Graphic Guide To Infectious Disease Brian T Kloss Full Chapter

Graphic guide to infectious disease
Brian T. Kloss
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2015v1.0
Brian Kloss, DO, JD, PA-C
Associate Professor
Department of Emergency Medicine
SUNY Upstate Medical University
Syracuse, New York
Travis Bruce, BFA

1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
GRAPHIC GUIDE TO INFECTIOUS DISEASE ISBN: 978-0-323-44214-5
Copyright © 2019 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical,
including photocopying, recording, or any information storage and retrieval system, without permission in writing from
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found at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as
may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our
understanding, changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using
any information, methods, compounds, or experiments described herein. In using such information or methods they
should be mindful of their own safety and the safety of others, including parties for whom they have a professional
responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most current
information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered,
to verify the recommended dose or formula, the method and duration of administration, and contraindications.
It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make
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safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability
for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or
from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Names: Kloss, Brian T., author, editor. | Bruce, Travis, illustrator.

Title: Graphic guide to infectious disease / Brian Kloss, Travis Bruce.
Description: Philadelphia, PA : Elsevier, [2019] | Includes bibliographical
references and index.
Identifiers: LCCN 2018006370 | ISBN 9780323442145 (hardcover : alk. paper)
Subjects: | MESH: Communicable Diseases | Infection | Pictorial Works
Classification: LCC RC111 | NLM WC 17 | DDC 616.9--dc23 LC record available at https://lccn.loc.gov/2018006370
Executive Content Strategist: James Merritt

Senior Content Development Manager: Kathryn DeFrancesco
Content Development Specialist: Angie Breckon
Book Production Manager: Jeff Patterson
Project Manager: Lisa A. P. Bushey
Book Designer: Patrick Ferguson
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

LIST OF REVIEWERS/
CONTRIBUTOR
CONTRIBUTING AUTHOR: GUEST REVIEWERS FOR DIAGNOSTIC TESTING:

Hernan Rincon-Choles, MD, MSCI Kanish Mirchia, MD
Assistant Professor Department of Pathology
Department of Nephrology and Hypertension SUNY Upstate Medical University
Cleveland Clinic Lerner College of Medicine of the
Case Western Reserve University Rochelle Nagales-Nagamos, MD, MBA
Medical Director, Ohio Renal Care Group Huron Department of Pathology
Dialysis Center SUNY Upstate Medical University
Attending Physician, Glickman Urological and Kidney
Institute Alexandria Smith-Hannah, MD, MS, MPH
Department of Pathology
Topics written by Hernan Rincon: SUNY Upstate Medical University
Echinococcosis
Melioidosis
Granuloma Inguinale
Tularemia
Plague
Legionellosis
Scabies
Rabies
Ebola
Rift Valley Fever
Hanta Virus Pulmonary Syndrome
Hemorrhagic Fever with Renal Syndrome
Crimea Congo Hemorrhagic Fever
Colorado Tick Fever
Rocky Mountain Spotted Fever
Lyme Disease
Babesiosis
Ehrlichiosis
Anaplasmosis
v
ACKNOWLEDGEMENTS
The authors would like to thank our friends, family, and all the staff at Elsevier for their support.
Thanks to Alex Seldes and Sabre Mrkva for being great friends and permitting us to draw Cleo with all those pediatric illnesses.
Thanks to Karen Cyndari, MD/PhD candidate, for website development and support. Thanks to Kara Welch and David
Rothman for assistance with the references and suggested reading section.
Very special thanks to Zubin Damania, MD, a.k.a. ZDoggMD, for making a cameo in our Zika Fever illustration; Mike Cadogan,
MD, from the Life in the Fastlane Emergency Medicine website and blog for making a cameo in our Melioidosis illustration;
and Jawad Kassem, MD, for making a cameo in our Middle Eastern Respiratory Syndrome illustration. Lastly, many thanks to
Rob Guillory, Eisner Award-winning comic book artist for Chew, for his support and serving as a guest illustrator for our Avian
Flu illustration. The guest appearances, celebrity cameos, and pop culture references contained in this textbook are intended to
be works of satire and parody.
vii
INTRODUCTION
Kloss and Bruce combine real medical education with comic book–style illustrations to create beautiful artistic images that
enhance learning. Realizing that many medical professionals are visual learners, Kloss and Bruce enhance learning by breaking
down complex medical conditions and diseases into illustrated scenes. As children of the eighties and with a passion for comic
books, pop culture, nostalgia, and humor, their illustrations exceed boundaries set by other medical illustrations. Irreverent,
provocative, and unconventional are terms that have been used to describe their campy, tongue-in-cheek approach to medical
education. Their visual aids are colorful, comical, and boundary pushing, all of which make learning more fun and memorable.
Dr. Brian Kloss, a professor and emergency medicine physician, and Travis Bruce, a talented illustrator and designer, aim to
educate physicians, physician assistants, nurses, medical students, and other healthcare providers using humor and comic
book–style illustrations.
Their process is simple. First, Dr. Kloss pencils a rough draft of a medical syndrome, disease, or illness and hands it over to
Travis. Travis then draws out the illustration and adds clarity and color. The end result is a helpful educational tool that is both
comical and informative.
The dynamic duo has been collaborating since connecting at a house party in Brooklyn during the turn of the century. Their
first educational product, Toxicology in a Box, was published by McGraw-Hill in 2013 and is available in Kindle version
on Amazon.com. Toxicology in a Box is a set of 150 full-color flashcards geared toward teaching medical providers how to
recognize and treat various toxic exposures ranging from the bizarre to the mundane.
Kloss and Bruce, in collaboration with Elsevier, are pleased to present their latest work: Graphic Guide to Infectious Disease. This
body of text and illustrations represents 4 years of late nights, highly caffeinated beverages, deadline extensions, revisions, and
more deadline extensions. While they’re admittedly no Rick and Morty, they needed a few deadline extensions.
Their only request is that you loosen your collar, sit back, relax, and enjoy learning high-yield medicine via a truly unique
medium. Welcome to Kloss and Bruce: Medical Education Through Comic Illustration.
Brian Kloss, DO, JD, PA-C

Associate Professor
Department of Emergency Medicine
SUNY Upstate Medical University
Travis Bruce, BFA
To learn more about us, please visit www.KlossandBruce.com
ix
ABOUT THE AUTHORS
Brian Kloss, DO, JD, PA-C, is an Emergency Medicine Physician and Associate Professor at the SUNY Upstate Medical
University and VA Medical Center in Syracuse, New York. He holds a Certificate in Radiologic Technology from Morristown
Memorial Hospital in New Jersey, an Associate of Science in Chemistry from the County College of Morris, a Bachelor of Science
in Physician Assistant Studies from Gannon University, a Juris Doctor for the University at Buffalo School of Law, and a
Doctor of Osteopathic Medicine from UMDNJ-SOM (Rowan). He completed a postgraduate Physician Assistant Fellowship
in Gastroenterology, is Board Certified in Emergency Medicine, and completed a Wilderness Medicine Fellowship at SUNY
Upstate. Brian likes vintage video games, comic books, action figures, and old-school hip hop.
Travis Bruce is an artist, illustrator, and designer living in Queens, New York. He graduated with a BFA in illustration from
the School of Visual Arts, with a focus on graphic narratives and children’s books. Along with illustration, he has designed
tabletop products and giftware for the past 15 years.
xi
TABLE OF CONTENTS
PART 1 | VIRAL HEPATITIS PART 3 | CHILDHOOD ILLNESSES
Chapter 1.1 Hepatitis A 2 Chapter 3.1 Measles 52

Chapter 1.2 Hepatitis B 4 Chapter 3.2 Mumps 54
Chapter 1.3 Hepatitis B Serum Markers 6 Chapter 3.3 Rubella 56
Chapter 1.4 Hepatitis C 8 Chapter 3.4 Erythema Infectiosum 58
Chapter 1.5 Hepatitis D 10 Chapter 3.5 Exanthem Subitum 60
Chapter 1.6 Hepatitis E 12 Chapter 3.6 Chickenpox 62
Chapter 3.7 Congenital and Perinatal Infections 64
Chapter 3.8 Pertussis 68
Chapter 3.9 Hand, Foot, and Mouth Disease 70
PART 2 | INFECTIOUS DIARRHEA Chapter 3.10 Bronchiolitis 72
Chapter 3.11 Kawasaki Disease 74
Section 2.1 Bacterial Chapter 3.12 Croup 76
Chapter 2.1.1 Shigellosis 18
Chapter 2.1.2 Salmonellosis 20
Chapter 2.1.3 Cholera 22
Chapter 2.1.4 Campylobacteriosis 24
PART 4 | TICK-BORNE ILLNESSES
Chapter 2.1.5 Enterohemorrhagic Escherichia coli 26
Chapter 4.1 Tick-Borne Illness and Ticks
Chapter 2.1.6 Enterotoxigenic Escherichia coli 28
as Vectors 80
Chapter 2.1.7 Yersiniosis 30
Chapter 4.2 Rocky Mountain Spotted Fever 84
Chapter 2.1.8 Clostridium difficile Infection 32
Chapter 4.3 Lyme Disease 86
Chapter 2.1.9 Vibriosis 34
Chapter 4.4 Ehrlichiosis 88
Section 2.2 Viral Chapter 4.5 Anaplasmosis 90
Chapter 4.6 Babesiosis 92
Chapter 2.2.1 Norovirus 38
Chapter 4.7 Tularemia 94
Chapter 2.2.2 Rotavirus 40
Chapter 4.8 Crimean-Congo Hemorrhagic Fever 96
Section 2.3 Protozoan Chapter 4.9 Colorado Tick Fever 98
Chapter 2.3.1 Giardiasis 44
Chapter 2.3.2 Cryptosporidiosis 46
Chapter 2.3.3 Amebiasis 48
xiii
xiv TABLE OF CONTENTS
PART 5 | WORMS Chapter 7.6 Trachoma 180

Chapter 7.7 Reactive Arthritis 182
Section 5.1 Roundworms Chapter 7.8 Herpes Simplex 184
Chapter 5.1.1 Ascariasis 104 Chapter 7.9 Trichomoniasis 186
Chapter 5.1.2 Filariasis 106 Chapter 7.10 Scabies 188
Chapter 5.1.3 Onchocerciasis 110 Chapter 7.11 Chancroid 190
Chapter 5.1.4 Pinworm 112 Chapter 7.12 Donovanosis 192
Chapter 5.1.5 Hookworm 116 Chapter 7.13 Vaginitis 194
Chapter 5.1.6 Whipworm 118 Chapter 7.14 Molluscum Contagiosum 196
Chapter 5.1.7 Trichinosis 120 Chapter 7.15 Lymphogranuloma Venereum 198
Chapter 5.1.8 Dracunculiasis 122
Chapter 5.1.9 Cutaneous Larva Migrans 124
Chapter 5.1.10 Threadworm 126
PART 8 | PULMONARY
Section 5.2 Tapeworms
Chapter 8.1 Middle Eastern Respiratory
Chapter 5.2.1 Pork Tapeworm and Cysticercosis 130
Syndrome 202
Chapter 5.2.2 Broad Fish Tapeworm 132
Chapter 8.2 Tuberculosis 204
Chapter 5.2.3 Beef Tapeworm 134
Chapter 8.3 Legionnaires’ Disease 206
Chapter 5.2.4 Echinococcosis 136
Chapter 8.4 Psittacosis 208
Chapter 5.2.5 Dwarf Tapeworm 138
Chapter 8.5 Avian Influenza 210
Section 5.3 Flatworms Chapter 8.6 Influenza 212
Chapter 8.7 Severe Acute Respiratory Syndrome 214
Chapter 5.3.1 Schistosomiasis 142
Chapter 5.3.2 Liver Fluke 144
Chapter 5.3.3 Lung Fluke 146
PART 9 | MOSQUITO-BORNE ILLNESSES
Chapter 9.1 Zika Fever 218

