Select a bacterial group below to view its detailed comparison table.
| Category / Feature | Staphylococcus aureus | Streptococcus pyogenes (GAS) | Streptococcus pneumoniae |
|---|---|---|---|
| I. Introduction | |||
| Discovery/Naming | Discovered by A. Ogston (1880)Sir Alexander Ogston identified it in surgical abscesses. Rosenbach later named it *aureus* (1884) from Latin for 'golden', due to colony pigment. A major opportunistic pathogen. | Described by T. Billroth (1874)Theodor Billroth described cocci from erysipelas. Pasteur later named genus *Streptococcus* from Greek for 'twisted berry/chain'. Significant human pathogen. | Isolated by Pasteur/Sternberg (1881)Independently isolated from saliva by Louis Pasteur and George Sternberg. Initially called *Diplococcus pneumoniae*. Key cause of pneumonia. |
| Taxonomy Snippet | Genus Staphylococcus ("Bunch of Grapes")Greek *staphyle* (bunch of grapes) reflects cluster arrangement. Family Staphylococcaceae. Compare vs Coagulase-Negative Staphylococci like *S. epidermidis*. | Genus Streptococcus ("Twisted Chain")Greek *streptos* (twisted) reflects chain arrangement. Family Streptococcaceae. Compare vs *S. agalactiae* (Group B Strep), Viridans group streptococci. | Species pneumoniae ("Lung")Member of *Streptococcus* genus, within the Mitis group of Viridans streptococci. Distinguished by specific features. |
| Key ID Grouping | Coagulase Positive StaphylococcusPrimary clinical differentiator from other staphylococci (CoNS). Many strains also produce golden pigment (staphyloxanthin). | Lancefield Group A Streptococcus (GAS)Defined by the Group A carbohydrate antigen in its cell wall. Prototype β-hemolytic Streptococcus. | Alpha-Hemolytic Streptococcus (Pneumococcus)Typically lacks Lancefield group antigens. Key α-hemolytic species identified by optochin susceptibility and bile solubility. |
| Epidemiology Snippet | Common Hospital- & Community-Acquired InfectionsFrequent human colonizer (anterior nares, skin). Causes opportunistic infections globally. Methicillin-Resistant *S. aureus* (MRSA) is a major public health concern. | Human Reservoir; Causes Pharyngitis/Skin InfectionsSpread person-to-person via respiratory droplets or direct contact. Leading bacterial cause of pharyngitis ("strep throat") and common cause of skin infections (impetigo, erysipelas, cellulitis). | Nasopharyngeal Carriage Common; Endogenous SourceCarried in upper respiratory tract by many healthy individuals. Infection often follows aspiration into lungs or spread to adjacent sites (ears, sinuses), especially after viral illness or with host risk factors. |
| Primary Distinction Test | Catalase PositiveProduces catalase enzyme (bubbles with H₂O₂). Differentiates all Staphylococci from Streptococci and Enterococci. | Catalase Negative; β-HemolyticLacks catalase. Complete clearing (beta-hemolysis) on blood agar is characteristic. | Catalase Negative; α-HemolyticLacks catalase. Partial, greenish hemolysis (alpha-hemolysis) on blood agar is characteristic. |
| II. Morphology | |||
| Gram Stain & Shape | Gram-Positive Cocci in ClustersSpherical cells dividing in multiple planes form grape-like clusters. | Gram-Positive Cocci in ChainsSpherical/ovoid cells dividing in one plane form pairs and chains. | Gram-Positive Lancet-shaped DiplococciOvoid cocci, often in pairs (diplococci) with slightly pointed adjacent ends ('lancet' shape). Can form short chains. |
| Motility/Spores | Non-Motile, Non-Spore-FormingLacks flagella, does not form endospores. | Non-Motile, Non-Spore-FormingLacks flagella, does not form endospores. | Non-Motile, Non-Spore-FormingLacks flagella, does not form endospores. |
| Capsule Presence | Microcapsule Present (Variable)Often a thin polysaccharide capsule (serotypes 5 and 8 most common). Contributes to virulence and biofilm formation. | Hyaluronic Acid Capsule (Mucoid Strains)Some strains have a capsule of hyaluronic acid, which is non-immunogenic (host mimicry) and anti-phagocytic. Gives mucoid appearance. | Polysaccharide Capsule Present (Key Virulence Factor!)Major virulence factor. Anti-phagocytic. Basis for >90 distinct serotypes, used in vaccine formulations. |
| III. Culture Characteristics | |||
| Atmosphere/Growth | Facultative Anaerobe; Grows EasilyGrows readily on basic laboratory media like Blood Agar and Nutrient Agar, with or without oxygen. | Facultative Anaerobe; Needs EnrichmentRequires enriched media (Blood Agar) for optimal growth. Growth often enhanced by CO₂ atmosphere. | Facultative Anaerobe; Needs CO₂ & EnrichmentConsidered capnophilic (requires 5-10% CO₂). Needs enriched media (Blood or Chocolate Agar). |
| Colony Appearance | Medium; Golden/White; Opaque; ButteryTypically 1-3 mm colonies. Staphyloxanthin pigment gives yellow color in many strains. Smooth, convex. | Small (Pinpoint); Gray-White; TranslucentOften less than 1 mm colonies. Typically associated with a relatively large zone of beta-hemolysis. Matte or glossy surface. | Small; Grayish; Umbilicated ('Draughtsman')Around 1 mm colonies, alpha-hemolytic. Older colonies often show central depression (autolysis). Mucoid if heavily encapsulated. |
| Hemolysis (Blood Agar) | Beta-Hemolysis (Complete Clearing)Typically complete lysis of red blood cells due to production of hemolysins (e.g., alpha-toxin). | Beta-Hemolysis (Strong, Wide Zone)Characteristically strong and wide zone of complete lysis due to Streptolysin S and O. | Alpha-Hemolysis (Partial, Greenish)Incomplete lysis with green zone due to H₂O₂ production converting hemoglobin to methemoglobin. |
| Selective Medium Reaction | Grows on Mannitol Salt Agar (+ Mannitol Fermentation)Salt tolerant (grows). Ferments mannitol, turning phenol red indicator yellow around colonies. | Inhibited by High Salt (No Growth on MSA)Does not tolerate high salt concentrations of Mannitol Salt Agar. | Inhibited by High Salt (No Growth on MSA)Does not tolerate high salt concentrations of Mannitol Salt Agar. |
| IV. Key Biochemical Identifiers | |||
| Catalase Test | Catalase PositiveBubbles form with H₂O₂. Key differentiator for Staphylococci. | Catalase NegativeNo bubbles with H₂O₂. Typical for Streptococci. | Catalase NegativeNo bubbles with H₂O₂. |
| Coagulase Test | Coagulase PositiveClots plasma. Defines *S. aureus* versus Coagulase-Negative Staphylococci. | Coagulase NegativeDoes not clot plasma. | Coagulase NegativeDoes not clot plasma. |
| PYR Hydrolysis | PYR NegativeDoes not hydrolyze L-pyrrolidonyl-β-naphthylamide. | PYR PositiveHydrolyzes substrate (red color). Key ID for GAS and Enterococcus. | PYR NegativeDoes not hydrolyze substrate. |
| Bacitracin Susceptibility ('A' Disk) | ResistantNot inhibited by 0.04 U Bacitracin disk. | SusceptibleInhibited (zone). Presumptive ID for Group A Streptococcus. | ResistantNot inhibited by Bacitracin disk. |
| Optochin Susceptibility ('P' Disk) | ResistantNot inhibited by Optochin disk. | ResistantNot inhibited by Optochin disk. | SusceptibleInhibited (zone ≥14mm). Key ID for *S. pneumoniae*. |
| Bile Solubility | InsolubleDoes not lyse in bile salts (remains turbid). | InsolubleDoes not lyse in bile salts. | SolubleLysed by bile salts (clearing). Key ID for *S. pneumoniae*. |
| V. Key Virulence Factors | |||
| Adherence/Colonization | MSCRAMMs (e.g., FnBPs), Protein ASurface proteins bind host matrix molecules. Protein A binds antibodies. Biofilm formation aids colonization. | M Protein, Lipoteichoic Acid (LTA), Protein FMediate adherence to epithelial cells, fibrinogen binding (M Protein). | Adhesins (PsaA, PspC/CbpA...), PiliBind to host cell receptors (e.g., pIgR), mucus. Choline Binding Proteins anchor adhesins. |
