Wednesday, 9 March 2011

VINCHUCA BUG (Chagas disease)

From Wikipedia, the free encyclopedia

Chagas disease (Portuguese: doença de Chagas, Spanish: enfermedad de Chagas-Mazza, mal de Chagas in both languages; also called American trypanosomiasis) is a tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. T. cruzi is commonly transmitted to humans and other mammals by an insect vector, the blood-sucking bugs of the subfamily Triatominae (family Reduviidae) most commonly species belonging to the Triatoma, Rhodnius, and Panstrongylus genera.The disease may also be spread through blood transfusion and organ transplantation, ingestion of food contaminated with parasites, and from a mother to her fetus.
The symptoms of Chagas disease vary over the course of an infection. In the early, acute stage, symptoms are mild and usually produce no more than local swelling at the site of infection. The initial acute phase is responsive to antiparasitic treatments, with 60-90% cure rates. After 4–8 weeks, individuals with active infections enter the chronic phase of Chagas disease that is asymptomatic for 60-80% of chronically infected individuals through their lifetime. The antiparasitic treatments also appear to delay or prevent the development of disease symptoms during the chronic phase of the disease, but 20-40% of chronically infected individuals will still eventually develop life-threatening heart and digestive system disorders. The currently available antiparasitic treatments for Chagas disease are benznidazole and nifurtimox, which can cause temporary side effects in many patients including skin disorders, brain toxicity, and digestive system irritation.
Chagas disease is contracted primarily in the Americas, particularly in poor, rural areas of Mexico, Central America, and South America; very rarely, the disease has originated in the Southern United States. The insects that spread the disease are known by various local names, including vinchuca in Argentina, Bolivia, Chile and Paraguay, barbeiro (the barber) in Brazil, pito in Colombia, chinche in Central America, chipo in Venezuela, chupança, chinchorro, and "the kissing bug". It is estimated that as many as 8 to 11 million people in Mexico, Central America, and South America have Chagas disease, most of whom do not know they are infected. Large-scale population movements from rural to urban areas of Latin America and to other regions of the world have increased the geographic distribution of Chagas disease, and cases have been noted in many countries, particularly in Europe. Control strategies have mostly focused on eliminating the triatomine insect vector and preventing transmission from other sources.


Signs and symptoms

Gross anatomy of a heart that has been damaged by chronic Chagas disease. See also: Chagas heart, radiology
The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years.
The acute phase lasts for the first few weeks or months of infection. It usually occurs unnoticed because it is symptom free or exhibits only mild symptoms that are not unique to Chagas disease. These can include fever, fatigue, body aches, headache, rash, loss of appetite, diarrhea, and vomiting. The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands, and local swelling (a chagoma) where the parasite entered the body. The most recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or accidentally rubbed into the eye. Rarely, young children, or adults may die from the acute disease due to severe inflammation/infection of the heart muscle (myocarditis) or brain (meningoencephalitis).The acute phase also can be severe in people with weakened immune systems.
If symptoms develop during the acute phase, they usually resolve spontaneously within 3–8 weeks in approximately 90% of individuals.Although the symptoms resolve, even with treatment the infection persists and enters a chronic phase. Of individuals with chronic Chagas disease, 60-80% will never develop symptoms (called indeterminate chronic Chagas disease), while the remaining 20-40% will develop life-threatening heart and/or digestive disorders during their lifetime (called determinate chronic Chagas disease). In 10% of individuals the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease.
The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two thirds of people with chronic symptoms have cardiac damage, including cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may be the first symptom of digestive disturbances and may lead to malnutrition. Twenty to fifty percent of individuals with intestinal involvement also exhibit cardiac involvement. Up to 10% of chronically infected individuals develop neuritis that results in altered tendon reflexes and sensory impairment. Isolated cases exhibit central nervous system involvement, including dementia, confusion, chronic encephalopathy and sensitivity and motor deficits.
The clinical manifestations of Chagas disease are due to cell death in the target tissues that occurs during the infective cycle, by sequentially inducing an inflammatory response, cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases due to heart muscle damage.


