Advances in Knowledge of Poultry Diseases Over the Past Fifty Years*

Advances in Knowledge of Poultry Diseases Over the Past Fifty Years* H.

J.

STAFSETH

Department of Microbiology and Public Health, Michigan State University, East Lansing, Mich. INTRODUCTION

M

BACTERIAL DISEASES

Pullorum Disease. Advances of great scientific and economic importance were the discoveries of the cause (Rettger, 1900) and mode of transmission (Rettger and Stoneburn, 1909) of pullorum disease. This was the first time a bacterial disease had been proved to be egg-borne. The importance of the application of the macroscopic agglutination test to the detection of carriers of Salmonella pullorum (Jones, 1913b; Gage et al., 1914; Rettger et al., 1914) is well known to all concerned with poultry husbandry and control of disease. Important contributions toward the control and eradication of pullorum disease have been made by several organizations: 1. The Conference of Investigators and Workers in Bacillary White Diarrhea Control (W.R.H. 1928; Anon., 1930) greatly improved the agglutination test and other diagnostic and control procedures. 2. The Conference of Research Research Workers in Animal Diseases of * This is the fourth in a series of special articles being published in celebration of the fiftieth anniversary of the Poultry Science Association.

North America (Anon., 1933) formulated "Standard Methods of Diagnosis of Pullorum Disease in Barnyard Fowl." These methods were adopted by the Conference and also by the United States Livestock Sanitary Association in 1932. 3. The United States Department of Agriculture, through the National Poultry Improvement Plan (1941), has activated the above mentioned control measures on a large scale. The whole-blood, stained antigen test was developed independently by Schaffer et al. (1931) U.S.D.A., and Coburn and Stafseth (1931), Michigan State University. The simplicity of this test and the quickly obtained results have given it wide acceptance. Roznowski and Foltz (1958) reported on flocculation tests for pullorum disease. The antigen is a cholesterol-lecithin extract of S. pullorum and the test may be carried out as a microscopic slide-flocculation test or as a macroscopic tube-flocculation test. Results are clear-cut and easily read. The diagnosis of pullorum disease by bacteriological examination is relatively simple when fresh specimens are available, inasmuch as S. pullorum will grow on standard beef infusion agar. When specimens that very likely contain a number of different organisms are to be examined, enrichment and selective media have been found useful. Among these are: brilliant green liver infusion agar (Mallmann, 1929), tetrathionate broth, selenite broth, S S, and MacConkey agar. As an aid to quick identification of a newly isolated culture one might use an S. pullorum

741

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

OST of what we know about poultry diseases has been learned in the past fifty years. By now, the pertinent literature is voluminous. A review article of reasonable length, that is supposed to cover these fifty years of very productive research and learning, can do no more than touch upon the most significant advances, made in that period.

742

H. J. STAFSETH

Improved methods of incubator sanitation have materially advanced pullorum disease control. Formaldehyde fumigation of incubators, when properly done, has proved very effective in preventing spread of S. pullorum in hatcheries (Bushnell et al., 1929; Bushnell and Payne, 1931; Graham, 1941; Gwatkin, 1927; Insko et al., 1941; Burton, 1946). However, excessive formaldehyde fumigation may be harmful and has been proved to be so for poults (Bierer, 1958). Chemotherapy has met with limited success in the control of pullorum diseases. Several sulfonamides will reduce mortality, especially in young stock, but the number of reactors is not reduced, nor does chemotherapy eliminate the carrier state (Severens el al., 1945; Botorff and Kiser, 1946; Gwatkin, 1946; Anderson et al., 1948; Cole, 1948; Dickinson and Stoddard

1949; Grumbles et al., 1950; Cooper et al., 1951; Chang and Stafseth, 1950). In testing the efficacy of antibiotic therapy Chang and Stafseth (1950) found that streptomycin is bactericidal for S. pullorum and that its action was enhanced by the use of sulfadiazine. However, its effectiveness in eliminating the carrier state was no better than that of the sulfonamides. Smyser and VanRoekel (1957) treated naturally infected adult chickens with furazolidone at the rate of 40 mg./kg. of body weight. Agglutination titers were not reduced and 75 percent of the birds yielded S. pullorum at necropsy 6 and 8 weeks after the initial treatment. Much better results were obtained with experimentally infected chickens. The authors suggest that this drug may be of value in conjunction with the testing method. Dalowy el al. (1958) used 0.011 percent furazolidone in mash for chickens inoculated with S. pullorum (intermediate strain). At the level used furazolidone did not affect the agglutination titers, nor did it affect the recoverability of the organism. Beldingand Mayer (1958) obtained better results in poults. Fowl Typhoid. Fowl typhoid has many things in common with paratyphoid and pullorum disease. It is found in several European countries and in North and South America (Pfeiler and Rehse, 1913; and Van Straaten and te Hennepe, 1918). Egg transmission of Salmonella gallinarum was reported by Beaudette (1925), and by Beach and Davis (1927). These findings have been confirmed by many investigators; there is also evidence of contact infection and infection from contaminated premises. The disease is widespread in the poultry producing areas of this country, especially in the Eastern states. Glover and Henderson (1946) reported an outbreak which is believed to be the first in Canada.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

antiserum (Stafseth and Corbutt, 1940). However, the complex and related antigenic structures in the members of the genus Salmonella (Edwards and Bruner, 1946) limits the accuracy of this procedure. Burr et al. (1957) found that S. heidelberg will produce cross reactions in the standard pullorum agglutination test. Williams (1951) described a spot test for the diagnosis of pullorum disease. This test may make it possible to differentiate between false positive or nonspecific reactions on the one hand and true positives on the other. Wright et al. (1957) reported that the whole-blood test was not reliable for the detection of 5. pullorum in turkeys beyond 8-10 weeks after infection. In some cases the serum plate test with polyvalent antigen seemed more reliable. 5. pullorum was not isolated from artificially inoculated turkeys beyond 35 weeks after infection. Rhoades and Hanson (1957) studied the antigenicity and pathogensis of S. pullorum in growing chickens.

REVIEW OF POULTRY DISEASES

The clinical diagnosis of fowl typhoid is, therefore, relatively simple and can easily be confirmed by bacteriological examination and serological tests.

The methods of control and eradication are the same as for pullorum disease. Immunization, using bacterins, has been employed with variable results. Lambert (1933) experimented with breeding for resistance and showed that mortality could be materially reduced by selecting breeding stock for resistance. This sytem proved to be mutually effective against both fowl typhoid and pullorum disease. Depopulation is too costly when highly developed breeding stock is concerned. Treatment with sulfonamides and antibiotics have been tried with conflicting results. Certain sulfa drugs have been claimed to be quite effective in reducing mortality. Titkemeyer and Schmittle (1957) found that therapeutic doses of various drugs, notably furazolidone, reduced the percentage of recovery of S. gallinarum from artificially infected White Leghorn chicks. Paratyphoid Infections. By the term paratyphoid infections we mean, as far as poultry is concerned, those caused by salmonellae other than S. pullorum and S. gallinarum. Within recent years numerous such salmonellae have been isolated from poultry and identified by the KaufTmann-White system of serological typing (Edwards and Ewing, 1955). These infections have become very important in poultry, economically and with respect to public health. Salmonellae cause loss of production, death losses and confusing results in the tests for carriers of S. pullorum some of them have been responsible for outbreaks of food poisoning in human beings. Darby and Stafseth (1942) reviewed the literature on Salmonella infections common to man, animals and birds. Up to that time, 35 species had been isolated from fowl. By now, this number has been practically doubled. New ones are encountered from time to time in various

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

European workers report that the disease is more prevalent than before World War I. They also report on its seasonal occurrence, which apparently varies in different localities (Truche, 1923; te Hennepe and Van Straaten, 1921). S. gallinarum and S. pullorum are so closely related antigenically and with respect to biochemical activity that several European workers have considered them to be the same (Van Heelsbergen, 1929; Manninger, 1930; Miessner, 1930; Wagener, 1934; Haupt, 1935). In this country a considerable amount of literature has been published on the biochemical properties and pathogenic characteristics of this organism which suggests that they are different. However, in the 7th edition of Bergey's Manual of Determinative Bacteriology these two organisms are considered identical under the name S. gallinarum. To this writer, the most convincing indications that this organism is not identical with S. pullorum is found in its pathogenicity and in the symptoms and lesions produced. Generally S. gallinarum produces a more acute disease than does S. pullorum. The anemic comb and wattles are rather typical of fowl typhoid. Most of all, the changes in the liver, spleen and kidneys are rather characteristic, especially those in the liver and spleen. Depending on the degree of acuteness and stage of the disease, the color of the liver may be red to greenish brown or bronze. The liver, spleen and kidneys are usually swollen. Miliary necrotic foci in the liver and myocardium are also seen, besides pericarditis, peritonitis and catarrhal enteritis. This pathological picture is not at all characteristic of pullorum disease.

743

744

H. J. STAFSETH

Salmonella infections present a difficult diagnostic problem. Signs and lesions are not pathognomonic. Serological tests are of limited value because of the numerous related antigens that exist within this group. The only reliable diagnostic procedure is isolation and serological typing of the causative organism. Elimination of the infection from a flock is difficult, even when one resorts to depopulation and restocking with what is thought to be clean birds. The reason for this is that there are carriers of salmonellae, not only among chickens and

turkeys, but among guinea fowl, ducks, geese, pigeons, reptiles, cats and flies. Treatment with various sulfonamides and nitrofurans has been found valuable in reducing morbidity and mortality. However, following treatment, a certain number of carriers will remain. Therefore, birds that have recovered from an attack of paratyphoid should not be used for breeding stock even if they have been treated with apparent success; unless specific serological tests prove them to be free from the Salmonella infection concerned. Sulfonamides, if improperly used may be toxic. Antibiotics apparently have no value as remedies for paratyphoid infection. Sieburth (1957) found that furazolidone (0.005 percent) seemed to hasten the elimination of S. typhi-murium. A 0.01 percent level apparently limited the infection to the intestinal tract. This drug suppressed production of agglutinins but not indirect hemaggglutinins for 5. typhimurium in chickens infected by mouth. Furazolidone did not decrease the number of intestinal carriers. For a more comprehensive review and list of references, see Fenstermacher(1952).Mundtand Tugwell (1958), concluded that paratyphoid infections of egg meats is improbable. Contamination of the shells of the eggs takes place in the cloaca as a result of contact with surfaces on which salmonellae are present. Paracolon Infection. A relatively recently recognized arrival on the scene of poultry diseases is paracolon infection. Lewis and Hitchner (1936) isolated paracolon bacteria from young chicks affected with an infection resembling pullorum disease. The mortality rates in several broods from the same hatchery ranged from 32 to 50 percent. The disease was reproduced in one-day-old chicks by oral administration and subcutaneous inoculation. Peluffo et al. (1942) and Edwards et al.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

localities. For example, in the Diagnostic Laboratory of the College of Veterinary Medicine, Michigan State University, the following species were isolated and were typed at the Regional Salmonella Typing Station, Michigan Department of Health: From chickens, S. orion, S. heidelberg, S. infantis, and ,S. Copenhagen; from turkeys, S. cerro, S. san diego, S. reding, S. kaposvar and S. kottbus. This was done during 1957 and up to March 12, 1958. Dr. Charles F. Hall, Department of Veterinary Pathology, Michigan State University, kindly supplied the following information from the Diagnostic Laboratory at the University of Arkansas for 1954: S. Chester, 27 isolations from chickens, 9 from sick birds, 18 from pullorum reactors. 5. schwarzengrund, 6 isolations, 5 from sick birds and 1 from a pullorum reactor. One Salmonella, with the antigenic structure XVI: Z 29, was isolated from chicken dropping brought in from a poultry farm for bacteriological examination. S. schwarzengrund and S. Worcester were isolated from turkeys. Besides these salmonellae, 17 others were isolated and identified serologically in 1952. Undoubtedly other isolations have been made elsewhere, but time and page limitations presently will not permit further elaboration on this phase of the subject.

REVIEW OF POULTRY DISEASES

invader when found in the tissues. History of the outbreak, symptoms and lesions must all be considered. Control, eradication and treatment must be based on the same principles as those employed against paratyphoid and pullorum diseases (Williams, 1952). Coli-granuloma (Hjarre's Disease). This disease was reported by Hjarre and Wramly in Sweden in 1945. Similar granulomas have been observed in the United States (Hofstad, 1952). Ulcerative Enteritis. This is a disease of quail. Schillinger and Morley (1934) thought it was cased by Escherichia coli, but Bass (1939, 1941) isolated a "quail disease bacillus." Kirkpatrick el al. (1950, 1952, 1953) reported encouraging results from treatment with streptomycin (Barger el al., 1958). Escherichia coli Infection of the Chicken Eye. Gross (1957) observed E. coli infection of the eyes of chickens in the course of studies on pericarditis and perihepatitis caused by this organism. Gross and microsocopic pathological changes were described. Avian Tuberculosis. The distribution of avian tuberculosis is world-wide. In the United States it occurs most frequently in the North Central region. Mycobacterium avium evidently is not affected by cold weather. Schalk (1928) buried carcasses of tuberculous birds in manure and in various depths of soil and was able to recover the organism after three, six, nine and twelve (one case) months. This, at least partly, accounts for the persistence of tuberculosis on certain farms. This disease is important, not only to the poultry industry, but also to swine growers. Moreover, the avian tubercle bacillus will sensitize cattle to mammalian tuberculin (Feldman, 1939; and McCarter et al., 1940). Much work has been done on the various characteristics of M. avium and on

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

(1943) isolated Arizona paracolon bacteria from poults and adult turkeys suffering .from natural infection. The mortality rate, where determined, ranged from 15 to 60 percent. The cultures isolated from the same group of birds belonged to the same serological type and the birds came from the same hatchery. Hinshaw and McNeil (1944, 1946a,b) reported the isolation of types 8, and 10 of Arizona group of paracolon bacteria from poults and snakes. On one ranch the mortality reached 70 percent, the greatest losses occurring during the first three weeks of life. Losses continued for five weeks. Edwards et al. (1943) ,Hinshaw and McNeil (1946b) and Edwards et al. (1947) indicated that paracolon infections in turkeys may be egg-borne. Infected poults may carry the infection until they are adult and may remain carriers for a long time. Infection may become established in a hatchery and from there be spread to distant locations (Edwards et al., 1947). Paracolon bacteria have been isolated from the ovaries of adult turkey hens and frequently from egg powder (Arizona type) (Edwards et al., 1947). The latter illustrates the distribution of these bacteria in chickens throughout the country. Symptoms and lesions in paracolon infections cannot be distinguished from those of salmonellosis with one exception; eye lesions, resulting in opacity and partial blindness, occur rather commonly in certain types of paracolon infections (Hinshaw and McNeil, 1946a). The only means of diagnosis is isolation and identification of the causative organism. Even this method may be questionable at times because of the wide distribution of these organisms and the difficulty in deciding whether the one isolated is the cause or merely a harmless parasite, when found in the digestive tract, or a secondary

745

746

H. J. STAFSETH

ported by Shook and Bunyea (1939). Some interesting enzootiological studies were carried out on fowl cholera byPritchett et al. (1930) and Pritchett and Hughes (1932). Some strains, introduced intranasally, produced cholera in 40 percent of the birds but did not survive in the nasal cleft and did not spread; others, similarly introduced, did not kill the birds but survived in the nasal cleft and spread, infecting susceptible birds. The organism may be spread by mites (Patton, 1926) and by flies (Skidmore, 1932). Opinions differ as to the value of drugs and vaccines (Barger et al., 1958). Heller (1957) found that geese can act as carriers of Pasteurella. Richey and Morgan (1957) reported results indicating that Chloromycetin may be useful in the control of fowl cholera in turkeys, if administered at the onset of an outbreak. Avian Listeriosis. According to Seastone (1935), Listeria monocytogenes was first isolated from chickens by Ten Broeck in 1932. Since then it has been found in several locations in the United States and several other countries. Malewitz et al. (1957) produced listeriosis in poults by intraperitoneal injection with L. monocytogenes. The organism was recovered from the hearts, livers and brains of four of the five poults injected. Symptoms and lesions were described. Since this work was done L. monocytogenes has been isolated from two separate turkey flocks in Michigan. Paterson (1940), using the agglutination test, found four serological types, while Drew (1946) found two with the precipitin test. Paterson (1940) also reported on experimental infection of the chick embryo with organisms of the genus Listerella. Few clinical symptoms are exhibited; adults may die suddenly, whereas young, naturally infected chickens may show a

