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Nocardia infection of a joint prosthesis complicating systemic lupus erythematosus

Identifieur interne : 002792 ( Istex/Corpus ); précédent : 002791; suivant : 002793

Nocardia infection of a joint prosthesis complicating systemic lupus erythematosus

Auteurs : C. Arnal ; H. Man ; F. Delisle ; P. M'Bappe ; J-J Cocheton

Source :

RBID : ISTEX:60BDBC727CAF2BC04E271985E14516081D3A8CBD

English descriptors

Abstract

The authors report the case of a 43-year-old woman suffering from severe systemic lupus erythematosus treated with long-term prednisone, who developed Nocardia nova infection on a hip prosthesis. Sepsis occurred about two years after an episode of pulmonary nocardiosis with the same Nocardia species, that was successfully treated by 12 months of antibiotics. A good outcome of the joint infection was observed in response to antibiotics and removal of the prosthesis. Nocardiosis is a rare infection, acting as an opportunisticinfection, facilitated in the present case by systemic lupus erythematosus and chronic corticosteroid therapy. Nocardia infections mainly affect the lungs, skin and central nervous system; these last two sites are mostly due to haematogenous spread, a frequent event. Treatment is based on antibiotics, usually continued for 3 ‐ 12 months, especially because of the risk of relapse. The imipenem ‐ amikacin combination appears to be more effective than trimethoprim ‐ sulfamethoxazole. To our knowledge, this is the first case report of Nocardia nova joint prosthesis infection also presenting as late septic spread of pulmonary nocardiosis, complicating corticosteroid-treated systemic lupus erythematosus.

Url:
DOI: 10.1191/096120300680198917

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ISTEX:60BDBC727CAF2BC04E271985E14516081D3A8CBD

