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Microbiology - Key Organisms (Apurba Sastry Style)
Content sourced from Medical Microbiology 9e and Sherris & Ryan's Medical Microbiology, 8th Edition.
1. SYPHILIS (Treponema pallidum)
Organism
- Thin, motile spirochete; obligate human pathogen
- Cannot be grown on artificial culture media
- Corkscrew motility; binds fibronectin via adhesins
Transmission
- Sexual contact with active primary/secondary lesions (>50% transmission rate when lesion present)
- Transplacental (congenital syphilis) - throughout latency
- Needle sharing (IV drug users)
- Tertiary syphilis is NOT infectious
Pathogenesis
- Enters through microabrasions in mucosa → multiplies in subepithelium → minimal initial reaction (few outer membrane antigens)
- Stimulates endarteritis (endothelial swelling/proliferation of arterioles) → necrosis, ulceration
- Disseminates via blood → systemic manifestations
Clinical Stages
| Stage | Key Features |
|---|
| Primary | Painless indurated ulcer = Chancre (genitalia/cervix/anal/oral); regional painless lymphadenopathy; heals in 4-6 weeks; incubation ~3 weeks |
| Secondary | 2-8 weeks after chancre; symmetric maculopapular rash on trunk, extremities, palms, soles, face; generalized lymphadenopathy; fever, malaise; condylomata lata (warty perineal lesions); teeming with spirochetes; resolves spontaneously |
| Latent | No clinical signs; serologically positive; early latent (<4 yr) - relapses possible; late latent (>4 yr) - no relapses, resistant to reinfection; 1/3 never progress |
| Tertiary | ~15-20 years later (1/3 of untreated); neurosyphilis, cardiovascular syphilis, gummas |
Tertiary Syphilis - Details
- Neurosyphilis: Chronic meningitis, cortical degeneration (psychosis, dementia), tabes dorsalis (demyelination of posterior columns → ataxia, wide-based gait, loss of sensation), paresis (mnemonic: Personality, Affect, Reflexes, Eyes, Sensorium, Intellect, Speech)
- Cardiovascular syphilis: Aortitis → aortic aneurysm (ascending/transverse aorta), aortic valve incompetence
- Gummas: Localized granulomas in skin, bone, joints, viscera
Congenital Syphilis
- Fetus susceptible after 4th month of gestation
- Features: rhinitis ("snuffles"), rash, bone changes (saddle nose, saber tibia, Hutchinson's teeth)
Diagnosis
- Dark-field microscopy (primary/secondary lesions)
- Serology: Non-treponemal (VDRL, RPR) for screening; Treponemal (FTA-ABS, TPHA) for confirmation
- HIV co-infection: syphilitic lesions are a portal for HIV transmission
Treatment
- Benzathine penicillin G is drug of choice for all stages
- Neurosyphilis: IV aqueous penicillin G
2. STAPHYLOCOCCUS AUREUS
Key Trigger Words
Coagulase, cytotoxins, exfoliative toxins, enterotoxins, toxic shock syndrome toxin (TSST), MRSA
Biology & Virulence
- Gram-positive cocci in clusters (grape-like); catalase positive; coagulase positive
- Survives on dry surfaces for long periods (thick peptidoglycan, no outer membrane)
- Virulence factors: structural (protein A - binds IgG Fc region, avoids phagocytosis; capsule; biofilm) and toxins/enzymes
Key Toxins
| Toxin | Disease |
|---|
| Coagulase | Clots fibrinogen; hallmark of S. aureus |
| Exfoliative toxin (A & B) | Scalded Skin Syndrome (SSS) - serine proteases that cleave desmoglein-1 |
| Enterotoxins (A-G) | Food poisoning - heat stable, preformed toxin, rapid onset (1-6 hr) |
| TSST-1 | Toxic Shock Syndrome - superantigen, massive cytokine release |