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

avian tuberculosis in general. Dr. William H. Feldman has written an excellent review on this subject in Diseases of Poultry (Biester and Schwarte, eds. 1952). Here the more important advances in our knowledge, of a practical nature, will be discussed. An intradermal tuberculin test was developed by Van Es and Schalk (1914). As in the case of most tests, it is not infallible, but, when administered by competent people and with understanding, it is a valuable adjunct to our means of combating this disease. Moses et al. (1943) and Karlson et al. (1950) reported the development and application of a rapid agglutination test. Richey el al. (1954) experimented with a hemagglutination test. This test, in its present state, has no value in the control and eradication of avian tuberculosis, but may be a useful experimental tool. In attempts at controlling avian tuberculosis, vaccination with the B.C.G. (Bacillus of Calmette and Guerin) has been done with reported success by French workers. Doyle (1930) did not get satisfactory results by the use of reduced doses of B.C.G. Fowl Cholera. Advances in our knowlege of fowl cholera are rather limited. Webster (1930) found that there are three distinct types of Pasteurella moltocida: 1. The fluorescent, highly virulent; 2. The intermediate, moderately virulent; and 3. The blue, only slightly pathogenic. Besides the more or less acute form of cholera, long known, local infections have been observed. These are respiratory tract infections, also referred to elsewhere in this article, edema of the wattles, abscesses in the legs (Hilbert and Weiter, 1936), ovarian abnormalities (Beach, 1922; Hoffman 1933; and Shook and Bunyea, 1939). An apparently effective whole-blood stained-antigen agglutination test was re-

REVIEW OF POULTRY DISEASES

The most pathognomonic symptom is the turgid, reddish purple snood or caruncle (Rosenwald and Dickinson, 1941). Treatment with sulfanilamide has proved uniformly unsuccessful. Vaccines, anti-swine erysipelas serum and antibiotics have been used with results varying from good to indifferent (Levine, 1952; Cooper et al., 1957; Barger et al., 1958). Boyer and Brown (1957) reported on experimental E. rhusiopathiae infection in 732 turkeys. Infection was produced via the following routes (in order of mortality rates): intravenous, subcutaneous, foot pad scarification, breast skin scarification, intramuscular and feather follicle. Young poults and adults, regardless of sex, were about equally susceptible. "Duovax" bacterin produced considerable resistance. Bacitracin, furazolidone, terramycin and streptomycin gave inadequate protection in pilot trials. Aureomycin and procaine penicillin reduced mortality from 30-100 percent. Morbidity was high in aureomycin fed birds. In another publication Boyer and Brown (1957) reported success with oral antibiotic therapy in laboratory and field research on treatment for erysipelas in turkeys. Pseudotuberculosis. This is a contagious disease caused by Pasteurella pseudotuberculosis. It is characterized by an acute septicemia of short duration followed by a chronic focalized infection, giving rise to tubercular lesions in various organs. The literature on this disease has been reviewed by Stafseth (1952). Since then the following reports have been published, Clapham (1953) observed pseudotuberculosis among Stockdoves in Hampshire, England, during December, January and February. In a search for the source of this infection, P. pseudotuberculosis was isolated from a lark, a wood pigeon, a jackday and a rook. The organism was also isolated from a rabbit in Hertford-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

slow wasting disease. Massive necrosis of the heart muscle and generalized edema and necrotic foci in the liver are the most conspicious lesions. No success has been achieved in treatment with drugs or vaccines (Levine, 1952). Botulism. Fowls are susceptible to the toxins of types A and C of Clostridium botulinum which is commonly found in soil, especially soil fertilized with the manure of herbivorous animals. According to Quortrup and Sudheimer (1943a), there appears to be a strong symbiotic relationship between CI. botulinum and Pseudomonas aeruginosa, which is an oxygen-consuming and alkali-producing organism. Through such activities Ps. aeruginosa creates favorable conditions for C. botulinum where the latter would otherwise be unable to live, as, e.g., under more than one foot of water in masses of decomposing vegetation. The specific antitoxin is an effective prophylactic, when given before symptoms have developed. One pound of epsom salts in the drinking water per 100 birds will flush out the intestines and may also act as a preventive, if administered early enough (Barger el al., 1958; Levine, 1952). Erysipelas Infection. Acute or subacute infection with Erysipelothrix rhusiopathiae has become more and more common in turkeys. This organism has a wide host range among birds and mammals, including man. I t is capable of surviving for long periods in certain types of soil. One may expect outbreaks of erysipelas in turkeys, especially where they are in close contact with swine or sheep, and where the ground has been contaminated with the droppings of infected birds or mammals. Males are much more susceptible than females (Madsen, 1937; Rosenwald and Dickinson, 1939; Stiles, 1946).

747

748

H. J. STAFSETH

Staphylococcic Infections. Staphylococci have been found to cause such disorders as: arthritis, peritonitis, vesicular dermatitis, bumblefoot and omphalitis in

fowls. Staphylococcus aureus and Staphylococcus citreus have been incriminated. Sulfonamides and vaccines have not proved effective. Antibiotics may be of value in treating highly developed breeding stock (Hafstad, 1952; Barger et al., 1958). Streptococcic Infections. Streptococcic infections in fowls have been reported from the United States, Sweden and Germany. An acute form has been referred to as apoplectiform septicemia, and a subacute form as sleeping sickness. Idiopathic peritonitis and chronic peritonitis and salpingitis have also been reported. The organisms encountered are: Streptococcus gallinarum, Streptococcus zooepidemicus and Streptococcus pyogenes. No successful treatment has been reported (Hofstad, 1952; Barger el al., 1958). RESPIRATORY DISEASES

Introduction. The respiratory diseases, collectively, are a most serious economic problem for the modern poultryman. For this, there are several reasons; some of these diseases are highly contagious, producing a high rate of morbidity and, at times, a high mortality rate. This may be of serious consequence to modern, large poultry plants, especially the oversized broiler establishments. No branch of, or activity within, the poultry industry is immune to the ravages of these diseases because of the ease with which they may be spread and the many channels along which this may take place. Van Roekel (1955) has written an excellent review article on this subject. Fortunately, notable progress has been made in the prevention of several of these diseases and here we shall deal mainly with advances along these lines. Fowl Pox. Fowl pox may appear in two forms, 1. the cutaneous, characterized by wart-like eruptions on the unfeathered

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

shire and from two pigeons from Norfolk, during this period. Previously, the authors had isolated this organism from grey partridge, pheasant and bob white. Dorsen (1952) isolated P. pseudotuberculosis from a bantam hen that had died. Marthedal and Villing (1954) observed this disease among pigeons in Denmark in 1950. There has been one case in a turkey and seven outbreaks in ornamental birds. Mathey and Siddle (1954) isolated P. pseudotuberculosis from an 8-month-old torn turkey which died, showing lesions, typical of pseudotuberculosis. Brucellosis. Whether brucellosis in poultry is of any consequence is still a question. Some of the diagnoses, made of brucellosis in fowls, have been based on postive agglutination reactions, most of them weak (Anczykowski, 1954). Shklair and Stafseth (1954) came to the conclusion that positive agglutination reactions alone cannot be accepted as proof of Brucella infection. Some diagnoses have been based on the fact that the chickens involved had been in close contact with infected herds of cattle. Huddleson and Emmel (1929) reported having found natural infection in four flocks. Much of the literature on this subject deals with more or less successful attempts at producing artificial infection (Jurado et al,, 1951). Galuzo and Rementsova (1955) have reviewed the literature on brucellosis with special reference to sources of the infection. They are of the opinion that not only mammals, but birds, reptiles, amphibians and even fish may act as natural reservoirs. For more complete review of and references to the literature on brucellosis, see Stafseth (1952).

REVIEW OF POULTRY DISEASES

749

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

ducing pure virus by cultivating it on the chorioallantoic membrane of the developing chick embryo. Now, commercial vaccines are available and, when properly used, have served to eliminate fowl pox as a serious problem both in chickens and turkeys. Inasmuch as fowl pox vaccine produces a systematic reaction, especially when the feather follicle method of application is used, it is not recommended for laying birds; in them pigeon pox vaccine may be used, always by the follicle method. In turkeys, fowl pox vaccine must be used. When young turkeys are vaccinated the immunity developed does not last much beyond 6 months. Therefore, birds that are to be kept for breeders or beyond 6 months for other purposes, must be vaccinated at 6-7 months of age (Hinshaw, 1952). A comprehensive review of the literature on fowl pox has been written by Cunningham (1952). Infectious Coryza. This disease has been known for a long time as roup. The term infectious coryza correctly describes the nature of the disease. A microorganism, Hemophilus gallinarum plays a role in the causation of the disease (de Blick, 1931). This is evidently not the only organism involved. Nelson (1935) isolated "coccobacilliform bodies," an organism which also was able to cause coryza. This organism had previously been found by de Blick (1931). Later Nelson (1938) showed that H. gallinarum produces a coryza of rapid onset and short duration, that coryza of slow onset and long-duration is caused by the coccobacilliform bodies and that a third form, with rapid onset and long duration, may be caused by infection with both organisms. Adler and Yammamoto (1956) obtained essentially the same results as Nelson described in 1936 and 1938. Nelson (1953) conSince then, Woodruff and Goodpasture sidered the possibility that chronic re(1931) have developed a method of pro-

portions of the skin, and, 2. the diphtheritic form in which false membranes or cankers appear on the mucous membranes of the mouth and throat. Both forms may appear in the same bird. Marx and Sticker (1902) proved that the cause is a filterable virus. Besides the flowl pox virus, there are two other avian pox viruses, the pigeon pox virus and the canary pox virus (Beaudette, 1949a). The fowl virus affects chickens, turkeys, guinea fowl, pheasants and peafowl, but is only mildly infective for pigeons. Pigeon pox virus produces only local swelling at the point of infection in chickens, but no systemic reaction. Canary pox virus is pathogenic only for canaries and other passerine birds. Extensive studies have been made of these viruses, many of them in attempts at developing a satisfactory vaccine. De Blieck and van Heelsbergen (1923) reported on the use of antidiphtherin to be used for cutaneous vaccination. Stafseth (1930) reviewed work done in this country and Canada with various forms of fowl pox vaccine and reported on the use of a vaccine containing 100-200 mg. of dried, ground pox scabs in 100 ml. diluent, consisting of glycerinated 0.85 percent NaCl solution. The vaccine was successfully applied by swabbing it into a few feather follicles on one leg or by the stab method in the wing web. The wing web method is very satisfactory in chickens, but may be objectionable in turkeys because of their habit of putting their heads under the wing, when going to sleep. After preparation the vaccine was held for at least 24 hours before being used. By so doing, the number of contaminating bacteria was reduced while the virus remained active. Thus, the danger of secondary infection was reduced to a minimum.

750

H. J. STAFSETH

McKay (1948) added 1 teaspoonful of Lugol's solution per gallon of drinking water and obtained marked beneficial results in the control of this disease on five large poultry farms (25,000 birds), experiencing persistent outbreaks. Fowls which recover become carriers. Therefore, young stock must be kept away from older birds that have had coryza, and, for the same reason, 100 percent replacement of layers each year may result in freedom from this disease (Barger et al., 1958). Pasteurella multocida sometimes produces coryza-like infections in poultry. The only way to differentiate Pasteurella respiratory infection from those produced by other causes is a bacteriological examination (Van Roekel, 1955). Infectious Laryngotracheitis. This disease has been recognized in North America since 1922 and may have existed here previously. Beaudette, in 1930, first reported that the disease, which then was called infectious bronchitis, is caused by a filterable virus. This was conclusively proved by Beach in 1931. About this time, at a meeting of the Conference of Research Workers in Animal Diseases of North America, Stafseth questioned the use of the name bronchitis, inasmuch as the bronchi were not involved, the lesions being confined to the larynx and trachea, and suggested that a more proper name would be largyngotracheitis. Buck of the Bureau of Animal Industry, U.S.D.A. concurred in this opinion. Since then this disease has been called laryngotracheitis. Certain symptoms and lesions are quite pathognomonic. These are the characteristic rhythmic gasping, blood stained mucus in the trachea and loosely attached caseous plugs or casts in the larynx and trachea. In most cases the visible, severe inflammatory changes do not extend beyond 1.5 to 2 inches down through the trachea. Pirozok et al. (1957) described a

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

spiratory disease (CRD) and infectious coryza may be the same disease and it has been suggested that the coccobacilliform bodies may be the same as the pleuropneumonia-like organism (PPLO). McKay and Taylor (1954) advanced the idea that the cause of CRD and infectious sinusitis (IS) is not a pleuropneumonialike organism but an L phase of a true bacterium similar to H. gallinarum. This needs further study. It is difficult to differentiate this disease from other respiratory diseases, fowl pox, laryngotracheitis, CRD and the respiratory type of fowl cholera (Seddon, 1953a). As a means of a differential diagnosis, Hofstad (1952) recommended the inoculation of susceptible chicks with suspected material followed by isolation of the organism. This may not be satisfactory in complicated cases in which more than one organism is involved. This is a highly contagious disease and is not readily subject to control by ordinary sanitary practices. Unfavorable environmental conditions are contributory causes, and, whenever possible, should be avoided. Individual treatment may be successful, but is obviously impractical in large flocks. Borstein and Samberg (1955) reported remarkable clinical recovery in 48 hours and prompt resumption of egg production after intramuscular injection in hens of 0.2 gm. of dihydrostreptomycin sulfate. Flock treatment is obviously less successful because of the difficulty in administration of proper doses-of drugs by that method. Heiman (1943) kept cold infections down to a maximum of 20 percent by feeding sulfathiazole at the rate of 7 ounces to 100 pounds of feed. Untreated birds showed a morbidity rate of 90 percent. When the treatment was discontinued the morbidity increased to 80 percent within 7 days. Growth was better in sulfa treated birds.

