Lecture Notes: Tropical Medicine

This book is dedicated to Dr Dion Bell, author

and later editor of the first four editions of this

book, a gifted teacher of tropical medicine,

and an inspiration to generations of doctors

working in the tropics.

Lecture Notes

Tropical Medicine

EDITED BY

Geoff GillProfessor of International MedicineLiverpool School of Tropical MedicineLiverpool, UK

Nick BeechingSenior Lecturer in Infectious DiseaseLiverpool School of Tropical MedicineLiverpool, UK

Sixth Edition

A John Wiley & Sons, Ltd., Publication

This edition first published 2009, © 2009 by Blackwell Publishing LtdPrevious editions: 1981, 1985, 1990, 1995, 2004

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Library of Congress Cataloging-in-Publication Data

Lecture notes. Tropical medicine. — 6th ed. / [edited by] Geoff Gill, Nick Beeching. p. ; cm. Rev. ed. of: Lecture notes on tropical medicine. 5th ed. 2004. Includes bibliographical references and index. ISBN 978-1-4051-8048-1 1. Tropical medicine. I. Gill, Geoffrey V. II. Beeching, N. III. Lecture notes on tropical medicine. IV. Title: Tropical medicine. [DNLM: 1. Tropical Medicine. WC 680 L471 2009]RC961.L42 2009616.9’883 —dc22 2008042562

ISBN: 978-1-4051-8048-1

A catalogue record for this book is available from the British Library.

Set in 8/12 pt Stone Serif by Charon Tec Ltd (A Macmillan Company), Chennai, IndiaPrinted in Singapore

1 2009

Contributors, vii

Preface, ix

List of Abbreviations, x

New Drug Names, xiii

Part 1: A General Approach to Syndromes/Symptom Complexes

1 Gastrointestinal presentations 3

2 Respiratory presentations 11

3 Neurological presentations 17

4 Febrile presentations 26

5 Dermatological presentations 32

6 The patient with anaemia 36

7 A syndromic approach to sexually

transmitted infections 40

8 Splenomegaly in the tropics 49

Part 2: Major Tropical Infections

9 Malaria 55

10 Visceral leishmaniasis 73

11 Cutaneous leishmaniasis 80

12 Tuberculosis 85

13 HIV infection and disease in the tropics 101

14 Onchocerciasis, filariasis and loiasis 133

15 African trypanosomiasis 148

16 South American trypanosomiasis—

Chagas’ disease 155

17 Schistosomiasis 158

18 Leprosy 171

Part 3: Other Tropical Diseases

Gastrointestinal

19 Amoebiasis 185

20 Bacillary dysentery 192

21 Cholera 195

22 Giardiasis and other intestinal protozoal

infections 199

23 Intestinal cestode infections (tapeworms)

including cysticercosis 204

24 Soil-transmitted helminths 208

25 Viral hepatitis 215

26 Liver and intestinal flukes 226

27 Hydatid disease 229

Respiratory

28 Pneumonia 233

29 Lung flukes 241

30 Tropical pulmonary eosinophilia 244

Neurological

31 Pyogenic meningitis 246

32 Cryptococcal meningitis 254

33 Encephalitis 256

34 Acute flaccid paralysis 261

35 Spastic paralysis 264

36 Rabies 267

37 Tetanus 272

Fever

38 Brucellosis 275

39 Typhoid and paratyphoid fevers 280

40 Arboviruses 287

41 Viral haemorrhagic fevers 289

42 Dengue and yellow fever 296

43 Relapsing fevers 301

44 Rickettsial infections 304

45 Leptospirosis 306

46 Melioidosis 309

Miscellaneous

47 Tropical ulcer 311

48 Buruli ulcer 313

49 Myiasis 316

50 Cutaneous larva migrans 318

51 Scabies and lice 320

52 Strongyloidiasis 322

v

Contents

53 Guinea worm infection (dracunculiasis) 326

54 Histoplasmosis 328

55 Other fungal infections 330

56 Haemoglobinopathies and red cell

enzymopathies 333

57 Haematinic deficiencies 338

58 Bites and stings 342

59 Non-communicable diseases 347

60 Refugee health 365

61 Syndromes of malnutrition 373

Index 380

Contents

vi

Imelda Bates Senior Lecturer, Liverpool School of

Tropical Medicine, Pembroke Place, Liverpool

L3 5QA

Chapters 6, 8, 56, 57

Nick Beeching Senior Lecturer, Liverpool

School of Tropical Medicine, Pembroke Place,

Liverpool L3 5QA; Clinical Lead, Tropical &

Infectious Disease Unit, Royal Liverpool

University Hospital, Liverpool L7 8XP

Chapters 1, 5, 18, 25, 29, 31, 38, 53

Tom Blanchard Honorary Senior Lecturer in

Infection & Immunity, University of Liverpool;

Honorary Fellow, Liverpool School of Tropical

Medicine; Consultant in Infectious Diseases &

Tropical Medicine, North Manchester General

Hospital, Delaunays Rd, Manchester M8 5RB

Chapter 4

Martin Dedicoat Chief Specialist Physician,

Polokwane Mankweng Hospital Complex,

Polokwane, Limpopo 0700, South Africa

Chapter 13

Tom Doherty Senior Lecturer, London School

of Hygiene & Tropical Medicine, London

WC1E 7HT; Consultant Physician, Hospital

for Tropical Diseases, Mortimer Market Centre,

Capper Street, London WC1E 6AU

Chapter 61

Neil French Director, Karonga Prevention Study,

Box 46, Chilumba, Malawi; Reader in

Infectious Disease Epidemiology, London

School of Hygiene & Tropical Medicine,

London WC1E 7HT

Chapters 2, 28, 30

Geoff Gill Professor, Liverpool School of Tropical

Medicine, Pembroke Place, Liverpool L3 5QA;

