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Case Report
Food Animal
2025
:5;
10
doi:
10.25259/RVSM_5_2025

Clinical Management and Recovery of a 2-Year-Old West African Dwarf Doe with Peste des Petits Ruminants

Department of Veterinary Medicine, Bayero University, Kano, Nigeria
Department of Veterinary Pharmacology, Ahmadu Bello University, Zaria, Nigeria
Department of Veterinary Medicine, Ahmadu Bello University, Zaria, Nigeria
Department of Clinical, Vetco Diagnostix, Kaduna, Nigeria.
Author image

*Corresponding author: Collins Chimezie Udechukwu, Department of Veterinary Medicine, Bayero University, Kano, Nigeria. sancollinoconsult92@gmail.com

Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Udechukwu CC, Jolayemi KO, Danbirni S, Yusuf A. Clinical Management and Recovery of a 2-Year-Old West African Dwarf Doe with Peste des Petits Ruminants. Res Vet Sci Med. 2025;5:10. doi: 10.25259/RVSM_5_2025

Abstract

Peste des petits ruminants (PPRs) is a highly contagious disease threatening small ruminant production and rural livelihoods in Africa. While most Nigerian reports focus on herd-level outbreaks, detailed single-animal case studies integrating clinical, hematological, and molecular findings remain limited. This report aimed to document and highlight the diagnostic and therapeutic steps involved in managing an individual goat with PPR, demonstrating the value of early diagnosis and structured supportive care in improving recovery outcomes. A 2-year-old West African Dwarf doe presented with anorexia, necrotic oral lesions, and profuse diarrhea. Clinical examination revealed pyrexia (41.6°C), tachycardia, lymphadenopathy, and dehydration. Hematology indicated moderate anemia and lymphocytosis, while real-time reverse transcription polymerase chain reaction targeting the PPR virus F-gene confirmed infection (cycle threshold [Ct] 29.21). Following timely supportive interventions, full recovery occurred within seven days. This case underscores the importance of early recognition, molecular confirmation, and targeted supportive management to enhance survival and guide field veterinarians in resource-limited endemic settings.

Keywords

Flock surveillance
Nigeria
Peste des petits ruminants
Real-time reverse transcription polymerase chain reaction
West African Dwarf goat

INTRODUCTION

Peste des petits ruminants (PPR) is a highly contagious viral disease of small ruminants that threatens livestock production and rural livelihoods across Africa, the Middle East, and Asia.[1,2] It is caused by the PPRs virus (PPRV), a morbillivirus in the family Paramyxoviridae, closely related to rinderpest and canine distemper viruses.[3] The World Organization for Animal Health classifies PPR as a transboundary animal disease of major global concern due to its rapid spread, high morbidity, and severe socio-economic consequences.[4] Goats are particularly susceptible, with morbidity often approaching 100% and mortality exceeding 70% in naïve populations.[5,6] The disease typically manifests with pyrexia, oculonasal discharge, necrotizing stomatitis, diarrhea, bronchopneumonia, and progressive emaciation.[7,8] In sub-Saharan Africa, small ruminants play a key role in food security and household income. However, the persistence of PPR continues to limit productivity and exacerbate poverty among livestock-dependent communities.[9,10] In Nigeria, despite the availability of an effective live attenuated vaccine, control efforts remain hampered by poor vaccination coverage, weak veterinary infrastructure, and logistical challenges.[11-13] A large-scale serosurvey covering 12 states and all agro-ecological zones revealed an overall PPRV antibody prevalence of 23.16% among small ruminants (sheep and goats), showing significant variation among the states.[14] Most published Nigerian studies describe outbreaks at the flock or regional level, focusing primarily on mortality rates, prevalence, and epidemiological patterns.[15] In contrast, detailed single-animal reports that integrate day-by-day clinical progression, basic hematology, and molecular confirmation are rarely documented, especially in West African Dwarf goats. Such reports are critical for improving field recognition of PPR, guiding case management decisions, and serving as educational resources for veterinary practitioners and students. This case is unique because it not only documents the clinical and laboratory findings of a naturally infected goat but also demonstrates how timely molecular confirmation and structured supportive therapy can result in complete recovery in a resource-limited setting. The indications of this study are to provide veterinarians and livestock owners with practical guidance for the early detection and effective management of individual cases, thereby helping to reduce within-flock spread and mortality while supporting broader PPR control strategies in endemic regions. This report aimed to document and highlight the diagnostic and therapeutic steps involved in managing an individual goat with PPR, demonstrating the value of early diagnosis and structured supportive care in improving recovery outcomes.

