Diseases of the foal

20.1. Prematurity/dysmaturity

Gestational length

• •Normal gestational length varies from 320 to 360 days.
• •Significant variations exist between horses, and gestational length alone is not a good indicator of readiness for birth.
• •When assessing maturity, clinical appearance and gestational age must be evaluated in combination.

Definitions

• 1. Prematurity: foal less than 320 days’ gestation.
• 2. Dysmaturity: signs of immaturity/prematurity in foals more than 320 days’ gestation. Commonly low birth weight, despite normal gestational age.
• 3. Postmaturity: foal greater than 360 days’ gestation. Normal to large axial skeletal size, but thin/emaciated.

Risk factors

• 1.Elective early induction of labour or early caesarean section.
• 2.Placentitis.
• 3.Systemic disease in the mare.
• 4.In utero disease of the foetus.
• 5.Fescue endophyte toxicity (risk for postmaturity).

Clinical characteristics of prematurity

• •Small for gestational age.
• •Soft/silky hair coat.
• •Floppy ears.
• •Increased range of joint motion; lax flexor tendons.
• •Abnormal progression through normal events subsequent to foaling (e.g. standing, suckling).
• •Weakness or ‘floppiness’.
• •Domed forehead.
• •Poor thermoregulation.
• •Increase chest wall compliance.

Clinical characteristics of postmaturity

• •Large axial skeletal size, but thin or emaciated.
• •Long hair coat.
• •Erupted incisors.
• •Flexor tendon contracture.

Pathophysiology and diagnostic findings

• 1.
  Immature adrenal cortical function:

  • •
    Low cortisol concentrations.
  • •
    Poor response to adrenocorticotrophic hormone (ACTH).
  • •
    Neutropenia, lymphocytosis, decreased neutrophil:lymphocyte ratios.
• 2.Poor glucose regulation.
• 3.Poor vascular tone and responsiveness; hypotension is common.
• 4.Immature renal function, low urine output.
• 5.
  Pulmonary immaturity:

  • •
    Decreased lung compliance.
  • •
    Increased chest wall compliance.
  • •
    Weak respiratory muscles.
  • •
    Surfactant deficiency.
  • •
    Thoracic radiographs: a diffuse, ‘ground glass’ appearance is seen with surfactant deficiency (Figure 20.1 ).
• 6.Gastrointestinal immaturity: unable to handle oral diet; poor absorption of colostrum.
• 7.Musculoskeletal immaturity: lack of cuboidal bone ossification seen on carpal and tarsal radiographs (Figure 20.2 ).
• 8.Susceptibility to infection; depressed immunity.

Figure 20.1.

Thoracic radiograph of a premature foal (310 days) with evidence of pulmonary immaturity, including atelectasis and lack of alveolar expansion.

Figure 20.2.

Radiographs of a premature foal (310 days) showing incomplete ossification of carpal cuboidal bones.

Treatment (see Chapter 26)

The treatment of premature foals remains one of the most challenging problems presented to the equine practitioner.

• 1.
  Supportive care is of primary importance:

  • •
    Maintain warm environment: blankets, lamps, heating pads, etc.
  • •
    General nursing care to prevent decubital ulcers.
• 2.
  Respiratory support:

  • •
    Maintain sternal recumbency.
  • •
    Intranasal oxygen if hypoxaemic.
  • •
    Mechanical ventilation may be needed.
  • •
    Surfactant treatment if deficient.
• 3.
  Cardiovascular support if necessary:

  • •
    Intravenous fluids.
  • •
    Vasopressors may be needed.
  • •
    Maintain adequate perfusion.
• 4.
  Nutritional support:

  • •
    Intravenous dextrose.
  • •
    Enteral nutrition if gastrointestinal function is mature.
  • •
    Parenteral nutrition if gastrointestinal function is immature or dysfunctional.
• 5.Adrenocortical axis support: corticosteroids may be used if adrenal insufficiency is suspected.
• 6.
  Physical therapy:

  • •
    Bandages, splints, braces, etc., as needed for musculoskeletal support.
  • •
    Exercise should be limited if hypoplasia of the carpal or tarsal bones is present.
• 7.
  Prevention of infection:

  • •
    Determine adequacy of passive transfer of immunoglobulin.
  • •
    Administer colostrum or plasma if necessary.
  • •
    Broad-spectrum antimicrobials.
• 8.
  Determine the underlying cause of prematurity if possible:

  • •
    Infection.
  • •
    Placental abnormalities.
  • •
    Cause is often undetermined.

Prognosis

• •Survival of foals induced before 320 days is poor.
• •Survival greater than 70% is reported for spontaneous birth between 280 to 322 days’ gestation.
• •Prognosis is better if cause of prematurity/dysmaturity is in utero infection or placentitis.
• •Concurrent disease (e.g. sepsis, asphyxia) may reduce the prognosis.
• •Respiratory immaturity is often the limiting factor to survival.
• •The prognosis is guarded if the neonate does not develop a righting reflex or suckle reflex.

Prevention

Prevention is based upon good management practices and on identification of maternal problems that may influence foetal viability and/or the onset of parturition.

• 1.Identification and treatment of placental infections. Treatment may include antimicrobials, anti-inflammatory drugs, and progesterone.
• 2.Avoid induction of parturition unless necessary, as readiness for birth is very difficult to predict.
• 3.Corticosteroids have been successfully used in humans and sheep to encourage foetal maturation. They have not been shown to be effective in the mare.
• 4.Monitoring foetal heart rate can give an indication of foetal well-being.
• 5.To prevent postmaturity, remove mares from endophyte-infected fescue pasture or administer dopamine receptor antagonists.

20.2. Systemic diseases involving multiple body systems

Sepsis

Sepsis is a common cause of morbidity and mortality in the neonatal foal, and is one of the most common reasons for neonatal foal presentation at referral clinics.

Definitions

• 1.Systemic inflammatory response syndrome (SIRS): characterized by fever, tachycardia, tachypnoea, and leucopenia or leucocytosis.
• 2.Sepsis: SIRS with a source of confirmed or suspected infection.
• 3.Septic shock: septicaemia with hypotension refractory to fluid resuscitation.

Aetiology

• 1.Although sepsis can also be secondary to viral or fungal infection, the term sepsis in the foal generally refers to systemic spread of bacteria through the bloodstream. Infection may arise in utero or postnatally.
• 2.Failure of transfer of passive immunity (FTPI) may predispose to infection (see Section 20.11).
• 3.Other risk factors include poor hygiene, maternal illness, prematurity, and immunosuppression.
• 4.Infections are generally a result of opportunistic organisms from the foal's environment, skin, or the mare's genital tract.
• 5.Portals of entry into the body include the respiratory tract, umbilicus, gastrointestinal tract, and placenta.
• 6.
  Gram-negative infections predominate. The most common organisms vary with the geographical location. Commonly encountered bacteria include:

  • •
    Escherichia coli.
  • •
    Salmonella.
  • •
    Klebsiella.
  • •
    Enterobacter.
  • •
    Actinobacillus.
• 7.
  Gram-positive infections are common, but less frequent than Gram-negative infections. Commonly encountered bacteria include:

  • •
    Beta- and alpha-haemolytic Streptococcus.
  • •
    Staphylococcus spp.
  • •
    Clostridium spp.

Clinical signs

• 1.Early signs are non-specific and include depression, weakness and decreased suckling.
• 2.Fever, hypothermia, or normothermia may be present, depending on the severity and stage of the disease.
• 3.Localizing signs of infection: uveitis, hypopyon, pneumonia, enteritis, meningitis, omphalophlebitis, septic arthritis, and osteomyelitis.
• 4.Injection, petechiation or ecchymotic haemorrhages on the mucous membranes. Subclinical coagulopathy is common.
• 5.Severe cardiovascular collapse (shock, stupor, coma), with associated tachypnoea, tachycardia, and hypotension. Bradycardia may be present in the late stages of septic shock.

Diagnosis

• 1.Blood culture. A positive blood culture is definitive, but a negative culture does not rule out sepsis; periods of bacteraemia may be intermittent and brief.
• 2.Culture of other body fluids may be beneficial, e.g. transtracheal aspirates, cerebrospinal fluid, faeces, urine, and synovial fluid.
• 3.History (risk factors) that may predispose to sepsis includes placentitis or vulvar discharge in the mare, maternal problems during gestation, dystocia, low birth weight, and prematurity.
• 4.Clinical findings: foals with early disease may present with few and subtle signs; advanced disease may progress to shock and coma.
• 5.
  Complete blood count (haematology):

  • •
    Leucopenia (neutropenia) is common.
  • •
    White cell count may be normal early in the disease.
  • •
    Differential cell counts may be more useful than total cell count, e.g. relative neutropenia or neutrophilia, presence of band forms and toxic changes.
  • •
    Repeat cell counts are helpful.
• 6.
  Other laboratory findings:

  • •
    Hypoglycaemia.
  • •
    Metabolic acidosis.
  • •
    Low plasma immunoglobulin concentrations (FTPI).
• 7.Sepsis score includes historical, clinical, and clinicopathological information.

Treatment

• 1.
  Antibiotic therapy should be initiated as soon as possible. It is often prudent to suspect sepsis until proven otherwise.

  • •
    The initial choice of antibiotics should be broad spectrum with an emphasis on the Gram-negative spectrum.
  • •
    Changes in therapy can be made when and if culture and sensitivity results are available.
  • •
    Therapy should be long-term in an attempt to prevent localization of infection (secondary complications).
• 2.FTPI should be treated with immunoglobulin therapy (plasma).
• 3.
  Supportive care (see Chapter 26):

  • •
    Nursing care is critical.
  • •
    Regulate environmental temperature (provide heat source).
  • •
    Nutritional support; hypoglycaemia is often present; glycogen and fat stores are poor in the foal.
• 4.Address any underlying infections.
• 5.Cardiovascular support if needed.

Prognosis

• 1.Reported survival is in the range 30–80%.
• 2.Prompt recognition of sepsis and referral for appropriate treatment increases the prognosis.
• 3.Foals with multiple septic joints have a guarded prognosis for future athletic performance.

Prevention

Good management practices:

• •Clean environment.
• •Healthy mares.
• •Check quality of colostrum and monitor for FTPI.
• •Umbilical hygiene.

Shock (see Chapter 26)

Shock is inadequate cellular energy production that results in cell dysfunction and death. Rapid recognition and treatment for shock are important in the prevention of organ system failure. The recognition and treatment of shock in the foal do not differ significantly from those in the adult horse.

Classifications

It is rare for shock to be categorized under a single classification, but the following groupings are useful for categorizing the pathophysiology and treatment targets:

• 1.
  Distributive shock.

  • •
    Decrease in systemic vascular resistance resulting from maldistribution of vascular volume.
  • •
    Secondary to sepsis (septic shock), infection, strangulating intestinal lesions, anaphylaxis.
• 2.
  Cardiogenic shock.

  • •
    Failure of the heart to act as a pump.
  • •
    Congestive heart failure.
  • •
    Cardiac arrhythmia.
  • •
    Congenital heart disease.
• 3.
  Hypovolaemic shock.

  • •
    Blood loss.
  • •
    Third space loss.
  • •
    Severe dehydration.
• 4.
  Hypoxaemic shock.

  • •
    Severe pulmonary disease.
  • •
    Anaemia.

Clinical signs

• 1.
  Early, compensated phase of shock.

  • •
    Difficult to recognize.
  • •
    Hyperdynamic: injected mucous membranes, rapid capillary refill time.
  • •
    Tachycardia.
  • •
    Tachypnoea.
  • •
    Bounding pulses.
  • •
    Decreased perfusion to gastrointestinal tract and other organs.
• 2.
  Decompensated phase of shock.

  • •
    Prolonged capillary refill time.
  • •
    Cold extremities.
  • •
    Tachycardia may change to bradycardia.
  • •
    Irregular respiration.
  • •
    Poor pulse pressure.
  • •
    Abnormal mentation.
  • •
    Lack of urine production.

Treatment

• 1.
  Fluid administration is the single most important treatment for hypovolaemic and distributive shock.

  • •
    The goal of fluid therapy is to optimize the vascular volume and restore circulatory function and tissue perfusion.
  • •
    The most appropriate fluid choice is balanced electrolyte solution containing acetate or lactate (e.g. lactated Ringers solution, Hartmann's solution, Plasma-Lyte 148).
  • •
    Polyionic fluids remain effective in restoring vascular volume if the PCV remains greater than 20% and the total protein greater than 35 g/L.
• 2.Hypertonic solutions cause rapid, transient volume expansion; however, hypertonic saline solution is not recommended, as neonatal foals are unable to handle large amounts of sodium.
• 3.Colloid fluids (Hetastarch or plasma) may be needed in cases of low colloid oncotic pressure.
• 4.The rate of administration of fluids is variable; crystalloid fluids may be given in boluses of 20 mL/kg, the boluses being repeated if needed after clinical reassessment.
• 5.In severe cases as much as 90 mL/kg may need to be administered rapidly.
• 6.
  Inotropes and vasopressors may be needed if the foal does not respond to fluid therapy:

  • •
    Dobutamine can be used to increase cardiac output.
  • •
    Norepinephrine can be used to increase systemic vascular resistance and increase stroke volume.
  • •
    Vasopressin.
• 7.
  Anti-endotoxic therapy.

  • •
    Polymyxin B.
  • •
    Non-steroidal anti-inflammatory drugs (e.g. flunixin meglumine).
  • •
    Anti-endotoxin plasma.
• 8.In haemorrhagic shock, whole-blood replacement may be necessary if adequate response is not achieved with crystalloids only.
• 9.Intranasal oxygen if hypoxaemic shock exists. Mechanical ventilation may be needed in cases of severe pulmonary disease.

Perinatal asphyxia

This is a mutifactorial problem that develops secondary to impairment of tissue oxygen delivery. It is most commonly seen in the neonate shortly after birth when oxygen delivery to the tissues is interrupted (see ‘maladjustment syndrome’ in section 20.5 of this chapter).

Causes

• 1.
  Prepartum.

  • •
    Placental insufficiency.
  • •
    Premature separation of the placenta.
  • •
    Severe maternal disease.
• 2.
  Delivery.

  • •
    Dystocia.
  • •
    Caesarean section.
  • •
    Compression/torsion of the umbilical cord.
• 3.
  Postpartum.

  • •
    Severe cardiopulmonary disease in the foal.
  • •
    Premature separation of the placenta.
  • •
    Neonatal isoerythrolysis.

Pathophysiology

Two major mechanisms may result in cellular deprivation of oxygen, namely, ischaemia and hypoxaemia. Ischaemia (lack of blood flow) is generally more severe than hypoxaemia, because during hypoxaemia some blood flow and oxygen delivery persist. With a lack of blood flow, anaerobic metabolites are not removed from the tissues which may result in severe local and/or cellular acidosis.

Organ dysfunction

• •Central nervous system: encephalopathy associated with cerebral necrosis, oedema and haemorrhage, although consistent cerebral abnormalities have not been reported.
• •Renal: acute tubular necrosis.
• •Gastrointestinal ischaemic necrosis; necrotizing enterocolitis.
• •Cardiovascular and respiratory systems are less commonly affected.

Clinical signs

Signs range from mild depression/transient behavioural abnormalities to severe seizures and generalized organ failure. Many foals do not show obvious clinical signs until 12–24 hours of age. Disorientation, loss of suckle, and tongue protrusion are common physical exam findings.

Resuscitation

• 1.
  Airway:

  • •
    Ensure patent airway.
  • •
    Provide intranasal oxygen.
• 2.Breathing: if the foal is not breathing or if breaths are infrequent or shallow, provide mechanical ventilation with an endotracheal tube or mask (endotracheal tube is preferable).
• 3.Cardiovascular support and correction of metabolic disturbances (see previous section on the treatment of shock).

Treatment

• 1.
  Supportive care.

  • •
    Provide nutrition if unable to nurse.
  • •
    Prevent self-trauma.
• 2.Seizure control.
• 3.
  Prevent further brain injury.

  • •
    Osmotic agents.
  • •
    Magnesium sulphate.
• 4.Respiratory support if foal has hypoventilation.
• 5.Antimicrobial drugs to reduce the risk of bacterial translocation and septicaemia.

Prognosis

With appropriate care, prognosis is good (approximately 75%), although will worsen with severe organ dysfunction or concurrent disease (e.g. sepsis).

20.3. Diseases of the cardiovascular system (see Chapter 7)

Examination

Physical examination

Part of the physical examination of the newborn should include a complete assessment of the cardiac and respiratory systems.

