Endemic mite-transmitted dermatoses and infectious diseases in the south.
MATERIALS AND METHODS
A MEDLINE search, 1966-2009, of the world's scientific literature of case reports, case series, original articles, and reviews was conducted in order to determine the epidemiology, outcomes, clinical manifestations, preferred diagnostic interventions, management and prevention strategies for mite-transmitted infestations and infectious diseases. In addition, a clinical classification of mite-transmitted infestations and infections was developed to assist clinicians in assessing potential mite-transmitted skin and systemic diseases. Mite infestations and infections were classified into the following distinct clinical and etiological categories: (1) scabies; (2) chiggers; (3) rickettsioses; (4) follicle mite infestations; (5) dust mite allergies; (6) animal or zoonotic mite infestations; and (7) plant mite infestations.
Taxonomy of Mites and Disease Ecology of Mite-Transmitted Infectious Diseases
Mites may be commonly classified as scabies mites, trombiculid mites (also called chiggers, red bugs, or itch mites), human follicle mites, dust mites, and a variety of animal and plant mites (Table 1). Most mite species develop close generational associations with their ecosystems and zoonotic reservoirs, often referred to as "mite islands".1 Trombiculid mite islands usually border cleared land and scrub brush with grassy vegetation with warm soil temperatures and high humidity, frequently visiting rodent hosts to feed larval mites, and sufficient small insect fauna to feed nymph and adult mites. Hikers stumbling onto mite islands are at significantly higher risks of larval chigger bites (also known as "chiggers" or trombidiosis) worldwide or scrub typhus, only in the endemic regions of Eurasia, Asia, and the South Pacific. Animal and plant mites establish their mite islands in animal dens, bird nests, trees, on fruits and vegetables, and even on breads and cheeses.
The Epidemiology, Clinical Manifestations, Diagnosis, and Management of Mite Infestations and MiteTransmitted Infectious Diseases
Scabies, an infestation by the itch or scabies mite, Sarcoptes scabiei var. hominis, has remained a major public health problem worldwide (Figure 1). Scabies has now become a significant re-emerging ectoparasitosis in its most severe form, crusted or Norwegian scabies, in both the developing world among those immunocompromised by acquired immunodeficiency syndrome (AIDS) and human T-cell lymphotropic virus Type 1 (HTLV-1) infections, and in the developed world, among the homeless, institutionalized, mentally retarded, and immunocompromised. (1)
The worldwide prevalence of scabies has been estimated to be about 300 million cases/year. (2) Although more often associated with crowding, homelessness, and institutionalization, scabies occurs worldwide in both sexes, at all ages, and among all ethnic and socioeconomic groups. Scabies is hyperendemic throughout the developing world, especially in sub-Saharan Africa, India, the Aboriginal regions of northern Australia, and the South Pacific Islands, especially the Solomon Islands. (2, 4, 5)
Scabies infestations and super-infestations with crusted (or Norwegian) scabies are more prevalent among several specific high risk groups including: (1) men who have sex with men; (2) patients treated in sexually-transmitted disease clinics; (3) homeless patients with AIDS; (4) and patients with HTLV-1 infections. (3, 6, 7) Many experts now recommend evaluating all high risk patients with crusted scabies for human immunodeficiency virus (HIV) and HTLV-1 infections.7, 8 In summary, descriptive epidemiological studies have now identified several high-risk groups for classical (typical) and crusted (atypical) scabies outbreaks including (1) long-term residents in institutions for the aged, demented, and disabled; (2) displaced, homeless, and often malnourished, persons; and (3) all immunocompromised persons, particularly those with HIV and HTLV-1 infections.1, (2-8)
Scabies mites cannot jump or fly, but can crawl at a rate of 2.5 cm per minute on warm, moist skin (Figure 1). (1, 2) They can survive in the natural environment for 24 to 36 hours at room temperature and average humidity and remain capable of infesting humans. (9) Scabies is most easily transmitted by close skin-to-skin contact as with sex partners, children playing, or health providers examining highly infectious patients with crusted scabies. The more mites there are on a human host, the greater the risks of transmission by close direct contact, more so than by indirect contact with fomites, such as shared bedding, clothing, and personal grooming items.2 Although rare, the indirect transmission of scabies by fomites occurs and is more common among immunocompromised hosts with AIDS, family members of a highly infectious atypical (crusted) index case, and within the institutional settings described.1, 2 Scabies mites have not been demonstrated to transmit HIV, HTLV-1, or any other infectious agent.
