B2 Flashcards
Compare & contrast the CSF changes in septic vs aseptic meningitis ( appearance , protein , glucose , WBC present / PCR result , causative agents )
S. Pneumoniae , N. Meningitidis & H. Influenza are transmitted via (……………)
S. Pneumoniae , N. Meningitidis & H. Influenza are transmitted via ( droplet inhalation )
State & explain about the virulence factor of S. pneumoniae
1) Capsule : principal virulence factor - protect from phagocytosis , autolysis & antibiotics
2) Pneumolysin ( Ply ) - inhibits neutrophils chemotaxis & phagocytosis
3) Autolysin - amidase enzyme that can cleaves the bacteria’s own peptidoglycan
- release cell wall fragments -> perpetuate inflammatory responses -> aids in Pathogenesis
4) C - carbohydrates antigens ( C - polysaccharides ) - component of cell wall - binds with CRP to achieve complement-mediated phagocytosis
5) IgA protease - cleaves IgA1
6) Pneumococcal surface proteins ( PspA, PspC ) - prevents binding of C3 onto pneumococcal surfaces - prevent compliment activation
7) Neuraminidase - aid colonisation by revealing receptors for adherence , modifies surfaces by competing bacteria , modified function of host clearances glycoprotein
8) Pneumococcal surface adhesin A ( PsaA ) - provide resistance to oxidative stress
State & explain the virulence factor of N . Meningitidis
1) Capsule x principal virulence factor
- protects the bacteria from complement-mediated phagocytosis
2) Lipopolysaccharide and endotoxin
3) Others - Ig A protease
- transferrin binding protein for iron uptake - adhesins
4) Porin proteins - found in outer membrane of Gram negative bacteria
State the virulence factors of Haemophilis influenza type B
1) Capsule - prevent complement-mediated phagocytosis
2) Endotoxin
3) Porin proteins
4) IgA1 protease
5) Pili & other adhesion proteins
6) Catalase
7 Oxidase
Describe the parhophysiology of meningitis
- Bacteria ( S. pneumonia , N. Meningitidis , H , influenzae ) colonies the upper RT& invades into the bloodstreams bacteria multiply , causing bacteremia
- The bacteria then cross BBB invading the meninges & CNS
- Bacteria induces increased permaebility of the BBB , invading neutrophil invasion & pleocytosis , leading to edema & increased intracranial pressure ( inflammation occurs )
- Leukocytes & other host cells release pro-inflammatory compounds which leads to neuronal injury & clinical manifestations of meningitis
State they clinical manifestations of meningitis ( Sign & symptoms )
Symptoms :
1) Intense headache
2) Photophobia
3) Phonophobia
4) Fever
5) Vomiting
6) Altered consciousness & mental status
Signs
1) Nuchal rigidity / stiff neck - pathognomic sign of meningeal irritation - neck resists passive flexion
2) Kernig sign - inability to straighten the leg when hip is flexed to 90’ due to hamstring stiffness - Knee extension is painful
3) Brudzinski sign - neck flexion cause spontaneous flexion of hips & knee
4) In infants - bulging frontalle - fever , irritability
5) In meningococal infections - purpurin rashes