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Oral Pathology Exam 2 > 4. Bacterial, Fungal, and Granulomatous Ds Etiology > Flashcards

4. Bacterial, Fungal, and Granulomatous Ds Etiology Flashcards

1
Q

What is Impetigo’s etiology and method of infection?

A
  • Strep. pyogenes*
  • Staph. aureus*

entering broken skin

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2
Q

What is the etiology and method of transmission of Erysipelas?

A

B-hemolytic streptococci - Group A

via lymphatics

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3
Q

What are the possible etiologies of Tonsillitis and Pharyngitis, and what is their method of transmission?

A
  • Viral: adenovirus, enterovirus, influenza, parainfluenza, EBV
  • Bacterial: Group A B-hemolytic streptococci

Respiratory droplet or oral secretions

2-5 day incubation

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4
Q

What is the etiology and method of transmission of Scarlet Fever?

A

Group A - B hemolytic streptococci

Erythrotoxin - toxin attacks the blood vessels

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5
Q

What is the etiology of Syphilis, and what are the 3 methods by which it can be spread?

A

Treponema pallidum

Spread by:

  • intimate sexual contact
  • transplacental transmission
  • contaminated blood exposure
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6
Q

What is the etiology of Gonorrhea?

A

Neisseria gonorrhoeae

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7
Q

What is the etiology and transmission method of Tuberculosis?

A

Mycobacterium tuberculosis

droplet transmission

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8
Q

What are the historical and current etiologies of Scrofula?

A
  • Historically = infection with mycobacterium bovis from contaminated milk
  • Now = mycobacterial infection involving cervical nodes
    • Adults - M. tuberculosis
    • Children - nontuberculous mycobacterial infection
      • ​Usually don’t have pulmonary symptoms
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9
Q

What is the etiology and method of transmission of Cat Scratch Disease?

A

Bartonella henselae

Follows scratch from a kitten with fleas

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10
Q

What are the etiologies of Bacillary Angiomatosis?

A
  • Bartonella hensalae*
  • Bartonellla quintana*
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11
Q

What is the etiology of Lyme Disease?

A

Borrelia burgodorferi

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12
Q

What is the etiology and method of transmission of Histoplasmosis?

A

H. capsulatum

bird and bat droppings - Ohio and Mississippi River Valleys

Spore Inhalation

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13
Q

What is the etiology of Blastomycosis and where is it found?

A

Blastomyces dermatitidis

grows as mold in soil

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14
Q

What is the etiology of Coccidioidmycosis?

A

Coccidioides immitis

  • Dimorphic
    • Humans - yeast
    • In the ground - mold
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15
Q

What is the etiology and method of transmission of Cryptococcosis?

A

Cryptococcus neoformans

  • Grows as yeast, with a prominent mucopolysaccharide capsule
  • Pigeon droppings contain spores which are inhaled
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16
Q

What are the etiologies (4) of Zygomycosis (Mucor), and where are they found?

A

Zygomycetes Class - Absidia, mucor, Rhizomucor, Rhizopus

grow in decaying organic material

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17
Q

What is the etiology of Aspergillosis?

A

A. fumigatus

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18
Q

What is the etiology of Toxoplasmosis, and what is the host?

A

Toxoplasma gondii

Host = cat

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19
Q

In what population is Impetigo common? (4)

A
  • Children
  • Crowded living conditions
  • Poor Hygiene
  • Hot/Humid Climates
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20
Q

Where is the skin infection of Impetigo seen on the body?

A

Skin of Face or Extremities

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21
Q

What is the clinical presentation of the lesions of Impetigo?

A
  • Range from:
    • Fragile vesicles
    • Flaccid bullae that rupture and leave an amber to “honey-colored” crust
  • Typically more than 1 lesion
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22
Q

What is the DD for Impetigo? (3)

A
  • Exfoliative Cheilitis
  • Recurrent Herpes Simplex
  • Mimic Child Abuse (burning skin)
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23
Q

What is the tx for isolated Impetigo lesions?

A

Topical mupirocin

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24
Q

What is the tx for bullous or more extensive Impetigo lesions?

A
  • 1 wk course of systemic oral antibiotics
    • Augmentin
    • PCN Allergy = clindamycin
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25
Q

What population is susceptible to Erysipelas?

A
  • Young and Elderly
    • particulary the debilitated or diabetic
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26
Q

What is the clinical presentation of Erysipelas? (5)

A
  • Occurs anywhere on the skin, common in areas of previous trauma
  • Common on face, bridge of nose butterfly-shaped rash
    • Mimics LE
  • Edema of eyelid
    • Mimics Angioedema
  • Painfull, bright red, warm, well-circumscribed, swollen, indurated
    • Mimics a Dental Infection
  • Fever, increased WBC count, nausea and vomiting possible
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27
Q

What is the treatment for Erysipelas?

A

Penicillin

Lesion often enlarges at the start of therapy, then rapid resolution within 48 hrs

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28
Q

What are the common symptoms that Children with Tonsillitis and Pharyngitis have? (5)

A
  • Headache
  • Anorexia
  • Abdominal pain
  • Malaise
  • Vomiting
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29
Q

What symtoms of Tonsillitis and Pharyngitis suggest a viral etiology? (6)

A
  • Conjunctivitis
  • Cough/Hoarseness
  • Diarrhea
  • No Fever
  • Rhinorrhea
  • Viral Exanthema
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30
Q

If the clinical features of Tonsillitis and Pharyngitis suggest a bacterial origin what is the protocol?