[FIGURE 1 OMITTED]
The human scabies mite is an obligate ectoparasite and must complete its entire life cycle on its human hosts, as females burrow intradermally to lay eggs and larvae emerge and mature to re-infest the same or new hosts. Female mites burrow preferentially into thinner areas of the epidermis by dissolving the stratum corneum with proteolytic secretions to penetrate to the stratum granulosum. Female mites then lay their eggs at the end of tunneled burrows 5-10 mm long, and larvae hatch two to three days after eggs are laid. The entire incubation period from eggs to full grown mites lasts about 14-15 days. (10) The human incubation period from initial infestation to symptom development is three to six weeks in initial infestations and as short as one to three days in re-infestations as a result of prior sensitization to mite antigens. (2)
Classical or typical scabies presents as generalized, intense nocturnal itching in a characteristic topographical distribution as 10-15 fertile female mites are transferred from infected patients to new hosts. The more significant, intensely pruritic skin eruptions in re-infestations and atypical scabies are considered consequences of both anamnestic hypersensitivity reactions to mite antigens and self-inflicted scratching. (2)
In classical scabies, the preferred distribution of skin eruptions includes hairless areas with a thin stratum corneum, such as the sides and interdigital web spaces of fingers and toes, popliteal fossae, flexor surfaces of the wrists, buttocks, and female breasts (Figure 2). (2) Although inflammatory, pruritic papules are present at most infested sites, the pathognomonic linear-to-serpiginous intradermal burrows, 5-10 mm long, dotted with fecal lithes (pellets) or scybala, and terminating in raised papules hiding ovipositing females are often absent. (2) Nonspecific secondary lesions occur commonly as a result of scratching and secondary infection and include self-inflicted excoriations, eczematization, lichenification, and impetigo.
Scabies may also present in three atypical forms, especially in high risk immunocompromised patients with HIV or HTLV-1 infections. The atypical forms of scabies include (1) scalp scabies, most common in infants, (2) crusted (Norwegian) scabies, more common in immunocompromised patients, and (3) sexually transmitted nodular scabies. Scabietic nodules will develop in 7%-10% of patients with sexually-transmitted scabies infestations, usually in males on the penis and scrotum, and appear as darkened, tender nodules 5-20 mm in diameter, often with a raised female mite burrow on top.
The diagnosis of scabies is made predominantly by epidemiological considerations and clinical observations. A clinical diagnosis may be confirmed by low power microscopic examination of a burrow skin scraping which excavates female mites, 0.2-0.5 mm in length, translucent with brown legs, and too small to be seen without magnification (Figure 1). Eggs (0.02-0.03 mm in diameter), smaller eggshell fragments, and fecal lithes or pellets may also be identified in microscopic specimens of burrow scrapings. (2) In atypical scabies cases, skin biopsy confirms the diagnosis. (2) Newer diagnostic methods for scabies now under investigation include enhanced microscopy (epiluminescence microscopy, noncomputed dermoscopy); immunological detection of specific scabies antibodies by enzyme-linked immunosorbent assay (ELISA); and molecular identification of scabies DNA by polymerase chain reaction (PCR). (2, 11-13)
[FIGURE 2 OMITTED]
Topical or oral scabicides should be used to treat all infested persons and their close personal contacts simultaneously, regardless of the presence of symptoms.2 Currently recommended treatment options for scabies are listed in Table 2. The most effective topical treatments for scabies are 5% permethrin cream and 1% lindane cream or lotion, with permethrin safer and slightly more effective than lindane, an organochlorine pesticide capable of causing seizures and sudden death on over-applications or accidental ingestions. (14, 15, 16)
The topical treatments for scabies may not be well accepted or tolerated by some patients for many reasons including severe burning and stinging (with benzyl benzoate and 5% permethrin) in cases of secondarily excoriated or eczematous infestations. In such cases, a single oral dose of ivermectin, 200 mcg/kg, may offer a more acceptable and equally effective alternative. (17) Nevertheless, ivermectin is not ovicidal, and a second course of oral treatment at adult maturation time of 14-15 days, is recommended. (2, 17)
