Notes: Introduction and Fundamentals of Veterinary Pathology
Introduction to Veterinary Pathology
Veterinary pathology is a medical specialty studying lesions and mechanisms of disease across animal species.
In North America, veterinarians with a DVM or VMD train an additional years in pathology and are certified by examination as either:
anatomic pathologists (necropsy/postmortem and histology)
clinical pathologists (cytology, microscopic and biochemical analyses of blood, bone marrow, urine, and other body fluids/aspirates).
Similar certification programs exist in Europe and Japan.
Although there is overlap, this book focuses on anatomic pathology; clinical pathology is usually taught separately with dedicated texts.
Pathology aims to answer a question or solve a problem, with several investigation contexts:
Diagnostic pathology (autopsy/necropsy) to determine cause of death or explain decreased production in groups.
Surgical pathology via tissue biopsy or fine-needle aspirate to diagnose living animals and guide prognosis/therapy.
Forensic pathology to determine cause of death for legal purposes.
Experimental pathology in research settings to correlate morphology with clinical, genetic, immunologic, and biochemical data to elucidate pathogenesis.
Regardless of specialization, veterinary pathologists share a common goal: teaching pathology to students, conducting rounds and seminars, and contributing to textbooks.
Most graduates practice internal medicine or surgery; pathology remains an integral part of veterinary education and public health.
Pathology links basic sciences (anatomy, physiology) to clinical sciences and underpins lifelong learning.
The veterinary clinician and pathologist form a team at the forefront of animal and public health.
Information Fundamentals for Effective Use of this Book
Pathology is the investigation of disease, encompassing recognition and interpretation of structural/functional alterations (lesions) of cells, tissues, and organs, and the underlying microbial, parasitic, biochemical, genetic, and molecular mechanisms.
This book is divided into two sections to aid learning:
General pathology: chapters (Cellular and Molecular Mechanisms of Disease).
Systemic pathology: chapters (Pathology of Organ Systems).
An extensive online E-section contains appendices addressing fundamentals of veterinary diagnostic pathology (e.g., Appendix C: Postmortem Examination; Appendix D: Recognition and Interpretation of Macroscopic Lesions).
The general pathology section examines responses of cells/tissues to injury, focusing on:
cellular adaptations (degeneration, regeneration, restoration),
vascular disorders,
inflammation,
neoplasia,
mechanisms of infectious diseases,
and disorders of immunity.
The living body presents overlapping vascular, inflammatory, immune-mediated responses and disturbances of growth that occur concurrently or sequentially.
Diagnoses in Veterinary Pathology
Table I.1 summarizes the types of diagnoses and the information used:
Clinical diagnosis: relies on signalment, history, and physical examination; even with lab/imaging data, it may be tentative.
Gross (macroscopic) diagnosis: based on physical/endoscopic findings, exploratory surgery, or autopsy; can be definitive for some injuries (e.g., fractures).
Morphologic diagnosis: concise naming of a lesion pattern observed grossly or microscopically, derived from DDDEMT observations (see Table I.2).
Differential diagnosis: a ranked list (most likely to least likely) of diseases that could cause the observed findings, usually 3–5 entities based on clinical data and postmortem findings.
Definitive diagnosis: identifies the exact disease; may be morphologic in some cases (e.g., certain neoplasms) or require ancillary tests.
Etiologic diagnosis: emphasizes the cause (e.g., a specific infectious agent) rather than the lesion pattern; may be less useful than a definitive diagnosis.
Example given: Tyzzer’s disease (Clostridium piliforme) illustrating the progression from morphologic to etiologic and definitive diagnoses.
Ancillary tests (microbiology, parasitology, chemical analyses, immunohistochemistry, PCR) refine differential diagnoses toward a definitive diagnosis.
Neoplastic diseases can yield a morphologic diagnosis that is also definitive (e.g., a well-differentiated tumor) in certain contexts; traumatic lesions can also provide definitive morphologic diagnoses; nutritional/toxic lesions are often less specific and require differential diagnoses.
Language of Veterinary Pathology
Five essential terms to understand:
Cell: the smallest unit capable of independent survival and function.
Tissue: structural groupings of cells; four main types: connective, muscle, nervous, epithelial. Epithelial tissue contains many cell types (e.g., keratinocytes, enterocytes, hepatocytes).
Organs/organ systems: functional units formed during embryologic development.
Structure: organization and roles of cells/tissues/organs in homeostasis and response to injury.
Function: metabolic, biochemical, and genomic processes in homeostasis and disease.
