avian medicine: princilpes and...

ompanion and aviary birds frequently de-velop clinical signs associated with the cen-tral or peripheral nervous system. Thesechanges may include depression, blindness,

opisthotonos, head tilt, circling, tremors, ataxia, con-vulsions, paresis and paralysis. Neurologic changesin birds may occur from primary or secondary dis-eases including genetic abnormalities, neoplasms,metabolic diseases, malnutrition, exposure to toxins,trauma and bacterial, viral, fungal or parasitic infec-tions.

In a retrospective study of avian patients withneurologic disorders, the clinical signs most fre-quently observed were seizures, ataxia, paresis, pa-ralysis, intention tremors, circling, head tilt, nystag-mus, abnormal mentation and visual deficits.General supportive care for patients in this studyincluded antibiotic therapy, fluid support, parenteralvitamin therapy and gavage feeding for nutritionalsupport. The two most common etiologies were leadtoxicity and hypocalcemia/vitamin D3 deficiency.Many other neurologic problems resolved with gen-eral supportive care and vitamin supplementation.87

Diagnostic tests that may be of value in determiningthe etiology of neural lesions, as well as the prognosisfor recovery in some cases, include CBC, biochemis-tries, specific tests for detecting levels of toxins, ra-d i o g ra p hs , e l e c t ro e n ce p h a log rams , e l e c-tromyograms, auditory evoke potentials, CT scansand MRI. Some of these diagnostic techniques re-quire specialized equipment, but their efficacy in di-agnosing neurologic diseases in birds has been docu-mented. Many of the advanced neurologic diagnostictests are available at veterinary colleges, and casereferral should be considered when one of these tech-niques is needed to evaluate a patient.

C C H A P T E R

28NEUROLOGY

R. Avery Bennett

Neuroanatomy69

Meninges

As in mammals, birds have three meninges: pia mater,arachnoid and dura mater. The subarachnoid spacecontains cerebrospinal fluid that may be collected fromthe cisterna magna; however, birds have a large venoussinus located dorsal to the cisterna that is easily dam-aged during a spinal tapping procedure and, if dis-rupted, will cause severe hemorrhage.

Brain

The brain of birds is agyric, with virtually no convo-lutions (Figure 28.1). The vallecula arises near therostral end of the median fissure and extendscaudad. The sagittal eminence is a prominence me-dial to the vallecula. The lateral ventricles are dis-placed dorsally by the large corpus striatum.83 Theolfactory bulbs are pointed at the rostral extent of thebrain, and the olfactory center of the brain is ratherunderdeveloped.28 The cerebral cortex is also under-developed (being two to three cell-layers thick, <1mm); however, when compared with mammals, thecorpus striatum is well developed and is consideredthe main center for association in birds (Figure 28.2).Consequently, instincts dominate avian behavior,which may account for some of the self-mutilationthat occurs in companion birds. Birds have no corpuscallosum nor septum pellucidum.

The diencephalon is the location of the pineal body,which lies dorsal and medial between the caudal as-pects of the cerebral hemispheres. It is composed ofsecretory cells, which resemble rudimentary photore-ceptors. The nonmyelinated axons are responsive tolight. The pathway for stimulation courses from theoptic nerve to the cranial cervical ganglion, which hasaxons to the pineal body. Interestingly, these axons arestill responsive to light even if the bird’s eyes areremoved and the cranial cervical ganglion is removed.The pineal body is involved in reproduction, migrationand circadian rhythms. Its secretions exert their effecton the hypothalamus. The hypothalamus is locatedcaudal (or ventral) to the optic chiasm.

MidbrainThe midbrain is the location of the optic tectum. Theavian optic lobes are massive and responsible for thewell developed, though monocular, vision of mostbirds (Figure 28.2). The optic tectum is equivalent tothe rostral colliculus of mammals and birds have nocaudal colliculus. Cranial nerves III and IV exit fromthe midbrain. Large motor afferent, efferent andoptic fiber systems originate, decussate and termi-nate in the mesencephalon and myelencephalon.There is complete decussation of tectospinal (motor)and rubrospinal (modulation) tracts in the midbrain,while the tracts of the pons and medulla do notdecussate.1

CerebellumAs in mammals, the cerebellum is the center forcoordination of movements and is correspondinglylarge. It has a single median lobe with transversesulci and is divided into three main lobes (not four asin mammals) by the fissura prima and fissurasecunda, which are deeper transverse sulci. Smallertransverse sulci divide it into ten primary lobules.Each lobule is believed to be responsible for coordina-tion of a specific part of the body. For example, lobulesII and III control leg coordination. The lateral floccu-lus (lobule X) with the paraflocculus (lobule IX) arelocated at the rostral aspect. The rostral and caudalcerebellar peduncles attach the cerebellum to themedulla. There may also be a cerebellar peduncle.

PonsThe pons is poorly developed and is present only as abroad band of fibers at the rostral portion of themedulla oblongata. There is no pyramid as found inmammals. Cranial nerves V through XII arise fromthe medulla.

FIG 28.1 The brain of birds is agyric with virtually noconvolutions.

SECTION FOUR INTERNAL MEDICINE

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Cranial Nerves

The cranial nerves of birds corre-spond to those found in mammals(Figure 28.3). The olfactory nerve(CN I) is sensory and passes througha single hole in the skull (the olfac-tory foramen) rather than a cribri-form plate. The optic nerve (CN II) issensory and large in order to accom-modate the visual acuity birds re-quire. It is usually more than halfthe diameter of the spinal cord. Theoculomotor nerve (CN III) is motor tothe dorsal, ventral and medial rectusmuscles and the ventral obliquemuscle of the eye. It also supplies themuscles of the eyelids. It has para-sympathetic fibers to the gland of thethird eyelid, the choroid, the iris andthe pecten (triangular pleated mem-brane extending forward from theoptic disc). The trochlear nerve (CNIV) is motor to the dorsal obliquemuscle of the eye.

The trigeminal nerve (CN V) con-tains both sensory and motor fibers.The ophthalmic branch is sensoryand consists of two components. Thedorsal component innervates the up-per eyelid and the skin of the fore-head. The ventral component is sen-sory to the nasal cavity and upperbeak. The maxillary branch is sen-sory and innervates the upper eyelid

before branching to supply the lower eyelid, palate,skin of the upper beak, nasal cavity and infraorbitalsinus. The mandibular branch is motor but may havesome sensory fibers. It innervates the muscles ofmastication and the skin and the mucosa at thecommissures of the beak.

FIG 28.2 a) Ventral and b) lateral view of the brain. 1) cranialnerve I 2) cranial nerve II 3) eye 4) cranial nerve IV 5a) cranialnerve V (ophthalmic branch) 5b) cranial nerve V (maxillarybranch) 5c) cranial nerve V (mandibular branch) 6) cranial nerveVI 7) cranial nerve VII 8) cranial nerve VIII 9) cranial nerve IX 10)cranial nerve X 11) cranial nerve XI 12) cranial nerve XII 13)olfactory lobe 14) pituitary gland 15) cerebral hemisphere 16) opticlobe 17) pons 18) medulla oblongata 19) spinal cord 20) cervicalnerve 1 21) cervical nerve 2 22) trigeminal ganglion 23) ventricularsystem 24) lateral ventricle 25) corpus striatum 26) arbor vitae 27)cerebellum 28) roof of medulla oblongata 29) central canal 30) floorof medulla oblongata 31) optic chiasm and 32) pineal body.

CHAPTER 28 NEUROLOGY

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The abducent nerve (CN VI) is motorto the lateral rectus muscles andmuscles of the third eyelid. The facialnerve (CN VII) is motor with a smallsensory component and parasympa-thetic fibers. It is not involved intaste as in mammals, but suppliesthe hyoid and the cutaneous neckmuscles. The vestibulocochlearnerve (CN VIII) has separate gangliafor the vestibular and the cochlearnerves. The glossopharyngeal nerve(CN IX) is sensory and motor. Cra-nial nerves IX, X, XI arise from a rowof small roots. Cranial nerves X andXI combine in a common ganglion.The lingual branch of the glosso-pharyngeal nerve receives sensoryinput from taste fibers.

The pharyngeal branch has fibersthat join with the vagus nerve to in-nervate the larynx and trachea. Theesophageal branch courses along theneck with the jugular vein, supplyingthe esophagus. The vagus nerve (CNX), CN XI and jugular vein course down the neck ina common sheath to the level of the nodose ganglion.The spinal accessory nerve (CN XI) is enclosed withthe vagus and supplies the superficial muscles of theneck. The hypoglossal nerve (CN XII) and CN IXinnervate the tracheal muscles. The former has alingual branch that innervates the tongue musclesand a syringeal branch that courses to the syrinx andtracheal muscles.

Spinal Nerves

Because birds of different species have varying num-bers of vertebrae, spinal nerves are numbered by thevertebra caudal to it in numerical order regardless ofwhether it is cervical, thoracic, lumbar, sacral orcoccygeal. In discussions of plexuses, it is customaryto refer to the roots making up the plexus by theordinal number of their cranial to caudal location(Figure 28.4). The lumbar spinal cord contains adorsal gelatinous structure (glycogen body), which isnestled in a deep cleft between the dorsal columns.83

The brachial plexus is formed by ventral branches ofthree to five spinal nerves. The ram communicanslateralis and medialis connect the second to the thirdnerve roots and the fourth to the fifth roots (if pre-sent). These are sympathetic nerve fibers. The sec-

FIG 28.3 a) Lateral and b) caudal view of the cranium showing theposition of the cranial nerves. 1) cranial nerve I 2) cranial nerve II3) cranial nerve III 4) cranial nerve IV 5a) cranial nerve V (oph-thalmic branch) 5b) cranial nerve V (maxillary branch) 5c) cranialnerve V (mandibular branch) 6) cranial nerve VI 7) cranial nerveVII 8) cranial nerve VIII 9) cranial nerve IX 10) cranial nerve X11) cranial nerve XI 12) cranial nerve XII 13) cervical nerve 1 14)cervical nerve 2 15) lingual branch 16) pharyngeal branch 17)internal carotid artery 18) jugular vein 19) corda tympani 20)sphenopalatine ganglion and 21) infraorbital nerve.


