Accidental Occupational Exposure to Burkholderia pseudomallei in South Korea Did Not Result in Melioidosis

To the Editor—Melioidosis is caused by Burkholderia pseudomallei and presents a high mortality rate of up to 40%. ¹ B. pseudomallei is endemic in Southeast Asia and northern Australia. In Korea, there have been several imported cases; however, there have been no autochthonous cases. ²

B. pseudomallei is regarded as a biothreat, and to date, 2 cases of laboratory-acquired melioidosis have been reported. ³ When laboratory workers are exposed to B. pseudomallei, postexposure monitoring and/or postexposure prophylaxis (PEP) according to the risk are recommended. ³ However, data are limited regarding the incidence of the development of melioidosis after accidental occupational exposure outside the laboratory.

On June 10, 2016, a 64-year-old Korean man presented with right second-toe pain, cough, sputum, and fever at the tertiary-care center in Ulsan, South Korea. He had been living in Singapore and Indonesia for 20 years. He was a sailor and had recently worked carrying sand in Indonesia. He returned from Indonesia to Korea because of his illness, 1 day before admission. He had been diabetic for the previous 18 years. Magnetic resonance image (MRI) of his foot showed an abscess and osteomyelitis in the second toe, and computed tomography scans of the chest revealed dense consolidation in the left upper lobe and multiple cavitary nodules in both the lungs. We performed incision and drainage of the abscess in the toe multiple times.

On June 15, Burkholderia cepacia was observed in the blood culture performed on June 10, which was identified using VITEK 2 (BioMerieux, Lyon, France). It was not identifiable via matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) (BioMerieux, Lyon, France). However, to differentiate between B. cepacia and B. pseudomallei, we performed 16S rRNA sequencing, as previously described. ⁴ Nucleotide BLAST searches (http://blast.ncbi.nlm.nih.gov/Blast.cgi) of the isolate sequences showed the following matches: B. pseudomallei strain 982 chromosome 2 (GenBank accession number CP012577.1), 99% (1471 of 1472 bp); B. pseudomallei strain 982 chromosome 1 (GenBank accession number CP012577.1), 99% (1471 of 1472 bp). The patient had persistent B. pseudomallei bacteremia from June 10 to June 20, and his sputum and pus culture from the wounds also yielded B. pseudomallei. We administered ceftazidime, and the patient survived with prolonged antibiotic therapy.

After we identified B. pseudomallei infection, we contacted HCWs who were at risk, and classified them as low or high risk, according to the modification of recommendations by Peacock et al. ³ Low-risk exposures included (1) plate sniffing, opening of the lid of an agar plate growing B. pseudomallei outside a biological safety cabinet, (2) possible contact with the blood or body fluid (pus or urine) with intact skin or protected body and hands without evidence of aerosols, and (3) spillage of small volumes of liquid culture (1 mL) within a biological safety cabinet. High-risk exposures included (1) a penetrating injury with contaminated equipment, (2) any splash causing contamination of the mouth or eyes, (3) contact with the blood or body fluid (pus or urine) with nonintact skin, and (4) aerosol-generating activities performed outside a biological safety cabinet. Exposure of laboratory workers with certain health conditions, such as diabetes mellitus and chronic liver or kidney disease, in the absence of proper personal protective equipment, was also considered high risk. Serological testing of exposed HCW was performed using indirect hemagglutination assay (IHA) as previously described. ⁵ Thirty HCWs were exposed during 21 days; 5 were classified as high risk because they had been possibly exposed to the patient’s blood and pus through nonintact skin during venipuncture or dressing wounds, and 25 including 2 laboratory workers were classified as low risk, mainly due to contact of blood with intact skin during venipuncture or dressing wounds. Laboratory workers inadvertently opened the lid of an agar plate growing B. pseudomallei outside a biologic safety cabinet. High-risk HCWs were offered trimethoprim/sulfamethoxazole for 21 days. All 30 HCWs were monitored to ascertain whether symptoms developed until September 5, and IHA was performed on July 7–11 (2 weeks or 4 weeks after exposure), July 25 (4–6 weeks after exposure), August 5 (6–8 weeks after exposure), and September 5 (11–13 weeks after exposure). None of the HCWs showed seroconversion or had the symptoms of melioidosis.

There have been 2 laboratory-acquired cases to date. ³ One occurred after sonication outside a safety hood, and the other after cleaning up a centrifuge spillage of B. pseudomallei culture with bare hands. This HCW had an ulcerative lesion on the finger at the time of exposure. During 2008–2013, there were 261 persons at risk for occupational exposure to B. pseudomallei while performing laboratory diagnostics in the United States; however, no infection occurred. ⁶ In addition, a review of work in a clinical laboratory in an endemic area suggests low risk to laboratory workers. ⁷ Our data suggest that the possibility of development of melioidosis after exposure to patient’s body fluid on nonintact skin outside the laboratory may be low.

Notably, not following standard precautions led to many exposures identified in this study. Using appropriate personal protection equipment when performing dressing and venipuncture, expecting to contact patient urine or body fluids, or HCWs having nonintact skin, cannot be overemphasized. In addition, considering potentially false-negative antibody testing, lack of performing longer-term postexposure follow-up is a limitation of our study.

In conclusion, delayed diagnosis of melioidosis and not following standard precaution led 30 HCWs to be exposed to patient’s blood or body fluids; however, none developed melioidosis.