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13 Cards in this Set

  • Front
  • Back
Actinomycetes:
Actinomycosis:
type of bacteria?
enter tissue how?
Present as an? characterized by?
dx?
tx?
- gram + filanmentous anaerobic, 50% cervicofacial
-actinomyces israelii-normal oral flora
-through opening via trauma
-acute deep suppurative abscess with draining sinus tract(acute response)
-colonies of actinomycotic organisms surrounded by neutrophils
-sulfar granules: yellowish flecks seen clinically representing colonies of actinomyces

dx: histology+culture
tx: surgican drainage/debridement and antibiotics
Noma
-type of infection frrom?
-common in?
-clinical manifestation
-result
-tx?
-opportunistic infection from normal oral flora in severly immunodeficient

-malnourished in 3rd world
-aids

-necrotizin ulcerative gingivitis extends to involve adjacent soft issue and beyond
-extensive necrosis and makred tissue destruction, facial disfigurement

-death

-tx: correct underlyin disease, debridement antibioti
• HIV-Associated Kaposi’s Sarcoma

most common?
compared to non HIV Kaposis?
type of tumor? caused by?
manfiests as?
what can be seen in the oral cavity?
requires a ___ for dx?
Therapy?
o The most common malignancy in HIV patients
 Non-HIV associated in older/lower extremeties
 HIV-assoicated: younger, on trunk, mucous membranes and internal organs
o A malignant vascular tumor caused by HHV8/KSHV
 Vascular proliferation
o Manifest as multiple lesions of the skin. oral mucosa & viscera
o Oral cavity: palate, tongue & gingiva
 starts as purple macular lesions on skin and later develops into nodules
 Invade bone
o Biopsy is necessary
o HAART has significantly reduced KS prevalence
• HIV-associated Non-Hodgkin’s Lymphoma

-how common is it?
-caused by?
-majority are what type?
-occur where?
o The 2nd most common malignancy in HIV patients
o Caused by EBV (KSHV?)
o Majority are high grade B-cell lymphoma
o Usually occur in extranodal locations
 CNS is the most common location
o Human Papillomavirus
- clinical manifesation
- HAART has what affect?
- Normal vs. HIV
-normal do occur in
Verruca vulgaris (common wart) and oral squamous papilloma
• Multiple exophytic on papillary nodules
 HAART treated patients show increased prevalence of HPV-related lesion
 More exaggerated in HIV patients
• Surface corrugated and covered with keratin
• Lesions merge together(usually single isolated)never happens in normal patient
Aphthous Ulcerations “canker sore”
HIV patients see?
HIV patients have increased frequency to develop all forms of aphthous ulcer (minor, major and herpetiform)
 In contrast to normal patients, most HIV patients develop major or herpetiform variants
• Herpetiform: resembles herpetic ulcer, cluster of small pinheadlesions
Cytomegalovirus-transmission?
immunocomrpomised patients?
histpathology?
Transmission:
 exchange of body fluid, organ transplant
 Infection ubiquitous, most subclinical
o Immunocompromised patients: affects many organs
 Oral manifestation:
• Chronic oral ulcer: often co-infect with HSV
• Cytomegaloviral sialadenitis
o Histopathology:
 CMV infected cells are massively enlarged. They contain intranuclear and cytoplasmic inclusions and exhibit “owl eye” alteration
 Attacks salivary gland too
• Acute Lymphonodular Pharyngitis

clinical:
nodules caused by?
treatment?
o Clinical: sore throat and flue-like symptom(similar to strept pharyingitis)
 Low number of yellow nodules develop in oropharynx area
 No vesiculation or ulceration
o Nodules are caused by lymphoid hyperplasia
o Tx: self limiting
Chronic Hyerplastic Candidiasis
clinical?
sx?
dx?
histology?
o Clinical:
 White plaque that is not removable, background may be red and inflamed
• White from hyperplastic epithelium and increased keratin
o Sx
 Usually asymptomatic
o Dx
 Biopsy is necessary: clinically resemble premalignant lesions
o Histology: candidal hyphae penetrating the hyperparakeratotic layer of the epithelium
Acute Atrophic Candidiasis
-occurs after?
-clinical?
-sx?
tx?
Often after broad spectrum antibiotics, or suffer from xerostomia
• Diffuse loss of the filiform papillae of the dorsal tongue
o Burning tongue sensation
o Sensitive to spices
• White area is normal area
• Red area = no filiform papillae
• Tx:
o Antifungals or treat underlying cuase(stop antibiotics or treat xerostomia)
• Mucocutaneous Candidiasis

-immunological disorders
-complications
• Mucocutaneous Candidiasis
o Immunological disorders
 Congenital immunodeficient patients: Patients develop immune disorder during the first few years in life
 Candidal infections of the mouth, nails, skin and other mucosal surfaces
 Endorince-candidiasis syndrome, autoimmune polyendocrinopathy-candidasis-ectodermal dystrophy
• Some patient develop autoantibody attacking endocrine glands
• Develop endocrine abnormalities later in the life: hypothroidism, hypoparathyroidism, Addison’s disease and DM etc
• Patients need to be periodically evaluated for their endocrine function.
• Histoplasmosis, Coccidiodomycosis & Cryptococcosis : Oral Lesions

clinical features:
DDH:
Dx?
histopathlogy?
tx?
Clinical features:
 chronic non-healing ulcer(s), may penetrate bone
o DDH for non-healing ulcer:
 Deep fungal infections, oral squamous cell carcinoma, tramatic ulceration, oral TB and primary syphilis have similar clinical pictures
o Biopsy is needed. Serology and cultures are also helful.
o Histopathology:
 granulomatous inflammation. Special stains are used to demonstrate the fungus.
 Oral lesion is not the primary lesion
o Tx: antimicrobial agents
Zygomycosis
type of organisms?
also know as?
-type of infection which infects?
-pathogensis
-histology
Zygomycosis(Zebra)
o Caused by fungal organisms of the phylum Zygomycota
o Also called “mucormycosis”, “phycomycosis”
o An opportunistic infection affecting
 Uncontrolled diabetes mellitus patients that develop ketoacidosis –thrive in iron
 Immunocompromised patients
o Angiotropic: Invade/grow the arterial wall, result in ischemia, infarction and necrosis
o Histology:
 extensive tissue necrosis and the characteristic fungal hypahe