Rhodnius prolixus is the principal vector in Colombia, Venezuela, Guatemala, Honduras and some parts of Nicaragua and El Salvador.
In Chagas-endemic areas, the main mode of transmission is through an insect vector called a triatomine bug.[1] A triatomine becomes infected with T. cruzi by feeding on the blood of an infected person or animal. During the day, triatomines hide in crevices in the walls and roofs. The bugs emerge at night, when the inhabitants are sleeping. Because they tend to feed on people’s faces, triatomine bugs are also known as “kissing bugs.” After they bite and ingest blood, they defecate on the person. Triatomines pass T. cruzi parasites (called trypomastigotes) in feces left near the site of the bite wound. Scratching the site of the bite causes the trypomastigotes to enter the host through the wound, or through intact mucous membranes, such as the conjunctiva. Once inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, which are then released into the bloodstream. This cycle is repeated in each newly infected cell. Replication resumes only when the parasites enter another cell or are ingested by another vector.[1] (See also: Life cycle and transmission of T. cruzi)
Dense vegetation (such as that of tropical rainforests) and urban habitats are not ideal for the establishment of the human transmission cycle. However, in regions where the sylvatic habitat and its fauna are thinned by economical exploitation and human habitation, such as in newly deforested areas, piassava palm culture areas, and some parts of the Amazon region, a human transmission cycle may develop as the insects search for new food sources.[8]
T. cruzi can also be transmitted through blood transfusions. With the exception of blood derivatives (such as fractionated antibodies), all blood components are infective. The parasite remains viable at 4°C for at least 18 days or up to 250 days when kept at room temperature. It is unclear whether T. cruzi can be transmitted through frozen-thawed blood components.[9]
Other modes of transmission include organ transplantation, through breast milk,[10] and by accidental laboratory exposure. Chagas disease can also be spread congenitally (from a pregnant woman to her baby) through the placenta, and accounts for approximately 13% of stillborn deaths in parts of Brazil.[11]
In 1991, farm workers in the state of Paraíba, Brazil, were infected by eating contaminated food; transmission has also occurred via contaminated açaí palm fruit juice and sugar cane juice.[12][13][14] A 2007 outbreak in 103 Venezuelan school children was attributed to contaminated guava juice.[15]


Photomicrograph of Giemsa-stained Trypanosoma cruzi (CDC)
The presence of T. cruzi is diagnostic of Chagas disease. It can be detected by microscopic examination of fresh anticoagulated blood, or its buffy coat, for motile parasites; or by preparation of thin and thick blood smears stained with Giemsa, for direct visualization of parasites. Microscopically, T. cruzi can be confused with Trypanosoma rangeli, which is not known to be pathogenic in humans. Isolation of T. cruzi can occur by inoculation into mice, by culture in specialized media (e.g., NNN, LIT); and by xenodiagnosis,[16] where uninfected Reduviidae bugs are fed on the patient's blood, and their gut contents examined for parasites.[2]
Various immunoassays for T. cruzi are available and can be used to distinguish among strains (zymodemes of T.cruzi with divergent pathogenicities). These tests include: detecting complement fixation, indirect hemagglutination, indirect fluorescence assays, radioimmunoassays, and ELISA. Alternatively, diagnosis and strain identification can be made using polymerase chain reaction (PCR).[2]


