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Microbiology & Infection - Microbiologie & Infection - Microbiologia & Infezione

SIMPLE CONTENTS * = Clinically Important

NEWS & UPDATES
MAPS
OVERVIEW
BACTERIA
VIRUSES
FUNGI
PARASITES : PROTOZOA, HELMINTHS (NEMATODES, TREMATODES, CESTODES), ARTHROPODS
SYSTEMS
ANTIMICROBIALS
REFERENCES

TOC
DETAILED CONTENTS

NEWS & UPDATES
MAPS
OVERVIEW

IMMUNOLOGY
LABORATORY DIAGNOSIS

BACTERIOLOGY
STRUCTURES
CLASSIFICATION
GENETICS
METABOLISM & GROWTH
PATHOGENESIS

IMPORTANT BACTERIAL GENERA

GRAM +

GRAM + COCCI
STAPHYLOCOCCUS S aureus S epidermidis S saprophyticus
STREPTOCOCCUS & ENTEROCOCCUS S pyogenes S agalactiae S pneumoniae

GRAM + BACILLI  Listeria Bacillus Corynebacterium Clostridium Cutibacterium (formerly Propionibacterium)

MYCOBACTERIUM & RELATED ACID-FAST

BACTERIAL DISEASES

VIROLOGY
CLASSIFICATION

VIRAL  DISEASES
SLOW
ONCOGENIC
PRIONS

MYCOLOGY
FUNGAL DISEASES

PARASITOLOGY
PROTOZOA
HELMINTHS
PARASITIC DISEASES
ARTHROPODS

SYSTEMS

ANTIMICROBIALS

REFERENCES

MAPS

CONTENTS
(Hawley BRS) V1 PDF

OVERVIEW
Classification
Normal Flora
Pathogenicity
Diagnostic   
Sterilization & Disinfection

MEDICAL MICROBIOLOGY
HISTORY
COMMONLY TREATED INFECTIOUS DISEASES
CAUSES & TRANSMISSION OF INFECTIOUS DISEASES

DIAGNOSTIC TESTS
MICROBIAL CULTURE
MICROSCOPY
BIOCHEMICAL TESTS
POLYMERASE CHAIN REACTION

TREATMENTS

TECHNIQUES IN CLINICAL MICROBIOLOGY


ISOLATION AND CULTURE

IDENTIFICATION AND TESTING

EQUIPMENT


TOC
IMMUNOLOGY

CONTENTS

DIVIRDEPT
IMMUNE CELL CHARACTERISTICS
T, B, AND OTHER CELLS
ANTIBODY
COMPLEMENT CASCADE
CYTOKINES
INNATE IMMUNITY & INFLAMMATION
IMMUNE RESPONSES
TH1 VERSUS TH2
HYPERSENSITIVITY REACTIONS : PART ONE
HYPERSENSITIVITY REACTIONS : PART TWO
IMMUNE RESPONSE TO INFECTIOUS AGENTS
VACCINES

COMPONENTS OF THE IMMUNE SYSTEM
ROLE OF T CELLS IN IMMUNE RESPONSES
IMMUNOGLOBULINS & THEIR PRODUCTION BY B CELLS
NORMAL & ABNORMAL IMMUNE RESPONSES
LABORATORY TESTS FOR DIAGNOSIS

END OF CONTENTS

COMPONENTS OF THE IMMUNE SYSTEM

TYPES & GOALS OF HOST DEFENSE MECHANISMS

NONSPECIFIC (INNATE) IMMUNITY
Innate immunity : antigen independent; first defense
Innate protections are immediate
Innate protections may be triggered by microbial structures

SPECIFIC (ACQUIRED) IMMUNITY
Specific immunity: antigen dependent
Activation, expansion, and movement of specific immunity to an infection takes time
CMI response : T cells
Humoral response: B cells → plasma cells → antibodies

IMMUNE ORGANS
Thymus: maturation of T cells
Bone marrow, fetal liver: maturation of B cells
B cells: located in germinal centers
M cell: “door keeper” to Peyer patches

IMMUNE SYSTEM CELLS
Cell surface determinants
Actions: activate, suppress, and kill
Role of cell and type of response
Products: cytokines, antibodies, etc.
ANTIGEN-RECOGNIZING LYMPHOID CELLS
B cells: surface antibodies recognize antigen
T cells: T cell receptors recognize antigen
Helper T cell : CD4 surface marker
Cytolytic T cell : CD8 surface marker
GRANULOCYTES
Neutrophil: phagocytic; first line of cellular defense
Neutrophils die and make pus
Eosinophils: allergic reactions; destroys intestinal worms
Basophils, mast cells: release histamine
MYELOID CELLS
DCs initiate, direct and control the T cell response through interactions and cytokines
Langerhans cells: DCs of skin; process antigens
Macrophages: follow neutrophils in inflammation; phagocytose; process antigen
Macrophages eat (phagocytize) and secrete (cytokines) but must be angry to kill
Asplenic individuals are prone to infections with encapsulated bacteria
NATURAL KILLER (NK) CELLS
NK cells: large granular lymphocytes; direct cytotoxicity; ADCC
NK cells provide an early, rapid defense against virus-infected and tumor cells
NK cells and cytotoxic T cells have similar killing mechanisms, but NK killing is turned off by MHC, and cytotoxic T cells are targeted to MHC

COMPLEMENT SYSTEM
Complement is the earliest antibacterial response
Complement kills, opens the vasculature (C3a, C4a, C5a), and attracts cell-mediated protections (C3a, C5a)
Activation of alternate and lectin pathways: microbial surfaces, cell surface components (e.g., endotoxin)
Classical pathway: activated by antigen- antibody complexes
For complement cleavage products: b means binding (e.g., C3b); a means attract, “anaphylact” (e.g., C3a, C4a, C5a)
MAC: punctures cell membranes
Individuals with C1 to C4 deficiencies are prone to pyogenic infections; those with C5 to C9 deficiencies are prone to neisserial infections
Hereditary angioedema: C1 esterase inhibitor deficiency
Paroxysmal nocturnal hemoglobinuria: deficiency of DAF

PHAGOCYTIC CLEARANCE OF INFECTIOUS AGENTS
Opsonins: IgG, C3b
Oxygen-dependent myeloperoxidase system: most potent microbicidal system

INFLAMMATION : INDUCED BY TISSUE DAMAGE DUE TO TRAUMA, INJURIOUS AGENTS, OR INVASION OF MICROBES; MEDIATED PRIMARILY BY INNATE AND IMMUNE CELLS, CYTOKINES, & OTHER SMALL MOLECULES
Acute inflammation: chemical, vascular, cellular (neutrophil) components
Classic signs of local acute inflammation: rubor (redness), calor (heat), tumor (swelling), and dolor (pain)
Inflammatory response and phagocytic killing are sufficient to contain and resolve many infections by extracellular bacteria

ROLE OF T CELLS IN IMMUNE RESPONSES

T CELL SURFACE MOLECULES
Cell it is on
Ligand it binds
Action it causes
Purpose in immunity
T CELL RECEPTOR (TCR) COMPLEX
TCR: associated with CD3 on T cells
TCRs resemble immunoglobulins but have to be presented with antigen by MHC
ACCESSORY MOLECULES
CD4: binds to class II MHC
CD8: binds to class I MHC

DEVELOPMENT & ACTIVATION OF T CELLS
ANTIGEN-INDEPENDENT MATURATION
ANTIGEN-DEPENDENT ACTIVATION
Leads to proliferation and differentiation of naive T cells (clonal expansion) into effector cells and memory T cells
Effective stimulation requires primary and coactivating signals (fail-safe mechanism) that trigger intracellular signal transduction cascades, ultimately resulting in new gene expression
Signal 1 (primary): specificity—dependent on antigen and MHC
Signal 2 (coactivating): permission—independent of antigen and MHC
Signal 3 (determines nature of response): direction—cytokine from dendritic cell (DC) or APC
Antigen specificity (TCR- MHC) + permission (CD28-B7) + direction (cytokine) = T cell activation
ANTIGEN PROCESSING AND PRESENTATION BY CLASS I & II MHC MOLECULES
Class II MHC presents phagocytized protein trash to CD4 T cells
Class I MHC presents intercellular protein trash to CD8 T cells

T CELL EFFECTOR MECHANISMS
CYTOKINE PRODUCTION BY CD4 T CELLS
TH1-produced cytokines mediate “early (1st), local” cell-mediated responses; defense against viral infections and intracellular bacteria
TH2-produced cytokines mediate “later (2nd), systemic” responses; defense against extracellular bacteria and parasites
TH17-produced cytokines mediate antibacterial, antifungal, inflammatory, and autoimmune responses when TGF-β and acute phase cytokines are present
CYTOTOXIC T LYMPHOCYTE (CTL)-MEDIATED KILLING OF TARGET CELLS
CTLs kill by apoptosis with perforin and granzymes or Fas ligand binding to Fas on target cell
Apoptosis: “clean” cell death involving breakdown of DNA and release of small, apoptotic bodies
Necrosis: “messy” cell death from injury in which cell swells and bursts; intracellular contents induce local inflammatory response

MHC AND THE IMMUNE RESPONSE TO TRANSPLANTED TISSUE
CLINICAL CLASSIFICATION OF ALLOGRAFT REJECTION
GRAFT-VERSUS-HOST DISEASE (GVHD)
GVH reaction: jaundice, diarrhea, dermatitis
GVHD develops most commonly after allogeneic bone marrow transplantation
DETERMINATION OF TISSUE COMPATIBILITY

CYTOKINES
CYTOKINE FUNCTIONS AND SOURCES
CYTOKINE-RELATED DISORDERS
Cytokine storm can be due to excessive IL-1, TNF, and other cytokines adn lead to sepsis, and systemic failures
Cardiac myxoma: IL-6 responsible for fever, weight loss, ↑ antibody synthesis
TAX protein product of the virus stimulates IL-2

IMMUNOGLOBULINS & THEIR PRODUCTION BY B CELLS

IMMUNOGLOBULIN STRUCTURE & FUNCTIONS
CHAIN STRUCTURE OF IMMUNOGLOBULINS
Heavy chains define the specificity of the immunoglobulin
FUNCTIONAL REGIONS OF ANTIBODY MOLECULES
Papain cleaves immunoglobulin G (IgG) into two monovalent Fab and one Fc fragment
Pepsin cleaves IgG into one divalent F(ab′)2 and one Fc fragment
Fab interacts with antigen, and Fc interacts with complement and immune cells
Fc is sometimes referred to as: fragment, crystallizable
PROPERTIES OF IMMUNOGLOBULIN ISOTYPES
IgM: first immunoglobulin produced after antigen exposure (e.g., bacteria)
IgM has capacity for binding 10 antigenic epitopes
IgG is the most abundant immunoglobulin
IgG: only immunoglobulin to cross the placenta
IgA: only immunoglobulin with a secretory component
IgE: mediator for type I hypersensitivity reactions
ANTIGENIC DETERMINANTS ON ANTIBODIES
Everyone has the same (iso) types (IgG, IgM, IgD, IgE, IgA) of immunoglobulin. “All’o” us have our own personal immunoglobulins
Just as in the world, there are many “idiot types” of immunoglobulin in each of us for all the different variable regions

DEVELOPMENT & ACTIVATION OF B CELLS
ANTIGEN-INDEPENDENT MATURATION OF B CELLS
All the antibodies produced by an individual B cell have the same antigenic specificity
Light chain gene has VJC segments
Heavy chain gene has VDJC segments
IgM and IgD come from the same mRNA
IgM and IgD are the only immunoglobulins that are expressed on the same cell
STIMULATION BY T-INDEPENDENT (TI) ANTIGENS
TI antigens are repetitive structures, like bacterial surface molecules
STIMULATION BY T-DEPENDENT (TD) ANTIGENS
IgG, IgE, and IgA production require T cell help
Direct B cell–TH cell interaction and cytokines secreted by TH cells are required for B cells to respond to most antigens
Memory response is faster than primary response
Antibody diversity is generated during random recombination of VDJ regions, nucleotide insertion during recombination, and somatic mutation
Somatic mutation during B cell proliferation and clonal selection of the producing cells improves the antibody product, and isotype switching changes its biologic properties
Isotype switching: IgM-producing plasma cell now produces IgG or other immunoglobulins
T cell help induces generation of memory
B cells and antibody-secreting plasma cells
TH1 responses include IgG
TH2 responses include IgG, IgE, and IgA