A
  • Rapid Antigen Detection Test
    • Good Sensitivity and Specificity
  • If the rapid test is negative, then get a throat culture
  • Antibiotic should only be Rx in confirmed bacterial infection
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31
Q

What does Scarlet Fever begin as?

A
  • Streptococcal tonsillitis with pharyngitis
  • Skin rash (exanthema)
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32
Q

In what population is Scarlet Fever common in?

A

Children (3-12 yrs)

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33
Q

What is the incubation period for Scarlet Fever?

A

Ranges from 1-7 days

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34
Q

What occurs within the 1st 2 days of Scarlet Fever? (4)

A
  • High Fever (~103 F)
  • Oropharynx
    • ​Erythematous, edematous, yellowish exudate in tonsillar crypts
    • Scattered petechiae may be seen on the soft palate
  • Skin
    • ​Rash (exanthema) on the trunk and extremities, sparing the face
    • Circumoral Pallor
  • Tongue
    • ​white strawberry tongue
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35
Q

What occurs during day 4-5 of Scarlet Fever?

A

Strawberry Tongue

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36
Q

What occurs after 1 week of having Scarlet Fever?

A
  • Rash subsides, followed by:
    • Desquamation of skin from face to extremites ensues for 3-8 wks
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37
Q

What is the Diagnosis and Treatment for Scarlet Fever?

A

Same as Tonsillitis and Pharyngitis

Rapid antigen detection test, if positive then give antibiotics

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38
Q

What population has the most cases of Syphilis?

A

Men having sex with men

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39
Q

When does Primary Syphilis develop?

A

3-90 days after exposure

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40
Q

What is the clinical presentation of Primary Syphilis?

A
  • Relatively painless ulceration becomes a chancre
    • Chancre mostly affecting genital region
  • 4% are oral
    • Lip, tongue, palate, gingiva, tonsils
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41
Q

What is the treatment for Primary Syphilis?

A

Spontaneously Resolves in 3-8 wks

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42
Q

When does Secondary Syphilis develop?

A

4-10 wks after initial infection

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43
Q

What is the Clinical Presentation of Secondary Syphilis? (3)

A
  • Erythematous, maculopapular, cutaneous eruption
  • Painless, generalized Lymphadenopathy
  • Oral Mucosa:
    • Mucous patches
    • Condyloma lata
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44
Q

When does Tertiary Syphilis develop?

A

Latency period of 1-30 years

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45
Q

What are the Clinical Features of Tertiary Syphilis? (5)

A
  • Affects 30% of pts with Syphilis
  • May affect any tissue, including CNS and vasculature
  • Gumma formation in multiple areas
    • Bone and Soft tissue
    • Interstitial glossitis
  • Luetic Glossitis of dorsal tongue
    • Atrophy, loss of papillae, and hyperkeratosis
  • Palatal Perforation may occur (esp in opiate addicted pts)
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46
Q

What are the classic clinical features of Congenital Syphilis? (3(5))

A
  • Saddle Nose Deformity (no bridge of nose)
  • Saber Shins (anterior bowing of tibia)
  • Hutchinson’s Triad
    • Malformed incisors and molars = Hutchinson’s Incisors and Mulberry Molars
    • Ocular Interstitial Keratitis
    • 8th nerve Deafness
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47
Q

What is used to Diagnosis Syphilis? (3)

A
  • Screening Tests
    • VDRL (veneral disease research laboratory)
    • RPR (rapid plasma reagin)
  • Specific Antibody Tests
    • FTA (fluorescent treponemal antibody)
  • Dark-field Microscopy
    • For non-oral lesions
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48
Q

What is the use of Screening Tests (VDRL, RPR) for Syphilis?

A
  • Test for Reinfection
  • Positive during the 1st 2 stages, then tapers off
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49
Q

What are the implications of the Specific Antibody Test (FTA) for Syphilis?

A

Positive for Life

Can’t use to test for reinfection

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50
Q

What is the histology seen in Primary and Secondary Syphilis?

A

Intense plasmacytic infiltrate

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51
Q

What is the histology seen in Tertiary (gumma) Syphilis?

A

Granulomatous inflammation

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52
Q

How can spirochetes (associated with the diagnosis of syphilis) be identified histologically?

A
  • Warthin-Starry Stain, or
  • Immunohistochemistry (IHC)
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53
Q

What is the drug of choice for treating Syphilis?

A

Parenteral Penicillin G

mega dose intramuscularly

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54
Q

What is use to treat syphilis in a patient with a penicillin allergy?

A

Doxycycline

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55
Q

What is the most common reportable bacterial infection?

A

Gonorrhea

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56
Q

Where does Gonorrhea occur in men, and women?

A
  • Men = urethra
  • Women = cervix (may lead to PID)
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57
Q

What can occur in a baby that was delivered by a mom who didn’t know she had gonorhhea?

A

Gonococcal Opthalmia Neonaturm

can cause blindness

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58
Q

What are the features of oral involvement in patients with Gonorrhea?

A

Oropharynx, tonsils, uvula

  • Usually transmitted via oral to genital contact
  • Oropharyngeal diffuse erythema with punctate pustules, and sore throat
  • Occasionaly looks like ANUG but without the odor
  • Patients with septicemia, the bacteria spreads through their bloodstream to the oral cavity, present with aphthous-like ulcers
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59
Q

How is Gonorhea Diagnosed?

A
  • Gram stain of exudate
  • Culture
  • PCR
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60
Q

What is the treatment for Gonorrhea?

A

Systemic Antibiotic

fluoroquinolone

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61
Q

What population is affected with Tuberculosis?

