Explanation:

Ludwig's angina is a rapidly progressing cellulitis involving the submandibular, sublingual, and submental spaces without abscess formation. It is a life-threatening condition that requires prompt recognition and management due to its potential for airway compromise. Correct Answer (b): Trismus (restricted mouth opening) is not a typical feature of Ludwig's angina unless the infection spreads to involve the parapharyngeal space134. This distinguishes it from other deep neck infections where trismus may be more common.

Option a: While Streptococcus species are common pathogens in Ludwig’s angina, including Streptococcus viridans, it is typically polymicrobial, involving a mix of aerobic and anaerobic organisms such as Staphylococcus and Bacteroides46. Thus, this statement oversimplifies the etiology.

Option c: The infection usually originates from odontogenic sources such as infections of the second or third mandibular molars, not the parotid gland35.

Option d: Ludwig’s angina involves diffuse cellulitis without abscess formation; this characteristic helps differentiate it from other deep neck infections13.

Option e: Airway management is often required due to the high risk of airway compromise from swelling and posterior displacement of the tongue16. This makes airway monitoring and intervention a priority in management.

Further Reading:

McDonnough JA et al. Epidemiology and resource utilization of Ludwig angina ED visits in the United States 2006–2014. Laryngoscope. 2019;129(9):2041–2044.

Cheng AG et al. Submandibular Space Infection (Ludwig Angina). MSD Manual Professional Edition. 2024: Feb 8 update.

Sasaki CT et al. Ludwig's Angina: Clinical Presentation and Management Strategies. PMC. 2022;9267709.

Additional Concepts:

Airway Management in Ludwig’s Angina:

Airway compromise is the leading cause of mortality in Ludwig’s angina6. Early involvement of an anesthesiologist or otolaryngologist is crucial for airway evaluation and management.

Flexible nasotracheal intubation or tracheostomy may be necessary in severe cases5.

Empirical Antibiotic Therapy:

Broad-spectrum antibiotics targeting aerobic and anaerobic bacteria are essential until culture results are available.

Common regimens include penicillin with beta-lactamase inhibitors (e.g., amoxicillin-clavulanate) or carbapenems combined with clindamycin or metronidazole for anaerobic coverage67.

Role of Imaging in Diagnosis:

Contrast-enhanced CT or MRI can help delineate soft tissue involvement, rule out abscesses, and assess airway compromise27.

Complications of Ludwig’s Angina:

Potential complications include mediastinitis, aspiration pneumonia, necrotizing fasciitis, sepsis, and death if untreated58. Early surgical drainage may be indicated if medical therapy fails or abscesses develop.

This question assesses higher-order thinking by requiring candidates to integrate clinical features with pathophysiology while distinguishing Ludwig's angina from other deep neck infections based on nuanced presentations like trismus absence or presence only with specific spread patterns.

Explanation:

The patient’s presentation is consistent with acute bacterial rhinosinusitis (ABRS), characterized by symptoms persisting beyond 10 days or worsening after initial improvement (double sickening). The most common bacterial pathogens responsible for ABRS in adults are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Among these, Streptococcus pneumoniae is the most frequently implicated pathogen, accounting for approximately 20–43% of cases134. Correct Answer (c): Streptococcus pneumoniae is a gram-positive, facultatively anaerobic bacterium that is the leading cause of ABRS in adults. It is part of the normal nasopharyngeal flora but can invade the sinuses under conditions conducive to bacterial growth, such as mucosal inflammation and obstruction14.

Distractor Analysis:

a. Staphylococcus aureus: While this pathogen can cause sinusitis, it is more commonly associated with sphenoid sinusitis or chronic rhinosinusitis rather than acute cases14.

b. Pseudomonas aeruginosa: This gram-negative organism is typically associated with nosocomial infections or immunocompromised patients and is not a common cause of community-acquired ABRS4.

d. Moraxella catarrhalis: This gram-negative diplococcus accounts for approximately 2–10% of ABRS cases in adults, making it less common than S. pneumoniae34.

e. Klebsiella pneumoniae: This organism is rarely implicated in ABRS and is more commonly associated with nosocomial infections or immunocompromised hosts4.

Further Reading:

Brook I. Microbiology and management of sinusitis. J Clin Microbiol. 2005;43(2):2429-2435.

Rosenfeld RM et al. Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2015;152(2 Suppl):S1-S39.

Fokkens WJ et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinology. 2020;58(Suppl S29):1-464.

