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However, other bacteria are extremely virulent pathogens with the ability to cause infectious diseases, including cholera (Vibrio cholerae), tuberculosis (Mycobacterium tuberculosis), tularemia (Francisella tularensis), leprosy (Mycobacterium leprae) and syphilis (Treponema pallidum).
NB have been described as potential pathogens with the ability to initiate extraskeletal calcification in vivo, and recent reports have flagged alarm concerning their widespread presence, filterability, self-replication, and blood-borne infectivity [see for example refs. 4], [7], [and 49].
Several infectious diseases, including tuberculosis, are caused by pathogens with the ability to survive in low metabolic activity states, which extends and complicates therapeutic drug regimens.
Fibronectin is a ligand for at least a dozen members of the β1 integrin family, where α5 β1 is the major integrin involved in indirect recognition of bacterial pathogens with the ability to bind to fibronectin [ 6, 8].
In S. aureus, L. monocytogens, or B. subtilis, it has been shown that increased intracellular c-di-AMP endowed these pathogens with the ability to resist β-lactam antibiotics whereas decreased intracellular c-di-AMP concentrations made the bacteria susceptible to antibiotics that target bacterial cell wall synthesis.
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In fact, E. durans has been hypothesized to act as a primary enteric pathogen with the ability to clear the way for other pathogens [ 23].
Influenza virus is a prime example of a pathogen with the ability to infect not only its avian reservoirs but also mammalian species such as swine, horses, dogs, cats, ferrets, whales, and humans.
The Mycobacterium avium complex comprises a group of environmental and opportunistic intracellular pathogens [ 1] with the ability to persist within macrophages and escaping the host's killing mechanisms [ 2].
Although mucosal immunity will account for some instances of asymptomatic carriage of particular pathogens, the presence of mucosal antibodies may also interfere with the ability to detect pathogens when using EIA.
The gradual accumulation of slightly deleterious mutations, slowly degrading the genome over time, may make the endosymbiont unable to compete with relatively benign pathogens that have the ability to participate in the mutualism.
These include regulation of intestinal microbial homeostasis, maintenance of the gastrointestinal barrier function, interference with the ability of pathogens to colonize [16], [17], [18], [19], [20], [21], [22] and finally modulation of local and systemic immune responses [23].
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