Parvovirus B19 Infection

Updated: Oct 11, 2019
Author: David J Cennimo, MD, FAAP, FACP, FIDSA, AAHIVS; Chief Editor: Russell W Steele, MD 



Parvovirus B19 (B19V) is a single-stranded DNA virus of the family Parvoviridae and genus Erythrovirus. Although parvoviruses commonly cause disease in animals, it was only in 1975 that the first human pathogen of this family was discovered by Cossart and colleagues while screening normal blood bank donors' sera for the hepatitis antigen (one of the donors' serum samples was coded B19).[1, 2]

The presence of immunoglobulin antibodies to this virus in the serum of half of the adult population was established by epidemiological surveys, suggesting acquisition of immunity during childhood. Evidence of recent infection (viral antigen, immunoglobulin M [IgM]-specific antibodies to the virus) was first found in the blood of Jamaican children living in London, England, all of whom presented with transient aplastic crisis (TAC) of sickle cell disease.[3]

Later, Serjeant et al confirmed the close association of parvovirus and aplastic crisis in a large retrospective study of sera from sickle cell disease patients with this complication.[4] Later, human parvovirus B19 was shown to be the etiologic agent of erythema infectiosum in hematologically normal persons.[5, 6] Erythema infectiosum was originally named Fifth disease because it was the fifth of 6 classic exanthematous diseases of childhood to be described. Later, cases of nonimmune hydrops fetalis were reported when infection in a woman occurred during pregnancy[7] . Parvovirus B19 has also been associated with multiple other conditions.[8, 2, 5, 9, 10]

The images below provide examples of symptoms observed with parvovirus B19 infection.

Note the right side of this boy's face displaying Note the right side of this boy's face displaying signs of erythema infectiosum, or Fifth disease. Image courtesy of CDC.
Elementary school child with Fifth Disease. Image Elementary school child with Fifth Disease. Image courtesy of CDC.


The incubation period from infection to initial, nonspecific symptoms ranges from 4-14 days; but cases have been reported as long as 21 days after exposure. The rash and joint symptoms usually occur 2-3 weeks after initial infection. Patients are most contagious in the few days preceding rash. Patients with aplastic anemia are considered contagious before the onset of symptoms and for at least 1 week.[5, 9, 8, 11]

Parvovirus B19 has a unique tropism for human erythroid progenitor cells. The virus requires the P blood antigen receptor (also known as globoside) to enter the cell. Rare individuals who lack the P antigen are immune to parvovirus B19 infection. Once inside the host cell, viral DNA enters the nucleus. The 3' end of the DNA strand folds back on itself, forming a hairpinlike bend that functions as a self-primer for viral DNA replication. The virus is cytotoxic to host cells.[2, 12] This, coupled with the tropism for rapidly dividing erythrocyte precursors (particularly pronormoblasts and normoblasts, wherein they replicate to high titers), leads to the suppression of erythrogenesis seen during infection. No reticulocytes (immature erythrocytes) are available to replace aging or damaged erythrocytes as they are cleared by the reticuloendothelial system.[5, 2]

Although decreases in hemoglobin levels of greater than 1 g/dL are rare in healthy children infected with parvovirus B19, decreases of 2-6 g/dL may be observed in patients with hemoglobinopathies or hemolytic anemias. Occasionally, the virus infects leukocytes (especially neutrophils).[13] Parvovirus B19 does not infect megakaryocytes; however, in vitro, parvovirus B19 proteins have a cytotoxic effect on megakaryocytes. Although B19V infection may manifest with pancytopenia, it is not believed to contribute significantly as an etiology of true aplastic anemia.[9, 11]

Fetal myocardial cells are known to express P antigen and may become infected with parvovirus B19. This may explain some of the direct myocardial effects seen in fetal infection.[2, 14]



United States

Parvovirus B19 infection is extremely common. Seropositivity rates are 5-10% among young children (aged 2-5 years), increasing to 50% by age 15 years and 60% by age 30 years. A small percentage of adults acquire infection every year, resulting in an incidence of approximately 90% in adults older than 60 years.[8, 6] The annual seroconversion rate among pregnant women without parvovirus B19 is 1.5%.[9]

Clinical cases of parvovirus B19 infection (erythema infectiosum) may be sporadic or may occur in outbreaks in the late winter through early spring. Attack rates during school outbreaks may be as high as 60%,[8] and secondary spread through nonimmune household contacts is common. Infection can be an occupational hazard in child care workers, with a rate of 20% reported in some studies.[9] A cyclic increase in the number of infections is also observed, peaking every 3-4 years.[8]


Parvovirus B19 infection is common worldwide. The age distribution is similar to that observed in the United States. A small number of groups, living in remote geographical locations, have not been exposed to human parvovirus.[2]


Parvovirus B19 infection in otherwise healthy children and adults has an extremely low mortality rate.[5, 2, 11]

Morbidity is as follows:

  • Erythema infectiosum (Fifth disease) is described in clinical manifestations below.

