Forwarded from امراض
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
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
unilateral or bilateral sinusitis may be observed, and prevents birds from opening the eyes and thus impairs feed intake. Morbidity is often high, and the mortality varies according to the age of birds and the occurrence of surinfections.
In the early stages of infection, the lesions are limi ted to a catarrhal inflammation of the airways and a beaded appearance or edema of the air sacs. Then, a fibrinous inflammation of air sacs and sometimes internal organs (peritoneum, hepatic capsule) may be observed. In turkeys, the sinuses are filled with an abundant serous mucus and then caseous material. Lesions of the respiratory tract can be severe in birds showing few clinical signs. Lesions of pneumonia, keratoconjunctivitis, teno- synovitis, arthritis or salpingitis have been occasionally reported
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
unilateral or bilateral sinusitis may be observed, and prevents birds from opening the eyes and thus impairs feed intake. Morbidity is often high, and the mortality varies according to the age of birds and the occurrence of surinfections.
In the early stages of infection, the lesions are limi ted to a catarrhal inflammation of the airways and a beaded appearance or edema of the air sacs. Then, a fibrinous inflammation of air sacs and sometimes internal organs (peritoneum, hepatic capsule) may be observed. In turkeys, the sinuses are filled with an abundant serous mucus and then caseous material. Lesions of the respiratory tract can be severe in birds showing few clinical signs. Lesions of pneumonia, keratoconjunctivitis, teno- synovitis, arthritis or salpingitis have been occasionally reported
Mycoplasma synoviae
The first signs of infection by MS consist of pale- ness of the comb, stunting, and swollen joints (hence the name of «infectious synovitis»). The acute joint damage includes edema of synovial membranes, periarticular tissue and tendon sheaths. In turkeys, a viscous exudate, then creamy even cheesy or fibrino-purulent, is found in the joints of the legs, which are amyotrophied, and in more severe forms, in the skull and cervical verte- brac. Breast blisters are frequently observed. In chronic forms, the joints remain swollen and the birds are reluctant to move. Morbidity is around 10% but varies widely depending on the virulence of strains, sometimes leading to very important condemnations in the slaughterhouse. The infec- tion of the respiratory system by MS is mostly sub- clinical, but many birds are carriers. When clini- cally expressed, the clinical signs and lesions of the respiratory tract are similar to those observed with MG but are usually less severe.
Mycoplasma meleagridis
Mycoplasma meleagridis infects only turkeys and causes, in congenital infections, airsacculitis cha- racterized by swelling and sometimes a yellowish exudate on the thoracic air sacs. These lesions then spread to the cervical and abdominal air sacs. In young birds, the infection may remain subclinical or cause stunting, abnormal feathering and defor- mity of the vertebrae or tarsometatarsal bones. In adult birds, the infection is often subclinical but hatchability may be reduced because of late embryonic mortality. Synergies between MM &Mor MS have been described and are respectively the source of airsacculitis or sinusitis.
The first signs of infection by MS consist of pale- ness of the comb, stunting, and swollen joints (hence the name of «infectious synovitis»). The acute joint damage includes edema of synovial membranes, periarticular tissue and tendon sheaths. In turkeys, a viscous exudate, then creamy even cheesy or fibrino-purulent, is found in the joints of the legs, which are amyotrophied, and in more severe forms, in the skull and cervical verte- brac. Breast blisters are frequently observed. In chronic forms, the joints remain swollen and the birds are reluctant to move. Morbidity is around 10% but varies widely depending on the virulence of strains, sometimes leading to very important condemnations in the slaughterhouse. The infec- tion of the respiratory system by MS is mostly sub- clinical, but many birds are carriers. When clini- cally expressed, the clinical signs and lesions of the respiratory tract are similar to those observed with MG but are usually less severe.
Mycoplasma meleagridis
Mycoplasma meleagridis infects only turkeys and causes, in congenital infections, airsacculitis cha- racterized by swelling and sometimes a yellowish exudate on the thoracic air sacs. These lesions then spread to the cervical and abdominal air sacs. In young birds, the infection may remain subclinical or cause stunting, abnormal feathering and defor- mity of the vertebrae or tarsometatarsal bones. In adult birds, the infection is often subclinical but hatchability may be reduced because of late embryonic mortality. Synergies between MM &Mor MS have been described and are respectively the source of airsacculitis or sinusitis.
