Clinical management of apisination in dogs--a report of 2 patients.
Each year large number of companion animals fall victim to honey bee (Apoidea) stings usually in the spring and then late summer (September to October and April to May) especially in wooded hilly areas, groves, caves, high walled buildings and parks where swarms of bees are found hanging. Honey bees attack usually to protect their hives or when a sound, smell or a color or something has provoked them. It could be dogs barking, children playing or working of noisy equipments like tractors, lawn movers or thrashers (Muhammad et al., 2000). They attack usually during the day while they are out and tending their hives and rarely attack during the evening and night hours. The sting may be single or multiple (hundreds). As we do not yet have safe, efficacious anti-venom, we have to develop guidelines for the most appropriate care aimed at reducing the risk of death among these patients.
The present paper reports toxic envenomation due to multiple stings by rock honey bee (Apisination) in two dogs and describes treatment guidelines that comprise emergency care, drugs, and the proper removal of stingers and local treatment.
History and Observations
A 7 yr old Pomeranian and 4 months old German shepherd pup belonging to the same owner were presented with history of both being attacked by a swarm of rock honey bees while playing in a park. At the time of presentation (i.e. 20 min after the stings), both dogs were dyspnoeic, hypotensive, comatosed and seizuring with multiple stings and dead honey bees all over the body. Vomiting, defecation, urination, muscle weakness and difficulty in breathing were noticed during transportation. Most of the stings were on areas covered by sparse hairs i.e. inner surface of ear pinna (Fig. 1) and ventral aspect of neck (Fig. 2), abdomen (Fig. 3) and tail (Fig. 4). There were dead rock honey bees all over the body (Fig. 5).
Since toxic envenomation / anaphylaxis is always an emergency following aggressive treatment was under taken, as the first 60 minutes is the critical period to save life of animals (Almeida et al., 2011):
The animals were initially stabilised by Inj. Adrenaline 1:1000 @ 0.5 ml s/c repeated every 30 minutes for three times and Inj. Aminophylline @ 10 mg/kg b. wt. I/M to reduce bronchospasm. Inj. Methyl Prednisolone Sodium Succinate @ 10/ kg. b. wt. I/V was administered followed by 2 mg/ kg for next two days, every 12 hours followed by tapering of dose. Inj. Chlorphenaramine maleate @ 0.5 mg/kg b. wt. I/M twice daily were used as antihistaminics. Inj Diazepam (1 mg/ kg. b. wt.) and Inj. Tramadol (1mg/kg b.wt.) were used as anticonvulsant and analgesic. Oro-tracheal intubation with assisted ventilation (oxygenation) was done for initial two hours of presentation. Inj. Ceftriaxone with Tazobactum @ 15 mg / kg b.wt. I/ V (Intacef Tazoa) was advocated to avoid secondary infections.The total hemodynamic stabilization was maintained with administration of inj. Ringers lactate solution (initial 90 ml/kg/hr). Removed stingers one by one, paying attention to not to squeeze the sac to avoid inoculating the venom they contain by using the razor to scrap close to the skin. Applied Potassium permanganate at 1:40,000 dilution for antisepsis of the stung areas. Then a cream containing mixture of Lidocaine jelly, Corticosteroid lotion, calendula oint, NaHCO3 and Vaseline was used to relieve pain and unpleasant burning sensation.
Animals responded well to the above treatment and condition stabilized. Over the following 12 hrs, both dogs developed azotemia, elevated liver enzyme levels, hypertension, hemoglobinurea and hematochezia. Hemolysis and Rhabdomylosis was suspected. To reduce the effect on kidney and heart, the above treatments (except Adrenaline) were repeated every 12 hrs for three days.
Osmotic diuresis was induced with 20% Mannitol, @ 10 ml/kg. b. wt. I/V every 12 hrs for two days along with I/V Fluids. Inj. Ranitidine @ 2mg /kg. b. wt. I/V was administered alkalinized the urine with Sodium bicarbonate solution at a dose of 1 to 2m g/kg weight/dose every 12h to prevent renal lesions caused by Hemoglobinuria and Myoglobinuria.
Both dogs returned to normalcy by fourth day with ongoing polyuria and polydipsia. The polydipsia and polyuria resolved by 7 days.
The rock honey bees (Apis dorsata) are notoriously famous for their swarming capacity, aggressiveness and en masse attacking behavior and have caused serious and fatal accidents both in humans and other animals. The inoculated quantity resulting from massive attacks causes serious envenomations and development of an acute syndrome characterized by release of large quantity of pro-inflammatory mediators including cytokines, thus causing a sharp inflammatory response that triggers disturbances in immune system, heart, liver, kidneys, central nervous system, bone marrow, blood vessels and skeletal muscles, among others (Bresolin et al., 2002 and Betten et al., 2006). Massive envenomation as seen in swarm attacks, can likewise cause death in nonallergic individuals. The estimated lethal dose is about 20 stings / kg in most mammals (Manoquerra et al., 2001).
