Fundamentals of veterinary nosology, etiology and pathogenesis of livestock animal diseases

What is nosology: from norm and homeostasis to the pre-disease state

Nosology represents the study of diseases and forms of organism vital activity. In practical veterinary medicine, two main forms of interaction between a livestock animal and the environment are distinguished — health and disease. Health is defined as the prosperous state of the organism and its regulatory systems, which ensure the dynamic constancy of the internal environment (homeostasis). This allows the animal to adapt to changing external conditions without loss of productivity and performance.

Optimal vital activity indicators of healthy livestock reflect its living conditions and directly depend on four main factors:

• housing conditions;
• nutritional adequacy;
• breeding;
• competent economic management.

As reserve adaptation forces are depleted, physiological regulation ceases to cope with external stresses. The organism enters a state of pre-disease — a period of high susceptibility to the development of pathologies. Timely diagnosis of this state is critically important for conducting preventive measures, preventing morbidity and the loss of livestock animals.

Disease, dysregulation, and compensation mechanisms

A disease arises when exposed to adverse environmental factors that disrupt the regulation of homeostasis. In a diseased organism, physiological regulation is replaced by dysregulation — a pathological change in functions, where the activation of protective and adaptive mechanisms occurs simultaneously with the damage to structural elements. Each independent disease forms a nosological entity with a specific cause, pathogenesis, and symptomatology, accompanied by a drop in the productivity and economic value of the livestock animal.

The organism's response to the impact of a pathogenic agent can occur in several forms:

• Compensated state: the disruption of one organ or system is made up for by the increased functioning of another element. For example, in anemia, a decrease in the oxygen transport capacity of the blood is compensated by a drop in peripheral vascular resistance and improved blood flow. Under excessive loads, reserves are depleted and decompensation occurs.
• Pathological reaction: a short-term inadequate response of tissues or systems to a stimulus (temperature, allergic, vascular, or leukocyte reactions).
• Pathological state: a stable morphological change that has become the consequence of a past process and thereafter practically does not develop (scars, bone calluses after fractures, heart defects, absence of organs or limbs). Under increased load, it easily reverts back into a pathological process.

Classification of pathological processes and animal diseases

A pathological process represents a local change in the structure and function of tissues, organs, or systems with metabolic disturbance (wound and inflammatory processes, atrophy, degeneration). Unlike a disease as a whole, it is limited in nature and has the property of reversibility. For example, joint inflammation (arthritis) with timely treatment ends in the restoration of its structure and function. Without therapeutic intervention, the outcome becomes ankylosis — complete immobility of the joint, that is, a persistent pathological state.

For quick orientation and the correct choice of treatment tactics, several principles of disease classification are applied in veterinary medicine:

• By etiology: non-contagious, infectious, invasive (parasitic), and zoonoses (infections common to animals and humans).
• By treatment method: therapeutic, surgical, obstetric-gynecological (the division is conditional, since, for example, lung pathologies may also require surgical intervention).
• By level of damage: molecular, chromosomal, tissue, systemic, and diseases of the integral organism.
• By localization (systems and organs): diseases of the digestive system (enterology), respiratory system (pulmonology), nervous system (neurology), endocrine system (endocrinology), and liver (hepatology).
• By species affiliation: diseases of cattle, horses, pigs, poultry, fur-bearing animals, fish, bees, as well as a separate group of diseases in young animals.

Dynamics, forms, and stages of disease progression

The form and nature of a disease's progression depend on its duration, the degree of symptom manifestation, and the reactivity of the organism. When housing, feeding, or immune status conditions change, one form can transition into another.

Disease form	Duration	Progression features and examples
Acute	From several hours to 2–3 weeks	Rapid and intense clinical manifestation (strangles in horses, croupous pneumonia, poisoning)
Subacute	From 3 to 6 weeks	Intermediate position between acute and chronic forms
Chronic	Over 6 weeks	Lasts for months and years with weakly expressed clinical signs (tuberculosis, brucellosis)

Diseases with a characteristic set of symptoms are called typical, while those without clear signs are atypical. If the course of a disease is uneven and periods of improvement are replaced by a sharp exacerbation, such a period is called a paroxysm (crisis), and the disease is termed paroxysmal.

In the process of pathology development, the following phenomena may occur:

• Complication — the addition of a new pathological process to the main pathology (for example, pneumonia complicated by tuberculosis).
• Relapse — a recurring manifestation of a disease after apparent recovery (characteristic of non-infectious pathologies and malignant tumors).
• Reinfection — a secondary infection of the organism by the same infectious agent (brucellosis, tuberculosis).