Additional Concepts:

Pathophysiology of ABRS: Viral upper respiratory infections often precede ABRS by causing mucosal inflammation, which obstructs sinus drainage pathways and creates an environment conducive to bacterial overgrowth12.

Role of Imaging in Diagnosis: Imaging studies such as CT scans are not routinely recommended for uncomplicated ABRS but may be useful in suspected complications (e.g., orbital or intracranial extension)28.

Antibiotic Resistance Trends: Increasing resistance among common pathogens like S. pneumoniae to penicillin and macrolides highlights the importance of judicious antibiotic use based on local resistance patterns45.

Management Guidelines: Antibiotics are reserved for patients with severe symptoms, prolonged illness (>10 days), or worsening symptoms after initial improvement (double sickening). Amoxicillin-clavulanate remains first-line therapy for most patients23.

Explanation:

The clinical presentation of a "slapped-cheek" rash sparing the nasolabial folds, combined with mild systemic symptoms such as fever and irritability, is characteristic of erythema infectiosum (Fifth disease). This condition is caused by parvovirus B19 and commonly affects children. The rash typically progresses to a lacy, reticular pattern on the extremities after appearing on the cheeks27. Why this is correct: Erythema infectiosum (Fifth disease): The hallmark "slapped-cheek" appearance, along with sparing of the nasolabial folds and mild systemic symptoms, strongly supports this diagnosis. Parvovirus B19 infection often presents in this manner in children27. Why others are incorrect: a. Measles: Measles presents with a high fever, cough, coryza, conjunctivitis, and a maculopapular rash that starts on the face and spreads downward. Koplik spots inside the mouth are diagnostic but absent in this case16.

c. Roseola (Sixth disease): Roseola typically begins with a high fever lasting 3–5 days, followed by a maculopapular rash that starts on the trunk and spreads outward as the fever resolves. The slapped-cheek appearance is not characteristic38.

d. Scarlet fever: This condition is associated with group A streptococcus infection and presents with sore throat, fever, and a scarlatiniform rash that feels like sandpaper. A "strawberry tongue" may also be present, but these findings are absent here4.

e. Atopic dermatitis: This chronic condition presents with pruritic eczematous lesions often in flexural areas or on exposed skin but does not cause a slapped-cheek appearance or systemic symptoms like fever5.

Further Reading:

Heininger U, Seward JF. Varicella. Lancet. 2006;368(9544):1365-1376.

Young NS, Brown KE. Parvovirus B19. N Engl J Med. 2004;350(6):586-597.

Cherry JD, Harrison GJ, Kaplan SL, et al., editors. Feigin and Cherry's Textbook of Pediatric Infectious Diseases. 8th ed. Philadelphia: Elsevier; 2019:1390-1400.

Additional Concepts:

Parvovirus B19 Complications: In immunocompromised individuals or those with hemolytic disorders (e.g., sickle cell anemia), parvovirus B19 can cause transient aplastic crisis or chronic anemia27.

Pregnancy Risks: Parvovirus B19 infection during pregnancy can lead to fetal complications such as hydrops fetalis due to severe fetal anemia2.

Transmission and Prevention: The virus spreads via respiratory droplets and has an incubation period of 4–14 days; patients are most contagious before the onset of rash7.

Differential Diagnosis for Pediatric Rashes: Clinicians should consider other viral exanthems such as rubella or enteroviral infections when evaluating febrile children with rashes to avoid misdiagnosis16.

Explanation:

Epiglottitis is a life-threatening condition characterized by inflammation of the epiglottis and surrounding supraglottic structures, typically caused by bacterial infection. The clinical presentation includes fever, severe sore throat, odynophagia (painful swallowing), dysphagia (difficulty swallowing), muffled "hot potato" voice, drooling, and stridor in severe cases. The tripod position and anxiety suggest impending airway obstruction, a hallmark of epiglottitis267.

Why the correct answer is correct:

Epiglottitis: The patient's symptoms—progressive sore throat, fever, muffled voice, drooling, and the indirect laryngoscopic findings of a swollen erythematous epiglottis—are classic for epiglottitis. This condition requires urgent airway management and intravenous antibiotics27.

Why the other options are incorrect:

Peritonsillar abscess: While this condition can cause sore throat, fever, and difficulty swallowing, it usually presents with unilateral tonsillar swelling that displaces the uvula to the opposite side. The absence of these findings makes this diagnosis less likely38.

