Department of Pathology,

UVAS, Lahore-Pakistan.

INFECTIOUS STUNTING SYNDROME OF BROILER CHICKS INCIDENCE, FEED CONSUMPTION

AND GROWTH TRAITS

By

G. MUSTAFA; S.A. KHAN and M. YOUNUS

(Received at 19/12/2004)

SUMMARY

120, day old commercial broiler chicks were obtained and divided into two equal groups i.e. control (A) and treatment (B). Each chick of both groups was weighed and then dosed with one ml of either tryptose phosphate broth (A) or prepared inocula (B) at the same day. Chicks of both groups were housed separately under similar standard and managemental conditions. In the subsequent period of the experiment, it was observed that these severely effected birds had few ruffled, short broken shaft, mature wing feathers and in the later stages of experiment, these birds had pale combs, wattles and shanks. During 28 days experiment, 20% of the inoculated birds died while none of the bird died amongst control group. To determine the “Feed Conversion Ratio” FCR sufficient amount of feed was provided to each group and the remaining feed in feeding troughs was calculated at the same weekly intervals. It was statistically concluded that Feed Conversion Ratio was severely impaired in birds of group B which remained significantly lighter in the weight at all the stages of the experiment. Hence we can estimate a successful induction of the syndrome by a crude intestinal homogenate prepared of the affected birds under local conditions.

Key words: Infectious stunting syndrome, broiler chicks, feed consumption.

INTRODUCTION

            Infectious stunting syndrome (ISS) is a condition causing growth retardation in young broiler chickens and more rarely in other strains of domestic fowl. It was first seen in Pakistan in 1983 in a few flocks, but now appears wide spread in the commercial broiler chickens in the whole of the country. The disease is of high economic significance and losses increase with age since the stunted birds eat well but do not gain weight (Jaffery et al, 1990.

            Clinically the syndrome is characterized by high early mortality, stunted growth, poor feed conversion, poor featherings, leg weakness and high incidence of lameness due to femoral head necrosis. Different clinical manifestations seem across the world have produced a variety names for the syndrome, like due to disturbance of growth and feathering it is called, “Runting and Stunting syndrome or Infectious stunting syndrome (Brace well et al 1984).

            The microscopic lesions during infectious stunting syndrome of broiler chicks consisted of lymphocytic renal and pancreatic interstitial infiltrates, dilated or cystic duodenal and jejunal crypts of lieberkuhn, increased crypt depth and increased cellularity in the intestinal lamina propria (Montgomery et al., 1997)

            The pathogenesis of this divasting syndrome of poultry is poorly studied in Pakistan. That is why the present project was designed to elucidate metabolic derangement and pathological changes is visceral organs of broilers suffering from experimentally induced infections stunting syndrome.

MATERIALS and METHODS

            120, one day old commercial broiler chicks were obtained from a commercial hatchery. Chicks were divided randomly into two equal groups, one as a control group (A) and the other as an inoculated group (B). Chicks at the same day of age were weighed and dosed per os one ml of either tryptose phosphate broth (Group A) or inoculum prepared from a crude intestinal homogenate of diseased birds (Group B). Birds were housed separately in two pens under similar standard managemental conditions. Feed and water were provided.

            Feed consumption of both the groups were determined at the end of every seven days, starting from day 1-28 of the experiment. A measured amount of sufficient feed was put to each group and the remaining feed in the feeders was weighed at the end of each week.  Feed consumption = total given feed – remaining feed in feeders. To demonstrate the weight gain, each chick of both groups was weighed individually at the end of every seven days. Thus, the correlation between the feed consumption and weight gain of both groups was determined separately throughout the period of investigation. 

            The tissues were processed for histopathology, prior to processing, the bones were incubated at 37^o C in 10 % formic acid for 2 hours for decalcification (Bancroft and Stevens, 1983 and Bancroft and Gamble, 2002).

            The data collected was analyzed statistically by applying students unpaired t-test- (Steel and Torrie 1980; Wayne and Daniel 1995, and Roger et al., 2003)

RESULTS and DISCUSSION

            During the present study it was observed that a higher number of birds died in the beginning i.e. post inoculation which gradually decreased in the subsequent weeks of the experiment. The mortality which took place in the present experiment was 20%. Generally, mortality is a feature of early acute phase of infectious stunting syndrome (Kouwenhoven et al, 1978 and Vertomen et al, 1980).

            Martland, 1989 stated that between 7 and 10 days, variation in size becomes more pronounced and at around 10 days of age mortality may increase again.  From approximately 14 days of age the syndrome enters a chronic phase which usually persists until the birds are slaughtered but results of our study differ from the report of Martland (1989).

            Stunting syndrome was induced successfully as judged by severely depressed weight gain, reduced consumption of feed and impaired feed conversion in inoculated poults (Angel et al 1989). Sell, 1991 observed that inoculation with the infective material had a dramatic impact on poults growth within a very short time.

It was also observed that weight gain was reduced by infection to a much greater extent rather than feed intake.