| Immune Evasion | Protein A (Binds Immunoglobulin G Fc), CapsuleProtein A prevents opsonization. Capsule inhibits phagocytosis. Coagulase may form protective clot. | M Protein (Anti-phagocytic!), HA Capsule, C5a PeptidaseM protein inhibits complement/phagocytosis. Hyaluronic acid capsule camouflages. C5a peptidase dampens neutrophil recruitment. | Polysaccharide Capsule!, PspA, IgA ProteaseCapsule is primary anti-phagocytic factor. PspA inhibits complement. IgA protease cleaves IgA on mucosa. |
| Cytotoxins | Alpha, Beta, Delta, Gamma Toxins; PVLDamage host cell membranes. Alpha toxin key pore-former. Panton-Valentine Leukocidin linked to severe infections. | Streptolysin O (SLO) & Streptolysin S (SLS)Pore-forming toxins lyse RBCs, WBCs. SLO antigenic (ASO test). SLS oxygen-stable hemolysin. | Pneumolysin (PLY)Major cytotoxin released on lysis. Cholesterol-dependent pore-former, damages respiratory cells, triggers inflammation. |
| Superantigens | TSST-1, Staphylococcal Enterotoxins (SEs)Cause non-specific T-cell activation, massive cytokine release (Toxic Shock Syndrome, Food Poisoning effects). | Strep Pyrogenic Exotoxins (SpeA, C, F...)Cause rash of Scarlet Fever, contribute to Strep Toxic Shock Syndrome (STSS). | Not ApplicableS. pneumoniae does not produce recognized superantigens. |
| Other Key Toxins/Enzymes | Exfoliative Toxins (ETA/B); Spreading FactorsETA/B cause Scalded Skin Syndrome. Hyaluronidase, Kinase, Lipase, DNase aid spread/damage. | SpeB (Cysteine Protease); Spreading FactorsSpeB crucial for tissue destruction (Necrotizing Fasciitis). Streptokinase, Hyaluronidase, DNases aid spread. | Autolysin (LytA); NeuraminidaseLytA releases Pneumolysin. Neuraminidase aids spread/adherence. Hyaluronidase present. |
| VI. Pathogenesis & Disease | |||
| Hallmark Lesion | Abscess (Localized Pus Collection)Coagulase aids localization. Necrosis surrounded by inflammation. | Spreading Inflammation (Cellulitis/Erysipelas)Rapid spread through tissues aided by enzymes. Less localized than Staph abscess. | Lobar Consolidation (Pneumonia)Alveoli fill with edema fluid, RBCs, PMNs due to inflammation/bacterial products. |
| Key Local Diseases | Skin/Soft Tissue Infections (Boils, Impetigo!)Most common cause of folliculitis, furuncles, carbuncles, wound infections. | Pharyngitis ("Strep Throat")!, Impetigo, CellulitisLeading bacterial cause of pharyngitis. Also erysipelas. | Otitis Media!, Sinusitis, ConjunctivitisLeading bacterial cause of middle ear and sinus infections. |
| Key Invasive Diseases | Bacteremia/Sepsis, Endocarditis, Pneumonia, OsteomyelitisSerious bloodstream infections and seeding of distant sites. | Necrotizing Fasciitis!, Bacteremia/Sepsis, PneumoniaLife-threatening deep tissue infection. Can cause severe sepsis. | Pneumonia!, Meningitis!, Bacteremia/SepsisMost common bacterial Community-Acquired Pneumonia cause. Leading cause of bacterial meningitis (post-Hib vaccine). |
| Key Toxin-Mediated Syndromes | Toxic Shock Syndrome!, Scalded Skin!, Food PoisoningSystemic effects caused by TSST-1, Exfoliatins, or Enterotoxins respectively. | Scarlet Fever!, Strep Toxic Shock Syndrome!Rash related to Spe production. Severe systemic illness with invasive disease. | Not ApplicablePneumococcal disease primarily driven by inflammation and direct cytotoxicity of Pneumolysin. |
| Immunologic Sequelae | Not CharacteristicPost-infectious immune syndromes are not typically associated with *S. aureus*. | Acute Rheumatic Fever! Glomerulonephritis!ARF follows pharyngitis; PSGN follows pharyngitis or skin infection. Caused by immune response (cross-reaction / immune complexes). | Not CharacteristicPost-infectious immune syndromes are not associated with *S. pneumoniae*. |
| VII. Laboratory Diagnosis | |||
| Microscopy Finding | Gram(+) Cocci in Clusters (from clinical site)Direct Gram stain highly suggestive if seen with PMNs in pus. | Gram(+) Cocci in Chains (often unreliable)May be seen in clinical samples, but less reliable/sensitive than culture. | Gram(+) Lancet Diplococci (CSF, Sputum)Highly suggestive, especially in CSF Gram stain for meningitis. |
| Culture & Identification Keys | Catalase(+), Coagulase(+), MSA(+) YellowStandard identification pathway for *S. aureus*. | β-hemolysis, Catalase(-), Bacitracin(S), PYR(+)Typical findings for Group A Streptococcus confirmation. | α-hemolysis, Catalase(-), Optochin(S), Bile Soluble(+)Required tests to differentiate *S. pneumoniae* from Viridans streptococci. |
| Rapid Diagnostic Tests | Rapid Coagulase/Latex tests; PCR (MRSA detection)Tests for specific surface components or *mecA* gene. MALDI-TOF rapid ID from culture. | Rapid Antigen Detection Test (RADT) for Throat SwabDetects Group A antigen directly from swab; useful for rapid diagnosis of pharyngitis. | Urine Antigen Test; CSF Antigen/PCR TestsUrine antigen useful for adult pneumonia. CSF tests aid meningitis diagnosis. |
| VIII. Treatment | |||
| Drug of Choice (Susceptible) | Anti-Staphylococcal Penicillin (e.g., Nafcillin, Oxacillin) or 1st Gen CephalosporinFor Methicillin-Susceptible *S. aureus* (MSSA). | Penicillin or AmoxicillinStill uniformly susceptible; preferred narrow-spectrum agents. | Penicillin or Amoxicillin (IF susceptible)Use depends on susceptibility results; resistance common. |
| Treatment for Resistant Strains | MRSA: Vancomycin (Severe); Oral options (e.g., Clindamycin, TMP-SMX, Doxycycline) for SSTIVancomycin standard for invasive MRSA. Community Skin and Soft Tissue Infection options vary by local resistance. Linezolid, Daptomycin alternatives. | Macrolide (e.g., Azithromycin) or Clindamycin (if Penicillin Allergic)Check susceptibility as resistance exists. Cephalosporins possible for non-anaphylactic allergy. | Ceftriaxone, High-Dose Penicillin/Amox, Respiratory Fluoroquinolones, VancomycinChoice depends on MIC/resistance level & site (esp. meningitis). Often combination needed empirically. |
| Important Adjunctive Therapy | Incision and Drainage of Abscesses!Crucial for localized collections of pus. | Surgical Debridement for Necrotizing Fasciitis!Urgent removal of dead tissue is life-saving. | Supportive Care (e.g., Oxygen); Dexamethasone (Meningitis)Maintain oxygenation for pneumonia. Steroids reduce inflammation/sequelae in meningitis. |
| IX. Prophylaxis | |||
| Vaccine Availability | None Currently EffectiveNo licensed vaccine provides broad protection despite efforts. | None AvailableNo vaccine currently available (M protein diversity a challenge). | Yes! Pneumococcal Vaccines (Conjugate & Polysaccharide)PCV (infants/adults) and PPSV23 (adults/risk groups) target capsular polysaccharides. Highly effective. |
| Chemoprophylaxis Uses | MRSA Decolonization (Situational)Nasal Mupirocin +/- CHG washes in specific high-risk scenarios (e.g., pre-surgery). | Penicillin for Rheumatic Fever Recurrence PreventionLong-term prophylaxis needed after episode of Acute Rheumatic Fever. | Penicillin for Asplenia/Splenic DysfunctionTo prevent overwhelming post-splenectomy infection (OPSI). |
| Category / Feature | Neisseria gonorrhoeae (Gonococcus) | Neisseria meningitidis (Meningococcus) |
|---|---|---|
| I. Introduction | ||
| Discovery/Naming | Neisser (1879); Gonorrhea AgentAlbert Neisser identified in purulent exudates. Causative agent of the sexually transmitted infection Gonorrhea. | Weichselbaum (1887); Meningitis AgentAnton Weichselbaum identified from cerebrospinal fluid of meningitis patients. Major cause of epidemic bacterial meningitis and sepsis. |
| Taxonomy/Significance | Genus Neisseria; Strictly Human PathogenFamily Neisseriaceae. Exclusively infects humans, causing significant morbidity related to sexual and reproductive health. | Genus Neisseria; Human Pathogen (often Carrier)Exclusively infects humans. Can be carried asymptomatically in nasopharynx, but causes life-threatening invasive disease (meningitis/sepsis). |
