Introduction

Nerium oleander is an ornamental plant (Figure 1) that is potentially lethal and belongs to the Apocynaceae family (¹). Its primary cytotoxic components are digitoxigenin, folinerin, neriin, rosagenin, and oleandrin, which are cardiac glycosides of vegetal origin with a glycolipid nature (², ³, ⁴, ⁵). Due to their perennial foliage, these toxic molecules are present throughout the year and are found on stems, flowers, and leaves, both dry and green (6, ⁷). Reports of poisonings have been described in several species, such as geese, horses, dogs, and bears (⁸, ⁹, ¹⁰, ¹¹, ¹²). However, the frequency and severity of mortality have been mostly studied in ruminants due to their production system and accessibility, with reported mortalities between 41-100 % (¹, ¹³, ¹⁴). N. oleander is described as an unpalatable plant because it releases a type of triterpenoid glycoside (saponins) when the fresh leaves are chewed, which produces an unpleasant burning sensation on contact with the oral mucosa (¹⁵). However, it can be consumed voluntarily by animals when they are hungry (¹⁶) or during periods of prolonged drought since oleander is one of the few species available because it is a highly resistant perennial plant (³). Nevertheless, the palatability of its leaves improves after they are detached from the bushes, pruned, or treated with herbicides, which makes them more likely to be consumed voluntarily. There are reports of accidental poisonings after consuming dry leaves intermixed with grass, bales, and/or rolls of hay since the toxicity of the plant is maintained for prolonged periods (¹, ³).

Source: own work

Figure 1 Nerium oleander in the summer; its toxicity is due to its primary cytotoxic components such as digitoxigenin, folinerin, neriin, rosagenin, and oleandrin. 

The purpose of this case report is to reveal an episode of mortality in dairy goats due to the consumption of N. oleander administered by the feedlot manager. This form of poisoning is classified as atypical because the animals were in corrals, and this was the only forage resource available to them, so they were forced to ingest it regardless of its low palatability. The authors have no knowledge of poisoning by the plant in this locality, which mainly supports goat production. Workers, technicians, and veterinarians must recognize it and eliminate it from the animal’s diet.

Materials and methods

In the town of Peldehue that is located in the Metropolitan Region of Santiago, Chile (33°10’17’’S70°37’53’’O), a mortality episode of adult goats kept for intensive dairy production was reported during the summer. Those affected were fed with remains of pruned trees and ornamental plants in an area close to the farm. At 12 hours’ post-ingestion (pi), it was reported that 15 % of the animals that had access to this trough were found dead (Figure 2), and 11 % had clinical signology. Mortality lasted 84 hours, at which time a visit was requested. Autopsies of the animals were performed on-site, and the person in charge indicated weakness, sternal decubitus, and increased heart rate. Several tissue fragments were extracted from the heart, lung, kidney, lymph node, and digestive system, including rumen, reticulum, omasum, abomasum, duodenum, and jejunum, which were fixed with 10% buffered formaldehyde. These fragments were processed with routine protocol and included in paraffin, from which cuts of 4-5 microns thick were obtained, stained with Hematoxylin and Eosin and observed under an optical microscope. Corrals were visited in order to visually analyze the type and species of plants available in the trough.

Source: own work

Figure 2 Adult female goats found dead 12 h after ingesting feed that was administered in troughs. 

Results

It was determined that 54% of the flock showed clinical signs that include agalactia, apathy, sternal decubitus, severe dehydration, anorexia, and/or cranial pressure (Figure 3). The autopsy findings revealed pale areas without clear limitations and a slightly elevated level of ventricular myocardium and papillary muscles on the left side. Both lungs showed an increase in their touch consistency and a presence of foam in the bronchial bifurcation and first tracheal portion. They also showed marked ruminal and abomasal distension with solid content and a fibrous aspect with remains of leaves that could not be identified at that time, as well as petechiae, hemorrhage in the abdominal serosa, duodenal mucosa, and the first portion of jejunum with marked congestion and slightly thickened walls and edematized in the first duodenal portion and its lumen. The large intestine presented greenish to brown content of low liquid consistency as well as reddened and enlarged mesenteric lymph nodes (twice its normal size). There were no alterations in size and morphology at the hepatic level. Histopathological lesions included marked multifocal necrosis of contractile myocardiocytes with heterogeneous coloration, pale and eosinophilic areas, pycnotic nucleus, rupture of myofibrils, mild lymphoplasmacytic infiltration, incipient fibrosis areas in more affected areas, and structures compatible with Sarcocystis spp (Figure 4 A-B). In the lung, edema and mild diffuse interstitial hemorrhage were found. In the kidney, interstitial hemorrhage and mild tubular degeneration with the presence of intraluminal cell debris were found. In the reticulum, rumen, omasum, and abomasum, mild mononuclear inflammatory infiltrate, hyperemia, congestion, and bleeding in the lamina propria were also noted. Hepatocytes, hydrophilic and vacuolar degeneration was found in the centrilobular area. During the inspection of the farm, N. oleander leaves were found mixed with the other forage in the troughs. Some of them were green while others were dry, and they showed evident marks of having been chewed.

