See also Enzootic Pneumonia of Calves Enzootic Pneumonia of Calves Enzootic pneumonia of calves is the most common respiratory disease seen in young dairy, veal, or beef calves. The disease is caused by a variety of viral and bacterial pathogens and environmental... read more and see Acute Respiratory Distress Syndrome (Acute Bronchointerstitial Pneumonia) in Foals Acute Respiratory Distress Syndrome (Acute Bronchointerstitial Pneumonia) in Foals Acute respiratory distress syndrome is a rare and rapidly progressive cause of respiratory failure in foals and is characterized by acute onset of respiratory distress and high mortality. A... read more .
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). It is more common in neonates with failure of transfer of passive immunity (FTPI). 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 result from inhalation pneumonia (airborne transmission of viral, bacterial, or fungal pathogens), aspiration of infected amniotic fluid secondary 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.
In neonates, localizing clinical signs of lung infection may be absent even in the presence of extensive disease. Dyspnea may occur 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 marked resistance/struggling during handling or restraint. Results of thoracic auscultation 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 severe pneumonia can have minimal abnormal findings on auscultation.
Mucous membranes should be examined for color, moisture, hyperemia (due to injected vessels), and cyanosis (e.g., due to severe hypoxemia with partial pressure of oxygen < 40 mm Hg). In addition, weakness, depression, anorexia, weak or absent suckle reflex, signs of 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 clinical signs of lung dysfunction may also be associated with nonrespiratory conditions including metabolic derangements (eg, severe acidosis), pain, acute abdomen, fever, high environmental temperatures, or excitement.
Diagnosis of Neonatal Pneumonia in Foals
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 preferable to assess the extent of hypoxemia and hypercarbia. 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 aid identification and localization (e.g., affected side) of peripheral lung consolidation, pleural effusion, and abscesses in foals with pneumonia.
Treatment of Neonatal Pneumonia in Animals
Broad-spectrum antimicrobial treatment of foals with bacterial pneumonia and possible sepsis should be initiated before culture results are available and is targeted toward the most common pathogenic bacteria ( see Treatment and Control Treatment and Control Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, there is critical reduction in tissue perfusion; acute failure... read more , above). In addition, intranasal oxygen therapy and cardiovascular support (including goal-directed fluid therapy) are essential in treatment of affected foals. Specific respiratory support may further include judicious respiratory 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 ultrasonography, which can also presumptively exclude umbilical infection. 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 ultrasonography and subsequent identification of bacteria in tissue samples. The normal equine umbilical stump is usually < 18 mm in diameter at 24 hours old, and it decreases to < 15 mm at 7 days old. The umbilical vein (as it courses cranially to the liver) should be < 10 mm in diameter at 24 hours after birth and is slightly smaller than the arteries; these vessels can be examined via ultrasonography 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, apparent abscessation of the stump or a single vessel, gas shadowing indicative of an anaerobic infection, edema of structures, and hematoma formation.
Treatment and Prognosis of Omphalitis, Omphalophlebitis, and Patent Urachus
A congenital patent urachus and many milder cases of patent urachus secondary to omphalitis may respond to local treatment (chemical cautery with silver nitrate, topical procaine penicillin G, cauterization) and systemic antimicrobials. However, caution must be used not to place caustic agents deeper 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 [eg, 10-14 days] systemic antimicrobials) and surgical options (umbilical resection). Foals that should be referred to surgery include those with substantial abscessation or venous involvement that extends to the liver. Mixed infections are likely, and common isolates include gram-negative bacteria (eg, E coli, Klebsiella, and Enterococcus), gram-positive organisms (especially beta-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 may produce poorer outcomes. Septic peritonitis or uroperitoneum are considered rare complications.
Prevention of Omphalitis, Omphalophlebitis, and Patent Urachus
After an uncomplicated birth, it is ideal to allow the umbilical cord to sever 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 of the eye 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 and induce clinical signs of 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, without permanent injury to the uveal tract once the corneal insult resolves.
Clinical signs of anterior uveitis generally consist of conjunctival hyperemia, ciliary flush, corneal edema, aqueous flare, hyperemia and swelling of the iris, miosis, and decreased intraocular pressure. Signs of ocular pain, blepharospasm, increased lacrimation, and photophobia are variable; whereas hyphema, hypopyon, and intraocular fibrin deposition occur in cases of severe inflammation. Intraocular fibrin formation occurs because of egress of essential clotting factors into the aqueous and vitreous humor during uveal inflammation. Furthermore, the regulation of fibrinolysis is altered in patients with endotoxemia. A prolonged increase in plasminogen activator inhibitor may increase coagulation activity 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 occur. The vitreous also tends to appear hazy on ophthalmic examination, with blurring of fundus details, because of 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 this 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 chronicity.