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Acariasis

Acariasis is a condition characterized by infestation with or disease caused by mites of the subclass Acari, a diverse group of microscopic arachnids that includes species capable of parasitizing human and animal tissues.^[1]^[2] These parasites can invade the skin, respiratory tract, gastrointestinal system, or urinary tract, leading to a spectrum of clinical manifestations ranging from mild irritation to severe systemic effects.^[3] The most common form in humans is cutaneous acariasis, exemplified by scabies, an intensely pruritic skin infestation caused by the mite Sarcoptes scabiei var. hominis.^[4] This mite burrows into the epidermis, where females deposit eggs, triggering an allergic response to mite feces and saliva that results in characteristic papular rashes, burrows, and nocturnal itching, often affecting interdigital spaces, wrists, and genitals.^[5] Transmission occurs primarily through prolonged skin-to-skin contact, though shared bedding or clothing can also spread it, with higher incidence in crowded or institutional settings.^[6] Diagnosis is confirmed by microscopic identification of mites, eggs, or scybala in skin scrapings, while treatment involves topical scabicides like permethrin cream or oral ivermectin, alongside washing infested items in hot water to eliminate mites.^[7]^[8] Less common but notable are internal forms of acariasis, such as intestinal acariasis from ingesting mite-contaminated foods like flour or grains, which invades the gastrointestinal mucosa and causes symptoms including abdominal pain, diarrhea, and anal burning.^[3] Pulmonary acariasis, often due to inhalation of domestic mites in dusty environments, presents with respiratory distress like dry cough, wheezing, dyspnea, and chest pain, particularly among agricultural workers exposed to organic dust.^[3] Urinary and otic variants may lead to dysuria, hematuria, or ear discomfort, respectively, with treatments tailored to the site, including ivermectin for intestinal cases or supportive antibiotics for secondary infections.^[3] Overall, acariasis underscores the zoonotic potential of mites, with prevention emphasizing hygiene, food storage practices, and prompt treatment to curb outbreaks.^[3]

Overview

Definition

Acariasis refers to the infestation of human or animal tissues by mites belonging to the subclass Acari of the class Arachnida within the phylum Arthropoda. These mites, which are microscopic arthropods characterized by eight legs in their adult stage, can burrow into or reside on the skin, leading to dermatological conditions, or invade internal organs such as the gastrointestinal tract, respiratory system, or urinary tract, resulting in invasive infections.^[9]^[10]^[11] Unlike ascariasis, which is a helminthic infection caused by the nematode roundworm Ascaris lumbricoides, acariasis specifically involves arachnids rather than worms, highlighting the distinction between arthropod and helminth parasitism. Mites of the subclass Acari are not insects, as they lack antennae and possess a fused body structure with chelicerae for feeding, often enabling them to penetrate host tissues.^[1]^[12]^[10] The condition affects both humans and a wide array of veterinary species, including over 100 mammals, birds, and reptiles, where it manifests as skin rashes from superficial infestations or internal migrations causing organ-specific pathology. Common examples include cutaneous lesions like those seen in scabies or mange, and rarer internal cases such as mites detected in sputum from pulmonary involvement or in urine from urinary tract invasions.^[9]^[3]^[13]

Terminology

The term acariasis originates from New Latin, derived from "Acari," the taxonomic subclass encompassing mites within the class Arachnida, combined with the suffix "-iasis," which indicates a pathological condition or disease process resulting from such infestation.^[14] This nomenclature reflects the 19th-century recognition of mite-induced disorders in medical and veterinary contexts, emphasizing the arthropod's role in causing dermal or systemic pathology.^[1] Common synonyms for acariasis include "mite infestation" and "acarodermatitis," the latter highlighting skin-specific inflammatory responses.^[9] In veterinary practice, particularly for animal hosts, the condition is often termed "mange," with subtypes such as sarcoptic mange (caused by Sarcoptes scabiei) and demodectic mange (caused by Demodex species), denoting contagious or follicular mite involvement, respectively.^[15] These terms underscore the zoonotic potential and shared etiological framework across species.^[14] Specialized terminology delineates particular mite groups and manifestations: gamasoidosis (or avian mite dermatitis) refers to ectoparasitic dermatitis from hematophagous mites in the suborder Mesostigmata, such as Dermanyssus gallinae or Ornithonyssus species, typically acquired from bird reservoirs.^[16] Similarly, trombidiosis (or trombiculiasis) denotes pruritic lesions from larval chigger mites of the family Trombiculidae, often seasonal and linked to environmental exposure.^[17] Acariasis is further categorized as ectoparasitic, involving surface-dwelling mites on skin, feathers, or mucous membranes, versus endoparasitic, where mites invade internal sites like respiratory tracts, though the latter is rarer in most hosts.^[14]

