Common Bacterial and Fungal Infections: Symptoms and Treatments

Posted on Dec 24, 2024 in Biology

Clinical Condition: Gas Gangrene (Clostridial Myonecrosis)

Etiological Agents:

  • Clostridium perfringens (most common)
  • Clostridium septicum
  • Clostridium novyi
  • Clostridium histolyticum
  • Clostridium sordellii

Pathogenesis

  1. Entry: Clostridial spores enter deep, anaerobic tissue (crushed muscles contaminated with soil).
  2. Anaerobic Growth: Necrotic tissue and poor blood supply provide an anaerobic environment for spore germination.
  3. Toxin Production:
    • Alpha-toxin (lecithinase): Damages cell membranes, causes hemolysis and tissue destruction.
    • Theta-toxin: Causes further tissue necrosis and systemic effects.
  4. Rapid Spread: Toxins degrade tissue, causing gas production (CO2, H2), edema, crepitus, and severe pain.
  5. Systemic Effects: Toxins enter the bloodstream, leading to shock, multi-organ failure, and death if untreated.

Laboratory Diagnosis:

  • Clinical Clues: Crepitus, foul-smelling discharge, rapid progression of edema and necrosis.
  • Microscopy: Gram-positive bacilli without inflammatory cells (due to toxin-induced lysis).
  • Culture: Anaerobic culture showing Clostridium growth (double-zone hemolysis on blood agar for C. perfringens).
  • Imaging: X-ray/CT may show gas in soft tissue.

Treatment:

  • Surgical Intervention: Immediate and aggressive debridement of necrotic tissue.
  • Antibiotics: IV penicillin G (high-dose), plus clindamycin for toxin suppression.
  • Supportive Care: IV fluids, vasopressors if needed for shock.
  • Hyperbaric Oxygen Therapy (HBOT): Provides oxygen to inhibit anaerobic growth and toxin production.

Case of Annular Ring-Shaped Skin Lesion

Clinical Diagnosis: Tinea Corporis (Ringworm of the Body)

Clinical Manifestations Produced by Trichophyton rubrum:

  1. Tinea Corporis: Classic ring-shaped lesions with central clearing and raised, scaly, pruritic borders. Seen on non-hairy, glabrous skin (e.g., arms, legs, trunk).
  2. Tinea Cruris: Also called “Jock Itch.” Involves the groin, perineum, and inner thighs. Itchy, red scaly patches with active edges.
  3. Tinea Pedis: Known as “Athlete’s Foot.” Causes maceration, itching, and scaling between toes (interdigital spaces).
  4. Tinea Capitis: Fungal infection of the scalp and hair follicles, causing alopecia, scaling, and kerion formation.
  5. Tinea Unguium (Onychomycosis): Infection of the nails causing thickening, yellow discoloration, and crumbly nails.
  6. Tinea Manuum: Scaly lesions of the palms and fingers.

Laboratory Diagnosis:

  • KOH Mount (Direct Microscopy): Skin scrapings mixed with 10–20% potassium hydroxide reveal hyaline, septate branching hyphae.
  • Culture on Sabouraud Dextrose Agar (SDA): Colonies appear velvety white on the surface and show red pigment on the reverse.
  • Microscopy shows:
    • Microconidia: Teardrop-shaped, numerous.
    • Macroconidia: Long, pencil-shaped, thin-walled.
  • Wood’s Lamp Examination: Dermatophyte infections caused by Microsporum fluoresce under UV light, but Trichophyton rubrum does not.

Treatment:

  • Topical Antifungals (Mild Cases): Clotrimazole, Miconazole, or Terbinafine (apply twice daily for 2–4 weeks).
  • Oral Antifungals (Severe or Extensive Cases): Terbinafine (250 mg/day) or Griseofulvin (500–1000 mg/day) for 4–6 weeks.
  • Preventive Measures: Keep skin clean and dry, avoid sharing personal items, and treat family members if infected.

Case of Calf Pain with Pus Discharge

Clinical Diagnosis and Causative Organism:

  • Diagnosis: Furuncle/Carbuncle
  • Causative Organism: Staphylococcus aureus

Infections Caused by S. aureus:

  1. Skin Infections: Furuncles, carbuncles, impetigo, cellulitis.
  2. Systemic Infections: Sepsis, pneumonia, osteomyelitis.
  3. Toxin-Mediated Diseases: Toxic Shock Syndrome (TSS), food poisoning, Scalded Skin Syndrome (SSSS).

Virulence Factors:

  1. Protein A: Prevents phagocytosis.
  2. Enzymes: Coagulase, hyaluronidase, DNase.
  3. Toxins: Hemolysins, exfoliative toxins, enterotoxins, TSST-1.

Laboratory Diagnosis:

  1. Microscopy: Gram-positive cocci in clusters.
  2. Culture: Golden-yellow, beta-hemolytic colonies on blood agar.
  3. Tests:
    • Catalase Test: Positive.
    • Coagulase Test: Positive.
  4. Antibiotic Sensitivity: MRSA testing (oxacillin resistance).

