40 Advances in Environmental Biology, 2(1): 40-48, 2008 ISSN 1995-0756

40
Advances in Environmental Biology, 2(1): 40-48, 2008
ISSN 1995-0756
© 2008, American-Eurasian Network for Scientific Information
This is a refereed journal and all articles are professionally screened and reviewed
O RIGINAL A RTICLE
Necrotic Araneism. A Review of the Loxosceles Genus. II. Clinical Findings, Diagnosis
and Treatment
1
Héctor Gabriel Ramos Rodríguez and 2José D. Méndez
1
Medical Gerontology Module. “Tlalpan” Family Medicine Clinic, ISSSTE, School of Geography. Faculty of
Philosophy and Letters, National Autonomous University of Mexico (UNAM)
2
Medical Research Unit in Metabolic Diseases, 21 st Century National Medical Center, Mexican Institute of Social
Security P.O. Box A-047, 06703 Mexico City, D.F., Mexico.
Héctor Gabriel Ramos Rodríguez and José D. Méndez,: Necrotic Araneism. A Review of the Loxosceles
Genus. II. Clinical Findings, Diagnosis and Treatment: Adv. Environ. Biol., 2(1): 40-48, 2008
ABSTRACT
Spider bites are the result of an incidental and accidental encounter between the arachnid and humans and
usually happens when unused shoes and clothing are put on or secretly while sleeping. Diagnosis is often made
by examining the lesion after the bite and rarely is a spider identified at the time of the attack. Loxosceles sp has
been implicated in causing necrotic skin lesions, secondary complications, and in some instances, even considered
life-threatening. Fatalities are rare but are much more common in children, the ill, and the elderly. No treatment
has been medically proven for Loxosceles poisoning.
Key words: Arachnidism, Loxosceles, Necrotic arachnidism, Necrotic ulcer, “Violin” spider, Venomous spiders,
Spider envenomation
Introduction
Skin loxoscelism
Often times, spider bites go unnoticed[1]. In
general terms, the victim feels no pain for the first 2-3
hours[2]. On certain occasions (20%)[3,5], it only
causes transitory pain, reddening and local
swelling (marmoreal plaque in the form of a
volcano[6,7]) in the first 10 minutes[8]. On the
average, the victim requires medical care after the first
3-8 hours, when the pain and itching are intense (a
burning sensation is felt)[9,11]. There are two types of
skin loxoscelism, the necrotic (75%) and edematous
(4%)[5]. The signal that identifies the bite are two
micro punctures (points) separated at least by 6
mm[12]. In mild cases, the local reaction is erythema
and edema with an itching sensation[13,14]. The
edematous appearance, depending on the severity, is
characterized by an edema of extraordinary
dimensions with a minor component of necrosis and
erythema (in general, the godet sign is negative) and
is the best prognostic tool[15,17]. Frequently, it
extends to downward surfaces, a phenomenon seen
when bitten in the face, neck or sectors proximal
to the extremities[17]. The intense inflammatory
response is media te d by ara chidonic a cid,
prostaglandins and the chemotactic infiltration of
neutrophils which is amplified by the intrinsic vascular
cascade that involves the reactive protein C and the
activation of the complement[9]. After 6-8 hours, the
affected area is painful and itchy, showing a central
indurate area surrounded by a pale ischemic zone and
another exterior erythematous section that conforms
the typical bull’s-eye sign (red-white-blue)[18,20], a
liveloid plaque (purple stain) secondary to the
gravitational dissemination of the venom (Figure 1)
[5,9,21].
Corresponding Author
José D. Méndez, 21st Century National Medical Center, Mexican Institute of Social Security
P.O. Box A-047, 06703 Mexico City, D.F., Mexico.
Telephone Number: +52 55 5627 6900 ext. 21561 Fax Number: +52 55 5227 6109
E-mail: [email protected]
Adv. Environ. Biol., 2(1): 40-48, 2008
41
Ski n-visceral Loxoscel ism (Systemic Loxoscel ism)
(SVL)
Fig. 1: Liveloid plaque, red or purple, of irregular
borders and variable dimensions[22].
In the majority of the cases, the lesion disappears
without treatment after 2-3 days[1,14,23]. For the first
24-72 hours[24], fever of variable intensity may occur,
with chills, weakness, nausea, vomiting, muscle pain,
joint pain, rash, sleep disorders and petechia together
with leukocytosis and thrombocytopenia[25,27].
It may be similar to having influenza[28]. In order of
importance, the arms, legs, neck or lower part of the
abdomen are the anatomical regions mainly
affected[3,14,16]. However, the majority of the times
the victims seeks medical care after some time[3].
