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PARVOVIRUS B19

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Parvovirus B19(Footnote 1-Footnote 4).

SYNONYM OR CROSS REFERENCE: Erythrovirus B19, B19V, fifth disease, human parvovirus (HPV), human serum parvovirus-like virus, erythaema infectiosum, slapped-cheek disease, hydrops foetalis, "gloves and socks" syndrome, and "Nakatani virus" in Japan(Footnote 1-Footnote 7).

CHARACTERISTICS: Parvovirus 19 is a member of the family Parvoviridae, sub-family Parvovirinae, and genus Erythrovirus(Footnote 4). It is classified into three genotypes: genotype 1 (classical B19 strains), genotype 2 (prototype K71- and A6-like strains), and genotype 3 (prototype V9 virus)(Footnote 5,Footnote 8). Parvovirus B19 is an icosahedral (20 to 25 nm diameter), non- enveloped, single-stranded DNA virus(Footnote 2,Footnote 5,Footnote 9). The virus targets rapidly growing erythroid progenitor cells, which are found in human bone marrow, foetal liver, human umbilical cord, and peripheral blood(Footnote 6). The virus is also found in platelets, and tissues from the heart, liver, lung, kidney, endothelium, and synovium(Footnote 10).

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Many persons with parvovirus B19 infection are asymptomatic (about 25% of adults and children during outbreak), or exhibit mild, non-specific, cold-like symptoms that are never linked to the virus(Footnote 1-Footnote 4,Footnote 6). The clinical conditions associated with the infection include erythema infectiosum (Fifth Disease), arthropathy, transient aplastic crisis, chronic red cell aplasia, hydrops foetalis, and papular, purpuric eruptions on the hands and feet ("gloves and socks" syndrome). Complications t hought to be associated with parvovirus B19 infection include encephalopathy, epilepsy, meningitis, myocarditis, dilated cardiomyopathy, and autoimmune hepatitis(Footnote 1,Footnote 6).

Erythema infectiosum (Fifth Disease) is the most recognizable presentation of parvovirus B19 infection. It consists of a rash that generally affects children between 4 and 10 years of age, although a less-pronounced rash can occur in adults. Prodromal symptoms are mild, and include fever, coryza, headache, and nausea. The first stage of the rash presents as erythaema of the cheeks ("slapped-cheek" rash). After 1 to 4 days, t he second stage appears as a maculopapular rash of the extremities and trunk. Central clearance of the rash is possible, giving it a lacy, reticular pattern. The second-stage rash usually lasts 1 to 6 weeks. The third stage may continue for the following 1 to 3 weeks and resolves spontaneously with no permanent sequelae(Footnote 6).

Arthropathy may be a complication of erythaema infectiosum or a primary presentation of infection. Approximately 8% of children infected with the virus have arthralgia; however, it is more common in adolescents and adults, affecting up to 60% of those infected. The pattern of arthropathy differs between adults and children. In children, the pattern can be symmetric or asymmetric and usually involves the knees (82% of patients) and ankles. In adults, the pattern is 2 symmetric and polyarticular and usually involves the proximal interphalangeal and metacarpophalangeal joints. Arthropathy generally resolves within three weeks but can last from months to years, especially in women(Footnote 6).

Transient aplastic crisis as a result of parvovirus B19 infection may occur in persons with decreased erythrocytes, for example due to iron deficiency anaemia, sickle cell disease, HIV, spherocytosis, or thalassaemia. Chronic red cell aplasia may occur in immunocompromised persons infected with parvovirus B19 in the absence of rashes and arthropathy(Footnote 6).

In young adults, infection can be associated with papular, purpuric, "gloves and socks" syndrome, which presents as symmetric, painful erythaema and oedema of the feet and hands. A hallmark of the syndrome is a sharp demarcation of the rash at the wrists and ankles, although other areas (e.g., cheeks, elbows, knees, inner thighs, glans of the penis, buttocks, or vulva) may also be involved. Patients may experience fever, arthralgia, or both. Symptoms usually resolve within 1 to 3 weeks without scarring(Footnote 6).

A major concern with foetal infection is the development of foetal anaemia. Thrombocytopenia may be present in addition to anaemia. Infection in the first trimester may result in foetal loss or miscarriage. Infection in the second and third trimester may result in foetal anaemia, myocarditis, high output cardiac failure, hydrops foetalis, and stillbirth. Foetal death may occur in up to 10% of infected foetuses(Footnote 11).