  • Polyarthropathy syndrome is mostly seen in adult women with acute infection. Patients develop acute symmetric arthritis affecting the small joints of the hands and feet, typically lasting for 1-3 weeks. In a small number, the arthritis may be prolonged, lasting for months. These symptoms can be confused with rheumatoid arthritis and further complicated by transient rheumatoid factor production during parvovirus B19 infection.[15] For this reason, parvovirus B19 infection should be considered in the differential diagnosis of newly diagnosed rheumatoid arthritis. Studies have not shown a causal link between parvovirus B19 infection and rheumatoid arthritis, and parvovirus B19 does not cause degenerative joint changes.[8]

  • In patients with hemoglobinopathies or hemolytic anemias, in whom the duration of erythrocyte survival is decreased, a decrease in the reticulocyte count to less than 1% (usually to 0%) may precipitate TAC. Such a crisis is characterized by profound anemia caused by a temporary halt in new erythrocyte production.[4] Abnormal erythrocytes, such as those associated with hemoglobinopathies, have a significantly shortened half-life because they are removed from circulation by the reticuloendothelial system. Any interruption in new erythrocyte production may trigger a crisis.

  • The bone marrow during TAC reveals an absence of erythroid precursors and the presence of striking giant pronormoblasts; rarely, necrosis may occur.[16] Parvovirus B19 is the only infectious cause of TAC known and has been shown to be the cause of aplastic crisis in over 80% of patients with sickle cell disease.[2, 8] .

  • Patients who are immunocompromised (eg, receiving chemotherapy or immunosuppressive drugs or have immune defects [congenital and acquired]) may develop chronic parvovirus B19 infection that results in chronic anemia. Pure red cell aplasia (PRAC) persists until the virus is cleared and should be distinguished from the transient anemia described above.[8, 5, 6, 10] Chronic parvovirus B19 infection in transplant recipients has been linked to anemia, other hematologic abnormalities, myocarditis, and pneumonitis.[17] Pediatric patients with hematologic malignancies and parvovirus B19 infection have suffered prolonged anemia that interferes with chemotherapy timing[18] .

  • Parvovirus B19 has been linked to other hematologic abnormalities. Thrombocytopenia, leukopenia, or both may be seen in acute infection, even in immunologically normal hosts. Cases of immune thrombocytopenic purpura, Henoch-Schönlein purpura, and the hemophagocytic syndrome have been attributed to parvovirus B19. However, transient erythroblastopenia of childhood and true aplastic anemia are not associated with infection.[8, 19, 11]

  • Hydrops fetalis, perhaps the most serious complication of parvovirus B19 infection, may occur when a nonimmune woman is infected, usually in the first 20 weeks of pregnancy.

    • Parvovirus B19 infection is the most common cause of nonimmune hydrops fetalis and can result in fetal death in 2-6% of cases.[9, 20]

    • As many as 50% of women of childbearing age may not be immune to parvovirus B19 and are susceptible to infection.[5] The seroconversion rate in the same group is 1.5% per year.[9] The vertical infection rate is estimated at 25-50%. The rate of fetal loss is estimated to be 1.6-9%.[5, 21, 22, 23] Of fetuses infected in the first half of pregnancy, 85% develop hydrops develops within 10 weeks (mean 6-7 wk). In one case series, no fetus infected after 21 weeks' gestation developed severe anemia.[24]

    • The most critical gestational age appears to be 13-16 weeks' gestation, when the fetus has the highest rates of hepatic hematopoiesis.

    • Historically, hydrops had a 30% mortality rate; however, newer data demonstrate a resolution of 94% of cases within 6-12 weeks and a mortality rate of less than 10% if the fetus can be supported by transfusion.[25]

    • Investigators have also called attention to the occurrence of severe anemia in fetuses with hydrops and suggest this may complicate the transfusion procedure.[24]

    • Intrauterine growth retardation, myocarditis, and pleural and pericardial effusions may also occur; however, parvovirus B19 is not associated with a congenital malformation.[9, 8, 14, 22]

    • Infection in the pregnant patient is further covered below.

