Bonhoeffer, Jan

Heininger, Ulrich

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150 • CID 2008:46 (1 January) • CORRESPONDENCEFondo Interno Ricerca Scientifica e Tecnologica(FIRST), University of Milan.Potential conflicts of interest. All authors: noconflicts.Laurenzia Ferraris,1 Giusi Maria Bellistri,2Valentina Pegorer,2 Camilla Tincati,2Luca Meroni,1 Massimo Galli,1Antonella d’Arminio Monforte,2 Andrea Gori,3and Giulia Marchetti21Department of Clinical Sciences, “Luigi Sacco”Hospital, and 2Department of Medicine, Surgeryand Dentistry, Clinic of Infectious Diseases,“San Paolo” Hospital, University of Milan, Milan,and 3Division of Infectious Diseases, “San Gerardo”Hospital, Monza, ItalyReferences1. Moore RD, Keruly JC. CD4+ cell count 6 yearsafter commencement of highly active antiret-roviral therapy in persons with sustained vi-rologic suppression. Clin Infect Dis 2007; 44:441–6.2. Grabar S, Le Moing V, Goujard C, et al. Clin-ical outcome of patients with HIV-1 infectionaccording to immunologic and virologic reas-ponse after 6 months of highly active antiret-roviral therapy. Ann Intern Med 2000; 133:401–10.3. Egger M, May M, Chene G, et al. Prognosisof HIV-1–infected patients starting highly ac-tive antiretroviral therapy: a collaborativeanalysis of prospective studies. Lancet 2002;360:119–29.4. Florence E, Lundgren J, Dreezen C, et al. Fac-tors associated with a reduced CD4 lympho-cyte count response to HAART despite fullviral suppression in the EuroSIDA study. HIVMed 2003; 4:255–62.5. Kaufmann GR, Furrer H, Ledergerber B, et al.Characteristics, determinants, and clinical rel-evance of CD4 T cell recovery to !500 cells/microL in HIV type 1–infected individuals re-ceiving potent antiretroviral therapy. ClinInfect Dis 2005; 41:361–72.6. Anthony KB, Yoder C, Metcalf JA, et al. In-complete CD4 T cell recovery in HIV-1 in-fection after 12 months of highly active an-tiretroviral therapy is associated with ongoingincreased CD4 T cell activation and turnover.J Acquir Immune Defic Syndr 2003; 33:125–33.7. Benveniste O, Flahault A, Rollot F, et al. Mech-anisms involved in the low-level regenerationof CD4+ cells in HIV-1-infected patients re-ceiving highly active antiretroviral therapywho have prolonged undetectable plasma viralloads. J Infect Dis 2005; 191:1670–9.8. Marchetti G, Gori A, Casabianca A, et al.Comparative analysis of T-cell turnover andhomeostatic parameters in HIV-infected pa-tients with discordant immune-virological re-sponses to HAART. AIDS 2006; 20:1727–36.9. Alves NL, Arosa FA, van Lier RA. Commongamma chain cytokines: dissidence in the de-tails. Immunol Lett 2007; 108:113–20.10. Fry T, Mackall C. Interleukin-7: from benchto clinic. Blood 2002; 99:3892–904.Reprints or correspondence: Dr. Giulia Marchetti, Dept. ofMedicine, Surgery and Dentistry, Clinic of Infectious Diseases,“San Paolo” Hospital, University of Milan, via A. di Rudinı`,8- 20142 Milan, Italy (giulia.marchetti@unimi.it).Clinical Infectious Diseases 2008; 46:149–50 2008 by the Infectious Diseases Society of America. Allrights reserved. 1058-4838/2008/4601-0029$15.00DOI: 10.1086/524087Cholera or Choleric?To the Editor—The cover of the 1 Sep-tember 2007 issue of Clinical InfectiousDiseases shows a 14th-century paintingbased on an 11th-century Arabic bookthat was described as an illustration of atreatment of cholera. However, there is noevidence that the disease that we now callcholera, caused by Vibrio cholerae, existedin Europe or Arabia at those times. Thefirst evidence of the presence of this dis-ease spreading westward outside the In-dian subcontinent arose in the early 19thcentury [1].Prior to the emergence of what we nowknow as cholera, the term “cholera” wassometimes applied to what were then con-sidered to be various disorders traceableto disturbances of bile, including a “chol-eric” or angry disposition [2]. It appearsto be likely that the cover illustration wasintended to show treatment of that dis-order, because the patient appears to beagitated, with breasts exposed, and seemsto be biting a towel. There is no sign ofthe diarrhea, vomiting, dehydration, orcollapse that are associated with what wenow know as cholera.AcknowledgmentsPotential conflicts of interest. D.R.N.: noconflicts.David R. NalinReferences1. Pollitzer R. Cholera. Geneva: World Health Or-ganization Monograph, 1959.2. Barua D, Greenough WB III, eds. Cholera. NewYork: Plenum, 1992.Reprints or correspondence: Dr. David R. Nalin, 100 LuckyHill Rd., West Chester, PA 19382 (davidnalin@aol.com).Clinical Infectious Diseases 2008; 46:150 2008 by the Infectious Diseases Society of America. Allrights reserved. 