ANTIBODY EFFECTOR MECHANISMS
NEUTRALIZATION OF VIRUSES AND TOXINS
OPSONIZATION (IGG)
COMPLEMENT ACTIVATION (IGG AND IGM)
ANTIBODY-MEDIATED AGGLUTINATION (IGM) OF BACTERIA
ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY
BINDING OF SECRETORY IGA TO MICROBES AT MUCOSAL SURFACES
HYPERSENSITIVITY REACTIONS

ANTIGEN-ANTIBODY REACTIONS
PRECIPITATION-BASED ASSAYS
AGGLUTINATION-BASED ASSAYS

NORMAL & ABNORMAL IMMUNE RESPONSES

CASCADE OF EVENTS IN TYPICAL IMMUNE RESPONSES
Trigger
Inducer
Cells
Time course
Outcome
Cytokines
LOCALIZED ANTIGEN-NONSPECIFIC RESPONSES AT SITE OF ANTIGEN EXPOSURE
Acute phase (proinflammatory) cytokines are IL-1, IL-6, and TNF-α
IL-12 production signals need for local cellular and antibody protections (TH1)
PRIMARY ANTIGEN-SPECIFIC RESPONSES
Primary antibody response: slow onset, initially IgM, low titer
Presence of IgM is good indication of a primary response
Acute inflammation produces painful swelling of lymph nodes
Secondary antibody response: fast onset, primarily IgG, high titer
SECONDARY IMMUNE RESPONSE

HYPERSENSITIVITY REACTIONS
Type I: Soluble mediators, preformed actors—fast reactions of less than 30 minutes
Type II : soluble mediators, cellular actors—slower reactions of less than 8 hours
Type III: soluble mediators, cellular actors—slower reactions of less than 8 hours
Type IV: cellular mediators, cellular actors—slow reactions of more than 1 day
TYPE I (IMMEDIATE) HYPERSENSITIVITY
Type I hypersensitivity: IgE; mast cell degranulation; rapid local (allergic) or systemic (anaphylactic) effects
TYPE II HYPERSENSITIVITY
Type II hypersensitivity: complement fixation on cells; acute inflammation
Production of C3a and C5a during Types II and III hypersensitivity attract and activate inflammatory neutrophils
TYPE III HYPERSENSITIVITY
Type III hypersensitivity: deposition of immune complexes; complement activation; acute inflammation
Large amount of hepatitis B surface antigen (HBsAg) and antibody during hepatitis B infection can cause immune complexes and type III hypersensitivity
TYPE IV (DELAYED-TYPE) HYPERSENSITIVITY
Type IV hypersensitivity: cytokines from CD4 TH1 cells; activated macrophages; skin reactions (acute); granulomatous and rejection reactions (chronic)

ANTIMICROBIAL & ANTITUMOR HOST DEFENSES
ANTIBACTERIAL RESPONSES
Increase in number of banded (immature) versus segmented neutrophils in complete blood count, referred to as a left shift, usually accompanies bacterial infection
Neutrophils always eat and kill bacteria; macrophages eat but must be activated to kill bacteria
Antibody is the primary antigen-specific protection
Antibody blocks toxin action and opsonizes and initiates complement reactions to bacteria
ANTIVIRAL RESPONSES
IFN-α, IFN-β, and NK cells may be sufficient to stop virus infection
IFN-α and IFN-β cause the flu-like symptoms associated with prodrome of many viral diseases
Double-stranded RNA is the best inducer of IFN-α and IFN-β activation of the antiviral state
Antibody cleans up free virus, and cell-mediated immunity kills virus factories to resolve infection
Vaccine-induced antibody prevents viremic spread of virus to disease target organ
ANTIPARASITE AND ANTIFUNGAL RESPONSES
ANTITUMOR RESPONSES

VACCINES & IMMUNIZATION
PASSIVE IMMUNIZATION
Passive immunization is common treatment for individuals exposed to tetanus toxin, botulinum toxin, rabies virus, or hepatitis A or B virus
ACTIVE IMMUNIZATION
Vaccine-induced cell- mediated immune responses are not dependable before 12 months of age
Thus, attenuated measles- mumps-rubella (MMR) and varicella-zoster virus (VZV) vaccines commonly are administered at 15 months
Killed vaccines are safer than live attenuated vaccines for immunodeficient individuals
Live vaccines induce both cellular and antibody responses and better memory

AUTOIMMUNE RESPONSES
CAUSES OF AUTOIMMUNE DISORDERS
MECHANISMS OF AUTOIMMUNE PATHOLOGY
ASSOCIATION BETWEEN HLA ALLELES AND AUTOIMMUNITY

TRANSPLANTATION
PREGNANCY
BLOOD TRANSFUSION
Blood transfusions: type O is the universal donor but picky about transfusions
O has antibodies to A and B; A has antibodies to B; B has antibodies to A
SOLID ORGAN
TREATMENTS

IMMUNODEFICIENCY DISEASES
OVERVIEW
PHAGOCYTE DISORDERS
COMPLEMENT ABNORMALITIES
LYMPHOCYTE DEFICIENCIES
Antibody deficiencies → increased susceptibility to bacterial infections, especially by encapsulated bacteria
T cell deficiencies → increased susceptibility to opportunistic infections by viruses, intracellular bacteria, and fungi
Inherited deficiency of adenine deaminase (ADA) causes one form of severe combined immunodeficiency disease
(SCID). ADA-SCID has been treated successfully with gene therapy

LABORATORY TESTS FOR DIAGNOSIS

LABORATORY ASSAYS FOR DETECTING NUCLEIC ACIDS
SOUTHERN BLOTTING FOR DNA & NORTHERN BLOTTING FOR RNA DETECT ELECTROPHORETICALLY SEPARATED GENOME SEQUENCES
IN SITU HYBRIDIZATION DETECTS VIRAL DNA OR RNA WITHIN INFECTED CELLS
POLYMERASE CHAIN REACTION (PCR) (DNA), REVERSE TRANSCRIPTASE (RT)-PCR (RNA), & RELATED TECHNOLOGIES PERMIT DETECTION, IDENTIFICATION, ANDAMPLIFICATION OF SPECIFIC NUCLEIC ACID SEQUENCES
PCR is a rapid, sensitive, and specific means for detecting microbes and distinguishing microbial strains
PCR of cerebrospinal fluid (CSF) replaced immunofluorescence of a brain biopsy for confirmation of herpes simplex virus (HSV) encephalitis
RT-PCR is the method of choice for detecting most RNA viruses
Viral load of human immunodeficiency virus (HIV) is determined by quantitative RT-PCR of patient serum

IMMUNOLOGIC ASSAYS
ANTIBODY-ANTIGEN BINDING
IgG anti-Rh antibodies, which are nonagglutinating, are detected by the Coombs test
This test employs antihuman antibody to cause agglutination of red blood cells (RBCs)
IMMUNOFLUORESCENCE (IF) AND ENZYME IMMUNOASSAY (EIA) DETECT PROTEINS EXPRESSED ON THE SURFACE OR INSIDE OF CELLS
DIRECT VERSUS INDIRECT ASSAYS
ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) AND RADIOIMMUNOASSAY (RIA) CAN BE USED TO DETECT AND QUANTITATE ANTIGEN OR ANTIBODY
ELISA can detect antigen or antibody depending on the adhered molecule used to capture the sample
WESTERN BLOT CAN DETERMINE TRUE-POSITIVE ELISA REACTIONS BY SHOWING THE SPECIFIC PROTEINS RECOGNIZED BY PATIENT SERA
ANTIBODY INHIBITORY TESTS: HEMAGGLUTINATION INHIBITION, VIRUS OR TOXIN NEUTRALIZATION

SEROLOGY (HISTORY OF THE INFECTION)
SEROLOGIC TESTING CAN DETERMINE THE TYPE & TITER OF ANTIVIRAL ANTIBODIES IN SERUM & THE IDENTITY OF VIRAL ANTIGENS

FLOW CYTOMETRY
LIGHT SCATTER MEASUREMENTS CAN DISTINGUISH LYMPHOCYTES, MACROPHAGES, AND GRANULOCYTES
DNA-BINDING FLUORESCENT DYES CAN BE USED TO EVALUATE CELL CYCLE
IMMUNOFLUORESCENCE MEASUREMENTS INDICATE THE PHENOTYPE OF THE CELL

TOC
BACTERIOLOGY
(Moi Bacteriology) V1 PDF
(Moi Bacteria Classification) V1 PDF
(Moi Bacteria Laboratory) V1 PDF
(Moi Bacteria G+) V1 PDF
(Moi Bacteria G-) V1 PDF
(Moi Bacteria Anaerobic) V1 PDF
(Moi Bacteria Mycobac) V1 PDF
(Moi Bacteria Pleomorphic) V1 PDF
(Moi Bacteria Spirochetes) V1 PDF

CONTENTS

BACTERIAL STRUCTURE
BACTERIAL MORPHOLOGY
BACTERIAL ULTRASTRUCTURE
PEPTIDOGLYCAN
LIPOPOLYSACCHARIDE

BACTERIAL GROWTH, GENETICS, & VIRULENCE
PROLIFERATION OF BACTERIAL CELLS
BACTERIAL GENETICS
MECHANISMS OF BACTERIAL VIRULENCE
ANTIBACTERIAL IMMUNOPATHOGENESIS

DIAGNOSIS, THERAPY, AND PREVENTION OF BACTERIAL DISEASES
LABORATORY IDENTIFICATION OF BACTERIA
ANTIMICROBIAL DRUGS
ANTIBACTERIAL VACCINES

END OF CONTENTS

BACTERIAL STRUCTURE

BACTERIAL MORPHOLOGY
OVERVIEW
SIZE OF BACTERIAL CELLS
SHAPE AND ARRANGEMENT OF COMMON BACTERIA
GRAM STAINING
Purple = P = gram Positive
Red = not P = gram negative

BACTERIAL ULTRASTRUCTURE - BACTERIAL STRUCTURES

APPENDAGES
PILI (FIMBRIAE)
Glycoprotein - Mediate adherence to cell surface; sex pilus forms during conjugation - Major virulence factor - especially in UTIs
FLAGELLA
Proteins - Motility

SPECIALIZED STRUCTURES
ENDOSPORES - SPORE-FORMING BACTERIA
Keratinlike coat, dipicolinic acid, peptidoglycan, DNA - Survival: resist dehydration, heat, chemicals
Some gram ⊕ bacteria can form spores when nutrients are limited - gram-negative bacteria cannot sporulate
Spores lack metabolic activity & are highly resistant to heat & chemicals
Core contains dipicolinic acid (responsible for heat resistance)
Spores are resistant to boiling & many chemicals (including common disinfectants) & can survive in soil for long times
Must autoclave to kill spores (as is done to surgical equipment) by steaming at 121°C for 15 minutes - and by aldehyde- containing disinfectants - Hydrogen peroxide & iodine-based agents are also sporicidal
Examples: B anthracis (anthrax), B cereus (food poisoning), C botulinum (botulism), C difficile (pseudomembranous colitis), C perfringens (gas gangrene), C tetani (tetanus)
Autoclave to kill Bacillus and Clostridium (ABC)

INTERNAL BACTERIAL STRUCTURES
RIBOSOME
major antimicrobial target; 30s subunit targeted by tetracycline and aminoglycosides; 50s subunit by chloramphenicol and macrolides, ketolides, and azalides

