Micro 61 Cns Infections And Micro 66 Sepsis

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Micro 61

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CNS Infections

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infection of brain parencyhma

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encephalitis or brain abscess

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infection of meningitis

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meningitis

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infection of spinal cord tissue

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myelitis

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postinfectious encephalitis (ADEM)

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Acute disseminated encephalomyelitis occurs weeks after viral infection may result from cross reaction from immune factors against components of normal brain

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prion

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abnormally folded proteins that cause chronic progressive uniformaly fatal disease

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bacteria that classically cause meningitis

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S. pneumonia, H. influenzae, N. meningitidis

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bacteria that classicly cause brain abscesses

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S. aureus ; Anaerobic streptococci

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viruses that cause encephalitis

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mostly HSV

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virus that more commonly causes meningitis

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enteroviruses

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K1 antigen

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found in capsule of E Coli that invade CNS , rich in sialic acid

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sialic acid in capsule facilitates CNS infection how

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adherence, antiphagocytic, inhibits complement

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3 routes for CNS infection

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hematogenous, neural pathway, direct innoculation (trauma/congental defect)

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path of pathogen to CNS in hematogenous spread

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blood, choroid plexus, ventricular CSF, epenymal cells, periventricular tissue

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compliment in the CSF

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very low, so complement dependent lysis in brain does not readily occur

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intrinsic immunologic surveillance mechanism of brain

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microglia

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virchow robin spaces

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perivascular sheeths surrounding blood vessels as they enter brain. Contain lymphocytes and macrophages

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PML

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progressive multifocal leukoencephalopathy is caused by reactivation of JC virus, seen in those with acquired immunodeficiency

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most common bacterial meningitis of neonates

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GBS , E Coli (in that order)

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listeria monocytogenes bacterial meningitis seen in

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neonates and elderly

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most common bacterial meningitis 3-60mo

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S. pneumonia, N. Meningitidis, HIB

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Most common bacterial meningitis after cranial surgery

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S. aureus

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Most common bacterial meningitis of immunosupressed

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L. monocytogenes, Gram negative organisms

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arborvirus peaks in what months

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summer

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enteroviral infections peak when

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late summer early fall

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most common cause of sporadic viral encephalitis in adults

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HSV

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characteristic inflammatory response of CNS

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infiltration of microglia ; proliferation of astrocytes

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causes of neurologic symptoms in CNS infections

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focal tissue destruction, cerebral edema/herniation

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why is prevalence of HIB meningitis decreasing

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vaccination against HIB

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acute meningitis are caused by

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bacteria and viruses

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subacute and chronic meningitis is most ofton caused by

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fungi and mycobacteria

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emperic treatment of bacterial meningitis (meningiococcal) is to include

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vancomycin and ceftriaxone

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prophylactic treatment of those in contact with meningiococcal meninigitis patients is

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rifampin , ceftriaxone or cipro

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why does bacterial meningitis warrant aggressive treatment

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high morbidity and mortality

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CSF findings in Bacterial and Viral meningitis

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viral associated with brief window of elevated PMNs but usually <300 ; with a shift to lymphocytes after 24 hours, glucose is normal in viral meningitis as well as protein. In bacterial meninigitis PMNs are through the roof, glucose is low and protein is high

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how are pneumococcal and meningococcal meningitis acquired

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respiratory route

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deficiency in _____________ is associated with susceptibility to neisseria

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late compliment (C5-9 MAC)

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associated with thick accumulations of pus that can block CSF flow raising ICP

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Enterobacteriacae and Pneumococci

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ICP in meningococcal meningitis

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only mildly elevated

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common sequellae of HIB meningitis

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deafness

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class frequently used to treat bacterial meningitis

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Beta Lactam

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b lactam antibiotics that are particularly good at fighting CNS infections due to better BBB penetration

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cefotaxime and ceftriaxone

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why do we use vancomycin in emperic therapy against bacterial meningitis

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infection is so dangerous we must use the high efficacy drug until we rule out cephlosporin resistance

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useful drug to combat cerebral edema from bacterial meningitis

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dexamethasone

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meningiococci that we don’t have a vaccine for

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type B

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most common cause of aseptic meningitis

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viruses

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differences b/w viral and bacterial meningitis

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viral is lymphocyte rich, milder disease, self limiting

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treatment for tuberculosis meningitis

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4 drug therapy (at least 3 INH, rifampin, pyrazinamide, streptomycin ; steroids to reduce inflammation

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CSF differences in tuberculosis and acute bacterial meningitis

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TB has more lymphocytes and monocytes

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acute onset of febrile illness accompanied by headache and altered mental status

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halmark of encephalitis

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most frequent etiology of sporadic encephaltiis

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HSV

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distinguishes meningitis from encephalitis

