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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effective treatment of deep wound infection without removal of a previously implanted foreign body is difficult. The Neurocybernetic Prosthesis (NCP) System (Cyberonics Inc., Webster, TX, U.S.A.), implanted for vagus nerve stimulation in patients with medically refractory epilepsy, uses coil-like electrodes placed around the left vagus nerve after exposure of the nerve in the carotid sheath. Infection within this compartment endangers the contained structures and makes removal of the system hazardous. We report the case of one patient implanted with the NCP who underwent successful open wound treatment without removal of the system. A 35-year-old man had local signs of wound infection 5 weeks after implantation of a vagus nerve stimulator. Systemic signs of infection were absent. C-reactive protein was slightly elevated, but all other laboratory values were normal. After open wound debridement and thorough rinsing with bacitracin-containing solution, the wound was packed with 3% iodoformized gauze. The NCP was left in place. Systemic antibiotic therapy with fosfomycin and cefmenoxim was started. Cultures confirmed an infection with Staphylococcus aureus. The wound was rinsed daily with 3% hydrogen peroxide solution and 5% saline until cultures were sterile and granulation tissue started to fill the wound. Delayed primary closure was performed 2 weeks later. Wound healing was accomplished without removal of the device. No signs of recurrent infection were observed during a follow-up of 1 year. Open wound treatment without removal of the implanted vagus nerve stimulator is feasible in cases of deep cervical wound infection and can be an alternative if removal of the device appears hazardous.
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PMID:Deep wound infection after vagus nerve stimulator implantation: treatment without removal of the device. 1120 97

Acute hematogenous osteomyelitis in children is a relatively uncommon but potentially serious disease. Improvements in radiologic imaging, most notably magnetic resonance imaging, and a heightened awareness of this condition have led to earlier detection and resultant marked decreases in morbidity and mortality. Staphylococcus aureus, which has the ability to bind to cartilage, produce a protective glycocalyx, and stimulate the release of endotoxins, accounts for 90% of infections in all age groups. Infections with Haemophilus influenzae have become rare in immunized children. A careful history and a thorough physical examination remain important. Positive cultures are obtained in only 50% to 80% of cases; the yield is improved by the use of blood cultures and evolving molecular techniques. Improvements in antibiotic treatment have lessened the role of surgery in managing these infections. Sequential intravenous and high-dose oral antibiotic therapy is now an accepted modality. Evaluation of response to treatment by monitoring C-reactive protein levels has decreased the average duration of therapy to 3 to 4 weeks with few relapses. The emergence of antibiotic resistance, particularly resistance to methicillin and vancomycin by S aureus organisms, is of increasing concern. Long-term sequelae and morbidity are primarily due to delays in diagnosis and inadequate treatment.
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PMID:Acute hematogenous osteomyelitis in children. 1142 74

The objective of this study is to determine the plasma concentrations and diagnostic accuracy of interleukin-6 (IL-6) and interleukin-8 (IL-8) in newborn infection. One hundred and one newborn infants with clinical signs of infection during their primary hospitalization were investigated with the minimum of a blood culture, C-reactive protein (CRP), full blood examination (FBE), and cytokine concentrations (IL-6 and IL-8). Infection in infants was classified without knowledge of cytokine levels into four groups-definite (n = 11), probable (n = 12), uncertain (n = 52), and nil (n = 26). The median concentrations of IL-6 and IL-8 were significantly higher in the definitely infected group compared with the other three groups (p <0.05). At the cut-off concentration of highest accuracy, IL-6 (>175 pg/mL) and IL-8 (>28 pg/mL) had similar sensitivities (80 and 82%, respectively) and specificities (91 and 81%, respectively). Cut-off concentrations could be identified with improved sensitivities (90% for IL-6 and 100% for IL-8) that maintained specificity >50%. However, the confidence intervals were wide for all sensitivities and specificities. IL-6 and IL-8 had little diagnostic accuracy in infants with probable infection. IL-6 and IL-8 concentrations increase early in newborn infants with definite infection.
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PMID:Interleukin-6 and interleukin-8 in newborn bacterial infection. 1160 49

Infection after total hip or knee arthroplasty is a major concern for the orthopedic surgeon. Because postoperative recovery in patients undergoing hip or knee replacement is always characterized by a shift in basal laboratory parameters, the value of the routine use of these parameters in the detection of this major complication is controversial. The aim of this study was to evaluate the physiological behavior of these parameters, the most reliable of which are C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cell count (WBC). The pattern of these parameters was observed for 60 days after surgery in 74 patients (48 males and 26 females) who underwent total hip or total knee arthroplasty. Mean age was 65.4 years. ESR reached a peak on day 5 and then decreased as much as 3-fold by day 60. CRP displayed even greater sensitivity with a peak level on day 3 followed by a rapid return to basal levels. WBC also peaked on day 1. No significant differences were found between total hip arthroplasty and total knee arthroplasty. Observation of the pattern of these parameters identifies any nonphysiological modifications and enables suitable measures to be adopted.
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PMID:Postoperative physiopathological analysis of inflammatory parameters in patients undergoing hip or knee arthroplasty. 1177 79

