AOSpine Masters Series, Volume 10: Spinal Infections (eBook)

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Epidemiology, Microbiology, and Pathology of Spinal Infections

Abdulrazzaq Alobaid and Abdulaziz Al-Mutair

Introduction

Spinal infections are a difficult problem, manifesting either as a dreaded postoperative complication or present as diskitis and osteomyelitis in the absence of previous surgery. Its incidence varies between 1:100,000 and 1:250,000 in developed countries, and its estimated mortality rate ranges between 2% and 4%.1 The majority of spinal infections are bacterial monomicrobial with an incidence between 30% and 80%.2–4 Antibiotics are always an important aspect of successful treatment, whether or not surgery is deemed necessary. Establishing the causative organism is of great importance in guiding the selection of the antibiotic and the duration of its administration, because species-specific antibiotics are much preferred over broad-spectrum antibiotics due to optimal efficacy and decreased risk to the patient. Risk factors for spinal infections include poor nutrition, immune suppression, human immunodeficiency virus (HIV) infection, cancer, diabetes, and obesity. Spinal infections can be classified by the anatomic location involved: the vertebral column, intervertebral disk space, the spinal canal, and adjacent soft tissues.

Vertebral osteomyelitis is the most common form of vertebral infection. It can develop from bacteria that spreads to a vertebra, from direct open spinal trauma, and from infections in surrounding areas.

Intervertebral disk space infections involve the space between adjacent vertebrae. Disk space infections can be divided into three subcategories: adult hematogenous (spontaneous), childhood (diskitis), and postoperative.

Spinal canal infections include spinal epidural abscess, which is an infection that develops in the space around the dura (the tissue that surrounds the spinal cord and nerve root). Subdural abscess is far rarer and affects the potential space between the dura and arachnoid (the thin membrane of the spinal cord, between the dura mater and pia mater). Infections within the spinal cord parenchyma (primary tissue) are called intramedullary abscesses.

Adjacent soft tissue infections include cervical and thoracic paraspinal lesions and lumbar psoas muscle abscesses. Soft tissue infections generally affect younger patients and are not seen often in older people. This chapter discusses the epidemiology, microbiology (including brucellosis and tuberculosis), and pathology of spinal infections.

Epidemiology

Spinal infections are among the most troublesome and complex conditions. They may occur in 2 to 7% of patients with musculoskeletal infections.1,5,6 The incidence peaks in patients younger than 20 years of age and again in patients between 50 and 70 years of age.2,7 Furthermore, male/female ratios of 2:1 to 5:1 have been reported.8,9

Previous spine surgery, a distant infectious focus, diabetes mellitus, advanced age, intravenous drug use, HIV infection, immunosuppression, an oncological history, renal failure, rheumatologic diseases, and liver cirrhosis have been identified as the main predisposing factors.10,11

Of late, an increased incidence has been reported, possibly due to the combined effect of an increase in susceptible populations (particularly patients with a history of previous spine surgery) and improved accuracy in diagnosis.3 Postprocedural diskitis represents up to 30% of all cases of pyogenic spondylodiskitis and has been related to almost all spine surgery techniques.12,13

Microbiology

The major agents identified for spinal infections are as follows: bacteria, which cause pyogenic infections; tuberculosis and fungi, which are responsible for granulomatosis infections; less commonly, parasites. With the advances in the diagnosis and treatment of tuberculosis, the incidence of spinal tuberculosis has been reduced, especially in the last 50 years. Bacterial monomicrobial14,15 spinal infections caused by Staphylococcus aureus have an incidence of 30 to 80%.2–4 Up to 25% of spinal infections are due to gram-negative bacteria such as Escherichia coli.2 S. aureus being the most common causative organism, it accounts for about half of all cases.6 The next most common organism is Staphylococcus epidermidis. Gram-negative organisms such as E. coli and Pseudomonas aeruginosa are less common and seem to be associated with genitourinary infections and procedures as well as with intravenous drug use. Anaerobes are involved rarely. Multiple-organism infections are unusual. Organisms of low virulence, such as skin flora, sometimes are found on culture, and it may be difficult to determine whether they are contaminants or causative organisms. It should be kept in mind that these organisms can cause vertebral osteomyelitis; therefore, caution should be used when proclaiming them as contaminants.