Over 80% of the patients see their physician six hours
after the bite and almost 60% does it after 12
hours[29].
In severe cases (approximately 10%)[18], in
a lapse of 24 - 48 hours, the erythema disseminates
and the center of the lesion appears hemorrhagic,
necrotic and with a flictena in the upper part, of
sero us or serohemorrhagic content[13 ,14,17].
Peripheral necrotic areas (satellite ulcers) with
hemorrhages may form[1] without involving
ganglia[17] and later skin, subcutaneous tissue or
even muscle destruction [25, 28, 30]. Necrosis is
significant in areas with fat as in the gluteus, thighs
and abdominal wall[9]. A black scab forms, which
falls off after several weeks with large tissue loss,
leaving several residual ulcers of 1-25 cm in
diameter[14,31]. Finally, about three weeks are needed
for a wide and depressed (deformed) scar to form,
time during which pain is of importance[1,14,25].
Healing
takes place 3-6 months later but may
continue for up to three years if there is extensive
affection of adipose tissue.
Systemic reactions are severe (14-22%), with
several deaths being reported [16, 21, 32]. Acute cases
that place lives in danger generally limit themselves to
children with manifestations such as intravascular
hemolysis, anemia, hemoglobinuria, hematuria,
hyperkalemia, petechia, jaundice, high fever (39.742.0°C)[17], nausea, vomiting, joint pain, muscle pain,
chills, hypotension[22], seizures, kidney failure
(oliguria/anuria), hypercatabolic syndrome[33],
multiple organic failure, respiratory distress[34],
pulmonary edema and shock[1,14,21,25], maybe due
to a lesser body area venom distribution[16].
Classically, there will be slight macular erythema
(exanthema) on the chest and extremities[35].
W hen there is visceral involvement, massive
hemorrhagic lesions are seen in the liver and kidneys.
Shock and anaphylaxis are seen in severe cases,
especially in children, the elderly and weak
patients[3,36]. Kidney failure can be induced by
disseminated intravascular coagulation, but also seems
to be linked to the action of metallo-proteins that
degrade the extra-cellular matrix and damage the
integrity of the basal membranes of the kidney’s blood
vessels[5]. The majority of the cases of SVL (73.5%)
show signs indicative of hemolysis within the first six
hours of evolution[29]. The blood abnormalities
include hemolytic anemia, thrombocytopenia and
leukocytosis[16]. Urine is often walnut brown[17].
Other risk factors related to this type of presentation
are: chest and abdominal bites, fever, nausea and
vomiting in the first 24 hours[33].
Among the results of loxoscelism are: 1) death,
almost exclusively restricted to skin-visceral or
visceral-hemolytic cases (15%), is also related to
massive hemolytic anemia associated to acute renal
failure. In the Chilean series, 23.5% mortality has
been reported in this group of patients and 3.7% of
the total cases of loxoscelism. In relation to the
temporary handicap, in the majority of those affected,
the disease resolved within the first three weeks,
although there are cases that may extend for six or
more weeks[5,29,33]. In general, recovery of an attack
leaves behind complete systemic immunity against
subsequent accidents, although there may be an
intense local reaction with skin loss[37].
Complications
Approximately half evolve and form a necrotic
scab. Of these, two thirds become ulcers; the majority
heals spontaneously without leaving sequelae.
Only 8% evolve and form a keloid scar. The
prop ortion of patients that develop ulcers
(approximately 50%) is greater in those that develop
a liveloid plaque from the start, than those with an
Adv. Environ. Biol., 2(1): 40-48, 2008
erythematous plaque (16 %). Consequently, the final
evolution to a scar with sequelae is proportionally
greater in individuals with a liveloid plaque, in
comparison to those with an erythematous plaque
(approximately 12% vs. 3%). The exception could be
the predominantly erythematous form – edema as the
only skin manifestations, especially in facial accidents
– but the scarcity of cases does not allow scientists to
reach a conclusion. Palpebral lesions have been
described that often require grafts (Figure 2)[22,38].
Myonecrosis, pseudoepitheliomatous hyperplasia
and gangrenous pioderm are often seen as
complications[6]. Diaphragmatic paralysis is rare[39].
Other local sequelae include lesions to the nerves and
secondary infections (Figure 3). The presence of
Clostridium perfringens is associated to the necrotic
process. All of the forms of skin loxoscelism are
painful to the touch[22,38].