PART 6 | FUNGAL
Chapter 9.2 Dengue 220
Chapter 9.3 Yellow Fever 222
Chapter 6.1 Sporotrichosis 150
Chapter 9.4 Malaria 224
Chapter 6.2 Paracoccidiomycosis 152
Chapter 9.5 Mosquito-Borne Encephalitis 228
Chapter 6.3 Coccidioidomycosis 154
Chapter 9.6 Chikungunya 232
Chapter 6.4 Blastomycosis 156
Chapter 6.5 Histoplasmosis 158
Chapter 6.6 Tinea Infections of the Skin 160
Chapter 6.7 Tinea Versicolor 162
Chapter 6.8 Aspergillosis 164
PART 10 | RAT-, FLEA-, LOUSE-, AND
Chapter 6.9 Mucormycosis 166
CHIGGER-BORNE ILLNESSES
Chapter 10.1 Hemorrhagic Fever with Renal

Syndrome 236
Chapter 10.2 Hantavirus Pulmonary Syndrome 238
PART 7 | SEXUALLY TRANSMITTED DISEASES
Chapter 10.3 Plague 240
Chapter 10.4 Leptospirosis 242
Chapter 7.1 Gonorrhea 170
Chapter 10.5 Rat Bite Fever 244
Chapter 7.2 Condyloma Acuminata 172
Chapter 10.6 Trench Fever 246
Chapter 7.3 Pubic Lice 174
Chapter 10.7 Scrub Typhus 248
Chapter 7.4 Syphilis 176
Chapter 10.8 Epidemic Typhus 250
Chapter 7.5 Chlamydia 178
Chapter 10.9 Endemic Typhus 252
Chapter 10.10 Arenaviridae 254
TABLE OF CONTENTS xv
PART 11 | OROPHARYNGEAL INFECTIONS Chapter 13.3 Pediculosis 292

Chapter 13.4 Naegleriasis 294
Chapter 11.1 Peritonsillar Abscess 258 Chapter 13.5 Prion Diseases 296
Chapter 11.2 Diphtheria 260
Chapter 11.3 Herpangina 262
Chapter 11.4 Thrush 264
Chapter 11.5 Streptococcal Pharyngitis 266 PART 14 | BACTERIAL
Chapter 14.1 Anthrax 300

Chapter 14.2 Botulism 302
PART 12 | VIRAL Chapter 14.3 Brucellosis 304
Chapter 14.4 Typhoid Fever 306
Chapter 12.1 Ebola 270 Chapter 14.5 Cat Scratch Fever 308
Chapter 12.2 Rabies 272 Chapter 14.6 Leprosy 310
Chapter 12.3 AIDS: Opportunistic Infections 274 Chapter 14.7 Infective Endocarditis 312
Chapter 12.4 Smallpox 280 Chapter 14.8 Tetanus 314
Chapter 12.5 Mononucleosis 282 Chapter 14.9 Listeriosis 316
Chapter 12.5 Polio 284 Chapter 14.10 Q Fever 318
Chapter 14.11 Melioidosis 320
PART 13 | PARASITES AND PRIONS

BIBLIOGRAPHY AND SUGGESTED READING
Chapter 13.1 Chagas Disease 288
Chapter 13.2 African Sleeping Sickness 290
PART 1
VIRAL
HEPATITIS
PART 1 VIRAL HEPATITIS
Disease Name: Hepatitis A

Synonyms: Infectious Hepatitis
Causative Agent: Hepatitis A Virus (HAV)
Reservoir: Humans
Incubation Period: 15-50 days; Average: 28 days
Geographic Regions Affected: Worldwide
Description: HAV is a vaccine-preventable fecal-orally transmitted RNA virus that causes acute
hepatitis. Hepatitis A is never chronic, is often asymptomatic in younger patients,
and causes fulminant hepatic failure in ,1% of cases. Risk factors include travel to
endemic regions, ingestion of contaminated food or water (raw shellfish), work in
day care centers (exposure to feces/diaper changing), close contact with infected
patients, and men who have sex with men.
Signs and Symptoms: Typically, the younger the patient, the fewer symptoms he or she exhibits. Most infants
will show little to no signs of infection, whereas most adults become symptomatic.
Symptomatic patients experience nausea, vomiting, malaise, abdominal pain, and fever
followed by scleral icterus and jaundice several days later. Symptoms often last for less
than 2 months; however, the disease may be prolonged or can relapse over a 6-month
period. Infection confers lifelong immunity.
Diagnostic Testing: Labs will reveal a hepatocellular pattern with ALT/AST elevations ,1000, rising
before an increase in bilirubin and alkaline phosphatase is seen. ALT, being more
specific to the liver, is often higher than AST. IgM rises in acute infection, and IgG
begins to rise in convalescence. Fulminant hepatic failure, a serious consequence of
infection characterized by altered mental status (hepatic encephalopathy) and
elevations of PT/INR, is more common in older patients and those with preexisting
liver disease (chronic hepatitis B and/or C).
Treatments: Supportive. The disease is preventable by two doses of a vaccine given at least
6 months apart. Depending on the manufacturer, the second dose of the vaccine
can be given up to 12 or 18 months after the first dose. Postexposure vaccine can
be given in healthy persons aged 1–40 years within 14 days to prevent infection.
Postexposure immune globulin is recommended within 14 days for unvaccinated
patients with immunodeficiency, chronic liver disease, adults .41 years, and
children ,12 months old.
Pearls: There have been several food-related outbreaks of hepatitis A in the United States.
Five hundred people became ill in 2003 after consuming salsa made with green
onions at a now-bankrupt Mexican food chain restaurant.
2
CHAPTER 1 HEPATITIS A
Hepatitis A
IgM IgG
3
Disease Name: Hepatitis B

Synonyms: Serum Hepatitis
Causative Agent: Hepatitis B Virus (HBV)
Incubation: 60–150 days; Average: 90 days
Geographic Regions Affected: Worldwide, Higher Incidence in Asia
Reservoir: Humans
Description: HBV is a double-stranded DNA virus that causes acute and chronic hepatitis. The
disease can be transmitted vertically at birth or through contact with infected
bodily fluids, such as blood, semen, and vaginal secretions. Hepatitis B can be
transmitted sexually and through IV drug use. Healthcare workers are at risk of
infection from needlestick injuries.
Signs and Symptoms: Acute: Most infants and young children with acute infections are asymptomatic. Older
patients are more likely to show symptoms, which include fever, malaise, anorexia,
nausea, vomiting, abdominal pain, and jaundice. Approximately 70% of acutely infected
adults will have symptoms. Symptoms can last for several weeks. The incidence of
fulminant hepatic failure is ,1%. Chronic: Chronic hepatitis B is often asymptomatic
but patients can have symptomatic flairs. If untreated, the disease can be spread to
others, cause cirrhosis, and predispose patients to hepatocellular carcinoma. The
likelihood of developing chronic hepatitis B is inversely proportional to age at time of
infection. The risk of vertical transmission is very high and is dependent on the mother’s
HBeAg/HBeAb status. Those women who are HBeAg1 and HBeAb2 are more likely
to pass on the infection. The Centers for Disease Control and Prevention report that
infected newborns develop chronic hepatitis B approximately 90% of the time,
whereas children infected between the ages of 1 and 5 years have a 25%–50% chance
of developing chronic disease. Older children and adults are more likely to clear the
disease and have a 5%–10% chance of chronicity.
Diagnostic Testing: Acute and chronic hepatitis B are diagnosed by specific serum markers and HBV
viral load testing using PCR. Chronic hepatitis B is defined as the presence of HBsAg
detectable in serum for 6 months or longer after symptom onset. Please see our
summary of hepatitis B markers for more information.
Treatments: Treatment of acute disease is supportive, except in cases of fulminant hepatic failure,
wherein nucleoside/nucleotide analog medications are indicated. In chronic hepatitis
B infections, treatment options and the decision to treat are highly dependent on
individual patient factors, such as viral load, presence/absence of cirrhosis or
hepatocellular cancer, HBeAg/HBeAb status, pregnancy status, patient age, and
biochemical markers. Treatment options for chronic hepatitis B include PEGylated
interferon or nucleoside/nucleotide analogs. Nucleoside/nucleotide analogs include
lamivudine, adefovir, entecavir, telbivudine, and tenofovir. The authors recommend
referencing current American Association for the Study of Liver Diseases (AASLD)
and/or European Association for the Study of the Liver (EASL) guidelines prior to
initiating treatment. Hepatitis B is vaccine preventable, and infection after acute
exposure can be prevented with vaccination and immune globulin.
4
CHAPTER 2 HEPATITIS B
Hepatitis B
I'm going to get the post-

exposure immune globulin
and start the vaccine
series <12 hours after
needle stick or <2 weeks I was vaccinated Day 0,
after sexual exposure. 1 M & 6 M and I am
HBsAb+
By the way,
I have Hepatitis B!
High Rate of Vertical Transmission
Give me vaccine &

immune globulin
≤12 hours.
5
Disease Name: Hepatitis B Serum Markers

Hepatitis B Surface Antigen HBsAg is the first serum marker to appear and is detectable prior to the onset of
(HBsAg): clinical symptoms. It peaks approximately 12 weeks after exposure and should become
undetectable within 24 weeks (6 months). The elimination of HBsAg and seroconversion
to hepatitis B surface antibody (HBsAb) indicates that the infection has resolved.
If HBsAg persists in the serum for .6 months, the patient has a chronic infection.
Hepatitis B e Antigen HBeAg is associated with viral replication and is detectable within 6–14 weeks after
(HBeAg): exposure. In chronic hepatitis B, HBeAg serves as a marker of both disease activity
and infectivity. Patients who are HBeAg+ (HBeAb2) have higher viral loads and
greater disease activity and are more infectious. In pregnancy, HBsAg+ women are
more likely to pass the infection on to their infants. Any infant born to a mother
with chronic HBV should be vaccinated and given immune globulin, ideally within
12 hours.
Hepatitis B Virus Core HBcAb is the first antibody to be detected via serum. Although there is a core
Antibody (HBcAb): antigen, it is intracellular and cannot be detected in serum. HBcAb exists as both
IgM (signifying acute infection or significant reactivation of chronic disease) and IgG
(indicating a past exposure to the hepatitis B disease). Because HBcAb can only exist
in those exposed to the disease, it is used when screening donated blood and/or
distinguishing whether a person is immune from disease exposure or vaccination.
Because the HBV vaccine consists only of HBsAg, those patients who have been
successfully vaccinated will test HBsAb1 and HBcAb2. This indicates that they have
antibodies to the hepatitis B surface antigen but have never been exposed to the full
virus. Patients who are HBsAb1 and HBcAb1 have been exposed to the full hepatitis B
virus, had the disease to some extent, and are now immune.
Hepatitis B e Antibody Antibodies to the e antigen are associated with decreased viral loads and herald
(HBeAb): convalescence. Seroconversion to HBeAb occurs early in acute disease but can be
delayed for years in chronic infection. Those patients with chronic hepatitis B that
are HBeAb2 seroconvert to HBeAb1 at a rate of approximately 0.5% per year.
HBsAb: HBsAb confirms immunity, either via vaccination or resolved infection. HBsAb begins
to elevate after HBsAg levels taper off. Again, presence of HBsAg and absence of
HBsAb at 6 months indicates chronic infection. In some cases, there is a window when
neither HBsAg nor HBsAb can be detected. In this case an HBcAb IgM level can be
obtained to evaluate for acute infection.
Hepatitis B Serum DNA: PCR can be used in either a qualitative (yes or no) or quantitative (How much?)
fashion when determining the presence or absence of HBV DNA in serum samples.
In patients who contract HBV infection and seroconvert to an HBsAb1 state, HBV
DNA should be 100% cleared from their serum. Those patients with chronic hepatitis
B will have detectable HBV DNA in their serum, the amount highly dependent on
their HBeAg/HBeAb status. HBV DNA quantitative studies, HBeAg/HBeAb status,
and liver biopsy results (to grade liver damage) are important in determining
treatment eligibility and options.
6
CHAPTER 3 HEPATITIS B SERUM MARKERS
Hepatitis B Markers
Chronology of Serum Markers

s Ag
pB
He
S
(Surface) g
B eA
p
He
E Ab
(Earth) c
pB
He
Ab
C
(Core) He
pB
e
E sAb
(Earth) pB
He
S
(Surface)
7
Disease Name: Hepatitis C

