Knemidocoptiasis in birds
This article reviews the recent literature, common clinical presentations, and current recommendations on diagnosing and treating knemidocoptiasis.
Many types of mites can inhabit birds' feathers, quills, skin, subcutaneous tissue, and respiratory tracts.1,2 Mites of the genus Knemidocoptes, which parasitize only birds, are burrowing mites that cause disfiguring dermatitis and thickening of the skin. If the mites are not identified and eliminated, the damage can be severe.
Knemidocoptes2,3 (also known as Knemidokoptes and Cnemidocoptes) is a genus in the class Arachnida, subclass Acari, order Sarcoptiformes, suborder Astigmata, family Epidermoptidae, and subfamily Knemidokoptinae.3 Taxonomically, knemidocoptic dermatitis in birds can be compared to sarcoptic dermatitis (mange) in mammals, but most birds lack the classic intense pruritus seen in animals with scabies.
Knemidocoptes species mites have been reported mainly in galliform (e.g. chickens, turkeys), passerine (e.g. finches, canaries, sparrows, robins, wrens), and psittacine birds (e.g. parrots, macaws, parakeets, budgerigars), but they also occur in piciform (e.g. woodpeckers, toucans) and anseriform (e.g. ducks, geese, swans) birds, raptors, and others. The prevalence of subclinical infections is largely undocumented in domestic and free-ranging birds. More common in a wide range of captive bird species, clinical infestation is rarely identified in wild birds. Knemidocoptiasis is fairly common in small pet birds; bird fanciers also call it scaly face and scaly leg or tassel foot. The condition was once thought to be caused by a fungal infection.
Other than knemidocoptic dermatitis in budgerigars, ectoparasitism is rare among psittacines. The earliest reports date back to the 1950s, but over the last 15 years, many more species of birds have been found to be affected, and several new Knemidocoptes species have been identified.4 This article reviews the recent literature, common clinical presentations, and current recommendations on diagnosing and treating knemidocoptiasis.
LIFE CYCLE AND TRANSMISSION
Knemidocoptes species mites spend their entire three-week life cycle on their bird hosts. The females are viviparous. The larvae have three pairs of legs (Figure 1). After two nymphal stages, the mites mature into adults that have four pairs of legs.5 The mites burrow into the feather follicles and stratum corneum, primarily on the face, feet, and cere, where they feed on keratin. Most commonly, the unfeathered regions (beak, eyelids, legs, vent) are affected. As the mites burrow, they form tunnels.
The mites are transmitted from bird to bird through prolonged close or direct contact. Although the mites are primarily transmitted from parent to unfeathered nestlings, knemidocoptiasis appears to be more opportunistic than infectious. As with Demodex species infections in dogs, not all nestlings will become clinically affected. Genetic susceptibility, stressors, or a compromised immune system likely result in clinical manifestation. Unlike many parasitic infections in birds, clinical infestation with Knemidocoptes species occurs more frequently in older birds.
Indirect forms of transmission, such as face rubbing on perches and contact with contaminated seed, are possible but less common. It is unknown whether interspecies transmission occurs, but infestation probably does not cross orders of birds.
KNEMIDOCOPTES SPECIES AND AFFECTED BIRDS
There are currently six genera in the subfamily Knemidokoptinae: Knemidocoptes, Neocnemidocoptes, Procnemidocoptes, Evansacarus, Picicnemidocoptes, and Micnemidocoptes.3 Clinically, the most common species are Knemidocoptes pilae, Knemidocoptes jamaicensis, and Knemidocoptes mutans. Knemidocoptes intermedius and others are less common (Table 1).6
Table 1 Knemidocoptes Species Common Names and Affected Birds
Scaly leg and face mites
Three species are known to infect both the legs and faces in birds: K. pilae, K. mutans, and Procnemidocoptes janssensi.