CASE REPORT

History

On April 5th, 2025, a 2-year-old West African Dwarf doe weighing approximately 15 kg was presented to the Large Animal Unit of the Magajin Gari Zonal Veterinary Hospital, Kaduna State, Nigeria. The doe was managed semi-intensively with one buck and fourteen other does and was fed wheat bran, bean husk, and hay. According to the owner, the animal had been off feed for three days, with progressive weakness, oral sores, and profuse foul-smelling diarrhea. No vaccination history against PPRs was reported in the flock. Importantly, no similar illness was observed among the other animals at the time of presentation, suggesting that the case was an isolated occurrence within the herd.

Clinical findings

On physical examination, the doe appeared weak, dull, and reluctant to move. The body condition score was assessed as 2/5; there was bilateral serous nasal discharge and extensive ulcerations of the lips, gums, and buccal mucosa, with a heavily soiled perineum due to projectile diarrhea with a fetid odor [Figure 1]. Bilateral sublingual lymphadenopathy was palpable. The mucous membranes were pale with a capillary refill time (CRT) of approximately 3 s, consistent with poor perfusion. Vital parameters revealed pyrexia (41.6°C), tachycardia (100 beats/min), and tachypnea (35 cycles/min). Dehydration was estimated at 6–8% based on skin tenting, sunken eyes, and delayed CRT, indicating moderate fluid loss.

Clinical presentation of a West African Dwarf doe with peste des petits ruminants (PPR). (a) Extensive necrotic ulcerations (orange arrow) of the oral mucosa and lips with excessive salivation observed on Day 0 (presentation). (b) Projectile, foul-smelling diarrhea with perineal soiling (orange arrow) on Day 0. Images were captured after obtaining owner consent and were anonymized to remove any identifying information.
Figure 1:
Clinical presentation of a West African Dwarf doe with peste des petits ruminants (PPR). (a) Extensive necrotic ulcerations (orange arrow) of the oral mucosa and lips with excessive salivation observed on Day 0 (presentation). (b) Projectile, foul-smelling diarrhea with perineal soiling (orange arrow) on Day 0. Images were captured after obtaining owner consent and were anonymized to remove any identifying information.

Differential diagnosis

At presentation, several differential diagnoses were considered due to the overlapping clinical signs observed. Contagious caprine pleuropneumonia (CCPP) was considered due to the fever and respiratory signs, but the absence of severe respiratory distress, pleuritic pain, and fibrinous exudates made this less likely. Bluetongue and foot-and-mouth disease (FMD) were also included in the differentials due to the oral ulcerations and salivation; however, FMD was discarded as there were no vesicular lesions on the feet or teats, and bluetongue was unlikely given the lack of cyanosis of the tongue and absence of vector exposure history. Contagious ecthyma (orf) was considered for the oral lesions, but the lesions observed were deep, necrotic ulcers typical of PPR rather than the proliferative crusty lesions of orf. Gastrointestinal diseases such as salmonellosis, coccidiosis, or severe gastrointestinal parasitism were considered due to the profuse diarrhea, yet these conditions typically do not present with severe necrotizing stomatitis or ocular/nasal discharge [Table 1].