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ond through fourth roots give off rami musculares toinnervate the neck muscles. The nerves arising fromthis plexus innervate the muscles of the wing.

There are three nerve plexuses in the lumbosacralregion (lumbar, ischiatic and pudendal). These nerveroots lie embedded in the foveae of the pelvis sur-rounded by the kidneys (see Anatomy Overlay). All

three plexuses are connected to thesympathetic chain. The lumbarplexus is composed of three to fournerve roots (the last two lumbar andfirst sacral roots). It innervates thecranial thigh muscles and the mus-cles of the body wall. The obturatornerve, femoral nerve, cranial glutealnerve and saphenous nerve arisefrom this plexus.

The ischiatic plexus or sacral plexusis usually made up of six sacral nerveroots, but occasionally four, five orseven roots. The first root arises withthe last root of the lumbar plexus.The roots combine to form the isch-iatic nerve, which is the largestnerve in body. This nerve should befaintly striated and a loss of stria-tions is suggestive of an inflamma-tory process. The caudal glutealnerve also arises from the sacralplexus.83

The pudendal plexus is formed byfive thin coccygeal nerve roots andsupplies the cloaca and tail.

NeurologicExamination

Two of the primary objectives in per-forming a neurologic examinationare to determine if the neuropathy isfocal or diffuse, and to localize focallesions. The examination should beperformed in a consistent, logicalmanner that starts with a completehistory (see Chapter 8). Neuropa-thies are particularly common secon-dary to trauma, exposure to toxins

and malnutrition. Subtle changes in cranial nervefunction and abnormal reflexes are difficult to appre-ciate and interpret in birds. Assessment of segmentalreflexes may be difficult in avian patients, makingevaluation of muscle tone, strength and atrophy anessential part of the neurologic examination.

FIG 28.4 Ventrodorsal view of the spinal nerves and autonomic nervous system. The rightkidney has been removed to show their relationship with the lumbar plexuses. 1) vagus2) cervical spinal nerves 3) brachial plexus 4) thoracic spinal nerves 5) greater splanchnicnerves 6) lumbar plexus 7) obturator nerve 8) sacral plexus 9) pudendal plexus 10) cloaca11) ischiatic nerve 12) cranial division of kidney 13) autonomic ganglion and 14) humerus.


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Neurologic evaluation of neonates is particularly dif-ficult, and making a “side-by-side” comparison witha “normal” clutchmate is the best way to detect sub-tle changes. Useful tests include evaluation of thefeeding response, menace reflex, use of wings to bal-ance, vocalization, perching ability, pain perceptionand hopping response.65

Mental Status

The patient’s mental status and level of conscious-ness should be evaluated. Any personality changesreported by the owner should be noted. The bird’sability to perform normal activities and its aware-ness of its surroundings should be assessed. Clientsmay indicate that the bird acts sleepy, dull, uneasy,nervous, anxious, aggressive or dizzy. It is difficult todifferentiate between seizures and syncope based onthe history; however, either may suggest an intracra-nial lesion. Seizures may be characterized by ataxia,disorientation and falling off a perch followed bytonic clonic convulsions.

Cranial Nerves

An evaluation of the cranial nerves may help localizea focal brain lesion (individual nerves involved) or ageneralized encephalopathy (several nerves in-volved). Olfaction (CN I) is difficult to assess becausebirds have a poor sense of smell; however, most nor-mal birds will react negatively to noxious odors (eg,alcohol pledget). Birds with CN I dysfunction mayexhibit an altered appetite or feeding response.

An ophthalmic examination is essential for detectingneurologic abnormalities (see Chapter 26). Failure toavoid obstacles may indicate vision impairment. Bi-lateral blindness without ocular lesions may indicateneoplasm, abscess or granuloma formation in thebrain.97 The menace reflex can be used to evaluateCN II and VII; however, depending on the circum-stances, the absence of a menace response does notalways indicate dysfunction of these cranial nerves.The pupillary light response evaluates CN II and III.Because there is complete decussation of the opticnerves at the chiasm, birds do not have a consensualpupillary light response. 68

Birds have some degree of voluntary control of pupilsize because of skeletal muscles in the iris.28,68 Ex-cited birds will voluntarily dilate and constrict theirpupils. The presence of anisocoria may indicate dys-function of CN III or a sympathetic neuropathy. Nor-mal eye movements require the coordination of CN

III, IV, VI and VIII as well as the cerebellum andbrain stem.87 The presence of nystagmus or strabis-mus may indicate an abnormality in this system(vestibular). A fundic examination may be performedwith the aid of d-tubocurarine. Its action on the avianpupil may be to inhibit the iris constrictor musclesallowing the myoepithelial dilator action to domi-nate.68 In some birds, intracameral injection of 0.045-0.09 mg d-tubocurarine chloride produces mydriasiswithin five minutes without systemic effects.68

Cranial nerve V is responsible for facial sensation,movement of the mandible and blinking of the eye-lids. Diminished beak strength may indicate an ab-normality in CN V. Eye blink involves both CN V andVII. A defect in CN VIII will cause deafness or a headtilt toward the affected side. Cranial nerves IXthrough XII are involved in normal tongue move-ment, swallowing and beak strength. Dysfunction ismanifested by dysphagia. Deviation of the tongue oratrophy of its muscles is observed with damage to CNXII.

Loss of normal physiologic nystagmus may occurwith bilateral CN VIII lesions or with severe brainstem lesions.87 Altered consciousness is usually anaccompanying sign with brain stem lesions. Abnor-mal, spontaneous nystagmus may result from ves-tibular lesions. Strabismus may indicate vestibularsystem dysfunction or a lesion in CN III, IV or VI.87

Horner’s syndrome may occur with intracranial le-sions or with a lesion in the cervical sympathetictract or the brachial plexus.87

Locating Lesions

Reflexes are evaluated to help determine if a lesionis central (upper motor neuron) or peripheral (lowermotor neuron). Wing droop, inability to fly and di-minished or absent pain perception may be presentwith either central or peripheral lesions. Pain per-ception in the wing requires intact peripheral nervesand the cervical spinal cord. Wing withdrawal is asegmental reflex that is present with intact periph-eral nerves, but does not require an intact cervicalspinal cord. A spinal cord lesion should cause hyper-reflexia; however, hyperreflexia is difficult to distin-guish from normoreflexia.

In most situations, it is sufficient to determine if areflex is present or absent. Weakness in the legs,knuckling over and an inability to grasp perches withthe feet may be observed with either upper motor


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neuron lesions or lower motor neuron lesions. Thepatellar reflex is difficult to assess in birds; however,the withdrawal reflex is also a segmental reflex andshould be intact with lesions affecting only the spinalcord.87

Conscious proprioception requires an intact periph-eral and central nervous system. A lesion in eitherwill result in the bird knuckling over. The vent re-sponse is a segmental reflex, and the sphinctershould be responsive to stimulation if a spinal cordlesion is present and the nerve roots are not affected.A crossed extensor reflex generally indicates a lesionin the spinal cord with a loss of normal central inhibi-tory pathways.

With cervical spinal cord lesions, dysfunction of thewings, legs and cloaca may be observed while headfunction and cranial nerves appear normal (Figure28.5). Weakness in the wings and legs with intact legand wing withdrawal and vent response would beindicative of a cervical spinal cord lesion. Lesionsaffecting the thoracolumbar spinal cord will cause legand cloacal dysfunction without affecting the head,cranial nerves or wings. Cloacal sphincter hyper-tonia, incontinence and soiling of the vent without

signs of head, wing or leg dysfunction are indicativeof a lumbosacral spinal cord lesion.

Loss of pain perception indicates a poor prognosis forrecovery.87 It is crucial to differentiate pain percep-tion from withdrawal reflex. Because withdrawal ofa stimulated extremity is a segmental reflex anddoes not require an intact spinal cord for a normalresponse, movement does not indicate the patient isable to feel the stimulus. Some type of consciousrecognition of the stimulus must be identified (eg,vocalization, attempting to bite or escape behavior).This part of the examination is generally reserved forlast so that the painful stimulus does not influencethe patient’s response to other segments of theneurologic examination.

Diagnostic Techniques

The results of the neurologic examination will sug-gest which diagnostic tests should be performed. A

CBC and serum chemistry profileare indicated if an infectious or me-tabolic neuropathy is considered. La-paroscopy and organ biopsy may beindicated to further define metabolicneuropathies. Serum for viral dis-eases or chlamydiosis, and blood lev-els for heavy metals are indicated insome cases. Radiographs are indi-cated if spinal trauma or heavy met-al intoxication is suspected. TSHstimulation test may be helpful ifhypothyroidism is suspected. Elec-tromyograms, nerve conduction ve-locities, spinal evoked potentials andnerve or muscle biopsies are helpfulin evaluating neuropathies.

Electrodiagnostics

Electrodiagnostic studies are usedcommonly in mammals for localizingneurologic lesions and aiding inprognostic assessment. When avail-able, electrodiagnostic techniquesare valuable in avian patients fordistinguishing between a neuropa-thy and a myopathy, localization of

FIG 28.5 A mature Amazon parrot was presented for emergency evaluation after beingbitten by a dog. The bird had several large puncture wounds in the thorax. The bird wasrecumbent, and a deep pain response could not be elicited from either pelvic limb.Radiographs indicated a puncture wound through the lung (arrow) with an increased softtissue density (blood) in portions of the lung parenchyma. The bird was placed onbroad-spectrum antibiotics and steroids. A deep pain response was noted five days afterthe initial injury, and the bird slowly improved with a complete return to normal functionover a three-month period.


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neurologic lesions and determining the prognosis forreturn to normal function.

