See also Enzootic Pneumonia of Calves and Shipping Fever Pneumonia and see Acute Bronchointerstitial Pneumonia in Foals.
Hematogenous infection of the lung occurs in association with sepsis, which may be acquired in utero from placental infection or perinatally through environmental contamination (eg, omphalitis, omphalophlebitis), and is more common in neonates with failure of passive transfer (FTP). Escherichia coli, Klebsiella spp, Actinobacillus equuli, Salmonella spp, and Streptococcus spp are some of the more common bacteria involved in neonatal pneumonia in foals. Descending respiratory infections may be related to inhalation pneumonia (transmission of viral, bacterial, or fungal airborne pathogens), aspiration of infected amniotic fluid due to placental infection, aspiration of gastric reflux, iatrogenic aspiration (oil, medication, oral supplements), and aspiration of milk and meconium. Aspiration of meconium occurs in utero in foals that experience fetal distress.
Early in life, localizing clinical signs of lung infection may be absent even in the presence of extensive disease. Dyspnea may be seen in severely affected foals and manifest as an increase in respiratory rate, effort, or thoraco-abdominal asynchrony (paradoxical breathing). However, signs of respiratory distress and hypoxemia are frequently vague. Even some severely hypoxemic foals may show only restlessness or considerable resistance/struggling during handling or restraint. Auscultation of the lung fields in newborn foals can be very misleading. Fluid sounds are normal immediately after birth, as are crackles due to simple atelectasis of the “down” lung during lateral recumbency. Conversely, foals with significant pneumonia can have minimal abnormal findings on auscultation. Mucous membranes should be examined for color, moisture, injected vessels, and the presence of cyanosis (which likely indicates severe hypoxemia with a PaO2 <40 mmHg). Additionally, weakness, depression, anorexia, weak or absent suckle reflex, dehydration, and fever may be noted in foals with respiratory disease. Cough and nasal discharge are usually absent in the early stages of neonatal pneumonia. Apparent signs of lung dysfunction may also be associated with nonrespiratory conditions such as metabolic derangements (eg, severe acidosis), pain, abdominal crisis, fever, high environmental temperatures, or excitement.
Thoracic radiographs are often essential to establish the presence of respiratory disease and determine the type and extent of lung involvement in neonates. Arterial blood gas analysis is preferentially used to assess the degree of hypoxemia and hypercarbia. The more common arterial blood sampling sites in neonatal foals include the dorsal metatarsal artery, the brachial artery on the medial aspect of the elbow, the carotid artery, and the transverse facial artery. Thoracic ultrasonography may further identify the presence and location (affected side) of peripheral lung consolidation, pleural effusion, and abscesses in foals with pneumonia.
Broad-spectrum antibiotic treatment of septic pneumonia should be initiated before culture results are available and is targeted toward the most common pathogenic bacteria (see Treatment, Control, and Prevention, above). Additionally, intranasal oxygen therapy and cardiovascular support (including goal-directed fluid therapy) are essential in treatment of compromised foals. Specific respiratory support may further include judicious suctioning, coupage, bronchodilators (eg, albuterol inhalants), and mucolytic agents. Recumbent foals should be maintained in a sternal position to limit positional atelectasis.
Omphalitis, Omphalophlebitis, and Patent Urachus
A patent urachus is the most common umbilical abnormality in neonatal foals. Diagnosis may be based on visual appearance (urine dripping from the umbilicus) or on umbilical ultrasound examination, which can also exclude umbilical infections. Clinical signs of infection may include discharge, pain, and heat and swelling of the umbilicus, although some infections of deeper structures may only be confirmed via ultrasound. The normal equine umbilical stump is usually <18 mm in diameter at 24 hr of age, and it decreases to <15 mm at 7 days of age. The umbilical vein (as it courses cranially to the liver) should be <10 mm in diameter at 24 hr after birth and is slightly smaller than the arteries, which can be followed via ultrasound as they course caudally on either side of the bladder. Ultrasonographic abnormalities consistent with omphalitis or omphalophlebitis in foals include enlargement of the vessels beyond normal limits, asymmetry of arteries with enlargement, abscessation of stump or single vessel, gas shadowing indicative of an anaerobic infection, edema of structures, and hematoma formation.
