Emergency Medicine Investigations

Volume 2017; Issue 09
19 Jun 2017

Emergency Dermatoses

. Review Article

KeijiSugiura*, Mariko Sugiura

Department of Environmental Dermatology and Allergology, Daiichi Clinic, Nakaku, Nagoya, Japan

*Corresponding author:KeijiSugiura, Department of Environmental Dermatology and Allergology, Daiichi Clinic, Nakaku, Nagoya, Japan. Tel:+81522040834, E-mail: ksugiura@daiichiclinic.jp

Received Date:3April, 2017; Accepted Date: 3 May, 2017; Published Date: 11 May, 2017





Suggested Citation



Some dermatoses require emergency treatment. A previous report found that 15% – 20% of patients visiting family physicians and emergency departments developed dermatoses[1], and Anatoli [1] reported that about 5% to 8% of all emergency department visitors have skin complaints. Because many dermatoses are visible, acute dermatoses are very prominent and induce patients to seek treatment. Most dermatoses are not life-threatening diseases; although rare cases requiring emergency treatment are occasionally seen.


Here, we describe some emergency dermatoses induced by infection, allergy, and trauma, to help make many physicians aware of emergency dermatoses and to improve the care of people with these conditions.


Keywords:Allergy; Dermatoses; Emergency; Infection; Trauma






Necrotizing fasciitis


Necrotizing fasciitis can occur after trauma or surgery, and lead to rapidly progressive necrosis of the deep fascia and subcutaneous tissue. Skin manifestations include swelling with pain, erythema and burgundy skin color with bulla and hematoma, and indurated edema with bad-smelling. General symptoms include high fever with an anguished look. The two types of bacteria that cause this disease are group A beta-hemolytic streptococciand Staphylococcus aureusin type 2, and non-group A streptococci, gram-negative enterococci or aerobic bacilli, peptostreptococcus and mixed anaerobes in type1[2-4]. The risk factors of this fasciitis are diabetes, immunosuppression, vascular disease, drinking alcohol, and trauma. If physicians suspect this condition, early treatment by surgical debridement of necrotizing tissue and broad-spectrum antibiotics with hospitalization is needed. Without rapid, correct treatment, patients develop shock, sepsis, organ failure and poor prognosis.  It has been reported that up to 70% of patients develop sepsis [2,3].




Tetanus is a common acute neurological disease in developing countries. Tetanus is caused by clostridium tetani infection via a cutaneous wound. A venom, tetanospasmin, affects the peripheral and central nerves, thus resulting in sympathetic nerve activation such as general cramps, arrhythmia, changes in blood pressure, respiratory arrest and hyperhidrosis. It is important to keep the wound clean, and one way to prevent tetanus is to cleanse the wound promptly. This disease can be prevented by a vaccine; the World Health Organization (WHO) recommends the administration of three doses of a tetanus toxoid [5].






Anaphylaxis was first described in 1902 [6]. The incidence of anaphylaxis ranges from 1.5 to 7.9 per 100,000 person-years, and about 0.3% (95% CI 0.1-0.5) of the European population was reported to experience anaphylaxis [7]. Most cases of anaphylaxis are caused by food products (32.2%), drugs (29.2%), and insect venom (19.3%) [8].


There are three main clinical types of food allergy, including anaphylaxis, Food-Dependent Exercise-Induced Anaphylaxis (FDEIA), and Oral Allergy Syndrome (OAS) [9]. Anaphylaxis and FDEIA are life-threating reactions. Worm [10] reported that in children, the most frequent trigger is food, and in adult cases insect venom and drugs are frequent triggers.  A previous report showed that the most common foods to induce these reactions were shellfish and peanuts [11], and another report showed the most common food allergens to be cow milk, egg, peanuts, tree nuts, soy, and shellfish [12]. The kinds of foods that cause anaphylaxis vary depending on eating habits, religion, country, and local area.


The most common drugs that cause anaphylaxis have been found to be Nonsteroidal Anti-Inflammatory Drugs (NSAID) and antibiotics [13,14]. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are life-threating drug allergy.


