Pulmonary adiaspiromycosis in a European hedgehog (Erinaceus europaeus) in Portugal

ADIASPIROMYCOSIS (haplomycosis) is a self-limiting pulmonary mycosis caused by the dimorphic fungi Chrysosporium parvum var crescens and C parvum var parvum (Burek 2001, Carter 2002) that occurs worldwide in small mammals (Turner and others 1999, Travis and others 2002). The disease has been reported in 124 mammal species and subspecies (Acha and Szyfres 1989) of the Carnivora, Rodentia and Insectivora (Burek 2001). The infection is widespread, especially among rodents of the Arvicolidae and Muridae families, but it rarely occurs in the Sciuridae and Cricetidae (Fischer 2001); the Mustelidae appear to be particularly susceptible to the infection (Simpson and GavierWiden 2000, Burek 2001). C parvum has also been found in dogs (Jones and others 1997, Carter 2002) and goats, and several cases of adiaspiromycosis have been reported in human beings since 1964 (Jones and others 1997). Human infection is uncommon (England and Hochholzer 1993, Turner and others 1999, Travis and others 2002), but cases have been reported in the USA, Europe, the former Soviet Union, and Central and South America (Chandler and Watts 1988). Most human infections are attributed to C parvum var crescens (Chandler and Watts 1988, Travis and others 2002), but two reports documented disseminated disease caused by C parvum var parvum in patients with AIDS (Echevarria and others 1993, Turner and others 1999). This short communication describes a case of adiaspiromycosis due to C parvum var crescens in a European hedgehog (Erinaceus europaeus). In May 2001, a young male European hedgehog was found dead in a road near Vila Real in northern Portugal. The animal was collected and submitted for postmortem examination at the Histopathology Laboratory of Tras-os-Montes e Alto Douro University. The animal was in normal body condition, weighing 638 g. Postmortem examination revealed multiple traumatic lesions in the mandible and ribs, and rupture of the abdominal wall with evisceration. The pericardial sac was ruptured. The lungs were detached from their normal anatomical position and free in the thoracic cavity. They presented multiple sites of damage, oedema, congestion and extensive haemorrhagic areas, and various grey-white, nodular, focal lesions, measuring 0·5 to 1·0 mm in diameter, were disseminated on the surfaces of both lungs. The lesions appeared to have no predilection for particular areas or lobes of the lungs. No significant abnormalities were observed in the thymus. The liver was pale and friable, and had multiple ruptures, and the spleen was also damaged. The small intestine was ruptured at four points, and its contents had spilled into the peritoneal cavity. Samples of the organs were fixed in 10 per cent buffered formalin and processed for light microscopy using standard methods. Paraffin sections (2 μm) for histological examination were stained with haematoxylin and eosin and by Grocott’s technique. Microscopically, the lung presented atelectasis, emphysema and numerous granulomatous lesions in the interstitium (Fig 1), each containing one or two spherical adiaconidia surrounded by epithelioid cells, giant multinucleated cells in a palisade arrangement, and fibrous tissue. The diameter of the fungi ranged from 119 to 285 μm. The double contour, refractile wall had a thickness of 38 to 59 μm. The outer third of the trilaminar wall was eosinophilic and refractile, and there was a non-staining layer between the outer and inner walls that appeared black with Grocott’s technique (Fig 2). The interior of the adiaconidia was either empty or contained small eosinophilic globules. The structures were consistent with descriptions of the morphology of the adiaspores of C parvum var crescens (Chandler and Watts 1988, Jones and others 1997, Burek 2001, Travis and others 2002). The hedgehog also had a verminous bronchitis. No adiaspores were observed in the regional lymph nodes. The liver showed lipidosis, and the kidney presented pigmentary nephrosis and interstitial nephritis. No significant lesions were observed in the remaining organs. Adiaspiromycotic infection is believed to occur as a result of the inhalation of dustborne spores (conidia) found in soil, which accumulate in the bronchioles and alveoli (England and Hochholzer 1993, Burek 2001, Travis and others 2002). The genus Chrysosporium consists of ubiquitous fungi, which produce 2 μm to 4 μm conidia in the saprophytic form (Simpson and Gavier-Widen 2000, Travis and others 2002). When inhaled by a mammalian host, the conidia progressively enlarge to form thick-walled spherules, designated as adiaconidia or adiaspores (Acha and Szyfres 1989, Simpson and Gavier-Widen 2000, Fischer 2001). The adiaspores of C parvum var parvum grow to up to 20 to 40 μm (Burek 2001), whereas the C parvum var crescens adiaspores have a diameter ranging from 200 to 700 μm (Chandler and Watts 1988, Simpson and Gavier-Widen 2000, Travis and others 2002). C parvum var crescens has also a broader host range and geographical distribution than C parvum var parvum (Peterson and Sigler 1998, Burek 2001). Adiaconidia seem to be incapable of replication or dissemination in the host (Chandler and Watts 1988, Travis and others 2002), yet massive infections have been observed in small mammals (Burek 2001). The disease is not contagious (Jones and others 1997), thus each adiaspore constitutes a separate infection (Simpson and Gavier-Widen 2000). The infection resembles foreign-body inhalation pneumonia, with a granulomatous reaction due to the inhaled spores (Chandler and Watts 1988, Travis and others 2002). The severity of the disease depends on the number of spores inhaled (Acha and Szyfres 1989, England and Hochholzer 1993) and the immune response of the host (Chandler and Watts 1988, Jones and others 1997). When clinical signs are present, they can be attributed to mechanical displacement of the tissues and the inflammatory reaction caused by the proVeterinary Record (2006) 158, 274-275