Cutaneous papillomavirus infection was diagnosed in a 6-year-old female Boxer dog that was under long-term corticosteroid therapy for atopic dermatitis. Multiple black, rounded papules were present on the ventral skin. Spontaneous regression occurred within 3 weeks after cessation of corticosteroids. Histologically, the lesions consisted of well-demarcated cup-shaped foci of epidermal endophytic hyperplasia with marked parakeratosis. In the upper stratum spinosum and in the stratum granulosum, solitary or small collections of enlarged keratinocytes were observed with basophilic intranuclear inclusion bodies and a single eosinophilic fibrillar cytoplasmic inclusion, Ultrastructurally, viruslike particles (40-45 nm in diameter) were observed within the nucleus, free or aggregated in crystalline arrays. Undulating fibrillar material, thought to be a modified keratin protein, was observed in the cytoplasmic inclusion. Immunohistochemistry, restriction enzyme analysis, and molecular hybridization experiments indicated that these distinctive clinical, histologic, and cytologic features were associated with a novel canine papillomavirus.

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

Chronic hypertrophic gastritis, proliferative gastritis, or hyperplastic gastritis are generic terms in dogs for rare conditions characterized by a marked thickening of gastric rugae due to mucosal hyperplasia. The lesions may predominantly involve the mucosa of the body of the stomach, as in Menetrier’s disease in human beings,14 or the antral mucosa, as the name antral pyloric hypertrophy syndrome implies4 Similar gastric lesions have been seen as isolated findings, in Zollinger-Ellison syndrome, as part of the gastrointestinal disease affecting Basenji dogs and dogs with mast cell tumors.’ The causes are unknown; however, immune or hormonal disorders, environmental factors, and genetic predispositions may be involved in the pathogenesis.

A raised, hairless cutaneous nodule was found incidentally at necropsy of a 24-month-old CD1 mouse. Histologically there was infiltration of the epidermis by a monomorphic population of moderate to large lymphocytoid cells. Many large cells had bizarre convolutions of the nuclear membrane and resembled the so-called Sézary or mycosis cells seen in epidermotropic T-cell proliferative disorders. The pattern of cutaneous involvement and the presence of the large cells with convoluted nuclei is characteristic of pagetoid reticulosis. No previous reports of such cutaneous lymphoid neoplasms in mice were found in an extensive literature search.

