Ard, Kevin Lee

Chan, Brian Tan

Farmer, Paul Edward

Koenig, Serena Patricia

Milner, Danny Arnold

Emerging Infectious Diseases

PubMed

Harvard University - DASH 

 Peritoneal Tuberculosis in a Pregnant Woman from Haiti,United States  (Article begins on next page)The Harvard community has made this article openlyavailable.Please share how this access benefits you. Your storymatters.Citation Ard, Kevin Lee, Brian Tan Chan, Danny Arnold Milner, PaulEdward Farmer, and Serena Patricia Koenig. 2013.“Peritoneal Tuberculosis in a Pregnant Woman from Haiti,United States.” Emerging Infectious Diseases 19 (3) (March):514–516. doi:10.3201/eid1903.121109.http://dx.doi.org/10.3201/eid1903.121109.Published Version doi:10.3201/eid1903.121109Accessed February 19, 2015 3:49:55 PM ESTCitable Link http://nrs.harvard.edu/urn-3:HUL.InstRepos:12114767Terms of Use This article was downloaded from Harvard University'sDASH repository, and is made available under the terms andconditions applicable to Other Posted Material, as set forth athttp://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAALETTERS2012 probably represent only the so-called tip of the iceberg. Nevertheless, PCR analysis to detect Schmallenberg virus in samples from animals with clinical signs is a valuable method for identifying first cases in areas where Schmallenberg virus infections have not previously been found. AcknowledgmentWe gratefully acknowledge the farm-ers, diagnosticians in the regional labora-tories,  and  veterinary  officials  who  pro-vided data on reemerging Schmallenberg virus cases.Franz J. Conraths, Doris Kämer, Kathrin Teske, Bernd Hoffmann, Thomas C. Mettenleiter,  and Martin BeerAuthor	 affiliations:	 Friedrich-Loeffler-Insti-tut,	Greifswald-Insel-Riems,	Germany	DOI:	http://dx.doi.org/10.3201/eid1903.121324References  1.   Hoffmann B, Scheuch M, Höper D, Jung-blut R, Holsteg M, Schirrmeier H, et al. Novel orthobunyavirus in cattle, Europe, 2011. Emerg Infect Dis. 2012;18:469–72 http://dx.doi.org/10.3201/eid1803.111905.    2.    Garigliany MM, Bayrou C, Kleijnen D, Cassart D, Desmecht D. Schmallenberg virus in domestic cattle, Belgium, 2012. Emerg Infect Dis. 2012;18:1512–4 http://dx.doi.org/10.3201/eid1809.120716.  3.   Muskens J, Smolenaars AJ, van der Poel WH, Mars MH, van Wuijckhuise L, Hol-zhauer M, et al. [Diarrhea and loss of pro-duction on Dutch dairy farms caused by the Schmallenberg virus]. [in Dutch] Tijd-schr Diergeneeskd. 2012;137:112–5.  4.   Elbers AR, Loeffen WL, Quak S, de Boer-Luijtze E, van der Spek AN, Bouwstra R, et al. Seroprevalence of Schmallenberg virus antibodies among dairy cattle, the Netherlands, winter 2011–2012. Emerg Infect Dis. 2012;18:1065–71 http://dx.doi.org/10.3201/eid1807.120323.  5.   European  Food  Safety  Authority. “Schmallenberg” virus: analysis of the epidemiological data and impact assess-ment. EFSA Journal. 2012;10: 2768. doi:10.2903/j.efsa.2012.2768. www.efsa.europa.eu.efsajournal.  6.   World  Organisation  for  Animal  Health. OIE technical factsheet, May 2012 [cited 2013 Jan 3]. 1. Schmallenberg virus. www.oie.int/.../A_Schmallenberg_virus.pdf   7.   Ducomble T, Wilking H, Stark K, Takla A, Askar M, Schaade L, et al. Lack of evi-dence for Schmallenberg virus infection in highly exposed persons, Germany, 2012. Emerg Infect Dis. 2012;18:1333–5 http://dx.doi.org/10.3201/eid1808.120533.    8.   Rasmussen LD, Kristensen B, Kirkeby C, Rasmussen TB, Belsham GJ, Bød-ker R, et al. Culicoids as vectors of Schmallenberg virus. Emerg Infect Dis. 2012;18:1204–6 http://dx.doi.org/10.3201/eid1807.120385.  9.   Bilk S, Schulze C, Fischer M, Beer M, Hlinak A, Hoffmann B. Organ distri-bution of Schmallenberg virus RNA in malformed newborns. Vet Micro-biol. 2012;159:236–8. http://dx.doi.org/10.1016/j.vetmic.2012.03.035Address for correspondence: Franz J. Conraths,  Friedrich-Loeffler-Institut,  Federal Research Institute for Animal Health–Institute of Epidemiology, Seestrasse 55, Wusterhausen 16868, Germany; email: Franz.Conraths @fli.bund.dePeritoneal  Tuberculosis in a Pregnant Woman from Haiti,  United StatesTo the Editor: A 29-year-old woman at 23 weeks’ gestation during her first pregnancy came to our hos-pital’s obstetrics clinic after 6 days of vaginal bleeding and abdominal pain. She had not experienced fever, sweats, weight loss, contractions, or other symptoms. She was otherwise