The Acari (mites and ticks) represent a large array of organisms that exhibit very diverse lifestyles. This article deals with the acarines that are of importance to human health, a group that includes human parasites, natural parasites of other mammals and birds that in particular situations may bite humans, and acarines whose fecal matter, body secretions, and disintegrating bodies are sources of potent allergens.
The parasitic Acari of vertebrates are physiologically dependent on their host and must obtain nourishment from tissue fluids, blood, and cytoplasm from the host to survive, complete the life cycle, and reproduce. Thus, these are obligate parasites. Some species are temporary parasites (e.g., ticks), which visit and feed on the host intermittently. In contrast, other species of parasitic Acari (e.g., scabies and follicle mites) are permanently associated with the host and perish if they become separated from the host. For some species, only one life stage in the life cycle is a parasite (e.g., chiggers), whereas for other species each life stage must feed from a vertebrate host to complete the life cycle (e.g., scabies mites and ticks).
There is usually an intimate interrelationship between acarine parasites and their hosts. Specific host factors, such as carbon dioxide, body odor, and temperature, allow the parasite to locate a host. For example, scabies mites are attracted to the host by body odor and temperature. Permanent parasites may be directed to specific areas of the host’s body by factors in the skin. The host-parasite interactions for most parasitic acarines have not been well studied and thus are not well understood. This article discusses mites that bite humans, live in the skin of humans, or produce substances that induce immune and/or inflammatory reactions. Because acarine parasites can induce inflammatory and adaptive immune responses, an understanding of the relationship between these two responses is important if one is to understand the symptoms associated with bites from parasitic mites or reactions to body parts, secretions, and fecal matter.
INFLAMMATORY AND IMMUNE RESPONSES
When feeding from the host’s skin surface, acarine parasites inject or secrete into the host an array of immunogenic and phar-macokinetic molecules. Likewise, acarine parasites that live in the skin, hair follicles, sebaceous glands, and respiratory tree and lungs release immunogenic molecules both while living and after death, from their disintegrating bodies. Substances injected or released may induce an inflammatory (i.e., innate) and/or immune (i.e., adaptive) response by the host. Pharmacokinetic molecules can modulate specific aspects of the host’s immune or inflammatory responses.
Innate Immune Response
After a person has been bitten by a parasitic acarine, a red (or ery-thematous), swollen (i.e., edema), and irritated (i.e., painful) lesion may develop at the bite site. These symptoms may be the result of a localized innate inflammatory reaction and not an adaptive immune reaction. In an inflammatory reaction, components of the saliva and body secretions of mites that feed from the skin surface or in tissue (e.g., follicle or scabies mites) cause cells of the skin (epidermis and dermis) such as keratinocytes, fibroblasts, and antigen-presenting cells (Langerhans, macrophages, natural killer cells) to release an array of chemical mediators (cytokines, kinins, and others). These substances cause arterioles to dilate, which results in increased blood flow to the tissue. Increased blood flow to the skin where a mite has bitten or is located imparts a red appearance. In addition, the tight junctions between endothelial cells of the post capillary venule wall become less tight, which allows fluid from the blood to leak from the venule lumen into the surrounding tissue, causing it to swell. These cytokines also cause local endothelial cells in the venule and white blood cells that pass by in the venules to express or increase expression of adhesion molecules (i.e., the receptors) in their surface membranes. White blood cells in the blood vessels stop and adhere to the endothelial cells of the venule. These cells (cellular infiltrate) then migrate out of the venule space between endothelial cells to the source of the molecules that induced the reaction. The infiltrating cells may include neutrophils, eosinophils, macrophages, and lymphocytes. The molecules from damaged or stimulated cells and secreted cytokines from the infiltrating cells stimulate pain receptors in the vicinity, causing an irritative sensation. This type of host response is referred to as innate immunity, and it is not altered with repeated exposure to a particular mite or tick. The time and intensity of the response reaction is the same each time the individual is challenged.
Adaptive Immune Response
In contrast, the molecules introduced into the body by acarine parasites may induce an adaptive immune response that is highly specific for a particular epitope (sequential or structural) on an immuno-genic molecule (antigen) from the parasite. An epitope is the part of the antigen that is recognized by receptors on B and T lymphocytes. The adaptive immune response is stronger and quicker with successive exposures and involves T and B lymphocytes and memory cells of each type. It may also be accompanied by an inflammatory reaction that can be delayed. With the help of type 2 T-helper cells (Th2) B cells become plasma cells that produce antibody directed at the offending molecules from the mite. Activated Th1-type helper cells activate cytotoxic T cells (Tc) that perform functions that kill the parasite directly or damage it. Helper T cells release specific cytokines such as interleukin 2 (IL-2), interferon y (IFN-y), and other interleukins (IL-4, IL-6, IL-10, and IL-13), which act as signals to activate Tc and B cells.
