- Email: [email protected]
Bacterial respiratory disease of poultry
Bacterial Respiratory Diseases of Poultry JOHN R. GLISSON1 Department of Avian Medicine, University of Georgia, Athens, Georgia 30602-4875 ABSTRACT Bacterial pathogens play an important role in causing respiratory disease in domestic poultry species. In many cases, the bacterial component of a respiratory disease colonizes the respiratory system only after a primary viral or environmental insult. Colonization of the airsacs of a chicken by Escherichia coli following an infectious bronchitis virus infection is an
example of secondary bacterial invasion. In other cases, the bacterial component of the respiratory disease is the primary initiating cause of the disease. Examples of primary bacterial respiratory disease are infectious coryza in chickens and fowl cholera in chickens and turkeys.
(Key words: respiratory system, bacteria, poultry)
INTRODUCTION Diseases of the respiratory tract are a significant component of the overall disease incidence in poultry. In many cases, respiratory disease observed in a flock may be a component of a multisystemic disease or it may be the predominant disease with lesser involvement of other organ systems. In some cases, such as infectious coryza or infectious laryngotracheitis, the disease may be limited to the respiratory system, at least initially. Various pathogens may initiate respiratory disease in poultry, including a variety of viruses, bacteria, and fungi. Environmental factors may augment these pathogens to produce the clinically observed signs and lesions. This review will confine itself to several diseases of the respiratory tract caused by bacteria for which the predominant organ system affected is the respiratory tract.
FOWL CHOLERA Fowl cholera, caused by infection with Pasteurella multocida (PM), is a disease of many avian species. Chickens, turkeys, ducks, and quail are the most important domestic avian species involved and the disease is of economical significance. Although PM may induce lesions in multiple organ systems, respiratory pathology is the most important facet of the disease. Pasteurella multocida is a common organism found in the oral cavity of a variety of animals, including dogs,
Received for publication August 3, 1997. Accepted for publication January 19, 1998. 1To whom correspondence should be addressed: [email protected]. uga.edu
cats, and rodents. Various animals, particularly cats and rodents, are a common source for the introduction of the organism into commercial poultry (Rimler and Glisson, 1997). Pasteurella multocida is not a common organism found in feed, water, or litter. Therefore, proper rodent control and elimination of contact of poultry with other animals, such as cats, is an important measure for the prevention of the introduction of PM into a poultry flock. Pasteurella multocida is capable of multiplication in the bloodstream of a bird. As a result of this bacteremia, the organism may quickly colonize many organs, contributing to the typical purulent exudative lesions of fowl cholera seen in the joints, wattles, ovaries, brain, liver, spleen, and lungs. A detailed description of the lesions has been compiled (Rimler and Glisson, 1997). Shortly before a bird succumbs to the disease, PM will typically multiply to very high levels in the bloodstream and tissues (Rimler and Glisson, 1997). As many domestic poultry species tend to be cannibalistic, carcasses of birds that have died of fowl cholera serve as a source of PM to infect the remainder of the flock. Therefore, removal of dead birds from a flock with an active PM infection is an important means of impeding the spread of the infection within a flock. Vaccination to prevent fowl cholera is an important aspect of controlling the disease, particularly in broiler breeders and turkeys. There are two broad categories of vaccines commercially available, live vaccines of low virulence and inactivated vaccines. There are a wide variety of vaccination programs utilized that minimize the impact of fowl cholera on a flock.
Abbreviation Key: HA = hemagglutination antigen; HI = hemagglutination-inhibition; HPG = Haemophilus paragallinarum; OR = Ornithobacterium rhinotracheale; PM = Pasteurella multocida.
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typically effective for treating fowl cholera. Penicillin susceptibility is also common. Fluoroquinolones are the most effective class of antimicrobial compound for the treatment of fowl cholera.