Mycoplasma iowae
In natural conditions, the infection of turkeys by M is associated with a reduction of 5% to 20% of hatchability due to late embryonic mortality (18 to 24 days of incubation). The dead embryos are small, congested, and present a swelling of the head and the neck, urate deposits on the surface of the body and in the ureters, and hepatitis. Experimental infection of one day-old turkeys leads to airsacculitis, growth retardation, feather abnormalities and leg deformities (chondrodystro- phy, curvature of bones, ruptures of the flexor ten- dons of the feet.
In natural conditions, the infection of turkeys by M is associated with a reduction of 5% to 20% of hatchability due to late embryonic mortality (18 to 24 days of incubation). The dead embryos are small, congested, and present a swelling of the head and the neck, urate deposits on the surface of the body and in the ureters, and hepatitis. Experimental infection of one day-old turkeys leads to airsacculitis, growth retardation, feather abnormalities and leg deformities (chondrodystro- phy, curvature of bones, ruptures of the flexor ten- dons of the feet.
Because mycoplasma infections may remain sub- clinical or cause non-specific clinical signs and lesions, screening or diagnosis of infection should be performed in the laboratory. Detection of the bacteria can be performed by cultures from live birds (tracheal, cleft palate, sinuses, oviducts or cloaca swabs, semen); or sacrificed or dead birds (sinuses, trachea, air sacs, lungs, etc.). If typical mycoplasma colonies appear on culture, they may either be identified using immunofluorescence or immuno-enzymatic techniques, or be cloned and identified by determination of antigenic (growth inhibition assay for example), biochemical or genetic (PCR) characteristics. Cultures must be kept for at least three weeks before being conside- red negative. The methods of polymerase chain reaction (PCR) are sensitive and specific to detect the presence of mycoplasma DNA. Their interest lies in the rapidity of obtaining results and the abi- lity to identify mycoplasmas in samples contami- nated with bacteria or carrying several species of mycoplasma, or coming from birds treated with antibiotics, which makes it difficult to diagnose by culture.
The detection of mycoplasma infections can also be based on serological methods. During infection, systematic or local antibodies are produced, their protective role remaining limited. Immunoglobulin (Ig), class G mainly, are transmitted to the chick via the yolk. Antibodies can be detected during the first two weeks of life of the chick. The humoral immune response towards MI seems insignificant and there is no currently reliable serological test for this mycoplasma.
DIAGNOSIS
The detection of mycoplasma infections can also be based on serological methods. During infection, systematic or local antibodies are produced, their protective role remaining limited. Immunoglobulin (Ig), class G mainly, are transmitted to the chick via the yolk. Antibodies can be detected during the first two weeks of life of the chick. The humoral immune response towards MI seems insignificant and there is no currently reliable serological test for this mycoplasma.
DIAGNOSIS
The rapid plate agglutination (RPA) test is widely used because of its simplicity and its low relative cost. The main advantage of this method is its car- liness as it detects IgM, but its lack of specificity is sometimes a problem. Thus, for example, the pre- sence of genes and antigens common to several species of mycoplasma, particularly between MG and MS may cause cross-reactions interfering with the interpretation of serological results.
Various precautions in taking samples, the method of analysis and the interpretation of results are =recommended. When in doubt, repeat sampling can be used and analyzed after fifteen days, or other serological tests such as hemagglutination inhibition (HAI) or enzyme-linked immunosorbent assay (ELISA) can be performed. The HAI is indeed more specific than the RPA but detects mainly IgG that appears later. The difficulty of using HAI is related to the preparation and preser- vation of antigens. ELISA tests available now are more specific than the first kits marketed, but their relatively high cost still limits their use.
Chapter 41
TREATMENT & CONTROL
The methods of mycoplasma infection control must take into account the particularities of these microorganisms relatively low resistance in the environment, persistence in the infected animal, and mode of transmission (horizontal and espe- cially vertical). Depending on the type of flock (genetic stock, breeders, meat-birds), the objective may be to eradicate or to simply reduce the level of infection in order to limit the economic conse- quences of mycoplasmosis.