PARASITIC MITES
Family Trombiculidae Chiggers are the parasitic larval stage of prostigmatid mites that belong to the family Trombiculidae (Fig. 1). Chiggers are also known as harvest bugs in Europe and scrub-itch mites in Asia and Australia. Trombiculid mites are prevalent in moist, warm temperate climates and in tropical climates worldwide. These mites live in moist soil covered with vegetation such as grassy and weedy areas. More than 3000 species of chiggers are known, but only about 15 species frequently bite humans and cause a cutaneous reaction.
Unlike many mites, male and female chiggers do not copulate directly. Instead, males deposit a stalked spermatophore (sperm packet) on the substrate. Females insert it into their genital pores to fertilize the eggs, which are then deposited on moist soils. Larvae emerge from the eggs and complete development into an active hexapodal (six-legged) larva (chigger). The larva is parasitic and must
FIGURE 1 Tromicula alfreddugesi, the mite that causes chiggers.
feed from a mammal, bird, reptile, or amphibian host before development can progress to the nymphal stages and the adult. Larvae of some species will feed on humans. The active nymphal stages and adults are free-living predators and prey on small arthropods (insects and mites) or their eggs. The chigger is small (100-300 |im in length) while the nymphs and adults are much larger.
Chiggers can cause dermatitis and transmit the bacteria Orientia tsutsugamushi, which causes scrub typhus in humans. Scrub typhus is characterized by an ulcer at the site of the bite, high fever, and headache. Scrub typhus is present in tropical climates such as parts of India, Pakistan, Southeast Asia, Philippines, Indonesia, Korea, Japan, China, some Pacific Islands, and coastal Queensland, Australia. The principal vectors are species of the chigger genus Leptotrombidium. The chiggers that vector scrub typhus to humans feed mainly on wild rodents (rats and field mice) but these species many also parasitize birds. The primary reservoir hosts for this disease are rodents. In nature, the pathogen is transferred from rodent to rodent by many chigger species. Humans become infected when they venture into an enzootic area and are bitten by an infected larva. The larval stage feeds only once and acquires the pathogen from infected moles, mice, rats, and other small rodents. Therefore, chiggers can only acquire the pathogen or, if they were already infected, transmit it, but not both. The pathogen acquired by the larva is carried (trans-stadially) throughout the developmental stages to the adult. Pathogens acquired by the larva multiply in the subsequent developmental life stages and infect the ovaries of the adult, from which they are passed to the egg (transo-varially) and then to the larvae of the next generation. The pathogens in transovarially infected larvae infect the salivary glands and are transmitted to humans when the larvae feed. Because O. tsutsugamushi is transferred transovarially and trans-stadially in the mite’s life cycle, it may be that the mites themselves are the reservoir for the pathogen.
The chigger does not burrow into the skin but feeds from the surface of the skin much like a tick. Its piercing mouthparts (chelicerae) are inserted through the epidermis into the dermis. Saliva is introduced into the host during feeding. In humans, these salivary components induce both an innate inflammatory reaction and an adaptive immune response. These reactions are characterized by the production of circulating antibody and by cellular infiltration into the feeding lesion. Repeated exposures result in a more rapid and intense adaptive immune response. It is unclear whether chiggers induce an innate inflammatory response independent of the immune response. Clinically, however, the bite manifests as a reddish (erythematous), swollen (edema), and epider-mally thickened papular and irritating lesion. Histologically, the feeding lesion appears as a cylinder of tightly packed cells surrounding a strawlike channel that extends from the dermis to the skin surface where the chigger is located. The chigger sucks fluids from the surface of the channel until it is engorged, and then it drops off the host. Chiggers do not feed on blood; rather, they feed on extracellular fluid from the dermis.