and Honorary Consultant Physician, Aintree

University Hospital, Liverpool L9 1AE

Chapters 44, 47, 49–52, 54, 59

Stephen Gordon Senior Lecturer, Liverpool

School of Tropical Medicine, Pembroke Place,

Liverpool L3 5QA

Chapters 2, 28, 30

Rachel Kneen Consultant Paediatric Neurologist,

Alder Hey Children’s NHS Foundation Trust,

Alder Hey, Liverpool L12 2AP

Chapters 3, 33, 34

David Lalloo Clinical Director and Reader,

Liverpool School of Tropical Medicine,

Pembroke Place, Liverpool L3 5QA

Chapters 15, 16, 32, 37, 46, 55, 58

Diana Lockwood Professor, London School of

Hygiene & Tropical Medicine, London WC1E

7HT; Consultant Physician and Leprologist,

Hospital for Tropical Diseases, Mortimer Market

Centre, Capper Street, London WC1E 6AU

Chapter 18

Alastair Miller Honorary Fellow, Liverpool

School of Tropical Medicine; Consultant

Physician, Tropical & Infectious Disease Unit,

Royal Liverpool University Hospital, Liverpool

L7 8XP

Chapter 45

Malcolm Molyneux Professor, Liverpool

School of Tropical Medicine, Pembroke Place,

Liverpool L3 5QA

Chapter 9

vii

Contributors

Tim O’Dempsey Senior Lecturer, Liverpool

School of Tropical Medicine, Pembroke Place,

Liverpool L3 5QA

Chapters 10, 11, 14, 19, 20, 22–24, 26, 27,

43, 48, 60

Chris Parry Senior Lecturer, Department of

Medical Microbiology and Genitourinary

Medicine, University of Liverpool, Duncan

Building, Liverpool L69 3GA

Chapter 39

Paul Shears Consultant Microbiologist, Sheffield

Teaching Hospitals NHS Foundation Trust,

Sheffield S10 2JF

Chapter 21

Rebecca Sinfield Clinical Lecturer, Child and

Reproductive Health, Liverpool School of

Tropical Medicine, Pembroke Place, Liverpool

L3 5QA

Chapter 61

Tom Solomon Professor, Division of Neurological

Science, University of Liverpool, Liverpool L9 7LJ

Chapters 3, 33–36, 40–42

Bertie Squire Reader, Liverpool School of

Tropical Medicine, Pembroke Place, Liverpool

L3 5QA

Chapters 12, 17

Miriam Taegtmeyer Senior Lecturer, Liverpool

School of Tropical Medicine, Pembroke Place,

Liverpool L3 5QA

Chapters 7, 13

Maureen Wilkinson Consultant Psychiatrist,

Cheshire and Wirral Partnership NHS

Foundation Trust, Countess of Chester Health

Park, Chester CH2 1BQ

Chapter 59

Contributors

viii

The first edition of Lecture Notes in Tropical

Medicine was published in 1981, conceived and

entirely written by Dr Dion Bell of the Liverpool

School of Tropical Medicine. It rapidly became

a highly successful ‘classic’ due to its practical,

authoritative and entertaining style. The next

two editions continued as single author books,

but by the time of the fourth edition in 1994,

the spectrum of tropical disease had consider-

ably expanded—HIV/AIDS in particular had

become a major health problem. In view of this,

other authors from the Liverpool School became

involved to cover specific topics.

Dion Bell was one of the greatest tropical physi-

cians and teachers of his time, and it has been a

privilege for us to take over editorship of this book

following his retirement and sadly his subsequent

death. In the fifth edition, we continued the proc-

ess of multi-authorship, though all contributors

were either staff of the Liverpool School of Tropical

Medicine or teachers on the Liverpool DTM&H

course. We also introduced syndromic chapters on

fever, splenomegaly, skin problems, etc., as well as

new chapters on the emerging problems of non-

communicable diseases and refugee health.

In this, the sixth edition, all chapters have

been updated, and a new chapter on nutritional

syndromes has been added, and a section on

mental health has been included in the chapter

on non-communicable diseases. We continue

to use bullet points, tables and boxes, and lists

of recommended reading, including websites.

We say goodbye in this edition to three valued

retiring authors Professor Charlie Gilks, Dr Fred

Nye, and Dr George Wyatt and welcome to our

team Dr Tom Doherty, Dr Rebecca Sinfield and

Dr Maureen Wilkinson.

As well as continuing the style and philoso-

phy of Lecture Notes in Tropical Medicine begun by

Dr Dion Bell 28 years ago, we have also continued

the same financial arrangements with the pub-

lishers. No author or editor of the book has ever

accepted payment and all royalties are paid to the

Liverpool School and used to award medical stu-

dent bursaries for elective periods in the tropics.

We hope that this new edition is useful to both

students and practitioners of tropical medicine. As

always, we welcome any comments and criticisms.