Rate and rhythm

• 1.Immediately after delivery the heart rate is 60–80 beats/min, increasing to 120–150 within hours to stabilize at 80–100 in the first week of life.
• 2.Sinus dysrhythmias are frequently found on auscultation and ECG in the immediate postpartum period, probably as a result of increased parasympathetic tone and myocardial hypoxia. Physiological (functional) murmurs are typically crescendo/decrescendo in time (grade 1–3/6), with maximal intensity over the semilunar valves.
• 3.Other dysrhythmias (ventricular premature contractions, ventricular tachycardia, supraventricular tachycardia) are occasionally auscultated immediately after delivery, but they disappear within 15–30 minutes postpartum.
• 4.To determine the clinical significance of any dysrhythmia, consideration should be given to the clinical, metabolic and haemodynamic status of the foal.

Murmurs

• 1.Because of the foal's thin chest, the apex beat is quite prominent, and heart sounds and flow murmurs are louder than in the adult horse. Murmurs are frequent in newborn foals, and in general are not pathological (i.e. functional). In the immediate postpartum period (15 min) most foals have a continuous murmur from blood shunting through the ductus arterious. This represents a transition from the intrauterine fetal circulation in which there is pulmonary hypertension, to an extrauterine circulation in which there is a decrease in vascular resistance from alveoli opening and prostaglandin release.
• 2.Murmurs are often heard in newborn foals but are not considered pathological unless they persist beyond 4 days of age. Holosystolic ejection-type murmurs are not uncommon and most of the time are physiological (innocent flow murmurs), rather than due to a patent ductus arteriosus (PDA).
• 3.Innocent murmurs may acquire unusual tones if the foal is in lateral recumbency, or is haemodynamically compromised.
• 4.Functional closure of the ductus arteriosus occurs shortly after birth in most foals.
• 5.Murmurs that persist after the first week of age should be further investigated. Likewise, murmurs associated with cyanosis should be evaluated immediately.

Echocardiography

See Chapter 7.

Electrocardiography

See Chapter 7.

Congenital heart disease

See Chapter 7.

Ventricular septal defect (VSD)

This is the most common and important congenital cardiac defect in the foal. There appears to be a genetic basis for VSD as it is more often documented in Arabians, Standardbreds, and Quarter Horses. VSDs are often incidental findings when foals are evaluated for other conditions. Foals with VSDs can appear normal or present for depression, respiratory disease, cyanosis, or failure to thrive. There is a grade 3–5/6 harsh, pansystolic murmur, typically louder on the right side, below the tricuspids valve. A left base ejection murmur from pulmonic stenosis is often present. Older foals may develop congestive heart failure, with or without atrial fibrillation. The intensity of the heart murmurs is not associated with the severity of the VSD. Other murmurs and dysrhythmias may be present if the VSD is associated with other developmental abnormalities. VSDs are present in tetralogy of Fallot, pseudotruncus arteriosus, and occasionally in foals with ASDs and tricuspid atresia.

Patent ductus arteriosus (PDA)

Functional closure of the ductus occurs shortly after birth in most foals (up to 72 hours in some). PDA is a rare cardiac abnormality in foals; however, a left-to-right PDA should not be considered pathological if it persists for a few days postpartum in an otherwise healthy foal. In some cases, a left-to-right PDA may become apparent a few days after birth, in particular in foals with systemic disease. Sick and premature foals with pulmonary hypertension as well as foals of mares treated with prostaglandin inhibitors are prone to PDA. Typical findings of a left-to-right PDA include a continuous, machinery-type murmur, with a thrill over the pulmonary artery.

Atrial septal defect (ASD)

Atrial septal defects are rare in foals and are in general associated with other congenital anomalies. Small ASDs may have no clinical significance (except for performance horses). If the ASD is large, with left-to-right blood shunting, right-sided volume overload ensues, leading to pulmonary over-circulation and atrial fibrillation as the foal ages.

Tetralogy of Fallot

Four characteristic lesions of tetralogy of Fallot include: VSD, right ventricular outflow tract obstruction (pulmonic stenosis), dextroposition of the aorta with overriding, and right ventricular hypertrophy. Foals with this complex pathology are small and ill-thrift. PaO₂ is decreased, and cyanosis is variable. On auscultation there is a loud systolic murmur over the left side from pulmonic stenosis, with a palpable thrill. A machinery-type murmur can be present from continuous blood shunting if there is a PDA. Prognosis is poor.

Tricuspid atresia

Atresia of the tricuspid valve is usually associated with a patent foramen ovale, ASD, VSD, hypoplastic right ventricle, hyperplastic mitral valve and left ventricle. There is cyanosis from right-to-left shunting through the ASD or the foramen ovale. Most of these foals die at an early age from severe hypoxaemia. The ones that survive for several months often have a VSD. These foals are in poor condition, intolerant to mild physical activity, and cyanotic. On echocardiography there is dilation of the right atrium, a small tricuspid valve, and a small right ventricle.

Truncus arteriosus

This condition is rare in foals. Early in development there is a failure of the truncus arteriosus to divide into the aorta and pulmonary arteries. The aorta, pulmonary, and coronary arteries originate from the single truncus. Clinical signs depend on pulmonary blood flow. If pulmonary vascular resistance is low clinical signs might be mild, with no evidence of cyanosis. In contrast, increased pulmonary vascular resistance leads to decreased pulmonary blood flow and hypoxaemia. The foals can be normal or lethargic and in poor body condition. There is a systolic murmur, with or without cyanosis. On echocardiography a single truncus is identified.

Patent foramen ovale

In the foetus, oxygenated blood from the placenta flows back to the heart via the caudal vena cava to the right atrium, and then through the foramen ovale to reach the left atrium. Lung inflation after birth leads to a drop in pulmonary vascular resistance, closure of the ductus arteriosus, and obliteration of the foramen ovale. Anatomic closure in foals occurs between 15 days and 9 weeks postpartum. Clinical signs of patency of the foramen ovale are rare unless associated with other cardiac defects, or with persistent pulmonary hypertension (reversion to foetal circulation) from various pulmonary diseases.

Acquired cardiac defects

Acquired cardiac defects are uncommon in the foal. Inflammatory or degenerative changes may be identified at necropsy. See Chapter 7 for more detailed descriptions.

Pericardial disease

Diseases of the pericardium are rare in foals. Exudate accumulation within the pericardial sac occurs from inflammation of the pericardial and epicardial surfaces. Pericardial effusion can also be present in foals with evidence of systemic inflammation/sepsis.

Myocardial disease

In foals, myocardial disease is associated with ischaemia, hypoxia, septicaemia, metabolic diseases, nutritional deficiencies (white muscle disease), and respiratory diseases. In white muscle disease (vitamin E and selenium deficiency – see Chapter 21), in addition to muscle weakness, dysphagia, and respiratory dysfunction, some foals may develop a dilated cardiomyopathy. The role of viral infections in myocardial disease is unclear. The clinical presentation of myocardial dysfunction is variable but includes murmurs from valvular incompetency, arrhythmias, atrial and ventricular premature depolarization, exercise intolerance, congestive heart failure, and sudden death. Arrhythmias are a common manifestation of myocardial disease. Diagnostics should include electrocardiography, echocardiography, assessment of serum electrolytes, creatine kinase activity (MB isoenzyme if possible), lactate dehydrogenase, and measurement of cardiac troponin I concentrations. If there is dysphagia or muscle weakness, measurement of vitamin E and selenium should be considered. Myoglobin can be present in urine if there is severe myocardial necrosis.

Supraventricular and ventricular arrhythmias

These are more common in adult horses.

Acquired heart murmurs

These may be due to aortic insufficiency, mitral insufficiency, tricuspid insufficiency, or endocarditis in septic foals.

White muscle disease

See Chapter 21.

Pulmonary hypertension/cor pulmonale

This is right ventricular hypertrophy in response to pulmonary hypertension; it can develop in response to severe pulmonary disease, in newborns with reversion to foetal circulation, and in left-sided heart failure. See section on asphyxia above.

Congestive heart failure

Clinical signs may include jugular vein distension, ventral oedema, pulmonary oedema, nasal discharge, and ascites.

20.4. Diseases of the respiratory system (see Chapter 6)

Examination

Respiratory rate

Respiration should begin immediately after birth. The respiratory rate of the neonatal foal is approximately 60–80 breaths/minute in the immediate neonatal period, and declines to 30–40 breaths/minute within 1–2 hours after birth.

Palpation

Palpation of the thorax should be performed to determine whether fractured ribs are present. One must be careful when assessing fractured ribs as pulmonary damage (pneumothorax, haemothorax) and cardiac damage can be induced. Most fractures are in ribs 3–6, and crepitus or a clicking noise can be heard on auscultation.

Thoracic auscultation

Thoracic auscultation is not as reliable an indicator of lower respiratory disease in the neonate as in adults, because often only subtle changes in lung sounds are appreciable on auscultation, even in the presence of very severe pulmonary disease. An elevation of respiratory rate, increased effort, and abnormalities of breathing pattern (nostril flaring, an abdominal component to the respiratory pattern, respiratory stridor) are more appreciable than auscultatory changes in foals with respiratory disease.

Lung sounds

Lung auscultation in the period immediately postpartum reveals crackles as airflow increases in a fluid-filled environment.

Arterial blood gas analysis

Arterial blood gas analysis aids in the characterization of the cause of lower respiratory disorders and cardiovascular disease and assists in the most appropriate course of therapy as well as response to treatment.

Radiography

Radiography provides a good diagnostic method to assess the type and extent of pulmonary disease. Evidence of pulmonary disease in the immediate postpartum period indicates in utero infections, septicaemia, peripartum stress (meconium aspiration), or prematurity.

• 1.Bacterial pneumonias may be characterized by alveolar, bronchoalveolar, and/or interstitial patterns. There is not a pathognomonic radiographic pattern produced by viral diseases, although in adult horses often an interstitial pattern is typical.
• 2.Ventral distribution of pathological changes may be indicative of bacterial or aspiration pneumonia (bacterial, meconium, milk). If there evidence of aspiration pneumonia, a complete evaluation of the mouth (cleft palate) and upper airways is indicated.
• 3.A ‘cotton ball or nodular’ pattern in the mid to dorsal thorax in young foals suggests fungal pneumonia. In older foals (>3 months) this pattern can be consistent with interstitial pneumonia. Foals with interstitial pneumonia can also have a miliary interstitial pattern.
• 4.Premature or dysmature foals with evidence of pulmonary disease may have pulmonary atelectasis (“ground-glass” appearance), indicating decreased surfactant production and/or bacterial infection.

Depending on the clinical presentation, thoracic radiography should be performed before trans-tracheal aspiration as pneumo-mediastinum may develop after trans-tracheal aspiration.

Ultrasonography

Thoracic ultrasonography has become a routine diagnostic method in foals with evidence of respiratory diseases (respiratory distress, diaphragmatic hernias, haemothorax) and systemic diseases (fever, sepsis).

• 1.In the foal with pulmonary disease it is preferable to perform ultrasonography with the foal in sternal recumbency or standing. This is particularly important for conditions such as diaphragmatic hernia, haemothorax, and pleural effusion.
• 2.Rib fractures can be identified as disruptions of the cortical surfaces of the rib, above but not involving the costochondral junction. Hypoechoic regions in the adjacent lung surface indicate pulmonary trauma. Homogeneous, slightly echogenic (cellular) fluid within the thorax is consistent with haemothorax. Pleural effusion is variable, from hypoechoic fluid when cellularity is low, to a hyperechoic fluid that can be homogeneous or filled with cellular debris and fibrin. The presence of gas echoes (hyperechoic) in the pleural fluid indicates either a pulmonary laceration (haemothorax) or a pleuritis/pleuropneumonia with involvement of anaerobic microorganisms.
• 3.Ultrasonography, like radiography, is not specific in the identification of pulmonary parenchymal disease. Thoracic ultrasonography in young foals with pulmonary disease, regardless of the aetiology, often reveals non-specific findings. Artefacts such as ‘comet tails’ from excessive reverberation indicate roughening of the pleural surfaces. Cavitary lesions (abscesses) and pulmonary consolidation are often identified by ultrasound.

Transtracheal aspirate

• •The goal is to identify the aetiological agent and its antimicrobial sensitivity.
• •Cytology can help differentiate the type of inflammatory response.
• •The previous use of antimicrobial drugs decreases the success of a positive culture.
• •Common sense should be used: in foals with severe pulmonary disease performing a transtracheal aspirate may be contraindicated.
• •Perform after radiography.

Endoscopy

Endoscopy is indicated in upper-airway disease (obstruction, laryngeal dysfunction, guttural pouch disease) and malformations (cleft palate, laryngeal and tracheal malformation).

Thoracocentesis

Thoracocentesis is indicated in haemothorax, pneumothorax, and pleural effusion.

• •A short intravenous catheter is safer than a needle. Depending on the type of exudates, a larger-bore catheter or a teat cannula can be used.
• •Ultrasound guidance is preferable.

Lung biopsy

Percutaneous lung biopsy can be considered in conditions in which there is evidence of pulmonary parenchymal disease but routine diagnostic tests are negative. This is not a procedure routinely performed in young foals as its indications include pulmonary neoplasia and fungal pneumonia. Do not perform in foals with tachypnoea or evidence of poor ventilation, or in foals with infectious pulmonary disease. Haemothorax and epistaxis can develop after lung biopsy.

Respiratory distress syndrome (RDS)

Neonatal RDS, also known as hyaline membrane disease, is a respiratory disorder of premature/dysmature neonates in which there is pulmonary immaturity, with alveolar collapse, impaired alveolar gas exchange, hypoxaemia, hypercapnia, tachycardia, tachypnoea, and cyanosis. Reduced lung compliance and diffuse atelectasis are central to the pathogenesis of RDS.

Predisposing factors

• 1.
  Prematurity/dysmaturity.

  • •
    Surfactant is critical for alveolar function. In foals, surfactant production begins at 100–150 days of gestation, being complete in most foals by 290–310 days of gestation, but in some foals it may not be complete until delivery. This process is variable, and gestational age should not be used as an indicator of pulmonary maturation. Foals with normal gestation length and evidence of incomplete organ maturation (respiratory, musculoskeletal) are considered dysmature.
  • •
    Alveolar collapse and subsequent respiratory distress occur from the absence of surfactant.
  • •
    Additional complicating factors in premature/dysmature foals with pulmonary disease include excessive compliance of the chest wall with poor compliance of the lung parenchyma, making the foal work harder during inspiration, which can lead to diaphragmatic fatigue.
• 2.
  Decreased respiratory efficiency.

  • •
    Factors that lead to increased demand or fatigue.
  • •
    Failure to establish functional residual capacity shortly after birth.
  • •
    Increased vascular permeability, decreased surfactant, and oedema.
  • •
    Cardiac anomalies (VSD, PDA, tricuspid valve atresia).
  • •
    Gastrointestinal tympany (enteritis, meconium impaction), diaphragmatic hernia.
  • •
    Is not unusual for premature/dysmature foals or foals with peripartum hypoxia to have a decreased respiratory rate and abnormal breathing patterns.
  • •
    Viral or bacterial pneumonia.
• 3.Dystocia or other problems at or during foaling: premature placental separation, umbilical cord compression, fractured ribs, prolonged parturition, perinatal hypoxia.
• 4.Any condition that results in prolonged recumbency and atelectasis.
• 5.Reversion to foetal circulation.

Clinical signs

• •Flared nostrils, tachycardia, tachypnoea, and increased respiratory effort.
• •Auscultation reveals poor air movement.
• •Cyanosis may be present.
• •PaO₂ <50 mmHg. PaCO₂ >60 mmHg.

Treatment

• •Oxygen therapy alone is often not sufficient, and mechanical ventilation may be necessary.
• •Cardiovascular support and correction of metabolic disorders.
• •Treatment of the underlying condition and surfactant replacement in premature foals.
• •Glucocorticoid replacement therapy (hydrocortisone, dexamethasone) – with the rationale of increasing surfactant production – should be considered.

Meconium aspiration

Meconium is the first faecal material of the neonate and consists of ingested and intestinal epithelial cells, amniotic fluid, and mucus. The foetal lung is normally protected from aspiration by the continuous movement of fluids up the trachea. During vaginal delivery, compression of the thorax and closure of the glottis help prevent aspiration.