REVIEW OF POULTRY DISEASES

The literature on infectious laryngotracheitis has been reviewed fully by Hofstad (1952), Van Roekel (1955) and by Barger et al. (1958). Infectious Bronchitis. Infectious bronchitis was first described by Schalk and Hawn in 1931. Their work was confirmed

by Beach and Schalm in 1933, and 1936, Beaudette and Hudson (1937), Delaplane and Stuart (1939) and others (Van Roekel et al., 1950). The causative virus is present in bronchial, tracheal and nasal exudates of affected chicks and has been found in the liver, spleen, kidneys and blood. It is of interest to note that, when cultivated on the chorio-allantoic membranes of the developing chicken embryo, the virus of bronchitis does not produce gross lesions, such as are produced by the viruses of fowl pox and laryngotracheitis (Beaudette and Hudson, 1937; Delaplane and Stuart, 1939). As far as presently known, this disease affects chickens only. Birds from 10 to 120 days are equally susceptible (Beach and Schalm, 1933). Delaplane and Stuart, in 1939, stated that the disease is found most frequently in semimature and adult chickens, less commonly in brooder chicks. Reid et al. (1958) found that Ascaridia galli infection aggravates infectious bronchitis. Symptomatically the disease does not differ much from Newcastle disease and laryngotracheitis. A positive diagnosis can be made by the isolation of the virus in embryonated chicken eggs and characterization of the virus by cross neutralization tests and cross-immunity tests. Fabricant (1957) described a simple embryo inoculation technique for the isolation of viruses from birds with respiratory disease. In young chicks the mortality may reach 70-80 percent while in older birds death losses are not great. Birds that have recovered may carry and spread the virus for 35 days (Hofstad, 1947). Sevoian and Levine (1957) made a comprehensive report on the effects of infectious bronchitis on the reproductive tracts, egg production and egg quality of

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

rapid histological technique for the diagnosis of infectious avian laryngotracheitis. Cover and Benton (1957) isolated a virus, similar to or identical with the laryngotracheitis virus, from chickens showing symptoms of chronic respiratory disease. At certain stages of the research the virus seemed similar to that of Crowley. Hudson and Beaudette, in 1932, reported that chickens and pheasant are the only recognized hosts. The virus has been cultivated in embryonated chicken and turkey eggs, but not in pigeon, guinea fowl or duck eggs. The lesions produced in eggs were described by Beaudette et al. in 1948 and by Burnet et al. in 1937. The characteristic lesions are grayish plaques on the chorioallantoic membrane. Besides the identification of the cause and the characterization of this highly contagious and often deadly disease, a most important discovery was made by Hudson and Beaudette in 1932 when they found that vaccination by application of virus to the cloacal membrane is safe and effective, if properly done. Interestingly, this disease, which in the early twenties was widespread in the United States and parts of Canada and is still most serious in some areas (Barger et al., 1958), is now reported very infrequently in the various laboratories in this country (Van Roekel, 1955). Kingsbury and Jungherr (1958) reported an extensive outbreak in which human beings were responsible for the spread of the disease and the persistence of the outbreak.

751

752

H. J. STAFSETH

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

spiratory disease (CRD). Delaplane and Stuart, in 1943, first described this disease of chickens. It is characterized by persistent respiratory symptoms, such as: discharge from the nostrils, foamy or bubbly discharge in the eyes, clear or mucoid secretion in the swelling of the sinuses, sometimes to the extent of closing one or both eyes. This secretion may become cheesy and yellow. When the bronchi and lungs are involved, there will be labored breathing. The appetite will be decreased, but the birds will eat as lqjig as they can see. There will be loss of weight and reduction in egg production. The disease is widely distributed in the United States and Canada. It has also been reported from Australia, England and the Union of South Africa. Thus, the disease is of great economic importance. Several microorganisms are capable of producing what clinically may be called CRD. Markham and Wong, in 1952, propagated a microorganism on cell free media from such cases. They suggested that the organism might belong to the pleuropneumonia group (PPLO). Several authors have confirmed these findings. Several media, including chick embryos have been used and the biochemical reChang et al. (1957) found the following actions of the organism have been studied. criteria useful in evaluating immunity The gross and histopathology of the disagainst infectious bronchitis: respiratory ease has also been studied, as has the symptoms, gross and microscopic lesions mode of transmission. Immunity studies in the trachea, and recovery of the virus in the tracheal exudate. Each criterion have also been carried out (Van Roekel, was valid for only a limited period and 1955). none was effective over the total test Another cause of CRD, a virus, was period. isolated by Fahey and Crawley in 1954. For review of and references to the Symptoms were typical of CRD and perliterature on infectious bronchitis, see: sisted for 8-10 weeks. Grumbles et al., in Hafstad (1952), Van Roekel (1955), 1952, stated that the gravity of the disCunningham (1957) and Barger et al. ease may be determined by several contributing causes or stress factors, such as: (1958). caponizing, vaccination reactions, dietary Chronic Respiratory Disease. More than one microorganism can cause what clin- disturbances, other infections, changes in ically may be diagnosed as chronic re- environment and other debilitating fac-

laying chickens. The effects are far reaching. Egg production and egg weights and quality are reduced. There are also gross and microscopic alterations in the reproductive tracts. There is no specific medicinal treatment for bronchitis. In the New England states a program of control has been used successfully, consisting of deliberately inoculating 5 to 10 percent of the flock with the virus at 6 to 14 weeks of age (Van Roekel et al, 1950). This is to be used only in areas where the disease prevails, because a flock so vaccinated may spread the disease to adjacent flocks. The use of a modified live virus vaccine, applied individually by the intranasal or intraocular route, or by spray, dust or addition to drinking water, has not met with general approval because of irregular results. Dickinson and Babcock (1957) reported on a symposium on immunization aginst infectious bronchitis virus. Definite measures are proposed for controlling this disease. Christian and Mack (1957) reported on successful experiments with a beta-propiolactone inactivated infectious bronchitis virus vaccine.

REVIEW OF POULTRY DISEASES

vitro antibiotic activity by several of the drugs. Olesiuk et al. (1957) found that aureomycin, furazolidone, magnamycin and terramycin, out of ten drugs tried, exerted some inhibition on the severity of the disease. The other drugs were ineffective. Price et al. (1958) confirmed previous reports to the effect that oxytetracycline will modify the course of CRD. This drug does not eliminate the organism from the respiratory tract of the carrier birds. The treatment caused a lag in antibody production but there was a significant improvement in weight gain over the infected control group. The authors consider the PPLO an initiating agent which paves the way for infection by other organisms. Sullivan et al. (1957), on the basis of laboratory analyses of birds from nine flocks, where outbreaks of CRD occurred, found that multiple etiological agents could be demonstrated, bacterial and viral. Limited experience with commercially prepared PPLO agent for serological diagnostic purposes is mentioned. Taylor et al. (1957) found that modified Grumble's medium is the best for primary isolation of the PPLO from tracheal exudate. At a recent symposium on chronic respiratory disease of poultry, Adler et al. (1958) reported on methods of isolation and identification of pleuropneumonialike organisms of avian origin. Inasmuch as organisms of this type have been isolated, which differ in physiological and pathological characteristics from the standard pathogenic strains isolated from chickens and turkeys, a re-evaluation of present laboratory procedures is suggested. Gross (1958) reported that Escherichia coli is an important complicating factor in CRD and other respiratory diseases. Van Roekel et al. (1958) dealt with the epizootiology of CRD. Transovarian in-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

tors. Carey and Adler (1957) found that the PPLO is capable of producing encephalitis in turkeys characterized by vasculitis and focal necrosis. The host range of the viral agent evidently has not been determined; that of the PPLO is a limited multiple one; chickens, turkeys, pheasant, partidges and pigeons have exhibited spontaneous cases. Jungherr et al., in 1953, found guinea fowl to be susceptible to experimental infection and rats and mice are susceptible to PPLO toxins. Wichmann (1957) found PPLO infection in chuckar partridges. Van Roekel (1953) and Fahey (1954) were of the opinion that egg transmission is the main source of natural outbreaks. The results obtained by Calnek and Levine (1957) create some doubt as to the importance of egg transmission of CRD. Undoubtedly aerosol and contaminated feed, water and litter must be considered as means of transmission. Besides clinical observations, the isolation and identification of the causative organism are required for a reliable diagnosis. Van Roekel, in 1955, stated that serological tests may be used for identifying the PPLO organism. Good hygienic management practices help in controlling the disease. The results of antibiotic treatment through the feed have been termed encouraging by some and inconclusive by others. Crawley and Fahey, in 1955 and 1957, indicated that it may be possible to obtain PPLO free flocks by the injection of breeding stock with streptomycin and then rearing the chicks out of contact with infected birds. Hamdy et al. (1957) studied the effects of antibiotics on PPLO in vitro and in vivo. Twenty large white turkeys infected with this organism and showing typical signs of infectious sinusitis became asymptomatic and 18 of 20 recovered. They also found various degrees of in

753

754

H. J. STAFSETH

Newcastle disease virus and the virus found in California. However, the first published report to that effect was made by Beach in 1944. In 1945 the disease was found on the East coast and by 1947 it had been recognized in most regions of the United States. Since then, so much work has been done and so many papers published on this disease that it will be impossible to do justice to all this work, and the workers, in a short review paper. Those who wish more complete information on Newcastle disease are referred the following excellent reviews: Beaudette (1943; 1950, 1951); Brandly (1952); Van Roekel (1955); Barger et al. (1958). The first symptoms are respiratory and resemble those of bronchitis; these are followed by nervous manifestations: muscular incoordination, neck and leg tremors, shaking of entire body, and partial paralysis of one or both legs. At times, there may be a combination of all these symptoms and others. Abnormalities of eggs laid by affected birds have been noted by several workers. Postmortem findings are: clouding and thickening of the air sacs, mesentery and internal membranes, yellowish discoloration of the tissues may be seen and they may be covered with a frothy, adherent exudate. There are also changes in the respiratory tract: clear or yellowish mucus in the mouth, trachea and bronchi; small hemorrhages may appear in internal organs and egg yolk may appear in the abdomonal cavity. Symptoms and lesions may be rather pathognomonic, but the following laboratory tests may be used to obtain a reliable diagnosis: 1. Isolation of the virus, 2. hemagglutination test (HA), 3. hemagglutination inhibition test (HI) and 4. serum neutralization test. Schmittle and Millen, in 1948, found hemagglutinationinhibiting antibodies in uninoculated eggs.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

fection is a common mode of spread; antibiotics did not inhibit egg transmission of CRD. Partial flock testing was found to be ineffective in determining the flock status with respect to this disease. In commercial flocks CRD may become widespread prior to sexual maturity of the birds. Jungherr (1958) discussed control of CRD by means of hygienic measures, antibiotic treatment and various types of tests. Naturally, PPLO occur in two forms: hemagglutinating (HA+) and nonhemagglutinating (HA — ). The former is usually highly pathogenic, the latter less so. The eye test and homologous and heterologous agglutination test may be used for differentiation. Osborn et al. (1958) discussed infectious sinusitis of turkeys. This disease continues to be important. Progress has been made in our understanding of the cause, mode of spread and, to a degree, in preventive measures. For review of and references to the literature on chronic respiratory disease, see Hofstad (1952), Van Roekel (1955) and Barger et al. (1958). Newcastle Disease. Kraneveld, in 1926, first described this disease in the Dutch East Indies, and Doyle, in the same year, isolated the causative virus from chickens in an outbreak near Newcastle-on-Tyne in England; hence, its name. It soon became recognized in several parts of the world. In 1940 a similar but much milder disease was observed in California. There, it was first designated as a respiratory-nervous disorder and later as pneumoencephalitis by Beach in 1942, and also by Stower in 1942. This is a descriptive and meaningful name, something that cannot be said for the name, Newcastle disease. From personal acquaintance with the work of Dr. F. R. Beaudette it appears to me that he was the first to discover the identity of

REVIEW or POULTRY DISEASES

that vaccinated birds may spread the disease to nonvaccinated stock. For this reason vaccinated birds should be kept away from nonvaccinated birds for a least six weeks. Dardiri et al. (1957) compared the values of three types of Newcastle disease vaccine. An aluminum hydroxideabsorbed, killed ND vaccine administered at 10 days of age showed 98.6 percent protection against challenge at 16 weeks of age. This was the most effective vaccine tested. Bankowski et al. (1957) reported that a single administration of the B-l strain of ND virus to birds 8.2 weeks of age, in the absence of parental or residual immunity, induced immunity to intramuscular challenge with a virulent NDV in 80 percent of the birds approximately 56.5 weeks later. Favorable results with infectious bronchitis vaccine are also reported. Winterfield et al. (1957) reported on results of vaccination with Bl, F and LaSota strains of ND virus administered through drinking water. The LaSota strain produced the highest hemagglutination inhibition titers and a slightly higher degree of immunity. Infectious Sinusitis. This disease was first reported as occurring in turkeys in England by Dodd in 1905 and later in the United States by Tyzzer in 1925. The name infectious sinusitis was suggested by Dickinson and Hinshaw in 1938. The disease is characterized by swelling of the infraorbital sinuses and inflammatory changes throughout the respiratory tract including the air sacks. The cause is evidently the PPL organism or one very closely related to it. A good review of the studies on this organism, and symptoms, pathology and transmission of the disease has been written by Van Roekel (1955). Egg transmission was suggested by Jerstad et al., in 1949, Mataney et al., in 1955, and Hofstad (1957) clearly demonstrated that such transmission takes

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

They treated egg yolk with ethylene chloride and ether and used it in place of serum. By this test they could determine accurately the previous presence of Newcastle disease. This test has obvious advantages. Gentry (1957) described an accurate and direct method of determining the eight unit antigen level for the hemagglutination-inhibition test (the beta or Lederle technique). McCollum et al. (1957) found that agglutination patterns formed by potassium periodate treated Newcastle disease virus remained stable for at least 12 hours. Thus, the periodate destroyed the elution property of the NDV without appreciably reducing its hemagglutinative capacity. Newcastle disease virus is air-borne and may also be transmitted through the egg. Besides these avenues of spread, there are several of the usual types of transmission of infectious diseases, including carriers. Newcastle disease virus has a wide host range including birds, mammals and even man (Van Roekel, 1955). For information on the resistance or susceptibility of the virus to physical and chemical agents the reader is referred to Brandly's review (1952). Boyd and Hanson (1958) reported on studies on the sterile or nonsterile survival of NDV in nature. The virus was found to survive in soil for 22 days maintained at 20° + 2C. at 100 percent relative humidity. It survived for 8 days at zero and 15 and 100 percent relative humidity. There is no medicinal treatment for Newcastle disease but several vaccines have been developed which have proved valuable in the control of this disease (Van Roekel, 1955; Barger et al., 1958). Live virus vaccines are generally considered superior to killed virus vaccines. However, live virus vaccination has the drawback

755

756

H. J. STAFSETH

the sources of the infection and other poor hygienic conditions undoubtedly are contributing factors. With improved poultry hygiene this disease has decreased in prevalence. There is no known medicinal treatment (Van Roekel, 1955; Bullis, 1952; Bargere/aZ., 1958). Duck Plague. Duck plague was first reported in Holland by Jansen and Kunst (1949). The cause is a virus, distinct from the fowl plague and Newcastle disease viruses. The disease has not been encountered outside of Holland. The duck hepatitis virus isolated by Levine (1952) differs antigenically from that of duck plague. Quail Bronchitis. A virus, distinct from other avian respiratory viruses, was isolated by Olson (1950). This virus causes bronchitis in quail, the only susceptible species. Dougherty's Long Island Duck Disease. A new and serious disease in ducks was discovered by Dougherty (1953) on Long Island. The cause has not been identified. Characteristic manifestations are mild cough, and, later, ataxia, diarrhea and paresis. The respiratory and nervous symptoms resemble those of Newcastle disease (Hilbert and Kiser, 1948). Some of the pathological manifestations are: fibrinous perihepatitis, aerocystitis, peritonitis and caseous pneumonia. Sulphonamide therapy has proved to be beneficial to a degree but antibiotics have so far failed. Careful management and sanitary practices have been helpful. Goose Influenza. This disease has been observed in Germany. Reis and Nobrega (1936a) reviewed the literature on the disease. Gerriets (1953) described the disease as an exudative septicemia. Serofibrinous exudate occurs on the serous membranes of the air sacs and the bronchi. There are also cattarrhal inflammatory changes in the intestinal mucosa. The

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

place. This is a serious disease in turkeys which runs a chronic course and may persist in a flock for weeks. Therefore, though it is not considered highly contagious, a certain amount of contagion must take place and environmental factors, as in CRD, may also play an important role in its propagation. Hofstad (1957) has reviewed previous work on diagnostic methods and investigated serological tests (tube agglutination, rapid plate test and hemagglutinationinhibition) as to their usefulness in work with this disease. Effects of treatment with antibiotics on antibody titer were noted. In such a case one must consider the possibility of other fowl on the premises being carriers of the PPLO. For comprehensive reviews and references to the literature on infectious sinusitis, see: Hinshaw (1952), Van Roekel (1955) and Bargere*aZ. (1958). S. pullorum and other salmonellae have been found to cause respiratory symptoms (Van Roekel, 1955). Aspergillosis. Aspergillus fumigatus has long been known to produce respiratory disease in poultry, especially in young birds. Other species of this genus have also been incriminated. Ophthalmic aspergillosis was reported by Hudson in 1945, Sperling in 1953 and by Moore in the same year. Moore, in 1953, reported that he had observed a higher incidence of aspergillosis among males than among females. In 1952, Pomeroy reported that accumulation of exudate occurs often in the air sacs of turkey poults. Dougherty, in 1953 reported that aspergillosis may be a serious disease in ducklings, 2 weeks or less in age. An unusual form of mycosis, encephalomalasia, in turkeys was reported in 1944 by Jungherr and Gifford. Reis and Nobrega, in 1936, reported that aspergilli may invade several tissues of the body and produce lesions. Moldy litter and feed are

REVIEW OF POULTRY DISEASES

PROTOZOAN DISEASES

Coccidiosis. This is one of the most prevalent of poultry diseases. The literature on this disease has become very voluminous. Johnson (1923,1938), Tyzzer (1929) and Tyzzer et al. (1932) have contributed much to our knowledge of species and life cycles of coccidia, and Johnston (1927) was the first to call attention to the development of immunity, resulting from continued exposure to nonlethal infection. Eight specie of the genus Eimeria infect chickens. Eimeria tenella produces cecal (bloody) cocidiosis, particularly serious in four-week-old chicks. The other seven species produce more or less chronic infection in the intestinal tract, anterior to the ceca. Seven species of Eimeria infect turkeys in which the disease is of a more or less chronic nature. The goose, quail, pheasant and pigeon, each has its own species of Eimeria and the duck is susceptible to Tyzzeria perniciosa. Inasmuch as birds frequently carry coccidia without ill effects a diagnosis of coccidiosis must not be based exclusively on the finding of coccidia, but on the presence of symptoms and typical lesions as well.

