Diagnosis, Treatment, and Control of Common Parasites in Companion and Aviary Birds

Victoria L. Clyde, DVM, and Sharon Patton, PhD

This article presents a brief review of clinical syndromes, diagnostic techniques, suggested treatments, and control measures for common parasite problems of companion and aviary birds. Copyright9 1996by W. B. Saunders Company. Key words: Antiparasitics, birds, ectoparasites, endoparasites.

Flagellated Protozoa
Giardia Psittaci
Giardiapsittaci 2,5s is a c o m m o n protozoal parasite of small birds such as budgerigars, lovebirds, and cockatiels. It has a direct life cycle in which the infective cyst is shed in feces and remains viable in organic matter for several weeks. After ingestion and excystation, the parasites live in the small intestine and reproduce by binary fission. In heavy infections, trophozoites may interfere with absorption and fat metabolism. Clinical syndrome. Asymptomatic carriers are extremely common. Affected birds show chronic to intermittent diarrhea with loose, malodorous, mucoid stools. O t h e r signs such as lethargy, anorexia, stunting, and mortality occur more frequently in juveniles. Dry skin, pruritis, and feather picking may occur secondary to malabsorption. Diagnosis. A single negative sample does not rule out infection, as cysts and trophozoites are shed irregularly in feces. A fresh fecal sample (less than 10 minutes old) will assist in diagnosis. Motile trophozoites have a gliding motion on direct saline smear examination. Two "eyespots" or nuclei can be identified by light microscopy. Visualization of trophozoites can be improved by iodine staining of fresh feces or trichrome staining of feces stored in polyvinyl alcohol. Occasionally, trophozoites will be identified on a routine Gram's stain of feces (Fig 1). Zinc sulfate flotation concentrates cysts. An enzyme-linked irnmunosorbent assay test that detects Giardia-specific antigen in aqueous extracts of h u m a n feces is From the Department of Comparative Medicine, College of VeterinaryMedicine, The University of Tennessee, Knoxville, TN. Address reprint requests to Victoria L. Clyde, DVM, PO Box 1071, Knoxville, TN37901-1071. Copyright 9 1996 by W. B. Saunders Company. 1055-937X/96/0502-000455. 00/0 75

arasitic infections are infrequently diagosed in caged birds. Captive-born birds maintained in raised-floor cages have little access to many parasites. However, parasitism may be overlooked even when present because of the similarity in clinical signs to diseases o f other etiology or the practitioner's unfamiliarity with parasites in birds. Although several chapters have been devoted to avian parasites, x-3 this report highlights the clinical syndromes observed most frequently in companion and aviary birds and suggests practical methods of diagnosis for general practice. Treatment of avian parasitism remains an art. Not all parasitic infections result in clinical disease, and few antiparasitic agents have been evaluated for safety and efficacy in psittacines and passerines. The sensitivity of avian parasites to antiparasitic treatment is variable, and it is imperative that birds be retested after treatment to assess efficacy. Because reinfection can mimic resistance, appropriate hygiene and control measures must be instituted in conjunction with drug therapy. Whenever possible, direct administration of the drug is strongly preferred over food or water treatment, which can result in erratic or inappropriate dosing of birds. Dosages in this r e p o r t have been derived from the listed references and emphasize readily available drugs of lower toxicity. T h e reader is referred to a recent review of avian antiparasitic agents for more detail. 4

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Figure 1. Giardiapsittaci trophozoite seen on routine Gram's stain of avian feces. Note appearance of two nuclei and multiple flagella. Trophozoites appear red-pink because of safranin counterstain (1000 X). available, b u t its use in d i a g n o s i s o f avian g i a r d i a sis r e m a i n s c o n t r o v e r s i a l . Treatment. All e x p o s e d b i r d s s h o u l d b e t r e a t e d with m e t r o n i d a z o l e (Table 1). U n f o r t u n a t e l y , r e s i s t a n c e a n d r e l a p s e is c o m m o n , a n d a d m i n i s t r a t i o n o f m e t r o n i d a z o l e in d r i n k i n g w a t e r is n o t effective. 7 F e n b e n d a z o l e at h i g h doses also m a y b e effective. 9 Control. R e i n f e c t i o n is c o m m o n a n d c a n b e m i s i n t e r p r e t e d as t r e a t m e n t failure b e c a u s e cysts

