BLACKWELL'S
NDERGROUND CLINICAL VIGNETTES
MICROBIOLOGY
VOL II, 3E
VIKAS BHUSHAN, MD
University of California. San Francisco. Class of 1991
Series Editor. Diagnostic Radiologist
VISHAL PALL, MBBS
Government Medical College. Chandigarh. India. Class of L990
Series Editor, U. of Texas, Galveston, Resident in Internal Medicine &
Preventive Medicine
TAO LE, MD
l nivciMH of California. San Francisco. Class of 1996
HOANG NGUYEN, MD, MBA
Northwestern University, Class of 2001
SONAL SHAH, MD
Ross University. Class of 2000
b
Blackwell
Science
CONTRIBUTORS
Sandra Mnn
University of Texas Medical Branch, Class of 2002
Shalin Patel, MD
McGraw Medical Center, Northwestern University, Resident in Internal
Medicine
Ashraf Zaman, MBBS
New Delhi, India
Vipal Soni, MD
UCLA School of Medicine, Class of 1999
FACULTY REVIEWER
Warren Levinson, MD, PHD
Professor of Microbiology and Immunology, UCSF School of Medicine
© 2002 by Blackwell Science. Inc.
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Blackwell's Underground Clinical Vignettes:
Microbiology II. 3e
ISBN 0-632-04549-3
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Library of Congress Cataloging-in-Publication Data
Bhushan. Vikas.
Blackwell's underground clinical vignettes.
Microbiology / Author. Vikas Bhushan.- 3rd ed.
p. : cm, - (Underground clinical vignettes)
Rev. ed. of: Mirrobiology/Vikas Bhushan ... [el al.].
2nd ed, cl999-. ISBN 0-632-04547-7 (alk. paper)
1. Medical microbiology- Case studies.
2. Physicians - Licenses - United States -
Examinations - Study guides.
[DNLM: I. Microbiology - Case Report.
2. Microbiology- Problems and Exercises. QW 18.2
B575b 2002] I. Tide: Microbiology. II. Tide:
Underground clinical vignettes. Microbiology.
III. Microbiology. IV. Title. V. Series.
QR46 .B465 2002
616'.01'076-dc21
2001004932
.Ml rights reserved. No part of this book may be
reproduced in any form or by any electronic or
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from the publisher, except by a reviewei who may
quote brief passages in a review.
Notice
IIk authors "I this volume have taken can' that the inhumation contained herein is accurate and compati-
ble with the standards generally accepted at the time ol publication. Nevertheless, it is difficult to ensure
thai all the information given is entirely accurate lor all circumstances. The publisher and authors do nol
guarantee the contents ol this book .m<\ disclaim any liability, loss, or damage incurred as a consequence,
direi ih or indirectly, ol the use and application ol any of die contents ol this vol nine.
CONTENTS
Acknowledgments x
Preface to the 3rd Edition xiii
How to use This Book xvi
Abbreviations xvii
Immunology
Infectious Disease
Anaphylaxis
Chronic Granulomatous Disease
Hereditary Angioedema
Selective IgA Deficiency
Severe Combined Immunodeficiency (SCID)
X-Linked Hypogammaglobulinemia
Histoplasmosis
Human T-Cell Leukemia
Virus Type 1 (HTLV-1)
Inclusion Conjunctivitis
Infectious Mononucleosis
Influenza
Jarisch-Herxheimer Reaction
Legionella Pneumonia
Leishmaniasis
Leprosy — Lepromatous
Leprosy— Tuberculoid
Leptospirosis (Weil's Disease)
Listeriosis
Lyme Disease
Lymphatic Filariasis
Lymphogranuloma Venereum
Malaria
Measles
Meningococcemia
Mucormycosis
Mumps
Mycoplasma Pneumonia
Necrotizing Fasciitis
Nocardiosis
Nosocomial Enterococcal Infection
Onchocerciasis
Overwhelming Postsplenectomy Infections
Pasteurella multocida
Plague
Pneumococcal Pneumonia
Pneumocystis carina Pneumonia
Proctocolitis
ESI
m
Psittacosis
Pyogenic Liver Abscess
Q Fever
Rabies
Rat Bite Fever
Relapsing Fever
Rocky Mountain Spotted Fever
RSV Pneumonia
Rubella — Congenital
Rubella (German Measles)
Salmonella Septicemia with Osteomyelitis
Scabies
Scarlet Fever
Schistosomiasis
Schistosomiasis — Urinary
Shigellosis
Shock — Septic
Sporotrichosis
Strongyloidiasis
Subdiaphragmatic Abscess
Syphilis — Congenital
Syphilis — Primary EE1
Syphilis — Secondary
Syphilis — Tertiary (Tabes Dorsalis)
Tetanus
Tetanus Neonatorum
Tick Paralysis
Toxoplasmosis 133
Trichinosis liftl
Tuberculosis — Miliary |sf]
Tuberculosis — Pulmonary
Tularemia
Typhoid Fever
Urethritis — Nongonococcal
Urinary Tract Infection (UTT)
UTI with Staphylococcus saprophytics
Varicella (Chickenpox)
Visceral Larva Migrans
Whooping Cough
Yaws
Yellow Fever
Neonatology Listeria Meningitis in the Newborn KEI
Nephrology/ Urology Acute Cystitis
Epididymitis
Orchitis
Neurology
Gynecology
Obstetrics
Orthopedics
Poststreptococcal Glomerulonephritis
Prostatitis — Acute
Prostatitis — Chronic
Pyelonephritis — Acute
Brain Abscess
Cysticercosis
Herpes Simplex Encephalitis
Japanese Encephalitis
Lymphocytic Choriomeningitis (LCM)
Meningitis — Bacterial (Adult)
Meningitis — Bacterial (Pediatric)
Meningitis — Cryptococcal
Meningitis — Tubercular
Poliomyelitis
Progressive Multifocal
Leukoencephalopathy
Ramsay Hunt Syndrome
St. Louis Encephalitis
Subacute Sclerosing Panencephalitis
Bacterial Vaginosis
Breast Abscess
Human Papillomavirus (HPV)
Pelvic Inflammatory Disease
Pelvic Tuberculosis
Toxic Shock Syndrome (TSS)
Chorioamnionitis
HIV Transmission in Pregnancy
Osteomyelitis
Septic Arthritis — Gonococcal
EH
E3
EH
EE
ACKNOWLEDGMENTS
Throughoui the production of this book, we have had the sup-
port of many friends and colleagues. Special thanks to our sup-
port team including Anu Gupta, Andrea Fellows, Anastasia
Anderson, Srishti Gupta, Mona Pall, Jonathan Kirsch and Chirag
Ainin. For prior contributions we thank Gianni Le Nguyen,
Tarun Mathur, Alex Grimm, Sonia Santos and Elizabeth
Sanders.
We have enjoyed working with a world-class international pub-
lishing group at Blackwell Science, including Laura DeYoung,
Amy Nuttbrock. Lisa Flanagan. Shawn Girsberger, Lorna Hind
and Gordon Tibbitts. For help with securing images for the
entire series we also thank Lee Martin, Kristopher Jones, Tina
Panizzi and Peter Anderson at the University of Alabama, the
Armed Forces Institute of Pathology; and many of our fellow
Blackwell Science authors.
For submitting comments, corrections, editing, proofreading,
and assistance across all of the vignette tides in all editions, we
collectively thank:
Tara Adamovich, Carolyn Alexander. Kris Alden, Henry E.
Aryan, Lynman Bacolor, Natalie Barleneva, Dean Bartholomew,
Debashish Behera, Sumit Bhatia, Sanjay Bindra, Dave Brinton,
Julianne Brown, Alexander Brownie, Tamara Callahan, David
Canes, Bryan Casey, Aaron Caughey, Hebert Chen.Jonadian
Cheng, Arnold Cheung, Arnold Chin. Simion Chiosea, Yoon Cho,
Samuel Chung, Gretchen Conant. Vladimir Coric, Christopher
Cosgrove, Ronald Cowan, Karekin R. Cunningham, A. Sean
Dalit y. Rama Dandamudi, Sunil Das, Ryan Armando Dave. John
David, Emmanuel de la Cruz, Robert DeMello, Navneel Dhillon.
Sharmila Dissanaike, David Donson, Adolf Etchegaray, Alea
Eusebio, Priscilla A. Frase, David Frenz, Kristin Gaumer,
Yohannes Gebreegziabher, Anil Gehi, Tony George, L.M.
Gotanco, Parul Goyal, Alex Grimm, Rajeev Gupta, Ahmad
Halim. Sue Hall. David Hasselbacher, Tamra Heimert, Michelle
Higley, Dan Hoit, Ericjackson, Tim Jackson, Sundarjayaraman,
Pei-Nijone, Aarchan Joshi. Rajni K. Julia, Faiyaz Rapadi, Seth
Karp, Aaron S. Kesselheim. Sana Khan, Andrew Pin-wei Ko,
Francis Kong, Paul Konitzky, Warren S. Krackov. Benjamin H.S.
Lau, Ann LaCasce, Connie Lee, Scott Lee, GuiUermo Lehmann,
Kevin Leung, Paul Levett, Warren Levinson. Eric Ley, Ken Lin,
Pavel Lobanov, J. Mark Maddox, Aram Mardian, Samir Mehta,
Gil Melmed, Joe Messina. Robert Mosca, Michael Murphy, Vivek
Nandkarni, Siva Naraynan, Carvell Nguyen, Linh Nguyen,
Dcanna Nobleza, Craig Nodurft, George Noumi, Darin T.
Okuda. Adam L. Palance, Paul Pamphrus, Jinha Park, Sonny
Palel, Ricardo Pietrobon, Riva L. Rahl. Aashiia Randeria,
Radian Reddy, Beatriu Reig, Marilou Reyes, Jeremy Richmon,
Tai Roe, Rick Roller. Rajiv Roy, Diego Ruiz, Andiony Russell,
Sanjay Sahgal, Urmimala Sarkar,John Schilling, Isabell Schmitt,
Daren Schuhmachcr, Sonal Shah, Fadi Abu Shahin, Mae Sheikh-
Mi, Kdie Shen. Justin Smith. John Stulak. Lillian Su, Julie
Sundaram, Rita Suri, Seth Sweetser, Antonio Talayero, Merita
Tan. Mark Tanaka, Eric Taylor, Jess Thompson, Indi Trehan,
Raymond Turner, Okafo L'chenna, Eric Uyguanco, Richa
Vai ma, John Wages, Alan Wang, Eunice Wang. Andv Weiss, Amy
Williams. Brian Yang, Hairy Zaky, Ashraf Zanian and David Zipf.
For generously contributing images to the entire Underground
Clinical Vignette Step 1 series, we collectively thank the staff at
BlackweU Science in Oxford. Boston, and Berlin as well as:
• Axford, J. Medicine. Osney Mead: BlackweU 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'"' Edition.
Osney Mead: BlackweU Science Ltd, 2000. Figures 2.8, 3.4,
5.28, 18.10, W5.32, W5.6.
• Berg D. Advanced Clinical Skills and Physical Diagnosis.
BlackweU 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: BlackweU Science
Ltd, 1996. Figures 13.19. 18.22, 18.33.
• Gillespie SH, Bamford K. Medical Micmbiology and Infection at a
Crlance. Osney Mead: BlackweU Science Ltd, 2000. Figures 20, 23.
• Ginsberg L. Lecture Notes on Neurology, 7"' Edition. Osney Mead:
BlackweU Science Ltd. 1999. Figures 12.3, 18.3, 18.3b.
•
Elliott T. Hastings M, Desselbetgei l\ Lecture \ote\ on Medical
Microbiology, 3"' Edition. Osney Mead: BlackweU 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. Ihii>matolog\ nl n (llanre. 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
series. 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
And 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 Atlas (Step 1) includes over 250
color plates, divided into gross pathology, microscopic pathol-
ogy (histology), hematology, and microbiology (smears).
• The I 'CV-Clinical Science Colin- Alias (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 = Anatomy
BS = Behavioral Science
BC = Biochemistry
M I = Microbiology, Vol. I
M2 - Miciiiliicilnj>y. Vul. II
PI = Pathophysiology, Vol. I
P2 = Pathophysiology, Vol, II
P:s = Pathophysiology;, Vol. Ill
PH = PIkutji.h < llog)
Step 2 Book Codes are: ER = Emergency Medicine
IM1 = Internal Medicine. Vol. I
IM2 = Internal Medicine. Vol. II
NKI ' - Neurology
OB = OB/GYN
PEL) - Pediatrics
SUR = Surgery
PSY = Psychiatry
MC = MiniCase
Case Number
I I I I M-P3-032A
Indicates Type of Image: H = Hematology
M = Microbiology
PG = Gross Pathology
I'M Microscopic Pathology
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
number of images possible, we have chosen to cross link the
Step I and 2 series.
• If the link is bold-faced this indicates that the link is direct
(i.e.. Siep 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 for
the USAILE Step 1 (Appleton & Lange/McGraw-Hill) and First
Mil for tlw USM1.F. Step 2 (Applelon & I.ange/ McGraw-Hill)
book will be linked to the corresponding L'CV 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 for quizzing —
captions are descriptive and do not give away the case name
direcdy.
We hope the updated UCV series will remain a unique and well-
integrated study tool dial 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-
tion 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 acknowledgment in
the revised book. If you submit over 20 high-quality corrections,
additions or new vignettes we will also consider inviting you to
become a "Contributor" on the book of your choice. If you are
interested in becoming a potential "Contributor" 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
elect tonic mail to UCVteam@yahoo.com. Please include
"Underground Vignettes" as the subject of your message. If you
do not have access to e-mail, use the following mailing address:
Rlackwell Publishing. Ann: UCV Editors. 350 Main Street,
Maiden, MA 02 148. USA.
Vikas Bhushan
Yishal Pall
Too Le
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
USMLE Step 1 (Appleton & Lange/McGravv Hill) and First Aid
for the USMLE 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 the authors and reviewers.
Although each case tends to present all the signs, symptoms,
and diagnostic findings for a particular illness, patients gener-
ally will not present with such a "complete" picture 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 within the
vigneties in (smali < ys) 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
5-aminosalicylic acid
ABGs
arterial blood gases
ABVD
adriamycin/bleomycin/vincrisUne/dacarbazine
ACE
angiotensin-converting enzyme
ACTH
adrenocorticotropic hormone
AD II
antidiuretic hormone
AFP
alpha fetal protein
AI
aortic insufficiency
AIDS
acquired immunodeficiency syndrome
ALL
acute lymphocytic leukemia
ALT
alanine transaminase
AML
acute myelogenous leukemia
ANA
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
BUN
blood urea notrogen
GAD
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
GT
computed tomography
CVA
cerebrovascular accident
CXR
chest x-ray
DIG
disseminated intravascular coagulation
DIP
distal interphalangeal
DKA
diabetic ketoacidosis
DM
diabetes mellitus
DTRs
deep tendon reflexes
DVT
deep venous thrombosis
EBV Epstein-Barr virus
ECG electrocardiography
Echo echocardiography
11- ejection fraction
EGD esophagogastroduodenoscopy
EMG electromyography
ERCP endoscopic retrograde cholangiopancreatography
ESR erythrocyte sedimentation rate
FEV forced expiratory volume
FNA fine needle aspiration
FTA-ABS lluorescent treponemal antibody absorption
FVC forced vital capacity
GFR glomerular filtration rate
GH growth hormone
(■I gastrointestinal
GM-CSF granulocyte macrophage colony stimulating
factor
GU genitourinary
HAY hepatitis A virus
hcG human chorionic gonadotropin
HEENT head, eyes, ears, nose, and throat
HIV human immunodeficiency virus
HLA human leukocyte antigen
HPI history of present illness
HR heart rate
HRIG human rabies immune globulin
HS hereditary spherocytosis
ID/CC identification and chief complaint
1DDM insulin-dependent diabetes mellitus
Ig immunoglobulin
IGF insulin-like growth factor
IM intramuscular
JVP jugular venous pressure
KUB kidneys/ureter/bladder
LDH lactate dehydrogenase
LES lower esophageal sphincter
I I I s liver function tests
LP lumbar puncture
LV left ventricular
I,VH left ventricular hypertrophy
Lytes electrolytes
MCHC mean corpuscular hemoglobin concentration
MCV mean corpuscular volume
MEN multiple endocrine neoplasia
MGUS
monoclonal gammopathy of undetermined
significance
MHC
major histocompaiibility complex
MI
myocardial infarction
MOPP
mechloreihamine/vincristine (Oncovorin)/
procarbazine/prednisone
MR
magnetic resonance (imaging)
MIL.
non-Hodgkin's lymphoma
NIDDM
non-insulin-dependent diabetes mellitus
NPO
nil per os (nothing by mouth)
NSAID
nonsteroidal anti-inflammatory drug
PA
posteroanterior
PIP
proximal interphalangeal
PBS
peripheral blood smear
PE
physical exam
PFTs
pulmonary function tests
PMI
point of maximal intensity
PMN
polymorphonuclear leukocyte
PT
prothrombin time
PTCA
percutaneous transluminal angioplasty
PTH
parathyroid hormone
pit
partial thromboplastin time
PUD
peptic ulcer disease
RBC
red blood cell
RPR
rapid plasma reagin
RR
respiratory rale
RS
Reed-Stern berg (cell)
RV
right ventricular
RVH
right ventricular hypertrophy
SBFT
small bowel follow-through
S1ADH
syndrome of inappropriate secretion of ADH
SLE
systemic lupus erythematosus
STD
sexually transmitted disease
TFTs
thyroid function tests
tPA
tissue plasminogen activator
TSH
thyroid-stimulating hormone
TIBC
total iron-binding capacity
TIPS
uansjiigular intrahepatic portosystemic shunt
TPO
thyroid peroxidase
TSH
thyroid-stimulating hormone
TTP
thromboiic thrombocytopenic purpura
I'A
urinalysis
UGI
upper C.l
US
ultrasound
VDRL Venereal Disease Research Laboratory
VS vital signs
VT ventricular tachycardia
WBC white blood cell
WPW Wolff-Parkinson-White (syndrome)
XR x-ray
ID/CC A 30-year-old female presents to the KR with severe, sudden-
onset shortness of breath and an extensive pruritic skin rash.
HPI She was prescribed cotrimoxazole by her general physician for a
LI I: she took die first close only a few minutes before developing
symptoms.
PE VS: hypotension. PE: severe respiratory distress; central cyanosis;
extensive urticaria] wheals noted all over body.
Labs IgE antibody demonstrated to sulfonamides by RAST.
Treatment Epinephrine (1:1000); antihistaminics; steroids; ventilatory
support; adequate IV fluid administration or vasopressor agents
to treat hypotension.
Discussion Systemic anaphylaxis is the most serious and life-threatening
IgE-mediated type I hypersensitivity reaction; its recognition and
prompt treatment are critical to survival.
o
o
en
-<
ANAPHYLAXIS
ID/CC A 2-year-old male is admitted to the hospital for evaluation of a
suspected immune disorder.
HPI He has a history of recurrent fungal diaper rashes and
staphylococcal cervical furunculosis requiring multiple incisions
and drainage in addidon to antibiotics. His mother also reports
chronic diarrhea and a prior perianal fistula.
PE Cervical lymphadenopathy: mild hepatomegaly and
splenomegaly; no pallor, purpuric patches, or sternal
tenderness.
Labs CBC/PBS: neutrophilic leukocytosis. Elevated ESR; normal
serum immunoglobulins; absence of respiratory burst (negative
nitroblue tetrazolium lest and chemoluminescence assay);
negative Mantoux test.
Imaging
Micro Pathology
CXR: hilar lymphadenopathy. US. abdomen: hepato-
splenomegaly; hepatic and splenic nodular lesions (due to
granulomas).
Characteristic granuloma formaiion with phagocytes, giant cells,
and occasional histiocytes in lymph nodes, liver, spleen, and
lungs.
Treatment Long-term TMP-SMX prophylaxis, -y-interferon.
Discussion Chronic granulomatous disease is most commonly an X-linked
disorder of ntuirophil function (may have variable inheritance
patterns) that is due to a deficiency of NADPH oxidase.
Neutrophils of affected padents demonstrate normal
chemotaxis, degranulation. and phagocytosis but cannot use the
oxygen-dependent myeloperoxidase system for microbial killing,
making patients susceptible to recurrent staphylococcal infections.
CHRONIC GRANULOMATOUS DISEASE
ID/CC A 19-year-old male has recurrent attacks of bilateral periorbital
and hand swelling coupled with respiratory difficulty that lasts
up to 24 hours and often requires hospitalization.
HPI He does not, however, complain of itching. His father and his
aunt both suffer from a similar illness.
PE Physical examination unremarkable.
Labs Decreased C4 (besi screening test); decreased CI inhibitor
(confirmatory test) and C2; normal C3; normal IgE.
Treatment Synthetic androgens (e.g., dana/ol), fresh frozen plasma.
Discussion CI esterase inhibitor deficiency is inherited as an autosomal-
dominant u ail; death may result from laryngeal edema. Also
known as hereditary angioedema.
O
en
-<
HEREDITARY ANGIOEDEMA
ID/CC A 25-year-old white female is referred to an internist by her
family doctor for a workup of recurrent sinusitis, chronic otitis
media, one episode of pneumonia that required hospitalization,
and recurrent bouts of watery diarrhea.
HPI She has seen an allergy specialist for several years and has
received desensitization shots for multiple allergies, including
pollen, dust, and cat hair.
PE Normal except for hypopigmented spots on neck and arms
(VITILIGO).
Labs Markedly decreased serum IgA; normal IgG and IgM.
Imaging XR, sinus: opacification of paranasal sinuses (due to chronic
sinusitis).
