Aberrant Mesenteric Migration of Spirocerca lupi Larvae Causing Necrotizing Eosinophilic Arteritis, Thrombosis, and Intestinal Infarction in Dogs.

This report presents a novel canine condition in 32 dogs in which aberrant migration of Spirocerca lupi larvae through mesenteric arteries, instead of gastric arteries, led to small or large intestinal infarction. This form of spirocercosis was first recognized in Israel in 2013 and is currently ongoing. Typical clinical signs were anorexia and weakness of 3 to 4 days and, less frequently, vomiting and diarrhea, followed by collapse, bloody diarrhea, and severe vomiting. Exploratory laparotomy showed 1 or more infarcted and often perforated intestinal segments in all cases. Microscopically, there was intestinal mucosal to transmural coagulative necrosis and mesenteric multifocal necrotizing eosinophilic arteritis, thrombosis, hemorrhage, and early fibroplasia. Third-stage S. lupi larvae were identified by morphologic features in 9 of 32 (28%) cases, and the species was confirmed by polymerase chain reaction in 4 cases. Nearly 50% of the dogs had been receiving prophylactic therapy, which did not prevent this form of spirocercosis.

[Secondary vasculitis to infection by Fasciola hepatica]. / Vasculitis secundaria a infección por Fasciola hepática.

There is a case of a 38 year-old male patient coming from an area where hepatic fascioliasis is endemic in Peru. He was hospitalized because he showed 4 weeks of symptoms like fever, intense myalgias, erythematous and painful injuries on limb extensions. The electromyography and nerve conduction velocity showed a global inflammatory myopathy. A skin biopsy showed polyarteritis nodosa-type vasculitis. During the evaluation process prior to the immunosuppressive therapy, hepatic Fasciola eggs were found in the parasitological examination of stools. The fascioliasis diagnosis was confirmed by fas2-ELISA: 0.46 (VN <0.20). Clinical symptoms started to subside after treatment with ticlabendazol. Contact with the patient was maintained for a year and there was no evidence of disease recurrence, and he was asymptomatic.

Vasculitis secundaria a infección por Fasciola hepática / Secondary vasculitis to infection by Fasciola hepatica

Se presenta el caso de un paciente varón de 38 años, procedente de una zona endémica para fascioliasis hepática en el Perú. Fue hospitalizado por presentar un cuadro de cuatro semanas de evolución; con fiebre, mialgias intensas, lesiones eritematosas y dolorosas en las regiones de extensión de las extremidades. La electromiografía y la velocidad de conducción nerviosa mostraron una miopatía inflamatoria global. La biopsia de piel evidenció una vasculitis de tipo poliarteritis nodosa. En el proceso de evaluación previa a la terapia inmunosupresora, se hallaron huevos de Fasciola hepática en el examen coproparasitológico. El diagnóstico de fascioliasis se confirmó con fas2-ELISA: 0,46 (VN <0,20). El cuadro clínico remitió luego del tratamiento con ticlabendazol. Se mantuvo contacto con el paciente durante un año y no se evidenció recurrencia de la enfermedad, manteniéndose asintomático.

There is a case of a 38 year-old male patient coming from an area where hepatic fascioliasis is endemic in Peru. He was hospitalized because he showed 4 weeks of symptoms like fever, intense myalgias, erythematous and painful injuries on limb extensions. The electromyography and nerve conduction velocity showed a global inflammatory myopathy. A skin biopsy showed polyarteritis nodosa-type vasculitis. During the evaluation process prior to the immunosuppressive therapy, hepatic Fasciola eggs were found in the parasitological examination of stools. The fascioliasis diagnosis was confirmed by fas2-ELISA: 0.46 (VN <0.20). Clinical symptoms started to subside after treatment with ticlabendazol. Contact with the patient was maintained for a year and there was no evidence of disease recurrence, and he was asymptomatic.

Canine leishmaniasis associated with systemic vasculitis in two dogs.

Two cases of canine leishmaniasis associated with systemic necrotizing vasculitis are described. The main macroscopic lesions were haemorrhagic in type; histopathological changes confirmed a vascular lesion affecting small arteries of several organs (skin, intestinal tract, kidney, urinary bladder, mesenteric lymph nodes, adrenal gland, myocardium, lung, eye and choroid plexus). The presence of the parasite was confirmed with a specific immunocytochemical stain. The possibility of an immunological aetiology of the vasculitis and its classification is discussed.

Trichinosis-related polyarteritis nodosa.

During an outbreak of trichinosis, two young men--one with established trichinosis and the other with suspected infection--were found to have clinical, radiologic and histologic stigmata of a systemic necrotizing vasculopathy equivalent to classic polyarteritis nodosa. The parasitosis manifested as a pentad of fever, myalgias, facial edema, eosinophilia and hyperimmunoglobulinemia E. Features of the arteritis included mononeuritis multiplex, pain in the abdomen and joints, weight loss, hypertension, leukocytosis, thrombocytosis, microhematuria and raised alkaline phosphatase levels. A sustained remission was achieved by the administration of thiabendazole, prednisone and cyclophosphamide. Pathogenetic links between the two diseases are presented: (1) deposition of circulating immune complexes in the vessel wall; (2) adjuvant activity with cross reaction between parasitic antigen and human vessel wall; (3) immunoglobulin E (IgE) aggregates and soluble antigen IgE complexes precipitation in vessel wall; and (4) hypereosinophilia-induced tissue damage. A causal relationship of trichinosis to polyarteritis nodosa is persuasive, and we suggest that cases of hepatitis B surface antigen (HBsAg) negative polyarteritis nodosa, especially those in which myalgias and eosinophilia are prominent, may be related to trichinosis and that, conversely, patients with trichinosis and multiorgan disease should be studied for polyarteritis nodosa.

[Polyarteritis nodosa: general aspects and occurrence in domestic animals, particularly in association with nosematosis in blue foxex (author's transl)]. / Polyarteritis nodosa: generalle aspekter og forekomst hos husdyr, spesielt i forbindelse med nosematose hos blårev

A survey of polyarteritis nodosa in domestic animals is presented, including a description of the patho-morphological lesions and a discussion on the causal factors. This vascular disease occurs in domestic animals in association with both viral infections (infectious plasmacytosis in mink), bacterial infections (erysipelas in swine), and protozoan infections (nosematosis in blue foxes). The conclusion is drawn that the observations in domestic animals support the view that immunological disturbances are involved as pathogenetic mechanisms. Nosematosis is dealt with in more detail; the infecting agent (fig. 1), Nosema cuniculi (Encephalitozoon cuniculi), is a widespread mamalian parasite, which causes cerebral and renal lesions in blue foxes of the same type as in animals of other species. In addition, the vascular system throughout the body is affected, resulting in patho-morphological alterations corresponding to classical polyarteritis nodosa (Fig. 2). In the early stages of involvement, masses of parasitic organisms are regularly found within the walls of affected arteries (Fig. 3). This disease is frequently lethal, and always accompanied by elevated values of gamma globulins. Both the hypergammaglobulinemia and the tissue lesions, seem at times, at least in part, to be reversible.