m a y b e p a s s e d in t h e feces 3 to 5 days a f t e r r e i n f e c t i o n . P r e v e n t r e i n f e c t i o n by l i m i t i n g access to c o n t a m i n a t e d feces a n d m a i n t a i n i n g immunocompetence through good nutrition and a p p r o p r i a t e s t o c k i n g density. Cages m u s t h a v e a g r a t e to p r e v e n t access to feces. Elevate f o o d bowls to p r e v e n t fecal c o n t a m i n a t i o n , a n d c l e a n a n d disinfect cages o n a r e g u l a r basis. Q u a t e r n a r y a m m o n i u m c o m p o u n d s a r e effective in i n a c t i v a t i n g cysts, s ' Zoonotic. Z o o n o t i c p o t e n t i a l r e m a i n s u n c l e a r . G psittaci m a y b e h o s t r e s t r i c t e d a n d t e m p e r a t u r e a d a p t e d , b u t a p r e s u m p t i v e case o f h u m a n infect i o n has b e e n r e p o r t e d . 7

Trichomonas Gallinae and Related Species

T r i c h o m o n i a s i s l~ is a c o m m o n i n f e c t i o n in columbiformes and falconiformes that can be s e e n s p o r a d i c a l l y in p s i t t a c i n e s a n d passerines. Clinical syndrome. W h i t e p l a q u e s o r n e c r o t i c masses a r e n o t e d in the o r a l cavity a n d e s o p h a gus. A f f e c t e d b i r d s m a y s h o w a n o r e x i a , d y s p n e a , d e b i l i t a t i o n , a n d r e g u r g i t a t i o n . N e o n a t e s inf e c t e d t h r o u g h p a r e n t a l f e e d i n g p r e s e n t with poor growth and acute death.

Table 1. Avian Antiparasitics Antiparasitic

Amprolium Carnidazole Chlorsulon Fenbendazole

Dosage
2-4 mL 9.6% soln/gal drinking water 20 mg/kg PO 20 mg/kg PO q 14 days 3 treatments 25 mg/kg PO repeat in 14 days 50 mg/kg PO q 24 h for 5 day~ 50 mg/kg PO q 24 h for 3 days 50 mg/kg PO q 24 h for 3 days 0.2-0.4 mg/kg PO, SQ, IM 15 mg/kg PO or 5 mg/kg SQ

Cemn~zts
5 days/month For trichomoniasis in pigeons For trematodes For ascarids For capillariasis For giardia; efficacy unproven For flukes For nematodes, ectoparasites; may be given topically in small species Toxic reactions include regurgitation, ataxia, death Use only if less toxic anthelmintics are ineffective For giardiasis, trichomoniasis For cestodes, some trematodes Repeat in 14 days 40-80 rag/1 drinking water, 100 mg/kg food; supplement folate and B vitamins Follow with 3 days folate/vitamin B6 supplementation; repeat cycle 4 times For coccidians

Ivermectin Levamisole

Metronid~ole Praziquantel Primaquine Pyrantel pamoate Pyrimethamine Sulfachlorpyrazine

25 mg/kg q 12 h PO for 5-10 days 50 mg/kg q 24 h PO for 5-10 days 10 mg/kg PO 0.03 mg/kg PO q 24 h for 3 days 7 mg/kg PO 0.5 mg/kg PO q 12 h for 14-28 days

1 g 30% powder/1 drinking water 5 days Trimethoprim-sulfanmthoxazole 30 mg/kg PO q 12 h for 5-10 d

NOTE. Dosages listed are guidelines only and are derived from references listed in text as well as from the authors' experience. No antiparasitics are approved for use in companion avian species, and owners should be informed of off-label usage and associated hazards. Abbreviations: PO, by mouth; S% subcutaneous; IM, intramuscular.

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Diagnosis. Motile, pyriform trophozoites seen on direct saline smear of oral lesions have one nucleus or "eyespot," a polar flagella, and an undulating m e m b r a n e . The jerky motion of trichomonads are markedly different f r o m the gliding m o v e m e n t s o f Giardia spp. Treatment and control Administer oral metronidazole (Table 1). Relapses after cessation of treatment occur m o r e c o m m o n l y in psittacines than columbiformes. Carnidazole tablets (Spartrix; Wildlife Pharmaceuticals, Inc, Fort Collins, CO) are available for t r e a t m e n t of affected pigeons. Successful t r e a t m e n t has b e e n obtained with dimetronidazole, ipronidazole, and ronidazole, but these drugs are not available in the United States. Control disease by t r e a t m e n t or elimination of carriers, p r o t e c t i o n of water sources f r o m contamination by wild birds, and avoidance of overcrowding.

