Neurology Flashcards
What toxin(s) does Clostridium botulinum produce?
Botulinum neurotoxin (BoNT/A, BoNT/B etc.)BoNT mosaic toxins (BoNT/CD and BoNT/DC)
List the antigenic types of C. botulinum and which types have been reported to cause disease in large animals.
C. botulinum type A, B, C1, C2, D, E, F, G;Types A, B, C1 and D.
What type of bacteria are C. tetani and C. botulinum?
Gram positive, anaerobic, spore-forming bacilli.
List the three types of C. botulinum infection and the antigenic type commonly implicated in each.
1) Forage botulism: ingestion of pre-formed toxin i.e. pasture/forage/silage/haylage contaminated with soil (A&B) or animal carcasses (C&D); phosphorus deficient cattle chewing on bones with some muscle attached (D).2) Toxicoinfectious botulism: colonisation of GIT by C. botulinum in neonates, toxins prod in GIT & absorbed (B).3) Wound botulism: C. botulinum colonises wound and multiplies under anaerobic conditions and prod toxins.
Which antigenic type of C. botulinum is most frequently associated with botulism outbreaks in horses in the USA?
Type B (>85% cases).
Describe the mechanism of action of BoNT.
BoNT accessory proteins facilitate absorption across intestinal epic cells –> blood stream –> presynaptic cholinergic nerve terminal esp somatic neuromuscular endplate –> internalised into cytosol –> inactivates the SNARE complex –> vesicles do not undergo exocytosis –> acetylcholine not released at the NMJ –> flaccid paralysis.
List the two types of Stringhalt reported in horses and how they can be distinguished on clinical examination.
- Australian Stringhalt - BILATERAL hindlimb disease.2. Classical Stringhalt - UNILATERAL hindlimb disease.
List the plants reported to cause Australian Stringhalt by their scientific and common names.
- Hypochaeris radicata (false dandelion, flatweed, cat’s ear, castear).2. Taraxacum officinale (dandelion)3. Marva parviflora (mallow).4. Lathyrus odoratus (sweet pea) NB experimental infection.
What is the characteristic gait abnormality observed in cases of Stringhalt?What factors can exacerbate this gait abnormality?
Sudden, exaggerated flexion of one or both pelvic limbs during the swing phase of locomotion. Varies from slightly excessive flexion to violent movements during which the fetlock or toe will contact the abdomen, thorax and occasionally the elbow.Backing, sharp turns, going downhill, sudden stops, transition for halt to walk, cold weather, excitement.
Describe clinical signs which may be seen in cases of Australian Stringhalt in addition to bilateral hindlimb hyperflexion.
- Mild to severe muscle atrophy of the hindlimbs.- Laryngeal paralysis (‘roaring’), stridor or change in voice.- Bilateral knuckling over on the forelimbs (generalised weakness; ‘atypical stringhalt’).- Generalised muscle atrophy and marked weight loss despite a good appetite.
Describe the proposed pathophysiology of Classical Stringhalt.
Trauma to the proximal dorsal metatarsus, may be months before Stringhalt is observed; additional proposed risk factors: foot conditions, articular lesions of the hock or stifle; likely cumulative result of interference with limb reflexes, mechanical effects of adhesions involving digital extensors of the pelvic limb, painful conditions of the hock or distal limb.
Describe the pathophysiology of Australian Stringhalt.
Ingestion of toxic weed –> distal neuropathy involving myelinated axons of the peripheral nervous system –> progressive degeneration of axons incl alpha motor neurons to skeletal muscle, 1A and 1B sensory neutrons from muscle spindles and Golgi tendon organs and gamma efferents to muscle spindles.
Name the three nerves most commonly affected in cases of Australian and Stringhalt and the most common signalment of affected patients.
- Recurrent laryngeal nerves.2. Peroneal branch of the sciatic nerve.3. Tibital branch of the sciatic nerve.Tall adult horse > young horses, shorter horses and ponies as LONG nerves affected (has been reported in Shetlands).
List the typical findings on electromyography in cases of Stringhalt.
- Increased insertion activity of affected muscle.- Abnormal spontaneous activity e.g. fibrillation potentials, positive sharp waves, in affected muscles.- Slowed nerve condition velocity in peroneal nerves.
List the typical gross and histologic pathology findings in long-standing cases of stringhalt.
