Impairment of erythrocyte viscoelasticity is correlated with levels of glycosylated haemoglobin in diabetic patients.

Erythrocytes from diabetic patients exhibit impaired viscoelastic properties when estimated by various methods. We determined erythrocyte filterability through 5-microm pores, in 51 patients with non-insulin-dependent diabetes mellitus, 18 healthy controls, 15 patients with homozygous beta-thalassemia and 15 with beta-thalassemia traits. The filtration measurements were made with a Hemorheometer, which uses the "initial flow rate" principle. To determine the Index of Rigidity (IR) of the red blood cells, we measured the passage time of white blood cell-free erythrocyte suspensions, 8% per volume, through the filter. Diabetic patients had significantly increased IR in comparison to healthy controls and to patients with beta-thalassemia trait, but not at the level found in patients with homozygous beta-thalassemia. In diabetic patients, a strong correlation between IR and the percentage of glycosylated haemoglobin was found (r=0.737, P < 0.0001), and a weaker one with serum unconjugated bilirubin (r=0.363, P=0.0097) and serum total lipids (r=0.321, P=0.0286). Patients with severe retinopathy also had significantly increased IR, in comparison to those with or without mild retinopathy. Anaemic diabetic patients, especially those with the anaemia of chronic disease, also had significantly increased IR in comparison to non-anaemic diabetics. No correlation between IR, MCV, MCH, MCHC, RDW, RBC morphology, serum LDH or the presence of erythrocyte inclusions after incubation with nitrous sodium solution was found. Our findings suggest that glycosylation of skeletal proteins probably contributes significantly to the increased membrane rigidity of diabetic erythrocytes.

Experimentally induced septic arthritis in chimpanzees infected with Mycoplasma hominis, Mycoplasma pneumoniae, and Ureaplasma urealyticum.

Mycoplasma hominis was isolated in pure culture from septic synovial aspirates from an individual (patient A) during 16 different bouts of exacerbation over a 70-month period of observation. Two isolates, 10(7) and also 10(6) color-changing units (CCU) of the 1620 isolate and 5 x 10(4) CCU of the 1628 isolate, caused inflammation in chimpanzees inoculated intraarticularly. Inflammation was also induced with 10(7) CCU of the 2010B isolate, serovar VII of Ureaplasma urealyticum, recovered from an agammaglobulinemic individual (patient B) with septic polyarthritis and with 3 x 10(6) CCU of the PI-1428 isolate of Mycoplasma pneumoniae. Inflammation persisted for up to 36 days and was self-limiting. The aspirates contained up to 220,000 white blood cells/mm3 and up to 10(7) CCU/mL. There was good correlation between the severity of inflammation and the numbers of organisms, but antibody was not detected in aspirates during the peak severity of disease. As the numbers of organisms, decreased, detectable levels of antibody increased, thus suggesting that antibody may have been bound to antigen. Chimpanzees previously infected with either the 1628 isolate of M. hominis or the 2010B isolate of U. urealyticum were protected on challenge with > 100 times the minimal dose causing arthritis. Chimpanzees showed little or no inflammation when inoculated intraarticularly with 5 x 10(8) CCU of the type strain PG-21 of M. hominis or with the type strain CO of U. urealyticum or when inoculated intravenously with 3 x 10(8) CCU of the arthrogenic 1620 isolate of M. hominis.

Experimentally induced Mycoplasma pneumoniae pneumonia in chimpanzees.

Eight chimpanzees were examined. Two served as negative control and six inoculated with Mycoplasma pneumoniae became colonized. Colonization persisted for 28-68, 16-50 and 21 days with an average duration of 47, 32.5 and 21 days in the oropharyngeal, tracheal and lung tissues, respectively. Mycoplasma titers ranged from 10(8) to 10(1) color-changing units per specimen during the course of the infections. Seroconversion occurred within 12-15 days and peak antibody titers ranged from 1.256 to 1.1024 and developed between days 28 and 48 post-inoculation. Positive cold agglutinin titers were detected between 12 to 15 days and peak titers ranged from 1:80 to 1:640. Significant increases in sIgA and IgG immunoglobulin antibody levels were detected in lung lavage fluids. Unlike the many other experimentally infected animals examined, chimpanzees infected with M. pneumoniae had positive X-ray findings, developed cold agglutinins and showed overt signs of disease. These signs include persistent cough, low grade fever, rhinitis, oropharyngitis, diarrhea, and loss of appetite. Peak severity of disease corresponded with peak lung colonization, and the detection of cold agglutinins and positive X-ray findings. The microbiological, serological and clinical aspects of pneumonia induced in chimpanzees was similar to naturally occurring primary atypical pneumonia in humans.