CELL ENVELOPE = CYTOPLASMIC MEMBRANE + CELL WALL CW + CAPSULE
Flagellin, lipopolysaccharide (LPS), lipoteichoic acid (LTA), & peptidoglycan are PAMPs that stimulate TLRs
Teichoic acids are present only in G+
LPS is present only in G- & porin
Mycoplasma lack cell walls
Chlamydia have an outer membrane with LPS but no peptidoglycan
ENCAPSULATED BACTERIA
Discrete layer usually made of polysaccharides (and rarely proteins) - Protects against phagocytosis - major virulence factor - and extends the bacteria’s time in the bloodstream
Examples are Pseudomonas aeruginosa, Streptococcus pneumoniae A , Haemophilus influenzae type b, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, & group B Strep - Please SHiNE my SKiS
Their capsules serve as an antiphagocytic virulence factor
Capsular polysaccharide +/– protein conjugate can serve as an antigen in vaccines
A polysaccharide antigen alone cannot be presented to T cells; immunogenicity can be enhanced by conjugating capsule antigens to a carrier protein
Are opsonized, and then cleared by spleen
Asplenics (No Spleen Here) have ↓ opsonizing ability and thus ↑ risk for severe infections; need vaccines to protect against : N meningitidisƒ S pneumoniae H influenzae

SLIME (S) LAYER
Loose network of polysaccharides - Mediates adherence to surfaces, plays a role in biofilm formation (eg, indwelling catheters)
IN VIVO BIOFILM-PRODUCING BACTERIA
S epidermidis - Catheter and prosthetic device infections
Viridans streptococci (S mutans, S sanguinis) - Dental plaques, infective endocarditis
P aeruginosa - Respiratory tree colonization in patients with cystic fibrosis, ventilator-associated pneumonia - Contact lens–associated keratitis
Nontypeable (unencapsulated) H influenzae - Otitis media

CELL WALL
Peptidoglycan is a sugar backbone with peptide side chains cross-linked by transpeptidase - Netlike structure gives rigid support, protects against osmotic pressure damage
CYTOPLAMIC MEMBRANE
Phospholipid bilayer sac with embedded proteins (eg, penicillin-binding proteins [PBPs]) and other enzymes - Site of oxidative and transport enzymes; PBPsinvolved in cell wall synthesis

CW OF G-
G- OUTER MEMBRANE
Outer leaflet: contains endotoxin (LPS/LOS) - Embedded proteins: porins & other outer membrane proteins (OMPs) - Inner leaflet: phospholipids
G ⊝ only - Endotoxin: lipid A induces TNF and IL-1; antigenic O polysaccharide component - Most OMPs are antigenic - Porins: transport across outer membrane, small and hydrophilic molecules but block others - Antibiotic’s ability to permeate porin channels determines sensitivity & resistance
G- PERIPLASM
Space between cytoplasmic membrane & outer membrane in G ⊝ (thin peptidoglycan in middle) - Accumulates components exiting G ⊝ cells, including hydrolytic enzymes (eg, β-lactamases)

CW OF G+
G+ CYTOPLAMIC MEMBRANE
Lipoteichoic acids (gram positive) only extend from membrane to exterior - Lipoteichoic acids induce TNF-α and IL-1

CW OF MYCOBACTERIUM
An acid-fast stained bacillus in sputum is a mycobacterium

PIGMENT-PRODUCING BACTERIA
Actinomyces israelii—yellow “sulfur” granules,which are composed of filaments of bacteria - Israel has yellow sand
S aureus—golden yellow pigment - Aureus (Latin) = gold
P aeruginosa—blue-green pigment (pyocyanin and pyoverdin) - Aerugula is green
Serratia marcescens—red pigment - Think red Sriracha hot sauce

COMPARISON OF GRAM-POSITIVE & GRAM-NEGATIVE BACTERIA - CELL ENVELOPE

PEPTIDOGLYCAN
STRUCTURAL PARTS OF PEPTIDOGLYCAN (MUCOPEPTIDE, MUREIN)
Lysozyme in tears and mucus degrades peptidoglycan.
Outer membrane protects against lysozyme; therefore, only gram- positive bacteria are sensitive
BIOSYNTHESIS OF PEPTIDOGLYCAN
ANTIBIOTICS THAT INHIBIT PEPTIDOGLYCAN SYNTHESIS
Cross-linking of peptidoglycan is the target for β-lactam antibiotics, vancomycin, and bacitracin

LIPOPOLYSACCHARIDE
STRUCTURAL PARTS OF LPS
Lipid a is endotoxin
Neisseria species shed Los, which mediates endotoxin action
SYNTHESIS OF LPS

BACTERIAL GROWTH, GENETICS, & VIRULENCE

PROLIFERATION OF BACTERIAL CELLS

BACTERIAL GROWTH CURVE

GROWTH REQUIREMENTS

OVERVIEW

OXYGEN REQUIREMENT
OBLIGATE AEROBES REQUIRE OXYGEN FOR GROWTH
Mycobacterium tuberculosis, Neisseria, Nocardia species, & Pseudomonas aeruginosa
ANAEROBES DO NOT REQUIRE OXYGEN FOR GROWTH
Examples include Clostridium, Bacteroides, Fusobacterium, and Actinomyces israelii -  Can’t Breathe Fresh Air - Treponema, & Propionibacterium - Some Clostridium species are aerotolerant
They lack catalase and/or superoxide dismutase & are thus susceptible to oxidative damage
Generally foul smelling (short-chain fatty acids), are difficult to culture, and produce gas in tissue (CO2 and H2)
Anaerobes are normal microbiota in GI tract, typically pathogenic elsewhere (eg, causes aspiration pneumonia)
AminO2glycosides antibiotics (e.g., streptomycin and gentamicin) are ineffective because these antibiotics require O2 to enter into bacterial cell
FACULTATIVE ANAEROBES CAN GROW UNDER AEROBIC OR ANAEROBIC CONDITIONS
May use O2 as a terminal electron acceptor to generate ATP, but can also use fermentation and other O2-independent pathways
Facultative anaerobes include Escherichia coli & Staphylococcus aureus - Streptococci, staphylococci, & enteric gram ⊝ bacteria

INTRACELLULAR BACTERIA
Obligate intracellular
Rickettsia, Chlamydia, Coxiella - Rely on host ATP - Stay inside (cells) when it is Really Chilly & Cold
Facultative intracellular
Salmonella, Neisseria, Brucella, Mycobacterium, Listeria, Francisella, Legionella, Yersinia pestis - Some Nasty Bugs May Live FacultativeLY

NUTRIENT REQUIREMENTS
TEMPERATURE REQUIREMENTS

CELL DIVISION
Bacteria initiate new DNA synthesis before cell division (they are born pregnant)

BACTERIAL GENETICS

BACTERIAL CHROMOSOME

OTHER GENETIC ELEMENTS
Plasmids
Bacteriophages
Lytic phages kill their host; lysogenic phages live in their host but can “jump ship” if the bacteria are sick
Transposons

MECHANISMS OF GENETIC TRANSFER
Horizontal gene transfer is the main mechanism for transfer of antibiotic resistance among bacteria
TRANSFORMATION
Transformation : uptake of a segment of naked DNA and its incorporation into the bacterial chromosome
CONJUGATION
Conjugation: direct transfer of DNA from a donor (male) cell to a recipient (female) cell through sex (F) pilus, which is encoded by F plasmid in donor cell
TRANSDUCTION
Transduction: uptake of DNA packaged in phage particles and its incorporation into the bacterial chromosome
TRANSPOSITION
Transposition: movement of a transposon (nonreplicable DNA segment) from one DNA site to another, resulting in inactivation of the recipient gene into which it inserts

RECOMBINATION
Salmonella species cellular entry biodevices are encoded within pathogenicity islands turned on by acidic pH and temperature

MECHANISMS OF BACTERIAL VIRULENCE “EAT RICE” - BACTERIAL PATHOGENESIS
“EAT RICE”
Enzymes : degradative enzymes
Adherence : pili, M protein, lipoteichoic acid, MSCRAMM (microbial surface components recognizing adhesive matrix molecules)
Toxins : exo and endo
Resistance to antibiotics
Invasion of normally sterile body sites
Circulation (septicemia/bacteremia) : spread through host
Evasion of immune responses : capsule, intracellular growth, catalase, evasion of lysosomal action

ADHERENCE
Pili promote adherence

INVASION
Sterile sites: blood, cerebrospinal fluid, brain, organ parenchyma, lower lung airways, joint spaces, bone

TISSUE DAMAGE
Bacterial tissue damage can be caused by metabolic byproducts, degradative enzymes, inhibitors of cell processes, growth on top of cells, and intracellular growth

CIRCULATION THROUGH THE BLOOD (BACTEREMIA)
Bacteria in blood release cell wall molecules & activate inflammatory processes, including fever

PATHOGEN-ASSOCIATED MOLECULAR PATTERNS (PAMPS)
Cell wall components are PAMPS that activate TLRs to promote acute phase responses

ENDOTOXIN
LPS found in outer membrane of gram ⊝ bacteria (both cocci and rods)
Composed of O-antigen + core polysaccharide + lipid A (the toxic component)
Neisseria have lipooligosaccharide
Released upon cell lysis or by living cells by blebs detaching from outer surface membrane (vs exotoxin, which is actively secreted)
Three main effects: macrophage activation (TLR4/CD14), complement activation, and tissue factor activation
Edema
Nitric oxide
DIC/Death
Outer membrane
TNF-α
O-antigen + core polysaccharide + lipid A
eXtremely heat stable
IL-1 and IL-6
Neutrophil chemotaxis
Shock + fever

EXOTOXINS - BACTERIA WITH EXOTOXINS
The B subunit of A-B toxins Binds to the receptor and the A subunit Acts on the cell
Superantigens and sepsis induce a cytokine storm that dysregulates the immune response, causing hypotension and shock
INHIBIT PROTEIN SYNTHESIS
Corynebacterium diphtheriae
Pseudomonas aeruginosa
Shigella spp
Enterohemorrhagic E coli
INCREASE FLUID SECRETION
Enterotoxigenic E coli
Bacillus anthracis
Vibrio cholerae
INHIBIT PHAGOCYTIC ABILITY
Bordetella pertussis
INHIBIT RELEASE OF NEUROTRANSMITTER
Clostridium tetani
Clostridium botulinum
LYSE CELL MEMBRANES
Clostridium perfringens
Streptococcus pyogenes
SUPERANTIGENS CAUSING SHOCK
Staphylococcus aureus
Streptococcus pyogenes

BYPRODUCTS OF GROWTH (ACID & GAS)

MAIN FEATURES OF EXOTOXINS & ENDOTOXINS
Source
Certain species of gram ⊕ and gram ⊝ bacteria
Outer cell membrane of most gram ⊝ bacteria
Secreted from cell
Yes
No
Chemistry
Polypeptide
Lipid A component of LPS (structural part of bacteria; released when lysed)
Location of genes
Plasmid or bacteriophage
Bacterial chromosome
Toxicity
High (fatal dose on the order of 1 µg)
Low (fatal dose on the order of hundreds of micrograms)
Clinical effects
Various effects
Fever, shock (hypotension), DIC
Mode of action
Various effects
Induces TNF, IL-1, and IL-6
Antigenicity
Induces high-titer antibodies called antitoxins
Poorly antigenic
Vaccines
Toxoids used as vaccines
No toxoids formed and no vaccine available
Heat stability
Destroyed rapidly at 60°C (except staphylococcal enterotoxin and E coli heat- stable toxin, and B cereus emetic toxin)
Stable at 100°C for 1 hr
Typical diseases
Tetanus, botulism, diphtheria, cholera
Meningococcemia; sepsis by gram ⊝ rods