A

More common in foreign-born persons

1/3 of the worlds population is infected

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62
Q

What are the clinical features of Tuberculosis? (4)

A

Only 5-10% of infected pts progress to active disease

  • Low grade fever, night sweats, fatigue
  • Weight loss
  • Chronic bloody cough
  • Enlarged lymph nodes
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63
Q

What are the features of Scrofula?

A
  • Enlargement of oropharyngeal lymphoid tissue and cervical lymph nodes
  • May see tissue necrosis causing fistulas which can calcify and be seen on PANX
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64
Q

What are the features of TB Oral Lesions? (4)

A
  • Rather uncommon
  • May be due to hematogenous spread or direct implantation of organisms
  • Most common on Gingiva and Tongue
  • Solitary chronic painless ulcer
    • ​Similar to SCCA, which is more common
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65
Q

How is Tuberculosis diagnosed?

A

+ Tuberculin Skin Test

  • If you recieved the BCG vaccine you will get a +TST, so get a blood test to confirm
  • Need a further workup: exam, chest xray, sputum sample
  • Culture or PCR to characterize the organism
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66
Q

What does the histology of TB show? (3)

A
  • Caseous Necrosis = Necrotizing granulomatous inflammation; cheesy necrotic center
  • Multinuclead Giant Cell
  • Organisms stain using the acid fast method (Ziehl-Neelsen Stain)
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67
Q

What is the Treatment protocol for patients with active TB?

A

Combo of antibiotics

  • Isoniazid (INH) + rifampin + pyrazinamide (+/- ethambutol)
    • For 8 weeks
  • Then, INH + rifampin
    • For 16 weeks
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68
Q

What is the Treatment protocol for patients with latent TB, that are at risk for developing the active ds (immunocomprimised pts)?

A

INH +/- rifampin or rifapentine

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69
Q

What is the etiology of Actinomycosis?

A
  • Any of several Actinomyces species that normally inhabit the mouth
  • Often associated with local trauma
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70
Q

What areas may be affected by Actinomycosis? (3)

A
  • Abdominal (25%)
  • Pulmonary (15%)
  • Cervicofacial (55%)
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71
Q

What is the initiating factor causing Cervicofacial Actinomycosis?

A

Dental Extraction or Untreated Dental Disease

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72
Q

What is the clinical presentation of Cervicofacial Actinomycosis?

A
  • Diffuse swelling
  • Erythema
  • Broad-like firm fibrosis with central soft abscess
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73
Q

In Cervicofacial Actinomycosis where are the organisms draining out of?

A

Sinus tracts

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74
Q

What is in the purulent exudate in Cervicofacial Actinomycosis?

A

Sulfur Granules

Colonies of organisms in purulent exudate

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75
Q

What is the histology o Actinomycosis?

A
  • Filamentous, club-shaped, anaerobic bacterial colonies forming radiating rosettes “Ray Fungus” surrounded by neutrophils
  • Adjacent tissue may show Granulomatous Inflammation or Granulation Tissue
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76
Q

What is the general treatment for Actinomycosis?

A

Remove offending tooth

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77
Q

What is the treatment for localized and periapical Actinomycosis lesions?

A

Remove infected tissue

If surgery fails - PCN

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78
Q

What is the treatment for chronic cases of Actinomycosis?

A

Prolonged, high doses of antibiotics

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79
Q

What is the treatment for Cervicofacial Actinomycosis lesions?

A

IV PCN for a couple of weeks, then oral dosing for 5-6 weeks

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80
Q

What is the treatment for deep-seated Actinomycosis lesions?

A

Oral PCN for a year

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81
Q

What is the most common cause of Chronic Regional Lymphadenopathy in Children?

A

Cat Scratch Disease

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82
Q

What population is usually affected by Cat Scratch Disease?

A

Males < 18 yrs old

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83
Q

What is the clinical presentation of Cat Scratch Disease?

A
  • Erythematous papule at the site of scratch
  • Followed by Tender Lymphadenopathy
    • Usually what is noticed by parents
  • Fever or Malaise may also be present
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84
Q

What is the Histology of Cat Scratch Disease? (3)

A
  • Necrotizing Granulomatous Inflammation localized to lymph nodes
  • Warthin-Starry staining method shows pleomorphic bacilli
  • Can do IHC for Bartonella henselae
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85
Q

How is Cat Scratch Disease Diagnosed?

A
  • Serologic Testing - indirect fluorescent antibody assay or ELISA testing
  • Rule out other cases of Lymphadenopathy
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86
Q

What is the Treatment for Cat Scratch Disease?

A
  • No definitive tx - resolves spontaneously after weeks to months
  • In prolonged cases, antibiotics may be used
  • Large necrotic nodes may require drainage
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87
Q

What is the clinical presentation of Bacillary Angiomatosis?

A
  • Painful, subcutaneous red/purple plaques (vascular growths)
  • Occasional oral lesions that occur in AIDS pts
    • Resembles Kaposi Sarcoma
      • Warthin-Starry stain highlights the bacillus
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88
Q

What is the clinical presentation of Lyme Disease?

A
  • “Bulls Eye” skin rash = Erythema Migrans
  • Fever, Headache, Fatigue
  • May spread to joints, heart and nervous system
    • Any CN can be involved
    • TMJ Pain
  • May cause facial palsy mimicking Bell’s Palsey
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89
Q

What is the treatment for Lyme Disease?

A

Doxcycline or Amoxicillin

Early in course

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90
Q

What is the etiology of Oral Candidiasis?

A
  • Chronic infection with Candida albicans
  • Dimorphic = yeast and hyphal forms
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91
Q

What is the most common oral fungal infection?

