Trichothecene Mycotoxins

Trichothecene Mycotoxins are powerful inhibitors of protein synthesis in host. Trichothecenes are different from most other potential weapons toxins because they can act through the skin.

Compared with some of the other mycotoxins such as aflatoxin, the trichothecenes do not appear to require metabolic activation to exert their biological activity.

Trichothecene Mycotoxins occurs fairly frequently in commercial poultry but at naturally occurring levels does not cause mortality.

Etiology

• The trichothecenes are a very large family of chemically related toxins produced by various species of Fusarium, Myrotecium, Trichoderma, Cephalosporium, Verticimonosporium, and Stachybotrys.
• There were been chemically related sesquiterpinoid trichothecane mycotoxins identified so far.
• Amongst 12,13-epoxytrichothecanes T-2 hydroxy T-2 (HT-2) diacetoxyscipenol (DAS Anguidine) and deoxynivalenol (DON, Vomitoxin) and Zearalenone (F2) through known for its effects but have minimal effects on commercial poultry.

Epidemiology

Prevalence of infection

• Tricothecene producing fungi grows at many temperature but toxin production is highest in cold (<20ºc) and  moist conditions.
• So, Trichothecenes are associated with Northern climates, particulary when grain harvests have been delayed into the winter months or infected grain has been stored in cold conditions.

Economic impact

• Losses due to reduced feed intake.
• Decrease growth and immunosuppression.

Sources of infection

• This type of toxins present frequently in wheat, corn (maize) and other poultry feed grains.
• Many species of Fusarium and  stachybotrys produces this toxins.
• Environmental conditions favours Fusarium and Stachybotrys growth and trichothecare production are distinct from those for Aflatoxin or Ochratoxin production.

Transmission

• Direct dermal application or oral ingestion, the trichothecene mycotoxins can cause rapid irritation to the skin or intestinal mucosa.

Host Affected

• All mammalian species and birds including chickens, animals and human beings are susceptible.

Pathogenesis

• Trichothecene mycotoxins produce their effects by two pathogenic mechanisms.
  • Direct epithelial necrosis
  • Radiomimetic effects that destroy rapidly dividing cells

T-Z Trichlorothecane Mycotoxin: Once the trichothecene mycotoxins enter the systemic circulation, regardless of the route of exposure they affect rapidly proliferating tissues. The trichothecene mycotoxins are cytotoxic to most eukaryotic cells. A minimum of 24 to 48 hours is required to measure the effects of the trichothecene mycotoxins on cell viability. It  causes epithelial necrosis of mucous membranes following contact. Ulcers occurs in organ having contact with contaminated food stuff. Thus erosions and ulcers on the hard palate, tongue, oropharynx and chemical burns on the tip of the tongue are due to the direct caustic effects of T-Z.

• DAS is epithelionecrotic but its effects are milder than T-Z.
• Trichothecane severely inhibits protein synthesis and mimic the lesions of acute severe radiation poisoning (radiometric).
• Tissue with short life spans and high turnover rates are affected by trichothecane.
• This accounts for T-2 suppression of haematopoiesis to produce anaemia and pale bone marrow.
• Lymphopoiesis is suppressed producing bursal and thymic atrophy and immunosuppression.
• Feather follicle epithelium replication is reduced producing breaks in shaft plumage on feathers.
• In severe cases replication of enterocytes is affected producing ulcerations in the intestine.
• T-Z very effectively produces oral ulcers at  low doses and produces radiomimetic  effects at slightly higher doses.
• DAS produces systematic radiomimetic effects at  low doses but is an inefficient producer of oral ulcers.
• DON is relatively non-toxic in poultry and produces no oral ulcers no feed refusal and no radiometric effects  at naturally occurring doses.

Clinical Signs

In Poultry

• Develop ulcers at the commissures of mouth, hard palate, adjacent to the peak, palantine cleft and on the dorsal surface of the tongue >2.0 ppm 7-2.
• Ulcers are not usually produced further beyond the oesophagus unless the birds ingest large quantity of toxic material containing feed stuff.
• Depends on the doses of toxin, ulcers appear in 3-4 days after initial toxin intake and continued as long as exposure persists.
• Ulcerative stomatitis leads to decreased feed intake, reduced gain and decreased feed efficiency.
• Intoxicated birds have poor feathering with breaking of shaft due to interruption of feathers growth.
• Birds become anaemic, immunosuppressed and depressed growth rate (>2.00 ppm T-Z).
• Intoxicated adult birds are more resistant but will develop oral ulcers and decreased egg production.
• The DON and T-Z in chicken produced lethargy, wing paresis, dysmetria and seizures.

In Animals

• Acute oral, parenteral, dermal, or aerosol exposures to trichothecene mycotoxins produces gastric and intestinal lesions.
• Hematopoietic and immunosuppressive effects.
• Central nervous system toxicity causes anorexia, lassitude, and nausea and suppression of reproductive organ function.
• Acute vascular effects leading to hypotension and shock.
• Corneal injury, inflammation and cutaneous irritations.
• Desquamation of the skin and considerable local irritation.
• Itching, pain, nasal discharge, epistaxis, cough, hemoptysis and dyspnea.
• Vomiting, diarrhoea, melena, abdominal pain, and acute gastroenteritis with hematemesis could be related to ingestion of toxin that was deposited in the upper respiratory tract and tracheobronchial region.

Necropsy Findings

• Causes epithelial necrosis of mucous membranes following contact.
• Ulcers occurs in organ having contact with contaminated food stuff.
• Thus erosions and ulcers on the hard palate, tongue, oropharynx and chemical burns on the tip of the tongue are due to the direct caustic effects of T-Z.

Diagnosis

• Based on clinical signs and blood biochemical parameters such as anemia, elevated liver enzymes, serum bile acids, albumin:globulin ratio; prothrombin activity.
• Demonstration of toxin and measurement of concentration.
• A number of cytotoxicity assays have been developed and include survival and cloning assays, measuring protein and deoxyribonucleic acid (DNA) synthesis by radio labeling procedures, and a neutral red cell–viability assay.

Differential Diagnosis

• Aspergillosis
• Ochratoxicosis
• Aflatoxicosis
• Other Mycotoxicoses

Treatment

• Remove infected materials.
• Wash the affected areas.
• Discard contaminated items.
• No vaccine for trichothecosis.
• Toxin binders shall be added in the feed materials.

Prevention

• Prevention by avoiding exposure
• Decontamination of feed materials
• Immunological prophylaxis
• Enzymatic prophylaxis
• Detoxification in feed materials

Control

• Provision of support therapy and antibiotics with antifungals.