Bit & Bridle

Equine Sepsis (Septicemia)

Other Names

  • Septicaemia
  • Bacteraemia
  • Systemic inflammatory response syndrome (SIRS)
  • Neonatal sepsis (in foals)

What is Sepsis in Horses?

Equine sepsis — also called septicaemia — is a life-threatening systemic condition characterised by a dysregulated, overwhelming immune response to infection, leading to widespread inflammation, organ dysfunction, and potentially death. While sepsis can affect horses of all ages, it is most clinically significant and most commonly fatal in neonatal foals, in whom it represents the leading cause of death in the first few weeks of life.

In sepsis, bacteria (or other pathogens) enter the bloodstream and trigger a systemic inflammatory cascade that, if unchecked, progresses to septic shock — a state of dangerously low blood pressure and inadequate tissue perfusion. Multiple organ failure involving the kidneys, liver, lungs, intestines, and joints can follow, making rapid intervention essential.

What Causes Sepsis in Horses?

Sepsis requires both an infectious source and a host that is unable to contain the infection locally. In horses, the most common scenarios are:

Neonatal Foal Sepsis

Foals are born without circulating immunoglobulins — they are entirely dependent on colostrum ingested within the first few hours of life for their initial immune protection (passive transfer). If a foal fails to receive adequate colostrum — due to the mare not producing sufficient colostrum, a weak or rejected foal not nursing, or premature colostrum run-off before foaling — the foal has no meaningful immune protection and is highly susceptible to bacterial infection from the environment.

The most common bacteria isolated from septicaemic foals include Escherichia coli, Klebsiella pneumoniae, Actinobacillus equuli, Salmonella spp., Streptococcus spp., and Enterococcus spp. Infection typically enters via the gastrointestinal tract, umbilicus, or respiratory tract.

Adult Horse Sepsis

In adult horses, sepsis most commonly arises as a complication of:

  • Severe gastrointestinal disease — particularly strangulating colic, large colon volvulus, or severe enterocolitis — where the gut wall is compromised and bacteria translocate into the bloodstream (endotoxaemia and bacteraemia)
  • Severe wounds or infected joints (septic arthritis)
  • Pneumonia and pleuropneumonia
  • Post-operative complications
  • Retained placenta with metritis in postpartum mares

Signs and Symptoms of Sepsis in Horses

The clinical presentation varies with the severity of the condition and the age of the horse:

Neonatal Foal

  • Depression, weakness, and failure to nurse
  • High fever (above 39.4°C) or hypothermia (below 37°C) — both are warning signs
  • Increased respiratory rate and effort
  • Injected (brick-red) or pale mucous membranes
  • Swollen joints (septic arthritis) — particularly hocks, fetlocks, and stifles
  • Diarrhoea or distended abdomen
  • Abnormal umbilicus (swelling, discharge, pain)
  • Cloudy eyes (uveitis)
  • Seizures in severe cases
  • Rapid deterioration — foals can go from mildly dull to critically ill within hours

Adult Horse

  • Fever, depression, and profound lethargy
  • Rapid heart rate (tachycardia) and rapid respiratory rate
  • Injected or toxic (purple-tinged) mucous membranes with prolonged capillary refill time
  • Extremities that feel cold (peripheral vasoconstriction in shock)
  • Collapse or inability to stand in severe cases
  • Signs related to the primary source: colic, respiratory distress, joint swelling, etc.

Diagnosis

Rapid diagnosis is essential given the speed at which sepsis can progress:

  • Blood culture: The gold standard for confirming bacteraemia. Multiple blood samples should be collected aseptically before antibiotics are started, and submitted for aerobic and anaerobic culture. Results take 24–72 hours.
  • Haematology: In foals, haematological changes consistent with sepsis include neutropenia (low neutrophil count), hyperfibrinogenaemia, and a left shift. The Sepsis Score (combining physical parameters including temperature, heart rate, white blood cell count, fibrinogen, and presence of diarrhoea, joint swelling, or respiratory distress) is a validated clinical scoring tool for foal sepsis assessment.
  • Serum IgG: All foals should have immunoglobulin G levels checked at 12–24 hours of age using a validated ELISA or immunoturbidimetric assay. A level below 400mg/dL indicates failure of passive transfer (FPT) and is a strong risk factor for sepsis.
  • Biochemistry: Elevated lactate (lactic acidosis) indicates inadequate tissue perfusion. Kidney and liver values assess organ dysfunction. Blood glucose should be monitored in foals as hypoglycaemia is common.
  • Imaging: Ultrasound of joints, abdomen, chest, and umbilicus to identify infection foci. Radiography of joints if septic arthritis is suspected.

