Listeriosis Recovery in a Nigerian Dwarf Goat

Listeriosis is a globally significant zoonotic disease caused by bacteria of the genus Listeria, of which Listeria monocytogenes is the primary pathogen affecting both humans and animals (Radoshevich and Cossart, 2018; Swaminathan and Gerner-Smidt, 2007). The genus has expanded to include multiple species, including L. ivanovii and L. welshimeri, although L. monocytogenes remains the principal cause of clinical disease (Orsi and Wiedmann, 2016). First described by Murray et al. (1926) and later renamed by Pirie (1940), Listeria spp. are small Gram-positive, non-spore-forming, facultatively intracellular rods that are catalase-positive, oxidase-negative, β-hemolytic, and motile at lower temperatures (Vázquez-Boland et al., 2001).

Listeriosis has a worldwide distribution and affects a broad range of hosts, including humans, ruminants, pigs, and wildlife, with more than 40 species reported to be susceptible (Koopmans et al., 2023). In humans, it is a major foodborne disease with high case mortality rates, particularly amongst immunocompromised individuals, pregnant women, and neonates (Sharma et al., 2025). In livestock, ruminants; especially sheep, goats, and cattle, are most frequently affected, with clinical syndromes including encephalitis, abortion, and septicemia (Constable et al., 2016). The encephalitic form is the most common presentation in small ruminants and results from invasion of the central nervous system following ingestion of contaminated feed, particularly poorly fermented silage or spoiled forage (Low and Donachie, 1997).

Clinically, neurologic listeriosis is characterized by asymmetric cranial nerve deficits, head tilt, circling, nystagmus, dysphagia, and progression to recumbence, which is widely associated with a guarded prognosis (Ersdal, 2026; Radostits et al., 2006). Disease progression is often rapid, and mortality remains high despite treatment, particularly in advanced cases. Standard therapeutic protocols include high-dose penicillin or ampicillin, often combined with thiamine and supportive care; however, treatment success is variable due to factors such as delayed diagnosis, limited antimicrobial penetration across the blood–brain barrier, and the intracellular nature of the pathogen (Plumb, 2015; Radoshevich and Cossart, 2018).

Listeria monocytogenes is notable for its environmental resilience and ability to survive under adverse conditions, including refrigeration temperatures, high salt concentrations, and acidic environments, as well as its capacity to form biofilms that enhance persistence and resistance to disinfectants (Carpentier and Cerf, 2011). Although antimicrobial resistance in Listeria spp. has historically been uncommon, emerging reports suggest increasing variability in susceptibility profiles, raising questions about the predictive value of in vitro testing for clinical outcomes (Wilson et al., 2018). Interpretation may be particularly challenging when a non-monocytogenes Listeria species is isolated from a non-CNS site, because such species generally have limited recognized pathogenicity and antimicrobial susceptibility varies among Listeria spp. (Korsak and Szuplewska, 2016; Troxler et al., 2000). Transmission to humans may occur through ingestion of contaminated food or direct contact with infected animals or tissues, posing an occupational risk to veterinarians and livestock handlers (Sharma et al., 2025).

This case is notable for describing severe neurologic disease consistent with listeriosis in a recumbent goat, from which Listeria welshimeri was isolated. Despite the reported in vitro antimicrobial resistance, the goat experienced a favorable clinical outcome. However, L. welshimeri was isolated from feto-placental fluids rather than the CNS, making its etiologic relationship to the neurologic disease uncertain. This creates a clinical dilemma when in vitro resistance conflicts with the use of penicillin, a standard therapy for listeriosis (Troxler et al., 2000). Reports involving non-monocytogenes Listeria species in neurologic disease of small ruminants are exceedingly rare, and their clinical relevance remains poorly defined. This case therefore highlights the need to interpret non-classical Listeria isolates and antimicrobial susceptibility results in conjunction with the clinical presentation and source of isolation.

