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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- infectious coryza
International Common Names
- English: Avibacterium paragallinarum, infectious coryza in chickens; contagious catarrh of fowls; coryza; coryza infectiosa gallinarum; haemophilus paragallinarum, infectious coryza in chickens; infectious coryza of chickens; infectious rhinitis of fowls
Local Common Names
- Indonesia: snot
Pathogen/sTop of page
OverviewTop of page
Avibacterium paragallinarum (formerly Haemophilus paragallinarum) is the causative agent of infectious coryza (IC), a disease of the upper respiratory tract in chickens (Yamamoto, 1984). The disease occurs in growing chickens and layers, and is of economic importance due to an increased number of culls and a marked reduction (10-40%) in egg production (Blackall et al., 1997). The disease is characterized by a swelling of the face, inflammation of infra orbital sinuses and conjunctivae with clear or purulent discharge from the nostrils in the acute stage of the disease (Blackall et al., 1997). In many parts of the world, IC has become a major problem that affects all ages of chickens of both indigenous (native chickens) and laying hens in poultry farms.
As early as 1920, Beach believed that IC was a distinct clinical entity. The aetiological agent eluded identification for a number of years, as the disease was often masked in mixed infection, and with fowl pox in particular (Blackall et al., 1997). DeBlieck (1932) isolated the causative agent and named it Bacillus hemoglobinophilus coryzae gallinarum (Blackall et al., 1997). Elliot and Lewis (1934) and Delaplane et al. (1934) independently proposed the binomial Haemophilus gallinarum (Yamamoto, 1991). Based on studies conducted during the 1930s, the causative agent of IC was classified as Haemophilus gallinarum because its requirement for both x-(haemin) and v-(nicotinamide adenine dinucleotide, NAD) factors for growth (Beach and Schalm, 1936; Blackall et al., 1997). Page (1962) found that all isolates recovered from cases of IC required only v-factor for growth. This led to the proposal and general acceptance of a new species, Haemophilus paragallinarum (Zinneman and Biberstein, 1974) for an organism requiring only the V-factor. Following a phenotypic and genotypic investigation of the taxonomy of H. paragallinarum, the bacterium was reclassified as Avibacterium paragallinarum (Blackall et al., 2005).
Host AnimalsTop of page
Hosts/Species AffectedTop of page
Chickens are primarily affected, although the disease has occasionally been reported in pheasants and guinea fowls (Charlton et al., 2000) and Japanese quails (Reece et al., 1981; Thenmozhi and Malmarugan, 2013). All ages of chickens are susceptible. The disease is seen more frequently on intensive chicken farms, especially on large-scale egg production complexes and breeding farms (Charlton et al., 2000).
On farms where multiple age groups are brooded and raised, spread of the disease to successive age groups usually occurs within 1-6 weeks after birds are moved from the brooder house to growing cages nearby to older groups of infected birds. Chickens are the natural host for A. paragallinarum (Blackall et al., 1997). IC does not occur in turkeys (Blackall et al., 1997). Indigenous domestic native fowls, sometimes referred to as village chickens are also susceptible to A. paragallinarum infection (Zaini and Kanameda, 1991; Lin et al., 1996; Poernomo et al., 2000).
