Pictorial review of foal diseases

Summary

There are more similarities between foal diseases of differing aetiologies than differences. This talk will review the clinical signs evident in prematurity, septicaemia, perinatal asphyxia syndrome, colic, enterocolitis, ruptured bladder, neonatal isoerythrolysis, cleft palate and pharyngeal dysfunction. Aspects shared between the diseases and those unique to a particular condition will be highlighted.

Prematurity

Foals that are premature often have distinct clinical features: Domed heads, fine silky hair, floppy ears, lax tendons and incomplete ossification of the small tarsal and carpal bones. They may also be dyspnoeic or have high or low respiratory rates.
Ossification of the small tarsal and carpal bones has great bearing on the future athletic ability of these foals, and foals with little ossification are unlikely to become athletes.

Foal can be very small for their age. Thoroughbred foals less than 25kg are unlikely to survive. The reversed neutrophil:lymphocyte ratio found in many premature foals can lead to confusion with sepsis. The serum amyloid A should be low in premature foals (<30mg/L) and high in septic foals (>100mg/L).

Septicaemia

Septicaemia has no specific clinical signs. The foal may be slightly depressed yet still be nursing in the early stages of sepsis. Septicaemia results in changes to the coagulation system and circulation, and manifestations of these changes may be seen in some affected foals. The main circulatory changes seen are injection of the oral mucous membranes and conjunctiva. Capillary leak syndrome, manifested by generalised oedema, can also be seen.
Coagulation problems can result in petechiation of the aural pinnae, mucous membranes and muzzle.

Infection can settle out in a number of sites in the foal, and the joints and the umbilicus are the most common. Joint infection can progress to osteomyelitis, or infection can settle in the bone with no obvious synovial involvement.

Perinatal asphyxia syndrome

Predisposing factors are dystocia, requiring resuscitation at birth, birth by C-section, premature placental separation and illness of the mare prior to parturition. However, many cases occur without any of these predisposing factors being present.
There is a range of clinical signs, and foals may show any or all of them as they progress through the disease. In the mildest forms, there is reduced nursing activity and/or poor affinity for the mare. Incoordination of the suck response and “tongue-lolling” is also very common. General poor coordination, which can lead to inability to get up and down, and inability to walk can also be seen. The most severely affected foals are unable to rise, with either extensor rigidity or coma.

Seizure activity can occur with perinatal asphyxia syndrome, and is not always accompanied by other severe signs. A foal that is able to walk and nurse can show seizure activity. It is important to remember that, although it is the most common cause of seizures, it is not the only one.

Colic

Almost all foals show colic in the same way, no matter what the cause. They tend to roll onto their backs and stay there for a while, rather than rolling violently like an adult horse. The most common cause of colic in foals less than 36 hours old and that have not passed meconium is a meconium impaction. These usually respond well to an enema, or failing that, an acetylcysteine retention enema. Occasionally the meconium can be higher up the gastrointestinal tract, and therefore will not respond to an enema.

However, it is important to remember that meconium impaction is not the only cause of colic in this age of foal, and never occurs in older foals. Atresi ani, recti or coli can present similar to a meconium impaction. A digital rectal examination will reveal no faeces in the rectum and may reveal a blind ended sac. Sometimes a definitive diagnosis needs to be made by a barium enema. Meconium impaction almost never results in gastric reflux, and if the foal is refluxing, small intestinal lesions such as volvulus or intussusception should be suspected.

Enterocolitis

The most common condition we see in foals less than 6 weeks old is enterocolitis. The causes vary with age. In the first week of life, generalized septicaemia is the most common cause. Between 1 and 4 weeks of age, we see a lot of rotavirus. Also in this age group, and up to 6 weeks of age are specific gastrointestinal pathogens, chiefly the Enterobacteriaceae. We also see a fair number of Clostridial infections, especially in foals previously treated with antibiotics for another condition. Foals with enterocolitis present with a wet tail, and faeces down their hind quarters. Often foals with chronic diarrhoea will have hairloss over the hindquarters. Occasionally other signs will accompany the enterocolitis, such as rectal prolapse or vulval swelling.