| Epidemiology/Transmission | Sexually Transmitted Infection (STI); High Global BurdenVery common STI worldwide. Spread via sexual contact (vaginal, anal, oral) or perinatally. Asymptomatic infections common, aiding spread. Rising antibiotic resistance is a major concern. | Respiratory Droplets; Nasopharyngeal Carriage; EpidemicsSpread via close contact (respiratory/oral secretions). Endemic/epidemic meningitis, especially in close quarters ('meningitis belt', dorms). Peak incidence in infants and adolescents/young adults. |
| II. Morphology & Structure | ||
| Gram Stain & Shape | Gram-Negative Diplococci (Kidney-Bean Shape)Pairs of cocci with adjacent sides flattened. Often found intracellularly within neutrophils in urethral exudate. | Gram-Negative Diplococci (Kidney-Bean Shape)Similar morphology to gonococcus. Often found intracellularly and extracellularly in cerebrospinal fluid during meningitis. |
| Key Structures | Pili, Outer Membrane Proteins (Opa, Por), LOS, IgA ProteasePili: Essential for attachment, undergo antigenic variation. OMPs: Mediate adherence (Opa), form pores (Por). LOS: Lipooligosaccharide (endotoxin), contributes to inflammation, variable structure aids immune evasion. IgA Protease: Cleaves IgA. NO Capsule. | Polysaccharide CAPSULE!, Pili, OMPs, LOS, IgA ProteaseSimilar Pili, OMPs (Por, Opa), LOS (endotoxin!), IgA Protease as gonococcus. CRITICAL DIFFERENCE: Possesses a major **Polysaccharide Capsule** (serogroups A, B, C, W, Y, X main causes of disease), which is anti-phagocytic and basis for vaccines. |
| III. Culture & Metabolism | ||
| Atmosphere/Growth | Aerobic; Capnophilic; FastidiousRequires oxygen and enriched CO₂ (5-10%). Nutritionally demanding. | Aerobic; Capnophilic; FastidiousRequires oxygen and enriched CO₂. Nutritionally demanding. Optimal temp 35-37°C. |
| Key Media | Chocolate Agar; Selective (Thayer-Martin) EssentialGrows on enriched Chocolate Agar. **Selective media** (e.g., Thayer-Martin, Martin Lewis) containing antibiotics are essential to isolate from contaminated urogenital/rectal/pharyngeal sites. | Chocolate Agar or Blood Agar; Selective Media Not Needed for Sterile SitesGrows well on Chocolate or Blood Agar. Often isolated from normally sterile sites (CSF, blood), so selective media less critical than for gonococcus (but can be used). |
| Key Biochemical Tests | Oxidase Positive, Catalase Positive; Utilizes ONLY GlucoseProduces cytochrome C oxidase. Produces catalase. Utilizes glucose by oxidation but does **NOT** utilize maltose, sucrose, or lactose. | Oxidase Positive, Catalase Positive; Utilizes Glucose AND MaltoseProduces cytochrome C oxidase and catalase. Utilizes **BOTH** glucose and maltose by oxidation. Does not utilize sucrose or lactose. Maltose utilization is key differentiator from gonococcus. |
| IV. Virulence & Pathogenesis | ||
| Key Virulence Factors | Pili (Attachment/Variation), Opa Proteins (Adherence/Invasion), LOS (Endotoxin/Inflammation), IgA ProteaseEmphasis on mucosal attachment and inflammation. Lack of capsule restricts invasiveness compared to meningococcus. Antigenic variation aids immune evasion. | Polysaccharide Capsule (Anti-phagocytic/Invasion!), Pili, Opa, LOS (Endotoxin!), IgA ProteaseEmphasis on invasion enabled by capsule preventing phagocytosis/complement. LOS release contributes significantly to sepsis severity (endotoxic shock, DIC). |
| Key Diseases Caused | Gonorrhea (Urethritis, Cervicitis etc), PID, DGI, Ophthalmia NeonatorumPrimarily mucosal infections: Urethra, cervix, pharynx, rectum, conjunctiva. Ascending infection causes Pelvic Inflammatory Disease (PID). Disseminated Gonococcal Infection (DGI) involves skin/joints. Eye infection in newborns. | Meningitis and/or Meningococcemia (Sepsis)!Invasive disease following bacteremia from nasopharyngeal colonization. Causes purulent meningitis and/or life-threatening sepsis with characteristic petechial/purpuric rash (due to LOS). High mortality if untreated. |
| V. Laboratory Diagnosis | ||
| Primary Diagnostic Method | Nucleic Acid Amplification Test (NAAT)!NAAT (e.g., PCR) on urine, vaginal/cervical swabs, or other site swabs is the preferred method due to high sensitivity and specificity. Gram stain of male urethral discharge is useful. Culture needed for susceptibility. | CSF and Blood Culture!Culture of Cerebrospinal Fluid (CSF) and Blood from symptomatic patients is the gold standard for confirming invasive disease. Gram stain of CSF is critical for rapid presumptive diagnosis. |
| Supportive Lab Findings | Gram Stain (Intracellular Gram-Negative Diplococci); Culture IDPresence of typical GNDC within neutrophils strongly suggests diagnosis in males. Culture confirms species via Oxidase/sugars. | CSF Analysis (PMNs, ↑Protein, ↓Glucose); Antigen/PCRCSF typically shows high white cells (neutrophils), elevated protein, low glucose. CSF antigen detection (latex) or PCR provide rapid supportive evidence. |
| VI. Treatment | ||
| Recommended Treatment | Ceftriaxone (IM, High Dose) - Resistance is MAJOR issue!Single dose Intramuscular Ceftriaxone (500mg) currently recommended due to widespread resistance to older agents (Penicillins, Tetracyclines, Fluoroquinolones) and rising Azithromycin resistance. Co-treatment for Chlamydia often given (Doxycycline). | Ceftriaxone (IV) or Penicillin G (if susceptible)Empiric treatment for suspected invasive disease typically involves Intravenous 3rd generation cephalosporins (e.g., Ceftriaxone). Penicillin G can be used if isolate known susceptible. Supportive care critical for sepsis/shock. |
| Resistance Considerations | Alarming resistance levels globally; Susceptibility testing vitalResistance via multiple mechanisms (PBP alteration, efflux pumps, plasmid-mediated resistance) severely limits treatment options. Surveillance crucial. | Penicillin resistance exists (altered PBP); Cephalosporin resistance rareWhile penicillin resistance occurs, high-level resistance or resistance to third-generation cephalosporins remains uncommon currently. |
| VII. Prophylaxis & Prevention | ||
| Vaccine | None AvailableVaccine development challenging due to antigenic variation of surface proteins. | Yes! Effective Conjugate & Protein Vaccines Available**MenACWY conjugate vaccines** protect against serogroups A,C,W,Y. **MenB recombinant protein vaccines** protect against serogroup B. Routinely recommended for adolescents and high-risk groups. |
| Chemoprophylaxis | No Routine Use (Partner treatment essential)Post-exposure prophylaxis not routinely recommended. Emphasis on treating diagnosed cases and their sexual partners. | Yes! Crucial for Close ContactsAntibiotic prophylaxis (e.g., Rifampin, Ciprofloxacin, Ceftriaxone) recommended for close contacts of patients with invasive meningococcal disease to eliminate carriage. |
| Other Prevention | Safe Sex Practices (Condoms); ScreeningCondom use reduces risk. Screening asymptomatic high-risk individuals. Ophthalmia Neonatorum prevention via Erythromycin eye ointment at birth. | Droplet Precautions (Hospital); Vaccination CampaignsStandard/Droplet precautions for hospitalized patients. Public health surveillance and vaccination programs key to controlling outbreaks. |
| Category / Feature | Corynebacterium diphtheriae | Clostridium tetani | Clostridium botulinum | Clostridium perfringens | Clostridioides difficile |
|---|---|---|---|---|---|
| I. Introduction | |||||
