Parvovirus Infection.presentation for pediatric patients

Contains info about PARVO virus infection in pediatric patients

1. Parvovirus Infection Presented by: Vilina Hemant Gangolli Group 9a, Semester 12, TSMU

2. Introduction Parvovirus B19 is a virus that only infects humans. It is known to cause fifth disease, also known as erythema infectiosum or slapped cheek syndrome, which occurs mostly in young children (but can occur in adults). It can also cause an aplastic crisis in those with certain anemias, hydrops fetalis in pregnant women, polyarthropathy , and papular -purpuric gloves and socks syndrome (PPGSS) in young adults.

3. Epidemiology Parvovirus B19 infection occurs worldwide and is most common in school-aged children.  The prevalence of parvovirus B19 in developed countries in children younger than five years is 2-10%, 40-60% in adults > 20 years, and 85% or more in people >70 years. Infections with parvovirus B19 tend to occur more often in the late winter, spring, and early summer. Mini-outbreaks of parvovirus B19 infection occur about every 3-4 years.

4. Viral Characteristics and Transmission Parvovirus B19 is a non-enveloped, single-stranded DNA virus belonging to the  Parvoviridae  family. The virus exhibits a strong tropism for erythroid progenitor cells , leading to its characteristic clinical manifestations. The mechanism of spread most commonly involves inhalation of respiratory droplets . However, vertical transmission from mother to fetus and transfusion-related exposure via infected blood or blood products are also documented routes of infection

5. Pathogenesis Parvovirus B19 binds to host cell receptors in the respiratory tract. It enters the cell and translocates its genome to the host nucleus, causing DNA replication, RNA transcription, and assembly of the virus. Lastly, the cells lyse and release the mature virions. Viremia occurs within 5-7 days and creates the viral prodrome. Parvovirus is  tropic to bone marrow  and replicates i n erythroid precursors . The  P antigen  is the cellular receptor for parvovirus B19 that causes erythema  infectiosum  in children. Once inside, the virus uses host DNA polymerase during the S phase to replicate its genome causing cell death via apoptosis and temporary arrest of erythropoiesis. The IgM antibody appears when viremia resolves, which is approximately 8-10 days post-inoculation. During the viremic period, reticulocytopenia occurs for 7-10 days. During peak viremia, reticulocyte count drops to undetectable levels as the virus kills red cell precursors in bone marrow. Recovery occurs within 7–10 days, usually leading to a transient fall in hemoglobin (~1g/dL or 0.6mmol/L). In those with pre-existing hemolytic disorders, the rapid erythroid shut down causes a transient aplastic crisis. One week after the appearance of the IgM antibody, the IgG antibody appears and coincides with the appearance of the rash and arthralgia.

6. Clinical Course Parvovirus B19 infection produces a biphasic clinical course and the host’s hematologic and immunologic status determines disease severity. Incubation : 4-14 days, patient is  infectious during this period 1.Viremic Phase: ~7 days after exposure (intranasal inoculation or natural infection). Virus replicates in erythroid progenitor cells in the bone marrow resulting in viremia, with high viral titers in the blood. Virus is also shed from the respiratory tract, allowing transmission. Symptoms: Mild, nonspecific “flu-like” illness with low-grade fever, malaise, myalgia, pruritus and fatigue. 2.Immune-Mediated Phase: 17–18 days after infection. As virus-specific antibodies appear, immune complex formation triggers systemic reactions. Symptoms: Rash, pruritus  and arthralgia/arthritis , particularly in adults, due to immune complex deposition in joints. Resolution:  Typically 1–3 weeks, sometimes longer for rash recurrences.

7. Virologic, immunologic, and clinical course

8. Erythema Infectiosum / Fifth Disease The most common and classic presentation of erythema infectiosum is a mild febrile illness with a rash . Initial symptoms of infection can include fever, malaise, myalgias, diarrhea, vomiting , and headache . After initial viremia, the classic erythematous malar rash involving the cheeks with surrounding oral pallor develops. This rash does not appear early in the disease process. The lesion is classically described as a “slapped-cheek rash” and may be the only clinical diagnostic finding. This facial rash lasts 4 to 5 days and is thought to be immune-mediated. By the time the facial rash develops, the patient usually feels well and the viremia has resolved.