- Atrophy of muscles of the pelvic limbs and the larynx.- Peripheral nerves: demyelination, perineurial fibrosis, accumulation of myelin debris (lesions worst distally).- +/- evidence of nerve regeneration: regenerating nerve clusters, onion bulbs, Schwann cell proliferation.
List two medications with reported success in treatment of Stringhalt and their mechanisms of action.
- Phenytoin (10-15mg/kg PO q12-24h): inhibits voltage-gated Na channels.2. Mephenesin: inhibits polysynaptic reflexes in the spinal cord (limited success).
Describe surgical therapy for treatment of Stringhalt and the prognosis for return to function.
Lateral digital extensor myotenectomy: surgical removal of the distal muscle belly and tension of insertion of the lateral digital extensor; 50-85% success rate.
What is the prognosis for recovery from Stringhalt?
- Few reports re Classical Stringhalt - presumed to persist in majority (1 resolved, 2/4 improved in one case study).- Australian Stringhalt: many cases resolve after removal from weeds; some die (recumbency; unable to walk to feed/water); some have persistent CSx; recovery takes on average 6-12mo (3d-3yr).
Identify ticks capable of causing tick paralysis, the countries in which they are located and the domestic animal species affected.
- Ixodes holocyclus - Australia - cats, dogs, foals, horses, calves, sheep, pigs.2. Dermancentor spp - USA - dogs, humans, cattle, camelids.3. Ixodes rubicundus & Rhipicephalus evertsi - Africa - small ruminants.
Outline the pathophysiology of tick paralysis.
Neurotoxin in saliva of female tick –> inoculated into affected animal when tick feeds –> inhibits release of acetylcholine from nerve terminals at the NMJ.
Describe the clinical signs of tick paralysis.
Progressive generalised flaccid paralysis –> recumbency and death (respiratory paralysis) over hours to day. Early signs include ataxia, paraparesis, change in voice.
Describe the treatment of tick paralysis.
- Identify and REMOVE ticks!!! (Px good for Dermancentor if removed before animal is moribund) –> tick search x3, clip, spray with fipronil.2. Administer hyperimmune serum - 0.5ml/kg horses (NB canine product; potential for anaphylaxis).3. Supportive care: NPO (dysphagic!), sternal, oxygenation, +/- IVF, deep bedding, stand and turn frequently.
What is the alternate name for Atypical Myopathy (AM) and in what countries does it occur?
Atypical myopathy (Europe); seasonal pasture myopathy (US).Largely UK and Northern Europe; isolated cases reported in USA, Australia, Falkland Islands.N.B. mal seco = clinically and pathologically identical disease in South America (mainly Chile).
What is the causative agent of AM and where does it originate from?
Hypoglycin A (toxic metabolite = methylenecyclopropyl acetic acid; MCPA).Seeds of Acer negundo (box elder) and Acer pseudoplantanus (sycamore maple) trees.
List risk factors for development of AM.
- Presence of box elder or sycamore maple trees.- Young adults: peak incidence 2-7yo.{- Dec risk if previous hx of contact/co-grazing with an EGS horse (+ inc risk young age = acquired immunity?)}- Previous occurrence of cases on the premises, increased soil nitrogen content, pasture disturbance (e.g. construction) and an increased number of horses- Grazing at pasture.- Recent movement to a new premises (esp first 2wk).- Change of feed type or quantity during the 14 days prior to disease and the use of an ivermectinanthelmintic at the ultimate and penultimate treatments.- Cooler, drier weather and irregular ground frosts.
List potential gross pathologic findings on post-mortem of a horse affected by EGS.
- Multiple abnormalities related to GI dysfunction e.g.: * Acute cases: stomach/SI fluid distension, reflux oesophagitis. * Subacute: firm, corrugated impactions of the large colon and caecum, the outer surface of which often shows a characteristic black coating. * Subacute and chronic: mucus-coated hard faeces in the small colon and rectum.- Poor body condition: dysphagia, anorexia, cachexia.- Marked, bilateral rhinitis sicca in some chronic cases.
Describe the typical lesions identified on histologic examination of nerves in EGS cases.
- Findings are indicative of neuronal degeneration.- Extensive chromatolysis, with loss of Nissl substance, eccentricity or pyknosis of the nuclei, neuronal swelling and vacuolation, accumulation of intracytoplasmic eosinophilic spheroids and axonal dystrophy.
In which organs is neuronal loss/damage observed in EGS? In addition to decreased numbers of neurons, what else is present in decreased numbers?
