ArticlePDF Available

Abstract

Three years old female pug was presented to the clinics with sudden onset of muscle tremors, salivation, vomitions, panting, restlessness and polyuria from last night. Dog had history of ingestion of dark coloured chocolates. Examination of saliva and faecal samples revealed brown colour with chocolate odour. Based on the history, clinical signs and laboratory examination condition was diagnosed as acute chocolate poisoning. Dog was treated with inj. DNS, inj. ranitidine along with antibiotic and activated charcoal for about three days. After completion of three days of therapy dog was free from toxicity.
International Journal of Veterinary Health Science & Research, 2013 © 16
B.Sudhakara Reddy, L.S.S.Varaprasad Reddy ,Sivajothi. (2013) .Chocolate Poisoning in a Dog, Int J Vet Health Sci Res, 01(03), 16-17.
International Journal of Veterinary Health Science & Research (IJVHSR)
ISSN 2332-2748
Chocolate Poisoning In A Dog
Review Article
B.Sudhakara Reddy1*, L.S.S.Varaprasad Reddy2, S.Sivajothi3
1* Assistant Professor (Veterinary Medicine), Teaching Veterinary Clinical Complex, Sri Venkateswara Veterinary
University, Proddatur, Y.S.R.District, Andhra Pradesh, India.
2 Assistant Professor, Dept. of Veterinary Physiology, Sri Venkateswara Veterinary University, Proddatur,
Y.S.R.District, Andhra Pradesh, India.
3 Assistant Professor, Dept. of Veterinary Parasitology, Sri Venkateswara Veterinary University, Proddatur,
Y.S.R.District, Andhra Pradesh, India.
*Corresponding Author:
B.Sudhakara Reddy,
Assistant Professor (Veterinary Medicine), Teaching Veterinary Clini-
cal Complex, Sri Venkateswara Veterinary University, Proddatur,
Y.S.R.District, Andhra Pradesh, India.
E-mail: bhavanamvet@gmail.com.
Received: October 30, 2013
Accepted: November 27, 2013
Published: November 29, 2013
Citation: B.Sudhakara Reddy, L.S.S.Varaprasad Reddy ,Sivajothi. (2013)
.Chocolate Poisoning in a Dog, Int J Vet Health Sci Res, 01(03), 16-17.
Copyright: B.Sudhakara Reddy © 2013. This is an open-access article
distributed under the terms of the Creative Commons Attribution Li-
cense, which permits unrestricted use, distribution and reproduction in
any medium, provided the original author and source are credited.
Introduction
Chocolate poisoning is one of the toxicological emergencies in
dogs. Chocolate is derived from the roasted seeds of the plant
Theorem cacao. The seeds contain substances known as methylxan-
thines, which includes the CNS stimulants theobromine (3, 7-di-
methylxanthine) and caffeine (1, 3, 7-trimethylxanthine), both of
which are toxic to dogs. Although both constituents may contrib-
ute to clinical signs of chocolate toxicity, the former is the major
cause as its concentration in chocolate is 3-10 times higher than
that of caffeine and its half life signicantly longer [1]. Chocolate
toxicity is not dependent on the amount of chocolate ingested
but it is depend on the type of ingested chocolate [2]. Different
concentrations of methylxanthines are present in different prod-
ucts and range from low levels as in white chocolate to cocoa
beans which contain the highest levels[3]. The LD50 of caffeine
and theobromine for dogs is 100–500 mg/kg [4]. At a low dose
of 20–40 mg/kg mild signs may appear (restlessness, vomiting),
from a dose of 40–50 mg/kg cardio-toxic effects can be observed
such as rhythm disturbances, seizures might be evident from a
dose of about 60 mg/kg, while higher doses than that may be
lethal [5]. The present article describes the theobromine toxicity
in a dog due to consumption of chocolate.
Case History and Observations
Three years old female pug was presented to Veterinary Hospital,
Proddatur with muscle tremors, salivation, vomition, increased
thirst, panting, restlessness, frequent urination from last night.
