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| CASE REPORT |
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| Year : 2016 | Volume
: 18
| Issue : 1 | Page : 40-43 |
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A case of melioidosis from splenic abscess
Ashish Jitendranath, L Bhargavi, JT Ramani Bai, R Radhika
Department of Microbiology, Sree Gokulam Medical College and Research Foundation, Trivandrum, Kerala, India
| Date of Web Publication | 28-Jun-2016 |
Correspondence Address:
Ashish Jitendranath
Department of Microbiology, Sree Gokulam Medical College and Research Foundation, Trivandrum, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0972-1282.184765
Melioidosis is a suppurative chronic infection caused by a Gram-negative bacterium, Burkholderia pseudomallei. A 41-year-old male diabetic patient presented with fever and abdominal pain. On computed tomography scan, he was found to have splenic abscess. Culture of splenic tissue yielded B. pseudomallei. He was treated with Ceftazidime and Cotrimoxazole. Keywords: Burkholderia pseudomallei, melioidosis, splenic abscess
How to cite this article:
Jitendranath A, Bhargavi L, Ramani Bai J T, Radhika R. A case of melioidosis from splenic abscess. J Acad Clin Microbiol 2016;18:40-3 |
| Introduction | |  |
Burkholderia pseudomallei orWhitmore's bacillus, earlier known as Pseudomonas pseudomallei, has emerged as a significant pathogen in the past few years.[1] Melioidosis was an important cause of morbidity and mortality in foreign troops fighting in Southeast Asia. About 100 cases occurred among French forces in Indochina between 1948 and 1954. By 1973, 343 cases had been reported in American troops fighting in Vietnam. Concerns of reactivation of latent infection in soldiers returning from Vietnam, with estimates from serology studies of approximately 225,000 potential cases, resulted in melioidosis being called the “Vietnamese time bomb.”[1]
Melioidosis, an infectious disease caused by B. pseudomallei, is a soil saprophyte. It was originally restricted to tropical and subtropical areas of Southeast Asia and Australia,[2] where it causes infections with protean manifestations.[3] Now, it is an emerging infectious disease in India.[4] In acute form, it has no pathognomonic features. The differential diagnosis is very wide, and definite diagnosis depends on culture.[5],[6]
| Case Report | | |
A 41-year-old male patient from Pathanamthitta, Kerala, India, working in Kuwait since 2010, who was on treatment for diabetes mellitus for 15 years, presented with high-grade fever, left-sided upper abdominal pain and left shoulder pain of five months duration. Complete blood count showed neutrophilic leucocytosis (TC = 29,500 cells/mm 3) and erythrocyte sedimentation rate was 103 mm.
Computed tomography abdomen showed multiple well defined, hypodense regions within the spleen. Minimal perisplenic fat stranding and nodularity was seen along the anterior aspect of spleen in the mid region. Small peripheral enhancing 14 × 9 mm hypodense collection was seen in left sub-phrenic space.
He was advised surgery and was started on Cefoperazone Sulbactam. Splenectomy was done. Tissue samples were sent for culture and biopsy.
Biopsy of the tissue showed suppurative palisading granulomatous lesion with central necrosis. Acid-fast bacill were not seen on Ziehl–Neelsen staining. Gomori's methenamine silver and periodic acid staining for fungal elements were negative. Differential diagnosis included cat scratch diseases, Brucellosis More Details, tularaemia, atypical mycobacteria and lymphogranuloma venereum.
Tissue sample and a wound swab from post-operative site were sent for culture and sensitivity.
Direct microscopy showed numerous pus cells and short Gram-negative bacill with bipolar staining.
Blood agar showed minute greyish white, non-haemolytic smooth colonies with a slight metallic sheen after 24 h incubation which turned into large, flat, dry, wrinkled colonies with umbonation after 72 h [Figure 1].
Nutrient agar showed minute greyish white, smooth colonies with a slight metallic sheen after 24 hrs incubation which turned into large, flat, dry, wrinkled colonies with umbonation after 72 hrs [Figure 2].
On MacConkeys agar, non-lactose-fermenting colonies were seen, which on further incubation became pale pink, flat, dry and wrinkled colonies [Figure 3] and [Figure 4].
Ashdown agar showed smooth colonies with slight metallic sheen on overnight incubation which transformed into wrinkled, rough purple colonies with central umbonation and characteristic corn flower-head appearance after 72 h.
The isolate was identified as B. pseudomallei based on the following:
- Bipolar appearance on Gram staining [Figure 5] and [Figure 6]
- Characteristic identifying features
- Positive oxidase reaction
- Motile
- Grows at 42°C
- Indole negative
- Citrate utilised
- Triple sugar iron agar - no change
- Mannitol not fermented, nitrate is reduced
- Arginine dihydrolase positive
- Resistant to Gentamicin and Colistin
- Sensitive to Amoxicillin-Clavulanate and Ceftazidime
Antibiotic susceptibility testing was performed by the disk diffusion test according to the CLSI guidelines. It was sensitive to Ceftazidime, Meropenem, Amoxicillin – Clavulanate, Imipenem, Cotrimoxazole and Tetracycline and resistant to Gentamicin, Amikacin, Netilmicin and Colistin [Figure 7].