Classification

Dermatological Acariasis

Dermatological acariasis refers to ectoparasitic infestations of the skin by mites, representing the predominant manifestation of acariasis in humans due to their direct interaction with the cutaneous surface.^[18] These infestations are characterized by mites that either burrow into the epidermis, reside in hair follicles, or deliver transient bites, often leading to localized dermatological reactions such as pruritus and inflammatory lesions. Unlike rarer internal forms that may involve systemic dissemination, dermatological cases are typically confined to the skin and transmitted through close personal contact or environmental exposure.^[19] The primary types of dermatological acariasis include scabies, demodicosis, and gamasoidosis, each caused by distinct mite species with unique pathogenic mechanisms. Scabies is induced by the burrowing mite Sarcoptes scabiei var. hominis, which excavates tunnels in the stratum corneum, depositing eggs and feces that provoke an intense allergic response manifested as severe nocturnal itching and erythematous papules, particularly in interdigital spaces, wrists, and genitals.^[20] This ectoparasite is estimated to affect more than 200 million people globally at any given time, with over 400 million cases cumulatively each year, and higher prevalence in crowded or unhygienic settings such as institutional environments or resource-limited communities.^[21] Transmission occurs primarily via prolonged skin-to-skin contact, though fomites like bedding can facilitate indirect spread.^[18] Demodicosis involves infestation by Demodex folliculorum or Demodex brevis, elongated mites that inhabit sebaceous glands and hair follicles, often asymptomatically colonizing the face and eyelids.^[19] These commensal organisms become pathogenic in immunocompromised individuals or those with underlying conditions like rosacea, where overproliferation leads to folliculitis, erythema, and scaling; prevalence in healthy adults ranges from 23% to 100%, increasing with age due to cumulative exposure.^[19] Unlike scabies, demodex mites are not readily transmitted person-to-person, as they rely on facial skin contact with colonized individuals or fomites, and their ectoparasitic nature is more opportunistic than invasive.^[22] Gamasoidosis, also known as avian or rodent mite dermatitis, results from bites by hematophagous mites such as Dermanyssus gallinae (poultry red mite) or Ornithonyssus species from birds and rodents, causing transient, pruritic papules without burrowing.^[23] These infestations are ectoparasitic and environmental in origin, occurring when mites seek alternative hosts in proximity to infested animal nests or poultry facilities, with human cases often self-limiting upon removal of the source; prevalence is low but notable in urban or agricultural settings with bird infestations, affecting up to 19% of exposed poultry workers with contact dermatitis.^[24] Transmission happens through direct contact with infested environments rather than sustained human-to-human spread. Representative examples of dermatological acariasis include human equivalents of canine or feline sarcoptic mange, where S. scabiei variants from pets cause zoonotic pseudoscabies with similar burrowing and itching in exposed individuals.^[25] Additionally, papular urticaria can arise from hypersensitivity to bites by non-burrowing mites like those in gamasoidosis, presenting as clustered, wheal-like papules that resolve without scarring but recur with re-exposure.^[26] These conditions underscore the ectoparasitic adaptability of mites, thriving in conditions of close contact or poor hygiene that facilitate their proliferation on human skin.^[27]

