13.1.1 Avipoxvirus

Avian pox is an infectious disease of domestic and wild birds, caused by the genus Avipoxvirus from the family Poxviridae. Avipoxviruses are large (250 × 350 nm), enveloped, oval‐shaped viruses that contain linear, double‐stranded DNA [1]. Avipoxvirus (APV) has been detected in 374 avian species in 23 orders, including pheasants [2, 3], partridges [4–6], quail [7–9], guineafowl [10], and peafowl [1].

Infected birds are the main reservoir for avipoxviruses. The most frequent route of infection is via biting insects – midges and mosquitoes – but pecking trauma to skin, objects contaminated with viable poxviruses, and inhalation or ingestion of dust, infected skin scabs and aerosols are other possible routes [11]. Mosquito‐borne infections are considered to be the most common route of transmission [12]. In some instances, cutaneous or diphtheritic pox lesions can develop as a result of viremia rather than direct inoculation [13]. APV infections can be introduced to captive populations from wild birds, newly introduced captive birds, fomites or arthropod vectors. Infected carrier birds with no clinical signs have been shown to spread APV infection in aviaries after a 10‐day quarantine [14]. Outbreaks of poxvirus are more commonly observed in warm, humid seasons (summer, fall) when the vector population is at the highest point [11]. Reported mortality in gamebirds affected by avipoxvirus is usually low [5]; however, mortality can vary depending on age, host, and strain of avipoxvirus [12]. In most reports of poxvirus in gamebirds, the infected birds are usually juveniles that have not developed full innate immunity or were not previously immunized from a virus exposure during the previous season [11, 14].

The duration of infection in individual birds is poorly understood. It may vary according to virus strain and host. For example, poxvirus isolates from bobwhite quail were shown to cause temporary skin lesions when inoculated into the skin of chicks and poults, but were nonpathogenic for coturnix quail [12].

The varying susceptibility of birds to avipoxviruses depends on the presence of host‐adapted strains and differences in virulence of the avipoxviruses [15]. Mosquito‐borne transmission is the most important route of infection [12]. Avian pox can occur in two forms: the cutaneous (dry) form and the diphtheritic (wet) form. Both forms of the disease can occur in the same birds [16]. The cutaneous form is caused by virus entry into breaks in the nonfeathered skin over the cere, eyelids, head, legs, and feet. These lesions are usually self‐limiting unless the extent of skin lesions is overwhelming and interfere with sight or prehension of feed. Eyelids can be sealed by the accumulation of dried exudate and secondary bacterial conjunctivitis [7]. The diphtheritic form develops on the mucous membrane of the oral cavity, nasal passage, and upper respiratory tract. The wet lesions are usually more severe than the cutaneous forms and can interfere with respiration as well as swallowing.

At a minimum, affected birds can be expected to show reduced activity and weight loss [17], but signs can be more severe if lesions are extensive. Pox infections can cause high mortality with both dry and wet forms in captive quail [9]. Brower et al. described severe beak necrosis and deformation in Hungarian partridges caused by avipoxvirus and likely exacerbated by the placement of beak bits [6]. In one report, peafowl chicks incurred high mortality from large scabs developing on the eyelids, nostrils, beak, and legs [18] which is typical for avipoxviral disease (Figure 13.1). Additionally, a poxvirus closely related to fowlpox virus caused high mortality from beak and periocular lesions in captive peafowl [19]. Kirmse showed that most cutaneous pox lesions disappear in 3–4 weeks, but some can remain for up to 10 weeks [15]. Davidson et al. also indicated that typical pox skin lesions regress spontaneously after 6–12 weeks [7].

Diagnosis is based on clinical signs, gross lesions, and a variety of tests that confirm the presence of poxvirus, including histopathology, immunohistochemistry, transmission electron microscopy, virus isolation, and PCR of affected tissue [16]. Histopathology of both cutaneous and diphtheritic lesions will reveal extensive epithelial hyperplasia with subepithelial fibrosis and infiltrates of heterophils and macrophages. The epithelial cells have ballooning degeneration with prominent eosinophilic intracytoplasmic inclusions (Bollinger bodies) [18] as shown in Figure 13.2. Inflammation and necrosis of the skin lesions caused by secondary bacterial infection is commonly observed in histologic sections.

