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Introduction Herein, concurrent true bacteremia with S. epidermidis andB. pseudomallei was managed appropriately in a healthy woman. Case report A thirty-two-year-old previously well farmer presented with a 2-day history of fever and malaise. Having low blood pressure (90/60 mmHg) with a high pulse rate (104 beats/minute) she was admitted to the intensive care unit suspecting sepsis. Two blood cultures from 2 different venipuncture sites were collected and empiric intravenous (i.v.) ceftriaxone was commenced. On day 2, C-reactive protein (CRP) was 320 mg/dL and procalcitonin (PCT) was 128 ng/dL and both cultures yielded methicillin resistant S. epidermidis (MESE), subsequently, vancomycin was added. On day 5, she developed breakthrough fever despite adequate therapy. The CRP level decreased to 110 mg/dL, however, PCT rose to 148 ng/dL. Subsequently, meropenem was added replacing ceftriaxone. Two sets of repeated blood cultures yielded MRSE and MRSE with B. pseudomallei, respectively. B. pseudomallei-IgM antibody titer was 1:5600 (cut off 1:320). Oral cotrimoxazole was added. On day 7, CRP and PCT decreased to 140 mg/dL and 67 ng/dL, and by day 9 only B. pseudomallei was isolated. Vancomycin was continued for a total of 10 days. Following 21 days of meropenem, the patient was discharged with oral cotrimoxazole for 90 days. Conclusions Concurrent bloodstream infection with S. epidermidis and B. pseudomallei is rare and not documented in the literature. Clinical vigilance has provided an opportunity to detect the pathogens in advance and proceed to a complete cure.
Melioidosis is an endemic disease in Southeast Asia and northern Australia.1 Melioidosis is caused by Burkholderia pseudomallei, a Gram-negative bacterium found in soil and water. In most cases, the infection is acquired by direct inoculation, and inhalation or ingestion considered minor portals of entry.2 The host immunity and response determine the outcome of infection as it can range from asymptomatic to fulminant sepsis and death.3
Staphylococcus epidermidis is a commensal, found ubiquitously on human skin and mucous membranes, animals and in the environment. Often bloodstream infections (BSI) are consequences of colonization of percutaneous devices or implanted medical devices.4Compared to B. pseudomallei, S. epidermidis is regarded as a low virulence pathogen and isolation of S. epidermidis from blood is presumed to be caused by contamination or rarely it causes true bacteremia.5
Concurrent BSI by two bacteria is less frequent, and it is rarely observed in an immunocompetent individual.6,7 Herein, concurrent true bacteremia with S. epidermidis and B. pseudomallei was detected and managed appropriately in a previously healthy woman.
Case report
A thirty-two-year-old previously well farmer presented with a 2-day history of fever and malaise. The clinical examination was insignificant except for low blood pressure (90/60 mmHg) with a high pulse rate (104/ minute). Therefore, she was admitted to intensive care unit with suspected sepsis without a specific focus of infection. She had not had any recurrent chest, middle ear or any focus of infections. There was no family history of immunodeficiency and no history of recent hospitalization. Dobutamine infusion was initiated. Two peripheral venous cannulas were inserted. Two blood cultures were taken from two different venipuncture sites and empirically intravenous (i.v.) ceftriaxone 1 g 12 hourly was commenced. Her C-reactive protein (CRP) was 320 mg/dL, procalcitonin (PCT) 128 ng/dL, a full blood count (FBC) of 16000 cells/µL with profound neutrophilia (94%) were found. Following 4 and 8 hours of incubation, both blood cultures became positive. On day 2, organisms were identified as S. epidermidis, and antimicrobial susceptibility profile suggests both were methicillin-resistant. Parenteral vancomycin 15 mg/kg 12 hourly was added.
On day 4 the patient became hemodynamically stable, she was weaned off the inotrope infusion and her CRP and PCT dropped to 120 mg/dL, 68 ng/dL suggesting a clinical response. Both i.v. ceftriaxone and vancomycin were continued [serum creatinine (SCr) 0.6 mg/L]. On day 5, she remained hemodynamically stable but developed breakthrough fever despite adequate therapy. Two blood cultures were collected. The patient’s CRP was 110 mg/dL, however, her PCT rose to 148 ng/dL. Parenteral ceftriaxone was stopped, empirically i.v. meropenem 1 g 8 hourly was added to the vancomycin treatment. Following 6 and 8 hours of incubation, blood cultures became positive, and S. epidermidis and S. epidermidis with B. pseudomallei were isolated from the respective cultures. At day 7, oral cotrimoxazole 1920 mg 12-hourly was added. By using trans-thoracic 2-D echocardiography, infective endocarditis was excluded. Ultrasound scan abdomen and pelvis, chest X-rays, CT-chest and bone scan were normal. The B. pseudomallei-IgM antibody titer was 1:5600, suggesting a highly positive result (cut off 1:320). On day 7, CRP and PCT were 140 mg/dL and 67 ng/dL, respectively. Two blood cultures were drawn on day 9 and after 18- and 22-hour incubation only B. pseudomalleiwas isolated and identified using VITEK2, culture based phenotypic tests and 16S rRNA sequencing. CRP and PCT dropped to 90 mg/dL and 38 ng/dL, respectively. Erythrocyte sedimentation rate (ESR) was 110 mm. Parenteral vancomycin was continued for a total of 10 days (SCr 0.9 mg/L). On day 12, two blood cultures were collected, and both remained negative following 120 hours of incubation. On day 16 CRP, PCT and ESR dropped to 50 mg/dL, 0.5 ng/dL and 88 mm/first hour, respectively. Since melioidosis without a focus of infection was isolated later, i.v. meropenem was given for 21 days instead of 14 days and the patient was discharged with oral cotrimoxazole 1920 mg 12-hourly for 90 days.7The response to treatment and complications for oral cotrimoxazole was monitored during monthly clinic visits and using ESR, CRP, and FBC, respectively (Table 1).
