Despite the progress in antimicrobial therapy, pyogenic infections of the CNS remains a serious disease, with significant mortality and morbidity. The neurosurgeon encounters these infections as intra-cranial and spinal abscesses and post-traumatic and post-operative infections. In addition, neurosurgeons are often associated with management of bacterial meningitis.

1 ) Spontaneous bacterial meningitis:

Almost three-quarters of the spontaneous meningitis are due to Streptococcus pneumoniae ( pneumococcus ), Haemophilus influenzae ( Haemophilus ) and Nisseria meningococcus infection; certain organisms tend to predominate with the age of the patient.

 Pathogenesis:

Haematogenous spread is the most common, either venous or arterial. The organisms appear to enter the CSF through choroid plexus, aggregate in and around cerebral draining veins and archnoidal villi and cause cerebral phlebitis and arachnoid villous dysfunction which may lead to increased ICT. Pial cell necrosis, small vessel arteritis and phlebitis are frequently associated.

Retrograde propagation ( infected thrombi within emissary veins )  from sinusitis, otitis and mastoiditis and direct spread from trauma and adjacent infective foci are other modes of infection.

Clinical features:

The typical symptoms include fever, headache, photophobia, stiff neck, nausea and vomiting, lethargy or altered mental status.

On examination, in addition to fever, there may be rashes ( meningococcus ).There may be resistance of neck flexion (Kerning's sign ) and passive flexion may cause flexion of hips and knees (Brudzinski's sign ). Altered sensorium and focal neurological deficit may be noted.

Infants do not usually have neck stiffness. 

Examination should also include a search for a primary focus, such as mastoiditis, sinusitis, otitis and endocarditis.

Diagnosis:

SAH and Neuroleptic malignant syndromes are sometimes confused with meningitis. Very occasionally a posterior fossa tumor may present in a similar way. Tuberculous and Viral meningitis may have to be ruled out only by investigations at times. 

Direct examination of the CSF provides the diagnosis. Decrease in glucose content, elevation of proteins and polymorphonuclear leukocytosis are the expected findings. A relative increase in mononuclear leucocytosis or lymphocytes may suggest viral or tuberculous etiology respectively. Organisms may be detected on a Gram's stain and  grow in culture and their antibiotic sensitivities are essential for management. AFB staining should be carried out as a routine in these days of AIDS.

Additional tests such as blood cultures and counterimmunoelectrophoresis or agglutination tests may help when partial treatment prevents the growth of bacteria in culture. A lactate content of more than 3.8 mmol/l in the CSF and C-reactive protein greater than 100 ng/ml will also help in differentiating bacterial from viral meningitis.

A mild diffuse rise in ICT is common in meningitis and should not prevent a lumbar puncture. Decrease in the level of consciousness or a focal neurological deficit suggest presence of increased IC in most. Absence of papilledema does not exclude a significant increase in ICT.
	Subdural empyema-rt.frontal& parafalcine	Cerbellar -epidural abcess	Meningeal enhancement-CT

When suspected, associated intra-cranial abscess or hydro-cephalus, should be ruled out with CT or MRI scan.

Imaging with CT and MRI is useful in evaluating the leptomeningeal involvement and complications of meningitis.

Treatment:

Adequate antibiotic therapy, initially empirical, then according to culture studies is the treatment.

Empirical antibiotic therapy is based on epidemiological information, age and CSF gram's stain studies and should be started with broad-spectrum antibiotics. Intrathecal and intraventricular instillation may be reserved for systemic treatment failure.

Other appropriate supportive management  is mandatory. Surgery may be needed to tide over a crisis, such as hydrocephalus.

Uncomplicated cases require 2 weeks of antibiotics following a satisfactory response.

Recurrence within a few weeks should prompt a search for a persistent focus or immune deficiency status. Careful examination for anomalies such as congenital dermal sinus, enteric cysts, encephalocele  and meningocele is warranted.

2 ) 'Neurosurgical' bacterial meningitis:

Headache, nuchal rigidity and altered sensorium are less reliable in meningitis in neurosurgical patients. Pre-existing neurological deficits and effects of surgery may cloud the clinical picture. They are characterised by different aetiology and require a different management on occasions.

