Case Studies in Infectious Disease: Echinococcus Spp

17 Pages·2009·1.517 MB·English

by  Lydyard, Peter;Cole, Michael;Holton, John;Irving, William L

Echinococcus spp.
Peter M. Lydyard
Michael F. Cole
John Holton
William L. Irving
Nino Porakishvili
Pradhib Venkatesan
Katherine N. Ward
This edition published in the Taylor & Francis e-Library, 2009.
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Vice President: Denise Schanck Peter M. Lydyard, Emeritus Professor of
Editor: Elizabeth Owen Immunology, University College Medical
Editorial Assistant: Sarah E. Holland School, London, UK and Honorary
Senior Production Editor: Simon Hill Professor of Immunology, School of
Typesetting: Georgina Lucas Biosciences, University of Westminster,
Cover Design: Andy Magee London, UK. Michael F. Cole, Professor
Proofreader: Sally Huish of Microbiology & Immunology,
Indexer: Merrall-Ross International Ltd Georgetown University School of
Medicine, Washington, DC, USA.
JohnHolton, Reader and Honorary
©2010 by Garland Science, Taylor & Francis Group, LLC Consultant in Clinical Microbiology,
Windeyer Institute of Medical Sciences,
University College London and University
This book contains information obtained from authentic and highly College London Hospital Foundation Trust,
regarded sources. Reprinted material is quoted with permission, and London, UK. William L. Irving, Professor
sources are indicated. A wide variety of references are listed. and Honorary Consultant in Virology,
Reasonable efforts have been made to publish reliable data and University of Nottingham and Nottingham
information, but the author and the publisher cannot assume University Hospitals NHS Trust,
responsibility for the validity of all materials or for the consequences of Nottingham, UK. Nino Porakishvili,
their use. All rights reserved. No part of this book covered by the Senior Lecturer, School of Biosciences,
copyright heron may be reproduced or used in any format in any form University of Westminster, London, UK
or by any means—graphic, electronic, or mechanical, including and Honorary Professor, Javakhishvili
photocopying, recording, taping, or information storage and retrieval Tbilisi State University, Tbilisi, Georgia.
systems—without permission of the publisher. Pradhib Venkatesan, Consultant in
Infectious Diseases, Nottingham University
Hospitals NHS Trust, Nottingham, UK.
The publisher makes no representation, express or implied, that the Katherine N. Ward, Consultant Virologist
drug doses in this book are correct. Readers must check up to date and Honorary Senior Lecturer, University
product information and clinical procedures with the manufacturers, College Medical School, London, UK and
current codes of conduct, and current safety regulations. Honorary Consultant, Health Protection
Agency, UK.
ISBN 978-0-8153-4142-0
Library of Congress Cataloging-in-Publication Data
Case studies in infectious disease / Peter M Lydyard ... [et al.].
p. ; cm.
Includes bibliographical references.
SBN 978-0-8153-4142-0
1. Communicable diseases--Case studies. I. Lydyard, Peter M.
[DNLM: 1. Communicable Diseases--Case Reports. 2. Bacterial
Infections--Case Reports. 3. Mycoses--Case Reports. 4. Parasitic Diseases--
Case Reports. 5. Virus Diseases--Case Reports. WC 100 C337 2009]
RC112.C37 2009
616.9--dc22
2009004968
Published by Garland Science, Taylor & Francis Group, LLC,
an informa business
270 Madison Avenue, New York NY 10016, USA,
and 2 Park Square, Milton Park, Abingdon, OX14 4RN, UK.
Visit our web site at http://www.garlandscience.com
ISBN 0-203-85380-6 Master e-book ISBN
Preface to Case Studies
in Infectious Disease
The idea for this book came from a successful course in a medical school
setting. Each of the forty cases has been selected by the authors as being
those that cause the most morbidity and mortality worldwide. The cases
themselves follow the natural history of infection from point of entry of
the pathogen through pathogenesis, clinical presentation, diagnosis, and
treatment. We believe that this approach provides the reader with a logi-
cal basis for understanding these diverse medically-important organisms.
Following the description of a case history, the same five sets of core ques-
tions are asked to encourage the student to think about infections in a
common sequence. The initial set concerns the nature of the infectious
agent, how it gains access to the body, what cells are infected, and how the
organism spreads; the second set asks about host defense mechanisms
against the agent and how disease is caused; the third set enquires about
the clinical manifestations of the infection and the complications that can
occur; the fourth set is related to how the infection is diagnosed, and what
is the differential diagnosis, and the final set asks how the infection is man-
aged, and what preventative measures can be taken to avoid the infection.
