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IdentityTop of page
Preferred Scientific Name
- infectious laryngotracheitis
Other Scientific Names
International Common Names
- English: avian infectious laryngotracheitis; avian infectious laryngotracheitis; avian laryngotracheitis
OverviewTop of page
Gallid herpesvirus 1, better known as infectious laryngotracheitis virus (ILTV), is a member of the genus Iltovirus, subfamily Alphaherpesvirinae of the family Herpesviridae (Davison et al., 2009). ILTV is a pathogen of the respiratory tract of poultry, producing peracute, subacute and chronic or mild disease outbreaks (Guy and Garcia, 2008). All ages of poultry are susceptible to infection, and mortalities in peracute outbreaks may exceed 50%. Respiratory signs predominate, although decreased egg production may also occur in layers. Virus persists in a latent state in recovered birds, being shed intermittently. Where the virus is present, management often relies on the use of live attenuated vaccines. Vaccinal strains also establish latency and can be subsequently shed. Vaccinal strains have the potential to revert to virulence, and vaccinated and non-vaccinated birds should therefore not be mixed.
The distribution section contains data from OIE's WAHID Interface database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Hosts/Species AffectedTop of page
ILTV is predominantly a pathogen of chickens (Bagust and Guy, 1997). Although all ages are susceptible, the most characteristic signs of disease are seen in adult birds. Disease has also been reported in pheasants and peafowls (Cranshaw and Boycott, 1982). Experimentally induced infection of young turkeys has also been reported associated with an age-related resistance (Winterfield and So, 1968). Other species, including closely related galliforms are refractory to infection.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||NULL||OIE, 2000a; OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease not reported||NULL||OIE, 2000a; OIE, 2009|
|Bangladesh||Disease not reported||OIE, 2009|
|Bhutan||No information available||OIE, 2009|
|Brunei Darussalam||No information available||OIE, 1996; OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Restricted distribution||NULL||GenChen et al., 1997; OIE, 2009|
|-Hong Kong||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Georgia (Republic of)||Last reported||1990||OIE, 2000a; OIE Handistatus, 2005|
|India||Disease not reported||NULL||OIE, 1997; OIE, 2009|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Disease not reported||2000||OIE, 2000a; OIE, 2009|
|Iraq||Disease not reported||OIE, 2009|
|Israel||Disease not reported||2005||OIE, 2000a; OIE, 2009|
|Japan||Present||NULL||OIE, 2000a; OIE, 2009|
|Jordan||Disease not reported||1991||OIE, 2000a; OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||OIE Handistatus, 2005|
|Korea, Republic of||Disease not reported||20050214||OIE, 2000a; OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||NULL||OIE, 1999; OIE, 2009|
|Laos||No information available||OIE, 2009|
|Lebanon||Present||NULL||OIE, 2000a; OIE, 2009|
|Malaysia||Disease not reported||200705||OIE, 2000a; OIE, 2009|
|-Peninsular Malaysia||Disease not reported||OIE, 1996; OIE Handistatus, 2005|
|-Sabah||Last reported||2002||OIE, 2000a; OIE Handistatus, 2005|
|-Sarawak||Reported present or known to be present||OIE, 2000a; OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Nepal||Disease not reported||2004||OIE, 1997; OIE, 2009|
|Oman||Disease not reported||OIE, 2009|
|Pakistan||No information available||NULL||OIE, 2000a; OIE, 2009|
|Philippines||Present||NULL||OIE, 2000a; OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||No information available||NULL||OIE, 1998; OIE, 2009|
|Singapore||Disease not reported||1989||OIE, 2000a; OIE, 2009|
|Sri Lanka||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Syria||No information available||OIE, 2009|
|Taiwan||Reported present or known to be present||Chang et al., 1997; OIE Handistatus, 2005|
|Tajikistan||Disease not reported||OIE, 2009|
|Thailand||Disease not reported||2004||OIE, 2000a; OIE, 2009|
|Turkey||No information available||OIE, 2009|
|Turkmenistan||No information available||OIE Handistatus, 2005|
|United Arab Emirates||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Uzbekistan||Reported present or known to be present||OIE, 1996; OIE Handistatus, 2005|
|Vietnam||No information available||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||1989||OIE, 2000a; OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2009|
