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

MSK Infections and Anti-Microbial Therapy Flashcards

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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
Q

Pathogens in Gaucher’s osteomyelitis?

A

If there is bone crisis, sterile

If infected, Staph. aureus

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26
Q

Importance of SAPHO and CRMO?

A

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
Q

Signs of SAPHO and CRMO?

A

Fever, weight loss and generalised malaise; there is a history of exacerbations/remissions

Raised inflammatory markers

Lytic lesions on X-ray

28
Q

Sites inv. with SAPHO/CRMO?

A

Chest wall (majority), pelvis, spine, lower limb

The osteitis is multi-focal with various, off sites being affected

29
Q

Describe vertebral osteomyelitis

A

Mostly a haematogeneous infection that causes spondylodiscitis and disc space infection

It may be assoc. with epidural abscess or psoas abscess

30
Q

Pathogens in vertebral osteomyelitis?

A

Staph. aureus (most important one)

Gram -ve aerobic bacilli

Strep.

Mycobacterium TB

31
Q

In who/what situation does vertebral osteomyelitis occur?

A

PWIDs

IV site infection and GU ifnection

SSTI (Skin and Soft Tissue Infections)

Post-operative

32
Q

Presentation of vertebral osteomyelitis?

A

Most people have insidious pain and tenderness; half have a fever

Sometimes, there are neuological signs

33
Q

Ix for vertebral osteomyelitis?

A

Raised inflammatory markers

Raised WCC (sometimes)

Abnormal plain film

MRI (BEST Ix), Ga-67 scan

34
Q

Treatment of vertebral osteomyelitis?

A

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
Q

Only situations where the MRI is repeated?

A

Unexplained increase in inflammatory markers

Increasing pain

New anatomically related signs/symptoms

36
Q

Describe vertebral TB

A

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
Q

Dissemination of TB tests?

A

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
Q

Risk factors for prosthetic joint infection?

A

RA, diabetes, malnutrition, obesity

39
Q

Mechanism of prosthetic joint infection?

A

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
Q

Different time frames of prosthetic joint infections?

A

Early (within one month) with a haematoma/wound sepsis

Late (after one month) with a contamination at the time of operation

41
Q

Infection with PVL Staph. aureus?

A

Panton Valentine Leukocidin Toxin; present in both MSSA and MRSA

42
Q

Presentation of PVL producing Staph. aureus infection?

A
  1. Skin infections
  2. Necrotising pneumonia
  3. Invasive infections, e.g: bacteraemia, septic arthritis

These patient are disproportionately unwell

43
Q

Treatment of PVL producing Staph. aureus infection?

A

Flucloxacillin + anti-toxin antibiotic (e.g: clindamycin or linezolid)

44
Q

Side effects of clindamycin and linezolid use?

A

Clindamycin - C. diff infection assoc.

Linezolid - must limit use to 4 weeks other there is a risk of bone marrow failure

45
Q

Describe planktonic vs sessile bacteria

A

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
Q

Ix for prosthetic joint infection?

A

CRP and inflammatory markers

Blood culture

Multiple peri-operative tissue samples; if they all grow the same organism, it is pathogenic

Radiology

47
Q

Treatment of prosthetic joint infections?

A

Removal of prosthesis and cement; therapy for at least 6 weeks

Re-implant the joint after aggressive antibiotic therapy

48
Q

Pathogens in prosthetic joint infection?

A

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
Q

Treatment of Staph. epidermidis prosthetic joint infection?

A

Initially, vancomycin

50
Q

4 ways in which septic arthritis can spread?

A
  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
Q

What is septic arthritis?

A

Inflammation of the joint space (normally sterile) caused by infection

52
Q

Bacterial causes of septic arthritis?

A

Staph. aureus (most important)

Strep. and coag -ve Staph. (prosthetic joints)

Neisseria gonorrheae (in sexually active patients)

H. influenzae (uncommon now)

53
Q

Presentation of septic arthritis?

A

Severe pain with a red, hot and pus-swollen joint

Limited movement

54
Q

Ix for septic arthritis?

A

Microscopy of joint fluid

If pyrexial, do a blood culture

Exclude crystals (gout and pseudogout)

55
Q

Treatment of septic arthritis?

A

FLUCLOXACILLIN (high dose to cover all Staph. aureus)

If < 5 years, add Ceftriaxone (to cover H. influenzae)

Adjust once organisms are confirmed

56
Q

Describe knee bursitis

A

Most are not infective but, if they are, give antibiotics (flucloxacillin)

57
Q

What is pyomyositis?

A

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
Q

What is tetanus?

A

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
Q

Consequences of tetanus infection?

A

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
Q

Incubation period of tetatnus?

A

4 days to several weeks

61
Q

Treatment of tetanus?

A

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
Q

Prevention of tetanus?

A

Route vaccination with a toxoid vaccine (2,3,4 months old)

63
Q

2 situations where anti-microbials are administered before culture?

A

Sepsis syndrome

Soft tissue infection

Year 2 Microbiology (7 decks)

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