Dog was regularly dewormed, vaccinated and regularly feeding
with adult pedigree feed. There was no change in the feeding
habits, but 12-14 hours back owners offered rst time, imported
dark chocolates to the dog. Clinical examination of the dog re-
vealed rise in body temperature (103.7ºF), increased heart rate
(142/min), increased respiration (36/min), dehydration, muscle
tremors, congested congenctival mucus membranes, with normal
lymph nodes. Coffee coloured with chocolate odour vomitous,
saliva and faeces was observed. Faecal samples, peripheral blood
smear, serum and whole blood with EDTA were collected for
laboratory examinations. Examination of peripheral blood smear
and feacal samples did not reveal any abnormalities. Haemotology
revealed total leucocytes count (9200/cumm), neutrophils (6256/
cumm), lymphocytes (2760/cumm), eosinophils (184/cumm),
haemoglobin (13 g/dl), TEC (6.2 x 106/cumm), PCV (43%). Ex-
amination of the faecal samples for presence of parvo viral anti-
gen with ScanVet kit (Intas) revealed negative results.
Treatment and Discussion
Based on the feeding history, prophylactic measures, clinical signs,
laboratory examination the condition was diagnosed as acute
chocolate poisoning. Dog was treated with Inj. DNS (@ 20 ml/kg
b.wt, IV), Inj. Amoxicillin and cloxacillin (@ 25 mg/kg b.wt, IM,
BID), Inj. ranitidine (@ 0.5mg/kg b.wt, IM) and activated char-
Abstract
Three years old female pug was presented to the clinics with sudden onset of muscle tremors, salivation, vomitions, panting, restlessness and
polyuria from last night. Dog had history of ingestion of dark coloured chocolates. Examination of saliva and faecal samples revealed brown
colour with chocolate odour. Based on the history, clinical signs and laboratory examination condition was diagnosed as acute chocolate poi-
soning. Dog was treated with inj. DNS, inj. ranitidine along with antibiotic and activated charcoal for about three days. After completion of
three days of therapy dog was free from toxicity.
Key Words: Chocolate Poisoning; Pug; Treatment
International Journal of Veterinary Health Science & Research, 2013 © 17
B.Sudhakara Reddy, L.S.S.Varaprasad Reddy ,Sivajothi. (2013) .Chocolate Poisoning in a Dog, Int J Vet Health Sci Res, 01(03), 16-17.
coal (@ 1gm/kg b.wt orally) on the day of presentation. Advice
was given to continue the administration of activated charcoal at
every 4 hours interval up to the next day to reduce the continued
resorption and recirculation of theobromine. By the next day dog
was free from the salivation and excitement. Above therapy was
continued up to three days, after completion of therapy dog was
free from toxic signs of chocolate poisoning.
Most poisonings from methylxanthines occur as a result of choc-
olate ingestion. Chocolate is toxic to animals, serious poisoning
happens more frequently in domestic animals especially to dogs,
which metabolise theobromine much more slowly than humans.
Though a toxic dose will vary depending on factors like size of
the dog (highly toxic in smaller breeds), sensitivity of the dogs
to chocolate, ingestion of chocolate with empty stomach and af-
ter food and the type of chocolate (dark chocolate is more toxic
than milk chocolate). The most important toxic component of
chocolate – the methylxanthines alkaloid theobromine is present
in variable concentrations dependent on the quality of the choco-
late – the darker or richer in cocoa solids the more dangerous the
preparation. Cocoa powder and cooking chocolate are the most
toxic forms. Theobromine and caffeine are readily absorbed from
the GI tract and are widely distributed throughout the body. They
are metabolized in the liver and undergo enterohepatic recycling
and then excreted in the urine as both metabolites and unchanged
parent compounds. The half-lives of theobromine and caffeine in
dogs are 17.5 h and 4.5 h, respectively. Methylxanthines increase
intracellular calcium levels by increasing cellular calcium entry
and inhibiting intracellular sequestration of calcium by the sarco-
plasmic reticulum of striated muscles. The net effect is increased
strength and contractility of skeletal and cardiac muscle[1]. Theo-
bromine action is through competitive inhibition of cellular aden-
osine receptors, leading to vasoconstriction, dieresis, tachycardia
and CNS stimulation[6]. Hooser and Beasley [7] observed choco-
late toxicity in dogs with clinical signs of restlessness, hyperacidity,
mild hyperesthesia, emesis, diarrhea, stiffness, muscle twitching,
tonic to tetanic convulsion, polypnea, tachycardia, hyperthermia
which observed similar ndings in the present case. Osweiler [8]
reported that treatment of chocolate toxicity included detoxica-
tion via gastric emptying, activated charcoal, osmotic cathartic,
uid therapy and lidocaine. But, present case was treated with ac-
tivated charcoal, uid therapy along with supportive therapy. In
dogs, the half life of theobromine is 17.2 hours, but in severe cas-
es, clinical symptoms of theobromine poisoning can persist for
72 hours [3]. The dog was presented to the clinics immediately af-
ter noticing of toxic signs, which accompanied timely therapy. So,
early response was noticed within 24 hours. Though intoxication
can also occur in cats and other species [9], dogs are mainly af-
fected because of their appetite for sweet foods, and smaller dogs
appear to be more susceptible to intoxication than larger dogs
[10]. If the ingested chocolate is highly fatty, gastrointestinal signs
of intoxication include vomiting, diarrhoea, abdominal disten-
tion, and pancreatitis [2,9]. Increased diuresis and haematuria are
reported and can progress to more detrimental cardio-respiratory
and neurological signs such as tachycardia, rhythm disturbances,
seizures, cyanosis and tachypnoea [2,4,9]. Death is caused mainly
due to arrhythmias, hyperthermia, respiratory failure, congestion
and oedema[11].
