Bacterial CNS Flashcards
4 major causes of bacterial meningitis
Strep pneumo, neisseria meningitidis, H Flu, Listeria monocytogenes
CSF in bacterial meningitis usually associated with
large numbers of polys
reduced glucose
elevated protein
Streptococci morphology
Gram positive spherical bacteria that occur in pairs
strep pneumo
- also known as pneumococcus
- Normal inhabitants of the upper respiratory tract but MOST COMMON cause of bacterial meningitis in US
Strep pyogenes
Also known as group A strep, also normal inhabitants of URT
Strep Agalactiae
Group B strep
Viridans Streptococci
dental pathogen
Lancefield classification
An antigenic carbohydrate found in cell walls that determines the Lancefield groups
Capsular polysaccharide is used to classify what?
Antigenic specificity of S. Pneumoniae
Strep pneumo disease
- pneumonia (lobar type)
- bacteremia (invasion of tissues and multiplication in the blood)
- Otitis media- infectionsof the ear
- Meningitis: systemic infection which crosses the bbb
case fatality rate of 30 %
Strep pneumo can alter vascular permeability to allow access to blood stream leading to bacteriemia. Can then directly invade endothelial cells. Cross the blood brain barrier by binding to cerebral capillaries, then transmigrate and enter CSF leading to meningitis
ok…KNOW
Strep pneumo virulence factors
- Capsule- interferes with phagocytosis by leukocytes. Interferes with binding of complement to cell surface
- Pilli: The initial event in invasive pneococcus disease is the attachment of encapsulated pneumococci to epithelial cells in the URT.
- Cell wall components-
- Choline binding proteins: major pneumococcal adhesin. Intereacts with carbohydrates on the pulmonary epithelial surface. Important in crossing the blood brain barrier during development of meningitis
- Hemolysins: cause lysis of host cells and activate complement
- Hydrogen peroxide
- Neuraminidase and IgA proteas: Importan tin invasion and destruction of secreted IgA at the mucosal surface.
Two vaccines for strep pneumo
1) Pneumovax: MULTIVALENT, NON-CONJUGATED, 23 capsule types, for older patients and high risk groups like: HIV, cardiopulmonary, transplant patients, splenic disorders.
Lasts 5-7 years
not effective in infants and young
Protects against invasive pneumococcal disease
2) Prevnar: Heptavalent, 13 groups, conjugated
safe but expensive. Good for infants
Neisseria morphology
gram negative, non-motile that occur in pairs (diplococci)
Many Neisseria are part of normal flora
- Two pathogenic neisseria:
Neisseria Gonorrhoea- high prevalence, low mortality
Neisseria Meningitidis: cause of meningococcal meningitis and sepsis. Low prevalence but high mortality
So if someone is talking about meningococcus meningitis they are referring to what bacteria
Neisseria meningitidis
N. Meningitidis has a prominent antiphagocytic polysaccharide capsule. This differentiates it from N Gonorrhaea
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What Neisseria meningitidis subgroups cause sporadic (small) outbreaks
B,C,Y
N.M is grouped on the basis of their capsular polysaccharide into 12 serogroups. Those associated with disease are
A, B, C, Y W125
Epidemic neisseria meningitidis?
Serotype A
Meningitis belt
sub-saharan africa
- epidemics occur every 5-12 years, last for 2-3 dry seasons and die out during intervening rainy season
Pathogeneisis of fulminant meningitis from neisseria
Begins abruptly with sudden high fever, stiff neck, chills, myalgias, weakness, NAUSEA, VOMITTING, and headache. Aprehension, restlessness, delirium. Widespread petechial and skin lesions appear suddenly.
Pulmonanry insufficiency then develops and patients will die
Major toxin of N Meningitidis=
lipooligosaccharide- endotoxin (elicit strong immune response)
the antiphagocytic capsule is also important
Only known reservoir of N meningitidis
human nasopharynx…spread via respiratory droplets. Aspiration of the infective particles
Meningococci attach to the nonciliated columnar epithelium of the nasopharynx. Attachment is mediated by pili and possibly other outer membrane components. Invasion of the mucosal cells occurs by a mechanism that involves phase variation (turning off capsule genes then turning them back on once they get in the bloodstream.
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