|Burkina Faso||No information available||NULL||OIE, 1999; OIE, 2009|
|Burundi||No information available||OIE Handistatus, 2005|
|Cameroon||Reported present or known to be present||OIE, 2000a; OIE Handistatus, 2005|
|Cape Verde||No information available||OIE, 1997; OIE Handistatus, 2005|
|Central African Republic||No information available||OIE Handistatus, 2005|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||No information available||OIE Handistatus, 2005|
|Côte d'Ivoire||Disease not reported||OIE Handistatus, 2005|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||Disease not reported||1991||OIE, 1996; OIE, 2009|
|Eritrea||Disease not reported||200702||OIE, 2000a; OIE, 2009|
|Ethiopia||Disease not reported||OIE, 2009|
|Gabon||Disease not reported||NULL||OIE, 1997; OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||No information available||NULL||OIE, 2000a; OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||No information available||OIE, 2009|
|Lesotho||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Libya||Disease not reported||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||NULL||OIE, 1996; OIE, 2009|
|Mauritius||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Morocco||No information available||NULL||OIE, 2000a; OIE, 2009|
|Mozambique||Disease not reported||NULL||OIE, 1998; OIE, 2009|
|Namibia||Disease not reported||2007||OIE, 2000a; OIE, 2009|
|Nigeria||No information available||OIE, 2009|
|Réunion||No information available||OIE Handistatus, 2005|
|Rwanda||No information available||OIE, 2009|
|Sao Tome and Principe||CAB Abstracts data mining||OIE, 1999; OIE Handistatus, 2005|
|Senegal||No information available||NULL||OIE, 2000a; OIE, 2009|
|Seychelles||Disease not reported||OIE Handistatus, 2005|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||Disease not reported||200804||OIE, 2000a; OIE, 2009|
|Sudan||Disease never reported||OIE, 2009|
|Swaziland||Disease not reported||OIE, 2009|
|Tanzania||No information available||NULL||OIE, 1996; OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease not reported||1998||OIE, 2000a; OIE, 2009|
|Uganda||Absent, reported but not confirmed||NULL||OIE, 2000a; OIE, 2009|
|Zambia||Disease not reported||OIE, 2009|
|Zimbabwe||Disease never reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Present||NULL||OIE, 2000a; OIE, 2009|
|-New Brunswick||Present||Alexander et al., 1998|
|-Ontario||Present||Alexander et al., 1998|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Present||NULL||OIE, 2000a; OIE, 2009|
|USA||Restricted distribution||NULL||OIE, 2000a; OIE, 2009|
|-Delaware||Present||Keeler et al., 1993|
|-Georgia||Present||Andreasen et al., 1990|
|-Maryland||Present||Keeler et al., 1993|
|-North Carolina||Present||Guy, et al., 1989|
|-Pennsylvania||Present||Keller et al., 1992|
|-Virginia||Present||Keeler et al., 1993|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease not reported||OIE Handistatus, 2005|
|Costa Rica||Present||NULL||OIE, 1998; OIE, 2009|
|Cuba||Disease not reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||Disease never reported||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||Disease never reported||OIE, 2009|
|Jamaica||Disease not reported||OIE, 2009|
|Martinique||No information available||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||No information available||OIE, 2009|
|Saint Kitts and Nevis||No information available||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Reported present or known to be present||OIE Handistatus, 2005|
|Argentina||Restricted distribution||NULL||OIE, 2000a; OIE, 2009|
|Bolivia||Absent, reported but not confirmed||NULL||OIE, 1996; OIE, 2009|
|Brazil||Disease not reported||OIE, 2009|
|Chile||Present||NULL||OIE, 2000a; OIE, 2009|
|Colombia||Disease not reported||200703||OIE, 2000a; OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease not reported||OIE, 2009|
|Guyana||Disease not reported||OIE Handistatus, 2005|
|Paraguay||Disease not reported||OIE, 1996; OIE Handistatus, 2005|
|Peru||Present||NULL||OIE, 1996; OIE, 2009|
|Uruguay||Present||NULL||OIE, 2000a; OIE, 2009|
|Venezuela||Disease not reported||OIE, 2009|
|Albania||No information available||OIE, 2009|
|Andorra||No information available||OIE Handistatus, 2005|
|Austria||No information available||OIE, 2009|
|Belarus||Disease not reported||200502||OIE, 2000a; OIE, 2009|
|Belgium||Disease not reported||200709||OIE, 2000a; OIE, 2009|