A 3.5-year-old Nigerian Dwarf doe (Boba Fetta) weighing 10.9 kg (24 lb) presented with acute onset neurologic dysfunction following abortion during her second pregnancy. The interval between abortion and onset of neurologic signs was approximately 2 days. Primary clinical concerns included lateral recumbence, severe torticollis, and vertical nystagmus, suggestive of central vestibular involvement (Figure 1). Neurologic examination included assessment of mentation, posture, ocular position and movement, menace response, pupillary light and palpebral reflexes, facial symmetry, swallowing, and tongue movement. Severe postural dysfunction was evident, with inability to maintain an upright position or ambulate independently, while no additional cranial nerve abnormalities were recorded. The patient originated from a small herd of six goats with no similar clinical signs reported. Environmental history revealed exposure to wet hay used as bedding following recent weather fluctuations (cold stress, heavy rainfall, and subsequent heat), representing a significant risk factor for listerial contamination. There was no prior history of neurologic disease, and the doe had previously completed a normal gestation. No recent dietary changes, toxin exposure, or trauma were reported.

Over the first 48 hours of hospitalization, the patient remained recumbent but stable. By day five of hospitalization, vital parameters were within acceptable ranges for the species, including a temperature of 100.4°F, heart rate of 120 bpm, respiratory rate of 30 breaths per minute, capillary refill time of 2 seconds, and pink, moist mucous membranes. Body condition score was 3/9. Neurologic abnormalities persisted. Neurologic examination revealed central vestibular signs, including head tilt, vertical nystagmus, and loss of balance, without evidence of peripheral ear disease. Mentation was dull but responsive, and cranial nerve deficits included abnormalities consistent with brainstem involvement, notably vestibular dysfunction (cranial nerve VIII), with suspected involvement of adjacent cranial nerves (V and VII), although detailed cranial nerve testing was limited by recumbence. Gastrointestinal function remained intact, with defecation and eructation observed; urination was also normal. Despite a guarded prognosis, the patient demonstrated gradual clinical improvement.

Comprehensive diagnostic evaluation was undertaken to identify the underlying cause of acute neurologic dysfunction following recent abortion. Because cerebrospinal fluid (CSF) analysis was not performed and Listeria was not isolated from the central nervous system, the etiologic diagnosis remained presumptive.

Abdominal ultrasonography was performed at presentation due to the recent history of abortion to evaluate for retained fetal or placental tissues. No abnormalities were detected, reducing concern for retained fetal or placental material, although this finding did not establish the cause of the neurologic signs.

Serial hematologic and serum biochemical evaluations revealed marked leukocytosis indicating systemic inflammation but not specifically supporting CNS infection. The recent abortion and associated physiologic stress were also considered potential contributors to the leukocytosis. Elevated creatine kinase (CK) concentrations were noted, likely secondary to muscle damage associated with prolonged recumbence. Additional findings included mild anemia, elevated aspartate aminotransferase (AST) indicative of tissue injury, and hypocalcemia (Table 1).

Bacteriological analysis was performed using standard aerobic culture techniques on selective media for Listeria spp. (Oxford/Palcam agar), followed by incubation at 35-37 °C. The sample used for bacterial culture was obtained from fetoplacental fluids/tissues. Therefore, isolation of Listeria from this site provided evidence of reproductive tract exposure/infection but could not establish that the organism was responsible for the concurrent neurologic disease. Presumptive colonies were identified based on characteristic morphology and confirmed using an automated identification system, the Matrix-Assisted Laser Desorption/Ionization Time-of-Flight (MALDI-TOF) mass spectrometry, which identified Listeria welshimeri with high confidence (Bizzini and Greub, 2010). CSF collection was not performed during the acute clinical period. Consequently, CSF cytology, protein analysis, and bacterial culture were unavailable to support CNS infection. This represents an important diagnostic limitation of the case. Antimicrobial susceptibility testing was conducted using a standardized Kirby-Bauer disk diffusion method and interpreted according to the Clinical and Laboratory Standards Institute (CLSI) guidelines for Listeria spp. (Hudzicki, 2009). The isolate demonstrated in vitro resistance to benzylpenicillin, while susceptibility to trimethoprim-sulfamethoxazole was observed. Interpretation of antimicrobial susceptibility was extrapolated from available guidelines, as standardized breakpoints for Listeria welshimeri are not well established (Davis and Jackson, 2009).