Internal Acariasis

Internal acariasis refers to rare infestations where mites penetrate and parasitize internal human organs, such as the gastrointestinal tract, lungs, or urinary system, leading to invasive pathology distinct from superficial skin involvement. Reports, primarily from older studies in regions like China (as of early 2000s), indicate rarity, with limited recent global data confirming ongoing but sporadic cases.^[28] However, reports of internal acariasis are primarily from China and some other regions, with debate in broader medical literature on whether detected mites represent true invasive parasitism or transient contaminants/pseudoparasites.^[14] ^[28] These cases often arise from accidental ingestion or inhalation of acaroid mites, which can survive in human tissues and cause mechanical damage, allergic responses, or secondary infections.^[29] While uncommon globally, internal acariasis is more frequently documented in regions with poor food storage practices or occupational exposure to contaminated grains and herbs.^[30] Intestinal acariasis primarily involves mites invading the gastrointestinal mucosa and musculature following ingestion of contaminated foodstuffs like grains, flour, dry fruits, or traditional Chinese medicines. Common causative agents include Acarus siro and Tyrophagus putrescentiae, which can persist in the intestinal environment and provoke symptoms such as diarrhea, abdominal pain, and lassitude.^[29] In a study from Anhui Province, China, 225 out of 3,416 stool samples (6.59%) tested positive for mites, with a higher detection rate of 28.29% among 152 patients presenting with diarrhea; species identified encompassed A. siro, T. putrescentiae, Dermatophagoides farinae, and Glycyphagus domesticus.^[30] These infestations are often underdiagnosed, with 63.33% of cases initially misattributed to other gastrointestinal disorders.^[29] Pulmonary acariasis occurs when mites are inhaled, typically in dusty environments, leading to their presence in sputum or lung tissues and causing respiratory distress. Involved species include T. putrescentiae, A. siro, Aeuroglyphus ovatus, and Tarsonemus spp., which may trigger cough, chest pain, dyspnea, hemoptysis, and eosinophilia.^[28] A Chinese investigation of 363 individuals exposed to grain stores and medicinal herbs found 92 (25.3%) with mites in sputum, 65 of whom exhibited symptoms attributable to the infestation; treatment with metronidazole cleared mites from sputum in 94.4% of cases and resolved clinical and radiographic signs.^[31] Additional reports from China include a single case of bronchiectasis linked to Tyrophagus and Tarsonemus mites.^[28] Urinary acariasis represents an exceedingly rare form, where mites appear in urine or affect the bladder, potentially stemming from ingested contaminants that migrate systemically. Mites such as A. siro, T. putrescentiae, D. farinae, and up to 17 other species have been detected, associated with conditions like pyelonephritis and pyelocystitis.^[13] In Anhui Province, China, a survey of 1,994 individuals revealed 37 cases (1.86%) positive for mites solely in urine and 32 (1.60%) in both urine and stool, with occupational groups like medicinal herb storehouse workers showing a 15.89% positivity rate.^[32] One historical report documented seven cases involving numerous mites and eggs in urinary sediment, leading to primary infections and ulcerative complications.^[28] These internal infestations are frequently tied to occupational hazards, particularly among grain mill workers, rice storehouse staff, and processors of traditional medicines, where exposure rates can reach 12.96% to 25%.^[13] Poor storage of foodstuffs exacerbates risks by allowing mite proliferation, and in some urinary cases, mites may migrate from the gastrointestinal tract to other systems post-ingestion.^[28] Prevention emphasizes improved hygiene in food handling and storage to mitigate these invasive threats.^[30]

Etiology and Transmission

Causative Agents

Acariasis is caused by various species of mites within the subclass Acari, which belongs to the class Arachnida in the phylum Arthropoda. These mites encompass two major superorders, Acariformes and Parasitiformes, with the former including most parasitic forms relevant to human infestations. The Acari are characterized by their eight-legged adult form and chelicerae for feeding, distinguishing them from insects.^[14] Parasitic mites in the Acari are typically microscopic, ranging from 0.2 to 0.4 mm in body length, enabling them to inhabit skin pores, follicles, or ingested food particles without immediate detection. Their life cycle generally progresses through four active stages—egg, hexapod larva, octopod nymph, and adult—though some species include resting (pharate) phases between nymphal instars. Development time varies from 10 to 36 days depending on temperature, humidity, and host availability, with females often producing 40–100 eggs over their 4–8 week lifespan. Key parasitic adaptations include specialized chelicerae and ambulacra for burrowing into host tissues or attaching to surfaces, as well as the secretion of enzymes and allergens from salivary glands or feces to facilitate feeding and evade immune responses.^[14] Among the implicated families, Sarcoptidae (order Sarcoptiformes, suborder Astigmata) includes burrowing ectoparasites like Sarcoptes scabiei, the agent of human scabies, which measures 0.2–0.4 mm and completes its life cycle in 10–15 days by tunneling into the stratum corneum to deposit eggs.^[33] Demodicidae (order Trombidiformes) features follicle-dwelling species such as Demodex folliculorum, a 0.3–0.4 mm long mite that resides in sebaceous hair follicles, with a life cycle of about 14 days and adaptations for lipid-rich environments via an elongated, worm-like body and reduced legs.^[19] Pyroglyphidae (order Astigmata) comprises free-living or semi-parasitic house dust mites like Dermatophagoides pteronyssinus, approximately 0.3 mm in size, with a 25–36 day life cycle involving protonymph and tritonymph stages; these mites produce potent fecal allergens and can contribute to ingestional acariasis through contaminated dust.^[34] Acaridae (order Astigmata), represented by storage mites such as Acarus siro, are 0.4–0.5 mm long pests of grains and flours, featuring a 10–20 day life cycle under humid conditions (70–85% RH) and hypopal (dispersal) stages for migration between food sources.^[35]

