```markdown Orofacial Infections In Paediatric Dentistry DENT 5312 Paediatric Dentistry Module Dr Jilen Patel Specialist Paediatric Dentist Senior Lecturer, Clinical Dentistry UWA Dental School ``` #### Course Information - **Course Code:** DENT 5312 - **Module:** Paediatric Dentistry Module #### Presenter Details - **Dr Jilen Patel** - Specialist Paediatric Dentist - Senior Lecturer, Clinical Dentistry - UWA Dental School # Orofacial Infections in Paediatric Dentistry - **MUST READ** - Handbook of Pediatric Dentistry, Cameron and Widmer 4th Ed - Ebook available through UWA Onesearch - Chapter 10: Paediatric oral medicine, oral pathology and radiology <img src="https://i.imgur.com/8X9jJzG.png" alt="Cover of the Handbook of Pediatric Dentistry, 4th Edition, edited by Angus C. Cameron and Richard P. Widmer, published by Mosby Elsevier, with a foreword by Roger K. Hall. The cover features a child holding a toothbrush and a smiling tooth character." />  #### Required Reading - **Handbook of Pediatric Dentistry** - Authors: Cameron and Widmer (4th Edition) - Access: Ebook available through UWA Onesearch #### Specific Study Areas - **Chapter 10:** Paediatric oral medicine, oral pathology and radiology Cover of the 'Handbook of Pediatric Dentistry' 4th Edition, edited by Angus C. Cameron and Richard P. Widmer, featuring a child holding a toothbrush and a smiling tooth character. The cover includes the Mosby Elsevier logo and a foreword by Roger K. Hall. ```markdown Diagnostic Sieve <img src="https://i.imgur.com/1.png" alt="Diagnostic Sieve Diagram"/> The University of Western Australia ``` ```html <table border="1" cellpadding="10" cellspacing="0" style="border-collapse: collapse; width: 100%; text-align: left;"> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">V</th> <td style="text-align: left; vertical-align: top;">VASCULAR</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">I</th> <td style="text-align: left; vertical-align: top;">INFLAMMATORY</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">T</th> <td style="text-align: left; vertical-align: top;">TRAUMATIC</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">A</th> <td style="text-align: left; vertical-align: top;">AUTOIMMUNE</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">M</th> <td style="text-align: left; vertical-align: top;">METABOLIC</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">I</th> <td style="text-align: left; vertical-align: top;">INFECTION</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">N</th> <td style="text-align: left; vertical-align: top;">NEOPLASTIC</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">D</th> <td style="text-align: left; vertical-align: top;">DEGENERATIVE</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">I</th> <td style="text-align: left; vertical-align: top;">IDIOPATHIC</td> </tr> <tr> <th style="text-align: center; vertical-align: middle; background-color: #f2f2f2;">C</th> <td style="text-align: left; vertical-align: top;">CONGENITAL</td> </tr> </table> ```  #### The Diagnostic Sieve (VITAMIND IC) The diagnostic sieve is a structured framework used to categorize potential causes of a clinical presentation. | Letter | Category | | :--- | :--- | | **V** | VASCULAR | | **I** | INFLAMMATORY | | **T** | TRAUMATIC | | **A** | AUTOIMMUNE | | **M** | METABOLIC | | **I** | INFECTION | | **N** | NEOPLASTIC | | **D** | DEGENERATIVE | | **I** | IDIOPATHIC | | **C** | CONGENITAL | The image displays a diagnostic sieve diagram titled 'Diagnostic Sieve' from The University of Western Australia. It features a vertical list of medical categories represented by the acronym VITAMIN D I C, with each letter corresponding to a condition type (Vascular, Inflammatory, Traumatic, Autoimmune, Metabolic, Infection, Neoplastic, Degenerative, Idiopathic, Congenital). A red oval labeled 'SURGICAL SIEVE (VITAMIN DIC)' is connected to the list, suggesting a flow or filtering process for diagnosis. # Orofacial Infections - **Bacterial** - **Viral** - **Fungal** <img src="https://i.imgur.com/8ZzZzZz.png" alt="University of Western Australia logo">  Orofacial infections in paediatric dentistry are generally categorized into three primary types: - **Bacterial** - **Viral** - **Fungal** The University of Western Australia logo, featuring a shield with a swan and the institution's name in blue text. # Orofacial Infections ## Differential Diagnosis ### Bacterial infections - Odontogenic - dental caries - periodontal disease - Scarlet fever - Tuberculosis - Atypical mycobacterial infection - Actinomycosis - Syphilis - Impetigo - Osteomyelitis ### Viral infections - Primary herpetic gingiva-stomatitis - Herpes labialis - Herpangina - Hand, foot and mouth disease - Infectious mononucleosis - Varicella ### Fungal infections - Candidosis  - **Odontogenic Infections** - Dental caries - Periodontal disease - **Systemic and Localized Bacterial Infections** - Scarlet fever - Tuberculosis - Atypical mycobacterial infection - Actinomycosis - Syphilis - Impetigo - Osteomyelitis - Candidosis A table titled 'Differential Diagnosis' categorizing orofacial infections into three types: bacterial, viral, and fungal. Under bacterial infections, it lists conditions such as odontogenic (dental caries, periodontal disease), scarlet fever, tuberculosis, atypical mycobacterial infection, actinomycosis, syphilis, impetigo, and osteomyelitis. Under viral infections, it includes primary herpetic gingiva-stomatitis, herpes labialis, herpangina, hand, foot and mouth disease, infectious mononucleosis, and varicella. Under fungal infections, it lists candidosis. # Orofacial Infections ## Differential Diagnosis ### Bacterial infections - Odontogenic - dental caries - periodontal disease - Scarlet fever - Tuberculosis - Atypical mycobacterial infection - Actinomycosis - Syphilis - Impetigo - Osteomyelitis ### Viral infections - Primary herpetic gingiva-stomatitis - Herpes labialis - Herpangina - Hand, foot and mouth disease - Infectious mononucleosis - Varicella ### Fungal infections - Candidosis  #### Bacterial and Viral Differential List - **Bacterial** - Odontogenic (dental caries, periodontal disease) - Scarlet fever - Tuberculosis - Atypical mycobacterial infection - Actinomycosis - Syphilis - Impetigo - Osteomyelitis - **Viral** - Primary herpetic gingiva-stomatitis - Herpes labialis - Herpangina - Hand, foot and mouth disease - Infectious mononucleosis - Varicella #### Fungal - Candidosis The image contains a structured list under the heading "Differential Diagnosis" that categorizes orofacial infections into three types: bacterial, viral, and fungal. The bacterial infections include odontogenic (dental caries, periodontal disease), scarlet fever, tuberculosis, atypical mycobacterial infection, actinomycosis, syphilis, impetigo, and osteomyelitis. The viral infections listed are primary herpetic gingiva-stomatitis, herpes labialis, herpangina, hand, foot and mouth disease, infectious mononucleosis, and varicella. The fungal infection mentioned is candidosis. # Viral Infections <table border="1" class="dataframe"> <thead> <tr style="text-align: left;"> <th>Virus</th> <th>Disease</th> </tr> </thead> <tbody> <tr> <td>Herpes Simplex Virus Type 1 (HSV)</td> <td>• Primary herpetic gingivostomatitis<br>• Herpes labilis</td> </tr> <tr> <td>Epstein Barr virus (EBV)</td> <td>Infectious mononucleosis</td> </tr> <tr> <td>Coxsackie A, B, enterovirus 71</td> <td>Hand foot and mouth disease</td> </tr> <tr> <td>Coxsackie A</td> <td>Herpangina</td> </tr> <tr> <td>Varicella Zoster Virus (VZV)</td> <td>Chickenpox</td> </tr> </tbody> </table>  | Virus | Disease | | :--- | :--- | | Herpes Simplex Virus Type 1 (HSV) | • Primary herpetic gingivostomatitis<br>• Herpes labialis | | Epstein Barr virus (EBV) | Infectious mononucleosis | | Coxsackie A, B, enterovirus 71 | Hand foot and mouth disease | | Coxsackie A | Herpangina | | Varicella