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Infectious diseases of birds of prey (Proceedings)
This paper will provide an overview of selected infectious diseases that avian practitioners are likely to see in a clinical avian practice.
This paper will provide an overview of selected infectious diseases that avian practitioners are likely to see in a clinical avian practice.
Pododermatitis—Pododermatitis (bumblefoot) is an inflammatory condition of the feet that most commonly involves the plantar surfaces. It is characterized by local abrasion to the foot pad, ulceration and swelling and erythema of one or more of the digital or metatarsal pads.1-3 Predisposing factors include trauma (self-inflicted talon puncture, bite wounds or fighting), inappropriate perch size or substrate, obesity, sedentary lifestyle, poor environmental hygiene and nutritional deficiencies.1,4 These factors then culminate in a destructive infectious/inflammatory disease process which may involve the skin, underlying soft tissues, and even bone. Staphylococcus aureus is commonly isolated from pododermatitis lesion; however, Escherichia coli, Klebsiella and Proteus sp have also been identified in foot lesions.1,3,5 Swelling, inflammation and pain are the hallmark of pododermatitis. Clinically the raptor will favor one leg over the other or lay down in sternal recumbency if the pain associated with infectious severe. Pododermatitis is often classified as follows:. Type I—Serious, chronic infection with diffuse cellulitis of the metatarsal pads of one or more digits.1 Type 2—Similar to Type 1; appears as a localized lesions of the digital or metatarsal pads.1,2 Type 3—Demonstrates discrete lesion(s) with hyperkeratinization, localized swelling, and reddening, while Type 4—Marked enlargement of the distal digital pads as a sequelae to flexor tendon rupture. Effective treatment requires: reduction of swelling and inflammation, debridement of necrotic tissue, draining and removing abscesses if present, identifying and eliminating the underlying cause (pathogens and husbandry related etiologies), protecting the wound from further infection or trauma and promoting the development of healthy granulation tissue and further healing with bandaging and dressings.1,2 Antibiotic therapy is based upon bacterial culture and sensitivity. Remple (2006) suggest a four-pronged therapeutic regime consisting of (1) systemic antibiotic therapy, (2) direct intralesional antibiotic delivery, (3) surgical debridement, and (4) post-operative protective foot-casting has offered the most effective therapy for the treatment of bumblefoot (Remple).6
Poxvirus—Poxviruses are large DNA viruses that cause diseases in many different species of birds of prey.7,8 The hallmark of avian poxviruses are the large intracytoplasmic, lipophilic inclusion bodies (Bollinger bodies) that are found in epithelial cells of the integument, respiratory tract and oral cavity, resulting in hypoplasia of the affected cells.
Poxvirus infections cause several different clinical forms: (1) a cutaneous form which creates mild to severe proliferative lesions on unfeathered skin around the eyes, beak, nares, and legs, (2) a diphtheritic form which produces lesions on the mucosa, tongue, laryngeal mound as well as other areas of the oropharynx larynx, and (3) a septicemic form characterized by a lethargy, depression, cyanosis, anorexia, and wart-like lesions of the skin.7,8 Raptors most commonly demonstrate the cutaneous form of the disease. Transmission of avian pox requires viral contamination of broken skin.7 Since the virus is rather large transmission from bird to bird requires a vector (mosquitoes and other blood sucking arthropods) to get through the skin. Diagnosis of an infection with poxvirus is confirmed by signalment, history, clinical signs, histopathologic examination and demonstration of Bollinger bodies in affected tissues and electron microscopy.5,8 Culture may be necessary to confirm a diagnosis in septicemic infections.8 Therapy is non-specific and may involve antibiotic therapy to prevent or treat secondary bacterial infections.5,7,8 High frequency radio waves from radiosurgical units on low settings may speed healing of skin lesions. Vaccination is the best method of controlling poxvirus infections in gallinaceous birds; however, further evaluation of autogenous and heterologous vaccine efficacy in raptors is needed.7,8 Natural infections are thought to provide lengthy immunity. Infected birds should be isolated from uninfected birds if possible.