Clinical syndrome. Subclinical infection is common, but stressed, overcrowded young birds may develop a mucoid or bloody diarrhea with resultant dehydration. In severe cases, destruction of intestinal epithelium may induce malabsorption, anemia, and hypoproteinemia. A few species of Eimeria can parasitize the liver, kidney, and lungs. Diagnosis. Oocysts can be identified on routine fecal flotation (Fig 2). However, most intestinal tract d a m a g e occurs before the p r o d u c t i o n of oocysts. Asexual stages (merozoites) can be observed at necropsy in the intestinal mucosa. Treatment and control. Affected birds can be treated with t r i m e t h o p r i m / s u l f a m e t h o x a z o l e (Table 1). Control involves breaking the fecaloral cycle through raised-floor cages, decreased stocking density, a n d hygiene. A m p r o l i u m may be used as a preventative (Table 1), but resistance can develop. Cryptosporidium spp
In contrast to o t h e r coccidia, Cryptosporidium spp 2a3 develop intracellularly but extracytoplasmically just u n d e r the surface of the host cell m e m b r a n e . Infective, sporulated oocysts are shed in the feces, and transmission occurs by direct ingestion or inhalation with subsequent ingestion of the oocyst. E n d o g e n o u s sporulation of the oocyst in the gut can result in autoinfection of a parasitized host. Clinical syndrome. Cryptosporidial infections are usually self-limiting. Prolonged or severe clinical disease is seen most c o m m o n l y in juve-

Apicomplexan Protozoa~The Coccidia

lsospora spp and Eimeria spp

Isospora spp and Eimeria spp 2 can be f o u n d in both psittacine and passerine hosts, especially in aviary-housed canaries, finches, mynahs, toucans, and lories. These parasites are not commonly seen in caged birds because the oocyst that is passed intermittently in the feces must sporulate in the e n v i r o n m e n t to b e c o m e infective. Once produced, the oocyst may remain infective in the e n v i r o n m e n t for months.

Figure 2. (A) Atoxoplasma spp oocyst from a Bali Mynah, which appears similar to oocysts of Isospora spp and Eimeria spp (1000 X); (B) typical appearance of an avian ascarid egg (400 X); (C) typical spiruirid egg surrounded by several bipolar Capillariaspp eggs (200 X); (D) egg of Syngamus spp, commonly called "gapeworm" (200 X).

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nile cockatiels and may be secondary to immunosuppression induced by other agents such as polyoma virus or psittacine feather and beak disease. Affected birds show regurgitation and weight loss secondary to gastroenteritis. Cryptosporidiosis is usually limited to the gastrointestinal tract of psittacines but may also involve the respiratory and urinary epithelial surfaces. Diagnosis. The oocyst can be overlooked easily because it is very small (4 to 6 txm) and floats in a higher plane than other parasite products. However, it is readily concentrated by sugar flotation, after which the oocyst and its sporozoites have a "pink glow" when viewed with the microscope. Although numerous other stains have been r e p o r t e d to facilitate cyst identification, sugar flotation is the preferred m e t h o d in general practice. Treatment and control. Supportive care and limiting reexposure may be the only available treatments. Recently, paromomycin has been reported as an effective treatment for cryptosporidiosis in a cat when given orally at 165 m g / k g every 12 hours for 5 days. 14 This aminoglycoside has low toxicity, is poorly absorbed from the gastrointestinal tract, and shows promise in the treatment of this disease. Control is difficult as oocysts are infective when shed and are resistant to many disinfectants. Some aviaries prefer to cull persistently infected birds to limit spread. Zoonotic. Avian Cryptosporidium spp appear to be temperature- and species-adapted, and do not present a risk to humans. But Cryptosporidium spp infecting mammals are zoonotic. Atoxoplasma spp

