Retrospective evaluation of wobbly hedgehog syndrome in 49 African pygmy hedgehogs (Atelerix albiventris): 2000–2020

Gabriela A. Gonzalez Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC

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Julie A. Balko Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC

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Miranda J. Sadar Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO

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Amy B. Alexander Department of Comparative, Diagnostic, and Population Medicine, College of Veterinary Medicine, University of Florida, Gainesville, FL

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Julie D. Sheldon Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN

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Grayson A. Doss Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI

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Krista A. Keller Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL

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Sara M. Gardhouse Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS

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Olivia A. Petritz Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC

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Abstract

OBJECTIVE

To retrospectively evaluate the prevalence and clinical progression of wobbly hedgehog syndrome (WHS) and concurrent incidence of neoplasia in a cohort of African pygmy hedgehogs (Atelerix albiventris).

ANIMALS

49 hedgehogs.

CLINICAL PRESENTATION AND PROCEDURES

Medical records of hedgehogs from 7 institutions across the US over a 20-year period (2000 to 2020) were retrospectively reviewed. Inclusion criteria were hedgehogs of any sex or age with postmortem CNS histopathology consistent with WHS. Collected data included sex, age at onset and euthanasia, major histopathologic findings, reported neurologic clinical signs, and treatments administered.

RESULTS

24 males and 25 females were included. Fifteen of 49 (31%) individuals had subclinical WHS with no reported antemortem neurologic clinical signs. In neurologically affected (clinical) hedgehogs (n = 34), the mean ± SD age at onset was 3.3 ± 1.5 years with a median (range) time from onset to euthanasia of 51 days (1 to 319 days). In neurologically affected hedgehogs, the most commonly reported clinical signs were ataxia (n = 21) and pelvic limb paresis (16) and the most commonly administered treatment was meloxicam (13). Overall, 31 of 49 (63%) hedgehogs had a concurrent histopathologic diagnosis of neoplasia outside of the CNS.

CLINICAL RELEVANCE

The prognosis for hedgehogs with WHS is poor. No treatment had a significant effect on survival time, and neoplasia was a common comorbidity in the current cohort. A small but clinically relevant subset of neurologically normal hedgehogs had a histopathologic diagnosis of WHS.

Abstract

OBJECTIVE

To retrospectively evaluate the prevalence and clinical progression of wobbly hedgehog syndrome (WHS) and concurrent incidence of neoplasia in a cohort of African pygmy hedgehogs (Atelerix albiventris).

ANIMALS

49 hedgehogs.

CLINICAL PRESENTATION AND PROCEDURES

Medical records of hedgehogs from 7 institutions across the US over a 20-year period (2000 to 2020) were retrospectively reviewed. Inclusion criteria were hedgehogs of any sex or age with postmortem CNS histopathology consistent with WHS. Collected data included sex, age at onset and euthanasia, major histopathologic findings, reported neurologic clinical signs, and treatments administered.

RESULTS

24 males and 25 females were included. Fifteen of 49 (31%) individuals had subclinical WHS with no reported antemortem neurologic clinical signs. In neurologically affected (clinical) hedgehogs (n = 34), the mean ± SD age at onset was 3.3 ± 1.5 years with a median (range) time from onset to euthanasia of 51 days (1 to 319 days). In neurologically affected hedgehogs, the most commonly reported clinical signs were ataxia (n = 21) and pelvic limb paresis (16) and the most commonly administered treatment was meloxicam (13). Overall, 31 of 49 (63%) hedgehogs had a concurrent histopathologic diagnosis of neoplasia outside of the CNS.

CLINICAL RELEVANCE

The prognosis for hedgehogs with WHS is poor. No treatment had a significant effect on survival time, and neoplasia was a common comorbidity in the current cohort. A small but clinically relevant subset of neurologically normal hedgehogs had a histopathologic diagnosis of WHS.