Acute viral pharyngitis: Viral pharyngitis typically causes mild symptoms such as sore throat, rhinorrhea, and cough but lacks the severe systemic signs (e.g., drooling or tripod positioning) seen in this case16.

Laryngeal carcinoma: This condition can cause dysphagia and hoarseness but usually develops over months rather than days. It is also associated with risk factors like chronic smoking and alcohol use but lacks acute inflammatory signs like fever or drooling4.

Infectious mononucleosis: Caused by Epstein-Barr virus (EBV), this condition presents with fever, pharyngitis, lymphadenopathy, and fatigue. However, it lacks the hallmark findings of epiglottitis (e.g., swollen epiglottis) and typically involves tonsillar exudates56.

Further Reading:

Brook I. "Acute bacterial infections of the head and neck." N Engl J Med. 2002;346(15):1137–1142.

Berger G et al. "Adult acute epiglottitis: its course and the need for airway intervention." Laryngoscope. 2003;113(4):708–711.

Schwartz SR et al. "Clinical practice guideline: Evaluation of dysphonia (hoarseness)." Otolaryngol Head Neck Surg. 2018;159(1_suppl):S1–S42.

Additional Concepts:

Airway Management in Epiglottitis: Airway obstruction is the most serious complication of epiglottitis. Early involvement of an otolaryngologist or anesthesiologist for potential intubation or tracheostomy is critical27.

Role of Imaging: While clinical diagnosis is paramount, lateral neck radiographs (showing a "thumbprint sign") or CT scans may confirm swelling of the epiglottis if the airway is stable6.

Antibiotic Therapy: Broad-spectrum antibiotics like ceftriaxone are essential to target likely pathogens such as Haemophilus influenzae type B (HiB), Streptococcus pneumoniae, or Staphylococcus aureus7.

HiB Vaccine Impact: The incidence of pediatric epiglottitis has declined significantly due to widespread HiB vaccination; however, cases in adults are increasing2.

Explanation:

The Jarisch-Herxheimer reaction (JHR) is a well-documented inflammatory response that occurs in patients undergoing antimicrobial treatment for spirochetal infections such as syphilis. It is caused by the rapid destruction of Treponema pallidum, which releases endotoxin-like substances that trigger an immune response. This reaction typically occurs within 24 hours of initiating treatment and is characterized by fever, chills, headache, and exacerbation of skin lesions—symptoms consistent with this patient's presentation126.

Why other options are incorrect:

a. Allergic reaction to penicillin: Allergic reactions typically present with urticaria, angioedema, or anaphylaxis rather than fever and worsening of pre-existing lesions. Symptoms such as fever and chills occurring hours after treatment are more indicative of JHR than an allergic response38.

c. Secondary syphilis manifestation: The progression to secondary syphilis involves systemic symptoms such as rash on palms and soles or mucosal lesions but does not occur acutely following treatment initiation48.

d. Systemic lupus erythematosus flare-up: While lupus flares can cause fever and systemic symptoms, this patient has no history or clinical features suggestive of lupus (e.g., malar rash, joint pain). Moreover, the temporal association with penicillin treatment strongly points to JHR18.

e. Neurosyphilis: Although neurosyphilis can present with systemic symptoms, it does not develop acutely following treatment and is more likely in untreated or late-stage syphilis cases46.

Further Reading:

Loveday HP, Bingham JS. The Jarisch-Herxheimer reaction in syphilis. BMJ. 1967;1(5537):384-385.

CDC Guidelines for the Treatment of Syphilis. Syphilis - STI Treatment Guidelines - CDC. 2024.

Putkonen T et al. Studies on the Jarisch-Herxheimer Reaction in Syphilis Patients Treated with Penicillin. BMJ. 1967;1(5537):384-385.

Additional Concepts:

Pathophysiology of JHR: The release of lipoproteins from T. pallidum during antibiotic therapy induces cytokine release (e.g., TNF-alpha, IL-6), causing systemic inflammation28.

Management of JHR: The reaction is self-limiting and resolves within 24 hours without specific treatment; however, antipyretics like ibuprofen may be used for symptom relief13.

Differentiating from allergic reactions: Allergic reactions typically involve pruritus, hives, or respiratory symptoms and occur within minutes to hours after exposure to the allergen3.

Prognostic implications: JHR is a sign that the antibiotic therapy is effectively targeting the infection and does not necessitate discontinuation of treatment unless symptoms are severe57.

