Histoplasma capsulatum is a dimorphic fungus growing in soils, bat guano and bird faeces (Aidé, 2009;Kauffman, 2007). Its dimorphism is induced by temperature variations during its growth phase. Histoplasma capsulatum growth involves a filamentous phase and a yeast phase, and the transition from the former to the latter entails changes in both cell form and cell wall composition. This transformation determines the virulence of dimorphic fungi such as H. capsulatum (Klein & Tebbets, 2007).Histoplasma capsulatum has three distinct variants based on morphology and geographic distribution. Histoplasma capsulatum var. capsulatum is pathogenic to humans, H. capsulatum var. duboisii causes disease in primates, and H. capsulatum var. farciminosum

Ricinus communis is a shrub of the family Euphorbiaceae popularly known in Brazil as “mamona” or “carrapateira”. It is an oleaginous plant whose seeds have been used mainly in biodiesel production. Plant seed oil can be extracted mechanically or using solvents, generating castor bean cake and castor bean meal as by-products, respectively. Accidental ingestion of these by-products can cause poisoning in animals and humans, characterized by digestive signs resulting from the presence of a toxalbumin called ricin. Seed toxicity varies among animal species; in horses, the lethal dose of seeds is 0.1 g/kg of body weight. The literature presents plenty of studies addressing poisoning by R. communis in different animal species and in humans; however, reports are scarce and little information is available on the pathological aspects of poisoning regarding equines. Therefore, the present study aimed to describe the epidemiological, clinical and pathological aspects observed in an outbreak of accidental poisoning with castor bean cake in horses. The equines were supplemented with palm kernel (Elaeis guianeesis) cake; however, in the purchase of a new batch, there was an error in the order, and castor bean cake was requested instead. Four horses that received castor bean cake presented clinical signs indicative of colic, which started about 21 hours after administration. Three of these horses died, with clinical evolution from 2 to 4.5 hours; the other animal was treated with intravenous fluid and antibiotic therapy and non-steroidal anti-inflammatory drugs and recovered after five days. In the necropsy of two of these horses, the main lesions were found in the small intestine, where mucosae with pronounced redness and covered with a thin layer of yellow fibrous material were observed. In the intestinal lumen, there was a large amount of bloody liquid. The stomach was full, and dark lumps similar to crushed castor bean seeds were observed in the contents. The adrenal glands of both horses presented congestion and hemorrhage in the cortex. In microscopy, the main lesion was an acute, diffuse and accentuated fibrin-necrotic enteropathy affecting the jejunum. The diagnosis of castor bean cake poisoning was based on the circumstantial evidence of by-product consumption supported by clinical and pathological aspects. The results indicate that castor bean cake commercially available as fertilizer is extremely toxic when ingested, and there is a need for appropriate detoxification or labeling informing of its toxicity.

A pig was in left lateral recumbency with limb spasticity, accentuated prostration, and strabismus, and was euthanized. During autopsy, yellowing of the leptomeninges at the ventral pons to medulla oblongata was noted. In the cerebellar peduncles, there was a focally extensive black-to-yellow area at the level of the vestibular nuclei. Histologic examination revealed a cross-section of a nematode larva, consistent with Stephanurus dentatus, bordered by edema and marked infiltration of mononuclear cells, plasma cells, and a few eosinophils. Vacuolation of the neuropil, with rare gitter cells and axonal spheroids, was also observed. We diagnosed parasitic encephalitis caused by S. dentatus migration based on the pathology findings and characterization of the parasite.