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First_Aid_Step1. Antibodies bind to cell-surface antigens  cellular destruction, inflammation, and cellular dysfunction. Cellular destruction—cell is opsonized (coated) by antibodies, leading to either: Phagocytosis and/or activation of complement system. NK cell killing (antibody-dependent cellular cytotoxicity). Inflammation—binding of antibodies to cell surfaces  activation of complement system and Fc receptor-mediated inflammation. Cellular dysfunction—antibodies bind to cell surface receptors  abnormal blockade or activation of downstream process. Direct Coombs test—detects antibodies attached directly to the RBC surface. Indirect Coombs test—detects presence of unbound antibodies in the serum Examples: Hemolytic disease of the newborn Examples: Hyperacute transplant rejection Examples: Immune complex—antigen-antibody (mostly IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes.


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First_Aid_Step1. Examples: Hyperacute transplant rejection Examples: Immune complex—antigen-antibody (mostly IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes. Can be associated with vasculitis and systemic manifestations. Serum sickness—the prototypic immune complex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibody-antigen complexes form and deposit in tissues  complement activation • inflammation and tissue damage. Arthus reaction—a local subacute immune complex-mediated hypersensitivity reaction. Intradermal injection of antigen into a presensitized (has circulating IgG) individual leads to immune complex formation in the skin (eg, enhanced local reaction to a booster vaccination). Characterized by edema, necrosis, and activation of complement. In type III reaction, imagine an immune complex as 3 things stuck together: antigenantibody-complement. Examples:


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First_Aid_Step1. In type III reaction, imagine an immune complex as 3 things stuck together: antigenantibody-complement. Examples: Poststreptococcal glomerulonephritis Fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 1–2 weeks after antigen exposure. Serum sickness-like reactions are associated with some drugs (may act as haptens, eg, penicillin) and infections (eg, hepatitis B). Two mechanisms, each involving T cells: 1. Direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells. 2. Inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation-inducing cytokines (shown in illustration). Response does not involve antibodies (vs types I, II, and III). Examples: contact dermatitis (eg, poison ivy, nickel allergy) and graft-versus-host disease. Tests: PPD for TB infection; patch test for contact dermatitis; Candida skin test for T cell immune function. 4T’s: T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis).


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First_Aid_Step1. Tests: PPD for TB infection; patch test for contact dermatitis; Candida skin test for T cell immune function. 4T’s: T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis). Fourth (type) and last (delayed). Allergic/ Type I hypersensitivity Within minutes Allergies: urticaria, anaphylactic reaction against plasma to 2-3 hr (due to pruritus reaction proteins in transfused release of preformed Anaphylaxis: blood inflammatory wheezing, IgA-deficient individuals mediators in hypotension, should receive blood degranulating mast respiratory arrest, Donor plasma proteins, Host mast cell Acute Type II hypersensitivity During transfusion Fever, hypotension, hemolytic reaction or within 24 hr tachypnea, transfusion Typically causes (due to preformed tachycardia, reaction intravascular hemolysis antibodies) flank pain, Donor RBC with A and/ Host anti-A, anti-B IgG, incompatibility) (intravascular), jaundice (extravascular)


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First_Aid_Step1. Donor RBC with A and/ Host anti-A, anti-B IgG, incompatibility) (intravascular), jaundice (extravascular) Febrile Cytokines created by Within 1-6 hr (due Fever, headaches, nonhemolytic donor WBCs accumulate to preformed chills, flushing transfusion during storage of blood cytokines) More common in reaction products children Donor WBC releases Reactions prevented by leukoreduction of blood products Respiratory distress, noncardiogenic pulmonary edema Generally self limited and clinically silent Mild fever, hyperbilirubinemia Donor RBC with Host IgG foreign antigens Antinuclear (ANA) Nonspecific screening antibody, often associated with SLE Anticardiolipin, lupus anticoagulant SLE, antiphospholipid syndrome Anti-dsDNA, anti-Smith SLE Antisynthetase (eg, anti-Jo-1), anti-SRP, anti-Polymyositis, dermatomyositis helicase (anti-Mi-2) IgA anti-endomysial, IgA anti-tissue Celiac disease transglutaminase, IgA and IgG deamidated gliadin peptide


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First_Aid_Step1. IgA anti-endomysial, IgA anti-tissue Celiac disease transglutaminase, IgA and IgG deamidated gliadin peptide Anti-glutamic acid decarboxylase, islet cell Type 1 diabetes mellitus cytoplasmic antibodies Antiparietal cell, anti-intrinsic factor Pernicious anemia Ataxia-telangiectasia A Defects in ATM gene  failure to detect DNA damage  failure to halt progression of cell cycle mutations accumulate; autosomal recessive Triad: cerebellar defects (Ataxia), spider Angiomas (telangiectasia A ), IgA deficiency  sensitivity to radiation (limit x-ray exposure) AFP  IgA, IgG, and IgE Lymphopenia, cerebellar atrophy  risk of lymphoma and leukemia Hyper-IgM syndrome Most commonly due to defective CD40L on Th cells  class switching defect; X-linked recessive Severe pyogenic infections early in life; opportunistic infection with Pneumocystis, Cryptosporidium, CMV Normal or  IgM  IgG, IgA, IgE Failure to make germinal centers


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First_Aid_Step1. Defect in lysosomal trafficking PLAIN: Progressive Giant granules ( B , arrows) in regulator gene (LYST) neurodegeneration, granulocytes and platelets. Microtubule dysfunction in Lymphohistiocytosis, Pancytopenia phagosome-lysosome fusion; Albinism (partial), recurrent Mild coagulation defects autosomal recessive pyogenic Infections, Bacteria Sepsis Encapsulated (Please SHINE my SKiS): Pseudomonas aeruginosa, Streptococcus pneumoniae, Haemophilus Influenzae type b, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, Group B Streptococcus Some Bacteria Encapsulated Produce No species with early Serious granules: complement Staphylococcus, deficiencies Burkholderia cepacia, Neisseria with late Pseudomonas complement (C5– aeruginosa, Nocardia, C9) deficiencies Serratia Viruses CMV, EBV, JC Enteroviral N/A N/A virus, VZV, chronic encephalitis, infection with poliovirus respiratory/GI viruses (live vaccine


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First_Aid_Step1. Viruses CMV, EBV, JC Enteroviral N/A N/A virus, VZV, chronic encephalitis, infection with poliovirus respiratory/GI viruses (live vaccine Fungi/parasites Candida (local), PCP, GI giardiasis (no IgA) Candida (systemic), N/A Cryptococcus Aspergillus, Mucor Note: B-cell deficiencies tend to produce recurrent bacterial infections, whereas T-cell deficiencies produce more fungal and viral infections.


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First_Aid_Step1. Hyperacute A Within minutes Pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction), activate complement Widespread thrombosis of graft vessels (arrows within glomerulus A ) ischemia/necrosis Graft must be removed Acute B Weeks to months Cellular: CD8+ T cells and/ or CD4+ T cells activated against donor MHCs (type IV hypersensitivity reaction) Humoral: similar to hyperacute, except antibodies develop after transplant Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate B Prevent/reverse with immunosuppressants Chronic C Months to years CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC Both cellular and humoral components (type II and IV hypersensitivity reactions) Recipient T cells react and secrete cytokines proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis Dominated by arteriosclerosis C Organ-specific examples: Chronic allograft nephropathy


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First_Aid_Step1. and secrete cytokines proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis Dominated by arteriosclerosis C Organ-specific examples: Chronic allograft nephropathy Bronchiolitis obliterans Accelerated atherosclerosis (heart) Vanishing bile duct syndrome Graft-versus-host disease Varies Grafted immunocompetent T cells proliferate in the Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly reject host cells with “foreign”


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First_Aid_Step1. For immunocompromised patients, irradiate blood products prior to transfusion to prevent GVHD Immunosuppressants Agents that block lymphocyte activation and proliferation. Reduce acute transplant rejection by suppressing cellular immunity (used as prophylaxis). Frequently combined to achieve greater efficacy with  toxicity. Chronic suppression  risk of infection and malignancy. Cyclosporine Calcineurin inhibitor; Psoriasis, rheumatoid Nephrotoxicity, binds cyclophilin arthritis hypertension, Blocks T-cell activation hyperlipidemia, by preventing IL-2 neurotoxicity, gingival transcription hyperplasia, hirsutism Tacrolimus (FK506) Calcineurin inhibitor; Similar to cyclosporine, binds FK506 binding  risk of diabetes protein (FKBP) and neurotoxicity; Blocks T-cell activation no gingival by preventing IL-2 hyperplasia or transcription hirsutism Both calcineurin inhibitors are highly nephrotoxic, especially in higher doses or in patients with decreased renal function


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First_Aid_Step1. Both calcineurin inhibitors are highly nephrotoxic, especially in higher doses or in patients with decreased renal function Sirolimus (Rapamycin) mTOR inhibitor; binds “PanSirtopenia” Kidney “sir-vives.” FKBP (pancytopenia), Synergistic with Blocks T-cell insulin resistance, cyclosporine Basiliximab Monoclonal antibody; Edema, hypertension, blocks IL-2R tremor Azathioprine Antimetabolite Rheumatoid arthritis, Pancytopenia 6-MP degraded by precursor of Crohn disease, xanthine oxidase; 6-mercaptopurine glomerulonephritis, toxicity  by Mycophenolate Reversibly inhibits Lupus nephritis GI upset, Associated with Mofetil IMP dehydrogenase, pancytopenia, invasive CMV preventing purine hypertension, infection synthesis of B and T hyperglycemia cells Less nephrotoxic and  transcription of


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First_Aid_Step1. Mofetil IMP dehydrogenase, pancytopenia, invasive CMV preventing purine hypertension, infection synthesis of B and T hyperglycemia cells Less nephrotoxic and  transcription of Many autoimmune and inflammatory disorders, adrenal insufficiency, asthma, CLL, non-Hodgkin lymphoma Cushing syndrome, osteoporosis, hyperglycemia, diabetes, amenorrhea, adrenocortical atrophy, peptic ulcers, psychosis, cataracts, avascular necrosis (femoral head) Demargination of WBCs causes artificial leukocytosis Adrenal insufficiency may develop if drug is stopped abruptly after chronic use “Support bacteria. They’re the only culture some people have.” “What lies behind us and what lies ahead of us are tiny matters compared to what lies within us.” —Henry S. Haskins “Infectious disease is merely a disagreeable instance of a widely prevalent tendency of all living creatures to save themselves the bother of building, by their own efforts, the things they require.”


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First_Aid_Step1. Microbiology questions on the Step 1 exam often require two (or more) steps: Given a certain clinical presentation, you will first need to identify the most likely causative organism, and you will then need to provide an answer regarding some features of that organism or relevant antimicrobial agents. For example, a description of a child with fever and a petechial rash will be followed by a question that reads, “From what site does the responsible organism usually enter the blood?” This section therefore presents organisms in two major ways: in individual microbial “profiles” and in the context of the systems they infect and the clinical presentations they produce. You should become familiar with both formats. When reviewing the systems approach, remind yourself of the features of each microbe by returning to the individual profiles. Also be sure to memorize the laboratory characteristics that allow you to identify microbes.


