South Dakota State University Open PRAIRIE: Open Public Research Access Institutional Repository and Information Exchange Agricultural Experiment Station Technical Bulletins SDSU Agricultural Experiment Station 1959 Studies on Control of Fowl Cholera T.A. Dorsey G.S. Harshfield Follow this and additional works at: http://openprairie.sdstate.edu/agexperimentsta_tb Recommended Citation Dorsey, T.A. and Harshfield, G.S., "Studies on Control of Fowl Cholera" (1959). Agricultural Experiment Station Technical Bulletins. 34. http://openprairie.sdstate.edu/agexperimentsta_tb/34 This Article is brought to you for free and open access by the SDSU Agricultural Experiment Station at Open PRAIRIE: Open Public Research Access Institutional Repository and Information Exchange. It has been accepted for inclusion in Agricultural Experiment Station Technical Bulletins by an authorized administrator of Open PRAIRIE: Open Public Research Access Institutional Repository and Information Exchange. 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Technical Bulletin 23 May 1959 Studies on Control of Fowl Cholera Veterinary Department CONTENTS Introduction ------------------------------------------------------------------- 1 Nature of Disease__________________________________________________________ 1 Occurrence ----------------------------------------- ---------------------- 1 Symptoms and Lesions______________________________________ 2 Epizootiology --------------------------------------------------------------- 2 Experimental Studies --------------------------------------------- 4 Studies of Pasteurella Multocida Strains_ _________________ 4 Detection of Carriers by Agglutination Test________________ 6 Immunization ---------- ----- ------------- 8 Treatment ------------------------- - - ----------- -------- 12 Summary and Conclusions____ ________ ______________________ __ 16 Bibliography ---------------------------------------- 16 lM-5-59-6661 Siudies on Conlrol of Fowl Cholera 1 T. A. DORSEY and G. S. HARSHFIELD 2 INTRODUCTION NATURE OF THE DISEASE Fowl cholera is a contagious dis­ Occurrence ease of domestic fowls and many Fowl cholera ranked with fowl wild birds caused by a bacterium, leuko.sis and coccidiosis to consti­ Pasteurella multocida. It is one of tute the three most frequently oc­ the oldest known infectious diseases curring diseases in poultry exam­ of poultry. Many reports on different ined at the South Dakota State phases of research on the disease College veterinary diagnostic labo­ have been published, dating to a ratory. It occurred at all seasons of period before Louis Pasteur, whose the year but was most prevalent name is associated with early during late summer, fall, and early studies of fowl cholera . Although winter months from August through the disease has received much at­ January ( figure 1 ). tention for over 100 years, its oc­ Most of the outbreaks of the dis­ currence is still widespread and ease in South Dakota poultry flocks control measures have generally were acute. In outbreaks of this na­ lacked effectiveness. ture, a heavy death loss occurred In South Dakota, fowl cholera early in the outbreak; then less has been a poultry disease of major acute, and sometimes chronic, cases importance for many years. Experi­ developed after the disease had mental work was undertaken at this been in progress for several days. station in 1944 to study fowl chol­ A few outbreaks were more chronic era as related to this area and to 1This study was financed in part by funds investigate the development or im­ from the North Central Regional Experi- provement of control measures to ment Station Cooperative Research Proj­ more effectively prevent losses from ect IC-6. 2Associate Veterinarian and Veterinarian, this disease. This bulletin is a re­ respectively, South D akota Agricultural port of that work. Experiment Station. 1 2 South Dakota Experiment Station Technical Bulletin 23 10 9 8 7 6 Cl) w Cl) 5 0 z ~ 0 4 LL 0 a::: 3 w CD ~ ::J 2 z 0 J F M A M J J A s 0 N D Figure 1. Average number of diagnoses of fowl cholera by month, 1949-58. from the onset. With these, the lameness resulting from swollen death rate was not so rapid, al­ joints ( figure 3). though duration of the outbreak Birds that died suddenly, showed was more prolonged. It was not un­ few lesions on necropsy. A few usual in flocks affected with chronic petechiae were found on the heart cholera for the disease to suddenly and serous membranes, particularly become acute with a heavy death over the gizzard fat. Small necrotic loss. foci also were found in the liver in Symptoms a nd Lesions less acute cases ( figure 4). Lesions Symptoms were lacking in most associated with the chronic disease acute cases. Birds would be found were characterized by accumula­ dead with no earlier sign of dis­ tions of a yellowish, caseous exu­ ease. In the chronic form, birds date in affected parts such as the air were affected in different ways. sacs, ears, ear lobes, wattles, or Respiratory involvement was com­ joints. mon and torticollis ("wry-neck") Epizootiology was observed