Introduction

African pygmy hedgehogs (Atelerix albiventris) are insectivorous mammals native to West and Central Africa. Despite being illegal to own in 5 states, they have been growing in popularity as household pets in the US.1 In 1991, it became illegal to import hedgehogs into the US as this species can be subclinically infected with foot and mouth disease virus, which is a serious economic threat to livestock.2 Consequently, all companion hedgehogs in the US are captive bred and inbreeding has become a noteworthy problem as breeders struggle to keep up with the demands of the hedgehog companion trade.3 The resulting limited genetic diversity in hedgehogs may play a role in many diseases that affect this species, potentially including wobbly hedgehog syndrome (WHS).4

Wobbly hedgehog syndrome is a fatal neurodegenerative disease observed in an estimated 10% of companion hedgehogs.1 Interestingly, WHS has not been reported in wild African pygmy hedgehogs.5 While the etiology of this disease remains unknown, genetic, nutritional, and autoimmune causes have been suggested.1,6 Wobbly hedgehog syndrome can occur at any age, but the disease typically affects animals under 2 years old.1 Clinical signs of WHS, such as ataxia and paresis, are nonspecific and can resemble CNS neoplasia, intervertebral disc disease, trauma, or infectious or toxic processes, among other etiologies. In a retrospective study7 of 106 African pygmy hedgehogs, WHS was the most common cause of ataxia.

Hedgehogs with confirmed WHS can become emaciated and have neurogenic muscle atrophy and hepatomegaly but typically do not have gross lesions in the brain or spinal cord.1,5 The hallmark histologic lesion of WHS is vacuolization of the white matter tracts of the cerebrum, cerebellum, brainstem, and spinal cord.1 Myelin degeneration, axonal loss, and astrocytosis have also been reported, which can help to distinguish this disease from other nonspecific causes of white matter vacuolization such as delayed fixation or improper handling of the tissues during the fixation process.5,8 Currently, no antemortem diagnostic tests exist for WHS and definitive diagnosis requires postmortem histopathology of the brain and/or spinal cord. Without a definitive antemortem diagnostic option, veterinarians rely on a clinical diagnosis by ruling out other diseases that can produce neurologic signs. Treatment for WHS focuses on supportive care and management of clinical signs. While numerous treatments such as NSAIDs, antibiotics, and steroids have been attempted, there is no therapy proven to treat, manage, or delay the progression of WHS and it remains a progressive, fatal disease.

A previous retrospective study1 characterized the incidence, progression, clinical signs, administered treatments, and pathology findings in a cohort of 40 African pygmy hedgehogs with histopathologically confirmed WHS. While the previous retrospective was comprehensive in nature, the data are currently over 15 years old and span a shorter time frame. Furthermore, as the genetic diversity of companion hedgehogs continues to degenerate while veterinary medicine rapidly evolves, it is necessary to reevaluate disease presentation, potential therapies, and prognosis to optimize clinical management. The objective of this retrospective study was to evaluate the prevalence, clinical progression, and histopathologic findings of African pygmy hedgehogs presented to veterinary teaching hospitals over a 20-year period with histopathologically confirmed WHS.

Materials and Methods

Case selection

Medical records from 7 veterinary teaching hospitals (North Carolina State University, Colorado State University, University of Tennessee, Kansas State University, University of Florida, University of Illinois, and University of Wisconsin-Madison) were retrospectively reviewed to identify hedgehogs with WHS from January 1, 2000, to December 31, 2020. Inclusion criteria were African pygmy hedgehogs of any sex or age with postmortem CNS histopathology consistent with WHS.

Medical records review

For each hedgehog that met the inclusion criteria, the medical record was reviewed. Sex, spay or neuter status (if known), age at onset and euthanasia, neurologic clinical signs at presentation, and administered treatments were recorded. Age at onset was defined as age at presentation to a veterinarian for clinical signs (either neurologic [clinical] or nonneurologic [subclinical]) or owner-reported age at onset of clinical signs from the medical record. Death was defined as either death by natural causes or euthanasia. Survival was defined as the time between onset of neurologic (clinical) or nonneurologic (subclinical) clinical signs and death. Hedgehogs were classified as subclinical if there were no antemortem neurologic clinical signs at presentation, but lesions consistent with WHS were reported on necropsy. Histopathology was performed by board-certified veterinary pathologists at the individual institutions, and relevant findings were recorded. Wobbly hedgehog syndrome was histopathologically confirmed when vacuolization of the white matter tracts of the cerebrum, cerebellum, brainstem, and/or spinal cord were reported. Documented neoplastic processes were classified using the Exotic Species Cancer Research Alliance neoplasia classification guide.9

Statistical analysis

Statistical analysis was performed using a computerized statistical program (R version 4.2.2 with survival package; R Foundation for Statistical Computing). Analysis of time to onset and survival was conducted using a Cox proportional hazards model. For considerations of sex, the P value was generated from a binomial distribution with a null hypothesis of an even split between male and female. Significance was set at P < .05. A Fisher exact test was used when sex and spay/neuter status were considered in tandem; of note, this approach to sex only holds if the population of companion hedgehogs is evenly split between male and female, as any preference from hedgehog owners for one over the other could affect the split.