Among the trombiculid chiggers including the scrub typhus-transmitting Leptotrombidium species, only the larvae are human and animal ectoparasites. The larger chigger nymphs and adults are free-living and feed on small insects and their eggs. All trombiculid larvae exhibit a unique method of feeding on hosts and transmitting salivary secretions, which may contain Orientia tsutsugamushi, the causative agent of scrub typhus, only in tropical endemic regions. Larvae pierce the skin with sharp mouthparts and inject tissue-dissolving saliva to create a pool of lymph, other body fluids, and dissolved epithelial cells to aspirate from. The repeated injection of saliva into bite wound incites a host reaction forming a straw-like hollow tube, the hypostome or stylostome, which extends downwards into the host's skin firmly anchoring the mite. (1, 18)
All of the noninfectious chigger larvae can cause scrub itch or trombidiosis with the American chigger mite, Eutrombicula alfreddugesi, being the most common culprit in the southern US. Initially painless, chigger bites will cluster where clothing is tight against the skin, especially on the genitalia, thighs, buttocks, flanks, waists, and ankles. Localized itching and discomfort ensue when the larvae withdraw their mouthparts and depart after feeding for three to six hours for most noninfectious chiggers. Although some trombiculid larvae remain attached to and feeding on human hosts for up to a month, the larval vectors of scrub typhus feed for two to 10 days before dropping to the ground engorged, and ready to mature into free-ranging nymphs.
Forcibly removing feeding chiggers often decapitates larvae leaving mouthparts embedded to cause further inflammation.1 Untested strategies for removing feeding, engorged chiggers intact have included painting chigger bite sites with colloidion, clear fingernail polish, or Liquid Skin[R]; drying the sites with a hair dryer; and then peeling the coated and dried chiggers off the skin intact.
Localized intense itching will be followed by an eruption of intensely pruritic erythematous papules by 10-12 hours, and crusting and healing by 24-48 hours. (1, 18) Treatment is supportive with soap and water cleansing, warm water soaks, and topical local anesthetics and antihistamines. Impetigo and other secondary infections are potential complications that would necessitate antibiotic treatment. Tetanus prophylaxis is recommended, if indicated. Although not reported in mite infestations, tetanus has occurred in jigger flea infestations (tungiasis) in unvaccinated persons. (19)
Only biting larvae of Asian scrub typhus chiggers (Leptotrombidium species) transmit scrub typhus caused by Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi); and only biting house-mouse mites (Liponyssoides sanguineus) transmit rickettsialpox caused by Rickettsia akari. Both scrub typhus mites and house-mouse mites are, like ticks, capable of inheriting bacterial infections by transovarial transmission and maintaining infections in several mite generations, as bacteria are passed from adults to juveniles (nymphs and larvae) by transstadial transmission. Scrub typhus chiggers are the main environmental reservoirs of O. tsutsugamushi in tropical endemic regions with much smaller secondary reservoirs in wild rodents. (1) Common house mice are the zoonotic reservoirs of R. akari, not only in crowded urban apartment buildings in the US, but also in all mice-infested buildings in more rural locations worldwide, including the southern US. (20, 21)
The house-mouse mite, Liponyssoides sanguineus, maintains a rickettsial zoonosis in its preferred house mouse (Mus musculus) reservoir, and can transmit rickettsialpox caused by Rickettsia akari through bites. (1, 18) Although initially described in clusters in crowded apartment buildings in large US cities, including New York, Boston, Cleveland, Philadelphia, and Pittsburgh, rickettsialpox has now been reported in rural areas of the southern US (North Carolina) and eastern Europe.19-21 Many experts now feel that rickettsialpox is underreported and distributed in silent sylvan cycles worldwide.21, 22 The incubation period and initial clinical manifestations of rickettsialpox mirror those of scrub typhus with eschar formation at the bite site within 10-12 days, followed by fever, chills, severe headache, conjunctival injection, and truncal maculopapular then vesicular rash (Figure 3). (21, 22) Unlike scrub typhus, hearing loss does not occur, and regional lymphadenopathy is also uncommon. Unlike scrub typhus, complications are rare, but may include thrombocytopenia and interstitial pneumonia. (21, 22)