ANTIBIOTIC RESISTANCE

ESCAPE OF HOST ATTEMPTS AT ELIMINATION
Evasion of host defenses permits bacteria to remain in the host longer, thereby causing more damage
ENCAPSULATION WITH POLYSACCHARIDE (SLIME) LAYER
The capsule produced by certain gram-positive & gram-negative bacteria is a significant virulence factor that helps bacteria avoid immune detection, phagocytosis, & intracellular killing
Patients lacking a spleen are more susceptible to encapsulated bacteria
BIOFILMS ARE STICKY WEBS OF POLYSACCHARIDE THAT CAN PROTECT THE BACTERIA FROM HOST DEFENSES & ANTIMICROBIALS
P. aeruginosa and Streptococcus mutans (dental plaque) make biofilms when a quorum of bacteria are present
INTRACELLULAR GROWTH WITHOUT INACTIVATION (ESPECIALLY IN MACROPHAGES)
REDUCTION OF PHAGOCYTIC CELL FUNCTION
Bacteria escape phagocytes by preventing uptake, detoxifying or preventing production of reactive oxygen species, or preventing lysosome function
INACTIVATION OF ANTIBODY
Bacteria escape antibody control by changing their antigens, by inactivating the antibody, or by hiding within cells
INHIBITION OF COMPLEMENT ACTION
ANTIGENIC VARIATION BY DNA REARRANGEMENT INVOLVING HOMOLOGOUS RECOMBINATION

VIRULENCE  FACTORS
These promote evasion of host immune response
Capsular polysaccharide
Highly charged, hydrophilic structure
Acts as barrier to phagocytosis and complement-mediated lysis
Major determinant of virulence
Protein A
Binds Fc region of IgG
Prevents opsonization and phagocytosis
Expressed by S aureus
IgA Protease
Enzyme that cleaves IgA, allowing bacteria to adhere to and colonize mucous membranes
Secreted by S pneumoniae, H influenzae type b, and Neisseria (SHiN)
M protein
Helps prevent phagocytosis
Expressed by group A streptococci
Sequence homology with human cardiac myosin (molecular mimicry); possibly underlies the autoimmune response seen in acute rheumatic fever

ANTIBACTERIAL IMMUNOPATHOGENESIS
Host immune responses cause the disease for some bacteria
INFLAMMATION
BACTERIA THAT INDUCE TISSUE-DAMAGING IMMUNE RESPONSES
CROSS-REACTING ANTIBACTERIAL ANTIBODIES
DEPOSITION OF IMMUNE COMPLEXES
SEPSIS
SUPERANTIGENS

DIAGNOSIS, THERAPY, AND PREVENTION OF BACTERIAL DISEASES

LABORATORY IDENTIFICATION OF BACTERIA

STAINS

GRAM STAIN
Purple is positive; red is negative
Gram variability occurs with old culture and β-lactam–treated bacteria
First-line lab test in bacterial identification
Bacteria with thick peptidoglycan layer retain crystal violet dye (gram ⊕); bacteria with thin peptidoglycan layer turn red or pink (gram ⊝) with counterstain
These bugs do not Gram stain well (These Little Microbes May Unfortunately Lack Real Color But Are Everywhere)
Treponema, Leptospira - Too thin to be visualized
Mycobacteria - Cell wall has high lipid content
Mycoplasma, Ureaplasma - No cell wall
Legionella, Rickettsia, Chlamydia, Bartonella, Anaplasma, Ehrlichia - Primarily intracellular; also, Chlamydia lack classic peptidoglycan because of ↓ muramic acid

GIEMSA STAIN
H pylori, Chlamydia, Borrelia, Rickettsia,Trypanosomes A , Plasmodium - Help! Certain Bugs Really Try my Patience
Clumsy Rick Tripped on a Borrowed Helicopter Plastered in Gems

PERIODIC ACID–SCHIFF STAIN
Stains glycogen, mucopolysaccharides; used to diagnose Whipple disease (Tropheryma whipplei)
PaSs the sugar

ZIEHL-NEELSEN STAIN (CARBOL FUCHSIN)
Acid-fast bacteria (eg, Mycobacteria C , Nocardia; stains mycolic acid in cell wall); protozoa (eg, Cryptosporidium oocysts) - Auramine-rhodamine stain is more often used for screening (inexpensive, more sensitive)

INDIA INK STAIN
Cryptococcus neoformans D; mucicarmine can also be used to stain thick polysaccharide capsule red

SILVER STAIN
Helicobacter pylori, Legionella, Bartonella henselae, and fungi (eg, Coccidioides E , Pneumocystis jirovecii, Aspergillus fumigatus)
HeLiCoPters Are silver

FLUORESCENT ANTIBODY STAIN
Used to identify many bacteria, viruses, Pneumocystis jirovecii, Giardia, and Cryptosporidium - Example is FTA-ABS for syphilis

SPECIAL CULTURE REQUIREMENTS - MEDIA FOR ISOLATING OR IDENTIFYING SELECTED BACTERIA - SELECTIVE / DIFFERENTIAL MEDIA

GROWTH & ISOLATION OF BACTERIA
CULTURE MEDIA
Chocolate Agar - H influenzae - Factors V (NAD+) and X (hematin)
Thayer-Martin (VCN) Agar - N gonorrhoeae, N meningitidis - Selectively favors growth of Neisseria by inhibiting growth of gram ⊕ organisms with vancomycin, gram ⊝ organisms except Neisseria with trimethoprim and colistin, and fungi with nystatin - Very typically cultures Neisseria
Bordet-Gengou Medium Agar (Bordet for Bordetella) - B pertussis - Potato extract
Regan-Lowe medium - B pertussis - Charcoal, blood, and antibiotic
Tellurite agar, Löffler medium - C diphtheriae
Lowenstein-Jensen agar - Middlebrook medium, rapid automated broth cultures - M tuberculosis
Eaton agar - M pneumoniae - Requires cholesterol
MacConkey Agar - Lactose-fermenting enterics - Fermentation produces acid, causing colonies to turn pink - distinguishes normal flora enterobacteria (lactose positive—purple colonies) from Salmonella, Shigella, Pseudomonas and other genera (lactose negative— gray colonies)
Eosin-Methylene Blue Agar - E coli - Colonies with green metallic sheen
Charcoal yeast extract agar buffered with cysteine and iron - Brucella, Francisella, Legionella, Pasteurella - The Ella siblings, Bruce, Francis, a legionnaire, and a pasteur (pastor), built the Sistine (cysteine) chapel out of charcoal and iron
Sabouraud agar - Fungi - “Sab’s a fun guy!”
Mannitol salt agar
Hektoen enteric (HE) agar
Bile Esculin Agar
BCYE agar
COLONY CHARACTERISTICS

BIOCHEMICAL TESTS

METABOLIC TESTS FOR FERMENTATION OF VARIOUS SUGARS & PRODUCTION OF BYPRODUCTS (E.G.,ACID OR GASES)
Neisseria species fermentation: meningitidis has an m and a g for maltose and glucose
Gonorrhoeae has only a g for glucose

TESTS FOR ENZYMES

CATALASE TEST : + REACTION = BUBBLES (GAS FORMATION) - CATALASE-POSITIVE ORGANISMS
Catalase degrades H2O2 into H2O and bubbles of O2 before it can be converted to microbicidal products by the enzyme myeloperoxidase
People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with certain catalase ⊕ organisms
Catalase ⊕ organisms include Candida, Pseudomonas, Nocardia, Bordetella pertussis, Burkholderia cepacia, Helicobacter pylori, Aspergillus, Staphylococci, Serratia, Listeria, E coli
Catalase Positive: Notoriously Big Bubbling HASSLE

COAGULASE TEST : + REACTION = PRECIPITATE/GEL FORMATION

OXIDASE TEST : + REACTION = BLUE COLOR

UREASE-POSITIVE ORGANISMS
Proteus, Cryptococcus, H pylori, Ureaplasma, Nocardia, Klebsiella, S epidermidis, S saprophyticus
Urease hydrolyzes urea to release ammonia and CO2 → ↑  pH
Predisposes to struvite (magnesium ammonium phosphate) stones, particularly Proteus
Pee CHUNKSS

HEMOLYSIS

LACTOSE FERMENTATION (+)
LACTOSE FERMENTATION (-)
NEISSERIA: SUGAR FERMENTATION

IMMUNOLOGIC TESTS

ANTIBIOTIC SENSITIVITY ASSAYS
SERIAL DILUTION ASSAY
MIC: lowest concentration that inhibits growth. MBC: lowest concentration that kills
KIRBY-BAUER ASSAY
Kirby-Bauer method only for achievable blood levels of antibiotic
E-TEST USES A GRADUATED DIFFUSION METHOD TO GIVE MIC VALUES FOR BACTERIA GROWN ON AGAR PLATES

ANTIMICROBIAL DRUGS
OVERVIEW
INHIBITORS OF PEPTIDOGLYCAN SYNTHESIS
PEPTIDE ANTIBIOTIC DISRUPTERS OF BACTERIAL MEMBRANES
INHIBITORS OF NUCLEIC ACID SYNTHESIS
INHIBITORS OF PROTEIN SYNTHESIS
ANTIMETABOLITE DRUGS

ANTIBACTERIAL VACCINES
PASSIVE IMMUNIZATION
ACTIVE IMMUNIZATION

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GRAM +

LAB ALGORITHM

BACILLI
AEROBIC
ANAEROBIC

COCCI
CATALASE -
Hemolysis
CATALASE +
Coagulase

BRANCHING FILAMENTS
AEROBIC
ANAEROBIC

GRAM-POSITIVE COCCI ANTIBIOTIC TESTS
Staphylococci
Novobiocin
Streptococci
Optochin
Bacitracin

HEMOLYTIC BACTERIA
α - hemolytic bacteria
Partial oxidation of hemoglobin → greenish or brownish color without clearing around growth on blood agar
Streptococcus pneumoniae & viridans streptococci
β - hemolytic bacteria
Complete lysis of RBCs → pale/clear area surrounding colony on blood agar
Include Staphylococcus aureus, Streptococcus pyogenes (group A strep), Streptococcus agalactiae (group B strep), Listeria monocytogenes

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BACILLOTA (LOW-G+C) G+

BACILLI

LACTOBACILLALES(CAT-)
STREPTOCOCCUS & ENTEROCOCCUS

BACILLALES (CAT+)

CLOSTRIDIA
MOLLICUTES

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ACTINOMYCETOTA G+
ACTINOMYCINEAE
CORYNEBACTERINEAE
BIFIDOBACTERIACEAE

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BACILLALES (CAT+)
STAPHYLOCOCCUS
BACILLUS
LISTERIA

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GRAM + COCCI

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STAPHYLOCOCCUS - GRAPELIKE CLUSTERS
COAGULASE +
S. aureus (Staphylococcal scalded skin syndrome - Toxic shock syndrome - MRSA)
COAGULASE -
novobiocin susceptible S. epidermidis
novobiocin resistant S. saprophyticus

SHARED STAPHYLOCOCCAL PROPERTIES
Ubiquitous distribution; part of normal flora; responsible for many nosocomial infections

VIRULENCE FACTORS
Protein A, coagulase, teichoic acid adherence, β-lactamase,
resistance to salt (growth on salted meats); toxins: enterotoxin,
exfoliative toxin, toxic shock toxin (superantigen), leukocidin

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STAPHYLOCOCCUS AUREUS * growth on mannitol salts
S. aureus is normal flora of skin and the anterior nares
S. aureus : catalase, coagulase, grape-like clusters, MRSA, pus, 3-hour gastroenteritis, toxins, TSST

PATHOGENESIS
DISEASES CAUSED BY S. AUREUS
S. aureus : major cause of nosocomial and wound infections
S. aureus ferment mannose, other staph don’t
Staphylococcal food poisoning due to preformed toxin is quick acting (<3 hours)
Staphylococci are salt tolerant & grow on picnic meats and other foods
CA-MRSA also carries Panton valentine leukocidin gene
S. aureus uses many different virulence mechanisms to degrade tissue
Staphylococci & streptococci cause pus- forming (suppurative) infections
TRANSMISSION OF S. AUREUS
TREATMENT
Antibiotics and staphylococci: most staphylococci are resistant to penicillin (produce a β-lactamase)
Resistance to methicillin means resistance to all β-lactams

