Nosocomial infections Flashcards
Ignaz Semmelweiss 1847
-Introduced hand washing to reduce chilbed fever (puerperal sepsis) -Streptococcus pyogenes
Joseph Lister 1865
- antiseptic phenol spray
- to reduce post-operative bacterial sepsis of wounds
Exogenous sources
other patients, medical staff, food, air, dust, water, catheters, instruments and equipment
Endogenous sources
another site within the patient
Hospital aquired infections
- increased incidence when patients are elderly, immunocompromised etc
- about 10% patients suffer
Mainly caused by opportunistic pathogens
- staphylococcus aureus
- clostridium difficile
- norovirus (winter vomiting virus)
What % of nosocomial infections are preventable?
about 15-30%
Risk Factors:
- age
- length of stay in hospital
- MRSA -previous exposure to abs
- surgery
- indwelling catheters
- C.difficile
MRSA
Methicillin Resistant Staphylococcus aureus
Staphylococcus aureus
- gram +ve coccus
- grow in grape-like clusters
- golden colonies
- non-fastidious, facultative anaerobe
- survives drying, salt tolerant
- commonly found in nose &skin of healthy humans
- spread by contact& airborne routes
Gram stained film of S.aureus would show…
-gram +ve cocci both intracellular and extracellular to polymorphonuclear leukocytes (PMN)
Virulence factors:
TOXINS:
- enterotoxins(v&D)
- toxic shock syndrome toxin (TSST)
- ‘superantigens’, trigger cytokine release, causing ‘shock’
- Various cell-destroying and tissue-destroying enzymes and toxins (e.g. alpha toxin, leukocidin, oxfoliative toxin, panton-valentine leukocidin)
Staphylococcus virulence factors:
- ->Adherence -fibronectin-binding proteins etc
- ->Anti-chemotaxis - chemotaxis inhibitory protein of staphylococci (CHIPS) , Extracellular adhesion protein (EAP)
- -> Anti-opsonic &anti-phagocytic-
- ->Degradative enzymes
- -> IRON uptake systems
Adhesins
Microbial surface components recognising adhesive matrix proteins
-bind to host proteins, may aid adherence to host tissues, and serum-coated plastic
Capsule:
- formation of biofilms
- adherence to plastic
what is Protein A?
- evasion mechanism
- binds Fc of IgG, to prevent opsonisation
opsonisation
- immune process where particles such as bacteria are targeted for destruction by phagocyte
- process will identify the invading particle
Antibiotic Resistance
-first appeared in 1950s
–Emergence of Methicillin-resistant Staphylococcus aureus (MRSA) in the last 30years
-
Mechanism of Resistance -Acquisition off mecA gene
mecA gene:
- encodes mutant penicillin-binding protein (PBP2a) with lower affinity for Beta-lactam antibiotics
- replaces normal penicillin binding proteins(enzymes involved in peptidoglycan synthesis) to which penicillin normally targets
mecA gene
located on a transposon known as SCCmecIV (jumping gene)
- resistant to all other B-lactam antibiotics
- often resistant to other types of antibiotics (multiply-resistant)
Epidemic MRSA (EMRSA)
- MRSA are no more virulent than antibiotic-sensitive strains
- they are more difficult to treat
Community acquired MRSA
- younger age group
- severe skin infections and lethal haemolytic pneumonia
- panton-valentine leukocidin makes pores (holes) in membranes of immune cells
Treatment and Prevention
- vancomycin
- emergence of VISA strains: vancomycin intermediate sensitivity
- vansomycin-resistant S.aureus (VRSA - vanA from VRE)
Recent approach
screening of hospital patients and decolonisation prior to admission
Clostridium difficile
-grem +ve rod
-strict anaerobe, spore-forming
-resistant to cleaning disinfectants
found in gut of:
-<1% people outside hospitals
-5-10% of hospital patients
Clostridium difficile: Disease
- diarrhoea
- abdominal pain
-life threatening pseudomembranous colitis
(extensive inflammation and necrosis of the colonic mucosa)
C. difficile infection development
- disease induced by disruption of normal flora
- broad spectrum antibiotics
- diarhhoea, ulceration of colon, death
Symptoms due to…
Toxin A (enterotoxin) cause hypersecretion of fluid Toxin B (cytotoxin) damage and destroys cells