Systems AffectedTop of page
digestive diseases of poultry
respiratory diseases of poultry
DistributionTop of page
IC is a disease of economic significance in many parts of the world. Within the USA, the disease is most prevalent in California and the Southeastern States (Blackall et al., 1997). It is likely that IC has a worldwide distribution.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Algeria||Absent, No presence record(s)|
|Congo, Democratic Republic of the||Absent, No presence record(s)|
|Djibouti||Absent, No presence record(s)|
|Libya||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Sudan||Absent, No presence record(s)|
|Tunisia||Absent, No presence record(s)|
|Uganda||Absent, No presence record(s)|
|Bahrain||Absent, No presence record(s)|
|Georgia||Absent, No presence record(s)|
|India||Present||Original citation: Anjaneya, et al. (2014)|
|Iran||Absent, No presence record(s)|
|Kazakhstan||Absent, No presence record(s)|
|Mongolia||Absent, No presence record(s)|
|North Korea||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Uzbekistan||Absent, No presence record(s)|
|Belarus||Absent, No presence record(s)|
|Cyprus||Absent, No presence record(s)|
|Czechia||Absent, No presence record(s)|
|Estonia||Absent, No presence record(s)|
|Finland||Absent, No presence record(s)|
|France||Absent, No presence record(s)|
|Greece||Absent, No presence record(s)|
|Isle of Man||Absent, No presence record(s)|
|Jersey||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|Luxembourg||Absent, No presence record(s)|
|Moldova||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Norway||Absent, No presence record(s)|
|Russia||Absent, No presence record(s)|
|Serbia and Montenegro||Absent, No presence record(s)|
|Slovakia||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Spain||Absent, No presence record(s)|
|Ukraine||Absent, No presence record(s)|
|Barbados||Absent, No presence record(s)|
|Belize||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Present|
|Trinidad and Tobago||Absent, No presence record(s)|
|French Polynesia||Present||CAB Abstracts Data Mining|
|New Caledonia||Present||CAB Abstracts Data Mining|
|Falkland Islands||Absent, No presence record(s)|
|French Guiana||Absent, No presence record(s)|
|Guyana||Present, Serological evidence and/or isolation of the agent|
PathologyTop of page
A. paragallinarum produces an acute catarrhal inflammation of mucous membranes of nasal passages and sinuses. There is frequently a catarrhal conjunctivitis and subcutaneous oedema of face and wattles. Typically, pneumonia and airsacculitis are rarely present; however, some reports of outbreaks in broilers have indicated significant levels of condemnations (up to 69,8%) due to airsaculitis even in the absence of any other recognized viral or bacterial pathogens (Droual et al., 1990; Blackall et al., 1997).
Essential change in the nasal cavity, infra orbital sinuses, and trachea consisted of sloughing, disintegration and hyperplasia of mucosal and glandular epithelia, oedema, and hyperaemia with heterophil infiltration in the tunica propria of the mucous membranes. Pathologic changes first observed at 20 hours reached maximum severity by 7-10 days after infection, with subsequent repair occurring within 14 -21 days. In birds with involvement of the lower respiratory tract, acute catarrhal bronchopneumonia was observed, with heterophils and cell debris filling the lumen of secondary and tertiary bronchi; epithelial cells of air capillaries were swollen and showed hyperplasia, catarrhal inflammation of air sacs was characterized by swelling and hyperplasia of the cells, with abundant heterophil infiltration. In addition, a pronounced infiltration of most cells was observed in the lamina propria of the mucous membrane of the nasal cavity. The products of most cells, heterophil, and macrophages may be responsible for the severe vascular changes and cell damage leading to coryza. A dissecting fibrinopurulent cellulitis similar to that seen in chronic fowl cholera has been reported in broiler and layer chickens. In infectious coryza, lesions were confined to the upper respiratory tract (Reid and Blackall, 1984; Droual et al.,1990; Blackall et al., 1997).
DiagnosisTop of page
Diagnosis is based on recognizing the clinical signs, postmortem findings, and bacteriological examinations of the suspected causal agent leading to isolation, and identification of the causative agent.
In susceptible chickens the symptoms first appear about 36-48 hours after exposure to infection. The disease affects the upper respiratory tracts of chickens (Yamamoto, 1984). The disease occurs in growing chickens and layers. The typical symptoms are a swollen face and sinuses with a clear discharge progressively becoming purulent. There is marked conjunctivitis and in some cases the eyes are partially or completely closed, and lacrimation results in an inability of the chicken to eat and drink. Infection may involve one or both sinuses. Mortality is low, but morbidity may reach 100%. Affected chickens have variable size of swelling of the infraorbital sinus and face, nasal discharge, difficulty in breathing and coughing. In layers infection causes a drop in egg production; in broilers there may be an increased need to cull birds (Bains, 1979). A. paragallinarum produces an acute catarrhal inflammation of mucous membranes of nasal passages and sinuses. There is frequently a catarrhal conjunctivitis and subcutaneous oedema of face and wattles.
Consistent lesions associated with IC are acute catarrhal inflammation of the nasal passage and sinusitis. There is frequently a catarrhal conjunctivitis and subcutaneous oedema of face and wattles. In chronic cases, an accumulation of 'cheesy' material in the infraorbital sinus may be present (Bain, 1979; Droual et al., 1990).
Ideally, the isolation and identification of the causative bacterium is used to confirm a diagnosis of infectious coryza. The methods used include examination of the satellite phenomenon with a feeder culture of Staphylococcus epidermidis or Staphylococcus hyicus, biochemical tests, fermentation tests of carbohydrates, and serological tests (Page, 1962; Blackall and Reid, 1982; Poernomo et al., 1997a, b).