| Key Distinguishing Feature | Potent Diphtheria Toxin (Phage Mediated)Produces A-B exotoxin inhibiting protein synthesis, requires lysogenic phage conversion. | Potent Tetanospasmin NeurotoxinProduces tetanus neurotoxin (plasmid-encoded) causing spastic paralysis (Tetanus). | Potent Botulinum Neurotoxin (Most Lethal!)Produces diverse BoNTs (phage/plasmid), blocks Acetylcholine release causing flaccid paralysis (Botulism). | Multiple Toxins (Alpha Toxin!); Gas Gangrene AgentProduces many toxins, Alpha toxin (lecithinase) essential for myonecrosis (Gas Gangrene). Also causes food poisoning (Enterotoxin CPE). | Toxins A (Enterotoxin) & B (Cytotoxin)Produces TcdA/TcdB damaging colonic mucosa causing antibiotic-associated diarrhea and pseudomembranous colitis (CDI). |
| Reservoir/Transmission | Humans Only; Droplets/ContactNasopharynx/skin reservoir. Respiratory droplet or direct contact transmission. | Soil, Dust, Animal Feces; Wound ContaminationUbiquitous spores contaminate wounds (puncture, crush injury). | Soil, Sediment; Foodborne (Toxin), Infant (Spores), WoundTransmission via ingestion of pre-formed toxin (improper canning) or spores (esp. infants, honey), or wound contamination. | Soil, Gut Flora; Wound Contamination / FoodborneSpores in soil contaminate wounds (Gas Gangrene). Spores/vegetative cells ingested in food cause food poisoning. | Gut Flora (Minority) / Environment (Spores!); Fecal-Oral (Nosocomial!)Small numbers in healthy gut. Spores persist in environment (hospitals!). Fecal-oral spread, esp. after antibiotic disruption of normal flora. Major hospital-acquired infection. |
| II. Morphology & Structure | |||||
| Gram Stain & Shape | Gram(+) Pleomorphic Rod (Club, Palisades)Variable staining. Irregular 'Chinese letter' or parallel arrangements. Contains granules. | Gram(+) Slender RodMay be hard to Gram stain. Flagellated. | Gram(+) RodFlagellated. | Gram(+) Large "Boxcar" RodRelatively large rods, often parallel. Non-motile. Capsule often present in vivo. | Gram(+) RodMay be difficult to Gram stain. Flagellated. |
| Endospores | Non-Spore-FormingDoes not produce endospores. | Yes! Terminal, Spherical ('Drumstick')Produces round terminal spore, swelling the sporangium. | Yes! Subterminal, OvalProduces oval spores in subterminal position, may swell cell. | Yes! Subterminal, Oval (RARELY seen in vitro)Forms spores, but often not observed readily in standard lab culture conditions or clinical samples. | Yes! Subterminal, OvalForms spores that persist in environment/transmit infection. |
| III. Culture & Metabolism | |||||
| Oxygen Requirement | Aerobe / Facultative AnaerobeGrows well in presence of oxygen. | Obligate (Strict) AnaerobeRequires absence of oxygen for growth. Oxygen is toxic. | Obligate (Strict) AnaerobeRequires anaerobic conditions. | Aerotolerant AnaerobePrefers anaerobic but tolerates some oxygen. Grows rapidly under anaerobic conditions. | Obligate (Strict) AnaerobeRequires anaerobic conditions. |
| Culture Notes | Grows on BA; Selective: Tellurite Agar (Black colonies)Loeffler's medium enhances granule formation. CTBA inhibits normal flora. | Difficult/Slow; Anaerobic Blood Agar; RCM BrothSwarming on agar may occur. Hemolysis common. | Difficult/Slow; Anaerobic Media (Egg Yolk Agar - Lipase)Requires specialized anaerobic techniques. Lipase activity helps ID group I. | RAPID Growth; Anaerobic Blood Agar; Double Zone Hemolysis!Very fast doubling time. Characteristic dual zone of hemolysis is highly suggestive. Stormy fermentation in milk. | Difficult; Selective CCFA Agar (Yellow, "Horse Manure" Smell)Requires anaerobic conditions. Cycloserine-Cefoxitin-Fructose Agar inhibits fecal flora. Smells characteristic. |
| Key Biochemicals | Catalase(+), Nitrate Reduct(+), Urease(-)Ferments glucose/maltose. | Catalase(-), Indole(-), Ferments few sugarsProteolytic. Biochemically relatively inert. | Catalase(-), Variable ferm/proteolysisDiverse groups (I-IV) based on proteolysis/sugars. Lipase useful ID marker for some. | Catalase(-), Lecithinase(+) (Nagler test), Ferments Sugars (Gas!)Strong fermentation (stormy clot in milk). Gelatinase(+). Nagler test detects alpha-toxin lecithinase activity. | Catalase(-), Indole(-)Characteristic profile on selective media/API tests. |
| IV. Key Virulence & Disease | |||||
| Primary Toxin(s) | Diphtheria Toxin (DT)A-B toxin; inhibits protein synthesis (ADP-ribosylates EF-2). | TetanospasminA-B neurotoxin; blocks inhibitory neurotransmitter release (glycine/GABA). | Botulinum Neurotoxin (BoNT)A-B neurotoxin; blocks Acetylcholine release at neuromuscular junction. Types A-G. | Alpha Toxin (CPA); Enterotoxin (CPE); OthersCPA=Lecithinase (myonecrosis). CPE=Diarrhea. Beta, Epsilon, Iota toxins important in subtypes/animals. | Toxin A (TcdA); Toxin B (TcdB)Large glucosylating toxins disrupting cytoskeleton, tight junctions causing enterocyte death/inflammation. TcdB more potent cytotoxin. Some strains = Binary Toxin (CDT). |
| Primary Disease | Diphtheria (Respiratory or Cutaneous)Pseudomembrane formation, potential systemic cardiac/neurologic toxicity. | TetanusSpastic paralysis ("lockjaw", opisthotonos), muscle rigidity/spasms. | Botulism (Foodborne, Infant, Wound)Descending flaccid paralysis, respiratory failure. | Gas Gangrene (Myonecrosis); Food PoisoningRapidly progressive muscle necrosis with gas production. Self-limited watery diarrhea (food poisoning). | Antibiotic-Associated Diarrhea; Pseudomembranous Colitis (CDI)Ranges from mild diarrhea to severe, potentially fatal colitis following antibiotic use. |
| V. Laboratory Diagnosis | |||||
| Key Diagnostic Approach | Culture (Tellurite) + TOXIN Detection (Elek/PCR)!Isolating organism AND proving toxigenicity is essential. | Clinical Diagnosis Primary!; Culture DifficultDiagnosis based on characteristic symptoms. Lab confirmation hard/slow. Toxin detection not routine. | Clinical Dx; Toxin Detection in Serum/Stool/Food (Mouse Bioassay/Immunoassay)!Identifying toxin is key. Culture supports. | Clinical Picture (Gas Gangrene); Anaerobic Culture (Nagler); CPE Toxin Assay (Food Poisoning)Gas gangrene diagnosis often clinical/imaging. Culture confirms. Toxin assay on stool/food confirms food poisoning. | Toxin Detection in Stool (EIA/NAAT)!; Culture +/-Detecting Toxin A/B or their genes (NAAT/PCR) in stool of symptomatic patient is standard. Culture can be done but not sufficient alone. Glutamate Dehydrogenase (GDH) antigen test is sensitive screen. |
| VI. Treatment | |||||
| Key Treatment Modality | Antitoxin! + AntibioticsDiphtheria Antitoxin (DAT) is crucial. Erythromycin or Penicillin also given. | Antitoxin (TIG)! + Antibiotics + Supportive CareHuman Tetanus Immune Globulin. Metronidazole or Penicillin. Debridement. Control spasms. | Antitoxin! + Supportive Care (Ventilation!)Equine antitoxin or BabyBIG for infants. Respiratory support paramount. Antibiotics only for wound botulism. | Surgical Debridement! + Antibiotics (Penicillin + Clindamycin)Urgent surgery is life-saving for gas gangrene. Hyperbaric O₂ secondary. Food poisoning supportive only. | Oral Vancomycin or FidaxomicinStop offending antibiotic. Metronidazole secondary choice now. Fecal Microbiota Transplant (FMT) for recurrence. |
| VII. Prophylaxis | |||||
| Vaccine | Yes! (Diphtheria Toxoid)In DTaP/Tdap/Td vaccines. Very effective. | Yes! (Tetanus Toxoid)In DTaP/Tdap/Td vaccines. Requires boosters. Very effective. | None routinely used (Equine Toxoid exists for high risk)No routine human vaccine. | None availableNo human vaccine. | None availableNo vaccine currently available. |
| Other Prevention | Vaccination; Respiratory IsolationMaintain high vaccine coverage. | Vaccination; Proper Wound Care; TIG Post-ExposureEnsure adequate booster status. Clean wounds. TIG if wound high risk & uncertain vax status. | Proper Food Canning/Heating; Avoid Honey (<1yr)Heat inactivates toxin. Infant botulism risk from honey. | Proper Wound Care; Safe Food TemperaturesPrevent contamination; cook/reheat food adequately for food poisoning prevention. | Judicious Antibiotic Use; Infection Control (Hand Wash - Soap!; Contact Precautions)Spores resistant to alcohol hand gels. Environmental cleaning critical. |
