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BACTERIAL/FUNGAL/VIRAL INFECTIONS SYPHILIS SYPHILIS • Chronic infection caused by Treponema pallidum • Transmitted by sexual contact or from mother to fetus • Proceeds through three stages: primary, secondary, and tertiary • Patient is infectious in the primary and secondary stages SYPHILIS • Primary syphilis – Chancre • Usually solitary; arises 3-90 days after exposure • Papular lesion with a central ulceration • Most common on the lip • Regional lymphadenopathy • Heals in 3-8 weeks SYPHILIS • Secondary syphilis – Occurs 4-10 weeks after initial infection – Systemic symptoms: painless lymphadenopathy, sore throat, malaise, headache, weight loss – Diffuse, painless, maculopapular cutaneous rash SYPHILIS • Secondary syphilis – Mucous patches (exocytosis and spongiosis) in the oral mucosa – Condylomata lata – Multiple lesions are common – Spontaneous resolution occurs in 3-12 weeks SYPHILIS • Tertiary syphilis – Develops 1-30 years after a latent stage (latent syphilis) – Serious complications: cardiovascular system and central nervous system – Granulomatous inflammation of the skin, mucosa, soft tissue, bones, and organs SYPHILIS • Tertiary syphilis – Gumma: active sites of granulomatous inflammation – Intraoral lesions involve the palate and tongue: palatal perforation and luetic glossitis SYPHILIS • Congenital syphilis – Hutchinson’s triad: • Hutchinson’s teeth (Hutchinson’s incisors and mulberry molars) • Ocular interstitial keratitis • Eighth nerve deafness SYPHILIS • Histopathologic features – Primary and secondary forms: • Perivasculitis (lymphocytes and plasma cells) • Corkscrew-like organisms – Tertiary form: • Granulomatous inflammation • Organisms are hard to identify SYPHILIS • Diagnosis – VDRL (Venereal Disease Research Laboratory) and RPR (rapid plasma reagin): serologic screening tests - nonspecific; only positive in the first two stages – FTA-ABS (fluorescent treponemal antibody) and TPHA (T. pallidum hemagglutination assays): serologic tests - specific; positive in all three stages SYPHILIS • Treatment and prognosis – Penicillin – Erythromycin or tetracycline: penicillin allergy TUBERCULOSIS TUBERCULOSIS • Chronic infectious disease caused by Mycobacterium tuberculosis • Acquired by direct person-to-person spread through airborne droplets from a patient with active disease • Primary tuberculosis: – Occurs in a previously unexposed individual – Almost always involves the lungs TUBERCULOSIS • Primary tuberculosis: – Chronic inflammatory reaction – Fibrocalcified nodule at the initial site of involvement – Viable organisms may be present for life • Secondary tuberculosis: – Reactivation of organisms in a previously infected person – Causes active disease TUBERCULOSIS • Secondary tuberculosis: – Usually associated with immunosuppression • Old age, poverty, crowded living condition, AIDS • Clinical and radiographic features: – Primary tuberculosis • Asymptomatic • Fever, pleural effusion TUBERCULOSIS • Clinical and radiographic features: – Secondary tuberculosis • Low-grade fever, malaise, weight loss, night sweats, cough, hemoptysis • Extrapulmonary lesions: –Skin, skeletal system, CNS, kidneys, cervical lymph nodes, larynx, middle ear TUBERCULOSIS • Clinical and radiographic features: – Secondary tuberculosis • Oral lesions –Chronic painless ulcer –Due to hematogenous spread or exposure to infected sputum –Gingiva, tongue, palate, lip TUBERCULOSIS • Clinical and radiographic features: – Secondary tuberculosis • Scrofula –Enlarged oropharyngeal lymphoid tissue and cervical lymph nodes –Due to contaminated milk –Fistulas of the overlying skin –Calcified lymph nodes TUBERCULOSIS • Histopathologic features – Granulomatous inflammation – Central caseous necrosis TUBERCULOSIS • Diagnosis – Mantoux or PPD skin test: indicates exposure to the organisms – Culture of infected sputum or tissue TUBERCULOSIS • Treatment and prognosis – Multiagent therapy • Isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin ACTINOMYCOSIS ACTINOMYCOSIS • Acute, rapidly progressing or chronic, slowly spreading infection associated with Actinomyces israelii • 55% of cases occur in the cervicofacial region • Organisms enter the tissue through an area of prior trauma: soft tissue injury, periodontal pocket, nonvital tooth, extraction socket, or infected tonsil ACTINOMYCOSIS • Organisms spread by direct extension through soft tissue producing draining fistulas to the skin surface • Sulfur granules: yellowish flecks • Most frequent site: skin overlying the angle of the mandible • Salivary gland involvement ACTINOMYCOSIS • Bone involvement – Actinomycotic osteomyelitis; illdefined radiolucency – Periapical involvement; anterior maxillary teeth > mandibular first molars ACTINOMYCOSIS • Histopathologic features – Inflamed granulation tissue – Colonies of organisms surrounded by a collection of neutrophils ACTINOMYCOSIS • Diagnosis – Culture – Biopsy ACTINOMYCOSIS • Treatment and prognosis – Prolonged high dose antibiotics (penicillin) – Abscess drainage and excision of sinus tracts – Early lesions respond in 5-6 weeks – Deep seated infections may take 12 months to resolve CAT-SCRATCH DISEASE CAT-SCRATCH DISEASE • Infectious disorder that begins in the skin and spreads to the adjacent lymph nodes • Most common cause of chronic regional lymphadenopathy in children • Arises after contact with a cat • Causative organism is Bartonella henselae • Papule or pustule along the initial scratch line • Lymphadenopathy occurs within 3 weeks CAT-SCRATCH DISEASE • Fever and malaise • Papule or pustule has often resolved by the time the lymphadenopathy is apparent CAT-SCRATCH DISEASE • Histopathologic features – Stellate suppurative necrosis surrounded by histiocytes and neutrophils CAT-SCRATCH DISEASE • Diagnosis – Serologic tests • Indirect fluorescent antibody assay: antibodies to B. henselae • ELISA: IgM antibodies to B. henselae • PCR: polymerase chain reaction CAT-SCRATCH DISEASE • Treatment and prognosis – Self-limiting disease; resolves in 4 months – Antibiotics: erythromycin or doxycycline – Local heat, analgesics – Aspiration of the node CANDIDIASIS CANDIDIASIS • Most common oral fungal infection in humans • Majority of cases are caused by Candida albicans • 30%-60% of patients carry the organism in their mouths • 3 factors determine if clinical infection occurs: – Immune status of the host – Oral mucosal environment – Strain of C. albicans CANDIDIASIS • Pseudomembranous candidiasis – “Thrush”; milk curds – Underlying mucosa is normal or erythematous – Often caused by exposure to broad-spectrum antibiotics or an impaired immune system – Symptoms are mild and consist of burning or an unpleasant taste – Common on the buccal mucosa, palate, and dorsal tongue CANDIDIASIS • Erythematous candidiasis – Several subtypes: • Acute atrophic or “antibiotic sore mouth” • Central papillary atrophy or median rhomboid glossitis • Chronic multifocal • Angular cheilitis • Denture stomatitis CANDIDIASIS • Acute atrophic candidiasis – Occurs after the use of broad-spectrum antibiotics – Mouth feels as if a hot beverage has scalded it – Diffuse loss of the filiform papillae if the dorsal tongue is affected CANDIDIASIS • Central papillary atrophy – Median rhomboid glossitis – Failure of the tuberculum impar to involute – Midline, posterior dorsal tongue; symmetrical – Asymptomatic – Loss of the filiform papillae CANDIDIASIS • Angular cheilitis – Involvement of the angles of the mouth – Erythema, fissuring, and scaling – Older individuals with reduced vertical dimension – 20% caused by C. albicans alone – 60% caused by C. albicans and S. aureus – 20% caused by S. aureus alone CANDIDIASIS • Denture stomatitis – Chronic atrophic candidiasis – Localized to the denture-bearing areas – Patient wears the denture continuously – Must rule out improper denture design, allergy to the denture base, or inadequate curing of the acrylic CANDIDIASIS • Chronic hyperplastic candidiasis – Candidal leukoplakia – Cannot be removed by scraping – Least common form of candidiasis – Usually located on the anterior buccal mucosa CANDIDIASIS • Histopathologic features – Exfoliative cytology or tissue sections – PAS stain • Hyphae or pseudohyphae (elongated yeast) • Hyperparakeratosis, acanthosis, neutrophilic abscesses, chronic inflammation in the connective tissue CANDIDIASIS • Treatment and prognosis – Topical antifungal medications • Nystatin, clotrimazole – Systemic antifungal medications • Fluconozole, itraconozole HISTOPLASMOSIS HISTOPLASMOSIS • Most common systemic fungal infection in the United States • Caused by Histoplasma capsulatum • Organisms grows in soil enriched with bird or bat excrement • Common in the Ohio and Mississippi River valley regions • Organisms are inhaled and germinate in the lungs HISTOPLASMOSIS • Most cases are asymptomatic or produce few symptoms • Organisms are ingested by macrophages and T-lymphocyte immunity develops in 2-3 weeks • Antibodies against the organisms appear several weeks later • 3 forms: acute, chronic, disseminated HISTOPLASMOSIS • Acute histoplasmosis – Self-limited pulmonary infection – Fever, headache, myalgia, cough – Patients are ill for 2 weeks – Calcification of the hilar lymph nodes HISTOPLASMOSIS • Chronic histoplasmosis – Primarily affects the lungs – Elderly or immunosuppressed patients – Similar to tuberculosis – Cough, weight loss, fever, dyspnea, hemoptysis HISTOPLASMOSIS • Disseminated histoplasmosis – Progressive spread to extrapulmonary sites – Elderly and immunosuppressed patients – Oral lesions: tongue, buccal mucosa, palate • Painful ulceration of several weeks’ duration HISTOPLASMOSIS • Histopathologic features – Diffuse infiltrate of macrophages containing organisms (yeasts) – Granulomas HISTOPLASMOSIS • Diagnosis – Tissue sections or culture HISTOPLASMOSIS • Treatment and prognosis – Acute form: supportive – Chronic and disseminated forms: amphotericin B, ketoconazole, or itraconazole – Mortality is 7%-23% with the disseminated form ZYGOMYCOSIS ZYGOMYCOSIS • Opportunistic fungal infection caused by one of four genera of Zygomycetes: Absidia, Mucor, Rhizomucor, and Rhizopus • Organisms are found in decaying organic material • Spores are liberated into the air and inhaled • Common in uncontrolled diabetics and immunocompromised individuals ZYGOMYCOSIS • Common symptoms include: nasal obstruction, bloody nasal discharge, facial pain or headache, proptosis • Involvement of the cranial vault leads to blindness, lethargy, seizures, and death • Massive tissue destruction with palatal perforation, swelling of the maxillary alveolar process, opacification of the sinuses ZYGOMYCOSIS • Histopathologic features – Extensive necrosis – Large branching, nonseptate hyphae ZYGOMYCOSIS • Treatment and prognosis – Radical surgical debridement – Amphotericin B – Control underlying disease – Prognosis is poor HERPES SIMPLEX VIRUS HERPES SIMPLEX VIRUS • Two types of HSV: HSV-1 and HSV -2 • Two patterns of infection: primary and secondary or recurrent • Primary infection – Initial exposure