In this text, a foal is defined as up to 4 weeks of age from the time of birth. Juveniles are defined as age 1 month to 12 months.
I. Foal Disorders and Diseases
1. Congenital abnormalities
Congenital abnormalities affect many organ systems. Many are life threatening. Only the most important are presented in this chapter. Less common abnormalities are listed at the end of the chapter.
Figure 2.1. Neonatal Foal. Body. Umbilical Hernia. This abnormality displays an open abdomen and eviscerated abdominal organs along the ventral midline.
Figure 2.2. Neonatal Foal. Head. Hydrocephalus. The head is disfigured from protruding brain markedly filled with central nervous system (CNS) fluid.
Figure 2.3. Foal. Spinal Cord. Hamartomatous Myelodysplasia. A spinal cord tissue protrusion at the laterodorsal aspect of L1 resulted in cord compression. (Courtesy Dr. J. Roberts, National Zoo, Washington DC.)
Figure 2.4. Foal. Mouth. Cleft Palate (Palatoschisis). Both the soft and hard palates are open and directly connected with the nasal cavity. The large size of the cleft leads to aspiration of ingesta and subsequent aspiration pneumonia.
Figure 2.5. Foal. Trachea. Cleft Palate. Milk Aspiration. The distal trachea in this foal with cleft palate is filled with milk.
Figure 2.6. Foal. Lung. Aspiration Pneumonia. Secondary to cleft palate. The lungs are mottled, and major portions are consolidated.
Figure 2.7. Foal. Large Intestine. Atresia Coli. The tubular misconnection of colonic segments resulted in a distal thin and empty colon with portions of the right and left ventral colons markedly distended with feces.
Figure 2.8. Foal. Large Intestine. Atresia Coli. Atresia occurred at the site of the transverse colon distending the entire large colon with feces. (Reprinted with permission from Animal Technology Institute Taiwan, Republic of China.)
Figure 2.9. Foal. Rear. Atresia Ani. Absence of tail.
Figure 2.10. Overo Foal. Large Intestine. Intestinal Aganglionosis. The absence of myenteric ganglia in the terminal ileum, cecum, and entire colon in white foals born to overo spotted parents is known as lethal white syndrome. The large intestinal tract is impacted by green meconium.
Figure 2.11. Overo Foal. Colon. Aganglionosis. Myenteric plexus ganglia are missing between the two layers of the tunica muscularis. (H&E)
Figure 2.12. Foal. Liver. Portosystemic Shunt. Microscopic findings include fibrosis and duplication of arterioles in portal triads. (H&E)
Figure 2.13. Foal. Urachus. Patent Urachus. Failure of the urachus to involute after birth leads to dribbling of urine. The condition is susceptible to infection and rupture leading to uroperitoneum.
Figure 2.14. Foal. Urinary Bladder. Rupture. This condition occurs typically in newborn male foals. The site of rupture is the dorsal aspect of the urinary bladder. The condition has been postulated to result from weakness of the musculature at this site, which is particularly susceptible to trauma during birth. Uroperitoneum is the fatal outcome.
Figure 2.15. Foal. Thyroid Gland. Hyperplasia/Goiter. The round contour of an enlarged thyroid gland is visible protruding the skin of the lateral cranial neck. The condition has been reported to lead to mandibular prognathism, skeletal malformations (contraction of forelimbs), and dysmaturity in carpal and tarsal bone ossification and is known as thyroid hyperplasia-musculoskeletal deformity syndrome or hypothyroidism and dysmaturity syndrome. It may be diet related in a mare deficient in iodine or due to toxic plants like locoweed (Astragalus mollissimus) or fescue.
Figure 2.16. Foal. Skeletal System. Thyroid Hyperplasia and Skeletal Deformities. There is evidence of deformities of the limbs. Nasal bones and the spine may also be involved.
Figure 2.17. Foal. Thyroid Glands. Hyperplasia. Both thyroid glands are bilaterally and symmetrically enlarged. This condition can be seen in iodine deficiency.