Post-traumatic:

Streptococcus pneumoniae is more often associated with dural tears following skull fractures. Penetrating injuries may precipitate Gram negative bacilli, such as klebsiella, E.coli, Pseudomonas and other enterobacteriaceae.

Treatment includes surgical repair of the dural tear, in addition to appropriate antibiotics.

Postoperative:

The incidence of postoperative meningitis varies between 1-15 %. The most common microbes involved were Pseudomonas, Klebsiella, E.coli and rarely other enterobactericeae.

It is claimed that third generation cephalosporins at the start of surgery reduce the incidence of post-operative meningitis.

Shunt infections:

The incidence varies in different series with an average of 10%. Staphylococcus epidermidis and aureus (the non pathogenic skin flora ) are often the culprits.

In addition to antibiotic therapy, the shunt may have to be removed.

Congenital anomalies:

Ruptured meningomyelocoele or a persistent dermal sinus in the craniospinal axis may be the cause for recurrent meningitis. Unusual and mixed pathogens should alert the surgeon.

They require appropriate surgery in addition to antibiotics.

3 ) Epidural and subdural empyemas:

These are rare these days.

Epidural empyemas are often associated with osteomyelitis of the skull. Frontal sinusitis, depressed fractures and penetrating injuries are the usual causes. Aspiration of these well localized collections and appropriate antibiotics give good results. Associated skull osteomyelitis must be eradicated.

Subdural empyemas are an emergency. Paranasal sinusitis is the common cause. Subdural effusions and hematomas may get infected and become empyema. Aspiration and appropriate antibiotics is the treatment. Attention to predisposing factors should follow immediately.

4 ) Brain abscess:

Incidence is about 8% of the ICSOLs  in India and on the rise in developed countries as well with the advent of AIDS.

Pathogenesis:

Bacteroides and anaerobic streptococci are the most common causative bacteria.

The majority of them are caused by spread from adjacent sites. Frontal and ethmoid sinusitis can lead to frontal abscesses, maxillary sinusitis to temporal lobe abscesses, sphenoid sinusitis to frontal or temporal abscesses, and mastoiditis to temporal lobe or cerebellar abscesses. Abscesses from the sinuses are commonly caused by Streptococci.

Those of otic origin is mostly by a combination of aerobes and anaerobes and is the commonest cause in India.

Trauma, especially with retained foreign bodies, is also a significant cause. Staphylococcus aureus is often the causative organism. 

Metastatic abscesses from a remote site are by hematogenous route, the commonest cause in developed countries. They are often multiple and typically occur at the junction of the white and gray matter, where the capillary blood flow is the slowest. They are more commonly seen in the distribution of the middle cerebral arteries and the parietal lobes, where the regional blood flow is the highest. The common systemic sites are chronic pulmonary infections, skin pustules, bacterial endocarditis and osteomyelitis. Those with a right to left vascular shunt as a result of congenital heart disease or pulmonary arteriovenous malformations are particularly susceptible. These abscesses contain a mixed flora. 

In about 25 % of patients, the source is unknown.

As the infection reaches the brain, there is immediate inflammatory response with edema and increased vasculairty; thrombophlebitis may block venous drainage and edema worsens; small vessels get thrombosed; areas of necrosis appear; reactions from the surrounding brain form a capsule and the infection get localized as the capsule gets thicker. 

It is suggested that there is early cerebritis on days 1 to 3, late cerebritis on days 4 to 9, early capsule formation on days 10 to 13, and late capsule formation after day 14.

Meningitis may precede or complicate an abscess. An abscess may rupture into the ventricles causing ventriculitis which is often fatal.

Clinical features:

They mimic any other ICSOL with seizures, focal deficits and features of raised ICT, such as headache, vomiting. There is no specific feature. Low grade fever may be seen in some, especially in early stages. Associated causative conditions may suggest an abscess.

Diagnosis:

Suspicion is the first step.

There may be leucocytosis in early stages; ESR is usually raised; plasma C-reactive protein is elevated.