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altered mental status

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focal lesions of herpes encephalitis often seen where

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frontal and temporal lobe

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CSF of HSV encephalitis

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mononuclear pleocytosis with RBCs and increased protein , normal glucose

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additional methods for diagnosing HSV encephalitis

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EEG abnormalities, MRI, PCR of CSF

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treatment of HSV encephalitis

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acyclovir

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focal infection of brain parenchyma

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brain abscess, causes include bacteria, fungi, parasites

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subdural empyema

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poorly localized subdural abscess ; can resolve on its own

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epidural abscess

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external to dura, may be complication of epidural anesthesia can spread to bone

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contents of acute CNS abscesses

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mixed bacterial flora, strict and facultative anaerobes

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why should patients with acute CNS abscess receive emperic therapy for anaerobes

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they are hard to culture so may come back as false negative

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can be isolated from brain abscess in septic emboli

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staph

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chronic brain abscesses are most commonly caused by

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mycobacteria, cryptococcus, other fungi

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LP in patient suspected to have a brain abscess

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contraindicated because increased ICP could cause brainstem herniation with lumbar decompression, LP is also not usually diagnostic

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Micro 66

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Sepsis

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progression of septic syndromes

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generalized inflammation, systemic inflammatory response syndrome, sepsis, severe sepsis, septic shock, multiorgan dysfunction syndrome

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criteria for SIRS

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fever, leukopenia or leukocytosis, tachycardia. Tachypnea

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criteria for sepsis

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SIRS plus confirmed infection

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criteria for severe sepsis

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sepsis with low BP corrected by fluids

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criteria for septic shock

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sepsis plus persistant hypotension nonresponsive to aggressive fluid recisitation , drugs to increase vascular tone requried

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criteria for MODS

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septic shock with evidence of coagulapathy, end organ dysfunction, accumulation of metabolic products that cannot be cleared (lactic acidosis)

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first proinflammatory cytokines to be released at induction of injury/infection

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TNF alpha, IL1 ; IL6 and 8 too

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physioligic effects of TNFa

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mimics sepsis syndrome, marginates neutrophils

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physiologic effects IL1

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fever, increased adhesiveness of endothelial cells and leukocytes, procoagulant activity

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physiologic effects of IL2,6,8

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hypotension and capillary leak, synthesis of acute phase proteins and leukocyte chemotaxis

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physiologic effect of compliment cascade

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neutrophil chemotaxis, aggregation, cap leak

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endorphins cause s

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hypotension and capillary leak, synthesis of acute phase proteins and leukocyte chemotaxis

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leukotrienes and thromboxane cause

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platelet aggregation, neutrophil adhesion, cap leak, decreased myocardial contractility

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Pg E2/I2 cause

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hypotension, neutrophil adhesion, fever, muscle ache, muscle proteolysis

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bradykinin effects

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hyoptension and capillary leak

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serotonin effect

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pulmonary HTN, capilalry leak

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hitamine effect

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hypotension, capillary leak

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PAF effect

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hypotension , cap leak, platelet aggregation, leukocyte activation, decreased myocardial contractility

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endothelin 1 activity

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kidney vasoconstriction

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compensatory anti-inflammatory response includes

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IL4,10,11, and TGF B (all anti-inflammatory cytokines)

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most potent bacterial stimulator of cytokines

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LPS

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PAMPs and DAMPs

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activate Pattern recognition receptors on immune cells (PRRs such as toll like receptors NOD-LRR_

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effect of sepsis on vasculature

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systemic vascular resistance decreases and there is venous pooling leading to extravasation of fluids, drop in BP and increase in cardiac work

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effect of sepsis on heart

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depressio of mitochondria and myocardial contractility, leading to a drop in stroke volume, meaning increase BP (tachycardia) is required to maintain BP

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warm shock

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in early sepsis low BP and high HR , called warm because skin is flushed and warm ,

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cold shock

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in late sepsis CO begins to drop and periphery constricts to shunt blood to try to give blood to vital organs, turn a blue purple color

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effect of sepsis on lungs

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fluid escapes into alveoli and neutrophils that are activated release free radicals this makes lungs damaged and edemous (Adult respiratory distress syndrome), must mechanically ventilate pt at this point

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kidney effect of sepsis

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hypotension + infection = acute tubular necrosis and renal failure…. Leads to buildup of dangerous metabolites

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effect of sepsis on liver

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leads to necorsis and jaundice, lowering of albuim, more edema…etc

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endocrine and metabolic effects of sepsis

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massive catabolic state due to stress hormones , sometimes adrenals cant keep up (relative adrenal insufficency ; lactic acidosis

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treatment for sepsis

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fluid resucitation , vasopressors, broad spectrum antibiotics (bacteriocidal)

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look over table 66-2 for a bad time

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