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Neurology > Neuro Micro > Flashcards

Neuro Micro Flashcards

1
Q
A
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1
Q

CNS infections routes of entry

A
  1. hematogenous 2. direct extension: sinuses 3. penetrating trauma (S. Aureus) 4. ascending neural route: rabies 5. opportunistic infection
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2
Q

most common bacterial meningitis for neonates**

A

E.Coli, Group B strep

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3
Q

most common bacterial meningitis for elderly **

A

S. Pneumonia and listeria monocytogenes

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4
Q

most common bacterial meningitis for young adults **

A

N. meningitidis

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5
Q

most common bacterial meningitis for immunocompromised **

A

Klebsiella

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6
Q

children who have not been vaccinated are at risk for this bacterial cause of meningitis

A

H. Influenza

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7
Q

Symptoms of meningitis

A

Headache, photophobia, irritability, neck stiffness (because of inflammation of meninges), mental status changes.

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8
Q

CSF changes for bacterial meningitis

A

increased neutrophils, increased protein, decreased glucose. bacterial may be seen on smear. positive cultures

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9
Q

Waterhouse Fridericksen **

A

septicemia, meningitis, petechia, and adrenal hemorrhage usually seen with meningococcal and pneumonococcal infection.

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10
Q

bean shaped Gram negative cocci in pairs

A

N. meningitidis

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11
Q

gram positive cocci in clusters

A

staph

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12
Q

gram negative coccobacillus

A

H. influenza

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13
Q

facultative, intracellular motile gram positive rod

A

L. Monocytogenes

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14
Q

lancet shaped gram positive cocci found in pairs

A

S. pneumonia

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15
Q

patients are at increased risk for meningitis caused by S. pneumonia

A

alcoholics, sickle cell, asplenic, poor health. those whom have had pulmonary infection or mild respiratory infection.

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16
Q

this bacterial cause of meningitis is the most common cause of bacterial meingitis in adults of all ages

A

S. pneumo

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17
Q

bacterial menigitis morphology

A
  1. purulent exudate with leptomeninges over the surface of the brain. 2. neutrophils fill the subarachnoid space. may extend into the brain. may cause hydrocephalus.
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18
Q

bacterial menigitis with prediliction for basal distribution**

A

H. influenza

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19
Q

bacterial menigitis with involvement of cerebral convexities**

A

pneumococcal

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20
Q

chronic adhesive arachnoiditis

A

capsular polysaccharide seen in pneumococcal meningitis. causes adhesions along the arachnoid with infections with pneumococcal meningitis

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21
Q

acute aspectic meningitis

A

also known as viral meningitis (certain drugs (NSAIDs)/nonsteroidals can also cause this but to a lesser extend). will have a less severe clinical course. usually viral in origin. CSF: lymphocytes, moderate protein increase and normal glucose. usually self limiting. Often an enterovirus (coxsackievirus, echovirus, poliovirus, enterovirus)

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22
Q

subdural empyema

A

bacterial or fungal cause: may cause a mass effet. (puss under the dura)

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23
Q

(arthropod-borne viral encephalitis) name the pathogen (what family of viruses). the virus, found locally. host and vector. CSF changes. and gneral symptoms

A

arbovirus is a common cause in the tropics. locally west nile virus. animal host and most vectors are mosquitos and some ticks. CSF: slight increase in pressure, initially neutrophils then lymphocytes, increase protein, glucose is normal. generalized neurologic defects, seizures, confusion, delerium, stupor, and coma.

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24
Q

conditions associated with down’s syndrome

A

early onset of Alzhemiers due to 3 copies of chormosome 21 (codes for APP), acute leukemias (AML and ALL), congenital heart disease- endocardial cushion defects- VSD, ASD) (boards). GI defects- duodenal atresia, hirschsprung disease

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25
Q

Poliomyelitis

A

(destruction of anterior horns). type of enterovirus. mononuclear cell perivascular cuffs, neurophagia of the anterior horn motor neurons. cranial nerves sometimes involved. Symptoms- flacid paralysis, muscle weakness. acutely may have paralysis of respiratory muscles.

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26
Q

name conditon based on histology: neuronophagia with group of inflammatory cells surrounding an anterior horn cell. can lead to anterior horn cell loss or bulbar lower motor neuron loss during the acute stage

A

poliomyelitis

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27
Q

name disease: severe encephalitis, cerebral edema, vascular congestion. inflammation of midbrain and floor of the 4th ventricle. Negri bodies

A

bite from a rabid animal. Negri bodies: cytoplasmic round to oval eosinophilic inclusions in the hippocampus and Purkinje cells of the cerebellum (RABIES is the disease)

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28
Q

this severe encephalitis causing virus enters the CNS along peripheral nerves from wound site.

A

rabies (rabdovirus)

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29
Q

pt presents to the ER with malaise, fever, HA, local parasthesias around a bite wound. they have report that even the fines touches are painful. They feel like their throught is tight and that he can’t swallow. You notice some foaming at the mouth and the patient has hydrophobia. After a few hours, the patient has a manic episode, followed by stupor and then slips into a coma. The patient soon dies from respiratory failure. What did he have?

A

Rabies:: virus enters CNS along peripheral nerves from wound site. Malaise, fever, HA local parasthesias around the wound site. CNS excitability: slightest touch is painful. Contraction of pharyngeal musculature makes swallowing difficult and causes foaming from the mouth and hydrophobia. Periods of mania and stupor progress to coma and death from respiratory center failure.

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30
Q

primary and secondary tx for trigmeninal neuralgia

A

primary tx: carbamazepine (ADR- p450 inducer, can cause aplastic anemia):: secondary Tx: baclofen, Valproic Acid

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31
Q

Negri bodies

A

in a Purkinje cell cytoplasm but can also be seen in pyramidal cells of the hippocampus. the virus travels intraaxonally from the peripheral nerves to the CNS in 1-3 mths (retrograde transport- dynein:: kinesin is antergrade transport along microtuble)

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32
Q

brain abscesses: who gets them

A

20% are unassociated with conditons predisposing to bacterial invasion of CNS. Reminder occur in pts with pyogenic infections at extraneural sites, anatomic anomalies, penetrating trauma, or neurosurgery.