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First_Aid_Step1. Flagellum Proteins Motility Pilus/fimbria Glycoprotein Mediate adherence of bacteria to cell surface; sex pilus forms during conjugation Spore Keratin-like coat; dipicolinic acid; Gram ⊕ only peptidoglycan, DNA Survival: resist dehydration, heat, chemicals Capsule Discrete layer usually made of polysaccharides Protects against phagocytosis (and rarely proteins) Slime (S) layer Loose network of polysaccharides Mediates adherence to surfaces, especially foreign surfaces (eg, indwelling catheters) Outer membrane Outer leaflet: contains endotoxin (LPS/LOS) Gram ⊝ only Embedded proteins: porins and other outer Endotoxin: lipid A induces TNF and IL-1; membrane proteins (OMPs) antigenic O polysaccharide component Inner leaflet: phospholipids Most OMPs are antigenic Porins: transport across outer membrane


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First_Aid_Step1. Periplasm Space between cytoplasmic membrane Accumulates components exiting gram and outer membrane in gram ⊝ bacterial ⊝ cells, including hydrolytic enzymes (peptidoglycan in middle) (eg, β-lactamases) Cell wall Peptidoglycan is a sugar backbone with peptide Net-like structure gives rigid support, protects side chains cross-linked by transpeptidase against osmotic pressure damage Cytoplasmic Phospholipid bilayer sac with embedded Site of oxidative and transport enzymes; PBPs membrane proteins (eg, penicillin-binding proteins involved in cell wall synthesis [PBPs]) and other enzymes Lipoteichoic acids induce TNF-α and IL-1 Lipoteichoic acids (gram positive) only extend from membrane to exterior


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First_Aid_Step1. Gram stain 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 Mycoplasma, Ureaplasma No cell wall India ink stain Cryptococcus neoformans D ; mucicarmine can also be used to stain thick polysaccharide capsule red Silver stain Fungi (eg, Coccidioides E , Pneumocystis jirovecii), Legionella, Helicobacter pylori Properties of growth media The same type of media can possess both (or neither) of these properties. Selective media Favors the growth of particular organism while preventing growth of other organisms. Example: Thayer-Martin agar contains antibiotics that allow the selective growth of Neisseria by inhibiting the growth of other sensitive organisms.


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First_Aid_Step1. Aerobes Use an O2-dependent system to generate ATP. Examples include Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis, and Bordetella pertussis. Reactivation of M tuberculosis (eg, after immunocompromise or TNF-α inhibitor use) has a predilection for the apices of the lung. Anaerobes Examples include Clostridium, Bacteroides, Fusobacterium, and Actinomyces israelii. They lack catalase and/or superoxide dismutase and 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 Can’t Breathe Fresh Air. Anaerobes are normal flora in GI tract, typically pathogenic elsewhere. AminO2glycosides are ineffective against anaerobes because these antibiotics require O2 to enter into bacterial cell.


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First_Aid_Step1. Anaerobes are normal flora in GI tract, typically pathogenic elsewhere. AminO2glycosides are ineffective against anaerobes because these antibiotics require O2 to enter into bacterial cell. Examples are Pseudomonas aeruginosa, Streptococcus pneumoniae A , Haemophilus influenzae type b, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, and group B Strep. Their capsules serve as an antiphagocytic virulence factor. Capsular polysaccharide + protein conjugate serves as an antigen in vaccines. Please SHiNE my SKiS. 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: Some vaccines containing polysaccharide capsule antigens are conjugated to a carrier protein, enhancing immunogenicity by promoting T-cell activation and subsequent class switching. A polysaccharide antigen alone cannot be presented to T cells.


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First_Aid_Step1. Pneumococcal vaccines: PCV13 (pneumococcal conjugate vaccine), PPSV23 (pneumococcal polysaccharide vaccine with no conjugated protein). H influenzae type b (conjugate vaccine). Meningococcal vaccine (conjugate vaccine). Catalase-positive Catalase degrades H2O2 into H2O and bubbles of O2 A before it can be converted to microbicidal organisms products by the enzyme myeloperoxidase. People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with certain catalase ⊕ organisms. Examples: Nocardia, Staphylococci, Serratia, Candida, Listeria, E coli, Burkholderia cepacia, Pseudomonas, Aspergillus, Helicobacter pylori, Bordetella pertussis. 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


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First_Aid_Step1. P aeruginosa Respiratory tree colonization in patients with cystic fibrosis, ventilator-associated pneumonia Contact lens–associated keratitis Some gram ⊕ bacteria can form spores A when nutrients are limited. Spores lack metabolic activity and are highly resistant to heat and chemicals. Core contains dipicolinic acid. Must autoclave to kill spores (as is done to surgical equipment) by steaming at 121°C for 15 minutes. Examples: B anthracis (anthrax), B cereus (food poisoning), C botulinum (botulism), C difficile (pseudomembranous colitis), C perfringens (gas gangrene), C tetani (tetanus). Bacterial virulence factors These promote evasion of host immune response. pieces of environmental naked bacterial chromosomal DNA (from bacterial cell lysis). The transfer and expression of newly transferred genes is called transformation. A feature of many bacteria, especially S pneumoniae, Hinfluenzae type b, and Neisseria (SHiN).


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First_Aid_Step1. Adding deoxyribonuclease degrades naked DNA, preventing transformation. into bacterial DNA of part of the chromosome bacterial chromosomal DNA, termed high- frequency recombination (Hfr) cell. Transfer of leading part of plasmid and a few flanking F+ cell F– cell Hfr cellF– cell Hfr cell F– cell Hfr cell Recombinant chromosomal genes. High-frequency recombination may integrate some of those bacterial genes. Recipient cell remains F– but now may have new bacterial genes. Generalized A packaging “error.” Lytic phage infects Cleavage of Bacterial DNA packaged bacterium, leading to cleavage of bacterial phage DNA. Parts of bacterial chromosomal DNA may become packaged in phage capsid. Phage infects another bacterium, transferring these genes. Release of new phage Infects other Genes transferred from lysed cell bacteria to new bacteria


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First_Aid_Step1. Release of new phage Infects other Genes transferred from lysed cell bacteria to new bacteria Specialized An “excision” event. Lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome. When phage DNA is excised, flanking bacterial genes may be excised with it. DNA is packaged into phage capsid and can infect another bacterium. Genes for the following 5 bacterial toxins are encoded in a lysogenic phage (ABCD’S): Group A strep erythrogenic toxin, Botulinum toxin, Cholera toxin, Diphtheria toxin, Shiga toxin. Release of new phage Infects other Genes di˜erent from from lysed cell bacteria donor and recipient (specialized segment of DNA), which can copy and excise itself and then insert into the same DNA molecule or an unrelated DNA (eg, Integration of genes Transposon plasmid or chromosome). Critical in creating plasmids with multiple drug resistance and DNA transfer across species lines (eg, Tn1546 with vanA from Enterococcus to S aureus).


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First_Aid_Step1. Main features of exotoxins and endotoxins Bacteria with exotoxins Downstream cellular reaction Exotoxin TNF, IL-1, IL-6 Host cell Endotoxin Toxin prevents release of inhibitory (GABA and glycine) neurotransmitters from Renshaw cells in spinal cord  spastic paralysis, risus sardonicus, trismus (lockjaw) Toxin prevents release of stimulatory (ACh) signals at neuromuscular junction  flaccid paralysis (floppy baby) aAn AB toxin (aka, two-component toxin [or three for anthrax]) with B enabling binding and triggering uptake (endocytosis) of the active A component. The A components are usually ADP ribosyltransferases; others have enzymatic activities as listed in chart. Bacteria with exotoxins (continued) Clostridium Alpha toxin Phospholipase (lecithinase) Degradation of phospholipids  myonecrosis perfringens that degrades tissue and (“gas gangrene”) and hemolysis (“double zone” cell membranes of hemolysis on blood agar)


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First_Aid_Step1. Streptococcus Streptolysin O Protein that degrades cell Lyses RBCs; contributes to β-hemolysis; pyogenes membrane host antibodies against toxin (ASO) used to diagnose rheumatic fever (do not confuse with immune complexes of poststreptococcal glomerulonephritis) Cross-links β region of TCR to MHC class II on APCs outside of the antigen binding site  overwhelming release of IL-1, IL-2, IFN-γ, and TNF-α • shock Toxic shock syndrome: fever, rash, shock; other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (heat-stable enterotoxin) Toxic shock–like syndrome: fever, rash, shock; scarlet fever


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First_Aid_Step1. Toxic shock–like syndrome: fever, rash, shock; scarlet fever Endotoxin LPS found in outer membrane of gram ⊝ bacteria (both cocci and rods). Composed of O antigen + core polysaccharide + lipid A (the toxic component). 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. ENDOTOXINS: 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 IL-1, IL-6 Fever Fever and hypotension HypotensionNitric oxide TNF-α hemolysis, hemolysis, Important tests are in bold. Important pathogens are in bold italics. Note: Enterococcus is either ˜or °-hemolytic. (No hemolysis, grows in bile) Novobiocin sensitivity


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First_Aid_Step1. Important tests are in bold. Important pathogens are in bold italics. Note: Enterococcus is either ˜or °-hemolytic. (No hemolysis, grows in bile) Novobiocin sensitivity Growth in 6.5% NaCl and PYR Status -hemolytic bacteria Gram ⊕ cocci. Partial oxidation of hemoglobin causes greenish or brownish color without clearing around growth on blood agar A . Include the following organisms: -hemolytic bacteria Gram ⊕ cocci. Complete lysis of RBCs  pale/clear area surrounding colony on blood agar A . Include the following organisms: Gram ⊕, β-hemolytic, catalase ⊕, coagulase ⊕ cocci in clusters A . Protein A (virulence factor) binds Fc-IgG, inhibiting complement activation and phagocytosis. Commonly colonizes the nares, ears, axilla, and groin. Causes: Inflammatory disease—skin infections, organ abscesses, pneumonia (often after influenza virus infection), endocarditis, septic arthritis, and osteomyelitis.


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First_Aid_Step1. Causes: Inflammatory disease—skin infections, organ abscesses, pneumonia (often after influenza virus infection), endocarditis, septic arthritis, and osteomyelitis. Toxin-mediated disease—toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin), rapid-onset food poisoning (enterotoxins). MRSA (methicillin-resistant S aureus)— important cause of serious nosocomial and community-acquired infections; resistance due to altered penicillin-binding protein. mecA gene from staphylococcal chromosomal cassette involved in penicillin resistance. TSST-1 is a superantigen that binds to MHC II and T-cell receptor, resulting in polyclonal T-cell activation and cytokine release. Staphylococcal toxic shock syndrome (TSS)— fever, vomiting, rash, desquamation, shock, end-organ failure. TSS results in  AST, • ALT,  bilirubin. Associated with prolonged use of vaginal tampons or nasal packing.


