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Practical Medical Microbiology for Clinicians E-Book

Frank E. Berkowitz

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Herausgeber: John Wiley & Sons
Kategorie: Wissenschaft und neue Technologien
Sprache: Englisch

Beschreibung

Infectious diseases constitute a major portion of illnesses worldwide, and microbiology is a main pillar of clinical infectious disease practice. Knowledge of viruses, bacteria, fungi, and parasites is integral to practice in clinical infectious disease.

Practical Medical Microbiology is an invaluable reference for medical microbiology instructors. Drs. Berkowitz and Jerris are experienced teachers in the fields of infectious diseases and microbiology respectively, and provide expert insight into microorganisms that affect patients, how organisms are related to each other, and how they are isolated and identified in the microbiology laboratory. The text also is designed to provide clinicians the knowledge they need to facilitate communication with the microbiologist in their laboratory.

The text takes a systematic approach to medical microbiology, describing taxonomy of human pathogens and consideration of organisms within specific taxonomic groups. The text tackles main clinical infections caused by different organisms, and supplements these descriptions with clinical case studies, in order to demonstrate the effects of various organisms.

Practical Medical Microbiology is an invaluable resource for students, teachers, and researchers studying clinical microbiology, medical microbiology, infectious diseases, and virology.

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Leseprobe

Cover

Title Page

Preface

Acknowledgments

SECTION I: Laboratory methods in clinical microbiology

CHAPTER 1: Introduction

Taxonomy

Purposes of the clinical microbiology laboratory

Principles of diagnostic testing

How do we know the true state (disease or no disease)?

Antimicrobial resistance

Further reading

CHAPTER 2: Microbiology laboratory methods

Reasons for making a microbial diagnosis

Basic methods used in microbiology

Bacteriologic methods

How precise should a microbiologic diagnosis be?

Virologic methods

Detecting and identifying fungi

Detecting and identifying parasites

Laboratory safety

Further reading

Resource

SECTION II: Prions and viruses

CHAPTER 3: Prions

Diagnosis

Further reading

CHAPTER 4: General virology

Properties of viruses

Taxonomy of viruses

Further reading

CHAPTER 5: DNA viruses (excluding hepatitis B virus)

Herpesviruses (Herpesviridae)

Adenoviruses (Adenoviridae)

Polyomaviruses (Polyomaviridae)

Papillomaviruses (Papillomaviridae)

Poxviruses (Poxviridae)

Parvoviruses (Parvoviridae)

Reference

Further reading

CHAPTER 6: RNA viruses (excluding hepatitis viruses, arthropod-borne viruses, and bat and rodent excreta viruses)

Picornaviruses (Picornaviridae)

Orthomyxoviruses (Orthomyxoviridae)

Paramyxoviruses (Paramyxoviridae)

Coronaviruses (Coronaviridae)

Reoviruses (Reoviridae) (Respiratory Enteric Orphan viruses)

Caliciviruses (Caliciviridae)

Astroviruses (Astroviridae)

Rhabdoviruses (Rhabdoviridae)

Togaviruses (Togaviridae)

Retroviruses (Retroviridae)

Further reading

CHAPTER 7: Hepatitis viruses

Hepatitis A virus (HAV)

Hepatitis B virus (HBV)

Hepatitis C virus (hepacivirus)

Hepatitis delta (D) virus

Hepatitis E virus

Further reading

CHAPTER 8: Arthropod-borne viruses (arboviruses), hantaviruses, arenaviruses, and filoviruses

Flaviviruses (Flaviviridae)

Togaviruses (Togaviridae)

Bunyaviruses (Bunyaviridae)

Reoviruses (Reoviridae)

Arenaviruses (Arenaviridae)

Filoviruses (Filoviridae)

Further reading

SECTION III: Bacteriology

CHAPTER 9: Bacteriology

Structure of bacteria

Genetic changes

Bacterial virulence factors

Mechanisms of resistance

Antibacterial agents

Further reading

CHAPTER 10: Gram-positive cocci

Staphylococci

Streptococci

Enterococci

Other Gram-positive cocci

Further reading

CHAPTER 11: Gram-negative cocci

Neisseria

Further reading

CHAPTER 12: Gram-positive rods

Sporogenous Gram-positive rods

Non-sporogenous Gram-positive rods

Other Gram-positive rods

Further reading

CHAPTER 13: Gram-negative rods

General features

Enterobacteriaceae

Non-Enterobacteriaceae Gram-negative rods from the environment

Non-Enterobacteriaceae Gram-negative rods from humans or animals

Further reading

CHAPTER 14: Anaerobic bacteria

General properties of anaerobes

Sporulating gram-positive rods

Non-sporulating Gram-positive rods

Gram-negative rods

Gram-positive cocci

Gram-negative cocci

Further reading

CHAPTER 15: Mycoplasmas, Chlamydiae, Rickettsiae, and Ehrlichiae

Mycoplasmas and Ureaplasma

Chlamydia and Chlamydophila

Rickettsiales

Coxiella burnetii

(see Chapter 13)

Further reading

CHAPTER 16: Spirochetes

Syphilis

Endemic treponematoses

Leptospirosis

Borrelia

Spirillum minus

Further reading

CHAPTER 17: Mycobacteria

Taxonomy

Tuberculosis

Non-tuberculous mycobacteria

Leprosy (Hansen’s disease)

Further reading

SECTION IV: Mycology

CHAPTER 18: Fungi

General properties of fungi

Laboratory perspectives for mycelial fungi

Detection of fungal components in body fluids

Further reading

CHAPTER 19: Yeasts

Candida

Cryptococcus

Malassezia

Other yeasts

Pneumocystis

Further reading

CHAPTER 20: Dimorphic endemic fungi

Histoplasma capsulatum

Blastomyces dermatitidis

Coccidioides

Paracoccidioides brasiliensis

Sporothrix schenkii

Penicillium marneffei

(penicilliosis)

Other dimorphic endemic fungi

Further reading

CHAPTER 21: Molds

Aspergillus

Mucorales

Fusarium

Scedosporium

Dermatophytes

Subcutaneous mycoses

Further reading

SECTION V: Parasitology

CHAPTER 22: Parasitology

General description of parasites

Life cycle

Diagnostic tests

Taxonomy of internal parasites

Antiparasitic drugs

Further reading

CHAPTER 23: Intestinal protozoa

Flagellates

Amebae

Ciliates

Apicomplexa (sporozoa)

Blastocystis hominis

Microsporidium

Diagnostic tests

Further reading

CHAPTER 24: Tissue and blood protozoa

Apicomplexa

Hemoflagellates

Tissue flagellate

Tissue amebae

Further reading

CHAPTER 25: Helminths

Introduction

Intestinal nematodes

Tissue nematodes

Flukes (Order: Trematoda)

Tapeworms (Order: Cestoda)

Further reading

CHAPTER 26: Ectoparasites

Flies

Fleas

Mites

Bed bugs

Lice

Further reading

SECTION VI: Clinical cases

CHAPTER 27: Cases

Case 1

Case 2

Case 3 (hypothetical)