Table 1: The key differentials, associated clinical features, and the rationale for ruling in or excluding each condition.
Clinical sign/history Possible differential diagnoses Reason ruled in/out
High fever, nasal discharge, oral necrotic ulcers PPR, FMD, Bluetongue, Orf PPR supported by necrotizing stomatitis and rapid systemic spread; FMD unlikely due to absence of foot/teat lesions; bluetongue unlikely due to no tongue cyanosis or insect vector exposure; orf ruled out as lesions were ulcerative, not proliferative.
Profuse foul-smelling diarrhea PPR, Salmonellosis, Coccidiosis, Parasitism PPR likely with concurrent mucosal lesions and systemic illness; coccidiosis and parasitism less likely due to sudden onset and severe mucosal necrosis.
Tachypnea, mild respiratory signs PPR, CCPP, Pasteurellosis CCPP unlikely due to absence of pleuritic pain, fibrinous pleural exudate, and herd outbreak signs.
Rapid progression in unvaccinated goat PPR, Salmonellosis, FMD PPR favored as unvaccinated herd member and classic disease course; FMD not supported by lesion pattern or spread to other animals.
Lymphadenopathy PPR, Systemic bacterial infection PPR most consistent due to concurrent viral stomatitis and systemic signs.

FMD: Foot-and-mouth disease, PPR: Peste des petits ruminants, CCPP: Contagious caprine pleuropneumonia

Laboratory investigations

Hematology

Blood samples were collected aseptically through jugular venipuncture using 21-gauge needles directly into vacuum tubes containing ethylenediaminetetraacetic acid as an anticoagulant. Samples were kept at 4–8°C in a cool box and transported immediately to the laboratory, where analysis was performed within 2 h of collection to minimize hemolysis and cellular degradation. Hematological evaluation was conducted using an automated veterinary hematology analyzer (Mindray BC-2800Vet, Shenzhen, China), which was calibrated for small ruminants following the manufacturer’s instructions at the Veterinary Pathology Laboratory, Ahamdu Bello University, Zaria. Goat-specific reference intervals were obtained from both the analyzer’s factory-set values and local laboratory reference data for West African Dwarf goats routinely maintained by the diagnostic unit. The reference intervals used were as follows: Packed cell volume (PCV) 24–50%, hemoglobin (Hb) 8–15 g/dL, red blood cell (RBC) 5–15 × 1012/L, white blood cell (WBC) 4–12 × 109/L, neutrophils 10–50%, lymphocytes 40–75%, monocytes 0–6%, eosinophils 0–10%, basophils 0–3%, and plasma protein 6.0–7.9 g/dL. These ranges were applied to interpret the results of the affected goat and are shown alongside patient values, as shown in Table 2.

Table 2: Hematological parameters of the affected goat.
Parameters Patient value Reference value Interpretation
PCV (%) 23 24–50 Low (anemia)
Hb (g/dL) 7.0 8.0–15.0 Low
RBC (×1012/L) 5.0 5.0–15.0 Lower limit of normal
MCV (fL) 46.0 23–50 Normal
MCH (pg) 14.0 8–12 Slightly high
MCHC (g/dL) 30.4 30–36 Normal
WBC (×109/L) 13.0 4.0–12.0 High (leukocytosis)
Lymphocytes (%) 76 40–75 High (lymphocytosis)
Neutrophils (%) 14 10–50 Low (neutropenia)
Monocytes (%) 4 0–6 Within normal limits
Eosinophils (%) 4 0–10 Within normal limits
Basophils (%) 2 0–3 Within normal limits
Plasma protein (g/dL) 6.4 6.0–7.9 Within normal limits
RT-PCR
Parameters Patient value Reference value Interpretation
Ct (Sample K) 29.21 ≤35 Positive

PCV: Packed cell volume, Hb: Hemoglobin, RBC: Red blood cell count, WBC: White blood cell count, MCV: Mean corpuscular volume, MCH: Mean corpuscular hemoglobin, MCHC: Mean corpuscular hemoglobin concentration, RT-PCR: Real-time reverse transcription polymerase chain reaction

