Persistent parvovirus b19 infection resulting in carpal tunnel syndrome

A woman showing chronic arthropathy after a parvovirus B19 infection was followed for 1 year with quantitative determination of parvoviral DNA, and specific immunoglobulin (Ig)M and IgG in blood. B19 arthopathy resulted in carpal tunnel syndrome, needing surgery, after 8 months of persistent B19 viraemia, when IgM was already cleared but IgG values were still high.

Case history

Carpal tunnel syndrome (CTS) is the most common peripheral compression neuropathy, but many aspects of its aetiology are not at all clear. CTS is often termed as idiopathic but it has also been attributed to a variety of underlying disorders and processes, and sometimes CTS has been reported as secondary to infectious diseases of bacterial, mycotic and viral origin, including parvovirus B19. Parvovirus B19 in humans can cause acute infections but also persistent infections with continuous virus production both in immunocompetent and in immunosuppressed individuals.¹ Parvovirus B19 is generally associated with erythema infectiosum, arthritis and arthralgias, hydrops fetalis and transient aplastic crisis,¹ but also, in a few reports, it has been suggested to have a role in the development of CTS. In fact. Samii et al.² described three cases of acute bilateral CTS associated with B19 infection diagnosed by serological data and, in one case, by detection of B19 DNA in serum by PCR. Moreover Gendi et al.³ found three cases of CTS in adults in whom 1 year previously a parvovirus infection had been diagnosed by specific immunoglobulin (Ig)M. Recently, two cases of CTS in two female patients with prolonged arthalgia and chronic fatigue syndrome following a previous acute B19 infection have been described by Kerr et al.⁴ Two principal difficulties with the hypothesis that B19 can be an infectious agent which can trigger CTS can arise, however: (1) the causal relationship, as CTS is generally found a long time after laboratory detection of acute infection; and (2) the limitation of the methods of detection of recent or past B19 infections.

In the present report we describe a case of a woman, followed for 1 year with quantitative determination of parvoviral DNA,⁵ specific IgM and IgG in blood,⁶ who showed persistent parvovirus B19 viraemia for 8 months, with chronic B19 arthopathy and occasionally recurrent fugaceous erythemas, which led to CTS, needing surgery. This, apparently immunocompetent, 42‐year‐old woman was followed for B19 infection markers (fig. 1, table 1) for 12 months after exposure to her child who had B19 infection.

Figure 1 B19 infection markers (viral load, IgM, IgG) and onset of CTS in the patient.

Table 1 B19 viral load, IgM, IgG and clinical features in the patient.

Months	Parvovirus B19		B19 IgM		B19 IgG		Clinical features
	Viral load (geq/ml)	Test result	OD/cut‐off	Test ratio result	OD/cut‐off ratio	Test result
0	1.30E+06	Pos	9.44	Pos	16.30	Pos	Arthralgias
1	8.41E+05	Pos	7.64	Pos	15.99	Pos	Arthralgias
2	6.25E+05	Pos	7.00	Pos	11.73	Pos	Arthralgias
3	1.50E+05	Pos	2.62	Pos	13.16	Pos	Arthralgias
4	1.00E+05	Pos	0.86	BL	8.41	Pos	Arthralgias Transient rash
5	7.23E+04	Pos	0.53	Neg	10.26	Pos	Arthralgias
6	1.61E+04	Pos	0.38	Neg	10.42	Pos	Arthralgias
7	3.02E+04	Pos	0.34	Neg	9.88	Pos	Arthralgias Transient rash
8	1.24E+04	Pos	0.40	Neg	9.07	Pos	Arthralgias CTS
9	1.00E+00	Neg	0.29	Neg	8.96	Pos
10	1.00E‐01	Neg	0.33	Neg	7.49	Pos
11	1.00E‐01	Neg	0.22	Neg	8.00	Pos
12	1.00E‐01	Neg	0.38	Neg	7.89	Pos

BL, borderline; CTS, carpal tunel syndrome; geq, genome equivalent; Neg, negative; OD, optical density; Pos, positive.

At the onset of the illness, B19 arthritis affecting bilaterally the small joints of the hands, wrists and elbows occurred. Symptoms persisted for 8 months with pain, stifness and swelling. The patient was always afebrile and no anaemia was observed. At the beginning of the observation period, no rash was observed but, during the 8 months in which the parvovirus was present in the blood, transient rashes occurred. Concomitant with the presence of arthritis symptoms, B19 DNA was always detectable by real‐time PCR. B19 IgG was always present, with similar titres throughout the study, while IgM was cleared at month 4. Between month 7 and 8, CTS developed. After month 8, concomitant with CTS surgery, but in our opinion not consequent to it, B19 virus cleared from the patient's blood without any intravenous immunoglobulin (IVIG) treatment, and the patient fully recovered without any other sign of B19 arthalgias.

It is possible to speculate that in this case at month 7–8, cell‐mediated immunity finally became effective, or antibody maturation occurred, possibly with transient autoimmunity relevant to CTS development. The hypothesis of a possible role for B19 in CTS is consistent with the fact that a variety of manifestations, similar to CTS, have been reported in subjects with B19 infection such as pain, effects on soft tissues with swelling, persistent finger paraesthesia and slowing of nerve conduction velocities.⁷,⁸ The prevalence of B19 arthralgias, moreover, is similar to CTS prevalence, being greater for middle‐aged women than for children and men.¹ To establish the role of parvovirus B19 in the development of CTS and to determine if long‐lasting B19 infections in patients with chronic arthritis can lead to CTS, it would be important to include research on B19 chronic infections with the presence of low levels of B19 DNA as a concurrent disease which could interact with secondary CTS.

Acknowledgements

We are grateful to Dr Jonathan Kerr for discussion of the data and valuable comments.