Electromyogram (EMG)Diseases of motor neuron cell bodies, ventral nerveroots, nerve plexuses, peripheral nerves, neuromus-cular junctions and muscle fibers may alter the elec-tromyogram (EMG), which is a recording of the elec-trical activity in striated muscle.27 Normal activityconsists of insertion potentials, motor unit potentialsand spontaneous waves, which occur infrequently.When the electrode is inserted into the muscle, theintrafascicular nerve branches and muscle fibers arestimulated, creating a brief burst of electrical activ-ity, which ceases immediately after the electrodestops moving. If the electrode is moved, insertionalactivity will again be recorded. Large positive wavesare occasionally observed. If the electrode is insertedcoincidentally near a motor endplate, a low continu-ous level of electrical activity will be recorded with anauditory component sounding like a distant beachsurf. Motor unit potentials occur during involuntarymuscle contraction or when a motor nerve is stimu-lated (an M response). The M response has twophases and represents the sum of the electrical activ-ity of all of the muscle fibers in that motor unit.

Fibrillation potentials, positive sharp waves, myopa-thic potentials and reinnervation potentials are ab-normal EMG recordings. Prolonged insertional activ-ity due to muscle hyperexcitability occurs six to tendays following peripheral nerve injury, then gradu-ally decreases. Fibrillation potentials are mono- orbiphasic and occur five to seven days following den-ervation. These spontaneous, repetitive action poten-tials from muscle fibers, not produced by nerve im-pulses, occur because of the instability of the cellmembrane at the endplate. Fibrillation potentialsincrease for several weeks after denervation, thendecrease as muscle atrophy and fibrosis occur. Theystop if reinnervation occurs.

Positive sharp waves are generally associated withdenervation, but may be observed with primarymyopathies. They are characterized by an initialpositive deflection followed by a slower negative po-tential with a “dive bomber engine” auditory compo-nent. They may be single or multiple. Myopathicpotentials are generally indicative of a primarymyopathy but may be observed with fibrillation po-tentials following denervation. They are continuousdischarges with varying amplitude, duration and fre-quency with a waxing and waning auditory compo-nent sounding like an attacking then retreating dive

bomber. As reinnervation occurs, motor unit poten-tials are initially low amplitude and polyphasic butbecome larger than normal motor unit potentials andare an indicator of a good prognosis for recovery.

Nerve conduction velocities (NCV) can provide infor-mation regarding delayed transmission along anerve as well as the location of a peripheral nervelesion. A nerve stimulator is used to generate an Mresponse at two different locations along the courseof a peripheral nerve. The distance between the sitesis divided by the latency difference in the two Mresponses to determine the velocity with which theimpulse travels along the nerve (m/s). Where there isa peripheral neuropathy such as demyelination, thevelocity is slow and the M responses are polyphasicand prolonged. If the nerve has been transected, thestimulation distal to the site will produce an M re-sponse, while stimulation of the site proximal to thelesion will not.

Standard EMG equipment may be used to evaluateH-wave and F-wave reflexes. The H-wave reflexevaluates both the afferent and efferent pathways. Aperipheral site is stimulated and sensory impulsesare carried to the spinal cord, where the alpha motorneurons are activated and discharged, resulting in acompound muscle section potential. The F-wave re-flex is evaluated by stimulating the peripheral nervewith a lower intensity than that required to cause anH-wave production, activating the motor neuron togenerate an efferent impulse. The H-wave and F-wave reflexes are used in combination to evaluatenerve root avulsion.

Signal-averaging capabilities are required for soma-tosensory-evoked potentials, spinal-evoked poten-tials and motor-evoked potentials. Somatosensory-evoked potentials correspond clinically to thepresence or absence of pain perception. They may beutilized to determine if failure to react to a painfulstimulus is the result of other more painful injuries,stoicism or denervation. This procedure is performedby stimulating a peripheral nerve and recording theresponse in the cervical spinal cord or cerebral cor-tex. It is important to recognize that these evokedpotentials evaluate sensory, not motor nerve func-tion. A response may persist after permanent loss ofmotor function.

Spinal-evoked potentials are utilized to determinethe location of a spinal cord lesion. Stimuli are ap-plied to peripheral nerves and the responses arerecorded by an electrode inserted near the spinal


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cord. They can discretely evaluate the sensory path-way of a focal segment of spinal cord such that loss ofresponse cranial to a specific vertebra identifies thelocation of the lesion. Spinal-evoked potentials alsoevaluate only sensory function. Motor-evoked poten-tials are capable of evaluating motor function, buttechniques are not well established for animal use.They are currently being evaluated for safety, effectsof anesthetics and correlation with injury.

ElectroencephalogramsElectroencephalograms (EEG) are continuous re-cordings of the electrical activity of the cerebral cor-tex. They vary with head size, environment, re-straint techniques and state of consciousness of thepatient. They may be beneficial in monitoring pro-gress in response to brain lesions or injury. Auditory-evoked potentials evaluate the brainstem responseto auditory stimuli. They may be used to assesshearing ability and brainstem function (Figure 28.6).

Neuropathies

Nutritional

Hypovitaminosis E and Selenium DeficiencyDeficiencies of vitamin E and selenium have beenreported to cause a wide variety of clinical signs andpathologic lesions in birds of all ages. In a survey ofcentral nervous system lesions from animals in azoological collection, birds had a higher incidence ofdisease than mammals, and encephalomalacia his-tologically compatible with hypovitaminosis E wasthe most common lesion observed.130

FIG 28.6 a) A Barn Owl was presented with a progressive head tiltand ataxia. Physical examination revealed a discharge of necroticdebris from the right ear canal that contained gram-negative rods. b)Auditory-evoked potentials indicated a centralized inflammatory dis-ease (see Color 14).


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Vitamin E is a fat-soluble vitaminand depletion of body stores occursslowly in adult birds, while youngbirds may develop clinical signs asso-ciated with acute deficiency. In youngbirds, hypovitaminosis E may causeencephalomalacia, exudative diathe-sis or muscular dystrophy. Encepha-lomalacia results in ataxia, head tilt,circling and occasionally convulsionsand is particularly common in hatch-ling budgerigars.51 Exudative diathe-sis and muscular dystrophy (whitemuscle disease) occur also with defi-ciency of vitamin E or selenium. Themyositis associated with hypovitami-nosis E may cause clinical changesd i f f icu lt t o di s t ingui sh fromneurologic signs.

Clinical signs associated with vitamin E and sele-nium deficiencies include tremors, ataxia, incoordi-nation, abnormal head movements, reluctance towalk and recumbency. 14,63 Postmortem findings sug-gestive of encephalomalacia include cerebellaredema or hemorrhage (petechia) with flattening ofthe convolutions.14 Histologically, there is edema, in-terruption of vascular integrity with associated cap-illary hemorrhage and hyaline thrombosis, and cere-bellar demyelination with degeneration and necrosisof neurons.14 Focal or multifocal poliomyelomalaciaof the spinal cord may also occur.40,63 Diagnosis ofhypovitaminosis E is frequently presumptive basedon clinical signs, history and gross and microscopicpathology. Hypovitaminosis E and selenium defi-ciency should be considered with pathologic lesions ofdemyelination and malacia in birds with vague clini-cal signs or in birds that are found dead in theirenclosures with no premonitory signs.

Muscular dystrophy is characterized by light-coloredstreaks in the muscle fibers (Figure 28.7). Earlyhistologic changes include hyaline degeneration, mi-tochondrial swelling, loss of striations and centralmigration of the nucleus.14 In more chronic cases,muscle fibers are disrupted transversely and macro-phages are present engulfing debris from necroticmyocytes.

This deficiency has also been incriminated as theetiology of cockatiel paralysis syndrome. This condi-tion appears to occur most frequently in lutino cocka-tiels infected with Giardia sp. or Hexamita sp. Vita-min E- and selenium-responsive neuropathies have

been reported in a variety of other species includingBlue and Gold Macaws, Severe Macaws, EclectusParrots and African Grey Parrots.

Clinical signs include slow or incomplete eye blinkdue to paresis of the lower eyelid, weak jaw muscles,paresis of the tongue, poor digestion with passage ofpartially digested food, diminished playful activity,hyperactivity, clumsiness and weak grip, low-pitchedand weak vocalization, delayed crop-emptying,spraddle leg, death of young in nest, weak hatchlings,

FIG 28.7 a) A two-year-old domestically raised Eclectus Parrotwas presented with a one-month history of progressive difficultiesin ambulating. At presentation, the bird was recumbent and hadstiff, nonmotile thoracic and pelvic limbs, but was bright, alert andresponsive. The muscle masses associated with all limbs wereatrophied and firm. b) EMG findings included fibrillation poten-tials and positive sharp waves suggestive of denervation. His-topathology indicated severe, progressive, generalized muscle fi-brosis of undetermined etiology.


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increased dead-in-shell, increased egg binding that isnot responsive to vitamin A and calcium supplemen-tation and decreased fertility. Cockatiels and otherpsittacine birds showing these clinical signs haveresponded to vitamin E and selenium supplementa-tion and antiprotozoal therapy. In one study, treat-ment of giardiasis resulted in an increase in serumvitamin E levels from a deficiency state into thenormal range.49

A selenium-responsive progressive ascending paraly-sis in fledgling mocking birds fed a commercial catfood has been reported.85 Necropsy findings weresuggestive of a viral encephalitis; however, clinicalsigns were similar to vitamin E- and selenium-re-sponsive paralysis in cockatiels. All affected birdsresponded to parenteral administration of seleniumfollowed by oral vitamin supplementation. Otherspecies of birds being raised at this facility were notaffected.

