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Lecture 17
Infections of the CNS
| Question | Answer |
|---|---|
| Definition of meningitis | Inflammation of the leptomeninges |
| Classic triad of symptoms for meningitis | (1)Fever (2)Headaches (3)Nuchal rigidity |
| Brudzinski's sign | Sign of meningeal irritation. The sign is elicited by passive flexion of the neck induces flexion of the hip or knees. |
| Kernig's sign | Sign of meningeal irritation. A positive sign is described as resistance to passive extension of the knee while the hip is flexed. |
| Clinical symptoms of CNS abscess | (1)Headache (2)lethargy (3)fever (4)focal neurologic deficits |
| How are CNS abscesses diagnosed? | Contrast-enhanced CT or MRI |
| Clinical symptoms of encephatlitis | (1)Fever (2)headache (3)altered mental status (4)sezures (5)focal neurologic deficits |
| Diffuse or localized inflammation of the brain, resulting from direct viral invasion | Encephalitis |
| Mode of transmission of CNS infections | (1)Hematogenous (2)Direct extension from adjacent structures (3)Direct implantation(trauma or from surgeries) (4)Centripetal spread (retrograde from the PNS, axonal transportation) |
| Most common mode of transmission of CNS infections | Hematogenous |
| Most common route of entry for bacterial meningitis | Most common route is from hematogenous spread from upper respiratory tract |
| Most common agents responsible for bacterial meningitis infection of newborns | (1)Group B streptococci (2)E. coli (3)Listeria |
| Most common agents responsible for bacterial meningitis in children (>1 mo) to adults (60 yrs) | (1)Neisseria meningitides (2)Streptococcus pneumoniae (3)Haemophilus influenza type b |
| Most common agent responsible for bacterial meningitis in the elderly population | Gram negative bacilli |
| Most common cause of bacterial meningitis associated with closed skull fractures | S. pneumoniae |
| Most common cause of bacterial meningitis associated with open skull fractures | S. aureus |
| Most common cause of bacterial meningitis associated with neurosurgical procedures | S. aureus |
| How do most people acquire meningococcus meningitis? | Meningococcous is present in the nasopharyns of 5% of people and spread by respiratory droplets and close contact |
| What populations are susceptible to H. influenzae meningitis? | (1) Immunocompromised (2) unvaccinated individuals |
| CSF profile of acute bacterial meningitis | (1)presence of PMN (2)High cellularity (10-10,000 cells/mm3) (3) low glucose (<40 mg/dl) (4) High protein (>50 mg/dl) (5) visualization of bacteria by gram stain |
| Complications of bacterial meningitis | (1)Cerebral infarcts (2) Hydrocephalus (3) Abscesses (4) Hearing loss (5) Mental retardation |
| Mechanism of cerebral infarcts as a complication of bacterial meningitis | The vasculitis elicited by bacterial meningitis affects the small cortical vessels resulting in thrombosis and eventual ischemic infarction |
| Mechanism of hydrocephalus secondary to bacterial meningitis | Chronic phases of bacterial meningits causes leptomeningeal fibrosis, which results in obstruction of CSF flow |
| Disease characterized by inflammation of the meninges with CSF lymphocytic pleocytosis with negative CSF stains and bacterial cultures | Aseptic meningitis |
| Most common cause of aseptic meningitis | Viruses |
| CSF profile of viral meningitis | (1)low cellularity (mainly mononuclear cells) (2)normal glucose (3)normal protein (4)negative gram stain |
| Most common agents for viral meningitis | Enteroviruses: Coxsackie B, echovirus, poliovirus |
| Mode of transmission of viral meningitis | (1) direct contact (2) oral-fecal transmission |
| Most common cause of viral menigitis worldwide | Mumps (paramyxovirus) |
| (T or F) Tuberculous meningitis is primarly seen during primary infection in children. | True. The most common type of CNS involvement by Mycobacterium tuberculosis manifests as menigitis. In children, most commonly occurs between birth and 5 years. In the US, it is most commonly seen in the elderly and immunocompromised patients. |