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First_Aid_Step1. Compare with Streptococcus pyogenes TSS (a toxic shock–like syndrome associated with painful skin infection). S aureus food poisoning due to ingestion of preformed toxin  short incubation period (2–6 hr) followed by nonbloody diarrhea and emesis. Enterotoxin is heat stable  not destroyed by cooking. S aureus makes coagulase and toxins. Forms fibrin clot around itself  abscess. Gram ⊕, catalase ⊕, coagulase ⊝, urease ⊕ cocci in clusters. Novobiocin sensitive. Does not ferment mannitol (vs S aureus). Normal flora of skin; contaminates blood cultures. Infects prosthetic devices (eg, hip implant, heart valve) and IV catheters by producing adherent biofilms. Staphylococcus Gram ⊕, catalase ⊕, coagulase ⊝, urease ⊕ cocci in clusters. Novobiocin resistant. saprophyticus Normal flora of female genital tract and perineum. Second most common cause of uncomplicated UTI in young women (most common is E coli). Gram ⊕, α-hemolytic, lancet-shaped diplococci


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First_Aid_Step1. Second most common cause of uncomplicated UTI in young women (most common is E coli). Gram ⊕, α-hemolytic, lancet-shaped diplococci A . Encapsulated. IgA protease. Optochin sensitive and bile soluble. Most commonly causes: Pneumococcus is associated with “rusty” sputum, sepsis in patients with sickle cell disease, and asplenic patients. No virulence without capsule. Gram ⊕, α-hemolytic cocci. Optochin resistant and bile insoluble. Normal flora of the oropharynx. Streptococcus mutans and S mitis cause dental caries. S sanguinis makes dextrans that bind to fibrin-platelet aggregates on damaged heart valves, causing subacute bacterial endocarditis. Viridans group strep live in the mouth, because they are not afraid of-the-chin (op-to-chin resistant). Sanguinis = blood. Think, “there is lots of blood in the heart” (endocarditis). Gram ⊕ cocci in chains A . Group A strep cause: Pyogenic—pharyngitis, cellulitis, impetigo (“honey-crusted” lesions), erysipelas


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First_Aid_Step1. Gram ⊕ cocci in chains A . Group A strep cause: Pyogenic—pharyngitis, cellulitis, impetigo (“honey-crusted” lesions), erysipelas Toxigenic—scarlet fever, toxic shock–like syndrome, necrotizing fasciitis Immunologic—rheumatic fever, glomerulonephritis Bacitracin sensitive, β-hemolytic, pyrrolidonyl arylamidase (PYR) ⊕. Hyaluronic acid capsule and M protein inhibit phagocytosis. Antibodies to M protein enhance host defenses against S pyogenes but can give rise to rheumatic fever. ASO titer or anti-DNase B antibodies indicate recent S pyogenes infection. “Ph”yogenes pharyngitis can result in rheumatic “phever” and glomerulonephritis. Strains causing impetigo can induce glomerulonephritis. Scarlet fever—blanching, sandpaper-like body rash, strawberry tongue, and circumoral pallor in the setting of group A streptococcal pharyngitis (erythrogenic toxin ⊕).


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First_Aid_Step1. Scarlet fever—blanching, sandpaper-like body rash, strawberry tongue, and circumoral pallor in the setting of group A streptococcal pharyngitis (erythrogenic toxin ⊕). Bacillus anthracis Gram ⊕, spore-forming rod that produces anthrax toxin (an exotoxin consisting of protective antigen, lethal factor, and edema factor). Has a polypeptide capsule (poly d-glutamate). Colonies show a halo of projections, sometimes referred to as “medusa head” appearance. Cutaneous anthrax Painless papule surrounded by vesicles  ulcer with black eschar A (painless, necrotic)  uncommonly progresses to bacteremia and death. Pulmonary anthrax Inhalation of spores, most commonly from contaminated animals or animal products, although also a potential bioweapon  flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis (CXR may show widened mediastinum), and shock. Also called woolsorter’s disease.


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First_Aid_Step1. Gram ⊕ cocci, bacitracin resistant, β-hemolytic, colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies. Produces CAMP factor, which enlarges the area of hemolysis formed by S aureus. (Note: CAMP stands for the authors of the test, not cyclic AMP.) Hippurate test ⊕. PYR ⊝. Screen pregnant women at 35–37 weeks of gestation with rectal and vaginal swabs. Patients with ⊕ culture receive intrapartum penicillin/ampicillin prophylaxis. Bacillus cereus Gram ⊕ rod. Causes food poisoning. Spores survive cooking rice (reheated rice syndrome). Keeping rice warm results in germination of spores and enterotoxin formation. Emetic type causes nausea and vomiting within 1–5 hours. Caused by cereulide, a preformed toxin. Diarrheal type causes watery, nonbloody diarrhea and GI pain within 8–18 hours. Management: supportive care (antibiotics are ineffective against toxins).


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First_Aid_Step1. Clostridia Gram ⊕, spore-forming, obligate anaerobic rods. Tetanus toxin and botulinum toxin are proteases that cleave SNARE proteins involved in neurotransmission. Clostridium tetani Produces tetanospasmin, an exotoxin causing Tetanus is tetanic paralysis. tetanus. Tetanospasmin blocks release of GABA and glycine from Renshaw cells in spinal cord. Causes spastic paralysis, trismus (lockjaw), risus sardonicus (raised eyebrows and open grin), opisthotonos (spasms of spinal extensors). Prevent with tetanus vaccine. Treat with antitoxin +/− vaccine booster, antibiotics, diazepam (for muscle spasms), and wound debridement. Produces a heat-labile toxin that inhibits ACh release at the neuromuscular junction, causing botulism. In adults, disease is caused by ingestion of preformed toxin. In babies, ingestion of spores (eg, in honey) leads to disease (floppy baby syndrome). Treat with human botulinum immunoglobulin.


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First_Aid_Step1. Symptoms of botulism (the 4 D’s): Diplopia, Dysarthria, Dysphagia, Dyspnea. Botulinum is from bad bottles of food, juice, and honey (causes a descending flaccid paralysis). Local botulinum toxin A (Botox) injections used to treat focal dystonia, hyperhidrosis, muscle spasms, and cosmetic reduction of facial wrinkles. Produces α-toxin (lecithinase, a phospholipase) that can cause myonecrosis (gas gangrene A ; presents as soft tissue crepitus) and hemolysis. If heavily spore-contaminated food is cooked but left standing too long at < 60°C, spores germinate • vegetative bacteria • heat-labile enterotoxin • food poisoning symptoms in 10-12 hours, resolution in 24 hours. Perfringens perforates a gangrenous leg. Produces toxins A and B, which damage enterocytes. Both toxins lead to watery diarrhea B . Often 2° to antibiotic use, especially clindamycin or ampicillin; associated with PPIs.


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First_Aid_Step1. Produces toxins A and B, which damage enterocytes. Both toxins lead to watery diarrhea B . Often 2° to antibiotic use, especially clindamycin or ampicillin; associated with PPIs. Diagnosed by PCR or antigen detection of one or both toxins in stool. Complications: toxic megacolon. Difficile causes diarrhea. Treatment: oral vancomycin, metronidazole, or fidaxomicin. For recurrent cases, consider repeating prior regimen or fecal microbiota transplant. Gram ⊕ rods occurring in angular arrangements; transmitted via respiratory droplets. Causes diphtheria via exotoxin encoded by β-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2, leading to possible necrosis in pharynx, cardiac, and CNS tissue. Symptoms include pseudomembranous pharyngitis (grayish-white membrane A ) with lymphadenopathy. Toxin dissemination may cause myocarditis, arrhythmias, neuropathies.


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First_Aid_Step1. Symptoms include pseudomembranous pharyngitis (grayish-white membrane A ) with lymphadenopathy. Toxin dissemination may cause myocarditis, arrhythmias, neuropathies. Lab diagnosis based on gram ⊕ rods with metachromatic (blue and red) granules and ⊕ Elek test for toxin. Toxoid vaccine prevents diphtheria. on Löffler media). Black colonies on cystine-tellurite agar. ABCDEFG: Elongation Factor 2 Granules Treatment: antibiotic therapy +/– diphtheria antitoxin. Gram ⊕, facultative intracellular rod; acquired by ingestion of unpasteurized dairy products and cold deli meats, transplacental transmission, by vaginal transmission during birth. Grows well at refrigeration temperatures (“cold enrichment”). Forms “rocket tails” (red in A ) via actin polymerization that allow intracellular movement and cell-to-cell spread across cell membranes, thereby avoiding antibody. Characteristic tumbling motility in broth.


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First_Aid_Step1. Can cause amnionitis, septicemia, and spontaneous abortion in pregnant women; granulomatosis infantiseptica; meningitis in immunocompromised patients, neonates, and older adults; mild, self-limited gastroenteritis in healthy individuals. Treatment: ampicillin. Nocardia vs Both are gram ⊕ and form long, branching filaments resembling fungi. Actinomyces Found in soil Normal oral, reproductive, and GI flora Causes pulmonary infections in Causes oral/facial abscesses that drain through immunocompromised (can mimic TB but sinus tracts; often associated with dental caries/ with ⊝ PPD); cutaneous infections after extraction and other maxillofacial trauma; trauma in immunocompetent; can spread to forms yellow “sulfur granules”; can also cause CNS PID with IUDs Treat with sulfonamides (TMP-SMX) Treat with penicillin Treatment is a SNAP: Sulfonamides—Nocardia; Actinomyces—Penicillin


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First_Aid_Step1. Treat with sulfonamides (TMP-SMX) Treat with penicillin Treatment is a SNAP: Sulfonamides—Nocardia; Actinomyces—Penicillin Gram ⊕ acid fast rods (pink rods, arrows in A ). Mycobacterium tuberculosis (TB, often resistant to multiple drugs). M avium–intracellulare (causes disseminated, non-TB disease in AIDS; often resistant to multiple drugs). Prophylaxis with azithromycin when CD4+ count < 50 cells/ mm . M scrofulaceum (cervical lymphadenitis in children). M marinum (hand infection in aquarium handlers). TB symptoms include fever, night sweats, weight loss, cough (nonproductive or productive), hemoptysis. Cord factor creates a “serpentine cord” appearance in virulent M tuberculosis strains; activates macrophages (promoting granuloma formation) and induces release of TNF-α. Sulfatides (surface glycolipids) inhibit phagolysosomal fusion.


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First_Aid_Step1. Healing by fbrosis Progressive primary tuberculosis Calcifcation (AIDS, malnutrition) (PPD false positives from BCG vaccination. PPD ⊕ if current infection or past exposure. PPD ⊝ if no infection and in sarcoidosis or HIV infection (especially with low CD4+ cell count). Caseating granulomas with central necrosis and Langhans giant cell (single example in A ) are characteristic of 2° tuberculosis. Leprosy Also called Hansen disease. Caused by Mycobacterium leprae, an acid-fast bacillus that likes cool temperatures (infects skin and superficial nerves—“glove and stocking” loss of sensation A ) and cannot be grown in vitro. Diagnosed via skin biopsy or tissue PCR. Reservoir in United States: armadillos. Leprosy has 2 forms (many cases fall temporarily between two extremes):


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First_Aid_Step1. Lepromatous—presents diffusely over the skin, with Leonine (Lion-like) facies B , and is communicable (high bacterial load); characterized by low cell-mediated immunity with a largely Th2 response. Lepromatous form can be Lethal. Tuberculoid—limited to a few hypoesthetic, hairless skin plaques; characterized by high cell- mediated immunity with a largely Th1-type response and low bacterial load. Treatment: dapsone and rifampin for tuberculoid form; clofazimine is added for lepromatous form. Important tests are in bold. Important pathogens are in bold italics. aPleomorphic rod/coccobacillus Neisseria Gram ⊝ diplococci. Metabolize glucose Acid production: MeninGococci—Maltose and and produce IgA proteases. Contain Glucose; Gonococci—Glucose. lipooligosaccharides (LOS) with strong endotoxin activity. N gonorrhoeae is often intracellular (within neutrophils) A . No vaccine due to antigenic variation of pilus Vaccine (type B vaccine available for at-risk proteins individuals)


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First_Aid_Step1. A . No vaccine due to antigenic variation of pilus Vaccine (type B vaccine available for at-risk proteins individuals) Causes gonorrhea, septic arthritis, neonatal Causes meningococcemia with petechial conjunctivitis (2–5 days after birth), pelvic hemorrhages and gangrene of toes B , inflammatory disease (PID), and Fitz-Hugh– meningitis, Waterhouse-Friderichsen Curtis syndrome syndrome (adrenal insufficiency, fever, DIC, Diagnosed with NAT Diagnosed via culture-based tests or PCR Condoms  sexual transmission, erythromycin Rifampin, ciprofloxacin, or ceftriaxone eye ointment prevents neonatal blindness prophylaxis in close contacts Treatment: ceftriaxone (+ azithromycin Treatment: ceftriaxone or penicillin G or doxycycline, for possible chlamydial coinfection)


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First_Aid_Step1. Treatment: ceftriaxone (+ azithromycin Treatment: ceftriaxone or penicillin G or doxycycline, for possible chlamydial coinfection) Small gram ⊝ (coccobacillary) rod. Aerosol transmission. Nontypeable (unencapsulated) strains are the most common cause of mucosal infections (otitis media, conjunctivitis, bronchitis) as well as invasive infections since the vaccine for capsular type b was introduced. Produces IgA protease. Culture on chocolate agar, which contains factors V (NAD+) and X (hematin) for growth; can also be grown with S aureus, which provides factor V via RBC hemolysis. A , can be “cherry red” in children; “thumb sign” on lateral neck x-ray B ), Meningitis, Otitis media, and Pneumonia. Vaccine contains type b capsular polysaccharide (polyribosylribitol phosphate) conjugated to diphtheria toxoid or other protein. Given between 2 and 18 months of age. Does not cause the flu (influenza virus does).