Results

Over a 20-year period (2000 to 2020), a total of 1,414 hedgehogs were presented to 6 veterinary institutions and WHS was diagnosed histopathologically in 47 (3.32%) hedgehogs. For the seventh institution, a subset of medical records (2000 to 2010) was unavailable for review; thus, these data were not included in the total prevalence calculation. Prevalence at this institution over a 10-year period (2010 to 2020) was 2 of 228 (0.87%) hedgehogs. Of the 49 hedgehogs with WHS from all 7 institutions, a clinically relevant subset had no reported antemortem neurologic clinical signs (15/49 [31%]); these animals were labeled “subclinical” and euthanized due to other comorbidities. The remaining animals (34/49 [69%]) had reported neurologic clinical signs and hereafter are referred to as “clinical” hedgehogs.

Signalment

Of the 49 WHS-confirmed hedgehogs, 23 were intact females, 21 were intact males, 2 were spayed females, and 3 were castrated males. Neither males nor females were more likely to be clinically affected by WHS (P = .775), and spay or neuter status did not increase the likelihood of disease (P = .642). In hedgehogs without antemortem neurologic clinical signs, there was no tendency for either sex (P = .217) or spay or neuter status (P = .571) to increase disease likelihood.

Wobbly hedgehog syndrome most commonly (75%) occurred in hedgehogs under 4.7 years of age (Q1 = 1.8 years, Q3 = 4.7 years) based on age at onset. In subclinical hedgehogs (15/49), mean ± SD at age of death was 3.1 ± 1.3 years (range, 0.7 to 5.1 years). In clinical hedgehogs (34/49), mean ± SD age at onset was 3.3 ± 1.5 years (range, 0.7 to 7.6 years) and mean ± SD age of death was 3.6 ± 1.6 years (range, 1.2 to 7.6 years). A significant relationship was found between the age at onset and the time from onset to death (P = .04), with each additional month of age at onset leading to a 2% increase in the hazards ratio. In other words, for each additional month of age, a hedgehog was 2% more likely to die before a hedgehog 1 month younger. For both clinical and subclinical hedgehogs, the median (range) time from onset of neurologic or nonneurologic clinical signs, respectively, to death was 51 days (1 to 319 days). Whether a hedgehog was subclinical or clinical for WHS did not have a significant relationship with the age at which they were presented to a veterinarian for clinical signs (P = .26) or the amount of time from onset of these signs to death (P = .283).

Clinical history

In clinical hedgehogs, the most commonly reported neurologic clinical signs were ataxia (21/34) and hind limb paresis (16/34; Table 1). Other reported neurologic clinical signs included “falling over” (6/34), focal and/or generalized seizures (4/34), circling (4/34), and decreased proprioception in either the pelvic limbs or all 4 limbs (4/34). Of the 4 hedgehogs with proprioceptive deficits, 2 had decreased to absent proprioception in both forelimbs and pelvic limbs, and the other 2 had decreased proprioception in the pelvic limbs exclusively. Clinical signs reported 3 or fewer times included lethargy, lateral recumbency, cervical pain, paralysis, nystagmus, head pressing, and the inability to “ball up.”

Table 1

Frequency of neurologic clinical signs in 34 of 49 total African pygmy hedgehogs (Atelerix albiventris) with histopathologically confirmed wobbly hedgehog syndrome presented to veterinary teaching hospitals across the US from 2000 to 2020. The remaining hedgehogs (n = 15) did not have antemortem neurologic clinical signs.

