Peripheral blood markers of sepsis in foals born from mares with experimentally induced ascending placentitis

Abstract

<jats:sec><jats:title>Background</jats:title><jats:p>Neonatal sepsis is a leading cause of neonatal death during the first-week postfoaling. Despite recent advancements in the diagnosis and treatment of sepsis in the newborn foal, the non-specific clinical signs and subtle nature of this disease may result in delayed diagnosis until severe progression of the disease; thus, early detection of sepsis remains critical for a favourable outcome. This study aimed to identify early blood markers as predictive of sepsis on foals.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Thirty-five foals were allocated into three groups: healthy control foals (n=7) and foals born from mares with placentitis: septic foals (n=9) and non-septic foals (n=19). Blood samples were obtained immediately after foaling and at 12, 24 and 48 hours. All samples were assessed for glucose, lactate, triglycerides, total cholesterol, urea, creatinine, total solids, fibrinogen, gamma-glutamyl transferase (GGT), serum amyloid A (SAA) and alpha-fetoprotein (AFP) concentrations.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>At foaling, glucose and GGT concentrations were lower in septic foals (P&lt;0.001). Of interest, SAA, AFP, creatinine and total cholesterol were higher in septic foals at parturition (P&lt;0.05). At 12 hours, lactate, triglycerides and total cholesterol concentrations were higher in septic foals. When evaluated at 24 and 48 hours, higher concentrations of SAA and AFP were found in placentitis foals than in the control group.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Total cholesterol and lactate appear to be suitable markers for sepsis during the first 24 hours postpartum. Septic foals displayed altered energy metabolisms as determined by increased triglycerides and cholesterol concentrations, hypoglycaemia at birth and reduced activity of the GGT and increased lactate and urea concentrations. Sepsis was associated with high concentrations of SAA and AFP.</jats:p></jats:sec>

Use of serum amyloid A in equine medicine and surgery

“…These slightly higher concentrations could be associated with passive transfer of SAA, as SAA has been found in colostrum, 31,32 or from endogenous production as a consequence of the foal sustaining mild trauma while passing through the birth canal. It is not clear whether placentitis in the mare will give rise to increases in serum SAA concentration in the foal, as both normal 58,59 and slightly elevated concentrations 60 have been demonstrated in nonseptic foals and fetuses from mares with placentitis. It is not clear at which age SAA concentrations level out, but presumably within a few weeks after birth.…”

“…White blood cell count (×10 mare will give rise to increases in serum SAA concentration in the foal, as both normal 58,59 and slightly elevated concentrations 60 have been demonstrated in nonseptic foals and fetuses from mares with placentitis. It is not clear at which age SAA concentrations level out, but presumably within a few weeks after birth.…”

Effects of intravenous administration of peripheral blood‐derived mesenchymal stromal cells after infusion of lipopolysaccharide in horses

“…4 In horses, sepsis is often caused by gram-negative bacterial infection and is associated with increased proinflammatory cytokine gene expression, acute-phase protein production, and oxidative stress. [5][6][7][8][9] Low-dose lipopolysaccharide (LPS; endotoxin) administered IV to horses results in moderate and transient clinical signs and clinicopathological abnormalities typical of sepsis. [10][11][12] This model of equine endotoxemia increases pro-inflammatory cytokine gene expression as well as serum amyloid A (SAA) and reactive oxygen species (ROS) production.…”

“…A systemic and dysregulated host immune response to infection can lead to multiple organ failure and death despite pathogen elimination 4 . In horses, sepsis is often caused by gram‐negative bacterial infection and is associated with increased pro‐inflammatory cytokine gene expression, acute‐phase protein production, and oxidative stress 5‐9 . Low‐dose lipopolysaccharide (LPS; endotoxin) administered IV to horses results in moderate and transient clinical signs and clinicopathological abnormalities typical of sepsis 10‐12 .…”

The fecal bacterial microbiota of healthy and sick newborn foals

“… 1 , 2 , 3 , 4 , 5 Factors associated with the development of sepsis in equine neonates include maternal disorders, abnormal gestation length, failure of transfer of passive immunity (FTPI), poor environmental hygiene, and inadequate umbilical care. 6 Maternal disorders including dystocia, placentitis, gastrointestinal or respiratory diseases have an essential role in the development of bacteremia in foals 7 , 8 , 9 ; however, the importance of other routes of infection such as umbilical structures, or the gastrointestinal tract (GIT) and respiratory system are not completely understood.…”