Brittany Vivian, a Biomedical student at the Ontario Veterinary College, contributed to this section by writing a literature review on this topic.
Giguère S, Weber EJ, Sanchez LC. Factors associated with outcome and gradual improvement in survival over time in 1065 equine neonates admitted to an intensive care unit. Equine Vet J. 2017 Jan;49(1):45-50.
Melissa C. MacKinnon, DVM, DACVS; Louise L. Southwood, BVSc, PhD, DACVS, DACVECC;
Megan J. Burke, DVM; Jonathan E. Palmer, VMD, DACVIM (2103) Colic in equine neonates: 137 cases (2000–2010). J Am Vet Med Assoc 2013;243:1586–1595
Objective—To document causes of colic in equine neonates, evaluate clinical features of neonates managed medically versus surgically, determine short- and long-term survival rates for neonates with specific medical and surgical lesions, and assess ability of patients to achieve intended use.
Design—Retrospective case series.
Animals—137 client-owned equine neonates (< 30 days old) with a history of colic or signs of colic within 1 hour after hospital admission examined between 2000 and 2010.
Procedures—Signalment, history, results of physical examination, laboratory data, ancillary diagnostic tests, details of treatment, primary diagnosis, concurrent diseases and shortterm survival rate were obtained from the medical records. Long-term follow-up information was obtained through phone survey.
Results—137 neonates with colic were included. The majority (122 [89%]) of neonates were managed medically. The 3 most common diagnoses associated with colic were enterocolitis (37 [27%]), meconium-associated colic (27 [20%]), and transient medical colic (26 [19%]). The most common reason for surgery was small intestinal strangulating obstruction, and these neonates were more likely to have severe, continuous pain and were less responsive to analgesics. Concurrent diseases were common (87 [64%]) but did not significantly impact survival rate. Short-term survival rate was not significantly different between medically (75%) and surgically (73%) managed neonates. Long-term survival rate was excellent (66/71 [93%]) for horses that survived to hospital discharge. Most neonates surviving to maturity were used as intended (49/59 [83%]).
Conclusions and Clinical Relevance—Most neonates examined for signs of colic can be managed medically. Short-term survival rate in medically and surgically treated neonates was good. Long-term survival rate of foals discharged from the hospital was excellent, with most achieving intended use.
Because the external environment is often much lower than usual, newborns must maintain their temperature. A reduction from normal of 2 to 3°C will result in reduced consciousness, movement and general behaviour. The metabolism of brown fat is important in maintaining temperature but muscle movement and general activity is also important. Any situation that alters vigour can result in hyperthermia and create a vicious cycle.
Common in normal foals. Abraham et al (2014) found that 10 of 14 standardbred foals has asymptomatic intussusceptions.
Abraham M, Reef VB, Sweeney RW, Navas de Solí C (2014) Gastrointestinal Ultrasonography of Normal Standardbred Neonates and Frequency of Asymptomatic Intussusceptions. J Vet Intern Med 2014; 28: 1580–1586.
The term neonatal encephalopathy (NE) has been used to encompass all neonatal foals that exhibit neurological abnormalities. It is important to note that Hypoxic Ischemic Encephalopathy is a specific type of NE, and not all NE cases are caused by hypoxia ischemia.
Fetuses that are neurologically mature at birth – the herbivores in particular, are maintained in a slit like unconscious state.
There are many names for this situation of hypoxia and ischemia in perinatal foals. They include HIE, NMJ, perinatal asphyxia syndrome, dummy foals, and
The incidence in foals is reported to be 1–2% of all births.1 There have been no direct studies of HIE in foals, and hence, knowledge of the condition has been extrapolated from studies in humans and other animal models with attendant limitations. Because the basic pathophysiology of brain injury in many species shares common features, the purpose of this review is to summarize the pathophysiology, diagnosis, and treatment of HIE in human neonates.
The origin of hypoxic ischemic brain injury results from a reduction in cerebral blood flow and oxygenation during the antepartum, peripartum, or postnatal period. Evidence suggests that approximately 70–80% of cerebral palsy cases are the result of antepartum injury, with birth asphyxia responsible for only 20%. Hypoxia can develop during labor because of compression of the umbilical cord, insufficient uteroplacental circulation, cord prolapse, uterine rupture, shoulder dystocia, or vaginal breech delivery. Most preventative measures and therapies target the birth asphyxia group, as there is a limited time period after insult to prevent or reduce injury, and often with antepartum injury that period has passed by the time the infant is born. Risk factors for the development of hypoxic brain injury in foals include prolonged dystocia, premature placental separation (red bag delivery), and need for resuscitation after cesarean section.8
Diesch and Mellor (2013) provide a detailed review of the normal periparturient transition from aquatic to terresterial enviroment, and discuss the causes and treatment of the neonatal maladjustment syndrome.
