Background. Fungemia due to Rhodotorula mucilaginosa is rare and highly resistance to antifungal therapy. Since most cases of R. mucilaginosa fungemia are attributed to medical devices, limited information is currently available on infection without central venous catheter (CVC) implantation. We herein report a case of R. mucilaginosa fungemia without implantation of CVC, successfully treated by liposomal amphotericin B (L-AMB). Case Presentation. An 81-year-old man with a history of chronic obstructive lung disease and rheumatoid arthritis was admitted with dyspnea and fever. The present case had no previous history of CVC implantation. Candidemia was suspected based on yeast and salmon-pink colonies in blood cultures, and thus, micafungin (MCFG) was administered. The isolated yeast was identified as R. mucilaginosa, which exhibited resistance to MCFG. Therefore, antifungal therapy was changed to L-AMB. The sterile blood culture and defervescence were observed from the initiation of L-AMB. Conclusion. Although the obvious entry point was unclear, long-term immunosuppressive therapy for RA may have damaged the gastrointestinal tract, which leading to the bacterial translocation of R. mucilaginosa. An early class switch to L-AMB was effective. Physicians need to consider the administration of L-AMB in cases suspected of R. mucilaginosa fungemia following the detection of salmon-pink colonies in blood cultures.

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Background Guillain–Barré syndrome (GBS) and spinal epidural abscess (SEA) are known as mimics of each other because they present with flaccid paralysis following an infection; however, they differ in the main causative bacteria. Nevertheless, the two diseases can occur simultaneously if there is a preceding Campylobacter infection. Here, we report the first case of SEA with GBS following Campylobacter coli infection. Case presentation A 71-year-old Japanese man presented with progressive back pain and paralysis of the lower limbs following enteritis. Magnetic resonance imaging showed a lumbar epidural abscess that required surgical decompression; therefore, surgical drainage was performed. Blood cultures revealed the presence of C. coli. Despite surgery, the paralysis progressed to the extremities. Nerve conduction studies led to the diagnosis of GBS. Anti-ganglioside antibodies in the patient suggested that GBS was preceded by Campylobacter infection. Intravascular immunoglobulin therapy attenuated the progression of the paralysis. Conclusions We report a case of SEA and GBS following Campylobacter infection. A combination of the two diseases is rare; however, it could occur if the preceding infection is caused by Campylobacter spp. If a cause is known but the patient does not respond to the corresponding treatment, it is important to reconsider the diagnosis based on the medical history.

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