Aetiology

• •Under physiological conditions meconium is not evacuated before birth. In utero, asphyxia, foetal stress, or mechanical factors during delivery may result meconium release into the amniotic fluid.
• •Deep gasping or failure of protective mechanisms can result in aspiration.
• •Meconium obstructs airways, resulting in air trapping and atelectasis, mechanical irritation, and chemical bronchopneumonia.

Clinical signs

• •Meconium-stained foal with yellow-brown discoloration of the hair coat.
• •Brown-tinged nasal discharge.
• •Staining with meconium does not imply that aspiration has occurred, but therapeutic measures to prevent a potential pneumonia should be considered.

Treatment

• •Respiratory and nursing care as needed.
• •Antibiotics should be considered as secondary infections often occur.

Idiopathic tachypnoea and hyperthermia

This syndrome is seen in Arabian, Thoroughbred, Belgian, Friesian, and Miniature foals and is more frequent during hot and humid weather. The pathophysiology is unknown but may be related to a problem with the central control of thermoregulation and/or respiratory rate.

Clinical signs

• •Sudden onset of clinical signs in an apparently healthy foal.
• •Tachypnoea and fever (38.9–42.2°C, 102–108°F). The respiratory pattern may resemble panting, and the rate may be as high as 80 breaths/minute.

Diagnosis

• •Other causes of respiratory disease must be ruled out via a complete respiratory evaluation. All other values should be within normal limits.
• •Respiratory and systemic infections or pain must be ruled out.
• •Haematology, fibrinogen concentrations, and serum chemistry may aid in the diagnosis as in most cases, except for an increase in haematocrit and a stress leukogram, these are normal.
• •Metabolic acidosis and other causes of tachypnoea must be ruled out.

Treatment

• •Temperature control: provide a cool environment; body clipping; alcohol baths.
• •Antipyretics in general are not successful but should be considered.
• •Antibiotics should be used if there is suspicion of infection.
• •The condition usually resolves spontaneously in days to weeks.

Reversal to foetal circulation

This condition, also known as persistent pulmonary hypertension, is failure by the newborn foal to make the transition from foetal to extrauterine circulation.

Aetiology

There is right-to-left shunting through the foramen ovale and/or the ductus arteriosus, hypoxaemia, hypercapnia, and pulmonary hypertension. In neonates, pulmonary vascular resistance decreases, and pulmonary blood flow increases during and immediately after delivery. As gas exchange increases, pulmonary blood pressure decreases; however, a failure in the mechanisms that regulate the decrease in pulmonary blood pressure leads to hypertension. Reversal to foetal circulation can occur with intrauterine foetal diseases, premature placental separation, prematurity/dysmaturity, peripartum asphyxia, respiratory distress syndrome, meconium aspiration, severe sepsis, and pneumonia.

Clinical signs

There is a tachypnoea, nasal flaring in severe cases, and tachycardia with systolic murmurs of variable degrees. Cyanosis may be present.

Diagnosis

Clinical findings include respiratory acidosis, hypoxaemia, and hypercapnia. On echocardiography a persistent foramen ovale or PDA, with pulmonary artery dilation (with or without right ventricular hypertrophy), is a consistent finding of pulmonary hypertension.

Treatment

Treatment includes oxygen insufflation, correction of the respiratory acidosis, and mechanical ventilation in severe cases. Other treatments that have been proposed or used include vasodilators (prostacyclin, nitric oxide) and bronchodilators. Bronchodilators are controversial as they can induce ventilation/perfusion mismatch, worsening the clinical signs.

Upper respiratory tract (URT) disease

There are many causes of upper airway obstruction in the foal. However, the prevalence is low. Many obstructions of the URT are partial and may go unnoticed until the foal is exercised. A more thorough discussion of URT disease is found in Chapter 5.

Nasal passages and paranasal sinuses

• •Deviation of the premaxilla (wry nose).
• •Deviation or thickening of the nasal septum.
• •Epidermal inclusion cysts.
• •Paranasal sinus cysts.

Pharynx and guttural pouches

• •Retropharyngeal infection.
• •Persistent dorsal displacement of the soft palate.
• •Pharyngeal cyst.
• •Guttural pouch tympany.
• •Choanal atresia.
• •Pharyngeal collapse.

Larynx

Obstructive conditions involving the larynx of young foals are uncommon.

• •Unilateral or bilateral paresis or paralysis.
• •Fourth branchial arch defects.
• •Congenital laryngeal web defect.

Trachea

• •Tracheal rupture (traumatic).
• •Tracheal stenosis and tracheal collapse.

Viral diseases

See also Chapter 19.

Equine herpesvirus 1 (rhinopneumonitis)

Aetiology

• •EHV-1 is the main aetiological agent of herpes infections in foals.
• •Occasionally associated with EHV-4.
• •Infection occurs in utero or in the early postnatal period.
• •IMPORTANT: foals suspected of EHV-1 or any viral infection should be placed in quarantine immediately.

Clinical signs

• •Foals may be born normal and show acute onset of respiratory disease in the first days of life. A number of foals are born sick, weak, dysmature, depressed, with tachypnoea or respiratory distress.
• •The virus infects other systems, and signs of gastrointestinal disease (diarrhoea) and liver disease (icterus) may be present. Leukopenia with lymphopenia is common from lymphoid tissue necrosis.
• •Secondary bacterial infections are frequent in foals that live for a few days.

Diagnosis

• •Clinical history and findings. It can present as a single sick foal, as an outbreak of sick foals, abortions, or horses with respiratory disease.
• •Virus isolation (inconsistent).
• •Serology, using paired samples. This may not be practical as most foals die within days. Serology should be performed in the dam and other horses in the premises.
• •Polymerase chain reaction (PCR).
• •Histopathology: inclusion bodies in cells of the respiratory epithelium, liver, intestinal mucosa and adrenal gland; interstitial pneumonia; hypoplasia or necrosis of the thymus/spleen; and hepatic abnormalities. Immunofluorescence and immunohistochemistry.

Treatment

• •General nursing care.
• •Antibiotics to prevent secondary bacterial infections.
• •Antiviral drugs. Acyclovir and valacyclovir have been used in foals and adult horses. Valacyclovir has a better bioavailability than acyclovir.

Control measures

• •Disinfect or dispose of tools and instruments that have been in contact with sick horses.
• •Isolate sick foals and horses exposed to sick foals.
• •Follow appropriate isolation protocols.
• •Vaccinate non-exposed mature horses.
• •Designate specific personnel to work with pregnant mares to avoid cross-contamination.

Equine viral arteritis

As with EHV-1, the equine viral arteritis (EVA) virus infects foals at an early age or in utero; the mortality rate is high. Most cases of EVA occur in adult horses. Foals with EVA infections are weak, depressed, with evidence of interstitial pneumonia and enteritis. Preventive and medical practices are similar to those for EHV-1; however, treatment is restricted to nursing support; no antiviral drug is effective against the EVA virus.

See also Chapter 19.

Adenovirus

Adenoviruses are considered opportunistic, and infections occur in horses with a compromised immune system. Adenovirus infections are almost limited to Arabian foals with severe combined immunodeficiency. Occasionally critically ill immunocompromised foals may get infected by adenovirus.

Bacterial disease

Bacterial infections are a common cause of pneumonia in the neonate and older foals. In the neonate, pneumonia is commonly associated with septicaemia. Severe pneumonia or septicaemia may lead to pleuropneumonia.

Routes of infection

• •Placenta (placentitis); aspiration during birth; umbilicus.
• •Inhalation, especially in dusty, poorly ventilated environmental conditions.

Common pathogens

• •Gram-negative enteric organisms (Escherichia coli, Salmonella, Klebsiella, Citrobacter).
• • Actinobacillus, Pasteurella.
• • Streptococcus spp.
• • Rhodococcus equi (see Chapter 6).
• •Mixed infections often occur.
• •Anaerobes may be present in mixed severe infections.

Clinical signs

Variable and dependent on the severity of the infection and organs involved.

• •Elevated respiratory rate and fever are highly suggestive. The absence of fever should not rule out bacterial pneumonia.
• •Other signs that may or may not be seen: cough, nasal discharge, depression, mucous membrane changes.
• •In chronic disease: weight loss, unthriftiness, poor doing.

Diagnosis

• •Clinical signs.
• •Abnormal auscultation (crackles, wheezes); deep inspiration may be necessary to identify sounds; the absence of abnormal sounds does not rule out pneumonia.
• •Radiology: interstitial or alveolar pattern, consolidation, abscess(es), fluid accumulation.
• •Ultrasonography is particularly useful to evaluate the superficial lung fields and to assess the pleural space for fluid or exudate accumulation.
• •Transtracheal aspirates: cytology and culture.

Treatment

• •Appropriate antibiotic therapy based on culture and sensitivity.
• •
  Supportive care as needed which may include:

  • ▪
    Intranasal oxygen.
  • ▪
    Environmental temperature regulation.
  • ▪
    Bronchodilators.
  • ▪
    Non-steroidal anti-inflammatory drugs.
  • ▪
    Nutritional support.

Interstitial pneumonia

This is an acute, highly fatal syndrome of foals between 2 and 6 months of age, associated with respiratory distress; most foals die within one week.

Aetiology

• •Unknown.
• •Many agents have been implicated including viruses (influenza, EHV-1, -4, -5), fungi, plants, toxins, R. equi, heat stress, atypical response to bacterial disease, and an exaggerated immune response (hypersensitivity).

Clinical signs

• •These foals often are presented for respiratory distress.
• •Foals have fever, nasal discharge, increased and harsh lung sounds and wheezing, respiratory effort (expiratory primarily, abdominal component).

Diagnosis

• •History, physical examination.
• •Haematological changes are non-specific (leukocytosis, neutrophilia), and fibrinogen can be normal or increased.
• •Serology is non-specific.
• •Ultrasonography may reveal pleural roughening or pulmonary consolidation.
• •Radiography is the method of choice when there is diffuse interstitial infiltration. Some foals may also have a bronchoalveolar component (bronchointerstitial pneumonia). On radiography some lesions may look similar to those of fungal pneumonia or metastatic disease (structured pattern, cotton balls).

Treatment

• •Oxygen.
• •Glucocorticoids: systemic (dexamethasone, prednisolone) or inhaled (beclomethasone, fluticasone). This is central in the treatment for interstitial pneumonia.
• •Non-steroidal anti-inflammatory drugs.
• •Bronchodilators (clenbuterol, ipratropium, albuterol).
• •Appropriate antibiotic therapy based on culture and sensitivity.

Prognosis

• •Poor. Most foals with interstitial pneumonia die despite aggressive treatment.
• •Foals that recover from acute disease may develop chronic pneumonia.

Necropsy

• •Bronchointerstitial pneumonia, with pulmonary consolidation and atelectasis.

20.5. Diseases of the nervous system

See also Chapter 11.

Examination

The neurological examination should not be considered in isolation from that of the other body systems as it is part of the general physical examination. This is particularly important in newborn foals where systemic diseases can be associated with neurological dysfunction. As in adult horses, the neurological examination should begin with a good clinical history and assessment of the mental status, progressing to evaluation of the head (position, orientation, movement), cranial nerves, trunk, limbs, and motion. While standing, normal foals have a base-wide stance.

Signalment and history

A good clinical history is central in recognizing neurological disease in foals. Critically ill neonates are often weak, depressed or recumbent, and may show neurological signs secondary to other diseases. These foals must be differentiated from those with primary neurological disease. Important information in the clinical history includes duration of gestation, pregnancy problems, history of premature lactation or placental separation, complications at partum, time to get up and nurse, IgG concentrations, fever, trauma, and duration of clinical signs. Behavioural observation is also crucial as disorientation or lack of maternal recognition can be the first detectable sign of neurological disease in some foals.

Physical examination

An important aspect of the neurological examination is observation (behaviour, response to external stimuli, stance). Healthy foals keep the head in a flexed position, and their response to stimuli is quick, exaggerated, with jerky movements, and some foals may show disorientation.

Cranial nerve evaluation

Evaluation of the cranial nerves is performed as in the adult horse. However, a few normal variations should be kept in mind:

• •Immediately after birth the foal should have a strong righting reflex (withdrawal).
• •The palpebral reflex is present shortly after birth.
• •The menace response does not develop until several weeks of age; however, the foal should withdraw its head from a menacing gesture.
• •The pupillary light reflex is slow in foals.
• •Auditory response is present immediately after birth.
• •Suckle reflex is present 5–15 minutes after birth.
• •The capacity to swallow can be evaluated by observing the ability to nurse. Lip and tongue tone and recognition of the udder are also necessary for adequate nursing. If a foal appears to be nursing but large amounts of milk are seen coming from the mouth or nostrils, then a swallowing deficit should be considered (also cleft palate and white muscle disease).
• •Facial innervation is assessed by observation (facial symmetry, eye and eyelid positioning, ear positioning) and response to stimulation (reflexes).
• •The facial reflex evaluates trigeminal and facial innervation. A delayed response indicates lesions in the brain stem or in the nerve paths, which can be caused by CNS infection, trauma, or perinatal asphyxia.
• •The cervicofacial reflex evaluates cervical sensory and facial innervation. A delayed response indicates lesions in the cranial cervical spinal cord, brain stem, or the nerve paths.
• •Tongue tone should be strong in newborn foals.
• •The slap test is unreliable in foals.

Reflex testing

Testing of reflexes is very useful in localizing a spinal cord lesion.

• 1.It is important to keep in mind that neonates and young foals have a hyperreflexive response to stimulation (compared to adults).
• 2.In the pelvic limb, the patellar reflex, flexor, gastrocnemius and cranial tibial reflexes can be tested.
• 3.The patellar reflex is tested with the foal in lateral recumbency and the limb to be tested supported in relaxed flexion. A brisk extension of the limb (stifle) is expected when the patellar ligaments are struck with the side of the hand. This reflex involves the L4–L5 spinal segments and is mediated through the femoral nerve.
• 4.The pelvic limb flexor or withdrawal reflex involves the L5–S3 spinal segments and is mediated through the sciatic nerve. Pinching the skin of the distal limb, the coronary band or the bulbs of the heel should elicit a withdrawal of the limb and/or a central recognition of pain.
• 5.The gastrocnemius reflex is performed by bluntly striking the gastrocnemius tendon and observing for extension of the hock. This reflex involves spinal cord segments L5–S3 and is mediated through the tibial branch of the sciatic nerve.
• 6.The cranial tibial reflex is performed by holding the limb in relaxed extension and balloting the cranial tibial muscle. The expected response is flexion of the hock.
• 7.Reflex testing in the thoracic limbs includes evaluation of the flexor and triceps reflexes. The triceps reflex is tested by holding the limb in relaxed flexion and tapping the triceps tendon above its insertion at the olecranon. This reflex is mediated by the radial nerve through the cervical intumescence (C6–T1).
• 8.The flexor or withdrawal reflex of the thoracic limb is mediated through the last three cervical and first two thoracic spinal cord segments. The expected response is a flexion of the digit, carpus, elbow and shoulder. A response to pain should be observed.
• 9.
  Thoracolumbar lesions can be localized by evaluating the cutaneous reflex along the lateral body wall:

  • •
    Gentle pinching or poking of the skin along the lateral thorax elicits a twitching of the cutaneous trunci muscle.
  • •
    The sensory input is carried to the spinal cord at the level of stimulation. It then travels cranially in the spinal cord white matter to the last thoracic and first cervical segments and synapses with the lower motor neurons of the lateral thoracic nerve.
  • •
    The lateral thoracic nerve innervates the cutaneous trunci muscle. Damage to any portion of this pathway results in an absence of the cutaneous trunci reflex.
• 10.The perineal reflex evaluates the last sacral segments and the caudal spinal cord segments. Stimulation of the perineal area results in flexion of the tail and closure of the anus.

Gait

The gait of the foal should be examined for the presence of weakness, stiffness, and ataxia. The normal newborn foal has a choppy, hypermetric gait, and while standing it has a base-wide stance.

Ancillary diagnostic testing

Additional ancillary testing of the neurological patient includes blood analysis, radiography, cerebrospinal fluid analysis, myelography, computed tomography (CT), magnetic resonance imaging (MRI), electromyography, and electroencephalography (see Chapter 11).

Central nervous system disorders

Neonatal maladjustment syndrome (NMS)

The NMS represents a broad term associated with clinical manifestations of CNS dysfunction in newborn foals. Other terms used include dummy foal, wanderer, barker, hypoxic ischaemic encephalopathy, peripartum asphyxia syndrome, and neonatal maladjustment syndrome. NMS is the most common CNS disturbance in newborn foals. It is mportant to mention that NMS often manifests with involvement of other organs (gastrointestinal, renal).

