Lecture 8 Gram positive bacteria – Topic 3 Staphylococcus Flashcards
The Firmicutes Low GC gram-positive bacteria
Non Spore forming bacteria
The lactic acid bacteria
Streptococcus
Lactobacillus
Staphylococcus
Listeria
Mycoplasma
The spore forming bacteria
Clostridium
Bacillus
Actinobacteria –
the high GC gram positive bacteria
Streptomyces
Nocardia
Corynebacteria
Mycobacteria
STAPHYLOCOCCI
Gram+ non-motile cocci (>30 species)
Facultative anaerobe capable of both fermentation and
respiration
Ferment sugars with the formation of lactic acid as one of
the major products but not part of the lactic acid group. G + C (30 - 40%) content similar to lactic
acid bacteria - less restrictive growth requirements.
Staphylococci test
Catalase positive (distinguishes from Streptococcus)
Staphylococcus aureus
Beta-hemolysis on blood agar
Coagulase positive
-distinguishes from S. epidermidis and micrococcus)
-causes plasma to clot by conversion of fibrinogen to fibrin, staph aureus is coagulase positive so produces an enzyme that turns fibrinogen into fibrin and it is this conversion that produces the fibrin sac around staph aureus furuncles (pus filled boils)
Used to be performed in a tube or on a slide
now usually performed using latex
bead agglutination
Only S.aureus is coagulase positive
Staph. aureus diseases:
.
Major components of normal flora –skin -nose
* can cause Pneumonia and septicaemia in new-born and
immunocompromised patients (also a problem in burns units).
*can also cause Skin infections. Organism invades subcutaneous tissue with the
aid of lipases - inflammation -> white blood cells -> organisms release
toxins that kill cells - > pus -> organisms releases coagulase - >
fibrin barrier -> boils, carbuncles. Also can cause Skin infections such as Impetigo
the bacteria can find a little abrasion in the skin as the possible site of infection and will start reeplicating in the skin, this causes immune cells and macrophages to produce inflammatory signals which attract more immune cells from the local capillaries and squeeze out of the capillaries and move through the tissues towards the target infection however staph aureus produces leukocidin, a toxin that kills white blood cells; forming pus as a result
Staph. aureus more diseases:
- Pneumonia and septicaemia in new-born and
immunocompromised patients (e.g. burns units). - Skin infections. Organism invades subcutaneous tissue with the
aid of lipases - inflamation -> white blood cells -> organisms relesaes
toxins that kill cells - > pus -> organisms releases coagulase - >
fibrin barrier -> boils, carbuncles. Also impetigo. - Osteomyelitis
- Septic arthritis
- Endocarditis
*Wound infections, absesses. Common hospital acquired infection
- can be transmitted by hospital personnel, but usually patient.
Major cause of nosocomial infections.
Coag+ staphs carried by 20-30% population but
approx. 50% hospital staff (unless “decolonised”).
Septic arthritis
this is when steph aureus gets into the joint perhaps after trauma or surgery or through blood via a hematogenous route (spread through the bloodstream)
- Staphylococcal septic arthritis - babies and
young children- older individuals could be many different bacteria - Serious – damage though infection and inflammatio to joints, bones and cartilage
- Bacteria gain access
– Via the bloodstream.
– From an injury that cuts into the joint
– During surgery.
group A strep can cause all these infections as well so doing testing for differential diagnosis is important
Osteomyelitis
this is an infection specifically of the bone itself and can also be caused by Strep A diseases
can occure commonly in children as there are growth plates in children gowing and likely to have thrombosis at the capillaries in the bones so bacteria in the blood can get caught there and hematogenous seeding of bacteria can occur in the bone thus forming a pussy legion and possible sepsis
Direct inoculation
or
Bacteria introduced
during trauma or surgery
Hematogenous osteomyelitis
Scalded skin syndrome (SSSS)
A toxin produced by phage group 2 Staphylococcus aureus (usually)
the staph carries the bacteria phage; a bacteria phage is a virus that infects a bacteria, the bacteria phage has genes encoding for an exfoliating toxin which causes desquamation. the toxin is produced at a certain site such as the mouth or umbilicus however the effects of the toxin can be remote from the sote of the infection
Initial infection in the mouth, nasal cavities, throat, or umbilicus
A lytic toxin (exfoliatin A or B, usually) is produced which affects the skin at remote
Sites leading to desquamation
Mostly in young children
particularly neonates
It heals up in a matter of weeks
Staph. aureus diseases:
- Pneumonia and septicaemia in new-born and
immunocompromised patients (e.g. burns units). - Skin infections. Organism invades subcutaneous tissue with the
aid of lipases - inflamation -> white blood cells -> organisms relesaes
toxins that kill cells - > pus -> organisms releases coagulase - >
fibrin barrier -> boils, carbuncles. Also impetigo - Septic arthritis
- Osteomyelitis
- Endocarditis- steph aureus is a possible cause for endocarditis
*Wound infections, absesses. Common hospital acquired infection
- can be transmitted by hospital personnel, but usually patient.
Major cause of nosocomial infections.
In an unscreened health setting,Coag+ staphs carried
by 20-30% pop but 50-70% hospital staff
Pathogenicity examples: Staph. aureus diseases
key one for steph aureus funnucle- leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages
Pathogenicity:
* hemolysins - (lyse erythrocytes) - toxins - will damage a large number of cell types.
* leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages.
* exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis.
* enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea
and vomiting. Heat stable - resist boiling.
* TSST-1 - superantigen. Stimulates T-cells to activate macrophages to release TNF ->
shock.
* lipases - lipid hydrolysing enzymes - allows organisms to invade tissues
* fibrolysin - disolves fibrin clots -> spread
* extracellular coagulase - may be involved in forming fibrin wall of abscess
Panton Valentine Leukocidin
example of a leukocidin
produced by strains carrying
the lukF and lukS genes
on a phage
Associated with community
acquired infections in the
young and healthy.
Occasionally hospital outbreaks
Acts with other leukocidins to
lyse host cell membranes.
Invasive soft tissue infections
key Pathogenicity
- exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis.
- enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea
and vomiting. Heat stable - resist boiling.
Food poisoning
staphylococcal food poisoning can be caused by enterotoxins A,B and D, staph aureus enterotoxins are heat stable so can resist boiling
- not a human infection
- caused by ingestion of preformed toxin
- food contaminated from humans
– bacterial growth
– enterotoxin production - onset and recovery both occur within few hours
– Very rapid - acts on emetic receptor site ->
vomiting - Inhibits water absorption → ‘explosive’ diarrhoea.
- Toxin is not destroyed by normal cooking.
key Pathogenicity
TSST-1 – toxic shock syndrome toxin is a superantigen. Stimulates T-cells to
activate macrophages to release TNF -> shock.
Panton Valentine Leukocidin pathogenicity
- hemolysins - (lyse erythrocytes) - toxins - will damage a large number of cell types.
- leukocidin - toxin acts on polymorphonuclear leukocytes and macrophages.
key * exfoliatin - plasmid encode skin toxin – produces wrinkling and peeling of epidermis.
key * enterotoxins A,B & D - exotoxins that cause a food poisoning - severe diarrhoea
and vomiting. Heat stable - resist boiling. - TSST-1 - superantigen. Stimulates T-cells to activate macrophages to release TNF ->
shock. - lipases - lipid hydrolysing enzymes - allows organisms to invade tissues
- fibrolysin - disolves fibrin clots -> spread
- extracellular coagulase - may be involved in forming fibrin wall of abscess
