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Lumbar spondylodiscitis secondary to Enterobacter cloacae septicaemia after extracorporeal shock wave lithotripsy
  2. S SAHIN,
  1. S FELEK
  1. Department of Physical Medicine and Rehabilitation
  2. School of Medicine
  3. Firat University, Elazig, Turkey
  4. Department of Clinical Microbiology and Infectious Diseases
  5. Firat University
  1. Dr A Kamanli, Firat Universitesi Firat Tip Merkezi, 23119 Elazig, Turkey akamanli{at}

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Infections of the lumbar spine may affect either the intervertebral disc or the vertebral body. Most infections of the intervertebral disc occur as an extension of vertebral osteomyelitis or direct inoculations during diagnostic or surgical procedures, or include urinary tract infections and septicaemia. This paper reports a case of L5-S1 spondylodiscitis secondary toEnterobacter cloacae septicaemia after extracorporeal shock wave lithotripsy (ESWL).

A 52 year old man presented with side pain, pollakiuria, haematuria, and nocturia. He had been treated with ciprofloxacin for acute pyelonephritis and nephrolithiasis as an outpatient. One week later, the patient was admitted to hospital by the urology department with symptoms of left side pain, fever, chills, shaking, and dysuria. Right renal and right ureter distal lithiasis and right hydronephrosis due to the lithiasis were diagnosed. One week after ESWL the patient was sent to the physical medicine and rehabilitation clinic with chills, shaking, high fever, and low back pain complaints. Lumbar movements were found to be restricted. There was an increase in severe pain at rest. The patient could not stand or walk. No neurological deficit was present. Body temperature was 39°C, pulse 110 beats/min, blood pressure 130/70 mm Hg, breathing 20 breaths/min.

Laboratory findings were as follows: haemoglobin 133 g/l, packed cell volume 0.31, white blood cells 18×109/l, platelets 316×109/l, erythrocyte sedimentation rate 110 mm/1st h, antistreptolysin O 25 IU, C reactive protein 12.3 mg/l, rheumatoid factor negative. Urea was 14 mmol/l of urea, creatinine 170 μmol/l. Glucose and electrolytes were normal and serum aspartate aminotransferase was 80 U/l, serum alanine aminotransferase 44 U/l, lactate dehydrogenase 321 U/l, total bilirubin 22 μmol/l, direct bilirubin 10 μmol/l. A considerable number of leucocytes and erythrocytes were noticed in urine microscopy.Enterobacter cloacae was isolated from blood and urine. The isolated pathogen was sensitive to ceftriaxone and amikacin. Figure 1shows magnetic resonance imaging (MRI) pictures obtained two weeks after the septicaemia.

Figure 1

(A, B) Magnetic resonance imaging findings, obtained two weeks after Enterobacter cloacae septicaemia are as follows: inflammation in the L5-S1 intervertebral disc and adjacent vertebral corpuses, decreased height of intervertebral disc, and destruction of adjacent vertebral corpus end plates. The signal intensity of the intervertebral disc and adjacent vertebral corpuses is oedematous. Inflammatory soft tissue component, extending to perivertebral region and spinal epidural space causing neuronal compression or irritation, or both. (C) Contrast enhanced mid-sagittal slice shows enhancement in the L5-S1 intervertebral disc, adjacent vertebral corpus medullary bone, and inflammatory soft tissue component.

Amikacin (1500 mg/day) and indometacin (150 mg/day) were given, but amikacin was stopped because nephrotoxicity developed after seven days of treatment. Later, ceftriaxone 2 g twice a day was given for one week, and then maintained at 1 g/day for three months. The patient used a lumbosacral support.

The clinical and laboratory findings of the patient improved and pain was relieved after a two month rehabilitation programme. The control MRI findings obtained 27 months later shown degeneration of the L5-S1 intervertebral disc and adjacent vertebral corpus end plates. Grade 1 spondylolisthesis is the sequel to the infection. Lumbar spondylodiscitis has not recurred after two years' follow up.

Staphylococcus aureus is reported as the major agent of spondylodiscitis. Streptococcus viridans, Streptococcus pyogenes, Salmonellaspp, Enterococcusspp, Pseudomonas aeruginosa, andBrucella spp are other possible causative agents. In most cases, isolation of an agent is difficult. In a limited number of cases an agent may be isolated in biopsy materials or in blood.1

We found two reported cases of spondylodiscitis caused byEnterobacter cloacae.2 ,3Generally, S aureus is the causative agent.4 However, Salmonella enteritidis, 5 Candida albicans, 6 Streptococcusspp,7 and Enterococcusspp8 are rare isolated pathogens. In our case, acute pyelonephritis was diagnosed before spondylodiscitis. Furthermore, worsening of the symptoms after ESWL seems important. Haematoma, contusion, petechial haemorrhagic focuses in the liver are reported as side effects of ESWL.9 Whether the spine infection was present before lithotripsy is not clear to us. There was insufficient time between the lithotripsy and diagnosis of the spine infection. Thus we think that the infection was present before the lithotripsy. ESWL may cause the spread of vertebral osteomyelitis or acceleration of sepsis. Because the case seems to originate through the haematogenous route, it may be more appropriate to state that it represents an extension of vertebral osteomyelitis.

Spinal infections should always be considered in severe back and lumbar pain.1 ,10 The patients should be monitored in a clinical and laboratory setting after invasive therapeutic procedures. Prophylactic antibiotic treatment should be given in an ESWL procedure.