| Panton-Valentine Leukocidin (PVL) | Tissue necrosis, destroys leukocytes; associated with MRSA |
| Alpha toxin | Cell membrane disruption; hemolysis |
Epidemiology
- Normal flora on skin and mucosal surfaces (nose - 30% of population are carriers)
- MRSA = now most common cause of community-acquired skin/soft-tissue infections
- Risk factors: foreign body (catheter, prosthesis), prior surgery, immunosuppression, antecedent viral respiratory infection
Diseases
- Toxin-mediated: Food poisoning, TSS, Scalded Skin Syndrome
- Pyogenic (localized): Impetigo, folliculitis, furuncles, carbuncles, wound infections
- Systemic: Bacteremia, endocarditis, osteomyelitis, septic arthritis, pneumonia, meningitis
Diagnosis
- Gram stain (gram-positive cocci in clusters)
- Mannitol-salt agar / Chromogenic agar (selective media)
- Coagulase test (tube coagulase = definitive)
- NAAT for MRSA screening
Treatment
- Localized: Incision & drainage
- Systemic: Empirical MRSA coverage
- Oral: TMP-SMX, doxycycline, clindamycin, linezolid
- IV: Vancomycin (DOC); alternatives: daptomycin, tigecycline, linezolid
- Food poisoning: Symptomatic only
3. CLOSTRIDIUM SPECIES
All are anaerobic, gram-positive, spore-forming rods
A. Clostridium difficile
Trigger Words: Spore former, antibiotic-associated diarrhea, pseudomembranous colitis, Toxin A & B
| Feature | Detail |
|---|
| Toxins | Toxin A (enterotoxin) - attracts neutrophils, stimulates cytokines; Toxin B (cytotoxin) - increases intestinal permeability → diarrhea |
| Pathogenesis | Antibiotics (clindamycin, cephalosporins, fluoroquinolones) suppress normal flora → C. diff overgrowth |
| Epidemiology | <5% carriage in healthy adults; spores resist decontamination |
| Disease | Antibiotic-associated diarrhea; Pseudomembranous colitis (profuse diarrhea, fever, whitish plaques on colonic mucosa) |
| Diagnosis | Detect cytotoxin/enterotoxin or toxin genes in feces (NOT culture alone) |
| Treatment | Discontinue offending antibiotic; metronidazole or vancomycin (oral) for severe disease; fecal transplant for recurrent disease |
| Note | Relapse common - antibiotics don't kill spores; second course usually required |
B. Clostridium perfringens
Trigger Words: Spore former, myonecrosis (gas gangrene), sepsis, food poisoning
| Feature | Detail |
|---|
| Biology | Large gram-positive rods; rapid growth; spores rarely visible |
| Toxins | Alpha toxin (lecithinase/phospholipase C) - main virulence factor; lysis of blood cells, tissue destruction, massive hemolysis; heat-sensitive enterotoxin (food poisoning) |
| Epidemiology | Ubiquitous (soil, water, intestines); Type A = most human infections |
| Diseases | Gas gangrene (myonecrosis) - surgical/traumatic wounds; Food poisoning - contaminated meat (beef, poultry, gravy) held at 5-60°C; Sepsis |
| Diagnosis | Large rectangular gram-positive rods on Gram stain; characteristic hemolytic colonies |
| Treatment | Severe: Surgical debridement + high-dose penicillin; food poisoning = symptomatic |
C. Clostridium tetani
Trigger Words: Spore former, neurotoxin, contaminated wound, tetanus, vaccine
| Feature | Detail |
|---|
| Toxin | Tetanospasmin (heat-labile neurotoxin) - blocks release of inhibitory neurotransmitters (GABA, glycine) → spastic paralysis |
| Spore | Drumstick/terminal spores; extremely oxygen-sensitive organism |
| Disease | Tetanus: trismus (lockjaw), risus sardonicus, opisthotonus, spastic paralysis; neonatal tetanus (umbilical stump infection) |
| Diagnosis | Clinical; culture very difficult (strict anaerobe) |
