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The induction of antiviral effector proteins as part of a homeostatically controlled innate immune response to infection plays a critical role in limiting the propagation and transmission of respiratory pathogens. However, the prolonged induction of this immune response can lead to lung hyperinflammation, tissue damage, and respiratory failure. We hypothesized that tissues exposed to the constant threat of infection may constitutively express higher levels of antiviral effector proteins to reduce the need to activate potentially harmful innate immune defences. By analysing transcriptomic data derived from a range of human tissues, we identify lung tissue to express constitutively higher levels of antiviral effector genes relative to that of other mucosal and non-mucosal tissues. By using primary cell lines and the airways of rhesus macaques, we show the interferon-stimulated antiviral effector protein TRIM22 (TRIpartite Motif 22) to be constitutively expressed in the lung independently of viral infection or innate immune stimulation. These findings contrast with previous reports that have shown TRIM22 expression in laboratory-adapted cell lines to require interferon stimulation. We demonstrate that constitutive levels of TRIM22 are sufficient to inhibit the onset of human and avian influenza A virus (IAV) infection by restricting the onset of viral transcription independently of interferon-mediated innate immune defences. Thus, we identify TRIM22 to confer a pre-existing (intrinsic) intracellular defence against IAV infection in cells derived from the respiratory tract. Our data highlight the importance of tissue-specific and cell-type dependent patterns of pre-existing immune gene expression in the intracellular restriction of IAV from the outset of infection.

Over the last 60 years poultry production has intensified in response to increased demand for meat. In modern systems, chicks hatch without contacting chickens and their gut bacteria. Consequently, they are colonized by environmental bacteria that may cause disease. The normal bacteria that live in the gut, or intestinal microbiota, play an important role in the development of the immune system. Therefore, it is essential to find easy ways to expose chicks to the more appropriate bacteria at hatching. This experiment investigated whether spraying eggs with adult cecal contents was sufficient to transfer an adult microbiota to chicks. Our findings show that spore-forming bacteria were transplanted, but other members of the microbiota were not. In this respect, the spray application was partially successful, but the timing of the spray needs to be modified to ensure that more bacteria are transferred., The intestinal microbiota plays an essential role in the metabolism and immune competence of chickens from the first day after hatching. In modern production systems, chicks are isolated from adult chickens, instead hatching in a clean environment. As a result, chicks are colonized by environmental bacteria, including potential pathogens. There is a need to investigate methods by which chicks can be exposed to a more appropriate microbial community at hatching. Such methods must be easy to apply in a hatchery and produce consistent results. The development of the intestinal microbiota of chicks hatched from eggs sprayed with dilute adult cecal content during incubation was observed at 0, 3, 7, and 14 days posthatching (dph) across two experiments. High-throughput Illumina sequencing was performed for the V4 hypervariable region of the 16S rRNA gene. A topical treatment of dilute adult cecal content was sufficient to transplant spore-forming bacteria such as Lachnospiraceae and Ruminococcaceae. However, this treatment was not able to transplant other taxa that are considered to be core elements of the chicken cecal microbiota, such as Bacteroidaceae, Lactobacillaceae, Bifidobacteriaceae, and Burkholderiaceae. The topical treatment significantly altered the microbiota of chicks immediately posthatching and accelerated the normal development of the microbiota with earlier colonization by Ruminococcaceae in the cecum and “Candidatus Arthromitus” in the ileum. The effect of the treatment on the cecal microbiota was maximal at 3 dph but diminished over time. IMPORTANCE Over the last 60 years poultry production has intensified in response to increased demand for meat. In modern systems, chicks hatch without contacting chickens and their gut bacteria. Consequently, they are colonized by environmental bacteria that may cause disease. The normal bacteria that live in the gut, or intestinal microbiota, play an important role in the development of the immune system. Therefore, it is essential to find easy ways to expose chicks to the more appropriate bacteria at hatching. This experiment investigated whether spraying eggs with adult cecal contents was sufficient to transfer an adult microbiota to chicks. Our findings show that spore-forming bacteria were transplanted, but other members of the microbiota were not. In this respect, the spray application was partially successful, but the timing of the spray needs to be modified to ensure that more bacteria are transferred.