Treatment Largely supportive; antibiotic therapy; try to avoid blood or plasma
transfusion (anaphylaxis or serum sickness due to presence of
antibodies to IgA) .
Discussion Selected IgA deficiency is the most common congenital
immunodeficiency, especially in patients of European descent.
Diarrhea is usually caused by Giardia lambda; recurrent
sinopulmonary infections are caused by Streptococcus pneumoniae,
Haemophilus influenzae, or Staphylococcus aureus; associated with
an increased incidence of allergies and autoimmune diseases
such as SLE and rheumatoid arthritis. Selective IgA deficiency
may be due to a specific defect in isotype switching.
SELECTIVE IgA DEFICIENCY
"
ID/CC A 4-month-old male presents with chronic diarrhea and failure
to thrive.
HPI The infant was diagnosed with extensive mucocutaneous
candidiasis in the early neonatal period and shortly thereafter
developed a fulminant Pseudomonas septicemia that required
intravenous antibiotic therapy for an extended period of time. A
paternal cousin had developed similar and equally devastating
bacterial and fungal infections in the neonatal period and
subsequently died.
PE Emaciated; mucocutaneous candidiasis noted; tonsils not seen;
lymph nodes not palpable despite recurrent infections.
Labs CBC: severe lymphopenia. PBS: lack of mature lymphocytes.
Tests for cutaneous delayed hypersensitivity and contact
sensitization negative; serum immunoglobulin levels (IgG, IgA,
and IgM) low; adenosine deaminase (ADA) deficiency demon-
strated in red cells.
Imaging ( 1XR: absent thymic shadow.
Gross Pathology
Micro Pathology
Treatment
Discussion
Thymus fails to descend into the anterior mediastinum from the
neck and resembles fetal thymus of 6 to 8 weeks.
No lymphoid tissue in the lymph nodes, spleen, tonsils, and
appendix.
Bone marrow transplant from an HLA-identical sibling; IV
immunoglobulin; infusion of normal ADA-containing erythro-
cytes (ADA-PEG is also very successful); antibiotics; gene therapy
for ADA; genetic counseling (SCID caused by ADA deficiency
can be diagnosed prenatally by amniocentesis) .
Severe combined immunodeficiency syndrome is characterized
by marked depletion of the cells that mediate bodi humoral
(B-cell) and cellular (T-cell) immunity. SCID may be transmitted
as either an autosomal-recessive trait or an X-linked recessive
trait, or it may be sporadic; half of the cases inherited in an
autosomal-recessive manner are caused by a deficiency in ADA.
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SEVERE COMBINED IMMUNODEFICIENCY (SCID)
ID/CC A 7-month-old male is admitted for a workup of recurrent upper
respiratory tract and skin infections of several months' duration.
HPI His parents state that he has had recurrent URIs, one episode of
Haemophilus influenzae pneumonia, and severe odtis media.
PE Low weight and height for chronological age; chronic bilateral
suppurative otitis media; asymmetric arthritis of knees; no tonsillar
tissue seen; no lymphadenopathy or hepatosplenomegaly.
Labi Panhypogamrnaglobulinernia: very low IgG; IgA and IgM
undetectable.
Treatment Parenteral gamma globulin; monitor pulmonary function to
guard against chronic lung disease.
Discussion An X-linked disease (manifests only in males) characterized by a
selective B-cell defect with recurrent bacterial infections. Also
known as Bruton's disease, X-linked hypogammaglobulinemia is
due to a genetic defect in tyrosine kinase receptor found on
antibody precursors, resulting in impaired maturation and
development of antibodies. Male infants demonstrate infections
when maternal antibodies have cleared from their system.
X-LINKED HYPOGAMMAGLOBULINEMIA
ID/CC A 27-year-old white female complains of mouth ulcers,
prolonged fever, flulike symptoms, and increasing fatigue and
weight loss over the past 2 months.
HPI She recently moved from a large metropolitan area to a farm in
Ohio, where she spent 1 week cleaning a pigeons' loft.
PE VS: fever (38.5°C). PE: pallor; weight loss; enlarged liver and
spleen; generalized lymphadenopathy: sc altered sibilanl rales
over lung fields.
Labs
Imaging
Gross Pathology
Micro Pathology
( !'>( :/PBS: anemia; leukopenia. Small, budding fungus found
intracellularly in reticuloendothelial cells (macrophages) on silver
stain; elevated l.DH; positive blood culture for dimorphic
fungus.
CXR: nonsegmental shifting pneumonic infiltrates; mediastinal
adenopathy with popcorn calcifications; bilateral hilar adenopa-
thy. CT, abdomen: splenic calcifications.
Nodules with granuloma formation; central area of necrosis and
caseation with sclerosis and calcification; any organ may be in-
volved, mainly reticuloendothelial system (RES) and adrenals.
Granulomas with epithelioid cells, Eanghans' giant cells, and
organisms within macrophages; in disseminated disease,
organisms present in RES throughout body with proliferation.
Treatment Itraconazole; amphotericin B.
Discussion Histoplasmosis is a systemic fungal infection sometimes resembling
TB that is caused by Hislojilasiiia ai/i.\ulatam, a dimorphic fungus.
The \east form is found intracellularly: the mold form is found
in soil associated with bird or bat feces. Transmitted by inhalation
of mold spores, it varies in intensity from asymptomatic to fulmi-
nant (in immunocompromised patients). The disease is most
prevalent in the southeastern, mid-Atlantic, and central regions
of the United States.
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HISTOPLASMOSIS
ID/CC A 57-year-old black male complains to his doctor of increasing
weakness, swollen glands in the armpits and groin, and a feeling
of heaviness in the abdomen (due to hepatosplenomegaly) .
HPI The patient is an immigrant from Trinidad and Tobago and has
a history of nonresolving skin rashes and recurrent respiratory
infections.
PE Marked pallor; extensive papular skin rash with few erythematous
plaques over abdomen; generalized lymphadenopathy and
hepatosplenomegaly.
Labs CBC/PBS: marked leukocytosis (83,000) with relative lymphocy-
tosis and atypical lymphocytes. Increased LDH; hypercalcemia.
Imaging CXR: normal.
Micro Pathology Skin biopsy reveals infiltration by leukemic CD4+ T lymphocytes.
Treatment Aggressive combination chemotherapy.
Discussion Adult T-cell leukemia/lymphoma (ATLL) is associated with
HTLV-1 type C, a retrovirus that has a higher incidence in
blacks from the Caribbean and southeastern United States as
well as in people from southern Japan and sub-Saharan Africa.
The infection is acquired via transmission from mother to child
(breast milk), from sexual activity, from blood transfusion, or
from IV drug use.
HUMAN T-CELL LEUKEMIA VIRUS TYPE 1 (HTLV-1)
ID/CC A 2-day-old neonate is evaluated for an eye discharge.
HPI The baby's mother is a prostitute who did not receive any
prenatal cervical cultures during pregnancy.
PE Normal Ml-term male neonate; mucoid eye discharge, conjunctival
congesdon, and chemosis noted in both eyes; nonfollicles seen
on palpebral conjunctiva (due to absence of subconjunctival
adenoid layer at this age); mild superficial keradds also present.
Labs Gram stain of swab reveals increased PMNs and no bacteria;
characteristic intracellular inclusion bodies demonstrated by the
DIF test; cell culture yields Chlamydia trachomatis serotypes D
through K; chlamydia also grown from maternal cervical swab.
Treatment Erythromycin syrup; azithromycin suspension has also been
shown to be beneficial; no topical therapy.
Discussion Chlamydia trachomatis is an important cause of preventable
blindness; its strains can be further differentiated into 18
serotypes by mieroimmunofluorescence tests. Serotypes A, B,
Ba, and C are principally associated with endemic trachoma in
developing countries; serotypes D through K primarily cause
sexually transmitted infections in adults and inclusion
conjunctivitis and pneumonia in infants, transmitted through an
infected birth canal; and serotypes LI, L2, and L3 cause
lymphogranuloma venereum.
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INCLUSION CONJUNCTIVITIS
ID/CC
HPI
A 20-year-old male college student complains of sore throat,
fatigue, fever, swollen lymph nodes on the back of his neck,
anorexia, cough, and malaise of 10 days' duration.
He was initially given ampicillin by his school nurse, after which
he developed an extensive skin rash.
PE VS: fever. PE: enlargement of submaxillary and cervical lymph
nodes; exudadve tonsillitis: petechiae on soft palate; slightly-
enlarged spleen and liver.
Labs
Gross Pathology
Micro Pathology
CBC/PBS: anemia; thrombocytopenia; leukocytosis with absolute
lymphocytosis (50%); atypical lymphocytes. Elevated ALT, AST,
and bilirubin; positive heterophil antibody test (Paui.-Bunni .i I.
TEST); IgM antibodies to viral capsid andgen/monospot positive.
Enlarged spleen, lymph nodes, and, to lesser extent, liver;
hepatitis may be present along with brain involvement; splenic
rupture rare complication.
Proliferation of reticuloendothelial system; infiltration of spleen
by atypical lymphocytes.
Treatment Supportive.
Discussion
Infectious mononucleosis is a systemic viral infection that is
caused by Epstein-Barr virus (EBV). a herpesvirus, and is
transmitted through respiratory droplets and saliva. In developed
countries, it most commonly affects teenagers and young adults
("kissing disease"); in underdeveloped countries, it is seen as a
subclinical infection of early childhood. EBV infection is associ-
ated with an increased risk of Burkitt's lymphoma, Hodgkin's
disease, and nasopharyngeal carcinoma.
Atlas Links
H-M2-010
...J f. ! IM2-022
J3 INFECTIOUS MONONUCLEOSIS
ID/CC A 65-year-old male presents with a high fever, headache, extreme
prostration, a nonproductive cough, and severe breathlessness.
HPI He had been receiving chlorambucil for treatment of chronic
lymphocytic leukemia (CLL) and was in an extremely
debilitated state.
PE VS: fever; tachypnea; cyanosis. PE: conjunctival congestion;
pharyngeal inflammation; rales and wheezes heard on auscultation
over both lung fields; splenomegaly and lymphadenopathy (due
to CLL).
Labs
Imaging
Treatment
Discussion
No organisms seen or cultured from sputum; fluorescent
antibody directed against influenza virus was positive; viral
cultures of nasopharyngeal washings grew influenza virus;
fourfold rise in hemagglutination inhibition antibody titer
against influenza virus demonstrated.
CXR (PA view): bilateral, diffuse interstitial infiltrates suggestive
of atypical pneumonia.
Amantidine or rimantadine for influenza A (zanamivir or
oseltamivir for influenza A and B); ventilatory support, antipyretics,
and IV fluids. Secondary staphylococcal pneumonia should be
treated with parenteral antibiotics; yearly vaccination prevents
excessive morbidity and mortality, especially among the elderly.
Influenza viruses are medium-sized spherical RNA viruses
termed orthomyxoviruses; influenza A and B viruses each con-
tain 8 RNA segments and ID viral proteins. Influenza infection is
most common in winter, with the severity of a given outbreak
depending on the status of immunity in the community.
Previous natural infection or immunization with viruses that are
immunologically dose to the current strain limits new infection,
bin if antigenic drift results in reduced cross-reactivity, the new
strain will spread more rapidly. New strains produced by
antigenic shift account for most major outbreaks. Influenza
affects all segments of the population, but severe infections and
major complications are most common in patients who are
young, elderly, or debilitated.
INFLUENZA
ID/CC A 30-year-old female presents with fever, chills, malaise,
headaches, and myalgias.
HPI She was diagnosed as suffering from secondary syphilis with an
extensive nonpruritic skin rash, condylomata lata, and mucous
patches in the mouth, for which she received a dose of
intramuscular penicillin 6 hours ago.
PE VS: fever; tachycardia; mild hypotension.
Treatment No specific treatment; symptoms subside in 24 hours.
Discussion The Jarisch-Herxheimer reaction consists of fever, chills, mild
hypotension, headache, and an increase in the intensity of
mucocutaneous lesions 2 hours after initiating treatment of
syphilis with penicillin or another effective antibiotic; symptoms
usually subside in 12 to 24 hours. The reaction occurs in 50% of
patients with primar\ syphilis .mil in 90% oJ [hose with secondary
syphilis. The Jarisch-Herxheimer reaction also occurs after
treatment of other spirochetal diseases (e.g., louse-borne relapsing
lever caused b\ Borrelia recurrentis) . It has been suggested that
the release of treponemal lipopolysaccharides might produce
this symptom complex.
JARISCH-HERXHEIMER REACTION
ID/CC A 40-year-old male smoker complains of acute-onset high fever,
chills, a nonproductive cough, tachypnea, and pleuritic chest
pain.
HPI A number of similar cases have been reported in his workplace
in recent months. The patient admits to significant alcohol and
tobacco consumption and uses a humidifier at night.
Pt
Labs
Imaging
VS: fever; dyspnea. PE: rales present bilaterally on auscultation.
Sputum exam with Gram stain reveals no pathogenic organisms.
CBC: neutrophilic leukocytosis. Cold agglutinins absent; indirect
fluorescent antibody technique reveals stable titer of > 1:256
(considered diagnostic); direct immunofluorescent staining of
sputum confirms presence of Legionella.
CXR, PA: bilateral diffuse, patchy infiltrates and ill-defined
nodules.
Gross Pathology Nodular areas of consolidation that may progress to involvement
of one or more lobes of the lung.
Micro Pathology Alveolar exudate with PMNs, macrophages, and fibrin; in more
severe cases, destruction of alveolar septa.
Treatment Erythromycin or an active fluoroquinolone.
Discussion Legionnaire's disease is caused by Legionella pneumophila, a
filamentous, flagellated, aerobic gram-negative, motile bacillus,
and is more common in immunocompromised patients.
Epidemiologic studies have established drinking water and air
conditioners as the sources of outbreak.
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LEGIONELLA PNEUMONIA
ID/CC A 30-year-old Pakistani immigrant complains of chronic fever,
weight loss, increased abdominal girth, a feeling of heaviness,
and appetite loss.
HPI Almost a year ago, the patient had a small, pruritic red papule on
his left arm that was caused by an insect bite and disappeared
spontaneously.
PE Skin darkening; trophic changes in hair; massive nontender,
hard splenomegaly; hepatomegaly without jaundice; generalized
lyinphadenopathy: peripheral edema; ecchynaosis.
Labs CBC/PBS: anemia, leukopenia, thrombocytopenia
(pancytopenia), and monocytosis; amastigotes in buffy coat.
Hypergammaglobulinemia; decreased albumin; increased ALT
and AST.
Imaging CT/US, abdomen: splenomegaly.
Gross Pathology
Micro Pathology
Massively enlarged spleen; also greatly increased in weight, dark
colored, and congested with Leishman-Donovan bodies.
Proliferation of reticuloendothelial system cells; biopsy or
aspiration reveals parasite-filled macrophages in infected locations.
Treatment Pentavalent antimony (e.g., sodium stibogluconate):
amphotericin B or pentamidine iscthionate.
Discussion Also known as kala azar, leishmaniasis is a zoonosis that is produced
by Ijoshmania donovani and is transmitted through the bite of
the Phlebotomuh sandfly. It is associated with a high fatality rate
when left untreated.
Atlas Links Lih.U M-M2-014A, M-M2-014B, M-M2-014C, H-M2-014
LEISHMANIASIS
ID/CC A 30-year-old male from India presents with slowly progressive
hypopigmented skin patches and nodules together with a
peculiar deformity of the nose.
HPI The patient has a history of nasal stuffiness and bloody nasal
discharge; he also complains of loss of libido.
PE Leonine facies (thickened facial and forehead skin); loss of
eyebrows and eyelashes (MADAROSIS); scleral nodules; depressed
nasal bridge ("SADDLE-NOSE* DEFORMITY); gynecomastia; testicular
atrophy; numerous symmetrical, hypopigmented macules with
vague edges and erythematous, smooth, shiny surfaces; skin
plaques and nodules; partial loss of pinprick and temperature
sensation (HYPOESTHESIA); no anhidrotic changes; symmetrically
enlarged ulnar and common peroneal nerves.
Labs CBC: mild anemia. ESR elevated; slil skin smears reveal
numerous acid-fast bacilli on modified ZN staining.
Micro Pathology
Dermis massively and diffusely infiltrated with foamy histiocytes
with bacilli and globi (masses of acid-fast bacilli) containing
Vii chow giant cells; bacilli found only rarely in epidermis and in
subepidermal "clear zone"; epidermis thinned out widi flatten-
ing of rete ridges.
Treatment Multidrug iherapy with rifampicin, dapsone, and clofazimine.
Discussion The discovery of one or more of the following is pathogno-
monic of leprosy: (1) anesthetic skin lesions (found in all tuber-
culoid and many lepromatous cases): (2) thickening of one or
more nerves (found in many lepromatous and some tuberculoid
cases); and (3) the presence of acid-fast bacilli in skin smears
(found in all lepromatous and some tuberculoid cases).
Myrobiictrrium Irpmehas not been cultured in vitro thus far.
Frequent complications include hand crippling (secondary to
nerve damage) and blindness. It is currently believed dtat in
most instances, the mode of transmission is via person-to-person
contact.
Atlas Links LU.CE3 :J MC-179A, MC-179B
LEPROSY— LEPROMATOUS
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ID/CC A 26-year-old male from India presents with a hypopigmented,
anesthetic skin patch over the left side of his face.
HPI He also complains of an occasional "electric current"-like
sensation radiating from his left elbow to his hand.
PE Dry, hypopigmented. anesthetic patch over left cheek; left ulnar
nerve enlarged and palpable; eye, ear, nose, and throat exam
normal; testes normal (vs. signs that are often demonstrable in
lepromatous leprosy).
Labs Glucose-6-phosphate dehydrogenase (G6PD) levels within
normal range (done to prevent dapsone-associated hemolysis);
slit skin smears reveal few acid-fast bacilli; skin biopsy from
patch diagnostic of tuberculoid leprosy.
Gross Pathology Single or small number of lesions with macular or raised edges.
Micro Pathology
Skin biopsy reveals many well-formed epithelioid granulomas
with very few acid-fast bacilli.
Treatment Chemotherapy with rifampin and dapsone.
Discussion Caused by Mycobacterium leprae, an acid-fast bacillus. The orga-
nism has two unique propenies: il is thermolabile. growing best
31 27°C to 30°C, and it divides very slowly; generation time is 12
to 14 days. Consequently, leprosy in humans typically evolves
very slowly. Tuberculoid leprosy predominantly affects the skin
with limited nerve involvement (most commonly ulnar - and per-
oneal); lepromatous leprosy has diffuse involvement of the skin,
eyes, nerves, and upper airway with disfigurement of the hands
and face (leonine facies).
Atlas Links mcmzi MC-179A, MC-179B
LEPROSY— TUBERCULOID
ID/CC A 35-year-old Britisli dairy farmer complains of a high remittent
fever with chills, severe muscle aches, decreased urine output,
and dark-colored urine for the past 2 days.
HPI He also complains of an extensive skin rash and nasal bleeding
(epistaxis). A careful history reveals that the area in which he
works is infested with rodents.
PE VS: fever; tachycardia; hypotension. PE: icterus; extensive hem-
orrhagic maculopapular skin eruption; conjunctival suffusion;
lymphadenopathy.
Labs CBC: leukocytosis with neutrophilia; thrombocytopenia. Mild
hyperbilirubinemia, predominantly conjugated; increased
alkaline phosphatase; elevated BUN and creatinine. UA:
proteinuria, casts, and RBC.s. Blood culture (positive during first
10 days of illness) and urine culture (positive after second week
of infection) on Fletcher's medium isolated Ixtptospira interrogans;
serologic diagnosis (positive during second week of illness):
microscopic slide agglutination demonstrated significant titer of
antibody to /.. interrogans.
Imaging CXR: patchy alveolar infiltrates consistent with alveolar
hemorrhage.
Gross Pathology Severe infection damages both the liver and kidneys.
Micro Pathology
Liver biopsy shows focal centrilobular necrosis with focal lympho-
cytic infiltration and disorganization of liver cell plates together
with proliferation of Kupffer cells with cholestasis; kidney biopsy
reveals mesangial proliferation with PMN infiltration.
Treatment Penicillin (dose modified due to presence of renal failure),
doxycycline; hemodialysis.
Discussion Weil's disease, a severe form of leptospirosis caused by LejHospira
interrogans complex, is characterized by fever, jaundice, cuta-
neous and visceral hemorrhages, anemia, azotemia, and altered
consciousness; major vectors to humans are rodents.
Transmission occurs through direct contact with the blood, tis-
sue, or urine of infected animals. Person-to-person transmission
is highly unlikely. Preventive measures include limiting the ro-
dent population and vaccinating animals.
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LEPTOSPIROSIS (WEIL'S DISEASE)
ID/CC A 2-week-old female is brought to the emergency room because
of high fever and convulsions.
HPI She also has an extensive skin rash on her legs and trunk.
PE VS: fever. PE: generalized hypotonia: extensive maculopapular
skin rash; nuchal rigidity; involuntary flexion of hips when
flexing neck (Brudzinski's sign).
Labs CBC: neutrophilic leukocytosis. LP: elevated CSF cell count
(750 cells/ mL), mostly neutrophils; elevated CSF protein; low
CSF sugar. Cram-positive, facultative, intracellular, nonsporulat-
ing motile bacilli on Cram stain and culture.
Gross Pathology Purulent meningitis.
Micro Pathology
Bacillus provokes both acute suppurative reaction with neu-
trophilic infiltration and chronic granuloma formation with
focal necrosis.
Treatment IV antibiotics (high-dose ampicillin).
