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Prevalence of human parvovirus B19 infection in children with Henoch-Schnlein purpura.

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ARTHRITIS & RHEUMATISM
Vol. 39, No. 5, May 1996, pp 880482
6 1996, American College of Rheumatology
880
CONCISE COMMUNICATIONS
Prevalence of human parvovirus B19 infection in
children with Henoch-Schonlein purpura
Henoch-Schonlein purpura (HSP) is an acute leukocytoclastic vasculitis of unknown etiology that primarily
affects children. Although epidemiologic studies suggest that
infections may cause or contribute to the pathogenesis of
HSP, an infectious agent is not identified in most cases (1,2).
Several reports have described acute human parvovirus B19
infection in some patients with HSP (3-7), but to date, there
are no controlled studies concerning the role of B19 infection
in HSP. The present study was therefore performed to
determine the prevalence of B 19 infection among children
with HSP compared with healthy control children.
Serum samples were obtained from 27 children (14
female and 13 male) with acute HSP who were seen at the
University of Virginia Health Sciences Center between 1986
and 1993. The patients ranged in age from 3 to 12 years
(mean 6.4 years). All had typical cutaneous purpura, 26
(96%) had arthritis, 17 (63%) had abdominal pain, 8 (30%)
had gastrointestinalbleeding, and 9 (33%) had nephritis. The
median interval from the onset of symptoms to the collection
of serum was 10 days, with a range of 1-62 days.
Control sera were obtained between 1987 and 1990
from 25 healthy children (15 females and 10 males) ranging in
age from 1 to 16 years (mean 7.9 years). Controls consisted
of children who were evaluated for musculoskeletal complaints that proved to be either functional in origin or
secondary to minor orthopedic problems, and children who
were evaluated because of a history of recurrent upper
respiratory infections who were otherwise healthy and found
to be immunologically normal. None of the controls had a
history of arthritis or vasculitis.
Sera were tested for B19-specific IgM and IgG antibodies by an enzyme immunoassay as previously described
(8,9). Sera were considered positive for B19-specific IgM or
IgG if they had absorbance values that were >5 SD above
the mean absorbance values for known seronegative controls. Recent B19 infection was defined by the presence of
serum IgM antibody, with or without IgG antibody, to B19.
Past B19 infection was defined as the presence of B19specific IgG antibody in the absence of IgM antibody. HSP
and control sera that were positive for IgM antibody to B 19
were tested for the presence of B19 DNA by means of a
nested polymerase chain reaction, as previously described
(10,ll).
Data were analyzed for statistical significance using
Fisher’s exact test, and confidence intervals (CI) were
calculated using the binomial distribution.
The results of B19 IgM and IgG antibody testing in
patients and controls are shown in Table 1. Recent B19
infection was documented in 3 of the 27 HSP patients (11%;
95% CI 2-29%) and in 2 of the 25 controls (8%; 95% CI
1-26%) (P= 0.54). All were weakly positive, and B19 DNA
was not detected in any of these 5 IgM-positive sera.
Evidence of past infection was present in 5 HSP
patients (19%; 95% CI 638%) and in 6 controls (24%; 95%
CI 945%) (P = 0.74).
Table 1. Prevalence of recent and past B19 infection based on IgM
and IgG antibody to B19 in patients with HSP and controls*
HSP patients (n = 27)
Healthy controls (n = 25)
Recent B 19
(I@+)
Past B19
( W + , IgM-1
3 (11)
2 (8)
5 (19)
6 (24)
* Values are the number (%) positive. HSP = Henoch-Schonlein
purpura.
B19 is an important human pathogen, with a wide
range of clinical manifestations, including erythema infectiosum, transient or chronic erythroid hypoplasia, arthritis, and
hydrops fetalis (12). The cellular receptor for B19 has been
identified as the erythrocyte P antigen, which is also expressed on vascular endothelial cells (13). Thus, B19 may be
capable of producing vasculitis by direct invasion of vascular
endothelial cells. Indeed, there is evidence indicating that
B19 is involved in the pathogenesis of necrotizing vasculitis,
including polyarteritis nodosa and Wegener’s granulomatosis, in some children (11).