We hypothesized that increased expression of antiviral host factors at portals of viral entry may protect exposed tissues from the constant threat of invading pathogens. Comparative transcriptomic analysis identified the broad-acting restriction factor TRIM22 (TRIpartite Motif 22) to be among the most abundantly expressed antiviral host factors in the lung, a major portal of entry for many respiratory pathogens. This was surprising, as TRIM22 is currently considered to be an interferon stimulated gene (ISG) product that confers protection following the activation of pathogen-induced cytokine-mediated innate immune defences. Using human respiratory cell lines and the airways of rhesus macaques, we experimentally confirmed high levels of constitutive TRIM22 expression in the lung. In contrast, TRIM22 expression in many widely used transformed cell lines could only be observed following immune stimulation. Endogenous levels of TRIM22 in non-transformed cells were sufficient to restrict human and avian influenza A virus (IAV) infection by inhibiting the onset of viral transcription independently of cytokine-mediated innate immune defences. Thus, TRIM22 confers a pre-existing (intrinsic) tissue-specific immune barrier to IAV infection in the respiratory tract. We investigated whether the constitutive expression of TRIM22 was a characteristic shared by other ISGs in human lung tissue. Transcriptomic analysis identified a large group of ISGs and IAV immuno-regulatory host factors that were similarly enriched in the lung relative to other mucosal tissues, but whose expression was downregulated in transformed cell-lines. We identify common networks of immune gene downregulation which correlated with enhanced permissivity of transformed cells to initiate IAV replication. Our data highlight the importance of tissue-specific and cell-type dependent patterns of pre-existing immune gene expression in the intrinsic intracellular restriction of IAV; findings highly relevant to the immune regulation of many clinically important respiratory pathogens.Author SummaryThe respiratory tract is a major portal of virus entry for many clinically important viruses, including seasonal and pandemic influenza A virus (IAV). We reasoned that cells within the respiratory tract might differentially express antiviral host factors to protect against the constant challenge of viral infection. We found the broad-acting antiviral protein TRIM22, conventionally regarded as an interferon stimulated gene (ISG) product upregulated in response to virus infection, to be constitutively expressed to high levels in the lung. We found that constitutive expression of TRIM22 restricted the initiation of human and avian IAV infection independently of cytokine-mediated innate immune defences. We identified pre-existing tissue-specific and cell-type dependent patterns of constitutive immune gene expression that strongly correlated with enhanced resistance to IAV replication from the outset of infection. Importantly, we show that these constitutive patterns of immune gene expression are lost or downregulated in many transformed cell lines widely used for respiratory virus research. Our data highlight the importance of pre-existing tissue-specific and cell-type dependent patterns of constitutive antiviral gene expression in the intracellular restriction of respiratory viral pathogens not captured in conventional cell culture model systems of infection.

Cases of arthropod-infested, abandoned or abused animals are sometimes brought to the attention of veterinarians by animal welfare authorities, with the requirement for a full postmortem examination towards criminal or civil proceedings. In these situations, entomology is an important support tool for the pathologists' investigation since the presence of arthropod life cycle stages serve as reliable forensic markers, especially for blowflies which form the first waves of activity following death. In the present study, 70 cadavers from a total of 544 referred to the Institute of Veterinary Science, University of Liverpool, between 2009 and 2014 displayed evidence of infestation. Here, the authors introduce principles of applied entomology and simplified approaches for estimating the minimum time since death, relevant in the context of routine submissions and the broad remit of individual cases. Despite often limited availability of scene of the crime and local thermal data, the interpretation of the minimum postmortem interval has nonetheless proved valuable as an adjunct to the expert pathology report. However, future developments and enhanced accuracy in this area of animal welfare require resource and training in expertise, and agreed standardisation of both laboratory and field procedures.

