**1. Introduction**

Brucellosis, an infectious disease caused by the *Brucella* bacteria in both humans and animals, leads to a significant impact on the public health and the animal industry [1]. Since 1950, comprehensive measures against Brucellosis were undertaken in China and a great number of achievements had been made in its prevention and control [2]. It, however, remains a serious public health issue, and much remains to be accomplished to reach the goal of controlling human and animal Brucellosis in China. As the most common and significant osteoarticular presentation of human Brucellosis, Brucellar spondylodiscitis has a variable course with a long latency between the onset of symptoms and the radiologic changes' appearance with and unspecific clinical symptoms, hindering an early intervention to prevent irreversible neurologic deficits and spinal deformities (**Figure 1**) [4, 5]. It is an endemic disease in areas of sheep farming, which is also widespread among farmers, animal breeders, veterinarians, and veterinary technicians as an occupational disease [6, 7]. Due to the late-onset radiological findings, slow growth rate in blood cultures, and complexity of the serodiagnosis, timely and accurate diagnosis of Brucellar spondylodiscitis is still a challenge for clinicians [8, 9].

Preclinical models exhibiting symptoms comparable to those in humans are essential for the translation of preclinical findings into clinical practice [10–13]. Relevant aspects of the Brucella pathogenesis have been intensively investigated in both *in vitro* and preclinical *in vivo* models. Several preclinical models are available to mimic Brucellar spondylodiscitis and provide beneficial platforms allowing the

#### **Figure 1.**

*A typical case of noncontiguous multiple-level Brucellar spondylodiscitis with an epidural abscess in a 57 year-old man with a 6-month history of low back pain, restricted range of motion, fever, chills, and night sweating. (A) the midsagittal magnetic resonance imaging revealed increased signal intensity (arrows) involving the T2-T3, T8–9, T11–12, and L4–5 disks and vertebral bodies. (B) Pathologic signal changes were identified, compatible with a 14 × 8-mm paraspinal abscess (L5), with low signal intensity on T1-weighted images, high signal intensity on T2-weighted images, and post-contrast peripheral enhancement (arrow) [3].*

management and exploration of translational investigations of medical device and novel therapeutics [14–16].

This chapter focuses on these preclinical models of Brucellar spondylodiscitis. The requirements for preclinical models of Brucellar spondylodiscitis, pearls and pitfalls of the preclinical model establishment, and comprehensive analyses of Brucellar spondylodiscitis in animal models are also deliberated.