Case 4

Case 5

Case 6

Case 7

Case 8 (hypothetical)

Case 9

Case 10

Case 11

Case 12

Case 13

Case 14

Case 15 (hypothetical)

Case 16

Case 17

Case 18

Case 19

Case 20

Case 21

Case 22

Case 23

Case 24 (hypothetical)

Case 25

Case 26

Case 27

Case 28 (hypothetical)

Case 29

Case 30

Case 31

Further reading

SECTION VII: Appendices

APPENDIX 1: Taxonomy of infectious agents infecting humans and lists of infectious agents according to their source

Human (close contact – other than sexual, droplet)

Human (sexual contact)

Human (endogenous bacteria)

Ingestion (human feces-contaminated food, water, or soil)

Ingestion (animal excreta-contaminated food, water, or soil)

Ingestion (uncooked animal tissue)

Animal (contact with animal, animal tissue, animal excreta, bite, scratch)

Fresh water (non-enteral exposure)

Sea water (enteral)

Sea water (non-enteral)

Inanimate environment, non-enteral (soil, air)

Inanimate (human fecal-contaminated)

Mother

Hospital

Blood

Tissue

Arthropod-transmitted infections

Acknowledgment

APPENDIX 2: Clinical syndromes and their causative organisms

APPENDIX 3: General references and online resources

General references

Specific references for Tables A2.7 and A2.10

Index

End User License Agreement

List of Tables

Chapter 01

Table 1.1 Structure of a table used to determine the diagnostic parameters and interpretation of diagnostic tests.

Chapter 02

Table 2.1 Specimen description: abscess. Site: flank; Gram stain: white blood cells; rare Gram-positive cocci in clusters Culture:

Staphylococcus aureus

Table 2.2 Specimen description: abscess. Site: thigh Gram stain: white blood cells; rare Gram-positive cocci in clusters Culture:

Staphylococcus aureus

PBP 2a detected; presumptive methicillin-resistant

Staphylococcus aureus

Table 2.3 Specimen description: blood. Culture: Streptococcus pneumoniae

Table 2.4 Specimen description: cerebrospinal fluid. Gram stain: white blood cells; Gram-positive cocci in pairsCulture: Streptococcus pneumoniae

Table 2.5 Specimen description: cerebrospinal fluid. Site: cerebrospinal fluid Gram stain: many white blood cells, moderate Gram-positive cocci in pairs Culture: Streptococcus pneumoniae

Table 2.6 Specimen: blood. Culture: Escherichia coli

Table 2.7 Specimen: blood. Culture: Escherichia coli

Table 2.8 Specimen: blood. Culture: Enterobacter cloacae

Table 2.9 Viral agents, common clinical syndromes, diagnostic tests, and specimen types. The tests for each virus are listed in Table 2.10.

Table 2.10 Tests used for detecting different viruses.

Chapter 05

Table 5.1 Infections caused by herpesviruses, diagnostic tests, and treatment.

Table 5.2 Serological responses to different EBV antigens and the timing of their presence.

Table 5.3 Development of anemia and then recovery in a child with sickle cell disease who developed an “aplastic crisis” caused by parvovirus B19.

Chapter 07

Table 7.1 Markers of hepatitis B infection.

Chapter 08

Table 8.1 Arthropod-borne viruses, listed by virus family, showing their geographic distributions, vectors, clinical syndromes they cause, and diagnostic methods.

Chapter 10

Table 10.1 Gram-positive cocci, their main characteristics, diseases they cause, and antimicrobial susceptibilities.

Chapter 11

Table 11.1 Key laboratory tests to differentiate the most common Gram-negative cocci.

Chapter 13

Table 13.1 Enterobacteriaceae most commonly encountered, according to tribe (sometimes used in their taxonomy), their usual sources, and the infections they cause.

Table 13.2 Enterobacteriaceae and their usual antimicrobial susceptibilities. With increasing antimicrobial resistance, there may be resistance to some of these drugs.

Table 13.3 Environmental Gram-negative rods, the clinical diseases they cause, and their usual antimicrobial susceptibilities.

Table 13.4 Gram-negative rods from humans or animals, their sources, diseases they cause, and their antimicrobial susceptibilities.

Chapter 15

Table 15.1 Chlamydiae and Chlamydophilas, and their main clinical syndromes.

Table 15.2 Rickettsial infections, their vectors, and distribution.

Table 15.3 Tick-borne diseases in America, their vectors, and distributions.

Chapter 16

Table 16.1 Spirochetes pathogenic in humans, modes of transmission, clinical syndromes, and diagnostic tests.

Chapter 17

Table 17.1 Antituberculous drugs and their major adverse effects.

Chapter 18

Table 18.1 Mechanisms of action of antifungal agents, and mechanisms of resistance to them.

Table 18.2 Commonly used mycology media.

Chapter 23

Table 23.1 Parallels between the life cycles of different apicomplexan parasites.

Table 23.2 Diagnostic tests used for intestinal protozoa.

Chapter 24

Table 24.1 Differences between the different species of plasmodium.

Table 24.2 Comparison of the hemoflagellates.

Chapter 25

Table 25.1 Treatment for individuals with platyhelminth infections.

Chapter 27

Table 27.1 Antibiotic susceptibilities of the

E. coli

isolate.

Table 27.2 Data for the PCR test and rapid test.

Table 27.3 How sensitivity, specificity, positive predictive value, and negative predictive value are calculated.

Table 27.4 Results of arbovirus testing.

Appendix 1

Table A1.1 Taxonomy of human pathogens, their usual sources, and the main clinical syndromes they cause.

Table A1.2 Arthropods as vectors of infectious agents.

Appendix 2

Table A2.1 Causative organisms of bloodstream infections according to the type of host.

Table A2.2 Respiratory tract infections and their causative organisms, including in special hosts.

Table A2.3 Eye infections and their causative organisms.

Table A2.4 Infections of the nervous system and their causative agents.

Table A2.5 Cardiovascular infections and their causes.

Table A2.6 Intraabdominal infections and their causative organisms.

Table A2.7 Infections of the gastrointestinal tract and their microbial causes.

Table A2.8 Urinary tract infections and their causes.

Table A2.9 Skeletal, skin, and soft tissue infections and their causative organisms.

Table A2.10 Genital tract and sexually transmitted infections and their causative organisms.

Table A2.11 Bites wounds: their causative organisms according to the inflicting animal.

†

Table A2.12 Viruses transmitted by rodent excreta (“rodex” viruses) and bat excreta (“batex” viruses), according to virus family, their geographic distributions, and animal sources.

Table A2.13 Bacterial infections for which serologic tests are used for diagnosis.

List of Illustrations

Chapter 01

Fig. 1.1 Decision thresholds.

Fig. 1.2 SNout for Sensitivity.

Fig. 1.3 SPin for specificity.

Fig. 1.4 A sensitive “net.”

Fig. 1.5 A specific “net.”

Fig. 1.6 The tension between sensitivity and specificity.

Fig. 1.7 How exposure to an antibiotic results in the resistant organisms becoming the dominant organisms and then the only organisms.

