DSA 30 CNS Infections (Vuitch) Flashcards
what pathogen causes acute pyogenic (bacterial) meningitis in neonates?
e.coli and group B strep
what pathogen causes acute pyogenic (bacterial) meningitis in infants/children?
s. pneumoniae
what pathogen causes acute pyogenic (bacterial) meningitis in adolescents/young adults?
neisseria meningitidis (aka meningococcal disease)
what pathogen causes acute pyogenic (bacterial) meningitis in the elderly?
s. pneumoniae and listeria monocytogenes
what is the clinical presentation of acute pyogenic (bacterial) meningitis?
fever, headache, photophobia, clouded sensorium, neck stiffness
what are the characteristics of CSF in acute bacterial meningitis?
purulent, neutrophils and organisms, increased protein, decreased glucose
what is the expected protein and glucose level in the CSF of patient with viral meningitis?
moderate increase in protein, normal glucose
what is the most common etiology of viral meningitis?
enteroviruses
what are the principal organisms involved in brain abscess?
streptococcus and staphylococcus
what is clinical presentation of brain abscess?
focal neurologic deficits and signs of increased ICP
what would be seen with an older brain abscess?
fibrous capsule surrounded by reactive gliosis and marked vasogenic edema (results from disruption of BBB)
what are characteristics of CSF in brain abscess?
high WBC count, increased protein, normal glucose
with prompt diagnosis and treatment, what is the residuum of subdural empyema?
thickened dura
what causes subdural empyema?
bacterial/fungal infection of skull bones or air sinuses spreads to subdural space
what can result from untreated subdural empyema?
focal neurologic signs, lethargy, and coma
what is the clinical presentation for tuberculous meningitis?
headache, malaise, mental confusion, and vomiting
what are characteristics of CSF in tuberculous meningitis?
pleocytosis of mononuclear cells or mix of neutrophils and mononuclear cells, increased protein, moderately decreased or normal glucose
what are complications of chronic tuberculous meningitis?
arachnoid fibrosis → hydrocephalus. obliterative endarteritis → arterial occlusion and infarction.
what is meningovascular neurosyphilis?
chronic meningitis involving the base of the brain, more variably cerebral convexities and spinal leptomeninges
what is paretic neurosyphilis?
caused by invasion of brain by t. pallidum
what is the clinical manifestation of paretic neurosyphilis?
insidious but progressive cognitive impairment associated with mood alterations that terminate in severe dementia. parenchymal damage of cerebral cortex in frontal lobe.
identify: these lesions are characterized by loss of neurons, proliferation of microglia, gliosis, and iron deposits
paretic neurosyphilis
what causes tabes dorsalis?
damage to the sensory axons in the dorsal roots → impaired joint position sense and ataxia, loss of pain sensation (Charcot joints), lightning pains, no DTRs.
identify: symptoms include aseptic meningitis, facial nerve palsies, other polyneuropathies, and encephalopathy.
neuroborreliosis (Lyme disease)
what is Waterhouse-Friderichsen syndrome?
results from mengitis-associated septicemia with hemorrhagic infarction of adrenal glands and cutaneous petechiae
what is the clinical presentation of arthropod-borne viral encephalitis?
generalized neurologic deficits: seizures, confusion, delirium, stupor, coma.
focal signs: ocular palsy, reflex asymmetry.
identify: CSF is colorless with slightly elevated pressure, increased protein, normal glucose, neutrophilic pleocytosis → lymphocytosis.
arthropod-borne viral encephalitis
what are the symptoms of meningoencephalitis caused by HSV-1?
alterations in mood, memory, and behavior
in which demographic do you predominantly see meningoencephalitis caused by HSV-1?
children and young adults
what areas of the brain are affected by meningoencephalitis caused by HSV-1?
inferior and medial regions of the temporal lobes; orbital gyri of the frontal lobes
what can HSV-2 cause in patients with active HIV infection?