Systemic allergies against insects have been reported in up to 3-8.9% of adults and 1% of children [15-19]. Insect allergies are well-known to be caused by Hymenoptera and formicidae[14]. Hymenoptera stings can result in very severe anaphylaxis [20]. Bees are divided into apids and vespids, and vespids can sting repeatedly. Aphids usually sting once and leave the stinger in the skin. In cases of vespid stings, the clinical symptoms are more severe than with aphid stings. Anaphylaxis requires rapid treatment with hospitalization. If the patient does not receive medical treatment, he or she will develop shock symptoms. It is recommended that outdoor laborers and patients with bee allergies always have an epinephrine auto-injector (EpiPen®) in their possession.


Stevens-Johnson Syndrome (SJS) andToxic Epidermal Necrolysis (TEN)


SJS and TEN are life-threating drug allergies. Most cases of SJS and TEN are drug induced [21], with 80-90 % of TEN cases [22] caused by drugs including sulfa drugs, antibiotics, NSAIDs, and antiepileptic agents [23]. SJS is also referred to as mucocutaneoocular syndrome; MCOS, and it is a serious erythema multiforme type of drug-induced eruption. This is an epidermal necrotizing disorder characterized by as erythema, bulla, epidermal necrosis, mucosa erosion, and desquamated skin. SJS can often progress to TEN, and the incidence of death is approximately 20-30%. In such cases, widespread skin disorders can be seen, and it can result in fluid loss, electrolyte imbalance, skin barrier breakdown, easily infection (bacteria, fungal), ocular disability, corneal ulcerations, and an inability to regulate body temperature. These symptoms can result in high fever, hypotension, painful burning, tachycardia, conjunctivitis, melena, renal failure, respiration failure, and coma.


Food-Dependent Exercise-Induced Anaphylaxis(FDEIA)


The first case of this anaphylaxis was reported in 1979 [24]. It is triggered by exercise (physical activity) after the consumption of allergenic foods. Common allergens that can cause FDEIA are tomatoes, peanuts, cereals, shellfish, oranges, milk, mushrooms, flour and soybeans [25-29]. Most cases of FDEIA occur within 2-3 hours after eating. Often, when students develop FDEIA, it occurs in physical education class after lunch. It is important for individuals with FDEIA to avoid allergens before exercise. Patients who consume allergens should rest quietly for at least 2-3 hours afterward.




Urticaria or angioedema with respiratory symptoms (dyspnea, wheezing, cough) or interstitial symptoms (abdominal pain, diarrhea) involve not only urticaria but also edema of the respiratory or gastrointestinal tract. These symptoms can lead to suffocation or ileus depending on the case. It is recommended that a fast-acting steroid injection be administered




Extensive or Airway (Respiratory Tract) Burn


Extensive burns can cause dehydration within 1 hour and infection can develop within 48 hours, and such cases require intensive care. Replenishment of water and infection prevention are essential treatments in the early stage of an extensive burn. Extensive burns can have many different causes, such as traffic accidents, occupational burns and even to taking an excessively hot bath.


Airway (respiratory tract)burns lead to inflammation or necrosis of the mucus membrane of the trachea. Signs of airway burns include scorched skin around the mouth and nose and the scorching of nose hairs. Airway burns can be caused by accidental explosions, fire, smoking under oxygen treatment and others. When a physician sees a patient with these signs, it is important to maintain the airway for breathing, even just in suspected cases.


Chemical Burns


Chemical burns make up 3-5% of all burns [30] and cause 30% of burn-associated deaths[31,32]. Chemical burns can be caused by six different processes, namely reduction, oxidation, corrosion, vesication, desiccation, and protoplasmic poisoning, and such burns result in protein denaturation [33,34]. Denatured tissue protein can’t regenerate as protein; it needs to be removed. Chemical substances remain and cause progressive destruction of tissue until they are inactivated by tissue reactions [35], and this often results in deep burns. A widespread chemical burn can lead to organ failure in other organs. Because the depth of the burn and the failure of other organs depend on the duration of the contact with chemical compounds [36-39], the wound must be washed and debrided immediately.There are various compounds causing chemical burns as follows [40]:


