Abstract
Background
Marburg Virus Disease (MVD) is a highly virulent zoonotic infection associated with high case fatality rates and multi-organ dysfunction. Early recognition, timely supportive care, and appropriate clinical management are important in improving outcomes. We describe the clinical presentation, laboratory features, management strategies, and outcomes of five confirmed MVD survivors.
Case presentation
We present a case series of five patients with laboratory-confirmed MVD who recovered following treatment at Jinka General Hospital/MVD Treatment Center between November and December 2025. The cohort included four females and one male (median age: 18 years). All patients presented with fever, headache, and gastrointestinal (GI) symptoms, with three exhibiting hemorrhagic manifestations. Key laboratory findings included leukopenia (White Blood Cell (WBC) nadir 1.55 × 10³/µL), thrombocytopenia (platelet nadir 65 × 10³/µL), and elevated transaminases (Aspartate Aminotransferase (AST) peak 1,153 U/L). One patient developed severe neutropenia (Absolute Neutrophil Count (ANC) 107 cells/µL).
Management and outcome
All patients received remdesivir (in varying regimens) and supportive care. Viral clearance was confirmed by two consecutive negative Reverse Transcription Polymerase Chain Reaction (RT-PCR) tests within 48 h, achieved between days 6 and 12. All five patients (100%) achieved complete clinical recovery and were discharged.
Conclusion
This case series demonstrates that recovery from confirmed MVD is achievable with early diagnosis, comprehensive supportive care, and antiviral therapy, even in the presence of severe gastrointestinal hemorrhage. Dynamic monitoring of liver enzymes and viral clearance is essential. These findings underscore the potential for favorable outcomes with early diagnosis and antiviral treatment even in resource-limited settings.
Keywords: Hemorrhagic fever, Resource-limited setting, Antiviral therapy, Outbreak response, Clinical management
Background
Marburg virus disease (MVD) is a severe, often fatal hemorrhagic fever caused by the Marburg virus, a member of the Filoviridae family [1–3]. Marburg virus disease was first recognized in 1967 following simultaneous outbreaks among laboratory workers in Marburg and Frankfurt, Germany, and Belgrade, Yugoslavia (now Serbia), associated with laboratory work involving African green monkeys imported from Uganda [4–6]. The natural reservoir is the Egyptian fruit bat, with human infection associated with high case fatality rates (CFRs) ranging from 24% to 90%, depending on the specific viral strain, host response, and treatment availability [4, 5].
The clinical course of MVD typically involves a nonspecific febrile phase that rapidly progresses to severe gastrointestinal symptoms (vomiting, diarrhea, abdominal pain) [7]. Advanced stages are characterized by coagulation abnormalities, increased vascular permeability, and hemorrhagic manifestations, ultimately leading to multi-organ failure and shock. Laboratory hallmarks commonly include leukopenia, thrombocytopenia, and elevated liver enzymes, reflecting the systemic nature of the infection [8–10].
Despite decades of research, there are currently no widely approved vaccines or antiviral therapies for MVD [5, 11]. Management remains primarily supportive, focusing on fluid resuscitation and the management of specific complications, which is particularly challenging in remote, resource-limited settings [5, 11]. Experimental therapeutics, such as remdesivir, have shown promise in preclinical models, but robust clinical trial data are lacking [5, 11, 12].
The most recent outbreak of MVD was in Rwanda in 2024. The country was able to contain the disease outbreak rapidly. The availability of diagnostic tests, antiviral treatment, and public awareness through social media and other news outlets has helped significantly [13]. The outbreak in Ethiopia was mostly in one region. Following the laboratory confirmation of an index case in Jinka town on October 23, 2025, the Ethiopian Ministry of Health declared a Marburg Virus Disease outbreak [14].
During the outbreak, 19 cases were identified, including 14 laboratory-confirmed MVD cases and five probable cases [14, 15]. Among the 14 laboratory-confirmed cases, nine patients died and five survived. Given the limited published data on survivors of Marburg virus disease, this case series aims to detail the clinical, laboratory, and therapeutic characteristics of the five laboratory-confirmed survivors treated at Jinka General Hospital/MVD Treatment Center [14–16].
