CLINICAL SIGNS & LESIONS
Mycoplasma gallisepticum
Alone or in combination with other pathogens, MG is the agent of the CRD. Under experimental conditions, the incubation period is around five to ten days, but under natural conditions, this duration is sometimes much higher. Birds from infected breeders (especially if they or their eggs were trea- ted with antibiotics) can present clinical signs and/or seroconvert only after several months.
Clinical signs include coryza, sneezing, nasal dis- charge, coughing, tracheal rales and dyspnea. The most severely affected birds remain prostrate, with open mouth breathing. Growth rate is slo- wed, the rate of lay decreases (about 10-15 eggs less per hen), and the percentage of poor quality eggs increase. In turkeys, an infra-orbital
Mycoplasma gallisepticum
Alone or in combination with other pathogens, MG is the agent of the CRD. Under experimental conditions, the incubation period is around five to ten days, but under natural conditions, this duration is sometimes much higher. Birds from infected breeders (especially if they or their eggs were trea- ted with antibiotics) can present clinical signs and/or seroconvert only after several months.
Clinical signs include coryza, sneezing, nasal dis- charge, coughing, tracheal rales and dyspnea. The most severely affected birds remain prostrate, with open mouth breathing. Growth rate is slo- wed, the rate of lay decreases (about 10-15 eggs less per hen), and the percentage of poor quality eggs increase. In turkeys, an infra-orbital
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Introduction
Many mycoplasma species can infect birds, but only Mycoplasma gallisepticum (MG), M. synoviae (MS), M. meleagridis (MM) and M. iowae (MI) are considered pathogenic in chickens and turkeys, and can cause economic losses due to stunted growth, condemnations associated with lesions, or synovi- tis, airsacculitis, decreased egg production, and decreased hatchability. Worldwide, the incidence of mycoplasma infection is favored by the intensifica- tion of poultry production.
ETIOLOGY
Mycoplasma spp.
Mycoplasma bacteria are small (about 200 nm) without a cell wall, bounded by a single cell mem- brane and possessing a small genome (about 600 to 1300 kbp). Consequently, their biosynthetic capabi- lities are limited and these organisms require com- plex culture media containing serum, a source of cholesterol and fatty acids. On agar, viewed with some magnification, typical colonies show a «fried egg morphology after several days of incubation. The absence of a cell wall explains the fragility of these microorganisms and their insensitivity to anti- biotics degrading or inhibiting bacterial cell wall synthesis, such as ß-lactamines or cephalosporins.
Many mycoplasma species can infect birds, but only Mycoplasma gallisepticum (MG), M. synoviae (MS), M. meleagridis (MM) and M. iowae (MI) are considered pathogenic in chickens and turkeys, and can cause economic losses due to stunted growth, condemnations associated with lesions, or synovi- tis, airsacculitis, decreased egg production, and decreased hatchability. Worldwide, the incidence of mycoplasma infection is favored by the intensifica- tion of poultry production.
ETIOLOGY
Mycoplasma spp.
Mycoplasma bacteria are small (about 200 nm) without a cell wall, bounded by a single cell mem- brane and possessing a small genome (about 600 to 1300 kbp). Consequently, their biosynthetic capabi- lities are limited and these organisms require com- plex culture media containing serum, a source of cholesterol and fatty acids. On agar, viewed with some magnification, typical colonies show a «fried egg morphology after several days of incubation. The absence of a cell wall explains the fragility of these microorganisms and their insensitivity to anti- biotics degrading or inhibiting bacterial cell wall synthesis, such as ß-lactamines or cephalosporins.
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Other factors
Chronic respiratory disease (CRD) in chicken results from infection with MG often associated with other infectious agents, such as wild-type or vaccine viruses (Newcastle disease, coronavirus, metapneumovirus, etc.) or bacteria (Escherichia coli, Haemophilus spp., Pasteurella spp., Ornithobacterium rhinotracheale, other Mycoplasma, etc.) or fungi (Aspergillus, etc.). Similarly, the pathogenicity of MS is exacerbated in association with bacteria or viruses with similar respiratory or articular tropism (reovirus, etc.). Poor environmental conditions (excessive levels of ammonia, dust, humidity, misadjusted ventilation, efc.) stress on birds (social stress, handling, vacci- nations, selection, beak conditioning, etc.), nutri- tional deficiencies and parasitism could also be predisposal or aggravating factors.
Chronic respiratory disease (CRD) in chicken results from infection with MG often associated with other infectious agents, such as wild-type or vaccine viruses (Newcastle disease, coronavirus, metapneumovirus, etc.) or bacteria (Escherichia coli, Haemophilus spp., Pasteurella spp., Ornithobacterium rhinotracheale, other Mycoplasma, etc.) or fungi (Aspergillus, etc.). Similarly, the pathogenicity of MS is exacerbated in association with bacteria or viruses with similar respiratory or articular tropism (reovirus, etc.). Poor environmental conditions (excessive levels of ammonia, dust, humidity, misadjusted ventilation, efc.) stress on birds (social stress, handling, vacci- nations, selection, beak conditioning, etc.), nutri- tional deficiencies and parasitism could also be predisposal or aggravating factors.