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First_Aid_Step1. Does not cause the flu (influenza virus does). Treatment: amoxicillin +/− clavulanate for mucosal infections; ceftriaxone for meningitis; rifampin prophylaxis for close contacts. Acinetobacter Gram ⊝, strictly aerobic, oxidase ⊝ coccobacillus. Commensal opportunist but increasingly baumannii associated with resistant hospital-acquired infections, especially in ICU. Can cause ventilator-associated pneumonia and septicemia in immunocompromised patients. Gram ⊝ rod. Gram stains poorly—use silver stain. Grow on charcoal yeast extract medium with iron and cysteine. Detected by presence of antigen in urine. Labs may show hyponatremia. Aerosol transmission from environmental water source habitat (eg, air conditioning systems, hot water tanks). No person-to-person transmission. Treatment: macrolide or quinolone. Gram ⊝, aerobic coccobacillus. Virulence factors include pertussis toxin (disables Gi), adenylate cyclase toxin ( cAMP), and tracheal cytotoxin. Three clinical stages:


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First_Aid_Step1. Gram ⊝, aerobic coccobacillus. Virulence factors include pertussis toxin (disables Gi), adenylate cyclase toxin ( cAMP), and tracheal cytotoxin. Three clinical stages: Catarrhal—low-grade fevers, Coryza. Paroxysmal—paroxysms of intense cough followed by inspiratory “whooP” (“whooping cough”), posttussive vomiting. Convalescent—gradual recovery of chronic cough. Prevented by Tdap, DTaP vaccines. May be mistaken as viral infection due to lymphocytic infiltrate resulting from immune response. Treatment: macrolides; if allergic use TMP-SMX. Gram ⊝, aerobic coccobacillus. Transmitted via ingestion of contaminated animal products (eg, unpasteurized milk). Survives in macrophages in the reticuloendothelial system. Can form noncaseating granulomas. Typically presents with undulant fever, night sweats, and arthralgia. Treatment: doxycycline + rifampin or streptomycin.


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First_Aid_Step1. Treatment: doxycycline + rifampin or streptomycin. Think of a French legionnaire (soldier) with his silver helmet, sitting around a campfire (charcoal) with his iron dagger—he is no sissy (cysteine). Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in chronic lung disease. Pontiac fever—mild flu-like syndrome. Aeruginosa—aerobic; motile, catalase ⊕, gram ⊝ rod. Non-lactose fermenting. Oxidase ⊕. Frequently found in water. Has a grape-like odor. PSEUDOMONAS is associated with: Pneumonia, Sepsis, Ecthyma gangrenosum, UTIs, Diabetes, Osteomyelitis, Mucoid polysaccharide capsule, Otitis externa (swimmer’s ear), Nosocomial infections (eg, catheters, equipment), Addicts (drug abusers), Skin infections (eg, hot tub folliculitis, wound infection in burn victims). Mucoid polysaccharide capsule may contribute to chronic pneumonia in cystic fibrosis patients due to biofilm formation.


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First_Aid_Step1. Mucoid polysaccharide capsule may contribute to chronic pneumonia in cystic fibrosis patients due to biofilm formation. Produces PEEP: Phospholipase C (degrades cell membranes); Endotoxin (fever, shock); Exotoxin A (inactivates EF-2); Pigments: pyoverdine and pyocyanin (blue-green pigment A ; also generates reactive oxygen species). Corneal ulcers/keratitis in contact lens wearers/ minor eye trauma. Ecthyma gangrenosum—rapidly progressive, necrotic cutaneous lesion B caused by Pseudomonas bacteremia. Typically seen in immunocompromised patients. Treatments include “CAMPFIRE” drugs: Polymyxins (eg, polymyxin B, colistin) Fluoroquinolones (eg, ciprofloxacin, levofloxacin) ThIRdand fourth-generation cephalosporins (eg, ceftazidime, cefepime) Extended-spectrum penicillins (eg, piperacillin, ticarcillin)


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First_Aid_Step1. Fluoroquinolones (eg, ciprofloxacin, levofloxacin) ThIRdand fourth-generation cephalosporins (eg, ceftazidime, cefepime) Extended-spectrum penicillins (eg, piperacillin, ticarcillin) Yersinia enterocolitica Gram ⊝ pleomorphic rod/coccobacillus. Usually transmitted from pet feces (eg, puppies), contaminated milk, or pork. Can cause acute bloody diarrhea, pseudoappendicitis (right lower abdominal pain due to mesenteric adenitis and/or terminal ileitis), reactive arthritis in adults. Gram ⊝ rod; intestinal flora that causes lobar pneumonia in alcoholics and diabetics when aspirated. Very mucoid colonies A caused by abundant polysaccharide capsules. Dark red “currant jelly” sputum (blood/mucus). Also cause of nosocomial UTIs. Associated with evolution of multidrug resistance (MDR). ABCDE’s of Klebsiella: Aspiration pneumonia aBscess in lungs and liver “Currant jelly” sputum Diabetes EtOH abuse


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First_Aid_Step1. ABCDE’s of Klebsiella: Aspiration pneumonia aBscess in lungs and liver “Currant jelly” sputum Diabetes EtOH abuse Campylobacter jejuni Gram ⊝, comma or S shaped (with polar flagella) A , oxidase ⊕, grows at 42°C (“Campylobacter likes the hot campfire”). Major cause of bloody diarrhea, especially in children. Fecal-oral transmission through person-to-person contact or via ingestion of undercooked contaminated poultry or meat, unpasteurized milk. Contact with infected animals (dogs, cats, pigs) is also a risk factor. Common antecedent to Guillain-Barré syndrome and reactive arthritis.


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First_Aid_Step1. Common antecedent to Guillain-Barré syndrome and reactive arthritis. Vibrio cholerae Gram ⊝, flagellated, comma shaped A , oxidase ⊕, grows in alkaline media. Endemic to developing countries. Produces profuse rice-water diarrhea via enterotoxin that permanently activates Gs,  cAMP. Sensitive to stomach acid (acid labile); requires large inoculum (high ID50) unless host has  gastric acidity. Transmitted via ingestion of contaminated water or uncooked food (eg, raw shellfish). Treat promptly with oral rehydration solution. Curved, flagellated (motile), gram ⊝ rod A that is triple ⊕: catalase ⊕, oxidase ⊕, and urease ⊕ (can use urea breath test or fecal antigen test for diagnosis). Urease produces ammonia, creating an alkaline environment, which helps H pylori survive in acidic mucosa. Colonizes mainly antrum of stomach; causes gastritis and peptic ulcers (especially duodenal). Risk factor for peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma.


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First_Aid_Step1. Most common initial treatment is triple therapy: Amoxicillin (metronidazole if penicillin allergy) + Clarithromycin + Proton pump inhibitor; Antibiotics Cure Pylori. Bismuth-based quadruple therapy if concerned about macrolide resistance. Jarisch-Herxheimer Flu-like syndrome (fever, chills, headache, myalgia) after antibiotics are started; due to killed reaction bacteria (usually spirochetes) releasing toxins. Chlamydiae cannot make their own ATP. They are obligate intracellular organisms that cause mucosal infections. 2 forms: Elementary body (small, dense) is “Enfectious” and Enters cell via Endocytosis; transforms into reticulate body. Reticulate body Replicates in cell by fission; Reorganizes into elementary bodies. A , nongonococcal urethritis, PID, and reactive arthritis. Chlamydophila pneumoniae and Chlamydophila psittaci cause atypical pneumonia; transmitted by aerosol.


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First_Aid_Step1. A , nongonococcal urethritis, PID, and reactive arthritis. Chlamydophila pneumoniae and Chlamydophila psittaci cause atypical pneumonia; transmitted by aerosol. Chlamydial cell wall lacks classic peptidoglycan (due to reduced muramic acid), rendering β-lactam antibiotics ineffective. Chlamys = cloak (intracellular). C psittaci—has an avian reservoir (parrots), causes atypical pneumonia. Lab diagnosis: PCR, nucleic acid amplification test. Cytoplasmic inclusions (reticulate bodies) seen on Giemsa or fluorescent antibody– stained smear. Treatment: azithromycin (favored because one-time treatment) or doxycycline. Add ceftriaxone for possible concomitant gonorrhea. Rickettsial diseases and vector-borne illnesses Treatment: doxycycline. Rickettsia rickettsii, vector is tick. Despite its name, disease occurs primarily in the South Atlantic states, especially North Carolina. Rash typically starts at wrists A and ankles and then spreads to trunk, palms, and soles.


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First_Aid_Step1. Classic triad—headache, fever, rash (vasculitis). Palms and soles rash is seen in Coxsackievirus A infection (hand, foot, and mouth disease), Rocky Mountain spotted fever, and 2° Syphilis (you drive CARS using your palms and soles). Q fever is caused by a Quite Complicated Bug because it has no rash or vector and its causative organism can survive outside in its endospore form. Not in the Rickettsia genus, but closely related. Classic cause of atypical “walking pneumonia” (insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate). Occurs frequently in those <30 years old; outbreaks in military recruits, prisons, colleges. X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate RBCs. Treatment: macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since Mycoplasma has no cell wall). Not seen on Gram stain. Pleomorphic A . Bacterial membrane contains sterols for stability. Grown on Eaton agar.


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First_Aid_Step1. Not seen on Gram stain. Pleomorphic A . Bacterial membrane contains sterols for stability. Grown on Eaton agar. Mycoplasma gets cold without a coat (no cell wall). Can cause atypical variant of Stevens-Johnson syndrome, typically in children and adolescents. Mississippi and Ohio Macrophage filled River Valleys with Histoplasma (smaller than RBC) Eastern and Central Broad-based budding US, Great Lakes of Blastomyces (same size as RBC) Southwestern US, Spherule (much larger California than RBC) filled with endospores of Coccidioides Latin America Budding yeast of Paracoccidioides with “captain’s wheel” formation (much larger than RBC) Palatal/tongue ulcers, splenomegaly, pancytopenia Disseminates to bone/ skin (may mimic SCC) Disseminates to skin/ bone Similar to blastomycosis, males > females Histo hides (within macrophages) Associated with bird or bat droppings (eg, spelunking) Associated with dust exposure in endemic areas (eg, archeological excavations, earthquakes)


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First_Aid_Step1. Associated with bird or bat droppings (eg, spelunking) Associated with dust exposure in endemic areas (eg, archeological excavations, earthquakes) Paracoccidio parasails with the captain’s wheel all the way to Latin America alba = white. Dimorphic; forms pseudohyphae and budding yeasts at 20°C A , germ tubes at 37°C B . Systemic or superficial fungal infection. Causes oral C and esophageal thrush in immunocompromised (neonates, steroids, diabetes, AIDS), vulvovaginitis (diabetes, use of antibiotics), diaper rash, endocarditis (IV drug users), disseminated candidiasis (especially in neutropenic patients), chronic mucocutaneous candidiasis. Treatment: oral fluconazole/topical azoles for vaginal; nystatin, azoles, or, rarely, echinocandins for oral; fluconazole, echinocandins, or amphotericin B for esophageal or systemic disease. E . 5–10 μm with narrow budding. Heavily encapsulated yeast. Not dimorphic.


