Pathology (CNS infection)

Card Set Information

Author:
amirh899
ID:
237893
Filename:
Pathology (CNS infection)
Updated:
2013-09-30 16:39:09
Tags:
Pathology CNS infection
Folders:

Description:
Pathology (CNS infection)
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user amirh899 on FreezingBlue Flashcards. What would you like to do?


  1. ................spread is the most common means of entry of organism into CNS
    Hematogenous (arterial)
  2. What are the routes of entry of microorganisms into CNS?
    • Hematogenous spread is the most common means of entry;arterial, retrograde venous sprea through anastomoses with veins of the face. 
    • Direct implantation (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 (Rabies, VZV)
  3. Meningitis refers to an inflammatory process of the.....................................
    leptomeninges and CSF within the subarachnoid space
  4. What is mcc of bacterial meningitis?
    Strep. pneumo
  5. What are the causes of bacterial meningitis?
    • Neonates, -->Escherichia coli and the group B streptococci
    • Elderly--> Streptococcus pneumoniae  and Listeria monocytogenes
    • Adolescents and in young adults--> Neisseria meningitidis is the most common pathogen, with clusters of cases
    • S. pneumoniae--> the most prevalent organism.
  6. What is the finding in CSF of bacterial and viral meningitis?
    • Bacterial--> cloudy or frankly purulent CSF, under increased pressure, with as many as 90,000 neutrophils per cubic millimeter, an increased protein concentration, and a markedly reduced glucose content
    • Viral--> clear, lymphocytic pleocytosis, Some elevation in protein, NORMAL GLUCOSE
  7. What is Waterhouse-Friderichsen syndrome?
    • meningitis-associated septicemia with hemorrhagic infarction of the adrenal glands and cutaneous petechiae
    • It occurs most often with meningococcal and pneumococcal meningitis
  8. The location of exudate in H.I and Strep Pneumo are........ and.............
    • Basal/ cerebral convexities near the sagittal sinus
  9. What are the pathological findings in fulminant meningitis?
    • Ventriculitis
    • Focal cerebritis (due to involvement of leptomeningeal veins)+ venous thrombosis and hemorrhagic infarction of the underlying brain.
  10. What is a pathological indicator of severe meningitis?
    Neutrophils fill the subarachnoid space in severely affected areas and are found predominantly around the leptomeningeal blood vessels in less severe cases
  11. What is the major pathological complication of meningitis?
    Leptomeningeal fibrosis+hydrocephalus
  12. What is chronic adhesive arachnoiditis?
    in pneumococcal meningitis, large quantities of the capsular polysaccharide of the organism produce a particularly gelatinous exudate that encourages arachnoid fibrosis, called chronic adhesive arachnoiditis.
  13. What are the findings in chemical meningitis?
    An aseptic meningitis–like picture may also develop subsequent to rupture of an epidermoid cyst into the subarachnoid space or the introduction of a chemical irritant (“chemical” meningitis). In these cases the CSF is sterile, there is pleocytosis with neutrophils and an increased protein concentration, but the sugar content is usually normal.
  14. What are the routes causing brain abscess?
    • Direct implantation of organisms,
    • local extension from adjacent foci (mastoiditis, paranasal sinusitis),
    • hematogenous spread (usually from a primary site in the heart, lungs, or distal bones or after tooth extraction).
  15. What are the predisposing factors for brain abscess?
    • 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;
    • immunosuppression
  16. Which predisposing condition tends to produce multiple abscess?
    Acute bacterial endocarditis
  17. Why CHD+ right-left shunt cause abscess in the brain?
    due to loss of pulmonary filtration of organisms
  18. What is the morphology of brain abscess?
    • 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.
  19. What are the clinical findings associated with brain abscess?
    • Progressive focal deficits in addition to the general signs of raised intracranial pressure.
    • The CSF is under increased pressure, the white cell count is raised, and protein concentration is increased, but the glucose content is normal.
