Abraham and Bauquier (2021) reviewed perinatal mortality. They included late term abortion, stillbirth and death after birth.
Mouncey et al (2022) reported on 144 horse that died between birth and 18 months of age. The majority died in the first day of life. The causes were congenital abnormalities (predominantly limb deformaties), pneumonia, neonatal sepsis/maladjustment, enteritis, GI obstruction/rupture, fractures and omphalitis
Mouncey et al (2022) extended their 2022 study by examining the data from 7 farms. There were 275 foals and musculoskeletal disease required intervention or was responsible for death. 3 were stillborn, 3 died in the first 24 hours, The next mortality event was 180 days.
Ricard et al (2023) reported on death in foals from birth to 7 days. They had 360 cases in Canada that were submitted to diagnostic laboratories. 213 came from Ontario. 195 were foals that died in the first 48 hours. Of these the majority were noninfectious. 33% were idiopathic, 16% had respiratory disease, 14% were traumatic, 10 were congenital, and 7.5% were nutritional. Bacterial (85%) and viral (15%) were the infectious diseases.
Abraham M, Bauquier J. Causes of equine perinatal mortality. The Vet J 2021; 273: 105675
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.
Mouncey R, Arango-Sabogal JC, de Mestre AM, Foote AK, Verheyen KL. Retrospective analysis of post-mortem findings in Thoroughbreds aged from birth to 18 months presented to a UK pathology laboratory. The Vet J 2022; 281
Mouncey R, Arango-Sabogal JC, de Mestre AM, Verheyen KL. Incidence of disease, injury and death in Thoroughbred foals and yearlings on stud farms in the UK and Ireland. Vet Rec. 2023; 192: e2994.
Ricard RM, St-Jean G, Atwal HK, Wobeser BK. A retrospective study of equine perinatal loss in Canada (2007 to 2020). Canadian Vet J 2023: 64; 933-939
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.
After birth, normal foals develop a prooxidant state - beginning 5 minutes after birth. (de Souza et al 2021)
de Souza DF, Alonso MA, Brito MM, Meirelles MG, Francischini MCP, Nichi M. Fernandes CB. Oxidative state in equine neonates: Anti- and pro-oxidants. Equ Vet J 2021; 53: 379-384
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
Birth trauma occurs during dystocia and also normal foaling. Thoracic trauma is common - particularly fractures ribs and diaphramatic hernia. Fractured ribs can lead to hemorrhage, perforation of lungs and pneumothorax.
Abraham M, Bauquier J. Causes of equine perinatal mortality. The Vet J 2021; 273: 105675
Apparent pain in the abdomen (colic) occurs periodically in foals.
MacKinnon et al (2013) reported on 137 cases less than 30 days old. Enterocolitis was the most common cause identified (27%). meconium retention (20%) and colic of a short duration that responded medically were the top 3 causes.
MacKinnon MC, Southwood LL, Burke MJ, DVM; Palmer JE. Colic in equine neonates: 137 cases (2000–2010). J Am Vet Med Assoc 2013;243:1586–1595
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.
This syndrome results in postnatal hypocalcemia and subsequent muscle fasciculation and seizures.Originally it was called idiopathic hypocalcemia, as calcium infusion would result in clinical improvement. It was found that foals had a nonsense variant of Rap Guanine Nucleotide Exchange Factor 5 (RAPGEF5c.2624C>A p.Ser875*; EquCab 3.0. chr4: g.54108297G>T
Elcombe ME, Bellone RR, Magdesian KG, Finno CJ. Prevalence of the RAPGEF5 c.2624C>A and PLOD1 c.2032G>A variants associated with equine familial isolated hypoparathyroidism and fragile foal syndrome in the US Thoroughbred population (1988-2019). Equine Vet J. 2023;55(4):666-671. doi:10.1111/evj.13883
About 1% of Thoroughbred and 2% of Standardbred foals develop this.