Clinical signs

Clinical signs are variable and range from disorientation and inappropriate nursing behaviour to seizures and coma. Foals may wander, exhibit blindness, star gaze, or infrequently produce abnormal vocalizations. Some foals may appear normal at birth but exhibit CNS signs at 12–48 hours of age.

Diagnosis

Specific criteria have not been established. However, it is generally the working diagnosis for a foal exhibiting CNS signs without any other specific neurological disease.

• •The history often suggests a problem during late gestation, parturition or immediately post-foaling.
• •Blood analyses are non-specific. Elevated creatinine may suggest placental insufficiency.
• •Sophisticated neurodiagnostic techniques (CT scans and/or MRI scans) may be helpful, if available.

Aetiopathogenesis

The aetiology remains unclear. It has been proposed that impaired oxygen delivery before, during or after birth, with subsequent hypoxic–ischaemic injury to the CNS, is the primary cause of the syndrome.

• •Intracranial haemorrhage as a result of excessive pressures during foaling may be a causative factor.
• •Impaired oxygen delivery may result from placental problems before birth (placental separation, placentitis, maternal diseases), problems during birth (dystocia, umbilical cord compression, etc.) or postpartum events (isoerythrolysis).
• •Most of the brain damage occurs subsequent to the hypoxia during the period of reperfusion (12–24 hours after the initial insult). Oxygen deprivation leads to abnormal membrane ion gradients, with excessive sodium and calcium influx (cytotoxic). In addition, the production of free radicals (reperfusion injury), activation of N-methyl-D-aspartic acid (NMDA) receptors by excitatory neurotransmitters (glutamate) with subsequent calcium influx, and decreased NMDA receptor blockade by magnesium have been proposed. These events lead to neuronal death.
• •Foals with NMS are prone to sepsis for several reasons. Often they do not nurse because of neurological dysfunction, missing the timing for immunoglobulin absorption. If the NMS is the result of premature placental separation it is also likely that there was premature lactation and therefore no colostrum. If the cause was the result of hypoxia during or immediately after birth it is also possible that there was hypoxia to the intestinal tract, leading to epithelial denudation and bacterial entrance. A combination of these processes is common.

Treatment

Treatment is symptomatic and supportive:

• •Control seizures. Diazepam (5–10 mg IV) or midazolam (0.1–0.4 mg/kg IV) are good initial choices as they work fast and are safe. Long-acting anticonvulsants such as phenobarbitone or phenytoin may be necessary as the duration of benzodiazepines is short. Phenobarbitone (2–10 mg/kg IV, over 15–20 min) is administered until seizures are controlled; it may not be necessary to repeat this for 12–24 hrs as it has a long half-life. Phenytoin is administered at 5–10 mg/kg IV q 6 h.
• •Non-steroidal anti-inflammatory drugs (flunixin meglumine), antioxidants (vitamin E), free-radical scavengers (DMSO), magnesium sulphate, mannitol, thiamine, and more recently ketamine have been recommended.
• •Fluid and nutritional support (fluids should be administered cautiously as excessive fluid therapy may worsen cerebral oedema).
• •Supportive care, including antimicrobials.

Prognosis

Prognosis is dependent upon the degree of hypoxic damage:

• •If severe, rapid death may ensue.
• •If neurological signs are not severe or can be controlled, then the prognosis is good if nursing care is adequate and secondary complications can be avoided.
• •Additional complications from systemic hypoxia, including gastrointestinal disease (enterocolitis, ileus, septicaemia) or renal disease may complicate the outcome.
• •In general, the athletic future of foals that recover is not impaired.

Developmental disorders

See Chapter 11.

Hydrocephalus, anencephaly, spina bifida, meningomyelocele, hemivertebra.

Bacterial meningoencephalitis (septic meningitis, suppurative meningitis) (See Chapter 11)

• •Meningitis may occur in foals with septicaemia (haematogenous).
• •Often these foals have a failure of transfer of passive immunity.
• •The clinical signs are variable but may include fever, depression, weakness, ataxia, disorientation, seizures, and cranial or spinal-cord nerve deficits. Similar signs may be present in foals with other neurological conditions (hypoxia, trauma).
• •Aetiology: Escherichia coli, Salmonella spp, Actinobacillus spp, Enterobacter spp, Klebsiella spp, Pseudomonas spp, Streptococcus spp and Rhodococcus equi in older foals.
• •The incomplete blood–brain barrier in the neonate favours bacterial invasion.
• •The presence of bacteria in the CNS leads to inflammation and development of the clinical signs.
• •Diagnosis: clinical findings and collection of cerebrospinal fluid (CSF) for cytology and culture are necessary for an appropriate diagnosis and subsequent treatment.
• •Treatment: medical support, control seizures (diazepam, midazolam, phenobarbitone), non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen), and antimicrobials. Proper antimicrobial selection depends on bacterial sensitivity and antimicrobial properties. Most infections are caused by Gram-negative bacteria. Aminoglycosides and penicillins have poor CNS penetration unless there is extensive meningeal inflammation; third-generation cephalosporins (ceftiofur, ceftriaxone, ceftazidime), chloramphenicol, and trimethoprim–sulfonamides have good CNS penetration. If leucocyte count in the CSF is elevated, regardless of culture and Gram-staining results, a good initial option is a third-generation cephalosporin. The use of glucocorticoids remains controversial but should be considered in foals with evidence of severe inflammation.

Viral encephalitis (EHV-1)

EHV-1 is a rare cause of diffuse cerebral disease in the neonate.

Vascular disorders

Meningeal or parenchymal haemorrhages of the CNS can result in a variety of neurological signs depending on the location and severity. The aetiology is variable and includes metabolic disturbances, trauma, hypertension, endothelial dysfunction (sepsis, vasculitis), and blood-flow abnormalities.

Liver disease

See Chapter 3 and the hepatobiliary diseases section, below. Relevant diseases include hepatic encephalopathy, Tyzzer's disease, and portosystemic shunts.

Juvenile idiopathic epilepsy (See Chapter 11)

Juvenile idiopathic epilepsy is a neurological condition of Arabian foals. Most foals show clinical signs in the first week of life, but it has been reported in foals up to 6 months of age. Typical signs include disorientation, tonic and clonic motor activity, unconsciousness, and blindness. The aetiology of idiopathic seizures remains unknown, but is more often reported in Egyptian Arabian foals, suggesting that it is heritable. Seizures can be controlled in the short term with benzodiazepines, but for the long term phenobarbitone or potassium bromide should be considered. Seizures usually cease by the time the horses is one year old.

Lavender foal syndrome

Coat colour dilution lethal, also known as the lavender foal syndrome (LFS), is a genetic disease of Egyptian Arabian foals characterized by inability to stand, weakness, recumbency, tetany, epilepsy, and death. The coat colour in these foals ranges from a dilute lavender to a pale chestnut. Most of the foals show neurological signs immediately after birth. This is in contrast to juvenile idiopathic epilepsy, another neurological disease of Egyptian Arabian foals, in which clinical signs show days or months after birth, and have no coat colour dilution. The other difference is that LFS is lethal, whereas most foals with idiopathic epilepsy survive with proper treatment.

LFS is a pathological condition of autosomal recessive inheritance caused by an inactivating mutation of the myosin Va (MYO5A) gene. Myosin Va is important in the movement of organelles and secretory granules in neurons and in melanosome transfer to keratinocytes. LFS should be suspected in any Arabian foal presented for weakness, inability to stand, neurological disease, and coat colour dilution. There is no treatment, and these foals die hours or days after birth or have to be euthanized.

Narcolepsy–cataplexy

• •Narcolepsy, also known as the fainting disease, is a neurological disorder characterized by cataplexy (acute loss of muscle tone) and sleep. In foals, the condition primarily occurs in Suffolk horses (Suffolk Punch) and Shetland ponies, indicating that it is inherited. Occasionally it may present in other breeds. It is believed that complete inhibition of skeletal muscle tone during acute sleep episodes is associated with abnormal function of the sleep–awake centre. In horses, episodes of cataplexy can be triggered by grooming, initiation of various activities, changes in environment, etc. Information on the pathogenesis in foals or horses is limited.
• •In general, clinical signs present in foals several months old. The foal may show weakness, or collapse. Sleep cycles can last from seconds to 10–15 minutes, and foals are normal between episodes.
• •The diagnosis is clinical as most laboratory and imaging tests are non-diagnostic. Electroencephalography may assist in confirming the diagnosis, although this is a low-yield test. The physostigmine provocation test (0.05–0.1 mg/kg IV over 10 minutes) may precipitate episodes of cataplexy 3–10 minutes after administration in adult horses, but the effect in foals is unknown. Any condition associated with acute collapse, in particular heart disease, should be considered. Cerebral damage from peripartum hypoxia may produce similar signs in some foals. Imipramine (0.5–1.0 mg/kg IV) has been used in adult horses to treat narcolepsy with variable success. Atropine sulphate (0.04–0.08 mg/kg IV) may provide temporary control for up to 24 hours. Foals with early-onset narcolepsy (Thoroughbreds and miniature breeds) may recover, whereas in ponies the frequency of episodes may decrease although the condition persists throughout life.

Other causes of CNS disease

See Chapter 11.

• •Toxins.
• •Trauma.
• •Rabies.
• •Parasite migration.
• •Heat stroke.
• •Lightning strike.
• •Leukoencephalomalacia.
• •Metabolic disorders.
• •Equine degenerative myeloencephalopathy (EDM).
• •Tetanus.

Cranial nerve disorders

Visual dysfunction

• 1.Assessment of vision. Assessment of vision in the neonate is difficult as the menace response is not easy to evaluate. Signs of blindness may include attempts to nurse from incorrect sites, walking into obstacles, and signs of disorientation.
• 2.
  Causes of blindness.

  • •
    Diffuse cerebral disease can result in bilateral blindness, usually with other signs of cerebral dysfunction.
  • •
    Postictal blindness may occur subsequent to seizures.
  • •
    Acute trauma, leading to cerebral lesions or optic nerve compression or avulsion.
  • •
    Severe uveitis in septic foals may lead to blindness.
  • •
    Congenital diseases, including stationary blindness, optic nerve hypoplasia, ocular dysgenesis, retinal dysplasia, microphthalmia, and cataracts.
• 3.
  Congenital stationary night blindness. This is a poorly understood condition that is most commonly seen in the Appaloosa but has been reported in other breeds including Thoroughbreds and Paso Finos.

  • •
    Visual impairment varies from poor vision during reduced light conditions during the day with blindness at night.
  • •
    A history of poor vision and an abnormal fundus allow for a presumptive diagnosis.
  • •
    Other clinical signs may include dorsal medial strabismus, nystagmus, mild microphthalmia and holding the head in a ‘stargazing’ position when attempting to visualize objects.
  • •
    In the Appaloosa this disease appears to be recessive and associated with the leopard complex of coat patterns, thus supporting a defect in neural crest cell (rods, melanocytes) migration during development.
• 4.Anterior segment dysgenesis. This is a condition described primarily in Rocky Mountain and Saddlebred horses, in which there is congenital megalocornea, ciliary and retinal cysts, hypoplastic iris, cataracts, and retinal detachment. Most of the time this condition goes unnoticed unless signs of visual impairment are detected.

Other cranial nerve abnormalities

See Chapter 11.

Cerebellar disease

See Chapter 11.

• 1.
  Cerebellar abiotrophy.

  • •
    Cerebellar abiotrophy is the most common cerebellar disease in foals. It is a congenital disease of Arabian foals, with no gender predilection. Most foals develop clinical signs after 1 month of age, rarely immediately after birth. At birth the cerebellum appears to be normal in size, with normal neurons; however, as the foal ages there is degeneration and depletion of the Purkinje cells. The exact mechanism for the development of cerebellar abiotrophy is unknown, but decreased trophic stimulation and free radical injury have been proposed. In foals with severe disease the cerebellum is small.
  • •
    Clinical signs include head tremors that worsen with external stimulation or blindfolding (intentional tremors), progressive ataxia, wide-based stance and gait, dysmetria with a hypermetric goose-stepping gait, hypometria, spasticity, inability to perform precise movements (apprehension, nursing), delayed or absent menace response, falling over, and inability to stand in severe cases. There are no changes in mentation, and nystagmus is rarely observed. These foals eventually have to be euthanized.
  • •
    The diagnosis is clinical and post-mortem. The cerebellum can be normal or small in size, and on histology the Purkinje cells are absent or decreased in number. A genetic test to detect carriers is currently available (University of California Davis Genetics Laboratory).
  • •
    A syndrome similar to cerebellar abiotrophy has been reported in Gotland ponies, Australian ponies, and Oldenberg foals.
• 2.
  Other cerebellar diseases.

  • •
    Cerebellar hypoplasia has been reported in Haflinger, Arabian and Thoroughbred foals. A condition similar to the Dandy–Walker syndrome (midline cerebellar defect with cystic dilatation of the fourth ventricle, partial absence of the vermis) has been documented in Arabian and Thoroughbred foals. These foals are abnormal from birth, with difficulty rising, seizures, and absent suckle reflex, and their forehead may be domed. A progressive degenerative cerebellar disease has been reported in Thoroughbred and Paso Fino foals.

Ataxia or paresis of the limbs (See Chapter 11)

Different conditions can be associated with ataxia or paresis in foals, including infections, trauma, and brain, spinal cord, and nerve diseases.

Spinal cord and vertebral trauma

Trauma to the vertebral column, with or without vertebral fracture, is relatively common in the foal.

• •Physical examination may identify external signs of trauma, such as skin abrasions, swellings or haematomas, epistaxis and haemorrhage from the ears. However, it is not uncommon to find no external evidence of trauma. With cervical trauma, neck pain may be present.
• •Neurological signs may include varying degrees of ataxia and/or paresis to paralysis. A combination of thoracic limb extensor hypertonia and pelvic limb paralysis (Schiff-Sherrington phenomenon) has been reported with caudal thoracic vertebral fracture.

Vertebral osteomyelitis

Aetiopathogenesis

This disorder involves the systemic spread of bacteria which localize in the vertebrae, leading to vertebral pain and spinal cord compression as the condition progresses. Meningitis may be present. The history includes a previous infection, although this is often not noticed. In foals with septicaemia, Gram-negative bacteria (Escherichia coli, Salmonella spp.) are the most common cause of osteomyelitis. In older foals, Gram-positive organisms (Streptococcus) are more likely to be isolated. Rhodococcus equi is a common cause of osteomyelitis in endemic areas.

Physical examination

There may be a stiff neck, neck or back pain, fever, depression, and/or unthriftiness.

Neurological examination

• •If spinal cord compression is present then paresis/paralysis or ataxia may be seen.
• •Areas of hypo- or hyperreflexia, patches of sweating, lordosis, kyphosis, or scoliosis may be seen.

Diagnosis

• •Radiographs may reveal bony changes; however, osteomyelitis is often not identified early in the disease.
• •CT or MRI, if available, are great imaging modalities.
• •Cerebrospinal fluid analysis may identify a neutrophilic pleocytosis.
• •Scintigraphy may aid in localizing the lesion.

Occipitoatlantoaxial malformation (See Chapter 11)

This condition is primarily reported in Arabian foals but it also has been reported in Quarter Horses, Appaloosas, Standardbreds, Morgans, and miniature horses. It appears that the condition in Arabian horses is congenital. The atlas is fused to the occipitus, and its caudal aspect is rounded, while the axis looks more like the atlas. Clinical signs are primarily the result of spinal cord compression, typically spastic paresis, and the neck can be flexed or extended, but in a fixed position. On palpation there is no movement of the atlanto-occipital joint. Radiography reveals a malformation, and in general myelography is not necessary.

Myoclonia / myotonia

A form of stimulus-induced inherited myoclonia has been documented in Peruvian Paso Fino foals. Inactivation of the glycine receptor is believed to be responsible for this condition. Congenital myotonia occurs in a number of equine breeds, including Quarter horses and Ponies. A mutation in a chloride channel was documented in a New Forest pony.

See also Chapter 11.

Paresis or paralysis of one limb

See also Chapter 11.

