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Year : 2020  |  Volume : 8  |  Issue : 2  |  Page : 99-101

Parvo virus infection − an unusual cause of pleural efusion in an immunocompetent patient

Yashoda Superspecilaity Hospital, Kaushambi, Uttar Pradesh, India

Date of Submission17-Dec-2018
Date of Decision02-Nov-2019
Date of Acceptance26-Mar-2020
Date of Web Publication10-Sep-2020

Correspondence Address:
Dr. Arjun Khanna
MD, DNB, DM, Consultant Pulmonologist and Intensivist, Yashoda Superspecilaity Hospital, Kaushambi, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacp.jacp_25_18

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Pleural and pulmonary manifestations of Parvo virus infection are exceedingly rare. Here, we describe an immunocompetent patient with Parvo virus infection who presented with lymphocytic, exudative effusion. Though, this presentation is rare, it may be looked for, if a patient presents with rash and pleural effusion.

Keywords: Parvo virus, Pleural effusion

How to cite this article:
Khanna A. Parvo virus infection − an unusual cause of pleural efusion in an immunocompetent patient. J Assoc Chest Physicians 2020;8:99-101

How to cite this URL:
Khanna A. Parvo virus infection − an unusual cause of pleural efusion in an immunocompetent patient. J Assoc Chest Physicians [serial online] 2020 [cited 2022 Aug 18];8:99-101. Available from: https://www.jacpjournal.org/text.asp?2020/8/2/99/294584

  Introduction Top

Pleural effusion has both non infective and infective etiologies. Infective etiologies, range from frank bacterial empyemas, to transient pleural effusions, caused by viruses. Human parvovirus (HPV) B19 is an endemic viral infection worldwide and it only infects humans. HPV B19 is linear, negative sense, single stranded DNA virus which belongs to genus erythrovirus and family Parvoviridae. Majority of the infections caused by HPV B19 in immunocompetent host remains asymptomatic or presented as simple flu like illness or erythema infectiosum (fifth disease). But in few cases, mostly in immunocompromised host it can present as pure red cell aplasia, transient aplastic crisis, glomerulopathy, nonimmune hydrops fetalis, anemia in end stage renal disease etc. Pleural and pulmonary manifestations of this virus are exceedingly rare. Here, we report an otherwise healthy patient with HPVB19 infection who presented with moderate pleural effusion.

  Case report Top

A previously healthy 30 year female presented to her local physician with 7-10 days history of fever and cough. The fever was high grade, intermittent and it was not associated with any joint pain or skin rashes. There were no significant past medical history, drug history or any family history. General physical examination showed a female with average built female and pallor. Chest auscultations revealed absent breath sounds in left infrascapular region with no added sound. Other systemic examinations were normal.

Her initial laboratory investigation showed pancytopenia with Hemoglobin − 6.1g/dl, total leukocyte count of 3100 cells/mm3, with 63% polymorphs, 28% lymphocytes, 6% monocytes and platelet count of 16,000cells/mm3. Serum ferritin, vitamin B12 and folate levels were all normal. Her kidney and liver function tests were also normal. Her peripheral smear for malarial parasite and malarial antigen were negative. Dengue serology including dengue NS1 antigen were negative. Viral markers for anti-HCV and HBsAg were negative and non-reactive for HIV 1&2.Scrub typhus serology was negative and urine examination was unremarkable. Her chest roentgenogram showed blunting of the left costophrenic angle with moderate pleural effusion. Pleural fluid evaluation was done, which was suggestive of lymphocytic, exudative fluid. Total 300 cells (90% lymphocytes), protein 4.1g/dl, sugar 88g/dl, gram stain and ZN stain, non contributory. With this history and radiology she was started on Anti tubercular treatment with rifampcin, isoniazid, ethambutol and pyrazinamide as per weight along with pyridoxine 20 mg. On the fourth day of anti-tubercular treatment she developed an erythematous rash involving face, trunk and parts of all four limbs. With this history and erythematous rash she was referred to our center. On evaluation, Her rash was involving the face, trunk and extremities and it was lacy, macular and erythematous. A diagnosis of ATT induced rash was entertained and ATT was stopped. Despite stopping the ATT, her rash continued to progress and it became very pruritic. A repeat chest X-ray was done, which showed near complete resolution of the pleural effusion. Repeat blood investigations again revealed persistence of pancytopenia. In view of the erythematous rash and transient pleural effusion, the possibility of autoimmune and viral etiologies was entertained. To find the etiology of persistent pancytopenia we performed serological analysis for many viruses including cytomegalovirus, Rubella, Epstein Barr virus, Hepatitis A and Parvovirus B19. IgM antibodies against Parvovirus B19 were detected using semi-quantitative ELISA (Euroimmun, Medizinische Labordiagnostika AG, Germany), as per manufacturer’s instructions, with appropriate controls. The serum specimen was negative for Parvovirus IgG antibodies. All other viral serologies and autoimmune work up was non contributory.[Figure 1]
Figure 1 Picture demonstrating the fine, erythematous, reticular rash on the leg of the paitent

