Bacterial Diseases

Basics of Bacterial Taxonomy

Bacterial taxonomy is the scientific classification of bacteria, which helps in understanding their relationships, characteristics, and roles in disease. The classification system is hierarchical and includes several key ranks.

• Domain: The highest taxonomic rank, splitting organisms into three kingdoms: Bacteria, Archaea, and Eukarya. Our focus is Bacteria.

• Kingdom: The second rank, with six categories: Fungi, Plantae, Animalia, Protista, and Prokaryotae. Our focus is Eubacteria.

Shapes and Arrangements in Bacteria

Bacteria are classified by their shapes and arrangements, which are important for identification and understanding their pathogenic mechanisms.

• Coccus (spherical):

  • Single coccus

  • Diplococci: pairs

  • Tetrad: group of 4

  • Sarcina: cube-like shape

  • Streptococci: chain-like

  • Staphylococci: grape-like clusters

• Bacillus (rod-shaped):

  • Single bacillus

  • Diplobacilli: pairs

  • Palisades: cluster-like or folded groups

  • Streptobacilli: chain-like

• Spiral:

  • Vibrio: comma-shaped

  • Spirochete: flexible, spiral-shaped with endoflagella

  • Spirillum: rigid, corkscrew-shaped

Cellular Structure of Bacteria

Bacterial cells have unique structures that contribute to their survival and pathogenicity.

• Cell wall: Made of peptidoglycan (thick in Gram-positive, thin in Gram-negative bacteria).

• Plasma membrane: Lipid bilayer responsible for transport of ions, nutrients, and waste.

• Capsule: Protective outer shell; helps camouflage from host immune system.

• Fimbriae: Bristle-like projections for attachment.

• Cytoplasm: Gelatinous material containing cytosol, inclusions, ribosomes, and sometimes a cytoskeleton.

• Ribosome: Site of protein synthesis.

• Nucleoid: Region containing bacterial DNA (usually a single, circular chromosome).

Exotoxins and Endotoxins

Bacteria produce toxins that contribute to disease. These are classified as exotoxins (secreted proteins) and endotoxins (components of the bacterial cell wall).

• Exotoxins:

  • Type I: Superantigens (intense immune response, cytokine release)

  • Type II: Membrane-disrupting toxins (lyse host cells, e.g., hemolysins, leukocidins)

  • Type III: A-B toxins (enzyme part A, binding part B)

  • Type IV: Genotoxins (damage DNA, disrupt cell division, can lead to cancer)

• Endotoxins:

  • Lipid A of LPS (from Gram-negative bacteria): released when cells die, causing fever, vasodilation, inflammation, shock, and blood clotting.

Necrotizing Fasciitis – Streptococcus pyogenes

Etiology

• Colony morphology: Shiny, grayish-white, translucent; Gram-positive cocci in chains; beta-hemolytic; facultative anaerobe.

Virulence Factors

• Invasion:

  • Streptokinase: Dissolves clots, spreading infection.

  • Hyaluronidase: Breaks down hyaluronic acid, aiding spread.

  • Deoxyribonuclease: Breaks up DNA from damaged host cells.

• Attachment:

  • M protein: Destabilizes complement, interferes with opsonization and lysis.

  • Protein F (fimbriae): Binds to host cells.

• Evasion (antiphagocytic factors):

  • M protein and capsule: Camouflage bacteria; hyaluronic acid capsule is ignored by WBCs.

  • Streptolysins: Lyse RBCs, WBCs, platelets; release lysosomes from phagocytes.

• Exotoxins:

  • Exotoxin A: Superantigen, activates T cells, massive cytokine release.

  • Pyrogenic exotoxins: Cause fever.

  • Erythrogenic toxin: Causes rashes.

  • Exotoxin B (SPE B): Protease, kills host cells by apoptosis.

Clinical Features

• Signs: Redness, fever, edema, bullae (fluid-filled sacs), ecchymosis (subcutaneous bleeding), crepitus (crackling sound), necrosis, anesthesia (no pain in late stage).

• Symptoms: Intense pain disproportionate to appearance.

Transmission, Diagnosis, and Treatment

• Transmission: Entry through skin breaks, especially in immunocompromised.

• Diagnosis: Gram stain and culture on blood agar.

• Treatment: Penicillin and clindamycin; surgical debridement of dead tissue.

• Prevention: Difficult due to commonality of S. pyogenes.

