Thursday, November 30, 2023
|
Characteristics |
Total, n = 130 |
C. striatum, n = 27 |
MRSA, n = 103 |
p value |
|---|---|---|---|---|
| Sex | ||||
| M | 92 (70.8) | 18 (66.7) | 74 (71.8) | 0.60 |
| F | 38 (29.2) | 9 (33.3) | 33 (32.0) | |
| Median age (interquartile range) | 71.0 (63.8–77.0) | 72.0 (66.0–80.0) | 71.0 (63.0–76.0) | 0.17 |
| Underlying disease or condition† | ||||
| Solid cancer | 32 (24.6) | 4 (14.8) | 28 (27.2) | 0.18 |
| Diabetes mellitus | 30 (23.1) | 6 (22.2) | 24 (23.3) | 0.91 |
| Structural lung disease | 24 (18.5) | 4 (14.8) | 20 (19.4) | 0.78 |
| Chronic obstructive lung disease | 12 (9.2) | 3 (11.1) | 9 (8.7) | 0.71 |
| Interstitial lung disease | 5 (3.8) | 0 | 5 (4.9) | 0.58 |
| Bronchiectasis | 4 (3.1) | 0 | 4 (3.9) | 0.58 |
| Destroyed lung due to tuberculosis | 1 (0.8) | 0 | 1 (1.0) | 1.00 |
| Pneumoconiosis | 1 (0.8) | 0 | 1 (1.0) | 1.00 |
| Bronchiolitis obliterans | 1 (0.8) | 1 (3.7) | 0 | 0.21 |
| Hematologic malignancy | 13 (10.0) | 5 (18.5) | 8 (7.8) | 0.14 |
| Liver cirrhosis | 11 (8.5) | 2 (7.4) | 9 (8.7) | 1.00 |
| End-stage renal disease | 7 (5.4) | 2 (7.4) | 5 (4.9) | 0.64 |
| Chronic renal failure | 6 (4.6) | 3 (11.1) | 3 (2.9) | 0.10 |
| Congestive heart failure | 3 (2.3) | 1 (3.7) | 2 (1.9) | 0.51 |
| Alcoholism | 2 (1.5) | 0 | 2 (1.9) | 1.00 |
| Cerebrovascular attack | 12 (9.2) | 5 (18.5) | 7 (6.8) | 0.13 |
| Solid organ transplantation | 2 (1.5) | 0 | 2 (1.9) | 0.63 |
| Hematopoietic stem cell transplantation | 3 (2.3) | 2 (7.4) | 1 (1.0) | 0.11 |
| Immunocompromised state‡ | 41 (31.5) | 14 (51.9) | 27 (26.2) | 0.01 |
| Recent chemotherapy | 23 (17.7) | 7 (25.9) | 16 (15.5) | 0.26 |
| Recent surgery, ≤1 mo | 19 (14.6) | 2 (7.4) | 17 (16.5) | 0.36 |
| Active smoker | 10 (7.7) | 1 (3.7) | 9 (8.7) | 0.69 |
| Neutropenia, <500 cells/mL | 8 (6.2) | 4 (14.8) | 4 (3.9) | 0.06 |
| Category of pneumonia | ||||
| Community-acquired | 6 (4.6) | 1 (3.7) | 5 (4.9) | 1.00 |
| Healthcare-associated | 37 (28.5) | 4 (14.8) | 33 (32.0) | 0.08 |
| Hospital-acquired | 63 (48.5) | 19 (70.4) | 44 (42.7) | 0.01 |
| Ventilator-associated | 24 (18.5) | 3 (11.1) | 21 (20.4) | 0.40 |
Table 1. Characteristics of adult patients with severe pneumonia caused by Corynebacterium striatum, Seoul, South Korea, 2014–2019*
*Values are no. (%) except as indicated. MRSA, methicillin-resistant Staphylococcus aureus.
†Patients could have ≥1 underlying disease or condition.
