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24 Cards in this Set
- Front
- Back
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What is the general pathophysiology of bacterial meningitis?
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Usually results from bacteremia/sepsis and then the bacteria seeds the meninges by binding to receptors on the meningeal cells, initiating an inflammatory response. Sometimes direct innoculation from surgery or trauma can occer.
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What pathogens are commonly seen in neonatal bacterial meningitis?
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1) Group B Streptococcus
2) E. coli K1 3) Lysteria monocytogenes |
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What pathogens are seen in premature infant bacterial meningitis?
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1) Streptococcus pneumonia (gram +)
2) Neisseria meningitidis (Gram -) 3) H. infuenzae (Gram -) only in unvaccinated populations 4) Coagulase negative stapholococci 5) Candida albicans (Fungus) |
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Group B Streptococcus and bacterial meningitis
a) Where is it found? b) What is the mode of transmission c) What age population is this bacteria responsible for meningitis and why? d) Prevention/At risk mothers |
a) Group B streptococcus is normal flora of mother
b) During child birth with prolonged rupture of membranes child can aspirate bacteria leading to bacteremia/ Early onset --> pneumonia and sepsis, late onset --> meningitis via binding receptors c) Neonates do not have normal IgG, complement, or PMN function necessary for phagocytosis d) Those at risk include colonized mom's, pre-term babies, and mutliple births. Mothers should be cultured in third trimester and if positive given Ampicillin to pretreat baby. |
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E. coli K1 and bacterial meningitis
1) What does the K1 refer to? 2) Bacterial appearance 3) Where is it found? 4) Name it's primary virulence factor 5) Transmission/pathogenesis |
1) The specific capsular type of E. coli
2) Gram negative rod 3) Mother's commensual flora 4) K1 capsule is not very antigenic because it resembles human protein and there for most individuals do not have IgG specific for it. This leads to K1 strain being significantly more associated with bacteremia than other E. coli strains. 5) Same as Group B Strep |
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Listeria monocytogenes and bacterial meningitis:
a) In what population group is this seen? b) Bacterial characteristics? c) Where is it found/transmission? d) Does mother show sxs? |
1) Neonates
2) Gram positive bacilius, motile 3) It is found in food grown with use of manure as fertilizer. 4) Mother shows flu like symptoms |
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What is treatment for suspected bacterial meningitis in neonates?
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Must cover gram negatives, listeria and group B Streptococcus (gram positive)
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Stapholococcus pneumonia and bacterial meningitis:
1) In what population is this normally found? 2) How are organisms acquired? 3) Site/method of colonization What mucosal defense may prevent adherance and what does bacteria produce to prevent this? 4) Virulence factors |
1) Infants and adults, with low IgG counts (IgG specific to capsule necessary to immunity)
2) Droplets in air 3) SP attaches to specific glycoconjugate receptors on epithelial surface. IgA can inhibit binding but SP produces IgA proteases. 4) a) Polysaccharide capsules allows for complement and phagocytic evasion. b)LTA, peptidoclygan, CpG motifs in cell wall all insite inflammatory response. c) Pneumolysin--> neuronal apoptosis d) S. pneumo binds and activates PAF (platelet activating factor) --> local clotting, lack of perfusion, acidosis |
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Stapholococcus pneumonia and bacterial meningitis:
5) How does bacteria get into meninges? 6) What causes the pathology of meningitis? |
5) Unknown
6) The host immune response. Bacteria in CSF are free to replicate due to lack of Ab and compliment. The membrane/capsular components of bacteria --> inflammatory response including upregulation of selectins and integrins to recruit PMNs. Activated leukocytes secrete ROS and elastase (-->cause directs damage to tissue) as well as LKTs, PGs (which disturb the blood brain barrier and CSF) |
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Stapholococcus pneumonia and bacterial meningitis:
What changes in CSF are due to PMN's and inflammation? |
1) Edema
2) Elevated CSF protein (seen on LP) 3) Increased intracranial pressure leading to a loss of perfusion to brain, and greater glucose metabolism 4) Break down of the blood brain barrier which leads to both low glucose levels (due to increased metabolism --> lactate production) and loss of autoregulation (BP control in brain, normally maintained separately from rest of body) |
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Stapholococcus pneumonia and bacterial meningitis:
Treatment |
1) Must address inflammation with steroids
2) Antibiotics Problem is steroids decrease the amount of Ab reaching infection so must increase dose |
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Stapholococcus pneumonia and bacterial meningitis:
Prevention a) For infants/children b) Adults |
a) Prevnar-conjugate vaccine with 7 common pneumococcal antigens linked to protein carriers to elicit T cell dependent Ab response
b) 23 valen pneumococcal vaccine- based on carbohydrate Ag of capsule |
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Neisseria Meningitidis and bacterial meningitis