Diagnosis. Diagnosis is rarely made by fecal examination because mortality usually occurs before the production of oocysts. Asexual stages may be identified in buffy coat smears, liver biopsies, or postmortem tissue samples. T h e small oocysts (20 ~zm) may be intermittently shed in the feces by asymptomatic carriers but are difficult to distinguish from many Isospora spp of birds (Fig 2). Treatment and control. No consistently effective treatment is readily available. Primaquine may suppress the tissue forms, and sulfachlorpyrazine may suppress fecal shedding (Table 1). Sulfachlorpyrazine is not available in the United States. Toxoplasma Gondii Toxoplasma gondii1~19is a ubiquitous coccidian parasite with both a direct and an indirect life cycle. Oocysts are produced only in the enteroepithelial cycle of felids. Birds become infected by the ingestion of infective oocysts from the envir o n m e n t or tissue cysts in raw or u n d e r c o o k e d meat. The parasites multiply asexually in cells as tachyzoites before becoming quiescent in tissue cysts as bradyzoites. Clinical syndrome. T gondii is an u n c o m m o n parasite of caged birds. Some early reports of avian toxoplasmosis may have been atoxoplasmosis. Acute onset of generalized "sick bird synd r o m e " with possible neurological signs or acute death is the c o m m o n presentation. Specific signs are highly variable because of the wide variety of body systems that can be infected. At necropsy, lesions include muscular atrophy and myositis, fibrinous serositis, p u l m o n a r y congestion, airsac: culitis, myocarditis, hepatosplenomegaly, enteritis, ophthalmitis, and meningoencephalitis. Diagnosis. Birds are an intermediate host and do not p r o d u c e oocysts. Tachyzoites travel through the vascular system and spread to other organ systems. Tissue cysts containing bradyzoites are encysted in multiple tissues. Diagnosis is obtained through serological tests or histological examination of tissues. Immunoperoxidase staining is helpful in the identification of tissue stages. Treatment and control. Treatment can be attempted with trimethoprim-sutfamethoxazole and pyrimethamine (Table 1). Zoonotic. Sources of contamination for birds (cat feces, u n c o o k e d meat products) can also be

Atoxoplasma spp 2,15 are small coccidian parasites of canaries and other passeriformes such as finches and mynahs. Each bird species is infected by a different Atoxoplasma spp, and cross-infection should not occur. Asexual reproduction of the organism in vital organs such as the lung, liver, spleen, and intestine incites a m o n o n u c l e a r inflammatory response. Sexual stages in the intestine result in the passage of oocysts that sporulate in the environment. Clinical syndrome. Clinical signs and mortality are greatest in juveniles, which can show diarrhea, anorexia, weight loss, ill-thrift, ruffled feathers, abdominal distention caused by hepatomegaly, and acute death. Adults are often asymptomatic shedders.

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sources of contamination for people. Birds do not p r o d u c e infective oocysts, therefore, pet birds are not contagious to people.

Sarcocystis falcatula Sarcocystis falcatula 2,2~ is a coccidian parasite that u n d e r g o e s sexual multiplication in the intestine of the opossum (Didelphis virginiana) in North America. Infective sporocysts are shed in opossum feces that may be deposited into aviaries directly or t r a n s p o r t e d by cockroaches. Asexual r e p r o d u c t i o n of the parasite in the psittacine intermediate host results in a severe vasculitis and pneumonitis. Clinical syndrome. Peracute death is c o m m o n . Marked dyspnea a n d yellow urates may be observed before death. Old World Psittacines are very susceptible to clinical disease. Adult New World Psittacines have m o r e resistance, but neonates can be fatally infected. P u l m o n a r y e d e m a and h e m o r r h a g e is a consistent necropsy finding. Diagnosis. P o s t m o r t e m evaluation is required for the identification of schizonts or merozoites in p u l m o n a r y tissue. These tissue stages may be overlooked by inexperienced pathologists. Treatment and control. T r e a t m e n t can be att e m p t e d with t r i m e t h o p r i m - s u l f a m e t h o x a z o l e and p y r i m e t h a m i n e (Table 1). Control disease by limiting access of opossums to aviaries, removing food f r o m cages overnight, and cockroach control.

relatively endoparasite free and will r e m a i n that way t h r o u g h o u t their lives. O f m o r e c o n c e r n are wild-caught individuals that may have b e e n infected before capture or aviary birds that are kept outside in dirt or grass enclosures.

Cestodes
Cestodes occur occasionally in parrots. They are diagnosed most frequently in wild-caught cockatoos, African Grey Parrots, or birds kept in dirt enclosures. Fecal flotations are usually negative for eggs, which are trapped in proglottids and not c o m m o n l y distributed t h r o u g h o u t the feces (Fig 3). Proglottids are shed.infrequently but may be observed by owners. Straining or unthriftiness may also be noted. Tapeworms can be treated effectively with praziquantel (Table 1).

