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Vermiculite toxicity in leos
Death in leopard geckos (Eublepharismacularius) following ingestion of vermiculite S. L. PUGSLEY, D. SPRATT& J. H. SAMOUR Department of Veterinary Science, Institute of Zoology, Zoological Society of London, Regent'sPark, London NWI4RY, United Kingdom Summary This paper details the clinical and post-mortem findings of leopard geckos following ingestion of vermiculite bedding material. Death was attributed to the high magnesium content of the vermiculite. Keywords; Lizards; Poisoning; Magnesium; Animal husbandry In recent years considerable efforts have been made by herpetologists to breed and rear reptiles in captivity. and a wide range of incubation, hatching and rearing methods have been proposed. Various bedding materials on which to place eggs for incubation have been tried out, and in recent times vermiculite has been the material of choice for use with reptile eggs, which are prone to desiccation. Vermiculite is the geological name given to a group of hydrated laminar minerals consisting of alumi- niumiron magnesium silicates. Vermiculite has the ability to absorb and then gradually release water by evaporation, thus providing a humid environment for incubation. The ReptileHouse at London Zoo has in recent years maintaineda breeding colony of Leopard ground geckos (Eublepharismacularius). Increased hatching rate and successful rearing of young has been achieved asaresultof careful monitoring of incubation. Various bedding materials have been tested for provision of adequate humidity and hygiene. In this paper we report the ingestion of vermiculite byabreedinggroup of geckos and their subsequent death, probably as a result of its toxic properties. Clinical observations 5 adult geckos were presented for post-mortem examination. The animals had been breeding prior to death: 4 of the animals died withina 3-week period, and each had been observed voluntarily ingesting large quantities of vermiculite on a regular basis prior to death. Many other members of the breeding colony were also seen ingesting vermiculite. The average weekly consumption per gecko was Received 24 lalluary /985. Accepled 23 April/985. estimated to be 20 g. 8 members of the breeding group became lethargic following vermiculite ingestion. Appetite of the clinically affected animals became depressed, and they lost bodyweight rapidly. Their faeces contained much stringy mucus, blood and vermiculite, and the urate content became more solid and darkcr than usual. Many of the geckos developeda flaccid paralysis of the hind limbs. 3 geckos recovered following force-feeding with a solution of electrolytes and glucose. Post-mortem and histological examinations Full gross post-mortem examinations were performed on the 5 geckos and, where possible, histological examination was also conducted. Samples of organs were placed into 10%neutral buffered formalin, and were subsequently embedded in paraffin wax and sectioned. Sections were routinely stained withhaematoxylin and eosin. Selected histochemical staining techniques were also employed and includedmagneson II and titan yellow for magnesium, andsolochromeazurine for aluminium (Pearce, 1972). Bacteriological and parasitological examinations of the major organs were also performed. Gross post-mortem and histological findings are shown in Table 1. The post-mortem appearance and microbiology results did not indicate any infectious aetiology, but the clinical and post-mortem findings suggested vermiculite toxicity may have been involved. The chemical composition of vermiculite would suggest that the only components capable of exerting a toxic effect were aluminium oxide and magnesium oxide. These represented 12%and 23% respectively of the dry weight of vermiculite. In the absence of measurements of blood levels of these substances, histochemical techniques were used to determinne whether aluminium and/or magnesium were present in high concentrations within body tissues. These techniques indicated abnormally high concentrations of magnesium in the kidneys of 3 cases (Table 1; Fig. 1). Histochemical determination of aluminium in liver, kidney, heart and lung of the geckos (215,399 and 395) proved negative (solochromeazurine, method Pearce, 1972). Vermiculite toxicity in geckos 285 Tahle I. Pust·murtem IIndingsul'theleupardgrnundgeckus Discussion Aluminium and magnesIum oxides and hydrates forma valuable group of drugs used clinically in human medicine for their antacid