Knemidocoptes pilae predominantly parasitizes psittacine birds, and many of these birds are Pacific distribution species. Most reports involve budgerigars (Melopsittacus undulatus), but K. pilae has also been found in Alexandrine parakeets, ring-necked parakeets (Psittacula species), scarlet-chested parrots (Neophema splendida), Princess parrots (Polytelis alexandrae), yellow-fronted Kakariki (Cyanoramphus auriceps), cockatiels (Nymphicus hollandicus), and cockatoos, especially palm (Probosciger species) and sulphur-crested (Cacatua species).4,7 Knemidocoptes pilae has also been seen in several South American birds, such as green-winged macaws (Ara chloroptera) and Amazon parrots (Amazona species).8 Knemidocoptes pilae is smaller than K. mutans, has a heavier chitinous dorsal shield with distinct edges, and is covered by minute punctiform dots.
Knemidocoptes mutans is common in domestic fowl and has been confused with K. pilae.9 Chickens, turkeys, pheasants, and other gallinaceous birds are commonly affected, as are several raptor species. Knemidocoptes mutans can range in size from 350 to 450 μm x 280 to 380 μm in females and 200 to 240 μm x 145 to 160 μm in males. Typically, adult females are 0.5 mm in diameter.9,10 Knemidocoptes mutans has a strongly striated epidermis; dorsal striations are not interrupted. The shield edges are indistinct, and the anterior shield is devoid of the minute punctiform dots seen in K. pilae.
Procnemidocoptes janssensi has been found in lovebirds (Agapornis species).11
Scaly leg mites
Two species most commonly infect the legs in birds: K. jamaicensis and K. intermedius.
Knemidocoptes jamaicensis is the scaly leg mite in passerines, primarily in canaries (Serinus canaria), Gouldian finches (Chloebia gouldiae), and mynahs. Knemidocoptes jamaicensis has also been reported in blackbirds, grackles, crows, catbirds, woodpeckers, towhees, and several other species in the United States and Canada.4 In the 1990s, several episodes of unusual morbidity with mortality were discovered in migratory American robins (Turdus migratorius) from Oklahoma, Florida, and Georgia. As much as 60% to 80% of the population was affected.12 Similar epizootics have occurred in the United States in evening grosbeaks (Coccothraustes vespertinus) and in Europe in migrating chaffinches (Fringilla coelebs).12
Knemidocoptes intermedius has been identified as the cause of skin lesions around tibiotarsal joints in several wild passerine species from Australia and the United Kingdom.13-15
Three mite species are known to infect primarily the feathers in birds: Knemidocoptes gallinae, Knemidocoptes laevis, and Neocnemidocoptes gallinae.
Knemidocoptes gallinae is smaller than K. mutans (the adult female averages 0.3 mm in diameter) and burrows into the basal shafts and feathers on the epidermis of chickens, pigeons, and pheasants. It appears to be more prevalent in the spring and summer. Knemidocoptes gallinae has interrupted dorsal striations, forming raised sculpturing.9
Knemidocoptes laevis is a depluming mite in pigeons, and N. gallinae affects pheasants, chickens, pigeons, and geese.9
In budgerigars, canaries, and other small birds, the mites cause scaly, crusty, gray to tan lesions on unfeathered skin, especially the legs, feet, and around the beak, eyelids, and periocular areas. Mites directly penetrate feather follicles, skin folds, and the epidermis, causing pouchlike cavities and producing secondary pouches, resulting in a honeycombed lesion. Usually, the birds are not noticeably pruritic. In severe cases, the beak, feet, and toes may become malformed. The mites also affect passerines, poultry, and raptors.
Knemidocoptiasis was first described in budgerigars by Lavoipierre and Griffiths in 1951. Male and female budgerigars of all ages may be affected, but the disease is most common in fledglings and young adults.4 Some affected birds do not have obvious lesions. An affected bird may develop lesions after appearing normal for many months, and disease progression is relatively slow.
Figures 2A & 2B
Lesions usually start at the commissures of the beak and have a honeycomb appearance. In the early stages, lesions are confined to the cere and the base of the beak (Figures 2A & 2B). Make sure to rule out brown hypertrophy of the cere in female birds. Brown hypertrophy typically has crusty layers, similar to the shell of an oyster, without the honeycomb tunnels that are distinctive of K. pilae mites. An important and unusual differential diagnosis is carcinoma of the cere and beak.
As the disease progresses in budgerigars, whitish, scaly, epithelial proliferations develop, forming raised, thickened, yellowish, craterlike encrustations that sometimes cause nasal obstruction. Mites burrowing into the germinal layer of the beak can ultimately cause distorted growth, especially in the upper mandible.