Causative Agent: Hepatitis C Virus, HCV
Reservoir: Humans
Description: HCV is a single-stranded RNA virus responsible for both acute and chronic viral
hepatitis, with up to 85% of infections becoming chronic. Risk factors for HCV
transmission include IV drug use, blood transfusions and organ transplantation
before July 2012, receiving clotting factors before 1987, intranasal drug use (cocaine),
long-term hemodialysis, unsterile tattoos (e.g., prison), and vertical transmission.
Sexual and household transmission can occur but is low.
Signs and Symptoms: Acute: Approximately 85% of acute infections are asymptomatic, and about 85% of
hepatitis C infections become chronic. Acute symptoms can include malaise, fatigue,
nausea, vomiting, abdominal pain, and jaundice. Chronic: Often asymptomatic but
can cause malaise and fatigue. People with chronic HCV infections can develop
cirrhosis and are predisposed to developing primary hepatocellular carcinoma.
Extrahepatic manifestations of chronic HCV can include diabetes, cryoglobulinemia,
and glomuleronephritis.
Diagnostic Testing: People with chronic hepatitis C may have normal liver enzymes. Hepatitis C antibody
testing screens for the disease, and positive results should be followed by PCR testing
for viral load and genotype. Positive HCV antibody tests with negative viral load
may indicate a false-positive antibody test or identify a patient who previously had
hepatitis C and cleared the virus either spontaneously or via treatment.
Treatments: Since the treatment for hepatitis C is continuously evolving, the authors recommend
consulting the American Association for the Study of Liver Disease (AASLD) and/or the
Infectious Disease Society of America (IDSA) for current guidelines. Initially, PEGylated
interferon combined with oral ribavirin provided about 50% sustained virologic response
(SVR) or “cure” rate. Direct-acting antivirals (DAAs) are now the preferred treatment and
include oral agents: elbasvir/grazoprevir, ledipasvir/sofosbuvir, simeprevir/sofosbuvir, and
sofosbuvir/velpatasvir.
Treatment is often based on genotype, viral load, presence/absence of cirrhosis,
previous treatment failures, and insurance formularies. New drugs are constantly
entering the development pipeline, and many patients may be offered enrollment
in clinical trials. All patients with chronic hepatitis C should be vaccinated against
hepatitis A virus and hepatitis B virus to prevent additional liver disease from these
infections.
8
CHAPTER 4 HEPATITIS C
Hepatitis C
Simplified Testing Algorithm
HCV Risk Factors
ALT
HCV Ab
6 Main
Genotypes
HCV Viral Load Quant Consider 1–6
HCV Genotype Repeating in
3-6 Months
Consider Liver Biopsy

Referral to ID/GI
= 2% Vertical Transmission
Blood Clotting
Transfusion Factors
< July 1992 < 1987
Intranasal
Cocaine
1992
Genotype 2
Genotype 3
10%
10%
type
Geno
4,5,6
Genotype 1
75%
1a 60%
1b 15%
Genotype
9
Disease Name: Hepatitis D

Causative Agent: Hepatitis D Virus (HDV), Delta Virus
Incubation: Coinfection: 45–160 days; Average: 90

Superinfection: 2–8 weeks
Geographic Regions Affected: Worldwide; Higher incidences where hepatitis B is endemic. Hepatitis D is rare in
the United States.
Reservoir: Humans with hepatitis B virus (HBV)/HDV coinfections.
Description: Hepatitis D is a “defective” single-stranded RNA virus that requires the machinery
and assistance of hepatitis B to replicate. HDV is acquired as either a coinfection
(simultaneously acquired with hepatitis B) or as a superinfection (acquired by a
person who already has chronic hepatitis B).
Signs and Symptoms: When acquired as a coinfection, HDV can increase the likelihood of severe illness and
fulminant hepatic failure. Coinfections are less likely to result in chronic hepatitis D.
Superinfections are more likely to cause chronic hepatitis D and can worsen preexisting
liver disease.
Diagnostic Testing: Since patients cannot have hepatitis D without hepatitis B, patients will test positive
for hepatitis B serum markers. IgM and IgG anti-HDV antibody testing is available
in the United States, and an elevated anti-HDV IgG titer can be seen in chronic
hepatitis D infections. Patients testing positive for HDV antibodies can be followed
up with HDV viral levels via PCR technology.
Treatments: Vaccination against hepatitis B is also preventative against hepatitis D. PEGylated

interferon is the only treatment that is effective for chronic hepatitis D, but successful
clearance of the virus with treatment is low (approximately 20%–25%).
Pearls: HDV infections cannot exist without hepatitis B. The incubation period for
hepatitis D coinfection is identical to that of acute hepatitis B (the HDV infection
occurs concurrently with HBV). The presence of HBsAg and IgM anti-HBc is
essential for the diagnosis of HDV infections.
10
CHAPTER 5 HEPATITIS D
Hepatitis D
Co-infection occurs
when Hep B + D
arrive simultaneously.
It’s indistinguishable
from acute Hep B.
Super-infection occurs
when D is introduced into a
chronic HBsAg carrier and
presents as severe acute
hepatitis or exacerbation of a
chronic hepatitis.
Miss B, may I
super-infect you
with D?
11
Disease Name: Hepatitis E

Causative Agent: Hepatitis E Virus, HEV
Geographic Regions Affected: Central America, Africa, Middle East, India, and Asia
Reservoir: Swine and small rodents may serve as an animal reservoir.
Description: HEV is a fecal-oral (genotype 1 and 2) and foodborne (genotype 3 and 4) single-stranded
RNA virus responsible for acute viral hepatitis. There are four major viral genotypes,
each associated with specific regions and unique clinical presentations. Genotype 3
is found in developed countries, tends to affect those patients .40 years old or
immunocompromised, and can cause chronic infections. Genotypes 1, 2, and
4 more commonly affect younger adults. HEV infections can occur as sporadic
outbreaks affecting many people or as isolated cases affecting isolated individuals.
Signs and Symptoms: Most cases are asymptomatic, with fewer than 5% of patients showing signs of acute
infection. When symptomatic, patients may exhibit malaise, fever, nausea, vomiting,
abdominal pain, arthralgia, and jaundice. Fulminant hepatic failure can occur in up
to 3% of infections and is more common in pregnant females and in those with
preexisting liver disease.
Diagnostic Testing: There are no commercially approved tests for HEV in the United States. Some
countries have access to IgM, IgG, and HEV PCR testing capabilities. Acute
infection would be determined by a positive IgM and HEV PCR viral load. IgM
is elevated in the acute setting and indicates recent exposure to the HEV virus,
whereas IgG increases during convalescence and confirms past exposure. In
chronic HEV infections, HEV RNA will be detectable via PCR in serum or stool
more than 6 months after initial infection.
Treatments: Supportive. Ribavirin may be beneficial in the treatment of chronic HEV infection.
There is an HEV vaccine that is licensed in China.
Pearls: Acute hepatitis E infection during pregnancy has a high mortality rate (up to 25%).
12
CHAPTER 6 HEPATITIS E
Hepatitis E
NA Virus
ssR
4G
eno t ypes
25%
Mortality
13
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PART 2
INFECTIOUS
DIARRHEA
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PART 2
Section 1
BACTERIAL
PART 2 INFECTIOUS DIARRHEA
Disease Name: Shigellosis

BACTERIAL
Synonyms: Bacillary Dysentery
Causative Agent: Four serogroups of Shigella, broken down into group A: S. dysenteriae; group B:
S. flexneri; group C: S. boydii; and group D: S. sonnei.
Transmission: Transmission is fecal-oral. Because a very small inoculum of bacteria (10–100 organisms)
is required for transmission, infected food handlers can easily spread the disease.
Person-to-person transmission is common. Consumption of contaminated water,
food, or produce grown where sewage is used as fertilizer often results in illness.
Given the low inoculum required for transmission, there can be rapid spread in
closed quarters such as military campaigns, refugee camps, day care centers, and
households.
Geographic Regions Affected: Worldwide—more common in developing nations.
Description: An acute bacterial hemorrhagic diarrheal illness caused by any one of four Shigella
serogroups. Key symptoms include bloody diarrhea, abdominal pain, and fever.
Severe dehydration is uncommon.
Signs and Symptoms: Diarrhea, fever, abdominal pain and cramps, tenesmus, malaise, nausea, and
vomiting. Diarrhea is initially watery and nonbloody then becomes mucoid and
bloody as the infection transitions into the large bowel. Symptoms typically last
5–7 days without treatment. Complications can include hemolytic uremic
syndrome (HUS), seizures in children, and reactive arthritis.
Diagnostic Testing: Shigella should be suspected in patients presenting with bloody diarrhea, abdominal
pain, fever, and small, frequent stool volumes. Stool can be cultured or tested using
PCR.
Treatments: Antibiotics can reduce the duration of symptoms in infected patients. Because
antibiotic resistance to TMP/SMX and ampicillin is commonplace, current
recommendations call for either azithromycin or ciprofloxacin. However, providers
should be aware of emerging resistance to these antibiotics as well. Antispasmodics
should be avoided.
Pearls: Shigella is the most infectious bacterial diarrheal disease, commonly passed via
person-to-person transmission. S. dysenteriae serotype 1 (formerly Shigella shigae)
tends to be a more aggressive pathogen, whereas S. sonnei tends to cause milder
disease. S. sonnei is more common in developed nations, and S. flexneri is more
common in less-developed nations.
18
CHAPTER 7 SHIGELLOSIS
Shigellosis
Shigella
BACTERIAL
(Bacillary Dysentery) 4 Serogroups
A: S. dysenteriae
B: S. flexneri
C: S. boydii
D: S. sonnei
Incubation: 1-7 Days
Average: 3 Gram Rod
Diarrhea: 5-7 Days
Military Street meats!
Campaigns Handmade,
hand served!
Fever
Nausea Food
Vomiting
Contaminated Abdominal Pain