Explanation:

The patient's presentation of refractory oral candidiasis, despite adequate treatment with topical antifungals such as nystatin and miconazole, necessitates a step-up in management to systemic antifungal therapy. Oral fluconazole is the first-line systemic treatment for extensive or treatment-resistant oral candidiasis in immunocompetent patients due to its high efficacy, good tolerability, and broad spectrum of activity against Candida species125. Correct Answer (b): Oral fluconazole is recommended at a dose of 50-100 mg daily for at least 14 days in cases of refractory or severe oral candidiasis12. It is effective in eradicating fungal infections that have not responded to topical therapies and can address deeper mucosal involvement.

Incorrect Options:

a. Prescribe higher doses of topical nystatin: Increasing the dose of nystatin is unlikely to be effective since the infection has already demonstrated resistance to topical therapy5.

c. Prescribe a hydrogen peroxide mouthwash: While hydrogen peroxide may have mild antifungal properties, it is not an evidence-based treatment for refractory oral candidiasis and does not address systemic fungal infections6.

d. Prescribe oral metronidazole: Metronidazole is an antibiotic effective against anaerobic bacteria but has no activity against fungal infections like candidiasis6.

e. Initiate broad-spectrum intravenous antifungal therapy: This approach is reserved for critically ill or immunocompromised patients with systemic fungal infections, such as candidemia, and is not appropriate for localized oral candidiasis in an otherwise healthy patient35.

Further Reading:

Pappas PG et al. Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2016;62(4):e1-e50.

Patil S et al. Current treatment of oral candidiasis: A literature review. J Contemp Dent Pract. 2014;15(4):524-530.

Akpan A, Morgan R. Oral candidiasis. Postgrad Med J. 2002;78(922):455-459.

Additional Concepts:

Role of Fluconazole Resistance: Although fluconazole is highly effective, resistance can occur, particularly in patients with recurrent or chronic infections or those previously treated with azoles36. In such cases, alternative agents like itraconazole or newer azoles (e.g., voriconazole) may be considered after susceptibility testing6.

Predisposing Factors: Persistent or recurrent candidiasis warrants investigation for underlying risk factors such as undiagnosed diabetes, iron deficiency, or immune dysfunction4. Addressing these factors is critical for long-term management and prevention of recurrence5.

Topical vs Systemic Therapy: Topical agents like nystatin and miconazole are effective for mild cases but have limited penetration into deeper tissues or biofilms, which may necessitate systemic therapy in refractory cases25.

Adjunctive Measures: Improving oral hygiene, discontinuing predisposing medications (e.g., inhaled corticosteroids), and dietary modifications (e.g., reducing carbohydrate intake) are essential adjuncts to antifungal therapy for optimal outcomes46.

Explanation:

Biofilms are structured communities of bacteria encased in a self-produced extracellular matrix that confer resistance to antibiotics and host defenses. In chronic otitis media (COM) with cholesteatoma, biofilm formation is a key pathogenic mechanism contributing to persistent infection and treatment failure. Correct Answer: e. Pseudomonas aeruginosa

Pseudomonas aeruginosa is the most commonly identified organism in biofilms associated with cholesteatomas. Studies have demonstrated its robust biofilm-forming capacity, which explains its persistence in chronic infections despite antibiotic therapy12. The unique ability of Pseudomonas aeruginosa to form biofilms within the keratin matrix of cholesteatomas makes it a significant pathogen in these cases3.

Incorrect Options:

a. *Staphylococcus aureus*: While S. aureus can form biofilms and is implicated in some cases of COM, it is less frequently associated with cholesteatoma-related infections compared to Pseudomonas aeruginosa23.

b. *Streptococcus pneumoniae*: This organism is more commonly associated with acute otitis media rather than chronic infections or cholesteatomas3.

c. *Haemophilus influenzae*: Similar to S. pneumoniae, this bacterium is primarily involved in acute otitis media and rarely forms biofilms in cholesteatomas3.

d. *Escherichia coli*: Although capable of forming biofilms, it is not a common pathogen in middle ear infections or cholesteatomas2.

Further Reading:

Chole RA, Faddis BT. Evidence for microbial biofilms in cholesteatomas. Otolaryngol Head Neck Surg. 2002;127(5):409-413.

Homøe P, Rosborg J, Djurhuus BD. Biofilm formation in chronic otitis media and cholesteatoma: A systematic review. Int J Pediatr Otorhinolaryngol. 2009;73(9):1211-1217.