Family Demodicidae
The prostigmatid mites of the family Demodicidae are small (approximately 100 |im in length) and have an elongated, transversely striated wormlike body (opisthosoma). The podosoma bears retractable, short, stumpy, telescoping legs. Two species, Demodex folliculo-rum and D. brevis, parasitize humans and are commonly called follicle mites. Both species are most often obtained from the face, particularly along the nose, forehead, scalp, and eyelids. D. folliculorum lives in the hair follicle alongside the hair shaft and is positioned with its capitulum (mouthparts) down in the follicle. D. brevis resides in the sebaceous gland off the follicle. The entire life cycle is completed in the follicle and sebaceous gland. The mites pierce host cells lining the follicle and sebaceous gland with their needlelike chelicerae and ingest the cell contents. Generally, these mites cause little pathology in humans who practice good facial hygiene and are not immunocompromised. However, they may be associated with acne, blackheads, and acne rosa-cea. A high percentage of humans are infected. They are likely transferred between humans by intimate contact (e.g., mother to infant).
Families Laelaptidae, Dermanyssidae, and Macronyssidae
The Mesostigmata contains many species of mites that are parasitic on reptiles, birds, and mammals. Included are hematophagous (blood-feeding) species in the families Laelaptidae, Dermanyssidae, and Macronyssidae. Among these are Dermanyssus gallinae (chicken mite), Ornithonyssus bacoti (tropical rat mite), O. bursa (tropical fowl mite), O. sylviarum (northern fowl mite), Echinolaelaps echidninus (spiny rat mite), Liponyssus sanguineus, Haemogamasus pontiger, and Eulaelaps stabularis. These species are attracted to warm objects and usually live on their host or in the nest of their host. Some of these species will attack humans if their normal hosts are not available. This situation may result after roosts and nests of birds (e.g., pigeons, sparrows, starlings) and nests of rodents (mice, rats, squirrels) in homes (attics, behind shutters, etc.) are destroyed. In the absence of a natural host, the mites invade homes and attack humans. Also, species that infest poultry (O. sylviarum, O. bursa, and O. gallinae) can be a problem for workers who handle infested chickens and turkeys. Bites of these mes-ostigmatid mites can cause an irritating inflammatory reaction. There may also be an allergic reaction in some individuals, but this remains to be confirmed. Siponyssoides sanguineus parasitizes house mice and rats and can transmit Rickettsia abari, which causes rickettsial pox in humans. Western equine encephalitis and St. Louis encephalitis viruses have been isolated from D. gallinae, but there are no documented cases of transmission of these viruses to humans.
Species in the families Rhinonyssidae, Entonyssidae, and Halarachnidae live in the nasal cavity and lungs of birds and some mammals (e.g., dogs, monkeys, seals, and baboons). Human infections by these mites have not been reported.
Family Sarcoptidae
The astigmatid mites, Sarcoptes scabiei, are permanent obligate parasites that live in the stratum corneum of the skin of at least 17 families of mammals. These mites cause a disease known as scabies. Scabies is a common contagious disease of humans. There is little morphological difference between the strains of S. scabiei that parasitize different host mammals, and at this time, the strains from different host species are not considered to be different species by most experts. However, the strains from different host species are host specific and generally cannot permanently infest an unnatural host. For example, the strain from dogs causes only temporary self-limiting infestations in humans, cats, pigs, cattle, goats, and mice, yet scabies naturally occurs on these host species. The host factors and physiological differences between mite strains that do not allow one strain to establish an infestation on strange hosts are not known.
Scabies mites are small. The males and females are 213-285 |im and 300-504 |im in length, respectively. The life cycle, consisting of egg, larva, protonymph, tritonymph, and adult males and females, is completed in about 10-13 days on the host. All active stages are oval, with a characteristic tortoiselike body with stout dorsal setae, cuticu-lar spines, and cuticular striations.
When separated from the host at room temperature, scabies mites must infest a new host within 24-36h to survive. Under cool (4°C or 10°C) and humid conditions, females of the strain that infests humans (var. hominus) remain infective for at least 4 days. Therefore, fomites (i.e., clothing, bedding, and furniture that harbor dislodged mites) can be important sources of infection for humans. Body odor and temperature attract these mites to a host. Once on the host’s skin, females begin to burrow into the skin within minutes, and they can be completely submerged within the stratum corneum within a half hour. Males, nymphs, and larval stages penetrate more quickly than females.
Scabies is common in nursing homes, day care centers, and among the general population in the United States. It often mimics other skin diseases and is difficult to diagnose. Scabies is prevalent in some populations in Africa, Central America, South America, Egypt, India, and Australia. Human scabies infestations are manifested in the vicinity of the burrowing mite by itching, red, papular and vesicular lesions. These symptoms generally develop in 6-8 weeks after a primary (first) infestation, but they are evident within a few days of a subsequent infestation. Lesions most commonly occur on the interdigits, elbows, and chest (breast area) skin. However, other areas that may be infested are the penis, buttocks, knees, soles and insteps of the feet, wrists, waistline, and axillae. Clinical scabies mimics many other diseases and can be misdiagnosed. A positive diagnosis is made by recovering mites, eggs, mite fecal material, and mite burrows in skin scrapes.
