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Biomedical subjects

G H Bornside

Publications and source records attributed to G H Bornside.

At least 37 records · Page 2Linked to original sources
PubMed1972

Development of tetracycline-resistant Staphylococcus aureus in gnotobiotic mice.

Germ-free mice were colonized with a pigmented, tetracycline-sensitive strain of Staphylococcus aureus and maintained in flexible plastic isolators. Treatment of the gnotobiotic mice with oral tetracycline (20 mg/ml) resulted in the development of staphylococci resistant to tetracycline (5 mug/ml or higher). Resistant staphylococci did not appear in feces until several days after exposure of mice to the antibiotic and persisted for as long as specimens were collected (64 days subsequently). Resistance developed after a single exposure of gnotobiotes to antibiotic. Resistant staphylococci were present in the intestinal tracts of mice at counts of 10(3) per g of contents, whereas sensitive organisms coexisted at counts of 10(5) to 10(11) per g. Resistant staphylococci were isolated only from treated mice and not from untreated mice in adjacent cages. Initial colonization of germ-free mice with sensitive staphylococci interfered with subsequent colonization by resistant staphylococci and provided an example of bacterial interference. Resistance to tetracycline was not associated with resistance to chloramphenicol, penicillin, ampicillin, erythromycin, streptomycin, or kanamycin. Hydrolysis of gelatin was the only biochemical characteristic in which isolates varied but was not correlated with resistance to tetracycline or pigmentation of colonies. A nonpigmented, gray variant of S. aureus appeared in all specimens after colonization with the original, pigmented strain. Only the nonpigmented strain was obtained from gnotobiotes colonized with the nonpigmented variant. Contact between bacteria and antibiotic in the intestinal tract of gnotobiotes was considered to be essential for the development of tetracycline-resistant staphylococci.

Animals↗
PubMed1970

Treatment of experimental burn wound sepsis by postburn immunization with polyvalent Pseudomonas antigen.

1. Vaccination with a new heptavalent Pseudomonas aeruginosa antigen was found to reduce mortality rates from experimental pseudomonal burn wound sepsis. 2. Adjunctive use of the heptavalent vaccine improved survival of animals with pseudomonal sepsis which were treated with topical antibiotics. 3. Elevated antibody titers following vaccination could be correlated with survival in this model.

Animals↗
PubMed1968

Synergistic antibacterial activity of ampicillin-cloxacillin mixtures against Proteus morganii.

Synergistic antibacterial effects of mixtures of ampicillin and cloxacillin and induced penicillinases were investigated in 48 strains of Proteus. The serial tube dilution method was used to determine the minimal inhibitory concentration of ampicillin, cloxacillin, and 2:1 and 1:1 mixtures of ampicillin and cloxacillin. Production of penicillinases was determined by the cellulose acetate membrane method, with ampicillin, cloxacillin, mixtures of ampicillin and cloxacillin, penicillin G, and cephalothin as inducing agents and as substrates for penicillinase. Synergism occurred against P. morganii, but against no other species. The 1:1 ampicillin-cloxacillin combination was synergistic against 13 of 17 P. morganii strains; the 2:1 combination was synergistic against only 9 strains. Penicillinases, demonstrated in all species except P. mirabilis, hydrolyzed penicillin G and cephalothin. Although only P. vulgaris hydrolyzed ampicillin, no species of Proteus hydrolyzed cloxacillin or the ampicillin-cloxacillin mixtures. Penicillinases were, however, induced by ampicillin, cloxacillin, and the mixtures. There was no relationship between production of penicillinase and synergism with mixtures of ampicillin and cloxacillin.

Ampicillin↗
PubMed1968

Hemoglobin and Escherichia coli, a lethal intraperitoneal combination.

Intraperitoneal injection into mice of approximately 8 x 10(6) washed cells of Escherichia coli suspended in a lysate of washed human red blood cells or an aqueous solution of crystalline hemoglobin was lethal. E. coli suspended in washed intact erythrocytes, whole blood, plasma, or saline was innocuous. Fractionation of non-hemoglobin proteins from hemoglobin in lysates showed that only hemoglobin promoted a lethal infection. Overwhelming intraperitoneal growth of E. coli was attained in about 12 hr in lethal infections. The polymorphonuclear leukocytic response was ineffective against this rapid growth. The lethal mechanism is hypothesized to center on a unique role for free hemoglobin in inhibiting peritoneal absorption and stimulating an intraperitoneal exudate which supports luxuriant bacterial growth. Death is attributed to a lethal intoxication from bacterial endotoxins. This role for hemoglobin involves neither enhanced bacterial virulence nor lowered host resistance, and it would be of importance not only in peritonitis but also in problems where hemolysis and infection coexist.

Animals↗