9. Erythema  Infectiosum / Fifth Disease

10. Erythema  Infectiosum / Fifth Disease Days after the facial rash develops, a maculopapular rash usually appears on the trunk and limbs . This rash is nonpruritic and typically lasts about 1 week. As it resolves, the rash may take on a lacy or reticular appearance , often more prominent on the extensor surfaces . The palms of the hands and soles of the feet are typically unaffected and exposure to sunlight or heat may exacerbate the rash.

11. Erythema  Infectiosum / Fifth Disease The infection may also present with arthralgias  more commonly in adults than in children, with women being more affected than men. Affected joints are usually symmetric and include the hands, feet, wrists, knees, and elbows . Patients often complain of joint stiffness . It typically occurs later in the disease course and resolves after about 3 weeks of symptom onset. Immunocompromised individuals typically do not exhibit rash or joint symptoms. Due to an inadequate immune response, these patients may experience chronic parvovirus B19 infection, which can lead to neutropenia, thrombocytopenia, or complete bone marrow suppression . Key characteristics of the rash include its potential to cause pruritus in adults, frequent appearance in children (with less than 50% of adults affected), and cessation of infectiousness once it manifests.

12. Hematologic Complications a. Transient Aplastic Crisis (TAC):  Occurs in patients with chronic hemolytic disorders (e.g., sickle cell disease, thalassemia, hereditary spherocytosis). Parvovirus B19 infects and destroys erythroid progenitor cells in the bone marrow which halts red blood cell (RBC) production for 7–10 days. This results in abrupt, severe anemia (often life-threatening) and reticulocytopenia. Symptoms: Pallor, fatigue, dizziness, shortness of breath, tachycardia, heart failure signs. b. Pure Red Cell Aplasia (PRCA):  Occurs in immunocompromised patients (HIV, post-transplant, chemotherapy) due to persistent infection (inability to clear the virus)leading to chronic suppression of erythropoiesis. Symptoms:   Severe chronic anemia, markedly reduced or absent reticulocytes, normal white cells and platelets c. Thrombocytopenia / Pancytopenia:  Occurs due to temporary suppression of bone marrow or immune-mediated platelet destruction characterized by bruising, petechiae, mucosal bleeding. It can mimic or trigger  idiopathic thrombocytopenic purpura (ITP) .

13. Fetal / Obstetric Complications a. Hydrops Fetalis Maternal infection before 20 weeks gestation carries the highest risk. Fetal infection involves destruction of fetal RBC precursors, causing severe anemia and high-output cardiac failure resulting in generalized edema (hydrops). Symptoms: Fetal ascites, pleural and pericardial effusions, skin edema. May cause intrauterine fetal death or spontaneous abortion.

14. Dermatologic Complications a. Papular -Purpuric “Gloves and Socks” Syndrome (PPGSS) Usually occurs in adolescents and young adults due to immune complex deposition and endothelial injury. Features: Painful redness and swelling on hands and feet, sharply demarcated at wrists/ankles, with petechiae, purpura, or blisters. Occasionally involves genitals, cheeks, or elbows and resolves in 1–3 weeks without scarring. b. Other Rash Variants: Erythema multiforme-like lesions Purpuric rash Pruritus of soles

15. Other Complications Cardiovascular Complications a. Myocarditis / Dilated Cardiomyopathy:  Direct viral infection of myocardial cells or immune-mediated inflammation leading to necrosis and fibrosis.  Reported inimmunocompromised or transplant patients. Presentation:   Chest pain, arrhythmias, dyspnea, signs of heart failure. It can be acute and reversible or progress to chronic dilated cardiomyopathy .  b. Endothelial Dysfunction:  Parvovirus B19 infects endothelial cells causing inflammation and impaired vascular relaxation. Neurologic Complications:  more common in immunocompromised or pediatric patients. Usually reversible but maycause prolonged deficits in severe cases. Central Nervous System:  Encephalitis, meningitis, seizures, cerebellitis. Peripheral Nervous System:  Peripheral neuropathy, Guillain–Barré–like syndrome, mononeuritis.