Differential diagnoses considered for the acute central vestibular/brainstem signs included listerial encephalitis, polioencephalomalacia, caprine arthritis encephalitis (CAE), intracranial abscessation, and toxic encephalopathy. The acute onset, vertical nystagmus, severe postural

Table 1: Selected hematologic and biochemical findings.

WBC: white blood cell count; K/µL: ×10³ cells per microliter; CK: creatine kinase; U/L: units per liter; AST: aspartate aminotransferase; Ca²⁺: ionized calcium; mg/dL: milligrams per deciliter.

Table 2: Comprehensive multimodal therapeutic protocol for case management and clinical rationale.

IU/kg: international units per kilogram; SC: subcutaneous; IV: intravenous; PO: per os (oral); q6-8h: every 6-8 hours; q12h: every 12 hours; q24h: every 24 hours; PRN: as needed; CNS: central nervous system; OU: oculus uterque (both eyes); Bo-Se: selenium and vitamin E injectable preparation.

dysfunction, history of abortion, and environmental exposure to wet hay increased clinical suspicion for listeriosis; however, these findings were not pathognomonic. In the absence of CSF analysis, advanced neuroimaging, or histopathology, the alternative neurologic differentials could not be definitively excluded.

Accordingly, neurologic listeriosis was considered a presumptive clinical diagnosis based on neurologic localization, environmental history, temporal association with abortion, and isolation of L. welshimeri from fetoplacental material. The fetoplacental isolate cannot be considered definitive evidence of CNS infection, and its causal relationship to the neurologic syndrome remains uncertain.

As detailed in Table 2 below, an integrated approach targeting infection control, neuroprotection, and clinical recovery, included antimicrobial, neurologic, anti-inflammatory, and supportive therapies with defined dosing regimens.

The patient demonstrated progressive clinical improvement during hospitalization, transitioning from lateral recumbence to independent ambulation, with restoration of voluntary feeding, drinking, and normal rumination by discharge. Clinical improvement was evaluated based on restoration of posture, ability to stand unassisted, normalization of appetite, and resolution of nystagmus. A structured neurological assessment of mentation, posture, nystagmus, ambulation, and feeding showed normalization of four of five domains at discharge, with only a mild residual head tilt.

Neurologic assessment revealed marked resolution of deficits, with only mild residual head tilt. Treatment adherence was ensured through continuous in-hospital monitoring and structured nursing care, while post-discharge compliance was facilitated by clear owner instructions; the therapeutic regimen was well tolerated, with no evidence of gastrointestinal or systemic intolerance. At 2–3-week follow-up, independent ambulation and normal feeding and rumination were maintained, with no recurrence of neurologic.

This case highlights several important clinical and pathophysiological aspects of neurologic listeriosis in small ruminants. The likely source of infection, wet hay used as bedding following rapid environmental changes, aligns with well-established epidemiologic risk factors, as Listeria spp. proliferate in poorly fermented or spoiled forage under fluctuating temperature and moisture conditions (Constable et al., 2016; Low and Donachie, 1997). Following ingestion, the organism may invade damaged oral mucosa and ascend to the brainstem via cranial nerves, particularly the trigeminal nerve, resulting in the characteristic neurologic manifestations of listerial encephalitis (Huff et al., 2024; Zhang et al., 2024).

The observed neurologic signs, particularly torticollis and vertical nystagmus, are consistent with brainstem encephalitis and central vestibular dysfunction, which are hallmarks of listerial infection in goats and sheep (Ersdal, 2026; Radostits et al., 2006). Although Listeria welshimeri was isolated, its role as the primary causative agent remains uncertain, as this species is typically considered non-pathogenic and may represent environmental contamination or an opportunistic organism. This observation contrasts with the established understanding that L. welshimeri is predominantly an environmental species with minimal pathogenic potential and lacking key virulence determinants required for neuroinvasion, such as internalins and listeriolysin O (Orsi and Wiedmann, 2016; Radoshevich and Cossart, 2018). Listerial encephalitis typically results from ingestion of contaminated feed or bedding, followed by invasion of damaged oral or pharyngeal mucosa and retrograde axonal migration along cranial nerves, particularly the trigeminal nerve, to the brainstem, leading to inflammation and characteristic vestibular signs (Wei et al., 2020).