INFLAMMATORY
skin infections, organ abscesses, pneumonia (often after influenza virus infection), infective endocarditis, septic arthritis, and osteomyelitis
TOXINS
toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin), rapid-onset food poisoning (enterotoxins)
MRSA (METHICILLIN-RESISTANT S AUREUS)
STAPHYLOCOCCAL TOXIC SHOCK SYNDROME (TSS)
TREATMENT
β-Lactamase–resistant drugs: methicillin, nafcillin,
oxacillin; methicillin-resistant: vancomycin, trimethoprim-
sulfamethoxazole, daptomycin

Localized skin infections
- Sty
- Furuncles or boils
- Carbuncles
Diffuse skin infection-impetigo (pyoderma)
Deep, localized infections
- Osteomyelitis
- "Septic joint"
Other infections
- Acute endocarditis, septicemia, necrotizing pneumonia
Toxinoses
- Toxic shock syndrome
- Gastroenteritis
- Scalded skin syndrome (bullous impetigo)
Ubiquitous, normal flora

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"On the office’s “STAPH” retreat, there was NO StRESs"
NOVOBIOCIN +
S. EPIDERMIDIS *
S. epidermidis : catalase, catheters, coagulase negative, shunts
Infections of catheters & heart valves
Skin, normal flora Artificial heart valves, catheters, shunts, prosthetic joints
Vancomycin treatment
NOVOBIOCIN -
S. SAPROPHYTICUS *
Cystitis in women Urinary tract infection

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Staphylococci = catalase (positive); streptococci = catalase (negative)
STREPTOCOCCUS & ENTEROCOCCUS - PAIRS OR CHAINS
Most common streptococcal pathogens in humans are S. pyogenes, S. agalactiae, viridans group, and S. pneumoniae

LACTOBACILLALES(CAT-)

STREPTOCOCCUS
ALPHA
Optochin susceptible
S. pneumoniae (Pneumococcal infection)
Optochin resistant
Viridans streptococci : S. mitis S. mutans S. oralis S. sanguinis S. sobrinus S. anginosus group
BETA
A bacitracin susceptible
S. pyogenes (Group A streptococcal infection - Streptococcal pharyngitis - Scarlet fever - Erysipelas - Rheumatic fever)
B bacitracin resistant, CAMP test+
S. agalactiae (Group B streptococcal infection)
Ungrouped
Streptococcus iniae (Cutaneous Streptococcus iniae infection)
GAMMA
D BEA+ : Streptococcus bovis = gallolyticus

ENTEROCOCCUS
BEA+ : Enterococcus faecalis (Urinary tract infection) - Enterococcus faecium

SHARED STREPTOCOCCAL PROPERTIES
Gram-positive spherical or football-shaped cocci in pairs or chains
Catalase negative
Species-dependent hemolysis in blood agar
Lancefield classification - Groups based on serologic identification of group-specific C-carbohydrates on cell wall

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α PARTIAL HEMOLYSIS, GREEN

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(P DISK OPTOCHIN SENSTIVE & BILE SOLUBILITY) +
STREPTOCOCCUS PNEUMONIAE * (ENCAPSULATED) DIPLOIDS Football-shaped diplococcus
S. pneumoniae is normally present in the throat and nasopharynx
S. pneumoniae: α-hemolytic, capsule, gram-positive diplococci, meningitis, otitis media, P disk (Optochin) sensitive, polysaccharide vaccine, pneumonia

IDENTIFICATION
Strep pneumo; Optichin sensitive (P-disk; pneumoniae)
Quellung reaction indicates capsule on S. pneumoniae
PATHOGENESIS
PNEUMOCOCCAL DISEASES
S. pneumoniae and Haemophilus influenzae : most common bacterial causes of acute otitis media and sinusitis
S. pneumoniae, H.influenza, Neisseria meningitidis, and Cryptococcus neoformans (yeast) have capsules and cause meningitis
EPIDEMIOLOGY OF PNEUMOCOCCAL INFECTION
PREVENTION AND TREATMENT

DISEASES MC MOPS
Meningitis The capsule prolongs the bacteria’s presence in the blood and eventually reaches the meninges: meningitis
Otitis media
Acute bacterial Pneumonia CAP adults
Sinusitis
bacteremia
VIRULENCE FACTORS
Adhesins;
enzymes: immunoglobulin A protease, pneumolysin;
teichoic acid, peptidoglycan promotes inflammation through alternate C′ pathway and Toll-like receptors;
capsule
EPIDEMIOLOGY
Normal flora
PREVENTION
Anticapsular vaccine: 23 capsular polysaccharides or multiple (at least nine) polysaccharides conjugated to protein
TREATMENT
Penicillin, amoxicillin, fluoroquinolones, macrolides

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(OPTOCHIN & BILE SOLUBILITY) -
VIRIDANS STREP (NO CAPSULE)
S. mutans
Dental caries
Dental caries, subacute endocarditis, heart valve disease,
intraabdominal infections
S. mitis
Infective endocarditis
"OVRPS (overpass)"

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β COMPLETE HEMOLYSIS, CLEAR
(A DISK -GROUP A- BACITRACIN SENSITIVE & PYR) +
STREPTOCOCCUS PYOGENES * CHAINS or singly
S. pyogenes: Bacitracin (A disk-group A) sensitivity, β hemolysis, gram-positive cocci in chains, necrotizing fasciitis, pus, streptolysin O and S

IDENTIFICATION
PATHOGENESIS
GROUP A STREPTOCOCCAL DISEASES
S. pyogenes: causes pharyngitis, scarlet fever, toxic shock, rheumatic fever, acute glomerulonephritis
Group A streptococci must be treated to prevent sequelae
Sequelae of group A streptococci are rheumatic fever and acute glomerulonephritis
TRANSMISSION OF S. PYOGENES
TREATMENT
Group A streptococci are still sensitive to penicillin

ESSENTIAL FACTS
Serotypic different M proteins can determine different diseases.
Toxic shock syndrome is caused by a superantigen that binds MHC II to the T-cell receptor and nonspecifically activates a large amount of cytokine production, causing systemic symptoms
LAB ID
Catalase negative; β-hemolytic; bacitracin sensitive (A disk), rapid strep antigen tests, ASO titer for rheumatic fever
VIRULENCE FACTORS
S. pyogenes has most of the potential virulence mechanisms, including adherence, toxins (including superantigens), manipulation of the immune response, capsule, and degradative enzymes.
M protein: adhesion, antiphagocytic, degrades complement C3b
Capsule
Lipoteichoic acid binds to epithelial cells
F protein: adheres to epithelial cells
Streptolysins O and S: lyse leukocytes, platelets, and red blood cells
Streptokinase: lyses blood clots, promotes spread
Toxic shock toxin: superantigen
DISEASES
“Ph”yogenes pharyngitis can result in rheumatic “phever” and glomerulonephritis
Pyogenic
pharyngitis
cellulitis, impetigo (“honey-crusted” lesions)
erysipelas
Toxigenic
scarlet fever
toxic shock–like syndrome
necrotizing fasciitis
Immunologic
rheumatic fever
glomerulonephritis

Pharyngitis, scarlet fever, skin and tissue disease (impetigo,
erysipelas, cellulitis), necrotizing fasciitis, toxic shock syndrome;
postinfection sequelae: rheumatic fever, acute glomerulonephritis

Acute PHaryngitis or pharyngotonsillitis (Strep throat)
Acute rheumatic   PHever
Impetigo
- GlomerulonePHritis
Erysipelas
Puerperal sepsis
Invasive Group A Streptococcal (GAS) disease
- Necrotizing fasciitis/myositis
-"Flesh-eating bacteria."

EPIDEMIOLOGY
Ubiquitous, fomites, direct contact

TREATMENT
Penicillin, cephalosporin, erythromycin

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(BACITRACIN & PYR) -
GROUP "B" = GBS
S. agalactiae *

IDENTIFICATION
PATHOGENESIS
GROUP B STREPTOCOCCAL DISEASES
Group B streptococci acquired at birth cause bacteremia, pneumonia, and meningitis within first week
TREATMENT

Meningitis & Septicemia in Neonates "Babies"
Adults
- Endometritis
- Septicemia or pneumonia
in individuals with impaired immune systems
Diabetic foot infections

Neonatal group B streptococcal infection
– Early onset: neonatal meningitis, pneumonia, and
bacteremia (sepsis)
– Late onset: (1 week to 3 months) bacteremia with meningitis
Pregnant women: urinary tract infection (UTI), postpartum sepsis
Diabetics and individuals with compromised immune responses: bacteremia, pneumonia, bone and joint infections, skin and soft tissue infections
"B-BRAS"

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GROUP B STREPTOCOCCI & S. VIRIDANS

IDENTIFICATION
VIRIDANS STREPTOCOCCAL DISEASES
Viridans streptococci cause dental plaque, caries
Damaged heart valves are a risk factor for viridans strep endocarditis
TREATMENT OF STREPTOCOCCAL ENDOCARDITIS

Usually β-hemolytic
Causes disease in immune-deficient host
Usually normal flora in upper respiratory, lower gastrointestinal (GI), and urinary tracts. Colonizes 60% of newborns
Vaccine, special quarantine or disinfection procedures
Penicillin ± aminoglycoside

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γ NO HEMOLYSIS, GROWS IN BILEBILE

ENTEROCOCCUS
IDENTIFICATION
Enterococci grow in bowel and resistant to bowel conditions: bile and salt
ENTEROCOCCAL DISEASES
TREATMENT
Enterococci are inherently resistant to many antibiotics

(GROWTH 6.5% NaCl & PYR) +
Enterococcus * either α or γ  (previously Group D Strep)
E. faecium sometimes β
E. faecalis sometimes α UTI
Nosocomial infections

(GROWTH 6.5% NaCl & PYR) -
Nonenterococcus
Group D
S. bovis sometimes α = Streptococcus gallolyticus
"Bovis in the Blood = Cancer in the Colon"

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GRAM + BACILLI TOXIGENIC

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BACILLALES (CAT+)
STAPHYLOCOCCUS
BACILLUS
xxxxxxxxxxxxxxxxxxxxxxxxx
LISTERIA

CLOSTRIDIA

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GRAM-POSITIVE RODS BACILLI
SPORULATING
Bacillus (Aerobic) (Bacillales Catalase +)
anthracis (Cutaneous & Pulmonary)
cereus
Clostridia (tetani botulinum perfringens Clostridioides difficile) (Anaerobic)
NONSPORULATING
Corynebacterium diphtheriae (Aerobic)
Listeria monocytogenes (Aerobic) (Bacillales Catalase +)

Cutibacterium ( or microaerophilic) (formerly Propionibacterium acnes) (Anaerobic)
Lactobacillus (Aerobic)
Erysipelothrix rhusiopathiae (Aerobic)

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BACILLUS

BACILLUS ANTHRACIS *
Cutaneous anthrax
Pulmonary anthrax (woolsorter’s disease)
Gastrointestinal form

BACILLUS CEREUS
Food poisoning

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LISTERIA & RELATED GRAM-POSITIVE BACTERIA

LISTERIA MONOCYTOGENES *
(Listeriolysin)
Listeriosis

ERYSIPELOTHRIX RHUSIOPATHIAE

CORYNEBACTERIUM DIPHTHERIAE *
Diphtheria
ADP-ribosylation
β-prophage
Corynebacterium
Diphtheriae
Elongation Factor 2
Granules

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CLOSTRIDIUM Spore-Forming Anaerobic

CLOSTRIDIUM CLOSTRIDIOIDES DIFFICILE *
Pseudomembranous colitis DIarrhea

CLOSTRIDIUM PERFRINGENS * (Non Motile)
Myonecrosis (gas gangrene)
PERForates a gangrenous leg
Acute Food poisoning
Anaerobic cellulitis
(Necrotic enteritis
Clostridial endometritis)

CLOSTRIDIUM TETANI * (TetanoSPASmin)
Tetanus SPAStic paralysis

CLOSTRIDIUM BOTULINUM * BOTtles
Botulism (food poisoning)
& FLOPPY baby syndrome
FLACCID paralyis
Diplopia
Dysarthria
Dysphagia
Dyspnea

MYCOBACTERIUM & RELATED ACID-FAST BACTERIA

GRAM-POSITIVE BRANCHING ORGANISMS
Nocardia vs Actinomyces
MYCOBACTERIUM
Mycobacteria
Tuberculosis
Leprosy

GRAM + BRANCHING FILAMENTS RIGID FILAMENTOUS

AEROBIC Nocardia (weakly acid fast) Nocardia asteroides Nocardia brasiliensis

ANAEROBIC Actinomyces israelii (not acid fast)

SNAP Sulfonamides-Nocardia Actinomyces-Penicillin

GRAM-NEGATIVE LAB ALGORITHM

GRAM-NEGATIVE COCCI

GRAM - DIPLOCOCCI AEROBIC

MALTOSE ACID DETECTION + Neisseria meningitidis * MeninGococci Maltose & Glucose Meningitis - Meningococcemia - Purulent Waterhouse-Friderichsen syndrome

MALTOSE ACID DETECTION - Neisseria gonorrhoeae * Glucose GoNOcocci NO polysaccharide capsule NO maltose acid detection NO vaccine due to antigenic variation of pilus proteins Gonorrhea - Salpingitis  - PID Ophthalmia neonatorum Septic arthritis Moraxella catarrhalis Respiratory system, middle ear, eye, CNS, and joints.

