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| CASE REPORT |
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| Year : 2023 | Volume
: 3
| Issue : 2 | Page : 61-63 |
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Melioidosis with amoebic coinfection presenting as multifocal liver and splenic abscess
R Aravind1, Dinu Abirami Premkumar1, Lokeshwari Gopal2, Joy Varghese1
1 Department of Hepatology and Transplant Hepatology, Gleneagles Global Health City, Chennai, Tamil Nadu, India
2 Department of Microbiology, Gleneagles Global Health City, Chennai, Tamil Nadu, India
| Date of Submission | 01-Jan-2023 |
| Date of Decision | 31-Jan-2023 |
| Date of Acceptance | 02-Feb-2023 |
| Date of Web Publication | 09-Mar-2023 |
Correspondence Address:
Joy Varghese
Department of Hepatology and Transplant Hepatology, Gleneagles Global Health City, Chennai - 600 100, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ghep.ghep_2_23
We present a case of chronic calcific pancreatitis with diabetes mellitus who presented with multifocal liver and splenic abscesses which were found to be a coinfection of Entamoeba histolytica and Burkholderia pseudomallei. The existence of concurrent infection by two such unrelated organisms provides an example of the enigma of infections in areas of decreased host resistance.
Keywords: Burkholderia pseudomallei, Entamoeba histolytica, liver abscess
How to cite this article:
Aravind R, Premkumar DA, Gopal L, Varghese J. Melioidosis with amoebic coinfection presenting as multifocal liver and splenic abscess. Gastroenterol Hepatol Endosc Pract 2023;3:61-3 |
How to cite this URL:
Aravind R, Premkumar DA, Gopal L, Varghese J. Melioidosis with amoebic coinfection presenting as multifocal liver and splenic abscess. Gastroenterol Hepatol Endosc Pract [serial online] 2023 [cited 2023 Mar 27];3:61-3. Available from: http://www.ghepjournal.com/text.asp?2023/3/2/61/371275 |
| Introduction | |  |
Melioidosis is a common infection in Southeast Asia and is increasingly recognized in India. The presentation may vary from localized to disseminated abscesses, pneumonia, and sepsis. India is endemic to amoebiasis and amoebic liver abscess accounts for 3%–9% of all cases of amoebiasis.[1] One of the serious complications of amoebic liver abscess is a secondary bacterial infection which occurs in approximately 20% of cases. Amoebiasis presenting as multiple liver and splenic abscesses are not uncommon and can be superinfected with pyogenic organisms.[2] Gram-negative rods such as Escherichia coli and Klebsiella pneumoniae are the most common organisms cultured from these abscesses.[3] The existence of concurrent infection by two such unrelated organisms provides an example of the enigma of infections in areas of decreased host resistance.[4] In our case, we were able to isolate entamoeba trophozoites and culture Burkholderia pseudomallei from the aspirated liver abscess.
| Case Reports | | |
A 53-year-old male, a known case of chronic calcific pancreatitis with diabetes mellitus for the past 7 years was referred to our institute as he was diagnosed with liver abscess. He was not on regular treatment for diabetes mellitus. He did not have the habit of consuming alcohol or smoking tobacco. He had high-grade fever with chills for 15 days with vague right hypochondrium discomfort for 1 week. There was no diurnal variation in the pattern of fever. The fever subsided transiently with antipyretics. He was admitted to a hospital elsewhere. His laboratory investigations were as mentioned in [Table 1].
His contrast-enhanced computed tomography abdomen revealed multiple splenic and liver abscesses. He was referred to our hospital for further management.
Positron emission tomography revealed an ill-defined Fluoro-Deoxy Glucose (FDG) avid conglomerate hypodense lesion with peripheral rim enhancement measuring approximately 36 mm × 28 mm × 35 mm in segment V of the liver with maximum standardized uptake value of 9.6 [Figure 1] and multiple small sub-centimetric ovoid hypodense lesions in segment VI, VIII, and VII. There was an ill-defined faintly FDG avid lesion in the splenic hilar region–suggestive of multiple Liver and splenic abscesses.