Trematodes
Infection of birds with digenetic trematodes requires the c o n s u m p t i o n of an i n t e r m e d i a t e host and thus is rarely seen in c o m p a n i o n birds. Cases usually involve imported, wild-caught, Old World Psittacines. T r e a t m e n t can be a t t e m p t e d with praziquantel or chlorsulon (Table 1).

Nematodes
N e m a t o d e s are occasionally seen in companion a n d aviary birds. Because most infections require access to larvated eggs, intermediate hosts, or feces of other species, n e m a t o d e problems occur m o s t frequently in birds kept in dirt-floored enclosures. W h e n present, infections usually r e s p o n d to treatment with anthelmintics such as pyrantel pamoate, fenbendazole, or ivermectin (Table 1). Ascarids Eggs are not infective until they larvate 2 to 3 weeks after passage in feces, but they can persist in moist environments for p r o l o n g e d periods. Ascarid infections 2&24'25are most c o m m o n l y seen in psittacines with access to the ground. Clinical syndrome. Intestinal ascaridiasis can cause anorexia and diarrhea with resultant malabsorption, weight loss, and stunting. Heavy infections can result in gastrointestinal obstruction and death (Fig 4). Cerebrospinal nematodia-

Hemoparasites
Avian hemoparasites include Hemoproteus spp, Plasmodium spp, Leukocytozoon spp, as well as flagellated trypanosomes. These parasites are c o m m o n l y observed in wild-caught birds but are often nonpathogenic. Avian hemoparasites are rare in captive-born caged birds. T h e reader is directed to other references for review of these parasites.l-3,93

Helminths
Many helminth parasites have an indirect life cycle requiring an intermediate host. These parasites are o f little i m p o r t a n c e to birds that are caged with limited exposure to feces or intermediate hosts. Indeed, m a n y captive-born birds are

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Figure 3. Appearance of avian tapeworm eggs after flotation. (A) Pulluterina spp; (B) Raillietiaspp. Note the presence of "hooklets" within embryos (200 X). sis is caused by a b e r r a n t larval migration of the raccoon r o u n d w o r m (Baylisascarisprocyonis). Central nervous system migration in affected birds will result in ataxia, torticollis, and death. Diagnosis. Intestinal ascaridiasis is c o n f i r m e d by finding typical ascarid eggs on a routine flotation of feces (Fig 2). No eggs are passed in cerebrospinal nematodiasis; therefore, diagnosis is based on clinical signs with confirmation by p o s t m o r t e m examination of neural tissue. Treatment and control. Intestinal ascaridiasis is treated with routine antiparasitic agents. Intestihal blockage and death may occur after treatm e n t o f heavily parasitized birds. Cerebrospinal nematodiasis is untreatable. Owners should limit access of birds to feces, k e e p birds in raised-floor cages whenever feasible, provide a dry environment, and prevent access of raccoons and o t h e r m a m m a l s to the aviary.

CapiUaria spp

Capillaria spp 2'26 are tiny, threadlike n e m a todes. Most CapiUaria spp of caged birds have a direct life cycle, Species with an indirect life cycle c o m m o n l y require earthworms as an intermediate host. Eggs larvate in 2 weeks and r e m a i n infective in the e n v i r o n m e n t for p r o l o n g e d periods. Clinical syndrome. Adults burrow into the mucosa of the intestinal tract, causing anorexia, regurgitation, diarrhea, and weight loss. Heavy infections can result in ulceration, anemia, a n d death. Infections o f the esophagus can cause gaping and difficulty in swallowing. Diagnosis. Bipolar eggs are seen on routine fecal flotation (Fig 2). Control. Prevent access to ground.
Spiruroidea

Figure 4. Gastrointestinal obstruction secondary to intestinal ascaridiasis was the cause of death in this parrot.

Spirurids 2,3,27 are a diverse g r o u p of n e m a todes usually requiring an invertebrate intermediate host for c o m p l e t i o n of their life cycle.

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Several syndromes reflecting infection by spirurids are noted infrequently in psittacines (Fig 2). Proventricular and ventricular (gizzard) worms, such as Spiroptera spp and Dispharynx spp, infect the u p p e r gastrointestinal tract inducing epithelial hyperplasia. Penetration of the mucosa can lead to coelomitis. Conjunctival nematodiasis results from infections with adult spirurids including Oxyspirura spp, Thelazia spp, Caratospira spp, and Annulospira spp. These parasites can be killed by treating the infected bird with ivermectin (Table 1). Manual removal of killed parasites requires anesthesia and conjunctival flushes. Syngamus Trachea

by transillumination of the trachea. Eggs can sometimes be identified in feces or sputum. Treatment and control. Ivermectin is an effective treatment (see Ivermectin Therapy). Eggs from infected Lady Gouldian Finches can be raised by mite-free Society Finches.

