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A controlled prospective study was made of a group of patients with chronic bronchitis, in which serum antibodies against a group of viruses and Mycoplasma pneumoniae were estimated at regular intervals. Sixteen significant rises in antibody titre were shown, of which eight were associated with clinical acute exacerbations of bronchitis. In individual patients no correlation was found between the number of acute exacerbations or the aetiological agent and persistent change in ventilatory function as expressed by the F.E.V.(0.75).This study was compared with the results of a previous parallel investigation of the same patients done to study the significance of rhinovirus infections. In the present investigation 12% of the acute exacerbations were associated with the 11 agents tested compared with 14% associated with rhinoviruses in the earlier work.

The agents of meningopneumonitis (MN) and of trachoma (TR) purified from chick embryo allantoic fluids and yolk sacs, respectively, were shown to produce CO(2) from the C(1) positions of pyruvate and glutamate, but not from the other carbon atoms. The reaction with pyruvate did not require did not require the addition of cofactors, but was stimulated to a small extent by alpha-lipoic acid and, in the case of TR, also by diphosphothiamine, and nicotinamide adenine dinucleotide (NAD). The reaction of MN with glutamate was greatly stimulated by the addition of NAD and pyruvate, and resulted in the accumulation of alanine. The reaction of TR with glutamate was also greatly enhanced by added NAD, but was not affected by added pyruvate. When eight intermediates of the citric acid cycle were added to MN cells incubated with glutamate-C(14), plus NAD and pyruvate, they reduced to varying degrees the evolution of C(14)O(2). It was shown by chromatography that the C(14) label extended to alpha-ketoglutarate and succinate, but not to fumarate and malate. A net gain in adenosine triphosphate could not be demonstrated in MN cells incubated with combined glutamate, pyruvate, oxaloacetate, and various cofactors. These results furnish additional examples of real or apparent gaps in enzyme sequences in Chlamydia.

Northern Illinois experienced an outbreak of chlamydial infection in 1963, 1964, and 1965, as reflected by an increase in the number of patients showing antibody to this group of agents during the period. Among these individuals, a disproportionately large number with PMD showed serologic activity against Chlamydia. This suggests that there was something distinctive about the response of the PMD patients in the face of this outbreak. The clinical manifestations of heart disease in PMD patients were similar regardless of their serologic status, i.e., whether or not they had antibody of Chlamydia. Specific serum reactivity to Chlamydia was verified by: (1) use of multiple chlamydial antigens, (2) application of both complement-fixation and RIP test systems, and (3) absence of reactivity to uninfected egg tissue or to egg tissue infected with Newcastle disease virus. Reactivity to Chlamydia persisted in our PMD population for periods of months to more than five years. While the evidence cited in this paper linking chlamydial agent to the PMD is inferential and no direct evidence of chlamydial infection was found in the tissue of 12 hearts examined, epidemiologic considerations strongly suggest an etiologic relationship.

conjunctival cells. Although viruses closely related to psittacosis occur in many avian and mammalian species, as described by Meyer (1962), the only viruses morphologically similar to psittacosis which are known to be pathogenic for the conjuctiva occur in man as trachoma and inclusion conjunctivitis. They are described by Thygeson (1959). The present paper describes (a) the isolation of 14 strains of a virus subse