He underwent ultrasound-guided aspiration of segment V liver abscess which revealed anchovy sauce pus. The wet mount of the collected pus sample revealed trophozoites of Entamoeba histolytica [Figure 2]. Pus culture also revealed the growth of B. pseudomallei [Figure 3] which was sensitive to the carbapenem group of antibiotics. The patient received injection metronidazole 750 mg and injection meropenem 1 g intravenously three times a day. His clinical condition improved within 5 days of therapy. He was discharged with IV antibiotics. Now, he is on regular follow-up. | Figure 2: Wet mount showing Trophozoites of Entamoeba histolytica (marked by blue arrow) with an eccentrically placed nucleus and ingested red blood cells
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 | Figure 3: Pinkish dry non lactose fermenting colonies with definite metallic sheen seen at 48 h of incubation in MacConkey agar plate
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| Discussion | | |
Liver abscesses are the most common type of visceral abscess. The annual incidence of the liver abscess has been estimated at 2.3 cases per 100,000 people and is higher among men than women (3.3 vs. 1.3 per 100,000 people).[5] The incidence is higher in east Asian countries (up to 17.6/100000 people).[6] Melioidosis is caused by B. pseudomallei a Gram-negative bipolar, safety pin-shaped bacillus. Familiarity with different presentations of this infection is essential for early diagnosis as delayed diagnosis contributes to increased mortality and morbidity. Diabetes mellitus is found in up to 60.9% of affected patients.[7] In our case uncontrolled diabetes could have been the important risk factor. The spectrum of clinical presentations ranges from asymptomatic or minor localized abscess or nodule to severe, fulminant diseases such as shock, multi-organ abscesses, and death. Treatment of melioidosis has two phases, the intravenous intensive phase, followed by the eradication phase. In deep-seated collection, intensive phase is for 4 weeks with injection of ceftazidime 2 g IV thrice daily or injection meropenem 1 g IV 8th h followed by 3 months of maintenance therapy. In severe infections including neurological disease, initial intensive therapy is prolonged for 6–8 weeks. It is followed by an eradication phase with oral cotrimoxazole for the next 6 months.[8]
E. histolytica infection can be contracted through consumption of fecal contamination of water or food, containing mature cysts. The parasite releases trophozoites in the small intestine, that penetrate the mucosa of the colon causing flask-shaped ulcers (intestinal disease). These trophozoites can infect various organs by gaining access to the portal venous system (extraintestinal disease). The amoeba triggers an inflammatory reaction thereby necrotizing the hepatocytes to form an abscess. This occurs in 3%–9% of entamoeba infections.[9] The difference between amoebic liver abscess and pyogenic liver abscess is described in [Table 2].
Our case is by far the first case report of B. pseudomallei coexistence with E. histolytica in a liver abscess.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Sharma MP, Sarin SK. Amoebic liver abscess in a North Indian hospital – Current trends. Br J Clin Pract 1987;41:789-93.  |
| 2. | Tayal A, Lal P, Uppal B. Single and multiple liver abscesses in adults in Delhi are amoebic in origin: A clinical and microbiological study. Trop Doct 2013;43:77-9. |
| 3. | Kurland JE, Brann OS. Pyogenic and amebic liver abscesses. Curr Gastroenterol Rep 2004;6:273-9. |
| 4. | Kakeya H, Izumikawa K, Yamada K, Obata Y, Nishino T, Takazono T, et al. Three cases of concurrent infection with Mycobacterium tuberculosis and Cryptococcus neoformans. Intern Med 2014;53:1685-92. |
| 5. | Huang CJ, Pitt HA, Lipsett PA, Osterman FA Jr., Lillemoe KD, Cameron JL, et al. Pyogenic hepatic abscess. Changing trends over 42 years. Ann Surg 1996;223:600-7. |
| 6. | Tsai FC, Huang YT, Chang LY, Wang JT. Pyogenic liver abscess as endemic disease, Taiwan. Emerg Infect Dis 2008;14:1592-600. |
| 7. | White NJ. Melioidosis. Lancet 2003;361:1715-22. |
| 8. | Sullivan RP, Marshall CS, Anstey NM, Ward L, Currie BJ. 2020 review and revision of the 2015 Darwin melioidosis treatment guideline; Paradigm drift not shift. PLoS Negl Trop Dis 2020;14:e0008659. |
| 9. | Espinosa-Cantellano M, Martínez-Palomo A. Pathogenesis of intestinal amebiasis: From molecules to disease. Clin Microbiol Rev 2000;13:318-31. |
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]
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