S. epidermidis was identified using Vitek 2 (bioMérieux, France) platform with 99% probability. In addition, manual methods including Gram staining, coagulase testing, and DNAse were also employed. The antimicrobial susceptibility profile was obtained using Vitek 2 and results indicated that it was sensitive to vancomycin, cotrimoxazole, and amikacin. It was identified as resistant to cefoxitin, cephalosporins, and quinolones. Vancomycin minimal inhibitory concentration (MIC) ranged from 0.12-0.25 mg/dL, and was measured using E-strips. Using E-test and glycopeptide resistance detection E-tests vancomycin hetero-resistance was not detected. Using ccrand the mec gene complexes M-PCR assays was performed, identifying SCCmectype V and that the S. epidermidis strains carried the mecA gene. The multilocus sequence typing (MLST) result resolved the sequence type as ST58 and pulsed-field gel electrophoresis (PFGE) proving that the same S. epidermidis pulsotypes were responsible for bacteremia in all 4 occasions. Screening swabs were taken from the patient’s skin (nasal, axillary, and antecubital areas), family members, admission bed linen, contacted health caregivers, and PFGE analysis suggested similar isolate was found from a family member who had been discharged from a tertiary care hospital in 10 days earlier (Figure 1).
B. pseudomallei was initially identified by the Vitek 2 platform with 80% probability and later confirmed with API 20NE (bioMérieux) and 16s-RNA sequencing.2,13 Using CLSI breakpoints the isolate was sensitive to meropenem, cotrimoxazole and resistant to amikacin, gentamicin, and colistin. Her fasting blood sugar was 76 mg/dL, HbA1c was 5.2% and the patient’s liver, renal, serum immunoglobulin profile, and neutrophil function was normal. Her anti-retroviral screening was negative and having common acquired and inherent immunodeficiencies may be excluded.
The majority of blood stream infections (BSI) are monomicrobial, but a recent study reported, bacteremia following polymicrobial infections accounts for 6%–34% of BSI8. The focus of infection following polymicrobial BSI are often associated with severe intra-abdominal, genitourinary, or skin and soft tissue infections. Compared to monomicrobial BSI, polymicrobial BSI are associated with high morbidity and mortality9. Polymicrobial BSI are usually caused by aerobic or facultative Gram-positive and Gram-negative bacteria10. In addition, a combination of aerobic and anaerobic bacteria is also documented11. Polymicrobial BSI are frequently found in elderly patients and also patients with underlying multiple chronic diseases.
Herein, concurrent BSI with S. epidermidis and B. pseudomallei was detected in a young, previously healthy woman. It is rare, and concurrent BSI with S. epidermidisand B. pseudomallei is a rare event and not documented in the literature. If the same strain of S. epidermidiswas recovered from two or more separate venipuncture samples, then it may be considered as a probable pathogen.12 This strain was continuously isolated from multiple blood samples taken from different venipuncture sites at different time intervals thereby suggesting the occurrence of true BSI. Further PFGE and MLST confirmed all 4 isolates were similar. The patient had developed S. epidermidis bacteremia without a focus, and the possible source of infection could be the skin. As S. epidermidis is part of human normal flora, following minor skin abrasions bacteremia can be developed. Since the patient is a farmer, the possibility of developing skin abrasions is high.
In contrast, B. pseudomallei is always regarded as a true pathogen and is found in Sri Lanka.1-3 Farming in the tropics poses a risk of acquiring B. pseudomallei. It can be contracted following inoculation through minor skin abrasions or inhalation of contaminated dusts. Also, it can be found following reactivation due to S. epidermidis bacteremia. However, our patient had not had fever or any symptoms in past 3 to 4 years, which suggests a low possibility of reactivation.13The development of co-infection following S. epidermidis may pose several source possibilities, and results from PFGE pulsotypes showed similar isolate was found in a family member who had been discharged from a tertiary care hospital 10 days previously. However, based on the PFGE finding we cannot guarantee the original source and probably the isolate could be found in the normal flora of both the patient and the family member.
Even with appropriate S. epidermidisantimicrobial therapy, persistence of bacteremia, associated breakthrough fever, and rise of CRP and PCT suggested the possibility of super-infection, cryptic infection, or the emergence of vancomycin resistance.14 The presence of B. pseudomallei in a subsequent blood culture highlighted the occurrence of concurrent bacteremia. Having high anti-B. pseudomalleititer also confirmed the disease. Vancomycin MIC did not creep. No recent hospitalization, foreign body insertion and transthoracic-2D-echocardiography was insignificant, suggesting S. epidermidis bacteremia without a focus.The chest-CT, chest X-rays, USS abdomen/pelvis and bone scan were normal and were not able to find the focus of infection for melioidosis. Clinical vigilance has provoked to conduct repeated blood cultures and in turn was able to identify a fatal pathogen and to treat appropriately.2-3
The development of polymicrobial BSI in an immunocompetent patient is rare. Furthermore, the co-infection of S. epidermidis and B. pseudomallei is rare. Clinical vigilance has provided an opportunity to detect the possibly fatal pathogen in advance and ultimately proceed to complete cure.
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https://doi.org/10.14202/IJOH.2017.7-11
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