Letters20 March 2012Occupational Syphilis Following Scalpel InjuryJan D. Raguse, MD, Christian Camerer, MD, Frank Bergmann, MD, Christiane Schewe, MD, and Dirk Schürmann, MDJan D. Raguse, MDFrom Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Search for more papers by this author, Christian Camerer, MDFrom Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Search for more papers by this author, Frank Bergmann, MDFrom Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Search for more papers by this author, Christiane Schewe, MDFrom Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Search for more papers by this author, and Dirk Schürmann, MDFrom Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-156-6-201203200-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Background: Previous reports have described many cases of occupational syphilis in health care personnel, but virtually all such reports were published before 1950 (1). In those reports, contact with a mucosal lesion was the most frequent route of transmission, but injuries from sharp devices were also reported to be routes of transmission (1).Education and prevention have made occurrences of occupational syphilis exceedingly rare (1). A review of the literature (2) found only 1 report of transmission through sharps injury. That report, however, did not involve a health care worker but a family caregiver who stuck herself with a needle ...References1. Meyer GS. Occupational infection in health care. The century-old lessons from syphilis. Arch Intern Med. 1993;153:2439-47. [PMID: 8215748] CrossrefMedlineGoogle Scholar2. Franco A, Aprea L, Dell'Isola C, Faella FS, Felaco FM, Manzillo E, et al. Clinical case of seroconversion for syphilis following a needlestick injury: why not take a prophylaxis? Infez Med. 2007;15:187-90. [PMID: 17940403] MedlineGoogle Scholar3. Palmer HM, Higgins SP, Herring AJ, Kingston MA. Use of PCR in the diagnosis of early syphilis in the United Kingdom. Sex Transm Infect. 2003;79:479-83. [PMID: 14663125] CrossrefMedlineGoogle Scholar4. Kent ME, Romanelli F. Reexamining syphilis: an update on epidemiology, clinical manifestations, and management. Ann Pharmacother. 2008;42:226-36. [PMID: 18212261] CrossrefMedlineGoogle Scholar5. Ficarra G, Carlos R. Syphilis: the renaissance of an old disease with oral implications. Head Neck Pathol. 2009;3:195-206. [PMID: 20596972] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAuthors: Jan D. Raguse, MD; Christian Camerer, MD; Frank Bergmann, MD; Christiane Schewe, MD; Dirk Schürmann, MDAffiliations: From Charité|Universitätsmedizin Berlin, Berlin 13353, Germany.Disclosures: Dr. Raguse: Board membership: Sanofi Aventis, Merck Serono. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySexually transmitted infections and female reproductive healthSyphilis transmission: a review of the current evidenceBlood and Body Fluid Exposures in Health-Care Settings: Risk Reduction Practices and Postexposure Prophylaxis for Health-Care Workers 20 March 2012Volume 156, Issue 6Page: 475-476KeywordsBiopsyHIV infectionsHepatitis C virusLesionsPolymerase chain reactionResearch laboratoriesSexually transmitted diseasesSurgeonsSyphilisUlcers ePublished: 20 March 2012 Issue Published: 20 March 2012 Copyright & PermissionsCopyright © 2012 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

Background For patients infected with the human immunodeficiency virus type 1 (HIV-1), the clinical course and overall health risk after 2009 H1N1 influenza virus infection is not well established. Objective Describe the clinical course, kinetics of viral shedding, and the H1N1 influenza-specific humoral immune response among HIV-infected children. Methods Observational study after an outbreak of 2009 H1N1 influenza virus infections among a travel group of 15 HIV-infected children (aged 8.9–16.8 years) in Germany in October 2009. All children had been treated with highly active antiretroviral therapy and had CD4 cell counts exceeding 350/µL. Disease symptoms were recorded and shedding of H1N1 influenza virus was assessed by detection of virus-specific RNA and culture of virus from nasal secretions. Serum levels of H1N1-specific antibodies were determined at 6 weeks after symptom-onset. Results In all 15 children of the travel group, infection with the 2009 H1N1 influenza virus was confirmed by viral culture and reverse transcriptase polymerase chain reaction from nasal secretions (n=11) and/or detection of 2009 H1N1-specific antibodies. Fourteen children (93%) had symptoms of disease, mostly consisting of low-grade fevers and cough. Five children (33%) had high-grade fevers (>39°C) and, thus, were treated with oseltamivir. Among the 11 children in whom viral shedding was assessed, viral RNA was detected for 4 versus 8 days (p=0.005), and cell cultures tested positive for 3 versus 6 days (p=0.005), respectively, among oseltamivir-treated (n=5) and non-treated (n=6) children. At 6 weeks after symptoms-onset, all children had developed H1N1 virus-specific antibodies. Conclusions Clinical course, kinetics of viral shedding, and rate of emergence of virus-specific antibodies among school-aged HIV-infected children with 2009 H1N1 influenza virus co-infection did not appear to be different from those described for healthy children. Oseltamivir shortens the duration of H1N1 influenza virus shedding in HIV-infected children.