    • A guideline reviewed the evidence relating to the effects of parvovirus B19 on the pregnant woman and fetus, and also the management of women who are exposed to, who are at risk of developing, or who develop parvovirus B19 infection in pregnancy. Investigation for parvovirus B19 infection was recommended apart from the standard workup for fetal hydrops or intrauterine fetal death.[26, 27]


No racial predilection is known.


In general, parvovirus B19 infection affects males and females in equal numbers. Adult females are more likely to develop postinfectious arthritis.


Parvovirus B19 infection is common in school-aged and younger children who attend daycare facilities. In general, children transmit the virus to parents and siblings. In young children, the antibody seroprevalence ranges from 5-10%. This increases to 50% in adolescents and approaches 90% in the elderly.[9, 2]




Common symptoms of parvovirus B19 (B19V) infection include a mild nonspecific prodromal illness that may consist of fever (15-30% of patients), malaise, headache, myalgia, nausea, and rhinorrhea; typically beginning 5-7 days after initial infection.[8, 28] These symptoms correspond to the initial viremia and dissipate in 2-3 days.[5] Approximately 1 week later, a bright red macular exanthem appears on the cheeks and is often associated with circumoral pallor.[9, 5] A diffuse maculopapular rash can appear 1-4 days later and fades to a lacy erythematous rash, which may be pruritic and may spread gradually toward the distal extremities. Most seropositive patients have no history of this classic biphasic illness. The clinical symptoms widely vary, and the classic "slapped cheek" rash is much more common in young children.[8]  More recently, parvovirus B19 has been recognized as a cause of atypical rash illness in adults,[29] as well as a host of less common manifestations.[30]

  • The cause of parvovirus B19 rash is believed to be immunologically mediated, and the rash corresponds to the appearance of immunoglobulin M (IgM) in the serum. This signals the clearance of viremia. Recurrence of the rash (lasting for weeks or more) may be provoked by sunlight, stress, or exercise and does not indicate relapsed infection.[2, 5]

  • Alternatively, parvovirus B19 infection may manifest with purpuric rash, erythema multiforme, or pruritus of the soles of the feet. Parvovirus B19 may cause a papular-purpuric "gloves-and-socks" syndrome (PPGSS), which manifests as an erythematous exanthem of the hands and feet with a distinct margin at the wrist and ankle joints. It is mainly seen in young adults and initially presents with painful erythema and induration of the hands and feet. Less commonly, the penis, vulva, thighs, cheeks, and elbows may be involved. This syndrome occurs exclusively with parvovirus B19 infection and is an uncommon manifestation. The skin changes may progress to petechia, purpura, and bulla with skin sloughing. PPGSS usually resolves in 1-3 weeks without scaring.[5, 6, 31, 32, 33]

  • Transient small joint arthropathy may be the main clinical presentation of parvovirus B19 in adults. Most have some joint pain, but few progress to frank arthritis. In general, the timing of joint symptoms coincide with the expected onset of rash in children. Arthritis usually improves in 1-3 weeks but may persist for months. Parvovirus B19 infection is not associated with chronic degenerative arthritis.[8, 2, 6] Less than 10% of children experience arthropathy; however, in those who do, the knees are most commonly involved.[9]

  • Patients with severe anemia due to transient aplastic crisis (TAC) may present with pallor, fatigue, or signs of an aplastic crisis. Underlying hemoglobinopathies should be sought in these patients. Patients with thrombocytopenia may exhibit bruising.[8, 11, 2, 13]

  • Rarely, parvovirus B19 infection manifests as myocarditis, vasculitis, glomerulonephritis, or encephalitis. B19V infection has been reported in association with idiopathic thrombocytopenia purpura, Henoch-Schönlein purpura, and pseudoappendicitis. It has also been reported to precipitate hemophagocytic syndrome.[5, 8, 2, 11] In rare cases, parvovirus B19 has been implicated in fatal myocarditis in transplant patients,[17] and has been implicated as a cause of endothelial dysfunction in patients with diastolic dysfunction.[34]

  • Parvovirus B19 infection in pregnant women may result in hydrops fetalis, particularly when infection occurs before 20 weeks' gestation. In the United States, the most common etiology of hydrops fetalis is parvovirus B19 infection.[25, 9, 8, 22]

  • Neurologic manifestations associated with parvovirus B19 infection widely vary.[5] Peripheral nervous system involvement such as neuropathy may be seen more frequently in older immunocompetent individuals. CNS involvement, including meningitis, encephalitis, and seizure, has been demonstrated in younger children and immunocompromised patients.[35]

  • Many individuals may experience asymptomatic or unrecognized infection.[5]


Parvovirus B19 infection may be indistinguishable from other viral illnesses in the absence of the classic exanthem.