T. J. Diesch TJ, Mellor J. (2013) Birth transitions: Pathophysiology, the onset of consciousness and possible implications for neonatal maladjustment syndrome in the foal. Equine Vet J 2013; 45: 656–660
Gold JR. Perinatal asphyxia syndrome. Equine Vet Edu 2017; 29: 158-164
The birth process in foals, as with any other species, required a transition from an aquatic to a terresterial environment and hypoxia is a normal part of that process. Prolonged hypoxia had many effects on the foal and often it is manifest as hypoxic ischemic encephalopathy, which is part of neonatal encephalopathy (see above).
Gold (2017) wrote a review about this syndrome.
Gold JR. Perinatal asphyxia syndrome. Equine Vet Edu 2017; 29: 158-164
Selenium deficiency can result in nutritional myodegeneration and if severe, death of the foal from hyperkalemia and myoglobinuria.
It appears that many foals are born with serum selenium concentration below the reference range. Some develop myodegeneration. If there is concurrent hypovitaminosis E, they may go on to develop equine degenerative myeloencephalopathy/neuroaxial dystrophy.
Finno CJ, Estell KE, Katzman S, Winfield L, Rendahl A, Textor J, Bannasch DL, Puschner B. Blood and Cerebrospinal Fluid α-Tocopherol and Selenium Concentrations in Neonatal Foals with Neuroaxonal Dystrophy. J Vet Intern Med. 2015; 29: 1667-1675.
MacQuarrie J. Congenital nutritional myodegeneration in a neonatal foal. Can Vet J. 2016; 57: 781-784
Koikkalainen K, Knuuttila A, Karikoski N, Syrja P, Hewetson M (2014) Congenital hypothyroidism and dysmaturity syndrome in foals: First reported cases in Europe. Equ Vet Educat 2014; 26: 181-189
Congenital hypothyroidism and dysmaturity syndrome (CHD) in neonatal foals was first described in western Canada in 1981 and remains an important problem for the western Canadian horse industry. This syndrome is characterised by hyperplasia of the thyroid gland, increased gestational length and multiple congenital musculoskeletal abnormalities. This case series describes the first confirmed cases of CHD in Europe and challenges contemporary opinion which suggests that this syndrome is distinct from congenital hypothyroidism associated with visible goitre.
Abnormalites of the eyes at birth include congenital anomalies and induced abnormalities that occur at birth.
Ocular anomalies are seen with some frequency - in other words, they happen. Barsotti et al (2013) reported on the types of anomalies in standardbred foals. 36% had an abnormality - hemorrhage mostly. 1 had a congenital cataract.
Microphthalmos is one of the more common congenital abnormalites.
Barsotti G, Sgorbini M, Marmorini P, Corazza M. Ocular abnormalities in healthy Standardbred foals Vet Ophthol 2013 16: 245-250
Greenberg SM, Plummer CE, Sledge D, Komine M, Craft SL. Conway JA (2015) Bilateral microphthalmos with cyst in a neonatal foal. Vet Ophthalmology 2015;
Koskinen and Hewetson (2017) report on a case where the larynx did not develop normally resulting in neonatal respiratory distress.
Koskinen M, Hewetson M Equine laryngeal dysplasia as a cause of acute respiratory distress in a neonatal foal. Equine Veterinary Education 2017; 29: 87-91.
About 10 % of foals dont receive sufficient passive immunity (AVJ 73:201). Foals with insufficient serum immunoglobulin or which have a heavy infectious 'burden' have an increased susceptibility to joint ill, pneumonia, and septicemia.
There does not appear to be an effect on the prevalence of diarrhea, or Rhodococcus pneumonia.
By using a single cut off value, Liepman et al (2015) found an increased likihood of death if the concentration of protein was <8g/L.
Liepman RS, Dembek KA, Slovis NM, Reed SM, Toribio RE. Validation of IgG cut-off values and their association with survival in neonatal foals. Equine Vet J. 2015; 47: 526-530.