Acinetobacter baumanii (Coccobacillus) Nosocomial (hospital-acquired)

Neisseria
GRAM-NEGATIVE RODS CAUSING RESPIRATORY AND MUCOSAL INFECTIONS
Haemophilus influenzae
Burkholderia cepacia complex
Acinetobacter baumannii
Bordetella pertussis
Legionella pneumophila
ENTERIC GRAM-NEGATIVE PSEUDOMONACEAE
Pseudomonas aeruginosa
ENTERIC GRAM-NEGATIVE RODS ENTEROBACTERIACEAE
Salmonella vs Shigella
Yersinia enterocolitica
Lactose-fermenting enteric bacteria (Citrobacter, E coli, Enterobacter, Klebsiella, Serratia)
Escherichia coli
Klebsiella
ENTERIC GRAM-NEGATIVE RODS VIBRIONACEAE
Campylobacter jejuni
Vibrio cholerae
Helicobacter pylori
SPIROCHETES Leptospira, Treponema, & Borrelia
Lyme disease
Leptospira interrogans
Syphilis
Diagnosing syphilis VDRL false positives
Jarisch-Herxheimer reaction
CHLAMYDIAE & RICKETTSIAE
Chlamydiae
Chlamydia trachomatis serotypes
Gardnerella vaginalis
Rickettsial diseases and vector-borne illnesses
MYCOPLASMA
Mycoplasma pneumoniae
ZOONOTIC BACTERIA
Brucella G-

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VIROLOGY
(Moi Virology) V1 PDF
(Moi Virus Classification) V1 PDF
(Moi Virus DNA RNA) V1 PDF
(Moi Hepatitis) V1 PDF
(Moi Retrovirus HIV Aids) V1 PDF

LABORATORY DIAGNOSIS OF VIRAL DISEASES
Microscopic Examination of Clinical Specimens
Viral Isolation (growth in tissue culture)
Laboratory Assays for Detecting Viral Proteins
Viral Nucleic Acids
Serology

Viral structure—general features
Viral genetics
Recombination
Reassortment
Complementation
Phenotypic mixing
DNA viral genomes
RNA viral genomes
Naked viral genome infectivity
Viral envelopes
CLASSIFICATION
DNA VIRUSES All replicate in the nucleus (except poxvirus). “Pox is out of the box (nucleus).”
DNA virus characteristics HHAPPPPy DS Linear genomes Icosahedral
Herpesvirus
Herpes Simplex Virus 1 (HSV-1) Cold Sores
Herpes Simplex Virus 2 (HSV-2) Genital
HSV identification
Varicella-Zoster Virus (HHV-3) (VZV, Chickenpox, Zoster, Shingles)
Epstein-Barr Virus (HHV-4) (EBV, Infectious Mononucleosis) LYMPHOME DE BURKITT
Cytomegalovirus (HHV-5) (CMV) Mononucleosis & Pneumonia
ROSEOLA Human Herpesviruses 6 and 7 (HHV-6, HHV-7, ROSEOLA) Sixth disease (roseola infantum or exanthem subitum)  ESANTEMA CRITICO O FEBBRE DEI TRE GIORNI
Human Herpesvirus 8 (HHV-8, KSHV or Kaposi Sarcoma–Associated Herpesvirus)
Receptors used by viruses
Poxvirus Complex Carries own DNA-dependent RNApolymerase
Smallpox (Variola) VAIOLO
Molluscum Contagiosum
Hepadnaviruses Circular Incomplete
Hepatitis B Virus, HBV
Adenoviruses
Papillomaviruses Circular Supercoiled
Human Papillomavirus
Polyomaviruses Circular Supercoiled
BK and JC viruses
Parvoviruses SS
Parvovirus B19
RNA VIRUSES All replicate in the cytoplasm (except retrovirus and influenza virus). “Retro flu is outta cyt (sight).”
POSITIVE (SINGLE)-STRANDED RNA VIRUSES—SS (+) RNA
Hepevirus
Hepatitis E (Enteric Hepatitis)
Picornavirus PicoRNAvirus = small RNA virus. PERCH on a “peak” (pico)
Polioviruses
Echovirus
Rhinovirus Rhino has a runny nose
Coxsackieviruses
Hepatitis A (HAV)
Flaviviruses
Hepatitis C (HCV, Infectious Hepatitis)
Matonavirus (Togaviruses)
RUBELLA (German Measles) three-day measles RUBEOLE 3EME MALADIE - ROSOLIA
Arboviruses transmitted by Aedes mosquitoes
Chikungunya virus Toga
Dengue virus Flavi
Yellow fever virus Flavi
Zika virus Flavi
Retroviruses
Human Immunodeficiency Virus (HIV)
HIV diagnosis
Time course of untreated HIV infection
Common diseases of HIV-positive adults
Caliciviruses
Coronaviruses
Severe acute respiratory syndrome coronavirus 2
NEGATIVE (SINGLE)-STRANDED RNA VIRUSES—SS (–) RNA  Always Bring Polymerase or Fail Replication
Paramyxoviridae Palivizumab for paramyxovirus (RSV) prophylaxis in preemies
Parainfluenza  Acute laryngotracheobronchitis
Respiratory Syncytial Virus
(RUBEOLA) MEASLES 4 C’s of measles: Cough Coryza Conjunctivitis “C”oplik spots ROUGEOLE - MORBILLO
Mumps Mumps makes your parotid glands and testes as big as POM-Poms
Orthomyxoviridae (Influenza A, B, and C Viruses)
Genetic/antigenic shift
Genetic/antigenicdrift
Rhabdoviridae (Rabies)
Filoviruses
Ebola
Bunyaviruses
Delta virus SS ⊝ circular HDV
Arenaviruses SS ⊕ and ⊝ circular 2 segments
DOUBLE-STRANDED RNA VIRUSES
Reoviruses
Rotavirus Rotavirus = right out the anus
Segmented viruses Bunyaviruses (3 segments), Orthomyxoviruses (influenza viruses) (8 segments), Arenaviruses (2 segments), and Reoviruses (10–12 segments)
HEPATITIS VIRUSES
Extrahepatic manifestations of hepatitis B and C
Hepatitis serologic markers

TOC
PRIONS
(Moi Prions) V1 PDF
Prions
Creutzfeldt-Jakob disease
Bovine spongiform encephalopathy
Kuru

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MYCOLOGY
(Moi Fungi) V1 PDF
(Moi Mycoses) V1 PDF
(Hawley BRS Mycology & Fungal Diseases) V1 PDF

SYSTEMIC MYCOSES (ENDEMIC)
Histoplasmosis
Blastomycosis
Coccidioidomycosis
Para-coccidioidomycosis
OPPORTUNISTIC FUNGAL INFECTIONS
Candida albicans
Aspergillus fumigatus
Cryptococcus neoformans
Mucor and Rhizopus spp
Pneumocystis jirovecii
SUBCUTANEOUS MYCOSES
Sporothrix schenckii
CUTANEOUS MYCOSES
Dermatophytes
Malassezia furfur

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PARASITOLOGY

TOC
PROTOZOA
(Moi Protozoa 1) V1 PDF
(Moi Protozoa 2) V1 PDF
(Hawley BRS Protozoan & Worms) V1 PDF

GASTROINTESTINAL INFECTIONS
Giardia lamblia
Entamoeba histolytica
Cryptosporidium
CNS INFECTIONS
Toxoplasma gondii
Naegleria fowleri
Trypanosoma brucei
HEMATOLOGIC INFECTIONS
Plasmodium
Babesia
VISCERAL INFECTIONS
Trypanosoma cruzi
Leishmania spp
SEXUALLY TRANSMITTED INFECTIONS
Trichomonas vaginalis

TOC
HELMINTHS
(Moi Helminths) V1 PDF

NEMATODES (ROUNDWORMS)
Nematode routes of infection
Intestinal
Enterobius vermicularis (pinworm)
Ascaris lumbricoides (giant roundworm)
Strongyloides stercoralis (threadworm)
Ancylostoma spp, Necator americanus (hookworms)
Trichinella spiralis
Trichuris trichiura (whipworm)
Tissue
Toxocara canis
Onchocerca volvulus
Loa loa
Wuchereria bancrofti, Brugia malayi
CESTODES (TAPEWORMS)
Taenia solium
Diphyllobothrium latum
Echinococcus granulosus
TREMATODES (FLUKES)
Schistosoma
Clonorchis sinensis
PARASITE HINTS

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ARTHROPODS & ECTOPARASITES
(Moi Ectoparasites) V1 PDF

ARACHNIDA
Ticks (Ixodida)
Mites
INSECTS
Lice (Anoplura)
Bugs (Heteroptera)
Mosquitoes and Flies (Diptera: Nematocera and Brachycera)
Fleas (Siphonatera)

Sarcoptes scabiei
Pediculus humanus and Phthirus pubis
Cimex lectularius and Climex hemipterus

TOC
SYSTEMS
(Moi Systems) V1 PDF
(Moi Systems italian) V1 PDF

NORMAL BACTERIAL FLORA
CONGENITAL AND PERINATAL INFECTIONS
DIARRHEAL DISEASES
FOOD POISONING AND WATERY DIARRHEA
BLOODY DIARRHEA AND PARASITE DIARRHEA
ENCEPHALITIS AND OTHER CNS DISEASES
MENINGITIS
IMMUNE DEFICIENCY DISEASES: INHERITED DISORDERS OF INNATE RESPONSE
IMMUNE DEFICIENCY DISEASES: PRIMARY LYMPHOCYTE IMMUNODEFICIENCIES
INFECTIONS ASSOCIATED WITH DEFECTS IN IMMUNE RESPONSES
OPPORTUNISTIC DISEASES IN AIDS
ORGAN SYSTEMS
LIVER DISEASES
MUSCLE, BONE, AND JOINT
OCULAR INFECTIONS
RESPIRATORY INFECTIONS
PNEUMONIA
SEXUALLY TRANSMITTED DISEASES
URINARY TRACT INFECTIONS
SKIN LESIONS AND RASHES
SKIN LESIONS AND RASHES: PART TWO
ZOONOSES AND ARTHROPOD-ASSOCIATED DISEASES

