Bacterial meningitis: pathogenesis, pathophysiology, and progress.
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Biomedical subjects
Publications and source records attributed to V Quagliarello.
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Bacterial meningitis continues to cause morbidity and mortality despite bactericidal antibiotic therapy. Experimental studies of pathophysiology reveal the bacteria and their surface components within cerebrospinal fluid (CSF) induce the release of inflammatory cytokines that promote CSF inflammation, injure the cerebral microvasculature and cause brain edema. Adjunctive corticosteroids reduce inflammation, ameliorate the pathophysiology, and improve neurologic outcome in children. Practical recommendations are made for children and selected adults regarding current and future directions of adjunctive therapy.
Endovascular infections that involve the right side of the heart present their own unique etiologies, pathophysiologies, clinical manifestations, and therapeutic issues. The pathology of the vegetations of right-sided endocarditis is identical to that of left-sided endocarditis. These vegetations are irregular, friable masses of varying size the contain platelets, fibrin, RBCs, and microorganisms. These lesions serve as a nidus for deep-seated infection and produce sustained bacteremia. Right-sided endocarditis occurs in 5% to 10% of all cases of endocarditis. The most common predisposing factors are IV drug abuse and congenital heart disease. S. aureus is the most common pathogen. The clinical manifestations include fever, chills, rigor, dyspnea, pleuritic pain, productive cough, and hemoptysis. The cardiac manifestations can be notably absent early in the course of the disease, with only 20% of patients initially showing a significant murmur on physical examination. Peripheral embolic lesions can be seen. Echocardiography is helpful in identifying vegetations on the tricuspid valve in a significant proportion of patients. The chest radiograph is characteristic, showing features typical of multiple septic pulmonary emboli. The radiograph shows multiple, small, fuzzy, patchy, peripherally located densities that can change rapidly on serial films. Complications of right-sided endocarditis include pulmonary infarction, pulmonary abscess, progressive right-sided heart failure, and renal abnormalities. The treatment of right-sided endocarditis includes prolonged therapy, with high doses of IV bactericidal antibiotics. Four weeks of antibiotic therapy is generally required, but newer regimens using combination antibiotic therapy can be successful in sensitive strains of viridans group streptococci and S. aureus. Surgical resection of the tricuspid valve is recommended for organisms that do not respond to initial antibiotic therapy, fungal endocarditis, resistant relapsing organisms, or coexistent infection with S. aureus and P. aeruginosa. The prognosis of right-sided endocarditis is generally favorable when compared with left-sided endocarditis. The prognosis is especially favorable in IV drug abusers infected with S. aureus. Patients infected with fungal organisms, Pseudomonas or Serratia, have a worse prognosis. The presence of significant right-sided heart failure also imparts a worse prognosis.