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Student Paper Communication tudiante

Polioencephalomalacia in a llama

Chelsea G. Himsworth

Abstract A 5-year-old, female llama(Lama glama) developed acute, progressive neurological disease, character-

ized by recumbency, muscle fasciculations, intermittent convulsions/opisthotonos, and absent menace responses.

Postmortem histopathologic lesions, limited to the cerebral cortex, consisted of necrosis of the superficial and deep

laminae. The clinical disease and microscopic lesions were consistent with polioencephalomalacia.

Rsum Polio-encphalomalacie chez un lama. Une femelle lama(Lama glama) ge de 5 ans a dvelopp

une maladie neurologique aigue et progressive caractrise par un dcubitus, de la fasciculation musculaire, des

convulsions/opisthotonos intermittents et labsence de rponse la menace. Les lsions histopathologiques post-

mortem, limites au cortex crbral, comprenaient une ncrose des laminae superficielle et profondes. Les signes

cliniques et les lsions microscopiques taient compatibles avec une polio-encphalomalacie.

(Traduit par Docteur Andr Blouin)

Can Vet J 2008;49:598600

I n early August 2006, a 5-year-old, female llama(Lama glama)with an unknown breeding history was found recumbent andunwilling to rise by the owners, leading to concerns about pos-

sible dystocia. The llama was kept with a number of other llamas

in an earthen pen with no access to pasture. All were fed a grass

and timothy hay mix, which was occasionally supplemented

with small amounts of oats, and they were given water from a

nearby well. No other llamas were affected.

Upon examination, the llama was in sternal recumbancy and

unwilling or unable to rise. The head and neck were held stifflyerect, and marked, diffuse muscle fasciculations were present.

The neck would intermittently become limp, and the llama

would assume an opisthotonos-like position. Menace response

was absent bilaterally; however, pupillary light reflexes were

intact. The temperature was 39.1C (normal, 37.5C to 38.9C)

and the heart rate 84 beats/min (normal; 60 to 90 bpm).

The respiratory rate could not be assessed, due to the muscle

fasciculations.

The history and neurologic signs were indicative of a fore-

brain lesion; initial differential diagnoses included polioencepha-

lomalacia, due to either thiamine deficiency or sulfate toxicity;

pregnancy toxemia; lead poisoning; West Nile virus infection;

rabies; bacterial encephalitis; hepatic encephalopathy; and head

trauma. Blood samples were taken and submitted to Prairie

Diagnostic Services in Saskatoon, Saskatchewan, for examina-

tion (Table 1). The llama was prescribed treatment for polioen-

cephalomalacia: administration of thiamine (Thiamine HCL;

Rafter 8, Calgary, Alberta), approximately 8 mg/kg bodyweight(BW), IM, q4h for 4 treatments. However, the llama was found

dead before the 3rd treatment.

Results from analysis of the blood sample revealed a moder-

ate leukocytosis, characterized by marked neutrophilia, with

left shift and toxic change. In addition, there was moderate

lymphopenia, and mild nonregenerative anemia (Table 1).

These results were interpreted to be indicative of either a chronic

inflammatory process or a severe stress response with superim-

posed anemia. Additionally, there was marked hyperglycemia

(glucose, 12.7 mmol/L, normal: 2.8 to 6.0 mmol/L), which

might also have been indicative of a stress response. Serum bio-

chemical analysis showed no evidence of liver disease.

West ern College of Vete rina ry Medicine , Uni vers ity of

Saskatchewan, Saskatoon, Saskatchewan S7N 5B4.

Address all correspondence to Dr. Chelsea G. Himsworth;

e-mail: chelsea.himsworth@usask.ca

Dr. Himsworths current address is 74127 Banyan Crescent,

Saskatoon, Saskatchewan S7V 1G5.

Reprints will not be available from the author.

Dr. Himsworth will receive 50 free reprints, courtesy of

The Canadian Veterinary Journal.

Table 1. Results rom the clinical pathologic examination

ReferenceResult interval Units

ErythrocytesHct 0.228 0.2500.445 L/LReticulocytes 0.1 %

LeukocytesWBC 50.1 7.222.0 3 109/LSegmented neutrophils 44.1 2.915.0 3 109/LBand neutrophils 5.0 0.00.1 3 109/L

Toxic change 11 Lymphocytes 0.5 1.07.6 3 109/L

Plasma total solidsTotal solids 61 4773 g/LFibrinogen 1 1.05.8 g/LTotal solids: fibrinogen ratio 61:1

Hct hematocrit; WBC white blood cells

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The llama was submitted to Prairie Diagnostic Services for

necropsy. A cerebrospinal fluid (CSF) sample was collected from

the atlanto-occipital space for possible future antibody testing.

