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Oral Pathology > Oral Bacterial and Fungal Infections > Flashcards

Oral Bacterial and Fungal Infections Flashcards

1
Q

Etiology of streptococcal infections…

A
  • Lancefield group A beta-hemolytic streptococcus (S. pyogenes) causes streptoccal pharyngitis, scarlet fever, and cellulitis. It is also responsible for acute rheumatic fever and post-streptococcal glomerulonephritis.
  • Group A streptococci produce erythrogenic exotoxins
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2
Q

Lancefield group A beta-hemolytic streptococcus (S. pyogenes) causes…

A
  • Streptococcal pharyngitis
  • Scarlet fever
  • Cellulitis
  • Acute rheumatic fever
  • Post-streptococcal glomerulonephritis
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3
Q

Group A streptococci produce…

A

Erythrogenic exotoxins

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4
Q

Diagnosis of streptococcus pyogenes…

A
  • Group A streptococcal antigens are detected by RADT (rapid antigen detection tests) on a throat swab.
  • Culture is more sensitive than RADT
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5
Q

Treatment for scarlet fever

A

Antibiotics (penicillin or erythromycin)

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6
Q

Complications of scarlet fever

A

Acute rheumatic fever and post-streptococcal glomerulonephritis.

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7
Q

Demography of scarlet fever…

A

Occurs mostly in children, but is less common in recent years

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8
Q

Incubation period for scarlet fever…

A

The incubation period ranges from one to 7 days

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9
Q

Onset of fever in scarlet fever occurs when?

A

Fever starts abruptly on the second day and lasts about 6 days

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10
Q

Characteristic circumoral pallor is evident in…

A

Scarlet Fever

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11
Q

Scarlet fever infection causes…

A
  • Pharyngitis
  • Tonsillitis
  • Stomatitis
  • Lymphadenitis
  • Systemic manifestations
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12
Q

The erythrogenic toxins produced by S. pyogenes in Scarlet Fever causes what?

A
  • Causes vascular dilatation and damage, which is responsible for the erythematous macular “sandpaper” rash
  • Usually clears within one week and then the skin desquamates over a period of several weeks
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13
Q

Paraoral and oral changes in Scarlet Fever involving the throat entails…

A

“Strep throat”:
• redness and swelling of the pillars, tonsils, uvula, and pharynx
• white or yellow patches of exudate on the tonsils
• (Tonsillitis and pharyngitis with a similar clinical presentation are also caused by common viral infections, often secondarily affected by bacteria)

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14
Q

Paraoral and oral changes in Scarlet Fever involving the tongue

A

Tongue appearance is characteristic:
• “Strawberry” tongue is due to edematous and hyperemic fungiform papillae projecting through a white coating
• “Raspberry” tongue develops when the white coat is lost and the red, swollen papillae are exposed
- The underlying mucosal surface is a glistening deep red.

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15
Q

Paraoral and oral changes in Scarlet Fever involving the soft palate

A

Scattered petechiae may be seen on the soft palate

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16
Q

Define cellulitis

A

• Cellulitis is an acute edematous inflammatory reaction which is rapidly spreading (rather than well-localized like an abscess)

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17
Q

How does virulent bacteria spread in Cellulitis?

A
  • Virulent bacteria, such as S. pyogenes
  • Produce enzymes that allow rapid spread through tissues and along fascial planes
  • Results in a firm, painful swelling
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18
Q

Appearance of cellulitis

A

The surface is discolored red or purple and there is regional lymphadenitis.

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19
Q

What is Ludwig’s angina?

A

This is a cellulitis involving the submandibular, sublingual, and lateral pharyngeal spaces.