In order to facilitate the learning process, each case includes summary bul-
let points, a reference list, a further reading list and some relevant reliable
websites. Some of the websites contain images that are referred to in the
text. Each chapter concludes with multiple-choice questions for self-test-
ing with the answers given in the back of the book.
In the contents section, diseases are listed alphabetically under the
causative agent. A separate table categorizes the pathogens as bacterial,
viral, protozoal/worm/fungal and acts as a guide to the relative involve-
ment of each body system affected. Finally, there is a comprehensive glos-
sary to allow rapid access to microbiology and medical terms highlighted
in bold in the text. All figures are available in JPEG and PowerPoint® for-
mat at www.garlandscience.com/gs_textbooks.asp
We believe that this book would be an excellent textbook for any course in
microbiology and in particular for medical students who need instant
access to key information about specific infections.
Happy learning!!
The authors
March, 2009
Table of Contents
The glossary for Case Studies in Infectious Disease can be found
at http://www.garlandscience.com/textbooks/0815341423.asp
Case 1 Aspergillus fumigatus
Case 2 Borellia burgdorferi and related species
Case 3 Campylobacter jejuni
Case 4 Chlamydia trachomatis
Case 5 Clostridium difficile
Case 6 Coxiella burnetti
Case 7 Coxsackie B virus
Case 8 Echinococcus spp.
Case 9 Epstein-Barr virus
Case 10 Escherichia coli
Case 11 Giardia lamblia
Case 12 Helicobacter pylori
Case 13 Hepatitis B virus
Case 14 Herpes simplex virus 1
Case 15 Herpes simplex virus 2
Case 16 Histoplasma capsulatum
Case 17 Human immunodeficiency virus
Case 18 Influenza virus
Case 19 Leishmania spp.
Case 20 Leptospira spp.
Case 21 Listeria monocytogenes
Case 22 Mycobacterium leprae
Case 23 Mycobacterium tuberculosis
Case 24 Neisseria gonorrhoeae
Case 25 Neisseria meningitidis
Case 26 Norovirus
Case 27 Parvovirus
Case 28 Plasmodiumspp.
Case 29 Respiratory syncytial virus
Case 30 Rickettsiaspp.
Case 31 Salmonella typhi
Case 32 Schistosomaspp.
Case 33 Staphylococcus aureus
Case 34 Streptococcus mitis
Case 35 Streptococcus pneumoniae
Case 36 Streptococcus pyogenes
Case 37 Toxoplasma gondii
Case 38 Trypanosoma spp.
Case 39 Varicella-zoster virus
Case 40 Wuchereia bancrofti
Guide to the relative involvement of each body system affected
by the infectious organisms described in this book: the organisms
are categorized into bacteria, viruses, and protozoa/fungi/worms
Organism Resp MS GI H/B GU CNS CV Skin Syst L/H
Bacteria
Borrelia burgdorferi 4+ 1+ 1+
Campylobacter jejuni 4+ 2+
Chlamydia trachomatis 2+ 4+ 2+
Clostridium difficile 4+
Coxiella burnetti 4+ 4+
Escherichia coli 4+ 4+ 4+ 4+
Helicobacter pylori 4+
Leptospira spp. 4+ 4+ 4+
Listeria monocytogenes 2+ 4+ 2+ 4+
Mycobacterium leprae 2+ 4+
Mycobacterium tuberculosis 4+ 2+
Neisseria gonorrhoeae 4+ 2+
Neisseria meningitidis 4+ 4+
Rickettsia spp. 4+ 4+ 4+
Salmonella typhi 4+ 4+
Staphylococcus aureus 1+ 1+ 2+ 1+ 4+ 1+
Streptococcus mitis 1+ 4+
Streptococcus pneumoniae 4+ 4+
Streptococcus pyogenes 3+ 4+ 3+
Viruses
Coxsackie B virus 1+ 1+ 4+ 1+
Epstein-Barr virus 2+ 4+
Hepatitis B virus 4+
Herpes simplex virus 1 2+ 4+ 4+
Herpes simplex virus 2 4+ 2+ 4+
Human immunodeficiency virus 2+ 2+ 4+
Influenza virus 4+ 1+ 1+
Norovirus 4+
Parvovirus 2+ 3+ 4+ 2+
Respiratory syncytial virus 4+
Varicella-zoster virus 2+ 2+ 4+
Protozoa/Fungi/Worms
Aspergillusfumigatus 4+ 1+ 2+
Echinococcus spp. 2+ 4+
Giardia lamblia 4+
Histoplasmacapsulatum 3+ 1+ 4+
Leishmania spp. 4+ 4+
Plasmodium spp. 4+ 4+
Schistosoma spp. 4+ 4+ 4+
Toxoplasma gondii 2+ 4+
Trypanosoma spp. 4+ 4+ 4+
Wuchereria bancrofti 4+
The rating system (+4 the strongest, +1 the weakest) indicates the greater to lesser involvement of the body system.
