Oral Infections (Candida, TB, Syphilis, HIV)

Oral Infections: Candida, TB, Syphilis, HIV – NEET MDS Study Guide

Oral infections are a significant component of Oral Pathology & Microbiology, frequently tested in NEET MDS. This comprehensive guide covers key aspects of Candidiasis, Tuberculosis, Syphilis, and HIV-associated oral manifestations, focusing on exam-relevant details.

1. Oral Candidiasis

Definition: Oral candidiasis is an opportunistic fungal infection primarily caused by Candida albicans, a commensal yeast in the oral cavity. It becomes pathogenic when host defenses are compromised or the oral microenvironment changes.

Classification/Types & Clinical Features:

• Acute Pseudomembranous Candidiasis (Thrush): ⭐This is the most common form of oral candidiasis. Clinically presents as white, soft, elevated plaques resembling cottage cheese, often on the buccal mucosa, palate, or tongue. These plaques can be easily wiped off, revealing an erythematous (red) and sometimes bleeding underlying mucosa. Common in infants, immunocompromised individuals (e.g., HIV, chemotherapy), and those on broad-spectrum antibiotics or corticosteroids.
• Acute Erythematous Candidiasis (Atrophic Candidiasis): Characterized by red, painful areas, often on the dorsal tongue (leading to atrophic glossitis with depapillation) or palate. It's often associated with antibiotic use or denture wear (denture stomatitis).
• Chronic Hyperplastic Candidiasis (Candidal Leukoplakia): Presents as persistent white plaques that are firm and cannot be easily scraped off. Commonly found on the buccal mucosa, commissures, or lateral tongue. It can be precancerous in some cases.
• Chronic Erythematous Candidiasis (Denture Stomatitis): Seen in denture wearers, presenting as erythema and edema of the palatal mucosa beneath a denture. Often asymptomatic or mildly burning.
• Angular Cheilitis (Perleche): Erythema, cracking, and fissuring at the commissures of the mouth, often bilateral. It can be associated with *Candida* and/or *Staphylococcus aureus* infection, often due to reduced vertical dimension or drooling.
• Median Rhomboid Glossitis: A well-demarcated erythematous, often rhomboid-shaped area on the midline of the dorsal tongue, typically devoid of filiform papillae. Often asymptomatic, but can be associated with *Candida* colonization.

Histopathology:

Microscopic examination reveals hyphae and pseudohyphae of *Candida* within the superficial layers of the epithelium, often associated with an inflammatory infiltrate (neutrophils). PAS (Periodic Acid-Schiff) stain is used to highlight the fungal elements.

Differential Diagnosis:

Leukoplakia, chemical burns, geographic tongue, oral hairy leukoplakia.

Treatment:

Topical antifungals (Nystatin, Clotrimazole) for mild cases. Systemic antifungals (Fluconazole, Itraconazole) for severe, recurrent, or immunocompromised patients. Addressing predisposing factors (e.g., denture hygiene, diabetes control, discontinuing offending medications) is crucial.

2. Oral Tuberculosis (TB)

Definition: Tuberculosis is a chronic granulomatous infectious disease caused by Mycobacterium tuberculosis. Oral lesions are relatively rare and usually represent secondary manifestations of pulmonary tuberculosis.

Classification/Types & Clinical Features:

• Primary Oral TB: Rare, typically seen in children or young adults. Presents as a single, painless ulcer often associated with cervical lymphadenopathy.
• Secondary Oral TB: More common, usually occurs in adults with active pulmonary TB, often due to autoinoculation of sputum. Presents as a painful, chronic, irregular ulcer with undermined edges, commonly affecting the tongue, palate, or gingiva. The base of the ulcer may have a yellowish, caseous appearance. Regional lymphadenopathy is common. It can mimic squamous cell carcinoma.

Histopathology:

Characterized by a granulomatous inflammatory reaction with central caseous necrosis. Key cellular components include Langhans giant cells (multinucleated giant cells with nuclei arranged in a horseshoe shape), epithelioid cells, and lymphocytes. Acid-fast bacilli (AFB) can be identified within the tissue using Ziehl-Neelsen stain, confirming the diagnosis.

Differential Diagnosis:

Squamous cell carcinoma, traumatic ulcer, deep fungal infections, syphilis (gumma).

Treatment:

Multi-drug anti-tubercular therapy (ATT) typically for 6-9 months, involving drugs like Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol (RIPE regimen).

3. Oral Syphilis

Definition: Syphilis is a sexually transmitted infection (STI) caused by the spirochete Treponema pallidum. It progresses through distinct stages, each with characteristic oral manifestations.

Classification/Types & Clinical Features:

• Primary Syphilis: Oral manifestations occur 2-3 weeks after exposure. A chancre appears as a painless, firm, solitary ulcer with raised borders and an indurated base. It is highly infectious. Common oral sites include the lip, tongue, and tonsils. Regional lymphadenopathy (cervical) is typically firm and non-tender.
• Secondary Syphilis: Develops 4-10 weeks after the primary chancre appears. Oral lesions, known as mucous patches, are common. These are grayish-white, slightly raised, highly infectious lesions often described as having a 'snail-track' appearance due to superficial ulceration. They can be found on the palate, tongue, buccal mucosa, or tonsils. Generalized skin rashes and condyloma lata (wart-like lesions) may also be present.
• Tertiary Syphilis: Occurs years after the initial infection in untreated individuals. Oral manifestations include:
  • Gumma: A destructive, granulomatous lesion with central necrosis, which can lead to palatal perforation. It is non-infectious.
  • Interstitial Glossitis: Atrophy of the dorsal tongue papillae, leading to a smooth, lobulated, or fissured tongue, sometimes called 'luetic glossitis'. This carries an increased risk of squamous cell carcinoma.
  • Syphilitic Leukoplakia: White, non-scrapable lesions with a risk of malignant transformation.
• Congenital Syphilis: Transmitted from an infected mother to the fetus. Oral manifestations are part of ⭐Hutchinson's Triad:
  • ⭐Hutchinson Teeth: Permanent incisors are peg-shaped or screwdriver-shaped with a central notch (notched incisors), and molars are dome-shaped with poorly developed cusps (mulberry molars).
  • Interstitial Keratitis: Inflammation of the cornea leading to blindness.
  • Eighth Nerve Deafness: Sensorineural hearing loss.
  Other features include rhagades (fissures radiating from the mouth) and saddle nose deformity.

Histopathology:

Primary and secondary lesions show a perivascular infiltrate of lymphocytes and plasma cells, along with endarteritis obliterans (thickening of vessel walls). Spirochetes can be demonstrated using silver stains (e.g., Warthin-Starry) or immunohistochemistry. Tertiary lesions (gumma) show granulomatous inflammation with central necrosis.

Differential Diagnosis:

Chancre: Traumatic ulcer, SCC, aphthous ulcer. Mucous patch: Candidiasis, geographic tongue. Gumma: SCC, deep fungal infection, TB.

Treatment:

Penicillin G is the drug of choice. Dosage and duration vary with the stage of syphilis.

4. Oral HIV Infection & AIDS

Definition: Human Immunodeficiency Virus (HIV) infection can progress to Acquired Immunodeficiency Syndrome (AIDS), leading to severe immunosuppression. Oral manifestations are common, often among the earliest clinical signs, and can indicate disease progression.

Clinical Features & Associated Lesions:

Oral lesions in HIV are often opportunistic infections or neoplastic processes due to the compromised immune system.

• Fungal Infections:
  • Oral Candidiasis: Very common, often persistent and recurrent. Can be pseudomembranous, erythematous, hyperplastic, or angular cheilitis. Its presence often indicates a declining CD4 count.
• Viral Infections:
  • ⭐Oral Hairy Leukoplakia (OHL): Presents as white, corrugated, or 'hairy' plaques that are non-scrapable, typically found on the lateral borders of the tongue. It is caused by the Epstein-Barr Virus (EBV) and is considered ⭐pathognomonic for HIV infection. It does not have malignant potential.
  • Herpes Simplex Virus (HSV) Infections: Often present as chronic, persistent, and extensive ulcers that may not heal.
  • Varicella-Zoster Virus (VZV): Can cause herpes zoster (shingles) in the trigeminal nerve distribution, often unilateral and painful.
  • Human Papillomavirus (HPV): Leads to warts, papillomas, or condylomas, which can be multiple and widespread.
• Bacterial Infections:
  • Necrotizing Ulcerative Gingivitis (NUG) and Necrotizing Ulcerative Periodontitis (NUP): Rapidly progressive, extremely painful, and destructive periodontal diseases with significant soft tissue and bone necrosis.
  • Linear Gingival Erythema (LGE): A distinct band of erythema along the free gingival margin, unresponsive to conventional plaque control.
• Neoplastic Lesions:
  • Kaposi's Sarcoma (KS): The most common HIV-associated malignancy. Caused by Human Herpesvirus 8 (HHV-8). Oral lesions appear as red, purple, or brownish macules, patches, nodules, or tumors. The palate is the most common oral site.
  • Non-Hodgkin Lymphoma (NHL): Can occur in the oral cavity, often as rapidly enlarging masses.
• Other Lesions:
  • Recurrent Aphthous Ulcers: Can be larger, deeper, and more persistent (major aphthous ulcers).
  • Xerostomia (Dry Mouth): Due to salivary gland dysfunction or medications.
  • Salivary Gland Enlargement: Often bilateral parotid enlargement, sometimes associated with benign lymphoepithelial cysts.

Histopathology:

• OHL: Characterized by hyperparakeratosis, acanthosis, and 'ballooning' cells in the spinous layer. There is often minimal inflammation. EBV can be detected by in-situ hybridization.
• Kaposi's Sarcoma: Proliferation of spindle cells, slit-like vascular spaces, extravasated red blood cells, and hemosiderin deposition.

Differential Diagnosis:

OHL: Frictional keratosis, leukoplakia. KS: Hemangioma, pyogenic granuloma.

Treatment:

Highly active antiretroviral therapy (ART) is the cornerstone of managing HIV infection and often leads to improvement or resolution of oral lesions. Specific oral lesions are treated symptomatically (e.g., antifungals for candidiasis, antivirals for HSV, excisional biopsy for KS or NHL).

Exam Tips for NEET MDS:

• Always correlate oral lesions with the patient's immune status for Candidiasis and HIV.
• Know the specific causative agents for each infection (Candida albicans, Mycobacterium tuberculosis, Treponema pallidum, EBV for OHL, HHV-8 for Kaposi's Sarcoma).
• Memorize the characteristic clinical features and histopathological findings for each stage/type.
• Pay special attention to the high-yield facts like Hutchinson's Triad, OHL as pathognomonic for HIV, and the most common type of candidiasis.
• Understand the differential diagnosis to avoid misdiagnosis, especially with SCC.