Infectious Diseases

One Liner

1. Koplik spots = Measles
2. Pyogenic granuloma = Attached gingiva

💡FUNGAL INFECTIONS

💡Oral candidiasis

Causative organism

Candida albicans is the most common cause of oral candidiasis.

• It is a dimorphic fungus: yeast and hyphal forms.
• It may be present as a commensal in healthy individuals.
• Disease develops when local or systemic factors favor overgrowth.
• The germ-tube test: C. albicans can produce germ tubes in serum at 37°C within approximately 2–3 hours.

Predisposing factors

FCPS tip: Oral candidiasis in an adult without an obvious local cause may warrant evaluation for underlying immunosuppression, diabetes or nutritional deficiency.

💡Types of oral candidiasis

A. Pseudomembranous candidiasis (thrush)

• White, creamy plaques on the oral mucosa.
• Plaques can be wiped away, revealing an erythematous or bleeding surface.
• May affect the tongue, buccal mucosa and palate.
• Symptoms include burning, soreness and altered taste, although it may be asymptomatic.
• Can occur after antibiotic use or in immunocompromised patients.

B. Erythematous (atrophic) candidiasis

• Red, smooth or depapillated areas, commonly on the dorsal tongue and palate.
• May follow broad-spectrum antibiotic use.
• Often more painful than pseudomembranous candidiasis.

C. Denture stomatitis

• Erythema beneath the fitting surface of a denture, classically an upper denture.
• Frequently asymptomatic.
• Associated with denture biofilm, continuous denture wear and poor denture hygiene.
• Newton classification:

Management includes denture hygiene, overnight removal, appropriate denture disinfection and antifungal treatment when indicated.

D. Chronic hyperplastic candidiasis (candidal leukoplakia)

• Presents as a non-removable white plaque.
• Commonly affects the buccal mucosa and commissural region.
• May show epithelial dysplasia and has potential malignant significance.
• Biopsy is important to assess dysplasia and exclude other pathology.
• Persistent lesions require reassessment even if antifungal treatment is given.

E. Angular cheilitis

• Erythema, fissuring and soreness at the corners of the mouth.
• Often involves mixed infection with Candida and Staphylococcus aureus.
• Predisposing factors include reduced vertical dimension, ill-fitting dentures and iron, B12 or folate deficiency.

FCPS tip: Miconazole cream covers Candida and Staphylococcus. Medication choice must account for interactions, especially with warfarin.

Master comparison

Remember: A non-removable white lesion should not automatically be assumed to be candidiasis. Persistent lesions need appropriate assessment and often biopsy.

💡Diagnosis of oral candidiasis

💡Antifungal treatment

These are the regimens recorded in the uploaded notes, not individualized prescriptions. Actual dose and duration depend on the formulation, patient, severity and current local guidance.

Important interaction: Miconazole, including oral gel, can increase warfarin anticoagulation and bleeding risk. Check the patient's medications before prescribing.

💡VIRAL INFECTIONS

💡Herpes simplex virus type 1 (HSV-1)

Primary herpetic gingivostomatitis

Usually occurs in children aged approximately 1–5 years during the first recognized HSV-1 infection.

Clinical features

• Fever, malaise and cervical lymphadenopathy.
• Widespread vesicles that rapidly ulcerate.
• Painful ulcers involving multiple oral mucosal surfaces.
• Acutely inflamed, red and swollen gingiva with spontaneous bleeding.
• Poor oral intake and dehydration may occur.

The illness commonly resolves over approximately 10–14 days without scarring.

Recurrent herpes labialis

HSV remains latent in the trigeminal ganglion and can reactivate following triggers such as sunlight, stress, fever, trauma or immunosuppression.

Intraoral recurrence

• Typically affects keratinized, firmly attached mucosa, such as the hard palate or attached gingiva.
• Recurrent intraoral HSV usually produces localized clusters of painful ulcers.

Treatment

Aciclovir and valaciclovir for recurrent herpes labialis, with greatest benefit when started during the prodrome. Primary gingivostomatitis is often managed supportively; systemic antivirals may be appropriate in severe or high-risk cases.

FCPS tip: HSV can affect keratinized and non-keratinized mucosa during primary infection. Recurrent intraoral HSV classically affects keratinized mucosa.

💡HSV vs recurrent aphthous stomatitis (RAS)

Exam pearl: Fever + generalized gingivitis + vesicles/ulcers suggests primary HSV; recurrent ulcers on non-keratinized mucosa without vesicles suggest RAS.

