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Year 2 Microbiology > MSK Infections and Anti-Microbial Therapy > Flashcards

MSK Infections and Anti-Microbial Therapy Flashcards

1
Q

What is osteomyelitis?

A

Inflammation of bone and the medullary cavity, usu. located in one of the long bones

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2
Q

Classifications of osteomyelitis?

A

Acute/chronic

Contiguous (adjacent to) / haematogeneous (blood spread)

Host status, e.g: presence of vascular insufficiency

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3
Q

What are the most common causes of osteomyelitis?

A

STAPH. AUREUS

In prosthetic joint infection, coagulase -ve Staphylococci are the most important

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4
Q

6 situations in which osteomyelitis occurs?

A
  1. Open fractures
  2. Diabetes/vascular insufficiency
  3. Haematogeneous osteomyelitis (blood-borne)
  4. Vertebral osteomyelitis
  5. Prosthetic joint infection
  6. Specific hosts and pathogens
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5
Q

Describe open fractures

A

There is a break in the skin producing a high infection risk; this is CONTIGUOUS

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6
Q

Treatment of open fractures?

A

Early management is key, inc. aggressive debridement, fixation and soft tissue cover

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7
Q

Clinical clues with infected open fractures?

A

Non-union and poor wound healing

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8
Q

Bacteria causing osteomyelitis in open fractures cases?

A
  • Staph. aureus

* Aerobic gram -ve bacteria

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9
Q

Describe diabetes/venous insufficiency

A

Often, this is a contiguous infection and tends to be polymicrobial (due to necrosis)

If the patient has an ulcer for longer than 2 months and >2 cm diameter, they probably have osteomyelitis; this is definitely the case if a tendon can be seen

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10
Q

Features of diabetes and vascular insufficiency?

A
  • Microneurovascular dysfunction with loss of nociceptive reflex (feel no pain) and inflammatory response
  • Loss of apocrine/eccrine gland function (no sweating)
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11
Q

Diagnosis of diabetic/vascular insufficiency

A

Probe to bone

MRI can be used to determine extent

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12
Q

Treatment of osteomyelitis in diabetics/vascular insufficiency?

A

Debridement and anti-microbials

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13
Q

Pathway for evaluation for the presence of osteomyelitis?

A

ADD PATHWAY PICTURE

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14
Q

In which groups of patients does haematogeneous osteomyelitis occur?

A
  • Pre-pubertal children
  • PWID
  • Central lines / dialysis / elderly
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15
Q

Epidemiology of haematogeneous osteomyelitis in PWIDs?

A

Contiguous, haematogeneous, direct inoculation

Tends to occur in unusual sites, e.g: sternoclavicular joint, sacroiliac joints, pubic symphisis, etc

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16
Q

Organisms in haematogeneous osteomyelitis in PWIDs?

A

Staphylococcus

Streptococci

Unusual pathogens:
• Pseudomonas 
• Candida 
• Eikenella corrodens (oral flora)
• Mycobacterium TB (in endemic areas)
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17
Q

Pathway for assessment and treatment of osteomyelitis?

A

ADD PATHWAY treatment PICTURE

TEE = trans-oesophageal echo

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18
Q

Treatment of acute and chronic osteomyelitis?

A

Acute - flucloxacillin; if the patient is known to have MRSA, vancomycin (otherwise avoid as it gives inferior outcomes)

Chronic - avoid empiric therapy unless the patient is septic or has extensive skin/soft tissue involvement

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19
Q

Epidemiology of haematogeneous osteomyelitis in dialysis patients?

A

E.g: can be with tunneled line; there are high Staphylococcal colonisation rates

Patient tend to have co-morbidities, e.g: PVD, diabetes

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20
Q

Pathogens in haematogeneous osteomyelitis in dialysis patients?

A
  • Staph. aureus (most common)

* Aerobic gram -ve bacteria

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21
Q

Unusual sites of osteomyelitis to be aware of?

A

Osteitis pubis (pubic symphisis) - urogynae procedures can predispose to bacterial causes; also, aspetic osteitis pubis can be triggered by surgery (can occur up to 18 months later) and athletes can get it

Clavicle osteo - risk factors inc. neck surgery and subclavian vein catheterisation

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22
Q

Describe sickle cell osteomyelitis

A

Occurs in people with sickle cell anaemia and tends to present as acute long bone osteomyelitis; there is a risk of septic arthritis

It may be mistaken as bone infarction

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23
Q

Pathogens in sickle cell osteomyelitis?

A
  • Salmonella

* Staph. aureus

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24
Q

What is Gaucher’s disease?

A

A paediatric lysosomal storage disorder that may mimic bone crisis; it often has osteomyelitis affecting the tibia