Diagnosis
Anamnesis is important in searching for the
geographical location of the accident (rural or urban
area), whether domiciliary or peridomiciliary, time of
day, place of work, activity carried out at the time of
the bite, animal characteristics if seen, whether the
spider is caught, history of bites or stings by other
animals, addictions, allergic and pathologic history,
etc.[40].
No laboratory tests exist that confirm diagnosis.
Its diagnosis is eminently clinical and necessary for
the identification of the arachnid[15,21]. The spider is
seen in 80% of the cases and identified in 13%[5].
Nonetheless, there is a need to determine and monitor
hemolysis data, conducting a hemogram for platelet
count, prothrombin time (PT), partial prothrombin
time (PTT), kidney function (urea and creatinine) and
serum electrolytes (especially potassium)[20,21].
The urinalysis may show some evidence of systemic
in vo lv e m e nt ( h em oglo binuria, m yo glo bin uria ,
hematuria). Gram stain and wound culture should be
done on wounds for identifying contaminating
microorganisms[9,41]. Similarly, hepatic functionality
test, fibrinogen and fibrin degradation products should
be measured[16].
If treatment with dapsone is considered, G-6-PD
levels should be measured[9]. The ELISA-specific
passive hemaglutination inhibition test has been
developed for detecting the venom at the site of the
bite and IgG-specific in serum, although none is
available in the clinical practice[6,16]. Similarly, there
is a fast ELISA test for detecting the venom in skin
and hairs up to four days after the bite[42]. There are
crossed reactivity tests for the Loxosceles venom and
from other arthropods with similar poisoning
strategies, with sensitivity for detecting up to 40 ng
[43]. The differential diagnosis should be done with
problems that cause similar lesions (Table 1).
42
Treatment
General Measures
The initial management is antisymptomatic and
consists in cleaning the wound locally (washing with
cold water and mild soap), placing colds pads or ice,
sterile bandage, avoiding or decreasing physical
activity, elevating or mild immobilization of the
affecte d a rea ( R IC E ). D o n o t ap ply
tourniquets[6,31,44]. Hot pads on the affected area
must be avoided (this may accelerate tissue
destruction), as well as lotions with steroids, nor
remove the venom using suction, incisions or
e le ctro the ra p y[2 0 ,4 5 ] . S in c e the a ctio n o f
sphingomyelinase D is dependent on temperature
(more active at 37°C) the use of cold pads should be
continued until the progression of the necrotic process
is stopped[9]. If necessary, administer analgesics,
antihistamines (in skin cases), hemorrheologics
(pentoxifilin), a ntim icro b ials and a tetanus
shot[13,14,30,33]. Solutions and dextran may be used
if the patient so requires[1]. Chloropheniramine is
indicated at a dose of 5-10 mg/tid/i.v. for 2 days
(0.4 mg/kg/day/qid) and 10 mg every 8, 12 or 24
hours v.o.[3] or dextrochlorophenamine at a dose of
0.15 mg/kg/day for the time necessary until the
disappearance of pain, edema and the delimitation of
necrosis[5]. Hydroxicin, at a dose of 25 mg/tid/vo is
effective if there is morbiliform rash and itching[9].
Diphenhydramine is used at a dose of 50-75
mg/v.o./i.m. in adults and 1-2 mg/kg/v.o./i.m. in
children[9]. Morphine and other opium derivatives
should be avoided since they can increase the effect of
the venom[36]. Insufficient data to justify the use of
nitroglycerin is unavailable[9]. Tetracycline, a
metalloproteinase inhibitor, may help in avoiding cell
death and the subsequent destruction of tissues[46].
Recently, importance has been given to the use of
da psone and cholc hic in[4,26], inhibitors of
polymorphonuclear leukocytes[21]. If the local
reaction progresses rapidly or ulcers appear, dapsone
is administered orally at a dose of 50-200 mg/bi/10-25
days[5,6], previous exclusion of a deficit of glucose-6phosphate dehydrogenase[13,14,31,35]. The pediatric
dose is 1-2 mg/kg/d/v.o. without exceeding 100
mg/d[9]. Precaution must be taken with collateral
effects such as general malaise, nausea and hemolysis
that may be confused with the systemic effects of the
venom[47]. Cholchicin is administered at a dose of
1.2 mg/v.o., followed by 0.6 mg/2 h/2 days and then
0.6 mg/4 h/2 days more[5]. Previously, in persons
bitten by spiders (or by unidentified species) that
develop skin lesions within the first 12 hours and that
increased in size during the following 12 hours,
dexamethasone is recommended at a dose of 4
mg/quid/i.m. during the acute phase and then in
decreasing doses based on standard practice[30].
