Infections of the Nervous System

289 Pages·1987·5.681 MB·English

by  Peter G. E. Kennedy and Richard T Johnson (Eds.)

Butterworths International Medical Reviews
Neurology 8
Published tides
1 Clinical Neurophysiology
Erik Stâlberg and Robert R. Young
2 Movement Disorders
C. David Marsden and Stanley Fahn
3 Cerebral Vascular Disease
Michael J. G. Harrison and Mark L. Dyken
4 Peripheral Nerve Disorders
Arthur K. Asbury and R. W. Gilliatt
5 The Epilepsies
Roger J. Porter and Paolo L. Morselli
6 Multiple Sclerosis
W. I. McDonald and Donald H. Silberberg
7 Movement Disorders 2
C. David Marsden and Stanley Fahn
Infections of the
Nervous System
Edited by
Peter G. E. Kennedy, MD, PhD, MRCP
Senior Lecturer in Neurology and Virology, University of Glasgow; Consultant Neurologist,
Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK
and
Richard T. Johnson, MD
Eisenhower Professor of Neurology and Professor of Microbiology and Neuroscience, The
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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First published, 1987
© Butterworth & Co. (Publishers) Ltd, 1987
British Library Cataloguing in Publication Data
Infections of the nervous system.
(Butterworths international medical reviews.
Neurology, 8)
1. Nervous system — Diseases
2. Communicable diseases
I. Kennedy, Peter G. Ε. II Johnson,
Richard T.
616.8 RC346
ISBN 0-407-02293-7
Photoset by Butterworths Litho Preparation Department
Printed and bound by Robert Hartnoll (1985) Ltd, Bodmin, Cornwall
Foreword
For almost a quarter of a century (1951-1975), subjects of topical interest were
written about in the periodic volumes of our predecessor, Modern Trends in
Neurology. Although both that series and its highly regarded editor, Dr Denis
Williams, are now retired, the legacy continues in the present Butterworths series
in Neurology. As was the case with Modern Trends, the current volumes are
intended for use by physicians who grapple with the problems of neurological
disorder on a daily basis, be they neurologists, neurologists in training, or those in
related fields such as neurosurgery, internal medicine, psychiatry, and rehabilita-
tion medicine.
Our purpose is to produce annually a monograph on a topic in clinical neurology
in which progress through research has brought about new concepts of patient
management. The subject of each monograph is selected by the Series Editors
using two criteria: first, that there has been significant advance in knowledge in that
area and, second, that such advances have been incorporated into new ways of
managing patients with the disorders in question.
This has been the guiding spirit behind each volume, and we expect it to
continue. In effect we emphasize research, both in the clinic and in the
experimental laboratory, but principally to the extent that it changes our collective
attitudes and practices in caring for those who are neurologically afflicted.
C. D. Marsden
A. K. Asbury
Series Editors
ν
Contributors
Larry Ε. Davis, MD
Chief, Neurology Service, Albuquerque Veterans Administration Medical Center;
Professor of Neurology and Microbiology, University of New Mexico School of
Medicine, Albuquerque, New Mexico, USA
Diane E. Griffin, MD, PhD
Professor of Medicine and Neurology, The Johns Hopkins University School of
Medicine, Baltimore, Maryland, USA
John W. Griffin, MD
Professor of Neurology and Neuroscience, The Johns Hopkins University School of
Medicine, Baltimore, Maryland, USA
Richard T. Johnson, MD
Eisenhower Professor of Neurology and Professor of Microbiology and Neurosci-
ence, The Johns Hopkins University School of Medicine, Baltimore, Maryland,
USA
Peter G. E. Kennedy, MD, PhD, MRCP
Senior Lecturer in Neurology and Virology, University of Glasgow; Consultant
Neurologist, Institute of Neurological Sciences, Southern General Hospital,
Glasgow, UK
Roman S. Kocen, TD, FRCP
Consultant Physician, National Hospitals for Nervous Diseases, Queen Square and
Maida Vale, London, UK
J. S. Kroll, MA, MRCP
Lister Institute Research Fellow and Honorary Senior Registrar, Oxford
University Department of Paediatrics, John Radcliffe Hospital, Oxford, UK
S. Looareesuwan, MD
Associate Professor, Hospital for Tropical Diseases, Faculty of Tropical Medicine,
Mahidol University, Bangkok, Thailand
vii
D. W. R. Mackenzie, BSC, PhD
Director, Mycological Reference Laboratory, (Central Public Health Laborator-
ies), Colindale, London; Visiting Professor of Medical Mycology, London School
of Hygiene and Tropical Medicine, London, UK
W. B. Matthews, DM, FRCP
Professor of Clinical Neurology, University of Oxford, The Radcliffe Infirmary,
Oxford, UK
E. Richard Moxon, MA, MB, BChir, FRCP
Professor and Head of Department, Oxford University Department of Paediatrics,
John Radcliffe Hospital, Oxford, UK
Bradford A. Navia, MD
Fellow in Neurology, Memorial Sloan-Kettering Cancer Center, New York,
New York, USA
Richard W. Price, MD
Associate Member, Memorial Sloan-Kettering Cancer Center; Associate Professor
of Neurology, Cornell University Medical College, New York, New York, USA
Louis Reik Jr, MD
Associate Professor of Neurology, University of Connecticut School of Medicine,
Farmington, Connecticut, USA
Julio Sotelo, MD