Molecular detection by real-time reverse transcription polymerase chain reaction (RT-PCR)

Nasal swabs were collected aseptically using sterile polyester-tipped swabs, which were immediately placed in HiViral Transport Medium (HiMedia Laboratories, India). The samples were kept on ice (4°C) and transported to the central diagnostic laboratory, National Veterinary Institute, Vom, Nigeria. On arrival, they were stored at −80°C and processed for RNA extraction within 24 h to preserve viral RNA integrity. Viral RNA was extracted using the Qiagen RNeasy Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer’s protocol. RNA quantity and purity were assessed using a NanoDrop spectrophotometer (Thermo Fisher Scientific, USA). Extracted RNA concentrations ranged between 18 and 25 ng/µL with A260/A280 ratios of 1.9–2.0, indicating high purity suitable for downstream real-time reverse transcription polymerase chain reaction (RT-qPCR) analysis. RT-qPCR targeting the fusion (F) gene of PPRV was performed on a Bio-Rad CFX96 Touch real-time polymerase chain reaction (PCR) Detection System using the Qiagen QuantiTect Probe RT-PCR Kit. The primers and probe were those validated by Flannery,[16] designed to detect all four PPRV lineages: Forward primer 5'-AGTACAAAAGATTGCTGATCACAGT-3', reverse primer 5'-GGGTCTCGAGGCTTCATTTT-3', and probe 5'-FAM-ACAGGCAATCTGTCACCTGTTGGTTBHQ1-3'. Each 25 µL reaction mixture contained 12.5 µL of ×2 QuantiTect Probe RT-PCR Master Mix, 0.5 µL of each primer (final concentration 400 nM), 0.5 µL of probe (final concentration 200 nM), 0.25 µL of RT Mix, 5 µL of RNA template, and nuclease-free water to make up the final volume. Cycling conditions were reverse transcription at 50°C for 30 min, initial denaturation at 95°C for 15 min, followed by 40 cycles of denaturation at 95°C for 15 s and annealing/extension at 60°C for 1 min. A positivity threshold of Ct ≤35 was selected based on validation data reported by Flannery,[16] which established this cutoff for reliable discrimination of true positives from background noise. The amplification plot showed a strong, sigmoidal curve with a single peak, confirming specific amplification and absence of primer-dimer formation. Positive control RNA amplified within the expected Ct range, while both the non-template control and extraction blank showed no amplification, validating assay performance. The nasal swab sample from the doe yielded a Ct value of 29.21, confirming active PPRV infection.

Laboratory findings

Hematological analysis of the affected doe revealed moderate anemia, as indicated by a PCV (23%) and Hb concentration (7 g/dL), both below the lower limits of the reference range. The total RBC count was 5 × 1012/L, which, although within the normal reference interval, was at the lower threshold, further supporting the presence of anemia. WBC count was elevated at 13 × 109/L compared with the reference range of 4–12 × 109/L, consistent with leukocytosis [Table 2]. Differential leukocyte evaluation showed a pronounced lymphocytosis (76%), exceeding the upper reference limit of 75%, accompanied by mild neutropenia (14%) and normal proportions of monocytes, eosinophils, and basophils. Plasma protein concentration remained within the normal range (6.4 g/dL) [Table 2]. Taken together, these hematological alterations reflected a viral infection characterized by anemia, leukocytosis, and marked lymphocytosis, which aligned with the clinical suspicion of PPR.

Molecular testing by RT-PCR provided definitive confirmation of infection. The nasal swab sample from the doe yielded a Ct value of 29.21 [Table 2], which fell well below the positivity cut-off of ≤35 established for the assay. This result indicated the presence of PPR viral RNA in the sample.