Atherosclerotic plaques were likened histologically to healing inflammatory lesions by Russell Ross, who proposed a "response to injury" hypothesis for their formation. More recently, intraplaque inflammation has been postulated to play a role in thinning of the fibrous cap, plaque rupture, and superadded thrombosis. Potential causes for vascular injury include mechanical stress, smoke exposure, hypercholesterolemia, hyperhomocysteinemia, and chronic infection (direct, or indirect). Blood levels of inflammatory markers (e.g., C-reactive protein [CRP]; serum amyloid A [SAA]; fibrinogen; plasma viscosity; erythrocyte sedimentation rate [ESR]; leukocyte count, low serum albumin) have been associated with vascular risk factors and with prevalent and incident atherothrombotic cardiovascular disease (CVD) (coronary heart disease, [CHD]; stroke; and peripheral arterial disease). More recently, cytokines (e.g., interleukin-6 [IL-6]) and soluble adhesion molecules (e.g., intercellular adhesion molecule-1, vascular cell adhesion molecule-1) have been associated with both risk factors and disease; and offer potential therapeutic targets for nonspecific "anti-inflammatory" treatment of arterial disease. Infections associated with arterial disease include specific infections (Chlamydia pneumoniae, Helicobacter pylori) and nonspecific infections (periodontal infections, respiratory tract infections). Recent meta-analyses have shown that associations of serum markers of C. pneumoniae and H. pylori with arterial disease, risk factors, or potential intermediary mechanisms for disease are weaker than was first suggested by early reports. Likewise, further studies and meta-analyses are required to evaluate the epidemiologic relationships of CVD to periodontal infection and disease and to chronic pulmonary infections and disease. The weaker the associations between chronic infections and CVD, the larger is the size of randomized controlled trials required to establish (or exclude) a preventive effect of infection treatment. While control of chronic infection in the mouth, stomach or lungs is appropriate for its local effects, proving its efficacy in prevention of CVD presents a continuing challenge to medical science.
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PMID:The relationship between infection, inflammation, and cardiovascular disease: an overview. 1188 52

Sero-epidemiological case control studies have observed positive relations between infections with Chlamydia pneumoniae, Helicobacter pylori or cytomegalovirus (CMV) and the occurrence of coronary artery disease (CAD) and stroke. Moreover, positive relations between 'infection burden' and CAD and the role of inflammation have recently been described. However, the relations between infection, inflammation and the occurrence of peripheral arterial disease (PAD) have not been reported so far. We performed a multi-centre population-based case-control study, using serum samples of 228 young female PAD patients and 643 control women to determine IgG antibody titres and C-reactive protein. The odds ratios for PAD in women with serological evidence for infection with C. pneumoniae, H. pylori or CMV were 2.0 (95% CI; 1.3-3.1), 1.6 (95% CI; 1.1-2.2) and 1.6 (95% CI; 1.1-2.3), respectively. The cumulative number of infections was positively related to the risk of PAD; the odds ratio was 1.5 (95% CI; 1.0-2.4), 2.7 (95% CI; 1.6-4.4) and 3.5 (95% CI; 1.5-8.1) for women with one, two or three infections, respectively. This increased risk, related to the 'infection burden', was found again in the subgroup of women with a high CRP level, but not in the subgroup with a low CRP level. Infections might be a causal component in the development of PAD. The risk of PAD is not only related to a single pathogen in particular, but also to the cumulative number of infections. The positive relation between 'infection burden' and PAD was only found in women with a high CRP level, which indicates that inflammation might be involved in the process that leads to PAD.
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PMID:Chlamydia pneumoniae, Helicobacter pylori and cytomegalovirus infections and the risk of peripheral arterial disease in young women. 1204 33