‡Defined as ≥1 of the following conditions: daily receipt of immunosuppressants, including corticosteroids; HIV infection; solid organ or hematopoietic stem cell transplant recipient; receipt of chemotherapy for underlying malignancy during the previous 6 months; or underlying immune deficiency disorder.
|
Pathogens identified |
No. (%) patients |
p value* |
|||
|---|---|---|---|---|---|
|
2014–2015, n = 200 |
2016–2017, n = 180 |
2018–2019, n = 185 |
Total, n = 565 |
||
| Total | 88 (44.0) | 66 (36.7) | 75 (40.5) | 229 (40.5) | 0.35 |
| Staphylococcus aureus | 27 (13.5) | 15 (8.3) | 8 (4.3) | 50 (8.8) | <0.01 |
| Methicillin-susceptible | 3 (1.5) | 0 | 3 (1.6) | 6 (1.1) | 0.24 |
| Methicillin-resistant | 24 (12.0) | 15 (8.3) | 5 (2.7) | 44 (7.8) | <0.01 |
| Corynebacterium striatum | 2 (1.0) | 7 (3.9) | 10 (5.4) | 19 (3.4) | 0.05 |
| Streptococcus pneumoniae | 4 (2.0) | 2 (1.1) | 1 (0.5) | 7 (1.2) | 0.43 |
| Legionella pneumophila | 1 (0.5) | 1 (0.6) | 0 | 2 (0.4) | 0.61 |
| Moraxella catarrhalis | 0 | 0 | 1 (0.5) | 1 (0.2) | 0.36 |
| Streptococcus pyogenes | 0 | 1 (0.6) | 0 | 1 (0.2) | 0.34 |
| Nocardia species | 0 | 0 | 1 (0.5) | 1 (0.2) | 0.36 |
| Enteric gram-negative bacilli | 18 (9.0) | 22 (12.2) | 20 (10.8) | 60 (10.6) | 0.59 |
| Klebsiella pneumoniae | 13 (6.5) | 14 (7.8) | 16 (8.6) | 43 (7.6) | 0.73 |
| Escherichia coli | 4 (2.0) | 4 (2.2) | 3 (1.6) | 11 (1.9) | 0.92 |
| Enterobacter cloacae | 1 (0.5) | 3 (1.7) | 2 (1.1) | 6 (1.1) | 0.54 |
| Citrobacter freundii | 1 (0.5) | 2 (1.1) | 0 | 3 (0.5) | 0.34 |
| Klebsiella oxytoca | 0 | 0 | 2 (1.1) | 2 (0.4) | 0.13 |
| Hafnia alvei | 0 | 0 | 1 (0.5) | 1 (0.2) | 0.36 |
| Nonenteric gram-negative bacilli | 47 (23.5) | 22 (12.2) | 37 (20.0) | 106 (18.8) | 0.02 |
| Acinetobacter baumannii | 24 (12.0) | 13 (7.2) | 23 (12.4) | 60 (10.6) | 0.20 |
| Pseudomonas aeruginosa | 19 (9.5) | 6 (3.3) | 11 (5.9) | 36 (6.4) | 0.047 |
| Stenotrophomonas maltophilia | 4 (2.0) | 2 (1.1) | 7 (3.8) | 13 (2.3) | 0.22 |
| Burkholderia cepacia | 0 | 0 | 1 (0.5) | 1 (0.2) | 0.36 |
| Acinetobacter lwoffii | 0 | 1 (0.6) | 0 | 1 (0.2) | 0.34 |
| Chryseobacterium indologenes | 0 | 1 (0.6) | 0 | 1 (0.2) | 0.34 |
| Chryseobacterium meningosepticum | 1 (0.5) | 0 | 0 | 1 (0.2) | 0.40 |
| Chlamydia pneumoniae | 1 (0.5) | 0 | 0 | 1 (0.2) | 0.40 |
Table 2. Bacterial pathogens detected among 565 adult patients with severe hospital-acquired pneumonia, Seoul, South Korea, 2014–2019
*p value based on χ2 test for trend.