| Category / Feature | Escherichia coli | Klebsiella pneumoniae | Proteus mirabilis | Salmonella enterica | Shigella spp. |
|---|---|---|---|---|---|
| I. Introduction | |||||
| General Family Traits | Facultative Anaerobes, Gram(-) Rods, Glucose Ferm(+), Oxidase(-), Nitrate Reduct(+)All members share these core characteristics. They grow readily on standard media and are typically found in the GI tract or environment. Many species, huge clinical impact (UTI, Sepsis, GI). | ||||
| Common Associations | #1 Urinary Tract Infection Cause; Diarrhea Types; Neonatal Meningitis; SepsisUbiquitous commensal but major opportunistic pathogen. Diverse pathotypes cause different diseases. | Pneumonia (CAP/HAP); UTI (Catheter); Liver AbscessProminent capsule is key feature. Often affects hospitalized or immunocompromised patients (alcoholics, diabetics). | Urinary Tract Infection (esp. Complicated); Kidney Stones!Potent urease activity leads to struvite stone formation. Common cause of catheter-associated UTI. | Gastroenteritis (Non-typhoidal); Enteric Fever (Typhoidal)Many serovars cause self-limited diarrhea. *S. Typhi* and *Paratyphi* cause systemic Typhoid/Paratyphoid Fever. | Dysentery (Shigellosis)!Humans only reservoir. Low infectious dose causes inflammatory colitis with bloody, mucoid stools. |
| II. Morphology & Key Structures | |||||
| Shape | Straight RodTypical GNR. | Straight RodTypical GNR. | Straight Rod (often pleomorphic)Can show variability in length. | Straight RodTypical GNR. | Straight RodTypical GNR. |
| Motility | Motile (Most Strains)Typically motile via peritrichous flagella (H antigen). Some exceptions (e.g., certain pathogenic strains). | NON-MOTILE!Characteristically lacks flagella. Important diagnostic feature. | Highly Motile (SWARMING!)Characteristic rapid "swarming" motility across agar surface due to peritrichous flagella. | Motile (Most Serovars)Typically motile via peritrichous flagella.*S. Gallinarum* & *S. Pullorum* are non-motile. | NON-MOTILE!Characteristically lacks flagella. Key differentiator from *E. coli* and *Salmonella*. |
| Capsule (K Antigen) | Variable (e.g., K1 type = meningitis)Presence and type vary. K1 capsular antigen strongly associated with neonatal meningitis and sepsis strains. | Prominent Polysaccharide Capsule!Produces a large mucoid capsule contributing to virulence (anti-phagocytic) and characteristic colony appearance. | Usually No CapsuleCapsule not typically a major feature. | Vi Antigen (*S. Typhi*)Capsular Vi antigen present in *S. Typhi*, important virulence factor (inhibits complement/phagocytosis). Other serovars generally non-encapsulated. | No CapsuleLacks a capsule. |
| Pili / Fimbriae | Yes (Type 1, P Pili etc)Crucial for adherence, esp. in UTIs (P pili) and gut colonization (Type 1, others). | Yes (Type 1, Type 3)Mediate adherence to respiratory/urinary epithelium, contribute to biofilm. | Yes (e.g., MR/P Fimbriae)Important for adherence and biofilm formation in urinary tract. | Yes (e.g., Type 1 Fimbriae)Important for adherence to intestinal epithelium. | Not Major Virulence Factor (relative to invasion)Relies more on direct invasion mechanisms. |
| III. Key Culture & Biochemical Identifiers | |||||
| Lactose Fermentation (on MacConkey Agar) | Lactose Fermenter [+] (Pink/Red Colonies)Rapidly ferments lactose, producing acid -> pink/red colonies. | Lactose Fermenter [+] (Mucoid Pink Colonies)Rapidly ferments lactose -> pink colonies, often very mucoid due to capsule. | Non-Lactose Fermenter [-] (Pale/Colorless)Does not ferment lactose -> pale colonies. May swarm over plate. | Non-Lactose Fermenter [-] (Pale/Colorless)Does not ferment lactose -> pale colonies. | Non-Lactose Fermenter [-] (Pale/Colorless)Does not ferment lactose -> pale colonies. *S. sonnei* is a late lactose fermenter. |
| Indole Production (IMViC 'I') | Indole Positive [+]Produces indole from tryptophan (red color with Kovac's reagent). | Indole Negative [-]Does not produce indole. | Indole Variable*P. mirabilis* is typically Negative, *P. vulgaris* is Positive. | Indole Negative [-]Does not produce indole. | Indole VariableMost are negative; *S. sonnei* can be positive. |
| Citrate Utilization (IMViC 'C') | Citrate Negative [-]Cannot use citrate as sole carbon source (remains green on Simmons Citrate Agar). | Citrate Positive [+]Can use citrate (turns Simmons Citrate Agar blue). | Citrate Positive [+]Typically positive. | Citrate Positive [+]Can use citrate. | Citrate Negative [-]Cannot use citrate. |
| Urease Production | Urease Negative [-]Does not hydrolyze urea. | Urease Positive [+] (Variable Speed)Produces urease (pink color on Urea Agar), but slower than Proteus. | Urease RAPID Positive [+]!Characteristically produces large amounts of urease rapidly -> bright pink on Urea Agar. | Urease Negative [-]Does not produce urease. | Urease Negative [-]Does not produce urease. |
| Hydrogen Sulfide (H₂S) Production (on TSI Agar) | H₂S Negative [-]Does not produce H₂S (no black precipitate in TSI tube butt). | H₂S Negative [-]Does not produce H₂S. | H₂S Positive [+]Produces H₂S (blackening of TSI butt). | H₂S Positive [+]!Characteristically produces H₂S (black precipitate in TSI). *S. Typhi* produces only a small amount. | H₂S Negative [-]!Characteristically does NOT produce H₂S. Key differentiator from *Salmonella*. |
| IV. Virulence & Pathogenesis | |||||
| Lipopolysaccharide (LPS) / Endotoxin | Yes (O Antigen varies)Contributes to sepsis/inflammation. O antigen used in serotyping (e.g., O157:H7). | YesCauses inflammation, fever, potential shock. | YesEndotoxin effects contribute to systemic response in UTI/sepsis. | YesContributes to fever/inflammation in gastroenteritis and systemic effects in Enteric Fever. | YesContributes to inflammation and fever during dysentery. |
| Key Adherence / Colonization Factors | Type 1 Pili, P Pili, Others (Pathotype specific)Mediate attachment to urinary tract (P pili) or gut (various types depending on pathotype, e.g., BFP in EPEC). | Type 1 & Type 3 Fimbriae, CapsuleMediate binding to various epithelial surfaces (respiratory, urinary). Capsule prevents phagocytosis. Biofilm. | Fimbriae (MR/P, UCA...), Flagella (Motility)Adherence to uroepithelium, catheter surfaces. Swarming aids ascent. Biofilm. | Type 1 Fimbriae, others; Invasion factorsAttachment to enterocytes/M cells necessary prior to invasion. Flagella aid movement. | Invasion Plasmid Antigens (Ipa proteins); Direct cell contactRelies heavily on direct invasion mediated by T3SS injecting Ipa proteins. Adherence less emphasized. |
| Major Toxins (Excluding Endotoxin) | Pathotype Dependent! (LT/ST, Stx, Hemolysin...)ETEC: Heat-Labile (LT, like cholera) / Heat-Stable (ST) toxins -> watery diarrhea. EHEC/STEC: Shiga Toxin (Stx1/Stx2) -> bloody diarrhea, Hemolytic Uremic Syndrome (HUS). UPEC: Alpha-Hemolysin. | Few Specific ToxinsVirulence primarily mediated by capsule and LPS/inflammation. No major exotoxins defining pathogenicity. | Hemolysin; Urease effectsProteus Hemolysin (HpmA). Ammonia from urease is cytotoxic. IgA protease. | None Defining (compared to others)Pathogenesis primarily driven by invasion (T3SS) and resulting inflammation/systemic spread (Enteric Fever). No major exotoxins like Cholera or Shiga Toxin. | Shiga Toxin (Stx - esp. *S. dysenteriae* 1)!A-B toxin inhibits protein synthesis, damages endothelial cells -> Contributes to bloody diarrhea & potential HUS. Other species have less/no Stx. |