M. Mallicote*, A. M. House and L. C. Sanchez (2012) A review of foal diarrhoea from birth to weaning. EQUINE VETERINARY EDUCATION. Equine vet. Educ. 2012, 24(4): 206-214
Foal heat diarrhoea is itself a misnomer for short periods of diarrhoea seen between one and 2 weeks of age in otherwise systemically healthy foals. Attempts to identify a causative agent in mare’s milk around the time of oestrus have been unsuccessful (Johnston et al. 1970). Further, orphans and foals maintained on milk replacer often also experience a similar episode of diarrhoea, effectively ruling out the mare as a cause (Cymbaluk et al. 1993; Magdesian 2005). A more likely theory involves the normal development of gastrointestinal flora, particularly as the foal begins to ingest other feeds and inoculates its gastrointestinal tract via coprophagy (Masri et al. 1986). Recent work examining bacterial flora and occurrence of diarrhoea in neonatal foals further supports this theory and failed to demonstrate an association between foal heat in dams and onset of diarrhoea in the foal (Kuhl et al. 2011). Affected foals will continue to suckle readily, are afebrile and have no clinical abnormality other than diarrhoea. Thus, owner education and benign neglect are ideal treatments.
Dietary issues can occur in both orphan and mare-fed foals. Overfeeding associated with high milk-producing mares results in a large amount of undigested lactose reaching the large intestine, where its fermentation can lead to osmotic diarrhoea. Foals receiving inappropriate or incorrectly prepared milk replacer can develop diarrhoea, secondary to overadministration of lactose or electrolytes (Cymbaluk et al. 1993). Primary lactose intolerance in foals is very rare, but has been reported (Koterba 1990; Roberts et al. 2008; Sloet van Oldruitenborgh-Oosterbaan 2008). There is also a suggested, although still unproven, association between secondary lactose intolerance and enterocolitis of clostridial or rotaviral origin (Weese et al. 1999). Some foals willingly ingest large amounts of sand or other abrasive material which can be extremely irritating and damaging to intestinal mucosa. Foals with significant colonic sand can present for diarrhoea, with or without colic. Most cases resolve with medical therapy but severe cases may require surgical intervention. Previous work in adult horses has shown that removal of the animal from a sandy environment may be equally efficacious as medical treatment but results are conflicting (Leib 1997; Hammock et al. 1998; Hotwagner and Iben 2007). Perinatal asphyxia syndrome (PAS) can also cause gastrointestinal mucosal damage. Hypoxia and hypoperfusion of the gastrointestinal tract can result in signs of enterocolitis, even in the absence of evidence of hypoxia to other body systems. Similar to treatment of the neurological signs of PAS, these foals require supportive care, prevention of sepsis and cautious enteral feedings. A syndrome of necrotising enterocolitis is recognised in human premature and term neonates and reported in foals. In foals (although not infants), the syndrome has been loosely linked to clostridial infection (Bueschel et al. 1998; East et al. 1998). Regardless of aetiology, the disease is characterised by symptoms of ileus, evidence of pneumatosis intestinalis and necrotic intestinal mucosa/ submucosa (Cudd and Pauly 1987; Eser et al. 2002; Magdesian 2005). Affected foals are generally very compromised and can progress rapidly to death.
N. M. SLOVIS, J. ELAM, M. ESTRADA† and C. M. LEUTENEGGER*†Infectious agents associated with diarrhoea in neonatal foals in
central Kentucky: A comprehensive molecular study. Equine Vet J 2014: 46:311-316
Reasons for performing study: Diarrhoea caused by infectious agents is common in foals but there is no comprehensive molecular work-up of the relative prevalence of common agents and appearance of coinfections.
Objectives: To determine the prevalence of 9 infectious agents in gastrointestinal (GI)-diseased and healthy foals with ages ranging from 1 to 20 weeks of age and to what degree coinfections are associated with clinical signs of GI disease.
Study design: Retrospective controlled observational study.
Methods: The population consisted of 88 Thoroughbred foals aged 2 days to 17 weeks born on 32 different studfarms in Kentucky. Healthy (n = 37) and GI-diseased (n = 51) foals were identified based on clinical presentation. Faecal samples were analysed for 9 infectious agents by real-time PCR: equine rotavirus, equine coronavirus, Clostridium difficile toxins A & B, Neorickettsia risticii, Clostridium perfringens alpha toxin, Lawsonia intracellularis, Rhodococcus equi, Cryptosporidium spp., and Salmonella spp. Salmonella was also cultured from overnight selenite enrichment broth.
