatism they found a leucocytosis of 12,000 to 15,000 per c.mm., very rarely exceeding 20,G00 per c.mm. Wilson and Kopel9 found that the average leucocyte count in children with a history of previous rheumatic infection, was 7,000 per c.mm.; in children with evidence of an organic