Awareness and prevention campaign poster in Cayenne, French Guiana, 2008
There is currently no vaccine against Chagas disease[17] and prevention is generally focused on fighting the vector Triatoma by using sprays and paints containing insecticides (synthetic pyrethroids), and improving housing and sanitary conditions in rural areas.[18] For urban dwellers, spending vacations and camping out in the wilderness or sleeping at hostels or mud houses in endemic areas can be dangerous; a mosquito net is recommended. Some stepstones of vector control include:
  • A yeast trap tested for monitoring infestations of certain species of triatomine bugs (Triatoma sordida, Triatoma brasiliensis, Triatoma pseudomaculata, and Panstrongylus megistus).[19]
  • Promising results were gained with the treatment of vector habitats with the fungus Beauveria bassiana.[20]
  • Targeting the symbionts of Triatominae through paratransgenesis.[21]
A number of potential vaccines are currently being tested. Vaccination with Trypanosoma rangeli has produced positive results in animal models.[22] More recently, the potential of DNA vaccines for immunotherapy of acute and chronic Chagas disease is being tested by several research groups.[23]
Blood transfusion was formerly the second most common mode of transmission for Chagas disease, but the development and implementation of blood bank screening tests has dramatically reduced this risk in the last decade. Blood donations in all endemic Latin American countries undergo Chagas screening, and testing is expanding in countries, such as France, Spain and the United States, that have significant or growing populations of immigrants from endemic areas.[24][25] In Spain, donors are evaluated with a questionnaire to identify individuals at risk of Chagas exposure for screening tests.[25] The US FDA has approved two Chagas tests including one recently approved in April 2010, and has published guidelines that recommend testing of all donated blood and tissue products.[25][26] While these tests are not required in U.S., it is estimated that 75-90% of the blood supply is currently tested for Chagas, including all units collected by the American Red Cross which accounts for 40% of the U.S. blood supply.[26][27] The Chagas Biovigilance Network reports current incidents of Chagas positive blood products in the United States, as reported by labs using the screening test approved by the FDA in 2007.[28]


There are two approaches to treating Chagas disease, antiparasitic treatment, to kill the parasite; and symptomatic treatment, to manage the symptoms and signs of infection.


Antiparasitic treatment is most effective early in the course of infection, but is not limited to cases in the acute phase. Drugs of choice include azole or nitro derivatives such as benznidazole[29] or nifurtimox. Both agents are limited in their capacity to effect parasitologic cure (a complete elimination of T. cruzi from the body), especially in chronically infected patients, and resistance to these drugs has been reported.[30] Studies suggest that antiparasitic treatment leads to parasitological cure in about 60-85% of adults and more than 90% of infants treated in the first year of acute phase Chagas disease. Children (age 6 to 12-years) with chronic disease have a cure rate of about 60% with benznidazole. While the rate of cure declines the longer an adult has been infected with Chagas, treatment with benznidazole has been shown to slow the onset of heart disease in adults with chronic Chagas infections.[2][4]
Treatment of chronic infection in women prior to or during pregnancy does not appear to reduce the probability the disease will be passed on to the infant. Likewise, it is unclear whether prophylactic treatment of chronic infection is beneficial in persons who will undergo immunosuppression (e.g., organ transplant recipients) or in persons who are already immunosuppressed (e.g., those with HIV infection).[2]


In the chronic stage, treatment involves managing the clinical manifestations of the disease. For example, pacemakers and medications for irregular heartbeats, such as the anti-arrhythmia drug amiodarone, may be life saving for some patients with chronic cardiac disease,[31] while surgery may be required for megaintestine. The disease cannot be cured in this phase, however. Chronic heart disease caused by Chagas disease is now a common reason for heart transplantation surgery. Until recently, however, Chagas disease was considered a contraindication for the procedure, since the heart damage could recur as the parasite was expected to seize the opportunity provided by the immunosuppression that follows surgery.[32] It was noted that survival rates in Chagas patients could be significantly improved by using lower dosages of the immunosuppressant drug ciclosporin. Recently, direct stem cell therapy of the heart muscle using bone marrow cell transplantation has been shown to dramatically reduce risks of heart failure in Chagas patients.[33]

Experimental treatments

Several experimental treatments have shown promise in animal models. These include inhibitors of oxidosqualene cyclase and squalene synthase,[34][35] cysteine protease inhibitors,[34][36] dermaseptins collected from frogs in the genus Phyllomedusa (P. oreades and P. distincta),[37] the sesquiterpene lactone dehydroleucodine (DhL) which affects the growth of cultured epimastigote–phase Trypanosoma cruzi,[38] inhibitors of purine uptake,[34] and inhibitors of enzymes involved in trypanothione metabolism.[39] It is hoped that new drug targets may be revealed following the sequencing of the T. cruzi genome.[40]