Zoster Virus (VZV) | Chickenpox | A table listing various viruses and the diseases they cause, under the heading 'Viral Infections'. The table has two columns: 'Virus' and 'Disease', with entries including Herpes Simplex Virus Type 1 (HSV) causing primary herpetic gingivostomatitis and herpes labialis, Epstein Barr virus (EBV) causing infectious mononucleosis, Coxsackie A, B, and enterovirus 71 causing hand foot and mouth disease, Coxsackie A causing herpangina, and Varicella Zoster Virus (VZV) causing chickenpox. <img src="https://i.imgur.com/5QvZ9dE.png" alt="Four images showing oral lesions, likely herpes simplex virus infection, with redness, blisters, and ulcerations on the lips and tongue.">     Visual clinical markers of viral orofacial infections often include redness, blisters, and ulcerations on the lips and tongue, characteristic of the Herpes Simplex Virus family. Close-up photograph of oral lesions on the lips, showing redness, blisters, and ulcerations, likely indicative of a herpes simplex virus infection. Photograph of oral lesions on the inner lip, with visible redness, blisters, and ulcerations, consistent with a herpes simplex virus infection. Image of a tongue with multiple small, raised lesions and areas of ulceration, suggesting a viral infection such as herpes simplex. Photograph of severe oral lesions on the lips and tongue, showing extensive redness, blistering, and ulcerations, characteristic of a herpes simplex virus infection. # Primary Herpetic Gingivostomatitis **THE UNIVERSITY OF WESTERN AUSTRALIA** ## Etiology - Herpes simplex type 1 virus - Herpes simplex type 2 virus (occasional cases) - due to genital herpes - cases of sexual abuse ## Age and gender - Primary infection usually occurs after 6 months of age - The peak incidence is between 12 and 18 months of age - No gender predilection #### Viral Agents - Herpes simplex type 1 virus - Herpes simplex type 2 virus (occasional cases related to genital herpes or sexual abuse) #### Demographics - **Age:** Primary infection usually occurs after 6 months of age, with peak incidence between 12 and 18 months. - **Gender:** No gender predilection. # Primary Herpetic Gingivostomatitis **Clinical presentation** (Amir et al. 1997, Amir et al. 1999) ## General - Febrile illness with a raised temperature of 100-102 °F (37.8-38.9 °C) - Headaches, malaise, irritability - Cervical lymphadenopathy ## Oral - Oral pain, mild dysphagia - Stomatitis - *Intraepithelial fluid-filled vesicles appear* (characteristic feature) - Site of vesicles: tongue, lips, buccal, and palatal mucosa - *Solitary ulcers*: usually small (3 mm) & painful with an erythematous margin - *Larger ulcers*: irregular margins, result from coalescence of individual lesions #### General Systemic Features - Febrile illness (37.8-38.9 °C / 100-102 °F) - Headaches, malaise, and irritability - Cervical lymphadenopathy #### Oral Manifestations - Oral pain and mild dysphagia - Stomatitis - **Vesicles:** Characteristic intraepithelial fluid-filled vesicles appearing on the tongue, lips, buccal, and palatal mucosa. - **Ulcerations:** - Solitary ulcers: Small (3 mm), painful, with erythematous margins. - Larger ulcers: Irregular margins resulting from the coalescence of individual lesions. **Primary Herpetic Gingivostomatitis** <img src="https://i.imgur.com/1234567.jpg" alt="Four images showing oral lesions characteristic of primary herpetic gingivostomatitis.">     Clinical presentation of Primary Herpetic Gingivostomatitis typically involves widespread oral lesions and significant gingival inflammation. A close-up photograph showing oral lesions with red, inflamed gums and ulcerations, characteristic of primary herpetic gingivostomatitis. A clinical photograph depicting multiple small vesicles and erosions on the inner lip and buccal mucosa, consistent with the presentation of primary herpetic gingivostomatitis. A photograph showing a tongue with multiple white, ulcerated lesions and surrounding erythema, indicative of the viral infection. A close-up photograph of the mouth with extensive ulcerations on the gums and tongue, illustrating severe symptoms of primary herpetic gingivostomatitis. ```markdown Primary Herpetic Gingivostomatitis <img src="https://i.imgur.com/placeholder1.jpg" alt="Painful, enlarged & erythematous palatal gingiva" /> Painful, enlarged & erythematous palatal gingiva <img src="https://i.imgur.com/placeholder2.jpg" alt="Painful, enlarged & erythematous facial gingiva" /> Painful, enlarged & erythematous facial gingiva Note erosions of the free gingival margin ```   #### Gingival Involvement - Painful, enlarged, and erythematous palatal gingiva. - Painful, enlarged, and erythematous facial gingiva. - Notable erosions of the free gingival margin. A close-up photo showing painful, enlarged, and erythematous palatal gingiva with visible erosions on the free gingival margin. A close-up photo displaying painful, enlarged, and erythematous facial gingiva with noticeable erosions at the free gingival margin. # Primary Herpetic Gingivostomatitis - **Incubation time** 3–5 days (with a prodromal 48-h history of irritability, pyrexia & malaise) - **Transmission** - Direct contact with the lesions - Contact with infected oral secretions (droplet infection) - **Course of disease** - Disease is self-limiting - Ulcers heal spontaneously without scarring within 10-14 days (Amir et al. 1997; Pinto and Hong, 2013) #### Incubation and Transmission - **Incubation Time:** 3–5 days, often preceded by a 48-hour prodromal history of irritability, pyrexia, and malaise. - **Transmission:** - Direct contact with active lesions. - Contact with infected oral secretions (droplet infection). #### Disease Course - The disease is self-limiting. - Ulcers typically heal spontaneously without scarring within 10–14 days. # Primary Herpetic Gingivostomatitis THE UNIVERSITY OF WESTERN AUSTRALIA ## Histology Tzanck cells: multinucleated giant cells with jig saw nucleus ## Diagnosis - History, clinical features & age group of the affected children - Exfoliative cytology: presence of multinucleated giant cells and viral inclusion bodies can be used for rapid diagnosis - Viral antigen - Viral culture - Viral antibody detection in blood samples <img src="https://i.imgur.com/8XJZJjL.png" alt="Microscopic image of Tzanck cells showing multinucleated giant cells with jagged nuclei." /> <img src="https://i.imgur.com/9Q7kKqS.png" alt="Microscopic image showing viral inclusion bodies (red arrows) and multinucleated giant cells (blue arrow) in a tissue sample." />   #### Histopathological Features - **Tzanck Cells:** Multinucleated giant cells with a "jig-saw" nucleus. - **Viral Inclusion Bodies:** Present within affected tissues. #### Diagnostic Methods - **Clinical Assessment:** Based on history, clinical features, and the age group of the child. - **Exfoliative Cytology:** Rapid diagnosis via identification of multinucleated giant cells. - **Laboratory Testing:** - Viral antigen testing - Viral culture - Viral antibody detection in blood samples Microscopic image showing multinucleated giant cells with jagged nuclei, consistent with Tzanck cells, in a tissue sample. The image highlights the histological features relevant to primary herpetic gingivostomatitis. Microscopic image displaying viral inclusion bodies (indicated by red arrows) and multinucleated giant cells (indicated by blue arrow) in a tissue sample, supporting the diagnosis of primary herpetic gingivostomatitis through exfoliative cytology. ```markdown # Primary Herpetic Gingivostomatitis ## Differential Diagnosis - Necrotizing ulcerative gingivitis - Erythema multiforme - Herpangina ## Complications Rare but severe complications of the infection - Aseptic meningitis - Encephalitis <img src="https://i.imgur.com/placeholder.jpg" alt="Image of oral cavity showing inflamed gums and teeth"/> ```  #### Differential Diagnosis - Necrotizing ulcerative gingivitis - Erythema multiforme - Herpangina #### Complications While rare, severe complications can include: - Aseptic meningitis - Encephalitis A close-up photograph of an oral cavity showing inflamed gums and teeth, illustrating the clinical presentation of primary herpetic gingivostomatitis. The image is positioned next to text discussing differential diagnoses and complications of the condition. # Primary Herpetic Gingivostomatitis **Management** - **Symptomatic care** - Encourage oral fluids - Bed rest and a soft diet - **Analgesics** - Paracetamol 15 mg/kg, 4-6 hourly - Topical therapies for pain control (e.g. 2% viscous lidocaine) are not recommended due to concern over systemic overdose & the inability of the young child to spit - Topical benzocaine gel should be avoided in children < 6 years to prevent methaemoglobinaemia (So and Farrington, 2008, Chung et al. 2010; Pinto and Hong 2013) #### Symptomatic Care - Encourage high fluid intake. - Recommend bed rest and a soft diet. #### Analgesics and Pain Control - **Paracetamol:** 15 mg/kg, every 4-6 hours. - **Topical Therapy Precautions:** - 2% viscous lidocaine is not recommended due to systemic overdose risks and the child's inability to spit. - Topical benzocaine gel should be avoided in children under 6 years old to prevent methaemoglobinaemia. # Primary Herpetic Gingivostomatitis **Management** **Mouthwashes** - In young children with severe ulceration: 0.2% chlorhexidine can be swabbed over the affected areas with cotton wool swabs - For older children – chlorhexidine gluconate, 0.2%, 10 mL 4-hourly - In children over 12 years of age: tetracycline or minocycline mouthwashes may be beneficial - A mouthwash containing benzadamine hydrochloride 0.15% & chlorhexidine 0.12% (Difflam C™) may offer some advantages over chlorhexidine alone (So and Farrington, 2008, Chung et al. 2010; Pinto and Hong 2013) #### Mouthwashes - **Young Children (Severe Ulceration):** 0.2% chlorhexidine may be swabbed over affected areas using cotton wool. - **Older Children:** Chlorhexidine gluconate 0.2%, 10 mL every 4 hours. - **Children Over 12 Years:** Tetracycline or minocycline mouthwashes may be beneficial. - **Combination Therapy:** Benzadamine hydrochloride 0.15% & chlorhexidine 0.12% (Difflam C™) may offer advantages over chlorhexidine alone. # Primary Herpetic Gingivostomatitis **Management** **Antiviral chemotherapy** - Oral and intravenous acyclovir is approved for use in children for management of primary herpetic gingivostomatitis (Arduino and Porter 2006) - Evidence for its use via the oral route in children < two years of age is limited - Some evidence that the administration of aciclovir in the first 72 - 96 h of the infection may be beneficial (Pinto and Hong 2013) - Dose: PO: 20mg/kg body weight 5 hourly TDS, or IV 10mg/kg body weight #### Antiviral Chemotherapy - **Aciclovir:** Approved for use in children for managing primary herpetic gingivostomatitis. - **Timing:** Administration within the first 72–96 hours of infection provides the most benefit. - **Dosage:** - **Oral (PO):** 20 mg/kg body weight, 5 times daily (or TDS depending on clinical guidance). - **Intravenous (IV):** 10 mg/kg body weight. - **Note:** Evidence for oral use in children under two years of age is limited. ```markdown Recurrent Herpes Simplex infections (Secondary herpes, recrudescent herpes) Herpes Labialis Alternative names: cold sore, fever blister Etiology: Herpes simplex type 1 virus Site: Vermilion border and adjacent skin of the lips Triggering factor - ultraviolet light - trauma <img src="https://i.imgur.com/7QZzv9L.jpg" alt="Image of herpes labialis with blisters on the lip"> <img src="https://i.imgur.com/8QZzv9L.jpg" alt="Image of herpes labialis with crusty lesions on the lip"> ```   #### Etiology and Site - **Agent:** Herpes simplex type 1 virus. - **Common Names:** Cold sore, fever blister. - **Site:** Vermilion border and adjacent skin of the lips. #### Triggering Factors - Ultraviolet (UV) light - Physical trauma A close-up photo showing herpes labialis with multiple small, fluid-filled blisters on the vermilion border of the lip, illustrating an active outbreak of the infection. A close-up photo depicting a more advanced stage of herpes labialis with crusted, ulcerated lesions on the lip, demonstrating the progression of the infection. # Herpes Labialis **THE UNIVERSITY OF WESTERN AUSTRALIA** ## Prodrimal signs and symptoms - Symptoms are most severe in the first 8 hours - Pain, burning, itching, tingling, localized warmth - Erythema of the involved epithelium arise 6-24 hrs before the lesions develop - Multiple small, erythematous papules develop - Form clusters of fluid-filled vesicles - Vesicles rupture and crust within 2 days ## Course of disease - Self limiting, Healing usually occurs within 7 to 10 days #### Prodromal Phase - Symptoms are most severe in the first 8 hours. - Sensations: Pain, burning, itching, tingling, and localized warmth. - Erythema appears 6–24 hours before lesions develop. #### Lesion Development - Multiple small, erythematous papules develop. - These form clusters of fluid-filled vesicles. - Vesicles typically rupture and crust within 2 days. #### Course of Disease - Self-limiting; healing usually occurs within 7 to 10 days. ```markdown # Herpes Labialis ## Prodrromal signs and symptoms - Symptoms are most severe in the first 8 hours - Pain, burning, itching, tingling, localized warmth - Erythema of the involved epithelium arise 6-24 hrs before the lesions develop - Multiple small, erythematous papules develop - Form clusters of fluid-filled vesicles - Vesicles rupture and crust within 2 days ## Course of disease - Self limiting, Healing usually occurs within 7 to 10 days ``` #### Clinical Progression Summary - **Initial 8 Hours:** Peak prodromal symptoms (tingling, itching). - **6–24 Hours:** Erythema of the involved epithelium. - **Vesicular Stage:** Formation of fluid-filled clusters. - **Crusting Stage:** Rupture and crusting within 48 hours. - **Resolution:** Spontaneous healing in 7–10 days. # Infectious mononucleosis Alternative terminology: Mono; Glandular Fever; Kissing Disease Etiology: Epstein-Barr virus (EBV or HHV-4) Transmission: The infection usually occurs by intimate contact - Main route of transmission is by blood or saliva - Intrafamilial spread is common, and once a person is exposed, EBV remains in the host for life - Children: infected through contaminated saliva on fingers, toys, or other objects - Adults: contract the virus through direct salivary transfer, such as shared straws or kissing Age and Gender: children ages 1 to 5 - not all children develop symptoms #### Etiology - **Agent:** Epstein-Barr virus (EBV or HHV-4). - **Terminology:** Mono, Glandular Fever, Kissing Disease. #### Transmission - Occurs via intimate contact, primarily through blood or saliva. - **Children:** Often infected via contaminated saliva on fingers, toys, or objects. - **Adults:** Direct salivary transfer (e.g., shared straws, kissing). - **Persistence:** Once exposed, EBV remains in the host for life. #### Demographics - Common in children aged 1 to 5 (often asymptomatic). - No specific gender predilection noted. # Infectious mononucleosis - **Clinical presentation**: It varies by age - Most infected children are typically asymptomatic - Young adults are at greatest risk for symptomatic disease **Symptoms includes** - Low-grade fever - Hepatosplenomegaly - Rhinitis or cough - Malaise, headache - Cervical lymphadenopathy and tenderness **Oral lesions**: oral ulcers, palatal petechiae and gingival ulcerations (necrotizing ulcerative gingivitis), tonsillitis with or without pharyngitis **Course of disease**: The disease is self-limiting (resolve in one to two weeks) (Pinto and Hong 2013) #### Systemic Symptoms - Low-grade fever - Hepatosplenomegaly - Rhinitis or cough - Malaise and headache - Cervical lymphadenopathy and tenderness #### Oral Lesions - Oral ulcers - Palatal petechiae - Gingival ulcerations (Necrotizing Ulcerative Gingivitis) - Tonsillitis with or without pharyngitis #### Disease Course - Self-limiting; typically resolves within one to two weeks. Young adults are at the highest risk for symptomatic disease.    