- Stomach, duodenum, jejunum, ileum, caecum, large colon, small colon and, more variably, the rectum.- Acute: widespread; greatest in ileum.- Chronic: less extensive in jejunum and small colon.- Interstitial cells of Cajal dec in ileum and pelvic flexure.
Describe the location of affected neurons in EGS.
- Lesions are most evident in the prevertebral and paravertebral ganglia of the ANS and ENS; somatic motor neurons also affected.- ANS: ciliary ganglion, cranial cervical ganglion, caudal cervical ganglion, stellate ganglion, thoracic and abdominal sympathetic trunk, coeliaco-mesenteric or coeliac/cranial mesenteric ganglion, the caudal mesenteric ganglion and the parasympathetic terminal cardiac ganglion.- ENS: myenteric and submucous plexuses.- CNS: CN III, V, VI, VII, VIII, X, XII, spinal cord lowermotor neurons and spinal cord intermediolateral horn neurons.
List the clinical signs of EGS.
- All forms: dullness, anorexia, dysphagia, tachycardia, ptosis, patchy sweating, muscle fasiculations.- Acute: colic, large volumes NGT reflux.- Subacute: colic, no/small volume NGT reflux, impactions.- Chronic: weight loss, ‘tucked up’ appearance, progressive myasthenia (base narrow stance, leaning against walls, weight shifting), rhinitis sicca.
The prognosis is very poor for recovery from EGS and treatment consists only of supportive care until some normal GI/muscle function is regained. List the criteria used to select appropriate candidates for treatment.
Criteria:1. Willingness to attempt to drink and swallow food.2. Retention of some ability to drink and swallow food.3. Absence of continuous, moderate to severe colic signs.
Describe the clinical signs of botulism in horses.
Dysphagia (poor tongue tone, milk/feed in nostrils or trachea, persistent DDSP), lethargy, weakness, mydriasis and sluggish PLRs, increased time spent recumbent and hypometric gait –> recumbency and dyspnoea.
What is the common name for (USA) endemic toxicoinfectious botulism of foals and what antigenic type causes it?
Shaker Foal Syndrome.C. botulinum type B.
What are the principles of treatment of a horse or foal with botulism?
- Bind the toxin: trivalent BoNT anti-toxin (A, B, C) - 20,000IU/foal and 50,000IU/adult (one dose as 12d t1/2); 98% died w/out vs 96% foals and >70% adults survived with early anti-toxin tx.- Eliminate the source of infection: removal of contaminated feed; lance, drain, debride, lavage wounds. - Supportive care: deep bedding/turn/sling recumbent horses; keep head above level of heart several hours/day if standing (prevent oedema); nutrition (oral, NGT, PPN); urinary catheter BID/remove faeces if required.- ABs only to tx known infection ONLY (penicillin/metro contradicted as > BoNT release) e.g. asp pneumonia, cystitis or in heavily instrumented foals.- InO2 or ventilation of foals.
In animals that survive, how long does it take the clinical signs of botulism to reverse?
- Recumbent animals: (death usually w/in 3d) recumbency resolves in 1-4 weeks; complete recovery weeks to months,- Non-recumbent animals: dysphagia, limb weakness, sluggish PLRs recover in days to weeks.
What vaccine is available to prevent against Botulism in horses and what is the recommended vaccine schedule?
- BoNT/B toxoid; highly effective vaccine (NB no BoNT/C or multivalent licensed in USA).- Adults: 2 doses 4 weeks apart then annually.- Broodmares: 4-6 weeks pre-foaling.- Foals: 3 doses 4 weeks apart; usually commence at 2-3mo BUT maternal antibody doesn’t interfere with vacc, therefore high risk foals should commence at 2wo.
Which two toxins are produced by Clostridium tetani?
Tetanolysin and tetanospasmin (TeNT).
Describe the pathophysiology of tetanus.
Deep wound, injection site, post-foaling uterus (RFM), Sx site, umbilicus etc. contaminated with C. tetani –> growth of C. tetani spores in anaerobic environment –> elaboration of exotoxins –> neurologic deficits.
Describe the actions of tetanolysin within the body.
Damages tissue, reduced redox potential, increases expansion of infection.
Describe the actions of tetanospasmin within the body.
