There 2011). M bovis is an intracellular pathogen, which

There are two common
pathways for infection with M.bovis.
The primary route of infection for M.
bovis is inhalation, which allows bacteria to infect cattle at the mucous
membranes of the lower respiratory tract or in the alveolar spaces of the lungs (Domingo et al. 2014). Ingestion of the M. bovis from contaminated sources is
another way that cattle can become infected (Domingo et al.
2014). This infection stimulates both the
innate and adaptive immune responses (Widdison et al.
2009). The innate immune response is the first to respond and is
non-specific for the invading organism (Domingo et al.
2014). During the innate immune response
Toll-like receptors assist macrophages in recognizing the M. bovis as foreign and phagocytize it (Krutzik and Modlin 2004; Widdison et al. 2009). Neutrophils contain granules that release enzymes to help
kill pathogens and they also release substances that produce fibers in the
surrounding tissues that help to encapsulate the bacteria (Widdison et al. 2008). This allows for granulomas to grow at the infection site
(Krutzik and Modlin 2004). At the same time the mycobacteria are capable of producing
components that can inhibit maturation of the host immune response (Krutzik and Modlin 2004; Widdison et al. 2008, 2011). M bovis is an
intracellular pathogen, which means that it is capable of growing inside
macrophages helping it to avoid being killed by the immune system (Domingo et al.
2014). When this happens the surviving M. bovis can travel through the lymphatic system to lymph nodes and
establish a secondary infection site usually in the retropharyngeal or
mesenteric lymph nodes (Domingo et al.

In the adaptive immune response cytokins and chemokins are released
by dendritic cells, which are important to help initiate the T-helper type-1
(Th1) and cytotoxic T-cell response (a cell-mediated response) (Widdison et al. 2009, 2011). This release of cytokins and chemokins help to stimulate
other immune cells to the site of infection and activate the T-cells (Widdison et al. 2009). Animals maintaining a Th1 response tend to have more
controlled disease (Pollock et al. 2005) while those shifting into Th2 response develop more severe
disease that spreads throughout the body (Widdison et al. 2009).

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Encapsulated bacteria can persist in the cattle without any
clinical signs of the disease (Pollock and Neill 2002). Stresses on cattle such crowded
conditions (in barns and/ or transportation to slaughter house), extreme
temperatures, or exposure to poor quality air can impact a cow’s immune system (Grandin 1997). When cattle are stressed those infected with M. bovis, that are not showing any
clinical signs, can experience with a progressive development of lesions or
tubercles. Lesions or tubercles are commonly found in the lungs and lymph
nodes, but they can also be found in other organs (Ayele et al. 2004). Animals that have more infectious lesions will
shed more bacteria into the environment which results in a higher chance of
spreading disease among the herd (Castillo-Velázquez et al. 2013). If left untreated, bTB causes a general state of
unwellness and eventual death in cattle.

Not all bovines are equally susceptible
to bTB. Studies have identified presence of certain genes such as tumor
necrosis factor ? (TNF-?) and toll-like receptors (TLR1) to be associated with
susceptibility to bTB in Holstein cattle (Cheng et al. 2016). TNF- ? plays an important role in the immune response
to M. bovis (Cheng et al. 2016). It stimulates inflammation and helps to regulate
other cytokines necessary to fight off infection (Cheng et al. 2016). TLR1 helps
the immune system recognize mycobacteria allowing macrophages to engulf the
bacteria during the innate immune response (Cheng et al. 2016). They also help to control the production of
cytokines required to stimulate the adaptive immune system (Cheng et al. 2016). In Holstein cattle, mutations of these two genes
have shown to disrupt normal TNF- ? and TLR1
function, leading to poor recognition f mycobacteria and poor immune response (Falfán-Valencia et
al. 2015; Cheng et al. 2016).

One study evaluated naturally resistant
or susceptible animals by determining macrophage phagocytic activity,
intracellular bacterial survival, and cytokine gene expressions against M. bovis (Castillo-Velázquez
et al. 2013). This study examined the susceptibility of cattle
to M.bovis based on the cattle’s macrophage
capacity (Castillo-Velázquez
et al. 2013). Macrophages in cattle
considered ‘susceptible’ allow on average 125% intracellular growth of M. bovis compared to about 60% growth in
‘resistant’ cattle (Castillo-Velázquez et al. 2013). Resistant animals showed the highest
phagocytosis index, microbial control, pro-inflammatory markers, and
anti-inflammatory markers (Castillo-Velázquez
et al. 2013). Transmission of bTB in a herd
can be highly variable due to many conditions affecting bacterium and
resistance or susceptibility of the host (Pollock and Neill 2002). For example, the bacteria thrive and survive for longer
periods in warm, humid, low light conditions (Castillo-Velázquez et al. 2013). In future
breeding, looking at the benefits of breeding animals that are more resistant
to disease, especially if it doesn’t affect genetic progress or productivity of
the animal could be beneficial.