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<p>The authors report the case of a 43-year-old woman suffering from severe systemic lupus erythematosus treated with long-term prednisone, who developed Nocardia nova infection on a hip prosthesis. Sepsis occurred about two years after an episode of pulmonary nocardiosis with the same Nocardia species, that was successfully treated by 12 months of antibiotics. A good outcome of the joint infection was observed in response to antibiotics and removal of the prosthesis.</p>
<p>Nocardiosis is a rare infection, acting as an opportunisticinfection, facilitated in the present case by systemic lupus erythematosus and chronic corticosteroid therapy. Nocardia infections mainly affect the lungs, skin and central nervous system; these last two sites are mostly due to haematogenous spread, a frequent event. Treatment is based on antibiotics, usually continued for 3 ‐ 12 months, especially because of the risk of relapse. The imipenem ‐ amikacin combination appears to be more effective than trimethoprim ‐ sulfamethoxazole. To our knowledge, this is the first case report of Nocardia nova joint prosthesis infection also presenting as late septic spread of pulmonary nocardiosis, complicating corticosteroid-treated systemic lupus erythematosus.</p>
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<meta-value> CASE REPORT Nocardia infection of a joint prosthesis complicating systemic lupus erythematosus C Arnal1 *, H Man1 , F Delisle2 , P M'Bappe1 and J-J Cocheton1 1 Service de MeÂdecine Interne and 2 Laboratoire de BacteÂriologie, HoÃpital Tenon, Paris, France The authors report the case of a 43-year-old woman suffering from severe systemic lupus erythematosus treated with long-term prednisone, who developed Nocardia nova infection on a hip prosthesis. Sepsis occurred about two years after an episode of pulmonary nocardiosis with the same Nocardia species, that was successfully treated by 12 months of antibiotics. A good outcome of the joint infection was observed in response to antibiotics and removal of the prosthesis. Nocardiosis is a rare infection, acting as an opportunistic infection, facilitated in the present case by systemic lupus erythematosus and chronic corticosteroid therapy. Nocardia infections mainly affect the lungs, skin and central nervous system; these last two sites are mostly due to haematogenous spread, a frequent event. Treatment is based on antibiotics, usually continued for 3 ± 12 months, especially because of the risk of relapse. The imipenem ± amikacin combination appears to be more effective than trimethoprim ± sulfamethoxazole. To our knowledge, this is the ®rst case report of Nocardia nova joint prosthesis infection also presenting as late septic spread of pulmonary nocardiosis, complicating corticosteroid-treated systemic lupus erythematosus. Lupus (2000) 9, 304±306 Keywords: nocardiosis; recurrence; joint prosthesis; systemic lupus erythematosus; corticosteroid therapy Introduction Nocardiosis is a rare infection caused by strict aerobic actinomycetes of the Nocardia genus present in the soil, that are not commensal organisms for animals or man. In man, they are responsible for acute, subacute or chronic suppurative infections, essentially pulmon- ary and disseminated infections.1 It occurs with predilection in debilitated or immunodepressed sub- jects and has been described, in particular, in the course of systemic lupus erythematosus (SLE)2 and corticosteroid treatments.3 We report a case of Nocardia infection of a hip prosthesis, two years after prolonged treatment of pulmonary nocardiosis in a patient with SLE. Case report Mrs B, 43 y old, was admitted to the Internal Medicine Department in January 1999 for investigation of hip pain. She had been followed since December 1987 for SLE with various combinations of manifestations: cutaneous (alopecia, vespertilio, discoid lupus, distal vasculitis), articular, pericardial (two episodes of pericarditis, with one constrictive episode in Novem- ber 1998 requiring surgical drainage), gastrointestinal (steroid-sensitive exudative enteropathy) and haema- tological (autoimmune haemolytic anaemia, leuko- penia and lymphopenia). She also suffered from renal disease. A renal biopsy performed in January 1993 because of persistent, isolated proteinuria up to 2.2 gad, revealed class V lupus nephritis according to the WHO classi®cation (membranous glomerulone- phritis). In September 1996, she developed neph- rotic syndrome (proteinuria of up to 4 gad, serum albumin: 21 gal, microscopic haematuria, renal failure with serum creatinine of 150 mmolal) and hyperten- sion; renal biopsy showed class Vc lupus nephritis *Correspondence: Dr C