Diffuses from tissue to vascular system –> somatic NMJ and autonomic ganglia –> binds to nerve terminals –> internalised –> transported retrograde in axons –> CNS –> binds irreversibly to presynaptic inhibitory interneurons (‘Renshaw cells’) –> cleaves synaptobrevin (SNARE) –> inhibits release of glycine and GABA –> spastic paralysis.
Describe possible post-mortem findings in a horse with tetanus.
- Gram stain of wound exudates –> gram +ve, spore-forming bacilli (30% cases).- Gross pathology non-specfic e.g. secondary muscle damage, pulmonary congestion, atelectasis etc.- IHC detection of TeNT antigen in spinal cord ventral or intermediate horn cells.
List clinical signs of tetanus in the horse.
CSx develop 1-60d post inoculation; commence with head & neck, may remain localised/mild or –> death; include:- Trismus, risus sardonicus, 3rd eyelid prolapse, lockjaw, neck stiffness.- Rigid extension of limbs/back/neck (sawhorse stance).- Stiff tail.- +/- colic (bloat in ruminants).- Tonic-clonic muscle spasms following stimuli.- Dysphagia.- Fluctuant HR/BP.- Recumbency.- Death: rest failure, aspiration, autonomic overactivity (cardiac dysrhythmias).
What are the principles of treatment of a horse or foal with tetanus?
- Neutralise unbound toxin: tetanus anti-toxin 20IU/kg/day for 5d; horses only: intrathecal admin (lumbosacral) 400-1000IU/kg.2. Eliminate the infection: open, drain, debride, lavage wound; metronidazole > penicillin for 3-5d.3. Provide muscle relaxation: pack ears, dim lights, minimal handling etc.; acepromazine, diazepam, midazolam, dantrolene, Mg (blocks neuromuscular transmission, interferes with catecholamine release, dec catecholamine receptor responsiveness, anticonvulsant).4. Ensure good footing: non-slip floor, +++ padding, sling?5. Maintain hydration and nutritional status.
What is the prognosis for horses with tetanus?
68-75% fatality.NB ~50% dairy cattle, >80% small ruminant.
What vaccine(s) is/are available to prevent against Botulism in horses and what is the recommended vaccine schedule?
Tetanus toxoid (TT): - Adults: 2 doses 4 weeks apart then annually; repeat if wounded or undergoing Sx >6mo after last booster.- Broodmares: 4-6 weeks pre-foaling.- Foals: 4-6mo, 2nd dose 4wk later, 3rd dose 10-12mo.Tetanus anti-toxin (TAT):- Give to wounded, un-vaccinated horses (+TT) or foals (TAT only)
Which antibiotic should be avoided in horses with botulism and why?
Aminoglycosides, as they may potentiate the neuromuscular blockade caused by BoNT.
What is Equine Motor Neuron Disease (EMND?)
An acquired neurodegenerative disorder of the ventral horns of the grey matter of the spinal cord and selected brainstem nuclei of adult horses resulting in skeletal muscle weakness and atrophy.
What is the aetiology of EMND?
Vitamin E deficiency (+/- selenium deficiency).
What age of horse is most at risk for EMND?
Reported cases: mean 9yo (2-27); highest risk 16yo.NB CSx develop after at least 18 months of being on a Vitamin E deficient diet.
List the risk factors associated with development of EMND.
- Use of pelleted feed.- Frequent supplementation with vitamin/mineral supplements lacking Vitamin E/selenium.- Lack of absorption of Vitamin E despite appropriate diet i.e. GI or hepatic disease.- Unknown if low vitamin E diet is the only nutritional or management factor responsible for influencing development of EMND.
Describe the pathophysiology of EMND.
Hypovitaminosis E –> systemic oxidative stress –> cellular damage.Evidence: dominant involvement of oxidatively active type I myofibres in atrophied skeletal muscles, abundant deposits of ceroid lipofuscin in retinal pigmented epithelium and the endothelium of spinal cord capillaries.
What are the clinical signs of EMND?
CSx reflect denervation of skeletal muscle: muscle weakness,+/- muscle wasting, trembling of anti-gravity muscles, sweating, ‘horse on ball’ stance, shifting weight, difficulty standing still, hypometric gait but not ataxic, neck low, tail head elevated.40% cases horizontal band of pigment above the optic disc at the tapetal-nontapetal junction.
How do you diagnose EMND ante-mortem?
