Experimental model of toxin-induced subclinical mastitis and its effect on disruption of follicular function in cows

Ori Furman, Gabriel Leitner, Zvi Roth, Yaniv Lavon, Shamay Jacoby, David Wolfenson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

This study establishes an experimental model for subclinical mastitis induced by Gram-positive (G+) exosecretions of Staphylococcus aureus origin or Gram-negative (G-) endotoxin of Escherichia coli origin to examine its effects on follicular growth and steroid concentrations in Holstein dairy cows. Cows were synchronized with the Ovsynch protocol followed by a series of follicular cycles that included GnRH and PGF doses administered every 8days. Cows received small intramammary doses of either G+ (10μg, n=10) or G- (0.5μg, n=6) toxin, or saline (n=6; uninfected control) every 48hours for 20days. Follicular fluids were aspirated from preovulatory follicles before (aspiration one: control), at the end of (aspiration two: immediate effect), and 16days after the end of (aspiration three: carryover effect) toxin exposure. During the 3weeks of subclinical mastitis induced by G+ or G-, no local inflammatory signs were detected in the mammary gland and no systemic symptoms were noted: body temperatures of the treated cows did not differ from controls; plasma cortisol and haptoglobin concentrations were not elevated and did not differ among groups. Somatic cell count was higher in the treated groups than in controls, and higher in the G- versus G+ group. For analysis of reproductive responses, cows were further classified as nonaffected or affected based on an more than 20% decline in follicular androstenedione concentration in aspiration two or three relative to the first, control aspiration. Most G- (5/6) and 40% of G+ (4/10) cows were defined as affected by induced mastitis. An immediate decrease in the number of medium-size follicles was recorded on Day 4 of the induced cycle, toward the end of the 20-day mastitis induction, in the affected G+ compared with uninfected control group (1.0±0.5 vs. 3.0±0.4 follicles; P<0.05); the affected G- and nonaffected G+ subgroups exhibited a similar numerical decline in the number of follicles. A carryover (but not immediate) decrease to 51% and 62% in follicular estradiol concentrations in G- affected group and G+ affected group was detected relative to controls (P<0.05). The nonaffected G+ subgroup did not differ from its control counterparts. Based on the current experimental model, subclinical IMI induced by G+ or G- toxin disrupts follicular functions, and it seems that the ovarian pool of early antral follicles is susceptible to subclinical mastitis.

Original languageAmerican English
Pages (from-to)1165-1172
Number of pages8
JournalTheriogenology
Volume82
Issue number8
DOIs
StatePublished - 1 Nov 2014

Bibliographical note

Funding Information:
The authors thank O. Krifucks for his technical assistance and E. Ezra for his help in the statistical analysis. This research was funded by the Israeli Dairy Board (grant number 820-0271).

Publisher Copyright:
© 2014 Elsevier Inc.

Keywords

  • Follicular development
  • Steroid
  • Subclinical mastitis

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