A polymerase chain reaction (PCR) test, which can be applied either to suspect colonies or directly to samples from chickens, is available (Chen et al., 1997, 1998). Although most isolates of A. paragallinarum are dependent upon v-factor for growth in artificial media (meaning they show the traditional satellite growth), some isolates are v-factor-independent (Monahid et al., 1992; Bragg et al., 1993; Horner et al., 1995; Miflin et al., 1995; Jacobs and Van der Werf, 2000). This variation in growth factor requirements, along with the existence of non pathogenic v-factor-dependent organisms, highlights the need for biochemical identification or the use of the new generation PCR test; serotyping of isolates is an important guide in the use of vaccines (Blackall and Yamamoto, 1998).
A range of serological tests to detect antibodies have been described (Blackall et al., 1997), and haemagglutination inhibition (HI) tests are in widespread use (Blackall and Yamamoto, 1998). A blocking ELISA-kit has also been developed (Zaini et al., 1995; Miao et al., 1999; Zhang et al., 1999; Miao et al., 2000). A. paragallinarum bacteria can be detected on the epithelium of the nasal passage and sinuses by using immunoperoxidase tests (Nakamura et al., 1993).
Isolation and Identification of the Causative Agent
Many different media have been developed to support the growth of A. paragallinarum. Specimens should be taken from two or three chickens in the acute stage of the disease. A sterile cotton swab is inserted deep into the sinus cavity where the organism is most often found in its pure (uncontaminated) form. Tracheal or air sac exudates may also be taken on a sterile swab. The swab is streaked on a blood agar plate, which is then cross-streaked with Staphylococcus epidermidis or Staphylococcus hyicus (Page, 1962; Blackall and Reid, 1982) and incubated at 37°C in a partially evacuated large screw-cap jar. Staphylococcus epidermidis or S. hyicus which are commonly used as 'feeders' should be pre-tested because not all strains actively produce the v-factor (Blackall et al., 1997).
At the simplest level, IC may be diagnosed on the basis of a history of a rapidly spreading disease in which coryza is the main manifestation. A smear of sinus exudates should be made and Gram stained. It should reveal Gram-negative bipolar-staining rods with a tendency toward filament formation and pleomorphism and combined with the isolation of a catalase-negative bacterium showing satellite growth. Another efficient diagnostic procedure is to inoculate the sinus exudates or culture into two or three young normal chickens by the infraorbital sinus (intra sinus). The typical signs and lesion associated with coryza may develop in 24-28 hrs or longer (3-5 days); however, the incubation period may be delayed up to 1 week if only a few organisms are present in the inoculum (Blackall et al., 1997; Charlton et al., 2000). Better equipped laboratories should attempt a more complete biochemical identification; serological tests for serotyping of A. paragallinarum isolates is important for epidemiological investigations and an invaluable prerequisite to management programs based on vaccination (Blackall et al., 1997). Chickens that have recovered from active infection of coryza develop varying degrees of immunity. Pullets that have experienced IC during their growing period are generally protected against a later drop in egg production. Resistance to re-exposure among individual birds may develop as early as 2 weeks after initial exposure by the intrasinus route. Oral administration of doses of 1010 cells of attenuated A. paragallinarum serotype A, effectively induces production of serum haemagglutination-inhibition antibodies in chickens and protects from subsequent infection (Nakamura et al., 1994; Blackall et al., 1997).
IC must be differentiated from chronic respiratory disease, chronic fowl cholera, fowl pox, and hypovitaminosis A, which produce similar clinical signs. In some areas A. paragallinarum infection must also be differentiated from infection due to Ornithobacterium rhinotracheale. A. paragallinarum often occurs in mixed infections, with chronic IC having a number of contributory agents. One should consider the possibility of other bacteria or viruses as complicating factors, particularly if mortality is high and the disease takes a prolonged course (Blackall and Yamamoto, 1998).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Digestive Signs / Diarrhoea||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sign|
|Respiratory Signs / Change in voice, vocal strength||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Respiratory Signs / Coughing, coughs||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Respiratory Signs / Purulent nasal discharge||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Respiratory Signs / Sneezing, sneeze||Poultry|Cockerel; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
Disease CourseTop of page
The principle lesion manifested by A. paragallinarum infection is an acute catarrhal inflammation of the upper respiratory tract, mainly of the nasal cavity and paranasal sinuses. Infiltration of a large number of most cells into the lamina propria of the mucous membrane of the nasal cavity is also characteristic. Numerous organisms are found on the cilia or on the surface of the epithelial cells of the nasal mucosa. Chickens with the lesions often have severe coryza. Adherence to and colonization of the encapsulated variant on the nasal mucosa seems to be a first step of infection (Sawata et al., 1985a). Colonization of the nasal mucosa by encapsulated A. paragallinarum is probably essential to induce morphological changes in the nasal mucosa (Sawata et al., 1985b).