Eradication programs must include the strict obser- vance of the classic rules of biosecurity (disinfec tion, downtime, isolation and protection of the flock, «all-in, all-out production, etc.) as well as appropriate programs of vaccination or prevention of the other bacterial and viral infections. Regular testing on a sufficient number of birds is made to ensure the absence of mycoplasma infections, and infected flocks have to be quickly eliminated. In some countries, official procedures describe these dispositions to control mycoplasma infections in the context of improving the health status of herds or trade between countries.
breeder flocks are infected and the elimina- tion of the flock is not economically feasible, it might be possible to reduce vertical transmission with antibiotics such as macrolides (erythromycin,
Various precautions in taking samples, the method of analysis and the interpretation of results are =recommended. When in doubt, repeat sampling can be used and analyzed after fifteen days, or other serological tests such as hemagglutination inhibition (HAI) or enzyme-linked immunosorbent assay (ELISA) can be performed. The HAI is indeed more specific than the RPA but detects mainly IgG that appears later. The difficulty of using HAI is related to the preparation and preser- vation of antigens. ELISA tests available now are more specific than the first kits marketed, but their relatively high cost still limits their use.
Chapter 41
TREATMENT & CONTROL
The methods of mycoplasma infection control must take into account the particularities of these microorganisms relatively low resistance in the environment, persistence in the infected animal, and mode of transmission (horizontal and espe- cially vertical). Depending on the type of flock (genetic stock, breeders, meat-birds), the objective may be to eradicate or to simply reduce the level of infection in order to limit the economic conse- quences of mycoplasmosis.
Eradication programs must include the strict obser- vance of the classic rules of biosecurity (disinfec tion, downtime, isolation and protection of the flock, «all-in, all-out production, etc.) as well as appropriate programs of vaccination or prevention of the other bacterial and viral infections. Regular testing on a sufficient number of birds is made to ensure the absence of mycoplasma infections, and infected flocks have to be quickly eliminated. In some countries, official procedures describe these dispositions to control mycoplasma infections in the context of improving the health status of herds or trade between countries.
breeder flocks are infected and the elimina- tion of the flock is not economically feasible, it might be possible to reduce vertical transmission with antibiotics such as macrolides (erythromycin,
spiramycin, josamycin, lincomycin, tylosin), tetra- cyclines (tetracycline, chlortetracycline, oxytetra- cycline, doxycycline), spectinomycin, tiamulin or quinolones (where allowed). Treatments can be administered to adults or chicks, by injection or orally, in food or drinking water. The treatment of incubating eggs by dipping or injection of antibio- tics has also been described, but the effects of these methods must be thoroughly evaluated, especially in terms of selection of antibiotic-resistant bacte- ria. Another technique consists of heating hatching eggs at a temperature of 46-47°C for approxima- tely 12 hours, which limits infection but also reduces hatchability. All these procedures can reduce but not totally eliminate the level of conta- mination. These options must therefore be evalua- ted.
In production flocks, treatments are administered either at a suspected infection of the flock during critical periods of breeding, or at the onset of the clinical signs. The antibiotics must reach sufficient concentrations in organs and tissues of the respira- tory or genital tract and joints, and must also be effective against secondary bacterial infections.
The economic consequences of mycoplasma infec- tion and the difficulty of controlling it, especially in multi-age farms, have generated interest in vac- cine development. Thus, many types of vaccines have been developed for MG. Inactivated vaccines are marketed in some countries. They induce a humoral immune response but do not prevent the infection of birds. A local inflammatory reaction is observed at the injection site. Live vaccines have also been developed. The MG vaccine strain F, of
In production flocks, treatments are administered either at a suspected infection of the flock during critical periods of breeding, or at the onset of the clinical signs. The antibiotics must reach sufficient concentrations in organs and tissues of the respira- tory or genital tract and joints, and must also be effective against secondary bacterial infections.
The economic consequences of mycoplasma infec- tion and the difficulty of controlling it, especially in multi-age farms, have generated interest in vac- cine development. Thus, many types of vaccines have been developed for MG. Inactivated vaccines are marketed in some countries. They induce a humoral immune response but do not prevent the infection of birds. A local inflammatory reaction is observed at the injection site. Live vaccines have also been developed. The MG vaccine strain F, of
moderate virulence, administered by different routes can spread in the farm; its residual pathoge- nicity is worth mentioning and it limits its use. The MG vaccine strains TSII and MG 6/85, are less virulent and may also be employed They spread less and induce a low humoral response. Under experimental conditions, it can be shown that some of these vaccine strains prevent infection by a wild strain and successive rounds of immunization may eventually eliminate the wild strain from a flock. Inactivated or live vaccines should be used only as a last resort when traditional measures of biosecu- rity do not control the infection. The last category of vaccines are vectored vaccines. They offer pro- tection while not spreading to other flocks since they only contain fractions of the genome and not the whole mycoplasma. This makes it possible to use antibiotics at the same time if necessary.
