Enfermedades infecciosas aviares.pdf

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ASPERGILLOSIS

Aspergillosis is an infectious but not contagious diseaseof pet and wild birds that is caused by the ubiquitoussoil saprophyte Aspergillus. Infection generally occurs viainhalation of spores, resulting in primary lesions in thethoracic and abdominal air sacs and in the large airways(syrinx). Dissemination to other organ systems oftenoccurs. Two forms of the disease, acute and chronic,commonly are seen.

• The acute form, which is seen most often in wild birdsor psittacine birds under poor sanitary conditions,occurs after inhalation of an overwhelming numberof spores. Severe dyspnea may result, with rapid progression to death.

• The chronic form, seen most often in psittacines,usually follows a stressful event or immunosuppressedstate. Signs are often nonspecific and depend on thelocation of the infection and the immune status ofthe bird.

• The most common species isolated is Aspergillus fumi-gatus. A. flavus, A. niger, and other species play a lesserrole.

� Key Point Aspergillosis is an opportunistic disease,requiring predisposing immunosuppressive factorssuch as stress, malnutrition, and environmentalfactors.

EtiologyPredisposing factors include the following:

• Stress, as may occur in shipping, quarantine, or move-ment to an unfamiliar environment. Stress also mayresult from a prolonged illness, such as chlamydiosis,or after a traumatic event, such as an injury or smokeinhalation.

• Malnutrition or vitamin deficiencies, especially hypo-vitaminosis A, often occur in birds on diets consistingof seed only.

• Prolonged antibiotic or corticosteroid use may cause under-lying immunosuppression. For example, aspergillosismay occur after treatment for chlamydiosis owing to

the immunosuppressive effects of tetracycline in con-junction with the debilitated state of a diseased bird.

� Key Point Suspect aspergillosis when clinical signs do not respond to or worsen with antibiotictreatment.

• Environmental factors:• Poor ventilation in conjunction with damp litter

(especially corn-cob litter) soiled with feces pro-motes spore formation.

• Poor sanitation, such as when nest boxes and incu-bators are cleaned inadequately, can predisposebirds to aspergillosis.

Clinical SignsAcute Form• Signs include anorexia, dyspnea, and cyanosis.• Sudden death may occur without signs.

Chronic FormThe onset is insidious, and signs vary depending on thelocation of the infection.

Respiratory SystemSigns depend on the area affected. Respiratory signs willonly occur if lesions impede airflow, for example,aspergillus granuloma formation in the syrinx, air sacthickening, and exudate accumulation in the air sacs.

Upper Respiratory Tract Signs

• Signs include a change in voice, reluctance to talk,and a respiratory click that can be heard when lesionsinvolve the main airways, especially the syrinx.

• Severe, life-threatening dyspnea often occurs if thelesions are large enough to occlude the trachea orsyrinx. In some cases, these may be the only lesionspresent.

• Mucoid to mucopurulent nasal discharge occurs inbirds with Aspergillus rhinitis or sinusitis.

• Erosion of the nasal conchae and misshapened naresare seen in advanced cases of nasal aspergillosis.

169 Avian Infectious DiseasesDon J. Harris / Barbara L. Oglesbee

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� Key Point Suspect aspergillosis when the ownerdescribes the bird as having “laryngitis.”

Lower Respiratory Tract Signs

• With mild to moderate aspergillus airsacculitis, theair sacs are usually able to function normally (i.e.,inflate and deflate to move air through the lungs). Inthese birds, respiratory signs are mild or absent, especially in birds that are sedentary.

• Dyspnea or exercise intolerance is seen in birds withextensive pneumonia or air sac involvement. Air sacsmay become thickened or filled with caseousexudate, inhibiting their ability to move air.

• Respiratory signs are more likely to occur earlier inbirds that are permitted to fly, as oxygen demand isgreater in these birds.

� Key Point Birds with lower respiratory tractinvolvement often do not exhibit respiratory signsuntil disease is extensive. The most common clin-ical signs in birds with lower respiratory tractaspergillosis are nonspecific, such as weight loss,depression, and poor feathering.

Liver and KidneysDiarrhea, anorexia, and polyuria may be seen. Greendiscoloration of the urates (biliverdinuria) and hepa-tomegaly occasionally are seen.

Nervous SystemAtaxia, torticollis, and paralysis may indicate centralnervous system (CNS) involvement. Compression of thesciatic nerve by a granulomatous Aspergillus lesion hasresulted in unilateral paralysis.

Nonspecific SignsThese are the most common signs. Weight loss, musclewasting, depression, lethargy, and poor feathering oftenare the only clinical signs.

DiagnosisHistory• The history may identify an underlying environmen-

tal or immunosuppressive factor.

Physical Examination• Examine the mouth and nares for mucus, exudates,

or deformation of the nares. Take samples from thetrachea or choana for fungal culture.

• Palpate the breast muscles and weigh the bird for evidence of weight loss and muscle wasting.

• Palpate the abdomen for evidence of organomegaly.• Auscultate the trachea and chest for abnormal respi-

ratory sounds and a respiratory click.

Laboratory Tests• A severe leukocytosis often ranging from 25,000 to

100,000 white blood cells (WBCs) per microliter isoften present.

• The differential count usually reveals heterophilia,monocytosis, lymphopenia, and anemia of chronicdisease. Occasionally, the complete blood count(CBC) is normal.

• Increased serum total protein with an increased betaor gamma globulin portion is seen on plasma proteinelectrophoresis (EPH) in birds with chronic disease.

• Aspartate aminotransferase (AST), lactate dehydro-genase (LDH), and creatine phosphokinase (CPK)levels usually are increased, especially with hepaticinvolvement.

Endoscopy

� Key Point Endoscopy is invaluable for the diagno-sis of aspergillosis.

• When there are episodes of severe dyspnea, trachealendoscopy may reveal a single lesion occluding thesyrinx.

• If a thick, white discharge or plaque is seen in thetrachea, obtain a sample for cytologic examinationand culture on Sabouraud’s dextrose agar.

• Endoscopy of the abdominal air sacs may revealdiffuse cloudiness or white to yellow plaques. Theseplaques may become covered with a green-gray pigmented mold; obtain samples for culture andcytology.

• Samples for culture and cytology may sometimes beobtained by performing an air sac wash.

Radiography• Radiographic changes may not be visible in early

cases.• Radiographs are generally not sensitive for defining

tracheal granulomas, although if a soft tissue mass is seen within the trachea, aspergillosis should be suspected.

• In birds with nasal or sinus aspergillosis, performcranial imaging such as skull radiographs, computedtomography (CT), or magnetic resonance imaging(MRI) to assess for the presence of granulomatous orcaseated masses. Skull radiographs are less sensitivefor picking up small lesions but are more readily avail-able than CT or MRI.

• In advanced disease, radiographic abnormalities can include loss of definition of the air sacs, asymmetry of the air sacs due to air sac collapse orhyperinflation, and focal densities in the lungs or air sacs.

• Hepatomegaly or renomegaly may be visible radi-ographically when there is involvement of theseorgans.

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1742 Section 12 / Diseases of Avian and Exotic Pets

TreatmentTreatment is most successful with early lesions confinedto the nares or syrinx and when aggressive treatment isinstituted early. A combination of topical treatmentsuch as tracheal injection, sinus flush or nebulization(depending on the site of infection), systemic treat-ment, and debridement are usually necessary for suc-cessful outcome. Treatment is prolonged, requiringweeks to months of outpatient therapy. Continue treat-ment until clinicopathologic changes normalize andradiographic and endoscopic lesions resolve.

Antifungal Agents• For birds with severe infections, administer ampho-

tericin B (Fungizone, Squibb), 1.5mg/kg q8h IV, for3 to 7 days. Mask the bird with isoflurane anesthesia,and maintain an IV catheter for each injection.

• In birds with syringeal lesions, administer ampho-tericin B by intratracheal injection, using a tomcaturinary catheter (Sherwood Medical) at a dosage of1mg/kg q12h for up to 1 month.

• For nasal aspergillosis, a solution of 0.05mg ofamphotericin B per milliliter of sterile water may beused to flush the nares.

• For mycotic airsacculitis, make a solution of 1mg ofamphotericin B per milliliter of sterile water and neb-ulize q12h for 15 minutes. Alternatively, nebulize withclotrimazole (10mg/ml in polyethylene glycol).