The control of avipoxvirus infection is based on prevention rather than treatment. Poor husbandry conditions in the pen along with abundance of blood‐sucking arthropods can trigger APV infection; hence, maintaining adequate air movement to reduce the amount of dust and dander in the house is important [20]. Increased bird activity, bright lights, and increased stocking density can increase bird‐to‐bird contact and exacerbate skin trauma. Effective insect control measures in the house or pen are also indicated.

Vaccination of commercial gamebirds is generally not practiced, but it might be effective in high‐risk situations. Commercial poxvirus vaccines are generally administered by subcutaneous injection of the wing web. Commercial vaccines are not available for all specific strains of avipoxvirus that affect gamebirds; however, as an example, a commercial fowlpox vaccine was shown to protect bobwhite quail against the bobwhite quail strain of APV [12]. Additionally, a live commercial fowlpox vaccine has been used to control avipoxvirus infection in 16‐week‐old breeder bobwhite quail [21]. Fatunmbi et al. showed that chickens vaccinated with various avipoxvirus strains (multivalent vaccines) show the greatest resistance to challenge with fowlpox virus [22], and perhaps a similar use of multiple strains of avipoxvirus would be effective in gamebirds. However, one study indicated that administration of a combination of live pigeonpox and fowlpox vaccines in coturnix quail did not protect the birds from challenge with a quail strain of poxvirus [9]. Captive peafowl that were previously vaccinated with fowlpox virus still broke with cutaneous pox lesions affecting the beak and periocular skin, even though the field virus infecting the peafowl was shown to be nearly identical to fowlpox [19]. To effectively determine if a vaccine would be successful one should attempt to isolate and genetically characterize the field virus, then differentiate it from other avipoxvirus strains by cross‐immunity and pathogenicity tests [3].

13.1.2 Staphylococcosis

Staphylococcal infection of the foot (pododermatitis) was addressed in Chapter 12, but this microorganism deserves further attention here because of the association with breast blisters, cellulitis, and omphalitis in gamebirds. The microorganisms are Gram‐positive cocci (0.5–1.5 μm diameter) belonging to the family Staphylococcaceae and genus Staphylococcus. These microorganisms are often observed as pairs, tetrads or grape‐like clusters, and are readily isolated on blood agar.

More than 50 species and subspecies have been described [23] but Staphylococcus aureus is the most important and common isolate from poultry. This microorganism is a common inhabitant of the skin and mucous membranes, but a break in the integrity of those tissues will allow this opportunistic bacterium to penetrate the skin or membrane, colonize the subcutis and, in some instances, progress to sepsis [24]. Skin that is chronically wet (high humidity, leaking drinkers, wet litter) is more pliable and subject to puncture wounds and lacerations. Common forms of S. aureus infection in poultry include omphalitis, necrotic dermatitis, tenosynovitis/arthritis, pododermatitis, and osteomyelitis in chickens and turkeys [25]. In terms of gamebirds, particularly pheasants, the authors have most often isolated Staphylococcus spp. (S. aureus, S. hyicus, S. intermedius), with or without coliforms (Escherichia coli), in cases of omphalitis (Figure 13.3), cellulitis and breast blisters. Raidal described staphylococcal dermatitis with crust formation on the beak, eyelids, and nares in captive‐reared Japanese quail experiencing 8% mortality and a nutritional deficiency [26].

Reduction of staphylococcal infection is based on reducing trauma in the flock: mitigate cannibalism and feather picking, eliminate sharp objects, avoid crowding, avoid wet litter or leaking drinkers, and have adequate feeder space so that birds do not crowd or climb on each other when taking a meal. In general, flocks under conditions of high humidity, wet litter, and skin trauma can develop staphylococcal disease. Antibiotics might be effective in reducing lesions in problem flocks, but attention should be given to appropriate culture and antibiotic sensitivity testing [25].

13.1.3 Lice (Phthiraptera)

Lice (Insecta: Phthiraptera) are wingless, dorsoventrally flattened insects that are divided into two groups: sucking lice and chewing lice (Mallophaga). Many chewing lice parasitize birds and, in fact, birds serve as hosts for only chewing lice [27]. The lice feed by ingesting host feathers, skin secretions and skin dander, using their broad mandibles to fragment the feather or dander into bite‐size pieces. Different genera of lice usually colonize different areas of the body. Lice are small (350 μm to 10 mm long in adult stage) and normally rest on the feathers, but they quickly disperse from feathers onto skin if they are disturbed. Immature lice (nymphs) resemble the adults, but they are smaller and lack external genitalia. Immature lice increase in size after each nymphal molt. At least six species of chewing lice are found on domestic fowl, particularly chickens [27], and many lice have been described on pheasants, partridges, quail, guineafowl, and pea fowl (Table 13.1).