Adv. Environ. Biol., 2(1): 40-48, 2008
43
Table 1: Pathologies that cause sim ilar necrotic lesions to those produced by Loxosceles
Pyoderm ias (Staph. and Strept.)
Poison ivy
Lym e disease
Poisonous oak
H erpes sim plex
Gonococci derm atitis-arthritis
D iabetic ulcer
Rocky m ountain fever
W orm bites
Stevens-Johnson syndrom e
Acarus bites
Lym phom atoid papulosis
Tick bites
Sporotrichosis
W asp sting
Adverse reactions to drugs
Fly bites
H erpes zoster
Bites by other spiders
Lym phom as
Focal vasculitis
Fulm inant purpura
Syphilitic chancre
Anthrax
Chickenpox
Traum a
Angioneurotic edem a
Skin lupus erythem atosus
Throm boem bolic phenom ena
Chem ical burns
N odule erythem a
W arfarin poisoning
H eparin poisoning
N odule periartheritis
M ultiform erythem a
Toxic epiderm al necrolysis
Pressure ulcers
Skin m ycosis
Squam ous cell Carcinom a
Varicose ulcers
N ecrotizing fascitis
Erysipela
Fig. 2: Chronology and characteristics of injuries caused by the Loxosceles bite. The clinical evolution is
variable and is in relationship to the species involved, the patient's response, treatment and complications
established aggregate. The images relate to people of both sexes and different ages, several anatomical
regions affected, various therapeutic schemes and different places of residence.
The parenteral route is preferred due to the affection
of the gastrointestinal mucosa which would damage
the absorption of drugs[17]. Low doses of aspirin
(100 mg/day) are recommended[48].
Patients will remain under observation at hospitals
when they have a rapid expansion of lesions or have
evidence of systemic toxicity which requires
conservative wound care, immobilization, elevation
Adv. Environ. Biol., 2(1): 40-48, 2008
44
Fig. 3: Sequence of day 3 to 10 of the lesions after a Loxosceles bite in the hand of a male patient with severe
tissue destruction[9].
and proper treatment if a bacterial infection occurs[9].
The skin-visceral cases require hospitalization for
proper antishock and antitoxic management, carrying
out the rigorous handling of fluids and electrolytes,
with an indication of blood transfusion when
necessary[5,9]. Although the efficacy of local or
system ic gluco co rtico id s has n o t b e e n
demonstrated[1,14], when used they are administered
immediately to counteract severe reactions[13,36]
(80 mg of methylprednisone/i.m./during transportation
to the hospital[34]); hydrocortisone succinate
(1g/qid/i.v./48 h, later continuing, if necessary, with
prednisone 40-100 mg/v.o. (1-2 mk/kg/d), once a day
during the mornings for four to five days, in
decreasing amounts of 10 mg/d associating it with an
antihistamine orally administered[49,51]. A short oral
scheme of prednisone may decrease hemolysis.
Methylprednisone is administered at a dose of 2-60
mg/d and 1 mg/kg/d/v.o. in adults and children,
respectively[9]. Another scheme is that of 80
mg/d/i.m. immediately after the bite, continued for a
week and with decreases of 40 mg, 20 mg and 10
mg/d for a total of 10 days[34]. If there is
anaphylactic shock, adrenaline is injected at 1:1000
s.c. at the dose and frequency based on the severity
and response[49,50,51]. In case of severe hypotension
or shock: adrenaline 0.3-0.5 mg/s.c. (with local
massage to improve absorption), 11 mg/i.m. for adults
and 0.001 mg/kg to a maximum of 0.3 mg in children.
The dose can be repeated after 10-15 minutes based
on evolution. In severe cases an ampulla of adrenaline
can be used (1 mg/i.v. diluted in 9 c.c. of
physiological solution in bolus repeated in 2-3 ml,
equivalent to 0.2-0.3 mg[48].
Heparin’s real use has not been proven[1].
Sa tis fa c to ry re s ults we re a chie ve d through
Adv. Environ. Biol., 2(1): 40-48, 2008
hemodialysis and / or peritoneal dialysis in patients
with skin-visceral loxoscelism[17].
After 72 hours a urinalysis and complete blood
count to detect any evidence of systemic toxicity is
recommended. In case of fever or dark urine, the
patient must return to the hospital immediately[9].