1058-4838/2008/4601-0030$15.00DOI: 10.1086/524088Interstrain AntigenicVariability of Mumps VirusesTo the Editor—We would like to con-gratulate Peltola et al. [1] on their excellentreview. As the authors emphasize, protec-tion from clinical disease is not perfect,even after 2 doses of mumps componentvaccine; both primary and secondary vac-cine failure were discussed as potential rea-sons. Another possibility for lack of pro-tection after mumps vaccination (andwild-type virus infection) is the existenceof heterologous mumps viruses that mayescape immune protection because of in-terstrain antigenic variability [2, 3]. Here,we report 3 such laboratory-confirmedcases of symptomatic mumps virus infec-tion in patients with documented pre-ex-isting immunity.The first case occurred in a 12-year-oldgirl who had received 2 mumps vaccina-tions (with Jeryl-Lynn vaccine strain inboth July 1990 and April 1997) and pre-sented with a lymphadenitis colli. At thattime, antimumps IgG antibodies were de-termined in a serum specimen (IgG an-tibody concentration, 1400 IU/mL; IgMantibody negative). Two weeks later, bi-lateral parotid swelling appeared; a secondELISA performed in the same laboratoryrevealed a 17-fold increase in antimumpsIgG antibody concentration to 24,000 IU/mL (IgM antibody negative).The second case occurred in a 9-year-old boy who had received 2 documentedmumps vaccinations (with Rubini vaccinestrain in July 1995 and with Jeryl-Lynnvaccine strain in March 2000) and pre-sented with acute bilateral parotid swell-ing; his antimumps IgG antibody concen-tration was 2900 IU/mL (IgM antibodynegative). Four weeks later, convalescent-phase serologic examination revealed aCORRESPONDENCE • CID 2008:46 (1 January) • 1515.5-fold increase in antimumps IgG an-tibody concentration to 16,000 IU/mL.The third case occurred in a 30-year-old male pediatric resident with no historyof mumps vaccination who had mumpsdisease during childhood. He had an an-timumps IgG antibody concentration of33 IU/mL in a serum sample obtained forscreening for newly employed health careworkers at our institution. One year later,the patient developed acute bilateral pa-rotid swelling. Examination of a serumsample obtained at that time revealed an8.5-fold increase in IgG antibody concen-tration to 277 IU/mL; this sample wastested together with the previous sampleand was antimumps IgM antibody nega-tive. Neutralizing assays confirmed rein-fection, despite pre-existing neutralizingantimumps serum antibodies. Ten dayslater, the patient’s 26-year-old female part-ner (with no history of mumps disease orvaccination) developed a primary mumpsinfection (IgM antibody positive). Thesecases illustrate that symptomatic mumpsreinfection may occur in the presence ofpre-existing specific mumps virus serumantibodies.AcknowledgmentsWe thank A. Tischer for providing the neu-tralizing assays.Potential conflicts of interest. U.H. and J.B.:no conflicts.Ulrich Heininger and Jan BonhoefferUniversity Children’s Hospital Basel,Basel, SwitzerlandReferences1. Peltola H, Kulkarni PS, Kapre SV, Paunio M,Jadhav SS, Dhere RM. Mumps outbreaks inCanada and the United States: time for newthinking on mumps vaccines. Clin Infect Dis2007; 45:459–66.2. Nojd J, Tecle T, Samuelsson A, Orvell C.Mumps virus neutralizing antibodies do notprotect against reinfection with a heterologousmumps virus genotype. Vaccine 2001; 19:1727–31.3. Rubin S, Mauldin J, Chumakov K, Vanderzan-den J, Iskow R, Carbone K. Serological andphylogenetic evidence of monotypic immuneresponses to different mumps virus strains. Vac-cine 2006; 24:2662–8.Reprints or correspondence: Dr. Ulrich Heininger, InfectiousDisease and Vaccines, University Children’s Hospital Basel(UKBB), Postbox, 4005 Basel, Switzerland (Ulrich.Heininger@unibas.ch).Clinical Infectious Diseases 2008; 46:150–1 2008 by the Infectious Diseases Society of America. Allrights reserved. 