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First_Aid_Step1. E . 5–10 μm with narrow budding. Heavily encapsulated yeast. Not dimorphic. Found in soil, pigeon droppings. Acquired through inhalation with hematogenous dissemination to meninges. Highlighted with India ink (clear halo G ) and mucicarmine (red inner capsule H ). Latex agglutination test detects polysaccharide capsular antigen and is more sensitive and specific. Causes cryptococcosis, cryptococcal meningitis, cryptococcal encephalitis (“soap bubble” lesions in brain), primarily in immunocompromised. Treatment: amphotericin B + flucytosine followed by fluconazole for cryptococcal meningitis. Irregular, broad, nonseptate hyphae branching at wide angles I .


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First_Aid_Step1. Treatment: amphotericin B + flucytosine followed by fluconazole for cryptococcal meningitis. Irregular, broad, nonseptate hyphae branching at wide angles I . Causes mucormycosis, mostly in ketoacidotic diabetic and/or neutropenic patients (eg, leukemia). Inhalation of spores  fungi proliferate in blood vessel walls, penetrate cribriform plate, and enter brain. Rhinocerebral, frontal lobe abscess; cavernous sinus thrombosis. Headache, facial pain, black necrotic eschar on face J ; may have cranial nerve involvement. Treatment: surgical debridement, amphotericin B or isavuconazole.


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First_Aid_Step1. Treatment: surgical debridement, amphotericin B or isavuconazole. Pneumocystis jirovecii Causes Pneumocystis pneumonia (PCP), a diffuse interstitial pneumonia A . Yeast-like fungus (originally classified as protozoan). Most infections are asymptomatic. Immunosuppression (eg, AIDS) predisposes to disease. Diffuse, bilateral ground-glass opacities on chest imaging, with pneumatoceles B . Diagnosed by bronchoalveolar lavage or lung biopsy. Disc-shaped yeast seen on methenamine silver stain of lung tissue C or with fluorescent antibody. Treatment/prophylaxis: TMP-SMX, pentamidine, dapsone (prophylaxis as single agent, or treatment in combination with TMP), atovaquone. Start prophylaxis when CD4+ count drops to < 200 cells/mm3 in HIV patients.


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First_Aid_Step1. Causes sporotrichosis. Dimorphic fungus. Exists as a cigar-shaped yeast at 37 ºC in the human body and as hyphae with spores in soil (conidia). Lives on vegetation. When spores are traumatically introduced into the skin, typically by a thorn (“rose gardener’s disease”), causes local pustule or ulcer with nodules along draining lymphatics (ascending lymphangitis A ). Disseminated disease possible in immunocompromised host. Treatment: itraconazole or potassium iodide (only for cutaneous/lymphocutaneous). Think of a rose gardener who smokes a cigar and pot. Toxoplasma Immunocompetent: gondii mononucleosis-like symptoms, ⊝ heterophile antibody test Reactivation in AIDS  brain abscesses usually seen as multiple ring-enhancing lesions on MRI A Congenital toxoplasmosis: classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications Cysts in meat (most Serology, biopsy Sulfadiazine + common); oocysts (tachyzoite)


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First_Aid_Step1. Plasmodium P vivax/ovale P falciparum P malariae A B Malaria—fever, headache, anemia, splenomegaly P vivax/ovale—48-hr cycle (tertian; includes fever on first day and third day, thus fevers are actually 48 hr apart); dormant form (hypnozoite) in liver P falciparum—severe; irregular fever patterns; parasitized RBCs occlude capillaries in brain (cerebral malaria), kidneys, lungs P malariae—72-hr cycle (quartan) Anopheles mosquito Blood smear: trophozoite ring form within RBC A , schizont containing merozoites; red granules (Schüffner stippling) B throughout RBC cytoplasm seen with P vivax/ovale Chloroquine (for sensitive species); if resistant, use mefloquine or atovaquone/ proguanil If life-threatening, use intravenous quinidine or artesunate (test for G6PD deficiency) For P vivax/ovale, add primaquine for hypnozoite (test for G6PD deficiency) Babesia C Babesiosis—fever and hemolytic anemia; predominantly in northeastern United States; asplenia  risk of severe disease Ixodes tick


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First_Aid_Step1. add primaquine for hypnozoite (test for G6PD deficiency) Babesia C Babesiosis—fever and hemolytic anemia; predominantly in northeastern United States; asplenia  risk of severe disease Ixodes tick (also vector for Borrelia burgdorferi and Anaplasma spp) Blood smear: ring form C1 , “Maltese cross” C2 ; PCR Atovaquone + azithromycin


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First_Aid_Step1. Intestinal tapeworm Ingestion of larvae encysted in Praziquantel undercooked pork Cysticercosis, Ingestion of eggs in food Praziquantel; albendazole for neurocysticercosis (cystic contaminated with human neurocysticercosis CNS lesions, seizures) D (“eggshell Ingestion of eggs in food Albendazole calcification”) in liver E ; cyst contaminated with dog feces rupture can cause anaphylaxis Sheep are an intermediate host Liver and spleen enlargement (S mansoni, egg with lateral spine A ), fibrosis, inflammation, portal hypertension Chronic infection with S haematobium (egg with terminal spine B ) can lead to squamous cell carcinoma of the bladder (painless hematuria) and pulmonary hypertension Snails are intermediate host; Praziquantel cercariae penetrate skin of humans in contact with contaminated fresh water (eg, swimming or bathing) Associated with cholangiocarcinoma


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First_Aid_Step1. Associated with cholangiocarcinoma Sarcoptes scabiei Mites burrow into stratum corneum and Common in children, crowded populations cause scabies—pruritus (worse at night) and (jails, nursing homes); transmission through serpiginous burrows (lines) often between skin-to-skin contact (most common) or via fingers and toes A . fomites. Treatment: permethrin cream, washing/drying all clothing/bedding, treat close contacts. Pediculus humanus/ Blood-sucking lice that cause intense pruritus Phthirus pubis with associated excoriations, commonly on scalp and neck (head lice), waistband and axilla (body lice), or pubic and perianal regions (pubic lice). Body lice can transmit Rickettsia prowazekii (epidemic typhus), Borrelia recurrentis (relapsing fever), Bartonella quintana (trench fever). Treatment: pyrethroids, malathion, or ivermectin lotion, and nit B combing. Children with head lice can be treated at home without interrupting school attendance.


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First_Aid_Step1. Treatment: pyrethroids, malathion, or ivermectin lotion, and nit B combing. Children with head lice can be treated at home without interrupting school attendance. Biliary tract disease, cholangiocarcinoma Clonorchis sinensis Brain cysts, seizures Taenia solium (neurocysticercosis) Naked virus Enveloped virus Enveloped virus Bacteriophage with icosahedral capsid with icosahedral capsid with helical capsid Generally, enveloped viruses acquire their envelopes from plasma membrane when they exit from cell. Exceptions include herpesviruses, which acquire envelopes from nuclear membrane. Naked (nonenveloped) viruses include Papillomavirus, Adenovirus, Parvovirus, Polyomavirus, Calicivirus, Picornavirus, Reovirus, and Hepevirus. Purified nucleic acids of most dsDNA viruses (except poxviruses and HBV) and ⊕ strand ssRNA (≈ mRNA) viruses are infectious. Naked nucleic acids of ⊝ strand ssRNA and dsRNA viruses are not infectious. They require polymerases contained in the complete virion.


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First_Aid_Step1. DNA = PAPP; RNA = CPR and hepevirus. Give PAPP smears and CPR to a naked hippie (hepevirus). Enveloped DNA viruses Have Helpful Protection (Herpesvirus, Hepadnavirus, Poxvirus). Some general rules—all DNA viruses: DNA viruses All replicate in the nucleus (except poxvirus). “Pox is out of the box (nucleus).” Papillomavirus No DS and circular HPV–warts (serotypes 1, 2, 6, 11), CIN, cervical cancer (most commonly 16, 18) (PML) in HIV BK virus—transplant patients, commonly targets kidney JC: Junky Cerebrum; BK: Bad Kidney Parvovirus No SS and linear B19 virus—aplastic crises in sickle cell disease, (smallest DNA virus) “slapped cheek” rash in children (erythema infectiosum, or fifth disease); infects RBC precursors and endothelial cells  RBC destruction • hydrops fetalis and death in fetus, pure RBC aplasia and rheumatoid arthritis–like symptoms in adults Herpesviruses Enveloped, DS, and linear viruses


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First_Aid_Step1. Herpesviruses Enveloped, DS, and linear viruses Herpes Respiratory Gingivostomatitis, keratoconjunctivitis A , Most commonly latent in trigeminal simplex secretions, saliva herpes labialis (cold sores) B , herpetic ganglia virus-1 whitlow on finger, temporal lobe encephalitis, Most common cause of sporadic esophagitis, erythema multiforme encephalitis, can present as altered mental status, seizures, and/or aphasia Herpes Sexual contact, Herpes genitalis C , neonatal herpes Most commonly latent in sacral simplex perinatal ganglia virus-2 Viral meningitis more common with HSV-2 than with HSV-1 Varicella-Respiratory Varicella-zoster (chickenpox D , shingles E ), Latent in dorsal root or trigeminal Zoster virus secretions, encephalitis, pneumonia ganglia; CN V1 branch (HHV-3) contact with fluid Most common complication of shingles is post-involvement can cause herpes Epstein-Barr Respiratory virus (HHV-4) secretions, saliva; aka “kissing disease,” (common in teens, young adults)


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First_Aid_Step1. Epstein-Barr Respiratory virus (HHV-4) secretions, saliva; aka “kissing disease,” (common in teens, young adults) Mononucleosis—fever, hepatosplenomegaly F , pharyngitis, and lymphadenopathy (especially posterior cervical nodes); avoid contact sports until resolution due to risk of splenic rupture Associated with lymphomas (eg, endemic Burkitt lymphoma), nasopharyngeal carcinoma (especially Asian adults), lymphoproliferative disease in transplant patients Infects B cells through CD21, “Must be 21 to drink Beer in a Barr” ⊕ Monospot test—heterophile antibodies detected by agglutination of sheep or horse RBCs Use of amoxicillin in mononucleosis can cause characteristic maculopapular rash HSV identification Viral culture for skin/genitalia. CSF PCR for herpes encephalitis. Tzanck test—a smear of an opened skin vesicle to detect multinucleated giant cells A commonly seen in HSV-1, HSV-2, and VZV infection. PCR of skin lesions is test of choice. Tzanck heavens I do not have herpes.


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First_Aid_Step1. Tzanck heavens I do not have herpes. Intranuclear eosinophilic Cowdry A inclusions also seen with HSV-1, HSV-2, VZV. HIV CD4, CXCR4, CCR5 Rhinovirus ICAM-1 (I came to see the rhino) RNA viruses All replicate in the cytoplasm (except retrovirus and influenza virus). “Retro flu is outta cyt (sight).” SS, single-stranded; DS, double-stranded; ⊕, positive sense; ⊝, negative sense; a= arbovirus, arthropod borne (mosquitoes, ticks). Influenza viruses Orthomyxoviruses. Enveloped, ⊝ ssRNA viruses with 8-segment genome. Contain hemagglutinin (binds sialic acid and promotes viral entry) and neuraminidase (promotes progeny virion release) antigens. Patients at risk for fatal bacterial superinfection, most commonly S aureus, S pneumoniae, and H influenzae. Reformulated vaccine (“the flu shot”) contains viral strains most likely to appear during the flu season, due to the virus’ rapid genetic change. Killed viral vaccine is most frequently used.