INFECTIOUS CORYZA Infectious coryza is an upper respiratory disease of chickens caused by infection with Haemophilus paragallinarum (HPG). The disease is characterized by swollen infraorbital sinuses, nasal discharge, and depression. The disease is seen most commonly in adult chickens and can cause a very significant reduction in the rate of egg production. The HPG organism does not survive well outside of its host; therefore, the infection does not spread readily from farm to farm without movement of contaminated people or fomites from farm to farm. An infection flock may potentially shed the organism for the life of the flock. For this reason, HPG infection may endure indefinitely on farms having multiple-age chickens, particularly multiple-age layer or breeder farms. Protection of flocks against infectious coryza involves the use of both biosecurity and vaccination. Good biosecurity procedures should prevent exposure of chickens to HPG infection; however, in many cases, as with multiple-age farms on which HPG infection is endemic, vaccination must be used to minimize the impact of the disease. There is some disagreement concerning the antigenic (serological) classification of HPG isolates. A scheme based on a plate agglutination test classified isolates into three serovars, A, B, and C (Page, 1962). A new classification system, based on the hemagglutinationinhibition (HI) test, changed serovars A, C, and B to serogroups I, II, and III and formed at least seven serovars within the three subgroups (Kume et al., 1983). Immunity induced by inactivated HPG bacterins is serogroup-specific and this specificity is closely associated with the hemagglutination antigen (HA) detected in the HI test. The antigenic structure and the immune response of HPG have been reviewed (Yamamoto, 1991). Commercially available infectious coryza vaccines are inactivated whole-cell bacterins emulsified in an oil adjuvant or adsorbed on to aluminum hydroxide. They may contain one or several isolates representing the various serogroups. Because heterologous serogroup protection is not induced by inactivated HPG bacterins, a bacterin that contains isolates representing all known serogroups is desirable; however, there is much controversy concerning the need for an isolate which represents serogroup III (serovar B) in a bacterin because it has been speculated that those isolates are simply serovar A or C organisms that have lost their type-specific antigen (Kume et al., 1980). In many instances, autogenous bacterins are made from local isolates.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
Inactivated PM bacterins are whole cell suspensions of inactivated PM emulsified in an oil adjuvant. These products induce an immune response specific to the serotype of the organism in the bacterin. For instance, if the bacterin contains Serotype 1, it will induce a protective immune response only against Serotype 1. This concept is very important because there are 16 serotypes of PM. The PM bacterins available commercially contain primarily Serotypes 1, 3, and 4. Because those are the most common serotypes found in commercial poultry, PM bacterins generally induce an adequate protective immune response. However, if birds that were vaccinated with a standard PM bacterin are challenged by a PM serotype other than Serotypes 1, 3, and 4, disease may result. There are three live PM vaccines available. The vaccines vary in virulence. The M-9 vaccine is the least virulent, the CU vaccine is the most virulent, and the PM-1 vaccine is intermediate in virulence. All three vaccines are serotype 3, 4 which means that they possess antigenic characteristics of PM Serotypes 3 and 4. All PM live vaccines readily infect turkeys orally, therefore, they can be administered in the drinking water. However, live PM vaccines do not readily infect chickens orally and must be applied by wing-web stab. Unlike inactivated vaccines, live PM vaccines induce an immune response that is not serotype-specific. Birds immunized with a live PM vaccine are protected against all PM serotypes. There are several advantages and disadvantages to the use of inactivated or live PM vaccines. The live PM vaccines are low virulent organisms and have the potential to induce chronic fowl cholera in both chickens and turkeys. However, various management factors can be utilized to minimize the incidence of fowl cholera induced by live PM vaccines. Live vaccines provided orally to turkeys induce only a transient immune response. This necessitates frequent vaccination in order to maintain adequate protection. The inactivated PM bacterins do not induce disease but have the disadvantage of providing protection limited to the serotypes in the bacterin. With either a live vaccine or an inactivated bacterin, a bird must be vaccinated at least twice to obtain an adequate immune response. As both types of vaccines have some limitations, a wide variety of vaccination programs have been developed to accommodate different management situations. Broiler breeder pullets should be vaccinated twice at least 4 wk apart with either two inactivated vaccines, two live vaccines, or one live vaccine and one killed vaccine. Young meat turkeys are typically vaccinated with a live vaccine at about 6, 10, and 14 wk of age. Fowl cholera can be effectively treated with several different antibiotics (Rimler and Glisson, 1997). Antibiotic susceptibility patterns vary among field isolates of PM; therefore, it is important that antibiotic susceptibility profiles be used to direct the choice of antibiotic to be used to treat a flock. Tetracyclines and sulfonamides are
SYMPOSIUM: INFECTIOUS POULTRY DISEASES
COLIBACILLOSIS Respiratory colibacillosis is a respiratory disease caused by secondary infection with pathogenic Escherichia coli. Escherichia coli is a ubiquitous organism in poultry production. Any insult to the respiratory tract of chickens and turkeys creates a climate for potential colonization of the respiratory tract by E. coli. The initial insult may be viral (such as infectious bronchitis virus), or bacterial (such as PM) or it may be an environmental insult such as elevated ammonia levels. The interaction of E. coli in respiratory diseases of poultry has recently been reviewed (Barnes and Gross, 1997).