|
Pathogens |
No. (%) co-infecting pathogens |
p value* |
||
|---|---|---|---|---|
|
Total, n = 130 |
C. striatum, n = 27 |
MRSA, n = 103 |
||
| Any | 50 (38.5) | 13 (48.1) | 37 (35.9) | 0.25 |
| Other bacteria | 28 (21.5) | 2 (7.4) | 26 (25.2)† | 0.045 |
| Pseudomonas aeruginosa | 7 | 0 | 7 | |
| Acinetobacter baumannii | 6 | 0 | 6 | |
| Klebsiella pneumoniae | 5 | 0 | 5 | |
| Escherichia coli | 4 | 1 | 3 | |
| Haemophilus influenzae | 2 | 0 | 2 | |
| Streptococcus pneumoniae | 2 | 0 | 2 | |
| Citrobacter freundii | 1 | 0 | 1 | |
| Enterobacter cloacae | 1 | 1 | 0 | |
| Elizabethkingia meningosepticum | 1 | 0 | 1 | |
| Klebsiella aerogenes | 1 | 0 | 1 | |
| Stenotrophomonas maltophilia | 1 | 0 | 1 | |
| Virus | 24 (18.5) | 9 (33.3)‡ | 15 (14.6)§ | 0.047 |
| Influenza virus | 8 | 4 | 4 | |
| Influenza virus A | 3 | 3 | 0 | |
| Influenza virus B | 1 | 1 | 1 | |
| Parainfluenza virus type 3 | 4 | 1 | 3 | |
| Rhinovirus | 3 | 1 | 2 | |
| Adenovirus | 3 | 1 | 2 | |
| Respiratory syncytial virus | 2 | 1 | 1 | |
| Respiratory syncytial virus A | 1 | 1 | 0 | |
| Respiratory syncytial virus B | 1 | 0 | 1 | |
| Human coronavirus | 2 | 1 | 1 | |
| 229E | 1 | 1 | 0 | |
| OC43/HKU1 | 1 | 0 | 1 | |
| Human metapneumovirus | 2 | 1 | 1 | |
| Bocavirus | 1 | 0 | 1 | |
| Enterovirus | 1 | 0 | 1 | |
| Fungus | 4 (3.1) | 4 (14.8)¶ | 0 | <0.01 |
| Aspergillus species | 4 (3.1) | 4 (14.8) | 0 | |
| Pneumocystis jirovecii | 1 (0.8) | 1 (3.7) | 0 | |
Table 3. Additional pathogens detected among adult patients with severe Corynebacterium striatum pneumonia and methicillin-resistant Staphylococcus aureus pneumonia, Seoul, South Korea, 2014–2019*
*Categories of co-infection were not mutually exclusive; some cases were associated with ≥2 categories of pathogens.
†Three patients were co-infected with 2 bacteria: H. influenzae and S. pneumoniae; E. coli and K. pneumoniae; and A. baumannii and K. pneumoniae.
‡One patient was co-infected with influenza A virus and human metapneumovirus.
§One patient was co-infected with bocavirus and rhinovirus.
¶One patient was co-infected with Aspergillus species and P. jirovecii.
|
Characteristics |
Total, n = 130 |
C. striatum, n = 27 |
MRSA, n = 103 |
p value |
|---|---|---|---|---|
| Clinical manifestation | ||||
| Dyspnea | 106 (81.5) | 25 (92.6) | 81 (78.6) | 0.16 |
| Fever, temperature >38°C | 103 (79.2) | 18 (66.7) | 85 (82.5) | 0.07 |
| Sputum | 92 (70.8) | 16 (59.3) | 76 (73.8) | 0.14 |
| Cough | 57 (43.8) | 11 (40.7) | 46 (44.7) | 0.72 |
| Altered mental status | 46 (35.4) | 10 (37.0) | 36 (35.0) | 0.84 |
| Diarrhea | 4 (3.1) | 2 (7.4) | 2 (1.9) | 0.19 |
| Septic shock at ICU admission | 81 (62.3) | 12 (44.4) | 69 (67.0) | 0.03 |
| Mechanical ventilation | 127 (97.7) | 27 (100) | 100 (97.1) | 1.00 |
| APACHE II score, mean (SD) | 25.6 (8.1) | 26.4 (11.9) | 26.0 (7.0) | 0.72 |
| SOFA score, mean (SD) | 9.5 (3.7) | 9.5 (3.4) | 9.5 (3.7) | 0.99 |
| Bacteremia | 19 (14.6) | 1 (3.7) | 18 (17.5) | 0.12 |
| Laboratory findings, median (IQR) | ||||
| Leukocyte count, cells/mL | 10,950 (7,800–15,625) | 11,600 (4,800–15,900) | 10,700 (8,400–15,600) | 0.26 |
| Platelets, × 103/mL | 159 (81–242) | 123 (55–230) | 171 (102–245) | 0.14 |
| C-reactive protein, mg/dL | 11.3 (5.5–19.3) | 13.6 (8.0–19.8) | 10.8 (5.4–18.6) | 0.61 |
| Procalcitonin, ng/mL | 1.1 (0.3–3.9) | 0.3 (0.1–1.3) | 1.8 (0.4–4.2) | <0.01 |
Table 4. Clinical and laboratory characteristics of patients with severe Corynebacterium striatum pneumonia and methicillin-resistant Staphylococcus aureus pneumonia, Seoul, South Korea, 2014–2019*
*Values are no. (%) except as indicated APACHE, acute physiology and chronic health evaluation; BAL, bronchoalveolar lavage; ICU, intensive care unit; IQR, interquartile range; MRSA, methicillin-resistant Staphylococcus aureus; SOFA, sequential organ failure assessment.