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25
Pathogens in Gaucher's osteomyelitis?
If there is bone crisis, sterile If infected, Staph. aureus
26
Importance of SAPHO and CRMO?
Synovitis Acne Pustulosis Hyperostosis Osteitis (adults) and Chronic Recurrent Multifocal Osteomyelitis (children) Potentially caused by Propionibacterium This can present in a similar manner to osteomyelitis and this must be ruled out
27
Signs of SAPHO and CRMO?
Fever, weight loss and generalised malaise; there is a history of exacerbations/remissions Raised inflammatory markers Lytic lesions on X-ray
28
Sites inv. with SAPHO/CRMO?
Chest wall (majority), pelvis, spine, lower limb The osteitis is multi-focal with various, off sites being affected
29
Describe vertebral osteomyelitis
Mostly a haematogeneous infection that causes spondylodiscitis and disc space infection It may be assoc. with epidural abscess or psoas abscess
30
Pathogens in vertebral osteomyelitis?
Staph. aureus (most important one) Gram -ve aerobic bacilli Strep. Mycobacterium TB
31
In who/what situation does vertebral osteomyelitis occur?
PWIDs IV site infection and GU ifnection SSTI (Skin and Soft Tissue Infections) Post-operative
32
Presentation of vertebral osteomyelitis?
Most people have insidious pain and tenderness; half have a fever Sometimes, there are neuological signs
33
Ix for vertebral osteomyelitis?
Raised inflammatory markers Raised WCC (sometimes) Abnormal plain film MRI (BEST Ix), Ga-67 scan
34
Treatment of vertebral osteomyelitis?
Avoid empiric antibiotics, unless septic, until the biopsy is done Drainage of large paravertebral/epidural abscesses Anti-microbials for 6 weeks (expect a >50% decreased in ESR); duration is extended is the case is complicated
35
Only situations where the MRI is repeated?
Unexplained increase in inflammatory markers Increasing pain New anatomically related signs/symptoms
36
Describe vertebral TB
If TB is in the vertebrae, it is called Pott's disease; often, there are NO systemic symptoms (only half have skin & soft tissue infection and less than half have pulmonary TB)
37
Dissemination of TB tests?
In children, check to see if they have a predisposition to dissemination (check for reduced IFN-γ, IL-12, etc) In adults, always offer a HIV test
38
Risk factors for prosthetic joint infection?
RA, diabetes, malnutrition, obesity
39
Mechanism of prosthetic joint infection?
Direct inoculation at the time of surgery Manipulation of the joint at the time of surgery Seeding of a joint at a layer time
40
Different time frames of prosthetic joint infections?
Early (within one month) with a haematoma/wound sepsis Late (after one month) with a contamination at the time of operation
41
Infection with PVL Staph. aureus?
Panton Valentine Leukocidin Toxin; present in both MSSA and MRSA
42
Presentation of PVL producing Staph. aureus infection?
1. Skin infections 2. Necrotising pneumonia 3. Invasive infections, e.g: bacteraemia, septic arthritis These patient are disproportionately unwell
43
Treatment of PVL producing Staph. aureus infection?
Flucloxacillin + anti-toxin antibiotic (e.g: clindamycin or linezolid)
44
Side effects of clindamycin and linezolid use?
Clindamycin - C. diff infection assoc. Linezolid - must limit use to 4 weeks other there is a risk of bone marrow failure
45
Describe planktonic vs sessile bacteria
Planktonic (bacteria in a free existence, i.e: in blood) - causes bacteraemia Sessile bacteria forms after the phenotypic transformation of planktonic bacteria, forming communities with biofilm and EC matrix around them (looks like goo), e.g: when the bacterium goes from blood to a joint
46
Ix for prosthetic joint infection?
CRP and inflammatory markers Blood culture Multiple peri-operative tissue samples; if they all grow the same organism, it is pathogenic Radiology
47
Treatment of prosthetic joint infections?
Removal of prosthesis and cement; therapy for at least 6 weeks Re-implant the joint after aggressive antibiotic therapy
48
Pathogens in prosthetic joint infection?
Staph. aureus and epidermidis (MOST IMPORTANT ones) Propionibacterium acnes (upper limb prostheses) Rarely, Strep. and Enterococcus sp. Gram negatives: E.coli and Pseudomonas Fungi and mycobacterium (perhaps, in immunosuppressed patients)
49
Treatment of Staph. epidermidis prosthetic joint infection?
Initially, vancomycin
50
4 ways in which septic arthritis can spread?
1. Direct invasion through a penetrating wound 2. Haematogeneous spread 3. Spread from infectous focus, e.g: cellulitis, abscess, in adjacent soft tissues 4. Spread from focus of osteomyelitis in adjacent bone
51
What is septic arthritis?
Inflammation of the joint space (normally sterile) caused by infection
52
Bacterial causes of septic arthritis?
Staph. aureus (most important) Strep. and coag -ve Staph. (prosthetic joints) Neisseria gonorrheae (in sexually active patients) H. influenzae (uncommon now)
53
Presentation of septic arthritis?
Severe pain with a red, hot and pus-swollen joint Limited movement
54
Ix for septic arthritis?
Microscopy of joint fluid If pyrexial, do a blood culture Exclude crystals (gout and pseudogout)
55
Treatment of septic arthritis?
FLUCLOXACILLIN (high dose to cover all Staph. aureus) If < 5 years, add Ceftriaxone (to cover H. influenzae) Adjust once organisms are confirmed
56
Describe knee bursitis
Most are not infective but, if they are, give antibiotics (flucloxacillin)
57
What is pyomyositis?
Bacterial infection of the skeletal muscles which results in a pus-filled abscess; usually, it is Staph. In tropical environments, MSSA immune competent Temperate - immunosuppressed, e.g: β-haemolytic Strep., entercoccus In contaminated wounds, consider Clostridial infection
58
What is tetanus?
Caused by Clostridium tetani (gram +ve rods and strictly anaerobic); spores at the ends of the rods make it look tennis-racket shaped and this organism found in soil, gardens, etc
59
Consequences of tetanus infection?
Produces a neurotoxin that causes spastic paralysis (binds to inhibitory neurones and presents release of neurotransmitters), i.e; it leads to LOCK JAW (risus sardonicus) These organisms are non-invasive and the illness is TOXIN RELATED
60
Incubation period of tetatnus?
4 days to several weeks
61
Treatment of tetanus?
Surgical debridement Anti-toxin Supportive treatment (must be in ICU as any trigger can cause muscle spasm; also, resp arrest can occur) Antibiotics (penicillin/metronidazole) Booster vaccination
62
Prevention of tetanus?
Route vaccination with a toxoid vaccine (2,3,4 months old)
63
2 situations where anti-microbials are administered before culture?
Sepsis syndrome Soft tissue infection

Year 2 Microbiology (7 decks)

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