A comparison of clinical virulence of nosocomially acquired methicillin-resistant and methicillin-sensitive Staphylococcus aureus infections in a university hospital.

OBJECTIVES: To compare the clinical virulence of nosocomially acquired methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-sensitive S aureus (MSSA) infections in 1989. DESIGN: A retrospective comparison of host factors, in-hospital exposures, sites of infections, and outcomes of patients with nosocomial MRSA and MSSA infections. SETTING: University of Illinois Hospital, Chicago, Illinois. PARTICIPANTS: Forty-four adult patients with nosocomial S aureus infections. RESULTS: The 22 MRSA-infected and 22 MSSA-infected persons were similar regarding mean age, gender, underlying diseases, and exposure to surgery. Before developing infection, MRSA-infected persons were more likely to have received antibiotics (73% compared with 27%, odds ratio = 7.1, 95% confidence interval [CI95] = 2.0-25.8 p = .003) and to have stayed in the hospital > 2 weeks (64% compared with 18%, odds ratio = 7.9, CI95 = 2.0-31.6, p = .002). Bacteremia was the most common presentation in the MRSA and MSSA groups (55% and 59%, respectively). Infectious complications and death were infrequent in both groups. CONCLUSIONS: MRSA and MSSA strains infect patients with similar demographic features and underlying diseases, but MRSA infections are significantly more common among patients with previous antibiotic therapy and a prolonged preinfection hospital stay. Clinical presentations and outcomes did not differ significantly between the 2 groups. Thus, similar to studies in the early 1980s, our findings do not suggest greater intrinsic virulence of MRSA.     

Comparative study of the efficacy and safety of intranasal DDAVP administered to normal blood donors

A study of the efficacy and safety of intranasal 1-deamino-8-D-arginine vasopressin (DDAVP; 300 micrograms) in normal blood donors was carried out in a double-blind, controlled, comparative study. In addition, the effect of heparin or citrate anticoagulation of blood on the recovery of factor VIII (FVIII) in plasma, cryoprecipitate, and a FVIII concentrate was assessed. Citrated plasma from placebo (CP) or DDAVP-treated donors (CD) contained 1103 +/- 73 and 1470 +/- 141 units per liter of FVIII, respectively (p less than 0.01), whereas the heparinized plasma from placebo (HP) or DDAVP-treated donors (HD) contained 1328 +/- 130 (p less than 0.01) and 2023 +/- 358 units per liter (p less than 0.01), respectively. The FVIII could be recovered in both cryoprecipitate and cold-reprecipitated cryoprecipitate (CRC) fractions. DDAVP treatment improved FVIII recovery by 41 percent in the concentrate from citrated plasma (p less than 0.01) and by 127 percent in that from heparinized plasma (p less than 0.01). The specific activity of concentrates from the CP, CD, HP, and HD groups was 0.95 +/- 0.1, 1.4 +/- 0.1 (p less than 0.01), 0.9 +/- 0.1, and 1.47 +/- 0.2 U per mg of protein (p less than 0.01), respectively. The stability of the final product was the same, regardless of the method of treatment or collection. The side effects of intranasal treatment were mild and transient and occurred with similar frequency in both placebo and DDAVP treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rifampicin-associated acute renal failure: pathophysiologic, immunologic, and clinical features

A 71-year-old woman was treated for a relapsing pulmonary tuberculosis with reinstitution of rifampicin after a medication-free interval of 2 years. After ingestion of the second dose, she developed severe hemolytic anemia and acute renal failure (ARF) necessitating dialysis. We demonstrated the presence in the patient's serum of rifampicin-dependent immunoglobulin G (IgG) and IgM antibodies, which caused red blood cell lysis through interaction with the I antigen on the erythrocyte surface. A review of the literature yielded 48 cases of rifampicin-associated renal failure. A subgroup of 37 patients could be distinguished, which, analogous to our case, suddenly developed ARF and frequently also developed hemolytic anemia and/or thrombocytopenia during intermittent or interrupted treatment. Regarding the pathogenesis of the ARF, renal biopsy consistently revealed tubular lesions. Although intravascular hemolysis with hemoglobinuria may play a role, it is not uniformly present. Our demonstration of an antibody with anti-I specificity provides a possible explanation. The I antigen is also expressed on tubular epithelium and may, therefore, be the target structure through which rifampicin-antibody complexes lead to tubular cell destruction. The other cases of rifampicin-associated ARF were unrelated to this subgroup: two cases of rapidly progressive glomerulonephritis, five cases of acute interstitial nephritis, and four cases of light chain proteinuria were recorded.     

Monocyte chemotactic protein-1 is a proinflammatory chemokine in rat skin injection sites and chemoattracts basophilic granular cells

Chemokines may control mast cell infiltrates found in many inflammatory diseases. These cells act through at least two main functions: migration and degranulation. Here we show that human recombinant monocyte chemotactic protein (MCP)-1 (10 ng/50 microliters) induces, after 4 h, an inflammatory vascular permeability and cellular extravasation reaction, determined by Evan's blue dye (1% in saline) injected into the tail vein of the rat, when injected intradermally in the rat skin. The blue color accumulating at the sites of injection provides evidence of vascular permeability and cellular extravasation. The colored areas of the skin were then enucleated and immersed in a fixative solution. Slides were prepared with sections of tissue colored with toluldine blue and analyzed under an optical microscope. A significant number of basophilic cells migrated to the injected area where MCP-1 (10 ng/50 microliters) was used compared to the control PBS treatment. Cell recruitment was slightly less than N-formyl-methionine- leucyl-phenylalanine (used at 10(-6) M/50 microliters). Electron microscopy studies confirmed the presence of basophilic granular cells where MCP-1 was intradermally injected. After preparation of a histidine decarboxylase (HDC) probe, a Northern blot analysis was determined for HDC mRNA in the enucleated tissue injected with MCP-1 (10 ng/50 microliters). Steady-state levels of HDC mRNA levels were induced after 4 h. These results were confirmed by the higher amount of histamine release, compared to the control PBS, in the enucleated tissue from the MCP-1 injection sites. Our results suggest that MCP-1 could play a significant role in diseases characterized by basophilic cell accumulation and migration to sites of tissue damage. Moreover, we show for the first time that MCP-1 is a pro-inflammatory chemokine that induces basophilic cell migration in rat skin injection sites.