• Amphotericin B is potentially nephrotoxic and maycause bone marrow suppression. Monitor serum uricacid concentration to detect toxicity.

• Administer itraconazole (Sporanox, Janssen), 10mg/kg q12h (with food) alone, in conjunction with, orfollowing amphotericin B treatment. Usually at least6 to 8 weeks of treatment are necessary; some birdsmay require treatment for months. Obtain a plasmabiochemistry profile every 2 to 4 weeks to monitor forhepatotoxicity during treatment. African grey parrotsappear to be more sensitive to the hepatotoxic effectsof itraconazole. Use with caution, and discontinueuse if anorexia occurs.

• Alternatively, administer fluconazole (Diflucan,Roerig), 15mg/kg q24h PO, for up to 6 weeks withor after amphotericin B. Fluconazole is usually not aseffective as itraconazole, but it may be better toler-ated by some species, especially African grey parrots.

• Terbinafine (Lamisil, Novartis), 10mg/kg q12h, POhas been anecdotally used to successfully treataspergillosis in birds.

• 5-Fluorocytosine (Ancobon, Roche Labs), 50 to 150mg/kg q12h PO, in conjunction with or after ampho-tericin B treatment has been used to treat aspergillo-sis in raptors. Give the higher dosage for activeinfections; use the lower dosage, often prophylacti-cally, for 10 to 14 days in high-risk patients.

Antibiotic Therapy• Antibiotic treatment based on culture and suscepti-

bility testing may be necessary if a secondary bacter-ial infection is present.

Surgical Treatment• Surgical removal of large accumulations of caseous

material from air sacs in conjunction with systemictreatment and nebulization is often necessary for successful treatment.

• Surgical debridement of devitalized material fromthe upper airways and sinuses may facilitate topicaltherapy.

Supportive Care• Fluid therapy, forced alimentation (see Chapter 168),

and a warm environment are required for debilitatedbirds.

Prognosis• The prognosis is poor to grave, depending on the

severity of the disease.

Prevention• Because Aspergillus is an opportunistic pathogen,

attempt to reduce predisposing immunosuppressivefactors such as stress and malnutrition.

• Treat birds with prolonged antibiotic therapy orother birds at risk with 5-fluorocytosine prophylacti-cally (as previously described).

� Key Point To avoid inhalation of an overwhelmingnumber of Aspergillus spores, house birds in awell-ventilated area. Do not use organic materialsas bedding in nest boxes.

CHLAMYDIOSIS

Avian chlamydiosis is known as psittacosis when occur-ring in psittacine species and ornithosis when occurringin passerine species. The incidence in pet birds is highand is reportedly 15% to 30% of those tested.

EtiologyAvian chlamydiosis is caused by the obligate intra-cellular bacteria Chlamydophila psittaci. The organisminfects many species of wild, domestic, and exotic birds, domestic mammals, and humans. Manifestation of thisdisease varies from subclinical to fatal, depending on the strain of C. psittaci involved and the species ofbird affected.

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� Key Point Chlamydiosis is potentially zoonotic anda reportable disease in many states. A valuableresource for practicing veterinarians, the com-pendium of psittacosis control is updated yearly bythe Association of Public Health Veterinarians andis available at www.avma.org/.

Life Cycle and TransmissionChlamydophila have a biphasic life cycle.

• Infectious, extracellular elementary bodies are shedin oral or nasal secretions and feces and may surviveoutside the host for a month or longer. Dissemina-tion may occur via shared food dishes or aerosolizedfecal dust.

• Elementary bodies are inhaled or ingested and enterhost cells, where they undergo cellular rearrange-ment to form reticulate bodies, the replicating form ofthe organism.

• After replication, initial bodies reorganize to forminfectious elementary bodies, which are released onrupture of the host cell. Elementary bodies then maybe disseminated to cells of the liver, spleen, lungs,intestines, kidneys, gonads, and CNS.

Clinical Signs

� Key Point Clinical signs vary greatly, depending onthe organ system affected, virulence of the organ-ism, and immune status of the host.

• Inapparent carriers are common. These may be birdsthat have recovered from clinical illness or that mayhave never shown signs. High numbers of organismsmay be shed intermittently from the feces or nasal ororal secretions, putting other pet birds and humansat risk.

• Clinical signs may develop in these carriers when theyare stressed or otherwise immunocompromised.

Acute Form• The acute form of the disease is seen more often in

young or immunosuppressed birds. Signs mayinclude the following:• Liver or gastrointestinal (GI) signs, such as in-

appetence, green-gray diarrhea, biliverdinuria(lime-green urates), and occasionally vomiting orregurgitation

• Respiratory signs, including serous to purulentnasal or ocular discharge, labored breathing, ble-pharitis, and conjunctivitis

• Nonspecific signs, including ruffled feathers,weight loss, and depression

• Without treatment, signs may progress over a fewweeks, leading to prostration and death.

Chronic Form• Nonspecific signs such as muscle wasting, poor feath-

ering, lethargy, and inappetence may be the onlysigns. These signs are most often seen in birds withchronic hepatopathy.

• Recurrent conjunctivitis and mild respiratory signsare often seen.

• Occasionally, CNS signs (e.g., torticollis, seizures, andrear limb paresis or paralysis) may be seen alone.

DiagnosisHistory• Recently acquired birds may be at higher risk because

of the increased exposure and stress associated withtransport.

� Key Point Recently acquired birds are not the onlyones at risk; birds may harbor the disease formonths and even years before manifestation ofclinical signs.

Physical Examination• Findings may be normal in inapparent carriers.• Suspect chlamydiosis in birds with poor feathering,

weight loss, or signs of GI or respiratory disease.

� Key Point Lime-green urates are highly suggestiveof chlamydiosis.

Laboratory Tests• Leukocytosis, often >40,000 WBC per microliter

demonstrating heterophilia with toxic heterophils,usually is seen in acute disease. Relative monocytosisand reactive lymphocytes and basophilia are oftenpresent.

• The WBC count may be normal in subclinical cases.• A low packed cell volume is common in both acute

and chronic disease.• Serum protein usually is elevated as a result of

chronic inflammatory stimulation. Plasma proteinelectrophoresis may demonstrate hypergammaglobu-linemia and hypoalbuminemia.

• AST, LDH, bile acids, creatine kinase, and/or uricacid levels may be elevated, depending on the organsystem affected.

Radiography• Hepatosplenomegaly is the most common radi-

ographic feature.• Diffuse clouding of the air sacs may be present with

airsacculitis.• Often, no radiographic abnormalities are seen with

chronic disease.

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Antigen CaptureImmunoassay

• An immunoassay (IDEIA antigen system, CaliforniaAvian Laboratories, Citrus Heights, CA) may be usedto detect chlamydial antigen in naso-ocular dis-charges, pharyngeal swabs, and feces. The chlamydialorganisms do not have to be viable for antigen to bedetected.

• Shedding of organisms is often intermittent, produc-ing false-negative results.

• Shedding is inhibited temporarily in birds testedwithin 1 to 2 weeks of treatment with erythromycin(e.g., Ornacyn, available in pet stores), doxycycline,tetracyclines, penicillins, chloramphenicol, tylosin,and quinolones.

• False-positive results also are common owing to cross-reactivity with some gram-negative bacteria. Confirmpositive results using another method of testing.

SerologyComplement Fixation

• In the complement fixation (CF) test (Texas Veteri-nary Medical Diagnostic Laboratory, College Station,TX), single serum samples are of value if the titer issufficiently high.

• Titers up to 1:8 are considered negative, 1:16 to 1:32is suspicious, and >1:64 is positive. A fourfold rise intiter over a 4-week period is considered most signifi-cant. Titers may remain high following successfultreatment.

• Young birds, budgerigars, cockatiels, canaries, andfinches with chlamydiosis may not produce antibodytiters high enough to be detectable by CF, makingnegative results unreliable in these birds.

• False negatives may occur when birds are tested earlyin the course of the disease, before sufficient anti-body formation.

Latex Agglutination

• This test detects serum immunoglobulin M (IgM),which indicates a current infection.

• False-negative results are common in cockatiels, love-birds, budgerigars, and some young birds, as well asin later stages of the disease.

Elementary Body Agglutination (Texas VeterinaryMedical Diagnostic Laboratory)

• This test primarily detects IgM and is more sensitivethan latex agglutination.

• IgM appears in the early phase of infection and wanesafter approximately 3 weeks.

• False positives are rare, but false negatives arecommon.