Knemidokoptic Mites

Clinical syndrome. Syngamus trachea1 (gapeworm) infections are rare in psittacine birds. When present, young birds are most often affected and can display voice changes, coughing, marked dyspnea, and bloody tracheal secretions. Diagnosis. Tracheal transillumination can demonstrate large, bright red worms that appear Y shaped because of p e r m a n e n t coitus of the small male with the larger female. Direct evaluation of tracheal secretions or flotation of feces will show characteristic double operculated eggs (Fig 2).
Filariidea
The filarid nematodes 2,21,2s,z9have a migrating microfilarial stage with adults located subcutaneously or in the body cavity, ocular chambers, heart, or air sacs. A n t e m o r t e m diagnosis is usually limited to subcutaneous filariasis by Pelecitus spp in which aspiration or surgical exploration of nodules on the feet and legs of birds shows microfilariae or adult filarids. Treatment requires surgical removal of adults and ivermectin to kill microfilarial stages (Table 1).

Clinical syndrome. The "scaly leg and face" mite (Knemidokoptes spp)1-3 seen in budgerigars, canaries, and other small birds induces proliferative, honey-combed masses of the n o n f e a t h e r e d skin, especially a r o u n d the beak and on the legs. Diagnosis. The clinical appearar~ce in commonly affected species is p a t h o g n o m o n i c (Fig 5). Knemidokoptic mites in other species of birds may incite only pruritis and feather loss around the head and neck without the characteristic proliferative lesions. In these cases, diagnosis can also be made by visualizing mites in skin scrapings, by biopsy, or by clinical response to treatment. Treatment and control. Treat all exposed birds with ivermectin (see Ivermectin Therapy).

Other External Parasites

O t h e r than knemidokoptic mites, external parasites are rare in captive-born pet birds. 2 The mite protectors and sprays sold in pet stores are unnecessary and may induce hepatic damage. Clients should be counseled to remove these products from their bird's environment. In the unusual instance of infestation with other mites, ivermectin treatment should be administered as outlined next. Less c o m m o n mites, such as red mites (Dermanyssus spp), spend time in the envir o n m e n t and may be better treated by light dustings of the bird with pyrethrin powder combined with premise treatments. Birds are very sensitive to organophosphates and aerosolised toxins and must be removed before premise treatment.

Arthropods
Tracheal Mites

Sternostoma tracheacolum1,2 infects the trachea of canaries, finches, parakeets, and cockatiels. Lady Gouldian Finches are commonly infected. Clinical syndrome. Dyspnea, coughing, and sneezing may occur. Signs are most severe in neonates and juveniles. Diagnosis. Tiny black mites can be visualized

Ivermectin Therapy
Ivermectin at 0.2 m g / k g can be administered orally, topically, or parenterally3 ~ T r e a t m e n t of small birds often requires dilution. Propylene glycol is the r e c o m m e n d e d diluent because ivermectin is not soluble in water or saline. However,