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20
Q

Describe the spread of infection in Ludwig’s angina if the infection originates in the periapical tissues of lower incisors…

A
  • It penetrates the lingual plate above the level of the mylohyoid attachment, and thereby enter the sublingual space.
  • If it spreads posteriorly, it reaches the posterior border of the mylohyoid muscle and extends into the submandibular and lateral pharyngeal spaces.
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21
Q

Describe the spread of infection in Ludwig’s angina if the infection arises from the periapical tissues of a lower molar…

A
  • May have similar results as if the infection were to originate from lower incisors
  • Penetration of the lingual plate occurs below the mylohyoid attachment and infection may spread to involve all three spaces.
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22
Q

Clinical presentation of Ludwig’s angina

A
  • The area is brawny hard
  • When the tongue is pushed up and back, there may be respiratory obstruction
  • There are accompanying fever and malaise
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23
Q

What is Erysipelas?

A

This is a sharply demarcated cellulitis, often due to trauma

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24
Q

What causes Erysipelas?

A

It is usually caused by S. pyogenes.

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25
Q

Butterfly pattern similar to that seen in lupus erythematosus is visible on the face, especially the malar area, over the bridge of the nose in this disease…

A

Erysipelas

** Note: the butterfly pattern may also extend onto the labial mucosa

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26
Q

Clinical presentation of erysipelas…

A
  • Edematous, hot, shiny, red, tender, slightly elevated plaque
  • May be an orange peel texture due to involvement of superficial lymphatics
  • Butterfly pattern on face
  • May have fever, chills, malaise
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27
Q

Necrotizing gingivostomatitis includes…

A
  • NUG (necrotizing ulcerative gingivitis)
  • NUP (necrotizing ulcerative periodontitis)
  • Necrotizing stomatitis

Note: They are similar clinically, histologically, and bacteriologically. They differ in underlying systemic factors and extent of necrosis.

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28
Q

Necrotizing ulcerative gingivitis (NUG) is limited to…

A

Gingiva with no loss of perio attachment

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29
Q

Necrotizing ulcerative periodontitis (NUP) is confined to…

A

Gingiva, PDL, and alveolar bone

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30
Q

Necrotizing stomatitis has progression beyond…

A

Progression beyond the mucogingival junction

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31
Q

Etiological factors of necrotizing gingivostomatitis

A
  • Microorganisms
  • Reduced host resistance
  • Atypical reaction to microorganisms
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32
Q

This is a “Fusospirochetal” infection…

A

Necrotizing Ulcerative Gingivitis (NUG)

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33
Q

“Constant flora” in NUG includes…

A
  • Treponema spp.
  • Selenomas spp.
  • Fusobacterium sp.
  • B. melaninogenicus ss intermedius (Prevotella intermedia)
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34
Q

“Variable flora” in NUG includes…

A

Heterogeneous bacterial types

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35
Q

Importance of spirochetes and fusobacteria in NUG

A
  • Presence of spirochetes and fusobacteria is not evidence of primary etiologic importance.
  • They occur in healthy mouths and mouths with “ordinary” gingivitis and chronic periodontitis.
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36
Q

Role of endotoxins in NUG

A

• Liberated by large masses of gram-negative bacteria
• May cause tissue destruction both by direct toxic effects and indirectly by activating and modifying host responses
- Indirectly, endotoxins may act as antigen and elicit immune reactions –> activate complement and release chemotoxins –> activate macrophages and lymphocytes –> interfere with cytokines they produce

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37
Q

What disease is known as “tench mouth” and why?

A 
• NUG
• It was common in WWI when solders were exposed to:
     - Smoking
     - Local trauma
     - Poor oral hygiene
     - Poor nutrition
     - Lack of sleep
     - Recent illness
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38
Q

Etiology of necrotizing ulcerative gingivitis (NUG)

A
  • Microorganisms
  • Impaired local and systemic host resistance are of major importance in this disease
  • Stress: steroid hormones –> alter T4/T8 ratios –> decreased neutrophil chemotaxis & phagocytosis
  • HIV infection is by far the most important predisposing systemic disease
  • Measles, chicken pox, tuberculosis, malaria, and infectious mononucleosis are important in some cases
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39
Q

Differential diagnosis for NUG

A
  • Primary herpetic gingivostomatitis

* Desquamative gingivitis (MMP etc)

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40
Q

Histology of NUG

A

There is non-specific intense inflammation covered by coagulation necrosis and colonies of microorganisms.