Results: The prevalence of infectious pathogens under studywas between 0% (Lawsonia intracellularis) and 34.6% (equine rotavirus). The overall prevalence for any infectious agent was 63.2% in the GI-diseased group and 43.2% in the healthy group. Coinfections were significantly more frequent in the sick group (15 monoinfections vs. 22 coinfections) than in the healthy group (12 vs. 4, respectively, P = 0.0002). Six of the 8 infectious agents were associated with the GI-diseased group, the other 2 were not (equine coronavirus and R. equi).
Conclusions: The use of panels rather than individual tests in combination with quantitative toxin gene analysis enables detection of coinfections
significantly associated with risk of disease. Several infectious diseases previously not tested for or considered unimportant were found at high prevalence and require further investigation.
Sepsis and the effects of endotoxemia are very important neonatal diseases. Much has been written about them. There are reviews written by Dunkel and Corley (2015)
Dunkel B, Corley KTT. Pathophysiology, diagnosis and treatment of neonatal sepsis. Equine Vet Edu 2015; 27: 92-98
The systemic inflammatory response syndrome is the result of cytokine release that affects the systemic function of organs and processes. DAMPs and PAMPs initiate a cascade of pro and antiinflammatory substances and cytokines resulting in systemic illness.
Omphalitis is inflammation of the umbilicus. Traditionally, it is considered an important portal for bacteremia and sepsis.
In a study of 40 foals with omphalitis, Rampacci et al (2017) found that 13 of the 38 had Streptococcus equi zooepidemicus, and 11 of 38 had Escherichia coli (there were 2 foals that were negative but they had been on antibiotics). About 10% were bacteremic with the same pathogen.
Rampacci E, Passamonti F, Bottinelli M, Stefanetti V, Cercone M, Nannarone S, Gialletti R, Beccati F, Coletti M, Pepe M. Umbilical infections in foals: microbiological investigation and management. Vet Rec. 2017 Jun 3;180(22):543.
Sepsis is very common in newborn foals. Foals that fail to get adequate colostrum or receive maternal antibodies of an inadequate quality are more likely to develop septicaemia. The list of potential bacteria is very long and some of the classics include Salmonella typhimurium, Streptococcus zooepidemicus, Actinobacillus equuli, and Escherichia coli.
Infection of the umbilicus is a common starting point for infection and subsequent spread throughout the body. Bacteria may also enter from the gastrointestinal tract and either enter the portal vein or the lymphatics. Lymphangitis is reported.
Normal foals may develop bacteremia. Hackett et al (2015) found that 4 of 7 normal foals had culturable bacteria in their blood. Bacillus, Propionibacterium, Streptococcus and Staphylococcus were the genera recovered. These foals were cultured 10 times in a 72 hour period..
Hackett ES, Lunn DP, Ferris RA, Horohov DW, Lappin MR, McCue PM. Detection of bacteraemia and host response in healthy neonatal foals. Equine Vet J. 2015; 47: 405-409.
Pulmonary alveolar macrophages don’t operate for the first few days of life.
Much less exudation of leukocytes and fluids than adult.
J Vet Diagn Invest 12: 173-176
Pneumonia was predominant finding.
Foals infected in late gestation with Leptospires usually abort or are stillborn, but weak foals with icterus, hepatomegaly and petechia can be found. The range of lesions are those seen in failure of pregnancy.
Ortega J, Daft B, Assis RA, Kinde K et al (2007) Infection of internal umbilical remnant in foals by Clostridium sordellii. Vet Pathol 44: 269-275
Haemorrhage, fibrin edema and fibrosis around umbilical vessels.
Fibrin in pericardial sac.
Lohr CV, PolsterU, Kuhnert P, Karger A, Rurangirwa FR, Teifke JP (2012) Mesenteric lymphangitis and sepsis due to RTX toxin-producing Actinobacillus spp in two foals with hypothyroidism-dysmaturity syndrome. Vet Pathol 2012, 49: 592-601.
Neospora caninum JVDI: 509:507
J Vet Diagn Invest 12: 153-156
Enterocolitis in 5 day old foal