Case presentation
During the outbreak, 19 cases were identified, including 14 laboratory-confirmed MVD cases and five probable cases. Among the 14 laboratory-confirmed cases, nine patients died, corresponding to a case fatality rate of 64.3%, while five patients survived. Of the 14 confirmed patients, 10 received remdesivir and four did not; all four patients who did not receive remdesivir died. Among the 10 patients who received remdesivir, the five patients who presented early in the course of illness and received treatment promptly survived, whereas five patients who presented later with more advanced disease and subsequently received remdesivir did not survive. The temporal course of remdesivir treatment and virological clearance among the five survivors is summarized in Fig. 1.
Fig. 1.
Temporal course of remdesivir treatment and virological clearance among the five MVD survivors
Case 1
A 15-year-old presented with three episodes of hematemesis, high-grade fever, headache, generalized weakness, cough, and abdominal pain without diarrhea. Her symptoms developed five days after direct contact with an individual who died of suspected MVD.On examination, she appeared ill but was conscious (Glasgow Coma Scale 15/15), with a systolic blood pressure of 120 mmHg, a respiratory rate of 36 breaths/min, and a palpable pulse of good volume. Scattered erythematous maculopapular skin lesions were observed without active external bleeding.
Initial laboratory tests revealed hemoglobin 8.9 g/dL, white blood cell count 5,000/µL with 59% neutrophils, and platelets 323,000/µL. Coagulation profile and electrolytes were within normal limits. After five days, laboratory tests showed alkaline phosphatase 184 U/L, AST 25 U/L, ALT 15 U/L, creatinine 0.72 mg/dL, hemoglobin 9.6 g/dL, and platelet count 525,000/µL. RT-PCR confirmed Marburg virus infection.
She received remdesivir (loading dose 200 mg IV once, followed by 100 mg IV twice daily for seven days). Supportive care included intravenous fluid resuscitation, paracetamol 1 g orally four times daily, omeprazole (80 mg IV loading followed by 40 mg IV twice daily), and metoclopramide 10 mg IV three times daily. Serial RT-PCR testing every 48 h showed the first negative result approximately one week after admission to the treatment unit on the third repeat test, with two additional consecutive negative tests 48 h apart confirming viral clearance. She was discharged after 12 days with complete clinical recovery.
Case 2
A 17-year-old male patient presented with a one-day history of fever, generalized headache, nausea, chills, fatigue, and dark-colored urine. Epidemiologic history revealed high-risk household exposure: the patient’s father was a probable MVD case, and an uncle had a confirmed Marburg-related death.
On admission, the patient appeared ill but with stable vital signs. No hemorrhagic manifestations, abdominal tenderness, or organomegaly were noted. Laboratory investigations showed significant abnormalities: WBC 1.63 × 10³/µL, platelets 104 × 10³/µL, hemoglobin 17 g/dL, and hematocrit 51%, indicating leukopenia, thrombocytopenia, and hemoconcentration. Liver function tests were mildly elevated (ALT 135 U/L, AST 142 U/L), with ALP 55 U/L. Renal function remained normal (creatinine 0.98 mg/dL, urea 17 mg/dL) (Table 1).
Table 1.
