In immunocompetent patients, the diagnosis is based on the presence of IgM antibodies (Knipe and Howley 2007). The presence of IgG alone may only suggest previous infection. The virus can be detected by the polymerase chain reaction (PCR) assay for months to years after infection. There may be a transient drop in the reticulocyte count and hemoglobulin concentration in week 1 or 2, but the numbers normalize after a month (Doyle et al. 2000).

In acute lung involvement, the diagnosis may be easily missed and misinterpreted as vasculitis or an autoimmune disease or another etiology. Suspicion is needed to determine if PV is the cause of the respiratory failure using serology and DNA evidence of PV infection. This may be difficult because IgM may be persistent from a previous self-limited infection and PV DNA can persist for months. PV is a very prevalent disease in the general population and has been demonstrated in several types of lung damage patterns thought to possibly be related to the ANCA-positive vasculitic syndromes associated with PV. PV has also been reported in idiopathic interstitial pulmonary fibrosis and may be related to capillary damage. PV has a known affinity for capillary endothelium (Magro et al. 2006).

PV symptoms prior to the appearance of the rash are nonspecific and thought to represent influenza or a rhinoviral infection. If the rash appears, in children it can be mistaken for rubella. The polyarthropathy can be confused with rheumatoid arthritis especially since patients may have a transient increase in serum rheumatoid factor (Tello-Winniczuk et al. 2011).

PVB19 can be misdiagnosed as Systemic Lupus Erythematosus (SLE). In an initial presentation of a patient, the symptoms of PVB19 may overlap greatly with SLE. Both PVB19 and SLE patients may have cytopenia, anti-DNA antibodies, antinuclear antibodies (ANA), and hypocomplementemia. However, patients with PVB19 will have symptom resolution in several weeks. There may be an increase of infections with PVB19 in patients with known SLE due to intrinsic immunosuppression or immunosuppressive therapies, with lower levels of circulating PV IgM and IgG (Bengtsson et al. 2000). In the lung, the changes may be similar to collagen vascular diseases, infections due to other viruses, and even lepidic adenocarcinoma. The differential diagnosis includes many entities which may cause acute respiratory distress syndrome. The transient or rapid anemia with or without skin rash can help in recognizing the infection. Because PV can create an environment with lower resistance to other opportunistic pathogens, a concurrent fungal or bacterial pneumonia may overshadow the effects of PV B19.

Prevention of acute illness is often difficult. When outbreaks are recognized, decrease of exposure to body fluids of the infected patient is useful. Recognized viral illness with fevers and rashes in children should result in their removal from the day-care or school environment (Leppard et al. 2007). Disinfection is not always effective due to the hardiness of the virus. The US Food and Drug Administration (FDA) issued a recommendation in July 2009 that makers of plasma-derived products (which include plasma-derived factor VIII and factor IX concentrates) begin screening for human PVB19 by performing nucleic acid testing.

Treatment is symptomatic in most cases. Other treatments related to the varied clinical symptoms may include blood transfusions for aplastic crisis or intrauterine infections. Intravenous immunoglobulin may be used in immunocompromised patients or in placental exchanges of infected pregnant women with fetal distress (Kurtzman et al. 1989; Mouthon et al. 2005). Antiretroviral therapies are important in HIV patients to prevent aplastic crisis. In patients with lung involvement, early recognition is needed for provided pulmonary support, antiviral therapies, and antibiotics to prevent secondary bacterial infections which may result in sepsis and demise. Despite these measures, the disease may be fatal, especially if the patient is immunocompromised.

Effective vaccines are available for animal strains of PV, but currently, there is no approved vaccine available for humans. There is progress for their development and use in young children. Technology to express viral proteins VP1 and VP2, derived from a copy of the parvovirus B-19 genome (strain Au) obtained from a child with sickle cell disease and transient aplastic crisis, was developed at the National Heart, Lung, and Blood Institute. Individual viral proteins were expressed in a baculovirus system and, when recombinant vectors are cotransfected into insect cells, VP1 and VP2 spontaneously assemble into empty viral-like particles. The vaccine consists of two viral proteins (VP1 and VP2) in separate baculovirus vectors that are coinfected at the correct multiplicity of infections (MOIs) into Spodoptera frugiperda (Sf9) cells and that, upon expression, self-assemble into immunogenic viruslike particles. Phase 1 trials have been completed, but mass production is needed for testing (Bernstein et al. 2011).

A common childhood disease which is often unrecognized, parvovirus infection causes an influenza-like illness which can be associated with a rash known as erythema infectiosum (fifth disease). Ultrastructurally, the viral agent, a member of the family Parvoviridae, is a small single-stranded DNA virus that uniquely infects human erythroid progenitor cells. The clinical presentations may vary from irritative (upper respiratory infections and rashes) to severe (diffuse alveolar damage with ARDS, arthropathy, cardiomyopathy, fulminant hepatitis, hydrops fetalis, and aplastic crisis). A definitive diagnosis can be made with detection of IgM by serology and specific PVB19 DNA PCR. A previous infection results in lifelong immunity unless the patient is immunocompromised.