  20. What are the mcc of brain abscess?
    Staph, strep
  21. What are the complications of brain abscess?
    The increased intracranial pressure and progressive herniation can be fatal, and abscess rupture can lead to ventriculitis, meningitis, and venous sinus thrombosis
  22. What is the cause of subdural empyema?
    Bacterial or occasionally fungal infection of the skull bones or air sinuses can spread to the subdural space, producing a subdural empyema
  23. In subdural empyema....................... are usually unaffected
    arachnoid and subarachnoid spaces
  24. What are the complications of subdural empyema?
    • thrombophlebitis may develop in the bridging veins that cross the subdural space, resulting in venous occlusion and infarction of the brain.
    • Mass effect
  25. Which veins may be involved in subdural empyema?
    Bridging veins
  26. What is the only finding in resolved subdural empyema?
    thickened dura
  27. What are the manifestations of subdural empyema?
    • Fever, headache, neck stiffness
    • The CSF profile is similar to that seen in brain abscesses
  28. Extradural abscess is the result of which pathology?
    commonly associated with osteomyelitis, often arises from an adjacent focus of infection, such as sinusitis or a surgical procedure
  29. What is the main cause of TB meningoencephalitis?
    Hematogenous from the lung
  30. What is the mc manifestation of TB CNS involvement?
    Diffuse Meningoencephalitis
  31. What are the histological findings of TB CNS involvement?
    • gelatinous or fibrinous exudate, most often at the base of the brain, obliterating the cisterns and encasing cranial nerves
    • white granules scattered over the leptomeninges
    • mixtures of lymphocytes, plasma cells, and macrophages, granuloma, and GC
    • Arteries running through the subarachnoid space may show obliterative endarteritis
    • may spread to the choroid plexus and ependymal surface through CSF
    •  In cases of long-standing duration, a dense, fibrous adhesive arachnoiditis may develop, most conspicuous around the base of the brain+hydrocephalus
    • wellcircumscribed intraparenchymal mass (tuberculoma)--> central caseous necrosis
  32. What are the manifestations of TB meningoencephalitis?
    • headache, malaise, mental confusion, and vomiting.
    • Moderate CSF pleocytosis made up of mononuclear cells or a mixture of polymorphonuclear and mononuclear cells; the protein concentration is elevated, often strikingly so; and the glucose content typically is moderately reduced or normal
  33. What are the most important complications of TB meningoencephalitis?
    • Arachnoid fibrosis producing hydrocephalus, and obliterative endarteritis producing arterial occlusion and infarction of underlying brain.
    • Spinal cord subarachnoid space: nerve roots 
    • With tuberculomas, the symptoms are typical of space-occupying lesions
  34. The major patterns of CNS involvement in neurosyphilis are .....................
    meningovascular neurosyphilis, paretic neurosyphilis, and tabes dorsalis (mc--> taboparesis)
  35. Individuals infected with .........are at increased risk for neurosyphilis, particularly as an acute syphilitic meningitis or meningovascular disease, because of impaired cell-mediated immunity
    HIV
  36. What are the histology of meningovascular syphilis?
    • involves the base of the brain and more variably the cerebral convexities and the spinal leptomeninges.
    • In addition, there may be an associated obliterative endarteritis (Heubner arteritis) accompanied by a distinctive perivascular inflammatory reaction rich in plasma cells and lymphocytes.
    • Cerebral gummas (plasma cell–rich mass lesions) may also occur in the meninges and extend into the parenchyma.
  37. What are the features of neurosyphilis?
    • Paretic neurosyphilis is caused by invasion of the brain by Treponema pallidum and is clinically manifested as insidious but progressive mental deficits associated with mood alterations (including delusions of grandeur) that terminate in severe dementia (general paresis of the insane).
    • Parenchymal damage in the cerebral cortex (particularly the frontal lobe) characterized by loss of neurons, proliferations of microglia (rod cells), gliosis, and iron deposits. The latter are demonstrable withthe Prussian blue stain perivascularly and in the neuropil, and are presumably the sequelae of small bleeds stemming from damage to the microcirculation.