Prevention and successful treatment may be accomplished by the use of drugs, such as: nicarbazin, nitrofurazone, nitrophenide and sulfaquinoxaline. The purpose of using these drugs is to keep the infection mild enough to be harmless, but sufficient for the development of immunity. Rosenberg et al., in 1941 and 1954, and Champion, in 1945, showed that it is possible to breed for resistance to coccidiosis. However, this method of control is not practical under ordinary poultry husbandry conditions. For comprehensive reviews of and references to the literature on coccidiosis, see: Becker (1952); Hinshaw (1952); and Barger et al. (1958). Hexamitiasis. Hexamita sp. was first observed in pigeons by Noller and Buttgereit, in 1923 and in ducks by Kotlan in 1923. Hinshaw el al., first identified the disease in turkeys in California in 1938. McNeil et al., in 1939, found it in quail and partridges and McNeil and Hinshaw, in 1941, reported having observed it in pigeons for the first time in the United States. Hexamita mileagridis is the name of the organism in turkeys and Hexamita columbae is the name for the one in pigeons. There is some limited cross transmission of these organisms among several species of birds. Symptoms are entirely nonspecific and lesions consist of catarrhal enteritis in the upper portion of the small intestines. Microscopic demonstration of the organism is the only means of diagnosis. This must be done on fresh specimens. The organism dies quickly in decomposing material. Mangrum et al., in 1955, discovered that furazolidone, 50 mg. per pound of feed, may be effective in controlling the disease. Lund (1956) found that aureomycin, 180 to 200 grams per ton of feed or 10 grams of the soluble forms in 50 gallons of water,

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

cause is a gram negative, slender rod and yields to sufathiazol treatment. Gapeworm Infestation. Respiratory symptoms are produced by Syngamus trachea in chickens, guinea fowls, turkeys and a number of wild birds (Wehr, 1952). Griffiths et al. (1954) reported heavy losses due to Cyathostoma bronchitis among goslings. There was severe respiratory distress and mortality of 80 percent. Survivors were retarded in growth. Life cycles and treatment have been studied by a number of authors. Barium antimonyl tartrate proved 98 percent effective in 10 experiments, when administered as a dust to chicks in jars (Barger et al., 1958).

757

v

758

H. J. STAFSETH

Trichomonas gallinarum causes trichomoniasis of the lower portion of the digestive tract. Turkeys are the most severely affected. Chickens and guineas are also susceptible. Symptoms are nonspecific. The most striking lesions are found in the liver and ceca where there may be irregular, elevated, granular and cheesy areas. These can be distinguished from blackhead lesions if carefully examined. Microscopic examination for the presence of T. gallinarum is desirable. Fever therapy (keeping turkeys in a chamber at approximately 104°F. with a relative humidity of 60 to 70 percent) has been found effective, Olson and Allen (1940), Becker (1952); Hinshaw (1952) Barger et al. (1958). Stabler et al. (1958) found 2-amino-5-nitrothiazole (Enheptin) effective in the treatment of trichomoniasis in domestic pigeons. Infectious Enterohepalitis (Blackhead).

This disease is an important one to turkey growers. Turkeys, especially young birds, are highly susceptible. Chickens are also susceptible, but suffer less serious effects. However, the fact that chickens may carry the infection without showing evidence thereof, may be of considerable consequence, if such chickens are allowed to run with turkeys or if turkeys are placed on ground, contaminated by the droppings of chickens. The cause of infectious enterohepatitis, Histomonas meleagridis, may be present in eggs of the cecal worm, Heterakis gallinae. This may explain the long survival of H. meleagridis, in soil (Graybill and Smith, 1920). Lesions in the liver and ceca are usually as nearly pathognomonic as lesions can be. The causative organism can be found by microscopic examination of suitable preparation from the liver and ceca. Malewitz and Calhoun (1957) reported that changes in the blood picture accompany histomoniasis in poults. The changes are: decrease in total red blood cell count, hemaglobin and white cell count. The heterophiles increased while the lymphocytes decreased. Leucocylozob'n Infection. Wickware described this disease in ducklings in 1915, and, in 1934, Clark reported high mortality among young grouse in Canada, apparently caused by leucozytozoa. In 1939 Johnson described the disease in turkeys. The organism affecting ducks is called Leucocytozoon simondi and the one in turkeys, Leucocytozoon smilhi. The disease may be acute and fatal. The symptoms and lesions are alike regardless of which of the two organisms are involved. Neither symptoms nor lesions are pathognomonic, the diagnosis being dependent on the demonstration of the organisms in the leucocytes in properly stained blood smears. Johnson found that the disease is

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

gave good results. For comprehensive reviews of and references to the literature on hexamitiosis (infectious catarrhal enteritis, see: Hinshaw (1952) and Barger et al. (1958). Trichomoniasis. Wehr and Christensen (1942) have written an excellent review of the literature on trichomoniasis. Trichomonas gallinae is the cause in turkeys, chickens and pigeons. Some authors prefer the name Trichomonas columbae for the organism in pigeons. The disease is characterized by necrotic ulceration in the esophagus, crop and proventriculus. Symptoms are nonspecific. The diagnosis depends on microscopic demonstration of the organism and observation of symptoms, and especially the characteristic lesions. Hinshaw (1937) found a 1 to 2000 solution of copper sulfate (in soft water and earthenware vessels), in place of drinking water, the only successful treatment.

REVIEW or POULTRY DISEASES

MYCOSES

Aspergillosis, being primarily a respiratory disease, has been discussed earlier in this article; Hubben (1958) reported three outbreaks of aspergillosis in turkeys and ducks, in which meningoencephalitis occurred. Favus, caused by Acharion favus, is primarily a skin disease of rather common occurrence. It is characterized by yellowish-white scaly lesions on the unfeathered parts of the head. However, it is not confined there. The infection may spread over the neck, and elsewhere over the body, making the feathers so brittle

that they may break off. Beach and Halpin, in 1918, produced artificial infection by rubbing material, containing the organism, into the skin but not by feeding or by intravenous injection. They reported that an ointment, made of 5 percent of formalin (by weight) and petroleum jelly, was effective in approximately 50 percent of cases treated. Riedel, in 1950, successfully treated artificially produced cases with a 2 percent solution of a quaternary ammonium compound, consisting of equal parts of alkyl-dimethylbenzyl-ammonium chloride and alkyldimethyl-dichlor-benzyl-ammonium chloride. This preparation did not show any evidence of harmful effects on the skin or in the eyes. Human beings are susceptible and due care should be taken when handling affected birds, especially when there are breaks in the skin of the hand. Thrush, ordinarily caused by Candida albicans, and occasionally by species of the genus Oidium, is not generally an important disease of poultry. Jungherr, in 1933, encountered some severe outbreaks, showing losses as high as 64 percent, among young chicks. Turkeys, pigeons, pheasant, quail and grouse have been found to suffer from this disease. Characteristic lesions are: whitish ulcers of pseudomembranes in the crop, ulcers in the gizzard, brownish and mucoid deposits in the proventriculus. In chicks the lesions are often almost imperceptible. Jungherr was able to reproduce the disease by feeding of fecal material from diseased chicks and by the injection of cultures. The fungus could be isolated from affected areas, and from the gall bladder and intestines. Yeastlike fungi have also been isolated from the cloaca of laying hens affected with "vent gleet." Saunders considers the Candida a normal inhabitant of the digestive tracts

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

spread by black-flies, Simulium occidentale and Simulium nigroparvum, and West and Starr, in 1940, suggested that lice may be vectors. Keeping turkeys in fly-proof shelters may be the only means of prevention (Becker, 1952; Barger el al., 1958). Spirochetosis. Spirochetosis affects several species of birds, including chickens and turkeys. The disease is widely prevalent in Europe (Krijgsman, 1929), and South America, and is found in some parts of the United States. The cause is Borrelia gallinarum which is transmitted by Argas persicus and possibly Dermanyssus gallinae (Becker, 1952). The symptoms resemble those of fowl typhoid. Swelling of the liver and spleen may be conspicuous on necropsy. The liver may show small, white necrotic foci. The diagnosis depends on the demonstration of the spirochetes in properly stained blood smears, or in dark-field preparations. Drugs and vaccines have been tried with variable results. Good results with penicillin have been obtained when given in single doses of 10,000 units intramuscularly. Eradicating the vector is the most effective preventive measure (Barger el al., 1958).

759

760

H. J. STAFSETH

of animals and man. Presumably, invasion of tissues requires predisposing causes. To obtain a reliable diagnosis one must resort to histological or wet preparations. There is no known effective therapeutic agent for this infection. For comprehensive reviews of and references to the literature on Mycoses see: Bullis (1952) and Barger et al. (1958). VIRAL AND RICKETTSIAL DISEASES

Fowl Plague. Fowl plague was intro-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Avian Encephalomyelitis. This disease also known as epidemic tremor, was first described by Jones (1932, 1934), who suggested that it is caused by a virus. The viral etiology has been verified by a number of workers. The disease has been observed over a large area in the United States and in Australia. Natural infection seems to be limited to chickens, but ducklings, young pigeons and poults have been infected artificially. The name epidemic tremor is based on the most characteristic symptoms. Chicks may show evidence of the disease as soon as 24 hours after hatching. No gross lesions are seen, but microscopic changes have been observed. Recently, Peckham (1957) observed lens opacities in fowls, possibly associated with epidemic tremor. A diagnosis may be established on the basis of symptoms and the microscopic lesions in the brain. Van Roekel et al., in 1941, were able to transmit the disease to chicks by inoculating eggs prior to hatching. Thus, egg transmission may be one means of spread, otherewise nothing is definitely known about it. Jungherr and Minard, in 1942, found that the mortality may be very high when chicks are affected during the second week of life. The mortality ranges from 3 to 67 percent. Flowers et al. (1957) reported cataracts as a new flock problem in Texas. Bridges and Flowers (1958) described iridocyclitis associated with encephalomyelitis in chickens.

Equine Encephalomyelitis. The possibility that birds may be natural sources of the equine encephalomyelitis viruses is of public health, as well as economic importance. Many workers have found the virus in pheasants and some have found other birds susceptible (Giltner, 1952; Barger et al, 1958). Woodring (1957) reported naturally occurring infection with this virus in turkeys in Nebraska, causing high morbidity and mortality. Infectious Synovitis. Wills first discovered and described this disease in Texas in 1954. Olson et al., in 1954, reported it from West Virginia. The cause is thought to be a large virus. The agent was found in almost any body tissue tested, following intravenous or intramuscular inoculation of chickens. It was not found in intestinal contents, in the bile or in the synovical membranes. There was a viremia 48 hours after injection and it persisted for ten days. Chickens and turkeys are susceptible and develop lameness and swollen joints, among other general symptoms. To establish a diagnosis the virus must be isolated, because other organisms may cause similar manifestations. Contact infection has been proved to take place. Thayer et al. (1958) concluded that hatching egg transmission of the infectious synovitis virus is definitely indicated. Chlortetracycline and oxytetracycline will reduce mortality if administered early (Barger et al., 1958). Bletner et al. (1957) found that the efficacy of chlortetracycline depended on the time of medication in relation to exposure and dosage. Olson et al. (1957) described blood changes occurring in infectious synovitis, pleuropneumonia-like-organism synovitis and in cases of a combination of these two infections. These two infections could not be differentiated on the basis of alterations in the blood picture.

REVIEW OF POULTRY DISEASES

sion and watery diarrhea. Outstanding changes, noted at necropsy, are: chalky appearance of the pancreas, deposits of urates on the viscera and accumulation of crystals of uric acid in the ureters. The kidneys are usually enlarged and the liver may show necrotic foci. Waller isolated a virus from the blood and livers of birds in the acute stages of the disease. This finding has not been corroborated by others. Beneficial results have been claimed for treatment with potassium dichromate, molasses, muriate of potash, aureomycin and terramycin (100 grams per ton of feed) (Jungherr, 1952; Barger et al., 1958). Bluecomb Diseases of Turkeys. Pomeroy and Sieburth, in 1953, described a disease in turkeys which resembles avian monocytosis. Young poults may be severely affected, the mortality ranging from 10 to 100 percent. Turkeys of all ages are susceptible. This disease has been described as non-specific enteritis, mud fever and transmissible enteritis. A filterable agent was demonstrated by Tumlin el al. in 1957 and by Sieburth and Johnson in 1957. Antibiotics appear to have therapeutic value (Barger et al., 1958). The Avian Leukosis Complex. The avian leukosis complex is a descriptive name, chosen to designate a disease which expresses itself in several forms, or several diseases, which in one way or another, may be related. Butterfield (1905) described a disease of chickens encountered in the District of Columbia and in Michigan, which may have been visceral lymphomatosis. One form of this complex, fowl paralysis, was first described by Marek in 1907. Ellermann, in 1920, first studied avian leukosis. Biely and Palmer in 1932, Jarmai in 1934, Olson in 1940, Engelbreth-Holm in 1924, Furth in 1946, Jungherr (1952) and Winton et al. (1955) have written reviews of the literature on this disease. Jungherr's review is comprehensive with re-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

duced into the United States in 1924, and appeared to have been eradicated in 1925. It reappeared in 1929 in New Jersey but was promptly eradicated. Since then it has not been reported in the United States. The disease remains enzootic in some of the southeastern European Countries. Occasionally it is introduced into the northern European countries, but, for some reason, it does not become established there (Kotlan, 1925). The disease may spread rapidly under certain favorable conditions but usually disappears, and, therefore, seems to be selflimiting (Stubbs, 1955). Symptomatically the disease seems somewhat similar to Newcastle disease, fowl cholera and fowl typhoid. The cause is a virus which is not pathogenic for rabbits. A definite diagnosis can be obtained by microbiological examination and animal inoculation. Moreover, the generalized hemorrhagic lesions, usually observed at necropsy, especially in the proventriculus, the edematous condition about the head and neck and the high mortality, all suggest fowl plague. As far as presently known, the infected bird is the main source of infection. Inasmuch as the disease does not persist for long periods, except in enzootic areas, carrier birds are probably not the perpetuating agents of the infection (Barger et al., 1958). Avian Monocytosis. This is a relatively recently recognized disease. For some time it was known by such names as pullet disease, blue comb or X disease, etc. Jungherr and Matterson, in 1944, proposed the name avian monocytosis. All these names are suggestive of some characteristics of the disease. X disease indicated that its cause and true nature were unknown. As one popular name indicates, pullets are most frequently affected, though the disease occurs in both sexes. Cyanosis (blue comb) is one of the conspicuous symptoms: others are depres-

