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The object of this investigation was to evaluate the use of aureomycin in obstetric patients. Since the advent of the sulfonamide drugs and penicillin investigators have continued to search for new antibiotics which would be effective and less toxic. One of the products of this search, aureomycin, was discovered by Duggar in 1948.1 Extensive bacteriologic and clinical studies have established the effectiveness of this agent in a wide variety of infections. Its mode of action, as determined in vitro, is predominately bacteriostatic, but it also possesses bactericidal properties at high concentration. Because of the promising results reported with aureomycin, including its use in obstetric complications,2 a study of this drug and its effect on the bacteriologic flora and infections during pregnancy and the puerperium was believed warranted. MATERIAL AND METHODS Aureomycin was prescribed according to various dosage schedules as noted under the individual descriptions. The in vitro studies

Primary atypical nonbacterial pneumonia has been reported with increasing frequency during the past fifteen years.1 This disease has since received particular attention. The intensive studies on disease of the respiratory tract conducted during World War II served to differentiate "primary atypical pneumonia" from similar pulmonary infections of established bacterial, viral or rickettsial causes.2 Clinically, diseases caused by the viruses of influenza, psittacosis, ornithosis and the rickettsiae of Q fever resemble atypical pneumonia.2 No causative agent has been isolated from patients suffering from this disease, although pooled sputum from patients has been shown to be capable of inciting the disease in human volunteers, even after it was passed through Corning sintered glass or Seitz filters.3 At present, there is no specific laboratory procedure available for confirming the clinical diagnosis. It has been noted that cold hemagglutinins and agglutinins for Streptococcus MG often develop in the serum of

Aureomycin is an antibiotic derived from a strain of Streptomyces aureofaciens).1 It has been found to protect mice and guinea pigs infected with the rickettsia of Q fever, Rocky Mountain spotted fever, murine typhus and rickettsial pox.2 The drug is readily absorbed after oral administration. Although quantitative assay in the body fluids has not been satisfactory, low levels (0.3 to 2.5 micrograms per millimeter) have been detected in the blood serum and levels up to 320 micrograms per milliliter3 in the urine. Pharmacologic studies in animals have shown that the toxicity of the drug is low except after intravenous administration where hemoglobinuria and anemia have been noted.4 In human beings, therapeutic doses up to 60.0 milligrams per kilogram of body weight per day given orally have not been associated with any toxic manifestations except for occasional nausea and vomiting.5 The latter has been transient and

An analysis of some of the physiological factors active in Maitland tissue cultures has been presented in the hope that it may be of some value in clarifying the principles underlying tissue cultures in general. It has been found that the empirically determined necessity of using relatively small amounts of tissue in such cultures is dependent upon the fact that excessive tissue leads to a rapid change of reaction toward the acid side. Whereas tissue may remain viable in an environment as alkaline as pH 9 and over, viability is rapidly destroyed when the reaction approaches pH 6. Evidence is presented to indicate that the changes in electrode potentials which take place in Maitland cultures are not, as has been suggested, the determining factors upon which virus multiplication depends, although they may, of course, be incidentally important. It has been shown that there are fundamental differences between those conditions in Maitland cultures which favor the multiplication of a typical virus and those upon which the growth of the Rickettsiae of typhus fever depends. The virus which we have studied (equine encephalitis virus, western type) multiplies during the period of active tissue metabolism. The maximum virus titrations are obtained at about the time at which metabolism has come to a standstill. Thereafter the virus not only ceases to increase but rapidly deteriorates. The period of viability of the tissue cells themselves is shortened by several days in the presence of virus multiplication. There is some evidence that a temporary acceleration of oxygen uptake takes place during the time of active virus multiplication. Technical difficulties in controlling such experiments prevent certainty in regard to this point. In contrast with the conditions determining the growth of a virus agent in the Maitland cultures the multiplication of Rickettsiae does not begin to any determinable extent until after active cell metabolism has either become stabilized or has ceased. The Rickettsiae continue to grow at a time when the cells are no longer viable. It appears likely that these organisms find the most favorable conditions for growth in cells which are no longer metabolically active but in which some delicately heat-susceptible elements have not yet been disturbed. As a consequence of these observations, frozen and preserved embryonic tissues have been successfully used for Rickettsia cultivation. A report on these experiments will be made in a separate communication.

The presence of riboflavin, pantothenic acid, and biotin could not be demonstrated in significant amounts in moderately concentrated solutions of purified tobacco-mosaic virus.

Local tetanus limited to one leg was studied in cats after intramuscular injection of tetanus toxin. 1. The electric and mechanical response of the affected muscle after a single stimulus to the intact sensory-motor nerve is greater in amplitude and duration than the response of the corresponding muscle of the unaffected leg (Fig. 1). 2. This augmented response of the muscle is associated with an augmented response arising from the ipsilateral portion of the spinal cord, while the contralateral part of the cord is unaffected, as demonstrated by electrographic records from the motor nerves (Figs. 2 to 5). 3. The augmented muscular response is abolished when the reflex arc is broken, but the augmented response in the spinal cord is independent of changes in the muscle, the neuromuscular junction, the afferent and efferent peripheral nerves, and the dorsal root ganglia. 4. The augmented spinal response develops in the absence of the peripheral signs of local tetanus. Hence the pathogenesis of the altered state in the spinal cord is independent of the peripheral effects of the toxin. 5. In local tetanus, therefore, the toxin injected intramuscularly acts selectively upon the segments of the spinal cord which supply the innervation of the injected area. 6. The augmented spinal response may be prevented by section of the nerve trunks supplying the area of injection prior to the injection of the toxin. 7. It is concluded that in local tetanus the toxin is carried to the spinal cord by way of peripheral nerves.