Bee venom is a complex mixture of biologically active components, primarily consisting of proteins, enzymes and amines. The major components of honeybee venom are Mellitin, (a direct hemolysin, cytotoxic and cardiotoxic; is a protein that hydrolyzes cell membranes, alters cellular permeability and causes histamine release and also responsible for local pain), Phospholipase [A.sub.2] (the major allergenic component and causes intravascular hemolysis), Peptide 401 (or mast cell degranulating peptide-causes mast cells to degranulate, releasing histamine and vasoactive amines), Apamin (a neurotoxin that acts on spinal cord), Adolapin (inhibits prostaglandin synthetase and Hyaluronidase (causes changes in cell permeability by altering cell membranes and disrupts collagen, allowing other venom components to penetrate into victim's tissues). The venom also contains vasoactive amines, such as histamine, dopamine and non epinephrine and other unidentified proteins (Fitzgerald and Flood, 2006).
Typically, honeybee stings are manifested as localized painful edema without a systemic reaction. Generally the small local reaction of erythema, edema, and pain at the site of sting is a self-limiting, non-IgE-mediated condition, which spontaneously resolves within 24 hours and application of ice will suffice. Occasionally, more severe type of reaction is a systemic, anaphylactic response caused by an immediate hypersensitivity reaction occurs. For dogs, Signs typically are seen within 15 minutes of sting and if a systemic reaction has not started within the first 30 minutes, it is unlikely to occur. Fatalities typically occur within 60 minutes of initial sting. The signs of anaphylaxis are attributable to antigen-induced IgE release and formation of chemical mediators that target smooth muscle and blood vessels (Hahn and Lewin, 2002).
Extraction of stings together with their poison sacs as soon as possible is most essential and important step in treatment of honey bee stinging. The honey bees possess capability to sting using a modified ovipositor found on terminal end of their abdomen. Honeybees can only sting once; After they sting, a barbed stinger and a venomous sac stays behind in victim's skin tearing bee's abdomen and soon after insect dies. The longer the sting stays in the skin the more poison passes into body. Therefore sting should be pulled out as soon as possible without compressing. Instead scrapping sideways with blade, card board or plastic is recommended (Muhammad et al., 2000).
When bees sting they deposit an alarm pheromone that triggers other bees to sting at same site leading to en masse attach. The pheromone (Isopentyl acetate) has an odour that smells like ripe bananas (Hahn and Lewin, 2002). So, ripened bananas should not be carried to picnic spots as they are likely to attract honey bees.
Almeida, R.A. M.B., Olivo, T.E.T., Mendes, R.P., Barraviera, S.R.C.S. and Barraviera B. (2011).
Africanized honeybee stings: how to treat them. Revista da Sociedade Brasileira de Medicina Tropical. 44: 755-61.
Betten, D.P., Richardson, W.H., Tong, T.C. and Clark, R.F. (2006). Massive honey bee envenomation-induced rhabdomyolysis in an adolescent. Pediatrics 117: 231-35.
Bresolin, N.L., Carvalho, F.C., Goes, J.C., Fernandes, V. and Barotto, A.M. (2002). Acute renal failure following massive attack by Africanized bee stings. Pediatr Nephrol. 17: 625-27.
Fitzgerald, K. T. and Flood, A. A. (2006) Hymenoptera Stings. Clin Tech Small Anim Pract. 21: 194-204.
Franca, F.O., Benvenuti, L.A. and Fan, H.W. (1994). Severe and fatal mass attacks by "killer" bees in Brazil: Clinicopathological studies with measurement of serum venom concentrations. Q J Med 87: 269-282.
Hahn, I. and Lewin, N.A. (2002). Arthropods, in Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds). Goldfrank's Toxicologic Emergencies (ed 7). New York: McGraw-Hill,
Manoquerra, A.S. (2001). Hymenoptera stings, in Ling L, Clark R, Erickson T, et al (eds): Toxicology Secrets. Philadelphia, Hanley and Belfus,
Muhammad, G., Saqib, M. and Mallick, S.H. (2000). Honey bee stinging (Apisination): what medicinal and veterinary professionals ought to know. Pakistan Vet J. 20: 209-11.
Association of Indian Zoo and Wildlife Veterinarians (AIZWV) and Indian Council of Agricultural Research are organising International Symposium on Ecology and Health Management of Asiatic Elephant in its landscape at NASC Complex D.P.S. Marg, Pusa New Delhi -110012, India on 10-11th November' 2015
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A.S. Patil (1), Suvarna Patil (2), Sangeetha Jadhav (3), B. N. Nagaraja (4) and
L. Ranganath (5)
College of Agriculture
University of Agriculture Sciences (UAS)
(1.) Assistant Professor and Corresponding author
(2.) Assistant Professor, Horticulture Entamologist, COHB, UHS, Bagalkot
(3.) Veterinary Officer, Dept of AH and VS, Karnataka
(4.) Professor, Dept of Surgery, Veterinary College, KVAFSU, Bengaluru
(5.) Professor and Head, Dept of Surgery, Veterinary College, KVAFSU, Bengaluru
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|Title Annotation:||Clinical Article|
|Author:||Patil, A.S.; Patil, Suvarna; Jadhav, Sangeetha; Nagaraja, B.N.; Ranganath, L.|
|Date:||Jan 1, 2015|
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