Treatment and clinical course

The doe was immediately isolated and commenced on a multimodal supportive treatment plan to stabilize vital functions, prevent secondary complications, and promote recovery. Tylosin (20%) (Tylodox®, Kepro B.V., Netherlands) was administered intramuscularly at 10 mg/kg once daily for 3 consecutive days as an empirical prophylactic measure against secondary bacterial pneumonia caused by opportunistic pathogens such as Pasteurella and Mannheimia spp., which frequently complicate PPR. Although thoracic auscultation did not reveal adventitious lung sounds at presentation, tylosin was included due to the high risk of bacterial overgrowth in immunocompromised animals. DIASTOP-plus (Novax®, Afgon Hydrotec, Nigeria), an oral combination antidiarrheal preparation containing oxytetracycline (25 mg), furazolidone (1.5 mg), mebendazole (1.4 g), sulfadimidine B.P.C (1.5 g), and light kaolin (2.5 g) per 15 mL, was given at 7.5 mL orally twice daily for 5 days to empirically control mixed enteric bacterial and protozoal infections associated with profuse diarrhea. This product was used due to local availability and clinical urgency; however, the goat was not intended for food production, and the owner was explicitly informed that furazolidone is prohibited for use in food animals under the National Agency for Food and Drug Administration and Control (NAFDAC) in Nigeria’s regulations due to carcinogenic residue concerns. To address concurrent helminthiasis, which can worsen immunosuppression and delay recovery, Rafoxanide (3%) (Rafoxidad®, DADVet, Jordan) was administered orally at 15 mg/kg once. The flock had a known history of fasciolosis and strongyle infestations, and although a fecal egg count was not performed at presentation due to logistical constraints, empirical deworming was justified based on regional parasite prevalence and field practice guidelines. Multivitamin supplementation (V-Multinor®, Jubaili Agrotec, China) was given intramuscularly at 1 mL/10 kg once daily for five days to support immune function and enhance recovery.

Given the presence of moderate dehydration (estimated at 6–8% based on skin tenting and sunken eyes) and ongoing gastrointestinal losses, Ringer’s lactate (Baxter Healthcare, Belgium) was administered intravenously at 80 mL/kg/day, divided into four doses (≈300 mL every 6 h). The calculated requirement included estimated deficit (0.9–1.2 L) + maintenance (0.75 L/day) + estimated ongoing diarrheal losses (~0.25 L/day). Clinical monitoring included CRT, mucous membrane color, skin tenting, body weight, urine output, and daily PCV and total protein to guide fluid adjustment and prevent overload. For analgesia and anti-inflammatory care, flunixin meglumine (Flumeg®, Bimeda, Ireland) was administered intramuscularly at 1.1 mg/kg once daily for 3 days to reduce mucosal pain, pyrexia, and systemic inflammation. This was given after initiating fluid therapy to minimize the risk of renal compromise, and the animal was closely monitored for adverse effects such as melena or signs of gastrointestinal irritation. Oral ulcerative lesions were irrigated once daily with a 0.01% potassium permanganate (KMnO4) solution (Merck KGaA, Germany) prepared by dissolving 0.1 g of crystals in 1 L of clean water. Care was taken to avoid ingestion of excessive solution and aspiration. Handlers wore protective gloves and eyewear due to the caustic nature of concentrated KMnO4. Rapid improvement was observed: Pyrexia and tachycardia resolved within 48 h, appetite and water intake normalized by day 3, diarrhea resolved by day 5, and complete clinical recovery was achieved by day 7 [Table 3]. Because this goat was not intended for human consumption, meat and milk withdrawal times were not applicable. In food-producing goats, withdrawal periods would be required for each drug class: Tylosin (minimum 8–14 days for meat), oxytetracycline (21–28 days for meat), sulfonamides (7–14 days), flunixin (4–8 days), and rafoxanide (28 days) based on Nigerian and international veterinary drug regulations.