Discussion Listeriosis is caused by Listeria monocytogenes. Bacteiial infection
may occur early (acquired in utero) or later (drinking contami-
nated milk) in neonatal life. Maybe rapidly fatal if disseminated.
Also occurs in adults immunocompromised by disease (e.g.,
renal disease or HIV). Escherichia coii and group B streptococcus
are two other common causes of neonatal meningitis.
LISTERIOSIS
ID/CC A 12-year-old male presents with fatigue, fever, headache,
fleeting joint pain, and a reddish rash on his trunk and left leg
of 1 week's duration.
HPI The patient is a native of Connecticut and attended a summer
camp in the state's national park 2 weeks ago. He recalls having
noticed a tick bite on his leg about 2 weeks ago.
PE VS: fever. PE: red macule on site of bite that has grown circum-
ferentially; acdve border and central clearing (ERYTHEMA
CHRON1CUM MIGRANS); femoral lymphadenopadiy; mild neck
stiffness; normal CNS exam.
Labs Posidve IgM ELISA for Borrelia burgdorferi; diagnosis confirmed
by Western blot assay. ECG: normal. LP: lymphocytic pleocytosis;
increased proteins. B. burgdorferi grown on Noguchi medium.
Gross Pathology
Erythema chronicum migrans (ECM) is characteristic of Lyme
disease; must be minimum of 5 cm in diameter for diagnosis to
be made; center may desquamate, ulcerate, or necrose; satellite
lesions sometimes seen; may spontaneously disappear with time.
Treatment Doxycycline: amoxicillin; ceftriaxone.
Discussion The most common disease transmitted by vectors in the United
States, Lyme disease is caused by Borrelia Imrgdorferi,, a spiro-
chete, and is transmitted through Ixodes species dck bites. Ticks
acquire B. burgdorferi from deer mice, which are the natural
reservoir. There are three recognized stages: stage 1 consists of
ECM and constitutional symptoms; stage 2, cardiac or neuro-
logic involvement; and stage 3, persistent migratory arthrids,
synovitis, and atrophic patches on the distal extremities
(At RODliRMATITIS CHK( >\'ICl'M ATROPHICANS) .
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LYME DISEASE
ID/CC A 57-year-old black female from Kenya complains of increasing
weight and edema of the lower legs with difficult)' walking.
HPI Over the years she has had episodes of fever with swelling of
inguinal lymph nodes and itching. She has also had numerous
attacks of malaria.
PE Inguinal lymph nodes indurated and slightly increased in size;
marked deformity in both legs with thickening of skin and
greatly increased diameter; rubbery consistency.
Labs
Imaging
Gross Pathology
Micro Pathology
Treatment
Discussion
PBS: several microfilariae; prominent eosinophilia.
Lymphangiogram: partial lymphatic obstruction at iliac level.
Presence of adult worms in lymphatics; marked fibrosis sur-
rounding obstructed vessels.
Granulomatous reaction with plasma cell and lymphocytic infil-
tration; giant cell formation: intense fibroblastic hyperplasia.
Ivermectin; diethylcarbamazine; surgery in advanced cases.
Lymphatic filariasis is a chronic disease that is due to lymphatic
obstruction and is caused by several types of filarial round-
worms, mainly Wuchereria bavoo/li and Brugiri malayi; it is trans-
mitted by female mosquito bites. Also known as elephantiasis.
Atlas Link EOT '1 M-M2-020
LYMPHATIC FILARIASIS
ID/CC A 25-year-old male complains of swollen, tender masses in his
groin and very painful genital ulcers of 1 week's duration.
HPI The patient admits to having had unprotected sex with multiple-
partners.
PE Swollen, erythematous, tender inguinal nodes, usually bilateral,
with draining sinuses (inguinal adenitis, buboks); multiple small
genital lesions.
Labs
Gross Pathology
Micro Pathology
Treatment
Discussion
Inguinal node biopsy diagnostic; positive complement fixation
test; positive immunofluorescence test.
Primary lesion is ulcerated nodule; gives rise to inguinal bubo,
an enlarged lymph node sometimes characterized by fistulous
tract formation; balanitis, phimosis, and rectal involvement with
stricture may also be present.
Neutrophilic infiltration of primary lesion with areas of necrosis;
lymphoid hyperplasia of lymph nodes with foci of macrophage
accumulation; abscess formation with fibrosis.
Doxycycline; tetracycline; azithromycin; erythromycin; TMP-
SMX; ceftriaxone; ciprofloxacin.
Lymphogranuloma venereum is an STD that is due to
Chlamydia trachomatis (LI, L2, L3). Counseling should be
given about other STDs (e.g., AIDS, syphilis, gonorrhea).
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LYMPHOGRANULOMA VENEREUM
ID/CC A 30-year-old missionary conies to the emergency room
complaining of high fever, chills, severe headache, and
confusion.
HPI Upon returning from Africa 2 weeks ago. he began to feel
weak and experienced backaches, pain behind the eyes, and
sleepiness.
PE VS: fever (39°C); tachycardia. PE: pallor; profuse sweating; mild
splenomegaly without lymphadenopailiy.
Labs CBC/PBS: anemia; thrombocytopenia; plasmodia in
erythrocytes on thick peripheral blood smear. Slight
hyperbilirubinemia and hypoglycemia.
Gross Pathology Liver and spleen moderately enlarged and soft in consistency,
with sequestration and hemolysis of erythrocytes and
macrophages; hyperplasia of Kupffer cells; malarial pigment in
spleen and liver; brain capillaries may show thromboses.
Micro Pathology Hypertrophy of phagocytic system: ischemic necrosis
surrounding occluded blood vessels in brain.
Treatment Chloroquine; quinine for cerebral malaria; sulfadiazine-
pyrimethamine, mefloquine, tetracycline for areas with
chloroquine-resistant strains; primaquine for radical treatment.
Discussion Malaria is transmitted by female Anopheles mosquitoes.
Plasmodium falciparum may be lethal, producing cerebral
malaria. Other types include P. vivax, P. ovale, and P. malarmr.
Atlas Links ._.! .:_] H-M2-022A, H-M2-022B, H-M2-022C
MALARIA
ID/CC A 3-year-old female is brought to the emergency room with a
high fever of 7 days' duration, accompanied by redness of die
eyes, persistent dry cough, and coryza.
HPI Her family doctor had treated her illness as a viral URI, but no
improvement was seen. One day before her admission, her
mother noticed a skin rash starring behind her ears and face
that has now spread to her trunk and extremities.
PE Pallor; injected conjunctiva; hyperemic throat; erythematous
maculopapular rash on face, neck, trunk, and extremities;
retroauricular lymphadenopaihy; bluish-gray spots surrounded
by erythematous areola on buccal mucosa in region of first
molar (KOPLIK'S SPOTS) .
Labs CBC: leukopenia.
Gross Pathology
Micro Pathology
Koplik's spots pathognomonic of measles; appearance presages
rash by approximately 2 days; uniform lesions (vs. varicella).
Lymphocytic dermal infiltration; multinucleated giant cells in
reticuloendothelial system (WARTHIN-FINKELDEY CELLS) .
Treatment No specific antiviral therapy available; treat complications.
Discussion
Atlas Links
Also called rubeola; not to be confused with rubella. Measles is
produced by a paramyxovirus and is transmitted by respiratory
droplets; a live attenuated vaccine is available. Measles has an in-
cubation period of 10 to 14 days. Sequelae include encephalitis,
subacute sclerosing panencephalitis (SSPE), and giant cell
pneumonia.
PED-030A, PED-030B
MEASLES
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ID/CC A 12-year-old white female is brought to the emergency room
because of sudden fever with chills, severe headache, pain in
the extremities and back, stiff neck, and generalized rash; she
also fainted while in school.
HPI She had been well until admission, with no relevant history. In
the emergency room, she vomits bright red blood twice.
PE VS: tachycardia; hypotension (BP 70/50). PE: altered senso-
rium; pallor; moist, cold skin; nuchal rigidity and positive
Kernig's sign; petechial rash all over body; minimal papilledema
on funduscopic exam; no focal neurologic signs.
Labs Hypoglycemia. Lytes: hyponatremia; hyperkalemia. CBC/PBS:
thrombocytopenia; neutrophilic leukocytosis. l.F: CSF cloudy
and under increased pressure; increased proteins; low sugar.
Gram-negative diplococci (Neisseria meningitidis) seen within and
outside WBCs on Gram stain; negative India ink and ZN stain;
growth of meningococci later revealed on blood culture.
Imaging CT, head: normal. CT, abdomen: bilateral adrenal hemorrhage.
Gross Pathology Bilateral adrenal hemorrhagic necrosis; skin necrosis; pyogenic
meningitis.
Micro Pathology
Meningeal hyperemia with abundant purulent exudate;
diplococcus-containing PMNs; acute hemorrhagic necrosis
of adrenal glands.
Treatment Steroid replacement; IV fluids; dopamine; IV penicillin G;
prophylactic rifampin for close contacts.
Discussion Meningococcemia is a fulminant disease caused by several
groups of Neisseria meningitidis; the cause of death is adrenal
necrosis with vascular collapse. A meningococcal vaccine is
available. Also known as Waterhouse-Friderichsen syndrome.
Atlas Link mcra2i IM2-024
MENINGOCOCCEMIA
ID/CC A 24-year-old white female with insulin-dependent diabetes
meilitus (IDDM) is hospitalized for ketoacidosis following a
night out drinking: on (he fifth day she develops right
periorbital swelling and a mucopurulent postnasal discharge
that fails to respond to antibiotics.
HPI She admits to irregular adherence to glucose control and
insulin dosing.
PE Right periorbital and paranasal edema; swelling of conjunctiva
(( i ii mosi.s): exophthalmos; black ulceration of nasal mucosa;
third cranial nerve (CN III) palsy.
Labs Large, irregular, nonseptate hyphae branching at wide (> 90°)
angles on nasal culture.
Imaging
Gross Pathology
Micro Pathology
Treatment
Discussion
XR, plain: opacification of paranasal sinuses.
Necrotic destruction of paranasal sinuses and orbit with dissemi-
nation to lung and brain.
Purulent arteritis with thrombi composed of hyphae; inflamma-
tion and necrosis with polymorphonuclear infiltrate.
Maintain tighter glucose control; amphotericin B; surgical
drainage.
Mucormycosis is a phycomycosis produced by Mucor and
Rhizopus molds: it should be suspected in cases of antibiotic-
resistant sinusitis, especially in the presence of underlying
diabetes, burns, lymphoma, or leukemia.
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Atlas Link LUCta I I M-M2-025
MUCORMYCOSIS
ID/CC A 6-year-old white male presents with fever, nausea, vomiting,
swelling, and tenderness of the mandibular angle; he finds it
difficult to talk, eat, or swallow.
HPI Two of his classmates were diagnosed with mumps 2 weeks ago.
There is no vaccination record.
PE VS: fever. PE: outward and upward displacement of ear; obliter-
ated mandibular hollow; orifice of Stensen's duct swollen and
hyperemic; right testicle enlarged and painful.
Labs
Gross Pathology
Micro Pathology
Treatment
Discussion
MUMPS
CBC: leukopenia with lymphocytosis. Hyper amylasemia; positive
complement fixation antibodies.
Parotid glands enlarged with areas of necrosis and mononuclear
infiltrate; encephalitis, orchitis, oophoritis, meningitis, and
pancreatitis may also be present.
Examination of parotid glands reveals perivascular mononu-
clear, lymphocytic, and plasma cell infiltrate with necrosis;
ductal obstruction and edema; testicular interstitial edema;
perivascular cerebral lymphocytic cuffing.
Supportive; analgesics for pain; treat complications.
A systemic infection caused by the mumps virus, an RNA
paramyxovirus, mumps is transmitted by droplets and direct
contact. Bilateral testicular involvement may lead to sterility;
one of the most common causes of pancreatitis in children.
A vaccine is available with measles and rubella (MMR).
ID/CC A '20-year-old male college student presents with a productive
cough, headache, malaise, runny nose, and fever.
HPI He has a history of sore throat preceding the onset of the
cough, which initially was nonproductive.
PE VS: lever. PK: mild respiratory distress; auscultation reveals fine
to medium rales over right lower lobe.
Labs Gram stain of sputum negative; routine cultures of both blood
and sputum negative. CBC: leukocyte count normal. Fourfold
rise in complement fixation titer in paired sera; cold agglutinin
titer > 1:128.
Imaging CXR: patchy alveolar infiltrates involving right lower lobe; ap-
pears worse than the clinical picture.
MYCOPLASMA PNEUMONIA
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Gross Pathology Unilateral lower lobe pneumonia with lirm. red pulmonary
parenchyma in affected areas. ^
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Micro Pathology Bronchial mucosa congested and edematous; inflammatory re-
sponse consists of perivascular lymphocytes initially and PMNs
later in infection. Organism lacks cell wall (thus penicillins and
cephalosporins are ineffective).
Treatment Erythromycin.
Discussion Mycoplasma pneumoniae is the most common cause of primary
atypical pneumonia. Transmission is by droplet spread; rapidly
infects those living in close quarters.
ID/CC A 50-year-old diabetic male presents with fever, pain, and a
necrotizing swelling over his left leg.
HPI His symptoms began about a week ago with redness and swelling
of the left leg followed by bronze discoloration of the skin and
the appearance of hemorrhagic bullae.
PE Extensive cutaneous gangrene observed over left leg with many
ruptured bullae; black necrotic eschar with surrounding ery-
thema resembles a third-degree burn.
Labs Swab staining reveals presence of chains of gram-positive cocci;
culture isolated (J-hemolvtic group A streptococcus (Streptococcus
pyogenes) .
Micro Pathology
Treatment
Discussion
Biopsy specimen reveals areas of necrosis in dermis and subcuta-
neous fat. infiltration with PMNs, and vasculitis and thrombosis
in vessels in the superficial fascia.
Treatment includes rapid surgical excision of necrotic tissue in
combination with appropriate antibiotics.
Streptococcal gangrene is a group A streptococcal cellulitis that
rapidly progresses to gangrene of the subcutaneous ussue and
necrosis of the overlying skin; the disease process usually
involves an extremity. Necrotizing fasciitis is also recognized as a
polymicrobial infection that is caused by aerobes and anaerobes
("SYNERGISTIC NECROTIZING CELLULITIS"). Infection spreads quickly
through various fascial planes, the venous system, and
lymphatics. Predisposing etiologies include surgery, trauma,
and diabetes.
NECROTIZING FASCIITIS
ID/CC A 45-year-old white male undergoing chemotherapy for
Hodgkin's lymphoma is brought to the emergency room by his
wife because of shortness ol breaih and cyanosis.
HPI For the past 3 months, he has been complaining of intermittent
weakness, fever with chills, and foul-smelling, thick greenish
sputum.
PE VS: fever (38°C); tachypnea; tachycardia. PE: pallor; mild
cyanosis; localized dullness with bronchial breathing; dimin-
ished breaih sounds over left lower lobe.
Labs
Imaging
Gross Pathology
Micro Pathology
CBC: leukocytosis with neutrophilia; anemia. Sputum culture
reveals gram-positive, filamentous, partially acid-fast staining
bacteria (due to Nocardia).
CXR; nodular infiltrate in left lower lobe with air-fluid level
(abscess) and left pleural effusion.
Lung lesions or disseminated lesions (brain, liver, kidney, subcu-
taneous tissue) consist of necrotic centers within regions of
consolidation and abscess formation resembling pyogenic
pneumonia.
Consolidation of alveoli with pus formation (exudate of PMNs
and fibrin) and surrounding granulomatous reaction.
Treatment Six-month course of TMP-SMX; surgery.
Discussion A chronic bacterial infection seen in diabetics, leukemia and
lymphoma patients, and immunocompromised patients, nocar-
diosis usually involves the lungs with possible dissemination to
the brain, subcutaneous tissue, and other organs. It is caused by
Nocardia asteroides, a branching, aerobic, gram-positive orga-
nism that is weakly acid fast and is sometimes confused with
Mycobacterium tuberculosis.
NOCARDIOSIS
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ID/CC A 60-year-olcl male who was hospitalized following a stroke pre-
sents with a high-grade fever with chills and obtundation.
HPI He had been catheterized due to urinary incontinence and was
receiving cephalosporin for treatment of aspiration pneumonitis.
PE VS: fever.
Labs Blood culture grew Enterococcus fecalis (morphologically indis-
tinguishable from streptococci and immunologically similar to
members of group D streptococci, the enterococci are metaboli-
cally unique in their ability to resist heat, bile, and 6.5% NaCl);
urine culture also isolated Streptococcus fecalis.
Treatment Ampicillin with gentamicin (vancomycin can be substituted for
ampicillin in patients with penicillin allergies).
Discussion Enterococci constitute a relatively common cause of UTIs,
wound infections, and peritonitis and intra-abdominal abscesses;
they have also become an increasingly prominent cause of
bacteremia, which usually originates from a focus in the urinary
tract or abdomen. The incidence of nosocomial bacteremias
caused by these organisms is also increasing, particularly in
patients who have received cephalosporins or other broad-
spectrum antibiotics. All clinically significant isolates should be
subjected to testing for 3-lactamase production, high-level
aminoglycoside resistance, and vancomycin resistance to deter-
mine if an alternative therapy is necessary. Infections caused by
enterococci that produce fi-lactamase are treated with an antimi-
crobial agent that combines a penicillin with a P-lactamase
inhibitor; infections caused by strains that are highly resistant
to aminoglycosides are treated with vancomycin.
NOSOCOMIAL ENTEROCOCCAL INFECTION
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ID/CC A 56-year-old white female is referred to an ophthalmologist for
an evaluation of diminished visual acuity.
HPI She has spent most of her adult life as a missionary in rural
Senegal and Mali. She admits to chronic generalized itching,
mostly while showering.
PE Wrinkling and loss of elastic tissue in skin; marked hypopigmen-
tation of shins; 2- to 3-cm, nonfixed, firm, nontender subcuta-
neous nodules on iliac bones, knees, and elbows; chronic
conjunctivitis, sclerosing keratitis, and chorioretinal lesions on
eye exam.
Labs CBC/PBS: eosinophilia. Fifty-milligram dose of diethylcarba-
mazine produces severe pruritus, rash, fever, and conjunctivitis
(positive Mazzotti reaction).
Micro Pathology Skin biopsy at iliac crest shows microfilariae.
Treatment Ivermectin; suramin.
Discussion Onchocerciasis is caused by Onchocerca volvulus and is transmit-
ted by the blackfly (SlMUUVM). which breeds near rivers; hence it
is also known as "river blindness." 1-arvae migrate through sub-
cutaneous tissue, producing painless soft tissue edema (CALABAR
EDEMA); with time, subcutaneous nodules form and filariae ob-
struct dermal h/mphatics, producing atrophy and hypopigmen-
tation. Microfilariae concentrate in the eyes, leading to
chorioretinitis and blindness.
ONCHOCERCIASIS
ID/CC A 9-year-old male is admitted for an evaluation of a suspected
underlying immune deficiency.
HPI He has been hospitalized and treated several times for recurrent
life-threatening septicemia due to Streptococcus pneumoniae,
meningococcus, and Haemophilus influenzae. Careful history
reveals that a few years ago he underwent an emergency
splenectomy following traumatic splenic rupture in a motor
vehicle accident.
PE Left paramedian postsurgical scar seen on abdomen.
Labs Reduced IgM levels; reduced antibody production when chal-
lenged with particulate antigens; PBS reveals Howell-Jolly
bodies.
Imaging US, abdomen: spleen is absent.
Treatment Pneumococcal vaccine and prophylactic antibiotics (penicillin,
amoxicillin, TMP-SMX).
Discussion Patients who have undergone splenectomy or who are function-
ally asplenic are at increased risk for overwhelming bacteremia;
pathogens include organisms that possess a polysaccharide
capsule, such as meningococcus, Staphylococcus, the DF2 bacillus,
and, especially. Streptococcus pneumoniae and Haemophilus
influenzae type B. Such functionally asplenic patients include
individuals with sickle cell disease and those who have
undergone splenic irradiation. Pneumococcal vaccine is
indicated in all patients who have undergone splenectomy,
particularly children and adolescents.
OVERWHELMING POSTSPLENECTOMY INFECTIONS
ID/CC A 12-year-old girl arrives in the emergency room with pain,
swelling, and limited motion of her left hand; she also complains
of fever and chills.
HPI The girl was bitten by a cat yesterday while playing at a friend's
house.
PE Hand is ei yilicmalous, shiny, and markedly edematous; on
palpation, hand is tender with fluctuation (cellulitis); limited
passive and active motion; yellowish-green purulent fluid drains
from wound; left epitrochlear and axillary lymphadenitis without
lymphangitis.
Labs Gram-negative rods with bipolar staining of abscess aspirate;
catalase and oxidase positive (PasteurelUi multoada) .
Imaging XR. plain: soft tissue swelling; no periostitis or erosions (vs.
osteomyelitis).
Treatment Incision and drainage, amoxicillin/clavulanate; tetracycline;
penicillin.
Discussion Pasteurelia multocida is the most common bacterium isolated
from cat bite wounds and may progress to osteomyelitis. Human
bite infections are most commonly caused by EikeneBa mrrodens
and are treated with penicillin.
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PASTEURELLA MULTOCIDA
ID/CC A 44-year-old male archaeologist presents with high fever,
malaise, intense headache, severe myalgia, and painful swelling
in the inguinal region.
HPI He recently returned from a trip to Arizona.
PE VS: tachycardia. PE: drowsy looking; no meningeal signs; pustule
seen at site of an insect bite on left upper arm: inguinal lymph
nodes enlarged, fluctuant, and tender (buboes); no lesion on
external genitalia.