Modes of Transmission

Acariasis transmission varies by the type of infestation and the mite species involved, primarily occurring through direct or indirect contact for dermatological cases and ingestion for internal cases. Dermatological acariasis, such as scabies caused by Sarcoptes scabiei, spreads mainly via prolonged skin-to-skin contact, facilitating the transfer of gravid females between hosts.^[4] In contrast, internal acariasis results from the ingestion of acaroid mites contaminating stored foods or dust, allowing mites to enter the gastrointestinal tract.^[13] Direct contact is the predominant mode for many dermatological infestations, including scabies and demodicosis. For scabies, transmission requires extended personal interaction, such as in household or institutional settings, where mites burrow into the skin of new hosts.^[36] Demodex mites (Demodex folliculorum and D. brevis) transfer through close facial contact, often from mother to infant during close physical contact after birth or via shared grooming items affecting hair follicles and sebaceous glands.^[19] These pathways are enhanced in overcrowded environments with poor hygiene, promoting outbreaks in families or communal living.^[4] Indirect transmission plays a secondary role in dermatological acariasis but is more significant in crusted (Norwegian) scabies, where thousands of mites contaminate fomites like bedding, clothing, or furniture, enabling spread without direct contact.^[37] For certain ectoparasitic mites like Dermanyssus gallinae (poultry red mite), indirect transfer occurs via environmental reservoirs such as infested bird nests or animal bedding.^[14] In internal acariasis, indirect routes involve inhalation or incidental ingestion of mite-laden dust from storage areas, though direct food contamination remains primary.^[29] Zoonotic transmission links animal reservoirs to human cases, particularly for dermatological acariasis. Sarcoptic mange mites from dogs (S. scabiei var. canis) or cats (Notoedres cati) can infest humans through pet contact, though infestations are typically self-limiting as these mites do not reproduce on human skin.^[14] Cheyletiella mites ("walking dandruff") from infested pets spread via direct animal handling or shared environments, affecting up to 20% of exposed owners.^[14] Internal acariasis has limited zoonotic reports, but environmental mites from agricultural settings may originate from animal feed storage.^[13] Environmental and occupational factors significantly influence transmission across acariasis types. Poor sanitation and overcrowding facilitate dermatological spread in communal settings like nursing homes or prisons.^[4] For internal cases, humid and warm conditions in food storage facilities, such as grain silos or herbal warehouses, promote mite proliferation, with higher infection rates among workers (e.g., 15.89% in medicinal herb handlers).^[13] Occupational exposure in agriculture or food processing heightens risk for both types through contaminated dust or animal proximity.^[29]