Table 3: Timeline of clinical parameters and interventions during treatment.
Day Temperature (°C) Heart rate (bpm) Appetite/Hydration Fecal consistency Key interventions
0 (Presentation) 41.6 100 Anorexic, severely dehydrated Profuse, watery, foul-smelling diarrhea Diagnosis initiated, intravenous fluids started, tylosin, DIASTOP-plus®, rafoxanide, flunixin
1 40.5 95 Poor, minimal water intake Profuse diarrhea Continued fluids, flunixin, oral lesion irrigation
2 39.8 90 Slight improvement in appetite Diarrhea persists, slightly less foul Continued fluids and medications
3 39.2 85 Moderate appetite, hydration improving Soft, partially formed feces Continued fluids, flunixin discontinued after Day 3
4 38.9 80 Good appetite Soft feces Fluids tapered
5 38.7 78 Normal appetite and hydration Formed feces DIASTOP-plus discontinued
6 38.6 76 Normal Normal Supportive vitamins only
7 38.5 76 Normal Normal Complete recovery

A 21-day follow-up was conducted to monitor the remainder of the herd for evidence of new infections. During this period, the 14 other does and one buck were observed closely for clinical signs of PPR, including fever, nasal or ocular discharge, oral lesions, or diarrhea. No additional animals developed clinical illness, suggesting that early isolation of the index case was effective in preventing immediate spread. However, due to logistical and resource constraints, serologic screening and RT-PCR testing of the apparently healthy cohort animals were not performed, and the presence of subclinical or incubating infections could not be ruled out. Following the recovery of the affected doe, the owner was counseled on the importance of preventive measures. Flock vaccination with the live attenuated PPR vaccine was strongly recommended and was scheduled. The recovered doe was kept in isolation for three weeks post-recovery, and the pen, feeding troughs, and water sources were disinfected using a 1% sodium hypochlorite solution. The owner was advised to implement strict biosecurity, including footbaths at entry points, restriction of animal movement, and proper disposal of bedding and manure from the isolation area to minimize environmental contamination and reinfection risk.

DISCUSSION

This case report describes the successful diagnosis and management of PPRs in a West African Dwarf goat through the integration of clinical assessment, hematology, and molecular confirmation, followed by targeted supportive care. The novelty of this work lies in its detailed documentation of the day-by-day clinical course and laboratory changes in a naturally infected goat, which is rarely reported in Nigeria, where most studies focus on flock-level outbreaks. By providing a stepwise clinical timeline, this study serves as a practical guide for veterinarians managing individual PPR cases in resource-limited settings.

The clinical signs observed in this doe (pyrexia, serous nasal discharge, necrotizing stomatitis, foul-smelling diarrhea, lymphadenopathy, and progressive weakness) were consistent with classical PPR presentations described in previous studies across sub-Saharan Africa.[17,18] The rapid progression within 3 days of anorexia and diarrhea emphasizes the virulent nature of the disease and the urgent need for early recognition. Importantly, no other animals in the herd exhibited clinical illness, suggesting that prompt isolation may have prevented spread, though subclinical infections cannot be ruled out. This underscores the value of early detection and segregation in controlling within-flock transmission.[5,15]

The hematological profile of moderate anemia, leukocytosis, and pronounced lymphocytosis provided key supportive evidence of viral infection. The lymphocytosis observed reflects a strong host immune response to active viral replication, aligning with earlier reports where goats in the early phase of PPR exhibit marked lymphocyte proliferation before lymphoid tissue depletion occurs in advanced disease.[19] The coexistence of leukocytosis with lymphocytosis also ruled out stress-induced leukograms, where lymphopenia would be expected.[20] This finding strengthens the interpretation that the doe was in an early stage of infection, which likely contributed to the favorable recovery outcome when treatment was initiated promptly.