Arnal, Service de MeÂdecine Interne, HoÃpital Tenon, 4 rue de la Chine, F-75970, Paris Cedex 20, France. Tel: ( 33) (1) 56 01 66 14; Fax: (+33) (01) 70 82 Received 7 August 1999; accepted in revised form 6 December 1999 Lupus (2000) 9, 304±306 ß 2000 Macmillan Publishers Ltd All rights reserved 0961-2033/00 $15.00 www.nature.com/lup (membranous glomerulonephritis with segmental sclerosis). Immunological assessment revealed anti- nuclear, anti-DNA, anti-RNP and anti-SSA antibodies associated with low serum complement C3 and C4. Treatment of systemic lupus erythematosus consisted of prednisone at dosages adapted to the course of the disease, continuous from December 1987 to July 1997, then restarted in November 1998, in combina- tion with hydroxychloroquine. Intravenous boluses of methylprednisolone (10 mgakgad for 2 ± 3 consecu- tive days) were also administered during severe acute episodes of the disease. The clinical course was complicated by numerous infections (Salmonella sp septicaemia in November 1988, Streptococcus pneumoniae and Staphylococcus aureus cavitating pneumonia in November 1996, Pseudomonas aeruginosa laryngitis and pneumonia in December 1998) and aseptic necrosis of the femoral heads in December 1990, requiring total arthroplasty in June and September 1991. Left breast cancer was treated by mastectomy and axillary lymph node dissection in January 1993. In February 1997, she was admitted to our Internal Medicine Department with bilateral cavitating Nocar- dia nova pneumonia. Initial treatment by cotrimox- azole was discontinued due to deterioration of her renal function and was replaced by a combination of amoxicillin (3 gad, per os) and doxycycline (200 mgad, per os) for one month. The clinical and radiological course was favourable, allowing subse- quent treatment with oral amoxicillin 3 gad for 11 months. In November 1998, the patient complained of pain of the left hip and proximal extremity of the left thigh, with a mechanical chronology. She was afebrile and presented no laboratory signs of infection (no modi®cation of white blood cell count and no elevation of CRP). X-rays allowed the pain to be attributed to loosening of the prosthesis, secondary to probable granulomas (titanium prosthesis). It was decided to wait and see, especially as corticosteroids were reintroduced because of an episode of lupus pericarditis. In January 1999, deterioration of pain and appear- ance of a fever of 38 ± 38.5 g, combined with a laboratory in¯ammatory syndrome, suggested a pros- thesis infection, although the patient was receiving antibiotics for a recent Pseudomonas aeruginosa infection. She was also taking 20 mgad equivalent of prednisone for treatment of her systemic lupus erythematosus. Standard X-rays of the hip and femur were unchanged compared to those performed in November 1998. Gallium scintigraphy revealed in- creased uptake in the acetabulum and proximal part of the left femoral diaphysis. Hip aspiration revealed a purulent ¯uid and, after six days of growth at 37 g on blood agar, showed small white colonies identi®ed as Nocardia nova. Identi®cation was con®rmed by the 'Centre National de ReÂfeÂrence des ActinomyceÁtes' (National Actinomycetes Reference Centre) at Institut Pasteur in Paris; this bacterial strain was identical to the strain isolated in February 1997. The disk diffusion technique was used to determine antibiotic susceptibility; these strains were resistant to amox- icillin, amoxicillinclavulanic acid, cefotaxime, to- bramycin, cipro¯oxacin, cotrimoxazole, but sensitive to imipenem, erythromycin and amikacin. Antibiotic treatment, adapted to renal function, combining imipenem (1500 mgad) and amikacin (300 mgad), was started and surgical removal of the hip prosthesis with traction of the limb was performed 10 d later. After surgery, antibiotic therapy consisted of erythro- mycin (4 gad) combined with imipenem (1500 mgad) for 35 d then erythromycin alone for two months, with a favourable course allowing the patient to walk with support six months after the operation. Discussion Human contamination by Nocardia is essentially airborne, which explains the predominant clinical manifestations of pneumonia (70 ± 80%), frequently associated with multiple sites and lung abscesses.1 Haematogenous spread is frequent (50%), predispos- ing to central nervous system involvement (35%) and soft tissue and skin infections (20%). Skin involve- ment is sometimes secondary to direct contamination via a wound. Antibiotic therapy of nocardiosis is based on empirical recommendations due to the absence of correlation between the in vitro ef®cacy of antibiotics and their clinical ef®cacy and the absence of controlled clinical trials.4 