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Toxemia and endotoxemia

  1. Toxemia and endotoxemia Prof. Dr. Mohamed Ghanem
  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?