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BLACKWELL'S

KI.H;TH;r*l ll?l.ltHI?ir^l*'JM?l*Wrei

MICROBIOLOGY
VOL. I, 3E

VIKAS BHUSHAN, MD

University oi 'California, San Francisco, Class of 1991
Series Editor, Diagnostic Radiologist

VISHAL PALL, MBBS

Government Medical College. Chandigarh. India. Class ol 1990
Series Editor, U. of Texas, Galveston. Resident in Internal Medicine &
Preventive Medicine

TAO LE, MD

University of California, San Francisco, Class of 1990

HOANG NGUYEN, MD, MBA

Northwestern University, Class oi 2001

Blackwell
Science

CONTRIBUTORS

Sandra Mini

University of Texas Medical Branch. Class of 201)2

Beth Ann Fair, MD

Eastern Virginia Medical School, Resident in F.mergencv Medicine

Kristen Lem Mygdal, MD

I Diversity of Kansas School of Medicine. Resident in Radiology

Mae Sheikh-Ali, MD

University o( Damascus, Syria, ( II ass of 1099

Shaiin Patel, MD

M<< .raw Medical Center, Northwestern University, Resident in Internal
Medicine

Jose M. Fierro, MD

la Salle University, Mexico City

FACULTY REVIEWER

Warren Levinson, MD. PHD

Professor of Microbiology and Immunology. UCSF School of Medicine

Editorial Offices:

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( lover design bv Leslie Haiines

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Typeset by TechBooks

Printed and bound by Capital City Press

Blackwell's Underground Clinical Vignettes:
Microbiology I, 3e

ISBN 0-632-04547-7

Printed in the United Stales oi America
02 03 04 05 5 4 3 2 1

The Blackwell Science logo is a trade mark of
Blackwell Science Lid., registered at the Linked
Kingdom Trade Marks Registry

Library of Congress Calaloging-in-Publication Data

Bluishan. Vikas.

lilackwell's underground clinical vignettes.

Microbiology Author, Vikas Bliiislian. - 3rd ed.

p. ; cm. - (Underground clinical vignettes)
Rev. ed. of: Microbiology / Vikas Bhushan ... let at.].
2nd ed. cl999-. ISBN 0-632-04547-7 (alk. paper)

1. Medical microbiology - Case studies.

2. Physicians - Licenses - United Slates -
Examinations- Study guides.

[DNLM: 1. Microbiology - Case Report.
2. Microbiology - Problems and Exercises.
QW 18.2 B575b 2002) I. Title: Microbiology.

II. ride: Underground clinical vignettes.
Microbiology. III. Microbiology. IV. Title. V. Series.

QR46 .B465 2002

0UV.oro70-dc21

200100-1032

All rights reserved. No part of this book may be
reproduced in any form or by any electronic or
mechanical means, including information storage
and retrieval systems, without permission in writing
trom the publisher, except by a reviewer who may
quote brief passages in a review.

Notice

I lie .111 1 hr >is nl ill is Mil 111 in- have taken care thai [he information contained herein is an urate and compali-
hle with the standards generally accepted at the lime Of publii ation. Nevertheless, it is difficult to ensure
that all the information given is entirely accurate For all circumstances. The publisher and authors do not
guarantee die contents ol this book and disclaim an) liability, loss, or damage incurred as a consequent e,
directly or indirectly, of the use and application ol any of the contents ol this volume.

CONTENTS

Acknowledgments x

Preface to the 3rd Edition xiii

How to Use This Book xvi

Abbreviations xvii

Cardiology

Dermatology

ENT/ Ophthalmology

Gastroenterology

Acute Bacterial Endocarditis

Myocarditis — Viral

Pericarditis — Acute

Prosthetic Valve Endocarditis

Subacute Bacterial Endocarditis

Cellulitis

Erysipelas

Erysipeloid

Erythema Infectiosum

Impetigo

Molluscum Contagiosum

Pityriasis Versicolor

Roseola Infantum

Scalded Skin Syndrome

Tinea Corporis (Ringworm)

Urticaria

Acute Conjunctivitis

Acute Sinusitis

Allergic Rhinitis (Hay Fever)

Common Cold (Viral Respiratory Infection)

Herpes Zoster Ophthalmicus

HSV Keratitis

Otitis Externa

Otitis Media

Pharyngitis — Adenovirus

Pharyngitis — Streptococcal

Fitz-Hugh-Curtis Syndrome

Gastroenteritis — Staphylococcus aureus

Hepatitis A

Hepatitis B— Acute

Hepatitis C — Chronic Active

Hookworm

Necrotizing Enterocolitis

Neutropenic Enterocolitis

Peptic Ulcer Disease (H. pylori)

Pinworm Infection

Rotavirus Diarrhea in Infants

m
m

Kil

Genetics
Hematology/ 'Oncology

Infectious Disease

Salmonella Food Poisoning

Spontaneous Bacterial Peritonitis

Traveler's Diarrhea

B81

Vibrio parahaemolyticus Food Poisoning

Efl

Vibrio vulnificus Food Poisoning

Whipple's Disease

Yersinia Enterocolitis

Chediak-Higashi Syndrome

Anemia — Aplastic Crisis (Parvovirus B19)

Anemia — Diphyllobothrium latum

Graft-Versus-Host Disease

PEl

Hemolytic-Uremic Syndrome (HUS)

Actinomycosis

Acute Bronchiolitis

Acute Rheumatic Fever

African Trypanosomiasis

AIDS-Related Complex (ARC)

Amebic Colitis

Amebic Liver Abscess

Amebic Meningoencephalitis

Anthrax

Aspergillosis

Aspergillosis— Allergic Bronchopulmonary

Aspiration Pneumonia with Lung Abscess

Atypical Mycobacterial Infection

Bacillus cereus Food Poisoning

Bartonellosis

Blastomycosis

Botulism

Brucellosis

Campylobacter Enteritis

Candidiasis

BCl

Cat-Scratch Disease

Chagas' Disease

Chlamydia Pneumonia

Chlamydia trachomatis

Cholera

CMV— Congenital

CMV Pneumonitis

CMV Retinitis

Coccidioidomycosis

Colorado Tick Fever

Croup

ETil

Cryptosporidiosis

Diphtheria

Echinococcosis

Ehrlichiosis

Endemic Typhus

Epidemic Typhus

Epiglottitis

Gas Gangrene — Traumatic

Giardiasis

Gonococcal Ophthalmia Neonatorum

Gonorrhea

Granuloma Inguinale

H. influenzae in a COPD Patient

Hantavirus Pulmonary Syndrome EQ

Hemorrhagic Fever— Crimean-Congo 158

Hemorrhagic Fever — Dengue

Hemorrhagic Fever — Ebola Virus fcfri

Hemorrhagic Fever — Renal Syndrome EE1

Herpangina

Herpes Genitalis

Herpes Zoster (Shingles)

ACKNOWLEDGMENTS

Throughout the production of this book, we have had the sup-
port of man\' friends and colleagues. Special thanks to our sup-
port team including Ann Gupta, Andrea Fellows, Anastasia
Anderson, Srishti Gupta, Mona Pall, Jonathan Kitsch and Ghirag
Amin. For prior contributions we thank Gianni L.e Nguyen,
Tarun Mathur, Alex ( .1 imm. Souia Santos and Elizabeth
Sanders.

We have enjoyed working with a world-class international pub-
lishing group at Blackwcll Science, including I. aura DeYoung,
Amy Nuttbrock, Lisa Flanagan, Shawn Girsberger, I.orna Hind
and Gordon Tibbitts. For help with securing images for the
entire series we also thank Lee Mai tin. Kristopher Jones, Tina
Pani/./.i and Peter Anderson at the University of Alabama, the
Aimed Forces Institute of Pathology, and many ol our fellow
Blackwell Science authors.

For submitting comments, corrections, editing, proofreading,
and assistance across all of the vignette titles in all editions, we
( ollec liveh thank:

Tara Adamovich, Carolyn Alexander, Kris Alden, Henry E. Aryan,
l.vmnan Bacolor, Natalie Barteneva. Dean Bartholomew,
Debashish Behera, Sumit Bhatia. San jay Bindra. Dave Brinton,
|ulianne Brown. Alexander Brownie. Tamara Callahan, David
Canes, Bryan Casey, Aaron Caughey, Hebert Chen, Jonathan
Cheng, Arnold Cheung, Arnold Chin. Simion Chiosea, Yoon Cho,
Samuel Chung, Grelchen Conant. Vladimir Coric, Christopher
Cosgrove, Ronald Cowan, Karckin R. Cunningham, A. Sean
Dalley. Rama Dandamudi. Sunil Das, Ryan Armando Dave, John
David, Emmanuel de la Cruz, Robert DeMello, Navneet Dhillon.
Sharmila Dissanaike. David Donson, Adolf Etchegaray, Alea
Eusebio, Priscilla A. Frase. David Frenz. Kristin Gaumer,
Yohannes Gebreeg/.iabher, Anil Gehi, Tony George, L.M.
Gotanco, I'arul Goval. Alex Grimm. Rajeev Gupta, Ahmad
I lalim. Sue I [all, David Hasselbacher, Tamra Heimert, Michelle
Higley, Dan Hoit, Eric Jackson, Tim Jackson, Sundarjayaraman,
Pei-Ni (one. Aarchan Joshi. Rajni K. Jutla, Faiyaz Kapadi, Seth
Karp. Aaron S. Kesselheim, Sana Khan. Andrew Pin-wei Ko.
Francis Kong, Paul Konitzky. Wanen S. Krackov, Benjamin H.S.
I.au. .Ann LaCasce, Connie Lee. Scon Lee. Guillcrmo l.ehmann.
Kevin Leung'. Paul Levett. Warren Levinson. Eric Lev. Ken Lin.

Pavel Loban ov, J. Mark Maddox, Aram Mardian. Sarair Mehta,
Gil Melmed,Joe Messina, Robert Mosca, Michael Murphy, Vivek
Nandkami. Siva Naraynan, Carvell Nguyen, l.inh Nguyen,
Deanna Nobleza, Craig Nodurft, George Noumi, Darin T.
Okuda, Adam L. Palance, Paul Paniphrus, Jinha Park, Sonny
Patel. Ricardo Pietrobon, Riva L. Rahl, Aashita Randeria.
Rachan Reddy, Beatriu Reig, Marilou Reyes, Jeremy Richmon,
Tai Roe. Rick Roller, Rajiv Roy, Diego Ruiz, Anthony Russell.
Sanjay Sahgal, Urmimala Sarkar, John Schilling. Isabel] Schmitt,
Daren Schuhmacher, Sonal Shah, Fadi Abu Shahin, Mae Sheikh-
Ali, Edie Shen, JusUn Smith, John Slulak. Lillian Su, Julie
Sundaram, Rita Suri, Seth Sweetser. Antonio Talayero, Merita
Tan, Mark Tanaka. Eric Taylor, Jess Thompson, Inch Trehan,
Raymond Turner, Okafo Uchcnna, Eric Uyguanco. Richa
V'arma, John Wages, Alan Wang, Eunice Wang, Andy Weiss, Amy
Williams. Brian Yang, I lain Zaky, Ashraf Zaman and David Zipl.

For generously contributing images 10 the entire Underground
Clinical Vignette Step 1 series, we collectively thank the stair at
Blackwell Science in Oxford, Boston, and Berlin as well as:

• Axford, J. Medici iii: Osney Mead: Blackwell Science Ltd, 1996.
Figures 2.14, 2.15, 2.16, 2.27. 2.28. 2.31, 2.35. 2.36. 2.38, 2.43,
2.65a, 2.65b, 2.65c, 2.103b, 2.105b. 3.20b, 3.21, 8.27, 8.27b,
8.77b, 8.77c, 10.81b, 10.96a, 12.28a, 14.6, 14.16, 14.50.

• Bannister B, Begg N, Gillespie S. Infectious Disease, 2 wl Edition.
Osney Mead: Blackwell Science Ltd, 2000. Figures 2.8, 3.4,
5.28, 18.10, W5.32, W5.6.

• Berg D. Advanced Clinical Skills and Physical Diagnosis.
Blackwell Science Ltd., 1999. Figures 7.10, 7.12, 7.13, 7.2, 7.3,
7.7.7.8,7.9,8.1.8.2,8.4,8.5,9.2, 10.2, 11.3,11.5, 12.6.

• Cuschieri A, Hennessy TPJ, Greenhalgh RM, Rowley DA,
Grace PA. Clinical Surgery. Osney Mead: Blackwell Science
Ltd, 1996. Figures 13.19, 18.22, 18.33.

• Gillespie SH, Bamford K. Medical Microbiology and Infection al n
Giant*. Osney Mead: Blackwell Science Ltd, 2000. Figures 20, 23.

• Ginsberg L. Lecture Notes on Neurology. 7' Edition, Osney Mead:
Blackwell Science Ltd, 1999. Figures 12.3, 18.3, 18.3b.

• Elliott T. Hastings M. Desselberger V. Lecture . Wiles on Medical
Microbiology, >"' Edition. Osney Mead: Blackwell Science Ltd,
1997. Figures 2, 5, 7, 8, 9, 11, 12, 14. 15, 16. 17, 19, 20, 25, 26,
27, 29, 30, 34, 35, 52.

• Mehta AB, Hoffbrand AV. Haonalolooy at a Glance. Osney
Mead: Blackwell Science Ltd, 2000. Figures 22.1. 22.2, 22.3.

Please lei us know if your name has been missed or misspelled
and we will be happy to make the update in the next edition.

PREFACE TO THE 3RD EDITION

We were very pleased with the overwhelmingly positive student
feedback for the 2nd edition of our Underground Clinical Vignettes
scries. Well over 100,000 copies of the UCV books are in print
and have been used by students all over the world.

Over the last two years we have accumulated and incorporated
over a thousand "updates" and improvements suggested by you,
our readers, including:

• many additions of specific boards and wards testable content

• deletions of redundant and overlapping cases

• reordering and reorganization of all cases in both series

• a new master index by case name in each Atlas

• correction of a few factual errors

• diagnosis and treatment updates

• addition of 5-20 new cases in every book

• and the addition of clinical exam photographs within UCV- —

Anatomy

Arid most important of all. the third edition sets now include
two brand new COLOR ATLAS supplements, one for each
Clinical Vignette series.

• The UCV-Basic Science Color Alias (Step 1) includes over 250
color plates, divided into gross pathology, microscopic pathol-
ogy (histology)- hematology, and microbiology (smears).

• The UCV-Clinical Science Color Atlas {Step 2) has over 125 color
plates, including patient images, dermatology, and fundus-
copy.

Each atlas image is descriptively captioned and linked to its cor-
responding Step 1 case, Step 2 case, and/or Step 2 MiniCase.

How Atlas Links Work:

Step 1 Book Codes are: A = Analom)

BS = Bili.uioi.il Science
BC = Bini licinisii \
Ml = Microbiology, Vol. 1
Ml' - Microbiology, Vol. II
PI = Pathophysiology, Vol. I
P2 = Pathophysiology, Vol. II
P I Pathophysiology, Vol, 111
PH = Pharmacology

Step 2 Book Codes are: ER = Emergency Medicine

IM I = Internal Medicine. Vol. I
IM2 = Internal Medicine, Vol. U

NHl ' - Neurology
OB = OB/GYN
PED Pediatrics
SUR = Surgei \
PSY= Psvchialrx
MC = MiniCasc-

Case Number

M-P3-032A

Indicates Type of Image: II = Hematology
M = Microbiolog)
I'c. - ( »ross Pathology
I'M - Microscopii Patholog)

ER-035A, ER-035B

Indicates UCV1 or UCV2 Series

• If the Case number (032. 035. etc.) is not followed by a letter,
then there is only one image. Otherwise A, B. C, D indicate
up to 4 images.

Bold Faced Links: In order to give you access to the largest
□umber of images possible, we have chosen to cross link the

Step 1 and 2 series.

• If ihe link is bold-faced I h is indicates that the link is direct
(i.e.. Step 1 Case with the Basic Science Step 1 Atlas link).

• If the link is not bold-faced this indicates that the link is indi-
rect (Step 1 case with Clinical Science Step 2 Atlas link or vice
versa).

We have also implemented a few structural changes upon your
request:

• Each current and future edition of our popular First Aid far
the USMLESle/i 1 (Appleton & Lange/McGraw-Hill) and First
Aid for the USMLESlej/ 2 (Appleton & Lange/McGraw-Hill)
book will be linked to the corresponding UCV case.

• We eliminated UCV — ► First Aid links as they frequently
become out of date, as the First Aid books are revised yearly.

• The Color Atlas is also specially designed l< ir quizzing —
captions are descriptive and do not give away the case name
directly.

We hope the updated UCV series will remain a unique and well-
integrated study tool that provides compact clinical correlations
to basic science information. They are designed to be easy and
fun (comparatively) to read, and helpful for both licensing
exams and the wards.

We invite your corrections and suggestions for the fourth edi-
lion of these books. For the first submission of each factual cor-
rection or new vignette that is selected for inclusion in the
fourth edition, you will receive a personal acknowledgement in
die revised book. If you submit oxer 21) high-quality corrections,
additions or new vignettes we will also consider inviting you to
become a "Contributor" on the book of your choice. Lf you are
interested in bet oming .1 potential "Contribitti >r" or "Author"
on a future UCV book, or working with our team in developing
additional books, please also e-mail us your CV/resume.

We prefer that you submit corrections or suggestions via
electronic mail to UCVteam@yahoo.com. Please include
"Underground Vignettes" as the subject of vour message. If you
do not have an ess to e-mail, use the following mailing address:
Blackwell Publishing, Attn: UCV Editors, 350 Main Street,
Maiden, MA 02148, USA.

1/7,7/ s Hh iish tin
\ "tshal Pall
Too Lf
October 2001

HOW TO USE THIS BOOK

This series was originally developed to address the increasing
number of clinical vignette questions on medical examinations.
including the USMLE Step 1 and Step 2. It is also designed to
supplement and complement the popular First Aid for the
I 'SMLE Step 1 (Appleton & Lange/McGraw Hill) and First Aid
for the l 'SMLE Step 2 (Appleton & Lange/McGraw Hill).

Each UCV 1 book uses a series of approximately 100 "supra-
prototypical" cases as a way to condense testable facts and
associations. The clinical vignettes in this series are designed to
incorporate as many testable facts as possible into a cohesive
and memorable clinical picture. The vignettes represent
composites drawn from general and specialty textbooks,
reference books, thousands of USMLE style questions and the
personal experience of die authors and reviewers.

Although each case lends to present all the signs, symptoms.
.iikI dia^nosti< lindings foi a parti< ulal illness, patients gener-
ally will not present with such a "complete" pichire either clini-
cally or on a medical examination. Cases are not meant to
simulate a potential real patient or an exam vignette. All the
boldfaced "buzzwords" are for learning purposes and are not
necessarily expected to be found in any one patient with the
disease.

Definitions of selected important terms are placed widiin the
vignettes in (SM \t I < IAPS) in parentheses. Other parenthetical
remarks often refer to the pathophysiology or mechanism of
disease. The format should also help students learn to present
cases succinctly during oral "bullet" presentations on clinical
rotations. The cases are meant to serve as a condensed review,
not as a primary reference. The information provided in this
book has been prepared with a great deal of thought and care-
ful research. This book should not, however, be considered as
your sole source of information. Corrections, suggestions and
submissions of new cases are encouraged and will be acknowl-
edged and incorporated when appropriate in future editions.