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41
Q

Treatment for NUG

A
  • Debridement
  • Rinses
  • Antibiotics
  • Treat any underlying disease
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42
Q

What rinses can be used to treat NUG?

A

Chlorhexidine, available commercially as Peridex

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43
Q

What antibiotics can be used to treat NUG?

A 
• Metronidazole
     - Used against a wide range of anaerobic bacteria and protozoa
• Tetracycline
• Penicillin
• Erythromycin
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44
Q

Prognosis for NUG

A
  • After appropriate therapy, NUG usually resolves more rapidly than most forms of periodontal disease.
  • NUG may develop into NUP or necrotizing stomatitis.
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45
Q

Clinical features of gingiva in NUG

A

• Gingivae intially red (hyperemic) and painful.
- Linear gingival erythema
• Later, punched out erosions of interdental papillae
• Covered by grey necrotic pseudomembrane
• Ulcerations spread along gingival margin

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46
Q

Describe the linear erythema observed in NUG

A

The zone between the marginal necrosis and unaffected gingiva may exhibit a well demarcated narrow erythematous zone, sometimes designated as “linear erythema”

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47
Q

Discuss linear gingival hyperemia in NUG

A
  • Red band gingivitis
  • Bleeding and pain
  • In HIV infection
  • Chronic candidiasis infection?
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48
Q

Is there loss of periodontal attachment in NUG?

A

There is no loss of periodontal attachment (which occurs when NUG develops into NUP).

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49
Q

Other clinical features of NUG include…

A
  • Powerful odor

* Fever, malaise, lymphadenopathy, etc.

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50
Q

What is necrotizing ulcerative periodontitis (NUP)?

A
  • Similar clinical presentation to NUG, but also loss of clinical attachment and alveolar bone.
  • Destructive form of periodontitis.
  • Gingival ulceration and necrosis with rapidly progressing loss of periodontal attachment.
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51
Q

Most distinguishing features of NUP includes…

A
  • Rapid rate of attachment loss (loss of alveolar bone)

* Lack of response to conventional perio treatment

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52
Q

Additional clinical features of NUP….

A
  • Edema
  • Severe pain
  • Spontaneous hemorrhage
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53
Q

Pocket depth in NUP…

A

• Deep pockets are not seen because gingival necrosis coincides with alveolar bone loss

54
Q

NUP may develop into…

A

necrotizing stomatitis

55
Q

Treatment for NUP…

A
  • Failure to respond to standard treatment for chronic periodontitis suggests underlying disease.
  • Debridement requires removal of necrotic tissue and extensive providone-iodine irrigation
  • Antimicrobial therapy: chlorhexidine rinses with metronidazole in severe cases
  • Follow-up care and long-term maintenance are essential
56
Q

Synonyms for necrotizing stomatitis

A
  • Noma

* Cancrum oris

57
Q

Etiology of necrotizing stomatitis…

A
  • A rapidly progressive polymicrobial opportunistic infection caused by normal oral flora that become pathogenic during compromised immune status.
  • A destructive, necrotizing often fatal condition dominated by the same mixed fusospirochetal flora mentioned in NUG
58
Q

Mechanism for massive necrosis in necrotizing stomatitis…

A

The mechanism for massive necrosis has not been fully elucidated, but the bacteria appear to induce an uncontrolled release of cytokines.

59
Q

Where does necrotizing stomatitis mainly occur?

A
  • It occurs mainly in developing countries, especially in children with malnutrition and systemic diseases.
  • Occasional cases occurred in association with AIDS in this country.
  • The concept that it always develops from pre-existing NUG has been challenged.
60
Q

Necrotizing stomatitis often begins as ___ and it may extend into adjacent soft tissue to form areas of ___________ __________ _________.