- Typical CSx, age >2yo, diet low in green forage and high in carbohydrates.- Serum: low vitamin E, mild to mod inc CK and AST.- Muscle biopsy: sacrocaudalis dorsalis tailhead muscle –> neurogenic muscle atrophy characterised by variable numbers of atrophied angular fibres (type I predominate); 90% sensitivity, low specificity.- Nerve biopsy: 5cm section of ventral branch of spinal accessory n as it courses over the sternocephalicus m –> mild to severe Wallerian degeneration of axons and Schwann cell proliferation; PPV 75%, NPV 90%.
List post-mortem examination findings in horses with EMND.
Widespread degeneration and loss of somatic motor neurons in the ventral horns of the spinal cord accompanied by degnerative axonal changes in the ventral roots and peripheral nerves.All brainstem CN somatic motor nuclei, except III, IV and VI are involved.Minimal to no lesions in autonomic nervous system.
What is the recommended treatment for EMND?
Vitamin E (at least 10IU/kg/da); natural (RRR-alpha-tocopherol) has higher bioavailability than synthetic (all-rac-alpha-tocopherol or dl-alpha-tocopherol).Good quality grass and alfalfa hay (rich in vitamin E).High quality and quantity pasture, hay and concentrates due to higher caloric requirements.
List the three potential outcomes for horses with EMND
- 40% of cases progressive deteriorate and are euthanised.- 40% improve markedly; look normal on PE but may ‘recrudesce’ with intensive training or competition.- 20% stabilise with permanent muscle wasting and emaciaton.
Damage to which locations within the central nervous system (CNS) can result in upper motor neuron (UMN) bladder dysfunction?
Thoracolumbar spinal cord, cerebrum, cerebellum or brain stem.
Damage to which locations within the nervous system can result in lower motor neuron (LMN) bladder dysfunction?
Sacral spinal cord or pelvic nerve.Detrusor muscle atony.
A cat has a firm, distended bladder on abdominal palpation which is difficult to express manually. Which of the following diseases could cause this clinical finding?A) Cerebral tumour.B) Proximal tail fracture.C) L3 fracture.D) Detrusor atony secondary to dysauntonomia.
A and C.UMN bladder signs.
A horse presents with urine scalding of both pelvic limbs. On rectal palpation a full bladder is identified which empties easily of urine when the bladder is manually compressed. The horse had a history of prior spinal cord trauma following a racing accident. At which level of the spinal cord did the trauma most-likely occur?
The sacral spinal cord.LMN bladder signs.
What genus and family do the Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE) and Venezuelan Equine Encephalitis (VEE) viruses belong to?
- Genus: Alphavirus.- Family: Togaviridae.- Unsegmented, single-stranded, positive-sense RNA viruses.
List the clinical signs of Horner’s Syndrome in the horse.
Unilateral sweating, regional hyperthermia, ptosis, miosis, enophthalmus, protrusion of the third eyelid, congested mucous membranes, inspiratory stridor, dermatitis caused by chronic sweating.
List primary conditions which can result in Horner’s Syndrome in the horse.
- Guttural pouch disease.- Perivascular injection (jugular v).- Thoracic inlet masses.- Trauma to the basisphenoid area or cervical trauma.- Otitis media.- Periorbital masses or abscesses.- Parotid duct obstruction and inflammation.- Oesophageal rupture.- Complications associated with carotid a ligation.- Polyneuritis equi (rarely).
Horner’s Syndrome results from interruption of ocular sympathetic pathways. Describe the anatomy of this pathway.
- 1st order: tectum of midbrain –> axons descend to T1-T3 –> enter grey matter of dorsal horn, synapse on…- 2nd order: pre-ganglionic sympathetic motor neurons –> cervicothoracic and middle cervical ganglia –> ascend in cervical sympathetic trunk to cranial cervical ganglion (guttural pouch)–> synapse on…- 3rd order: post-ganglionic sympathetic nerve –> fibres distributed to sweat glands of head, ciliary muscles, periorbital smooth muscles.
Correlate the site of damage with classification of Horner’s Syndrome by ‘order’.
- 1st order: brainstem or spinal cord.- 2nd order: cranial thoracic nerve roots or spinal nerves or cervical sympathetic trunk.- 3rd order: cranial cervical ganglion, the skull, behind the eye.
Describe how you can use ocular pharmaceutics to determine the level of sympathetic interruption in a horse with Horner’s Syndrome.
