N.farcinica is a Gram–positive, branching, filamentous bacillus causing many localized and disseminated infectious in humans, including pulmonary and wound infections, brain abscesses, and bacteraemia. Immunocompromised hosts and patients undergoing immunosuppressive therapies are more commonly affected by this bacterium [2].
Anton Y. Peleg et al. described the risk factors of N. farcinica infection in organ transplant recipients. In this case series, patients with Nocardia infection had significantly higher prednisone dosages (p 0.007), lower lymphocyte counts (p 0.003), and higher neutrophil counts (p 0.006) at the time of infection, compared with control subjects [13]. In our case, the patient had undergone therapy with prednisone in the preceding 12 months because of leprosy reaction. At admission he had WBC 14,500/μL with neutrophils 87% (11800/mmc), lymphocytes 4.1% (500/mmc), CD4 cells 34.6% (463/mmc), CD8 cells 24.8% (322/mmc).
The relative frequency of infections caused by the different Nocardia species are difficult to determine retrospectively and may vary geographically. N. farcinica has been reported to constitute 13,8% and 19% of Nocardia isolates in Italy from 1982 to 1992 [14] and from 1993 to 1997 [7], respectively. It is not possible to estimate the actual number of Italian cases due to the potential bias of referrals to public health authorities and also because Nocardia strains are not collected at the National Reference Centre.
The clinical manifestations of N. farcinica are different. The lung is the most common site of infection (43%). Torres et al. observed infections of cutaneous and sub-cutaneous tissues in 10% of cases. In the case of disseminated infections, it was possible to detect a metastatic focus or, more frequently, a primary lesion after traumatic injury. In other cases, the patients had sub-clinical or transient primary pulmonary infection followed by dissemination to the brain, skin, bones, and kidney [15]. In our case, as in the 7/26 cases described in an Italian report about human Nocardiosis between 1993 and 1997 [7], it was not possible to observe previous pulmonary involvement.
Concerning the epidemiology, Nocardiae are ubiquitous in the environment and can be found worldwide in fresh and salt water, in a variety of soil types, dust, decaying vegetation, and decaying faecal deposits from animals [2]. Bittar et al. described a Nocardia infection in a man who was an active gardener [16]. Our patient had gardening as a hobby, which led us to speculate that he could have acquired the infection in this way.
Unfortunately, we did not identify the organism with the cultures and could not perform susceptibility testing. However, previous studies have identified multi-drug-resistance patterns in isolates of N. farcinica, characterized by resistance to most beta-lactam antibiotics [17] and susceptibility mainly to amikacin, imipenem, trimethoprim/sulfamethoxazole, and fluoroquinolones [2]. Hansen G. et al. reported that fluoroquinolones had variable activity against clinical strains of Nocardia, and the newer fluoroquinolones such as moxifloxacin, gatifloxacin, and gemifloxacin, had increased in vitro activity compared to ciprofloxacin [17].
Laboratory identification and speciation for Nocardia are challenging, and the methodology continues to evolve. Before 2000, Nocardia isolates were identified primarily through phenotypic methods. In 2000, the identification of Nocardia was enhanced through the use of 16SrRna gene sequencing in research centres [18–20]. In the reported case, it is interesting to underline that our patient presented clinical and radiological improvement after the initiation of therapy with daptomycin. Since no cases of N. farcinica treated with daptomycin have been described in literature (there are only sensitivity studies in vitro) [21], we started empirical antibiotic combination therapy with imipenem plus trimethoprim-sulfamethoxazole. Information on the duration of treatment is inadequately documented in most reports, varying from 3 to 12 months with a median of 4 months. Primary cutaneous Nocardiosis may be treated with therapy for 2 to 4 months, but only after bone involvement has been excluded [4, 6].
In summary, Nocardiosis remains a severe and sometimes potentially life-threatening complication in the immunocompromised host. It is relevant to consider this microorganism in the differential diagnosis of infections, even in cases with unusual presentations such as this one. Because of the aggressiveness, tendency to disseminate, and resistance of the organism to antibiotics, delayed diagnosis can have serious consequences.
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