Clinical Features

Symptoms

Acariasis, an infestation by mites of the subclass Acari, manifests through a range of clinical signs depending on the site of infestation and the specific mite species involved. Dermatological acariasis, the most common form in humans, typically presents with intense pruritus that often worsens at night, accompanied by burrows, papules, and vesicles on the skin. In scabies caused by Sarcoptes scabiei, the rash commonly affects interdigital spaces, wrists, elbows, and genitals, with burrows appearing as thin, wavy lines. Demodicosis, due to Demodex mites, frequently features folliculitis with papules and pustules around hair follicles, particularly on the face, alongside scaling and erythema, though low-burden infestations may remain asymptomatic. Internal acariasis is rarer but can involve multiple organ systems. Intestinal acariasis leads to abdominal pain, diarrhea, and weight loss, sometimes with mucous or bloody stools and a burning sensation around the anus. Pulmonary acariasis causes cough, hemoptysis, and dyspnea, potentially progressing to wheezing, chest pain, and fatigue in severe cases. Urinary acariasis results in dysuria and frequent urination, often associated with pyelonephritis or cystitis-like symptoms. Otic acariasis presents with severe itching and a sensation of insects crawling in the ear.^[3] General symptoms across acariasis types include allergic reactions to mite bites or saliva, such as hives and, rarely, anaphylaxis with swelling and shortness of breath. Secondary bacterial infections frequently arise from scratching, leading to impetiginized lesions or cellulitis. Symptom severity varies; low-density Demodex infestations are often subclinical, while immunocompromised individuals experience exacerbated presentations, including widespread dermatitis or systemic involvement.

Complications

Untreated acariasis, particularly scabies caused by Sarcoptes scabiei, often leads to secondary bacterial infections due to intense scratching of infested skin lesions, which breaches the skin barrier and allows entry of pathogens such as Staphylococcus aureus and Streptococcus pyogenes.^[20] These infections commonly manifest as impetigo, characterized by honey-crusted sores, or progress to cellulitis, involving deeper tissue inflammation with symptoms like swelling, redness, and fever.^[21] In severe cases, such as in resource-limited settings, these bacterial superinfections can escalate to systemic complications including abscesses, lymphadenopathy, or even septicaemia, a life-threatening bloodstream infection.^[20] Chronic internal acariasis, including intestinal infestations by acaroid mites like Acarus siro, can result in malnutrition through persistent gastrointestinal disturbances such as diarrhea, abdominal pain, and loss of appetite, leading to weight loss and fatigue over time.^[3] Pulmonary acariasis, involving mite migration to the respiratory tract, may cause respiratory distress, wheezing, dyspnea, and bronchiectasis, potentially predisposing individuals to secondary pneumonia if bacterial colonization occurs.^[3] Similarly, urinary acariasis from mites in the genitourinary tract can lead to renal impairment via associated pyelonephritis or pyelocystitis, presenting with frequent urination, pain, and risk of chronic kidney damage.^[3] Allergic sequelae from acariasis extend beyond local reactions, with mite allergens, such as those from house dust mites or Sarcoptes scabiei, exacerbating asthma in sensitized individuals by triggering airway inflammation, hyperreactivity, and increased risk of acute episodes.^[38] In immunocompromised patients, such as those with HIV, crusted (Norwegian) scabies represents a hyperinfestation state with millions of mites, leading to thick, crusted plaques that foster severe secondary infections and heightened transmission risk.^[20] Scabies-associated streptococcal infections further contribute to post-streptococcal glomerulonephritis, causing acute renal damage in up to 10% of affected children in endemic areas, and rheumatic heart disease through immune-mediated cardiac inflammation.^[21] Rare complications include anaphylaxis, as seen in oral mite anaphylaxis (pancake syndrome) from ingestion of mite-contaminated food, resulting in angioedema, wheezing, and systemic shock.^[3] Zoonotic spread of acariasis, particularly from animal-derived mites, can precipitate community outbreaks, amplifying infection rates in crowded or institutional settings.^[20]