Key laboratory and virological findings among five patients with laboratory-confirmed Marburg virus disease
| Laboratory parameter | Case 1 | Case 2 | Case 3 | Case 4 | Case 5 |
|---|---|---|---|---|---|
| WBC (×10³/µL) | 5.00 → 6.50 | 1.63 → 4.60 | NR | NR* | 2.03 → 6.41 |
| Hemoglobin (g/dL) | 8.9 → 9.6 | 17.0 → 15.1 | 9.0 → 10.7 | NR* | NR |
| Hematocrit (%) | NR | 51 → 44 | NR | NR | NR |
| Platelets (×10³/µL) | 323 → 525 | 104 → 195 | 161 → 429 | NR* | 97 → 332 |
| ALT (U/L) | 15 → 15 | 135 → 304 | 596 → 55 | NR* | 124 → 50 |
| AST (U/L) | 25 → 25 | 142 → 124 | 554 → 48 | NR* | 149 → 29 |
| ALP (U/L) | 184 | 55 | 524 → 371 | NR* | NR |
| Creatinine (mg/dL) | 0.72 | 0.98 → 0.91 | 1.07 → 0.96 | NR* | 0.68 → 0.68 |
| Urea (mg/dL) | 7 | 17 → 4 | NR | NR* | NR |
| RT-PCR / Ct | Positive → negative† | Positive → negative | Positive → negative‡ | Ct 20.8 → 35 → negative | Positive → negative |
| First negative RT-PCR | Approximately 1 week after admission | Day 6 | NR | Day 12 | Day 8 |
| Confirmed clearance | Two additional negatives 48 h apart | Two consecutive negative tests | Two consecutive negative tests within 48 h | Confirmatory negative on Day 14 | Two additional negative tests |
The patient received remdesivir (200 mg IV loading dose on day one, followed by 100 mg IV daily for ten days). Empiric antibiotic therapy with ceftriaxone 1 g IV twice daily and metronidazole 500 mg IV three times daily was administered for seven days because of clinical concern for a superimposed bacterial gastrointestinal infection. Supportive care included intravenous fluid resuscitation to replace gastrointestinal fluid losses, paracetamol for fever management, oral rehydration solution after episodes of diarrhea, omeprazole 40 mg IV twice daily, and metoclopramide 10 mg IV three times daily. The patient also developed marked anxiety, panic, frustration, and difficulty sleeping during the illness and received diazepam 5 mg orally at night for five days for symptomatic management of anxiety and insomnia. Diazepam was not administered for seizures or suspected encephalitis, and there were no documented clinical features suggestive of encephalitis. Strict isolation and infection-control measures were maintained.
Hematologic parameters improved over five days (WBC 4.32 × 10³/µL, platelets 189 × 10³/µL, hemoglobin 15.5 g/dL, hematocrit 45%). ALT progressively increased during recovery, while AST showed a modest decline (ALT 304 U/L, AST 124 U/L). Serial RT-PCR testing confirmed viral clearance, with the third test on day six negative. The patient was discharged after ten days following two consecutive negative RT-PCR results (Table 1).
Case 3
A 35-year-old female patient with confirmed MVD was admitted on November 25, 2025, following extended caregiver exposure to two siblings: one laboratory-confirmed MVD case (deceased) and one probable MVD case (deceased). She presented with high-grade fever, severe headache, bloody diarrhea, and a history of upper gastrointestinal bleeding. On admission, she was febrile but hemodynamically stable without shock or organ failure.
On day 5 after admission, she developed a critical illness phase with persistent fever (39.5 °C) and severe hepatic injury. Laboratory findings showed AST of 1,153 U/L, ALT 596 U/L (initial), ALP 578 U/L, creatinine 1.20 mg/dL, hemoglobin 8.8 g/dL, and platelets 176 × 10³/µL. Coagulation profile and electrolytes were unavailable due to reagent shortages.
Management included strict isolation, intravenous fluids, ceftriaxone 1 g IV twice daily and metronidazole 500 mg IV three times daily for seven days because of clinical concern for a superimposed bacterial gastrointestinal infection. Additional supportive treatment included omeprazole 40 mg IV twice daily, tranexamic acid, vitamin K, fresh-frozen plasma, and metoclopramide. Remdesivir was initiated with a 200 mg IV loading dose followed by 100 mg IV once daily. After five days of treatment, remdesivir was temporarily discontinued because of marked elevation of liver enzymes. Following a five-day interruption and improvement in liver function, remdesivir was reinitiated at 100 mg IV once daily for a further five days, resulting in a total of 10 days of remdesivir treatment.
The patient achieved full clinical recovery and was discharged after two consecutive negative PCR tests within 48 h, with final laboratory values showing AST 48 U/L, ALT 55 U/L, ALP 371 U/L, creatinine 0.96 mg/dL, hemoglobin 10.7 g/dL, and platelets 429 × 10³/µL (Table 1).
