Toxaemia:

• Toxaemia is a clinical systemic state caused by widespread activation of host defence mechanism to presence of toxins produced by bacteria or injury to tissue cells.
• It doesnot include disease caused by toxic substances produced by plants or insects or ingested organic or inorganic poisons.
• Most common form of toxaemia in large animals is endotoxaemia. It is caused by the presence of LPS of gram-ve bacteria in blood and characterized clinically by abnormalities of many body systems.
• Abnormalities of endotoxaemia includes:
  • Marked alterations in cardiopulmonary function
  • Abnormalities in leukon (neutropenia and lymphopenia) and thrombocytopenia that may lead to coagulopathies
  • Increased vascular permeability
  • Decreased organ blood flow and metabolism, leading to heart and renal failure
  • Decreased gastrointestinal motility
  • Decreased perfusion of peripheral tissues
  • High case fatality rate

Etiology:

• Bacterial infection: coli, Pasteurella spp, Histophilus somni
• Exotoxins produced by Clostridium sps
• Enterotoxins produced by E. coli affecting intestine
• Endotoxins as found in coliform mastitis
• Coliform septicemia in calves
• Metabolic toxins produced due to incomplete elimination of toxic materials produced by body

Pathogenesis:

• These toxins are normally present in intestines and intestinal mucosa provides efficient barriers and prevents toxin gets absorbed in circulation.
• Small quantities are absorbed into blood which are removed by liver.
• Endotoxemia results when liver starts failing and when mucosal barrier of intestine gets disrupted due to ischemia, necrosis, trauma, ionizing radiation, bacterial overgrowth or inflammatory disease.
• Toxins escaped from intestine gets access to peritoneum and gets access to blood stream and toxins appears in peripheral blood.

Endotoxemia also occurs when gram-ve bacteria containing LPS gains access into tissue /blood. Most of these organism liberate endotoxin during their proliferation and gains access to blood from primary foci of systemic or superficial tissue infections.

Clinical Findings:

Acute toxemia:

• Depression, anorexia, muscular weakness
• Calves donot suck voluntarily and may not have suckling reflex
• Scanty feces or low volume diarrhoea is present
• Increased heart rate, weak pulse
• Fever is common in early stages but later temperature may be normal or sub-normal.
• Animals collapses and death occurs with coma or with convulsions.

Endotoxemia:

• Severe peripheral vasodilatation with consequent fall in blood pressure
• Pallor of mucosa
• Hypothermia, tachycardia
• Pulse of small amplitude
• Muscle weakness
• Hyperthermia followed by hypothermia
• Decreased systemic blood pressure
• Cool skin and extremities
• Diarrhoea
• Congested mucus membrane with increased CRT
• Muscle weakness leading to recumbency
• Renal failure characterized by anuria
• If DIC develops, it is characterized by petechial and ecchymotic hemorrhages and sclerae with tendency to bleed from venipuncture sites.

Chronic toxemia:

• Lethargy
• Separation from rest of group
• Failure to grow or produce
• Emaciation

Laboratory Findings:

• Leukocytosis and neutrophilia in mild cases
• In severe case, neutropenia and lymphopenia
• Low plasma glucose concentration, high serum urea concentration, low serum albumin and total protein concentration in acute toxemia

Treatment:

• Principles of treatment of endotoxemia is aimed at:

1. Removal of foci of infection
2. Administration of antibiotics
3. Aggressive fluid and electrolyte therapy
4. NSAID or corticosteroids to reduce products of cyclooxygenase pathway

1. Removal of foci of infection:

• Bacterial toxins present in body system should be eliminated and infection foci should be removed.
• In case of ingestion of toxin, activated charcoal can be used to adsorb toxin preventing its absorption to bloodstream.
• Gastric lavage can be carried out in case of ingestion or hemodialysis in case of blood infection

2. Administration of antibiotics:

• Β-lactam antibiotics or aminoglycosides are useful in controlling bacterial infection and killing bacteria.
• NSAID should also be administered concurrently to remove inflammatory products and reduces pain, swelling in body.

3. Aggressive fluid and electrolyte therapy:

• Maintenance of peripheral tissue perfusion is important in treatment of endotoxemia.
• Large amount of isotonic fluids such as ringer’s lactate solution or other balanced fluid should be administered continuously over hours
• Hypertonic salines such as 7.5% NaCl rapidly increases blood volume, tissue perfusion and gives rapid response than isotonic fluids.

4. Administration of NSAID:

• These drugs suppress the production of thromboxane and prostaglandin and reduce acute hemodynamic response to endotoxemia
• Flunixin meglumine is most commonly used NASID in treatment of horses and cattle. Dose: 1.1-2.2 mg/kg, b.wt. IV/IM OD for 5 days’ maximum. In horse, it is administered @ 1.1 mg/kg, b.wt., BID, IV/IM
• Corticosteroid; dexamethasone @ 1mg/kg, b.wt., IV, OD improves tissue perfusion, decreases activation of complement, decrease neutrophil aggregation, protect against hepatic injury.