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1.  Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit 
Pathophysiological studies in bacterial meningitis in man have been limited by clinical variability and the necessity for immediate therapy. After the development of a reliable animal model of pneumococcal meningitis, we studied respiration and circulation in 25 anesthetized New Zealand white rabbits during untreated pneumococcal meningitis and in 33 healthy controls. In meningitis, we found increased lactic acid in cerebrospinal fluid (CSF). Increased ventilation, perhaps due to CSF lactic acid accumulation, resulted in respiratory alkalosis; the concomitant lowering of Pco2 acted as a homeostatic mechanism to restore pH toward normality in the CSF. Hyperventilation increased with the duration of the illness. Cardiac output was also increased with decreased peripheral vascular resistance but with only slight reduction in mean systemic and pulmonary arterial pressures. In the final hour of life, peripheral vascular resistance fell further; ventilation declined and then abruptly ceased while cardiac activity continued. Lactic acid accumulation in the CSF, found in both experimental and human pneumococcal meningitis, may cause the hyperventilation found in this disease and may contribute to death.
PMCID: PMC301520  PMID: 4152001
2.  Evaluation of Cefazolin, a New Cephalosporin Antibiotic 
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 μg 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 μg 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 μg or less of cefazolin per ml; however, 25 μg/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.
PMCID: PMC444440  PMID: 4790605
3.  Minocycline in the Chemoprophylaxis of Meningococcal Disease 
An outbreak of meningococcal disease occurred among basic combat trainees at Fort Lewis, Wash., in the first 3 months of 1971. After five recruits developed meningitis within a 2-week period, 8,721 recruits were given 100 mg of minocycline every 12 hr for 5 days. No new cases of meningococcal disease occurred for almost 5 weeks. Then six additional cases occurred among recruits who had entered training after the initial course of minocycline and who had not received the drug. Minocycline was given to all 6,130 of these men, and again occurrence of new cases was halted abruptly. One week later, group C polysaccharide vaccine was administered to all recruits in the first 6 weeks of training and subsequently to all new entering trainees. No new cases of meningitis occurred in the next 3 months. Surveys showed that minocycline significantly lowered the meningococcal carrier rate for 4 to 5 weeks. No strains of Neisseria meningitidis, among 341 isolated after minocycline treatment, were resistant to the drug. Prophylaxis with minocycline clearly interrupted the course of this outbreak due to sulfa-resistant meningococci. Although immunization is the preferred method of prophylaxis, minocycline may be useful until a suitable polyvalent vaccine is available.
PMCID: PMC444231  PMID: 4670480
4.  The Clostridial Syndrome 
Western Journal of Medicine  1978;129(2):134-136.
PMCID: PMC1238284  PMID: 18748272

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