to the virus – No antibodies in the circulation – Occurs at a young age – Often is asymptomatic (80%) HERPES SIMPLEX VIRUS • Secondary or recurrent infection – Reactivation of the virus via axons of sensory nerves – Precipitated by old age, UV light, stress, pregnancy, allergy, or trauma – 50%-60% of adults are HSV-1 seropositive HERPES SIMPLEX VIRUS • Acute herpetic gingivostomatitis – Most common pattern of symptomatic primary HSV infection – Peak age: 2-3 years of age – Cervical lymphadenopathy, chills, fever, nausea, anorexia – Resolves in 7-14 days HERPES SIMPLEX VIRUS • Pharyngotonsillitis – Primary infection in adults – Sore throat, fever, malaise, headache – Vesicles and ulcerations on the tonsils and posterior pharynx – Resembles streptococcal pharyngitis or mononucleosis HERPES SIMPLEX VIRUS • Secondary or recurrent infection – Usually occurs at the site of primary inoculation – Herpes labialis: 15%-45% of the US population – Oral mucosa: keratinized mucosa – Resolves in 7-10 days HERPES SIMPLEX VIRUS • Histopathologic features – Acantholysis, nuclear clearing, nuclear enlargement (ballooning degeneration), multinucleation – Tzanck cells HERPES SIMPLEX VIRUS • Diagnosis – Clinical presentation – Viral culture: 2 weeks for results – Antibody titers: positive 4-8 days after exposure – Cytologic smear – Tissue biopsy HERPES SIMPLEX VIRUS • Treatment and prognosis – Primary disease • Acyclovir suspension • Nonsteroidal anti-inflammatory medications – Secondary disease • Acyclovir, valacyclovir, famciclovir, penciclovir, foscarnet VARICELLA VARICELLA • Primary infection with VZV • Virus is spread through air droplets or direct contact • 5-9 years of age • Most cases are symptomatic: rash begins on face and trunk and then spreads to extremities • Erythema, vesicle, pustule, and crust VARICELLA • Oral lesions – Common on palate and buccal mucosa – Painless • Complications – Reye’s syndrome, skin infections, encephalitis, pneumonia VARICELLA • Histopathologic features – Same as HSV VARICELLA • Diagnosis – Cytologic smear – Tissue biopsy – Viral culture – Antibodies to VZV VARICELLA • Treatment and prognosis – Supportive – Acyclovir, valacyclovir, famciclovir – VZIG: varicella-zoster immune globulin • Immunocompromised patients – VZV vaccine HERPES ZOSTER HERPES ZOSTER • Reactivation of VZV; 10%-20% of individuals • Single recurrence • Predisposing factors – Cytotoxic drugs, radiation, malignancies, old age, alcohol abuse • Three phases – Prodrome, acute, and chronic HERPES ZOSTER • Prodrome: 90% of patients – Intense pain in the area innervated by the affected sensory nerve – Present 1-4 days before exanthem – Fever, malaise, headache • Acute – Vesicles, ulcerations, crusts: midline – Resolves in 2-3 weeks HERPES ZOSTER • Acute – Oral lesions • Movable or nonmovable mucosa • In conjunction with skin lesions • Maxillary involvement may cause devitalization of teeth HERPES ZOSTER • Acute – Ocular lesions • May cause blindness – Ramsay Hunt syndrome • Lesions of the external auditory canal and facial paralysis HERPES ZOSTER • Chronic – Postherpetic neuralgia • Neuralgia-associated pain persists for more than 3 months • 15% of patients • 50% of patients over 60 years of age • Most cases resolve in 1 year HERPES ZOSTER • Histopathologic features – Same as varicella and HSV HERPES ZOSTER • Diagnosis – Clinical presentation – Viral culture – Cytologic smear – Antibodies to VZV HERPES ZOSTER • Treatment and prognosis – Supportive – Acyclovir, valacyclovir, famciclovir INFECTIOUS MONONUCLEOSIS INFECTIOUS MONONUCLEOSIS • Caused by Epstein-Barr virus (EBV) • Children: contaminated saliva on fingers or toys • Adults: direct salivary transfer such as