Plexus and peripheral nerve trauma

Aetiology

Trauma to the brachial or lumbosacral plexus occurs most frequently at birth (during difficult deliveries) but can be caused by other physical accidents. The clinical signs are associated with the location of the lesion, type of injury, number of nerves involved, and severity of nerve damage (neuropraxia, axonotmesis, and neurotmesis). Neuropraxia is a mild nerve injury (concussion), with interruption of nerve conduction, but is reversible (days, weeks). In axonotmesis there is loss of axonal continuity with myelin layer disruption (more severe than neuropraxia), leading to Wallerian degeneration, with loss of motor and sensory function that can be reversible or not (weeks to months). Neurotmesis is a severe lesion leading to denervation.

Clinical signs

Signs include unilateral or bilateral hypotonia with depressed or absent reflexes, limb dragging, inability to get up or stand. If there is major involvement of motor innervation, muscle atrophy can become evident in 1–2 weeks.

Diagnosis

This is by physical examination, neurological examination, and assessment of motor and sensory activity. Signs include unilateral or bilateral hypotonia with depressed or absent reflexes, limb dragging, or inability to get up or stand. On electromyography, prolonged insertional activity with fibrillation potentials indicates muscle denervation of >7 days. Nerve conduction can also be evaluated in peripheral nerves. Depending on the location of the lesion, radiography should be considered to assess the extent of the lesion and to rule out fractures.

Treatment

• •Non-steroidal anti-inflammatory drugs, glucocorticoids in the acute stage.
• •Physical therapy.
• •Splints may allow the foal to bear weight and prevent limb contracture and additional trauma.

Prognosis

The prognosis is dependent upon the location and severity of trauma. Spinal root injury has a worse prognosis than plexus or peripheral nerve injury.

Other diseases of the nervous system

See Chapter 11.

Botulism (shaker foal syndrome)

See Chapter 11.

Aetiology

• •Botulism is a progressive muscular weakness caused by a Gram-positive, anaerobic, exotoxin-producing rod, Clostridium botulinum, a microorganism ubiquitous to the soil.
• •Botulinum toxin is a neurotoxin that blocks the release of acetylcholine from the motor endplate at the myoneural junction causing muscular paralysis.
• •There are seven neurotoxins identified: A, B, C, D, E, F, and G. In the USA, particularly in the mid-Western states and mid-Atlantic seaboard, most cases are caused by type B toxin. Type A botulism is primarily reported on the west coast. Type C is associated with decomposing carcasses and is less frequent. Types B, C and D have been reported in Europe.
• •In foals, the disease results from the ingestion of preformed toxin or toxin production from the organism within the body. Necrotic lesions within the gastrointestinal tract may allow colonization; umbilical infections as well as wounds are other possible foci of infection.

Pathogenesis

• •In foals, typically there is ingestion of spores which then produce toxin in the gastrointestinal tract. Unlike adult horses, the toxin can be detected in the faeces of 30% of foals. The toxin gets access to terminal ends and may travel to the CNS by retrograde axonal transport.
• • C. botulinum toxin comprises a light and a heavy chain. The light chain is an endopeptidase that interferes with acetylcholine release by inhibiting proteins necessary for the fusion of synaptic vesicles to the neuromuscular junction. The binding of the toxin is irreversible, and therefore resolution of the clinical signs is dependent on the synthesis of new endplates.

Clinical signs

• •Foals at any age can be infected, but they are usually more than 1 week of age.
• •Presentation varies with the amount of toxin ingested or elaborated.
• •The toxin produces a flaccid neuromuscular paralysis.
• •Affected foals are centrally bright and alert. The initial signs include a stiff gait, with the foal spending only short periods standing, and/or dysphagia (milk dripping from the sides of the mouth). The foal may progress to trembling or shaking when standing to total paralysis. Some foals may present for respiratory disease from aspiration pneumonia. If severe, respiratory failure and rapid death may occur from diaphragmatic paralysis.

Physical examination

• •Foals are bright and alert and typically afebrile unless there is a secondary infection.
• •There is a flaccid neuromuscular paralysis, trembling, poor eyelid, tongue and tail tone.

Diagnosis

• •Presumptive, based on clinical signs.
• •Demonstration of C. botulinum spores or the preformed toxin in the gastrointestinal content would be ideal, but this rarely is possible despite clinical evidence of the disease.
• •Attempts to identify the toxin in peripheral blood have been unsuccessful.
• •Toxin can be identified in necrotic wounds.
• •The mouse bioassay is the most sensitive method available to look for the presence of the toxin in serum.

Differential diagnosis

• •Any neurological disease associated with weakness.
• •White muscle disease.
• •Electrolyte abnormalities.
• •Cleft palate (no evidence of muscle weakness).
• •Hyperkalaemic periodic paralysis.

Treatment

• •Potassium or sodium penicillin (22 000–44 000 IU/kg IV QID) or metronidazole (20 mg/kg PO TID–QID). Caution must be taken when using drugs that may potentiate neuromuscular blockade (aminoglycosides, procaine penicillin, tetracyclines). Aminoglycosides may be necessary in foals with secondary infections.
• •Good nursing and supportive care are essential. A nasogastric tube may be placed for feeding.
• •Polyvalent antitoxin greatly increases the chance of survival, although it is very expensive. Alternatively, in regions where the most common type of botulism is known, monovalent antitoxin is a great alternative.
• •Assisted ventilation may be necessary if respiratory paralysis has developed.

Prognosis

• •Dependent on the severity. If severe and treatment is not aggressive, mortality is high.
• •Mild cases can recover without antitoxin therapy, but antitoxin enhances the chance of survival.
• •Severe cases can have a good prognosis if therapy is aggressive (mechanical ventilation, antibiotics, nutritional support, and meticulous nursing care).

Prevention

• •Vaccination of mares with C. botulism toxoid to provide colostral immunity in endemic areas. A type B toxoid is available in the United States. Type C and D toxoids have been evaluated in Switzerland. It is recommended to vaccinate mares in the last trimester of gestation with two additional doses 2–4 weeks apart.
• •If mares are unvaccinated then foals can be vaccinated early in life.

Tetanus

See Chapter 11.

20.6. Musculoskeletal disease

See Chapters 15, 16 and 17Chapter 15Chapter 16Chapter 17.

Examination

• 1.In the newborn foal, examination of the musculoskeletal system evaluates maturity and/or gestational age. Floppy ears, absence of hair or a silky hair coat, and joint laxity can indicate immaturity, prematurity or dysmaturity.
• 2.Assessment for birth trauma involves palpation for rib, mandible, or limb fractures as well as any soft tissue injury.
• 3.Congenital abnormalities include flexural and angular limb deformities, lateral luxation of the patella, prognathia/brachygnathia, wry nose, polydactyly, kyphosis, and scoliosis.
• 4.Careful palpation for lameness, joint effusion, physeal pain/swelling, and heat over joints is critical as neonates are at risk of septic arthritis.

Incomplete cuboidal bone ossification

Radiographs are needed to diagnose incomplete ossification (Figure 20.2). Manage with strict exercise restriction until there is evidence of adequate ossification. Splints or casts may be used for cases of severe laxity, but do not incorporate the foot in the splint.

Fractured ribs

Fractured ribs (dystocia or trauma at birth) are one of the more frequent injuries in the newborn foal, although brachial plexus injuries and ruptured gastrocnemius tendons/muscle are seen occasionally.

• •Fractured ribs may be bilateral but usually involve one side of the rib cage only.
• •A single rib may be fractured, but multiple ribs are usually involved.
• •Dislocations at the costochondral junctions may occur, and are of less clinical concern as the surrounding structures are usually left undamaged.
• •Multiple dislocated rib fractures are easily identified, causing pain, swelling, and/or a flail chest.
• •Careful palpation of the thorax can identify individual and non-displaced fractures. Swelling or crepitus may be present. Auscultation may reveal a rubbing sound.
• •Fractured ribs may be difficult to identify radiographically. Ultrasound is useful to assess whether fractures are displaced, and to monitor healing.
• •The importance of identifying fractured ribs should not be underestimated as they can result in numerous life-threatening complications.
• •Internal fixation may be needed for multiple rib fractures or displaced rib fractures that cause respiratory compromise.

Brachial plexus injuries and tendon ruptures

Clinical signs of brachial plexus injuries vary with the severity of injury. However, they generally result in some degree of radial nerve paralysis. The foal is unable to bear weight on the limb and is unable to extend the carpus or digit. Rupture of the gastrocnemius muscle can occur during foaling and is identified as a swelling above the hock in the area of the gastrocnemius muscle. A complete disruption of the gastrocnemius allows flexion of the hock when the stifle is in an extended position. Ultrasonography identifies muscle tearing.

Angular limb deformities

See Chapters 16 and 17Chapter 16Chapter 17.

Angular limb deformity (ALD) is deviation of the limb from the normal axis in the frontal plane.

• •Carpal valgus is the most common form of ALD.
• •Perinatal factors include soft-tissue/ligamentous laxity and incomplete ossification of the cuboidal bones.
• •Developmental factors include unbalanced nutrition, uneven weight-bearing, and excessive exercise or trauma.

Flexural limb deformities

Flexural limb deformity (FLD) is deviation of the limb from the normal axis in the sagittal plane and can be either hyperflexion or hyperextension.

• •FLD may be due to congenital or acquired factors.
• •Abnormalities at the distal interphalangeal, metocarpophalangeal, metatarsophalangeal and carpal joints are most common.
• •Treatment for hyperextension consists of controlled exercise, protection of soft-tissue structures, and shoes with heel extensions.
• •Treatment for hyperflexion in the neonatal foal consists of physical therapy, bandages, splints or casts, and oxytetracycline.

Septic arthritis

Septic arthritis in foals is most often haematogenous in origin and results in joint effusion, pain, and lameness.

• •Joint fluid analysis usually reveals increased leukocyte count (>10 000/µL, and typically >30 000/µL with >90% neutrophils) and elevated total protein (>4 g/dL).
• •Cultures of synovial fluid and blood are recommended.
• •Treatment consists of joint lavage, local and systemic antimicrobials, and pain management.

Hyperkalaemic periodic paralysis

See Chapter 21.

20.7. Diseases of the alimentary system

Examination

Physical examination

• 1.External abdominal palpation. This can be of diagnostic benefit in small foals as impactions or other masses may occasionally be palpated.
• 2.Abdominal auscultation. Gastrointestinal sounds (borborygmi) can normally be heard on both sides of the abdomen. Fluid sounds may indicate enteritis. Gas distension can be confirmed by percussion with a resulting ‘ping’.
• 3.Ballotment can be useful for determining the presence of free abdominal fluid.

Clinical pathology

Leukopenia, hypoglycaemia and metabolic acidosis are common findings in foals with enteritis.

Nasogastric intubation

Nasogastric intubation should be part of the assessment in foals with colic with or without abdominal distension. The gastric content can be variable, from a normal white–yellowish material to a dark–haemorrhagic content in foals with severe enteritis. In some instances the gastric content can be submitted for bacterial culture (Salmonella spp., Clostridium spp.).

Radiography

• 1.Useful in cases of gastric reflux, abdominal distension, or signs of colic.
• 2.Abdominal radiographs are most easily taken with the foal in a standing position, although left or right lateral recumbency views are possible in small foals.
• 3.
  Abnormal radiographic findings:

  • •
    Gas/fluid distension: ileus or intestinal displacements with resultant obstruction (intussusception, meconium impaction, congenital malformations).
  • •
    Free peritoneal fluid: fluid lines can often be seen in standing radiographs.
  • •
    Free peritoneal gas (pneumoperitoneum): may indicate gastrointestinal rupture.
• 4.
  Contrast studies are useful in certain cases of suspected gastrointestinal obstruction (duodenal strictures) or gastrointestinal ulceration.

  • •
    Withhold food 4–12 hours or empty the stomach by nasogastric intubation prior to the study.
  • •
    Barium sulphate suspension: 5 mL/kg via nasogastric tube.
  • •
    Radiographs should be taken at 1, 15 and 30 minutes, then every 2 hours until the barium has passed the area of interest.
  • •
    Barium should have left the stomach within 2 hours in a normal foal. Delayed gastric emptying can indicate pyloric outflow obstruction. However, sick foals may have delayed gastric emptying due to decreased gastrointestinal motility.
  • •
    Barium swallow may be performed if oesophageal disease is suspected. Administer 100–120 mL barium sulphate suspension (liquid or paste) via dose syringe. This is contraindicated if oesophageal perforation or dysphagia is suspected.
  • •
    Barium enema can be useful in diseases of the distal gastrointestinal tract such as atresia coli or other obstructive lesions (meconium impaction). Barium sulphate (180 mL) suspension is administered via an enema tube, and radiographs are taken immediately.

Ultrasonography

Ultrasound examination of the abdomen is useful for the evaluation of the bladder, umbilicus, kidneys, spleen, liver and gastrointestinal tract, as well as to look for the presence of peritoneal fluid.

• •Free peritoneal fluid is dark and anechoic. Increased echogenicity may indicate peritonitis or gastrointestinal rupture. Presence of large amounts of anechoic fluid is highly suggestive of a ruptured bladder.
• •An intussusception can sometimes be diagnosed with ultrasound by identifying the characteristic bulls-eye appearance on cross-section.
• •Small intestinal distension caused by obstruction or ileus can also be identified with ultrasound.
• •Assessment of intestinal wall thickness is important when assessing enteritis. In older foals this is important in the diagnosis of various forms of protein-losing enteropathies, including proliferative enteropathy caused by Lawsonia intracellularis.

Endoscopy

Endoscopic examination is useful to evaluate the oesophagus, stomach and pylorus.

• •For optimal visualization, withhold feed or empty the stomach via nasogastric intubation prior to the examination.
• •Gastric ulcerations are common in sick, stressed foals.

Abdominocentesis

• 1.Indicated in colic or where peritonitis or ruptured bladder is suspected.
• 2.
  The technique is the same as in the adult but with special considerations:

  • •
    The foal must be adequately restrained.
  • •
    The procedure can be performed with the foal standing or in lateral recumbency.
  • •
    Care must be taken to prevent perforation of the bowel. The intestinal walls in the foal are thinner and more friable than the adult. Guidance with ultrasonography can be helpful.
• 3.
  Normal peritoneal fluid analysis is similar to that in the adult:

  • •
    Colour: clear or pale yellow.
  • •
    White blood cell count: <3 × 10⁹/L.
  • •
    Protein: <25 g/L.

  Caution should be used in the evaluation of peritoneal fluid to differentiate medical and surgical cases, as elevations of protein and WBCs can occur in a number of conditions, as well as with enteritis.

• 4.
  Abnormal peritoneal fluid:

  • •
    Increased protein and WBCs:

    • –
      Enteritis.
    • –
      Ischaemic intestinal lesions such as intussusceptions, volvulus.
    • –
      Peritonitis.
    • –
      Urachal or bladder infections.
  • •
    Increased RBCs or haemorrhagic fluid:

    • –
      Splenic tap.
    • –
      Haemoperitoneum.
    • –
      Haemorrhage from vessels in the abdominal wall.
  • •
    Food material or ingesta:

    • –
      Enterocentesis.
    • –
      Bowel rupture.
• 5.Cytology is also useful to detect bacteria (which may indicate peritonitis, bowel rupture or bowel tap). Urine crystals can sometimes be seen in cases of uroperitoneum.
• 6.If uroperitoneum is suspected, the serum creatinine should be compared to the abdominal fluid creatinine.

Faecal analysis

• 1.
  Examination for parasites or protozoa.

  • •
    Faecal flotation: Stronyloides westeri, Parascaris equorum, and strongyles.
  • •
    Direct faecal examination: protozoa or oocysts (e.g. Cryptosporidium).
  • •
    Normal foals older than 2 weeks should have an active faecal protozoal population.
• 2.
  Faecal cultures.

  • •
    Salmonella spp. using selective media.
  • •
    Multiple cultures should be performed as shedding of the organism appears to be intermittent.
  • •
    Other organisms that can also be selectively cultured for include Clostridium spp, Campylobacter spp.
  • •
    Polymerase chain reaction (PCR) for Salmonella spp, Clostridium spp, and Lawsonia intracellularis.
• 3.
  Assays for clostridial toxins.

  • •
    Clostridium difficile toxins A and B.
  • •
    Clostridium perfringens toxins.
• 4.
  Analysis for viruses, especially rotavirus.

  • •
    Electron microscopy.
  • •
    Enzyme-linked immunosorbent assay (ELISA).

Congenital problems of the alimentary system

Cleft palate

See Chapter 1.

Oesophageal stenosis

Congenital stenosis is rare and considered to be secondary to persistent right aortic arch.

Atresia

See Chapter 2.

