CNS Infections - PDF

Infections of CNS Dr. Salmeen Abdulla Aljeffree  Infections of CNS With infection, damage to nervous tissue may be the consequence of direct injury of neurons or glia by the infectious agent or may occur indirectly through the elaboration of microbial toxins, destructiv...

Infections of CNS Dr. Salmeen Abdulla Aljeffree  Infections of CNS With infection, damage to nervous tissue may be the consequence of direct injury of neurons or glia by the infectious agent or may occur indirectly through the elaboration of microbial toxins, destructive effects of the inflammatory response, or the result of immune- mediated mechanisms. There are four principal routes by which infectious microbes enter the nervous system. Hematogenous spread is the most common means of entry; infectious agents ordinarily enter through the arterial circulation, but retrograde venous spread can occur through anastomoses with veins of the face. Direct implantation of microorganisms is almost invariably traumatic or is associated with congenital malformations (such as meningomyelocele). Local extension can come from any of several adjacent structures (air sinuses, an infected tooth, cranial or spinal osteomyelitis). Transport along the peripheral nervous system occurs with certain viruses, such as rabies and herpes zoster.  Meningitis Meningitis: is an inflammation of the membranes (meninges) surrounding your brain and spinal cord.  Importance of early recognize CNS infection High mortality Permanent disability Features of both meningeal and brain involvement to various degrees Common features in presentation and sequelae – Bacterial meningitis – Tuberculous meningitis – Viral meningoencephalitis – Brain abscess – Fungal – polio Important meningeal signs  Acute bacterial Meningitis (ABM) Very common & serious Medical emergency 100% curable if treated adequately or 100% fatal High index of suspicion important Dx by CSF examination  ABM : Etiology Streptococcus pneumoniae (pneumococcus). This bacterium is the most common cause of bacterial meningitis in infants, young children and adults in the United States. It more commonly causes pneumonia or ear or sinus infections. A vaccine can help prevent this infection. Neisseria meningitidis (meningococcus). This bacterium is another leading cause of bacterial meningitis. These bacteria commonly cause an upper respiratory infection but can cause meningococcal meningitis when they enter the bloodstream. This is a highly contagious infection that affects mainly teenagers and young adults. It may cause local epidemics in college dormitories, boarding schools and military bases. A vaccine can help prevent infection.  ABM : Etiology Haemophilus influenzae (haemophilus). Haemophilus influenzae type b (Hib) bacterium was once the leading cause of bacterial meningitis in children. But new Hib vaccines have greatly reduced the number of cases of this type of meningitis. Listeria monocytogenes (listeria). These bacteria can be found in unpasteurized cheeses, hot dogs and lunchmeats. Pregnant women, newborns, older adults and people with weakened immune systems are most susceptible. Listeria can cross the placental barrier, and infections in late pregnancy may be fatal to the baby. Anatomic defects (# base of skull, pilonidal sinus), immunodeficiency others  ABM: Epidemiology Max in 1st 5 yrs Risk Factors: Colonization Crowding: person to person droplet infection Poverty Male Absence of breast feeding  ABM: Pathology Bacterial colonization of nasopharynx  bacteremia  choroid plexus  meninges Meningeal exudates, ventricultis, perivascular inflammatory exudates, venous occlusion, infarction, necrosis, ↑ICT Pyogenic meningitis. A thick layer of suppurative exudate covers the brainstem and cerebellum and thickens the leptomeninges  ABM: Clinical Features Sudden onset high fever, headache, anorexia, myalgia, photophobia, meningeal signs, convulsions, stupor, coma ↑ICP: hypertension, bradycardia, bulging AF, 3rd/6th cranial nerve palsy, posturing, breathing abnormalities. Papilledema Purpuric rash s/o meningococcus Septic foci  ABM Diagnosis – High index of suspicion very important – Confirm by CSF examination – LP referred if there is contraindication – Start empirical antibiotics on suspicion CSF: ↑Pressure, turbid, ↑cells (mostly polys), ↑protein, ↓sugar to < 40% of blood sugar Gram stain, culture Latex Imaging CSF  ABM Complications – Subdural effusion – Subdural empyema – Ventricultis – Abscess – Hydrocephalus – Infarcts Sequelae – Neurological deficits – Deafness – MR – Epilepsy – hydrocephalus  ACUTE FOCAL SUPPURATIVE INFECTIONS Brain Abscess Brain abscesses may arise by direct implantation of organisms, local extension from adjacent foci (mastoiditis, paranasal sinusitis), or hematogenous spread (usually from a primary site in the heart, lungs, or distal bones or after tooth extraction). Predisposing conditions include acute bacterial endocarditis, which tends to produce multiple abscesses; congenital heart disease with right-to-left shunting and loss of pulmonary filtration of organisms; chronic pulmonary sepsis, as can be seen with bronchiectasis; and immunosuppression. Streptococci and staphylococci are the most common offending organisms identified in nonimmunosuppressed populations  Morphology. Grossly, abscesses are discrete lesions with central liquefactive necrosis surrounded by fibrosis and swelling. On microscopic examination there is exuberant granulation tissue with neovascularization around the necrosis that is responsible for marked vasogenic edema. A collagenous capsule is produced by fibroblasts derived from the walls of blood vessels. Outside the fibrous capsule is a zone of reactive gliosis with numerous gemistocytic astrocytes.  