healthy; she was taking no medica-tions, but was taking iron and multi-vitamin supplements. She had legally immigrated to the United States from Haiti 8 months previously and had no known tuberculosis contacts. Physical examination disclosed brown vaginal discharge and a closed cervix. Obstet-ric ultrasound was normal, and vagi-nal swab samples were negative for Neisseria gonorrhea and Chlamydia trachomatis.Over the ensuing 2 weeks, her vaginal bleeding and abdominal pain worsened. She was admitted to the hospital. Physical examination re-vealed vaginal bleeding, but her con-dition was otherwise unchanged. Rou-tine laboratory studies were normal. Repeat obstetric ultrasound showed a viable fetus, ascites, and a 15 × 15 × 3–cm rind of echogenic material an-terior to the uterus. This abnormality was in the upper abdomen, an area not imaged on her previous ultrasound. Abdominal magnetic resonance imag-ing revealed moderate ascites and a 21 × 14 × 3–cm omental mass of interme-diate intensity on T1 and T2 sequenc-es; there was no lymphadenopathy (Figure). A tiny left pleural effusion was seen on chest radiograph. Routine HIV and tuberculin skin test results had been negative 4 months previ-ously, and pre-immigration examina-tion results and chest radiograph had been normal.Fine-needle aspiration of the omental mass was nondiagnostic. The patient’s vaginal bleeding and abdom-inal pain persisted, and her cervix di-lated. She had an oral temperature of 38.9° Celsius. Exploratory laparotomy demonstrated a friable omental mass with implants on the small bowel; a partial omentectomy was performed at 26 weeks’ gestation. During this procedure, the patient gave birth to a male infant.Multiple granulomata, some containing acid-fast bacilli, were identified  upon  histologic  examina-tion of the omentum (Technical Ap-pendix Figure, wwwnc.cdc.gov/EID/article/19/3/12-1109-Techapp1.pdf). Transcription-mediated  amplifica-tion of the specimen was positive for Mycobacterium tuberculosis rRNA; cultures later grew M. tuberculosis susceptible to all first-line antitubercu-losis medications. Sputum smears and cultures were not performed. The pa-tient’s treatment began with isoniazid, rifampin, ethambutol, and pyrazin-amide; her fevers and abdominal pain 514	 Emerging	Infectious	Diseases	•	www.cdc.gov/eid	•	Vol.	19,	No.	3,	March	2013LETTERSresolved. Her son was admitted to the neonatal intensive care unit and was placed on antimycobacterial therapy. He also recovered and was discharged after 135 days.This case highlights several is-sues related to tuberculosis epidemi-ology and diagnosis. Although pul-monary disease is the most common manifestation of tuberculosis overall, extrapulmonary tuberculosis accounts for a significant and increasing propor-tion of cases in the United States (1). Pregnancy is associated with greater likelihood of extrapulmonary disease; extrapulmonary infection accounts for 13% of all cases worldwide (2) but 50% of cases in pregnancy, according to a recent study (3).The frequency of peritoneal tu-berculosis in pregnancy is unknown; few cases have been reported in the literature (4–7), although we know of 3 additional cases from Haiti (online Technical Appendix Table). However, cases are likely underdiagnosed or di-agnosed late in the course of illness. Underdiagnosis and delayed diagno-sis may be caused by the nonspecific nature of symptoms, commonly ab-dominal pain and ascites, which can be attributed to pregnancy itself or obstetrical complications. These erro-neous explanations for symptoms are reflected in this patient, whose symp-toms were initially attributed to abrup-tion and who was not diagnosed with tuberculosis until >3 weeks after seek-ing medical assistance. Such delays in diagnosis are typical of peritoneal tuberculosis and are associated with increased death rates (8). In many cas-es, clinical features cannot distinguish peritoneal tuberculosis from malig-nancy, necessitating more extensive evaluation (7).Failure to diagnose peritoneal tu-berculosis, in pregnancy or otherwise, might also stem from the insensitiv-ity of noninvasive diagnostic testing. Paracentesis with acid-fast staining detects only a minority of cases (8). The sensitivity of mycobacterial cul-tures of ascites fluid varies, and cul-ture results are often not available for weeks (8).  