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| Year : 2016 | Volume
: 59
| Issue : 3 | Page : 417-419 |
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| Neurological melioidosis presenting as intracranial abscess |
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Deepak Madi1, Santosh P. V. Rai2, K Vidyalakshmi3, K Nithyananda Chowta1
1 Department of Internal Medicine, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India
2 Department of Radiology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India
3 Department of Microbiology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India
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| Date of Web Publication | 10-Aug-2016 |
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 Abstract | | |
Melioidosis is an emerging disease in our country caused by the bacteria Burkholderia pseudomallei. Melioidosis can virtually affect any organ. It has varying clinical presentations ranging from pneumonia to fatal sepsis. Central nervous system (CNS) involvement in melioidosis is rare. We present a case of CNS melioidosis from South India. As the incidence of diabetes is increasing in our country varying manifestations of melioidosis will be seen in routine clinical practice. Melioidosis should be considered in the differential diagnosis of intracranial abscess and meningoencephalitis, especially in diabetics. Keywords: Burkholderia pseudomallei, central nervous system, intracranial abscess, melioidosis
How to cite this article:
Madi D, Rai SP, Vidyalakshmi K, Chowta K N. Neurological melioidosis presenting as intracranial abscess. Indian J Pathol Microbiol 2016;59:417-9 |
| Introduction | |  |
Melioidosis is an infection caused by the bacteria Burkholderia pseudomallei. B. pseudomallei is an environmental saprophyte. Melioidosis is endemic in Southeast Asia and Northern Australia. It has varying clinical presentations ranging from pneumonia to visceral abscesses. Central nervous system (CNS) involvement in melioidosis is rare.[1] The incidence of CNS involvement in one of the largest case series from India was 1%.[2] We present a case of CNS melioidosis from South India.
| Case Report | | |
A 54-year-old man who was a watchman presented with fever and headache of 5 days duration. He did not have any comorbid illness in the past.
On examination, his pulse was 80/min, blood pressure - 180/100 mm Hg, and temperature 100.4°F. A swelling of 3 cm × 2 cm was present over the right frontal region. Systemic examination was normal. Investigations revealed hemoglobin - 13.3 g/dl, total count - 9500 cells/cu mm, platelets - 3.41 lakhs/cu mm, and erythrocyte sedimentation rate 44 mm. Fasting blood sugar - 251 mg/dl, postprandial blood sugar - 404 mg/dl, and glycosylated hemoglobin - 11.9%.
Renal function test, electrolytes, liver function tests, chest X-ray, and ultrasound abdomen was normal. Malaria and dengue - IgM was negative. Blood culture did not reveal any organism.
On the 4th day of admission, he had a seizure. Antiepileptic was started. Magnetic resonance imaging (MRI) of the brain showed a collection in extracalvarial soft tissue [Figure 1] in a right frontal region measuring about 37 mm with focal areas of the altered signal intensity of right frontal marrow. There was an associated subdural collection in the frontal region with associated meningeal enhancement. The MRI features were suggestive of scalp abscess with bone osteomyelitis and intracranial spread of abscess with focal patchy leptomeningitis. | Figure 1: Axial magnetic resonance imaging brain showed an area of restricted diffusion in the scalp (white arrow a) which is an encapsulated collection in extracalvarial soft tissue in right frontal region measuring about 37 mm with focal areas of altered signal intensity of right frontal marrow. There is an associated subdural collection in the frontal region with associated meningeal enhancement (postcontrast axial magnetic resonance T1-weighted images white arrow b and c) along right fronto temporal dura flax cerebri cortical sulci and the frontal region (coronal magnetic resonance imaging T1-weighted images white arrow d). The features appeared even more distinct on the magnetic resonance imaging postcontrast fluid-attenuated inversion recovery images which showed distinct enhancement of the scalp collection (white arrow e) and the meninges (white arrow f). The magnetic resonance imaging features are suggestive of scalp abscess with bone osteomyelitis and intracranial spread of abscess with focal patchy leptomeningitis
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Incision and drainage of the extracalvarial collection in the right frontal region were done, and pus was sent to the laboratory for culture. Meanwhile, our patient was started on parenteral meropenem 1 g thrice daily. Gram-staining revealed numerous polymorphonuclear leukocytes and a few Gram-negative Bacilli, some of them showing bipolar staining. Culture on blood, chocolate and MacConkey's agar [Figure 2] showed colonies with a slight metallic sheen after 48 h; colonies turned rough with the wrinkled surface after 4 days. Based on positive oxidase test, resistance to gentamicin and polymixin B, the wrinkled appearance and pink color of colonies on MacConkey's agar, a presumptive identification of B. pseudomallei was made. Identification was confirmed by the Vitek 2 Compact system (BioMe´rieux). The isolate was sensitive to cotrimoxazole, ceftazidime, imipenem, meropenem, doxycycline, and piperacillin-tazobactam. Parenteralmeropenem (1 g thrice daily) was continued for 4 weeks. He was discharged on oral trimethoprim/sulfamethoxazole (TMP-SMX) (160/800 mg) twice daily and doxycycline (100 mg twice daily). He was treated with insulin for diabetes. Antihypertensive medications were also started. Oral antibiotics were given for 3 months. Our patient was asymptomatic at the end of 3 months, and repeat imaging showed resolution of the lesions. | Figure 2: Colonies of Burkholderia pseudomallei on chocolate agar plate (a) and MacConkey's agar plate (b) after 4 days of incubation; showing rough, wrinkled surface and pink color on MacConkey's agar
