الفهرس 
Classifications of pyogenic and fungal CNS infectionsOnly 14 pages are availabe for public view
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Abstract
Classifications of pyogenic and fungal CNS infections
Despite major medical advances in the past century, infections of the central nervous system remain a major burden on society. A high index of suspicion, early recognition, and prompt treatment by the clinician remain the best tools to save lives and decrease resultant morbidity from these infections. However, multiple drug-resistant microbes are emerging with the broad-spectrum use of medications, and thus appropriate clinically focused diagnosis and treatment should be the ultimate goal and standard of care.
There are four main causes of infections of the Central Nervous System (CNS): bacterial , viral, fungal and protozoal .The most important bacterial infections include bacterial meningitis, intracranial suppurations and intracranial complications of extracranial infections like otitis media , leprosy, neuroborreliasis, tuberculosis and neurosyphilis .
Classifications of Bacterial infections of the CNS
According to entry routes: Direct from other adjacent source of infections.
And hematogenic Awhich is through arterial and venous routes .
according to pus formation :
1 • Pyogenic infections: mean that infections by organisms (e.g. streptococcae, meningnococcae) which can produce pus which is an acute, exsudative process with massive infiltration of neutrophilic granulocytes.
Types of pyogenic Infections of the CNS include:
•Brain abscess
• Epidural Abscess
• Subdural Abscess and Empyema
• Purulent Leptomeningitis and
Meningoencephalitis.
• Encephalitis and Pyocephalus
2 • Non-pyogenic infections (e.g. mycobacteriae, treponema) : Subacute or chronic granulomatous inflammation.
Types of pyogenic Infections of the CNS include:
•Bra
• Epidural Abscess
• Subdural Abscess and Empyema
• Purulent Leptomeningitis and
Meningoencephalitis. in abscess
• Encephalitis and Pyocephalus
2 • Non-pyogenic infections (e.g. mycobacteriae, treponema) : Subacute or chronic granulomatous inflammation.
The likelihood of CNS fungal infection is generally underestimated because of the nonspecific symptoms and the difficulty in diagnosis. Cryptococcal meningitis is the most common CNS fungal infections. Clinically relevant fungi include yeasts, filamentous fungi and dimorphic fungi. Yeasts are unicellular organisms and include the relatively common Candida species and Cryptococcus species, and less common pathogens such as Trichosporon species. The filamentous fungi are characterized by branching hyphae, which are either septate or aseptate and are further subdivided into the hyalinized and the dematiaceous groups. These classes include the more common Aspergillus species and the zygomycetes, including Rhizopus, Rhizomucor and Mucor. Less common pigmented molds that infect the Central Nervous System (CNS) include Pseudallescheria and Fusarium species. Finally, the dimorphic, or so-called ‘endemic’, fungi are filamentous at 258°C and yeasts or spherules in host tissue or when incubated at 358°C, and include Blastomyces, Histoplasma, Coccidioides, Paracoccidioides and Penicillium marneffei .
Recent methods of diagnosis of pyogenic and fungal CNS infections
The patient with pyogenic and fungal central nervous system infections presents with generalized signs of infection, features of raised intra-cranial tension and focal neurological signs depending upon the location of the abscess. In any patient having one of the underlying causes, features suggestive of meningitis, raised intracranial tension or focal neurological deficit should suggest the possibility or brain abscess. Lumbar puncture should not be routinely done in such cases since the risk or coning is high. Moreover the CSF may not show diagnostic changes in the case of localized abscess.
Reduced level of consciousness is a common clinical finding in acutely sick patients. In the majority of cases a cause for the encephalopathy is readily identifiable. Frequently, the onset of encephalopathy is associated with, or follows, infection. The mechanisms through which infection leads to encephalopathy are diverse. They range from direct microbial invasion of the brain or its supporting structures, to remote, infection- triggered mechanisms such as acute disseminated encephalo- myelitis. However, Most common is the encephalopathy caused through a remote effect of systemic sepsis (septic encephalopathy).
The diagnosis can be confirmed by CT Scan which should be done of an early stage. X-ray skull may give evidence of sinusitis and rarely gas in the abscess cavity, if the abscess is caused by gas-producing organisms or the abscess is communicating with the paranasal sinuses. Cranial MRI is now the imaging study of choice, being superior to cranial CT scan in outlining the extent of lesions and demonstrating the convexity and interhemispheric collections. MRI also shows greater morphological detail than CT scan. The sensitivity of MRI is improved by using gadolinium contrast medium.