Pathology focuses on disease and lesions; a lesion is a structural abnormality, not the entire disease. The phrase “no pathology is observed” is better written as “no lesion is observed.”
While many terms are shared with other veterinary courses, some terms carry different meanings across disciplines; precision in terminology is essential.
The root terms commonly used in pathology:
-itis: inflammatory diseases (e.g., steatitis, bronchitis, hepatitis)
-opathy: noninflammatory diseases (e.g., neuropathy, hepatopathy)
-osis: noninflammatory conditions and ongoing processes (e.g., cirrhosis, steatosis); includes degenerative states (e.g., calcinosis)
-omegaly: enlargement (e.g., splenomegaly, hepatomegaly)
-ectasis: dilation of tubular structures (e.g., bronchiectasis)
-penia: deficiency (e.g., cytopenia)
-plasia: formation/growth (e.g., hyperplasia, hypoplasia)
-trophy: nourishment or development (e.g., atrophy, hypertrophy)
-genesis: beginning or production (e.g., osteogenesis, carcinogenesis, pathogenesis)
-cele: distended space or sac (e.g., meningocele)
-oma: mass or tumor (e.g., granuloma, fibroma)
Necrosis is defined as cell death and the structural changes that follow cell death within tissues; it is central to recognizing many lesions. The term is extensively discussed in Chapter 1 and throughout.
The Greek-based noun- combining forms underlie the naming of disease processes (e.g., -itis, -opathy, -osis, -oma).
Important vocabulary caveats:
Pathology vs lesion: a lesion is a structural abnormality; pathology is the study of disease.
Context matters: the same word can have different meanings in different courses or tissues (e.g., malacia: brain liquefactive necrosis vs bone softening).
The book also covers inflammatory, noninflammatory, degenerative, proliferative processes, and other responses to injury.
Recognition and Interpretation of Lesions
Veterinary pathologists often view lesion recognition as problem solving, akin to detectives: obtain history, develop a diagnostic strategy, evaluate biopsy or postmortem specimens, and integrate nonmorphologic data (pathogen identification, toxin levels, chemistry, genetics) to reach a diagnosis.
Nonmorphologic techniques complement lesion interpretation:
Microbiology to identify infectious agents; toxicology; genetic tests; chemical analyses; immunohistochemistry; molecular diagnostics (e.g., PCR).
A complete diagnostic workflow may lead to a definitive diagnosis; however, in some cases, a definitive diagnosis remains elusive, and a differential diagnosis is provided.
In postmortem work, recognition/interpretation hinges on morphologic changes observed macroscopically and microscopically.
Foundations for recognizing lesions come from general pathology and are reinforced in systemic pathology chapters.
The concept of pattern recognition (see Table I.3) is central to building morphologic diagnoses and understanding pathogenesis.
Pattern Recognition in Postmortem Examinations
STEP 1: Assess signalment and history (species, age, sex, breed; diet, housing/environment, clinical signs).
Examples illustrate differences across animals (e.g., growing pig, young cat, older dog).
STEP 2: Identify and describe gross (macroscopic) lesions.
Examples show various lesion patterns in different species and contexts.
STEP 3: Characterize the pattern(s) of the lesions using key elements observed in STEP 2:
Key Elements: Distribution, Quantity, Color, Shape, Size, Firmness (density), Surface texture.
The combination of these elements forms a diagnostic picture when integrated with case context.
Pattern patterns can be tissue-specific (e.g., lungs, liver) or systemic.
STEP 4: Develop morphologic diagnoses and diagnostic reports by interpreting the observed patterns.
Examples (from Table I.3) illustrate differential MAGNITUDEs and pathogenetic pathways:
Example 1: Morphologic diagnosis = Suppurative and lobular bronchopneumonia; Causative agent = Mycoplasma hyopneumoniae; Mechanism = Inhalation leading to bronchial/bronchiolar damage and bronchopneumonia; Common disease name = Porcine enzootic pneumonia.
Example 2: Morphologic diagnosis = Fibrinous and granulomatous peritonitis, pleuritis, and vasculitis; Common disease name = Feline infectious peritonitis; Causative agent = Feline infectious peritonitis virus; Mechanism = Viral infection with macrophage involvement leading to polyserositis.
Example 3: Morphologic diagnosis = Chronic tubulointerstitial nephritis; Common disease name = Chronic interstitial nephritis; Causative agent/Mechanism = (illustrative; various etiologies possible, often immune-mediated or infectious; table shows pathogenesis pathways).
Mechanisms illustrated in Table I.3 include inhalation/infection leading to bronchopneumonia, viral infection and macrophage trafficking leading to vasculitis and polyserositis, and septicemia/toxemia leading to tubular injury and interstitial nephritis.