Chapter 02

Fig. 2.1 Gram-positive cocci in pus.

Fig. 2.2 Gram-negative rods in CSF.

Fig. 2.3 A blood smear stained with Wright’s stain showing diplococci. This was from a fatal case of

Streptococcus pneumoniae

sepsis.

Fig. 2.4 Gram stain of a smear of the same blood as in the previous figure, showing Gram-positive diplococci.

Fig. 2.5 Acridine orange preparation showing orange-staining bacteria, which are staphylococci.

Fig. 2.6 Petri dishes with blood agar (5% sheep blood) on the left and MacConkey agar on the right.

Fig. 2.7 A specimen being inoculated onto a blood agar plate.

Fig. 2.8 Various biochemical tests used to identify bacteria, in this case

Salmonella typhi.

Fig. 2.9 A microtiter well plate with biochemical tests used to identify Gram-positive organisms, and to test for their antimicrobial susceptibilities.

Fig. 2.10 The flow of bacterial isolation and identification.

Fig. 2.11 The flow of bacterial isolation and identification using blood culture.

Fig. 2.12 Broth being removed from a blood culture bottle, to be smeared on a slide for Gram stain, and to be inoculated onto agar plates.

Fig. 2.13 A simplified algorithm for bacterial identification.

Fig. 2.14 The essence of hybridization of a nucleic acid target with a specific complementary probe. When target molecules are present, hybridization occurs and in this assay light is emitted and detected.

Fig. 2.15 The polymerase chain reaction (PCR).

Fig. 2.16 A MALDI-TOF instrument.

Fig. 2.17 The MALDI-TOF process. (1) Colonies are mixed with the matrix chemical on a template. (2) The template is placed in the instrument, where it is subject to (3) a laser burst, resulting in “soft” ionization of proteins; (4) these ionized particles are drawn by a vacuum, flying at a speed determined by their size and charge (m/hz), towards the mass spectrometer, where (5) a spectral pattern is produced. (6) The pattern is compared with those in a database to provide an identification.

Fig. 2.18 Enzyme-linked immunosorbent assay (ELISA). A known antigen is attached to the surface of the microtiter well; the test serum (possibly containing antibodies) is added. During an incubation step, the antibody, if present, attaches to the antigen. After a wash, an antibody to human immunoglobulin, raised in a different animal, e.g. a goat, and to which an enzyme has been linked, is added, with a second incubation step and wash. Then a substrate to the enzyme is added. When acted upon by the enzyme, this produces a color, the intensity of which is measured by a spectrophotometer. The result is expressed as an optical density (OD).

Fig. 2.19 Tube dilution measurement of minimal inhibitory concentration (MIC). Bacterial growth is indicated in blue. In this case the MIC is 1 μg/mL.

Fig. 2.20 Demonstrating why “microbiologic resistance” (rising MICs) does not necessarily constitute “clinical resistance.” Bacterial growth is indicated in blue. If clinical resistance were defined by a minimal inhibitory concentration (MIC) greater than 1 μg/mL, then only the isolate in the third row would be considered resistant (MIC of 2 μg/mL), although the isolate in the second row (MIC of 0.5 μg/mL) is less susceptible than that in the first row (MIC of 0.125 μg/mL).

Fig. 2.21 A tube dilution MIC test on

Staphylococcus aureus

performed in a microtiter well plate. The top row is for daptomycin in which there is growth in the 0.5μg/mL well but not in the 1 μg/mL well. The MIC is therefore 1 μg/mL. The lower row is for vancomycin. There is growth in 0.25, 0.5, and 1 μg/mL wells, but not in the 2 μg/mL well. Therefore the MIC is 2 μg/mL.

Fig. 2.22 A tube dilution MIC test on

Pseudomonas aeruginosa

performed in a microtiter well plate. There is growth (green due to the production of pyocyanin) in all the wells containing Aug, which is Augmentin

(amoxicillin/clavulanic acid) and A/S, which is ampicillin/sulbactam, as expected for this organism, and no growth in the wells containing Cp (ciprofloxacin) and Lvx (levofloxacin). The MIC for ciprofloxacin is <= 1 μg/mL, and to levofloxacin is <= 2 μg/mL.

Fig. 2.23 Kirby–Bauer test using

Pseudomonas aeruginosa

as the test organism. Note the zones of inhibition around the disks.

Fig. 2.24 An E-test.

Fig. 2.25 The color change caused by β-lactamase acting on nitrocefin. The right disk is a negative control, and the left disk is a positive.

Fig. 2.26 A fibroblast monolayer with cytopathic changes (“rounding up” of cells) caused by herpes simplex virus. Courtesy of PHIL, CDC.

Fig. 2.27 Principle of immunofluorescence tests for antigen detection.

Fig. 2.28 Immunofluorescence for herpes simplex virus.

Fig. 2.29 Tissue from mouth biopsy of an immunocompromised boy with herpes zoster. Note the eosinophilic intranuclear inclusions. This is not easily appreciated.

Fig. 2.30 The same tissue as shown in Figure 2.29 showing the positive immunoperoxidase staining for varicella zoster virus.

Chapter 05

Fig. 5.1 Cutaneous herpes simplex infection in a newborn infant.

Fig. 5.2 A normal child with varicella. Note different staged lesions.

Fig. 5.3 Zoster in a teenage boy.

Fig. 5.4 Tzanck preparation, showing a multinucleate giant cell, which can occur with herpes simplex and varicella zoster virus infections.

Fig. 5.5 Cytomegalovirus infection of the lung in a patient with AIDS, showing a large cell with an intranuclear inclusion.

Fig. 5.6 African child with Burkitt lymphoma.

Fig. 5.7 Large “atypical lymphocyte” called Downy type II cells, in a teenage boy with infectious mononucleosis.

Fig. 5.8 Anal warts (condylomata acuminata).

Fig. 5.9 Electron micrograph of smallpox virus.

Fig. 5.10 A child with smallpox.

Fig. 5.11 The typical reaction to vaccination with vaccinia virus.

Fig. 5.12 Patient with monkeypox during an outbreak in the Democratic Republic of the Congo in 1996.

Fig. 5.13 Child with molluscum contagiosum.

Fig. 5.14 Young girl with erythema infectiosum, showing the characteristic lacy rash.

Fig. 5.15 Liver tissue of a newborn dying of hydrops fetalis caused by parvovirus B19 infection. Note the intranuclear inclusions caused by the virus.

Chapter 06

Fig. 6.1 Child with weakness due to polio.

Fig. 6.2 Rash of a child with hand-foot – mouth disease, occurring during a community outbreak of Coxsackie A 6 infection.

Fig. 6.3 Electron micrograph of an influenza virus.

Fig. 6.4 Model of influenza virus. The dark blue structures represent neuraminidase and the light blue ones represent hemagglutinin.

Fig. 6.5 Immunofluorescence microscopy showing respiratory syncytial virus-infected cells.

Fig. 6.6 Mumps virus: electron microscopy, negative staining.

Fig. 6.7 Measles virus.

Fig. 6.8 Child with measles, showing the conjunctivitis and miserable appearance.

