Mite‐Transmitted Dermatoses and Infectious Diseases in Returning Travelers

James H. Diaz MD, MPH&TM, Dr PH
DOI: 21-31 First published online: 1 January 2010

Mites are among the smallest arthropods with most barely visible without magnification. 1 Mites are closely related to ticks, but they are tissue‐juice feeders, not blood‐feeders, and do not transmit as broad a variety of infectious microbial diseases. 1 In fact, the only infectious diseases transmitted by mites are rickettsialpox and scrub typhus. 1 The most common ectoparasitic dermatoses caused by mites are chiggers and scabies. 1 Travelers are uniquely predisposed to contracting several mite‐transmitted dermatoses and infectious diseases including: (1) scabies mites from close personal contacts; (2) zoonotic scabies from domestic or wild animals and pets; (3) rickettsialpox from sleeping in or visiting mice‐infested dwellings; and (4) chiggers and scrub typhus after stumbling onto trombiculid larvae‐infested “mite islands” in endemic regions worldwide. This review will describe the epidemiology, clinical manifestations, and management of the most common mite‐transmitted dermatoses and infectious diseases in returning travelers.

Materials and Methods

A MEDLINE search, 1966 to 2008, of the world's scientific literature of case reports, case series, original articles, reviews, and observational and longitudinal studies was conducted to determine the epidemiology, outcomes, clinical manifestations, preferred diagnostic interventions, and management for mite‐transmitted dermatoses and infectious diseases in returning travelers. In addition, a clinical classification of mite‐transmitted infestations and infections was developed to assist clinicians in assessing potential mite‐transmitted skin and systemic infectious diseases in travelers.


Classification of Mites and Disease Ecology of Mite‐Transmitted Dermatoses and Infectious Diseases

Mite infestations and infections were classified into the following distinct clinical and etiological categories: (1) the mite‐transmitted dermatoses caused by human mites: scabies and follicle mite infestations (also known as demodecidosis or demodicosis); (2) the mite‐transmitted dermatoses caused by non‐human mites: chiggers, zoonotic scabies, animal and plant and plant insect mite infestations, and dust mite allergies; and (3) the mite‐transmitted systemic infectious diseases: scrub typhus and rickettsialpox (Table 1). Only two non‐human, animal mites may transmit infectious diseases: (1) chiggers or trombiculid larval mites may transmit scrub typhus caused by the rickettsia‐like bacterium, Orientia tsutsugamushi; and (2) house‐mouse mites may transmit rickettsialpox caused by the rickettsial microorganism, Rickettsia akari.