Pattern recognition helps distinguish acute vs chronic changes, focal vs multifocal vs diffuse involvement, and primary vs secondary processes.
Appendix D expands on macroscopic lesion recognition/interpretation details.
Specular Highlights in Gross Photography
Specular highlights are bright white areas on tissue surfaces in gross photographs.
They can occur on surfaces that are normal or lesion-bearing and must be distinguished from actual lesions.
Characteristics:
Bright white areas of varied sizes/shapes (RGB 255,255,255).
More prominent on smooth, shiny, or wet surfaces (serosae, e.g., pleurae, peritoneum).
Can be smaller (pinpoint) on roughened surfaces; hedge around underlying texture.
Cut surfaces illuminated during photography may show highlights due to exposed internal structures.
Highlights can be a mix: central solid area with peripheral pinpoints on surfaces that are irregular or curved (e.g., intestines).
Causes of roughened or irregular surfaces (leading to non-specular patterns) include:
Active hyperemia, fibrinogenesis, inflammation, granulation tissue, fibrosis.
Post-cut irregular exposure of internal microstructures (e.g., glomeruli, tubules).
Important diagnostic caveat: distinguish specular highlights from lesions such as fibrin, fibrosis, mineralization, or inflammatory exudates.
Figures in the book (e.g., Fig. I.1) illustrate various highlight patterns; additional materials discuss the physics of specular vs diffuse reflection (linked to a Physics Classroom resource).
Colors of Normal Tissues and Organs
Normal tissues/organs display colors resulting from a mix of five primary color groups and the microcirculation within tissues.
The book categorizes colors as:
White to gray: attributable to proteins and lipids in cells; includes some pigments and differences due to microarchitecture.
Yellow: related to lipids, carotene pigments, cytochromes, lipochromes, bilirubin, amyloid, hemosiderin.
Red: due to blood and erythrocyte presence in microcirculation; well-oxygenated blood is pink to red; poor oxygenation reddens or darkens blood.
Brown: melanin, myoglobin, cytochromes, bilirubin, hemosiderin, hematin.
Black: melanin, hematin, or exogenous pigments.
The natural color of a tissue also depends on its unique microcirculation (blood supply) and the presence of erythrocytes within the tissue.
Mechanisms shaping tissue color:
Colors of molecules/substances within cells: pigments such as melanin, myoglobin, cytochromes, bilirubin, iron, lipofuscin, and carotenoids contribute to tissue hues.
Erythrocytes and microcirculation: oxygenation status and flow influence tissue color; well-oxygenated erythrocytes yield pinking; poor oxygenation yields darker red tones; the amount of erythrocytes and flow rate also modulate color.
The text provides cross-references to E-Table D.1 for colors of normal organs and E-Table D.3 for colors in lesions; Appendix E offers photographs of normal organs for reference.
Colors of Lesions and Mechanisms of Color Change
Colors of lesions arise from variations in the five basic color groups, modified by pathogenesis and duration of disease.
Examples illustrating color changes:
Normal lung: pale pink.
Acute pulmonary congestion: red to darker red.
Chronic passive pulmonary congestion with hemosiderin accumulation: intermixed red/darker red and yellow/brown.
Pulmonary calcinosis: pinkish-white to pinkish-white-gray due to calcium deposition; may be pale overall.
Other color changes and their meanings:
Red: congestion, acute passive congestion, active hemorrhage; thrombosis; hyperemia; infarction (in certain contexts).
Brown: congestion (chronic passive), pigmentation (melanin, bilirubin, hemosiderin, hematin).
Black: endogenous pigments (melanin, hematin) or exogenous pigments (e.g., carbon).
In solid organs like kidney and liver, color density reflects parenchymal cell makeup and endogenous pigments; congestion darkens the tissue due to trapped erythrocytes; pale colors may indicate reduced perfusion, anemia, or generalized organ involvement.
In neoplasia, masses are often white to grayish or yellow (lipid content); neoplasms are often highly vascular and may appear pink; exceptions include melanomas (brown/black due to melanin) and hemangiosarcomas (red to blue-purple due to vascular channels and slow blood flow).
Mechanisms of color alteration in tissues (summary): intensity and hue changes reflect alterations in pigmentation, perfusion, tissue composition, hematologic factors, and mineralization; reference to detailed mechanisms in later chapters.
Mechanisms Involved in Alterations of Colors of Tissues and Organs
Entire-tissue color alteration patterns are often observed early in postmortem exams and reflect global changes:
Pale to almost white: anemia, hypovolemia, poor tissue perfusion.