KEY:
Resp = Respiratory: MS = Musculoskeletal: GI = Gastrointestinal
H/B = Hepatobiliary: GU = Genitourinary: CNS = Central Nervous System
Skin = Dermatological: Syst = Systemic: L/H = Lymphatic-Hematological
Echinococcus spp.
A 28-year-old Kurdish refugee complained of upper
abdominal pain for 4 months. He had recently noticed
some pain on the right side of his chest. He had not
noticed any fever and his weight was stable. His doctor
requested a chest X-ray. This showed a mass lesion in the
right lung. He was referred to the Thoracic Surgical
Department at the local hospital. A CT scan of his chest
and abdomen was requested. This demonstrated a cystic
structure in his liver, with another cyst in his chest
(Figure 1). The surgeons excised the lung lesion. The
histopathologists reported that it was a hydatid cyst. The
patient was referred to the Infectious Diseases
Department. A serological test was positive for
Echinococcus. He was given treatment with albendazole
and his remaining cyst was monitored serially on scans.
Figure 1. Pulmonary hydatid cysts. Chest X-ray showing
hydatid cysts (opaque areas at center right and center
left) in a patient’s lungs. The cysts are caused by the
parasitic tapeworm Echinococcussp. Humans are not a organ in the body. Large pulmonary cysts may cause
natural host for the parasite, but may become infected from symptoms, including shortness of breath, chest discomfort
ingesting eggs shed in the feces of an infected dog or other and sometimes wheeze. Treatment involves giving anti-
canids. Cysts may be formed in the liver, lungs or any other parasitic drugs and careful surgical resection when possible.
1. What is the causative agent, how does it enter the body and
how does it spread a) within the body and b) from person to
person?
Causative agent
Echinococcusspecies are tapeworms, also known as cestodes. Adults are only
3–8.5 mm in length. Two species are responsible for the majority of human
infections. Echinococcus granulosusarises from dogs and other canids and has
been described worldwide. It causes cystic echinococcosis. Echinococcus
multilocularis arises from arctic or red foxes and is restricted to the
Northern Hemisphere. It causes alveolar echinococcosis. Infection with
the latter seems to be spreading as red fox populations have been growing.
Adult tapeworms live in the intestines of the dog or wild canid hosts. They
attach to the mucosa with suckers and hooks. There are different parts to
the structure of the tapeworm, and these are shown in Figure 2. The adult
tapeworms lay eggs, which pass out in the feces and contaminate the soil.
2 ECHINOCOCCUS SPP.
sucker uterus with eggs These may be swallowed by an intermediate host such as sheep for E. gran-
ulosusand small mammals for E. multilocularis.
Echinococcus granulosus Entry and spread within the body
Humans are infected if they accidentally swallow eggs. The eggs have a
Figure 2. An adult tapeworm of
tough shell that breaks down and releases a larval form called the
Echinococcus granulosus.
oncosphere. The oncosphere burrows into the intestinal wall and then
spreads to other parts of the body along blood vessels or lymphatics. The
liver is the commonest site of infection as most of the intestinal drainage of
blood is along the portal vein to the liver. However, infection could arise
anywhere in the body.
When the oncosphere lodges in an organ it develops into a vesicle. This
progressively grows into a cyst. The cyst wall includes an inner germinal
layer. From this buds a stage called protoscolex within brood capsules.
