Staphylococcal mastitis in dairy cows

Abstract

Bovine mastitis is one of the most common diseases of dairy cattle. Even though different infectious microorganisms and mechanical injury can cause mastitis, bacteria are the most common cause of mastitis in dairy cows. Staphylococci, streptococci, and coliforms are the most frequently diagnosed etiological agents of mastitis in dairy cows. Staphylococci that cause mastitis are broadly divided into Staphylococcus aureus and non-aureus staphylococci (NAS). NAS is mainly comprised of coagulase-negative Staphylococcus species (CNS) and some coagulase-positive and coagulase-variable staphylococci. Current staphylococcal mastitis control measures are ineffective, and dependence on antimicrobial drugs is not sustainable because of the low cure rate with antimicrobial treatment and the development of resistance. Non-antimicrobial effective and sustainable control tools are critically needed. This review describes the current status of S. aureus and NAS mastitis in dairy cows and flags areas of knowledge gaps.

Keywords: Staphylococcus aureus; antimicrobial resistance of staphylococci; bovine staphylococcal mastitis; control; dairy cow; host immune responses; non-aureus staphylococci; staphylococcal virulence factors.

Figure 1

Staphylococcus aureus Universal Virulence Regulators. AgrA: accessory gene regulator A; AIP: Autoinducing peptide (AIP); SarA: staphylococcal accessory regulator A; SaeRS: S. aureus exoprotein expression locus RS; AgrAC: accessory gene regulator AC AgrAC; Rot: repressor of toxin; SigB: the alternative sigma factor; ArlRS: the autolysis regulated locus RS., Spa: Staphylococcal protein A, psms: phenol-soluble modulins, sRNAs: Small RNA regulators, TSST-1: toxic shock syndrome toxin-1. The S. aureus global regulators consist of the agr, ArlRS, SaeRS, and the SarA homologs (SarA, Rot and MgrA). The agr system induction causes expression of toxins and enzymes.The AIP is encoded from AgrD. The AgrD is processed to AgrB by SpsB peptidase. The extracellular AIP is detected by histidine kinase AgrC. This induced phosphorylation that transfers phosphate to AgrA that induces activation and binding to the P2 and P3 promoters inducing expression of RNAII and RNAIII, respectively. The RNAII comprises agrBDCA operon that encodes AgrB, AgrD, AgrC and AgrA. RNAIII is the major effector of the agr system through inducing target genes. Activated AgrA binds to promoters of PSMs genes and induces their expression. The SaeRS induce expression of exo-proteins. The SaeS phosphorylates its associated response regulator SaeR. This cause activation of SaeR which binds to the promoter region and induce expression of different virulence factors. The sae gene consists of saeP, saeQ, saeR and saeS that are under the control of the P1 promoter. SarA: sarA is induced from P1, P2 and P3 promoters and trigger expression of exo-proteins but represses spa. The alternative sigma factor σB (SigB) induces sarA through binding to the P3 promoter and prevents agr activity. The SarR binding to all three promoters prevents expression. SarA is an inducer of the agr system, and it represses the three SarA-like proteins SarH1, SarT and Rot. Rot regulates toxins and extracellular proteases and agr activation prevents Rot translation. MgrA: Induces expression of efflux pumps and capsule but represses surface proteins. The ArlRS induced by unknown factor and then activate MgrA but represses agr and autolysis. It down-regulates surface proteins, enabling ClfA/ClfB to interact with fibrinogen.