infectious dz Flashcards
How are patients with bacterial meningitis initially treated
Start appropriate empiric antibiotic therapy urgently (within 60minutes of arrival to the ER) after patient’s arrival at the hospital
Bacterial meningitus classic triad
Only ~45% of patients have the complete classic triad of fever,decreased conciousness and neck stiffness (nuchal rigidity/meningismus) but nearly 100% of patients have at least 2 of 4 symptoms (fever, headache, nuchal rigidity, altered mental status).
Bacterial meningitis findings other than triad
seizures, nausea/vomiting, myalgias, cranial nerve palsies (III, VI, VII, VIII) and focal deficits (hemiparesis, ataxia, gaze preference), papilloedema in <1% cases
Median age of patients with bact meningitis
42 yrs- use to be 1yr but Hib vaccine has eliminated meningitis in children mostly
bacterial meningitis pathogenesis
A. Bacteria can reach the subarachnoid space from: (1) the bloodstream (most common) (2) adjacent intracranial infection (sinusitis, mastoiditis, otitis) (3) congenital, traumatic or surgical defects in skull/spinal column.
B. Bacterial meningitis is a disease of the subarachnoid space. Bacterial cell wall components stimulate pro-inflammatory cytokines (e.g. TNF, IL-1), increase BBB permeability, and recruit neutrophils (PMNs). PMNs add to purulent exudates, and enhance cytotoxic edema via reactive oxygen species. Hydrocephalus and infarction from vasculitis can occurA. Bacteria can reach the subarachnoid space from: (1) the bloodstream (most common) (2) adjacent intracranial infection (sinusitis, mastoiditis, otitis) (3) congenital, traumatic or surgical defects in skull/spinal column.
B. Bacterial meningitis is a disease of the subarachnoid space. Bacterial cell wall components stimulate pro-inflammatory cytokines (e.g. TNF, IL-1), increase BBB permeability, and recruit neutrophils (PMNs). PMNs add to purulent exudates, and enhance cytotoxic edema via reactive oxygen species. Hydrocephalus and infarction from vasculitis can occurA. Bacteria can reach the subarachnoid space from: (1) the bloodstream (most common) (2) adjacent intracranial infection (sinusitis, mastoiditis, otitis) (3) congenital, traumatic or surgical defects in skull/spinal column.
B. Bacterial meningitis is a disease of the subarachnoid space. Bacterial cell wall components stimulate pro-inflammatory cytokines (e.g. TNF, IL-1), increase BBB permeability, and recruit neutrophils (PMNs). PMNs add to purulent exudates, and enhance cytotoxic edema via reactive oxygen species. Hydrocephalus and infarction from vasculitis can occur
Most common organisms causing meningitis in Pt <2 months
*Streptococcus agalactiae (Group B Strep)
*Gram-Negative Rods (e coli)
Listeria monocytogenes
Streptococcus pneumoniae (pneumococcus)
Hemophilus influenzae (H flu)
(0-5%) Neisseria meningitidis (meningococcus)
(0-1%) Staphylococcus speciesStreptococcus agalactiae (Group B Strep)
*Gram-Negative Rods (e coli)
Listeria monocytogenes
Streptococcus pneumoniae (pneumococcus)
Hemophilus influenzae (H flu)
(0-5%) Neisseria meningitidis (meningococcus)
(0-1%) Staphylococcus speciesStreptococcus agalactiae (Group B Strep)
*Gram-Negative Rods (e coli)
*Listeria monocytogenes
Streptococcus pneumoniae (pneumococcus)
Hemophilus influenzae (H flu)
(0-5%) Neisseria meningitidis (meningococcus)
(0-1%) Staphylococcus species
Most common organisms causing meningitis in Pt 2-23months
(50%) Streptococcus pneumoniae (pneumococcus)
(10-15%) Neisseria meningitides (meningococcus)
(10-15%) Streptococcus agalactiae (Group B Strep) E coli
(5-10%) Haemophilus influenzae (nontypable H. flu)
(1-2%)Listeria monocytogenes
(0-5%) Staphylococcus species
(50%) Streptococcus pneumoniae (pneumococcus)
(10-15%) Neisseria meningitides (meningococcus)
(10-15%) Streptococcus agalactiae (Group B Strep) E coli
(5-10%) Haemophilus influenzae (nontypable H. flu)
(1-2%)Listeria monocytogenes
(0-5%) Staphylococcus species
(50%) Streptococcus pneumoniae (pneumococcus)
(10-15%) Neisseria meningitides (meningococcus)
(10-15%) Streptococcus agalactiae (Group B Strep) E coli
(5-10%) Haemophilus influenzae (nontypable H. flu)