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33
Q

sources of primary infection leading to brain abscess development

A

sources: 1/2. paranasal cavities and mastoids arising from retrograde movement of bacteria through veins. usually solitary. only 40-50% are febrile on presentation. 3. frontoethmoid sinusitis can cause abscess in anterobasal frontal lobes. 4. otitic infections spread to temporal lobes or cerebellar hemispheres. 5. sphenoid sinusitis spread to frontal and temporal regions. 6. dental sepsis and pyogenic infections of the scalp and face. 7. odontogenic abscesses follow tooth extraction or dentla manipulations.

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34
Q

Organisms causing brain abscesses.

A

Steptococcus intermedius bacteroides, proteus, e.coli, klebsiella, mixed infections are common

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35
Q

dental infections leading to brain abscesses are caused by

A

Fusobacterium, bacteroides, Strep

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36
Q

facial or scalp infections leading to brain abscesses can be caused by these pathogens

A

S. aureus, often complicated by cavernous sinus thrombosis

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37
Q

mandibulofacial Actinomycosis may lead to

A

brain abscesses

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38
Q

CNS abscesses from distant foci usually result in a

A

multiplicity of abscesses (often the distant foci is the thorax ie lung abscesses and bronchiectasis are common causes:: less common: endocarditis, osteomyelitis, infections of the deep pelvic organs or abdominal viscera)

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39
Q

the abscesses from distant foci often are found in areas of

A

middle cerebral arteries- most germinate bw cortical mantle and underlying white matter. (often the distant foci is the thorax ie lung abscesses and bronchiectasis are common causes:: less common: endocarditis, osteomyelitis, infections of the deep pelvic organs or abdominal viscera)

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40
Q

this can cause secondary polycthemia resulting in microcirculatory sludging and regional brain hypoxia therefore predisposing to abscess formation

A

cyanotic congential heart disease with right to left shunts

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41
Q

Osler Weber Rendu disease

A

contributes to abscesses in a way similar to right to left shunts. (aka hereditary hemorrhagic telangiectasia (HHT)- genetically (AD) determined disorder that affects blood vessels throughout the body and results in a tendency for bleeding (vascular dysplasia and hemorrhage).mainfests by mucocutaneous telangiectasias and AVMs, a potential source of serious morbidity and mortality. Lesions can affect the nasopharynx, CNS, lungs, etc)

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42
Q

iatrogenic causes of brain abscesses

A

instrumentation of esophagus

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43
Q

pulmonary sepsis

A

actinomycotic and nocardia, fusobacterium, bacterioides, strep

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44
Q

congential heart disease

A

strep and haemophilus

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45
Q

bacterial endocarditis

A

S. aureus

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46
Q

penetrating cranial trauma

A

S. aureus and Salmonella

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47
Q

clinical aspect of brain abscess

A

diagnostic challenge. appearance is nonspecifc, more common signs and symptoms consistent with expanding intracranial mass.

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48
Q

sx of brain abscess

A

(mimics a tumor) H/A, mental status change, N/V.

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49
Q

Brain abscess CT or MRI

A

hypodensity with ring enhancement but findings are similar to neoplasms or some demyelinating disease

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50
Q

one of the worst complications of brain abscesses

A

intraventricular discharge of purlent matter

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51
Q

morphology of abscesses

A

begin as ill defined zones of bacterial multiplication and PMN infiltration. situated in white matter at the jxn with subcortical ribbon. over time fibroblasts surround a central mass of fibrinopurlent debris. eventually produces a collagenous capusle. capsule surrounded by edematous chronically inflammed gliottic brain tissue. rate at which a capusle forms varies (ie with survival of pt). Heamtogenous seeding of brain from distant sites produces less well formed capsules. Nocardial lesions- also form a poor capusle. Capular organization most advanced along superifical juxtacortical perimeter. Capsules less likely to form near ventricles due to less extensive vasculature. intraventricular purulent material often results in fatal complications.

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52
Q

epidural abscesses (epidemiology)

A

mostly occur in the spine. 50% thorax, 33% lumbar region and remainder in cervical and sacral region. 30-40% arise spontaneously. the remiander from secondary infections at distant sites, spinal surgery or trauma. predisposing infections: vertebral osteomyelitis, psoas and perinephric abscesses, decubitus ulcers.

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53
Q

clinical features of epidural abscesses- who’s at risk

A

DM, ETOH, renal failure

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54
Q

clinical symptoms of epidural abscesses

A

H/A, fever, malaise. may progress to radiculopathy, sensorimotor, sphincter disturbances and paralysis. S. Aureus most common cause

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55
Q

CNS TB

A

myocobacterium TB: (Seen in IVDA). produce caseating granulomas. arise in low thoracic or lumbar region. often arise from extension of TB vertebral osteomyelitis or disk infection. Also called Pott’s disease

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56
Q

Tuberculoma

A

mycobacterium Tuberculosis. encapuslated granulomatous central caseating mass. these often present intracranially

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57
Q

bulbar encephalitis can be caused by

A

listeria monocytogenes

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58
Q

cerebral Whipple’s disease

A

Tropheryma whippelii produces foamy macrophages with granular cytoplasm with rod shaped baccilli and reactive astrogliosis (GI component- malnutrition)

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59
Q

this organism causes a space occupying inflammatory lesion associated with immunodeficiency

A

Bartonella Henselae

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60
Q

CNS mycoses cases have risen dramatically due to all the people with HIV living forever with anti-viral therapy. So what organims are most often associated with these intracranial and intraspinal lesions often associated with diffuse meningeal or systemic infection

A

cryptococcus neoformans and Candida species

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61
Q

single most common CNS mycosis and where in the brain will you find it

A

Cryptococcus neoformans. in the brain may present as choroid plexus based masses- cryptococcomas. often consist of gelatinous material due to capsular mucopolysaccharides

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62
Q

on autopsy- brain is dissected out and you see thick mucoid exudate in the subarachnoid space, ventricles and brain parenchyma. CSF has leukocytosis, elevated protein and decreased glucose. You know from the patients HX that he was HIV +. What organism due you suspect to be responsible for the gelatinous material seen on the brain specimen?