Wang EW, Jung JY, Pashia ME, et al. Biofilm formation by middle ear pathogens facilitates chronic infection in experimental otitis media model systems. J Clin Microbiol. 2010;48(10):3470-3476.

Additional Concepts:

Pathogenesis of Cholesteatoma: Cholesteatomas are keratinizing epithelial lesions that can erode bone and cause complications such as hearing loss, facial nerve paralysis, or intracranial infections due to their invasive nature and association with chronic inflammation and infection13.

Role of Biofilms in Chronic Otitis Media: Biofilms protect bacteria from antibiotics and immune responses, necessitating surgical intervention (e.g., tympanomastoidectomy) for eradication in cases of COM with cholesteatoma12.

Diagnostic Tools for Biofilms: Advanced techniques like scanning electron microscopy (SEM) and polymerase chain reaction (PCR) are used to identify biofilms and their bacterial constituents, though they are not routinely available23.

Treatment Implications: The presence of biofilms often necessitates surgical removal of infected tissue combined with targeted antibiotic therapy based on culture and sensitivity results to prevent recurrence3.

Explanation:

The patient’s risk factors (chronic inhaled corticosteroid use, methotrexate-induced immunosuppression), laryngoscopic findings of white plaques, and histopathological evidence of pseudohyphae strongly support Candida albicans as the causative organism. Inhaled corticosteroids impair local mucosal immunity, predisposing to candidiasis, while methotrexate further suppresses systemic immunity. Pseudohyphae formation is pathognomonic for Candida species in tissue samples. Why other options are incorrect:

a. Histoplasma capsulatum: Presents as intracellular yeast within macrophages (not pseudohyphae) and is endemic to the Ohio/Mississippi River Valleys. Patients typically have exposure to bird/bat droppings.

b. Aspergillus fumigatus: Demonstrates septate hyphae with acute-angle branching on histopathology, commonly seen in immunocompromised hosts but rarely isolated to the larynx without pulmonary involvement.

d. Blastomyces dermatitidis: Causes broad-based budding yeast forms and is endemic to the Ohio/Mississippi River Valleys and Great Lakes. Laryngeal involvement is rare and associated with disseminated disease.

e. Coccidioides immitis: Endemic to the southwestern US, it forms spherules containing endospores on histology. Laryngeal involvement is exceedingly uncommon.

Further Reading:

Thompson GR, Young JAH. Laryngeal candidiasis in immunocompromised hosts: A diagnostic and therapeutic challenge. Laryngoscope Investig Otolaryngol. 2023.

Kim EJ, Park HS. Fungal laryngitis: Clinical and histopathological correlations. Ann Otol Rhinol Laryngol. 2021.

Miller RH, Sneed WF. Inhaled corticosteroids and laryngeal complications: Mechanisms and mitigation strategies. Chest. 2020.

Additional Concepts:

Risk Factors for Fungal Laryngitis: Chronic inhaled/oral steroid use, diabetes, HIV/AIDS, and immunosuppressive therapies (e.g., methotrexate) disrupt mucosal integrity or systemic immunity, facilitating fungal overgrowth.

Histopathological Clues: Candida pseudohyphae appear as elongated, branching structures without true septae, distinct from Aspergillus (septate hyphae) or Blastomyces (broad-based budding).

Differential Diagnosis: Includes laryngeal leukoplakia, squamous cell carcinoma, and granulomatous diseases (e.g., tuberculosis). Biopsy with fungal stains (PAS, GMS) is critical for differentiation.

Treatment: First-line therapy involves oral fluconazole; refractory cases may require voriconazole or amphotericin B. Concurrent reduction of immunosuppressive agents, if feasible, improves outcomes.

Explanation:

The clinical presentation and imaging findings are suggestive of a juvenile nasopharyngeal angiofibroma (JNA), a benign but locally aggressive vascular tumor that primarily affects adolescent males but can occasionally present in adults. The hallmark features include unilateral nasal obstruction, recurrent epistaxis, and a vascular mass on imaging without bony destruction. Correct Answer (b): Preoperative embolization followed by surgical resection is the standard treatment for JNA. Embolization reduces intraoperative bleeding by occluding the tumor’s blood supply, which is critical given the highly vascular nature of this tumor. Surgical resection is then performed to remove the tumor completely.

Incorrect Options:

a. Endoscopic sinus surgery: While endoscopic approaches are often part of the surgical management for JNA, preoperative embolization is essential to minimize bleeding risk during surgery.

c. Radiation therapy: This is reserved for unresectable or recurrent cases and not used as first-line treatment.

d. Systemic corticosteroids: These are not effective in managing JNA as it is not an inflammatory condition.

e. Chemotherapy: This is not indicated for benign tumors like JNA.