امراض
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INTRODUCTION
Viral arthritis/tenosynovitis is one of the clinical manifestations of avian reovirus infection in chickens, particularly in meat-type chickens. Other manifestations are hepatitis, myocarditis and hydropericardium.
Enteric problems, such as enteritis and proventri- culitis that are commonly described as malabsorp- tion syndrome, have been found to be sometimes caused by avian reovirus. However, other viruses such as enteroviruses, parvoviruses, caliciviruses as well as some bacteria have been implicated as possible causative or contributing agents in malab- sorption syndrome.
In 1998, a reovirus was isolated in Poland (proto- type 238/98 - polish strain) in broilers (some were from breeders that had been vaccinated with cur- rently available reovirus vaccines) with malab- sorption syndrome, hepatitis, myocarditis, pan- creatitis, proventriculitis, tenosynovitis, enteritis& neurological signs (and also in layers with decreased production). Increased mortality was associated with concurrent infections (Escherichia coli, adenovirus). This virus was classified as ente- ric reovirus strain (ERS). A series of variants, much different from vaccine strains and associated with leg problems in broilers, has also been identi- fied in different regions of North America and other countries like France since 2012. The emer- gence and reemergence of reovirus-related diseases over the years in poultry make this virus a pathogen of interest as primary or secondary agent.
ETIOLOGY & EPIDEMIOLOGY
Avian reovirus has been a known cause of viral arthritis/tenosynovitis in chickens since 1969 and, more recently, in turkeys as well. It is occasionally seen in commercial layers. It is important to note that this virus is often isolated from clinically nor- mal birds.
The fowl reovirusesare double-stranded RNA non enveloped viruses, with a common group antigen. The viral particle is proximally 75-80 nm in diame- ter. The name «reovirus» comes from «respiratory. enteric orphan, being first isolated from these sites in humans who were not showing clinical signs. This virus is resistant to heat (it withstands 60°C for 8-10 hours) and to pH 3. It has been shown to survive at least 10 days on feathers, wood
Viral arthritis/tenosynovitis is one of the clinical manifestations of avian reovirus infection in chickens, particularly in meat-type chickens. Other manifestations are hepatitis, myocarditis and hydropericardium.
Enteric problems, such as enteritis and proventri- culitis that are commonly described as malabsorp- tion syndrome, have been found to be sometimes caused by avian reovirus. However, other viruses such as enteroviruses, parvoviruses, caliciviruses as well as some bacteria have been implicated as possible causative or contributing agents in malab- sorption syndrome.
In 1998, a reovirus was isolated in Poland (proto- type 238/98 - polish strain) in broilers (some were from breeders that had been vaccinated with cur- rently available reovirus vaccines) with malab- sorption syndrome, hepatitis, myocarditis, pan- creatitis, proventriculitis, tenosynovitis, enteritis& neurological signs (and also in layers with decreased production). Increased mortality was associated with concurrent infections (Escherichia coli, adenovirus). This virus was classified as ente- ric reovirus strain (ERS). A series of variants, much different from vaccine strains and associated with leg problems in broilers, has also been identi- fied in different regions of North America and other countries like France since 2012. The emer- gence and reemergence of reovirus-related diseases over the years in poultry make this virus a pathogen of interest as primary or secondary agent.
ETIOLOGY & EPIDEMIOLOGY
Avian reovirus has been a known cause of viral arthritis/tenosynovitis in chickens since 1969 and, more recently, in turkeys as well. It is occasionally seen in commercial layers. It is important to note that this virus is often isolated from clinically nor- mal birds.
The fowl reovirusesare double-stranded RNA non enveloped viruses, with a common group antigen. The viral particle is proximally 75-80 nm in diame- ter. The name «reovirus» comes from «respiratory. enteric orphan, being first isolated from these sites in humans who were not showing clinical signs. This virus is resistant to heat (it withstands 60°C for 8-10 hours) and to pH 3. It has been shown to survive at least 10 days on feathers, wood
shavings, egg shells and feed; and over 10 weeks in drinking water.