acute hemorrhagic and necrotizing encephalitis
what two populations are affected by CMV infections in the nervous system?
fetuses and immunosuppressed
how does CMV manifest in utero?
periventricular necrosis → severe brain destruction → microcephaly and periventricular calcification
what are Negri bodies and what infection are they involved in?
cytoplasmic eosinophilic inclusions found in rabies infection
where can Negri bodies be found?
pyramidal neurons in hippocampus and Purkinje cells in cerebellum
what are the clinical features of rabies infection?
malaise, headache, fever, and local paresthesias around the wound initially. progression to extraordinary CNS excitability, foaming at the mouth, hydrophobia, flaccid paralysis.
alternating mania and stupor → coma → death from respiratory failure.
what is HIV encephalitis?
chronic inflammatory reaction associated with widely distributed microglial nodules often containing multinucleated giant cells. foci of tissue necrosis and reactive gliosis
what causes progressive multifocal leukoencephalopathy?
JC polyomavirus
what cells are preferentially affected in PML and what is the result?
oligodendrocytes, demyelination
identify: focal and progressive neurologic signs and symptoms. extensive lesions in hemispheric or cerebellar white matter
progressive multifocal leukoencephalopathy
identify: this CNS infection occurs in children or young adults after an initial infection with measles.
subacute sclerosing panencephalitis
identify: CNS infection chracterized by widespread gliosis and myelin degeneration, viral inclusions in nucleus of oligodendrocytes and neurons, inflammation of white and gray matter, and neurofibrillary tangles.
subacute sclerosing panencephalitis
what is the clinical presentation of subacute sclerosing panencephalitis?
cognitive decline, spasticity of limbs, and seizures
what organisms can cause fungal meningoencephalitis, specifically vasculitis?
mucor species and aspergillus; directly invade the blood vessels
which fungal species can cause fungal meningoencephalitis, specifically parenchymal invasion?
candida and cryptococcus, often cause granulomas or abscesses
cryptococcal meningitis is seen in what clinical setting?
it is common in AIDS patients
identify: soap bubbles (small cysts within parenchyma) seen in basal ganglia.
chronic meningitis resulting from cryptococcal infection
identify: abnormal forms of cellular protein that cause rapidly progressive neurodegenerative disorders that may be sporadic, familial, or transmitted.
prions
what is the pathogenesis and molecular biology of prion diseases?
conformational change of normal neuronal protein PrP. resistant to protease digestion, induces more protein molecules to change conformation
what is the clinical course of CJD?
rapid progression of dementia with gait abnormalities and myoclonus. spongiform change, neuronal loss, no inflammation.
what pathologically characteristic of vCJD?
extensive cortical plaques surrounded by halo of spongiform change
name 3 ways in which vCJD differs from CJD.
- ) affects young adults
- ) behavioral disorders in early stages
- ) neurologic syndrome progresses more slowly
idenfity: onset is linked to consumption of bovine spongiform encephalopathy agent in contaminated foods.
vCJD
identify: cerebral gummas (plasma cell-rich mass lesions)
meningovascular neurosyphilis
what is common pattern of meningeal involvement in pneumococcal meningitis?
outer surfaces of cerebral hemispheres (cerebral convexities)
CSF findings in TB meningitis?
normal glucose, high protein, lymphocytes
what are common complications of TB meningitis?
obliterative endarteritis, hydrocephalus, destruction of cranial nerves
identify: this organism is most common CNS organism seen in AIDS patients. imaging shows ring-enhancing lesions. CSF has high protein, normal glucose, no organisms.
toxoplasma gondii
how can you use CSF findings to differentiate between toxoplasma gondii and cryptococcus infection?
toxoplasma gondii organisms will not be present in CSF while cryptococcus organisms will be present in CSF
identify: cell type with CD4 coreceptor and CCR5 or CXCR4 chemokine receptors
microglia