  • Acids: acid burns cause coagulative necrosis;
  • Alkalis: alkalis cause liquefactive necrosis that may progress to deeper tissues;
  • Bases: bases lead to deep burns and cause liquefactive necrosis of the tissue;
  • Organic solutions: organic solutions are absorbed quickly and cause disorders in other organs;
  • Phenol (carbonic acid): phenol absorption causes cardiac arrest, renal failure, and liver failure;
  • Hydrofluoric acid: hydrofluoric acid affects cell membranes and produces coagulation necrosis with severe pain;
  • Chromic acid: chromic acid penetrates cell membranes and causes coagulative necrosis, renal failure, and liver failure;
  • Cement: cement is a common cause of chemical burns and is classified as an alkali;
  • Tar: tar causes liquefactive necrosis; and
  • Hydrochloric and sulphuric acids: hydrochloric and sulphuric acids cause coagulative necrosis.


The essential treatments and management techniques for chemical burns are wound evaluation[36-39], neutralization[41], removal of the chemicals, debridement, and re-assessment of the injury[40].


Jellyfish, Snake and Spider with Venom Bite


Jelly Fish Stings


There are about 150 million cases of jellyfish stings per year [42].


There are five classes in the phylum Cnidaria: Cubozoa (box jellyfish), Scyphozoa (true jellyfish), Hydrozoa (Portuguese Man O’ War, fire corals, and hydroids), Anthozoa (sea anemones and true corals), and Staurozoa (Stauromedusae) [43,44].  Cubozoa (box jellyfish) are the most dangerous jellyfish; they are found in harbors and shallow waters [44, 45]. The venom of Cubozoa is a cardiotoxin, and Cubozoa stings can lead to death in less than 30 seconds [46].


Cubozoa are divided two subgroups: Carybdeids with four smaller tentacles, and Chirodropids with large multi-tentacles [47,48].


Carybdeid stings cause severe life-threatening systemic symptoms which are collectively referred to as Irukandji syndrome [49,50].


Chirodropids are the most life-threatening animal in the world and are found in the summer months in both the Northern and Southern Hemispheres. They sting in shallow water and cause envenomation [49]. A few hours after being stung by a Chirodropid, swelling, blistering, and necrosis occur. If the victim does not rapidly receive first aid or medical treatment, he or she will stop breathing within a few minutes after the envenomation and die [49]. The Australian Resuscitation Council (ARC) recommends vinegar application, tentacle removal, and ice-pack application.


Snake bites


Snake bites cause many symptoms depending on the kind of snake or venom encountered.


The frequency of snake envenomation was 421,000 to 1,842,000 cases and the number of deaths among these cases was 20,000 to 94,000 each year [51]. The prevalence of snake bites is 13.33 in South and Southeast Asia, 12.59 in Latin America and 11.11 cases in sub-Saharan Africa / 100,000 inhabitants [52-54]. Most snake bites occur in South and Southeast Asia, Sub-Saharan Africa, and Latin America [55-57]. Surprisingly, in only one country, India, which has the most snake bite deaths in the world, the number of deaths ranges between 15,000 and 50,000 a year [58]. The mortality rate of snake bites depends upon the species and size of the snakes, the amount of venom, the site of the bite, the presence of bacteria in the mouth of the snake, and the human action taken after the snake bite [58].


The gender breakdown of snake bite victims shows that more males than females suffer from snake bites, most likely because males engage in more outdoor activities than do females [59,60]. Most snake-bite victims are farmers and laborers, especially in rural areas; also, 55% of snake bites occur in the early morning (before 6 am) [58]. One possible explanation for this timing is that farmers and laborers start working early in the morning and most snakes are active in the night and early morning.


At present, there is a global antivenom crisis. The WHO estimates that it needs about 10 million vials of antivenom each year to control the effects of snakebite envenomings[56, 61], although low prospects for commercial returns and a lack of interest have hampered the advance of antivenom technology [62].


Spider Bites


There are more than 50,000 spider species in the world, and about 4% of them are considered dangerous to humans [63-67].


