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This study was carried out to investigate the pattern of lectin binding in the cerebellum of calves poisoned with Solanum fastigiatum var. fastigiatum. For the experimental reproduction of the illness, S. fastigiatum var. fastigiatum was collected from farms where the intoxication occurs. The dried ground plant was administered to two 1-year-old cattle by a ruminal cannula. The animals received 5 g/kg b.w. daily, 5 days a week, during periods of 107 and 140 days. After these periods the animals were bled to death. For the histological study, transverse sections of the cerebellum were used. Paraffin-embedded sections were incubated with the following biotinylated lectins with different specificity: Concanavalia ensiformis (Con-A). Glycine max (SBA). Dolichos hiflorus (DBA), Ulex europeus-I (UEA-I). Triticum vulgaris (WGA), succynyl-WGA (sWGA). Arachis hypogaea (PNA), Ricinus communis-I (RCA-I) and Bandeirea simplicifolia-I (BS-I). Avidin-biotin-peroxidase complex was applied as a detection system. Purkinje cells showed vacuolation in the pericaryon. The stored material present in the cells reacted strongly with the following lectins: Con-A. sWGA, WGA and RCA-I. An irregular affinity was observed with PNA and DBA. The lectin-binding pattern was compatible with a glycolipid storage disease.

A congenital progressive cerebellar disorder is described in Holstein calves. The clinical signs were progressive and were characterized by ataxia, hypermetria, a wide stance and fine head tremors. When the affected cattle were forced to run, the signs were exacerbated, leading to epileptiform attacks. Histological lesions consisted of a very selective cerebellar cortical degeneration, almost exclusively affecting the Purkinje cells. The disease affected 6 out of 200 Holstein calves from the same bull. However, results of mating tests of the bull with his daughters and granddaughters suggested that it was not hereditary (p = 0.0062) although an environmental-genetic interaction could not be ruled out.

In southern Brazil, cattle are affected by a disease known locally as Lechiguana and characterized by large subcutaneous swellings. Eighteen cases were examined clinically; 17 of the cattle had a single swelling, and one had two swellings. In 14 of the 18 cases, the swellings were located over the scapula and adjacent regions. The subcutaneous masses reached maximum dimensions of 45 x 50 cm, with heights above the skin surface of 5-25 cm. Growth was rapid, often taking place in 15 to 60 days. Histologically, all lesions were focal proliferative fibrogranulomatous panniculitis and consisted of focal proliferation of fibrous tissue that was infiltrated by plasma cells, eosinophils, lymphocytes, and sometimes neutrophils. An eosinophilic lymphangitis was also present, which sometimes resulted in the destruction of the lymphatics and the formation of eosinophilic microabscesses. Small granulomas, sometimes containing radiating clubs, and Splendore-Hoeppli material were present in the regional lymph node. Pasteurella granulomatis was isolated from the subcutaneous masses of 14 of the 18 natural cases. All 11 of these cases recovered following treatment with 3 g of chloramphenicol daily for 5 days. Untreated animals died. Because the area of anatomic distribution is similar to that infested by Dermatobia hominis, we postulate that this insect may transmit the causative agent. In one steer, a subcutaneous injection of P. granulomatis caused a large subcutaneous swelling consisting of interlacing bundles of collagen infiltrated by neutrophils, eosinophils, and some lymphocytes. Microabscesses, but not lymphangitis and granulomas, were detected. In all 11 cattle inoculated either intramuscularly or subcutaneously with P. granulomatis, purulent abscesses were produced at the sites of the injection, and P. granulomatis was recovered from all lesions.

Congenital lymphedema is described in Hereford cattle. The disease was characterized by edema of the hind limbs, sometimes forelimbs, tail, and prepuce. Lymphatic system lesions were hypoplasia and aplasia of lymph vessels and prescapular, iliofemoral, and popliteal lymph nodes. Test matings demonstrated the transmission of the disease by an autosomal dominant trait with variable expressivity and incomplete penetrance.