Close-up photograph of the throat showing hyperplastic pharyngeal tonsils with yellowish crypt exudates, indicating a case of infectious mononucleosis. Photograph of the oral cavity displaying hyperplastic pharyngeal tonsils with yellowish crypt exudates, a characteristic finding in infectious mononucleosis. Image of the soft palate showing numerous petechiae, a common clinical sign associated with infectious mononucleosis. # Infectious mononucleosis **Histopathological features** Downey cells – atypical lymphocytes diagnostic feature **Differential Diagnosis** - Trauma - Reactive gingival lesions - Hematologic disorders - thrombocytopenia - platelet disorders - hereditary hemorrhagic telangiectasia <img src="https://i.imgur.com/8X8X8X8.png" alt="Microscopic image showing Downey cells (atypical lymphocytes) among red blood cells.">  #### Histopathology - **Downey Cells:** Atypical lymphocytes; considered a diagnostic feature. #### Differential Diagnosis - Trauma - Reactive gingival lesions - **Hematologic Disorders:** - Thrombocytopenia - Platelet disorders - Hereditary hemorrhagic telangiectasia Microscopic image showing Downey cells (atypical lymphocytes) with prominent purple-stained nuclei, surrounded by red blood cells. This histopathological feature is highlighted as a diagnostic characteristic of infectious mononucleosis. # Infectious mononucleosis **Diagnosis** - History and clinical features - Atypical lymphocytes on blood film - Positive heterophile antibody test - Monospot test (mononucleosis spot test) - Paul–Bunnell agglutination test - Indirect immunofluorescent assays - Real-time PCR #### Diagnostic Criteria - Clinical history and presentation. - Identification of atypical lymphocytes on a blood film. - **Heterophile Antibody Tests:** - Monospot test - Paul–Bunnell agglutination test - **Advanced Testing:** - Indirect immunofluorescent assays - Real-time PCR # Infectious mononucleosis **Treatment** - Most cases resolves within 4 to 6 weeks - Symptomatic treatment - bed rest - maintenance of fluid intake - adequate nutrition - analgesia - antipyretics #### Treatment Protocol - Most cases resolve spontaneously within 4 to 6 weeks. - **Supportive Care:** - Bed rest - Maintenance of fluid intake and adequate nutrition - Analgesia and antipyretics # Infectious mononucleosis **Complications:** Possible significant complications include - Splenic rupture - Thrombocytopenia - Autoimmune hemolytic anemia - Aplastic anemia - Neurologic problems - Myocarditis - Hemophagocytic lymphohistiocytosis - Patients experience fatigue lasting for several weeks to months (< 10% cases) - Increases the risk for developing multiple sclerosis later in life #### Significant Complications - Splenic rupture - Thrombocytopenia - Autoimmune hemolytic anemia - Aplastic anemia - Neurologic problems - Myocarditis - Hemophagocytic lymphohistiocytosis - Chronic fatigue (lasting weeks to months in <10% of cases) - Increased risk for developing multiple sclerosis later in life    A black-and-white photograph showing a group of individuals, including a man in a suit examining a patient in a hospital bed, with others observing in a clinical setting. A close-up black-and-white photograph of a child's face showing symptoms of a severe illness, likely related to the Epstein Barr Virus, with visible facial swelling. A black-and-white photograph of a large audience seated in a lecture hall or auditorium, facing a stage with a screen, suggesting a presentation or conference setting. # Epstein Barr Virus ## M A Epstein, B G Achong and Y S Barr in 1964 <img src="https://i.imgur.com/9ZQ9V9z.jpg" alt="M A Epstein, B G Achong and Y S Barr in 1964"> ## Electron micrograph of thin sectioned EBV particles <img src="https://i.imgur.com/9ZQ9V9z.jpg" alt="Electron micrograph of thin sectioned EBV particles. Immature virions (above) cut in various planes in an infected cell. Inset (below) a mature enveloped particle. These images led to the virus being immediately recognized as a member of the herpesvirus family"> Electron micrograph of thin sectioned EBV particles. Immature virions (above) cut in various planes in an infected cell. Inset (below) a mature enveloped particle. These images led to the virus being immediately recognized as a member of the herpesvirus family      #### Historical Context - Discovered by M.A. Epstein, B.G. Achong, and Y.S. Barr in 1964. #### Virology - Electron microscopy reveals immature virions and mature enveloped particles. - Identified as a member of the herpesvirus family based on structural characteristics. Black and white portrait photo of M A Epstein, B G Achong, and Y S Barr in 1964, identified as the discoverers of the Epstein-Barr virus. Black and white portrait photo of B G Achong, one of the scientists who discovered the Epstein-Barr virus in 1964. Black and white portrait photo of Y S Barr, a researcher involved in the discovery of the Epstein-Barr virus in 1964. Black and white photo of an electron microscope, the instrument used to visualize the Epstein-Barr virus particles. Electron micrograph of thin-sectioned EBV particles showing immature virions in an infected cell and a mature enveloped particle in the inset, leading to the recognition of EBV as a herpesvirus. ```markdown Herpangina July 1941 HERPANGINA JOHN ZAHORSKY, M.D. » Author Affiliations Am J Dis Child. 1941;62(1):169. doi:10.1001/archpedi.1941.02000130180018 **Abstract** To the Editor:—The interesting article by Dr. B. B. Breese Jr. entitled "Aphthous Pharyngitis" (AM. J. Dis. CHILD. 61:669 [April] 1941) impels me to report that this disorder, which I regard as a specific disease, was described by me in two articles entitled "Herpetic Sore Throat" (South. M. J. 13:1871, 1920) and "Herpangina" (Arch. Pediat. 41:181, 1924). Naturally, I am gratified to find that other pediatricians, such as Levine, Hoerr and Allanson (J. A. M. A. 112:2020 [May 20] 1939) and, more recently, Breese, have corroborated my earlier observations. ``` #### Historical Background - First described as "Herpetic Sore Throat" (1920) and later named "Herpangina" (1924) by Dr. John Zahorsky. - Also historically referred to as "Aphthous Pharyngitis." ```html <table border="1" class="dataframe"> <thead> <tr style="text-align: right;"> <th>year</th> <th>technology</th> </tr> </thead> <tbody> <tr> <td>1890s</td> <td>filtration</td> </tr> <tr> <td>1929</td> <td>complement fixation</td> </tr> <tr> <td>1948</td> <td>tissue culture</td> </tr> <tr> <td>1970s</td> <td>monoclonal antibodies</td> </tr> <tr> <td>1985</td> <td>polymerase chain reaction (PCR)</td> </tr> <tr> <td>2000s</td> <td>high throughput sequencing</td> </tr> </tbody> </table> ```   #### Evolution of Diagnostic Technology | Year | Technology | | :--- | :--- | | 1890s | Filtration | | 1929 | Complement fixation | | 1948 | Tissue culture | | 1970s | Monoclonal antibodies | | 1985 | Polymerase chain reaction (PCR) | | 2000s | High throughput sequencing | Figure 1 shows two discovery curves for human viruses. (a) Virus discovery curve by species, displaying the cumulative number of species reported to infect humans, with statistically significant upward breakpoints indicated by vertical lines. (b) Virus discovery curve by family, showing the cumulative number of families containing species reported to infect humans. Table 1 lists major developments in the technology of virus discovery, including the year and corresponding technology: filtration (1890s), complement fixation (1929), tissue culture (1948), monoclonal antibodies (1970s), polymerase chain