ORNITHOBACTERIUM RHINOTRACHEALE Ornithobacterium rhinotracheale (OR) is a bacterium that was recently named and it has been associated with respiratory disease in both chickens and turkeys. This subject has recently been reviewed (Chin and Droual, 1997). The organism causes a potentially severe disease in turkeys characterized by respiratory distress, facial edema, and swelling of infraorbital sinuses. The most striking lesion is unilateral or bilateral fibrinopurulent pneumonia. Its role in producing respiratory disease in young chickens is less clear. It may be that OR plays only a secondary role in respiratory disease in young chickens. In older chickens, particularly breeders, it produces a mild respiratory disease associated with a decrease in egg production (Chin and Droual, 1997). Attempts to control the disease have used primarily chemotherapeutics and vaccination. For the most part, vaccination has been unsuccessful. Treatment utilizing penicillin, tetracyclines, sulfonamides, and fluoroquinolones, has typically been very successful. Antibiotic choice should be based on antibiotic susceptibility profiles.
BORDETELLOSIS Bordetellosis is an upper respiratory disease, primarily seen in young turkeys, caused by infection with Bordetella avium. This subject has recently been reviewed (Skeels and Arp, 1997). The disease is characterized in young turkeys by sneezing, oculonasal discharge, mouth breathing, tracheal collapse, and stunted growth. The disease is most commonly referred to as turkey coryza because its clinical appearance is somewhat similar to the clinical signs of infectious coryza in chickens. Bordetella avium infects and causes disease in turkeys, chickens, and Japanese quail. The disease in chickens is mild in comparison to the disease in turkeys and B. avium may play only a secondary role in respiratory disease in young chickens. In young turkeys, the disease is very contagious and acute signs of upper respiratory disease spread rapidly through a flock. Morbidity may reach 100% but the mortality rate is typically 5% or less. Feed intake and body weight gain are negatively impacted, which contributes to the overall poor performance of a B. avium-infected young turkey flock. The signs of the respiratory disease typically abate in 2 to 4 wk. Vaccination of turkeys to prevent bordetellosis has had only limited success. Inactivated B. avium whole cell bacterins have been used to immunize turkey breeder hens for the purpose of producing high levels of maternal antibodies in the progeny. Although it appears that maternal antibodies delay the onset of infection in the progeny, they do not successfully prevent infection nor eliminate the signs of the disease. A temperaturesensitive live vaccine has also been extensively used to immunize young poults. The use of the vaccine has generally been less than successful. It may be that poults are incapable of responding adequately to B. avium antigens at a very young age. Antibiotic treatment of flocks suffering with bordetellosis has provided minimal clinical improvement.
