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A deadly thorn: a case of imported melioidosis
iron-deficiency patients for coeliac disease by duodenal biopsy. Richard J Farrell, *J Thomas LaMont Division of Gastroenterology, Beth Israel Deaconess Medical Centre, Harvard Medical School, Boston, MA 02215, USA. 1
Catassi C, Ratsch IM, Fabiani E, et al. Coeliac disease in the year 2000: exploring the icebeurg. Lancet 1994; 343: 200–03. 2 Kepczyk T, Kadakic SC. Prospective evaluation of gastrointestinal tract in patients with iron deficiency anemia. Dig Dis Sci 1995; 40: 1283–89. 3 Gordon SR, Smith SE, Power GC. The role of endoscopy in the evaluation of iron deficiency anaemia in patients over the age of 50. Am J Gastroenterol 1994; 89: 1963–67. 4 Ferguson A. Coeliac disease, an eminently treatable condition, may be underdiagnosed in the United States. Am J Gastroenterol 1997; 92: 1252–54. 5 Fasano A. Where have all the Americans coeliacs gone? Acta Pediatr Suppl 1996; 412: 20–24.
A deadly thorn: a case of imported melioidosis Sir—David Dance and colleagues (Jan 16, p 208)1 highlight an increase in the frequency of imported melioidosis, and list 15 cases occurring from 1988 to 1998. We report further details of one of these cases, with particular reference to the suspected mode of acquisition and ultimate outcome. A previously healthy 61-year-old man returned from a 2-week holiday in Thailand, having stayed on the popular tourist island of Phuket. He did not walk barefoot during the holiday, swam only in the hotel swimming pool, and was well throughout. While gardening the day after he returned from Thailand, he stood on a large thorn. This thorn penetrated his left heel through the sole of his shoe. At the time, he was wearing the rubber-soled canvas shoes that he had worn throughout his holiday. He removed the thorn (with difficulty) using a sewing needle. 2–3 days later he developed a fever, and over the next 7 days he had rigors, sweating, malaise, and weight loss, but no respiratory symptoms. On day 12 after his return to the UK, he developed scattered pustular skin lesions, and was admitted to hospital. Apart from the pustular lesions, examination was unremarkable, although his temperature later rose to 40°C. Chest radiograph, full blood count, electrolytes, and glucose were normal, but a gram-negative bacillus was isolated from blood cultures. He was treated empirically with oral ciprofloxacin 500 mg every 12 h, before further identification revealed
1016
the organism to be B u r k h o l d e r i a pseudomallei, which was resistant to amoxycillin, gentamicin, and ciprofloxacin, but sensitive to ceftazidime and augmentin. He was then given intravenous ceftazidime 2 g every 8 h, which was later increased to 2 g every 6 h after the development of epididymitis. After 2 weeks of intravenous therapy, he was changed to tablets containing amoxycillin 500 mg and clavulanic acid 125 mg (three tablets every 8 h) and discharged to complete 4 months of treatment. He was reviewed regularly as an outpatient and seemed to respond satisfactorily. 3 months later he developed severe back pain and died suddenly at home. A n e c r o p s y revealed a ruptured abdominal aorta, with histological evidence of acute inflammation and periaortic abscess formation. Melioidosis is a common cause of septicaemia in rural Thailand, particularly in rice farmers during the rainy season. Transmission is mainly through skin abrasions exposed to soil and water containing B pseudomallei.2 Our patient’s skin and shoes were probably colonised with B pseudomallei in Thailand, and the bacteria were then inoculated by the thorn. Puncture wounds of the foot are often associated with Pseudomonas a e r u g i n o s a, which has been successfully cultured from the shoes of such patients.3 B pseudomallei i s phylogenetically similar to P aeruginosa and occupies similar environmental n i c h e s . 4 Death from a ruptured mycotic aneurysm has been previously reported in melioidosis.5 This case serves as a reminder that the mortality remains high despite long-term treatment with recommended antibiotics, and that even short-stay tourists are at risk from this deadly disease. *James K Torrens, Paul H M McWhinney, David S Tompkins *Department of Infectious Diseases, Seacroft Hospital, Leeds LS14 6UH, UK; and Public Health Laboratory, York Road, Leeds (e-mail: [email protected]) 1
Dance DAB, Smith MD, Aucken HM, Pitt TL. Imported melioidosis in England and Wales. Lancet 1999; 353: 208. 2 Chaowagul W, White NJ, Dance DAB, et al. Melioidosis: a major cause of community-acquired septicaemia in northeastern Thailand. J Infect Dis 1989; 159: 890–99. 3 Fisher MC, Goldsmith JF, Gilligan PH. Sneakers as a source of Pseudomonas aeruginosa in children with osteomyelitis following puncture wounds. J Pediatr 1985; 106: 607–09. 4 Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology. Washington, DC: ASM Press, 1995.