| Clinical symptoms of TB meningitis | (1)low-grade fever (2)headache (3)nausea (4)drowsiness that may progress to stupor and coma (5) Positive Kernig's and Brudzinski's sign |
| What areas are involved in TB meningitis | (1) base of the brain (2) cranial nerves |
| (T or F) TB meningitis is characterized by purulent subarachnoid exudates | False. TB meningitis is characterized by gelatinous subarachnoidal exudates |
| Complications of TB meningitis | (1) Focal or diffuse infarcts (2) Tuberculomas (3) Hydrocephalus |
| Infectious agent responsible for Lyme disease | Borrelia burgdorferi |
| Neurological manifestations during the early phase of Lyme disease | (1)Lymphocytic meningitis or meningoencephalitis (2) Cranial neuritis (Bell's palsy) (3) Senosry or motor radiculoneuropathies |
| Neurological manifestations during the late phase of Lyme disease | (1) Mild encephalopathy (2) Peripheral polyneuropathy |
| (T or F) Majority of fungal infections of hte CNS are opportunistic. | True. Major concern in fungal meningitis is in immunocompromised patients. |
| Most common fungal agent associated with meningitis in AIDS or immunocompromised patients | Cryptococcus sp |
| Most common fungal agent associated with meningitis in Hodgkin's lymphoma patients | Cryptococcus sp |
| Agents of fungal meningitis in immunocompetent patients | Blastomyces dermatitidis and Coccidiodes immitis |
| Radiographic appearance of CNS abscesses | Ring-enhancing lesion in contrast-enhanced CT and MRI |
| Pathogenesis of brain abscess | Brain abscesses are most commonly a secondary infection spread by hematogenous dissemination, from direct extension from adjacent structures, introduced by trauma or surgical procedures, or cryptogenic. |
| Complications of brain abscesses | (1) Herniations (2) Severe cerebral edema (3) Ventriculitis (4) CSF dissemination (5) Secondary abscess |
| Most common non-purulent bacterial agent of CNS abscesses | Tuberculosis |
| Most common fungal agents of CNS abscesses | Candida, Aspergillus, Cryptococcus, Zycomycosis, Blastomycosis, Coccidiodomycosis |
| Most common parasitic agent of CNS abscesses | Toxoplasmosis, Amebiasis |
| Bacterial agents associated with brain abscesses secondary to otitis media and mastoiditis | Streptococci, Bacteroides fragilis, Enterobacteria |
| Bacterial agents associated with brain abscesses secondary to frontoethomoidal and sphenoidal sinusitis | Streptococci, Bacteroid spp, Enterobacteria, Staphylococcus aureus, Haemophilus sp |
| Bacterial agents associated with brain abscesses secondary to dental abscesses | Mixed fusobacterium, Bacteroids, and Streptococcus sp |
| Bacterial agents associated with brain abscesses secondary to penetrating head trauma or post-surgical infection | Staphylococcus aureus, Streptococci, Enterobacteria, Clostridium sp |
| Bacterial agents associated with brain abscesses secondary to congential heart disease | Streptococci (viridans, anaerobic, or microaerophilic), Haemophilus sp |
| Bacterial agents associated with brain abscesses secondary to lung abscess, empyema, bronchiectasia | Fusobacterium, Actinomyces, BActeroides, Streptococcus, Nocardia asteroides |
| Bacterial agents associated with brain abscesses secondary to bacterial endocarditis | Stphylococcus aureus, Streptococcus sp |
| Diffuse or localized inflammation of the brain | Encephalitis |
| Diffuse or localized inflammation of the brain and leptomeninges | Meningoencephalitis |
| Diffuse or localized inflammation of the brain and spinal cord | Encephalomyelitis |
| Symptoms of diffuse encephalopathy | (1) Altered mental status (2) delirium (3) convulsions (4) coma |
| Route of infection for viral encephalitis | (1) Hematogenous (2) Centripetal spread (retrograde form the PNS or retrograde from mucosal surface) |
