Cover page

Table of Contents

Title page

Copyright page

Contributors

Preface

Acknowledgments

1: The Equine Necropsy

I. General considerations

II. Techniques

III. Tissue collection

IV. Recording of findings of routine cases

2: Diseases of Foals and Juveniles

I. Foal Disorders and Diseases

II. Diseases of juveniles

3: Diseases of the Nervous System and Peripheral Nerves

I. Central nervous system

II. Peripheral nervous system

4: Diseases of the Respiratory System

I. Upper respiratory tract

II. Lower respiratory tract

5: Diseases of the Cardiovascular System

I. Heart

II. Vessels

6: Diseases of the Gastrointestinal System

I. Diseases of the oral cavity

II. Diseases of the esophagus

III. Diseases of the stomach

IV. Noninfectious diseases of the intestinal tract

V. Diseases of the intestinal tract: Infectious disorders

VI. Diseases of the peritoneum

7: Diseases of the Liver and Pancreas

I. Liver

Summary

II. Pancreas

8: Diseases of the Urinary System

I. Kidney

II. Lower urinary tract

9: Diseases of the Muscular System

I. Genetic muscle disorders

II. Myotonic myopathy

III. Dietary and conditioning-associated muscle diseases

IV. Myonecrosis/myodegeneration

V. Myositis

VI. Neurogenic myopathy

VII. Immune-mediated myopathy

VIII. Hormonal imbalance myopathy

IX. Trauma

X. Neoplasia

10: Disease of the Skeletal System

I. Congenital/developmental lesions

II. Traumatic lesions (fractures)

III. Infectious/inflammatory lesions

IV. Idiopathic, ischemic/vascular-associated lesions and laminitis

V. Degenerative lesions

VI. Proliferative and neoplastic disease

VII. Metabolic bone disease

Acknowledgments

11: Diseases of the Endocrine System

I. Pituitary gland

II. Thyroid gland

III. Adrenal gland

12: Disease of the Reproductive System

I. Male

II. Female (nonpregnant)

III. Female (pregnant)

IV. Noninfectious abortion diseases

V. Infectious abortion diseases

VI. Choice of samples and diagnostic methods for abortion investigation

13: Diseases of the Skin (Integument)

I. Congenital and hereditary disorders

II. Disorders of epidermal differentiation

III. Disorders of pigmentation

IV. Physiochemical and actinic injury to the skin

V. Immune-mediated dermatoses

VI. Helminthic diseases of the skin

VII. Viral diseases of skin

VIII. Bacterial diseases of the skin

IX. Fungal diseases of skin

X. Oomycete diseases of the skin: pythiosis

XI. Protozoal diseases of the skin

XII. Ectoparasites: Mange

XIII. Miscellaneous skin disorders

XIV. Neoplasia of the skin

14: Diseases of the Eye and Ear

I. Eyes

II. Ears

15: Diseases of the Hemolymphatic System

I. Diseases of the bone marrow

II. Diseases of circulating blood cells

III. Diseases of the thymus

IV. Chylothorax

V. Diseases of lymph nodes and lymphangitis

VI. Diseases of the spleen

Appendix A: Equine Diseases without Pathology

I. Botulism

II. Tetanus

III. Japanese yew (Taxus)

IV. Selenium toxicity

Appendix B: List of Equine Neoplasms

Appendix C: List of Equine Infectious Diseases Foreign to North America

Index

Title page

Contributors

Julia A. Conway, DVM, DACVP

Clinical Assistant Professor

Department of Infectious Diseases and Pathology

University of Florida

Gainesville, FL 32611-0880

 

Julie B. Engiles, VMD, DACVP

Assistant Professor of Pathology

School of Veterinary Medicine

University of Pennsylvania

Kennett Square, PA 19348

 

Pamela Eve Ginn, DVM, DACVP

Associate Dean

Office of Students & Instructions

College of Veterinary Medicine

University of Florida

Gainesville, FL 32611-0125

 

Ingeborg Maria Langohr, DVM, PhD, DACVP

Associate Professor

Department of Pathobiological Sciences

College of Veterinary Medicine

Louisiana State University

Baton Rouge, LA 70803

 

Donald J. Meuten, DVM, PhD, DACVP

Professor Department of Population, Health and Pathobiology

College of Veterinary Medicine

North Carolina State University

Raleigh, NC 27606

Preface

Native Dancer, 1950–1967, most celebrated and successful Thoroughbred racehorse and stallion.

fpref-fig-5001

The atlas is intended as a reference for readers interested in the pathology of equine diseases. It features macroscopic digital images of equine diseases supplemented by microscopic transparencies and a text highlighting the main aspects of equine diseases and disorders. The atlas is structured according to different body systems and emphasizes pathologic aspects of diseases in the neonate, juvenile, and adult horse. While attempting to incorporate as many diseases for which information and illustrations were available, the editors are aware that some may have been omitted by chance. Not all images are of best quality as these are from historic entities for which better examples were not available. For very unique equine diseases, contributions from colleagues in the field were solicited. We gratefully acknowledge their willingness to share their material and knowledge.

