Compared with a 9-month isoniazid regimen, a 4-month rifampin regimen was associated with a higher percentage of patients completing treatment and a lower percentage of patients with clinically recognized adverse reactions. Additional studies are warranted to determine efficacy and effectiveness of rifampin therapy for LTBI.
Reliable data on the risk of transmission of N. gonorrhoeae would enhance our understanding of the importance of host defenses against gonorrhea and would aid in the evaluation of prophylactic measures. This paper examines the risk of transmission of gonorrhea from infected female to male and the role that variables such as race, prophylaxis and amount of exposure play in the development of gonococcal urethritis. Volunteer crew members of a large naval vessel were followed prospectively as a cohort to study their risk of acquiring gonococcal infection during a four-day liberty period in the Far East. At the same time the prevalence of N. gonorrhoeae was determined in a population of females to whom the sailors were exposed. The calculated risk of transmission per exposure with an infected partner was .19 for whites and .53 for blacks. A statistically significant relationship was noted between the risk of transmission of gonorrhea and both the number of partners and the frequency of sexual intercourse. Further, the increasing infection rate with increasing numbers of exposures in men who had a single sex partner suggests that the majority of men are in fact susceptible to gonorrhea if the quantity of exposure is sufficient.
In a prospective evaluation of antibiotic prophylaxis against gonorrhea, 1080 men were given 200 mg of oral minocycline or placebo after sexual intercourse with prostitutes in a Far Eastern port. Later, at sea, gonococcal infection was detected in 57 of 565 men given placebo and 24 of 515 men given minocycline (P less than 0.001). Minocycline prophylaxis completely prevented infection by gonococci susceptible to 0.75 microgram or less of tetracycline per milliliter, reduced the risk of infection or prolonged the incubation period in men exposed to gonococci susceptible to 1.0 to 2.0 micrograms per milliliter, but did not prevent infection or prolong incubation in men exposed to gonococci resistant to 2.0 micrograms. Minocycline did not increase the proportion of asymptomatic infections. Minocycline prophylaxis would probably have limited effectiveness as a public-health measure because of the tendency to select resistant gonococci.
Cefazolin sodium was tested in vitro against 308 isolates of Enterobacteriaceae, Pseudomonas aeruginosa, Neisseria meningitidis, Haemophilus influenzae, Staphylococcus aureus, and enterococcus. Broth and agar dilution and disk diffusion techniques were used with at least two sizes of inocula of organisms. Cefazolin was also studied in the treatment of 85 hospitalized patients with a variety of serious infections. In concentations of 5 sg or less/ml, cefazolin inhibited and killed more than 90% of isolates of Enterobacteriaceae with the exception of indole-positive Proteus and Enterobacter species. No isolate of P. aeruginosa and only a few of Enterobacter and enterococci were killed by 25 ug of cefazolin/ml, a concentration readily attainable in serum with a 500-mg dose given intramuscularly. Penicillin-susceptible as well as penicillin-resistant isolates of S. aureus were killed by 1 ug or less of cefazolin per ml; however, 25 ug/ml was required to kill 100% of the strains when the inoculum size was increased 100-fold. Cefazolin treatment appeared effective in 82 of 85 patients, including four with endocarditis. Pain was minimal after intramuscular injection, and thrombophlebitis was not observed in those treated intravenously. No patient developed a positive Coombs test, and no evidence of renal toxicity was apparent in clinical studies.
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