Figure 2.18. Foal. Fore Leg. Distal Limb. Joint and Tendon Laxity. The distal limb is deviated and held in palmar flexion position (angular deformity). There are two forms of deformity: deep flexor contracture and superficial flexor contracture. The congenital tendon contractures usually are the result of uterine malpositioning. They can also be acquired, such as from trauma.
Figure 2.19. Foal. Luxation Patella. The foal exhibits a spastic leg.
Figure 2.20. Foal. Extremities. Segmental Hypoplasia of Distal Phalanx and Angular Limb Deformity of Hind Legs. Fetlocks are involved. The front limbs are overextended.
2. Acquired diseases
a. Neonatal isoerythrolysis
Mares sensitized to fetal incompatible alloantigens develop alloantibodies such as agglutinins and hemolysins in the serum and colostrum. When colostrum is ingested by suckling foals during the first 2 days postpartum, isoimmune hemolytic disease develops in the foal. It may occur in newborn mules as well. Characteristic gross findings are shown in the accompanying figures.
Figure 2.21. Foal. Oral Cavity. Mucous Membranes. Neonatal Isoerythrolysis. These are yellow from bilirubinemia secondary to hemolysis.
Figure 2.22. Foal. Vulva. Mucous Membranes. Neonatal Isoerythrolysis. These are yellow from bilirubinemia secondary to hemolysis.
Figure 2.23. Foal. Body as Whole. Neonatal Isoerythrolysis. Icterus. Abdominal and subcutaneous fat are diffusely yellow, and the kidney is a deep blue color suggesting pigmentary nephrosis from hemolysis.
Figure 2.24. Foal. Abdominal Organs. Neonatal Isoerythrolysis. The spleen is enlarged, the urinary bladder is distended by burgundy-red urine suggesting hemoglobinuria, and the thoracic vertebrae and aorta are yellowish discolored.
Figure 2.25. Foal. Kidney. Neonatal Isoerythrolysis. Pigmentary Nephrosis. The cortex is deep red from hemolysis and the medulla yellow from icterus.
b. Actinobacillosis
The multisystem disease caused by Actinobacillus equuli is also known as “navel ill,” shigellosis, or sleepy foal syndrome. The bacterium is one of the causes of neonatal septicemia and usually enters through an open and inappropriately cared for umbilicus to typically shower the lung, kidneys, and multiple joints. Failure of passive transfer is an important predisposing factor.
Figure 2.26. Foal. Umbilicus. Abscess. The wall of the opened umbilicus is covered by clotted blood admixed with fibrin and pus.
Figure 2.27. Foal. Lung. Multifocal Suppurative Pneumonia. Actinobacillus equuli bacterial emboli caused these multiple brownish abscesses via capillary colonization.
Figure 2.28. Foal. Kidney. Embolic Glomerulonephritis. Multiple microabscesses. Actinobacillus equuli showering into the capillary bed of glomeruli caused multifocal embolic glomerulonephritis. Differential bacterial etiologies include Staphylococcus sp., E. coli, Streptococcus equi subsp. zooepidemicus, or Klebsiella pneumoniae.
Figure 2.29. Foal. Kidney. Bacterial Emboli. Myriads of A. equuli bacteria are entrapped within glomerular capillaries. (H&E)
Figure 2.30. Foal. Hock Joint. Fibrinopurulent Synovitis. Although causing lameness, it may resolve if the foal survives because there is no damage to the articular cartilage.
c. Tyzzer’s disease
This liver disease of foals is caused by Clostridium piliforme with rodents and adult horses serving as the reservoir. The organism is obligatory intracellular and transmitted through the fecal-oral route from a contaminated environment.
Figure 2.31. Foal. Liver. Tyzzer’s Disease. Hepatic Necrosis. The liver is markedly enlarged.
Figure 2.32. Foal. Liver. Tyzzer’s Disease. On cross section, multiple small, white, and yellowish coalescing areas are present suggesting necrosis and inflammation.