Chagas in Latin America (A:Endemic zones)
Chagas disease affects 8-10 million people living in endemic Latin American countries, with and additional 300,000-400,000 living in non-endemic countries including Spain and the United States. An estimated 41,200 new cases occur annually in endemic countries and that 14,400 infants are born with congenital Chagas disease annually. About 20,000 deaths are attributed to Chagas disease each year.[2][4]
The disease is present in 18 countries on the American continents, ranging from the southern United States to northern Argentina.[1] Chagas exists in two different ecological zones. In the Southern Cone region the main vector lives in and around human homes. In Central America and Mexico the main vector species lives both inside dwellings and in uninhabited areas. In both zones Chagas occurs almost exclusively in rural areas, where triatomine breed and feed on the over 150 species from 24 families of domestic and wild mammals, as well as humans, that are the natural reservoirs of T.cruzi.[41] Although Triatominae bugs feed on birds, they appear to be immune against infection and therefore are not considered to be a T. cruzi reservoir. Even when colonies of insects are eradicated from a house and surrounding domestic animal shelters, they can re-emerge from plants or animals that are part of the ancient, sylvatic (referring to wild animals) infection cycle. This is especially likely in zones with mixed open savannah, with clumps of trees interspersed by human habitation.[42]
Disability-adjusted life year for chagas disease per 100,000 inhabitants in 2004.[43]
  no data
  < 10
  > 450
The primary wildlife reservoirs for Trypanosoma cruzi in the United States include opossums, raccoons, armadillos, squirrels, woodrats and mice.[44] Opossums are particularly important as reservoirs because the parasite can complete its life cycle in the anal glands of the animal without having to re-enter the insect vector.[44] Recorded prevalence of the disease in opossums in the U.S. ranges from 8.3%[44] up to 37.5%.[45] Studies on raccoons in the Southeast have yielded infection rates ranging from 47%[46] to as low as 15.5%.[44] Armadillo prevalence studies have been described in Louisiana and range from a low of 1.1%[45] up to 28.8%.[47] Additionally small rodents including squirrels, mice and rats are important in the sylvatic transmission cycle because of their importance as bloodmeal sources for the insect vectors. A Texas study revealed 17.3% percent T. cruzi prevalence in 75 specimens representing four separate small rodent species.[48]
Chronic Chagas disease remains a major health problem in many Latin American countries, despite the effectiveness of hygienic and preventive measures, such as eliminating the transmitting insects. However, several landmarks have been achieved in the fight against Chagas disease in Latin America including a reduction by 72% of the incidence of human infection in children and young adults in the countries of the Southern Cone Initiative, and at least three countries (Uruguay, in 1997, and Chile, in 1999, and Brazil in 2006) have been certified free of vectorial and transfusional transmission.[2][49][50] In Argentina vectorial transmission has been interrupted in 13 of the 19 endemic provinces.[49] and major progress toward this goal has also been made in both Paraguay and Bolivia.
Screening of donated blood, blood components, solid organ donors, as well as donors of cells, tissues and cell and tissue products for T. cruzi is mandated in all Chagas endemic countries and has been implemented.[51] Approximately 300,000 infected people live in the United States, which is likely the result of immigration from Latin American countries.[52] With increased population movements, the possibility of transmission by blood transfusion became more substantial in the United States. Transfusion blood and tissue products are now actively screened in the U.S., thus addressing and minimizing this risk.[53]


