Poster Presentation The 3rd Prato Conference on the Pathogenesis of Bacterial Diseases of Animals 2014

Pathogenesis of abortion by leptospirosis (#12)

Bibiana Brihuega 1 2 , Agustin Venzano 1 , Sylvia Grune 1 , Mara Martinez 1 , Graciela Romero 1 , Luis Samartino 1 2
  1. National Institute of Agricultural Technology, Ciudad Autonoma De Buenos Aires, Argentina
  2. Microbiology, University of Salvador, Pilar, Buenos Aires, Argentina

Introduction

The pathogenesis of abortion by Leptospira sp. may have a multifactorial origin and a wide array of physiopathological mechanisms could be involved. In vivo assays have been done in this survey in order to study such mechanisms in guinea pigs. 

Materials and methods

Samples of placenta from aborted animals infected by Leptospira interrogans serovar Pomona were collected and fixed in 10% buffered formalin, embebbed in paraffin wax, sectioned at 5 µm and stained with hematoxylin and eosin (HE), Warthin-Starry, Periodic acid-Schiff (PAS) and Masson`s trichrome modified by Lillie. Observations were focused both on blood vessels and perivascular areas.

Results

Masson-stained tissues exhibited fibrinoid material and granular proteinaceous deposits on the vessel walls, whereas PAS colored ones showed thickened basal membranes as well as rupture and disorganization of other vascular components.

Placental changes consisted of vacuolar degeneration of the arterial endothelium, disseminated vascular coagulation, neutrophilic histiocytic vasculitis, fibrinoid degeneration of blood vessels and trophoblast necrosis. At the uteroplacental union were observed necrosis, neutrophilic infiltration and haemorrhage together with degenerative change of large arteries including proliferation of sincytotrophoblasts that invaded both wall and lumen.

Warthin-Starry placental tissues showed aggregations of leptospiras adhering to the vascular endothelium

Conclusion

This study leads to a better understanding of the pathological consequences of leptospiral infection.  Direct participation of these bacteria has been suggested as a crucial factor in cell lesion, characterized by the presence of inflammatory cells, endothelial damage by proteinaceous deposits and adhesion of leptospires to the vascular wall of the placenta. These factors interfere with the mother- fetal exchange disrupting the mother- fetal nutrient flow mostly in the later pregnancy states, thus finally triggering hypoxia and cell death. These events lead to fetal death.

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