Scrub typhus and rickettsialpox present similarly temporally and clinically. Both infections respond to treatment with oral tetracycline, oral doxycycline, or intravenous chloramphenicol, which is not recommended, except in life-threatening infections, due to its bone marrow toxicity. (20)
[FIGURE 3 OMITTED]
Follicle Mite Infestations
Scabies and follicle mites are the only exclusively human ectoparasitic mites and do not transmit infectious diseases. Less serious than scabies are infestations with the two follicle mites, Demodex folliculorum, which inhabit hair follicles, and Demodex brevis, which inhabit sebaceous glands. These diminutive (0.1-0.4 mm in length) human mites feed on sebum and exfoliated skin, while lodged in human hair follicles or sebaceous gland pores. Demodex mites cluster in follicles on the nose, eyelids, nasolabial folds, and ears. (1, 23, 24) All of the developmental stages of Demodex mites occur over an egg-to-egg cycle of 13-15 days entirely within hair follicles or sebaceous glands, especially in females over-using cream-based facial cosmetics. (1, 24) Other than causing comedones or "blackheads", Demodex infestations cause few adverse symptoms, and rarely need treatment, other than soap and water washing to reduce infestations; unless infestations are associated with acne, blepharitis, impetigo, rosacea, or seborrheic dermatitis. (1), 24 Scalp and eyelash infestations will respond to washes with 0.5% selenium- or 10% sulfur-containing creams, lotions, or shampoos, with care to avoid ocular instillation. Super-infestations with Demodex mites may cause chronic blepharitis (demodicosis) or rosacea-like dermatitis which may require systemic therapy with a single oral dose of ivermectin, 200 mcg/kg, in addition to topical miticides.
Dust Mite infestations
Dermatophagoides species dust mites have highly allergenic exoskeletons, body fragments, and feces; all of which are aerosolized during bed-making and pillow-fluffing. Allergens from dust mites frequently cause allergic rhinitis and asthmatic bronchitis in predisposed, atopic persons. (18) The American house dust mite, D. farinae, is distributed worldwide, as is the European house dust mite, D. pteronyssinus. (18) House dust mites prefer to reside in bedrooms, mattresses, and carpets year-round in warm, humid homes. They exhibit maximum growth and reproduction during seasonal warming cycles at ambient temperatures at or above 25[degree] C. and relative humidity at or above 75%.18 House dust mite allergies may be managed by immunotherapy with house dust mite extracts.
Animal Mite Infestations
Although of limited clinical significance, a number of animal and plant mite infestations can cause bothersome, usually self-limited, erythematous, papulovesicular eruptions. Bites from the red chicken or poultry mite, Dermanyssus gallinae, can cause a pruritic dermatitis, usually on the backs of the hands and forearms in farmers and poultry workers. (23) Bites from the rat mite, Ornithonyssus bacoti, ubiquitous in the temperate areas of Europe and the Americas, can cause a papulovesicular dermatitis in stockyard and warehouse visitors and workers. (23) The bird mite, Ornithonyssus bursa, is a common ectoparasite of pigeons and other nesting birds worldwide and a frequent cause of mite infestations in attics and buildings with bird nests. (23, 24) Human bird mite infestations are also self-limited and characterized by maculopapular dermatitis of the finger webs and axillae, most commonly in pigeon-breeders, bird fanciers, and travelers sleeping in bird-infested facilities.24 Most animal and plant mite bites can be managed symptomatically with topical agents, unless active infestations are present, which can be controlled with topical 10% crotamiton, 25% benzyl benzoate, or topical 1% lindane or 1% malathion preparations.
[FIGURE 4 OMITTED]
Several nonhuman species of sarcoptid mites can cause human scabies, particularly in immunocompromised individuals, with itching, inflammation, and alopecia. Animal scabies or mange occurs commonly in domestic pets and animals, especially in cats, dogs, pigs, horses, and camels. Animal scabies mites are facultative ectoparasites in humans, cannot effectively complete their life cycles in human dead-end hosts, and cause self-limited infestations in humans. Symptomatic infestations may be treated with 5% permethrin lotion, 10% crotamiton cream or lotion, or oral ivermectin.