kissing or shared straws • Childhood exposure is usually asymptomatic • Adulthood exposure is symptomatic INFECTIOUS MONONUCLEOSIS • Fever, lymphadenopathy, pharyngitis, tonsillitis • Hepatosplenomegaly • Oral lesions – Palatal petechiae (25% of patients) – Necrotizing ulcerative gingivitis INFECTIOUS MONONUCLEOSIS • Diagnosis – Clinical presentation – WBC count is elevated – Lymphocytosis, atypical lymphocytes – Paul-Bunnell heterophil antibody (90%) – EBV-specific antibodies INFECTIOUS MONONUCLEOSIS • Treatment and prognosis – Resolves in 4-6 weeks – Supportive HERPANGINA HERPANGINA • • • • Caused by coxsackievirus A 1 to 6, 8, 10, or 22 Most cases arise in the summer or early fall Fecal-oral route of transmission Acute phase: may be transmitted through saliva or respiratory droplets • Infection confers immunity against reinfection to that one strain HERPANGINA • Sore throat, dysphagia, fever • Oral lesions – Vesicles or ulcers on the soft palate or tonsillar pillars – Resolve in 7-10 days HERPANGINA • Histopathologic features – Intracellular and intercellular edema – Intraepithelial and subepithelial vesicles – Epithelial necrosis and ulceration HERPANGINA • Diagnosis – Clinical features – Viral culture • Treatment and prognosis – Self-limiting – Supportive HAND-FOOT-AND-MOUTH DISEASE HAND-FOOT-AND-MOUTH DISEASE • • • • Caused by coxsackievirus A 16 Most cases arise in the summer or early fall Fecal-oral route of transmission Acute phase: may be transmitted through saliva or respiratory droplets • Infection confers immunity against reinfection to that one strain HAND-FOOT-AND-MOUTH DISEASE • Skin rash and oral lesions are associated with flulike symptoms: sore throat, dysphagia, fever • Skin lesions: macular, vesicles, crusts • Oral lesions – Buccal mucosa, labial mucosa, tongue – Vesicles and ulcers – Resolve in 1 week HAND-FOOT-AND-MOUTH DISEASE • Histopathologic features – Intracellular and intercellular edema – Intraepithelial and subepithelial vesicles – Epithelial necrosis and ulceration HAND-FOOT-AND-MOUTH DISEASE • Diagnosis – Clinical features – Viral culture • Treatment and prognosis – Self-limiting – Supportive HIV INFECTION HIV INFECTION • HIV-associated periodontal disease – Linear gingival erythema – Necrotizing ulcerative gingivitis – Necrotizing ulcerative periodontitis – Necrotizing stomatitis HIV INFECTION • Linear gingival erythema – Linear band of erythema involving the free gingival margin – Punctate or diffuse erythema of the alveolar mucosa HIV INFECTION • Necrotizing ulcerative gingivitis (NUG) – Ulceration and necrosis of one or more interdental papillae – No loss of periodontal attachment – Gingival necrosis, bleeding, pain and halitosis HIV INFECTION • Necrotizing ulcerative periodontitis (NUP) – Gingival ulceration and necrosis associated with rapidly progressing loss of periodontal attachment – Multiple isolated defects – Edema, severe pain, hemorrhage – No deep pocketing – Does not respond to conventional periodontal therapy HIV INFECTION • Treatment of NUG and NUP – Debridement combined with povidone-iodine irrigation – Antimicrobial therapy: metronidazole, chlorhexidine – Follow-up care – Long-term maintenance HIV INFECTION • Necrotizing stomatitis – Massive areas of tissue destruction – May involve soft tissue or bone – Results in sequestration HIV INFECTION • Oral hairy leukoplakia – Associated with EBV – White mucosal lesions that do not rub off – Lateral border of the tongue HIV INFECTION • Histopathologic features – Parakeratosis with or without candidiasis – Surface corrugations – Acanthosis with “balloon cells” – Nuclear beading HIV INFECTION • Treatment – None – Acyclovir, desiclovir – Zidovudine (AZT)