Plasma concentrations of procalcitonin (PCT) have been shown to be elevated in bacterial and fungal infections. In contrast to C-reactive protein (CRP), PCT is not elevated in inflammations of noninfectious origin. Febrile inflammatory conditions are frequent in patients with hemato-oncological diseases. A reliable marker to discriminate infectious inflammations from drug-related and tumor-associated fever is still lacking. To evaluate the impact of PCT in this setting, PCT and CRP were prospectively measured in 95 febrile hemato-oncological patients. Infections could be identified in 40 of 95 patients: 38 of 95 had fever of unknown origin (FUO), 9 patients were suspected to suffer from drug-related fever, and 8 patients from tumor-associated fever. In the noninfection group (drug-related and tumor-associated fever), PCT levels were significantly lower than in patients with infections (P<0.001) or FUO (P<0.001). Differences were still highly significant comparing patients with suspected drug-related or tumor-associated fever alone with the infection or the FUO cohort. All eight patients with tumor-associated fever as well as eight of the nine patients with drug-related fever had PCT levels within the normal range (<0.5 micro g/l). CRP values only partially allowed discrimination between the various subgroups. Differences were significant between patients with drug-related fever and the infection (P=0.001) or FUO group (P=0.004). However, as CRP levels were far above the normal range also in the patients with drug-related fever, the significance of individual values was rather limited. In conclusion, PCT may provide useful additional information to assess the clinical significance of febrile conditions. PCT may facilitate the decision on when to initiate antimicrobial or cytotoxic therapy.
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PMID:Procalcitonin: a useful discriminator between febrile conditions of different origin in hemato-oncological patients? 1260 88

In patients with diarrhea caused by Vibrio parahaemolyticus, antibody-secreting cell responses to thermostable direct hemolysin (TDH), lipopolysaccharide (LPS), and whole-cell bacteria were seen. TDH- and LPS-specific responses were seen in serum samples, and immunoglobulin A antibody responses were observed in stool. Levels of C-reactive protein and nitric oxide metabolites increased in the systemic circulation at the onset of illness. Tumor necrosis factor-alpha and lactoferrin levels were high during the acute stage in mucosal secretions and in plasma, whereas interleukin-1beta levels were high only in mucosal secretions. Duodenal and rectal biopsy specimens obtained at the onset of illness showed an acute inflammatory response. The lamina propria showed edema, congestion of blood vessels, and hemorrhage, with an increase in levels of polymorphonuclear neutrophils and macrophages. Strains belonging to different serotypes exhibited varying resistance to killing by serum; the O8:K21 strain was most sensitive. Infection with V. parahaemolyticus results in B cell responses and an acute inflammatory response that is self-limiting.
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PMID:Adaptive and inflammatory immune responses in patients infected with strains of Vibrio parahaemolyticus. 1266 Sep 23

Pleural fluid rarely occurs in patients with progressive systemic sclerosis (PSS) or polymyositis (PM) with no lesions in the pulmonary area. Pleural fluids in patients with autoimmune diseases are mostly dominated by monocytes and lymphocytes but very rarely contain increased eosinophils. We report a 55-year-old male with PSS-PM overlap syndrome and eosinophilic pleural effusion. Air invasion into the pleural cavity and the antituberculous therapy could be ruled out as causes for the patient's eosinophilic pleural effusion, because the differential eosinophil count was already as high as 19% from the first thoracentesis before the start of antituberculous therapy. Infections and malignant tumor also were unlikely causes based upon the negative pleural fluid results and the negative pleural biopsy findings, except for nonspecific inflammation. After the administration of corticosteroid, the pleural effusion decreased promptly, with normalization of serum creatine phosphokinase and C-reactive protein concentrations.
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PMID:Progressive systemic sclerosis-polymyositis overlap syndrome with eosinophilic pleural effusion. 1272 42

Infections are common in systemic lupus erythematosus (SLE), and remain a source of mortality. The types of infections (such as pneumonia, urinary tract infection, cellulitis, and sepsis) in SLE patients are similar to the general population and include the same pathogens (Gram-positive and Gram-negative). SLE patients may also develop opportunistic infections, especially when treated with immunosuppressive agents. As a high-risk population, identification and treatment of chronic infections such as tuberculosis, hepatitis B, or human immunodeficiency virus (HIV), are important prior to the institution of immunosuppression to prevent reactivation or exacerbation of the infection. A common caveat is to distinguish between a lupus flare and an acute infection; judicious use of corticosteroids and cytotoxic drugs is critical in limiting infectious complications. The risk factors associated with susceptibility to disease include severe flares, active renal disease, treatment with moderate or high doses of corticosteroids and/or immunosuppressive agents, and others. Genetic factors (complement deficiencies, mannose-binding lectin, Fcgamma III, granulocyte macrophage colony-stimulating factor [GM-CSF], osteopontin) may predispose certain SLE patients to develop infections. Parameters including C-reactive protein (CRP) and adhesion molecules may help to differentiate an infectious disease from an exacerbation of the disease. Finally, the mechanism of molecular mimicry by specific microbial agents may play a role in the induction of SLE.
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PMID:SLE and infections. 1279 59


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