Brain Abscess Predisposing features: – Congenital cyanotic heart disease – Meningitis – Penetrating head injury – Local extension from mastod, otitis, sinusitis, soft tissues of face and scalp Etiology: – S aureus – Micro aerophilic strep – Other aerobic & anaerobics – Mixed infections in 35% Clinical Features: – Fever – Headache – Vomiting – Focal deficits – ↑ICT Lab – Blood counts non specific – EEG: focal slowing – CT scan diagnostic Treatment: – IV antibiotics – cover anaerobes (CP + Chloro) – Surgical drainage  Chronic meningitis Slow-growing organisms (may be caused by M. tuberculosis, T. pallidum, and Borrelia species.) that invade the membranes and fluid surrounding your brain cause chronic meningitis. Chronic meningitis develops over two weeks or more. The signs and symptoms of chronic meningitis — headaches, fever, vomiting and mental cloudiness — are similar to those of acute meningitis.  Tuberculous meningitis (TBM) Most dreaded and dangerous form of TB Risk Factors: – Young age – Household contact – Recent infection – Measles Pathophysiology – Primary infection  bacillemia  hematogenous seeding of meninges (Rich’s foci)  rupture – Thick exudates in basal cisterns – Arteritis  TBM: Clinical Features 3 stages – Stage 1: prodromal stage with nonspecific symptoms 1-4 weeks – Stage 2: neurological manifestations – seizures, deficits, meningeal signs – Stage 3: coma Decerebrate posturing, cranial nerve palsies, optic atrophy, extrapyramidal signs, hydrocephalus (communicating or obstructive) more common  TBM DDx – Partially treated bacterial meningitis – Other CNS infections Dx – CSF examination - ↑pressure, cells upto 500 /cu mm, mostly lymphos, ↑protein, sugar ↓upto ½ of concommitant blood sugar – AFB – Culture – CXR – Skin test – Newer Tests: Tuberculostearic acid Adenosine deaminase test Bromide partition test NBT ELISA for antibody/antigen PCR Intrerferon gamma release assays  TBM Complications & sequelae: – Hydrocephalus – Optic neuritis – Focal deficits – Epilepsy – MR Treatment – 4 anti TB drugs for initial 2 months + 3 drugs for 6-7 months – DOTS ?? – Steroids initially for 6 weeks – Shunt surgery for hydrocephalus  Viral meningitis Viral meningitis is usually mild and often clears on its own. Most cases in the United States are caused by a group of viruses known as enteroviruses, which are most common in late summer and early fall. Viruses such as herpes simplex virus, HIV, mumps, West Nile virus and others also can cause viral meningitis. VIRAL MENINGOENCEPHALITIS Encephalitis and meningitis are 2 ends of the spectrum Neurotropic & non neurotropic viruses can cause VME – Arbo: JE/ west nile/ dengue – Entero – Herpes:HSV1, EBV, CMV, HHV-6, Varicella zoster – Myxo – Paramyxo – Adeno – Rhabdo  VME: Clinical features 3 stages – Prodromal: fever, vomiting, diarrhea, anorexia, malaise – Acute encephalitic stage: convulsion. Coma, neurodeficits, raised ICT, death – Convalescent stage: improving coma, extrapyramidal  Characteristically, there is a lymphocytic meningoencephalitis (sometimes with neutrophils), and a tendency for inflammatory cells to accumulate perivascularly. Multiple foci of necrosis of gray and white matter are found; in particular, there is evidence of single-cell neuronal necrosis with phagocytosis of the debris (neuronophagia). Microglial cells form small aggregates around foci of necrosis, called microglial nodules. In severe cases there may be a necrotizing vasculitis with associated focal hemorrhages. While some viruses reveal their presence by inclusion bodies, the identification of viral pathogens is most often by a combination of ultrastructural, immunohistochemical, and molecular methods Characteristic findings of viral encephalitis include perivascular cuffs of lymphocytes (A) and microglial nodules (B).  Herpes encephalitis Commonest sporadic encephalitis in west Severe, fulminant course Focal deficits Focal features on EEG Imaging: temporal hypodensities Specific antiviral Treatment available: acyclovir 10 mg/kg/d x 14-21 days Herpes encephalitis showing extensive destruction of inferior frontal and anterior temporal lobes. B, Necrotizing inflammatory process characterizes acute herpes encephalitis  Viral (aseptic) meningitis Mild, self limited Etiology: – Mumps – Entero – EBV – Arbo – M pneumoniae Clinical features: – Fever – Headache – Irritability – Vomiting – Convulsion (rare) – Meningeal signs Lab: CSF clear, pleocytosis, ↑protein, normal sugar Tt: supportive only