Water Hand to Mouth Cramps
Tenesmus
Reactive Arthritis
HUS Seizures in Children
Shiga Blood & Pus

Toxin Common
Rapid Intra-Family Spread

Refugee camps 100 Bacteria Cause Illness
19
Disease Name: Salmonellosis

BACTERIAL
Synonym: Nontyphoidal Salmonella
Causative Agents: Salmonella bongori, Salmonella enterica
Reservoir: Poultry is the most common. Some reptiles.
Transmission: Typically foodborne via consumption of undercooked poultry, foodstuffs in contact

with raw/undercooked poultry (contaminated cutting board), raw eggs, and raw/
unpasteurized milk. There have been several major U.S. foodborne outbreaks traced
back to commercially packaged chicken, peanut butter (Peanut Corporation of
America in 2008), and ice cream (Schwan’s in 1994). Reptiles such as turtles, lizards,
and snakes may be carriers of salmonella (S. bongori).
Incubation: 12–48 hours
Description: An acute, febrile, bacterial diarrheal illness often transmitted by undercooked poultry
(chicken/raw eggs) and characterized by watery and/or bloody diarrhea.
Signs and Symptoms: Typical symptoms include fever, malaise, nausea, vomiting, abdominal pain/cramps,
tenesmus, and diarrhea. Bloody diarrhea can also occur and is more common in
children. The illness is often self-limiting, and symptoms typically resolve within
3–7 days. More severe infections are seen with larger bacterial inoculums, in young
children and older adults, and the immunocompromised. Salmonella may become
invasive and can cause bacteremia, meningitis, septic arthritis, and osteomyelitis (sickle
cell patients are at increased risk). Postinfectious irritable bowel syndrome and reactive
arthritis may occur in some patients.
Diagnostic Testing: Stool culture is the gold standard for diagnosis.
Treatments: The mainstay of treatment is often supportive and consists of fluids and a gentle diet.
Antibiotics are indicated in cases of severe illness, persistent fever, high-risk patients
(extremes of age, weakened immune systems), and those with invasive disease.
Treatment options may include fluoroquinolones (ciprofloxacin or levofloxacin),
macrolides (azithromycin), or cephalosporins (ceftriaxone or cefotaxime). Resistance
to TMP/SMX and other antibiotics is on the rise.
Pearls: The Food and Drug Administration has banned the sale of pet turtles less than 4 inches
in length since 1975 to reduce the incidence of salmonellosis in children. The Centers
for Disease Control and Prevention estimates that 100,000 cases of the disease have been
prevented as a result of this ban.
20
CHAPTER 8 SALMONELLOSIS
Salmonellosis
BACTERIAL
(Non-typhoidal Salmonella)
Salmonella
2 species High Risk:
Incubation:
S. bongori
12-48 Hours
S. enterica
Diarrhea: 3-7 Days
Gram rod
Sickle Cell =
Fever Osteomyelitis
Nausea
Vomiting
Non-typhoidal Salmonella
Abdominal (NTS)
Pain/Cramps
Tenesmus Reactive Arthritis
S. bongori
Diarrhea: Watery/Bloody
1994
2008
21
Disease Name: Cholera

BACTERIAL
Synonym: Blue Death
Causative Agent: Vibrio cholerae
Transmission: Fecal-oral transmission can occur through consumption of contaminated water,

foodstuffs, or naturally contaminated shellfish.
Incubation: 1–5 days; Average: 2–3 days
Geographic Regions Affected: Resource-poor countries, mostly in Africa, Asia, the Caribbean, and Central and
South America. Peaks are seen before and after rainy seasons.
Description: An acute, afebrile, painless, bacterial diarrheal illness characterized by profound fluid
loss and the passage of “rice water stools.” Severe cases can cause severe electrolyte
abnormalities, renal failure, acidosis, hypovolemic shock, circulatory collapse, and
death.
Signs and Symptoms: Cholera is a spectrum disease with diarrheal symptoms ranging from asymptomatic
or mild to severe. Severe illness causes hypovolemic shock and death. After a brief
incubation period, patients develop nausea, vomiting, painless diarrhea, and lethargy.
Fever is uncommon. Diarrhea is nonbloody, may contain flecks of mucus (rice water
stools), and has a fishy odor. Volume losses of 10–20 liters per day can occur in
adults, resulting in hypovolemic shock, sunken eyes, and loss of skin turgor and
elasticity (washerwoman hands). Severe acidosis secondary to bicarbonate loss can
trigger Kussmaul respirations.
Diagnostic Testing: Clinical signs and symptoms, specifically in the setting of an outbreak of watery
diarrhea, should raise suspicions to the diagnosis. Darkfield microscopy may show
motile Vibrio bacteria. Rapid diagnostic tests can identify the O1 and/or O139
antigens in stool samples. Labs from severely ill patients will reflect the electrolyte,
pH, and renal abnormalities associated with severe dehydration and acidosis.
Ultimately, a positive stool culture is considered the gold standard for diagnosis.
Treatments: The mainstay of treatment consists of IV fluid resuscitation with lactated Ringer’s
solution followed by transition to oral rehydration salts once tolerated. Antibiotics can
shorten the duration of illness in severe disease and include doxycycline, azithromycin,
tetracycline, or erythromycin. Vaccines are available in endemic areas of the world
and for those U.S. travelers headed to endemic regions (relief workers, extended
medical missions, etc.).
Pearls: There was a significant outbreak of cholera in Haiti after a major earthquake in
2010. Patients with blood group O may have worse disease. Cholera epidemics are
associated with O1 and O139 serogroups; O139 is only found in Asia.
22
CHAPTER 9 CHOLERA
Cholera ibr
io cholera
BACTERIAL
V
e
(Blue Death) Rice
Water
Incubation: Gr
am Rod
1-5 Days
Diarrhea: 4-6 Days
Severe Cholera = Peaks before and
Shock w/i 24 Hours after rainy seasons
Lethargy
Sunken Eyes
Fever
Massive IVF Uncommon
Washerwoman Hands
Nausea (Very Thin Fingers)
Vomiting
Hypotension
Kussmaul
Respirations
Oral Rehydration
Painless Diarrhea Cholera Toxin
(CT)
Rice Water
Fishy Odor
Stools
10-20 L/Day Diarrhea

Blood Group O = Worse Disease
V. cholerae O1
Epidemics
V. cholerae O139
23
Disease Name: Campylobacteriosis

BACTERIAL
Causative Agents: Campylobacter jejuni, Campylobacter coli
Reservoir: Gastrointestinal tract of animals and livestock; poultry is the most common. Domestic
dogs and cats may also be colonized.
Transmission: Typically foodborne via consumption of undercooked poultry, foodstuffs in contact

with raw/undercooked poultry, raw/unpasteurized milk, chicken paté, or fecal-oral
transmission from symptomatic individuals.
Description: An acute, febrile, bacterial diarrheal illness characterized by watery diarrhea that
frequently becomes bloody after a few days.
Signs and Symptoms: Patients may have a febrile prodrome before the diarrhea occurs. Typical symptoms
include fever, malaise, abdominal pain/cramps, tenesmus, and watery diarrhea that
often becomes bloody. Nausea and vomiting may occur in some patients. The illness
is often self-limiting and symptoms typically resolve within 7 days. In the acute
setting, some patients may develop right lower quadrant abdominal pain prior to
the onset of diarrhea (pseudoappendicitis). Postinfectious complications can include
Guillain-Barré syndrome and reactive arthritis.
Diagnostic Testing: Stool culture is the gold standard for diagnosis. Darkfield or phase-contrast microscopy
may reveal the motile, gram-negative, curved/helical-shaped rods. There are some stool
antigen and PCR tests available as well.
Treatments: The mainstay of treatment is often supportive and consists of fluids and a gentle diet.
Antibiotics will decrease the duration of illness and options include azithromycin
500 mg daily 3 3 days or erythromycin 500 mg four times daily 3 5 days. There is
worldwide emerging campylobacter resistance to fluoroquinolones, specifically in
Southeast Asia.
24
CHAPTER 10 CAMPYLOBACTERIOSIS
Campylobacteriosis
BACTERIAL
lobacter
py lobact je
py e
Cam
ju coli
ni
r
Cam
Gra m
Rod
Average: 3 Days
Diarrhea 7 Days
d
He e
lical-shap
C. jejuni is in my guts
and I don’t get sick!
Cook me!
Fever
Nausea
Vomiting
Guillain-Barré
Syndrome
Tenesmus
Reactive Arthritis
Watery/Bloody
Diarrhea
Pseudoappendicitis
Watery Diarrhea Bloody after 2-3 Days
25
Disease Name: Enterohemorrhagic Escherichia coli

BACTERIAL
Causative Agent: Escherichia coli bacteria strains capable of producing Shiga toxin, known as “Shiga
toxin–producing E. coli” (STEC). Strains identified in significant outbreaks have
included E. coli O157:H7 (most common in North America, Jack in the Box in 1993),
O104:H4 (Germany and Europe in 2011), and O26 (Chipotle in 2015).
Reservoir: Ruminant animals: Cattle, goats, sheep, deer, and elk. Cattle are the main reservoir.
Transmission: Transmission is fecal-oral, most commonly from the consumption of foodstuffs

like leafy green vegetables, undercooked meat, and raw milk
Description: An acute bacterial hemorrhagic diarrheal illness caused by STEC. Key symptoms
include bloody diarrhea, abdominal pain, cramps, leukocytosis, and absence of
fever.
Signs and Symptoms: Bloody diarrhea, abdominal pain, cramps, tenesmus, malaise, and anorexia. Fever
is notably absent. Symptoms typically resolve over 5–7 days without intervention.
Hemolytic uremic syndrome (HUS), a triad of hemolytic anemia, renal failure, and
thrombocytopenia, occurs in 5%–10% of cases. HUS is more common in children
under 10 years old (affecting about 15%) and those treated with antibiotics (up to
25% of children). HUS typically occurs 5–10 days after the onset of diarrhea, just
as the diarrhea is becoming less frequent.
Diagnostic Testing: STEC should be suspected in patients presenting with bloody diarrhea, abdominal
pain, and absence of fever. Stool can be cultured using sorbitol-MacConkey agar.
Enzyme-linked immunosorbent assays for Shiga toxin 1 and 2. PCR for Shiga toxin
gene, anti-LPS (anti-lipopolysaccharide) IgM and IgG antibodies can also be obtained.
Treatments: The mainstay of treatment is supportive and consists of fluids. Antispasmodics

should be avoided, as they increase the likelihood of systemic complications like
HUS and seizure. Ciprofloxacin and TMP/SMX have been shown to increase the
release of Shiga toxin from bacteria, thus increasing the likelihood of HUS. If an
antibiotic is used, azithromycin is probably the safest choice.
Pearls: There have been several infamous outbreaks of STEC in the United States associated
with fast food restaurants, including Jack in the Box in 1993 and Chipotle in 2015.
26
CHAPTER 11 ENTEROHEMORRHAGIC ESCHERICHIA COLI
Enterotohemorrhagic E. coli
BACTERIAL
(EHEC)
erichia c
ch
ol
Es
i
Average: 3-4 Days
Diarrhea: 5-7 Days Gr
am Ro
d
Fever Uncommon 2015
1993
Abdominal Pain/Cramps
Shiga Toxin 1&2
O157:H7
Tenesmus O104:H4
O26
Anorexia
ABX HUS
in Children
27
Disease Name: Enterotoxigenic Escherichia coli

