The genus Brucella encompasses a group of Gram-negative facultative intracellular coccobacilli belonging to the family Brucellaceae, order Rhizobiales, class Alphaproteobacteria, phylum Proteobacteria. Brucella organisms are responsible for one of the most widespread bacterial zoonoses, named brucellosis. The disease affects several species of animals, including humans[1]. The sick animals are characterized by infertility, abortion, and a decline in milk production, resulting in great economic losses to the livestock husbandry industry[2].
The genus Brucella currently comprises twelve species differentiated by their tropism, pathogenicity, and host phenotypic traits[3]. The majority of human brucellosis infections are caused by two Brucella species, B. melitensis and B. abortus, which exhibit marked livestock host preferences. Brucellosis in small ruminants (sheep and goats) is primarily caused by B. melitensis, whilst in cattle the infection is mostly caused by B. abortus. However, in areas where cattle are kept in close association with sheep or goats, as is common in many mixed-livestock-keeping populations, infection in cattle may also be caused by B. melitensis, and in small ruminants by B. abortus[4]. Although some Brucella strains are highly infectious for humans, humans are an incidental host, and human-to-human transmission is extremely rare[5]. Human infection usually results from direct contact with tissues or blood from infected animals or by consumption of contaminated animal products, including unpasteurized milk and cheeses[6]. The disease caused by infection is characterized by non-specific acute symptoms, such as fever, malaise, chills, weight loss, and arthralgia. In some cases, brucellosis can evolve into chronic signs, which can affect a large number of systems and cause osteomyelitis, orchitis, and endocarditis, among other manifestations[7]. Despite surveillance and eradication programs recommended by the World Health Organization, the Food and Agricultural Organization, and the World Organization for Animal Health, the disease remains endemic in many regions of the world[8].
Brucella lacks well-known or classical virulence factors such as spores, fimbriae, cytolysins, exotoxins, secreted proteases, antigenic variation, resistance forms, phage-encoded toxins, virulence plasmids, and capsules. The virulence factors that have been reported to be necessary for invasion, the establishment of infection, as well as intracellular survival and replication of Brucella are cyclic β-1,2-glucan, VirB T4SS, pathogen-associated molecular patterns, two-component sensory and regulatory system BvrS/BvrR, and lipopolysaccharide. Other virulence factors include outer membrane proteins, BacA, SagA, BmaC, BetB, BtaE, MucR, and a genomic island associated with Brucella pathogenicity[9].
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[2] Xiong X, Li B, Zhou Z, et al. The VirB System Plays a Crucial Role in Brucella Intracellular Infection[J]. Int J Mol Sci, 2021, 22(24): 13637.
[3] Coloma-Rivero R F, Flores-Concha M, Molina R E, et al. Brucella and Its Hidden Flagellar System[J]. Microorganisms, 2021, 10(1): 83.
[4] Akoko J M, Pelle R, Lukambagire A S, et al. Molecular epidemiology of Brucella species in mixed livestock-human ecosystems in Kenya[J]. Sci Rep, 2021, 11(1): 8881.
[5] Roop R M, 2nd, Barton I S, Hopersberger D, et al. Uncovering the Hidden Credentials of Brucella Virulence[J]. Microbiol Mol Biol Rev, 2021, 85(1): e00021-19.
[6] de Figueiredo P, Ficht T A, Rice-Ficht A, et al. Pathogenesis and immunobiology of brucellosis: review of Brucella-host interactions[J]. Am J Pathol, 2015, 185(6): 1505-17.
[7] Pereira C R, Cotrim de Almeida J V F, Cardoso de Oliveira I R, et al. Occupational exposure to Brucella spp.: A systematic review and meta-analysis[J]. PLoS Negl Trop Dis, 2020, 14(5): e0008164.
[8] Garin-Bastuji B, Mick V, Le Carrou G, et al. Examination of taxonomic uncertainties surrounding Brucella abortus bv. 7 by phenotypic and molecular approaches[J]. Appl Environ Microbiol, 2014, 80(5): 1570-9.
[9] Huy T X N, Nguyen T T, Kim H, et al. Brucella Phagocytosis Mediated by Pathogen-Host Interactions and Their Intracellular Survival[J]. Microorganisms, 2022, 10(10): 2003.