Surgical Procedure
Certain authors recommend the surgical excision
of the wound as soon as possible[26], preferably
within the first 24 hours[1,25]. Others mention that
this may be damaging and that the debridation as well
as the use of a skin graft is recommended after the
acute inflammation subsides, once necrotic damage is
extensive[14,35,36]. If the necrotic tissue is to be
removed, this must be extensive, with daily wound
washings using saline solution until granulation is
achieved[3]. Preferably, a conservative debridement
should be done, once the wound margins are welldefined, since a wider excision may be disabling,
disfiguring and rarely indicated[9]. Only 3% heal with
scars that require excision[52].
Occasionally, the intervention of a plastic surgeon
is required, especially in extensive areas with dermonecrotic compromise[53,55]. W hen a total thickness
defect is caused, the definite surgical treatment
involves a skin graft or a total flap, depending on the
base area and its extension[56].
Antimicrobials
Initially, the wound is not infected for the first
two or three days, but may become contaminated
when the patient scratches the wound due to intense
itching[57].
Others proposed indications are: daily washing of
the ulcerate wounds with 3% oxygenated water,
submerging in Burrow solution at 1:20/tid for 15
minutes or apply a triple watery coloring (brilliant
green 1:400, genciana violet 1:400 and acriflavin
1:1000) three times a week, as in the case of crotale
bites.
The use of ointments containing polymixin,
neomycin and bacitracin during the evenings is also
recommended[30].
If an additional infectious process is suspected,
due to the slow evolution of the dermonecrotic
process, this makes it inclined to G ram positive
microorganisms (streptococci and staphylococci)
attraction, considering the use of cloxacylin,
flucloxacylin, cefalexin, oral penicillin or clindamycin
necessary. Gram negative agents and anaerobes are
less frequent[58,59]. The use of erythromycin
prophylactically is universally accepted to avoid
additional wound infections[56]. In 11 cases of
children, the administration of dicloxacylin plus
45
dapsone 1 mg/kg/d was effective, since none evolved
systemically[60].
Biologics
If in some countries the development of antidotes
against the Loxosceles venom has started they have
not been approved for their use due to the lack of
satisfactory clinical assessments. Nonetheless, 10
ampoules of antiloxoscelic serum/i.v.[4,14,25] are
recommended. In Brazil, a polyvalent hyperimmune
ecquine serum is used against Phoneutria nigri venter,
Loxosceles gaucho, Tityus serrulatus and T. bahiensis
(scorpions)[36,61], indicating that 1 ml neutralizes less
than 6 necrotizing minimum doses and 1 ml of
lexoscelic serum (made from L. intermedia) for 15
DMN[61]. The monovalent antisera derived from
different Loxosceles species share their abilities for
neutralizing the dermonecrotic activity. Particularly,
those produced from L. intermedia and L. gaucho
maintains their properties when faced with L.
laeta[29].
In Peru, depending on the severity of the case, the
dose recommended for children as well as adults is 1
or 2 ampoules of antiloxoscelic serum/s.c. in the
interscapulary zone or i.v. at a 1:3 dilution with
physiologic serum[40].
In Mexico, a technique named Fabotherapy
(portions of Fab2 of immunoglobulins) has been
developed and perfected with a high level of
specificity neutralizing venoms while avoiding adverse
reactions of first and second generation sera[62]. It is
suggested that the application of the antiloxoscelic
serum as soon as possible within the first 2-4 hours
after the accident is the best measure possible, which
is not always easy. In cases of skin loxoscelism, 5
ampoules/i.v. are applied and 5-10 ampoules for the
s k in -v is c e r a l fo r m [ 5 ,6 ,1 7 ] . T h e p o lyv a le n t
phototherapeutic antiarachnid (Latrodectus and
Loxosceles) by slow i.v. or i.m. at a dose of 5-15 ml
(one to three bottles), that can be increased depending
on the severity, possesses the neutralizing ability of
6,000 L D 5 0 [63]. Currently, Bioclon-Silanes produce a
specific fabtherapeutic to counteract the poisoning of
the Loxosceles (Loxmyn), obtained from recombinant
toxins from spiders from the United States, M exico
and Peru that may be useful against the “violinists”
from the American continent[64].
The only mention on adverse events is found in
the Brazilian series from Santa Catarina reporting
6.5% (8/125) reactions catalogued as mild: skin
rashes, facial rubor, nausea and vomiting, rash, chills
and bronchial spasm[29]. From the antidote of
hyperimmunized equine, the reactions are of the
anaphylactic type and anaphylactoid and occur in a
higher frequency in persons treated with the
product[22].