Vitamin E deficiency also occurs in piscivorous birdsfed an unsupplemented diet of frozen fish (especiallysmelt). In birds of the family Ardeidae (herons andbitterns), the deficiency manifests initially as fatnecrosis accompanied by steatitis. In pelicans,myodystrophy predominates.105

Supplementation with injectable and oral vitamin Eis the recommended treatment; however, the patientmay or may not respond depending on the severity ofdamage. Muscular dystrophy may resolve with sup-plementation, but encephalomalacia rarely respondsto therapy. 14

Hypovitaminosis B1 (Thiamine)Clinical signs of hypothiaminosis include anorexia,ataxia, ascending paralysis and opisthotonos.51 Opis-thotonos (“star-gazing”) may result from paralysis ofthe anterior muscles of the neck resulting in pseudo-hypertonus of the muscles of the dorsal aspect of theneck (see Color 48). Histologically, thiamine defi-ciency causes a polyneuritis with myelin degenera-tion of peripheral nerves. Adrenal hypertrophy andedema of the skin are also characteristic of thiaminedeficiency. Affected birds generally respond withinhours of oral or parenteral administration of vitaminB1. A response to treatment provides a presumptivediagnosis. Administration of thiamine is a usefuladjunct to therapy in many nonspecific neurologicdisorders.

Hypovitaminosis B2 (Riboflavin)Curled toe paralysis occurs in poultry and is seen innestling budgerigars with riboflavin deficiency (seeColor 48). Other signs include weakness, emaciationin the presence of a good appetite, diarrhea, walkingon the hocks with toes curled inward and atrophy ofleg muscles. Chicks fed a deficient diet may developclinical signs as early as 12 days of age.61 Histologi-cally, a demyelinating peripheral neuritis is observedwith edema of the nerves (especially the ischiatic andbrachial nerves). There is Schwann cell proliferationand swelling, perivascular leukocytic infiltration andsegmental demyelination accompanied by accumula-tion of osmophilic debris in the cytoplasm ofSchwann cells.61 Gliosis, chromatolysis in the spinalcord and degeneration at the neuromuscular end-plate may also be observed. Treatment involves ad-ministration of oral or parenteral riboflavin and dietcorrection; however, many of the changes are irre-versible, especially in chronic cases.

Hypovitaminosis B6 (Pyridoxine) Neurologic signs associated hypovitaminosis B6 arecharacteristic, with the bird exhibiting a jerky, nerv-ous walk progressing to running and flapping thewings. The bird then falls with rapid, clonic tonichead and leg movements. These convulsions are se-vere and may result in death due to exhaustion.51

Hypovitaminosis B12 (Cyanocobalamine)Deficiency in a Nanday Conure was reported to causesubacute, multifocal white matter necrosis.51

Traumatic

Concussion LesionsConcussive head trauma is fairly common in free-ranging as well as companion and aviary birds. Headtrauma may occur at night when a panicked bird fliesinto an enclosure wall or if birds fly into windows ormirrors. Injured birds may remain on the bottom ofthe enclosure and exhibit depression, head tilt, cir-cling or paresis of a wing or leg. Blood may be presentin the mouth, ears or anterior or posterior chamberof the eye. Anisocoria and delayed pupillary lightresponse may be present and convulsions may occurif the bird is disturbed.

Fractures of the skull or scleral ossicles may be de-tected radiographically. In some cases, a bruisemight be visualized on the head that is the result ofmeningeal hemorrhage seen through the cranium.Blood actually leaks into bone and is not subdural(see Color 14).51 If the vessels in the neck are rup-


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tured, the pneumatic spaces in the skull may fill withblood obscuring evidence of trauma. It is very rare forhemorrhage to occur within the brain parenchyma.Unconsciousness with a loss of normal physiologicnystagmus indicates a brainstem lesion with a poorprognosis.88

Treatment is supportive and involves maintainingthe bird in a dark, quiet, cool area with no distur-bances. Dexamethasone appears to be the most im-portant therapeutic agent. The prognosis is guarded-to-poor if the bird is convulsing.

Compressive LesionsPigmented calvarium is characterized by a yellowdiscoloration (hemosiderin) in the skull, especiallythe pneumatic spaces of the temporal bones. Thesepneumatic cavities help regulate CSF pressure.There is no definitive correlation as yet between thiscondition and neurologic signs. Inflammation of thefrontal bone was reported as a cause of opisthotonosand depression with violent convulsions. 51 Jugularstasis occurs secondary to thyroid enlargement andresults in increased intracranial pressure. Hydro-cephalus and intracranial masses cause compressiveinjury to the brain or spinal cord. With hydrocepha-lus, the cortex over the lateral ventricles has a “blis-ter-like” appearance at necropsy.84 Imaging tech-niques (CT or MRI) and EEG studies may be helpfulin diagnosing these conditions.

Spinal AbnormalitiesSpinal fractures may be the result of injury or meta-bolic bone disease and may cause compression of thespinal cord. Tumors may affect the spinal cord bydirect invasion or compression. MRI, CT scans andscintigraphy are useful imaging modalities for iden-tifying these lesions, which may not be visible withplain radiographs, especially in the acute phase.

The junction of the fixed synsacrum with the moreflexible portion of the thoracolumbar spine is a loca-tion susceptible to mechanical stress and vertebralsubluxation. In broiler chickens, a congenital defectof the vertebral facets of T6 and T7 allows ventraldisplacement of T7, producing spondylolisthesis andvarying degrees of spinal cord compression.148 In aKing Penguin, spondylolisthesis was believed to bethe result of trauma because no articular defectswere observed.

The intervertebral discs of birds differ from those ofmammals. They consist of a fibrocartilaginous cen-tral region surrounded by a “C”-shaped synovial cav-

ity that extends around the dorsal and lateral mar-gins of the disc. A fibrocartilaginous, wedge-shapedmeniscus protrudes into the joint cavity from thedorsal and lateral margins.37 This zygapophysealjoint has hyaline cartilage with an interveningsynovial cavity. With intervertebral disc rupture, thismeniscus is driven into the spinal canal along withthe fibrocartilaginous disc material (see Color 14).

In a Black Swan, cervical intervertebral degenera-tive joint disease and spondylosis caused spinal cordcompression and associated neurologic signs. Inmammals with spondylosis, ventral and lateralosteophyte formation result in osseous bridging be-tween adjacent vertebrae, while dorsal and dorsolat-eral osteophyte formation, as occurred in this swan,are rare. Spondylosis is believed to be the result ofdegenerative changes in the annulus fibrosis and inter-vertebral disc as a result of continuous heavy stress. Inbirds, the joints between vertebral bodies are synovialand in this swan, noninflammatory, degenerativechanges were associated with the spondylosis. Thedegeneration, rupture and atrophy of the synovial-lined, fibrous intervertebral meniscus may have beeninvolved in the pathogenesis of this disease.57

Dexamethasone and forced rest are the only recom-mended therapies for birds with spinal lesions.Myelography and spinal surgery have rarely beenperformed in birds. Naloxone and thyrotropin releas-ing hormone are beneficial in mammalian patientswith spinal cord trauma, but their effects in avianpatients are unknown.

Peripheral Nervous System

TraumaConcussive peripheral nerve trauma occurs as a re-sult of long bone fractures or impact trauma. Thelevel of nerve injury (eg, neurapraxia, neurotmesis,axonotmesis or complete transection) determines theprognosis. In many instances, nerve dysfunction istransient; however, as in the case of brachial plexusavulsion, the damage may be permanent.

Brachial plexus avulsion occurs most commonly intraumatized free-ranging birds (Figure 28.8).34,46

Clinically, there is evidence of denervation of theaffected wing including lack of pain perception, pa-ralysis with loss of withdrawal reflex and atrophy ofthe muscles of the affected wing and the ipsilateralpectoral muscles. Signs of Horner’s syndrome may bepresent including ptosis and a dropped “horn” on theaffected side of “horned” owls such as Screech and


734

Great Horned Owls. Because of the skeletal musclein the avian iris, miosis is not a consistent feature ofHorner’s syndrome. Interruption of the sympatheticpathway from T1 and occasionally T2 segments re-sults in these clinical signs.

A long bone fracture may or may not be associatedwith peripheral nerve injuries. It may be difficult todetermine the level of nerve injury in birds presentedwith clinical signs associated with a unilateral pe-ripheral neuropathy involving one extremity. Typi-cally, birds with neurapraxia improve clinicallywithin two to four weeks, while those with axonot-mesis and neurotmesis (as with avulsion injury)would not.34 EMG and spinal-evoked potentials canhelp determine the degree of injury. If these are notavailable, it is prudent to treat with supportive carefor approximately one month, with weekly evalu-ation for signs of improved neurologic function.

Abdominal MassesCompressive peripheral nerve trauma generally oc-curs secondary to an expanding mass that appliespressure to the nerve (see Figure 25.10). Because thepelvic nerves pass through the renal parenchyma,tumors or infection of the kidneys can damage thenerves (see Color 21). Ovarian tumors, if very largeor invasive, have also been reported to damage thesenerves. Of 74 budgerigars with abdominal tumors, 64had paresis of one or both legs.104 Paresis is usuallyunilateral in the early stages and is accompanied byabdominal distention.

Renal adenocarcinomas occur more commonly inmales than females and the incidence is higher inpsittacine than passerine birds (see Color 25). Themost common sign is a unilateral leg paresis pro-gressing to paralysis. Affected birds may demon-strate an abdominal lift. The paresis may becomebilateral, but systemic signs usually develop beforethe contralateral limb is affected. The bird may havea palpable abdominal mass with polydypsia andpolyuria. Grossly, these tumors are 1 to 2.5 cm indiameter, irregular, ovoid, globular, white or off-white with cysts or necrotic foci. They may metasta-size to the liver (see Color 25).

The biologic behavior, clinical signs and gross ap-pearance of embryonal nephromas are similar to re-nal adenocarcinoma. They usually contain morecysts and necrotic foci and are less frequently associ-ated with paralysis. They occur in younger birds(three to five years old). Ovarian adenocarcinomasand granulosa cell tumors usually cause anorexia,weight loss and diarrhea, but can invade the kidneysand compress the pelvic nerves. If these tumors causeparalysis, the patient is likely to show an abdominallift.

