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Overview of Avian Metapneumovirus

(Turkey rhinotracheitis, Avian pneumovirus, Swollen head syndrome)

By Silke Rautenschlein, DVM, PhD, Clinic for Poultry, University of Veterinary Medicine-Hannover

Avian metapneumovirus (aMPV) causes turkey rhinotracheitis, an acute respiratory tract infection of turkeys. It is also associated with swollen head syndrome in broilers and broiler breeders, as well as egg production losses in layers. The virus was first detected in turkeys in South Africa in the late 1970s and has spread to all the major poultry-producing areas in the world except for Australia. aMPV has been detected not only in chickens and turkeys but also in pheasants, Muscovy ducks, and guinea fowl. Geese, most other duck species, and possibly pigeons are suggested to be refractory to disease. Epidemiologic studies provide evidence for the circulation of aMPV in wild birds, especially water-associated species. Some outbreaks have been attributed to vaccine-derived viruses, which may persist for several months in the environment. Infection with aMPV is often complicated by secondary bacterial infections, leading to high economic losses. In 2001 the first human metapneumovirus (hMPV) was isolated and classified as a member of the genus Metapneumovirus, which causes respiratory infections in people. Experimental studies suggest that turkeys also may be susceptible to hMPV. Complete genome sequencing confirmed that the genomic organization of hMPV is similar to that of aMPV. Overall, little is known about the cross-species pathogenicity of these two viruses.


aMPV is a member of the family Paramyxoviridae and of subfamily Pneumovirinae, which consists of the genus Pneumovirus (including the human and bovine respiratory syncytial viruses) and the genus Metapneumovirus. Currently the genus Metapneumovirus comprises aMPV and hMPV.

Isolates of aMPV are grouped in subtypes A to D. The sequence of the attachment glycoprotein (G protein) can be used to subtype different strains. Based on the phylogenetic analysis of F protein sequences, it was suggested that the European subtypes A, B, and D are all more closely related to each other than to subtype C. More recently, aMPV subtype C isolates were also identified in pheasants in Korea and water-associated bird species in Europe. The latter was shown to be of a different genetic lineage than the USA subtype C isolates. Irrespective of the differences within subtype C, isolates of this subtype display a higher amino acid sequence homology to hMPV than to European aMPV subtypes A, B, and D.

Transmission and Epidemiology:

The spread of aMPV appears to depend on the poultry population density, standard of hygiene, and biosecurity. Within or between poultry flocks, aMPV may spread rapidly horizontally by direct contact or by contact with contaminated material. aMPV is assumed to be highly contagious. The enveloped virus is rapidly destroyed after release from the host to the environment. Because aMPV affects mainly ciliated epithelial cells of the upper respiratory tract, transmission is most likely to be airborne, especially by aerosol. But ciliated cells of the reproductive tract and possibly macrophages also may be target cells of aMPV. Metapneumovirus subtype C was isolated from eggs of experimentally infected SPF turkeys, but it was suggested that the vertical route may be short-lived and may play only a minor role in viral transmission.

Birds appear to shed aMPV for only a few days after infection. This short period of shedding suggests that there is no latency or carrier status under experimental conditions. There is evidence that on farms aMPV may persist for longer periods. Reconvalescent flocks may be repeatedly reinfected with aMPV within one fattening period.

Clinical Findings:

aMPV induces an acute, highly contagious infection of the upper respiratory tract of turkeys and chickens. The disease affects all age groups, although younger birds seem to be more susceptible. In fattening turkeys the upper respiratory tract is predominantly affected, while in laying hens only a mild respiratory infection with a drop in egg production and egg quality has been seen. Coughing associated with lower respiratory tract involvement may lead to prolapses of the uterus in laying turkeys.

Typical respiratory signs in young turkeys include serous, watery nasal and ocular discharge; frothy eyes; and conjunctivitis. At later stages, signs include mucopurulent, turbid nasal discharge; plugged nostrils; swollen infraorbital sinuses; and snicking, sneezing, coughing, or tracheal rales. These respiratory signs are accompanied by depression, anorexia, and ruffled feathers.

The incubation period is 3–7 days, and morbidity in birds of all ages may reach 100%. Mortality may be 1%–30% depending on age and constitution of the flock as well as secondary infections. Birds without secondary infections with good constitution may recover within 7–10 days. However, in birds with secondary infections and under poor management, the disease may be prolonged and exacerbated by airsacculitis, pericarditis, pneumonia, and perihepatitis.

Infection in chickens and pheasants is less clearly defined and may not always be associated with clinical signs. aMPV is associated with swollen head syndrome in chickens. This condition is characterized by swelling of the peri- and infraorbital sinuses, frothy eyes, nasal discharge, torticollis, and opisthotonos due to ear infection. Typically, <4% of the flock is affected, although respiratory signs may be widespread. Mortality is rarely >2%. In broiler breeders and commercial layers, egg production and quality are frequently affected.


