Microbiology Encyclopedia

Staphylococcus aureus

Methicillin-resistant Staphylococcus aureus (MRSA) — Photo: CDC (Unsplash License, free to use)

A catalase-positive, coagulase-positive Gram-positive coccus arranged in clusters. The leading Staphylococcal pathogen, capable of causing disease in otherwise healthy hosts.

• Virulence factors: coagulase, Protein A, hemolysins, Panton-Valentine leukocidin (PVL), enterotoxins, TSST-1, exfoliatin.
• Classic diseases: skin abscesses, toxic shock syndrome, food poisoning (rapid-onset vomiting), infective endocarditis, scalded skin syndrome (neonates).
• Diagnosis: coagulase-positive on culture; novobiocin-sensitive.
• Resistance concern: MRSA (mecA gene → altered PBP2a) resists virtually all beta-lactams.

Staphylococcus epidermidis

Coagulase-negative, novobiocin-sensitive skin commensal. Normally harmless, but a classic opportunist once it gains access to indwelling devices.

• Mechanism: forms protective biofilms on catheters and prosthetic material.
• Classic disease: catheter-associated bloodstream infection, prosthetic valve endocarditis.

Staphylococcus saprophyticus

Coagulase-negative but, unlike S. epidermidis, novobiocin-resistant — the key lab distinction between the two.

• Classic disease: uncomplicated urinary tract infection in young, sexually active women.

Streptococcus pyogenes (Group A)

Beta-hemolytic, catalase-negative coccus in chains. Its major virulence factor, M protein, both resists phagocytosis and underlies a serious autoimmune complication.

• Classic diseases: pharyngitis, cellulitis, necrotizing fasciitis, scarlet fever.
• Post-infectious sequelae: acute rheumatic fever (molecular mimicry between M protein and cardiac tissue) and post-streptococcal glomerulonephritis.
• Diagnostic marker: elevated ASO (anti-streptolysin O) titer confirms recent infection.

Streptococcus agalactiae (Group B)

Beta-hemolytic Group B Streptococcus, notable for maternal colonization and vertical transmission.

• Classic disease: early-onset neonatal sepsis and meningitis.

Streptococcus pneumoniae

Alpha-hemolytic, optochin-sensitive, encapsulated diplococcus.

• Virulence factor: polysaccharide capsule (also the vaccine target — PCV/PPSV23); capsular switching can evade vaccine immunity.
• Classic diseases: pneumonia, otitis media, meningitis.

Viridans Streptococci

Alpha-hemolytic, optochin-resistant group of normal oral flora streptococci.

• Classic disease: subacute infective endocarditis on a previously damaged heart valve after dental procedures.

Escherichia coli

Normal gut flora and the most common Gram-negative pathogen overall; specific pili mediate uroepithelial attachment.

• Classic diseases: UTI, traveler's diarrhea (ETEC via heat-labile/heat-stable toxins), neonatal meningitis, hemolytic uremic syndrome (EHEC O157:H7, Shiga-like toxin).

Klebsiella pneumoniae

Encapsulated Enterobacteriaceae member with a prominent antiphagocytic polysaccharide capsule.

• Classic disease: pneumonia (especially in alcoholics), UTI.

Salmonella

Motile, non-lactose-fermenting, H2S-producing rod that survives and disseminates inside macrophages.

• Classic diseases: enteric (typhoid) fever via S. typhi, gastroenteritis via non-typhoidal serotypes.

Shigella

Non-motile rod with a very low infective dose thanks to acid resistance and efficient colonic epithelial invasion.

• Classic disease: bacillary dysentery (bloody diarrhea with few ingested organisms needed).

Proteus mirabilis

Urease-positive, swarming-motile rod.

• Mechanism: urease alkalinizes urine, promoting struvite (staghorn) stone formation in UTI.

Pseudomonas aeruginosa

Obligate aerobe, intrinsically multidrug-resistant, classic opportunist of compromised patients.

• Classic diseases: burn/ICU infections, ventilator-associated pneumonia, malignant otitis externa.

Vibrio cholerae

Alkaliphile (pH 8.5–9.0), causative agent of cholera.

• Toxin mechanism: cholera toxin ADP-ribosylates Gs, permanently activating adenylate cyclase → raised cAMP → massive Cl⁻/water secretion → "rice-water" diarrhea.
• Treatment: aggressive oral/IV rehydration is the life-saving intervention; antibiotics only shorten illness duration.

Campylobacter jejuni

Campylobacter sp. — causes campylobacteriosis — Photo: CDC (Unsplash License, free to use)

Microaerophilic curved rod, a leading cause of bacterial diarrhea.

• Important association: antecedent trigger of Guillain-Barré syndrome via molecular mimicry with peripheral nerve gangliosides.

