INACTIVATION OF INFECTIOUS LARYNGOTRACHEITIS VIRUS BY DISINFECTANTS

The effect of several commercial disinfectants on the infectivity of infectious laryngotracheitis virus was studied. Benzalkonium chlorides did not cause any detectable inactivation of the virus when their concentration was less than 0.001%, but at concentrations greater than 0.01% no surviving virus was detected. At 0.00015% 2,4-dichloro-meta-xylenol did not detectably inactivate virus, while no virus survived in the presence of 0.01% of the compound. In the presence of 1% skim milk, ten times as much disinfectant was needed to inactivate the same amount of virus. An anthelmintic and an anti-histomonad had no detectable effect on virus infectivity at concentrations of 0.32% and 0.025% respectively. The significance of the findings in relation to vaccination of poultry against infectious laryngotracheitis via drinking water is discussed.     

REPLICATION OF INFECTIOUS LARYNGOTRACHEITIS VIRUS IN CHICKENS FOLLOWING VACCINATION

SUMMARY The site of replication of infectious laryngotracheitis vaccine virus (ILTV) was studied in chickens vaccinated by drinking water (DW), intraconjunctival (IC) and cloacal (CL) routes. The anatomical sites exposed to vaccine were determined by simulating vaccination with rhodamine red dye. Virus replication was determined by recovering virus from various organs at necropsy.
The dye simulation studies clearly demonstrated that DW vaccination did not usually expose susceptible target organs to virus while the CL and IC routes flooded susceptible organs with vaccine.
Virus replication was confined to the cloaca in CL vaccinated birds while in IC and DW vaccinated birds most replication took place in the nasal cavity. Vaccine virus did not always become established in DW vaccinated birds and its establishment did not appear to be related to the amount of vaccine these birds were exposed.
It was concluded that DW vaccination depends for its success upon the accidental contamination of the nasal cavity with vaccine virus during the act of drinking.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

An association was demonstrated between the development of clinical infectious avian encephalomyelitis (IAE), the persistence and titre of infectious avian encephalomyelitis virus (IAEV) in the brain of the chicken, the duration of detectable viraemia and the age of the chicken at the time of infection with the virus. The older the chicken at the time of infection the milder the disease, the lower the virus titre in the brain and the shorter the period of viraemia. IAEV serum neutralising antibody was produced earlier after infection in older chickens, and its detection was associated with decreasing virus titres in the brain and the cessation of detectable viraemia. Treatment of chickens with testosterone in ova, to inhibit the development of antibody synthesis, prevented the onset of age-associated resistance and testosterone treated birds were as susceptible to clinical IAE as baby chickens. The results suggested that the ability to produce IAEV serum neutralising antibody was an important component of age-associated resistance to IAE.     

SPRAY VACCINATION OF CHICKENS USING INFECTIOUS LARYNGOTRACHEITIS VIRUS

Day-old chickens were vaccinated with the SA2 strain of infectious laryngotracheitis vaccine using a coarse spray and 14-day-old chickens were vaccinated using a coarse or a fine (Turbair Vaccinair 240) spray. The Conjunctiva was the most common site of infection in all cases but this almost invariably led to involvement of the nasolacrimal ducts. Other sites in the nasal cavity were affected less frequently. The clinical consequences of infection in day-old chickens were too severe for field use but the mortality (0 to 1.4% in different experiments) in 14-day-old chickens may be acceptable in some circumstances although about 9% developed infection of the trachea. It is concluded that a less pathogenic vaccine is needed if spray vaccination with ILT is to be recommended as a routine procedure particularly for day-old chickens.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

Infectious avian encephalomyelitis virus (IAEV) maternal antibody was detected in the serum of chickens for up to 21 days following hatching. This antibody protected chickens against clinical IAE after intracerebral inoculation with van Roekel strain or oral administration of the NSW-1 strain of IAEV. Maternal antibody to IAEV also protected testosterone bursectomised chickens against the development of clinical disease. IAEV maternal antibody also influeced the pattern of virus excretion in faeces and serological responsiveness. This influence on antibody responses persisted beyond the time that IAEV maternal antibody could be detected. The importance of IAEV maternal antibody on the strategy of vaccination against IAE is discussed.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

The age of the chicken at the time of infection with infectious avian encephalomyelitis virus (IAEV) and the route of the administration of the virus had a marked effect on the development of the clinical disease. Chickens given the virus by intramuscular, intraperitoneal and oral routes exhibited a decreased susceptibility to development of clinical disease with increasing age. Irrespective of age, chickens were consistently susceptible to intracerebral inoculation of IAEV. Chickens infected with the virus at 1-, 7- and 14-days of age developed lower neutralising antibody titres to IAEV than chickens infected at 21 and 28 days. A relationship between the ability to produce specific neutralising antibody to IAEV and susceptibility to the development of clinical disease is discussed.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

Normal chickens given infectious avian encephalomyelitis virus (IAEV) orally at 1, 7 or 14 days of age developed infectious avian encephalomyelitis (IAE), whereas those dosed with the virus at 21, 28 and 35 days of age did not. Chickens in all of these age groups that had been treated with cyclophosphamide or testosterone developed clinical IAE. Intraperitoneal inoculation of IAEV immunoglobulin at the time of dosing with the virus, or 48 hours later, protected normal and immunosuppressed chickens against the onset of clinical IAE. The titre of IAEV serum neutralising antibody was found to be lower in normal chickens given the virus at 1, 7 and 14 days of age in older chickens. These results suggest a significant role for the humoral immune system in the pathogenesis of IAE and in the development of immunity to the disease.     

鸡传染性喉气管炎病毒(江苏株)的分离与初步鉴定

本研究从江苏省某养鸡场采集临床疑似鸡传染性喉气管炎(infectious laryngotracheitis,ILT)的病鸡喉头气管,接种鸡胚绒毛尿囊膜分离病毒,命名为LJS091151。以分离毒人工感染SPF鸡,于攻毒后d3出现了ILT的典型临床症状,剖检亦可见喉头气管黏膜充血肿胀、消化道空虚、黏膜充血等病理变化。根据GenBank发表的鸡传染性喉气管炎病毒(Infectiouslaryngotracheitis virus,ILT)gB、TK基因保守序列设计2对引物对分离株基因组DNA进行扩增和序列测定。序列分析表明,获得的核苷酸序列及其推导的氨基酸序列与GenBank发表的序列相似性均在99%以上,证明了分离株LJS091151为鸡传染性喉气管炎病毒。