Ochratoxicosis

Ochratoxicosis occurs seldom in poultry. It is more lethal in acute toxicity. It caused by Aspergillus ochraceus that interferes with functions of kidney, proventriculus and gizzard by Ochratoxin toxin.

Ochratoxin is carcinogenic to humans. And type A is weakly mutagenic by induction of oxidative DNA damage. It causes immunosuppression and immunotoxicity in animals.

Etiology

• Ochratoxin is produced by the fungus Aspergillus ochraceous.
• This toxin is also produced by Penicillum veridicatum, five species of Aspergillus and six species of Penicillium.
• Toxin is derivatives of dihydroisocoumarin which is connected to L.β Phenylalanine.A and  dechlorinated B form of Ochratoxin  are naturally produced toxins in which A is the important toxin produced in large quantities.

Epidemiology

Prevalence of infection

• Problems occur worldwide, but especially climates with high temperature, high humidity and where grain is harvested with high moisture content.
• It is found in wide range of raw and processed food commodities all over the world.
• OTA production by A. ochraceus favoured by relatively high temperatures (13oC to 37oC).
• It is considered to be storage fungi, rather than field contaminants or plant pathogens.
• Toxin production occurs mainly when susceptible commodities are stored under inappropriate conditions, particularly at high moisture levels.

Economic impact

• Economic impact is considerable in some countries.

Predisposing factors

• High grain humidity, damage due to insects, and poor storage conditions are major predisposing causes.

Source of infection

• It was first reported in cereals, but has since been found in other products, including coffee, dried fruits, wine, beer, cocoa, nuts, beans, peas, bread and rice.
• It has also been detected in meat, especially pork and poultry, following transfer from contaminated feed.

Transmission

• The route of infection is by ingestion of fungal spores, which are readily carried in the air.
• Inhalation of spores also occurs.

Host affected

• Chickens, turkeys, ducklings are susceptible.
• Young birds are mostly susceptible to Ochratoxin.
• Ducks are seven times more sensitive to the acute effects of the toxin than chickens.
• Quails and turkeys are more sensitive than chickens.

Pathogenesis

• OTA is a potent nephrotoxin and causes both acute and chronic effects in the kidneys of all mammalian species tested.
• A level of 200 µg/kg in feed over three months is sufficient to cause acute damage to the kidneys of pigs and rats.
• OTA is also genotoxic (damages DNA) and teratogenic (damages the foetus) and is considered a probable carcinogen, causing renal carcinoma and other cancers in a number of animal species.
• Ochratoxin inhibits protein synthesis, produce acute proximal tubular epithelial necrosis in kidneys.
• Inhibits normal toxic acid secretion.
• Affected kidneys are white to tan, swollen, hard and may have pin- point urate crystals.
• Extensive damage may causes renal failure.
• There is dehydration, hyper uraemia & visceral urate deposition.
• Pasty white urates are deposited.
• Pericaridial, perihepatic, peritoneal and articular surfaces.
• These deposits may be mistaken for inflammatory exudate, but their true nature can be determined by microscopic examination of impressions smears.
• In surviving birds after renal failure, kidneys is enlarged, fibrotic and pale.
• In addition to the renal lesions there is mild to moderate fatty changes and glycogen deposition in hepatocytes resulting in yellow enlarged livers.
• Bursa and thymus reduced in size with immuno-suppression.

Clinical Signs

• No direct mortality caused by the Aflatoxin but more than 10.0 ppm may be lethal to the birds.
• Growing birdsDecreased growth rate.
• Poor feed conversion (>1.0 ppm).
• Decreased resistance to infections such as Salmonellosis, Coccidiosis, Infectious bursal disease and candidiasis.
• Increased condemnation during processing >0.5 ppm.
• Loss of pigmentation & increased bruising (>0.5 ppm).
• Diarrhoea.
• Paralysis or incoordination.
• Reduced feed efficiency.
• Reduced weight gain or egg production/hatchability.
• Increased condemnations.
• Pale shanks, combs, bone marrows.
• Poor egg shell quality and kidney poisoning.
• Adult chicks Adult birds may show decreased testicular weights, poor quality semen, decreased numbers of sperm counts & decrease fertility.
• Signs vary with the species affected, the mycotoxin, the dose ingested and the period of exposure.

Necropsy Findings

• Lesions also vary in accordance with the same factors as signs.
• Mycotoxins can cause damage to mucosae with which they come in contact.
• They can also be absorbed and affect blood coagulation, resulting in petechiae and larger haemorrhages in various tissues.
• Liver and kidney lesions- livers may be enlarged and fatty or show bile retention or tumours.
• Enteritis of variable degree may be seen.
• Mycotoxicosis- Liver is enlarged and haemorrhagic and gall bladder is distended with bile or with chronic exposure, this organ will be pale and friable with a small gall bladder.
• Mycotoxicosis- Loss of pigmentation in peak and feet Hydropericardium.
• Pale bone marrow.
• Regression of the bursa of Fabricius.
• Gizzard erosions.

Diagnosis

• Based on clinical signs and blood biochemical parameters such as anemia, elevated liver enzymes, serum bile acids, albumin:globulin ratio; prothrombin activity.

Differential Diagnosis

• Aspergillosis
• Other mycotoxicoses

Treatment

• The most effective treatment is removal of the source of toxins.
• Addition of antifungal feed preservatives is also helpful.
• Increasing protein level in the feed until mortality reduces may also be beneficial.
• Administration of soluble vitamins and selenium (0.2 ppm), along with finely divided copper sulphate in the feed 1 kg/ton for 7 days (where approved) has been used.

Prevention

• OTA is destroyed by acid and alkaline hydrolysis and by the action of some oxidising agents.

Control

• Mycotoxicoses may be prevented by careful choice of feed raw materials, reduction in water content of the raw materials and hygienic storage.
• Antimycotic feed additives may also be used but may not deal with toxins already formed.
• Feeds with high levels of fishmeals are particularly susceptible and should not be stored for more than 3 weeks.
• Pelletising feed may reduce fungal counts but does not affect toxins.
• Certain minerals additives have been shown to bind mycotoxins and reduce their effects.
• Good stock control, management of feeders and bins, and avoidance of feed spillage are all important.