Ascites  fluid  adenosine deaminase has shown promise as a reliable, minimally invasive diagnos-tic test in resource-poor countries, but was insensitive in a United States study (9). In addition, although tu-berculin skin testing and interferon gamma release assay performance are not affected by pregnancy (10), nei-ther can distinguish active from latent infection. Without diagnostic clinical features or sensitive noninvasive tests, the diagnosis of peritoneal tuberculo-sis might only be confirmed through laparoscopy or laparotomy, as in our case. Such invasive testing methods and facilities, equipment, and person-nel might not be readily available in resource-poor settings.This case also illustrates the on-going threat of tuberculosis in coun-tries of all income levels. It is not clear where our patient contracted tuberculosis; she was most likely ex-posed in Haiti, but transmission with-in her Haitian community in the Unit-ed States, or from another source, is also possible. Regardless, as in her case, a majority of tuberculosis cas-es within the United States occur in foreign-born persons. Given the ease and frequency of travel, lapses in tu-berculosis control in any locale are likely to have effects more broadly. Wherever they work, clinicians must maintain vigilance for tuberculosis in all of its protean forms.AcknowledgementsThe authors thank Walter Pieciak and Andrew Onderdonk for providing the molecular diagnostic testing used for this patient.Kevin L. Ard, Brian T. Chan, Danny A. Milner, Jr.,  Paul E. Farmer, and  Serena P. KoenigAffiliations:	Brigham	and	Women’s	Hospi-tal,	Boston,	Massachusetts,	USA	(K.L.	Ard,	B.T.	Chan,	D.A.	Milner	Jr,	P.E.	Farmer,	S.P.	Koenig);	and		Massachusetts	General	Hos-pital,	Boston	(K.L.	Ard,	B.T.	Chan)DOI:	http:/dx.doi.org/10.3201/eid1903.121109References    1.    Albalak R, O’Brien RJ, Kammerer JS, O’Brien SM, Marks SM, Castro KG, et al. Trends in tuberculosis/human   immunodeficiency  virus  comorbid-ity, United States, 1993–2004. Arch   Intern Med. 2007;167:2443–52.   http://dx.doi.org/10.1001/archinte. 167.22.2443  2.   World Health Organization. Global Tuber-culosis Control: WHO Report 2011. 2011 [cited 2012 Dec 5].  http://www.who.int/tb/publications/global_report/2011/gtbr11_full.pdf.    3.    Knight M, Kurinczuk JJ, Nelson-Piercy C, Spark P, Brocklehurst P. Tu-berculosis in pregnancy in the UK. BJOG. 2009;116:584–8. http://dx.doi.org/10.1111/j.1471-0528.2008.02097.x	 Emerging	Infectious	Diseases	•	www.cdc.gov/eid	•	Vol.	19,	No.	3,	March	2013	 515Figure.	 T2-weighted	 magnetic	resonance	 imaging	 sequence	 of	the	abdomen	of	a	pregnant	woman	from	 Haiti.	 An	 omental	 mass	 of	intermediate	intensity	(white	arrow)	is	shown	anterior	to	the	uterus.LETTERS  4.   Coden J. Tuberculous peritonitis in preg-nancy. BMJ. 1972;3:153. http://dx.doi.org/10.1136/bmj.3.5819.153  5.   Brooks JH, Stirrat GM. Tuberculous perito-nitis in pregnancy. Case report. Br J Obstet Gynaecol. 1986;93:1009–10. http://dx.doi.org/10.1111/j.1471-0528.1986.tb08027.x  6.   Lee GS, Kim SJ, Park IY, Shin JC, Kim SP. Tuberculous peritonitis in preg-nancy. J Obstet Gynaecol Res. 2005;31: 436–8. http://dx.doi.org/10.1111/j.1447-0756.2005.00316.x  7.   Sakorafas  GH,  Ntavatzikos A,  Konstan-tiadou I, Karamitopoulou E, Kavatha D, Peros G. Peritoneal tuberculosis in pregnancy mimicking advanced ovarian cancer: a plea to avoid hasty, radical and irreversible surgical decisions. Int J In-fect Dis. 2009;13:e270–2. http://dx.doi.org/10.1016/j.ijid.2008.11.003  8.   Chow KM, Chow VC, Hung LC, Wong SM, Szeto CC. Tuberculous peritonitis-associated mortality is high among pa-tients waiting for the results of mycobac-terial cultures of ascitic fluid samples. Clin Infect Dis. 2002;35:409–13. http://dx.doi.org/10.1086/341898  9.   Hillebrand  DJ,  Runyon  BA,  Yasmineh WG, Rynders GP. Ascitic fluid adenosine deaminase insensitivity in detecting tu-berculous peritonitis in the United States. Hepatology. 1996;24:1408–12. http://dx.doi.org/10.1002/hep.51024061710.   Lighter-Fisher J, Surette AM. Perfor-mance of an interferon-gamma release assay to diagnose latent tuberculosis infection during pregnancy. Obstet Gy-necol. 