Foals develop haemolysis and jaundice - and systemic hypoxia.
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
Selenium deficiency can result in nutritional myodegeneration and if severe, death of the foal from hyperkalemia and myoglobinuria. It affects both the striated syncitial muscle and the cardiac muscle. Many foals with this will die, and usually it is foals in the first month of life. Severe cases cause cardiac failure. Less severe cases result in skeletal myodegeneration. Muscles with high physiological activity such as the diaphragm, intercostal muscles, gluteal muscles, the tongue, and masticatory muscles are usually most severely affected.
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.
Delesalle C, de Bruijn M, Wilmink S, Vandendriessche H, Mol G, Boshuizen B, Plancke L, Grinwis G. White muscle disease in foals: focus on selenium soil content. A case series. BMC Vet Res. 2017 3;13(1):121.
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
Fragile foal syndrome is a cutaneous asthenia/Ehler-Danlos-like syndrome. The mutation is a missense mutation in the PLOD1 (c.2032G>A; p.Gly678Arg gene) that effects collagen fibril formation. Homozygous animals are affected.
Elcombe ME, Bellone RR, Magdesian KG, Finno CJ. Prevalence of the RAPGEF5 c.2624C>A and PLOD1 c.2032G>A variants associated with equine familial isolated hypoparathyroidism and fragile foal syndrome in the US Thoroughbred population (1988-2019). Equine Vet J. 2023;55(4):666-671. doi:10.1111/evj.13883
Savage et al (2018) reported on a 10 day old foal with 2 large masses in the abdomen. These were diagnosed as neoplasia of lymphatic vessels. They were well circumscribed, and located in the mesentry, in the intercolic fold and in the inguinal region.
Savage VL, Cudmore LA, Russell CM, Railton DI, Begg AP, Collins NM, Adkins AR. Intra-abdominal cystic lymphangiomatosis in a Thoroughbred foal. Equine Vet Educ 2018; 30: 403–408
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.
Cleft palate/palatoschisis
Foals with cleft palate may go unnoticed as identification can occur only after several months or even after 1 year of age. Surgical repair is only possible in about 11% of cases. The cleft can be of the hard palate, soft palate or both. Aspiration pneumonia is a common complication.
Shaw SD, Norman TE, Arnold CE, Coleman MC. Clinical characteristics of horses and foals diagnosed with cleft palate in a referral population: 28 cases (1988-2011). Can Vet J. 2015; 56: 756-760.
Hamartoma
Borel et al (2014) reported on a foal that developed nervous signs at 1 day of age. It had a vascular hamartoma of the obex
Borel N, Grest P, Junge H, Wehrli Eser M. Vascular hamartoma in the central nervous system of a foal. J Vet Diagn Invest. 2014; 26: 805-809.
Anomalies 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;
Mouncey et al (2022) reported on 144 horse that died between birth and 18 months of age. The majority died in the first day of life. The largest category of causes was congenital abnormalities (predominantly limb deformaties),
Mouncey R, Arango-Sabogal JC, de Mestre AM, Foote AK, Verheyen KL. Retrospective analysis of post-mortem findings in Thoroughbreds aged from birth to 18 months presented to a UK pathology laboratory. The Vet J 2022; 281
Laryngeal dysplasia
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.
Fragile Foal Syndrome (FFS)
Fragile skin of foals is reported in warmblood horses and now in Thoroughbreds. It was called Warmblood Fragile Foal Syndrome (WFFS).
It is a mutation in procollagen-lysine, 2-oxoglutarate 5-diosygenase 1 (PLOD1) gene. It causes thin and fragile skin.
Umbilical cord anomalies
Anomalies of the umbilical cord in newborn foals are similar to those of aborted or stillborn fetuses.
Acland HM, Mann PC, Robertson JL, Divers TJ, Lichtensteiger CA, Whitlock RH. Toxic hepatopathy in neonatal foals. Vet Pathol. 1984 Jan;21(1):3-9. doi: 10.1177/030098588402100102. PMID: 6710809.