Lesions similar to those described above may also occur on the legs, feet, and skin of other parts of the body (especially around the eyes and vent). In chronic cases affecting the face, horny protuberances may develop. Severe pruritus is seldom observed.
Budgerigars with leg bands may develop necrosis of the limb distal to the band as the lesions grow and press into the band, constricting the leg's blood vessels. Podoacariasis (or more specifically podoknemidocoptiasis) is more common in canaries,4 in which the legs and feet exhibit yellow-white, tassel-like projections. Serous exudate is produced in response to the tunneling mites, which hardens and lifts the scales on the feet and legs, causing reduced flexibility. When the feet are involved, lameness may be seen in advanced cases because of ankylosis of the hock and other joints, necrosis and sloughing of toes, swollen nail beds, and twisted nails.
Because disease can be seen in inbred birds, a genetic predisposition or selective immunosuppression has been suggested but not proved.
In Alexandrine parakeets (Psittacula eupatria), the mites may cause itching and feather loss, but no scaly lesions.4 Knemidocoptes pilae has been associated with feather picking and feather loss around the neck, keel and ventral abdomen, and dorsum.4 Postinfection feather loss and eyelid damage may result. Early or mild lesions caused by Knemidocoptes species may resemble lesions caused by vitamin A deficiency; however, chronic or advanced knemidocoptiasis lesions are much larger and more extensive than those associated with vitamin A deficiency.
Occasionally, in other parrot species, knemidocoptiasis is associated with concurrent psittacine circovirus infection or other immunosuppressive diseases (mycobacteriosis). In macaws with knemidocoptiasis, pruritus of the hocks and feet occurs and may lead to self-mutilation.8
An unclassified Knemidocoptes species (not K. pilae or Neoknemidocoptes laevis) has been found in the feathers of red-fronted parakeets (Cyanoramphus novaezelandiae).16 Birds exhibit generalized patchy feather loss with hyperemic skin on the head, neck, and cheeks. Mites are found embedded in the thickened calamus portion of the shaft of affected feathers. Mites have been identified in adult and immature birds, but only the adults develop clinical signs.16
Canaries and finches
The earliest reports of knemidocoptiasis in canaries and finches attributed infection to K. mutans, while later reports described disease due to K. pilae.4,8 Recent investigations have identified K. jamaicensis in these birds and, thus, may actually represent taxonomic reclassification.12
Figures 3A & 3B
In canaries, lesions are usually confined to the legs and digits and begin as crusts that form on the plantar surfaces of the feet and gradually thicken. Marked lameness results, and perching becomes difficult. Birds with leg bands are in danger of serious tarsometatarsal constriction. Knemidocoptes jamaicensis is also seen in wild finches and sparrows.12
Differential diagnoses include infestation with other mite species, dermatophytosis, and poxvirus or papillomavirus infection, with the latter probably being the most common. Proliferation of scales on the feet seen in aging passerine birds is distinctly different from the dramatic tassel foot changes seen with knemidocoptiasis (Figures 3A-4C). Keep in mind that tassel foot in European goldfinches (Carduelis carduelis) is primarily due to a papillomavirus,17 but Knemidocoptes species infestation is an important differential diagnosis. Dual infection can occur.
A retrospective examination of banding records in Hong Kong showed infestation in Eurasian tree sparrows (Passer montanus), black-faced buntings (Emberiza spodocephala), spotted doves (Streptopelia chinensis), and Eastern great reed warblers (Acrocephalus species). Adult tree sparrows were affected more often than juveniles were, and males were affected more commonly than females were. Lesions on juveniles usually involved the feet, while lesions on adults were found on the legs and beak.18 Robins may lose all or part of their feet and digits.12 Most of the advanced, chronic lesions are pathognomonic, but early, acute lesions resemble or are indistinguishable from the wartlike proliferative skin lesions of avian poxvirus.