A

Candidiasis

92
Q

What are the clinical features of Pseudomembranous candidiasis (Trush)?

A
  • Removeable cheesy, white plaques on buccal mucosa, palate, and tongue
  • Burning sensation or bad taste in the mouth
  • Acute Onset with Antibiotic exposure
  • Slower Onset with Immunosuppresion
93
Q

What are the clinical features of Acute Atrophic Candidiasis?

A
  • “Antibiotic Sore Mouth”
  • Scalded/burning sensation to tongue
  • Diffuse loss of filiform papillae on dorsal tongue
94
Q

What are the clinical features of Central Papillary Atrophy (Median Rhomboid Glossitis)?

A
  • Well-demarcated red zone, flat, smooth, often symmetric
  • Posterior dorsal tongue, in the midline
  • Often asymptomatic
95
Q

What are the clinical features of Chronic Multifocal Candidiasis?

A
  • Central Papillary Artophy (Median Rhomboid Glossitis) + Additional Site
    • ​Kissing lesion on palate OR angular cheilitis
96
Q

What are the clinical features of Angular Cheilitis (Perleche)?

A
  • Erythema, fissuring and scaling of the angles of the mouth
  • Waxes and wanes
  • Can occur alone or with other forms of Erythematous candidiasis
97
Q

What are the possible etiologies of Angular Cheilitis?

A
  • 20% Candida alone
  • 60% Candida + Staph Aureus
    • ​Usually not just candida alone
  • 20% Staph Aureus alone
98
Q

What is the term for Angular Cheilitis that shows more extensive perioral involvement, spreading all the way around the lips?

A

Cheilocandidiasis

99
Q

What is the etiology of Denture Stomatitis (Chronic Atrophic Candidiasis)?

A
  • May be related to continuous denture wear
  • Mostly a tissue response rather than a true infection of mucosa
    • Denture is often contaminated with Candida organisms
100
Q

What are the clinical features of Denture Stomatitis (Chronic Atrophic Candidiasis)?

A
  • Erythema of palatal denture-bearing area
  • Typically asymptomatic
101
Q

What can predispose to erythematous or pseudomembranous candidiasis of the hard/soft palate?

A

Steroid Inhalers

102
Q

What are the clinical features of Chronic Hyperplastic Candidiasis?

A
  • Non-removable, white plaques
  • Most common sites are buccal mucosa, tongue
  • If superimposed on pre-neoplastic lesion (Leukoplakia), often speckled appearance
103
Q

What is the etiology/pathogenesis of Mucocutaneous candidiasis?

A
  • Rare, immunologic defect leading to infection
  • Usually sporadic, but can be inherited
104
Q

What is the clinical presentation of Mucocutaneous candidiasis?

A
  • Onset early in life with infections of mouth, skin, nails and other mucosal sites
    • Skin infections
      • ​Rough, foul-smelling, plaques/nodules
    • Oral infections
      • ​Thick, white oral plaques, chronic hyperplastic appearing
  • May develop endocrine abnormalities OR iron deficiency anemia
    • ​follow-up indicated
105
Q

What is the treatment for Mucocutaneous candidiasis?

A

Control with systemic antifungals

106
Q

What may develop in Mucocutaneous candidiasis pts?

A

Endocrine-Candidiasis Syndrome

107
Q

What endocrine problems may develop, months to years after candida infections are noted, in Endocrine-Candidiasis Sx? (4)

A
  • Hypothyroidism
  • Hypoparathyroidism
  • Hypoadrenocorticism (Addison’s Ds)
  • Diabetes Mellitus
108
Q

In the diagnosis of Candidiasis what technique is more sensitive, capturing the most cases possible?

A

Culture

2-3 days to grow colonies (2-3mm creamy white) - yeast form

109
Q

In the diagnosis of Candidiasis what are the characteristics of KOH preparation - Cytology? (4)

A
  • Quick (mins) and Inexpensive
  • Not as sensitive as culture or stained slide
  • Not permanent
  • Can’t asses epithelial cells
110
Q

In the diagnosis of Candidiasis what are the characteristics of Stained Slide (periodic acid schiff) - Cytology? (3)

A
  • Next Day results
  • Permanent record
  • Fix cells to slide with alcohol and send to lab for staining
111
Q

What is the histology of Candidiasis? (5)

A
  • Hyperkeratosis
  • Elongation of rete ridges
  • Chronic inflammation in CT
  • Neutrophils forming “microabscesses” in the parakeratin (trying to attack hyphae)
  • Hyphae embedded in keratin, rarely penetrate into viable epithelium
112
Q

What is the Histochemistry used for Candidiasis? How does it stain?

A
  • Periodic Acid Schiff (PAS)
    • Stains carbohydrate wall magenta
  • Grocott-Gomori Methanamine Silver (GMS)
    • Stains black
113
Q

What antifungal medications are the Polyene Agents?

A

Nystatin, Amphotericin B

Soak partial dentures

114
Q

What is the downside to polyene agents?

A

Have to use 5x/day

115
Q

How do polyene agents work?

A

BINDS to ergosterol leading to cell permeability and cell death

116
Q

What antifungal medications are the Imidazole Agents?

A

Clotrimazole (Mycelex), Ketoconazole, and Micronazole (denture pt, dissolves in mouth)

10mg troches (lozengens)

useful for treating all types

117
Q

When do Imidazole agents work well?

A

if not responding to nystatin or fluconazole

118
Q

How do Imidazole Agents work?