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First_Aid_Step1. Reformulated vaccine (“the flu shot”) contains viral strains most likely to appear during the flu season, due to the virus’ rapid genetic change. Killed viral vaccine is most frequently used. Live attenuated vaccine contains temperature-sensitive mutant that replicates in the nose but not in the lung; administered intranasally. Treatment: supportive +/– neuraminidase inhibitor (eg, oseltamivir, zanamivir). Rubella virus A togavirus. Causes rubella, once known as German (3-day) measles. Fever, postauricular and other lymphadenopathy, arthralgias, and fine, maculopapular rash that starts on face and spreads centrifugally to involve trunk and extremities A . Causes mild disease in children but serious congenital disease (a TORCH infection). Congenital rubella findings include “blueberry muffin” appearance due to dermal extramedullary hematopoiesis.


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First_Aid_Step1. Paramyxoviruses Paramyxoviruses cause disease in children. They include those that cause parainfluenza (croup), mumps, measles, RSV, and human metapneumovirus, which causes respiratory tract infection (bronchiolitis, pneumonia) in infants. All contain surface F (fusion) protein, which causes respiratory epithelial cells to fuse and form multinucleated cells. Palivizumab (monoclonal antibody against F protein) prevents pneumonia caused by RSV infection in premature infants. Palivizumab for Paramyxovirus (RSV) Prophylaxis in Preemies.


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First_Aid_Step1. Acute Also called croup. Caused by parainfluenza viruses. Virus membrane contains hemagglutinin laryngotracheobronchitis (binds sialic acid and promotes viral entry) and neuraminidase (promotes progeny virion release) antigens. Results in a “seal-like” barking cough and inspiratory stridor. Narrowing of upper trachea and subglottis leads to characteristic steeple sign on x-ray A . Severe croup can result in pulsus paradoxus 2° to upper airway obstruction. Mumps virus Uncommon due to effectiveness of MMR Mumps makes your parotid glands and testes as vaccine. big as POM-Poms. Symptoms: Parotitis A , Orchitis (inflammation of testes), aseptic Meningitis, and Pancreatitis. Can cause sterility (especially after puberty).


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First_Aid_Step1. Symptoms: Parotitis A , Orchitis (inflammation of testes), aseptic Meningitis, and Pancreatitis. Can cause sterility (especially after puberty). A . Negri bodies (cytoplasmic inclusions B ) commonly found in Purkinje cells of cerebellum and in hippocampal neurons. Rabies has long incubation period (weeks to months) before symptom onset. Postexposure prophylaxis is wound cleaning plus immunization with killed vaccine and rabies immunoglobulin. Example of passive-active immunity. Travels to the CNS by migrating in a retrograde fashion (via dynein motors) up nerve axons after binding to ACh receptors. Progression of disease: fever, malaise • agitation, photophobia, hydrophobia, hypersalivation • paralysis, coma • death. Infection more commonly from bat, raccoon, and skunk bites than from dog bites in the United States; aerosol transmission (eg, bat caves) also possible.


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First_Aid_Step1. Infection more commonly from bat, raccoon, and skunk bites than from dog bites in the United States; aerosol transmission (eg, bat caves) also possible. A filovirus A that targets endothelial cells, phagocytes, hepatocytes. Following an incubation period of up to 21 days, presents with abrupt onset of flu-like symptoms, diarrhea/vomiting, high fever, myalgia. Can progress to DIC, diffuse hemorrhage, shock. Diagnosed with RT-PCR within 48 hr of symptom onset. High mortality rate. Transmission requires direct contact with bodily fluids, fomites (including dead bodies), infected bats or primates (apes/monkeys); high incidence of nosocomial infection. Supportive care, no definitive treatment. Strict isolation of infected individuals and barrier practices for health care workers are key to preventing transmission. Extrahepatic manifestations of hepatitis B and C Anti-HBe Antibody to HBeAg; indicates low transmissibility. Relative concentration of reactants Level of detection


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First_Aid_Step1. Extrahepatic manifestations of hepatitis B and C Anti-HBe Antibody to HBeAg; indicates low transmissibility. Relative concentration of reactants Level of detection Incubation Prodrome, period acute disease gp120: gp41: Diploid genome (2 molecules of RNA). The 3 structural genes (protein coded for): p17: Matrix protein • env (gp120 and gp41): • Formed from cleavage of gp160 to form Lipid envelope envelope glycoproteins. • gp120—attachment to host CD4+ T cell. p24: • gp41—fusion and entry. RNA proteins, respectively. • pol—Reverse transcriptase, Integrase, Protease; RIP “Pol” (Paul) Reverse transcriptase synthesizes dsDNA from genomic RNA; dsDNA integrates into host genome. Virus binds CD4 as well as a coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on T cells (late infection). Homozygous CCR5 mutation = immunity. Heterozygous CCR5 mutation = slower course.


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First_Aid_Step1. Homozygous CCR5 mutation = immunity. Heterozygous CCR5 mutation = slower course. Presumptive diagnosis made with HIV-1/2 Ag/ Western blot tests are no longer recommended Ab immunoassays. These immunoassays by the CDC for confirmatory testing. detect viral p24 Ag capsid protein and IgG Abs HIV-1/2 Ag/Ab testing is not recommended in to HIV-1/2. Very high sensitivity/specificity. babies with suspected HIV due to maternally Viral load tests determine the amount of viral transferred antibody. Use HIV viral load RNA in the plasma. High viral load associated instead. with poor prognosis. Also use viral load to monitor effect of drug therapy. Use HIV genotyping to determine appropriate therapy. AIDS diagnosis: ≤ 200 CD4+ cells/mm3 (normal: 500–1500 cells/mm3) or HIV ⊕ with AIDS-defining condition (eg, Pneumocystis pneumonia). HIV-1 NAT HIV-1 NAT NAT: nucleic acid test


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First_Aid_Step1. AIDS diagnosis: ≤ 200 CD4+ cells/mm3 (normal: 500–1500 cells/mm3) or HIV ⊕ with AIDS-defining condition (eg, Pneumocystis pneumonia). HIV-1 NAT HIV-1 NAT NAT: nucleic acid test Time course of untreated HIV infection +/– Acute HIV infection Skin and mucous Systemic immuno-Viral dissemination membrane defciency/AIDS-Seeding of lymphoid organs Clinical latency infections defning illnesses Dashed lines on CD4+ count axis indicate moderate immunocompromise Four stages of untreated infection: (< 400 CD4+ cells/mm3) and when AIDS-defining illnesses emerge (< 200 1. Flu-like (acute) CD4+ cells/mm3). 2. Feeling fine (latent) Most patients who do not receive treatment eventually die of complications of 3. Falling count HIV infection. 4. Final crisis During clinical latency phase, virus replicates in lymph nodes


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First_Aid_Step1. Most patients who do not receive treatment eventually die of complications of 3. Falling count HIV infection. 4. Final crisis During clinical latency phase, virus replicates in lymph nodes Common diseases of  CD4+ cell count  reactivation of past infections (eg, TB, HSV, shingles), dissemination of HIV-positive adults bacterial infections and fungal infections (eg, coccidioidomycosis), and non-Hodgkin lymphomas. Prions Prion diseases are caused by the conversion of a normal (predominantly α-helical) protein termed prion protein (PrPc) to a β-pleated form (PrPsc), which is transmissible via CNS-related tissue (iatrogenic CJD) or food contaminated by BSE-infected animal products (variant CJD). PrPsc resists protease degradation and facilitates the conversion of still more PrPc to PrPsc. Resistant to standard sterilizing procedures, including standard autoclaving. Accumulation of PrPsc results in spongiform encephalopathy and dementia, ataxia, and death.


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First_Aid_Step1. Creutzfeldt-Jakob disease—rapidly progressive dementia, typically sporadic (some familial forms). Bovine spongiform encephalopathy—also called “mad cow disease.” Kuru—acquired prion disease noted in tribal populations practicing human cannibalism. Normal flora: Neonates delivered by C-section have no flora but are rapidly colonized after birth. dominant B cereus Reheated rice. “Food poisoning from reheated rice? Be serious!” (B cereus) C botulinum Improperly canned foods (toxins), raw honey (spores) Salmonella Poultry, meat, and eggs S aureus Meats, mayonnaise, custard; preformed toxin a V vulnificus can also cause wound infections from contact with contaminated water or shellfish. Common causes of pneumonia Common causes of meningitis Give ceftriaxone and vancomycin empirically (add ampicillin if Listeria is suspected). Viral causes of meningitis: enteroviruses (especially coxsackievirus), HSV-2 (HSV-1 = encephalitis), HIV, West Nile virus (also causes encephalitis), VZV.


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First_Aid_Step1. Viral causes of meningitis: enteroviruses (especially coxsackievirus), HSV-2 (HSV-1 = encephalitis), HIV, West Nile virus (also causes encephalitis), VZV. In HIV: Cryptococcus spp. Note: Incidence of Group B streptococcal meningitis in neonates has  greatly due to screening and antibiotic prophylaxis in pregnancy. Incidence of H influenzae meningitis has  greatly due to conjugate H influenzae vaccinations. Today, cases are usually seen in unimmunized children. Assume if no other information is available S aureus (most common overall) Vertebral involvement S aureus, M tuberculosis (Pott disease) IV drug abuse S aureus; also Pseudomonas, Candida Elevated ESR and CRP sensitive but not specific. Radiographs are insensitive early but can be useful in chronic osteomyelitis ( A , left). MRI is best for detecting acute infection and detailing anatomic involvement ( A , right). sigNs aND symPtoms No inflammation Thin, white discharge


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First_Aid_Step1. sigNs aND symPtoms No inflammation Thin, white discharge A with fishy odor lab FiNDiNgs Clue cells pH > 4.5 ⊕ KOH whiff test Inflammation (“strawberry Inflammation cervix”) Thick, white, “cottage cheese” Frothy, yellow-green, foul-discharge B pH normal (4.0–4.5) pH > 4.5 Metronidazole Azoles Treat sexual partner(s) TORCH infections Microbes that may pass from mother to fetus. Transmission is transplacental in most cases, or via delivery (especially HSV-2). Nonspecific signs common to many ToRCHHeS infections include hepatosplenomegaly, jaundice, thrombocytopenia, and growth retardation. Other important infectious agents include Streptococcus agalactiae (group B streptococci), E coli, and Listeria monocytogenes—all causes of meningitis in neonates. Parvovirus B19 causes hydrops fetalis. Red rashes of childhood Sexually transmitted infections Top bugs—Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrhoeae (acute).