Neurologic clinical signs Frequency (%)
Ataxia 21 (61.8)
Hind limb paresis 16 (47.1)
“Falling over” 6 (17.6)
Circling 4 (11.8)
Decreased proprioception 4 (11.8)
Reduced activity 4 (11.8)
Seizures and/or tremors 4 (11.8)
Lateral recumbency 2 (5.9)
Cervical pain 1 (2.9)
Head pressing 1 (2.9)
Nystagmus 1 (2.9)
Paralysis 1 (2.9)
Unable to “ball up” 1 (2.9)

Treatment and case outcome

Diagnostic imaging was limited in hedgehogs with neurologic clinical signs (6/34). Treatments, as reported in medical records, were grouped into global treatment categories. These included the following: NSAIDs (meloxicam, 18/49 [36.7%]; and piroxicam, 1/49 [2.0%]), antibiotics (enrofloxacin, 4/49 [8.2%]; orbifloxacin, 1/49 [2.0%]; sulfamethoxazole/trimethoprim, 4/49 [8.2%]; and amoxicillin-clavulanate, 6/49 [12.2%]), steroids (prednisolone, 5/49 [10.2%]), gastrointestinal medications (omeprazole, 2/49 [4.1%]; famotidine, 1/49 [2.0%]; and sucralfate, 1/49 [2.0%]), and additional supportive therapies (trazodone, 1/49 [2.0%]; gabapentin, 1/49 [2.0%]; fluid therapy, 5/49 [10.2%]; vitamin E supplementation, 1/49 [2.0%]; and silymarin, 1/49 [2.0%]; Table 2). In clinical hedgehogs, no treatment was found to have a significant effect on the time from onset of neurologic clinical signs to death (P = .607). The majority of hedgehogs in the current cohort were euthanized (48/49), with only 1 hedgehog reported to die from natural causes at 183 days from onset of clinical signs. Euthanized hedgehogs had a median (range) of 46 days (1 to 319 days) from onset of clinical signs to death.

Table 2

Treatments administered to 49 African pygmy hedgehogs (A albiventris) with wobbly hedgehog syndrome that were evaluated at tertiary teaching hospitals from 2000 to 2020. No treatment was found to have a significant effect on the time from onset of neurologic clinical signs to death.

Treatment group No. of hedgehogs (%)
NSAIDs 19 (38.8)
Antibiotics 15 (30.6)
Steroids 6 (12.2)
Gastrointestinal medications 4 (8.2)
Anxiolytics 2 (4.1)
Supportive care 7 (14.3)

Pathology

Overall, 31 of 49 (63%) hedgehogs from both subclinical and clinical groups had a histopathologic diagnosis of neoplasia outside of the CNS. No hedgehogs had a diagnosis of CNS neoplasia. Tumor types and incidence are reported (Table 3). There was no significant difference in incidence of neoplasia between subclinical (11/15 [73.3%]) and clinical (24/34 [70.6%]) hedgehogs. Twenty-eight hedgehogs with neoplasia had malignant tumors (28/31 [90.3%]), with gastrointestinal being the most common anatomic location (15/28 [53.6%]). Benign neoplasia was found in 9 hedgehogs (9/31 [29.0%]) and, of these, urinary and vascular sites were most common. Six hedgehogs (6/31 [19.4%]) had both benign and malignant neoplasms.

Table 3

Frequency of neoplasia outside of the CNS diagnosed by histopathology in 49 African pygmy hedgehogs (A albiventris) with histopathologically confirmed wobbly hedgehog syndrome presented to veterinary teaching hospitals across the US from 2000 to 2020. Six hedgehogs had both benign and malignant neoplasms and were reported more than once.

System Benign (n) Malignant (n)
Gastrointestinal 1 15
Genital 1 6
Hemolymphatic/histiocytic 1 4
Mesenchymal 1
Musculoskeletal 4
Ocular 1
Respiratory 1
Urinary 3 2
Vascular 2 4

There was no significant difference in the age at onset between the neoplasia and nonneoplasia groups (P = .9349). The nonneoplasia group had a median age at onset of 3.5 years (Q1 = 1.7 years, Q3 = 4.8 years), while the neoplasia group had a median age at onset of 3.4 years (Q1 = 2.1 years, Q3 = 4.4 years). Age at death was not significantly different between hedgehogs that did or did not have neoplasia (P = .553). There was also no significant effect of concurrent neoplasia on time from presentation to a veterinary hospital until death (P = .28). For all hedgehogs (n = 49), the nonneoplasia group had a median survival of 43 days (Q1 = 8.75 days, Q3 = 117.75 days) while the neoplasia group had a median survival of 52 days (Q1 = 5.6 days, Q3 = 66 days).