|Bosnia-Hercegovina||Disease not reported||OIE Handistatus, 2005|
|Bulgaria||Disease not reported||1994||OIE, 1998; OIE, 2009|
|Croatia||Disease never reported||OIE, 2009|
|Cyprus||Disease not reported||2004||OIE, 2000a; OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Present||NULL||OIE, 2000a; OIE, 2009|
|Estonia||Disease not reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|France||No information available||NULL||OIE, 2000a; OIE, 2009|
|Germany||Present||NULL||OIE, 2000a; OIE, 2009|
|Greece||Disease not reported||2000||OIE, 2000a; OIE, 2009|
|Hungary||Disease not reported||20080304||OIE, 2000a; OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||1997||Graham et al., 2000; OIE, 2009|
|Isle of Man (UK)||Disease not reported||OIE Handistatus, 2005|
|Italy||No information available||NULL||OIE, 2000a; OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|Luxembourg||Disease not reported||NULL||OIE, 2000a; OIE, 2009|
|Macedonia||No information available||OIE, 2009|
|Malta||Disease not reported||2004||OIE, 1999; OIE, 2009|
|Moldova||Last reported||1992||OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Netherlands||Present||NULL||OIE, 2000a; OIE, 2009|
|Norway||Disease not reported||2005||OIE, 2000a; OIE, 2009|
|Poland||No information available||NULL||OIE, 1997; OIE, 2009|
|Portugal||Disease not reported||200801||OIE, 2000a; OIE, 2009|
|Romania||Disease not reported||1999||OIE, 2000a; OIE, 2009|
|Russian Federation||Disease not reported||2006||OIE, 2000a; OIE, 2009|
|Serbia||No information available||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||No information available||NULL||OIE, 1999; OIE, 2009|
|Sweden||Present||NULL||OIE, 2000a; OIE, 2009|
|Switzerland||Present||NULL||OIE, 2000a; OIE, 2009|
|UK||Present||NULL||Hughes et al., 1991a; Graham et al., 2000; OIE, 2009|
|-Northern Ireland||Reported present or known to be present||OIE Handistatus, 2005|
|Ukraine||Disease not reported||2004||OIE, 2000a; OIE, 2000b; OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease not reported||OIE Handistatus, 2005|
|Australia||Present||NULL||OIE, 2000a; OIE, 2009|
|Cook Islands||Present||OIE, 1997|
|French Polynesia||Present||OIE, 2009|
|Guam||Reported present or known to be present||OIE, 2000a|
|Kiribati||Reported present or known to be present||OIE, 1998|
|New Caledonia||Disease not reported||NULL||OIE, 1996; OIE, 2009|
|New Zealand||Present||NULL||OIE, 2000a; OIE, 2009|
|Samoa||Disease not reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE, 2000a; OIE Handistatus, 2005|
PathologyTop of page
In the peracute form, postmortem changes are largely confined to the upper respiratory tract, with haemorrhagic tracheitis and blood clots and blood stained mucus in the lumen of the trachea (Tripathy, 1998; OIE, 2000b). In some birds, pneumonitis and air sacculitis may also be seen.
In the subacute form of the disease, postmortem findings are less severe, with mucoid exudate, possibly containing blood, being present in the trachea. Caseous yellow diptheritic membranes may be present on the mucosa of the larynx and upper trachea.
In the chronic/mild form, diptheritic and caseous necrotic plaques and plugs in the trachea, larynx and mouth are the predominant lesions. The sequence of histopathological changes that occurs in the trachea following infection begins with loss of cilia from, and enlargement of, epithelial cells accompanied by the disappearance of mucus glands. Syncytial formation in the mucosal epithelium with development of intranuclear type A inclusions occurs, with hyperaemia and congestion of the lamina propria and associated infiltration of lymphocytes and macrophages. This is followed by connective tissue proliferation and stratification of epithelium, with sloughing of epithelial cells into the lumen. Haemorrhage may also be evident. The luminal exudate additionally contains heterophils, macrophages, mucus, fibrin, cellular debris and erythrocytes. In more chronic stages, the tracheal mucosa may be replaced by a fibrinonecrotic membrane. In the lungs, lesions of bronchointerstitial pneumonia may be present. These include congestion and interstitial oedema with infiltration of macrophages and lymphocytes. Sloughing of the mucosa, syncytial formation with intranuclear inclusion bodies, and luminal exudate may be seen in the bronchi. Syncytial formation with intranuclear inclusion bodies may also occur in conjunctival mucosa (Jordan, 1966; Linares et al., 1994; Abbas and Andreasen, 1996).