Patients infected with human immunodeficiency virus type 1 (HIV-1) are considered to be at increased risk for 2009 H1N1 influenza-related complications. We performed an observational study after an outbreak of 2009 H1N1 influenza virus infection among a group of 15 HIV-1-infected school-aged children in Germany in October 2009. Clinical course, kinetics of viral shedding, and antibody response among children with CD4 cell counts >350 cells/μL and 2009 H1N1 influenza virus coinfection did not appear to differ from that among healthy children. Oseltamivir shortened the duration of viral shedding.

In non-endemic areas, malaria is rare and locally acquired infections, particularly with Plasmodium falciparum, are exceptional events. The diagnosis is, therefore, likely to be delayed or missed in patients without a relevant travel history. This report describes a case of falciparum malaria in Berlin, Germany, in a patient who had not been to an endemic area for more than a decade. Potential routes of vector-related and direct transmission were evaluated, particularly with regard to a possible danger to the public. A review of the literature was conducted regarding possible routes of transmission and their probability assessed. Genotyping of parasite isolates of this and another patient with malaria admitted 16 days before revealed homology between the two strains. In a local entomological survey, anopheline vectors on the hospital grounds as well as in the residential area of both patients were found. Despite intensive investigations, the mode of transmission remained obscure. In this context, possible routes of vector-borne and direct occupational/accidental transmission in a major European city are reviewed and discussed, providing information and guidance in case other similar events occur elsewhere. Examples for investigations and measures to be taken in such a situation are provided. When local malaria transmission within a large non-immune population cannot be ruled out, genotyping of parasite isolates, local entomological surveys, preparedness for secondary cases, expert consultations in a multidisciplinary team and careful information management are essential. Malaria acquired in non-endemic areas remains an unlikely, but possible event for which awareness needs to be maintained.

Editor, Toxoplasmic chorioretinitis is the most common cause of retinochoroiditis in humans worldwide and the second most common infectious cause of ocular lesions in HIV-infected patients (Lanska 1999). Until now, ocular toxoplasmosis (OT) as the presenting manifestation of HIV infection has been rarely reported (Holland et al. 1988; Cochereau-Massin et al. 1992). The patient reported in this study (a 36-year-old, White man who was a former i.v. drug abuser) had known he was infected with HIV for 7 years prior to presentation at our institution. This report and the data accumulation process informing it were approved by the Ethical Committee of Charité-Universitätsmedizin Berlin, Humboldt University of Berlin. All research followed the tenets of the Declaration of Helsinki. Informed consent was obtained from the patient, whose identity and observation times have been concealed. On staging, Toxoplasma gondii serology was positive for IgG but negative for IgM, thus indicating previous (asymptomatic) infection. Fundoscopy of both eyes showed no evidence of retinitis or scarring. At that time, the subject's CD4 cell counts were consistently above 400/µl, indicating continuing sufficient cellular immunity, and he did not receive any antiretroviral therapy. One year later, he developed blurred vision and frontal cephalgia. Differential diagnosis included toxoplasmosis, varicella-zoster virus, herpes simplex virus 1/2, lues, and foreign body reaction. Treatment with ganciclovir was initiated. A week later, findings were consistent with OT (central inflammation with infiltration of the vitreous body), and T. gondii IgM turned positive (Table 1). Cranial computerized tomography analysis did not reveal any intracerebral lesions corresponding to central nervous system toxoplasmic encephalitis. Antitoxoplasmic therapy with clindamycin, pyrimethamine and folinic acid in standard doses was given over 1 month and switched to maintenance therapy with sulphadoxin/pyrimethamine 1 tablet twice weekly when the retinal lesions had resolved to scars but clouding of the vitreous body persisted. Three months later, blurred vision occurred in the left eye, and a fresh central toxoplasmic lesion was diagnosed. Again, acute therapy was initiated as above, but clindamycin was replaced by 4 × 1 g sulphadoxin 3 weeks later when the focus showed no regression. Another month later, the patient showed no sign of active toxoplasmic retinitis in the left eye, but a central scotoma and synechiae remained, with almost complete loss of vision. Secondary prophylaxis was initiated again, but the patient did not completely adhere to it, particularly when his i.v. drug abuse recurred. No further episodes of OT disease occurred over the next 3 years. Relevant clinical data recorded during the OT episodes described here are summarized in Table 1. Plasma samples from this patient were routinely collected for more than 4 years. Interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) bioactivities were analysed by B9 and WEHI-164 bioassays, respectively, as described (Prada et al. 1993). Nitric oxides (NO) were evaluated as nitrite by a compensated Griess reaction, and neopterin was assayed by enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed using Student's t-test and Pearson's correlation coefficient (PCC). The highest levels of IL-6, TNF-α and NO were always detected during the OT episodes described (Fig. 1). The levels of IL-6 were much higher than those of TNF-α or NO, and were statistically significant (p = 0.0049) compared with the other recorded IL-6 values. The best correlation was observed between TNF-α and NO (PCC = 0.4), whereas IL-6 presented a PCC of 0.3, both with TNF-α and NO. Neopterin did not correlate with any of the other molecules analysed (PCC = 0.0). (A) Interleukin-6 (IL-6) bioactivities and concentrations of neopterin, and (B) tumour necrosis factor (TNF)-α bioactivities and accumulation of nitric oxides (NO) in plasma samples collected from an HIV patient presenting with episodes of ocular toxoplasmosis (OT). Values are means of triple measurements of triplicates with standard error of the mean < 5% of the means. IL-6 and TNF-α are both expressed in bioactivity units/ml plasma. Neopterin and NO are recorded as µmol neopterin/ml and nmol nitrite/ml plasma, respectively. The year number in the dates corresponds to the order number of the year of observation after admission. OT episodes = period when OT episodes were observed. The IL-6 increases observed during OT were statistically significant (p = 0.0049) compared with the other recorded IL-6 values. TNF-α and NO showed a Pearson's correlation coefficient (PCC) of 0.4 with one another, and IL-6 presented a PCC of 0.3, both with TNF-α and NO. Neopterin did not correlate with any of the other parameters analysed (PCC = 0.0). These results agree with previous observations at the mRNA level in a murine model of OT (Lyons et al. 2001), where transcripts for inflammatory mediators, such as IL-6, TNF-α and iNOS (inducible NO-synthase), were increased during chronic infection with T. gondii parasites. As reported in the OT murine model, the increased IL-6 levels during OT may provide a protective effect for the host by controlling the number of T. gondii parasites as well as the development of ocular inflammation. The highest IL-6 levels detected also corresponded with critical events during OT, such as extended conjunctivitis, vitreous turbidity and/or temporary blindness. Thus, high levels of IL-6 and, in a minor extension, also of TNF-α and NO (but not of neopterin), seem to represent interesting markers for assessing the development of critical ocular complications during the course of OT in HIV patients. The authors are especially grateful to B. Dominik, Department of Internal Medicine, Section of Infectiology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, for excellent technical assistance in the collection of the plasma samples. J. Prada was partially supported by the Rudolf Siedersleben−Otto Wolff Foundation, Cologne, Germany. Part of this work was presented as a poster at the European Association for Vision and Eye Research (EVER) Meeting 2006, Vilamoura, Portugal, October 4−7th, 2006.