Although primarily a disease concern of chickens. reoviruses have been isolated from other avian spe- cies (turkeys, geese, ducks, pigeons, psittacines, etc.). Based on sequence analysis of selected genes, turkey and duck reoviruses are classified in different subgroups from chicken reoviruses. Chickens are most susceptible to pathogenic reovi- ruses at 1 day of age..
Avian reovirus can be transmitted horizontally by infected chickens or turkeys. Reoviruses can be excreted from both the intestinal and the respira- tory tracts for at least 10 days post-infection, with newly hatched chicks being more susceptible to the respiratory route. Transmission through broken skin in the foot has been shown experimentally. When done this way, the incubation period is very short (1 day); but it is normally between 9 and 13 days. The vertical transmission through the eggs of reovirus-infected breeders can be important in the epidemiology of the infection. Vertically infected chicks can easily become a nucleus of infection for hatchmates. Replication of the virus may occur in several tissues, but the intestine, the tibio-tarsome- tatarsal joint, and the liver are the main sites.
When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.
Morbidity is normally high, but mortality rarely exceeds 6%. Lesions of arthritis take a long time to be observed macroscopically. This may explain why they are usually not seen before four weeks of age. In turkeys, lesions have been seen mainly in males at least 14 weeks old, although it has been seen as well in poults only five weeks of age.
Although primarily a disease concern of chickens. reoviruses have been isolated from other avian spe- cies (turkeys, geese, ducks, pigeons, psittacines, etc.). Based on sequence analysis of selected genes, turkey and duck reoviruses are classified in different subgroups from chicken reoviruses. Chickens are most susceptible to pathogenic reovi- ruses at 1 day of age..
Avian reovirus can be transmitted horizontally by infected chickens or turkeys. Reoviruses can be excreted from both the intestinal and the respira- tory tracts for at least 10 days post-infection, with newly hatched chicks being more susceptible to the respiratory route. Transmission through broken skin in the foot has been shown experimentally. When done this way, the incubation period is very short (1 day); but it is normally between 9 and 13 days. The vertical transmission through the eggs of reovirus-infected breeders can be important in the epidemiology of the infection. Vertically infected chicks can easily become a nucleus of infection for hatchmates. Replication of the virus may occur in several tissues, but the intestine, the tibio-tarsome- tatarsal joint, and the liver are the main sites.
When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.
Morbidity is normally high, but mortality rarely exceeds 6%. Lesions of arthritis take a long time to be observed macroscopically. This may explain why they are usually not seen before four weeks of age. In turkeys, lesions have been seen mainly in males at least 14 weeks old, although it has been seen as well in poults only five weeks of age.
CLINICAL SIGNS & LESIONS
Viral arthritis
Avian reovirus infections cause symptoms of lame- ness and reluctance to move with visible swelling of the tarsal and metatarsal tendons. Sometimes the hock joint are also swollen, but not as severe as when secondary staphylococcus arthritis exists.
Later, fibrosis of the tarsal and metatarsal tendons will develop. can develop into rupture of the gastrocnemius tendon and subsequent subcuta neous hemorrhage followed by a fibrotic lump above the hock joint.
Much of the tendon sheath tissue will be granulo- matous and eventually replaced by fibrous connec- tive tissue. Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.
Secondary infections with bacteria such as Staphylococcus will aggravate the lesions with for- mation of a more purulent exudate and extensive hock joint swelling. If the birds are Mycoplasma synoviae (MS) positive, the synovitis can also be caused by MS as a co-factor. Reovirus may also exacerbate clinical signs caused by pathogens such as chicken anemia virus, Escherichia coli, and some respiratory viruses.
When the infection is acute, stunting may be obser- ved, while lameness is more pronounced. Lesions at slaughter (enlargement of gastrocnemius/digital flexor tendon area; green discoloration of the skin over the site of tendon rupture) may involve only a low percentage of birds, but flocks with over 10% of affected carcasses have been reported.
Arthritis, with epicarditis and tenosynovitis, have been reported in young geese, usually 2-3 weeks of age
Viral arthritis
Avian reovirus infections cause symptoms of lame- ness and reluctance to move with visible swelling of the tarsal and metatarsal tendons. Sometimes the hock joint are also swollen, but not as severe as when secondary staphylococcus arthritis exists.
