Emily Brouwer
Animal Health Laboratory, University of Guelph, Guelph, ON.
AHL Newsletter 2025; 29(3):17.
A stillborn foal was submitted to the Animal Health Laboratory for diagnostic workup for suspected infectious placentitis. There had been concerns on the farm for the previous three breeding seasons, with the submitting veterinarian reporting increased incidence of placentitis cases estimated at 1-2 per season out of 15-25 mares. Some of the foals born to mares with diagnosed placentitis have been poor doers, and one was suspected to have in utero sepsis.
The dam of this foal was reported to have a one week history of mucohemorrhagic vulvar discharge, and was diagnosed with placentitis based on elevated combined thickness of the uterus and placenta via transrectal ultrasound (14.3 mm). The mare was treated with trimethoprim sulfa, flunixin meglumine, and altrenogest (Regu-Mate). The mare subsequently had a red bag delivery of a stillborn foal at 329 days gestation.
On gross examination, the placenta was noted to be diffusely edematous, up to 1 cm thick in the non-gravid horn, and there were tortuous, dilated lymphatic vessels on the allantoic surface. The chorionic surface was opaque, diffusely tan-brown and thickened with scattered petechial hemorrhages. The umbilical cord was 54 cm long with no twists. The amnion was unremarkable.
On internal examination, the pericardial sac was distended and taut, and contained approximately 200 mL of clotted blood. There was a focal, elliptical rent in the pulmonary artery measuring 22 mm x 5 mm on the serosal surface that was surrounded by intramural hemorrhage (Fig 1.). On cut section, the defect in the intimal surface measured approximately 5 cm x 1 cm, and had ragged edges (Fig. 2).
Figure 1. Pulmonary artery rupture, serosal surface.
Figure 2. Pulmonary artery rupture, intimal surface
On gross examination, the foal was diagnosed with pulmonary artery rupture and severe hemopericardium, as well as placental edema.
Histologically, the placenta was severely, diffusely edematous and the vessels were markedly dilated. There was no histologic evidence of an inflammatory or infectious process in the sections of placenta or fetal tissues. Bacterial culture of the placenta isolated low numbers of E. coli in mixed culture (interpreted as contamination), and there were no bacterial pathogens isolated from either the fetal lung or stomach content. Leptospira spp., equine arteritis virus, and equid herpesvirus 1 (both neuropathogenic and non-neuropathogenic variants) were not detected by PCR.
Based on these findings, spontaneous vascular rupture was suspected to be the result of vascular fragility- either related to an inherited collagen defect (such as Marfan syndrome) or copper deficiency. Fetal copper levels were elevated (89 μg/g, reference 4.0-7.5 μg/g), which was considered normal as fetuses will store copper at the expense of the dam. This finding ruled out copper deficiency as a cause of vascular fragility. Fragile foal syndrome type 1, an inherited disease that results in fragile skin, hematomas, and accumulation of fluid (among other lesions) was considered, but ultimately was not tested for due to the signalment. The mutation responsible for fragile foal syndrome type 1 has been reported predominantly in warmbloods, and much less frequently in other breeds such as Thoroughbreds, American Sport Ponies, Knabstruppers, and Haflingers.
In the absence of an inflammatory component associated with the placental edema, the placental lesions were suspected to be the result of impaired fetal circulation related to cardiac tamponade. The underlying cause of vascular rupture was not identified.
Reference
1.Reiter S, et al. Distribution of the warmblood fragile foal syndrome type 1 mutation (PLOD1 c.2032G>A) in different horse breeds from Europe and the United States. Genes (Basel) 2020;11(12):1518.