As editors professionally engaged in a high number of equine necropsies and tissue biopsies, we acquired a substantial knowledge base and collected a plethora of pathologic illustrations during our careers. We would like to convey this richness of professional experience to the readership. We are thankful for having enjoyed the opportunity to first share the equine pathology with veterinary students, trainees in veterinary pathology, and clinicians at our institutions. With this volume, we strive to make our material and expertise available to a wider veterinary and equine community, especially general practitioners, farm managers, and veterinary pathologists. Although we attempted to keep most illustrations at the macroscopic pathologic level, we saw the need for microscopic, immunohistochemistry, and graphic support in disease entities where gross changes are usually absent or overlap and when morphologic aspects for differential diagnoses had to be clarified. We selected chapter contributors as experts in the field where we felt incomplete in our image collection and knowledge base. We also solicited individual transparencies from individual sources and made every effort to obtain their permission as copyright owners. We are aware that some diseases are incompletely covered and that we did not expand the geographic scope of our work beyond North America. We refer to other resources describing global equine diseases in more details. Resources to complement disease aspects in the atlas are available on the website as Dr. John M. King's Necropsy Show and Tell, Cornell University or Noah's Arkive, University of Georgia.

Finally we are grateful to our equine patients for providing us a large range of disease examples and the stimulus to engage in putting the atlas together.

Claus D. Buergelt, Gainesville, Florida

Fabio Del Piero, Baton Rouge, Louisiana

Acknowledgments

The core collection presented in this atlas is derived from the files of our institutions: Louisiana State University, the University of Florida, and the University of Pennsylvania. We thank our educational institutions for providing the cases.

Many people from other institutions around the world have generously contributed to the contents of the atlas. Our thanks and appreciation go to their support starting foremost with those who contributed chapters to the atlas: Julia Conway, Pamela Ginn, Julie Engiles, Ingeborg Langohr, and Donald Meuten.

In addition, with utmost appreciation and gratitude, we acknowledge Ted Clark (Canada), Perry Habecker (USA), John M. King (USA), and John Roberts (USA) for their enthusiasm for this work and for providing images from their files.

From the following individual educational institutions and practices we received contributions.

United States: R. Alleman, N. Allison, T.A. Banner, A. Boone, M. Calder­wood Mays, W. Carlton, J. Cooley, S. Diab, M. Drost, J. Edwards, P. Hambleton, J. Harvey, T. Haskett, A. Hattel, P. Isenbarg, J. Kennedy-Peters, M. Law, D. Meuten, S.A. Montgomery, J. Neel, L. Perryman, S. Petersen-Jones, M. Pozor, D. Richardson, L. Roth-Johnson, M. Sebastian, F. Shahriar, R. Smedley, P. Stromberg, F. Uzal, B. Valentine, B. Williams, N. Williams.

Brazil: D. Driemeier and R. Fighera.

Canada: S. Ashburner and R. Foster.

Italy: C. Cantile and R. Rossi.

United Kingdom: D.T. Blunden and E. Milne.

Switzerland: F. Ehrensperger.

M. Kiupel, Diagnostic Center for Population and Animal Health, Michigan State University, performed and provided the immunostaining of mesothelioma and hepatoblastoma cases.

The editors of the Journal of the American Veterinary Association, Cambridge University Press, and Elsevier gave us permission to use several illustrations. The Animal Technology Institute Taiwan granted permission to reprint images originally published in an Atlas of Alimentary Tract Pathology, by C.D. Buergelt, R.M. Chu, and R.C.T. Lee.

We thank Ingeborg Langohr, Michigan State University, for reviewing the manuscript and for ideas and suggestions for improvement; J. Abbot for improving images; Nancy Buergelt for encouragement, patience, computer help, and sharing interest in the project; and Susan Engelken and Erica Judisch at Wiley Blackwell for their advice, support, and patience in helping make this atlas possible.

C.D.B.

F.D.P.