Scabies mites induce both cell-mediated (Th1) and circulating antibody (Th2) immune responses and an associated inflammatory reaction. The cell-mediated/inflammatory response is characterized by a mixed cellular infiltrate in the skin lesion that consists of plasma cells, lymphocytes, mast cells, neutrophils, Langerhans cells, and eosinophils.
An infestation with scabies induces some immune resistance to subsequent infestations. The balance between the Th1 and Th2 responses appears to be a key aspect in protective immunity. Hosts that develop protective immunity exhibit up-regulated Th1 and weaker Th2 responses. In contrast, hosts that do not develop protective immunity exhibit strongly up-regulated Th2 response (circulating antibody) but a weaker Th1-cell-mediated response. Infected hosts produce serum antibodies to at least 12 antigens from sarcoptic mites. Some of these antigens are cross-reactive with antigens from the related house dust mites, Dermatophagoides farinae, D. pteronyssinus, and Euroglyphus maynei. In some humans, antigens from S. scabiei can also induce an IgE-mediated allergic reaction and circulating IgE-type antibody.
Family Pyemotidae
Pyemotid mites are prostigmatids that have an elongate cigar-shaped body with the first two pair of legs widely spaced from the posterior two pair of legs. They have needlelike chelicerae and are usually parasitic on the larvae of some moths, beetles, bees and other insects. Unlike other mites, pyemotid female mites retain internally the eggs from which the larvae hatch and pass through all developmental stages while still inside the female. As a result, the female’s opisthosoma (region behind the last pair of legs) becomes enormously swollen before the offspring are born. Males are born first and then they copulate with females as they emerge.
Pyemotes tritici (straw itch mite or grain itch mite) are parasitic on the larvae of grain moths, boring and stored grain beetle larvae, and other insects. The saliva contains toxins that paralyze their prey larva while the mite feeds. Humans may contact these itch mites when working with grain and hay. Also, hordes of these mites may emerge from the flowers of cattails that are brought into a home to make floral arrangements. These mites will attack humans, and while they attempt to feed, the saliva that is injected into the skin causes a red, itchy inflammatory dermatitis.
NONPARASITIC MITES
Family Pyroglyphidae
The family Pyroglyphidae contains mainly species of astigmatid mites that live in the nests of birds and mammals, where they feed on the epidermal detritus (skin, feathers) left by the host. Three species, Dermatophagoides farinae, D. pteronyssinus, and Euroglyphus may-nei, are commonly found in homes of humans. In homes, these mites are most prevalent in high-use areas, where shed skin scales collect and serve as their food. Therefore, the greatest densities are found in carpets around sofas and easy chairs, in fabric-covered overstuffed furniture, and in mattresses. However, they may also be found in bedding, on pillows, on clothing, on automobile and train seats, and sometimes in schools and in the workplace. Each species is the source of multiple potent allergens that sensitize and trigger allergic reactions in predisposed people. These allergens cause perennial rhinitis, asthma, and atopic dermatitis.
Ambient relative humidity is the key factor that determines the prevalence and geographical distribution of these mites. This is because water vapor in humid air is the main source of water for their survival. They survive and thrive well at relative humidities above 50% but desiccate and die at relative humidities below this. Therefore, dust mites and the allergies they cause are a significant problem only for people who live in humid, tropical, and temperate geographical areas. D. farinae and/or D. pteronyssinus are prevalent in homes in the United States, Europe, South America, and Asia. Most homes are coinhabited by multiple species. However, the most prevalent species varies both between homes in a geographical area and between geographical areas. For example, in the United States, both D. farinae and D. pteronyssinus are prevalent in homes but D. farinae is more prevalent in homes in northern humid climates than D. pteronyssinus. However, in South America, D. pteronyssinus is prevalent in homes, whereas D. farinae is not.
In temperate climates, population densities of D. farinae and D. pteronyssinus exhibit pronounced seasonal fluctuations that parallel the seasonal fluctuations in indoor relative humidity. High densities occur during the humid summer months and low densities during winter when relative humidity is low in homes.
