Granulomatous enteritis in a dromedary (Camelus dromedarius) due to green algal infection.

Abstract

In mammals, infections caused by unicellular algae are rare, and most have been due to the achlorophyllous microorganisms Prototheca spp. Pathogenicity of green algae in animals was first recognized in 1973 by Cordy, who reported a case of necrotizing hepatitis in ~ h e e p . ~ Since then, the infection has been recognized in slaughtered and sheep2+’ by incidental lesions involving predominantly the retropharyngeal lymph nodes in cattle and the liver and the hepatic lymph nodes in sheep. Subcutaneous infections in a beaver’ and in a woman6 have also been described. Characteristically, the macroscopic lesions are green. Although definitive specific identification of the etiologic agents has thus far been hampered by the absence or inconclusiveness of cultural studies, these organisms are considered to belong to the genus Chlorella, order Chlorococcales, based on their morphologic appearance and life cycle.* Recently, Zakia et a1.10 reported the first documented case of chlorellosis in Sudan, which occurred in a sheep that presented the typical distribution of lesions for this species. This report describes another case of green algal infection that occurred in Sudan. This is the first report of such an infection in a camel and the first associated with granulomatous enteritis in any species. An 8-year-old female one-humped camel (Camelus dromedarius), weighing approximately 4 10 kg, was slaughtered at Gedarif abattoir, Sudan, after a history of persistent chronic diarrhea. At necropsy, which was performed immediately after death, macroscopic findings were limited to the gastrointestinal tract and consisted of irregular areas of green mucosal discoloration along the distal part of the ileum (over 50 cm from the ileocecal junction), the cecum, and the proximal half of the right colon (Fig. 1). The mucosal folds were markedly thickened and had scattered circular ulcers. The mesenteric lymph nodes were enlarged and green, especially those located at the ileocecaljunction. The liver was normal. Sections of ileum and colon were fixed in 10% neutral buffered formalin, processed routinely in an automatic tissue processor, embedded in paraffin, sectioned at 4-6 pm, and stained with hematoxylin and eosin (HE), periodic acid-Schiff (PAS) with and without diastase, Gridley fungus (GF), GOmori methenamine silver (GMS), and Ziehl Neelsen methods. Deparaffinized replicate sections were examined by the fluorescent antibody (FA) technique for the presence of Prototheca wickerhamii and Prototheca zopjii9 at the Centers for Disease Control in Atlanta, Georgia, (USA). For electron microscopic examination, 1 -mm3 formalin-fixed samples were immersed in 2.5% glutaraldehyde in 0.1 M phosphate buffer (pH 7.37), post-fixed in 2% osmium tetroxide, and embedded in epoxy resin. Semithin sections were stained with toluidine blue, and ultrathin sections were stained with uranyl acetate and lead citrate and examined with a Zeiss EM109 electron microscope. Microscopically, the intestines were variously affected. More severe lesions were characterized by a marked thickening of the mucosa and submucosa (Fig. 2), which were