In HIV-positive patients, Mycobacterium tuberculosis accounts for up to 60% of identified pathogens. In cases of penetrating trauma of the spine, anaerobic agents are also a cause of infections.16 In one third of cases, the infectious agent is never identified.17,18 Brucellosis and tuberculosis have a high incidence in some endemic areas, such as the Mediterranean countries and in Eastern European countries, and should be given due consideration. Turunc et al,19 in their prospective study of 75 spondylodiskitis patients, found that tuberculosis was the cause in 13 patients (17.3%), brucellosis was the cause in 32 patients (42.7%), and other bacterial agents were the cause in 30 patients (40%).

Brucellosis is a systemic disease, and many organ systems (e.g., the nervous system, the heart, the skeletal system, and the bone marrow) may become involved following hematogenous dissemination. However, osteoarticular involvement is the most common complication of brucellosis. Osteoarticular involvement has been reported in 10 to 85% of patients in most series.20 Arthritis and sacroiliitis usually reflect the acute form of brucellosis and frequently respond to the standard therapeutic regimens. In contrast, the spinal column is generally affected in the subacute and chronic forms of brucellosis.21 Moreover, spinal brucellosis usually affects elderly patients, whereas sacroiliitis and arthritis are usually reported in those in the first three decades of life. The incidence of spinal brucellosis is highly variable (2–54%) depending on the study population.20 Radiographic abnormalities generally develop 3 to 12 weeks after the onset of clinical symptoms. The spinal column can be affected at any joint, but the lumbar spine is the most commonly involved site, particularly the L4-L5 and L5-S1 junctions.20 In a review of the literature from Turkey, the authors evaluated 452 spinal brucellosis cases. However, detailed information on the anatomic location of the lesions was available for only 305 cases. Of these lesions, 7% were cervical, 14% were thoracic, 2% were thoracolumbar, 68% were lumbar, 9% were lumbosacral, and 0.3% were sacral. In the majority of patients (98%), a solitary lesion was diagnosed, whereas multiple lesions were diagnosed in only 2%.6 However, the incidence of multiple site involvement has been reported as 9 to 30%.22 Abscess formation had rarely been reported in the past, but it has become a common finding (21–42%) following the development of highly sensitive diagnostic techniques such as computed tomography (CT) and magnetic resonance imaging (MRI). The main causes of morbidity in spinal brucellosis are epidural abscess, radiculoneuritis/myelitis, and demyelinating neuropathy.20

Pathology

Bacterial infection causing vertebral osteomyelitis can arise from a number of sources. It can occur through direct inoculation, contiguous spread from a nearby infection, or hematogenous seeding. Penetrating injuries and per cutaneous or open spinal procedures (e.g., chemonucleolysis, diskography, diskectomy) performed on the intervertebral disk can account for the direct inoculation. Intra-abdominal and retroperitoneal abscesses can lead to the local spread of bacteria or fungi. As the number of spinal procedures performed increases, the local spread from direct inoculation of bacteria into the spinal canal becomes more prevalent. But the most common mechanism of spinal infection is still hematogenous seeding of infection. Skin and soft tissue infections, infected vascular access sites, and the urinary tract can be potential sources of pathogenic organisms.

The two major theories for hematogenous dissemination are the venous theory and the arteriolar theory. The venous theory was proposed by Batson,23 who demonstrated retrograde flow from the pelvic venous plexus to the perivertebral venous plexus via valveless meningorrhachidian veins, using both live animal and human cadaveric models. Wiley and Trueta24 proposed the arteriolar theory, specifically that bacteria can become lodged in the end-arteriolar capillary loops. Both mechanisms are likely significant in the establishment of an infectious focus in the spinal column. An extensive prevertebral pharyngeal venous plexus in the cervical spine also may act as a conduit for the spread of bacteria.25

There are a variety of ways in which the infection can spread locally. The infection adjacent to the end plate of one vertebral body can rupture through it into the adjoining disk and infect the next vertebral body. The bacterial enzymes can rapidly destroy the relatively avascular disk...