Treatment of Sepsis in Horses

Sepsis treatment must be prompt, intensive, and multifaceted:

  • Broad-spectrum antibiotics: Started immediately — before culture results are available — using combinations with good gram-negative and gram-positive cover. In foals, the combination of a penicillin-class antibiotic (amikacin or gentamicin, with careful monitoring of renal function given nephrotoxicity risk) and a beta-lactam (ampicillin or ticarcillin-clavulanate) is standard. Antibiotic choice should be revised when culture results are available.
  • Plasma transfusion: In foals with confirmed failure of passive transfer (IgG below 400mg/dL), intravenous plasma transfusion from an immunised donor horse provides immediate immunoglobulin supplementation. This is one of the most impactful interventions in foal sepsis management.
  • Intravenous fluid therapy: Essential for correcting dehydration, electrolyte abnormalities, hypoglycaemia (supplement dextrose as needed), and supporting blood pressure. Colloidal support (plasma, synthetic colloids) may be added if there is significant protein loss.
  • Anti-inflammatory treatment: NSAIDs (flunixin meglumine) to manage fever, pain, and endotoxin effects. Used carefully to avoid exacerbating renal compromise in volume-depleted animals.
  • Nutritional support: Septic foals may not nurse — enteral feeding via nasogastric tube or intravenous parenteral nutrition may be needed to maintain energy substrate availability.
  • Treatment of infection foci: Septic joints require joint lavage (flushing under general anaesthesia or standing sedation) to remove bacteria and inflammatory debris. Infected umbilical structures may require surgical resection.
  • Intensive monitoring: Blood glucose, electrolytes, blood pressure, urine output, and clinical status should be monitored closely and managed dynamically.

Prevention of Sepsis in Horses

Prevention of foal sepsis is based on ensuring adequate passive transfer and minimising neonatal infection risk:

  • Ensure colostrum intake: All foals should nurse from the mare within 2 hours of birth and have IgG levels checked at 12–24 hours. If the foal is unable to nurse or IgG is inadequate, supplemental colostrum (ideally equine frozen colostrum from a bank) or plasma transfusion should be administered without delay.
  • Vaccinate mares: Vaccination of mares with relevant vaccines (tetanus, equine herpesvirus, rotavirus where available) in the last trimester boosts colostral antibody levels, providing passive immunity to the foal.
  • Foaling environment hygiene: Foaling should occur in a clean, dry, disinfected environment. The foal’s umbilical stump should be treated with dilute chlorhexidine or iodine solution shortly after birth to reduce the risk of umbilical infection (omphalophlebitis).
  • Monitor high-risk foals: Foals from mares with premature udder development, mastitis, or those that ran milk before foaling may have received insufficient colostrum. These foals should have IgG levels checked proactively.

Prognosis

Prognosis for equine sepsis depends critically on the speed of diagnosis and treatment. In foals, survival rates for sepsis treated aggressively at a specialist neonatal intensive care unit are 50–80%, depending on the severity of disease and number of organs involved. Without intensive treatment, most severely septic foals will die within 24–48 hours. In adult horses, prognosis depends on the underlying cause — horses with sepsis secondary to strangulating colic carry a more guarded prognosis than those with a localised source that can be treated surgically. Long-term sequelae in recovered foals include damaged joints from septic arthritis, which may require ongoing management.

When to Call the Vet

Call your vet immediately if a foal shows:

  • Failure to stand within 1–2 hours of birth or failure to nurse within 2–3 hours
  • Depression, weakness, or unwillingness to nurse
  • Swollen joints
  • Fever, abnormal temperature (very high or very low), or rapid breathing
  • Any diarrhoea in the first 24 hours (as opposed to normal foal heat scours later)

In adult horses, call your vet urgently if the horse is profoundly depressed, has a high fever, and you are aware of a potential infectious source (colic, contaminated wound, retained placenta). Sepsis is a veterinary emergency at any age.

Frequently Asked Questions

What is failure of passive transfer and why does it matter?

Failure of passive transfer (FPT) occurs when a foal does not absorb sufficient immunoglobulins (IgG) from the mare’s colostrum in the first 12–24 hours of life. The gut’s ability to absorb intact immunoglobulin molecules closes rapidly — by 12 hours absorption is declining, and by 24 hours it is essentially complete. A foal with FPT has no circulating antibodies and is highly vulnerable to bacterial infection. IgG levels below 400mg/dL are considered inadequate, and levels below 200mg/dL represent complete FPT. Plasma transfusion is the treatment — acting quickly before infection establishes is critical.

Can adult horses recover from sepsis?

Yes, but recovery from severe sepsis is a significant undertaking. The underlying infectious source must be identified and treated, and intensive supportive care is required. Many horses that survive acute sepsis suffer organ damage — kidney injury and laminitis are two important sequelae. With early, aggressive treatment, survival is achievable, but the financial cost of intensive care is considerable and owners should be counselled about prognosis and cost early in the process.

How quickly can a foal deteriorate from sepsis?

Very quickly — this is what makes neonatal sepsis so dangerous. A foal that appears mildly dull at morning feed can be in septic shock by evening. In some peracute cases, foals deteriorate from subtle lethargy to recumbency within hours of the first signs. This is why any foal that is not nursing normally, appears depressed, or has a fever requires same-day veterinary attention, not a “wait and see” approach.

Is umbilical dipping important in preventing foal sepsis?

Yes. The umbilical stump is an important portal of entry for bacteria in the neonatal period. Dipping or spraying the navel stump with 0.5% chlorhexidine solution (diluted from 2% stock, or use a proprietary product) or dilute povidone-iodine (10%) within the first hour of birth and repeating 2–3 times in the first 24 hours significantly reduces the incidence of omphalophlebitis (navel ill) and ascending umbilical infection. Avoid using strong undiluted iodine, which can cause tissue damage and slow drying of the stump.