- Hydroxyamphetamine 1%: results in release of NE from intact post-ganglionic neurons –> mydriasis.- 0.1ml 1:1000 epinephrine: mydriasis in 20mins post-ganglionic lesion vs 40 mins pre-ganglionic lesion.
Describe treatment and prognosis of Horner’s Syndrome in horses.
- Usually irreversible, unless associated with perivascular xylazine inj.- If perivascular inj: infiltrate large volumes of saline into perivascular tissues. - Anti-inflammatory doses of flunixin and dexamethasone.- Drain abscesses.- Treat GP mycosis.
What is the causative agent of parasitic myelopathy (a.k.a. ‘meningeal worm’) of camelids?
Parelaphostrongylus tenuis (nematode).
Describe the life cycle of P. tenuis.
Definitive host = white-tailed deer: adults living in subdural space and associated vessels lay eggs –> hatch in pulmonary capillaries –> L1 migrate to alveoli, coughed up and swallowed –> L1 passed in feces –> ingested by intermediate host = snails –> molt x 2 –> snails containing L3 ingested by definitive hosts or aberrant hosts e.g. camelids.
Describe the pathophysiology of P. tenuis infection in camelids.
in snails ingested by camelid –> migration to CNS parenchyma –> scattered foci of haemorrhagic necrosis and parenchymal loss –> CSx in ~40-50d.
List the neurologic deficits reported in camelids with parasitic myelopathy.
- Typical CSx: wide-based hindlimb stance, hindlimb ataxia +/- progressing to recumbency; BAR.- Lesions vary: can see FL or lateralised deficits.- Atypical form: brain involvement –> acute-onset brain or vestibular signs including depression, seizures,circling, leaning, head tilt, and slow PLRs.
How do you diagnose parasitic myelopathy in a camelid anti-mortem?
- CSF: eosinophilic pleocytosis with inc protein in most cases.- CBC: usually WNL +/- inc CK and AST.
At what time of year is parasitic myelopathy most frequently observed and in what age group of camelids?
Autumn and Winter (Oct to Mar).Adults > young animals.
Describe the characteristic lesions of parasitic myelopathy observed on post-mortem of affected camelids.
Lesions of parasite migration: randomly distributed axonal degeneration that progresses to pannecrosis characterised by axon and axon sheath swelling, axon drop out, axonophagia, accumulation of gitter cells.Lesions mainly in white matter.Larvae rarely seen.
Outline the treatment of parasitic myelopathy in camelids.
- Fenbendazole 50mg/kg PO for 5 days.- NSAIDs e.g. flunixin meglumine 1mg/kg q24-48h.- DMSO in severe cases.- Vitamin E and B (non-specific therapy).- IVF if required.- Physical therapy.
What is the prognosis for survival in cases of parasitic myelopathy of camelids?
- Good if able to stand with assistance.- Poorer if recumbent.- Guarded with brain lesions.
What segment of the spinal cord is most frequently affected by trauma in camelids and was is the most common source of the trauma?
- Cervical spinal cord.- Fence-related injuries.
Describe clinical examination findings in a camelid with cervical trauma.
- ‘Lump’ or ‘kink’ in neck (fibrosis, periosteal reaction).- Abnormal head and neck posture.- UMN/LMN deficits in FLs, UMN deficits in HLs.- May not see CSx after acute inflammation resolves due to wide spinal canal.
List treatment options for traumatic lesions of the cervical spinal cord in camelids?
- Supportive care: NSAIDs, confinement.- Sx may be indicated in young, growing animals to stabilise vertebral canal –> aim to produce fusion between neighbouring vertebrae.
List possible aetiologies of otitis media in camelids.
- Ascending infection up the eustachian tubes.- Extension of otitis interna.- Spinous ear ticks (Texas).- Most common bacteria isolated: Arcanobacter pyogenes, Staphylococcus app and Bacillus spp.
What abnormalities may be identified on neurologic examination of a camelid with otitis media?
Head tilt, facial nerve deficits (e.g. droopy ear, flaccid facial muscles, ptosis, inability to blink), circling, ataxia, nystagmus.
How do you diagnose otitis media in a camelid?
- CT ideal.- Radiographs may be helpful if bony changes present.- CSF to rule out other causes of vestibular dz e.g. listeriosis; protein inc in 50% cases.
What is the frequency of occurrence and prognosis associated with listeriosis in camelids?
- Not very common.- Guarded px, with most failing to respond even to aggressive therapy.
List the clinical signs of listeriosis in camelids.