A

Cryptococcal infection.

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63
Q

define molds

A

fungi existing in pure hyphal form at both room temp and 37 degrees celcius are termed molds

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64
Q

what are some CNS mold pahtogens

A

aspergillus and mucoraceae- these are opportunistic infections which rarely attact other healthy people. usually will be intraparenchymal vs meningeal.

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65
Q

Pts most at risk for Aspergillus and mucoracea infections of the intraparenchymal areas of brain-

A

alcoholics, IVDA, pts on corticosteroids (and of course AIDs pts). (orbital or paranasal sinus infection may spread to the meninges)

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66
Q

these pathogens may occlude, invade, and trigger thrombosis leading to multifocal stroke

A

MOLDS!!! fungi can migrate through damaged blood vessels. lesions usually seen in cerebral hemispheres, cerebellum and brainstem.

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67
Q

pt died- you look at their brain and you notice there are areas of brain swelling, hemorrhage and midline shift. On histology, you find branchin septate hyphae. There is vascular invasion, thromvosis and infarction. you suspect the patient had

A

aspergilosis. (branching septate hyphae are prone to cause vascular invasion, thrombosis, and infarction)

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68
Q

this is one of the most common CNS mycoses in immunocompromised pts

A

Candida- many are only found at autopsy resulting from fungemia. often small supperative lesions. may form macroabscesses. may only involve the meninges.

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69
Q

neurocysticerosis

A

caused by larvae of pork tapeworm (taenia solium)- most common parasitic cerebral infection (note that parasitoses refers to protozoal and helminthic infections). solitary enceysteoscolex. often associated with seizures. prominent investing tegument, smooth muscle fibers. the thing has four suckers

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70
Q

parasitoses

A

infection is acquired by ingestion of food or water contaminated by feces containing the cestode’s ova. seizures are common bc the infection involves the cerebral cortex. hydrocephalus and increases in ICP: due to involvement of ventricular system. appearance of cysticerci almost pathognemonic: small diameter, fibrous pseudocapsule, single larval scolex.

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71
Q

Toxoplasmosis

A

toxoplasma gondii: intracellular protozoan (think HIV). often seen as a space occupying lesion in AIDs pts. favors neuron rich areas such as cerebral cortex, basal ganglia, brainstem. Central necrotic mass surrounded by edema and inflammation. Perivascular intramural lymphoid infiltrates. endothelial swelling, thrombosis, fibrinoid necrosis and fibrous obliteration. 2 protozoal forms: tachyzoite and bradyzoite: tachyzoite- causes tissue injury. bradyzoite- fills cysts and pseudocyts collect around neurons and perivascular macrophages

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72
Q

HIV pt presents to ER with new onset seizures, hemiparesis, cranial nerve deficits. the pt described also experiencing H/A, a fever, and lethargy. On CT you see several space occupying ring enhancing lesions with areas of edema. THE PATIENT HAS HIV. What do you suspect

A

Toxoplasmosis- note infections can be congenital in neonates but in adults is associated with an immunocompromised state- kids may present with neurologic changes early on if not tested.

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73
Q

histology: basophilc structures (bradyzoite) fill the protozoal pseudocyts. often have surrounding inflammatory cells consisting of lymphocytes, plasma cells, and macrophages.

A

Toxoplasmosis

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74
Q

Treponema pallidum causes

A

syphilis, neurosyphilis (spirochetes)

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75
Q

lyme disease is caused by

A

Borrelia burgdorferi (spirochete)

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76
Q

gummas

A

necrosis and fibrosis seen in syphilis (Treponema pallidum- a spirochete)

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77
Q

ventricular surface is studded with many ependymal granulations. may cause chronic pressure hydrocephalus. perivascular inflammation has plasma cells and lymphocytes which can cause focal ischemia and infarction. What is the likely diagnosis

A

neurosyphilis- think of vascular involvement and RICH PLASMA CELL INFILTRATION AROUND THE VASCULATURE.

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78
Q

focal, necrotizing hemorrhagic encephalits. fever, disordered affect, seizures, deterioration of consciousness. often localized to one or both frontotemporal regions, insulae, and cingulate gyrus. CSF has antigens of the virus. What is the likely virus

A

Herpes simplex (condition described- herpes simplex encephalitis)- remember necrotizing hemorrhagic encephalitis. know that it’s in the frontotemporal regions, insulae and cingulate gyrus

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79
Q

this virus causes neuronal shrinkage, eosinophilia, vascular congestion and pallor, eosinophilic intranuclear inclusion bodies, lymphocytes and plasma cells colonize meninges, cuff blood vessels and migrate into the cortex. monocytes converge on infected neurons and form neuronophagic nodules. often seen in the frontotemporal region, insulae and cingulate gyrus. name the condition

A

herepes simplex encephalitis

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80
Q

viral encephalitis - viral infections usually involve the

A

cortex and sometimes the meniges: you get lymphocytic infiltarte in parenchyma as well as around the cerebral vessels

81
Q

most perinatal cases of encephalitis is caused by this virus

A

HSV-2

82
Q

most adult cases of encephalitis is caused by this virus

A

HSV-1 (sporadic onset)

83
Q

Progressive multifocal leukoencephalopahty

A

opportunistic demylinating disease of the CNS caused by some DNA viruses such as JC and HIV-1. almost always associated with defective cell mediated immunity. sx: motor deficits, cognitive decline, visual loss. usually found in cerebral hemispheric white matter. Attracted to oligodendrolions; causing enlargement of nuclei, dissolution of chromatin and replacement of basophilic “ground glass” material. develops into expanding zone of oligodendroglial loss and infiltration of macrophages ingesting myelin. Yellowish gray discoloration of white matter. may progress to white matter cavitation. florid astrogliosis with bizarre nuclei- large cytologic alteraitons, infiltration of foamy macrophages. perivascular monocyte infiltrates, astrocytosis and bizarre astrocytes, lipid laden macrophages. large oligodendrocytes with a ground glass appearance due to infection with the JC virus.

