025) Bacterial Infections of Bones, Joints and Muscles Flashcards
Describe organism’s morphology and name it
Staphylococcus species
- Gram-positive cocci arranged in clusters
Staphylococcus are catalase (+/-) bacteria
Catalase (+)
How can catalase + staphylococcy be further classified ?
By Coagulase test
Coagulase (+) staphylococcy ?
Staph. aureus
Coagulase (-) staphylococcy ?
-S. epidermidis
-S. saprophyticus
…. Causes ~75% of cases of osteomyelitis
Staph. aureus (coagulase positive)
…… are skin commensals that cause most cases of osteomyelitis associated with prosthetic joints.
Staph. epidermidis (Coagulase-negative)
Virulence factors of Staph. aureus ?
• Coagulase
• Staphylokinase
• Leucocidins
• Hyaluronidase
• Haemolysins
• Epidermolytic toxins
• Enterotoxins
• Toxic shock toxin
• Biofilm production
Invasins of Staph. aureus ?
• Staphylokinase
• Leucocidins
• Hyaluronidase
Exotoxins of Staph. aureus ?
• Epidermolytic toxins
• Enterotoxins
• Toxic shock toxin
Major Virulence factor of Coagulase -ve Staphylococci ?
• Biofilm production – cause 10-40% of prosthetic hip infections
Pathogenesis of S. aureus osteomyelitis ?
• Sluggish flow at the metaphysis
• Adhesion of S. aureus
• Acute inflammation at the site
• Avoidance of host defences
• Growth in biofilm
• Necrosis of tissue
• Abscess formation
• Further necrosis due to compromised blood supply
Treatment of S. aureus osteomyelitis ?
-SURGERY :
Drainage (release) any pus WITHOUT DELAY
and :
- CHEMOTHERAPY :
Vigorous use of antibacterial agents ;
•Flucloxacillin +/- Fusidic acid (Fucidin) or
•Teicoplanin
CHEMOTHERAPY of staph.aures ostemomyolitis needs to be continued for…. Weeks
(6-8 weeks)
Treatment of pott’s disease ?
- CHEMOTHERAPY :
Treatment for at least 6 months and possibly up to 9–12 months for extensive bone infections eg rifampicin + izonaziad + pyrazinamide + ethambutol (2months or more) then rifampicin and izonaziad (up to 10 months)
Pott’s disease treatment often needs …. Time
Treatment for at least 6 months and possibly up to 9–12 months for extensive bone infections
In Management of Septic Arthritis : Antimicrobials must be continued for…… weeks
3 to 6
How can Catalase (-) Streptococcus be further classified ?
Haemolysis
Beta haemolytic Streptococcy ?
-S. Pyogenes (GAS)
-S. Agalactiae (GBS)
Alpha haemolytic Streptococcy ?
-S. pneumoniae
-S. viridans
what’s the haemolysis ?
Gamma
Name organism and describe morphology
Streptococcus pyogenes (GAS) ;
Morphology: Gram-positive cocci, arranged in chains
Virulence factors of Strep pyogenes ?
• M-protein – adhesin, antiphagocytic
• Lipoteichoic acid – adhesin
• Fibronectin-binding protein (Protein-F)
• Streptococcal pyrogenic exotoxins A,B,C superantigens
• Streptolysin, O, S – haemolysins
• Streptokinase
• DN’ase
• Hyaluronidase
• Proteases e.g. C5a peptidase
Adhesion factors of Strep pyogenes ?
• M-protein – adhesin, antiphagocytic
• Lipoteichoic acid – adhesin
• Fibronectin-binding protein (Protein-F)
Invasion factors of Strep pyogenes ?
• Streptococcal pyrogenic exotoxins A,B,C superantigens
• Streptolysin, O, S – haemolysins
• Streptokinase
• DN’ase
• Hyaluronidase
• Proteases e.g. C5a peptidase
Superantigens are often produced by :
Staphylococci, Group A Streptococci and Mycoplasmas
How does Superantigens cause damage ?
• Potent immunomodulators (overstimulation of the immune system)
• Overproduction of cytokines ……………Tissue Damage
• Divert T cells into polyclonal activation which is immunologically unhelpful.
Cells secreting TNF, IL-1 ?
macrophages, fibroblasts
Cells secreting IL-8 ?
epithelial cells
Cells secreting Histamine ?
Mast cells
What secretes NAD dehydrogenase ?
mitochondria
Cells secreting Leucotrienes, prostaglandins ?
all cells
Pathogenesis of Streptococcal infections ?
• Penetrate tissue
• Adherence
• Avoid host defenses
• Produce enzymes/toxins to destroy tissue
• Cause thrombosis of perforating arteries
• Activate immune cells non-specifically
Cellulitis ?
Comment on the demarcation of cellulitis
an irregular line of demarcation (not well demarcated)
Pathogens of Necrotizing fasciitis ?
• Streptococcus pyogenes (group A strep)
(flesh-eating bacteria)
• Mixed infections with facultative anaerobes
• Rarely other organisms e.g. E. coli
Presentations of Necrotizing fasciitis ?
• Acute inflammatory response
• Very painful
• Erythema spreads rapidly
• Patient is “toxic”
Treatment of S. pyogenes infections ?
• Penicillins are the drugs of choice benzylpenicillin (BP)
Treatment of S. pyogenes Necrotizing fasciitis ?
• Prompt Radical excision of necrotic tissue (surgical debridement)
• Aggressive Local and systemic antibiotics –
clindamycin + BP
Pathogens of Gas Gangrene ?
• Clostridium perfringens
• Mixed facultative and strict anaerobes
Presentations of Gas Gangrene ?
• Dark red skin with large bullae
• Very painful
• Erythema spreads
• Patient is “toxic”
• Very little inflammation
comment on morphology and define the organism
Clostridium perfringens ;
Gram-positive rods
……. Produces acid and gas by fermentation of carbohydrates (saccharolytic)
Clostridium perfringens
…… Can form spores (under unfavourable conditions)
Clostridium perfringens
While most Clostridiums are saccharolytic , others are …..
proteolytic
Clostridium perfringens is a strict (aerobe/anaerobe)
Anaerobe
Virulence Factors of Clostridium perfringens ?
1-Exotoxins
2- Spreading enzymes: Collagenase & Hyaluronidase
Exotoxins of Clostridium perfringens ?
(~17 all with Greek letters)
• Alpha toxin :(phospholipase C or Lecithinase)
• Theta toxin: O 2 labile hemolysin
Pathogenesis of Clostridium perfringens ?
Treatment of Clostridium perfringens (Gas gangrene) ?
- surgical debridement
• Hyperbaric oxygen chamber
• Benzylpenicillin is an adjunctive therapy not an alternative to surgery
What is Hyperbaric oxygen chamber/therapy ?
Hyperbaric oxygen therapy increases the amount of oxygen your blood can carry. With repeated scheduled treatments, the temporary extra high oxygen levels encourage normal tissue oxygen levels, even after the therapy is completed.
