Youngstock diseases — an immunological perspective

Current understanding of the development of the immune system in neonatal calves emphasises the importance of reducing stress and avoiding inappropriate antibiotic use.

At birth, calves are reliant on protection via passive immunity (antibodies from the mother's colostrum) and their own innate immune system (non-specific pathogen recognition), until the development of adaptive immunity (anti-bodies, T and B cells). It can take weeks for adaptive immune responses to reach protective levels. Since maternal antibodies begin to decline from day seven, there is an ‘immunity gap’ which must be covered by the innate immune system. Appropriate early life vaccinations can be used to help bridge this gap.

Innate immunity comprises physical barriers (skin and mucosa), antimicrobial peptides (e.g. lactoferrin), complement, cytokines (e.g. interferons and interleukins) and phagocytic and granulocytic cells. A key first responder is the mucosa — particularly the lining of the alimentary and respiratory tract.

The mucosal epithelial cells are the cornerstone of the mucosal response. They function to maintain tight junctions between cells, interact with commensal flora and export antimicrobial peptides and IgA/IgG.