occasionally ( figure Histories which were obtained 2). Some birds had swollen eyes, concerning individual outbreaks wattles, or ear lobes. Some showed of fowl cholera often suggested that Figure 2. Chronic infection in the ear causes torticollis. Figure 3. Localized chronic infection in the foot. Figure 4. Acute fowl cholera showing petechiae on the heart and small, ne­ the source of infection could have c11otic foci on the liver. been birds which were apparently normal, but were carriers of the spe­ cific organism. Some outbreaks oc­ curred after birds of a healthy flock had been exposed to another flock in which there may have. been birds carrying infection acquired during a previous outbreak. Others fol- 4 South Dakota Experiment Station Technical Builetill 23 lowed the introduction of cockerels Rosenbusch and Merchant ( 24 ) or pullets from another flock. Many made a study of a number of P. mul­ of the outbreaks occurred in late tocida strains of mammalian and summer or fall months after the as.­ avian origin and divided them into sociation of susceptible pull~ts three groups according to their raised on the farm with the older ability to ferment xylose, arabinose, flock, on range or in the poultry and dulcitol. This grouping was house. In some instances, a history correlated by tube agglutination of an earlier outbreak in the older tests. birds was provided but this was not A similar study was made at this always the case. laboratory with 364 P. multocida A source of infection could not strains of fowl origin. Fermentation always be determined, nor could it of xylose, arabinose, and dulcitol be explained why a latent infection was determined by color change in in a flock would suddenly develop Difeo purple broth base to which into an explosive outbreak with a 0.5% of each sugar that was filter heavy death loss. It was not deter­ sterilized had been added. Three mined whether such occurrences tubes, each containing 2.5 milliliters resulted from a sudden increase in of purple broth and the respective the virulence of P. multocida in the sugar, were inoculated with each P. carri r birds, from lowered resist­ multocida strain and incubated at ance of the birds, or perhaps a com­ 37°C. The final reaction was re­ bination of these and other fatcors. corded on the seventh day. Fmther EXPERIMENTAL STUDIES incubation was not carri d out be­ cause of evaporation. Studies of Pasteurella Multocida Table 1 shows the basis for Strains grouping these strains according to Most of the strains of P. multo­ fermentation reactions, and the cicla isolated from fowls submitted number and percent of strains for for diagnosis during the past 10- each group. year period were retained. Isola­ A few more xylose - negative tions were made from blood, liver, strains could have been included in or suggestive lesions on blood agar group I but were omitted because and identification was made bv their biochemical characteristic{s Table 1. D istribution of Avian P. multo­ and morphology. Subcultures from cida Strains According to Fermentation each new isolation were made on Reaction Difeo stock culture agar slants and Fermentation incubated 24 hours at 37°C. The Reaction Number tubes were sealed with waxed corks Xy- Ara- Dul- of Per- and then stored at room tempera­ Group lose binose c:tol Strains cent ture. Many strains were held in this I + + 306 84.06 manner for 3 years or longer with­ II + + 53 14.57 out transfer. Only a few strains be­ or - came nonviable by this procedure. III + + + 5 1.37 Studies on Control of Fowl Cholera 5 of their inability to ferment arabi­ lated intravenously with two 1 milli­ nose and/ or dulcitol. liter doses of each culture given 5 Reciprocal agglutination tests days apart. These birds were nega­ were made to determine whether tive to agglutination tests with the agglutination reactions might be different antigens prior to inocula­ correlated with biochemical reac­ tion. About 1 week after the last in­ tions in classifying these P. multo­ oculation the birds were bled from cida strains. Rapid, somatic anti­ the heart. The .serum was separated gens were prepared from group I, from the blood and preserved with II, and III P. multocida strains. The merthiolate. Agglutination tests method for preparing these anti­ were conducted by mixing one gens is described under the section, drop of antigen with .02 milliliter "D etection of Carriers by Aggluti­ of serum. Antisera of strains of each nation Test." group were tested with each anti­ The same strains of P. multocida gen. The results of these tests are that were used to prepare the rapid shown in table 2. antigens were used to inoculate These tests showed that the so­ chickens to . produce agglutinins. matic antigens of strains of group I Difeo tryptose phosphate broth was and group III were very similar. inoculated with the different strains They were not closely related to and incubated 24 hours at 37°C. those of group II. Group II strains, Incubation was then continued for 33 and 338, fermented xylose but 96 hours at 56°C. to remove the not arabinose and dulcitol.