84
Q

Varicella zoster encephalitis

A

immunocompromised pts. seen mostly in cerebral hemispheric white matter. multifocal expanding lesion with demyelination variable axonal loss. may have small infarcts from vascular involvement. astrocytes have COWDRY A TYPE INTRANUCLEAR INCLUSIONS. oligodendrocytes have ground glass appearance but DO NOT ENLARGES AS THEY DO IN PML. may cause cerebral vasculitis leading to stroke and aneurysm. may have hemnorrhagic lesions in ganglia from reactivation. encephalitis can occur in immunocompromised individuals.

85
Q

HIV encephalitis

A

replicates in macrohpages and microglia. vasocentric inflammatory infiltrate in cerebral hemispheric white matter, basal ganglia and rostral brainstem. mononucleate and multinucleate macrophages. these cells harbor and release virions. diffuse astrogliosis and microglial activation. pallor of the cerebral white matter and brain atrophy. perivascular multinucleated cells which can be infected by HIV. few lymphocytes due to infection (due to stage of HIV- therefore wont have as much of lymphocytosis as you might expect). infection of the brain is carried out by macrophages.(look for multinucleated giant cells and tons of astrogliosis!!)

86
Q

3 major bacterial causes of meningitis

A

N. meningitidis (A,B,C, Y, W-135: quadrivalent vaccine), H. INfluenzae (b serotype: vaccine Hib), S. pneumoniae (many serotypes: vaccine: pneumovax and Prevnar13) - capsulation is central to ability to infect CNS

87
Q

3 major viral causes of meningitis

A

Common causes: HSV-1 (boards love this one), VZV, EBV: less common causes: arboviruses (rabies) and enteroviruses

88
Q

what fungus causes meningitis

A

crytococcus neoformans (chronic meningitis) and the endemic mycoses-> coccidioides immitis and histoplasma capsulatum

89
Q

how do you tell if you are dealing with a fungal, bacterial, viral cause of meningitis?

A

based on the presence of leukocytes vs PMNs, concentration of CSF glucose and protein

90
Q

chronic meningitis (characterized by slow onset, symptoms developing over several wks, and granulomatous inflammatory disease) is most likely to be caused by

A

mycobacteria or fungi, occasionally parasites

91
Q

viral meningitis, or aspectic meningitis is likely to causes

A

encephalitis and meningoencephalitis.

92
Q

common causes of bacterial meningitis in newborns

A

Group B strep (most common) ( a gram positive, diplococci), E Coli (gram negative rod), Listeria monocytogenes (beta hemolytic, Gram positive, rod)

93
Q

common causes of bacterial meningitis in infants and children

A

S. Pneumoniae, N. Meningitidis, H. Influenza

94
Q

most common causes of bacterial meningitis overall

A

S. Pneumoniae, N. Meningitidis, H. Influenza (b/c there are vaccines to both N. Meningitidis and H. Influenza- S. Pneumoniae is the most common right now)- characteristics shared by all 3 organisms- non pathogenic strains are pt of the normal flora of the nasopharynx. pathogenic strains can transiently colonize the nasopharynx.

95
Q

nosocomial causes of meningitis

A

(ie- ICU pts): gram nagative Bacilii, S. Aureus

96
Q

newborn, viral causes of meningitis most often associated with this

A

HSV-II

97
Q

infants and children, viral cause of meningitis

A

Enteroviruses (most common), arboviruses, HIV (early after infection)

98
Q

Adults, viral causes of meningitis

A

HIV (early after infection), Arboviruses

99
Q

can lyme disease cause a chronic meningitis, what’s the causative organism

A

Borrelia burgdorferi- chronic meningitis when these dimorphic endemic mycosis disseminate

100
Q

brain abscess caused by fungus

A

blastomyces dermatitidis (endemic mycosis- causes meningitis when they disseminate)

101
Q

parasitic pathogens that can cause Brain abscess (not on test)

A

toxoplasma gondii, Tanenia solium (neurocysticerosis)

102
Q

HIV asscoiated dementia is caused by HIV as Subacute sclerosing panencephalitis is caused by

A

Measles

103
Q

congenital infection or SSPE-type disease (chronic viral encephalitis)

A

Rubella

104
Q

progressive mutifocal leukoencephalopathy caused by (likes on boards)

A

JC polyomavirus (ppl with HIV)

105
Q

bacterial or virus? Stiff neck, confusion; disorientation, loss of consciousness, n/v, HA, fever, decrease glucose in CSF

A

bacterial (note stiff neck, confusion; disorientation and loss of consciousness more likely to be seen with bacterial meningitis)

106
Q

describe the consequences of bacterial infection on CNS

A

influx PMNs (inflammation), increase permeability of BBB (leakage of serum into CSF (not CSF normally has low protein concentration) permability= increase protein in CSF), edema leading to increased ICP, altered glucose transport (leading to decrease glucose in CSF relative to serum)

107
Q

CSF analysis (state most likely causative agent): increased lymphocytes, and normal glucose with a moderate increase in protein (less than 150mg/dL). Pt has meningitis

A

viral infection

108
Q

CSF analysis in a pt with meningitis (what is the causitive agent): PMNs, glucose <25mg/dL, protein 150-1000mg/dL.