Circling, ataxia, leaning to one side, nystagmus, recumbency, depression, seizures.
What CSF changes are reported in cases of listeriosis in camelids?
Monocytosis, elevated protein and CK concentrations.
Outline the components of aggressive therapy of a camelid with listeriosis.
IVFT, anti-inflammatories, thiamine, oxytetracycline (20mg/kg SID for 5d) or Na/K penicillin IV (80mg/kg q6h), nursing care.
In what age group of camelids is meningitis or meningoencephalitis most frequently reported?
Neonates; secondary to sepsis.
What organisms have been associated with meningitis in camelids?
- Neonates: Listeria monocytogenes, Escherichia coli, Salmonella newport, Streptococcus bovis.- One reported of cryptococcal meningitis in an 8yo alpaca in Australia.
Describe the typical CSF analysis findings in a cria with bacterial meningitis.
Leukocytosis, especially with suppurative inflammation.
Describe clinical signs associated with meningitis in crias.
- Vague and variable!- Weakness, depression, inability to stand or elevate the head, tremors, ataxia, opisthotonus and seizures.- Death in 100% reported cases.
Outline the clinical signs and signalment of crias with vertebral abscessation.
- HL ataxia, paresis or paralysis (thoracolumbar abscess)- Reported in several crias under 6mo.
Why are llamas more prone to heat stress than alpacas?
Both are poorly adapted to hot and humid climates, but llama breeders tend to barrel clip only vs alpaca breeders which completely shear.
Describe presenting clinical signs in a camelid with heat stress.
- Elevated body temperature >105F (may be up to 108F).- Respiratory distress.- Tachycardia.- Inability to rise (FLs weaker than HLs).Check for CSx of underlying dz
List the common abnormalities identified on serum biochemistry of an alpaca with heat stress.
- Elevated CK and AST.- Hypoproteinaemia despite haemoconcentration (cell damage).- Severe electrolyte imbalances esp hypokalaemia.- Metabolic acidosis.
Outline therapy for a camelid with heatstress.
- Completely shear the animal.- Hose with cold water; ice packs in inguinal and axillary regions.- Judicious fluid therapy: hypoalb + cell damage –> pulmonary oedema.- NSAIDs: analgesic (muscle pain) and anti-inflammatory.- Vitamin E: anti-oxidant.
What is the aetiologic agent of Ryegrass Staggers in camelids?
Lolitrems = tremorogenic toxins produced by endophytes infecting ryegrass.
What are the clinical signs of Ryegrass Staggers in camelids and the prognosis for complete recovery?
- Head tremor +/- ataxia.- Normally recover fully when removed from pasture but prolonged exposure may result in permanent damage.
What agents induce polioencephalomalacia (PEM) in camelids?
- Dietary change.- Excessive carbohydrate ingestion.- Amprolium overdosage (thiamine analogue).- Often unknown.
What are the clinical signs of PEM in camelids?
- Acute-onset blindness (cortical).- Depression.- Circling and head tremors.- Atypical presentation: charge walls, aggression.
How is PEM treated in camelids?
- Thiamine hydrochloride 10-15mg/kg q4h then daily for several days after resolution of signs.- Supportive and nursing care.
Which viral encephalidites reported in other species can also occur in camelids?
- Horses: EEE, WNV, EHV-1 (NB severe brain dz).- Sheep: ‘louping ill’ a.k.a. ovine encephalomyelitis.- Rabies.
Can camelids be vaccinated against viral encephalidites?
No registered vaccines, however equine EEE, WNV and rabies results in production of neutralising antibodies.
List differential diagnoses for ruminants with an elevated white blood cell count in their CSF.
- Neutrophils: bacterial meningitis.- Lymphocytes: viral encephalitis, listeriosis.- Macrophages: trauma, polioencephalomyelitis.- Eosinophils: parasite migration.
List clinical signs of cerebral disease in ruminants.
- Excitement, mania.- Seizures.- Compulsive behaviour.- Stupor. - Coma.- Abnormal vocalisation.- Central blindness.- Hyperaesthesia.
What is the most common cause of symmetric cerebral disease in ruminants?
Metabolic abnormalities incl dehydration, acid-base abnormalities, electrolyte disturbances.
Outline aetiologic agents of polioencephalomalacia (PEM) in ruminants.
- Thiamine deficiency.- Sulphur toxicity.- Lead toxicity.- Salt toxicity.