Discussion

Wobbly hedgehog syndrome continues to be a prevalent disease in companion African pygmy hedgehogs, with a short time from the onset of clinical signs to death, no proven treatment strategies, and a grave prognosis. This retrospective study reports prevalence of histopathologically confirmed WHS and updates decades-old knowledge of clinical signs, treatments, and concurrent neoplasia prevalence with this disease. Statistical correlation of these factors to mortality provides clinicians with updated information to relay to clients when making decisions regarding their companion animal. Wobbly hedgehog syndrome prevalence in the current study (3.32% [ 47/1,414]) is lower than previously described in the literature; however, it is still high relative to other diseases, especially since it is a fatal disorder without a known etiology or effective treatment. A retrospective study of 106 captive African pygmy hedgehogs conducted from 1994 to 2013 at Kansas State University College of Veterinary Medicine reported a prevalence of 8.49%.7 Similarly, a survey of hedgehog owners between 2000 and 2005 reported 10% (n = 676) of hedgehogs to have progressive paralysis.1 Potential hypotheses for these differences include differences in sample size, genetic variation among geographic locations, changes in prevalence over time, and the use of histopathology in the current study. It is possible that the lower prevalence found in this study may have been because previous studies included clinical signs of WHS in addition to histopathology-confirmed cases when reporting prevalence.1

Similar to past studies, no gender bias was found for WHS in the current cohort.1 Therefore, if the etiology of WHS has a genetic component due to inbreeding,6 it is unlikely to be sex linked. Similarly, spay and neuter status was also not significant, but this was likely limited by the small number of surgically sterilized hedgehogs in the current cohort (n = 5). Evaluation of a larger number of surgically sterilized hedgehogs would be needed to elucidate any potential influence of sterilization.

The average life-span of companion African pygmy hedgehogs is 4 to 6 years.10 Previous literature reported that WHS occurs most frequently in African pygmy hedgehogs under 2 years of age with a mean age at onset of 1.5 years.1 In contrast, the mean age at onset in the current cohort was 3.3 years, and this was of clinical relevance from both a diagnostic and prognostic standpoint for veterinarians. This difference may have been due to an increased number of hedgehogs being presented to veterinary hospitals and improved medical care leading to potentially increased life-spans. The older age range may also have been influenced by the exclusion of the 15 subclinical hedgehogs that had WHS but did not have antemortem neurological deficits, as these had a younger mean age at time of death.

Previous research did not find a correlation between the age at onset and the progression rate of WHS.1 In the current study, however, increased age translated to decreased survival (2% increase in hazards ratio) and this may have been influenced by several factors. First, older animals may have decreased responses to stress and infection and decreased organ reserve capacity, which may make them more likely to succumb to progressive diseases such as WHS.11 Second, owners may be more likely to euthanize an older pet compared to a younger pet, especially if the animal has other comorbidities. Third, the sample size or sampling cohort in the current study may reflect population differences not identified in the aforementioned study. The median time from onset of clinical signs to death in the current cohort was 51 days. Survival time has not been explicitly reported in previous studies, but another benchmark of progression, time from the onset of ataxia to immobility, was reported as 15 months for the majority (90%) of cases (n = 3,740) in a prior study.1 This contrasts with the much shorter 51-day median time from onset of neurologic signs to death in the current study. Although the mechanism(s) of death were not reported in the aforementioned study, the high prevalence of euthanasia in the current cohort (48/49 hedgehogs) likely influenced this disparity. Since knowledge of this disease has progressed over time, owners may be more likely to euthanize neurologically affected hedgehogs with a suspected poor prognosis before the disease advances to complete immobilization. Due to the retrospective nature of this study, however, owners’ rationale behind their decision to euthanize was unobtainable.