    • The spirochetes may be seen
    • There is often an associated hydrocephalus with damage to the ependymal lining and proliferation of subependymal glia, called granular ependymitis
  38. What are the findings in Tabes dorsalis?
    • Damage by the spirochetes to the sensory nerves in the dorsal roots, which produces impaired joint position sense and resultant ataxia (locomotor ataxia); loss of pain sensation, leading to skin and joint damage (Charcot joints); other sensory disturbances, particularly the characteristic “lightning pains”; and absence of deep tendon reflexes.
    • On microscopic examination there is loss of both axons and myelin in the dorsal roots, with corresponding pallor and atrophy in the dorsal columns of the spinal cord.
    • Organisms are not demonstrable in the cord lesions
  39. What are the manifestations of neuroboreliosis?
    aseptic meningitis, facial nerve palsies and other polyneuropathies, encephalopathy
  40. What is the hallmark of viral encephalitis?
    Invariably associated with meningitis
  41. Latency is seen in .......................CNS infection
    VZV, PML
  42. What infections in the CNS is the result of immune reaction to virus?
    Acute Disseminated Encephalomyelitis and Acute Necrotizing Hemorrhagic Encephalomyelitis
  43. What is the vector and reservoir for most arboviruses?
    Mosquito/birdss
  44. Which arbovirus can cause involvement of spinal cord and a polio like syndrome?
    WNV
  45. What is the CSF feature in arboviral infections?
    The CSF is usually colorless but with a slightly elevated pressure and, initially, a neutrophilic pleocytosis that rapidly converts to lymphocytes; the protein concentration is elevated, but glucose content is normal.
  46. What are the pathological features of arboviral meningoencephalitis?
    • lymphocytic meningoencephalitis
    • Perivascular
    • single-cell neuronal necrosis with phagocytosis of the debris (neuronophagia).
    • Microglial cells form small aggregates around foci of necrosis, called microglial nodules
    • Severe--> necrotizing vasculitis
    • cuffs of lymphocytes (A) and microglial nodules (B).
  47. What are the features of HSV-1 encephalitis?
    • children and young adults
    • 10% history of prior herpes
    • alterations in mood, memory, and behavior
    • inferior and medial regions of the temporal lobes and the orbital gyri of the frontal lobes
    • necrotizing and often hemorrhagic
    • Perivascular
    • Cowdry type A intranuclear viral inclusion bodies may be found in both neurons and glia.
  48. What is the mc manifestation of HSV-2 in CNS of adults?
    Meningitis
  49. In what situation HSV-2 can cause encephalitis?
    • In 50% of neonates born by vaginal delivery to women with active primary HSV genital
    • Active HIV infection
  50. VZV become latent in ................
    dorsal root or trigeminal ganglia
  51. Who is at increased risk for PHN?
    >60 years
  52. Which virus can cause granulomatous arteritis in CNS?
    VZV
  53. In immunosuppressed individuals, herpes zoster may cause .................
    acute encephalitis with numerous sharply circumscribed lesions characterized by demyelination followed by necrosis.
  54. Who is at risk for CMV CNS infection?
    fetuses and immunosuppressed individuals
  55. What is the major CNS involvement in CMV infection of the fetus?
    periventricular necrosis that produces severe brain destruction followed later by microcephaly and periventricular calcification
  56. What is the mc manifestation of CNS CMV in immunosuppressed patients?
    subacute encephalitis
  57. What is the major morphologic involvement of CMV in the CNS?
    • paraventricular subependymal regions
    • severe hemorrhagic necrotizing ventriculoencephalitis and a choroid plexitis.