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First_Aid_Step1. Red rashes of childhood Sexually transmitted infections Top bugs—Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrhoeae (acute). C trachomatis—most common bacterial STI in the United States. Signs include cervical motion tenderness, adnexal tenderness, purulent cervical discharge A . PID may include salpingitis, endometritis, hydrosalpinx, and tubo-ovarian abscess. Salpingitis is a risk factor for ectopic pregnancy, infertility, chronic pelvic pain, and adhesions. Can lead to perihepatitis (Fitz-Hugh–Curtis syndrome)—infection and inflammation of liver capsule and “violin string” adhesions of peritoneum to liver B . Nosocomial infections E coli (UTI) and S aureus (wound infection) are the two most common causes. Rash Beginning at head and moving down with Rubella virus postauricular lymphadenopathy Beginning at head and moving down; preceded by Measles virus cough, coryza, conjunctivitis, and Koplik spots


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First_Aid_Step1. Rash Beginning at head and moving down with Rubella virus postauricular lymphadenopathy Beginning at head and moving down; preceded by Measles virus cough, coryza, conjunctivitis, and Koplik spots Can also lead to myalgia and paralysis Poliovirus Tetanus Muscle spasms and spastic paralysis (eg, lockjaw, Clostridium tetani Branching rods in oral infection, sulfur granules Actinomyces israelii Chronic granulomatous disease Catalase ⊕ microbes, especially S aureus Human bite Human oral flora (eg, Eikenella, Fusobacterium) Neutropenic patients Candida albicans (systemic), Aspergillus Pneumonia in cystic fibrosis, burn infection Pseudomonas aeruginosa Puncture wound, lockjaw Clostridium tetani Pus, empyema, abscess S aureus


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First_Aid_Step1. Fluoroquinolones Ciprofoxacin Levofoxacin, etc Quinolone Nalidixic acid Chloramphenicol Clindamycin Linezolid Macrolides Azithromycin Clarithromycin Erythromycin Streptogramins Quinupristin Dalfopristin Rifampin Aminoglycosides Gentamicin Glycylcycline Tigecycline Neomycin Amikacin Tobramycin Streptomycin Tetracyclines Tetracycline Doxycycline Minocycline PROTEIN SYNTHESIS Penicillinase-sensitive penicillins Penicillin G, V Ampicillin Amoxicillin Penicillinase-resistant penicillins Oxacillin Nafcillin Dicloxacillin Antipseudomonal Ticarcillin Piperacillin Cephalosporins (I-V) 1st—Cefazolin, etc 2nd—Cefoxitin, etc 3rd—Ceftriaxone, etc 4th—Cefepime 5th—Ceftaroline PEPTIDOGLYCAN SYNTHESIS CELL WALL SYNTHESIS MEMBRANE INTEGRITY GYRASEDNA INTEGRITY (via free radicals) mRNA SYNTHESIS (RNA polymerase) Carbapenems Imipenem Meropenem Ertapenem Doripenem Monobactams Aztreonam PEPTIDOGLYCAN CROSS-LINKING Glycopeptides Vancomycin Bacitracin 30S SUBUNIT 50S SUBUNIT 50S 30S30S 50S 30S 50S


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First_Aid_Step1. polymerase) Carbapenems Imipenem Meropenem Ertapenem Doripenem Monobactams Aztreonam PEPTIDOGLYCAN CROSS-LINKING Glycopeptides Vancomycin Bacitracin 30S SUBUNIT 50S SUBUNIT 50S 30S30S 50S 30S 50S Sulfonamides Sulfamethoxazole Sulfsoxazole Sulfadiazine FOLIC ACID SYNTHESIS AND REDUCTION (DNA methylation) PABA DHF THF Trimethoprim Cellmembrane Cellwall BACTERIAL CELL DNA mRNA DNA gyrase Ribosomes RNA polymerase – – – – – – – – – Metronidazole – Daptomycin (gram ˜) Polymyxins (gram °)


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First_Aid_Step1. Penicillin G, V Penicillin G (IV and IM form), penicillin V (oral). Prototype β-lactam antibiotics. mecHaNism D-Ala-D-Ala structural analog. Bind penicillin-binding proteins (transpeptidases). Block transpeptidase cross-linking of peptidoglycan in cell wall. Activate autolytic enzymes. cliNical Use Mostly used for gram ⊕ organisms (S pneumoniae, S pyogenes, Actinomyces). Also used for gram ⊝ cocci (mainly N meningitidis) and spirochetes (mainly T pallidum). Bactericidal for gram ⊕ cocci, gram ⊕ rods, gram ⊝ cocci, and spirochetes. β-lactamase sensitive. aDVerse eFFects Hypersensitivity reactions, direct Coombs ⊕ hemolytic anemia, drug-induced interstitial nephritis. resistaNce β-lactamase cleaves the β-lactam ring. Mutations in PBPs. aDVerse eFFects Hypersensitivity reactions, rash, pseudomembranous colitis. mecHaNism oF resistaNce Penicillinase (a type of β-lactamase) cleaves β-lactam ring. Penicillinase-resistant penicillins Dicloxacillin, nafcillin, oxacillin.


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First_Aid_Step1. mecHaNism oF resistaNce Penicillinase (a type of β-lactamase) cleaves β-lactam ring. Penicillinase-resistant penicillins Dicloxacillin, nafcillin, oxacillin. mecHaNism Same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring. cliNical Use S aureus (except MRSA). “Use naf (nafcillin) for staph.” aDVerse eFFects Hypersensitivity reactions, interstitial nephritis. mecHaNism oF resistaNce MRSA has altered penicillin-binding protein target site. Antipseudomonal penicillins Piperacillin, ticarcillin. mecHaNism Same as penicillin. Extended spectrum. Penicillinase sensitive; use with β-lactamase inhibitors. cliNical Use Pseudomonas spp. and gram ⊝ rods. aDVerse eFFects Hypersensitivity reactions. 4th generation (cefepime)—gram ⊝ organisms, with  activity against Pseudomonas and gram ⊕ organisms.


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First_Aid_Step1. cliNical Use Pseudomonas spp. and gram ⊝ rods. aDVerse eFFects Hypersensitivity reactions. 4th generation (cefepime)—gram ⊝ organisms, with  activity against Pseudomonas and gram ⊕ organisms. 5th generation (ceftaroline)—broad gram ⊕ and gram ⊝ organism coverage; unlike 1st–4th generation cephalosporins, ceftaroline covers MRSA, and Enterococcus faecalis—does not cover Pseudomonas. aDVerse eFFects Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency. Low rate of cross-reactivity even in penicillin-allergic patients. • nephrotoxicity of aminoglycosides. mecHaNism oF resistaNce Inactivated by cephalosporinases (a type of β-lactamase). Structural change in penicillin-binding proteins (transpeptidases).


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First_Aid_Step1. • nephrotoxicity of aminoglycosides. mecHaNism oF resistaNce Inactivated by cephalosporinases (a type of β-lactamase). Structural change in penicillin-binding proteins (transpeptidases). cliNical Use Gram ⊕ cocci, gram ⊝ rods, and anaerobes. Wide spectrum and significant side effects limit use to life-threatening infections or after other drugs have failed. Meropenem has a  risk of seizures and is stable to dehydropeptidase I. aDVerse eFFects GI distress, rash, and CNS toxicity (seizures) at high plasma levels. mecHaNism oF resistaNce Inactivated by carbapenemases produced by, eg, K pneumoniae, E coli, E aerogenes. mecHaNism Less susceptible to β-lactamases. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.


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First_Aid_Step1. cliNical Use Gram ⊝ rods only—no activity against gram ⊕ rods or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides. aDVerse eFFects Usually nontoxic; occasional GI upset. mecHaNism Inhibits cell wall peptidoglycan formation by binding D-Ala-D-Ala portion of cell wall precursors. Bactericidal against most bacteria (bacteriostatic against C difficile). Not susceptible to β-lactamases. cliNical Use Gram ⊕ bugs only—for serious, multidrug-resistant organisms, including MRSA, S epidermidis, sensitive Enterococcus species, and Clostridium difficile (oral dose for pseudomembranous colitis). aDVerse eFFects Well tolerated in general but NOT trouble Free. Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse Flushing (red man syndrome A idiopathic reaction largely preventable by pretreatment with antihistamines), DRESS syndrome.


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First_Aid_Step1. mecHaNism oF resistaNce Occurs in bacteria (eg, Enterococcus) via amino acid modification of D-Ala-D-Ala to D-Ala-D-Lac. “If you Lack a D-Ala (dollar), you can’t ride the van (vancomycin).” Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits), leaving human ribosome (80S) unaffected. All are bacteriostatic, except aminoglycosides (bactericidal) and linezolid (variable). Chloramphenicol, Clindamycin Erythromycin (macrolides) Linezolid “Buy AT 30, CCEL (sell) at 50.” cliNical Use Severe gram ⊝ rod infections. Synergistic with β-lactam antibiotics. Neomycin for bowel surgery. aDVerse eFFects Nephrotoxicity, Neuromuscular blockade (absolute contraindication with myasthenia gravis), Ototoxicity (especially with loop diuretics), Teratogenicity. mecHaNism oF resistaNce Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation. Tetracyclines Tetracycline, doxycycline, minocycline.


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First_Aid_Step1. mecHaNism oF resistaNce Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation. Tetracyclines Tetracycline, doxycycline, minocycline. mecHaNism Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA. Limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not take tetracyclines with milk (Ca2+), antacids (eg, Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit drugs’ absorption in the gut. cliNical Use Borrelia burgdorferi, M pneumoniae. Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne. Doxycycline effective against community-acquired MRSA. aDVerse eFFects GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.


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First_Aid_Step1. aDVerse eFFects GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy. mecHaNism oF resistaNce  uptake or  efflux out of bacterial cells by plasmid-encoded transport pumps. mecHaNism Tetracycline derivative. Binds to 30S, inhibiting protein synthesis. Generally bacteriostatic. cliNical Use Broad-spectrum anaerobic, gram ⊝, and gram ⊕ coverage. Multidrug-resistant organisms (MRSA, VRE) or infections requiring deep tissue penetration. aDVerse eFFects GI symptoms: nausea, vomiting. mecHaNism Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic. cliNical Use Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and rickettsial diseases (eg, Rocky Mountain spotted fever [Rickettsia rickettsii]). Limited use due to toxicity but often still used in developing countries because of low cost.


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First_Aid_Step1. aDVerse eFFects Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronosyltransferase). mecHaNism oF resistaNce Plasmid-encoded acetyltransferase inactivates the drug. mecHaNism Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic. aDVerse eFFects Pseudomembranous colitis (C difficile overgrowth), fever, diarrhea. mecHaNism Inhibits protein synthesis by binding to 50S subunit and preventing formation of the initiation complex. cliNical Use Gram ⊕ species including MRSA and VRE. Macrolides Azithromycin, clarithromycin, erythromycin. mecHaNism Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic. cliNical Use Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STIs (Chlamydia), gram ⊕ cocci (streptococcal infections in patients allergic to penicillin), and B pertussis.


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First_Aid_Step1. cliNical Use Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STIs (Chlamydia), gram ⊕ cocci (streptococcal infections in patients allergic to penicillin), and B pertussis. aDVerse eFFects MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT interval, acute Cholestatic hepatitis, Rash, eOsinophilia. Increases serum concentration of theophylline, oral anticoagulants. Clarithromycin and erythromycin inhibit cytochrome P-450. mecHaNism oF resistaNce Methylation of 23S rRNA-binding site prevents binding of drug. Polymyxins Colistin (polymyxin E), polymyxin B. mecHaNism Cation polypeptides that bind to phospholipids on cell membrane of gram ⊝ bacteria. Disrupt cell membrane integrity  leakage of cellular components  cell death. cliNical Use Salvage therapy for multidrug-resistant gram ⊝ bacteria (eg, P aeruginosa, E coli, K pneumoniae). Polymyxin B is a component of a triple antibiotic ointment used for superficial skin infections.


