Rickettsial Infection and Immunity

257 Pages·2002·9.215 MB·English

by  Burt Anderson (auth.), Burt Anderson, Herman Friedman, Mauro Bendinelli (eds.)

Rickettsial Infection
and Immunity
INFECTIOUSAGENTS AND PATHOGENESIS
SeriesEditors: Mauro Bendinelli, University of Pisa
Herman Friedman, University of South Florida
COXSACKIEVIRUSES
A General Update
Edited by Mauro Bendinelli and Herman Friedman
DNA TUMOR VIRUSES
Oncogenic Mechanisms
Edited by Giuseppe Barbanti-Brodano, Mauro Bendinelli, and
Herman Friedman
ENTERIC INFECTIONS AND IMMUNITY
Edited by Lois J. Paradise, Mauro Bendinelli, and Herman Friedman
FUNGAL INFECTIONS AND IMMUNE RESPONSES
Edited by Juneann W. Murphy, Herman Friedman, and
Mauro Bendinelli
MICROORGANISMS AND AUTOIMMUNE DISEASES
Edited by Herman Friedman, Noel R. Rose, and Mauro Bendinelli
MYCOBACTERIUMT UBERCULOSIS
Interactions with the Immune System
Edited by Mauro Bendinelli and Herman Friedman
NEUROPATHOGENIC VIRUSES AND IMMUNITY
Edited by Steven Specter, Mauro Bendinelli, and Herman Friedman
PSEUDOMONAS AERUGINOSA AS AN OPPORTUNISTIC
PATHOGEN
Edited by Mario Campa, Mauro Bendinelli, and Herman Friedman
PULMONARY INFECTIONS AND IMMUNITY
Edited by Herman Chmel, Mauro Bendinelli, and Herman Friedman
RICKETTSIAL INFECTION AND IMMUNITY
Edited by Burt Anderson, Herman Friedman, and Mauro Bendinelli
VIRUS-INDUCEDIMMUNOSUPPRESSION
Edited by Steven Specter, Mauro Bendinelli, and Herman Friedman
A Continuation Order Plan is available for this series. A continuation order will bring
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Rickettsial Infection
and Immunity
Edited by
Burt Anderson
University of South Florida
Tampa, Florida
Herman Friedman
University of South Florida
Tampa, Florida
and
Mauro Bendinelli
University of Pisa
Pisa, Italy
Kluwer Academic Publishers
NewYork, Boston, Dordrecht, London, Moscow
eBookISBN: 0-306-46804-2
Print ISBN: 0-306-45528-5
©2002 Kluwer Academic Publishers
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Contributors
BURT ANDERSON • Department of Medical Microbiology and Immunol-
ogy, College of Medicine, University of South Florida, Tampa, Florida
3361 2
OSWALD G. BACA • Department ofBiology, The University of New Mexi-
co, Albuquerque, New Mexico 87131
PHILIPPE BROUQUI • Unité des Rickettsies, CNRS-UPRES-A, Faculté de
Médecine, 13385 Marseille cedex 5, France
THOMAS D. CONLEY • Cardiology Section, The University of Oklaho-
ma Health Sciences Center, Oklahoma City, Oklahoma 73104. Present ad-
dress: University of Arkansas for Medical Science, Little Rock, Arkansas
72204
J. STEPHEN DUMLER • Division of Medical Microbiology, Department of
Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland
21287-7093
CAYLE C. GRAUMANN • Department ofMolecular Microbiology and Im-
munology, School of Medicine, University of Missouri, Columbia, Missouri
6521 2
KAREN K. HAMILTON • Cardiology Section, The University of Oklaho-
ma Health Sciences Center, Oklahoma City, Oklahoma 73104. Present ad-
dress: Cardiology Associates of Corpus Christi, Corpus Christi, Texas
78412
ROBERT A. HEINZEN • Department of Molecular Biology, University of
Wyoming, Laramie, Wyoming 82071-3944
THOMAS R. JERRELLS • Department of Pharmaceutical Sciences, col-
lege of Pharmacy, Washington State University, Pullman, Washington
991 64-651 0
v
vi CONTRIBUTORS
GREGORY A. MCDONALD • Department of Molecular Microbiology and
Immunology, School of Medicine, University of Missouri, Columbia, Mis-
souri 65212
LOUIS P. MALLAVIA • Department of Microbiology, Washington State
University, Pullman, Washington 99 164
MICHAEL F. MINNICK • Division of Biological Sciences, The University of
Montana, Missoula, Montana 59812-1002
DIDIER RAOULT • Unité des rickettsies, Centre National de la Recherche
Scientfique EP J 0054, Faculté de Médecine, 13385 Marseilles, France
VERONIQUE ROUX • Unité des rickettsies, Centre National de la Re-
cherche Scientifique EP J 0054, Faculté de Médecine, 13385 Marseilles,