1

The Equine Necropsy


I. General considerations
II. Techniques
1. Positioning, examining, and opening of the carcass
2. Evisceration of the abdominal, pelvic, and thoracic organs
a. Cranial mesenteric artery
3. Removal of the brain and spinal cord
4. Examination of the locomotor system
5. Examination of the placental membranes and the fetus
III. Tissue collection
IV. Recording of the findings of routine cases

I. General considerations

A necropsy can be defined as the orderly, systematic dissection of a cadaver. It should have as its objective to determine the cause of death or nature of a disease process. A necropsy always should be thorough and complete to obtain the best possible answer to the cause of disease or death. A partial necropsy yields only partial answers. Gross examination alone frequently provides an incomplete diagnosis. Additional microscopic, toxicologic, parasitologic, bacteriologic, virology, or molecular biologic assays are ancillary tests to obtain the most accurate final diagnosis. There are many methods to perform a complete necropsy. Regardless of the choice, to generate the most accurate outcome, the approach should always be the same so that no organs or tissues are overlooked.

Equine necropsies can be divided into three types: the disease-oriented necropsy, the insurance necropsy, and the medicolegal necropsy, each of them requiring a modified approach. The events of a necropsy should be documented by records of the physical findings and by photography, radiographs, collected specimens, and laboratory findings. Protective attire and the right set of instruments are important prerequisites for the adequate performance of a necropsy, so is the optimal environment under field conditions. The necropsy should be conducted within a reasonable time frame after death to avoid tissue decomposition. If euthanasia is performed, the animal should be bled out before the postmortem examination is begun to avoid spilling of blood into organs to be examined.

At the end of the necropsy, all observations should be written down or recorded. All findings should be documented objectively because the signed necropsy record becomes a legal document. The results of all ancillary tests including histopathology should be accompanied by a narrative and interpretation of the findings.

The necropsy procedure described in this chapter is taught at the University of Florida. Other methods are described elsewhere.

II. Techniques

1. Positioning, examining, and opening of the carcass

After the body weight is determined or estimated, the animal is positioned in left lateral recumbency. For identification purposes, a whole-body photograph is taken. If there is a tattoo or brand, these are recorded. The external examination involves all body orifices, mucous membranes including the lining, ocular sclera, the hooves, ears, eyes, and the condition of the hair coat. Valuable information concerning disease of internal organs can be obtained by observing color changes of visible mucous membranes. The gross examination should also include the nutritional status of the animal.

A ventral midline incision extending from the pelvis to the head facilitates the subsequent skinning of the carcass and reflection of the right front leg and hind leg. In the male horse the prepuce is reflected and testes removed from the scrotal sac. This is followed by opening of the abdominal cavity by incision through the abdominal wall.

2. Evisceration of the abdominal, pelvic, and thoracic organs

The abdominal viscera, in particular the intestinal tract, are checked for expected anatomic position. The amount and character of the peritoneal fluid (100–200 mL normal, clear, and straw colored) is assessed. After examination of the cranial mesenteric root, the entire gastrointestinal tract is removed to inspect and remove the remaining organs from the abdominal cavity. Individual organs are assessed for color, consistency, symmetry, and, where appropriate, aspect of the cut surface. Individual organs can be weighed and measured under certain circumstances.

Figure 1.1. Horse. Gastrointestinal Tract. The length of the gastrointestinal tract requires separation into four segments: stomach, small intestinal loops, large colon, cecum, and transverse small colon. (Reprinted with permission from Equine Medicine and Surgery, Colahan et al., Figure 3-55, Page 122, Copyright Elsevier, 1999.)

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The bones of the pelvic cavity are cut with a handsaw for removal of the organs of the pelvic cavity including the urinary bladder, rectum, and genital tract.

The right rib cage is removed from the chest using strong rib cutters. The entire pluck is removed en bloc, starting with loosening of the tongue from the oral cavity. The tongue is left attached to the esophagus, which is cut at the diaphragmatic hiatus and removed from the opened thorax together with trachea, lungs, and the heart. Trachea, lungs, and heart are separately examined.

Figure 1.2. Horse. Normal Heart. There are several methods of orderly dissection of the heart. Care should be taken not to mutilate major anatomic structures and pathologic alterations of the heart. The left and right heart sides should be identified before the atria and ventricles are opened. The pointed apex is entirely formed by the left ventricle.

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Figure 1.3. Horse. Opening of the Left Heart. The left ventricle is opened longitudinally by placing the cutting knife at the free lateral side. The cut is directed toward the left atrium, the tip of the instrument passing underneath the mitral valve leaflet toward the aortic ostium.