Geoff Gill

Nick Beeching

Liverpool, UK

ix

Preface

x

AAFB acid- and alcohol-fast bacilli

Ab antibody

ABC abacavir

ACE angiotensin-converting enzyme

ACR adequate clinical response

ADLA acute dermatolymphangioadenitis

AFB acid-fast bacilli

AFL acute filarial lymphangitis

Ag antigen

AgB antigen B

AIDP acute inflammatory demyelinating

polyneuropathy

AIDS acquired immune deficiency syndrome

ALA amoebic liver abscess

ALB albendazole

AMAN acute motor axonal neuropathy

APOC African Programme for Onchocerciasis

Control

ARC AIDS-related complex

ARI annual risk of infection

ART antiretroviral therapy

ARV antiretroviral drug

AZT zidovudine

BB borderline leprosy

BCG bacille Calmette–Guérin

b.d. twice daily

BI bacterial index

BL borderline lepromatous leprosy

BMI body mass index

BP blood pressure

b.p.m. beats per minute

BT borderline tuberculoid leprosy

cAMP cyclic adenosine monophosphate

CATT card agglutination test for trypanosomes

CBT cognitive behaviour therapy

CCHF Crimean–Congo haemorrhagic fever

ComDT Community directed treatment with

ivermectin

CFT complement fixation test

CHE complex humanitarian emergency

CHK chikungunya virus

CIATT card indirect agglutination test for

trypanosomes

CL cutaneous leishmaniasis

CM cryptococcal meningitis

CMI cell-mediated immunity

CMR crude mortality rate

CMV cytomegalovirus

CNS central nervous system

COPD chronic obstructive pulmonary disease

CRP C-reactive protein

CSF cerebrospinal fluid

CT computerized tomography

CTC community based therapeutic care

CTF Colorado tick fever

CVP central venous pressure

CXR chest x-ray

DAT direct agglutination test

d4T stavudine

DCL diffuse cutaneous leishmaniasis

ddi didanosine

DD5 double diffusion test for arc 5

DEN dengue virus

DDS 4,4-diaminodiphenylsulphone

DDT dichlorodiphenyl-trichloroethane

DEC diethylcarbamazine citrate

DF dengue fever

DHF dengue haemorrhagic fever

DHFR dihydrofolate reductase

DHPS dihydropteroate synthetase

DIC disseminated intravascular coagulation

DKA diabetic ketoacidosis

DOT directly observed therapy

DOTS directly observed short course therapy

DSS dengue shock syndrome

DTH delayed-type hypersensitivity

List of Abbreviations

xi

DTM&H diploma in tropical medicine and

hygiene

DTP diptheria, tetanus and pertussis

EBV Epstein–Barr virus

ECG electrocardiogram

EEE eastern equine encephalitis

EEG electroencephalography

EFV efavirenz

EIA enzyme immunoassay

EITB enzyme-linked immunoelectrotransfer blot

ELISA enzyme-linked immunoabsorbent assay

EMF endomyocardial fibrosis

ENL erythema nodosum leprosum

EPI extended programme of immunization

ERCP endoscopic retrograde

cholangiopancreatography

ESR erythrocyte sedimentation rate

ETF early treatment failure

FAR fever–arthralgia–rash

FBC full blood count

FCPD fibrocalculous pancreatic diabetes

FES fasciola excretory–secretory

FEV1 forced expiratory volume in 1 second

FGM female genital mutilation

FGT formol gel test

FTC emtricitabine

FUO fever of unknown origin

FVC forced vital capacity

G6PD glucose-6-phosphate dehydrogenase

GABA γ-aminobutyric acid

GAELF Global Alliance for the Elimination of

Lymphatic Filariasis

GAVI Global Alliance for Vaccines and

Immunization

GBS Guillain-Barré syndrome

GCS Glasgow coma score

GDP gross domestic product

GTT glucose tolerance test

HAART highly active antiretroviral therapy

HAV hepatitis A virus

HbA adult haemoglobin

HbF fetal haemoglobin

HbS sickle haemoglobin

HBeAg hepatitis B ‘e’ antigen

HBIg hepatitis B immunoglobulin

HBsAg hepatitis B surface antigen

HBV hepatitis B virus

HCC hepatocellular carcinoma

HCV hepatitis C virus

HDCV human diploid cell vaccine

HDV hepatitis D virus

HEV hepatitis E virus

HFRS haemorrhagic fever with renal

syndrome

Hib Haemophilus influenzae type b

HIV human immunodeficiency virus

HLA human leucocyte antigen

HNK hyperosmolar non-ketotic coma

HPV human papilloma virus

HTLV-1 human T lymphotrophic virus type 1

HUS haemolytic uraemic syndrome

ICT immunochromatographic card test

IDP internally displaced person

IFAT indirect fluorescent antibody test

IFN interferon

Ig immunoglobulin

IGRA interferon gamma release assays

IL interleukin

i.m. intramuscular

IMAI Integrated Management of Adult Illness

strategy

IMCI Integrated Management of Childhood

Illness strategy

INR international normalized ratio

IPT intermittent presumptive therapy

IRD immune reconstitution disease

IRIS immune reconstitution inflammatory

syndrome

i.v. intravenous

IVDU intravenous drug use

IVM ivermectin

JEV Japanese encephalitis virus

KS Kaposi’s sarcoma

LACV La Crosse virus

LBRF louse-borne relapsing fever

LED light emitting diode

LF lymphatic filariasis

LL lepromatous leprosy

LP lumbar puncture

LR leishmaniasis recidivans

LRTI lower respiratory tract infection

LTF late treatment failure

MAEC minianion exchange column technique

MAT microscopic agglutination test

List of Abbreviations

xii

MCH mean corpuscular haemoglobin

MCHC mean corpuscular haemoglobin

concentration

MCL mucocutaneous leishmaniasis

MCV mean corpuscular volume

MDR multidrug resistant

MDT multidrug therapy

Mf/mL microfilariae per millilitre

MHCT microhaematocrit

ML mucosal leishmaniasis

MMDM malnutrition-modulated diabetes

mellitus

MOTT mycobacteria other than tuberculosis

MRDM malnutrition-related diabetes mellitus

MRI magnetic resonance imaging

MSF Médecins sans frontières

MTB Mycobacterium tuberculosis

MTCT mother to child transmission

MUAC mid-upper arm circumference

MVE Murray Valley encephalitis

NCD non-communicable disease

NGO non-governmental organizations

NK natural killer

NNN Novy, MacNeal and Nicolle’s medium

NNRTI non nucleoside reverse transcriptase

inhibitor

NRTI nucleoside reverse transcriptase inhibitor

NSAID non-steroidal anti-inflammatory drug

NTS non-typhi Salmonella

NVP nevirapine

OCP Onchocerciasis Control Programme

OEPA Onchocerciasis Elimination Program for

the Americas

OLM ocular larva migrans

ONN o’nyong nyong virus

ORS oral rehydration solution

ORT oral rehydration therapy

OTF outpatient treatment facility

OTP outpatient therapeutic programme

PAS periodic acid–Schiff

PCECV purified primary chick embryo cell vaccine

PCP Pneumocystis jirovecii (formerly P carinii)

pneumonia

PCR polymerase chain reaction

PCV packed cell volume

PDEV purified duck embryo vaccine

PE pre-erythrocytic

PEG pegylated

PI protease inhibitors

PID pelvic inflammatory disease

PF peak flow

PGL persistent generalized lymphadenopathy

PHC primary health clinic

PKDL post-kala-azar dermal leishmaniasis

PML progressive multifocal leucoencephalopathy

PMTCT prevention of mother to child

transmission

PPD purified protein derivatives

PTSD post traumatic stress disorder

PUO pyrexia of unknown origin

PVCV purified vero cell vaccine

PVRV purified Vero cell vaccine

QBC quantitative buffy coat

q.d.s. four times a day

QTc corrected QT interval (electrocardiographic)

RAPLOA rapid assessment procedures for loiasis

RDT rapid diagnostic test

RIG rabies immune globulin

r.p.m. revolutions per minute

RR respiratory rate

RRV Ross River virus

RUTF ready to use therapeutic food

RVF Rift Valley fever

SACD subacute combined degeneration of the

spinal cord

SAM severe acute malnutrition

SAT standard agglutination test

SFP selective feeding programme

SLE systemic lupus erythematosus

SLE St Louis encephalitis

SMB suckling mouse brain

SP sulfadoxine–pyrimethamine

STD sexually transmitted disease

STI sexually transmitted infection

TB tuberculosis

TBE tick-borne encephalitis

TBRF tick-borne relapsing fever

TCBS thiosulphate citrate bile salt sucrose

TDF tenofovir

t.d.s. three times daily

TFC therapeutic feeding centre

TIF thiomersal, iodine and formol

TNF tumour necrosis factor

TPE tropical pulmonary eosinophilia

List of Abbreviations

xiii

TT tuberculoid leprosy

U&E urea and electrolytes

UFM under-fives mortality

UN United Nations

UNICEF United Nations Children’s Fund

UTI urinary tract infection

VCT voluntary counselling and testing

VEE Venezuelan equine encephalitis

VHF viral haemorrhagic fever

VIMTO vascular, infectious, metabolic, tumours

trauma and toxins, other

VL visceral leishmaniasis

VLM visceral larva migrans

W/H weight-for-height index

WBC white blood cell count

WBCT20 20-min whole blood clotting test

WHO World Health Organization

WNV West Nile virus

XDR extremely drug resistant

YF yellow fever

New Drug Names

New Old

aciclovir acyclovir

amoxicillin amoxycillin

anthelmintic antihelminthic

beclometasone beclomethasone

chlorphenamine chlorphenyramine

hydroxycarbamide hydroxyurea

lidocaine lignocaine

nonoxinol ‘9’ non-oxynol 9

phenobarbital phenobarbitone

sulfamethoxazole sulphamethoxazole

tiabendazole thiabendazole

thioacetazone thiacetazone

List of Abbreviations

Part 1

A General Approach to Syndromes/Symptom Complexes

3

Lecture Notes: Tropical Medicine, 6th edition. By G.V. Gill and N.J. Beeching. Published 2009 by Blackwell Publishing, ISBN: 978-1-4051-8048-1.