| Treatment | Wound debridement + penicillin/metronidazole + antitoxin (TIG) + tetanus toxoid vaccination |
| Prevention | 3 doses toxoid + booster every 10 years |
D. Clostridium botulinum
Trigger Words: Spore former, neurotoxin, flaccid paralysis, foodborne/infant botulism, NO vaccine
| Feature | Detail |
|---|
| Toxin | Botulinum toxin (types A, B most common; E, F also) - blocks release of acetylcholine at peripheral cholinergic synapses → flaccid paralysis |
| Contrast with Tetanus | Tetanus = spastic; Botulinum = flaccid |
| Diseases | Foodborne botulism (blurred vision, dry mouth, constipation, descending flaccid paralysis); Infant botulism (contaminated honey/soil); Wound botulism; Inhalation botulism |
| Spores | Found in soil worldwide; heat resistant |
| Toxin | Heat labile - destroyed by heating at 60-100°C for 10 min |
| Diagnosis | Toxin in food, serum, feces, or wound |
| Treatment | Penicillin/metronidazole + trivalent botulinum antitoxin + ventilatory support |
4. PNEUMONIA (Streptococcus pneumoniae - Pneumococcus)
Biology & Virulence
- Gram-positive lancet-shaped diplococci (pairs)
- Catalase negative, alpha-hemolytic on blood agar (green zone)
- Key virulence factor: Polysaccharide capsule (>90 serotypes; inhibits phagocytosis; anticapsular antibodies are protective)
- Other: pneumolysin, IgA protease, surface adhesins
Epidemiology
- Carried asymptomatically in nasopharynx (25-50% of children, less in adults)
- Spreads via respiratory droplets
- Peak incidence: winter/spring (cool months)
- At-risk groups: children <5 yr, elderly, asplenic/hyposplenic, hypogammaglobulinemia, HIV, chronic lung disease, alcoholism, DM, CHF
- WHO estimate: >750,000 children <5 yr die annually from pneumococcal pneumonia/meningitis
Pathogenesis
Oropharyngeal colonization → aspiration into lower airways → rapid multiplication in alveolar edema fluid → erythrocyte/neutrophil/macrophage accumulation → lobar consolidation → resolution when anticapsular antibodies form
Predisposing factors: antecedent viral illness (influenza), chronic pulmonary disease, alcoholism, CHF, diabetes, renal disease, splenectomy (unable to clear encapsulated organisms)
Clinical Diseases
- Lobar Pneumonia (most classic): Abrupt onset; severe shaking chill + sustained fever 39-41°C; productive cough with blood-tinged/rust-coloured sputum; pleuritic chest pain; consolidation in lower lobes; preceded by viral URTI 1-3 days prior
- Meningitis - most common bacterial meningitis in adults
- Otitis Media - most common cause in children
- Sinusitis
- Bacteremia
Diagnosis
- Gram stain of sputum: gram-positive lancet-shaped diplococci, with PMNs
- Culture on blood agar: alpha-hemolytic colonies; optochin sensitive (distinguishes from other streptococci); bile solubility positive
- Urinary antigen test (rapid, sensitive for adults)
- Blood cultures for bacteremia
Treatment
- Community-acquired pneumonia: Penicillin G or amoxicillin (if sensitive); macrolides/respiratory fluoroquinolones for atypicals or resistant strains
- Increasing penicillin resistance - ceftriaxone, levofloxacin, moxifloxacin
Prevention (Vaccines)
- PPSV23 (Pneumovax): 23-valent polysaccharide vaccine for adults ≥65 yr and high-risk groups
- PCV13/PCV20 (Prevnar): Conjugated vaccine for children and adults; broader protection including herd immunity
5. DIPHTHERIA (Corynebacterium diphtheriae)
Biology & Key Features
- Gram-positive rod with clubbed ends (palisade/Chinese-letter arrangement on stain)