761

762

H. J. STAFSETH

Doyle, in 1928, and McGaughey and Downie, in 1930, expressed the opinion that fowl paralysis is transmissible through eggs. This opinion did not gain support at first. The infectious nature of lymphomatosis has now been well established. Burmester (1955) studied bioassay of the virus on 3,566 chickens. He found that, under given conditions, a 9-week period appeared to be the optimum for such an assay. The role of eggs in the transmission of lymphomatosis has been

established by Burmester and Waters (1955, 1956) and Burmester et al. (1955). Burmester et al. (1956) have also shown that transovarian transmission of lymphomatosis virus may sufficiently contaminate live virus Newcastle vaccine to make this immunizing agent a means of spread of lymphomatosis. This virus has also been found in the saliva and feces of chickens, thus, making pen-contact infection another natural avenue of spread (Burmester, 1956, 1957). Hutt et al., in 1944, showed that raising chicks at least 100 feet from adult fowls reduced the incidence of lymphomatosis noticeably below that of chicks kept closer to adult chickens. The effect of innate resistance to lymphomatosis on the incidence of lymphomatosis was studied by Taylor et al., in 1943, Hutt et al, in 1945, Waters, in 1945, 1947, and 1956, and Waters and Prickett, in 1946. Burmester (1955) and Burmester el al. (1957) showed that the progeny of immunized females possessed a significantly increased resistance to lymphomatosis, osteopetrosis included. Hutt and Cole (1957) clearly demonstrated the effects of breeding for resistance and susceptibility. In the genetically resistant stock the mortality is now 0.8 to 1.5 percent, whereas in the susceptibile stock the mortality was 38.8 percent. Experiments with isolated stock showed that egg transmission of the virus is relatively unimportant in comparison to genetic susceptibility and mass exposure following hatching. Barger et al. (1958) have prepared a good review of and a list of references to the literature on this disease. Neoplastic Diseases of Chickens. An excellent review of the literature on neoplastic diseases of chickens, with a complete bibliography, has been written by Feldman and Olson in Diseases of Poul-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

spect to coverage of the literature and listing of references. Since the twenties the disease has become widely recognized and is one of the poultryman's greatest problems. Benton and Cover (1957) have reported an increase in the incidence of visceral lymphomatosis in broilers and replacement birds. The forms in which this disease complex expresses itself are: 1. lymphomatosis, neural, ocular, viseral and osteopetrotic; 2. Erythroblastosis; 3. Granuloblastosis; 4. Myelocytomatosis. In a recent report (Burmester, 1958) prepared by a group of pathologists, hematologists and virologists, following a joint study of pathologic blood and tissues, at the U. S. Regional Poultry Research Laboratory, it was concluded that visceral lymphomatosis is an extravascular multicentric neoplasia of the cells in lymphocytic developmental series which manifests itself in a wide range of malignancy. Transmission experiments with cell-free material at the laboratory have demonstrated that propagated virus strains elicit a response identical with that of the most malignant naturally occurring cases. These strains also cause erythroblastosis which is regarded as a malignant intravascular neoplasia of the proerythroblast in the bone marrow; an aleukemic state is invariably present in this disease.

REVIEW OF POULTRY DISEASES

psiltaci. This organism sometimes plays a role in the respiratory disease complex in poultry. The infection is spread through body discharges. According to Davis et al. (1957), eggs play no part in transmission. Davis and Delaplane, in 1955, reported on the use of high levels of chlortetracycline in the feed of young poults with success. Successful treatment with chlortetracycline, oxytetracycline, chloramphenicol, and erthromycin was reported by Loosli in 1955. Meyer, in 1955, found tetracycline in the feed of parakeets effective against psittacosis. Davis el al. (1958) found furazolidone to be ineffective against ornithosis in turkeys. Excellent reviews of the literature on this disease have been published by Meyer (1952), Beaudette (1955) and by Barger el al. (1958). NUTRITIONAL DISEASES

Norris (1958) has covered, very adequately, the advances made in our knowledge of nutritional factors and the role they play in the health and diseases of poultry. The following remarks on this subject are merely supplementary to his review. Pyridoxine (vitamin Be) deficiency results in dermatitis and nervous disorders. The disease is rare because natural feed stuffs contain adequate amounts of pyridoxine. The requirement per pound of feed is 1,000 micrograms, but the poults showed higher mortality and slower growth than those from mothers receiving one milligram per pound of feed. Anti-Gizzard Erosion Factor. Gizzard erosion, degeneration of the horny layer of the gizzard, was first observed in experiments dealing with vitamin K. The causative agent has not been isolated. Sources of anti-gizzard erosion factor are: wheat, bran, fresh kale, oats, whole wheat, barley

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

try, edited by Biester and Schwarte, Iowa State College Press, Ames (1952). Duck Virus Hepatitis. This virus disease of ducks was first described by Levine and Fabricant in 1950 (Levine, 1952). The epizootiology of the disease is not completely known. Duck virus hepatitis has been reported from several states and from England, Canada, Germany, Egypt and the Netherlands. The pathology of the disease has been described by Fabricant et al. (1955, 1957). The significant gross changes are enlargement, paleness and softness of the liver which is also sprinkled with petechial and ecchymotic hemorrhages. Serum therapy has proved an effective means of control. Avian Infectious Hepatitis. This disease was evidently first observed in 1953 when it was mistaken for fowl typhoid (Moore, 1958). Marthedral (1953) described hepatitis in chickens as a presumably noncontagious disease. The disease is characterized by primary liver degeneration and is caused by a virus. Several drugs have shown prophylactic effects, especially furazolidone, (Sevoian et al., 1958; Winterfield et al., 1958; and Moore, 1958). Ornithosis (Psittacosis). The original name of this disease is psittacosis, because it was first observed in psittacine birds. More than 70 species of birds have been found to be susceptible, including pigeons, ducks, chickens and turkeys, hence the name ornithosis. Inasmuch as the disease is transmissible to man it has considerable public health significance, besides being of economic importance to the poultry industry. Some serious outbreaks in man have been reported as resulting from handling and processing of poultry by Irons et al. in 1951; and by Andrews in 1957. The disease is caused by a rickettsial filterable organism, named Miyagawanella

763

764

H. J. STAFSETH

Goiter. This disease is practically unknown in most states. However, it does occur. Kernkamp encountered 2 cases of simple goiter in Minnesota in 1925. According to Welch the disease is common in Montana. On Long Island and in Sumter, S. C , many cases have been observed in pigeons. These workers found that small amounts of potassium iodide in the ration cured and prevented goiter

in adult and newly hatched squabs. Wilgus et al, in 1948, found that 0.5 to 1.0 milligram of iodine per pound of ration is required for the prevention of iodine deficiency. Wilder et al., in 1933, found that the amount of iodine fed determined the iodine content of eggs (Barger et al., 1958). For reviews of and references to the literature on these nutritional deficiencies, see: Sherwood and Couch (1952) and also, Norris and Scott (1952). Necrosis of the Beak. Necrosis of the beak is a condition which may result from the use of a too finely ground all-mash ration. Impaction takes place under the tongue and some of the masses of mash may adhere to the upper and lower mandibles. Thus, irritation with secondary infection will develop. Cleaning out these masses, disinfecting the inflamed areas and using a coarser feed will remedy this condition (Barger et al., 1958). Toxic Disease in Broilers. A disorder of chickens, probably due to a toxic feed, has recently been described by Schmittle et al. (1958). The disease occurs in broiler chicks in different locations in the United States. It manifests itself by droopiness, ruffled feathers, labored breathing and progressively increasing morbidity and mortality. Postmortem changes are: marked hydropericardium, hydroperitoneum, swollen liver with a roughened surface and discoloration with alternate areas of yellow and red tissue. The kidneys are swollen and pale and there is often subcutaneous edema in the ventral portion of the body. Exhaustive laboratory examinations failed to reveal any infectious agent. The toxic agent appears to be stable in storage for eight months and tolerates 121°C. for 20 minutes. Further research is in progress. Weiss and Fisher (1957) found deranged lipid metabolism resulting from feeding 5-10 percent animal fat.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

and hempseed meal. Other anti-gizzard erosion factors are cholic acid, and alcocholic extract of chicken feces, the factor possibly being bile. Lansing and Miller, in 1940, produced gizzard erosion by ligation of the bile ducts in adult birds. Folic Acid Deficiency. Stockstad and Manning, in 1938, discovered that folic acid is necessary for chicks. Richardson et al., in 1945, described the symptoms of folic acid deficiency in poults as a type of cervical paralysis. Requirements for folic acid have been stated as follows: chicks up to six weeks of age, 115 micrograms per pound of feed. This is the requirement for survival; for hemoglobin formation and growth up to four weeks of age, the requirement is 200 micrograms. For hemoglobin formation up to six weeks of age, 160 micrograms, but for feathering at six weeks, 250 micrograms of folic acid for normal feathering, hemoglobin, and prevention of cervical paralysis. New Hampshire chicks receiving a synthetic diet, required 700 to 900 micrograms of folic acid per pound of diet. Robertson, from limited data, in 1946, found that commercial feeds contained 450 micrograms of folic acid per pound of ration. Boucher thought it unlikely that poultry rations, made up of natural feed stuffs, would produce folic acid deficiency. Turkey hens, receiving 0.2 milligrams of folic acid per pound of feed, showed no signs of deficiency. They layed well and the eggs hatched.

REVIEW OF POULTRY DISEASES

PARASITES

Raggi and Levine (1957) reported the occurrence of Tetrameres americana in domestic pigeons. Comprehensive reviews of and refer-

ences to the literature on internal parasites have been published by Wehr (1952), Price (1952) and by Barger et al. (1958). MISCELLANEOUS

Saunders and Moore (1957) reported blindness in turkeys due to granulomatous chorioretinitis. The cause was not determined. Dougherty and Rickard (1957) reported on a non-infectious abnormality in the livers of slaughtered White Pekin ducks, characterized by whitish spots on the medial, cardiac portion of the right lobe. The cause is evidently rough handling during machine feather picking, resulting in rupture of small bile ducts. Gentry (1958) reported on the toxic effects of some antibiotics and of furazolidone for chicken embryos. Quirox and Hanson (1958) studied physical chemical treatments of inocula as means of separation and identification of avian viruses. They found that certain mixtures could be resolved by such treatments. Newberne and Buck (1957) studied the effects of nicarbazin in young chickens and observed the following symptoms: inanition, ataxia, jerky incoordination, stilted gait and loss in weight gains. Cover (1957) has reviewed the chemotherapy of avian viral and bacterial infections. Wilson (1957) reported that a condition, characterized by a rounded heart with dimpled apex and a dark liver is on the increase in Britain. It has also been reported in Europe, Canada and in New York. The cause has not been found. In some ways the disease behaves similarly to neurolymphomatosis. A great contribution to poultry pathology and prevention of avian diseases is the book Diseases of Poultry, edited by Biester and Schwarte, Veterinary Re-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

External Parasites. Considerable progress has been made in the control of external parasites. This is due partly to improved housing and partly to better hygienic management and intelligent use of insecticides. This subject is well covered in Diseases and Parasites of Poultry by Barger et at. (1958), and by Benbrook in Diseases of Poultry, Biester and Schwarte (1952). Melathion is effective against lice and certain mites. Furnam (1957) reported excellent results through its use in the control of northern fowl mite (Ornithonyssus sylviarum), a very harmful ectoparasite of poultry which apparently has been spreading. Internal Parasites. Internal parasites evidently are not as much of a problem as they once were. The main reason for this must be attributed to the function of sanitation and hygiene in modern poultry management (Turk, 1958). Advances in our knowledge of the life cycles of internal parasites have made it possible to outline effective preventive measures. This statement should not be interpreted to mean that anthelmintics are of no value. Internal parasites do, at times, create serious health problems in which the use of the better chemical remedies will facilitate control and prevention of parasitism. Piperazine derivatives, for example, have been found effective against Ascaridia galli and somewhat less so against Heterakis gallinae (Horton-Smith and Long, 1955; Shumard, 1956; Edgar et al., 1957; and Enzie et al., 1957). Phenothiazine is highly effective against H. gallinae and, thus, aids in the prevention of blackhead, the cause of which is transmitted by the cecal worm (Wehr, 1958).

765

766

H. J. STAFSETH

search Institute, Iowa State College and published by the Iowa State College Press., Ames, Iowa. The 4th edition of this book will appear soon. SELECTED REFERENCES

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Adler, H. E., and R. Yamamoto, 1956. Studies on chronic coryza (Nelson) in the domestic fowl. Cornell Vet. 45: 337-343. Adler, H. E., J. Fabricant, R. Yamamoto and J. Berg, 1958. Symposium on chronic respiratory disease of poultry. I. Isolation and identification of pleuropneumonia-like organisms of avian origin. Am. J. Vet. Res. 19: 440-447. Anczykowski, F., 1952. Brucellosis in fowls. II. Serology, III. Agglutination tests with serum of fowls with concurrent 5. pullorum and Br. abortus infection. Roczn. Nauk. rol. Ser. E. 66: 303-317. Anderson, G. W., J. B. Cooper, J. C. Jones and C. L. Morgan, 1948. Sulfonamides in the control of pullorum disease. Poultry Sci. 27: 172-174. Anonymous, 1930. Eastern States Conference of Laboratory Workers in Pullorum Disease Control. J. Am. Vet. Med. Assn. 77: 259-263. Anonymous, 1933. Report of the conference of official research workers in animal diseases of North America on standard methods of pullorum disease in barnyard fowl. J. Am. Vet. Med. Assn. 82:487-491. Bankowski, R. A., R. W. Hill and L. G. Raggi, 1957. Response of eight-week-old susceptible chickens to Newcastle disease (B-l) and infectious bronchitis viruses. Avian Dis. 1: 195-207. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Avian monocytosis. Diseases and Parasites of Poultry, 5th ed., pp. 281-282, 304-305. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Blackhead. Diseases and Parasites of Poultry, 5th ed., pp. 234-240, 256-258. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Coccidiosis. Diseases and Parasites of Poultry, 5th ed., pp. 224-233, 252-256. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Equine encephalomyelitis. Diseases and Parasites of Poultry, 5th ed., pp. 208-209, 222-223. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Fowl plague. Diseases and Parasites of Poultry, 5th ed., pp. 196-200, 219. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958.

Gapeworms. Diseases and Parasites of Poultry, 5th ed., pp. 348-352, 360, 363. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Goiter. Diseases and Parasites of Poultry, 5th ed., pp. 276-280. Necrosis of the beak, p. 299. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Infectious coryza. Diseases and Parasites of Poultry, 5th ed., pp. 128-131, 156-157. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Infectious laryngotracheitis. Diseases and ParaParasites of Poultry, 5th ed., pp. 171-188, 211213. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Infectious bronchitis. Diseases and Parasites of Poultry, 5th ed., pp. 200-203, 219-220. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Chronic respiratory disease complex. Diseases and Parasites of Poultry, 5th ed., pp. 117-119, 159. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Infectious synovitis. Diseases and Parasites of Poultry, 5th ed., pp. 206-207, 221-222. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Internal parasites. Diseases and Parasites of Poultry, 5th ed., pp. 333-363. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. External parasites. Diseases and Parasites of Poultry, 5th ed., pp. 364-387. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Leucocytozoon infection. Diseases and Parasites of Poultry, 5th ed., pp. 247-248, 259-260. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Mycoses. Diseases and Parasites of Poultry, 5th ed., pp. 284-289, 302-305. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Newcastle disease. Diseases and Parasites of Poultry, 5th ed., pp. 191-196, 217-219. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Ornithosis and psittacosis. Diseases and Parasites of Poultry, 5th ed., pp. 203-205, 220-221. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Spirochetosis. Diseases and Parasites of Poultry, 5th ed., pp. 248-250, 260-261. Lea and Febiger, Philadelphia.

