Lecture notes
staphylococci
- Module
- Medicine
- Institution
- Cambridge University (CAM)
staphylococci disease characteristics lab diagnosis Treatment And everything you need to know
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Staphylococci1. Staph. Aureus :
● Characteristics :
i. Gram +ve \ catalase +ve \ coagulase +ve \ cocci in clusters \
haloduric "tolerate salts" \ beta hemolytic ,
mannitol fermenter .
ii. Optimum growth temp. 35 c
iii. Non capsulated "but some are, thus serotyping isn’t that useful".
iv. Have a golden color in blood agar, this is due to production of
carotenoid pigment called staphyloxanthin , that inactivate
bactericidal products of the WBCs.
v. Normally found as commensal in the nose or in female genitals
tract.
● Virulence factors :
● Structural :
a. Protein A , principle of coagulase test, binds to Fc portion
of IgG, thus activation of complement system is
prevented, and thus opsonization and phagocytosis are
prevented.
b. Teichoic acid, mediate adherence to mucosal membranes,
Lipoteichoic acid is important in induction of septic shock
by inducing the release of cytokines like IL‐1 and TNF,
from macrophages .
c. Peptidoglycans , has an
endotoxin like activity, by binding
to macrophages it induce the release of cytokines and
coagulation cascade, explains why Sta. Aureus can cause
septic shock without having endotoxins.
d. Fibronectin binding protein : enables the bacteria to bind
to the fibronectin of the endocardium of the heart volves,
(the only cause of acute endocarditis)
● Toxins :
a. Superantigens :
i. Enterotoxin ,
heat stable, acid resistant, that cause
release of large amounts of IL‐1 and IL‐2 from
macrophages and helper T cells, respectively, this
stimulates enteric neurons to stimulate the vomiting
center in the brain.
ii. TSST‐1 , causes toxic shock syndrome, only 20 % of
staph. Aureus have the gene for this toxin. TSST is a
superantigen and causes toxic shock by stimulating
, the release of large amounts of IL‐1, IL‐2, and TNF,
antibodies against TSST are found.
b. Exfoliatin , cause separation of the skin at stratum
granulosum, causing scalded skin syndrome and
impetigo
.
c. Leukocidins toxins , are two:
i. Alpha toxin , forms a hole in the cells causing
necrosis of skin and hemolysis, by forming pores on
the cell membrane.
ii. P‐V leukocidin , it’s gene is located in a lysogenic
phage, this toxin form a hole in cell membrane
causing death of cells especially WBCs, causes of
necrotizing pneumonia.
● Enzymes :
a. Beta lactamase , the cause of penicillin resistance.
b. Catalase , causes the break of H 2O
2.
c. Hyaluronidase , spreading factor, causes breaking of
hyaluronic acid thus make penetration easy to
subcutaneous tissue.
d. Coagulase , either
i. bound "clumping factor," facilitate binding to
surfaces and cause clumps in plasma.
ii. releasable , induce formation of plasma clot that
forms a protective wall around the bacterium
inhibiting leukocytes migration, by activating
prothrombin to thrombin, which activate fibrinogen
to fibrin.
e. Fibrinolysin , AKA staphylokinase , breaks blood clots.
● Diseases:
i. Pyogenic diseases :
● Conjunctivitis typically presents with unilateral burning eye
pain, hyperemia of the conjunctiva, and a purulent
discharge."most common cause".
● Sepsis, with clinical features that of gram ‐ve rods.
● Acute Endocarditis may occur on normal or prosthetic heart
valves, especially right‐sided endocarditis (tricuspid valve) in
intravenous drug users.
● Osteomyelitis and septic arthritis (old individuals and children)
may arise either by hematogenous spread from a distant
infected focus or be introduced locally at a wound site, the most
common cause of septic arthritis in adults is S. Aureus .
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