ABBREVIATIONS

5-ASA f)-aniinosalicylic acid

ABGs arterial blood gases

ABVD adriamycin/bleomycin/vincristine/dacarbazine

ACE angiotensin-con verting enzyme

ACTH adrenocorticotropic hormone

ADH antidiuretic hormone

AFP alpha fetal protein

AI aortic insufficiency

AIDS acquired immunodeficiency syndrome

ALL acute lymphocytic leukemia

ALT alanine transaminase

AML acute myelogenous leukemia

AN \ antinuclear antibody

ARDS adult respiratory distress syndrome

ASD atrial septal defect

ASO anti-streptolysin O

AST aspartate transaminase

AV arteriovenous

BE barium enema

BP blood pressure

111 \ blood urea nitrogen

CAD coronary artery disease

CALLA common acute lymphoblastic leukemia antigen

CBC complete blood count

CHF congestive heart failure

CK creatine kinase

CLL chronic lymphocytic leukemia

CML chronic myelogenous leukemia

CMV cytomegalovirus

CNS central nervous system

COPD chronic obstructive pulmonary disease

CPK creatine phosphokinase

CSF cerebrospinal fluid

CT computed tomography

( 'V A cerebrovascular accident

CXR chest x-ray

DIC disseminated intravascular coagulation

DIP distal interphalangeal

DKA diabetic ketoacidosis

DM diabetes mellitus

I) I Rs deep tendon reflexes

DVT deep venous thrombosis

I .UN Epstein— Barr virus

ECG electrocardiography

Echo echocardiography

EF ejection fraction

1- < .1 ) esophagogastroduodenoscopy

EMG electromyography

ERCP endoscopic retrograde cholangiopancreatography

KSR er\ throe) le sedimentation rate

FEV forced expiratory volume

FNA line needle aspiration

FTA-ABS fluorescent treponemal antibody absoi ption

FVC forced vital capacity

GFR glomerular filtration rate

GH growth hormone

(il gastrointestinal

GM-CSF granulocyte macrophage colony stimulating

factor

GU genitourinary

HA\" hepatitis A virus

hcG human chorionic gonadotrophin

HEENT head, eves, ears, nose, and throat

HIV human immunodeficiency virus

HLA human leukocyte antigen

IIP1 history of present illness

HR heart rate

HRIG human rabies immune globulin

1 IS hereditary spherocytosis

ID/CC identification and chief complaint

IDDM insulin-dependent diabetes mellitus

Ig immunoglobulin

IGF insulin-like growth factor

IM intramuscular

JVP jugular venous pressure

KUB kidneys/ ureter/bladder

I.DH lactate dehydrogenase

LES lower esophageal sphincter

LFTs liver function tests

LP lumbar puncture

LV left ventricular

I VI I left ventricular hypertrophy

I aics electrolytes

MCHC mean corpuscular hemoglobin concentration

MCV mean corpuscular volume

MEN multiple endocrine neoplasia

MIS US monoclonal gammopathy of undetermined

significance

\l 1 1< major histocompatibility complex

MI myocardial infarction

MOPP mcchlorcthamine/vincristine (Oncovorin)/

procai ba/ine/ prednisone

MR magnetic resonance (imaging)

\ 1 i I . non-Hodgkin's lymphoma

NIDDM non-insulin-dependent diabetes mellitus

NPO nil per os (nothing by mouth)

NSAID nonsteroidal anti-inllammalory drug

PA posteroanterior

PIP proximal interphalangeal

I'li.s peripheral blood smear

PE physical exam

PFTs pulmonary function tests

I'M I point of maximal intensity

PMN polymorphonuclear leukocyte

PT prothrombin lime

I'l ( A percutaneous transluminal angioplasty

PTII parathyroid hormone

Pi T partial thromboplastin time

PUD peptic ulcer tlisease

RB< : red blood cell

RPR rapid plasma reagin

RR respiratory rate

RS Reed-Sternberg (cell)

RV tight ventricular

RVH r 'g nl ventricular hypertrophy

SBFT small bowel follow-through

SIADH syndrome of inappropriate secretion of ADH

SLE systemic lupus erythematosus

S I I ) sexually transmitted disease

TFTs thyroid function tests

I PA tissue plasminogen activator

TSH thyroid-stimulating hormone

TIBC total iron-binding capacitv

TIPS transjugular intrahepatic portosystemic shunt

TPO thyroid peroxidase

TSH thyroid-stimulating hormone

TTP thrombotic thrombocytopenic purpura

UA urinalysis

UCSI upper GI

I S ultrasound

\ I ) \i I Venereal Disease Research Laboratory

VS vital signs

VT ventricular Uichvcardia

\\1'.( white blood cell

W'I'W Wolff-Parkinson-White (syndrome)

XR x-ray

ID/CC A 25-year-old IV drug abuser presents with a high fever with

chilis, malaise, a productive cough, hemoptysis, and right-sided
pleuritic chest pain.

HPI He also reports multiple skin infections at injection sites.

PE VS: fever. PK: stigmata of intravenous drug abuse at multiple
injection sites; skin infections: thrombosed peripheral veins;
splenomegaly and pulsatile hepatomegaly; ejection systolic
murmur, increasing with inspiration, heard in tricuspid area.

Labs CBC; normochromic, normocytic anemia. UA: microscopic
hematuria. Blood culture yields Staphylococcus aureus.

Imaging Echo: presence of vegetations on tricuspid valve and tricuspid
incompetence. CXR: consolidation.

Treatment High-dose intravenous penicillinase-resistant penicillin in

combinalion with an aminoglycoside. If the isolated .V. aureus
strain is methicillin resistant, vancomycin is the drug of choice.

Discussion In drug addicts, the tricuspid valve is die site of infection more
frequently (55%) than the aortic valve (35%) or the mitral valve
(30% ): these findings contrast markedly with the rarity of right-
sided involvement in cases of infective endocarditis (hat are not
associated with drug abuse. Staphylococcus aureus is responsible
for the majority of cases. Certain organisms have a predilection
for particular valves in cases of addict-associated endocarditis;
for example, enterococci, other streptococcal species, and
non-albicans Candida organisms predominantly affect the valves
of die left side of the heart, while S. aureus infects valves on both
the right and the left side of the heart. Pseudomonas organisms
are associated with biventricular and multiple-valve infection in
addicts. Complications of endocarditis include congestive heart
failure, ruptured valve cusp, myocardial infarction, and
myocardial abscess.

>
o

Atlas Link

PG-M1-001

ACUTE BACTERIAL ENDOCARDITIS

ID/CC A 25-year-old male complains of increasing shortness of breath
and ankle edema thai have progressively worsened over the past

'_' weeks.

HPI He also complains of fatigue, palpitations, and low-grade fever.
His symptoms followed a severe URL He denies any history <>l
joint pain or skin rash (vs. rheumatic fever).

PE JVP elevated; pitting pedal edema; fine inspiratory crepitations
heard at both lung bases; mild hepatosplenomegaly.

Labs ASO titers not elevated. CBC: lymphocytosis. EGG: first-degree
AV block. ESR elevated; increased tilers of antibodies to
coxsackievirus demonstrated in serum.

Imaging CXR: cardiomegaly and pulmonary edema. Echo: dilated
cardiomyopathy with low ejection fraction.

Gross Pathology Dilated heart with foci of epicardial, myocardial, and
endocardial petechial hemorrhages.

Micro Pathology Endomyocardial biopsy reveals diffuse infiltration by

mononuclear cells, predominantly lymphocytes; focal fibrosis.

Treatment Manage congestive heart failure and arrhythmias: cardiac
transplant in intractable cases.

Discussion Coxsackie B is most often implicated in viral myocarditis.

Nonviral causes of myocarditis include bacteria such as Borrelia
burgdorferi (Lyme disease I, parasites such as Trypanosoma rruzi
(Chagas' disease), hypersensitivity reaction (systemic lupus
erythematosus, drug reaction), radiation, and sarcoidosis; may
also be idiopathic (giant cell myocarditis).

Atlas Link LZLLLJ M-Ml-002

MYOCARDITIS— VIRAL

ID/CC A 35-year-old male complains of fever, nonproductive cough,
and chest pain.

HPI Ht- slates llial (he chest pain developed after lie had a severe
cold for 1 week. He describes the pain as severe, crushing, and
constant over the anierior rhesi and adds that it worsens with
inspiration and is relieved by sitting up and bending forward.

PE VS: low-grade fever; sinus tachycardia. PE: triphasic pericardial

friction rub (systolic and diastolic components followed by a third
component in late diastole associated with atrial contraction):
elevated JVP; inappropriate increase in JVP with inspiration

(RussMAt'i.'s Mt.\): pulsus paradoxus may also be seen.

Labs Moderately elevated transaminases and I.f)H: elevated ESR;

serum CPK-MB normal. CBC: neutrophilic leukocytosis. ECG:
diffuse ST-segment elevation (vs. myocardial infarction);
PR-segment depression.

Imaging Echo: pericardial effusion. CXR: apparent cardiomegaly (due to
effusion).

Gross Pathology

In long-standing cases, pericardium may become librotic.
scarred, and calcified.

Micro Pathology

Pericardial biopsy reveals signs of acute inflammation with
increased leukocytes, vascularity, and deposition of fibrin.

Treatment Analgesics for pain; steroids in resistant cases; indomeihacin:
surgical stripping of scarring in severe cases.

Discussion Acute pericarditis is commonly idiopathic. Known infectious

causes include coxsackievirus A and B, tuberculosis, staphylococcal
or pneumococcal infection, amebiasis, or actinomycosis;
noninfectious causes include chronic renal failure.
collagen-vascular disease (systemic lupus erythematosus,
scleroderma, and rheumatoid arthritis), neoplasms, myocardial
infarction, and trauma. Long-term sequelae include chronic
constrictive pericarditis.

Atlas Link mem i PG-Mi-003

PERICARDITIS— ACUTE

ID/CC A 64-year-old male presents with rapidly progressive dyspnea
and fever.

HPI He has a history of orthopnea and paroxysmal nocturnal

dyspnea and also reports pink, frothy sputum (HEMOPTYSIS).
One month ago he underwent a bioprosthetic valve replace-
ment for calcine aortic stenosis. He is not hypertensive and has
never had oven cardiac failure in the past.

PE VS: fever; hypotension. PE: bilateral basal inspiratory crackles
heard: cardiac auscultation suggestive of aortic incompetence
(early diastolic murmur heard radiating down left sternal edge).

Labs CBC: normochromic, normocyiic anemia. Three consecutive
blood cultures yield coagulase-negative Staphylococcus
epidermidis: si rain found to be methicillin resistant.

Imaging CXR (PA view): suggestive of pulmonary edema. Echo: confirms
presence ol prosthetic aoriic valve dehiscence leading to

incompetence and poor left ventricular function.

Treatment High-dose parenteral antibiotics — vancomycin (drug of choice
For meihicillin-resistant .S". aureus), gentamicin, and oral
rifampiciu; surgical replacement of damaged prosthetic valve;
prophylactic antibiotics (amoxicillin) for patients receiving
oral/ dental treatments to prevent transient bacteremia.

Discussion Prosthetic valve endocarditis is subdivided into two categories:
early prosthetic valve endocarditis (EPVE), which becomes
clinically manifest within 60 days after valve replacement (most
commonly caused by Staphylococcus epidermidis, followed by
gram-negative bacilli and Candida), and late prosthetic valve
endocarditis (LPVE). which is manifested clinically more than
60 days after valve replacement (most commonly caused by
viridans streptococci).

PROSTHETIC VALVE ENDOCARDITIS

ID/CC A 25-year-old female complains of low-grade fever and myalgia
of 3 weeks' duration.

HPI She has a history of rheumatic heart disease (RHD). One month
ago, she underwent a dental extraction and did not take the
antibiotics that were prescribed for her.

PE VS: fever. PE: pallor; small peripheral hemorrhages with slight
nodular character (Janeway 1-F.sions); small, tender nodules on
finger and toe pads (Osler's nodes); subungual linear streaks
(splinter hemorrhages); petechial hemorrhages on conjunctiva,
oral mucosa, and upper extremities; mild splenomegaly; apical
diastolic murmur on cardiovascular exam; fundus exam shows
oval retinal hemorrhages (Roth's spots).

Labs CBC/PliS: normocytic, normochromic anemia. UA: microscopic
hematuria. Growth of penicillin-sensitive Streptococcus viridans
on five of six blood cultures.

Imaging Echo: vegetal ions along atrial surface of mitral valve.

Gross Pathology

Micro Pathology

Treatment

Discussion

Embolism from vegetative growths on valves may embolize
peripherally (left-sided) or to the lung (right-sided).

Bacteria form nidus of infection in previously scarred or
damaged valves; bacteria divide unimpeded once infection takes
hold with further deposition of fibrin and platelets; peripheral
symptoms such as Osier's nodes are believed to result from
deposition of immune complexes.

IV 3-lactamase-resistant penicillin and gentamicin; bacteriostatic
treatments ineffective.

S. viridans is the most common cause of subacute infective
endocarditis, while Staphylococcus aureus is the most common
cause of acute bacterial endocarditis. Prophylactic antibiotics
should be given to all RHD patients before any dental procedure.
The disease continues to be associated with a high mortality rate.

Atlas Link [~1 TT PG-M1-005

C~l

•— * W

o §

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SUBACUTE BACTERIAL ENDOCARDITIS

ID/CC A ."> l-Ycar-uld (finale who underwent a led mastectomy with
axillary lymph node dissection a year ago presents with pain
together with rapidly spreading redness and swelling of the left
arm.

HPI One year ago, she was diagnosed and operated on for stage 1
carcinoma of die left breast.

PE Left forearm swollen, indurated, pink, and markedly tender;

overlying temperature raised: margins and holders of skin lesion
ill defined and not elevated (vs. erysipelas).

Labs Needle aspiration from advancing border of the lesion, when

stained and cultured, isolated (3-hemolytic group A streptococcus.

Treatment I'enicillinasc-rcsistaut penicillin (nafcillin/oxacillin).

Discussion ( ielluliiis is an acute spreading infection ol the skin that

predominantly affects deeper subcutaneous tissue. Group A
streptococci and Staphylococcus aureus .we the most common
etiologic agents in adults: Uai'wo/i/i/lus in/lumz/w infection is
common in children. Patients with chronic venous stasis and
lymphedema of any cause (lymphoma, filariasis. post-regional
lymph node dissection, radiation therapy) are predisposed:
recently, recurrent saphe nous-vein donor-site cellulitis was
found to be attributable to group A. C, or G streptococci.

CELLULITIS

ID/CC A Ki-vear-okl U'cnager presents to the outpatient clinic with a
painful facial rash and fever.

HPI One week ago, the paiient went on a camping trip and

scratched liis lace on some low-lying tree branches. There is no
medical history of diabetes, cancel, or oilier chronic conditions.

PE VS: fever (39.0 a C); tachycardia (HR 110): BP normal. PE :
erythematous, warm, plaque-like rash extending across cheeks
and face bilaterally with sharp, distinct borders and facial
swelling.

Labs ( IB( : leukocytosis with neutrophilia. ESR elevated.

Treatment

Discussion

Atlas Link

ERYSIPELAS

Antibiotics with sufficient coverage for penicillinase-producing
Streptococcus nui\ Staphylococcus spp. (e.g., cephalexin):
analgesics/antipyretics; elevate the affected part to reduce
swelling.

Erysipelas is an acute inflammation of the superficial layers of
the connective tissues of the skin, usually on the face, almost
always caused by infection with Group A Streptococcus which is
part of normal bacterial skin flora. Risk factors include any
breaks in the skin or lymphedema.

mct'j-i MC-136

o
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i —

o
en

ID/CC A 30-year-old slaughterhouse worker presents with a painful red
swelling of the index finger of his right hand.

HPI The swelling developed 4 days alter he was injured with a knife
while slaughtering a pig.

PE Well-defined, exquisitely tender, slightly elevated violaceous
lesion seen on right index finger; no suppuration noted; right
epitrochlear and right axillary lynipliadenopalhv noied.

Labs Biopsy from edge of lesion yields Erysipelothrix rhusiopathiae,
a thin, pleomorphic, nonsporulating, microaerophilic gram-
positive rod.

Treatment Penicillin G or ciprofloxacin in penicillin-allergic patients.

Discussion Erysipeloid refers to localized cellulitis, usually of the fingers

and hands, caused by Erysipelothrix rhusiopathiae; infection in
humans is usually the result of contact with infected animals or
their products (often fish). Organisms gain entry via cuts and
abrasions on the skin.

ERYSIPELOID

ID/CC A 10-year-old male complains of a spreading skin rash and
painful swelling of both wrists.

HPI The patient's mother states that die rash began with erythema
of the cheeks ("slapped-chkkk appearance") and subsequently
progressed to involve the trunk and limbs.

PE Erythematous lacy/reticular skin rash involving face, trunk, and
limbs: bilateral swelling and painful restriction of movement at
bodi wrist joints.

Labs Serology detects presence of specific IgM antibody to parvovirus;
ASO titer (to rule out acute rheumatic fever) normal:
rheumaioid factor (to rule out rheumatoid arthritis) negative.

Treatment Self-limiting disease.

Discussion A small (20- to 26-nm), single-stranded DNA virus, parvovirus B19
causes erythema infectiosum (fifth disease) in schoolchildren,
aplastic crises in persons with underlying hemolytic disorders
(e.g., sickle cell anemia), chronic anemia in immunocompromised
hosts, arthralgia/ arthritis in normal individuals, and fetal loss in
pregnant women.

Atlas Link i»icl r MC-299

o
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ERYTHEMA INFECTIOSUM

ID/CC A 5 year-old whin- male presents with golden-yellow, crusted
lesions around his mouth and behind his ears.

HPI He has a history of intermittent low-grade lever, frequent "nose
picking." and purulent discharge from his lesions. Me lias no
history of hematuria (due to increased risk of poststreptococcal
glomerulonephritis).

PE Characteristic "honey-colored" crusted lesions seen at angle of
mouth, around nasal orifices, and behind ears.

Labs Gram-positive cocci in chains (si REPTOCOCCt) in addition to pus
cells on Gram stain of discharge; (i-hciuolwic streptococci
(group A streptococci) on blood agar culture: ASO liter negative.

Gross Pathology Krvthematous lesions surrounding natural orifices with whitish
or yellowish purulent exudate and crust formation.

Micro Pathology Inflammatory infiltrate of I'MNs with varying degrees of necrosis.

Treatment Cephalosporin, penicillin, or erythromycin if allergic.

Discussion Impetigo is a highly communicable infectious disease that is

most often caused bv group A streptococci, occurs primarily in
preschoolers, and may predispose to glomerulonephritis. It
occurs most commonly on the face (periorbital area), hands,
and arms. Staphylococcus aureus ma) coexist or cause bullous
impetigo: group !'■ streptococcal impetigo may be seen in
newborns'

IMPETIGO

ID/CC A 30-year-old male homosexual visits his family doctor

complaining of a nonpruritic skin eruption on his upper limbs,
trunk, and anogenital area.

HPI He has been HIV positive for about 3 years and admits to
having continued unprotected intercourse.

PE Multiple painless, pearly-white, dome-shaped, waxy, umbilicated
nodules 2 to 5 mm in diameter on arms, trunk, and anogenital
area; palms and soles spared.

Gross Pathology Firm, umbilicated nodules containing thick yellowish material.

Micro Pathology

Treatment

Discussion

Atlas Link

Stained histologic sections confirm diagnosis with large
cytoplasmic inclusions (mou.l'scim bodies) in materia]

expressed from lesions.

Lesions may resolve spontaneously or be removed by curettage.
cryotherapy, or podophyllin; no antiviral drug or vaccine
available.

Molluscum contagiosum is a benign, autoinoculable skin disease
of children ;\\t(\ young adults; ii is caused b\ a poxvirus (DNA
virus) and is transmitted through sexual contact, close bodily
contact, clothing, or towels. It is one of many opportunistic
infections seen in AIDS patients (difficult to eradicate).

MC-143

o
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O
CD

MOLLUSCUM CONTAGIOSUM

ID/CC A 30-year-old black male presents with a nonpruritic skin rash
on the trunk, upper arm, and neck.

HPI The patient is otherwise in excellent health.

PE Multiple hypopigmented, scaling, confluent macules seen on

trunk, upper arms, and neck; no sensory loss demonstrated over
areas of hypopigmentation; Wood's lamp examination of skin
macules displays a pale yellow to blue-white fluorescence.

Labs Examination of KOH mounting of scales from lesions

demonstrates the presence of short, thick, tangled hyphae with
clusters of large, spherical budding yeast cells with characteristic
"spaghetti-and-meatballs" appearance.