reaction (PCR) (1985), and high throughput sequencing (2000s). # Herpangina - Herpangina was first described in the 1920s but the viral etiology was not established until 1951 (Zahorsky, 1920; Huebner et al. 1951) - Etiology: Coxsackie group A viruses - Age and sex - Mainly affecting children up to 10 years of age - No gender predilection - Transmission: Fecal-oral route - Incubation time: 4 to 7 days #### Etiology - **Agent:** Coxsackie group A viruses. #### Epidemiology and Transmission - **Age:** Primarily affects children up to 10 years of age. - **Gender:** No gender predilection. - **Transmission:** Fecal-oral route. - **Incubation Time:** 4 to 7 days. # Herpangina **Clinical Presentation** - General symptoms - Low-grade fever, malaise, headache - Sore throat, dysphagia, anorexia, rhinorrhea, vomiting, diarrhea, myalgia - Oral lesions - Appearance of the red macules (usually 2-6), which form fragile vesicles that rapidly ulcerate (2-4 mm) - Site: palate, pillars of the fauces and pharynx - Herpangina lesions do not coalesce to form large areas of ulceration - Course of disease: self-limiting healing occurs within 1-2 weeks #### General Symptoms - Low-grade fever, malaise, and headache. - Sore throat, dysphagia, anorexia, and rhinorrhea. - Gastrointestinal distress (vomiting, diarrhea) and myalgia. #### Oral Manifestations - **Lesions:** Red macules (typically 2–6) that form fragile vesicles and rapidly ulcerate (2–4 mm). - **Site:** Palate, pillars of the fauces, and pharynx. - **Distinction:** Unlike other infections, herpangina lesions do not coalesce into large ulcerated areas. #### Course of Disease - Self-limiting; healing occurs within 1–2 weeks. ```markdown Herpangina <img src="https://i.imgur.com/placeholder.jpg" alt="Numerous aphthous-like ulcerations of the soft palate"/> Numerous aphthous-like ulcerations of the soft palate ```  #### Clinical Appearance - Numerous aphthous-like ulcerations localized to the soft palate. A close-up clinical photograph showing numerous aphthous-like ulcerations on the soft palate, consistent with herpangina. The image displays inflamed, red mucosal tissue with multiple small, white or yellowish lesions, illustrating the characteristic appearance of the condition. # Herpangina **Herpangina** **Histopathological** - Intraepithelial vesicles contain eosinophilic exudate - Nuclear ballooning degeneration of epithelial cells **Differential diagnosis** - Other viral mucosal ulcers (e.g., HSV, CMV and EBV) **Diagnosis** - Clinical appearance and history - Known epidemic - Viral culture from swab (Pinto and Hong 2013) #### Histopathology - Intraepithelial vesicles containing eosinophilic exudate. - Nuclear ballooning degeneration of epithelial cells. #### Diagnosis - Based on clinical appearance and history. - Recognition of known epidemics. - Viral culture from a swab. #### Differential Diagnosis - Other viral mucosal ulcers including Herpes Simplex Virus (HSV), Cytomegalovirus (CMV), and Epstein-Barr Virus (EBV). ```html <table border="1" cellpadding="5" cellspacing="0" style="border-collapse: collapse; width: 100%;"><tr><td colspan="2" style="text-align: center; font-size: 2em; font-weight: bold;">Herpangina</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">THE UNIVERSITY OF WESTERN AUSTRALIA</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">Sci Rep. 2016; 6: 35388.</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">Published online 2016 Oct 18. doi: 10.1038/srep35388</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">PMCID: PMC5067559</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">PMID: 27752104</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">Large outbreak of herpangina in children caused by enterovirus in summer of 2015 in Hangzhou, China</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">Wei Li, 1,* Hui-hui Gao, 1,* Qiong Zhang, 1 Yu-jie Liu, 1 Ran Tao, 1 Yu-ping Cheng, 1 Qiang Shu, 1 and Shi-qiang Shang a, 1</td></tr><tr><td colspan="2" style="text-align: center; font-size: 1em; font-weight: bold;">• Author information • Article notes • Copyright and License information Disclaimer</td></tr><tr><td style="text-align: center; font-size: 1em; font-weight: bold;">ELSEVIER</td><td style="text-align: center; font-size: 1em; font-weight: bold;">Clinical Microbiology and Infection</td></tr><tr><td style="text-align: center; font-size: 1em; font-weight: bold;">Volume 18, Issue 5, May 2012, Pages E110-E118</td><td style="text-align: center; font-size: 1em; font-weight: bold;">Original Article</td></tr><tr><td style="text-align: center; font-size: 1em; font-weight: bold;">Virology</td><td style="text-align: center; font-size: 1em; font-weight: bold;">Outbreak of hand, foot and mouth disease/herpangina associated with coxsackievirus A6 and A10 infections in 2010, France: a large citywide, prospective observational study</td></tr><tr><td style="text-align: center; font-size: 1em; font-weight: bold;">A. Mirand a, b , C. Henquell a, C. Archimbaud a, b, S. Ughetto c, D. Antona d, J.-L. Bailly b, H. Peigue-Lafeuille a, b</td><td style="text-align: center; font-size: 1em; font-weight: bold;"></td></tr></table> ```  #### Epidemiological Reports - Significant outbreaks have been documented globally, including large-scale events in Hangzhou, China (2015) and France (2010). - Outbreaks are frequently associated with Coxsackievirus A6, A10, and other enteroviruses. A small figure in the top right corner of the page, likely a thumbnail or cover image for a related article, showing a colorful diagram with text labels and a blue bar at the bottom. # Herpangina **Management** - Symptomatic care - Adequate hydration - Analgesia for pain control - Antipyretics **Complications:** Potential complications include - Pneumonia - Pulmonary edema - Hemorrhage - Acute flaccid paralysis - Encephalitis meningitis - Carditis #### Management - Symptomatic care focusing on adequate hydration. - Use of analgesics for pain and antipyretics for fever. #### Potential Complications - Pneumonia and pulmonary edema. - Hemorrhage. - Acute flaccid paralysis. - Encephalitis and meningitis. - Carditis. # Hand Foot and Mouth Disease **THE UNIVERSITY OF WESTERN AUSTRALIA** - **Etiology**: either - Coxsackie A virus - Coxsackie B virus - or enterovirus 71 - **Age and gender** - Mainly affecting children up to 10 years of age - No gender predilection #### Etiology - Coxsackie A virus - Coxsackie B virus - Enterovirus 71 #### Epidemiology - **Age:** Primarily affects children up to 10 years of age. - **Gender:** No gender predilection. # Hand Foot and Mouth Disease **THE UNIVERSITY OF WESTERN AUSTRALIA** ## Clinical Presentation ### General - Low-grade fever, malaise - Sore throat, dysphagia - Occasional cough, rhinorrhea, anorexia, vomiting, diarrhea, myalgia, and headache ### Oral lesions - Resemble those of herpangina (more numerous and frequently involve anterior regions of the mouth) - Appearance of the red macules (usually 2-6), which form fragile vesicles that rapidly ulcerate (2-4 mm) - Number of lesions ranges from 1 to 30 - Common sites: buccal mucosa, labial mucosa, and tongue, palate, pillars of the fauces and pharynx #### General Symptoms - Low-grade fever and malaise. - Sore throat and dysphagia. - Occasional cough, rhinorrhea, anorexia, vomiting, diarrhea, myalgia, and headache. #### Oral Manifestations - **Appearance:** Resemble herpangina but are typically more numerous (1 to 30 lesions). - **Lesions:** Red macules that form fragile vesicles and rapidly ulcerate (2–4 mm). - **Sites:** Frequently involves anterior regions including buccal mucosa, labial mucosa, and tongue, as well as the palate, fauces, and pharynx. # Hand Foot and Mouth Disease THE UNIVERSITY OF WESTERN AUSTRALIA ## Clinical Presentation - Cutaneous lesions: Range from a few to dozens - Site: borders of the palms and soles and the ventral surfaces and sides of the fingers