Carlos Chagas, in his laboratory at the Instituto Oswaldo Cruz.
The disease was named after the Brazilian physician and infectologist Carlos Chagas, who first described it in 1909,[54][55][56][57] but the disease was not seen as a major public health problem in humans until the 1960s (the outbreak of Chagas disease in Brazil in the 1920s went widely ignored[58]). He discovered that the intestines of Triatomidae (now Reduviidae: Triatominae) harbored a flagellate protozoan, a new species of the Trypanosoma genus, and was able to prove experimentally that it could be transmitted to marmoset monkeys that were bitten by the infected bug. Later studies showed that squirrel monkeys were also vulnerable to infection.[59]
Chagas named the pathogenic parasite Trypanosoma cruzi[54] and later that year as Schizotrypanum cruzi,[56] both honoring Oswaldo Cruz, the noted Brazilian physician and epidemiologist who fought successfully epidemics of yellow fever, smallpox, and bubonic plague in Rio de Janeiro and other cities in the beginning of the 20th century. Chagas’ work is unique in the history of medicine because he was the only researcher so far to describe solely and completely a new infectious disease: its pathogen, vector, host, clinical manifestations, and epidemiology.
Nevertheless, he believed (falsely) until 1925 that the main infection route was by the bite of the insect—and not by its feces, as was proposed by his colleague Emile Brumpt in 1915 and assured by Silveira Dias in 1932, Cardoso in 1938, and Brumpt himself in 1939.[citation needed] Chagas was also the first to unknowingly discover and illustrate the parasitic fungal genus Pneumocystis, later infamously to be linked to PCP (Pneumocystis pneumonia in AIDS victims).[55] Confusion between the two pathogens' life-cycles led him to briefly recognize his genus Schizotrypanum, but following the description of Pneumocystis by others as an independent genus, Chagas returned to the use of the name Trypanosoma cruzi.
In Argentina, the disease is known as Mal de Chagas-Mazza, in honor of Salvador Mazza, the Argentine physician who in 1926 began investigating the disease and over the years became the principal researcher of this disease in the country. Mazza produced the first scientific confirmation of the existence of Trypanosoma cruzi in Argentina in 1927, eventually leading to support from local and European medical schools and Argentine government policy makers.[60]
It has been hypothesized that Charles Darwin might have suffered from Chagas disease as a result of a bite of the so-called Great Black Bug of the Pampas (vinchuca) (see Charles Darwin's illness). The episode was reported by Darwin in his diaries of the Voyage of the Beagle as occurring in March 1835 to the east of the Andes near Mendoza. Darwin was young and generally in good health, though six months previously he had been ill for a month near Valparaiso, but in 1837, almost a year after he returned to England, he began to suffer intermittently from a strange group of symptoms, becoming incapacitated for much of the rest of his life. Attempts to test Darwin's remains at the Westminster Abbey by using modern PCR techniques were met with a refusal by the Abbey's curator.

Chilean recluse (SPIDER)

From Wikipedia, the free encyclopedia
Chilean recluse spider
Scientific classification
Species:L. laeta
Binomial name
Loxosceles laeta
(Nicolet, 1849)
Scytodes laeta
Scytodes rufipes
Scytodes nigella
Omosita bicolor
Loxosceles similis
Loxosceles longipalpis
Loxosceles nesophila
Loxosceles yura
Loxosceles rufipes
The Chilean recluse spider is a venomous spider, Loxosceles laeta, of the family Sicariidae (formerly of the family Loxoscelidae). In Spanish, it (and other South American recluse spiders) is known as araña de rincón, or "corner spider"; in Portuguese, as Aranha-marrom or "brown spider". This spider is considered by many to be the most dangerous of the recluse spiders, and its bite is known to frequently result in severe systemic reactions, including death.


Description and habitat

The Chilean recluse is one of the larger species of recluse spiders, generally ranging from 8–40 mm in size (including legs). Like most recluses, it is brown and usually has markings on the dorsal side of its thorax, with a black line coming from it that looks like a violin with the neck of the violin pointing to the rear of the spider resulting in the nickname "fiddleback spider" or "violin spider" in English-speaking areas. Coloring varies from light tan to brown and the violin marking may not be visible. Since the "violin pattern" is not diagnostic, it is far more important, for purposes of identification, to examine the eyes. Contrary to most spiders, which have 8 eyes, recluse spiders have 6 eyes arranged in pairs (dyads) with one median pair and 2 lateral pairs.
The Chilean recluse spider is native to South America (it is common in Chile, and can be found throughout South America), and can now be found worldwide, including in North and Central America, Finland, and Australia. The spider is known to have established itself in the Los Angeles area, and infestations have been reported in Vancouver, British Columbia, Cambridge, Massachusetts, and Florida.
Like other recluse spiders, the Chilean recluse builds irregular webs that frequently include a shelter consisting of disorderly threads. Unlike most web weavers, they leave these webs at night to hunt. People get bitten when they unintentionally squeeze them in clothing and bedding. These spiders frequently build their webs in woodpiles and sheds, closets, garages, and other places that are dry and generally undisturbed. The spider frequently is found in human dwellings. The spiders can last a long time without food or water , a fact that encourages their worldwide spread.