Fig. 6.9 A child with measles.

Fig. 6.10 Diagram showing how Nipah virus spreads from flying foxes to humans.

Fig. 6.11 Flying fox (Courtesy of PHIL/CDC).

Fig. 6.12 Electron micrograph showing rotavirus.

Fig. 6.13 Electron micrograph of noroviruses.

Fig. 6.14 A man with rabies.

Fig. 6.15 Negri bodies (cytoplasmic inclusions) in neuron of a rabies victim.

Fig. 6.16 Congenital cataracts due to the congenital rubella syndrome.

Fig. 6.17 Newborn infant with congenital rubella infection, showing the “blueberry muffin” skin lesions, due to extramedullary erythropoiesis.

Fig. 6.18 Electron micrograph of HIV.

Fig. 6.19 Oral candidiasis (note white patches on inner aspects of the lips and on the palate) in a teenage boy with HIV infection.

Fig. 6.20 Kaposi sarcoma.

Fig. 6.21 Electron micrograph of HTLV and HIV.

Chapter 07

Fig. 7.1 Geographic distribution of hepatitis B .

Chapter 08

Fig. 8.1 Distribution of yellow fever in Africa.

Fig. 8.2 Distribution of yellow fever in South America.

Fig. 8.3

Aedes aegypti

Fig. 8.4 Liver histology in yellow fever. Note the eosinophilic “Councilman” bodies.

Fig. 8.5 Distribution of dengue in the Western hemisphere.

Fig. 8.6A Distribution of dengue in Asia and Oceania.

Fig. 8.6B Distribution of dengue in Africa.

Fig. 8.7 The rash occurring in dengue.

Fig. 8.8 The distribution of Japanese B encephalitis.

Fig. 8.9 Distribution of tick-borne encephalitis.

Fig. 8.10 Radiologic appearance of the lungs in a patient with hantavirus pulmonary syndrome.

Fig. 8.11 Appearance of the lung in hantavirus pulmonary syndrome. Note the intraalveolar fluid.

Fig. 8.12

Peromyscus maniculatus

Fig. 8.13 Ebola virus.

Chapter 09

Fig. 9.1 Structure of a bacterial cell.

Fig. 9.2 Basic structure of Gram-positive and Gram-negative cell walls.

Fig. 9.3 Sites of action of different classes of antibacterial agents. DNA, deoxyribose nucleic acid; RNA, ribose nucleic acid; 30S, 30S ribosomal subunit; 50S, 50S ribosomal subunit.

Fig. 9.4 The basic structure of penicillins.

Fig. 9.5 The basic structure of cephalosporins.

Fig. 9.6 The mechanisms of action of folate synthesis antagonists.

Chapter 10

Fig. 10.1 Gram-positive cocci in chains, in this case

Streptococcus pyogenes

Fig. 10.2 Diagram showing how Gram-positive cocci are differentiated.

Fig. 10.3 A positive catalase test (bubbles) on the left (staphylococcus), and a negative test (no bubbles) on the right (streptococcus).

Fig. 10.4 A slide coagulase test to differentiate coagulase-positive

Staphylococcus aureus

(

left-hand panel

) from coagulase-negative staphylococci (

right-hand panel

Fig. 10.5 A child with impetigo caused by

Staphylococcus aureus

Fig. 10.6 Child with left distal femoral osteomyelitis caused by

Staphylococcus aureus.

Fig. 10.7 Child with infective endocarditis caused by

Staphylococcus aureus

. Note the embolic lesions on the sole.

Fig. 10.8 Radiograph of a child with pneumonia and pleural effusion caused by

Staphylococcus aureus

, complicating influenza.

Fig. 10.9 Newborn infant with staphylococcal scalded skin syndrome.

Fig. 10.10 Infant with thigh infection.

Fig. 10.11 Gram stain showing Gram-positive cocci in clusters.

Fig. 10.12 Culture showing golden (aureate) colonies produced by

Staphylococcus aureus

Fig. 10.13 The “D” test. In each plate the erythromycin disk is on the left, and the clindamycin disk is on the right. The plate on the left shows both erythromycin and clindamycin susceptibility (large zones of inhibition); the plate on the right shows erythromycin resistance (no zone of inhibition), and inducible clindamycin resistance (a flatter zone of inhibition on the side of the clindamycin disk closer to the erythromycin disk).

Fig. 10.14 β-Hemolysis (complete); note the zone of inhibition around the A disk, which is bacitracin, which identifies this isolate as

Streptococcus pyogenes

Fig. 10.15 Agglutination with Group A antiserum.

Fig. 10.16 Sites of infection caused by

Streptococcus pyogenes

Fig. 10.17 A rapid

Streptococcus pyogenes

antigen detection test. The blue line indicates a positive test and the red line is the negative control.

Fig. 10.18 Patient showing submandibular cellulitis.

Fig. 10.19 A Gram-stained smear of cerebrospinal fluid of a 4-month-old infant, showing many leukocytes and Gram-positive cocci in pairs and chains, which were

Streptococcus agalactiae.

Fig. 10.20 Colonies of

Streptococcus agalactiae

on blood agar. Note the small zone of β-hemolysis.

Fig. 10.21 Diagram showing how α-hemolytic streptococci are differentiated.

Fig. 10.22 α-Hemolytic streptococci, with a zone of inhibition around the optochin disk (optochin susceptibility), indicating that this is

Streptococcus pneumoniae.

Fig. 10.23 Gram stain of cerebrospinal fluid, showing Gram-positive cocci in pairs (

Streptococcus pneumoniae

Fig. 10.24 α-Hemolytic colonies, showing central umbilication (

Streptococcus pneumoniae

Fig. 10.25 Enterococci growing on blood agar. Note the absence of hemolysis.

Fig. 10.26 The pyrrolidonyl arylamidase (PYR) test for identifying enterococci. The disk on the left is negative, and that on the right is positive.

Fig. 10.27 CT scan showing an epidural abscess in the right frontal area.

Fig. 10.28 Pus and many Gram-positive cocci in chains.

Chapter 11

Fig. 11.1 Child with meningococcemia, showing a hemorrhagic rash.

Fig. 11.2 Child with meningococcal meningitis showing a macular rash.

Fig. 11.3 Child with meningococcemia and vascular occlusion affecting the left upper limb. (These affected the right upper limb and both lower limbs as well.)

Fig. 11.4 Autopsy specimen of a child dying of meningococcemia, showing adrenal hemorrhage (Waterhouse–Friderichsen syndrome).

Fig. 11.5 Child with meningococcal meningitis, showing a subconjuctival petechia.

Fig. 11.6 Gram stain of cerebrospinal fluid showing leukocytes containing

Neisseria meningitidis

Fig. 11.7 Gram stain of a skin aspirate, showing Gram-negative cocci (

Neisseria meningitidis

Fig. 11.8 Eye of a newborn infant showing severe conjunctivitis caused by

Neisseria gonorrhoeae

Fig. 11.9 Gram-stained smear from the eye of the patient in Fig. 11.8. It shows characteristic Gram-negative cocci, both inside and outside leukocytes.

