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At least 1,099 records · Page 61Linked to original sources
PubMed1994

Serious Pseudomonas aeruginosa infections in patients infected with human immunodeficiency virus: a case-control study.

We conducted a case-control study to determine the incidence and clinical features of and risk factors for Pseudomonas aeruginosa infections in patients infected with human immunodeficiency virus (HIV). Twenty-five patients who had 37 episodes of P. aeruginosa infection from 1990 through 1992 were identified. Most of the patients (92%) were homosexual men with low CD4+ lymphocyte counts and a history of AIDS. The annual incidence rates of P. aeruginosa infection were 3.5% (1990), 6.3% (1991), and 8.7% (1992). Most infections were community-acquired (68%) and involved the respiratory tract (73%). Patients were more likely than HIV-infected controls to have AIDS and had more AIDS-defining opportunistic illnesses. The overall mortality was 36%. Recurrent episodes were common (39%). We conclude that P. aeruginosa infections may be an increasing problem in patients with extremely advanced HIV infection. Clinicians should consider including antibiotics with activity against P. aeruginosa in the empirical treatment for suspected bacterial infection in patients with advanced HIV infection.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Protection of immunosuppressed mice against infection with pseudomonas aeruginosa by monoclonal antibodies to outer membrane protein OprI.

Two monoclonal antibodies (mAbs) designated 2A1 and 6A4 which had been shown to be directed against Pseudomonas aeruginosa outer membrane lipoprotein I were tested in cyclophosphamide treated mice for their protective ability against P. aeruginosa infection. Pretreatment of mice with either 2 mg of 2A1 or 4 mg of 6A4 in combination with lethally irradiated human leucocytes reduced the mortality after subsequent subcutaneous injection of 100 living P. aeruginosa organisms to 50% of the controls. Without leucocytes only mAb 2A1 (isotype IgG2b) showed protection (47%). Irradiated leucocytes alone without mAb did not protect the mice significantly from fatal P. aeruginosa infection.

Animals↗
PubMed2006

Deficiency of mannose-binding lectin greatly increases susceptibility to postburn infection with Pseudomonas aeruginosa.

Burn injury disrupts the mechanical and biological barrier that the skin presents against infection by symbionts like the Pseudomonas aeruginosa, a Gram-negative bacteria. A combination of local factors, antimicrobial peptides, and resident effector cells form the initial response to mechanical injury of the skin. This activity is followed by an inflammatory response that includes influx of phagocytes and serum factors, such as complement and mannose-binding lectin (MBL), which is a broad-spectrum pattern recognition molecule that plays a key role in innate immunity. A growing consensus from studies in humans and mice suggests that lack of MBL together with other comorbid factors predisposes the host to infection. In this study we examined whether MBL deficiency increases the risk of P. aeruginosa infection in a burned host. We found that both wild-type and MBL null mice were resistant to a 5% total body surface area burn alone or s.c. infection with P. aeruginosa alone. However, when mice were burned then inoculated s.c. with P. aeruginosa at the burn site, all MBL null mice died by 42 h from septicemia, whereas only one-third of wild-type mice succumbed (p = 0.0005). This result indicates that MBL plays a key role in containing and preventing a systemic spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans maybe a premorbid variable in the predisposition to infection in burn victims.

Animals↗
PubMed2004

Limited role for interleukin-18 in the host protection response to pulmonary infection with Pseudomonas aeruginosa in mice.

We report that clearance of Pseudomonas aeruginosa, accumulation of neutrophils, and synthesis of tumor necrosis factor alpha and macrophage inflammatory protein 2 in the infected lung were not largely different in interleukin-18 (IL-18) knockout or transgenic mice compared with control mice. Our results suggest a limited role for IL-18 in the host defense against P. aeruginosa.

Animals↗
PubMed1990

[Role of alveolar macrophages and neutrophils in the defense system against infection of Pseudomonas aeruginosa in the respiratory tract and the effect of derivative of muramyl dipeptide].

We investigated the role of alveolar macrophages and neutrophils on the defense system against infection of Pseudomonas aeruginosa (P. aeruginosa) in the lower respiratory tracts of rats. Intratracheal inoculation of formalin-inactivated P. aeruginosa to normal rats showed an increased number of neutrophils in bronchoalveolar lavage (BAL) fluid obtained at 24 hours after the inoculation. This response of neutrophils was induced by intravenous administration of MDP-Lys, which is muramyl dipeptide. Phagocytic activity of neutrophils for P. aeruginosa was higher than that of alveolar macrophages, indicating that neutrophils are essential phagocytes in the defense system against P. aeruginosa infection in the lower respiratory tract. Alveolar macrophages released neutrophil chemotactic factor after phagocytosis of P. aeruginosa. This function of alveolar macrophages was increased by MDP-Lys administration. These results indicated that alveolar macrophages play an important role in neutrophil accumulation by release of neutrophil chemotactic factor after the P. aeruginosa phagocytosis in the lower respiratory tract. Moreover MDP-Lys can amplify the neutrophil-dependent defense system against P. aeruginosa by activation of the alveolar macrophage function in vivo.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1991

Protection of immunosuppressed mice against infection with Pseudomonas aeruginosa by recombinant P. aeruginosa lipoprotein I and lipoprotein I-specific monoclonal antibodies.

Outer membrane protein I (OprI) is one of the major proteins of the outer membrane of Pseudomonas aeruginosa. The protective effect of OprI vaccination and that of three OprI-specific monoclonal antibodies (MAbs) against infection with P. aeruginosa were tested in immunosuppressed mice. The combination of Oprl and MAb 2A1 protected the mice against a challenge with a 96-fold 50% lethal dose. The binding site of MAb 2A1 was mapped, resulting in the identification of a protective epitope (amino acids 7 to 20).

Animals↗
PubMed1989

Once-daily versus thrice-daily administration of netilmicin in combination therapy of Pseudomonas aeruginosa infection in a man-adapted neutropenic animal model.

A granulocytopenic mouse model was used to elucidate the impact of dose spacing on the activity of netilmicin against Pseudomonas aeruginosa. A thigh infection was produced and then treated with netilmicin combined with azlocillin. Netilmicin was injected subcutaneously at decreasing doses every 20 min to result in plasma-concentration-time curves similar to those observed in patients on intravenous netilmicin treatment. A once-daily regimen was simulated and compared to a simulated conventional schedule of every 8 h. Identical total amounts of drug were used in both groups of comparatively treated mice. Therapeutic efficacy was quantitated by repeated determinations of surviving organisms in thigh homogenates. Combination therapy was significantly more effective than azlocillin treatment alone. In combination regimens the simulated once-daily netilmicin schedule killed the target organisms faster than the simulated thrice-daily regimen and was significantly more efficacious by 24 and 32 h in two out of three strains of Pseudomonas aeruginosa tested. It is concluded that the results of combination therapy of severe Pseudomonas aeruginosa infections in the immunocompromised host might be improved by choosing an aminoglycoside dosage interval of 24 h instead of the conventional 8 h.

Animals↗