Case 4
A 32-year-old female healthcare worker at a Marburg Treatment Center in Jinka, Ethiopia, had direct occupational exposure to confirmed MVD patients for approximately two weeks, followed by seven days of work in a pre-triage area. She reported appropriate use of personal protective equipment while caring for patients in the treatment unit. A confirmed MVD patient was managed in the treatment unit during this period, and the patient was involved in her delivery-related care, representing a potential occupational exposure. No contact with confirmed MVD cases in the patient’s private or community setting was identified based on the available epidemiological history. Seven days after her last documented occupational exposure, she developed acute fever, chills, rigors, and marked fatigue. Initial malaria testing was negative, and empiric antimalarial therapy failed to improve her symptoms.
On admission, RT-PCR confirmed Marburg virus infection with an initial cycle threshold (Ct) value of 20.8, indicating a high viral burden. From day 3, she developed severe gastrointestinal symptoms, including refractory vomiting, profuse diarrhea, anorexia, and generalized weakness, resulting in substantial gastrointestinal fluid losses. Intravenous crystalloid resuscitation with dextrose-containing fluids was therefore provided to replace ongoing fluid losses and maintain intravascular volume. Laboratory evaluation showed progressive liver enzyme elevation (AST peak 468 U/L, ALT peak 221 U/L) and hematologic abnormalities, including profound leukopenia, severe neutropenia, and thrombocytopenia.
She received remdesivir (200 mg IV loading dose, then 100 mg IV daily for maintenance). Due to severe neutropenia, meropenem 1 g every 8 h was initiated for broad-spectrum bacterial coverage. GI symptoms were managed with ondansetron 10 mg IV every 8 h, metoclopramide 10 mg IV every 8 h, and omeprazole 40 mg IV every 12 h. Supportive care included intravenous crystalloid resuscitation with dextrose-containing fluids, potassium supplementation, and vitamin B-complex. N-acetylcysteine was administered for hepatic dysfunction according to a standard intravenous protocol (150 mg/kg loading dose, followed by 50 mg/kg over 4 h and 100 mg/kg over 16 h).
Serial RT-PCR showed a progressive increase in Ct values, with the first negative result on day 12 and a confirmatory negative on day 14. No hemorrhagic complications developed. She achieved complete recovery and was discharged.
Case 5
An 18-year-old female presented with a one-day history of acute-onset fever, profound fatigue, and anorexia following high-risk household exposure to a suspected MVD case that died one week prior. Shortly after admission, she developed significant upper gastrointestinal bleeding, indicating progression to the hemorrhagic phase of the disease. Despite the bleeding, she remained conscious (GCS 15/15) with stable respiratory function. The initial hemoglobin concentration was 11.6 g/dL. Serial measurements increased to 12.6 g/dL and subsequently 14.6 g/dL following control of the bleeding, with no documented fall in hemoglobin during the available measurements.
She received remdesivir (200 mg IV loading dose followed by 100 mg daily for 10 days). Hemostatic management of the upper gastrointestinal bleeding included fresh-frozen plasma, tranexamic acid (1 g IV loading dose followed by 1 g three times daily), and vitamin K. GI protection included omeprazole (80 mg IV loading followed by 40 mg twice daily), and metoclopramide 10 mg IV three times daily was used for symptom control. The patient received intravenous fluid resuscitation and continuous hemodynamic monitoring. The upper gastrointestinal bleeding subsequently resolved, and hematological parameters normalized.
Serial RT-PCR became negative on day 8, confirmed by two additional negative results (Fig. 1). Upper gastrointestinal bleeding resolved during hospitalization, and hematological parameters normalized. The patient achieved full clinical recovery and was discharged after 14 days.