Nevertheless, emerging genomic and experimental evidence suggests that certain non-monocytogenes Listeria spp., including L. welshimeri, may possess limited or atypical virulence potential under specific conditions, possibly through acquisition or expression of partial virulence-associated factors (Cheong et al., 2026; Zakrzewski et al., 2020). These findings raise the possibility that, although uncommon, such species may occasionally be associated with clinical presentations indistinguishable from classical listeriosis. Therefore, although a possible association cannot be excluded, the isolation of L. welshimeri from fetoplacental material does not establish it as the cause of the neurologic disease.

Clinical recovery occurred despite the reported in vitro penicillin resistance; however, the diagnostic uncertainty prevents attributing this response specifically to treatment of L. welshimeri. This apparent discordance between antimicrobial susceptibility testing and clinical outcome has been increasingly recognized with intracellular pathogens such as Listeria, where pharmacokinetic and pharmacodynamic factors; particularly high-dose administration and tissue penetration into the central nervous system, play a critical role (Plumb, 2015; Radoshevich and Cossart, 2018). Penicillin remains the first-line therapy for listeriosis due to its bactericidal activity and ability to achieve therapeutic concentrations when administered aggressively, and clinical response may not always correlate with laboratory susceptibility profiles (Wilson et al., 2018). The case suggests that clinical response should be considered alongside in vitro susceptibility findings, although it provides limited evidence because the causative organism was not definitively established.

The favorable outcome observed is particularly notable given that prolonged lateral recumbence is typically associated with poor prognosis in small ruminant listeriosis (Constable et al., 2016; Ersdal, 2026). Early intensive therapy and supportive care may have contributed to recovery, although their specific effects cannot be determined. Similar reports emphasize that survival in advanced neurologic cases depends not only on antimicrobial therapy but also on meticulous nursing care and maintenance of physiologic stability (Plumb, 2015). Overall, the favorable clinical outcome is noteworthy, but the absence of definitive CNS confirmation requires cautious interpretation of both the etiologic diagnosis and treatment response. Definitive diagnosis was limited by the absence of cerebrospinal fluid analysis, CNS isolation of Listeria, or postmortem confirmation, representing a major limitation of this case. Therefore, the diagnosis remained presumptive and based on clinical presentation, neurologic findings, environmental exposure, and isolation of L. welshimeri from fetoplacental material rather than the CNS.

This case describes the clinical recovery of a goat from severe neurologic signs of uncertain etiology, with a presumptive diagnosis of listeriosis. The isolation of Listeria welshimeri and its in vitro antimicrobial resistance profile highlights the complexity of interpreting laboratory findings in relation to clinical response. However, the absence of definitive CNS confirmation limits conclusions regarding the pathogenic role of L. welshimeri and the clinical significance of its antimicrobial resistance.

The authors thank the microbiology and biochemistry laboratory technicians at Tuskegee University College of Veterinary Medicine for performing the diagnostic analyses, and the large animal hospital technicians and veterinary students for their assistance with patient care and clinical monitoring.

This report documents recovery from lateral recumbence to independent ambulation within 12 days in a Nigerian Dwarf doe with presumptive neurologic listeriosis, alongside isolation of Listeria welshimeri reported as benzylpenicillin-resistant from fetoplacental material. The case highlights a diagnostic and therapeutic dilemma: how to interpret an atypical isolate and its susceptibility profile when the sampling site differs from the suspected site of disease. Although central nervous system infection was not confirmed, the documented recovery during multimodal treatment provides a clinically informative account of managing severe neurologic disease under diagnostic uncertainty.

VH: Writing, review and editing, writing original draft, resources, methodology, formal analysis, conceptualization. DM: Writing review and editing, writing supervision. AE, BOO: Writing review and editing. FB: Writing review and editing, writing original draft, supervision, methodology, conceptualization.

From the owner’s perspective, the doe showed progressive recovery from severe neurologic dysfunction, transitioning from recumbence to normal feeding and mobility. The owner reported good compliance with treatment and expressed satisfaction with the outcome despite the initially guarded prognosis.

No funding was received for this manuscript.

The data that support the findings are available on request from the corresponding author.

The authors declare that no generative AI and AI assisted technology was used in the creation of this manuscript.

The authors have declared no conflicts of interest.