Mite Infestations by Ectoparasites of Plant and wood-Feeding Insect Larvae
The North American straw itch mite, Pyemotes tritici (formerly Pyemotes ventricosus), feeds preferentially on the larvae of insects that infest cane, hay, straw, and some grains, especially rice. In 1965, Fine and Scott were the first investigators to describe Pyemotes tritici dermatitis in the southern US, where hay rides, caned furniture, and straw rugs are popular. (25) Such exposures frequently place patients in skin contact with infested hay, straw, or furniture during peak mite feeding and breeding seasons in the spring and summer. (25) Straw itch mite dermatitis is characterized by pruritic, maculopapulovesicular eruptions on the limbs and trunk, which resolve rapidly with topical corticosteroid therapy. (25)
In 2004, a close relative of the North American straw itch mite, P. tritici, the oak leaf gall mite (Pyemotes herfsi), which preferentially feeds on insect larvae in oak trees, caused an outbreak of plant insect mite dermatitis in the US. (26) Over 300 residents of Pittsburg, Kansas, sought immediate medical attention for an intensely pruritic, erythematous maculopapular rash clustering on the face, neck, and limbs (Figure 4). (26) All lesions healed within days following topical treatment with antihistamines and corticosteroids. (26)
In summary, human infestations with Pyemotes mite ectoparasites of insect pests of plants, trees, and non-living plant and wood products, such as cane, hay, straw, and indoor furniture are common causes of annoying pruritic, erythematous maculopapular rashes. (25, 26) Plant insect mite dermatitis may become chronic or recur on indoor or outdoor mite re-exposure on the heads, limbs, and trunks of backpackers, campers, and resort vacationers during peak mite-feeding and breeding seasons in the spring and summer.
The Prevention of Mite Infestations and Mite-Transmitted Infectious Diseases
Prevention and control strategies for scabies include: (1) aggressive treatment of infested patients and all close household, institutional, and sexual contacts; (2) disposal of or hot wash-dry sterilization of all index case contaminated clothing and bedding by machine washing and drying at 60[degree]C. or higher (Most household clothes dryers, whether gas or electric, can reach average high temperatures of 90[degree] C. [194[degree]F.]. See www.cpsc.gov/library.); (3) provision of improved access for personal hygiene and health care for all displaced, homeless, or institutionalized persons; and (4) aggressive control of outbreaks of zoonotic scabies with the potential for human transmission caused by the sarcoptid mites of various wild and domestic animals, especially cats, dogs, camels, pigs, horses.
Prevention and control strategies for other mite infestations include: (1) household and campsite spraying of pyrethrin and pyrethroid-containing insecticides; (2) spraying or impregnating pyrethrin and pyrethroidcontaining repellants on clothing; (3) applying diethyl toluamide (N, N-diethyl-methyl-toluamide, [DEET]) or picardin-containing insect repellants to exposed skin; (4) gently washing exposed or infested areas of the body with soap and water to remove stylosome-attached mites without decapitating them; (5) improving rodent reservoir control in campgrounds, cabins, homes, apartments, barns, sheds, and, especially, in crowded public housing; (6) removing all bird nests from the exterior of buildings and rodent dens from crawl spaces to prevent animal mite infestations; (7) treating straw beds, straw mattresses, and hay-ride wagons with pyrethrin and pyrethroid-containing insecticides; and (8) vacuuming bedrooms and mattresses and washing bed linens regularly, and encasing mattresses and pillows in plastic covers to minimize house dust mite levels. Although there are no vaccines for scrub typhus or rickettsialpox, weekly doses of 200 mg of doxycycline can prevent O. tsutsugamushi infections in endemic areas of the Asiatic-Pacific tropics. (20)
In summary, mites are mostly ubiquitous, bothersome pests with few species of medical importance, and, of these, most are scabies mites, trombiculid larvae, and animal and plant mites (Table 1). All patients with scabies and their close household, institutional, and sexual contacts should be informed that scabies is a highly transmissible ectoparasitic infestation and that several topical treatments and an effective oral treatment are readily available and highly effective at present (Table 2). Sexually active patients with scabies should be screened for other sexually transmitted diseases, particularly HIV and HTLV-1 infections. Lastly, only the Asian and Eurasian Leptotrombidium species of trombiculid larvae (chiggers) can transmit scrub typhus in endemic regions of Asia, Eurasia, and the South Pacific, and only the house-mouse mite can transmit rickettsialpox in both urban and rural dwellings worldwide, including the southern US.
(1.) Service MW. Scrub typhus mites (Trombiculidae). In: Medical Entomology for Students. London: Chapman & Hall;1996:256-262.
(2.) Chosidow O. Scabies. N Engl J Med 2006;354:1718-1727.