DiagnosisTop of page
Clinical signs of coughing and gasping with bloody nasal discharges are highly suggestive of ILT in peracute cases. The respiratory signs in subacute and chronic/mild cases are less characteristic, but the presence of coughing and gasping is again suggestive of ILT.
Whilst not in itself diagnostic for ILT, the presence of haemorrhagic tracheitis is highly suggestive of this diagnosis.
ILT, particularly in the subacute and mild forms, needs to be differentiated from a number of other respiratory pathogens. These include infectious bronchitis virus, avian rhinotracheitis virus, influenza A virus, paramyxovirus type 1, fowlpox virus, fowl adenovirus, Aspergillus spp. and avian mycoplasmosis.
Laboratory diagnosis is based on isolation of ILTV, demonstration of the presence of virus, viral proteins, viral DNA or inclusion bodies, or the detection of virus-specific serum antibodies (OIE, 2000b; Guy and Garcia, 2008).
The polymerase chain reaction and other approaches to the amplification of DNA/RNA are being used increasingly for ILT diagnosis. In addition to being very sensitive and not requiring prior isolation and growth of the virus in vitro, these techniques provide DNA that can be analysed to provide additional information to identify strains and to help put them into epidemiological and phylogenetic contexts (Guy and Garcia, 2008). Multiplex PCRs have been developed to detect ILTV and other avian viruses simultaneously (Tadese et al., 2007; Rashid et al., 2009; Mahmoudian et al., 2011) whilst real-time PCRs permit quantification of ILTV (Callison et al., 2007) and provide DNA for restriction-fragment analysis (Creelan et al., 2006) or sequencing. PCR can also be used to detect ILTV in formalin-fixed, paraffin-embedded tissues (Humberd et al., 2002). Real-time PCRs have also been developed using minor groove binder technology (Corney et al., 2010; McMenamy et al., 2011) and compared with a loop-mediated isothermal amplification assay (Ou et al., 2012). PCRs are also used for purity testing of avian viral vaccines (Ottiger, 2010).
Virus isolation may be performed on the dropped chorio-allantoic membrane (CAM) of 10-12 day old embyronated fowl eggs or on monolayered cultures of chicken embryo liver (CEL), chicken embryo kidney (CEK), chicken embryo lung (CELu) or chicken kidney (CK) cells. Of these, CEL and CK have been shown to be the most sensitive for primary isolation (Hughes and Jones, 1988). Virus replication in CAMs results in the production of characteristic pocks, whilst in cell cultures a characteristic syncytial cytopathic effect develops. Definitive confirmation of the isolation of ILTV may be made by electron microscopy, immunofluorescent staining, or virus neutralisation. Appropriate samples for virus isolation include tracheal swabs or tissue in transport medium containing antibiotics or tracheal tissue. Virus isolation is sensitive but requires appropriate facilities and may be time consuming, with samples in some cases requiring multiple passage before yielding a positive result.
Electron microscopy (EM) can be used to demonstrate the presence of virus particles in tracheal scrapings or exudate. EM is relatively insensitive compared to virus isolation, requiring 103.5/0.1ml of infectious virus (Hughes and Jones, 1988). However, it is a rapid test and has the advantage of not being unduly hindered by the presence of bacterial contamination or other viruses (Williams et al., 1994).
Immunofluorescent or immunoperoxidase staining of viral proteins may be performed either directly or indirectly using specific polyclonal or monoclonal antibodies. Tests may be performed on acetone-fixed tracheal scrapes or cryostat sections. The same methodology may be used to confirm the identity of viral isolates. Although both tests are typically less sensitive than virus isolation, they are quick to perform, giving a result in a matter of hours. Immunoperoxidase staining may be more sensitive than immunofluoresence, and has the added advantage of not requiring fluorescent microscope facilities (Guy et al., 1992; Abbas and Andreasen, 1996).
Agar gel immunodiffusion (AGID) may also be used to detect virus directly in tracheal samples, or alternatively in infected CAMs or cell cultures following initial amplification in the laboratory. Lines of precipitation (reactions of identity) are observed between a central well containing hyperimmune antiserum and peripheral wells containing ILTV antigen. AGID is relatively cheap and straightforward to perform, but is less sensitive than isolation techniques (York and Fahey, 1988) due to the greater amount of virus required to yield a positive result.
Antigen-capture enzyme-linked immmunosorbent assay (ELISA) may also be used to detect ILTV (York and Fahey, 1988). ELISA tests are relatively straightforward to run, and have the advantage of giving a result within a matter of hours. Sensitivity is reported to be comparable to virus isolation.