NORMAL FLORA: DOMINANT
BUGS CAUSING FOOD-BORNE ILLNESS
S aureus and B cereus food poisoning starts quickly and ends quickly
BUGS CAUSING DIARRHEA
Bloody diarrhea
Watery diarrhea
COMMON CAUSES OF PNEUMONIA
Special groups
COMMON CAUSES OF MENINGITIS
CEREBROSPINAL FLUID FINDINGS IN MENINGITIS
INFECTIONS CAUSING BRAIN ABSCESS
OSTEOMYELITIS
RED RASHES OF CHILDHOOD
Coxsackievirus type A
Human herpesvirus 6
Measles virus
Parvovirus B19
Rubella virus
Streptococcus pyogenes
Varicella-zoster virus
URINARY TRACT INFECTIONS
COMMON VAGINAL INFECTIONS
SEXUALLY TRANSMITTED INFECTIONS
TORCH INFECTIONS
PELVIC INFLAMMATORY DISEASE
NOSOCOMIAL INFECTIONS HEALTHCARE-ASSOCIATED INFECTIONS
BUGS AFFECTING UNVACCINATED CHILDREN
BUG HINTS

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ANTIMICROBIALS

ANTIBACTERIAL AGENTS
IMPORTANT TERMS

TOC
REFERENCES

DIDACTIC

Le. First Aid USMLE Step 1. Microbiology. 34e. 2024. 30e. 2020.
Le. First Aid Basic Sciences General Principles. Microbiology. 3e. 2017.
Gillespie. Medical Microbiology & Infection at a Glance. 4e. 2012. [ Download ] [ Resources ]
Cornelissen. LIR Microbiology. 4e. 2019. [ Download ]
Hawley. HY Microbiology & Infectious Diseases. 2e. 2006. [ Read 2e ] [ Read 1e ]
Hawley. BRS Microbiology & Immunology. 6e. 2013. [ 320 pages ] [ Download ] [ Read 6e ] [ Read 5e ]
Rosenthal. Medical Microbiology & Immunology Flash Cards. 2e. 2016. [ Download ] [ Download ] [ Download ]
Rosenthal. RR Microbiology & Immunology. 3e. 2010. [ 237 pages ] [ Download ]
Murray & Rosenthal. Medical Microbiology. 9e. 2020. [ 872 pages ] [ Download ] [ Download 8e ] [ Download ]
Murray. Murray's Basic Medical Microbiology : Foundations and Clinical Cases. 2e. 2023. [ 304 pages ]  [ Download ]
Gladwin. Clinical Microbiology Made Ridiculously Simple.
Harpavat. Microcards: Microbiology Flash Cards. [ Download ]
Somers. Lange Microbiology and Infectious Diseases Flash Cards. 3e. 2018. [ Download ]
Levinson. amazon.com/Review-Medical-Microbiology-Immunology-Seventeenth

Murray. Microbiologia medica. 9e. 2021. [ 872 pages ]

TOPICS

OVERVIEW
https://en.wikipedia.org/wiki/Medical_microbiology
https://en.wikipedia.org/wiki/Infection

BACTERIA
https://en.wikipedia.org/wiki/Staphylococcal_infection
https://en.wikipedia.org/wiki/Pathogenic_bacteria
https://en.wikipedia.org/wiki/Growth_medium

VIRUS
https://en.wikipedia.org/wiki/Viral_disease
https://en.wikipedia.org/wiki/Virus_classification

UNSORTED
microbiologyinfo.com/top-and-best-microbiology-books
Microbiologynutsandbolts.co.uk
http://www.nature.com/nrmicro/index.html
http://www.nature.com/nmicrobiol/
https://twitter.com/NatureRevMicro
http://www.microbiologynutsandbolts.co.uk/the-bug-blog/old-moania-double-pneumoniawhats-wrong-with-just-plain-pneumonia
http://www.microbiologynutsandbolts.co.uk/the-bug-blog/how-to-spit-polish-your-diagnosis
WayBack Machine (old version)

MORE REFERENCES

NEWS & UPDATES
WayBack Machine

GRAM - RODS Respiratory & Mucosal

Bartonella quintana Bartonella henselae (Zoonotic) HaEMOPhilus influenzae * (Coccobacillus) Epiglottitis Meningitis Otitis media Pneumonia Upper respiratory tract infections Sinusitis Haemophilus ducreyi Bordetella pertussis * (Coccobacillus) Pertussis (whooping cough) Catarrhal phase Coryza Paroxysmal phase “whooP” Bordetella parapertussis

Pasteurella multocida (Coccobacillus) Brucella  * (Zoonotic) (Coccobacillus) Brucella abortus Brucella canis Brucella melitensis Brucella suis Brucellosis UNdulant fever UNpasteurized milk Francisella tularensis * (Zoonotic) (Coccobacillus) Tularemia

Legionella pneumophila * Legionnaires disease Pontiac fever Yersinia pestis * (Zoonotic) Bubonic (septicemic) plague - Buboes Pneumonic plague Gardnerella vaginalis "I don’t have a clue why I smell fish in the vagina garden!"

GRAM - BACILLI LACTOSE FERMENTATION + "MacConKEY agar LACTOSE is KEY" Enteric

FAST Escherichia coli * Urinary tract infection (UTI) Diarrhea EnteroInvasive EIEC - Dysentery EnteroToxigenic ETEC (EnteroToxins) - "Traveler’s diarrhea" EnteroPathogenic EPEC - Pediatrics EnteroHemorrhagic EHEC O157:H7 Hamburgers - Dysentery - Hemorrhagic colitis - Hemolytic uremic syndrome (Shiga like toxin) Meningitis in infants Klebsiella pneumoniae Klebsiella oxytoca A aBscess in lungs and liver “Currant jelly” sputum Diabetes EtOH abuse Enterobacter

SLOW Citrobacter Serratia marcescens

GRAM - BACILLI LACTOSE FERMENTATION - Enteric

OXIDASE + PSEUDOMONACEAE (NON ENTERIC) Pseudomonas AER(obic)uginosa * Localized infections Systemic infections Pneumonia Sepsis Ecthyma gangrenosum UTIs Diabetes Osteomyelitis, Mucoid polysaccharide capsule Otitis externa  Nosocomial infections Addicts Skin infections

OXIDASE - H2S production on TSI agar + Salmonella enterica Serovars Enteritidis & Typhimurium * Enterocolitis (gastroenteritis, food poisoning) Salmonella enterica Serovar Typhi * Enteric (typhoid) fever & paratyphoid fever "Flagella Salmon Swim" Proteus mirabilis

OXIDASE - H2S production on TSI agar - Shigella sonnei * Shigella dysenteriae * (Shiga toxin) Shigella flexneri * Shigella boydii * Shigella : Bacillary dysentery (shigellosis) Fingers, Flies, Food, Feces Yersinia enterocolitica (Pleomorphic rod/coccobacillus) Yersiniosis (gastroenteritis) Septicemia Yersinia pseudotuberculosis

OTHER ENTEROBACTERIACEAE Morganella Edwardsiella Providencia

BACTEROIDIACEAE ANAEROBIC (ENTERIC) Bacteroides fragilis

Anaerobes : "Can’t - Clostridium G+ Breathe - Bacteroides G- Fresh - Fusobacterium G- Air - Actinomyces israelii G+ "

GRAM - CURVED RODS OXIDASE + VIBRIONACEAE

GROWS IN 42°C HOT CAMPfire CAMPylobacter jejuni * Acute enteritis - Traveler's diarrhea - Pseudoappendicitis Campylobacter fetus

GROWS IN ALKALINE MEDIA Vibrio cholerae * (Cholera toxin) Cholera - Rice-water stools Vibrio parahaemolyticus

PRODUCES UREASE Triple + : Catalase Oxidase Urease Helicobacter pylori * Acute gastritis - Duodenal & gastric ulcers - Gastric carcinoma & Gastric B-cell lymphoma

RIGID FILAMENTOUS MYCOBACTERIA (Poorly G +)

Mycobacterium tuberculosis * Tuberculosis

Mycobacterium leprae * Hansen disease (leprosy) - Tuberculoid - Lepromatous - - Leonine - - Lethal

Atypical Mycobacteria Mycobacterium abscessus Mycobacterium avium-intracellulare Mycobacterium bovis Mycobacterium chelonei Mycobacterium fortuitum Mycobacterium kansasii Mycobacterium marinum Mycobacterium scrofulaceum Mycobacterium ulcerans

LACKING CELL WALL MYCOPLASMA

Mycoplasma pneumoniae * Primary atypical pneumonia

Mycoplasma genitalium Mycoplasma hominis Ureaplasma urealyticum Genital

Mycoplasma incognitus

RIGID CELL WALL SIMPLE UNICELLULAR OBLIGATE INTRACELLULAR CHLAMYDIA Elementary Body (small, dense) is “Enfectious” & Enters cell via Endocytosis; transforms into RB Reticulate Body Replicates in cell by fission; Reorganizes into EB

Chlamydia pneumoniae * Community-acquired respiratory infection

Chlamydia psittaci * (Zoonotic) Psittacosis (ornithosis) Parrots Atypical Pneumonia

Chlamydia trachomatis * ABC = Africa, Blindness, Chronic infection Nongonococcal urethritis NGU D-K - PID Trachoma ABC - Chronic keratoconjunctivitis Inclusion conjunctivitis of the newborn ICN Lymphogranuloma venereum LGV L1 L2 L3

RIGID CELL WALL SIMPLE UNICELLULAR OBLIGATE INTRACELLULAR RICKETTSIA Obligate intracellular : Rickettsia, Chlamydia, Coxiella "Stay inside when it is Really CHilly and COld" Facultative intracellular : Salmonella, Neisseria, Brucella, Mycobacterium, Listeria, Francisella, Legionella, Yersinia pestis "Some Nasty Bugs May Live FacultativeLY"

Rickettsia rickettsii * Rocky Mountain spotted fever Rickettsii on the wRists

Rickettsia akari Rickettsia canadensis Rickettsia conorii Rickettsia sibirica Rickettsia prowazekii Rickettsia typhi Typhus on the Trunk

Ehrlichia chaffeensis Ehrlichia equi Monocytes Anaplasma phagocytophilum Neutrophils MEGA berry

Coxiella burnetii Q fever

FLEXIBLE SPIROCHETES "BLT Borrelia is Big"

Treponema pallidum * Syphilis - Chancre - Maculopapular rash - Condylomas - Syphilitic hepatitis,     meningitis, nephritis & chorioretinitis - Gummas Congenital VDRL false positives Jarisch-Herxheimer reaction Nonvenereal Treponemal Infections

Borrelia burgdorferi * Lyme disease Facial nerve palsy (typically bilateral) Arthritis Cardiac block Erythema migrans

Borrelia reccurrentis and other Borrelia species Relapsing fever

Leptospira interrogans * Leptospirosis  = Infectious jaundice, Marsh fever, Weil disease, Swineherd's disease

BACTERIAL INFECTIONS

FUNGI

GENERAL CHARACTERISTICS

MORPHOLOGY Yeast Filamentous

TRUE PATHOGENS

CUTANEOUS SUPERFICIAL DERMATOPHYTES Epidermophyton species Microsporum species Trichophyton species Malassezia furfur

SUBCUTANEOUS Phialophora & Cladosporium Chromomycosis Madurella grisea Mycetoma (“Madura foot”) Actinomadura madurae Sporothrix schenckii Sporotrichosis

SYSTEMIC ENDEMIC Blastomyces dermatitidis Coccidioides immitis Histoplasma capsulatum Paracoccidioides brasiliensis

OPPORTUNISTIC

Candida albicans Cryptococcus neoformans Aspergillus fumigatus Rhizopus oryzae (R. arrhizus) Pneumocystis jiroveci (formerly known as Pneumocystis carinii)

Absidia corymbifera Rhizomucor pusillus Microsporidia Mucor and Rhizopus

FUNGAL INFECTIONS MYCOSES

Superficial Skin

Cutaneous

Mucocutaneous Candidiasis

Subcutaneous

Pneumonias/Systemic

Opportunistic

Immunocompetent Non Systemic Symptoms

Immunocompetent Systemic Symptoms

Immunocompromised Symptoms

PROTOZOA

INTESTINAL Entamoeba histolytica (Ameba) Amebic dysentery Giardia lamblia (Flagellate) Giardiasis Cryptosporidium parvum, Cyclospora & Cystoisospora (Sporozoan) Cryptosporidiosis Balantidium coli (Ciliate) Balantidiasis