1) Name different types and whether they are seen sporadically or endemically? 2) Affects what age group? 3) Who becomes ill/ who does not? 4) How is is taken up? Transmission? 5) Virulence factors 6) How quickly does disease manifest? 7) Risk factors 8) Vaccine |
1) Type B is sporadic, while Type A and C are epidemic
2) Peak ages are less than 1 yr and elderly 3) Those without specific anticapsular Ab will become ill. Many have the Ab from N lactamica strains which are part of commensual flora. These individuals will serve as carriers. 4) By air. Plus gram (-) LPS leads to the rapid uptake by epithelial cells via endocytosis 5) IgA protease Capsule= antiphagocytic (need both IgG and complement for phagocytosis) b) sialylated glyco-conjugates that mimic neuronal adhesion molecules and thus do not trigger immune response 6) The disease progresses extremely rapidly: it is referred to as fulminant sepsis 7) Those promoting bacterial colonization: previous viral infections, poor living conditions, asplenic, non-immune individuals (children, military). Also more common in individuals with low terminal complement levels (important in clearing organism from blood) 8) Vaccines contain types A, C, Y, and W135 but not B. It is recommended for those at risk, including asplenic individuals, those with lack in terminal compliment, travelers, military recruits, college freshman. Not B because very much like host neuronal tissue. |
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Haemophilus influenzae type B and bacterial meningitis:
1) In which age group is this common? 2) Site/means of colonization factors |
1) Neonates
2) Attaches to specific glycoconjugate receptors on epithelial surface |
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Haemophilus influenzae type B and bacterial meningitis:
4) Vaccination 5) type B vs. nontypable: what does this refer to and what disease mainfestations are associated with each? |
4) Disease has virtually been eradicated in developed world do to conjugate vaccine (HiB-PRP) to polyribose phosphate capsule. Conjugate implies it provokes a T-cell mediated Ab response
5) type B refers to the presense of the poly ribose phophate capsule (this is associated with bacteremia, pneumonia, and meningitis. Nontypable= non type B or without a capsule and this generally leads to otitis media |
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Haemophilus influenzae type B and bacterial meningitis:
3) Pathogenesis and Virulence |
3) Like S. pneumonia, after aspiration bacteria gets access to blood stream. Capsule makes bacteria resistant to phagocytosis and complement. Bacteremia develops and there is spread to subarachnoid space. Here an inflammatory response is stimulated by cell wall fragments. LPS both stimulates expression of selectins and integrins, PMN migration, as well as secretion of TNF alpha and IL-1. Active leukocytes then secrete ROS and elastase (which cause direct damage), LKTs (which lead to PAF to thrombosis, loss of blood flow and O2 to depletion of glucose and formation of lactic acid) and PGs disturbing the BBB, leading to edema, increased protein leves in CSF, increased blood pressure as well as intracranial pressure, etc.
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Neonatal bacterial meningitis:
1) Why are neonates at increased risk? 2) Sxs? |
1) Because they do not have Ab (only a bit of IgG from mother if full term), have defects in PMN chemotaxis and bacterial killing. They also do not have a highly developed blood brain barrier
2) May be nonspecific, but often lethargy, irritability, and eventually seizures and vomiting. |
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Children with bacterial meningitis:
Sxs |
Fever
Headache Lethargy Vomiting Seizures Stiff neck Back pain Some simply looked flushed Some have altered consciousness, stiff neck, Kernig and Bruzinski signs |
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Bacterial meningitis in adults:
sxs |
Severe headache and altered mental status most common.
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Bacterial meningitis: Diagnosis
1) Appearance of CSF 2) Cell count in CSF 3) glucose and protein levels in CSF |
1) CSF appears cloudy due to PMN. Normally appears clear. Can appear yellowish due to RBC breakdown or increased protein
2) WBC is elevated. There shouldn't be any PMNs in CSF so cell counts in CSF (PMNs, monocytes, and lymphocytes indicated meningitis) 3) Glucose is low (less than 50% of plasma glucose levels, normally 0.6), protein is elevated |
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Long term effects of bacterial meningitis in children
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The amount of inflammation, vascular insult, and parenchymal damage determines child's risk for future losses in development, hearing, learning, hemiplegias, deafness, and blindness.
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What CSF tests can you run if you are not sure it is a bacterial meningitis and may be meningitis due to another organism?
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Screen for mycobacterial infection
Fungal infection, cryptococcus (with india ink stain) Viral culture PCR for virus Antibody-Western blot |
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Bacterial meningitis and imaging
CT MRI |
CT- can see increased intracranial pressure, ventricular size, and infacts
MRI-used later in management for diagnostic purposes no in care of acute infection |
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What are the key aspects of bacterial meningitis that must be managed in treatment?
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Inflammation: with steroids
Specific pathogen: antimicrobials Fluid: CNS pressure management Shock: Septic shock managemtnet And public health considerations, who has been exposed? |