BACTERIAL
Synonyms: Traveler’s Diarrhea, Montezuma’s Revenge, Delhi Belly, Turista
Causative Agent: Escherichia coli bacteria strains capable of producing one of two toxins: heat-stable
(ST) enterotoxin, which increases intracellular cGMP, and heat-labile (LT) enterotoxin,
which increases intracellular cAMP. These toxins stimulate the intestines to increase
fluid secretion, causing non-bloody diarrhea. Enterotoxigenic Escherichia coli (ETEC)
bacteria may produce either or both toxins.
Transmission: Transmission is fecal-oral, through the consumption of contaminated foodstuffs,

drinking water, or ice. Following the “Boil it, cook it, peel it, or forget it” mantra
reduces the odds of getting ill.
Incubation: 8 hours–3 days
Geographic Regions Affected: Worldwide. Most common cause of “traveler’s diarrhea.”
Description: An acute, profuse watery diarrheal illness caused by ST or LT toxin producing strains
of E. coli (ETEC) bacteria. Key symptoms include watery diarrhea, abdominal pain,
cramps, malaise, anorexia, and absence of fever.
Signs and Symptoms: Profuse watery diarrhea, abdominal pain and cramps, tenesmus, malaise, and
anorexia. Fever is notably absent. Symptoms typically resolve over 3–4 days without
intervention.
Diagnostic Testing: ETEC or “traveler’s diarrhea” is often diagnosed based on patient’s symptoms and
history of recent travel. Often, by the time the patient comes to a healthcare provider’s
attention, symptoms have begun to resolve. Since both bacterial and viral causes of
“traveler’s diarrhea” have very short incubation periods, giardia or other parasites
should strongly be considered in those patients who develop diarrhea 1–2 weeks
after returning from travel.
Treatments: The mainstay of treatment is supportive and consists of fluids and a gentle diet.
Handwashing, drinking bottled water, and avoiding street meats/street vendors, iced
drinks, salads (uncooked vegetables), and fruits may reduce risk of transmission.
Bismuth subsalicylate taken prophylactically may reduce likelihood of infection.
Azithromycin 1000 mg as a single dose or 500 mg daily 3 3 days, ciprofloxacin
750 mg twice daily for 1–3 days, or levofloxacin 500 mg daily for 1–3 days can be
prescribed to travelers to take if they develop diarrhea while abroad. Since the actual
cause of “traveler’s diarrhea” cannot be determined in the field, while the traveler is
abroad, azithromycin is the preferred antibiotic—it covers campylobacter, a bacterium
with emerging resistance to fluoroquinolones, specifically in Southeast Asia.
28
CHAPTER 12 ENTEROTOXIGENIC ESCHERICHIA COLI
Enterotoxigenic E. coli
BACTERIAL
(ETEC/Traveler’s Diarrhea/Montezuma’s Revenge)
erichia c
ch
ol
Es
i
Incubation: 8-72 Hours
Diarrhea: 3-4 Days Gr
am Ro
d
Fever Uncommon
Malaise
Heat-Stable
Abdominal Pain/Cramps Enterotoxin (ST)
Activates cGMP
Heat-Labile
Enterotoxin (LT)
Tenesmus Activates cAMP
Watery Diarrhea
Contaminated Water Anorexia
Non-bloody
29
Disease Name: Yersiniosis

BACTERIAL
Causative Agents: Yersinia enterocolitica, Yersinia pseudotuberculosis
Reservoir: Pigs, rodents, rabbits, sheep, horses, dogs, and cats. Pigs are the most important.
Transmission: Fecal-oral or foodborne transmission via the handling or consumption of

undercooked pork (especially chitterlings), raw/unpasteurized milk, or contaminated
water.
Description: Yersiniosis may have a variety of presentations. Y. enterocolitica often causes an acute,
febrile, bacterial diarrheal illness characterized by nausea, vomiting, abdominal pain,
and bloody diarrhea. Y. pseudotuberculosis often presents as pseudoappendicitis,
occasionally without diarrhea.
Signs and Symptoms: Infants and children often have worse disease than adults. Infants may develop
necrotizing enterocolitis. Typical symptoms in children and adults include fever,
malaise, abdominal pain, cramps, tenesmus, nausea, vomiting, and bloody diarrhea.
The illness is often self-limiting, and symptoms typically resolve within 1–3 weeks.
Y. enterocolitica may present as pharyngitis without diarrhea. Some patients may
develop right lower quadrant abdominal pain secondary to mesenteric lymphadenitis
and present as pseudoappendicitis. Bacteremia and hematogenous spread can occur
and is more common in infants and the immunocompromised. Postinfectious
complications include erythema nodosum and reactive arthritis.
Diagnostic Testing: Culture from the source of infection (stool, pharynx, blood, etc.) is the gold standard
for diagnosis. Serologic testing is used in Europe and Japan, but it is not widely
available in the U.S.
Treatments: For diarrheal illness, the mainstay of treatment is often supportive and consists of
fluids. Antibiotics are indicated for severe infections and include doxycycline
combined with an aminoglycoside, TMP/SMX, or fluoroquinolones.
Pearls: Hemochromatosis and iron overload states predispose patients to yersinia infections.
Desferrioxamine therapy increases disease severity and should be discontinued in
infected patients.
30
CHAPTER 13 YERSINIOSIS
Yersiniosis
BACTERIAL
Yersinia enterocolitica
Yersinia pseudotuberculosis
Incubation: 1–14 Days
Average: 4–6 Days
Diarrhea: 1–3 Weeks
Gram Rod
Although I’m the Plague

Doctor, Yersinia pestis
(Plague) is an entirely
different disease.
Nausea
Vomiting Diarrhea can be
absent in
Y. pseudotuberculosis
Abdominal Pain/ Reactive
Cramps Arthritis
Tenesmus
Watery/Bloody
Symptoms in Infants
Diarrhea
& Children > Adults
Pseudoappendicitis
31
Disease Name: Clostridium difficile Infection

BACTERIAL
Synonyms: Pseudomembranous Colitis, C. diff
Causative Agent: Clostridium difficile
Incubation: Varied
Description: Clostridium difficile is a gram-positive spore and toxin-forming bacteria that can
colonize the human gastrointestinal tract and causes antibiotic-associated diarrhea.
The infection is a spectrum disorder, with symptoms ranging from asymptomatic
colonization to severe colitis. The disease is more common in elderly patients and is
associated with antibiotic use. Antibiotics decrease normal colonic flora and can
allow for C. diff overgrowth and symptom manifestation. The antibiotics most
associated with C. diff include clindamycin, fluoroquinolones, and second-generation
(and above) cephalosporins.
Signs and Symptoms: Watery diarrhea beginning during or after recent antibiotic use is the classic disease
manifestation. Other symptoms include fever, malaise, abdominal pain, cramps, and
tenesmus. Severe disease can cause profound dehydration, hypotension, shock, acidosis,
abdominal distension, and toxic megacolon (which may lead to perforation).
Diagnostic Testing: Leukocytosis is common. Leukocytosis, elevated creatinine, decreased albumin, and
elevated lactate are markers for disease severity. Fecal leukocytes will be positive.
Stool can be cultured and/or sent for PCR analysis and/or EIA testing for Toxin A
and B. Since only Toxin B is associated with diarrheal illness, PCR and EIA testing
may be limited to that toxin in some institutions.
Treatments: Discontinue the offending antibiotics if possible. Treatment of C. diff can be with oral
metronidazole, vancomycin, or fidaxomicin. Severe disease requires intravenous (IV)
metronidazole. IV vancomycin is not effective for C. diff. Fecal microbial transplant
is being investigated as another treatment option.
Pearls: Proton-pump inhibitors (PPIs) and H2 acid blockers are associated with increased
risk of C. diff. If colonoscopy is performed, mucosal friability, edema, inflammation,
and pseudomembranes will be visualized. Only liquid stool is sent for culture/PCR
testing, as diarrhea with solid/semi-solid stool is not consistent with C. diff infection.
32
CHAPTER 14 CLOSTRIDIUM DIFFICILE INFECTION
Clostridium difficile Infection
BACTERIAL
(Pseudomembranous Colitis)
idiu m diffi
str c
Clo
ile
Spore-Forming
WBC
Creatinine = BAD
Albumin Gr
am + Rods
+
Clindamycin
Fluoroquinolones = Worst Offenders
Pseudomembrane 2nd-Gen + Cephalosporins
Fever
Stop the offending
antibiotics!
>6 cm
Toxic Megacolon Perforation
Risk
Abdominal Pain/
Cramps Diarrhea +
Recent ABX Use = C. diff
Fecal Tenesmus
Transplant >3 Watery Stools <24 Hrs.
EIA Toxin A PPI & H2

EIA Toxin B Blockers = Risk
Toxin A Toxin B
PCR
Stool Culture
Fecal Leukocytes
33
Disease Name: Vibriosis

BACTERIAL
Causative Agents: Vibrio parahaemolyticus, Vibrio vulnificus
Incubation: 24–72 hours
Description: Vibrio bacteria are common to marine and brackish waters (estuaries, saltwater
marshlands), and shellfish living in these waters concentrate the bacteria, making
vibrio a common cause of shellfish-associated diarrhea. Since bacterial concentration
increases as water temperatures rise, highest disease incidence is noted in the United
States between April and September. In addition to causing gastrointestinal illness,
vibrio can also cause significant wound infections and/or septicemia. Vibrio
infection tends to be worse in the immunocompromised, those with chronic
liver disease, and alcoholics.
Signs and Symptoms: Gastroenteritis: Vibriosis should be suspected when watery diarrhea begins shortly
after recent raw or undercooked shellfish consumption (oysters and clams are most
common). Other symptoms include abdominal pain, cramps, nausea, and vomiting.
Diarrhea may become bloody. Soft Tissue Infection: Wound exposure to vibrio can
occur if cut while swimming in marine or brackish waters or when handling infected
shellfish. In severe cases, cellulitis can expand rapidly, cause hemorrhagic bullae and/or
necrotizing fasciitis. Septicemia: High-risk patients exposed to vibrio may develop
bacteremia and sepsis after consumption of infected shellfish or secondary from a
wound infection. Shock rapidly follows the onset of sepsis and patients have an
extremely high mortality. This pathologic process is most common in those with
compromised immune systems and/or chronic liver disease.
Diagnostic Testing: Stool, wound, or blood cultures confirm the diagnosis.
Treatments: Gastroenteritis: Mild to moderate disease can be treated with intravenous or oral
hydration. Antibiotics may shorten the duration of illness in more-severe cases. Soft
Tissue Infections and/or Septicemia: Doxycycline or minocycline 100 mg twice daily
1 ceftriaxone 2 grams IV daily is the suggested regimen for severe infections.
Intravenous cefotaxime 1 ciprofloxacin and fluoroquinolone monotherapy are
alternatives. Aggressive treatment is necessary in soft tissue infections and sepsis.
Pearls: While either species can present in any of the above scenarios, V. parahaemolyticus is
more commonly associated with gastroenteritis and V. vulnificus is more commonly
implicated in severe soft tissue infections and septicemia. Most restaurant menus
warn consumers with chronic liver disease and/or immunodeficiency to avoid raw
shellfish for this reason.
34
Another random document with
no related content on Scribd:
limit of Mr. Chanler’s journey, and from whence he sighted Lorian.
Pushing forward with renewed vigour, we finally reached it, and
looked round with eager eyes, fully expecting to get a glimpse of our
long-sought-for goal.
Not a sign of the swamp could be seen! The river, scarcely half a
dozen yards in width, meandered eastwards, flowing smoothly and
sluggishly between its low banks. On every side stretched the silent
plains, in some places perfectly bare, and in others covered by
patches of dried reeds, while a few solitary thorny acacias stood like
ragged sentinels amid the general desolation.
Lorian had vanished!
1. Head of old bull buffalo. The horns are very rugged, one being
broken at the tip.
2. Waller’s gazelle.
3. Thompson’s gazelle.
4. Greater Koodoo.
5. Grant’s gazelle shot south of Kenia.
6. Lichtenstein hartebeeste.
7. Grant’s gazelle shot near the Waso Nyiro.
CHAPTER XV.
RETURN FROM THE LORIAN JOURNEY.
An interrupted night’s rest—Photography under difficulties—We go