France
DAVID J. SILVERMAN • Department of Microbiology and Immunology,
University of Maryland School of Medicine, Baltimore, Maryland 21201
LEONARD N. SLATER • Infectious Diseases Section, The University of
Oklahoma Health Sciences Center, and The Department of Veterans Af-
fairs Medical Center, Oklahoma City, Oklahoma 73104
JOSEPH J. TEMENAK • Department of Molecular Microbiology and Im-
munology, School of Medicine, University of Missouri, Columbia, Missouri
6521 2
JENIFER TURCO • Department of Biology, Valdosta State University, Val-
dosta, Georgia 31698-0015
MATTHEW F. WACK • Infectious Diseases Section, The University of
Oklahoma Health Sciences Center, and The Department of Veterans Af-
fairs Medical Center, Oklahoma City, Oklahoma 73104. Present address: In-
fectious Disease of Indiana, Indianapolis, Indiana 46202.
DAVID F. WELCH • Pediatric Infectious Diseases Section, The University of
Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104. Pre-
sent address: Laboratory Corporation of America, Dallas, Texas 75230
HERBERT H. WINKLER • Laboratory of Molecular Biology, Department
of Microbiology and Immunology, University of South Alabama College of
Medicine, Mobile, Alabama 36688
Preface
Historically, rickettsial diseases have had a profound impact on civilized man.
Epidemic typhus has been one of the most devastating infectious diseases affecting
humanity. The effects of this disease were most evident during times of war and
famine and influenced the outcome and mortality of many wars fought in Europe
and Russia before World War II. During and immediately following World War
I, over 3 million lives were lost to epidemic typhus in Europe and present-day
Russia. In modern times, insecticides have greatly reduced the spread of epidemic
typhus by disrupting transmission from the vector, the human body louse, to
man. Nevertheless, the disease is still present in Africa and South America. The
etiologic agent of epidemic typhus, Rickettsia prowazekii, has been isolated from the
flying squirrels, Glaucomys volans, and their ectoparasites in the southeastern
United States. Thus, a reservoir of R. prowazekii exists in the United States for
transmission to man. Although this naturally occurring reservoir has not resulted
in outbreaks of typhus in this region of the country, the possibility must not be
discounted. Should conditions of social upheaval or famine occur, epidemic ty-
phus could resurface in the United States, much like the recent resurgence of
tuberculosis.
Although the past has provided dramatic historical evidence for the mortal-
ity associated with rickettsial diseases, perhaps the most exciting aspect of rickett-
sial research is currently under way. The advent of modern molecular biology
methods has greatly facilitated the study of these obligate intracellular bacteria.
Molecular cloning has provided the means by which individual rickettsial genes
and the corresponding proteins can be studied without the need of cultivating
rickettsiae and purifying them from host cell debris. Polymerase chain reaction
amplification has allowed specific genes to be amplified and sequenced without
the need to cultivate the organisms. Individual antigens of the etiologic agent of
Rocky Mountain spotted fever (Rickettsia rickettsii) have been cloned and expressed
in bacterial and other expression systems. The resulting recombinant expressed
antigens have been used to study the immune response elicited during infection
vii
viii PREFACE
with R. rickettsii. In this fashion potential vaccine candidate proteins have been
identified and shown to confer protection in animal models. Likewise, molecular
tools have advanced recent research efforts aimed at understanding the mecha-
nisms of pathogenesis and the biochemistry of the rickettsiae. The role of individ-
ual proteins such as phospholipases, adhesins, invasins, and factors that may
affect host-cell signal transduction are areas of current active research.