Herpesvirus—Herpesviruses (primarily betaherpesvirinae) may also affect a wide range of mammalian and avian species.. Herpesvirus infections reported in raptors include Inclusion Body Hepatitis of Falcons (FHV-Falcon Herpesvirus), Hepatosplenitis Infectosa Strigorum (OHV-Owl Herpesvirus), and Eagle Herpesvirus.8,9 FHV preferentially affects reticuloendothelial cells and hepatocytes causing marked depression, anorexia and high mortality. Multifocal hepatic necrosis is the hallmark of this disease as well as necrosis of the pancreas, lung, kidney and brain.8 OHV occurs in both wild and captive owls in Europe, Asia and the United States.8 This disease as been reported as a naturally occuring infection in the great horned owl (Bubo virginianus) and snowy owl (Nyctea scandiaca).8 Although OHV usually affects epithelial and mesenchymal cells, clinical signs and histopathologic lesions may resemble FHV. Necrotic foci are seen within the liver, spleen, intestine and jugular veins.8 Diagnosis of herpesviruses in raptors is based upon clinical signs, histologic lesions, serologic identification and virus isolation. Acyclovir (Zorivax®) (333 mg/kg orally, ever 12 hours for 7-14 days) may be effective in infected raptors.10 Supportive care and empirical antibiotic therapy are also warranted.
Adenovirus—Adenoviruses are well known for their ability to also affect a wide range of avian species including raptors. Recently Schrenzel and coworkers (2005) described an outbreak of adenovirus in a captive raptor breeding facility. Species affected in this outbreak include Northern Aplomado falcons (Falco femoralis septentrionalis) between 9 and 35 days of age and peregrine falcons (Falco peregrinus) between 14 and 25 days of age.11 The affected birds appeared dehydrated, had diarrhea, were anorexic and died acutely.11 The etiologic agent appeared to be a new species of adenovirus related to group I aviadenovirues.11 Subsequent to the initial outbreak adenovirus infection was determined to be the cause of deaths of various other species of falcons in Wyoming, Oklahoma, Minnesota and California.11,12 Serum neutralization testing suggests that peregrine falcons were the primary host and reservoir for this adenonvirus.11,12 Wild peregrine falcons demonstrated a seropositivity rate of 80-100%.11,12 At necropsy the lesion associated with this disease are very similar to those observed with FHV.
West Nile Virus—West Nile virus infection is caused by a Flavivirus (Family Flaviviridae) and was first isolated from a woman in the West Nile region of Uganda in 1937.13 Although many species of birds can be infected and affected with WNV, the American crow (Corvus brachyrhynchos) and other corvids commonly suffered high morbidity and mortality.
Transmission of WNV occurs primarily through C. pipiens in Europe and North America Ingestion of infected prey species (house sparrows and pigeons) may also serve as a means of acquiring the WNV.
