7_Gram Positives I Flashcards
1
Q
how can staph aureus be transmitted?
(4 different ways)
A
-
carrier
- asymptomatic carriage on skin or mucous membranes of anterior nares
-
infection
- localized surface
- furuncles, carbuncles
- impetigo
- stye
- deep
- osteomyelitis
- arthritis
- systemic
- pneumonia
- endocarditis
- UTI
- entrocolitis
- septicemia
- localized surface
-
intoxication
- toxin ingestion (e.g. food poisoning)
- emesis or diarrhea (gastroenteritis)
-
infection and intoxication (toxin produced during infection)
- toxic shock syndrome
- scalded skin syndrome
2
Q
can S. aureus be carried on the skin?
A
Yes! It can be carried as part of the normal flora on the skin
Asymptomatic carriage on the skin or mucous membranes of anterior nares
3
Q
types of surface lesions?
A
- impetigo: crusting lesion
- furuncle (boil): hair follicle infection
- stye: single boil in the eye
- carbuncles: multiple boils together
4
Q
what is key characteristic of an S. aureus lesion?
A
produces a large amount of pus
5
Q
steps/process of surface infection?
A
- the bacteria bind via fibronectin binding proteins –> adheres to fibronectin
-
coagulase causes fibrin to clot walling off the bacteria
- induces fibrin clotting on bacteria protecting the cell from phagocytosis
- protein A binds the Fc portion of IgG helping to protect the bacteria from the immune response/ phagocytosis
6
Q
how does S. aureus spread?
production of a number of toxins, including….
A
- fibrinolysin, which lysis the fibrin
- hylauronidase, which promotes spread through connective tissue
- hemolysins
- toxins for nutrient scavenging
7
Q
cellulitis:
define
A
- DEEP LESION
- common, potentially serious bacterial skin infection
- affected skin appears swollen, red, typically painful and warm to the touch
- usually affects the skin on the lower legs, but it can occur in the face, arms and other areas
8
Q
osteomyelitis:
define
A
- DEEP LESION
- infection of the bone; rare but serious
- typically caused by S. aureus
- Infection in one part of the body may spread through the bloodstream into the bone, or an open fracture or surgery may expose the bone to infection
9
Q
arthritis:
define
A
- DEEP LESION
- inflammation of one or more of your joints
- main symptoms of arthritis are joint pain and stiffness, which typically worsen with age
10
Q
pneumonia:
define
A
- systemic infection
- an infection that inflames the air sacs in one or both lungs
- Sxs: air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing.
- Can be caused by a variety of organisms, including bacteria, viruses and fungi
11
Q
endocarditis:
define
A
- systemic infection of the heart’s inner lining, usually involving the heart valves
- usually occurs when germs from elsewhere in the body travel through the blood and attach to damaged areas of the heart
- Sxs vary based on severity of infxn, may include fevers, chills, and fatigue
- Tx: antibiotics or surgery
12
Q
bacteremia:
define
A
- systemic infection
- aka septicemia;
- the presence of bacteria in the blood. Blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly accomplished by blood cultures) is always abnormal.
13
Q
Name the 2 superantigens discussed
A
- Toxic Shock Syndrome Toxin-1 (TSST-1)
- Staphylococcal Enterotoxins (SE)
14
Q
how do superantigens cause toxic shock/ cytokine storm?`
A
- bind the outside of the Vbeta chain of the TCR and crosslink it to MHC class II
- all T cells with the appropriate Vbeta chain will be activated
- activation does not require antigen
- activation causes release of a massive amount of cytokines that lead to toxic shock
15
Q
how to toxic shock and endotoxic shock differ?
A
- toxic shock is similar to endotoxic shock except:
- toxic shock is mediated by an exotoxin
- endotoxic shock is mediated by LPS
16
Q
symptoms of toxic shock syndrome
A
- fever,
- malaise,
- rash,
- multi-organ changes, and
- lethal hypotension
17
Q
what causes toxic shock syndrome?
A
- caused by SEs and TSST-1
- (staphylococcal enterotoxins, and toxic shock syndrome toxin-1)
- originally assoc. w/ high absorbancy tampon use, but there are other cases of TSS not involving tampon use
- can be caused by local cause, like a boil
18
Q
CC: staphylococcal scalded skin syndrome
A
- disease usually following upper respiratory tract infxn, inner ear infxn, or conjunctivitis
- associated with the production of exfoliative toxin
- Sxs: fever, malaise, lethargy, rash on head and neck which spreads
- blisters develop on up to 90% of the body surface
- after blistering –> the skin is shed
- found in children and neonates
19
Q
what are persistent carriers, w/ regards to S. aureus?
what about intermittent carriers?
A
-
persistent: ALWAYS carry S. aureus
- high CFUs in anterior nares
- consistent strain
-
intermittent: sometimes carry S. aureus
- exchange of carrier
- strains over time
20
Q
how can carriers spread S. aureus?
A
- direct contact
- contamination of fomites (surfaces)
- contamination of food
- *can also infect themselves
27
Q
what are the key distinguishing features of S. aureus?
A
- Gram-positive cocci in grape-like clusters
- Catalase positive
- Coagulase positive
- Beta (b) hemolytic usually slightly yellowish/gold colonies
28
Q
S. epidermis
forms what?
A
- part normal flora
- forms biofilms on indwelling devices
29
Q
what is the cause of recurrent bouts of septicemia?
A
- because S. epidermidis in biofilms are hard to kill w/ Abx –> therefore usually not cleared
- Septicemia in this case is due to planktonic (free-living) bacteria that can be killed by antibiotics
- Killing is not as effective as the biofilm, so the biofilm survives and can cause anotehr bout of septicemia
- ONLY WAY TO CLEAR THE INFXN (typically) is to remove the indwelling device
31
Q
S. epidermidis
distinguishing features
A
- gram-positive cocci in grape-like clusters
- catalase positive
- coagulase negative
- gamma hemolytic
43
Q
examples of non-invasive disease
A
- pharyngitis (tonsillits, strep throat)
- erysipelas
- impetigo
- may be superinfected w/ s. aureus
- cellulitis
- can occur when S. pyogenes infects chicken pox lesions (secondary infection)
44
Q
CC: necrotizing fasciitis, aka “flesh-eating bacteria”
A
- destructive deep tissue infection that rapidly eats away underlying muscle
- can occur after a small injury
- develops rapidly and is extremely painful
- rare complication
45
Q
CC: sueprantigen disease
A
- predominantly SpeA
- toxic shock-like syndrome (TSLS) or streptococcal toxic shock syndrome STSS – similar to toxic shock mediated by staphylococci
- scarlet fever
48
Q
S. pyogenes have a number of diff’t strains.
How are these grouped, and what makes them different?
A
- Grouped by M-types (antigenic type of M-protein), which is antigenically highly variable
- Diff’t strains can be genetically very different, including:
- SNPs (single nucleotide polymorphism) –> may account for cyclic nature of disease and changes in virulence
- Up to 30% of genome varies –> pan-genome or supragenome for S. pyogenes
49
Q
Which M proteins are associated w/ invasive disease?
A
M1 and M3
50
Q
Streptococcus pyogenes
defining characteristics
A
- Group A strep
- Gram positive cocci in chains
- Beta hemolytic on (blood agar plate) BAP
- catalase negative (distinguish from Staph)
- bacitracin sensitive (A disk)
- PYR positive (enterococci + GAS)
- Strep quick test directed against surface antigens