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PATHOGENICITY
The pathogenicity of avian mycoplasmas depends on several factors (host, species and strain of Mycoplasma, etc.). Thus, for example, MI is patho- genic for turkeys and not for chickens, and there are low pathogenic strains of MG naturally or arti ficially used as vaccines. Avian mycoplasmas have tropism for the respiratory tract, the joints and the genital tract especially in turkeys. Studies reveal the sophistication of the pathogenic mechanisms implemented by these bacteria. They have genetic systems allowing them to quickly change the nature and structure of their surface membrane proteins: membrane antigens may differ in their expression (+/-), their characteristics (size varia- tion) and accessibility of their epitopes. These phe- nomena can be observed in vitro as well as in vivo. This variability seems to be a crucial evaluative mechanism allowing this microorganism to escape from the immune reactions of the host and explains its persistence. Attachment of Mycoplasma to cells of the host through adhesins, genes encoded in multiple copies of MG and MS, ciliostasis pheno- mena, release of toxins, nucleases or peroxides and consumption of essential metabolites for the host cells are other virulence factors.
EPIDEMIOLOGY
In the modern poultry world, the selection or bree- ding flocks are most often free of MG and MS. But Mycoplasma spp. contamination is still common in production flocks, especially if located in areas with high poultry density.
Generally considered as fragile bacteria, the avian mycoplasmas can nevertheless survive for several days in the external environment, in particular on feathers or diverse materials: for example, MG is viable for 61 days under dry conditions at 4°C, or 5 days in the water of wells; MI survives 6 days on human hair. On farms, the most frequent mode of infection for MG or MS is the respiratory route. Transmission occurs primarily by direct contact between sick or latent carriers and susceptible birds. Indirect transmission through human acti- vity, wild birds or insects or livestock equipment is also possible.
In addition, MG and MS can be transmitted verti- cally through the egg, either by contamination of the embryo by blood route, or because of conti- guity between the oviduct and the infected air sacs. The percentage of infected eggs remains limited but probably allows the spread of infection in the hatchery and then the farms. The rate of vertical transmission would be greater in the first weeks of infection.
The location of MM and MI in turkeys' genital tract of provides an important venereal transmission through the infected semen with artificial insemi- nation, as well as vertical transmission due to the contamination of the oviduct. The number of infec- ted eggs appears to be lower at the beginning and the end of the laying period. Horizontal transmis- sion is also possible either by direct contact bet- ween birds or through intervention teams (sexing, insemination). The transmission rate of infection in poultry depends on the density of the flock and the extent of the reservoir. Environmental factors that exacerbate the disease, such as high levels of ammonia or concurrent infections may increase the excretion of Mycoplasma and hence the speed of transmission.
In some cases, the development of infection may be more or less severe as a result of various stresses (transfers, at the onset of laying, etc.). Dissemination of MS seems generally faster than that of MG. However some strains of MG or MS show a low transmissibility and development of infection in a flock with these strains is slower
The pathogenicity of avian mycoplasmas depends on several factors (host, species and strain of Mycoplasma, etc.). Thus, for example, MI is patho- genic for turkeys and not for chickens, and there are low pathogenic strains of MG naturally or arti ficially used as vaccines. Avian mycoplasmas have tropism for the respiratory tract, the joints and the genital tract especially in turkeys. Studies reveal the sophistication of the pathogenic mechanisms implemented by these bacteria. They have genetic systems allowing them to quickly change the nature and structure of their surface membrane proteins: membrane antigens may differ in their expression (+/-), their characteristics (size varia- tion) and accessibility of their epitopes. These phe- nomena can be observed in vitro as well as in vivo. This variability seems to be a crucial evaluative mechanism allowing this microorganism to escape from the immune reactions of the host and explains its persistence. Attachment of Mycoplasma to cells of the host through adhesins, genes encoded in multiple copies of MG and MS, ciliostasis pheno- mena, release of toxins, nucleases or peroxides and consumption of essential metabolites for the host cells are other virulence factors.
EPIDEMIOLOGY
In the modern poultry world, the selection or bree- ding flocks are most often free of MG and MS. But Mycoplasma spp. contamination is still common in production flocks, especially if located in areas with high poultry density.
Generally considered as fragile bacteria, the avian mycoplasmas can nevertheless survive for several days in the external environment, in particular on feathers or diverse materials: for example, MG is viable for 61 days under dry conditions at 4°C, or 5 days in the water of wells; MI survives 6 days on human hair. On farms, the most frequent mode of infection for MG or MS is the respiratory route. Transmission occurs primarily by direct contact between sick or latent carriers and susceptible birds. Indirect transmission through human acti- vity, wild birds or insects or livestock equipment is also possible.
In addition, MG and MS can be transmitted verti- cally through the egg, either by contamination of the embryo by blood route, or because of conti- guity between the oviduct and the infected air sacs. The percentage of infected eggs remains limited but probably allows the spread of infection in the hatchery and then the farms. The rate of vertical transmission would be greater in the first weeks of infection.
The location of MM and MI in turkeys' genital tract of provides an important venereal transmission through the infected semen with artificial insemi- nation, as well as vertical transmission due to the contamination of the oviduct. The number of infec- ted eggs appears to be lower at the beginning and the end of the laying period. Horizontal transmis- sion is also possible either by direct contact bet- ween birds or through intervention teams (sexing, insemination). The transmission rate of infection in poultry depends on the density of the flock and the extent of the reservoir. Environmental factors that exacerbate the disease, such as high levels of ammonia or concurrent infections may increase the excretion of Mycoplasma and hence the speed of transmission.
In some cases, the development of infection may be more or less severe as a result of various stresses (transfers, at the onset of laying, etc.). Dissemination of MS seems generally faster than that of MG. However some strains of MG or MS show a low transmissibility and development of infection in a flock with these strains is slower