Indian Journal of Pathology and Microbiology

: 2015  |  Volume : 58  |  Issue : 1  |  Page : 130--132

Tubercular pleural effusion complicated with Elizabethkingia meningoseptica infection in a diabetic male

Gitanjali Sarangi1, Gautam Patnaik1, Padma Das2, Nirupama Chayani1, Jyoti Patnaik3,  
1 Department of Microbiology, S. C. B. Medical College and Hospital, Cuttack, Odisha, India
2 Department of Microbiology, AIIMS, Raipur, Chhattisgarh, India
3 Department of Pulmonary Medicine, S. C. B. Medical College and Hospital, Cuttack, Odisha, India

Correspondence Address:
Dr. Gitanjali Sarangi
Department of Microbiology, S. C. B. Medical College and Hospital, Cuttack - 753 007, Odisha

How to cite this article:
Sarangi G, Patnaik G, Das P, Chayani N, Patnaik J. Tubercular pleural effusion complicated with Elizabethkingia meningoseptica infection in a diabetic male.Indian J Pathol Microbiol 2015;58:130-132

How to cite this URL:
Sarangi G, Patnaik G, Das P, Chayani N, Patnaik J. Tubercular pleural effusion complicated with Elizabethkingia meningoseptica infection in a diabetic male. Indian J Pathol Microbiol [serial online] 2015 [cited 2022 Jan 23 ];58:130-132
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Full Text


Elizabethkingia meningoseptica is a nonfermentative, nonmotile, oxidase positive Gram-negative rods that are widely distributed in nature. In 1959, an American bacteriologist Elizabeth O. King at Centers for Disease Control (CDC), Atlanta discovered it and named it as Flavobacterium meningosepticum or CDC-IIa. Subsequently in 1994 it was renamed as Chryseobacterium menigosepticum by Van Damme et al. [1] The organism mostly causes meningitis in premature and newborn infants and rarely causes pneumonia, endocarditis, and meningitis associated with severe underlying illness in adults. Accurate diagnosis of E. menigoseptica is important because the species is usually resistant to multiple antibiotics including extended spectrum beta-lactam agents and aminoglycosides. Here, we report a case of tubercular pleural effusion complicated with E. meningoseptica infection in a diabetic male.

A 46-year-old man presented to the outpatient department of pulmonary medicine with complaints of left sided chest pain for 2 days. The patient was also experiencing a mild degree of fever with nonproductive cough and dyspnea since 2 weeks. He did not have a headache, nausea, dysphagia, or dysuria. The patient had no history of smoking or alcohol intake. He was a known case of diabetes mellitus (type 2) for last 6 years and under treatment with oral hypoglycemic.

On clinical examination, he had a temperature of 38°C, heart rate 112 beats/min, blood pressure of 130/70 mm Hg and respiratory rate of 22 breaths/min. Auscultation of the chest revealed poor air entry with the crepitation in the left lower hemi-thorax of the lung and heart rhythm was normal without any murmur. The abdomen was soft with normal bowel sounds. Chest X-ray [Figure 1] and computed tomography scan of the chest [Figure 2] showed left sided pleural effusion. Routine hemogram showed a white cell count of 12.3 × 10 3 /mm 3 , differential count N53, L38, E7, M2, B0, hemoglobin = 10.5 g/dl, and a total platelet count of 300 × 10 3 /ml, 1 st h erythrocyte sedimentation rate-55 mm; fasting blood sugar-195 mg/dl and 2 h postprandial blood sugar-282 mg/dl. Other parameters such as blood urea, creatinine and liver function test were within normal limits. The pleural fluid was drained aseptically and sent for routine investigation and culture. Biochemical evaluation of pleural fluid revealed a pH of 7.2, glucose 58 mg/dl, protein 4.6 g/dl, lactate dehydrogenase 382 U/L, adenosine deaminase (ADA) >70 U/L with lymphocytic predominance. No growth was detected in the conventional aerobic culture method. Examination of sputum was negative for acid-fast bacillus, and no growth was detected on routine aerobic culture. Based on the clinical signs and symptoms and elevated ADA level, the patient was diagnosed to be a case of tubercular pleural effusion with uncontrolled diabetes mellitus. He was treated with insulin and antitubercular drugs. However, the patient remained febrile with breathlessness even after 2 weeks of treatment with antituberculosis treatment (ATT). Pleural fluid was again drained aseptically and sent to the microbiology department for investigation. Simultaneously a blood culture was also sent. Biochemical analysis of the pleural fluid revealed a pH of 6.9, glucose 48 mg/dl, protein 3.3 g/dl, ADA 60 U/L. Gram stain examination of pleural fluid showed a good number of pus cell with few Gram-negative bacilli. Culture on blood agar showed small translucent low convex nonhemolytic colonies after 48 h of aerobic incubation. On nutrient agar smooth circular (diameter 1-2 mm) yellow pigmented colonies were observed, but no growth was seen on Mac Conkey agar.{Figure 1}{Figure 2}

The organism was identified to be E. meningoseptica by conventional biochemical reactions and was confirmed by a VITEK ID-GNB (Vitek 2, Bio merieux, France) identification system. The blood culture also revealed growth of the same organism on first sub-culture.