The gastrointestinal tract is incomplete. A defect may occur at the anus (atresia ani), small colon (atresia coli) or rectum (atresia recti).

Lethal white syndrome (ileocolonic aganglionosis, overo lethal white syndrome)

Autosomal fatal disorder of white foals born from two overo American Paint horses. It is caused by a mutation of the endothelin receptor B. This results in absence of submucosal and myenteric ganglia in the small and large intestines. Most foals appear normal at birth, are white, with unpigmented skin, have blue irises, do not pass meconium and develop signs of colic with abdominal distension within hours to one day. These foals die or have to be euthanized. On necropsy there is intestinal impaction, distension, and a hypoplastic intestinal tract from the lack of intrinsic innervation (aganglionosis). This condition is similar to the Hirschsprung's disease of humans, in which there is a mutation of the endothelin B receptor, which impairs the proper migration of melanocytes to the skin and neurons to the intestinal tract. The diagnosis in foals is straightforward, based on clinical findings and abnormalities. There is a PCR-based test to identify carriers of this mutation.

Foal diarrhoea

Clinical signs

• •Faeces can range from soft consistency to profuse watery, yellowish, dark haemorrhagic diarrhoea depending on the severity and cause.
• •Increased borborygmi may be noticed before the onset of diarrhoea. Some foals may have decreased intestinal sounds.
• •Depression, fever, anorexia, colic, dehydration, congested mucous membranes.
• •Abdominal distension may be present.

Laboratory data

• •Increased PCV and serum creatinine concentrations from dehydration and/or prerenal azotaemia. The presence of azotaemia (increased BUN and creatinine) should be addressed as it can be prerenal or renal. This is relevant to prognosis but also to the treatment plan, in particular for drug selection.
• •Neutropenia with a left shift is a frequent finding, in particular in foals with evidence of endotoxaemia. Neutropenia can also be present in foals with viral diarrhoea from intestinal inflammation and absorption of endotoxins.
• •Electrolyte imbalances include hyponatraemia, hypochloraemia, hypokalaemia, and metabolic acidosis.
• •Hypoglycaemia is a frequent finding.
• •Low total serum protein: total protein can be increased in foals with severe dehydration but is rare.
• •L-lactate concentrations are increased in foals with poor perfusion.

Aetiologies of diarrhoea

Identifying the aetiological agents is often difficult. Predisposing conditions include peripartum asphyxia (maladjustment), failure of transfer of passive immunity (FTPI), septicaemia, and poor farm management.

• 1.
  Infectious causes of diarrhoea.

  • •
    Bacterial:

    • ▪
      Salmonella spp are a common cause of bacterial enteritis. Can cause enterocolitis with severe diarrhoea, colic, depression and fever. Concurrent sepsis, septic arthritis, or osteomyelitis can occur.
    • ▪
      Escherichia coli is probably not a primary cause of diarrhoea in foals, but it is frequently a cause of sepsis, and diarrhoea can develop secondarily to this.
    • ▪
      Clostridium perfringens (types A and C) and C. difficile are the most common causes of clostridial diarrhoea in foals. Usually sporadic, but occasionally can present as outbreaks. In general the diarrhoea is severe may be haemorrhagic, and may cause rapid death. Some foals may have severe necrotizing enterocolitis and present for acute colic with no evident diarrhoea (per acute death). C. difficile diarrhoea can present in foals as early as 1 day of age, and faeces vary from yellowish to haemorrhagic.
    • ▪
      Other bacteria that have been associated with diarrhoea in the neonatal foal include Rhodococcus equi, which can cause diarrhoea in foals 1–4 months of age; it is more commonly associated with pneumonia and lung abscesses, and can also cause septic arthritis, physitis, uveitis and abdominal abscesses. Lawsonia intracellularis (proliferative enteropathy) occurs in foals older than 2 months; affected foals are presented for poor body condition, weight loss, ventral oedema, and diarrhoea; treatment is administration of a macrolide (erythromycin or clarithromycin) with rifampin or a tetracycline (oxytetracycline or doxycycline) for 3 weeks. Response to this treatment is good. Plasma transfusion may be required. (See Chapter19: L. intracellularis.) Actinobacillus equuli and Klebsiella spp are usually associated with septicaemia.
  • •
    Viral causes of diarrhoea:

    • ▪
      Rotavirus is the most common viral cause of diarrhoea in foals. It causes a profuse watery diarrhoea in foals usually <1 month of age; most foals are younger than 2 weeks of age. Many foals on the farm are affected within 3–5 days. Diarrhoea is usually profuse and watery. The virus induces denudation of the epithelial cells of the proximal intestine, resulting in increased secretion and decreased absorption of fluids and electrolytes. These cells also produce disaccharidases such as lactase; thus, lactose is not digested in the small intestine but is broken down by bacteria in the large intestine. This worsens the diarrhoea as glucose pulls water into the intestine (osmotic diarrhoea).
    • ▪
      Blood abnormalities include metabolic acidosis, hyponatraemia, hypochloraemia, and hypokalaemia.
    • ▪
      As gastroduodenal ulcers may develop, anti-acid drugs should be considered, especially when entral feeding is decreased.
    • ▪
      As foals with rotavirus infection can dehydrate quickly, rapid intervention is required. Therapy should include balanced electrolyte solutions and sodium bicarbonate. Enteral feeding should be restricted or reduced.
    • ▪
      Other viruses that have been isolated from foals with diarrhoea include coronavirus, parvovirus and adenovirus. Their pathogenicity in foals is unknown. These viruses are typically isolated from immunocompromised foals and do not cause outbreaks.
  • •
    Parasitic causes of diarrhoea (see Chapter 19).

    • ▪
      Strongyloides westeri is a nematode that may cause mild diarrhoea in the foal at 1–4 weeks of age.
    • ▪
      Heavy infestation with strongyles or Parascaris equorum may cause diarrhoea but uncommonly.
    • ▪
      Cryptosporidium may occur in immunocompromised foals. This has zoonotic potential. Treatment is by supportive care.
• 2.
  Foal heat diarrhoea.

  • •
    Self-limiting diarrhoea that occurs between 6 and 14 days of age.
  • •
    Affected foals are not systemically ill, and usually no treatment is necessary.
  • •
    Resolves in <1 week.
• 3.
  Nutritional causes of diarrhoea.

  • •
    Over-eating or over-feeding, sudden changes in diet, or ingestion of sand or dirt can cause diarrhoea.
  • •
    Lactose intolerance is uncommon as a primary condition. Usually this is a transient condition secondary to infectious diarrhoea.
• 4.
  Antibiotic-associated diarrhoea.

  • •
    The administration of antimicrobial drugs can alter the normal microflora of the gastrointestinal tract which can lead to colonization by pathogenic bacteria. This is rarely a problem in newborn foals, but can occur in foals at a few weeks of age.
  • •
    Antibiotics associated with diarrhoea include macrolides (erythromycin, azythromycin), oxytetracycline, trimethoprim–sulphonamides, penicillins, and third-generation cefalosporins.
  • •
    There is a low incidence of antibiotic-related diarrhoea in foals; therefore these antibiotics should still be used if needed. If diarrhoea develops, consider discontinuing the antibiotic.

Diagnosis

• •Diagnosis of the aetiological agent is often difficult despite testing. In most cases of foal diarrhoea an aetiological agent is not identified.
• •Faecal cultures, faecal analysis for parasites, viruses, pathogen DNA (PCR) and blood cultures are indicated.

Treatment

Initial treatment is supportive with the goal of correcting hydration, acid–base and electrolyte imbalances, and hypoglycaemia.

• 1.
  Intravenous fluids. There are many options on the market, but balanced isotonic replacement solutions such as lactated Ringer's solution, Plasma-Lyte 148, Normosol R, or Isolyte S are good initial options. Saline solution (0.9%) can be used in some cases. Another aspect to consider when using these solution is the pH; while replacement solutions have a pH of >6.0, pH of 0.9% saline solution is 4.0. This may be relevant in foals with metabolic acidosis.

  • •
    Administration of KCl should be considered in severe hypokalaemia. KCl administration should not exceed 0.25–0.5 mEq/kg/h as a rapid rate may lead to cardiac dysrhythmias. Mild hypokalaemia is often corrected with restoration of the hydration status, and intravenous or oral supplementation of KCl may not be necessary.
  • •
    Supplementation becomes more important in foals with metabolic acidosis, as low pH leads to overestimation of serum K concentrations. As the pH increases K moves into the cells and vice versa.
  • •
    Severe acidosis may require intravenous administration of isotonic sodium bicarbonate. It is preferable to administer sodium bicarbonate alone than to mix it with other solutions, in particular those with calcium and magnesium salts as they may precipitate. Rapid administration of sodium-containing fluids to foals with severe hyponatraemia may lead to neurological signs.
  • •
    Dextrose may be added to fluids for hypoglycaemic foals. Typical solutions include 5% dextrose or 2.5% dextrose + 0.45% saline. Dextrose can also be added to other solutions to create a 2.5–5% concentration. Injectable hypertonic dextrose comes as a 25% or 50% solution.
  • •
    Hypocalcaemia is a frequent abnormality in foals with gastrointestinal disease. Isotonic solutions can be supplemented with calcium gluconate (23%) at 10 mL/L.
• 2.
  Oral electrolyte solutions.

  • •
    Not as effective in correcting severe electrolyte and acid–base imbalances, especially if absorption is impaired from enteritis. However, oral supplementation of potassium chloride and sodium bicarbonate is an effective and cheaper way to correct electrolyte concentrations in foals with mild abnormalities.
  • •
    Older foals may be able to maintain hydration and correct mild electrolyte imbalances if free-choice water and electrolytes (in water or salt block with trace minerals) are provided.
  • •
    If the foal is not interested in drinking, fluids and electrolytes may be administered via nasogastric tube.
• 3.
  Nutrition/caloric intake is very important in foals. Supplementation should be considered if the foal is not nursing or eating, of if the foal has evidence of proximal intestinal disease or lactose intolerance (idiopathic, rotavirus).

  • •
    If the foal is interested in eating, controlled nursing is important as excessive milk intake may worsen the clinical signs. Excess of lactose in a dysfunctional small intestine may lead to bacterial breakdown of lactose to glucose and galactose. Glucose is osmotically active, drawing more water into the intestine. In addition, this increase in luminal glucose can lead to bacterial overgrowth.
  • •
    If the foal is not interested in nursing, a small-bore feeding tube can be placed. These tubes have the advantage that the foal can nurse without problems, and they can be left in place for many days.
  • •
    Bottle feeding should be done by experienced personnel as in some situations it may lead to aspiration pneumonia.
  • •
    If there is no evidence of improvement and the foal does not tolerate enteral feeding, parenteral nutrition should be considered.
• 4.
  Antibiotics.

  • •
    There are several factors to take into consideration in the selection of antimicrobial drugs, including current disease, aetiological agent, drug interactions, toxicity, and cost. The initial choice should be a broad-spectrum combination, unless the aetiological agent and sensitivity are known.
  • •
    A combination of penicillin (or ampicillin) and an aminoglycoside (gentamicin or amikacin) is the most frequently used combination. It is important that the foal is well hydrated and that there is no evidence of renal disease, as aminoglycosides are nephrotoxic, particularly if there is dehydration and concurrent use of other nephrotoxic drugs (e.g. flunixin meglumine).
  • •
    Third-generation cefalosporins such as ceftiofur (4.4–8.8 mg/kg IV BID), cefotaxime (40 mg/kg IV TID–QID), ceftazidime (40 mg/kg IV TID–QID), or ceftriaxone (10 mg/kg IV BID).
  • •
    Metronidazole (20 mg/kg PO TID–QID) should be considered in foals with haemorrhagic diarrhoea, as this is a common finding in clostridial diarrhoea.
• 5.
  Anti-endotoxin therapy.

  • •
    Flunixin meglumine (0.25 mg/kg IV TID) or polymyxin B (3000–6000 IU/kg IV BID, in 5% dextrose solution) should be considered in foals with severe sepsis or evidence of endotoxaemia.
• 6.Intestinal protectants. The use of these products is controversial, but protectants to consider are bismuth subsalicylate, kaolin, pectin, and activated charcoal. More recently, smectite-based products (Bio-Sponge) have been claimed to show good results in treating foal diarrhoea.
• 7.
  Non-steroidal anti-inflammatory agents.

  • •
    Flunixin meglumine if there is evidence of endotoxaemia (0.25 mg/kg IV TID) or fever, pain, inflammation (0.25–1.1 mg/kg IV).
  • •
    Ketoprofen (1.1–2.2 mg/kg IV) is a good choice in foals with fever and pain. It is less ulcerogenic than other non-steroidal drugs.
• 8.Plasma transfusion may be indicated in cases of FTPI or in foals with hypoproteinaemia.
• 9.Additional therapeutic measures.

• Oral supplementation with lactase should be considered in foals with watery diarrhoea, foals with rotavirus infection, or in foals that do not tolerate enteral feeding. Anti-acid drugs such as cimetidine, ranitidine, or omeprazole can be used as foals are prone to developing gastric ulcers.

Gastroduodenal ulcers

Predisposing factors include stress, previous illness, decreased feeding, and treatment with non-steroidal anti-inflammatory drugs.

Clinical signs

• •Diarrhoea and abdominal pain are the most common signs.
• •Signs of colic/pain, bruxism (grinding teeth), salivation, dorsal recumbency.
• •History of stress such as recent shipping or previous illness.

Diagnosis

• •Often based on clinical signs.
• •Faecal occult blood test can be positive but is not diagnostic.
• •Endoscopic examination is the test of choice. Feed intake should be restricted for 4–6 hours in foals. The pyloric region and duodenum can be difficult to visualize in foals. Ulcers frequently occur in the squamous mucosa near the margo plicatus and along the lesser curvature and cardia in older foals.
• •Contrast radiographic studies may be indicated if duodenal stricture is suspected.

Treatment

• 1.
  Drugs to decrease gastric acid secretion.

  • •
    Histamine type-2 receptor antagonists: cimetidine and ranitidine, available in oral or IV preparations.
  • •
    Omeprazole: blocks HCl secretion by inhibiting the hydrogen ion pump and thereby blocking all receptor types for gastric acid secretion. May be indicated when gastric ulcers are not responsive to H2 blockers. A cheap way to give it is by using the adult formulation and dosing on the basis of body weight.
• 2.
  Mucosal protectants.

  • •
    Sucralfate. There is no evidence that sucralfate is effective in foals unless the presence of gastric ulcers is confirmed. It has been suggested that sucralfate should be given 1 hour before H2 blockers because it is most effective in an acid environment. It can be expensive.
  • •
    Anti-acids such as magnesium hydroxide, aluminium hydroxide, or calcium bicarbonate are rarely used in equine practice.

Prognosis

The prognosis is good with treatment and reduction of stress, unless complications develop.

Sequelae

• •Perforation: gastric or duodenal ulcers may perforate, resulting in severe peritonitis and death.
• •Oesophageal stricture: secondary to chronic reflux oesophagitis.
• •Duodenal stricture: results in delayed gastric emptying. These foals present for chronic abdominal pain. Surgery to bypass the stricture may be attempted.

Meconium impaction/retention

Meconium consists of the intestinal secretions, cellular debris, and digested amniotic fluid that accumulate in the intestinal tract during gestation. Normally it is completely passed during the first 24–48 hours of life.

Clinical signs

• •Straining to defecate: the foal usually stands with the back arched upwards, whereas foals straining to urinate stand more stretched out.
• •Tail swishing, restlessness.
• •Decreased nursing.
• •Abdominal pain. With time, abdominal distension develops.

Diagnosis

• •In mild cases, diagnosis is often based on the clinical signs and response to treatment.
• •Digital rectal examination may reveal firm meconium in the rectum, and help to rule out congenital abnormalities such as atresia.

Treatment

• 1.
  Enemas. Care must be taken not to irritate or damage the rectal mucosa. Over-distension of the rectum can result in rectal tears.

  • •
    Warm water and soapy water enemas.
  • •
    Commercial phosphate enemas. Should be used with care as some foals may develop hyperphosphataemia.
  • •
    Acetylcysteine retention enemas are effective for refractory impactions. Acetylcysteine (4% solution) is administered via Foley catheter and retained for 10–30 minutes.
• 2.
  Oral laxatives.

  • •
    Mineral oil via nasogastric tube.
• 3.IV fluids if the foal is dehydrated.
• 4.Surgical therapy may be required in cases with severe abdominal distension or bowel compromise.

