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Toxemia and
endotoxemia
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
 Neutropenia, lymphocytopenia
 Decreased organ blood flow and metabolism
 Increased vascular permeability
 Decreased GIT motility
 Decreased perfusion of peripheral tissue leading to shock
 A high case fetality
Etiology
Etiology
Antigenic Metabolic
Exotoxins
clostridia
Enterotoxin
E.Col
i (intestine MM)
Endotoxin
LPS (E.Coli
Salmonella)
Abnormal
metabolism
Normal
incomplete
excretion
Exotoxins
 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.
Enterotoxins
 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.
Endotoxins
 The endotoxins of several species of Gram-negative
bacteria are a major cause of morbidity and mortality in
farm animals.
 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.
Metabolic toxin
 These may accumulate as a result of
incomplete elimination of toxic materials
normally produced by body metabolism,
or by abnormal metabolism
 Normally,
toxic products produced in the alimentary
tract or tissues are excreted in the urine
and feces or detoxified in the plasma and
liver.
 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
acute endotoxemia.
 Calves do not suck voluntarily and may not have a suck reflex.
 Scant feces are common but a low-volume diarrhea may also
occur.
 The heart rate is increased and initially the intensity of the heart
sounds is increased, but later as the toxemia worsens the intensity
may decrease.
 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:
 Depression
 Hyperthermia followed by hypothermia
 Tachycardia followed by decreased cardiac output
 Decreased systemic blood pressure
 Cool skin and extremities
 Diarrhea
 Congested mucosae with an increased capillary refill time
 Muscular weakness, leading to recumbency.
Chronic toxemia
 Lethargy, separation from the group, inappetence,
failure to grow or produce and emaciation are
characteristic signs of chronic toxemia.
Haematological changes
 Leukocytosis and neutrophilia occur with mild
endotoxemia
 leukopenia, neutropenia and lymphopenia increase
in severity and duration with increasing severity of
endotoxemia.
Serum biochemistry
 A low plasma glucose concentration, high serum
urea concentration (nonprotein nitrogen)
 Low albumin and protein
 Adults have :
 Low ca
 Low Mg
 Low Ph
 Low K
Treatment
 Removal of foci of infection (ambilicus infection in
calves)
 Antimicrobial agent with Gm-ve spectrum
 Streptomycine
 Gentamycin
 Polymyxin B
 Aggressive fluid therapy IV to restore cardiac
output and increase urine output.
 Lactated ringer solution
 Isotonic saline solution
Treatment (cont)
 Hypertonic saline (7.5 % Nacl) or sod. Bicarb may
enhance tissue perfusion.
 NSAID (analgesic, antipyretic and anti-inflammatory
effect)
 Phenylbutazone (phenylo-ject)
 Flunixin (fendyne)
 Glucocorticoid such as dexamethazone to improve
cellular metabolism and gluconeogenesis
 Antisera (hyperimmune serum)
 Anti-lipid antibodies to bind to LPS preventing inflammatory
cascade
Questions
What is the difference between antigenic and
metabolic toxemia?

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Toxemia and endotoxemia

  • 2. 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
  • 3. 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  Neutropenia, lymphocytopenia  Decreased organ blood flow and metabolism  Increased vascular permeability  Decreased GIT motility  Decreased perfusion of peripheral tissue leading to shock  A high case fetality
  • 4. Etiology Etiology Antigenic Metabolic Exotoxins clostridia Enterotoxin E.Col i (intestine MM) Endotoxin LPS (E.Coli Salmonella) Abnormal metabolism Normal incomplete excretion
  • 5. Exotoxins  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.
  • 6. Enterotoxins  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.
  • 7. Endotoxins  The endotoxins of several species of Gram-negative bacteria are a major cause of morbidity and mortality in farm animals.  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.
  • 8. Metabolic toxin  These may accumulate as a result of incomplete elimination of toxic materials normally produced by body metabolism, or by abnormal metabolism  Normally, toxic products produced in the alimentary tract or tissues are excreted in the urine and feces or detoxified in the plasma and liver.  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
  • 9. 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 acute endotoxemia.  Calves do not suck voluntarily and may not have a suck reflex.  Scant feces are common but a low-volume diarrhea may also occur.  The heart rate is increased and initially the intensity of the heart sounds is increased, but later as the toxemia worsens the intensity may decrease.  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.
  • 10. 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:  Depression  Hyperthermia followed by hypothermia  Tachycardia followed by decreased cardiac output  Decreased systemic blood pressure  Cool skin and extremities  Diarrhea  Congested mucosae with an increased capillary refill time  Muscular weakness, leading to recumbency.
  • 11. Chronic toxemia  Lethargy, separation from the group, inappetence, failure to grow or produce and emaciation are characteristic signs of chronic toxemia.
  • 12. Haematological changes  Leukocytosis and neutrophilia occur with mild endotoxemia  leukopenia, neutropenia and lymphopenia increase in severity and duration with increasing severity of endotoxemia.
  • 13. Serum biochemistry  A low plasma glucose concentration, high serum urea concentration (nonprotein nitrogen)  Low albumin and protein  Adults have :  Low ca  Low Mg  Low Ph  Low K
  • 14. Treatment  Removal of foci of infection (ambilicus infection in calves)  Antimicrobial agent with Gm-ve spectrum  Streptomycine  Gentamycin  Polymyxin B  Aggressive fluid therapy IV to restore cardiac output and increase urine output.  Lactated ringer solution  Isotonic saline solution
  • 15. Treatment (cont)  Hypertonic saline (7.5 % Nacl) or sod. Bicarb may enhance tissue perfusion.  NSAID (analgesic, antipyretic and anti-inflammatory effect)  Phenylbutazone (phenylo-ject)  Flunixin (fendyne)  Glucocorticoid such as dexamethazone to improve cellular metabolism and gluconeogenesis  Antisera (hyperimmune serum)  Anti-lipid antibodies to bind to LPS preventing inflammatory cascade
  • 16. Questions What is the difference between antigenic and metabolic toxemia?