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
Non infectious
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
Summary
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
Family Pasteurellaceae; Actinobacillus equuli subsp equuli and subsp haemolyticus
Bacteria of the genus Actinobacillus are normal inhabitants of the alimentary and reproductive tract of horses. They can cause septicemia and reproductive disease (endometritis and failure of pregnancy). They are often recovered with Streptococcus equi subsp zooepidemicus.
The lesions in foals are classically recognised as embolic nephritis, but lesions can be found in any location including the umbilicus. Thus omphalitis, peritonitis, pleuritis, pneumonia, lymphadenitis, meningoencephalitis and orchitis are all reported.
Layman QD, Rezabek GB, Ramachandran A, Love BC, Confer AW. A retrospective study of equine actinobacillosis cases: 1999-2011. J Vet Diagn Invest. 2014; 26: 365-375.
Neonatal foals with severe respiratory disease in the immediate postpartum period due to Chlamydia psittaci are reported. The foal have severe clinical disease and often die.
Begg et al (2022) reported on 13 cases of perinatal/neonatal mortality where Chlamydia psittaci was considered the cause of death.
Begg AP, Carrick J, Chicken C, Blishen A, Todhunter K, Eamens K, Jenkins C. Fetoplacental pathology of equine abortion, premature birth, and neonatal loss due to Chlamydia psittaci. Vet Pathol. 2022; 59: 983-996.
Gough SL, Carrick J, Raidal SL, Keane S, Collins N, Cudmore L, Russell CM, Raidal S, Hughes KJ. Chlamydia psittaci infection as a cause of respiratory disease in neonatal foals. Equine Vet J. 2020; 52: 244-249.
Willis et al (2019) provides retrospective information about Enterococcus bacteria isolated from 75 foals admitted to a Veterinary Hospital (UC Davis) aged from 0 to 30 days (neonatal period). Enterococcus faecium was the most common; E faecalis was the second. Culture of multiple bacteria was common and found in 53 of the 75. Other bacteria were E. coli, Klebsiella, Actinobacillus, Clostridium (perfringens or other species), and Enterobacter bacteria.
They found infection of the umbilicus (umbilical veins and arteries and urachus) and bladder.Only a small number were cultured from blood. Half of the foals did not survive.
Willis AT, Magdesian KG, Byrne BA, Edman JM. Enterococcus infections in foals. Vet J. 2019; 248:42-47.
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.
Salmonella enterica subsp enterica Abortusequi
Grandolfo et al (2018) published a case report of an outbreak of abortion, perinatal mortality and neonatal mortality in a herd of 40 Murgese mares10 of 34 newborns died and 7 foals developed disease and died in the first 10 days, and 4 developed disease up to 20 days of age.
Disease included diaorrhea and lameness with diffuse pneumonia, arthritis, and hemorrhagic cecocolitis.
Grandolfo E, Parisi A, Ricci A, Lorusso E, de Siena R, Trotta A, Buonavoglia D, Martella V, Corrente M. High mortality in foals associated with Salmonella enterica subsp. enterica Abortusequi infection in Italy. J Vet Diagn Invest. 2018; 30(3): 483-485.
Lawhon et al (2014) wrote a case report about a 2 day old foal with sepsis, septic arthritis and septic tenosynovitis. This foal developed an arterial thrombus and the affected limb developed avascular necrosis.
Lawhon SD, Lopez FR, Joswig A, Black HC, Watts AE, Norman TE, Porter BF. Weissella confusa septicemia in a foal. J Vet Diagn Invest. 2014; 26: 150-153.
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.
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.
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.
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
8 foals
Haemorrhage, fibrin edema and fibrosis around umbilical vessels.
Peritonitis
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.
Neosporum caninum
Neospora caninum JVDI: 509:507
J Vet Diagn Invest 12: 153-156
Enterocolitis in 5 day old foal