Clinical signs of WNV infection are highly variable and sometimes dependent upon the age of the raptor. Infected birds may show signs ranging from slight depression and weight loss to marked depression, anorexia, blindness, ataxia, head tremors, seizures an sudden death.14 The University of Minnesota Raptor Center classifies clinical signs as follows:
Phase 1: Depression, anorexia, weight loss, sleeping, pinching off of blood feathers, elevated white cell count.13
Phase 2: In addition to the above, head tremors, green urates, mental dullness/central blindness, general lack of awareness of surroundings, ataxia, weakness in the legs.13
Phase 3: More severe tremors, seizures.13
Ante mortem diagnosis of WNV infection can be difficult at best especially if the clinical signs may be attributable to any number of infectious, inflammatory, metabolic, nutritional or toxic etiologies. Serum neutralization test may indicate an antibody response to infection. Clinical signs coupled with Paired samples submitted 2-4 weeks that demonstrate a rise in antibody levels coupled with clinical signs may allow for a more definitive diagnosis. Fundic examination may reveal optic neuritis, anterior uveitis, vitritis and chorioretinitis.14 Unfortunately, most cases are confirmed through post-mortem examination. Kidney and brain are good samples to submit for histopathologic evaluation. Nemeth et al, (2006) reported the most common histopathologic lesions in naturally and experimentally infected raptors included subacute myocarditis and encephalitis.15 Several birds had a more acutely severe disuse characterized by arteritis and associate tissue degeneration and necrosis.15
There is no specific treatment available for WNV, and treatment is often unrewarding. Preventative measures (vaccinations) involve the use of a vaccine available for equids (Fort Dodge). However, there is no definitive data evaluating the long term efficacy of this vaccine in birds. The Centers for Disease Control has provided a killed vaccine that has been in several avian species including endangered species. The following recommendations for use of the Fort Dodge product is given: Birds > 300 grams receive 1.0 ml IM; birds < 300 grams receive 0.3-0.5 ml IM.17 A "booster" vaccination is given 3 weeks later.13 A third vaccination may be necessary in areas with large vector populations. Moving birds indoors, covering outdoor enclosures with mosquito netting, isolating infected birds and appropriate disposal of carcasses are also effective means of control.
Aspergillosis—Aspergillosis is probably the most common mycotic disease reported in raptors. Goshawks (Accipiter gentilis), gyrfalcons (Falco rusticolus) and red-tailed hawks (Buteo jamaicensis) are commonly infected. Aspergillus fumigatus is the most common etiological agent reported followed by A. flavus and A. niger.16 Given the ubiquitous nature of Aspergillus sp, infections are considered to occur secondarily to any event that acutely or chronically compromises the raptor's immune system. Aspergillosis may present as an acute form, a tracheal form, a more chronic granulomatous form or a systemic form.2,17,18 Clinical signs are usually associated with the respiratory system or organ(s) affected. Initially, the most common clinical signs are depression and anorexia; however, respiratory signs quickly follow. Dyspnea, change or loss of voice, exaggerated respiratory effort ("tail bob") are frequently reported. In addition, weight loss or emaciation may be seen in more chronic disease. The prognosis for most cases of aspergillosis is fair to guarded. Therefore, rapid detection and aggressive therapy are necessary to increase long-term survivability. Diagnosis of aspergillosis can be difficult at best and requires a thorough clinical exam involving a history, physical examination, laboratory diagnostics, radiography, endoscopic and laparoscopic examination of the respiratory tract, protein electrophoresis, serological testing, cytologic examination and fungal culture. Endoscopic examination of the coelomic cavity and upper respiratory tract, demonstration of aspergillosis lesions and identification of the organism by cytology or culture is the most definitive way to diagnose this insidious disease. Many therapeutic regimens have been proposed including the use of amphotericin B (1.5 mg/kg IV every 8 hours for 3 days, 1.0 mg/kg within the trachea (IT) every 8-12 hours or 0.5 mg/ml sterile water nasal flush), miconazole, clotrimazole (0.2 ml equaling 2 mg/kg IT once daily for 5 days or nebulize 1% solution for 30-60 minutes), fluconazole (5-15 mg/kg orally every 12 hours for 14-60 days), enilconazole, itraconazole (10 mg/kg orally every 24 hours)10,19 Newer antifungal medications, such as voriconazole (10 mg/kg q 12 hours), are showing promise in the treatment of this disease.20 Therapy is usually long-term with patient response and serological testing used to monitor progress.