The life stages of the dust mites are egg, larva, protonymph, tri-tonymph, and adult male and female. The length of the life cycle is temperature dependent when relative humidity is above 60%. At 23°C the life cycle takes 34 and 36 days to complete for D. farinae and D. pteronyssinus, respectively. Females produce 2 or 3 eggs daily during the reproductive period at 23°C. D. pteronyssinus takes 23 and 15 days to complete development at 16°C and 35°C, respectively. D. farinae does not develop well at 16°C and 35°C.
A desiccant-resistant quiescent protonymphal stage can develop that allows survival during long periods (months) under dry (low relative humidity) conditions. When relative humidity conditions become optimal, the quiescence is broken and development continues.
Allergens from these mites are associated with fecal material (e.g., enzymes), body secretions (e.g., chitinase), and body anatomy (e.g., muscle tropomyosin). Twenty different groups of mite allergens have been characterized. The frequency of reactivity to most of these allergens is above 50% among patients sensitive to dust mites. The prevalence of sensitivity to house dust mites is about 27.5% in the U.S. population. Sensitivity to allergens varies both within and between individuals. Allergens from one species may be species specific, or they may cross-react with allergens from another mite species. Most patients with mite sensitivities are allergic to multiple allergens of a species and to multiple mite species.
Families Acaridae, Glycyphagidae, Carpoglyphidae, Echimyopididae, and Chortoglyphidae
Many species of the astigmatid families Acaridae, Glycyphagidae, Carpoglyphidae, Echimyopididae, and Chortoglyphidae are medically important because they are the sources of potent allergens. Many species of these mites are often referred to as ” storage mites ” because they occur in stored hay, grain, and straw, in processed foods made from grain (flour, baking mixes), and in dust in grain and hay at storage, transfer, and livestock feeding facilities. Also, stored product mites may occur in homes in significant numbers. Thus, humans may be exposed to storage mites and their allergens, occupationally and in the home. Inhalation or contact on the skin or mucus membranes of the eyes with allergens from storage mites can induce allergic reactions. These mites and their allergens can also occur in bread, pancakes, cakes, pizza, pasta, and bread made from ingredients contaminated with mites. Humans have had anaphylactic reactions after eating these mite-contaminated foods.
Species known to be the sources of allergens include Blomia tropi-calis (Echimyopididae); Acarus siro, Tyrophagus putrescentiae, T. lon-gior, and Aleuroglyphus ovatus (Acaridae); Lepidoglyphus destructor and Glycyphagus domesticus (Glycyphagidae); Carpoglyphus spp. (Carpoglyphidae); Chortoglyphus arcuatus (Chortoglyphidae); and Suidasia medanensis (Suidasiidae). Sensitivity to T. putrescentiae is at least 6.5% in southwest Ohio. B. tropicalis is common in house dust in tropical climates and may be more prevalent than pyroglyphid mites and is a significant cause of sensitivity. This species has been reported to occur in small numbers in some homes in the southern subtropical United States. Sensitivity to storage mites may be 6-22% in urban and rural populations in Europe. There is little cross-reactivity between storage mites and house dust mites. However, many patients are sensitive to both storage mites and the pyroglyphid house dust mites.
Families Tetranychidae and Eriophyidae
Many species of prostigmatid mites such as those in the families Eriophyidae and Tetranychidae parasitize plants and can become an economic problem on food crops (e.g., fruit trees; vegetable and grain crops) and yard/garden and green houseplants. Humans come into contact with these mites when working in fields, orchards, greenhouses, gardens, and yards, when handling infested food crops/produce, or by living near an area in which food crops are grown. The importance to human health of most of these pest species has yet to be determined. However, it is clearly documented that a few species are the source of allergens that induce allergic reactions in predisposed individuals. Farmers working in greenhouses, grape vineyards, and in apple orchards and children living around citrus orchards have become sensitized and/or had allergic reactions to Tetranychus urticae (two-spotted spider mite) and Panonychus ulmi (European red mite), and P. citrilis (citrus red mite).
Family Phytoseiidae
Humans come into contact with predaceous mites that are used for biological control of pest species such as the tetranychids just mentioned. The predaceous mite Phytoseiulus persimilis, which feeds on spider mites, can cause allergic reactions.
Family Hemisarcoptidae
Hemisarcoptes cooremani is an astigmatid mite that is a predator of scale insects that parasitize woody plants. The body of this mite is the source of at least two allergenic proteins. Close contact with these mites can result in production of serum IgE and allergic symptoms. Therefore, gardeners and nursery workers may become sensitized to this mite and have allergic reactions.