View this table:
Table 1

Mites of medical importance

Family Genus, speciesCommon names (human, animal, or plant mite)Geographic distributionMaintenance in natureClinical manifestationsInfectious disease transmission
Sarcoptes scabiei var. hominisScabies (itch) mite (human mite)WorldwideObligate ectoparasite of man, human reservoirClassical scabiesNone
Atypical scabies
Neotrombicula autumnalisEuropean harvest mite (animal mite)EuropeFree‐living ectoparasites of small mammals and birdsScrub itch (Trombidiosis)None
Eutrombicula alfreddugesiAmerican chigger mite (animal mite)Western hemisphereFree‐living ectoparasites of small mammals and birdsScrub itch (Trombidiosis)None
E sarcinaAsian chigger mite (animal mite)Asia and AustraliaFree‐living ectoparasites of small mammals and birdsScrub itch (Trombidiosis)None
Leptotrombidium delienseAsian rodent chigger (animal mite)Southeast Asia, Japan, Philippines, South Pacific, and AustraliaFree‐living ectoparasites of rodents and insectivores, transovarial‐transstadial passage of ID agentScrub typhus (tsutsugamushi disease)Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi) causative agent of scrub typhus
Leptotrombidium akamushi, Leptotrombidium pallidum, and Leptotrombidium scutellarisJapanese rodent chiggers (animal mites)JapanSameSameSame
Leptotrombidium arenicola and Leptotrombidium fletcheriMalaysian rodent chiggers (animal mites)MalaysiaSameSameSame
Leptotrombidium pavlovskyiRussian rodent chigger (animal mite)Far east of former Soviet UnionSameSameSame
Demodex folliculorumHair follicle mite (human mite)WorldwideObligate ectoparasite of man, human host reservoir in hair folliclesBenign follicular (scaling) dermatitisNone
Chronic blepharitis possible
Demodex brevisSebaceous gland mite (human mite)WorldwideObligate ectoparasite of man, human host reservoir in sebaceous glands.May potentiate granulomatous acneNone
Dermatophagoides pteronyssinusEuropean house dust mite (human mite)WorldwideFree‐living ectoparasites of man; live in human bedrooms, especially in mattresses; feed on human skin detritusHouse dust mite allergies and asthmaNone
Dermatophagoides farinaeAmerican house dust mite (human mite)WorldwideSameSameNone
Liponyssoides sanguineus (formerly Allodermanyssus sanguineus)House‐mouse mite (animal mite)North America, Northern Europe and Asia, and AfricaFree‐living ectoparasites of field mice, transovarial‐transstadial passage of ID agentRickettsialpoxRickettsia akari
Dermanyssus gallinaeRed poultry (chicken) mite (animal mite)WorldwideFree‐living ectoparasites of domestic and wild birdsPoultry workers' dermatitis of handsNone
Ornithonyssus bacotiTropical rat mite (animal mite)Temperate and tropical regions worldwideFree‐living ectoparasites of large rodents: Rattus rattus and Rattus norvegicusUrticarial papulovesicular to pustular dermatitisNone
Ornithonyssus bursaTropical fowl mite (animal mite)SameFree‐living ectoparasites of domestic and wild birdsPruritic papules in a scabietic distribution: finger webs, axillae, groin, and buttocksNone
Laelaps echidninaSpiny rat mite (animal mite)Worldwide, the most prevalent rodent mite species in the United StatesFree‐living ectoparasites of large rodents: R rattus and R norvegicusNon‐specific mite‐bite dermatitisNone
Pyemotes tritici (formerly Pyemotes ventricosus)North American straw itch mite (plant insect mite)Introduced into the southern United States from EuropeFree‐living ectoparasites of straw, hay, grain, and rice‐eating larval moths, beetles, and weevilsGrain workers' pruritic vesicular eruptionNone
P ventricosusEuropean straw itch mite (plant insect mite)Southern EuropeFree‐living ectoparasites of furniture beetles, Anobium punctatumIntensely pruritic erythematous maculopapular lesions with central micropustules and comet signs (see text for discussion)None
Peymotes herfsiOak leaf gall mite (plant insect mite)Free‐living ectoparasites of gall‐making larvae of oak treesPruritic, erythematous, vesicular eruptions of limbs, face, and neckNone

Most mite species develop very 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 bush with grassy vegetation, warm soil temperatures, and high humidity. “Mite islands” have frequently visiting rodent hosts for larval chiggers to feed upon and sufficient small insect fauna to feed nymphs and adults. Travelers stumbling onto mite islands are at significantly higher risks of larval chigger bites (also known as “chiggers” or trombidiosis) worldwide or scrub typhus in endemic regions of Asia, Eurasia, and the South and West Pacific. Animal and plant mites establish their mite islands in animal dens, bird nests, trees, on fruits and vegetables, and even on cheeses and furniture.

The Epidemiology of Mite‐Transmitted Dermatoses in Returning Travelers

The epidemiology of arthropod‐associated dermatoses in travelers returning from tropical countries has been studied extensively by investigators at the Hôpital Pitié‐Salpêtrière in Paris. 2,3 The investigators concluded that dermatoses in travelers returning from tropical countries were common; accounted for one third of cutaneous disorders; and were significantly influenced by traveler status (age, sex, and nationality) and region visited. 2,3 In summary, the epidemiological investigations of dermatoses in returning travelers have now demonstrated the following: (1) arthropod‐induced dermatoses are common in travelers returning from the tropics; (2) many of these dermatoses are caused by human mites, particularly scabies mites; and (3) other pruritic skin conditions, particularly pruritus of unknown origin (PUO) and pruritic arthropod‐reactive dermatitis or prurigo, may be caused by several species of non‐human mites including zoonotic scabies mites, other animal mites, and plant and plant insect mites. 2,3

The Clinical Manifestations, Management, and Prevention of Human Mite‐Transmitted Dermatoses


Scabies, an infestation by the itch or scabies mite, Sarcoptes scabiei var. hominis, remains a major public health problem worldwide and a common cause of PUO in returning travelers. 3,4 The worldwide prevalence of scabies has been estimated to be about 300 million cases/y. 4 Although more often associated with crowding, homelessness, institutionalization, and immunodeficiency, scabies occurs worldwide in both sexes, at all ages, and among all ethnic and socioeconomic groups.