The antibiotic susceptibility of the isolate was determined by the disk diffusion method. The Clinical and Laboratory Standards Institute criteria for Gram-negative and Gram-positive bacteria were used to interpret the antimicrobial susceptibility as no recommendations regarding breakpoints are available for this pathogen. The isolate was sensitive to vancomycin, levofloxacin, piperacillin-tazobactam, trimethoprim-sulfamethoxazole, ceftazidime and resistant to amikacin ceftriaxone and penicillin.

An environmental sampling was also done, and culture found to be negative for E. meninigoseptica.

The patient was successfully treated with ceftazidime for 2 weeks and trimethoprim-sulfamethoxazole for 4 weeks and recovered completely. The patient was advised to continue ATT and insulin injection with regular interval of check-ups. Subsequent visits were uneventful.

The genus Chryseobacterium originally comprised of six species of yellow pigmented nonmotile, catalase positive, oxidase positive, nonglucose fermenting Gram-negative bacilli that are ubiquitous in nature and are found in plants, soil, food and both fresh and marine water. Six species of Chryseobacterium that are more commonly isolated from clinical specimen are: C. meningosepticum, C. odoratum, C. multivorum, C. brevi and group IIb Chryseobacterium species which includes C. indulgenes and C. gleum. However, in 2005 C. meningosepticum and C. miricola were placed in a different genus Elizabethkingia based on 16S rRNA sequence. [2] E. meningoseptica is the most pathogenic member of the genus.

Strains of Elizabethkingia have rarely been reported to cause infection among immunocompetent adults accounting for only 1-2% of Gram-negative rods isolated in microbiologic culture. Immunocompromised status including malignancy, neutropenia, diabetes, organ transplant, steroid use, malnutrition or being on dialysis may predispose to infection. [3] Colonization in patients via contaminated medical devices such as respirators, endotracheal or tracheostomy tubes, mist tents, humidifiers, incubators for new-born, syringes, etc. has been demonstrated. In the literature most of the reported cases of E. meningosepticum infection were found to be a hospital acquired, and they had usually occurred in immunodeficient patients. The infection that has been described here was considered to be a hospital acquired as the initial pleural fluid culture was sterile, and the subsequent pleural fluid culture was positive for this organism. The isolation of E. meningoseptica from the blood culture, further confirms the pathogenicity and excludes the possibility of a particular isolated strain as a contaminant in this particular case. The possible source of infection could not be traced as the environmental sample culture for E. meninigoseptica was negative. There are also several reports where no source could be identified despite extensive investigations and culture of environmental samples. [4]

Elizabethkingia meningoseptica has unusual resistance pattern and mechanism. They are resistant to multiple antimicrobials, especially to the β-lactams. There is always a discrepancy in sensitivity pattern by disk diffusion and broth dilution. However, in one study a good correlation was found between agar dilution and disc diffusion method for piperacillin, ceftazidime, and ciprofloxacin against E. meniningoseptica and disk diffusion break point were proposed. [5] In our case, we could able to perform a disk diffusion test and the pa tient was treated successfully with a combination of ceftazidime and trimethoprim-sulfamethoxazole.

To conclude, E. meningoseptica can be considered as a potential opportunistic pathogen and should always be kept in mind as a possible etiological agent of suspected nosocomial infections especially in patients with immunocompromised status. Proper management of infection by this rare organism warrants correct identification and sensitivity testing of such isolate by the microbiology laboratory personnel.


1Hsueh PR, Hsiue TR, Wu JJ, Teng LJ, Ho SW, Hsieh WC, et al. Flavobacterium indologenes bacteremia: Clinical and microbiological characteristics. Clin Infect Dis 1996;23:550-5.
2Kim KK, Kim MK, Lim JH, Park HY, Lee ST. Transfer of Chryseobacterium meningosepticum and Chryseobacterium miricola to Elizabethkingia gen. nov. as Elizabethkingia meningoseptica comb. nov. and Elizabethkingia miricola comb. nov. Int J Syst Evol Microbiol 2005;55:1287-93.
3Abrahamsen TG, Finne PH, Lingaas E. Flavobacterium meningosepticum infections in a neonatal intensive care unit. Acta Paediatr Scand 1989;78:51-5.
4Maraki S, Scoulica E, Manoura A, Papageorgiou N, Giannakopoulou C, Galanakis E A. Chryseobacterium meningosepticum colonization outbreak in a neonatal intensive care unit. Eur J Clin Microbiol Infect Dis 2009;28:1415-9.
5Chang JC, Hsueh PR, Wu JJ, Ho SW, Hsieh WC, Luh KT. Antimicrobial susceptibility of flavobacteria as determined by agar dilution and disk diffusion methods. Antimicrob Agents Chemother 1997;41:1301-6.