Parasitic And Protozoal Diseases
Trichomoniasis—Trichomoniasis ("frounce"), is caused by Trichomonas gallinae and is a significant disease of both captive and wild raptors.2,5 Pigeons (Columba livia) and doves (Zenaidura macroura) are incriminated as "resevoirs" of this organ and are usually involved in transmitting the organism to birds of prey. Infections are seen in captive raptors fed a diet of freshly killed pigeons and wild raptors that feed on pigeons (goshawks, falcons, and a some species of owls).2, 5 Classic infections with T. gallinae typically cause caseous plaques in and around the oropharynx; however, lesions have also been describe in the lungs, air sacs, sinuses, ear canal and kidneys.21,22 Raptors that are affected often have difficulty swallowing and may flick pieces of food.2 Diagnosis is based upon history, clinical signs and demonstration of the organisms cytologically. Treatment with metronidazole (30-50 mg/kg q 24 hrs for five to seven days) or Carnidazole (Spartrix®, Wildlife Pharmaceuticals, Inc., Fort Collins, CO) (30 mg/kg every 12 hrs for three days; 20-30 mg/kg orally once or 20 mg/kg orally, once daily for 2 days) is often effective.2,10
Helminths—Nematodes are the most common helminths that affect birds of prey and include capillarids, ascarids, spirurids, and tracheal and air sac nematodes.23 Clinical signs are associated with the species of nematode and its preferred site of infectivity. Single or multiple fecal examinations are require to demonstrate ova, eggs, oocysts or adult worms with in the feces, or in other areas of the gastrointestinal tract. These must be differentiated from parasites that originate from prey species. Most nematode infestation can be treated with ivermectin give orally, intramuscularly, or subcutaneously at a dose of 0.2–0.4 mg/kg.
Coccidia—Caryospora spp. Cryptosporidium spp, Eimeria spp, Fenkelia spp, Sarcocystis spp. and Toxoplasma gondii are reported in birds of prey. In most instances they are non-pathogenic; however, they may cause severe disease in juvenile or immunocompromised birds. Clinical signs of infestation include lethargy, depression, diarrhea, hematochezia, weight loss, emaciation or even death. Diagnosis requires demonstration of oocysts in the feces or the organisms in tissue. Several medications may be used to effectively treat coccidial infestations. Sulfadimethoxine (Albon®; at 25-55 mg/kg orally, once daily for 3-7 days); Pyrimethamine (Daraprim®) especially effective against toxoplasmosis, Atoxoplasmosis and sarcocystis, or toltrazuril (Baycox®;at 7 mg/kg orally), once daily for 2-3 days.10
Hemoparasites—Leukocytozoon sp. and Hemoproteus sp. are seen in both captive and wild birds of prey. Often infections are associated with some degree of compromise to the immune system, although large numbers do not necessarily cause apparent disease.2,24 Plasmodium sp. is of clinical significance, especially in gyrfalcons and snowy owls, and may cause depression, weight loss, respiratory distress, anemia, and anorexia. Mosquitoes are the primary vectors for host to host transmission. Its is believed that passerine species may serve as natural resevoirs.2 Diagnosis is usually made by coupling appropriate clinical signs and demonstration of the organism in blood cells. Correction of the underlying problem(s) often resolves Leukocytozoon and Hemoproteus infections; however, management of Plasmodium sp. infestations requires supportive care (fluid therapy, blood transfusions and diphenhydramine (Benedryl®) and the administration of Chloroquine (Aralen®,) in combination with Primaqine. Chloroquine is given parenterally at a dose of 20mg/kg, then at a dose of 10 mg/kg PO at 6, 18 and 24 hours in combination with oral primaquine (1 mg/kg) given q 24 hours for 2 days.25 This regimen is repeated as necessary at weekly intervals for 3–5 weeks to prevent relapses. Once the bird is stable a preventative regime of chloroquine (10 mg/kg PO) and primaquine (1 mg/kg) are given weekly. Other treatment regimes include Mefloquine HCl (Lariam®) 30 mg/kg given at 0, 12, 24, 48, and 72 hours then weekly for 6 months25 or Quinacrine (Atabrine®) at a dose of 5-10mg/kg IM once daily for 7 days.
References provided on request.