Chapter 1

Gastrointestinal presentations

The most important gastrointestinal presentation

in the tropics is diarrhoea, and the majority of

this chapter is devoted to this problem. However,

other presentations of gastrointestinal disease are

discussed first.

Dysphagia

Significant recent-onset dysphagia should always

raise the possibility of oesophageal carcinoma.

This malignancy is particularly common in cer-

tain parts of the tropics, for example, some areas

of Central and East Africa. Oesophageal can-

didiasis (AIDS-related) is also a common cause

of tropical dysphagia. In South America, the

mega-oesophagus of Chagas’ disease should be

considered. Finally, peptic strictures, corrosive

chemical ingestion and foreign bodies (fish bones

especially in some areas) may also be important

causes of impaired swallowing.

Haematemesis

In all areas of the world, an upper gastrointestinal

haemorrhage can be caused by peptic ulceration,

gastritis, oesophagitis and gastric or oesophageal

carcinoma. Gastritis, gastric erosions and gastric

ulcers may be drug related, for example, corti-

costeroids and non-steroidal anti-inflammatory

drugs (NSAIDs). Helicobacter pylori is recognized

globally as a major cause of gastric and duode-

nal inflammation and/or ulceration. Oesophageal

varices may be a particularly common cause of

haematemesis in many tropical areas—at least

25% of all cases in some series. The underlying

liver disease can be the late result of chronic viral

hepatitis or schistosomal hepatic fibrosis.

Abdominal pain

In ‘western’ populations, severe abdominal pain

can result from appendicitis, mesenteric adeni-

tis, perforated peptic ulcers, biliary colic, chole-

cystitis and intestinal obstruction (commonly

because of adhesions or malignancy). This list is

far from exhaustive, but serves to demonstrate

that the spectrum of causes in the tropics is much

wider. The following ‘exotic’ causes of acute severe

abdominal pain may need to be considered.● Abdominal tuberculosis (TB)● Typhoid (including typhoid perforation)● Hydatid cyst rupture● Amoebic colitis (including perforation)● Amoebic liver abscess (which may rupture)● Intestinal obstruction caused by Ascaris

lumbricoides● Ectopic ascariasis (e.g. biliary and/or pancreatic

obstruction)

Chapter 1 Gastrointestinal presentations

4

● Sickle cell crisis● Splenic rupture● Hyperinfection syndrome of strongyloidiasis.

Malabsorption

Malabsorption can be a feature of infection with

Giardia lamblia, Strongyloides stercoralis, intestinal

TB, as well as AIDS. Perhaps the most common

cause, however, is the temporary lactase-defi-

cient situation that may occur after any signifi-

cant acute infective diarrhoeal illness. Milk and

milk products may need to be avoided, although

yoghurt is usually tolerated, because of its high

bacterial lactase content.

Tropical sprue

A particularly well-described form of tropical

malabsorption is ‘tropical sprue’. This occurs pre-

dominantly in India and South East Asia, as well

as in the Caribbean and Central America. Patients

develop non-bloody diarrhoea (sometimes steator-

rhoea) often with abdominal bloating and signifi-

cant weight loss. There may be a history of initial

acute diarrhoeal illness, which is thought to be

the precipitant (although the exact mechanism is

unknown). Duodenal biopsy, as well as biochemi-

cal features of malabsorption, typically shows par-

tial villous atrophy. The illness can be prolonged

and debilitating. Traditional treatment with tetra-

cycline (for associated bacterial small bowel over-

growth) and folic acid is often highly effective.

Diarrhoea

Diarrhoeal illness is one of the most important

causes of morbidity and mortality in the tropics,

causing over six million deaths per year, and is

clearly linked with poor hygiene and contamina-

tion of water and food. A wide variety of viral, bac-

terial and parasitic pathogens have been implicated

in the pathogenesis of diarrhoea, but it is impossible

and unnecessary to test for all these in individual

cases. Systematic review of epidemiological, clinical

and host factors usually enables a sensible work-

ing aetiological diagnosis to be established. The

working diagnosis can be used to decide whether

specific investigation should be performed, or to

direct empirical antimicrobial therapy in the minor-

ity of cases in which it is required. The mainstay of

management of diarrhoeal illness is the assessment

and maintenance of adequate hydration and elec-

trolyte balance, irrespective of the aetiology, as well

as the introduction of control measures in an epi-

demic setting to prevent further cases.

History

It is essential to establish that both the doctor

and the patient are talking about the same thing,

especially if interpreters are being used to take

the clinical history. A useful working definition

of diarrhoea is the passage of three or more loose

or watery bowel motions in 24 h. The distinction

between soft and loose diarrhoea is more difficult,

but bowel motions can be described as diarrhoeal,

when they assume the shape of the collecting con-

tainer. This definition works with acute diarrhoeal

illness but is less satisfactory with chronic diar-

rhoeal illness related to malabsorption in which

bulky, sticky soft bowel motions are abnormal but

may not be fluid enough to move around in the

container. Key features in the history are the pres-

ence or absence of visible blood in the stool (dys-

entery), the presence and degree of abdominal

pain, the presence of tenesmus and the presence of

fever. The duration of illness is important—chronic

diarrhoea can usefully be defined as diarrhoea last-

ing more than 14 days, although a more precise

definition (especially in the context of an immuno-

compromised host) is the passage of three or more

loose or watery stools a day for 28 days or more.

In the historical assessment of fluid balance, the

volume and frequency of faecal loss should be esti-

mated together with the frequency and approxi-

mate volume of any vomiting. The amount of

fluid intake should be checked, as should the fre-

quency of urinary output during the last 24 h.

The epidemiological setting is important. Illness

in close family contacts should be ascertained, and

enquiry should be made about whether the patient

has attended any functions or eaten unusual foods

in the preceding 48–72 h. If so, have any other

Gastrointestinal presentations Chapter 1

5

guests had similar illness? Point source outbreaks

can be caused by toxin-mediated food poisoning

in which case vomiting is often a predominant

feature and incubation periods are usually shorter

than 24 h. This may be difficult to distinguish from

outbreaks of norovirus infection in which vom-

iting is a predominant feature and contacts are

readily infected. Unusual systemic pathogens (e.g.

anthrax of the gut) or non-infectious poisoning

caused by adulterated or contaminated food prod-

ucts must always be considered. Bacterial patho-

gens causing small or large bowel diarrhoea usually

have intermediate incubation periods of 12–72 h.