A

BLOCK ergosterol synthesis by enzyme inhibition

119
Q

What antifungal medications are the Triazoles? (4)

A

Fluconazole (Diflucan), itraconazole, voriconazole, and posaconazole

long 1/2 life, good absorption

120
Q

What is the upside to triazoles?

A

once a day pill

121
Q

What is the downside to triazoles?

A

More chance for side effects since it is a systemic drug

122
Q

How do triazoles work?

A

BLOCK ergosterol synthesis by enzyme inhibition

Same as Imidazole Agents

123
Q

How do Echinocandins work?

A

Block beta-(1,3)-glucan synthesis

124
Q

What are other antifungal medications that can be used to treat candidiasis?

A

1% Iodoquinol + hydrocortisone cream

use for Angular Cheilitis if it is the only area involved

125
Q

What is the newer antifungal drug, Posoconazole used for?

A

Oropharyngeal Candidiasis in HIV+ pts

Expensive

126
Q

What is the new antifungal class, Echinocandins used for?

A

IV use ONLY, for life-threatening candida and aspergillus infections

ex. caspofungin, micafungin, anidulafungin

127
Q

What can deep fungal infections mimic in the oral cavity?

A

malignancy

128
Q

What is used to treat advanced deep fungal infections?

A

Amphotericin B

129
Q

What is the most common systemic fungal infection in the US?

A

Histoplasmosis

130
Q

What is the etiology of Histoplasmosis? (3)

A
  • H. capsulatum dimorphic:
    • Humans = yeast
    • Nature = mold
  • Bird, Bat droppings in Ohio and Mississippi River Valley
  • Spore inhalation - germinate in lungs
131
Q

How does Histoplasmosis present clinically?

A
  • 1-2 wks of flu-like illness
    • ​Organisms normally destroyed, but may remain viable within macrophages
    • Can recur with immuno suppression
132
Q

What are the characteristics of Acute Histoplasmosis?

A
  • Self-limited pulmonary infection
    • # of exposed pts affected depends on concentration of spores inhaled
133
Q

What is the treatment for Acute Histoplasmosis?

A

No treatment indicated

134
Q

In what population is Chronic Histoplasmosis most common?

A
  • Primarily a lung infection in the:
    • Elderly
    • Immunosuppresed
    • Pts with Emphysema
135
Q

What is Chronic Histoplasmosis similar to?

A

TB

cough, weight loss, fever, dyspnea, upper lobe infiltrates, calcification

136
Q

What is the Prognosis for Chonic Histoplasmosis?

A
  • Up to 50% recover spontaneously
  • Progressive pulmonary damage without tx
  • Up to 20% mortality
137
Q

What is the preferred treatment for Chronic Histoplasmosis?

A

IV amphotericin B

Itraconazole - used in non-immunocomprimised pts

138
Q

What are the characteristics of Disseminated Histoplasmosis? (2)

A
  • Uncommon - 1:2,000 - 5,000 pts with acute symptoms
  • Extrapulmonary spread - context of most oral lesions
139
Q

What is the prognosis for pts with Disseminated Histoplasmosis, in those that are treated vs. untreated?

A
  • Untreated = 90% mortality
  • Treated with Amphotericin B = 7-23% mortality
140
Q

What are the characteristics of the Oral Lesions of Histoplasmosis, what can it mimic? (3)

A
  • Most affected sites = tongue, palate, buccal mucosa
  • Solitary, +/- Painful, Ulceration of Short Duration (weeks)
  • Firm, rolled margins, in areas of ulceration mimic malignancy of SCCA
141
Q

What is the Histology of Histoplasmosis? (2)

A
  • Granulomatous Inflammation, often with multinucleated giant cells
  • PAS and SIlver Stain (GMS) show 1-4 um yeasts inside macrophages
142
Q

What is the etiology of Blastomycosis?

A

Blastomyces dermatitidis

Dimorphic fungus - grows as a mold in soil

143
Q

What is the pathogenesis of Blastomycosis?

A
  • Fungal mold spores inhaled and grow as yeasts within the lungs, where infection is normally maintained
    *
144
Q

What are the clinical features of Blastomycosis? (2)

A
  • Usually subclinical or mild pulmonary symptoms
  • Dissemination through blood to skin, bone, prostate, oral mucosa, and abdominal organs, can occur
145
Q

What is the clinical presentation of Acute Blastomycosis?

A
  • Pneumonia-like symptoms:
    • high fever, malaise, productive cough (purulent sputum), night sweats, chest pain
146
Q

What is the treatment for Acute Blastomycosis?

A
  • Only Treat if:
    • Seriously ill
    • No improvement
    • Extended illness (> 2-3 wks)
147
Q

What type of Blastomycosis is more common?

A

Chronic Blastomycosis

148
Q

What is the clinical presentation of Chronic Blastomycosis? (2)

A
  • Mimics TB
    • low-fever, night sweats, weight loss, productive cough
  • Chest Films are: normal, with diffuse infiltrates or pulmonary mass, and no calcifications
    • Like in Histoplasmosis and TB
149
Q

What is the treatment for Chronic Blastomycosis?

A
  • Mild/Moderate Infection = itraxonazole
  • Severe Infection = amphotericin B
150
Q

What are the clinical features of Cutaneous Blastomycosis? (2)

A

May be spread of infection

  • Expanding erythematous nodule that becomes verrucous or ulcerated
151
Q

What is the clinical appearance of oral lesions of blastomycosis?

A
  • Irregular white/red lesion or ulceration with rolled borders
  • Mimicks malignancy
152
Q

What is the Histology of Blastomycosis? (3)

A
  • Often mixed inflammation (acute or granulomatous) with 8-20 um yeasts (bigger than Histoplasmosis)
  • Double refractile cell wall, broad budding pattern
  • PEH
153
Q

What is the treatment and prognosis of Blastomycosis?

