calca-protein--human and Pneumococcal-Infections

The induction of C-reactive Protein (CRP) may be attenuated by corticosteroids, whereas Procalcitonin (PCT) appears to be unaltered. We investigated, whether in community-acquired pneumonia (CAP) a combined antibiotic-corticosteroid therapy may actually lead to different slopes of decline of these inflammatory markers.. We studied the slopes of decline of PCT and CRP serum levels during 7 consecutive days as well as clinical parameters in a group of patients with CAP on or off corticosteroids. Patients with underlying COPD received systemic corticosteroids (n = 10), while non-COPD patients (n = 10) presenting with CAP alone formed the control group. All patients were treated with antibiotics.. At baseline, relevant clinical and laboratory characteristics of the two groups were similar. Regarding the decreasing shapes of the curves from PCT and CRP, no significant differences were found (p-value = 0.48 for the groups for CRP, respectively 0.64 for PCT). All patients showed an uneventful recovery.. In patients with COPD and CAP, the time courses over 7 days of PCT and CRP showed a nearly parallel decline compared to non-COPD patients with CAP. Contrary to the induction phase, corticosteroids do not modify the time-dependent decay of PCT and CRP when the underlying infectious disease (CAP) is adequately treated.

Topics: Aged; Anti-Bacterial Agents; Anti-Inflammatory Agents; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Community-Acquired Infections; Drug Therapy, Combination; Female; Humans; Longitudinal Studies; Male; Methylprednisolone; Middle Aged; Pilot Projects; Pneumococcal Infections; Pneumonia; Prednisone; Protein Precursors; Pulmonary Disease, Chronic Obstructive

Procalcitonin (PCT) is expressed in nonthryoidal tissues of humans during severe infections. Serum PCT levels are measured to diagnose and guide therapy, and there is some evidence that PCT may also contribute to the pathogenesis of sepsis. We tested whether disruption of the gene encoding PCT in mice affected the course of sepsis. Mice with exons 2-5 of the gene encoding calcitonin/calcitonin gene-related polypeptide α (Calca) knocked out and congenic C57BL/6J control mice were challenged with aerosolized Streptococcus pneumoniae or Pseudomonas aeruginosa, or injected intraperitoneally with S. pneumoniae. There were no significant differences in the survival of knockout and control mice in the two pneumonia models, and no significant differences in weight loss, splenic bacterial counts, or blood leukocyte levels in the peritoneal sepsis model. To verify disruption of the Calca gene in knockout mice, the absence of calcitonin in the serum of knockout mice and its presence and inducibility in control mice were confirmed. To evaluate PCT expression in nonthyroidal tissues of control mice, transcripts were measured in multiple organs. PCT transcripts were not significantly expressed in liver or spleen of control mice challenged with aerosolized P. aeruginosa or intraperitoneal endotoxin, and were expressed in lung only at low levels, even though serum IL-6 rose 3,548-fold. We conclude that mice are not an ideal loss-of-function model to test the role of PCT in the pathogenesis of sepsis because of low nonendocrine PCT expression during infection and inflammation. Nonetheless, our studies demonstrate that nonendocrine PCT expression is not necessary for adverse outcomes from sepsis.

Topics: Animals; Bacterial Load; Calcitonin; Calcitonin Gene-Related Peptide; Exons; Gene Deletion; Interleukin-6; Lung; Mice; Mice, Inbred C57BL; Mice, Knockout; Peritonitis; Pneumococcal Infections; Protein Precursors; Pseudomonas aeruginosa; Pseudomonas Infections; Sepsis; Severity of Illness Index; Spleen; Streptococcus pneumoniae