In addition to chronic necrotizing vasculitis, B19 has
been anecdotally implicated in the pathogenesis of HSP
(3-7), but the present study is the first to systematically
examine the prevalence of B 19 infection among children
with HSP compared with healthy control children. Our
results indicate that HSP may be associated with acute B19
infection in a few children, but the vast majority of HSP
patients had no serologic evidence of recent B19 infection.
In fact, the prevalence of recent and past B19 infection was
not significantly different among children with HSP compared with healthy control children. Our results are consistent with those of Farley et a1 (2), who investigated a cluster
of HSP cases in Connecticut and concluded that there was
no evidence to support a role of B19 in the outbreak of HSP.
In that study, none of the 19 patients tested were B19 IgM
positive, and only 2 were B19 IgG positive. However, no
control sera were tested for B19 antibody.
In summary, the results of this study indicate that
only a small minority of children with HSP had evidence of
a recent B19 infection. Moreover, the prevalence of recent
and past B19 infection was virtually identical among children
with HSP and healthy control children. We conclude that
B19 is not a common cause or contributing factor in the
pathogenesis of HSP in children.
Polly J. Ferguson, MD
Frank T. Saulsbury, MD
University of Virginia Health Sciences Center
Charlottesville, VA
Scott F . Dowell, MD, MPH
Thomas J. Torok, MD
Dean D. Erdman, DrPH
Larry J. Anderson, MD
Centers for Disease Control and Prevention
Atlanta, GA
CONCISE COMMUNICATIONS
1. Nielsen HE: Epidemiology of Schonlein-Henoch purpura. Acta
Paediatr Scand 77:125-131, 1988
2. Farley TA, Gillespie S, Rasoulpour M, Tolentino N, Hadler JL,
Hunvitz E: Epidemiology of a cluster of Henoch-Schonlein
purpura. Am J Dis Child 143:798-803, 1989
3. Lefrere JJ, Courouce AM, Muller JY, Clark M, Soulier JP:
Human parvovirus and purpura (letter). Lancet 2:730, 1985
4. Mortimer PP, Cohen BJ, Rossiter MA, Fairhead SM, Rahman
AF: Human parvovirus and purpura (letter). Lancet 2:730-731,
1985
5. Lefrere JJ, Courouce AM, Soulier JP, Cordier MP, Guesne
Girault MC, Polonovski C, Bensman A: Henoch-Schonlein
purpura and human parvovirus infection. Pediatrics 78: 183-184,
1986
6. Schwarz TF, Bruns R, Schroder S, Wiersbitzky S, Roggendorf
M. Human parvovirus B19 infection associated with vascular
purpura and vasculitis. Infection (Munchen) 17:170-171, 1989
7. Veraldi S, Rizzitelli G: Henoch-Schonlein purpura and human
parvovirus B19. Dermatology (Basel) 189:213-214, 1994
8. Erdman DD, Usher MJ, Tsou C, Caul EW, Gary GW, Kajigaya
S, Young NS, Anderson LJ: Human parvovirus B19 specific
IgG, IgA, and IgM antibodies and DNA in serum specimens
from persons with erythema infectiosum. J Med Virol 35: 110115, 1991
9. Kajgaya S, Fujii H, Field A, Anderson S, Rosenfeld S, Anderson LJ, Shimada T, Young NS: Self-assembled B19 parvovirus
capsids, produced in a baculovirus system, are antigenically and
immunologicallysimilar to native virions. Proc Natl Acad Sci U
S A 88:4646-4650, 1991
10. Durigon EL, Erdman DD, Gary GW, Pallansch MA, Torok TJ,
Anderson LJ: Multiple primer pairs for polymerase chain reaction (PCR) amplification of human parvovirus B19 DNA. J Virol
Methods 44:155-166, 1993
11. Finkel TH, Torok TJ, Ferguson PJ, Durigon EL, Zaki SR,
Leung DYM, Harbeck RJ, Gelfand EW, Saulsbury FT, Hollister RJ, Anderson LJ: Chronic parvovirus B19 infection and
systemic necrotising vasculitis: opportunistic infection or aetiologic agent? Lancet 343: 1255-1258,1994
12. Torok TJ: Parvovirus B19 and human disease. Adv Intern Med
37:431455, 1992
13. Brown KE, Anderson SM, Young NS: Erythrocyte P antigen:
cellular receptor for B19 parvovirus. Science 262:114-117, 1993
Mycobactenum kansasii septic arthritis in a patient
with acquired immunodeficiency syndrome
Nontuberculous mycobacterial diseases are an important cause of morbidity and mortality in patients with
acquired immunodeficiency syndrome (AIDS). Infections
due to Mycobacterium kansasii are more frequent and more
severe in these patients (1,2). The microorganism usually
causes isolated respiratory disease, but disseminated infections have been reported (3). Musculoskeletal infections are
very rare, and we have found only one case of arthritis in a
patient with AIDS (4). We present here a case of M kansasii
septic monarthritis of the knee in an AIDS patient, which
probably developed as a result of hematogenous spread from
pulmonary disease.