• An elementary body agglutination titer of 80 suggestsan active infection. Titers of 10 to 40 may be seen with

low-grade infections, exposure, or recently treatedinfections.

Immunofluorescent Antibody

• This test primarily detects IgG, which appears in laterstages of infection.

• False positives are more common than with othertests.

DNA Probe

• A highly sensitive and specific DNA probe for thedetection of Chlamydophila infection is commerciallyavailable. Samples may be taken from blood, theoropharynx or cloaca.

• A positive result indicates an active infection, as falsepositives are unlikely.

• For Chlamydophila organisms to be detected inoropharyngeal secretions or cloacal swabs, the birdmust be actively shedding organisms. Therefore, false-negative results are possible. However, a DNA probeis significantly more sensitive for detecting sheddingthan any other available method.

• For Chlamydophila organisms to be detected in bloodsamples, the bird must be bacteremic. Therefore,false-negative results are possible.

• To increase the likelihood of detecting infection,submit samples from the oropharynx, cloaca, andblood simultaneously.

Isolation on Culture• Isolation requires live Chlamydia organisms.• Success is highly dependent on proper transport

medium, transport conditions, and previous anti-biotic treatment.

• The chlamydial agent may be propagated in tissueculture, mice, or embryonated chicken eggs. Obtainpostmortem samples from the spleen, liver, or airsacs.

• Isolation may be possible from antemortem exudateor fecal samples; however, shedding often is inter-mittent. This is the most reliable postmortem confirmation.

� Key Point False-negative results are commonwhen testing for Chlamydophila organisms owingto intermittent shedding, administration of inhi-bitory antimicrobials, and production of low anti-body titers in the face of active disease. Base thediagnosis of chlamydiosis on a combination ofDNA probe and serologic testing, clinical signs,hematology, serum biochemical profile, plasmaprotein electrophoresis, and radiography.

TreatmentTetracyclines are the most effective antibiotics againstChlamydophila.

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� Key Point Tetracyclines must be administered for45 days to be effective in eliminating infection.Client compliance is often a problem, especiallywhen once- or twice-daily oral administration isprescribed. Treat clinically ill birds by a parenteralor direct oral route. Use food- and water-baseddosage regimens in stable birds only. Monitorthese birds to ensure that the treated food or wateris being appropriately consumed.

• Doxycycline (Vibramycin, Pfizer) is the drug of choicefor treatment of Chlamydophila. It is available in anoral (suspension, solution, or capsules) or IV form inthe United States. The IV form should not be injectedIM or SC.• The dosage of doxycycline varies, depending on

the species. Administer 25mg/kg q24h to macawsand cockatoos and 35 to 50mg/kg q24h to Africangrey parrots, cockatiels, and Amazon parrots.Senegal parrots require 30mg/kg q12h. Somebirds will regurgitate on higher doses. Doxycyclinemay be mixed with a small amount of a favoritefood, as long as that food is immediately and completely consumed.

• For cockatiels and budgerigars, doxycycline may be added to a mixture of hulled millet seed and oats. Lightly coat the seed-oat mixture with sunflower oil, and add doxycycline at a rate of 300mg/kg of seed mix. Feed birds this mix exclu-sively for 45 days. Use this route only in stable birds.Monitor birds to ensure that they are eating thisdiet.

• Doxycycline for IM injection (Vibravenos, Pfizer) isavailable in countries outside of the United Statesand may be imported for use in birds. Administer75 to 100mg/kg IM every 7 days for 6 weeks.

• Doxycycline may be effective for some birds whenadded to the drinking water. Use this route only instable birds, and carefully monitor the birds toensure that the water is palatable and that waterconsumption is normal. Birds may overconsumewater during hot, dry periods or while on dry orpelleted diets, resulting in overdosage. Under-dosage, resulting in treatment failures and possiblydehydration, may occur if birds refuse to drinktreated water. Species that normally consume verylittle water, such as budgerigars cannot be effectivelytreated using water-based medication. Dosages are available for a limited number of species andinclude 300 to 400mg/L water for cockatiels, 400mg/L water for Goffin’s cockatoos, and 600 to800mg/L water for African grey parrots.

• Secondary mycotic or bacterial infections owing toalterations of the normal enteric flora, stress, andimmunosuppression are a common problem in birdstreated with doxycycline.

• Thoroughly clean the environment following treat-ment to remove chlamydia organisms and preventreinfection.

• Treat all birds sharing the same air space as birdsdiagnosed with Chlamydophila for 45 days.

Supportive Care• Many birds with acute chlamydiosis are seriously ill

and require supportive care such as fluid therapy,forced alimentation (see Chapter 168), and heat, aswell as antibiotic therapy if secondary bacterial infec-tion is present.

Prevention• Because inapparent carriers are common and an

accurate screening test is not available, it is difficultto prevent the introduction of Chlamydia organismsinto a flock when purchasing new birds. A combina-tion of serology and DNA probe to screen for chla-mydiosis is recommended, with repeated yearly testing.

PSITTACINE VIRAL DISEASES

Psittacine Circovirus: Psittacine Beak and Feather DiseasePsittacine beak and feather disease (PBFD) is an infec-tious, sometimes fatal disease characterized by featherloss, feather dystrophy, occasional beak deformity, and destruction of the thymus and bursa. Originallybelieved to affect only white and pink cockatoos and afew other South Pacific psittacine birds, the disease hasbeen reported in more than 30 species of Asian andSouth Pacific psittacine birds and is believed to becapable of causing disease in many others. Occurrencein Central and South American psittacine birds is rare.Death is attributed to secondary bacterial, viral, ormycotic infections or to general debilitation.

Etiology• PBFD is caused by a non-enveloped, single-stranded

DNA virus (PBFDV) that is structurally similar to theporcine circovirus and chicken anemia agent.

Transmission

• Virus may be recovered in the feces, crop secretions,and feather dust of infected birds. Being non-enveloped, PBFDV is thought to be extremely stablein the environment and may be resistant to many disinfectants.

• Infection may occur by inhalation or ingestion of thevirus.

• PBFDV is believed to spread throughout the body of an infected bird via circulating WBCs. There is evidence that inapparent carriers may exist.

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� Key Point Feather dust is a major method of trans-mission and environmental persistence of PBFDV.Feather dust may be dispersed through natural airflow and may contaminate food dishes, cages, birdcarriers, insects, and human clothing.

Clinical SignsPBFDV may cause peracute, acute hematologic, acutedermatologic, or chronic disease.

Peracute FormThis form is seen in neonates, most often cockatoos andAfrican grey parrots, and may be associated with cropstasis, pneumonia, diarrhea, weight loss, and rapiddeath. There are few feather lesions.

Acute Hematologic FormThis form is seen almost exclusively in African greyparrots and on occasion in other African species.

• Patients usually present near or just after weaning agewith severe weakness and depression.

• The primary hematologic feature is a marked pancy-topenia, with WBCs sometimes absent and the hema-tocrit dropping to as low as 4%.

• Recovery is rare but has occurred with supportivecare.

Acute Dermatologic FormThis form is seen in birds as young as 30 days of age,when feathers begin to replace neonatal down.

• Feather lesions include fractures, necrosis, hemor-rhage, curvature, and premature shedding ofaffected feathers.

• GI signs include diarrhea, crop stasis, and anorexia.There may be few feather lesions, especially in youngcockatoos, lovebirds, and African grey parrots.

• Death may follow the onset of clinical signs withindays to several weeks.

Chronic FormThis form usually is recognized in psittacines youngerthan 3 years of age but has been reported in birds asold as 20 years of age. Birds may live for months to yearsbefore succumbing to secondary infections or chronicdebilitation.

• Progressive feather abnormalities may be accompa-nied by beak lesions.

• Feather lesions include retained feather sheaths,bleeding within the pulp cavity, fractured feathers,clubbed feathers, circumferential constrictionswithin the feather shaft, curled or deformed feathers,and stress lines within feather vanes.

• Feather loss typically begins with powder down feath-ers. Contour, crest, wing, and tail feather loss is

roughly symmetrical and progresses with each molt.Some birds become completely bald and remain sountil death (months to years).

• Beak lesions often occur in galahs and Moluccan andsulfur-crested cockatoos but are not routinely seen inother species. Lesions may include oral ulcerationand elongation and fractures of the beak, oftenaccompanied by secondary mycotic or bacterial infec-tions. Beak lesions usually occur after chronic featherloss but also can occur in birds with mild featherlesions. In cockatoos, the beak may appear shiny andblack because of the absence of powder that settleson the beak during preening.