Acute uncomplicated coryza is characterized by a short duration, with signs usually clinically visible for 7-11 days, and subsequently results in birds being refractory to reinfection. Chronic disease is usually found in complicated coryza and in this case clinical signs can persist for a month and longer. Chronic coryza can be produced experimentally, by creating a combined infection of Mycoplasma gallisepticum and A. paragallinarum (Rimler et al., 1977).
IC may occur in growing chickens and layers. There is usually a rapid onset and morbidity is high in the flock, decreased feed and water consumption, retarded growth in young stock and reduced egg production in laying flocks. The most common clinical signs are nasal discharge, facial swelling, lacrimation, anorexia, conjunctivitis with some adherence of eyelids, respiratory noise, swollen infraorbital sinuses and exudates in the conjunctival sac, occasionally diarrhoea (Blackall et al., 1997; Charlton, 2000). There has been a recent emergence of disease in meat chickens in the USA and a swollen head-like syndrome associated with A. paragallinarum infection has been reported (Droual et al., 1990); similar symptoms have been reported in South America (Sandoval et al., 1994). Additionally, arthritis and septicaemia, possibly complicated by the presence of other pathogens, have been reported in broiler and layer flocks in South America (Sandoval et al., 1994). A foul odour may be detected in flocks in which the disease has become chronic and complicated with other bacteria (Blackall et al., 1997). A. paragallinarum/A. gallinarum infection also may involve the trachea and bronchi, causing rales and difficult breathing (Beach and Schalm, 1936).
EpidemiologyTop of page
The disease is observed primarily during the autumn and winter months in subtropical climates, or during the rainy season in a tropical climate. All age groups of chickens are susceptible, but the disease appears to be more severe in birds of 4 weeks old and upwards. Morbidity is high (80-100%) and mortality is low (0-1%), unless there is complication with other infections, such as infectious bronchitis virus, Mycoplasma gallisepticum and Pasteurella spp. The presence of disease in growing birds may result in poor growth, and reduced egg production. Chronic or apparently healthy carrier birds have been recognized as the main reservoirs of infection. Spread within a flock is rapid via contact with infected birds, through ingestion of contaminated feed or water, and by the airborne route. Recovered birds are frequently carriers. No mechanical or biological carriers (vectors) have been demonstrated. The organism does not survive longer than 4-5 hours in the environment outside its hosts (Anon., 1971; Charlton et al., 2000). Susceptible birds exposed to infected birds may show signs of the disease within 24-72 hours (Rimler et al., 1977; Blackall et al., 1997). Chickens inoculated with cultures of A. paragallinarum or exudate, will show the characteristic features of coryza after 24-48 hours (Blackall et al., 1997).
Impact: EconomicTop of page
IC occurs in all ages of growing chickens and is of economic importance due to an increased number of culls and a marked reduction (10-40%) in egg production (Blackall et al., 1997).
IC is often regarded as a disease that has its greatest impact in intensively raised chickens. In Indonesia, the disease was formerly not considered to be widespread in village chickens. However the isolation of A. paragallinarum in village chickens has indicated that the disease can be present in less intensive production systems (Poernomo et al., 2000). In China, it has been estimated that over a three year period, 1986-1988, the disease caused cases of about 1000 million Yen (approximately US $18 million) at the 1992 exchange rate (Chen et al., 1993).
Disease TreatmentTop of page
Various sulfonamides and antibiotics have been used to treat IC, usually in feed or drinking water. Birds usually respond to treatment but relapses may occur when treatment is discontinued. Many drugs and antibiotics have been used, including streptomycin, erythromycin, sulfodimethoxine, tylosin tartrate and spectinomycin (Charlton et al., 2000). Drug combinations found effective for the treatment of IC include sulfachloropyridazine/trimethoprim (Poernomo and Ronohardjo, 1987), and sulfamethoxazol/trimethoprim (Takahashi et al., 1990; Poernomo et al., 1997). It should be noted that sulfa drugs may cause a temporary drop in egg production and overdoses may be toxic. Similarly, streptomycin causes severe stress in chickens, which can last for 24 hours (Bains, 1979). Erythromycin and oxytetracycline are two commonly used antibiotics (Blackall et al., 1997). Other antibiotics found effective in the treatment of IC include norfloxacin (Lublin et al., 1993), enrofloxacin, ciprofloxacin, ampicillin (Prabhakar et al., 1998), and gentamycin (Muhammad et al., 1998). Some strains of A. paragallinarum are resistant to various antibiotics, including cloxacillin, erythromycin, ampicillin, lincomycin (Prasad et al., 1999), neomycin, cotrimoxazol, amikacin, and cephalexin (Prabhakar et al., 1998). Strains of A. paragallinarum resistant to various antibiotics have not been found to carry plasmids (Blackall, 1988).
