7_Gram Positives I Flashcards
how can staph aureus be transmitted?
(4 different ways)
-
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
can S. aureus be carried on the skin?
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
types of surface lesions?
- impetigo: crusting lesion
- furuncle (boil): hair follicle infection
- stye: single boil in the eye
- carbuncles: multiple boils together
what is key characteristic of an S. aureus lesion?
produces a large amount of pus
steps/process of surface infection?
- 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
how does S. aureus spread?
production of a number of toxins, including….
- fibrinolysin, which lysis the fibrin
- hylauronidase, which promotes spread through connective tissue
- hemolysins
- toxins for nutrient scavenging
cellulitis:
define
- 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
osteomyelitis:
define
- 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
arthritis:
define
- DEEP LESION
- inflammation of one or more of your joints
- main symptoms of arthritis are joint pain and stiffness, which typically worsen with age
pneumonia:
define
- 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
endocarditis:
define
- 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
bacteremia:
define
- 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.
Name the 2 superantigens discussed
- Toxic Shock Syndrome Toxin-1 (TSST-1)
- Staphylococcal Enterotoxins (SE)
how do superantigens cause toxic shock/ cytokine storm?`
- 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
how to toxic shock and endotoxic shock differ?
- toxic shock is similar to endotoxic shock except:
- toxic shock is mediated by an exotoxin
- endotoxic shock is mediated by LPS
symptoms of toxic shock syndrome
- fever,
- malaise,
- rash,
- multi-organ changes, and
- lethal hypotension
what causes toxic shock syndrome?
- 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
CC: staphylococcal scalded skin syndrome
- 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
what are persistent carriers, w/ regards to S. aureus?
what about intermittent carriers?
-
persistent: ALWAYS carry S. aureus
- high CFUs in anterior nares
- consistent strain
-
intermittent: sometimes carry S. aureus
- exchange of carrier
- strains over time
how can carriers spread S. aureus?
- direct contact
- contamination of fomites (surfaces)
- contamination of food
- *can also infect themselves
CC: food poisoning
define, and process of infection
- intoxication; transient and self-limiting disease
- process
- A carrier of S. aureus prepares food.
- Food is left at warm temp–>bacteria grow & produce Staphylococcal enterotoxins
- SEs are heat stable (whether food is eaten raw or cooked makes no difference after the toxin is formed)
- SEs act as superantigens at the intestinal lining causing increased permeability of the GI tract –> diarrhea and vomiting.
- Because cooking has killed bacteria, the disease is transient and self-limiting.
Methicillin Resistant S. Aureus
- contains which gene encoding for alternative penicillin binding protein?
- what Abxs is it resistant to?
- contains mecA gene encodes an alternative penicillin binding protein (PBP2a)
- resistant to all beta-lactam antibiotics
CC: Hospital-Associated MRSA
found where? what is it resistant to?
- found in hospitals
- often resistant to other antibiotics
CC: Community-Associated MRSA
found where? associated w/ what?
- found predominantly in the community
- associated w/ death of healthy individuals, such as athletes
why are s. aureus infections so common?
S. aureus can survive on surface, increasing the likelihood of infection in the hospital and in the community
which Abx can S. aureus be resistant to?
and why?
Resistant to most antibiotics
- Penicillin
- due to changes in PBP (MRSA) mecA gene
- beta-lactamases (on plasmids)
- Chloramphenicol
- production of acetylases, methylases, or phosphorylases
- efflux pumps
- Erythromycin
- changes in ribosome proteins
- Sulfonamides
- alternate pteridine synthetase
what are the key distinguishing features of S. aureus?
- Gram-positive cocci in grape-like clusters
- Catalase positive
- Coagulase positive
- Beta (b) hemolytic usually slightly yellowish/gold colonies
S. epidermis
forms what?
- part normal flora
- forms biofilms on indwelling devices
what is the cause of recurrent bouts of septicemia?
- 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
where can S. epidermidis form biofilms?
- prosthetic valves
- contact lenses
- intravascular catheters
- artificial hearts
- joint replacements
- endotracheal tubes
- voice prosthesis
S. epidermidis
distinguishing features
- gram-positive cocci in grape-like clusters
- catalase positive
- coagulase negative
- gamma hemolytic
S. saprophyticus:
normal, and pathogenic forms?
virulence factors?
- normally urinary tract normal flora/ GI tract normal flora
- pathogenic
- upper UTI: pylonephritis
- lower UTI: cystitis
- virulence
- urease
- multi-drug resistance
S. saprophyticus:
defining features
- Gram-positive cocci in clusters
- coagulase negative
- multi-drug resistant
- causes UTI, esp in sexually active women –> produces urease
how are Streptococci classified?
by serotypic against surface structures
- Lancefield serogrouping – cell wall specific polysaccharides or LTA components
- S. pyogenes serotyped based on M-protein serotypes
- S. agalactiae and S. pneumoniae serotyped based on capsular polysaccharide antigenicity
Lancefield grouping and subspecies of:
Streptococcus pyogenes
Group A streptococci
Subspecies:
- M protein > 80 serotypes
- T antigen
- R antigen
Lancefield grouping and subspecies of:
Streptococcus agalactiae
Group B; neonatal sepsis
Subspecies:
- capsular polysaccharides
Lancefield grouping of:
Enterococcus faecalis and faecium
(now a separate genus)
Group D; assoc w/ endocarditis and UTIs
Lancefield grouping of:
Streptococcus sanguis
Group H; assoc w/ endocarditis
Two examples of non-Lancefield pathogens and associated disease
- Streptococcus pneumoniae –> pneumoniae
- Virdons streptococci (S. mutans) –> dental caries
examples of S. pyogenes Group A strep diseases:
Localized infection on 1) surface or 2) deep
1) Surface
- tonsilitis
- impetigo
- erysipelas
2) Deep - necrotizing fasciitis
examples of S. pyogenes Group A strep diseases:
Toxin produced during infection
- streptococcal toxic shock syndrome
what is post-streptococcal sequelae?
immune response
- rheumatic fever
- rheumatic heart disease
- glomerulonephritis
examples of non-invasive disease
- pharyngitis (tonsillits, strep throat)
- erysipelas
- impetigo
- may be superinfected w/ s. aureus
- cellulitis
- can occur when S. pyogenes infects chicken pox lesions (secondary infection)
CC: necrotizing fasciitis, aka “flesh-eating bacteria”
- destructive deep tissue infection that rapidly eats away underlying muscle
- can occur after a small injury
- develops rapidly and is extremely painful
- rare complication
CC: sueprantigen disease
- predominantly SpeA
- toxic shock-like syndrome (TSLS) or streptococcal toxic shock syndrome STSS – similar to toxic shock mediated by staphylococci
- scarlet fever
CC: S. pyogenes
causes what? when does it occur?
- causes post-streptococcal sequelae
- acute rheumatic fever
- rheumatic heart disease
- glomerulonephritis
- occurs following active infection
define the following S. pyogenes sequelae:
- acute rheumatic fever
- rheumatic heart disease
- glomerulonephritis
- acute rheumatic fever – antibodies that recognize the alpha helical structure of M protein cross react with the heart sarcolemma usually following throat infection
- rheumatic heart disease is a chronic condition resulting for vavular heart damage due to ARF
- glomerulonephritis – deposition of immune complexes in the kidney leading to kidney inflammation and damage using following skin infection
S. pyogenes have a number of diff’t strains.
How are these grouped, and what makes them different?
- 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
Which M proteins are associated w/ invasive disease?
M1 and M3
Streptococcus pyogenes
defining characteristics
- 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