💡Varicella-zoster virus (VZV)

VZV causes chickenpox during primary infection and herpes zoster following reactivation.

A. Chickenpox

• Generalized vesicular eruption.
• Oral vesicles and ulcers may affect the tongue, palate and buccal mucosa.
• Lesions occur at different stages of development.
• The illness is usually self-limiting in otherwise healthy children.

B. Herpes zoster (shingles)

VZV reactivates in a sensory ganglion and produces a unilateral dermatomal eruption.

Key clinical features

• Burning or severe neuropathic pain may precede the rash by 2–4 days.
• Unilateral vesicles or ulcers follow the distribution of the affected nerve.
• Lesions generally do not cross the midline.
• Trigeminal zoster can produce unilateral facial and oral lesions.
• Toothache may precede the rash; teeth can occasionally become non-vital without caries due to nerve-related injury.
• Persistent pain after the rash resolves is called postherpetic neuralgia.

Important syndromes

Treatment

Valaciclovir 1 g three times daily for seven days, ideally initiated within 72 hours of rash onset. Treatment and dosing should be individualized, particularly for renal impairment.

FCPS tip: Unilateral painful vesicles following a dermatome that do not cross the midline strongly suggest herpes zoster.

💡Epstein–Barr virus (EBV / HHV-4)

A. Infectious mononucleosis

EBV commonly causes infectious mononucleosis, particularly in adolescents and young adults.

Classic triad

1. Fever.
2. Severe pharyngitis or tonsillitis.
3. Cervical lymphadenopathy.

Oral findings

• Palatal petechiae, especially near the junction of the hard and soft palate.
• Tonsillar enlargement with exudate.
• General malaise and fatigue.
• Splenomegaly may occur.

Important examination point

Avoid amoxicillin or ampicillin when infectious mononucleosis is suspected, because a maculopapular rash frequently develops after exposure. This does not necessarily indicate a true penicillin allergy.

Patients with splenomegaly should avoid contact sports until medically cleared because of the risk of splenic rupture.

B. Oral hairy leukoplakia

• Caused by EBV.
• Appears as white, corrugated or vertically ridged plaques, classically on the lateral borders of the tongue.
• Usually bilateral.
• Cannot be wiped off.
• Strongly associated with immunosuppression, especially HIV infection.
• Unlike conventional leukoplakia, it is not considered a premalignant lesion.

FCPS tip: Non-removable corrugated white plaques on the lateral tongue in an immunocompromised patient = oral hairy leukoplakia.

💡Cytomegalovirus (CMV / HHV-5)

Clinical features

• Infection is often asymptomatic in immunocompetent individuals.
• Advanced immunosuppression, particularly in HIV, can produce chronic painful oral ulcers.
• CMV can also cause retinitis, esophagitis and colitis.

Diagnosis

• Biopsy may demonstrate characteristic owl's-eye intranuclear inclusions.
• Tissue diagnosis is important when CMV is suspected as the cause of an oral ulcer.

Treatment

Ganciclovir or valganciclovir for clinically significant CMV disease, under specialist supervision.

FCPS tip: Large, persistent oral ulcers in a severely immunocompromised patient + owl's-eye inclusions = CMV.

💡HHV-8 — Kaposi sarcoma

Kaposi sarcoma is associated with HHV-8 and is an AIDS-defining malignancy in the appropriate clinical context.

Oral presentation

• Begins as flat red, purple or brown macules.
• May progress to raised nodules and ulcerated, bleeding masses.
• The hard palate is a classic and common oral site.
• Lesions may be the first clue to previously undiagnosed HIV infection.

Histology and diagnosis

• Spindle-cell proliferation.
• Slit-like vascular spaces.
• Extravasated red blood cells.
• LANA immunohistochemistry supports confirmation of HHV-8-associated disease.

Treatment principles

• Antiretroviral therapy (ART) is central in HIV-associated disease.
• Local treatment may include intralesional therapy or radiotherapy.
• Disseminated disease may require systemic chemotherapy.

FCPS tip: Violaceous lesion on the hard palate in an immunocompromised patient = Kaposi sarcoma until appropriately investigated.

💡BACTERIAL INFECTIONS

💡Acute necrotizing ulcerative gingivitis (ANUG)

ANUG is an acute necrotizing gingival infection associated with a fusospirochetal bacterial community.