The observation of classical Cowdry type A intranuclear inclusion bodies in epithelial cells on histological examination of haematoxylin and eosin-stained tracheal sections may be used to diagnose ILT (OIE, 2000b). However, the reading of histology is a specialised task and requires the availability of appropriate facilities for preparation and cutting of sections. While the specificity of histopathology is high, the sensitivity tends to be low relative to virus isolation (Guy et al., 1992; Abbas and Andreasen, 1996).
Immunology and Serology
Following infection, serum antibody responses appear five to seven days post infection, peak around two weeks later and wane slowly thereafter. Detection of specific ILTV antibodies therefore provides indirect evidence of infection. Serological tests based on virus neutralization (VN), indirect immunofluorescence (IFA), AGID and ELISA have been described. In a comparative study, VN, IFA and ELISA were found to have comparable performance, with AGID less sensitive, although still satisfactory on a flock basis (Adair et al., 1985).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|General Signs / Discomfort, restlessness in birds||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Increased mortality in flocks of birds||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Sign|
|General Signs / Oral cavity, tongue swelling, mass in mouth||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Head shaking, headshaking||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Pain / Discomfort Signs / Pain, pharynx, larynx, trachea||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Poultry:Mature female||Sign|
|Reproductive Signs / Soft, thin egg shell||Poultry:Mature female||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Diagnosis|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Diagnosis|
|Respiratory Signs / Coughing, coughs||Diagnosis|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Diagnosis|
|Respiratory Signs / Haemoptysis coughing up blood||Diagnosis|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Respiratory Signs / Sneezing, sneeze||Diagnosis|
Disease CourseTop of page
Infectious laryngotracheitis (ILT) is a respiratory disease, principally of the upper respiratory tract. Following natural infection, disease signs appear in 6-12 days (Jordan, 1966). Peracute, subacute and chronic (or mild) forms of the disease may occur (Tripathy, 1998; OIE, 2000b). The peracute form is characterised by sudden onset and rapid spread with high morbidity. In such outbreaks, mortality may exceed 50% (Jordan, 1966). Affected birds show characteristic clinical signs associated with respiratory distress. Birds may sneeze, gasp or cough, sometimes producing clots of blood. Gurgles, rattles and rales may be heard due to tracheal obstruction.
In the subacute form, morbidity is again high, but mortalities are typically lower, varying from 10% to 30%. The spread of disease and the development of clinical signs occurs more slowly, with respiratory signs observed for some days before deaths occur. Affected birds may also show conjunctivitis with associated lacrimation and swelling of the infra-orbital sinuses. The chronic/mild form of ILT may be seen subsequent to peracute and subacute outbreaks or as a distinct disease entity. Mortality rates are typically 1-2%, with losses occurring over a period of months. Affected birds may be unthrifty, with bouts of gasping and coughing accompanied by nasal or oral discharges. A considerable drop in egg production may also be seen in laying birds (Jordan, 1966).
EpidemiologyTop of page
ILTV is primarily a pathogen of fowl, although natural infection has also been reported in pheasants and peafowl (Cranshaw and Boycott, 1982). Turkey poults may also be infected experimentally (Winterfield and So, 1968). All ages of fowl are susceptible to infection, with disease having been reported in broilers, pullets and layers in birds from eight days to four years of age (Kingsbury and Jungherr, 1958; Jordan, 1966; Linares et al., 1994).
Infection with both field and vaccinal strains of ILTV results in a carrier state characterized by latency in the trigeminal ganglia interspersed with brief periods of spontaneous virus shedding over an extended period of time (Bagust, 1986; Hughes et al., 1987; Hughes et al., 1991b; Williams et al., 1992). Natural stress factors including re-housing, mixing and the onset of lay are recognised factors that will trigger recrudescence and shedding of latent virus (Hughes et al., 1989).
ILTV may be transmitted directly by contact with other fowl that are shedding virus, or indirectly. Of particular importance in relation to direct transmission is the mixing of vaccinated and non-vaccinated naïve fowl. Recrudescence and shedding of vaccinal virus under such conditions leads to infection of susceptible fowl. Although vaccinal strains of virus are of low virulence, serial passage of such strains through a susceptible population can produce highly virulent virus within six to ten passages (Guy et al., 1990; Guy et al., 1991; Kotiw et al., 1995). Indirect transmission of the virus may be effected by movements of people or equipment from farm to farm and by mechanical transmission by vermin, scavenging birds, or dogs in the absence of adequate disinfection, hygiene and biosecurity (Kingsbury and Jungherr, 1958; Jordan, 1966). In regions of intensive production, ILTV is usually well controlled by vaccination in commercial fowl, but may persist in backyard and fancier flocks (Bagust and Guy, 1997).