(3.) Tijoe M, Vissers WH. Scabies outbreaks in nursing homes for the elderly: recognition, treatment options and control of reinfestation. Drugs Aging 2008;25:299-306.
(4.) Mahe A, Faye O, N'Diaye HT, et al. Definition of an algorithm for the management of common skin diseases at primary health care level in sub-Saharan Africa. Trans R Soc Trop Med Hyg 2005; 99:39-47.
(5.) Lawrence G, Leafasia J, Sheridan J, et al. Control of scabies, skin sores and haematuria in children in the Solomon Islands: another role for ivermectin. Bull World Health Organ 2005;83:34-42.
(6.) Otero L, Varela JA, Espinosa E, et al. Sarcoptes scabiei in a sexually transmitted infections unit: a 15-year study. Sex Trans Dis 2004; 31:761-765.
(7.) Blas M, Bravo F, Wenceslao C, et al. Norwegian scabies in Peru: the impact of human T cell lymphotropic virus type 1 infection. Am J Trop Med Hyg 2005;72:855-857.
(8.) Del Guidice P, Sainte Marie D, Gerard Y, et al. Is crusted (Norwegian) scabies a marker of adult T cell leukemia/lymphoma in human T-lymphotropic virus type 1-seropositive patients? J Infect Dis 1997;176:1090-1092.
(9.) Arlian LG, Runyan RA, Achar S, et al. Survival and infectivity of Sarcoptes scabiei var. canis and var. hominis. J Am Acad Dermatol 1984;11:210-215.
(10.) Walton SF, Holt DC, Currie BJ, et al. Scabies: new future for a neglected disease. Adv Parasitol 2004;57:309-376.
(11.) Argenziano G, Fabbrocini G, Delfino M. Epiluminescence microscopy: a new approach to in vivo detection of Sarcoptes scabiei. Arch Dermatol 1997;133:751-753.
(12.) Prins C, Stucki L, French L, et al. Dermoscopy for the in vivo detection of Sarcoptes scabiei. Dermatol 2004;208:241-243.
(13.) Walton SF, McBroom J, Mathews JD, et al. Crusted scabies: a molecular analysis of Sarcoptes scabiei variety hominis populations from patients with repeated infestations. Clin Infect Dis 1999;29:1226-1230.
(14.) Strong M, Johnstone PW. Interventions for treating scabies. Update of Cochrane Database of Syst Rev 2007: CD000320.
(15.) Singal A, Thami GP. Lindane neurotoxicity in childhood. Am J Therapeu 2006;13:277-280.
(16.) Sudakin DL. Fatality after a single dermal application of lindane lotion. Arch Environ Occup Health 2007;62:201-203.
(17.) Sule HM, Thacher TD. Comparison of ivermectin and benzyl benzoate lotion for scabies in Nigerian patients. Am J Trop Med Hyg 2007;76:392-395.
(18.) Goddard J. Mites. In: Physician's Guide to Arthropods of Medical Importance, 4th edition. Boca Raton: CRC Press; 2002:229-246.
(19.) Obengui P. La tungose et le tetanus au C.H. U. de Brazzaville. Dakar Med J 1989;34:44-48.
(20.) Watt G, Walker DH. Scrub typhus. In: Guerrant RL, Walker DH, Weller PF, (editors). Tropical Infectious Diseases: Principles, Pathogens & Practice, 2nd edition. Philadelphia: Elsevier Churchill Livingston;2006:557-562.
(21.) Krusell A, Comer JA, Sexton DJ. Rickettsialpox in North Carolina: a case report. Emerg Infect Dis 2002;8:727-728.
(22.) Ozturk MK, Gunes T, Kose ET, et al. Rickettsialpox in Turkey. Emerg Infect Dis 2003;9:1498-1499.
(23.) Neva FA, Brown HW. Class Arachnida-ticks, mites, spiders, scorpions. In: Basic Clinical Parasitology. East Norwalk: Appleton & Lange;1994:300-311.
(24.) Kong TK, To WK. Bird-mite infestation. N Engl J Med 2006;354: 1728.
(25.) Fine RM, Scott HG. Straw itch mite dermatitis caused by Pyemotes ventricosus: comparative aspects. South Med J 1965;58:416-420.
(26.) Hansen G, Taylor C, Goedeke J, et al. Outbreak of pruritic rashes associated with mites-Kansas, 2004. Morb Mort Week Rep; 54:952-955.
