Biomedical subjects
Publications and source records attributed to G M Kalmanson.
L-forms of Streptococcus faecalis, Escherichia coli and Proteus mirabilis showed significantly less chemotactic activity for normal human leucocytes than did parent bacterial forms which were strongly chemotactic. Mycoplasma pneumoniae and Mycoplasma hominis did not demonstrate chemotactic activity.
Histological and serological data were obtained from a group of 160 mice given intravenous inoculations of 3.5 X 10(7) colony-forming units of Mycoplasma pulmonis and studied for 46 weeks. The basic pathology was that of an initial acute inflammatory response within the joint and periarticular tissues, slowly changing to a chronic inflammatory response seen predominantly in subsynovial areas with marked synovial proliferation. Occasional lymphoid follicles and plasma cells were seen in the subsynovial spaces. Titers of antibody to M. pulmonis were determined by both metabolic inhibition and indirect hemagglutination techniques. By the metabolic inhibition method, titers were highest between two and 22 weeks, and by indirect hemagglutination between four and 42 weeks. Antibodies to synovial antigens were present between nine and 26 weeks as determined by indirect hemagglunination. Serologic cross-reactions were found between M. pulmonis and normal mouse synovium in sera from infected mice and, by indirect hemagglutination, metabolic inhibition, and immunodiffusion techniques, in sera of rabbits or mice immunized with either M. pulmonis or mouse synovium.
A strain of Klebsiella pneumoniae virulent for mice was serially passaged in vitro as a penicillin-induced L-form. Periodically, the L-form was reverted to the bacterial form by removal of penicillin, and the revertant was tested for virulence. Virulence was gradually reduced, and after 109 passages the revertant was totally avirulent. Virulence was not restored by 40 passages of the revertant through mouse peritoneum. The revertant grew less vigorously and did not infect mice when inoculated subcutaneously; in contrast, the parental form was found in all tissues examined. After phagocytosis in vitro or in vivo, the revertant survived but did not increase in numbers, whereas the parental form did increase in numbers. The revertant had a much smaller capsule than did the parental form. Immunization with the live revertant resulted in type-specific protection against infection with the parental form.
Murine cytomegalovirus was inhibited by 0.6 to 1.2 mug of cytosine arabinoside per ml and by 0.3 to 0.6 mug of 5-iodo-2'-deoxyuridine in mouse embryo fibroblast cells. Human cytomegalovirus was inhibited by similar concentrations of the two drugs in WI-38 cells. Intraperitoneal inoculation of suckling mice with 10(4.5) plaque-forming units of murine cytomegalovirus provides a model for disseminated human cytomegalovirus infection in human newborn infants and is characterized by a widespread infection involving the liver, spleen, lung, kidney, and brain with a 70 to 90% mortality in 7 to 9 days. Treatment with 12.5 mg of cytosine arabinoside per kg or 25 mg of 5-iodo-2'-deoxyuridine per kg twice daily for 8 days had no effect on final mortality or the pathogenesis of the infection with the exception of reduced viral titers in the spleen of 5-iodo-2'-deoxyuridine-treated animals. These data indicate that neither cytosine arabinoside nor 5-iodo-2'-deoxyuridine are effective in the treatment of murine cytomegalovirus infections in suckling mice and suggest that they may be of limited value in the treatment of severe cytomegalovirus infections in human neonates.
A study has been done of immunization against Streptococcus faecalis pyelonephritis in the rat. Intravenous, subcutaneous, and bladder immunizations were tested with intravenous and retrograde challenge. Logarithmic and stationary growth phase organisms were used separately for both immunization and challenge. The only instance of significant, but incomplete, protection was in animals immunized subcutaneously or intravenously and challenged intravenously with log phase organisms. No correlation was found between circulating antibody response and infection. Serum bactericidal activity was not increased by immunization or infection.