Adv. Environ. Biol., 2(1): 40-48, 2008
46
Indications for applying the biologics are: 1. the
aggravating animal is a spider with morphological
attributes to the Loxosceles genera; 2. the patient does
not have the arthropod but refers that the bite was by
a spider within the home and has loxoscelism
manifestations; 3. the subject does not pinpoint the
origin nor the circumstances that made the accident
possible but the place where it presumably started
points to spider webs, or identifiable spider remains;
4. without any data, the victim reveals a clinical
pattern compatible with loxoscelism, and 5. in all
severe clinical presentations[40].
6.
Results and discussion
12.
If in the majority of the cases of arachnidism, the
spider is not identified, it has been currently seen that
a greater number of people develop necrotic ulcers
probably due to the great variety of species found
distributed throughout the Mexican Republic or even
the introduction of dangerous species such as L.
recluse and L. laeta that cause severe poisoning in the
United States and South America. As the attacks
usually occur, the bite is produced accidentally when
dressing or sleeping with no differences found in
gender. Therefore, since the lesions produced by the
“violin” spider bites are unspecified, the following
observations should be considered for a definite
diagnosis: potential exposure to these spiders, their
detailed identification, the characteristics of the lesions
and the clinical course[18], due, it is known that the
poison from other genera such as Phoneutria, Lycosa,
Tegenaria and Chiracanthium contain necrotoxins
References
1.
2.
3.
4.
5.
M oye de Alba, C.E., 1997. En: Manual de
Terapéutica M édica y P rocedimientos de
Urgencia. Aguilar S C, Prado C E, Cañedo C S,
Chevoile R J, Saucedo J, Kaplan S.M., Díaz A,
Eraña G J (Eds). México: McGraw Hill-I
nteramericana.
Nieuwenhuys, E., 2001. Spiders an Immunology.
University of Florida. Department of Entomology
and Nematology.
Vázquez, O.V., 1992. En: Arañas de Chiapas.
Alvarez del Toro M (Ed). M éxico: Universidad
Autónoma de Chiapas.
Olson, K.R., 1994. En: Diagnóstico Clínico y
Tratamiento. Tierney L M, McPhee S J,
Papadakis M A, Schroeder S A (Eds). México:
Manual Moderno.
Rodrìguez, D.D., R.J. Mogollòn, J. Guevara, A.
Rodrìguez, A.C. Eslava and M .F. Valdivia,
Envenenamiento por arañas. Facultad de Medicina
de la Universidad Privada “AntenorOrrego”. Perù.
www.monografias.com/trabajos16/aracn idosveneno/aracn idosveneno.shtml
7.
8.
9.
10.
11.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
Quintana, C.J.C. and P.R. Otero, 2002.
Envenenamiento aracnídico en las Américas.
MEDUNAB, 5(13): 1-9.
V orlesu
ngsskripte
Zoop hysiolo gie.www.
sinnesphysiologie.de/kanal/iono07.htm
Spiders Bite., 2002. Brown Recluse Spiders. Pest
Management. University of California.
Arnold T., 2002. Loxosceles in the United States.
eMedicine Journal, 3(4): 2-11.
Omundo da aranha., 1974. www.geocities.com/
~esabio/ aran ha/aranha_princi pal. htm.
Potter M., 2002. Brown Recluse Spider. College
of Agricultura. University o Kentucky.
Bücherl, W ., 1969. Biology and venoms of the
most important South American spider of genera
Phoneutria, Loxosceles, Lycosa and Latrodectus.
Am Zool, 157-159.
Goodard, J., 1993. Physician’s Guide to
Arthropods of Medical Importante. USA: CRC
Press.
Maguire, J.H., 1998. Spielman A. En: Principios
de Medicina Interna. Vol. II. Fauci A S,
Braunwald E, Isselbacher K J, W ilson J D, Martin
J B, Kasper D L, Hauser S L, Longo D L.
España: McGraw Hill-Interamericana.
Phillip, S., 1995. Araneismo (brown spider). Am
Emerg Med., 25: 363-368.
W alley, S and C. Johnston, 1997. Loxosceles
reclusa y loxoscelismo: The Brown Recluse
Spider and Envenomation Reactions. Annals of
Emergency Medicine, 30: 28-32.
Schenone, F.H., 2003. Cuadros tóxicos producidos
por mordeduras de araña en Chile: Latrodectismo
y loxoscelismo. Rev Méd Chile, 131: 437-444.
W ilson, C.D. and E.L. King, 1999. Arthropod
Bites and Stings. In: Dermatology in General
Medicine. Vol. II. Freedberg I.M ., Eisen
A.Z., Wolff K., Austen K.F., Goldsmith L.A.,
Katz
S.I.,
Fitzpatrick
T.B., (Eds). USA:
McGraw Hill.