First-line treat- ment usually consists of trimethoprim ± sulfamethox- azole (TMP ± SMX), which is frequently effective in vitro but often only minimally active in vivo, particularly on N. nova.5,6 The imipenemamikacin combination appears to be clinically more effective than cotrimoxazole, regardless of the species respon- sible.4,6 Antibiotics must be continued for 3 ± 12 months, depending on the severity of the clinical features. Surgery, especially for drainage of an abscess or pleurisy, is sometimes justi®ed. Relapses can occur at any time, especially in pulmonary sites.7 Cerebral or multi-organ lesions are associated with a poor prognosis. The opportunistic behaviour of Nocardia facilitates the development of infection in high-risk contexts (cancers, haematological malignancies, particularly Nocardia infection of joint prosthesis C Arnal et al 305 Lupus lymphoid, chronic respiratory diseases, immunosup- pressant and corticosteroid treatments, transplant recipients). Mok et al2 recently evaluated the pre- valence of nocardiosis in SLE patients to be 2.8%. Systemic lupus erythematosus had usually been diagnosed for several years and, in more than 80% of cases, was complicated by severe nephropathy with renal failure andaor requiring immunosuppressant therapy. In this study, all patients were receiving corticosteroids andaor immunosuppressants, which could constitute a factor of poor prognosis of nocardiosis.1 Sites of Nocardia infections are the same in immunocompetent and immunodepressed patients, but cutaneous nocardiosis has been described more frequently than central nervous system nocardiosis in SLE patients.2 Rare sites have been reported (lymph nodes, ocular, renal, splenic, laryngeal, hepatic), but always in combination with at least one of the three 'classical' sites. Two cases of Nocardia tibiotarsal arthritis have been reported in lupus patients treated with prednisone following an episode of pulmonary nocardiosis.8 To our knowledge, no other cases of nocardiosis of a joint prosthesis in the context of SLE has been previously reported. We also found only one case of primary Nocardia infection of a joint prosthesis, in a non-immunodepressed subject, in whom sepsis occur- red only six weeks after arthroplasty.9 In our case, articular nocardiosis occurred a long time after the pulmonary infection: 23 months after the onset of pneumonia and 11 months after stopping antibiotics. Recurrence of nocardiosis during SLE has never been described. Navarro et al10 reported a case of pulmonary nocardiosis relapsing after six months of treatment with cotrimoxazole in a patient with autoimmune haemolytic anaemia and strongly posi- tive antinuclear antibodies, but no clinical or other immunological feature allowing con®rmation of the diagnosis of SLE. However, the follow-up of cases of Nocardia infection, whether or not complicating SLE, is usually too short or unknown to allow reliable estimation of the recurrence rate. Wallace et al11 considered that relapses are rare when antibiotic therapy is prolonged (3 months), particularly with the TMP ± SMX combination. However, the ef®cacy of these antibiotics remains controversial, particularly on N. nova,5,6 in contrast with the amoxicillindoxycy- cline combination used in our case to treat the pulmonary infection.12 Furthermore, the risk of haematogenous spread during nocardiosis is not decreased by antibiotic therapy.1 Various elements in our case argue in favour of haematogenous spread from the pulmonary site of nocardial infection to the hip prosthesis: the frequency of this form of spread, identi®cation of the same strain of Nocardia, absence of hip pain before the episode of pulmonary nocardiosis, absence of signs of prosthetic loosening or appearance of granuloma on X-rays performed three months before the pneumonia. Conclusion Nocardial infection is rare, but has an unpredictable course, even in response to treatment. We report the ®rst case of recurrence of pulmonary nocardiosis in an extrapulmonary site in a patient with corticosteroid- treated systemic lupus erythematosus. This case emphasizes both the opportunistic behaviour of Nocardia infections, which often occur in a context of immunodepression, facilitated in this case by systemic lupus erythematosus and prolonged corti- costeroid therapy, and the risk of recurrence even after prolonged treatment of an initial site of infection. We suggest that the amikacinimipenem combination might be the treatment of choice for nocardiosis in lupus patients. This case also emphasizes the frequency of opportunistic and non-opportunistic infections in systemic lupus erythematosus and the need for precise assessment of lupus patients present- ing with suspected infection. References 1 Lerner PI. Nocardia species. In: Mandell GL, Bennett JE, Dolin R (eds). Mandell, Douglas and Bennett's principles and practice of infectious diseases. 