Bruhn, H.

Frahm, J.

Thorwirth, V.

Weber, T.

English

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1610All patients were nursed in isolation and no secondary casesoccurred. The klebsiella strains showed resistance to cefotaxime andaztreonam, and up to five further classes of antibiotics. Resistance tothird-generation cephalosporins was successfully transferred toEscherichia coli J62 from the K pneumoniae strains from the first twocases, consistent with these ESBLs being plasmid-mediated; andplasmids of 60 and 70 MD, respectively, were found on agarose gelelectrophoresis.These three cases illustrate the possible origins of organismsproducing ESBLs-namely, international transfer with the patient,inter-hospital transfer, and selection of the resistant strain withina hospital. Nosocomial outbreaks of ESBL-producingEnterobacteriaceae with multiple resistance2 to a range of antibioticclasses have occurred in Europe3,4 and the USA. The continued useof third-generation cephalosporins exerts substantial selectionpressure in favour of ESBL-producing organisms and also for theevolution of ESBLs. This, together with the introduction of similaroral cephalosporins, such as ceflxime, into the community, shouldprompt laboratory surveillance for such strains. We suggest avariation of the double-disc synergy test3 on isolates showingmoderate resistance to cefotaxime. Should the use of third-generation cephalosporins be restricted?7We thank Dr T. L. Pitt, Central Public Health Laboratory, for serotypingthe isolates, and Prof J. M. T. Hamilton-Miller and Dr S. H. Gillespie foradvice and comments.Department of Medical Microbiology,Royal Free Hospital,London NW3 2QG, UKA. A. MACDONALDP. A. C. MAPLEC. C. KIBBLERDivision of Hospital Infection,Central Public Health Laboratory,London NW9R. C. GEORGEA. P. JOHNSONDepartment of Medical Microbiology,Edinburgh University Medical SchoolS. K. DU BOISS. G. B. AMYES1 BSAC Working Party. In-vitro antibiotic sensitivity testing. J Antimicrob Chemother1988; 21: 701-10.2. Jacoby AJ, Sutton S. Properties of plasmids responsible for production ofextended-spectrum beta-lactamases. Antimicrob Agents Chemother 1991; 35:164-69.3. Sirot J, Chanal C, Pent A, Sirot D, Labia R, Gerband G. Klebsiella pneumoniae andother enterobacteriaceae producing novel plasmid-mediated beta-lactamasesmarkedly active against third-generation cephalosporins: epidemiologic studies.Rev Infect Dis 1988; 10: 850-59.4. Brun-Buisson C, Legrand P, Phillipon A, Montravers P, Ansquer M, Duval J.Transferable enzymatic resistance to third generation cephalosporins during anosocomial outbreak of Klebsiella pneumoniae. Lancet 1987; ii: 302-06.5. Rice LB, Willey SH, Papanicolaou GA, et al. Outbreak of ceftazidime resistancecaused by extended-spectrum beta-lactamases at a Massachusetts chronic-carefacility. Antimicrob Agents Chemother 1991; 34: 2193-99.6. Collatz E, Labia R, Gutmann L. Molecular evolution of ubiquitous beta-lactamasestowards extended-spectrum enzymes active against newer beta-lactam antibiotics.Mol Microbiol 1990; 4: 1615-20.7. Payne DJ, Amyes SGB. Transferable resistance to extended-spectrum beta-lactams: amajor threat or a minor inconvenience? J J Antimicrob Chemother 1991; 27: 255-61.In-vivo monitoring of neuronal loss inCreutzfeldt-Jakob disease by protonmagnetic resonance spectroscopySIR,-The advent of bovine spongiform encephalopathy hasrenewed interest in novel approaches to the clinical diagnosis ofspongiform encephalopathies such as Creutzfetdt-Jakob disease(CJD). We have seen a case of sporadic CJD where the onlymagnetic resonance imaging abnormalities were mild corticalatrophy and hyperintensities in the lentiform nuclei, as notedpreviously.’ By contrast, proton magnetic resonance spectroscopy(MRS) demonstrated significant metabolic alterations in corticalgrey matter and white matter and in striatum. Right frontal lobebiopsy, done 2 days after these scans, revealed fine vacuolation ofthe neuropil (spongiform change) in the deep grey-matter with aslight loss of neurons and gliosis, consistent with CJD.After a cold in August, 1990, a 53-year-old woman had difficultysleeping and complained of dizziness. When cycling she found ithard to keep her balance. A neurologist noted trunk and gait ataxiaand a tremor of her right thumb. By October she had becomeforgetful, had difficulty expressing herself, and her speech wasFig 1-Localised proton MR spectra of parietal white-matter.Upper: Patient with CJD, exhibiting reduction of NAA and PCr/Crandincrease in Ins.Lower controlMajor metabolites include N-acetylaspartate (NAA), glutamate (Glu),creatine (Cr), and phosphocreatine (PCr), choline-containingcompounds (Cho), and myo-inositol (Ins). Volume of interest 12 mlslurred. Nocturnal anxiety and paraspasticity ensued and she wasadmitted to hospital in November. Her ataxia worsened as did hermemory. Paranoid-hallucinatory states required treatment withhaloperidol for a week. In December a progressive left-sidedspasticity developed. Dysarthria further impeded her speech andshe became demented. CSF analysis revealed oligoclonal banding.EEGs revealed diffuse slow and a-range complexes with temporo-occipital sharp wave 6 and 8-complexes. No 1-2 Hz periodic sharpwave complexes (PSWC) were seen. In February, 1991, the patientwas in a coma and showed spontaneous myoclonus, predominantlyin her right arm. An EEG showed PSWCs, supporting thediagnosis of CJD. In March localised proton MRS was done with20 ms echo-time stimulated-echo sequences (2-0 T Siemens’Magnetom’).3 Measuring times were 6-5 min with 128accumulations and repetition times of 3 s.Fig 1 shows the proton MR spectrum of the left parietalwhite-matter of the patient, compared with that of a 56-year-oldhealthy female control. The N-acetylaspartate (NAA) peak wasreduced (40%), as was the creatine/phosphocreatine ratio (10%);there was an increase in inositol (30%). Similar findings wereobserved contralaterally and in frontal white-matter except forslightly lower values of choline-containing compounds. Twovolumes of interest in predominantly grey-matter were investigatedin paramedian frontal and parietal locations; only NAA wasdiminished (30%) (fig 2). MRS in the hyperintense region of thestriatum showed a fourfold loss of metabolites. The remainingmetabolite pattern exhibited a further reduction of NAA relative tocreatines and cholines.1611Fig 2-Localised proton MR spectra and paramedian grey-matter.Upper: Patient with CJD exhibiting reduction of NAA.Lower. control. Volume of interest 18 ml.The NAA data, a marker of vital neuronal tissue,’ indicate severeneuronal loss in CJD. Most notably, MRS in this patient revealedmetabolic alterations in regions of the brain that had appearednormal on magnetic resonance imaging. Structural preservation inthe presence of gross functional impairment in CJD is often seenwith computerised tomography. Positron emission tomography5,1reveals hypoperfusion and hypometabolism but proton MRS hasthe potential advantage of selectively indicating neuronal damage,the cell type most severely affected in the spongiformencephalopathies. This non-invasive investigation could be of usein the early diagnosis of CJD.Financial support by the Bundesminister fur Forschung und Technologie(grant 01 VF 8606/6) is gratefully acknowledged.Max Planck Institute for Biophysical Chemistry,D-3400 Gottingen, Germany,Neurological Clinic,University of Gottingen;and Klinik Schildautal, SeesenH. BRUHNT. WEBERV. THORWIRTHJ. FRAHM1. Pearl GS, Anderson RE. Creutzfeldt-Jakob disease: high caudate signal on magneticresonance imaging. South Med J 1989; 82: 1177-80.2. Levy SR, Chiappa KH, Burke CJ, Young RR. Early evolution and incidence ofelectrencephalographic abnormalities in Creutzfeldt-Jakob disease. J ClinNeurophysiol 1986; 3: 1-21.3. Frahm J, Michaelis T, Merboldt KD, Bruhn H, Gyngell ML, Hanicke W.Improvements m localized proton NMR spectroscopy of human brain: watersuppression, short echo times, and 1 ml resolution. J Magn Reson 1990; 90: 464-73.4. Bruhn H, Frahm J, Gyngell ML, Merboldt KD, H&auml;nicke W, Sauter R. Cerebralmetabolism in man after acute stroke: new observations using localized protonNMR spectroscopy. Magn Reson Med 1989; 9: 126-31.5. Hunter R, Gordon A, McLuskie R, et al. Gross regional cerebral hypofunction withnormal CT scan in Creutzfeldt-Jakob disease. Lancet 1989; i: 214-15.6. Holthoff VA, Sandmann J, Pawlik G, Schroder R, Heiss WD. Positron emissiontomography in Creutzfeldt-Jakob disease. Arch Neurol 