Causative organisms

• Fusobacterium nucleatum
• Treponema species, including organisms historically called Borrelia vincentii
• Prevotella intermedia

Classic triad

Predisposing factors include smoking, stress, poor oral hygiene, malnutrition and immunosuppression.

Treatment principles

• Gentle supragingival debridement is the primary intervention.
• Metronidazole may be indicated when systemic antibiotics are appropriate.
• Chlorhexidine rinses and oral hygiene measures may help.
• Provide analgesia and address smoking and other risk factors.

Exam pearl: Antibiotics alone are not sufficient; plaque and necrotic deposits must be managed.

💡Cervicofacial actinomycosis

Organism

Actinomyces israelii is a Gram-positive, branching, filamentous bacterium that may be part of the normal oral flora.

Predisposing events

• Dental extraction.
• Periapical infection or abscess.
• Pericoronitis.
• Other disruptions of the oral mucosal barrier.

Clinical features

• Slowly progressive, firm or “woody” swelling of the jaw or neck.
• Indurated tissues that may become adherent to the skin.
• Sinus tracts and draining pus may develop.
• Yellow-white sulfur granules may be present in the discharge.
• Lymphadenopathy may be absent or less prominent than expected.

Diagnosis

• Histology can show branching filamentous organisms.
• Gram stain is typically positive.
• Ziehl–Neelsen staining is negative, helping distinguish the condition from acid-fast organisms such as Mycobacterium tuberculosis.

Treatment

• Prolonged antibiotics are generally required.
• Amoxicillin for at least six weeks, often extending to several months depending on disease severity and response.
• Drainage or surgical management may be required for selected lesions.

FCPS tip: Woody jaw swelling + sinus tracts + sulfur granules = cervicofacial actinomycosis.

💡Syphilis — oral manifestations

Syphilis is caused by Treponema pallidum and progresses through recognized clinical stages.

Diagnosis

• Non-treponemal tests: VDRL and RPR.
• Treponemal tests: TPHA/TPPA and treponemal antibody tests.

Non-treponemal titres are useful for monitoring treatment response, while treponemal tests often remain positive after treatment.

Treatment principles

• Benzathine penicillin G is the standard treatment for many stages of syphilis.
• Regimen depends on stage, duration, pregnancy status and whether neurological or ocular involvement is present.
• Suspected syphilis should be referred and managed according to current STI guidance.

FCPS tip: Hutchinson's incisors + interstitial keratitis + sensorineural deafness form Hutchinson's triad in congenital syphilis.

💡Tuberculosis — oral manifestations

Oral tuberculosis is uncommon but may occur in primary or secondary infection.

Clinical features

• Chronic, irregular ulcer, classically on the tongue.
• Ulcer may have undermined edges.
• It can mimic squamous cell carcinoma.
• Cervical lymphadenopathy may coexist.
• Pulmonary or systemic symptoms may or may not be present.

Histopathology

• Caseating granulomas.
• Epithelioid histiocytes.
• Langhans-type giant cells may be seen.

Diagnosis and management

• Biopsy and appropriate microbiological testing are important.
• Assessment for pulmonary TB and systemic disease is necessary.
• Rifampicin is a potent CYP450 inducer and can reduce the effectiveness of various medications, including some drugs used in HIV treatment.
• Dental care should be planned with infection-control precautions and appropriate coordination with the treating team.

FCPS tip: Chronic non-healing oral ulcer with undermined edges + caseating granulomas = consider TB, but biopsy is needed to distinguish it from malignancy and other causes.

💡Bacterial sialadenitis

A. Acute suppurative parotitis

Most common organism: Staphylococcus aureus.

Predisposing factors

• Dehydration.
• Xerostomia.
• Sjögren syndrome.
• Salivary stasis or obstruction.

Clinical features

• Painful, swollen salivary gland.
• Purulent discharge from Stensen's duct on gland massage.
• Fever and tenderness may occur.

Treatment principles

• Hydration.
• Appropriate antibiotics based on severity, local resistance and patient factors.
• Salivary flow stimulation where appropriate.
• Drainage or specialist assessment if abscess or obstruction is suspected.

B. Submandibular sialolithiasis

• Approximately 80–90% of salivary calculi occur in the submandibular gland.
• The long, uphill course of Wharton's duct and the characteristics of submandibular saliva favor stone formation.
• Swelling and pain may occur around mealtimes due to stimulated salivary flow.
• A stone may sometimes be palpable in the floor of the mouth.
• Radiopaque calculi may be visible on appropriate radiographs.

