Infectious Laryngotracheitis

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Presentation transcript:

Infectious Laryngotracheitis

Etiology Herpes virus

Epidemiology Disease common Natural host chicken Men are more sensitive More in hot seasons Animals of all ages are sensitive, but older than 6 weeks are more sensitive Three months in active exudates, 20 days in submerged, live exudate for years

Sensitive to disinfectants Transmission is via direct and indirect respiratory route The disease spreads rapidly in the poultry Poultry transmission is slower No vertical infection Incubation 3-12 days Causes significant economic loss due to the fall in egg yield and mortality in chickens

Clinical findings and macroscopic lesions Peracuet form (severe epizootic form) : Respiratory depression, oral mucus morbidity and high mortality (70%) Light enzootic form: Trachea inflammation, sinusitis, conjunctivitis, low death. Inflammation and haemorrhage is the most important finding in the conjunctiva. Mortality is low (5-10%)

AVI POX DİSEASE

Etiology The avian influenza virus (avipox virus), which is the disease-specific influenza, has paternalized adventitious pathogens (such as chicken flower virus, turkey flower virus, canary flower virus, pigeon flower virus, etc.). The chicken flower virus reproduces on the chorioallophilic membrane (CAM) of the embryonic eggs, bringing gray-white foci (pock). In addition, the embryo can produce in fibroblast and kidney cells and form cytopathic effects (CPE). The inclusion bodies (Bollinger bodies) and the virus particles (Borrel particles) in the cytoplasm of the cells that are matured can be easily seen with light microscopes (1500x magnification).

The virus resists environmental conditions, drying and some disinfectants. They can stay alive on the scar, in skin rashes, on fur and dust, and they can protect their infectivity for a long time (months, sometimes years). It has been described that some strains of poultry chicken flower viruses (chicken and pigeon flower viruses) have hemagglutination ability. It was found that the chicken flower virus was able to withstand phenol (1%) and formalin (0.1%) for up to 9 days, and 50oC. 30 min. and 60 ° C. 8 min was reported to be inactive.

Epidemiology Infection can be found in almost every season - deaths can go up to over 50%. If there are parasitic, bacterial, viral, latent, or chronic infections in the animals, deaths resulting from disease may be even greater. Young people are more susceptible to infection. More males can be observed in males than females (especially in those who are fighting). Viruses can easily enter and initiate infection from lesions that occur in skin and mucous membranes. Cracks, hard foods, scratches, microscopic and macroscopic lesions at the end play an important role at the entrance of the virus into the body and at the exit of the infection.

Up to now more than 60 species of wild flowers have been reported flower disease. Contagion is usually caused by direct contact with the in-body portraits or by dusts, droplets, very thin fur, etc. with aerogenes on the ground. In addition, viruses, wind, wild birds, insect flies and insects, etc., can be transported away and spread the infection. Infected pigeons can infect and infect the virus with their viruses through viruses in flower lesions found in food borrows, crops and phyla, while feeding their offspring.

Clinical Findings 1) Skin form (cutaneous form): It is a flower form that grows in the appearance of small lesions and bubbles in the face, comb, beard, mouth and eye of chickens, hairless areas of the body. Significant clinical manifestations can not be observed in the mild forms of the disease and at the beginning. However, reductions in egg production and growing strains can be noticed. As the lesions grow and the numbers increase, they become weak and deaths become severe (in severe form).

2) Diphteric form: lesions in this form of the disease are more commonly found in mucous membranes. Mouth, tongue, pharynx, food conduit, larynx, crayfish, trachea yellow, necrotic pseudomembranes develop. These also grow over time and can merge with each other. These membranes are held with a pencil, and when they are removed, the bleeding surfaces come out. These lesions also cause weakness, wheezing and difficult breathing, asphyxia, and deaths in animals because they prevent nourishment and breathing.

Diagnosis 1) Clinical and necropsy findings : Lesions that develop in flower disease, skin and mucous membranes may be sufficient to diagnose the disease. However, some bacterial (CRD, infectious cirrhosis, chronic cholera, infectious sinusitis, etc.), viral (ILT, IB, ND, etc.), fungi (moniliasis, aspergillosis, . 2) Laboratory examinations: a) Microscopy b) Virus isolation c) Serologic tests d) Biotechnological methods e) Animal experiment

Treatment Because flower disease is a viral infection, it can not be treated with antibiotics. However, broad-spectrum antibiotics can be used to prevent bacterial contamination and secondary infection.

Protection and Control Biosecurity Vaccination