• Heat stress;
  • Sheep;
  • Spinal cord;
  • Summer


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References


We detected a pattern of lambs presenting with hyperthermia and neurological signs during the summer.


The main objectives of this study were to compare clinical findings and results of diagnostic testing and to identify a potential etiology.


Fifteen clinical cases of lambs less than 12 months of age presenting with neurological signs, tachypnea, and hyperthermia over 4 summers.


Retrospective case series. Medical records were searched for lambs less than 12 months of age that presented with neurological signs including the following: kyphosis, pelvic limb hyperextension, treading of feet, muscle tremors and recumbency, and hyperthermia of greater than 104°F. A grading system was established to describe severity of presenting neurological signs. Weather data were collected from weather stations near the farm of origin for 3 days prior to presentation.


The lambs were from 7 flocks in central Texas. All cases occurred between July and September, with a median heat index of 90.5 for the 3 days before presentation. Complete blood count, serum chemistry, necropsy examination, rumen content, virology, brain MRI, liver copper, selenium, and vitamin E failed to identify a consistent etiology for the signs presented. The only common factor was high heat and humidity. Histopathological examination identified axonal degeneration and skeletal muscle necrosis in some lambs.

Conclusions and Clinical Importance

These clinical cases appeared similar to the Australian disease humpyback and indicate that lambs exposed to high environmental temperatures and humidity might be at risk of developing the described clinical presentation.


agar gel immunodiffusion


aspartate transferase


bluetongue virus


creatinine kinase


cerebrospinal fluid


fluid attenuated inversion recovery


gamma glutamate transferase


gradient recall echo


immunofluorescence antibody testing


magnetic resonance imaging


short tau inversion recover


total carbon dioxide


turbo spin echo

Hyperthermia is defined as a rise of core body temperature above the hypothalamic set point.[1] In humans, heat stress syndromes include, in increasing order of pathology, heat cramps, heat exhaustion, and heat stroke.[1, 2] Neurologic dysfunction in humans is attributed to metabolic disturbances, metabolic encephalopathy, and cerebral edema and ischemia.[1] Long-term neurologic deficits occur in 20% of patients.[1] Similar presentations have been reported in other species. Heat stroke in working dogs can result from dehydration, high environmental temperatures and humidity, long work shifts, hair coat length, and potential exposure to toxins.[3] Heat stroke has been induced in sheep as a human model by high environmental temperatures and exercise, resulting in clinical signs that included hyperventilation, restlessness, cyanosis, and convulsions.[4] High environmental temperatures have been linked to adverse effects on productive capabilities[5] and deaths[6] in ruminants. The upper critical threshold at which cattle performance and health are compromised ranges from 73.4 to 86°F (23–30°C) depending on production stage.[5] Diet[7]and genotype (Bos indicus versus Bos taurus)[8] also influence heat tolerance in cattle.

During the summer months of 2009–2012, a number of lambs presented to the Texas A&M Veterinary Medical Teaching hospital with clinical signs of high rectal temperature and neurologic disease. The severity of disease ranged from mild neurologic signs characterized by a postural kyphosis, limb hyperextension, and paddling pelvic limbs progressing to sternal recumbency. Increased spinal reflexes were observed in all cases. Neurologic examination of these cases localized the lesion to the spinal cord or cerebellum. In 2012, a similar syndrome of hyperthermia, tachypnea, muscle fasciculation, and hunched back was reported in sheep in Oklahoma.[9] There are similarities between this observed syndrome and “humpyback disease”, which has been reported in Merino wethers in Australia.[10] Humpyback disease appears to affect sheep in full fleece walked for distances for shearing after a period of significant rainfall 6–10 weeks prior.[11] Solanum esuriale has been suggested to be involved in the etiology of this disease.[11] In this report, we describe the clinical and pathologic findings, and some epidemiological observations in 15 lambs less than 12 months of age that presented with neurologic signs and hyperthermia.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References

From 2009 to 2012, medical records were examined for sheep admitted that fit the case definition of a lamb under 12 months old presenting with the neurologic signs described below coupled with increased rectal temperature greater than 104°F (40.0°C) on presentation. Data retrieved from these cases included physical and neurologic examination findings, complete blood count and chemistry panels, cerebrospinal fluid (CSF) analysis, serological and molecular testing for viruses, liver Vitamin E, copper and selenium concentrations, advanced imaging findings, pathological findings, rumen content analysis, and historical environmental conditions.

