COLOMBA, Claudia

GIAMMANCO, Giovanni

INGRASSIA, Daniela

RUBINO, Raffaella

SAPORITO, Laura

SPICOLA, Daria

TITONE LANZA DI SCALEA, Lucina

Archivio istituzionale della ricerca - Università di Palermo

Downloaded from www.microbiologyresearch.org byIP:  147.163.72.194On: Sun, 17 Sep 2017 18:39:53Case Report Severe Mediterranean spotted fever complicatedby acute renal failure and herpetic oesophagitisLaura Saporito,1 Giovanni M. Giammanco,2 Raffaella Rubino,1Daniela Ingrassia,1 Daria Spicola,1 Lucina Titone1 and Claudia Colomba1CorrespondenceLaura Saporitolaura.sapo@tin.itReceived 11 September 2009Accepted 20 May 20101Dipartimento di Scienze per la Promozione della Salute, Sezione di Malattie Infettive,Universita` di Palermo, Via del Vespro 129, 90127 Palermo, Italy2Dipartimento di Scienze per la Promozione della Salute, Sezione di Microbiologia,Universita` di Palermo, Via del Vespro 129, 90127 Palermo, ItalyMediterranean spotted fever (MSF) is a tick-borne disease caused by Rickettsia conorii. Recently,complicated cases have been more frequently reported, even in previously healthy patients. Wedescribe a case of severe MSF complicated by acute renal failure and associated with herpeticoesophagitis. Acyclovir therapy resulted in remission of oesophageal symptoms within 48 h.IntroductionMediterranean spotted fever (MSF) is a tick-borne diseasecaused by Rickettsia conorii. In Italy about 400 cases arereported every year. Nearly half occur in Sicily, which isone of the most endemic regions. MSF is typicallycharacterized by fever, skin rash and a black eschar at thesite of the tick bite (‘tache noire’). At present, severe formsare more frequently described and the current fatality ratefor MSF is increasing (Brouqui et al., 2007; Rovery et al.,2008). Complications are described mainly in adultpatients, and include hepatic, renal, cardiac and neuro-logical impairment. Severe complications can be preventedby a prompt and efficacious antibiotic treatment. Diagnosisis based on epidemiological, clinical and laboratory criteria(Brouqui et al., 2007). We describe a case of severe MSFcomplicated by acute renal failure and associated withherpetic oesophagitis.Case reportIn August 2008 a 50-year-old Italian man was admitted tothe Infectious Diseases Unit of the University Hospital ofPalermo, Italy, because of continuous-remittent fever andmalaise of 6 days duration. A diffuse rash had appearedthe day before admission. An antibacterial therapy withamoxicillin/clavulanate had been started at home withoutan improvement of the symptoms.In the patient’s medical history there was no evidence ofcardiac illness, diabetes mellitus, or hepatic, gastric or renaldysfunctions. On admission, the patient appeared acutelyill, with a maculo-papular rash with some petechialelements involving the trunk and the extremities, includingpalms and soles. Herpetiform skin lesions of 565 cm werepresent on the upper lip and the nose. A single lesion of20 mm in diameter surrounded by an inflammatory halowith a small central crust was observed on the right leg.Physical examination showed a diffusely tender abdomenwith significant splenomegaly and lower extremitiesoedema. Results of cardiovascular, respiratory and neuro-logical examinations were unremarkable. The patient’sblood pressure was 120/70 mmHg and his body temper-ature was 39.5 uC.Laboratory examination demonstrated normal white andred blood cell counts and a normal haemoglobin value, witha low platelet count (51 000 cells ml21), and increased serumurea (191 mg dl21), creatinine (6.1 mg dl21), aspartateaminotransferase (469 IU l21), alanine aminotransferase(229 IU l21) and C-reactive protein (26.77 mg dl21).Coagulation parameters were within normal limits.Creatinine clearance was 12.8 ml min21.Chest X-ray showed a bilateral pleural effusion. Anabdominal ultrasound scan showed splenomegaly (trans-verse diameter 17 cm) and a normal aspect of bothkidneys.Because of a rash that was evocative