    • painful radiculoneuritis
    • intranuclear and intracytoplasmic inclusions
  58. What is the morphology of polyomyelitis infection?
    mononuclear cell perivascular cuffs and neuronophagia of the anterior-horn motor neurons of the spinal cord and CN motor nuclei
  59. What are the manifestations of polio infection?
    CNS infection manifests initially with meningeal irritation and a CSF picture of aseptic meningitis. The disease may progress no further or advance to involve the spinal cord. When the disease affects the motor neurons of the spinal cord, it produces a flaccid paralysis with muscle wasting and hyporeflexia in the corresponding region of the body—the permanent neurologic residue of poliomyelitis. In the acute disease, death can occur from paralysis of the respiratory muscles, and a myocarditis sometimes complicates the clinical course
  60. What is the morphology of rabies infection?
    • intense edema and vascular congestion.
    • widespread neuronal degeneration and an inflammatory reaction that is most severe in the brainstem. 
    • Negri bodies, the pathognomonic microscopic finding, are cytoplasmic, round to oval, eosinophilic inclusions that can be found in pyramidal neurons of the hippocampus and Purkinje cells of the cerebellum, sites usually devoid of inflammation 
  61. What are the symptoms of the rabies infection?
    • Since the virus enters the CNS by ascending along the peripheral nerves from the wound site, the incubation period (commonly between 1 and 3 months) depends on the distance between the wound and the brain.
    • The disease begins with nonspecific symptoms of malaise, headache, and fever, but the conjunction of these symptoms with local paresthesias around the wound is diagnostic.
    • As the infection advances, the affected individual exhibits extraordinary CNS excitability; the slightest touch is painful, with violent motor responses progressing to convulsions. Contracture of the pharyngeal musculature on swallowing produces foaming at the mouth, which may create an aversion to swallowing even water (hydrophobia).
    • There is meningismus and, as the disease progresses, flaccid paralysis.
    • Periods of alternating mania and stupor progress to coma and death from respiratory center failure.
  62. What are the common manifestations of HIV infection of the CNS?
    • Acute retroviral syndrome--> meningitis (aseptic)
    • Chronic--> encephalitis and Dementia
  63. What is the histological hallmark of HIV infection?
    • Microglial nodules
  64. What is the histology of HIV brain infection?
    • Microglial nodules +MNGC
    • blood vessels, show abnormally prominent endothelial cells and perivascular foamy or pigment-laden macrophages
    • subcortical white matter, diencephalon, and brainstem
    • HIV is detected in MQ and microglia
  65. What is the most important determinants of AIDS dementia?
    Magnitude of microglial involvement
  66. What are the features of PML?
    • JC polyomavirus
    • Oligodendrocyte
    • Demyelination
    • immunosuppressed 
    • reactivation of virus in the setting of immunosuppression
    • patch of demyelination, most often in a subcortical location, in the center of which are scattered lipid-laden macrophages and a reduced number of axons
    • At the edge of the lesion are greatly enlarged oligodendrocyte nuclei with glassy amphophilic intranuclear inclusions
  67. What are the features of SSPE?
    • progressive clinical syndrome characterized by cognitive decline, spasticity of limbs, and seizures
    • months or years after an initial, early-age acute infection with measles
    • Persistant nonproductive infection with defective virus
    • widespread gliosis and myelin degeneration; viral inclusions, largely within the NUCLEI, of oligodendrocytes and neurons; variable inflammation of white and gray matter; and neurofibrillary tangles
  68. What is the hallmark of inclusion in SSPE?
    It is intranuclear
  69. How is brain involved in fungal infection?
    • Fungal disease of the CNS is encountered primarily in immunocompromised individuals.
    • The brain is usually involved when there is widespread hematogenous dissemination of the fungus, most often Candida albicans, Mucor species, Aspergillus fumigatus, and Cryptococcus neoformans.
    • In endemic areas, pathogens such as Histoplasma capsulatum, Coccidioides immitis, and Blastomyces dermatitidis may involve the CNS after a primary pulmonary or cutaneous infection; again, this often follows immunosuppression.
