staphylococci Flashcards
- staphylococcus is a genus in gram — bacteria and it appears to be – shaped and from in —-
- they are —
- traditionally divided into – groups based on their ability to —-
1- —– staphylococci ( S.aureus) can colonise nasal passages and other moist skin areas ( ex. axilla , groin )
2- —- staphylococci ( >20 other species)
are common in human skin commensals ( ex. S. epidermidis)
- positive
- spherical ( cocci )
- forms in clumps/ clusters
- facultative anaerobes
-2 groups - ability to clot plasma ( the coagulase reaction/test)
- Coagulase-positive staphylococci
- Coagulase-negative staphylococci
-A laboratory test used to differentiate S. aureus (coagulase +ve) from other staphylococci (negative) ——
- —– is an enzyme that can cause blood clot formation (converting fibrinogen to fibrin) which allows the bacteria to coat its surface w — and possibly resists —
- coagulase test
- coagulase
- fibrin
- phagocytosis
-Used to differentiate staphylococci from streptococci (also a Gram-positive coccus) —–
-presence of a —- is determined by the ability of the bacteria to reduce — into water and oxygen which results in the production of —-
- catalase test
- catalase ( aka an enzyme )
- reduce hydrogen peroxide
- bubbles
( staphylococci = catalase + )
- staphylococcus aureus is found in —– and about —– healthy humans colonised.
- its increased with:
- its distinguished as being — or resistant to —–
1- Resistance to usual treatment results from production of an —–
2- usually a — infection , — at higher risk ( colonisation vs infection ) - can also be resistant to other —-
- in hospital:
- moist skin folds, mucosal surfaces, nasopharynx
- 20-40%
- increased if:
- Diabetes mellitus
- Injecting drug use
- Where a foreign body/implant is present
- methicillin-sensitive (MSSA) or
resistant (MRSA) - altered penicillin-binding protein (PBP2a)
- healthcare associated infections
- elderly
- antimirobial classes
- isolate / cohort w contact precautions
S. aureus pathogenesis:
- portal of entry:
1——
2- —– by:
- a —- in a skin or from enters through —–membranes allowing access to adjoining tissue
- attaches to cells by:
1- —- which facilitates attachment
2- —- as it inhibits —- and facilitates — to implants
3- —– biding protein which is — , its for the attachement to — and —-
4- —– ex: — which promotes collagen attachment and found in strains that causes —–
- ingestion
- penetration
- break
- mucous membrane
- surface cell
- capsule
- inhibits chemotaxis and phagocytosis
- facilitates the adherence to implants
- fibrin/fibrongen binding protein which is a clumping factor
- blood clot and traumatised tissue
- matrix binding protein
- adhesins
- osteomyelitis or septic arthritis
s. aureus pathogenesis :
-it can invade/defeat the —- which causes inhibition of —- with the survival within —–
- production of —- that promotes —- as:
- immune ssytem
- phagocytosis
- within phagocytes
- extracellular substance
- invasion
- invasins and enzymes
S/ aureus can can damage to the host cells by:
1- — damage through —-
2- —
3- — as:
- —- which are super antigens
- —–
- —– 8 antigenic type ( A-E , G-I) causes food poisoning and will be converted to GIHEP module
- —- toxins which causes scalded skin syndrome
- others as :
S. aureus can also cause damage by getting out and spread further to:
- direct damage by peptidgoglcycan wall
- enzymes
- toxins
- exotoxins
- toxic shock sydrim toxin (TSST-1)
- endotoxin
- exfoliative toxin
- cytokines ( alpha beta leukocidin _)
- person-to-person: – direct contact via skin carriage, especially hands
- environment: shed on to surface
classification of staphylococcal infection:
- Skin & soft tissue
- Systemic – invasive
- Toxin-mediated
-a) Food Poisoning / Gastroenteritis
- Short incubation period,
self-limiting
- Covered in GIHEP module
- b) Scalded Skin Syndrome