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Figure 1.4. Horse. Opening of the Left Heart. The mitral valve leaflet is cut and the ascending aorta is opened. Rinsing with water facilitates the assessment of various internal structures of the left heart. The entire heart is weighed and measurements of valvular circumferences and ventricular and atrial muscular thickness can be taken.

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Figure 1.5. Horse. Opening of the Right Heart. An incision is made by knife following the ventricular septum. The instrument is turned along the ventricular septum into the right atrium. Inspection of the internal structures is similar to the procedure listed for the left heart.

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a. Cranial mesenteric artery

After dissection of the perivascular tissue, the vascular branch is opened with scissors. The mesenteric arterial root lumen is checked for patency and smoothness of its intima to rule out the presence of Strongylus vulgaris larvae.

3. Removal of the brain and spinal cord

Before removing the head, cerebrospinal fluid can be collected by syringe from the atlanto-occiptal cistern for analysis to aid in the diagnosis of central nervous system disease. Decapitation is performed at the level of the atlanto-occipital joint. The guttural pouches near the occipital condyles are inspected. The cranial cervical ganglion is located next to the carotid artery in the dorsocaudal aspect of the medial compartment of the guttural pouches and can be felt as a bulge in the fold of tissue at that site.

The severed head is placed tightly into a vice or on a solid surface against a rigid object such as a wall or raised table corner.

Figure 1.6. Horse. Head. For a field necropsy, a simple method to access the brain is to perform a transverse craniotomy via handsaw through the middle of the head caudal to the last visible molar tooth toward the palatine bone and oral cavity, thus splitting the head into rostral and caudal parts.

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Figure 1.7. Horse. With the cranium open, both rostral and caudal portions of the brain can be removed with a gentle push. This technique is easier to perform if the mandible is removed at the temporomandibular joints and across the pterygomandibular folds to reduce the bulkiness of the equine head.

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Figure 1.8. Horse. Spinal Cord. Removal. Field Technique. (Reprinted from Equine Medicine and Surgery, Colahan et al., Figure 3-65, page 127, Copyright Elsevier, 1999.)

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For the removal of the spinal cord, institutional facilities use an electric band saw. The spinal cord can also be safely harvested with a handsaw under field conditions. After fleshing, it is preferred to divide the vertebral column into three to four major segments (cervical, two thoracic, lumbar). Depending on the suspected location of the pathologic process, one or all of these segments are cut transversely through the arches and bodies of adjacent vertebrae, leaving the intervertebral articulations intact.

Figure 1.9. Horse. Spinal Cord. The vertebral canal is exposed and the spinal cord segment is removed with scissors. This can be repeated on as many vertebrae as necessary.

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Figure 1.10. Horse. Spinal Cord. Normal. This piece measures the length of one vertebra and has the dura mater removed for better fixation.

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4. Examination of the locomotor system

As part of a routine necropsy, one should open a regular set of joints. This examination should be extended when clinical history identifies their involvement in lameness. Similarly, muscles and tendons are examined when indicated. Knowledge of joint anatomy facilitates a direct, safe approach to any joint. The skin over the selected joint should be removed to guarantee better visibility and sterility should there be the need to collect joint fluid for culture. Under normal condition, a slight amount of viscous straw-colored fluid oozes from an opened joint. A healthy articular cartilage has a moist, smooth, light bluish-white surface. The synovial fossae vary in size depending on joint location and age of the animal. In cases of laminitis, the hooves are separated proximal to the coronary band and the pedal bone can be exposed by splitting the hooves into halves with a handsaw or electric bandsaw.

5. Examination of the placental membranes and the fetus

Placentation in the mare is classified at the gross level as diffuse. The placenta is composed of chorioallantois, allantoamnion, and the umbilical cord. The examination of placental membranes is critical in determining events that led to abortion, stillbirth, premature birth, or prolonged gestation. Ideally, intact, noncontaminated, and completely preserved placental membranes are needed for meaningful diagnostic analysis. The total placenta should be weighed.

Figure 1.11. Horse. Placental Membranes. Both membranes are spread out; the chorionallantois as an “F” and the amnion as a flat membrane to which a small portion of umbilicus is attached. The visible chorionic surface on the bottom is velvety and reddened because it is rich in vasculature. The amnion on the top is normally thin and translucent and contains coiled muscular arteries. A yellow hippomane (allantoic calculus) is present between the placental membranes. Hippomanes contain lipids, cellular debris of desquamated fetal membranes, and mineral deposits. Their function is unclear.