Knemidocoptes mutans primarily affects the unfeathered skin of the legs in chickens and, occasionally, the comb and wattles. Disease is more common in older birds; affected chickens exhibit severe weight loss and decreased egg production.4,19 Knemidocoptes mutans has also recently been found to cause digit necrosis.10 Birds with knemidocoptiasis from K. mutans are predisposed to secondary bacterial and fungal pyoderma. Compared with chickens, Knemidocoptes species infestation in turkeys is relatively rare.20
Figures 5A & 5B
Knemidocoptes gallinae causes intense irritation, resulting in affected birds pulling out their body feathers. Weight loss and reduced egg production are reported.4
Knemidocoptes mutans was first identified in great horned owls (Bubo virginianus) exhibiting bilateral proliferative papillary hyperkeratosis of the feet.21 Examples of the lesions and mites are seen in Figures 5A-6B. Knemidocoptes mutans has subsequently been found in snowy owls (Nyctea scandiaca) and several accipiters such as goshawks and sparrowhawks. A Swainson's hawk (Buteo swainsoni) had severe crusting of the skin on the medial thigh and ventral body.22 This case was unusual in that the Knemidocoptes species infestation appeared to be localized to the feathered regions of the body. The stress of captivity may induce disease in affected individuals.
Figures 6A & 6B
Scaly face in the budgerigar is considered pathognomonic for knemidocoptiasis. A diagnosis is usually easily confirmed by identifying the mites on a skin scraping under the microscope. With a small scalpel or a spatula, carefully obtain a small sample of keratinized debris, scales, and crusts from the affected area. Then place the sample onto a slide premoistened with a drop of mineral oil. For birds with thickened leg scales, gently remove a loose leg scale, and examine the underside with a magnifying lens. Interfering with the base of any large crusts on passerines can result in hemorrhage and should be performed carefully. Occasionally, you can directly see adult mites in honeycomb tunnels with a high-quality operating microscope.
The mites are recognized by their globoid shape and stubby legs that barely extend beyond the body's lateral margins.23 Knemidocoptes species mites are sexually dimorphous. Adult females are large and round (up to 0.5 mm in diameter), with short legs and no stalks on the ends of the legs. The smaller male has long, unjointed stalks with pretarsi (resembling those of Sarcoptes species) on each leg (Figures 1 & 6A). Larvae have stalked pretarsi, and nymphs lack stalks. Compared with Sarcoptes and Notoedres species, Knemidocoptes species lack scales and spines on the dorsal surface. Their tarsal segments have clawlike structures and tactile hairs instead of pediculated suckers. Look for larvae, nymphs, and adult mites; female mites are found more commonly than males. Also, mite feces and shed nymphal skins may be seen in heavy infestations.
Occasionally, biopsy or tissue samples obtained at necropsy and submitted for histologic examination will yield more mites. Mites cause papillomatous proliferation of the epidermis (acanthosis) and cystic degeneration of the feather follicles. Both orthokeratotic and parakeratotic hyperkeratosis are seen and contribute to superficial keratin sloughing. Mites are seen within all layers of the stratum corneum in heavy infestations, as demonstrated in the histologic sections in Figures 4A-4C.10,19,24
Rarely, mites will not be identified on cytologic or histologic examination in birds with classic lesions. In those cases, a positive response to treatment confirms the diagnosis.
TREATMENT AND PREVENTION
Isolate and treat all birds with lesions and any birds that have had direct contact with symptomatic birds.
Ivermectin is the drug of choice and may be given orally, topically, or by injection.25-27 Topical or oral dosing is recommended for small birds. Ivermectin may be toxic if given intramuscularly, especially in small birds, and death may occur.28 Two large-animal injectable propylene-glycol–based formulations of ivermectin (Ivomec—Merial) are available for extralabel use in birds in 1% (10 mg/ml) and 0.27% (2.7 mg/ml) concentrations.
