Respiratory diseases Flashcards
Respiratory organs
Nasal cavity and sinuses- infra-periorbital sinus Larynx Trachea Bronchi Lungs Air sacs
Avian metapneumoviral diseases
avian rhinotracheitis, ART, TRT, SHD
Pathogen of the 3 diseases:
• Paramyxoviridae, Pneumovirinae, Metapneumovirus genus
• avian pneumovirus - A, B, C (Colorado), D (France) serotype
• Infection:
– direct contact with the virus shed in the nasal and tracheal discharge
– aerogenous way, aerosol inhalation
Avian metapneumoviral diseases
(avian rhinotracheitis, ART, TRT, SHD)
Pathogenesis
• Pathogenesis:
– virus 1st replicate in the epithelial cells of the airway– very fast replication cycle
– the replication induces increased mucus production in the air ways
• 1st the microvilli & cilia disappear, later the epithelial cells degenerate too=>necrotized cells detach and mix into the respiratory discharge (serous-catarrhal)
– epithelial layer of the air ways is destroyed
-secondary infection
Viral inflammation of the air ways occur
• hyperaemia, hemorrhages, exudation
• epithel necrosis, large amount of mucus
– serous-catarrhal inflammation
– sneezing, snuffling, nasal discharge
– lacrimation, laboured breathing
• some birds suffocate from the production of thick inflammatory mucous exudate in the air ways
HEAD:
• accumulation of sero-mucus discharge in the infra-, intra- & periorbital sinuses
– in the subcutaneous CT surrounding the sinuses perifocal edema develops=> swelling and enlargement of the head
– Swollen Head Disease in chickens
• after replication cycles in the air ways VIRAEMIA occurs!!!
– lethargy, emaciation, ruffled feathers
– serous, sero-fibrinous (!!) exudate in the body cavity
• If no complications=> the respiratory epithelial layer regenerates rapidly
– there is still excess mucus production for some time
– Viscous discharge from the choanas can obturate the airways
– Because of suffocation the pectoral muscles are often markedly pale
Avian metapneumoviral diseases
Predisposing factors
Predisposing factors needed for severe clinical symptoms to develop – overcrowding – bad microclimate – exhausted animals due to production – other infectious agents • adult (layer-)flock • decrease in egg production – it gets back to normal after few weeks • the color of the layed eggs is lighter than before – it gets back to normal after few weeks
Pathology of the bronchi
• Developmental anomalies • Circulatory disturbances • Regressive changes • Proliferative changes • Inflammations (different forms) –Diseases with bronchitis • Accomodation – Vitamin A deficiency • Parasites – Syngamus tracheae
Infectious bronchitis of chicken
Pathogen
coronavirus (Nidovirales, Coronaviridae)
• RNA, rounded-oval (irregular, pleomorph) with helical symmetry
• on it’s capsid - 20 nm sized spike peplomers (solar-corona)
• around 120 nm in diameter
– chicken and pheasant susceptible
Resistance of the virus: low (easily prevented)
• after infection the survived birds shed the virus
– for 1 month from the respiratory tract
– for 3-5 months with feces & urine
• Infection:
– mainly aerogenous • aerosol, dust in the air
– or per os • contaminated feed or water
The virus is not uniform
– besides Massachusetts and Connecticut strains
– Other strains exist: 4/91, 793B, D274, D1466, QX-virus
• Virus variants
– different virulence
– different affinity (airways, kidneys, genitals)
• The chicken is susceptible in all age
– disease in day-old
– disease in broilers
– disease in adults
Infectious bronchitis of chicken
Pathogenesis
Main feature of the disease:
– 1st virus replicates in the respiratory tract (same with metapneumovirus)
– viraemia follows
– then the virus replicates in all other organs
• the viral replication cycle is very short
– 3-4 hours after infection new viral particles are produced
– 12 hours after infection the virus leaves the cells
• Different forms:
– respiratory form
• the virus replicates 1st in lower third of the trachea & the macrobronchi!!!
• then spreads towards the upper part of the trachea and nasal cavity
– urinary=> nephrosonephritis= inflammatory and regressive changes & urolithiasis
– genital=> young birds> tract won’t develop= False Layer Syndrome (degenerated follicles and oviduct
=>adult layers: decresed quality and quantity of eggs + lighter colour
– gastro-intestinal=> proventriticulis and enteritis
Infectious bronchitis
respiratory form
• the virus replicates in the cytoplasm of the epithelial cells (in the mucous membrane of the air ways) …. • degeneration of the epithelial cells, • exudation and mucus production follow • tissue debris closes the air ways • other pathogens might get activated • the basic lesions change – secondary invadors, complications
Infectious laryngotracheitis
Pathogen
• ILT
• susceptible– chicken, pheasant, turkey, peacock
Pathogen:
• Herpesviridae, Alphaherpesvirinae
• Gallid herpesvirus 1 (GaHV-1)
• the pathogen is 80-100 nm,
– hexagonal nucleocapsid
– icosahedral symmetry
– thick capsomere
– in final form huge virus - 195-250 nm
• different strains with different virulence!!!
VIRUS REMAINS IN BRID=> in trigeminal ggl
– severe and less severe diseases in flocks
– sometime almost symptomless disease
Infectious laryngotracheitis
Pathogenesis
• Infection:
– aerogenous (aerosol)
– through the conjunctiva
Pathogenesis:
– replication of the virus takes place in the epithelial
cells of the air ways and the conjunctiva
• no viraemia!!!
• The most effected air ways are:
– Larynx and the upper third of the trachea
– some lesions occur in other parts too
– the virus has cytocid effect!=> epithelial layer of the mucous membrane gets destroyed=> blood vessels reach the denudated surface
=>serum and blood leaks from the vessels=> fibrinous pseudomembranes, clotted blood in the trachea
• fibrin clots, blood cylinders
– conjunctivitis
– consequence: suffocation
• severe cases
– sick animals stand with extended neck, try to get air with open beak
• sneezing, snuffling, head shaking, conjunctivitis
• swollen hyperaemic mucous membrane with petechiae
• the eyelids are infiltrated with exudate
Infectious laryngotracheitis
• Main feature of the disease:
– the virus replicates in the air ways only
– rhinitis, laryngitis, tracheitis and macrobronchitis occur
– plus conjunctivitis
Pathology:
• in acute case
– catarrhal inflammation in the larynx and trachea
– petechiae in the mucous membrane
• later: hemorrhages and pseudomembranes are formed on the same areas
– croupous-diphteroid inflammation
Conjunctivitis
• swollen, hyperaemic mucous membrane
• petechiae
• edema of the eyelids
HISTOPATH:
– loss of cilia
– disturbances of water metabolism in the cells
– desquamation and necrosis of the epithelial cells
– intranuclear inclusion bodies!
• larynx, trachea, bronchi, conjunctiva
– infiltration of the mucous membrane by macrophages and immune cells
Infectious laryngotracheitis
sever/ chronic
• keratitis – ulceration • endophtalmitis – fibrinous-purulent • thickening of the edge of the eyelids – almond eye • mild inflammation of the infraorbital sinus
Infectious laryngotracheitis
mild
• Disease caused by the less virulent strains
– conjunctivitis, edema of the eyelids, sneezing
– mortality below 5%
– Serves as predisposing factor for other pathogens
• Clinical signs:
– the disease caused by the mild virulent strains increases the effect of other bacteria
• Mycoplasma
• Ornithobacterium
• E. coli bacteria