REVIEW OF POULTRY DISEASES

Becker, E. R., 1952. Leucocytozoon infections. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd ed., pp. 995-998, Iowa State College Press, Ames. Becker, E. R., 1952. Protozoa. Coccidiosis of the chicken. Coccidiosis of the turkey. Coccidiosis of ducks. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 943-977. Iowa State College Press, Ames. Belding, R. C-, and M. L. Mayer, 1958. Furazolidone in the treatment of salmonella infections of turkeys. 1. Effect of acute pullorum disease of poults. 2. Effect on acute paratyphoid infection in poults. Poultry Sci. 37: 459-467. Benbrook, E. A., 1952. External parasites of poultry. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 787-833. Iowa State College Press, Ames. Benton, W. J., and M. S. Cover, 1957. The increased incidence of visceral lymphomatosis in broilers and replacement birds. Avian Dis. 1: 320-327. Benton, W. J., and M. S. Cover, 1958. Experimental treatment of infectious sinusitis in turkeys with nitrofurans and antibiotics. Am. J. Vet. Res. 19: 489^93. Bierer, B. W., 1958. The ill effects of excessive formaldehyde fumigation on turkey poults. J. Am. Vet. Assn. 132:174-176. Bletner, J. K., D. C. Shelton, N. O. Olson and C. E. Weakley, Jr., 1957. Control of infectious synovitis. 3. The efficacy of chlortetracycline with relation to time of experimental infection. Poultry Sci. 36: 1016-1022. Borstein, S., and Y. Samberg, 1955. The therapeutic effect of streptomycin in high dosage on egg production and growth of birds affected with infectious coryza. Poultry Sci. 34:896-904. Botorff, C. A., and J. S. Kiser, 1946. The use of sulfonamides in the control of pullorum disease. Poultry Sci. 25:397. Boyd, R. J , and R. P. Hanson, 1958. Survival of Newcastle disease virus in nature. Avian Dis. 2: 82-93. Boyer, C. I., Jr., and J. A. Brown, 1957. Oral therapy for erysipelas in turkeys. Avian Dis. 1: 275290. Boyer, C. I., Jr., and J. A. Brown, 1957. Studies on erysipelas in turkeys. Avian Dis. 1: 42-52. Brandly, C. A., 1952. Newcastle disease. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 331-368. Iowa State College Press, Ames. Bridges, C. H., and A. I. Flowers 1958. Iridocyclitis and cataracts associated with an encephalomyelitis in chickens. J. Am. Vet. Med. Assn. 132: 79-84.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Staphylococcic and streptococcic infections. Diseases and Parasites of Poultry, 5th ed., pp. 140146. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. The avian leukosis complex. Diseases and Parasites of Poultry, 5th ed., pp. 180-191, 213-217. Lea and Febiger, Philadelphia. Barger, E. H., L. E. Card and B. S. Pomeroy, 1958. Ulcerative enteritis. Diseases and Parasites of Poultry, 5th ed., pp. 147-149. Lea and Febiger, Philadelphia. Bass, C. C , 1939. Observations on the specific cause and the nature of "quail disease" or ulcerative enteritis in quail. Proc. Soc. Exp. Biol. Med. 42: 377-380. Bass, C. C , 1941. Specific cause and nature of ulcerative enteritis in quail. Proc. Soc. Exp. Biol. Med. 46: 250-252. Beach, J. R., 1922. Observations on the occurrence of fowl cholera in California. Poultry Sci. 1: 186195. Beach, J. R., and D. E. Davis, 1927. Acute infection of chicks and chronic infection of the ovaries of hens caused by the fowl typhoid organism. Hilgardia, 2:411-424. Beaudette, F. R., 1925. The possible transmission of fowl typhoid through the egg. J. Am. Vet. Med. Assn. 67: 741-745. Beaudette, F. R., 1943. A review of the literature on Newcastle disease. Proc. Forty-Seventh Ann. Meet. TJ. S. Livestock San. Assn., pp. 122-177. Beaudette, F. R., 1949. Twenty years of progress in immunization against virus diseases of birds. J. Am. Vet. Med. Assn. 115: 232-244. Beaudette, F . R., 1950. Recent literature on Newcastle disease. Proc. Fifty-Fourth Ann. Meet. U. S. Livestock. San. Assn., pp. 132-153. Beaudette, F. R., 1951. Current literature on Newcastle disease. Proc. Fifty-Fifth Ann. Meet. U. S. Livestock San. Assn., pp. 108-174. Beaudette, F. R., 1955. Psittacosis, Diagnosis, Epidemiology and Control. Rutgers University Press, New Brunswick. Becker, E. H., 1952. Aegyptianella pullorum infections. Spirochete infections. In Diseases of Poultry (Biester and Schwarte, eds.) 3rd ed., pp. 1009-1013. Iowa State College Press, Ames. Becker, E. R., 1952. Intestinal flagellates. Trichomonas infections. In Diseases of Poultry (Biester and Schwarte, eds.) 3rd ed., pp. 10171020,1025-1026. Iowa State College Press, Ames. Becker, E. R., 1952. Protozoa. In Diseases of Poultry (Biester and Schwarte, eds.) 3rd. ed., pp. 1009-1013. Iowa State College Press, Ames.

767

768

H. J. STAFSETH tumors of the hen. Folia Haematol. 2: 649-657. Burton, W. H., 1946. Control of pullorum disease transmission in hatcheries by formaldehyde fumigation. Proc. 18th Ann. Conf. Lab. Workers in Pullorum Disease Control, p. 1. Bushnell, L. D., and L. F . Payne, 1931. Dissemination of pullorum disease in the incubator. Kansas Agr. Exper. Sta. Tech. Bui. 29. Bushnell, L. D., L. F . Payne and C. J. Coon, 1929. Fumigation of forced-draft incubators. J. Am. Vet. Med. Assn. 75: 611-625. Calnek, B. W., and P. P. Levine, 1957. Studies on experimental egg transmission of pleuropneumonia-like organisms in chickens. Avian Dis. 1: 208-222. Chang, Kuan-How, and H. J. Stafseth, 1950. Influence of various factors on the bacteriostatic and bactericidal action of streptomycin on Salmonella pullorum. Poultry Sci. 29: 130-138. Chang, Kuan-How, and H. J. Stafseth, 1950. Influence of serum of normal and pullorum infected birds on the bacteriostatic and bacteriocidal action of streptomycin on Salmonella pullorum. Poultry Sci. 29: 139-145. Chang, P. W., A. H. Dardiri, D. Fry and V. J. Yates, 1957. A study of the criteria for evaluating infectious bronchitis immunity. Avian Dis. 1: 304311. Christian, R. T., and W. N. Mack, 1957. An experimental infectious bronchitis virus vaccine inactivated with beta-propiolactone. Poultry Sci. 36: 1177-1181. Clapham, P. A., 1953. Pseudotuberculosis among stock-doves in Hampshire. Nature, 172: 353. Coburn, D. R., and H. J. Stafseth, 1931. A field test for pullorum disease. J. Am. Vet. Med. Assn. 79: 241-243. Cole, R. K., 1948. Sulfonamides versus Salmonella pullorum in adult chickens. Poultry Sci. 27: 427429. Cooper, J. B., C. L. Morgan, G. W. Anderson and J. C. Jones, 1951. Effect of sulfamerazine on pullorum reactors. Poultry Sci. 30: 249-254. Cooper, M. S., G. R. Personeus and R. C. Percival, 1957. Laboratory studies on erysipelas. 4. Duration of immunity in turkeys vaccinated with an absorbed bacterin. Poultry Sci. 36: 266-269. Cordy, D. R., and H. E. Adler, 1957. The pathogenesis of the encephalitis in turkey poults produced by a neurotropic pleuropneumonia-like organism. Avian Dis. 1: 235-245. Cover, M. S., 1957. A review of the chemotherapy of avian viral and bacterial infections. Jour. Am. Vet. Med. Assn. 131: 465-469.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Bullis, K. L., 1952. Diseases caused by fungi. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 435-452. Iowa State College Press, Ames. Burmester, B. R. 1955, Immunity to visceral lymphomatosis in chicks following injections of virus into dams. Proc. Soc. Exp. Biol. Med. 88: 153— 155. Burmester, B. R., 1955. Bioassay of the virus of visceral lymphomatosis. I. Use of short experimental period. J. Natl. Cancer Inst. 16: 1121— 1127. Burmester, B. R., 1956. The shedding of the virus of visceral lymphomatosis in the saliva and feces of individual normal and lymphomatous chickens. Poultry Sci. 35: 1089-1099. Burmester, B. R., 1957. Routes of natural infection in avian lymphomatosis. New York Acad. Sci. 68:487-495. Burmester, B. R., 1957. Transmission of tumor inducing avian viruses under natural conditions. Texas Repts. Biol. Med. 15: 540-558. Burmester, B. R., 1958. Personal communication. Burmester, B. R., 1957. Recent studies on the natural transmission of visceral lymphomatosis in chickens. J. Am. Vet. Med. Assn. 131:496-499. Burmester, B. R., R. F. Gentry and N. F. Waters, 1955. The presence of virus of visceral lymphomatosis in embryonated eggs of normal appearing hens. Poultry Sci. 34: 609-617. Burmester, B. R., C. H. Cunningham, G. E . Cottral, R. C. Belding and R. F. Gentry, 1956. The transmission of visceral lymphomatosis with live virus Newcastle disease vaccines. Am. J. Vet. Res. 17: 283-289. Burmester, B. R., and N. F . Waters, 1955. The role of the infected egg in the transmission of visceral lymphomatosis. Poultry Sci. 34: 1415-1429. Burmester, B. R., and N. F. Waters, 1956. Avian lymphomatosis. (U. S. Dept. Agr. Yearbook, pp. 466^74. Burmester, B. R., W. G. Walter and A. K. Fontes, 1957. The immunological response of chickens after treatment with several vaccines of visceral lymphomatosis. Poultry Sci. 36: 79-87. Burmester, B. R., and N. F. Waters, 1956. Variation in the presence of the virus of visceral lymphomatosis in the eggs of the same hen. Poultry Sci. 35: 939-944. Burr, W. E., M. Tourtellotte, R. E. Luginbuhl and E. L. Jungherr, 1957. Salmonella heidelberg infection as a problem in pullorum disease control. Avian Dis. 1: 298-304. Butterfield, E. E., 1905. Aleukaemic lymphadenoid

R E V I E W OF POULTRY D I S E A S E S

The efficacy of some piperazine compounds in the elimination of helminths from experimentaflyand naturally-infected poultry. Poultry Sci. 36: 495-510. Edwards, P . R., W. B. Cherry and D. W. Bruner, 1943. Further studies in coliform bacteria serologically related to the genus Salmonella. J. Infect. Dis. 73: 229-238. Edwards, P. R., and W. H. Ewing, 1955. Identification of Enterobacteriaceae. Burgess Publishing Co., Minneapolis. Edwards, P. R., M. G. West and D. W. Bruner, 1947. Arizona group of paracolon bacteria. Kentucky Agr. Exper. Sta. Bui. 499. Enzie, F. D., M. L. Colglazier and E. H. Wilkens, 1957. Newer treatments for helminthic infections. Vet. Med. 52: 267-281, 387. Fabricant, J., 1957. A modified chicken embryo inoculation technique for the isolation of viruses from the respiratory tract of chickens. Avian Dis. 1: 62-66. Fabricant, J., C. G. Pickard and P . P. Levine, 1957. The pathology of duck virus hepatitis. Avian Dis. 1:256-275. Feldman, W. H., 1939. The role of the avian tubercle bacillus in the sensitization of cattle to tuberculin. J. Am. Vet. Med. Assn. 95: 152-157. Fenstermacher, R., 1952. Paratyphoid infections. In Diseases of Poultry, (Biester and Schwarte, ed.) 3rd. ed., Iowa State College Press, Ames, pp. 261-300. Flowers, A. J., L. C. Grumbles, R. T. Du Bose and J. P. Delaplane, 1957. Cataracts: a new flock problem in chickens. Poultry Sci. 36: 1117; also, 37: 420^22. Furman, D. P., and W. S. Coates, 1957. Northern fowl mite control with malathion. Poultry Sci. 36:252-255. Gage, G. E., B. H. Paige and H. W. Hyland, 1914. On the diagnosis of infection with Bacterium pullorum in the domestic fowl. Massachusetts Agr. Exp. Sta. Bui. 148. Galuzo, I. G., and M. N . Rementsova, 1955. Reservoir of animal brucellosis amongst wild animals and birds in the light of studies on foci of infection. Trud. Inst. Zool., Alma-Alta, 3 : 12-26. Gentry, R. F., 1957. A simplified method for the titration of antigen in the beta hemagglutinationinhibition test. Avian Dis. 1: 75-81. Gentry, R. F., 1958. The toxicity of certain antibiotics and furazolidone for chicken embryos. Avian Dis. 2: 76-82. Gerriets, E., 1953. Antibiotica und Chemotherapie bei einen Fall von Septicaemia anserum exuda-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Cover, M. S., and W. J. Benton, 1957. The isolation of a viral agent from chickens showing respiratory distress. Avian Dis. 1: 54-61. Cover, M. S., and W. J. Benton, 1957. The distribution of the infectious synovitis agent in the tissues of artificially infected chickens. Avian Dis. 1: 312-319. Cunningham, C. H., 1952. Fowl pox. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., Iowa State College Press, Ames, pp. 629-667. Cunningham, C. H., 1957. Symposium on immunization against infectious bronchitis virus. 1. Some basic properties of infectious bronchitis virus. Am. J. Vet. Res. 18: 648-654. Darby, C. W., and H. J. Stafseth, 1942. Salmonella infections common to man, animals and birds. Proc. 46th Ann. Meet. U. S. Livestock Sanit. Assn., pp. 189-202. Dardiri, A. H., P. W. Chang and D. E. Fry, 1957. Immunity study of three types of Newcastle disease vaccine for broilers and caponettes. Am. J. Vet. Res. 18: 400-404. Davis, D. E., J. P . Delaplane and J. R. Watkins, 1957. The role of turkey eggs in the transmission of ornithosis. Am. J. Vet. Res. 18: 409^13. Davis, D. E., J. R. Watkins and J. P. Delaplane, 1958. Research note—The ineffectiveness of furazolidone as a prophylactic agent against turkey ornithosis. Avian Dis. I I : 117-119. de Blieck, L., 1931. Een haemoglobinophile bacterrie als oorzaak van coryza infectiosa gallinarum. Tijdsch. Diergeneesk. 58: 1-5. de Blieck, L., and T. van Heelsbergen, 1923. Impfung gegen Diphtherie und Gefliigelpocken bei Huhnern. Deutsch. tierarztl. Wochenschr. 31: 85. Dickinson, E. M., and E. D. Stoddard, 1949. Sulfamerazine against Salmonella pidlorum in adult chickens. Poultry Sci. 28: 153-155. Dougherty, E., I l l , 1953. Disease problems confronting the duck industry. Proc. Book Am. Vet. Med. Assn., pp. 359-365. Dougherty, E., I l l , and C. G. Rickard, 1957. An artefact resembling focal necrosis in the livers of slaughtered White Pekin ducks. Avian Dis. 1: 130-135. Doyle, T. M., 1930. Immunization of fowls against tuberculosis with B.C.G. vaccine. Vet. J. 86: 9096. Drew, R. M., 1946. Occurrence of two immunological groups within the genus Listeria. Studies based upon precipitation reactions. Proc. Soc. Exper. Biol. Med. 61: 30-33. Edgar, S. A., D. C. Davis and J. A. Frazier, 1956.