Dark red to purple: poorly oxygenated erythrocytes, reduced venous flow, passive congestion.
Bright red or brown: chemically induced alterations in hemoglobin (e.g., carbon monoxide poisoning, methemoglobinemia).
Lung-specific notes:
The lung’s pink color in homeostasis results from an extensive microcirculation; inflation state at death affects perceived pinkness (fully inflated vs deflated changes intensity).
Pulmonary yellow staining indicates icterus (hyperbilirubinemia).
Kidneys and liver are solid organs; congestion from cardiac/vascular dysfunction darkens color due to entrapped erythrocytes; pale kidneys/livers indicate reduced microvascular perfusion or reduced erythrocyte presence.
Area- or region-specific color changes include:
White/gray-white: necrosis/infarction, cell swelling, inflammation, neoplasia.
Yellow: icterus, amyloid, bilirubin, lipid (steatosis).
Red: congestion, hemorrhage, thrombosis, hemorrhagic infarction.
Tan/brown: bilirubin, hemosiderin/hemosiderin deposition.
Neoplasms generally appear as masses that are white/gray to light pink to yellow; melanomas can be brown/black; hemangiosarcomas appear dark red to blue-purple due to vascular channels.
Shapes of Lesions (Key Element 4)
Shape and size are often interrelated; shape is a component of the morphologic diagnosis.
Shapes observed:
Nodules/nodular/mass: circumscribed, space-occupying.
Solid nodules/masses: tumors, granulomas, neoplastic or microbial emboli.
Cysts/abscesses: sacs of fluid or exudate with potential nodular appearance.
Hematomas: localized blood accumulations.
Noncircumscribed/poorly circumscribed: malignant tumors, hematopoietic diseases, inflammation, healing tissue.
Depressions/erosions/ulcerations: surface changes due to necrosis or disease processes.
Elevated/raised/plaquelike: nodular growths, fibrous or inflammatory surfaces.
Wedge-shaped/rhomboidal: typical of infarcts.
Shape assessment often occurs together with size and distribution to guide diagnosis.
Sizes of Lesions (Key Element 5)
Relative organ size and lesion sizes are assessed:
Organ size changes reflect vascular congestion, hypertrophy/hyperplasia, infiltrative neoplasms, or accumulation of substances; shrinkage (atrophy) often results from reduced blood flow, cell loss, or metabolic changes.
Lesion size ranges provide clues about lesion age:
Small lesions (roughly mm) are typically acute (necrosis, acute inflammation, edema) and may be hours to days old.
Larger lesions indicate more extended evolution (days to weeks or longer) and healing processes such as fibroplasia, fibrosis, granulomatous formation, or bone metaplasia.
In practice, lesion size alone is non-specific; distribution, color, shape, surface, and texture often yield more diagnostic value.
Some contexts: a solid, solitary mass > cm may be interpreted as benign; malignant tumors can be solitary but often invasive and rapidly growing; multiple masses of similar size throughout an organ suggest metastasis rather than a single primary tumor.
Firmness (Density) of Lesions (Key Element 6)
Soft lesions indicate acute processes (necrosis, inflammation, hemorrhage, edema, or fat).
Firmer lesions indicate chronic or organized processes (fibrosis, granulation tissue, granulomatous inflammation, proliferating cells, amyloid, mineralization, or bone).
Surface Texture of Lesions (Key Element 7)
External surface characteristics help differentiate lesions:
Fibrin overlays, rough/granular surfaces, capsules, and defined vs invasive edges.
Benign neoplasms tend to have confined/encapsulated edges; malignant neoplasms often have invasive, irregular, and haphazard edges.
Erosions/ulcerations indicate superficial necrosis and are prominent on mucosal surfaces.
Thorough examination of mucocutaneous junctions and mucosal surfaces is critical for detecting erosions/ulcerations during postmortem exams.
Diagnostic Pathology and Laboratory Reports
Diagnostic laboratories affiliated with veterinary schools are essential sources of case-based knowledge.
Students gain experience recognizing macroscopic and microscopic lesions in diagnostic settings and refine skills during clinical rotations.
Practicing veterinarians rely on pathology reports to understand macroscopic and microscopic findings and often consult pathologists.
The reporting framework in this book emphasizes:
Macroscopic (gross) reports and Microscopic reports.
The use of morphological terminology to describe lesions and to name patterns.
The role of positive planimetric and descriptive language in clinical decision-making.
Key reporting elements (macroscopic and microscopic) mirror the seven key elements described earlier and are elaborated in Appendix D and in the systemic chapters.