Cytologic analysis of the CSF was also performed; the results

were unremarkable. No significant abnormalities were seen

on gross examination, but it was noted that the llama was not

pregnant and was in fair body condition, with hay and a small

amount of whole grain present in the C1 gastric compartment

(1st of 3 gastric compartments in camelids). The brain was

examined under ultraviolet (UV) light at 365 nm, but no areas

of fluorescence characteristic of polioencephalomalacia (PEM)

were detected.Immunohistochemical staining and fluorescent antibody tests

for rabies were conducted, the results from both of which were

negative. The lead concentration in liver collected at necropsy

was within normal limits.

Histopathologic examination of the brain revealed moderate

perineuronal vacuolation in the superficial and deep laminae of

the cerebrum (Figure 1). In addition, several necrotic, shrunken

neurons with eosinophilic cytoplasm were observed, resulting

in a final diagnosis of PEM.

Polioencephalomalacia is a common degenerative neurologic

disease of ruminants, characterized by laminar necrosis of

grey matter in the cerebral cortex (1). Although PEM is rarelyreported in camelids, the clinical signs and histopathologic

findings in this case were consistent with other published cases

in these species (24).

Historically, PEM in ruminants is most often attributed to a

relative thiamine deficiency (2). Neurologic signs are a caused by

cerebrocortical degeneration resulting from energy depletion, as

thiamine is a cofactor required for carbohydrate metabolism in

the brain (5). Since gastric microbes in ruminants and camelids

are able to synthesize thiamine, thiamine deficiency in these

species is believed to be due, not to deficient dietary intake but

rather to metabolic abnormalities. These may include produc-

tion of thiaminase enzymes by microbes in the forestomach,

the ingestion of plants containing thiaminase, or decreased

intestinal absorption or increased fecal excretion of thiamine (5).

In this case, since the llama was not allowed access to pasture

and had been fed a low carbohydrate and high roughage diet,

with no history of recent diet change, a disruption in thiamine

metabolism may not be the most likely cause of the PEM.

Additionally, treatment with thiamine, 250 to 1000 mg, IM,

q4-12h, is usually highly effective in llamas with PEM caused

by thiamine deficiency (2). In this case, the lack of response totreatment may indicate an alternative etiology.

More recently, excess intake of dietary sulfur has been associ-

ated with PEM in ruminants (1,6). The proposed mechanism

involves metabolism of ingested sulfur compounds to hydro-

gen sulfide gas by ruminal microbes. This toxic gas is either

absorbed though the ruminal wall or eructated and inhaled (1).

Hydrogen sulfide is thought to affect cytochrome oxidase and

inhibit aerobic metabolism in the brain. However, it may also be

involved in the formation of free radicals or act as an exogenous

neuromodulator (1). In this case, a possible source of excessive

dietary sulfur intake could be the drinking water. Cases of

sulfur-induced PEM resulting from high water sulfate levelshave been reported in beef herds in central Saskatchewan; they

are believed to be more prevalent in the summer when increased

ambient temperature leads to increased water consumption

(1,6). It was suggested to the owners that they have the water

tested for sulfate levels; however, the results of this testing were

not forwarded to the clinician.

Rumen pH can effect the formation of hydrogen sulfide, with

acidic conditions favoring formation of the gas (1). Camelids

may be more resistant to sulfur-induced PEM than other species,

because effective gastric absorption of volatile fatty acids, along

with bicarbonate secretion by mucosal glands in the C1 gastric

compartment, results in buffering and the prevention of dra-matic fluctuations in gastric pH (3).

Although an unlikely alternative diagnosis in this case, it

should be noted that the history, clinical signs, and histological

findings are somewhat similar to those in Clostridium perfringens

type D enterotoxaemia. This is an invariably fatal disease of

young, fattening lambs and, less commonly, goat kids and

calves (5). It is usually associated with a sudden diet change

leading to intestinal overgrowth ofC. perfringens type D (5).