Spider venom can cause several tissue disorders; these venoms are divided into two main types, neurotoxins and necrotoxins[63,68]. Spider venom affects muscular systems and blood cells and results in breathing difficulties and death. Surprisingly, the toxicity of some spider venoms is 15 times than that of the typical viper [67].


Previous reports found that the frequency of spider bites is highest during warm seasons (August in the northern hemisphere) [69-73]and during times when spiders are active (8:00-20:00) [74].


The symptoms caused by spider bites include both local (erythema, edema, itching, burning, and pain) and systemic reactions (dyspnea, hypotension, anxiety, vomiting, diarrhea, and fever).




More than 12,500 species of ants have been reported [75]. Ants possess poison glands in the posterior part of their bodies [76], and the ant venoms that cause anaphylaxis are spray acids and alkaloids derived from piperidine [25, 26,77,78]. The poison glands of ants secrete a variety of chemicals which vary between ant queen and workers [76]. Sting reactions are normally immediate local reactions (pain, swelling, and erythema at sting sites within 1-4 hours after ant stings), immediate large reactions (a reaction larger than 10 cm in diameter persisting for longer than 24 hours), general cutaneous reactions (pruritus and urticaria), systemic reactions and delayed-type hypersensitivity [79], and life-threatening systemic reactions (anaphylaxis).


Systemic allergic reactions (anaphylaxis) were reported to occur in about 2% of fire-ant sting cases [80,81]. One way to prevent spider or formicids bites is to wear long-sleeved shirts, pants, and gloves sprayed with insecticide.



