|Year : 2010 | Volume
| Issue : 2 | Page : 94-98
Melioidotic pericardial effusion
Thomas S Kuruvilla, Meena Dias, Uttam Udayan, Zevita Furtado
Department of Microbiology, Father Muller Medical College, Mangalore, Karnataka, India
|Date of Web Publication||28-Mar-2012|
Thomas S Kuruvilla
Department of Microbiology, Father Muller Medical College, Kankanady, Mangalore - 575 002, Karnataka
Aim is to present a rare case of purulent pericardial effusion caused by Burkholderia pseudomallei. Pericardial sample was inoculated into Bactec Peds Plus/F broth of the Bactec automated system. After the system flagged positive, the broth was subjected to Gram stain, biochemical tests and drug susceptibility. The organism was identified as Burkholderia pseudomallei. Tuberculosis (TB) is the most common cause of pericarditis in countries where it remains a major public health problem, but in the western coastal districts of India, clinicians and microbiologists alike must be aware of Burkholderia pseudomallei a rare cause of pericarditis that can be misdiagnosed as TB pericarditis.
Keywords: Burkholderia, melioidosis, pericardial effusion, tubercular pericarditis
|How to cite this article:|
Kuruvilla TS, Dias M, Udayan U, Furtado Z. Melioidotic pericardial effusion. Indian J Med Sci 2010;64:94-8
| ¤ Introduction|| |
Burkholderia pseudomallei is a Gram negative bacterium, commonly found in the soil of tropical countries especially in the agricultural belts. These saprophytes are endemic in Southeast Asia and Northern Australia.  It causes a condition called melioidosis which is now an emerging infection in India. Melioidosis leads to abscesses in lungs, liver, spleen, musculoskeletal system, prostate and even sepsis. In some tourist destinations, such as parts of northern Thailand, it is the cause of 20% of community-acquired septicaemias, and 50% of sepsis-related deaths.  Infection may follow an acute or sub-acute course, and may affect one or more of any organ system, resembling a wide range of alternative infectious diseases, from tuberculosis to mumps. Hence, diagnosis relies on being able to identify those patients at risk, an accurate travel history, a high degree of clinical suspicion and an experienced laboratory. 
| ¤ Case Report|| |
A 37 year old male, residing near Mangalore, an agriculturalist by profession since ten years came to our hospital with 20 day history of high grade fever with chills and myalgia. He had associated breathlessness and chest pain. He has no past history of diabetes mellitus, bronchial asthma, tuberculosis or hypertension. On general physical examination he was febrile, pulse rate 72/min, blood pressure of 124/80 mm Hg. He had pedal edema. CVS: Heart sounds were muffled. RESP: On auscultation bilateral basal crepitations were heard. P/A: Abdomen was distended with tenderness in the right hypochondriac region. Free fluid was present. Investigations: The chest radiograph showed cardiomegaly and air space opacities in both lungs. Ultrasonography revealed congestive hepatomeagaly, mild to moderate ascites, bilateral pleural effusion (left > right) and significant pericardial effusion. Echocardiography revealed a large pericardial effusion with tamponade features. Blood investigations showed a total count of 23,600 cells/cumm and an ESR of 55 mm/hr. Other biochemical and hematological parameters were within normal limits. Pericardiocentesis was done and a turbid, blood tinged fluid with coagulum was obtained. The pericardial fluid analysis showed WBC count of 3,800/cumm with predominant lymphocytes (76%) and neutrophils (24%). Gram stain revealed moderate pus cells, occasional mononuclear cells and no bacteria. The smear was negative for acid fast bacilli. Blood culture, tests for malarial parasite and HIV were negative. Based on the pericardial fluid profile, he was provisionally diagnosed to have tubercular pericardial effusion. He was empirically started on Inj. Piperacillin - Tazobactam 4.5 gm I.V Q 12 h and anti-tubercular treatment while awaiting the culture report. The pericardial fluid was inoculated into Peds plus/F Bactec vial of the Bactec 9120 automated blood culture system and also into conventional blood culture bottles. The Bactec culture flagged a positive within 24 hrs and the Gram stain from the bottle showed Gram negative bacilli with a typical bipolar staining "safety pin appearance" [Figure 1] arousing a suspicion. The Bactec bottle contents were streaked onto MacConkey and blood agar. After 18-24 hrs minute non-lactose fermenting colonies on MacConkey's agar and pin point non-hemolytic colonies on blood agar were noticed. The organism was motile, oxidase and catalase positive, a non fermenter, utilized citrate and did not produce indole and H 2 S or hydrolyse urea. It was presumptively identified as Pseudomonas spp. other than Pseudomonas aeruginosa.