| Invasion / Intracellular Capability | Variable (EIEC invades; UPEC intracellular?; EPEC/EHEC attach)EIEC: Invades colonic epithelium like *Shigella*. UPEC: Can invade bladder cells, form intracellular bacterial communities (IBCs). EPEC/EHEC: Primarily extracellular, form attaching/effacing lesions. | Primarily ExtracellularCapsule inhibits phagocytosis. Does not typically rely on active invasion or intracellular replication. | Extracellular (Urinary Tract Infection focus)Does not typically invade systemically. Primarily infects the urinary tract lumen. | Invasive! (T3SS-mediated); Survives in MacrophagesActively invades enterocytes & M cells using **Type III Secretion System-1**. For *S. Typhi/Paratyphi*, survives/replicates within macrophages using **T3SS-2**, enabling systemic spread. | HIGHLY Invasive! (T3SS); Intracellular Spread!Invades colonic epithelial cells via **T3SS**, lyses phagosome, multiplies in cytoplasm, spreads cell-to-cell using host **actin polymerization**. |
| V. Treatment & Resistance Notes | |||||
| Resistance Concerns | Major Issue! ESBLs, Fluoroquinolone-Resistance common. CRE emerging.Susceptibility testing essential for guiding therapy, especially for serious infections. | Major Issue! ESBLs, Carbapenemases (KPC, NDM etc -> CRE!) Frequent!*K. pneumoniae* is a major source of dangerous resistance mechanisms. Limited treatment options for Carbapenem-Resistant Enterobacteriaceae (CRE). | Resistance Increasing (Fluoroquinolones, Trimethoprim-Sulfamethoxazole)ESBL production also occurs. Check susceptibility. | Fluoroquinolone Resistance Increasing Globally! (esp. Typhoid)Also resistance to older agents (Ampicillin, TMP-SMX). Requires susceptibility testing for Enteric Fever. Gastroenteritis often needs no antibiotics. | Fluoroquinolone & Azithromycin Resistance Rising Globally!Limits options for treatment of dysentery, esp. from travel. Susceptibility testing recommended if treating. |
| VI. Prophylaxis & Prevention | |||||
| Key Prevention | Hygiene, Safe Food/Water, Proper Catheter CareGeneral measures critical. Traveler's precautions. Urinary Tract Infection prevention strategies. | Infection Control! Hand Hygiene, Environmental CleaningCrucial in healthcare to prevent spread of resistant strains (esp. Carbapenem-Resistant Enterobacteriaceae - CRE). | Catheter Care, HygienePreventing catheter associated UTIs. Maintaining urine flow. Prevent stone formation. | Safe Food Handling (Poultry!), Safe Water, Hygiene; Typhoid Vaccine!Cook food thoroughly. Prevent cross-contamination. Vaccination for travelers/endemic areas (*S. Typhi*). | HANDWASHING!, Sanitation, Safe Food/WaterStrict hygiene critical due to low infectious dose. Prevent fecal-oral spread. |
| Category / Feature | Vibrio cholerae | Haemophilus influenzae | Bordetella pertussis | Brucella spp. |
|---|---|---|---|---|
| I. Introduction | ||||
| Key Association | Cholera Toxin / "Rice Water Diarrhea"Production of Cholera Toxin leads to massive fluid loss. Causes Cholera pandemics. | Needs X+V Factors / Hib Vaccine ImpactRequires specific growth factors. *H. influenzae* type b (Hib) impact greatly reduced by vaccine. Non-typeable strains (NTHi) now more prevalent clinical isolates. | Whooping Cough / Pertussis ToxinCausative agent of Pertussis. Virulence largely mediated by toxins, especially Pertussis Toxin. | Brucellosis / Undulant Fever (Zoonosis)Systemic zoonotic disease acquired from animals or unpasteurized dairy. Intracellular pathogen. |
| Oxygen Requirement / Key Metabolism | Facultative Anaerobe / Oxidase [+]Oxidase positive distinguishes from Enterobacteriaceae. Ferments Sucrose. | Facultative Anaerobe / Capnophilic / Oxidase [Variable]Requires CO₂. Oxidase variable. Does not typically ferment many sugars. | Strict Aerobe! / Oxidase [+]Requires oxygen. Fastidious metabolism, does not ferment carbohydrates. | Strict Aerobe! / Oxidase [+] / Urease [+]Requires oxygen. Positive for Urease production (key feature). |
| II. Morphology & Structure | ||||
| Gram Stain & Shape | Gram (-) Curved Rod (Comma)Characteristic shape. | Gram (-) Coccobacillus/Pleomorphic RodSmall, variable shape. | Gram (-) Tiny CoccobacillusVery small. Stains faintly. | Gram (-) Tiny CoccobacillusSmall, often stains poorly. |
| Key Structures | Polar Flagellum; Toxin Co-regulated Pili (TCP); Lipopolysaccharide (LPS)Flagellum allows motility. TCP essential for colonization and as phage receptor. O antigen defines serogroups (O1/O139). | Capsule (Hib=PRP!); Pili; LOS/LPSPolyribitol Phosphate capsule of type b is key vaccine target/virulence factor. Non-typeable strains lack capsule. LOS is major endotoxin component. | Adhesins (FHA, PRN)!; Toxins!; PiliFilamentous Hemagglutinin & Pertactin crucial for binding respiratory epithelium. Multiple toxins mediate disease. | Intracellular! (Facultative); Smooth/Rough LPSSurvival within macrophages key. LPS phase variation (Smooth=virulent). Lacks classical exotoxins/capsules. |
| III. Culture | ||||
| Key Media / Growth Conditions | TCBS Agar (Yellow colonies)!; Alkaline Peptone Water (APW)Selective/Differential TCBS (Thiosulfate Citrate Bile Sucrose) agar yields yellow colonies due to sucrose fermentation. APW for enrichment. Grows rapidly. | Chocolate Agar (Needs X+V factors)!; SatellitismRequires lysed blood (Chocolate agar) for X (hemin) and V (NAD+). Satellitism = growth near V-factor producing *Staph* on blood agar. Needs CO₂. | Regan-Lowe / Bordet-Gengou (Special Media!) Slow growthVery fastidious. Requires charcoal/potato/blood-based media with inhibitors. Takes 3-7+ days. Tiny "mercury drop" colonies. | Enriched Blood Agar; Slow Growth! Biosafety Level-3!Slow growth (days-weeks). Requires enriched media. **Handle in BSL-3 lab due to risk of lab-acquired infection.** |
| IV. Virulence & Disease | ||||
| Primary Virulence Factor(s) | Cholera Toxin (CTX)!; TCP PiliCTX causes massive fluid secretion via increased cAMP. TCP pili essential for intestinal colonization. | PRP Capsule (Hib!); Adhesins; IgA Protease; LOSCapsule prevents phagocytosis/complement (Hib). Adhesins (Pili, HMW1/2) bind respiratory cells. LOS causes inflammation. | Adhesins (FHA, PRN); Pertussis Toxin(PTx)!; ACT; TCTAdhesins attach to ciliated cells. PTx ADP-ribosylates Gi (↑cAMP, lymphocytosis). ACT forms pores, ↑cAMP. TCT damages ciliated cells. | Intracellular Survival! (Macrophages); LPS (Smooth type); Inhibition of Phagolysosome FusionEvades killing inside macrophages. Smooth LPS linked to virulence. May use Type IV Secretion System. |
| Key Disease(s) | Cholera! (Severe Dehydrating Watery Diarrhea)Profuse "rice water stool", leading to shock if untreated. | Meningitis/Epiglottitis(Hib pre-vac!); Otitis/Sinusitis/Pneumonia(NTHi!)Spectrum shifted from invasive Hib disease to mucosal NTHi disease post-vaccination. | Whooping Cough! (Pertussis)Prolonged coughing illness with characteristic 'whoop', esp. severe in infants. | Brucellosis! (Systemic, Undulant Fever, Granulomas)Febrile illness with wide range of potential focal complications (bone, joint, liver, spleen). Can be chronic. |
| V. Laboratory Diagnosis | ||||
| Primary Method | Stool Culture (TCBS!) / Serotyping O1/O139 / Rapid Ag TestsCulture confirms diagnosis. Rapid tests used in outbreaks. | Culture (Chocolate!) / Gram Stain (Sterile site) / PCR / X+V TestCulture confirms species, determines X/V needs. | PCR! (NP swab/aspirate); Culture Difficult/SlowPCR is now the diagnostic standard. Culture has low sensitivity and requires special handling. | Blood Culture! (Prolonged Incubation); Serology! (Agglutination/ELISA)Culture essential but slow/needs BSL-3. Serology plays key role in diagnosis. |
| VI. Treatment | ||||