4th ed. vol. 2. New York: Churchill Livingstone, 1995 pp. 2273 ± 2280. 2 Mok CC, Yuen KY, Lau CS. Nocardiosis in systemic lupus erythematosus. Semin Arthritis Rheum 1997; 26: 675 ± 683. 3 Frazier AR, Rosenow EC III, Roberts GD. Nocardiosis: a review of 25 cases occurring during 24 months. Mayo Clin Proc 1975; 50: 657 ± 663. 4 McNeil MM, Brown JM. The medically important aerobic actinomy- cetes: epidemiology and microbiology. Clin Microbiol Rev 1994; 7: 357 ± 417. 5 Lerner PI. Nocardiosis. Clin Infect Dis 1996; 22: 891 ± 905. 6 Boiron P. ActinomyceÁtes aeÂrobies. Rapport d'activite du Centre National de ReÂfeÂrence des mycoses humaines, des antifongiques et des actinomyceÁtes.. Unite de mycologie, Institut Pasteur, Paris, 1998. 7 Stropes L, Bartlett M, White A. Multiple recurrences of nocardial pneumonia. Am J Med Sci 1980; 280: 119 ± 122. 8 Wongthim S, Udompanich V, Charoenlap P et al. Pulmonary nocardiosis in Chulalongkorn Hospital. J Med Assoc Thai 1991; 74: 271 ± 277. 9 Robinson D, Halperin N. Nocardia asteroides infection of an Austin- Moore hemiarthroplasty in a nonimmunocompromised host. Bull Hosp Jt Dis Orthop Inst 1989; 49: 107 ± 110. 10 Navarro EE, Tupasi TE, Verallo VM et al. Disseminated histoplas- mosis with unusual cutaneous lesions in a patient from the Philippines. Am J Trop Med Hyg 1992; 46: 141 ± 145. 11 Wallace RJ Jr, Septimus EJ, Williams TW Jr et al. Use of trimethoprim-sulfamethoxazole for treatment of infections due to nocardia. Rev Infect Dis 1982; 4: 315 ± 325. 12 Wallace RJ Jr, Brown BA, Tsukamura M et al. Clinical and laboratory features of Nocardia nova. J Clin Microbiol 1991; 29: 2407 ± 2411. Nocardia infection of joint prosthesis C Arnal et al 306 Lupus</meta-value>
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<publisher>Sage Publications</publisher>
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<placeTerm type="text">Sage CA: Thousand Oaks, CA</placeTerm>
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<dateIssued encoding="w3cdtf">2000-05</dateIssued>
<copyrightDate encoding="w3cdtf">2000</copyrightDate>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
</language>
<abstract lang="en">The authors report the case of a 43-year-old woman suffering from severe systemic lupus erythematosus treated with long-term prednisone, who developed Nocardia nova infection on a hip prosthesis. Sepsis occurred about two years after an episode of pulmonary nocardiosis with the same Nocardia species, that was successfully treated by 12 months of antibiotics. A good outcome of the joint infection was observed in response to antibiotics and removal of the prosthesis. Nocardiosis is a rare infection, acting as an opportunisticinfection, facilitated in the present case by systemic lupus erythematosus and chronic corticosteroid therapy. Nocardia infections mainly affect the lungs, skin and central nervous system; these last two sites are mostly due to haematogenous spread, a frequent event. Treatment is based on antibiotics, usually continued for 3 ‐ 12 months, especially because of the risk of relapse. The imipenem ‐ amikacin combination appears to be more effective than trimethoprim ‐ sulfamethoxazole. To our knowledge, this is the first case report of Nocardia nova joint prosthesis infection also presenting as late septic spread of pulmonary nocardiosis, complicating corticosteroid-treated systemic lupus erythematosus.</abstract>
<subject>
<genre>keywords</genre>
<topic>nocardiosis</topic>
<topic>recurrence</topic>
<topic>joint prosthesis</topic>
<topic>systemic lupus erythematosus</topic>
<topic>corticosteroid therapy</topic>
</subject>
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<title>Lupus</title>
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<identifier type="ISSN">0961-2033</identifier>
<identifier type="eISSN">1477-0962</identifier>
<identifier type="PublisherID">LUP</identifier>
<identifier type="PublisherID-hwp">splup</identifier>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>9</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>304</start>
<end>306</end>
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</part>
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<identifier type="istex">60BDBC727CAF2BC04E271985E14516081D3A8CBD</identifier>
<identifier type="ark">ark:/67375/M70-3LWHMVJJ-V</identifier>
<identifier type="DOI">10.1191/096120300680198917</identifier>
<identifier type="ArticleID">10.1191_096120300680198917</identifier>
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