Prof. Dr. Mohamed Ghanem
Definition of toxemia
Toxemia is a clinical systemic state caused by a
widespread activation of host defense mechanisms
to the presence of toxins produced by bacteria or
injury to tissue
Toxemia does not include the diseases caused by
toxic substances produced by plants or insects or
ingested organic or inorganic poisons
Definition of endotoxemia
most common form of toxemia in animals, caused by
presence of lipopolysaccharide cell-components of
Gram-negative bacteria in the blood, and characterized
clinically by abnormalities of many body system
Alteration of cardiopulmonary function
Decreased organ blood flow and metabolism
Increased vascular permeability
Decreased GIT motility
Decreased perfusion of peripheral tissue leading to shock
A high case fetality
These are protein substances produced by
bacteria that diffuse into the surrounding medium.
The important bacterial exotoxins are those
produced by Clostridium spp., for which
commercial antitoxins are available.
They may be ingested preformed, as in botulism,
or produced in large quantities by heavy growth in
the intestines, such as in enterotoxemia, or from
growth in tissue, as in blackleg and black disease.
These are exotoxins that exert their effect
principally on the mucosa of the intestine, causing
disturbances of fluid and electrolyte balance.
The most typical example is the enterotoxin
released by enterotoxigenic E. coli, which causes a
hypersecretory diarrhea in neonatal farm animals.
The endotoxins of several species of Gram-negative
bacteria are a major cause of morbidity and mortality in
The endotoxins are lipo-polysaccharides found in the outer
wall of the bacteria.
Endotoxins are released into the immediate surroundings
when thebacteria undergo rapid proliferation with production
of unused sections of bacterial cell wall or, most commonly,
when the bacterial cell wall breaks.
Endotoxin gains access to the blood when there is a severe
localized infection, such as a coliform mastitis in dairy
cattle, or a disseminated infection, such as coliform
septicemia in newborn calves.
These may accumulate as a result of
incomplete elimination of toxic materials
normally produced by body metabolism,
or by abnormal metabolism
toxic products produced in the alimentary
tract or tissues are excreted in the urine
and feces or detoxified in the plasma and
When these normal mechanisms are
disrupted, particularly in hepatic dys
function, the toxins may accumulate
beyond a critical point and the syndrome
of toxemia appears.
Examples: ketonemia (ketosis) and lactic acidemia
Clinical signs of Acute toxemia
The syndrome varies with the speed and severity of the toxic
process but the variations are largely of degrees.
Depression, anorexia and muscular weakness are common in
Calves do not suck voluntarily and may not have a suck reflex.
Scant feces are common but a low-volume diarrhea may also
The heart rate is increased and initially the intensity of the heart
sounds is increased, but later as the toxemia worsens the intensity
The pulse is weak and rapid but regular.
A fever is common in the early stages of endotoxemia but later the
temperature may be normal or subnormal.
Terminally, there is muscular weakness to the point of collapse
and death occurs in a coma or with convulsions.
Clinical signs of endotoxemia
Endotoxemia is most commonly associated with bacteremia
or septicemia due to infection with Grain-negative
organisms, especially E. coli.
The clinical findings of severe endotoxemia include:
Hyperthermia followed by hypothermia
Tachycardia followed by decreased cardiac output
Decreased systemic blood pressure
Cool skin and extremities
Congested mucosae with an increased capillary refill time
Muscular weakness, leading to recumbency.
Lethargy, separation from the group, inappetence,
failure to grow or produce and emaciation are
characteristic signs of chronic toxemia.
Leukocytosis and neutrophilia occur with mild
leukopenia, neutropenia and lymphopenia increase
in severity and duration with increasing severity of
A low plasma glucose concentration, high serum
urea concentration (nonprotein nitrogen)
Low albumin and protein
Adults have :
Removal of foci of infection (ambilicus infection in
Antimicrobial agent with Gm-ve spectrum
Aggressive fluid therapy IV to restore cardiac
output and increase urine output.
Lactated ringer solution
Isotonic saline solution
Hypertonic saline (7.5 % Nacl) or sod. Bicarb may
enhance tissue perfusion.
NSAID (analgesic, antipyretic and anti-inflammatory
Glucocorticoid such as dexamethazone to improve
cellular metabolism and gluconeogenesis
Antisera (hyperimmune serum)
Anti-lipid antibodies to bind to LPS preventing inflammatory
What is the difference between antigenic and