Enterocolitis
Enterocolitis, or inflammation of the gastrointestinal tract, can be a sequela to septicemia, a cause of septicemia, or can occur due to non-infectious causes (Mallicote et al 2012). Primary infectious diarrhea is caused by organisms colonizing and destroying the cells that line the gastrointestinal tract. Foals with systemic sepsis can develop secondary diarrhea due to mucosal hypoperfusion of the gastrointestinal tract and the release of sepsis-related inflammatory mediators (Mallicote et al 2012). The translocation of enteric bacteria is possible but less common than gastrointestinal inflammation secondary to sepsis (Mallicote et al 2012). In foals with sepsis, 32 - 62% of foals showed signs of enterocolitis (Oliver-Espinosa 2018; Taylor 2015). Colitis occurs when there is an imbalance between the secretion by the crypt epithelium and the absorption by the surface epithelial cells of the colon. This balance is controlled by systemic hormones, the enteric nervous system, bacterial enterotoxins, and the immune system; all of which can be affected by preformed inflammatory mediators, such as those that occur with systemic infection. Reactive oxygen species are of specific concern as they can be cell damaging and increase mucosal permeability. One of the greatest risks to the gastrointestinal tract is damage to the tight junctions between epithelial cells. Damage to these tight junctions allows for solutes and inflammatory molecules to flow across a previously tightly regulated membrane (Mealey and Long 2018).
Clinical SignsSeptic foals can range from symptomatic to comatose, and these clinical signs can progress rapidly. Unfortunately, septic foals often present with nonspecific signs, so suspicion of sepsis should be on the differential list for any abnormal neonatal foal. Owners may report that the foal is sleeping more than usual, difficult to rouse, or is not nursing. Upon examination, the only clinical evidence of the foal’s anorexia may be an engorged udder or milk staining on the dam’s hind legs. As the sepsis progresses, foals can show the classic signs of shock, cold extremities, mucous membrane abnormalities, hypothermia, and dehydration (McKenzie 2018). Other clinical signs seen may depend on the organ system affected. Respiratory infection often leads to tachypnea with subsequent acid-base disturbances that may mask the severity of disease (Taylor 2015). Clinically, foals with colitis can present with a range of symptoms from diarrhea to dehydration to depression to sudden death. Some organisms, such as certain Clostridia spp., can cause acute colitis with toxemia and the foal may die acutely prior to physical evidence of diarrhea (Uzal et al 2022). Early in the disease foals often have physical examination findings consistent with colic or depression including, but not limited to, tachycardia, tachypnea, anorexia, bruxism, rolling, and pawing. Due to their small size and small glucose reserves, the foals can also develop weakness and ataxia from a lack of metabolizable energy (Oliver-Espinosa 2018). As the illness progresses into SIRS many foals show signs of cardiovascular shock in which they remain hypotensive despite adequate fluid resuscitation (Taylor 2015).
Foals are very prone to gastric ulcers when stressed. Septic or colitis cases can be stressed due to the pain from the inflamed gastrointestinal tract, fever, or anorexia. In self-propagating fashion, pain from the ulcers causes the foal to stop nursing, which causes more stress and more acid production. Gastric ulcers form from hydrochloric acid splashing upwards onto the squamous mucosa, leading to cell damage. This splashing can be due to movement, stress, or increased intra-abdominal pressure (Sykes et al 2015). Studies have shown the incidence of gastric ulcers in hospitalized foals to be between 3 and 51% (Furr et al 2012).
While it is less stressful for foals to be with their dams, colic may occur due to milk intake. Milk ingestion can cause physical discomfort due to gastrointestinal distention secondary to ileus or gas produced due to lack of lactose enzymatic digestion. As such, foals are sometimes muzzled, or the mare milked frequently to reduce foal intake for 12 - 24 hours allowing the gastrointestinal tract to rest (Oliver-Espinosa 2018). Inflammation of the foal gastrointestinal tract can lead to microvilli necrosis due to hypoxia secondary to changes in intestinal vascular perfusion (McKenzie 2018). This in turn reduces the foal’s ability to break down and digest lactose, also known as lactose intolerance.