Treatment Topical selenium sulfide: antifungal agents such as miconazole
and clotrimazole; oral itraconazole in recalcitrant cases.

Discussion Pityriasis versicolor, which is common in young adults, is a

relatively asymptomatic superficial skin infection caused by the
lipophilic fungal organism Pityrosporum orbiculare (also
termed Malassezia furfur) . The lesions, which usually have a
follicular origin, are small, hypopigmented-to-tan macules with a
branlike scale; the macules are distributed predominantly on
areas of the upper trunk, neck, and shoulders.

Atlas Links LTZIZLJ M-M 1-012 IT~m MC-148

PITYRIASIS VERSICOLOR

ID/CC An 18-month-old male is brought to the pediatrician following
the appearance of an extensive skin rash.

HPI Four days ago he suddenly developed a very high fever (4()°C)

with no other symptoms or signs. The fever continued for 4 days
until the day of his admission, when it abruptly disappeared,
coinciding with the onset of the rash.

PE Child looks well; in no acute distress; generalized rash apparent as
discrete 2- to 5-mm rose-pink macules and papules on trunk,
neck, and extremities (face is spared): lesions blanch on pressure;
no lymphadenopaUiy; splenomegaly may also be present.

Labs CBC/PBS: WBCs variable; relative lymphocytosis with atypical
lymphocytes.

Treatment Supportive; foscarnet.

Discussion Roseola infantum, also called exanthem subitum, is caused by
human herpesvirus 6. It is the most common exanthematous
disease in infants 2 years of age or younger and is a frequent
cause of febrile convulsions.

o
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ROSEOLA INFANTUM

ID/CC A 2-month-old female infant presents with extensive bullae and

large areas of denuded skin.

HPI I ler mother had suffered from staphylococcal mastitis 1 week
ago.

PE VS: fever. PE: large areas of red. painful, denuded skin on
periorbital and peribuccal areas; flaccid bullae with easy
dislodgment of epidermis under pressure (Nikolsky's sk ;n ) ;
mucosal surfaces largely uninvolved.

Labs Vesicle Quid sterile; Staphylococcus aureus on blood culture.

Treatment IV penicillinase-resistant penicillin (e.g., nafcillin, oxacillin).

I Veal with erythromycin Jl palieni is allergic lo penicillin.

Discussion Scalded skin syndrome is caused by the exfoliating effect of
staphylococcal exotoxin. The action of the exoioxin is to
degrade desmoglein in desmosomes in the skin.

SCALDED SKIN SYNDROME

ID/CC A 30-year-old man presents with a bilateral red pruritic skin
eruption in the groin area.

PE Bilateral, circular papulosquamous skin eruption on erythematous
base with active, advancing peripheral (serpiginous) border over
scrotum and perineum.

Labs Microscopic examination reveals long septate hyphae on KOH

skin scrapings.

Treatment Topical antifungal agents (Whitfield's ointment, clotrimazole.

miconazole); systemic therapy with oral griseofulvin, ketoconazole,
or itraconazole in resistant cases.

Discussion Tinea cruris and tinea corporis (common ringworm) occur

sporadically; Trichophyton ruhrum is the most common cause. The
inflammatory form, which is usually localized to the limbs,
chest, or back, is commonly caused by Microsporum canis or
Trichophyton mentagrophytes. Ringworm of the scalp, known as
tinea capitis, is commonly seen in children and is caused by
Trichophyton tonsurans.

Atlas Link mcmzi MC-151

TINEA CORPORIS (RINGWORM)

ID/CC A 28-year-old male presents with a red, pruritic skin eruption on
his Crunk and his upper and lower limbs of a few hours'
duration.

HPI One day earlier, he was prescribed cotrimoxazole for a UT1. He

has not experienced any dyspnea.

PE Erythematous, warm, urticarial wheals (hives) seen over trunk,
legs, and arms; no angioedema or respiratory distress.

Labs CBC: leukocytosis with eosinophilia. No parasites revealed on
stool exam.

Gross Pathology

Micro Pathology

Treatment

Discussion

Linear or oval, raised papules or plaque-like wheals up to several
centimeters in diameter.

Wide separation of dermal collagen fibers with dilatation Ol
lymphatics and venules.

Topical agents to reduce itching; avoidance of causative agent
(in this case, cotrimoxazole); antihistamines (primarily H|
blockers but also H 2 blockers) ; consider glucocorticoids.

Mast cells and basophils are focal to urticarial reaction. When
stimulated by certain immunologic or nonimmunologic
mechanisms, storage granules in these cells release histamine
and other mediators, such as kinins and leukotrienes. These
agents produce the localized vasodilatation and transudation of
fluid thai characterize urticaria.

Atlas Link IZIIO _J MC-021

URTICARIA

ID/CC A 7-year-old male is brought to his family physician complaining
of a thick yellowish discharge in his eyes that prevents him from
opening his eyes in the morning: for the past lew (lavs, his eyes
have been blood-red, painful, and watery. His eye pain is
exacerbated b\ exposure to light (PHOTOPHOBIA).

HPI Three of his classmates and a neighbor had a similar episode
about 7 days ago (suggesting a local epidemic of such cases).

PE VS: no fever. PE: normal visual acuity; erythematous palpebral
conjunctiva: watery eyes: remains of thick mucus found on inner
canthal area; no corneal infiltrate on slit-lamp exam; normal
anterior chamber; mild preauricular lymphadenopathy.

Labs Stained conjunctival smears reveal lymphocytes, giant cells,
neutrophils, and bacteria.

Treatment Topical antimicrobial eye drops; cool compresses; minimize

contact with others to avoid spread; avoid use of topical steroid
preparations, as these can exacerbate bacterial and viral eye

infections.

Discussion Conjunctivitis is a common disease of childhood that is mostly
viral (adenovirus) and self-limiting; it occurs in epidemics, and
secondary bacterial infections (staphylococci and streptococci)
may result. Visual acuity is not affected.

■<

ACUTE CONJUNCTIVITIS

ID/CC A 3f>-year-old woman complains of fever and pain in the face
and upper teeth (maxillary sinus), especially while leaning
forward.

HPI She has had a chronic cough, nasal congestion, and discharge
for the pasi lew months.

PE VS: fever. PE: halitosis: greenish-yellow postnasal discharge:
bilateral boggy nasal mucosa; bilateral percussion tenderness
and erythema over zygomatic arch; clouding of sinuses by
transillumination; denial and cranial nerve exams normal.

Labs Nasal cultures reveal Streptococcal pneumoniae.

Imaging CT, sinus: partial opacification of maxillary sinus with air-fluid
level.

Gross Pathology Erythematous and edematous nasal mucosa.

Micro Pathology Presence of organisms and leukocytes in mucosa.

Treatment Oral decongestants; amoxicillin, Bactrim, or fluoroquinolone.

Discussion Other pathogens include other streptococci, Haemophilus

influenzae, and Moraxella. The obstruction of ostia in the anterior
ethmoid and middle tneatal complex by retained secretions,
mucosal edema, or polyps promotes sinusitis. Staphylococcus
aureus and gram-negative species may cause chronic sinusitis.
Fungal sinusitis may mimic chronic bacterial sinusitis.
Complications include orbital cellulitis and abscesses.

ACUTE SINUSITIS

ID/CC A 1 7-year-old boy presents with itchy eyes, nasal stuffiness,

increased lacrimation, sneezing, and a watery nasal discharge.

HPI He has had similar episodes in tin- pasi that have corresponded
with changing of the seasons. His mother is known to have
bronchial asthma.

PE VS: no fever. PE: pallor; boggy nasal mucosa; nasal polyps present:
conjunctiva congested; no exudate.

Labs Conjunctival and nasal smear demonstrates presence of

eosinophils; no bacteria on Gram stain; no neutrophils. Allergen
skin tests (sensitized cutaneous mast cells) show positive
sensitivity.

Gross Pathology Nasal mucosa hyperemic and swollen with fluid transudation.

Micro Pathology

Treatment

Discussion

Local tissue inflammation and dysfunction of upper airway
because of type I. IgE-mediated hypersensitivity response.

Oral decongestants with intranasal corticosteroids;
antihistamines: intranasal cromolyn sodium, especially before
anticipated contact with allergen.

Allergic rhinitis is commonly caused by exposure to pollens,
dust content, and insect matter; symptoms arc mediated by the
release of vasoactive and chemotactic mediators from mast cells
and basophils (e.g., histamine and leukotrienes) with IgE
surface receptors.

O
"a

ALLERGIC RHINITIS (HAY FEVER)

ID/CC A 20-year-old male presents with a runny nose, nasal congestion,
sore throat, headache, and sneezing.

HPI He notes that his wife currently has similar symptoms.

PE VS: mild fever. PE: rhinorrhea; congested and inflamed
posterior pharyngeal wall; no lymphadenopathy.

Labs Routine tests normal; routine throat swah staining and culture
negative for bacteria.

Gross Pathology Nasal membranes edematous and erythematous with watery
discharge.

Micro Pathology Mononuclear inflammation of mucosa; focal desquamation.

Treatment Symptomatic.

Discussion Colds occur 2 to 3 times a year in the average person in the
United Slates; ihe peak incidence is in the winter months.
Rhinoviruses account for the majority of viral URIs, followed by
coronaviruses. Spread occurs by direct contact and respiratory
droplets.

COMMON COLD (VIRAL RESPIRATORY INFECTION)

ID/CC A 60-year-old male presents with swelling and a vesicular skin
eruption on the left side of his face.

HPI The patient reports that before the rash developed, he had

severe radiating pain on the left side of his face. He also recalls
having suffered an attack of chickenpox during his childhood.

PE Unilateral vesicular rash over left forehead and nasal bridge,
including the Up of the nose, indicating involvement of the
nasociliary branch of the trigeminal nerve (Hutchinson \s sign);
skin of lids red and edematous; slit-lamp examination reveals
numerous rounded spots composed of minute white dots
invoking epithelium and su'oma, producing a coarse subepithelial
punctate keratitis; cornea is insensitive.

Micro Pathology

Vesicular skin lesions with herpesvirus inclusions that are
intranuclear and acidophilic with a clear halo around them
(Cowdry type A inclusion bodies); syncytial giant cells also seen.

Treatment Acyclovir; steroids; cycloplegics. Trifluorothymidine for HSV
keratitis.

Discussion Herpes zoster ophthalmicus is caused by the varicella zoster

virus, which causes chickenpox as a primary infection. Zoster is
believed to be a reactivation of the latent viral infection. In
zoster ophthalmicus, the chief focus of reactivation is the
trigeminal ganglion, from which the virus travels down one or
more branches of the ophthalmic division such that its area of
distribution is marked out by rows of vesicles or scars left by
the vesicles. Ocular complications arise during subsidence of ihe
rash and are generally associated with involvement of the
nasociliary branch of the trigeminal nerve.

HERPES ZOSTER OPHTHALMICUS

ID/CC An 18-year-old male complains of severe irritation in the left eye,
blurred vision, excessive lacrimation, and photophobia.

HPI He reports that he lias had similar episodes in the past diat were
Healed with an antiviral drug. His records indicate thai he
suffered the first attack at the age of 7. at which time his
condition was diagnosed and treated as a severe follicular
keratoconjunctivitis; his records also indicate a history of
recurrent episodes of herpes labialis.

PE Examination of left eye reveals circumcorneal congestion;

fluorescein staining of cornea reveals infiltrates spreading in all
directions, coalescing with each other and forming a large,
shallow ulcer with crenated edges ("dendritic ii.cir"): cornea is
insensitive.

Labs HSV-1 demonstrated on immiirioftuorescent staining of
epithelial scrapings as well as in the aqueous humor.

Treatment Trifluridine eye drops; acyclovir has been shown to decrease
recurrences.

Discussion Most ocular herpetic infections are caused by HSV-1. It is also
the primary cause of corneal blindness in the United States.
Primary infections present as unilateral follicular conjunctivitis,
blepharitis, or corneal epithelial opacities; recurrences may lake
the form of keratitis (> 90% of cases are unilateral), blepharitis,
or keratoconjunctivitis. Branching dendritic ulcers, usually
detected by fluorescein staining, are virtually diagnostic; deep
stromal involvement may result in scarring, corneal thinning,
and abnormal vascularization with resulting blindness or
rupture of the globe.

HSV KERATITIS

ID/CC A 20-year-old male swimmer complains of severe pain and

itching in the right ear that is associated with a slight amount of
yellowish (purulent) discharge.

HPI The patient has no previous history of discharge from the ear
and no history of associated deafness or tinnitus.

PE Red. swollen area seen in right external auditory meatus that is
partially obliterating the lumen: movement of tragus is

exquisite!) painful ( i ragai sign).

Labs Gram stain of aural swab reveals presence of gram-negative rods;
culture isolates Pseudomonas aeruginosa.

Gross Pathology

Red, swollen area seen in cartilaginous part of external auditory
meatus; when visualized, tympanic membrane is erythematous
and moves normally with pneumatic otoscopy (vs. acute otitis
media).

Treatment Eardrops (either a combination of polymyxin, neomycin, and
hydrocortisone or ofloxacin); gentle removal of debris in ear.

Discussion Otitis externa is most common in summer months and is thought
to arise from a change in the milieu of the external auditory
im atus b\ increased alkali/ation and excessive moisture; this leads
to bacterial overgrowth, most commonly with gram-negative rods
such as Pseudomonas (also causes malignant otitis extei na)and
Proteus or fungi such as Aspergillus.

O
en

OTITIS EXTERNA

ID/CC An 18-month-old white female presents with irritability together
with a bilateral, profuse, and foul-smelling ear discharge of

2 months' duration.

HPI The patient had recurrent URIs last year, bin her mother did

not administer the complete course of antibiotics. The patient's
mother has a history of feeding her child while lying down.

PE Bilateral greenish-while ear discharge; perforated tympanic

membranes in anteroinferior quadrant of both ears: diminished
mobility of tympanic membrane on pneumatic otoscopy.

Labs Gram-negative coccobacilli on Gram stain of discharge from

tympanocentesis: Haemophilus influenzae seen on culture.

Gross Pathology

Micro Pathology

Possible complications include ingrowth of squamous
epithelium on upper middle ear (CHOLESTEATOMA) if long-
standing; conductive hearing loss; mastoiditis; and brain abscess.

Hyperemia and edema of inner ear and throat mucosa;
hyperemia of tympanic membrane; deposition of cholesterol
crystals in keratinized epidermoid cells in cholesteatoma.

Treatment Keep ear dry; amoxicillin-clavulanic acid; surgical drainage for
severe otalgia: myringoplasty.

Discussion Otitis media is the most common pediatric bacterial infection
and is caused by Escherichia coU, Staphylococcus aureus, and
Klebsiella pneumoniae in neonates; in older children il is usually
caused by pneumococcus (Streptococcus pneumoniae). II. influenzae.
MoraxeUa catarrhaUs, and group A streptococcus. Resistant strains
are becoming increasingly common.

OTITIS MEDIA

ID/CC A 6-year-old male presents with complaints of a mild sore throat
and eye irritation.

HPI His mother says that he has spent hours at the community
swimming pool this summer.

PE Mild rhinopharyngitis; bilateral conjunctival congestion with

scanty mucoid discharge.

Labs Viral culture of conjunctival and nasopharyngeal swab yields
adenovirus.

Treatment No specific treatment; self-limiting illness.

Discussion Adenovirus infections occur most often in infants and young
children, who acquire the virus by the respiratory or fecal-oral
route. The most common respiratory tract syndrome in this age
group is mild coryza with pharyngitis; in older children, these
symptoms may be accompanied by conjunctivitis. May also cause
hemorrhagic cystitis in children. On electron microscopy it is
seen as a double-stranded nonenveloped DNA virus surrounded
by a 20-faced icosahedral protein capsid from which 12 antenna-
like Fibers or pen tons extend radially.

PHARYNGITIS— ADENOVIRUS

ID/CC A 9-year-old male complains of pain during swallowing

(odynophagia) for 2 days, accompanied by muscle aches,
headache, and fever.

HPI Ik- has otherwise been in good health.

PE V'S: level - . PE: moderale erythema of pharynx; enlarged,
erydiematous tonsils covered with white exudate; tender
cervical adenopathy.

Labs CBC: neutrophilic leukocytosis. Streptococcus pyogenes isolated

On throat swab and culture.

Gross Pathology

Micro Pathology

1 Ivperemia and swelling ol upper respiraton i.ra< i mucosa; cryptic
enlargement of tonsils with purulent exudate; enlargement of
regional lymph nodes.

Acute inflammatory response with polymorphonuclear infiltrate,
hyperemia and edema with pus formation: hyperplasia of
regional lymph nodes; dilatation of sinusoids.

Treatment Oral penicillin V.

Discussion

Streptococcal pharyngitis is an acme bacterial inlei lion produced
In gram-positive cocci in chains (Streptococcus); pharyngitis is most
commonly caused by group A streptococcus. Complications due
to immune-mediated cross-reactivity and molecular mimicking
may include glomerulonephritis and rheumatic fever.

Atlas Link

M-Ml-026

PHARYNGITIS— STREPTOCOCCAL

ID/CC A 30-year-old female presents to the surgical ER complaining of
a stabbing right upper quadrant abdominal pain.

HPI She is a prostitute who has been receiving treatment for
gonococcal pelvic inflammatory disease.

PE Right upper quadrant tenderness; cervical motion tenderness
and mucopurulent cervicitis found on pelvic exam.

Labs Cervical swab staining and culture identifies Neisseria
gonorrhoeae.

Imaging US: no evidence of cholecystitis. Peritoneoscopy: presence of

"violin string" adhesions between liver capsule and peritoneum.

Gross Pathology Adhesions noted between liver capsule and peritoneum.

Treatment Antibiotic therapy (ceftriaxone and doxycycline) for paiieni
(and for partner if warranted).

Discussion Acute fibrinous perihepatitis (Fi r/.-Hicii-Ci ktis syndrome)
occurs as a complication of gonococcal and chlamydial pelvic
inflammatory disease and clinically mimics cholecystitis.

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FITZ-HUGH-CURTIS SYNDROME

ID/CC A 23-year-old male presents with sudden-onset, severe vomiting,
nausea, abdominal cramps, and diarrhea.

HPI He had returned home about 2 hours after attending a birthday
part) at which meat and milk were served in various forms. The
friend who was celebrating his birthday reported similar
symptoms.

PE VS: no fever. PE: mild dehydration; diffuse abdominal
tenderness; increased bowel sounds.

Labs Toxigenic staphylococcus recovered from culturing food.

( loagulase-positive staphylococcus cultured from nose of one of
the cooks at party.

Micro Pathology No mucosal lesions.

Treatment Fluid and electrolyte balance; antibiotics not indicated.

Discussion Staphylococcus /uncus food poisoning results from die ingestion
of food containing preformed heat-stable enterotoxin B.
Outbreaks of staphylococcal food poisoning occur when food
handlers who have contaminated superficial wounds or who are
shedding infected nasal droplets inoculate foods such as meat,
dairy products, salad dressings, cream sauces, and custard-filled
pastries. The incubation period ranges from 2 to 8 hours; the
disease is self-limited.

GASTROENTERITIS— STAPHYLOCOCCUS AUREUS

ID/CC An 11-year-old white male presents with jaundice and dark
yellow urine that has been present lor the last several days.

HPI He also complains of nausea, vomiting, and malaise. For the

past 2 weeks, he has had a low-grade level and mild abdominal
pain. He recently returned from a vacation in Mexico, where he
said he consumed a lot of shellfish.

PE Icterus; tender, firm hepatomegaly; no evidence of splenomegaly
or free fluid in the peritoneal cavity.

Labs Direct hyperbilirubinemia; elevated serum transaminases
(ALT > AST); moderately elevated alkaline phosphatase;
prolonged PT; increased urinary urobilinogen and bilirubin;
positive IgM antibody to hepatitis A (HAV) indicative of active
HAV infection.

Gross Pathology May often appear normal.