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| Discussion | | |
Melioidosis is an emerging disease in India. Infection results from percutaneous inoculation, inhalation or ingestion. Diabetes, chronic kidney disease, malignancy, and alcohol consumption are risk factors.[2] Sometimes, risk factors can be absent.[2],[3] Our patient had diabetes. Melioidosis can present as an acute or chronic illness with or without sepsis.[2],[3] Pulmonary Melioidosis (pneumonia) is the most common type of presentation in our country.[2]
The incidence of CNS involvement in melioidosis is 3% (14/540) according to the Darwin study.[3] No CNS involvement was documented among 32 patients in a recently published case series from India.[4] In Thailand, 1.5% (3/191) of patients with melioidosis had neurologic involvement.[5] In a study of 91 patients (culture confirmed) from Malaysia, 2% had neurologic involvement.[6]
Pathogenesis of CNS melioidosis has been debated.[1] The pathogenesis of CNS melioidosis is postulated to be due to direct bacterial invasionor due to hematogeneous spread.[3] Neurological manifestations range from meningoencephalitis, myelitis, spinal epidural abscess, and cerebral abscess to osteomyelitis.[3],[7],[8],[9] Melioidosis can mimic tuberculosis clinically, radiologically, and on histopathology.[2],[8]
The culture of B. pseudomallei is the sine qua non for the diagnosis of melioidosis.[10] In our case pus aspirated from the frontal region grew B. pseudomallei. The bacterium B. pseudomallei is nonfastidious, and grows well on routine culture media like MacConkey's agar, blood agar and chocolate agar; and these suffice for most clinical specimens. Modified Ashdown media is a selective media for B. pseudomallei[11],[12] Treatment consists of an intensive phase with parenteral antibiotics for 2–4 weeks followed by a maintenance phase with oral antibiotics for 3–6 months.[10] Ceftazidime or carbapenems are used in the intensive phase and TMP-SMX is used in the maintenance phase.[5],[10] We used meropenem for 4 weeks in our case. Amoxicillin–clavulanate and doxycycline can be used in the treatment of melioidosis in patients who cannot tolerate TMP-SMX. Mortality is 21–50% for neurological melioidosis.[3],[7] Survivors of CNS melioidosis may have significant long-term neurologic sequelae.[7] Recurrent melioidosis can occur if adherence to treatment is poor.[3]
Melioidosis can mimic various infectious diseases. Melioidosis can virtually affect any organ ranging from skin, lung, liver, spleen, prostate, bone, pericardium, and kidney to CNS. As the incidence of diabetes is increasing in our country varying manifestations of melioidosis will be seen in routine clinical practice. Melioidosis should be considered in the differential diagnosis of meningoencephalitis and intracranial abscess, especially in diabetics. In suspected cases of melioidosis, physicians must make a sincere effort to isolate the organism from body fluids so as to confirm the diagnosis. Timely initiation of appropriate antibiotics is needed to prevent a fatal outcome. Poor adherence to treatment can cause recurrence of the disease.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Hesstvedt L, Reikvam DH, Dunlop O. Neurological melioidosis in Norway presenting with a cerebral abscess. IDCases 2014;2:16-8.  |
| 2. | Vidyalakshmi K, Lipika S, Vishal S, Damodar S, Chakrapani M. Emerging clinico-epidemiological trends in melioidosis: Analysis of 95 cases from western coastal India. Int J Infect Dis 2012;16:e491-7. |
| 3. | Currie BJ, Ward L, Cheng AC. The epidemiology and clinical spectrum of melioidosis: 540 cases from the 20 year Darwin prospective study. PLoS Negl Trop Dis 2010;4:e900. |
| 4. | Gopalakrishnan R, Sureshkumar D, Thirunarayan MA, Ramasubramanian V. Melioidosis: An emerging infection in India. J Assoc Physicians India 2013;61:612-4. [ PUBMED] |
| 5. | Limmathurotsakul D, Chaowagul W, Wongsrikaew P, Narmwong A, Day NP, Peacock SJ. Variable presentation of neurological melioidosis in Northeast Thailand. Am J Trop Med Hyg 2007;77:118-20. |
| 6. | Hassan MR, Pani SP, Peng NP, Voralu K, Vijayalakshmi N, Mehanderkar R, et al. Incidence, risk factors and clinical epidemiology of melioidosis: A complex socio-ecological emerging infectious disease in the Alor Setar region of Kedah, Malaysia. BMC Infect Dis 2010;10:302. |
| 7. | Deuble M, Aquilina C, Norton R. Neurologic melioidosis. Am J Trop Med Hyg 2013;89:535-9. |
| 8. | Kumar GS, Raj PM, Chacko G, Lalitha MK, Chacko AG, Rajshekhar V. Cranial melioidosis presenting as a mass lesion or osteomyelitis. J Neurosurg 2008;108:243-7. |
| 9. | Muthusamy KA, Waran V, Puthucheary SD. Spectra of central nervous system melioidosis. J Clin Neurosci 2007;14:1213-5. |
| 10. | Wiersinga WJ, Currie BJ, Peacock SJ. Melioidosis. N Engl J Med 2012;367:1035-44. |
| 11. | Dance DA, Wuthiekanun V, Naigowit P, White NJ. Identification of Pseudomonas pseudomallei in clinical practice: Use of simple screening tests and API 20NE. J Clin Pathol 1989;42:645-8. |
| 12. | Cheng AC, Currie BJ. Melioidosis: Epidemiology, pathophysiology, and management. Clin Microbiol Rev 2005;18:383-416. |
Correspondence Address:
Dr. Santosh P. V. Rai
Department of Radiology, Kasturba Medical College and Hospital, Manipal University, Mangalore, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0377-4929.188118
[Figure 1], [Figure 2] |
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