The development of a disease is divided into successive periods. The latent (hidden) period continues from the moment of pathogen exposure to the first clinical signs. During this time, the organism actively fights the stimulus, and if the agent is eliminated, the disease may not develop.

Disease (condition)	Duration of the latent period
Burn	Several minutes
Influenza	Several hours
Tuberculosis	Several months

The latent stage is followed by the prodromal period — from the first symptoms to the full development of the disease. During this time, general symptoms predominate: elevated body temperature, rapid pulse and respiration, loss of appetite, and depression of the nervous system. Since specific signs of pathology are absent in the prodromal phase, precise diagnosis at this stage is extremely difficult.

The period of clinically manifest disease follows the prodromal period and ends at the time of recovery. All main signs of the condition, typical for a particular disease, develop (for example, spots on the skin in erysipelas, coughing in bronchopneumonia, diarrhea in dyspepsia). Thus, it becomes possible to form a fairly clear idea about the nature of the disease, the causes of its occurrence, and, therefore, to make a correct diagnosis.

The duration of the clinical period is also determined by the nature of the stimulus and the body's defenses: foot-and-mouth disease, erysipelas — several days; brucellosis, tuberculosis — several months.

It must be remembered that not all diseases proceed with characteristic external signs. And as symptomatology (the science of disease signs) testifies, the most frequent sign of a disease is pain ("disease" from the word "pain"), and this is a signal of distress in the organism. There is a multitude of signs: weakness, fever, swelling, redness, cyanosis, salivation, etc. There are signs that are barely noticeable and difficult to detect, especially in livestock animals, and for a number of diseases, there is a multitude of such signs.

It is important to know that groups of signs, constant and characteristic of individual diseases, are called syndromes. Pathognomonic signs are signs inherent only to specific diseases.

The final period of the disease (outcome) is characterized either by the recovery of the organism (complete, incomplete) or by death. With complete recovery, the organism and its organs are restored, both morphologically and functionally. However, the state of the organism does not always return to its original state, as the organism may acquire immunity or, conversely, hypersensitivity (allergy).

With incomplete recovery, the disruption of functions and structures that developed during the disease is not fully restored but is compensated for by the mobilization of the organism's reserves. Sometimes a pathological condition develops (kidney hardening, myocardial damage), whereby the animal is more susceptible to falling ill again.

Death occurs if the organism cannot adapt to the changed environmental conditions. The main causes of death are: 1) cessation of cardiac activity (damage to the heart or cardiac centers in the brain), 2) cessation of respiration (damage to the respiratory center in the brain). Death may occur instantaneously or gradually; in the latter case, it is accompanied by terminal states: agony and clinical death.

Agony is characterized by a profound disruption of all functions of the organism as a result of central nervous system dysfunction. In this state, respiration becomes intermittent, heartbeat is weakened, temperature is lowered, convulsions appear, and involuntary discharge of urine and feces occurs. It lasts from several hours to two days and transitions into clinical death.

Clinical death is characterized by the cessation of respiration and heartbeat; metabolic functions in cells are sharply inhibited. The duration of clinical death is 5-6 minutes, which is determined by the survival time of the higher parts of the nervous system (cerebral cortex) most sensitive to oxygen deprivation. Clinical death is a reversible process, and with certain interventions on the organism (on the heart and central nervous system), vital functions can be restored. Clinical death transitions into biological death, which is characterized by irreversible changes first in the central nervous system, and then in other organs and tissues.

1) algor mortis – at an ambient temperature of 18-20°C, the body temperature drops by 1°C per hour during the first 24 hours, and by 0.2°C during the second 24 hours;

2) rigor mortis - 8-10 hours after death;

3) livor mortis - as a result of tissue infiltration by hemolyzed blood;

4) putrefaction - grey-green spots appear (combination of hydrogen sulfide with iron).

Violent death in livestock animals can be the result of killing the animal by a human or another animal, or the result of an accident. Non-violent death occurs due to various diseases. It, in turn, can be sudden - the unexpected death of a healthy animal (cerebral hemorrhage, rupture of large vessels) or ordinary - the death of an animal after a more or less prolonged dying period in connection with various diseases.

Etiology (Gr. cause, study) — a section of general pathology that studies the general patterns, causes, and conditions of the emergence and development of diseases. In the study of disease, general etiology, which answers the questions of "why and how they arise," is one of the most important concepts in both scientific and practical terms.