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Figure 1.12. Horse. Placental Membranes. Several sites of tissue collection for histologic evaluation should be chosen from both placental membranes. (Courtesy Dr. J. Roberts, National Zoo, Washington DC.) (See also Chapter 12, “Diseases of the Reproductive Tract.”)

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The umbilicus severed from its attachment contains the urachus, two arteries, and, depending on the segment, covered by amnion or allantois, one or two veins, respectively. The length of the umbilicus should be measured. The umbilicus normally contains several twistings that should not be confused with pathologic twists.

The fetus should be weighed, its gender determined, and a crown-rump length established. A complete necropsy should be performed regardless of gestational age and tissue freshness. Autolysis rapidly occurs in kidneys and liver; lung and heart tissues stay relatively viable for some time.

III. Tissue collection

Depending on how much the complete necropsy reveals at the gross level, ancillary tests are required to determine the cause of death or nature of disease. These tests include histopathology, virology, bacteriology, toxicology, parasitology, serology, molecular biology, or postmortem radiology. Each test requires special handling of the selected specimen. Regarding histopathology, the collection of tissue should take into account sample size, fixation type, fixation time, and volume of fixative. There should be 10 times as much fixative as tissue volume.

IV. Recording of findings of routine cases

All observations should be recorded or written down at the end of the necropsy and ideally before the carcass and its remaining organs are disposed of. Gross abnormalities should be recorded in an objective and descriptive manner to allow the reader a mental image of what the prosector saw. The necropsy report should incorporate weights and measurements of organs as well as shape, color, texture, and aspect of the cut surface. The diagnoses should be listed in order of importance. At the end of the report, a comment should interpret the cause of death or nature of disease and explain possible inconsistencies between clinical history and pathologic findings. It should incorporate and interpret the results of all ancillary tests performed. Incidental findings, background pathology, or postmortem changes should be listed as such.


Equine necropsy – Fact sheet
Definition

Orderly dissection of a cadaver

Types
Objective

Performance of a complete necropsy to obtain a complete answer for the cause of death or nature of disease.

Special techniques for
Tissue collection
Recording

Dated and signed necropsy report


Selected reference

King R, Dodd N. 2009. The Necropsy Book. 5th ed. Guernee, IL: Charles Louis Davis DVM Foundation.

2

Diseases of Foals and Juveniles


I. Foal disorders and diseases
1. Congenital abnormalities
2. Acquired diseases
a. Neonatal isoerythrolysis
b. Actinobacillosis
c. Tyzzer’s disease
d. Clostridial enteritis
e. Salmonellosis and foal sepsis
f. Toxic hepatopathy
g. Immunodeficiency disease of Arabian foals
h. Patterns and comparison of foal lung diseases
i. Tumors
j. Miscellaneous disorders
II. Diseases of juveniles
1. Acquired diseases
a. Rhodococcus equi
b. Interstitial pneumonia
c. Gastroduodenal ulcer disease
d. Enteric bleeding events
e. Septic polyarthritis
f. Miscellaneous disorders

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.

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Figure 2.2. Neonatal Foal. Head. Hydrocephalus. The head is disfigured from protruding brain markedly filled with central nervous system (CNS) fluid.

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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.)

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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.

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Figure 2.5. Foal. Trachea. Cleft Palate. Milk Aspiration. The distal trachea in this foal with cleft palate is filled with milk.

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Figure 2.6. Foal. Lung. Aspiration Pneumonia. Secondary to cleft palate. The lungs are mottled, and major portions are consolidated.

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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.

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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.)

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Figure 2.9. Foal. Rear. Atresia Ani. Absence of tail.

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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.

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Figure 2.11. Overo Foal. Colon. Aganglionosis. Myenteric plexus ganglia are missing between the two layers of the tunica muscularis. (H&E)

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Figure 2.12. Foal. Liver. Portosystemic Shunt. Microscopic findings include fibrosis and duplication of arterioles in portal triads. (H&E)

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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.

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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.

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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.

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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.

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Figure 2.17. Foal. Thyroid Glands. Hyperplasia. Both thyroid glands are bilaterally and symmetrically enlarged. This condition can be seen in iodine deficiency.

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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.

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Figure 2.19. Foal. Luxation Patella. The foal exhibits a spastic leg.

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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.

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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.

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Figure 2.22. Foal. Vulva. Mucous Membranes. Neonatal Isoerythrolysis. These are yellow from bilirubinemia secondary to hemolysis.