On further incubation, the colonies on MacConkey's agar became pink, dry and wrinkled a typical feature of this organism [Figure 2]. The organism was characterized according to the standard procedures meant for Pseudomonas speciation. It utilized glucose, lactose and starch oxidatively, decarboxylated arginine, liquified gelatin, reduced nitrate and grew well at 42°C thus identifying it to be Burkholderia pseudomallei. Based on the antibiotic sensitivity pattern the patient was then started on Inj. Ceftazidime 1 gm IV q 8 h. The patients general condition improved dramatically over a week. Before discharge a repeat pericardiocentesis was done and no organism was isolated. On discharge he was advised oral Doxycycline 100mg twice daily and Trimethoprim-Sulfamethoxazole 160 mg/800 mg twice daily as eradication therapy for 20 weeks.
|Figure 1: Gram stain of pericardial fluid showing typical bipolar "safety pin appearance" of B. pseudomallei (arrows)|
Click here to view
| ¤ Discussion|| |
Burkholderia pseudomallei earlier known as Pseudomonas pseudomallei or Whitmore's bacillus, is a natural saprophyte widely distributed in soil, stagnant water of endemic areas. Burkholderia pseudomallei has emerged as a significant pathogen in the past few years.  Melioidosis which is a glanders like infectious disease of humans caused by B. pseudomallei presents with a varied clinical spectrum. Clinical manifestations are protean, varying from acute disseminated infection, to subacute, to chronic with high morbidity and mortality.  The predisposing risk factors for this infection is seen in agriculturalists, diabetics, chronic renal failure patients, prolonged steroid usage and alcoholics.  The mode of transmission is postulated to be through direct inoculation into damaged skin or mucous membranes or through inhalation.  The pathogenesis of melioidotic pericarditis is more likely to involve secondary seeding of the organisms after bacteremia, because two-thirds of cases studied by Ploenchan Chetchotisakd et. al had evidence of bacteremia (ie: The multifocal localized melioidosis and disseminated septicemic melioidosis cases) mainly affecting males. ,,, This was opposed to the presentation in our case as there was no bacteremia. Melioidosis can present clinically in acute or chronic forms.  Few cases of melioidosis pericarditis have been reported and most have presented as subacute to chronic, similar to a tuberculosis (TB) infection.  Melioidosis with cardiac involvement is rare and is often combined with septicemia, for which the mortality rate is 20-60%.  Our patient, had no features of septicaemia on arrival despite a 20 day history. The patient survived from cardiogenic and septic shock because of early intervention and aggressive treatment. Pericardial effusion should be drained to improve the tamponading effect, cardiac contractility and eventually improve cardiac output. Pericardiocentesis also lessens the likelihood of distinguishing TB and melioidosis and in the present study, the presence of underlying diseases considered to be a significant risk factor for melioidosis was not helpful in differentiating between the conditions clinically, by chest radiography or electrocardiography as there was no underlying disease in our case. The histology of the fluid analysis could speak in terms of tuberculosis but the major diagnostic test for melioidosis is pericardial fluid culture. By comparison, a pericardial histology examination is most useful when diagnosing TB, because almost 60% of patients will have positive acid-fast bacilli and 86% will have caseous granulomas or granulomatous inflammation. The latter pathological findings were not found in any of the patients with melioidosis pericarditis in Ploenchan Chetchotisakd et.al's study.  No growth was obtained from blood culture done during the initial period of illness and neither did we isolate B. pseudomallei from two sets of blood culture, during the course of the illness.