References
[1]. Merck Veterinary Manual (2005) (Toxicology/Food hazards section), Merk
& Co., Inc., Chocolate Poisoning.
[2]. Luiz JA, Heseltine J (2008) Five common toxins ingested by dogs and cats.
Compendium on Continuing Education for the Practicing Veterinarian 30,
578–587.
[3]. Gwaltney-Brant S (2001) Chocolate intoxication. Veterinary Medicine 96,
108–111.
[4]. Carson TL (2006) Methylxanthines. In: Peterson ME, Talcott PA (eds.)
Small Animal Toxicology. 2nd ed. Saunders, St. Louis, MO. 845–852.
[5]. Stidworthy MF, Bleakley JS, Cheeseman MT, Kelly DF (1997) Chocolate
poisoning in dog. Veterinary Record 141, 28.
[6]. Seran WE (1996) Drugs used in the treatment of asthma. In: Goodman and
Gilman’s e Pharmacologic basis of erapeutics, 9th ed. J.G.Hardman, et
al, eds. McGraw Hill , New Yark, NY, pp. 672-678.
[7]. Hooser SB, Beasley VR (1986) In Current Veterinary erapy IX (Ed.) Kirk,
R.W., W.B. Saunders Co., Philadelphia.
[8]. Osweiler GD (1996) Toxicology. Williams and Wilkins, A. Waverly Co.,
pp. 307.
[9]. Smit HJ (2011) eobromine and the pharmacology of cocoa. In: Fredholm
BB (ed.): Methylxanthines, Handbook of Experimental Pharmacology. 1st
ed. Springer Verlag, Berlin, Heidelberg. 201–234.
[10]. Kovalkovicova N, Sutiakova I, Pistl J, Sutiak V (2009) Some food toxic for
pets. Interdisciplinary Toxicology 2, 169– 176.
[11]. Jansson DS, Galgan V, Schubert B, Hard af Segerstad C (2001) eobro-
mine intoxication in a red fox and a European badger in Sweden. Journal of
Wildlife Diseases 37, 362–365.
... Kasus keracunan coklat pada anjing telah banyak dilaporkan di berbagai negara seperti Inggris (Berny et al., 2010), Jerman (McFarland et al., 2017), India (Reddy et al., 2013) dan Amerika Serikat (Gwaltney-Brant, 2012). Laporan kejadian di Indonesia secara resmi jarang sekali muncul karena kemungkinan coklat maupun makanan berbahan dasar coklat masih dianggap mahal sehingga jarang diberikan pada hewan kesayangan. ...
... Gejala klinis keracunan coklat pada anjing sangat bervariasi seperti dehidrasi, tremor, peningkatan nafsu minum (Reddy et al., 2013), muntah, diare, distensi abdomen (Luiz and Heseltine, 2008) aritmia, hyperthermia (Strachan and Bennett 1994) dan biasanya muncul 6-12 jam setelah mengkonsumsinya. Meskipun demikian, menurut pengamatan Finlay (2005), sebagian besar gejala klinis akan mulai muncul dalam dua jam setelah konsumsi, namun demikian karena theobromine dimetabolisme secara perlahan, maka diperlukan waktu sampai 24 jam untuk muncul gejala klinis dan hingga tiga hari untuk pemulihan. ...