The airway epithelium secretes proteins that function in innate defense against infection. Bactericidal/permeability-increasing fold-containing family member A1 (BPIFA1) is secreted into airways and has a protective role during bacterial infections, but it is not known whether it also has an antiviral role. To determine a role in host defense against influenza A virus (IAV) infection and to find the underlying defense mechanism, we developed transgenic mouse models that are deficient in BPIFA1 and used these, in combination with in vitro three-dimensional mouse tracheal epithelial cell (mTEC) cultures, to investigate its antiviral properties. We show that BPIFA1 has a significant role in mucosal defense against IAV infection. BPIFA1 secretion was highly modulated after IAV infection. Mice deficient in BPIFA1 lost more weight after infection, supported a higher viral load and virus reached the peripheral lung earlier, indicative of a defect in the control of infection. Further analysis using mTEC cultures showed that BPIFA1-deficient cells bound more virus particles, displayed increased nuclear import of IAV ribonucleoprotein complexes, and supported higher levels of viral replication. Our results identify a critical role of BPIFA1 in the initial phase of infection by inhibiting the binding and entry of IAV into airway epithelial cells.Mucosal Immunology advance online publication 17 May 2017; doi:10.1038/mi.2017.45.

Feline herpesvirus type 1 (FeHV-1) is one of the etiological agents of feline respiratory disease. FeHV-1 is an epitheliotropic and cytopathic virus that mainly causes rhinitis and conjunctivitis, although pneumonia is also occasionally seen. In this study, the authors investigated the pathogenesis of FeHV-1-associated pneumonia, comparing natural cases with viral infection of tracheal ring and cell cultures in vitro, using histology, immunohistology, double immunofluorescence, and transmission electron microscopy as investigative tools. The results confirm that FeHV-1 targets both respiratory epithelial cells and pneumocytes and indicate that FeHV-1 pneumonia is the consequence of continuous cell-to-cell viral spread from the upper airways via the trachea into the lungs. They provide strong evidence that FeHV-1–infected cells die primarily via apoptosis, following loss of cell-to-cell contact, rounding, and detachment. However, virus-induced lesions in vivo are dominated by marked neutrophil infiltration and extensive necrosis with less prominent apoptosis; in the airways, the tissue necrosis can extend into the submucosa. The necrosis appears to result from virus-induced neutrophil influx and release of proteolytic enzymes, such as matrix metalloproteinase-9, from the neutrophils.

BPIFA1 is a member the bactericidal/permeability-increasing (BPI) protein family and is structurally similar to other BPIF family members with demonstrated innate immune roles. It is produced mainly in the mammalian respiratory tract and has been implicated in airway host defense against respiratory pathogens. However, the function of this protein is yet unresolved in many species and by elucidating this will aid to clarify its physiological role within the lungs. The objective of this study was to assess BPIFA1 expression and function in the respiratory tract in response to Influenza A virus. Using BPIFA1 knockout mice, we have shown increased virus load and inflammation in the lungs of these mice infected with the X31 strain (H3N2) as compared with wild-type controls. Interestingly, there were large peri-vascular aggregations of B cells in the lungs of BPIFA1-/- mice suggesting a role of BPIFA1 in modulating antibody responses. Lung tissues from mice infected with different strains of varying pathogenicities of Influenza A virus were analysed by immunohistochemical methods at specific time points during the infection period. Imaging software was then used to quantify the level of protein expression within the respiratory epithelium. It was found that the level of BPIFA1 decreased in response to highly pathogenic H5N1 and H7N9 infections but not to low pathogenicity H5N1 or H1N1 viruses. This alteration in expression was associated with an inflammatory response within the respiratory tissue surrounding the epithelium. Our data indicate that BPIFA1 influences inflammation and possibly signals to immune cells during Influenza A virus infection.