(1-2%)Listeria monocytogenes
(0-5%) Staphylococcus species
Most common organisms causing meningitis in Pt 23 monts -34 yrs
(~40%) Neisseria meningitidis (meningococcus)
(~40%) Streptococcus pneumoniae (pneumococcus)
(5-10%) Hemophilus influenzae (H flu)
(<5%)Streptococcus agalactiae (Group B Strep)
(1-2%)Listeria monocytogenes
(1-2%) Staphylococcus species
(1-2%) Gram- Negative Rods
Most common organisms causing meningitis in Pt >35 yrs
(50-70%) Streptococcus pneumoniae (pneumococcus)
(10-25%) Neisseria meningitidis (meningococcus)
(1-10%) Hemophilus influenzae (H flu)
(5-10%)Listeria monocytogenes (25% of cases in age > 60yrs or immune compromise)
(1-10%) Staphylococcus species (more common w/ neurosurg, head trauma, shunts)
(1-10%) Gram- Negative Rods (more common as a nosocomial infection)
( 60yrs or immune compromise)
(1-10%) Staphylococcus species (more common w/ neurosurg, head trauma, shunts)
(1-10%) Gram- Negative Rods (more common as a nosocomial infection)
( 60yrs or immune compromise)
(1-10%) Staphylococcus species (more common w/ neurosurg, head trauma, shunts)
(1-10%) Gram- Negative Rods (more common as a nosocomial infection)
(<5%)Streptococcus agalactiae (Group B Strep)
Diagnostic tests for suspected meningitis
Complete LP immediately (no delay for neuroimaging) in all patients with suspected meningitis unless:
- decreased level of consciousness 2. focal neurologic deficits 3. papilloedema 4. new onset seizures 5. History of CNS disease or an associated condition (e.g. frontal sinusitis) that increases probability of brain abscess/ empyema. 6. Immunocompromised. If any of the above, get blood cultures and immediate empiric antibiotics while doing CT/MRI, prior to LPComplete LP immediately (no delay for neuroimaging) in all patients with suspected meningitis unless:
- decreased level of consciousness 2. focal neurologic deficits 3. papilloedema 4. new onset seizures 5. History of CNS disease or an associated condition (e.g. frontal sinusitis) that increases probability of brain abscess/ empyema. 6. Immunocompromised. If any of the above, get blood cultures and immediate empiric antibiotics while doing CT/MRI, prior to LPComplete LP immediately (no delay for neuroimaging) in all patients with suspected meningitis unless:
- decreased level of consciousness 2. focal neurologic deficits 3. papilloedema 4. new onset seizures 5. History of CNS disease or an associated condition (e.g. frontal sinusitis) that increases probability of brain abscess/ empyema. 6. Immunocompromised. If any of the above, get blood cultures and immediate empiric antibiotics while doing CT/MRI, prior to LP
Normal CSF profile of adults and newborns
Adult: WBC (predominately lymphs and monos) <150mg/dL, glucose 2/3 of serum glucose (variable)
Bacterial meningitis CSF profile (WBC, cell type, glucose, protein, useful test
WBC: 100-10,000. Cell type: PMNs (80-95%). Glucose: low (50mg/dl). Gram stain
Viral meningitis CSF profile (WBC, cell type, glucose, protein, useful tests
WBC: 10-2,000. cell type: mononuclear lymps. Glucose: normal. Protein: normal or slightly elevated. PCR
Viral encephalitis CSF profile (WBC, cell type, glucose, protein, useful tests
WBC: 10-2,000. cell type: mononuclear lymps. Glucose: normal. Protein: elevated. PCR, MRI
How are neonates/ infants (<1-3mos) treated for bacterial meningitis
Ampicillin and Cefotaxime or ampicillin and aminoglycoside
How are children/adults (3mos-50 yrs) treated for bacterial meningitis
Ceftriaxone OR Cefotaxime AND Vancomycin
How are adults >50 yrs treated for bacterial meningitis
Ceftriaxone or Cefotaxime AND Vancomycin AND Ampicillin
How are people treated for bacterial meningitis when it is hospital acquired, with recent head trauma/neurosurg, immunocompromised or alcholics
Vancomycin AND meropenem +/- Ampicillin
What does ampicillin treat
listeria
what does meropenem treat and what is an alternative
pseudomonas and other resistant gram negative rods. Cefepime is alternative
what does vancomycin treat
provides better coverage against penicillin/cephalosporin resistant pneumococci and coagulase-negative and methicillin-resistant staphylococci as well as enterococcus.