Helicobacter pylori

Urease-positive spiral organism that colonizes the stomach.

• Mechanism: urease converts urea to ammonia, locally buffering gastric acid to enable survival.
• Classic disease: peptic ulcer disease; associated with gastric cancer risk.

Mycobacterium tuberculosis

Drug-resistant Mycobacterium tuberculosis, 3D render — Photo: CDC (Unsplash License, free to use)

Obligate aerobe capable of surviving inside macrophages by evading phagolysosomal killing.

• Growth note: a notably long lag phase (may take days) compared to fast-growing organisms like E. coli.

Clostridium

Clostridioides difficile, medical illustration (CDC) — Photo: CDC (Unsplash License, free to use)

Obligate anaerobic genus, classic endospore former.

• Classic diseases: tetanus, gas gangrene, botulism (each caused by a different species) via resistant environmental spores.

Bacillus

Obligate aerobic genus, the other classic endospore former alongside Clostridium.

• Classic disease: anthrax (B. anthracis); food poisoning (B. cereus, both a preformed emetic toxin and a heat-labile diarrheal toxin).

Corynebacterium diphtheriae

Acquires its toxin gene via a lysogenic bacteriophage (phage conversion/specialized transduction) — a nontoxigenic strain can become toxigenic this way.

• Toxin mechanism: diphtheria toxin ADP-ribosylates elongation factor 2 (EF-2), halting host protein synthesis, producing the classic pharyngeal pseudomembrane.

Gram Stain

Differentiates bacteria by cell wall peptidoglycan content. Gram-positive organisms retain crystal violet (stain violet); Gram-negative organisms are decolorized and counterstained (stain pink/red).

Catalase Test

Detects the catalase enzyme, which breaks down hydrogen peroxide into water and oxygen (visible bubbling). Distinguishes Staphylococci (positive) from Streptococci (negative).

Coagulase Test

Detects the coagulase enzyme, which clots plasma. Distinguishes S. aureus (positive) from other Staphylococci (negative).

Novobiocin Sensitivity

Distinguishes coagulase-negative Staphylococci: S. epidermidis is sensitive, while S. saprophyticus is resistant.

Optochin Sensitivity

Distinguishes alpha-hemolytic Streptococci: S. pneumoniae is sensitive (and bile-soluble), while viridans Streptococci are resistant.

Hemolysis Patterns

Describes red cell lysis around a colony on blood agar.

• Alpha: partial lysis, greenish zone (S. pneumoniae, viridans strep).
• Beta: complete lysis, clear zone (S. pyogenes, S. agalactiae).
• Gamma: no hemolysis (Enterococcus).

Indole Test

Detects the enzyme tryptophanase, which breaks down tryptophan to indole. Reagent (Kovac's) turns pink/red at the surface if positive. E. coli is indole-positive; most other Enterobacteriaceae (Klebsiella, Salmonella, Shigella) are indole-negative — a key organism-differentiating test within the family.

Urease Test

Detects the urease enzyme, which hydrolyzes urea into ammonia and CO2, raising pH (color change with phenol red indicator). Positive in Proteus (strong/rapid), Helicobacter pylori, and Klebsiella (weaker); negative in E. coli, Shigella, Salmonella.

Hydrogen Sulfide (H2S) Production

Some Enterobacteriaceae reduce sulfur compounds to H2S, producing a black precipitate on TSI/SIM media. Salmonella and Proteus are classically H2S-positive; E. coli and Shigella are H2S-negative — useful for distinguishing Salmonella from Shigella in stool culture.

Beta-lactams (Penicillins)

Structurally mimic the D-Ala-D-Ala terminus of peptidoglycan precursors, irreversibly binding and inactivating penicillin-binding proteins (PBPs, transpeptidases), blocking cell wall cross-linking. Time-dependent killing.

Cephalosporins

A beta-lactam subclass with progressively broader Gram-negative coverage across "generations" (1st through 5th). Share the PBP-binding mechanism of penicillins but resist some beta-lactamases better, depending on generation. Commonly favored empirically when Gram-negative sepsis is suspected, since they better cross the Gram-negative outer membrane than narrow-spectrum penicillins.

Vancomycin

Binds the D-Ala-D-Ala terminus directly (rather than PBPs), blocking peptidoglycan cross-linking. Too large to cross the Gram-negative outer membrane (intrinsic resistance). Resistance in Enterococcus (VRE) arises from substituting the terminus to D-Ala-D-Lac (vanA gene), sharply reducing binding.

Aminoglycosides

Bind the 30S ribosomal subunit, causing misreading of mRNA. Require an active, oxygen-dependent electron transport chain for uptake — ineffective against strict anaerobes regardless of in vitro susceptibility. Concentration-dependent killing with a post-antibiotic effect, supporting extended-interval dosing.