Chapter 12

Fig. 12.1 Cutaneous anthrax.

Fig. 12.2

Bacillus anthracis

on Gram stain. Spores can be seen.

Fig. 12.3

Bacillus anthracis

growing on blood agar.

Fig. 12.4

Bacillus cereus colonies

growing on blood agar showing hemolysis.

Fig. 12.5A Gram stain of cerebrospinal fluid of a patient with Listeria monocytogenes meningitis, showing numerous leukocytes, and Gram-positive rods. Courtesy of Marylyn Addo M.D. Ph.D., Division of Infectious Diseases, Massachusetts General Hospital and Harvard Medical School, and Judith Holden, MT (ASCP) MPH, Micropathology Laboratory, Massachusetts General Hospital, Boston, MA. This image was first published on Partners’ Infectious Disease Images web site, whose content is copyrighted by Partners Healthcare System, Inc., and is used with permission. All rights reserved.

Fig. 12.5B Gram stain of

Listeria monocytogenes

growing in blood culture. Courtesy of Eileen Burd, PhD, D(ABMM),Director, Clinical Microbiology, Emory University Hospital.

Fig. 12.6

Corynebacterium diphtheriae

growing on agar containing tellurite.

Fig. 12.7

Corynebacterium diphtheriae

showing bipolar enhancement of staining.

Fig. 12.8 Inflammation and branching rods of Actinomyces.

Fig. 12.9

Nocardia

spp. in lung tissue, stained with the Kinyoun stain.

Fig. 12.10 “Clue cells.”

Chapter 13

Fig. 13.1 Pink colonies of

E. coli

on MacConkey agar due to lactose fermentation.

Fig. 13.2 Oxidase test. The panel on the left shows a positive test (

Pseudomonas aeruginosa

), and that on the right is a negative test (

E. coli

Fig. 13.3 A negative Hodge test (left disk is ertapenem, right disk is meropenem). Note that there is no growth close to the disk. Compare this with Fig. 13.4.

Fig. 13.4 A positive Hodge test (left disk is ertapenem, right disk is meropenem). Note growth up to the disk. Compare this with Fig. 13.3.

Fig. 13.5

Proteus mirabilis

swarming on agar.

Fig. 13.6 Reported cases of plague in the USA, 1970–2012.

Fig. 13.7 Patient with septicemic plague, showing peripheral gangrene.

Fig. 13.8 Blood smear of patient with septicemic plague, showing Gram-negative rods with bipolar staining, characteristic of

Yersinia pestis.

Fig. 13.9 Agar plate showing the blue pigment (pyocyanin) produced by

P. aeruginosa.

Fig. 13.10 Agar plate showing red pigment (pyorubrin) produced by

P. aeruginosa.

Fig. 13.11 A 6-day-old culture of

Legionella pneumophila

on charcoal-yeast extract agar.

Fig. 13.12 Indirect fluorescent antibody stain showing

Legionella pneumophila

in sputum.

Fig. 13.13

Chromobacterium violaceum

on blood agar.

Fig. 13.14

Chromobacterium violaceum

on MacConkey agar.

Fig. 13.15 Colonies of

Vibrio cholerae

on thiosulfate-citrate-bile salt (TCBS) agar. The left-hand plate has not been inoculated.

Fig. 13.16

Haemophilus influenzae

in cerebrospinal fluid (note small Gram-negative coccobacilli).

Fig. 13.17 Inguinal lymphadenopathy due to

Haemophilus ducreyi.

Fig. 13.18 Distribution of reported cases of tularemia within the USA from 2001 to 2010.

Fig. 13.19 Inoculation site in a case of cat-scratch disease.

Fig. 13.20 The rash of the patient with rat-bite fever in Fig. 13.19.

Fig. 13.21 A pustule on the patient with rat-bite fever in Fig. 13.19.

Fig. 13.22 Gram stain of colonies from culture of material from the pustule in Fig. 13.21, showing chains of Gram-negative rods, which were identified as

Streptobacillus moniliformis

Chapter 14

Fig. 14.1 Gram stain of peritoneal fluid from a child with peritonitis complicating a perforated appendix. Note the large Gram-negative rods, small Gram-negative coccobacilli, and Gram-positive cocci in pairs.

Fig. 14.2 A 5-day-old infant with tetanus, showing clenching of the fist and grimacing.

Fig. 14.3 Opisthotonus due to tetanus.

Fig. 14.4 Micrograph showing

Clostridium tetani

with terminal spores.

Fig. 14.5 An infant with marked hypotonia, due to botulism.

Fig. 14.6 Gram stain of

Clostridium botulinum

. Note the spores.

Fig. 14.7 Gram-positive rod in an aspirate from a bulla in a child with gas gangrene. This was identified as

Clostridium septicum

Fig. 14.8 The cytotoxic effect of

C. difficile

toxin in tissue culture.

Fig. 14.9 CT scan showing thickened loops of large bowel.

Fig. 14.10 The pieces of bamboo removed from the child’s nasal bridge.

Fig. 14.11 Gram stain of colonies of

Clostridium perfringens

cultured from the wound. Note the Gram-variable rods, some with subterminal spores.

Fig. 14.12

Propionibacterium granulosum

cultured from a brain abscess.

Fig. 14.13 CT scan showing a large intra-abdominal abscess.

Fig. 14.14 Gram stain of

Veillonella parvula

, cultured from an infant’s blood.

Chapter 15

Fig. 15.1 Chest X-ray of a teenage girl with

Mycoplasma pneumoniae

pneumonia.

Fig. 15.2 Life cycle of chlamydiae.

Fig. 15.3 Chlamydial cervicitis.

Fig. 15.4 Pathogenesis of intrapartum chlamydial infection. Red indicates area of chlamydial infection. 1. Cervical infection; 2. cervical infection, with fetus

in utero

; 3. infant passing through chlamydia-infected birth canal; 4. routes of spread of chlamydia in newborn infant.

Fig. 15.5 Chest X-ray of a young infant with

Chlamydia trachomatis

pneumonia. Note the bilateral patchy infiltrates.

Fig. 15.6

Chlamydia trachomatis

growing in tissue culture in McCoy cells, demonstrating inclusions stained with iodine.

Fig. 15.7 Rash in an individual with epidemic typhus.

Fig. 15.10 Rash in a boy with ehrlichiosis.

Fig. 15.11 Morulae in a mononuclear cell of the boy shown in Fig. 15.10.

Chapter 16

Fig. 16.1

Treponema pallidum

, the cause of syphilis.

Fig. 16.2 Chancre due to primary syphilis.

Fig. 16.3 Rash caused by secondary syphilis.

Fig. 16.4 Infant with snuffles due to congenital syphilis.

Fig. 16.5 Peeling of the soles in congenital syphilis.

Fig. 16.6 Pitting edema due to the nephrotic syndrome caused by congenital syphilis.

Fig. 16.7 Lower limb X-rays of a newborn infant showing periostitis due to congenital syphilis. Note the lucencies at the proximal ends of the tibias and the periosteal thickening of the femurs.