A
  • NUG

* necrotizing ulcerative mucositis

61
Q

Location of necrotic zones in necrotizing stomatitis…

A

Necrotic zones may also occur in soft tissue not contiguous with gingivae, especially in areas of trauma

62
Q

Clinical features of necrotizing stomatitis

A 
• There are extensive areas of discolored necrotic tissue
• Initially, destruction involves soft tissue but it may spread into bone, causing osteomyelitis.
• Necrosis does not follow tissue planes but spreads through anatomic barriers such as muscles.
• Common manifestations include: 
     - severe pain
     - fetid odor
     - fever
     - malaise
     - tachycardia
     - increased respiratory rate
     - anemia
     - leukocytosis
     - regional lymphadenopathy
63
Q

Additional lesions in necrotizing stomatitis may occur in…

A 
Distant sites:
• scalp
• neck
• ear
• perineum
• vulva
64
Q

What is Vincent’s angina?

A

An ulcerative pharyngitis, which may occur with NUG but is more often separate from it.

65
Q

Treatment for necrotizing stomatitis

A
  • Local wound care
  • Penicillin and metronidazole
  • Control of underlying disease
66
Q

What is metronidazole?

A

An antibiotic against a wide range of anaerobic bacteria and protozoa

67
Q

Periodontal disease associated with HIV infection include…

A
  1. Necrotizing ulcerative periodontitis
  2. Necrotizing ulcerative gingivitis
  3. Necrotizing stomatitis
  4. Linear gingival erythema (probably a form of candidiasis)

Note: there may be altered host immunity in addition to diminished resistance

68
Q

Suggested organisms involved in periodontal disease associated with HIV infection include…

A
  • Borrelia
  • Gram-positive cocci
  • beta-hemolytic streptococci
  • C. albicans
  • Cytomegalovirus
69
Q

Stages of syphilis

A
  • Primary
  • Secondary
  • Latency
  • Tertiary
  • Congenital
70
Q

75% of primary and secondary syphilis occurred among ___ who have sex with ___.

A

• Men who have sex with men

71
Q

Initial exposure of syphilis entails…

A
  • T. pallidum penetrates intact mucosa
  • In hours, enters lymphatic & blood vessels
  • Causes systemic infection and metastatic foci (but not clinical disease) long before primary lesions appear.
72
Q

Oral lesions in syphilis during the primary stage

A
  • Chancre at site of inoculation, some weeks after exposure
  • Erythematous macule –> Papule –> Indurated nodule –> Central crater
  • +/- pain
  • Regional lymph nodes painful and enlarged
73
Q

How long do chancres last in primary syphilis?

A

~ 2 to 6 weeks

74
Q

_. _______ present in lesion and its exudate in primary syphilis

A

T. pallidum

75
Q

When do antibodies appear in the primary stage of syphilis?

A

Antibodies appear 1 to 4 weeks after chancre.

76
Q

Diagnosis of syphilis entails…

A
  • Spiral T. Pallidum is too thin to be seen with conventional stains on smear or biopsy. It can be seen with silver stains, dark-field examination and immunofluorescent techniques.
  • Only immunofluorescence is reliable in the mouth because other spiral organisms are present. Specific immunofluorescence antibody demonstrates T. Pallidum T. Pallidum in smear or tissue.
  • Non-specific serologic screening tests are positive after 3 weeks but negative during the latency period.
  • Specific serologic tests are positive throughout life.
77
Q

What are the non-specific serologic screening tests done to diagnose syphilis?

A
  • Venereal Diseases Research Laboratories (VDRL)

* Rapid plasma regain (RPR)

78
Q

What are the specific serologic tests done to diagnose syphilis?

A
  • Fluorescent treponema antibody absorption (FTA-ABS)

* T. Pallidum hemagglutination assays (TPHA)

79
Q

Histology of syphilis

A

• Histology is not specific
• Probably an immune response to T. pallidum
• Proliferative endarteritis in all stages:
- Endothelial proliferation and hypertrophy
- Intimal fibrosis
- Perivascular lymphoplasmacytic infiltrate

80
Q

Stage one syphilis histology entails…

A

• Chancre surface epithelium ulcerated
• Lamina propria:
- Increased vascularity
- Dense plasma cell & lymphocyte infiltrate in perivascular pattern