properties, since they rapidly increase gastricpHwhen taken orally. In humans, magnesium oxide, given orally in large doses raises the serum magnesium significantly and may cause intoxication, especially inpatients with impaired renal function (Shearman, 1970). Alumi- niumhydroxideis generally accepted as not being absorbed from the gut, but.actively adsorbs pepsin. Aluminium hydroxide is regarded as practically non-toxicinhumans (Gosselin, 1976) however, large doses may lead to acute phosphate depletion (Rumack, 1980). Goodman (1980) stated that aluminium hydroxide maybe absorbed from the gut and in humans with impaired renal function alumi- niummay accumulate in a variety of tissues. No references to toxicity of oral aluminium oxide were found. Review of magnesium toxicity in humansindio catedmagnesium hydroxide to be slightly toxic and magnesium oxide moderately toxic (Gosselin, 1976). Repeated oral administration in humans with renal dysfunction can result in a dangerous degree of magnesium retention, causing neurological. Clioi'£' Adultfcmale, 30g
!15m-t) Adult female, 3X g (3')9/X.\) Adult male, 50g (3,)5/X.\) Adult female. :!5 g (.\:!3m.\) Adult female. :!5 g (363m.\) Filldillgs Liver: Markcdcytopbsmicfally changcthroughoutparcnchymal cclls. Kidncy: Thickcningof Bowman's capsules. Swollenglomcruli and lUhules. Hydropic cytoplasmic lubularchanges. Minute granular aggregationsdetccted within glomcruliandlubulecytopbsms- histochemically determined as magncsiulllby using Illagncson II and titan yellow methods (Fig. I). Lungs: Ilydropic cytoplasmic changes of muscle fihrcs. Similar findings toc;lse:! 15m.\. Cloacal infection by P.H'lIdoIlIlJl/IiS spp. Other findings similar tocasc :!15m.\. Pulmonaryhaemorrhage. Fatly liver. No histological examinationpossihle. Gastrich;lemorrhagc. No histological examination possible. neuromuscular and cardiovascular impairment (Jones, 1977). Between 5'}'0 and 15% of ingested magnesium maybe absorbed and in the normal human is rapidly excreted by the kidney (Miller, 1979; Gosselin, 1976). Systemically, magnesium produces depression, abolition of reflexes and death from respiratory paralysis. Gentry, Miller, Pugh, Neathery&Bynum (1978) reported toxic effects of feeding high magnesium (4%magnesium oxide in diet) to dairy calves and the clinical findings were similar to those observed in this study in geckos. Gentry el (/1. (I Y78) noted diarrhoea and reduced food intake, together with reduced weight gains. Traces of blood and stringy mucus were also noticed in the faeces and the calves were reported to be unthrifty and drowsy. Gross post-mortem examination revealed no abnor- malities. The demonstration of magnesium concentrated within the gecko kidneys, coupled with the clinical and other post-mortem observations, providesa strong basis fora diagnosis of magnesium toxicity. Magnesium toxicity in humans is more severe with concurrent renal dysfunction. Renal efficiency may have been an important factor in the magnesium toxicity in these geckos, particularly since the reptilian kidney is less well developed and is regarded as less efficient than that of the mammal. It is unfortunate that clinicalserUlll magnesium determinations were not possible in these geckos because the histological demonstrable levels in the kidneys would suggest high serum levels. The inability to demonstrate aluminium in the tissues suggests that it may not have been absorbed by the reptile gut. Alternatively, aluminium may have had to compete with magnesium for absorption, and/or maybe more widely distributed throughout the body, thus making the comparatively smaller alumi- niumdeposits histochemically undetectable. The severe hepatic fatty changes seen in the geckos is interesting and to the authors'knowledge, magnesium and aluminium toxicity has not been reported in manor animals to cause such changes. Therefore these liver changes may have been related to the reduced food intake, possibly compounded by aluminium'spropertyof reducing absorption of nutrients by binding proteolytic enzymes. Furthermore, it is possible that vermiculite induced changes in the gut flora which may have resulted in the production of bacterial toxins with a hepatotoxic effect. Severe fatty change is a common finding in reptiles and is especially seen incases of anorexia. As a result of these findings, vermiculite is no longer used as a bedding material for reptiles at the London Zoo. except for egg incubation The report suggests the need for caution in using this material with reptiles.
