Educational Workshops 2013 Bone and Joint Infections A Sore Back Dr George Jacob Dr Michael Millar Dr Jayshree Dave

History 4 year old Bangladeshi child was admitted with a 2/52 h/o Increasing lower back pain Difficulty in walking and weight bearing There was no history of fever, bowel or bladder disturbances and she was otherwise systemically well

Examination Afebrile Tenderness over lower back No other focal neurology No hip, knee or ankle joint abnormality

Investigations Routine bloods WCC 9.7 Neutrophils 4.9 CRP 6 ESR 70 Lumbar spine X- ray- Abnormal reduction of the intervertebral disc space between L3-L4 suggestive of lumbar discitis

What would you advise? Discussion -Aetiology -Investigations -Treatment

Management Empirical antibiotic therapy commenced with IV benzylpenicillin and flucloxacillin after blood cultures Screening for TB BCG scar present. CXR, Mantoux & T-spot NAD MRI spine- Abnormal inflammatory signal demonstrated in the L3-L4 disc consistent with infective discitis

Discussion What would you advise? -Management

Management CT guided biopsy performed. Samples were sent for MC&S, TB smear & cultures Microscopy of 13mls of blood stained fluid WCC 90 RBC 1800 Differential- 90% Neutrophils 10% degenerates Gram stain- Scanty gram negative rods (GNRs)

Discussion What would you advise? -Aetiology -Management

Management IV benzylpenicillin and flucloxacillin stopped. Commenced on empirical IV ceftriaxone pending cultures GNRs Ided as Kingella Kingae. Sensitive to amoxicillin, co-amoxiclav, cefuroxime, ceftriaxone, ceftazidime, gentamicin, amikacin and ciprofloxacin. Resistant to trimethoprim Smear and culture negative for TB

Discussion What would you advise? -Management

Management IV ceftriaxone continued. Screened for infective endocarditis (IE) with transthoracic echocardiogram (TTE) - NAD for IE Switched to PO ciprofloxacin after 3/52 of IVs as per clinical response and resolving inflammatory markers Completed a total of 8/52 of Rx with full recovery & resolution of clinical symptoms & signs. Repeat ESR 5 & CRP <5. Follow up MRI spine awaited.

Discussion Kingella kingae Microbiology Increasingly recognised as a common aetiology for paediatric osteoarticular infections in children younger than 4 years of age1,2 Facultative anaerobic, β-haemolytic, gram negative organism that appears as pairs or short chains with tapered ends3 Grows on routine sheep blood & chocolate agar3. Fails to grow on MacConkey agar3. Oxidase positive, urease & indole negative and produces acid from glucose & maltose3

Discussion Kingella kingae Pathogenesis Upper airway colonisation precedes the development of invasive disease4 Colonisation rate increases between the ages of 12 to 24 months and then gradually declines in older children suggesting an age related immune response that eradicates pharyngeal carriage in older children5,6 Day care centre attendance increases the risk for colonisation and transmission of K.kingae infections7-9

Discussion Kingella kingae Pathogenesis Pili facilitate adherence to respiratory epithelial cells aiding colonisation of the upper airways10,11 Concomitant viral infections and extracellular toxin production may cause disruptions in the respiratory epithelium and facilitate entry into the blood stream1,12,13 Extra-cellular polysaccharide capsule formation which hinders killing by opsonophagocytosis might be one of the defence mechanisms ensuring intravascular survival and dissemination to bone, joints & heart12

Discussion Kingella kingae Infections Children with invasive K. kingae infection may be febrile or afebrile13-15. Constitutional symptoms are commonly absent except in cases of infective endocarditis13-15. ESR & CRP rise may be mild, moderate or absent13-15 They commonly cause osteoarticular infections (OAIs), bacteraemias, endocarditis & respiratory tract infections in children12,15 Septic arthritis commonly involves large joints like knee, hip, ankle or shoulder12,15

Discussion Kingella kingae Infections Osteomyelitis commonly affects long bones, sternum, clavicle, calcaneum and talus12,15 25% of all haematogenous spondylodiscitis is caused by K.kingae in children under 4 years. It commonly affects the lumbar discs16-19. Patients commonly present with low back pain, limping, refusal to sit or walk and neurological symptoms/signs12 Routine echocardiographic evaluation of children from whom the organism has been isolated from a sterile site is recommended by some authors20

Discussion Kingella kingae Diagnosis K.Kingae can be cultured on sheep blood agar and chocolate agar3 The yield of cultures can be improved by inoculating clinical samples into aerobic blood culture vials and sub culturing the positive blood culture vials onto agar plates13 They are readily identified by commercial systems such as API NH or VITECK 2 (bioMѐrieux, France)12 16SPCR substantially improves detection in culture negative cases12

Discussion Kingella kingae Treatment Usually susceptible to penicillins, cephalosporins, aminoglycosides, fluroquinolones, macrolides, tetracyclines, trimethoprim-sulfamethoxazole and chloramphenicol12,21-23 Always resistant to trimethoprim and glycopeptides13,23. 40% of isolates are resistant to clindamycin23 Β-lactamase production reported in rare cases21-23

Discussion Kingella kingae Treatment Most patients with OAIs respond well to conservative treament with antibiotics without the need for invasive surgical procedures11 Antibiotic therapy is required for 2-3 weeks for septic arthritis, 3-6 weeks for osteomyelitis and 3-12 weeks for spondylodiscitis11 IV to PO switch of antibiotics is based on clinical response and resolving inflammatory markers12

Discussion Kingella kingae Treatment Post exposure prophylaxis for eradication of pharyngeal carriage can be considered in contacts aged 6 to 48 months when clusters of disease are detected in day care centre settings12 Rifampicin 20mg/kg twice daily for 2 days or in combination with amoxycillin 80mg/kg per day for 2 days-4 days is recommended for post exposure prophylaxis of contacts22-24