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. The disease has been identified in virtually all countries in which intensive poultry production occurs. It has been associated with several different enteric viruses and appears to be multifactorial, though the true etiology remains to be identified. Poor management may contribute to the problem.
Etiology and Transmission
The disease 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.
The disease is typically recognized in broiler chicks 1–3 wk old. It is characterized by uneven growth; temporary stunting; permanent runting; lack of pigmentation in the skin, feet, or beak; slow feathering; broken or twisted feathers (“helicopter wings”); undigested feed in the feces; and 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 vary with the particular agents or combinations of agents involved. Lesions often include enlarged proventriculi, small gizzards, pancreatic atrophy, 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. Because of the complex etiology and the presence of enteric viruses in normal flocks, laboratory investigations may be difficult to interpret, particularly because virus culture 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 severely affected birds. Good broiler farm hygiene will reduce the burden of challenge caused by multiple infectious organisms. Good flock nutrition and sanitation and avoidance of intercurrent disease are beneficial. No vaccines prevent malabsorption syndrome. Some reovirus vaccines are marketed to prevent the stunting and poor feed conversions due to pathogenic reoviruses. 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.
Last full review/revision September 2013 by Richard C. Jones, BSc, PhD, DSc, FRCPath