Fever

(Pyrexia, Febris)
Dr. Amar Nasir
Associate Professor (Medicine)
Department of Clinical Sciences
CVAS Jhang
Introduction
Humanity has but three great foes viz. fever, famine
and fight (war), of these the most terrible by far is
fever (William Osler)

Elevation of body temperature caused by stimulation

of thermoregulatory center under the influence of
pyrogens circulating in blood.
Characterized by increase in body temperature,
anorexia, depression and loss of milk production
Etiology
Different infections --- most common cause
Bacterial diseases
HS
BQ
Anthrax
Listeriosis
Mycoplasmosis
Brucellosis
Salmonellosis
Strangles
Glanders
Tetanus
Etiology
Viral Diseases
MCF
BVD
Rinderpest
Blue tongue
AHS (African Horse Sickness)
Rabies
Canine distemper
Canine hepatitis
Infectious coryza
ND
Etiology
Parasitic diseases
Babesiosis
Theileriosis
Anaplasmosis
Toxoplasmosis
Trypanosomiasis
Coccidiosis
Fungal
Aspergillosis, mycotoxicosis etc.
Etiology
Immune mediated disorders
Anaphylaxis
Drug allergies
Purpura hemorrhagica
Thrombocytopenia
Rheumatoid arthritis
Etiology
Septicemic and toxemic conditions
Mastitis
Metritis
Abscess formation
Endocarditis
Pericarditis
Arthritis
Pyelonephritis
Peritonitis
Pneumonitis
Hepatitis
Etiology
Tumors
Lymphosarcoma (Cancer of lymphocyctes &
Lymphoid tissues)
Squamous Cell carcinoma
Fibrosarcoma (malignant cancer of fibroblasts)
Melanomas
Etiology
Plant and chemical poisonings
Ergot
Mustard
Bracken fern
Castor beans
Gossypol
Thorn apple (Digitalis/Datura)
Drugs (levamisole, furazolidone)
Chemicals (iodides, arsenic, mercury)
Poisonous snakes, scorpions, spiders
Etiology
Miscellaneous
Massive burns
Trauma
Surgery
Intravascular hemolysis
Pathogenesis
Infectious agents, inflammatory lesions, massive tissue
damage or immune complexes--------release toxins
(exogenous toxins or pyrogens)
Lipopolysaccharides of gram –ve bacteria---most
common exogenous toxin
These, if present in blood ------- release low molecular
weight proteins from polymorphonuclear leukocytes,
lymphocytes, monocytes, macrophages
These proteins are endogenous pyrogens
Interleukin-I ---- most common, TNF
Pathogenesis
Endogenous pyrogens-----do not cross BBB directly
Bind to surface receptors on endothelial cells of blood
vessels close to neurons of hypothalamus.
This binding activates Ca channels ------leading to
influx of Ca ions into cells -------initiates activation of
phospholipase A2.
It along with cyclooxygenase -----production of PGE2.
PGE2 ----- release neurotransmitters ------- raise the
body temperature a new “set point or thermostatic
level.
Clinical findings
Rise in body temperature (>2F)
Depression
Loss of appetite
Constipation or diarrhea
Decrease in milk production
Chronic cases---emaciation and muscle wasting.
Signs can be distinguished with each stage of fever
Stages of fever
Stage-I: period of increment temperature or chill
Duration variable
Cutaneous vasoconstriction
Coldness and dryness of skin
Absence of sweating
Muscle shivering
Reduced respiration rate and urine production
Heart rate and core body temperature at increase
Stages of fever
Stage-II: period of constant temperature (Fastigium)
Body temperature remains constant but at higher set
point
Heat production and loss remains constant
Duration variable
 Stages of fever
Stage-III: Period of decrement temperature
(defervescence)
Vasodilatation
Sweating
Muscle flaccidity
Polyuria
Decrease in body temperature than stage-I
Diagnosis
CBC----leukopenia in early period
Leukocytosis with or without shift to left---later stages
Blood culture
Direct or stained smear
LFT
KFT
Abdominocentesis
Serology (virus)
Treatment
Specific treatment (Antibiotics, antiprotozoans,
antifungal, antitoxin or hyper-immune serum)
Symptomatic treatment (Antipyretics, steroids,
diuretics)
Sodium salicylate at 30-50mg/kg BW PO
Phenylbutazone at 10-20mg/kg SA, horses 2-4mg/kg
IV
Diclofenac sodium at 2.25mg./kg
Flunuxine meglumine 1.1-2.2mg/kg
Ketoprofen2-4mg/kg
Treatment
Adrenocortical hormones dexamethasone,
methylprednisolone and prednisolone
Diuretics (lower of body temperature and removal of
toxins)
Ammonium chloride, potassium nitrate, furosemide
Treatment
Fever mixture
Soda salicylate 30gm
Ammonium chloride 20gm
Potassium nitras 20gm
Magnesium sulfate 200gm
Water QS