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She was treated symptomatically for the fever and itching with paracetamol and oral fexofenadine. For severe anemia she was transfused with two packed red cell. Over the next few days her rash started eventually cleared and her pancytopenia improved .At the time of discharge her Hb was 10g/dl, WBC count 7000 cells/mm3 (PMN 55%, lymphocytes 40%, eosinophil 3%, monocytes 2%), and platelet count of 2.2 lacks cells/mm3. This case highlights the rare non hematological manifestations of parvovirus infection in an immunocompetent individual. HPV B19 should be considered as an important differential diagnosis in patients with fever and rash. This case also highlights the rampant use of empirical anti-tubercular drugs at primary healthcare level and need of further strengthening our Tuberculosis control program. The primary care physician must ensure, that the diagnosis of Tuberculosis is well established, before starting ATT.

  Discussion Top

Parvoviruses include many humanoid and zoonotic viruses. HPV B19, which infects only human being belongs to genus erythrovirus and family Parvoviridae. It is nonenveloped, icosahedral, nucleocapsid symmetric, spherical virus with a total diameter of 22–26 nm.[1] It has linear, negative sense, single stranded DNA of 5–6 kb in length. The predominant route of transmission is through respiratory route but it mainly replicates in erythroid progenitors as it contains primary B19V receptor, blood group P antigen. Increased viremia leads to viral induce toxicity causing cessation of red blood cell production. Most of the times this viremia and arrest of erythropoiesis are transient in immunocompetent host and it resolves with increasing IgM and IgG antibody response.[2] Majority of the infections caused by HPV B 19 remain asymptomatic in immunocompetent hosts but sometimes it can present as erythema infectiosum, transient aplastic anemia, arthropathy, hydrops fetalis, meningitis, myocarditis etc. Symptoms usually begin to show on the sixth day and erythema infectiosum or fifth disease remains the most common manifestation of HPV B19 infection. Along with fifth disease hematological disorders are well defined and very commonly described manifestations of HPV B19 infection. Non hematological manifestations were very less described and have been reported only in some case series or case report. Most common non hematological manifestations were found to be joint and skin involvement. In our literature search, we could not find a single case report of Parvovirus associated pleural effusion.

As most of the cases remain asymptomatic diagnosis is seldom required in immune competent people. In the appropriate patient diagnosis can be established by detection of B19V IgM and B19 DNA by PCR.[3] In immunocompromised individuals detection of viral DNA is pivotal for the diagnosis of parvovirus B19 as they may be negative for IgM or IgG based antibody response. Treatment of parvovirus infection remains symptomatic and no antiviral drug has been found to be effective against HBV B19.[4] Only in severe cases intravenous immunoglobulins have been tried, with variable success.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Gallinella G. Parvovirus B19 Achievements and Challenges. ISRN Virology. 2013, Article ID898730, 2013. Available at: https://doi.org/10.5402/2013/898730.  Back to cited text no. 1
Brown KE. Haematological consequences of parvovirus B19 infection. Baillieres Best Pract Res Clin Haematol 2000;13:245-59.  Back to cited text no. 2
Broliden K, Tolfvenstam T, Norbeck O. Clinical aspects of parvovirus B19 infection. J Intern Med 2006;260:285-304  Back to cited text no. 3
Young NS, Brown KE. Parvovirus B19. N Engl J Med 2004;350:586-97.  Back to cited text no. 4


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