Source: own work

Figure 3 Adult female goat, which presents loss of body condition, respiratory difficulty, and skull pressure 84 h post-ingestion of feed administered in troughs 

Source: own work

Figure 4 A-B: Histological sample of the heart: (A) Moderate to severe multifocal myocardial necrosis with myocardiocytes of hypereosinophilic cytoplasm and picnosis. Loss of continuity of myofibrils and areas of mild to moderate mononuclear inflammatory infiltrate (H&E, 10X) (B) Contractile myocardiocytes with hypereosinophilic cytoplasm, marked picnosis, and occasional absence of nucleus (H&E 40X). 

Discussion

N. oleander is not a plant that the animals consume voluntarily but, as indicated (¹,¹⁵), some factors make poisoning occur accidentally. One of them is that the leaves and branches of oleander were pruned, which made them palatable, and in this case, the leaves were mixed with forage that facilitated accidental consumption. It was administered in the ration because those in charge lacked knowledge about the plant’s toxicity. Although accidental cases have been reported in cattle (¹, ⁷), the cases analyzed in small ruminants only refer to experimental poisonings in which variable doses ranging from 0.05-1 g/Kg have been administered, with episodes of mortality starting at 4 hours and lasting up to 8 days (¹⁷, ¹⁸). As reported by other authors (⁶), it is not possible to determine the value of the lethal dose 50 (LD50). However, it is possible to determine with certainty that the temporal range of mortality began at 8 hours (pi) and was extended until 84 hours, coinciding with those reported. As in the present report, the literature indicates that clinical signology primarily affects the cardiovascular system, then the respiratory, renal, digestive, and central nervous systems (¹⁸). In the cardiovascular system, this is due to the tropism of the cardenolides by the cardiomyocytes, which act by binding and inhibiting the Na⁺/K⁺ -ATPase pump present in the membrane that causes an electrolyte imbalance consisting of an increase in extracellular K⁺ and intracellular Na⁺. Due to the latter’s increase, the functioning of the Na⁺/Ca²⁺ ion-exchange channel is disrupted and an increase in intracellular Ca²⁺ is generated, which leads to a markedly positive inotropic effect. It also generates macroscopically necrosed areas and marked multifocal necrosis of contractile myocardiocytes upon histopathological examination, as described by other authors (⁶, ⁷, ¹⁹). The increase in Ca²⁺ causes the modification of the resting membrane potential, increasing its positivity and generating spontaneous depolarizations (⁶). The main effect on the respiratory system was the discovery of bronchial and tracheal edema, as well as other cases studied in other species (⁷). These glycosides also generate necrosis in renal tubular epithelial cells, which is more evident in distal contoured tubules and collectors (¹⁸). In this case, the lesions reported were interstitial hemorrhage and mild tubular degeneration with the presence of intraluminal cellular debris, coinciding with the findings of other authors (⁶). According to other cases (¹⁸), oleandrin can cross the blood-brain barrier and accumulate in the central nervous system, which explains the signology of cranial pressure in one of the clinically affected animals. There are also reports of histopathological lesions such as cerebral hemorrhage and congestion (¹⁷), which were not observed in this case.

Conclusions

The presence of the plant, the evolution of mortality, clinical signology, macroscopic, and microscopic findings suggest that accidental poisoning was due to N. oleander in this farm and knowledge of this plant species is essential to arrive at a confirmatory diagnosis.