5
Steinmetz I, Stosiek P, Hergenrother D, Bar W. Melioidosis causing a mycotic aneurysm. Lancet 1996; 347: 1564–65.
Sir—David Dance and colleagues1 emphasise that the microbiologist should be aware of the characteristics of Burkholderia pseudomallei, a bacterium not well-known in nonendemic areas. Having been confronted with a fatal case of imported melioidosis, we had to cope with the reliable identification of this species. This task may be more complicated than Dance and colleagues mention.1 This difficulty arises because of the rapidly growing number of newly described, phylogenetically related, and often also medically important bacteria such as B cepacia ( s e n s u stricto), B gladioli, B multivorans, B t h a i l a n d e n s i s , 2 B vietnamensis, unpigmented Chromobacterium violaceum isolates, and Ralstonia pickettii. Some of these bacteria are not yet included in the database of commercially available biochemical test kits or are difficult to discriminate with standard biochemical or physiological tests in a clinical laboratory. Furthermore, Inglis and colleagues3 reported misidentification of B p s e u d o m a l l e i with such kits. 3 Determination of the fatty acid methylester pattern by gas chromatogaphy, a latex agglutination test, or both3 may help to avoid such misidentification with a consequently false diagnosis. Sequencing of the 16S rDNA is a reliable alternative but does not allow a distinction between B pseudomallei and B mallei.5 This distinction can be achieved by sequencing regions of the ITS or 23S r D N A . 5 Since melioidosis is an uncommon disease in temperate countries and often shows the phenomenon of latency, 1 measurement of specific antibodies can be helpful, as in our case, to achieve a rapid diagnosis and thus lowering of the high mortality rate from melioidosis. *Heidrun Peltroche-Llacsahuanga, Gerhard Haase Institute of Medical Microbiology, University Hospital RWTH Aachen, D-52057 Aachen, Germany (e-mail: [email protected]) 1
Dance DAB, Smith MD, Aucken HM, Pitt TL. Imported melioidosis in England and Wales. Lancet 1999; 353: 108. 2 Brett PJ, DeShazer D, Wodds DE. Burkholderia thailandensis sp nov, a Burkholderia pseudomallei-like species. Int J Syst Bacteriol 1998; 48: 317–20. 3 Inglis TJJ, Chiang D, Lee GSH, Chor-Kiang L. Potential misidentification of Burkholderia pseudomallei by Api 20NE. Pathology 1998; 30: 62–64.
THE LANCET • Vol 353 • March 20, 1999
Catassi C, Ratsch IM, Fabiani E, et al. Coeliac disease in the year 2000: exploring the icebeurg. Lancet 1994; 343: 200–03. 2 Kepczyk T, Kadakic SC. Prospective evaluation of gastrointestinal tract in patients with iron deficiency anemia. Dig Dis Sci 1995; 40: 1283–89. 3 Gordon SR, Smith SE, Power GC. The role of endoscopy in the evaluation of iron deficiency anaemia in patients over the age of 50. Am J Gastroenterol 1994; 89: 1963–67. 4 Ferguson A. Coeliac disease, an eminently treatable condition, may be underdiagnosed in the United States. Am J Gastroenterol 1997; 92: 1252–54. 5 Fasano A. Where have all the Americans coeliacs gone? Acta Pediatr Suppl 1996; 412: 20–24.
