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Pneumocystis pneumonia in humans is caused by P jiroveci not P carinii
  1. R Miller1
  1. 1Mortimer Market Centre, Camden PCT and Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, University College London, London WC1E 6AU, UK;
  1. R J Boyton2,
  2. D M Mitchell2,
  3. O M Kan2
  1. 2Chest and Allergy Department, St Mary’s Hospital NHS Trust, London W2 1NY, UK;

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I read with interest the illustrative case by Boyton et al1 on the subject of HIV associated pneumonia, which highlights the improved survival among HIV infected patients with Pneumocystis pneumonia (PCP) admitted to ICU since the introduction of both PCP prophylaxis and highly active antiretroviral therapy (HAART). This article will help inform physicians and intensivists about the optimal management of patients with PCP and respiratory failure and enable identification of individuals who will most benefit from ICU. The article raises two issues—firstly, the name used to describe human Pneumocystis infection and, secondly, the choice of second line treatment for PCP.

From its description by Chagas in 1909 until recently, Pneumocystis was thought to be a protozoan. In 1988, by DNA analysis, the organism was revealed to be a fungus.2 Additional DNA data have subsequently shown that Pneumocystis organisms derived from different mammalian host species are quite different3; furthermore, attempts at cross infection between host species have not been successful, indicating host species specificity and that Pneumocystis infection in humans is not a zoonosis. The organism that causes human PCP is now named Pneumocystis jiroveci Frenkel 1999—in honour of the Czech parasitologist Otto Jírovec who was one of the first researchers to describe Pneumocystis infection in humans.4,5Pneumocystis carinii is now only used to describe the rat derived infection.4,5 The acronym “PCP” used to describe the clinical syndrome of pneumonia in humans and other mammalian hosts still applies—PneumoCystisPneumonia. Pneumocystis jiroveci (pronounced “yee-row-vetsee”) is already widely used in publications describing human Pneumocystis infection.6–8

Some physicians caring for HIV infected patients would not use trimethoprim-dapsone as second line treatment for mild to moderately severe PCP, nor would they use intravenous pentamidine as second line treatment for severe PCP; instead clindamycin-primaquine would be second line treatment, regardless of disease severity. Evidence in support of this choice of second line treatment comes from two sources. In patients with mild and moderately severe PCP the efficacy of clindamycin-primaquine was shown in a multicentre randomised prospective trial to be similar to co-trimoxazole (76% and 79%, respectively), with clindamycin-primaquine being the better tolerated of the two regimens.9 In patients unresponsive to first line treatment for PCP, evidence for the efficacy of clindamycin-primaquine as “salvage” therapy comes from a meta-analysis of 27 drug trials, case series, and case reports.10 This analysis showed that clindamycin-primaquine (81–92% response rate) was better than atovaquone (80%), intravenous pentamidine (39%), or trimetrexate (30%).


Authors’ reply

We thank Dr Miller for his interest in the illustrative case of HIV associated pneumonia recently published in this journal.1 The case presented was that of a patient with HIV associated pneumonia successfully treated in the ICU. The improved mortality of HIV infected patients admitted to ICU since the introduction of PCP prophylaxis and highly active antiretroviral therapy (HAART) was also discussed.

Dr Miller quite correctly makes the point that at a Pneumocystis nomenclature meeting in 2001 at the Seventh International Workshops on Opportunistic Protists, it was recommended that the organism that causes Pneumocystis pneumonia in humans should be referred to as Pneumocystis jiroveci.2 We hope it will be appreciated that, in the interest of maintaining accessibility to general physicians who may not all be familiar with recent developments in Pneumocystis nomenclature, we opted for the more widely used and understood usage and stayed with the familiar term, Pneumocystis carinii. We should also point out that the key publication from Dr Miller and colleagues on the proposed change in nomenclature appeared while our manuscript was in press.3

The additional comment about the use of clindamycin-primaquine as second line treatment is well taken. The meta-analysis that Dr Miller cites showing the effectiveness of clindamycin-primaquine “salvage therapy” for patients with PCP unresponsive to conventional agents shows that this is an effective alternative treatment.4 As will be appreciated from the comments accompanying table 2 in our paper, our aim was to give an overview of the available options without being unduly prescriptive. In the paper we strongly promote close collaboration between general, respiratory, HIV, and intensive care physicians in order to deliver optimal care.


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