- Email: [email protected]
A fatal sandwich
Personal view 15 Dye C, Williams BG. Criteria for the control of drug-resistant tuberculosis. Proc Natl Acad Sci USA 2000; 97: 8180–85. 16 Farmer P, Kim JY. Community based approaches to the control of multidrug resistant tuberculosis: introducing “DOTS-plus”. BMJ 1998; 317: 671–74. 17 Bastian I, Rigouts L, Van Deun A, Portaels F. Directly observed treatment, short-course strategy and multidrug-resistant tuberculosis: are any modifications required? Bull World Health Organ 2000; 78: 238–51. 18 Teixeira L, Perkins MD, Johnson JL, et al. Infection and disease among household contacts of patients with multidrug-resistant tuberculosis. Int J Tuberc Lung Dis 2001; 5: 321–28.
Multidrug-resistant tuberculosis
19 Grange JM. Vaccination against tuberculosis: past problems and future hopes. Semin Respir Crit Care Med 1997; 18: 459–70. 20 Collins HL, Kaufmann SHE. Prospects for better tuberculosis vaccines. Lancet Infect Dis 2001; 1: 21–28. 21 Rose AM, Watson JM, Graham C, et al. Tuberculosis at the end of the 20th century in England and Wales: results of a national survey in 1998. Thorax 2001; 56: 173–79. 22 CDSC Report. Drug resistant tuberculosis in north London. Commun Dis Wkly Rep 2000: 10: 285–88. 23 Hayward AC, Coker RJ. Could a tuberculosis epidemic occur in London as it did in New York? Emerg Infect Dis 2000; 6: 12–16.
Clinical picture A fatal sandwich
A previously healthy 45-year-old man presented with a 2-day history of epigastric pain and bloody vomiting. These symptoms developed a few hours after eating a sandwich containing poorly conserved sausage. On admission, the patient was somnolent, blood pressure was 65/37 mm Hg, pulse rate was 98 beats per minute, and temperature was 36·7°C. The abdomen was painful, slightly distended with mild tenderness but no guarding. Bowel sounds were absent and rectal examination was normal. Lungs were clear and cardiac auscultation revealed no murmur. White blood cell count was 12 600/L. Arterial blood gas values were: pH 7·11, PaO2 60 mm Hg, PaCO2 32 mm Hg. Bicarbonate concentration was 12 mmol/L and serum creatinine concentration was 168 µmol/L. Creatine phosphokinase was 1964 UI/mL, alanine aminotransferase 59 UI/mL, aspartate
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aminotransferase 152 UI/mL, and amylase 449 UI/mL. Abdominal computed tomography (CT) scan disclosed gas in the enteric wall and portal vein (figure, arrows). Despite mechanical ventilation, administration of large amounts of intravenous fluids, vasopressors, and broad-spectrum antibiotics, the patient died 8 h after admission. On necropsy, the abdominal cavity contained serosanguinous liquid and pseudomembranes. Vessels were normal except for mesenteric ischaemia. The bowel seemed normal except for the duodenum wall, which was thickened. Histological examination showed necrosis of the mucosa of the duodenum and proximal jejunum, neutrophil infiltration of the duodenum, and presence of extracellular Gram-positive rods. Culture yielded no growth, but PCR amplification detected the gene encoding for the beta toxin of Clostridium perfringens, which confirmed the diagnosis of enteritis necroticans. Histological lesions were limited to the proximal bowel, which suggests that the virulence of C perfringens developed as soon as the bacteria or its toxin entered the intestinal wall. Clinicians must be aware of this fulminant yet rarely recognised entity. Prompt diagnosis by CT scan, and early treatment including aggressive resuscitation and intestinal necrosis resection are the only way to reduce mortality from enteritis necroticans. M Tonnellier, E Maury, J Guglielminotti, G Offenstadt Intensive care unit, Saint-Antoine Hospital, Paris, France Correspondence: Dr Marc Tonnellier, Service de réanimation médicale, Hôpital Saint-Antoine, 184 rue du Faubourg SaintAntoine, 75571 Paris cedex 12, France. Fax +33 1 49282145; email [email protected]
THE LANCET Infectious Diseases Vol 1 October 2001
For personal use. Only reproduce with permission from The Lancet Publishing Group.
Multidrug-resistant tuberculosis
19 Grange JM. Vaccination against tuberculosis: past problems and future hopes. Semin Respir Crit Care Med 1997; 18: 459–70. 20 Collins HL, Kaufmann SHE. Prospects for better tuberculosis vaccines. Lancet Infect Dis 2001; 1: 21–28. 21 Rose AM, Watson JM, Graham C, et al. Tuberculosis at the end of the 20th century in England and Wales: results of a national survey in 1998. Thorax 2001; 56: 173–79. 22 CDSC Report. Drug resistant tuberculosis in north London. Commun Dis Wkly Rep 2000: 10: 285–88. 23 Hayward AC, Coker RJ. Could a tuberculosis epidemic occur in London as it did in New York? Emerg Infect Dis 2000; 6: 12–16.
Clinical picture A fatal sandwich
A previously healthy 45-year-old man presented with a 2-day history of epigastric pain and bloody vomiting. These symptoms developed a few hours after eating a sandwich containing poorly conserved sausage. On admission, the patient was somnolent, blood pressure was 65/37 mm Hg, pulse rate was 98 beats per minute, and temperature was 36·7°C. The abdomen was painful, slightly distended with mild tenderness but no guarding. Bowel sounds were absent and rectal examination was normal. Lungs were clear and cardiac auscultation revealed no murmur. White blood cell count was 12 600/L. Arterial blood gas values were: pH 7·11, PaO2 60 mm Hg, PaCO2 32 mm Hg. Bicarbonate concentration was 12 mmol/L and serum creatinine concentration was 168 µmol/L. Creatine phosphokinase was 1964 UI/mL, alanine aminotransferase 59 UI/mL, aspartate
202
aminotransferase 152 UI/mL, and amylase 449 UI/mL. Abdominal computed tomography (CT) scan disclosed gas in the enteric wall and portal vein (figure, arrows). Despite mechanical ventilation, administration of large amounts of intravenous fluids, vasopressors, and broad-spectrum antibiotics, the patient died 8 h after admission. On necropsy, the abdominal cavity contained serosanguinous liquid and pseudomembranes. Vessels were normal except for mesenteric ischaemia. The bowel seemed normal except for the duodenum wall, which was thickened. Histological examination showed necrosis of the mucosa of the duodenum and proximal jejunum, neutrophil infiltration of the duodenum, and presence of extracellular Gram-positive rods. Culture yielded no growth, but PCR amplification detected the gene encoding for the beta toxin of Clostridium perfringens, which confirmed the diagnosis of enteritis necroticans. Histological lesions were limited to the proximal bowel, which suggests that the virulence of C perfringens developed as soon as the bacteria or its toxin entered the intestinal wall. Clinicians must be aware of this fulminant yet rarely recognised entity. Prompt diagnosis by CT scan, and early treatment including aggressive resuscitation and intestinal necrosis resection are the only way to reduce mortality from enteritis necroticans. M Tonnellier, E Maury, J Guglielminotti, G Offenstadt Intensive care unit, Saint-Antoine Hospital, Paris, France Correspondence: Dr Marc Tonnellier, Service de réanimation médicale, Hôpital Saint-Antoine, 184 rue du Faubourg SaintAntoine, 75571 Paris cedex 12, France. Fax +33 1 49282145; email [email protected]
THE LANCET Infectious Diseases Vol 1 October 2001
For personal use. Only reproduce with permission from The Lancet Publishing Group.