Pregnancy toxaemia as predisposing factor for development of mastitis in sheep during the immediately post-partum period

• Pregnancy toxaemia led to development of mastitis at the early stage of subsequent lactation period in ewes.
• Bacteriological, cytological and pathological methods were used.
• Impairment of mammary defence mechanisms was the likely cause.

Objective of the work was to evaluate the potential predisposing role of pregnancy toxaemia in development of mastitis in the immediately post-partum period. Ewes were allocated in subgroups A1 or A2 (with pregnancy toxaemia) or B1 or B2 (with no pregnancy toxaemia). Ewes in A1 or B1 were challenged, on the 5th day post-partum, by deposition of Mannheimia haemolytica into the teat duct, whilst ewes in A2 and B2 were controls. Clinical, bacteriological and cytological examinations were performed, as well as pathological examination of the inoculated teat (after mammelectomy) and both mammary parenchymas (after biopsy). Mastitis developed in 8/8 ewes of subgroup A1, in 1/8 ewe of subgroup A2, in 4/8 ewes in subgroup B1 and in 0/4 ewes in subgroup B2. Comparisons between subgroups revealed that isolations from A1 were greater than respective isolations from B1 (P < 0.08); bacteria were recovered more frequently from tissue samples from A1 than from B1 (P = 0.008). The characteristic lymphoid follicles at the border between teat duct and teat cistern were observed in 3/8 ewes in A1 and in 7/8 ewes in B1 (P = 0.019). In A1, cumulative score for macroscopic and histological pathological findings in the teat was 18 and 23 (max. 32), respectively; cumulative score for histopathological findings in the mammary parenchyma ipsilateral to the inoculated teat was 24, whilst scores for B1 were 5, 31 and 16 (P ≤ 0.05). The results confirm that pregnancy toxaemia can act as a predisposing factor for mastitis in the immediately post-partum period. Possibly, impairment of the lymphoid follicular structures present at the border between teat duct—teat cistern could have been the cause of reduced protection of the mammary gland.