REFERENCES Barnes, H. J., and W. B. Gross, 1997. Colibacillosis. Pages 131–141 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Chin, R. P., and R. Droual, 1997. Ornithobacterium rhinotracheale infection. Pages 1012–1015 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Kume, K., A. Sawata, T. Nakai, and M. Matsumotos, 1983. Serological classification of Haemophilus paragallinarum with a hemagglutinin system. J. Clin. Microbiol. 17: 958–964. Kume, K., A. Sawata, and Y. Nakase, 1980. Immunologic relationship between Page’s and Sawata’s serotype strains of Haemophilus paragallinarum. Am. J. Vet. Res. 41:757–760. Matsumoto, M., and R. Yamamoto, 1975. Protective quality of an aluminum hydroxide adsorbed broth bacterin against infectious coryza. Am. J. Vet. Res. 36:579–582. Page, L. A., 1962. Hemophilus infections in chickens. I. Characteristics of 12 Hemophilus isolates recovered from diseased chickens. Am. J. Vet. Res. 23:85–95.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
Broilers are seldom vaccinated against infectious coryza; however, replacement layers and breeders are routinely vaccinated in many countries. The usual program is two vaccinations, subcutaneously or intramuscularly, at least 4 wk apart, before 20 wk of age. The first vaccine is usually administered at 8 to 12 wk of age followed by a second injection at 16 to 18 wk of age. Such a vaccination program does not prevent infection by HPG but minimizes the clinical signs of the disease for up to 30 to 35 wk, but not an entire laying cycle (Matsumato and Yamamoto, 1975). For this reason, controlled exposure programs are practiced in some locations. Pullets are vaccinated once or twice with inactivated vaccine followed by controlled infection with the autogenous organism 2 to 4 wk later. At least one study has shown that heterologous serogroup immunity is induced by live infection with HPG; therefore, controlled exposure of vaccinated chickens may produce a very broad immune response (Rimler and Davis, 1977).
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Rimler, R. B., and R. B. Davis, 1977. Infectious coryza: In vivo growth of Haemophilus paragallinarum as a determinant for cross protection. Am. J. Vet. Res. 38:1591–1593. Rimler, R. B., and J. R. Glisson, 1997. Fowl cholera. Pages 143–159 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA.
Skeeles, J. K., and L. H. Arp, 1997. Bordetelleosis (Turkey coryza). Pages 275–287 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Yamamoto, R., 1991. Infectious coryza. Pages 186–195 in: Diseases of Poultry. B. W. Calnek, ed. Iowa State University Press, Ames, IA.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
example of secondary bacterial invasion. In other cases, the bacterial component of the respiratory disease is the primary initiating cause of the disease. Examples of primary bacterial respiratory disease are infectious coryza in chickens and fowl cholera in chickens and turkeys.
(Key words: respiratory system, bacteria, poultry)
INTRODUCTION Diseases of the respiratory tract are a significant component of the overall disease incidence in poultry. In many cases, respiratory disease observed in a flock may be a component of a multisystemic disease or it may be the predominant disease with lesser involvement of other organ systems. In some cases, such as infectious coryza or infectious laryngotracheitis, the disease may be limited to the respiratory system, at least initially. Various pathogens may initiate respiratory disease in poultry, including a variety of viruses, bacteria, and fungi. Environmental factors may augment these pathogens to produce the clinically observed signs and lesions. This review will confine itself to several diseases of the respiratory tract caused by bacteria for which the predominant organ system affected is the respiratory tract.
FOWL CHOLERA Fowl cholera, caused by infection with Pasteurella multocida (PM), is a disease of many avian species. Chickens, turkeys, ducks, and quail are the most important domestic avian species involved and the disease is of economical significance. Although PM may induce lesions in multiple organ systems, respiratory pathology is the most important facet of the disease. Pasteurella multocida is a common organism found in the oral cavity of a variety of animals, including dogs,
Received for publication August 3, 1997. Accepted for publication January 19, 1998. 1To whom correspondence should be addressed: [email protected]. uga.edu
cats, and rodents. Various animals, particularly cats and rodents, are a common source for the introduction of the organism into commercial poultry (Rimler and Glisson, 1997). Pasteurella multocida is not a common organism found in feed, water, or litter. Therefore, proper rodent control and elimination of contact of poultry with other animals, such as cats, is an important measure for the prevention of the introduction of PM into a poultry flock. Pasteurella multocida is capable of multiplication in the bloodstream of a bird. As a result of this bacteremia, the organism may quickly colonize many organs, contributing to the typical purulent exudative lesions of fowl cholera seen in the joints, wattles, ovaries, brain, liver, spleen, and lungs. A detailed description of the lesions has been compiled (Rimler and Glisson, 1997). Shortly before a bird succumbs to the disease, PM will typically multiply to very high levels in the bloodstream and tissues (Rimler and Glisson, 1997). As many domestic poultry species tend to be cannibalistic, carcasses of birds that have died of fowl cholera serve as a source of PM to infect the remainder of the flock. Therefore, removal of dead birds from a flock with an active PM infection is an important means of impeding the spread of the infection within a flock. Vaccination to prevent fowl cholera is an important aspect of controlling the disease, particularly in broiler breeders and turkeys. There are two broad categories of vaccines commercially available, live vaccines of low virulence and inactivated vaccines. There are a wide variety of vaccination programs utilized that minimize the impact of fowl cholera on a flock.