A Grading System was Established as to Severity of Neurologic Signs Upon Presentation

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References
  • Grade I: mild kyphosis, pelvic limb hyperextension, treading of feet, hyper-reflexive spinal reflexes in all limbs
  • Grade II: kyphosis, muscle tremors, treading of feet, increased time in recumbency, hyper-reflexive spinal reflexes in all limbs
  • Grade III: recumbent, hyper-reflexive spinal reflexes in all limbs

Eighteen sheep were admitted during this time period that fit the case definition. Three cases were excluded because of the lack of pertinent clinical data on admission. All cases were owner admitted without referral. Necropsy was performed on 6 animals. Serum chemistry was performed on 7 animals on the day of admittance. Cerebrospinal fluid was examined in 5 animals. Serological (agar gel immunodiffusion; AGID) or molecular testing for bluetongue virus (PCR and immunofluorescence antibody testing; IFAT), epizootic hemorrhagic disease (PCR) or both was performed in 4 animals. Liver copper concentrations were measured at necropsy in 4 animals, liver vitamin E in 5 animals and liver selenium concentrations in 4 animals. Two animals underwent brain and cervical spinal cord magnetic resonance imaging (MRI). Cervical and thoracic vertebral radiography was performed on 1 animal. Analysis of rumen content for toxic plants was performed on 6 animals, and feed was tested for ionophore levels from 1 herd. Cholinesterase activity was measured in 1 animal.

Weather data were collected from the closest weather station to the farm of origina for the 3 days before the admission of all animals. The maximum and minimum daily temperature and humidity were obtained. The minimum and maximum daily heat indices were calculated using the minimum daily temperature and maximum humidity and maximum daily temperature and minimum humidity respectively.b


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References

Epidemiological Aspects

The environment and animal husbandry of the animals varied. All animals were fed a form of concentrate feed (protein levels, origin, and amount varied) and differing amounts of forage in the form of coastal Bermuda, alfalfa or Sudan hay, and pasture. Animals were either kept at pasture with shade or housed, or a combination of both. Some animals had access to areas with fans. All animals had access to water-free choice. Animals were treated, before admission, by the owners with a variety of medications that included antibiotics, thiamine, flunixin meglumine, dexamethasone, anthelmintics, ammonium chloride, Vitamin B, and selenium. All but 1 herd reported animals showing similar signs in previous summer seasons. All cases occurred between July and September. Two herds reported the clinical signs also occurring in animals older than 1 year. All cases in this study were from Texas. The environment of 1 herd was assessed, and Solanum species were found to be present in the pasture.

All animals had rectal temperatures greater than 104°F (40.0°C) and were less than 12 months old, as per the case definition. Three cases in total were excluded because of incomplete physical examination data. The animals were from 7 herds. Seven animals presented as a group from a single owner and the other eight cases were presented individually.

All animals, irrespective of the severity of their neurologic signs, were bright and alert with good appetites.

The signalment, rectal temperature and respiration rate on presentation, month of presentation, and severity of clinical signs are presented in Table 1. The median age at presentation was 6 months, with a range of 4–6 months. The sex was not recorded for 6 animals. Of the animals where sex was recorded, 55.5% were female. Median rectal temperature on presentation was 106.2°F (41.3°C), range of 104.2°F (40.1°C) to 107.6°F (42°C). More lambs were presented in the month of August compared to July and September. Of the 14 animals, for which respiration rate was recorded on presentation, only 20% of cases had a respiratory rate less than 100 breaths per minute.

Table 1. Signalment, rectal temperature, respiratory rate on admission, month of admission, and survival to discharge in 15 sheep according to their grade of neurologic lesion
 Grade of Neurologic Clinical SignsPercentage
Blackface x11013
Age (months)
Rectal temperature (°F) on presentation
Survival to discharge
Month of presentation
Respiration rate
Total number per grade (%)6 (40)6 (40)3 (20) 