DiagnosisHistopathology

• In affected feathers, typically there are ballooningdegeneration and necrosis of epithelial cells in theepidermal collar and in the epidermal basal andintermediate zones of the developing rachis.

• Non-suppurative inflammation, characterized byperivascular accumulations of heterophils, plasmacells, lymphocytes, and macrophages, is the primarylesion seen in the feather pulp.

• Beak lesions histopathologically are similar to thoseseen in the feather shafts.

• The thymus and bursa typically are atrophied, withfocal areas of necrosis and degeneration. Theselesions are thought to cause immunosuppression.

Hematoxylin and Eosin Stain

• Basophilic intranuclear and intracytoplasmic inclu-sion bodies may be seen with hematoxylin and eosin(H&E) staining in the feathers, pulp, and follicularepithelium. These were once considered diagnosticfor PBFDV; however, other viruses (e.g., avian poly-omavirus) may induce similar intranuclear inclusionbodies.

DNA Probe

• A highly sensitive and specific viral DNA probe forthe detection of PBFDV infection is commerciallyavailable (Infectious Diseases Laboratory, Universityof Georgia, Athens, GA). Birds latently infected canbe detected by submitting 0.2 to 0.5ml of wholeunclotted blood. This test allows veterinarians toscreen for birds subclinically infected with PBFDV.

• Birds testing positive on a blood DNA probe forPBFDV with no feather lesions should be retested in90 days. If negative, the bird has cleared the virus andis likely immune. Birds continuing to test positiveafter 90 days are subclinically infected and maydevelop feather lesions at a later date.

• Birds testing positive on a blood DNA probe forPBFDV with feather lesions have an active infection.It is still possible that DNA-positive birds will mount

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an immune response, clear the infection, andbecome blood DNA negative. However, keep birdswith feather lesions strictly isolated until all feathersbecome normal. Abnormal-appearing feathers andtheir feather dust should be considered infectious.Monitor these birds for the development of normalfeathers.

• Birds with feather lesions that continue to test posi-tive and continue to grow abnormal feathers areunlikely to recover and will continue to be infectiousto other birds as long as abnormal feathers arepresent.

� Key Point Keep all birds with abnormal feathersstrictly isolated. Birds may become blood DNAnegative before all affected feathers are molted.However, as long as abnormal feathers and theirassociated feather dust are present, the bird is con-tinuing to shed virus and should be consideredcontagious.

Treatment• There is currently no effective treatment for PBFDV.• Provide supportive care (e.g., good nutrition,

debridement of lesions, beak trimming, and heat)and antimicrobial therapy for secondary bacterialand fungal infections for chronically infectedpatients.

Prevention

� Key Point Using the DNA probe, test all birds forPBFDV prior to admission to the aviary.

• Isolate all birds testing positive for PBFDV to preventcontact with non-infected birds.

• Isolate all birds with feather lesions caused by PBFDVfrom direct or indirect contact with other birds untilall abnormal feathers have been replaced withnormal feathers.

• Exercise care to prevent feather or fecal dust frominfected birds contaminating non-infected birds, particularly psittacine neonates.

• Viral particles, which are resistant to practically alldisinfectants, may remain viable for more than 3years in a contaminated environment.

PolyomavirusEtiologyPolyomavirus is responsible for major economic lossesin commercial budgerigar aviaries (budgerigar fledg-ling disease, BFD). Polyomavirus also has been reportedto cause clinical disease in nearly all species of largepsittacine birds and in passerine birds.

Budgerigars that survive BFD infection may developfeather abnormalities commonly referred to as “French

molt.” The lesions of French molt, however, also may becaused by psittacine circovirus.

Transmission

• Polyomavirus may be present in feces, feather dust,and oronasal and oral secretions. These contami-nated materials may be inhaled or ingested by susceptible birds.

• Infected hens may pass the virus to offspring throughthe egg.

• Latent infections are common in budgerigars and arebelieved to be responsible for spread of this virus.Clinically normal parents may transmit polyomavirusto their offspring, some of which also become inap-parent carriers.

• There is currently no evidence to support the exis-tence of persistent infections in larger psittacinebirds. However, some psittacine birds may becomeinfected without demonstrating clinical signs andshed virus before eliminating the infection. Thus,birds with subclinical infections may be responsiblefor viral outbreaks, especially in pet stores and breeding facilities where susceptible neonates areexposed.

Clinical SignsHatchling Budgerigars <15 Days Old

• Signs include abdominal enlargement, delayed cropemptying, subcutaneous hemorrhage, retardedgrowth, and abnormal feathers.

• Sudden death is common. Reported mortality ratesvary from 30% to 100% of affected hatchlings.

Budgerigars >15 Days Old

• Signs are similar to those described for hatchlings;however, the mortality rate is much lower.

• Fledglings may produce deformed primary flightfeathers that break off at the base, leaving the birdsunable to fly thus called “runners.”

Neonatal ParrotsNon-budgerigar psittacine neonates are extremely susceptible to polyomavirus and are likely to developclinical signs.

• Clinical signs usually develop at the time of weaningbut may be seen anywhere from 14 to 150 days of age.

• Sudden death with and without clinical signs iscommon; birds that develop clinical signs usually diewithin 12 to 48 hours.

• Signs include diarrhea, delayed crop emptying, depres-sion, anorexia, widespread hemorrhage, polyuria,and posterior paresis and paralysis.

• Unless immunosuppressed, adult non-budgerigarpsittacine birds demonstrate mild or no clinical signs and eventually eliminate the virus. However,

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these birds are likely to shed virus before recoveryand thus serve as a source of environmental contamination.

Diagnosis• Gross pathologic changes include hydropericardium,

cardiomegaly, pale kidneys, ascites, hepatomegaly,splenomegaly, and diffuse petechial and ecchymotichemorrhages in the subcutis, intestines, myocardium,epicardium, and serosal surfaces.

• Histopathologic demonstration of karyomegaly withbasophilic intranuclear inclusion bodies in thekidneys, liver, spleen, heart, or feather follicles suggests polyomavirus.

• Confirmatory diagnosis requires the identification ofviral antigen using virus-specific antibodies or thedetection of viral nucleic acid using virus-specificDNA probes.• Highly specific and sensitive viral DNA probes

(Infectious Diseases Laboratory, University ofGeorgia, Athens, GA or Avian Research AssociatesLaboratory, Milford, OH) can detect polyomavirusin infected tissue, cloacal swabs, and fresh feces of birds shedding virus. Identify birds that are shedding the polyomavirus by submitting a cloacalswab for testing. False-negative results may occur if the bird is not shedding virus at the time oftesting.

Treatment• Provide supportive care, as described for PBFD.

Prevention

� Key Point Quarantine all new birds for 30 daysbefore entrance into an aviary. Perform DNA probetesting on all birds before entrance into an aviary.Isolate birds testing positive.

• Do not keep budgerigars in the vicinity of unvacci-nated neonatal parrots.

• Do not mix neonates from different sources or returna neonate to the nursery after exposure to otherbirds.

• Disinfection with chlorine solution (50ml/L ofwater) or prolonged contact with iodophors inacti-vates the virus.

VaccinationA United States Department of Agriculture (USDA)approved inactivated avian polyomavirus is consideredsafe and effective (Biomune, Lenexa, KS). Administerthe vaccine subcutaneously. Mild injection site reactionshave been reported but should resolve within 3 to 6weeks after injection. Follow vaccination guidelines pro-vided by the manufacturer.

Pacheco’s DiseaseAlso known as herpes hepatosplenitis, Pacheco’s diseasecauses an acute, necrotizing hepatosplenitis that usuallyis rapidly fatal. The hallmark of Pacheco’s disease issudden death in birds that appear clinically normaluntil just before death. All species of psittacines of all ages, both imported and domestically raised, are susceptible.

Etiology• Several strains of antigenically unrelated herpesvirus

may cause Pacheco’s disease; herpesvirus persists byinducing latent disease, with periodic reactivationand shedding. Clinical disease is dependent on thevirus serotype, the species, and the immune status ofthe infected bird.

Transmission

• Although the exact route of Pacheco’s disease virustransmission is unknown, this virus is present in highnumbers in the feces and pharyngeal secretions ofsymptomatic and asymptomatic carrier birds. Thus,direct-contact contaminated aerosols and fecal-oralroutes are the most likely routes of virus transmission.