  70. What are the three main patterns of fungal infection?
    chronic meningitis, vasculitis, and parenchymal invasion
  71. Vasculitis is most frequently seen with which fungal infection?
    mucormycosis and aspergillosis
  72. What is the consequence of fungal vasculitis?
    The resultant vascular thrombosis produces infarction that is often strikingly hemorrhagic and that subsequently becomes septic from ingrowth of the causative fungus.
  73. The most commonly encountered fungi invading the brain are ........................
    Candida and Cryptococcus
  74. What is the pattern of brain involvement in candida?
    Candidiasis usually produces multiple microabscesses, with or without granuloma formation.
  75. What are the features of CSF in cryptococcal meningitis?
    • WBC<50
    • MN
    • Slightly elevated protein
    • Slightly decreased glucose
    • India ink preparations and in tissue sections by PAS, mucicarmine, and silver stains.
  76. What are the morphological features of cryptococcal meningitis?
    • Chronic meningitis affecting the basal leptomeninges, which are opaque and thickened by reactive connective tissue that may obstruct the outflow of CSF from the foramina of Luschka and Magendie, giving rise to hydrocephalus.
    • Sections of the brain disclose a gelatinous material within the subarachnoid space and small cysts within the parenchyma (“soap bubbles”), which are especially prominent in the basal ganglia in the distribution of the lenticulostriate arteries.
    • Parenchymal lesions consist of aggregates of organisms within expanded perivascular (Virchow-Robin) spaces associated with minimal or absent inflammation or gliosis.
    • A, Whole-brain section showing the numerous areas of tissue destruction (“soap bubbles”) associated with the spread of organisms in the perivascular spaces. B, At higher magnification it is possible to see the cryptococci in the lesions.
  77. What are the clinical features of cerebral toxoplasmosis?
    HIV--> Subacute, evolving during a 1- or 2-week period, and may be both focal and diffuse. Computed tomography and magnetic resonance imaging studies may show multiple ring-enhancing lesions

    Cerebritis in the fetus
    , with the production of multifocal cerebral necrotizing lesions that may calcify
  78. What is the mc location for cerebral toxoplasmosis abscess?
    erebral cortex (near the gray-white junction) and deep gray nuclei
  79. What are the morphological features of cerebral toxoplasmosis?
    • Acute lesions exhibit central foci of necrosis, petechial hemorrhages surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation. Both free tachyzoites and encysted bradyzoites may be found at the periphery of the necrotic foci. The blood vessels in the vicinity of these lesions may show marked intimal proliferation or even frank vasculitis with fibrinoid necrosis and thrombosis.
    • After treatment, the lesions consist of large, well-demarcated areas of coagulation necrosis surrounded by lipid-laden macrophages. Cysts and free tachyzoites can also be found adjacent to these lesions but may be considerably reduced in number or absent if therapy has been effective.
    • Chronic lesions consist of small cystic spaces containing scattered lipid- and hemosiderin-laden macrophages that are surrounded by gliotic brain. Organisms are difficult to detect in these older lesions.
  80. What are the major manifestations of amebic encephalitis?
    • Acute necrotizing encephalitis--> Naegleria
    • Chronic granulomatous meningoencephalitis --> Acanthamoeba
  81. What are Transmissible Spongiform Encephalopathies?
    Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), fatal familial insomnia, and kuru
  82. What is the major feature of PrP?
    infectious and transmissible.
  83. What is the pathological hallmark of TSE?
    intracellular vacuoles in neurons and glia
  84. What is the pathophysiology of prion disease?
    • Disease occurs when the PrP undergoes a conformational change from its normal α-helix-containing isoform (PrPc) to an abnormal β-pleated sheet isoform, usually termed PrPsc
    • Associated with the conformational change, PrP acquires resistance to digestion with proteases, such as proteinase K. Accumulation of PrPsc in neural tissue seems to be the cause of the pathology in these diseases
    • Western blotting of tissue extracts after partial digestion with proteinase K allows detection of PrPsc, which is diagnostic.