- Non-motile, non-spore-forming
- Produces diphtheria exotoxin (if lysogenised by beta-phage carrying tox gene)
- Toxin regulated by DTxR (diphtheria toxin repressor) - represses toxin at high iron concentrations
Diphtheria Toxin - Mechanism
- A-B subunit toxin:
- B subunit: Binds host cell receptor (heparin-binding EGF precursor); facilitates entry
- A subunit: Catalytic; ADP-ribosylates and inactivates Elongation Factor-2 (EF-2) → terminates host cell protein synthesis completely
- One toxin molecule can inactivate ALL EF-2 in a cell
Epidemiology
- Worldwide distribution; poor urban areas with crowding, low vaccination
- Transmitted via respiratory droplets or skin contact
- Reservoir: asymptomatic carriers in oropharynx/skin of immune individuals
- Humans are the only reservoir
- Largely eliminated in vaccinated countries; risk with travel to endemic areas (Indian subcontinent, Africa, SE Asia)
- ~200,000 cases/yr in 1921 USA; only 2 cases since 2003
Clinical Diseases
Respiratory Diphtheria
- Incubation: 2-4 days
- Sudden onset: malaise, sore throat, exudative pharyngitis, low-grade fever
- Exudate evolves into thick grey pseudomembrane (bacteria + lymphocytes + fibrin + dead cells) over tonsils/pharynx/larynx
- Pseudomembrane bleeds on attempted removal
- Toxin disseminates via blood → systemic disease (myocarditis, neuropathy)
- Bull-neck appearance (cervical lymphadenopathy + soft tissue edema)
- Laryngeal diphtheria: Hoarseness, croupy cough, risk of airway obstruction
Systemic Complications (from toxin)
- Myocarditis (2nd-3rd week) - most common cause of death
- Neuropathy: Palatal palsy → nasal voice/regurgitation; oculomotor palsy; peripheral neuropathy
- Adrenal involvement
Cutaneous Diphtheria
- Chronic, non-healing ulcers; less systemic toxicity
- Can transmit organism
Diagnosis
- Gram stain: metachromatic granules (Babes-Ernst granules) with Albert's stain (bluish-green organisms, dark granules)
- Culture on Loeffler's serum slope (rapid growth) and Tellurite agar (black colonies - selective)
- Elek test: Double immunodiffusion to detect toxin production (in vitro toxigenicity test)
- PCR for tox gene
Treatment
- Diphtheria antitoxin (DAT) - given immediately (neutralizes free toxin; does NOT reverse fixed toxin)
- Penicillin or erythromycin - kills the organism, eliminates carrier state
- Supportive: airway management, cardiac monitoring
Prevention
- DPT/DTP vaccine: Diphtheria toxoid (inactivated toxin - formaldehyde treated)
- Primary series: 3 doses + boosters
- Tetanus + Diphtheria (Td) booster every 10 years
Quick Comparison Table
| Feature | Syphilis | S. aureus | C. difficile | S. pneumoniae | C. diphtheriae |
|---|
| Morphology | Spirochete | GP cocci clusters | GP rod (anaerobe) | GP diplococci | GP rod (clubs) |
| Key toxin/factor | None (immune-mediated) | Coagulase, TSST | Toxin A + B | Capsule | Diphtheria toxin (EF-2 inhibition) |
| Culture | Cannot be cultured | Blood agar | Anaerobic culture | Blood agar (optochin sensitive) | Loeffler's / Tellurite agar |
| Key disease | Chancre → rash → tertiary | Abscess, TSS, food poisoning | Pseudomembranous colitis | Lobar pneumonia | Pseudomembrane, myocarditis |
| Treatment | Benzathine penicillin G | Vancomycin (MRSA) | Metronidazole/Vancomycin | Penicillin/Ceftriaxone | Antitoxin + Penicillin |
| Vaccine | No | No | No | PCV13, PPSV23 | DTP (toxoid) |
Sources: Medical Microbiology 9e (Murray/Rosenthal), Sherris & Ryan's Medical Microbiology 8th Edition