James H. Diaz, MD, MPH & TM, DrPH, FAAP FACPM Dr. Diaz is a professor of Public Health and Preventive Medicine, Program Head, Environmental and Occupational Health Sciences, School of Public Health, Louisiana State University Health Sciences Center (LSUHSC) in New Orleans.
Table 1. Mites of medical importance in the Southern United States. Family Genus, species Common Names (Human, Plant or Animal Mite) Sarcoptidae Scabies (itch) Sarcoptes scabiei var. mite (Human mite) hominis Demodicidae Hair follicle mite Demodex folliculorum Demodex brevis Sebaceous gland mite Pyroglyphidae European house Dermatophagoides dust mite (Human mite) pteronyssinus D. farinae American house dust mite (Human Mite) Dermanyssidae House mouse mite Liponyssoides sanguineus (formerly Allodermanyssus sanguineus) Dermanyssus Red poultry gallinae (chicken) mite Macronyssidae Tropical rat mite Ornithonyssus bacoti O. bursa Tropical fowl mite Laelapidae Spiny rat mite Laelaps echidnina Pyemotidae Pyemotes Grain (straw) itch tritici mite (formerly Pediculoides ventricosus) Peymotes herfsi Oak leaf gall mite Family Genus, species Maintenance in Nature Sarcoptidae Obligate ectoparasites of Sarcoptes scabiei var. man, human reservoir hominis Demodicidae Obligate ectoparasites Demodex folliculorum of man, human host reservoir in hair follicles Demodex brevis Obligate ectoparasites of man, human host reservoir in sebaceous glands Pyroglyphidae Free-living ectoparasites Dermatophagoides of man; live in human bedrooms, especially in pteronyssinus mattresses; feed on human skin detritus D. farinae Same Dermanyssidae Free-living Liponyssoides ectoparasites of field sanguineus (formerly mice, transovarial Allodermanyssus -transstadial passage of sanguineus) ID agent Dermanyssus Free-living ectoparasites gallinae of domestic and wild birds Macronyssidae Free-living ectoparasites Ornithonyssus bacoti of large rodents: Rattus rattus, Rattus norvegicus O. bursa Free-living ectoparasites of domestic and wild birds Laelapidae Free-living ectoparasites Laelaps echidnina of large rodents: Rattus rattus, Rattus norvegicus Pyemotidae Pyemotes Free-living ectoparasites tritici of straw, hay, grains (formerly Pediculoides (rice), cane and wicker ventricosus) furniture that eat moths, beetles, weevils in crops, plants, furniture Peymotes herfsi Free-living ectoparasites of gall-making larvae of oak trees Family Genus, species Clinical Manifestations Sarcoptidae Classical scabies Sarcoptes scabiei var. Atypical scabies hominis Demodicidae Benign follicular Demodex folliculorum (scaling) dermatitis Demodex brevis May potentiate granulomatous acne Pyroglyphidae House dust mite Dermatophagoides allergies and asthma. pteronyssinus D. farinae Same Dermanyssidae Rickettsialpox Liponyssoides sanguineus (formerly Allodermanyssus sanguineus) Dermanyssus Poultry workers' gallinae dermatitis of hands Macronyssidae Urticarial papulovesicular Ornithonyssus bacoti to pustular dermatitis O. bursa Pruritic papules in a characteristic scabietic distribution: finger webs, axillae, groin, buttocks Laelapidae Nonspecific mite-bite Laelaps echidnina dermatitis Pyemotidae Pyemotes Pruritic, erythematous, tritici microvesicular (formerly Pediculoides eruptions that ulcerate ventricosus) then crust on limbs, face, neck, trunk, and breasts with characteristic "comet signs" Peymotes herfsi Pruritic, erythematous, microvesicular eruptions of limbs, face, neck, trunk Family Genus, species Infectious Disease Transmission Sarcoptidae None Sarcoptes scabiei var. hominis Demodicidae None Demodex folliculorum Demodex brevis None Pyroglyphidae None Dermatophagoides pteronyssinus D. farinae None Dermanyssidae Yes-Rickettsia akari Liponyssoides sanguineus (formerly Allodermanyssus sanguineus) Dermanyssus None gallinae Macronyssidae None Ornithonyssus bacoti O. bursa None Laelapidae None Laelaps echidnina Pyemotidae Pyemotes None