  • Children are often febrile, but their appearance is nontoxic and the prodrome is nonspecific.

  • Patients with aplastic crisis have pallor and tachycardia secondary to anemia. Children with aplastic crisis usually do not have a rash.[9] The absence of rash may result from prolonged viremia and lack of anti–parvovirus B19 IgM. Another hypothesis is that patients in aplastic crisis often receive blood transfusions, and any rash may be attributed to a transfusion reaction.

  • A friction rub may be audible if pericarditis is present. Benign flow murmurs are common in anemic children with tachycardia. Patients with myocarditis or severe anemia may present with physical findings of heart failure.

  • The small joints of the hands, feet, elbows, and knees may exhibit signs of arthritis.

  • Painful pruritic papules and purpura may be present on the hands and feet as part of PPGSS.


Classic fifth disease, aplastic crisis, and PPGSS are caused almost exclusively by parvovirus B19. This virus, distributed worldwide, infects only humans. Transmission occurs via vertical transmission (birth), large droplet respiratory secretions, transfusion of blood products, and percutaneous exposure to blood.[9, 28]

  • Parvovirus B19 has been spread by blood products, such as intravenous immunoglobulin (IVIG), nonrecombinant clotting factors, platelets, and, to a lesser extent, packed RBCs. Because the virus lacks an outer lipid envelope and the genome is very stable, it is extremely resistant to heat, cold, and solvents. Since 2002, makers of plasma-derived products have screened for parvovirus B19.[2]

  • An investigation of parvovirus B19–seronegative recipients of blood components from donors who were positive for parvovirus B19 DNA using polymerase chain reaction (PCR) failed to demonstrate any evidence of transmission when the donors viral loads were below 106 IU/mL.[36] The authors concluded that screening of packed RBC (PRBC) transfusions may not be necessary.



Differential Diagnoses



Laboratory Studies

Most patients with parvovirus B19 (B19V) infection do not require laboratory studies because symptoms are mild and the illness resolves over 5-7 days.

  • Parvovirus serology (anti–parvovirus B19 immunoglobulin M [IgM] and immunoglobulin G [IgG] antibodies) can be determined using enzyme-linked immunoassay (ELISA), radioimmunoassay, or immunofluorescence. Results of IgM testing are particularly difficult to interpret. Standardization between laboratories is lacking. Even in a single laboratory, sensitivity and specificity are partly determined by operator skills. High-level viremia in acutely infected persons may cause virus-antibody complexes, which will result in a false-negative IgM test result.[37] In this setting, polymerase chain reaction (PCR) may be a better diagnostic modality.

  • PCR testing for parvovirus B19 is routinely available with increased sensitivity level. However, contamination and false-positive results are noted risks that lead to confusing interpretation. Low levels of B19 DNA may detectable for more than 4 months in serum after acute infection and for years in other tissues.[38, 39] . This test, a more useful clinical tool to diagnose chronic infection, detects viral DNA present in the blood or other tissues/fluids.[22] The interpretation, especially as it pertains to pregnant women is uncertain.[21, 25] The diagnosis of acute or chronic infection should be made on the basis of standard DNA hybridization or quantitative (real-time) PCR in combination with serologic assays for B19-specific IgG, IgM, or both.[8] Monitoring the quantitative PCR viral load in neonates with congenital parvovirus infection helps direct follow-up and the need for transfusions.

  • During experimental infection of volunteers, IgM antibodies were detected 10-12 days after inoculation, and IgG antibodies were detected at 2 weeks.[40] Ninety percent of patients with classic erythema infectiosum rash had IgM antibodies detected at initial presentation and IgG antibodies by day 7.[9] IgM remains detectable for months and IgG for life.[9, 8]

  • In patients with evidence of clinically significant anemia or transient aplastic crisis (TAC), obtain a CBC count with reticulocyte count.

    • Patients infected with parvovirus B19 have a low reticulocyte count (0-1%).

    • In an aplastic crisis, hemoglobin levels drop below the patient's baseline by at least 2 g/dL.