To study the clinical characteristics of children who suffered from Streptococcus pneumoniae (SP) septicemia and the drug sensitivity of SP strains.. A retrospective analysis was performed on the clinical data of 25 children with SP septicemia between January 2009 and December 2012.. Of the 25 cases, 16 (64%) were aged under 2 years, 5 (20%) were aged 2-5 years, and 4 (16%) were aged over 5 years. Fourteen cases (56%) were complicated by infection of other organs, and 5 cases (20%) had underlying chronic diseases. Fever was the most common clinical manifestation, and the majority presented with remittent fever. Eight patients with pneumonia or pyothorax had pulmonary symptoms. Five patients with purulent meningitis had neurological symptoms, five cases had hepatosplenomegaly and two cases had septic shock. Nineteen cases (76%, 19/25) had significantly elevated white blood cell (WBC) counts, twenty-one cases (84%, 21/25) had significantly elevated serum C-reactive protein (CRP) levels, and eight cases (50%, 8/16) had significantly elevated serum procalcitonin (PCT) levels. The drug sensitivity analysis showed that invasive SP had high resistance rates to penicillin (96%), clindamycin hydrochloride (88%) and erythromycin (84%), and it was completely sensitive to imipenem, vancomycin, levofloxacin and linezolid. The multi-drug resistance rate of invasive SP was up to 88%. Twenty-three cases (92%) were cured or improved after active treatment.. SP septicemia is commonly seen in children aged under 2 years. The most common clinical manifestation is fever, accompanied by elevated WBC count, CRP level and PCT level, and it is usually complicated by pulmonary or brain infection. Resistance to multiple antibiotics is very common in SP strains, so it is important to properly use antibiotics according to drug sensitivity test results. Patients who receive active treatment have a good clinical outcome.

Topics: Anti-Bacterial Agents; Bacteremia; C-Reactive Protein; Calcitonin; Calcitonin Gene-Related Peptide; Child; Child, Preschool; Female; Humans; Infant; Infant, Newborn; Male; Microbial Sensitivity Tests; Pneumococcal Infections; Protein Precursors; Retrospective Studies; Streptococcus pneumoniae

Topics: Anti-Infective Agents; Calcitonin; Calcitonin Gene-Related Peptide; Humans; Influenza A Virus, H1N1 Subtype; Influenza, Human; Pneumococcal Infections; Protein Precursors; Streptococcus pneumoniae

Plasma procalcitonin (PCT) increases rapidly during bacterial infections but remains low in viral infections and other inflammatory processes. High plasma PCT typically occurs in children with bacterial meningitis, severe bacterial infections, particularly in cases of septic shock or bacteremia, and in renal parenchymal damage. The aim of this study was to test the usefulness of plasma PCT analysis in the diagnosis of osteomyelitis, septic arthritis, and other skeletal inflammatory diseases in pediatric patients admitted because of fever and limping.. White blood cell count, erythrocyte sedimentation rate, C-reactive protein, and PCT levels were measured in children admitted to the pediatric department with fever, limping, and suspected osteomyelitis or septic arthritis. PCT levels were measured by an immunochromatography assay, based on monoclonal and polyclonal antibodies against katacalcin.. Forty-four children were evaluated: 12 (27.3%) were diagnosed with osteomyelitis, 11 (25%) had septic arthritis, 5 children (11.4%) were diagnosed as a soft tissue infection, and transient synovitis or reactive arthritis was diagnosed in another 6 children (13.6%). Four children (9.1%) were diagnosed as having juvenile rheumatoid arthritis, and 6 (13.6%) with different diseases. PCT value was elevated in 7 patients (58.3%) with osteomyelitis, and only 3 children (27.2%) with the diagnosis of septic arthritis had a mildly elevated value. Among the children with other diagnosis, there were no positive PCT values (P < 0.001 between skeletal infection and all other diagnosis).. In this study, PCT was found to be a useful marker in the diagnosis of osteomyelitis and not in septic arthritis. A larger group of patients needed to be studied to confirm our findings.

Topics: Adolescent; Adult; Arthritis, Infectious; Arthritis, Juvenile; Biomarkers; Calcitonin; Calcitonin Gene-Related Peptide; Child; Child, Preschool; Diagnosis, Differential; Female; Fever; Humans; Infant; Infant, Newborn; Male; Osteomyelitis; Pneumococcal Infections; Protein Precursors; Soft Tissue Infections; Staphylococcal Infections; Synovitis