Figure 2.33. Foal. Liver. Tyzzer’s Disease. Foci of coagulation necrosis are intermingled with mixed inflammatory cells. (H&E)
Figure 2.34. Foal. Liver. Tyzzer’s Disease. A silver stain demonstrates filamentous brown bacilli within hepatocytes with an “Asian Letter” arrangement. (Warthy-Starry)
Other causes of bacterial hepatitis are A. equuli, Rhodococcus equi, and S. equi subsp. zooepidemicus.
d. Clostridial enteritis
Foals with colic and bloody diarrhea may develop a necrotizing hemorrhagic enterocolitis caused by both pathogenic Clostridium perfringens and Clostridium difficile. Both produce enterotoxins responsible for the clinical and pathologic changes.
Five strains (types A–E) of C. perfringens are classified according to the enterotoxins produced by them. These are alpha, beta, epsilon, and/or iota enterotoxins. In foals, C. perfringens type C is generally associated with diarrhea. A commercial enzyme-linked immunosorbent assay (ELISA) is used to identify the enterotoxins in feces. It should be mentioned that C. perfringens type A can reside in the normal intestinal flora of horses.
As for C. difficile, an emerging enteric pathogen, toxins produced are toxin A, an enterotoxin, and toxin B, a cytotoxin. Most toxigenic strains producing disease secrete both toxins. The toxins are analyzed by fecal ELISA.
Figure 2.35. Foal. Abdominal Cavity. Clostridial Disease. Loops of the jejunum are markedly reddened. C. perfringens should be considered as cause. Small intestinal volvulus and C. difficile should be considered in the differential diagnosis.
Figure 2.36. Foal. Small Intestine. Clostridial Disease. The superficial mucosa has undergone diffuse necrosis, whereas the adjacent lamina propria is hyperemic and contains fibrin thrombi in some blood vessels. (H&E).
Figure 2.37. Foal. Small Intestine. Clostridial Disease. A gram stain will reveal gram-positive rods colonizing the necrotic mucosa as a dense monotonous layer. (Brown & Brenn).
Other enteric pathogens in foals include Salmonella, Campylobacter sp., R. equi, E. coli, Streptococcus durans, Aeromonas hydrophila, Lawsonia intracellularis, coronavirus, rotavirus, Cryptosporidium parvum, and Strongyloides westeri.
Figure 2.38. Foal. Pony Body. Rotavirus. Diarrhea is the main complaint clinically. The virus predisposes to bacterial enteric pathogens. The diagnosis of rotavirus diarrhea is made by ELISA or by transmission electron microscopic examination of negatively stained feces.
e. Salmonellosis and foal sepsis
Epizootic outbreaks of foal sepsis are the result of infection by a variety of bacteria and involve multiple organs and tissues. Many septicemias develop from infection by opportunistic bacilli taking advantage of immunocompromised foals or of foals with failure of passive transfer of colostral antibodies. Frequent bacteria isolated in septic foals are A. equuli, S. equi var. zooepidemicus, K. pneumoniae, E. coli, and Salmonella. The age of the foal is important as to the likelihood of which bacterium may be involved.
Figure 2.39. Foal. Whole Body. Sepsis. Stunted growth, emaciation, and especially dehydration can be external signs of foal sepsis.
Figure 2.40. Foal. Small Intestine. Salmonella Enteritis. The opened mucosa exhibits fibrinonecrotic diffuse enteritis with ecchymotic hemorrhage on the serosal surface indicating septicemia. Septicemic salmonellosis can occur between 1 and 3 months of age.
Figure 2.41. Foal. Meninges. Salmonella Septicemia. The meningeal surface exhibits ecchymotic hemorrhage and a faint cloudy exudate suggesting fibrinopurulent inflammation.
Figure 2.42. Foal. Heart. Salmonella Septicemia. The epicardium shows petechial and ecchymotic hemorrhage. Differential diagnosis: purpura hemorrhagica.
Figure 2.43. Foal. Heart and Lung. Salmonella Septicemia. The epicardium is covered by a fibrin clot. The lungs are wet from edema.
Figure 2.44. Foal. Adrenal Glands. Salmonella Septicemia. Typically, the cortex is hemorrhagic or ecchymotic. The condition is known as Waterhouse-Friderichsen syndrome in septic human infants.
- Umbilicus
- Digestive
- Respiratory
- Lung
- Kidney
- Joints
- Lymphoid system
- Central nervous system
- Liver
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