• Herpesvirus is an enveloped virus and is relativelyunstable in the environment. Anecdotal reportssuggest that humans can serve as vectors, even withrelatively long intervals between bird exposure. Anincubation period of 3 to 7 days is common.

� Key Point Asymptomatic carriers of viruses thatcause Pacheco’s disease are common and often areincriminated in disease outbreaks. Any psittacinebird that has been exposed to or recovered fromherpesvirus infection may potentially become acarrier.

Clinical Signs• Sudden death without premonitory signs has been

reported most frequently in Amazon parrots, cocka-toos, lovebirds, Pionus parrots, and parakeets.

• Nonspecific signs include lethargy, anorexia, vomit-ing, diarrhea (sometimes hemorrhagic), biliver-dinuria, naso-ocular discharge, and occasionally CNSsigns.

• Signs often progress to death within several days;however, recovery has been reported in some birdswith clinical signs consistent with Pacheco’s diseasevirus.

DiagnosisAntemortem Diagnosis

• Virus isolation from feces may reveal infection;however, viral shedding may be intermittent, makingit ineffective for the detection of carrier birds.

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• A reliable serologic test is not commercially available.• A DNA probe is currently available that theoretically

detects all known herpes serotypes affecting pet birds.Evidence suggests that the oral cavity or the cloaca isa highly reliable site for the collection of samples. Todetect virus, birds must be shedding virus at the timethe sample is taken, so false negatives are possible.The significance of a positive test is currently unclearat the time of this writing. A positive test result indi-cates that the bird is shedding a herpesvirus; however,what type of clinical disease, if any, that the detectedherpesvirus may cause is unknown.

Postmortem Diagnosis

• Gross lesions may include hepatomegaly, spleno-megaly, hemorrhagic enteritis, sinusitis, pneumonia,airsacculitis, and congestion and hemorrhage in thespleen, liver, and kidneys. Gross lesions may not beapparent in birds with peracute death.

• Histopathologic lesions often include hepatic andsplenic necrosis.

• Virus may be isolated from liver, spleen, small intes-tine, and pancreas.

� Key Point Basophilic and eosinophilic Cowdry typeA inclusion bodies, often present in the liver,spleen, kidneys, and pancreas, suggest herpes-virus infection.

Treatment• Oral administration of acyclovir (Zovirax, Burroughs

Wellcome) (80mg/kg q8h ¥ 7d) or the IV form givenIM (40mg/kg q8h) has been reported to decreasemorbidity and mortality during Pacheco’s diseaseoutbreaks.

• Supportive care, including fluids, heat, assisted ali-mentation, and antibiotic therapy for secondaryinfections, may be of some benefit.

Prevention• Do not mix susceptible birds with suspected carriers.• Sanitation is critical in disease prevention because

viral spread within an aviary occurs primarily bycontact with contaminated feces and pharyngealsecretions.

• Thoroughly clean water and feed dishes followed bytreatment with a disinfectant. Herpesvirus typically isinactivated by desiccation and through contact withmost disinfectants.

• Instruct all aviary personnel to practice soundhygiene by washing and disinfecting hands beforeentering the aviary and after handling individualbirds or cages.

• Reduce stress to help prevent shedding and spreadof the virus.

VaccinationLicensed Pacheco’s disease virus vaccine is currentlyavailable (Biomune, Lenexa, KS). Two vaccinations sub-cutaneously in the inguinal area 4 to 8 weeks apart followed by yearly boosters are recommended. Thevaccine is not effective against all avian herpesvirusserotypes.

Other HerpesvirusesThirteen different herpesviruses are known to affectbirds. The pathogenicity, host spectrum, and relation ofthese viruses largely are unknown.

• The only herpesvirus of known clinical significancein psittacine birds (besides those that cause Pacheco’sdisease) is Amazon tracheitis virus.• This virus causes a pseudomembranous tracheitis,

pharyngitis, and sinusitis.• Signs include dyspnea, change or loss of voice,

abnormal respiratory signs, and occasionallyhemoptysis.

• Base diagnosis on virus isolation or typical Cowdrytype A inclusion bodies in the tracheal mucosa atnecropsy.

• Treatment is similar to that discussed for Pacheco’sdisease virus.

• Based on histologic findings, another herpesvirushas been reported as the suspected etiology of wart-like lesions occurring on the feet of cockatoos.

• Limited success has been reported in these caseswith treatment with topical application of acyclovircream.

PoxvirusesPoxvirus is commonly seen in canaries, pigeons, andwild birds. It is rarely seen in pet psittacine birds due torecent restrictions on importation of these birds.

Two forms of clinical disease caused by avian pox-viruses commonly are encountered:

• Dry, or cutaneous, pox is characterized by discretenodules on unfeathered skin.

• The more common wet, or diphtheritic, pox is char-acterized by fibronecrotic lesions in the respiratorysystem, conjunctiva, and pharynx.

The type of disease that develops may depend on thestrain of infecting virus, route of infection, and thespecies, age, and condition of the host.

Etiology• Avipoxviruses replicate in the cytoplasm of epithelial

cells, inducing characteristic intracytoplasmic, lipo-philic inclusion bodies called Bollinger bodies.

• Host susceptibility and virulence of the virus varieswith the strain of avipoxvirus. Most poxvirus strainsare relatively host specific.

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Transmission

• Poxvirus is incapable of penetrating intact epithe-lium. Entrance into the host is gained through pre-existing traumatic lesions or often is introduced intoa flock via mosquito vectors.

• Virus is shed in epithelial crusts and exudates duringactive infection and in feces, skin, and feather quillsduring recovery and in latent infections.

• Virus transmission may occur through direct contactwith affected birds or through contact with contami-nated soil, food, or cages.

• Poxviruses are very resistant to desiccation, humidity,and light and may survive up to 1.5 years in the environment.

• Recurrence of poxvirus lesions has been reported insome species.

• It is postulated that asymptomatic carriers of poxvirusmay exist.

Clinical SignsDiphtheritic (Wet) Pox

• Yellow to gray-brown fibronecrotic plaques may occuron the mucosa of the mouth, choana, beak, esopha-gus, and trachea.• Multiple plaques may coalesce, forming tightly

adherent diphtheritic membranes, which, if forci-bly removed, leave a raw, hemorrhagic surface.

• Respiratory epithelium may be affected, with result-ing dyspnea, rales, serous to purulent naso-ocular discharge, lethargy, and anorexia.

• Death due to secondary bacterial bronchopneumo-nia is common.

Cutaneous (Dry) Pox

• Signs include papules, pustules, and scabs on theunfeathered portions of the skin.• Secondary bacterial and fungal infections are

common and may result in swelling or abscessation.• If no secondary bacterial infection occurs, the

lesions may resolve without scarring in 10 to 14days.

• In canaries and finches, wart-like lesions are commonon unfeathered skin.

Diagnosis• Clinical lesions suggest the diagnosis.• Epithelial hyperplasia with ballooning degeneration

and intraepithelial vesicles seen on histopathologicexamination suggest avian pox.

• Intracytoplasmic lipophilic Bollinger bodies arepathognomonic.

Treatment• Treatment of secondary fungal or bacterial infections

is based on culture and susceptibility testing.

• Birds often have systemic illness, and mortality ratesare high.

• Provide supportive care such as supplemental heat,fluid therapy, and assisted alimentation, if mouthlesions are present.

• Prophylactic administration of systemic broad-spec-trum antibiotics may prevent secondary bacterialinfections.

PreventionVaccination

Vaccines are available for canaries, pigeons, and domes-tic fowl. Use of these vaccines is restricted to high-riskpopulations, such as recently imported birds or birdsexposed to large numbers of mosquitoes. Adverse reac-tions, including sudden death, have been associatedwith the vaccine.

DisinfectionEffective disinfectants include 1% potassium hydroxide(KOH), 2% sodium hydroxide (NaOH), and 5%phenol.

• To control an outbreak, replace all wood items in theaviary and clean and disinfect all equipment, nets,cages, and breeding containers.

ReovirusesThere are 11 avian serotypes of reoviruses that are anti-genically distinct from each other and from reovirusesisolated from mammals. Of the common pet birds,African grey parrots have historically been the mostseverely affected.

Etiology• Avian reoviruses have been isolated or identified by

electron microscopy from asymptomatic psittacineand passerine birds.