How long are the following bacteria treated: Meningococcus, H. flu, Pneumococcus, Gram neg rod, Listeria
How long are the following bacteria treated: Meningococcus, H. flu, Pneumococcus, Gram neg rod, Listeria
Meningococcus: 7d; H. flu: 7d; Pneumococcus: 10-14 d; Gram neg rod: 21d; Listeria: 21+d (2 wks culture negative)
Use of corticosteroids in bacterial meningitis
Initiate corticosteroids in previously healthy and non-immunosuppressed patients suspected to have bacterial meningitis. Dexamethasone given Prior to or Simultaneously with the first dose of antibiotics reduces mortality and prevents hearing complications in developed countries. Benefit is seen exclusively in streptococcus pneumoniae
Initiate corticosteroids in previously healthy and non-immunosuppressed patients suspected to have bacterial meningitis. Dexamethasone given Prior to or Simultaneously with the first dose of antibiotics reduces mortality and prevents hearing complications in developed countries. Benefit is seen exclusively in streptococcus pneumoniae
Resistant bacteria in meningitis and how to treat
Pneumococci should be tested for resistance to penicillin and cephalosporins, If resistant, should have a repeat LP after 24-36 hrs of therapy to document sterilization of CSF culture
When should LPs be repeated
no clinical response in 48 hrs, resistant strains, gram negative rods or listeria (repeat 3 weeks after starting Rx or >2 weeks after negative culture)
Clinical features of viral encephalitis and meningitis
Both Typically Acute, Febrile Illnesses with Headache. Stiff Neck: Meningitis/Meningoencephalitis. Significantly Altered Mental Status, Focal Neurological Deficits, seizures all suggest brain parenchymal involvement (Encephalitis, Abscess/Empyema, etc.)
Describe two autoimmune encephalitis dzs
- Anti-NMDA Receptor Encephalitis: psychiatric symptoms, cognitive, seizures, orofacial dyskinesias, autonomic instability. CSF profile looks like viral encephalitis. Diagnosis: serum/CSF testing for the antibody. Treatment: immune suppression.2. Autoimmune limbic encephalitis: Antibodies to onco-neuronal antibodies or synaptic/neuronal cell surface antigens (VGKC, GAD, AMPAR, etc).
Viruses that cause meningitis vs encephalitis
Meningitis: enteroviruses, arboviruses (west nile), herpes (HSV-2, VZV), HIV, mumps, measles. Encephalitis: Arboviruses (West nile is most common cause of epidemic encephalitis), herpes (HSV-1 is most common cause of sporadic encephalitis, CMV, EBV), HIV, influenza, rabies
Diagnosis of viral meningitis
LP (PMNs rather than lymphocytes may predominate in ~50% of WNV cases. Low glucose is occasionally seen with Mumps, LCMV, and HSV 2. ), PCR amplification of viral genome from CSF, serology (CSF IgM diagnostic of many aroboviruses (WNV). )
Viral meningitis therapy
Acyclovir for HSV, VZV; Antiretrovirals for HIV; Foscarnet, ganciclovir and cidofovir for CMV; Rimantidine and others for flu; Pleconaril (non-FDA) for enteroviruses; supportive treatment for WNV.
How is west nile transmitted
Bird reservoir host > mosquito vector
Diagnosis of viral encephalitis
LP, EEG abnormal in 60-90%, CT/MRI identify focal encephalitis (ie. Herpes), PCR amplification of viral nucleic acid (HSV, VZV, CMV, EBV) or WNV IgM in CSF
west nile virus neuroimaging
early MRI often normal. Later: ~30% Abnormalities in deep gray nuclei . Subtle, symmetric findings in thalamus, basal ganglia, midbrain, brainstem
CSF in west nile virus
WBC: up to 2000 cells (250 mean). Cell type: PMNS predominate. Reactive lymphocytes. Protein: elevated (50-250mg/dl). Glucose: normal. Other: IgM (does not cross BBB), PCR
WNV therapy
No therapy of proven efficacy