|
Outcome |
Total, n = 130 |
C. striatum, n = 27 |
MRSA, n = 103 |
p value |
|---|---|---|---|---|
| Death | ||||
| Total | n = 103 | n = 27 | n = 103 | NA |
| 30 days | 41 (31.5) | 11 (40.7) | 30 (29.1) | 0.25 |
| 60 days | 57 (43.8) | 14 (48.1) | 44 (42.7) | 0.61 |
| 90 days | 68 (52.3) | 16 (59.3) | 52 (50.5) | 0.42 |
| In-hospital | 73 (56.2) | 19 (70.4) | 54 (52.4) | 0.09 |
| Death among patient categories | ||||
| Nonimmunocompromised patients | n = 89 | n = 13 | n = 76 | NA |
| 30 days | 21 (23.6) | 5 (38.5) | 16 (21.1) | 0.18 |
| 60 days | 31 (34.8) | 5 (38.5) | 26 (34.2) | 0.76 |
| 90 days | 40 (44.9) | 7 (53.8) | 33 (43.4) | 0.49 |
| In-hospital | 40 (44.9) | 7 (53.8) | 33 (43.4) | 0.49 |
| Immunocompromised patients | n = 41 | n = 14 | n = 27 | NA |
| 30 days | 20 (48.8) | 6 (42.9) | 14 (51.9) | 0.59 |
| 60 days | 26 (63.4) | 8 (57.1) | 18 (66.7) | 0.55 |
| 90 days | 28 (68.3) | 9 (64.3) | 19 (70.4) | 0.73 |
| In-hospital | 33 (80.5) | 12 (85.7) | 21 (77.8) | 0.69 |
| Median ICU stay, d (IQR) | 14.0 (8.0–26.3) | 14.0 (9.0–27.0) | 14.0 (8.0–26.0) | 0.33 |
| Median hospital stay after ICU admission, d (IQR) | 29.5 (14.0–57.0) | 30.0 (16.0–81.0) | 29.0 (14.0–55.0) | 0.48 |
Table 5. Outcomes of adult patients with severe Corynebacterium striatum and methicillin-resistant Staphylococcus aureus pneumonia, Seoul, South Korea, 2014–2019*
*Values are no. (%) except as indicated. ICU, intensive care unit; MRSA, methicillin-resistant Staphylococcus aureus; NA, not applicable.
This activity is intended for infectious disease clinicians, pulmonologists, internists, hospitalists, intensivists, and other clinicians who treat and manage patients with or at risk for severe Corynebacterium striatum pneumonia.
The goal of this activity is for learners to be better able to describe the proportion, clinical characteristics, and outcomes of severe Corynebacterium striatum hospital-acquired pneumonia (HAP) in adults compared with those of severe methicillin-resistant Staphylococcus aureus HAP, based on a retrospective study of 27 severe Corynebacterium striatum pneumonia cases during 2014 to 2019 in Seoul, South Korea.
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We investigated the proportion and characteristics of severe C. striatum pneumonia compared with severe MRSA pneumonia. Although the proportion of severe MRSA HAP greatly decreased during 2014–2019, the proportion of severe C. striatum pneumonia sharply increased and surpassed that of severe MRSA pneumonia. C. striatum pneumonia was more commonly associated with immunocompromise, viral co-infection, and fungal co-infection. Mortality rates between the C. striatum and MRSA groups were comparable.
