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At least 19 recordsLinked to original sources
PubMed1992

The effect of humoral and cell-mediated immunity in resistance to systemic Serratia infection.

Protection against experimental Serratia marcescens infection in mice was enhanced by prior injection of formalin-killed or viable bacteria of the same strain. From the first to the fourth week after vaccination, specific immunity was involved in the host defence against systemic serratia infection. The transfer of antiserum specific for S. marcescens increased bacterial clearance from the liver, but did not increase the survival of the mice. Bacterial clearance from the liver was also increased by the transfer of spleen cells from immunised mice, but, again, survival was not increased. However, the transfer of both antiserum and spleen cells from vaccinated mice increased both bacterial clearance from the liver and survival (p less than 0.01). These results suggest an additive effect of humoral immunity and T-cell-mediated immunity in protection against systemic serratia infection.

Animals↗
PubMed1989

Effects of vaccination against systemic Serratia infection.

Host defense against Serratia marcescens in experimental infection in mice was enhanced by vaccination with formalin-killed bacteria of the same strain. The enhancement appeared within 24 hr after vaccination, reached a peak seven days later and lasted four weeks. The enhanced resistance to Serratia infection was also observed in the early phase (within seven days) after vaccination with killed Escherichia coli or other Gram-negative strains, but the efficacy on Day 7 was inferior to that with killed S. marcescens. Phagocytic activities of both circulating neutrophils and peritoneal macrophages were measured by the chemiluminescence (CL) response, and the activity of tissue macrophages was evaluated by the carbon clearance test. The activities were significantly elevated in the early phase, that is, within two or three days for neutrophils, seven days for peritoneal macrophages and at least 14 days for tissue macrophages, after vaccination with killed Gram-negative bacteria. These results suggest that the enhancement of host defense in the early phase is dependent on phagocytic functions that are non-specifically activated by dead bacteria. In the late phase after vaccination, specific immunity might have been involved in the defense mechanism. However, transfer of high titer specific antiserum, in itself, did not render mice resistant to Serratia infection.

Animals↗
PubMedDate not supplied

Intracranial Serratia infection in preterm newborn infants.

Four cases of cerebral Serratia infection in preterm infants were diagnosed with the aid of real-time sector sonography. Three cases had brain abscesses and one case had ventriculitis. In two cases brain abscesses had ruptured into the ventricles. Serratia brain abscess was common in our series of brain abscesses. Sonographic patterns of cerebritis, abscess formation, and ventriculitis correlated well with computed tomographic scans. Bedside cerebral sonography proved to be useful for the diagnosis, location, and follow-up of intracranial Serratia infection.

Brain Abscess↗
PubMed1980

Serratia infection in a patient with bilateral subcondylar impacted third molars and associated dentigerous cysts: report of case.

A case of bilateral subcondylar impacted mandibular third molars is presented. Both impactions had associated dentigerous cyst, one of which was severely infected with Serratia marcescens and had a draining sinus tract. The patient also had uncontrolled diabetes mellitus and iron deficiency anemia, which altered her response to surgical treatment. This case illustrates the necessity for early identification of infective organisms and determining their antibiotic sensitivity, as well as the need for prophylactic removal of impacted teeth to prevent complications such as those presented.

Dental Fistula↗
PubMed1976

Sulfamethoxazole-trimethoprim-polymyxin therapy of serious multiply drug-resistant Serratia infections.

Nonpigmented multiply drug-resistant Serratia marcescens caused an extensive outbreak of infection at the Nashville Veterans Administration Hospital. Isolates were of one serotype resistant to all currently available antimicrobial agents for therapy of systemic infections except for occasional susceptibility to chloramphenicol and kanamycin. Frequently strains were susceptible to nalidixic acid, and all were susceptible to amikacin (BB-K8). Drug-resistant strains caused 130 infections, 12 bacteremias, and 7 infection-associated deaths. Combinations of antimicrobial agents were evaluated for synergism against Serratia strains from infected patients. "Checkerboard" isobolograms indicated in vitro static synergism between sulfamethoxazole, trimethoprim, and polymyxin (STP). Killing curves using clinically achievable concentrations of STP verified the bactericidal effect of STP against these strains. In a daily dosage of 1,600 mg of sulfamethoxazole and 320 mg of trimethoprim orally in combination with 100 to 300 mg of colistimethate parenterally, serum cidal levels at 1:8 or greater were achieved in five of six patients. Clinical improvement or microbiological cure was effected in four of six patients. STP may be potentially useful for selected Serratia infections for which single agents are unavailable or ineffective.