Treatment:

  • Mild Cases: Oral Cephalexin or Amoxicillin-Clavulanate.
  • MRSA: Trimethoprim-Sulfamethoxazole or Doxycycline.
  • Surgical Drainage: For large abscesses.

Diagnosis: Streptococcal Cellulitis

Etiologic Agent:

Streptococcus pyogenes (Group A Streptococcus, GAS)

Virulence Factors and Clinical Manifestations:

  1. Virulence Factors:
    • M Protein: Antiphagocytic, key in adhesion.
    • Streptolysin O and S: Cause hemolysis and tissue damage.
    • Hyaluronidase: Promotes tissue invasion.
    • Streptokinase: Facilitates fibrin breakdown.
    • Pyrogenic Exotoxins: Cause systemic effects like fever and shock.
  2. Clinical Manifestations:
    • Skin and Soft Tissue Infections:
      • Cellulitis: Red, warm, swollen, tender lesion (as in this case).
      • Impetigo: Honey-colored crusted lesions.
      • Erysipelas: Superficial, sharply demarcated, red rash.
      • Necrotizing Fasciitis: Rapidly progressing skin infection (flesh-eating disease).
    • Systemic Infections: Pharyngitis, scarlet fever, rheumatic fever, glomerulonephritis.

Laboratory Diagnosis:

  1. Microscopy:
    • Gram Stain: Gram-positive cocci in chains.
  2. Culture:
    • Blood Agar: Beta-hemolytic colonies.
  3. Biochemical Tests:
    • Catalase Test: Negative (differentiates from Staphylococcus).
    • Bacitracin Sensitivity: S. pyogenes is bacitracin-sensitive.
  4. Serology:
    • ASO Titer (Anti-Streptolysin O): Elevated in systemic infections like rheumatic fever.

Treatment:

  • Drug of Choice: Penicillin G or Amoxicillin.
  • For penicillin allergy: Erythromycin or Clindamycin.

Diagnosis: Herpes Simplex Virus (HSV) Infection

Most likely HSV-1 (Oral Herpes). The vesicles on the lips and mucosa, along with the presence of painful sores, suggest a primary HSV infection.

Other Agents Causing Similar Infections:

  1. Herpes Simplex Virus (HSV-1, HSV-2): HSV-1 causes oral herpes, HSV-2 is usually genital but can also affect the mouth.
  2. Varicella-Zoster Virus (VZV): Causes chickenpox and shingles, with vesicular lesions.
  3. Coxsackievirus (Hand, Foot, and Mouth Disease): Causes vesicles in the mouth, hands, and feet.
  4. Enterovirus (Herpangina): Produces vesicular lesions in the mouth with fever.

Laboratory Diagnosis:

  1. Microscopy (Tzanck Smear): Identifies multinucleated giant cells (Tzanck cells), indicative of a viral infection like HSV.
  2. Viral Culture: Gold standard for diagnosis, though time-consuming.
  3. Polymerase Chain Reaction (PCR): Highly sensitive, differentiates HSV-1 from HSV-2.
  4. Direct Fluorescent Antibody (DFA): Detects viral antigens in lesion scrapings.
  5. Serology: IgM for recent infection and IgG for past exposure.

Treatment:

  • Acyclovir (oral or topical) for viral suppression.
  • Symptomatic relief with pain management and hydration.

Clinical Diagnosis and Causative Agent:

  • Diagnosis: Cutaneous Anthrax
  • Causative Agent: Bacillus anthracis

Bacillus anthracis causes anthrax, and the papulo-vesicular lesion evolving into a coal-black necrotic wound suggests cutaneous anthrax, which is common in individuals exposed to infected animals or their products.

Pathogenesis and Clinical Presentation:

  • Pathogenesis:
    • Bacillus anthracis spores germinate on the skin, releasing toxins that cause tissue necrosis.
    • Infection usually occurs through direct contact with contaminated animal products or soil.
  • Clinical Forms:
    1. Cutaneous Anthrax: Small papule develops into a vesicle and then a necrotic ulcer with a black eschar.
    2. Inhalational and Gastrointestinal Anthrax: More severe forms involving respiratory or digestive symptoms, respectively.

Laboratory Investigations to Confirm the Diagnosis:

  1. Gram Staining: Gram-positive, rod-shaped bacilli in chains.
  2. Culture:
    • Blood agar: Grayish-white colonies with a “ground-glass” appearance and medusa-head pattern.
  3. Biochemical Tests: Catalase-positive, non-motile.
  4. PCR/Serology: PCR confirms Bacillus anthracis, and serology detects antibodies to the toxin.

Treatment:

  • Antibiotics: Ciprofloxacin or Doxycycline.
  • Supportive Care: Wound care and debridement.