Medical significance

As indicated by its name, this spider is not aggressive and usually bites only when pressed against human skin, such as when putting on an article of clothing. Like all sicariid spiders, the venom of the Chilean recluse contains the dermonecrotic agent, sphingomyelinase D, which is otherwise found only in a few pathogenic bacteria. According to one study, the venom of the Chilean recluse (along with the six-eyed sand spider), contains an order of magnitude more of this substance than that of other sicariid spiders such as the brown recluse.
Some bites are minor with no necrosis, but a small number produce severe dermonecrotic lesions (cutaneous loxoscelism) or even systemic conditions (viscerocutaneous loxoscelism); sometimes resulting in renal failure and in 3-4% of cases in a clinical study in Chile, death. (For a comparison of the toxicity of several kinds of spider bites, see the list of spiders having medically significant venom.)
The serious bites form a necrotising ulcer that destroys soft tissue and may take months, and very rarely, years to heal, leaving deep scars. The damaged tissue will become gangrenous and eventually slough away. Initially there may be no pain from a bite, but over time the wound may grow to as large as 10 inches (25 cm) in extreme cases. Bites may take up to seven hours to cause visible damage; more serious systemic effects may occur before this time, as venom of any kind spreads throughout the body in minutes. Deaths have been reported for the related South American species.
First aid involves the application of an ice pack to control inflammation, the application of aloe vera to soothe and help control the pain, and prompt medical care. If it can be captured, the spider should be brought with the patient in a clear, tightly closed container for identification. However, by the time the bite is noticed any spider found nearby is not likely to be the culprit.

Ohio State University Fact Sheet
1991 Kenny Road, Columbus, Ohio 43210

not actual size
Common Name
brown recluse spider Scientific Name
Loxosceles reclusa
Brown Recluse Spider
Susan C. Jones, Ph.D.
Assistant Professor of Entomology
Extension Specialist, Household & Structural Pests
The brown recluse spider is uncommon in Ohio. Nonetheless, OSU Extension receives numerous spider specimens that homeowners mistakenly suspect to be the brown recluse. Media attention and public fear contribute to these misdiagnoses.
The brown recluse belongs to a group of spiders that is officially known as the "recluse spiders" in the genus Loxosceles (pronounced lox-sos-a-leez). These spiders are also commonly referred to as "fiddleback" spiders or "violin" spiders because of the violin-shaped marking on the top surface of the cephalothorax (fused head and thorax). However, this feature can be very faint depending on the species of recluse spider, particularly those in the southwestern U.S., or how recently the spider has molted.
The common name, brown recluse spider, pertains to only one species, Loxosceles reclusa. The name refers to its color and habits. It is a reclusive creature that seeks and prefers seclusion.

The brown recluse spider and ten additional species of Loxosceles are native to the United States. In addition, a few non-native species have become established in limited areas of the country. The brown recluse spider is found mainly in the central Midwestern states southward to the Gulf of Mexico (see map). Isolated cases in Ohio are likely attributable to this spider occasionally being transported in materials from other states. Although uncommon, there are more confirmed reports of Loxosceles rufescens (Mediterranean recluse) than the brown recluse in Ohio. It, too, is a human-associated species with similar habits and probably similar venom risks (unverified).

