bacteria

Staphylococcus aureus Identification

Gram-positive cocci in grapelike clusters; Catalase-positive; Coagulase-positive; Beta-hemolytic.

Staphylococcus aureus Virulence Factors

Protein A (inhibits phagocytosis), Coagulase (clots blood to hide), Exfoliative toxin, Alpha-toxin (causes tissue necrosis), and beta-lactamase.

Staphylococcus aureus Clinical Findings

Folliculitis, SSSS (Scalded Skin Syndrome), Impetigo, Conjunctivitis, Sepsis, and MRSA.

Staphylococcus aureus Resistance & Treatment

>90% resistant to Penicillin G; MRSA contains the mecA gene; VRSA is treated with Daptomycin.

Staphylococcus epidermidis Identification

Gram-positive cocci; Coagulase-negative; Non-hemolytic; Salt-tolerant.

Staphylococcus epidermidis Virulence & Transmission

Slime layer (critical for adherence to plastic); Part of normal skin flora; Enters bloodstream via catheters or IV sites.

Staphylococcus epidermidis Clinical Findings

Almost always hospital-acquired: Prosthetic joint and implant infections, endocarditis, and catheter-site folliculitis.

Streptococcus pyogenes (Group A) Identification

Gram-positive cocci in chains; Catalase-negative; Beta-hemolytic; Sensitive to Bacitracin.

Streptococcus pyogenes Virulence Factors

M protein (antiphagocytic), Capsule, Hyaluronidase (cements/breaks down tissues), Streptolysin S, and Exotoxin A.

Streptococcus pyogenes Clinical Findings

Necrotizing fasciitis ("flesh-eating"), Strep throat, Cellulitis, Impetigo, and Rheumatic fever.

Streptococcus pyogenes Treatment

Necrotizing fasciitis requires urgent surgical removal and IV Penicillin.

Streptococcus pneumoniae Identification

Gram-positive diplococci; Alpha-hemolytic (produces green zone); Catalase-negative.

Streptococcus pneumoniae Virulence & Diagnostic Tests

Major polysaccharide capsule (antiphagocytic); Identified via capsular swelling (Quellung) test; Prevented with pneumococcal vaccine.

Streptococcus pneumoniae Clinical Findings

Leading cause of meningitis in adults (50% of cases); Pneumonia, Otitis media, and Sinusitis.

Streptococcus agalactiae (Group B) Identification

Gram-positive cocci; Beta-hemolytic; Catalase-negative.

Streptococcus agalactiae Virulence & Colonization

Capsule and Hemolysin; Colonizes normal flora in 30% of healthy adults.

Streptococcus agalactiae Clinical Findings & Treatment

Leading cause of sepsis and meningitis in newborns; Treated with IV Penicillin given 4 hours prior to delivery.

Neisseria meningitidis Identification

Gram-negative diplococci; Fastidious growth requirements (requires Chocolate Agar).

Neisseria meningitidis Virulence Factors

Pili (adhere to nose and pharynx), Capsule, and LOS Endotoxin.

Neisseria meningitidis Clinical & Epidemilogy

Causes Acute Meningitis (high fever, stiff neck, rash) and URT infections; Spreads in close quarters (military/college); Vaccine given at ages 11 and 16.

Haemophilus influenzae Identification & Requirements

Gram-negative coccobacillus; Fastidious (requires Heme/Factor X and NAD+/Factor V).

Haemophilus influenzae Virulence & Clinical

Capsule (primary virulence factor); Causes Meningitis (former leading childhood cause), Pneumonia, and Epiglottitis; 90% fatality if untreated; Prevented via Hib vaccine.

Pseudomonas aeruginosa Morphology & Pigments

Gram-negative rods; Beta-hemolytic; UV-fluorescent (Pyoverdin) and produces blue-green toxin/pigment (Pyocyanin).

Pseudomonas aeruginosa Virulence Factors

Pyocyanin toxin, Capsule, Fimbriae (biofilm formation), and Multidrug resistance.

Pseudomonas aeruginosa Clinical Findings & Mortality

Burn and surgical wound infections, Hot tub folliculitis, Cystic Fibrosis lung infections, and Malignant otitis externa; Opportunistic with 50% fatality in bacteremia.

Listeria monocytogenes Morphology & Virulence

Gram-positive rod; Beta-hemolytic; Intracellular; Uses Listeriolysin to escape phagosomes into cytosol.

Listeria monocytogenes Transmission & Clinical

Transmitted via cold contaminated food (deli meats, soft cheese); Replicates at refrigerator temperatures; Causes newborn meningitis, spontaneous abortion, and sepsis.