Describe the pathophysiology of thiamine deficiency in PEM of ruminants.
- Thiamine is produced by rumen microflora; production meets daily requirements; not stored.- Thiamine essential for cerebral glucose metabolism; it is a co-enzyme of the pentose-phosphate pathway.- Thiamine deficiency can be caused by rumen acidosis/disruption, thiamine inhibition or ingestion of plants containing thiaminases e.g. bracken fern, horsetail.
Describe the pathophysiology of suphur toxicity in PEM of ruminants.
- Sulphur in the rumen is either assimilated into microbial protein or combines with H to form H2S.- H2S is detoxified by the liver.- Excess H2S prod –> overwhelms liver, or eructated and excess H2S inhaled.- H2S inhibits cytochrome C oxidase –> no ATP –> neuronal swelling –> PEM.- Source of S: feed intake limiters e.g. gypsum, by-products of corn, beet and sugar cane extraction e.g. molasses, water sources, S-accum plants incl rape, kale, turnips. Lamb’s quarters, Burning bush.
Describe the pathophysiology of lead toxicity in PEM of ruminants.
- Lead has a profound effect on sulfhydryl-containing enzymes, the thiol content of erythrocytes, antioxidant defenses, and tissues rich in mitochondria –> cerebellar hemorrhage and edema associated w capillary damage.- Industrial pollution from smelting.- Junk piles: lead paint, gasoline and motor oil, insecticides, herbicides, lead batteries, shotgun pellets.
Describe the pathophysiology of salt toxicity in PEM of ruminants.
- May be due to true salt poisoning e.g. ingestion of salt-licks, but usually due to water restriction.- Alteration of cerebral energy metabolism –> dec pentose phosphate pathway activity –> dec ATP prod –> accum of Na –> oedematous swelling. - Brain’s immediate response to hypertonic state is to lose water; rapid correction occurs through accum of electrolytes then idiogenic osmoles and water.- RISK OF TX!! If you rapidly correct the hypertonic state cerebral oedema will occur due to the idiogenic osmoles.
List clinical signs of PEM in ruminants.
- Depression/stupor.- Central blindness.- Convulsions.- Head pressing.- Aimless wandering.- Inco-ordination.- Ataxia.- Muscle tremors.- Opisthotonos.- Dorsomedial strabismus.- Nystagmus.- Bruxism.
Outline test results for diagnosis of PEM in ruminants.
- CSx and Hx.- CBC/MBA/CSF cytology: rarely useful.- CSF may have subjectively inc pressure on collection.- Thiamine defic: blood thiamine (160mmol/L or CSF:serum >1.- Sulphur tox: rumen H2S, sulfur content of feed and water- Lead tox: blood or tissue lead, or if chronic and blood Pb no measure RBC δ‐aminolevulinic acid dehydratase; RBCs may show basophilic stippling.
Describe necropsy findings in ruminants with PEM.
- Gross lesions: brain swelling with gyral flattening and coning of the cerebellum due to herniation into the foramen magnum, slight yellowish discoloration of the affected cortical tissue, autofluorescent bands of necrotic cerebral cortex when viewed with ultraviolet illumination –> macroscopically evident cavitation of cerebrocortical tissue. - Histo: necrosis of cerebrocortical neurons; neurons are shrunken and have homogeneous, eosinophilic cytoplasm, nuclei are pyknotic, faded, or absent, vessel cells undergo hypertrophy and hyperplasia; later stages –> cortical tissue undergoes cavitation as macrophages infiltrate and necrotic tissue is removed.
Outline treatment options for PEM in ruminants.
- Thiamine: 10mg/kg IV q6h.- Diuretics: 20% mannitol.- Dexamethsone: 1-2mg/kg IV.- Chelation therapy for Pb: EDTA IV, oral MgSO4 forms insoluble lead sulphides.- IVFT as needed.
Describe the rabies virus.
- Family: Rhabdoviridae; bullet-shaped viruses.- Genus: Lyssavirus.- Non-segmented, negative-stranded RNA virus.
Describe transmission and incidence of rabies in the US.
- Distinct strains in raccoons (most common), skunk, bat, coyote, fox, canine.- Transmission by exposure to saliva containing rabies virus (bite or non-bite); possible all warm-blooded animals.- US 2012 cases: 5,669 wildlife, 115 cattle, 47 equids, 13 small ruminants, 1 human.