Later, fibrosis of the tarsal and metatarsal tendons will develop. can develop into rupture of the gastrocnemius tendon and subsequent subcuta neous hemorrhage followed by a fibrotic lump above the hock joint.
Much of the tendon sheath tissue will be granulo- matous and eventually replaced by fibrous connec- tive tissue. Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.
Secondary infections with bacteria such as Staphylococcus will aggravate the lesions with for- mation of a more purulent exudate and extensive hock joint swelling. If the birds are Mycoplasma synoviae (MS) positive, the synovitis can also be caused by MS as a co-factor. Reovirus may also exacerbate clinical signs caused by pathogens such as chicken anemia virus, Escherichia coli, and some respiratory viruses.
When the infection is acute, stunting may be obser- ved, while lameness is more pronounced. Lesions at slaughter (enlargement of gastrocnemius/digital flexor tendon area; green discoloration of the skin over the site of tendon rupture) may involve only a low percentage of birds, but flocks with over 10% of affected carcasses have been reported.
Arthritis, with epicarditis and tenosynovitis, have been reported in young geese, usually 2-3 weeks of age
Enteric problems
If reovirus is involved in a malabsorption syn- drome, diarrhea can be observed usually at 8-10 days of age. Pale birds and growth retardation (runting and stunting), abnormal feathering (heli- copter wings) and/or femoral head fractures (osteoporosis) can be observed.
The fecal matter frequently has an orange color and contains undigested feed. The intestines quently have a pale, "cement" colored appearance and an enlarged proventriculus can be found. Tenosynovitis also occurs in such chickens.
If reovirus is involved in a malabsorption syn- drome, diarrhea can be observed usually at 8-10 days of age. Pale birds and growth retardation (runting and stunting), abnormal feathering (heli- copter wings) and/or femoral head fractures (osteoporosis) can be observed.
The fecal matter frequently has an orange color and contains undigested feed. The intestines quently have a pale, "cement" colored appearance and an enlarged proventriculus can be found. Tenosynovitis also occurs in such chickens.
In turkeys, some studies have suggested that reovi- ruses could play a role in the poult enteritis morta- lity syndrome (PEMS) (see Chap.IV.72). A reovi- rus has been shown, experimentally, to produce intestinal lesions. The authors also proposed that this virus could as well increase the susceptibility of poults to other pathogens associated with PEMS. However, an epidemiological study conducted in three states in the USA could not demonstrate any relationship between the presence of reoviruses and PEMS.
Muscovy duck reovirus has been associated with diarrhea, high morbidity and mortality in 2-4 week-old ducklings (see Chap. VI.85).
Muscovy duck reovirus has been associated with diarrhea, high morbidity and mortality in 2-4 week-old ducklings (see Chap. VI.85).
Myocarditis associated with reovirus (see Chap. 11.39)
DIAGNOSIS
Sample collection
It is highly recommended to collect intact legs, including shanks and feet, from six birds per flock. Younger flocks (10 to 35 days) are preferred because they provide a higher probability of isola- ting viable virus. Legs must be placed on ice immediately at time of collection and then frozen in ziplock bags. It must be shipped frozen to the diagnostic laboratory.
Histopathology
Cross-sections of the metatarsal tendons will show typical microscopic tenosynovitis lesions, as des-
DIAGNOSIS
Sample collection
It is highly recommended to collect intact legs, including shanks and feet, from six birds per flock. Younger flocks (10 to 35 days) are preferred because they provide a higher probability of isola- ting viable virus. Legs must be placed on ice immediately at time of collection and then frozen in ziplock bags. It must be shipped frozen to the diagnostic laboratory.
Histopathology
Cross-sections of the metatarsal tendons will show typical microscopic tenosynovitis lesions, as des-
TREATMENT & CONTROL Although reovirus infections cannot be treated with antibiotics, in the case of co-existing secon- dary infections with Staphylococcus spp. and/or Mycoplasma synoviae, antibiotic treatment can be useful.