A

bacterial infection- glucose is low and protein is elevated

109
Q

CSF analysis in pt with meningitis (what is the causitive agent): lymphocytes in CSF, low glucose, and moderate increase in protein

A

chronic infection (TB and mycoses): both viral and chronic infection = lymphocytes and moderate protein increase but [glucose] will indicate which pathogen it is most likely to be

110
Q

CSF glucose levels are normally what fraction of serum glucose levels (CLinical Pearl)

A

2/3 of serum glucose level

111
Q

acute bacterial meningitis may follow this type of infection

A

respiratory (remember, 3 most common bacterial causes are normal flora in nose)- otitis media, sinusitis, pharyngitis, pneumonia. RESPIRATORY PATHOGEN causes a bacteremia, spreads to the CSF (infects choroid plexus epithelial cells, OVTs located here) which can then access CSF. migrate through or between cerebral capillary endothelial cells into CSF

112
Q

Patient has a history of recent otitis media and now appears to have meningitis, what is the most likely bacteriologic agent

A

S. pneumo, H. Flu

113
Q

Patient has a history of recent Pharyngitis and now appears to have meningitis, what is the most likely bacteriologic agent

A

N. Meningitis

114
Q

Patient has a history of recent pneumonia and now appears to have meningitis, what is the most likely bacteriologic agent

A

S. Pneumoniae

115
Q

Patient has a history of Rash and now appears to have meningitis, what is the most likely bacteriologic agent

A

N. Meningitis

116
Q

of the common bacterial causes of meningitis which can form a capsule, has an IgA protease, Pili, and secretes an endotoxin

A

N. Meningitis and H. INfluenzae

117
Q

of the common bacterial causes of meningitis which can form a Capsule and has an IgA protease but does NOT have a pili or secrete an endotoxin

A

S. PNEUMO

118
Q

children do not generate an effective antibody response to polysaccharide antigens (capsule of bacteria) until they are 2-3 years old. Therefore, early vaccines against N. Meningitis, Pneumo, and N. Meningitis were ineffective. what immunologic response should happen to the capuslar antigens once the child develops effective antibody response to the capusule?

A

opsonization

119
Q

this acid residue of certain bacterias inhibits the activation of complement. therefore they escape killing by opsonization

A

sialic acid residues

120
Q

important serotype in neonatal meningitis caused by group B strep (capsule is rich in sialic acid)

A

III

121
Q

important serotype in neonatal meningitis caused by E. Coli (has a capsule rich in sialic acid)

A

K1 (denotes the antigenicity of the capsule)

122
Q

Clinical question: patient presents with meningitis like symptoms to the ER. What should you do

A

draw blood and CSF fluid for culture and gram stain and before diagnosis is confirmed- begin antimicrobial therapy right away based on the most likely etiologic agent. once the diagnosis is confirmed, you can change the antimicrobial meds as needed. MUST measure protein and GLUCOSE levels in CSF. latex agglutination test on CSF supernate can identify the serotype of the pathogen- can be used to identify the organism even if the culture results are negative

123
Q

microbiologic question: H. INfluenza

A

fastidious organism, needs factor X & V on chocolate agar to grow

124
Q

microbology question: gram stain +, diplococci, and grows on both chocolate agar and blood agar- what is the organism

A

S. pneumoniae

125
Q

micro question: gram stain -, coccobacilli, and grows on chocolate agar but not on blood agar

A

H. Influenzae

126
Q

micro question: gram negative, diplococci, and grows on both chocolate agar and blood agar, oxidase positive

A

N. meningitidis

127
Q

what test can you use to differentiate between the different strains of N. Meningitidis

A

cystein trypticase agar test: stains are differentiated by their abilities to form an acid upon oxidation of different sugars. (GLUCOSE, MALTOSE, lactose, or sucrose. PHENOL RED indicator turns from red to yellow in the presence of acid). Serogroups lets you know the antigenicity of the polysaccharide capsule and agllutination test

128
Q

meningitis Y is the most common cause of

A

pneumonia

129
Q

what subtype of meningitis is the most common cause of epidemics in Asia and Africa

A

Asia and Africa= A subtype

130
Q

transmission of meningitis from

A

respiratory droplets from asymptomatic carriers (colonizes the nasopharynx of healthy people).

131
Q

individuals at high risk for meningitis disease

A

childre <5, instiutionalized individuals, pt with late complement deficiencies (C5-C9), asplenic individuals. (REMEMBER- antibody to the capusle provides protection via opsonization:: other bacteria can induce cross-reactive antibody ie E.Coli K1 antigen induces antibody that can cross react with group B capsular polysaccharide)

132
Q

meningococcemia

A

lipo-oligosaccharide (LOS) triggers an inflammatory response that leads to vascular damage, shock, DIC. Can be with or without concomitant meningitis. rash on trunk and lower extremities; can coalesce. B/L destruction of adrenal glands (WATERHOUSE-FRIDERICHSEN SYNDROME), 25% mortality

133
Q

TX of meningitis

A

Penicillins (DOC) ie Cephalosporins if resistance is prevalent (resistance to penicillin via altered pencillin binding proteins (more likely) and B-lactamase (rare) and Chemoprophylaxis give to close contacts ie Sulfonamides if susceptible, Rifampin if not.

134
Q

vaccine for meningitis for what age group (now)

A

routine vaccination for 11-18yo, 2-55 yr old increased risk for disease.

135
Q

micro question: H. Influenza: requires what growth factors and how do you culture it

A

requires GF: X factor-hematin and Y factor-NAD:: Culture on Chocolate agar or Blood agar with XV on disk- growth around disk. the fact that H. flu requires the disk to crow on blood agar differentiates it from the non-pathologic strains of influenza

136
Q

non-pathologic strains of Hemophilius Influenza live in the nasopharynx. what are some features of the nonpathogenic strains

A

non-capsulated (non-typable). less virulent and can see it act as an opportunistic infection or otitis media in children and acute bronchitis in adults.