Human toxocariasis is usually contracted by exposure to contaminated soil. This disease is rarely transmitted by raw meat or giblets of paratenic animals, such as chickens, lambs, or cows. We present a case of isolated cerebral toxocariasis presumably caused by the consumption of raw duck liver. This 55-year-old woman had sudden-onset hemiparesis of the right leg, eosinophilia of 30%, and markedly elevated total serum IgE levels. Magnetic resonance imaging demonstrated multiple cerebral hyperintense lesions on T2-weighed images. Tests for antibodies to Toxocara in serum and cerebrospinal fluid yielded highly positive results. Repeated courses of albendazole and corticosteroids led to significant clinical improvement.

Background ESPRIT is a randomized trial comparing the clinical impact of interleukin (IL)-2 plus antiretrovirals vs antiretrovirals alone. Identification of factors that influence the relationship between IL-2 and CD4 count recovery will enable better personalization of treatment with IL-2 in HIV-1-positive individuals. The IL-2 induction phase consists of three dosing cycles over 6-8 months (7.5 MIU twice a day, for 5 days every 8 weeks).Methods We included patients initiating IL-2 at the 7.5 MIU dose with an 8-month CD4 count, measured at least 30 days after their last cycle. We identified baseline predictors of CD4 count changes over 8 months using linear regression.Results Of 2090 patients assigned IL-2, 1673 (80%) were included in the analysis. The median (interquartile range) baseline CD4 count was 461 (370, 587) cells/mu L with a median increase of 233 (90, 411) cells/mu L at month 8. After adjustments, significant predictors of CD4 count change included CD4 nadir (29.8 cells/mu L greater increase per 100 cells/mu L higher; P < 0.0001), last CD4 count before baseline (mean 36.0 cells/mu L greater increase per 100 cells/mu L higher; P < 0.0001), time from antiretroviral start to baseline (8.3 cells/mu L smaller increase per year longer; P=0.001), age (11.7 cells/mu L smaller increase per 5 years older; P=0.005) and race (79.7 cells/mu L greater increase for black patients vs white patients; P=0.003). A linear relationship existed between total IL-2 dose in the first cycle and CD4 count change (73.1 cells/mu L greater increase per 15 MIU higher; P < 0.0001).Conclusions Prior nadir and current CD4 counts, age and IL-2 dose are major determinants of CD4 increases induced by with intermittent administration of IL-2 in HIV-1-positive individuals on antiretrovirals. The clinical function of these induced CD4 cells is under study.