Death in leopard geckos (Eublepharismacularius) following ingestion of vermiculite S. L. PUGSLEY, D. SPRATT& J. H. SAMOUR Department of Veterinary Science, Institute of Zoology, Zoological Society of London, Regent'sPark, London NWI4RY, United Kingdom Summary This paper details the clinical and post-mortem findings of leopard geckos following ingestion of vermiculite bedding material. Death was attributed to the high magnesium content of the vermiculite. Keywords; Lizards; Poisoning; Magnesium; Animal husbandry In recent years considerable efforts have been made by herpetologists to breed and rear reptiles in captivity. and a wide range of incubation, hatching and rearing methods have been proposed. Various bedding materials on which to place eggs for incubation have been tried out, and in recent times vermiculite has been the material of choice for use with reptile eggs, which are prone to desiccation. Vermiculite is the geological name given to a group of hydrated laminar minerals consisting of alumi- niumiron magnesium silicates. Vermiculite has the ability to absorb and then gradually release water by evaporation, thus providing a humid environment for incubation. The ReptileHouse at London Zoo has in recent years maintaineda breeding colony of Leopard ground geckos (Eublepharismacularius). Increased hatching rate and successful rearing of young has been achieved asaresultof careful monitoring of incubation. Various bedding materials have been tested for provision of adequate humidity and hygiene. In this paper we report the ingestion of vermiculite byabreedinggroup of geckos and their subsequent death, probably as a result of its toxic properties. Clinical observations 5 adult geckos were presented for post-mortem examination. The animals had been breeding prior to death: 4 of the animals died withina 3-week period, and each had been observed voluntarily ingesting large quantities of vermiculite on a regular basis prior to death. Many other members of the breeding colony were also seen ingesting vermiculite. The average weekly consumption per gecko was Received 24 lalluary /985. Accepled 23 April/985. estimated to be 20 g. 8 members of the breeding group became lethargic following vermiculite ingestion. Appetite of the clinically affected animals became depressed, and they lost bodyweight rapidly. Their faeces contained much stringy mucus, blood and vermiculite, and the urate content became more solid and darkcr than usual. Many of the geckos developeda flaccid paralysis of the hind limbs. 3 geckos recovered following force-feeding with a solution of electrolytes and glucose. Post-mortem and histological examinations Full gross post-mortem examinations were performed on the 5 geckos and, where possible, histological examination was also conducted. Samples of organs were placed into 10%neutral buffered formalin, and were subsequently embedded in paraffin wax and sectioned. Sections were routinely stained withhaematoxylin and eosin. Selected histochemical staining techniques were also employed and includedmagneson II and titan yellow for magnesium, andsolochromeazurine for aluminium (Pearce, 1972). Bacteriological and parasitological examinations of the major organs were also performed. Gross post-mortem and histological findings are shown in Table 1. The post-mortem appearance and microbiology results did not indicate any infectious aetiology, but the clinical and post-mortem findings suggested vermiculite toxicity may have been involved. The chemical composition of vermiculite would suggest that the only components capable of exerting a toxic effect were aluminium oxide and magnesium oxide. These represented 12%and 23% respectively of the dry weight of vermiculite. In the absence of measurements of blood levels of these substances, histochemical techniques were used to determinne whether aluminium and/or magnesium were present in high concentrations within body tissues. These techniques indicated abnormally high concentrations of magnesium in the kidneys of 3 cases (Table 1; Fig. 1). Histochemical determination of aluminium in liver, kidney, heart and lung of the geckos (215,399 and 395) proved negative (solochromeazurine, method Pearce, 1972). Vermiculite toxicity in geckos 285 Tahle I. Pust·murtem IIndingsul'theleupardgrnundgeckus Discussion Aluminium and magnesIum oxides and hydrates forma valuable group of drugs used clinically in human medicine for their antacid properties, since they rapidly increase gastricpHwhen taken orally. In