Virulence of 15 strains of Escherichia coli from the human upper urinary tract was compared with that of 16 strains from the lower urinary tract, using an ascending infection in the mouse. No significant difference was found. There was no significant difference in frequency of K antigen and ability to ferment dulcitol between 32 lower strains and 31 upper strains. However, 22 strains containing K antigen, regardless of anatomical site of localisation, were more significantly likely to cause infection than 9 strains with no antigen. Similarly, 23 dulcitolfermenting strains, regardless of site of localisation, were significantly more likely to cause infection than 8 non-fermenting strains.
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The effect of antimicrobial therapy on the histopathologic progression of experimental hematogenous pyelonephritis induced in rats by Streptococcus faecalis was studied. Treatment sufficient to render the renal parenchyma sterile strikingly decreased the incidence and severity of calyceal lesions, delayed the progression of papillary lesions but had little effect on the severity of cortical interstitial and tubular alterations. L-forms could not be demonstrated to participate in the pathogenesis of these lesions. Kanamycin had an independent nephrotoxic effect which complicated interpretation of the effect of therapy in animals receiving this agent.
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Earlier workers suggested that synergism of polymyxin and sulfonamides occurred because sulfonamides produced changes in the cell wall which permitted the more ready access of polymyxin. We tested this hypothesis by using L-forms, which lack cell wall. The demonstration that synergism of polymyxin and sulfonamides occurs in L-forms of Proteus mirabilis and Staphylococcus aureus suggested that the synergism is a result of some mechanism other than alterations of the cell wall.
Minimum inhibitory and bactericidal concentrations of four antibiotics and their combinations were determined for 38 strains of enterococci by a microtitration tube dilution technique. The drugs were ampicillin, vancomycin, gentamicin, and streptomycin; the combinations were ampicillin-gentamicin, ampicillin-streptomycin, vancomycin-gentamicin, and vancomycin-streptomycin. At achievable serum concentrations, ampicillin alone killed 60% of strains, whereas combination with streptomycin increased this to 90% and with gentamicin to 100%. Vancomycin alone showed striking inhibitory activity, but very poor bactericidal activity at achievable concentrations. Combination with one of the aminoglycosides increased the bactericidal activity substantially. When combined with ampicillin, gentamicin was both more active and showed synergistic bactericidal activity significantly more often (P < 0.01) than streptomycin.
The fatty acid composition of the membranes of three different penicillin-produced L-forms of Streptococcus faecalis was determined: (i) a stable (nonreverting) L-form (T(53)) cultured in brain heart infusion (BHI) with 0.5 M sucrose; (ii) a stable L-form (T(531)) cultured in BHI without sucrose; and (iii) an unstable L-form (T(9)) cultured in BHI with 0.5 M sucrose and 1,000 U of penicillin per ml. L-forms were obtained by centrifugation and lysed by washing in 1 mM tris(hydroxymethyl)aminomethane-hydrochloride buffer. The parent S. faecalis was also cultured in BHI and BHI containing 0.5 M sucrose, and washed with buffer. The fatty acid composition of L-forms of S. faecalis cultured in BHI without sucrose (370 mosmol) had higher C(18:1) and lower C(18) than L-forms cultured in the same media with added 0.5 M sucrose (950 mosmol) in both exponential and stationary cultures. In the stationary phase of growth, C(19) was reduced in the L-forms cultured without sucrose. Similar changes were seen in the parent S. faecalis cultured in the two types of media. These changes in membrane fatty acids may relate to osmo-regulation of the L-forms.
An L-form of Serratia marcescens has previously been shown incapable of producing the red pigment, prodigiosin, characteristic of the parent bacteria. Mutants of S. marcesens, unable to form one or the other of the two prodigiosin precursors, 4-methoxy-2,2'-bipyrrole-5-carboxaldehyde or 2-methyl-3-n-amylpyrrole, were used to test the nature of the L-form defect. The L-forms failed to form sufficient amounts of either precursor to be detected by the appropriate mutant, and, when furnished the precursors, failed to couple them to form prodigiosin.
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