Discussion
The outcomes observed in this case series should be interpreted in the context of the broader outbreak cohort. Among the 14 laboratory-confirmed MVD cases, five survived and nine died, corresponding to an overall case fatality rate of 64.3%. Ten confirmed patients received remdesivir, while four did not; all four patients who did not receive remdesivir died. Among the remdesivir-treated patients, the five survivors presented early in the course of illness and received treatment promptly, whereas five patients who presented later with more advanced disease and subsequently received remdesivir did not survive. These observations suggest that timing of presentation and initiation of antiviral therapy may have been important determinants of outcome. However, given the observational nature of the outbreak response, the small number of patients, and the likely influence of disease severity at treatment initiation, these findings cannot establish a causal effect of remdesivir on survival. Rather, they provide a clinically relevant context for the favorable outcomes observed in the five patients described in this series and support the need for further evaluation of early antiviral treatment in MVD.
The clinical presentations mirror the typical progression of MVD documented in recent outbreaks. The initial symptoms of fever, headache, and fatigue were common among all patients, consistent with the early, non-specific phase of the illness [7]. All patients in our series experienced prominent GI symptoms, such as vomiting, diarrhea, or abdominal pain. This aligns with the consistent documentation of GI symptoms as a hallmark of Marburg virus disease in recently published outbreak reports from multiple African nations, including Uganda (2017) [17], Equatorial Guinea (2023) [18, 19], Tanzania (2023) [20], and Rwanda (2024) [13]. Notably, hemorrhagic manifestations (hematemesis, bloody diarrhea, GI bleeding) occurred in three of our five patients, occurring between days 5–7 of illness, a timeline consistent with previous outbreaks [7, 18]. This series demonstrates that, contrary to being an automatic death sentence, hemorrhage can be managed effectively with aggressive supportive care.
The laboratory test results were consistent with those of the MVD test. Severe leukopenia and thrombocytopenia, observed in all patients, are classic hallmarks of filovirus infection, resulting from bone marrow suppression and immune dysregulation [10]. The marked transaminitis, particularly in Case 3 (AST 1,153 U/L), is consistent with the virus’s known hepatotropism, which causes direct hepatocellular injury [10]. In patients with severe GI involvement or profound neutropenia, empiric broad-spectrum antibiotics were administered in accordance with the Ethiopian MVD clinical management guideline. However, evidence supporting routine antibiotic use in MVD remains limited, and treatment is primarily guided by clinical suspicion of bacterial co-infection [21].
For patients with hemorrhagic manifestations (Cases 3, and 5), tranexamic acid was administered as an antifibrinolytic agent to help achieve hemostatic control. The Ethiopian MOH guideline recommends tranexamic acid for bleeding complications in MVD, alongside other measures such as vitamin K, fresh frozen plasma, and blood product support when indicated [21]. This approach is consistent with clinical practice during the 2024 Rwanda MVD outbreak, where oral, vaginal, and cannula site bleeding were similarly treated with vitamin K and tranexamic acid [11]. In our cohort, this management strategy contributed to the resolution of bleeding without apparent thromboembolic complications. However, evidence supporting its use specifically in MVD is limited, and its benefit in filovirus-associated bleeding remains uncertain.
All patients in this series received remdesivir in addition to supportive care. In Case 4, serial Ct values increased from 20.8 at admission to 25.4, 29, and 35 before the first negative RT-PCR on day 12, with confirmatory clearance on day 14. This temporal increase in Ct values, indicating declining viral load, was observed following remdesivir initiation and is hypothesis-generating [22]. This finding aligns with recent data from the 2024–2025 Rwanda outbreak, where remdesivir, alone or in combination with a monoclonal antibody, was associated with improved clinical outcomes and a case fatality rate of 23% among 66 confirmed cases [13, 23]. Additionally, a cohort study from the same Rwandan outbreak found that remdesivir was safe as post-exposure prophylaxis for healthcare workers, and the findings suggest it may lead to a clinically and statistically significant extension of the incubation period [24]. Collectively, these observations support the continued evaluation of remdesivir in clinical trials for MVD.