Abdominal abscesses

Aetiology

Most frequent aetiological agents include Streptococcus equi, S. zooepidemicus and Rhodococcus equi; occasionally enterobacteria are involved.

Clinical signs

• •Depression, fever, anorexia. Depending on the duration, poor body condition.
• •Colic due to compressive effects on the intestines or adhesion formation.
• •Peritonitis due to inflammation or rupture of abscess.

Diagnosis

• •Haematology may show neutrophilia with left shift. High fibrinogen.
• •Ultrasound or radiology may be helpful in locating an abscess.

Treatment

• •Medical treatment with long-term antibiotic therapy is often unrewarding.
• •If there is bowel involvement or if medical therapy is unsuccessful, surgery may be indicated to attempt resection of the abscess. Resection is ideal but may not be possible. In these cases, debulking and establishing drainage are performed by marsupialization or drain placement.
• •Antimicrobials should have good penetration. To consider for Streptococcus spp. and Rhodococcus equi abscesses are macrolides (erythromycin, clarithromycin, azythromycin) alone or in combination with rifampin, sulphonamides/trimethoprim, and tetracyclines. Penicillins and aminoglycosides have poor cure success for abscesses. Care should be taken when using macrolides in foals as the mares may develop clostridial enterocolitis.

Obstructive/strangulating lesions

These are similar to those in adults in causing signs of colic, tachycardia and abdominal distension. See Chapter 2.

Intussusceptions

These usually involve the small intestine: jejunojejunal or ileocaecal. Ultrasound may help diagnosis. Exploratory surgery with resection of the affected area is indicated.

Hernias

These may be diaphragmatic, inguinal/scrotal, intra-abdominal (mesenteric rent) or umbilical. Inability to reduce an umbilical or scrotal hernia constitutes an emergency, and surgical repair should be performed immediately to minimize bowel compromise.

Small intestinal volvulus

This strangulating lesion causes acute, severe pain, and rapid cardiovascular deterioration.

Large colon displacement and volvulus

These are not common in foals, but large colon displacements and volvulus can occur.

Functional obstruction: ileus

Ileus can result from electrolyte abnormalities (especially hypocalcaemia and hypokalaemia), intestinal irritation, enteritis and peritonitis. Ultrasound and radiography can be useful to determine the extent of abdominal distension. It is important to rule out mechanical obstruction as the cause of ileus. Treatment is aimed at removing the underlying cause and correcting any electrolyte imbalances.

Surgical treatment

Surgery is indicated if the foal is persistently in pain or has evidence of complete obstruction or strangulation. Reported short-term survival for foals undergoing colic surgery is approximately 65%.

20.8. Hepatobiliary diseases

Examination

Physical examination and clinical signs

See Chapter 3.

Laboratory investigations

See Chapter 3.

Ultrasonography

Ultrasonography is a very useful non-invasive tool.

• •The liver can be visualized on the right side of the ventral abdomen from the 6th to the 15th intercostal spaces.
• •Portal and hepatic vessels can normally be visualized in the parenchyma. Veins are very prominent in foals. Bile ducts are very small in normal liver and are often not seen.
• •In cholestatic disease it may be possible to see distended bile ducts.
• •In hepatocellular disease, inflammation or diffuse cellular infiltration results in increased echogenicity of the liver parenchyma.
• •Focal hepatic diseases such as abscesses can also be diagnosed using ultrasound and appear as masses with increased echogenicity.

Liver biopsy

Liver biopsy is a procedure rarely performed in foals unless severe parenchymal disease is suspected. See Chapter 3.

Infectious hepatobiliary diseases of the foal

Tyzzer's disease

This is an acute, highly fatal infectious hepatitis of foals.

Aetiology

The infectious agent is Clostridium piliforme (Bacillus piliformis), a Gram-negative (despite being a Clostridium sp.), filamentous, intracellular, anaerobic bacterium. Infection occurs via ingestion of contaminated soil or faeces. The mare is suspected to be the source of infection.

Clinical signs

• •Usually occurs in foals of 40–60 days of age.
• •Onset and progression of disease is very rapid, from hours to days.
• •Signs include depression, anorexia, recumbency, ataxia, seizures, icterus, fever, diarrhoea, coma, or sudden death. Classical signs are consistent with hepatic encephalopathy. Faeces may be white to grey.
• •Laboratory data are suggestive of liver failure and include increased liver enzymes, increased serum bilirubin, increased ammonia, hypoglycaemia, low BUN, prolonged clotting times, metabolic acidosis, neutropenia or neutrophilia.

Diagnosis

• •As this is an acute disease, antemortem diagnosis is difficult.
• •Liver biopsy may provide a diagnosis with identification of groups of parallel bacilli within hepatocytes, in particular around necrotic areas.
• •The organism is difficult to culture, but PCR methods are available.

Treatment

• •Usually not successful.
• •Intravenously administered antibiotics. The organism is susceptible to penicillins, oxytetracycline, streptomycin, erythromycin, and metronidazole.
• •Supportive treatment: IV fluids (with dextrose if hypoglycaemic).

Prognosis

The prognosis is grave despite treatment. Most foals die within 24 hours.

Equine herpesvirus 1

In utero infection during late gestation with EHV-1 most commonly causes abortion, but can cause interstitial pneumonia and necrotizing hepatitis in neonates. Clinical signs include weakness, depression, respiratory signs, liver failure and icterus. See Chapter 19.

Septicaemia

• •Bacteria (enterobacteria, Actinobacillus, Listeria monocytogenes, Clostridium spp.) can be isolated from the liver of septicaemic foals. Septicaemia and endotoxaemia interfere with normal hepatocyte function.
• •Hepatitis can also develop secondarily to septicaemia via the haematogenous route or ascending cholangitis.

Liver abscesses

• •Uncommon but can occur in the foal secondarily to septicaemia or via ascending infection of the bile ducts.
• •Clinical signs include weight loss, intermittent colic and fever.
• •Ultrasonography can be very beneficial in diagnosis. Liver enzymes can be elevated.

Toxic hepatobiliary disease

Iron fumarate toxicosis

Aetiology

Administration of iron (fumarate oral supplement) prior to colostrum intake, when intestinal absorption is high, has been associated with fatal hepatic necrosis. Foals are much more susceptible to iron toxicity than adults. There is no need to supplement healthy foals with iron.

Clinical signs

• •Usually occurs 2–5 days after administration of iron fumarate.
• •Signs include depression, icterus, hyperexcitability, blindness, ataxia, coma and death.

Diagnosis

• •History of iron supplementation.
• •The liver is smaller than normal.
• •Histopathology shows severe hepatic necrosis.

Treatment

Treatment is supportive.

Prognosis

The prognosis is poor if there is liver failure.

Pyrrolizidine alkaloid toxicosis

This is very rare in foals. See Chapter 3.

Congenital hepatobiliary conditions

Portacaval/portosystemic shunts

• •Few cases have been documented in the literature.
• •Portosystemic shunts can be internal or external. Shunts allow blood from the portal system to bypass the liver and drain into systemic circulation, via the caudal vena cava or the azygous vein.
• •Most affected foals are older than 1 month.
• •Foals present because of neurological signs, including ataxia, disorientation, and blindness associated with poor body condition.
• •On ultrasound the liver is small and hyperechoic. Occasionally external shunts may be observed.
• •Laboratory abnormalities include increased ammonia, increased bile acids, low BUN, normal liver enzymes.
• •Liver biopsy reveals hepatocyte atrophy, fibrosis, and biliary tract hyperplasia.
• •Portography (intraoperative) can be performed.
• •Treatment is surgical, and prognosis is poor.
• •On necropsy the liver is small, and the shunt can be observed (if external).

Biliary atresia

• •This is a rare condition in which there is incomplete formation of the biliary ducts.
• •Foals will present for depression, anorexia, poor body condition, icterus, fever, colic, polyuria, and polydipsia.
• •Laboratory tests reveal increased GGT (gamma-glutamyl transferase), increased direct bilirubin, and increased sorbitol dehydrogenase activity.
• •The liver is normal or larger than normal on necropsy. Canaliculi are distended, there is biliary hyperplasia, and the portal triad is not properly developed.

Biliary obstruction/cholangiohepatitis (See Chapter 3)

• •Ascending disease of the biliary tract and hepatic parenchyma associated with gastroduodenal ulcers that lead to duodenal strictures, common bile duct obstruction and cholestasis.
• •Strictures distal to the opening of the common bile duct into the duodenum (hepatopancreatic ampulla) are associated with cholestasis and reflux of ingesta into the common bile duct. Chronic cholestasis leads to cholangiohepatitis.
• •Depending on the degree of inflammation or obstruction, direct bilirubin and GGT concentrations are elevated.
• •Cholangiohepatitis from strictures should resolve with surgical correction, unless permanent hepatic damage has occurred.

Hepatic lipidosis

• •Sick pony foals, miniature horse foals, and donkey foal may develop hyperlipaemia from different diseases. Some foals may accumulate large amounts of triglycerides in the liver (hepatic lipidosis) leading to liver failure, encephalopathy, and death.
• •Clinical signs include depression, anorexia, blindness, seizures, ataxia, diarrhoea, and sudden death.
• •Laboratory abnormalities are those of liver disease, and serum triglycerides are elevated.
• •Medical treatment is supportive, based on dextrose and insulin to reduce the rate of fat mobilization.

20.9. Diseases of the urogenital system

Examination

Physical examination

• •The umbilicus should be carefully examined for any abnormalities such as urine leakage (indicating patent urachus), swelling or discharge (which may indicate umbilical infection).
• •Abdominal ballotment can be useful in detecting free abdominal fluid.
• •The external genitalia should be examined for any abnormalities such as congenital malformations. Some colts will have a persistent frenulum for the first week of life.

Serum biochemistry and electrolytes

See Chapter 8.

Urinalysis

See Chapter 8.

Healthy, nursing neonatal foals have a low urine specific gravity (1.001–1.010).

Radiography

• 1.Loss of serosal detail and presence of a fluid line (with standing radiographs) indicate free abdominal fluid.
• 2.
  Contrast studies can be helpful in determining the site of urinary tract disruption prior to surgery.

  • •
    A water-soluble contrast agent must be used (e.g. iohexol).
  • •
    The urinary bladder is catheterized (using aseptic techniques), and a suitable amount of contrast agent is injected to distend the bladder.
  • •
    Lateral and ventrodorsal (if possible) radiographs are taken. Contrast material within the peritoneal cavity indicates a ruptured bladder or urachal defect. Occasionally urachal tears can occur outside the peritoneal cavity and contrast material can be seen in the subcutaneous tissue around the umbilicus.
• 3.
  Excretory urography such as an intravenous pyelogram may be useful in diagnosing ectopic ureters.

  • •
    Caution should be used as the contrast material is potentially nephrotoxic, especially if there is dehydration or impaired renal function.
  • •
    Iodinated, water-soluble contrast material is used.

Ultrasonography

• •Very useful in evaluating the umbilicus for infection or abscesses.
• •Free abdominal fluid can be visualized to aid abdominocentesis. Free abdominal fluid and lack of visualization of a fluid-filled bladder are supportive of bladder rupture. However, visualization of a fluid-filled bladder does not rule out the possibility of a rupture as some cases may involve small tears, and the bladder is able to partially fill.
• •The kidneys should also be evaluated especially if nephritis or congenital abnormalities are suspected.

Abdominocentesis

• 1.Should be performed in cases of excessive free peritoneal fluid and when uroabdomen is suspected.
• 2.
  Uroperitoneum:

  • •
    Peritoneal fluid creatinine should be compared to serum creatinine to diagnose uroperitoneum. A ratio >2 : 1 is highly suggestive of uroperitoneum, although a normal ratio does not rule it out.
  • •
    Increased WBCs, increased total protein and/or bacteria in cases of uroperitoneum may indicate septic peritonitis.

Congenital urogenital defects

Ectopic ureter

• 1.Rare, but the most common congenital anomaly of the equine urinary tract. More common in fillies.
• 2.Primary clinical sign is persistent urinary incontinence which is present at birth. Affected foals often develop urine scalds in the perineal region and down the backs of the limbs.
• 3.Definitive diagnosis is by excretory urography or endoscopy.
• 4.Surgical correction is successful in some cases.

Cryptorchidism

See also Chapter 8.

Occurs in 2–8% of male horses. This condition is thought to have a heritable component.

Congenital hernias

See also Chapter 4.

Neonatal foals should be evaluated for the presence of congenital inguinal and umbilical hernias.

• 1.Small umbilical hernias usually close within the first few weeks of life. Large umbilical hernias and those that persist warrant surgical repair. Intestinal incarceration in an umbilical hernia requires emergency surgery.
• 2.Congenital inguinal hernias usually involve the small intestine, are easily reducible, and rarely require surgery. Non-reducible and ruptured inguinal hernias require immediate surgical repair.

Rare congenital defects

• 1.Renal dysplasia/hypoplasia: diagnosis by renal ultrasound and biopsy.
• 2.Rectovaginal and rectoureteral fistula: often associated with atresia ani.
• 3.Intersex: abnormal external and internal genitalia. The XX-male pseudohermaphrodite is the most common intersex in horses.

Patent urachus

See also Chapter 8.

• 1.Urine drips from the umbilicus when the foal urinates. The urachus may be patent at birth or may reopen due to infection.
• 2.The umbilicus should be kept clean using dilute chlorhexidine solution (0.5%), and systemically administered antimicrobials are used to treat or prevent infection.
• 3.Surgical resection of the umbilical remnants is recommended if infection is present or the urachus has not closed after 5–7 days of medical treatment.

Omphalitis/umbilical remnant infections

Infection can occur in umbilical remnants or urachal remnants.

Clinical signs

• •Swelling of the umbilicus and occasionally purulent discharge can be expressed from the umbilicus. Lack of external swelling does not rule out umbilical remnant infection as infection/abscess can occur internally.
• •Intermittent fever, leukocystosis, neutrophilia, and increased plasma fibrinogen are non-specific signs of infection that can be seen with umbilical infections.

Diagnosis

• •Can often be made on the basis of the clinical signs.
• •Ultrasonography is very helpful to diagnose infections of the internal portions of the umbilical remnants and to determine the extent of infection. Any foal with signs of inflammation and infection that cannot be localized should have an ultrasound evaluation of the umbilicus.

Treatment

• •Medical therapy with long-term, broad-spectrum antibiotics.
• •Surgical removal of infected umbilical remnants is indicated if there is not an adequate response to medical treatment, or the umbilicus is severely enlarged, or there is leakage of urine from the urachus.

Ruptured bladder

See Chapter 8.

Clinical signs

• •Frequent attempts to urinate. Progressive abdominal distension and colic.
• •Weakness, recumbency, and cardiovascular compromise occur as electrolyte abnormalities progress.
• •Signs are seen in the first 24–72 hours of life if the rupture occurs during parturition. Rupture can occur at days to weeks after birth when it is secondary to sepsis.

Diagnosis

• •Ultrasonography usually reveals a large amount of free abdominal fluid and a small urinary bladder.
• •Abdominocentesis reveals clear-yellow fluid with a creatinine concentration greater than twice that of the serum creatinine.
• •Electrolyte derangements include hyperkalaemia, hyponatraemia, and hypochloraemia.

Treatment

• •Surgical repair of the defect is not performed until the foal is medically stabilized.
• •Correction of electrolyte abnormalities, drainage of the uroperitoneum, and evaluation for concurrent disease, such as sepsis.

Primary renal disease

See also Chapter 8.

Aetiology

• 1.
  Sepsis-associated.

  • •
    Most common cause of renal failure in foals.
  • •
    Sepsis can cause renal failure via ischaemic damage and direct infection of the kidneys by the causative organism.
  • •
    Common organisms involved include Actinobacillus equuli, Escherichia coli and Klebsiella.
• 2.
  Nephrotoxic renal failure.

  • •
    Uncommon cause of renal failure but results from overdoses of potentially nephrotoxic drugs or administration of normal doses to a dehydrated patient.
  • •
    Aminoglycosides can cause renal tubular damage. Gentamicin is reportedly more nephrotoxic than amikacin.
  • •
    Oxytetracycline, especially when given at high dosages for treatment of contracted tendons, has been reported as a cause of renal failure in foals.
  • •
    Non-steroidal anti-inflammatory drugs (prostaglandin inhibition) can cause renal failure by reducing blood flow, resulting in ischaemia. They can also cause renal papillary necrosis (phenylbutazone).
  • •
    Haemoglobin in foals with haemolytic anaemia (isoerythrolysis). Haemoglobin causes renal vasoconstriction, acute tubular necrosis, and renal failure.
• 3.
  Ischaemic renal failure.