More detailed food histories are not otherwise very

helpful, except in the case of expatriates who have

unwisely overindulged in very spicy foods (‘tasting

the chilli twice’) or who have recently arrived in

the tropics (traveller’s diarrhoea). Diarrhoea devel-

oping in patients who are already hospitalized sug-

gests a nosocomial or antibiotic-associated cause,

while outbreaks of diarrhoeal illness in a refugee

or camp setting imply specific infections such as

shigellosis or cholera (see later) (Fig. 1.1).

Other illness

Diarrhoea can be a prominent feature of many sys-

temic illnesses, including malaria, pneumonia and

enteric fever, especially in children, and evaluation

of the patient should exclude these as potential

causes. Surgical and other intra-abdominal condi-

tions may mimic gastroenteritis, as can inflamma-

tory bowel disease. In older or immobile patients,

constipation with overflow diarrhoea must be

excluded. Alcohol and drugs frequently cause diar-

rhoea with or without nausea and vomiting.

Host factors

Conditions that cause hypochlorhydria (e.g. gastric

surgery, H2 antagonists and proton pump inhibi-

tors) reduce the gastric acid barrier to many bacterial

pathogens, so a smaller infective dose is required.

Patients with established cardiovascular or renal

disease are less likely to tolerate dehydration, as are

those on diuretics and patients with poorly con-

trolled diabetes. Pre-existing large bowel problems

such as inflammatory bowel disease predispose to

complications of dysenteric infections such as toxic

megacolon, signs of which may be partly masked

by concurrent steroid therapy. Bowel tumours can

produce diarrhoea with or without blood or weight

loss. Small bowel problems, including lymphoma,

can cause prolonged diarrhoea. Immunosuppression

of the patient, particularly by HIV, predisposes to

increased invasiveness (local and systemic) of bac-

terial pathogens such as non-typhoidal Salmonella,

increased recurrence of such pathogens and chronic

diarrhoea caused by a variety of protozoa.

Examination

General examination must include assessment

of the state of hydration. This is more difficult

to quantify clinically in adults than in children,

but key features are summarized in Table 1.1.

Measurement of any postural drop in blood pres-

sure (BP) is particularly useful. Rectal examination

should be performed, except in obvious cases of

cholera, and is particularly important in older

patients who are more likely to have non-infec-

tious bowel problems. Systemic causes of diar-

rhoea and signs of immunosuppression (e.g. zoster

scars and oral candidiasis) should be sought out.

Clinical syndromes of diarrhoea

Apart from acute toxin-mediated food poison-

ing, diarrhoeal illness can be broadly classi-

fied into small bowel secretory diarrhoea, small Figure 1.1 Though it looks like urine, this is the `ricewater’ stool from a patient with cholera.

Chapter 1 Gastrointestinal presentations

6

bowel malabsorption and large bowel inflamma-

tory diarrhoea. Each of these groups may be acute

or chronic, and there is considerable overlap (Table

1.2).

Small bowel secretory diarrhoea is exempli-

fied by cholera and non-invasive Escherichia coli

infections in which toxins specifically promote

secretion of water and electrolytes into the

bowel lumen and inhibit their reabsorption. Such

secretion can be competitively overcome by a

steady intake of balanced electrolyte solutions con-

taining adequate amounts of glucose but not too

much to produce an osmotic diarrhoea. This is the

scientific basis for the success of oral rehydration

therapy in which the correct quantities of salts and

glucose are added to sterile water for rehydration.

Table 1.1 Clinical classification of severity of dehydration in adults

Mild Moderate Severe

Subjective

General state Alert, active, up and

about

Weak, lethargic, able to

sit and walk

Dull, inactive, unable to sit or

walk

Ability to perform daily

activities

Able to perform

daily activities

without difficulty

Able to perform daily

activities with some

difficulty, for example,

stays away from work

and needs support

Unable to perform daily

activities, stays in bed or needs

hospitalization

Thirst Not increased Increased thirst Feels very thirsty

Objective

Pulse Normal Tachycardia Tachycardia

Blood pressure Normal Normal or decrease,

10–20 mmHg systolic

Decrease > 20 mm Hg systolic

Postural hypotension No Yes or no Yes

Jugular venous pressure Normal Normal or slightly flat Flat

Dry mucosa (mouth, tongue) No Slight Severe

Skin turgor Good Fair Poor

Sunken eye balls No Minimal Sunken

Body weight loss <5% 5–10% >10%

Table 1.2 Clinical features of inflammatory and non-inflammatory diarrhoea

Non-inflammatory Inflammatory

Symptoms

Nausea, vomiting; abdominal pain and fever not Abdominal pain, tenesmus, fever

major features

Stool

Voluminous, watery Frequent, small volume; blood-stained, pus cells

present, mucus

Site

Proximal small intestine Distal ileum, colon

Mechanism

Osmotic or secretory Invasion of enterocytes leading to mucosal

cell death and inflammatory response

Gastrointestinal presentations Chapter 1

7

Malabsorption is a common complication

of infectious diarrhoea in the tropics, as many

races have relatively low disaccharidase activity

in the small bowel enterocytes. Disruption of

‘normal’ bowel activity readily leads to failure

to break down sugars and a moderately pro-

longed lactose intolerance. This is particularly

common after infections that cause flattening of

the small bowel mucosa (such as giardiasis and

cryptosporidiosis). Large bowel diarrhoea is usu-

ally caused by direct invasion of the bowel by

pathogens such as Entamoeba histolytica, bacteria

such as Campylobacter species or Clostridium dif-

ficile after antibiotic therapy. Other parasites such

as Schistosoma mansoni can also cause prolonged

large bowel diarrhoea. In heavy Trichuris trichiura

infections, oedema of the rectal mucosa together

with continued efforts to defaecate resulting from

tenesmus can lead to rectal prolapse. A summary

of the major pathogens in inflammatory and non-

inflammatory diarrhoea is shown in Table 1.3.

Investigations

A useful algorithmic approach to individual

patient diagnosis and management is shown in

Figure 1.2. In most tropical settings, microbio-

logical investigation proves impossible or very

Table 1.3 Pathogens in inflammatory and non-inflammatory diarrhoea

Inflammatory Non-inflammatory

VirusesNil Rotavirus

Adenovirus 40/41

Astrovirus

Norovirus (Norwalk agent)

Calicivirus

Small round structureless virus

Coronavirus

Torovirus

Bredavirus

Picobirnavirus

BacteriaEnteroinvasive Escherichia coli (EIEC) Enterotoxigenic E. coli (ETEC)

Enterohaemorrhagic E. coli (EHEC), for example, 0157 Enteropathogenic E. coli (EPEC)

Enteroaggregative E. coli (EAggEC) Vibrio cholerae

Aeromonas hydrophila Vibrio parahaemolyticus

Campylobacter spp. Campylobacter spp.

Salmonella spp. Salmonella spp.