not actual size
Recluse spiders have six eyes that are arranged in pairs.
In the mature brown recluse spider as well as some other species of recluse spiders, the dark violin marking is well defined, with the neck of the violin pointing toward the bulbous abdomen. The abdomen is uniformly colored, although the coloration can range from light tan to dark brown, and is covered with numerous fine hairs that provide a velvety appearance. The long, thin, brown legs also are covered with fine hairs, but not spines. Adult brown recluse spiders have a leg span about the size of a quarter. Their body is about 3/8 inches long and about 3/16 inches wide. Males are slightly smaller in body length than females, but males have proportionally longer legs. Both sexes are venomous. The immature stages closely resemble the adults except for size and a slightly lighter color. Whereas most spiders have eight eyes, recluse spiders have six eyes that are arranged in pairs in a semicircle on the forepart of the cephalothorax (see close-up view). A 10X hand lens or microscope is needed to see this diagnostic feature. In order to determine the exact species of Loxosceles, the spider's genitalia need to be examined under a high-power microscope. This requires the skills of a spider expert.
Life Cycle and Habits
Egg laying primarily occurs from May through July. The female lays about 50 eggs that are encased in an off-white silken sac that is about 2/3-inch diameter. Each female may produce several egg sacs over a period of several months. Spiderlings emerge from the egg sac in about a month or less. Their development is slow and is influenced by weather conditions and food availability. It takes an average of one year to reach the adult stage from time of egg deposit. Adult brown recluse spiders often live about one to two years. They can survive long periods of time (about 6 months) without food or water.
The brown recluse spider spins a loose, irregular web of very sticky, off-white to grayish threads. This web serves as the spider's daytime retreat, and it often is constructed in an undisturbed corner. This spider roams at night searching for insect prey. Recent research at the University of Kansas indicates that the brown recluse spider is largely a scavenger, preferring dead insects. Mature males also roam in search of females.
Brown recluse spiders generally occupy dark, undisturbed sites, and they can occur indoors or outdoors. In favorable habitats, their populations are usually dense. They thrive in human-altered environments. Indoors, they may be found in attics, basements, crawl spaces, cellars, closets, and ductwork or registers. They may seek shelter in storage boxes, shoes, clothing, folded linens, and behind furniture. They also may be found in outbuildings such as barns, storage sheds, and garages. Outdoors, brown recluse spiders may be found underneath logs, loose stones in rock piles, and stacks of lumber.
The brown recluse spider is not aggressive, and it normally bites only when crushed, handled or disturbed. Some people have been bitten in bed after inadvertently rolling over onto the spider. Others have been bitten after accidentally touching the spider when cleaning storage areas. Some bites occur when people put on seldom used clothing or shoes inhabited by a brown recluse.
Bite Symptoms
The physical reaction to a brown recluse spider bite depends on the amount of venom injected and an individual's sensitivity to it. Some people are unaffected by a bite, whereas others experience immediate or delayed effects as the venom kills the tissues (necrosis) at the site of the bite. Many brown recluse bites cause just a little red mark that heals without event. The vast majority of brown recluse bites heal without severe scarring (
Initially, the bite may feel like a pinprick or go unnoticed. Some may not be aware of the bite for 2 to 8 hours. Others feel a stinging sensation followed by intense pain. Infrequently, some victims experience general systemic reactions that may include restlessness, generalized itching, fever, chills, nausea, vomiting, or shock. A small white blister usually initially rises at the bite site surrounded by a swollen area. The affected area enlarges and becomes red, and the tissue is hard to the touch for some time. The lesion from a brown recluse spider bite is a dry, blue-gray or blue-white, irregular sinking patch with ragged edges and surrounding redness--termed the "red, white, and blue sign." The lesion usually is 1½ inches by 2¾ inches or smaller. Characteristics of a bite are further discussed at
The bite of the brown recluse spider can result in a painful, deep wound that takes a long time to heal. Fatalities are extremely rare, but bites are most dangerous to young children, the elderly, and those in poor physical condition. When there is a severe reaction to the bite, the site can erupt into a "volcano lesion" (a hole in the flesh due to damaged, gangrenous tissue). The open wound may range from the size of an adult's thumbnail to the span of a hand. The dead tissue gradually sloughs away, exposing underlying tissues. The sunken, ulcerating sore may heal slowly up to 6 to 8 weeks. Full recovery may take several months and scarring may remain.