EPIDEMIOLOGY: Persons with blood group P antigen (the receptor for B19 erythroid cells) are universally susceptible to Parvovirus B19(Footnote 2). Virus strains are found in Western Europe, United States, and Brazil, with a lower prevalence of genotype 1 strain compared to the other strains. Genotype 3 is endemic in Ghana, West Africa(Footnote 5). Infection can occur in sporadic or epidemic forms, and can occur in any month of the year, and. In temperate climates, epidemic manifestations are more common in late winter, spring, and early summer, with epidemic peaks every 3 to 7 years in a given community. Over a 2 to 6 months observed outbreak period, the susceptibility rates are 50% in household contacts, and 10% to 60% in the day care or school settings. In the United States, 50 to 60% of adults have serological evidence of past infection, depending on age and location(Footnote 2,Footnote 4). Arthropathy appears to affect women twice as often as men(Footnote 6). The prevalence of IgG antibodies directed against B19 ranges from 2 to 15% in children 1 to 5 years old, 15 to 60% in children 6 to 19 years old, 30 to 60% in adults, and more than 85% in the geriatric population(Footnote 1). The infectiousness of the virus has also been observed in the occupational setting among hospital staff and research laboratories(Footnote 2,Footnote 3,Footnote 12,Footnote 13).

HOST RANGE: Humans(Footnote 1-Footnote 5).

INFECTIOUS DOSE: Unknown. In a study of B19 seronegative plasma pool-recipients, it was shown that only those recipients who received plasma containing greater than 10Footnote 7 genome copies/ml became infected or seroconverted(Footnote 14,Footnote 15); however, it has also been proposed that products with much lower virus DNA concentrations (e.g., 10Footnote 1 geq/ml or even lower) would transmit the virus(Footnote 16)

MODE OF TRANSMISSION: Transmission occurs most commonly by personal contact, via aerosols, respiratory secretions, or saliva droplets. It can also be transmitted vertically from mother to foetus or via transfusion of blood and contaminated blood products (especially pooled factor VIII and factor IX concentrates), and organ transplantation (iatrogenic nosocomial infections)(Footnote 2-Footnote 5,Footnote 10,Footnote 17). The risk of vertical transmission to the foetus is approximately 33%(Footnote 11).

INCUBATION PERIOD: Four to 14 days, but can last as long as 21 days(Footnote 2).

COMMUNICABILITY: Illness is most communicable before the onset of rash in people with rash illness alone, and probably not communicable thereafter because viraemia has been cleared by this point(Footnote 6). Patients are highly contagious during aplastic crisis and should be isolated to prevent transmission of the virus(Footnote 6). Individuals with aplastic crisis are communicable up to 1 week after onset of symptoms. Immunosuppressed people with chronic infection and severe anaemia may be infectious for months to years(Footnote 2).

SECTION III - DISSEMINATION

RESERVOIR: Humans(Footnote 2,Footnote 18).

ZOONOSIS: None.

VECTORS: None.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: None currently available(Footnote 18).

SUSCEPTIBILITY TO DISINFECTANTS: Treatment with formaldehyde or β-propiolactone destroys the antigenicity of the virus(Footnote 12). Parvovirus B19 may be sensitive to a 5 minute contact at room temperature with sodium hypochlorite (3,000 to 5,000 ppm free chlorine), and accelerated hydrogen peroxide (5,000 ppm)(Footnote 19-Footnote 21).

PHYSICAL INACTIVATION: Unknown. The physical properties contribute to viral resistance to various factors such as heat (80°C for 72 hours), solvent, and detergent treatments(Footnote 4,Footnote 7).

SURVIVAL OUTSIDE HOST: It is difficult to cultivate in vitro. Serum samples containing the virus can be stored for short periods at 4°C and for longer periods at -70°C for virus detection(Footnote 4).