FIG 28.8 a) An immature Red-tailed Hawk was found down andunable to fly near a highway. A severe wing droop was present andradiographs indicated a fractured coracoid. The wing was placedin a figure-of-eight bandage and the fracture healed without com-plication. When the bandage was removed, the bird still had asevere wing droop, no deep pain and muscle atrophy involving mostof the palpable muscle masses. b) At necropsy, swelling (arrows)and discoloration were present in the brachial plexus suggestiveof an avulsion-type injury.


735

All of these tumors are associated with a poor prog-nosis. Excision may be attempted but if neurologicsigns are present, the neoplasm is generally not ame-nable to resection. These tumors cause a peripheralneuropathy with a loss of withdrawal reflex not ob-served with a spinal cord lesion.

Egg binding or internal trauma associated withoviposition may result in hemorrhage and swellingaround the area of the pelvic plexus, causing a tran-sient paresis or paralysis secondary to neurapraxia.

Circulatory DisturbancesBoth peripheral and central neuropathies have beenas so c ia t e d wi th d imin i s he d c i r cu la t i on .Atherosclerosis occurs with some degree of frequencyin birds. Most commonly, no clinical signs are associ-ated with this condition, and affected birds are sim-ply found dead in their enclosure. In some cases,however, neurologic signs may be observed.Atherosclerosis of the carotid arteries has been de-scribed as a cause of ischemia and cerebral hyperten-sion.22,51,64

Neurologic signs associated with atherosclerosis in-clude a sudden onset of blindness, ataxia, paresis andseizures. A Blue-fronted Amazon Parrot, which had a90 to 95% reduction in lumen diameter in one carotidartery and a 60 to 70% reduction in the other due toatherosclerosis, presented with clinical signs of re-gurgitation once daily, an “aura-like” behavior andholding the right leg in front of the body while goinginto a semiconscious state. Another Blue-frontedAmazon Parrot with progressive hind limb paresiswas found to have severe atherosclerosis at ne-cropsy.64

Signs ranging from blindness and ataxia to opistho-tonos and seizures have been associated with cere-br ov ascular acc id e nts an d i s che mic in-farction.22,46,51,130 MRI, CT scans and EEG may beuseful in diagnosing these lesions.

Primary Neoplasms of the Nervous SystemGlioblastoma multiforme, choroid plexus tumors,Schwannomas and astrocytomas, pineal body tu-mors, undifferentiated sarcomas and hemangiomashave been described in the nervous system of com-panion birds.51,116,118,140 Clinical signs vary with thelocation of the neoplasm. Imaging with MRI or CTmay be useful in determining the location of themass; however, all neural tumors are associated witha grave prognosis. Phenobarbital for control of sei-zures and dexamethasone to decrease cerebrospinal

fluid production (thus, intracranial pressure) mayprovide symptomatic relief.

Pituitary adenoma or pituitary chromophobe ade-noma occurs in young (four years old), predominantlymale budgerigars with a two to three percent preva-lence. These tumors arise from chromophobe cellsand may or may not be functional, secreting tumors.The avian pituitary gland secretes LH, FSH, TSH,ACTH, growth hormone, melanocyte stimulatinghormone (MSH) and prolactin (in Columbiformes).These tumors are reported to cause a classic clinicalsyndrome described as somnolence with occasionalconvulsions, uncoordinated wing-flapping and clonicleg twitches, followed by unconsciousness.51 Clinicalsigns are usually the result of compression of thebrain and cranial nerves. Incoordination, tremorsand inability to perch have also been reported.91 Poly-dipsia and polyuria, cere color change, feather abnor-malities and obesity may occur with functional tu-mors. Exophthalmos, visual deficits, lack of pupillarylight response and mydriasis may be presentalso.97,140

A tentative diagnosis may be confirmed with con-trast-enhanced CT scanning of the skull. Becauseclinical signs are primarily related to compression ofthe brain and not to adrenal hypersecretion, therapywith o,p’-DDD is not generally indicated.140 Radia-tion therapy is effective in treating human and ca-nine pituitary tumors and may be efficacious in birds.A report suggests that this tumor is transmissible;however, this theory has not been confirmed.54

Metabolic Neuropathies

Hepatic EncephalopathyBirds with severe liver disease may demonstratesigns of hepatic encephalopathy. Hepatic lipidosis,mycotoxicosis, hemochromatosis and vaccine-in-duced hepatopathy have been reported to cause clini-cal signs of depression, ataxia, diminished consciousproprioception and seizures (see Color 20).98,110,135,146

With hepatic encephalopathy, these signs usually oc-cur shortly after eating when the blood levels ofneurotoxins absorbed from the gastrointestinal tract(and not properly processed by the liver) are high.Various compounds are believed to contribute to theclinical signs associated with hepatic encephalopa-thy including ammonia, glutamine, glutamate, alphaketoglutarate, aromatic amino acids, methionine,mercaptans and short chain fatty acids.18 In addition,abnormal neurotransmitters, alterations in theblood-brain barrier, alterations in neuroreceptors, al-


736

tered cerebral sensitivity and hypoglycemia contrib-ute to the development of clinical signs associatedwith hepatic encephalopathy.

Postprandial blood ammonia concentrations may beelevated and can be determined using a conspecificcontrol bird.135 In a Toco Toucan with hepaticencephalopathy, the three-hour postprandial bloodammonia level was 350 µg/dl, while the conspecificcontrol was only 86 µg/dl. Ammonia tolerance testsmay be beneficial in diagnosing some cases; however,a parallel test should be performed on an asympto-matic bird of the same species. Serum bile acidsassays are a more reliable and safer test of hepaticfunction.

Treatment should be directed toward the underlyingcause of hepatic failure. Lactulose syrup and a low-protein, high-carbohydrate, high-quality protein dietwith a vitamin supplement may provide sympto-matic relief while the underlying hepatopathy is cor-rected.135 Neomycin sulfate may decrease the forma-tion of ammonia by reducing the quantity ofgram-negative bacteria in the colon.

HypocalcemiaA syndrome characterized by opisthotonos, tonic ex-tension of the limbs and convulsions has been de-scribed in young (two- to five-year-old) African GreyParrots.43,53,95,101,122,123 Initially, an affected bird mayonly seem uncoordinated and fall from its perch. Thefrequency gradually increases, seeming to be precipi-tated by some external stimulation. Eventually, sei-zure activity is pronounced and may become constantor prolonged. Serum calcium levels are below 6.0mg/dl with concentrations as low as 2.4 mg/dl re-ported. It has been shown that parathyroidectomizedbirds begin to have seizures when the serum calciumconcentration falls below 5.0 mg/dl.127 Birds demon-

strating only intermittent incoordination may stillhave normal serum calcium levels. This conditionhas also been observed in Amazon parrots andconures.122

At necropsy, the parathyroid glands of affected Afri-can Grey Parrots are grossly enlarged, presumably inresponse to the low serum calcium concentrations(see Color 14). Parathyroid hyperplasia and degen-eration are prominent histologic findings. Vacuola-tion of the cells of the adrenal glands is a consistentfeature and may be an indication of stress. There isno skeletal demineralization present in this syn-drome.122 In most birds with signs of nutritional sec-ondary hyperparathyroidism, serum alkaline phos-phatase activity is increased; however, this changehas not been found to occur with the hypocalcemiasyndrome in African Grey Parrots.53

The etiology and pathogenesis of this condition re-mains speculative. Affected birds are usually wild-caught and are maintained on a diet deficient incalcium and vitamin D3 (usually a whole-seed diet).It appears that these birds are not able to mobilizebody calcium stores (as occurs in cows with “milkfever”). Vitamin A deficiency may also play a role, ashypovitaminosis A has been shown to inhibit osteo-clast activity.123 It has been postulated that a virusthat affects parathyroid function is the cause of thisproblem; however, attempts to demonstrate viralparticles using electron microscopy have failed. An-other hypothesis suggests that there is increasedrenal excretion of calcium.95,122

Diazepam may be used as an anticonvulsant, butbirds generally rapidly respond to the parenteraladministration of calcium gluconate. Seizure activitywould be expected to cease well before serum calciumlevels return to normal.53 Corticosteroids should notbe used in these patients because they increase uri-nary excretion and decrease intestinal absorption ofcalcium.

Once the serum calcium concentration has returnedto within normal limits, the patient should be placedon a proper diet with calcium and vitamin supple-mentation. Foods such as dairy products should beencouraged, while those high in fat such as seedsshould be eliminated. Serum calcium concentrationshould be evaluated periodically (every two to fourmonths) to determine if alterations in therapy areindicated. The prognosis for full recovery appears todepend on the severity of damage to the parathyroidglands. If the condition is detected before complete

CL IN ICAL APPL ICAT IO NSThe corpus striatum is well developed and is considered themain center for association in birds; consequently, instinctsdominate avian behavior, which may account for some of theself-mutilation that occurs in companion birds.

Birds are ten to twenty times more susceptible than mam-mals to acetylcholine inhibitors found in organophosphateand carbamate pesticides. Young birds and males are alsomore susceptible.

Because withdrawal of an extremity following stimulation isa segmental reflex that does not require an intact cervicalspinal cord for normal response, movement does not indi-cate the patient is able to feel the stimulus.


737

degeneration of the glands has occurred, the progno-sis is favorable.

Because it appears that these birds cannot mobilizebody stores of calcium, long-term prevention of recur-ring problems requires that birds receive adequatelevels of calcium in proper balance with phosphorus,as well as sufficient levels of vitamins A, D3 and E.

HypoglycemiaHypoglycemia may occur as a result of starvation ormalnutrition, hepatopathy, endocrinopathies andsepticemia. Blood glucose less than 150 mg/dl (or halfthe species’ normal value) may be an indication ofhypoglycemia.146 Seizure activity usually occurs oncethe blood glucose level falls below 100 mg/dl. Therapyshould consist of 1.0 ml/kg IV of a 50% dextrosesolution for acute relief of clinical signs, while theunderlying cause of the problem is being determinedand corrected. Dextrose solutions (>2.5%) should beadministered intravenously with caution becausethey are hypertonic and may cause tissue damage ifperivascular leaking occurs. Dextrose will compro-mise a patient’s acid-base balance and should not beused in dehydrated birds.