            Consequently feed to gain ratio which was much larger for the infected poults than for the control, illustrating that utilization of nutrients was impaired by the infection. During the present study, feed conversion ratio of both groups was also recorded by putting sufficient feed and calculating the remaining feed in the feeder at the end of every week. The difference in feed consumption to weight gain ratio increased through the experiment probably due to maldigestion and malabsorption. It was also observed that the overall weight of gastrointestinal tract of birds in control group was more, however, the percentage weight of gastrointestinal tracts of birds in inoculated group was significantly increased (Brace Well and Randall, 1984). Tang et al. (1987) observed that stunted birds exhibited severe weakness and had pale breast muscles. It was observed at necropsy that bird with swollen hock joint had transparent fluid in their synovial cavities and lesions of tenosynovitis were also observed. These findings are in agreement with earlier workers (Gouvea and Schnitizer, 1982, Dhillon et al,. 1986 and Tang et al,. 1987).

            The clinical and pathological observations were also alarming. Pancreas was of major significance as it presented a classical picture for understanding the pathogenesis of the syndrome. The affected pancreas was white or white to pink in colour and firm in consistency (Brace Well and Randall, 1984, Reece et al,. 1984, Derow, 1984 and Martland and Farmer, 1986). Much of work is needed to be done locally to understand the syndrome especially from the microbiological aspect. So, as to isolate the prevalent pathogens in our local environment to develop the control measures.

REFERENCES

Angel, C.; Roselina, Jerry L. sell and Darrellw. Trampel (1989): Stunting syndrome in Turkeys development of an experimental model. Avain Diseases 34: 447-453.

Bancroft J.D. and Stevens A.C. (1983): Decalcification of bone and the preparation of bone sections. Theory and practice of histological techniques, 305-306.

Bancroft, J.D. and Gamble M. (2002): Theory and practice of histological techniques, 5^th, Edi., Harcourt Pub. Ltd. pp: 63-125.

Brace Well, C.D. and Randal, C.J. (1984): The infectious stunting syndrome. Worlds Poultry Sci. J. 40: 31-37.

Dhillon, A.S.; Kibenge, F.S.B. and Page, R.K. (1987): Viral Arthritis in Fryers related to reo virus infection in Breeders. Avian disease 30: 613-616.

Gouvea, V. and Schnitzer, T.J. (1987): Pathogeneicity of avian reo viruses: Examination of six isolates and vaccine strain. Infect. Immun. 38: 731-738.

Jaffery, S.N.H.; Anjum, A.D. and Khan, M.Z. (1990): Stunting syndrome in commercial broiler chickens in Pakistan. P.V.M.A. 3^rd International Congress at Islamabad 199-204.

Kouwenhoven, B.F.G. Davelaor and Van. J. Walsum (1978): Infectious proventiriculitis causing runting in broilers. Avian pathol. 7: 183-187.

Martland, M.F. (1989): Advances in stunting and stunting and runting syndrome research. Prog. Vet. Microbiol. Immunol. Basal, Kargar 5: 108-131

Montgomery, R.D.; Boyle, C.R.; Maslin,W.R. and Magee, d.L. (1997): Avian diseases, 41(80-92) college of Vet. Medicine, Mississppi state University 39762-9825, USA.

Reece, R.L.; Hooper, P.T.; Tale, F.H.; Beddome, V.D.; Forsyth, W.M.; Scott, P.C. and Barr, D.A. (1984): Field clinical and pathological observations of runting and stunting syndrome in broilers. Vet. Rec. 115: 483-485.

Riddel, C. and Derow, D. (1984): Infections stunting and paneratic fibrosis in broile chickens in Saskatchewan. Avian diseases 29: 107-115.

Roger Mead, Robert N. Curnow and Anne, M. Hasted (2003): Statistical methods in Agriculture and Experimental biology, champion and Hall/CRC press company Boca Raton London New York, Washington, D.C.

Sell, J. (1991): Selected aspects of stunting syndrome in poultry zootexnica international, 50-53.

Steel, R.G.D. and Torrie, J.H. (1980): Principle and procedure of statistics. M.C Grew Hill Book Company Inc. New York.

Tang, N. Rai.; Fletcher, O.J. and Villegas, P. (1987): Comparative study of the Pathogenecity of avian reo viruses. Avian diseases 31: 577-583.

Vertomen, M.H.; Van ECK, H.H.; Kouwenhoven, B.N. Van Kol and ECK Van, J.H.H. (1980): Infectious stunting and leg weakness in broilers. Pathology and Bio-chemical changes in blood plasma. Avian Pathology, 2: 133-142.

Wayne, W. and Daniel (1995): Bio-statistics, a foundation for analysis in the wealth science. 6^th Edi. John willey and sons, New York.

To

                        Prof. Dr. Yehia Hefnawy

                   Secretary Board

                        Assiut Veterinary Medical Journal Faculty of Veterinary Medicine

1. A.    V. M.J./ISSN 1012-5973 Assiut University, Assiut Egypt

Dear Sir,

                        I am very highly obliged and thankful to your honour in regard of accepting my articles for publication in your Journal free of cost. It is submitted that I have corrected the research papers according to your kind direction, expect photographs which are not available.  Please find enclosed herewith two copies of research papers for publication in your well reputed  Journal and one floppy of disc (3.5) Microsoft Windows of research papers.

                        I appreciate your big favour in this regard.

With best wishes and compliments.

Yours Obediently.

Dr. Muhammad Younus  

Ph.D Scholar

Department of Pathology,

University of Veterinary and Animal Sciences, Lahore, Pakistan

E. Mail: Younusrana @ hotmail.com.