A

Most pts = no tx

Prognosis = good

154
Q

Where is Coccidioidomycosis most common?

A

Southwestern US

Desert soil

“Valley Fever”

155
Q

What is the clinical presentation of Coccidioidomycosis?

A
  • Most asymptomatic
  • ~40% have flu-like symptoms, lasting a few wks
    • similar to histomycosis and blastomycosis
  • Occasional EM or erythema nodosum
    • non-specific, painful, red bumps on extremities
156
Q

What is the common presentation of Disseminated (<1%) Coccidioidomycosis? (2)

A
  • Skin of face is a common site
    • Papules, verrucous plaques, and granulomatous nodules often around central face and nasolabial fold
  • Oral lesions uncommon
157
Q

What is the histology of Coccidioidomycosis?

A
  • 20-60 um (very large) round spherules containing endospores
    • ​Way bigger than Histo and Blasto
158
Q

How do you dx Coccidioidomycosis?

A

Biopsy - verrucous plaques

159
Q

What is the tx for Coccidioidomycosis?

A
  • Usually none
  • Amphotericin B
    • ​pts with immunosuppression, disseminated ds or life-threatening infection
160
Q

In what population are you most likely to find Cryptococcosis?

A

common life-threatening fungal infection in AIDs pts

(AIDs defining ds)

161
Q

What is a severe infection of Cryptococcosis called?

A

Fungal Meningitis

162
Q

What is common in Cryptococcosis, that isnt as common in histomycosis and blastomycosis?

A

Dissemination is common

  • Meninges, skin, bone, prostate
163
Q

What is often the first sign of fungal meningitis?

A
  • Fever, headache, neck stiffness, vomitting
164
Q

How is Fungal Meningitis dx?

A
  • Spinal tap to check CSF
    • Stain with PAS, to see if it is fungal (+)
    • Gram Stain - CSF should be sterile and not have gram (-) or gram (+) organisms
    • If both are negative then it is probably viral menengitis.
165
Q

What are the skin lesions of Cryptococcosis? (2)

A
  • Often H/N area
  • Erythematous papules/pustules - their discharge is full of organisms
166
Q

What are the oral lesions of Cryptococcosis?

A
  • Rare
  • Present as tender, non-healing ulcers
167
Q

What is the histology of Cryptococcosis? (3)

A
  • Granulomatous inflammation
  • Round to ovoid 4-6 um yeast surrounded by a clear halo (capsule)
  • PAS, GMS stain organisms, mucicarmine stain highlights the capsule (bright pink)
168
Q

What population does mucor most affect?

A

It is an opportunistic fungal infection

  • Poorly controlled Type I Diabetes
  • Immunocomprimised pt
169
Q

What form of Zygomycosis is most relevant to the dentist?

A

Rhinocerebral Form

170
Q

What is the initial presentation of Mucor?

A

Maxillary swelling

171
Q

What are the symptoms associated with Mucor? (6)

A
  • Nasal obstruction
  • Bloody discharge (epitaxis)
  • Vision alterations with proptosis
  • Facial Pain/headache
  • Facial Swelling
  • Facial Paralysis common if facial nerves involved
172
Q

What is the radiographic appearance of mucor?

A

Opacification of the sinus mimicking malignancy

173
Q

What may the disease progression of mucor lead to? (3)

A
  • Blindness
  • Seizures
  • Death
174
Q

What is the histology of mucor? (3)

A
  • Extensive necrosis with large (6-30 um), 90 deg branching, nonseptate hyphae
    • Candidia and Aspergillosis have septae
  • Tissue destruction due to invasion of small vessels leading to disruption of BF
    • Shows black necrosis
  • Variable neutrophilic response depending on immune status
175
Q

What is the tx for Mucor? (3)

A
  • Radical surgical debridement of necrotic tissue
  • High does Amphotericin B
  • Control of predisposing ds
176
Q

What is the prognosis for Mucor?

A

Poor

50% die

177
Q

What is the clinical presentation of Aspergillosis? (3)

A
  • Allergic Fungal Sinusitis
    • ​Painful swelling of sinus, can also affect lungs
  • Aspergilloma and Antolith
    • ​Instead of an immune response, they form a fungal mass which can calcify
  • Post-extraction or RCT of maxillary tooth
    • ​Painful gingival ulceration
    • Diffuse gray/purple swelling
178
Q

What are the features of Disseminated Aspergillosis? (3)

A
  • Immunocompromised pt - 1/3 survive
  • Chest pain, cough, fever
  • Hematogenous spread to:
    • CNS, eye, skin, liver, GI tract, bone, thyroid
179
Q

What is the histology of Aspergillosis? (3)

A
  • Branching at acute angles, septate hyphae (3-4 um) invading and occluding small vessels
  • Healthy pt - granulomatous response
  • Immunocompromised pt - minimal inflammation
180
Q

How is Aspergillosis diagnosed? (3)

A
  • Blood/sputum culture often negative despite disseminated ds
  • Tx based on clinical presentation
  • Biopsy showing organism is only suggestive
181
Q

What can infection with toxoplasmosis during the 1st trimest lead to?

A
  • Blindness
  • Mental retardation of baby
182
Q

How is Toxoplasmosis diagnosed?

A

Rising antibody titers in healthy pts 10-14 days after infection

183
Q

What is the treatment for Toxoplasmosis?

