IAI Accepts, published online ahead of print on 26 October 2009

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Infect. Immun. doi:10.1128/IAI.00965-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Acid phosphatases do not contribute to pathogenesis of Type A Francisella tularensis

Robert Child, Tara D. Wehrly, Dedeke Rockx-Brouwer, David W. Dorward, and Jean Celli^*

Tularemia Pathogenesis Section, Laboratory of Intracellular Parasites and Electron Microscopy Unit, Research Technologies Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA

^* To whom correspondence should be addressed. Email: jcelli{at}niaid.nih.gov.

The intracellular pathogen Francisella tularensis is the causative agent of tularemia, a zoonosis that can affect humans with potentially lethal consequences. Esssential to Francisella virulence is its ability to survive and proliferate within phagocytes through phagosomal escape and cytosolic replication. Francisella spp. encode a variety of acid phosphatases, whose roles in phagosomal escape and virulence have been documented yet remain controversial. Here we have examined in the highly virulent (Type A) tularensis strain Schu S4 the pathogenic roles of three distinct acid phosphatases, AcpA, AcpB, AcpC, that are most conserved between Francisella subspecies. Neither the deletion of acpA nor the combination of acpA, acpB and acpC deletions affected phagosomal escape or cytosolic growth of Schu S4 in murine and human macrophages, despite decreasing acid phosphatase activities by up to 95%. Furthermore, none of these mutants were affected in their ability to cause lethality in mice upon intranasal inoculation. Hence, the acid phosphatases AcpA, AcpB and AcpC do not contribute to intracellular pathogenesis, nor do they play a major role in virulence of Type A Francisella strains.