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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.

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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.

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Figure 2.25. Foal. Kidney. Neonatal Isoerythrolysis. Pigmentary Nephrosis. The cortex is deep red from hemolysis and the medulla yellow from icterus.

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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.

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Figure 2.27. Foal. Lung. Multifocal Suppurative Pneumonia. Actinobacillus equuli bacterial emboli caused these multiple brownish abscesses via capillary colonization.

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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.

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Figure 2.29. Foal. Kidney. Bacterial Emboli. Myriads of A. equuli bacteria are entrapped within glomerular capillaries. (H&E)

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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.

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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.

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Figure 2.32. Foal. Liver. Tyzzer’s Disease. On cross section, multiple small, white, and yellowish coalescing areas are present suggesting necrosis and inflammation.

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Figure 2.33. Foal. Liver. Tyzzer’s Disease. Foci of coagulation necrosis are intermingled with mixed inflammatory cells. (H&E)

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Figure 2.34. Foal. Liver. Tyzzer’s Disease. A silver stain demonstrates filamentous brown bacilli within hepatocytes with an “Asian Letter” arrangement. (Warthy-Starry)

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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.

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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).

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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).

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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.

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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.

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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.

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Figure 2.41. Foal. Meninges. Salmonella Septicemia. The meningeal surface exhibits ecchymotic hemorrhage and a faint cloudy exudate suggesting fibrinopurulent inflammation.

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Figure 2.42. Foal. Heart. Salmonella Septicemia. The epicardium shows petechial and ecchymotic hemorrhage. Differential diagnosis: purpura hemorrhagica.

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Figure 2.43. Foal. Heart and Lung. Salmonella Septicemia. The epicardium is covered by a fibrin clot. The lungs are wet from edema.

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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.

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Foal septicemia – Fact sheet
Definition: Inflammatory response of various organs to embolic dissemination of bacteria from a primary source (nidus)
Primary source
  • Umbilicus
  • Digestive
  • Respiratory
Organ systems involved in pathology
Frequent
  • Lung
  • Kidney
  • Joints
  • Lymphoid system
Less Frequent
  • Central nervous system
  • Liver
Infectious agents isolated
Frequent
  • Actinobacillus equuli
  • Coliforms
  • Klebsiella pneumoniae
  • Salmonella
  • Streptococcus sp.
Infectious agents isolated
Less frequent
  • Listeria monocytogenes
  • Candida albicans
  • Aspergillus fumigatus
Risk factors
  • Poor umbilical hygiene
  • Colostrum deprivation
  • Nutritional imbalance
  • Management practices

f. Toxic hepatopathy

In the early 1980s, a paste probiotic product introduced to the market for stimulating appetite in neonatal foals was found to cause clinical signs of liver failure and subsequent death. Further investigations incriminated iron fumarate overload as responsible for the liver failure due to severe panhepatic necrosis.

Figure 2.45. Foal. Liver. Degeneration and Necrosis. Iron Toxicosis. Discoloration and decrease in liver size. The liver surface appears flattened in the center of the lobes.

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Figure 2.46. Foal. Liver. Degeneration and Necrosis. Iron Toxicosis. On cross section, the parenchyma appears reduced because the vascular and biliary structures are relatively prominent. Yellow discoloration is the result of icterus.

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Figure 2.47. Foal. Liver. Hepatocellular Collapse. Iron Toxicosis. Hepatic cords are in disarray. Hepatocytes are vacuolated and disintegrated (necrosis). Sinusoids are dilated. (H&E)

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Other acutely lethal toxins in foals to consider as differential diagnoses for sudden death are mycotoxins, organophosphates, ethionine, gentamicin, cantharidin, red maple leaf, and Indigofera plants.

g. Immunodeficiency disease of Arabian foals

Severe combined immunodeficiency disease (SCID) of Arabian Foals affects both the cellular and humoral immune systems of these animals at a young age. The disease is inherited by a non–sex-linked gene in an autosomal recessive mode. Of such affected animals 25% may be carriers of the defective mutated gene. The deficiency affects both T and B lymphocyte lineages blocking their development. Affected foals suffer from secondary adenoviral pneumonia, sometimes complicated by superimposed infection with Pneumocystis jiroveci (formerly carinii) or Rhodococcus equi. Affected animals have a largely reduced or even grossly inapparent thymus, small lymph nodes, and a small spleen indicating hypoplastic lymphoid tissue. The disease has been largely eliminated by genetic testing and selective breeding. Clinical and morphologic parameters for the diagnosis of SCID include hypogammaglobulinemia, lymphopenia of peripheral blood, and hypoplasia of lymphoid tissues, particular the thymus.