Clinical Trials as Topic↗
PubMed1978

[The clinical significance of Serratia infections during the post-operative course (author's transl)].

A series of 25 cases of Serratia infections, during the period from november 1977 through aptile 1978, is reported. Serratia isolates were identified with increasing frequency from urine, surgical incisions and blood. All the patients had received antimicrobial therapy prior to the time Serratia was first isolated. These patients (92%) had had indwelling urinary catheters inserted during the post-operative course and Serratia was isolated predominantly from the urinary tract. In 3 patients who died, Serratia played a role in the ultimate demise of the patient. Prophylaxix and antimicrobial therapy are discussed.

Aged↗
PubMed1991

Serratia infections in patients with neutropenia.

We report on six cases of sepsis caused by Serratia marcescens in patients with neutropenia. Four cases showed an additional involvement of the upper respiratory and digestive tract with oral and pharyngeal mucositis, haemorrhagic laryngo-tracheo-bronchitis, and oedematous swelling of the face. One patient showed a Serratia marcescens carrier state in the pharynx over a period of months without neutropenia. The isolated strains showed a broad spectrum of resistance against antibiotics; only aztreonam and amikacin were effective in vitro against all isolates.

Adolescent↗
PubMed1978

[Serratia infection].

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Enterobacteriaceae Infections↗
PubMed1975

[Serratia infections].

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Enterobacteriaceae Infections↗
PubMed1985

Treatment of Pseudomonas and Serratia infections with ceftazidime.

The effectiveness and safety of parenterally administered ceftazidime were assessed in 20 patients with infections caused by Pseudomonas aeruginosa or Serratia marcescens. There were six infections involving the urinary tract, six wound infections, one respiratory tract infection, three septicaemias, one empyema, one mastoiditis and two infections of the epididymis. Sixteen of the isolates were resistant to at least one aminoglycoside antibiotic. Fifteen patients were clinically and bacteriologically cured, two patients improved, but had relapses and three patients showed no response. The lack of clinical response was due to the development of resistance by P. aeruginosa in two patients with osteomyelitis, one of whom also had diabetes mellitus. The third patient who had chronic lymphocytic leukaemia developed post-operative osteomyelitis and septicaemia with serratia. She did not respond to treatment. Side effects consisted of a positive direct Coomb's test without evidence of haemolysis in two patients and a mild maculopapular rash in one patient.

Adult↗
PubMed1987

Role of cell-bound hemolysin as a pathogenicity factor for Serratia infections.

The hemolytic activities of clinical isolates of Serratia marcescens, of Serratia liquefaciens, and of Escherichia coli strains containing a cloned hemolysin gene of S. marcescens were determined. Hemolysis was induced only by cells and not by spent media. The hemolytically active bacteria induced the release of the leukotriene C4 and of much less leukotriene B4 from polymorphonuclear leukocytes, the release of histamine from rat mast cells, and chemoluminescence of neutrophils. The hemolytic activity was correlated with the response of the leukocytes, but quantitative differences were recorded with regard to the release of the inflammatory mediators. Therefore, other factors in addition to the hemolysin contribute to the stimulation of leukotriene generation and histamine release. It is concluded that the hemolysin via these inflammatory mediators can increase vascular permeability, edema formation, and granulocyte accumulation and thus contributes to the pathogenicity of Serratia species.

Animals↗
PubMed1985

Clinical efficacy of a synergistic combination of cefotaxime and amikacin against multiresistant Pseudomonas and Serratia infections.

The synergistic activity of cefotaxime and amikacin against 21 highly resistant Pseudomonas aeruginosa and Serratia marcescens isolates was evaluated in-vitro by the checkerboard tube dilution method and in-vivo in five patients with serious infections caused by these organisms. All isolates were resistant to gentamicin, tobramycin, amikacin, and cefotaxime. Synergy was observed in 90% of isolates and occurred when the MIC of amikacin was less than 256 mg/l and of cefotaxime less than 1024 mg/l. A clinical response occurred in 100% and bacteriological cure in 80% of patients. Our results demonstrate a high degree of synergism between amikacin and cefotaxime in-vitro and clinical efficacy in the treatment of infections due to multiply-resistant Pseudomonas and Serratia species.

Aged↗