Article
Full-text available
Chocolate poisoning has long been recognized as a common cause mostly in dogs, although many species are susceptible. Contributing factors include indiscriminate eating habits and readily available sources of chocolate. In general, the poisoning resulted from a lack of public knowledge of the health hazard to dogs that may be imposed by these products.Chocolate is derived from the seeds of the plant Theobroma cacao, and the main toxic components are the methylxanthine alkaloids theobromine and caffeine, causing gastrointestinal, cardiovascular and central nervous signs. Diagnosis is based on history of exposure, along with clinical signs. Amphetamine or cocaine toxicosis, and ingestion of antihistamines, antidepressants, or other CNS stimulants should be considered in the differential diagnosis. Stabilization of symptomatic animals is a priority in treating chocolate toxicosis. Although there is no specific antidote, supportive management includes induction of vomiting and administration of activated charcoal, oxygen, and intravenous fluids. Preventing exposure is the key to reducing the incidence of these poisoning episodes. Therefore, it is important to increase the knowledge of dogs owners with regard to foodstuffs that must not be fed to dogs and should be stored outside their reach.
... The mean lethal dose of caffeine and theobromine for dogs is 100-500 mg kg, which corresponds to four bars of dark chocolate. At the low dose of 20-40 mg kg mild clinical signs may occur (hyperactivity, vomiting), the dose of 40-50 mg kg may result in cardio toxic effects such as cardiac arrhythmias, at the dose of 60 mg kg seizures may be develop, whereas higher doses can be fatal [21][22][23]. ...
Article
Full-text available
Background: This study investigated the clinical and pathological manifestations of kola nut on puppies. Kola nut which contains caffeine is used in some regions in Nigeria particularly the south-south to poison stray dogs. Keywords: Kola Nut; Dogs; Caffeine; Clinical Signs; Gross Lesions; Biochemical and Histopathology Materials and Methods: Aqueous extracts of Kola nut nitida was administered to dogs in order to investigate the possible effects on some organs of the dogs. Four dogs were used in the treatment group whereby two doses of the extract (400 mg/Kg and 800 mg/Kg) were daily administered orally to the test animals for a period of 2 weeks. Results: A dose related response was observed. Clinical signs observed include: excitement, polyuria, shivering, dull appearance, rough hair coat, emaciation/ body weight lost, drowsiness, tetanic convulsion, bloody diarrhea, aggressiveness, irritating mood, de�creased pulse rate, decreased body temperature, decreased respiratory rate, sunken eye ball and mucoid diarrhea. Severity of gross lesions in the liver, kidney, Brain, lymph nodes and small Intestine of animals in the infected groups. The laboratory result showed that kola nut extract can be toxic to dogs following the laboratory results gotten from this study as haematology result showed that there is a difference in Red Blood cells, white blood cell, Monocyte, Pack cell volume, Neutrophils, Lymphocyte and Hemoglobin which shows hypochromic condition, while the histopathological lesions shows neuronal necrosis and pyknosis in the brain, gastric erosion with hemorrhage in intestine, necrosis of the renal tubular epithelial cells of the kidney, necrotic myocyte in the heart, thickening of the alveolar septa in the lungs and in the liver necrosis of the hepatocytes. Some of the biochemical parameters showed great statis�tical significance: AST, Urea, Total protein and Creatinine are high compared with the control group. These signify kidney and liver damage. Conclusion: Despite the reported potentially beneficial effects of kola nut, its use as a medicinal plant should be with great caution because of the clinico-pathological manifestations seen in this study
... On abdominal palpation, there was mild pain in dogs affected with renal and hepatic disorders. Reddy and Reddy (2013) and Patel et al. (2018) recorded similar findings in dogs affected with vomition. ...
Article
Full-text available
The present study of etio-epidemiology of vomition in dogs was carried out amongst the dogs presented at Veterinary Clinical Complex, AAU, Anand. A total of 50 cases of vomiting dogs were selected for this study. Investigation of etiological factors associated with vomition revealed that 50.00% vomiting cases were due to dietary abnormalities, 24.00% due to Parvo viral infection, 10.00% due to parasitic infestation, 8.00% renal disorders, 6.00% due to hepatic disorders, and 2.00% due to pyometra. The epidemiological parameters like sex, breed, and age were recorded. During the sex-wise incidence of vomition was found more in male (64.00 %) than in female (36.00 %) dogs. The breed-wise incidence of vomition was recorded highest (32.00 %)in Mongrel, followed by Labrador Retriever (28.00 %), Spitz (12.00 %), Doberman Pinscher (8.00 %), German Shepherd (10.00 %), Great Dane 4%, Beagle (2.00 %), Lasa Aphso (2.00 %), and Pug (2.00 %). The age-wise incidence of vomition was recorded higher (58.00%) in 0-6 months age group, followed by (24%) in 7 months to 3 years age group and (18%) in 3-8 years age group. Clinical examination revealed dehydration, dullness, congested to anemic mucus membranes, inappetence to anorexia, tachycardia, melaena, haematemesis, diarrhea, and clear lungs. On abdominal palpation, there was mild pain in dogs affected with renal and hepatic disorders.