The book emphasizes the use of positional terminology (e.g., lateral, medial, dorsal, ventral) when describing lesions (see Fig. I.3: Directional Labels and Planes of the Animal Body).
Photographs and examples illustrate lesion descriptions; depth (z-axis) estimation is a skill often inferred from experience.
Macroscopic (Gross) Reports: Key Components
When evaluating gross lesions, pathologists consider:
Anatomic location and informative positional planes.
Colors of lesion tissue and adjacent normal tissue, particularly at interfaces.
Palpable characteristics (touch/feel).
Surface characteristics (color, texture).
Size of the lesion.
Shape of the lesion.
Density and distribution of lesions.
Structural arrangement of tissues/substances and their relationship to surrounding tissue.
Presence of expected normal materials (e.g., bile) or unexpected abnormal materials (e.g., fibrin, amyloid).
Odor or smell associated with the lesion (e.g., ammoniacal odor in uremia).
The process includes sampling lesions for further microbiological or histopathologic analysis as needed.
Microscopic Reports: Key Characteristics
Morphologic (microscopic) findings are described with:
Anatomic location of the lesion.
Size/volume and shape of affected cells and their nuclei.
Density and distribution of cells.
Structural arrangement of cells.
Nuclear and cytoplasmic chromatin characteristics.
Mitotic activity.
Tinctorial features with standard stains (e.g., hematoxylin and eosin): e.g., eosin staining rules, hematoxylin staining rules.
Normal materials (e.g., bile within hepatic canaliculi) or normal cells (e.g., lymphocytes in Peyer’s patches).
Abnormal materials (e.g., fibrin, amyloid), abnormal cells (inflammatory or neoplastic), or microbes (bacteria).
More detailed morphologic characteristics of lesions in specific disorders are presented throughout the organ-system chapters.
Color, Shape, and Pattern: Integration into Diagnosis
Colors, shapes, distributions, and other morphologic features are integrated with clinical history and ancillary tests to formulate diagnoses.
Pattern recognition teaches students to identify disease patterns that are characteristic of particular diseases or mechanisms (pathogenesis).
The book emphasizes that lesions exist in three-dimensional space (width, height, depth) and that depth estimation is often inferred.
The Plane, Planes, and Directional Labels (Fig. I.3)
Directional labels and planes of the animal body include:
Lateral, medial, dorsal, ventral; cranial and caudal; rostral and caudal; proximal and distal; plantar and palmar; dorsal/ventral planes; transverse, sagittal, and coronal-like references.
These terms help standardize lesion description across chapters and species.
In Conclusion: Application and Practice
Veterinary pathology blends descriptive morphology with clinical context to solve diagnostic puzzles.
The discipline trains students to write clearly, reason scientifically, manage data, and communicate with clients and colleagues.
The knowledge and skills acquired in veterinary pathology are transferable across companion, production, exotic, wildlife, and zoo animals.
Suggested Readings and further resources are provided online (www.expertconsult.com).
Appendix and Additional Resources Mentioned
Appendix C: Postmortem Examination (Autopsy) of Domestic Animal Species.
Appendix D: Recognition and Interpretation of Macroscopic (Gross) Lesions.
Appendix B: Photographic Techniques in Veterinary Pathology (lighting and specimen photography).
Online Appendices and resources include communication and collaboration in veterinary pathology (Online Appendix A).
Figures and tables referenced include:
Table I.1: Types of Diagnoses and Information Used.
Table I.2: DDDEMT nerve for constructing morphologic diagnoses (Degree, Duration, Distribution, Exudate, Modifiers, Tissue).
Table I.3: Pattern Recognition in Postmortem Examinations (Examples and Mechanisms).
Glossary of Key Concepts (Concise Reference)
Anatomic pathology: surgical/necropsy-based tissue diagnosis.
Clinical pathology: analysis of blood, urine, and other body fluids.
Morphologic diagnosis: naming a pattern of structural changes (gross or microscopic).
Etiologic diagnosis: naming the cause rather than pattern (e.g., a specific pathogen).
Differential diagnosis: a ranked list of plausible diseases producing the observed lesions.
DDDEMT: Degree, Duration, Distribution, Exudate, Modifiers, Tissue.
Specular highlights: bright white surface reflections in gross photos that must be distinguished from actual lesions.
Colors of normal tissues: white/gray, yellow, red, brown, black, influenced by pigments and microcirculation.
Pattern recognition: analytic process linking gross/microscopic lesions to diseases/mechanisms.
Planes/directions: anatomical terms used to describe lesion location and orientation.