Scabies mites cannot jump or fly, but can crawl at a rate of 2.5 cm/min on warm, moist skin. 1,4 They can survive in the natural environment for 24 to 36 hours at room temperature and at average humidity, and remain capable of infesting humans. 5 Scabies is most easily transmitted by close skin‐to‐skin contact, such as between sex partners. The more the mites 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 and clothing. 4 Scabies mites have not been demonstrated to transmit HIV, HTLV‐1, or any other infectious agent. 4

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 reinfest 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 to 10 mm long, and larvae hatch 2 to 3 days after eggs are laid. The entire incubation period from eggs to full grown mites lasts about 14 to 15 days. 6 The human incubation period from initial infestation to symptom development is 3 to 6 weeks in initial infestations and as short as 1 to 3 days in reinfestations as a result of prior sensitization to mite antigens. 4

Classical or typical scabies presents as generalized, intense nocturnal itching in a characteristic topographical distribution because 10 to 15 fertile female mites are transferred from infected patients to new hosts. The more significant, intensely pruritic skin eruptions in reinfestations and atypical scabies are considered as consequences of both anamnestic hypersensitivity reactions to mite antigens and self‐inflicted scratching. 4

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. 4 Skin eruptions are characterized by inflammatory, pruritic papules at infested sites; and the pathognomonic linear‐to‐serpiginous intradermal burrows. 4 Scabietic burrows are 5 to 10 mm long, dotted with fecal lithes (pellets) or scybala, and terminate in raised papules that may rarely hide ovipositing females. 4 Non‐specific secondary lesions occur commonly from scratching (self‐inflicted excoriations and lichenification); secondary infection (impetigo); or side effects of topical treatments (eczematization).

The diagnosis of scabies is made predominantly by epidemiological considerations and clinical and microscopic observations. A clinical diagnosis may be confirmed by low power microscopic examination of a burrow skin scraping which may excavate a female mite, 0.2 to 0.5 mm in length, translucent with brown legs, and too small to be seen without magnification. 4 Eggs (0.02–0.03 mm in diameter), smaller eggshell fragments, and fecal lithes may also be identified in microscopic specimens of burrow scrapings. 4 Newer diagnostic methods for scabies now under investigation include enhanced microscopy (epiluminescence microscopy and non‐computed dermoscopy); immunological detection of specific scabies antibodies by enzyme‐linked immunosorbent assay (ELISA); and molecular identification of scabies mite DNA by polymerase chain reaction (PCR). 4,7,8

Topical or oral scabicides should be used to treat all infested persons and their close personal contacts simultaneously, regardless of the presence of symptoms. 4 Currently, recommended treatment options for scabies are listed in Table 2. The most effective topical treatments for scabies are 5% permethrin cream, 10 to 25% benzoyl benzoate lotion, and 1% lindane cream or lotion. 9