Antimicrobial susceptibility using the disc diffusion method in our hospital is also widely practised in melioidosis endemic areas, but may overestimate resistance to trimethoprim/sulfamethoxazole. The E-test is a better tool as compared to disc diffusion method for antimicrobial susceptibility testing for Burkholderia pseudomallei. B. pseudomallei, an emerging pathogen, is overlooked in many cases due to the low index of suspicion and awareness among microbiologists and clinicians. Therefore, due consideration should be given to this organism to know the true magnitude of melioidosis in our country. As B. pseudomallei is a non fastidious organism without any exacting growth requirements, all non fermenters should be subjected to speciation as a part of routine microbiological work up. Melioidosis pericarditis should be considered in patients presenting with clinical presentations of subacute to chronic pericarditis and laboratory findings that cannot be differentiated from tuberculous pericarditis, except by the results of pericardial culture and pathology. 
In conclusion, early diagnosis, simple pericardiocentesis and appropriate antibiotic treatment for melioidosis can significantly reduce the mortality rate. As melioidosis has a propensity for multi-organ involvement, physicians should look for pericardial involvement and keep in mind that an infection with B. pseudomallei particularly in endemic regions can simulate tubercular pericarditis.
| ¤ References|| |
|1.||Northfield J, Whittyn CJ, MacPhee IA. Burkholderia pseudomallei infection, or melioidosis, and nephrotic syndrome. Nephrol Dial Transplant 2002;7:137-9. |
|2.||Walsh AL, Wuthiekanun V. The laboratory diagnosis of melioidosis. Br J Biomed Sci 1996;53:249-53. |
|3.||Sanford JP. Pseudomonas species (including melioidosis and Glanders) Chapter 197. In: Principles and Practice of Infectious diseases. 3 rd ed. Mandel, Douglas, Bennet, editors. London: Churchill Livingstone; 1990. p. 1693-4. |
|4.||Chetchotisakd P, Anunnatsiri S, Kiatchoosakun S, Kularbkaew C. Melioidosis pericarditis mimicking tuberculous pericarditis. Clin Infect Dis 2010;51: e46-9. |
|5.||How SH, Liam CK. Melioidosis: A potentially life threatening infection. Med J Malaysia 2006;61:386-94. |
|6.||Forbes BA, Sahm DF, Weissfield AS. Pseudomonas, Burkholderia and similar organisms Chapter 31 Bailey and Scott's Diagnostic Microbiology. 10th ed. St. Louis: Mosby Co.; 1998. p. 448-50. |
|7.||Ruff MJ, Lamkin N Jr, Braun J, Barnwell P. Melioidosis complicated by pericarditis. Chest 1976;69:227-9. |
|8.||Majid AA. Successful surgical management of a case of pulmonary and pericardial melioidosis. Aust N Z J Surg 1990;60:139-41. |
|9.||Lim KB, Oh HM. Melioidosis complicated by pericarditis. Scand J Infect Dis 2007;39:357-9. |
|10.||Chung HC, Lee CT, Lai CH, Huang CK, Lin JN, Liang SH, et al. Non-septicemic melioidosis presenting as cardiac tamponade. Am J Trop Med Hyg 2008;79:455-7. |
|11.||Wuthiekanun V, Cheng AC, Chierakul W, Amornchai P, Limmathurotsakul D, Chaowagul W, et al. Trimethoprim/sulfamethoxazole resistance in clinical isolates of Burkholderia pseudomallei. J Antimicrob Chemother 2005;55:1029-31. |
[Figure 1], [Figure 2]