137
Q

epiglottitis in child

A

type B H. Flu (sinusitis and otitis media in children- nontypable)

138
Q

what serotype of H. flu is associated with elderly or adult pts with chronic pulmonary disease (pneumonia)

A

nontypeable strains causing acute bronchitis

139
Q

capsular antigen of H. INfluenza is

A

PRP- polyribosylribitol phosphate (note current vaccines= PRP conjugated to a protein carrier ie PRP-OMP= meningococcal outer membrane protein or PRP-TT (tetanus toxoid). combination vaccines with DTap or with recombinat Hep B (HBV)

140
Q

look for a zone of inhibition (or clearing) around a “P” disk on a blood agar plate to confirm

A

S. Pneumoniae- a alpha hemolytic, gram positive cocci. susceptible to optochin. look for zone of clearing around a P disk on blood agar plate. soluble in bile salts (deoxycholate).

141
Q

most common disease caused by S. Pneumoniae

A

pneumonia, sinusitis, otitis and when pt becomes bacteremic–> potential development of meningitis due to increased permeability of BBB

142
Q

is neurologic sequalae common in survivors of P. Meningitis

A

yes: 30% fatility rate, but up to 80% in elderly. : since Hib vaccination, S. Pneumo has become the leading cause of bacterial meningitis in children <5yo

143
Q

compare: PPSV23 to PCV13

A

PPSV23: not effective in children less than 2. 60-70% protective against invasive disease. less effective in preventing pneumococaal pneumonia. PCV13- highly immunogenic in infants and young children- including high risk children, <90% effective in invasive disease, less effective against pneumonia and acute otitis media

144
Q

recommendation of PPV23 vs PCV13

A

PPV23: adults greater than or equal to 65 yo or children greater than 2 with risk factors (chronic ill, anatomic or functional asplenia, immunocompromised, HIV, environments or settings with increased risk, cochlear implant):: PCV 13: routin vac for children 2-59 mths: doses at 2,4,8, 6 mths and booster 12-15 mths.

145
Q

neonatal meningitis from Group B streptococci- one organism under this category is

A

S. agalactiae- most common cause of neonatal meningitis, Beta hemolytic, serotypes are determined by antigenicity of polysaccharide capsule: serotype III is most commonly associated with meningitis. colonizes the genitourinary and gastrointestinal tract (transmission is usually during birth or prior to birth- via amniotic fluid): bactermia, pnumonia, meningitis + sequale (blindness,etc)

146
Q

risk factors for GBS infection to neonate

A

heavily colonized mother wo specific antibody. PROM (premature reupture of membranes), preterm delivery, prolonged labor/complications. (screening of GBS colonization at 35-37 wks gestation is recommended- antibiotic prophylaxis for colonized mothers

147
Q

late onset of GBS to neoborn

A

occurs 1-3wks, nosocomial infection. risk factors lack of maternal antibody, poor hygine in nursery. baby can get bacteremia and meningitis. mortality low, neurologic complications are possible : quick review of GBS- III most common, transmission before, during or nosocomial after birth.

148
Q

encapsulated yeast on india ink prep of CSF with this organism. The yeast cell is in the center and there is a halo appearnce on the india ink. What is the organism?

A

Cryptococcus neoformans- (found worldwide in soil contaminated with pigeon droppings*- transmission via inhalation). pulmonary infection may be subclinical or a mild influenza-like illness

149
Q

Cryptococcus neoformans can cause lung infections. Where is it most likely to disseminate to and who is likely to get the disseminated disease>

A

Disseminates most commonly to CSF. This is an AIDS defining illness. (skin and bones are other sites)- symptoms HA, fever, stiff neck, and disorientation

150
Q

india ink preparation oF CSF fluid can be used to identify Cryptococcus infection. What other test can you do that is more sensitive than india ink?

A

Latex agglutination test- detects capsular antigen and more sensitive than india ink. latex is also quicker bc organism is pretty slow growing

151
Q

describe some interesting features of meningitis caused by Cryptococcus neofromans

A

neutrophils predominant in CSF (weird for a fungus). incubation 1-4 wks. (common- HA, stiffneck, photophobia): epidural injection- epidural abscess and increasing back pain: intraarticular injection- jt infection pain; erythema or swelling of jt

152
Q

brain abscesses (seen on CT or MRI scans) include the following symptoms most commonly

A

seizures, progressive loss of consciousness, focal deficits (depending on location of the lesion)

153
Q

acute abscesses tend to consist of

A

mixture of aerobes and anaerobic organisms such as staph, anaerobic streptococci, gram negaitve baccili

154
Q

chronic abscess tend to be caused by

A

mycobacteria, fungi or parasites

155
Q

immunocompetent pts get brain abscess most often from these pathogens

A

Strep (aerobic, anaerobic, viridans), Enterobacteriaceae (proteus, E.Coli, Klebsiella), Anaerobes (bacteroides, Fusobacterium), Staphylococcus

156
Q

immunocompromised patients get brain abscesses most often from these pathogens

A

Nocardia, Toxoplasma gondii, Aspergillus, Candida, Cryptococcus neoformans

157
Q

branching filamentous bacteria, gram positive rod, causes abscesses in the brain in immunocompromised hosts. Also may be associated with pulmonary disease -bronchopneumonia or cutaneous disease

A

Nocardia

158
Q

what is the most common nocardia species associated with pulmonary and CNS disease

A

N. asteroids

159
Q

what is the most common species of nocardia associated with cutaneous disease

A

N. brasiliensis

160
Q

spread from otitis media and causes an abscess in temporal lobes and cerebellum- name the common pathogens

A

strep, bacteroides, pseudomonas, Haemophilus, enterobacteriaceae

161
Q

spread from paranasal sinusitis and causes abscess in frontal lobes

A

strep , bacteroides, pseudomonas, haemophilus

162
Q

spread from dental infections and causes abscess in frontal lobes- most common pathogens

A

strep, staph, bacteroides, fusobacterium

163
Q

hematogenous abscess- usually multiple and in the posterior frontal or parietal lobes. these can cause infective endocarditis, lung infections, urinary sepsis. name the pathogen most likely to cause each.