81
Q

Oral lesions in secondary syphilis include…

A
  • Usually multiple lesions
  • May appear before chancre resolves
  • Mucous patches. Mucosa appears grey-white due to intense exocytosis and spongiosis. Necrosis of this epithelium produces an ulceration which is irregular in outline. It is surrounded by erythema. They may be multiple and sometimes painful. “Snail-track” ulcers are confluent mucous patches.
  • Papules (some of which are “split papules”)
  • Condyloma lata are papules which enlarge to become red-brown, broad based elevations having a flat top with a lobulated or warty surface. They are up to 3 cm in diameter. The surface exhibits papillary epithelial hyperplasia. The connective tissue shows endarteritis obliterans and perivascular cuffing with plasma cells. It is teeming with spirochetes.
  • Lues maligana occurs in immunocompromised cases. There are necrotic ulcerations on the face and scalp. The oral cavity is affected in up to 30% of cases.
82
Q

Describe the mucous patches found in secondary syphilis…

A
  • Mucosa appears grey-white due to intense exocytosis and spongiosis.
  • Necrosis of this epithelium produces an ulceration which is irregular in outline.
  • It is surrounded by erythema.
  • May be multiple and sometimes painful
  • “Snail-track” ulcers are confluent mucous patches.
83
Q

Describe the condyloma lata that are found in secondary syphilis…

A
  • Papules which enlarge to become red-brown, broad based elevations
  • Flat top and lobulated or warty surface.
  • Up to 3 cm in diameter.
  • Surface exhibits papillary epithelial hyperplasia.
  • Connective tissue shows endarteritis obliterans and perivascular cuffing with plasma cells.
  • Teeming with spirochetes
84
Q

Describe Lues maligna which is found in secondary syphilis…

A
  • Occurs in immunocompromised cases
  • Necrotic ulcerations on the face and scalp
  • Oral cavity is affected in up to 30% of cases
85
Q

After second stage of syphilis, latent period can range from _ to __ years

A
  • 1 to 30 years

* The tertiary stage occurs in 1/3 of patients

86
Q

Tertiary syphilis histology …

A
  • Surface ulceration with peripheral pseudoepitheliomatous hyperplasia
  • Underlying necrotizing granulomas
  • Organisms very difficult to identify
87
Q

Oral lesions in tertiary syphilis include…

A
  • Oral gummas start as small, firm, painless nodules, most in the palate or tongue.
  • Lesions are rubbery due to a semi-firm type of necrosis. This results in ulceration which may heal after several months.
  • Interstitial glossitis is thought to be result of contracture of lingual musculature after healing of gummas. Lobulated and irregular lesions may reach several cms in diameter.
  • Sometimes, the necrotic tissue in the ulcer base sloughs away leaving a punched-out defect. In the palate, this may produce an oro-nasal fistula.
  • Syphilitic (luetic) glossitis presents as a smooth, bald (depapillated) on the dorsum of the tongue with areas of leukoplakia. Microscopically, there is diffuse epithelial atrophy, loss of lingual papillae and hyperkeratosis. Surface epithelial premalignant and malignant changes are far less common than in the past due to the decline in late stage syphilis. (Arsenical agents and heavy metals used to treat syphilis before antibiotics may have caused some of the earlier cancers)
88
Q

Describe the oral gummas observed in tertiary syphilis…

A
  • Small, firm, painless nodules, most in the palate or tongue.
  • Lesions are rubbery due to a semi-firm type of necrosis. Ulceration may heal after several months.
89
Q

Describe interstitial glossitis observed in tertiary syphilis…

A
  • Thought to be result of contracture of lingual musculature after healing of gummas.
  • Lobulated and irregular lesions may reach several cms in diameter.
  • Sometimes, the necrotic tissue in the ulcer base sloughs away leaving a punched out defect.
  • In the palate, this may produce an oro-nasal fistula.
  • Microscopically, there is surface ulceration with peripheral pseudoepitheliomatous hyperplasia and underlying necrotizing granulomas. Organisms are very difficult to identify.
90
Q