and toes (primarily), buttocks, external genitals & legs (rarely) - Cutaneous lesions begin as erythematous macules that develop central vesicles and heal without crusting - nail loss or ridges (Beau lines) may ensue after several weeks - Course of disease: self-limiting healing occurs within 1 week #### Cutaneous Manifestations - **Sites:** Primarily the borders of palms and soles, and the ventral surfaces/sides of fingers and toes. Occasionally involves buttocks, genitals, and legs. - **Progression:** Erythematous macules develop central vesicles; these heal without crusting. - **Nail Changes:** Nail loss or Beau lines (ridges) may occur several weeks post-infection. #### Course of Disease - Self-limiting; healing typically occurs within 1 week. # Hand Foot and Mouth Disease <img src="https://i.imgur.com/1QzQzQz.jpg" alt="Multiple aphthous-like ulcerations of the mucobuccal fold"> <img src="https://i.imgur.com/2QzQzQz.jpg" alt="Numerous cutaneous vesicles on the sides of the fingers"> <img src="https://i.imgur.com/3QzQzQz.jpg" alt="Multiple vesicles of the skin of the toe">    #### Visual Clinical Markers - Multiple aphthous-like ulcerations in the mucobuccal fold. - Numerous cutaneous vesicles on the sides of the fingers and the skin of the toes. A close-up photo showing multiple aphthous-like ulcerations on the mucobuccal fold, with visible lesions on the oral mucosa near the teeth. A photo depicting numerous cutaneous vesicles on the sides of the fingers, showing small fluid-filled blisters on the skin. A photo illustrating multiple vesicles on the skin of the toe, highlighting small blisters on the toe's surface. # Hand Foot and Mouth Disease <img src="https://i.imgur.com/1QzQzQz.jpg" alt="Hand Foot and Mouth Disease - Nail changes shown in three images labeled A, B, and C."> Shin et al. 2014  #### Post-Infection Nail Changes Clinical evidence shows that Hand, Foot and Mouth Disease can lead to significant changes in the nail plate, including shedding or the development of deep ridges. Three photographic images labeled A, B, and C showing nail changes associated with Hand Foot and Mouth Disease. Image A displays multiple fingers with nail plate abnormalities, Image B shows a close-up of a single fingernail with a white line, and Image C depicts another fingernail with a similar white line and nail bed changes. # Hand Foot and Mouth Disease **THE UNIVERSITY OF WESTERN AUSTRALIA** ## Histopathology - Intraepithelial vesicles – early stages with intra-cytoplasmic eosinophilic inclusion bodies - Later stages - shallow ulcerations and erosions with regeneration of the marginal epithelium - Superficial inflammatory cell infiltrate in submucosa ## Differential diagnosis - Herpetic gingivostomatitis - Herpangina - Varicella - Aphthous stomatitis ## Diagnosis - Clinical appearance and history - Known epidemic - Viral culture from swab #### Histopathology - **Early Stages:** Intraepithelial vesicles with intra-cytoplasmic eosinophilic inclusion bodies. - **Later Stages:** Shallow ulcerations and erosions with marginal epithelium regeneration. - **Submucosa:** Superficial inflammatory cell infiltrate. #### Differential Diagnosis - Herpetic gingivostomatitis - Herpangina - Varicella - Aphthous stomatitis #### Diagnosis - Clinical appearance and history. - Recognition of epidemic patterns. - Viral culture from a swab. # Hand Foot and Mouth Disease **Management** - Symptomatic care - Adequate hydration - Antipyretics - Analgesia for pain control **Complications**: Potential complications include - Neurological complications - Viral meningitis - Encephalitis - Cerebellar ataxia *(Chang et al. 1999)* #### Management - Symptomatic care and hydration. - Antipyretics and analgesics for pain control. #### Complications - Neurological complications. - Viral meningitis. - Encephalitis. - Cerebellar ataxia. # Varicella (Chickenpox) **Varicella (Chickenpox)** - **Etiology**: varicella-zoster virus (VZV or HHV-3) - **Age and gender** - Two clinically distinct forms - Chicken pox: Children - Shingles: Older adults - No gender predilection - **Transmission** - Spread through air droplets - Direct contact with active lesions - **Incubation period** - 10 to 21 days (with an average of 15 days) <figure> <img src="https://i.imgur.com/1X7XzJt.png" alt="University of Western Australia logo"> <figcaption>The University of Western Australia</figcaption> </figure>  #### Etiology - **Agent:** Varicella-zoster virus (VZV or HHV-3). #### Transmission - Spread via air droplets. - Direct contact with active lesions. - **Incubation Period:** 10 to 21 days (average of 15 days). #### Epidemiology - **Chickenpox:** Primary form affecting children. - **Shingles:** Recurrent form affecting older adults. - **Gender:** No gender predilection. The University of Western Australia logo, featuring a shield with a black swan and the institution's name in blue text, located in the top-right corner of the slide. ```markdown Varicella (Chickenpox) Clinical Presentation - In immunized children: - General: low or no fever - Skin: a maculopapular, cutaneous rash with only a small number of lesions - Oral: few or no vesicles - Course of disease: a shortened disease course of approximately 4 to 6 days ``` #### Presentation in Immunized Children - **General:** Low or no fever. - **Skin:** Maculopapular cutaneous rash with a small number of lesions. - **Oral:** Few or no vesicles. - **Course:** Shortened duration of approximately 4 to 6 days. ```markdown Varicella (Chickenpox) Clinical Presentation - unimmunized individuals - General - malaise, pharyngitis, and rhinitis - headache, myalgia, nausea, anorexia, and vomiting (occasionally) - Skin - intensely pruritic exanthema (rash begins on the face and trunk and spreads to the extremities). - vesicular stage (classic presentation): each vesicle is surrounded by a zone of erythema and has been described as “a dewdrop on a rose petal” - Lesions continue to erupt for 4 or more days and old crusted lesions intermixed with newly formed, intact vesicles are commonplace <img src="https://i.imgur.com/1QZ2X9p.jpg" alt="Close-up of chickenpox rash on skin"/> <img src="https://i.imgur.com/3QZ2X9p.jpg" alt="Baby with chickenpox rash on face and body"/> ```   #### Presentation in Unimmunized Individuals - **General:** Malaise, pharyngitis, rhinitis, headache, myalgia, and nausea. - **Skin Rash:** - Intensely pruritic exanthema starting on the face/trunk and spreading to extremities. - **Vesicular Stage:** "Dewdrop on a rose petal" appearance (vesicle on an erythematous base). - Lesions erupt over 4+ days; various stages (crusted and new) appear simultaneously. Close-up photograph of chickenpox rash on skin, showing multiple vesicles surrounded by erythema, illustrating the classic 'dewdrop on a rose petal' appearance described in the text. Photograph of a baby with chickenpox, displaying widespread vesicular rash on the face and body, consistent with the clinical presentation of varicella in unimmunized individuals. # Varicella (Chickenpox) Clinical Presentation in unimmunized individuals ## Oral lesions - The lesions begin as 3- to 4-mm, white, opaque vesicles - Vesicles rupture to form 1- to 3-mm ulcerations - Site: vermilion border and palate (frequently), followed by the buccal mucosa and gingiva - Mild cases: ulcers may not be present or one or two oral ulcers that heal within 1 to 3 days - Severe infections: oral ulcerations are always present and numbering up to 30 and persisting for 5 to 10 days <img src="https://i.imgur.com/7kR0qZl.jpg" alt="Oral lesions of varicella (chickenpox)">  #### Oral Manifestations (Unimmunized) - **Lesions:** Begin as 3–4 mm white, opaque vesicles that rupture into 1–3 mm ulcerations. - **Sites:** Frequently the vermilion border and palate; also buccal mucosa and gingiva. - **Severity:** - Mild: 1–2 ulcers healing in 1–3 days. - Severe: Up to 30 ulcers persisting