Seizures and Idiopathic Epilepsy

Seizures in birds can have numerous etiologies andvarious clinical presentations (Table 28.1). A typicalseizure may consist of a short period of disorientationwith ataxia followed by falling to the enclosure flooras a result of the loss of the ability to grip the perch(Figure 28.9). The bird may remain rigid or havemajor motor activity for a few seconds or a few min-utes. Voiding may or may not occur. The postictalphase is variable.

TABLE 28.1 Common Causes of Seizures in Birds

Nutritional (Calcium, phosphorus and vitamin D3 imbalances, vi-tamin E and selenium deficiencies, thiamine deficiency, hypovi-taminosis B6)

Metabolic (Heat stress, hypocalcemia, hypoglycemia, hepaticencephalopathy)

Toxic (Heavy metals, insecticides)

Infectious (Bacterial, fungal, viral or parasitic)

Traumatic

Neoplastic

Hypocalcemic (African Grey Parrots)

Hypoglycemic (Raptors)

Idiopathic EpilepsyIdiopathic epilepsy is used as a diagnosis when othercauses of seizures have been ruled out. A syndromeof idiopathic epilepsy has been described in Red-loredAmazon Parrots that has been suggested to have agenetic basis.124 Seizures of undetermined cause oc-cur with some degree of frequency in Greater IndianHill Mynahs as well. Mild to severe seizure activitymay occur in these birds with signs ranging from“periodic trance-like states” and “stiffening up” togrand mal-type seizures.

Diazepam can be used to temporarily interrupt sei-zure activity.125,126,146 Long-term phenobarbital at adose of 4.5-6.0 mg/kg PO BID titrated to effect, ap-pears to be beneficial in reducing the frequency andseverity of seizures in these birds.124 Blood phenobar-bital concentration should be determined approxi-mately one month after institution of therapy toevaluate the dosage. Owners should be advised thatthe therapy does not “cure” the condition, and theyshould keep a calendar recording seizure activity andseverity.

The use of electroencephalograms in diagnosing epi-lepsy is difficult in any species of animal. The knowl-edge of normal electroencephalogram patterns foravian species is limited as is the availability of theequipment and trained personnel to make and evalu-ate the EEG. Even in species where EEG patternsindicative of epilepsy are established, it is recognizedthat between seizures, the EEG may be normal.146

Lafora Body Neuropathy

Lafora body neuropathy has been reported as a causeof fine, continuous myoclonus in one cockatiel andweakness, anorexia and dyspnea in another cocka-tiel.1,9,11 This disease is characterized by the forma-tion of glycoprotein-containing cytoplasmic inclusionbodies within neurons. This accumulation of glyco-proteins is believed to be the result of a defect inintracellular metabolism. In humans, the conditionis known as familial progressive myoclonic epilepsy.It has also been diagnosed as a cause of spontaneousconvulsions or epilepsy in beagles, miniature poodlesand basset hounds. The inclusions may be found inother organs including the liver, heart, skeletal mus-cle and sweat glands. In the affected cockatiel, La-fora-like particles were identified diffusely through-out the liver.9,11


738

Xanthomatosis

The etiology of xanthomatosis is unknown but itseems to develop as a response to deep inflammation(see Chapter 25). The clinical manifestation is thickyellow skin usually in the area of the sternum andventral abdomen. Xanthomatosis may affect thebrain where it appears in association with bloodvessels.51

Toxic Neuropathies

Heavy MetalsLead and zinc poisoning are the most common causesof toxicity in birds (see Chapter 37).92 In addition tocommon sources of lead contamination, chronic expo-sure to automobile exhaust has been shown to con-tribute to the cumulative lead concentrations in bodytissues.88

Clinical signs associated with lead intoxication aredependent on the amount ingested and the chronicityof the intoxication. Lead adversely affects all bodysystems by inhibiting enzyme activity and proteinformation.100 Nervous, digestive and hematopoieticsystems are most affected. Neurologic changes sug-gestive of plumbism include lethargy, depression,

weakness, ataxia, paresis, paralysis,loss of voice, head tilt, blindness, cir-cling and seizures.

Lead intoxication causes a demyeli-nation of the vagus nerve and a blockof presynaptic transmission by com-petitive inhibition of calcium. De-myelination produces the clinicalsigns associated with peripheralneuropathy. Lead encephalopathy isthe result of diffuse perivascularedema, increases in cerebrospinalfluid and necrosis of nerve cells.100

Histologically, neurologic lesions as-sociated with plumbism includene u ro n a l d e g e ne r at i o n w i thshrunken, angular, basophilic neu-rons of the cerebral cortex andedema of Virchow-Robin spaces andleptomeninges.59,106 Vacuolation ofthe neuropil of the cerebral cortex,optic lobes and medulla may be pre-s ent . Gro ss and microsco pi cneurologic lesions may be absent,even in birds with neurologic signs.32

Botulism (Limber Neck)Botulism in birds is usually the result of ingestion ofthe exotoxin of Clostridium botulinum type C. Occa-sionally C. botulinum type A and type E are involved.The organism is an anaerobic, spore-forming bacil-lus. Spores are present in the soil of many wetlandsand are numerous in marsh areas with a history ofthe disease. The spores are environmentally stable,can survive in the soil for years and are resistant toheat and chemical disinfectants.

Botulism is uncommon in companion birds, but oc-curs with some degree of frequency in waterfowl.Decaying organic matter provides adequate sub-strate for development of the clostridial spores. Thetoxin can persist for months under alkaline condi-tions (pH 9). Intoxication occurs following ingestionof contaminated food such as necrotic tissue (plant oranimal) or dipterous maggots and other inverte-brates. Maggots concentrate the toxin without beingaffected. Birds eat the toxin-laden maggots and dis-seminate the disease. It is generally the larval stagesof blowflies and fleshflies (Calliphoridae and Sarco-phagidae) that are found in high concentrations ondecomposing carcasses and carry the greatest con-centrations of toxin.39 In an outbreak in pheasants,

FIG 28.9 A mature Umbrella Cockatoo that was maintained in a dark room on a wild-bird-seed diet was presented for an acute onset of convulsions. The bird was severelydepressed and was unable to stand. Note the poor general condition of the feathers. Thebird did not respond to supportive therapy. Necropsy findings included microhepatia,hypertrophy of the parathyroid glands and enlarged adrenal glands.


739

20,000 maggots were collected from one carcass, eachcontaining 4x104 mouse MLD of type C toxin/g ofmaggots. It has been estimated that one ounce oftype C toxin could kill the entire population of theUnited States.95

The toxin interferes with the release of acetylcholineat motor endplates causing signs of peripheralneuropathy. All peripheral nerves, including cranialnerves, are affected. The classic clinical sign is alimber neck resulting from paralysis of the cervicalmusculature. Most birds exhibit hindlimb paresisfirst, which is characterized by sitting on their ster-num with legs extended behind their body.12 Paraly-sis of the wings followed by loss of control of the neckand head are observed in the terminal stages. Greendiarrhea with pasting of the vent are also commonwith botulism.12,39,48 Inconsistent clinical findingswith botulism are chemosis, swelling of the eyelidsand nictitans, ocular discharge and hypersaliva-tion.12,48

Gross and histologic examination generally fail toreveal any lesions. In some cases, maggots may beobserved within the proventriculus, and some birdshave a pericardial effusion.12,48 The toxin can be de-tected in stomach contents, serum or plasma. Themouse protection test is used to provide an an-temortem diagnosis in most cases. Mice are chal-lenged with the serum of an affected bird and controlmice are left untreated while others receive anti-toxin. A positive diagnosis is made if only unpro-tected mice die. This test is accurate approximately75% of the time.48,62 In an outbreak where toxin wasnot detected in serum, the toxin was recovered fromthe spleen and liver.39

Therapy is primarily supportive. Cathartics, laxa-tives and drenches are used to flush unabsorbedtoxins through the gastrointestinal tract. Tube-feed-ing provides nutritional support for birds that areunable to eat and drink. Antitoxin may be adminis-tered intraperitoneally, but it is not commerciallyavailable and its benefits are equivocal.12,48,72

Efforts should be made to prevent exposure of birdsto maggots and other sources of botulism toxin.Ponds and lakes should not be used for disposal ofcarcasses and organic debris. They should be dredgedperiodically, and a fountain or other means of aera-tion should be provided.

PesticidesThe United States Environmental Protection Agencyhas registered 36 different organophosphate and 46

carbamate compounds such as carbaryl (Sevin dust),dursban (chloropyrifos), diazanon, malathion, di-chlorvos and methyl carbamate.113 Both of these com-pound classes are acetylcholinesterase inhibitorsthat bind to and subsequently inactivate acetyl-cholinesterase causing an accumulation of acetyl-choline at the postsynaptic receptors. Organophos-phate bonds are considered irreversible, whilecarbamate bonds are slowly reversible (spontaneousdecay in several days). Acetylcholine is the neuro-transmitter found at autonomic ganglia (both sympa-thetic and parasympathetic); postganglionic para-sympathetic nerves affecting smooth muscle, cardiacmuscle and exocrine glands; and at neuromuscularjunctions of the somatic (skeletal muscle) nervoussystem.72,119

Birds are 10 to 20 times more susceptible to theseacetylcholine inhibitors than mammals. Young birdsand males are also more susceptible.94 The develop-ment of clinical signs is dependent on the concentra-tion of the pesticide, the route and proximity of expo-sure, the amount of ventilation, the species of birdand its physical condition.72 Exposure in companionbirds is generally accidental or the result of inappro-priate use of insecticide products. The most commonroute of exposure is inhalation.