Preventive vaccination of breeders is the most common procedure. Generally live reovirus vac- cines are given at 7 days and 5 weeks of age, fol- lowed by 2 applications of killed reovirus vaccine at 10 and 20 weeks of age, resulting in adequate antibody titers. Progeny chicks are protected by maternal antibodies for approximately 3 weeks, after which age resistance against lesion develop- ment following infection is usually the case. It should be noted that protection is effective against homologous serotypes only
If needed, broiler progeny will have to be vaccinated at 7-10 days of age, but this common procedure. The numerous outbreaks reovirus related teno synovitis in Eastern United States have been controlled by the concerted application of autoge nous vaccines and enhanced biosecurity and sani tation procedures (longer downtime, at least two weeks, complete washing and disinfection of infected premises and control of darkling beetles),
Viral arthritis/tenosynovitis has rarely been found in commercial layer chickens. If it occurs, reovirus vaccination of parent breeders is advisable.
Preventive vaccination of breeders is the most common procedure. Generally live reovirus vac- cines are given at 7 days and 5 weeks of age, fol- lowed by 2 applications of killed reovirus vaccine at 10 and 20 weeks of age, resulting in adequate antibody titers. Progeny chicks are protected by maternal antibodies for approximately 3 weeks, after which age resistance against lesion develop- ment following infection is usually the case. It should be noted that protection is effective against homologous serotypes only
If needed, broiler progeny will have to be vaccinated at 7-10 days of age, but this common procedure. The numerous outbreaks reovirus related teno synovitis in Eastern United States have been controlled by the concerted application of autoge nous vaccines and enhanced biosecurity and sani tation procedures (longer downtime, at least two weeks, complete washing and disinfection of infected premises and control of darkling beetles),
Viral arthritis/tenosynovitis has rarely been found in commercial layer chickens. If it occurs, reovirus vaccination of parent breeders is advisable.
Enteric problems, such as enteritis and proventri- culitis that are commonly described as malabsorp- tion syndrome, have been found to be sometimes caused by avian reovirus. However, other viruses such as enteroviruses, parvoviruses, caliciviruses as well as some bacteria have been implicated as possible causative or contributing agents in malab- sorption syndrome.
Reoviruses can be excreted from both the intestinal and the respira- tory tracts for at least 10 days post-infection, with newly hatched chicks being more susceptible to the respiratory route.
broken skin in the foot , the incubation period is very short (1 day);
but it is normally between 9 and 13 days.
Replication of the virus may occur in several tissues, but the intestine, the tibio-tarsome- tatarsal joint, and the liver are the main sites..
When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.
broken skin in the foot , the incubation period is very short (1 day);
but it is normally between 9 and 13 days.
Replication of the virus may occur in several tissues, but the intestine, the tibio-tarsome- tatarsal joint, and the liver are the main sites..
When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.When breeder chickens get infected with reovirus during production, they will not have any clinical signs themselves, but some of the progeny broilers will have viral arthritis/tenosynovitis, while hat- chability will also decrease for several weeks, until the breeders become immune to the reovirus. Different studies suggest that vertical transmission occurs principally between 5 and 19 days post- infection in breeders.
امراض
INTRODUCTION Viral arthritis/tenosynovitis is one of the clinical manifestations of avian reovirus infection in chickens, particularly in meat-type chickens. Other manifestations are hepatitis, myocarditis and hydropericardium. Enteric problems, such as…
INTRODUCTION
Respiratory Viral infection
resistant to heat (it withstands 60°C for 8-10 hours) and to pH 3.
survive at least 10 days on
feathers
wood shavings
egg shells
feed; and over 10 weeks in drinking water
ETIOLOGY & EPIDEMIOLOGY
(turkeys, geese, ducks, pigeons,
psittacines, etc.).
occasionally seen in commercial layers.
Chickens are most susceptible to pathogenic reoviruses at 1 day of age..
الانتقال
_ horizontally by infected chickens or turkeys.
_ vertical transmission through the eggs
Morbidity is normally high,
mortality rarely exceeds 6%.
Lesions of arthritis take a long time to be observed macroscopically.
that's why they are usually not seen before four weeks of age.
In turkeys, lesions have been seen mainly in males at least 14 weeks old, although it has been seen as well in poults only five weeks of age.
CLINICAL SIGNS & LESIONS
Viral arthritis
lameness
reluctance to move
visible swelling of the tarsal and metatarsal tendons.
hock joint swollen, but not as severe as when secondary staphylococcus arthritis exists.
, fibrosis of the tarsal and metatarsal tendons can develop into rupture of the gastrocnemius tendon and subsequent subcuta neous hemorrhage followed by a fibrotic lump above the hock joint.
tendon sheath tissue will be granulomatous
and replaced by fibrous connetive tissue.
Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.
Secondary infections with bacteria such as Staphylococcus will aggravate the lesions with formation of a more purulent exudate and extensive hock joint swelling.
with Mycoplasma synoviae (MS) , the synovitis can also be caused by MS as a co-factor
Reovirus may also exacerbate clinical signs caused by pathogens such as chicken anemia virus, Escherichia coli, and some respiratory viruses.
When the infection is acute,
stunting lameness is more pronounced.
Lesions at slaughter
_ enlargement of
•gastrocnemius
•digital flexor tendon area
_green discoloration of the skin over the site of tendon rupture
_Myocarditis
/tenosynovitis
hepatitis
myocarditis
hydropericardium.
_Arthritis
_epicarditis
_ tenosynovitis, have been reported in young geese, usually 2-3 weeks of age
Muscovy duck
diarrhea,
high morbidity
mortality in 2-4 week-old ducklings
TREATMENT & CONTROL
Immunity lifter
Preventive vaccination the most common procedure.
Live reovirus vaccines are given at 7 days and 5 weeks of age
followed by 2 applications of killed reovirus vaccine at 10 and 20 weeks of age
Viral arthritis/tenosynovitis has rarely been found in commercial layer chickens.
Respiratory Viral infection
resistant to heat (it withstands 60°C for 8-10 hours) and to pH 3.
survive at least 10 days on
feathers
wood shavings
egg shells
feed; and over 10 weeks in drinking water
ETIOLOGY & EPIDEMIOLOGY
(turkeys, geese, ducks, pigeons,
psittacines, etc.).
occasionally seen in commercial layers.
Chickens are most susceptible to pathogenic reoviruses at 1 day of age..
الانتقال
_ horizontally by infected chickens or turkeys.
_ vertical transmission through the eggs
Morbidity is normally high,
mortality rarely exceeds 6%.
Lesions of arthritis take a long time to be observed macroscopically.
that's why they are usually not seen before four weeks of age.
In turkeys, lesions have been seen mainly in males at least 14 weeks old, although it has been seen as well in poults only five weeks of age.
CLINICAL SIGNS & LESIONS
Viral arthritis
lameness
reluctance to move
visible swelling of the tarsal and metatarsal tendons.
hock joint swollen, but not as severe as when secondary staphylococcus arthritis exists.
, fibrosis of the tarsal and metatarsal tendons can develop into rupture of the gastrocnemius tendon and subsequent subcuta neous hemorrhage followed by a fibrotic lump above the hock joint.
tendon sheath tissue will be granulomatous
and replaced by fibrous connetive tissue.
Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.
Secondary infections with bacteria such as Staphylococcus will aggravate the lesions with formation of a more purulent exudate and extensive hock joint swelling.
with Mycoplasma synoviae (MS) , the synovitis can also be caused by MS as a co-factor
Reovirus may also exacerbate clinical signs caused by pathogens such as chicken anemia virus, Escherichia coli, and some respiratory viruses.
When the infection is acute,
stunting lameness is more pronounced.
Lesions at slaughter
_ enlargement of
•gastrocnemius
•digital flexor tendon area
_green discoloration of the skin over the site of tendon rupture
_Myocarditis
/tenosynovitis
hepatitis
myocarditis
hydropericardium.
_Arthritis
_epicarditis
_ tenosynovitis, have been reported in young geese, usually 2-3 weeks of age
Muscovy duck
diarrhea,
high morbidity
mortality in 2-4 week-old ducklings
TREATMENT & CONTROL
Immunity lifter
Preventive vaccination the most common procedure.
Live reovirus vaccines are given at 7 days and 5 weeks of age
followed by 2 applications of killed reovirus vaccine at 10 and 20 weeks of age
Viral arthritis/tenosynovitis has rarely been found in commercial layer chickens.
tendon sheath tissue will be granulomatous
and replaced by fibrous connetive tissue.
Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.
and replaced by fibrous connetive tissue.
Infiltration with mononuclear cells, plasma cells and macrophages acute stage with the presence of serous fluid in these tissues. The syno- vial surface of the tarso-metatarsal (hock) joint can have a typical granulation (pannus) formation, very similar to rheumatoid arthritis in humans. Inflammation degrades the quality of the synovial fluid and breaks down tendon and cartilage.