Firstly, all diseases arise under the influence of certain causative factors. Secondly, diagnosing correctly and in a timely manner and determining the causes of diseases means opening a path to understanding the nature of diseases, as well as the principles of their prevention and treatment.

In the vital activity of an organism, numerous environmental factors create the necessary conditions for its existence as an open physiological system, carrying out metabolism and energy exchange in constant interaction with the environment. However, a complex of external causes and unfavorable conditions exceeding physiological limits can manifest a pathogenic effect on the organism and cause the development of disease. They can act directly on cells and tissues or indirectly, through reflex and humoral influences.

Alimentary factors — these are disruptions in the feeding of animals, physiologically unjustified or nutritionally unbalanced in terms of quantity and quality:

• general caloric or water deficiency, starvation;
• excessive intake of nutrients (storage diseases).

Mechanical injuries: from tissue damage to traumatic shock

Poor-quality feeding and violations of zoohygiene directly undermine the herd's resistance to diseases. When the ration is unbalanced, and the premises are damp with poor ventilation or lack of bedding, the animals lose productivity and produce weak offspring. Young animals born in such conditions are non-viable and become easy targets for opportunistic microflora. The specialist's task is to strictly control management parameters, exercise regimens, and feed quality.

Mechanical injuries occur upon contact with blunt or sharp objects, as well as from gunshot wounds and technological accidents. All lesions are divided into closed (without damage to the skin integrity) and open — with wounds, cavity penetration, and open fractures. Pain during an injury is provoked not only by direct irritation of receptors but also by the action of toxic tissue decay products. An additional pain factor is the metabolic waste of microorganisms at the site of the lesion.

Severe mechanical impacts lead to contusions and traumatic shock. A contusion is a general injury of the organism caused by a shock wave; it is accompanied by coordination disorders, dizziness, and hearing loss even in the absence of open wounds. Traumatic shock develops when extensive areas of the body are damaged and is expressed by a sharp suppression of all vital functions. Long-term consequences of injuries include persistent scarring, muscular motor disorders, and failures in internal organ function.

• Secondary traumatic shock — 4–6 hours later
• Critical area for 2nd-degree burns — 1/3 of the body surface
• Temperature rise during hyperthermia — by 3–4 °C
• Stages of tissue frostbite — 3 stages

Physical factors: burns, overheating, and hypothermia

Physical factors of pathology include fluctuations in humidity, air, temperature, exposure to electric current, radiant energy, atmospheric pressure, and ionizing radiation. High temperature exerts both a local effect in the form of burns and a general one in the form of hyperthermia. Burns occur under the influence of flames, hot steam, molten metal, or electric current. Prolonged exposure of an animal's unprotected head to direct sunlight leads to sunstroke.

Degree of burn	Characteristic pathological changes
1st degree	Skin redness (erythema)
2nd degree	Formation of blisters and vesicles
3rd degree	Tissue death (necrosis)
4th degree	Tissue charring

The general effect of high temperature causes overheating of the body (hyperthermia), which sequentially passes through three phases and ends in heat stroke. Understanding the dynamics of this process allows for timely intervention before irreversible changes occur.

1. First phase: vessels dilate, perspiration, respiration, and pulse increase, but body temperature remains within the normal range.
2. Second phase: blood pressure drops, protein breakdown intensifies, and body temperature rises by 3–4 °C.
3. Third phase (heat stroke): under-oxidized metabolic products accumulate in the body, clonic convulsions develop, and death occurs due to respiratory or cardiac paralysis.

Exposure to low temperatures manifests as local frostbite or general hypothermia. Frostbite in livestock animals is most often localized on the extremities: ear pinnae, tail, teats of the udder, and genitals. Local damage includes three sequential stages: vascular spasm followed by vasodilation (redness), blister formation, and tissue necrosis.

The development of hypothermia is facilitated by exhaustion, low body condition, wind, precipitation, and high humidity. First, compensatory mechanisms are triggered (shivering, huddling), then vessels dilate, lethargy and drowsiness increase, body temperature drops, respiration and heart rate slow down, after which death occurs. Colds and bronchopneumonia develop due to a drop in resistance in drafts and cold conditions, especially during irregularities in feeding.

Etiological factors: chemical and biological threats

Chemical poisoning and biological infections are key external causes of diseases in livestock animals. Toxic substances enter the body in solid, dissolved, or gaseous states via feed, water, or air. By origin, these poisons are divided into organic and inorganic.