FCPS tip: Painful swelling during meals strongly suggests salivary obstruction; pus expressed from Stensen's duct suggests suppurative parotitis.

💡Gonorrhoea — oral manifestations

Organism

Neisseria gonorrhoeae, a Gram-negative diplococcus.

Oral presentation

• Often asymptomatic.
• May cause pharyngeal soreness, erythema or exudative pharyngitis.
• Oral transmission can occur through sexual contact.

Diagnosis

• NAAT is commonly used on an appropriate throat swab.
• Testing and treatment should follow current STI guidance.

Ceftriaxone plus azithromycin; this reflects its recorded regimen and should not be taken as a current universal prescription. Contemporary treatment recommendations may differ because of antimicrobial resistance.

FCPS tip: Pharyngeal gonorrhoea is often asymptomatic; NAAT on a throat swab is a key diagnostic test.

💡HIV / AIDS AND ORAL MANIFESTATIONS

💡HIV structure and important proteins

HIV is an enveloped, single-stranded RNA retrovirus. HIV-1 is responsible for the pandemic; HIV-2 is concentrated mainly in West Africa and generally progresses more slowly.

The principal target cells are CD4-positive T lymphocytes.

HIV replication cycle

1. gp120 binds CD4 and a coreceptor.
2. gp41 mediates fusion and viral entry.
3. Reverse transcriptase converts viral RNA into DNA.
4. Integrase inserts viral DNA into the host genome, creating a provirus.
5. The host cell produces viral RNA and proteins.
6. Protease processes viral polyproteins to produce mature infectious virions.

Remember: Integrated proviral DNA can persist in latent reservoirs. ART suppresses replication but does not eradicate latent HIV; treatment is generally lifelong.

💡HIV natural history and CD4 counts

The following table follows the approximate thresholds used in your uploaded notes. These are revision associations, not absolute diagnostic boundaries.

High-yield CD4 thresholds

Important update: Modern HIV care recommends ART for all people with HIV, regardless of CD4 count. Prophylaxis thresholds depend on the infection, viral load, ART status and current guidelines.

💡Oral manifestations of HIV

Important associations

• Candidiasis: may be an early manifestation of HIV, but it is not specific to HIV.
• Hairy leukoplakia: strongly associated with immunosuppression; classically on the lateral tongue.
• Linear gingival erythema: a persistent red gingival band that may not resolve with routine scaling alone.
• NUP: rapidly destructive periodontal disease that warrants assessment for immunosuppression.
• Kaposi sarcoma: purple or violaceous oral lesion; hard palate is a classic site.
• CMV: large, chronic oral ulcers in advanced immunosuppression.

FCPS tip: Oral lesions can be the first clue to HIV infection, but diagnosis requires appropriate HIV testing rather than clinical appearance alone.

💡Dental management of patients with HIV

HIV status alone is not a reason to refuse routine dental care.

General principles

• Use standard precautions for every patient.
• Assess the patient's medical status, medications and relevant laboratory results when indicated.
• Manage oral candidiasis, periodontal disease and caries appropriately.
• Coordinate care with the treating clinician when the patient has advanced immunosuppression, significant cytopenias or active opportunistic infection.

CD4-based framework

These bands are not automatic rules for withholding treatment. The decision depends on the patient's overall condition, blood counts, procedure and current clinical guidance.

💡Needlestick injury and HIV post-exposure prophylaxis (PEP)

Immediate management

1. Wash the exposed area with soap and water; do not aggressively squeeze or traumatize the wound.
2. Report the exposure immediately.
3. Assess the source and exposure risk.
4. Seek urgent assessment for HIV PEP.
5. Arrange baseline and follow-up testing according to the occupational exposure protocol.

Key examination points

• HIV transmission risk after a percutaneous needlestick from an infected source is low but not zero.
• PEP should be started as soon as possible, ideally within hours.
• Do not delay indicated PEP while waiting for all source test results.
• PEP is generally not initiated more than 72 hours after exposure; urgent expert assessment is still appropriate if the timing is uncertain.
• Follow the current recommended PEP regimen and testing schedule.

Drug interaction

Ritonavir as a CYP3A4 inhibitor. It can substantially increase concentrations of certain medicines, including midazolam. Check interactions before administering sedatives to a patient taking ritonavir-containing ART.

FCPS tip: HIV is not a contraindication to dental treatment; standard precautions apply universally. An occupational exposure requires immediate reporting and assessment for PEP.

💡MASTER COMPARISON TABLE

💡Oral infections