Fig. 16.8 Pneumonia alba caused by congenital syphilis.

Fig. 16.9 Hutchinson teeth due to congenital syphilis.

Fig. 16.10 Clutton’s joints due to congenital syphilis.

Fig. 16.11 Traditional and reverse sequence algorithms for syphilis testing. CIE, chemiluminescence immunoassay; EIA, enzyme immunoassay; RPR, rapid plasma reagin test.

Fig. 16.12 Histology showing spirochetes (

Treponema pallidum

) stained with a silver stain.

Fig. 16.13 Liver smear of a fatal case of leptospirosis stained with a silver impregnation stain and showing leptospira organisms.

Fig. 16.14 Patient with erythema migrans.

Fig. 16.15 Giemsa-stained blood smear showing

Borrelia hermsii

Chapter 17

Fig. 17.1 World map showing the global distribution of tuberculosis, according to incidence (cases per 100,000 population) as of 2012.

Fig. 17.2 Chest X-ray showing hilar lymphadenopathy due to tuberculosis in a young child.

Fig. 17.3 Chest X-ray showing left upper lobe pulmonary infiltrate with a cavity.

Fig. 17.4 Chest X-ray showing a tuberculous pleural effusion in a teenage boy.

Fig. 17.5 Acid-fast bacilli within a macrophage in a pleural biopsy of the patient shown in Fig. 17.4.

Fig. 17.6 Ziehl–Neelsen showing an acid-fast bacterium.

Fig. 17.7 An acid-fast bacillus stained with aureamine, appearing yellow.

Fig. 17.8 Colonies of

Mycobacterium tuberculosis

growing on a solid medium.

Fig. 17.9 A reactive tuberculin skin test (PPD).

Fig. 17.10 Colonies of a rapidly growing mycobacterium on chocolate agar.

Fig. 17.11 Hand deformity resulting from leprosy.

Fig. 17.12 Hypopigmented skin lesion of leprosy.

Fig. 17.13 Tissue specimen stained with an acid-fast stain showing

Mycobacterium leprae.

Chapter 18

Fig. 18.1 Steps in the synthesis of ergosterol.

Fig. 18.2

Aspergillus

spp. stained with Calcofluor white.

Fig. 18.3 Silver impregnation stain of sinus tissue, showing mold (

Bipolaris

spp.).

Fig. 18.4 Culture of

Trichophyton mentagrophytes

, showing the front side of the petri dish.

Fig. 18.5 Culture of

Trichophyton mentagrophytes

, showing the reverse side of the petri dish.

Fig. 18.6 Lactophenol cotton blue preparation showing conidia of

Bipolaris

spp.

Chapter 19

Fig. 19.1 Pseudohyphae of

Candida albic

ans in pus from a perivenous abscess caused by an intravenous catheter (see Fig. 19.3).

Fig. 19.2 Oral candidiasis (thrush) in a normal newborn infant.

Fig. 19.3 Perivenous abscess at an intravascular catheter site, caused by

Candida albicans

. The Gram stain of an aspirate is shown in Fig. 19.1.

Fig. 19.4 Gram stain of a buffy coat preparation obtained from a central venous catheter, showing budding yeasts, which were

Candida tropicalis

Fig. 19.5 “Foot processes” on colonies of

Candida albicans

Fig. 19.6 Germ tube production by

Candida albicans.

Fig. 19.7 Characteristic blue colonies of

Candida tropicalis

on CHROMagar

Fig. 19.8 Gram stain of cerebrospinal fluid showing

Cryptococcus neoformans.

Note budding.

Fig. 19.9 India ink preparation of cerebrospinal fluid, showing

Cryptococcus neoformans

with a large capsule.

Fig. 19.10

Cryptococcus neoformans

growing on agar.

Fig. 19.11 A teenager with pitryriasis versicolor due to

Malassezia

spp.

Fig. 19.12

Malassezia furfur

, showing yeast and hyphal forms (“spaghetti and meatballs”).

Fig. 19.13 The cysts of

Pneumocystis jiroveci

, in lung tissue from a child with AIDS, stained with Gomorri silver impregnation stain.

Fig. 19.14 The histologic appearance of the lung, stained with hematoxylin and eosin, caused by

Pneumocystis jiroveci

in a child with AIDS.

Chapter 20

Fig. 20.1 Distribution of cases of histoplasmosis in individuals >65 years in the USA, 1999–2008. Numbers are cases per 100,000.

Fig. 20.2 Chest radiograph of a patient with acute pulmonary histoplasmosis.

Fig. 20.3

Histoplasma capsulatum

in a histiocyte.

Fig. 20.4 Distribution of cases of blastomycosis in individuals >65 years old in the USA. Numbers are cases per100,000.

Fig. 20.5 Chest radiograph of a patient with blastomycosis.

Fig. 20.6 Silver-stained section showing a budding yeast form of

Blastomyces dermatitidis

Fig. 20.7 Distribution of coccidioidomycosis in individuals >65 years old in USA. Numbers are cases per 100,000.

Fig. 20.8 Arthroconidia, the infectious form of Coccidioides.

Fig. 20.9 Spherule of

Coccidioides immitis

, containing endospores.

Fig. 20.10 Face of a Brazilian child with

Paracoccidioides brasiliensis

infection.

Fig. 20.11 Budding yeast of

Paracoccidioides brasiliensis

in tissue.

Fig. 20.12 Conidiophores with conidia of

Sporothrix schenkii

cultured from peat moss.

Fig. 20.13 Cutaneous infection caused by

Sporothrix schenkii

Fig. 20.14 Yeast form of

Sporothrix schenkii

in culture.

Fig. 20.15

Penicillium marneffei

in human spleen, stained with Gomori methenamine silver stain.

Fig. 20.16 Culture of

Penicillium marneffei

Fig. 20.17 Conidiophores laden with conidia of

Penicillium marneffei

Chapter 21

Fig. 21.1 Aspergillus in lung tissue stained with Gomori silver impregnation stain.

Fig. 21.2 Aspergillus cultured from a lung biopsy and stained with Calcofluor white.

Fig. 21.3 Aspergillus hypha, cultured from a lung biopsy, and stained with lactophenol cotton blue. The preparation was made by applying tape to the mycelia of a culture. The round structures at the tips of the “aspergillum” are the conidia.

Fig. 21.4

Mucor

spp. showing wide angle branching and absence of septa.

Fig. 21.5 Sporangium of Mucor.

Fig. 21.6 Patient with mucormycosis affecting the paranasal sinus and orbit.

Fig. 21.7 Skin lesion (ecthyma gangrenosum) caused by

Mucor

spp. in a child with AIDS.

Fig. 21.8 Fusarium in a skin biopsy of the patient shown in Fig. 21.10. Although visible in this hematoxylin and eosin-stained section, the fungi are difficult to see well. Compare this with Fig. 21.9.

Fig. 21.9 The same biopsy material as shown in Fig. 21.8, but stained with Gomori–Grocott silver impregnation stain. Note how easily the fungi can be seen.

Fig. 21.10 Two-year-old girl with relapsed acute myeloid leukemia and neutropenia, illustrating skin lesions due to disseminated fusarium infection.