[11, 13] hepatotoxicity in Case 3. Distinguishing between viral hepatitis and drug-induced liver injury (DILI) is a major clinical challenge [25]. The decision to discontinue remdesivir in the face of rising liver enzymes, followed by successful re-challenge without recurrence, raises the possibility of reversible, drug-related hepatic stress, although hepatic injury related to MVD itself cannot be excluded. This pattern is well documented for remdesivir, which has been associated with transaminase elevations in a significant proportion of treated patients [26]. This case highlights the necessity for dynamic pharmacovigilance, including baseline and serial liver function monitoring in MVD patients receiving antivirals.
Finally, the epidemiological profile of this series, which includes three household contacts and one healthcare worker, underscores major transmission pathways. The high proportion of healthcare workers affected during filovirus outbreaks is well documented, as seen during the 2024 Marburg outbreak in Rwanda [11]. Our cases reinforce the urgent need for rigorous infection prevention and control measures, particularly in household and healthcare settings, to rapidly interrupt transmission chains in resource-limited environments. In Case 4, the healthcare worker reported appropriate use of PPE during patient care; however, the occurrence of infection despite reported adherence highlights the importance of continuous reinforcement of infection-prevention practices [11]. Optimization should include regular PPE training and competency assessment, supervised donning and doffing, minimizing unnecessary exposure time in high-risk areas, maintaining adequate PPE supplies, and ensuring strict adherence to infection-control protocols during high-risk procedures [11, 13].
Conclusion
These cases demonstrate that recovery from confirmed MVD is achievable with early diagnosis, supportive care, and antiviral therapy, even in the presence of severe GI hemorrhage and hepatic involvement. The successful outcomes in all five patients challenge the historical perception of MVD as a uniformly fatal disease. Dynamic monitoring of liver enzymes and viral clearance is essential for guiding safe antiviral use and determining patient discharge. These findings inform clinical management protocols and underscore the need for continued investment in clinical trials and outbreak preparedness to improve outcomes in resource-limited settings.
Acknowledgements
We thank the patients and their families for agreeing to give their consent to publish their clinical records for this series. We also acknowledge the Federal Ministry of Health of Ethiopia for its support, coordination, and assistance during the Marburg Virus Disease outbreak response.
Abbreviations
- ANC
Absolute neutrophil count
- ALP
Alkaline phosphatase
- ALT
Alanine aminotransferase
- AST
Aspartate aminotransferase
- CFR
Case fatality rate
- Ct
Cycle threshold
- DILI
Drug-induced liver injury
- GI
Gastrointestinal
- GCS
Glasgow Coma Scale
- IV
Intravenous
- MVD
Marburg virus disease
- MoH
Ministry of Health
- PCR
Polymerase chain reaction
- RT-PCR
Reverse transcription polymerase chain reaction
- WBC
White blood cell
Author contributions
Conceptualization: AAW, BTM, GWH. Methodology: AAW, BTM, CTM, SZT, MGT. Investigation: AAW, CTM, SZT, MGT, GWB, AAB, AJA, NKA, TGB, DGN, ASG, EBT, ER, GWH. Data curation: AAW, BTM, CTM, SZT, MGT, GWB. Formal analysis: AAW, BTM, CTM. Validation: CTM, SZT, MGT, GWH. Resources: GWB, AAB, AJA, NKA, TGB, ASG, EBT. Visualization: AAW, BTM, CTM. Writing – original draft: AAW, BTM. Writing – review & editing: CTM, SZT, MGT, GWB, AAB, AJA, NKA, TGB, DGN, ASG, EBT, ER, GWH. Supervision: BTM, GWH. Project administration: AAW, BTM.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Data availability
The data underlying the results presented in this work are available within the manuscript.
Declarations
Ethical approval and consent to participate
This retrospective case series used routinely collected clinical data from Jinka General Hospital/MVD Treatment Center and the relevant South Ethiopia Regional Health Bureau response structures. Institutional review board review and approval were waived/not required in accordance with the applicable institutional policy for retrospective reporting of clinical cases. All patient information was de-identified prior to analysis and reporting. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki and its subsequent amendments.
Consent for publication
Written informed consent for publication of the clinical details and accompanying images was obtained; the signed consent form is held by the corresponding author and can be made available to the Editor on request.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Data Availability Statement
The data underlying the results presented in this work are available within the manuscript.