Lymphomatoid granulomatosis is a rare human disease that has been recently reported in young dog^.',^.^.^ Lymphomatoid granulomatosis, as originally described in human beings by Liebow et al.,5 is an angiocentric and angiodestructive lymphoreticular proliferative and granulomatous disease that predominantly involves the lungs. Pathologically, it is a peculiar angiocentric lymphoid lesion with a lymphomalike appearance (lymphomatoid) in some areas and necrosis (granulomatosis) in others. The proliferative infiltrate is composed of atypical lymphoreticular cells admixed with variable proportions of lymphocytes, plasma cells, and histiocytes. A clinically normal, 8-month-old, male Beagle was not included in drug safety studies owing to a persistent eosinophilia (3.2-4.2 103/mm3). The dog was euthanatized at 15 months of age as a result of a sudden deterioration of its condition: a marked abdominal enlargement, a 3.7 kg increase in body weight during the last 2 weeks, and severe respiratory problems, including coughing. At necropsy, the abdomen contained about 2.5 liters of a clear fluid; the liver was congested. The accessory lobe of the right lung was enlarged (1 2 x 13 cm), firm, and pale yellow. The overlying pleura was smooth and dull. Cut sections revealed coalescing multinodular pale tissue centered around bronchi that compressed the remaining lung peripherally. Grey or dark-red patches were scattered throughout all lobes. A white, firm tissue replaced the markedly enlarged tracheobronchial lymph nodes (5 x 3 cm) and was found focally in the sternal lymph node. Other organs were unremarkable. Tissues were fixed in 10% neutral buffered formalin, routinely processed to paraffin sections, and stained with hematoxylin and eosin, and Gomori's trichrome stain with Weigert's stain for elastin fibers. Sections were stained immunocytochemically by the peroxidase anti-peroxidase technique using rabbit anti-bovine S100 protein (Dakopatts, Issy-les-Moulineaux, France) with a silver amplification (Amersham, Les Ulis, France), and by peroxidase-labeled protein A (New England Nuclear, Paris, France) with trypsinization, using goat anti-human a1 -anti-trypsin, goat antihuman lysosyme followed by a rabbit anti-goat immunoglobulin G (Nordic, Le Perray en Yvelines, France). For negative controls, duplicate sections were incubated with normal, nonimmune rabbit or goat serum instead of the primary antibody. Lymph node and brain were used as positive controls. Formalin-fixed portions of the accessory lobe of the right lung were divided into 1 mm3, 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. U1trathin sections were stained with uranyl acetate and lead citrate and examined with a Zeiss EM109 electron microscope. Microscopically, the tumor was composed of sheets of dense infiltrates of atypical pleomorphic lymphoid cells that obliterated normal structures (Fig. 1). Most cells were polygonal to oval and had a faintly basophilic, moderately abundant cytoplasm. Nuclei varied from rounded to slightly elongated. Chromatin was predominantly stippled and occasionally coarse. Many cells had up to four round amphophilic nucleoli. There were atypical vesicular or cleft nuclei. Scattered binucleated cells were present. The fine fibrovascular stroma was predominantly infiltrated by eosinophils, fewer plasmocytes, and occasional Mott cells. Individual cell necrosis was observed throughout the tissue. No immunoreactivity for lysozyme, a-I-antitrypsin or S-100 protein was seen in tumor cells. Many large blood vessels were infiltrated by pleomorphic lymphoid cells and eosinophils. Their centers were occupied by a variously-shaped fibrous tissue that delineated vascular channels and was connected to the fibrous wall that merged with the surrounding stroma (Fig. 2). They had no elastic lamina. There were occasional epithelial remnants of airways and necrotic foci up to 3 mm in diameter. The overlying pleura was thickened and fibrotic. Sections at the margins of the tumor revealed that the process originated from pulmonary arteries and compressed adjacent airways (Fig. 3). The intimae of some affected pulmonary arteries were thickened by edema, fibrosis, eosinophils, and atypical lymphoid cells. Histologic lesions of allergic bronchitis3 with a few, small, foreign-body granulomas corresponded to the patches seen at necropsy in the other lobes. Blood vessels in these areas were spared. The sternal lymph node was multifocally invaded by tumor cells. Histologic liver changes were consistent with acute passive congestion. Heart, kidney, spleen, thyroid, and muscle were unremarkable. Ultrastructurally, tumor cells lacked intercellular junctional complexes and pericellular basement membrane material (Fig. 4). A limited amount of cellular interdigitations was observed. Nuclei were ovoid or variably folded and had large, often multiple, nucleoli. The cytoplasm contained moderately abundant profiles of granular endoplasmic retic-

Cardiotoxicity is often a limiting factor in doxorubicin (D) treatment (Herman 1981). D causes damage in several cellular components such as mitochondria, cell membranes, lysosomes, and myofibrils (Buja et al. 1973). In order to diminish the cardiotoxicity of D, several compounds have been coadministered. However, results have been inconsistent (Rabkin et al. 1983; Wikman-Coffelt et al. 1983), partly because the extent of cardiac damage is not quantified in detail. As part of a more systematic approach, the quantification of cardiac damage induced by D was attempted using histochemistry and morphometry.

Wheat-germ lectin peroxidase conjugate was used to stain the liver of normal rats and rats given α-naphthylisothiocyanate (ANIT). Changes in patterns in bile duct and canalicular staining were compatible with the hypothesis that cell damage caused by ANIT is essentially restricted to bile ducts.

The ultrastructural features of a spontaneous malignant fibrous histiocytoma and three malignant histiocytomas in Sprague-Dawley rats are described. The ultrastructural features of the malignant histiocytomas (or histiocytic sarcomas) support origin from cells of the monocyte series. The histogenesis of more fibrous tumors (fibrous histiocytomas) remains uncertain.