Since 1998, an epidemic of avian influenza has occurred in the Iranian poultry industry. The agent was pathotyped as non-highly pathogenic and subtyped as an H9N2 avian influenza virus. Therefore it did not require eradication. However, frequent incidences of high mortality were observed commonly on broiler farms. No other species of bird were affected. The circulation of the virus and mixed infection with other respiratory pathogens, particularly infectious bronchitis virus and Mycoplasma gallisepticum, were incriminated in the high mortality on poultry farms and resulting great economic losses. Clinical signs in both field and experimental studies included swelling of the periorbital tissues and sinuses, nasal and ocular discharge, and severe respiratory distress. However, in the experimental study, the mortality rate was much lower than in the natural outbreak. Gross lesions identified included extensive congestion of the respiratory tissues, and exudation with cast formation in the tracheal bifurcation, which extended to the secondary bronchi. Severe necrotizing tracheatis was the predominate histological lesion. Ultrastructurally, orthomyxovirus-like particles were identified in the inoculum used for the experimental study. An inactivated H9N2 avian influenza vaccine prevented mortality in experimentally challenged chickens.

An epidemic of avian influenza (AI) (H9N2) occurred in broiler chicken farms in Iran during 1998-01. Mortality between 20% and 60% was commonly observed on the affected farms. Mixed infections of the influenza virus with other respiratory pathogens, particularly infectious bronchitis virus and Mycoplasma gallisepticum, were thought to be responsible for such high mortality, which resulted in great economic losses. Clinical signs included swelling of the periorbital tissues and sinuses, typical respiratory discharge, and severe respiratory distress. Gross lesions included extensive hyperemia of the respiratory system followed by exudation and cast formation in the tracheal biforcation extending into the secondary bronchi. Light microscopy lesions were characterized by severe necrotizing tracheatis. Serological examination using H9N2 AI viral antigen produced inconsistent results. Ultrastructural findings showed typical viral replication through budding processes on cell membranes of the tracheal epithelium.

Avian influenza virus of H9N2 subtype is pathotyped as a non-highly pathogenic virus. However, frequent incidences of avian influenza of high mortality that are caused by H9N2 viruses have been observed in broiler chicken farms in Iran and some other Asian countries. Coinfections or environmental factors may be involved in such cases. Infectious microorganisms have been implicating in taking part in the cases of coinfection. We studied the effect of experimental coinfection of H9N2 avian influenza virus with infectious bronchitis live vaccine, which is used extensively in chicken farms in Iran. Clinical signs, gross lesions, viral shedding and mortality rate of the experimentally infected birds were examined. Coinfection of infectious bronchitis live vaccine and H9N2 avian influenza virus led to an extension of the shedding period of H9N2 virus, increasing the severity of clinical signs and mortality rates, causing macroscopic lesions in the embryos.

Background:Campylobacter is one of the leading bacterial species causing foodborne illnesses in humans. Antimicrobial agents have been extensively used for treatment of Campylobacter infections; but in the recent years, both animal and human isolates of this bacterium have shown resistance to several antibiotics such as tetracycline.Objectives:The aim of this study was to investigate the presence of genetic determinants of tetracycline resistance in Campylobacter spp. recovered from poultry carcasses in Shiraz, Iran.Materials and Methods:Eighty-three thermophilic Campylobacter spp. Isolates were first identified based on multiplex polymerase chain reaction (PCR) and then screened for presence of tetracycline resistance genes (tet (A), tet (B), tet (O) and te (S)) by PCR.Results:The overall prevalence of Campylobacter jejuni and C. coli among the examined isolates was 51.8% and 48.2%, respectively. Tetracycline resistance genes of tet (B) and tet (S) were not seen among these Campylobacter spp. Isolates, whereas the most common tet gene identified was tet (O), found in 83.1% (69/83) of all the isolates. The tet (O) gene sequence comparison between C. jejuni and C. coli showed 100% similarity and these sequences (JX853721and JX853722) were also identical to the homologous sequences of other strains of Campylobacter spp. existing in the GenBank databases. In addition, tet (A) was found in 18% (15/83) of Campylobacter spp. isolates. To our knowledge, this represents the first report of tet (A) in Campylobacter spp. There was 100% homology between the sequences of tet (A) from this study (JX891463 and JX891464) and the tet (A) sequences mentioned for other bacteria in the GenBank databases.Conclusions:The high prevalence of tet (O) resistance gene along with new detection of tet (A) resistance gene in Campylobacter spp. isolated from poultry carcasses revealed an extensive tetracycline resistance among Campylobacter isolates from poultry in Iran. It emphasized the need for cautious use of tetracycline in poultry production to decrease the extension of tetracycline-resistant Campylobacter spp.

Infectious bronchitis (IB) is one of the most important viral diseases of poultry. The aim of this study was to investigate the distribution of avian infectious bronchitis virus isolate IRFIBV32 (793/B serotype) in experimentally infected chicken. Ninety-one-day-old commercial broilers were divided randomly into two groups (seventy in the experimental and twenty in the control group). Chicks in the experimental group were inoculated intranasally with 105 ELD50/0.1 mL of the virus at three weeks of age. The samples from various tissues were collected at1, 2, 3, 5, 7, 11, 13, 15, and 20 days postinoculation. Chickens exhibited mild respiratory signs and depression. Viral RNA was detected in the kidney, lung and tracheas on days 1 to 13 PI, in the oviduct between, days 3 and 13, in testes between days 1 and 11 PI, and in the caecal tonsil consistently up to day 20 PI. The most remarkable clinical signs and virus detection appeared on day 1 PI. Data indicated that the number of infected chickens and viral RNA detection from tissues was reduced with increasing antibody titer on day 20 PI. The results demonstrated that the IRFIBV32 virus has wide tissue distribution for respiratory, urogenital, and digestive systems.