Faculty Bibliography

By specific active or passive immunization, mice were protected against lethal infection with Serratia marcescens. Animals that were immunized against organisms of the challenge strain O serotype survived, whereas animals that were immunized against other serratia O serotypes did not survive. Protective sera (from convalescent partients or immunized rabbits) contained a specific complement-independent opsonin. These sera also contained passive hemagglutinating and bacterial agglutinating antibodies in high titer. The protective and complement-independent opsonizing antibodies were associated with IgG fractions of the serum, while the agglutinating antibodies were primarily associated with the IgM. Mice also survived infection with Serratia after immunization against the Re595 Salmonella minnesota mutant. However, complement-independent opsonizing antibody was not demonstrated in these cross-protective sera

Serratia marcescens strains isolated from clinical specimens can be divided into those which are sensitive or resistant to the bactericidal activity of normal human serum. Serum bactericidal activity is heat labile, cation dependent, and is absorbable by whole, serum-sensitive Serratia or ethanol-insoluble extracts of these organisms. Bacteremic Serratia infection is invariably caused by the serum-resistant strains. Serum resistant Serratia are ingested and killed by normal human leukocytes and fresh normal serum. Heating or preabsorption of serum with whole, heat-killed, or ethanol-insoluble antigen extracts of the serum-resistant Serratia diminishes opsonization and phagocytosis. Serratia opsonins in the serum of healthy individuals are type-specific IgM globulins which combine with the organism and activate complement by the alternate pathway

An abrupt increase in gentamicin-resistant isolates was noted in the Manhattan Veterans Administration Hospital in 1973 and 1974. Bacteraemic infection occurred in 17 patients, 9 of whom died. R factors mediating gentamicin resistance were demonstrated in 34 of 36 strains. Organisms from 9 of 11 patients transferred a resistance pattern common to all other isolates from that patient, suggesting in-vivo interbacterial spread of the R factor

Fungal endocarditis occurs in heroin addicts, patients who have undergone cardiovascular surgery, and patients who are treated for prolonged periods with intravenous fluids and broad spectrum antibiotics. The organisms associated with endocardial infection differ in each of these groups. Candida parapsilosis is the fungal species most commonly isolated from narcotics addicts, Aspergillus species are most frequently found in patients after cardiovascular surgery, and Candida albicans occurs most frequently in patients who have received prolonged courses of intravenous fluids and antibiotics. Despite the availability of antifungal antibiotics and surgery, over 80% of patients with documented fungal endocarditis die of this infection. Thus, early diagnosis of fungal invasion and prevention of established endocardial infection are essential. Antifungal therapy and/or careful followup should be considered in patients in whom 'transient fungemia' is documented by blood culture and serological and untrasonic techniques should be further evaluated as a means of early diagnosis

Five heroin addicts were treated for endocarditis caused by Pseudomonas cepacia. Two of these infections occurred in patients with no known heart disease whereas the others occurred at sites of previous endocarditis or valve prostheses. Infection was indolent in four patients but was associated with shock and skin lesions suggestive of ecthyma gangrenosum in the fifth. After failure of chloramphenicol and kanamycin, all patients were treated with a combination of sulfamethoxazole, trimethoprim and polymyxin plus heart valve resection or replacement

Resistance to gentamicin increased abruptly among nosocomial isolates of Klebsiella and Enterobacter at the New York Veterans Administration Hospital in 1973 and 1974. A prospective clinical survey revealed a greater incidence of true infection caused by Klebsiella than by Enterobacter. The initial site of implantation was usually the urinary tract. Multiple serotypes were involved, and one of these was found in rectal swabs of patients treated with antibiotics. Gentamicin resistance declined rapidly after the use of this antibiotic was restricted and increased several months after restrictions were removed. Gentamicin-resistant strains of Klebsiella were uniformly sensitive to amikacin; 75% were sensitive to polymyxin B and 70% to streptomycin. Antibiotic sensitivity among gram-negative pathogens might be preserved by a program in which the use of highly effective agents is periodically rotated

The major action of serum on gram-negative organisms is thought to be on the microbial envelope. We compared the effects of normal human and rabbit serum on the envelope lipids of two strains of Serratia marcescens, one sensitive and one resistant to the bactericidal effects of serum. During killing by either serum, the sensitive strain underwent rapid permeability changes coincident with degradation of microbial phospholipids. The resistant strain exhibited none of these effects. The phospholipid degradation that accompanies killing of the sensitive strain by serum could be caused by phospholipases present in serum or by Serratia's own phospholipid-splitting enzymes. The results indicate that phospholipid breakdown is caused by activation of bacterial of bacterial phospholipases and not by serum phospholipases. This conclusion is based upon the following findings.(i1 Although rabbit serum phospholipase A was at least 10 times more active than human serum phospholipase A, phospholipid degradation in the sensitive Serratia strain was comparable during (equally rapid) killing by human or rabbit serum. (ii) Heat treatment (56 C) of both sera eliminated bactericidal activity as well as microbial lipid degradation but abolished phospholipase activity of human serum only. (iii) Virtually complete removal of phospholipase A activity from human serum by adsorption onto autoclaved Micrococcus lysodeikticus had no effect on the extent of phospholipid hydrolysis or on bactericidal activity. Activation by serum of endogenous phospholipase activity in S. marcescens was accompanied by enhanced incorporation of lipid precursors into bacterial lipids. No evidence was found for increased turnover of protein or ribonucleic acid during killing by serum