Preoperatively, patient was started on Cefoperazone Sulbactam. There was a recurrence of fever 2 days after surgery, and he was started on Meropenem. Diagnosis of melioidosis was confirmed, and he was started on Ceftazidime and Doxycycline for 10 days. He improved symptomatically and was discharged after 10 days and advised to continue on Doxycycline for three months.
| Discussion | | |
Persons, who have regular contact with soil or ground water, most often get infection with B. pseudomallei, especially during the monsoon season, probably through pre-existing skin lesions or penetrating wounds, particularly, immunocompromised patients.[7]
Clinically melioidosis can present with fever, septicaemia and localised abscess in spleen, liver and lung.[4] Human infection occurs through direct inoculation, through direct contact with damaged skin or mucous membranes or through inhalation and ingestion of contaminated particles.[5] Diabetes is the single most important predisposing factor in meliodosis and our patient was diabetic since 15 years.[2],[8]
In regions where this disease is not endemic, it is often misidentified or discarded as environmental contaminants.[9]B. pseudomallei can be mistaken for Pseudomonas stutzeri species because they share several phenotypic characteristic and their colony morphology is very similar. Resistant pattern of B. pseudomallei is distinctive and helps in differentiating them from Pseudomonas species. Melioidosis may have a protracted course and a chance of relapse if proper antibiotic treatment is not continued for an adequate period of time. The bacteria are inherently resistant to many antibiotics that are commonly used against Gram-negative non-fermenters – such as Penicillin, Ampicillin, first generation and second generation Cephalosporins, Gentamicin, Tobramycin, Streptomycin and Polymyxin. Ertapenem, Tigecycline and Moxifloxacin – such as Tetracyclines, Chloramphenicol, the Quinolones and Ceftriaxone do not appear to be clinically useful in the intensive phase.[10]B. pseudomallei isolates are intrinsically resistant to all aminoglycosides (via an efflux pump mechanism), but sensitive to Amoxicillin Clavulanic acid. This pattern is not seen in Pseudomonas species.[11],[12],[13],[14]
The preferred antibiotics are Ceftazidime or Meropenem, especially in the initial intensive therapy stage given intravenously every 6-8 h. Ceftazidime was the first antibiotic to produce a well-defined improvement in mortality. Ceftazidime has been found to be more effective than other third generation Cephalosporins.[1],[9],[11] In cases of abscess, duration of initial intensive therapy is 10-15 days to achieve resolution and to avoid chances of relapse, there is an eradication oral therapy of Cotrimoxazole or Doxycycline for 20 weeks.[1],[3]
Over the years, there has been a steady increase of cases isolated from the Indian subcontinent with various clinical manifestations such as septicaemia, arthritis, liver abscess and splenic abscess.[9] Due to this upsurge in cases, a diagnosis of melioidosis should be considered in cases of abscess associated with predisposing factors.[9] Proper precautions need to be taken while diagnosing B. pseudomallei as it is Level III biohazard agent. Despite adequate antibiotic therapy, melioidosis is associated with high mortality rate. This case report highlights melioidosis as a cause of splenic abscess and stresses the need for early diagnosis because the treatment of this infection requires specific intensive and eradication therapy for longer periods.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Jesudason MV, Kumar RS, John TJ. Burkholderia pseudomallei- An emerging pathogen in India. Indian J Med Microbiol 1997;15:1-2. |
| 3. | Mukhopadhya A, Balaj V, Jesudason MV, Amte A, Jeyaman R, Kurian G. Isolated liver abscesses in melioidosis. Indian J Med Microbiol 2007;25:150-1. [ PUBMED]  |
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| 5. | Yee KC, Lee MK, Chua CT, Puthucheary SD. Melioidosis, the great mimicker: A report of 10 cases from Malaysia. J Trop Med Hyg 1988;91:249-54. |
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| 7. | Rode JW, Webling DD. Melioidosis in the Northern territory of Australia. Med J Aust 1981;1:181-4. |
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| 10. | E, Vidal DR, Girardet M, Cavallo JD. Antibiotic susceptibility of 65 isolates of Burkholderia pseudomallei and Burkholderia mallei to 35 antimicrobial agents. J Antimicrob Chemother 2004;54:1134-8. |
| 11. | Mukhopadhyay C, Eshwara VK, Hattangad VB. Melioidosis. J Acad Clin Microbiol 2013;15:11-8. |
| 12. | Dhodapkar R, Sujatha S, Sivasangeetha K. Burkholderia pseudomallei infection in a patient with diabetes presenting with multiple splenic abscesses and abscess in the foot: A case report. Cases J 2008;1:224. |
| 13. | CDC Guidelines on Treatment of Melioidosis, 2012. Available from: . [Last accessed on 2012 Jan 16]. |
| 14. | Moore RA, DeShazer D, Reckseidler S, Weissman A, Woods DE. Efflux-mediated aminoglycoside and macrolide resistance in Burkholderia pseudomallei. Antimicrob Agents Chemother 1999;43:465-70. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
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