Septicaemia - Foal

Introduction

Septicaemia in the foal is a serious and life-threatening condition that requires prompt diagnosis and treatment. It is caused by the presence of bacteria, or bacterial toxins in the blood. The infection can either be localised (ie to the joints or umbilicus) or generalised, with systemic signs.

Several bacteria can cause septicaemia, including grams negative organisms such as E-coli, Actinobacillus, and Klebsiella species,and gram positive organisms such as Streptococcus and Staphylococcus species. Occasionally anaerobic organisms such Clostridium species may also cause disease.

Signalment

Infection is via haematogenous spread following infection via the placenta, umbilicus, lungs or GI tract. Foals may be affected as early as the

Predisposing factors include:

Failure of passive transfer - due to failure of the foal to suckle adequate quantities of colostrum, or low volume/poor quality colostrum produced by the dam.
Dystocia
Premature/Dysmature foal
Over-crowding and poor hygiene
Artificial severance and ligation of the umbilicus
Failure to treat the umbilicus immediately after birth (with tincture of iodine)

Clinical Signs

Foals in the early stages of clinical disease may not show any specific signs, instead appearing 'off-suck' (inspecting the dams udder can give some indication of when the foal last suckled). This may be accompanied by lethargy, malaise, frequent recumbancy and pyrexia. The bacteria may localise in different organs, producing clinical signs directly related to that organ:

Ocular localisation produces hypopyon and iritis
Integumentary localisation produces anasarca
Locomotor localisation produces joint effusion and/or septic arthritis
Cardiac localisation produces tachycardia
Respiratory localisation produces polypnoea
Gastrointestinal localisation produces ileus, colic and diarrhoea
Urogenital localisation produces anuria
Neurological localisation produces seizures and depression

The disease may then advance to septic shock. Clinical signs include prolonged recumbancy, depression, dehydration, and tachycardia with cold extremities, weak thready pulses, slow capillary refill time and muddy mucous membranes, indicative of hypotension. Dependant on the organs affected, signs of individual or multiple organ dysfunction may be present.

Clinical signs can progress very rapidly therefore prompt recognition is necessary.

Diagnosis

Septicaemia scoring.... Clinical signs and history. Individual tests eg US,arthrocentesis etc related to organs affected Bloods neutropaenic with toxic change FPT measurements - serum IgG..... Positive blood culture confirms but negative does not rule it out

Treatment

The foal should be immediate treated with broad spectrum IV antibiotics until culture results are known. Multiple plasma transfusions may be required to raise IgG serum levels, and IV fluid therapy should be administered to treat endotoxic shock. Nutritional support is necessary, either by helping the foal suckle the dam or administration of the dams milk (or a substitute) via nasogastric tube. In addition, glucose levels should be measured frequently and dextrose added to the IV fluid therapy if necessary. The use of anti-endotoxin drugs (flunixin, anti-prostoglandin, polymyxin B) as an adjunct treatment has also been reported.

General supportive care, recumbant foal management and TLC is also necessary - this may continue for several weeks after infection. Organ-specific treatments such as joint lavage may also be needed.

If the umbilicus is a localised source of infection, it can surgically resected to reduce the spread of infection to distant organs.

Prevention

Ensuring adequate intake of colostrum in the first 12-24 hours of life. Levels can be checked by measuring serum IgG (>800mg/dl)
Appropriate treatment of the umbilicus with tincture of iodine promptly after birth.
Providing a clean, warm and well ventilated environment for the neonate.

Prognosis

Dependant on the severity of clinical signs and the individual organs affected. Early recognition and aggressive treatment are key to an improved prognosis.

References

Merck & Co (2009) The Merck Veterinary Manual (Ninth Edition), Merial

Captain M. Horace Hays FRCVS Veterinary Notes for Horse Owners (Revised Edition), Stanley Paul

RVC staff (2009) Urogenital system RVC Intergrated BVetMed Course, Royal Veterinary College

Mair, TS & Divers, TJ (1997) Self-Assessment Colour Review Equine Internal Medicine Manson Publishing Ltd