further down-stream—Still no signs of Lorian—Sad end of “Spot”
the puppy—Our men refuse to go further—Preparations for the
return journey—Reasons for our failure to reach Lorian—Return
to our Rendili camp—Somalis think of going north to Marsabit—
Ismail asks me to accompany him—I decline—The scare in
Ismail’s camp—Departure for M’thara.
We were bitterly disappointed at this unexpected turn of affairs, but,
after a short consultation, determined to proceed on the morrow still
further down-stream, in the hope of reaching the tantalizing swamp.
In our eagerness to reach the sycamore tree we had outstripped our
half-mutinous men, and they were slowly coming into camp in twos
and threes long after our arrival. Two of them had deserted during
the march, an M’kamba and the ruffian Sulieman, who happened to
be carrying a small black portmanteau which contained all George’s
and my kit. This he had cut open and had abstracted therefrom my
matches, fishing-line, and the whole of my stock of needles and
thread, so that we were left without the wherewithal to repair our
clothing. These desertions were the more serious in that they
necessitated our sending two of our remaining men back to the
Rendili camp so that Jumbi might apprehend the deserters, or, failing
that, to at least prevent him being deceived by a spurious message
purporting to come from us, to the effect that he was to hand over a
quantity of trade goods to Sulieman on the pretence that we required
them—a trick often practised by Swahili deserters from a party
operating away from their main camp. Sending these men away
reduced our already weak party by four men, whose loads had to be
distributed among the remainder; a proceeding which still further
increased their discontent.
That evening we dined on the hippopotamus tongue, which proved
a right royal dish. It was wonderfully fat and tender, and, as it
weighed about seven pounds, it afforded a substantial as well as a
very pleasant meal. We turned in early, and as I wished to change
the plates in my camera, I manufactured an extempore dark room by
throwing a blanket over a bush and creeping beneath it. I could not,
however, use it with safety till the moon had set, at 2 a.m., so I
instructed the sentry to call me at that time, and, getting out my
package of spare plates, placed them, together with my collapsible
ruby lamp, beside me, and endeavoured to sleep. We had arranged
our beds at the foot of the sycamore tree, and, as it turned out, right
in the path used by the hippopotamus and rhinoceros in their nightly
wanderings along the banks of the river.
We had slept for perhaps two hours, when a shout of alarm from
the men was followed by a stampede, as the two mules broke from
their picket ropes and bolted. Waking up with a start, I was surprised
to see El Hakim and George, clad in the very scantiest attire, come
flying across my bed as if they were practising the high jump. I
glanced round, and an instant later rose hurriedly from my blankets
and joined them. A rhinoceros, coming along the path, had rushed
among our sleeping men and charged through, scattering them right
and left. He then rushed at the fire and stamped on it, and when I
awoke was coming down with the speed of an avalanche to the spot
where we had been sleeping. We, however, with a sudden access of
modesty, due perhaps to the knowledge of our attire, bashfully
retreated to the other side of our friendly sycamore tree, where some
of our men were already perched among the branches, while the
rhinoceros passed on without further demonstration. Inquiries
revealed the fact that none of the men were hurt, with the single
exception of Docere ben Ali, who had grazed his shin. He said the
rhinoceros did it, but I rather inclined to the belief that he did it
himself in his haste to climb the tree at the commencement of the
stampede. We retired to our blankets, thanking our lucky stars that
nothing worse had happened. Not more than half an hour later, when
I had just got comfortably to sleep again, I was once more aroused
by El Hakim uttering my name in an intense whisper. In an instant I
was wide awake, and saw him and George standing on their
blankets gazing intently into the darkness. A cloud had temporarily
obscured the light of the moon, and it was at first somewhat difficult
to distinguish objects a few yards distant. When my eyes grew
accustomed to the darkness, I became aware of the presence of a
herd of hippopotamus standing irresolute within a dozen yards of my
bed. One, ahead of the others, was slowly advancing in a line that
would bring him right across our blankets, and was at that moment
not five yards away. We stood undecided; we did not wish to alarm
them, as they might have stampeded over us, and in that case we
might just as well have stayed at home and died an easier death
beneath a steam-roller. It was too dark to use a rifle with any effect,
while it was open to the same objection. Meanwhile the herd was
slowly advancing and the situation was becoming more and more
strained, when our dog sprang at the foremost with a snarl, while
“Spot,” the puppy, yelped defiance in his shrill treble. The herd
paused, turned, and disappeared like a flash in the opposite
direction, with a thundering of feet which constituted an unpleasant
reminder of what might have happened had they come in our
direction. The puppy took all the credit of the affair to himself, and
came up to be patted and stroked, wagging his diminutive tail in a
manner expressive of the utmost contempt for wild beasts in general,
and hippopotamus in particular. We turned in again and tried to sleep
once more.
I was called when the moon had set, and proceeded to rig up my
al fresco dark room. During the two alarms either El Hakim or
George had trodden on my ruby lamp and had stamped it out quite
flat. It took me some time to bend it back into something of its former
shape, while the sentry stood by and struck matches to enable me to
see. Finally the lamp was more or less satisfactorily adjusted and the
blanket placed in position. In the middle of the operation an excited
whisper of “Faru, bwana,” caused me to drop my apparatus and
scramble hurriedly out. I took one glance round, yelled to El Hakim
and George, and we all three hastily took up our position behind the
tree, while the oncoming rhinoceros danced through the camp at
fifteen miles an hour and disappeared.
We began to think that these visitations were becoming too much
of a good thing. The men, too, manifested an anxious desire to
emulate the fowls of the air and roost among the branches of our
friend in need, the sycamore tree.
Returning to my dark room, I completed the operation of changing
the plates, and once more sought my blankets, in the pious hope
that we should not be disturbed again.
But it was not to be. On two other occasions during that eventful
night we were compelled to rise hurriedly from our blankets and
betake ourselves to the shelter of the friendly sycamore, while a too
impetuous rhinoceros whirled past; and the dawn discovered us
blear-eyed and weary from the effects of our nocturnal gymnastics.
When the usual time for starting the day’s march arrived the men
flatly refused to go a step further. We argued the point with them,
and finally induced them to make one more march, promising that if
we did not find the “Siwa” (swamp) then we would return. With that
understanding we set out, marching at a good pace, as the ground
was rather firmer underfoot than hitherto.
Just before midday we passed a small herd of grantei, and I
managed to secure one at long range. An hour later a couple of bull
buffaloes were seen, quietly feeding on the opposite side of the river.
El Hakim put in some pretty shooting at fifty yards, bringing them
both down. We crossed the river and camped beside the carcases.
It was here that we sustained a loss which we all felt very deeply,
and which even now I cannot recall without a sigh. “Spot,” the puppy,
who had endeared himself to us all by his lovable disposition and
pretty ways, had gone to sleep in the grass while El Hakim was
engaged with the buffaloes. When we crossed the river he was
forgotten, and not until we were making our arrangements for
camping, did a shrill bark from the other side of the river call our
attention to the small owner thereof. We immediately sent a couple
of men across the river to bring him over, but they had to go fifty
yards or so lower down to do so. The gallant little chap would not,
however, wait for the men, but plunged boldly into the stream and
swam towards us, wagging his tail in infinite delight at his own
daring. He had scarcely got three-parts of the way across when he
gave a sudden sharp yelp of pain and disappeared under the surface
with a jerk, leaving us standing on the bank speechless with
consternation and distress. Ramathani ran up with a rifle, but I
waved him away in despair. A hundred rifles could not have restored
our gallant little dog to us, the crocodile which had seized him having
never shown itself above the water. There was nothing to do but to
turn sorrowfully away and console ourselves as best we might.
We called the men together after we had eaten and asked them if
they were willing to go on still further, but they were unanimous in
their determination not to go a yard further down the river. “Takufa
yote, bwana” (We shall all die, master); “Mangati tele hapa” (There
are many wild beasts here); “Afreeti winge hapa” (There are plenty of
devils about here); and “Tu’nataka kurudi, bwana” (We wish to
return, master), were among the remarks which greeted our ears at
the mere suggestion that we should go further down-stream. Finally
we compromised. We asked for two volunteers who would go down
the river, there and then, for some hours’ march, and see if they
could see anything of Lorian. If they discovered it they were to
return, and we would all go on together there, but if they saw nothing
of it, we would return to our Rendili camp on the following day. This
was agreed to, and two of the men, Asmani ben Selim and Kati (an
M’Nyamwezi), accordingly started off.
They returned late the same evening, and reported that they had
been some miles down the river and had seen no signs of the
swamp. We were greatly disappointed, but in accordance with our
agreement made arrangements to commence our return march on
the following day. We could not have done otherwise, as if we had
signified our intention of proceeding further to the eastward in
defiance of our promise, the men would have deserted in a body
during the night, and gone back to the Rendili camp.
It took Mr. Chanler nine days, starting from a point opposite our
Rendili camp, to reach the sycamore tree under which we had slept
—or rather tried to sleep—the night before, while the same distance
only occupied us five days, which is easily explained by the fact that
we had already a general idea of the course of the Waso Nyiro, while
Mr. Chanler had to feel every mile of his way. We were now a march
beyond the sycamore tree, which formed the limit of his journey, and
our men had been some miles farther still down the river and had not
seen the swamp. The only hypothesis I can advance which will
account for our failure to find Lorian at the place where Mr. Chanler
saw it on January 7th, 1893, is this.
In very wet seasons, or after a series of wet seasons, the Waso
Nyiro overflows its banks and covers a portion of the Kirrimar Plain,
forming a vast swamp, or more probably a chain of swamps, to
which the name of Lorian has been given by the natives. That the
portion of the Kirrimar Plain immediately adjoining the river is at
times under water, is beyond a doubt, as I have already mentioned in
the previous chapter. After a long drought, by which the supply of
water brought down by the Waso Nyiro would be materially curtailed,
these swamps dry up, those lying up-stream, owing to their higher
level, naturally drying up first, and consequently the western edge of
the swamp, or swamps, called Lorian, would gradually recede more
and more to the eastward as the drought increased. At the time of
our visit in September, 1900, there had been no rain in Samburuland
for three years, according to the Rendili, and it is therefore quite
reasonable to suppose that Lorian, for the reasons enumerated, had
receded many miles to the eastward of the point at which Mr.
Chanler turned back, having satisfied himself that Lorian was merely
a swamp and not a lake as he had supposed. It is quite possible that
the swamp seen by Mr. Chanler may not have been Lorian at all, but
may have been only one of the chain of swamps to the west of it and
higher up the river, and which had dried up prior to our visit. The
evaporation in that terribly hot climate (scarcely one degree north of
the Equator, and not more than 700 feet above sea-level) must be
enormous, and would be sufficient to dry up even a large lake
providing it was not well fed with water, as in the case of Lorian. A
shallow body of water with a very large surface-area, such as this
swamp, would be very easily dried up in one season if its river-borne
water-supply was much reduced.
On the morning of September 5th we reluctantly turned our backs
on the elusive Lorian, and retraced our steps. Nothing of interest
occurred on the return journey beyond the usual weary marches
over the desolate country already described, punctuated at intervals
with a rhino charge or a hunt for meat. I remember one rhinoceros
which amused us very much. We were making our way across a belt
of bush which somehow managed to draw sustenance from the
sand, when the familiar but subdued shout of “Faru” caused us to
glance hurriedly round. Facing us ten yards away a large rhinoceros
was stamping and snorting. In a few seconds he made up his mind
to investigate, and charged down upon us. Something impelled
George to place his fingers in his mouth and send forth a shrill ear-
piercing whistle. The charging rhinoceros stopped suddenly in mid-
career, so suddenly, indeed, that he almost sat on his hind quarters.
Such a look of porcine surprise came over its ugly features that we
involuntarily burst out into a roar of laughter, which apparently
completed the ungainly brute’s discomfiture, as it turned and
galloped away with every symptom of fear. We also shot every
crocodile we could get at on the return journey, as a set-off against
the loss of our lamented pup, but it failed to afford us any
satisfaction.
On the fifth day after we started on our return journey we arrived
half-starved and footsore at our Rendili camp. In the light of this
experience I can quite believe that the Rendili were right when they
asserted that they could reach Lorian in two days, always supposing
Lorian to be in the position roughly assigned to it, viz. read 1° 5’ 0” N.
lat. and 30° 30’ 0” E. long. A native perfectly acquainted with the
country would abandon the Waso Nyiro altogether, and cut across
the big curve which the river makes to the north and south-east, and
travelling across the desert in a direction east-north-east from the
Zambo Plateau, he would only have a fifty-mile march before him—
by no means a difficult matter for a native, as he would only require
to make two marches of twenty-five miles each in forty-eight hours. If
I ever make another trip down the Waso Nyiro I shall certainly adopt
that plan myself.
The moment we reached camp we ordered a sheep to be killed,
and when it was cooked the three of us sat down and finished it. We
were very hungry, and it was only a small sheep. While we were
satisfying our material wants, we summoned Jumbi that he might
give an account of his stewardship. It appeared that he had bought a
couple of hundred sheep in our absence. The Somalis under Ismail
Robli had moved their camp one march up the river, following the
Rendili and Burkeneji, who were moving their villages up-stream, the
adjacent pasture being finished. There was a recrudescence of
small-pox among the Rendili, and many were dying daily. Such was
the news.
On the following morning I rode over to Ismail’s camp to hear what
he had to say. I found the Somalis very despondent. Business was
decreasing, as, owing to the presence of two safaris, the market was
glutted with trade goods. They were buying camels, which was
necessarily a very slow process, as the camels could only be bought
for so many sheep. These sheep had first to be purchased for cloth
or wire, and Ismail was finding out that between the value of a sheep
he wished to buy, and that of a sheep he wished to sell, there was a
wide difference.
Ismail also informed me that a party of Wa’Embe had come to
trade with the Rendili and Burkeneji, and had stayed at a Burkeneji
village further up the river. When the Wa’Embe heard that the
Somalis were camped among the villages of their hosts, they
inquired of them why they had not attacked the Somalis and speared
them. “We have beaten them twice,” they said, “and killed many of
their men with our spears. Their bullets did not hurt us. Why do you
not spear them?” This advice was not lost on the Burkeneji, and they
would have probably acted upon it in the near future; but Ismail,
hearing the news from his spies, went forth to attack the mischief-
making Wa’Embe, who forthwith fled without giving battle.
The next day we also moved our camp up-stream, and pitched our
tents afresh on a spot a few yards from the river-bank and 500 yards
or so from Ismail’s boma. We understood from Ismail that he
intended going north to Marsabit, and for some reason he was very
anxious that I should leave El Hakim and George to return alone and
accompany him northward. He was very pressing in his invitation,
which, however, I consistently declined. If Jamah had been alive,
nothing would have pleased me better than an opportunity of
penetrating further northward to Marsabit and perhaps Reshiat and
Marle at the north end of Lake Rudolph, but I entertained such a
hearty contempt for Ismail, that the prospect of some months’
journey in his company did not offer sufficient inducement to warrant
me in altering my arrangements.
After we had settled down in our fresh camp we concentrated our
attention on exchanging the remainder of our cloth for sheep, so that
we might start on our return journey to Nairobi. El Hakim wished to
get back to Nairobi in November for personal reasons, otherwise we
should have gone back to M’thara, and after buying a fresh supply of
food there, and getting the forty odd loads of beads which were in
N’Dominuki’s charge, we had intended journeying to Lake Baringo
and thence northward into the country of the Turkana.
Business was very slack until El Hakim hit on a bright idea. He
called the Rendili chiefs Lubo, Lokomogo, Lomoro, and other lesser
lights together, and pointed out that although we had dwelt amongst
them for almost a month, so far only one of them, Lubo to wit, had
brought us a present. “It was well known,” continued El Hakim, “that
when ‘friends’ visited the Rendili they were always presented with
many sheep, and even camels, as a token of good-will.” He was
therefore reluctantly compelled to conclude that we and the Rendili
were not friends, a state of affairs which filled his heart with sorrow.
But still, it was not yet too late, and if those who had not yet brought
sheep as a present did so within the next few days all would be
forgotten and forgiven.
The effect was magical. Early the following day Lokomogo stalked
into camp, followed by a couple of men driving a small flock of
thirteen sheep, which, after much circumlocution, he introduced as
his present. El Hakim immediately made him a return present of a
quantity of cloth, wire, and beads, of the value of something like
twenty per cent. above the market price of the sheep. Lokomogo
was delighted, and departed with his present with every sign of
pleasure and good-will.
The other chiefs must have been waiting to see how Lokomogo’s
present was received, as the next day, finding it had been
satisfactory, the presents came in thick and fast, every present
consisting of exactly thirteen sheep, neither more nor less than that
brought by Lokomogo. Each donor received a return present over
and above the market value of the sheep, and business fairly
boomed, everybody being satisfied. Had we offered treble the value
of the sheep in the ordinary way of business, we could not have
bought any, as the market was glutted with trade goods. El Hakim,
however, touched them on their weak spot when he made a
ceremonial transaction of it, and the result fully justified his claim to a
certain amount of insight into the working of the native mind.
About this time I was prostrated with a very severe toothache,
which confined me to my tent for some days. By the time I was about
again our scheme for the exchange of presents had worked so well
that our cloth was almost exhausted, and we were nearly ready to
take our departure for M’thara. We had now upwards of 500 sheep,
and it promised to be a tedious task to transport them safely to
Nairobi; more especially as we were extremely doubtful of our
reception by the A’kikuyu of north-east Kenia.
Late in the evening two days before our departure from the Rendili
settlement, a couple of the Somalis came into our camp exhibiting
every symptom of alarm. They brought a message from Ismail to the
effect that the Burkeneji warriors had killed and eaten three sheep[15]
preparatory to attacking him and us. The attack was to take place
during the small hours of the same night. His information emanated
from some friendly Rendili.
We had already retired for the night, but we donned our clothes
and went over to the Somali camp to see Ismail.
The Somali camp was in a great state of excitement. Ismail
himself was serving out ammunition to his men with a lavish hand,
and others of the Somalis were cutting bush and otherwise
strengthening the boma. We did not quite believe their story, but as it
would do no harm to take ordinary precautions, we returned to our
own camp and proceeded to put it into a state of defence.
It was already well protected on two sides by a thick belt of bush,
so thickly interlaced as to be impenetrable, and by a large fallen
thorn tree, which, while easily seen through, formed a barrier as
impassable to naked savages as a barbed wire entanglement. More
thorn-bush was cut down and a strong barrier erected on the river
side. On the opposite side, where the men’s tents were situated, we
built another thorn fence, leaving the tents outside with the fires
burning as usual, in the hope that in the event of hostilities the
apparently unprotected tents would draw the first attack. We did not
think that the enemy would feel inclined to make a second.
The men all slept under arms in the centre of our boma, with the
exception of the sentries, whom we posted some distance outside
the camp. The 8-bore, loaded with slugs, was placed handy, together
with half a dozen of the blue flares, which would instantly light up the
scene for a hundred yards round with an intense radiance as awe-
inspiring to the enemy as it would be useful to ourselves. When our
defensive preparations were completed we retired fully dressed to
our blankets, and endeavoured to snatch a little sleep, with such
success that we did not wake till sunrise.
We temporarily demolished the “boma” on the side on which the
men’s tents stood, so that we should not give our scheme away
should we be visited during the day by any of the Burkeneji, as, for
all we knew, it might yet prove useful.
The Burkeneji were undoubtedly restless, as we found that they
were moving their villages down the river again, some of them going
as far as the eastern spur of the Zambo Plateau.
The next night we took the same precautions as on the previous
evening, but still nothing happened.
On September 20th we had finally disposed of all our stock, and
were now quite ready to leave for M’thara. Ismail informed us that he
was going north to Marsabit, and bade us good-bye.
When we retired that night we took the same precautions against
surprise. About eight o’clock in the evening we were aroused by the
report of a rifle from the direction of the Somali camp. After a short
interval we heard another, then another, and then a sound of rapid
firing mingled with shouts and yells. We sprang up and got our men
under arms and waited events. A dead silence succeeded the former
pandemonium, nor did we hear another sound. We concluded that
the Burkeneji had attempted to rush the Somali camp, and, finding
them prepared, had abandoned the attack.
Next morning we packed up in preparation for the start. While we
were thus engaged we were visited by Ismail, who came over to
explain the cause of the disturbance of the preceding night.
It appeared that the Somalis, as well as their men, were still very
nervous on account of the supposed hostility of the Burkeneji. After
they had gone to sleep, their cattle, which were corralled in a small
enclosure in the centre of their boma, were by some means
stampeded. Breaking out of their enclosure, the frightened animals
rushed hither and thither among the sleeping porters, who, waking
up under the impression that the Burkeneji were upon them, were
immediately stricken with panic, and crawling under blankets,
bushes, or anything that afforded them the slightest cover, they
yelled dismally for mercy, thus adding to the general confusion.
Ismail and his lieutenants seized their rifles and rushed out of their
tents, to find some of their men trying to break out of the boma,
some crawling about on their hands and knees, crying for mercy,
while others were brandishing spears and shouting defiance. They
likewise jumped to the conclusion that they were being attacked, and
that the enemy were actually within the boma; and under the
influence of a panic, no whit less than that of their men, they without
further ado raised their rifles and fired into the confused groups of
men, seen dimly in the flickering light of the camp-fires. After a time
order was restored, and it was found that there had been no attack
at all. Two of their porters were shot dead in the confusion, and one
Somali received a Snider bullet in the forearm; while a horse which
Ismail had bought from the Rendili, and of which he was very proud,
received a bullet in the chest and another in one of its hoofs. The
cattle were probably stampeded by the scent of a lion which had
been prowling round the boma, and which, some days before, had
actually, in broad daylight, seized and killed a cow belonging to
Ismail.
Congratulating Ismail on the state of his nerves and on the
discipline of his camp, we bade him adieu once more. We then
shook the dust of the Rendili settlement from our feet, and started
amid the joyous shouts of our men on our journey up the river en
route for M’thara.
FOOTNOTES:
[15] It is the custom of the natives to kill and eat meat before
setting out on a warlike expedition.
CHAPTER XVI.
RETURN TO M’THARA.
Departure from the Rendili settlement—Ismail’s porters desert—The

