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Previous epidemiologic studies have shown that most primary atypical pneumonia illnesses in which cold agglutinins develop are associated with the agent first described by Eaton, Meiklejohn, and van Herick in 1944 (1-8). In addition the agent causes a spectrum of effects ranging from inapparent infection to febrile respiratory disease without pneumonia (5, 6).Recent studies have established that the organism, previously known as "primary atypical pneumonia virus" or "Eaton agent", is not a virus but a member of the genus Mycoplasma (pleuropneumonia-like organisms) (9-11). Thus, at least 30 strains have been grown in cell-free semisolid or liquid medium containing bovine heart infusion, yeast extract, and horse serum (10-13). Growth does not occur in the absence of serum or a suitable substitute such as egg yolk (10, 14). The colonies which grow on semisolid *agar medium exhibit a colonial morphology and fine structure characteristic of Mycoplasma (10). Certain microbial inhibitors such as thallium acetate, penicillin, and amphotericin B do not affect growth of the organism (10, 11). The agent is inhibited, however, by the tetracycline group of antibiotics (15).Until recently only four species of mycoplasma were known to infect man. These are M. hominis type 1, M. hominis type 2, M. salivarium, and M. fermentans. (16-18). When the atypical pneumonia organism was compared with these species by immunofluorescence or complement-fixation tests it was antigenically distinct (10, 19-21). It resembles M. fermentans in utilizing glucose and other sugars (22). The agent differs biologically from the four recognized human species of Mycoplasma by its ability to produce rapid and complete hemolysis of guinea-pig and horse red cells (23, 24). Under 662 R. M. CHANOCK

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SummaryA report is represented on a 44-year-old patient suffering, since 1938, from very slowly progressive rheumatoid arthritis. Haemorrhagic manifestations have been seen since 1951 (large cutaneous and muscular haemorrhages, microhaematuria and macrohaematuria, possibly also articular haemorrhages). In addition to an extremely marked increase in γ-globulins to values above 8 g/100 ml (γ-globulins with a normal sedimentation constant S 7) a circulating anticoagulant was demonstrable, which is held responsible for the marked increase in clotting time, “prothrombin” time and thrombin time. The hypothesis is forwarded that this is a physiological anticoagulant showing a marked increase. Since it is different from the four antithrombins described by Seegers it is referred to as antithrombin-V. Antithrombin-V occurs both in the plasma and in the serum and appears to be bound to the (ß)γ-fraction. It is a thrombin inhibitor which, unlike antithrombin-II, has no direct effect on thromboplastin and thrombin formation. Antithrombin-V cannot be neutralized by protamine sulphate; it is heat-stable, not dialysable and not adsorbed onto BaSO4. Thrombelastography made it possible clearly to demonstrate that an increase in antithrombin-V is associated with a marked increase in clotting time but causes no pathological course of clot formation.Therapeutic results obtained with ACTH and cortisone are favourable: the activity of antithrombin-V decreases parallel with a decrease in γ-globulin values, and the clotting time is normalized. The patient has received, during the past 16 months, oral cortisone treatment (25 mg thrice daily), and is at present free of complaints, although clinical and laboratory findings show a gradual increase in symptoms respectively γ-globulin values with a slight increase in clotting time.The possible significance of the antithrombin-V activity in the protection against thrombo-embolism is briefly mentioned.

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