Abbreviation Key: HA = hemagglutination antigen; HI = hemagglutination-inhibition; HPG = Haemophilus paragallinarum; OR = Ornithobacterium rhinotracheale; PM = Pasteurella multocida.
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Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
1998 Poultry Science 77:1139–1142
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GLISSON
typically effective for treating fowl cholera. Penicillin susceptibility is also common. Fluoroquinolones are the most effective class of antimicrobial compound for the treatment of fowl cholera.
INFECTIOUS CORYZA Infectious coryza is an upper respiratory disease of chickens caused by infection with Haemophilus paragallinarum (HPG). The disease is characterized by swollen infraorbital sinuses, nasal discharge, and depression. The disease is seen most commonly in adult chickens and can cause a very significant reduction in the rate of egg production. The HPG organism does not survive well outside of its host; therefore, the infection does not spread readily from farm to farm without movement of contaminated people or fomites from farm to farm. An infection flock may potentially shed the organism for the life of the flock. For this reason, HPG infection may endure indefinitely on farms having multiple-age chickens, particularly multiple-age layer or breeder farms. Protection of flocks against infectious coryza involves the use of both biosecurity and vaccination. Good biosecurity procedures should prevent exposure of chickens to HPG infection; however, in many cases, as with multiple-age farms on which HPG infection is endemic, vaccination must be used to minimize the impact of the disease. There is some disagreement concerning the antigenic (serological) classification of HPG isolates. A scheme based on a plate agglutination test classified isolates into three serovars, A, B, and C (Page, 1962). A new classification system, based on the hemagglutinationinhibition (HI) test, changed serovars A, C, and B to serogroups I, II, and III and formed at least seven serovars within the three subgroups (Kume et al., 1983). Immunity induced by inactivated HPG bacterins is serogroup-specific and this specificity is closely associated with the hemagglutination antigen (HA) detected in the HI test. The antigenic structure and the immune response of HPG have been reviewed (Yamamoto, 1991). Commercially available infectious coryza vaccines are inactivated whole-cell bacterins emulsified in an oil adjuvant or adsorbed on to aluminum hydroxide. They may contain one or several isolates representing the various serogroups. Because heterologous serogroup protection is not induced by inactivated HPG bacterins, a bacterin that contains isolates representing all known serogroups is desirable; however, there is much controversy concerning the need for an isolate which represents serogroup III (serovar B) in a bacterin because it has been speculated that those isolates are simply serovar A or C organisms that have lost their type-specific antigen (Kume et al., 1980). In many instances, autogenous bacterins are made from local isolates.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
Inactivated PM bacterins are whole cell suspensions of inactivated PM emulsified in an oil adjuvant. These products induce an immune response specific to the serotype of the organism in the bacterin. For instance, if the bacterin contains Serotype 1, it will induce a protective immune response only against Serotype 1. This concept is very important because there are 16 serotypes of PM. The PM bacterins available commercially contain primarily Serotypes 1, 3, and 4. Because those are the most common serotypes found in commercial poultry, PM bacterins generally induce an adequate protective immune response. However, if birds that were vaccinated with a standard PM bacterin are challenged by a PM serotype other than Serotypes 1, 3, and 4, disease may result. There are three live PM vaccines available. The vaccines