Bacillus anthracis Morphology & Toxins

Large Gram-positive rods in chains; Spore-forming; Aerobic; Anthrax toxin consists of Edema factor and Lethal factor.

Bacillus anthracis Clinical Forms & Detail

Pulmonary anthrax (deadly, leads to hemorrhagic mediastinitis), Cutaneous anthrax (black eschar), and GI anthrax; Spores persist in soil for years.

Clostridium perfringens Morphology & Toxins

Large Gram-positive rods; Spore-forming; Obligate anaerobe; Produces 11 toxins that lyse cells and trigger shock.

Clostridium perfringens Clinical & Source

Causes Gas gangrene (blackened muscle, gas bubbles) and Necrotizing fasciitis; Found in soil and GI tract; Associated with war or accident wounds.

Clostridium botulinum Mechanism of Toxin

Gram-positive rod, spore-forming obligate anaerobe; Botulism neurotoxin blocks Acetylcholine release at neuromuscular junctions.

Clostridium botulinum Clinical & Infection Sources

Causes Botulism: Flaccid paralysis, blurry vision, and respiratory failure; Contaminated sources include honey (infants), improperly canned food, and wound drugs.

Clostridium tetani Mechanism of Toxin

Gram-positive rod, spore-forming obligate anaerobe; Produces Tetanospasmin neurotoxin which prevents muscle relaxation.

Clostridium tetani Clinical & Prevention

Causes Tetanus: Lockjaw, painful muscle contractions, and irregular HR/BP; Spores enter via wounds; Prevented by TT (Tetanus Toxoid) vaccine.

Rickettsia rickettsii Morphology & Pathophysiology

Gram-negative obligate intracellular bacterium; Directly damages endothelial cells lining blood vessels.

Rickettsia rickettsii Clinical & Transmission

Causes Rocky Mountain Spotted Fever: Acute fever, headache, and petechial rash starting on hands/feet (peripheral); Transmitted by dog and wood ticks; Treated with Doxycycline.

Borrelia burgdorferi Morphology & Transmission

Spirochete (thin-walled spiral structure with Gram-negative rod framework); Transmitted by tick bite requiring 24–48 hours of feeding to infect.

Borrelia burgdorferi Clinical Stages

Lyme Disease: Stage 1 (Bull’s eye rash/Erythema chronicum migrans); Stage 2 (Bell’s palsy); Stage 3 (Chronic arthritis).

Escherichia coli Pathophysiology

Gram-negative rod with thin cell wall; Contains Endotoxin (LPS) in its outer membrane.

Escherichia coli Clinical Significance

Causes Sepsis, UTIs, and diarrhea; Primary bacterial source of Endotoxins leading to fever, severe hypotension, and shock.

Mycobacterium tuberculosis Characteristics

Thick, waxy cell wall composed of Mycolic acid; Causes Tuberculosis; Requires Acid-Fast Stain with heat to melt waxy layer.

Mycoplasma pneumoniae Characteristics

Lacks a cell wall entirely; Pleomorphic shape; Causes atypical pneumonia; Naturally resistant to Penicillin (which targets cell walls).

Salmonella spp. Identification & Clinical

Gram-negative rods; Causes food poisoning primarily from poultry; Identified via ELISA or Agglutination tests.

Vibrio cholerae Mechanism & Clinical

Comma-shaped Gram-negative rods; Secretes Cholera toxin (enzyme inhibitor) causing massive fluid loss and rice-water diarrhea.

Lactobacillus Function

Composes 90% of normal vaginal microbiota; Produces protective environment against opportunistic pathogens.

Streptococcus mutans Virulence & Role

Produces a slime layer allowing strong adherence to teeth; Forms biofilms and primary component of dental plaque.

Bacterial Virulence Mechanisms

Adherence via pili, flagella, or adhesins; Tissue invasion facilitated by enzymes including collagenase, hyaluronidase, and keratinase.

Endotoxins vs. Exotoxins Differences

Endotoxins: LPS in outer membrane of Gram-negative bacteria only, released upon cell lysis, cause systemic shock. Exotoxins: Proteins secreted by living bacteria (e.g. botulism, cholera), treatable with antitoxins.

Bacterial Identification Diagnostic Methods

Gram staining (Purple = Positive, Pink = Negative), Biochemical testing (fermentation), Genetic testing (PCR), and Immunological tests (ELISA, Agglutination).

Bacterial Resistance Mechanisms (MRSA vs VRSA)

MRSA evolved via horizontal gene transfer of the mecA gene from Staphylococcus epidermidis; VRSA acquired Vancomycin resistance from enterococci via a plasmid.