... Methylxanthine poisoning cases have been reported after the ingestion of herbal supplements containing guarana (52), garden mulch made of cacao bean shells (53,54), caffeine tablets (55,56), and caffeine-containing bait (57). However, most poisoning cases occur as a result of chocolate ingestion (4,(58)(59)(60)(61)(62). Though the intoxication of cats may also occur, dogs are most commonly affected because of their indiscriminate eating habits (4). ...
Article
Full-text available
Several foods that are perfectly suitable for human consumption can be toxic to dogs and cats. Food-associated poisoning cases involving the accidental ingestion of chocolate and chocolate-based products, Allium spp. (onion, garlic, leek, and chives), macadamia nuts, Vitis vinifera fruits (grapes, raisins, sultanas, and currants), products sweetened with xylitol, alcoholic beverages, and unbaked bread dough have been reported worldwide in the last decade. The poisoning episodes are generally due to lack of public knowledge of the serious health threat to dogs and cats that can be posed by these products. The present review aims to outline the current knowledge of common food items frequently involved in the poisoning of small animals, particularly dogs, and provides an overview of poisoning episodes reported in the literature.
Article
Full-text available
Carob is the fruit, in the form of a pod, of an evergreen tree that is cultivated mainly in the Mediterranean area (Note 1). The ingredient panels of several canine nutritional products list carob, mostly with suffix, such as pods, meal, powder, chips or gum. Carob treats for dogs are generally positioned as chocolate replacers (Note 2). Two supplements and four complete dry foods make claims, based on their carob ingredient, going from digestive support to diarrhea management (Notes 3, 4). Carob gum is a thickening agent that is occasionally found in wet foods (Note 5). Carob pods have a wrinkled, leathery surface and softer inner portion that surrounds and separates the seeds. Pods can be divided into two parts: pulp (70-90%) and seeds. Carob pulp may undergo drying and grinding. It can also be dehulled, ground, roasted and milled into a powder, serving as chocolate substitute. During the roasting process the pulp obtains a cacao-like aroma. Isolated seeds' endosperm (nutritive tissue for the embryo/germ) serves as carob gum, also called locust-bean gum. Carob contains tannins, polyphenols that can bind proteins in the intestinal lumen and make them resistant to digestion. Dry dog foods with carob generally contain less than 3% pulp, which brings in tannin levels that slightly reduce net protein digestion, but do not jeopardize protein supply. There are no published dog studies providing any evidence for dietary carob as promoter of digestive health or as controller of diarrhea. Roasted carob pulp is used as chocolate replacer because of near comparable appearance and taste. Contrary to cacao in chocolate, carob does not contain theobromine, which can be toxic for dogs. Acute, chocolate poisoning in dogs occurs frequently, the signs being vomiting, diarrhea, excessive thirst, lack of coordination and irregular heartbeat. There is wide variation between individual dogs in their sensitivity to theobromine. Thus, keeping all dogs away from chocolate is prudent (Note 6). Some dog owners appear to fill the abstention with carob treats (Note 7), given their market supply (Note 2). Proximate composition Size, pulp:seed ratio and proximate compositon of carob pods depend on cultivar and horticultural condition (1-3). As a rough guide, carob pulp contains 5% crude protein, 1% crude fat, 7% crude fiber, 3% ash, 8% moisture and 76% soluble carbohydrates (nitrogen-free extract). The pulp's carbohydrate fraction has about 60% sucrose and 5% pinitol (4, Note 8). Seeds' germ and endosperm may contain 57 and 6% crude protein and 18 and 91% soluble carbohydrates (5, 6). The carbohydrates of endosperm (carob gum) comprise about 80% galactomannans (6), which provide gelling capacity.
