Viral Hemorrhagic Fevers (VHFs):
Introduction
Viral hemorrhagic fevers (VHFs) are zoonotic infections that can lead to life-threatening systemic illness. They are caused by RNA viruses, primarily transmitted through arthropod vectors or contact with infected animals/humans. Due to their potential for outbreaks and high fatality rates, VHFs pose significant public health challenges
Key viruses causing hemorrhagic fever include:
• Filoviridae (Ebola, Marburg)
• Arenaviridae (Lassa, Junin, Machupo)
• Bunyaviridae (Crimean-Congo HF, Rift Valley fever, Hantavirus)
• Flaviviridae (Dengue HF, Yellow fever, Kyasanur Forest disease)
These viruses induce endothelial dysfunction, coagulopathy, and immune dysregulation, leading to multi-organ failure and high mortality (up to 90% in untreated Ebola).
Modes of transmission:
• Person to person through direct contact with symptomatic patients, body fluids, or cadavers
• Inadequate infection control in a hospital setting (Crimean–Congo hemorrhagic fever, Lassa, Ebola)
• Slaughtering practices
• Consumption of raw meat from infected animals or unpasteurized milk (Crimean–Congo hemorrhagic fever, Rift Valley fever)
• Direct contact with rodents, or inhalation of or contact with materials contaminated with rodent excreta (Lassa)
• Mosquito bites (Rift Valley fever, Dengue) or ticks (Crimean–Congo hemorrhagic fever).
Pathophysiology:
• Endothelial damage → Loss of vascular integrity: Viral infection → upregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-8) → increased vascular permeability.
• Coagulopathy: thrombocytopenia (platelet consumption, marrow suppression). disseminated intravascular coagulation (DIC): Widespread microthrombi → ischemic organ damage.
• Immune dysregulation: Massive IL-6, IL-10, and TNF-α release → systemic inflammation → capillary leak syndrome, shock (cytokine storm).
• Multi-organ failure
Liver: Necrosis → elevated AST/ALT (AST > ALT in Ebola).
Kidneys: Acute tubular necrosis (ATN) → oliguric renal failure.
CNS: Encephalopathy due to microbleeds, edema.
Clinical Staging
Stage 1: Febrile Phase (Days 1–3)
• High fever (>39°C), chills, myalgia, headache.
• Conjunctival injection, facial flushing, pharyngitis.
• Mild petechiae, bruising (early coagulopathy).
Stage 2: Hemorrhagic Phase (Days 4–7)
• Mucosal bleeding (epistaxis, gingival hemorrhage).
• GI hemorrhage (hematemesis, melena).
• Hematuria, menorrhagia, intracranial hemorrhage (rare but fatal).
Stage 3: Organ Failure (Days 7–10)
• Hypotensive shock (SBP <90 mmHg, lactate >4 mmol/L).
• Hepatorenal syndrome (jaundice, oliguria, elevated Cr).
• ARDS, coma, seizures (CNS involvement).
Diagnostic Approaches
Laboratory Tests
• PCR (gold standard for viral detection)
• ELISA (IgM/IgG antibodies)
• Complete blood count : thrombocytopenia (<100,000/µL), leukopenia (WBC <4,000/µL) with atypical lymphocytes .
• Coagulation profile (prolonged PT/PTT, elevated D-dimer)
• Liver enzymes (elevated AST/ALT)
Imaging
• Chest X-ray: Pulmonary edema (ARDS).
• Ultrasound: Hepatosplenomegaly, free fluid (ascites).
• CT/MRI Brain: Diffuse edema, microhemorrhages.
Treatment Strategies
A-Supportive Care
• Fluid resuscitation (crystalloids, Ringer’s lactate, normal saline) to maintain good urine output.
• Blood product transfusion (platelets, Packed RBCs , FFP for DIC)
• Vasopressors for shock
B- Antiviral and Immunomodulatory Therapy
Antiviral Therapy (where available)
• Ribavirin (for Lassa fever, some arenaviruses)
• Monoclonal antibodies (e.g., Inmazeb for Ebola)
• Favipiravir (experimental for some VHFs)
Prevention and Infection Control
A. Infection Control Measures
• Contact + Droplet precautions (gown, gloves, N95, face shield).
• UV sterilization, 0.5% hypochlorite for surfaces.
• Safe burial practices (WHO protocols).
B. Vaccination
• Ervebo (rVSV-ZEBOV) – FDA-approved for Ebola.
• CYD-TDV (Dengvaxia) – For dengue seropositive individuals only.
HFs represent a critical global health threat due to their high mortality, epidemic potential, and lack of definitive treatments for many viruses. Early recognition, strict isolation, and aggressive supportive care remain the cornerstones of management.
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