Micro Pathology

Multifocal hepatocellular necrosis with Councilman bodies;
lymphocytic infiltrates around necrodc foci; loss of lobular
architecture.

Treatment Supportive management; passive vaccinadon available.

Discussion In hepatitis A infection, virus is shed 14 to 21 days before the
onset of jaundice; patients are no longer infectious 7 days after
tlu onset of jaundice. It is spread by fecal-oral transmission and is
endemic in areas where there are contaminated water sources.
There is no chronic carrier state; recovery takes place in 6 to
12 months. HAV is a naked, single-stranded RNA virus of the
picorna family. A killed vaccine is available; passive immunization
in the form of immune serum globulins is also available.

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HEPATITIS A

ID/CC A 25-year-old male medical student presents will) jaundice and
dark yellow urine.

HPI He admits to having experienced an accidental needle stick
2 months ago, which he did not report. He also complains of
nausea, low-grade fever, and loss of appetite.

PE Icterus; tender, firm hepatomegaly: no evidence of ascites or
splenomegaly.

Labs Direct hyperbilirubinemia: elevated serum transaminases

(ALT > AST): mildly elevated alkaline phosphatase: HBsAg
posidve; IgM anti-HBc positive (present during window period).

Imaging US, abdomen: hepatomegaly: increased echogenicity.

Gross Pathology

Micro Pathology

Treatment

Discussion

Atlas Links

Liver may be enlarged, congested, or jaundiced: in fulminant
cases of massive hepatic necrosis, liver becomes small, shrunken,
and soft (acute yellow atrophy).

Liver biopsv reveals hepatocellular necrosis with Councilman
bodies and ballooning degeneration; inflammation of portal
areas with infiltration of mononuclear cells (small lymphocytes,
plasma cells, eosinophils); prominence of Kupffer cells and bile
ducts; cholestasis with bile plugs.

Supportive care: follow up to determine continued presence of
HBsAg for at least 6 months as sign of chronic hepatitis: vaccine
available for prevention.

Hepatitis B immune globulin plus hepatitis B vaccine are

recommended for parenteral or mucosal exposure to blood and
for newborns of HBsAg-positive mothers. The infection is
divided into the prodromal, icteric, and convalescent phases;
5% proceed to chronic hepatitis with increased risk for cirrhosis
and hepatocellular carcinoma. Unlike hepatitis A. hepatitis B
has a long incubation period (3 months). Hepatitis B virus is an
enveloped, partially circular DNA virus of the hepadna family
that contains a DNA-dependent DNA polymerase. The
continued presence of HBsAg after infection has clinically
resolved indicates a chronic carrier slate.

M-Ml-030

HEPATITIS B— ACUTE

ID/CC A 30-year-old male is referred for an evaluation of intermittent
jaundice over the past 2 years.

HPI He also complains of diarrhea, skin rash, and weight loss. He

received a blood transfusion 3 years ago, when he was injured in
a motorcycle accident. He denies any IV drug use or any history
of neuropsychiairic disorders in his family.

PE Icterus: firm, tender hepatomegaly: splenomegaly: no evidence of
ascites; no Kayser— Fleischer rings found on slit-lamp examination
(vs. Wilson's disease).

Labs

Micro Pathology

Treatment
Discussion

Atlas Link

Dii eci hyperbilirubinemia; markedly raised serum transaminase
levels; hepatitis B (HBV) serology negative; enzyme immunoassay
of antibodies to structural and nonstructural enzyme proteins of
hepatitis C (C200, C33c, C22-3) positive.

On liver biopsy, presence of ballooning degeneration; fatty
changes; portal inflammation with necrosis of hepatocytes
within parenchyma or immediately adjacent to portal areas

( "I'll < :l UKAI NECROSIS") .

Ribavirin and a 2 |,-mterferon; supportive management.

Hepatitis C belongs to the flavivirus family and is currently the
most important cause of post-transfusion viral hepatitis: 90% of
cases involve percutaneous transmission. Greater than 50% of
cases progress to chronic hepatitis, leading to cirrhosis in 20%.

M-Ml-031

HEPATITIS C— CHRONIC ACTIVE

ID/CC A 1 0-year-old male complains of generalized weakness, faintness
on exertion, and occasional epigastric pain.

HPI His mother has noticed that he often eats soil and other
inedible things (i'K \).

PE Pallor; puffy face and dependent edema.

Labs CBC: microcytic, hypochromic anemia; eosinophilia. Low serum
iron and ferritin; elevated serum transferrin; reduced bone
marrow hemosiderin; hypoproteinemia: stool exam revealed
eggs of Ancylosloma duodenale (ovoid eggs with thin
transparent shell that reveal the segmented embryo within).

Treatment Albendazole or mebendazole; iron supplementation to treat iron
deficiency anemia.

Discussion

Infection with hookworms, either Ancylostoma duodenale or
Necator americanus, is more likely where insanitary conditions
exist: individuals at risk include children, gardeners, plumbers
or electricians who are in contact with soil, and armed-forces
personnel. Hookworm eggs excreted in the feces hatch in the
soil, releasing larvae that develop into infective larvae.
Percutaneous larval penetration is the principal mode of human
infection. From the skin, hookworm larvae travel via the
bloodstream to the lungs, enter die alveoli, ascend the
bronc hotracheal tree to the pharynx, and are swallowed. Although
transpulmonary larval passage may elicit a transient eosinophilic
pneumonitis (Lomi i:r's pm-i momiis). this phenomenon is much
less common with hookworm infections than with roundworm
infections. The major health impact of hookworm infection,
however, is iron loss resulting from the 0.1 to 0.4 mL of blood
ingested daily by each adult worm. In malnourished hosts, such
blood loss can lead to severe iron deficiency anemia.

HOOKWORM

ID/CC A 14-year-old malnourished child died soon after hospitalization
dui' Id in extensive small bowel rupture and shock.

HPI He had presented to the emergency room with massive bloody
diarrhea. His history at admission revealed the presence of
abdominal pain, fever, and diarrhea of a few days' duration; his
symptoms had developed after he ate leftover meat at a

fast-food restaurant.

PE He was dehydrated, pale, and hypotensive at lime of admission
and developed signs of peritonitis and shock shorllv before his
death.

Labs Culture and exam of necrotizing intestinal lesions isolated
Clostridium perfringens type C producing beta toxin.

Gross Pathology Autopsy revealed ruptured small intestine, mucosal ulcerations,
and gas production in the wall.

Micro Pathology Microscopic exam revealed necrosis and acute inflammation in

the ileum.

Treatment

Discussion

Patient died despite aggressive fluid and electrolyte replacement,
bowel decompression, and antibiotic therapy (penicillin,
clindamycin, or doxyevi line): surgery had been planned in view
of rupture ol the small bowel.

Necrotizing enterocolitis is a condition affecting poorly nourished
persons who suddenly feast on meat (pigbel). It is associated
with Clostridium perfringens type C and beta enterotoxin; beta
toxin paralyzes the villi and causes friability and necrosis of the
bowel wall. Immunization of children in New Guinea with
beta-toxoid vaccine has dramatically decreased the incidence of
the disease.

Atlas Links [ZLCIZ1 M-M1-033A, M-M1-033B, PG-M1-033

—I

NECROTIZING ENTEROCOLITIS

ID/CC A 7-year-old male who has been hospitalized for treatment of
acute lymphocytic leukemia complains of copious watery
diarrhea, right lower quadrant abdominal pain, and fever.

HPI He was diagnosed as neutropenic (due to aggressive cytotoxic

chemotherapy ) a few days ago.

PE VS: fever; tachycardia; tachypnea. PE: pallor; sternal tenderness;
axillary lymphadcnopathy; hepatosplenomegaly; abdominal
distention; moderate dehydration.

Labs CBC: severe neuu-openia; anemia; thrombocytopenia. PBS and
bone marrow studies suggest he is in remission: blood culture
grows Clostridium seplicum.

Imaging CT, abdomen; thickening of cecal wall.

Gross Pathology Mucosal ulcers and inflammation in ileocecal region of small
intestine.

Treatment Aggressive supportive measures; surgical intervention; appropriate
antibiotics (penicillin G. ampicillin. or clindamycin).

Discussion Neutropenic enterocolitis is a fulminant form of necrotizing

enteritis that occurs in neutropenic patients: neutropenia is often
related to cyclic neutropenia, leukemia, aplastic anemia, or
chemotherapy. In postmortem exams of patients who have died
of leukemia, infections of the cecal area (typhlitis) are
frequently found; Clostridium septicwm is the most common
organism isolated from the blood of such patients.

NEUTROPENIC ENTEROCOLITIS

ID/CC A 25-year-old male complains of midepigastric pain thai usually
brains I to 2 hours after eating and nci asionalh awakens him ai
night,

HPI The paiiem has heen diagnosed with duodenal ulcers several
limes in die past, but his symptoms have consistently recurred
even after therapy with H a blockers, antacids, and sucralfate.

PE \'S: stable. PE: pallor; epigastric tenderness on deep palpation.

Labs CBC: normocytic, normochromic anemia. Stool positive for
occult blood.

Imaging IK. II: ulcerations in annum ol stomach and duodenum: antral
biopsy specimens yield positive urease test.

Gross Pathology

Micro Pathology

Treatment

Discussion

Atlas Links

Grossly round ulcer (may also be oval) seen as sharply
punched-out defect widi relatively straight walls and slight
overhanging ol mucosal margin (heaped-up margin is
characteristic of a malignant lesion); smooth and clean ulcer base.

No evidence of malignancy; antral biopsies reveal presence of
chronic mucosal inflammation.

Triple iherap\ with amoxicillin, metronidazole, and bismuth
subsalicylate; triple therapy with clarithromycin, omeprazole,
and imidazole is now considered effective and relatively free of
side effects.

Helicobacter pylori grows overlying the antral gastric mucosal
cells; 40% of health) individuals and approximately 50% of
patients with peptic disease harbor this organism. Although
H. pylori does not breach die epithelial barrier, colonization of
the antral mucosal layer by this organism is associated with
structural alterations of the gastric mucosa and hence with a
high prevalence of antral gastritis. Despite the fact that //. pylori
docs not grow on duodenal mucosa, ii is strongly associated with
duodenal ulcer, and eradication of the organism in patients with
refractory peptic ulcer disease decreases the risk of recurrence.

M-M1-035A, M-M1-035B, M-M1-035C, PG-M1-035

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PEPTIC ULCER DISEASE (H. PYLORI)

ID/CC A 4-year-old male is brought to the physician by his parents, who
complain that the child has had intense perianal itching,
especially during the night.

HPI The child is otherwise healthy, and his developmental progress
is normal.

PE Perianal excoriation noted.

Labs Cellulose adhesive tape secured to perianal area during the
nighi reveals presence of Enterobius vermicularis eggs that
were flattened on one side, were embryonated, and had a thick
shell; no parasites found on stool exam.

Treatment Strict personal hygiene; drugs used include albendazole,
mebendazole, piperazine, and pyrantel pamoate.

Discussion Infection is caused by Enterobius vermicularis. Adult worms are
located primarily in the cecal region: female adult worms
migrate to the perianal area during the night and deposit their
eggs. Direct person-to-person infection occurs by ingestion and
swallowing of eggs; autoinoculation occurs by contamination of
fingers. The life cycle is completed in about 6 weeks.

PINWORM INFECTION

ID/CC A 10-month-old male presents with fever and severe vomiting
followed by watery diarrhea.

HPI His stools are loose and watery without blood or mucus.

PE VS: fever; tachycardia. PE: child is irritable; moderate
dehydration.

Labs Absence of leukocytes on fecal stain: rotavirus delected with
ELISA; electron microscopy with negative staining identifies
rotavirus on stool ultrafiltrates.

Micro Pathology

Major histopathologic lesions are characterized by reversible
involvement of the proximal small intestine; mucosa remains
intact with shortening of villi, a mixed inflammatory infiltration
of lamina propria, and hyperplasia of the mucosal crypt cells;
electron microscopy reveals distended cisterns of endoplasmic
reticulum, mitochondrial swelling, and sparse, irregular
microvilli.

Treatment Fluid replacement therapy.

Discussion Rotavirus group A is the single most important cause of

endemic, severe diarrheal illness in infants and young children
worldwide; it occurs with greater frequency during winter
months in temperate climates and during the dry season in
tropical climates. In die United States, rotavirus accounts for
50% of all childhood diarrheas, has an incubation period of
48 hours, is transmitted by the fecal-oral route, and lasts only a
few days. Some children subsequently develop lactose intolerance,
which lasts for a few weeks.

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ROTAVIRUS DIARRHEA IN INFANTS

ID/CC A 30-year-old male presents with sudden-onset, crampy
abdominal pain and diarrhea.

HPI The diarrhea is watery and contains mucus. The patient also
Complains of low-grade lever with chills, malaise, nausea, and
vomiting. ( iareful history reveals that he had ingested partially
cooked eggs at a poultry I'arm 2 1 hours before his symptoms
began.

PE VS: fever; tachycardia. PE: mild diffuse abdominal tenderness;
mild dehydration.

Labs Stool culture yields Salmonella typhimurium; stained stool
demonstrates PMNs.

Gross Pathology Intestinal mucosal erythema (limited to the colon) and some
superficial ulcers.

Micro Pathology Mixed inflammatory infiltrate in mucosa; superficial epithelial

erosions.

Treatment Fluid and electrolyte replacement therapy; antibiotics withheld,
as they prolong carrier state. Antibiotic therapy only for
malnourished, severely ill, bactcrcmic, and sickle cell disease
patients.

Discussion Salmonella infection is acquired through the ingestion of food
(eggs, meat, poultry) or water contaminated with animal or
human feces; individuals with low gastric acidity are also
susceptible.

SALMONELLA FOOD POISONING

ID/CC A 50-vear-old alcoholic white male presents with fever, abdominal
pain, and rapicllv progressive disieiiiion of the abdomen.

HPI He was diagnosed with alcoholic cirrhosis 1 month ago. when

he was admitted to the hospital wilh jaundice and hematemesis.

PE VS: fever. PE: icterus; on palpation, abdominal lenderness with
guarding; fluid thrill and shifting dullness to percussion (clue to
ascites): splenomegaly; decreased bowel sounds.

Labs CBC: leukocytosis. Ascitic fluid leukocyte count > 500/ cc;

PMNs (350/cc) elevated; ascitic proieins and glucose depressed:
gram-negative bacilli in ascitic fluid; Escherichia coli isolated in
culture; elevated AST and ALT (AST > ALT).

Imaging KUB: ground-glass haziness (due to ascites); no evidence of free
air. US, abdomen: cirrhotic shrunken liver; ascites;
splenomegaly; increased portal vein diameter and flow. EGD:
esophageal varices.

Gross Pathology Fibrinopurulcnt exudate covering surface of peritoneum;
fibrosis may lead to formation of adhesions.

Micro Pathology PMNs and fibrin on serosal surfaces in various stages with
presence of granulation tissue and fibrosis.

Treatment Specific organism-sensitive antibiotics or empiric therapy (such
as cefotaxime or B-lactamase-resislant penicillin) for
gram-negative aerobic bacilli and gram-positive cocci: supportive
treatment for cii i hosis.

Discussion The spontaneous or primary form of peritonitis occurs in

patients with advanced chronic liver disease and concomitant
ascites; /.. coliis the most common cause of secondary peritonitis.

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SPONTANEOUS BACTERIAL PERITONITIS

ID/CC A 25-year-old male U.S. citizen on vacation in Mexico presents
with abrupt-onset explosive watery diarrhea, abdominal cramps,
and a low-grade fever and chills.

HPI The patient does not complain of tenesmus or passage of blood
or mucus in his stools, but he does complain of a feeling of
urgency to defecate.

PE VS: low-grade fever. PE: unremarkable.

Labs No erythrocytes. VVBCs. or parasites seen in stained stool;

bioassays for enterotoxigenic Escherichia coli (ETEC) reveal
presence of the labile enterotoxin (LT) (tests available only for
research purposes) .

Treatment Fluid replacement; antibiotics (fluoroquinolone or TMP-SMX)
with loperamide; prevention with careful hygienic practices and
prophylactic fluoroquinolone or bismuth subsalicylate with
loperamide.

Discussion Traveler's diarrhea is a self-limited condition that develops

within 1 to 2 days of ingestion of contaminated food or drinks.
Over three-fourths of cases of traveler's diarrhea are caused by
bacteria, with enterotoxigenic E. coli the most frequent cause
(may also be caused by enteropathogenic /'.'. coli and, in Mexico,
by an enteroadherent E. coli ). Other common pathogens
include Shigella species. Campylobacter jejuni. Aeromonas species.
Plesiornonas shigelloides. Salmonella species, and noncholera
vibrios. Rotavirus and Norwalk agent are the most common viral
causes; C.iardia, Cryptosporidium, and. rarely, Entamoeba histolytica
are parasitic pathogens. Enterotoxigenic E. coli produce
enteroloxins that bind to intestinal receptors and activate
adenyl cyclase in the intestinal cell to produce an increase in the
level of the cyclic nucleotides cAMP (LT, labile toxin) and cGMP
(ST, stable toxin), which markedly augments sodium, chloride,
and water loss, diereby producing a secretory diarrhea.

53 TRAVELER'S DIARRHEA

ID/CC A 30-year-old male presents with sudden-onset fever, colicky
abdominal pain, and watery diarrhea.

HPI He had eaten raw oysters at a friend's party the day before
(incubation period 4 hours to 4 days).

PE VS: fever; tachycardia. PE: no dehydration: diffuse abdominal
tenderness; increased bowel sounds.

Labs Vibrio parahaemolyticus isolated from stool in a high-salt-
content (halophilic vibrio) culture medium; PMNs in stool;
Kanagawa phenomenon (beta-hemolysis on medium containing
human blood; done as an indicator for pathogenicity) positive.

Treatment Fluid and electrolyte balance; antibiodcs not required (since
they do not shorten course of infection).

Discussion Seafood is the main source of the organism. After ingestion.
Vibrio parahaemolyticus multiplies in the gut and produces a
diarrheal enterotoxin.

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VIBRIO PARAHAEMOLYTICUS FOOD POISONING

ID/CC A 35-year-old male presents to the emergency room with high-
grade fever, marked weakness, and a hemorrhagic vesiculobullous
skin eruption.

HPI He had just returned from deep-sea fishing in die Gulf of

Mexico, where he had consumed large quantities of seafood.
He has been diagnosed with chronic liver disease (due to
hemochromatosis).

PE VS: fever: hypotension; tachycardia. PE: icterus; vesiculobullous
skin lesions seen on an otherwise-bronzed complexion.

Labs Blood culture on high-salt medium (halophilic bacteria) reveals
growth of Vibrio vulnificus; evidence of hemochromatosis

( hyperglycemia, hyperbilirubinemia, increased serum iron).

Treatment Ceftazidime and doxycycline, ciprofloxacin; supportive.

Discussion Halophilic Vibrio vulnificus should be suspected and treated in any
individual with chronic liver disease who presents with sepdeemia
and skin lesions 1 to 3 days following seafood ingestion.

VIBRIO VULNIFICUS FOOD POISONING

ID/CC A 56-year-old white male complains of diarrhea and bloating for
several months along with ankle swelling.

HPI He also complains of memory loss, fever, arthritis in the knees
and hands, and weight loss.

PE VS: lever. PE: thin, gaunt male; muscle wasting; swollen, tender
right wrist and ankle; axillary and femoral lymphadenopathy;
ecchymoses ol < hesl and arms.

Labs CBC/PBS: macrocytic, hypochromic anemia; hypoalbnminemia;
increased fecal fat (steatorrhea).

Imaging l.'GI/SBFT: nonspecilic dilatation of small bowel.

Gross Pathology Atrophy of intestinal mucosa; inflammatory infiltrate in synovia
of joints.

Micro Pathology

Small bowel biopsy reveals characteristic macrophages
containing bacilli with PAS reagent staining: characteristic

gram-negative actinoinycete bacilli in macrophages, l'MNs. and
epithelial cells of lamina propria; dilated lymphatics; flattening
of intestinal villi.