769

770

H. J. STAFSETH Heller, O., 1957. Geese as carriers of fowl cholera. Monatssch. f. Vet. Med. May 1:218. Henderson, W., F . L. Walkey and G. L. Morehouse, 1958. Furazolidone treatment of experimental pullorum disease in adult chickens. Am. J. Vet. Res. 19: 196-199. Hilbert, K. F., and W. F. Witter, 1936. Report of the poultry disease laboratory at Farmington, Long Island. Ann. Rept. New York State Vet. Col. 1934-1935, p. 38. Hilbert, K. F., and J. S. Kiser, 1948. Chemotherapy of duck diseases with sulfonamides, Cornell Vet. 38: 148-155. Hinshaw, W. R., 1937: Diseases of turkeys. California Agr. Exp. Sta. Bui. 613:1-12. Hinshaw, W. R. Coccidiosis (of turkeys). 1952. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 1175-1178. Iowa State College Press, Ames. Hinshaw, W. R., 1952. Fowl pox. In Diseases of Poultry (Biester and Schwarte, eds.) 3rd. ed., pp. 1325-1332, Iowa State College Press, Ames. Hinshaw, W. R., 1952. Histomoniasis (infectious enterohepatitis, blackhead). In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 1168-1175. Iowa State College Press, Ames. Hinshaw, W. R., 1952. Hexamitiasis (infectious catarrhal enteritis). In Diseases of Poultry (Biester and Schwarte, eds.), pp. 1178-1184. Iowa State College Press, Ames. Hinshaw, W. R., and E. McNeil, 1944. Gopher snakes as carriers of salmonellosis and paracolon infections. Cornell Vet. 34: 248-254. Hinshaw, W. R., and E. McNeil, 1946a. The occurrence of type 10 paracolon in turkeys. Jour. Bact. 51: 281-286. Hinshaw, W. R., and E. McNeil, 1946b. Paracolon type 10 from captive rattlesnakes. J. Bact. 51: 397-398. Hoffman, H. A., 1933. Studies on the etiology of "ruptured yolk." Poultry Sci. 12: 189-200. Hofstad, M. S., 1952. Avian staphylococcosis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 428^30. Iowa State College Press, Ames. Hofstad, M. S., 1952. Avian streptococcosis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 427-428. Iowa State College Press, Ames. Hofstad, M. S., 1952. Coli-granuloma (Hjarre's disease). In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 432-434. Iowa State College Press, Ames. Hofstad, M. S., 1952. Infectious coryza. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 377-382. Iowa State College Press.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

tiva. Berlin, u. Munich, tierarztl, Wochenschr. 15: 261-265. Giltner, L. T., 1952. Equine encephalomyelitis virus in birds. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 629-634. Iowa State College Press, Ames. Glover, J. A., and W. Henderson, 1946. Fowl typhoid. Report on a recent outbreak in Ontario. J. Comp. Med. 10: 241-249. Goldwasser, R., and A. Kohn, 1957. Neutralization and titration of Newcastle disease virus in chicken embryo tissue cultures. Am. J. Vet. Res. 18: 390-395. Graham, R., 1941. Hatchery sanitation and incubator hygiene. Proc. Conf. Nat. Poultry Improv. Plan., Bur. An. Ind., U.S.D.A., 106-115. Graybill, H. W., and T. Smith, 1920. Production of fatal blackhead in turkeys by feeding embryonated eggs of Heterakis papulosa. J. Exp. Med., 31:647-655. Griffiths, N . J., R. M. Leary and R. Fenstermacher, 1954. A new record of gapeworm {Cyathostoma bronchialis) infection of domestic geese in North America. Am. J. Vet. Res. 15: 298-299. Gross, W. B., 1957. Escherichia coli infection of the chicken eye. Avian Dis. 1: 36-41. Gross, W. B., 1958. Symposium on chronic respiratory disease of Poultry. II. The role of Escherichia coli in the cause of chronic respiratory disease and certain other respiratory diseases. Am. J. Vet. Res. 19: 448-463. Grumbles, L. C , H. E. Levy and W. T. Oglesby, 1950. Sulfonamides in the control of pullorum disease in young chicks. Poultry Sci. 29: 236-239. Gwatkin, R., 1927. Some experiments on the disinfection of eggs and incubators. Ont. Vet. Coll. Rep. (1926) pp. 58-65. Gwatkin, R., 1946. Resume of studies relating to Younie strains of Salmonella pullorum. Proc. 18th Am. Conf. Lab. Workers in Pullorum Disease Control, p. 1. Hall, W. J., Fowl typhoid. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 301326. Iowa State College Press, Ames. Hamdy, A. H., L. C. Ferguson, V. L. Sanger and E. H. Bohl, 1957. Susceptibility of pleuropneumonia-like organisms to the action of the antibiotics erythromycin, chlortetracycline, hygromycin, magnamycin, oxytetracycline and streptomycin. Poultry Sci. 36: 748-754. Haupt, H., 1935. Zur Systematik der Bakterien. Die fur Mensch und Tier pathogenen gram-negativen alkalibildenden Stachenbakterien. Ergeb. Hyg. Bakt. Immunit u. Exper. Therap. 17: 175. Heiman, V., 1943. Sulfathiazole for colds in chickens. Vet. Med. 38: 2fi-?8.

REVIEW or POULTRY DISEASES

Jungherr, E.L., 1958.Symposium onchronic respiratory diseases of poultry, IV. The control of chronic respiratory disease. Am. J. Vet. Res. 19: 464-467. Jurado, F. R., C. A. Mazzini, V. C. F. Cedro and E. J. Torre, 1951. Experimental brucellosis in fowls. Proc. 5th Vet. Congr., Braz. Vet., Sao Paulo, 1950, 629-648. Karlson, A. G., M. R. Zinober and W. H. Feldman, 1950. A whole-blood rapid agglutination test for avian tuberculosis—a preliminary report. Am. J. Vet. Res. 11: 137-141. Kingsbury, F. W., and E. L. Jungherr, 1958. Indirect transmission of infectious laryngotracheitis in chickens. Avian Dis. 2: 54-63. Kirkpatrick, C. M., H. E. Moses and J. T. Baldini, 1950. Streptomycin studies in ulcerative enteritis in Bobwhite quail. Poultry Sci. 29: 561-569. Kirkpatrick, C. M., H. E. Moses and J. T. Baldini, 1952. Concentration of streptomycin in drinking water suppressing the experimental disease. Am. J. Vet. Res. 13: 102-104. Kirkpatrick, C. M., and H. E. Moses, 1953. The effect of streptomycin against quail disease in Bobwhites. J. Wildlife Mgmt. 17: 24-28. Kotlan, A., 1925. Personal communication. Krijgsman, B. J., 1929. Durch Spirochaten verursachte Krankheiten. In Handbuch der Gefliigelkrankheiten (van Heelsbergen), pp. 374-382. Ferdinand Enke, Stuttgart. Lambert, W. V., 1933. A preliminary study of the reaction of two disease resistant stocks of chickens after infection with their reciprocal pathogens. Iowa Acad. Sci. 40: 231. Levine, N. D., 1952. Avian listeriosis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 403-408. Iowa State College Press, Ames. Levine, N. D., 1952. Botulism. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 408-414, Iowa State College Press, Ames. Levine, N. D., 1952. Erysipelas. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 414-422. Iowa State College Press, Ames. Levine, P. P., 1952. Duck virus hepatitis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 689-694. Iowa State College Press, Ames. Levine, P. P., and J. Fabricant, 1950. A hitherto undescribed virus disease of ducks in North America. Cornell Vet. 40: 71-86. Lewis, K. H., and E. R. Hitchner, 1936. Slow lactose-fermenting bacteria pathogenic for young chickens. J. Infect. Dis. 59: 225-235. Madsen, D. E., 1937. An erysipelas outbreak in turkeys. J. Am. Vet. Med. Assoc. 91: 206208.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Hofstad, M. S., 1952. Infectious laryngotracheitis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 521-530, Iowa State College Press, Ames. Hofstad, M. S., 1952. Infectious bronchitis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd ed., pp. 509-519, Iowa State College Press, Ames. Hofstad, M. S., 1952. Chronic respiratory disease and coccobacilli from coryza. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 382-386. Iowa State College Press, Iowa. Hofstad, M. S., 1957. Egg transmission of infectious sinusitis in turkeys. Avian Dis. 1: 165-170. Hofstad, M. S., 1957. A serological study of infectious sinusitis in turkeys. Avian Dis. 1: 170-179. Horton-Smith, C , and P. L. Long, 1955. The anthelmintic effect of three piperazine derivatives on Ascaridia Galli (Schrank 1788). Poultry Sci. 35: 606-614. Hubben, K., 1958. A case report—Aspergillus meningoencephalitis in turkeys and ducks. Avian Dis. 2: 110-116. Hutt, F. B., and R. K. Cole, 1957. Control of fowl leukosis. J. Am. Vet. Med. Assn. 131: 491-495. Insko, W. M., D. G. Steele and C. M. Hinton, 1941. Effect of formaldehyde fumigation on mortality of chick embryos. Kentucky Agr. Exper. Sta., Bui. 416. Jansen, J., and H. Kunst, 1949. Is duck plague related to Newcastle disease or to fowl plague? Proc. 14th Intern. Vet. Congr., London 2: 263-265. Johnson, W. T., 1923. Avian coccidiosis. Poultry Sci. 2: 146-163. Johnson, W. T., 1927. Immunity or resistance of the chicken to coccidial infection. Oregon Agr. Expt. Sta. Bui. 230:1-31. Johnson, W. T., 1938. Coccidiosis of the chicken with special reference to species. Oregon Agr. Exp. Sta. Bui. 353: 1-33. Jones, E., 1932. An encephalomyelitis in the chicken. Science, 76: 331-332. Jones, E. E., 1934. Epidemic tremor, an encephalomyelitis affecting young chickens. J. Exp. Med. 59: 781-798. Jones, F. S., 1913. The value of the macroscopic agglutination test in detecting fowls that are harboring Bacterium pullorum. J. Med. Res. 27:471479. Jungherr, E. J., 1952. Avian monocytosis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd., ed. pp. 695-709. Iowa State College Press, Ames. Jungherr, E. J., 1952. The avian leukosis complex. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 453-507. Iowa State College Press, Ames.

771

772

H. J. STAFSETH National Poultry Improvement Plan, 1941. U.S.D.A., Misc. Pub. 300: 28. Nelson, J. B., 1935. Cocco-bacilliform bodies associated with an infectious fowl coryza. Science, 82:43-44. Nelson, J. B., 1936. Studies on uncomplicated coryza of the domestic fowl. VI. Coccobacilliform bodies in birds infected with the coryza of slow onset. VII. Cultivation of the coccobacilliform bodies in fertile eggs and in tissue cultures. VIII. The infectivity of fetal membrane and tissue culture suspensions of the coccobacilliform bodies. J. Exp. Med. 63: 512-522; 64: 749-758, 759-769. Nelson, J. B., 1938. Studies on an uncomplicated coryza of the domestic fowl. IX. The cooperative action of Hemophilus gallinarum and the coccobacilliform bodies in the coryza of rapid onset and long duration. J. Exp. Med. 69: 199-209. Nelson, J. B., 1953. Microorganisms of the pleuropneumonia group and their relation to chronic respiratory disease. Proc. 25th Ann. Conf. Lab. Workers in Pullorum Disease Control, Amherst. Newburne, P. M., and W. B. Buck, 1957. Studies on drug toxicity in chicks. 3. The influence of various levels of nicarbazin on growth and development of chicks. Poultry Sci. 36: 304-312. Norris, L. C , 1958. The significant advances of the past fifty years in poultry nutrition. Poultry Sci. 37:256-2.74. Olesiuk, O. M., H. Van Rockel and L. P. Boninato, 1957. Influence of chemotherapeutic agents on experimental chronic respiratory disease in chickens and turkeys. Poultry Sci. 36: 383-395. Olsen, M. W., and E. A. Allen, 1940. Treatment of cecal and liver trichomoniasis in turkeys by fever therapy. Proc. Soc. Exp. Biol. Med. 45: 875-876. Olson, N. O., 1950. A respiratory disease (bronchitis) of quail caused by a virus. Proc. 54th Ann. Meet. U. S. Livestock San. Assoc, pp. 171-174. Olson, N. O., D. C. Shelton, D. A. Munro and R. Beltner, 1957. Preliminary blood studies in chickens with a synovitis caused by the infectious synovitis agent, pleuropneumonia-like organism and a combination of the two agents. Avian Dis. 1: 82-91. Osborn, O. H., and B. S. Pomeroy, 1958. Symposium on chronic respiratory disease of poultry. V. Infectious sinusitis of turkeys. Am. J. Vet. Res. 19: 468^72. Paterson, J. S., 1940. The antigenic structure of organisms of the genus Listerella. J. Path. Bact. 51: 427-436. Paterson, J. S., 1940. Experimental infection of the chick embryo with organisms of the genus Listerella. J. Path. Bact. 51: 437-440.

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Malewitz, T. D., and M. L. Calhoun, 1957. The normal hematological picture of turkey poults and blood alterations caused by enterohepatitis. Am. J. Vet. Res. 18: 396-399. Malewitz, T. D., M. L. Gray and E. M. Smith, 1958. Experimentally induced listeriosis in turkey poults. Poultry Sci. 36: 416-419. Mallmann, W. L., 1929. Salmonella pullorum in the intestinal contents of baby chicks. J. Infect. Dis. 44: 16-20. Manninger, R., 1930. Hiihner typhus und bakterielle Kiickenruhr. Proc. Eleventh Internat. Vet. Cong. (London), Part 3: 724. Marthedal, H. E., and G. Villing, 1954. Pasteurellosis and pseudotuberculosis among fowls in Denmark. Nord. Vet. Med. 6: 651. Mathey, W. J., Jr., and P. J. Siddle, 1954. Isolation of Pasteurella pseudotuberculosis from a California turkey. J. Am. Vet. Med. Assn. 125: 482483. Marx, E., and A. Strieker, 1902. Untersuchungen iiber das Epithelioma contagiosum des Gefliigels. Deutsch. med. Wochenschr. 29: 79-80. McCarter, J. R., E. S. Hastings and B. A. Beach, 1940. The sensitization of cattle to mammalian tuberculin by an avirulent strain of avian tubercle bacillus. J. Am. Vet. Med. Assn. 96: 52-55. McCollum, W. H., E. R. Doll and J. T. Bryans, 1957. The use of periodate-treated Newcastle disease virus as antigens in the hemagglutinationinhibition test. Poultry Sci. 36: 855-858. McKay, W. M., 1948. Fowl coryza: treatment with iodine. Vet. J. 104: 70-74. McKay, K. A., and J. R. E. Taylor, 1954. The reversion of L type cultures previously described as pleuropneumonia-like and associated with chronic respiratory disease to an organism resembling Hemophilus gallinarum. Can. J. Comp. Med. Vet. Sci. 18: 7-12. Meyer, K. F., 1952. Ornithosis and psittacosis, 1952. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 569-618. Iowa State College Press, Ames. Miessner, H., 1930. Die Pullorum Infektion der Hiihner (Die weisse Ruhr des Kucken-Huhnertyphus. Deutsch. tierarztl. Wochenschr. 38: 517. Moore, R. W., 1958. Studies of an agent causing hepatitis in chickens. Avian Dis. 2:39-54. Moses, H. E., W. H. Feldman and F . C. Mann, 1943. Mycobacterial rapid agglutination antigens and their diagnostic value in tuberculosis in fowls. Amer. J. Vet. Res. 4: 390-394. Mundt, J. O., and R. L. Tugwell, 1958. The relationship of chicken egg to selected paratyphoids. Poultry Sci. 37: 415-420. -