Ureaplasma urealyticum colonization of full term infants: perinatal acquisition and persistence during early infancy.

In a prospective study 225 (35%) of 640 pregnant women who delivered at term had vaginal colonization with Ureaplasma urealyticum at the time of delivery. One hundred ninety-three full term infants born to U. urealyticum-colonized mother were cultured from the throat, eyes and vagina within the first 3 days of life. One hundred seven infants (55%) had at least one culture site positive for U. urealyticum (throat 41%, eyes 20%, vagina 40%). Rupture of membranes for greater than or equal to 12 hours and the mode of delivery did not affect vertical transmission of U. urealyticum. We were able to follow 108 infants during the first 3 months of life. Sixty-eight, 33 and 37% of the infants who were initially colonized with U. urealyticum in the throat, eyes and vagina, respectively, were still colonized when the follow-up cultures were obtained 3 months later. Fourteen of the 108 infants whom we followed developed a lower respiratory tract illness. In the pharyngeally colonized infants there was no increased risk for lower respiratory tract illness during early infancy compared with the pharyngeally noncolonized infants.

Lincomycin resistance in methicillin-resistant Staphylococcus aureus strains of hospital origin.

A total of 170 Staphylococcus aureus strains isolated during a one-year period at the University Hospital of Patras Medical School were examined for resistance to a battery of antimicrobial agents by disk diffusion and minimum inhibitory concentration (MIC) determination. Fifty-five isolates were lincomycin- and methicillin-resistant (LMRSA). In the group of 55 LMRSA isolates 13 were also resistant to vancomycin. All the LMRSA isolates were not typed by the international set and the experimental phages 88A and 25 at routine typing dilution (RTD), while 18 isolates were lysed by phages at 100XRTD and 1000XRTD. Reverse phage-typing and heat shock treatment of the LMRSA isolates had no effect on their typability. Plasmid profiles coupled with restriction endonuclease analysis of plasmid DNA established that the LMRSA isolates represent different strains. Membrane-protein profiles by polyacrylamide gel electrophoresis (PAGE) showed that LMRSA strains could belong to one group. This method proved useful and sensitive for characterization of LMRSA.

Lymphocyte subpopulations in megaloblastic anaemia due to vitamin B-12 deficiency.

Lymphocyte subpopulations were measured in the blood of 17 patients with megaloblastic anaemia due to vitamin B-12 deficiency. 14 patients had pernicious anaemia and 3 others were gastrectomized. By using monoclonal antibodies recognizing T cell surface markers and immunofluorescence microscopy, we found a significant decrease in the number of circulating suppressor T cells and an increase in the ratio of helper to suppressor T lymphocytes in pernicious anaemia patients. This finding may be related to other immune abnormalities found in pernicious anaemia, e.g. the presence of multiple autoantibodies.

Survey of immunoglobulin A protease activity among selected species of Ureaplasma and Mycoplasma: specificity for host immunoglobulin A.

Because immunoglobulin A (IgA) is the predominant immunoglobulin at mucosal surfaces, IgA proteases produced by pathogenic bacteria are considered potential virulence factors for organisms that cause disease or gain entry at mucous membranes. To determine the role of IgA protease in the pathogenicity of mycoplasmal disease, a variety of human and animal mycoplasma and ureaplasma species were examined for IgA protease activity with human, murine, porcine, and canine IgA. None of the mycoplasma species examined showed detectable IgA protease activity with any of the IgAs tested. Twenty-eight strains of Ureaplasma urealyticum isolated from human urogenital tissues cleaved human IgA1, but no cleavage of human IgA2 or murine, porcine, or canine IgA was observed. Ureaplasmas isolated from nonhuman hosts (feline, canine, avian, and bovine [Ureaplasma diversum]) did not cleave human IgA1. Two strains of canine ureaplasmas were able to cleave canine IgA, but not murine IgA. Thus, ureaplasmas from other species can produce IgA protease, but the specificity of the enzyme was restricted to the IgA of the appropriate host. This finding suggests that IgA proteases could play a role in the selective host specificity of mucosal pathogens.