Treatment Bactrim (TMP-SMX) or ceftriaxone for 1 year.

Discussion Caused by infection with Tropheryma whippelir. produces

malabsorption offal-soluble vitamins, protein, iron, folic acid.
and vitamin B| 2 .

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WHIPPLE'S DISEASE

ID/CC A 28-year-old female complains of painful swelling of both knees
and tender skin eruptions on both shins.

HPI For the past 2 weeks she has also had watery diarrhea that
developed after she consumed some raw pork. She also
complains of low-grade fever and mild abdominal pain.

PE VS: low-grade fever; tachycardia. PE: mild dehydration; swollen
and warm knee joints with painful restriction of all movements
(arthritis); multiple tender, erythematous plaques and nodules
(ERYTHEMA NODOSUM) seen over both shins.

Labs CBC: leukocytosis. Yersinia enterocolitica isolated from stool;
patient is HLA-B27 positive.

Micro Pathology

Oval ulcers with long axis in the direction of bowel flow, similar
to ulcers caused by typhoid fever (intestinal tubercular ulcers
are transverse).

Treatment Supportive; antibiotics (aminoglycosides, fluoroquinolones)
indicated in severe infections.

Discussion Yersinia mleroailitica is an invasive gram-negative intracellular
pathogen that causes gastroenteritis, most frequently involving
the distal ileum and colon (enterotoxin mediated), mesenteric
adenitis (due to necrotizing and suppurative gut lesions) and
ileitis (pseudoappendicitis), and sepsis; infection may trigger a
variety of autoimmune phenomena, including erythema
nodosum, i ca< live arthritis, and possibh < Waves' disease.
especially in HLA-B27-positive individuals. Spread is by the
fecal-oral route and occurs via contaminated milk products or
water, swine, or household pet feces.

YERSINIA ENTEROCOLITIS

ID/CC A 3-year-old albino male is referred to a specialist for an
evaluation of a suspected immune deficiency.

HPI His parents report recurrent respiratory, skin, and oral

infections with gram-negative and gram-positive organisms. He

also has a history of bruising easily.

PE Partial albinism; light-brown hair with silvery tint; nystagmus;
photophobia on eye reflex exam; chronic gingivitis and
periodontitis; purpuric patches over areas of repeated minimal
trauma; mild hepatomegaly; no lymphadenopathy.

Labs CBC/PBS: decreased neutrophil count with normal platelet
count: large cytoplasmic granules (c.ian i l.ysosomes) in WBCs
on Wright-stained peripheral blood smears. Prolonged bleeding
time: impaired platelet aggregation; normal clotting time and
PTT; normal nitroblue tetrazolium test.

Treatment Largely supportive; ascorbic acid, prophylactic antibiotics,
acyclovir.

Discussion Chediak-Higashi syndrome is an autosomal-recessive disorder
thai is due to a defect in polymerization of microtubules in
leukocytes that causes impairment of cbemotaxis, phagocytosis,
and formation of phagolysosomes. Patients with this disorder
usually present with recurrent pyogenic staphylococcal and
streptococcal infections.

CHEDIAK-HIGASHI SYNDROME

ID/CC An 8-year-old child with sickle cell anemia is seen with

complaints of sudden-onsel pallor of the skin and mucous
membranes, fatigue, and malaise.

HPI The- child suffered a mild prodromal illness before developing
severe pallor.

PE VS: no fever; tachycardia: tachypnea; BP normal. PE: severe
pallor; mild icterus; no lymphadenopathy, splenomegaly, or
hepatomegaly noted.

Labs CBC: severe anemia (Hb 2 g/dL); reduced leukocyte and

plaielei counts: mild hvperbilirubinemia; absent reticulocytes
and sickled RBCs on peripheral blood smear.

Micro Pathology

Bone marrow biopsy reveals increased numbers of giant
pronormoblasts (diagnostic of parvovirus infection).

Treatment Blood transfusions to tide over the crises. Spontaneous recovery

in 1 to 2 weeks.

Discussion Parvovirus infection is the cause of transient aplastic crises (may

also be due to folic acid deficiency) that occur in patients who have
severe hemolytic disorders; cessation of erythropoiesis for about 10
days in a normal adult as a result of parvovirus infection would
produce a 10% drop in hemoglobin concentration (i.e., a fall of
1% dailv would lead to a decline in hemoglobin concentration of I
to 2 g/dL after 10 days). A patient with severe hemolysis in
whom the bone mat 1 i >w is turning over at a rale seven times
normal would experience a 70% decrease in hemoglobin con-
centration (i.e., a drop from 10 g/dL to 3 g/dL) as a result of a
10-dav cessation of erythropoiesis. Although parvovirus can
affect all precursor cells, the red cell precursors are most
profoundly affected.

Atlas Link □ □ 1 H-Ml-046

ANEMIA— APLASTIC CRISIS (PARVOVIRUS B19)

ID/CC A 35-year-old Finnish man complains of easy fatigability and
shortness of breath.

HPI He often cats undercooked or raw freshwater fish. He also
reports vague digestive disturbances such as anorexia,
heartburn, and nausea.

PE PE: pallor.

Labs CB( /1'BS: megaloblastic anemia. Blood vitamin B, 2 levels low;
stool exam reveals presence of operculated eggs and proglottids
of Diphyllobothrium latum.

Treatment Niclosamide or praziquantel.

Discussion Diphyllobothrium latum (fish tapeworm) infection is found in cold
climates where raw or undercooked fish are eaten. The adult
worm attaches to the human jejunum and competes for
absorption of vitamin B, 2 . producing a deficiency that resembles
pernicious anemia. Prevention includes proper preparation of
fish.

ANEMIA— DIPHYLLOBOTHRIUM LATUM

ID/CC A 45-year-old male with refractory acute myeloid leukemia who
underwent a bone marrow transplant from a nonidentical
donor presents with an extensive skin rash, severe diarrhea, and
jaundice.

HPI Prior to the transplant, which occurred 2 months ago. he

received preparative chemotherapy and radiotherapy along with
broad-spectrum antibiotics. Engraftment was confirmed within
4 weeks by rising leukocyte counts.

PE VS: BP normal. PE: patient is cachectic and moderately
dehydrated: icterus noted; violaceous, scaly macules and
erythematous papules resembling lichen planus seen over
extremities.

Labs CBC: tailing blood counts; relative eosinophilia. Elevated direct
serum bilirubin and transaminases: stool exam reveals no
infectious etiology: skin biopsy taken.

Gross Pathology

Treatment

Discussion

Skin biopsy specimens reveal vacuolar changes of basal cell layer
with perivenular lymphocytic infiltrates (CD8+ T cells).

High-dose cyclosporine therapy, rabbit anti-thymocyte globulin,
methylprednisolone or anti-T-ceU monoclonal antibodies.

Approximately 30% of bone marrow transplant recipients
develop "lali-versus-host disease- ((AUD). This attack is primarily
launched bv immunocompetent T lymphocytes derived from
the donor's marrow against the cells and tissues of the recipient,
which it recognizes as foreign. Cyclosporin A is effective for
prevention of GVHD.

GRAFT-VERSUS-HOST DISEASE

ID/CC A 20-year-old male presents with an extensive purpuric skin rash,
oliguria, and marked weakness; he also complains of bloody
diarrhea of 1 week's duration.

HPI The patient ate a hamburger at a fast-food restaurant 2 to 3 days
prior to the onset of his diarrhea. He has no associated fever.

PE VS; no fever. PE: dehydration; pallor; extensive purpuric skin
rash.

Labs

Imaging

Micro Pathology

Treatment

Discussion

Atlas Link

Stool examination reveals presence of RBCs but no inflammatory
cells or parasites; culture isolates sorbitol-negative Escherichia
coli; serotyping studies and effect on HeLa cell culture reveal
presence of enterohemorrhagic E. coli (EHEC) serotype
0157:H7. elevated BUN and creatinine. CBC/PBS: microangio-
pathic anemia and thrombocytopenia. PT, PIT normal.

Sigmoidoscopy: moderately hyperemic mucosa with no evidence
of any ulceration.

Pathology localized to kidney, where hyaline thrombi were seen
in afferent arterioles and glomerular capillaries.

Dialysis and blood transfusion for management of HUS; Quid and
electrolyte maintenance; antimicrobial therapy. Most patients who
develop HUS as a complication of E. coli hemorrhagic colitis die
as a result of hemorrhagic complications.

Hemorrhagic colitis associaied with a Shiga-like toxin producing
EHEC 0157:H7 is characterized by grossly bloody diarrhea with
remarkably little fever or inflammatory exudate in stool; a
significant number of patients develop potentially fatal HUS.
EHEC infections can be largely prevented through adequate
cooking of beef, especially hamburgers.

Li _.] H-Ml-049

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HEMOLYTIC-UREMIC SYNDROME (HUS)

ID/CC A 34-year-old male presents to his primary care physician with a
hard, red, painless swelling on his left mandible that has slowly
been growing over die past few weeks and has now begun to
drain pus.

HPI The patient recendy had a tooth extracdon.

PE No acute distress; no other significant findings.

Labs Gram stain of exudate reveals branching gram-positive filaments
and characteristic "sulfur granules": non-acid-fast and anaerobic
(distinguishes actinomyces from Nocardia).

Imaging XR: no bony destruction.

Gross Pathology Sinus tracts from region of infection to surface with granular
exudate.

Micro Pathology

Treatment

Discussion

Granulation tissue and fibrosis surrounding a central suppurative
necrosis; granulation tissue may also enclose foamy histiocytes
and plasma cells.

Ampicillin followed by amoxicillin or penicillin G followed by
oral penicillin V and, if necessary, surgical drainage and removal
of necrotic tissue.

Actinomyces israelii is a part of the normal flora of the mouth
(crypts of tonsils and tartar of teeth), so most patients have a
history of surgery or trauma. There is no person-to-person
spread. Actinomycosis is a chronic suppurative infection and
can also involve the abdomen or lungs, especially following a
penetrating trauma such as a bullet wound or an intestinal
perforation. Pelvic disease is associated with 1UD use. Spread
occurs contiguously, not hcmatogenously.

Atlas Link L'KMI 1 1 M-Ml-050

ACTINOMYCOSIS

ID/CC A 7-month-old girl is brought to the pediatric clinic with

wheezing, respiratory difficulty, and nasal congestion of 3 hours'
duration.

HPI She has had rhinorrhea, fever, and cough and had been
sneezing for 2 days prior to her visit to the clinic.

PE VS: tachypnea. PR: nasal flaring; mild central cyanosis; accessory
muscle use during respiration; hyperexpansion of chest;
expiratory and inspiratory wheezes; rhonchi over both lung fields.

Labs CBC/PBS: relative lymphocytosis. ABGs: hypoxemia with mild

hypercapnia. Respiratory syncytial virus (RSV) demonstrated on

viral culture of lluoal swab.

Imaging CXR: hyperinflation; segmental atelectasis; interstitial infiltrates.

Micro Pathology Severe bronchiolitis produces bronchiolar epidielial necrosis,
lymphocytic infiltrate, and alveolar exudates.

Treatment Humidified oxygen, bronchodilators. aerosolized ribavirin.

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Discussion RSV is the most common cause of bronchiolitis in infants under
2 years of age; other viral causes include parainfluenza,
influenza, and adenovirus. RSV shedding may last 2 or more
weeks in children.

ACUTE BRONCHIOLITIS

ID/CC An 8-year-old female presents with pain and swelling of her knee
joints, elbows, and lower limbs along with fever for the past
2 weeks; she also complains of shortness of breath (dyspnea) on
exertion.

HPI The patient had a sore throat 2 weeks ago.

PE VS: fever. PE: blanching, ring-shaped erythematous rash over
trunk and proximal extremities (erythema marc.i.vyi I'M);
subcutaneous nodules at occiput and below extensor tendons in
elbow; swelling with redness of both knee joints and elbows
(POLYARTHRI i is); painfully restricted movement; pedal edema;
increased JVP; high-frequency apical systolic murmur with
radiation to axillae (mitral valve insufficiency due to carditis);
bilateral fine inspiratory basal crepitant rales; mild, tender
hepatomegaly.

Labs CBC: leukocytosis. Streptococcus pyogenes an throat swab; markedly
elevated ASO titers; elevated ESR; elevated C-reactive protein
(CRP); negative blood culture. EGG: prolonged P-R interval.

Imaging

Gross Pathology

Micro Pathology

CXR: cardiomegaly; increased pulmonary vascular markings.
Echo: vegetations over mitral valve with regurgitation.

Acute form characterized bv endo-, myo-, and pericarditis

( PAN( ARDrns); chronic form characterized by fibrous scarring with

calcification and mitral stenosis with verrucous fibrin deposits.

Myocardial muscle liber necrosis enmeshed in collagen;
characteristic finding is fibrinoid necrosis surrounded by
perivascular accumulation of mononuclear inflammatory cells

(AsCllOKKCItl-S).

Treatment Aspirin, corticosteroids, and diuretics; penicillin or

erythromycin.

Discussion Acute rheumatic fever is a sequela of upper respiratory infection
with group A, p-hemolytic streptococcus; it causes autoimmune
damage to several organs, primarily the heart. The systemic
effects of acute rheumatic fever are immune mediated and are
secondary to cross-reactivity of host antistreptococcal antibodies.

Atlas Link L_1_L_LJ M-Ml-052

ACUTE RHEUMATIC FEVER

ID/CC A 48-year-old missionary who has lived in Cameroon,

West Africa, for 20 years is airlifted home because of lethargy,
nuchal rigidity, persistent headache, and drowsiness that have
not responded to antibiotics and supportive treatment.

HPI He states that over the years he has been bitten in the neck
several times by a muttimutu, or tsetse fly (Gui.ss/\.\ palpaijs).
lie has also had intermittent, generalized erythematous rashes
accompanied by fever.

PE Alert but somewhat incoherent and confused; sometimes
delusional; nuchal rigidity and tremors of face and lips;
splenomegaly; generalized rubbery, painless lymphadenopathy,
predominantly in posterior neck and supraclavicular areas
(Wjnterbottom's sign).

Labs

Gross Pathology

Micro Pathology

PBS/LP: hypercellular, trypanosomal forms present;
lymphocytes in CSF. Elevated IgM.

Chancre with erythema and induration at bite site; chancre
resolves spontaneously; spleen and lymph nodes enlarged
during systemic stage; leptomeninges enlarged during CNS
involvement.

Skin: edema, mononuclear cell inflammation, organisms, and
endothelial proliferation; spleen and lymph nodes: histiocytic
hyperplasia; CNS: mononuclear cell meningoencephalitis.

Treatment Suramin; pentamidine or eflornithine.

Discussion Also called sleeping sickness. African trypanosomiasis is a

systemic febrile disease endemic to Africa whose chronic form
causes a meningoencephalitis. It is caused by the flagellated
protozoans Trypanosoma brucei gambiense (West African) and
Trypanosoma brum rhodesiense (East African), which are transmitted
by the tsetse fly.

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AFRICAN TRYPANOSOMIASIS

ID/CC A 28-year-old male homosexual complains of continuous

low-grade fever, weight loss, and diarrhea of 1 month's duration.

HPI He also complains of an extensive skin rash, mucous membrane
eruptions, recurrent herpes zoster infection, and oral
ulcerations. He reports practicing receptive anal intercourse.

PE VS: low-grade fever. PS: cachectic; generalized lymphadenopathy;
maculopapular rash: severe seborrheic dermatitis; aphthous
ulcers: while confluent patch with corrugated surface (oral.
HAIRY LEUKOPLAKIA) along lateral borders of tongue: penile warts

(i MMiM.nMAi \ v i mix m \ i; extensive multiple pruritic, pink.
umbilicaied papules 2 to 5 mm in diameter (molli si i m
contac.iosum).

Labs CBC: anemia; leukopenia with lymphopenia; thrombocytopenia.
Low CD4+ count; elevated CD8+ T-cell count; ELISA for HIV-1
positive; Western blot confirmatory; PCR for viral RNA

(investigation of choice in window period) positive.

Micro Pathology

Treatment

Oral hairy leukoplakia; lesions show keratin projections
resembling hairs, koilocytosis, and little aiypia; hybridization
techniques reveal Epstein-Barr virus in lesions.

Prophylactic antibiotics for prevention of opportunistic
infections while monitoring CD4+ T-cell counts; anthetioviral
drugs (zidovudine, didanosine, zalcitabine, and protease
inhibitors); counseling and rehabilitative measures.

Discussion AIDS-related complex (ARC) consists of symptomatic conditions
in an HIV-infected patient thai are noi included in the AIDS
surveillance case definition and that meet at least one of the
following criteria: (1) the conditions are indicative of a defect in
i ell-mediated immunity: oi ("_') the conditions have a ( linical
course or management that is complicated by HIV infection.

Atlas Link QUI Z-Ml-054

AIDS-RELATED COMPLEX (ARC)

ID/CC A 28-year-old male from India complains of gradual-onset, inter-
mittent, crampy abdominal pain with one to four foul-smelling,
frothy loose stools daily.

HPI His stools sometimes contain blood and mucus. He also

complains of flatulence, tenesmus, and, at times, alternating
diarrhea and constipation.

PE Slight tenderness during palpation of cecum and ascending
colon; no hepatomegaly.

Labs CBC: mild leukocytosis; no eosinophilia. Fresh stool examinadon
reveals presence of Entamoeba histolytica cysts and motile
hematophagous trophozoites; serology for antiamebic antibodies
is positive.

Imaging

Micro Pathology

Treatment

Colonoscopy: multiple colonic mucosal ulcers [hat are slightly
raised and covered with shaggy exudate; mucosa between ulcers
normal.

Biopsy specimens reveal lesions extending under adjacent intact
mucosa to produce classical "flask-shaped" ulcers; amebic
trophozoites demonstrated at base of ulcer.

Metronidazole (drug of choice) followed by paromomycin or
iodoquinol.

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Discussion Entamoeba histolytica cysts are infective and are transmitted

through contaminated water, raw vegetables, food handlers, and
fecal-oral or oral-anal contact. The siles of involvement, in order
of frequency, are the cecum and ascending colon, rectum,
sigmoid colon, appendix, and terminal ileum. Trophozoites are
the invasive form of the organism, causing colitis or distant
infection by hematogenous spread. Complications include
perforation of the bowel; liver abscess with pleural, pericardial,
or peritoneal rupture; bowel obstruction by ameboma; and skin
ulcers around the perineum and genitalia.

Atlas Link

M-Ml-055

AMEBIC COLITIS

ID/CC A 45-year-old male Peace Corps volunteer who recently spent
2 years in rural Mexico complains of a spiking fever, malaise,
headache, and right upper quadrant abdominal pain.

HPI He admits to having had bloody diarrhea with mucus

(nvsi-MiRY) and tenesmus dial disappeared with some pills that
he took several months ago.

PE VS: fever (39.6°C). PE: pallor: slight jaundice; tender 3 +
hepatomegaly with no rebound tenderness; pain on list
percussion of right lower ribs.

Labs CBC: leukocytosis with neutrophilia. Amebic cysts in stool

specimen (not concurrent with abscess); positive serology for
antibodies to Entamoeba histolytica.

Imaging

Gross Pathology

CXR: elevation of right hemidiaphragm; small right pleural
effusion. CT/US: cavitating lesion in right lobe of liver (due to

abscess).

Multiple colonic mucosal ulcers, slightly raised and covered with
shaggy exudate: enlarged liver with one large abscess on right
lobe containing chocolate-colored pus; abscess may rupture and
spread to lungs, brain, or other organs.

Micro Pathology Sierile pus; ann-b.i may be obtained from periphery of lesion.

Treatment Metronidazole; needle evacuation; surgery in case of treatment
failure or rupture.

Discussion Prior travel lo endemic areas plus a triad ol lever, hepatomegaly,
and right upper quadrani pain are hallmarks of hepatic liver
abscess. Colitis precedes the liver abscess: amebas llien invade
the gut wall and enter portal circulation.