In the other hand many recent scientific achievements in neuroimaging, molecular diagnosis, antibiotic therapy and neurointensive care have allowed more precise and earlier diagnoses and more efficient treatments, resulting in improved outcomes.
CSF sampling is indicated in all patients with meningitis and may show a lymphocytic pleocytosis (Cryptococcus and Candida), neutrophilic predominance (Aspergillus and Blastomycosis) or eosinophilia (Coccidioides). Care is required prior to sampling the CSF to ensure that increased intracranial pressure does not place the patient at undue risk from the lumbar puncture (e.g. non-communicating hydrocephalus) . In cases of neurosurgery or device-related Candida meningitis, pleocytosis may be absent. CSF glucose is generally low and protein high, with exceptionally high levels seen in cryptococcal infections. CSF antigen testing is available for Cryptococcus and Histoplasma, with sensitivity and specificity rates reported in some series above 90%. Testing for serum beta glucan may be useful for identifying the presence of an invasive fungal infection (with the notable exceptions of Cryptococcus and zygomycetes) with sensitivity rates, in some series, of 64-77%, although specificity may be decreased in the presence of concurrent bacteremia .While serum assay for galactomannan is reported in some series to have a 95% sensitivity and specificity for invasive Aspergillus infections. CSF assays for galactomannan are under investigation and may prove to have clinical utility . A positive serum galactomannan assay in the setting of a radiographic brain lesion should prompt empiric antifungal therapy targeted to treat invasive aspergillosis. If noninvasive methods fail to define a pathogen, the risks and benefit of brain biopsy should be weighed against empiric antifungal therapy
Treatment of pyogenic CNS infections
Control of infection is achieved by giving the appropriate antibiotic in high dosage, as in the case of purulent meningitis. Treatment of bacterial meningitis has two major goals. The first is the rapid administration of a bactericidal antibiotic with good CNS penetration to treat the neurologic infection.The second, in select cases, is the use of anti-inflammatory agents to suppress the sequelae of bacterial lysis. Empiric antibiotic choice is based on broad-spectrum coverage of common pathogens. The choice of antibiotics has to be made in consideration of the prevailing pathogens in the locality. Antibiotic prophylaxis is recommended for high-risk exposures to patients with Neisseria or Hib meningitis, with high-risk populations including household contacts, those with exposure to oral secretions, and those who have intubated the patient without a mask. Regimens include single-dose ciprofloxacin or ceftriaxone, or with rifampin, 600 mg every 12 hours for five doses. There is no indication for prophylaxis for exposure to pneumococcal meningitis. Quinolone resistance has been reported to Neisseria, and this class of antibiotics is no longer recommended for prophylaxis in parts of the United States .
As soon as the abscess is localized, it is aspirated through a burr hole. Antibiotics can be instilled into the abscess cavity. Excision of the abscess may be necessary in some cases.If left untreated, brain abscess is fatal. Complications include rupture into cerebral ventricles producing ventriculitis, meningitis, rise in intracranial tension and secondary epilepsy. If the abscess is diagnosed early and treated, full recovery may occur. Mortality is higher in brain abscess complicating congenital heart disease. The overall mortality in large series is 11-15%.
Treatment of fungal CNS infections
Antifungal therapy for CNS fungal infections typically requires a prolonged period, often months to years; thus, it is imperative to define the etiologic agent especially for resistant cases. Primary issues in the successful treatment of a CNS fungal infection are maintaining a high index of clinical suspicion and establishing a specific pathogen identification through antigen detection, histopathology or fungal culture obtained by lumbar puncture or biopsy. Effective empiric antifungal regimens are limited by significant toxicities and narrow therapeutic range. In addition, the patients at highest risk for fungal brain infections are often on a variety of other medications, including antiretrovirals or immunosuppressants, which have multiple drug-drug interactions. The goal of treatment is to cure the infection and reduce the risk of permanent damage. In the other hand many recent scientific achievements in neuroimaging, molecular diagnosis, antibiotic therapy and neurointensive care have allowed more precise and earlier diagnoses and more efficient treatments, resulting in improved outcomes.However, multiple drug-resistant microbes are emerging with the broad-spectrum use of medications, and thus appropriate clinically focused diagnosis and treatment should be the ultimate goal and standard of care.