Supporative treatment
 Hyperthermia

Heat stroke, heat prostration

Remarkable elevation in body temperature
Excessive heat production or absorption
Deficient heat loss
Cause –purely physical (not infectious)
Etiology
High environmental temperature and humidity
Observed in summer in tropics and subtropics
Severe muscular exertion, dehydration, electrolyte imbalance
(Pre-disposing factors)
Sweating-----absorbed heat loss
Decrease heat loss through sweating  >60% humidity
Ruminants -------suffer more -----unable to sweat
Exotic breeds -----less heat tolerant ------more prone
Fat animal with long hair coat or lactating animals ---more prone
Strychnine poisoning, damage to hypothalamus (neurological
hyperthermia)
Pathogenesis
Increased heat load or production
Homeostatic mechanism of temp regulation fail to
dissipate heat
Associated changes are:
Increased metabolic rate and non-protein nitrogen contents
in blood
Decreased liver glycogen and hypoglycemia
Increased heart and respiration rate (direct influence of
high temp and metabolic rate)
Critical point (108F)---depression of nervous activity and
respiratory center------sudden death
Clinical Findings
Sudden rise in body temperature
Increased heart and respiration rate
Dyspnea
Absence of sweating
Increased thirst
General depression
Month of high environmental temp and humidity---
indicative of heat stroke

Prolonged cases
Abortion
Early embryonic death
Renal or liver dysfunction
Myocardial necrosis
If untreated—convulsions, collapse , coma---death
Lab findings
No specific lab test
Liver, renal dysfunction may be observed
Differential diagnosis
Septicemic and toxemic conditions
HS
Anthrax
Black leg
Treatment
Continuous application of ice cold water
Ice cold water enemata
Fluid therapy (dextrose 5%, normal saline) at lower
body temp
Adequate drinking of ice cold water with common salt
Ice blocks to lick
Ventilated shelter---air movement or fan
Treatment
Antipyretics
Tranquilizers
Dextrose, multivitamins, minerals etc.----after
recovery from initial attack
Broad spectrum antibiotics---later stages
Avoid exercise, hard work, grazing during sunny days
with high humidity
Ad-libitum excess to drinking water
Hypothermia
Common in temperate areas
Lowering of body temperature than normal
Excessive heat loss or insufficient production
Cold, wet, windy weather
Cannot regulate body temp. by metabolic activity,
muscle tone or peripheral vasoconstriction
Etiology
Decreased muscular activity (newborns, old animals)
Metabolic conditions (hypoglycemia, hypocalcemia,
acidosis, electrolyte imbalance)
Damage to thermoregulatory center
Diseases causing hypoxia, peripheral vasodilatation,
cardiac dysfunction, coma, collapse)
Profuse diarrhea in winter
Over sedation/anesthesia
Exposure to cold/humid wind in winter
Emaciation –malnutrition----predisposing cause
Clinical Findings
Subnormal body temperature
Cold skin and extremities
Weak pulse
Shallow breathing
Depression and lethargy
Terminal stages ---- low cardiac output---hypoxemia,
coma—death

Development of hypothermia following hyperthermia

---bad prognosis
Treatment
Attempt to raise body temp
Avoid exposure to cold wet windy weather
Keep animal in pre-heated room or shed
Thermal blanket or heat pads
Pre-warmed dextrose solution (10, 25 or 50%)
Corticosteroids to prevent or treat shock
Hypoxia---warm humidified oxygen therapy
Rectal enemata with luke warm water
Raise body temperature slowly over period of time