of MSF, R. conoriiserological testing was performed and two blood samples werecollected for testing rickettsial DNA by real-time PCR usingprimers for the citrate synthase-encoding gene, gltA (Stenoset al., 2005). Treatment with 100 mg doxycycline twice dailywas started. Intravenous furosemide was administered(20 mg, three times daily, for 5 days) to reduce the oedemaof the lower extremities and the bilateral pleural effusion.The day after admission the patient complained of severeretrosternal pain and odynophagia and presented withmelena. Oesophagogastroduodenoscopy (OGD) evidencedsevere ulcerative lesions with raised edges and exudativebottoms throughout the entire oesophagus. There wasAbbreviations: HSV, herpes simplex virus; MSF, Mediterranean spottedfever; OGD, oesophagogastroduodenoscopy.Journal of Medical Microbiology (2010), 59, 990–992 DOI 10.1099/jmm.0.015891-0990 015891 G 2010 SGM Printed in Great BritainDownloaded from www.microbiologyresearch.org byIP:  147.163.72.194On: Sun, 17 Sep 2017 18:39:53redness and punctiform bleeding of the antral mucosa.Lesions were consistent with herpetic oesophagitis anderosive gastritis. Oral acyclovir (800 mg daily for 10 days)and omeprazole (20 mg twice daily for 7 days) wereprescribed, and remission of the oesophageal symptomswas obtained after 48 h treatment.Specific anti-rickettsia IgM and IgG determinations wereperformed by an indirect immunofluorescence assay withantigens obtained from a clinical isolate of R. conorii subsp.conorii freshly prepared as described by Vitale et al. (1989).An immunofluorescent antibody test for R. conorii showedan increase of titres in two sera obtained after a 2 weekinterval (first sample IgM 1 : 40 and IgG negative; secondsample IgM 1 : 1280 and IgG 1 : 640). Rickettsial DNA wasdetected from both full blood and buffy coat samples witha highly sensitive and specific real-time PCR assay for thedetection of spotted fever and typhus group Rickettsiaeusing primers to the citrate synthase-encoding gene, gltA(Stenos et al., 2005).The ETI-HSVK-G enzyme immunoassay kit (Diasorin/Sorin Diagnostics), a qualitative ELISA for the detection ofIgG antibodies to herpes simplex virus type 1 (HSV1) and/or type 2 (HSV2) gB-1 antigens in human serum,demonstrated a high titre of anti-HSV1 IgG.Blood cultures were negative for aerobic/anaerobic bacteria,mycobacteria and fungi. Results of serological tests werenegative for hepatitis viruses A, B and C, cytomegalovirus,Epstein–Barr virus, Brucella spp., Leptospira spp., Salmonellaspp. and human immunodeficiency virus infections.Immunological work-up showed normal CD4 levels.Monitoring laboratory tests were strictly performed andshowed a progressive reduction in haemoglobin values(7.5 g dl21) and diuresis (200 ml per day) for 1 week, whilea progressive defervescence and rash disappearance werealso observed.At discharge, haematochemical values were within normalranges. The follow-up OGD 1 month after dischargeshowed no oesophageal lesions.DiscussionDuring the last few years rickettsial diseases have emergedin several Mediterranean countries (Rovery et al., 2008;Schmulewitz et al., 2008; Boillat et al., 2008; Weinbergeret al., 2008). Until the 1980s, MSF was thought to be abenign illness with few complications and the propor-tion of deaths was ,1%. In recent times, complicatedMSF cases have been reported, even in the absence ofpredisposing conditions (Colomba et al., 2008; Leone et al.,2008; Tsiachris et al., 2008; Tzavella et al., 2006). Thepathogenesis of MSF complications results from vascularinjury, which may be responsible for the dysfunction ofdifferent organs (Brouqui et al., 2007; Rovery et al., 2008;Schmulewitz et al., 2008). Our patient was previouslyhealthy. In particular, he denied any history of renal orgastro-oesophageal disease. The only recognizable riskfactor for a severe form of MSF could be the inappropriateantibacterial therapy that had been started at home andthat could have