Labs CBC/PBS: normal; no malarial parasites. Gram-negative bacilli
with "safety pin" appearance seen in aspirates from buboes;
culture of aspirate reveals Yersinia pestis.
Gross Pathology
Enlarged lymph nodes are necrotic and suppurative; pneu-
monic form shows lobar consolidation.
Micro Pathology Numerous organisms in suppurative and necrotic lymph tissue.
Treatment Streptomycin; gentamicin; doxycycline prophylaxis for close
contacts; tetracycline.
Discussion
Plague is usually acquired alter contact with rodents and fleas in
endemic areas (southwestern United States). Septic shock,
pneumonia, DIG, and vascular collapse are life-threatening
sequelae. Death rapidly ensues in the absence of treatment.
PLAGUE
ID/CC An 1 1-year-old white male presents with a high-grade fever, a
productive, blood-tinged cough, mucoid sputum, and pleuritic
left-sided chest pain of a few days' duration.
HPI The child had previously been well and is fully immunized.
PE VS: fever; tachypnea. PE: use of accessory respiratory muscles;
central trachea; decreased left respiratory excursion; increased
vocal fremitus in left infrascapular area with dullness to
percussion; bronchia] breathing with coarse crackles heard over
left lung area.
Labs CBC: increased WBC count; preponderance of neutrophils.
ABGs: hypoxemia without hypercapnia. Gram-positive
diplococci in sputum; ct-hemolytic colonies of gram-positive
diplococci (Streptococcus pneumoniae) on blood agar culture.
Imaging
Gross Pathology
CXR: homogenous opacification of left lower lobe (LOBAR
CONSOLIDATION) with small left pleural effusion.
Consolidation of lung parenchyma passes through four stages:
congestion and edema, red hepatization, gray hepatization, and
resolution.
Micro Pathology Vascular dilatation with hyperemia and alveolar edema; PMNs
rich in purulent exudate; fibrin deposition; hardening of lung
parenchyma with fibrin clotting inside alveoli (consolidation).
Treatment Parenteral therapy with penicillin; monitor with radiologic
imaging; supplemental oxygen for respiratory distress.
Discussion S. pneumoniae is the most common cause of community-
acquired pneumonia and produces typical lobar pneumonia.
Atlas Links
CD M-M2-035A, M-M2-035B, M-M2-035C, PG-M2-035
PNEUMOCOCCAL PNEUMONIA
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ID/CC A 32-year-old HIV-positive male presents with progressively
increasing dyspnea over the past 3 weeks.
HPI He also complains of a dry, painful cough, marked fatigue, and
a continuous low-grade fever. He has been noncompliant with
cotrimoxazole prophylaxis.
PE VS: fever; marked tachypnea. PE: pallor; generalized lym-
phadenopathy; respiratory distress; intercostal retraction: mild
central cyanosis; nasal flaring; coarse, crepitant rales auscultated
at both lung bases.
Labs
Imaging
Gross Pathology
Micro Pathology
ABGs: hypoxemia out of proportion to clinical findings.
Pneumocystis am nit on methenamine silver stain of induced spu-
tum or bronchoalveolar lavage; ELISA/Western blot positive for
HIV. CBC: leukopenia with depressed CD4+ cell count. Serum
LDH typically elevated.
CXR: diffuse, bilaterally symmetrical interstitial and alveolar in-
filtration pattern, predominantly perihilar; no lymphadenopathy
or effusion.
Congestion and consolidation of lungs with hypoaeration.
Eosinophilic exudate in alveoli with multiple 4- to 6-mm cysts
containing oval bodies (mf.rozoites) on lung biopsy or
bronchial lavage; Pneumocystis abundant on Gomori
methenamine silver stain.
Treatment TMP-SMX; pentamidine; steroids for severe disease.
Discussion Pneumocystis carinii pneumonia is an opportunistic infection that
causes interstitial pneumonia in many immunocompromised
patients. Traditionally it has been classified as a protozoan;
however, P. carinii ribosomal RNA indicates that the organism is
fungal. It is seen in the upper lobes in patients receiving inhaled
pentamidine prophylaxis. Treat HIV patients prophylactically
with TMP-SMX for P. carinii pneumonia if the CD4 count
is < 200.
Atlas Links EUSIIE M-M2-036A, M-M2-036B, M-M2-036C
PNEUMOCYSTIS CARINII PNEUMONIA
ID/CC A 25-year-old HIV-negative homosexual male presents with rectal
burning, itching in the anal region, diarrhea, tenesmus, and a
bloody, mucopurulent discharge per rectum.
HPI One month ago he was hospitalized with severe febrile
proctocolitis that was diagnosed as lymphogranuloma venereum.
He has also been treated several times in the past for amebiasis
and shigella colitis and admits to having receptive anal
intercourse. Further history reveals that his most recent sexual
partner has been suffering from urethral pain and discharge.
PE Condylomata acuminata noted in perianal distribution; remain-
der of physical exam normal.
Labs Gram stain and culture of rectal swab reveals gram-negative
diplococci identified as Neisseria gonorrhoeae on Thayer-
Martin medium; urethral swab from partner also isolates
N. gonorrhoeae.
Imaging Sigmoidoscopy: proctitis with bloody mucopurulent discharge
noted.
Treatment Ceftriaxone and doxycycline (to treat likely concomitant
chlamydial infection) for bodi patient and partner. Most apparent
failures of correct antibiotic therapy are in fact due to reinfection;
in resistant cases, spectinomycin, fluoroquinolones, or other
cephalosporins can be used.
Discussion The term "gay bowel syndrome" is used in reference to enteric
and perirectal infections that are commonly encountered in
immune-competent homosexual men; in homosexuals with HIV,
opportunistic organisms play a more important role. Common
etiologic agents include Chlamydia trachomatis, lymphogranu-
loma venereum serovars, Neisseria gonorrhoeae, HSV, Treponema
pallidum, human papillomavirus, Campylobacter species, Shigella,
Entamoeba histolytica, and Giardia.
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PROCTOCOLITIS
ID/CC A 35-year-old male presents with high fever, malaise, headache,
and a hacking cough productive of a small amount of mucoid
sputum.
HPI Me has two pet parrots at home who have recentiy shown signs
of illness.
PE VS: fever; bradycardia. PE: auscultation of chest reveals crepitant
rales over both lower lung fields; splenomegaly with mild
hepatomegaly noted; multiple purpuric macules seen over
abdomen ("HORDER'S SPOTS").
Labs Greater than fourfold rise in complement-fixing antibody titer
to a group antigen suggestive of infection with Chlamydia
psittaci; definitive diagnosis of psittacosis was made from spu-
tum by isolation of C. psittaci in pretreated tissue culture cells.
Imaging CXR, PA: interstitial patchy, bilateral infiltrates.
Gross Pathology Principal lesions found in lungs, liver and spleen.
Micro Pathology
Pulmonary lesion is an interstitial pneumonitis; mononuclear
cells with ballooned cytoplasm containing inclusion bodies are
observed. In the liver, focal necrosis of hepatocyte occurs along
with Kupffer cell hyperplasia.
Treatment Azidiromycin or clarithromycin.
Discussion Psittacosis is an acute infection caused by Chlamydia psittaci: it
is characterized primarily by pneumonitis and systemic manifes-
tations and is transmitted to humans by a variety of avian
species, principally psittacine birds (parrots, parakeets). A his-
tory of contact with birds, particularly sick birds, or of employ-
ment in a pet shop or in the poultry industry provides a clue to
the diagnosis of psittacosis in a patient with pneumonia, espe-
cially if bradycardia and splenomegaly are also present.
PSITTACOSIS
ID/CC A 54-year-old female being treated in the ER is noted to have
developed progressively worsening abdominal pain and high-
grade fever with chills.
HPI She presented to the ER a few hours ago with colicky abdominal
pain and was diagnosed with choledocholithiasis.
PE VS: fever (39.5C), hypotension (BP 80/60); tachycardia
(HR 120). PE: toxic-looking; icteric: abdominal exam reveals
extremely tender RUQ with hepatomegaly.
Labs CBC; leukocytosis with neutrophilia. LFTs: markedly elevated
bilirubin, AST, ALT, alkaline phosphatase and GGT. Blood
cultures grew Escherichia coli.
Imaging CT, abdomen: multiple hepatic abscesses; distended gallbladder
with perihepatic and perieliolecvstic fluid collections.
Treatment Prolonged TV antibiotic therapy; emergent endoscopic (ERCP)
or surgical biliary decompression; surgical drainage of the
abscesses if no response to IV antibiotics.
Discussion A pyogenic liver abscess is a pus-filled cavity within the liver
caused by a bacterial infection, typically polymicrobial. The
causes of liver abscess include abdominal infection such as ap-
pendicitis, diverticulitis, or perforated bowel: sepsis; biliary tract
infection; or liver trauma leading to secondary infection. The
most common bacteria involved are E. coli, Klebsiella spp.,
Enterococcus, Staphylococcus spp., Streptococcus spp., and
Bacteroides. Positive blood cultures are found in about half
of patients with a pyogenic liver abscess and sepsis is a life-
threatening complication. There is significant mortality even in
treated patients and mortality is higher in those with multiple
abscesses.
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PYOGENIC LIVER ABSCESS
ID/CC A 30-year-old dairy farm worker presents widi complaints of
fever, headache, cough, pleuritic chest pain, and malaise.
HPI His work at the dairy involves milking cows and looking after
parturient cattle.
PE VS: fever; tachypnea. PE: mild icterus; bilateral crackles on chest
auscultation.
Labs CliC: normal WBC count. Mild elevation of serum bilirubin and
liver enzymes; greater than fourfold increase in complement-
fixing antibody (against Coxiella burnetii) titer between acute
and convalescent sera (IFA technique for early detection of spe-
cific IgM Ab is die serodiagnostic method of choice); negative
Weil-Felix reaction; C. burnetii isolated from sputum by inoculation
of cultured human fetal diploid fibroblasts.
Imaging CXR: right upper lobe rounded opacity that increased in size
over a few days and cleared completely with treatment.
Treatment Doxycycline is the first-line agent of therapy (erythromycin can
also be used).
Discussion Q fever is caused by the rickettsia-like organism Coxiella
burnetii and produces the clinical picture of primary atypical
pneumonia. Q fever differs from the odier human rickettsioses
in that rash is absent and transmission is usually by the airborne
route. C. burnetii localizes in die mammary glands and uterus of
pregnant cattle, sheep, and goats, in which infection is mild or
inapparent; infected placentas, postpartum discharges, and the
feces of these animals are the principal sources of contaminated
material in die environment. Humans acquire Q fever by
inhaling aerosolized particles from such substances; particularly
at risk are dairy and slaughterhouse workers.
Q FEVER
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ID/CC A 12-year-old while female is rushed to the emergency room
because of numbness of the right foot and leg followed by
fever and convulsions. The child refuses to drink any fluids
(HYDROPHOBIA).
HPI She had been camping 5 weeks ago. When questioned, her
molher recalls that one night the child had apparendy stepped
on a bat that bit her in the right foot.
PE VS: no fever. PE: child is disoriented, hyperventilating,
extremely agitated, and actively moving all four limbs; thus
difficult to restrain; no meningeal signs; fundus normal;
saliva viscous and foaming.
Labs LP: lymphocytic pleocytosis with mildly elevated proteins
and normal sugar in CSF. Positive rabies antigen in corneal
scrapings.
Micro Pathology
Treatment
Discussion
Characteristic cytoplasmic inclusion bodies (Negri bodies) in
corneal scrapings or Amnion's horn.
Supportive; almost always fatal; prevent with vaccine; postexpo-
sure prophylaxis with diploid cell vaccine and human rabies
immune globulin (HR1G).
Rabies is a fatal viral disease that is transmitted to humans by the
biles of bats, raccoons, skunks, foxes, coyotes, dogs, and cats.
Rabies virus is an enveloped, single-stranded RNA virus. Rabies
has a long incubation period (approximately 3 to 8 weeks);
death usually results from respiratory failure.
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Atlas Link tnc^iii M-M2-041
RABIES
ID/CC A 27-year-old male researcher presents with sudden-onset fever,
chills, headache, a skin rash, and painful swelling of multiple
limb joints.
HPI Careful history reveals that he was bitten by a rat in his labora-
tory a few days ago; the bite wound has now healed.
PE VS: fever. PE: morbilliform rash noted over extremities, particu-
larly the hands and feet; painful swelling and restriction of
movement noted over both wrist and knee joints.
Labs CBC: leukocytosis. Streptobacillus moniliformis isolated from
blood and synovial fluid of inflamed joints; agglutinins to S.
moniliformis demonstrated in significant titers.
Treatment Amoxicillin/clavulonic acid (doxycycline can also be used).
Discussion Rat bite fever, which is caused by Streptobacillus moniliformis,
is an acute febrile illness that is usually accompanied by a skin
rash; most cases result from the bites of wild or lab rats, although
mice, squirrels, weasels, dogs, and cats may also transmit the
disease by bites or scratches. The disease is called Haverhill
fever when S. moniliformis is transmitted by drinking rat-
excrement-contaminated milk. Distribution is probably
worldwide, with most cases occurring in crowded cities
characterized by poor sanitation.
RAT BITE FEVER
ID/CC A 30-year-old male who lives in the western part of the United
States presents with high fever, shaking chills, severe headache,
myalgias, and diarrhea.
HPI He reports having had similar symptoms 10 days ago that lasted
for 4 to 5 days, followed by defervescence accompanied by
drenching sweats and marked prostration. He had been hiking
in a tick-infested forest until about a week before the develop-
ment of symptoms.
PE VS: fever.
Labs Spirochetes found on thick smears of peripheral blood obtained
during febrile period and stained with Wright or Giemsa stain.
Treatment Doxycycline is the drug of choice (erythromycin may also be
used).
Discussion Relapsing fever is an acute louse-borne or tick-borne infection
that is caused by blood spirochetes of the genus Borrelitr, it is
characterized by recurrent febrile episodes separated by asymp-
tomatic intervals. Unlike other spirochetes, the etiologic agent
can readily be detected with Giemsa slain or Wright's stain.
B. recurrentis is the cause of louse-borne relapsing fever.
whereas a variety of different species produce the tick-borne
disease. In the United States, the predominant species are
B. kermsii and B. luricatae. Most patients experience the
Jaa im h-Herxheimer reaction within the first 2 hours of treatment
RELAPSING FEVER
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ID/CC A 6-year-old male presents with fever, intense headache, myalgia,
dry cough, and a rash that began peripherally (on his wrists and
ankles) but now involves the entire body, including the palms
and soles.
HPI The child lives in North Carolina and indicates that he was
bitten by an insect a few weeks ago while playing in the woods
near his home.
PE VS: fever. PE: lethargy; ill appearance: petechial rash all over
body, including palms and soles.
Labs
Gross Pathology
Micro Pathology
( KC: thrombocytopenia: prolonged bleeding and clotting time.
Positive Hess capillary test (RiMi'i.t.-I.i l DK i-hknomknON);
positive Proteus OX 19 and OX2 Weil-Felix reaction: specific
antibodies to Rickettsia rickettsii with positive complement
fixation. UA: proteinuria; hematuria.
Hemorrhagic necrosis in brain and kidneys; nodular formation
in glia.
Inflammatory lymphocytic and plasma cell perivascular infiltra-
tion; endothelial edema with abundant rickettsiae; microthrom-
bus formation with necrotic vasculitis.
Treatment Doxycycline or chloramphenicol.
Discussion Rickettsia rickettsii is the causative organism of Rocky Mountain
spotted fever; Dermacentor, a wood tick, is the vector. The orga-
nism's tropism for endothelial cells results in vasculitis, edema,
thrombosis, and ischemia. Ironically, Rocky Mountain spotted
fever is endemic to the East Coast of the United States.
ROCKY MOUNTAIN SPOTTED FEVER
ID/CC A 5-month-old male infant is brought to the pediatric clinic with
wheezing and respiratory difficulty of 3 hours' duration.
HPI He has had rhinorrhea, fever, and cough and had been sneezing
for 2 days prior to his visit to the clinic.
PE VS: tachypnea. PE: nasal flaring; mild central cyanosis; accessory
muscle use during respiration; hyperexpansion of chest; expira-
tory and inspiratory wheezes; rhonchi over both lung fields.
Labs CBC/PBS: relative lymphocytosis. ABGs: hypoxemia with mild
hypercapnia. Normal flora on bacterial culture of sputum;
respiratory syncytial virus (RSV) demonstrated on viral culture
of throat swab.
Imaging CXR; hyperinflation; segmental atelectasis; interstitial infiltrates.
Treatment Humidified oxygen; bronchodilators; aerosolized ribavirin.
Discussion RSV is the most common cause of bronchiolitis in infants under
2 years of age; other viral causes include parainfluenza, in-
lluenza. and adenovirus. Infections typically occur during the
fall and winter months. Transmission occurs via close contact
with contaminated fomites but can also occur after coughing or
sneezing. The majority of infections occur during an RSV
epidemic.
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RSV PNEUMONIA
ID/CC A 4-month-old girl brought in for a well-child visit is found to be
low in weight and height for her age and to have lens opacities
(due to congenital cataracts).
HPI Her mother had a skin rash and fever during her first trimester.
The mother states that when the child was born, she too had a
rash like a "blueberry muffin" and was jaundiced.
PE Deaf and globally retarded; malnourished; microcephaly and
bulging anterior fontanelle; microphthalmia with unilateral left
cataract: discrete black, patchy pigmentation found in retina on
funduscopic exam; hepatosplenomegaly; machinery murmur
heard at second intercostal space on left sternal border (due to
patent ductus arteriosus) .
Labs CBC/PBS: leukopenia; thrombocytopenia. Increased serum
bilirubin (both direct and indirect); rubella virus isolated from
urine and saliva; markedly increased IgM specific antibody for
rubella.
Imaging XR, plain: radiolucent (lytic) bone lesions (metaphyseal).
Treatment None.
Discussion Congenital rubella, transmitted in utero, is caused by rubella
virus, a single-stranded KNA togavirus. In children and adults it
is a transitory and unremarkable disease. If acquired in utero it
has devastating consequences.
RUBELLA— CONGENITAL
ID/CC A 10-year-old female Asian immigrant presents with a low-grade
fever and coryza of 3 days' duration.
HPI She also complains of arthralgias and a skin rash that began on
her face and spread to her trunk. Her mother says she cannot
remember any details of her vaccination history.
PE VS: fever. PE: maculopapular rash over face and trunk; enlarged
postauricular, posterior cervical, and occipital lymph nodes.
Labs CBC: leukopenia; thrombocytopenia. Rubella virus hemaggluti-
nation inhibition test demonstrates fourfold rise in titer to 1:32.
Gross Pathology
Erythematous skin rash resembling rubeola measles but lighter
in color and more discrete; similar distribution pattern in both.
Treatment Symptomatic treatment.
Discussion Rubella (German measles) is caused by a togavirus. Live attenu-
ated rubella virus vaccine (part of MMR) should be given to all
infants and to susceptible girls before menarche. The course of
illness is self-limiting and mild; in females the major implication
is the potential for congenital rubella syndrome. Females with
rubella can get polyarthritis secondary to immune complex
deposition.
Atlas Link □ I IM2-026
RUBELLA (GERMAN MEASLES)
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ID/CC A 14-year-old male who is known to have sickle cell anemia pre-
sents Willi throbbing pain, redness, and swelling ol the right
thigh.
HPI The patient also complains ol lever and chills of 1 week's dura-
tion. He has a lew pet turtles at home.
PE VS: fever; tachycardia. PE: pallor; redness, swelling, and tender-
ness over right thigh; effusion denionsiiaied in right knee joint;
limitation of range of motion of right knee.
Labs CBC: leukocytosis; elevated ESR. PBS: irreversible sickling;
blood culture reveals Salmonella typhimurium (most com-
mon); organism also isolated from pus aspirated from right
femur (diagnostic of osteomyelitis).
Imaging Nuc: increased uptake in metaphyseal region of right femur. XR
(usually normal during the first 10 days of illness) may reveal
changes of bone resorption, detached necrotic cortical bone
(SEQUESTRUM), and laminated periosteal new-bone formation
(IMOU'CRUM).
Gross Pathology Dense, pale, sclerotic-appearing area in shaft.
Micro Pathology Changes include suppurative and ischemic destructive necrosis,
fibrosis, and ultimate bone repair.
Treatment Parenteral antibiotics, with fluoroquinolones being first-line
agents (third-generation cephalosporins may also be used).
Discussion A striking association has been noted between diseases produc-
ing hemolysis (e.g., sickle cell anemia, malaria, and bartonel-
losis) and salmonella infections; elderly patients with impaired
host defense mechanisms, those with hcpatosplenic schistosomi-
asis, and AIDS patients are also at increased risk of severe and
recurrent salmonella bacteremia. Salmonella osteomyelitis in
sickle cell patients presents primarily in young individuals and
typically affects long bones. It is believed that die functional
asplenic state found in most sickle cell patients contributes
to the increased prevalence of salmonella osteomyelitis.
SALMONELLA SEPTICEMIA WITH OSTEOMYELITIS
ID/CC Ail Asian refugee family comprising a 30-year-old man, his wife,
and i wo schoolchildren present with complaints of severe
itching over their entire bodies except for their face; the itching
increases during the night.
HPI The male family members also report penile and scrotal skin
lesions. The family is of low socioeconomic status and lives in a
single room under crowded conditions.
PE Papulovesicular lesions; "burrows" seen in the dorsal interdigi-
lal web spaces and flexor aspects of both wrists; lesions also seen
around elbows, anterior axillary folds, periumbilical area, lower
buttocks, and thighs; face was spared; scrotal and penile lesions
seen in male members were nodular and reddish.