| Standard Treatment | REHYDRATION! (Oral/IV); Antibiotics Secondary (Doxycycline/Azithromycin)Fluid replacement is life-saving. Antibiotics shorten duration. | Amoxicillin-Clavulanate / Cephalosporins (due to β-lactamase)Check susceptibility. Serious infections = Ceftriaxone. | Macrolides (Azithromycin/Erythromycin - Esp. Early!)Treat to reduce transmission and maybe duration/severity if given early (catarrhal stage). | Doxycycline + Rifampin or Aminoglycoside (Combo Therapy Essential!)Combination required for cure and relapse prevention. Long duration (6+ weeks). |
| VII. Prophylaxis & Prevention | ||||
| Vaccine? | Yes (Oral Killed - targeted use)OCVs used in endemic areas/outbreaks. Not for routine travel. | Yes (Hib Conjugate - HIGHLY Effective!)Routine childhood vaccine against type b capsule. Does NOT protect against NTHi. | Yes (Acellular Pertussis in DTaP/Tdap)!Key component of childhood/adolescent/adult immunizations. Waning immunity requires boosters (Tdap). | No (Human); Yes (Animal Control)Human vaccine not available. Control via animal vaccination/testing/culling. |
| Other Prevention | Safe Water & Sanitation! Personal HygieneFundamental for controlling cholera transmission. | Hib Vaccine Schedule ComplianceCompleting series vital for protection. Rifampin prophylaxis rarely needed now for contacts. | DTaP/Tdap Vaccinations!; Droplet Precautions; Post-exposure Prophylaxis (Contacts)Macrolides for close contacts of active case. | Pasteurization!; Avoid Risky Contact (Animals/Tissues); Lab Safety!Handle animal products safely. High risk of lab acquired infection requires BSL-3. |
| Category / Feature | Mycobacterium tuberculosis complex | Mycobacterium leprae | Atypical Mycobacteria (NTM) Overview |
|---|---|---|---|
| I. Introduction | |||
| Defining Feature | Causes Tuberculosis!; Acid-Fast Bacilli (AFB)Chronic granulomatous disease. Cell wall rich in mycolic acids confers acid-fastness. | Causes Leprosy!; Unculturable AFBChronic disease primarily of skin and peripheral nerves. Cannot be grown in lab media. | Environmental AFB; Opportunistic InfectionsFound in environment (water/soil). Cause disease mainly in immunocompromised or those with underlying lung issues. |
| Transmission | Airborne Droplets (Human Reservoir)Inhalation of aerosolized particles from infected individuals. | Prolonged Contact (Resp Droplets?); Humans/Armadillos ReservoirNot highly contagious. Mode uncertain, likely respiratory. Armadillos are animal reservoir in Americas. | Environmental Exposure (Water, Soil); Generally Not Person-to-PersonAcquired via inhalation, ingestion, or inoculation from environmental sources. |
| II. Morphology & Structure | |||
| Staining / Wall | ACID-FAST Rods!; High Lipid / Mycolic Acid WallRequires Ziehl-Neelsen or Kinyoun stain (or fluorescent stain). Wall responsible for resistance. | ACID-FAST Rods! (Often weaker/in Globi); High Lipid Wall; PGL-1Often seen in clumps within macrophages/nerves. Specific Phenolic Glycolipid-1 present. | ACID-FAST Rods!; High Lipid / Mycolic Acid WallSimilar wall structure conferring acid-fastness. |
| Growth Pattern | "Cording" in liquid cultureCharacteristic serpentine cords linked to virulence (Cord Factor). | Forms "Globi" (clumps) in infected cellsLarge collections of bacilli within macrophages in lepromatous leprosy. | Variable (Smooth/Rough colonies; Pigment varies)Used in Runyon classification based on growth rate and pigment production (photo/scoto/non-chromogenic). |
| III. Culture & Metabolism | |||
| Oxygen / Growth Rate | Obligate Aerobe; VERY Slow Grower (Weeks)!Needs O₂. Divides approx every 18-24 hours. | Obligate Intracellular; Cannot be Cultured *In Vitro*!Has lost many genes needed for independent growth. | Aerobic; Variable Growth Rate (Slow / Rapid)!Key differentiator: Slow (>7 days) vs Rapid (<7 days) growers. |
| Media / Conditions | Lowenstein-Jensen (LJ) / Middlebrook Agar; 37°C; Slow GrowthComplex egg-based or agar-based media needed. Automated liquid systems (MGIT) faster. | Needs Animal Models (Mouse Footpad, Armadillo)Only way to propagate the organism for research. | LJ / Middlebrook; Temperature varies (e.g., 30°C for *M.marinum*)Culture requirements differ by species. Growth rate crucial for grouping. |
| Key ID Features | Niacin Accumulation(+), Nitrate Reduction(+)(Traditional biochem). Now NAAT (GeneXpert)/Probes/Sequencing primary from culture/specimen. | Unculturable; Diagnosed Clinically + Biopsy AFB/HistologyCannot use biochemicals. Relies on clinical signs and detecting AFB in lesions. | Growth Rate/Temp/Pigment; Molecular ID (hsp65, rpoB sequencing etc)!Biochemicals less reliable; precise species ID by molecular methods critical for treatment. |
| IV. Virulence & Disease | |||
| Key Virulence Mech. | Intracellular Survival!(Macs); Inhibit Phagolysosome; Cell Wall Lipids (LAM, Cord Factor)Resists macrophage killing, modulates immune response. Granuloma formation contains but allows persistence. | Intracellular Survival!(Macs/Schwann cells!); Nerve Tropism!; PGL-1Unique ability to infect peripheral nerve Schwann cells. Cell wall glycolipid PGL-1 involved. Immune response dictates spectrum. | Intracellular Survival; Resistance; Biofilm (some); Varies by speciesCan resist host defenses. Intrinsic drug resistance common in many NTMs. Biofilms aid environmental survival/colonization. |
| Primary Disease(s) | Tuberculosis! (Pulmonary mostly; Extrapulmonary possible), Latent Infection (LTBI) commonActive disease develops from primary infection or reactivation of LTBI. | Leprosy! (Hansen's Disease); Tuberculoid<->Lepromatous Spectrum; Nerve Damage!Chronic disease defined by host immune response. Nerve involvement leads to disability. | Pulmonary Disease (MAC! *kansasii*); Lymphadenitis (kids); Skin/Soft Tissue Infections; Disseminated Disease (AIDS/Immunocompromised)Wide spectrum depending on NTM species and host factors. |
| V. Diagnosis & Treatment | |||
| Diagnosis | AFB Smear/Culture/NAAT!; TST/IGRA (for Latent TB Infection)Need to detect organism (Active disease) or immune response (Latent infection). NAAT (e.g., GeneXpert) is rapid/sensitive. | Clinical Exam! + AFB Smear/Skin Biopsy!Diagnosis relies heavily on recognizing clinical signs plus demonstrating AFB in slit smears or biopsies. Culture impossible. | AFB Smear/Culture! + Molecular Species ID!; ImagingCulture essential for species ID and susceptibility. Molecular methods vital for identifying species accurately. Clinical/radiological context important. |
| Treatment Approach | Multi-Drug Therapy (MDT - RIPE!) + Long Duration!; MDR/XDR TB Threat!Standard 6-month regimen (Rifampin/Isoniazid/Pyrazinamide/Ethambutol). Longer/complex for resistance. Directly Observed Therapy critical. | Multi-Drug Therapy (MDT - Rifampicin/Dapsone/Clofazimine)! + Long DurationWHO regimens based on paucibacillary (6mo) vs multibacillary (12mo) classification prevent resistance. | Multi-Drug Therapy! + Very Long Duration! + Species & Susceptibility Dependent!Complex regimens based on species/resistance pattern. Often includes macrolide + ethambutol + rifamycin (e.g., MAC). *M. abscessus* very hard to treat. |
| VI. Prophylaxis & Prevention | |||
| Vaccine / Prevention | BCG Vaccine (Variable Efficacy); Latent TB Infection Treatment!; Infection ControlBCG protective vs severe childhood TB. Treating LTBI prevents active disease. Respiratory isolation key for pulmonary TB cases. | BCG Vaccine (Partial Protection?); Early Diagnosis/Treatment; Contact Prophylaxis?MDT stops transmission. Single-dose Rifampicin for contacts studied. | No Vaccine; Avoid Environmental Exposure (if high risk); Prophylaxis(AIDS/MAC)Prevention difficult. MAC prophylaxis (Azithro) for severe immunosuppression. Proper medical device sterilization. |
| Category / Feature | Treponema pallidum | Borrelia burgdorferi (Lyme) | Leptospira interrogans |