Figure 2.48. Arabian Foal. Head. SCID. Nasal and ocular discharges are indicators of a respiratory problem (pneumonia) in affected Arabian foals.

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Figure 2.49. Arabian Foal. Thymus. SCID. Hypoplasia. The thymus will be difficult to find grossly. Microscopically, it is characterized by paucity of lymphocytes in cortex and medulla. (H&E). (Courtesy Dr. L. Perryman, Colorado State University.)

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Figure 2.50. Arabian Foal. Spleen. SCID. Hypoplasia. The number of lymphocytes is reduced around the splenic arteriole because there is evidence of lack of connective tissue framework at the site of lymphoid follicles when compared to lymphoid atrophy of different etiology. (H&E)

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Figure 2.51. Arabian Foal. Lung. SCID. Adenovirus. Cranioventral Pneumonia. Plum-red discoloration of the cranioventral lung is suggestive of bronchointerstitial pneumonia by adenovirus infection.

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Figure 2.52. Arabian Foal. Lung. SCID. Bronchiolitis. Necrotizing bronchiolitis with intranuclear amphophilic viral inclusions. Intraluminal neutrophils can be observed. Adenoviral bronchiolitis is characterized by the presence of basophilic intranuclear viral inclusions in epithelial cells. (H&E)

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Figure 2.53. Arabian Foal. Lung. SCID. Adenovirus. Indirect immunohistochemistry demonstrates intranuclear adenovirus antigen within endothelial cells. (IHC)

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Figure 2.54. Arabian Foal. Lung. SCID. Pneumocystosis. Pneumocystis jiroveci is a frequent concomitant pathogen in SCID foals and can be detected by a special stain in alveoli markedly distended by highly proteinaceous fluid. (GMS). (Courtesy Dr. L. Perryman, Colorado State University.)

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Figure 2.55. Arabian Foal. Lung. SCID. Multifocal Caseous and Pyogranulomatous Pneumonia. P. jiroveci was detected microscopically in addition to R. equi.

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Hemogram of SCID foal obtained on three different days
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h. Patterns and comparison of foal lung diseases

Figure 2.56. Foal. Lung. Normal.

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Figure 2.57. Foal. Lung. Diffuse Atelectasis. The lung shows a uniform collapsed profile and brown color due to underperfusion and nonaeration.

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Figure 2.58. Foal. Lung. Cranioventral Necrosuppurative Bronchopneumonia. Consolidation of the cranial lung suggests aspiration or bacteria as causes.

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Figure 2.59. Foal. Lung. Locally Extensive Pneumonia. S. equi subsp. zooepidemicus was the cause.

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Figure 2.60. Foal. Lung. Abscesses. Hematogenous spread of bacteria such as A. equuli should be considered as the cause.

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Figure 2.61. Foal. Lung. Interstitial Pneumonia. Diffuse consolidation is present in all lobes. Such a lung feels firm on touch. The disorder results from type 2 pneumocyte proliferation and is of viral, bacterial, and/or toxic etiology.

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i. Tumors

Figure 2.62. Foal. Gum. Oral Congenital Hemangiosarcoma. There are small irregular fleshy growths in the gum next to the molars of the maxilla.

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Figure 2.63. Foal. Gum. Oral Congenital Hemangiosarcoma. Microscopic features that qualify for the diagnosis of hemangiosarcoma are bundles of spindled cells and plump and irregular endothelial cells lining small channels partially filled with red blood cells. (H&E)

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Figure 2.64. Foal. Liver. Hepatoblastoma. Multifocal, semi-firm brown/tan raised nodular growths extend throughout the liver lobes replacing the hepatic parenchyma.

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Figure 2.65. Foal. Liver. Hepatoblastoma. Microscopic features of the nodular tissue are packages of neoplastic round to polygonal hepatoid cells with no special histologic arrangement. Many of these cells have a vacuolar cytoplasm displacing the nuclei peripherally. Nuclei are round to ovoid to reniform with hyperchromatic chromatin. (H&E)

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Figure 2.66. Foal. Liver. Foal. Hepatoblastoma. The neoplastic cells show strong labeling for hepatocyte paraffin 1. (IHC)

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j. Miscellaneous disorders

Figure 2.67. Foal. Tongue. Parakeratosis. Candidiasis (Thrush). The surface of the tongue is affected by severe parakeratosis. Infection by the yeast Candida albicans is the cause of this lesion in immunocompromised animals. Bacteria such as S. equi subsp. zooepidemicus are differential agents in nonimmunocompromised foals.