Clinical signs of WHS appear to vary considerably, with some hedgehogs displaying neurologic signs of ataxia and hind limb paresis and others presenting with nonneurologic clinical signs (ie, subclinical disease). It is likely that a third group of WHS-afflicted hedgehogs, those without any clinical signs, exists; however, as this study only included deceased hedgehogs that presumably presented to veterinarians and were euthanized for disease of some capacity, this third cohort was not captured in the current study. The inability to ball up and close their hood has previously been named the earliest indicator of WHS disease1; however, only 1 African pygmy hedgehog in the current study was reported to have this clinical sign. It is worth noting that the large number (31%) of nonneurologically affected hedgehogs in the current study exceeded a previously reported subclinical WHS prevalence of 5% (2/40) in histopathology-confirmed WHS cases.1 The larger subclinical population in the current study may have been the result of enhanced veterinary care available for nondomestic species, including hedgehogs, leading to earlier identification of other diseases and decision to euthanize.

Neoplasia comprised over half of identified histopathology abnormalities, although surprisingly, having WHS and concurrent neoplasia did not significantly change the time until death. Therefore, a diagnosis of neoplasia in a suspected WHS hedgehog may not decrease prognosis, which may change clinical recommendations. This finding was likely related to the lack of antemortem diagnostic testing performed in these cases. Since limited imaging was performed in neurologically affected hedgehogs in the current study (6/35), it is likely that clinicians may not have been aware of concurrent neoplasia outside of the neurologic system until necropsy. Clinicians are encouraged to pursue additional antemortem diagnostic testing in this species because the high rate of concurrent neoplasia may change the owner’s decision to pursue supportive care in an animal that potentially has a fatal disease, such as WHS. Conversely, diagnostic testing may permit further therapy (radiation therapy, chemotherapy, or surgery) for identified neoplasia, especially in subclinical WHS cases. Common neoplasms reported in hedgehogs include mammary gland carcinoma, lymphoma, and oral squamous cell carcinoma, with prevalence for the latter ranging from 35.7% to 45.45%.3,4,7,12,13 Interestingly, gastrointestinal neoplasms were the most common neoplasia (53.6%) among African pygmy hedgehogs with WHS in the current study. The interface and connection between gastrointestinal and neurologic diseases has been an area of emerging research, and it is proposed that electrolyte imbalances and dietary deficiencies may lead to demyelination, as seen in WHS histopathology.1,14,15

This study was limited in its retrospective nature. The variation in medical records across multiple institutions over many years may have inadvertently impacted record accuracy. Due to a lack of evidence-based drug doses in hedgehogs, medical records had drug doses that varied widely and therefore were not included in this study. Data such as husbandry, diet regimens, and diagnostics could not be assessed due to record-keeping variability. In this study, many hedgehogs were treated supportively and had limited diagnostics performed to further elucidate a cause of neurologic disease. This may have been due to clinical suspicion of WHS making clinicians less likely to pursue additional diagnostics or challenges obtaining them due to patient size. Owners may also have been hesitant to elect diagnostics due to financial constraints, leading to limited diagnostic data in these cases. Although this study evaluated a large number of African pygmy hedgehogs with WHS, a larger population size may have exposed additional statistically significant results. While the patient population had a wide geographical range, patients were sampled solely from tertiary veterinary teaching hospitals and not all hedgehog owners elected to pursue intensive critical care or postmortem examination. Since WHS can only currently be diagnosed postmortem, it is likely that some hedgehogs had WHS but were not recorded, as a necropsy was not performed. Animal age was owner-reported, and euthanasia and natural death were used synonymously for the purpose of this study; thus, data relying on age may have been impacted. Further research using breeder and owner surveys is needed to estimate overall population numbers and subsequently perform genetic analyses and determine the prevalence of WHS. Future studies are warranted to evaluate the etiology, usefulness of antemortem diagnostics, and potential treatments for WHS.

Acknowledgments

The authors have nothing to declare.

This study was presented in abstract form at the ExoticsCon 2022 conference.

The authors would like to thank James Robertson for his contribution to the statistical analysis and Jocelyn Becker for medical record review.

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Contributor Notes

Corresponding author: Dr. Petritz (oapetrit@ncsu.edu)
  • 1.

    Graesser D, Spraker TR, Dressen P, et al. Wobbly hedgehog syndrome in African pygmy hedgehogs (Atelerix spp.). J Exot Pet Med. 2006;15(1):59-65. doi:10.1053/j.jepm.2005.11.010

    • Search Google Scholar
    • Export Citation
  • 2.

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