Impact: EconomicTop of page
Given that mortalities may exceed 50% (Jordan, 1966), ILT outbreaks can obviously have a significant economic impact. However there are little definitive data available on the cost of such outbreaks.
Zoonoses and Food SafetyTop of page
There is no evidence that ILTV is transmissible to humans or other mammals; it is not considered to be a food safety issue (Guy and Garcia, 2008).
Disease TreatmentTop of page
There are no effective means of treatment available for ILT. However, where a diagnosis is made early in the course of an outbreak, administration of vaccine may help reduce further morbidity and mortality (Kingsbury and Jungherr, 1958).
Prevention and ControlTop of page
Immunization and Vaccines
In regions with intensive poultry industries, ILT is often effectively controlled by the use of vaccines (Guy and Garcia, 2008). Typically, these are modified live vaccines containing virus strains that have been attenuated by serial passage in tissue culture (tissue culture origin [TCO] vaccines) or embryonated fowl eggs (chick embryo origin [CEO] vaccines) (Guy et al., 1990; Chang et al., 1997). Inactivated ILT vaccines are not used due to the high cost of production and application (Guy and Garcia, 2008). Recombinant viral vector vaccines against ILT are commercially available in some countries e.g. USA.
Vaccines given in the face of an outbreak will reduce virus spread and shorten the duration of disease (Bagust and Guy, 1997). In common with wild type virus, modified live vaccines are capable of establishing latent infections which may be followed by intermittent reactivation and shedding. Serial passage in susceptible birds can then lead to reversion to virulence, particularly in CEO vaccines (Guy et al., 1991), and vaccinal strains of virus have been implicated in many disease outbreaks (Guy et al., 1989; Guy et al., 1990; Keller et al., 1992; Chang et al., 1997; Graham et al., 2000). For this reason, modified live vaccines should not be used in regions where ILTV is not already present. The replication and transmissibility of two CEO ILT vaccines has been studied by experiment by Coppo et al., (2012a, b). Typically vaccines are given by eye drop to fowl at around four weeks of age, with revaccination of replacement birds at sixteen to twenty weeks of age. Vaccine needs to be stored and reconstituted properly to ensure that each bird receives an adequate dose of virus.
Commercially available virus vector vaccines for ILT based on herpesvirus of turkeys (HVT) and fowl poxvirus (FPV) have been developed and applied as they have advantages over modified live ILT vaccines; they are not transmitted from bird to bird, do not establish latent infections, and do not revert to virulence. The HVT-LT vaccine contains the ILTV genes for glycoproteins D and I, whilst the FPV-LT vaccine contains the ILTV genes encoding glycoprotein B and membrane-associated protein (Vagnozzi et al., 2012). The protection induced by these vector vaccines has been compared with that induced by live modified vaccine. Vagnozzi et al. (2012) reported that the vector vaccines, applied in ovo and subcutaneously, provided partial protection, and partially reduced clinical signs and virus replication in the trachea. The HVT-LT vaccine was more efficacious than the FPV-LT vaccine.
Husbandry Methods and Good Practice
Maintenance of adequate biosecurity is a prerequisite to preventing the introduction of ILTV onto poultry production sites (Guy and Garcia, 2008). Site quarantine and disinfection procedures should be used to prevent the introduction of virus on fomites such as clothing and personnel, vehicles, feed and equipment. The fabric of buildings should be maintained so as to prevent ingress of wild birds, and effective rodent and dog control protocols should be in place. Record keeping should be such as to prevent the possibility of vaccinated and non-vaccinated birds being mixed. Direct or indirect contact between commercial poultry and backyard or fancier flocks should be avoided. In the event of an outbreak, dead birds should be disposed of immediately, for example by burning or burying. Survival of the virus in the environment is variable, being influenced by a number of factors including dose, pH, temperature and exposure to light, but virus is considered readily inactivated by disinfectants and warm temperatures (Jordan, 1966; Bagust and Guy, 1997).
Cooperation between government and industry can facilitate effective control of outbreaks (Bagust and Guy, 1997), allowing rapid diagnosis, introduction of vaccination and initiation of biosecurity and movement controls to minimise further spread.
ReferencesTop of page
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