The two main components of the disc—nucleus pulposus and annulus fibrosus—are confined in the intervertebral space by the end-plate cartilage, a hyaline structure adherent to the vertebral metaphysis, and by the anterior and posterior longitudinal ligaments. With aging all these entities undergo multiple structural changes. At birth the disc is well vascularized and contains 80–90% water. The collagen and elastin fibers are organized in very complex networks. Proteoglycans are responsible for maintaining the osmotic pressure and disc hydration, which further allows the disc to maintain height when loaded. With time the fibers become less organized and lose their strength. Proteoglycans are degraded and subsequently the osmotic pressure and water content decrease [10].

At birth, branches of the segmental arteries penetrate the annulus and provide blood supply to the entire disc. Progressively the intradiscal vascular bed contracts. In the third decade of life, the disc becomes almost avascular, maintaining only limited blood supply to the outer margin of the annulus fibrosus. The adult disc receives nutrients by diffusion through the cartilaginous end plates and from its own poor peripheral vasculature. The innervation also regresses to the disc periphery. Nociceptive and mechanosensitive fibers accompanying the blood vessels or branching from the sinuvertebral nerves are found only in the outer third of the adult annulus. Cartilaginous end plates become more frail, prone to fissures, allowing disc material to herniate into adjacent vertebrae to form Schmorl’s nodes.

The disc starts to lose height and becomes more susceptible to degenerative, traumatic, and infectious processes.

In adults, the infection of the intervertebral disc is most frequently the result of hematogenous spread, from a distant source (genitourinary, endocardial, respiratory, gastrointestinal, cutaneous ulcers, etc.). Infected emboli reach the well-vascularized vertebral metaphysis via arterial or retrograde venous (Batson’s veins) blood flow, subsequently producing bone infarction, destruction, and osteomyelitis. From the subchondral area, the infection diffuses then into the intervertebral disc space to the avascular nucleus pulposus.

Direct hematogenous colonization of the disc occurs mostly in children, as their discs are still vascularized. Infection is often limited to the disc space [11]. The rich vascular supply allows good antibiotic penetration. Overall, in these very young patients, discitis has a better prognosis [12]. Less frequently, discitis is caused by direct iatrogenic or traumatic disc contamination. Spine surgery and intradiscal procedures are the most common iatrogenic causes of discitis. The incidence of post-discography infection varies from 1 to 4% [13].

Because discitis can be either preceded or complicated by vertebral osteomyelitis, the two conditions are frequently described as spondylodiscitis [14]. Most disc infections are bacterial, but mycobacterial and fungal etiology should be considered in specific circumstances.

Staphylococcus aureus, Staphylococcus epidermidis, and gram-negative Escherichia coli are some of the pathogens commonly isolated in the spinal infections involving the disc. Many predisposing comorbidities have been described, among them diabetes, immunocompromised states, malignancies, intravenous drug use, chronic alcoholism, previous spine surgery, infective endocarditis, etc.