Polioencephalomalacia (PEM) in calves associated with excess sulfur intake

Abstract

Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to-3-month-old calves. Occurrence of PEM is rare in calves at such a young age.

Polioencephalomalacia in Buffaloes in the Amazon Biome

“…The clinical signs were of a multifocal nature, involving all regions of the brain (e.g., cerebellum and brainstem), similar to the clinical signs in cattle [10][11][12], sheep [13], and goats [14,16]. In light of this symptomatology, Riet-Correa et al [5] suggest that the increase in intracranial pressure exerted by edema of the brain structures causes herniation of the cerebellum through the foramen magnum.…”

“…The ages of the animals studied ranged from two months to one year. Withoeft et al [12] diagnosed PEM in calves from 15 days to 1 year. This can be explained by primary thiamine deficiency, as the young cannot produce or ingest it in sufficient quantities [8,21].…”

“…In chronic cases, in which the animals survive for several days, necrosis becomes more evident and the brain is visibly reduced in size due to the loss of gray matter, with flattening of the convolutions, yellowish gelatinous consistency areas of the cortex, and cavitations [5,6]. Laminar necrosis of the cerebral cortex has also been found in cattle with PEM [10,12,24] and sheep intoxicated with sulfur [13].…”

“…The active form of thiamine is thiamine pyrophosphate, a cofactor of transketolase, which regulates the pentose phosphate pathway responsible for much of the ATP used in nerve cells [8], a fact that explains the triggering of PEM in these animals. In addition, sulfur intoxication cannot be ruled out as it leads to lesions in PEM conditions involving ruminal bacteria, transforming ingested sulfates to the toxic form (sulfides), which affects cellular respiration [12,21].…”

“…In Europe, the same lesion pertinent to PEM was called cerebrocortical necrosis [8], and there are even reports of the disease in llamas in Canada [9]. In Brazil, PEM has been described in bovines [10][11][12], ovine [13][14][15], goats [13,14,16], and buffaloes in the state of Mato Grosso, midwest Brazil [17].…”