Shigella spp. Plesiomonas shigelloides

Yersinia enterocolitica Bacillus cereus

Clostridium difficile Clostridium perfringens

ProtozoaEntamoeba histolytica Cryptosporidium spp.

Balantidium coli Giardia intestinalis

Cyclospora cayetanensis

Isospora belli

Microsporidia (e.g. Enterocytozoon bieneusi)

HelminthsSchistosoma spp. Strongyloides stercoralis

Chapter 1 Gastrointestinal presentations

8

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Gastrointestinal presentations Chapter 1

9

limited. Microscopic inspection of faeces for leuco-

cytes, suggestive of invasive pathogens in the large

bowel, is commonly advocated but is of question-

able time-effectiveness compared with macro-

scopic inspection of faeces for blood (and smell)

when resources are limited. However, cholera

vibrios may be observed with their characteristic

‘shooting star’ motility even without dark ground

facilities, and this is very useful when culture is

not available. Investigations for faecal parasites

should be limited to specific settings (e.g. chronic

diarrhoea complicating HIV) and are almost never

indicated in nosocomial diarrhoea. Fresh stool

microscopy for active trophozoites should only

be requested when amoebic dysentery is truly sus-

pected. Blanket requests for faecal microscopy for

‘ova, cysts and parasites’ on all patients are a waste

of time in most settings. Such requesting patterns

overload laboratories, demoralize their staff and

lead to reports of questionable quality with little

effect on clinical management decisions.

In an outbreak setting, full microbiological

identification of the pathogen and assessment

of the antimicrobial resistance patterns are very

helpful, and it should be pursued even if outside

assistance is required. In sporadic cases, detailed

microbiological tests may be inappropriate, but

clinicians need to be aware of the local antibi-

otic sensitivities of organisms such as Shigella,

Salmonella and Campylobacter if they are to use

empirical antimicrobial therapy in a responsible

and effective manner. Other investigations, such

as serum electrolytes, peripheral white cell count

and blood cultures, are performed in a hospital

setting but again may not be available routinely.

Management

Detailed management of individual pathogens is

beyond the scope of this chapter. The key is the

correction of fluid and electrolyte imbalance.

Severely dehydrated patients need rapid intrave-

nous replacement of fluid loss, preferably using

a physiologically balanced electrolyte solution

such as Ringer’s solution (see Chapter 21, p. 197).

Large volumes of dextrose solution can be dan-

gerous. Intravenous fluid can be supplemented

and rapidly replaced by oral rehydration, which

is more successful if small volumes of fluid are

taken steadily rather than large volumes at a time.

Specific World Health Organization (WHO) oral

rehydration solution (ORS) is ideal, but the water

in which it is dissolved must be clean and safe to

drink—preferably by prior boiling and cooling.

Alternative oral rehydration therapy mixtures can

also be used for adults, and food, including milk

products, is usually reintroduced as early as possi-

ble after initial resuscitation of children. Fluid bal-

ance should be carefully monitored, and a cholera

bed is useful for less mobile patients with profuse

diarrhoea. The fluid faeces can then be collected

through a hole in the middle of the bed directly

into a measuring bucket. If a large-bore disposable

Foley’s urinary catheter is available, this can be

inserted into the rectum when diarrhoea is pro-

fuse and watery (e.g. in cholera), removing the

need for frequent evacuation, and allowing accu-

rate measurement of faecal losses by volume.

Antidiarrhoeal agents such as codeine or lop-

eramide should be avoided in patients with acute

invasive or large bowel disease and should not

be used in young children. Antiemetics should

be used sparingly and again avoided in young

children. Zinc supplementation is beneficial for

children, but the roles of probiotics and use of

lactose-free feeds are less clear. Empirical or spe-

cific antimicrobial treatment should be reserved

for specific situations such as proven amoebiasis,

prolonged severe infection in a vulnerable host

or in outbreak settings—for example cholera or

shigellosis. Chronic diarrhoea presents a different

challenge and patients with HIV-related diarrhoea

often progress through successive therapeutic

trials of co-trimoxazole, metronidazole, fluo-

roquinolones, albendazole or nitazoxanide. Such

patients may need ‘hospital at home’ support

including provision of adequate antidiarrhoeal

medications.

In a refugee camp outbreak setting, logisti-

cal support must be requested at an early stage

for detailed epidemiological investigation, triage

and treatment facilities, as well as provision of an

adequate water supply, rehydration solutions and

latrines (Chapter 60).

Chapter 1 Gastrointestinal presentations

10

Further reading

Al-Abri SA, Beeching NJ, Nye FJ. Traveller’s diarrhoea.

Lancet Infect Dis 2005; 5: 349–360. [Overview

of aetiology, epidemiology, management and

prevention of this common problem for

travellers.]

Elliott EJ. Acute gastroenteritis in children. BMJ

2007; 334: 35–40. [Concise evidence based

review, very practical and useful.]

Hart CA. Introduction to acute infective diar-

rhoea. In: Cook GC, Zumla A, eds. Manson’s

Tropical Diseases, 21st edn. London: Elsevier

Science, 2003: 907–913. [Good overview with

references of both adult and paediatric diar-

rhoea causes and effects.]

Manatsathit S, DuPont H, Farthing M et al.

Guideline for the management of acute diar-

rhoea in adults. J Gastroenterol Hepatol 2002;

17 (Suppl): S54–S71. [Superb working party

report produced by acknowledged experts from

Thailand, India and Africa as well as ‘west-

ern’ authorities. Detailed definitions, practical

approaches and many references.]

Thomas PD et al. Guidelines for the investigation

of chronic diarrhoea, 2nd edition. Gut 2003; 52:

1–15. [British guidelines for assessment of both

infectious and non-infectious causes of chronic

diarrhoea.]

WHO. Handbook IMCI Integrated Management

of Childhood Illness. WHO 2005. Chapter 8

Diarrhoea—assessment and management of

diarrhoea in children in tropical settings pages

25–31. [Summary of WHO guidelines for use

at clinic level. Full manual and other IMCI

and nutrition-related resources freely down-

loadable from WHO child and adolescent

health development website http://www.who.

int/child_adolescent_health/topics/en/]

WHO. Implementing the New Recommendations on

the Clinical Management of Diarrhoea. Guidelines

for Policy Makers and Programme Managers. WHO

2006. [Summary of new recommendations for

use of the 2003 low osmolarity ORS mixture

and zinc supplementation, plus programme

guidance.]

WHO. The Treatment of Diarrhoea. A Manual for

Physicians and Other Senior Health Workers,

4th edn. WHO 2005. [Comprehensive review

with algorithms for assessment and manage-

ment of children and adolescents in particular,

appropriate for resource poor settings.]

11

Lecture Notes: Tropical Medicine, 6th edition. By G.V. Gill and N.J. Beeching. Published 2009 by Blackwell Publishing, ISBN: 978-1-4051-8048-1.