Eliastam, M., G.L. Sternbach and B.M. Jay, 1994.
Manual de Medicina de Urgencias. Quinta
Edición. España: Mosby/Doyma.
Keim, S.M., 2002. Spider bite, brown recluse.
eMedicine.com.
Echenique, G., 2003. Latrodectus mactans y
Loxosceles laeta. Ponencia. Animales Venenosos,
2003.
Loxoscelismo. Araña del rincón (Loxosceles
laeta). www.2udec .c l/~lpa lma /loxosc elism o/
loxoscelismo.html
Berger R.S., 1973. The unremarkable brown
recluse spider bite. JAMA, 225: 1109-1111.
Professional Pest Control Products. Brown
Recluse B ite. Spider E limination.
Petsproducts.net.
Harwood, R.F., M.T. James, 1987. Entomología
Médica y Veterinaria. México: Editorial Limusa.
Adv. Environ. Biol., 2(1): 40-48, 2008
26. Condom, F., 1992. Manual de Terapéutica
Quirúrgica. España: Editorial Salvat.
27. Brown recluse spiders. KU Department of
Entomology, 2001.
28. Swing, F.P., 1999. Acupunture for treatment of a
nonhealing brown recluse spider bite: a case
report. Medical Acupuntura a Journal for
Physicians for Physicians, 11(1): 1-6.
29. Araujo, M. and F. Otaiza, 2002. Efectividad del
suero anti-Loxosceles. Sìntesis de evidencia.
ETESA.
30. Russell, F.E., 1987. En: El Manual Merck.
Berkow R, Fletcher A). España: Ediciones
Doyma.
31. Hunt, T.K. and E. Jawetz, 1989. Intoxicaciones
en: Diagnóstico y Tratamiento Quirúrgicos ed.
W ay L W (Ed). México: Manual Moderno.
32. Murakami, M.T., P.M.F Fernandes, D.V.
Tambourgi and R.K. Arni, 2005. Structural Basis
for M etal-Ion Coordination and the Catalytic
Mechanism of Sphingomielynases D. ASBMB,
2005: 1-26.
33. Maquiña, V.C., J.C. Hinojosa, R. G utiérrez, C.
Henríquez and C. Ugarte, 2004. Enfermedades por
artrópodos. Parte I: Loxoscelismo cutáneo y
cutáneovisceral en el Perú. Dermatol Perú, 14(2):
1-10.
34. Villaveces, J.W ., 1968. Gangrenous Spider Bite in
Los Angeles County (Apparently by Loxosceles
recluse). California Medicine, 108(4): 305-308.
35. Ruiz Maldonado. Tratado de Dermatología
Pediátrica. México: Editorial I nteramericana,
1991.
36. Diniz, C.R., 1971. Venomous Animals and their
Venoms. Vol. III. USA: Academic Press.
37. Suárez, H.M., A.J.J. Pérez, M.T. Rodríguez and
M.E. Pena, 1998. Aracnoidismo sistémico. Rev
Cubana Med Gen Integr, 14(1): 1-5.
38. Monteiro, C.L.B, Rubel R., Cogo L.L.,
Mangili O.C., Gremski W ., Vega S.S., 2002.
Isolation and identification of Clostridium
perfringens in the venom and fangs of Loxosceles
intermedia (brown spider): enhancement of the
dermonecrotic lesion in loxoscelismo. Toxicon,
40: 409-418.
39. Pascolat, G., 2005. Animais Peçonhentos. Hospital
U n iv e rsitá rio E v a n g é l ic o d e C u ritib a .
www.pediatriaevangelico.com.br/cient/aula/pec.a
sp.
40. Di Nardo, L.C., C.A. González and R. Bertrand,
2005. Picadura por arácnidos del género
Loxosceles. Boletín Epidemiológico, 5: 6-8.
41. Hurtado, V.J.G, C.N. Sotelo and S.R. Ibarra,
2005. Envenenamiento por Loxosceles reclusa
(araña “parda”).Rev Mex Pediatr, 72(2): 85-88.
42. Miller, M.J., H.F. G ómez, R.J. Snider, E.L.
Stephens, R.M. Czop and J.S. W arren, 2000.
Detection of Loxosceles venom in lesional hair
47
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
shafts and skin: Application of a specific
im m u n o a s s a y t o i d e ntify d e rm o ne c ro tic
arachnidism. Am J Emerg Med., 18: 626-628.
Gómez, H.F., D.M. Krywko and W .V. Stoecker,
2002. A new assay for the detection of Loxosceles
species (brown recluse) spider venom. Ann Emerg
Med., 39(5): 469-474.