CT scan reveals a contrast enhancing ring lesion with non-enhancing hypodense center and surrounding edema. There may be gas inside the lesion and ventricular and meningeal enhancement.

frontal abscess-plain CT	frontal abscess-contrast CT	frontal abscess-ruptured into ventricle-plain CT	frontal abscess-ruptured into ventricle-contrast CT

MRI scan delineates the lesion better and also reveals additional micro-abscesses, if any. 

Isotope scan and PET (positron emission tomography ) scan may be of help to differentiate between an abscess and a tumor with necrotic center.                   

Treatment:

The management is still a controversial topic. Some studies suggest that with adequate antibiotic therapy, mortality rates (10 to 20%) are similar after aspiration alone, or  aspiration followed by excision, or primary excision. 

It is widely presumed that total excision reduces the recurrence rates and the incidence of seizures, but there is no evidence to support this .But excision does shorten the hospital stay and the antibiotic therapy.

Surgical therapy: 

Surgery establishes the diagnosis, removes the infected, and necrotic tissue, provides the material for microbiological studies, and relieves raised ICT.

The recommended procedures are aspiration, excision and drainage. 

Drainage using a flexible drain  is seldom used nowadays and has been replaced by aspiration and excision procedures. 

Total excision is a must in abscesses containing foreign material. Excision may be the primary procedure. Some prefer to aspirate, get the culture studies and excise the lesion after few days of appropriate antibiotics. Studies suggest that such preoperative antibiotics are of little benefit. The location and the stage of abscess, the condition of the patient need to be considered in choosing between aspiration and excision.

Total excision is not feasible if the capsule is not well formed or in deep and critical areas without significant morbidity and also in seriously ill patients. In such cases, stereotactic aspiration is recommended and it is also useful in multiple abscesses.

Medical therapy:

Blind antibiotic therapy may be of use in ' cerebritis ' stage. There are occasional reports claiming cure with antibiotics alone, either empirically or after blood and / or CSF studies, especially in microabscesses. With the advent of stereotactic facilities it is not recommended even in microabscesses.

Associated antiedema measures and other supportive therapy are indicated. 

Associated predisposing conditions should be eradicated.

Antibiotics should be continued for 6-8 weeks and patient should be followed up for about 6 months.

5 ) Skull Osteomyelitis:

Most are related to trauma and spread from adjacent sites, especially the frontal sinusitis. There are occasional case reports of hematogenous origin.

In acute osteomyelitis, the patient is toxic with tender swelling over the involved bone called " Pott's puffy tumor " and likely to involve the CNS.

Chronic ones often present with a lump in the scalp.

Treatment is wide excision of the involved bone until the normal bone is reached and appropriate antibiotics. Treatment of associated condition should follow. 

6 ) Bacterial infections of the spine:

It is uncommon.

The route of infection is hematogenous from usually the urinary tract by retrograde venous seeding through Batson's venous plexus, or direct extension from adjacent sites, or as a result of penetrating injury. Staphylococcus aureus is the most common organism. Gram negative organisms and anaerobes have also been implicated.

Iatrogenic causes such as post discectomy (1%), lumbar punctures are rare. This should be excluded in 'Failed back syndromes'.

It usually affects two adjacent vertebrae and the disc. Posterior elements are rarely involved. The lumbar and thoracic spines are more commonly affected.

Acute infections present with fever, backache and tender spines and the chronic ones with just pain.

Neurological complications, due to epidural extension and spinal deformity and instability, may occur.

X-rays show disc space narrowing in early stages and vertebral collapse in late stages with associated deformity.

Isotope and CT scans may pick up early lesions and the skip lesions. if any. 

CT guided aspiration and biopsy for diagnosis and microbiological studies are widely practiced.

MRI scans reveal the extent of the intra spinal extension.

Treatment is bed rest until pain subsides and antibiotics are administered for 6 to 8 weeks in uncomplicated cases.

Debridement, decompression and stabilization with bone grafting is recommended when there is a progressive neurological deficit and extensive vertebral or intraspinal involvement. Ideally an anterior or anterolateral approach is employed unless there is posterior involvement which is rare. Instrumentations are avoided.