Flashcards in Staphylococcus Deck (76):
Staphylococcus structure and physiology
-gram positive cocci
Staph aureus is the only medically important staph species that is ___________.
-so a negative coagulase staph means it is not s. aureus
What is coagulase?
-aka clumping factor
-it binds and cleaves fibronogen, converting it to insoluble fibrin which causes S. aureus to clump as a result
S. epidermidis is coagulase ______.
Like GAS, S. aureus expresses many virulence factors with overlapping functions allows for what 3 things?
-evasion of host defenses
Does S. aureus express a capsule? If so, why?
-prevents phagocytosis of bacterium by leukocytes and also plays a role in adherence of bacteria to catheters and other synthetic materials
Protein A (Spa): what is it, what does it do, and who has (doesn't have ) it?
-on surface of most S. aureus strains, but NOT coagulase negative staph
-binds very tightly to Fc region of antibodies and so prevents antibodies from binding to its antigens and then leading to phagocytosis
S. aureus produces many toxins that play a significant role in its virulence. What are some of their effects?
-invasive infection, skin exfoliation, food poisoning, TSS
Most toxins in S. aureus are encoded by ______.
Alpha toxin: function
-produced by most strains
-integrates into cell membranes and forms pores
-Na and Ca flow into cell, water follows, and cell undergoes osmotic lysis
-important role in tissue damage
Beta toxin: function
-present in most s.aureus strains
-by cleaving sphingomyelin in membranes of cells, it damages the membrane and can lead to cell lysis
-plays role in tissue destruction like alpha toxin
-important in Staph scolded skin syndrome (SSSS)
-proteases that are thought to digest proteins involved in cell to cell contacts
-associated with food poisoning and found in 30-50% of staph strains
-heat stable and resistant to hydrolysis by stomach and intestinal enzymes
-function as superantigens and nonspecifically activate T cells and cytokine release
What is the issue with enterotoxins begin heat stable?
-if food has toxin, you cannot eat it because even if cooked well, toxins will persist
What is thought to cause vomiting that is characteristic of staph food poisoning?
-stimulation of mast cell degranulation
Toxic Shock Syndrome Toxin
-very stable toxin
-superantigen and induces nonspecific and massive release of cytokines that lead to vascular permeability and falling BP
In addition to toxins, Staph can produce a number of enzymes that help it to penetrate tissues and spread. Such as...
-lipases, hemolysins, fibrinolysin, and hyaluronidase
How does coagulase help S. aureus create characteristic infections that S. epidermidis doesn't?
-coagulase helps it bind fibrin and formed walled off abscesses, a major feature of S. aureus infections that S. epidermidis doesnt do
Are coagulase positive or negative Staph more virulent?
Immunity and S. aureus
-adaptive immunity is ineffective and so recurrent infection is common
What tests distinguish between S. aureus and S. epidermidis
-coagulase and mannitol
T/F: All staphylococci are catalase negative.
-False; they are all POSITIVE
Describe s.aureus colonies on agar
-soft, round, convex colonies
-tend to become golden
Main features of S. epidermidis
-common skin flora
-common contaminant because skin is shed a lot
-catheter or device-related infections due to biofilm formation
Main features of S. aureus
-predominant nosocomial and community acquired pathogen
-infection control nemesis
-commonly carried in human nares and other surfaces
-numerous virulence factors
-causes wide spectrum of diseases: local and systemic
Name virulence factor allowing for Staph aureus to adhere to host cells
Name virulence factors that allow S. aureus to establish infection and evade host defense systems
Name virulence factors that allow entry of s. aureus into deeper tissue and/or blood
What makes S. aureus so heterogeneous and hard to treat?
-large number of virulence factors
-different strains express different virulence factors
3 patterns of S. aureus carriers
1. persistent carriers (20%)
2. Intermittent carriers (60%)
3. Almost never carriers (20%)
What is the primary nosocomial pathogen?
-MRSA since hospital antibodies kill off its competition
Nosocomial infections are those that occur ________ after admission.
3 categories of disease caused by S. aureus
1. superficial lesions: skin abscesses and wound infections
2. Systemic and deep-seated/sepsis: pneumonia and bacteremia
3. Toxin-mediated: toxic shock syndrome and food poisoning
Molecular typing technologies have shown that S. aureus infections are largely due to ...
-the success and expansion of genetically-related "clones"
-Ex USA300 MRSA
Where does S. Aureus most likely colonize?
Food intoxication-heat stable enterotoxins consumed resulting in rapid onset (2-6 hours) of symptoms such as ______________.
-emesis and diarrhea
Toxins involved in TSS
-TSST-1 or exotoxin B or exotoxin C
Staphylococcal scalded skin syndrome is a blistering disease caused by what?
-exfoliative toxins A or B (ETA or ETB) that are serine proteases that cause separation of epidermal layers
-associated with epidemics in nurseries
More invasive and disseminated disease (bacteremia, endocarditis, intravenous catheter infection, septic arthritis, osteomyelitis) result when _____________.