affray between Barri and the Somalis—Ismail wounded—A giraffe
hunt—Ismail’s vacillation—Another giraffe hunt—Journey up the
Waso Nyiro—Hippopotamus-shooting.
We marched steadily for nearly three hours, and then, selecting a
suitable spot, camped on the river-bank. En route we noticed several
stone cairns, which on inquiry I learnt were the burial-places of the
Rendili. Unlike the Wakamba, A’kikuyu, and Masai, they do not leave
their dead or dying relatives outside their villages, to the tender
mercies of the hyænas. They, on the contrary, dig a hole in the
ground, in which the corpse is placed in a sitting position. Stones are
then piled over the body till a cairn is formed, and finally a spear is
placed upright on the summit. In view of the utter dissimilarity
between the Rendili and the ordinary negro, and the lack of definite
information concerning their origin, it is to my mind a curious
coincidence at least that they should bury their dead in almost
precisely the same manner as the people who at one time inhabited
the banks of the Nile in Upper Egypt.[16]
I remember hearing in Cairo, in the early part of 1899, that
Professor Flinders Petrie had unearthed some graves which were
supposed to be those of a people so ancient as to be unacquainted
with the use of metals, and who buried their dead in a sitting
position, afterwards covering them by inverting a large earthen jar
over the body and then filling up the grave. These facts, taken in
conjunction with Mr. Seton Karr’s discovery of flint implements in
Somaliland resembling, I believe, those discovered by Professor
Petrie in Egypt may, in the hands of an antiquarian, throw an
interesting light on the antecedents of this remarkable people. It
would be interesting indeed could it be shown that the Rendili are the
modern representatives of the primitive race who manufactured clay
pottery and worked in flint on the banks of the Nile before the
pyramids were built.
When we had constructed a boma for the sheep, George and I
went down to bathe in the Waso Nyiro, a feat we successfully
accomplished to the accompaniment of the usual eccentric dance on
account of the leeches.
In the evening a young Somali, named Barri, came into camp. He
wished to return to Nairobi with us, and as he was not bound to
Ismail in any way, not receiving any pay, we consented to his doing
so. He was, indeed, a small trader on his own account, and with a
couple of cattle had accompanied Ismail in order to try to exchange
them for two tusks. This purpose he had not been able to carry out.
He therefore sold them to some of the other Somalis who
accompanied Ismail’s caravan on the same conditions as himself,
and, unknown to Ismail, proposed to return to Nairobi with us. We
did not know at the time that Ismail was unaware of the proposed
change, and as Barri had formerly been a personal servant of El
Hakim’s, and a very good man, we gave him permission to
accompany us on condition that he made himself useful.
Before sunrise on the following morning, Barri went away from
camp to try to procure some fresh milk for us at an isolated Burkeneji
village some little distance away. He borrowed my Martini and half a
dozen cartridges, as he had no more ammunition for his own
weapon, a carbine of Italian manufacture, and set out. An hour later,
as we were preparing to start on our march, Ismail Robli, who had
travelled all night, accompanied by a strong party of Somalis, all fully
armed, strode into our camp. He stated, none too politely, that most
of his remaining porters had deserted, and he had reason to believe
that they were accompanying our safari. Ignoring his discourtesy, we
politely informed him that such was not the case, nor had we seen
his men; but if it would in any way ease his mind he had our
permission to look through the camp. He proceeded to do so, and of
course found no traces of his missing porters.
In the meanwhile Barri was returning with the milk he had
purchased, and was approaching the camp, all unconscious of this
new aspect of affairs. He was sighted by two of Ismail’s armed
guards, who, slipping cartridges into their Sniders, rushed towards
him, demanding his instant surrender on pain of death. Barri’s reply,
more forcible than polite, was a shot from the Martini, which sent
them helter-skelter to the cover of the nearest bush. From that
comparatively safe position they held a parley with him, under cover
of which they sought an opportunity of shooting at him. He, however,
was aware of their amiable intentions, and, standing with his rifle at
the ready, threatened to shoot the first man who raised his weapon.
One of them tried it, but Barri instantly fired, which, though he
missed his man, effectually stopped any further attempt at such
treachery.
Ismail, busily searching for his absent porters, heard the shots,
and, momentarily desisting from his search, rushed out of camp to
see what was the matter. Fifty yards away he saw Barri with uplifted
rifle covering the two Somalis, who were cowering behind the bush.
If ever I saw murder written on a man’s face, I saw it then on Ismail’s,
and remembering what he was capable of, I went after him, followed
by El Hakim and George. Ismail was carrying a 12-bore shot-gun
loaded with ball cartridges, and as he ran at Barri he unslung the
weapon from his shoulder. Barri turned in the nick of time, and
without a second’s hesitation fired point-blank at him. Ismail
collapsed into a writhing heap on the ground, while Barri turned and
fled with the speed of a deer into the surrounding bush.
These events happened in such rapid succession that we had no
time to interfere and prevent the catastrophe, as we were only just
outside the camp when Ismail fell. Of the two Somalis who had
brought Barri to bay, one followed him, but, apparently very half-
heartedly, he soon returned, and the other ran to assist Ismail. That
swashbuckler and would-be assassin had struggled into a sitting
position, and was groaning with great vigour, punctuating his howls
at intervals with supplications to Allah, mingled with bitter curses on
the head of his assailant. We immediately examined him to ascertain
the extent of his injuries. He had sustained a nasty flesh-wound on
the inside of his right leg a few inches above the ankle. The bullet
had cut away the flesh and laid bare the bone, but fortunately had
not fractured it. El Hakim dressed and bound the wound, while I
superintended the construction of a litter in which Ismail could be
conveyed to his own camp.
His removal took place soon after midday. El Hakim accompanied
him to his camp, and, on arriving there, again dressed the wound,
returning to our own camp late in the evening. Ismail’s wound was by
no means serious, and would be quite well in a week or so, and as
many of his porters had deserted, he seemed inclined to accompany
us back to Kenia, and we decided, therefore, to make very short
marches for the next few days, primarily in order that Ismail could
communicate with us if necessary, and secondly, to gradually
accustom the sheep to marching in preparation for their long tramp
to Nairobi.
We did not pity Ismail in the least, as neither he nor any of his men
had a right to threaten Barri or in any way to control his movements,
and, in addition, I had ocular evidence that Barri had acted purely in
self-defence. Nevertheless, knowing that Ismail’s safari was now
numerically very weak, and the Wa’Embe, as already stated, were in
communication with the Burkeneji, we were strongly disinclined to
abandon his safari to perhaps further misfortune. This feeling, I must
admit, did not extend to Ismail personally, as he had shown himself
to be a vacillating bully, and a man of evil passions, which at times
entirely mastered him. But he had still some forty or fifty porters who
deserved a better fate, and in addition, a mishap to one safari
naturally mischievously affected any other which happened to be in
the district at or near the same time.
During the night we were much troubled by lions round the camp.
They were not roaring, or we should have had no apprehensions, as
Leo does not roar till he has killed. It was the peculiar low whining
grunt, which is so modulated that it is extremely difficult to estimate
the brute’s distance, or even locate his direction. The sheep were
very uneasy, and it required the utmost exertions of our men to
prevent them from stampeding. The fires were stirred up and fresh
wood piled upon them, but all night we were kept constantly on the