| Four common pathological features of viral encephalitis | (1)Mononuclear infiltrates (lymphocytic inflammation) (2)Microglia activaton (3) inclusion bodies (4) necrosis |
| (T or F) Some patients who recover from viral encephalitis have residual signs. | True. 20% of cases have residual signs after resolution such as mental deterioration, amnesic defect, personality change, recurrent seizures, and hemiparesis |
| Most common type of HSV responsible for majority of encephalitis infections | HSV-1 |
| Population most affected by HSV-2 encephalitis | Neonates |
| Mode of transmission of Herpes virus encephalitis | Centripetal or retrograde spread |
| Anatomical distribution of Herpes Encephalitis infection | Temporo-frontal and limbic distribution |
| What part of the year does arboviral encephalitis peak? | Summer: June through September |
| Family of viruses that cause arboviruses encephalitis | (1)Togaviridae (2) Flaviviridae (3) Bunyaviridae |
| Vector responsible for arbovirus encephalitis in the US | Mosquitoes |
| Geographic distribution of St. Louis Encephalitis | Nationwide, but especially along the Mississippi River |
| Geographic distribution of Eastern Equine Encephalitis | Eastern states, Atlantic coast, Gulf coast |
| Geographic distribution of Western Equine Encephalitis | West of Mississippi River |
| Geographic distribution of La Crosse Encephalitis | Great lakes states |
| Arbovirus encephalitis characterized by poliomyelitis-like and Parkinsonian symptoms | West Nile Encephalitis |
| Infectious agent responsible for Rocky Mountain Spotted Fever | Rickettsia rickettsii |
| Disease characterized by a macular rash involving the trunk and limbs, fever, and arthralgia | Rocky Mountain Spotted Fever |
| Neurologic manifestation of Rocky Mountain Spotted Fever | (1) Progressive stupor leading to coma (2) sustained fever (3) focal neurologic signs (4) Optic neuritis |
| Infectious agent responsible for subacute sclerosing panencephalitis (SSPE) | Measles |
| Infectious agent responsible for progressive multifocal leukoencephalopathy | JC virus |
| Pathogenesis of Progressive Multifocal Leukoencephalopathy | PML is caused by the reactivation of latent JC virus due to impaired cell-mediated immunity |
| A condition characterized by slowly or rapidly progressive dementia accompanied by abnormalities of motor function in AIDS/HIV patients | HIV encephalitis or AIDS dementia complex |
| (T or F) Only adult HIV/AIDS patients develop HIV encephalitis or AIDS dementia complex | False. Both pediatric and adult populations are affected by HIV encephalitis or AIDS dementia complex |
| Routes of infection of HIV encephalitis or AIDS dementia complex | Hematogenous route carried by T lympocytes and macrophages or invasion and persistence in the CNS (HIV reservoir) |
| Pathologic features of HIV encephalitis or AIDS dementia complex | (1)Mild diffuse cerebral atrophy (2)Diffuse and multifocal rarefaction of the cerebral white matter (3)diffuse lymphocytic infiltration (4)Macrophage reaction with microglial nodules, macrophages, multinucleated giant cells |
| (T or F) HIV genome/proteins can be detected in neurons | False. There has been no demonstration of the virus in neurons. Only multinucleated giant cells and macrophages in the CNS have been detected to have HIV genome/proteins. |
| (T or F) In HIV encephalitis or AIDS dementia complex, neuronal death is a result of direct neuronal infection. | False. Neuronal damage is not due to direct infection of the neuron. It is most likely due to secondary effects. |
| Infectious agents that make up the TORCH syndrome | T=Toxoplasmosis O=other R=Rubella C=CMV H=Herpes (HSV-2) and HIV |
| (T or F) Most TORCH infections are due to transplacental transmission. | True |
| Mode of transmission of HSV-2 meningoencephalitis in neonates | Transvaginal |
| Modes of transmission of HIVmeningoencephalitis in neonates | Transplacental and breast feeding |
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