A
  • Healthy pt - none
  • Pregnant women
    • Prevention - avoid raw meat and cat litter box
    • sulfadiazine and pyrimethamine often prevents transmission to fetus
    • Also used for immunosuppressed pts
184
Q

What type of infection is toxoplasmosis?

A

Protozoal

185
Q

What is the pathogenesis of Sarcoidosis? (2)

A
  • Multisystem granulomatous ds of unknown origin
  • Improper breakdown of antigens leading to granulomatous inflammation
186
Q

In what population does Sarcoidosis occur?

A
  • Blacks
  • 20-40 yrs
187
Q

What shows the most prominant symptoms in Sarcoidosis?

A

Pulmonary Symptoms

  • Dyspnea
  • Chest Pain
  • Dry Cough
    • Deep fungal inf have purulent coughs
  • Bilateral hilar lymphadenopathy seen on chest film
188
Q

What are the skin manifestations of Sarcoidosis?

A
  • “Lupus Pernio”
    • violacious, indurated lesions (purple, firm, plaques) on face and lips
  • Erythema Nodosum
    • ​non-specific, tender red nodules on lower legs
      • Also in Coccidioidomycosis
  • ***May cause Facial Paralysis
189
Q

What are the eye and salivary manifestations of Sarcoidosis?

A

Mimics Sjogren Sx

Eye

  • Keratoconjunctivitis sicca (dry eyes)
    • Most often anterior uveitis = inflammation of the middle layer of the eye - redness, pain, and blurred vision
  • Lacrimal involvement

Salivary Gland

  • Enlargement and Xerostomia of major and minor glands
190
Q

What are often the 1st signs of Sarcoidosis? (4)

A

Oral Lesions

  • Submucosal mass, papule, granular lesion
  • Brownish/red, violaceous, or hyperkeratotic lesion
  • Buccal mucosa, gingiva, lips, FOM, tongue, or palate
  • Can’t diagnose based on oral lesions, because they mimic alot of other diseases
191
Q

What is the presentation of the intraosseous lesions of Sarcoidosis?

A

​Never put in a DD for a RL jaw lesion, unless they have all other symptoms!

  • Ill-defined RL
  • Cortical erosion, with no expansion
192
Q

What is present in the histology of Sarcoidosis? (5)

A
  • Granulomatous inflammation with mngc
  • Epitheliod histiocytes with surrounding lymphocytes
  • Schaumann Bodies - ​laminated basophilic calcifications
  • Asteroid Bodies - ​stellate inclusions (stars inside giant cells)
  • No Bug (fungal, bacterial, foreign material)
    • PAS, GMS, Acid Fast are all negative
193
Q

How is Sarcoidosis diagnosed? (2)

A
  • Clinical and Radiographic findings
  • Elevated ACE levels + Pulmonary Involvement
    • ​Offers strong support
194
Q

What is the treatment for Sarcoidosis? (3)

A
  • Observation period (3-12 months) to asses disease course
  • 1st line therapy - corticosteroids effective in 20%
  • Refractory Ds
    • Chemo drugs: methotrexate, azathiprine, chlorambucil, cyclophosphamide
    • TNF-a antagonists (etanercept, infliximab)
    • Antimalarials (chloroquine)
195
Q

What is the prognosis for Sarcoidosis? (3)

A
  • Without Treatment - 60% resolve within 2 yrs
  • With Treatment - 10-20% don’t resolve
  • 10% die of pulmonary, cardiac, or CNS complications
196
Q

What is the pathogenesis of Orofacial Granulomatosis?

A
  • idiopathic - abnormal immune rxn
  • Must rule out other causes because it can be secondary to:
    • Local Factors
      • _​_Chronic oral infection
      • Foreign material (if localized to gingiva)
      • Allergy
    • Systemic Factors
      • Chronic Granulomatous Ds
      • Crohn’s Ds
      • Sarcoidosis
      • TB
197
Q

What is the classic presentation/main site of Orofacial Granulomatosis?

A

Lips

non-tender, persistent swelling, that doesn’t go away

DD: Angioedema usually goes away in 3 days

198
Q

What is it called when the lip signs of orofacial granulomatosis are combined with fissured tongue, and facial paralysis?

A

Melkersson-Rosenthal Syndrome

199
Q

What are the intraoral lesions of Orofacial Granulomatosis? (3)

A
  • Gingiva
    • Swelling, erythema, pain, erosions
  • Buccal Mucosa
    • Cobblestone appearance
    • linear ulcerations in the mucobuccal fold
  • Palate
    • Papules, hyperplastic tissue
200
Q

What is the histology of Orofacial Granulomatosis? (2)

A
  • Non-necrotizing granulomatous inflammation
  • Poorly formed, small granulomas around blood vessels
    • Lots of normal looking tissue in between the granulomas; spread apart
    • Nor as well formed as in Sarcoidosis
201
Q

What is the treatment for Orofacial Granulomatosis?

A
  • Eliminate trigger
  • Intralesional corticosteroids (triamcinolone)
  • Lesions may resolve spontaneously or progress in spite of therapy
202
Q

What is the age of people affected with Wegner’s Granulomatosis?

A

Wide age range

mean = 40 yrs

203
Q

When occurs in Classic Wegner’s Granulomatosis?

A
  • Initially - upper and lower respiratory tract involvement
  • If the condition remains untreated - rapid renal involvement
204
Q

When is Limited Wegner’s Granulomatosis diagnosed?

A
  • No Renal Involvement
  • Stays in respiratory tract and never goes to the kidney
205
Q

What is seen in Superficial Wegner’s Granulomatosis?