Labs Female adult mite was seen with a hand lens when teased out of
her burrow with a needle.
Treatment Apply lindane or permethrin (lindane is contraindicated in
small children and in pregnant women). All family members
must be treated; clothing, linen, and the like should be boiled
and washed: fingernails should be trimmed. Use antihistamines
or calamine lotion to help control itching.
Discussion Scabies is caused by infestation with Sarcoptes scabiei, a mite
that bores into the corneal layer of the skin, forming burrows in
which it deposits its eggs. The scabies organism does not survive
for more than 48 hours away from the host; modes of transmis-
sion include close contact with infected individuals, unsanitary
conditions, and sexual contact. In adults, certain areas of the
body are generally spared, including the face, scalp, and neck.
Atlas Links BED I M-M2-049
mcMzl MC-186
SCABIES
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ID/CC A 10-year-old white female complains of difficulty swallowing,
pain in both ears, and fever of 1 week's duration; she also
complains of an extensive skin rash.
HPI The child is fully immunized and has been well until now.
PE VS: fever. PE: extensive erythematous rash ( "goose-pimple
sunburn") on neck, groin, and axillae; desquamation and
peeling of fingertips; circumoral pallor; lines of hyperpigmenta-
tion with tiny petechiae (Pastia's sign) in antecubital fossae;
bright red lingual papillae superimposed on white coat
( "strawberry TONGUE") ; pharyngitis with exudative tonsillitis;
cervical lymphadenopalhy; normal eardrums.
Labs CBC: leukocytosis with neutrophilia. Group A B-hemolytic
Streptococcus pyogenes on throat swab and culture; elevated ASO
titer.
Gross Pathology Toxin-induced vasodilation; complications include otitis media,
pneumonia, glomerulonephritis, osteomyelitis, and rheumatic
fever.
Micro Pathology Inflammatory polymorphonuclear epidermal infiltrate; intersti-
tial nephritis; lymph node hyperplasia.
Treatment Penicillin; erythromycin.
Discussion Scarlet fever is a streptococcal infection that is characterized by
morbilliform rash due to hypersensitivity to erythrogenic toxin.
Atlas Links L'Jcmzi MC-187A, MC-187B
SCARLET FEVER
ID/CC A 27-year-old Peace Corps volunteer working in the Congo is
sent home after developing fever, sweats, and abdominal pain
that have not responded to antimalarial treatment.
HPI Five weeks ago, he developed severe itching and a macular rash
(swimmer's itch) after swimming in a nearby pond.
PE VS: fever. PE: moderate enlargement of liver and spleen; lender
abdomen but no peritoneal irritation.
Labs CBC/PBS: marked eosinophilia. Characteristic large parasite
eggs with lateral spines may be found in stool specimen.
Imaging Sigmoidoscopy: swollen and erythematous mucosa; many small
ulcerations. CT/US, abdomen: hepalosplenomegaly; portal vein
dilatation.
Gross Pathology
Skin and liver sites of principal lesions in acute stage; eggs may
be found in liver, lungs, intestines, pancreas, spleen, urogenital
organs, and brain; chronic stage characterized by granuloma
formation in bladder and liver (periportal fibrosis).
Micro Pathology Granulomatous reaction and fibrosis.
Treatment Praziquantel.
Discussion Schistosomiasis is among the most common parasitic diseases in
ihe world: infection with Schistosoma mansoni or S.japonicum is
acquired by swimming in snail-infested ponds and lakes. Long-
standing infection may lead to noncirrhotic portal fibrosis and
portal hypertension. Also known as bilharziasis.
Atlas Link LUcSaTJ M-M2-051
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SCHISTOSOMIASIS
ID/CC A 12-year-old immigrant from the Middle East presents with
terminal hematuria, dysuria, and increased frequency of
micturition.
HPI He remembers having played and bathed in snail-infested
streams while he was in his native country; on one occasion he
had developed an intensely pruritic skin eruption after bathing
in one such stream ("cercarial dermatitis").
PE Pallor noted.
Labs UA: hematuria; mild proteinuria and sterile (abacterial) pyuria.
Microscopic exam of urine and rectal biopsy reveals presence of
ellipsoid eggs with a sharp terminal spine containing a miracid-
ium surrounded by a thick, rigid shell.
Imaging XR: bladder wall calcification.
Treatment Praziquantel, metrifonate.
Discussion Three major species exist. Schistosoma mansoni, S. japonicum, and
S. haematobium infect humans. .S". mansoni is found in Africa, the
Arabian Peninsula, South America, and parts of the Caribbean;
S. japonicum is found in Japan, China, and the Philippines; and
S. haematobium is found in Africa and the Middle East.
Transmission of schistosomiasis cannot occur in the United
States because of the absence of the specific freshwater snail
that is an intermediary host. In .S'. haematobium infection, the
principal symptoms are terminal hematuria, dysuria, and fre-
quent urination; hydronephrosis, pyelonephritis, and squamous
cell carcinoma of the urinary bladder may develop as
complications. In S. mansoni and S. japonicum infection,
manifestations may include fever, malaise, abdominal pain,
diarrhea, or hepatosplenomegaly. Presinusoidal hepatic trapping
of eggs and the consequent granulomatous reaction induce
portal hypertension.
SCHISTOSOMIASIS— URINARY
ID/CC A 36-year-old male executive comes to the emergency room
because of the development of sudden nausea, vomiting, and
diarrhea with blood and mucus (dysentery) as well as crampy
abdominal pain for 2 clays.
HPI He had just returned from a business trip in South America.
PE VS: low-grade fever. PE: mild dehydration; hyperactive bowel
sounds; tender abdomen without definite peritoneal irritation.
Labs Leukocytes on stool examination; Shigella isolated on stool cul-
ture; on microbiology, organism does not ferment lactose and is
not motile.
Micro Pathology Shigella enterotoxin acts by activating adenylate cyclase;
organism invades intestinal mucosa.
Treatment Rehydration with antibiotic therapy (ampicillin orTMP-SMX).
Discussion Shigellosis outbreaks occur primarily in areas with overcrowding
and poor hygiene (fecal-oral transmission): arthritis, conjunctivitis,
and urethritis (Reiter's SVNDRf >mi- ) may be complications in
HLA-B27-positive individuals. Like Salmonella, Shigella causes
bloody diarrhea by invading the intestinal mucosa, causing
intestinal ulceration and inflammation.
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SHIGELLOSIS
ID/CC A 56-year-old hospitalized male is found to have an abrupt-onset
high-grade fever with chills a few hours after he underwent
nephrolithotomy.
HPI He was diagnosed with chronic nephrolithiasis with recurrent
UTIs: a surgery intern also noted poor urine output.
PE VS: fever; tachycardia: hypotension; tachypnea. PE: confused
and disoriented; hyperventilating: diaphoresis; hands warm and
pink with rapid capillary refill; pulse bounding: on chest
auscultation, air entry found to be bilaterally reduced.
Labs CBC: leukocytosis with left shift; neutrophils contain toxic
granulations, Dohle bodies, and cytoplasmic vacuoles; band
forms > 10%; thrombocytopenia. Prolongation of thrombin
lime, decreased fibrinogen, and presence ol D-dimers (suggest-
ing DIG); raised BUN and creatinine. ABGs: metabolic acidosis
(increased anion gap due to lactic acidosis) and hypoxemia
(due to ARDS). Blood and urine culture yields Escherichia coli.
Imaging CXR: evidence of noncardiogenic pulmonary edema (ARDS).
Treatment IV antibiotics (with adequate gram-negative coverage): manage-
ment of multiorgan failure (azotemia. ARDS, and DIG).
Discussion Almost anv bacterium can cause a bacteremia, including E. coli
(most common), Klebsiella, Proteus, Pseudoinonas (associated with
antibiotic therapy and burn wounds), Bacteroides fragilis (causes
of anaerobic septicemias). Staphylococcus aureus. Streptococcus
pneumoniae, and pediatric septicemia due to /;. coli and
Streptococcus agalacliae. Gram-negative bacteria release endotox-
ins; the release of endotoxin into the circulation leads to the
activation of macrophages and monocytes, which in turn release
cyiokines. These cytokines trigger cascade reactions that lead
to the clinical and biochemical manifestations of the sepsis
syndrome.
Atlas Links dEEE M-M2-054A, M-M2-054B
SHOCK— SEPTIC
ID/CC A 37-year-old gardener complains of lumps with red streaks on
his arm and swelling of the axillary lymph nodes.
HPI Two weeks ago, he pricked his hand with a thorn while pi lining
roses. A nodule then formed which subsequendy ulcerated and
filled wilh pus.
PE Nonpainful nodular lesion on dorsum of hand with ulcer forma-
tion and suppuration; tender, palpable inflammation and hard-
ening of lymph vessels (1 vuill WGITIS); swelling, inflammation.
and suppuration of lymph nodes (LYMPHADENITIS); nonulceraied
satellite nodules along course of lymphatics.
Labs Cigar-shaped budding cells (Sporotiirix SCHENCKIl) visible in pus;
diagnosis confirmed by culture of aspirate of nodule.
Gross Pathology Nonpainful, soft, ulcerated nodule at inoculation site
(SPOROTRK.IH n H t UANCRE): may extend to deep tissues and
bone with osteitis and synovitis.
Micro Pathology
Usually area of suppuration with polymorphonuclear infiltrate
surrounded by granulomatous reaction of varied intensity with
epithelioid and giant cell formation; chlamydospore asteroid
bodies present.
Treatment Itraconazole; potassium iodide.
Discussion Also called "rose gardener's disease," sporotrichosis is a fungal
infection caused by Sporothrix schenckii, a dimorphic fungus
that lives on vegetation. It is typically transmitted by ;i thorn prick
and causes localized infection with few systemic manifestations.
Atlas Link I i J M-M2-055
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SPOROTRICHOSIS
ID/CC A 7-year-old girl is seen by the embassy doctor in Nigeria for ab-
dominal pain, diarrhea, fever, dry cough, and marked dyspnea
of 2 weeks' duration.
HPI She is the daughter of an American diplomat working in
Nigeria. Despite her parent's admonitions, she frequently walks
barefoot.
PE VS: fever. PE: moderate respiratory distress; no cyanosis; no
clubbing; coarse, crepitant rales and wheezing beard over both
lung fields; mild abdominal tenderness.
Labs CBC/PBS: marked eosinophilia. Typical motile rhabditiform
larvae on sputum exam as well as in freshly passed stool; positive
filarial complement fixation test.
Imaging CXR: bilateral, transient migratory infiltrates.
Gross Pathology Pneumonitis produced by migration of larvae through respiratory
tract.
Treatment Ivermectin, thiabendazole.
Discussion Strongyloidiasis is seen in (he presence of poor hygiene and in
tropica] countries. Larvae penetrate the skin, gaining entrance
to the venous system and to the lungs, and then ascend to enter
die Gl tract.
Atlas Link f.Zl n M-M2-056
STRONGYLOIDIASIS
ID/CC A 54-year-old white female complains of spiking fever, chills,
loss of appetite, several bouts of diarrhea, and right upper
quadrant pain.
HPI Ten days ago she underwent an apparently uncomplicated
emergency surgery for suppurative cholecystitis and was subse-
quently discharged and sent home.
PE VS: fever. PE: pallor; slight icterus: pain on percussion of right
costal region: well-healed surgical wound with DO evidence of
infection: liver not palpable; crepitant rales on right lung base.
Labs CBC: elevated WBC count (17,000) with predominance of
neutrophils.
Imaging CXR: elevated right hemidiaphragm; slight right pleural
effusion. US/CT: complex fluid collection below diaphragm.
Treatment Percutaneous drainage under ultrasonic or fluoroscopic
guidance followed by regular blood and radiologic exams;
surgical exploration and drainage.
Discussion Subdiaphragmatic abscess most commonly occurs after abdomi-
nal surgery, mainly with septic, emergency procedures; it typi-
cally presents 1 week or more postoperatively.
SUBDIAPHRAGMATIC ABSCESS
ID/CC A 6-week-oId male, the son of a prostitute, is brought to the
family doctor because of persistent, sometimes bloody
mucopurulent nasal discharge, anal ulcers, and a generalized
rash.
HPI The child was delivered at home, and the mother did not
receive any prenatal care.
PE Weak-looking, icteric infant with hoarse cry; does noi move right
limb (pseudoparalysis); bloody purulent discharge evident at
nares; generalized lymphadenopathy; hcpatosplenomegaly;
maculopapular rash with desquamation on back and buttocks;
bullae on hands and feet.
Labs CBC: anemia. VDRL in both mother and child positive; direct
hyperbilirubinemia: negative Coombs' test: Treponema pallidum
seen on nasal exudate and anal ulcers.
Imaging
Gross Pathology
XR. plain: periostitis of long bones: bilateral moth-eaten lesions;
focal defect in proximal tibial epiphysis with increased density of
epiphyseal line (Wimberger's ska i.
Pathologic features seen if neonatal disease is left untreated in-
clude syphilitic chondritis and rhinitis (causes saddle-nose
deformity), pathologic fractures, bowing of the tibia (SABER
MUM. V-shaped incisors (HUTCHINSON'S TEETH), multicuspid
molars (MULBERRY MOLARS), interstitial keratitis, and deafness.
Treatment Penicillin.
Discussion Treponema pallidum is a spirochete; in utero vertical transmission
occurs from an infected mother to the fetus. Congenital syphilis
occurs maximally during 16 to 36 weeks of gestation and may
be the cause of stillbirth. Ii is preventable if the mother has
received adequate treatment.
SYPHILIS— CONGENITAL
ID/CC An 18-year-old while male presents with a painless ulcer on his
penis.
HPI He admits to having had unprotected intercourse with a prosti-
tute 3 weeks ago.
PE Painless, single, rounded, firm papule with well-defined margins
on dorsal aspect of glans penis that ulcerates ("hard chancrk");
nontender, rubbery bilateral inguinal lymphadenopathy.
Labs Treponemes on dark-field examination of exudate from chan-
cre; VDRL positive; FTA-ABS positive; ELISA for HIV negative.
Gross Pathology A 1.2-cm ulcerated papule with rolled edges and induration; re-
gional lymphadenopaihy.
Micro Pathology Capillary dilatation with plasma cell, PMN, and macrophage in-
filtration; fibroblastic reaction.
Treatment Benzathine penicillin G 1M. 2.4 ML' single dose.
Discussion An STD caused by Treponema pallidum, a spirochete, primary
syphilis is characterized by the appearance of a painless chancre
in the area of inoculation. If left untreated, secondary and terti-
ary syphilis may ensue. Other STDs, such as AIDS, are more
prevalent in patients with syphilis.
Atlas Link wcrazi Z-M2-059
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SYPHILIS— PRIMARY
ID/CC A 23-year-old female presents wilh a nonpruritic skin eruption,
hair loss, and generalized fatigue and weakness.
HPI She admits to having had multiple sexual partners and
unprotected sex. She has had two spontaneous abortions.
PE Extensive raised, copper-colored, maculopapular, desquamative
rash on palms and soles; generalized nontender lymphadenopathy
with hepatosplenomegaly; large, pale, coalescent, flat-topped
papules and plaques in groin (CONDYLOMATA lata); dull, erythe-
matous mucous patches in mouth: hair loss (ALOPECIA) in tail of
eyebrows.
Labs Skin lesions, mucous patches in mouth, and condylomata lata
positive for treponemes; positive VDRL; positive FTA-ABS;
ELISA negadve for HIV; CSF VDRL negative.
Treatment IM benzathine penicillin G.
Discussion Sexual partners must be treated.
Atlas Links i.uctgz\ IM2-027A, IM2-027B
|3 SYPHILIS— SECONDARY
ID/CC A 54-year-old man presents with ataxia, mental status changes,
grossly deformed ankle joints, and shooting pains in his
extremities.
HPI He remembers having had a "boil" on his penis (primary
syphii n u ( a i ANCRE) many years ago that went away by itself. He
also recalls having had a scaling rash on the soles of his feet and
die palms of his hands (due to secondary syphilis) some lime
ago.
PE Painless subcutaneous granulomatous nodules (GUMMAS);
reduced joint position and vibration sense in both lower
extremities (due to bilateral dorsal column destruction); loss of
deep tendon reflexes in both lower limbs; loss of pain sensation
and deformed ankle and knee joints with effusion (Charcot's
NEUROPATHIC ARTHROPATHY): broad-based gait; positive Romberg's
sign (due to sensory ataxia); pupillary light reflex lost but
accommodation reflex retained (ARGYLL ROBERTSON PUPILS}.
Labs Positive VDR1. and Treponema pallidum hemagglutination assay
(TP-HA) . LP: pleocytosis and increased proteins in CSF; VDRL
positive. Normal blood glucose levels.
Imaging CXR: "tree-bark calcification" of ascending aorta.
Gross Pathology Obliterative endarteritis and meningoencephalitis.
Micro Pathology Proliferation of microglia; demyelini/.ation and axonal loss in
dorsal roots and columns.
Treatment Penicillin.
Discussion Tabes dorsalis usually develops 15 to 20 years after initial
infection. There may also be visceral involvement (can cause
neurogenic bladder).
Atlas Link n~Y~\ 1 IM2-028
SYPHILIS— TERTIARY (TABES DORSALIS)
ID/CC A 12-year-old white male presents with stiffness of the jaw and
neck along with inability to swallow.
HPI Twelve days ago lie stepped on a rusty nail, which produced a
small puncture wound; the area is now red, hard, and swollen
with pus. He has been experiencing tingling sensations and
spasms in his calf muscles. He has not received any immunizations
within the past 10 years.
PE Jaw muscle rigidity ( trismus); facial muscle spasm (risus
SARDonicus); dysphagia; neck rigidity; normal deep tendon
reflexes; profuse sweating; patient alert, apprehensive, restless,
and hyperactive during PE; loud noise elicits painful spasms of
face, neck, abdomen, and back, the latter producing
opisthotonos.
Labs CBC, CSF, blood chemistries normal.
Gross Pathology There may be fractures of ribs or vertebrae with sustained
spasms.
Treatment Surgical debridement of wound; tetanus immune globulin intra-
muscularly or intrathecally; diazepam; phenobarbital; tetanus
toxoid; penicillin IV.
Discussion Tetanus is caused by tetanospasmin, a neurotoxin produced by
Clostridium tetani, an obligate anaerobic, spore-forming, gram-
positive rod; the toxin blocks the release of the inhibitory neu-
rotransmitter glycine in the anterior horn cells. Tetanus often
occurs in IV drug abusers; neonates of nonimmunized mothers
may become infected through the umbilical cord stump. The
disease may occur even years after injury or infection and may
also involve the autonomic nervous system (arrhythmias,
high/low blood pressure).
Atlas Link
W M-M2-062
TETANUS
ID/CC A 15-day-old infant is brought by his mother to the pediatric
emergency room in a state of marked muscle rigidity and spasm.
HPI The mother is illiterate and did not receive any prenatal care:
the delivery was conducted at home and, according to her, was
uneventful and full term. The child did not receive any
immunizations; directed questioning reveals that he has been
crying excessively for the past 2 weeks and has not been feeding
normally.
PE Extremely ill-looking infant in a state of generalized rigidity and
opisthotonus; on slightest touch or noise, spasm worsens and he
develops a stridor and becomes cyanosed.
Labs Diagnosis is largely clinical; culture of umbilical stump yields
Clostridium letani.
Treatment Ventilatory assistance; supportive management; maintenance of
nutritional, fluid, and electrolyte balance; tetanus antitoxin;
control of tetanic spasms with diazepam.
Discussion Tetanus neonatorum accounts for a considerable proportion of
infant deaths in developing countries, primarily owing to the
lack of availability of good prenatal care (no tetanus immuniza-
tion); untrained birth attendants in rural areas use contaminated
material to cut or anoint the umbilical cord. Tetanus is caused by
Clostridium letani, a gram-positive, motile, nonencapsulated,
anaerobic, spore-bearing bacillus; its effects are mediated
through production of a powerful neurotoxin (tetanospasmin).
The toxin acts principally on the spinal cord, altering normal
control of the reflex arc by suppressing the inhibition regularly
mediated by die internuncial neurons.
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ID/CC A 40-year-old male who recently went hiking in a forest in the
western United States presents with symmetric weakness of the
lower extremities that has now progressed over the past few days
to involve the trunk and die upper arms.
HPI The patient does not report any sensory symptoms.
PE Higher mental functions intact; symmetric flaccid paralysis with
an ascending pattern of spread noted; no sensory loss demon-
strated; <^n careful examination of hairy areas of the body, a tick
was found embedded in the scalp.
Labs LP: CSF normal. EMG: nerve conduction velocity and compound
muscle action potentials decreased.
Treatment Tick was detached without being squeezed, and this led to
resolution of symptoms over the next few days.
Discussion Feeding ticks may elaborate a neurotoxin that causes tick paraly-
sis; symmetric weakness of the lower extremities progresses to an
ascending flaccid paralysis over several hours to days, although
the sensorium remains clear and sensory function is normal.
TICK PARALYSIS
ID/CC A 40-year-old male diagnosed with AIDS presents with a severe
headache.
HPI He suffered a grand mat seizure 2 hours before his arrival in the
emergency room. He denies any history of seizures and adds
that he has many pets, including cats.
PE Generalized lymphadenopathy: bilateral papilledema; left-sided
hemiparesis with lnperactive deep tendon reflexes on lefi side;
positive Babinski's sign on left side.
Labs Positive indirect fluorescent antibody test for toxoplasmosis;
positive Sabin-Feldman dye test.