Chapter 2

Respiratory presentations

Disorders of the respiratory tract are the most

important cause of ill health in human popula-

tions around the world. The normal physiologi-

cal functioning of the respiratory tract exposes it

to prolonged and intimate contact with the exter-

nal environment, leading to a steady exposure to

airborne pollutants and pathogens with disease-

causing potential.

Infectious diseases dominate acute respiratory

illness in the tropics in all age groups; acute viral

and bacterial infections in childhood, and tubercu-

losis and bacterial pneumonia in adults. The enor-

mous global burden of respiratory impairment

due to chronic obstructive pulmonary disease

(COPD) has recently been described and shown to

be worst in South Africa and China, where the dis-

ease is mainly caused by the exposure to tobacco

smoke in men and by indoor air pollution from

cooking with biomass fuel in women. Global con-

cern regarding the health effects of tobacco smoke

has now resulted in important international trea-

ties to limit tobacco products.

Assessment

History

The predominant symptoms of respiratory illness

are breathlessness, cough and chest pain. Symptom

duration and the concurrence of fever are useful

discriminators—common presentations in adults

and children are summarized in Table 2.1.

Breathlessness

Shortness of breath should be characterized by

duration, progression and whether it is constant

or intermittent. Orthopnoea (breathlessness when

lying flat) suggests a cardiac cause or a structural

abnormality of the thoracic cage. Nocturnal dys-

pnoea is a feature of asthma and obstructive air-

ways disease.

The effort required to precipitate breathlessness

provides a good gauge of the level of respiratory

impairment. Breathlessness at rest or inability of

a young child to feed indicates severe restriction.

Shortness of breath in an adult should be quanti-

fied in terms of tasks completed or failed, or dis-

tance walked.

Cough

Cough is a reflex from any part of the vagal sup-

ply and a conscious act. Therefore, discriminating

between causes of cough can be difficult. Cough

may be productive or non-productive, but a ‘pro-

ductive’ cough is often evidence of pulmonary

infection.

The quantity of sputum produced may provide

diagnostic information about COPD or bron-

chiectasis. The expectoration of mucopurulent

Chapter 2 Respiratory presentations

12

material is an indicator of neutrophil activity and

infection.

Haemoptysis is often an indicator of seri-

ous underlying pathology, but it is important to

establish that blood is being coughed and not

coming from the upper airway or enteric tract.

Tuberculosis, bronchiectasis and neoplasia are

primary concerns.

Extreme paroxysms of coughing in a child,

particularly in association with the characteristic

whoop, indicates a diagnosis of whooping cough.

A ‘barking’ cough with inspiratory stridor is the

hallmark of laryngotracheobronchitis—croup.

Chest pain

Complaints of chest pain should be assessed for

their association with breathing and coughing.

Pain derived from the pleura will be noticeable

on breathing and is lateralized. Tracheal pain has

a tearing or burning quality and is felt retroster-

nally, particularly on coughing.

Respiratory history

In addition to the presenting symptoms, it is

important to enquire about● tobacco smoking (quantify in pack years);● occupation—identify occupationally related

symptoms and exposures including asbestos,

inhaled proteins and fumes;

● risk factors for HIV infection and contact with

tuberculosis cases, particularly in children failing

to thrive.

Non-respiratory illness

Non-respiratory illness may present with pre-

dominantly respiratory symptoms. Breathlessness

is a feature of metabolic acidosis which may be

caused by diabetic ketoacidosis, poisoning, severe

sepsis or renal failure. Chronic breathing difficul-

ties are a feature of anaemia and thyroid disease.

Alteration of breathing pattern and breathless-

ness can occur with neurological injury, during

the early stages of tetanus and botulism and fol-

lowing envenomation.

Examination in respiratory cases

A respiratory examination is used to test hypoth-

eses generated by the history. The signs elicited

are rarely diagnostic in isolation.

The general condition of an individual provides

clues to a diagnosis. In particular, cachexia, or fail-

ure to thrive in a young child, will indicate malnu-

trition or chronic underlying illness. Oral thrush,

skin rashes and old herpes zoster scars are highly

suspicious of HIV infection, heightening the possi-

bility of pneumococcal pneumonia or tuberculosis.

Tachypnoea (rapid breathing) can be a feature

of any respiratory illness. In the context of an

Table 2.1 Shortness of breath in adults and children

Sudden (hours) Acute (days) Chronic (weeks, months)

Adults

Pneumothorax Pneumonia Tuberculosis

Pulmonary embolus Bronchitis COPD

Asthma Lung abscess Kaposi’s sarcoma

Acute left ventricular failure Lung cancer

Allergic alveolitis Heart failure

Pulmonary eosinophilia Silicosis/asbestosis

Children

Pneumothorax Pneumonia Tuberculosis

Inhaled foreign body Bronchitis Heart failure

Asthma

Respiratory presentations Chapter 2

13

acute presentation, rates in adults above 30/min

suggest severe disease particularly in association

with systolic blood pressure below 90 mmHg

and/or a tachycardia in excess of 120 beats per

minute. The criteria for tachypnoea in childhood

are very different from adults. It is diagnosed

only if the respiratory rate is over 60/min before

the age of 2 months, over 50/min from 2 to 12

months, over 40/min from 1 to 5 years and over

30/min (as for adults) over the age of 5 years.

Cyanosis should be looked for in the oral

mucosa but is a difficult sign in pigmented

people. When present it indicates at least 10%

desaturation of haemoglobin and the need for

supplemental oxygen. Pulse oximetry is becom-

ing increasingly widespread and provides more

reliable information.

Altered consciousness and confusion

usually indicate severe acute disease and can

necessitate specific management to protect the

airway. Meningism can be found with severe

pneumonia, with or without pneumococcal

meningitis.

Percussion of the chest will identify a large

pleural effusion (dull note). Lobar consolidation

is common in pneumonia or tuberculosis and can

be diagnosed on the basis of bronchial breathing.

Many patients present with non-specific signs or

scanty chest signs. In these cases, a suggestive

history should lead to further investigation as a

normal chest examination does not exclude sig-

nificant pathology.

Investigation of respiratory disease

Chest X-ray

Limited resources must be carefully rationed in

order to optimally investigate respiratory patients

in the tropics. In particular, a chest X-ray should

be used to extend the examination in difficult

cases and not simply to confirm diagnosis made

confidently on auscultation. Patients with severe

acute respiratory illness or those who fail to

respond to therapy including smear-negative cases

of chronic cough are the ones most frequently

requiring a chest X-ray.

Sputum/respiratory secretions

Sputum examination is essential in the manage-

ment of suspected TB (see Chapter 12) and is of

less value in other cases. Ziehl–Neelsen stain-

ing for mycobacteria and Gram staining for

bacteria are the most common investigations.