AMEBIC LIVER ABSCESS

ID/CC A 15-year-old male who resides in Florida presents with nausea
and vomiting, fever, and marked neck stiffness.

HPI He also complains of a severe bifrontal headache. Careful

liisioi v reveals that he swam for several hours in brackish water

approximately a week ago.

PE VS: fever; tachycardia. PE: signs of meningeal irritation (neck
rigidity, positive Kernig's sign and Brudzinski's sign):
I'unduscopy reveals mild papilledema.

Labs

Gross Pathology

Micro Pathology

LP: bloody CSF (raised RBC count may also be due to examiner's
inability to recognize proliferating amebas) shows intense
neutrophilia, pleocytosis, high protein, and low sugar; no
organism seen on Gram, ZN. or India ink staining of CSF; wet
preparation of CSF reveals viable Naegleria trophozoites;
diagnosis confirmed using direct fluorescein antibody staining.

lesions are mostly present in the olfactory nerves and brain.
Focal hemorrhages, extensive fibrinoid necrosis, and blood
vessel thrombosis with nerve tissue necrosis.

Naegleria fowkri trophozoites seen as 10- to 20-u.in-diameter
oiganisms with large nucleus, small granular cytoplasm, distinct
ectoplasm, and bulbous pseudopodia.

Treatment Intracisternal and IV amphotericin B, miconazole, rifampin;
prognosis is very poor.

Discussion Primary amebic meningoencephalitis is caused by amebas of the
genus Niu-gfcrin or Arniilliamoi'l/ri. The former most often affects
children and voting adults, appears to be acquired by swimming
in warm, fresh/brackish water, and is almost always fatal, with
die ameba gaining entry into die arachnoid space through the
nasal cribriform plate. Acantkamoeba infections involve older,
immunocompromised individuals and are sometimes
characterized by spontaneous recovery.

AMEBIC MENINGOENCEPHALITIS

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ID/CC A 30-year-old male goes to the emergency room because of
dyspnea, cyanosis, hemoptysis, and chest pain.

HPI He lias had a high lever, malaise, and a nonproductive cough for
1 week. The patient is a sheep farmer who remembers having
been treated for dark black skin lesions in the past.

PE VS: fever. PE: dyspnea; cyanosis; bilateral rales heard over lungs.

Labs CBC: normal. Negative blood and sputum cultures; diagnosis
of anthrax confirmed by fourfold increase in indirect
microhemagglutination titer.

Imaging CXR: mediastinal widening. CT, chest: evidence of
"hemorrhagic mediastinitis."

Gross Pathology Patchy consolidation: vesicular papules covered by black eschar.

Micro Pathology Lungs show fibrinous exudate with many organisms but few
PMNs.

Treatment Isolate and treat with TV penicillin G or ciprofloxacin.

Discussion

Anthrax is caused by infection with Bacillus anthracis. A
cell-free anthrax vaccine is available to protect those employed
in industries associated with a high risk of anthrax transmission
(farmers, veterinarians, tannery or wool workers) .

ANTHRAX

ID/CC A 38-year-old male receiving cytotoxic chemotherapy

(immunosuppressed) for acute leukemia presents with pleuritic
chest pain, hemoptysis, fever, and chills.

HPI He also complains of dyspnea, tachypnea, and a productive
cough,

PE VS: fever: PE: severe respiratory distress; bilateral rales heard
over lungs.

Labs CBC: severe neutropenia. Negative blood and sputum culture
for bacteria.

Imaging CXR: necrotizing bronchopneumonia.

Gross Pathology Necrotizing bronchopneumonia: abscesses.

Micro Pathology Lung biopsy identifies Aspergillus -with septate, acutely branching
hvphae (visualized by silver stains); necrotizing inflammation;
vascular thrombi with hyphac (due to blood vessel invasion).

Treatment IV amphotericin B or itraconazole.

Discussion The most lethal form of infection, invasive aspergillosis, is seen
primarily in severely immunocompromised individuals, i.e.,
patients with AIDS: patients with prolonged, severe neutropenia
following cytotoxic chemotherapy; patients with chronic
granulomatous disease; and patients receiving glucocorticoids
and Other immunosuppressive drugs (e.g., transplant recipients).

Atlas Links UTEX M-M1-059A, M-M1-059B, M-M1-059C

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ASPERGILLOSIS

ID/CC A 50-year-old male presents to the ER with complaints of

recurrent, sudden-onset, severe breathlessness, wheezing, fever,
chills, and a productive cough (sometimes producing brown
bronchial casts) .

HPI The patient has had steroid-dependent chronic bronchial

asthma for many years and has no history of foreign travel or
contact with a TB patient. He has a history of occasional
hemoptysis.

PE VS: fever; marked tachycardia; severe tachypnea. PE: respiratory
distress; central cyanosis; wheezing: rhonchi and coarse rales
over both lung fields.

Labs CBC: eosinopbilia. Oxygen saturation low. Very high liters of
specific IgE antibodies against Aspergillus present (specific
marker for the disease); sputum cultures positive for Aspergillus;
skin tests to Aspergillus -antigens positive. PFI's: obstructive
picture (due to underlying asthma).

Imaging CXR: segmental infiltrate in upper lobes (these infiltrates are
segmental because they correspond directly to the affected
bronchi); branching, fingerlike shadows from mucoid impaction
of dilated central bronchi (virtually pathognomonic of allergic
bronchopulmonary aspergillosis). CT, chest: evidence of
proximal bronchiectasis.

Treatment Oral corticosteroids or beclomethasone.

Discussion Allergic bronchopulmonary aspergillosis (ABPA) is a

hypersensitivity disorder that primarily affects the central
bronchi: immediate and Arthus-type hypersensitivity reactions
are involved in its pathogenesis. The onset of the disease occurs
most often in the fourth and lillh decades, and virtually all
patients have long-standing atopic asthma. Untreated ABPA
leads to proximal bronchiectasis.

ASPERGILLOSIS— ALLERGIC BRONCHOPULMONARY

ID/CC A 50-year-old alcoholic male presents with a high-grade fever,
cough, copious, foul-smelling sputum, and pleuritic right-sided
chest pain.

HPI His wife reports that he was brought home in a semiconscious
state a few days ago, when he was found lying on the roadside
heavilv under the influence of alcohol.

PE VS: fever. PE: signs of consolidation elicited over right middle
and lower pulmonary lobes.

Labs Sputum reveals abundant PMN leukocytes and mixed oral flora;
culture yields Bacteroides melaninogenicus (Prevotella
melaninogenica ) and other Bacteroides species, Fusobacterium,
microaerophilic streptococci, and Peptostreptococcus.

Imaging ( ;XK: consolidation involving apical segment of right lower lobe
and posterior segments of middle lobe; large cavity with air-fluid
level (abscess) also seen.

Treatment Clindamycin.

Discussion Alcoholism, drug abuse, administration of sedatives or anesthesia.
head trauma, and seizures or other neurologic disorders are
most often responsible for the development of aspiration
pneumonia. Because anaerobes are the dominant flora of the
upper GI tract (outnumbering aerobic or facultative bacteria by
10 to I ), they are the dominant organisms in aspiration pneu-
monia; of particular importance are Bacteroides melaninogenicus
( Prevotella melaninogenica) and other Bacteroides species (slender,
pleomorphic, pale gram-negative rods), Fusoiia el 'mum nucleatum
(slender gram-negative rods with pointed ends), and anaerobic
or microaerophilic streptococci and Peptostreptococcus (small
gram-positive cocci in chains or clumps).

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ASPIRATION PNEUMONIA WITH LUNG ABSCESS

ID/CC A 38-year-old HIV-positive male is admitted to the hospital with
fever, rigors, night sweats, and diarrhea.

HPI He reports excessive weighi loss over the pasi few weeks. He was
treated lor Pneumocystis pneumonia a few weeks ago and still
reports a persistent productive cough.

PE \'S: lexer. PE: palieni is extremely emaciated: hcpaiosplenomegaly
and lymphadenopathy noted.

Labs

Imaging

Micro Pathology

CD4+ count < 50/cc: Mycobacterium aviutn-iiitracellulare
isolated on blood culture; smears of tissues obtained from
lymph nodes, bone marrow, spleen, liver, and lungs reveal
evidence of acid-fast bacilli, and cultures yield ML avium;
intestinal infection with M. avium proven by culture of stools
and colonic biopsy specimens.

CT. abdomen: hepatosplenomegaly; retroperitoneal

lymphadenopathy; bowel mucosal fold thickening.

Despite the presence of many mycobacteria and macrophages,
well-formed granulomas were typically absent due to profound
impairment of cell-mediated immunity.

Treatment The primary treatment regimen includes clarithromycin and

ethambutol with or without rifabutin. The failure rate of therapy
is high.

Discussion Mycobacterium avium complex is now the most frequent
opportunistic bacterial infection in patients with AIDS; it
typically occurs late in the course of the syndrome, when other
opportunist ii infections and neoplasia have already occurred.
Prophylaxis against M. avium-intrairltularea recommended in
AIDS patients with a CD4+ count of < LOO/ram 3 (administer
azithromycin, clarithromycin, or rifabutin).

ATYPICAL MYCOBACTERIAL INFECTION

ID/CC A 20-year-old male from India presents to the ER with severe
nausea and vomiting.

HPI Careful history reveals that 2 hours ago he ate some

unrefrigerated fried rice that his wife had cooked the night
before. He does not complain of any fever or diarrhea (may or
may not be present) .

PE VS: no fever. PE: mild dehydration; diffuse mild abdominal
tenderness.

Labs Fecal staining reveals no RBCs, WBCs, or parasites; Bacillus

cereus, a gram-positive rod, isolated from vomitus and stool and
shown to produce the emetogenic enterotoxin.

Treatment Supportive.

Discussion Bacillus cereus causes two distinct syndromes: a diarrheal form
(mediated by an Escherichia ro/JLT-type enterotoxin witb an
incubation period of 8 to lb hours: caused by meats and
vegetables) and an emetic form (mediated by a Staphylococcus
aureus-XYpe enterotoxin with an incubation period of 1 to
8 hours; caused by fried rice). Proper food handling and
refrigeraiion of boiled rice are largely preventive.

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BACILLUS CEREUS FOOD POISONING

ID/CC A MO-vcar-old male who recently emigrated from Peru presents
wiili an extensive nodular skin eruption, mild arthralgias, and
occasional fever.

HPI One month ago. the patient had a high-grade fever that was
accompanied by excessive weakness, dyspnea, and passage of
cola-colored urine; the fever subsided after '_' weeks, bill his
weakness has progressed since that lime.

PE Pallor; mild icterus; extensive skin rash comprising purplish
nodular lesions of varying sizes seen on face, trunk, and limbs;
mild hcpaiosplenomcgaly; lunduscopy reveals retinal
hemorrhages.

Labs

Micro Pathology

Treatment

Discussion

Intraerythrocytic coccobacillary-form bacteria \isible in thick
and thin 61ms stained wild Giemsa; bacteria seen and isolated
from skin lesions; indirect serum bilirubin elevated. PBS;
macrocytic, hypochromic anemia with poh/chromasia; marked
reticulocytosis (due io hemolytic anemia); Coombs' lest negative.

Skin biopsy of vascular skin lesions reveals endothelial proliferation
and histiocytic hyperplasia; electron microscopy of verrucous tissue
sin iws Bartonella bacilliformis in interstitial tissue.

Chloramphenicol, penicillin, erythromycin, norfloxacin, and
tetracycline are effective; rifampicin is indicated for treatment of
verrucous forms.

Bartonellosis is a sandfly-borne bacterial disease occurring only
on ihe western coast of South America at high altitudes: the
causative agent is a motile, pleomorphic bacillus, Bartonella
bacilliformis. Two stages of the disease are recognized: an initial
febrile stage associated with a hemolytic anemia (Oron \ 1 1 \ 1 k)
and a later cutaneous stage characterized by hemangiomatous
nodules (VERRUGA PERI ana).

BARTONELLOSIS

ID/CC A 32-year-old male is referred to a tertiary care center with
chronic pneumonia and warty lesions on his left upper limb.

HPI The patient is from the southeastern United States. His skin

Lesions are nonpruritic and painless. He also complains of
malaise, weight loss, night sweats, chest pain, breathlessness, and
hoarseness.

PE VS: fever; tachycardia; mild tachypnea. PE: bilateral rales and
rhonchi; raised, verrucous, and crusted lesions with serpiginous
border located on left upper extremity; small abscesses
demonstrable when superficial crust was removed.

Labs Sputum and pus from cutaneous lesions demonstrate spherical
cells (8 to 15 mm in diameter) that have a thick-walled,
refracdle double contour and show unipolar (broad-based)
budding: culture of pus and sputum on Sabouraud's agar yields
growth of Blastomyces; no evidence ol acid-fast bacilli found
either on staining or on culture; Gomori's methenamine silver
staining of lung tissue does not reveal Pneumocystis.

Imaging CXR: bilateral alveolar consolidations with air bronchogi urns.

Micro Pathology

Epithelioid macrophages and giant cells surrounding a
suppurative center; skin lesions show pseudoepiiheliomatous
hyperplasia very similar to squamous cell carcinoma.

Treatment Itraconazole is treatment of choice in most patients;

amphotericin B, fluconazole, and kctocona/.ole are alternative
drugs.

Discussion

Blastomycosis is a systemic mycotic infection ol humans and
dogs that is characterized b\ suppuration and granulomatous
lesions and is caused by the dimorphic fungus Blastomyces
dermatitidis, the disease is endemic in the southeastern and
south-central pordons of the United States, and several po< ki is
of infection extend north along the Mississippi and Ohio rivers
into central Canada. Clinical disease most commonly involves
the lungs (acquired by spore inhalation) and then, by
hematogenous dissemination, the skin, the skeletal system, and
the male genitourinary tract. Infection cannot be passed from
person to persi in.

Atlas Link LIT LJ M-Ml-065

BLASTOMYCOSIS

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ID/CC A 25-year-old male presents with sudden-onset double vision
(DIPLOPIA), dry mouth, weakness, dysarthria, and dysphagia.

HPI He has no previous history of episodic weakness or of dog or
rick bites (vs. myasthenia gravis, rabies, or Lyme disease). Last
night, he ate some home-canned food.

PE VS: no fever. PE: patient alert; ptosis; bilateral third and tenth
cranial nerve palsy; symmetric flaccid paralysis of all four limbs;
deep tendon reflexes reduced; no sensory loss seen; decreased
bowel sounds.

Labs Botulinum toxin detected in patient's serum and canned-food
sample with specific antiserum.

Treatment Antitoxin; close monitoring of respiratory status; intubation for
respiratory failure.

Discussion

The disease is characterized by gradual return of muscle
sircngth in most cases. Botulinum toxin is a zinc
metalloprotease that cleaves specific components of synaptic
vesicle docking and fusion complexes, thus inhibiting the
release of acetylcholine at the neuromuscular junction. The
disease in adults is due to ingestion of the toxin rather than to
bacterial infection. Botulism is also seen in infants secondary to
the ingestion of Clostridium bolulinuin spores in honey.

BOTULISM

ID/CC A 28-year-old while male visits his family doctor complaining of
acute pain in both hip joints together with weakness, backache,
myalgias, arthralgias, and undulating fever of 2 months'
duration; this morning he woke up with pain in his right testicle.

HPI For the past 3 years he has worked ai the largest dairy farm in
his slate. He enjoys drinking "crude" milk.

PE VS: fever. PE: pallor; marked pain on palpation of sacroiliac
joints; mild splenomegaly; generalized lymphadenopathy.

Labs CBC: relative lymphocytosis with normal WBC count. Positive
agglutination titer (> 1:160); rising serologic titer over time;
small gram-negative rod Brucella abortus on blood culture.

Imaging XR, hips: joint effusion and soft tissue swelling without
destruction. MR, spine: evidence of spondylitis.

Gross Pathology Lymphadenopathy and splenomegaly; hepatomegaly rare.

Micro Pathology Granulomatous foci in spleen, liver, and lymph nodes, with

proliferation of macrophages; epithelioid and giant cells may be

Treatment Combination therapy with doxycycline or TMP-SMX and
rifampin or streptomycin.

Discussion Also called Malta fever, a microbial disease of animals, brucellosis
is caused by several species of Brucella, a gram-negative, aerobic
coccobacillus. It is transmitted to humans through the drinking
ol Contaminated milk or through direct contact with products
or i issues from animals such as goats, sheep, camels, cows, hogs,
and dogs. The clinical picture is often vague; thus, a high index
of suspicion may be necessary for diagnosis.

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BRUCELLOSIS

ID/CC A 26-year-old female presents to the ER with intense, acute-onset
left lower quadrant crampy abdominal pain, foul-smelling stools
with streaks of blood, urgency, tenesmus, and fever.

HPI For the past 2 days, the patient has also had headaches and

myalgias. She frequently drinks unpasteurized ("raw") milk thai
she buys at a health-food store.

PE VS: fever (39°C); tachycardia; normal RR and BR PE: no

dehydration; diffuse abdominal tenderness more marked in left
lower quadrant.

Labs Stool smear shows leukocytes (due to invasive tissue damage in
I he colon) and gram-negative, curved bacilli, often in pairs, in
"gull-wing"-shaped pattern; dark-field exam shows motility;
culture in microaerophilic, 42°C conditions on special agar
yields Campylobacter jejuni, indicated by oxidase and catalase
positivity.

Gross Pathology Friable colonic mucosa.

Micro Pathology

Treatment

Discussion

Nonspecific inflammatory reaction consisting of neutrophils,
lymphocytes and plasma cells with hyperemia, edema and
damage to epithelium, glandular degeneration, ulcerations, and
crypt abscesses caused by colonic tissue invasion of the
organism.

Self-limiting disease. Severe cases (i.e., high fever, severe
diarrhea) can be treated with fluoroquinolones.

One of the primary causes of "traveler's diarrhea." Sources of
infection include undercooked food and contact with infected
animals and their excreta. Prevent by improving public
sanitation, pasteurizing milk, and proper cooking.

CAMPYLOBACTER ENTERITIS

ID/CC A 49-year-old morbidly obese, diabetic woman presents with
pruritus in the skin folds beneath her breasts.

HPI She admits to having this problem chronically, especially in the
warm summer months, when she perspires more heavily.

PE Superficially denuded, beefy-red areas beneath breasts with
satellite vesicopustules and whitish curd-like concretions on
surface.

Labs ( 'lusters of budding cells with short hyphae seen under high-
power lens after skin scales have been put in 10% KOH;
Candida albicans isolated in Sabouraud's medium.

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Gross Pathology

Rash has whitish-creamy pseudomembrane that covers an
erythematous surface.

Micro Pathology Yeast invades superficial layers of epithelium.

Treatment Keep affected areas dry; clotrimazole or other antifungal agents
locally.

Discussion Other superficial areas of infection include the oral mucosa
(thrush), vaginal mucosa (vaginitis), and esophagus (GI
candidiasis). Systemic invasive candidiasis may be seen with
immunosuppression, in patients receiving chronic broad-spectrum
antibiotics, in AIDS patients, or in those receiving
hyperalimentation.

CANDIDIASIS

ID/CC A 25-year-old female presents with painful lumps in her right
axilla and neck together with low-grade fever.

HPI Three weeks ago she was scratched on her right forearm by her
pet cat; an erythematous pustule initially developed at the site
but resolved spontaneously within 10 days.

PE VS: fever. PE: tender right axillary and cervical
lymphadenopathy.

Labs Lymph node biopsy diagnostic; serologic indirect immunofluo-
rescent antibody test for Bartonella henselae is positive.

Micro Pathology

Hematoxylin and eosin staining reveals granulomatous
pathology with stellate necrosis and surrounding palisades of
histiocytic cells; Warthin-Starry silver stain reveals clumps of
pleomorphic, strongly argyrophilic bacilli.

Treatment Symptomatic; fluctuant node may need aspiration; azithromycin
given to immunocompromised patients.

Discussion Bartonella henselae is the agent that causes cat-scratch disease.
Lymphadenopathy can persist for months and can sometimes
be mistaken for a malignancy. Individuals who are
immunocompromised may present with seizures, coma,
and meningitis.