Table 2 Diluting Ivermectin for Topical or Oral Use in Birds
For small and tiny birds, ivermectin can be diluted for safer oral or topical dosing. Many anecdotal dilutions are used; a 1:4 dilution is often recommended. See Table 2 for two easy-to-prepare ivermectin dilution formulas for oral or topical administration. Dilute the bovine preparation (which contains propylene glycol) with propylene glycol because the ivermectin will precipitate if mixed with water. Thoroughly mix the solution before administration because ivermectin settles out in propylene glycol. When given orally, propylene glycol has been associated with tracheal necrosis in some birds, and certain species are sensitive to propylene glycol, such as keel-billed toucans (Ramphastos sulfuratus).29
The suggested ivermectin dosing regimen is 200 to 400 μg/kg given orally or topically for two to three treatments at 10-day intervals.25-27 For most species, give 200 μg/kg, and repeat in 10 to 14 days. Canaries usually require a longer treatment period than budgerigars do; three to six treatments are often needed before resolution is achieved. Because topical ivermectin administration at 0.4 mg/kg was found to be toxic in finches, use the 0.2 mg/kg dose for passerines and other sensitive individuals.28
If diluted ivermectin is not available, moisten the feathers on the neck with water or an alcohol-soaked cotton ball, and apply one drop (0.01 ml) from an insulin syringe to the skin over the jugular furrow. Alternatively, apply a light coating of 0.1% ivermectin topically on the affected areas of skin (e.g. cere, feet) for three consecutive days, and repeat in one week.
Although autoclaving diluted ivermectin to obtain a sterile form for injection has been discussed by some practitioners, it is not recommended. The melting point of ivermectin (311 F [155 C]) is too close to typical autoclave temperatures (average 250 F [121 C]) to ensure drug stability, according to the manufacturer. In addition, the flash point of propylene glycol is 210 F (99 C), which may make it combustible in an autoclave.30
A water-soluble, 10-mg/ml liquid ivermectin (Eqvalan—Merial) available for horses has been used safely when given orally.27 However, when this product was given intramuscularly, it resulted in the death of finches and budgerigars.27
Pour-on or injectable moxidectin (Cydectin—Fort Dodge Animal Health) is also effective and available in 0.5% and 1% preparations, respectively. In one study, one or two topical treatments at 10-day intervals on the neck skin in budgerigars with 0.1 ml of the 10-mg/ml injectable was effective and showed no adverse effects in 30 birds.31 Pruritus disappeared within 10 days after the first treatment, while complete resolution of lesions took about 30 to 40 days, depending on lesion severity.31 In another study, two drops of a 1:20 dilution of 1% moxidectin applied topically to the neck once and then repeated 23 days later was effective in treating red-fronted parakeets.16 Spot-on 1,000 μg/ml moxidectin (Scatt—Vetafarm; 1 drop/30 g every 21 days for two or three treatments) has also been used with success and is popular among breeders and hobbyists.
Avoid using older topical parasiticides, such as rotenone-orthophenylphenol (e.g. Goodwinol ointment), crotamiton (Eurax cream), and lindane, which may be more toxic than efficacious. In the past, applying mineral oil to the lesions has been effective, but it is messy and can result in side effects, including oily feathers and aspiration of the mineral oil. Cage mite protectors have no efficacy against Knemidocoptes species. Although selamectin (Revolution—Pfizer) is effective for treating ear mites (Otodectes species) and sarcoptic mange in mammalian species, it has not been evaluated in birds and is not recommended for use in avian species at this time.
Adjunctive therapy includes softening crusts with water-soluble, nontoxic emollients, such as aloe vera gel, being careful not to plug the nares. If the nares are occluded with crusts, carefully remove them to restore normal airflow. Sparing use of topical antibiotic ophthalmic ointments in and around the eyes may be needed in severe cases, but avoid contact with the feathers. Birds with open sores may benefit from concurrent administration of systemic antibiotics and nonsteroidal anti-inflammatory drugs (0.1 to 0.5 mg/kg meloxicam orally b.i.d.) as well as perch adjustments that make perching more comfortable for birds with foot and leg lesions. If indicated, the bird's diet should be improved and supplemental vitamin A may be beneficial.32
Breeding should be discontinued until the infestation is eliminated, and some individuals may need to be culled. Disinfect cages, roosts, and perches to prevent spread to other birds. If possible, perform a full medical work-up for underlying conditions because Knemidocoptes species infection is often secondary to other immunosuppressive disease processes.
The following experts have been consulted for manuscript review and scientific accuracy:
Pathology: Shelley J. Newman, DVM, DVSc, DACVP, Department of Pathology, University of Tennessee, Knoxville, Tenn. Mite biology and taxonomy: Heather Proctor, BSc, MSc, PhD, and Wayne Knee, BSc, MSc candidate, Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.
Laura Wade, DVM, DABVP (avian practice)
Broadway Veterinary Clinic
Lancaster, NY 14086
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