Imaging MR/CT. head: single or multiple rounded mass lesions with ring
or nodular enhancement.
Gross Pathology Large brain abscesses with concomitant focal neurologic abnor-
malities, seizures, or altered mental status.
Micro Pathology Parasites appear in tissue as tachyzoites or encysted bradyzoites;
aggregates of nonencapsulated organisms constitute pseudocysts.
Treatment Pyrimethamine; sulfadiazine.
Discussion The definitive host of Toxoplasma gondii is the domestic cat. The
Intermediate hosts are many and varied, including humans.
Toxoplasmosis is also transmitted by ingestion of raw or
undercooked meal.
Atlas Links I'lcran M-M2-065
HICM 2 1 MC-191
TOXOPLASMOSIS
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ID/CC A 50-year-old man presents with generalized myalgia and a
persisteni low-grade fever.
HPI In addition, the patient recalled having severe abdominal pain
and diarrhea several weeks ago. The patient worked in a pig
slaughterhouse for many years.
PE VS: fever. PE: periorbital and facial edema; tenderness over calf,
thigh, and shoulder muscles; conjunctival and splinter hemor-
rhages; no neurologic deficit seen.
Labs CBC: eosinophilia. Normal ESR; elevated serum CPK, LDH,
and AST; latex agglutination test positive for THchinelia.
Gross Pathology Facial, neck, biceps, lower back, and diaphragm most frequently
affected muscles.
Micro Pathology Biopsy of sternocleidomastoid muscle reveals cysts of Trichinella
spiralis.
Treatment Albendazole; mebendazole; high-dose corticosteroids.
Discussion The organism causing trichinosis. Trichinella spiralis, can be
t ransmi tted when raw or undercooked pork is ingested. The
larvae develop only in striated muscle cells.
Atlas Link HJcLI 1 1 M-M2-066
TRICHINOSIS
ID/CC A 6-year-old male is brought lo the ER in a delirious state with
fever and marked dyspnea thai have rapidly progressed over the
past 2 days.
HPI 1 lis mother, an Asian immigrant, was diagnosed and treated for
pulmonary tuberculosis a few months ago. Me has had a low-
grade fever, cough, malaise, and night sweats for the past 2
months. The child has not received prophylactic isonia/.id or
BCG vaccination.
PE VS: fever; tachycardia: marked tachypnea; hypotension. PE:
toxic and stuporous; pallor; central cyanosis; extensive rales and
rhonchi bilaterally; hepatosplenomei'aly; lyinphadenopathy;
lunduscopy reveals choroidal tubercles.
Labs CBC: lymphocytosis; normochromic, normocytic anemia.
Increased ESR; Mantoux skin test negative (false negative may
occur during incubation and with severe ilisease); staining and
culture of transbronchial and bone marrow biopsy specimens
reveal presence of Mycobacterium tuberculosis; PCR for tuber-
i iilosis positive; EI.ISA for I IIV negative.
Imaging CXR: soft, uniformly distributed fine nodules throughout both
lung Fields (miliary mottlinc;) .
Gross Pathology Myriad 1- to 2-mm granulomas demonstrable in lungs, liver, and
bone marrow biopsy specimens.
Micro Pathology Granulomas with central caseous necrosis surrounded by
epithelial cells, Langerhan's cells, lymphocytes, plasma cells,
and fibroblasts in affected (issues.
Treatment Multidrug antitubercular therapy with isoniazid, rifampicin,
pyia/inamide, and ethambutol or streptomycin; steroids may be
indicated.
Discussion Miliary tuberculosis results from widespread hematogenous
dissemination and often presents with a perplexing fever,
dyspnea, anemia, and splenomegaly; the disease is more fulminant
in children than in adults.
Atlas Link ujcvj 1 1 PG-M2-067
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TUBERCULOSIS— MILIARY
ID/CC A 14-year-old male immigrant complains of malaise, weight loss,
fever, and night sweats of 6 weeks' duration; he also has a mild
cough that began to produce bloody sputum 3 days prior to his
admission.
HPI The patient's mother has been diagnosed with pulmonary
tuberculosis and is currently receiving treatment for it.
PE VS: mild fever. PE: malnourished; low height and weight for age;
bronchial breath sounds with crepitant rales heard over right
supramammary area.
Labs CBC/PBS: normocytic, normochromic anemia; WBC count
normal with relative lymphocytosis. Increased ESR; sputum
stained with ZN stain positive for acid-fast bacilli; positive radio-
metric culture for Mycobacterium tuberculosis; posidve ELISA for
TB; posidve intradermal tuberculin injection (Mantoux TEST).
CXR: small cavity with streaky infiltrates in right upper lobe;
hilar lymphadenopathy; calcified lung lesion (Ghon's LESION);
Ghon's lesion and calcified lymph node (Ranke complex).
Primary tuberculosis usually consists of lesions in lower lung
lobes and in subpleural locations; cavitation rare; secondary TB
or reinfection characterized by cavitary lesions usually located in
apical regions.
Multinucleated epithelioid Langerhan's cells surround core of
ensealing necrosis in lung parenchyma, producing fibroblastic
reaction at periphery with lymphocytic infiltration and
proliferation (TUBERCLE) .
Treatment Multiple drug dierapy with Lsoniazid (INH), rifampin, ethambutol,
pyrazinamide, and/or streptomycin.
Imaging
Gross Pathology
Micro Pathology
Discussion
Atlas Links
Pulmonary tuberculosis is caused by Mycobacterium tuberculosis,
an acid-fast, gram-positive aerobic bacillus. An increasing
incidence in AIDS patients has been observed; drug resistance is
becoming common.
LJ I . M-M2-068A, M-M2-068B, M-M2-068C, PG-M2-068A,
PG-M2-068B
E3
TUBERCULOSIS— PULMONARY
ID/CC A 12-year-old white male is brought to his pediatrician because
of an ulcer on his right wrist together with swelling of the lymph
nodes in the right axillae with suppuration.
HPI He had just returned from summer camp and, upon questioning,
admits to having played with rabbits at the camp's breeding
grounds. He has been suffering from fever, headache, and muscle
aches for almost a week.
PE VS: fever. PE: indurated erythematous nodule with ulcer
formation on right wrist; right axillary adenopathy with pus
formation; lymphangitis; mild splenomegaly; scattered rales in
both lung bases.
Labs CBC: normal WBC count. Increased ESR; elevated C-reactive
protein; positive agglutination test; Frana sella lularensis on direct
fluorescent antibody staining of material from ulcer.
Imaging CXR: bilateral basilar interstitial infiltrates.
Gross Pathology
Micro Pathology
Enlarged, indurated lymph nodes with necrosis and suppura-
tion; skin nodule at site of inoculation with ulcer formation.
Necrosis and suppuration of lymph nodes; pulmonary and
disseminated lesions; granulomatous nodules with central
caseating necrosis.
Treatment Streptomycin and gentamicin.
Discussion
Tularemia is an acute zoonosis caused by Francisella tularensis,
a nonmotile, aerobic, gram-negative bacillus; it is transmitted
through contact with rabbits, squirrels, or other rodents or tick
biles. It may be ulceroglandular, tonsillar, oculoglandular.
pneumonitic, or typhoidal.
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TULAREMIA
ID/CC A 27-year-old male is admitted to the hospital for evaluation of
increasing fever of unknown origin along with malaise,
headache, sore throat, cough, and constipation.
HPI He visited Southeast Asia 3 weeks ago but did not receive any
prior vaccinations.
PE VS: bradycardia; fever; fever charting reveals "stepladder"
pattern. PE: mild hepatosplenomegaly; faint erythematous
macules seen over trunk ("rose spots").
Labs CBC: neutropenia with relative lymphocytosis. Widal's test
positive in significant tilers; blood and stool cultures reveal
Salmonella typhi.
Gross Pathology Infection of Peyer's patches in terminal ileum leads to necrosis
of underlying mucosa, producing longitudinal oval ulcerations.
Micro Pathology Ulcers bordered by mononuclear cells; typhoid nodules with
lymphocytes and macrophages may be present in liver, spleen,
and lymph nodes.
Treatment Ciprofloxacin is curative.
Discussion
Because infection is acquired from contaminated food or water,
typhoid vaccine is recommended for all those traveling to areas
that have had typhoid epidemics. Three vaccines are available:
the parenteral vaccine containing the capsular polysaccharide
and the oral vaccine containing live attenuated organisms are
more effective than the parenteral vaccine containing whole
killed organisms. S. typhi is transmitted only by humans, whereas
all other Salmonella species have an animal as well as a human
reservoir.
Atlas Link
IM2-030
TYPHOID FEVER
ID/CC A 19-year-old male goes lo his health clinic complaining of
painful urination and discharge.
HPI The patient had casual sex with a classmate while at a party
2 weeks ago. He has had no previous STDs.
PE Watery yellowish-green discharge from meatus; no penile
ulcerations or inguinal lymphadenopathy.
Labs Numerous neutrophils but no bacteria on Gram stain of
discharge; positive direct immunofluorescence using mono-
clonal antibody against Chlamydia; routine bacterial cultures,
including Thayer-Martin, do not show growth.
Treatment Tetracycline; doxycycline; azithromycin; treat both patient and
sexual partner.
Discussion The most common cause of nongonococcal urethritis is
(Chlamydia trachomatis; less frequently it is caused by Urea-plasma
iimilyticum. It is frequently coincident with gonococcal urethritis.
Atlas Link mcra 1 1 M-M2-071
URETHRITIS— NONGONOCOCCAL
ID/CC A 25-year-old sexually active female complains of burning on
urination.
HPI She also complains of pain in the lower abdomen and increased
frequency of urination.
PE Mild suprapubic tenderness.
Labs UA: mild proteinuria; hematuria: WBCs but no casts seen. Urine
culture reveals > 100,000 Escherichia coli organisms present.
Gross Pathology Infection ascends the urinary tract (urethritis, cystitis,
pyelonephritis); mucosal hyperemia and edema.
Micro Pathology Urothelial hyperplasia and metaplasia.
Treatment Ciprofloxacin.
Discussion Eighty percent of UTIs are caused by E. coli; Staphylococcus
saprophytics is the second most common cause. Other causes, in
order of frequency, are Proteus, Klebsiella, Enterobacter, Serratia,
Pseudomonas, and Enterococcus; Chlamydia and Neisseria are also
causes of urethritis. Risk factors include female gender, sexual
activity, pregnancy, obstruction, bladder dysfunction,
vesicoureteral reflux, and catheterization.
URINARY TRACT INFECTION (UTI)
ID/CC A 25-year-old sexually active woman presents with burning
during micturition (dysuria), increased frequency and urgency
of micturition, and low-grade fever.
HPI She is otherwise in perfect health.
PE VS: fever.
Labs UA: abundant WBCs; mild proteinuria but no casts; staining of
sediment reveals presence of gram-positive cocci. Urine culture
isolates coagulase-negative Staphylococcus saprophyticus.
Treatment Antibiotics (ampicillin, cotrimoxazole, or ciprofloxacin).
Discussion Enterobacteriaceae such as Escherichia coli, Klebsiella species, and
Proteus and Pseudomonas species are die most common organisms
causing UTI. After E. coli. Staphylococcus saprophyticus is die most
common cause of primary nonobstructive UTI in sexually active
young women.
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UTI WITH STAPHYLOCOCCUS SAPROPHYTICUS
ID/CC A 5-year-old male presents with malaise, anorexia, fever, and a
pruritic rash on his scalp, face, and trunk.
HPI He also complains of a headache. Six of his classmates recently
missed school because of similar symptoms.
PE VS: fever (39°C). PE: skin lesions consist of macules, papules, vesi-
cles, pustules, and scabs, all present at same time, predominantly
over trunk, face, and scalp.
Labs Multinucleated giant cells on scraping samples from vesicles.
C.BC: leukopenia.
Gross Pathology
Micro Pathology
Macular, papular, vesicular, and pustular rash with scab
formation; characteristically, all lesions present at same time (vs.
variola) ; lesions appear in crops every 3 to 5 days; myocarditis
and pneumonitis may be present.
Intranuclear, acidophilic inclusion bodies (Lipschutz bodies) in
epithelial cells with clear halo around them and multinucleated
giant cells on histologic exam of skin lesions (on Tzanck smear) .
Treatment Acetaminophen; antihistamines and calamine lotion; hygienic
measures, including isolation.
Discussion A highly contagious dermotropic viral disease caused by
varicella-zoster virus, a DNA herpesvirus, chickenpox is
transmitted by respiratory aerosol or by direct contact.
Complications include secondary bacterial infection of the skin
and pneumonia; high-risk individuals may be protected passively
with immunoglobulin and/or acyclovir.
Atlas Links □ □ M-M2-074
L_l i J PED-035
VARICELLA (CHICKENPOX)
ID/CC An 8-year-old male is brought to a physician with complaints of
impairment of vision in the left eye, urticarial skin rashes, and
ill-defined muscle aches.
HPI The child's mother has caught the child eating dirt or soil on
many occasions (l'K \). The family also has a pel dog ai home.
PE Rounded swelling near the optic disk seen on fundus exam of
left eye: urticarial wheals observed on extremities and trunk;
mild hepatosplenomegaly noted.
Labs Leukocytosis with marked eosinophilia; enzyme immunoassay
using extracts of excretory-secretory products of Toxocara canis
larvae positive.
Micro Pathology
Treatment
Discussion
Biopsy of liver reveals larvae with granuloma and eosinophilic
infiltration.
Diethylcarbamazine; albendazole or mebendazole; steroids to
control symptomatic inflammatory response; laser photocoagu-
lation of visible ocular larvae.
When the nondefinitive human host is infected with parasites
that normally infect animals, the parasites do not mature com-
pletely, but the larvae introduced persist and induce an inflam-
matory reaction. The syndrome of visceral larva migrans
develops when nematode larvae of animal parasites (mostly cat
or dog ascarids such as Toxocara canis) migrate in human tissues;
the syndrome ol cutaneous larva migrans (creeping eruption)
develops when the larvae of various parasites (including the dog
or cat hookworm Ancylostoma hmzilinise) penetrate human skin
and form pruritic, serpiginous cutaneous lesions along the mi-
gratory tracts of the larvae.
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VISCERAL LARVA MIGRANS
ID/CC A 2-year-old female is brought to the emergency room because
of paroxysms and multiple coughs in a single expiration, fol-
lowed by a high-pitched inspiratory whisde or whoop.
HPI For the past 2 weeks she has had a runny nose, low-grade fever,
muscle pains, and headache. Her immunization schedule is
incomplete.
PE VS: fever. PE: child apprehensive and becomes cyanotic during
cough paroxysm; thick green mucus expelled with cough; con-
junctival injection.
Labs CBC: marked leukocytosis with lymphocytosis. Bardetella pertussis
on fluorescent antibody staining of nasopharyngeal secretions;
diagnosis confirmed by culture on Bordet-Gengou medium.
Gross Pathology Small conjunctival and brain hemorrhages may appear during
paroxysms; bronchiectasis may also be a complication.
Micro Pathology
Signs of acute inflammation in upper respiratory tract mucosa,
with erythema, petechiae, polymorphonuclear infiltrate, and
necrosis.
Treatment Largely supportive; erythromycin.
Discussion A bacterial infection of the upper respiratory tract caused by
Bordetella pertussis, a gram-negative coccobacillus, whooping
cough is transmitted by droplets and comprises three stages:
prodromal (catarrhal), paroxysmal (coughing), and convales-
cent. It is largely preventable with universally administered diph-
theria toxoid, tetanus toxoid, and pertussis a cellular (DTP)
vaccine. Pertussis toxin is a heat-labile exotoxin in which ADP
ribosylates the inhibitory G protein, thus inactivating it and
leading to constant activation of adenylate cyclase and increased
cAMP. The remarkable lymphocytosis is due to pertussis toxin
inhibiting chemokine receptors. As a result, lymphocytes are
unable to leave the blood stream.
WHOOPING COUGH
ID/CC A 10-year-old child who lives in tropical Africa presents with
multiple papillomatous skin lesions and pain in both legs.
HPI The first lesion had appeared on die leg as a small indurated
papule that ulcerated into a granulomatous papilloma.
PE Multiple papillomatous skin lesions seen, especially in interlrigi-
n mi is areas: lesions were painless and exuding .1 serous fluid;
painful hyperkeratotic lesions seen on palms and soles: both
dbia were tender to palpation.
Labs Dark-field microscopic examination of exudate from lesions
established the diagnosis by revealing organisms with the
characteristic morphology and rotational motion of pathogenic
treponemes; nonlreponemal serologic tests (i.e.. VDRL and RPR
tests) and treponemal tests (i.e., FTA-ABS test) were positive.
Imaging XR, legs: evidence of periostitis of the tibia.
Treatment Long-acting intramuscular benzatiiine penicillin G is the treat-
men I of choice.
Discussion
Yaws, the most common of the nonvenereal treponeniatoses, is a
chronic infection of skin and bones caused by livpoiirma
pertenue. Yaws occurs in tropical areas of Africa. Asia, and
Central and South America; ii is principalh a disease of child-
hood, and initial infection occurs between 5 and 15 years of age.
transmission is b\ direct contact with infected skin lesions con-
taining treponemes and is fostered by conditions of overcrowd-
ing and poor hygiene. The disease may occur in three stages:
primary, secondary, and tertiary. Only lesions of primary and
secondary yaws are infectious.
YAWS
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ID/CC
HPI
A 24-year-old while South American male develops sudden high
fever, chills, generalized aches and pains, retro-orbital
headache, nausea, and vomiting.
He gradually improves, but the fever returns 4 days later along
with a yellowing of his skin and eyes and an episode of fainting
and abundant coffee-ground emesis.
PE VS: fever (39°C); hypotension (BP 90/60). PE: jaundice; pe-
techiae on lower legs; swollen, bleeding gums; cardiomegaly;
hepatomegaly.
Labs CBC: leukopenia. UA: oliguria; albuminuria; hematuria.
Gross Pathology Normal-sized liver with yellowish hue and petechiae: pale,
swollen kidneys.
Micro Pathology Characteristic midzonal lobular necrosis, fatty accumulation,
and eosinophilic inlracytoplasmic Councilman bodies on liver
biopsy; hyperplasia of endothelial cells surrounding lymphoid
follicles ol spleen; severe renal tubular damage with epithelial
fatty degeneration and necrosis.
Treatment Symptomatic; prevention with mosquito control and live viral
vaccination.
Discussion Yellow fever is a viral hemorrhagic fever that is caused by a
flavivirus transmitted by Aedes mosquitoes: it is preventable by a
vaccine, which is required prior to travel to certain countries. It
is associated with a mortality rate of 5% to 10%, but most cases
are self-limiting and mild. It is similar to malaria but does not
recur.
3 YELLOW FEVER
ID/CC A neonate died shortly after birth.
HPI Review of the medical record reveals history of refusal to feed,
an extensive maculopapular skin rash on his legs and trunk,
respiratory distress, diarrhea, and seizures shortly after birth.
Discussion Neonatal listeriosis may occur early or late in neonatal life.
Infants may be acutely ill at birth and may die within hours as a
result of disseminated listeriosis, which is also called
granulomatosis infantiseptica. This condition is characterized
by hepatosplenomegaly, thrombocytopenia, generalized skin
papules, whitish pharyngeal patches, and pneumonia. Commonly,
a stained smear of meconium will reveal gram-positive bacilli,
suggesting the diagnosis.
Atlas Link lUCiMU PG-M2-079
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LISTERIA MENINGITIS IN THE NEWBORN
ID/CC A 2. r )-year-old woman visits her family physician because of
marked burning pain while urinating (UYSI'RIA). increased
frequency of urination with small amounts of urine
(POLLAKIURIA) , and passage of a few drops of blood-stained
debris at the end of urination (HEMATURIA).
HPI She got married 2 weeks ago and has just returned from her
honeymoon.
PE VS: no fever; BP normal. PE: no edema; no costovertebral angle
tenderness; moderate suprapubic tenderness with urgency.
Labs UA: urine collected in two glasses; second glass more turbid
and blood-stained; urine sediment reveals RBCs and WBCs;
no RBC orWBC casts: Gram stain of urine sediment reveals
gram-negative bacilli; Escherichia coH in significant colony count
(> 100,000) on urine culture.
Treatment Oral antibiotics (Bactrim, fluoroquinolone); adequate
hydration.
Discussion E. roliis the most common pathogen: Proteus. Klebsiella,
Staphylococcus saprophylicus, and Enterococcus are other common
bacteria causing cystitis. Hemorrhagic cystitis may result from
adenoviral infection.
ACUTE CYSTITIS
ID/CC A 28-year-old man comes to the F.R witli gradually worsening
and now severe scrotal swelling and pain radiating to the
inguinal area.
HPI Hie patient has no significant medical history. He reports pain
on urination (due to concomitant urethritis) and notes that he
is sexually active witli multiple partners. He also notes that the
pain is greater on standing and walking and is relieved by rest
and elevation of the legs.
PE VS: normal. PE: scrotal edema and erythema; right epididymis
enlarged and tender; induration present; elevation of scrotal
contents relieves pain (PBEHN'S SIGN).
Labs UA: pyuria. Culture negative; biopsy of epididymis inoculated
into cell cultures grows Chlamydia trachomatis, immunofliio-
i escencc reveals subtype D.
Imaging US: hypoechoic. enlarged epididymis with hyper vascularity.
Gross Pathology Nonspecific inflammation characterized by congestion and
edema.
Micro Pathology Earlv stage of the infection is limited to the interstitial connec-
tive tissue with white cell infiltration.
Treatment Antibiotics like doxycycline, minocycline for chlamydia. Course
of ofloxacin covers all possibilities ol causative organisms.