Two types of neuropathy and corresponding clinicalsigns have been described related to toxicosis withacetylcholinesterase inhibitors.72 Acutely, clinicalsigns are related to excessive stimulation of acetyl-choline receptors. Signs include anorexia, crop stasis,ptyalism, diarrhea, weakness, ataxia, wing twitchingand muscle tremors, opisthotonos, seizures, brady-cardia and prolapse of the nictitans.72,94,113,119 Brady-cardia and dyspnea with crackles and wheezes mayoccur as the toxicosis progresses. Respiratory failureis usually the cause of death and results from in-creased mucus secretion, bronchoconstriction andparalysis of respiratory musculature.

The second type of neuropathy is an organophos-phate ester-induced neuropathy, which is not associ-ated with an inhibition of acetylcholine.73 The onsetof clinical signs is delayed (7 to 21 days after expo-sure) and is the result of a symmetric distal primaryaxonal degeneration of the central and peripheralnervous systems, with secondary myelin degenera-tion. Clinical signs include weakness, ataxia, de-creased proprioception and paralysis.

Diagnosis of acetylcholinesterase inhibition is usu-ally based on clinical signs and a history of exposure


740

to these compounds. Cholinesterase assay may beperformed on blood, plasma, serum or brain tissue. Adecrease in acetylcholinesterase of 50% from normalis considered diagnostic.73 Normal avian plasmacholinesterase levels are reported to be greater than2000 IU/l. A new cholinesterase test requires only0.01 ml of serum and results may be available in fiveminutes.113

Intoxication is best treated with atropine, prali-doxime chloride (2 PAM) and supportive care (seeChapter 37).119

The exact mechanism of action of organochlorideinsecticides, such as DDT, is unknown, but clinicalsigns are usually neuromuscular, resulting fromeither stimulation or depression of the central nerv-ous system.11 There is no known antidote for organo-chloride intoxication. Birds with seizures or othersigns of CNS stimulation should be tranquilized orlightly anesthetized with a long-acting agent such asphenobarbital. In cases of CNS depression, stimu-lants may be beneficial. Cathartics, activated char-coal and general supportive care should be providedas necessary (see Chapter 37).

Therapeutic AgentsDimetridazole was commonly used to treat trichomo-niasis, giardiasis and histomoniasis. Toxicity resultsin birds with increased water consumption (in-creased intake of drug). Convulsions, wing flappingand opisthotonos have been reported in budgerigars,goslings, pigeons and ducks. Histologically, largeclear spaces are present around blood vessels, neu-rons and glial cells. Neurons have a pyknotic nucleusand eosinophilic cytoplasm. Dimetridazole is nolonger commercially available in the United States.

Metronidazole toxicity has been reported in dogs andcats, but not in companion birds. Clinical signs relateprimarily to the vestibular system and includeataxia, incoordination, proprioceptive deficits, nys-tagmus, depression, paresis, tremors and seizures.Treatment involves limiting further absorption of thedrug (eg, absorptives, emetics and cathartics), fluidtherapy to increase renal excretion, control of seizureactivity and supportive care.

Other NeurotoxinsMany plants are toxic to the nervous and digestivesystems. Generally, birds are more resistant thanmammals to plant-derived toxins (see Chapter 37).

Citreoviridin and tremorgens are two types of myco-toxins that primarily affect the neural system. Fusa-

riotoxins and ochratoxins also produce nervous dis-orders. A syndrome characterized by cervical paresisin free-ranging Sandhill Cranes has been associatedwith mycotoxicosis.107

Domoic acid poisoning was diagnosed as the cause ofdeath in Brown Pelicans and Brandt’s Cormorantsexhibiting neurologic signs. Twenty-seven of 39 af-fected birds died within 24 hours.153 Domoic acid is aneurotoxin produced by marine diatoms. It is anexcitatory toxin that binds to both pre- and postsy-naptic kainate receptors in the brain, resulting incontinuous depolarization of neurons until cell deathoccurs. It was theorized that this epornitic wascaused by the ingestion of contaminated anchovies,which had fed on the diatoms.

Infectious Neuropathies

Fungal

The nervous system may be a secondary site foraspergillosis lesions that may cause ataxia, opistho-tonos and paralysis. In infected birds, yellowish, my-cotic nodules may be grossly visible within the brainor spinal canal. Fungal granulomas may compress orinvade peripheral nerves and cause unilateral orbilateral paresis or paralysis (see Color 21).47 Spinalaspergillosis has been diagnosed in several penguinsat the San Francisco Zoological Gardens. Fungalelements are usually detected histologically (seeChapter 35).

Dactylaria gallopava has been reported in Grey-winged Trumpeter Swans and gallinaceous birds.The organism is present in wood chips and barklitter. Infections characterized by encephalomyelitisoccur following the inhalation of fungal spores.Cladosporius (Exophiala) and Mucomyces have alsobeen reported to cause meningoencephalitis.31

Parasitic

ToxoplasmaToxoplasma gondii infections are reported primarilyin Galliformes and Passeriformes with lesions in-volving the brain and skeletal muscles. Cats are theonly host known to excrete infectious oocysts.36 Con-sidering avian species, it would seem that raptors are


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most likely to become infected because they prey onthe same types of animals as cats. Although toxoplas-mosis has been reported in raptors, they appear to bemore resistant to infection than other birds.36,78

Clinical signs include anorexia, pallor, diarrhea,blindness, conjunctivitis, head tilt, circling andataxia. Infection may occur from ingestion of copro-phagic arthropods or food and water supplies con-taminated with feces from infected cats. Encapsu-lated cysts (round or oval) are found in the brainhistologically. A definitive diagnosis is made using alatex agglutination serum test or immunohisto-chemical staining of affected tissues. There is vari-ation among avian species with respect to the anti-body response generated against Toxoplasma sp.Chickens do not develop antibodies, while raptors,pigeons, canaries and finches have been shown todevelop positive agglutination antibody titers.36,70,144

In experimentally infected raptors, cysts were foundin the brain and muscles (skeletal and cardiac) evenwhen no clinical abnormalities were noted.

In canaries and finches, toxoplasmosis has beenshown to cause loss of myelinated axons in the opticnerve resulting in blindness and conjunctivitis.144

Tachyzoites could be demonstrated in the detachedand intact retinae, lenses and exudate from the vit-reous humor. Focal, disseminated, chronic inflamma-tion with accumulations of tachyzoites characterizedthe histologic findings in the brains (see Chapter 36).

SarcocystisSarcocystis spp. infect a broad range of hosts in sev-eral orders of birds. Infection in birds is reported tobe less common than in mammals; however, infectionhas been reported in over 60 species of birds, withOld World psittacines apparently more susceptible(see Chapter 36). Unlike many other species of Sar-cocystis, S. falcatula schizonts can persist in aviantissues for up to 5.5 months.36 It is believed thatcockroaches and flies may be transport hosts for theparasite.26,52 Raptorial species may become infectedby ingestion of prey containing the encysted organ-ism.1,36

Histologically, the organisms are elongated, spindle-or banana-shaped, and grouped into packets withina spherical- to spindle-shaped cyst. Granulomatousinflammation consisting of macrophages and lym-phocytes forming nodular and diffuse aggregates isassociated with these cysts. With electron micros-copy, characteristic polar rings and micronemes maybe discernable.58

SchistosomiasisGranulomatous encephalitis caused by the bloodfluke Dendritobilharzia sp. has been reported inswans.77,147 Neurologic signs included head tilt, cir-cling, weakness and extension of the head and neck.Granulomas containing macrophages, giant cells,lymphocytes and occasional heterophils and fi-broblasts were identified within the cerebrum andcerebellum of affected birds. Ova of the parasite wereidentified within these lesions. Adult flukes wereidentified within the blood vessels in one bird. Adultschistosomes usually live within veins; however,those of the genus Dendritobilharzia live within ar-teries. Adults have little host-specificity.

Baylisascaris sp.Baylisascaris procyonis is the ascarid of raccoons andis a zoonotic organism that can cause fatal menin-goencephalitis in humans. Over 40 species of mam-mals and birds have been shown to develop clinicalcerebrospinal nematodiasis following infection.4,5,68,99

Free-ranging birds are infected by ingesting raccoonfeces, while companion birds may become infected byingestion of food contaminated with parasite eggs.The eggs may remain viable and infective in theenvironment for years.

Clinical signs are nonspecific and include depression,ataxia and torticollis. The onset may be acute orchronic, possibly related to the number of larvaeinvolved. Prolonged migration of a single larvawithin the brain could produce chronic, progressivesigns. Treatment with ivermectin has been com-pletely ineffective.5

Gross lesions are generally absent. Edema of thebrain and spinal cord, encephalitis, encepha-lomalacia, eosinophilia around sections of larvae, de-generative foci with heterophils in the neuropil, peri-vascular cuffing and glial cell proliferation areobserved histologically.4,5,38,67,99 In some cases, a crosssection of the parasite may not be observed as thelarvae migrate even after host death.99

FilariaChandlerella quiscali is a filariid nematode of grack-les that has been reported to cause cerebrospinalnematodiasis in emus.7 Gnats are the vectors fornatural infection. The gnat is ingested and the larvaemigrate into the brain or spinal cord and then intothe lateral ventricles of the cerebrum where theymature and produce microfilaria. Affected emuchicks demonstrated torticollis, ataxia, recumbency


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and death. Circulating microfilaria were not detected(see Chapter 36).

Viral Neuropathies

The following viral diseases of birds have neurologicclinical or histologic abnormalities as part of theirpathophysiology; most produce lesions in other sys-tems as well. Only their effects on the nervous sys-tem will be discussed here. For a more completediscussion of these viruses, see Chapter 32.