1990; 47: 1035-38.High frequency of concomitant pancreatitisin salmonella enteritisSIR,-Dr Baird-Parker (Nov 17, p 1231) underscores theincreasing incidence of foodborne salmonellosis in many countriesof the western world.l We report some observations that arerelevant to the clinical picture and differential diagnosis of thisdiarrhoeal condition.Stimulated by a case of salmonellosis with severe concomitantpancreatitis we prospectively followed all culture-proven cases ofsalmonella enteritis for symptoms and laboratory signs ofconcomitant pancreatitis. Within 18 months we treated 47 patientswith salmonella enteritis (17 men, mean age 45 [range 16-79] years).16 patients had Salmonella typhimurium and 31 had S enteritidisinfections, 1 patient having both. The frequency of concomitantpancreatitis as assessed by raised serum amylase and lipase was:Concomitant pancreatitis No pancreatitisNo 29(62%) 18(38%)Men/women 8/21 9/9Mean age (range) 44.8 (18-79) 45-8 (16-71)Concomitant pancreatitis was found in 7 patients withS typhimurium and in 22 with S enteritidis (p < 005, Chi-squaretest). The course of pancreatitis was usually mild to moderate, withsome pancreatic enlargement, as shown by abdominal sonography,in about half the patients. Pancreatitis was unrelated to treatment ofsalmonellosis either by fluid replacement alone or antibiotics(mainly ciprofloxacin).The high frequency of concomitant pancreatitis in salmonellaenteritis in our series is in contrast with other publications. Ingastroenterological textbooks salmonella pancreatitis is notmentioned2 or is merely listed in tables.3 Only in paediatricpublications has some attention been paid to these forms ofpancreatitis complicating viral or bacterial infections.4 Thepathogenetic mechanisms are unknown as far as we are aware. Byanalogy to other infections, a haematogenous attack on parenchymalpancreatic cells seems probable.These observations indicate that patients with upper abdominalpain in salmonella enteritis should be investigated for concomitantpancreatitis, and in those with hyperamylasaemia and diarrhoea,salmonellosis should be considered as a possible explanation for thisclinical condition.Department of Medicine,Krankenhaus der Barmherzigen Schwestern,4910 Ried/l, AustriaFRIEDRICH RENNERCHRISTIAN NIMETHNIKOLAUS DEMMELBAUER1. World Health Organisation. Salmonellosis control: the role of animal and producthygiene. WHO Tech Rep Ser 1988, no 774.2. Soergel KH. Acute pancreatitis. In: Sleismger MH, Fordtran JS, eds. Gastrointestinaldisease, 3rd ed. Philadelphia Saunders, 1983: 1462-84.3. Creutzfeldt W, Lankisch PG. Acute pancreatitis: etiology and pathogenesis. In: BerkJE, ed. Bockus gastroenterology, 4th ed. Philadelphia: Saunders, 1985. 3971-92.4. Seifert G. Zur Pathologie der Pankreatitis im Kindesalter. Mschr Kinderheilk 1960;108: 225-29.Mega-dose methylprednisolone for chronicidiopathic thrombocytopenic purpuraSIR,-Dr Balint and colleagues (May 4, p 1106) mention, amongother approaches, conventional prednisolone (1-2 mg/kg daily)administration for the treatment of idiopathic thrombocytopenicpurpura (ITP).With colleagues, I have shown that such treatment for 2 weeks isnot effective in ITP; on the contrary it delays spontaneous recoveryin childhood acute ITP.1 Mega-dose oraF or intravenous1.3methylprednisolone (MDMP; 30 mg/kg daily for 3 days followedby 20 mg/kg for 4 days; each dose given before 0900 h) has, however,proved very effective. Platelet counts increased to over 150 000/&micro;lwithin 3 days in about two-thirds of patients.1,2 IntravenousMDMP has also been used successfully in children4-6 and adults7,Swith chronic ITP. We have used oral MDMP (30 mg/kg and 20mg/kg daily, each for 1 week; every dose before 0900 h) in 10children with chronic ITP (ie, duration longer than 6 months). 1child could not be followed. Platelet count increased to over150 000/&micro;l in 6 patients within 3 days and in 8 by 2 weeks.

In-vivo monitoring of neuronal loss in Creutzfeldt-Jakob disease by proton magnetic resonance spectroscopy

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In-vivo monitoring of neuronal loss in Creutzfeldt-Jakob disease by proton magnetic resonance spectroscopy

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