Molecular techniques have had a great impact on the identification and
characterization of new rickettsial pathogens as well. Rickettsiae and rickettsiae-
like organisms contain the largest number of recently identified human pathogens
of any bacteria. At least six new human pathogens (the agent of human granu-
locytic ehrlichiosis, the ELB agent, Ehrlichia chaffeensis, Rickettsia japonica, Bartonella
henselae,andB. elizabethae) have been described so far this decade. Two of these
agents, the agent of human granulocytic ehrlichiosis and E. chaffeensis, were previ-
ously viewed as agents primarily infecting animals. In the inaugural issue of
“Emerging Infectious Diseases,” the Centers for Disease Control and Prevention
names two agents included in this volume (E. chaffeensis andB. henselae) as major
etiologic agents of infectious diseases identified in recent years. The use of poly-
merase chain reaction amplification of the small subunit ribosomal RNA coupled
with sequencing has proven invaluable as a tool to detect and identify. new
rickettsial pathogens without the need for isolation of the organism. Because
rickettsiae are difficult to isolate and cultivate (some have still not been cultivated
in the laboratory), the possibility of identifying additional rickettsial pathogens is
very real. A number of other new organisms, belonging to almost every genus of
rickettsiae or rickettsiae-like organisms, have been isolated or detected in a variety
of animal or insect hosts. The ability of these newly described agents to cause
disease in man has not yet been extensively studied.
The strict definition of rickettsiae is that they are obligate intracellular bacte-
ria. Until recently the order Rickettsialescontained members that could be culti-
vated in the laboratory on cell-free media. A recently published proposal has been
to combine the genus RochalimaeawithBartonellaand to remove these facultatively
intracellular or epicellular bacteria to another order outside the Rickettsiales. Re-
gardless, for the purpose of this volume, rickettsiae-like organisms such as Bar-
tonella have been included. Perhaps the most exciting recent discovery is the
identification of the agent responsible for cat-scratch disease. Bartonellahenselae
(formerlyRochalimaea henselae) is most closely related to the agent of trench fever, B.
quintana(formerlyRickettsia quintana). The identification of the etiologic agent of
cat-scratch disease was the source of controversy for over 40 years. Compelling
evidence provided by PCR, serology, and culture indicates that B. henselae is the
primary agent responsible for cat-scratch disease. B. henselae andB. quintana are
also opportunistic pathogens of immunocompromised patients and both are eti-
ologic agents of bacillary angiomatosis. Bacillary angiomatosis is a disease seen
primarily in AIDS patients and results in unique skin lesions that are charac-
PREFACE ix
terized by proliferation of vascular endothelial cells. This pseudoneoplasia is also
the hallmark of the chronic stage (termed verruga peruana) of infection with B.
bacilliformisamong immunocompetent patients. This novel mechanisms of patho-
genesis shared by these organisms is fascinating. The factor or factors from these
organisms that mediates angiogenesis remains unidentified but is an area of active
research in several prominent laboratories. The possible exchange of DNA cod-
ing for virulence factors among these related organisms is under investigation.
Considering the recent interest in rickettsiae and rickettsiae-like organisms,
as well as the description of several new pathogens, the editors and authors of this
volume feel it is both timely and needed. We anticipate that this volume will be a
medium for the cohesive presentation of a variety of different aspects of rickettsial
pathogenesis and immunity. Few organisms, if any, offer such fertile grounds for
the study of diverse mechanisms of immunity and pathogenesis. It is our hope that
this volume summarizes our current knowledge and piques the interest of readers
who want to know more about these unusual organisms.
Contents
1. Molecular Rickettsiology: A Short History
BURT ANDERSON
1. Introduction .............................................. 1
2. Gene Structure and Expression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
2.1. Transcription Initiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
2.2. Translation Initiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
2.3. Posttranslational Modification ..................... ...... 5
3. Identification of New Species . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
3.1. Bacillary Angiomatosis/Cat-Scratch Disease . . . . . . . . . . . . . . . 7
3.2. Ehrlichiosis .......................................... 8
3.3. ELB Agent .......................................... 9
4. Epidemiology and Natural History of Rickettsial Diseases . . . . . . . . . 9
4.1. Ehrlichiosis .......................................... 9
4.2. Bartonella ........................................... 10
5. Summary/Conclusion ...................................... 11
References............................................... 11
2. Immunity to Rickettsiae (Redux)
THOMAS R . JERRELLS
1. Introduction .............................................. 15
2. Immune Responses to Intracellular Organisms ........................... 16
3. Role ofthe T Cell in Immunity to Rickettsiae................... 18
xi