Salmonella enterica serovar Virchow usually causes mild gastroenteritis in humans; however, it is frequently invasive and many isolates are resistant to a broad-range of therapeutic antimicrobials. Poultry meat is considered a major source of human infection. In this study, we characterize the infection biology and immune response to S. Virchow in chickens and determine protection against homologous and heterologous re-challenge, with S. Virchow or S. Typhimurium. Following oral infection of 7-day-old chickens, S. Virchow colonized the gastrointestinal tract and the spleen. Infection elicited an increase in specific IgA, IgG, and IgM antibodies and relative quantitative changes in several leukocyte populations, including CD3, CD4, CD8α, CD8β, MHC II, KuL01, and γδ TCR positive cells, both in the gastrointestinal tract and systemically. Increased expression of pro-inflammatory cytokines IL-1β and IL-6 and the chemokine CXCLi2 was also found. Primary infection with S. Virchow offered limited systemic protection against re-challenge with S. Virchow or S. Typhimurium, but no protection against cecal colonization. In conclusion, S. Virchow exhibits similar infection biology and immune responses in the chicken to that previously described for S. Typhimurium. Unlike S. Typhimurium, S. Virchow infection is poorly protective to homologous and heterologous re-challenge. These findings suggest that S. Virchow is capable of colonizing the chicken well and therefore, presents a risk of entering the food chain in meat production. Furthermore, the development of vaccines that protect effectively against S. Virchow and indeed multivalent vaccines that protect across all Salmonella serogroups in the chicken would appear to remain a challenging proposition.

Soft tissue sarcomas of the equine distal limb associated with joints, sheaths, or bursae have rarely been reported. Accurate diagnosis of these tumors is challenging in both human beings and veterinary species. Immunohistochemical staining and transmission electron microscopy have been used in human beings to reduce misdiagnosis. The current report describes 2 mature horses presenting with lameness and swelling associated with the dorsal aspect of the metacarpo(tarso)phalangeal joint. In both cases, surgical excision was performed with subsequent histological analysis of the masses to determine the tissue of origin. In both cases, immunohistochemical staining and transmission electron microscopy aided the definitive diagnosis of fibrosarcoma associated with the fetlock joints of 2 horses.

Feline calicivirus (FCV) is a pathogen of felids and one of the most common causative agents of feline upper respiratory disease (URD). Reports of natural FCV pneumonia in the course of respiratory tract infections are sparse. Therefore, knowledge on the pathogenesis of FCV-induced lung lesions comes only from experimental studies. The aim of the present study was to assess the type and extent of pulmonary involvement in natural respiratory FCV infections of domestic cats and to identify the viral target cells in the lung. For this purpose, histology, immunohistochemistry and RNA-in situ hybridisation for FCV and relevant cell markers were performed on diagnostic post-mortem specimens collected after fatal URD, virulent systemic FCV or other conditions. All groups of cats exhibited similar acute pathological changes, dominated by multifocal desquamation of activated alveolar macrophages (AM) and occasional type II pneumocytes with fibrin exudation, consistent with diffuse alveolar damage (DAD). In fatal cases, this was generally seen without evidence of epithelial regeneration. In cats without clinical respiratory signs, type II pneumocyte hyperplasia was present alongside the other changes, consistent with the post-damage proliferative phase of DAD. FCV infected and replicated in AM and, to a lesser extent, type II pneumocytes. This study shows that lung involvement is an infrequent but important feature of FCV-induced URD. AM are the main viral target cell and pulmonary replication site, and their infection is associated with desquamation and activation, as well as death via apoptosis.

