**4.2 Salmonellosis**

*Salmonella typhimurium* is a facultative intracellular bacterium that resides within modified phagosomes in macrophage promotes replication and escape from killing by ROS [108]. *S. typhimurium* infects a wide range of hosts, including animals, humans, and poultry. *S. typhimurium* causes acute gastroenteritis in humans and typhoid-like disease in mice. If left untreated, 100% fatal [50]. *Salmonella* infects the epithelial wall of the intestine and escapes from the innate immunity and ROS activity of the host. The SOD of *S. typhimurium* protects the bacterium from excessive ROS activity produced outside or inside of the host cell [109, 110]. Thus, SOD was considered a critical factor for bacterial survival by neutralizing the ROS activity [111]. The sod-A gene inactivation in *Salmonella* species is connected with limited protection from ROS and decreased virulence during mice infection [26, 109]. sod-A-deficient bacterium displayed a slightly lower growth rate compared to the wild-type strain. The loss of the sod-A gene in mutant bacteria harms the ability to infect the host cell. Consequently, the sod-A mutant bacterium is highly susceptible to the bactericidal action of host cells and has also shown attenuated virulence properties. More specifically, SOD-A plays a vital role in biofilm formation, increased resistance against oxidative stress, and overcome from bactericidal complement system of serum [51]. *Salmonella* combats phagocytic free radicals by producing the periplasmic superoxide dismutase. Periplasmic Cu, Zn-cofactor superoxide dismutase (SOD-C) protects *S. typhimurium* from extracellular phagocyte-derived oxidative damage by host cells. *Salmonella* deficient sod-C gene has shown abated survival inside the macrophage, increased ROS susceptibility, and attenuated virulence factor during in-vivo infection. Conclusively, SOD protects periplasmic or inner membrane targets by controlling the phagocytosisdependent oxidative burst or inducible nitric oxide synthase activities during in vivo infection [49]. The evolutionary acquisition of the sod-C gene in *Salmonella* species extends an increased virulence trait of bacterium [52].

However, cytosolic Mn-SOD enzyme is essential for detoxifying intracellular superoxide radicals but not involved virulence [112]. SOD of *Streptococcus suis* resistant to anti-oxidative stress and ROS-generating herbicides, which is known to cause a severe damage to DNA, RNA, and proteins molecules that might contribute to its virulence in mice [53].
