1,721,053 research outputs found
Lyme borreliosis. Skin and nervous system
No full textLyme borreliosis is the most frequent tick-borne disorder. Its discovery 25 years ago was a milestone in the field of infectious diseases. Children are especially prone to tick bites and therefore at special risk for Lyme borreliosis, Lyme borreliosis is a multisystem disorder which affects the skin in three-fourths of the cases (mainly erythema migrans) and the central nervous system and the joints clearly less frequently, In childhood acute peripheral facial nerve palsy and aseptic meningitis dominate the clinical spectrum of neuroborreliosis. Lyme borreliosis is a clinical diagnosis which is established on the basis of the history, the clinical findings, and the antibody results. Specific antibody diagnosis is complicated by the problem of insufficient sensitivity and specificity. The consequence is the risk of overdiagnosis and overtreatment. In neuroborreliosis the CSF findings are especially helpful. CSF pleocytosis is mandatory for the diagnosis of neuroborrehosis. Early and effective antibiotic treatment guarantees a good prognosis of Lyme borreliosis with quick resolvement of symptoms. Long-term sequelae of neuroborrehosis have not been proved in children, but cannot yet be excluded
Minimizing the release of proinflammatory and toxic bacterial products within the host: A promising approach to improve outcome in life-threatening infections
No full textVarious bacterial components (e.g., endotoxin, teichoic and lipoteichoic acids, peptidoglycans, DNA) induce or enhance inflammation by stimulating the innate immune system and/or are directly toxic in eukariotic cells (e.g., hemolysins). When antibiotics which inhibit bacterial protein synthesis kill bacteria, smaller quantities of proinflammatory or toxic compounds are released in vitro and in vivo than during killing of bacteria by beta-lactams and other cell-wall active drugs. In general, high antibiotic concentrations liberate lower quantities of bacterial proinflammatory or toxic compounds than concentrations close to the minimum inhibitory concentration. In animal models of Escherichia coli Pseudomonas aeruginosa and Staphylococcus aureus peritonitis/sepsis and of Streptococcus pneumoniae meningitis, a lower release of proinflammatory bacterial compounds was associated with a reduced mortality or neuronal injury. Pre-treatment with a bacterial protein synthesis inhibitor reduced the strong release of bacterial products usually observed during treatment with a P-lactam antibiotic. Data available strongly encourage clinical trials comparing antibiotic regimens with different release of proinflammatory/toxic bacterial products. The benefit of the approach to reduce the liberation of bacterial products should be greatest in patients with a high bacterial load. (c) 2005 Published by Elsevier B.V. on behalf of the Federation of European Microbiological Societies
Modulation of Release of Proinflammatory Bacterial Compounds by Antibacterials: Potential Impact on Course of Inflammation and Outcome in Sepsis and Meningitis
No full text
SUMMARY
Several bacterial components (endotoxin, teichoic and lipoteichoic acids, peptidoglycan, DNA, and others) can induce or enhance inflammation and may be directly toxic for eukaryotic cells. Bactericidal antibiotics which inhibit bacterial protein synthesis release smaller quantities of proinflammatory/toxic bacterial compounds than Β-lactams and other cell wall-active drugs. Among the Β-lactams, compounds binding to penicillin-binding protein 2 (PBP-2) release smaller amounts of bacterial substances than antibacterials inhibiting PBP-3. Generally, high antibiotic concentrations (more than 10 times the MIC) induce the release of fewer bacterial proinflammatory/toxic compounds than concentrations close to the MIC. In several in vitro and in vivo systems, bacteria treated with protein synthesis inhibitors or Β-lactams inhibiting PBP-2 induce less inflammation than bacteria treated with PBP-3-active Β-lactams. In mouse models of Escherichia coli peritonitis sepsis and of Streptococcus pneumoniae meningitis, lower release of proinflammatory bacterial compounds was associated with reduced mortality. In conclusion, sufficient evidence for the validity of the concept of modulating the release of proinflammatory bacterial compounds by antibacterials has been accumulated in vitro and in animal experiments to justify clinical trials in sepsis and meningitis. A properly conducted study addressing the potential benefit of bacterial protein synthesis inhibitors versus Β-lactam antibiotics will require both strict selection and inclusion of a large number of patients. The benefit of this approach should be greatest in patients with a high bacterial load.
</jats:sec
Successful management of malaria tropica with 50% parasitaemia
No full textHistory: A 52-year-old woman was hospitalized with fever after a 3-week stay in tropical Kenya. Prophylaxis against malaria had been carried out with chloroquine. Diagnosis: Falciparum malaria with 28% parasitaernia at first examination, rising to 50% after 3 hours. Treatment and course: Treatment with quinine dihydrochloride i.v. was initiated immediately after diagnosis. In addition, in view of increasing parasitemia of up to 50%, a partial exchange blood transfusion was carried out. No clinical signs of organ damage caused by malaria were observed. Because of a drop in blood pressure the patient needed catecholamine treatment for a short time. After decrease of the parasiterma the patient rapidly recovered and complete cure was achieved. Conclusion: Despite extremely high parasitemia the clinical signs were unusually mild. Standard treatment for severe malaria is intravenous administration of quinine. However, this drug is no longer sold in Germany, so that difficulty in obtaining it must be expected. A stockpiling of quinine is recommended for hospitals treating patients with malaria. Transfusion may improve outcome and must be considered if parasite counts are high or if there are clinical signs of malaria complications
Strategies for Increasing the Resistance of the central Nervous System against bacterial Infections
No full textUpdate Neuroborreliosis - New and Proven Options
No full textNeuroborreliosis is a nervous system infection caused by Borrelia burgdorferi sensu lato. Lyme disease is the most frequent tick-borne infectious disease in Europe affecting the skin, joints, heart, nervous system and rarely the eyes. Since the discovery of the causative pathogen Borrelia burgdorferi 30 years ago, the rapid accumulation of knowledge about this disease has resulted in well-evaluated clinical and microbiological diagnostic guidelines. Today, neuroborreliosis can generally be diagnosed and treated successfully. Progress in microbiological research has led to improved serological tests with higher sensitivity and new approaches for early diagnosis of Lyme disease. Erythema migrans is the most frequent manifestation of Borrelia infection. It is diagnosed clinically. Neuroborreliosis is diagnosed by the combination of typical neurological symptoms, cerebrospinal fluid pleocytosis and Borrelia-specific antibodies produced intrathecally. In adults, erythema migrans is treated with doxycycline, in children with amoxicillin. Standard treatment of neuroborreliosis is ceftriaxone or cefotaxime i.v. Recent studies show similar efficacy of oral doxycycline in early neuroborreliosis. An appropriate antibiotic treatment eliminates the pathogen effectively. Repeated episodes of acute manifestations of Lyme disease in treated patients are probably due to reinfection and not to relapse. Only in a small proportion of treated patients is recovery from neuroborrelioses incomplete. In addition to neurological residual sequelae recent studies have detected persistent neuropsychological deficits in a small subgroup of patients. Conversely, when borreliosis is suspected by patients suffering from non-specific symptoms, a thorough clinical and laboratory assessment is required to identify other underlying diseases
- …
