Background: Due to antibiotic overuse, numerous organisms have evolved multidrug resistance, a global health crisis. Klebsiella pneumoniae (K. pneumoniae) causes respiratory, biliary, and urinary infections. It initially impacts individuals with impaired immune systems. Main body of The treatment of K. pneumoniae clones poses significant challenges, highlighting the need for new, more effective pathogen control methods. Our understanding of the natural or acquired antibiotic resistance mechanisms in K. pneumoniae is inadequate. Therefore, it is crucial to continue searching for novel compounds to fight against K. pneumoniae and to understand its antibiotic resistance processes fully. Short conclusion: This review covers K. pneumoniae antibiotic resistance in detail. The review also identifies the molecular components of natural or acquired K. pneumoniae antibiotic resistance mechanisms. This study further digs into the novel pharmacological targets to offer therapy insights.

The Brucella species is the causative agent of brucellosis in humans and animals. So far, brucellosis has caused considerable economic losses and serious public health threats. Furthermore, Brucella is classified as a category B bioterrorism agent. Although the mortality of brucellosis is low, the pathogens are persistent in mammalian hosts and result in chronic infection. Brucella is a facultative intracellular bacterium; hence, it has to invade different professional and non-professional phagocytes through the host phagocytosis mechanism to establish its lifecycle. The phagocytosis of Brucella into the host cells undergoes several phases including Brucella detection, formation of Brucella-containing vacuoles, and Brucella survival via intracellular growth or being killed by host-specific bactericidal activities. Different host surface receptors contribute effectively to recognize Brucella including non-opsonic receptors (toll-like receptors and scavenger receptor A) or opsonic receptors (Fc receptors and complement system receptors). Brucella lacks classical virulence factors such as exotoxin, spores, cytolysins, exoenzymes, virulence plasmid, and capsules. However, once internalized, Brucella expresses various virulence factors to avoid phagolysosome fusion, bypass harsh environments, and establish a replicative niche. This review provides general and updated information regarding Brucella phagocytosis mediated by pathogen-host interactions and their intracellular survival in host cells.

Reyes AW, et al. J Vet Sci. 2021 Feb;22(2):e18. https://doi.org/10.4142/jvs.2021.22.e18