Treatment and Prognosis
A congenital patent urachus and many milder cases of patent urachus secondary to omphalitis may respond to local therapy (chemical cautery with silver nitrate, topical procaine penicillin G, and thermocautery) and systemic antimicrobials. However, caution must be used not to place caustic agents further than 1 cm into the stump, because ensuing tissue necrosis may predispose to further bacterial infection. Treatment of umbilical infections may include both medical (longterm systemic antimicrobials) and surgical options (umbilical resection). Foals that should be referred to surgery include those with substantial abscessation or venous involvement that extends as far as the liver. Mixed infections are likely, and common isolates include gram-negative bacteria (eg, E coli, Klebsiella, and Enterococcus), gram-positive organisms (especially β-hemolytic Streptococcus), and anaerobes (including Bacteroides and Clostridium), similar to organisms identified in generalized neonatal sepsis.
Overall survival rate with appropriate treatment is reported as 87%. However, severe concurrent disease such as secondary hepatic abscessation, sepsis, or multiple joint arthritis are suggestive of a poorer outcome. Septic peritonitis or uroperitoneum are considered rare complications. Umbilical infections are generally less common in neonatal camelids than in neonatal foals.
After an uncomplicated birth, it is ideal to allow the umbilical cord to break spontaneously when the dam rises. In foals, the cord is narrowest at ~5 cm from the body wall, which is the natural separation (break) point. If the cord has to be manually separated, it is best to provide steady traction on the cord while supporting the foal's abdomen at the umbilicus. Sharp transection of the cord with a clamp or ligature prevents retraction of the umbilical structures and may be associated with a greater incidence of subsequent umbilical complications. However, excessive hemorrhage can be addressed by transient ligation with umbilical tape or a clamp. After birth, 1% iodine or 0.5% chlorhexidine solution (preferred) should be applied 2–4 times daily to the umbilical stump until the umbilical remnant is dry.
Neonatal sepsis may initiate intraocular seeding or endogenous inflammation due to uveal tissue injury. Secondary ocular infection as well as endotoxemia, free radical formation, tissue hypoxia, and alterations in pH may trigger vascular damage at a cellular level and induce clinical uveitis. Various chemical mediators, including histamine, serotonin, plasmin, kinins, complement, and arachidonic acid derivatives mediate acute vascular changes. The ensuing increase in vascular permeability of the blood-ocular barrier allows cellular components, fluid, and plasma proteins to escape into the surrounding extravascular uveal stroma (edema), ocular fluid compartments (aqueous flare, plasmoid vitreous), and subretinal space (retinal detachment). Congenital and acquired adnexal disease, prolonged lateral recumbency, dehydration, and a decreased menace response in the neonate may also induce a reflex-mediated uveitis due to corneal trauma. Reflex-mediated uveitis is generally transient and leaves the uveal tract unaltered once the corneal insult resolves.
Clinical signs of anterior uveitis are more evident and generally consist of conjunctival hyperemia, ciliary flush, corneal edema, aqueous flare, hyperemia and swelling of the iris, miosis, and a decrease in intraocular pressure. Signs of ocular pain, blepharospasm, increased lacrimation, and photophobia are variable, whereas hyphema, hypopyon, and intraocular fibrin deposition are seen in cases of severe inflammation. Intraocular fibrin formation occurs due to egress of essential clotting factors into the aqueous and vitreous humor during uveal inflammation. Furthermore, the regulation of fibrinolysis is altered in endotoxemic animals. A prolonged increase in the activity of plasminogen activator inhibitor may favor coagulation and impede intraocular fibrinolysis.
Acute posterior uveitis is often overlooked if unaccompanied by apparent changes in the anterior chamber. Retinal vascular congestion, hemorrhage, edema, cellular infiltration, or retinal detachment may be seen. The vitreous also tends to appear hazy, with blurring of fundus details, due to cellular infiltration and proteinaceous debris. The type of inflammatory cell reaction is generally classified as neutrophilic (suppurative), granulomatous, or lymphocytic-plasmacytic. Neutrophilic inflammation is an acute response to bacterial infection and sepsis, although intraocular bacteria may not be present. Neutrophils can accumulate in the anterior chamber in the form of hypopyon, which is often sterile and thus indicative of inflammation rather than local infection. Proteases released from neutrophils may also induce corneal endothelial damage, thereby resulting in corneal edema. Lymphocytic-plasmacytic inflammation is often suggestive of an immune-mediated reaction and indicates some type of chronicity.
See Septic Arthritis.
Last full review/revision August 2015 by Daniela Bedenice, DVM, DACVIM, DACVECC