Discussion Differentiate epididymitis from testicular torsion and tumor
(scrotal ultrasonography or isotopic flow study max be needed
for differentiating). Transmitted sexually in young adults and
most often caused by Chlamydia trachomatis subtypes D
through K and Neisseria gonorrhoea*: In those older than 40,
Escherichia coli and I'seudomona.s cause most infectious. II associated
with rectal intercourse, it may be due to Enterobacteriaceae.
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EPIDIDYMITIS
ID/CC A 15-year-old male presents with painful bilateral swelling of the
parotid glands, left-sided scrotal pain, and fever.
HPI Nothing in the patient's history suggests that he had childhood
mumps. He has not received a measles-mumps-rubella (M.MR)
vaccination.
PE VS: fever. PE: bilateral parotid gland enlargement with oblitera-
tion of mandibular hollow; hyperemia and edema of Stensen's
duct (parotid duct) orifice; retroauricular lymphadenopathy;
left-sided scrotal and testicular swelling with tenderness.
Labs CBC: leukopenia with lymphocytosis; hyperamylasemia. Positive
complement fixation antibodies; positive serologic enzyme im-
munoassay (EIA) for mumps antibody (repeat test after 1 week
to demonstrate a fourfold rise).
Imaging Is, scrotum: increased color How and edema.
Gross Pathology Enlarged, edematous testicle.
Micro Pathology
Parotid glands show perivascular mononuclear, lymphocytic,
and plasma cell infiltrate with necrosis; ductal obstruction and
edema; testicular interstitial edema; perivascular cerebral
lymphocytic cuffing.
Treatment Scrotal support; analgesics, ice packs; corticosteroids.
Discussion
Atlas Link
Orchitis may be caused by bacterial infections such as Escherichia
coli and other enterobacteria; viral infections such as mumps;
STDs such as Chlamydia species or gonorrhea; or pathogens such
as Mycobacterium tuberculosis. Mumps orchitis may give rise to
sterility if bilateral.
PG-M2-082
ORCHITIS
ID/CC A 10-year-old child presents with complaints of acute-onset void-
ing o I tea-colored urine and reduced urinary output.
HPI The child was Heated 1 week ago lot streptococcal pyoderma
that was confirmed by culture. He also complains of puffiness
around the eyes and mild swelling of both feel.
PE VS: hypertension (BP 140/96); lexer, tachycardia. PE: perior-
bital swelling; mild pitting pedal edema; no ascites or kidney-
mass palpable.
Labs CBC: mild leukocytosis. Elevated BUN and creatinine; elevated
ASO titer: serum < rvoglobulins present. LA: RBC casts;
proteinuria. C3 levels reduced in blood.
Gross Pathology Smooth, reddish-brown cortical surface with numerous
petechial hemorrhages.
Micro Pathology
Biopsy shows diffuse glomerulonephritis resulting from prolifer-
ation of endothelial, niesangial. and epithelial cells: granular.
"starry-sky" pattern of IgG, IgM, and C3 on immunofluores-
cence: electron microscopy shows subepithelial "humplike"
deposits (antigen-antibody complexes).
Treatment Penicillin if still infected with Streptococcus-, diuretics, salt and
water restriction and antihypertensives.
Discussion Poststreptococcal glomerulonephritis is a classic immune
complex-mediated entity that is associated with acute nephritic
syndrome, which develops following infection with nephrogenic
group A 3-hemolvtie streptococci (e.g., types 1, 4, and 12, which
are associated with pharyngitis, and types 19, 55, and 57, which
arc associated with impetigo).
POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
ID/CC A 25-year-old male presents with complaints of sudden-onset
fever and chills, urgency and burning; on micturition (nv'SURlA),
and perineal pain.
HPI I lis symptoms developed a day after he underwent urethral
dilatation for a stricture.
PE VS: fever. PE: suprapubic tenderness; rectal exam reveals asym-
metrically swollen, firm, markedly tender, hot prostate; prostatic
massage is avoided owing to risk of inducing bacteremia; epi-
didymitis and extreme pain.
Labs Examination and culture of urine and prostatic secretions reveal
infection with Escherichia coli.
Gross Pathology
Edematous gland enlargement with suppuration of entire gland,
possibly abscesses and focal areas of necrosis that have coa-
lesced.
Micro Pathology Initially minimal leukocytic infiltration of stroma. Later, necrosis
of the gland may lead to gland fibrosis.
Treatment Antibiotic therapy as directed by urine and blood culture sensi-
tivity tests.
Discussion Escherichia coli is the most common cause of acute prostatitis;
mam cases follow the use of instrumentation for the urethra
and prostate (e.g., catheterization, cystoscopy, urethral dilata-
tion, transurethral resection). Remaining infections are caused
by Klebsiella, Proteus, Pseudomonas, and Serratia. Among the gram
positives, eiuenx i iccus and Staphylococcus aureus are frequent
causative organisms.
PROSTATITIS— ACUTE
ID/CC A 65-year-old male complains o I recurrent burning, urgency, and
frequency of micturition together with vague lower abdominal,
lumbar, and perineal pain.
HPI He also complains of a mucoid urethral discharge. He was
previously diagnosed via ultrasound with benign prostatic hyper-
trophy but does not report any severe symptoms of prostatism;
his medical history reveals frequent UTIs due to Escherichia coli.
PE VS: stable; no fever. FE: rectal exam reveals enlarged, nodular
prostate: biopsy obtained to rule out carcinoma.
Labs Examination and culture of expressed prostatic secretions reveal
leukocytosis and E. coli.
Imaging FvT/voiding cystourethrogram (to rule out underlying anatomic
cause): normal.
Gross Pathology Enlarged prostate with nodularity and calculi.
Micro Pathology
Chronic inflammation and few PMNs around glands and ducts on
biopsy; dilated ducts containing inspissated secretions (CORPORA
amyi.u i<a).
Treatment Antibiotics (TMP-SMX, carbenicillin. quinolones). High fluid in-
take and abstinence from alcohol. Recurrences are common.
Discussion Bacterial prostatitis is usually caused by the same gram-negative
bacilli that cause UTIs in females; 80% or more of such infec-
tions are caused by Escherichia coli. Chronic bacterial prostatitis is
common in elderly males with prostatic hyperplasia and is a fre-
quent cause of recurrent UTIs in males (most antibiotics poorly
penetrate the prostate; hence the bacteria are not totally eradi-
cated and continuously seed the urinary tract).
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PROSTATITIS— CHRONIC
ID/CC A 28-year-old black woman who is in her 27th week of pregnancy
complains of right flank pain, high-grade fever, malaise,
headac he, and dysuria.
HPI Thus far her pregnancy has been uneventful.
PE VS: fever. PE: no peripheral edema; right costovertebral angle
tenderness; acutely painful fist percussion on right lumbar area
(positive Giordano's ska).
Labs CBC: leukocytosis with neutrophilia. UA: proteinuria; hema-
turia; abundant WBCs and WBC casts; pyocytes on sediment; al-
kaline pH; urine culture > 1 00,000 colonies of Esclierichia coli.
Imaging US, renal: slightly enlarged kidney-
Gross Pathology Kidney enlarged, edematous, and hyperemic with microab-
scesses in medulla.
Micro Pathology
Pyocytes in tubules; light blue neutrophils on supravital stain
(GLITTER cells); PMN infiltration of interstitium.
Treatment Antibiotics according to sensitivity; ampicillin; in nonpregnant
patients, fluoroquinolone or ampicillin and an aminoglycoside
constitute initial treatment.
Discussion
An acute bacterial kidney infection caused mainly by gram-
negative bacteria such as E. coli, Klebsiella, Proteus, and
Eiiterobacter, acute pyelonephritis usually results from upward
dissemination of lower urinary tract bacteria.
Atlas Links Fl F"l PG-M2-086A, PG-M2-086B
PYELONEPHRITIS— ACUTE
ID/CC A 10-ycar-old female presents vviih a high fever, headache,
vomiting, and impaired consciousness.
HPI She suffered a generalized seizure about 45 minutes ago. She
was previously diagnosed with cyanotic congenital heart disease
(ventricular septal defect with Eisenmenger's syndrome).
PE VS: fever. PE: altered sensorium: papilledema: nuchal rigidity;
clubbing; central cyanosis; cardiac auscultation suggestive of
YSD with severe pulmonan arierial hvpertension.
Labs Blood culture reveals mixed infection will) Bacteroides, mi-
croaerophilic streptococci. Staphylococcus aureus, and Klebsiella:
staining and culture of pus aspirated from brain abscess confirm
p< ilvniii robial infection.
Imaging CT (with contrast): multiple ring-enhancing lesions with low
attenuation centers (ABSCESS) surrounding cerebral edema and
ventricular compression.
Gross Pathology Cavity filled with thick, liquefied pus surrounded by fibrous
capsule of variable thickness; pericapsular zone of gliosis and
edema.
Central portion contains degenerated PMNs and cellular debris;
capsule is composed of collagenous fibrous tissue with blood
vessels and mixed inflammatory cells.
Treatment High-dose, extended parenteral broad-spectrum antibiotic cov-
erage; CT-directed drainage of pus.
Micro Pathology
Discussion brain abscesses arise secondary lo hematogenous spread from
another infection (bronchiectasis, endocarditis), from contigu-
ous spread from adjacent infection (chronic otitis media, mas-
toiditis, sinusitis), or following direct implantation from trauma.
Patients with i ongenital heart disease with right-to-lcft shunt are
particularly predisposed because the normal filtering action of
tin- pulmonary vasculature is lost.
BRAIN ABSCESS
ID/CC A 43-year-old male Mexican migrant worker visits his ophthal-
mologist because of pain and loss of vision in his right eye.
HPI Recently he has also suffered from severe headaches and
projectile vomiting.
PE Papilledema on left funduscopic exam; free-floating cyst in vit-
reous body of right eye; chorioretinitis and disk hemorrhage;
multiple nontendcr subcutaneous nodules.
Labs CBC: eosinophilia. LP: lymphocytic and eosinophilic pleocytosis
in CSF with elevated protein and decreased glucose. Eggs of
Taenia solium in stool sample.
Imaging
Gross Pathology
Micro Pathology
XR, plain: small nodular calcifications. CT/MR, brain: charac-
teristic ring-enhancing intracranial cysts or calcifications: can
cause obstruction and hydrocephalus.
Fluid-filled cysts containing scolex surrounded by fibrous cap-
sule in anterior chamber of eye; intraventricular and parenchy-
mal invasion of brain, subcutaneous tissue, and striated muscle.
Inflammatory infiltration of cyst by PMNs; necrotic inflamma-
tion with calcification upon death of parasite.
Treatment Surgical removal of parasite from eye; albendazole, cortico-
steroids/praziquantel for brain disease.
Discussion Produced by Cystirerciis rellulosae, ihe larval form of the pork
tapeworm Taenia solium, neurocysticercosis is due to the inges-
tion of ova and spreads through fecal-oral transmission.
CYSTICERCOSIS
ID/CC A 30-year-old male presents with a high fever and chills,
headache, nausea, vomiting, and muscle aches.
HPI Yesterday he had an episode involving abnormal movements of
his right hand and face (FOCAL seizure) . I le also has difficulty
comprehending speech and has olfactory hallucinations. He has
no history of psychiatric illness.
PE VS: fever; tachycardia; mild tachypnea: BP normal. PE: confused
and disoriented; papilledema: mild nuchal rigidity; Kernig's sign
positive; paraphasic errors in speech; deep tendon reflexes nor-
mal and bilaterally symmetric.
Labs
Imaging
Gross Pathology
Micro Pathology
l.P: cells 400/uL with mononuclear pleocytosis; mildly elevated
protein; normal glucose; CSF PCR reveals herpes simplex virus
type 1 (HSV-1); serum complement-fixing antibody tiler >
1:1000. EF.G: spiked and slow waves localized to temporal lobes.
CT: characteristic changes of encephalitis seen over temporal
lobes.
Hemorrhagic, necrotizing encephalitis most severe along infe-
rior and medial regions of temporal lobes and orbitofrontal
gvri.
Brain biopsy reveals Cowdry intranuclear viral inclusion bodies
in both neurons and glial cells with perivascular inflammatory
infiltrates.
Treatment Intravenous acyclovir.
Discussion Herpes simplex virus is the most common cause of acute
sporadic encephalitis in the United States. In the newborn,
HSV-2 is usually the cause; after the neonatal period, most cases
result from HSV-1. Neonatal infection (usually HSV-2) occurs
after exposure to maternal genital infection at the time of
delivery. The precise pathogenesis of HSV-1 encephalitis in the
older child or die adult is not clear, but viral spread into the
temporal loin- l>\ both nlfac Ion and trigeminal routes has been
postulated.
Atlas Link UlcHI 1 1 M-M2-089
HERPES SIMPLEX ENCEPHALITIS
ID/CC An 1 1-year-old girl is brought to the ER with high fever, chills,
severe headache, vomiting, and obtundation.
HPI Her parents report that she suffered a generalized seizure about
an hour ago. A few days ago. the family had returned from a
.summer vacation in south India, where the child often played in
irrigated rice farms. She did not receive any immunizations
prior to her travel.
PE VS: fever. PE: patient is stuporous; neck stiffness and Kernig's
sign positive (due to meningeal irritation): mild papilledema;
tremors noted in hands.
Labs LP: CSF reveals pleocytosis with predominant lymphocytosis,
mildly elevated proteins, and normal sugar (suggestive of aseptic
meningitis); IgM enzyme immunoassay performed on acute and
convalescent sera and CSF reveals significant titer of antibodies
to Japanese encephalitis virus.
Imaging ( T. head: areas of low density in the thalamus and basal ganglia.
Treatment Supportive; experimental intrathecal a-interferon therapy.
Discussion Japanese encephalitis virus is a flavivirus that causes disease in
humans, horses and pigs. It is widely distributed in Asia from
Japan and Eastern Siberia to Indonesia and westward to India;
epidemics occur in summer months coincident with the abun-
dance of the mosquito vector Culex tritaenioHiychnus. The vec-
tor breeds in irrigated rice fields and bites preferentially at
sunset and sunrise; pigs are the amplifying hosts, whereas man is
the incidental "dead-end" host. A vaccine is available for routine
use for childhood immunization in Japan and in developed
counuies to protect travelers.
JAPANESE ENCEPHALITIS
ID/CC A 30-year-old male laboratory researcher presents with a high
fever, neck rigidity, retro-orbital pain, and severe myalgias of a
few days' duration.
HPI The patient also complains of a sore throat and photophobia.
His work in the lab involves close contact with experimental ani-
mals such as hamsters, white mice, and nude mice. He was ade-
quately vaccinated.
PE VS: fever. PE: neck stiffness and Kernig's sign positive (due to
meningeal irritation); pharyngeal inflammation but no exudate
noted.
Labs CBC: mild leukopenia. LP: CSF suggestive of aseptic meningitis;
LCM virus isolated from CSF. IgG and IgM antibodies detected
in serum by immunofluorescent assay.
Treatment Supportive; ribavirin may play a role.
Discussion Lymphocytic choriomeningitis virus is an arenavirus. Sporadic
cases occur after infection with feral mice, but the most
common sources of human infection are pet/lab rodents. The
virus is considered a major lab hazard, and care must be taken
to avoid accidental infection. There is no commercially available
vaccine.
LYMPHOCYTIC CHORIOMENINGITIS (LCM)
ID/CC A 50-year-old white male develops sudden fever with chills, pain
in the back and extremities, and neck stiffness; he vomited six
limes and had a convulsion prior to admission.
HPI The patient is a heavy smoker and is diabetic. Two weeks ago,
he had a URL He is also very sensitive to light (photophobia).
PE Markedly reduced mental status (obtunded); petechial rash
over trunk and abdomen; nuchal and spinal rigidity; positive
Kernig's and Brudzinski's signs; no local neurologic deficits.
Labs LP: elevated pressure; cloudy CSF; elevated protein; markedly
decreased glucose; high cell count with mostly WBCs. CSF Gram
stain reveals gram-positive diplococci. Spinal fluid culture grows
Streptococcus pneumoniae.
Imaging CT/MR, brain: meningeal thickening and enhancement.
Gross Pathology
Pia-arachnoid congestion results from inflammatory infiltrate;
thin layer of pus forms and promotes adhesions while obstruct-
ing normal CSF flow (can cause hydrocephalus); brain covered
with purulent exudate, most heavily on base.
Treatment Early empiric high-dose IV antibiotics; cefotaxime: vancomycin;
high-dose steroids.
Discussion Bacterial meningitis is a pyogenic infection of the CNS that re-
quires prompt treatment. Streptococcus pneumoniae is the most
common cause of adult meningitis.
Atlas Links QEH j ] PG-M2-092A, PG-M2-092B, M-M2-092
Cli. □' NEU-027
MENINGITIS— BACTERIAL (ADULT)
ID/CC A 4-year-old female presents with a 1-week history of fever, se-
vere headache, irritability, and malaise: 2 days ago she devel-
oped neck stiffness, and her parents report projectile vomiting
over the past 24 hours.
HPI The child is also very sensitive to light (photophobia). She is
fully immunized and has no history of ear, nose, and throat
infection, skin rashes, dog bites, or foreign travel.
PE VS: fever. PE: irritability; resistance to being louched or moved;
minima] papilledema of fundus; no focal neurologic signs; no
cranial nerve deficits; positive Kernig's and Brudzinski's signs.
Labs CBC: neutrophilic leukocytosis. LP: increased pressure; cloudy
CSF; neutrophilic pleocytosis; decreased glucose; increased
protein; gram-negative coccobacilli. Negative ZN and India ink
staining; normal scrum electrolytes; on chocolate agar, blood
culture grew Haemophilus influenzae; negative Mantoux.
Imaging CT/MR, brain: meningeal thickening and enhancement.
Gross Pathology Abundant accumulation of purulent exudate between pia mater
and arachnoid; meningeal thickening; cloudy to frankly
purulent CSF.
Micro Pathology Intense neutrophilic infiltrate.
Treatment IV antibiotics (ampicillin, cefotaxime); consider steroids.
Discussion A pyogenic infection of the nervous system primarily affecting
the meninges, bacterial meningitis is most commonly caused by
pneumococcus (Streptococcus pneumoniae, associated with sickle
cell anemia), meningococcus (Neisseria meningitidis, associated
with a petechial skin rash), and H. influenzae (most commonly in
children). It is less commonly caused by enterobacteria,
Streptococcus species, Staphylococcus species (due to dental infec-
tion), and anaerobic organisms (clue to trauma).
Atlas Link mcfc'j 1 1 M-M2-093
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?| MENINGITIS— BACTERIAL (PEDIATRIC)
ID/CC A 33-year-old HIV-positive white male is brought into the emer-
gency room by his mother because of a persistent headache.
HPI The patient's mother states that her son has been suffering for a
long tune from headaches and stiff neck as well as from fever
and chills.
PE VS: fever (39°C). PE: severe nuchal rigidity; lack of responsive-
ness 10 any command; positive Kemig's and Rrud/iiiski's signs;
diminished patellar and Achilles reflexes; clear lung sounds.
Labs LP: increased CSF pressure; variable pleocytosis (75 lymphocytes/
mm 1 ); elevated protein; decreased glucose. Heavily
encapsulated, nondimorphic spherical fungal cells
(CRYPTOC.occ.rs \t.oi-or\ia\s) revealed on India ink staining;
polysaccharide capsular antigen detected on latex agglutination
test; diagnosis confirmed by culture on Sabouraud's medium.
Imaging CT/MR. brain: multiple ring-enhancing lesions.
Gross Pathology
Micro Pathology
Granuloma and abscess formation, mainly at base of brain; CNS
primarily affected; lungs affected less commonly.
Abundant fungi in CSF and leptomeninges, with slight mononu-
clear inflammatory reaction; typical nodular granulomatous
meningitis with exudate.
Treatment Amphotericin B and 5-flucytosine; fluconazole.
Discussion Once called torulosis, cryptococcosis is the most common cause
of mycotic meningitis; it is acquired through the inhalation of
dried pigeon droppings and is usually seen in immunocompro-
mised patients.
Atlas Link L'JCL-a 1 1 M-M2-094
MENINGITIS— CRYPTOCOCCAL
ID/CC A 6-year-old male being treated for primary pulmonary
tuberculosis presents with diplopia, increasing drowsiness,
irritability, and unexplained, recurrent vomiting.
HPI The child has had a low-grade fever, loss of appetite, and a per-
sistent headache over the past few weeks.
PE VS: fever. PE: stuporous; signs of meningeal irritation noted
(neck rigidity, Kernig's sign); CN III and IV palsy on right side;
lunduscopy reveals papilledema.
Labs LP (guarded): CSF under increased pressure and turbid; on
standing, a "cobweb" coagulum formed at center of tube; ( !SF
studies reveal lymphocytic pleocytosis. greatly elevated protein,
and low sugar; ZN staining of CSF coagulum reveals presence of
acid-fast bacilli; radiometric culture yields Mycobacterium
tuberculosis.
Imaging
Gross Pathology
Micro Pathology
CT: suggests basal exudates, inflammatory granulomas, and a
communicating hydrocephalus; striking meningeal enhance-
ment noted in post-contrast studies.
Meningeal surface covered with yellowish-gray exudates and tu-
bercles that are most numerous at base of brain and along the
course of the middle cerebral artery; subarachnoid space and
arachnoid villi obliterated (leading to poor absorption of CSF
and hence a communicating hydrocephalus).
Subarachnoid space contains gelatinous exudate of chronic in-
flammatory cells, obliterating cisterns, and encasing cranial
nerves; well-formed granulomas occasionally seen, most often at
base of brain; arteries running through subarachnoid space
show "obliterative endarteritis."