View this table:
Table 2

Currently recommended treatments for scabies

Scabicides (trade names—United States)Pregnancy category*Dosing schedulesSafety profilesContraindications
5% Permethrin cream (Actin, Nix, and Elimite)BApply from neck down; wash off after 8–14 hoursExcellentPrior allergic reactions
Good residual activity, but second application recommended after 1 weekItching and stinging on applicationInfants < 2 months of age
Breast feeding
1% Lindane lotion or creamBApply 30–60 mL from neck down; wash off after 8–12 hoursPotential for CNS toxicity from organochlorine poisoning, usually manifesting as seizures, with over‐applications and ingestionsPreexisting seizure disorder
No residual activityInfants and children under 6 months of age
Increasing drug resistancePregnancy
Breast feeding
10% Crotamiton cream or lotion (Eurax)CApply from neck down on two consecutive nights; wash off 24 hours after second applicationExcellentNone
Not very effective
Exacerbates pruritus
2–10% Sulfur in petrolatum ointmentsCApply for 2–3 days then washExcellentPreexisting sulfur allergy
Not very effective
10–25% Benzoyl benzoate lotionNoneTwo applications for 24 hours with 1‐day to 1‐week intervalInexpensive and highly effectivePreexisting eczema
Exacerbates pruritus
Can induce contact irritant dermatitis and pruritic cutaneous xerosis
0.5% Malathion lotion (Ovide)B95% ovicidalFlammableInfants and children under 6 months of age
1% Malathion shampoo (unavailable in United States)Rapid (5 min) killing78% Isopropyl alcohol vehicle stings eyes, skin, and mucosaPregnancy
Good residual activityIncreasing drug resistanceBreast feeding
Increasing drug resistanceOrganophosphate poisoning risks with over‐applications and ingestions
Ivermectin (Stromectol), 0.8% lotion (unavailable in United States)C200 mcg/kg single po dose, may be repeated in 14–15 daysExcellentSafety in pregnancy uncertain
Not ovicidal and second dose highly recommended on day 14–15May cause nausea and vomiting; take on empty stomach with waterProbably safe during breast feeding
Recommended for endemic or epidemic scabies in institutions and refugee campsNot recommended in children weighing <15 kg
  • CNS = central nervous system.

  • *US Food and Drug Administration (FDA) Safety in Pregnancy Categories: A, safety established; B, presumed safe; C, uncertain safety; D, unsafe; X, highly unsafe.

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. 10 Nevertheless, ivermectin is not ovicidal, and a second course of oral treatment at adult maturation time of 14 to 15 days is recommended. 10

Follicle Mite Infestations or Demodecidosis

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 human follicle mites: (1) Demodex folliculorum, which inhabits hair follicles; and (2) Demodex brevis, which inhabits sebaceous glands. The follicle mites are diminutive (0.1–0.4 mm long), usually non‐pathogenic saprophytes, that feed on sebum and exfoliated skin while lodged in hair follicles and sebaceous glands on the eyelids, nasolabial folds, nose, and ears. 1 Although controversial, follicle mites may also be pathogenic agents of chronic blepharitis. 1,11 Other than causing comedones or “blackheads” in immunocompetent patients, demodecidosis causes few adverse symptoms and rarely needs treatment, other than soap and water washing to reduce infestations.

The Clinical Manifestations, Management, and Prevention of Non‐Human Mite‐Transmitted Dermatoses and Infectious Diseases


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 O tsutsugamushi, the causative agent of scrub typhus, in endemic regions. Larvae pierce the skin with sharp mouthparts and infuse tissue‐dissolving saliva to fill a pool of lymph, other body fluids, and dissolved epithelial cells to aspirate from (Figure 1). The repeated injection of saliva into bite wounds incites a host reaction forming a straw‐like hollow tube, the hypostome (stylostome), which extends downwards firmly anchoring the mite into the host's skin. 1

Figure 1

An intensely pruritic erythematous bleb 24 hours after a bite inflicted by a larval trombiculid species chigger mite. Although these species of lymph‐sucking mites do not transmit infectious diseases in the United States, many species of larval trombiculids will transmit scrub typhus or tsutsugamushi disease, caused by the rickettsial microorganism, Orientia (formerly Rickettsia) tsutsugamushi, throughout Southeast Asia and the South and West Pacific regions. Source: United States Department of Health and Human Services, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia USA and CDC Public Health Image Library, PHIL ID # 3806, no copyright permission required.

All of the non‐infectious chigger larvae can cause scrub itch or trombidiosis with the American chigger mite, Eutrombicula alfreddugesi, being the most common culprit in the United States; the European autumn harvest mite, Neotrombicula autumnalis, the most common culprit in Europe; and the Asian chigger, Eutrombicula sarcina, the most common culprit in Asia (Table 1). 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 3 to 6 hours for most non‐infectious 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 2 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 Several untested strategies for removing feeding, engorged chiggers intact have included painting chigger bite sites with colloidion, clear fingernail polish, or Liquid Skin, then drying the sites with a hair dryer and peeling the coated and dried chiggers off the skin intact.