Laboratory Analyses

Of the 8 animals with serum chemistry analyses, all had gamma glutamate transferase (GGT), creatinine kinase (CK), and aspartate transferase (AST) activities greater than the reported reference intervalc (GGT 128–149 μ/L reference interval 20–44; CK 126–1084 μ/L reference interval 7.7–101 μ/L; AST 143–353 μ/L reference interval 49–123 μ/L). One animal had mild hypoproteinemia, 4/6 had mild hypoalbuminemia, 5/6 had mild increase in total carbon dioxide (TCO2 23–31 mmol/L reference interval 20–27 mmol/L) indicating mild metabolic alkalosis, and 2 animals had mild hypokalemia (potassium 3.7–5.1 mmol/L reference interval 4.3–6.3 mmol/L. Hyperglycemia was recognized in 5 animals (glucose 73–110 mg/dL reference interval 44–81 mg/dL). Of the 7 animals that had a CBC performed, mild nonregenerative anemia was present in four. Nucleated red blood cells were present in 1 animal with anemia. Mild lymphopenia was present in 2 animals. Mild neutrophilia was present in 1 animal, and mild leukopenia was present in 1 animal. One of 4 animals had marginally low liver selenium (0.95 ppm reference interval 1.0–6.0 ppm). Copper levels were marginally increased in 2/4 animals (110 ppm and 139 ppm reference interval 25–100 ppm). Liver vitamin E levels (dry weight basis) ranged from 8.8 to 31.6 ppm in the 5 animals tested (reference interval 10–15 ppm). Levels were increased above the reference range in 2 animals and mildly decreased in 1 animal.

Rumen contents from the 6 euthanized animals were identified for toxic plants, and Solanum species were identified in 1 animal. Feed analysis from 1 herd did not identify an increased level of ionophores. Cholinesterase activity was tested on 1 animal from the herd that admitted 7 animals as a group, and the result was within normal intervals.

Cerebrospinal Fluid

Of the 5 cases, 2 had marked hemodilution, 2 had a mild mononuclear pleocytosis, and the 6th animal had a possible pleocytosis, but sample size was considered too small to be accurate. The site of CSF collection was recorded for 2 cases, one from the atlantooccipital space and one from the lumbosacral space. Coagulase negative Staphylococcus, Pasteurella, Enterococcus, and Bacillus species were cultured from the CSF obtained at necropsy in 1 animal that had a mild-to-moderate mononuclear pleocytosis and was considered contamination.

Serological Testing and Molecular Diagnostics

Two animals were weakly positive for bluetongue virus (BTV) on IFAT, but negative on PCR, another animal was negative on both. One animal was negative for BTV on AGID. All animals tested (3) were PCR negative for epizootic hemorrhagic disease.

Diagnostic Imaging

Magnetic resonance imaging of the brain and was performed on 2 animals immediately postmortem with a 3 Tesla system.d Precontrast T1 and T2 weighted fluid attenuated inversion recovery, T2- weighted turbo spin echo, T2* gradient recall echo, and short tau inversion recover (STIR) sequences were obtained in multiple planes. No lesions of the brain or 1st segment of the spinal cord were identified. The cerebral and cerebellar architecture, signal intensity, and gray-white matter distinction was normal. The brain stem, meninges, and cranial nerves were normal. Radiographs of the cervical and thoracolumbar vertebral column in 1 animal were normal.

Treatment and Outcome

All animals were admitted to the hospital that was air conditioned to an ambient temperature of 65–75°F (18.3–23.8°C). Treatments included cooling alone, or with a combination of any of the following medications: procaine penicillin G ceftiofur hydrochloride and florfenicol antimicrobials; thiamine; amprolium; flunixin meglumine; gabapentin; and intravenous fluids. Five of the 15 animals were euthanized, 3 for diagnostic purposes, 1 for deterioration of clinical signs, and 1 that presented as grade 3, for failure to improve. The lamb that deteriorated presented at grade 2 deteriorated to grade 3 (recumbency) following CSF collection at the lumbosacral space. One animal died under general anesthesia during the MRI procedure. The remaining 9 animals survived to discharge and all improved at least 1 clinical grade during hospitalization. The surviving animals presented with clinical grades 1 and 2 only. Of the 9 surviving animals, median duration of hospitalization was 7 days, mean 5.8 days (range 2–7 days).

Weather Data

Table 2 presents the range and median daily temperatures, humidity, and heat indices for the 3 days before presentation.