  1. Freiman A,Borsuk D,Sasseville D (2005) Dermatologic emergencies. CMAJ 173: 1317-1319.
  2. Usatine R, Smith MA, Mayeaux EJ,Chumley H, Tysinger J (2009) The Color Atlas of Family Medicine. McGraw-Hill, New York, NY.
  3. Centers for Disease Control and Prevention (2009) Group A Streptococcal(GAS) disease.
  4. Freiman A, Borsuk D, Sasseville D (2005) Dermatologic emergencies. CMAJ 173:1317-1319.
  5. Borrow R, Balmer P, Roper MH (2006) The Immunological Basis for Immunization Series-Module 3: Tetanus Update 2006, Geneva, WorldHealth Organization:1-63.
  6. Portier P, Richet C (1902) De I’ action anaphylactique de certainsvenins. C R SocBiol54: 170-172.
  7. Panesar SS, Javad S, de Silva D, Nwaru BI, Hickstein L, et al. (2013) The epidemiology of anaphylaxis in Europe: a systematic review. Allergy 68: 1353-1361.
  8. Beyer K, Eckermann O, Hompes S,Grabenhenrich L, Worm M (2012) Anaphylaxis in an emergency setting – elicitors, therapy and incidence of severe allergic reactions. Allergy 67:1451-1456.
  9. Moriyama T (2015) Diversity of Food Allergy. J Nutr Sci Vitaminol 61: S106-108.
  10. Worm M, Babina M, Hompes S (2013) Causes and risk factors for anaphylaxis. J DtschDermatolGes 11: 44-50.
  11. Yocum MW, Khan DA (1994) Assessment of patients who have experienced anaphylaxis: a 3-year survey. Mayo Clin Proc 69: 16-23.
  12. Turnbull JL, Adams HN, Gorard DA (2015) Review article: the diagnosis and management of food allergy and food intolerances. Aliment PharmacolTher 41: 3-25.
  13. Kemp SF, Lockey RF, Wolf BL, Lieberman P (1995) Anaphylaxis. A review of 266 cases. Arch Intern Med 155: 1749-1754.
  14. Cohglan-Johnston M, Lieberman P (2001) Dermographic and clinical characteristics of anaphylaxis. J Allergy ClinImmunol107: 557.
  15. Golden DB, Marsh DG, Kagey-Sobotka A, Freidhoff L, Szklo M, et al. (1989) Epidemiology of insect venom sensitivity. JAMA 262: 240-244.
  16. Stuckey M, Cobain T, Sears M, Cheney J, Dawkins RL (1982). Bee venom hypersensitivity in Busselton. Lancet 2: 41.
  17. Nittner-Marszalska M, Cichocka-Jarosz E (2015) Insect sting allergy in adults: key messages for clinicians 125: 929-937.
  18. Settipane GA, Newstead GJ, Boyd GK (1972) Frequency of Hymenopteraallergy in an atopic and normal population. J Allergy ClinImmunol50: 146-150.
  19. Björnsson E, Janson C, PlaschkeP, Norrman E, Sjöberg O (1995) Venom allergy in adult Swedes: a population study. Allergy 50: 800-805.
  20. Ollert M, Blank S (2015) Anaphylaxis to insect venom allergens: role of molecular diagnostics. Curr Allergy Asthma Rep 15: 26.
  21. Usatine RP, Sandy N (2010) Dermatologic emergencies. Am Fam Physician 82: 773-780.
  22. James WD, Berger TG, Elston DM, Odom RB (2006) Andrews’ Diseases of the Skin: Clinical Dermatology. In: 10, Saunders Elsevier, Philadelphia.
  23. Parrillo SJ (2007) Stevens-Johnson syndrome and toxic epidermal necrolysis. Curr Allergy Asthma Rep 7: 243-247.
  24. Maulitz RM, Pratt DS, Schocket AL (1979) Exercise-induced anaphylactic reaction to shellfish. J Allergy ClinImmunol 63: 433-434.
  25. Morita E, Kunie K, Matsuo H (2007) Food-dependent exercise-induced anaphylaxis. J Dermatol Sci 47: 109-117.
  26. Morita E, Matsuo H, Chinuki Y, Takahashi H, Dahlström J, et al. (2009) Food-dependent exercise induced anaphylaxis-importance of omega-5 gliadin and HMWglutenin as causative antigens for wheat-dependent exerciseinduced anaphylaxis. Allergol Int 58: 493-498.
  27. Du Toit G (2007) Food-dependent exercise-induced anaphylaxis in childhood. Pediatr Allergy Immunol 18: 455-463.
  28. Adachi A, Horikawa T, Shimizu H, Sarayama Y, Ogawa T, et al. (2009) Soybean beta-conglycinin as the main allergen in a patient with food-dependent exercise-induced anaphylaxis by tofu: food processing alters pepsin resistance. ClinExp Allergy 39: 167-173.
  29. Romano A, Di Fonso M, Giuffreda F, Papa G, Artesani MC, et al. (2001) Food-dependent exercise-induced anaphylaxis: clinical and laboratory findings in 54 subjects. Int Arch Allergy Immunol 125: 264-272.