Diagnosis

Diagnostic Methods

Diagnosis of acariasis relies on a combination of clinical evaluation and laboratory confirmation, tailored to whether the infestation is dermatological or internal. Clinical history plays a crucial role, particularly assessing exposure to potential sources such as contaminated food storage, animal contact, or environments with high mite populations like grain silos or bedding. For instance, patients with a history of occupational exposure to organic dust or recent consumption of mite-infested grains may prompt suspicion of internal acariasis.^[14]^[28] Microscopy remains the cornerstone for confirming mite presence across acariasis types. In dermatological cases, such as scabies caused by Sarcoptes scabiei, skin scrapings from burrows or lesions are collected and examined under low-power magnification (e.g., 40x) to identify mites, eggs, or scybala (fecal pellets); techniques like 10% potassium hydroxide digestion or flotation enhance visibility. Dermoscopy provides a non-invasive alternative or complement, revealing characteristic burrows with a "delta-wing" or "jetliner" sign indicative of mites, with specificity around 85-95%.^[39] For internal infestations, stool samples undergo saturated saline flotation to detect adult mites, larvae, eggs, or hypopi, with reported positive rates around 6% in endemic areas for species like Acarus siro and Tyrophagus putrescentiae. Pulmonary acariasis is diagnosed by microscopic examination of sputum for free-living mites, often in individuals exposed to dust, while urinary acariasis involves centrifugation and filtration of urine to isolate mites such as Aleuroglyphus ovatus. Bleach liquefaction may aid in processing sputum or stool for better mite recovery in internal cases.^[14]^[13]^[28] Imaging and endoscopic procedures provide supportive visualization, especially for internal sites. Bronchoscopy can reveal mites in pulmonary acariasis, allowing direct sampling from airways, while colonoscopy in intestinal cases may show pale mucosal walls, ulcers, and live mites or eggs. Cystoscopy similarly aids urinary diagnosis by detecting mites in the tract. These invasive methods are reserved for symptomatic patients where microscopy is inconclusive.^[13]^[28] Serological and allergy tests offer indirect evidence, particularly for dermatological acariasis. Skin prick tests for mite allergens, such as those from storage mites, show positivity rates up to 8-10% in exposed populations and correlate with clinical findings. In advanced settings, polymerase chain reaction (PCR) amplifies mite DNA from skin scrapings, stool, or sputum, enabling species-specific identification (e.g., universal PCR for S. scabiei with high sensitivity); however, it is not routinely used due to technical demands.^[13]^[14]^[40]

Differential Diagnosis

Acariasis, particularly its dermatological form such as scabies, must be differentiated from other pruritic skin conditions that present with similar erythematous rashes and intense itching. Common mimics include eczema, which features dry, scaly patches without linear burrows; psoriasis, characterized by well-demarcated silvery scales rather than excoriations from burrowing mites; pediculosis, involving nits and lice rather than microscopic mites; and allergic contact dermatitis, often linked to specific irritants without identifiable burrows.^[20]^[41] Distinction relies on the presence of characteristic S-shaped burrows in acariasis, absent in these alternatives, alongside confirmatory microscopy revealing Sarcoptes scabiei or related mites.^[41] For internal acariasis, differential diagnosis varies by site of involvement. Intestinal forms, caused by acaroid mites, mimic amoebiasis due to overlapping diarrhea and abdominal pain, helminthiasis such as ascariasis with similar worm-like debris in stool, and inflammatory bowel disease through chronic ulceration and bloody stools; however, mite identification in feces differentiates it.^[42]^[3] Pulmonary acariasis presents with cough and dyspnea, resembling tuberculosis via radiographic infiltrates, asthma through wheezing, or bronchitis with non-specific inflammation, but sputum examination for mites provides key differentiation.^[3] Urinary acariasis, featuring dysuria and hematuria, is often confused with bacterial urinary tract infections or pyelonephritis, resolved by detecting mites in centrifuged urine sediment.^[13] Key differentiators across forms include a history of exposure to infested environments, such as stored grains for internal cases or close contact for dermatological, and definitive microscopy showing acarine structures, unlike flea bites which lack burrows and show only punctate lesions without mite recovery.^[43]^[3] Challenges in diagnosis arise from the rarity of internal acariasis, leading to frequent misattribution to neurosis, allergies, or idiopathic conditions, particularly when symptoms like pruritus or vague abdominal discomfort predominate without initial mite detection.^[42]^[3]