Around the germinal layer is an acellular, laminated layer. For E. granulo-
susthis cyst is unilocular and known as a hydatid cyst. For E. multilocularis
the cyst is multilocular, or referred to as alveolar. Occasionally cysts can
rupture giving rise to secondary, ‘daughter’ cysts. The structure of a
hydatid cyst due to E. granulosus is shown in Figure 3.
Person to person spread
inflammatory cells germinal layer Humans do not spread Echinococcus spp. from person to person. Humans
fibrosis
acellular layer are an end host, with occasional exceptions.
Figure 3. Histopathology of the Intermediate hosts
structure of a hydatid cyst. Round
Animals such as sheep or cattle may ingest E. granulosus eggs shed in dog
protoscoleces are seen on the right. They
feces. They can act as intermediate hosts. When sheep or cattle are killed,
arise from a thin germinal layer, which is
dogs may eat their meat or offal. When the dogs swallow cysts within
surrounded by an acellular layer; the host
infected tissues the protoscoleces are released. They attach to the dogs’
inflammatory cells can be seen to the left
intestinal mucosa to mature into the adult tapeworms. Thus the life cycle
of this.
is completed (Figure 4). Dogs are the definitive hosts. This life cycle for
E. granulosus occurs on farms but for E. multilocularis there is a rural, or
sylvatic, life cycle with small mammals serving as the intermediate host
and arctic or red foxes as the definitive host.
Epidemiology
Given the life cycle, hydatid disease is most common where dogs and ani-
mals such as sheep and cattle mix. In the United Kingdom hydatid disease
has been mainly found in sheep farming areas such as North Wales.
Worldwide the Turkana district of Kenya has one of the highest incidences
of human cystic echinococcosis. Dogs are a key part of Turkana commu-
nities that herd cattle. The Turkana do not always bury their dead. Dogs
may then scavenge human remains and continue the life cycle.
2. What is the host response to the infection and what is the
disease pathogenesis?
Potentially the host may mount a response to the oncospheres, after they
have entered the intestine, or against the cysts, which become surrounded
by the acellular, laminated layer. There may also be a host response to fluid
that leaks from a ruptured cyst.
ECHINOCOCCUS SPP. 3
6 scolex attaches
to intestine 4
4
definitive host 1 adult in
dogs and other canidae small intestine
4
2
5 protoscolex
from cyst 4
ingestion of cysts
(in organs)
i
3
4
2 embryonated
egg in feces
ingestion of eggs
(in feces)
d
intermediate hosts
4 hydatid cysts in
sheep, goats, swine
liver, lungs, etc.
3 oncosphere hatches:
penetrates intestinal wall
i infective stage
d diagnostic stage
Little is known of the host response to the oncospheres. A single or small Figure 4. Life cycle of Echinococcus
number of oncospheres may not pose a sufficient antigenic stimulus to granulosus. Adult worms living in the dog
trigger an adaptive immune response. The innate immune response, uti- intestine shed eggs in dog feces. These
contaminate the environment and may be
lizing phagocytic cells or complement, may attack them after invasion of
ingested by intermediate hosts such as
the intestinal mucosa. Once a hydatid cyst has developed an antibody
sheep. In the intestine oncospheres hatch
response occurs that is initially IgM followed by an IgG and IgE
from the eggs and penetrate the intestinal
response. If these antibodies also recognize the oncospheres they could
wall. The oncosphere spreads to other
play a part in preventing further ingested oncospheres from causing addi-
organs and eventually matures into a cyst.
tional infection.
Within the cyst protoscolices develop.
When a cyst is ingested by a dog the
An inflammatory response occurs around the maturing cyst. This is trig-
protoscolices are released, attach to the
gered by complement activation. There is an infiltration of macrophages
intestinal mucosa as a scolex, and mature
and lymphocytes and these include both CD4+and CD8+T lymphocytes.
into adult worms.
Both Th1- and Th2-type cytokines are found, such as interferon
(IFN)-gg, interleukin (IL)-4, and interleukin-10. Eventually a host-
derived, fibrous layer forms around the cyst. Complement activation and
inflammation subside as the acellular layer accumulates. It is thought that
there is local immunomodulation with impaired macrophage responses,
impaired dendritic cell differentiation, and T-regulatory cells. Cyst-
derived antigens, including an antigen B, affect the maturation and func-
tion of dendritic cells, such that when they present antigen to lymphocytes
the immune response skews to a Th2 pattern. The latter is characterized
by IL-4 production and increased IgG and IgE levels.