    • The conformational change resulting in PrPsc may occur spontaneously at an extremely low rate (resulting in sporadic cases) or at a higher rate if various mutations are present in PrPc, such as occurs in familial forms of CJD and in GSS and fatal familial insomnia.
    • PrPsc facilitates, in a cooperative fashion, the conversion of other PrPc molecules to PrPsc molecules. It is this activity of PrPsc that accounts for the infectious nature of prion diseases.
  85. What is the genetic of prion disease?
    • The gene encoding PrP, termed PRNP, shows a high degree of conservation across species.
    • A variety of mutations in PRNP have been found to underlie familial forms of prion diseases.
    • In addition, a polymorphism at codon 129 that encodes either methionine (Met) or valine (Val) has been found to influence the disease: individuals who are homozygous for either Met or Val are over-represented among cases of CJD compared with the general population, implying that heterozygosity at codon 129 is protective against development of the disease
  86. What is the mc prion disease?
    Sporadic CJD
  87. How is CJD transmitted?
    corneal transplantation, deep implantation electrodes, and contaminated preparations of human growth hormone.
  88. What are the features of CJD?
    • The clinical onset is marked by subtle changes in memory and behavior followed by a rapidly progressive dementia, often with pronounced involuntary jerking muscle contractions on sudden stimulation (startle myoclonus).
    • Signs of cerebellar dysfunction, usually manifested as ataxia, are present in a minority of affected individuals
  89. What is the difference between CJD and vCJD?
    • vCJD affected young adults, behavioral disorders figured prominently in the early stages of the disease, and the neurologic syndrome progressed more slowly than in individuals with other forms of CJD
    • No alterations in the PRNP gene are present; nearly all affected patients are Met/Met homozygotes at codon 129
    • Pathologically, variant CJD (vCJD) is characterized by the presence of extensive cortical plaques with a surrounding halo of spongiform change.
  90. Pathologically, variant CJD (vCJD) is characterized by the presence of ......................................
    extensive cortical plaques with a surrounding halo of spongiform change.
  91. What is the CSF finding in sporadic CJD?
    positive 14-3-3 protein
  92. What are the histological features of CJD?
    • Little atrophy
    • Spongiform transformation of the cerebral cortex and, often, deep gray-matter structures (caudate, putamen); this multifocal process results in the uneven formation of small, apparently empty, microscopic intracytoplasmic vacuoles of varying sizes within the neuropil and sometimes in the perikaryon of neurons ( Fig. 28-32A )
    • No inflammatory infiltrate
    • Kuru plaques are extracellular deposits of aggregated abnormal protein; they are Congo red- and PASpositive and usually occur in the cerebellum ( Fig. 28-32B ) although they are present in abundance in the cerebral cortex in cases of vCJD surrounded by the spongiform changes ( Fig. 28-32C ).
    • In all forms of prion disease immunohistochemical staining demonstrates the presence of proteinase K–resistant PrPsc in tissue.
  93. What are the features of fatal familial insomnia?
    • Sleep disturbances that characterize its initial stages, is also caused by a specific mutation in the PRNP gene.
    • The mutation at residue 178 of PrPc, results in FFI when it occurs in a PRNP allele encoding methionine at codon 129, but causes CJD when present in tandem with a valine at this position.
    • In the course of the illness, which typically lasts fewer than 3 years, affected individuals develop other neurologic signs, such as ataxia, autonomic disturbances, stupor, and finally coma.
    • Unlike other prion diseases, FFI does not show spongiform pathology.
    • Instead, the most striking alteration is neuronal loss and reactive gliosis in the anterior ventral and dorsomedial nuclei of the thalamus; neuronal loss is also prominent in the inferior olivary nuclei.
    • Proteinase K–resistant PrPsc can be detected by immunostaining or western blotting

What would you like to do?

Home > Flashcards > Print Preview