Management

Treatment Approaches

Treatment approaches for acariasis are tailored to the specific type of mite infestation, such as scabies caused by Sarcoptes scabiei or demodicosis due to Demodex species, with the goal of eradicating the parasites while managing symptoms and preventing transmission.^[4] Pharmacological interventions form the cornerstone, often combining topical and systemic agents for optimal efficacy.^[21] Topical permethrin 5% cream is a first-line acaricide for scabies and certain demodex infestations, applied from the neck down to cover the entire body and left on for 8-14 hours before rinsing; a second application may be needed after 7-14 days.^[7] Oral ivermectin, dosed at 200 mcg/kg, serves as an effective alternative for classic scabies (administered in two doses 7-14 days apart) and is preferred for crusted scabies, frequently combined with topical permethrin to enhance clearance rates.^[44] For internal forms such as intestinal acariasis, oral ivermectin (200 mcg/kg, single or repeated doses) has shown efficacy in case reports.^[45] In demodicosis, topical ivermectin 1% cream or metronidazole gel targets skin and ocular involvement, while systemic ivermectin provides broader control in refractory cases.^[46] For pulmonary acariasis, treatments may include organoarsenic compounds like acetarsol or supportive antibiotics for secondary infections, while urinary acariasis can be managed with metronidazole or chloroquine.^[3] Systemic antiparasitics like lindane 1% lotion are occasionally used when first-line options fail, but they carry significant toxicity risks, including neurotoxicity, and are not recommended routinely due to safer alternatives.^[44] Secondary bacterial infections, which frequently complicate scabies through excoriations leading to impetigo, require antibiotics such as topical mupirocin or oral agents like cephalexin to resolve.^[21] Supportive measures address pruritus and inflammation, with oral antihistamines (e.g., hydroxyzine) or topical corticosteroids providing relief from allergic reactions and post-treatment itching that may persist for up to two weeks.^[47] Environmental decontamination is critical, involving hot-water machine washing (at least 50°C) and drying on high heat for all bedding, clothing, and towels used in the three days prior to treatment to eliminate surviving mites.^[7] In veterinary contexts, treatments for animal acariasis like sarcoptic mange parallel human approaches, employing subcutaneous or oral ivermectin (200-400 mcg/kg) or topical selamectin, with therapy continued until two consecutive negative skin scrapings and quarantine to curb zoonotic spread.^[48] Follow-up may include brief preventive measures to avoid reinfestation.^[8]

Prevention Strategies

Prevention of acariasis focuses on interrupting mite transmission pathways through personal hygiene, environmental controls, and targeted interventions tailored to specific mite types such as Sarcoptes scabiei (causing scabies), storage mites (leading to intestinal acariasis), and zoonotic species from birds or rodents.^[8]^[13] Hygiene practices form the cornerstone of individual prevention, particularly for scabies and intestinal forms. For scabies, avoiding direct skin-to-skin contact with infested individuals and not sharing clothing, bedding, or towels significantly reduces transmission risk; items used by affected persons should be washed in hot water (at least 50°C) and dried on high heat or dry-cleaned.^[8] Regular cleaning of living spaces, including vacuuming floors and upholstery, helps eliminate mites and their eggs from household environments.^[8] In the case of intestinal acariasis caused by acaroid mites like Tyrophagus species, proper food storage is essential—using sealed, airtight containers for grains, flour, and dried goods prevents mite contamination from stored products, while thorough washing and cooking of potentially exposed foods minimize ingestion of mites or their allergens.^[13]^[49] Occupational strategies are critical for workers in agriculture, food storage, or pest-prone settings where exposure to storage or zoonotic mites is elevated. Protective gear, such as long-sleeved clothing, gloves, and masks, shields against skin contact and inhalation of mite-laden dust in grain handling or farming activities.^[49] Environmental mite control measures, including periodic fumigation with approved acaricides and maintaining low humidity (below 13% moisture content) in storage facilities, effectively suppress mite populations in warehouses and silos.^[49] For zoonotic mites from birds or rodents, prompt removal of nests or infestations in work areas, combined with structural modifications like sealing entry points, prevents spillover to humans.^[50] Public health initiatives emphasize education, vector control, and screening to curb community-level spread, especially for zoonotic acariasis. Community education programs on recognizing zoonotic risks—such as avoiding contact with wild birds or rodents—and promoting hygiene in high-density settings like shelters or nursing homes reduce scabies outbreaks.^[51] Vector control efforts, including trapping and exclusion of rodents or birds near human habitats, limit infestations by species like Dermanyssus gallinae (poultry red mites) or Ornithonyssus bacoti (rodent mites).^[52]^[53] Screening high-risk groups, such as immunocompromised individuals or those in endemic areas, through routine dermatological checks or stool examinations enables early detection and isolation, preventing wider dissemination.^[51]^[13] No vaccines exist for acariasis, underscoring the reliance on non-pharmacological preventive measures; however, early detection through vigilant symptom monitoring and prompt environmental interventions remains key to averting severe infestations.^[8]^[52]