Fig. 21.11 Child with tinea capitis.

Fig. 21.12 Child with kerion, a hypersensitivity reaction to tinea capitis.

Fig. 21.13 Child with tinea corporis.

Fig. 21.14

Trichphyton tonsurans

hyphae and microconidia.

Fig. 21.15 Apiculate terminal chlamydospores of

Microsporum audouini

Fig. 21.16 Chromoblastomycosis caused by

Phialophora verrucosa

Fig. 21.17

Phialophora verrucosa

in culture.

Fig. 21.18 Histology of “black grain” eumycetoma due to

Madurella mycetomatis

, stained with Gridley stain.

Fig. 21.19 Histology of phaeohyphomycosis due to

Wangiella dermatitidis

, stained with PAS.

Fig. 21.20 Appearance of

Exophiala jeanselmei

in culture.

Fig. 21.21 Brazilian man with lobomycosis.

Fig. 21.22 Appearance of

Lacazia loboi

in tissue stained with Gomori silver impregnation stain.

Chapter 22

Fig. 22.1 Simple taxonomy of parasites.

Chapter 23

Fig. 23.1

Giardia intestinalis

trophozoite.

Fig. 23.2

Giardia intestinalis

cyst.

Fig. 23.3 Amebic ulcer. Note the undermining of the mucosa.

Fig. 23.4 Pathogenesis of amebiasis.

Fig. 23.5

E. histolytica

in a fresh stool specimen, examined by phase contrast microscopy, showing numerous ingested erythrocytes.

Fig. 23.6 Cyst of

E. histolytica

, stained with iodine.

Fig. 23.7

Balantidium coli

in colonic epithelium.

Fig. 23.8 Trophozoite of

Balantidium coli

in stool. Note the cilia on the outside.

Fig. 23.9 Wet preparation of stool showing cryptosporidium oocysts containing sporozoites.

Fig. 23.10 Cryptosporidium oocysts stained with a modified acid-fast stain.

Fig. 23.11 Cryptosporidium oocysts stained with auramine-rhodamine fluorescent stain.

Fig. 23.12 Autofluorescence of

Cyclospora cayetanensis

under ultraviolet light.

Fig. 23.13 Oocysts of

Cyclospora cayetanensis

stained with safranin.

Fig. 23.14

Cystoisospora belli

oocyst fluorescing under UV light.

Fig. 23.15

Cystoisospora belli

oocyst stained with an acid-fast stain.

Fig. 23.16

Blastocystis

spp. in stool, stained with trichrome stain.

Fig. 23.17 Polar tube of a microsporidium inserted into a host cell.

Fig. 23.18 Microsporidium stained with Chromotrope 2R.

Chapter 24

Fig. 24.1A Distribution of malaria in the Western Hemisphere.

Fig. 24.1B Distribution of malaria in the Eastern Hemisphere.

Fig. 24.2 Life cycle of Plasmodium.

Fig. 24.3 Thin blood smear with many ring forms of

Plasmodium falciparum.

This is a very high-grade parasitemia.

Fig. 24.4 Thick blood smear with multiple ring forms of

Plasmodium falciparum

. Note the difference in overall appearance from the thin smear.

Fig. 24.5 Thin blood smear showing a gametocyte of

Plasmodium falciparum

Fig. 24.6 Blood smear with a platelet lying on an erythrocyte, which could be mistaken for a malarial parasite by an inexperienced microscopist.

Fig. 24.7 Life cycle of

Babesia

spp.

Fig. 24.8 Blood smear showing

Babesia

spp.

Fig. 24.9 Blood smear showing tetrad forms of

Babesia

spp.

Fig. 24.10 Blood smear showing vacuolation in

Babesia

spp. parasites.

Fig. 24.11 Life cycle of

Toxoplasma gondii

Fig. 24.12 Tachyzoites of

Toxoplasma gondii

Fig. 24.13 Bradyzoites of

Toxoplasma gondii

inside a pseudocyst in cardiac muscle.

Fig. 24.14 Brain CT scan of an infant with congenital toxoplasmosis, showing hydrocephalus, and diffuse parenchymal calcification.

Fig. 24.15 Child whose CT scan is shown in Fig. 24.14, showing retinitis affecting the posterior pole of the eye.

Fig. 24.16 Life cycle of

Trypanosoma brucei.

Fig. 24.17 Giemsa-stained thin blood smear showing trypomastigotes of

Trypansoma brucei

Fig. 24.18 Life cycle of

Trypanosoma cruzi.

Fig. 24.19 Trypomastigote of

T. cruzi

in a Giemsa-stained blood smear.

Fig. 24.20

Phlebotomus papatasi

Fig. 24.21 Worldwide distribution of cutaneous leishmaniasis. With permission from the World Health Organization.

Fig. 24.22 Worldwide distribution of visceral leishmaniasis. With permission from the World Health Organization.

Fig. 24.23 Life cycle of

Leishmania

spp.

Fig. 24.24 Individual with cutaneous leishmaniasis.

Fig. 24.25 individual with mucocutaneous leishmaniasis causing destruction of the nasal septum and consequent nasal deformity.

Fig. 24.26 Bone marrow smear showing Leishmania amastigotes inside macrophages. The kinetoplasts are the small dots adjacent to the nucleus.

Fig. 24.27

Trichomonas vaginalis

trophozoite.

Fig. 24.28

Acanthmoeba polyphaga

viewed by scanning electron microscopy.

Fig. 24.29 Corneal scraping showing

Acanthamoeba polyphaga.

Fig. 24.30 Brain showing the damage caused by

Balamuthia mandrillaris.

Fig. 24.31

Naegleria fowleri

in brain tissue.

Chapter 25

Fig. 25.1 Eggs

of Enterobius vermicularis

obtained by tape.

Fig. 25.2 Eggs of

Enterobius vermicularis

Fig. 25.3 Adult

Trichuris trichiura.

Fig. 25.4 Egg of

Trichuris trichiura

in feces. Note the opercula at both ends.

Fig. 25.5 Life cycle of

Ascaris lumbricoides

. 1. Eggs are ingested in soil; 2. The eggs hatch in the intestine; 3. The larvae penetrate the intestine and enter the mesenteric venous system; 4. The larvae pass through the right side of heart and into the lung; 5. The larvae pass from the pulmonary capillary into the alveolus; 6. The larvae ascend the respiratory tree and are swallowed; 7. The larvae reenter the intestine; 8. The larvae mature into adults; 9. The female lays eggs, which are passed out in feces; 10. The eggs mature in soil, in which they are ingested, completing the cycle.

Fig. 25.6 Adult

Ascaris lumbricoides

worm.

Fig. 25.7

Ascaris lumbricoides

egg showing an embryo within.

Fig. 25.8

Toxocara

in liver tissue.

Fig. 25.9

Baylisascaris procyonis

in brain tissue.

Fig. 25.10 Head of adult

Ancylostoma duodenale

, showing teeth.

Fig. 25.11 Egg of hookworm in stool (wet preparation).

