130 -140 day old laying hensThirty hens were submitted for post mortem examination with a history of respiratory distress and high mortality from a flock of 25,000. During a high wind storm the roofs of 2 houses were damaged; numerous birds were outside and intermixing of birds from both houses occurred.
There was severe, catarrhal, hemorrhagic tracheitis.Â Caseous casts were present in the tracheas of several birds.Â Four had caseous plugs lodged in the larynx.
Trachea: The lumen contains large amounts of necrotic cellular debris (fig.Â 2-1), fibrin and mats of bacterial colonies.Â The mucosa has diffuse erosion to ulceration of psuedostratified epithelium and formation of large, angular multinucleate syncytia (fig.Â 2-2) within the mucosa and within sloughed luminal debris.Â Within syncytia, many nuclei contain large, eosinophilic nuclear inclusion bodies (fig.Â 2-3) that marginate chromatin.Â The submucosa is moderately expanded by congested blood vessels and dense lymphocytic infiltrates (fig.Â 2-4).
Diffuse, severe, necrotizing and catarrhal tracheitis with syncytia formation and nuclear inclusions (Infectious Laryngotracheitis)
No significant bacterial pathogens were culture.
PCR for Newcastle's Disease Virus (NDV) and Avian Influenza virus (AI) were negative.Â PCR for Infectious Laryngotracheitis virus (ILT) was positive.
Infectious laryngotracheitis (ILT) is a disease primarily of chickens caused by Gallid herpesvirus 1 , an alphaherpesvirus.Â The disease was first described in 1925 and was the first major avian viral disease for which an effective vaccine was developed.Â It has a worldwide distribution, causing the most characteristic signs in adult laying hens.Â Natural routes of infection are upper respiratory and ocular, although oral transmission can occur.Â Viral replication in limited to respiratory tissues.Â The trigeminal ganglion is the principle site of latency.Â LTV can persist as latent infections in recovered birds, and virus can be re-excreted in birds under stress.Â The virus may also persist as endemic infections in backyard and fancier chicken flocks.
Clinical signs vary from severe epizootic forms (as in this case) to mild endemic forms.Â Coughing, gasping and expectoration of blood-stained mucus characterize severe forms; mild forms show unthriftiness, decreased egg production nasal discharge and hemorrhagic conjunctivitis.Â Severe forms have high morbidity (90 -100%); mortality usually ranges from 10 -20%.Â Endemic forms have low morbidity and mortality.Â Although antigenically homogeneous, different virus strains with differing virulence have recently been differentiated by PCR-RFLP techniques5.Â Differential diagnoses for respiratory disease in chickens include the diphtheritic form of avian pox, NDV, AI, infectious bronchitis, fowl adenovirus infections and aspergillosis.
The most consistent gross lesions of ILT are in the larynx and trachea.Â In mild cases, the only lesions may beconjunctivitis, sinusitis and mucoid tracheitis.Â In severe forms, diphtheritic changes can be striking, consisting of mucoid casts along the entire length of the trachea.Â Mucoid plugs in the larynx (as seen in this case) are also common.Â In some cases, hemorrhage predominates.Â Histologicaly, early lesions consist of loss of goblet cells and mononuclear inflammation.Â As the lesions progress, respiratory epithelial cells loose cilia, enlarge and form multinucleate syncytia.Â Nuclear inclusion bodies are present only in early stages (1 - 5 days).Â Confirmatory diagnostic procedures include viral isolation on embryonated chicken eggs, serology and PCR.Â Control of the disease in laying flocks is generally by vaccination, whereas tight biosecurity and a shorting growing cycle will often make vaccination of broiler flocks unnecessary.Â Vaccines are usually modified live virus, and mixing of flock with different immunity levels can cause disease outbreaks.Â In this case, birds from a non-vaccinated house were mixed with vaccinated birds, causing a disease outbreak.Â Newer deletion mutant vaccines are underdevelopment that will not only provide a safer ILT vaccine but show promise as vector vaccines for other avian infectious diseases, such as AI 1.
Trachea: Tracheitis, necrotizing,
subacute, diffuse, moderate, with epithelial syncytia, intranuclear
inclusion bodies, and intraluminal serocellular
coagulum, chicken (Gallus domesticus), avian.
The contributor gives an excellent
overview of Infectious Laryngotracheitis (ILT).
Chickens and pheasants are the only natural hosts, although
isolation from peafowl and experimental infection
of turkeys has been described.1
Ultrastructural features are those of a typical herpes virion and include a DNA-containing core within a 100nm icosahedral capsid surrounded by a variably sized proteinaceous tegument layer and an outer envelope with incorporated viral glycoproteins.1 The viral glycoproteins appear as fine spikes projecting from the surface of the envelope.2 Viral particle sizes vary between 200- 350nm depending on the amount of incorporated tegument protein.1
Tegument proteins are common in enveloped viruses and are usually a combination of essential and non-essential proteins that are released shortly after viral entry into the cell.Â These proteins may aid in suppression of the immune response, suppression of host mRNA transcription, or transcribing/translating viral genes.Â Formation of tegument proteins is generally done late in the viral infectious cycle, following replication of viral genes.3
Viral replication of ILT is similar to that of other alphaherpes virus.1,2 Within the infected cell nucleus, viral capsids are formed and filled with viral DNA.Â These nucleocapsids are then enveloped by the inner nuclear membrane and deenveloped by the outer nuclear membrane when transported into the cytoplasm.1 Within the cytoplasm the capsids associate with an electron dense tegument and are enveloped by a second budding event in the trans-Golgi region.Â The mature virus particles are then released by exocytosis.1
A list of common veterinary alpha-herpesviral infections is included in table 2-1.4
Table 2-1.Â Alphaherpesviruses4
1.Â Fuchs W, Veits J, Helferich D, Granzow H, Teifke JP, Mettenleiter TC: Molecular biology of avian infectious laryngotracheitis virus.Â Vet Res 38:261-279, 2007.
2.Â Guy JS, Bagust TJ: Laryngotracheitis.Â In: Diseases of Poultry, ed.Â Saif YM, 11th ed., pp.Â 121-131.Â Iowa State Press, Ames, IA, 1997
3.Â Yeung BJ, McHamstein HY, McHamstein M: Herpes simplex virus tegument Protein V1 elucidation and formation around the nucleocapsid.Â J Virol 28:1262-1274, 2007
4.Â Murphy FA, Gibbs EPJ, Horzinek M, Studdert MJ: Herpesviridae.Â In: Veterinary Virology, 3rd ed., pp.Â 301- 325.Â Academic Press, San Diego, CA, 1999
5.Â Kirkpatrick NC, Mahmoudian A, Colson CA, Devlin JM, Noormohammadi AH: Relationship between mortality, clinical signs and tracheal pathology in infectious laryngotracheitis.Â Avian Pathol 35:449-453, 2006
6.Â Sellers HS, Garcia M, Glisson JR, Brown TP, Sander JS, Guy JS: Mild infectious laryngotracheitis in broilers in the southeast.Â Avian Dis 48:430-436, 2004