A

infective endocarditis: viridans streptococci, staph aureus. :: Lung infections: strep, staph, bacteroides, fusobacterium, enterobacteriaceae.:: urinary sepsis: enterobacteriaceae, Pseudomonas aeruginosa

164
Q

common vauses of viral meningitis in infants and children

A

Enteroviruses (most common), arboviruses

165
Q

common cause of meningitis in adults

A

arboviruses (HIV, early after infection)

166
Q

most common cause of neonatal meningitis

A

HSV-2

167
Q

relatively more common causes of acute viral encephalitis in the US include Arbovirus- name the three viruses under this headline

A

La Crosse virus, West Nile virus, St. Louis encephalitis virus (know that this are all spread by arthopod)

168
Q

enteroviruses less commonly causes viral encephalitis- name the ones implicated

A

poliovirus, Coxsackievirus (A,B), Echovirus, Enterovirus, Hepatitis A :: these viruses get in fecal-orally or through respiratory droplets

169
Q

spread fecal-orally and through respiratory secretions, most prevalent in the summer and fall, many infections are asymptomatic: usually symptoms include cold or flu-like illness, sometimes a rash, aspectic meningitis can occur with numerous serotypes, type of illness is determined by serotype of virus and age of immune status of the patient

A

general characteristics of enterovirus

170
Q

aseptic meningitis due to enteroviruses is most common cause in what age population

A

children -course of infection includes fever, severe HA, stiff neck, photophobia, drowsiness, confusion, N/V. duration is 7-10 days and rarely fatal . (causes aspectic meningitis)

171
Q

poliovirus epidemiology

A

crowding, poor hygine, and poor sanitiation–> infection in young children (less severe infection than older children) and infants: due to better hygine and sanitation –> infection in older age groups. w polio-endemic countries: nigeria, Afghanistan, and Pakistan (importation established PV transmission in 23 countries: India taken off the list)

172
Q

poliovirus course of infection

A

replication at site of entry: oropharynx and GI tract. dissemination of virus crosses the blood/brain barrier. infects via the axons of peripheral nerves- infects motor neurons, anterior horn of the spinal cord, medulla, and occasionally cerebellum and motor cortex

173
Q

abortive poliomyelitis

A

no dissemination to CNS. 7-14 day incubation pd. FEVER, MALAISE, DROWSINESS, HA, N/V, CONSTIPATION, SORE THROAT

174
Q

nonparalytic poliomyelitis (aspectic meningitis)

A

fever, malaise, drowsiness, HA, N/V, constipation, sore throat, stiff neck and pain in the back and neck. 2-10 day duration. complete recovery

175
Q

paralytic poliomyelitis

A

fever, malaise drowsiness, HA, N/V, constipation, sore throat, stiff neck and pain in the back and neck. + FLACCID PARALYSIS. spinal poliomyelitis, range of severity. temporary paralysis lasts less than 6mths. paralysis remaining after 6 mths is permanent.

176
Q

post-polio syndrome

A

prior paralytic poliomyelitis with evidence of motor neuron loss. a period of partial or complete functional recovery, followed by an interval (usually more than 15 yrs) of stable neuromuscular function. gradual onset of progressive and persistent new muscle weakness or fatigability. symptoms that persist for at least a year. exclusion of other Neuromuscular, medical, and orthopedic problems as causes of symptoms

177
Q

what virus is the most common cause of SPORADIC viral encephalitis

A

herpes simplex virus (HSV-1) (note that HSV-2 meningitis is more common than HSV1 in encephalitis of neonates and people with genital herpes. Occasionally EBV and VZV can cause meningitis)

178
Q

outbreaks of viral encephalitis are usually associated with

A

enteroviruses or arboviruses

179
Q

3 families of viruses under the arbovirus category. they cause viral encephalities (usually associated with outbreaks and are carried by arthropods)

A

togaviruses, flavivurses, bunyaviruses

180
Q

causes meningitis, +s RNA, icosahedral, eveloped (arbovirus)

A

Togavirus (genus- Alphavirus)

181
Q

causes meningitis, +s RNA, enveloped (arbovirus)

A

Flavicirdae (genus Flavivirus)- dengue is under this heading

182
Q

causes meningitis, -S RNA, 3 segments; helical, enveloped (arbovirus)

A

Bunyaviridae

183
Q

animal resevoirs for meningitis caused by the arboviruses are

A

squirls and birds (horses and people are considered incidental or dead end hosts)

184
Q

arbovirus course of infection

A

virus enters host via mosquito bite, replication in vascular endothelial cells and lymphatic cells- may be asymptomatic, virus may be cleared at this point. Viremia and dissemination to CNS or other organs can have flu-like illness during viremia phase. Systemic disease may be severe.

185
Q

clinical disease associated with arboviruses

A

most infections are asymptomatic. clinical disease is usually mild- fever, HA, fatigue, N/V. severe disease can involve coma, seizures, and paralysis- permanent brain damage is possible, fatality rate is usually less than 5%. EEE- more severe: fatality rate for encephalitis ~1/3

186
Q

outbreak of equine encephalitis may forewarn of human epidemic caused by these viruses

A

arboviruses - birds are monitored for WNV. West Nile Virus has replaced St. Louis encephalitis virus as the most important arbovirus in US. (St. Louis encephalitis is more common in children).