Epsilon toxin produced by the bacterium can act on the brain to

produce neurological signs, including recumbency, convulsions,

opisthotonos, and blindness, and histological lesions of focal

symmetrical encephalomalacia (FSE) (7,8). These lesions consistof noninflammatory necrosis of the brain, featuring numer-

ous eosinophillic degenerating neurons (7). The areas of the

brain most often affected in FSE include the internal capsule,

midbrain, thalamus, and cerebellar peduncles, and the lesions

are usually bilaterally symmetrical (7,8). This differs somewhat

from PEM, in which degenerative lesions can be asymmetrical

and are confined to the cortical grey matter, as seen in this case.

Also, since epsilon toxin acts on the vascular endothelium,

the lesions of FSE are often preceded by perivascular edema

and hemorrhages (8). Additionally, there are frequently other

postmortem lesions due to the systemic effect of the toxin,

including enterocolitis; pulmonary edema; pleural, peritoneal,

Figure 1. Cerebrum, superfcial lamina. Perineuronalvacuolation and numerous shrunken neurons. Hematoxylinand eosin, bar = 100 mm.

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and pericardial effusions; and rapid postmortem autolysis of the

kidneys, none of which were seen in this case (8).

Since the signalment and postmortem findings in this case

were inconsistent with FSE, PEM is the most likely diagnosis.

Nevertheless, C. perfringens enterotoxaemia could have been

ruled out in this llama by testing the intestinal contents and

tissue fluids for epsilon toxin. However, the results would have

had to have been interpreted in relation to the entire clinical

picture, since toxin testing is neither completely sensitive norspecific for this disease.

Several laboratory findings in this case were inconsistent

with the diagnosis of PEM. These included the absence of fluo-

rescence on UV light examination of the brain, as well as the

abnormalities seen on the complete blood (cell) count.

Although the leukogram could be interpreted as reflecting a

chronic inflammatory process, which would be inconsistent with

a diagnosis of PEM, other cases of PEM in llamas have included

a similarly abnormal leukogram with superimposed hyperglyce-

mia, suggesting that the observed changes may be stress induced

(4). Additionally, although nonregenerative anemia in llamas can

be associated with chronic disease, it is not uncommon for thisabnormality to be present without a known cause (9).

Fluorescence of cerebral lesions under UV light at 365 nm

is often used for rapid diagnosis of PEM. However, it is not

uncommon for fluorescence to be absent in early cases of

PEM, as may have been the case with this llama (10). This

is because the fluorescence results from autofluorescence of

ceroid-lipofuscin in lipophages as they engulf necrotic lipid

in the brain (10). In early cases of the disease, the lipophages

have not yet engulfed sufficient material to be visible under

UV light.

This report serves to further illustrate the unusual clinical and

laboratory findings of PEM in llamas, as well as possible causes

of the disease in this species.

Acknowledgments

The author thanks Drs. Nathalie Tokateloff and Chris Clark fortheir guidance. CVJ

References1. Gould DH. Polioencephalomalacia. J Anim Sci 1998;76:309314.2. Baum KH. Neurologic diseases of llamas. Vet Clin North Am Food

Anim Pract 1994;10:383386.3. Beck C, Dart AJ, Collins MB, Hodgson DR, Parbery J. Polioencepha-

lomalacia in two alpacas. Aust Vet J 1996;74:350352.4. Kiupel M, VanAlstine W, Chilcoat C. Gross and microscopic lesions

of polioencephalomalacia in a llama(Llama glama). J Zoo Wildl Med2003;34:309313.

5. McGavin MD, William WC, James FZ. Thomsons Special VeterinaryPathology, 3rd ed. St. Louis: Mosby, 2001:410412.

6. Haydock D. Sulfur-induced polioencephalomalacia in a herd of rotation-ally grazed beef cattle. Can Vet J 2003;44:828829.

7. Hartley WJ. A focal symmetrical encephalomalacia of lambs. NZ VetJ 1956;4:129135.

8. Buxton D, Morgan KT. Studies of lesions produced in the brains ofcolostrum deprived lambs byClostridium welcii (Cl. perfringens) type Dtoxin. J Comp Pathol 1976;86:435447.

9. Garry F, Weiser G, Belknap E. Clinical pathology of llamas. Vet ClinNorth Am Food Anim Pract 1994;10:201209.

10. Little PB. Identity of fluorescence in polioencephalomalacia. Vet Rec1978;103:76.

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