MuHV-4 is a natural pathogen of rodents of the genus Apodemus (e.g., wood mice, yellow-necked mice) and Myodes glareolus (bank voles). We report experimental MuHV-4 infection of bank voles in comparison with infection of A. sylvaticus (wood mice) and BALB/c mice. Like in wood mice, the level of productive replication in the lungs of bank voles was significantly lower than in BALB/c mice. In contrast to other hosts, however, the level of latent infection in the lung and spleen of bank voles was extremely low. These findings, together with those of previous studies, suggest that bank voles are an occasional and inefficient host for MuHV-4.

Murine γ-herpesvirus 68 (MHV-68) infection of Mus musculus-derived strains of mice is an attractive model of γ-herpesvirus infection. Surprisingly, however, ablation of expression of MHV-68 M3, a secreted protein with broad chemokine-binding properties in vitro, has no discernable effect during experimental infection via the respiratory tract. Here we demonstrate that M3 indeed contributes significantly to MHV-68 infection, but only in the context of a natural host, the wood mouse (Apodemus sylvaticus). Specifically, M3 was essential for two features unique to the wood mouse: virus-dependent inducible bronchus-associated lymphoid tissue (iBALT) in the lung and highly organized secondary follicles in the spleen, both predominant sites of latency in these organs. Consequently, lack of M3 resulted in substantially reduced latency in the spleen and lung. In the absence of M3, splenic germinal centers appeared as previously described for MHV-68-infected laboratory strains of mice, further evidence that M3 is not fully functional in the established model host. Finally, analyses of M3's influence on chemokine and cytokine levels within the lungs of infected wood mice were consistent with the known chemokine-binding profile of M3, and revealed additional influences that provide further insight into its role in MHV-68 biology., Author Summary Infection of inbred strains of laboratory mice (Mus musculus) with the rodent γ-herpesvirus MHV-68 continues to be developed as an attractive experimental model of γ-herpesvirus infection. In this regard, the MHV-68 protein M3 has been shown to selectively bind and inhibit chemokines involved in the antiviral immune response, a property expected to contribute significantly to virus infection and host colonization. However, inactivation of the M3 gene has no discernable consequence on infection in this animal host. Prompted by recent evidence that natural hosts of MHV-68 are members of the genus Apodemus, and that MHV-68 infection in laboratory-bred wood mice (Apodemus sylvaticus) differs significantly from that which has been described in standard strains of laboratory mice, we addressed whether M3 functions in a host-specific manner. Indeed, we find that M3 is responsible for host-specific differences observed for MHV-68 infection, that its influence on infection within wood mice is consistent with its chemokine-binding properties, and that in its absence, persistent latent infection - a hallmark of herpesvirus infections - is attenuated. This highlights the importance of host selection when investigating specific roles of pathogenesis-related viral genes, and advances our understanding of this model and its potential application to human γ-herpesvirus infections.

We report 4 cases of equine rhinosporidiosis in the United Kingdom. These cases provide evidence of spread of infectious agents from rhinosporidiosis-endemic areas to nonendemic areas by increased international movement of livestock. Surveillance should continue for this infective agent of potential relevance for numerous species, including humans.