|---|---|---|---|
| I. Introduction | |||
| Shape / Visualization | Thin, Tightly Coiled Helices; Darkfield Microscopy Needed!Requires live specimen microscopy to see characteristic motility. Stains poorly. | Larger Diameter, Wider Coils; Visible w/ Giemsa/Silver StainLarger spirochete, visible in blood smears (Relapsing Fever) or tissue stains. | Very Thin, Tightly Coiled, Hooked Ends!; Darkfield Needed!Ends often bent into a hook shape. Difficult to visualize. |
| Key Disease | Syphilis (Multi-stage Systemic)Primary, secondary, latent, tertiary stages affecting multiple organs. | Lyme Disease (Multi-system); Relapsing Fever (*Borrelia spp*)Early localized rash -> disseminated cardiac/neuro/arthritis. Different species cause Relapsing Fever. | Leptospirosis (Biphasic Systemic Illness; Weil's Disease)Febrile illness often followed by immune phase. Severe form involves jaundice/renal failure. |
| Transmission | Direct Contact (Sexual, Congenital); Humans Only ReservoirRequires direct contact with infectious chancre or lesion. | Tick Bite! (*Ixodes* spp.); Zoonosis (Rodents/Birds)Transmitted by bite of infected blacklegged ticks. | Contact w/ Contaminated Water/Soil/Animal Urine!; ZoonosisEnters through abraded skin or mucous membranes. Broad animal reservoir. |
| II. Structure & Culture | |||
| Key Structure | Axial Filaments (Endoflagella); Sparse Outer Membrane ProteinsCorkscrew motility via periplasmic flagella. 'Stealth pathogen' due to few surface proteins. | Axial Filaments; Many OM Lipoproteins (OspA/C); Linear Chromosome!Outer Surface proteins involved in host/tick adaptation. Unique linear genetic material. | Axial Filaments; Hooked Ends; LPS-like Molecules in OMRapid motility. Lipopolysaccharide-like substance contributes to inflammation. |
| Culture Difficulty | CANNOT Be Cultured *In Vitro*!Obligate parasite, requires host cells (rabbit model) for propagation. | Difficult! Needs Complex BSK Medium; Microaerophilic; SlowCulture rarely done clinically due to difficulty and slow growth (weeks). | Difficult! Needs Special EMJH/Fletcher's Medium; Aerobic; SlowCulture possible but slow (weeks) and requires special media. Aerobic. |
| III. Laboratory Diagnosis | |||
| Primary Method | SEROLOGY! (Non-treponemal screen VDRL/RPR + Treponemal confirm FTA/TPPA)!; Darkfield (Early Lesions)Antibody detection is mainstay. Darkfield useful only for specific lesion types. | Clinical Picture (EM Rash)! + SEROLOGY (Later Stages - 2 Tier ELISA/WB)!Erythema Migrans rash highly suggestive. Serology useful later but needs careful interpretation (two-tiered testing). | SEROLOGY (MAT gold standard)!; PCR / Culture less commonMicroscopic Agglutination Test detects antibodies but complex. PCR useful early. |
| IV. Pathogenesis | |||
| Key Mechanisms | Motility/Invasion; Inflammation (Endarteritis!); Immune EvasionPenetrates tissues, triggers inflammation leading to vascular damage in later stages. Slow clearance. | Motility/Dissemination; Inflammation (Host response to lipoproteins!); Antigenic Variation? Immune modulationDisseminates widely. Host response drives arthritis/neuropathy. | Direct Tissue Invasion (via motility); Inflammation; Vascular Damage (Severe Disease); Endotoxin-like effects?Damages endothelial cells causing hemorrhage. Renal tubular damage. Liver damage. |
| V. Treatment | |||
| Drug(s) of Choice | Penicillin G! (Especially Benzathine Penicillin G form)Remains highly effective for all stages; dosage/duration varies. | Doxycycline (Early)!; Amoxicillin; Ceftriaxone (Late/Severe)Antibiotic choice depends on stage and manifestations. | Doxycycline (Mild); Penicillin / Ceftriaxone (Severe)Treatment depends on disease severity. |
| Jarisch-Herxheimer Rxn | Common (Fever/Chills after Treatment start)Due to release of bacterial components. | Can occur (Less common than Syphilis/RF)Mild reaction possible. | Can occurPossible after starting antibiotics. |
| VI. Prevention | |||
| Main Strategy | Safe Sex Practices!; Screening (Pregnancy!)Condoms reduce risk. Early detection/treatment crucial. | Tick Avoidance!; Prompt Tick Removal; Personal ProtectionUsing repellents, protective clothing, checking for ticks. | Avoid Contaminated Water/Soil; Protective Gear; Animal Vaccination/ControlEspecially for occupational risk groups (farmers, sewer workers). |
| Category / Feature | Mycoplasma pneumoniae | Ureaplasma urealyticum / parvum |
|---|---|---|
| I. Introduction | ||
| Defining Feature | No Cell Wall!; Causes Atypical PneumoniaSmallest free-living bacterium. Lacks peptidoglycan. Major cause of 'walking pneumonia'. | No Cell Wall!; Urease Positive!; GU Tract Colonizer/PathogenLacks peptidoglycan. Produces urease. Common urogenital colonizer, role in some infections/preterm birth. |
| Transmission | Respiratory Droplets (Close Contact)Spread person-to-person via aerosols. Long incubation period. | Sexual Contact; Vertical (Mother-Infant during birth)Commonly acquired sexually or during passage through birth canal. |
| II. Structure & Culture | ||
| Wall / Morphology | No Peptidoglycan Wall!; Pleomorphic; Membrane requires Sterols!Variable shape. Cell membrane contains cholesterol derived from host. Gram stain useless. | No Peptidoglycan Wall!; Pleomorphic; Membrane requires Sterols!Similar basic structure to Mycoplasma. |
| Culture Notes | VERY Fastidious; Slow (Weeks!); Needs Glucose; "Fried Egg" Colonies!Requires special media (SP4), sterols, complex nutrients. Characteristic colony morph. Strict aerobe. | Fastidious; Faster (Days); Tiny 'T-strain' Colonies; Needs Urea!; MicroaerophilicRequires special media (A8, Shepard's), sterols AND Urea. Colonies extremely small. |
| III. Diagnosis | ||
| Preferred Method | PCR! (Respiratory Sample); Serology often used (slower)NAATs most sensitive/rapid. Serology (IgM/IgG) common but takes time to rise. Cold agglutinins insensitive/nonspecific. Culture rare. | PCR! (Urogenital Sample); Culture less commonNAATs available for detection in urine/swabs. Culture requires specialized media/expertise. |
| IV. Pathogenesis & Disease | ||
| Virulence Factors | P1 Adhesin!; Cell Damage (H₂O₂/ROS); CARDS Toxin?; InflammationAttaches via P1 to respiratory epithelium causing ciliostasis/damage. Produces reactive oxygen. CARDS toxin implicated. Host immune response contributes. | Adherence Factors; Urease (Ammonia toxicity?); Phospholipases?; Inflammation?Mechanisms less well understood. Urease activity, Phospholipase A/C production may contribute. Role in preterm birth debated. |
| Key Diseases | Tracheobronchitis; Atypical "Walking" Pneumonia!; Extrapulmonary manifestations possibleCommon cause of CAP. Can also cause skin (SJS), neuro, cardiac issues. | Non-Gonococcal Urethritis (NGU); Preterm Birth/Chorioamnionitis Link?; Neonatal InfectionsRole in NGU established. Association with adverse pregnancy outcomes controversial. Can cause pneumonia/sepsis/meningitis in premature newborns. |
| V. Treatment | ||
| Key Resistance Point | INTRINSICALLY RESISTANT TO CELL WALL AGENTS!All drugs targeting peptidoglycan synthesis (Penicillins, Cephalosporins, Carbapenems, Vancomycin etc.) are ineffective because these bacteria lack the target structure. | |
| Preferred Drug Classes | Macrolides (Resistance ↑); Doxycycline; FluoroquinolonesMacrolides (Azithro/Erythro/Clarithro) often used first-line, but resistance increasing globally. Alternatives effective. | Macrolides (Azithro); Doxycycline (Resistance documented)Erythromycin traditionally used for neonatal coverage. Check local patterns if possible. |
| VI. Prevention | ||
| Vaccine / Prophylaxis | None AvailableNo vaccine exists. | None Available (Safe Sex Practices reduce GU Spread)No vaccine. Condom use reduces transmission. |