A deadly thorn: a case of imported melioidosis Sir—David Dance and colleagues (Jan 16, p 208)1 highlight an increase in the frequency of imported melioidosis, and list 15 cases occurring from 1988 to 1998. We report further details of one of these cases, with particular reference to the suspected mode of acquisition and ultimate outcome. A previously healthy 61-year-old man returned from a 2-week holiday in Thailand, having stayed on the popular tourist island of Phuket. He did not walk barefoot during the holiday, swam only in the hotel swimming pool, and was well throughout. While gardening the day after he returned from Thailand, he stood on a large thorn. This thorn penetrated his left heel through the sole of his shoe. At the time, he was wearing the rubber-soled canvas shoes that he had worn throughout his holiday. He removed the thorn (with difficulty) using a sewing needle. 2–3 days later he developed a fever, and over the next 7 days he had rigors, sweating, malaise, and weight loss, but no respiratory symptoms. On day 12 after his return to the UK, he developed scattered pustular skin lesions, and was admitted to hospital. Apart from the pustular lesions, examination was unremarkable, although his temperature later rose to 40°C. Chest radiograph, full blood count, electrolytes, and glucose were normal, but a gram-negative bacillus was isolated from blood cultures. He was treated empirically with oral ciprofloxacin 500 mg every 12 h, before further identification revealed
1016
the organism to be B u r k h o l d e r i a pseudomallei, which was resistant to amoxycillin, gentamicin, and ciprofloxacin, but sensitive to ceftazidime and augmentin. He was then given intravenous ceftazidime 2 g every 8 h, which was later increased to 2 g every 6 h after the development of epididymitis. After 2 weeks of intravenous therapy, he was changed to tablets containing amoxycillin 500 mg and clavulanic acid 125 mg (three tablets every 8 h) and discharged to complete 4 months of treatment. He was reviewed regularly as an outpatient and seemed to respond satisfactorily. 3 months later he developed severe back pain and died suddenly at home. A n e c r o p s y revealed a ruptured abdominal aorta, with histological evidence of acute inflammation and periaortic abscess formation. Melioidosis is a common cause of septicaemia in rural Thailand, particularly in rice farmers during the rainy season. Transmission is mainly through skin abrasions exposed to soil and water containing B pseudomallei.2 Our patient’s skin and shoes were probably colonised with B pseudomallei in Thailand, and the bacteria were then inoculated by the thorn. Puncture wounds of the foot are often associated with Pseudomonas a e r u g i n o s a, which has been successfully cultured from the shoes of such patients.3 B pseudomallei i s phylogenetically similar to P aeruginosa and occupies similar environmental n i c h e s . 4 Death from a ruptured mycotic aneurysm has been previously reported in melioidosis.5 This case serves as a reminder that the mortality remains high despite long-term treatment with recommended antibiotics, and that even short-stay tourists are at risk from this deadly disease. *James K Torrens, Paul H M McWhinney, David S Tompkins *Department of Infectious Diseases, Seacroft Hospital, Leeds LS14 6UH, UK; and Public Health Laboratory, York Road, Leeds (e-mail: [email protected]) 1
Dance DAB, Smith MD, Aucken HM, Pitt TL. Imported melioidosis in England and Wales. Lancet 1999; 353: 208. 2 Chaowagul W, White NJ, Dance DAB, et al. Melioidosis: a major cause of community-acquired septicaemia in northeastern Thailand. J Infect Dis 1989; 159: 890–99. 3 Fisher MC, Goldsmith JF, Gilligan PH. Sneakers as a source of Pseudomonas aeruginosa in children with osteomyelitis following puncture wounds. J Pediatr 1985; 106: 607–09. 4 Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology. Washington, DC: ASM Press, 1995.
5
Steinmetz I, Stosiek P, Hergenrother D, Bar W. Melioidosis causing a mycotic aneurysm. Lancet 1996; 347: 1564–65.
Sir—David Dance and colleagues1 emphasise that the microbiologist should be aware of the characteristics of Burkholderia pseudomallei, a bacterium not well-known in nonendemic areas. Having been confronted with a fatal case of imported melioidosis, we had to cope with the reliable identification of this species. This task may be more complicated than Dance and colleagues mention.1 This difficulty arises because of the rapidly growing number of newly described, phylogenetically related, and often also medically important bacteria such as B cepacia ( s e n s u stricto), B gladioli, B multivorans, B t h a i l a n d e n s i s , 2 B vietnamensis, unpigmented Chromobacterium violaceum isolates, and Ralstonia pickettii. Some of these bacteria are not yet included in the database of commercially available biochemical test kits or are difficult to discriminate with standard biochemical or physiological tests in a clinical laboratory. Furthermore, Inglis and colleagues3 reported misidentification of B p s e u d o m a l l e i with such kits. 3 Determination of the fatty acid methylester pattern by gas chromatogaphy, a latex agglutination test, or both3 may help to avoid such misidentification with a consequently false diagnosis. Sequencing of the 16S rDNA is a reliable alternative but does not allow a distinction between B pseudomallei and B mallei.5 This distinction can be achieved by sequencing regions of the ITS or 23S r D N A . 5 Since melioidosis is an uncommon disease in temperate countries and often shows the phenomenon of latency, 1 measurement of specific antibodies can be helpful, as in our case, to achieve a rapid diagnosis and thus lowering of the high mortality rate from melioidosis. *Heidrun Peltroche-Llacsahuanga, Gerhard Haase Institute of Medical Microbiology, University Hospital RWTH Aachen, D-52057 Aachen, Germany (e-mail: [email protected]) 1
Dance DAB, Smith MD, Aucken HM, Pitt TL. Imported melioidosis in England and Wales. Lancet 1999; 353: 108. 2 Brett PJ, DeShazer D, Wodds DE. Burkholderia thailandensis sp nov, a Burkholderia pseudomallei-like species. Int J Syst Bacteriol 1998; 48: 317–20. 3 Inglis TJJ, Chiang D, Lee GSH, Chor-Kiang L. Potential misidentification of Burkholderia pseudomallei by Api 20NE. Pathology 1998; 30: 62–64.
THE LANCET • Vol 353 • March 20, 1999