Further Reading:

Nicolai P, Schreiber A, Bolzoni Villaret A. Juvenile angiofibroma: evolution of management. Int J Pediatr Otorhinolaryngol. 2009;73(Suppl 1):S28-S31.

Lloyd G, Howard D, Lund VJ, Savy L. Juvenile angiofibroma: The lessons of 20 years of modern imaging. J Laryngol Otol. 1999;113(2):127-134.

Snyderman CH, Pant H, Carrau RL, Gardner P, Prevedello DM, Kassam AB. Endoscopic approaches to benign sinonasal tumors including juvenile angiofibroma: A paradigm shift? Head Neck Surg Clin N Am. 2010;22(4):497-508.

Additional Concepts:

Imaging Features of JNA: CT and MRI are essential for diagnosis and surgical planning in JNA cases. CT typically shows a soft tissue mass with bone remodeling (e.g., widening of the sphenopalatine foramen), while MRI highlights its vascular nature with flow voids.

Vascular Supply: The tumor is primarily supplied by branches of the external carotid artery (e.g., internal maxillary artery). Preoperative angiography helps delineate the blood supply and guide embolization.

Staging Systems for JNA: The Radkowski staging system classifies JNA based on tumor extent and involvement of adjacent structures, guiding treatment planning.

Complications of Embolization and Surgery: Potential complications include cranial nerve injury, residual or recurrent disease, and postoperative epistaxis requiring further intervention.

Differential Diagnosis: Other causes of unilateral nasal masses include inverted papilloma, sinonasal carcinoma, and fungal sinusitis; histopathology is crucial for differentiation.

This question assesses higher-order thinking by integrating clinical presentation, imaging findings, pathology results, and management principles to arrive at an optimal treatment strategy for a complex ENT condition like JNA.

Explanation:

Noma is a rapidly progressive, necrotizing stomatitis most prevalent in malnourished children in developing regions, often following systemic illnesses like measles. Key features include full-thickness mucosal and cutaneous necrosis, foul odor, and a history of immunosuppressive triggers (e.g., malnutrition, recent infection). The buccal mucosa-to-skin destruction seen here is pathognomonic. a) Necrotizing ulcerative gingivitis (NUG): Limited to gingival tissues with interdental necrosis and bleeding but not extra-gingival tissue destruction. Systemic involvement (e.g., cutaneous extension) is absent137.

b) Herpetic gingivostomatitis: Presents with vesicular lesions before ulceration, typically in younger children, and lacks necrotic tissue sloughing or cutaneous perforation57.

d) Tuberculous ulceration: Usually presents as a single, indurated ulcer with a granular base and systemic TB symptoms (e.g., night sweats, weight loss). Biopsy would show granulomas15.

e) Recurrent aphthous stomatitis: Small, shallow, painful ulcers on non-keratinized mucosa; recurrent history and absence of necrosis/systemic signs distinguish it45.

Further Reading:

Marck KW. Noma: A neglected enigma. Lancet Glob Health. 2020;8(5):e610-e611.

Enwonwu CO, Falkler WA, Idigbe EO. Oro-facial gangrene (noma/cancrum oris): Pathogenetic mechanisms. Crit Rev Oral Biol Med. 2000;11(2):159-171.

Farah CS, Lynch N, McCullough MJ. Oral ulcerative lesions: Unraveling the mystery. Oral Dis. 2022;28(6):1539-1555.

Additional Concepts:

Differential Diagnosis of Rapidly Progressive Oral Necrosis: Include ANUG, noma, mucormycosis, and midline granuloma. Noma is distinguished by cutaneous perforation and epidemiologic risk factors67.

Management of Necrotizing Oral Conditions: Immediate broad-spectrum antibiotics (e.g., metronidazole + penicillin), fluid resuscitation, nutritional support, and surgical debridement for tissue preservation26.

Role of Malnutrition in Oral Pathology: Protein-energy malnutrition impairs mucosal immunity, enabling polymicrobial infections (e.g., Fusobacterium, Prevotella) to progress to necrosis26.

Biopsy Indications for Oral Ulcers: Persistent (>3 weeks), indurated, or solitary ulcers require biopsy to exclude malignancy or granulomatous diseases (e.g., TB, Crohn’s)45.