-tissue barriers are interrupted
SSSS primarily affects who?
-neonates and young children
Progression of SSSS
-abrupt onset; localized erythema often starts around the mouth and eventually can cover the entire body within 2 days
-skin can slough off as pressure is applied and large blisters form after which the skin desquamates
Is scarring an issue in SSSS?
-no, because it only impacts epidermis
A localized form of SSSS is called _________
-mostly infants and young children
-highly communicable, self resolving, localized blisters
T/F: like GBS, Staph aureus can cause a superficial crusting infection impetigo.
False; GAS and staph aureus can cause this
S. aureus causes a number of ________________.
-pyogenic skin infections
-if pus is present in an abscess think staph!!
2 types of pyogenic skin infections s. aureus causes
-infection of hair follicles
-called a stye if at base of eyelid
___________ are an extension of folliculitis.
-large, painful red nodules with dead tissue underneath
Carbuncles: what are they and what are they associated with?
-term used when there are multiple furuncles that coalesce
-assoc with fever and chills indicating more severe and systemic infection
S. aureus is particularly problematic when skin surface is damaged and organism _____________.
-gains access to deeper tissues
Where does bacteremia arise from and what is a major complication of it?
-arise from an innocuous skin infection
-endocarditis that is highly fatal due to rapid destruction of heart valves
Pneumonia and empyema due to S. aureus
-can occur from aspiration or from hematogenous spread
-presents like other pneumonias but abscesses and tissue destruction are more common due to array of enzymes produced by staph
Bacterial seeding in the blood that is common to S. aureus makes it the most common cause of ....
-bone infection, septic arthritis in young children, and intraarticular infections in those with abnormal or artificial joints
A common form of food poisoning is due to __________ rather than an infection.
-intoxication/ingestion of the toxin
What are the most commonly affected foods by S. aureus enterotoxins?
Contamination to foods by enterotoxin is most commonly due to...
-asymptomatic human carrier
Once contaminated with S. aureus, what needs to happen for food to become toxin filled?
-needs to be at room temp or higher long enough for the bacteria to grow and release the enterotoxin
-as the toxin is stable, even if prepared properly, the food is still contaminated
Symptoms of staph food poisoning
-severe vomiting, nonbloody diarrhea, abdominal pain, nausea
What causes TSS?
-localized growth of toxin-producing S. aureus producing TSST-1, with release of toxin into blood stream
Symptoms of TSS
-fever, hypotension, diffuse macular rash
-multiple organ failure due to hypotension
-skin can slough off late in disease
How to treat TSS?
-need to treat immediately with antibiotics
-patients who survive (95%) have antibodies to the toxin and are immune
S.epidermidis, as a very common colonizer of human skin, is frequently responsible for ___________.
-infections involving in-dwelling medical devices
Staph epi is a major cause of _______ of artificial heart valves. Where do the infections usually occur and what can happen as a result?
-more commonly takes root at sites where valve is sewn into heart which can lead to separation of heart valve at the annulus
-native valve infections are much less common
The presence of an _________________ on staph epi enables efficient attachment to artificial surfaces like catheters and shunts. Why is this such a worrisome issue?
-exopolysaccharide or slime layer
-indwelling catheters are used extensively especially in debilitated patients
-such colonization leads to persistent bacteremia and the organisms can be seeded most anywhere else in the body, leading to other localized infections
___________ is a significant cause of UTIs in sexually active women.
Almost all staph are resistant to _________. So what is used instead?
-penicillin due to acquisition of penicillinases, which hydrolyzes beta lactam ring of penicillin
-thus the methicillins were used instead but resistance was quickly acquired
MRSA acquired an altered PBP that was introduced by a _____________.
-phage rendering them resistant to all beta lactam antibiotics
Treatment of S. epidermidis
-often depends on removal of foreign body
-vancomycin is drug of choice is necessary
MRSA has driven the use of __________ in hospitals, which has contributed to the spread of ________.
-vancomycin resistance among some other bacteria
Methicillin resistance is defined by the presence of ______.
mecA gene which encodes for an altered penicillin binding proteins
-harbored on large mobile element
CA-MRSA outbreak populations
-children in daycare
-crystal meth users
-native americans, alaskan, pacific islanders
HA MRSA vs. CA MRSA
-HA: link to healthcare system, multidrug resistant, 5 major genetic backgrounds,SCCmec I,II, III, panton-valentine leukotoxin negative
CA: less resistant, 2 significant clones, SCCmec IV, Panton-valentine leukotoxin +, prone to cause severe pneumonia
Resistances of nosocomial MRSA
-all beta lactam resistant
->90% resistant to erythromyocin, fluoroquinoline, clinamycin
~50% susceptible to vancomycin
Vancomycin Resistant S. aureus (VRSA)
-acquired vanA operon like enterococcus
VRE: Vancomycin resistant enterococcus risk factors
-prior broad spectrum antibiotics (cephalosporins, vancomycin)
-admission to an intensive care unit
-renal failure needing dialysis