Rhinosporidium seeberi is the infective, waterborne agent that causes rhinosporidiosis, which commonly presents as polypoid masses of the nasal mucosa or conjunctiva in both human beings and animals (Arseculeratne and Atapattu 2004). Previously classified as a fungus, R seeberi has recently been grouped into the class Mesomycetozoa (order Dermocystida), which comprises 10 different parasitic and saprophytic microbes (Herr and others 1999). R seeberi is primarily a human pathogen, and rhinosporidiosis is predominantly seen in the tropics. The disease is endemic in southern India and Sri Lanka, and sporadic cases have been reported in Africa, the Americas and Europe (Fredricks and others 2000). Cases in the UK and other parts of Europe are rare and predominantly involve persons native to, or having travelled from, endemic areas (Mears and Amerasinghe 1992, van der Coer and others 1992). One outbreak was reported in northern Serbia (Vukovic and others 1995). Rhinosporidiosis has been reported occasionally in equids in South America (Londero and others 1977), southern USA (Smith and Frankson 1961, Myers and others 1964) and South Africa (Zschokke 1913), but also in other mammals, including cats (Moisan and Baker 2001, Wallin and others 2001), dogs (Mosier and Creed 1984, Easley and others 1986, Jimenez and others 1986), cattle (Moses and Balachandran 1987) and a pink river dolphin (Armed Forces Institute of Pathology [AFIP] 1998); it has also been reported in captive swans (Kennedy and others 1995). A surgical biopsy was taken from one of several, focally ulcerated, polypoid lesions (Fig 1) in the nasal mucosa of a six-year-old polo pony gelding recently imported from Argentina. The lesion was not associated with clinical signs. Tissue was fixed in formalin and routinely embedded in paraffin wax; 3 to 5 μm sections were stained with haematoxylin and eosin and periodic acid-Schiff (PAS). For transmission electron microscopy (TEM), fixed tissue was post-fixed in 2·5 per cent glutaraldehyde and routinely processed and embedded in epoxy resin. Semithin and ultrathin sections were examined. Multiple, 6 μm paraffin sections were treated with xylene, ethanol and proteinase K, and DNA was extracted using the DNeasy Tissue Kit, according to the manufacturer’s protocol (Qiagen). DNA extracted from the skin of an unaffected horse was used as a negative control. R seeberispecific primers for the 18S rDNA sequence was used in a 40 μl PCR, modified from Fredricks and others (2000). The PCR product was purified using the QIAquick PCR Purification Kit (Qiagen), and forward and reverse products were sequenced (Lark Technologies). Histologically, focal ulceration and multifocal hyperplasia of the nasal mucosa were seen. The mucosa and submucosa were expanded by spherical to polygonal organisms. The smaller (up to 100 μm in diameter), predominantly spherical structures had an eosinophilic and PAS-positive wall, enclosing eosinophilic to basophilic fibrillar material (juvenile sporangia; Fig 2). The larger (up to 300 μm in diameter), spherical to polygonal structures had a thin, eosinophilic wall with closely opposed basophilic stippled material and basophilic and eosinophilic ovoid structures in the central lumen (Fig 3). These are mature sporangia, containing endospores, which are known to be released via a pore (Fig 4) (Mendoza and others 1999). An intermediate stage (immature sporangia; Fig 3), in which the endospores were observed in the periphery, was also present. Surrounding these structures was a moderate, multifocal, lymphoplasmacellular, inflammatory infiltrate. Within some areas of tissue, free endospores were seen, associated with a pyogranulomatous inflammation (Fig 3). Ultrastructurally, juvenile sporangia with a nucleus, lipid bodies and laminated bodies (Fig 5), as well as mature endospores with electron-dense bodies (Fig 6) were observed. PCR yielded a product of the expected size (377 base pairs [bp]; Fredricks and others 2000), the sequences of which represented an exact match with 369 bp of the sequence for R seeberi (Herr and others 1999, Fredricks and others 2000). The diagnosis of rhinosporidiosis in this case was based on the characteristic morphological features of R seeberi (Gardiner and others 1998), and was confirmed by sequence analysis (Fredricks and others 2000). However, morphologically, fungal infections with Coccidioides immitis or Chrysosporium parvum (the causative agent of adiaspiromycosis, a rare pulmonary disorder), should be considered (Kennedy and others 1995, AFIP 1998). The natural habitat for R seeberi appears to be stagnant or lacustrine waters, although this has not been confirmed due to the failure to isolate R seeberi from such habitats (Arseculeratne 2002, 2005). It is current opinion that ‘elec

Felid herpesvirus 1 (FeHV-1) is an important feline pathogen of the upper respiratory tract which can be identified in clinical cases by virus isolation and PCR. Studies on the effect and mode of spread of FeHV-1 in the respiratory epithelium, however, have previously only been performed in infected cats. Feline tracheal organ cultures which were inoculated with FeHV-1 at varying multiplicity of infection (MOI) were established. A dose-dependent response was observed. Low MOIs induced multifocal infection in the otherwise viable respiratory epithelium, which allowed monitoring of viral growth over several days. Therefore, tracheal organ cultures represent a suitable model for further study of the morphological and functional effects of FeHV-1 on respiratory epithelium, mimicking the in vivo situation.