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Figure 2.68. Foal. Esophagus. Parakeratosis. Candidiasis (Thrush). White plaques are suggestive of C. albicans infection.

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Figure 2.69. Foal. Kidney. Multifocal, Necrotizing Nephritis. Candidiasis. Areas of tan bulging tissue representing yeasts are spread within the kidneys.

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Figure 2.70. Foal. Kidney. Intralesional Candida sp. A cluster of yeasts positive for periodic acid-Schiff is located within tubules. (PAS)

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Figure 2.71. Foal. Kidney. Nephrosis. The pale kidney is moist and swollen. The animal was treated with aminoglycosides.

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Figure 2.72. Foal. Kidney. Microabscesses. Hematogenously spread and bacterial in origin. Streptococcus equi subsp. zooepidemicus was isolated.

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Figure 2.73. Foal. Brain. Focal Cerebral Encephalopathy. Area of malacia. Affected foals may become lethargic, dummies, or wanderers. Focal lesions may result from peripartum trauma or asphyxia-hypoxia during parturition.

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Figure 2.74. Foal. Spinal Cord. Hypoxic Ischemic Encephalopathy (Neonatal Maladjustment Syndome). Severe frank subdural and intramedullary spinal cord hemorrhage may result from dystocia or fetal stress during or after birth. The affected animals are incoordinated, unable to stand, unable to nurse, stuporous or hyperexcitable. Similar changes may be present in the brain.

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Figure 2.75. Foal. Brainstem and Dura. Multifocal Hemorrhage. Eastern Equine Encephalitis (EEE). Multiple petechiae and ecchymoses are the indirect result of EEE alphavirus infection.

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Figure 2.76. Foal. Skull. Fracture. Traumatic.

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Figure 2.77. Foal. Brain. Hematoma. Traumatic.

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Figure 2.78. Foal. Intestine. Perforation. Focal necrosis due to thrombosis resulted in perforation and septic peritonitis.

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Figure 2.79. Foal. Mesentery. Postprandial lymphangiectasia.

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Figure 2.80. Foal. Larynx. Perilaryngeal Cyst deforming Larynx. (Courtesy Dr. P. Habecker, University of Pennsylvania.)

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Figure 2.81. Foal. Heart. Mitral Valve. Ruptured Chorda Tendinea. The rupture had occurred at the papillary muscle insertion site. Pulmonary edema is a fatal complication.

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Figure 2.82. Foal. Heart. Atrial Septum. Valvula Foraminis Ovalis.

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Figure 2.83. Foal. Neonate. Head. Vibrissae. Prolonged hair around lips indicates hypermaturity.

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Figure 2.84. Foal. Neonate. Head. Nasal Deformity. Traumatic or body pregnancy.

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Congenital abnormalities of foals
Central nervous system
  • Hydrocephalus
  • Cerebellar abiotrophy
  • Optic nerve hypoplasia/aplasia
Cardiovascular
  • Ventricular septal defect (VSD)
  • Truncus arteriosus
  • Tetralogy of Fallot
  • Patent ductus arteriosus (PDA)
  • Persistent right aortic arch
Respiratory
  • Tracheal dysplasia
  • Wry nose
  • Diaphragmatic hernia
Gastrointestinal
  • Palotoschisis
  • Megaesophagus
  • Intestinal atresia
  • Atresia ani
  • Aganglionosis
  • Meckel’s diverticulum
  • Mesodiverticular band
Liver
  • Portal shunts
  • Hepatic fibrosis
Urinary tract
  • Horseshoe kidney
  • Renal aplasia/hypoplasia
  • Polycystic kidneys
  • Persistent urachus
Reproductive tract
  • Turner syndrome
  • Parovarian cysts
  • Segmental aplasia of the uterus
  • Umbilical hernia
  • Cryptorchidism
Skeleton
  • Atlanto-occipital malformation
  • Lordosis, kyphosis, scoliosis
  • Inferior brachygnathism
Tendons
  • Contractions
  • Angular deformities
  • Arthrogryposis
Skin
  • Congenital porphyria
  • Hyperelastosis cutis
  • Lavender foal syndrome
  • Presumptive chronic progressive lymphedema in draft horses
Hematopoietic
  • Immunodeficiency
Eye
  • Microphthalmia
  • Dermoids
  • Iris hypoplasia
Ear
  • Aplasia/hypoplasia of external ear