for 5–10 days. A close-up photo of oral lesions in a patient with varicella (chickenpox), showing white, opaque vesicles on the mucosal surface of the mouth, consistent with the clinical presentation described in the text. ```markdown Varicella (Chickenpox) THE UNIVERSITY OF WESTERN AUSTRALIA National Immunisation Program Schedule From 1 April 2019 | Age | Disease | Vaccine Brand | |------------|-------------------------------------------------------------------------|----------------------------------| | Birth | • Hepatitis B (usually offered in hospital)ᵃ | H-B-Vax® II Paediatric or<br>Engerix B® Paediatric | | 2 months | • Diphtheria, tetanus, pertussis (whooping cough),<br>hepatitis B, polio, Haemophilus influenzae type b (Hib)<br>• Pneumococcal<br>• Rotavirusᵇ | Infanrix® hexa<br>Prevenar 13®<br>Rotarix® | | 4 months | • Diphtheria, tetanus, pertussis (whooping cough),<br>hepatitis B, polio, Haemophilus influenzae type b (Hib)<br>• Pneumococcal<br>• Rotavirusᵇ | Infanrix® hexa<br>Prevenar 13®<br>Rotarix® | | 6 months | • Diphtheria, tetanus, pertussis (whooping cough),<br>hepatitis B, polio, Haemophilus influenzae type b (Hib) | Infanrix® hexa | | 12 months | • Meningococcal ACWY<br>• Measles, mumps, rubella<br>• Pneumococcal | Nimenrix®<br>M-M-R® II or Priorix®<br>Prevenar 13® | | 18 months | • Haemophilus influenzae type b (Hib)<br>• Measles, mumps, rubella, varicella (chickenpox)<br>• Diphtheria, tetanus, pertussis (whooping cough) | ActHIB®<br>Priorix-Tetra® or ProQuad®<br>Infanrix® or Tripace® | | 4 years | • Diphtheria, tetanus, pertussis (whooping cough), polio | Infanrix® IPV or Quadrace®¹ | Additional vaccines for Aboriginal and Torres Strait Islander children (QLD, NT, WA and SA) and medically at-risk childrenᶜ | Age | Disease | Vaccine Brand | |------------|-------------------------------------------------------------------------|----------------------------------| | 12 months | • Hepatitis A | Vaqta® Paediatric | | 18 months | • Hepatitis A | Vaqta® Paediatric | | 4 years | • Pneumococcal | Pneumovax 23® | Additional vaccines for Aboriginal and Torres Strait Islander children (QLD, NT, WA and SA) Measles, Mumps, Rubella and Varicella Virus Vaccine Live ProQuad® NDC 0006-4171-00 10 Single-dose 0.5-mL Vials Measles vaccine: More attenuated Enders’ Edmonston strain. Chick cell tissue culture origin. Mumps vaccine: Jeryl Lynn™ strain. Chick cell tissue culture origin. Rubella vaccine: Wistar RA 27/3 strain. Human diploid cell (WI-38) culture origin. Varicella vaccine: Oka/Merck strain. Human diploid cell (MRC-5) culture origin. Contains no preservative. Contains trace quantities of neomycin. Rx only STORE FROZEN <img src="https://i.imgur.com/placeholder.jpg" alt="Measles, Mumps, Rubella and Varicella Virus Vaccine Live ProQuad® vial and packaging"> ```   #### Childhood Schedule (Selected Entries) - **12 Months:** Meningococcal ACWY; Measles, mumps, rubella (MMR); Pneumococcal. - **18 Months:** Hib; Measles, mumps, rubella, varicella (MMRV - e.g., Priorix-Tetra® or ProQuad®); DTPa. #### Vaccine Details (ProQuad®) - Combined live virus vaccine for Measles, Mumps, Rubella, and Varicella. - Varicella component: Oka/Merck strain. A detailed table of the National Immunisation Program Schedule from 1 April 2019, listing vaccines by age, the diseases they prevent, and the corresponding vaccine brands. The table includes childhood vaccinations and additional vaccines for Aboriginal and Torres Strait Islander children and medically at-risk children. A photograph of the Measles, Mumps, Rubella and Varicella Virus Vaccine Live ProQuad® packaging and a single-dose vial. The image shows the product label with storage instructions ('STORE FROZEN') and details about the vaccine components, including the strains used for each virus. ```markdown Varicella (Chickenpox) National Immunisation Program Schedule From 1 April 2019 | Age | Disease | Vaccine brand | | --- | --- | --- | | **Adolescent vaccination** (also see influenza vaccine) | | | | 12–<13 years (School programs<sup>d</sup>) | • Human papillomavirus (HPV)<sup>e</sup><br>• Diphtheria, tetanus, pertussis (whooping cough) | Gardasil<sup>®</sup>9<br>Boostrix<sup>®</sup> | | 14–<16 years (School programs<sup>d</sup>) | • Meningococcal ACWY | Nimenrix<sup>®</sup> | | **Adult vaccination** (also see influenza vaccine) | | | | 15–49 years<br>Aboriginal and Torres Strait Islander people with medical risk factors<sup>c</sup> | • Pneumococcal | Pneumovax 23<sup>®</sup> | | 50 years and over<br>Aboriginal and Torres Strait Islander people | • Pneumococcal | Pneumovax 23<sup>®</sup> | | 65 years and over | • Pneumococcal | Pneumovax 23<sup>®</sup> | | 70–79 years<sup>†</sup> | • Shingles (herpes zoster) | Zostavax<sup>®</sup> | | Pregnant women | • Pertussis (whooping cough)<sup>g</sup><br>• Influenza<sup>h</sup> | Boostrix<sup>®</sup> or Adacel<sup>®</sup> | ```  #### Adolescent and Adult Schedule - **12–13 Years:** HPV (Gardasil®9) and DTPa (Boostrix®). - **14–16 Years:** Meningococcal ACWY. - **70–79 Years:** Shingles (Zostavax®). - **Pregnant Women:** Pertussis and Influenza. A table detailing the National Immunisation Program Schedule from 1 April 2019, listing age groups, corresponding diseases to be vaccinated against, and the recommended vaccine brands. The table is organized into sections for adolescent and adult vaccination, with specific entries for HPV, diphtheria-tetanus-pertussis, meningococcal ACWY, pneumococcal, shingles, pertussis, and influenza vaccines. # Varicella (Chickenpox) **Histopathologic Features** - The cytologic alterations are virtually identical to HSV - The virus causes acantholysis, with formation of numerous free-floating Tzanck cells, which exhibit nuclear margination of chromatin and occasional multinucleation **Diagnosis** - Viral cytology - PCR (performed on vesicular fluid, cells from the base of a lesion, or a scab from a resolving skin lesion) - Direct fluorescent antibody assay <img src="https://i.imgur.com/7zJQ9Qm.png" alt="Histopathologic image of Varicella (Chickenpox) showing Tzanck cells">  #### Histopathology - Cytologic alterations are virtually identical to HSV. - Features include acantholysis and the formation of free-floating Tzanck cells with nuclear margination of chromatin and multinucleation. #### Diagnosis - Viral cytology. - **PCR:** Performed on vesicular fluid, lesion base cells, or scabs. - Direct fluorescent antibody assay. Histopathologic image showing Tzanck cells in a tissue sample, with nuclear margination of chromatin and occasional multinucleation, illustrating the cytologic alterations caused by the varicella virus. # Varicella (Chickenpox) - **Symptomatic treatment** (for relieve of pruritus) - Warm baths with soap, baking soda, or colloidal oatmeal - application of calamine lotion - antihistamines - **Antipyretic**: Acetaminophen - **Antiviral medications** (such as, acyclovir, valacyclovir, and famciclovir) have been shown to reduce the duration and severity of infection if administered within 24 hours of the rash #### Symptomatic Treatment - Relief of pruritus: Warm baths (with baking soda or oatmeal), calamine lotion, and antihistamines. - Antipyretic: Acetaminophen. #### Antiviral Medications - Agents: Acyclovir, valacyclovir, and famciclovir. - Effectiveness: Reduces duration and severity if administered within 24 hours of rash onset. # Varicella (Chickenpox) **Complications** - secondary skin infections Secondary skin infection with group A, β-hemolytic streptococci may progress to - Encephalitis - Pneumonia - Necrotizing fasciitis - Septicemia - Toxic shock syndrome - or other life-threatening conditions #### Complications - Secondary skin infections (often Group A β-hemolytic streptococci). - **Severe Systemic Conditions:** - Encephalitis - Pneumonia - Necrotizing fasciitis - Septicemia - Toxic shock syndrome Thank you Conclusion of clinical review on Varicella