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First_Aid_Step1. aDVerse eFFects Nephrotoxicity, neurotoxicity (eg, slurred speech, weakness, paresthesias), respiratory failure. Sulfonamides Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine. mecHaNism Inhibit dihydropteroate synthase, thus inhibiting folate synthesis. Bacteriostatic (bactericidal when combined with trimethoprim). Sulfonamides, dapsonecliNical Use Gram ⊕, gram ⊝, Nocardia. TMP-SMX for synthase simple UTI. aDVerse eFFects Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, Stevens-Johnson syndrome, kernicterus in infants, displace other drugs from albumin (eg, warfarin). mecHaNism oF resistaNce Altered enzyme (bacterial dihydropteroate synthase),  uptake, or  PABA synthesis. Trimethoprim, mecHaNism Similar to sulfonamides, but structurally distinct Purines Thymidine Methionine agent.


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First_Aid_Step1. Trimethoprim, mecHaNism Similar to sulfonamides, but structurally distinct Purines Thymidine Methionine agent. cliNical Use Leprosy (lepromatous and tuberculoid), DNA, RNA DNA Protein Pneumocystis jirovecii prophylaxis, or treatment when used in combination with TMP. aDVerse eFFects Hemolysis if G6PD deficient, methemoglobinemia, agranulocytosis. mecHaNism Inhibits bacterial dihydrofolate reductase. Bacteriostatic. cliNical Use Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMPSMX]), causing sequential block of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis. aDVerse eFFects Hyperkalemia (high doses), megaloblastic anemia, leukopenia, granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid). TMP Treats Marrow Poorly.


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First_Aid_Step1. aDVerse eFFects Hyperkalemia (high doses), megaloblastic anemia, leukopenia, granulocytopenia, which may be avoided with coadministration of leucovorin (folinic acid). TMP Treats Marrow Poorly. cliNical Use Gram ⊝ rods of urinary and GI tracts (including Pseudomonas), some gram ⊕ organisms, otitis externa. mecHaNism oF resistaNce Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps. mecHaNism Lipopeptide that disrupts cell membranes of gram ⊕ cocci by creating transmembrane channels. aDVerse eFFects Myopathy, rhabdomyolysis. mecHaNism Forms toxic free radical metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal. aDVerse eFFects Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste. Plasma Cell wall membrane Interior of cell Rifamycins Rifampin, rifabutin.


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First_Aid_Step1. Plasma Cell wall membrane Interior of cell Rifamycins Rifampin, rifabutin. mecHaNism Inhibit DNA-dependent RNA polymerase. Rifampin’s 4R’s: cliNical Use Mycobacterium tuberculosis; delay resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with H influenzae type b. aDVerse eFFects Minor hepatotoxicity and drug interactions ( cytochrome P-450); orange body fluids (nonhazardous side effect). Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation. Rifampin ramps up cytochrome P-450, but rifabutin does not. mecHaNism oF resistaNce Mutations reduce drug binding to RNA polymerase. Monotherapy rapidly leads to resistance. mecHaNism  synthesis of mycolic acids. Bacterial catalaseperoxidase (encoded by KatG) needed to convert INH to active metabolite. mecHaNism oF resistaNce Mutations leading to underexpression of KatG.


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First_Aid_Step1. mecHaNism oF resistaNce Mutations leading to underexpression of KatG. mecHaNism Mechanism uncertain. Pyrazinamide is a prodrug that is converted to the active compound pyrazinoic acid. Works best at acidic pH (eg, in host phagolysosomes). cliNical Use Mycobacterium tuberculosis. aDVerse eFFects Hyperuricemia, hepatotoxicity. mecHaNism  carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase. cliNical Use Mycobacterium tuberculosis. aDVerse eFFects Optic neuropathy (red-green color blindness, usually reversible). Pronounce “eyethambutol.” mecHaNism Interferes with 30S component of ribosome. cliNical Use Mycobacterium tuberculosis (2nd line). aDVerse eFFects Tinnitus, vertigo, ataxia, nephrotoxicity. Antimicrobial cliNicalsceNario meDicatioN prophylaxis Exposure to meningococcal infection Ceftriaxone, ciprofloxacin, or rifampin History of recurrent UTIs TMP-SMX


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First_Aid_Step1. Antimicrobial cliNicalsceNario meDicatioN prophylaxis Exposure to meningococcal infection Ceftriaxone, ciprofloxacin, or rifampin History of recurrent UTIs TMP-SMX Malaria prophylaxis for travelers Atovaquone-proguanil, mefloquine, doxycycline, primaquine, or chloroquine (for areas with sensitive species) Prevention of gonococcal conjunctivitis in Erythromycin ointment on eyes newborn Prevention of postsurgical infection due to Cefazolin Prophylaxis of strep pharyngitis in child with Benzathine penicillin G or oral penicillin V prior rheumatic fever Treatment of highly MRSA: vancomycin, daptomycin, linezolid, tigecycline, ceftaroline, doxycycline. resistant bacteria VRE: linezolid, tigecycline, and streptogramins (quinupristin, dalfopristin). Multidrug-resistantP aeruginosa, multidrug-resistantAcinetobacter baumannii: polymyxins B and E (colistin).


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First_Aid_Step1. aDVerse eFFects Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (“amphoterrible”). Hydration  nephrotoxicity. toxicity. mecHaNism Same as amphotericin B. Topical use only as too toxic for systemic use. cliNical Use “Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis. mecHaNism Inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase. cliNical Use Systemic fungal infections (especially meningitis caused by Cryptococcus) in combination with amphotericin B. aDVerse eFFects Bone marrow suppression. Azoles Clotrimazole, fluconazole, isavuconazole, itraconazole, ketoconazole, miconazole, voriconazole. mecHaNism Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol.


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First_Aid_Step1. mecHaNism Inhibit fungal sterol (ergosterol) synthesis by inhibiting the cytochrome P-450 enzyme that converts lanosterol to ergosterol. cliNical Use Local and less serious systemic mycoses. Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types. Itraconazole may be used for Blastomyces, Coccidioides, Histoplasma, Sporothrix schenckii. Clotrimazole and miconazole for topical fungal infections. Voriconazole for Aspergillus and some Candida. Isavuconazole for serious Aspergillus and Mucor infections. aDVerse eFFects Testosterone synthesis inhibition (gynecomastia, especially with ketoconazole), liver dysfunction (inhibits cytochrome P-450). mecHaNism Inhibits the fungal enzyme squalene epoxidase. cliNical Use Dermatophytoses (especially onychomycosis—fungal infection of finger or toe nails). aDVerse eFFects GI upset, headaches, hepatotoxicity, taste disturbance. Echinocandins Anidulafungin, caspofungin, micafungin.


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First_Aid_Step1. aDVerse eFFects GI upset, headaches, hepatotoxicity, taste disturbance. Echinocandins Anidulafungin, caspofungin, micafungin. mecHaNism Inhibit cell wall synthesis by inhibiting synthesis of β-glucan. cliNical Use Invasive aspergillosis, Candida. aDVerse eFFects GI upset, flushing (by histamine release). mecHaNism Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (eg, nails). cliNical Use Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm). aDVerse eFFects Teratogenic, carcinogenic, confusion, headaches, disulfiram-like reaction,  cytochrome P-450 and warfarin metabolism. mecHaNism Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.


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First_Aid_Step1. mecHaNism Blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia. cliNical Use Treatment of plasmodial species other than P falciparum (frequency of resistance in P falciparum is too high). Resistance due to membrane pump that  intracellular concentration of drug. Treat P falciparum with artemether/lumefantrine or atovaquone/proguanil. For life-threatening malaria, use quinidine in US (quinine elsewhere) or artesunate. aDVerse eFFects Retinopathy; pruritus (especially in dark-skinned individuals). Antihelminthic Pyrantel pamoate, Ivermectin, Mebendazole (microtubule inhibitor), Praziquantel ( Ca2+ therapy permeability,  vacuolization), Diethylcarbamazine. Helminths get PIMP’D. Zidovudine (ZDV, Acyclovir, etc (HSV, VZV) Oseltamivir, zanamivir mecHaNism Inhibit influenza neuraminidase  release of progeny virus.


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First_Aid_Step1. Zidovudine (ZDV, Acyclovir, etc (HSV, VZV) Oseltamivir, zanamivir mecHaNism Inhibit influenza neuraminidase  release of progeny virus. Infuenza A, B cliNical Use Treatment and prevention of influenza A and B. Beginning therapy within 48 hours of symptom onset may shorten duration of illness. Acyclovir, famciclovir, valacyclovir Ganciclovir mecHaNism 5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. cliNical Use CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability. mecHaNism Viral DNA/RNA polymerase inhibitor and Foscarnet = pyrofosphate analog. HIV reverse transcriptase inhibitor. Binds to pyrophosphate-binding site of enzyme. Does not require any kinase activation. cliNical Use CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV.


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First_Aid_Step1. cliNical Use CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV. aDVerse eFFects Nephrotoxicity, electrolyte abnormalities (hypoor hypercalcemia, hypoor hyperphosphatemia, hypokalemia, hypomagnesemia) can lead to seizures. mecHaNism oF resistaNce Mutated DNA polymerase. mecHaNism Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase. cliNical Use CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life. aDVerse eFFects Nephrotoxicity (coadminister with probenecid and IV saline to  toxicity).


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First_Aid_Step1. cliNical Use CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life. aDVerse eFFects Nephrotoxicity (coadminister with probenecid and IV saline to  toxicity). HIV therapy Antiretroviral therapy (ART): often initiated at the time of HIV diagnosis. Strongest indication for use with patients presenting with AIDS-defining illness, low CD4+ cell counts (< 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance: 2 NRTIs and preferably an integrase inhibitor. All ARTs are active against HIV-1 and HIV-2 with the exception of NNRTIs and enfuvirtide. Abacavir (ABC) Didanosine (ddI) Emtricitabine (FTC) Lamivudine (3TC) Stavudine (d4T) Tenofovir (TDF) Zidovudine (ZDV, Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group). Tenofovir is a nucleoTide; the others are nucleosides. All need to be phosphorylated to be active.


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First_Aid_Step1. ZDV can be used for general prophylaxis and during pregnancy to  risk of fetal transmission. Have you dined (vudine) with my nuclear (nucleosides) family? Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (didanosine). Abacavir contraindicated if patient has HLA-B*5701 mutation due to  risk of hypersensitivity. Hepatitis C therapy Chronic HCV infection treated with multidrug therapy that targets specific steps within HCV replication cycle (HCV-encoded proteins). Examples of drugs are provided. Grazoprevir Inhibits NS3/4A, a viral protease, preventing Grazoprevir: headache, fatigue Simeprevir viral replication Simeprevir: photosensitivity reactions, rash


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First_Aid_Step1. Grazoprevir Inhibits NS3/4A, a viral protease, preventing Grazoprevir: headache, fatigue Simeprevir viral replication Simeprevir: photosensitivity reactions, rash Ribavirin Inhibits synthesis of guanine nucleotides by Hemolytic anemia, severe teratogen competitively inhibiting IMP dehydrogenase Used as adjunct in cases refractory to newer medications Disinfection and Goals include the reduction of pathogenic organism counts to safe levels (disinfection) and the sterilization inactivation of all microbes including spores (sterilization). Autoclave Pressurized steam at > 120°C. Sporicidal. May not reliably inactivate prions. Alcohols Denature proteins and disrupt cell membranes. Not sporicidal. Chlorhexidine Denatures proteins and disrupts cell membranes. Not sporicidal. Chlorine Oxidizes and denatures proteins. Sporicidal. SAFe Children Take Really Good Care.


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First_Aid_Step1. Chlorhexidine Denatures proteins and disrupts cell membranes. Not sporicidal. Chlorine Oxidizes and denatures proteins. Sporicidal. SAFe Children Take Really Good Care. “Digressions, objections, delight in mockery, carefree mistrust are signs of health; everything unconditional belongs in pathology.” “You cannot separate passion from pathology any more than you can separate a person’s spirit from his body.”