delayed the correct treatment.Renal impairment has been frequently described as aconsequence of severe MSF. It has been observed that acuterenal failure was most strongly associated with a fataloutcome (Sousa et al., 2008).To the best of our knowledge, an association between MSFand oesophagitis has never been reported. Oesophagitisdue to HSV1 is a well-recognized entity in immunocom-promised patients but it has rarely been described inimmunocompetent hosts. It can represent either primaryinfection or reactivation. In our patient the diagnosis ofHSV1 oesophagitis due to a reactivation of a primaryinfection was based on the concomitant presence of herpeslabialis, characteristic endoscopic findings and HSV1serological results. In our patient ulcerative lesions werepresent throughout the entire oesophagus, and the follow-up OGD 1 month after discharge showed no oesophageallesions.Severe complications of herpetic oesophagitis, includingbleeding and oesophageal perforation, have rarely beenreported in immunocompetent hosts (Chien et al., 1992;Cronstedt et al., 1992). Antiviral treatment of herpeticoesophagitis in immunocompetent hosts is controversial(Kurahara et al., 1998; Ramanathan et al., 2000). Earlyinitiation of acyclovir therapy was beneficial for our patient,who had a striking response to the treatment within 48 h.Our patient was affected by a severe MSF, complicated byacute renal failure and associated with a rare clinicalpicture of HSV1 reactivation. It can be supposed that amore virulent R. conorii strain affected our patient, causingthe severe MSF. Acute renal failure could represent acofactor for a transient decline of immunological status sothat a latent herpetic infection could reactivate.In conclusion, complicated MSF has to be taken intoaccount even in individuals without any underlying riskfactor. Severe MSF can be accompanied by clinical featuresthat are more frequently observed in immunocompro-mised patients.ReferencesBoillat, N., Genton, B., D’Acremont, V., Raoult, D. & Greub, G. (2008).Fatal case of Israeli spotted fever after Mediterranean cruise. EmergInfect Dis 14, 1944–1946.Brouqui, P., Parola, P., Fournier, P. E. & Raoult, D. (2007). 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Emerg Infect Dis 14, 995–997.Sousa, R., Franc¸a, A., Do´ria No`brega, S., Belo, A., Amaro, M., Abreu, T.,Poc¸as, J., Proenc¸a, P., Vaz, J. & other authors (2008). Host- andmicrobe-related risk factors for and pathophysiology of fatal Rickettsiaconorii infection in Portuguese patients. J Infect Dis 198, 576–585.Stenos, J., Graves, S. R. & Unsworth, N. B. (2005). A highly sensitiveand specific real-time PCR assay for the detection of spotted fever andtyphus group Rickettsiae. Am J Trop Med Hyg 73, 1083–1085.Tsiachris, D., Deutsch, M., Vassilopoulos, D., Zafiropoulou, R. &Archimandritis, A. J. (2008). Sensorineural hearing loss complicatingsevere rickettsial diseases: report of two cases. J Infect 56, 74–76.Tzavella, K., Chatzizisis, Y. S., Vakali, A., Mandraveli, K., Zioutas, D.& Alexiou-Daniel, S. (2006). Severe case of Mediterranean spottedfever in Greece with predominantly neurological features. J MedMicrobiol 55, 341–343.Vitale, G., Di Stefano, R., Damiani, G. & Mansueto, S. (1989).Characterization of Sicilian strains of spotted fever group rickettsiaeby using monoclonal antibodies. J Clin Microbiol 27, 1081–1085.Weinberger, M., Keysary, A., Sandbank, J., Zaidenstein, R., Itzhaki, A.,Strenger, C., Leitner, M., Paddock, C. D. & Eremeeva, M. E. (2008).Fatal Rickettsia conorii subsp. israelensis infection, Israel. Emerg InfectDis 14, 821–824.L. Saporito and others992 Journal of Medical Microbiology 59

Severe Mediterranean spotted fever complicated by acute renal failure and herpetic oesophagitis.

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Severe Mediterranean spotted fever complicated by acute renal failure and herpetic oesophagitis.

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