Prevention and ControlTop of page
Recovered carrier birds are the main source of infection, so practices such as buying breeding males or started chicks from unknown sources should be discouraged. Only day-old chicks should be secured for replacement purposes unless the source is known to be free of IC. Isolation rearing and the housing away from old stock are desirable practices. To eliminate the agents from a farm, it is necessary to depopulate the infected or recovered flock(s), because birds in such flocks remain reservoirs of infection. After the cleaning and disinfecting of equipment and houses, the premises should be allowed to remain vacant for 2-3 weeks before restocking with clean birds (Blackall et al., 1997), raised, in so far as is possible, in quarantine (Charlton et al., 2000).
It is important to avoid the introduction of infected chickens to the farm and if this occurs then the early recognition of disease and institution of appropriate treatment is vital. Good husbandry and management procedures prevent spread of disease; isolation of age groups of chickens on an all-in, all-out basis (Bain, 1979).
It is necessary to depopulate flocks that have experienced the disease, because recovered birds remain reservoirs of infection. The method of eradication depends upon circumstances on the farm, the size of the flock, facilities, and purpose of the flock. The infected birds may be marketed at once and the premises cleaned before new chicks are brought onto the farm. Another more popular method is to treat the affected flock and keep it isolated until new stock has been raised in isolation as replacements. After the infected or recovered birds are marketed, the house should be cleaned and disinfected before housing clean stock. As the organism may survive in exudates for several days at low temperatures, it would be advisable to allow the cleaned house to remain vacant for about 1 week, particularly during the cooler periods of the year (Yamamoto, 1984).
Immunization and Vaccines
Vaccination is normally effective for the control of disease, but some outbreaks have been caused by vaccine failure. The mis-matching of challenge serovar with vaccine is the most likely explanation for these cases of vaccine failure. Other explanations such as improper vaccination technique may also have played a role. Where they occur there is a need for the active investigation of suspect infectious coryza vaccine failures, including the isolation and serotyping of suspect A. paragallinarum isolates.
Commercial bacterins prepared from chicken embryos or broth may be autogenous or may combine strains of 2-3 serotypes. The product is inactivated with formalin or merthiolate, and must contain at least 108 CFU/ml to be effective. They may contain adjuvants (Al(OH)3 gel or mineral oil), stabilizers, or saline diluent (Yamamoto, 1984). Bacterin/vaccine produced in broth protected more effectively than vaccine produced in chicken embryo (Terzalo et al., 1999). Bacterins are generally injected in birds between 10 and 20 week of age and yield optimal result when given 3-4 weeks prior to an expected natural outbreak. Two injections given approximately 4 weeks apart before 20 weeks of age results in better performance of layers than a single injection (Feng et al., 1988; Mouhid et al., 1991). Both subcutaneous and intramuscular injections have been found to be effective (Blackall and Reid, 1987). Injection of the bacterin into the leg muscle has been found to give better protection than when it is injected into breast muscle.
Inactivated IC bacterins provide protection only against the particular Page serovars included in the vaccine, so it is vital that vaccines contain all the serovars that may be present in infections in the target population (Blackall et al., 1997); Page serovar B has now been confirmed to be a true serovar with full pathogenicity. Serovar B is widespread and must be included in inactivated bacterins in areas where it is present (Tezalo et al., 1999; Poernomo et al., 2000). However, as different strains of serovar B provide only partial cross-protection among themselves it may be necessary to prepare an autogenous bacterin for use in areas where serovar B is endemic (Mouchid et al., 1991; Yamaguchi et al., 1990, 1991; Aly and Mousa, 2000; Poernomo et al., 2000).
ReferencesTop of page
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DeBlieck L, 1932. A haemophilic bacterium as the cause of contagious catarrh of the fowl (coryza infectiousa gallinarum). Veterinary Journal, 88:9-13.
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