Localized intense itching will often be followed by prurigo, an eruption of intensely pruritic erythematous papules by 10 to 12 hours, followed by crusting and healing by 24 to 48 hours. 1 Treatment of mild infestations is supportive with soap and water cleansing, warm water soaks, and topical local anesthetics and antihistamines. Prurigo should be treated specifically with topical corticosteroids, with oral corticosteroids indicated for severe cases. 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. 12

Zoonotic Scabies

Several non‐human species of sarcoptid mites can cause animal 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, camels, horses, pigs, and rabbits. 13 Humans may also contract zoonotic scabies from a variety of exotic animals including chamois (Rupicapra rupicapra), wombats, and koalas (Phascolarctos cinereus). 14–16 Animal scabies mites are facultative ectoparasites in humans, cannot effectively complete their life cycles in human dead‐end hosts, and cause self‐limiting infestations in humans. Symptomatic infestations may be treated with 5% permethrin lotion, 10% crotamiton cream or lotion, or oral ivermectin.

Other Animal Mite Infestations

Although of limited clinical significance, a number of other animal mite infestations can cause bothersome, usually self‐limited, erythematous, papulovesicular eruptions. Bites from the red chicken or poultry mite, Dermanyssus gallinae, can cause prurigo, usually on the backs of the hands and forearms in farmers and poultry workers. 17 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. 17 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. 17,18 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. 18 Most animal mite bites can be managed symptomatically with topical agents, specifically topical corticosteroids. 18

Dust Mite Allergies

Dermatophagoides species dust mites have highly allergenic antigens, such as fragments of chitinous exoskeletons and feces, which are easily aerosolized during bed‐making and pillow‐fluffing. 19 These allergens may cause allergic rhinitis and asthmatic bronchitis in predisposed, atopic persons. 19 The American house dust mite, Dermatophagoides farinae, is distributed worldwide, as is the European house dust mite, Dermatophagoides pteronyssinus. 19 House dust mites prefer to reside in bedrooms, mattresses, and carpets year‐round in warm, humid homes. 17 They exhibit maximum growth and reproduction during seasonal warming cycles at ambient temperatures at or above 25°C and relative humidities at or above 75%. 17 House dust mite allergies may be managed by antigen immunotherapy with house dust mite extracts.

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 P tritici dermatitis in the southern United States, where hay rides, caned furniture, and straw rugs are popular. 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. Straw itch mite dermatitis is characterized by pruritic, maculopapulovesicular eruptions on the limbs and trunk, which resolve rapidly with topical corticosteroid therapy. 17,20

In 2000, Bellido‐Blasco and colleagues 21 investigated three separate outbreaks of dermatitis afflicting over 100 patients caused by the European straw itch mite (P ventricosus) in Castellon, Spain. In 2006, Del Giudice and colleagues 22 described a similar outbreak, also suggestive of arthropod bite‐induced dermatitis in southeastern France. The dermatitis was characterized by solitary to multiple, highly erythematous pruritic macules, some of which were accompanied by contiguous, linear erythematous macular tracts that resembled “comet tails” (Figure 2). 22 In a 2007 outbreak investigation of an additional 42 cases of dermatitis with comet tail signs in the same region, Del Giudice and colleagues identified P ventricosus mites as causative agents and described the epidemiology and outcomes of P ventricosus infestations in homes and humans.

Figure 2

Photographs of six persons (A–F) with skin lesions of Pyemotes ventricosus dermatitis. Note the central microvesicles, ulcerations or crusts, and many lesions with the pathognomonic comet signs. (D) Lymphangitis‐like dermatitis. (E and F) Lesions resulting from natural infections of two of the investigators. Source: United States Department of Health and Human Services, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia USA; CDC Emerging Infectious Diseases; and Del Giudice and colleagues. 23 Available at: No copyright permission required.

