Lecture 18: Osteomyelitis Flashcards
What is osteomyelitis?
Infection and inflammation of the bone or bone marrow (Usually metapheseal area)
What are some common symptoms of osteomyelitis in children?
- Limping or inability to walk
- Fever and focal tenderness (b/c in blood)
- Sometimes visible redness and swelling around a bone.
What are the likely bugs for:
- Prosthetic joint infection
- Vertebral osteomyelitis
- Post-traumatic infection
- Diabetic foot infection
Staph aureus (amongst other things)
Whats the route of infection for osteomyelitis?
- Trauma (Join replacement, root canal etc)
- Spreading from local area of infection i.e SSTI, diabetic ulcer
- Hematogenous route (Bacteremia)
Whats the pathogenesis of osteomyelitis?
- Bacteria infect bone (Colonise and proliferate)
- Leukocytes infiltrate infected site and fight bacteria
- Inflammation and formation of pus
- Devascularisation, dead bone, abscess
- Bacteria might have invaded bone cells and evade immune system + drugs
- Bacteria might spread to joints (septic arthritis)
Whats of note when it comes to joint aspirate of septic athritis?
It will not be clear unlike rheumatic fever
Who is at risk for developing osteomyelitis?
- Diabetics with foot ulcers
- Patients with infections following trauma, bone surgery, joint replacement
- IV drug users
- Root canal treatment
- SSTI
- Can be children with chicken pox
What are the pathogens of osteomyelitis?
- ~80% will be staphylococcus aureus
OR
- GAS - S. pyogenes
- GBS
- Coagulase negative staphylococci
- Hemophilus influenzae
- Enterobacter spp
How is osteomyelitis diagnosed?
Complex…
- Specific symptoms: Pain/weakness of specific bones, redness, fever +/- bacteria in blood
- BLOODS: WBC high, elevated CRP, bacteria present
- Radiology, not great, MRI can confirm but expensive
- Bone biopsy is specific but invasive.
Whats a gram stain indicative of?
Positive = thick layer of peptidyglycan = sensitive to penicillins
Negative = extra outer membrane and insensitive to penicillins
Describe the subsequent tests following identification of gram status:
Gram +ive i.e staphylococcus -> Coagulase status.
Coag +ive = S. Aureus ONLY. Coag-ive (CONS): could be s. epidermis for example, but others.
Gram -ive i.e streptococcus -> Hemolysis study
Alpha hemolysis = S. pneumoniae or Viridians strep
Beta hemolysis = S Pyogenes
Gamma hemolysis = Enterococcus
Write some notes on staphylococcus aureus as a pathogen:
Habitat: Anterior nares, transiently on skin
Transmission: Human-human
Source of infection: Comm and hospital (one of the most nosocomial)
Diseases: SSTI, invasive disease, toxic shock and more
How can S. aureus cause skin infections?
Breaks in skin i.e splinter, cracks or via hair follicles
What are the virulence factors of S. aureus?
- Adhesins: For binding host tissues (Colonisation)
- Immune evasion factors: Neutralise certain parts of the immune response.
- Spreading factors: Allow bacteria to spread from local infection into deeper tissues or blood i.e proteases, DNAases, Hyaluronidase
Write some notes on Adhesins and their function, and examples:
MSCRAMS: Microbial Surface Components REcognising Adhesive Matrix Molecules
Binds structures such as ECM
What are some spreading factors of staph aureus?
Staphylokinase (Fibrinolysin): Causes fibrinolysis, dissolves fibrin clot (like streptokinase)
Lipases: Hydrolyse lipids
DNAses: Hydrolyse DNA, decreases viscosity of purulent material
Cytolysins: Destroy epithelial cells
What are the five immune evasion factors of staph aureus?
- Cytolysins
- Capsule
- Slime layer (Extracellular polysaccharide)
- Protein A
- Cell bound coagulase
And many more… theyre the masters of immune evasion
Write some notes on staph aureus cytolysins and capsule:
- Cytolysins: i.e hemolysin, leukocidin; Kills RBC, Leukocytes, tissue cells.
- Capsule: Thick layer outside cell wall prevents opsonisation with C3b or Ig and phagocytosis
Describe the slime layer of staph aureus:
- Microbial community with bacteria attatched to a substrate or interface to each other, embedded in a matrix of EPS.
Prevents antibiotics and immune components reaching the bacteria
Describe the function of protein A and cell bound coagulase in staph aureus:
Protein A: Binds IgG in wrong orientation (Via Fc), prevents opsonisation and phagocytosis.
Cell bound coagulase: Binds prothrombin and induces fibrin polymerisation, fibrin deposition on cell surface prevents opsonisation and phagocytosis.
What are superantigens, what do they do and what produces them?
Superantigens are a family of heat-resistant proteins that are nonspecific and highly potent T cell mitogens. (Think cytokine storm)
They trigger a strong pro-inflam response.
Synergisitc with endotoxins i.e LPS
= Systemic inflammation with tissue destruction, vascular leakage, multiorgan failure, toxic shock
Produced by S. aureus and S. pyogenes.
Whats the therapy for osteomyelitis with S. aureus?
- Prolonged antibiotic treatment i.e PIC line.
- > S. aureus resistant to penicillin and methicillin. Increasing resistance developing
- > Vancomycin last option.
-> Possible surgical debridement.
… start with augmentin till bacteria isolated.
How do beta lactams work?
Irreversible inhibition of transpeptidase (penicillin binding protein)
Beta lactamases are plasmid encoded enzymes that can be transferred between bacterial strains and species. That break down beta lactam antibiotics. Therefore, using an antibiotic that is not susceptible or combined with beta lactamase inhibitor.
Write some notes on what impetigo is:
Staph aureus purulent infection of the skin (contact based)
- Pustules, rupture and crusting, scratching causes secondary spread
Whats the prevention and treatment of impetigo?
Prevention: Good hygiene
Treatment: Wash with soapy water, air dry topical antibiotics or ointments
Write some notes on staph aureus caused folliculitis -> Furuncle and carbuncle:
Folliculitis: Pyogenic infection of hair follicles. Base of follicle is raised and reddened, pus beneath the epidermal surface.
Furuncle (Boil)
- Extension of folliculitis, large painful raised cutaneous nodule (pus filled)
Carbuncle
- Coalescence of furncles
- Progress of infection into deeper tissues
- Possibly systemic symtoms i.e fever, chills
Write some notes on staphylococcal scalded skin syndrome:
- Abrupt onset of localised perioral erythema over entire body
- Caused by exfoliative toxins
- Large bullae / cutaneous blisters over entire body
Write some notes on S. aureus cellulitis:
- Rapidly spreading pyogenic inflammation of dermis / subcutaneous tissue
- Often mild traumas, burns, surgical incision
- No sharp demarcation.
Treatment = Oral or IV antibiotics.
Write some notes on acute infective endocarditis:
- Infection of the inner tissue of the heart, including valves
- S. aureus most common cause of acute IE.
Write some notes on TSS:
Toxic shock syndrome is caused by toxic shock syndrome toxin produced by S. aureus. (Menstural TSS) - prolonged use of tampons.
Non-menstural TSS
- Caused by superantigens
- Systemic inflam
- bacteria through wounds