A
  • Mostly skin/mucosal signs, with slow development of systemic ds
  • This is usually what dentists see
206
Q

What is seen with upper respirtory involvement in Wegner’s Granulomatosis? (8)

A
  • Purulent nasal drainage
  • Chronic sinus pain
  • Nasal ulceration
  • Congestion
  • Fever
  • Otitis media
  • Sore throat
  • Epistaxis
207
Q

What is seen with lower respirtory involvement in Wegner’s Granulomatosis? (4)

A
  • Dry cough
    • ​Also in sarcoidosis (opposite of deep fungal infections)
  • Hemoptysis
  • Dyspnea
  • Chest Pain
208
Q

What seen with renal involvement in Wegner’s Granulomatosis?

A
  • Glomerulonephritis (nephrotic Sx) leads to proteinuria
  • Occurs late in the ds process
  • Most frequent cause of death
209
Q

What is the most frequent cause of death in Wegner’s Granulomatosis?

A

Renal involvement

210
Q

What are the uncommon oral lesions of Wegner’s Granulomatosis? (3)

A
  • Strawberry Gingivitis
    • ​Early sign of ds
    • Attached buccal gingiva
    • Isolated or multifocal
  • Salivary Enlargement
    • ​Early sign of ds
  • Non-Specific Ulceration
    • ​Late sign of ds
    • May cause palatal perforation
211
Q

What are other orofacial signs/symptoms of Wegner’s Granulomatosis? (3)

A
  • Facial Paralysis
  • Sinusitis
  • Can mimic toothache or TMJ arthralgia
212
Q

What is shown in the histology of Wegner’s Granulomatosis? (4)

A
  • Mixed inflammation (pmns, histocytes, lymphocytes, eosinophils, mngc) around blood vessels
    • Langerhan’s Histiocytosis also classically shows eosinophils
  • Leukocytoclastic Vasculitis = destroying wall of blood vessel
    • Necrosis and nuclear dust
  • RBC extravasation
  • Possible PEH
213
Q

How is Wegner’s Granulomatosis Diagnosed? (4)

A
  • Combo of clinical presentation + microscopic appearance
  • Confirm Disease Extent with:
    • Chest and sinus x-rays
    • Serum creatinine and urinalysis
  • Anti-Neutrophilic Cytoplasm Antibodies (ANCA)
    • p-ANCA - but it is seen in other vasculitides
    • c-ANCA (PR3-ANCA)
      • Most useful in dx, present in 90-95% of classic/generalized WG
  • Confirm with ELISA specific for antigen proteinase 3 (PR3)
214
Q

What is the treatment for Wegner’s Granulomatosis?

A

Oral cyclophosphamide (nasty drug) and predisone

215
Q

What is the prognosis for Wegner’s Granulomatosis without treatment?

A
  • Classic WG
    • Mean survival 5 months
    • 90% die within 2 yrs
  • Limited and Superficial WG
    • Much better prognosis
216
Q

What is the prognosis for Wegner’s Granulomatosis in pts who receive treatment?

A
  • 75% have prolonged remission
  • Cure for localized disease if dx and tx properly
217
Q

What is the pathogenesis of Crohn’s Disease?

A

Unknown Cause

Inflammatory and probably immunologically mediated

218
Q

In what population is Crohn’s ds diagnosed?

A

young adults and teenagers

219
Q

What sites does Crohn’s Disease affect?

A
  • Any part of the GI Tract (primarily likes the distal portion)
  • Extra-intestinal sites:
    • Skin, eyes, joints
  • Oral Mucosa in ~30% of cases
220
Q

What are the general signs/symptoms of Crohn’s Disease?

A
  • Abdominal cramping and pain, nausea and diarrhea, occasionally fever
  • Weight loss and malnutrition can lead to: anemia, decreased growth, and short stature
221
Q

What are the oral lesions assocaited with Crohn’s Disease? (3)

A

If GI is asymptomatic, this could be the 1st sign

  • Diffuse, or nodular oral mucosal swelling with a cobblestone appearance
    • Can resemeble histoplasmosis(?) and Orofacial Granulomatosis
  • CLASSIC - deep, granulomatous-appearing linear ulcers of buccal vestibule
  • Aphthous-like ulcers if dramatic and occuring frequently
222
Q

What is the histology present in Crohn’s Disease?

A
  • Non-necrotizing granulomatous inflammation (non-specific)
    • sarcoidosis and orofacial granulomatosis
  • Special stains needed to exclude:
    • Deep Fungal Infection
    • Tertiary Syphilis
    • TB
223
Q

What is the treatment for Crohn’s Disease? (4)

A
  • 1st Line
    • ​mesalamine or sulfa-type drug (sulfasalazine)
  • 2nd Line
    • _​_Systemic prednisone + azathioprine
  • Refractory Cases
    • + TNF-a inhibitor (infliximab)
  • Complications: bowel obsturction, fistula, abscess
    • Require surgery
    • Vitamin and mineral replacement may be neccessary
224
Q

What is Pyostomatitis Vegetans?

A

Oral manifestation of Ulcerative Colitis or Crohn’s Disease

225
Q

What is the classic lesion of pyostomatitis vegetans?

A
  • Yellowish, slightly elevated, linear, serpentine “snail tracks” set on an erythematous base
  • Variable discomfort
226
Q

What is the histology of Pyostomatitis Vegetans?

A
  • Marked edema with intraepithelial eosinophilic abscesses
    • ​normally neutrophils in abscesses
227
Q

What is the treatment for Pyostomatitis Vegetans?

A
  • sulfasalazine (anti-inflammatory) or systemic steroids
    • Clears the oral lesions

Oral Pathology Exam 2 (7 decks)

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