Table 2. Maximum, minimum, and median temperature (degrees Fahrenheit and Celsius), relative humidity (%), and calculated mean heat index for the 3 days before admission of the animals from 2009 to 2012
Temperature69 (20.5)105.5 (40.8)86 (30)
Relative humidity2010058
Heat indexb7010590.5


Of the 6 animals that were necropsied, 1 had gross muscle lesions. The lamb had pale areas in the muscle of the left lateral thigh. Other gross findings included pulmonary edema (3/6), mild hydropericardium (2/6), and haemonchosis (2/6). The abomasal worm burden was considered heavy in 1 animal and light in the second.

Histologically, lesions were most consistently found in the central nervous system (CNS), skeletal muscles, and liver. Central nervous system lesions consisted of minimal to mild axonal degeneration at all levels of the spinal cord, which was generally very subtle. Axonal degeneration was most frequent in the ventral and ventrolateral funiculi and was characterized by swollen myelin sheaths, some of which contained axonal debris and macrophages, and occasional swollen axons. In 1 case, minimal axonal degeneration was also evident within the midbrain and medulla oblongata. One case had occasional nodules composed of microglia within the brain stem.

Skeletal muscle necrosis was evident in 5/6 cases. The severity of the necrosis was minimal to mild in all 5 cases, generally limited to scattered individual myofibers, but 1 animal had moderate necrosis in the left triceps muscle, which was not associated with a known injection site. Affected myofibers were hypereosinophilic, fragmented, and were often surrounded by macrophages and proliferating satellite cells. Mineralization was not evident. In the case with no observable muscle necrosis, only 1 section of muscle was examined. The animal with gross pallor of the left lateral thigh musculature had only mild necrosis histologically.

The majority of cases (5/6) had a vacuolar change in the liver that was classified as severe in 4 cases and mild in 2 cases. Hepatocytes contained clear round vacuoles of varying size, with many cells having a single large vacuole. Some of these vacuoles were clear, consistent with lipid, whereas other contained a hyalinized to flocculent, eosinophilic material. The eosinophilic vacuoles were most conspicuous around portal areas in two of the more severely affected cases, and these 2 cases also had scattered individually necrotic hepatocytes and evidence of regeneration. The vacuoles were examined ultrastructurally in 1 case, and the results were consistent with dilated endoplasmic reticulum.


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References

The clinical signs in these animals consisted of increased spinal reflexes, normal to increased muscle tone, hindlimb extension, kyphosis, muscle fasciculation and, in some cases, recumbency. These findings, combined with normal cranial nerve examination and mental status, localized the lesions to the spinal cord, which correlated well with the histopathologic finding of mild spinal axonal degeneration in all 6 lambs. A cerebellar lesion was thought less likely with the lack of changes observed on MRI. The results of this retrospective study suggest that environmental factors of high ambient temperatures and humidity were the most likely cause of the described clinical signs. The seasonal presentation was in the hottest months of the year. The median temperature for the 3 days preceding admission of these cases was 86.0°F (30°C). Combined with humidity, the median heat index was 90.5, classified as “emergency” conditions for livestock.[12] These animals were also receiving concentrate feeds designed for high growth rates; therefore, it is likely that their metabolic rates were high resulting in increased susceptibility to heat stress. Feedlot cattle have been shown to suffer from heat stress, their high energy diets are thought to contribute to elevated metabolic heat production.[7] Heat stress in ruminants results in both decreased reproductive and weight-gain performance[5] and compromised welfare.[13] In feedlot cattle, heavier weight animals are more negatively affected by high heat indices than lightweight cattle.[13]

Heat stroke, the most severe form of heat illness, results from failure of thermocompensatory processes. Decreased central venous pressure and a shift of blood flow toward the muscles and skin away from splanchnic organs results in endotoxic shock like syndromes and multiorgan failure.[14] In humans, the diagnosis of heat stroke is made by a combination of hyperthermia and central nervous system dysfunction,[14] most commonly altered mental status.[15] Hyperthermia is known to cause of variety of degenerative lesions in the human brain.[16] The spinal cord has been rarely evaluated as a target of injury in human hyperthermia cases, but the spinal cord does appear to be susceptible to hyperthermic injury.[17] As in humans, heat stroke in the dog is associated with multiorgan failure and can include necrosis in the brain and other viscera.[18] Experimental heat stroke in sheep appears to result in similar biochemical and physiologic alterations as in humans, but the lesions induced by hyperthermia in this species have apparently not been explored.[17] Neurologic deficits have also been associated with heat stress in camelids, exhibited by weakness progressing to recumbency.e Significant histopathologic findings of heat stress camelids were described as mild-to-severe muscle necrosis and minimal to mild spinal axonal degeneration, as observed in the lambs in this study.e

