May, 2006- Dr. Guillermo Zavala of the Poultry Disease Research Center, University of Georgia, provided an update on research on Runting and Stunting Syndrome (RSS) at a special session of the Southern Conference of Avian Diseases held concurrently with the January 2006 meeting of the Southern Poultry Science Society in Atlanta. The syndrome first emerged during the late 1970s in Europe and appeared in U.S. broiler flocks during 1979. Despite intensive research the specific cause was never defined, although specific strains of avian reoviruses were implicated. The problem resolved gradually over a three-year period, presumably as reovirus vaccination was intensified and parent flocks were also naturally exposed to the infectious agent during rearing, resulting in protection of progeny by maternal antibody transfer during the critical first ten days after placement.

During the late 1990s, runting and stunting syndrome re-emerged in Europe, Central America and North Africa, but at this time the more extensive problem of ALV-J infection complicated field diagnosis and research. Scientists affiliated with Intervet in Holland isolated a highly pathogenic strain of reovirus (ERS), which has serologic and molecular similarities to isolates obtained from complexes demonstrating the condition in Georgia and adjoining states.

Dr. Zavala emphasizes that RSS is a syndrome and that the clinical appearance, lesions and impact on performance are extremely variable. Factors that can influence severity include concurrent infection, especially with immunosuppressive viruses, climatic extremes and deficiencies in management including biosecurity and hygiene.

Various viral agents have been implicated in the appearance of the condition, although specific reovirus strains appear to be most frequently associated with problem complexes and farms. Other potential pathogens that have been evaluated include astroviruses which are responsible for avian nephritis, caliciviruses, rotaviruses, coronaviruses, enteroviruses and non-defined “small round” viruses.

Due to the persistence of runting and stunting syndrome in a number of complexes located in North Georgia, the PDRC undertook an investigation aimed at defining the primary and contributory pathogens in order to develop appropriate recommendations for prevention. Extensive epidemiologic analyses based on performance data have eliminated nutritional causes including rendered animal protein ingredients, soybean meal, fish meal, soybean and sunflower meals or mineral deficiencies and imbalances. Evaluation of affected flocks shows an overall increase in mortality of approximately 0.5 percent, and a 20-point decline in feed conversion efficiency. Depressed performance is invariably attributable to the proportion of extremely stunted birds in a flock.

Characteristic post-mortem changes include pale, thin-walled intestines, reduction in the size of the liver, a large gall bladder and undigested feed in the terminal intestinal tract. Histological examination of jejunal tissue shows a reduction in the number and density of intestinal villi responsible for absorption. Characteristic cystic enteritis is observed, located in the crypts of the villi which are responsible for proliferation of enterocytes that line the intestinal tract. Catarrhal enteritis, which is characteristic of many viral infections and which also follows clostridial enterotoxemia-mild coccidiosis complex, is absent in RSS.

Field observations suggest that a low brooding temperature increases the inherent variability in flocks and is generally reflected in depressed weight at seven days. Suboptimal brooding and improper distribution of heat may exacerbate losses in flocks predisposed to RSS.

A series of fifteen trials has been completed by the PDRC under the direction of Dr. Zavala, in an attempt to understand the causation and pathogenesis of the condition. Early trials were designed to reproduce the disease and to develop a consistently reproducible model. Stunting can be induced by administration of either crude homogenates or filtered material derived from affected chicks by the oral route at day old, suggesting a viral etiology. It was clearly demonstrated that placing susceptible chicks on used litter from affected flocks resulted in significant depression in growth rate by 20 days of age. Early studies eliminated litter beetles as a possible reservoir of the RSS agent and that infection with enteropathogenic enterotoxic E. coli was not involved in RSS. Intensive surveillance of the purity of commercial vaccines failed to reveal any infectious agent which may have been associated with the condition, including leukosis virus, reticuloendotheliosis virus, chick anemia virus and reovirus. Hemorrhagic enteritis virus (adenovirus) of turkeys, which stimulates antibody in broiler parent flocks in the affected area, was also eliminated as a possible causal factor.

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The series of trials conducted at the PDRC during the past year has clearly shown that litter is infective and that the occurrence and severity in flocks are inversely proportional to the duration of the intercrop interval, especially with periods as low as one to three days. Reproducing runting and stunting syndrome over four successive cycles resulted in 70 percent non-uniformity compared to 10 percent in non-exposed control flocks. Severely affected birds weighed 160 g compared to 650 g for non-exposed controls.

Differences in clinical effect following exposure to contaminated litter were demonstrated among current broiler strains as shown in the accompanying table.

No differences were observed in the performance of progeny from two hatcheries, one of which was implicated in the occurrence and severity of RSS. Heating litter to a temperature of 90 F to 105 F for five successive days did not markedly affect infectivity despite the susceptibility of reovirus to elevated temperature under experimental conditions.

An important finding from the PDRC trials related to the age susceptibility of chicks. If batches of chicks were transferred to infected litter at ages ranging from 11 to 21 days, they were refractory compared to day-old placements, which showed characteristic depression in growth rate.

Based on the studies conducted to date, it is accepted that reovirus strains, different from those associated with arthritis and previously-encountered retardation in growth rate, are in all probability responsible for the emergence of RSS. Litter maintains infectivity for approximately seven days, and reducing the duration of the intercrop interval will obviously increase the severity of losses on farms with a history of infection.

Current studies at the PDRC and other centers will involve developing autogenous reovirus vaccines to be administered to immature parent flocks in specific complexes affected by the syndrome. Diligent vaccination against reovirus infection by administering currently available live priming vaccines at approximately seven days and at 20 to 40 days is recommended to stimulate the immune system of parent flocks. This should be followed by administration of at least one dose of multivalent reovirus vaccine prior to onset of lay and in some cases with a mid-cycle boost.

Since the problem is confined to specific complexes operated by four U.S. integrators and is limited in geographic extent, RSS should be regarded as an erosive condition impacting profitability but not representing a danger to the entire industry. Studies conducted by the PDRC, which have yielded interim results, indicate the ability of field and laboratory investigators to respond rapidly to an emerging multi-factorial health problem in commercial broilers.