  • •
    May be a consequence of perinatal asphyxia, severe dehydration, volume depletion.

Clinical signs

• •Depression, lethargy, anorexia, tachycardia, fever.
• •Oliguria.

Diagnosis

It is important to differentiate renal failure from urinary tract disruption such as ruptured bladder or obstruction.

• •Laboratory findings: azotaemia, hyponatraemia, hyperkalaemia and metabolic acidosis are commonly seen.
• •Urinalysis: urine gamma-glutamyl transferase/urine creatinine ratio may be elevated. This method is not considered reliable, but is used by some clinicians. Fractional excretions may be useful, but values are not as well established in foals. Urine cytology may reveal casts indicating renal tubular damage.

Treatment

The goals of therapy are to correct the underlying causes such as dehydration or sepsis, to correct electrolyte and metabolic imbalances, and to maintain urine output.

• 1.
  Fluid therapy. Care must be taken not to over-hydrate, especially in the oliguric patient.

  • •
    Fluid overload can result in oedema, hypertension, CNS swelling and death.
  • •
    Monitoring central venous pressure (CVP), urine output, PCV, and body weight can be helpful.
  • •
    Potassium-free fluid such as 0.9% saline solution is the best choice in hyperkalaemia.
• 2.Diuretics in foals with evidence of acute tubular necrosis (haemoglobinuria) may be used to try to improve urinary output in oliguric patients.
• 3.Diazepam or midazolam may be indicated to control seizures.
• 4.Peritoneal dialysis or haemodialysis has been proposed in anuric renal failure patient.

20.10. Endocrine/metabolic disorders

Neonatal hypothyroidism (goitre)

See Chapter 9.

Adrenal insufficiency (hypoadrenocorticism)

Adrenal insufficiency, also known as hypoadrenocorticism, is a poorly understood condition in foals. It occurs in premature, dysmature, and septicaemic foals. The dysfunction can be at the hypothalamus, pituitary gland, or adrenal gland. Most often it is the adrenal gland that has a poor response (cortisol release) to adrenocorticotropin (ACTH) stimulation. The adrenal cortex is not fully developed or functional in premature foals.

Cortisol has many essential functions, including regulation of intermediary metabolism (carbohydrates, proteins, lipids), immunomodulation, controlling inflammation, and in late gestation/early postnatal period is important for organ maturation. Aldosterone, another adrenal corticoid that is essential in regulating fluids and electrolytes, can be low.

• 1.Clinical signs: evidence of prematurity or dysmaturity, septicaemia, and respiratory dysfunction (see section on prematurity).
• 2.
  Diagnosis is based on clinical signs with supporting laboratory data.

  • •
    Normal plasma cortisol in healthy foals of 1–7 days of age is >2 µg/dL. Values of <2 µg/dL are suggestive of adrenal insufficiency but are not diagnostic unless a functional test is performed.
  • •
    ACTH stimulation test: no or minimal response to 100 µg of synthetic ACTH (cosyntropin). In foals with a normal adrenal gland function cortisol increases by 200% with this ACTH dose.
  • •
    Neutropenia and lymphocytosis may be present.
  • •
    Hyponatraemia and hyperkalaemia if aldosterone concentrations are low.
• 3.Treatment: glucocorticoid (hydrocortisone, dexamethasone) supplementation remains controversial but should be considered in foals with immature lungs and electrolyte and glucose abnormalities. Also necessary is supportive medical treatment.

Nutritional secondary hyperparathyroidism

See Chapter 9. This is not a problem in newborn foals.

20.11. Haemolymphatic and immunological disorders

Failure of transfer of passive immunity (FTPI)

Passive transfer of maternal antibodies does not occur transplacentally in the horse (epitheliochorial placenta). The mare's colostrum contains high concentrations of antibodies (primarily IgG); it usually contains up to five times the IgG concentration of plasma. The foal must ingest colostrum and absorb the antibodies. The foal's gastrointestinal tract is able to absorb proteins intact via specialized villus epithelial cells in the small intestine. Maximum absorption occurs within 8 hours following parturition, and the specialized epithelial cells are replaced by more mature cells unable to pinocytose proteins within 24–36 hours.

Causes of FTPI

• 1.
  Inadequate colostrum or inadequate concentration of IgG in colostrum.

  • •
    Mares that prematurely lactate (>24 hours prior to parturition) tend to have lower IgG concentration in the colostrum.
  • •
    Premature parturition: mares foaling prior to 320 days may not have adequate colostral antibodies.
  • •
    Mares on fescue pasture during late gestation can have agalactia, thickened foetal membranes, premature lactation, retained placenta, and weak foals.
• 2.Failure of the foal to ingest and absorb colostrum within the first 12 hours. Any illness or abnormality which causes the foal to be weak can result in lack of nursing.

Clinical signs

• •There are no signs specific for FTPI, but these foals are predisposed to septicaemia and other infections.
• •Neonatal maladjustment (dummy foals): these foals generally do not have a suckle reflex, are disoriented and unable to nurse.

Diagnosis

• 1.
  Immunoglobulin G concentrations should be measured at 24 hours of age (after antibody absorption is complete). Values <400 mg/dL are considered diagnostic of FTPI; 400–800 mg/dL is considered partial failure; >800 mg/dL is considered adequate.

  • •
    Methods to measure IgG include the zinc sulphate turbidity test, glutaraldehyde precipitation, ELISA (CITE^®, SNAP^®), and agar gel immunodiffusion (AGID, radial immunodiffusion). The zinc sulphate test is the least expensive; however, it is not a sensitive test, and false positives often occur. AGID is considered the most accurate method.
• 2.
  Measurement of IgG content of the colostrum.

  • •
    The specific gravity of colostrum directly correlates with the IgG content. Colostrum with a specific gravity >1.06 usually contains sufficient IgG.
  • •
    The specific gravity can be measured with a colostrometer.

Treatment

The treatment is dependent on the reason for FTPI and the age of the foal.

• 1.
  If the foal is <18–24 hours old:

  • •
    Frozen colostrum can be administered via bottle or nasogastric tube. At least 1 L should be administered within the first 12 hours of life, divided into several feedings. Frozen colostrum should not be thawed in a microwave.
  • •
    Lyophilized IgG is an oral IgG supplement. Variable absorption has been reported.
  • •
    Plasma can be administered orally, but it is not considered to be as effective as intravenous administration.
• 2.
  If the foal is >24 hours old or if colostrum is not available:

  • •
    Plasma transfusion.
  • •
    Approximately 20–40 mL/kg plasma is necessary to raise IgG levels to >400 mg/dL. If the foal is already sick, additional amounts are necessary.
  • •
    Ideally the plasma should be cross-matched if commercial cell-free plasma from anti-RBC negative donors is not being used.
  • •
    Serum IgG levels should be tested at 2–24 hours following administration, depending on the health status of the foal. Additional plasma should be administered if IgG concentration remains low.
  • •
    Caution should be taken not to cause fluid overload, especially in sick or very small foals.
  • •
    Before administering a large volume of plasma, a small amount (20 mL) should be given to assess for anaphylactic reactions. This manifests as tachycardia and tachypnoea, usually within 10–15 minutes. Urticaria is rare in foals.
  • •
    Avoid fluid overload, especially in sick or small foals.

Prevention

• •Mares should be removed from endophyte-infected fescue pastures 30–60 days before the expected foaling date.
• •The colostrum should be checked in mares. Stickiness is a better indicator of good quality than colour or thickness. It is best to measure the specific gravity.
• •The foal should be watched to ensure that it stands and nurses within a reasonable time after birth.
• •If there is any doubt, the foal's serum IgG levels should be measured.
• •Large breeding farms should establish a colostrum bank; 200–400 mL of colostrum can be taken from a normal mare without jeopardizing her foal's IgG levels. Also mares that die or lose their foals should be milked out and the colostrum frozen.

Severe combined immunodeficiency (SCID)

See Chapter 10.

• •Primary immunodeficiency of Arabian foals in which there is a failure to produce functional B and T lymphocytes.
• •The condition is autosomal recessive. There is a defect in an enzyme (DNA protein kinase) responsible for V(D)J recombination necessary for lymphoid tissue differentiation, and T-cell receptor and immunoglobulin production.
• •Foals with SCID are normal at birth, but over time and depending on maternal antibodies titres, develop infections (fungal, viral, bacterial, protozoal). Frequently these foals have infections by Cryptosporidium spp, Pneumocystis carinii, and Rhodococcus equi. Adenovirus is often isolated from the intestinal, respiratory, and urogenital systems.
• •Clinical signs are those of respiratory and gastrointestinal infections, including diarrhoea, fever, weight loss, nasal discharge, dyspnoea. Most foals die by 6 months of age.
• •Laboratory tests reveal lymphopenia and neutrophilia. Immediately after birth IgG and IgM concentrations can be normal (maternal), but after 2–4 weeks IgG is low and IgM is undetectable.
• •The diagnosis is clinical. Breed, lymphopenia, infections, no IgM, low IgG. There is a genetic test.
• •Treatment is supportive and questioned on an ethical basis.
• •As important is client education.

Neonatal isoerythrolysis (isoimmune or alloimmune haemolytic anaemia)

• •Haemolytic condition of neonatal foals in which the mare develops antibodies against the foal's erythrocytes.
• •Occurs when the foal inherits paternal RBC antigens that the mare does not have but has previously been exposed to these antigens.
• •In general multiparous mares. Exposure usually occurs in a previous gestation from the same stallion. Primiparous mares can develop antibodies if they have been exposed to antigens from a blood transfusion, a biological product, or from a ‘leaky placenta’.
• •After the foal nurses and absorbs colostral antibodies, severe haemolytic anaemia occurs.

Pathogenesis

• •The foal must have RBC paternal antigens different from those of the mare.
• •A highly antigenic blood group is necessary to mount a high immune response by the mare.
• •Factors Aa and Qa are the most immunogenic in horses, but it can happen with other blood groups. A ‘donkey factor’ is responsible for antigenicity in mule foals.
• •Mares that are negative for Aa or Qa are at high risk of producing foals that will develop isoerythrolysis.

Clinical signs

• •Foals are usually normal at birth. Signs develop from 8 hours to 4 days following parturition.
• •Weakness, icterus, tachycardia, tachypnoea. Urine can be dark.
• •Neonatal isoerythrolysis should be suspected in any foal younger than 1 week with icterus,.
• •Differentials for icterus include liver disease, anorexia, and haemolysis.
• •Seizures can occur if the anaemia/hypoxia is severe.
• •Foals may develop diarrhoea and septicaemia with severe hypoxia, compromising the intestinal mucosa.

Diagnosis

• •Laboratory findings include anaemia (PCV of 10–15%), leukocytosis from a stress response, hyperbilirubinemia (indirect), icteric to red-tinged plasma, and abnormalities from secondary complications.
• •Haemoglobinuria: in severe cases foals may develop acute tubular necrosis.
• •Indirect Coombs test to detect the presence of antibodies on the surface of the foal's RBCs.
• •Minor cross-match (foal's RBCs + mare's serum): positive agglutination suggests neonatal isoerythrolysis, although non-specific autoagglutination is frequent in foals with isoerythrolysis.

Treatment

• 1.If the foal is less than 24 hours old at the time of diagnosis, it should not be allowed to nurse the mare until it is 24–48 hours of age.
• 2.
  Blood transfusion:

  • •
    A transfusion should be considered if the anaemia is severe (PCV <15%) or if the foal is weak.
  • •
    Sources of blood for transfusion include the mare's blood (RBCs must be washed to remove any antibodies); other donors should be cross-matched with the foal's blood prior to transfusion. If a cross-match cannot be achieved, a gelding donor is less likely to cause a reaction.
  • •
    20–30 mL/kg of packed red blood cells usually raise the PCV to 15–20%.
  • •
    Transfused red blood cells have a very short-half life (2–4 days), therefore the PCV needs to be closely monitored as further transfusions may be needed.
• 3.Plasma transfusions may be necessary if the serum IgG concentration is low. Often foals with isoerythrolysis have a high IgG concentration.
• 4.Broad-spectrum antibiotics should be given to protect against opportunist infections.

Prevention

• •Blood-typing of mares: alloantigens Aa and Qa are responsible for most cases; therefore mares without these alloantigens are more likely to be at risk.
• •Mares can be tested late in gestation. The mare's serum can be tested against samples with known alloantigens (stallion). If there is consistent evidence of agglutination, colostrum should be withheld and the foal supplemented with colostrum from another mare that has not produced a foal by the same stallion.
• •Testing at birth: the foal can be tested at the time of birth, and colostrum withheld until the test results are known.

Immune-mediated thrombocytopenia and neutropenia

• •Syndrome of foals younger than 1 week of life. These foals appear clinically normal until they become depressed and develop spontaneous bleeding. They can present with thrombocytopenia alone, or thrombocytopenia and neutropenia. Often they have signs of sepsis.
• •The pathogenesis appears to be similar to neonatal isoerythrolysis, but antibodies are directed to the platelets and neutrophils. These foals rarely develop immune-mediated anaemia, although it may occur. Anaemia, if present, is often the result of blood loss.
• •Petechiation, epistaxis, haematomas, spontaneous bleeding.
• •Laboratory abnormalities include low platelet and neutrophil counts, as well as abnormalities secondary to organ complications (acidosis, electrolyte imbalances, sepsis).
• •As with isoerythrolysis, these mares are at risk of having foals with this condition in future gestations.
• •Foals should not be allowed to nurse colostrum. They should receive colostrum from another mare or transfused with plasma. After 48 hours they can be placed back with the mare. The colostrum should be removed from the mare.
• •These foals should be treated with antibiotics immediately as they have an incompetent immune system from the leukopenia and likely septicaemia.
• •In foals with neutropenia, the use of granulocyte colony-stimulating factor has been suggested.

Ulcerative dermatitis, thrombocytopenia, neutropenia syndrome of foals

• •Foals of <4 days of age present with ulcerative dermatitis, low platelet count (<30 000/µL), leukopenia (<3000/µL) and neutropenia (<2000/µL).
• •Reported in Thoroughbreds and Paint horses.
• •Lesions consist of oral, gingival and lingual ulcers, and erythema and exudative dermatitis on the face, around the eyes, mouth, inguinal, axillary, and perineal areas.
• •Petechiation is frequent. Spontaneous bleeding (haematomas, epistaxis, melaena, haematochezia) can be present.
• •Pathogenesis is unclear but it is believed that paternal antigenic stimulation of the mare and colostral antibodies are involved.
• •Treatment consists of glucocorticoids (dexamethasone), antibiotics, platelet-rich plasma transfusion, and blood transfusion.
• •With early intervention the prognosis is good.

Other immunopathies

Selective IgM deficiency

This has been documented in Arabians, Quarter Horses, and apparently in other breeds. Affected horses have enteritis, pneumonia, sepsis, and weight loss.

Transient hypogammaglobulinaemia

In this condition there is a delay in IgG production; it has been reported in Arabian and Thoroughbred foals. Foals develop bacterial and viral infections.

Agammaglobulinaemia

A condition – reported in Thoroughbreds, Standardbreds, and Quarter horses – in which the foals have no B cells and fail to produce immunoglobulins. Clinical presentations relate to impaired immune function and include gastrointestinal and respiratory disease. IgA and IgM are usually undetectable, and IgG is low (probably maternal).

20.12. Miscellaneous conditions

Steatitis (yellow fat disease)

Steatitis is a rare disease seen primarily in pony and donkey foals, usually between 1 and 6 months of age. The aetiology is uncertain but might be associated with selenium and/or vitamin E deficiency. Clinical signs include pyrexia, inappetence, depression, tachypnoea and weakness. Firm, indurated subcutaneous plaques are palpable over the body, and the ligamentum nuchae is thickened, hard and painful. Other signs that may be present include hyperlipaemia, ventral oedema and diarrhoea. There is no effective treatment.

Glycogen branching enzyme deficiency (GBED)

This is a lethal, autosomal recessive condition of fetuses and foals of Quarter horse and Paint horse breeds. It is caused by a mutation of the glycogen branching enzyme, disrupting the metabolism of glycogen. GBED is characterized by abortion or mortality, immediately post-partum. These foals are weak, have contracted tendons, develop seizures, or die suddenly from hypoglycemia or cardiorespiratory failure. Some foals may live for a few weeks but eventually have to be euthanized.