Organic poisons include fungal toxins, alkaloids and glycosides of poisonous plants, as well as venoms from snakes and insects, and toxins from microbes and helminths. Inorganic poisons include acids, alkalis, heavy metal salts, and poisonous gases. Biological pathogens penetrate the body when natural defensive barriers are weakened.

The group of biological risk factors includes the following agents:

• pathogenic microbes and fungi;
• viruses and prions;
• protozoa and helminths;
• arthropods.

Under unfavorable conditions of housing and feeding, biological agents actively multiply in tissues and release toxins. Prevention of infectious and invasive diseases requires specialists to regularly monitor microclimate, quality of rations, and the sanitary state of facilities.

Pathogenesis: from primary irritation to systemic failure

Pathogenesis describes the mechanisms of the origin, course, and outcome of diseases. It is divided into general (studying universal patterns of pathologies) and particular (investigating the features of a specific disease). Etiology and pathogenesis are inseparably linked: the trigger factor determines the nature of subsequent structural and functional disorders.

The primary mechanism for the development of pathologies in higher animals is reflex-based. Nerve receptors perceive the impact of a harmful environmental or internal factor and transmit excitation via afferent pathways to the central nervous system. From there, the signal travels along efferent pathways to the organs, altering their function. Initially, these changes are protective in nature, but in the case of insufficient compensation, they escalate into a pathological process. The form of the reaction depends directly on the quantity and type of receptors in the affected tissue.

Site of toxic irritant (bile) injection	Result of the organism's response
Spinal canal	Epileptic seizure
Vein	Increase in blood pressure, increased respiration rate
Artery	Drop in blood pressure, decreased respiration rate

Direct impact on the central nervous system occurs during the accumulation of carbon dioxide, toxic metabolic products in the blood, or during mechanical damage to the brain. A pathological process can originate in any part of the nervous system. For example, respiratory rhythm disturbance occurs upon irritation of the pulmonary branch of the vagus nerve, the respiratory center of the medulla oblongata, or the hypothalamus. A rise in blood sugar levels occurs due to irritation of the medulla oblongata or the central end of a severed sciatic nerve.

Disruption of the relationship between the cerebral cortex and subcortical centers increases the excitability of the latter. This provokes deviations in the activity of the heart, digestive tract, endocrine glands, and leads to tissue dystrophy. A strong external stimulus during feeding can cause loss of appetite, and a sudden change in environment can lead to a decrease in productivity. Isolated local processes do not exist: a common skin abscess arises due to a decrease in resistance against a background of poor feeding and housing, after which it causes a systemic reaction of the organism — leukocytosis and a rise in temperature.

Pathways of pathogen spread and compensatory reserves of the organism

Pathogenic agents and tissue decay products spread from the primary focus throughout the organism via several pathways: through intertissue spaces (for example, the transition of inflammation from the tracheal mucosa to the bronchi), through direct contact of organs (pulmonary and costal pleura), as well as through blood vessels, lymphatic vessels, and nerve trunks. Barrier organs — the liver, spleen, and lymph nodes — are the first to capture microbes, viruses, helminth larvae, and toxins. However, by accumulating irritants, they themselves often turn into secondary pathological foci.

In response to the penetration of disease-causing factors, the organism employs internal compensatory resources. Under normal conditions, a healthy livestock animal uses only a small part of its organ potential, preserving the main reserve for extreme situations.

Organ or system	Resource utilization under normal conditions, %
Cardiac muscle	17–20
Respiratory surface of the lungs	20–25
Absorptive surface of the intestine	20–25
Glomerular apparatus of the kidneys	20–25
Functional elements of the liver	12–15
Capillary bed	10–15
Blood hemoglobin	50–60

The functional capabilities of the nervous and endocrine systems under ordinary conditions are also consumed only to an insignificant degree. It is precisely because of these reserves that the organism remains viable even after the resection of a significant part of the stomach or intestine, the removal of a kidney, and severe blood loss.

Physiological protective reactions of the organism include:

• fever and inflammatory processes;
• regeneration of affected tissues;
• production of specific immunity;
• excretion of pathogens with feces, urine, sweat, and vomit.

In highly organized livestock animals, the activation of compensatory mechanisms is regulated by the central nervous system via a reflex pathway. The restoration of the CNS functions themselves under the influence of strong and prolonged irritants occurs through protective inhibition. Such inhibition, including natural sleep, prevents the exhaustion and death of cortical cells, playing a key role in the adaptation of the organism to pathology.