A seventy-nine-year-old man presented to our emergency service because of
fever and chills that he had had for eight days. The history included the use
of analgesics and a steroid (20 mg/day of prednisolone) for one year for the
treatment of chronic low back pain. On arrival, the patient was febrile
(38.4°C), with a blood pressure of 150/90 mm Hg. Physical examination
revealed a cushingoid habitus (moon face, truncal obesity, and paper-thin
skin), a pulsatile abdominal mass, and low back pain limiting his spinal
flexibility. Plain radiographs of the lumbar spine showed multiple traction
spurs along the anterior edges of the vertebrae and decreased disc height at
L3-L4 without overt evidence of osseous destruction
(Fig. 1). The patient had
leukocytosis with a left shift (a white blood-cell count of
12,600/mm3 [12.6 × 109/L], with 91.9%
granulocytes), an elevated erythrocyte sedimentation rate at 97 mm/hr (normal
value, <15 mm/hr), and a high C-reactive protein level at 121 mg/dL (1210
mg/L) (normal value, <5 mg/dL). The findings on the chest radiographs were
normal, and the patient denied having a history of pulmonary tuberculosis.
Cefazolin and gentamicin were empirically administered and then were switched
to ceftriaxone when the blood culture yielded Salmonella serotype B.
Because of persistent fever and back pain, and the pulsatile abdominal mass
on palpation, aortography and abdominal computed tomography were performed.
The studies disclosed bilateral psoas muscle abscesses and a saccular mycotic
aneurysm (5 cm in diameter) with an irregular margin located in proximity to
the anterior cortex of the L4 vertebra at the infrarenal aortic level
(Fig. 2). Aneurysmectomy,
endarterectomy of the abdominal aorta, placement of a synthetic bypass graft
with omental coverage, and débridement of both psoas muscles were
carried out. A 1-cm hole was found on the bulging necrotic posterior wall of
the aneurysm in which a tiny osseous fragment was trapped; the aneurysm
protruded toward but did not reach the L4 vertebra. Although cultures of
specimens of the aneurysmal wall and psoas abscesses were negative,
histopathological analysis of the aorta revealed acute inflammation with
polymorphonuclear cell infiltration.
Postoperatively, the patient had a nosocomial pneumonia, was found to be
malnourished, and required treatment in the intensive care unit for three
weeks. During the stay in the intensive care unit, he experienced persistent
back pain and had progressive weakness develop in both lower limbs (to grade 4
of 5 motor strength). Despite the ongoing antimicrobial therapy with
ceftriaxone, a new abscess was seen in the L3-L4 intervertebral disc and
paravertebral space on magnetic resonance imaging
(Fig. 3). Because of the
long-term steroid use, poor pulmonary function, and sepsis, the patient was
managed with computed tomography-guided percutaneous catheter drainage of the
L3-L4 disc space and paravertebral abscesses. Cultures and gram-staining of
the drained pus were both negative for bacteria. The patient had lower limb
weakness (grade 3 of 5 motor strength) and cauda equina syndrome develop one
week after the draining catheter was removed. A follow-up magnetic resonance
imaging scan showed progressive destruction of the end plate, collapse of the
vertebral body, and a large epidural abscess at the L2-L4 levels
(Fig. 4). Through a left
retroperitoneal approach, drainage of the psoas abscesses, sequestrectomy of
L3 and L4, and interbody arthrodesis with use of autologous iliac bone graft
was performed. The histopathological analysis of the vertebral specimens
revealed granulomatous inflammation with caseous necrosis, and culture of
these specimens subsequently grew Mycobacterium tuberculosis.
Polymerase chain reaction was negative for Mycobacterium tuberculosis
complex, which excluded Mycobacterium tuberculosis coinfection
of the mycotic aortic aneurysm wall. Antituberculosis chemotherapy was
instituted, and a staged posterior decompression and instrumental arthrodesis
was performed two weeks later. Unfortunately, the patient had funguria and
disseminated herpes zoster. With the infections controlled, spinal stability
reestablished, and the use of an interdisciplinary rehabilitation program, the
patient had a reduction in back pain. When he was released from the hospital
three months later, he had achieved grade 4 of 5 motor strength of the lower
limbs and had well-controlled sphincter function.
The diagnosis and treatment of coexistent mycotic aortic aneurysm and
spondylitis are difficult and
challenging1-2.
Infective spondylitis may develop when any paravertebral soft-tissue
inflammation emerges, although the inflammatory abnormality is near the
neighboring aortic mycotic
aneurysm2. In our
patient, the coexisting lesion of the contiguous spine was initially
overlooked despite the fact that the irregular margin of the aneurysm
protruded toward the anterior edge of the L4 vertebra, as shown by computed
tomography although no osseous destruction was seen on the lateral radiograph
of the lumbar spine. A computed tomography or magnetic resonance imaging scan
of the spine may have been helpful, as bone or disc destruction and abscess
formation may be obscured in the early stage of
infection4.
Salmonella species are the most common pathogens in infective spondylitis
associated with adjacent
aortitis1,5.
The granulomatous inflammation in Salmonella spondylitis may be
indistinguishable histopathologically from that seen in tuberculosis,
brucellosis, or fungal osteomyelitis, and the osseous lesions due to these
infectious etiologies bear many radiographic
similarities6-8.
To our knowledge, this is the first report of a patient with Salmonella and
Mycobacterium tuberculosis, which were separately involved in aortic
and adjacent spinal lesions, respectively. The case of this patient emphasizes
that, when the clinical response to the treatment of Salmonella mycotic
aneurysm is unsatisfactory, it is important for the clinician to be alert to a
possible concurrent infection and the related complications.
Mycobacterium tuberculosis may spread hematogenously and seed any
organ and become latent if the T-cell-mediated immunity of the host is
sufficiently
competent9. When
immunity becomes attenuated because of aging or disease, the latent
Mycobacterium tuberculosis may be
reactivated10. The
CD4+ T-lymphocytes play a pivotal role in combating the invading
intracellular bacteria such as mycobacteria and
Salmonella9.
Depletion of CD4+ T-lymphocytes in a mouse model resulted in rapid
reactivation of previously dormant Mycobacterium tuberculosis,
contributing to an augmented bacterial load and exacerbating the
tuberculosis11.
Patients with advanced AIDS (acquired immunodeficiency syndrome) who have
reduced numbers of CD4+ T-lymphocytes are at high risk for
acquisition of salmonellosis and reactivation of latent Mycobacterium
tuberculosis12,13.
The large population of patients with AIDS has led to a recent resurgence of
tuberculosis, which may involve the musculoskeletal
system14. We
believe that the compromised cellular-mediated immunity resulting from the
iatrogenic Cushing
syndrome15 in our
patient contributed to the concurrent Salmonella mycotic aneurysm and the
adjacent tuberculous spondylitis. In one recent series, only 15% of 532
patients with bone and joint tuberculosis had findings on a chest radiograph
suggestive of active pulmonary
tuberculosis16.
However, concurrent bone and joint tuberculosis still could not be excluded in
patients with normal findings on a chest radiograph.
In conclusion, the present case report describes tuberculous spondylitis
and an adjacent Salmonella mycotic aneurysm in an immunocompromised patient.
We believe that, in an immunocompromised patient with a poor clinical response
to appropriate antimicrobial therapy for Salmonella aortitis and spondylitis,
the clinician should be alert to the possibility of concurrent spinal
tuberculosis. ?
Notes: The authors thank Jien-Wei Liu, MD, for his critical
review of the manuscript.