1,721,224 research outputs found
Experimental meningitis by Streptococcus pneumoniae and Neisseria meningitidis in rodents
Bacterial meningitis (BM) is a global public health issue that affects patients of all ages. The two leading causes of BM worldwide are Streptococcus pneumoniae (the pneumococcus) and Neisseria meningitidis (the meningococcus). Despite the use of antibiotics and vaccines, both pneumococcal meningitis (PM) and meningococcal meningitis (MM) result in high case fatality rates and long-term neurological sequelae. Moreover, increasing resistance to first-line antibiotics, limited vaccine coverage, serotype replacement in vaccinated population, and lack of adjunctive therapies to control brain damage are all matters of concern in the management of PM and MM.
The availability of animal models of PM and MM is crucial to characterize the pathogenetic and pathophysiologic mechanisms of disease as well as to identify novel antimicrobial agents, adjuvant therapies and vaccine candidates. Historically, animal models of BM employed large animals to mimic the disease in humans, such as monkeys for MM and rabbits for PM. However, since the introduction of rodents, both rats and mice have demonstrated to be robust, reliable, and suitable species for modeling both PM and MM. Depending on the route of infection, the dose of bacterial inoculum, the animal age and strain, different experimental readouts are obtained that permit to answer specific scientific questions.
This chapter describes the main features of two models of PM and MM developed in the infant rat and adult mouse, respectively. Each model system presents unique characteristics that allow to study different aspects of the disease.
The broad range of different forms of brain injury that can be observed in the PM infant rat model enables to study the entire spectrum of the pathophysiology of brain damage in PM and allows to evaluate novel therapeutic strategies and their impact on long-term neurological sequelae. The MM mouse model is suitable to investigate the role of meningococcal virulence factors in the disease, the host–parasite interactions in the central nervous system, and the efficacy of drugs to control the infection and limit brain damage in MM
[A case from practice (305). Recurrent erysipelas--tinea pedis et unginum--chronic venous insufficiency]
[In search of strategies for preventing brain damage as a sequela of bacterial meningitis]
Multiplication of bacteria within the central nervous system compartment triggers a host response with an overshooting inflammatory reaction which leads to brain parenchyma damage. Some of the inflammatory and neurotoxic mediators involved in the processes leading to neuronal injury during bacterial meningitis have been identified in recent years. As a result, the therapeutic approach to the disease has widened from eradication of the bacterial pathogen with antibiotics to attenuation of the detrimental effects of host defences. Corticosteroids represent an example of the adjuvant therapeutic strategies aimed at downmodulating excessive inflammation in the infected central nervous system. Pathophysiological concepts derived from an experimental rat model of bacterial meningitis revealed possible therapeutic strategies for prevention of brain damage. The insights gained led to the evaluation of new therapeutic modalities such as anticytokine agents, matrix metalloproteinase inhibitors, antioxidants, and antagonists of endothelin and glutamate. Bacterial meningitis is still associated with persistent neurological sequelae in approximately one third of surviving patients. Future research in the model will evaluate whether the neuroprotective agents identified so far have the potential to attenuate learning disabilities as a long-term consequence of bacterial meningitis
[A case from practice (300). Lambliasis; possibly 2-year-old chronic infection. Maculopapillary pruritic exanthema of the hairy scalp and the sternum; seborrheic dermatitis; skin reaction to lambliasis? Horseshoe kidney].
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
[Meningitis (II)--acute bacterial meningitis]
Acute meningitis is a medical emergency, particularly in patients with rapidly progressing disease, mental status changes or neurological deficits. The majority of cases of bacterial meningitis are caused by a limited number of species, i.e. Streptococcus pneumoniae, Neisseria meningitis, Listeria monocytogenes, group B Streptococci (Streptococcus agalactiae), Haemophilus influenzae and Enterobacteriaceae. Many other pathogens can occasionally cause bacterial meningitis, often under special clinical circumstances. Treatment of meningitis includes two main goals: Eradication of the infecting organism, and management of CNS and systemic complications. Empiric therapy should be initiated without delay, as the prognosis of the disease depends on the time when therapy is started. One or two blood cultures should be obtained before administering the first antibiotic. Empiric therapy is primarily based on the age of the patient, with modifications if there are positive findings on CSF gram stain or if the patient presents with special risk factors. It is safer to choose regimens with broad coverage, as they can usually be modified within 24-48 hours, when antibiotic sensitivities of the infecting organism become available. Adjunctive therapy with dexamethasone is also administered in severely ill patients concomitantly with the first antibiotic dose. In patients who are clinically stable and are unlikely to be adversely affected if antibiotics are not administered immediately, including those with suspected viral or chronic meningitis, a lumbar puncture represents the first step, unless there is clinical suspicion of an intracerebral mass lesion. Findings in the CSF and on CT scan, if performed, will guide the further diagnostic work-up and therapy in all patients
An in vitro model of central nervous system infection and regeneration: neuronal stem cells as targets of brain damage and regenerative therapies in bacterial meningitis.
[Pneumococcal meningitis as a complication of maxillary sinusitis. Purulent conjunctivitis is linked to maxillary sinusitis].
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