16. Other Complications Renal and  Vasculitic  Complications Glomerulonephritis:  Immune complex deposition in glomeruli causing hematuria, proteinuria, mild renal impairment. Henoch–Schönlein purpura–like vasculitis:  Palpable purpura, abdominal pain, arthralgia. Polyarteritis nodosa–like presentation:  Rare; vessel wall inflammation and necrosis. Systemic / Immune Complications Hemophagocytic  Lymphohistiocytosis  (HLH):  Triggered by strong immune activation following infection and causes fever, hepatosplenomegaly,  cytopenias , high ferritin. Requires urgent recognition and treatment. Pseudoappendicitis:  Mesenteric adenitis mimicking appendicitis due to viral inflammation of lymph nodes.

17. Diagnosis Diagnosis of parvovirus B19 infection generally does not require testing due to the self-limiting nature of the disease and its mild symptoms. Blood tests for specific antibodies may be conducted . Anti-B19 IgM antibodies can confirm acute infection, typically appearing 7 to 10 days after virus exposure and remain detectable for 2-3 months following infection. If positive, it indicates infection within the previous 2-4 months. IgG antibodies begin to rise about 2 weeks after exposure and provide lifelong immunity once measurable. Testing is particularly useful in diagnosing aplastic crisis to confirm causality from acute parvovirus B19 infection. Additionally, testing for IgG antibodies is common in prenatal care to assess immunity status and evaluate the risk of potential congenital disabilities. PCR testing from the serum or tissue can also be used. 

18. Management The disease process typically resolves without intervention. Symptom control and supportive care form the foundation of treatment. Acetaminophen or NSAIDs may be used to manage fever, arthralgias, and headache when present.  Serial hemoglobin and hematocrit monitoring should be conducted if an aplastic crisis is identified on evaluation. Packed   RBC transfusions must be administered as needed throughout the course of infection. Effective therapy of pure red cell aplasia consists of IVIG / infusion of immunoglobulin (0.4 g/kg of body weight/day for 5 days or 1g/kg/day for 2 to 3 days) which provides rapid improvement in reticulocyte count and hemoglobin within 1–2 weeks. Close follow-up with an obstetrician is essential when a pregnant patient is diagnosed with acute parvovirus B19 infection early in gestation, including serial ultrasounds every 1–2 weeks for 8–12 weeks after maternal infection. If fetal hydrops or anemia develops, intrauterine transfusion (via cordocentesis) is indicated and can be lifesaving. In patients receiving immunosuppressive agents, temporarily decreasing the dose of immunosuppressive agents usually enables production of sufficient IgG to eradicate the infection and confer lifelong protection. In individuals with HIV infection, highly active antiretroviral therapy restores immune function, enabling resolution of chronic parvovirus B19 infection.

19. Prognosis Parvovirus B19 infection (Fifth disease) generally has an excellent prognosis in healthy individuals, being a self-limiting illness that resolves completely within 1–3 weeks. Once infected, patients develop lifelong immunity due to persistent IgG antibodies. Rash and joint symptoms may persist for a short period but cause no lasting damage. In patients with hemolytic disorders, the virus may trigger a transient aplastic crisis, which is fully reversible with supportive transfusions. In immunocompromised individuals, chronic infection can cause pure red cell aplasia, but most recover with IV immunoglobulin therapy. During pregnancy, maternal infection carries a small risk (<10%) of fetal hydrops or loss, especially before 20 weeks, but intrauterine transfusion significantly improves outcomes. Overall, with appropriate recognition and management, mortality is rare and long-term sequelae are uncommon.

20. References Macri A, Crane JS. Parvoviruses. [Updated 2023 Jun 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482245/ Syed HA, Waymack JR. Erythema Infectiosum . [Updated 2025 May 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513309/ Heegaard, E. D., & Brown, K. E. (2002). Human parvovirus B19. Clinical microbiology reviews, 15(3), 485–505. https://doi.org/10.1128/CMR.15.3.485-505.2002 https://emedicine.medscape.com/article/961063-overview Bouraddane M, Warda K, Zouhair S. Parvovirus B19 and Pregnant women: A bibliographic review. Open Journal of Obstetrics and Gynecology. 2021;11(11):1543-1564. doi:10.4236/ojog.2021.1111145 https://www.scirp.org/journal/paperinformation?paperid=113338