  30. Wasiak J, Spinks A, Ashby K, Clapperton A, Cleland H, et al. (2009) The epidemiology of burn injuries in an Australian setting, 2000-2006. Burns 35: 1124-1132.
  31. Pegg SP (2005) Burn epidemiology in the Brisbane and Queensland area. Burns 31: S27-S31.
  32. Watson WA, Litovitz TL, Rodgers GC Jr, Klein-Schwartz W, Reid N, et al. (2005) 2004-Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 23: 589-666.
  33. Jelenko C (1974) Chemicals that burn. J Trauma 14: 65-72.
  34. Elijah IE, Sanford AP, Lee JO (2012) Chemical Burns. In: Herndon DN, editor. Total Burns Care In:4, Elsevier, New York: 455-460.
  35. Sarabahi S, Bajaj SP (2008) Step by Step Management of Burns. In: 1, Chap. 10, Chemical Burns. Jaypee Brothers, New Delhi: 180.
  36. Zhang F, Zheng XF, Ma B, Fan XM, Wang GY, et al. (2015) Mass chemical casualties: treatment of 41 patients with burns by anhydrous ammonia. Burns 41: 1360-1367.
  37. Sykes RA, Mani MM, Hiebert JM (1986) Chemical burns: retrospective review. J Burn Care Rehabil 7: 343-347.
  38. Braue EH Jr, Graham JS, Doxzon BF, Hanssen KA, Lumpkin HL, et al. (2007) Noninvasive methods for determining lesion depth from vesicant exposure. J Burn Care Res 28: 275-285.
  39. Arturson G (1996) Mechanism of injury. In: Settle JAD, editor. Principles and practice of burns managemen. New York: Churchill Livingstone.
  40. Gnaneswaran N, Perera E, Perera M, Sawhney R (2015) Cutaneous chemical burns: assessment and early management. Australian Family Physician 44: 135-139.
  41. Yano K, Hata Y, Matsuka K, Ito O, Matsuda H (1994) Effects of washing with a neutralizing agent on alkaline skin injuries in an experimental model. Burns 20: 36-39.
  42. Boulware DR (2006) A randomized controlled field trial for the prevention of jellyfish stings with a topical sting inhibitor. J Travel Med 13: 166-171.
  43. Tibballs J (2006) Australian venomous jellyfish, envenomation syndromes, toxins and therapy. Toxicon 48: 830-859.
  44. Haddad JV, Silveira FL, Migotto AE (2010) Skin Lesions in Envenoming by Cnidarians (Portuguese Man-Of-War and Jellyfish): Etiology and Severity of Accidents on the Brazilian Coast. Rev Inst Med Trop Sao Paulo 52: 47-50.
  45. Tibballs J, Yanagihara AA, Turner HC, Winkel K (2011) Immunological and toxinological responses to jellyfish stings. Inflamm Allergy Drug Targets 10: 438-446.
  46. Rosson CL, Tolle SW (1989) Management of marine stings and scrapes. West J Med 150: 97-100.
  47. Williamson JA, FennerPJ, Burnett JW, Rifiin J (1996) Venomous and poisonous marine animals: a medical and biological handbook. New South Wales University Press, Sydney.
  48. Winkel KD, Hawdon GM, Fenner PJ, Gershwin LA, Collins AG, et al. (2003) Jellyfish antivenoms: Past, present, and future. J Toxic 2: 115-127.
  49. Fenner PJ (1998) Dangers in the Ocean: the traveler and marine envenomation. I. jellyfish. Journal of Travel Medicine 5: 135-141.
  50. Tibballs J, Li R, Tibballs HA, Gershwin LA, Winkel KD (2012) Australian carybdeid jellyfish causing Irukandji syndrome. Toxicon59: 617-625.
  51. Kasturiratne A, Wickremasinghe AR, de Silva N, Gunawardena NK, Pathmeswaran A, et al. (2008) The global burden of snakebite: a literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med 5: e218.
  52. Warrell DA (2010) Snake bite. Lancet 375: 77-88.
  53. Chippaux JP (2011) Estimate of the burden of snakebites in sub-Saharan Africa: a meta-analytic approach. Toxicon 57: 586-599.
  54. Avau B, Borra V, Vandekerckhove P, De Buck E (2016) The Treatment of Snake Bites in a First Aid Setting: A Systematic Review. PLOS Neglected Tropical Diseases 10: e0005079.
  55. Kasturiratne A, Wickremasinghe AR, de Silva N, Gunawardena NK, Pathmeswaran A, et al. (2008) The global burden of snakebite: a literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med 5: e218.
  56. World Health Organization (WHO) (2007) Rabies and Envenomings- A neglected public health issue. Geneva: WHO: 1-38.
  57. Mohapatra B, Warrell DA, Suraweera W, Bhatia P, Dhingra N, et al. (2011) Snakebite mortality in India: a nationally representative mortality survey. PLoSNegl Trop Dis 5: e1018.