2012;119:1088–95. http://dx.doi.org/10.1097/AOG.0b013e3182546affAddress for correspondence: Kevin L. Ard, Brigham and Women’s Hospital; 75 Francis St, PBB-A4, Boston, MA 02115, USA; email: kard@partners.orgMicrosporidial  Keratoconjunctivitis Outbreak among Athletes from Hong Kong Who Visited Singapore, 2012To the Editor: An international outbreak of microsporidial kerato-conjunctivitis related to soil contact in a Singapore sport venue during April was reported to Hong Kong Department of Health, People’s Republic of China, in May 2012. Microsporidia are obligate intracellular, unicellular, eukaryotic, parasitic protists related to fungi (1). Fourteen species of microsporidia have been detected in humans (1). Several species of microsporidia, such as Vittaforma corneae, can cause keratoconjunctivitis (1). An increasing incidence of microsporidial keratitis in Singapore that is strongly correlated with exposure to soil was reported during 2004–2007 (2). In a case series of 22 patients during 2006–2008 in Singapore, soil or mud were reported as predominant ocular contaminants that were contacted by athletes during sporting activities, such as playing rugby in muddy fields (3).The outbreak reported in May 2012 affected 34 (41%) of 82 rugby players from Hong Kong who had participated in a rugby tournament in Singapore during April 21–22, 2012. In addition to the affected athletes from Hong Kong, there were 89, 15, 13, and 9 affected players, respectively, from Singapore, Malaysia, Australia, and United Arab Emirates (4). We conducted a retrospective cohort study among players from Hong Kong to identify potential risk and preventive factors for microsporidial keratoconjunctivitis.The rugby tournament involved ≈1,600 boys and girls from 16 rugby clubs in Singapore, Hong Kong, Malaysia, Australia, and the United Arab Emirates. We invited 82 boys (8–16 years of age) from 2 Hong Kong  rugby clubs that participated in the tournament to participate in telephone interviews during May 18–25, 2012. Using a standardized questionnaire, we collected information describing demographics and potential risk and preventive  factors.  We  defined  a case-patient as any player who had eye redness and 1 of the following ocular signs or symptoms since April 21: pain, discharge, swelling, or itchiness. We interviewed 73 (89%) of the 82 players: 34 (47%) met the case definition.  The  median  age  of  case-patients was 13 years (range 9–16 years); these figures were not different from those of the cohort (median age 13 years, range 8–16 years).Onset of the reported 34 cases ranged from April 26 through May 22, peaking on May 7 (Figure). The distribution of onset of cases over time indicates a point-source outbreak and reflects a wide range of incubation periods. Symptom onset occurred a median of 15 days (range 5–31 days) after opening day of the tournament.Except for 2 players who had histories of asthma, all players reported good past health. Ocular signs and symptoms of the 34 case-patients were redness (100%), pain (53%), itchiness (53%), discharge (47%), and swelling (41%). Corneal scraping samples from 3 players were positive for V. corneae by PCR.Heavy  rainfall  on  playing  fields was reported on April 21, when all the players from Hong Kong participated in the games and were exposed to soil and muddy water. Some players washed their eyes after exposure to the  dirt  in  the  field.  We  identified the following as preventive factors for keratoconjunctivitis: individual eye washing by bottled or tap water (relative risk [RR] 0.38, 95% CI 0.23–0.62), bottled water (RR 0.44, 95% CI 0.25–0.76) and tap water (RR 0.50, 95% CI 0.27–0.92). Group eye washing with water from a hose held by a trainer was not preventive. It is possible that individual eye washing by the players was more thorough.The 47% attack rate among the players from Hong Kong is higher than the overall 10% (160/1,600) attack rate for tournament participants. Rugby players from Hong Kong might have been less aware of the risk of contracting microsporidial keratoconjunctivitis through soil or muddy water exposure than were players from other locations.516	 Emerging	Infectious	Diseases	•	www.cdc.gov/eid	•	Vol.	19,	No.	3,	March	2013

Peritoneal Tuberculosis in a Pregnant Woman from Haiti, United States

Kevin L. Ard

Brian T. Chan

Danny A. Milner

Paul E. Farmer

Serena P. Koenig

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Peritoneal Tuberculosis in a Pregnant Woman from Haiti, United States

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