1058-4838/2008/4601-0031$15.00DOI: 10.1086/524089Prevention of Traveler’sDiarrhea: A Call toReconveneTo the Editor—More than 40 years havepassed since the initial reports of traveler’sdiarrhea (TD), and much has been learnedabout the epidemiology of this illness,which is most often attributed to coloni-zation of the intestinal track with patho-genic bacteria of a broad variety [1, 2].Although our understanding has im-proved and effective treatment has beenmade available, individuals are still trav-eling from developed countries to lesserdeveloped countries, and ∼1 of 3 will ex-perience an acute illness; some of theseindividuals will be incapacitated, but mostwill improve within a few days [3].In addition, 150 years ago, the initialdescriptions of postinfectious functionalbowel disorders were reported [4, 5], andin the past decade, a proliferation of stud-ies summarized in 2 recent systematic re-views have concluded that ∼1 of 10 peoplewho develop TD will acquire postinfec-tious irritable bowel syndrome (PI-IBS),despite normal preexisting bowel habits[6, 7]. Although PI-IBS is perhaps not asdebilitating as less frequent sequelae of re-active arthritis [8], Guillain Barre´ syn-drome [9], or inflammatory bowel disease[10], the attributable burden of PI-IBS ismeasurable. A quick calculation revealsthat, among the 100 million travelers eachyear from industrialized countries who areat intermediate to high risk of diarrhea,∼30 million will develop TD, and 3 mil-lion new cases of PI-IBS will arise [11].PI-IBS has been reported to persist in 57%of patients 6 years after its onset in onestudy, and postinfectious functional boweldisorders (predominantly PI-IBS) per-sisted in 76% of patients 5 years after itsonset in another study [12, 13]. These ill-nesses not only decrease the quality of lifeof those afflicted, but the economic impactis considerable. In a review of 18 economicstudies conducted in the United States andthe United Kingdom, the direct cost perpatient-year was estimated to be US$348–$8750 (in 2002), the annual number oflost days of work was 9–22 days, and theindirect cost per patient-year was esti-mated to be $355–$3344 [14]. Unques-tionably, this represents significant socialand economic impact.In addition to travel-related PI-IBS, thefraction of cases of IBS secondary to do-mestically acquired foodborne illnessneeds to be considered. IBS is the mostcommon chronic medical illness, seen inup to 15% of the US population and ac-counting for nearly one-third of all costsin gastroenterology as a result of investi-gation, management, and work lossamong those seeking care [15–17]. Al-though the attributable fraction of IBScases caused by domestic foodborne illnessis unknown, it is likely to be large, giventhe frequency of these illnesses [18]. Thus,the traditional thought of foodborne ill-ness as a self-limited condition also needsserious reconsideration and should informfuture food security policy decisions.Finally, shortly after the first reports ofTD 40 years ago, reports of studies eval-uating agents for use in prophylaxis fol-lowed. A number of effective regimenshave been described; however, widespreaduse of prophylaxis, particularly antimicro-bial agents, has been discouraged—a po-sition formalized in a 1985 National In-stitutes of Health consensus meeting thathas been unchallenged [19]. We feel thatPI-IBS is a development that challengesthis consensus.The balance of chemoprophylaxis risk,compared with the consequences of TDand sequelae, needs reassessment. Al-though certain questions remain regardingthe natural history of PI-IBS, effectivetreatment, and consequences of chemo-prophylaxis, it is time that the questionsregarding what can be done to prevent TD

Interstrain Antigenic Variability of Mumps Viruses

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