DERMOID sinus (also termed pilonidal sinus, pilonidal cyst or dermoid cyst) is a developmental anomaly characterised by incomplete separation of the skin from the neural tube during embryonic development (Lord and others 1957, Mann and Stratton 1966, Antin 1970). Six different types of dermoid sinus exist and classification is based on their relationship to the supraspinous ligament (Mann and Stratton 1966, Kiviranta and others 2011). This short communication describes the clinical, MRI and histopathological features of a type IV dermoid sinus and spina bifida in a young Victorian bulldog. An 11-month-old male Victorian bulldog was referred for investigation of progressive paraparesis, moderate hindlimb ataxia and moderate proprioceptive deficits in both hindlimbs. At physical examination, it was noted that the hair was growing in a spiral fashion on the dorsal midline in the mid-thoracic region. A small, fluctuating mass was palpable subcutaneously and evoked considerable pain for the dog; the mass was continuous with a firm fistulous cord attached to the underlying tissues. A round-shaped opening in the skin (diameter 0.5 cm) containing no exudates was found after clipping of the hair. Radiographs of the thoracic and thoracolumbar spine were unremarkable. MRI scans (Vet-MR Grande; Esaote) of the dog's thoracic region were obtained in three planes of orientation before and after the intravenous administration of 0.1 mmol/kg gadolinium (Magnevist; Schering). Transverse T1-weighted and T2-weighted images revealed an invagination of the epidermal and dermal tissues towards the spinous process of T8. A fistular tract was visible connecting the spinal cord with the opened skin layers. The normal morphology of T8 was lost: this vertebra lacked a normal vertebral arch and the spinous process …

EQUINE multinodular pulmonary fibrosis (EMPF) is a relatively recently described condition in horses, characterised by a loss of functional pulmonary parenchyma due to extensive nodular to coalescing interstitial fibrosis; the remaining alveoli are lined by cuboidal epithelium and are filled with inflammatory cells (Williams and others 2007). EMPF was described first in the USA (Williams and others 2007, Hart and others 2008, Wong and others 2008), but more recently has been reported in Europe, in Germany and Austria (Poth and others 2009, Niedermaier and others 2010). A strong association between EMPF and equine herpesvirus type 5 (EHV-5) has been established, although the pathogenesis of the condition is still unclear (Williams and others 2007). EHV-5 is a DNA gammaherpesvirus, which has been detected in the USA, Australia, New Zealand and Europe in nasal swabs and peripheral blood lymphocytes (PBLs) from both healthy horses and those with respiratory signs, at highly variable rates (Agius and Studdert 1994, Reubel and others 1995, Franchini and others 1997, Borchers and others 1999, Dunowska and others 1999, Nordengrahn and others 2002, Bell and others 2006, Wang and others 2007, Torfason and others 2008, Fortier and others 2009). EHV-5 has also been identified in horses in the UK, where PCR yielded a positive result in PBLs from five of 21 healthy adult horses (Nordengrahn and others 2002). This short communication describes two cases of EMPF in the UK, and their association with EHV-5. The first case, an 11-year-old thoroughbred gelding, was presented in February 2010 with a two-week history of lethargy, listlessness and an increased respiratory rate. Radiographic and ultrasonographic examinations (Fig 1a, b) revealed nodular lesions throughout both lungs. The animal was euthanased. At postmortem examination, gross findings in the lungs were consistent …

Equine herpesvirus 5 and nodular pulmonary fibrosis – literature review and case report