Occasionally, an unstained wet preparation of

sputum examined under low power may be

useful for identifying Strongyloides, paragonim-

iasis or fungal elements. Cytology for malig-

nant cells can also be performed on sputum but

requires a skilled pathologist. Other sputum tests

include direct immunofluorescence for viruses

and Pneumocystis jirovecii, antigen detection for

pneumococci and molecular techniques for sev-

eral organisms including tuberculosis, but these

methods are not resource-efficient in developing

countries.

Sputum must be from the lower respiratory

tract and a macroscopic mucopurulent appear-

ance makes this probable. Microscopic sputum

quality assessment is described in Chapter 28.

Sputum samples are best collected in the open air

(outside) to limit the hazard of cross-infection.

When sputum cannot be produced, placing the

patient in a head down position or simple chest

physiotherapy (drumming) for 2–3 min will help.

Lung aspiration increases the diagnostic yield in

young children with lung consolidation. A nee-

dle and syringe primed with 1 mL normal saline

or sterile water is passed into the consolidated

tissue through the thoracic wall and aspirated.

The aspirated material can be smeared onto

slides for examination and injected into liquid

culture media. In young children when sputum is

difficult to collect, gastric washings may be con-

sidered for the investigation of possible tubercu-

losis (mycobacteria are gastric acid resistant).

Blood cultures

Blood cultures are a valuable investigation in all

febrile patients. Recovery of a pathogen allows

confident treatment and is frequently the inves-

tigation by which an unusual cause of pneumo-

nia is established, for example, Salmonella typhi,

Chapter 2 Respiratory presentations

14

Cryptococcus spp, Burkholderia pseudomallei (melio-

idosis), Rhodococcus equi.

Pleural fluid

Sampling of pleural fluid is simple to perform and

should be considered for most effusions, as the

management of simple effusion and empyema is

different. Fluid is aspirated by using a needle and

syringe, avoiding the neurovascular bundle at the

inferior margin of each rib. Occasionally, this fails

because pleural fluid is loculated and has formed

a thick empyema or the chest findings result from

chronic pleural scarring. Protein measurements

may be helpful in confirming an effusion to be a

transudate—a protein level below 30 g/dL and an

absence of inflammatory cells.

Lung function testing

Although lung function can now be measured

using hand-held technology and stored on a lap-

top computer, this is not yet widely used. Now

that asthma prevalence is increasing and COPD is

recognized as a significant burden of chronic dis-

ease in Africa, this may change.

Common presentations

In general, respiratory presentations in the

general medical clinic tend to fall into a small

number of syndromes.

Acute breathlessness and fever in a small child

Lower respiratory tract infection (LRTI) is a lead-

ing killer of children. Consequently, the early

assessment and management of this syndrome is

a core component of the Integrated Management

of Childhood Illness (IMCI) strategy promoted

by the WHO. Vaccination against pneumococcal

and Haemophilus infection are also global

priorities.

Simple assessment at the primary care level

using features of rapid breathing and subcostal

recession (chest indrawing) of a child with fever

and cough is used to distinguish children with an

LRTI who require antibiotics and possible hospital

admission, from those with an upper respiratory

tract infection (see Figure 28.1). Early initiation

of therapy is essential for a good outcome.

Although many LRTIs are initiated by viral

infections, amongst which respiratory syncytial

virus, parainfluenza, adenovirus and measles are

important, super-added bacterial infections are fre-

quent. Streptococcus pneumoniae and Haemophilus

influenzae type b are common. The presentation

of tuberculosis in infants is often occult.

Acute breathlessness, cough and fever in adults

Acute bacterial pneumonia is the principal diag-

nostic consideration, and the diagnosis and

management of this is covered in Chapter 28.

Non-infectious causes become more prevalent in

older adults.

Chronic cough and malaise

Most chronic respiratory problems present

in this way. It is important to exclude or

confirm tuberculosis which represents a seri-

ous public health threat but is readily treat-

able (Chapter 12). A small number of conditions

are specific to the tropics and may need to be

considered under the right epidemiological

circumstances: paragonimiasis in South East

Asia and restricted areas of West Africa (Chapter

29); endemic mycoses in South and Central

America (Chapter 54); and pulmonary compli-

cations of schistosomiasis in endemic regions

(Chapter 17). The incidence of tobacco smoking

associated lung cancer is increasing in developing

countries.

Breathlessness and wheeze

Asthma is an increasingly important problem

in the tropics, particularly in urban centres. The

Respiratory presentations Chapter 2

15

expiratory wheeze or whistling associated with

lower airways obstruction must be differentiated

from inspiratory phase stridor, which indicates

upper airway obstruction. The presence of parox-

ysmal or diurnal cough, breathlessness and wheeze

preferably supported by variation in peak flow

measurements reliably indicates airways obstruc-

tion. An important differential diagnosis of asthma

is tropical pulmonary eosinophilia (Chapter 30).

Although the symptoms are identical, a high

peripheral eosinophil count above 1 � 109/L, dem-

onstration of microfilaria in blood and clinical

response to filaricides support the diagnosis.

Pleural effusion

Symptoms associated with pleural effusions can

be of short or long duration depending on the

nature of the underlying problems, but large effu-

sions are straightforward to find on examination.

Pleural fluid should be sampled as described ear-

lier. In HIV endemic regions, TB is the most com-

mon cause of pleural effusion. Parapneumonic

effusions, empyema or tuberculous effusions

should be suggested by the history. Malignant

effusions must be considered when an infective

aetiology is not readily apparent. Effusions may

indicate extrapulmonary or systemic problems

(Table 2.2).

Respiratory disease in the HIV-infected adults

Respiratory problems head the list of conditions

leading to hospital admission of HIV-infected

adults (Table 2.3). Bacterial (particularly pneu-

mococcal) pneumonia is strongly associated with

HIV infection. It has a similar predictive value for

HIV infection in adults to herpes zoster—around

90% in eastern and southern Africa. HIV infection

Table 2.2 Causes of pleural effusion

Common Infrequent Rare

● Tuberculosis ● Neoplasia ● Thoracic duct damage● Parapneumonic – Lung carcinoma ● Pancreatitis● Empyema – Kaposis’s sarcoma ● Haemorrhagic fever● Heart failure – Burkitt’s lymphoma ● Filariasis

– Mesothelioma ● Hypothyroidism● Constrictive pericarditis

Table 2.3 Respiratory problems complicating HIV infection

Common Infrequent

● Bacterial pneumonia ● Pneumocystis jirovecii pneumoniaa

● Tuberculosis ● Rhodococcus equi infection● Acute bronchitis ● Nocardiasis● Sinusitis ● Lymphoid interstitial pneumonitisb

● Bronchiectasis ● Lymphoma● Pulmonary cryptococcosis ● Pulmonary hypertension● Pulmonary Kaposi’s sarcoma ● Penicillinosisc

● Melioidosisc

● Invasive mycosesd

aCommon in children under 1 year old.bCommon in children.cSouth East Asia.dSouth and Central America.