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Figure 5. Knemidokoptic mites induce pathognomonic proliferative masses on the nonfeathered skin of the face and legs of budgerigars and other small birds. m a n y clinicians dilute ivermectin in saline for immediate use after mixing and have n o t reported adverse effects. I f p r o p y l e n e glycol is used as the diluent, it can be sterilized by passing it through a m i c r o p o r e filter. Diluted p r o d u c t should be used immediately because stability of the diluted f o r m has not b e e n proven. Toxicity has b e e n observed in small birds treated with ivermectin intramuscularly, a n d this route is not r e c o m m e n d e d for birds weighing less than 500 g. Topical treatment in small birds (<100 g) is accomplished by placing one d r o p of diluted ivermectin (1 m g / m L ) on the featherless tract of cervical skin, and it appears to be clinically effective. H i g h e r doses u p to 0.4 m g / k g may be required if a lower dose is not efficacious. W h e n treating large n u m b e r s of birds or an inbred strain, it is advisable to test a t r e a t m e n t r e g i m e n on a small n u m b e r of individuals to check for signs of toxicity. diarrhea, weight loss, a n d stunting. Screening for G psittaci is r e c o m m e n d e d in all featherpicking birds, and empirical t r e a t m e n t with metronidazole or fenbendazole is frequently used. Resistance to metronidazole and the commercial inavailability of o t h e r nitroimidizoles have m a d e effective t r e a t m e n t m o r e challenging for the clinician. In most instances, protozoal infections only b e c o m e recognized as a clinical p r o b l e m when increased mortalities in an aviary p r o m p t a clinical workup. Control a n d prevention througfi improved hygiene and h u s b a n d r y practices are often m o r e i m p o r t a n t in disease m o d u l a t i o n than actual treatment. Treating large n u m b e r s of birds in aviaries is often difficult. Drugs are frequently administered through the food or water, but these routes are less effective than direct administration of medication. H e l m i n t h parasites are not c o m m o n in companion birds, although they may be seen in wild-caught specimens or in animals k e p t in o u t d o o r cages with dirt substrate. All new birds should be screened with fecal examinations, but annual reexamination of healthy birds may not be necessary for i n d o o r pets or animals kept in raised-floor cages. Cestode infections are overlooked frequently in wild-caught parrots. Prophy-

Summary
Protozoal parasites are m o r e c o m m o n in companion and aviary birds than helminths. Giardiasis in pet birds may be associated with featherpicking and self-mutilation, as well as causing

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lactic t r e a t m e n t with b r o a d s p e c t r u m a n t h e l m i n tics such as i v e r m e c t i n a n d p r a z i q u a n t e l s h o u l d be c o n s i d e r e d i n p a r r o t s with a n u n k n o w n envir o n m e n t a l history. C o m p a n i o n birds are f r e q u e n t l y p r e s e n t e d to the v e t e r i n a r i a n for t r e a t m e n t o f e x t e r n a l parasites w h e n f e a t h e r loss b e c o m e s a p p a r e n t . External parasites are rarely the cause o f f e a t h e r loss i n c o m p a n i o n birds, e x c e p t for k n e m o d i k o p t i c mites. Clinical w o r k u p of f e a t h e r loss in birds s h o u l d i n c o r p o r a t e s c r e e n i n g tests for b o t h internal a n d e x t e r n a l parasites. R e s p o n s e to p r o p h y lactic t r e a t m e n t c a n also b e a diagnostic tool. l v e r m e c t i n t r e a t m e n t s h o u l d e l i m i n a t e external parasites t h a t c o m p l e t e t h e i r life cycle o n the pet. T h e s t a n d a r d dose o f 0.2 m g / k g a p p e a r s safe, a l t h o u g h birds are f r e q u e n t l y d o s e d at 0.4 m g / k g . S i m u l t a n e o u s t r e a t m e n t o f all susceptible a n i m a l s is imperative. Eetoparasites t h a t c o m p l e t e t h e i r life cycle off the host c a n b e h a r b o r e d i n the e n v i r o n m e n t . T h e s e parasites m u s t be t r e a t e d by c o m b i n a t i o n t h e r a p y of the a n i m a l a n d the e n v i r o n m e n t . P y r e t h r i n o r carbaryl p r o d u c t s a p p r o v e d for kittens can o f t e n be u s e d safely i n birds, b u t the avian t h r e s h o l d for toxicity is lower a n d c a u t i o n m u s t b e exercised. O r g a n o p h o s p h a t e s with insect growth i n h i b i t o r s can be u s e d as p r e m i s e sprays, as l o n g as all pets, cages, a n d food are r e m o v e d as directed. Ventilate the e n v i r o n m e n t well b e f o r e r e t u r n i n g the birds a n d do n o t allow direct access to t r e a t e d surfaces for 48 hours. As a final n o t e , n o antiparasitics are a p p r o v e d for use in c o m p a n i o n avian species. As is freq u e n t l y the case i n avian a n d exotic a n i m a l m e d i c i n e , effective t h e r a p y r e q u i r e s j u d i c i o u s extralabel usage of drugs. A g o o d client-patientv e t e r i n a r i a n r e l a t i o n s h i p a n d effective c o m m u n i cation m u s t b e established b e f o r e the a d m i n i s t r a tion o f these drugs.

Acknowledgment
T h e a u t h o r s t h a n k C h u c k Faulkner, Kreis Weigel, a n d Phil Snow for t h e i r assistance i n photographic preparation.

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