    • IgM antibodies are usually present by day 3 of illness or the time of hematopoietic nadir. IgG antibodies are detectable around the time of the recovery of erythrogenesis.[8, 9, 28, 19]

    • Parvovirus B19 PCR demonstrates high level viremia during TAC.[8]

  • Immunodeficient patients with chronic B19V infection and pure red cell anemia (PRAC) also have signs of anemia. In contrast to TAC, PRAC is characterized by very low or absent antibody levels. PCR is the diagnostic test of choice to demonstrate viremia.[5, 8]

  • If a pregnant woman is exposed to parvovirus B19, obtain IgG and IgM serology as soon as possible.[25, 22]

    • Positive IgG results and negative IgM results indicate past infection (no risk to fetus).

    • Positive IgG and IgM results indicate infection within the last 7-120 days (possible risk to fetus).

    • Negative IgG results and positive IgM results indicate acute infection (higher risk to fetus).

    • Negative IgG and IgM results indicate that the mother is not immune and that no evidence of acute infection is noted. In this case, repeat the tests in 3 weeks. Subsequent development of IgM indicates an acute infection.

    • No standards have been established to evaluate parvovirus B19 PCR on maternal blood; low levels may be detected long after clinical infection.[39] PCR may be performed on fetal serum of amniotic fluid to detect virus.[21]

Imaging Studies

Routine imaging is not necessary.

Fetal ultrasonography may be useful in detecting hydrops. The timing and frequency of ultrasonography surveillance for infected pregnant women have not been conclusively determined.[22]



Medical Care

Treatment may include the following:

  • Acetaminophen or ibuprofen is effective for treating fever in patients with parvovirus B19 (B19V) infection. Fever does not always require treatment with antipyretics; however, consider antipyretics if a patient appears clinically uncomfortable.

  • Resolution of infection depends on the presence of immunoglobulins against parvovirus B19. Intravenous immunoglobulin (IVIG) has been used with good results for patients suffering pure red cell aplasia (PRCA). Patients should be monitored for relapsed viremia.[8, 2, 28, 41]

  • Patients in aplastic crisis require packed RBC transfusions.[9] In some studies, more than 80% of patients with sickle cell disease in transient aplastic crisis (TAC) have required transfusion.[8] IVIG is not recommended for TAC.

  • In patients receiving immunosuppressive agents, temporarily decreasing the dose of immunosuppressive agents usually enables the immune system to produce sufficient immunoglobulin G (IgG) to eradicate the infection and confer lifelong protection. In some individuals with human immunodeficiency virus (HIV) infection, highly active antiretroviral therapy restores immune function, enabling resolution of chronic parvovirus B19 infection.[28]

  • Although its use is controversial and carries many risks, intrauterine blood transfusions may be helpful in cases of hydrops fetalis.[2, 14, 22, 25, 42]


Consultations may include the following:

  • Hematologist: Patients who present with aplastic crisis require intensive monitoring and RBC transfusions to prevent death and should be evaluated by a hematologist.

  • Pediatric infectious disease specialist or immunologist: Patients with long-term or unusual parvovirus B19 infections can benefit from consultation with a pediatric subspecialist in infectious diseases or immunology. These patients may benefit from treatment with IVIG.


No dietary restrictions are necessary.


Patients with classic erythema infectiosum are no longer contagious after the rash has appeared.[9]

Patients with aplastic crisis, papular-purpuric "gloves and socks" syndrome (PPGSS), or immunosuppression and chronic parvovirus B19 infection with anemia should be isolated with droplet and standard precautions due to ongoing viremia.[9]

Maintain precaution for patients with TAC for 7 days or until the reticulocyte count rebounds to at least 2%, whereas those with chronic infection should be isolated for the duration of their stay.[9]

Pregnant staff should be alerted to the potential risks of parvovirus B19 infection when caring for these patients.[9]



Medication Summary

No antiviral therapy is available to treat parvovirus B19 (B19V) infections. Children rarely require specific therapy other than acetaminophen for fever.

In patients with postinfectious arthritis, acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) usually provide symptomatic relief. Because the use of aspirin in children with other viral illnesses has been associated with Reye syndrome, aspirin use is not recommended in children with B19V infection. If children have pruritus from the parvovirus B19 rash, oral antihistamines (eg, diphenhydramine) and starch baths typically provide relief.

Antipyretic agents

Class Summary

These agents decrease or eliminate fever by acting at the level of the hypothalamus (acetaminophen) or by decreasing the activity of the enzyme cyclooxygenase, thereby decreasing the production of prostaglandins (NSAIDs).