The patient was a 38-year-old white man whose
medical history disclosed intravenous drug abuse, human
immunodeficiency virus (HIV) infection with extrapulmonary tuberculosis, and Pneumocystis carinii pneumonia. His
CD4+ cell count was 30 cells/mm3,with a CD4:CD8 ratio of
0.1, and he was receiving prophylaxis with monthly aerosol-
88 1
ized pentamidine. In November 1992, he was admitted to the
hospital because of an infiltrate in the upper right lobe of the
lung without cavitation. M kansasii was identified in cultures
of sputum, and isoniazid and ethambutol were administered
for 18 months, with apparent resolution of the infection.
In June 1994, the patient reported progressive pain
and swelling in his left knee that had developed in the
previous 2 months. He denied having fever, asthenia, or
other symptoms. Results of a physical examination were
unremarkable, apart from a synovial knee effusion. Results
of laboratory studies were negative, except an erythrocyte
sedimentation rate of 76 mm in the first hour. Chest radiograph showed no abnormalities, and radiographs of the knee
demonstrated only soft tissue swelling. Magnetic resonance
imaging revealed an important knee effusion, with synovial
enlargement and a popliteal cyst. Arthrocentesis yielded 30
ml of inflammatory synovial fluid, with 20,000 leukocytes/
mm3 (75% neutrophils and 25% lymphocytes). Polarized
light microscopy showed no crystals. Ziehl stain revealed
the presence of acid-fast bacilli.
Treatment with isoniazid, rifampin, ethambutol, and
pyrazinamide was begun, and when Lowenstein cultures of
the synovial fluid showed growth of M kansasii, pyrazinamide was discontinued. The antibiogram revealed in vitro
resistance to both rifampin and high-concentrationisoniazid,
but treatment was not modified due to the good clinical
response. Arthrocentesis was performed regularly, and cultures of the synovial fluid were positive for mycobacteria
during the first 4 weeks, and then became negative. After 6
weeks of treatment, physical examination and radiographic
studies of the knee yielded normal results. After 1 year of
antimycobacterial therapy with 3 drugs, there has been no
evidence of relapse of M kansasii infection in this patient.
Treatment will be continued for at least 1 more year.
Among atypical mycobacteria, M kansasii is closely
related to Mycobacterium tuberculosis with respect to the
clinical manifestations and response to therapy (5,6). Pulmonary infection is a well-known entity that is usually recognized in patients with underlying respiratory disease. Disseminated infections have been reported infrequently;
however, any organ can be affected, usually occurring after
a primary lung infection followed by hematogenous spread
(6). M kansasii usually affects HIV-seropositive patients
when the diagnosis of AIDS is well established and the
CD4+ lymphocyte count is less than 200 cells/mm3 (6,7).
Musculoskeletal infections due to M kansasii are
very rare; a review of the literature in 1987 identified only 29
cases of articular and periarticular infections (8). The clinical
course in those patients was indolent, and delay in diagnosis
was very common. There were 2 different groups of patients:
healthy middle-aged adults, and patients with Underlying
diseases that predisposed them to the infection, such as
certain rheumatic diseases (especially rheumatoid arthritis)
or other causes of immunosuppression. Although full recovery in previously healthy patients is the rule, bone and joint
destruction are more frequent in those with underlying
diseases (8). We have found only one other report of M
kansasii arthritis in an AIDS patient. He was a 28-year-old
man with arthritis of the right elbow that showed a good
clinical response to antimycobacterial therapy (4). The discrepancy between clinical outcome and in vitro suscepti-
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purpura, henoch, schnlein, children, infectious, b19, human, prevalence, parvovirus
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