tritici (formerly Pediculoides ventricosus) Peymotes herfsi None Table 2. Currently recommended treatments for scabies. Scabicides (Trade Names-US) Pregnancy Category * 5% permethrin cream B (Actin [R], Nix [R], Elimite [R]) 1% lindane lotion or B cream 10% crotamiton cream C or lotion (Eurax [R]) 2%-10% sulfur in C petrolatum ointments 10%-25% benzoyl None benzoate lotion 0.5% malathion lotion B (Ovide [R]) (1% shampoo is unavailable in US) Ivermectin C (Stromectol [R]) (0.8% lotion is unavailable in US) Scabicides (Trade Names-US) Dosing Schedules 5% permethrin cream Apply from neck (Actin [R], Nix [R], down; wash off after Elimite [R]) 8-14 hours. Good residual activity, but second application recommended after one week. 1% lindane lotion or Apply 30-60 mL from cream neck down; wash off after eight to 12 hours. No residual activity. Increasing drug resistance. 10% crotamiton cream Apply from neck down or lotion (Eurax [R]) on two consecutive nights; wash off 24 hours after second application. 2%-10% sulfur in Apply for two to three petrolatum ointments days then wash. 10%-25% benzoyl Two applications for 24 benzoate lotion hours with one day to one week interval. 0.5% malathion lotion 95% ovicidal. (Ovide [R]) Rapid (five minutes) (1% shampoo is killing. unavailable in US) Good residual activity. Increasing drug resistance. Ivermectin 200-mcg/kg single (Stromectol [R]) (0.8% dose by mouth, may be lotion is unavailable in repeated in 14-15 days. US) Not ovicidal and second dose highly recommended on day 14-15. Recommended for endemic or epidemic scabies in institutions and refugee camps. Scabicides (Trade Names-US) Safety Profiles and Comments 5% permethrin cream Excellent. (Actin [R], Nix [R], Itching and stinging on Elimite [R]) application. 1% lindane lotion or Potential for central cream nervous system (CNS) toxicity from organochlorine pesticide poisoning, usually manifesting as seizures, with over-applications and ingestions. 10% crotamiton cream Excellent. or lotion (Eurax [R]) Not very effective. Exacerbates pruritus. 2%-10% sulfur in Excellent. petrolatum ointments Not very effective. 10%-25% benzoyl Irritant. benzoate lotion Exacerbates pruritus. Can induce contact irritant dermatitis and pruritic cutaneous xerosis. 0.5% malathion lotion Flammable 78% (Ovide [R]) isopropyl alcohol (1% shampoo is vehicle stings eyes, skin, unavailable in US) and mucosa. Increasing drug resistance. Organophosphate pesticide poisoning risks with over-applications and ingestions. Ivermectin Excellent. (Stromectol [R]) (0.8% May cause nausea and lotion is unavailable in vomitting; take on US) empty stomach with water. Scabicides (Trade Names-US) Contraindications 5% permethrin cream Prior allergic reactions. (Actin [R], Nix [R], Infants < two months Elimite [R]) of age. Breast feeding. 1% lindane lotion or Pre-existing seizure cream disorder. Infants and children under six months of age. Pregnancy. Breast feeding. 10% crotamiton cream None. or lotion (Eurax [R]) 2%-10% sulfur in Pre-existing sulfur petrolatum ointments allergy. 10%-25% benzoyl Pre-exising eczema. benzoate lotion 0.5% malathion lotion Infants and children (Ovide [R]) under six months of (1% shampoo is age. unavailable in US) Pregnancy. Breast feeding. Ivermectin Safety in pregnancy (Stromectol [R]) (0.8% uncertain. lotion is unavailable in Probably safe during US) breast feeding. Not recommended for children weighing < 15 kg. * US Food and Drug Administration (FDA) Safety in Pregnancy Categories: A-Safety established; B-Presumed safe; C-Uncertain safety; D-Unsafe; X-Highly unsafe.
|Printer friendly Cite/link Email Feedback|
|Author:||Diaz, James H.|
|Publication:||The Journal of the Louisiana State Medical Society|
|Date:||May 1, 2010|
|Previous Article:||Unexplained fever and worsening CNS symptoms.|
|Next Article:||Inverted liver with suprahepatic, anteriorly displaced gallbladder.|