Beruflich Dokumente
Kultur Dokumente
Sinung Bawono
Pembimbing : Prof. DR. Dr. Priyambodo, M.Sc
Introducing
Came from greece words that means: golden grape-
cluster berry
Coccus shape Positive gram staining Anaerob fakultatif Dangerous strain : MRSA
Genom
Involved of circulair chromosome ( 2800 bp), dan
prophages, plasmids, and transposons Gen that works on virulens resistence on AB laid on chromosome and extra chromosome elements Can be transfered to another strains
H2O and O2
www.aic.cuhk.edu.hk/ web8/mrsa.htm
http://textbookofbacteriology.net/staph. html
Factor Virulensi
concentrations gradient in order to the cell is more stable and not easy to lysis.
Polysacaryde and adhesin alter fagositosis. Petidoglikan make bacterial adhesion at the host cell
membrane
Protein A- Immunological disguise.
Invasive enzymes
Coagulase Complex-Seals off infection, preventing phagocytic
engulfment
bid to to cell wall surface, forms a pore, and cellular machinery of host cell leak out
- During the initial stages of infection, the expression of surface proteins that bind extracellular-matrix molecules favors successful colonization of host tissues, whereas the synthesis of exoproteins favors the spread to adjacent tissues
syndrome
Transmission
nosocomial infection -->exposure to the hands of
health care workers . Outbreaks may also result from exposure to a single long-term carrier or environmental sources,
staphylococci access to adjoining tissues or the bloodstream. (host -defense mechanism) The risk of infection is increased by the presence of foreign material :intravenous cathetersthrombusbacterial adherencenosocomial endocarditis
Invasive Infections
A. The endothelial cell is central to these pathogenic processes : target for injury Staphylococci avidly adhere to endothelial cells and bind through adhesinreceptor interactions
B.monocytes and macrophages (same as infection of gram bacteria) The monocytes release TNF and interleukin-1, interleukin-6, and interleukin-8 after contact with intact staphylococci.
Sepsis
cytokine and cellular activation the complement and
coagulation pathways are activated, arachidonic acid is metabolized, and platelet-activating factor is releasedcause fever, hypotension, capillary leak, disseminated intravascular coagulopathy, depression of myocardial function, and multiorgan dysfunctionseptic syndrome
Toxin-Mediated Disease
Pyrogenic-toxin superantigenshigh fever, shock,
capillary leak, and multiorgan dysfunction massive release of cytokines by both macrophages and T cells shock syndrome (endotoxin shock) tissue damage
adhesion molecules on endothelial cells migration of leukocytes to the site of infection - After infection, cytokines are first demonstrable within vessels, extending into tissues as inflammatory cells migrate to the sites of infection
intercellular adhesion molecule 1 (CD54), vascular-cell adhesion molecule 1 (CD106), and MHC class I
endovascular disorders. Bacteremia Mortality: 11 to 43 percent. age of more than 50 years, nonremovable foci of infection, serious underlying cardiac, neurologic, or respiratory disease
Endocarditis
25 to 35 percent of cases intravenous drug users, elderly patients, patients with prosthetic valves
Metastatic Infections
tends to bones, joints, kidneys, and lungs Suppurative collections at these sites serve as potential
Sepsis
advanced age, immunosuppression, chemotherapy,
and invasive procedures. similar to that of gram-negative sepsis, with fever, hypotension, tachycardia, and tachypnea the most common gram-positive pathogens in cases of sepsis.
disseminated intravascular coagulation, lactic acidosis, and death both gram-positive and gram-negative sepsis, the levels of circulating tumor necrosis factor , interleukin-1, and interleukin-6 are predictive of the outcome.
desquamation, hypotension, and multiorgan damage toxic shock syndrome toxin 1(>90%) associated with menstruation, other enterotoxins account for 50 percent of cases unrelated to menstruation ( localized infections, surgery, or insect bites) Mortality rate:nonmenstrual toxic shock syndrome>menstrual
Mechanism Of Resistance
http://www.jci.org/cgi/content/full/114/12/1693/F1
http://www.jci.org/cgi/content/full/114/12/1693/F1
Resisten cephalosporin
Resisten penicillin
Resisten Meticilin
high level of resistance requires the presence of the mec gene that encodes penicillin-binding protein 2a
suggesting the horizontal transfer of mec DNA The enterococcal plasmid-bearing gene for resistance to vancomycin has been transferred by conjugation to S. aureus in vitro.
http://www.bioteach.ubc.ca/Biodiversity/AttackO fTheSuperbugs
Nafcillin
Oxacillin
Cephalothin
Vancomycin
Allergy patient: fluoroquinolones, Drug of choice for isolated MRSA trimethoprim sulfamethoxazole, clindamycin, or minocycline If resisstent : quinolon, quinupristin dalfopristin, a new carbapenem, and a new family of antimicrobial drugs, oxzolidinones
Vancomycin
Combination -lactams and aminoglycosides increases invitro bacterial killing and in animal models with endocarditis.
Rifampicin
Potent Easy become enough for resistent in S. aureus single use
A capsular polysaccharideprotein conjugate antistaphylococcal vaccine has produced improved phagocytosis in vitro and improved survival in experimental models of staphylococcal infection
Universal precaution