Definitive diagnosis was achieved through RT-PCR targeting the PPRV F-gene, which yielded a Ct value of 29.21, confirming active infection. Molecular testing remains the gold standard for PPR detection due to its high sensitivity and specificity.[16,17] However, lineage characterization was not performed, which limits the epidemiological value of this report. Future studies should incorporate sequencing to track circulating lineages, as this information is vital for surveillance and eradication efforts.[10]

Management of PPR remains largely supportive, as no antiviral drugs are currently available. In this case, a multimodal treatment regimen combining intravenous fluids, antimicrobial prophylaxis, anthelmintics, multivitamins, and topical oral care resulted in complete recovery within seven days. The rapid improvement highlights the role of timely supportive care in mitigating dehydration, secondary bacterial infections, and metabolic complications, which are key factors that influence survival.[21,22] While spontaneous recovery is possible in mild cases, the structured treatment approach likely enhanced the doe’s resilience and prevented disease progression. This aligns with previous findings emphasizing that supportive therapy significantly improves survival rates when applied early in the clinical course.[21]

A notable finding was that no other animals developed clinical signs during the 21-day follow-up. This suggests that early isolation and biosecurity measures were effective in preventing immediate spread within the flock. However, since subclinical carriers can act as reservoirs, flock-level interventions such as vaccination, movement restriction, and periodic screening remain essential to achieve long-term control.[11,15] The lack of flock vaccination reported here reflects broader challenges in Nigeria, including poor vaccine coverage and weak veterinary infrastructure, which continue to impede eradication programs.[14]

The practical significance of this case lies in demonstrating how a single, well-managed case can provide valuable insights into field diagnosis and therapeutic strategies in endemic areas. Unlike outbreak-focused reports, this study offers a detailed model for recognizing and managing PPR at the individual animal level, especially for West African Dwarf goats, which are vital to rural livelihoods. The findings highlight the importance of equipping field veterinarians with accessible diagnostic tools, including hematology and RT-PCR, and promoting farmer awareness of early signs to facilitate rapid intervention. In summary, this study strengthens existing knowledge by linking early diagnosis with recovery outcomes, showing that molecular confirmation and timely supportive care can significantly improve prognosis. It also provides justification for strengthening surveillance and vaccination strategies to reduce the broader economic and animal health impacts of PPR.

Limitations

Although this case report confirmed PPRV infection through RT-qPCR, lineage characterization of the virus was not performed due to the unavailability of sequencing facilities and lineage-specific RT-PCR reagents at the time of analysis. Such data would provide greater epidemiologic utility by revealing circulating strains, and future investigations will incorporate partial F- or N-gene sequencing to strengthen molecular surveillance and support eradication efforts. The affected herd was observed for 21 days following isolation of the index case, and no serological or PCR testing was performed on apparently healthy animals. This limited the ability to detect subclinical infections or accurately determine the extent of viral circulation within the flock. Future case reports should include follow-up laboratory testing of in-contact animals to strengthen epidemiological interpretation and improve understanding of PPR transmission dynamics.

CONCLUSION

This case highlights the critical role of early clinical recognition, hematological evaluation, and molecular confirmation in the timely diagnosis and management of PPR at the individual animal level. The rapid recovery of the West African Dwarf doe following structured supportive care demonstrates that, even in resource-limited settings, well-coordinated interventions can significantly improve survival outcomes and reduce the risk of disease spread. Unlike herd-level outbreak reports, this study provides a practical framework for veterinarians and livestock owners to manage isolated cases effectively, bridging the gap between field diagnosis and laboratory confirmation. Moving forward, strengthening molecular surveillance, improving farmer education, and expanding vaccination coverage are essential to controlling PPR and safeguarding small ruminant populations.

Acknowledgments:

We acknowledge the client for giving us the approval to publish this case.

Authors’ contributions:

CCU, KOJ, SD, and AY: Handled the case, and analyzed the result; CCU, KOJ: Conducted, RT-PCR; CCU and KOJ: wrote the manuscript and all authors agreed to the final draft.

Ethical approval:

The ethical approval was obtained from the Ethics Committee of Veterinary and Livestock Services Department, Ministry of Agriculture, Kaduna.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Financial support and sponsorship: Nil.

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