A recent report described a similar syndrome in 8 lambs originating from a farm in Oklahoma.[9] These animals exhibited hyperthermia, an arched back, and muscle fasciculations in the rear limbs. Histologic findings included myodegeneration, renal tubular necrosis, chronic bronchointerstitial pneumonia, and a normal brain and spinal cord. Similarities to the present study suggest the possibility that both reports are describing the same disease, although some pathologic differences and the small number of cases receiving necropsies in both studies preclude any definitive conclusions.

The clinical signs in this study are similar to a disease observed in Australia called humpyback, which occurs with a reported morbidity of 3–5% in animals gathered for shearing in hot weather.[11] Humpyback disease occurs in animals in good condition, similar to the lambs receiving a high plane of nutrition in this study.[10, 11] The histopathologic lesions in the sheep presented in this study and those affected by humpyback are consistent with axonal degeneration in the CNS and myodegeneration.[10, 11] Also similar to humpyback disease, all sheep in this study received cooling by placing in an air-conditioned environment and the surviving animals improved at least 1 grade during hospitalization. The cause of humpyback is unknown, but ingestion of a toxic plant such as Solanum spp. is suspected.[7, 14].

A plant toxicity is considered unlikely as the inciting cause in these cases because of the lack of potential toxicologic plants consistently identified on rumen evaluation and the variable management systems involved. Contamination of the feed by a mycotoxin is another consideration. Ergot alkaloids are known to cause a hyperthermic syndrome in ruminants,[19] and this possibility might warrant further investigation. A nutritional etiology (ionophore toxicity and copper or selenium deficiency) is thought unlikely because of the lack of common abnormalities in all animals. An inherited degenerative disease or a genetic predisposition to heat sensitivity are also thought unlikely as there were at least 3 breeds involved. An infectious disease also seems unlikely. The lymphopenia present in 2 animals suggested viral disease or a stress leukogram; however, molecular diagnostics and serology did not indicate a viral infection. Cerebrospinal fluid analysis identified a mild mononuclear pleocytosis in 3 animals, which was inconsistent with viral or bacterial infection. Hematology showed mild nonregenerative anemia in four animals, but was not correlated with the severity of the disease (2 severely affected and 2 mildly affected).

Hyperthermia has been shown to result in myodegeneration and liver damage in a variety of species.[10, 12, 13, 15] Serum biochemistry in these lambs revealed increased muscle enzymes, consistent with the increased muscle activity from fasciculation, recumbency, and the histologic evidence of myodegeneration. Gamma glutamyl transferase activity was also increased in all animals tested. This change likely reflects the liver pathology observed. The vacuolar change observed within hepatocytes and interpreted as dilatation of endoplasmic reticulum is apparently a nonspecific change, but this change has been reported in the livers of human patients treated for malignancies with exogenous hyperthermia and in experimental hyperthermia studies in rats.[20, 21]

In conclusion, the syndrome described here has many similar attributes to humpyback disease observed in Australia. However, in the animals in this study, clinical signs were not induced by forced exercise. High planes of nutrition and high environmental temperatures might contribute to the disease, but the specific cause remains unclear. An unidentified toxin or other factor that renders affected animals more susceptible to the effects of high ambient temperatures cannot be excluded. Producers should be made aware of the risk of disease in rapidly growing sheep in hot climates and the potential benefit of rapid cooling to improve neurologic signs.


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References

This work was not supported by a grant and was not presented at a meeting.

Conflict of Interest: Authors disclose no conflict of interest.

  1. 1 Accessed on August 22, 2012

  2. 2
  3. 3

    Smith, B. Large Animal Internal Medicine, 4th ed. St. Louis, MO: Mosby Elsevier; 2009

  4. 4

    Siemens, MagnetomVerio, Malvern, PA

  5. 5

    Norton P, Gold J, Schulz K, et al. Camelid heat stress as a syndrome: 15 cases (2003–2011). Journal of Veterinary Internal Medicine 2012;26:761 (abstract)


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. A Grading System was Established as to Severity of Neurologic Signs Upon Presentation
  5. Results
  6. Discussion
  7. Acknowledgment
  8. References