Head, Research Division, Instituto Nacional de Neurologia y Neurocirugia,
Mexico City, Mexico
Nicholas J. White, BSC, MD, FRCP
Director, Wellcome-Mahidol University, Oxford Tropical Medicine Research
Programme, Hospital for Tropical Diseases, Faculty of Tropical Medicine,
Mahidol University, Bangkok, Thailand
C. M. Wiles, BSc, PhD, FRCP
Consultant Neurologist at St Thomas' Hospital, and National Hospitals for
Nervous Diseases, London, UK
1
Introduction
Peter G. Ε. Kennedy and Richard T. Johnson
Three striking developments on the subject of central nervous system (CNS)
infections have been evident over the last decade. These include: understanding of
disease processes provided by new technologies; new pathogens and the widening
spectrum of disease caused by familiar pathogens; and new therapeutic tools.
First, the pathogenesis of many infective neurological diseases has been clarified
by the use of powerful molecular biological techniques and by new methods of
imaging the human brain. Genetic mapping, monoclonal antibodies, immuno-
cytochemistry, and in situ and Southern blot hybridization have been used to
investigate the factors controlling neurovirulence of bacteria and viruses; they have
provided new information on the mechanisms of the demyelinating encephalomye-
litis that can follow viral infections, and they have given new insight into the
protean neurological manifestations of varicella-zoster virus infections and slow
infections of the nervous system. Computerized tomography has clarified both the
pathogenesis and the management of tuberculous meningitis and neurocysticer-
cosis, and dispelled the assumption that brain oedema is the central problem in
cerebral malaria. Magnetic resonance imaging may provide non-invasive diagnosis
for postinfectious encephalomyelitis and progressive multifocal leucoencephalo-
pathy and detect early central nervous system involvement in the acquired
immunodeficiency syndrome (AIDS).
Second, the remarkable diversity of infectious agents that can affect the nervous
system has been increasingly recognized by clinicians and scientists alike. Agents
such as spirochaetes and fungi have been known to cause neurological disease for
many decades. The range of species within these different groups has proved to be
wider than anticipated in the past; thus the spirochaete Borrelia burgdorferi has
been shown to cause Lyme disease, and some of its neurological features are
reminiscent of neurosyphilis. The increased therapeutic immunosuppression and
cytotoxic drugs have amplified the importance and the range of fungal infections, as
well as selective viral and bacterial infections. Botulism has recently been
recognized to occur not only from contaminated food, but also from the absorption
by toxin formed in the gastrointestinal tract. It has become the only documented
cause of the sudden infant death syndrome.
AIDS, which probably represents the most formidable challenge which the
world's public health services have ever had to face, has highlighted the extent to
1
2 Introduction
which an unusual organism can cause neurological disease and immunosuppression
in individuals. Whether, as many suspect, the causative agent in human
immunodeficiency virus (HIV) became prevalent in man by extending its host
specificity from the African green monkey, or whether it became a human
pathogen via some other mechanism is not yet known. However, it is clear from
retrospective and epidemiological studies that the disease is new. In view of the
estimates of the likely incidence of AIDS over the next decade, one can only hope
that intensive current investigative, preventative and therapeutic measures
employed by scientists, governments and public health services will have a
significant impact in halting the spread of this disease. It is particularly sobering to
note that many of the neurological complications may occur in individuals who do
not have established AIDS, but the AIDS-related complex, or those with
seropositivity for human immunodeficiency virus alone without other manifesta-
tions of the syndrome.
Third, significant advances in the treatment of infectious neurological diseases
have also been noteworthy. In general, these have been of two main kinds:
established, well-recognized therapy for newly recognized diseases, and newly
developed treatment for diseases which have been recognized for many years. In
the first category can be included penicillin therapy for Lyme disease, in which a
good clinical response can be anticipated in the majority of patients. The second
category includes recent antiviral therapy such as acyclovir for herpes simplex
encephalitis and the remarkable efficacy of the helminthicide praziquantel in
treating CNS cysticercosis. In addition, each new generation of antibiotics has
potential relevance to the treatment of acute and chronic bacterial infections of the
CNS. It can be readily appreciated that these three advances are not mutually
exclusive. For example, an increasing understanding of pathogenesis is likely to
lead to more rational therapy. Thus, the recent demonstration of a lack of cerebral
oedema in patients with cerebral malaria has led most clinicians to abandon
dexamethasone therapy in this condition.