- c) Toxic Shock Syndrome
systemic s.aureus infection:
- Bloodstream infection (BSI)
- Endocarditis
– Usually secondary to BSI - Bone/joint infections
– Ex. septic arthritis, osteomyelitis - Deep abscesses, e.g. brain, spine, psoas muscle
- Pneumonia
– Risk factors: viral respiratory infection, cystic fibrosis, ventilation,
aspiration
- toxin mediated : scaled skin syndrome:
1- spectrum of — skin disorder:
has localised —- , generalised —- of entire body surface , —- usually spared
2- —- toxin by which these toxins are spread —- from localised source , split — in skin layer ( middle layers )
3- most common in —-
4- its —-
5- mortality: –
- superficial blisering
- blister
- exfoliation
- mucous membrane
- heamatogenously
- intracellular bridge
- in children less than 6 yr mainly in neonates , immunuspressed adults and Renal failure
- its contagious
- Children <3% / Adults up to 60%
- scaled skin syndrome:
1- skin extremly —
2- large patches of — slide off underlying layer at the slightest pressure — sign
3- complication due to —–
4- managemt:
- painful
- necrotic epidermis
- nikolyski sign
- sepsis , 2ndary infection , dehydration
- management:
- Rehydration
- Wound care
- Antimicrobial treatment
Toxin-Mediated: Staphylococcal Toxic Shock Syndrome (TSS):
1-TSS toxin-1 acts as a —- –>
massive —– release
2- Historically associated with —-
3- its —— , —– , —– onset :
- ——
- —–
4- other organ involved:
- superantigen
-cytokines - high absorbency tampons
- rapid , dramati , fulminant onset
- pyrexia and hypertension
- rash w subsequent desquamation,
especially on palms and soles - other organs involved:
– Renal failure
– CNS (disorientation without focal
neurological signs)
– Muscular (severe myalgia, increase in CK)
labatory diagnosis:
1- day 0 aka — :
2- day 1+ aka —- :
3- 24 hours later aka — :
4- 24 hours later aka — :
1- patient specimens ( blood culture for example ) –> incubate at 37 degree c
2- postive signal –>
* Gram stain; bunches of grapes
* Set up culture plates in lab
* Team reviews patient
* ? PCR for earlier confirmation
3- culture result —>
* Read agar culture plates
* Coagulase test
* Phone team/patient reviewed
4- antibiotic suspeciability results –?
* Alter empiric antibiotic therapy as
appropriate
* If MRSA – infection control
precautions & decolonisation
management of s.aureus infection:
- History, especially timing and presentation of symptoms
- Clinical exam
a) Focus on a possible source or evidence of the spread of
infection if systemically unwell
b) Be sure to examine:
a) Skin: IV line sites or other indwelling devices, surgical wounds,
soft tissue infections or abscesses
a) Remember scars can indicate implantable devices or joint or valve
replacements
b) CVS: evidence of known or new / changed murmur on
auscultation
c) Musculoskeletal: new bone or joint pain, reduced range of motion
or limp, swelling, loss of function
c) Always consider the possibility of deep-seated infection - Investigations: (depends on the clinical presentation)
* General bloods: FBC, U&E, CRP, lactate
* Microbiological (specimen will depend on infection site)
– Abscess - pus or tissue better than skin swab
– BSI – blood cultures
– Pneumonia – sputum, broncho-alveolar lavage (BAL)
– Septic arthritis – joint fluid
– TSS (next slide)
– Food poisoning – food (not stool)
* Other investigations (as relevant):
– Imaging (ex. CXR, CT or MRI scans, Echocardiogram (ECHO))
TTS 0 investigation and management:
1- investigation:
- —- if febrile or systemically unwell which is rarley —-
- —- for culture if skin lesion
- other swabs for culture:
2- managemt:
- — quickly
- —– and —- input
- rapid —-
- source control :
- blood culture
- positive
- wound swab
- abcess , cervix/vagina
- recognise it
- Resuscitation & critical
care input - rapid IV antimicrobials
- sources: Debride infected or
necrotic wounds, drain
abscess etc