We found that the proportion of severe MRSA pneumonia decreased while severe C. striatum pneumonia greatly increased and that C. striatum emerged as one of the most common pathogens in patients with severe HAP. Strengthened infection control measures during the study period might have contributed to the decline of severe MRSA pneumonia[18]; however, severe C. striatum pneumonia demonstrated the opposite trend. Several possible explanations for this discrepancy exist. First, detection of C. striatum from respiratory specimens in clinical laboratories increased, possibly because experience among laboratory staff accumulated over time. Also, new reliable identification techniques, such as matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, were introduced and enabled precise and rapid detection and identification of bacteria in clinical samples, which might have contributed to the increased reports of severe C. striatum pneumonia[19,20]. Second, C. striatum can be resistant to infection control measures and can adhere to abiotic surfaces and form biofilms on various medical devices, such as feeding tubes, endotracheal tubes, and ventilators[21,22]. Some reports documented C. striatum strains with resistance to high-level disinfectants, such as 2% glutaraldehyde and other biocides[23,24]. These findings suggest that appropriate environmental infection control measures for C. striatum should be further investigated and implemented. Finally, hospital outbreaks also might have contributed to the seeming discrepancy. Colonized patients and contaminated inanimate objects could be reservoirs for prolonged outbreaks. However, when we chronologically analyzed the occurrence patterns according to time and place, we could not find any suggestions of notable outbreaks. Clinical observation alone creates difficulties and limitations in distinguishing outbreaks; therefore, future studies should include more detailed typing analysis of C. striatum isolates to identify and curb possible healthcare-associated outbreaks.
In this study, viral or fungal co-infection was more common in the C. striatum group, whereas other bacterial co-infection was more common in the MRSA group. This finding could represent the host factor because a greater proportion of C. striatum patients were in an immunocompromised state, which would make them vulnerable to opportunistic infections. Of note, fewer cases of bacterial coinfection were diagnosed in the C. striatum group, but the cause for this difference is uncertain. One possible explanation is that C. striatum might influence the behavior and fitness of other bacteria. A recent study reported that Corynebacterium species can reduce the toxicity of Staphylococcus aureus by exhibiting decreased hemolysin activity and displaying diminished fitness of in vivo coinfection[25]. Further targeted studies on this issue are needed.
We found that serum procalcitonin level was higher in the MRSA group than in the C. striatum group (median 1.8 ng/mL vs. 0.3 ng/mL). Some studies suggest that serum procalcitonin can be used as a marker for bacterial infection and to differentiate bacterial from viral infection or noninfectious causes of inflammation[26,27]. In 2017, a group of researchers in China reported that the median serum procalcitonin level of an S. aureus bacteremia group of patients was higher (1.18 ng/mL) than that of a coagulase-negative staphylococci bacteremia group (0.21–0.31 ng/mL)[28]. We speculate that infections caused by low-virulence bacteria, such as C. striatum in our study, might have low levels of procalcitonin and this warrants further investigation.
Mortality rates were similarly high in both groups, but septic shock at the time of initial clinical manifestation was less common in the C. striatum group. Immunocompromised conditions were more common in the C. striatum group, which could suggest that C. striatum is less virulent than MRSA. Host factor might contribute to the development of severe C. striatum–associated pneumonia and the subsequent outcomes; however, we noted no statistically significant differences in mortality rates between the 2 groups after stratification by immunocompromised conditions. The existence of co-infection and pathogen types (e.g., other bacteria, viruses, fungi) involved might have affected mortality rates, but we were unable to effectively evaluate each effect because of the small number of patients in each subgroup.
The first limitation of our study is that we used a single-center design and our results might not be replicable in other centers or hospital systems. In addition, as we mentioned previously, we were not able to effectively evaluate the sole contribution of C. striatum because co-infection with other pathogens was common among the patient cohort. Finally, we included all C. striatum isolates from sputum, endotracheal aspirate, and bronchoalveolar lavage, but the cultures were mostly semiquantitative, and some of the C. striatum isolates might have been nonpathogenic colonizers. A 2020 study from the United States reported that normal respiratory flora appears to have caused one quarter of CAP cases[29], which supports our finding that bacteria previously considered as colonizers or normal flora can be a cause of pneumonia.
In conclusion, we found C. striatum was associated with severe HAP. Patients with severe C. striatum pneumonia showed similar clinical and laboratory features as patients with severe MRSA pneumonia, and both infections were associated with high mortality rates. Further investigations could clarify incidence, clinical characteristics, and outcomes of severe C. striatum pneumonia in critically ill adults and determine whether infections are due to colonization, or community- or healthcare-acquired infections. Clinicians should be aware of this emerging pathogen as a possible cause for severe pneumonia, especially among immunocompromised patients.
