correspondence

PCI group) and hence the increased recorded incidence of refractory angina and nonfatal myocardial infarction. Since there was no core laboratory confirmation, what was the distribution of the severity of untreated lesions? What was the ejection fraction, and how many patients had systolic dysfunction and heart failure? What is needed is a trial comparing immediate PCI with staged, ischemia-driven PCI of noninfarct vessels. Until we have solid evidence, there is no reason for operators to deviate from the recommendation that noninfarct PCI should be performed only in patients whose condition is unstable.1 George V. Moukarbel, M.D. University of Toledo Medical Center Toledo, OH [email protected] No potential conflict of interest relevant to this letter was reported. 1. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA

Guideline for the Management of ST-Elevation Myocardial Infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:529-55. DOI: 10.1056/NEJMc1314696

Moukarbel is incorrect in stating that enzyme testing was reported as more frequent in the control group. His speculation that the reporting of primary end points may have been higher in the control group, in the absence of a treatment difference, is unlikely, given the single-blind design and the fact that the result was statistically significant for the hard end points of cardiac death and nonfatal myocardial infarction alone. Shah et al. make within-trial group comparisons across the different trials listed in Table 1 of their letter, which undermines the benefit of the randomized design that was adopted to avoid selection bias. Their cross-trial comparisons are biased, since the PRAMI trial was limited to multivessel disease with a poorer prognosis than that in the other four trials, which were not limited in this way. Hoebers et al. are incorrect in regarding procedural myocardial infarction and repeat PCI as part of the primary outcome. Dillinger et al. and White and Stewart request subset analyses, but given the size of the PRAMI trial, such analyses lack the statistical power to show different treatment effects according to the extent of coronary-artery stenoses.

David S. Wald, M.D. The authors reply: Our randomized trial Joan K. Morris, Ph.D. (PRAMI) showed that in patients with acute Nicholas J. Wald, F.R.S. STEMI, the use of preventive PCI resulted in a Barts and the London School of Medicine and Dentistry reduction of 65% in the primary trial outcome of London, United Kingdom cardiac death, nonfatal myocardial infarction, or [email protected] refractory angina (angina supported by objective for the PRAMI Investigators evidence of ischemia). The correspondents do not Since publication of their article, the authors report no furprovide evidence to indicate that this result is in- ther potential conflict of interest. valid or biased. DOI: 10.1056/NEJMc1314696

An Emmonsia Species Causing Disseminated Infection in South Africa To the Editor: Kenyon and colleagues (Oct. 10 issue)1 described 13 cases of disseminated disease caused by an emmonsia species; all 13 patients had advanced human immunodeficiency virus (HIV) infection. We describe two HIV-uninfected patients with disseminated emmonsiosis from the same geographic area. At our hospital, we reviewed patients with invasive fungal disease between 2008 and 2011. We identified emmonsiosis in two HIV-negative patients (Table 1), one

with no apparent risk factors and the other a renaltransplant patient receiving immunosuppressive therapy. A case of disseminated emmonsiosis in an apparently immunocompetent person (Patient 1) raises the question of whether this is a more virulent strain or a different species or whether the host had exposure to a large amount of the organism or had an undiagnosed immune disorder.2 Molecular techniques were needed to make the final diagnosis, and accurate identification

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The

n e w e ng l a n d j o u r na l

of

m e dic i n e

Table 1. Clinical Characteristics of HIV-Uninfected Patients with Emmonsiosis.* Variable

Patient 1

Age (yr)

Patient 2

52

Sex Risk factors for immune suppression

48

Male

Male

None known

Immunosuppressive therapy after renal transplantation, with transplant rejection

Clinical features

Headache, raised intracranial pressure, and ataxia

Productive cough, malaise, and skin lesions

Imaging results

Solid contrast-enhancing cerebellar ­lesion with multiple small abscesses

Mass in right upper lobe of lung

Diagnostic tests

Cerebellar biopsy showed budding yeast Transbronchial biopsy showed fungal elecells; tissue-culture assay initially identiments on histologic analysis; both tissue-­ fied blastomyces species, but PCR assay culture assay and PCR assay identified identified emmonsia species ­emmonsia species

Treatment

Intravenous amphotericin B followed by oral itraconazole

Outcome

Alive after 3 yr

Oral itraconazole Died 1 mo later

* PCR denotes polymerase chain reaction.

has been a problem in the past.3 Both cases highlight the fact that in this geographic area, emmonsiosis may appear outside the clinical realm of HIV-infected patients and warrants further investigation. Izak Heys, M.D. Jantjie Taljaard, M.D. Heidi Orth, M.D. University of Stellenbosch Cape Town, South Africa [email protected] Dr. Heys reports having received financial support from the President’s Emergency Plan for AIDS Relief–U.S. Agency for International Development through the Anova Health Institute. No other potential conflict of interest relevant to this letter was reported. 1. Kenyon C, Bonorchis K, Corcoran C, et al. A dimorphic fun-

gus causing disseminated infection in South Africa. N Engl J Med 2013;369:1416-24. 2. Al-Abdely HM. Management of rare fungal infections. Curr Opin Infect Dis 2004;17:527-32. 3. Anstead GM, Sutton DA, Graybill JR. Adiaspiromycosis causing respiratory failure and a review of human infections due to Emmonsia and Chrysosporium spp. J Clin Microbiol 2012;50:1346-54. DOI: 10.1056/NEJMc1314277

mary pathogen like Histoplasma capsulatum, although further investigations may have revealed an underlying immune deficiency in Patient 1. Heys et al. speculate that the emmonsia species that caused disease in Patient 1 may be a different species or a more virulent strain. However, perfect pairwise sequence alignment of a portion of the internal transcribed spacer region of this isolate to those reported in our case series suggests that this is the same species. Because its portal of entry is likely through inhalation, we hypothesize that this southern African emmonsia species may initially cause a pneumonic illness in immunocompetent persons who are exposed to a large inoculum. There is a need to determine the prevalence and full clinical spectrum of emmonsiosis in southern Africa. Chris Kenyon, M.D., Ph.D. University of Cape Town Cape Town, South Africa [email protected]

Craig Corcoran, F.C.Path. National Health Laboratory Service Johannesburg, South Africa

The authors reply: The description by Heys Nelesh P. Govender, M.D. and colleagues of two cases of invasive emmon- National Institute for Communicable Diseases siosis in HIV-uninfected persons, and in particu- Johannesburg, South Africa lar the case in a patient with no apparent immuSince publication of their article, the authors report no furnodeficiency, raises additional questions. The ther potential conflict of interest. new emmonsia species may potentially be a pri- DOI: 10.1056/NEJMc1314277

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An emmonsia species causing disseminated infection in South Africa.

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