SECTION V - FIRST AID / MEDICAL

SURVEILLANCE: If erythaema infectiosum is present, a clinical diagnosis can be made without laboratory testing(Footnote 6). Serum IgM testing is recommended to diagnose acute viral infection in immunocompetent patients. Elevated IgM antibodies will remain detectable for 2 to 3 months after acute infection. IgG testing is less useful because it only indicates previous infection and immunity. Viral DNA testing is crucial for the diagnosis of infection in patients in transient aplastic crisis or in immunocompromised patients with chronic infection(Footnote 6,Footnote 22). PCR assays are preferred over less sensitive nucleic acid hybridization assays(Footnote 6). ELISA- and haemagglutination-based assays have been developed to detect viral antigen during blood screening(Footnote 14). Other methods such as detection of B19 protein production by immunofluorescence staining and quantitative PCR methods have been developed for laboratory diagnosis(Footnote 23).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Erythaema infectiosum is usually self-limited and does not require treatment(Footnote 6). Generally, no specific therapy is required for parvovirus B19 infection in immunocompetent individuals(Footnote 10). Treatment of symptoms such as fever, pain, or itching may be required. Adults with joint pain and swelling may require rest and anti-inflammatory drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs), to relieve symptoms(Footnote 1). Pure red-cell aplasia and the underlying persistent infection may be terminated by discontinuing immunosuppressive therapy, or by instituting antiretroviral drug therapy in patients with AIDS(Footnote 3). Patients in transient aplastic crisis may require erythrocyte transfusions. Chronic red cell aplasia, if severe, may require intravenous immunoglobulin therapy. This treatment may improve the symptoms of anaemia, but it may precipitate a rash or arthropathy. Intravenous immunoglobulin G (IVIG) therapy has also been used in other cases of severe illness(Footnote 2,Footnote 6,Footnote 10).

IMMUNISATION: A vaccine has been developed, but is not yet available for use(Footnote 1,Footnote 2,Footnote 6,Footnote 18).

PROPHYLAXIS: Pregnant women with sick children at home are advised to wash hands frequently and to avoid sharing eating utensils(Footnote 2). Isolation of infected persons is impractical, with the exception of hospitalized patients(Footnote 3). Health care workers should be advised of the importance of following good infection control measures(Footnote 2).

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: Many cases of laboratory-acquired infection have been reported, and occupational exposure to infectious aerosols in laboratories is suspected. Infectious aerosols can be generated by centrifugation, during the resuspension of virus pellets, or in washing stages of solid phase immunoassays. It is suggested that parvovirus infection will remain a problem in the laboratory unless the antigen is inactivated beforehand or, as a minimum precaution, aerosols are contained(Footnote 12,Footnote 13).

SOURCES/SPECIMENS: Parvovirus B19 has been found in blood (serum or plasma), respiratory secretions (e.g., saliva, sputum, or nasal mucus), bone marrow aspirates, cord blood samples, amniotic fluid cells and biopsy specimens of placenta, foetal tissues, synovial fluid, cells and tissue of affected joints, and skin tissue from systemic sclerosis that is used for B19 DNA detection(Footnote 4,Footnote 6,Footnote 10,Footnote 22-Footnote 24).

PRIMARY HAZARDS: Exposure to infectious aerosols and needlestick injuries(Footnote 2,Footnote 9,Footnote 12).

SPECIAL HAZARDS: None.

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(Footnote 25).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infected or potentially infected materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes(Footnote 26).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities(Footnote 26).

SECTION VIII - HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, while wearing protective clothing, gently cover the spill with paper towels and apply appropriate disinfectant starting at the perimeter, working inwards towards the centre. Allow sufficient contact time before clean up(Footnote 26).

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and incineration(Footnote 26).

STORAGE: In sealed containers that are appropriately labelled(Footnote 26).

SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: November 2010.

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2010
Canada

REFERENCES:

Footnote 1
Heegaard, E. D., & Brown, K. E. (2002). Human parvovirus B19. Clinical Microbiology Reviews, 15 (3), 485-505.
Footnote 2
Heymann, D. L. (2004). In American Public Health Association (Ed.), Control of Communicable Diseases Manual (18th ed., pp. 196-199). Washington, D.C.: American Public Health Association.
Footnote 3
Young, N. S., & Brown, K. E. (2004). Mechanisms of disease: Parvovirus B19. New England Journal of Medicine, 350 (6), 586-597.
Footnote 4
Zerbini, M., & Musiani, M. (2003). Human Parvoviruses. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken (Eds.), Manual of Clinical Microbiology (8th ed., pp. 1534-1543). Washington, D.C.: ASM Press.
Footnote 5
Parsyan, A., & Candotti, D. (2007). Human erythrovirus B19 and blood transfusion - An update. Transfusion Medicine, 17 (4), 263-278.
Footnote 6
Servey, J. T., Reamy, B. V., & Hodge, J. (2007). Clinical presentations of parvovirus B19 infection. American Family Physician, 75 (3), 373-376+377.
Footnote 7
Clewley, J. P. (1984). Biochemical characterization of a human parvovirus. Journal of General Virology, 65 (1), 241-245.
Footnote 8
Servant, A., Laperche, S., Lallemand, F., Marinho, V., De Saint Maur, G., Meritet, J. F., & Garbarg-Chenon, A. (2002). Genetic diversity within human erythroviruses: Identification of three genotypes. Journal of Virology, 76 (18), 9124-9134.
Footnote 9
Kerr, J. R. (2000). Pathogenesis of human parvovirus B19 in rheumatic disease. Annals of the Rheumatic Diseases, 59 (9), 672-683.
Footnote 10
Corcoran, A., & Doyle, S. (2004). Advances in the biology, diagnosis and host-pathogen interactions of parvovirus B19. Journal of Medical Microbiology, 53 (6), 459-475.
Footnote 11
Ramirez, M. M., & Mastrobattista, J. M. (2005). Diagnosis and management of human parvovirus B19 infection. Clinics in Perinatology, 32 (3), 697-704.
Footnote 12
Cohen, B. J., & Brown, K. E. (1992). Laboratory infection with human parvovirus B19 [7]. Journal of Infection, 24 (1), 113-114.
Footnote 13
Cohen, B. J., Couroucé, A. M., Schwarz, T. F., Okochi, K., & Kurtzman, G. J. (1988). Laboratory infection with parvovirus B19. Journal of Clinical Pathology, 41 (9), 1027-1028.
Footnote 14
Brown, K. E. (2004). Detection and quantitation of parvovirus B19. Journal of Clinical Virology, 31 (1), 1-4.
Footnote 15
Brown, K. E., Young, N. S., Alving, B. M., & Barbosa, L. H. (2001). Parvovirus B19: Implications for transfusion medicine. Summary of a workshop. Transfusion, 41 (1), 130-135.
Footnote 16
Blu mel, J., Schmidt, I., Effenberger, W., Seitz, H., Willkommen, H., Brackmann, H. H., Lo wer, J., & Eis-Hu binger, A. M. (2002). Parvovirus B19 transmission by heat-treated clotting factor concentrates. Transfusion, 42 (11), 1473-1481.
Footnote 17
Eid, A. J., Brown, R. A., Patel, R., & Razonable, R. R. (2006). Parvovirus B19 infection after transplantation: A review of 98 cases. Clinical Infectious Diseases, 43 (1), 40-48.
Footnote 18
Broliden, K., Tolfvenstam, T., & Norbeck, O. (2006). Clinical aspects of parvovirus B19 infection. Journal of Internal Medicine, 260 (4), 285-304.
Footnote 19
Collins, C. H., & Kennedy, D. A. (1999). Decontamination. Laboratory acquired infections: History, incidence, causes and preventions (4th ed., pp. 160-186). Woburn, MA: Butterworth- Heinemann.
Footnote 20
Omidbakhsh, N., & Sattar, S. A. (2006). Broad-spectrum microbicidal activity, toxicologic assessment, and materials compatibility of a new generation of accelerated hydrogen peroxide-based environmental surface disinfectant. American Journal of Infection Control, 34 (5), 251-257.
Footnote 21
Favero, M. S., & Arduino, M. J. (2006). Decontamination and Disinfection. In D. O. Fleming, & D. L. Hunt (Eds.), Biological Safety: Principles and Practices (4th ed., pp. pp. 373-381). Washington, D.C.: ASM Press.
Footnote 22
Weir, E. (2005). Parvovirus B19 infection: Fifth disease and more. Canadian Medical Association Journal, 172 (6), 743.
Footnote 23
Wong, S., & Brown, K. E. (2006). Development of an improved method of detection of infectious parvovirus B19. Journal of Clinical Virology, 35 (4), 407-413.
Footnote 24
Ohtsuka, T., & Yamazaki, S. (2004). Increased prevalence of human parvovirus B19 DNA in systemic sclerosis skin. British Journal of Dermatology, 150 (6), 1091-1095.
Footnote 25
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
Footnote 26
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.