  58. Jarwani B, Jadav P, MadaiyaM (2013) Demographic, epidemiologic and clinical profile of snake bite cases, presented to Emergency Medicine department, Ahmedabad, Gujarat. J Emerg Trauma Shock 6: 199-202.
  59. Bakshi SA (1999) Snake bites in rural area of Maharashtra state, India. TropDoct 29: 104-105.
  60. Bambery P (2008) Snake Bites and Arthropod Envenomation. In: 8. Shah SN. API Textbook of Medicine. The Association of Physicians of India Publication, Mumbai: 1517-1520.
  61. Scheske L, Ruitenberg J, Bissumbhar B (2015) Needs and availability of snake antivenoms: relevance and application of international guidelines. Int J Health Policy Manag 4: 447-457.
  62. Williams DJ, Gutiérrez JM, Calvete JJ, Wüster W, Ratanabanangkoon K, et al. (2011) Ending the drought: new strategies for improving the flow of affordable, effective antivenoms in Asia and Africa. J Proteomics 74: 1735-67.
  63. Rash LD, Hodgson WC (2002) Pharmacology and biochemistry of spider venoms. Toxicon 40: 225-254.
  64. Isbister GK, Graudins A, White J, Warrel D (2003) Antivenom treatment in arachnidism. J ToxicolClinToxicol 41: 291-300.
  65. Diaz HJ (2004) The global epidemiology, syndromic classification, management, and prevention of spider bites. Am J Trop Med Hyg 71: 239-250.
  66. Bayram A, Yigit N, Danısman T, Corak I, Sancak Z, et al. (2007) Venomous spiders of Turkey (Araneae). J ApplBiol Sci 1: 33-36.
  67. Yigit N, GuvenT, Bayram A, Cavusoglu K (2004) A morphological study on the venom apparatus of the spiderAgelenalabyrinthica(Araneae, Agelenidae). Turk J Zool 28: 149-153.
  68. Yigit N (2005) The comparative protein profiles of venom and venom gland extracts of Agelenalabyrinthica (Araneae: Agelenidae). Gazi Univ J Sci 18: 555-561.
  69. Sezerino MU, Zannin M, Coelho LK, Gonçalves J, Grando M, et al. (1998) A clinical and epidemiological study of Loxosceles spider envenoming in Santa Catarina, Brazil. Trans Roy Soc Trop Med Hyg92: 546-548.
  70. Silva PHD, Silveira RBD, Appel MH, Mangili OC, Gremski W, et al. (2004) Brown spiders and loxoscelism. Toxicon44: 693-699.
  71. Forrester MB, Stanley SK (2004) Epidemiology of spider bites in Texas, 1998-2002. Public Health 118: 506-507.
  72. Cristiano PM, Cardoso CD, Raymundo MS (2009) Contextual analysis and epidemiology of spider bite in southern Santa Catarina State, Brazil. Trans Roy Soc Trop Med Hyg 103: 943-948.
  73. Cesaretli Y, Ozkan O (2011) A clinical and epidemiological study on spider bites in Turkey. Asian Pac J Trop Med 4: 159-162.
  74. Isbister GK, Gray MR (2002) A prospective study of 750 definite spider bites, with expert spider identification. Q J Med 95: 723-731.
  75. Potiwat R, Sitcharungsi R (2015) Ant allergens and hypersensitivity reactions in response to ant stings. Asian Pac J Allergy Immunol; 33: 267-275.
  76. Brindis Y, Lachaud JP, Gomez YGB, Rojas JC, Malo EA, et al (2008) Behavioral and olfactory antennal responses of Solenopsisgeminata(Fabricius) (Hymenoptera: Formicidae) workers to their dufour gland secretion. NeotropEntomol37: 131-136.
  77. Potiwat R, Sitcharungsi R (2015) Ant allergens and hypersensitivity reactions in response to ant stings. Asian Pac J Allergy Immunol 33: 267-275.
  78. Chen J, Cantrell CL, Shang HW, Rojas MG (2009) Piperideine alkaloids from the poison gland of the red imported fire ant (Hymenoptera: Formicidae). J Agric Food Chem; 57: 3128-3133.
  79. Stafford CT (1996) Hypersensitivity to fire ant venom. Ann Allergy Asthma Immunol 77: 87-95.
  80. Stafford CT, Hutto LS, Rhoades RB, Thompson WO, Impson LK (1989) Imported fire ant as a health hazard. South Med J 82: 1515-1519.
  81. Cho YS, Lee YM, Lee CK, Yoo B, Park HS, et al. (2002) Prevalence of Pachycondylachinensis venom allergy in an ant-infested area in Korea. J Allergy ClinImmunol 110: 54-57.
Suggested Citation


Citation: Sugiura K,Sugiura M (2017) Emergency Dermatoses. Emerg Med Inves 2017: EMIG-144.

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