Most residences of case‐patients with P ventricosus dermatitis were infested with live furniture beetles, Anobium punctatum, which do not bite or infest humans. Adult P ventricosus mites, common ectoparasites of furniture beetles, were present in stereomicroscopic examination of wood dust beneath beetle‐infested furniture. Confocal laser scanning microscopy (CLSM) of a central microvesicle in a maculopapular lesion on an experimentally infested co‐investigator demonstrated an ovoid foreign body consistent with a P ventricosus mite (Figure 2). Both naturally occurring and experimental infestations caused the characteristic maculopapular rash of P ventricosus dermatitis, again associated with comet signs (Figure 2). 23 Although oral prednisone (0.5 mg/kg) rapidly relieved pruritus, P ventricosus dermatitis would persist or recur in case‐patients until beetle‐infested furniture was removed from households or patients permanently vacated their infested residences, often in resort regions. 23

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 United States. 24 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 3). 24 All lesions healed within days following topical treatment with antihistamines and corticosteroids. 24

Figure 3

Close‐up photograph of the pruritic erythematous papulovesicular bite lesions inflicted by the European oak leaf gall mite on a resident of Pittsburg, Kansas, USA in late August 2004. Source: United States Department of Health and Human Services, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia USA and CDC MMWR. 24 Photo/A. Broce, L. Zurek, Kansas State University. Available at: No copyright permission required.

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. Plant insect mite dermatitis may become chronic or recur on indoor or outdoor mite reexposure 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 Non‐Human Mite‐Transmitted Infectious Diseases

Only biting larvae of Asian scrub typhus chiggers (Leptotrombidium species) transmit scrub typhus caused by O tsutsugamushi (formerly Rickettsia tsutsugamushi), and only biting house‐mouse mites (Liponyssoides sanguineus) transmit rickettsialpox caused by R akari. Although these two mite‐transmitted infectious diseases do share mites as vectors, their preferred mite vectors, disease ecologies, and clinical presentations are different, when compared with Table 3. Although initially classified in the genus Rickettsia, O tsutsugamushi was reclassified into a separate genus based on molecular evidence that its cell wall ultrastructure differed significantly from Rickettsia species. 25 Both scrub typhus and rickettsialpox respond to treatment with oral tetracycline, oral doxycycline, or intravenous chloramphenicol, which is not recommended due to its bone marrow toxicity. 25

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Table 3

The presentation, diagnosis, differential diagnosis, and management of mite‐transmitted scrub typhus versus rickettsialpox

Major mite‐transmitted infectious diseasesScrub typhusRickettsialpox
Bacterial agentO tsutsugamushi (formerly R tsutsugamushi)R akari
Mite vectorLarvae of Leptotrombidium species of Asian rodent chigger mitesCommon house‐mouse mites, L sanguineus
Incubation period8–10 days (range 8–20 days)10–12 days
Mite‐bite sitePainless initial bite, eschar at bite site (50%)Painless initial bite, eschar at bite site
Presenting constitutional symptomsFever, chills, headaches present (60%) versus headaches absent (40%), myalgia, and pathognomonic hearing loss (30%)Fever, chills, severe headache, myalgia, and no hearing loss
Conjunctival injectionPresentMay be present
Regional lymphadenopathyPresent regionally and tenderUsually absent
Associated rash exanthemaDelayed truncal onset, erythematous macules then maculopapules that spread peripherallyAbrupt truncal onset, erythematous macules that develop central vesicles in crops
Chest findingsCough, tachypnea, dyspnea, and bibasilar ralesAsymptomatic bibasilar rales
Chest X‐ray findingsInfiltrates commonUsually normal
Potential complicationsAdult respiratory distress syndrome, acute renal failure, disseminated intravascular coagulation, and encephalomyelitisThrombocytopenia
Differential diagnosesInfectious mononucleosis, leptospirosis, tularemia, anthrax, spotted fever group rickettsioses, murine typhus, and Q feverChickenpox, tularemia, anthrax, and Q fever
Diagnostic methodsScreening: rapid dipstick recombinant 56‐kd protein antigen testSerodiagnostic: immunofluorescent antibody assay for IgG to both R akari and R rickettsia with follow‐up cross adsorption testing for predominant antibodies
Serodiagnostic: indirect immunofluorescent antibody tests and immunoperoxidase assaysConfirmatory: isolation from skin biopsy
Confirmatory: microscopic isolation of causative agent from blood or tissues, polymerase chain reaction for causative agent DNA (or RNA)
Recommended treatmentsTetracycline 500 mg po qid × 1 week, or Doxycycline 100 mg bid × 1 week, or iv chloramphenicol, 50–75 mg/kg/day × 1 week (only for complicated cases)Doxycycline 100 mg po bid × 7–10 days
In childhood and pregnancy, consider the macrolides: clarithromycin, or roxithromycin
Outcomes = case fatality rates (%)1–15%< 1%