vary in virulence. The M-9 vaccine is the least virulent, the CU vaccine is the most virulent, and the PM-1 vaccine is intermediate in virulence. All three vaccines are serotype 3, 4 which means that they possess antigenic characteristics of PM Serotypes 3 and 4. All PM live vaccines readily infect turkeys orally, therefore, they can be administered in the drinking water. However, live PM vaccines do not readily infect chickens orally and must be applied by wing-web stab. Unlike inactivated vaccines, live PM vaccines induce an immune response that is not serotype-specific. Birds immunized with a live PM vaccine are protected against all PM serotypes. There are several advantages and disadvantages to the use of inactivated or live PM vaccines. The live PM vaccines are low virulent organisms and have the potential to induce chronic fowl cholera in both chickens and turkeys. However, various management factors can be utilized to minimize the incidence of fowl cholera induced by live PM vaccines. Live vaccines provided orally to turkeys induce only a transient immune response. This necessitates frequent vaccination in order to maintain adequate protection. The inactivated PM bacterins do not induce disease but have the disadvantage of providing protection limited to the serotypes in the bacterin. With either a live vaccine or an inactivated bacterin, a bird must be vaccinated at least twice to obtain an adequate immune response. As both types of vaccines have some limitations, a wide variety of vaccination programs have been developed to accommodate different management situations. Broiler breeder pullets should be vaccinated twice at least 4 wk apart with either two inactivated vaccines, two live vaccines, or one live vaccine and one killed vaccine. Young meat turkeys are typically vaccinated with a live vaccine at about 6, 10, and 14 wk of age. Fowl cholera can be effectively treated with several different antibiotics (Rimler and Glisson, 1997). Antibiotic susceptibility patterns vary among field isolates of PM; therefore, it is important that antibiotic susceptibility profiles be used to direct the choice of antibiotic to be used to treat a flock. Tetracyclines and sulfonamides are
SYMPOSIUM: INFECTIOUS POULTRY DISEASES
COLIBACILLOSIS Respiratory colibacillosis is a respiratory disease caused by secondary infection with pathogenic Escherichia coli. Escherichia coli is a ubiquitous organism in poultry production. Any insult to the respiratory tract of chickens and turkeys creates a climate for potential colonization of the respiratory tract by E. coli. The initial insult may be viral (such as infectious bronchitis virus), or bacterial (such as PM) or it may be an environmental insult such as elevated ammonia levels. The interaction of E. coli in respiratory diseases of poultry has recently been reviewed (Barnes and Gross, 1997).
ORNITHOBACTERIUM RHINOTRACHEALE Ornithobacterium rhinotracheale (OR) is a bacterium that was recently named and it has been associated with respiratory disease in both chickens and turkeys. This subject has recently been reviewed (Chin and Droual, 1997). The organism causes a potentially severe disease in turkeys characterized by respiratory distress, facial edema, and swelling of infraorbital sinuses. The most striking lesion is unilateral or bilateral fibrinopurulent pneumonia. Its role in producing respiratory disease in young chickens is less clear. It may be that OR plays only a secondary role in respiratory disease in young chickens. In older chickens, particularly breeders, it produces a mild respiratory disease associated with a decrease in egg production (Chin and Droual, 1997). Attempts to control the disease have used primarily chemotherapeutics and vaccination. For the most part, vaccination has been unsuccessful. Treatment utilizing penicillin, tetracyclines, sulfonamides, and fluoroquinolones, has typically been very successful. Antibiotic choice should be based on antibiotic susceptibility profiles.