Macroscopic lesions depend on the course of infection, especially on secondary bacterial infections, and are most prominent on days 4–10 after infection. Gross lesions induced after experimental infection are due to rhinitis, tracheitis, sinusitis, and airsacculitis. Infected birds may be free of gross lesions. Serous to turbid mucus may be observed in the nasal cavity, nasal turbinates, trachea, and in infraorbital sinuses. During the course of infection, the secreted mucus turns from clear and serous to turbid and purulent. Nonspecific signs of inflammation, such as swelling and hyperemia of the mucosa and excessive mucus, can be seen in the upper respiratory tract and in the air sacs. If secondary bacterial infections are present, copious inflammatory exudates are found in the respiratory tract. In addition, pneumonia, pericarditis, perihepatitis, splenomegaly, and hepatomegaly are seen. In the reproductive tract of laying turkeys, lesions can include egg peritonitis, ovary and oviduct regression, folded shell membranes in the oviduct, and misshapen eggs. Microscopic examination of the upper respiratory tract, including the secondary bronchi during the first 2 days after aMPV infection, reveals loss of cilia, increased glandular activity, congestion, and mild mononuclear infiltration of the submucosa. The most pronounced microscopic lesions are found in the mucosa or the nasal turbinates, which may be the most suitable tissue for microscopic evaluation and diagnosis of aMPV infection. Harderian glands and lacrimal glands may also show infiltration of lymphocytes and formulation of lymphoid follicle-like structures in the interstitial tissue and around the secondary collecting ducts.


Obtaining samples from the upper respiratory tract of birds in the early stages of the disease is extremely important when attempting virus isolation. Especially in broiler-type chickens, samples should be taken before the sixth day after infection. Once clinical signs are obvious, the isolation of replicating aMPV may not be successful. The most suitable samples for aMPV detection are tracheal and choanal swabs. Tracheal organ cultures prepared from turkey or chicken embryos, or 1- to 2-day-old chicks, are the most sensitive for primary isolation of aMPV. Ciliostasis may occur within 7 days of aMPV A and B but not subtype C inoculation or after passages. The virus has also been isolated after the inoculation of 6- to 8-day-old embryonated chicken or turkey eggs via the yolk sac route and identified by electron microscopy, virus neutralization test, or molecular techniques. Cell cultures have not proved successful for the primary isolation of the virus. However, once the virus has been isolated and adapted in the systems above, it will grow in a variety of avian and mammalian cultures.

Reverse transcriptase PCR (RT-PCR), as well as real-time RT-PCR, tests targeting the F, N, or G gene of aMPV have been developed and are widely used to detect the virus in clinical material, particularly respiratory swabs. Some nested RT-PCR tests have been constructed so that the subtype as well as the identity of virus can be determined from the clinical sample. Based on the growing amount of genome sequence data and access to sequencing techniques, detailed characterization and molecular differentiation of isolated aMPV strains is commonly done. Antigen detection tests have also been developed, including immunofluorescence and immunoperoxidase assays on both fixed and unfixed tissues.

Because of difficulties in isolation and identification of aMPV, serologic assays have been developed to confirm infection in commercial chickens and turkeys. A number of commercial ELISA kits are available and are commonly used, but other techniques, including virus neutralization and indirect immunofluorescence tests, have also been used. Both acute and convalescent serum samples should be submitted for analysis. Although ELISA systems that use either subgroup A or B strains as antigens detect antibodies to both of these subgroups because of some cross-reactivity, the homologous antigen should be used for the efficient detection of subgroup C. The subtype specificity of the applied test may result in limited or no detection of other subtypes or new emerging aMPV strains that do not cross-react.

Paramyxoviruses (particularly Newcastle diseaseand paramyxovirus 3 (see Newcastle Disease and Other Paramyxovirus Infections), infectious bronchitis virus (see Infectious Bronchitis), and influenza viruses (see Avian Influenza) may cause respiratory disease and egg production problems in chickens and turkeys that closely resemble aMPV infection. These viruses can be differentiated on the basis of morphology, hemagglutinating and neuraminidase activity, and molecular characteristics. A wide range of bacteria and Mycoplasma spp can cause signs very similar to those of aMPV. These agents are frequently present as secondary opportunistic pathogens and may mask the presence of the aMPV.

Prevention and Treatment:

Good management practices can significantly reduce the severity of infection, especially in turkeys; in particular, optimal ventilation, stocking densities, temperature control, litter quality, and biosecurity have a positive influence on the outcome of the disease. Some success in reducing disease severity by controlling secondary bacterial infections with antibiotics has also been reported.

Both live and inactivated vaccines are available for immunization of chickens and turkeys and are widely used in countries where the disease is endemic. Maternal antibodies do not provide sufficient protection against aMPV infection and do not interfere significantly with vaccination. Thus, a vaccination program should plan for the first immunization as soon as possible after hatching. It is crucial to achieve a homogenous state of immunization per flock and farm by application of an adequate vaccine dose to all birds.

Live vaccines, which may be applied by spray or drinking water in the field, stimulate both local respiratory and systemic immunity, and cross-protection between subtypes may occur. But live vaccines may induce only short-lived protection, especially for grow-out of toms, because of the fast decline of local immunity. Thus, repeated revaccination of turkeys is common practice. There is, however, a risk of reversion of the live vaccine stains to more virulent variants. Inactivated aMPV vaccines are often used for booster immunization of layer and breeder flocks after priming with live vaccines. While inactivated vaccines alone induce only partial protection against aMPV infection, the most efficient and long-lasting protection is achieved by a combined prime-boost vaccination program. This program comprises repeated priming with live attenuated vaccines and booster immunization with inactivated adjuvanted vaccines. As experimentally shown, in ovo vaccination may also be a promising strategy for effective, early induction of an immune response. Besides live attenuated and classical inactivated vaccines, some genetically engineered viruses, including recombinant vectored vaccines, have been designed and tested under experimental conditions. These have induced partial protection and need further development.