187
Q

this encephalitis virus is the most important worldwide- arbovirus group

A

Japanese Encephalitis virus

188
Q

this is a bunyavirus and has positive serology but shows a high increase in titers. this arbovirus belongs to the CA encephalitis serogroup. symptoms include fever, severe frontal headache, dizziness, left sided numbness tingling and weakness. What is it

A

Jamestown Canyon Virus (JCV)- bunyaviruses show positive serology for LACV and JCV- acute vs convalescent serum: greater increase in titer for JCV than LACV. (normally LACV is more common than JCV. also there can be cross reactivity in serum with flavivirus)

189
Q

west nile virus

A

flavivirus, related to SLE and JE. Usually causes milder disease than SLE and JE(japenese encephalitis) in people. usually not ivrulent for birds.

190
Q

this is a demylinating disease of CNS due to destruction of oligodendrocytes. The pt has been ruled out for MS. The patient is positive for JC virus and HIV. The patients condition rapidly progressed and he soon died. What did he have?

A

Progressive multifocal leukoencephalopathy (PML)- demylination of CNS due to destruction of oligodendrocytes. Associated with JC virus and seen in 2-4% of AIDS pts (reactivation of latent viral infection). Rapidly progressive, usually fatal. (the AIDs correlation- any immunocompromised host (lymphoma/leukemia) have higher risk for this condition)

191
Q

west nile virus can be spread via

A

mosquitos and contaminated blood- gave example of breastfeeding, organ transplant, blood transfusions

192
Q

-s RNA, helical, enveloped, and associated with the highest case fatality rate of any infectious disease

A

RABIES- rhabdovirus: no medical tx has been proven effective after the development of clinical signs

193
Q

according to Goljan what animal host is most like to be infected with rabies

A

skunks (all mammals can be hosts: domestic and wild: bats may carry virus but appear healthy). Cases in US due to transmission from wild animals- most associated with exposure to bats

194
Q

rabies course of infection

A

replicates in muscle and CT (3-8 wks incubation: range days to yr: shorter with bites on head and face- depends on viral inoculum.) enters peripheral nerves at Neuromuscular jxt- need to prevent dissemination to CNS to prevent fatality. travels via nerve axons to CNS- severe encephalitis >90% fatal: disseminates from CNS to salivary glands, other tissues. transmission via saliva. does not appear to be spread by viremia.

195
Q

pt presents to ER complaining of abn sensations near a bite wound from an animal. She is complaining of malaise, HA, nausea, vomiting, sore throat, fever. She has Hydrophobia, painful, spasmodic contractions of muscles involved in swallowing and drools to avoid swallowing. Her CNS exam was positive for dilated pupils, muscle spasms and hallucination. agitation, anxious, nervousness and depressed. Later on she had a seizure and fell into a coma. Three to five days later, she died as a result of respiratory paralysis. describe the shape and strand of the virus that caused her death.

A

nonsegmented, negative-stranded RNA genome, bullet shaped, helical and enveloped (Rabies virus): death was most likely caused by extensive CNS damage caused by the virus leading to demyelination of the cerebral cortex, cerebellum, hippocampus, dorsal spinal ganglia (destruction of respiratory center in medulla). –> common symptoms: difficulty swallowing; pharyngitis, fatigue, weakness pain altered mental status, agitated, confusion. spasms tremors. hallucinations. SOB. difficulty maintaining balance, symptoms consistent with encephalitis and flaccid paralysis- look at brain structures involved and sx make sense.

196
Q

a patient dies from Rabies. On brain biopsy, what would you expect to find and what tests would you want to do

A

Negri bodies- cytoplasmic inclusion bodies. aggregates of viral nucleocapsids (absence does not rule out rabies). IF staining for viral antigens-brain tissue, corneal epithelial cells, skin biopsy from thenape of the neck. isolate virus (brain or saliva, cell culture or inoculate infant mice). serology. RT- PCR (and sequencing)

197
Q

DX of rabies.

A
  1. samples sent to CDC (serum, CSF, saliva, nuchal skin biopsy), 2. serum and CSF + for rabies antibodies 3. rabies virus antigens often detected in the nucal skin biopsy by direct fluorescent antibody testing. 4. rabies virus RNA detected in the biopsy and saliva by RT-PCR sequencing ( viral antigen and RNA not detected from nuchal skin biospy and saliva samples of pt who surivived- serum and CSF were positive for antibodies. – doing all tests is important)
198
Q

this virus is part of the polymaviridae family. it’s a naked icosahedral virus, double stranded DNA. T antigens of the virus can bind and inactivate p53 and Rb- sends cells through the cell cycle, facilitates productive viral replication in permissive cells, may result in transformation in nonpermissive cells

A

JC VIRUS (do not get this confused with the arbovirus Jamestown Canyon Virus (JCV))

199
Q

JC virus, course of infection

A

thought to enter via respiratory tract, disseminates via viremia to the kidney. latent infection in the kidney, B cells and monocyte-lineage cells. Reactivation in immunocompromised individuals- secondary viremia and dissemination to the CNS, productive, lytic infection in oligodendrocytes leads to demyelination, JC virus may produce transformation in glial cells.

200
Q

a patient with lymphoma is sent to ICU from the floor and is found to have changes in speech, vision, coordination, mental ability and paralysis of her arms and legs. She is found to be infected by a virus with T antigens that can bind and inactivate p53 and Rb. It is a naked icosahedral virus. What is her prognosis?

A

she has progressive multifocal leukoencephalopathy (PML)- demyelinating disease occuring in immunocompromised patients. occurs in ~10% of AIDS pts (immunocompromised hosts). It is fatal in ~90% of all cases- mean survival after diagnosis is ~1-4 mths. Diagnosis is based on detection of viral DNA in CSF (PCR), MRI or CT evidence of lesion in white matter.

Neurology (6 decks)

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