Treatment Anlituberculous therapy with rifampin, isoniazid, ethambutol
and pyrazinamide; steroids; ventriculoperiloneal shunt to relieve
hydrocephalus.
Discussion Tuberculous infection reaches the meninges through the
hematogenous route, resulting in a clinically subacute form of
meningitis; it is often complicated by cranial nerve palsies, a
communicating hydrocephalus, decerebrate posturing,
convulsions, coma, and death.
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MENINGITIS— TUBERCULAR
ID/CC A 3-year-old male, the child of recent African immigrants, is
brought to the local health center because of asymmetrical legs.
HPI His parents give a history of incomplete immunization. They add
that 5 months ago the boy had fever and diarrhea that subsided
spontaneously; a few weeks later they noted that he could not
use his right leg.
PE Right leg thin, short, wasted, weak, and flaccid; absent deep
tendon reflexes in right leg; no sensory deficit; upper limbs
normal; mental status and cranial nerves normal.
Labs EMCi: chronic partial denervation with abnormal spontaneous
activity in resting muscle and reduction in number of motor
units under voluntary control; normal sensory conduction
studies.
Treatment Rehabilitation, supportive.
Discussion A symptomatic disease caused by poliovirus that is more com-
mon in infants and children, poliomyelitis can result in muscu-
lar atrophy and skeletal deformity. It attacks motor neurons in
the anterior horns and may affect cranial nerves (bulbar polio);
it is preventable by vaccine.
POLIOMYELITIS
ID/CC A 26-year-old nurse presented with headaches and recent-onset
seizures; she also complained of increasing right-sided
numbness and blurring of vision.
HPI A clinical diagnosis of HSV encephalitis had previously been
made, for which the patient was treated with two courses of acy-
clovir without any amelioration of symptoms; the disease contin-
ued to progress both radiologically and clinically. On serology
she tested HIV positive.
PE Neurologic exam reveals cognitive mental impairment; visual
Field defects and sensory dysphasia seen; an ill-defined sensory
loss on right side of body.
Labs HIV positive by ELISA and Western blot.
Imaging
Micro Pathology
Treatment
Discussion
MR (T2-weighted): patchy high-intensity lesions in the deep
white matter of left cerebral hemisphere involving temporal,
parietal, and occipital lobes.
Stereotactic biopsy sections show abnormal brain with rarefac-
tion, numerous reactive astrocytes, foamy histiocytes, and in-
flammatory infiltrate around some vessels; JC virus in situ
hybridization shows many positive nuclei; no herpesvirus inclu-
sions seen: electron microscopy demonstrates cells with typical
papovavirus structures in nucleus.
Disease was relentlessly progressive and resulted in death within
6 months.
Progressive multifocal leukoencephalopathy is a progressive
demyelinating disease related to JC papovavirus infection; the
largest number of cases occur in persons who are immunocom-
promised for any of a variety of reasons, including organ trans-
plantation, hematologic and other malignant diseases, chronic
immunosuppressive therapy, and AIDS.
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PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY
ID/CC A 30-year-old male is seen with complaints of a rash along with
pain in his left ear and inability to move the muscles of his face
with accompanying asymmetry.
HPI He suffered an attack of chickenpox during childhood but has
lid history either of a similar rash over his face or of any visual
symptoms (to rule out herpes zoster ophthalmicus).
PE Vesicular rash over left pinna (otitis kxtkrna); left-sided lower
motor neuron-type facial nerve palsy (patient is unable to frown
and unable to blink left eye; eyeballs roll up during attempt to
close eye; patient is unable to whistle; taste sensation over
anterior two-thirds of tongue lost on left side).
Labs Although the diagnosis is predominantly clinical, a Tzanck test
examining lesion scrapings (showing evidence of multinucleate
acanlholytic cells), direct culture, and immunohistochemical
identification of infected cells allow identification of the virus.
Gross Pathology Neuritis and vesicular skin lesions confined to distribution of
geniculate ganglion of facial nerve.
Micro Pathology
Vesicular skin lesions widi herpes viral inclusions, i.e.. intranu-
clear, acidophil inclusions with a halo around them (Cowdry
i mi A inclusions); syncytial cells also seen.
Treatment Systemic steroids are mainstay of management.
Discussion Herpes zoster of the geniculate ganglion, or Ramsay Hunt syn-
drome, presents as a vesicular rash on the pinna followed by
ipsilateral I.MN facial nerve palsy.
RAMSAY HUNT SYNDROME
ID/CC A 30-year-old male presents with a high fever, neck stiffness, and
drowsiness.
HPI He also complains of nausea and vomiting. He recently traveled
along the Mississippi-Ohio River basin.
PE V'S: fever. PK: neck stiffness and Kernig's sign positive (due to
meningeal irritation); right oculomotor nerve palsy noted; mild
papilledema.
Labs IgM enzyme immunoassay done on paired sera, and CSF con-
firms the diagnosis of St. Louis virus infection. LP: CSF exam
reveals pleocytosis with predominant lymphocytosis suggestive of
aseptic meningitis.
Micro Pathology
Inflammation and neuronal degeneration, principally in the
thalamus, midbrain, and brainstem.
Treatment Supportive treatment.
Discussion St. Louis encephalitis virus is the most common cause of
epidemic encephalitis in the United Stales: cases occur annuallv
as isolated events or in summer and autumn encephalitis
epidemics. Most infections are asymptomatic. The disease occurs
throughout the United States, but outbreaks have also occurred
in the Caribbean as well as in Central and South America.
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ST. LOUIS ENCEPHALITIS
ID/CC The case of a 12-year-old boy who died of a progressive degener-
ative neurologic disease was discussed at an autopsy meeting.
HPI The child had been developing normally up to 10 years of age,
when his teachers noted a progressive deterioration in intellect
and personality; this was followed by the development of
seizures akin to myoclonus, signs of pyramidal and extrapyrami-
dal disease, and finally a state of decerebrate rigidity. The child
died 7 months after the onset of symptoms. His history revealed
that he had had a severe attack of measles at the age of 2.
Labs LP: routine CSF profile normal. Gamma globulin level elevated:
markedly elevated levels of measles antibody present in both
serum and CSF; despite the elevated antibody liters, antibody to
the M protein was not present. EEC: pattern of burst
suppression and biphasic sharp and slow waves.
Imaging MR: nonspecific parenchymal abnormalities.
Micro Pathology
Histopathologically. the encephalitis involved both white and
gray matter and was marked by lymphocytic infiltration, nerve
cell degeneration, and demyelination; measles antigen demon-
strated by immunofluorescence analysis, and particles resem-
bling paramyxovirus were detected by electron microscopy.
Treatment No specific therapy available.
Discussion Subacute sclerosing panencephalitis (SSPE) is caused by a
defective (major defect is the lack or altered expression of the
M-matrix protein) form of measles virus (family Paramyxoviridae);
SSPE is a late complication of a measles infection that is not
eliminated from the host. Immunization against measles is the
only effective preventive tool.
SUBACUTE SCLEROSING PANENCEPHALITIS
ID/CC A 25-year-old recently married woman is concerned about a
scanty, offensively malodorous vaginal discharge.
HPI She states that the discharge is thin, grayish-white, and foul-
smelling. She does not complain of vulvar pruritus or soreness.
PE Pelvic exam confirms presence of a homogenous, grayish-white,
watery discharge adherent to the vaginal walls that yields a
"fishy" odor when mixed with KOH; no injection and excoria-
tion of the vulva, vagina, or cervix.
Labs Vaginal pH > 5; saline smear reveals presence of characteristic
"clue cells" (squamous epithelial cells with smudged borders
due to adherent bacteria).
Treatment Single dose of metronidazole (2 g) effective in treating the
infection. Oral clindamycin is an alternative drug.
Discussion Although bacterial vaginitis was originally thought to be caused
by Gardnerella vaginalis, this organism is now recognized to be
part of the normal vaginal flora. Bacterial vaginosis is now
known to result from a synergistic interaction of bacteria in
which the normal Lactobacillus species in the vagina is ultimately
replaced by high concentrations of anaerobic bacteria, including
Bacteroides, Peptostreptococcus, Peptococcus, and Mobiluncus
species along with a markedly greater number of G. vaginalis
organisms than is encountered in normal vaginal secretions.
Bacterial vaginosis is known to increase the risk of pelvic inflam-
matory disease, chorioamnionitis, and premature birth.
Atlas Link VlcVi 1 1 M-M2-101
BACTERIAL VAGINOSIS
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ID/CC A 25-year-old puerpera who was lactating her week-old infant
presents with pain and swelling in her left breast.
HPI The symptoms commenced acutely, and she does not recall any
previous breast lumps or swellings.
PE Skin overlying left breast is red, edematous, tender, and hot;
area of tense induration felt underlying inflamed skin.
Labs Culture of pus drained from breast abscess and nasopharyngeal
swab taken from the infant grew Staphylococcus aureus.
Imaging USG: nearly anechoic area with posterior enhancement.
Treatment Penicillinase-resistant antibiotic; incision (in a radial direction
over the affected segment) and dependent drainage of intra-
mammary abscess; breast feeding was temporarily discontinued.
Discussion Bacterial mastitis most commonly occurs in lactating women
due to infection of a hematoma or secondary infection of
plasma cell mastitis; the infecting organism is mostly
penicillin-resistant Staphylococcus aureus.
BREAST ABSCESS
ID/CC A 38-year-old while female visits her gynecologist for a routine
Pap smear.
HPI She admits to early sexual activity, many sexual partners, and
unprotected sex.
PE Pallor; cervical tenderness; a few small, raised, flat lesions on
cervix: genital warts also seen on vulva (condylomata
a< i WIN ATA).
Labs Presence of HPV in cervical cells revealed on DNA hybridization
and immunofluorescent antibody assays for viral antigen.
Micro Pathology
Rounded basophilic cells on Pap smear with large nuclei occupy-
ing most of surface; nuclei show mitoses and coarse clumping of
chromatin with perinuclear halo (severe KOILOCYTIC DYSPLASIA).
Treatment Cryotherapy, conization, or local excision with follow-up.
Discussion Infection with HPV types 16, 18, and 31 is strongly associated
with cervical cancer preceded by dysplasia. Spread of die infec-
tion to partners may be prevented by barrier contraception.
Atlas Links Ul< IT ; M-M2-103
L»JCk'i21 0B-011A, 0B-011B
HUMAN PAPILLOMAVIRUS (HPV)
ID/CC A 28-year-old sexually active woman presents with crampy lower
abdominal pain, yellowish vaginal discharge, and general
malaise.
HPI She also complains of continuous low-grade fever and reveals
thai the pain is exacerbated during and immediately after
menstruation (congestive DYSMENORRHEA). She uses a copper
intrauterine device for contraception.
PE VS: low-grade fever. PE: lower abdominal tenderness; bimanual
pelvic exam demonsuates purulent vaginal discharge, bilateral
adnexal tenderness, and pain on movement of cervix
(MUCOPURUl-ENT CERVICITIS).
Labs CBC: leukocytosis with left shift. Increased ESR; endocervical
swab sent for microscopic exam; staining and culture revealed
combined infection with Neisseria gonorrhoeae (cultured on
Thayer-Martin medium) arid Chlamydia trachomatis (identi-
fied on cell culture, immunofluorescence, and antigen capture
assay); laparoscopy ("gold standard" for diagnosis) confirmed
diagnosis.
Imaging USG: free pelvic fluid, dilated tubular structure in adnexa.
Gross Pathology Erythema and swelling of fallopian tubes on laparoscopy; sero-
purulent exudate noted on surface of tubes from Gmbriated end.
Micro Pathology
Treatment
Discussion
Endocervical swab reveals increased neutrophils and gram-
negative diplococci seen both intra- and extracellularly; cervical
biopsy reveals inclusions containing Chlamydia within columnar
cells.
Antibiotic therapy with cefoxitin (for N. gonorrhoeae) and doxycy-
cline (for chlamydial infection); male partners must be treated
for STDs.
Pelvic inflammatory disease usually occurs as a primary infec-
tion that ascends from the lower genital tract due to STDs
caused by Neisseria gonorrhoeae and Chlamydia trachomatis.
Sequelae of PID include peritonitis; intestinal obstruction due
to adhesions; dissemination leading to arthritis, meningitis, and
endocarditis; chronic pelvic pain; infertility; ectopic pregnancy;
and recurrent PID.
PELVIC INFLAMMATORY DISEASE
ID/CC A 20-year-old Asian woman presents with complaints of
infertility and heavy bleeding during menses (MENORRHAGIA).
HPI She was treated for pulmonary tuberculosis a few years ago. She
has been unable to conceive despite unprotected intercourse for
the past 2 years. Her husband's semen analysis is normal.
PE On pelvic exam, small, fixed adnexal masses are palpable that
are matted and fixed to uterus ("FROZEN PELVIS").
Labs Culture of endometrial cureitings yields Mycobacterium
tuberculosis; histologic examination of curettings reveals
presence of characteristic tubercles; Mantoux skin test strongly
positive.
Imaging
Gross Pathology
CXR: left apical fibrosis (evidence of old healed pulmonary
tuberculosis). (Hysterosalpingography [HSG] is contraindicated
in a proven case of tuberculosis. When done in asymptomatic-
cases, HSG yields certain typical findings, including a rigid,
nonperistaltic, pipelike tube; beading and variation in tilling
density; calcification of the tube; cornual block; jagged
fluffiness of the tubal outline; and vascular or lymphatic
extravasation of the dye.)
Tubes are enlarged, thickened, and tortuous; examination of
uterus reveals evidence of synechiae and adhesions (leading to
Asherman's syndrome) .
Micro Pathology Microscopic exam of tubes, ovaries, and endometrium reveals
evidence of granulomas with giant cells and caseation.
Treatment Four-drug therapy with isoniazid, pyrazinamide, ethambutol.
and i ilampicin; pyridoxine to prevent isoniazid-induced
deficiency.
Discussion Genital tuberculosis is almost always secondary to a focus
elsewhere in the body, with the bloodstream by far the most
common method of spread. The fallopian tubes are the most
frequently involved part of the genital tract, followed by the
uterus. Ninety percent of patients are cured with chemotherapy,
although only 10% regain fertility.
PELVIC TUBERCULOSIS
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ID/CC A 30-year-old woman presents to the F.R with an abrupt-onset
high fever, vomiting, profuse diarrhea, severe muscle aches, and
disorientation.
HPI One day ago she developed an extensive skin rash all over her
body. Her husband says she used a vaginal sponge for
contraception.
PE VS: fever; tachycardia; hypotension. PE: extremely toxic-looking;
drowsy but responding to verbal commands; extensive
scarlatiniform rash seen involving entire body; pharyngeal,
conjunctival, and vaginal mucosa congested (frank hyperemia);
no neck rigidity or Kernig's sign demonstrable; funduscopic
exam normal; no localizing neurologic deficits.
Labs CBC: leukocytosis; thrombocytopenia. UA: mild pyuria (in
absence of L'TI). BUN and creatinine elevated; blood cultures
sterile; culture of cervical secretions grows Staphylococcus
aureus. LP: CSF normal. Serology for Rocky Mountain spotted
lever, leptospirosis, and measles negative.
Treatment Vigorous IV fluids and parenteral penicillinase-resistant
penicillin or first-generation cephalosporins: patient in this case
recovered, and typical skin desquamation was seen over palms
and soles during convalescence.
Discussion Toxic shock syndrome results from infection with Staphylococcus
aureus. Its effects are mediated through the exotoxin TSST-1,
which functions as a superantigen, stimulating the production
of interleukm-1 and tumor necrosis factor. Staphylococcal TSS
has been associated with the use of vaginal contraceptive
sponges and with many types of localized staphylococcal soft
tissue infections. Most cases of TSS occur in menstruating women.
Atlas Links QJTEIll 0B-027A, 0B-027B
TOXIC SHOCK SYNDROME (TSS)
ID/CC A 28-year-old primigravida al 36 weeks' gestation presents with a
high fever.
HPI She was being monitored following a premature rupture of the
membranes.
PE VS: fever; fetal tachycardia. PE: uterine tenderness.
Labs Elevated maternal total lymphocyte count; vaginal swab culture
revealed colonization with group B streptococcus.
Treatment Presence of group B streptococcus in vagina after premature
rupture of membranes was an indicadon for immediate delivery
and treatment of the infant; mother was also treated with
intravenous antibiotics.
Discussion A significant proportion of the population is colonized in the
vagina and rectum with group B streptococcus, which is
correlated with preterm labor, premature rupture of
membranes (PROM), chorioamnionitis, and neonatal sepsis;
neonates widi group B streptococcus sepsis have a 25% mortality
rate. Among preterm neonates, this figure doubles to over 50%;
therefore antibiotic prophylaxis is recommended in the setting
of preterm delivery and PROM even without die diagnosis of
frank chorioamnionitis. When chorioamnionitis is suspected,
intravenous antibiotics are started and delivery is hastened.
CHORIOAMNIONITIS
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Treatment
Discussion
An 8-month-old male infant is brought to a pediatrician because
of severe, intractable chronic diarrhea and failure to thrive.
The mother died of AIDS shortly after the baby was delivered.
The baby was asymptomatic at birth.
VS: fever; tachycardia. PE: emaciated, grossly malnourished; oral
thrush; generalized lymphadenopathy; hepatosplenomegaly.
Decreased CD4+ cell count; increased serum immunoglobulin
level with impaired production of specific antibodies; ELISA and
Western blot for HTV-1 positive (could be due to placental
transfer of antibodies to HIV, but strongly supports diagnosis in
presence of symptoms); PCR for HTV* RNA positive (confirming
HIV infection).
Nutritional support, Pneumocystis carinii prophylaxis, azidothymi-
dine (zidovudine, or AZT) therapy (suppresses replication by
inhibiting viral reverse transcriptase), and anti-infective agents
for specific infections; IV serum immunoglobulin to reduce
frequency of bacterial infections; oral polio vaccine and BCG
contraindicated .
Vertical transmission of HIV-l may occur in utero through
transplacental passage of the virus, during delivery, or postnatally
through breast feeding; however, it is believed that most
infections are acquired at birth through contact with contami-
nated blood or secretions. Women who carry the virus should
thus be discouraged from becoming pregnant or from breast
feeding. The rate of transmission of HIV-l from mother to
infant has varied from 13% to 45%, with an average of 25%;
however, when AZT is administered to HIV-l -infected pregnant
women and to infants during the first 6 weeks of life, the risk of
maternal-infant transmission is significantly reduced.
HIV TRANSMISSION IN PREGNANCY
ID/CC A 4-year-old while male presents with fever, chills, malaise, pain.
and immobility of the right knee of 1 week's duration.
HPI Two weeks ago the child fell while playing, but no abnormality
was found by the school nurse.
PE ( )verlying skin warm and red; swelling of distal third of thi«h
and knee; tenderness on palpation.
Labs CBC: leukocytosis. Elevated ESR. Gram stain and culture con-
firm diagnosis and isolate pathogen.
Imaging XR, plain: early findings include soft tissue edema and thin line
running parallel to diaphysis (periosteal thickening); later find-
ings include bone erosion, subperiosteal abscess with periostitis,
and sequestrum formation (due to detached necrotic cortical
bone): involucrum formation (laminated periosteal reaction).
MR: marrow edema; abscess. Indium-labeled WBC, scan: hot
spot.
Gross Pathology New osteoblastic periosteal bone formation (INVOLUCRUM);
trapping of detached necrotic bone by involucrum
(SEQUESTRUM); isolated localized abscess (Broihe's abscess);
sinus tract formation, draining pus to skin.
Micro Pathology
Purulent exudate formation, usually metaphyseal, with ischemic
necrosis of bone due to increased pressure of pus in rigid bone
walls; vascular thrombosis.
Treatment IV* antibiotics according to sensitivity; surgical debridement.
Discussion Osteomyelitis is an acute pyogenic bone infection which, if left
untreated, produces functional incapacity and deformities. The
most common pathogen is Staphylococcus aureus; less fre-
quently .SV rcptoaicats and enterobacteria are involved. In sickle
cell anemia Escherichia roli and Salmonella species are seen; diabet-
ics are at risk for Pseudomonas infection. Immunocompromised
patients may show Sporolhrix schenckii osteomvelitis: human bites,
anaerobes; puncture wounds. Pseudomtmas aeruginosa; and cat-
bile wounds. I'aslntri'lla inullocida.
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OSTEOMYELITIS
ID/CC A 21-year-old female college student complains of low-grade
fever along with pain and swelling in the left knee of 5 days'
duration.
HPI She had been to her family physician 2 weeks ago because of
dysuria and a purulent vaginal discharge (due to gonococcal
infection) and was given an "antibiotic shot". She was
asymptomatic until 4 days ago. She then developed fever, chills.
and pain in both wrists and in her left ankle, which disappeared
when the pain appeared in her left knee (migratory poly-
arthralgia) .
PE Swollen, tender, warm left knee with limited range of motion;
white vaginal discharge.
Labs Intracellular, bean-shaped gram-negadve diplococci
((.( i\( «.:()( ( ij and markedly elevated WBC count on urethra]
smear and synovial fluid aspirate culture of synovial aspirate
grows gonococci.
Imaging XR, knee: soft tissue swelling.
Treatment IV ceftriaxone.
Discussion .Almost always accompanied by synovitis and effusion, gonococ-
cal arthritis can rapidly destroy ardcular cartilage and is often as-
sociated with skin rash and C5, C6, C7, and C8 complement
deficiencies. Single joints are usually affected, most often the
wrists, fingers, knees, and ankles.
SEPTIC ARTHRITIS— GONOCOCCAL
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