complications and management. [^1]: Original PDF page 1: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=1|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.1]] [^2]: Original PDF page 2: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=2|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.2]] [^3]: Original PDF page 3: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=3|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.3]] [^4]: Original PDF page 4: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=4|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.4]] [^5]: Original PDF page 5: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=5|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.5]] [^6]: Original PDF page 6: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=6|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.6]] [^7]: Original PDF page 7: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=7|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.7]] [^8]: Original PDF page 8: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=8|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.8]] [^9]: Original PDF page 9: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=9|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.9]] [^10]: Original PDF page 10: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=10|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.10]] [^11]: Original PDF page 11: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=11|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.11]] [^12]: Original PDF page 12: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=12|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.12]] [^13]: Original PDF page 13: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=13|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.13]] [^14]: Original PDF page 14: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=14|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.14]] [^15]: Original PDF page 15: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=15|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.15]] [^16]: Original PDF page 16: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=16|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.16]] [^17]: Original PDF page 17: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=17|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.17]] [^18]: Original PDF page 18: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=18|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.18]] [^19]: Original PDF page 19: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=19|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.19]] [^20]: Original PDF page 20: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=20|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.20]] [^21]: Original PDF page 21: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=21|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.21]] [^22]: Original PDF page 22: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=22|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.22]] [^23]: Original PDF page 23: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=23|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.23]] [^24]: Original PDF page 24: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=24|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.24]] [^25]: Original PDF page 25: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=25|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.25]] [^26]: Original PDF page 26: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=26|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.26]] [^27]: Original PDF page 27: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=27|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.27]] [^28]: Original PDF page 28: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=28|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.28]] [^29]: Original PDF page 29: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=29|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.29]] [^30]: Original PDF page 30: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=30|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.30]] [^31]: Original PDF page 31: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=31|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.31]] [^32]: Original PDF page 32: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=32|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.32]] [^33]: Original PDF page 33: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=33|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.33]] [^34]: Original PDF page 34: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=34|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.34]] [^35]: Original PDF page 35: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=35|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.35]] [^36]: Original PDF page 36: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=36|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.36]] [^37]: Original PDF page 37: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=37|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.37]] [^38]: Original PDF page 38: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=38|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.38]] [^39]: Original PDF page 39: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=39|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.39]] [^40]: Original PDF page 40: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=40|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.40]] [^41]: Original PDF page 41: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=41|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.41]] [^42]: Original PDF page 42: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=42|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.42]] [^43]: Original PDF page 43: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=43|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.43]] [^44]: Original PDF page 44: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=44|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.44]] [^45]: Original PDF page 45: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=45|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.45]] [^46]: Original PDF page 46: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=46|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.46]] [^47]: Original PDF page 47: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=47|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.47]] [^48]: Original PDF page 48: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=48|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.48]] [^49]: Original PDF page 49: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=49|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.49]] [^50]: Original PDF page 50: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=50|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.50]] [^51]: Original PDF page 51: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=51|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.51]] [^52]: Original PDF page 52: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=52|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.52]] [^53]: Original PDF page 53: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=53|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.53]] [^54]: Original PDF page 54: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=54|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.54]] [^55]: Original PDF page 55: [[Lecture 7 - Orofacial Infections in Paediatric Dentistry.pdf#page=55|Lecture 7 - Orofacial Infections in Paediatric Dentistry, p.55]]