BORDETELLOSIS Bordetellosis is an upper respiratory disease, primarily seen in young turkeys, caused by infection with Bordetella avium. This subject has recently been reviewed (Skeels and Arp, 1997). The disease is characterized in young turkeys by sneezing, oculonasal discharge, mouth breathing, tracheal collapse, and stunted growth. The disease is most commonly referred to as turkey coryza because its clinical appearance is somewhat similar to the clinical signs of infectious coryza in chickens. Bordetella avium infects and causes disease in turkeys, chickens, and Japanese quail. The disease in chickens is mild in comparison to the disease in turkeys and B. avium may play only a secondary role in respiratory disease in young chickens. In young turkeys, the disease is very contagious and acute signs of upper respiratory disease spread rapidly through a flock. Morbidity may reach 100% but the mortality rate is typically 5% or less. Feed intake and body weight gain are negatively impacted, which contributes to the overall poor performance of a B. avium-infected young turkey flock. The signs of the respiratory disease typically abate in 2 to 4 wk. Vaccination of turkeys to prevent bordetellosis has had only limited success. Inactivated B. avium whole cell bacterins have been used to immunize turkey breeder hens for the purpose of producing high levels of maternal antibodies in the progeny. Although it appears that maternal antibodies delay the onset of infection in the progeny, they do not successfully prevent infection nor eliminate the signs of the disease. A temperaturesensitive live vaccine has also been extensively used to immunize young poults. The use of the vaccine has generally been less than successful. It may be that poults are incapable of responding adequately to B. avium antigens at a very young age. Antibiotic treatment of flocks suffering with bordetellosis has provided minimal clinical improvement.
REFERENCES Barnes, H. J., and W. B. Gross, 1997. Colibacillosis. Pages 131–141 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Chin, R. P., and R. Droual, 1997. Ornithobacterium rhinotracheale infection. Pages 1012–1015 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Kume, K., A. Sawata, T. Nakai, and M. Matsumotos, 1983. Serological classification of Haemophilus paragallinarum with a hemagglutinin system. J. Clin. Microbiol. 17: 958–964. Kume, K., A. Sawata, and Y. Nakase, 1980. Immunologic relationship between Page’s and Sawata’s serotype strains of Haemophilus paragallinarum. Am. J. Vet. Res. 41:757–760. Matsumoto, M., and R. Yamamoto, 1975. Protective quality of an aluminum hydroxide adsorbed broth bacterin against infectious coryza. Am. J. Vet. Res. 36:579–582. Page, L. A., 1962. Hemophilus infections in chickens. I. Characteristics of 12 Hemophilus isolates recovered from diseased chickens. Am. J. Vet. Res. 23:85–95.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015
Broilers are seldom vaccinated against infectious coryza; however, replacement layers and breeders are routinely vaccinated in many countries. The usual program is two vaccinations, subcutaneously or intramuscularly, at least 4 wk apart, before 20 wk of age. The first vaccine is usually administered at 8 to 12 wk of age followed by a second injection at 16 to 18 wk of age. Such a vaccination program does not prevent infection by HPG but minimizes the clinical signs of the disease for up to 30 to 35 wk, but not an entire laying cycle (Matsumato and Yamamoto, 1975). For this reason, controlled exposure programs are practiced in some locations. Pullets are vaccinated once or twice with inactivated vaccine followed by controlled infection with the autogenous organism 2 to 4 wk later. At least one study has shown that heterologous serogroup immunity is induced by live infection with HPG; therefore, controlled exposure of vaccinated chickens may produce a very broad immune response (Rimler and Davis, 1977).
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Rimler, R. B., and R. B. Davis, 1977. Infectious coryza: In vivo growth of Haemophilus paragallinarum as a determinant for cross protection. Am. J. Vet. Res. 38:1591–1593. Rimler, R. B., and J. R. Glisson, 1997. Fowl cholera. Pages 143–159 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA.
Skeeles, J. K., and L. H. Arp, 1997. Bordetelleosis (Turkey coryza). Pages 275–287 in: Diseases of Poultry. 10th ed. B. W. Calnek, H. J. Barnes, C. W. Beard, L. R. McDougald, and Y. M. Saif, ed. Iowa State University Press, Ames, IA. Yamamoto, R., 1991. Infectious coryza. Pages 186–195 in: Diseases of Poultry. B. W. Calnek, ed. Iowa State University Press, Ames, IA.
Downloaded from http://ps.oxfordjournals.org/ at Kainan University on April 27, 2015