• Epidemiology: 700–1200 cases/year.

Botulism and Tetanus – Clostridium botulinum and Clostridium tetani

Etiology – Clostridium botulinum

• Gram-positive, anaerobic, bacillus, endospore-forming (spore subterminal).

Virulence Factors

• Botulinum toxin (Botox): Neurotoxin (exotoxin); blocks acetylcholine release at neuromuscular junction (NMJ), causing flaccid paralysis.

• Most potent toxin in nature: LD50 = 0.03 ng/kg (by person).

• Symptoms: Flaccid paralysis, fixed pupils, respiratory failure.

Transmission

• Spores found in soil, pond, and lake sediments.

• Contaminated food (especially home-canned products) is a common source.

Diagnosis and Treatment

• Diagnosis: Clinical symptoms, lab confirmation of toxin, mouse inoculation.

• Treatment: Mechanical ventilation, antitoxin, supportive care.

• Prevention: Proper canning, heating food to 100°C for 10 minutes.

• Epidemiology: ~110 cases/year in the U.S. (20% foodborne).

Etiology – Clostridium tetani

• Gram-positive, anaerobic, bacillus, endospore-forming (spore terminal, lollipop shape).

Virulence Factors

• Tetanospasmin: Neurotoxin (exotoxin); blocks inhibitory neurotransmitter release at NMJ, causing spastic paralysis.

Transmission

• Spores from soil enter through wounds, especially puncture wounds.

• Common in developing countries, often introduced to newborns via umbilical stump.

Diagnosis and Treatment

• Diagnosis: Clinical symptoms only.

• Treatment: Human tetanus immunoglobulin, supportive care, benzodiazepines.

• Prevention: Tetanus toxoid vaccine (part of DTaP).

• Epidemiology: Rare in U.S. (<50 cases/year), 1 million cases worldwide (200,000 deaths).

Strep Throat – Streptococcus pyogenes

Etiology

• Same as necrotizing fasciitis.

Virulence Factors

• Invasion: Streptokinase

• Attachment: M protein

• Evasion: M proteins, capsules, streptolysins

• Endotoxin: Superantigen, pyrogenic, erythrogenic

Transmission

• Spread via respiratory droplets.

Diagnosis and Treatment

• Diagnosis: Throat culture (gold standard), beta-hemolysis on blood agar.

• Treatment: Oral penicillin and related antimicrobials.

• Prevention: Handwashing, respiratory etiquette, staying home when ill.

• Epidemiology: Most common in winter and spring.

Gastritis/Ulcers – Helicobacter pylori

Etiology

• Spiral (vibrio) shape, Gram-negative, able to survive acidic stomach environment.

Virulence Factors

• Invasion:

  • Adhesins: Facilitate attachment to gastric epithelial cells.

  • Flagella: Enable burrowing through stomach lining.

  • Urease: Produces ammonia, neutralizing stomach acid.

• Evasion: Enzymes inhibit phagocytic killing.

Clinical Features

• Gastritis: Inflammation of the stomach lining, sharp or burning pain.

• Peptic ulcers: Lesions in the stomach or duodenum.

• Stomach cancer: Associated with chronic infection.

Transmission

• Likely oral-to-oral or oral-to-fecal route.

• 2/3 of the world's population is infected; higher prevalence in older adults.

Diagnosis and Treatment

• Diagnosis: Urease test, endoscopy, histology, sensitivity testing.

• Treatment: Antibiotics and acid-reducing agents.

• Prevention: Avoid fecal-oral transmission.

• Epidemiology: 25 million Americans will have an ulcer at some point; 500,000–800,000 new cases/year.

Gastroenteritis and Antimicrobial-Associated Diarrhea – Clostridium difficile

Etiology

• Bacillus, single bacillus, Gram-positive, endospore former.

• Part of normal microbiome in ~5% of adults.

Virulence Factors

• Pseudomembranous colitis: Toxin A breaks tight junctions between colon epithelial cells, causing inflammation and fluid loss. Toxin B kills cells, forming a pseudo-membrane.

Clinical Features

• Gastroenteritis: Inflammation of stomach and intestines, diarrhea.

• Antimicrobial-associated diarrhea: Often follows antibiotic use, due to loss of normal flora.

Table: Comparison of Major Bacterial Toxins

Additional info: Some explanations and context have been expanded for clarity and completeness, including definitions, clinical features, and mechanisms of action for toxins.