ParamyxovirusParamyxoviruses (PMV) 1, 2, 3 and 5 have beenisolated from companion birds, and groups 1 and 3have been associated with lesions of the central nerv-ous system.75 Pigeon paramyxovirus causes a non-suppurative encephalitis similar to that describedwith Newcastle disease virus.129

Clinical signs associated with PMV-1 in companionbirds are variable depending on the virulence of thestrain and the species of bird affected. In some cases,the only signs may be acute death and high mortality.Other signs are associated with abnormalities of therespiratory, digestive and nervous systems.23,24,30

Neurologic signs including depression, hyperexcita-bility, ataxia, incoordination, torticollis, head tremor,opisthotonos, muscle tremors and unilateral or bilat-eral wing or leg paresis or paralysis occur more com-monly in older birds and with chronic infections.24,30

Some birds clench their feet while others lose controlof the tongue and their ability to grip with the beak.23

All reflexes are depressed but neurologic signs areexacerbated by excitement. Seizures and runningmovements are often observed just prior to death.Neurologic signs generally persist in birds that sur-vive the acute infection.142

At necropsy, there may be petechiae on the surface ofthe cerebrum and cerebellum.23 Histologically, cen-tral nervous system lesions are commonly observedin the cerebellum, brainstem, midbrain and spinalcord. Neuronal degeneration, gliosis, endothelial cellhypertrophy and lymphocytic perivascular cuffingcharacterize the lesions.30,114

Lymphoplasmacytic meningoencephalitis outbreakshave been described in Pionus species and Neophemaspecies from a quarantine station. These deaths werecaused by an unclassified hemagglutinating virusthat morphologically resembles paramyxovirus.82,84

The disease produced high morbidity and moderate

mortality. Muscle tremors, circling, ataxia, torticol-lis, weakness, depression, paresis and paralysis werethe major clinical signs.

A yellowish periventricular discoloration was theonly abnormal gross brain lesion noted. Histologi-cally, there was lymphoplasmacytic perivascularcuffing adjacent to the ventricles, within the choroidplexus and around the central canal of the spinalcord, sometimes accompanied by edema of theneuropil. Some ependymal cells and few subependy-mal glial cells had equivocal eosinophilic Cowdrytype A inclusions. On electron microscopy, these con-tained virions compatible with paramyxovirus.

Neuropathic Gastric DilatationThere is strong evidence that neuropathic gastricdilatation is caused by a virus (possibly aparamyxovirus). Anorexia, regurgitation, changes infecal consistency, weight loss, pectoral muscle atro-phy and depression are presenting clinicalsigns.55,64,90,139,151 The clinical signs of this diseaseprimarily relate to the gastrointestinal system, withcentral and peripheral neurologic signs occurringonly occasionally.64,150 However, the main histologiclesions involve the nervous system.

Creatine kinase is an enzyme released from damagednerves and muscles. It has been reported that somebirds with neuropathic gastric dilatation have ele-vated serum CK levels; however, an elevation of se-rum CK activity is not specific for this disease andmay occur with septicemia, neuropathies and myopa-thies.60

Microscopic lesions generally involve the brainstem,the ventriculus and the proventriculus. Multifocallymphocytic encephalitis with lymphocytic perivas-cular cuffing, gliosis and neuronophagia characterizethe brainstem lesions.55 Asymmetric lymphocytic po-liomyelitis, lymphocytic perivascular cuffing andgliosis are present in the spinal cord. Multifocal lym-phocytic leiomyositis with smooth muscle degenera-tion and fibrosis are common in the ventriculus andproventriculus.

There is a general loss or depletion of myentericganglion cells (myenteric ganglioneuritis). The gan-glia of gastric and duodenal myenteric plexuses dem-onstrate round cell accumulations (lymphocytes,plasma cells, macrophages). Intranuclear and in-tracytoplasmic eosinophilic inclusion bodies havebeen described within the perikaryon of the celiacganglion and myenteric plexus.90 Virus particles associ-


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ated with the inclusions have been morphologicallysimilar to paramyxovirus particles.

Avian (Picornavirus) Encephalomyelitis This picornavirus has been associated with gastroin-testinal and neurologic signs in Galliformes, Anseri-formes and Columbiformes.8,51,89,132,133 Only one sero-type is recognized but strains vary in neurotropism.Clinical signs include depression, ataxia, paresis orparalysis and severe, but fine head and neck tremors.Neurologic signs occur only in birds less than 28 daysof age.51 No characteristic gross lesions are noted atnecropsy. Neuronal degeneration with lymphocyticperivascular cuffing and gliosis in the brain andspinal cord characterize the disease histologically.89

Polyomavirus (Budgerigar Fledgling Disease)Although not the primary lesions, tremors of thehead, neck and limbs, incoordination and ataxia havebeen associated with polyomavirus in infected birds.Histologically, large, slightly basophilic intranuclearinclusion bodies can be identified in the cerebellarganglionic layers.88,91,131

ReovirusReovirus is commonly reported in imported birds andprimarily affects African Greys, cockatoos and otherOld World Psittaciformes. Clinical signs includeuveitis, depression, emaciation, anorexia, incoordi-nation, ataxia, paresis and diarrhea. Histologically,multifocal necrosis of the liver is present. This is nota neurotropic virus, and the paresis or paralysis isthe result of vascular thrombosis of the extremities.

Togaviridae Viral encephalitis caused by a number of togaviruseshas been reported in numerous species of birds.Clinical signs include depression, ruffled feathers,decreased appetite, dyspnea, profuse hemorrhagicdiarrhea (in emus), ataxia, muscle tremors, weak-ness, unilateral or bilateral paresis or paralysis, tor-ticollis and death. At necropsy, the cerebral hemi-spheres may be softened. Histologically, lesionsinclude nonsuppurative encephalitis, patchy neuralnecrosis, cerebral vasculitis, leukocytic perivascularinfiltrates, microgliosis, meningitis, neuronal degen-eration and myocardial necrosis.121 These changeshave a rostral distribution contrary to most avianviral encephalitides. Vaccines are available and ap-pear to be beneficial in outbreaks.15,51,56,21,121,138

Marek’s DiseaseThis lymphoproliferative disease is caused by a her-pesvirus. Peripheral nerve dysfunction occurs secon-

dary to lymphoid infiltrates. Often birds display aspraddle-leg paralysis with one leg extended forwardand the other back. Grossly, the ischiatic nerves ap-pear enlarged with a loss of striations and a graydiscoloration. In a study of neoplasms of budgerigars,many birds with abdominal tumors also had evidenceof infection with avian leukosis virus; however, simi-lar findings were not confirmed in another study.43,104

Encephalomyelitis in LorikeetsEncephalomyelitis was described in free-rangingAustralian lorikeets.102 Affected birds demonstrateda progressive bilateral paralysis with clenched feet.Perivascular macrophage infiltrates, vascular endo-thelial cell proliferation, gliosis, neuronal necrosisand neuronophagia were observed in the brainstemand spinal cord of affected birds. Edema of the ischia-tic nerve was also a feature. A viral or protozoaletiology has been suggested.

Duck Viral EnteritisDuck viral enteritis is primarily a concern whereferal populations of ducks mingle with captive birds.Clinical signs include photophobia, ataxia, seizures,penile prolapse, lethargy, hemorrhagic diarrhea andserosanguinous nasal discharge. The most notablefinding at necropsy is hemorrhagic bands on thesmall intestine (see Color 14).

Duck Viral HepatitisDuck viral hepatitis is caused by a picornavirus.Clinical signs include lethargy, seizures, opistho-tonos and death. Ducklings suffer the highest mor-tality, and Muscovy Ducks appear to be resistant toinfection with this virus. At necropsy, the liver, spleenand kidneys are enlarged with petechial hemor-rhages. It is recommended to vaccinate breeders be-fore the onset of laying.

Bacterial Neuropathies

ListeriosisListeria monocytogenes is a small, gram-positive,nonsporulating, motile rod that is frequently con-fused with a hemolytic Streptococcus sp. The organ-ism is ubiquitous and can survive for years in theenvironment. Intracranial infections cause opistho-tonos, ataxia and torticollis (Figure 28.10).29 Brainlesions consist of microabscesses with heterophil andgiant cell infiltrates, diffuse gliosis, meningeal hy-peremia, degeneration of Purkinje cells and perivas-cular cuffing (see Chapter 33).


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ChlamydiosisOccasionally, Chlamydia psittaci will cause neu-rologic signs in birds that survive the acute respira-tory or gastrointestinal phase of the disease. Signs

include seizures, torticollis, tremorsand opisthotonos (see Chapter 34).88

GranulomasAvian tuberculosis can causeneurologic signs if the granulomasoccur intracranially or adjacent toperipheral nerves.51,108 Osteomyelitiscaused by mycobacterium may pro-duce a lameness that could be misin-terpreted as a neuropathy. Ab-scesses, granulomas, encephalitis,myelitis and meningitis may becaused by any bacterial organism.Salmonella, Streptococcus, Staphy-lococcus, Pasteurella multocida, My-coplasma and Clostridium spp. havebeen isolated.19,46,51,73 Clinical signsdepend on the location and extent ofthe lesions.

Otitis

Otitis media and interna in compan-ion birds may cause neurologic signs.Otitis interna produces a head tiltand circling toward the affected side(see Figure 28.6). If the infection pro-gresses, other cranial nerves and themidbrain may become affected.

CongenitalAbnormalities

The incidence of developmental ab-normalities of the avian nervous sys-tem is not well established. Studiesin poultry suggest that meningocoeleand other related anomalies resultfrom early malformation and forkingof the neural tube during embryonicdevelopment.79 In turkeys, hydro-cephalus, shortened beaks and ab-sence of the terminal digits have

been linked to an autosomal recessive semilethalgene.103 In laboratory animals, virus infections, cer-tain chemicals and malnutrition (hypovitaminosis A,hypervitaminosis A, hypovitaminosis B12 and B6 and

FIG 28.10 An adult Amazon parrot was presented with a history of progressive depres-sion, weight loss and ataxia. When undisturbed, the bird would exhibit repeated periodsof opisthotonos with shifting phase nystagmus. Abnormal clinicopathologic findingsincluded WBC=26,000 (toxic heterophils), PCV=26, total protein=7.5 and CPK=1200. Thebird did not respond to supportive care. Histopathology indicated a severe perivascularcuffing with neuronal necrosis of undetermined etiology.


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avian medicine: princilpes and...

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