Transmission

• Both horizontal and egg transmissions of reovirusoccur in chickens. However, little is known abouttransmission in psittacine birds; horizontal transmis-sion through oral and respiratory routes is believedto occur.

• The incubation period in experimental studies is 2 to15 days. After natural exposure, replication of thevirus occurs in the GI mucosa, followed by viremia(24–48 hours) and spread to other organ systems.

Clinical Signs• Severity of the disease, and thus clinical signs, varies,

depending on the age of the host, the virulence ofthe virus, the route of infection, and the presence orabsence of secondary infections.

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• Signs include anorexia, depression, yellow-orangeurates, diarrhea, dyspnea, and occasionally paresis,hind limb paralysis, and bloody nasal discharge.

Diagnosis• Gross pathologic changes include hepatospleno-

megaly with pale yellow mottling and multifocal gray-white foci.

• The typical histologic lesion is disseminated or focalcoagulative, necrotizing hepatopathy.

• A tentative histologic diagnosis may be confirmed byisolating the virus in cell culture from feces, liver, orspleen.

Treatment• Supportive care is the only treatment currently

available.

Prevention• There currently is no serologic test or commercial

vaccine available for reoviruses affecting pet birds.• Strict quarantine of newly arrived birds, especially

birds of African descent, may help prevent flockexposure. However, epidemiologic evidence suggeststhe existence of an asymptomatic carrier state.

• Viral infectivity can be reduced by prolonged contactwith phenols, aldehydes, ethanol, halides, a 0.5%iodine solution, and a temperature of 158∞F.

AdenoviridaeAdenovirus infections have been associated with depres-sion, diarrhea, anorexia, and acute death in budgeri-gars, Amazon parrots, macaws, cockatoos, lovebirds,and parakeets. Adenovirus infections typically produceeosinophilic and basophilic intranuclear inclusionbodies.

Adenovirus infections in psittacines commonly arereferred to as inclusion body hepatitis or inclusion body pan-creatitis, depending on the predominant organ systeminvolved.

Clinical Signs• Signs generally are nonspecific and vary with the

organ system affected. Signs include lethargy, depres-sion, fluffed feathers, yellow urates, diarrhea,anorexia, and sudden death.

Diagnosis• An enlarged, friable liver is the most consistent

feature recognized on gross necropsy examination.• Base definitive diagnosis on histologic examination

of affected tissues from necropsy specimens. Histo-logically, there is diffuse necrosis of parenchymatousorgans with eosinophilic and basophilic intranuclearinclusion bodies.

Treatment• There is no specific treatment.• General supportive care may be beneficial (warmth,

fluids, forced alimentation, and antibiotic therapy forsecondary infection).

Prevention• Disinfect cages and supplies with an aldehyde disin-

fectant (requires 1 hour of contact) to prevent spreadof the disease.

• Quarantine all new birds and strictly isolate affectedbirds.

Newcastle Disease Virus (Paramyxovirus-1)Newcastle disease virus (NDV) is of extreme economicimportance to the poultry industry. Legally importedbirds are placed in USDA quarantine stations for 30days. These were created to prevent the introduction ofvirulent forms of this virus into the United States.

� Key Point Smuggling of birds into the UnitedStates is the main source of NDV-infected birds.NDV should not be a problem for the serious avi-culturist who does not expose an aviary collectionto birds of questionable origin. NDV is a reportabledisease.

Etiology• There are nine serotypes of avian paramyxovirus

(PMV). The most significant pathogens are virulentserotypes of PMV-1, which has been isolated frommost species of domestic, aviary, and wild birds.

Transmission

• The respiratory and oral routes of transmission areequally important.

• Fecal contamination of eggshells may lead to viralspread. The virus infects the red blood cells and thenis spread throughout the body.

• The incubation period typically is 4 to 7 days.

Clinical Signs• Clinical signs depend on the virulence of the strain

of virus involved.• Predominant clinical signs in psittacine birds include

fluffed feathers, conjunctivitis, and CNS signs (e.g.,ataxia, wing and head tremors, and paralysis ofextremities).

• The mortality rate is 22% to 55% of affected birds.• Chronic NDV infection may develop in survivors.

Virus has been isolated from oral and cloacal swabs84 days to 1 year after exposure.

Diagnosis• Serologic testing using hemagglutination inhibition,

agar-gel immunodiffusion, or enzyme-linked immuno-

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sorbent assay can indirectly diagnose avian PMVinfection. However, serology is less effective in diag-nosing infections than viral isolation. Antibodies typ-ically appear 8 days after infection.• Hemagglutination inhibition is not specific for

PMV-1 (crossreaction may occur with other PMVs);however, suspect NDV in birds demonstrating hightiters.

• Base definitive diagnosis on virus isolation from fecesor oral secretions of live birds or from infected organsat necropsy.

Treatment• No treatment is available. Inform the USDA of any

birds positively diagnosed with NDV.

PreventionAll birds legally presented for importation into theUnited States are placed in a USDA-approved quaran-tine station for 30 days, at which time samples are takento detect hemagglutination viruses, including PMV andinfluenza. Birds with isolates of hemagglutination virusesthat are pathogenic to chickens are refused entry.

� Key Point The best prevention against NDV inpsittacine birds is avoidance of contact with birdsthat may have been smuggled into the country.

• No vaccine is available for psittacine birds.

SUSPECTED VIRAL DISEASES

Proventricular Dilatation DiseaseOther names for this disease include myenteric gan-glioneuritis, infiltrative splanchnic neuropathy, andmacaw wasting disease. The disease originally was seenonly in macaws but has been reported in almost allpsittacine species. Both ultrastructural findings and epi-demiologic evidence suggest that proventricular dilata-tion disease (PDD) has a viral etiology. The diseaseappears to have a protracted course, with low virulenceand extended incubation periods. The potential modeof transmission is unknown at this time.

Clinical Signs• Signs include intermittent regurgitation, diarrhea,

polydipsia or polyuria, depression, passage of undi-gested food, progressive weight loss, abdominal dis-tension, and central and peripheral neurologic signs.

• In birds with a severely dilated proventriculus, sec-ondary aspiration pneumonia may develop afterrepeated bouts of regurgitation.

� Key Point Once signs of PDD develop, the diseaseis usually fatal.

DiagnosisAntemortem Diagnosis

• A presumptive diagnosis may be based on clinicalsigns and radiographic identification of an enlargedproventriculus, and it may be made by ruling out allother possible causes of proventricular dilatation.

• Contrast radiography is usually necessary to positivelyidentify a dilated proventriculus.

• Rule out other causes of regurgitation, proventricu-lar dilatation, or passage of undigested food, such asGI foreign bodies, proventricular outflow obstruction(e.g., tumors and granuloma), heavy metal toxicity,proventriculus, enteritis, crop disorders, impaction,pancreatitis, and liver and kidney disease.

• Definitive diagnosis requires the identification oftypical histopathologic lesions on biopsy specimens.A biopsy of the crop is relatively non-invasive and mayprovide a diagnosis. When obtaining a biopsy, becertain to include mucosal blood vessels in thesample. This will increase the likelihood of obtaininga nerve, thus demonstrating histologic lesions. False-negative results are likely if nervous tissue is notobtained or if lesions are absent in the crop but arepresent in other areas of the GI tract.

• The CBC may demonstrate a leukocytosis and non-regenerative anemia.

• The serum biochemical profile may reveal increasedCK and hypoproteinemia.

Postmortem DiagnosisThe diagnosis is made by identification of characteris-tic lesions on necropsy.

• Gross pathologic changes include proventriculardilatation, ventricular ulcers, and undigested food inthe lower GI tract.

• Confirmation of the diagnosis requires identificationof accumulated lymphocytes and plasma cells in thenerves of the GI tract, brain, or spinal cord.• GI lesions include endoventriculitis, muscle atro-

phy, lymphocytic leiomyositis, and smooth muscledegeneration.

• Lesions may be found in the brain and peripheralnerves. Peripheral nervous tissue is affected mostoften, and lesions include lymphocyte and plasmacell infiltrates in the mesenteric plexus ganglia andin the intrinsic and extrinsic nerves of the proven-triculus and ventriculus and intranuclear and intra-cytoplasmic eosinophilic inclusion bodies in nervecells of intestinal ganglia.

• Other, less frequently encountered nervous tissuelesions include multifocal lymphocytic encephalitiswith gliosis; neuronophagia and perivascular cuff-ing in the cerebellum, medulla oblongata, brainstem, cerebrum, spinal cord, and meninges; visceralganglioneuritis; and lymphocytic poliomyelitis.