CAT-SCRATCH DISEASE

ID/CC An 8-year-old white female enters the emergency room

complaining of headache, malaise, and bipalpebral swelling of
the right eye.

HPI She recently returned from a year-long stay in Brazil, where her
father works as a logger in the Amazon forest. Over the past
week she had a high fever, which was treated at home as malaria.

PE VS: fever (39°C); tachycardia. PE: right eyelid swollen shut

(Romania's SIGN); markedly hyperemic conjunctiva; ipsilateral
retroauricular and cervical lymph nodes; hepatosplenomegaly.

Labs PBS: trypanosomes on thick blood smear. ECG: right bundle-
branch block; ventricular extrasystoles.

Gross Pathology Encapsulated, nodular area (chagoma) or Romana's sign may
be seen at point of entry, commonly the face.

Micro Pathology

Intense neutrophilic infiltrate with abundant macrophages at
site of entry: myocardial necrosis with mononuclear cell
infiltration; pseudocysts in infected rissues contain parasites thai
multiply within cells; denervation of myenteric gut plexus.

Treatment X'ifurtimox for acute disease.

Discussion C'.hagas' disease is a parasitic disease that is restricted to the
Americas (endemic in South and Central America) and is
produced by Trypanosoma cruzi. a thin, undulating flagellated
protozoan; it is transmitted by contamination of a reduviid
bug bite with injection of its feces. Also known as American
trypanosomiasis. Long-standing cases show myocardial
involvement with dilated cardiomyopathy, life-threatening
conduction defects, and apical aneurysm formation and may
also show megaesophagus or megacolon.

Atlas Link DEUE M-Ml-071

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CHAGAS' DISEASE

ID/CC A 35-year-old male complains of cough productive of
mucopurulent sputum and breathlessness.

HPI Before the onset of these symptoms, he had a sore throat with
hoarseness. He has no history of hemoptysis, sharp chest pain,
or high-grade fever.

PE Crepitations heard over left lung base.

Labs CBC: normal leukocyte count. Sputum exam revealed no bacterial
organism: microimmunofluorescence detected species-specific
antibodies directed against Chlamydia outer-membrane proteins;
cultivation of C. pneumoniae demonstrated on HEp-2 and HL
cell lines.

Imaging GXR: left lower lobe subsegmental infiltrate with interstitial
pattern.

Treatment Doxycycline is the drug of choice; erythromycin and
fluoroquinolones may also be used.

Discussion The peak incidence of chlamydia pneumonia is in young adults.
The mode of transmission would appear to be from person to
person.

CHLAMYDIA PNEUMONIA

ID/CC An 8-year-old male who recently emigrated from India presents
with bilateral eye irritation and photophobia.

HPI He reports recurrent episodes of similar eye irritation and
redness in the past.

PE Conjunctival congestion; multiple (> 5) follicles, each at least
0.5 mm in diameter, seen in upper tarsal conjunctiva;
inflammatory thickening of tarsal conjunctiva; new vessels
(pannus) seen in cornea at superior limbns; punctate keratitis.

Labs Diagnosis confirmed by demonstration of characteristic

cytoplasmic inclusion bodies (Halberstaedter-Prowa/kk BODIES)
in Giemsa staining of conjunctival scrapings.

Micro Pathology

Chlamydia trachomatis is typically seen in conjunctival scrapings in
colony form in the epithelial cells as H-P inclusion bodies.
I lisiologically there is lymphocytic infiltration involving the
whole adenoid layer of parts of the conjunctiva; special
aggregations of lymphocytes form follicles that tend to show
necrosis and certain large multinucleated cells (Leber's cells).

Treatment Topical tetracycline with systemic tetracycline/doxycycline/

erythromycin/azithromycin; prophylaxis of family contacts with
topical tetracycline'.

Discussion Chlamydia trachomatis causes a variety of ocular diseases, including
neonatal inclusion conjunctivitis, sporadic inclusion conjunctivitis
in adults, and sporadic as well as endemic trachoma: trachoma is
endemic in North Anica, in the Middle East, and among the
Native American population of the southwestern United States.
In endemic areas, trachoma is transmitted from eye to hand to
eye. especially among young i hildren in regions where standards
of cleanliness are poor. Sporadic U'achoma infection in
nonendemic areas as well as sporadic inclusion conjunctivitis in
adults results from transmission of the agent from the genital
tract to the eye. Trachoma is a major cause of blindness in
endemic areas.

Atlas Link mcra 1 1 m-mi-073

CHLAMYDIA TRACHOMATIS

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ID/CC A 30-year-old man has sudden severe, profuse (several liters per
day) watery diarrhea, protracted vomiting, and abdominal pain.

HPI He has just returned from a trip to rural India.

PE Severe dehydration; low urine output; generalized mild abdominal
tenderness with no signs of peritoneal irritation; stools have
characteristic "rice-water" appearance; (gray, slightly cloudy
fluid with flecks of mucus), with no blood.

Labs Stool culture reveals gram-negative rods with "darting motility";
Ol antigen detected; Vibrio cholerae isolated on culture media;
serum chloride levels decreased; serum sodium levels increased.

Treatment Vigorous rehydration therapy with oral and/or IV fluids;
tetracycline, ciprofloxacin, or doxycycbne.

Discussion A heat-labile exotoxin produced by Vibrio cholerae thai acts by
permanently stimulating G s protein via ADP ribosylation.
resulting in activation of intracellular adenylate cyclase, which in
turn increases cAMP levels and produces secretory diarrhea.

CHOLERA

ID/CC A newborn baby is referred to the pediatrician for further

evaluation of an unusually small head, low birth weight, and an
extensive erythematous rash.

HPI Intrauterine growth retardation was prenatal ly diagnosed on

ultrasound. The child's mother had a flulike episode during the
first trimester of her pregnancy.

PE Small for gestational age; generalized hypotonia with sluggish
neonatal reflexes; extensive "pinpoint" petechial skin rash
(MULBERRY MUFFIN RASH); microcephaly; chorioretinitis; mild
icterus; hepatosplenomegaly; sensorineural hearing loss in right

Labs CBC/PBS: mild thrombocytopenia; atypical lymphocytosis.

Moderately elevated direct serum bilirubin and transaminases.
UA: cells in urine found to have large intranuclear inclusions
(owl's eye inc.i.i skins); cytomegalovirus isolated on tissue
culture.

Imaging XR/CT, head: periventricular calcifications; microcephaly.

Treatment Ganciclovir (only for immunocompromised patients).

Discussion A congenital herpesvirus infection involving the CNS with eye
and ear damage, congenital cytomegalovirus is a common cause
of mental retardation.

CMV— CONGENITAL

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ID/CC A 1 3-year-old white female visits her pediatrician complaining of
fever, severe dyspnea, and a dry cough.

HPI She was recently diagnosed with acute lymphocytic leukemia, for
which she received a bone marrow transplant. She is currently
on immunosuppressive therapy.

PE VS: fever; tachypnea. PE: pallor; crepitant rales over both lung
fields; mild cyanosis: no hepatosplenomegaly.

Labs CBC/PBS: anemia; leukopenia. ABGs: hypoxemia. No organism
in induced sputum stained with Gram, Giemsa, ZN, and
methenamine silver.

Imaging
Gross Pathology
Micro Pathology

Treatment
Discussion

CXR: diffuse, bilateral interstitial infiltrates.
Interstitial pneumonitis; hepatitis.

Characteristic intranuclear inclusions with surrounding halo

(OWL'S- OR 1st 1 .1 's-ivi i ki is) on transbronchial lung biopsy.

Ganciclovir (CMV is resistant to acyclovir).

An enveloped, double-stranded DNA virus belonging to die
In' i pesvirus group; die mosi c< mimon cause ol pneumonia and
death in bone marrow transplant patients. It is also common in
AIDS patients.

Atlas Link U_D_. M-Ml-076

CMV PNEUMONITIS

ID/CC A 30-year-old homosexual white male presents to his family
physician with a rapidly progressive diminution of vision.

HPI He is known to be HIV positive and periodically comes in for
checkups.

PE Cotton-wool exudates, necrotizing retinitis, and perivascular
hemorrhages on funduscopic exam.

Treatment Ganciclovir; foscarnet (CMV is resistant to acyclovir).

Discussion CMV retinitis is an important treatable cause of blindness that
occurs in 20% of AIDS patients; 50% to 60% of patients develop
retinal detachment within 1 year. Toxoplasmosis and progressive
multifocal leukoencephalopathy (PML) are other important
causes of blindness in AIDS patients.

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CMV RETINITIS

ID/CC A 19-year-old migrant worker from the southwestern

United States is brought to the family doctor complaining of
cough, pleuritic chest pain, fever, and malaise.

HPI He also complains of a backache and headache along with an
erythematous skin rash (due to hypersensitivity reaction) in his
lower limbs.

PE VS: fever; tachypnea. PK: central trachea; coarse, crepitant rales
over both lung bases; tender, erythematous nodules over shins

(l.RYim-.MA \oiiosr\i); periarticular swelling of knees and ankles.

Labs Positive skin test with coccidioidin; dimorphic fungi (hyphae in
soil; spherules in body tissue); Coccidioides immitis on silver stain
and sputum culture; positive latex agglutination test. CBC/PBS:
eosinophilia.

Imaging CXR: nodular infiltrates and thin-walled cavities in both lower
lungs.

Gross Pathology Caseating granulomas; often subpleural and in lower lobes;
necrosis and cavitation may also be present.

Micro Pathology Silver-stained tissue sections show spherules filled with
endospores.

Treatment Amphotericin II or itraconazole.

Discussion Endemic in the southwestern United States, coccidioidomycosis
is produced by C. immitis and is transmitted by inhalation of
arthrospores. Systemic dissemination is frequent in blacks as
well as in immunosuppressed and pregnant patients. Meningitis
or granulomatous lung disease may result, which may lead to
death.

COCCIDIOIDOMYCOSIS

ID/CC A 28-year-old male who lives in the northwestern United States
complains of a high-grade fever with rigors, generalized aches,
myalgias, headache, and backache.

HPI Four days ago In- relumed from a hiking trip during which he
was bitten by a tick: he took amoxicillin as prophylaxis against
Lyme disease.

PE VS: fever.

Labs CBC: leukopenia; relative lymphocytosis. Viral antigen detected
in RBCs by immunofluorescence: Colorado tick virus cultured
in suckling mice by intracerebral inoculation of blood clot;
indirect fluorescent Ab test positive.

Treatment Symptomatic.

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Discussion Colorado tick fever virus is an 80-nm double-shelled reovirus
thai is covered with capsomeres; its icosahedral core contains
1 2 segments of dsRNA. The disease is a zoonosis that is
transmitted by a wood tick, Dermacentor andersoni. It occurs
primarily in the Rocky Mountain region, primarily affecting
hikers. Since no specific therapy exists, prevention is key (wear
clothing diat covers the body).

COLORADO TICK FEVER

ID/CC A 2-year-old male is brought to the F.R by his parents with sore
throat, inspiratory stridor, and a barking cough of 1 day's
duration.

HPI The patient has no significant past medical history.

PE VS: fever (38.6°C); tachypnea. PE: respiratory distress;

nasopharyngeal discharge; diffuse rhonchi and wheezes;
examination of extremities reveals some cyanosis.

Labs Throat and nasal swabs isolate parainfluenza virus; serocliagnosis
and hemagglutinin inhibition tests reveal type 1 (most common

cause) .

Imaging CXR: air trapping. XR, neck: subglottic narrowing.

Gross Pathology Inflammation and edema of larynx, trachea, and bronchi.

Treatment Most cases respond to supportive therapy such as humidified air,
removal of secretions, and bed rest. Severe cases may require
humidified oxygen, racemic epinephrine, or high-dose
corticosteroids.

Discussion Differentiate croup from Htiriiwp/i/hi.s influenzae type B and
influenza A virus. Modes of transmission include respiratory
droplets and person-to-person contact; tends to peak in the fall
and winter. Most cases of croup are due to parainfluenza virus
ivpe 1 ; type 3 is a prominent cause of bronchiolitis in babies.

CROUP

ID/CC A 30-year-old man with AIDS presents with chronic, recurrent
profuse, nonbloody, watery diarrhea.

HPI The diarrhea has recurred over the past 2 months with
intermittent cramping, and previous treatments have not
been effective.

PE VS: no fever. PS: moderate dehydration; thin; generalized
lymphadenopalhy.

Labs Acid-fast staining demonstrates oocysts of Cryptosporidium in
fresh stool.

Gross Pathology
Micro Pathology

Intestinal mucosa appears normal.

Blunting of intestinal villi; mixed inflammatory cell infiltrates
with eosinophils in lamina propria; organisms visible on brush
borders.

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Treatment No treatment found effective; supportive management with
maintenance of fluids and nutrition.

Discussion Cryptosporidium parvum infection presents as acute diarrhea
in malnourished children and as severe diarrhea in
immunocompromised patients (part of HIV wasting syndrome);
tin- disease is mild and self-limiting in immune-competent
patients. The disease is acquired through the ingestion of
oocysts (fecal-oral transmission) that may be killed by
chlori nation.

Atlas Link

:OZ1 M-Ml-081

CRYPTOSPORIDIOSIS

ID/CC A 5-year-old white male presents with malaise, anorexia, low-
grade fever, sore throat of 3 days' duration, and dyspnea on
exertion.

HPI The child was raised abroad. His immunization status cannot be
determined.

PE VS: fever; tachycardia with occasional dropped beats. PE:

cervical lymphadenopathy (bui.i.'s-nkck. appearance); smooth,
whitish-gray, adherent membrane over tonsils and pharynx; no

hepatosplenomegaly; diminished intensity of SI.

Labs Metachromatic granules in bacilli arranged in "Chinese character"
pattern on Albert stain of throat culture; C.orynebacterium
diphtheriae confirmed by growth observed on Ldffler's blood
agar; erythema and necrosis following intradermal injection of
(',. diphtheriae toxin (POSITIVE Schick's test); immunodiffusion
studies (Elek's) confirm toxigenic strains of C. diphtheriae. ECG:
ST-segment elevation; second-degree heart block.

Imaging Echo: evidence of myocarditis.

Gross Pathology

Micro Pathology

Treatment

Discussion

Pharyngeal membranes not restricted to anatomic landmarks;
pale and enlarged heart.

Polymorphonuclear exudate with bacteria: precipitated fibrin
and cell debris forming a pseudomembrane; marked hyperemia,
edema, and necrosis of upper respiratory tract mucosa;
exotoxin-induced myofibrillar hyaline degeneration; lysis of
myelin sheath.

Begin treatment on presumptive diagnosis; specific antitoxin
and penicillin or erythromycin; respiratory and cardiac support;
confirm eradication by repeating throat culture.

A bacterial infection of the throat, diphtheria is preventable by
vaccine and is caused by toxigenic Corynebacteriwn diphtheriae, a
club-shaped, gram-positive aerobic bacillus. Diphtheria toxin is
produced by B-pi ophage-infected corynebacteria; it blocks EF-2
via ADP ribosylation and hence ribosomal function in protein
synthesis. The toxin enters the bloodstream, causing fever,
myocarditis (within the first 2 weeks), and polyneuritis (many
weeks later) .

Atlas Links UJCta » I M-Ml-082

DIPHTHERIA

MTl MC-324

ID/CC A 5(>-ycar-old male professor of veterinary medicine from
New Zealand experiences sudden high fever with chills,
jaundice, and right upper quadrant pain while attending a
conference in the United Stales.

HPI I lis past history is unremarkable. He has been healthy and has
been physically active working in the field with sheep and
breeding dogs.

PE VS: fever; hypotension (BP 90/50). PE: hepatomegaly; jaundiced
sclera; on palpation of epigastrium and right hypochondrium,
abdomen is tender with no rebound tenderness.

Labs CBC: leukocytosis with neutrophilia; slight eosinophilia.

Strongly positive iinmunoblot test for antibodies to echinococcal
antigens; elevated direct bilirubin and alkaline phosphatase.

Imaging

Gross Pathology

CT/US, abdomen: multiple large septated liver cysts impinging
on bile ducts, producing biliary dilatation (due to obstruction).

Liver is most common site of invasion, but cysts may also form in
lungs, kidney, bone, and brain; each cyst contains millions of
scoleces and consists of two layers: an inner germinal layer and
an outer laminated layer; usually surrounded by fibrotic
reaction.

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Micro Pathology Giant cell reaction surrounding cyst with eosinophilic
infiltration.

Treatment Surgically remove cysts if possible; albendazole may be effective.

Discussion Echinococcosis is a zoonosis produced by Echinococcus

granulosus. It is acquired through the ingestion of food or drink
contaminated with the feces of dogs or odier carnivores that
have eaten contaminated meat; humans are die intermediate
host of parasitic larvae. Accidental spilling of cyst fluid, either
spontaneously or during surgery, may result in secondary
seeding or anaphylaxis and even death. Also known as hydatid
disease.

Atlas Link ID.

M-Ml-083

ECHINOCOCCOSIS

ID/CC A 28-year-old male who is a resident of the southeastern

United States presents with a high fever with chills, headache,
and myalgias.

HPI He remembers having been bitten by a tick a week before
developing his symptoms; however, he reports no skin rash.

PE VS: fever. PE: no skin rash noted.

Labs CBC: leukopenia and mild thrombocytopenia. Characteristic
intraleukocytic inclusion bodies and serologic response to
Ehrlichia antigens demonstrated; E. chaffeensis cultured from
blood and detected by PCR.

Treatment Doxycycline.

Discussion Ehrlichieae are gram-negative, obligately intracellular bacteria.
The two types of Ehrlichia species that affect humans are
/■,'. chaffeensis (which attacks macrophages and monocytes) and
an /.'. equWke organism (which attacks granulocytes). Preventive
measures include wearing clothing that covers the body and
using insect repellants.

EHRLICHIOSIS

ID/CC A 30-year-old male from Texas presents with fever and a skin
rash thai began about 2 weeks ago.

HPI The onset was gradual, with prodromal symptoms of headache,
malaise, backache, and chills. These symptoms were followed by
shaking chills, fever, and a more severe headache accompanied
by nausea and vomiting. A remittent pattern of fever
accompanied by tachycardia continued for 10 to 12 days, with
the rash appearing around the fifth day of fever. The patient
worked at a rat-infested food-storage depot this summer.

PE VS: fever. PE: discrete, irregular pink maculopapular rash seen
in axillae and on trunk, thighs, and upper arms; face, palms,
and soles only sparselv involved: mild splenomegaly noted.

Labs The Weil-Felix agglutination reaction for Proteus strain OX-19
was positive; complement-fixing antibodies to the typhus group
antigen were demonstrated; endemic typhus (due to Rickettsia
typhi) was confirmed serologically by using specific washed
rickettsial antigens in IFA tests.

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Treatment Antibiotic treatment with doxycycline (chloramphenicol is used
as an alternative).

Discussion Murine typhus is a natural infection of rats and mice by

Rickettsia typhi; spread of infection to humans by the rat flea is
incidental and occurs when feces from infected fleas are
scratched into the lesion. Cases can occur year-round; however,
most occur during the summer months, primarily in southern
Texas and California.

ENDEMIC TYPHUS

ID/CC A 28-year-old Guatemalan male is brought to the hospital

complaining of severe headache, photophobia, and fever over
the past 2 weeks.

HPI As a political dissident, he spent 4 months in a refugee camp in
soi u hern Mexico before entering the United States.

PE VS: fever (40°C). PE: papilledema and delirium; bilateral
swelling of parotid glands 1 week later; toxic facies;
maeulopapular rash on trunk and extremities; face, palms,
and soles spared; mild splenomegaly-
Labs Positive Weil-Felix reaction to OX-1 9 strains of Proteus; rise in
complement fixation titer for Rickettsia prowazekii; specific
antibodies. UA: proteinuria; microscopic hematuria.

Gross Pathology Myocarditis and pneumonia may be present; cerebral edema;
maeulopapular rash.