Ruptured bladder

Foals with ruptured bladders usually present at 3-5 days of age with a very swollen abdomen. Traditionally, this condition has been described to be much more prevalent in males. However, recent studies have shown ruptured bladder to also occur commonly in females. They may, however, present earlier or later in life than this. These foals may also show signs of colic, although despite great abdominal distension, this is not a universal sign. Very high potassium concentrations can result in cardiac arrhythmias, characterised by bradycardia and, on changes on an ECG trace.
These foals can get abdominal compartment syndrome, in which the increased pressure in the abdomen reduces diaphragmatic movement and puts pressure on the caudal vena cava, reducing blood return from the caudal body to the heart. The abdomen can be drained through a teat cannula through the abdominal wall. However, if the rent in the bladder wall is sufficiently large, the entire abdomen can be drained through an indwelling Foley catheter placed via the urethra into the bladder.
A differential for ruptured bladder is dysfunctional bladder syndrome, a single organ manifestation of perinatal asphyxia syndrome. Often no other signs of perinatal asphyxia syndrome are evident. In this condition, the bladder does not empty, and will increase in size until it ruptures. Very large volumes (>1.5L) can be removed by catheterisation. This condition is distinguished from a ruptured bladder by ultrasound examination of the bladder and abdomen. Treatment consists of placing an indwelling urinary catheter for 1-3 days.

Neonatal isoerythrolysis

Neonatal isoerythrolysis occurs when the mare makes antibodies to antigens on the foal’s red blood cells. This occurs when the stallion has a different blood type to the mare. The most common blood groups involved are Aa or Qa, when the stallion carries this antigen and the mare does not.
The first foal inherits the stallion’s blood type. During birth, some of the foals red blood cells cross into the mares bloodstream, causing her to make antibodies against the foals red blood cells. Typically these are not passed to the foal, and the first foal is unaffected.
When the mare has a second foal with the same blood type, antibodies are passed to the foal in the colostrum.
These then cause agglutination or lysis of the foals red blood cells. The most common clinical sign is icterus – yellow discolouration of the mucous membranes. This occurs due to accumulation of bilirubin, which is a breakdown product of haemoglobin. If there is intravascular haemolysis (which occurs if the antibody fixes complement), there may be haemoglobinuria.

Cleft palate and pharyngeal dysfunction

Cleft palate is an uncommon condition in foals. We typically see 1 to 2 cases per annum in our referral practice.
The usual presentation is milk coming out from the nostrils just after nursing. Foals may also present with signs of aspiration pneumonia.
The main differential diagnosis is pharyngeal dysfunction. In neonatal foals, this appears to be a single organ manifestation of perinatal asphyxia syndrome. Often no other signs of perinatal asphyxia syndrome are evident.
In older foals (and some neonatal foals treated extensively with antibiotics), pharyngeal dysfunction can occur secondarily to guttural pouch infection (bacterial or fungal). Foals with pharyngeal dysfunction may present with milk coming from the nostrils. They may also may make an inspiratory noise due to dorsal pharyngeal collapse, and show signs of aspiration pneumonia.
Diagnosis of cleft palate is by endoscopy. The two separated walls of the soft palate can be seen as “rolls” on either side of the nasopharynx. Depending on the extent of the soft palate cleft, it may be seen to separate from a rostral normal soft palate. Occasionally it is possible to see the cleft palate via an oral examination. However, it is hard to adequately open the jaw without anaesthetizing the foal. It is possible to do surgery if the cleft involves the soft palate only, and not the hard palate. However, there is a high risk of breakdown of the repair after surgery.
Treatment of pharyngeal dysfunction involves placement of an indwelling stomach tube, or parenteral feeding.
Any underlying guttural pouch infection should be treated.