Acetaminophen (Tylenol, Feverall, Tempra, Aspirin Free Anacin, Panadol)

Reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.

Ibuprofen (Motrin, Ibuprin, Advil)

One of the few NSAIDs indicated for reduction of fever.

Immunologic effectors

Class Summary

These agents are purified preparations of gamma globulin. Immunologic effectors are derived from large pools of human plasma and comprise 4 subclasses of antibodies, approximating the distribution of human serum.

Immunity to B19V infection appears to be purely humoral (ie, mediated via immunoglobulins). The role, if any, that cell-mediated immunity plays in providing immunity to B19V is unknown. As a result of the high seroprevalence of IgG against parvovirus among adults in the general population who have recovered from infection, the antiparvovirus IgG titer in IVIG is probably sufficient to provide passive immunity for the clearance of virus in immunocompromised hosts with chronic B19V infection.

Immune globulin, intravenous (Gammagard S/D, Carimune NF, Gammar-P)

Provides passive immunization against a broad spectrum of infectious agents. Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).


Class Summary

These agents decrease or prevent allergic symptoms caused by histamine receptors from mast cells.

Diphenhydramine (Benadryl)

First-generation antihistamine that binds to H1 receptors in the CNS and the body.

Competitively blocks histamine from binding to H1 receptors. As a result of CNS penetration, diphenhydramine frequently causes drowsiness. A small percentage of children paradoxically respond to diphenhydramine with agitation.



Further Outpatient Care

Patients with a resolved aplastic crisis or with a rash are no longer infectious.

Patients are no longer infectious after other symptoms resolve (usually by day 7 of illness). Thus, patients with a classic parvovirus B19 rash may return to school or daycare.[43, 9]

Further Inpatient Care

Patients rarely require admission for parvovirus B19 (B19V) infections unless they have underlying disease.

Consider the following factors for purposes of infection control:

  • Parvovirus B19 is spread via small respiratory droplets.

  • The attack rate in susceptible populations approaches 60%.

  • Parvovirus B19 is contagious from 24-48 hours before developing the viral prodrome and until the rash appears. The appearance of serum immunoglobulin (IgM) coincides with the appearance of the rash.[9]

  • See above for isolation precautions.


Patients with an aplastic crisis may require transfer to centers that provide pediatric critical care and hematology services.


Phase I clinical trials are currently evaluating vaccine candidates against parvovirus B19.[2, 8]

The risk of contagion in typical erythema infectiosum in the community is the highest during the early stages of the infection when symptoms are least specific and the disease more difficult to diagnose. Little rationale warrants excluding children with Fifth disease exanthem from daycare centers and school and adults from work.[43]

In addition to standard precautions, droplet precautions are recommended for hospitalized children with aplastic crises, children with the papular purpuric "gloves and socks" syndrome (PPGSS), and immunosuppressed patients with chronic infection and anemia for the duration of hospitalization.[9]


Complications include hydrops fetalis, chronic anemia, aplastic crisis, and death.

Immunocompetent individuals with a prolonged course of rash, fatigue, and arthralgias caused by persistent viremia have been reported. Symptoms in some of these patients respond to intravenous immunoglobulin (IVIG) therapy.


Most patients recover without sequelae.

Patient Education

Parvovirus B19 infects only humans. Approximately 60% of adults aged 30 years are immune to parvovirus B19, although few recall having had the infection. Symptoms include a low-grade fever, myalgias, arthralgias, headache, nausea, and rhinorrhea. As the symptoms disappear, children often develop a bright red rash on the cheeks (as if they had been slapped). The infection is contagious in children for a few days before symptoms begin and until the symptoms disappear. When the rash appears, the infection is no longer contagious. The presence of the parvovirus B19 rash is not a reason to keep children home from daycare or school.

If a pregnant woman is not immune to parvovirus B19 becomes infected, the probability of hydrops fetalis developing in the neonate is small (2-5%). Any pregnant woman who is exposed to an individual in whom parvovirus B19 infection is suspected should immediately contact their obstetrician.

In healthy adults and children, parvovirus B19 is not a serious infection. Exceptions include patients with cancer who are receiving chemotherapy, as well as patients with HIV infection and/or acquired immunodeficiency syndrome (AIDS), organ transplants, and other immunodeficient states.

For patient education resources, see the Children's Health Center, as well as Fifth Disease.


Questions & Answers


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