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Treatment• There are some reports of prolonged survival with

supportive care, a soft gruel diet, and nonsteroidalanti-inflammatory drugs (NSAIDs). In most cases,however, PDD eventually is fatal.

• The use of NSAIDs has alleviated clinical signs andprolonged life in mild to moderately affected birds.Drugs used include meloxicam (Metacam, Merial),0.1 to 0.5mg/kg PO q24h, or celecoxib (Celebrex,Pfizer), 10mg/kg PO q24h, for 6 to 12 weeks.

• It is currently unknown whether, but entirely possiblethat, birds treated with NSAIDs may continue to beinfectious, even after resolution of clinical signs. Continue to isolate birds definitively diagnosed withPDD.

Prevention• Because an etiologic agent, its transmission mode,

and the incubation period have not been identified,prevention is difficult.

• Strictly isolate birds with confirmed PDD from director indirect contact with other birds.

• Quarantine birds exposed to confirmed cases for atleast 6 months.

� Key Point Do not euthanize birds with radiographicevidence of proventricular dilatation unless adefinitive, histologic diagnosis of PDD has beenobtained. Rule out other causes of proventriculardilatation.

PapillomatosisPapillomas are proliferative, wartlike lesions that mayoccur on mucosal surfaces of the intestinal tract, includ-ing the oral cavity, esophagus, crop, proventriculus, andcloaca. Lesions are most commonly identified on thecloacal mucosa. Some birds develop internal papillo-matous disease, which results in multiple papillomasthroughout the GI tract, and, in some cases, neoplasiaof the liver or GI tract. The most common neoplasiaassociated with internal papillomatous disease is bileduct adenoma or adenocarcinoma. South and CentralAmerican birds such as Macaws, Amazon parrots, andconures are the species most frequently affected. Clini-cal signs have not been reported in South Pacific andAfrican parrots (cockatoos, cockatiels, parakeets, love-birds, and African grey parrots).

Etiology• A viral etiology is suspected because papillomas often

appear to spread through groups of birds. Currently,evidence suggests that a psittacine herpesvirus similarto that causing Pacheco’s disease may be at least inpart responsible for this condition. In one study, all

birds with cloacal papillomas tested positive forpsittacine herpesviruses. Psittacine herpesvirus hasalso been isolated from hepatic and GI tract neopla-sia in birds with papillomas.

Clinical SignsClinical signs vary with the location of the lesions. Clin-ical signs have only been reported in Central and SouthAmerican parrots.

• Signs of cloacal papillomas include straining to defe-cate, flatulence, malodorous and bloody stools, persistent enteric bacterial infections, and reducedfertility.• Cloacal papillomas may resemble granulation

tissue and can be difficult to distinguish fromcloacal prolapse.

• Oral papillomas may cause wheezing, dyspnea, exces-sive salivation, dysphagia, and persistent oral bacter-ial infections.

• Signs of esophageal, crop, and proventricular papil-lomas are less common and include vomiting, regur-gitation, and weight loss.

• Birds with hepatic or GI tract neoplasia exhibitweight loss, lethargy, or signs referable to the space-occupying effects of the mass.

Diagnosis• Base the diagnosis on the appearance of the lesions,

biopsy, and histopathology.

TreatmentIn some cases, the size and appearance of lesions waxand wane without treatment. Treatment is indicatedwhen clinical signs are evident or, in the case of cloacalpapillomas, if self-mutilation occurs.

• Cloacal papillomas may be gradually removed withchemical cauterization with silver nitrate sticks. Evertthe papilloma from the cloaca, and roll a silver nitratecautery stick onto the papilloma, taking extreme carenot to cauterize normal mucosa. Rinse thoroughlywith water. This procedure can be painful; therefore,anesthetize with isoflurane.

• Remove surgically by ligation and resection, electro-cautery, or cryosurgery. The technique used dependson the extent of the lesion.• Circumferential lesions of the cloaca may require

more than one procedure.• Take care to avoid the development of post-

operative strictures.• Treat secondary bacterial infections before surgical

removal.• Although a psittacine herpesvirus has been associated

with papillomas, treatment with acyclovir is not effective.

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Prevention• Because papillomas may be caused by an infectious

agent, carefully examine the cloaca and mouth of allbirds being added to a collection for the presence of papillomas. Those with lesions should be deniedentry.

• It may be difficult to detect birds that have had papil-lomas surgically removed. It is likely that a carrierstate exists if a herpesvirus is the cause of lesions.

• Until a greater understanding of the relationshipbetween psittacine herpesviruses and papillomasexists, avoid exposure of non-infected birds to birdsdiagnosed with herpesviruses.

BACTERIAL DISEASES

Gram-Negative InfectionsBacterial infections requiring treatment commonly areencountered in avian medicine, especially in birds thathave been stressed, are on a poor nutritional plane, orare housed in unsanitary conditions. Normal intestinalflora in most pet bird species consist primarily of gram-positive bacteria. Although small numbers of gram-negative bacteria may normally be found in healthybirds, many gram-negative bacteria are primary orpotentially opportunistic pathogens. Normal psittacineflora includes Lactobacillus, Bacillus, non-hemolytic Strep-tococcus, Micrococcus, Staphylococcus, Corynebacterium, andStreptomyces species and Pasteurella gallinarum.

EtiologyCommonly encountered gram-negative pathogensinclude Escherichia coli; Enterobacter, Klebsiella, Pseu-domonas, Salmonella, Proteus, and Campylobacter species;and Pasteurella multocida.

Clinical SignsClinical signs depend on the organ system affected.

• Respiratory, GI, or nonspecific signs such as inappe-tence, lethargy, and ruffled feathers may be seenalone or concurrently.

• Septicemia, especially from invasion of entericpathogens, is extremely common in pet birds.• Suspect septicemia in any severely depressed bird.

Diagnosis• If a bacterial cause of illness is suspected, perform a

Gram stain and culture on samples collected fromsites of infection.

• CBC usually demonstrates leukocytosis, with a relativeheterophilia. Toxic heterophils are often seen. Withchronic disease, the serum protein electrophoresismay demonstrate a hypergammaglobulinemia. The

serum biochemical profile may be helpful in identi-fying hepatic or renal involvement.

Respiratory System

• The rostral-most portion of the choana is a readilyaccessible site for collecting specimens from theupper respiratory system.

� Key Point Microbiologic analysis of samples fromthe choana is only significant if visible pathologyis present or if clinical signs of respiratory diseaseare evident.

• Other techniques for isolation of respiratory micro-bial agents include aspiration of the sinuses and tracheal washing (see Chapter 168).

• Direct culture of the air sacs or air sac flushing maybe performed via laparoscopy.

Gastrointestinal System

• Readily accessible sites for isolation of microbialagents include the crop, cloaca, and fresh feces.

• In large birds, the proventriculus and ventriculus maybe cultured directly using a rigid endoscope or smallflexible endoscope.

Other Organ Systems

• Organ systems such as the urogenital tract and liver,both common sites of bacterial infection, are accessi-ble only by more invasive techniques, such aslaparoscopy or exploratory laparotomy.

• Septicemic birds often are severely depressed and areunable to withstand invasive procedures. Aggressiveempirical treatment with antibiotics is often indicatedfor these birds.

TreatmentTreatment is indicated when potentially pathogenicbacteria are isolated from a bird with system-specificsigns or signs of septicemia.

� Key Point Identification of gram-negative organ-isms on samples taken from clinically healthy birdsdoes not usually warrant treatment. Monitor thesebirds for clinical signs and shifts in bacterial flora.

Selection of AntibioticsWhenever possible, select antibiotics based on cultureand susceptibility testing.

Kirby Bauer Susceptibility Test

• Bacterial isolates are classified as susceptible based onserum concentrations of antimicrobial agents that areachievable in humans.

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• Because it may not be possible to achieve thesehigh levels in pet birds, this test may not accuratelypredict the efficacy of the antibiotic chosen in vivo.

• Determining the minimum inhibitory concentration(MIC) of antibiotics allows a more accurate assess-ment of antimicrobial efficacy in pet birds; however,this test is not readily available. For this reason, theKirby Bauer test still is commonly used.

• When choosing an antibiotic based on standard KirbyBauer testing check the following:• The bacterial isolate should be susceptible to the

antibiotic.• The antibiotic preferably should be bactericidal,

known to penetrate into the site of infection, andeffective at very low serum concentrations.

