In addition, local administration of
corticosteroids, can also be a risk factor for bone
and joint infection, particularly when performed
in primary care and on patients with rheumatoid
arthritis. 3 However, the overall incidence of this
is low. 4
Taking both of these factors into consideration,
a thorough history and examination of new joint
swelling, joint or back pain and fever, in the case
of septic arthritis, and new back pain and fever
in the setting of vertebral osteomyelitis (VOM)
and a high index of suspicion on the part of the
clinician, is required to appropriately investigate
and manage the patient.
Investigation
Obtaining a microbiological diagnosis is the
cornerstone of investigation of bone and joint
infection.
Microbiological diagnosis
The main pathogens causing septic arthritis and
osteomyelitis are bacterial, with Staphylococcus
aureus infections in around three quarters of
patients being the most prevalent. Pathogens
and their risk factors are listed below.
For pyogenic bone and joint infections,
appropriate samples to take include fluid aspirate
for microscopy, Gram stain and culture, as well as
blood cultures. It is important to highlight that
Gram stain is positive in only 50% of patients, so
for those with a high clinical index of suspicion,
antimicrobials should be initiated/continued even
with a negative Gram stain result until culture
results are available. Intraoperatively, fluid
samples in septic arthritis or tissue samples
in VOM should also be sent to guide future
antimicrobial therapy.
In the setting of culture negative bacterial
bone and joint infection, 16sPCR can be used
to amplify and identify any bacterial DNA on
a sample. 5 It is important to understand the
limitations of molecular diagnostic tests – for
example, a positive sample may still be a
contaminant, and there are no commercially
available techniques at present to predict
sensitivity patterns even if a pathogen is isolated.
However, PCR may still be useful if an organism
is difficult to culture or if antimicrobials were
started before culture was taken.
If tuberculosis is suspected, samples should be
sent for Mycobacterial culture, and consideration of
PCR for MTB complex (where available). A careful
history and Imaging should be performed to elicit
any evidence of disseminated tuberculosis. In
patients with with suspected Lyme arthritis (that
is, risk factors such as a tick bite from an endemic
area), investigations should include Lyme
serology on serum. Fluid aspirate samples can
also be sent for PCR if locally available to aid
detection of Borrelia burgdorferi.
Fungal infection is a rare cause of septic
arthritis. If fungal infection is suspected, usually
in the setting of a highly immunosuppressed
patient or intravenous drug user, fluid should be
sent for fungal culture. If this culture is negative
– further tests could include 18sPCR, panfungal,
and fungal markers such as galactamman and
beta glucan in blood may be useful. In the setting
of appropriate travel history to North and South
America, serology for the diamorphic fungi, for
example, Histioplasma, Coccoides and Paracoccoides,
can also be useful.
Biomarkers
C-reactive protein (CRP) has been the mainstay
for detecting and monitoring inflammation and
infection for many years. However, there are
well described controversies with differentiating
between the inflammation of rheumatological
conditions and that of infection. There may also
TABLE 1
Pathogens and related at-risk groups
Pathogen
Staphylococcus aureus
(including MRSA)
At-risk group
No comorbidities; direct trauma/inoculation/IVDU;
damaged joint; prosthetic joint
Streptococcus sp
No comorbidities, direct trauma (group A); splenic
dysfunction (particularly for Streptococcus
pneumoniae)
Neisseria gonorrhoea
As per sexually transmitted Infections
Gut/urinary tract infections, particularly lumbar spine
Enterobactericea/
Pseudomonas
vertebral osteomyelitis
Immunosuppression with Pseudomonas
Salmonella sp
Haemaglobinopathies, paediatric population
Haemophilus influenzae Unvaccinated for serogroup B
Kingella kingae
Paediatric population
Immunosuppressed, urinary tract manipulation
Mycoplasma hominis
Zoonosis from contact with farm animals or drinking
Brucella sp
unpasteurised milk in endemic areas, for example,
Mediterranean, India, Middle East, Latin America
Travel or residence in an epidemic area, recent
Mycobacterium
tuberculosis immunosuppression
Immunosuppression
Non-tuberculous
Mycobacterium
Borrelia burgdorferi
Tick bite from endemic area
Fungal sp
Candida sp immunosuppression or intravenous drug
users, long line use; Coccoides/histoplasmosis-
endemic areas in the Americas
TABLE 2
Immunosuppressive /antimicrobial drug
interactions
Immunosuppressant Antimicrobial
Interaction
Methotrexate
Penicillins
Increased risk of bone
Ciprofloxacin
marrow toxicity
Sulphamethoxazole
Doxycycline
Trimethoprim
Corticosteroid
Macrolides
Action of corticosteroids
possibly inhibited
Isoniazid
Metabolism of
corticosteroids
accelerated
Hydroxychloroquine
Moxifloxacin
Increased risk of
ventricular arrhythmias
Azathioprine
Sulfamethoxazole
Increased risk of
Trimethoprim
haematological toxicity
Leflunomide
Rifampacin
Plasma concentration of
active metabolite
possibly increased by
rifampacin
Fluconazole and
Side effects of
Cyclophosphamide
itraconazole cyclophosphamide
possibly increased
18
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