R E V I E W OF POULTRY D I S E A S E S

erysipelas in turkeys. Am. J. Vet. Res. 2: 203213. Quiroz, C. A., and R. P. Hanson, 1958. Physicalchemical treatment of inocula as a means of separating and identifying avian viruses. Avian Dis. 2: 94-98. Quortrup, E. R., and R. L. Sudheimer, 1943. Some ecological relations of Pseudomonas aeruginosa to Clostridium botulinum Type C. J. Bact. 45: 551554. Raggi, L. G., and N. F. Baker, 1957. Case report— Tetrameres Americana (Cram, 1927) infection in domestic pigeons. Avian Dis. 1: 227-234. Reid, W. M., D. D. Pate and A. L. Kleckner, 1958. Effects of Ascaridia galli on chicks with infectious bronchitis. Avian Dis. 2: 99-109. Reis, J., and P . Nobrega, 1936. Spirochetosis. Tratado de doencas das Aves, Sao Paulo. Rettger, L. F., 1900. Septicemia among young chickens. New York Med. J. 71: 803. Rettger, L. F., and F . H. Stoneburn, 1909. Bacillary white diarrhea of young chicks. Storrs Agr. Exper. Sta. BuU. 178: 92-103. Rettger, L. F., W. F. Kirkpatrick and R. E. Jones, 1914. Bacillary white diarrhea of young chicks. (Fourth report) Storrs Agr. Exper. Sta. Bull. 77: 259-309. Saunders, L. Z., and E. N. Moore, 1957. Blindness in turkeys due to granulomatous chorioretinitis. Avian Dis. 1: 27-36. Schafer, J. M., A. D . MacDonald, W. J. Hall and H. Bunyea, 1931. A stained antigen for the rapid whole blood test for pullorum disease. J. Am. Vet. Med. Assn. 79: 236-240. Schalk, A. F., 1928. Results of some avian tuberculosis studies. J. Am. Vet. Med. Assn. 72: 852-863. Schillinger, J. E., and L. C. Morley, 1934. Studies on ulcerative enteritis in quail. J. Am. Vet. Med. Assn. 84: 25-33. Schmittle, S. C , H. M. Edwards and D. Morris, 1958. A disorder of chickens probably due to a toxic feed—preliminary report. J. Am. Vet. Med. Assn. 132: 216-219. Seastone, C. V., 1935. Pathogenic organisms of the genus Listerella. J. Exper. Med. 62: 203-212. Seddon, H. R., 1953. Bacterial diseases. Diseases of Domestic Animals in Australia. Dept. of Health, Canberra, A.C.T. Service Publication No. 9, Vol. 1, Part 5: 259-264. Severens, J. M., E. Roberts and L. E. Card, 1945. The effect of sulfonamides in reducing mortality from pullorum disease in the domestic fowl. Poultry Sci. 24: 155-158. Sevoian, M., and P. P. Levine, 1957. Effects of infectious bronchitis on the reproduction tracts,

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

Patton, J. W., 1926. Avian hemorrhagic septicemia (fowl cholera). J. Am. Vet. Med. Assn. 68: 581602. Peckham, M. C , 1957. Case report—Lens opacities in fowls possibly associated with epidemic tremor. Avian Dis. 1: 247-255. Peluffo, C. A., P. R. Edwards and D. W. Bruner, 1942. A group of coliform bacilli serologically related to the genus Salmonella. J. Infect. Dis. 70: 185-192. Pfeiler, W., and A. Rehse, 1913. Bacillus typhi gallinarum alcalifaciens und die durch ihn verursachte Hiihner Seuche. Mitt. a.d. Kaiser Wilhelm Institut f. Landwirtschaft zu Bromberg. 5: 306. Pirozok, R. P., C. F. Helmboldt and E. L. Jungherr, 1957. A rapid histological technique for the diagnosis of infectious avian laryngotracheitis. J. Am. Vet. Med. Assn. 130: 406-408. Poznowski, E. P., and V. D. Foltz, 1958. Flocculation tests for pullorum disease. Am. J. Vet. Res. 19:478^182. Price, K. E., Z. Zoli, Jr., W. B. Hardie and R. Owens, 1958. The influence of penicillin and oxytetracycline in the ration on mortality, lesions and predominating microflora in experimental CRD. Poultry Sci. 37: 472-478. Price, E. W., 1952. Trematodes of poultry. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 919-941. Iowa State College Press, Ames. Pritchett, I. W., F . R. Beaudette and T. P. Hughes, 1930. The epidemiology of fowl cholera. IV. Field observations of the "spontaneous" disease. J. Exper. Med. 51: 249-259. V. Further field observations of the spontaneous disease. J. Exper. Med. 51:259-274. Pritchett, I. W., and T. P . Hughes, 1932. The epidemiology of fowl cholera. VI. The spread of epidemic and endemic strains of Pasteurella avicida in laboratory populations of normal fowl. J. Exper. Med. 55: 71-78. Rhoades, H. E., and L. E. Hanson, 1957. Serological response of and pathogenesis of Salmonella pullorum in the growing chick. Poultry Sci. 36: 1065-1070. Richey, D. J., W. N. Mack and H. J. Stafseth, 1954. The hemagglutination reaction in avian tuberculosis. Poultry Sci. 33: 345-350. Richey, D. J., and C. L. Morgan, 1957. The effect of Chloromycetin and sulfaquinoxaline on fowl cholera in turkeys. Poultry Sci. 36: 536-538. Rosenwald, A. S., and E. M. Dickinson, 1939. A report on swine erysipelas in turkeys. Cornell Vet. 29:61-67. Rosenwald, A. S., and E. M. Dickinson, 1941. Swine

773

774

H. J. STAFSETH 1957. Laboratory analysis of several field outbreaks of chronic respiratory disease. Avian Dis. 1:94-100. Sullivan, J. F., E. Gill and O. M. Somer, 1958. Immune response of chickens to beta-propiolactonekilled Newcastle disease vaccines. Am. J. Vet. Res. XIV: 483-488. Taylor, J. R. E., J. Fabricant and P. P. Levine, 1957. A comparison of four in vitro methods for the isolation of the pleuro-pneumonia-like organism of chronic respiratory disease from tracheal exudate. Avian Dis. 1: 101-104. te Hennepe, B. J. C , and H. van Straaten, 1921. Fowl septicemia. Trans. First World's Poultry Cong. 1: 259. Thayer, S. C , R. S. Stroud and W. R. Dunlop, 1958. Observations on infectious synovitis. Poultry Sci. 37: 449-454. Titkemeyer, C. W., and S. C. Schmittle, 1957. The effect of drugs on the isolation of Salmonella gallinarum from inoculated chicks. Poultry Sci. 36: 1198-1206. Truche, C , 1923. De la typhose aviaire. Ann. de l'Inst. Pasteur, 37: 478^97. Turk, R. D., 1958. Anthelmintics for poultry. J. Am. Vet. Med. Assn. 132: 13-15. Tyzzer, E. E., 1929. Coccidiosis in gallinaceous birds. Am. J. Hyg. 10: 269-383. Tyzzer, E. E., H. Theiler and E. E. Jones, 1932. Coccidiosis in gallinaceous birds. I I . A comparative study of species of Eimeria of the chicken. Am. J. Hyg. 15:319-393. Van Dorsen, C. A., 1952. Pseudotuberculosis in a bantam fowl. Tijdschr. Diergeneesk. 77: 297. Van Heelsbergen, T., 1929. Hiihnertyphus. Handbuch der Gefliigelkrankheiten und Gefltigelzucht, Ferdinand Enke, Stuttgart, pp. 135-149. Van Straaten, H., and B. J. C. te Hennepe, 1918. Die Kleinsche Htihnerseuche. Folia Microbiol. 5: 103. Van Es, L., and A. F. Schalk, 1914. Avian tuberculosis. North Dakota Agr. Exper. Sta. Bui. 108. Van Roekel, H., 1955. Respiratory diseases of poultry. In Advances in Veterinary Science (Brandly and Jungherr, eds), 2: 64-105. Van Roekel, H., O. M. Olesiuk and L. P. Beninato, 1958. Symposium on chronic respiratory disease of poultry. III. Epizootiology of chronic respiratory diseases of chickens. Am. J. Vet. Res. 19: 453^63. Wagener, K., 1934. Ktickenruhr. Proc. Twelfth Internat. Vet. Cong. (New York) Part 3: 108. Waters, N . F., 1956. Genetics and Disease. U. S. Dept. Agr. Yearbook, pp. 46-54. Webster, L. T., 1930. The epidemiology of fowl chol-

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

egg production and egg quality of laying chickens. Avian Dis. 1: 136-164. Sevoian, M., R. W. Winterfield and C. L. Goldman, 1958. Avian infectious hepatitis. I. Clinical and pathological manifestations. Avian Dis. 2: 3-18. . Sherwood, R. M., and J. R. Couch, 1952. Vitamins and vitamin deficiencies. In Diseases of Poultry (Biester and Schwarte, eds.), pp. 163-213. Iowa State College Press, Ames. Shklair, I. L., and H. J. Stafseth, 1954. A study of serological cross reactions between Brucella and certain salmonellae. Michigan S. C. Veterinarian, 14: 130-142. Shook, W. B., and H. Bunyea, 1939. The detection of carriers of fowl cholera and its control by means of a stained antigen, rapid whole-blood test. Poultry Sci. 18: 146-149. Shumard, R. F., and D. F. Eveleth, 1956. Further studies on the anthelmintic action of piperazine citrate. Vet. Med. 51: 515-517. Sieburth, J. M., 1957. The effect of furazolidone on the cultural and serological response of Salmonella typhimurium infected chickens. Avian Dis. 1: 180-194. Sieburth, J. M., and E. P. Johnson, 1957. Transmissible enteritis of turkeys. 1. Preliminary studies. Poultry Sci. 36: 256-261. Skidmore, L. V., 1932. The transmission of fowl cholera to turkeys by the common house fly (Musca domestica Linn.) with brief notes on the viability of fowl cholera microorganisms. Cornell Vet. 22: 281-285. Smyser, C. F., and H. Van Roekel, 1957. The influence of furazolidone on experimental and natural pullorum infection in chickens. Avian Dis. 1: 328-337. Stabler, R. M., S. M. Schmittner and W. M. Marmon, 1958. Success of soluble 2-amino-5-nitrothiazole in the treatment of trichomoniasis in the domestic pigeon. Poultry Sci. 37: 352-355. Stafseth, H. J., 1930. Cutaneous immunization against fowl pox. Proc. Twenty-first Ann. Meet. Poultry Sci. Assn., Auburn, Alabama, Aug. 2023, 1929, pp. 80-88. Stafseth, H. J., and A. C. Corbutt, 1940. Identification of Salmonella pullorum colonies with immune serum by means of a macroscopic plate test. Am. J. Vet. Res. 1:76-77. Statseth, H. J., 1952. Brucellosis. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 387-392. Iowa State College Press, Ames. Stubbs, E. L., 1952. Fowl plague. In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 669-680. Iowa State College Press, Ames. Sullivan, J. F., E. Gill, A. Somer and K. Heddleston,

775

R E V I E W OF POULTRY D I S E A S E S

studies. 4. Vaccination of chickens with B l , F and La Sota strains of Newcastle disease virus administered through the drinking water. Poultry Sci. 36: 1076-1088. Winterfield, R. W., M. Sevoian and C. L. Goldman, 1958. Avian infectious hepatitis. I I . Some characteristics of the etiologic agent. Effect of various drugs on the course of the disease. Avian Dis. 2: 19-39. Winton, B., B. R. Burmester, E. M. Denington, A. M. Lucas, S. W. Lesher and N. F. Waters, 1955. Lymphomatosis in chickens. Circular No. 970, U. S. Dept. Agr., U. S. Gov. Print. Office, Washington 25, D. C. Woodring, F. R., 1957. Naturally occurring infection with equine encephalomyelitis virus in turkeys. J. Am. Vet. Med. Assn. 130: 511-512. Woodruff, A. M., and E. W. Goodpasture, 1931. The susceptibility of the chorio-allantoic membrane of chick embryos to infection with fowl pox virus. Am. J. Path. 7: 209-222. W. R. H., 1928. New England Conference of Laboratory Workers in Bacillary White Diarrhea Control. J. Am. Vet. Med. Assn. 73: 263-264. Zimmerman, W. J., 1957. Field studies on Eimeria species in Iowa chickens. Poultry Sci. 36: 184193.

NEWS AND NOTES NOMINATIONS—P.E.N.B. AWARD The Poultry and Egg National Board Research Achievement Award is given annually. The award has three principle objectives: (a) To recognize outstanding achievement in the fields of poultry products technology and marketing; (b) to encourage investigators to intensity their efforts in those areas of research which will lead to the increased consumption of poultry and eggs; and (c) to help publicize research in its contribution to Poultry and Egg National Board objectives. The recipient of the Poultry and Egg National Board Research Achievement Award will receive an appropriate plaque and will be honored at the Annual Meeting of P.E.N.B. to be held in April, 1959. Selection of the winner is based on the importance of poultry and/or egg research contributions concerning the processing, preservation, nutritive value, improved product development, and marketing leading to the increased use of poultry and eggs in the diet. Nominations should be supported by biographical

sketches of the nominees, including enumeration of contributions pertinent to the award objectives, a list of publications during the past ten years, and, if available, endorsement for seconds. Nominations should be sent to Milo H. Swanson, Chairman of the P.E.N.B. Technical Advisory Committee, Department and Poultry Husbandry, University of Minnesota, St. Paul 1, Minnesota, not later than November 15, 1958. ERRATUM In Table 2 of the article entitled "Some effects of arsanilic acid and/or penicillin upon egg production" by C. W. Carlson, on page 1072 of the September 1957 issue of POULTRY SCIENCE, the number of the

diet in experiment 2 containing penicillin and arsanilic acid fed to the S.C.XS.C.W.L. group should have been 211 not 212. VERMONT NOTES N. S. Cowan and C. A. Blackwood, graduates in 1958 from the University of Vermont, Burlington,

(Continued on page 801)

Downloaded from http://ps.oxfordjournals.org/ by guest on May 5, 2015

era. Experimental studies. I. Introduction. J. Exp. Med. 51:219-223. Wehr, E. E., 1952. Cestodes of poultry. In Diseases of Poultry (Biester and Schwarte eds.), 3rd. ed., pp. 887-918. Iowa State College Press, Ames. Wehr, E. E., 1952. Nematodes and acanthocephalids of poultry. In Diseases of Poultry (Biester and Schwarte eds.), 3rd. ed., pp. 835-885. Iowa State College Press, Ames. Wehr, E. E., 1952. Nematodes and acanthocephalids of poultry (Syngamidae). In Diseases of Poultry (Biester and Schwarte, eds.), 3rd. ed., pp. 842846. Iowa State College Press, Ames. Wehr, E. E., and J. F. Christensen, 1942. Trichomoniasis. U. S. Dept. Agr. Yearbook, 1019-1022. Wehr, E. E., M. M. Farr and D. K. McLaughlin, 1958. Chemotherapy of blackhead in poultry. J. Am. Vet. Med. Assn. 132: 439-445. Weiss, H. J., and H. Fisher, 1957. Plasma lipid and organ changes associated with the feeding of animal fat to laying chickens. J. Nutr. 61: 267-280. Wichmann, R. W., 1957. A case report—PPLO infection in chuckar partridges (Alectoris graeca). Avian Dis. 1: 222-226. Wilson, J. E., 1957. Round heart disease in chickens. J. Comp. Pathol. Therap. 67: 239-250. Winterfield, R. W., C. L. Goldman and E. H. Seadale, 1957. Newcastle disease immunization