• Antibiotics and dosages commonly used in pet birdsare listed in Table 169-1.

Route of AdministrationOral Administration

• Direct oral administration of medications often isused in pet birds, especially for palatable solutions orsuspension. However, this method is difficult forsome owners. Instruct owners on the proper restrainttechniques. Even after this, birds sometimes spit outthe medication, and aspiration is a possibility.

• Addition of medications to a small amount of favoritefood is a stress-free method and generally effective aslong as the entire portion is readily consumed.

• Administration of antibiotics via drinking water is theleast preferred method because most antibiotics areunpalatable and are not water soluble and becauseingestion of the medication is sporadic and effectiveconcentrations at the site of infection are rarelyachieved.

• When a bird is hospitalized and the intestinal tract isfunctioning properly, oral medications may beadministered via gavage tube.

Parenteral Administration

• Many antibiotics commonly used in avian medicineare poorly absorbed when given orally, necessitatingparenteral administration.

• Use injectable antibiotics in the following cases:• When a bird is unwilling to take oral medications• When GI motility is altered• In critically ill or septicemic birds

• The advantages of this method include precisedosing, rapid development of therapeutic serum con-centrations, and relatively stress-free administration.

• Some practitioners teach their clients to administerIM injections to their pets (the technique for IMinjection is described in Chapter 168).

Table 169-1. ANTIBIOTICS FOR USE IN AVIAN PATIENTS

Product NameGeneric Name (Manufacturer) Dosage Comments

Amikacin (250 mg/ml) Amiglyde (Bristol) 10–20 mg/kg q12h IM Potentially nephrotoxicSynergistic with penicillins

Piperacillin (injectable) Pipracil (Lederle) 100–200 mg/kg q6–8h IM, IV Effective against most gram-negative bacteriaSynergistic with aminoglycosidesFreeze after reconstitution until useGood activity against gram-negative bacteria

Cefotaxime Claforan (Hoechst-Roussel) 75 mg/kg q6–8h IM Broad-spectrum, low toxicityGood against gentamicin-resistant gram-negative

isolatesCeftiofur Naxel (Pharmacia & 75–100 mg/kg q6–8h IM, IV Synergistic with aminoglycosides

Upjohn) Reconstituted drug lasts 12 weeks in freezer, 10days in refrigerator

Broad-spectrum, penetrates into CNSEnrofloxacin Baytril (Bayer) 10–20 mg/kg q24h IM, PO Broad-spectrum, little toxicity

Irritating when injected IM—do not use for >3–5 days

Metronidazole Flagyl (Searle) 50 mg/kg q12h Effective against many anaerobic bacteriaTrimethoprim- Bactrim (Roche) 100 mg/kg q12h PO Good against many gram-negative and

sulfamethoxazole gram-positive isolates(suspension) Excellent for hand-feeding neonates

May cause emesis in some birds, especially macaws

CNS, central nervous system; IM, intramuscularly; IV, intravenously PO, orally (per os).

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MonitoringAssess antibiotic effectiveness by monitoring the reso-lution of clinical signs, serial hemograms, cytology, andculture. Serial fecal or cloacal Gram stains during andafter antibiotic administration are important becausedevelopment of secondary infections, especially can-didiasis or aspergillosis, are common.

Gram-Positive InfectionsGram-positive infections occur less frequently in petbirds. Pathogens include beta-hemolytic Streptococcus,Staphylococcus aureus, and Clostridium spp. Follow thesame principles for diagnosis and treatment as outlinedpreviously for gram-negative infections.

Avian TuberculosisEtiologyTuberculosis in psittacines, unlike that in mammals,usually is a primarily alimentary disease.

• Although a few cases of Mycobacterium tuberculosis andM. bovis have been reported in pet birds, the causativeagent usually is M. avium.

• These gram-positive, acid-fast granulated rods arecapable of causing disease in birds, pigs, guinea pigs,rabbits, and humans.

• Brotogeris parakeets (especially gray-checked para-keets) are particularly susceptible, followed byAmazon parrots, budgerigars, and Pionus parrots.

Transmission

• Transmission occurs primarily by ingestion of fecal-contaminated food, water, or soil; an aerosol route orwound contamination also is possible. The organismis capable of surviving in soil for up to 2 years.

• After ingestion, the organisms penetrate the GImucosa and colonize under the serosa.

• A primary bacteremia occurs (usually without clinicalsigns), and the organisms are phagocytized (but notkilled) by mononuclear phagocyte cells of the liver,spleen, and bone marrow. Multiplication within thesecells causes a local reaction by the cell-mediatedimmune system and the formation of nodules, whichmay calcify with time.

• Release of the organisms from the liver results in asecondary bacteremia, with localization in lungs,kidneys, gonads, and intestines. Tubercles in theintestinal wall may open into the intestinal lumen,resulting in shedding of large numbers of organismsin the feces.

Clinical Signs• Clinical signs include chronic weight loss (often

despite a good appetite), depression, chronic diar-rhea, polyuria, and poor feathering.

• Abdominal distension due to hepatomegaly anddilated, fluid-filled, thickened intestines is common.

• Subcutaneous and periorbital masses may be seen.• Lameness due to endosteal bone proliferation occa-

sionally is reported.• Signs often are nonspecific and slowly progressive.

DiagnosisHematology and Serum Biochemistry

• Severe leukocytosis (>20,000) with marked hetero-philia and monocytosis is common.

• Anemia and polychromasia usually are present.• AST levels usually are elevated with hepatic

involvement.

Histopathologic Lesions

• On postmortem examination, in addition to thegrossly visible nodules previously described, diffuseinfiltration of epithelioid or giant cells may result ina grossly thickened firm intestine, hepatomegaly, orsplenomegaly.

• Histologically, the intestinal villi may be club shaped,swollen, and filled with epithelioid cells containingacid-fast rods.

• Definitive diagnosis is based on identification of acid-fast rods and epithelioid cells on biopsy or post-mortem slide preparations. The liver is generally themost reliable source.

• Acid-fast staining or culture of feces also may demon-strate the organism, although false-negative resultsare common owing to intermittent shedding oforganisms.

• Cultures require 3 to 6 weeks for results.• Indirect diagnosis with intradermal tuberculin and

slide agglutination tests also frequently produce false-negative results.

Treatment• Euthanasia often is recommended because of the

potential human health hazard, especially toimmunocompromised owners.

• Successful treatment of pet birds with M. avium,mimicking human treatment protocols, has beenreported.

SUPPLEMENTAL READING

Aguilar RF, Redig PT: Diagnosis and treatment of avian aspergillosis.In Bonagura JD, Kirk RW (eds): Current Veterinary Therapy XII:Small Animal Practice. Philadelphia: WB Saunders, 1995, pp1294–1299.

Aranaz A, Liebana E, Mateos A, Dominguez L: Laboratory diagnosisof avian mycobacteriosis. Semin Avian Exot Pet Med 6:9–17, 1997.

Cross GM: Viral diseases. Semin Avian Exot Pet Med 4(2), 1995.

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Dorrestein GM: Bacteriology. In Altman RB, Clubb SL, DorresteinGM, Quesenberry K (eds): Avian Medicine and Surgery. Philadel-phia: WB Saunders, 1997, pp 225–280.

Flammer K: Chlamydia. In Altman RB, Clubb SL, Dorrestein GM,Quesenberry K (eds): Avian Medicine and Surgery. Philadelphia:WB Saunders, 1997, pp 364–379.

Gerlach H: Viruses. In Ritchie BW, Harrison GJ, Harrison LR (eds):Avian Medicine: Principles and Application. Lake Worth, FL:Wingers Publishing, 1994, pp 862–948.

Gregory CR, Latimer KS, Niagro FD, et al: A review of proventriculardilatation syndrome. J Assoc Avian Vet 8:69–75, 1994.

Ritchie BW: Papovaviridae. In Ritchie RW (ed): Avian Viruses: Func-tion and Control. Lake Worth, FL: Wingers Publishing, 1995, pp 127–170.

Ritchie BW: Herpesviridae. In Ritchie RW (ed): Avian Viruses Func-tion and Control. Lake Worth, FL: Wingers Publishing, 1995, pp 171–218.

VanDerHeyden N: New strategies in the treatment of avian mycobac-teriosis. Semin Avian Exot Pet Med 6:25–33, 1997.

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