Epidemiology and History

Epidemiology

Acariasis encompasses a range of mite infestations, with dermatological forms, particularly scabies caused by Sarcoptes scabiei, being the most prevalent globally. An estimated more than 200 million people are affected by scabies at any given time, with more than 400 million incident cases annually, with rates significantly higher in tropical and subtropical regions where environmental conditions favor mite survival.^[21] Internal acariasis, involving acaroid mites in the gastrointestinal or urinary tracts, remains rare worldwide, though localized studies in China have reported intestinal mite detection rates of approximately 6.22% in stool samples from at-risk populations exposed to contaminated stored grains and traditional medicines.^[54] The global distribution of acariasis is uneven, with endemic transmission concentrated in resource-limited areas of Asia, Africa, and parts of Latin America, driven by socioeconomic factors such as poverty, inadequate sanitation, and limited access to clean water.^[21] In these regions, scabies prevalence can exceed 10-20% in vulnerable communities, while internal forms are sporadically reported among those handling mite-infested foodstuffs. Outbreaks are common in high-density institutional settings like prisons, nursing homes, and refugee camps, where close contact facilitates rapid spread; for instance, a global meta-analysis indicates a pooled scabies prevalence of 6.57% (95% CI: 2.16–19.94%) among prisoners.^[55] Key risk factors for acariasis include overcrowding and poor personal hygiene, which enhance person-to-person transmission of scabies, as well as immunosuppression from conditions like HIV/AIDS, which increases susceptibility to severe infestations.^[56] Occupational exposure plays a role, particularly for internal acariasis among farmers, grain handlers, and workers in food storage facilities, where ingestion of mite-contaminated products is a primary route. Zoonotic transmission from animals such as dogs, cats, or livestock is more prominent in rural areas, contributing to sporadic cases of animal-derived scabies in agricultural communities.^[14] As of 2021, global scabies prevalence was estimated at 2.71% (95% CI: 2.41–3.04%), reflecting a decline in age-standardized prevalence rates in low- and middle-income countries due to improved sanitation and public health interventions, though absolute numbers have risen with population growth.^[57] In developed nations, endemic scabies has largely waned through better hygiene and housing standards, but localized outbreaks persist, compounded by emerging resistance to standard treatments like permethrin and ivermectin, which has been documented in multiple regions with failure rates up to 30% in resistant strains.^[58]^[59]

Historical Context

Acariasis, encompassing infestations by various mite species, has been recognized in human history for millennia, with early accounts suggesting skin conditions akin to scabies. Biblical texts, such as those in Leviticus dating to approximately 1200 BCE, describe infectious skin diseases involving itching and isolation protocols, which may refer to scabies-like infestations caused by mites.^[33] In ancient Greece, around 350 BCE, Aristotle documented small "lice of the flesh" emerging from skin pimples when pricked, a description consistent with Sarcoptes scabiei burrows.^[33] The modern understanding of acariasis began in the late 17th century with the identification of the scabies mite. In 1687, Italian physicians Giovan Cosimo Bonomo and Diacinto Cestoni observed mites in skin scrapings and demonstrated their role in causing scabies through experiments on volunteers, marking the first definitive link between a parasite and a human disease.^[33] Internal forms of acariasis were reported starting in the early 20th century, with intestinal cases documented in 1934 involving Tyrophagus longior mites in human feces; pulmonary acariasis in humans was noted in the 1940s, including mites detected in sputum from asthma patients.^[3] Key outbreaks highlighted the public health impact of acariasis during the 20th century. Scabies epidemics surged in crowded wartime conditions, such as World War II trenches, where poor hygiene led to widespread infestations affecting millions of soldiers across Europe and contributing to secondary bacterial infections.^[60] More recently, studies in the 2000s in Asia, particularly China, revealed storage mites like Acarus siro and Tyrophagus putrescentiae as causes of intestinal acariasis, often linked to contaminated traditional medicines and foods, with detection rates up to 6.59% in surveyed populations.^[29] The evolution of acariasis knowledge shifted from folklore remedies, such as sulfur applications described by Roman physician Celsus in 25 CE, to a scientific parasitological framework by the 19th century, aided by microscopy advances.^[61] The discovery of ivermectin in the late 1970s and its widespread adoption in the 1980s revolutionized control, offering an oral treatment effective against scabies mites and reducing global burdens in endemic areas.^[62]

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