It is difficult for a physician to accurately diagnose a "brown recluse bite" based simply on wound characteristics. It is absolutely necessary to have the spider for a positive identification. Necrotic wounds can result from a variety of agents such as bacteria (Staphylococcus, "flesh-eating" Streptococcus, etc.), viruses, fungi, and arthropods (non-recluse spiders, centipedes, mites, ticks, wasps, bedbugs, kissing bugs, biting flies, etc.). Necrotic conditions also can be caused by vascular and lymphatic disorders, drug reactions, underlying diseases states, and a variety of other agents. An annotated list of conditions that could be mistaken for a brown recluse spider bite is available at Misdiagnosis of lesions as brown recluse bites can delay appropriate care.
First Aid
If bitten, remain calm, and immediately seek medical attention (contact your physician, hospital and/or poison control center). Apply an ice pack directly to the bite area to relieve swelling and pain. Collect the spider (even a mangled specimen has diagnostic value), if possible, for positive identification by a spider expert. A plastic bag, small jar, or pill vial is useful and no preservative is necessary, but rubbing alcohol helps to preserve the spider.
An effective commercial antivenin is not available. The surgical removal of tissue was once standard procedure, but now this is thought to slow down wound healing. Some physicians administer high doses of cortisone-type hormones to combat hemolysis and other systemic complications. Treatment with oral dapsone (an antibiotic used mainly for leprosy) has been suggested to reduce the degree of tissue damage. However, an effective therapy has not yet been found in controlled studies.
Control of indoor infestations of the brown recluse spider can take a long time (6 months or more) and can be difficult because humans have a very low tolerance for this pest, it tends to be widely dispersed within infested buildings, and it seeks secluded sites. Control of spiders, including the brown recluse, is best achieved by following an integrated pest management (IPM) approach. IPM involves using multiple approaches such as preventive measures, exclusion, sanitation, trapping, and chemical treatment when necessary.
Preventing spider bites
Shake out clothing and shoes before getting dressed.
Inspect bedding and towels before use.
Wear gloves when handling firewood, lumber, and rocks (be sure to inspect the gloves for spiders before putting them on).
Remove bedskirts and storage boxes from underneath beds. Move the bed away from the wall.
Exercise care when handling cardboard boxes (recluse spiders often are found in the space under folded cardboard flaps).
Install tight-fitting screens on windows and doors; also install door sweeps.
Seal or caulk cracks and crevices where spiders can enter the house.
Install yellow or sodium vapor light bulbs outdoors since these attract fewer insects for spiders to feed upon.
Tape the edges of cardboard boxes to prevent spider entry.
Use plastic bags (sealed) to store loose items in the garage, basement, and attic.
Remove trash, old boxes, old clothing, wood piles, rock piles, and other unwanted items.
Eliminate clutter in closets, basements, attics, garages, and outbuildings.
Do not stack wood against the house.
Clean up dead insects that the brown recluse spider can feed on.
Non-chemical control
Use sticky traps or glueboards to capture spiders.
Dust and vacuum thoroughly to remove spiders, webs, and egg sacs (dispose of the vacuum bag in a container outdoors).
Use a rolled up newspaper or fly swatter to kill individual spiders.
There are many labeled pesticides for spider control. Some are labeled for homeowner use, while others are labeled only for the licensed, certified pesticide applicator. It would be prudent to enlist the services of a professional pest management company when dealing with an indoor infestation of the brown recluse spider.
Research indicates that recently developed pyrethroids (e.g., cyfluthrin, cypermethrin, etc.) are particularly effective against brown recluse spiders. Wettable powders and microencapsuled "slow-release" formulations of these chemicals provide residual activity and are preferable to using emulsion-type sprays. Insecticide treatments should be applied so that the chemical contacts as many spiders and webs as possible. Residual liquid sprays should be applied to the outside perimeter of the home (including under eaves, patios, and decks; behind window shutters), baseboards, undisturbed corners, and other suspected spider harborages. Residual dusts should be applied to voids and inaccessible areas where spiders may hide. Aerosol flushing agents such as pyrethrins, though ineffective by themselves in providing control, can cause spiders to move about so that they contact treated surfaces.
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Any opinions, findings, conclusions, or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the view of the U.S. Department of Agriculture
All educational programs conducted by Ohio State University Extension are available to clientele on a nondiscriminatory basis without regard to race, color, creed, religion, sexual orientation, national origin, gender, age, disability or Vietnam-era veteran status.
Keith L. Smith, Associate Vice President for Ag. Adm. and Director, OSU Extension.
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