Graphic Guide To Infectious Disease Brian T Kloss Full Chapter

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Graphic guide to infectious disease

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GRAPHIC GUIDE TO INFECTIOUS DISEASE ISBN: 978-0-323-44214-5

Copyright © 2019 by Elsevier, Inc. All rights reserved.

Library of Congress Cataloging-in-Publication Data

Names: Kloss, Brian T., author, editor. | Bruce, Travis, illustrator.

Executive Content Strategist: James Merritt

Last digit is the print number: 9 8 7 6 5 4 3 2 1

CONTRIBUTING AUTHOR: GUEST REVIEWERS FOR DIAGNOSTIC TESTING:

Brian Kloss, DO, JD, PA-C

PART 1 | VIRAL HEPATITIS PART 3 | CHILDHOOD ILLNESSES

Chapter 1.1 Hepatitis A 2 Chapter 3.1 Measles 52

PART 5 | WORMS Chapter 7.6 Trachoma 180

Chapter 9.1 Zika Fever 218

Chapter 10.1 Hemorrhagic Fever with Renal

PART 11 | OROPHARYNGEAL INFECTIONS Chapter 13.3 Pediculosis 292

Chapter 14.1 Anthrax 300

PART 13 | PARASITES AND PRIONS

Disease Name: Hepatitis A

Causative Agent: Hepatitis A Virus (HAV)

Incubation Period: 15-50 days; Average: 28 days

Geographic Regions Affected: Worldwide

Disease Name: Hepatitis B

Causative Agent: Hepatitis B Virus (HBV)

Incubation: 60–150 days; Average: 90 days

Geographic Regions Affected: Worldwide, Higher Incidence in Asia

I'm going to get the post-

High Rate of Vertical Transmission

Give me vaccine &

Disease Name: Hepatitis B Serum Markers

Chronology of Serum Markers

Disease Name: Hepatitis C

Incubation: 14–180 days; Average: 45 days

Geographic Regions Affected: Worldwide

Consider Liver Biopsy

Disease Name: Hepatitis D

Incubation: Coinfection: 45–160 days; Average: 90

Reservoir: Humans with hepatitis B virus (HBV)/HDV coinfections.

Treatments: Vaccination against hepatitis B is also preventative against hepatitis D. PEGylated

Disease Name: Hepatitis E

Incubation: 15–60 days; Average: 40 days

Reservoir: Swine and small rodents may serve as an animal reservoir.

Disease Name: Shigellosis

Synonyms: Bacillary Dysentery

Incubation: 1–7 days; Average: 3 days

Geographic Regions Affected: Worldwide—more common in developing nations.

Contaminated Abdominal Pain

HUS Seizures in Children

Shiga Blood & Pus

Rapid Intra-Family Spread

Disease Name: Salmonellosis

Synonym: Nontyphoidal Salmonella

Causative Agents: Salmonella bongori, Salmonella enterica

Reservoir: Poultry is the most common. Some reptiles.

Transmission: Typically foodborne via consumption of undercooked poultry, foodstuffs in contact

Incubation: 12–48 hours

Geographic Regions Affected: Worldwide

Diagnostic Testing: Stool culture is the gold standard for diagnosis.

Disease Name: Cholera

Synonym: Blue Death

Causative Agent: Vibrio cholerae