Vetter, R., 2005. How to identify and misidentify
a brown recluse spider. Dermatol Online J.,
5(2): 7.
Cantera, H.R., Cuidado con las mordeduras de
araña.Hospital Regional Docente de Trujillo.
www.peruprensa.org/Sp030806.htm
Paixão, C.D., C.W . van den Berg, F.M. de
Freitas, R.M. Gonçalves and D.V. Tambourgi,
2006. Role of Matriz Metalloproteinases in
HaCaT Keratinocytes Apoptosis Induced by
Loxosceles Venos Sphingomyelinase D. J Invest
Dermatol, 126: 61-68.
Ramos, R.H. and R.I. Vázquez, 1999. Arañismo
ocasionado por especies del género Loxosceles
(Araneae; Sicariidae). Rev Educ Salud, 29: 25-34.
Pastrana, J., R. Blasco and M.A. Pinillos, 2003.
Picaduras y Mordeduras de animales. Anales
Hosp. Navarra, 26(Supl. 1): 1-24.
Rook. Tratado de Dermatología. España: Editorial
Doyma, 1989.
Platnick, N., 1993. Advances in Spider Taxonomy
1988-1991. W ith Synonimies and Transfers 19401980. USA: New York Entomological Society,
American Museum of Natural History.
Brown, W .H., 1977. Parasitología Clínica.
México: Interamericana.
Fiddleback Spider., 1999. J Fam Pract, 48(7):
536-42.
Coyle, F.A., 1994. Brown Recluse Spider.
Loxosceles recluse. Animal Facts. W ildwnc.org.
Flaherty, C., 2003. Symptoms, diagnosis and
treatment of bite of aggressive house spider
(compared to brown recluse spider bite).
C om m unication Se rvices. M ontana S tate
University.
W irschum, S.R., K.D. do Rocio, C.D. María,
M.O. Carlos and S.I José, 2002. Differential
distribution of constitutive heterochromatin in two
species of brown spider: Loxosceles intermedia y
L. laeta (Araneae, Sicariidae) from the
metropolitan region of Curitiba, PR (Brazil). Acta
Biol Par, 31(1,2,3,4): 123-136.
Portilla, C.J., Q.M. Maresca, S.B. Hoyos, B.J.
Garcìa, M.J. Velez 2005., Lesiòn necròtica
palpebral por picadura de araña. Arch Soc Esp
Oftalmol, 80(2): 1-5.
Spider
bites.www.dermatology.
cdlib.org/cgibin/search. pl?query=Loxosceles %20
envenomation&index=doj .swish.
Guía Clínica para el Manejo de Mordedura de
Araña de Rincón o Araña Casera (Loxosceles
Adv. Environ. Biol., 2(1): 40-48, 2008
laeta). www.foros.mo nografias.com /archive/
index.ph p/t-32605.html (2006).
59. M artino, O., T. Orduna and M. Espinosa, 2002.
La Agresión de los Animales y su I mportancia en
la Salud. www.aps.org.ar/_private/
Laagresion(IParte).pdf.
60. Escalante, G.P., C.M .A. M ontoya, L.V.M .
Terroba, J.A. Nava and F.I. Escalante, 1999.
Loxoscelismo local dermonecrótico en niños
mordidos por la araña Loxosceles reclusa (araña
“violin ista”). Gac Méd Méx., 35(4): 426-436.
61. Braz, A., J. Minozzo, J.C. Abreu, I.C. Gubert and
C. Chávez-Olórtegui, 1999. Development and
evolution of the neutralizing capacity of horse
antivenom against the Brazilian spider Loxosceles
intermedia. Toxicon, 37: 1323-1328.
48
62. Silanes, 1999. Nueva tecnología para el
tratamiento de intoxicaciones por animales
ponzoñosos. Investigación y Desarrollo, 71: 12.
63. Secretarìa de Salud. Aclaraciòn a la Norma
O fic ia l M e x ic a n a N O M -0 3 6 -S S A 2 -2 0 0 2 ,
prevenciòn y control de enfermedades. Aplicaciòn
de vacunas, toxoides, sueros, antitoxinas e
inmunoglobulinas en el humano. Publicada el 17
de julio del 2003. Fecha de publicación 20 de
enero del 2004. www.salud.gob. mx/u nidades/cd
i/nom/compi/acl036ssa202.html.
64. Alagón, C.A., Anticuerpos terapéuticos: El caso
de los antivenenos. Instituto de Biotecnología,
UNAM. www.ibt.unam .mx.