Fig. 25.13

Strongyloides stercoralis

rhabditiform larva in stool. The red arrow shows the genital primordium.

Fig. 25.14 Life cycle of

Wuchereria bancrofti

Fig. 25.15 Individual with elephantiasis due to lymphatic filariasis.

Fig. 25.16 Thick blood smear showing microfilaria of

W. bancrofti

Fig. 25.17 Life cycle of

Onchocerca volvulus

Fig. 25.18 Histological section of a nodule showing multiple sections of worms (

Onchocerca volvulus

Fig. 25.19 Female Guinea worm being extracted from a patient’s limb.

Fig. 25.20 Life cycle of

Trichinella spiralis

Fig. 25.21

Trichinella spiralis

in human muscle.

Fig. 25.22 Head of

Gnathostoma spinegerum.

Fig. 25.23 Patterns of life cycles of flukes.

Fig. 25.24

Fasciola hepatica

from a bile duct.

Fig. 25.25 Operculated egg of

Fasciola hepatica

Fig. 25.26

Clonorchis sinensis

, showing its size.

Fig. 25.27 Egg of

Paragominus westermani

Fig. 25.28 World distribution of schistosomiasis. CDC, Yellow Book, 2014.

Fig. 25.29 Life cycle of

Schistosoma

spp. S. m,

Schistosoma mansoni

; S. h,

Schistosoma haematobium

; S. j,

Schistosoma japonicum

Fig. 25.30 Cercaria of

S. mansoni

Fig. 25.31 Female within the gynecophoric canal of the male.

Fig. 25.32 Intense inflammation around eggs in the bladder, caused by

S. haematobium

Fig. 25.33 Egg of

S. mansoni

; note the lateral spine.

Fig. 25.34 Egg of

S. haematobium

; note the terminal spine.

Fig. 25.35 Basic life cycle of cestodes.

Fig. 25.36 Life cycle of

Taenia solium

Fig. 25.38 Life cycle of

Echinococcus granulosus

Chapter 26

Fig. 26.1 Dermatobia larvae removed from the skin.

Fig. 26.2 Skin lesion caused by

Tunga penetrans

Fig. 26.3 Hand of an 8-year-old boy with scabies.

Fig. 26.4

Sarcoptes scabiei

in a skin scraping.

Fig. 26.5

Cimex lenticularius

Fig. 26.6 Skin lesion produced by a bed bug bite.

Fig. 26.7

Pediculus humanus capitis,

the human head louse.

Fig. 26.8

Pediculus humanus corporis,

the human body louse.

Fig. 26.9

Phthirus pubis

, the pubic louse.

Chapter 27

Fig. 27.1 Skin lesions in a febrile, neutropenic boy.

Fig. 27.2 Gram-stained smear from an aspirate of one of the skin lesions.

Fig. 27.3 Giemsa-stained thin blood smear.

Fig. 27.4 Giemsa-stained thin blood smear.

Fig. 27.5 Gram-stained smear of pus.

Fig. 27.6 Culture of the pus on blood agar.

Fig. 27.7 CT scan showing basilar skull fractures.

Fig. 27.8 Gram stain of CSF, showing small, pleomorphic Gram-negative rods.

Fig. 27.9 Rash on the child’s arm.

Fig. 27.10 Rash on the child’s trunk.

Fig. 27.11 Chest X-ray showing right upper lobe consolidation with cavitation.

Fig. 27.12 Gram stain of the CSF.

Fig. 27.13 Fecal smear, stained with methylene blue, demonstrating large numbers of leukocytes.

Fig. 27.14 Gram-stained smear of joint fluid.

Fig. 27.15 Skin lesions.

Fig. 27.16 Skin lesions on the infant’s foot.

Fig. 27.17 Rash on mother’s wrist.

Fig. 27.18 Chest X-ray.

Fig. 27.19 Large lymph node.

Fig. 27.20 Results of the tuberculin skin test.

Fig. 27.21 CT scan showing a large left parietal lobe abscess.

Fig. 27.22 Gram stain of the pus from the abscess.

Fig. 27.23 Chocolate agar showing pink/red colonies.

Fig. 27.24 Colonies growing on the blood and chocolate agar plates (

foreground

), but not on the MacConkey plate (

upper right

Fig. 27.25 Colonies on blood agar.

Fig. 27.26 Small Gram-negative coccobacilli.

Fig. 27.27 A positive oxidase test (

right

) and a positive indole test (

left

Guide

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Practical Medical Microbiology for Clinicians

Frank E. Berkowitz

Robert C. Jerris

Published by John Wiley & Sons, Inc., Hoboken, New Jersey

Published simultaneously in Canada

No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750-8400, fax (978) 750-4470, or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, (201) 748-6011, fax (201) 748-6008, or online at http://www.wiley.com/go/permissions.

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Library of Congress Cataloging-in-Publication Data:

Berkowitz, Frank E. (Frank Ellis), 1948–, author. Practical medical microbiology for clinicians / Frank E. Berkowitz, Robert C. Jerris. p. ; cm. Includes bibliographical references and index.

ISBN 978-1-119-06674-3 (pbk.)I. Jerris, Robert C., author. II. Title. [DNLM: 1. Microbiological Phenomena. 2. Microbiological Techniques. QW 4] QR46 616.9’041–dc23

2015028776

Cover image courtesy Robert Jerris

This book is dedicated to our wives, Zahava and Kerry.

Preface

Microorganisms cause a large proportion of human disease. Newly recognized organisms and newly recognized diseases caused by known organisms continue to be reported. Yet less time in medical school curricula is devoted to microbiology than previously.

The goal of this book, therefore, is to give clinicians, practicing in all branches of medicine, an insight into microorganisms that infect their patients, how these organisms are related to one another, what takes place in the microbiology laboratory to isolate and identify them, and how they can best utilize the laboratory for the benefit of their patients. It is designed to give clinicians the knowledge to facilitate their communication with the microbiologist in the laboratory. The approach is systematic, with a description of taxonomy of key (but not all) human pathogens and, for the most part, consideration of organisms within taxonomic groups. The emphasis of the book is not so much on the biology of the organisms, but rather on their epidemiology, and the use of the laboratory in managing individuals infected with them. It describes microorganisms and the diseases they cause, but it is not intended as a book about infectious diseases and their management.

Acknowledgments

We want to thank the following individuals who helped to make the writing of this book possible: the staff of the microbiology laboratory, Children’s Healthcare of Atlanta at Egleston, who helped gather material for many of the illustrations: Charles Ash, Theresa Stanley, Kathy Shauger, Becky De Ridder, Salome Tesfay, Mona Dillard, Scott Brown, Heather MacDonald, and Danielle Ingebrigtsen; the fellows in Pediatric Infectious Diseases, Emory University School of Medicine, for their assistance in obtaining some of the pictures, and for their stimulating questions; Carlos Abramowski MD, who provided several histologic pictures, and for his enthusiasm in teaching us the histology of infections; Satyen Tripathi, who helped with some of the illustrations; and Joni Lewis, who helped to prepare the manuscript.

SECTION ILaboratory methods in clinical microbiology

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