Equis ISSN 2398-2977

Foal: neonatal septicemia syndrome

Synonym(s): Equine neonatal septicemia

Contributor(s): Prof Derek Knottenbelt, Graham Munroe, Prof Jonathon Naylor, Kate Hepworth-Warren


  • CauseE. coli and other gram-negative organisms; gram-positive organisms, including Streptococcus spp and Staphylococcus spp.
  • Signs: lethargy, decreased or absent nursing, weakness, diarrhea, uveitis, lameness, injected mucous membranes, petechiation of pinnae or mucous membranes.
  • Diagnosis: history and clinical signs; bacteriology, hematology, biochemistry, foal sepsis scoring.
  • Treatment: nursing care, antimicrobials, fluid therapy, NSAIDs.
  • Prognosis: often poor, but improves if treatment is sought early. Mortality rate up to 50%.
  • Septicemia is defined as the development of systemic inflammatory response syndrome (SIRS) in response to an infection.
  • Bacteremia is the transient passage of bacteria through the bloodstream without obvious clinical signs.
  • Localized infection of lungs, joints, bones or GI tract may follow either septicemia or bacteremia.



  • Neonatal foals are exposed to pathogens from the moment they are born. Routes of inoculation with bacteria include ingestion, umbilical infection, placental transmission, respiratory, penetrating wound, etc.
  • The most commonly isolated organisms (blood culture/necropsy) are gram-negative bacteria, especiallyE. coli  Escherichia coli  , although gram-positive and anaerobic infections, or polymicrobial infections are also common.
  • Other gram-negatives that are often involved in septicemia:
  • The most common gram-positive organism cultured areStreptococcusspp (beta-hemolytic) andStaphylococcusspp, often in mixed infection with gram-negative organisms.
  • The sensitivity patterns of some of these organisms, particularly in gram-negatives, have changed and therefore culture and sensitivity should be used where possible to plan an appropriate choice of antibiotic therapy.

Predisposing factors

Foal factors
  • Identification of the so-called 'high risk foal'.
  • Failure of passive transfer of immunity   Foal: failure of passive transfer (IgG)  :
    • Inadequate intake of colostrum, eg dummy foals that cannot nurse, mares that reject their foals, mares that leak colostrum prior to foaling.
    • Poor quality colostrum.
  • Stress.
  • Premature or dysmature foals   Reproduction: prematurity / dysmaturity  .
  • Foals that have required resuscitation or are meconium stained.
  • Foals with abnormal behavior.
  • Prolonged gestation.
  • Poor feeding capacity/ability.
  • Twins.
Maternal factors

Parturition factors


  • Systemic bacterial infection of the neonate may develop as a result of anin uteroinfection, placentitis   Placenta: placentitis  , or post-parturient oral, respiratory, or umbilical inoculation.
  • Septicemia results when the foal's immunity is overcome by the bacterial challenge.
  • Usually involves opportunistic organisms found in the genital tract, perineum and udder of the mare.
  • Specific signs depend on the extent of the infection and organ predilection of the organism.
  • The route of infection is sometimes difficult to identify but about 50% of neonates are infectedin uteroand the rest during parturition or immediately after parturition.
  • The increased permeability of the gut to antibodies may also lead to increased permeability to ingested bacteria.
  • In uteroacquired infections are usually of a chronic nature leading to a placentitis and subsequent fetal infection. The placentitis may not be evident grossly.
  • Perinatal infection can enter via ingestion, inhalation and umbilical contamination, and is particularly associated with problems   →   perinatal stress.
  • Infections acquired post-parturition are especially associated with failure of passive transfer of immunity   Foal: failure of passive transfer (IgG)  , poor husbandry, endemic farm infections and high-risk neonatal foals.
  • The location of infection is most commonly the gastrointestinal tract, lungs, and skeletal system.


  • Clinical signs may be subtle or non-specific, but foals can decline rapidly into fatal septic shock.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Fielding C L & Magdesian K G (2015) Sepsis and septic shock in the equine neonate. Vet Clin North Am Equine Practice 31 (3), 483-496 PubMed.
  • Weber E, Sanchez L & Giguere S (2015) Re-evaluation of the sepsis score in equine neonates. Equine Vet J 47 (3), 275-278 PubMed.
  • Palmer J (2014) Fluid therapy in the neonate: not your mother's fluid space. Vet Clin North Am Equine Pract 20 (1), 63-75 PubMed.
  • Mapes et al (2007) Comparison of five real-time PCR assays for detecting virulence genes in isolates of Escherichia coli from septicemic nenoatal foals. Vet Rec 161 (21), 716-718 PubMed.
  • Perkins G, Ainsworth D M, Erb H N et al (2000) Clinical, haemotological and biochemical findings in foals with neonatal Equine herpesvirus- 1 infection compared with septic and premature foals. Equine Vet J 31 (5), 422-426 PubMed.
  • Wichtel M E et al (1999) Pharmacologic considerations in the treatment of neonatal septicaemia and its complications. Vet Clin North Am Equine Pract 15 (3), 725-746 PubMed.
  • Paradis M R (1994) Update on neonatal septicemia. Vet Clin North Am Equine Pract 10 (1), 109-135 PubMed.
  • Raisis A L, Hodgson J L & Hodgson D R (1996) Equine neonatal septicemia - 24 cases. Aust Vet 73 (4), 137-140 PubMed.