The life cycles of different avian lice can vary slightly but the wing louse (Lipeurus caponis) will be used here as an example of a typical life cycle. Eggs of the wing louse hatch 4–7 days after the female has cemented them to the base of a feather shaft. Each nymphal stage will each last 5–18 days and total generation time is 18–27 days [27]. Direct host contact (e.g., young in nest, copulation) is the primary route of transmission for lice; however, chewing lice can survive for days off the avian host [63]. Any time the lice spend off the host can promote transmission through contaminated nests, litter, cages, or truck beds.

The clinical signs observed with a louse infestation in a flock are hyperirritability, increased grooming, poor feathering or feather loss, weight loss, and reduced egg production. The gross lesions include red, irritated skin from the scratching activity of the lice and frayed feathers from mite chewing and excessive grooming. Large numbers of lice can debilitate the host. The lice are very active on the host, are larger than mites and are visible to the naked eye as they move about on the host (Figure 13.4a). Inspection of individual feathers can reveal the large masses of eggs (nits) glued to the feather shaft, generally toward the base (Figure 13.4b). Speciation of the lice is based on body morphology (Figure 13.5) [63, 64].

The approach to control and treatment of lice and mites is similar and will be addressed in the section on mites below.

13.1.4 Mites (Acari)

More than 250 species of mites are known to cause health‐related issues in domestic animals and humans. Based on the classification schemes described by Zhang [65], mites or Acari consist of two major groups: the superorder Parasitiformes (Anactinotrichida) and the superorder Acariformes (Actinotrichida). These superorders are further divided into six orders. The orders of mites that are known to contain species of veterinary importance are Ixodida, Mesostigmata, Trombidiformes, and Sarcoptifomes. Most of the mites identified on gamebirds are feather and skin mites or environmental mites that migrate onto captive birds. The list of gamebird mites is likely incomplete and new species will be identified in future surveillance studies. Knemidocoptes sp. is the scaly leg mite and will be described later in the chapter. In most poultry, feather mites can cause discomfort and excessive grooming and promote weight loss, reduced egg production, or mortality in severe cases [50, 66]. For example, feather loss from mites can reduce marketing of quail [50].

The life cycle of mites consists of the egg, prelarva, protonymph, deutonumph, tritonymph, and adult. Mites typically have four pairs of legs as nymphs and adults, but larvae have only three pairs. Surveys of ectoparasites in many types of wild and captive gamebirds have identified a variety of mites, and Ornithonyssus sylviarum, the northern fowl mite, and Dermanyssus gallinae, the red roost mite, are cited most often; therefore, these two mites will be emphasized in this section.

Feather and skin mites are usually identified by distribution on the host, by inspecting (usually with magnification) the entire feather and by scraping the feather exudate onto a glass slide with or without the use of mineral oil for microscopic examination (Figure 13.6) [66]. It should be noted that avian mites, particularly O. sylviarum and D. gallinae, are associated with “avian mite dermatitis” in humans. These blood‐sucking mites can use humans as a short‐term feeding host but will not reproduce on human hosts. Poultry workers and people residing close to bird nests are most often affected. Mite numbers in the surrounding environment are usually heavy if there are human infestations [67].

13.1.4.1 Northern Fowl Mite

Ornithonyssus sylviarum, a mite that spends its entire life on the avian host, is generally located on feathers of the tail, wing, and neck (Figure 13.7). Surveys have documented this this mite in at least 72 species of birds [68] and it can likely be spread to captive bird farms by wild birds [69]. The northern fowl mite is a blood feeder and has been documented in pheasants [29, 66], partridges [43], quail [47], and guineafowl [70]. Multiple surveys of ectoparasites in wild and captive peafowl failed to list feather mites [53, 54, 58]; however, because of the broad host range of the northern fowl mite and the red roost mite, it is likely that peafowl are susceptible to these mite species as well. Economic loss can result from discomfort, decreased egg production, reduced feed consumption, and reduced weight gain. Male birds tend to be more heavily infested than hens and the mites are readily spread between genders while breeding [30].

