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Evidence, Challenges, and Knowledge Gaps Regarding Latent Tuberculosis in Animals

Mycobacterium bovis and other Mycobacterium tuberculosis complex (MTBC) pathogens that cause domestic animal and wildlife tuberculosis have received considerably less attention than M. tuberculosis, the primary cause of human tuberculosis (TB). Human TB studies have shown that different stages of in...

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Detalles Bibliográficos
Autores principales: Ncube, Pamela, Bagheri, Bahareh, Goosen, Wynand Johan, Miller, Michele Ann, Sampson, Samantha Leigh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9503773/
https://www.ncbi.nlm.nih.gov/pubmed/36144447
http://dx.doi.org/10.3390/microorganisms10091845
Descripción
Sumario:Mycobacterium bovis and other Mycobacterium tuberculosis complex (MTBC) pathogens that cause domestic animal and wildlife tuberculosis have received considerably less attention than M. tuberculosis, the primary cause of human tuberculosis (TB). Human TB studies have shown that different stages of infection can exist, driven by host–pathogen interactions. This results in the emergence of heterogeneous subpopulations of mycobacteria in different phenotypic states, which range from actively replicating (AR) cells to viable but slowly or non-replicating (VBNR), viable but non-culturable (VBNC), and dormant mycobacteria. The VBNR, VBNC, and dormant subpopulations are believed to underlie latent tuberculosis (LTB) in humans; however, it is unclear if a similar phenomenon could be happening in animals. This review discusses the evidence, challenges, and knowledge gaps regarding LTB in animals, and possible host–pathogen differences in the MTBC strains M. tuberculosis and M. bovis during infection. We further consider models that might be adapted from human TB research to investigate how the different phenotypic states of bacteria could influence TB stages in animals. In addition, we explore potential host biomarkers and mycobacterial changes in the DosR regulon, transcriptional sigma factors, and resuscitation-promoting factors that may influence the development of LTB.