Biomedical subjects
Publications and source records attributed to A N Weinberg.
The physician's approach to the differential diagnosis of obscure, atypical pneumonias has changed. The physician needs to expand the diagnostic search when confronted with a perplexing, progressive atypical pneumonia. Diseases examined in this article include anthrax, psittacosis, Q fever, tularemia, pasteurellosis, melioidosis, Rocky Mountain spotted fever, and the plague.
The possibility that a perplexing febrile illness may represent a zoonotic infection should be explored. The history should include where the person has been, what he or she has done, what has been eaten and drunk, what contacts have occurred with vertebrates or arthropods in wild or domestic venues, and whether there has been exposure to unusual animal products. The preceding discussion emphasized, via some examples, mechanisms of spread as well as the physical and biologic conditions that enhance the probability of an encounter with a pathogen. From clues in the history and physical examination the appropriate diagnostic and therapeutic decisions can be made. These decisions may be life saving for the patient, and perhaps protect care providers and family from acquiring the same disease. Many of the infections mentioned in this article will be amplified in subsequent articles, which will deal with diseases encountered primarily in the United States.
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Bacterial meningitis is a medical emergency that is ordinarily rapidly progressive. We present three patients who had meningococcal meningitis with an indolent course. Symptoms were present from two days to four weeks before hospitalization. Cerebrospinal fluid cultures grew Neisseria meningitidis one to eight days before antibiotic therapy, yet all patients remained fully alert and clinically stable during this interval. All recovered after penicillin therapy. In the future earlier diagnosis should be facilitated by an awareness of differing manifestations of meningococcal meningitis, including benign CSF findings, intact sensorium, and an indolent progression. Immunologic studies will be required to clarify the pathogenesis of this syndrome.
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Enterococci exhibit two types of resistance to streptomycin. Moderately high-level resistance is observed in most naturally occurring strains and can be overcome by simultaneous exposure to penicillin. In addition, very high-level resistance is found in those strains against which penicillin plus streptomycin fail to produce synergism in vitro. To study the mechanism of streptomycin resistance in enterococci, ribosomes from a wild-type strain and from a highly streptomycin-resistant mutant were isolated, characterized, and studied in an in vitro amino acid incorporation system. The ribosomes from the organism with moderately high-level streptomycin resistance were sensitive to streptomycin in vitro, suggesting that this type of resistance is caused by failure of streptomycin to reach the ribosomes. Very high-level resistance (and lack of penicillin-streptomycin synergism), on the other hand, appears to be due to ribosomally mediated streptomycin resistance.
The mechanism by which agents that inhibit bacterial cell wall synthesis produce a synergistic effect against enterococci when combined with aminoglycoside antibiotics has not been elucidated. Using (14)C-labeled streptomycin, it could be shown that uptake of this aminoglycoside antibiotic was markedly enhanced in enterococci growing in the presence of penicillin or other agents which inhibit the synthesis of bacterial cell walls. There was no enhancement of streptomycin uptake when the cells were incubated with antibiotics which primarily affect the bacterial cell membrane or inhibit protein synthesis. Increased streptomycin uptake was produced by penicillin only in actively growing bacteria. These observations are consistent with the hypothesis that enterococci exhibit a natural barrier to the entry of streptomycin which can be overcome by agents which inhibit cell wall synthesis, thus producing a synergistic effect.
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