4

General systemic states

HYPOTHERMIA

Hypothermia is a lower than normal body temperature, which occurs when excess heat is lost or insufficient is produced.
Neonatal hypothermia is a major cause of morbidity and mortality in newborn farm animals within the first few days of life.
ETIOLOGY:

--Excessive loss of heat

Exposure to excessively cold air temperatures causes heat loss:
If increased metabolic activity, shivering and sustained muscular contraction and peripheral vasoconstriction are unable to compensate.
--Insufficient heat production
Insufficient body reserves of energy and insufficient feed intake result in insufficient heat production.
Hypothermia also occurs secondary to many diseases in which there may be a decrease in the ability to shiver and skeletal muscle contraction associated with decreased cardiac output, decreased peripheral perfusion and shock.
Examples:
include parturient paresis, acute ruminal acidosis (grain overload), and during anesthesia and sedation, and the reduction of metabolic activity that occurs in the terminal stages of many diseases.

Combination of excessive heat loss and insufficient heat production

A combination of excessive heat loss and insufficient heat production is often the cause of hypothermia. Insufficient energy intake or starvation of newborn farm animals in a cold environment can be a major cause of hypothermia.

HYPERTHERMIA

(HEAT STROKE OR HEAT EXHAUSTION)

Hyperthermia is the elevation of body temperature due to excessive heat production or absorption, or to deficient heat loss

ETIOLOGY

1- The major causes of hyperthermia are the physical ones of high
environmental temperature .
2- prolonged, severe muscular exertion, especially when the humidity is high,
the animals are fat, have a heavy hair coat or are confined with inadequate
ventilation, such as on board ship or during road transportation.

Other causes of hyperthermia:

3- Neurogenic hyperthermia damage to hypothalamus, e.g. spontaneous
hemorrhage, may cause hyperthermia or poikilothermia

4- Dehydration - due to insufficient tissue fluids to accommodate heat

loss by evaporation
5- Excessive muscular activity - e.g. strychnine poisoning
6- Miscellaneous poisonings, including levamisole and dinitrophenols


PATHOGENESIS
Unless the body temperature reaches a critical point, a short period of hyperthermia is advantageous in an infectious disease because phagocytosis and immune body production are facilitated and the viability of most invading organisms is impaired.
However, the metabolic rate may be increased by as much as 40-50%.
liver glycogen stores are rapidly depleted .
If anorexia ,there will be considerable loss of body weight and lack of muscle strength accompanied by hypoglycemia and a rise in non- protein nitrogen.
There is increased thirst due in part to dryness of the mouth.

An increase in heart rate occurs due directly to the rise in blood temperature and indirectly to the fall in blood pressure resulting from peripheral vasodilatation.

Respiration increases in rate and depth due directly to the effect of the high temperature on the respiratory center. An increased respiratory rate cools by increasing salivary secretion and the rate of air flow across respiratory epithelial surfaces, thereby increasing the rate of evaporative cooling.

Urine secretion is decreased because of the reduced renal blood flow resulting from peripheral vasodilatation, and because of physicochemical changes in body cells that result in retention of water and chloride ions.

When the critical temperature is exceeded, there is depression of nervous system activity and depression of the respiratory center usually causes death by respiratory failure. Circulatory failure also occurs, due to myocardial weakness, the heart rate becoming fast and irregular.

CLINICAL FINDINGS:

Elevation of body temperature
Increase in heart and respiratory rates,with a weak pulse of large amplitude, sweating and salivation occur initially, followed by a marked absence of sweating.
The animal may be restless but soon becomes dull, stumbles while walking and tends to lie down.
In the early stages there is increased thirst
Abortion. may occur if the period of hyperthermia is prolonged
and a high incidence of embryonic mortality has been recorded in sheep
that were 3-6 weeks pregnant. In cattle, breeding efficiency .


FEVER (PYREXIA )

Fever is an elevation of core body temperature above that normally maintained by an animal .

ETIOLOGY

Fevers may be septic, the more common type, or aseptic, depending on whether not infection is present.
Septic fevers
These include infection with bacteria, viruses, protozoa or fungi as:
Localized infection such as abscess, cellulitis, empyema.
Intermittently systemic, as in bacteremia, endocarditis.
Consistently systemic, as in septicemia.
Aseptic fevers
Chemical fevers, caused by injection of foreign protein, intake of
Dinitrophenols
Surgical fever, due to breakdown of tissue and blood
Fever from tissue necrosis, e.g. breakdown of muscle after injection
of necrotizing material
Severe hemolytic crises (hemoglobinemia)
Extensive infarction
Extensive necrosis in rapidly growing neoplasms such as multicentric
lymphosarcoma in cattle
Immune reactions - anaphylaxis, angioneurotic edema.


PATHOGENESIS:

Most fevers are mediated through the action of *endogenous pyrogens produced by granulocytes, monocytes and macrophages.

The most important and best known endogenous pyrogen is interleukin-1, produced by monocytes and macrophages. The febrile response is initiated by the introduction of an exogenous pyrogen to the body.
Exogenous pyrogens include pathogens such as bacteria, viruses, bacterial endotoxins, antigen-antibody complexes, hemoglobinemia in a hemolytic crisis, and many inorganic substances.
In hypersensitivity states, soluble antigen antibody complexes may act as mediators.
One of the most potent exogenous pyrogens is the lipopolysaccharide of Gram-negative bacteria.

Interleukin-1 initiates fever by inducing an abrupt increase in the synthesis of
prostaglandins, particularly prostaglandin E2, in the anterior hypothalamus.

The elevated prostaglandin levels in the hypothalamus raise the thermostatic set point and induce the mechanisms of heat conservation (vasoconstriction) and heat
production (shivering thermogenesis) until the blood and core temperature are
elevated to match the hypothalamic set point.

Effect of pyrogens on the hypothalamus

The effect of bacterial and tissue pyrogens is exerted on the thermoregulatory center of the hypothalamus so that the thermostatic level of the body is raised. The immediate response on the part of organs involved in heat regulation is the prevention of heat loss and the increased production of heat. This is the period of increment, or chill, which is manifested by cutaneous vasoconstriction, resulting coldness and dryness of the skin and an absence of sweating. Respiration is reduced and muscular shivering occurs, while urine formation is minimal. The extremities are cold to the touch and the rectal temperature is elevated and the pulse rate increased. When the period of heat increment has raised the body temperature to a new thermostatic level the second period of fever, the fastigium, or period of constant temperature, follows. In this stage the mechanisms of heat dissipation and production return to normal. Cutaneous vasodilatation causes flushing of the skin and mucosae, sweating
occurs and may be severe, and diuresis develops. During this period there is decreased forestomach motility in ruminants, metabolism is increased considerably to maintain the body temperature, and tissue wasting may occur.
There is also an inability to maintain a constant temperature when environmental
temperatures vary.
When the effect of the pyrogenic substances is removed, the stage of decrement, or fever defervescence, appears and the excess stored heat is dissipated. Vasodilatation, sweating and muscle flaccidity are marked and the body temperature falls.