Downloaded 10 times
Uploaded byRanjini Manuel
Infectious coryza/ fowl coryza
Infectious coryza, caused by Avibacterium paragallinarum, is a highly contagious upper respiratory disease in chickens characterized by nasal discharge, facial swelling, and reduced egg production, leading to significant economic losses. The disease, first diagnosed in 1931, is prevalent globally and primarily transmitted through contaminated environments, affecting all ages of chickens, with older birds showing more severe symptoms. Control measures include sanitation, biosecurity, and vaccination, with antibiotic susceptibility tests indicating resistance to certain antibiotics and sensitivity to others.
More Related Content
Similar to Infectious coryza/ fowl coryza
Infectious coryza/ fowl coryza
- 1. INFECTIOUS CORYZA FOWL CORYZA,ROUP, COLD, SWOLLEN HEAD DISEASE, WATTLE DISEASE BY RANJINI MANUEL
- 2. INTRODUCTION Highly contagious Acute disease of the upper respiratory tract of chickens – starts as acute and progresses as chronic Worldwide distribution Economic losses due to increased culling rate and reduction in egg production Limited to chickens and has no public health significance Disease is characterized by nasal discharge, facial swelling, sneezing, labored breathing and fetid odor of the exudates
- 3. HISTORY clinical syndromewas first diagnosed in 1931 by De Blieck. Since the disease proved to be infectious and primarily affected nasal passages, the name "infectious coryza" was adopted (Blackall, 1989)
- 4. HISTORY 1930’S –1960’S – causative agent – Haemophilus gallinarum It required X (haemin ) and V factor (nicotinamide adenine dinucleotide NAD) for the growth in vitro 1960- 1980’s – disease producing agent required only V factor – known as Haemophilus paragallinarum Later named to Avibacterium (Blackall et al., 2005) V factor independent H. paragallinarum was also prevalent
- 5. ETIOLOGY Avibacterium paragallinarum can be V factor dependent or independent Gram negative Non-motile Non spore forming Capsulated rod forming bacterium Microaerophilic and high humidity – promote the growth
- 6. PROPERTIES Ability toreduce nitrate to nitrite Ferment D- glucose without gas formation Inability to grow in MacConkey agar Indole negative, catalase positive, oxidase negative Do not hydrolyse urea and gelatin Organism is delicate difficult to survive outside the host- not more than 48hrs, 18-24 degrees
- 7. There aretwo serotyping schemes - page serotyping and kume serotyping Page serotyping scheme – serogroup A, B, C Kume serotyping scheme- serogroup A-1, A-2, A-3, A-4, B-1, C-1, C-2, C-3 and C-4 (Blackall et al., 1990).
- 8. EPIDEMIOLOGY World widedistribution Argentina, India, Morocco, South Africa, U.S and Thailand – common Prevalence of serotypes: Serogroups A and C have been reported in Japan, Australia Indonesia,and Malaysia In Germany, serogroups A and B have been identified Serogroup A has been reported in China (Chen et al.,1993), while serogroup C has been found in Taiwan(Lin et al., 1995). serovars A and C have been identified in India (Tongaonkar et al.,2003).
- 9. INDIA In Karnooldistrict of India, infectious coryza has been reported as the second most important bacterial disease associated with mortality after Salmonellosis (Shrinivasa et al., 1989) It has been reported as an epidemic in Madhya Pradesh. In India it is most common in areas of high altitude, Bihar plateau but may occur elsewhere in cold damp weather. (Rajurkar et al.,2009)
- 10. HOST Limited tochickens Cultured from pheasents, guinea fowls and quails All age and sex susceptible but older are more severely affected
- 11. TRANSMISSION Clinically affectedand carrier birds Direct and indirect contact Contaminated drinking water, feed, bedding material etc
- 12. PATHOGENESIS Organism adhere tocilia of URT Capsule and haemagglutinin - colonization toxins clinical signs If complicated – moves to LRT
- 13. CLINICAL SIGNS Incubationperiod – 1-3 days Clinical signs within 1-7 days If not complicated resolve within Mild – 10days Severe- 3 weeks Seromucoid nasal and ocular discharge Facial edema Severe – marked conjunctivitis with cosed eyes Swollen wattles Laboured breathing Low egg production (10-40 %)
- 14. A) Mild conjunctivitis. B)Conjunctivitis with partial closure of the eye and swelling of periorbital area and paranasal sinuses. C) & D) Conjunctivitis, eyelids closed but unbounded and obvious swelling of periorbital area and paranasal sinuses
- 16. LESIONS Catarrhal fibrinopurulentinflammation of the nasal passages Conjunctivitis Subcutenous edema of face and wattle Loss of cilia and microvilli, cell edema, degeneration and desquamation of mucosal and glandular epithelium
- 17. DIAGNOSIS Clinical signs Culture and identification Specimen- swab from sinuses, exudates, conjunctiva Swabbing the inside of the infraorbital sinus
- 18. Blood agaris used for culture After 24-48hrs – 37 degrees atm 5% carbon dioxide- presence of transluscent colonies PCR Agglutination FAT ELISA
- 19. Avibacterium paragallinarum colonies-onto agar Columbia with addition of 7% (v/v) hemolyzed horse blood – mucoid colonies
- 20. CONTROL DEPOPULATION SANITATION GOOD BIOSECURITY
- 21. DRUG THERAPY Antibioticsusceptibility pattern using six different antibiotics were carried out. All the isolates were sensitive to colistin, co-trimoxazole and cefalexin and resistant to tetracycline, ceftriaxone-tazobactam and enrofloxacin (N Sarika et al.,2018)
- 22. vaccination Currently inactivatedbivalent (serovars A-1 and C-1) or trivalent (A-1, B-1 and C-2) bacterins are used according to the incidence of serovars in different geographical regions Vaccination – inactivated sero grp specific first dose – 12- 16 weeks Second dose 3-4 weeks apart