The entire life cycle is completed in 5 days and in most instances the mite remains on the host bird for the entire life cycle and at all times of the day. The infestation and disease caused by the northern fowl mite are worse during cold months of the year because of the close contact of birds during these periods.

13.1.5 Knemidocoptes Infection (Scaly Leg Mites)

Scaly leg disease is a condition caused by Knemidocoptes mites that burrow into the nonfeathered skin of the feet and legs, resulting in hyperkeratosis and grossly thickened skin with disfigurement and loss of function in severe cases. There are a variety of burrowing mite species described in birds, and Knemidocoptes mutans is the major mite described in poultry. The primary Knemokoptinae described in gallinaceous birds are K. mutans and Neocnemidocoptes gallinae. Knemidocoptes jamaicensis is described in the green peafowl, while K. mutans has been described in the helmeted guineafowl [72]. Among gamebirds, K. mutans is most often reported in pheasants [29, 36]. Wild birds can serve as a source of knemidocoptic infection for confined poultry.

Mites are transmitted directly from bird to bird through contact. The mites spend their entire 3‐week life cycle on their bird hosts. Female mites are viviparous, producing nymphal offspring with three pairs of legs. There are two nymphal stages before adult mites develop with four pairs of legs, and then burrow into feather follicles and the epidermal stratum corneum of the nonfeathered feet, shanks, eyelids, and beak. The burrowing of adult mites causes increased hyperkeratosis and in extreme cases can cause discomfort and reduced function of the affected appendage. Severe hyperkeratosis of the affected skin can impair blood supply to result in eventual loss of digits or entire feet (Figure 13.8). Neocnemidocoptes gallinae, the depluming itch mite, burrows into the feather shafts of the head, neck, back, abdomen, and upper legs of gallinaceous birds to cause irritation, feather picking, and feather loss. The affected skin underneath the feathers can be hyperkeratotic and thickened, but hyperkeratosis of the legs, feet or face is not observed [66, 73].

The primary lesions described in pheasants are prominent hyperkeratosis of the skin of the legs causing discomfort and associated plucking of feathers, weight loss, and reduced egg production [36]. The hyperkeratotic skin lesions, if focal, can resemble poxvirus infection and should be differentiated by histopathology of extruded crust. In histologic sections, the round, short‐legged mites are embedded in pockets within keratin and range in size from 350–450 μm × 280–380 μm for females and 200–240 μm × 145–160 μm for males [74]. Diagnosis can also be made by cytologic examination of skin scrapings. In individual birds, ivermectin, as off‐label medication, has been administered orally at 200 μg/kg given three times, 2 weeks apart, to effectively reduce the lesions in peafowl and other poultry [75, 76]. Prevention should focus on preventing entry of wild birds into the pen, reducing stocking density and practicing routine pen hygiene of the ground, equipment, and feeders/drinkers.

13.1.6 Treatment and Prevention of Ectoparasites

Preventing the introduction of lice and mites onto a premises is most important because eradication can be difficult, medications are not readily available, and the use of insecticides may pose a risk to both human and bird health. Biosecurity should focus on insect control, rigid sanitation, regular removal of dead birds, and restricting movement of people and equipment from pen to pen or premise to premise. Litter should be thoroughly removed between flocks and dry cleaning and disinfection are essential [69, 77]. Wild birds and rodents that can serve as vectors for mites should be excluded. This can be difficult in a flight cage arrangement.

The authors have never encountered heavy mite loads on farmed gamebirds, but in instances of heavy infestation, one can consider chemical insecticide sprays, for which veterinary supervision is strongly recommended. The insecticides are available as wettable powders, emusifiable concentrates, soluble concentrates, granular and microencapsulated products. The spray must be at high enough pressure (100–125 psi with 1 gallon of water per 100 birds) to penetrate the feathers of the vent region. Commercial acaricides include pyrethroids (e.g., permethrin) and organophosphates such as tetrachlorviphos (Rabon^® or Ravap®) often contain wetting agents to help the active chemical penetrate to the feathers [78]. Commercial insecticide sprays should have a Material Safety Data Sheet (MSDS

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