Fluoroquinolones

Trap DNA gyrase and topoisomerase IV on bacterial DNA, generating lethal double-strand breaks.

Macrolides

Bind the 50S ribosomal subunit, blocking the translocation step of protein synthesis.

Tetracyclines

Bind the 30S ribosomal subunit, blocking aminoacyl-tRNA attachment.

Sulfonamides + Trimethoprim

Sulfamethoxazole inhibits dihydropteroate synthase; trimethoprim inhibits dihydrofolate reductase — sequential, non-redundant steps of the same folate pathway, producing synergistic bactericidal activity when combined (co-trimoxazole).

Rifampin

Binds the beta subunit of bacterial RNA polymerase, blocking transcription. A single rpoB point mutation confers high-level resistance, so it is never used as monotherapy (hence combination regimens in tuberculosis treatment).

Polymyxins (Colistin)

Disrupt the integrity of the bacterial outer and inner membrane. Reserved as a last-resort agent for multidrug-resistant Gram-negative infections due to their toxicity profile relative to other classes.

Herpes Simplex Virus 1 (HSV-1)

Establishes lifelong latency in the trigeminal ganglion.

• Classic disease: oral herpes (cold sores), keratitis, herpes encephalitis.

Herpes Simplex Virus 2 (HSV-2)

Establishes lifelong latency in the sacral ganglion.

• Classic disease: genital herpes.

Varicella-Zoster Virus (VZV)

Establishes latency in dorsal root ganglia after primary infection.

• Classic disease: chickenpox (primary infection); shingles (reactivation).

Epstein-Barr Virus (EBV)

Establishes latency within B lymphocytes via the LMP1 protein, a constitutively active CD40 mimic.

• Classic disease: infectious mononucleosis (heterophile-antibody positive).
• Oncogenic associations: Burkitt lymphoma (t(8;14) translocation), nasopharyngeal carcinoma.

Cytomegalovirus (CMV)

Establishes latency in monocytes/lymphocytes.

• Classic disease: heterophile-negative mononucleosis-like illness; congenital infection; serious disease in immunosuppressed patients.

Hepatitis A Virus (HAV)

Fecal-oral transmission; causes only acute infection, never chronic.

Hepatitis B Virus (HBV)

Transmitted via blood, sexual contact, and perinatally. Can become chronic, especially if acquired early in life.

• Key markers: HBsAg (active infection), Anti-HBs (immunity), Anti-HBc (marks natural infection exposure, absent after vaccination alone), HBeAg (high infectivity/replication).

Hepatitis C Virus (HCV)

Blood-borne transmission; has the highest chronicity rate among all hepatitis viruses.

• Diagnosis note: a positive Anti-HCV antibody only shows past exposure — HCV RNA testing confirms whether infection is currently active.

Hepatitis D Virus (HDV)

Requires HBV co-infection (uses HBsAg) to form complete virions and cause disease.

Hepatitis E Virus (HEV)

Fecal-oral transmission; typically acute, but can cause unusually severe/fulminant disease in pregnant women.

Human Immunodeficiency Virus (HIV)

Infects CD4+ T helper cells via gp120 (CD4 + co-receptor binding) and gp41 (membrane fusion). Reverse transcriptase converts its RNA genome to DNA, which integrates into the host genome as a provirus — the basis of lifelong infection.

• Co-receptors: CCR5 (R5-tropic, classically transmitted strains) and CXCR4 (X4-tropic, often emerging later in disease).
• AIDS-defining threshold: CD4 count below 200 cells/µL.
• Notable resistance variant: CCR5-Δ32 homozygosity confers strong resistance to R5-tropic HIV (basis of the "Berlin patient" functional cure).

Acyclovir

Requires activation by viral thymidine kinase before it can inhibit viral DNA polymerase — a key selectivity mechanism sparing uninfected cells. Resistance classically arises from thymidine kinase mutations.

Ganciclovir

Used against CMV; requires activation by the viral UL97 kinase (CMV's counterpart to HSV's thymidine kinase). Resistance classically arises from UL97 mutations.

Foscarnet

Directly inhibits viral DNA polymerase without requiring kinase activation — making it active against acyclovir/ganciclovir-resistant strains, though with significant nephrotoxicity.

Oseltamivir

Structurally mimics sialic acid, competitively blocking influenza neuraminidase and preventing release of new virions.

Reverse Transcriptase Inhibitors

Nucleos(t)ide analogs (e.g., zidovudine, tenofovir) lack a 3'-OH group, terminating DNA chain elongation once incorporated during reverse transcription.

Protease Inhibitors

Block cleavage of HIV polyprotein precursors into functional viral proteins. Ritonavir is notably also a potent CYP3A4 inhibitor, often used at low ("booster") dose to raise levels of a co-administered protease inhibitor.