Article
Full-text available
According to world statistics, dogs and cats are the species that owners most frequently seek assistance with potential poisonings, accounting 95–98% of all reported animal cases. Exposures occur more commonly in the summer and in December that is associated with the holiday season. The majority (>90%) of animal poisonings are accidental and acute in nature and occur near or at the animal owner's home. Feeding human foodstuff to pets may also prove dangerous for their health. The aim of this review was to present common food items that should not be fed (intentionally or unintentionally) to dogs, i.e. chocolate, caffeine, and other methylxanthines, grapes, raisins, onion, garlic, avocado, alcohol, nuts, xylitol contained in chewing gum and candies, etc. Onion and avocado are toxic for cats, too. The clinical effects of individual toxicants and possible therapy are also mentioned. Knowing what human food has the potential to be involved in serious toxicoses should allow veterinarians to better educate their clients on means of preventing pet poisonings. It can be concluded that the best advice must surely be to give animal fodder or treats specifically developed for their diets.
Article
Full-text available
A red fox (Vulpes vulpes) and a European badger (Meles meles) were found dead on a golf-course in October 1997 near Stockholm (Sweden). At necropsy, both animals were obese and the main finding was acute circulatory collapse. Theobromine intoxication was suspected as chocolate waste was available at a nearby farm and no other cause of death could be detected. Gastric contents and samples of liver from both animals were analyzed by reversed-phase high pressure liquid chromatography for the presence of methylxanthines. Theobromine and caffeine were detected in gastric contents and theobromine was identified in the liver samples from both animals. This appears to be the first report of theobromine intoxication in the red fox and the European badger.
Article
Pets may be exposed to a wide variety of chocolate and cocoa products, including candies, cakes, cookies, brownies, baking supplies (e.g. chocolate chips, cocoa powder), and cocoa bean mulches. Not surprisingly, most accidental chocolate exposures in pets occur around holidays, especially Valentine's Day, Easter, Halloween and Christmas, when chocolate is more prevalent in the household. Cocoa bean hull mulches are attractive to many dogs and may be ingested as dogs dig through them. 1 Because of their indiscriminate eating habits, dogs are far more commonly affected than cats. The toxic compounds in chocolate are methylxanthines, specifically theobromine and caffeine. Methylxanthines' mechanisms of action Competitive inhibition of cellular adenosine receptors is thought to cause most signs seen in animals with methylxanthine toxicosis, including central nervous system stimulation, diuresis, and tachycardia. 2 Methylxanthines also inhibit cellular calcium reuptake, which increases the free calcium concentration and enhances cardiac and skeletal muscle contractility. 2 Methylxanthines may also exert their effects by competing for benzodiazepine receptors within the central nervous system and by inhibiting phosphodiesterase, resulting in increased intracellular cyclic adenosine monophosphate. 2 Susceptibility and clinical signs The relative amounts of theobromine and caffeine vary with the form of chocolate (Table 1). In most chocolate compounds theobromine is the predominant toxic component, and caffeine is present in much lower concentrations. For animals that have ingested chocolate products made in the home or in bakeries or produced as a prepackaged mix, it may be difficult to identify the exact amount and type of chocolate used. In these cases estimate the methylxanthine dose based on a worst-case scenario. Likewise, with assorted chocolates -which include filled candies and chocolate-covered nuts -it is often safest to calculate the amount of chocolate as if the total amount were solid chocolate of the most concentrated form (e.g. if the assortment includes dark-chocolate-covered products, make calculations by using the theobromine concentration for dark chocolate). Add the theobromine and caffeine amounts to determine the total amount of methylxanthine ingested (Example 1).
Chapter
The effects of theobromine in man are underresearched, possibly owing to the assumption that it is behaviourally inert. Toxicology research in animals may appear to provide alarming results, but these cannot be extrapolated to humans for a number of reasons. Domestic animals and animals used for racing competitions need to be guarded from chocolate and cocoa-containing foods, including foods containing cocoa husks. Research ought to include caffeine as a comparative agent, and underlying mechanisms need to be further explored. Of all constituents proposed to play a role in our liking for chocolate, caffeine is the most convincing, though a role for theobromine cannot be ruled out. Most other substances are unlikely to exude a psychopharmacological effect owing to extremely low concentrations or the inability to reach the blood–brain barrier, whilst chocolate craving and addiction need to be explained by means of a culturally determined ambivalence towards chocolate. KeywordsChocolate-Cocoa-Comparative-Craving-Liking-Myths-Pharmacology-Psychology-Theobromine-Toxicology
Article
When a dog or cat ingests a common household toxin, rapid decontamination is critical. This article provides treatment recommendations for some of the most common toxicoses in dogs and cats, along with a summary table for quick reference.
Small Animal Toxicology
  • Tl Carson
Carson TL (2006) Methylxanthines. In: Peterson ME, Talcott PA (eds.) Small Animal Toxicology. 2nd ed. Saunders, St. Louis, MO. 845-852.