CNS Toxoplasma gondii (Sporozoan) Toxoplasmosis Naegleria fowleri (Ameba) Acanthamoeba castellanii (Ameba) Balamuthia mandrillaris (Ameba) Amebic encephalitis

HEMATOLOGIC Plasmodium species (Sporozoan) Malaria Babesia microti (Sporozoan) Babesiosis

VISCERAL Trypanosoma species (Flagellate) Trypanosomiasis Leishmania species (Flagellate) Leishmaniasis

SEXUALLY TRANSMITTED UROGENITAL Trichomonas vaginalis (Flagellate) Trichomoniasis

PROTOZOA INFECTIONS

HELMINTHS

Gut Tissues Nematode routes of infection Immune response to helminths Parasite hints

CESTODES (TAPEWORMS) FLAT SEGMENTED Diphyllobothrium latum (Broad fish tapeworm) Echinococcus granulosus (Dog tapeworm) Taenia saginata (Beef tapeworm) Taenia solium (Pork tapeworm)

TREMATODES (FLUKES) FLAT NONSEGMENTED Clonorchis sinensis (Chinese or Oriental liver fluke) Paragonimus westermani (Lung fluke) Schistosoma mansoni (Blood fluke) Schistosoma haematobium (Blood fluke) Schistosoma japonicum (Blood fluke)

NEMATODES (ROUNDWORMS) NON SEGMENTED INTESTINAL Ancylostoma duodenale Necator americanus (Old World and New World hookworms) Ascaris lumbricoides (Giant roundworm) Enterobius vermicularis (Pinworm) Strongyloides stercoralis (threadworm) Trichinella spiralis Trichuris trichiura (Whipworm)

NEMATODES (ROUNDWORMS) NON SEGMENTED TISSUE Brugia malayi Dracunculus medinensis (Guinea worm ) Loa loa (Filarial worm, or African eye worm) Onchocerca volvulus (Filarial worm) Toxocara canis (Dog worm) Wuchereria bancrofti (Filarial worm)

ARTHROPODES & ECTOPARASITES Sarcoptes scabiei Pediculus humanus / Phthirus pubis

VIRUSES

DNA NONENVELOPED SS LINEAR PARVOVIRIDAE Parvovirus B19 “PART-OF-A-VIRUS”

DNA NONENVELOPED DS CIRCULAR PAPOVAVIRIDAE PAPILLOMAVIRINAE Human Papillomavirus HPV * Hyperplastic epithelial lesions Cervical carcinoma Anogenital warts (condyloma acuminatum) Laryngeal papillomas Epidermodysplasia verruciformis Squamous cell carcinomas Common, flat, and plantar warts PAPOVAVIRIDAE POLYOMAVIRINAE BK virus JC virus "JC: Junky Cerebrum; BK: Bad Kidney"

DNA NONENVELOPED DS LINEAR ADENOVIRIDAE Adenoviruses * Respiratory tract diseases - Acute febrile pharyngitis Ocular diseases - Pharyngoconjunctival fever - Epidemic keratoconjunctivitis Gastrointestinal diseases - Infantile gastroenteritis

DNA ENVELOPED DS HERPESVIRIDAE ALPHAHERPESVIRINAE (herpes simplex group) Herpes Simplex Virus 1 * (HSV-1) Primary HSV-1 infections - Gingivostomatitis - Tonsillitis and pharyngitis - Keratoconjuctivitis - Encephalitis Latent HSV-1 infections - Herpes labialis - "Cold sores" or "fever blisters" Herpes Simplex Virus 2 * (HSV-2) Primary HSV-2 infections Latent HSV-2 infections Varicella-Zoster Virus * (VZV, Chickenpox, Zoster, Shingles) Varicella ("chickenpox") Zoster ("shingles")

DNA ENVELOPED DS HERPESVIRIDAE BETAHERPESVIRINAE  (cytomegalovirus group) Cytomegalovirus * (CMV) HCMV infectious mononucleosis Cytomegalic inclusion disease HCMV infection of immunosuppressed transplant recipients HCMV infection of AIDS patients Human Herpesviruses 6 and 7 (HHV-6, HHV-7, Roseola) = Exanthema subitum = Baby Measles Français = Roséole Italien = Sesta malattia

DNA ENVELOPED DS HERPESVIRIDAE GAMMAHERPESVIRINAE (lymphoproliferative group) Epstein-Barr Virus * (EBV, Infectious Mononucleosis) Infectious mononucleosis (IM) Association with Burkitt lymphoma and other human neoplastic diseases Human Herpesvirus 8 * (HHV-8, KSHV or Kaposi Sarcoma–Associated Herpesvirus)

DNA ENVELOPED DS POXVIRIDAE Smallpox (Variola) Virus Molluscum Contagiosum Virus   Vaccinia virus “Pox is out of the box (nucleus).” RNA viruses All replicate in the cytoplasm (except retrovirus and influenza virus). “Retro flu is outta cyt (sight).”

DNA ENVELOPED DS HEPADNAVIRIDAE Hepatitis B Virus * HBV Acute hepatitis Fulminant hepatitis Primary hepatocellular carcinomas (HCC; hepatomas)

RNA SS - CIRCULAR ENVELOPED Hepatitis D Virus (DELTA)

RNA SS + NONENVELOPED ICOSAHEDRAL CALICIVIRIDAE Hepatitis E Virus PICORNAVIRIDAE Hepatitis A Virus * Hepatitis A (“infectious hepatitis”)

RNA SS + ENVELOPED ICOSAHEDRAL FLAVIVIRIDAE Hepatitis C Virus * HCV Hepatitis C

RNA SS + NONENVELOPED ICOSAHEDRAL PICORNAVIRIDAE Enterovirus Coxsackievirus * Coxsackievirus infections Enterovirus Echovirus Enterovirus Poliovirus * Poliomyelitis - Flaccid paralysis - Respiratory paralysis Enterovirus Enterovirus Rhinovirus Hepatovirus Hepatitis A virus * - Hepatitis A (“infectious hepatitis”)

RNA SS + NONENVELOPED ICOSAHEDRAL CALICIVIRIDAE Hepatitis E virus Enteric Hepatitis Norwalk virus

RNA SS + ENVELOPED ICOSAHEDRAL TOGAVIRIDAE Alphavirus - Chikungunya virus - Eastern and Western equine encephalitis viruses - Venezuelan equine encephalitis virus Rubivirus - Rubella virus * - - German measles - - Congenital rubella Français = Rubéole Italien = Rosolia Spanish = Rubeola

RNA SS + ENVELOPED ICOSAHEDRAL FLAVIVIRIDAE Flavivirus - Dengue fever virus - Japanese encephalitis virus - St. Louis encephalitis virus - Tickborne encephalitis virus - West Nile virus - Yellow fever virus Hepatitis C virus Infectious Hepatitis

RNA SS + ENVELOPED ICOSAHEDRAL CORONAVIRIDAE Coronavirus

RETRO & AIDS RNA SS + ENVELOPED ICOSAHEDRAL RETROVIRIDAE Human immunodeficiency viruses 1 and 2 * - HIV infection - Acquired immune deficiency syndrome    (AIDS) Human T-cell lymphotropic viruses 1 and 2

RNA SS - HELICAL ENVELOPED RHABDOVIRIDAE Lyssavirus (rabies virus) * Rabies

RNA SS - HELICAL ENVELOPED PARAMYXOVIRIDAE PARAMYXOVIRINAE PARAMYXOVIRUS Human parainfluenza viruses types 1 & 3 * RUBULAVIRUS Human parainfluenza viruses types 2 & 4 * Parainfluenza virus 1 2 3 4 hPIV Respiratory tract infections croup, pneumonia, and bronchiolitis "common cold" Mumps virus * Mumps Français = Oreillons Italien = Parotite Epidemica Spanish = MORBILLIVIRUS Measles virus * Postinfectious encephalomyelitis Français = Rougeole Italien = Morbillo Spanish = Sarampión PARAMYXOVIRIDAE PNEUMOVIRINAE PNEUMOVIRUS Respiratory syncytial virus RSV * Respiratory tract infections Bronchiolitis Pneumonia Influenza-like syndrome Severe bronchitis with pneumonia

RNA SS - HELICAL ENVELOPED ORTHOMYXOVIRIDAE Influenza A B & C Viruses * Influenza (the "flu") Reye syndrome

RNA SS - HELICAL ENVELOPED FILOVIRIDAE Ebola virus Marburg virus

RNA SS - HELICAL ENVELOPED BUNYAVIRIDAE Bunyavirus California encephalitis virus LaCrosse encephalitis virus Hantavirus Hantaan viruses

RNA SS - HELICAL ENVELOPED ARENAVIRIDAE Lymphocytic chorio-meningitis virus Junin virus Machupo virus Lassa virus

DS RNA ENVELOPED ICOSAHEDRAL REOVIRIDAE “RepeatO-virus” Rotavirus "ROTAvirus = Right Out The Anus"

UNCONVENTIONAL AGENTS PRIONS

SYSTEMS

NORMAL FLORA

IMMUNOCOMPROMISED

OPPORTUNISTIC INFECTIONS OF HIV Mycobacterium avium complex Streptococcus pneumoniae Mycobacterium tuberculosis Salmonella species Candida species Histoplasma capsulatum Cryptococcus neoformans Pneumocystis jiroveci Cryptosporidium species Toxoplasma gondii Human herpesvirus type 8 (HHV-8) Herpes simplex virus (HSV) JC virus (JCV) Human cytomegalovirus (HCMV)

RESPIRATORY

COMMUNITY-ACQUIRED PNEUMONIA Streptococcus pneumoniae Haemophilus influenzae Staphylococcus aureus Influenza virus types A and B Parainfluenza viruses Respiratory syncytial virus

“ATYPICAL” PNEUMONIA Mycoplasma pneumoniae Chlamydia pneumoniae Legionella pneumophila Influenza viruses Respiratory syncytial virus (RSV) Adenovirus

SINUSITIS (BACTERIAL) Streptococcus pneumoniae Haemophilus influenzae Staphylococcus aureus Anaerobes Moraxella catarrhalis

CARDIOVASCULAR

BLOODSTREAM

GI

FOODBORNE ILLNESS (bacterial) Salmonella species Clostridium species Campylobacter jejuni Staphylococcus aureus Shigella species Vibrio species Escherichia coli

URINARY & REPRODUCTIVE

SEXUALLY TRANSMITTED DISEASES Chlamydia trachomatis Neisseria gonorrhoeae Treponema pallidum Ureaplasma urealyticum Haemophilus ducreyi Candida albicans Trichomonas vaginalis Herpes simplex virus type 2 (HSV-2) Human papillomavirus (HPV) Human cytomegalovirus (HCMV) Human immunodeficiency virus

URINARY TRACT INFECTIONS Escherichia coli Staphylococcus saprophyticus Other enterobacteria   Klebsiella species   Proteus species Pseudomonas aeruginosa

HEPATITIS Hepatitis B virus Hepatitis A virus Hepatitis C virus Hepatitis D virus Hepatitis E virus

BONES, JOINTS & SKIN

EYE AND EAR

DISEASES OF THE EYE Herpes simplex virus (HSV) Adenovirus Staphylococcus aureus Neisseria gonorrhoeae Chlamydia trachomatis

OTITIS MEDIA (ACUTE) Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis

NERVOUS

BACTERIAL MENINGITIS Streptococcus pneumoniae Neisseria meningitidis Haemophilus influenzae Streptococcus agalactiae Listeria monocytogenes

NOSOCOMIAL

CHILDREN

ZOONOTIC

ANTIMICROBIALS

ANTIBACTERIAL