humans, magnesium oxide, given orally in large doses raises the serum magnesium significantly and may cause intoxication, especially inpatients with impaired renal function (Shearman, 1970). Alumi- niumhydroxideis generally accepted as not being absorbed from the gut, but.actively adsorbs pepsin. Aluminium hydroxide is regarded as practically non-toxicinhumans (Gosselin, 1976) however, large doses may lead to acute phosphate depletion (Rumack, 1980). Goodman (1980) stated that aluminium hydroxide maybe absorbed from the gut and in humans with impaired renal function alumi- niummay accumulate in a variety of tissues. No references to toxicity of oral aluminium oxide were found. Review of magnesium toxicity in humansindio catedmagnesium hydroxide to be slightly toxic and magnesium oxide moderately toxic (Gosselin, 1976). Repeated oral administration in humans with renal dysfunction can result in a dangerous degree of magnesium retention, causing neurological. Clioi'£' Adultfcmale, 30g
!15m-t) Adult female, 3X g (3')9/X.\) Adult male, 50g (3,)5/X.\) Adult female. :!5 g (.\:!3m.\) Adult female. :!5 g (363m.\) Filldillgs Liver: Markcdcytopbsmicfally changcthroughoutparcnchymal cclls. Kidncy: Thickcningof Bowman's capsules. Swollenglomcruli and lUhules. Hydropic cytoplasmic lubularchanges. Minute granular aggregationsdetccted within glomcruliandlubulecytopbsms- histochemically determined as magncsiulllby using Illagncson II and titan yellow methods (Fig. I). Lungs: Ilydropic cytoplasmic changes of muscle fihrcs. Similar findings toc;lse:! 15m.\. Cloacal infection by P.H'lIdoIlIlJl/IiS spp. Other findings similar tocasc :!15m.\. Pulmonaryhaemorrhage. Fatly liver. No histological examinationpossihle. Gastrich;lemorrhagc. No histological examination possible. neuromuscular and cardiovascular impairment (Jones, 1977). Between 5'}'0 and 15% of ingested magnesium maybe absorbed and in the normal human is rapidly excreted by the kidney (Miller, 1979; Gosselin, 1976). Systemically, magnesium produces depression, abolition of reflexes and death from respiratory paralysis. Gentry, Miller, Pugh, Neathery&Bynum (1978) reported toxic effects of feeding high magnesium (4%magnesium oxide in diet) to dairy calves and the clinical findings were similar to those observed in this study in geckos. Gentry el (/1. (I Y78) noted diarrhoea and reduced food intake, together with reduced weight gains. Traces of blood and stringy mucus were also noticed in the faeces and the calves were reported to be unthrifty and drowsy. Gross post-mortem examination revealed no abnor- malities. The demonstration of magnesium concentrated within the gecko kidneys, coupled with the clinical and other post-mortem observations, providesa strong basis fora diagnosis of magnesium toxicity. Magnesium toxicity in humans is more severe with concurrent renal dysfunction. Renal efficiency may have been an important factor in the magnesium toxicity in these geckos, particularly since the reptilian kidney is less well developed and is regarded as less efficient than that of the mammal. It is unfortunate that clinicalserUlll magnesium determinations were not possible in these geckos because the histological demonstrable levels in the kidneys would suggest high serum levels. The inability to demonstrate aluminium in the tissues suggests that it may not have been absorbed by the reptile gut. Alternatively, aluminium may have had to compete with magnesium for absorption, and/or maybe more widely distributed throughout the body, thus making the comparatively smaller alumi- niumdeposits histochemically undetectable. The severe hepatic fatty changes seen in the geckos is interesting and to the authors'knowledge, magnesium and aluminium toxicity has not been reported in manor animals to cause such changes. Therefore these liver changes may have been related to the reduced food intake, possibly compounded by aluminium'spropertyof reducing absorption of nutrients by binding proteolytic enzymes. Furthermore, it is possible that vermiculite induced changes in the gut flora which may have resulted in the production of bacterial toxins with a hepatotoxic effect. Severe fatty change is a common finding in reptiles and is especially seen incases of anorexia. As a result of these findings, vermiculite is no longer used as a bedding material for reptiles at the London Zoo. except for egg incubation The report suggests the need for caution in using this material with reptiles.
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