It has been our intention in this volume to choose topics which reflect these
various developments. In particular, we wished to illustrate the major theme of the
series, namely to highlight areas or subjects in which significant advances have been
made which also have relevance to the treatment of patients. We believe that this
volume covers a number of important aspects of infectious diseases of the nervous
system, but in view of the selective nature of the reviews we have obviously not
attempted to produce a comprehensive review of the subject.
Our intention is that our selection of topics will appeal, not only to clinical
neurologists and neurosurgeons, but also to general physicians, those involved
primarily with infectious diseases, psychiatrists and microbiologists. Clearly, the
future promises to hold many challenges for those concerned with investigating and
treating neurological infections. We hope that this book will convey some of the
excitement which many of us feel as we brace ourselves to face these challenges.
Finally, we would like to thank our contributors for the rigour of their
contributions.
2
Acute bacterial meningitis
J. S. Kroll and Ε. R. Μοχοη
INTRODUCTION
There have been substantial additions to our understanding of the biology of
central nervous system (CNS) infections which are relevant to clinicians confronted
by, and concerned with, the many problems inherent in their diagnosis and
management.
Bacteria may cause acute infections of the CNS as a result of direct implantation,
contiguous infection from a local septic process or an infected foreign body (e.g. a
cerebrospinal fluid shunting device), or by haematogenous spread. CNS
derangement may also occur by the action of neurotoxins produced at a distant
focus of infection or as the result of the systemic effects of septicaemia.
The propensity of bacterial meningitis to cause death or permanent neurological
sequelae underlies the critical importance of biomedical research into these
problems.
In this chapter, some aspects of the present understanding of the host and
microbial determinants involved in bacterial meningitis are reviewed, emphasizing
current knowledge of its epidemiology, pathophysiology, diagnosis and preven-
tion.
EPIDEMIOLOGY
National surveillance of the organisms responsible for bacterial meningitis has
produced information of considerable practical importance and has proved to be a
vital tool in defining the relative incidence of the major causes of meningitis (Figure
2.1). Such data as age-specific attack rates, antibiotic susceptibility, and the
prevalence and geographical distribution of important phenotypic characteristics,
e.g. capsular type, are critical for the implementation of sensible antibiotic policies
and for planning and targeting preventive strategies such as immunoprophylaxis
and chemoprophylaxis. Examples of the sort of information documented include
the emergence since about 1973 of ß-lactamase-producing Haemophilus influenzae,
now accounting for about 20% of the type b strains causing meningitis in North
America and about 14% of strains in the UK. Monitoring of chloramphenicol
3
4 Acute bacterial meningitis
Figure 2.1 Relative incidence of aetiological agents causing bacterial meningitis. Total
number of cases reported: 7605. (Reprinted with the kind permission of Dr Ν. Noah, Public
Health Laboratory Service, Colindale, London, UK from Laboratory reports 1980-1984,
England, Wales and Ireland)
resistance shows this still to be rare in most Western countries, except Spain, where
in the vicinity of Barcelona more than 50% of H. influenzae type b strains are
chloramphenicol resistant (Campos, Garcia-Tornell and Sanfeliu, 1984). The
importance of monitoring trends for an increase in chloramphenicol resistance is
apparent since the drug is currently the mainstay of treatment for H. influenzae
meningitis. Group Β streptococci aand meningococci remain susceptible to
penicillin, but occasional (about 1%) strains of pneumococci are relatively resistant
to penicillin and therapeutic failures have been reported (Jackson et al., 1984). An
outbreak of multiply resistant pneumococci causing several cases of meningitis in
South Africa seems fortunately to have proved an exceptional occurrence
(Editorial, 1977). The multiple antibiotic resistance patterns of enteric bacilli,
especially Escherichia coli, which account for about one-half of the cases of
neonatal meningitis and many instances of nosocomial meningitis in adults, poses a
particularly difficult problem which is discussed later.
In addition to standard reporting of the kind described above, a variety of
laboratory techniques such as outer-membrane protein (Barenkamp, Granoff and
Munson, 1981) and isoenzyme typing (Musser et al., 1985) are being applied in
epidemiology. This has, for example, allowed the identification and tracking of a
particular strain of meningococcus (group B, serotype 15:PI. 16) of great concern in
Europe. This strain has resulted in a prolonged epidemic in Norway and is currently
the cause of substantial concern in the UK (Frasch, Zollinger and Poolman, 1985).
The recognition that particular surface polypeptides are characteristic of this strain
may be a prime consideration in developing a successful vaccine, since it belongs to
serogroup Β and immune responses to this capsular polysaccharide are particularly
poor.