Malabsorption syndrome is a transmissible disease characterized by stunted growth and a lack of skin pigmentation in growing chickens, most commonly broiler breeds. Turkeys may also be affected; in these birds, it resembles poult enteritis mortality syndrome.
Etiology and Transmission
Malabsorption syndrome in poultry has been reproduced with bacteria-free intestinal homogenates, suggesting a viral origin. Enteroviruses, parvoviruses, astroviruses, caliciviruses, arenaviruses, togaviruses, reoviruses, and rotaviruses have been implicated. Enteroviruses, reoviruses, and mycotoxins have been considered the most likely etiologic factors, although recent reports suggest an important role for astroviruses and unusual parvoviruses. A problem hampering the understanding of the etiology is the inability to isolate these viruses. Because the disease is seen in very young chicks, it is likely the viruses are vertically transmitted, although fecal/oral spread occurs after hatching. The involvement of feedborne mycotoxins is not well understood. Poor management may contribute to the problem.
Malabsorption syndrome in poultry is typically recognized in broiler chicks 1–3 weeks old. It is characterized by:
lack of pigmentation in the skin, feet, or beak
broken or twisted feathers (“helicopter wings”)
undigested feed in the feces
poor feed conversion ratios
Diarrhea is common during the initial phases, and eating feces is seen. Other signs include lameness, osteodystrophy, and secondary encephalomalacia.
Severely affected birds do not respond immediately to changes in feed or management practices and are usually culled from flocks before processing. The number affected in a flock can vary from a few to 90%.
The severity and type of lesions resulting from both field and laboratory infections with malabsorption syndrome vary with the particular agents or combinations of agents involved. Lesions often include enlarged proventriculi, small gizzards, atrophy of the pancreas, thymus and bursa, and orange mucus in the small-intestinal lumen. No consistent microscopic lesions are found, although cystic lesions in the small intestine have been described, and sometimes changes are present in the bursa and thymus. Encephalomalacia or rickets may be seen occasionally, presumably as a result of malabsorption or malassimilation of nutrients.
Clinical signs and postmortem lesions permit a presumptive diagnosis of malabsorption syndrome in poultry. Because of the complex etiology and the presence of enteric viruses in normal flocks, laboratory investigations may be difficult to interpret, particularly because culturing of the virus may be difficult or impossible. Poor early management of flocks (especially feed and water supply and temperature control) may lead to a similar picture in the absence of specific infection.
Prevention and Control
There is no effective treatment for birds severely affected by malabsorption syndrome. Good farm hygiene will reduce the burden of challenge caused by multiple infectious organisms.
No vaccines prevent malabsorption syndrome. Some reovirus vaccines are marketed to prevent the stunting and poor feed conversions due to pathogenic reoviruses.
Good flock nutrition and sanitation and avoidance of intercurrent disease are beneficial. Feeds should be analyzed for dietary toxins, and high levels of toxins should not knowingly be fed to commercial poultry. Antibiotics and vitamin supplements can be helpful.
There have been no reported zoonotic risks associated with malabsorption syndrome.
Malabsorption syndrome can cause significantly reduced growth in affected birds.
It is likely of viral etiology.
No specific prevention or treatment is available.