Micro Pathology

Zenker's degeneration of striated muscle: thrombosis and
endothelial proliferation of capillaries with abundant rickettsiae
and perivascular cuffing; accumulation of lymphocytes;
microglia and macrophages (typhus nodules) in brain.

Treatment Doxycycline; chloramphenicol.

Discussion Epidemic typhus is a febrile illness caused by Rickettsia prowazekii,
a gram-negative, nonmotile, obligate intracellular parasite; it is
transmitted via body lice and is associated with war, famine, and
crowded living conditions. The rash should be differentiated
from Rocky Mountain spotted fever, which starts peripherally on
the wrists and ankles and also includes the palms and soles.

Atlas Link L'jciazi MC-169

EPIDEMIC TYPHUS

ID/CC A 4-year-old male presents with fever, hoarseness, and

respiratory distress because of partial airway obstruction.

HPI Tlie child is also unable to speak clearly and has pain while
swallowing (oiiym iphagia) .

PE VS: fever; tachypnea. PE: patient is leaning forward wiUi neck
hyperextended and chin protruding; drooling; marked
suprasternal and infrasternal retraction of chest: inspiratory ^

stridor on auscultation. cz

Labs Culture of throat swab (no role in management of acute to

disease) reveals penicillinase-resislant Haemophilus influenzae; >

blood cultures also positive. m

Imaging XR, neck: marked edema of epiglottis and aryepiglottic folds
("thumbs-up" sign).

Gross Pathology Epiglottis is cherry-red, swollen, and "angry-looking." Rapid

cellulitis of epiglottis and surrounding tissue leads to progressive
blockage of airway.

Treatment Preservation of airway; IV cefuroxime.

Discussion The principal cause of acute epiglottitis in children and adults is
H. influenzae type b; other pathogens include II. parainfluenza
and group A streptococcus. Characterized by rapid onset.

Atlas Link "TFI" PG-M1-087

EPIGLOTTITIS

ID/CC A 30-year-old soldier who had been admitted for a gunshot

wound in the right ihigli presents with severe pain and swelling
at the site of his injury.

HPI The patients right lower limb had become discolored, and
several bullae had appeared on the skin. He has passed very
Utile urine over the past day. and the urine he has passed has
been dark ("cola-colored").

PE VS: low-grade fever; marked tachycardia. PE: diaphoresis; skin
of right thigh discolored (bronze to purple red); site of injury
exquisitely tender and tense and oozing a thin, dark, and
foul-smelling fluid; crepitus while palpating thigh.

Labs CBC: low hematocrit. Gram stain of exudate and necrotic

material at wound site reveals presence of large gram-positive
rods; anaerobic culture of exudate and blood yields Clostridium
perfringens type A: culture isolate demonstrates positive Nagler
reaction (due to presence of alpha toxin lecithinase): further
labs confirm presence of intravascular hemolysis, myo- and
hemoglobinuria, and acute tubular necrosis.

Imaging XR. right thigh: presence of gas in soft tissues.

Gross Pathology Overlying skin purple-bronze, markedly edematous with
vesiculobullous changes with little suppurative reaction.

Micro Pathology

Treatment

Discussion

Coagulative necrosis, edema, gas formation, and many large
gram-positive bacilli found in affected muscle tissue; relatively-
sparse infiltration of PMNs noted in the bordering muscle
tissue.

Surgical debridement: antibiotics (penicillin, clindamycin.
tetracycline, metronidazole); hyperbaric oxygen therapy and
polyvalent antitoxin; supportive management of associated
multiorgan failure.

A rapidly progressive myonecrosis caused by Clostridium
/irr/ringens type A, traumatic gas gangrene develops in a wound
with low oxygen tension (embedded foreign bodies containing
calcium or silicates cause lowering of oxygen tension, leading to
germination of the spores). The most important toxin is the alpha
toxin leciihinase, which produces hemolysis and myonecrosis.

Atlas Link MIL, PG-M1-088

GAS GANGRENE— TRAUMATIC

ID/CC A 4-year-old female is brought to the pediatrician because of
lack of appetite; nausea and vomiting; chronic, foul-smelling
diarrhea without blood or mucus; and a bloated sensation.

HPI She has been in several day-care centers over the past 3 years.

PE Low weight and height for age; mild epigastric tenderness.

Labs Binucleate, pear-shaped, flagellated trophozoites {GiARDlA

lAMiu.i.x) on freshly passed stool; cysts found on stool exam.

Treatment Metronidazole.

Discussion The most common protozoal infection in children in the United
States, giardiasis is transmitted mainly through contaminated
food or water and causes malabsorption.

Atlas Links ETIcra \ I M-M1-089A, M-M1-089B

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GIARDIASIS

ID/CC A 3-day-old female neonate presents with a thick eye discharge.

HPI The mother admits to having multiple sexual partners and

complains of a vaginal discharge. She did not receive adequate
antenatal care.

PE Exam of both eyes reveals a thick purulent discharge and
marked conjunctival congestion and edema; conjunctival
chemosis is so marked that cornea is seen at bottom of a
c rater-like pit; corneal ulceration noted.

Labs Conjunctival swabs on Gram staining reveal presence of gram-
negative diplococci both intra- and extracellularly in addition to
many PMNs; conjunctival swab and maternal cervical culture
yield Neisseria gonorrhoeae.

Treatment Aqueous penicillin G or ceftriaxone for a total of 7 days. Also
treat mother and her sexual contacts. Educate the mother
regarding the importance of safe sex.

Discussion Caused by Neisseria gonorrhoeae, gonococcal ophthalmia

neonatorum is contracted from a mother with gonorrhea as the
fetus passes down the birth canal; infection does not occur in
utero. Corneal inflammation is the major clinical sign that may
produce complications such as corneal opacities, perforation,
anterior synechiae, anterior staphyloma, and panophthalmitis. It
is now common practice to prevent this disease by treating the
eyes of the newborn with an antibacterial compound such as
erythromycin ointment or 1% silver nitrate; however, home
childbirth bypasses this prophylactic procedure, and thus some
cases are still occurring in the United States.

GONOCOCCAL OPHTHALMIA NEONATORUM

ID/CC A 19-year-old white male presents with burning urination;

profuse, greenish-yellow, purulent urethral discharge; staining
of his underwear; and urethral pain.

HPI Four days ago, he had unprotected sexual contact with a
prostitute.

PE Mucopurulent and slightly blood-tinged urethral discharge;
normal testes and epididymis; no urinary retention.

Labs Smear of urethral discharge reveals intracellular gram-negative
diplococci in WR( is; gonococcal infection confirmed by
inoculation into Thayer-Martin medium.

Gross Pathology Abundant, purulent urethral exudate.

Treatment Ceftriaxone plus doxycycline or erythromycin for possible
coinfection with Chlamydia.

Discussion A common STD caused by Neisseria gonorrhoeae, gonorrhea may
involve the throat, anus, rectum, epididymis, cervix, fallopian
tubes, prostate, and joints; conjunctivitis is also found in
neonates. Neonatal conjunctivitis may be prevented through the
instillation of silver nitrate or erythromycin eye drops at birth.

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Atlas Links H'lcyjn M-Ml-091

IM2-018

GONORRHEA

ID/CC A 28-year-old male immigrant presents with inguinal swelling
and a painless penile ulcer.

HPI He admits to unprotected intercourse with multiple sexual
partners, many of whom were prostitutes. He first noticed a
papule on his penis several weeks ago.

PE Soft, painless, raised, raw, beef-colored, smooth granulating
ulcer noted on distal penis: multiple subcutaneous swellings

(rsi i now ii( its) noted in inguinal region, some of which have
ulcerated.

Labs Giemsa-stained smear from penile and inguinal regions

demonsU'ate characteristic "closed safety pin" appearance
i >l en. apsulated organisms within a large histiocyte
(Donovan bodies).

Micro Pathology Characteristic histologic picture of donovanosis comprises some
degree of epithelial hyperplasia at margins of lesions; dense
plasma cell infiltrate scatters histiocyte-containing Donovan

b< idies.

Treatment Treat with doxycycline or double-strength TMP-SMX.

Discussion Granuloma inguinale, a slowly progressive, ulcerative,

granulomatous STD involving the genitalia, is caused by the
gram-negative bacillus Calymmatobacterium granulomatis
(formerly Donovdnia gmti.ulom/ilis): ii is seen in Giemsa-stained
sections as a dark-staining, encapsulated, intracellular rod-
shaped inclusion in macrophages, the so-called Donovan body.
The disease is endemic in tropical areas such as New Guinea,
southern India, and southern Africa.

GRANULOMA INGUINALE

ID/CC A 60-year-old male presents with cough productive of

mucopurulent sputum together with mild lever and worsening
breathlessness.

HPI He is a chronic smoker who has been diagnosed with COPD.

PE VS: lever. PE: in moderate respiratory distress; emphysematous
i hesi with obliterated cardiac and livei dullness; wheezing and
crackles heard over both lung fields.

Labs Haemophilus influenzae organisms seen as small, pleomorphic
gram-negative ba< illi on Gram stain of sputum; nontypahle
H. influenzae isolated on sputum culture (to grow in culture,
II influenzae requires both factor X-hematin and factor
V— nicotinamide nucleoside present in erythrocytes).

Treatment Amoxicillin/ampicillin therapy; TMP-SMX. azithromycin, and

clarithromycin arc also excellent drugs for the treatment of
clinically mild to moderate //. influenzae infections of the upper
respiratory tract.

Discussion Infections caused by nontypahle. or unencapsulated,

Haemophilus influenzae strains have been increasingly recognized
in pediatric and adult populations. Nontypable H. influenzae
strains are frequent respiratory tract colonizers in patients with
COPD and commonly exacerbate chronic bronchitis in these
patients; nontypable strains are also the most common cause of
acute otitis media in children.

H. INFLUENZAE IN A COPD PATIENT

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ID/CC A 25-year-old male presented with sudden-onset breathlessness,
cough, cyanosis, and high-grade fever.

HPI The patient failed to improve on 100% oxygen, became

hypotensive, and died of type 2 respiratory failure a few hours
after admission. He had been in perfect health and had been
hiking in several rodent-infested areas before falling ill.

PE On admission he was found to have fever, tachycardia, cyanosis,
hypotension, and rales on auscultation over both lung fields; no
meningeal signs or localizing CNS signs could be demonstrated.

Labs ABGs: respiratory acidosis with hypoxia and hypercapnia. CBC:
leukocytosis; hemoconcentration; thrombocytopenia; atypical
lymphocytosis. Increased LDH and ALT levels; prolonged PT
index; sputum exam and blood culture did not yield any
organism; IgM antibody to hantavirus and immunohistochemical
stains for hantavirus antigen in tissues confirmed infection with
the virus.

Imaging CXR: noncardiogenic pulmonary edema (bat-wing edema
pattern).

Micro Pathology

Histopathologic exam of lung tissues was suggestive of acute
respiratory distress syndrome (adult hyaline membrane disease).

Treatment Patient died despite intensive ventilatory support (Sin Nombre
virus most frequently causes hantavirus pulmonary syndrome in
the United States).

Discussion A virus closely related to the Hantaan virus (which produces
Korean hemorrhagic fever and hemorrhagic fever with renal
syndrome) has been recovered from mice in various regions of
the United States; rodents are the natural host for this group of
viruses. Infected rodents shed the virus in saliva, urine, and
feces for many weeks, and humans are believed to acquire the
infection via exposure to rodent excrement or saliva, either by
the aerosol route or by direct inoculation.

HANTAVIRUS PULMONARY SYNDROME

ID/CC A 35-year-old male who works as a U.N. health worker presents
with a high-grade fever and massive hematemesis.

HPI He recently returned from Zaire, where he worked in a
lick-infested forest.

PE VS: fever. PE: extensive ecchymosis.

Labs CBC: leukopenia; severe thrombocytopenia. LFTs: elevated AST.
Crimean-Congo virus isolated.

Treatment Treatment involves a 10-day course of ribavirin; platelet

transfusions; avoid salicylates; barrier nursing and containment
of infected secretions, since airborne infection may occur in
hospital environment.

Discussion The agent responsible for Crimean-Congo hemorrhagic fever is
a bunyavirus; reservoirs include wild and domesticated sheep,
cattle, goats, and hares. The disease is transmitted by a tick
vector, usually an ixodid of the genus Hyalomma; endemic areas
include the Middle East and western China. The disease targets
individuals of all ages and affects males and females equally.

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HEMORRHAGIC FEVER— CRIMEAN-CONGO

ID/CC A 10-year-old male is brought to the ER in a slate ol' shock
accompanied by massive hematemesis.

HPI The family had just returned from a vacation in Thailand. His
parents say that he had a high-grade fever for 5 to fi days, for
which he was receiving presumptive treatment for malaria.

PE VS: hypotension: tachycardia. V'S: tool, clammy extremities;
petechial skin rash over extremities, axillae, trunk, and face;

bleeding from venipuncture sites.

Labs CBC: thrombocytopenia; hematocrit increased by > 20%.

Abnormal clotting profile suggestive o I disseminated
intravascular coagulation (DIC); paired sera reveal significant
rise in liter of hemagglutination inhibition antibodies against
Dengue virus serotypes 1 and 2.

Imaging LIS: bilateral pleural effusion and ascites.

Treatment Symptomatic; manage shock with fluids and hemodynamic

monitoring: fresh blood/ plaieiei-rich plasma: avoid salicylates.

Discussion Dengue hemorrhagic fever is caused by a mosquito-borne {Aedes
aegypti) flavivirus and is characterized by four distinct dengue
serotypes (type 2 is considered the most dangerous). A. aegypti
has a domestic habitat (stagnant water in llovver pots, old jars, tin
cans, and old tires) and bites during the day. Dengue fever has
shown an increase in incidence in Southeast Asia, Central and
South America, and the Caribbean. Since no specific therapy
exists, prevent by avoiding contact with infected A. aegjpli.

Atlas Link i L : Z-Ml-096

HEMORRHAGIC FEVER— DENGUE

ID/CC A 58-year-old man who was hitchhiking through central and

southern Africa was admitted to a hospital in /.aire in a slate of
shock following massive hemorrhage from the GI tract
(hcmatemesis and melena); he died within 6 hours of
admission. Ten days later, a male doctor who had attended ihis
patient and had attempted resuscitation became ill with a
similar disease syndrome.

HPI Ai admission, he gave an 8-day hisiorv of progressive fever,
severe headaches, myalgias, and watery diarrhea. He also

reported an erythematous, measles-like skin rash that had
begun to desquamate.

PE VS: lever. PE: splenomegaly; hepatomegaly.

Labs CBC: leukopenia; Pelger-1 luet anomaly of neutrophils with

atypical mononuclear cells: thrombocytopenia widi abnormal
platelet aggregation. Markedly elevated AST and ALT: blood was
inoculated intraperitoneal!)' into young guinea pigs and into
various tissue culture cell lines, and Ebola virus was detected by
indirect immimofluorescent staining techniques.

Gross Pathology At autopsy, lymph nodes, liver, and spleen (bund to be most

conspicuously involved (replication of Ebola virus can occur in
virtually all organs); stomach and intestines filled with blood;
petechiae seen over bowel mucosa.

Micro Pathology

Treatment

Discussion

Severe congestion and stasis of spleen: widespread necrosis of
liver cells; electron microscopy of liver i cvealed pleomorphic
virus particles appearing in contrast preparations as long,
filamentous forms, U-shaped forms, and some circular forms
resembling a doughnut.

Supportive care, since no specific treatment exists: a prior
outbreak was brought under control bv isolating patients and
instituting Strict barrier nursing.

A hemorrhagic, febrile infection of humans due to infection with
the Ebola and Marburg viruses, both of which are liloviruses that
are structuralh indistinguishable but anligcnicallv distinct. This
disease is a zoonosis but the reservoir is unknown. Individuals can
become infected through person-to-person or nosocomial contact

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HEMORRHAGIC FEVER— EBOLA VIRUS

ID/CC A 25-year-old male woodcutter who lives in South Korea is

admitted to the ER in a state of shock and massive epistaxis.

HPI The patient had been complaining of fever, malaise, headache,
myalgias, back pain, abdominal pain, nausea, and vomiting for
the past week; he also complained of extremely reduced urine
output. Careful history revealed that before he fell ill. he and his
friend were cutting wood in the forest when they accidentally
disturbed a rodent-infested area.

PE VS: hypotension. PE: epistaxis; facial Hushing; pctechiae and
subconjunctival hemorrhages.

Labs Deranged RFTs suggestive of acute renal failure. CBC:

thrombocytopenia. Serology and culture identify hantavirus,
Hantaan serotype.

Treatment Supportive management in the form of dialysis (for renal

failure); management of shock and hemorrhage; IV ribavirin

(must start within first 4 days of manifestation of disease).

Discussion Korean hemorrhagic fever with renal syndrome is caused by the
Hantaan serotype of hantavirus. Its reservoirs are various
rodents that are found distributed over Europe and Asia;
humans acquire the disease mainly by inhaling aerosols of
rodeni virus.

HEMORRHAGIC FEVER— RENAL SYNDROME

ID/CC A 7-year-old male complains of a high fever and a very sore
throat.

HPI The pain is so severe thai the child refuses to swallow. He is
adequately immunized and achieved normal developmental
milestones.

PE VS: fever. PE: characteristic grayish-white vesicular lesions, some
of which have ulcerated, noted over soft palate and tonsils.

Labs Coxsackievirus A isolated from mucosal lesions.

Treatment Self-limiting condition.

Discussion In hand, foot, and mouth disease (HFMD), patients complain
of fever, weakness, and decreased appetite along with similar
1 i-M oils noted in tin- oral cavity, palms, soles, and buttocks.
Herpangina may be caused by coxsackievirus Al— A10. A16,
A22, and B1-B5. Outbreaks of HFMD are usually caused by
coxsackievirus A16.

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HERPANGINA

ID/CC A 25-year-old homosexual male visits a health clinic complaining
of headache, low-grade fever, and a painful skin rash in the
perianal area.

HPI He has no history of penile ulcerations and admits to
unprotected anal sex with multiple partners.

PE Perianal vesicular rash in clusters on erythematous base; no

penile ulceration; painful inguinal lymphadenopalhy.

Labs

Gross Pathology

Multinucleated giant cells with intranuclear inclusions

sin rounded by clear halo on Pap-stained section or Tzanck
preparation of scrapings from base of vesicles.

Clear liquid in vesicles: secondary bacterial infection may result;
painful ulcerations when vesicles rupture.

Micro Pathology Inflammatory infiltrate with abundant lymphocytes.

Treatment Acyclovir.

Discussion An enveloped, double-stranded DNA virus transmitted by sexual
contact, HSV 2 has a tendency to recur and can be transmitted
to the fetus through the birth canal. Condom use appears to be
one of the most effective means of preventing transmission.

Atlas Links mem 1 1 M-Ml-100

T Li; IM2-019A, IM2-0WB

HERPES GENITALIS

ID/CC A 45-year-old HIV-positive male is seen by his family doctor

following die appearance of a painful, burning skin rash on the
left side of his chest that is accompanied by a headache and
low-grade fever.

HPI The patient had chickenpox as a child. He had been well

until 1 year ago, when he was diagnosed with non-Hodgkin's
lymphoma, for which he is etirrendy undergoing chemotherapy.

PE Vesicular rash on erythematous base; in dermatomal distribution

(left T6-T8); exquisitely tender to touch.

Labs Acantholytic cells on Tzanck smear from base of vesicles.

Micro Pathology Intranuclear eosinophilic inclusions surrounded by clear halo

(CowdryA INCLUSIONS).

Treatment Acyclovir.

Discussion Shingles represents a reactivation of a latent infection with

varicella-zoster virus; the rash typically follows the distribution
of a nerve root. It is commonly seen in immunosuppressed
patients and is also associated with trauma, ultraviolet radiation,
hypothermia, and emotional stress. Postherpetic neuralgia is a
common complication in die elderly.

Atlas Links mcvj2i IM2-020A, IM2-020B

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HERPES ZOSTER (SHINGLES)

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