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, because bacteria are passed from adults to juveniles (nymphs and larvae) by transstadial transmission. 25 Scrub typhus chiggers are the main environmental reservoirs of O tsutsugamushi in endemic regions with much smaller secondary reservoirs in wild rodents. 1,25 Common house mice are the zoonotic reservoirs of R akari, not only in crowded urban apartment buildings in the United States but also in all mice‐infested buildings and sheds in more rural locations worldwide.

Scrub Typhus

Among the scrub typhus‐carrying Leptotrombidium larval chigger mites, Leptotrombidium deliense, the Asian rodent chigger, is a principal vector throughout eastern Asia and Eurasia. 25,26 Following scrub typhus‐infected chigger bites, there is an 8‐ to 10‐day incubation period before onset of classical clinical manifestations including bite‐eschar, regional lymphadenopathy, conjunctival injection, hearing loss, and centrifugal rash. 25,26 In the temperate regions of Eurasia, there is a definite scrub typhus seasonal transmission cycle determined by peaking temperatures and humidity during weeks of marked seasonal change between spring and summer and fall and winter. 27 In the tropics, scrub typhus transmission occurs year‐round. 25

In Asia, the most common endemic rickettsioses include scrub typhus, murine typhus, and Q fever, which may be difficult to differentiate clinically and also serologically due to cross‐reacting antigens. 25,26 Scrub typhus may present with a non‐specific influenza‐like prodrome of fever, chills, diaphoresis, headache (in approximately 60%), malaise, and weakness. In classical cases, this prodrome may be followed by skin rash, bite‐eschar(s), regional lymphadenopathy, conjunctival injection, icteric sclera, jaundice, and bradycardia. 25,27 Later, patients may develop potentially fatal complications including adult respiratory distress syndrome (ARDS), especially in older patients, hypotensive shock, acute renal failure, encephalomyelitis, and disseminated intravascular coagulation (DIC). 25

Frequently, patients presenting with similar constellations of constitutional symptoms and few pathognomonic signs (eschar, rash, and hearing loss) in rural scrub typhus‐hyperendemic areas are often treated preemptively and empirically with oral doxycycline. 26 Rural regions may have limited access to specific serological tests (immunofluorescent antibody assays and paired sera comparisons for rising specific antibody titers) required to differentiate scrub typhus from other endemic rickettsial diseases. 25,26 Weekly doses of 200 mg of doxycycline can prevent O tsutsugamushi infections. 25


The house‐mouse mite, L sanguineus, maintains a rickettsial zoonosis in its preferred house‐mouse (Mus musculus) reservoir, and can transmit rickettsialpox caused by R akari through bites. 1,27,28 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 United States and Eurasia. 27,28 Many experts now feel that rickettsialpox is underreported and distributed in silent sylvan cycles worldwide. 27,28 The incubation period and initial clinical manifestations of rickettsialpox mirror those of scrub typhus with bite‐eschar formation within 10 to 12 days, followed by fever, chills, severe headache, conjunctival injection, and truncal maculopapular, then vesicular, rash. 27,28 Unlike scrub typhus, complications are rare, but may include thrombocytopenia and interstitial pneumonia. 27,28 Hearing loss does not occur, and regional lymphadenopathy is uncommon in rickettsialpox. The clinical manifestations, diagnosis, and management of scrub typhus and rickettsialpox are contrasted in Table 3.


In summary, mites are mostly ubiquitous, bothersome pests, with few species of medical importance and, of these, most are scabies mites, trombiculid larvae, and rodent mites. 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. Finally, only the Asian and Eurasian Leptotrombidium species of trombiculid larvae (chiggers) can transmit scrub typhus in endemic regions of Asia, Eurasia, and the South and West Pacific; and only the house‐mouse mite can transmit rickettsialpox in both urban and rural dwellings worldwide.

Declaration of interests

The author has no acknowledgements or financial or other interests to disclose.


Support for Prof. Diaz was provided by departmental and institutional sources.


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