Describe the syphilitic (leutic) glossitis observed in tertiary syphilis…

A
  • Smooth, bald (depapillated) on the dorsum of the tongue with areas of leukoplakia
  • Microscopically, there is diffuse epithelial atrophy, loss of lingual papillae, and hyperkeratosis.
  • Surface epithelial premalignant changes are far less common than in the past due to the decline in late stage syphilis. (Arsenical agents and heavy metals used to treat syphilis before antibiotics may have caused some of the earlier cancers.)
91
Q

Residual stigmata of congenital syphilis include…

A
  • Hutchinsonian teeth
  • Abnormal facies: frontal bossing, saddle nose, small maxilla, rhagades (linear scars or furrows at corners of mouth and nose due to secondary bacterial infections of early facial skin lesions).
  • Nerve deafness
  • Optic atrophy
  • Corneal opacities (due to past interstitial keratitis)
  • TRIAD: eyes, ears, and teeth
92
Q

What is Hutchinsonian teeth?

A
  • Enamel hypoplasia of permanent teeth which start to calcify during first year.
  • Hutchinson’s incisors: small, barrel-shaped, tapered towards incisal edge which is notched.
  • Moon molars: dome-shaped crown
  • Mulberry molars: narrow crown with multiple small nodules (“cusps”)
93
Q

Oral tuberculosis…

A
  • Extrapulmonary lesions are more likely to occur in AIDS patients than in others.
  • Usually 2nd to pulmonary disease.
  • Dissemination via infected sputum.
  • Occasionally lymphohematogenous (exogenous is exceedingly uncommon).
  • Oral mucosal lesions: irregular, indurated erythematous or ulcerated nodules which are often painful.
  • Osteomyelitis: hematogenous or due to entry, via a tooth, into periapical tissues, and then into bone.
  • Cervical lymph nodes are the most common site in the head and neck.
94
Q

Describe scrofula, which is observed in tuberculosis..

A

• Mycobacterial lymphadenopathy of oropharyngeal and cervical nodes.
• Nodes may caseate with sinus tracts
• Nontuberculous mycobacterial infection
- Usually from contaminated milk

95
Q

Etiology of leprosy (Hansen’s disease)

A
  • Mycobacteria leprae which is tropic for histiocytes and Schwann cells. It was believed to localize in cool sites, but that concept has been challenged.
  • Involvement of Schwann cells leads to sensory loss.
  • Exposure to Mycobacteria leprae rarely causes disease because the organism has low infectivity.
96
Q

Forms of leprosy (Hansen’s disease).

A
  • Paucibacillary (tuberculoid): hypersensitivity to the organism. Occurs in patients able to mount a strong immune response. It is much more localized than the lepromatous form. This is a granulomatous inflammatory response. Limited number of well-circumscribed nodules.
  • Multibacillary (lepromatous): this occurs when there is reduced cell-mediated immune response. Organisms proliferate in huge foamy histiocytes (Lepra cells). Clinically, there are many poorly-demarcated macules, plaques, and nodules.
97
Q

Clinical features of leprosy (Hansen’s disease)

A
  • Face: Leonine appearance due to sagging skin (caused by coalescence of nodules). Also loss of eyebrows and pendulous earlobes.
  • Nose: collapse of nasal bridge and perforation of palate.
  • Oral: nodules (lepromas) which are red or yellow, hard or soft, sessile, often ulcerated. They heal by scarring, which results in microstomia. There is destruction of the premaxilla, odontodysplasia leprosa (in children), loose teeth, and gingival hyperplasia.
98
Q

Diagnosis for leprosy (Hansen’s disease)

A

• Demonstration of acid-fast organisms in smear or tissue sections.

99
Q

Treatment for leprosy (Hansen’s disease).

A

Cure can be achieved by a 3-drug combination (rifampin, dapsone, and clofazimine) for 2 years. There are now fewer than one million cases world wide.

100
Q

Etiology of actinomycosis…

A
  • This is a clinical syndrome caused by a group of anaerobic, gram positive, filamentous, branching higher bacteria.
  • Actinomyces israeli is the most common cause in humans.
  • Sulfur granules are 1 to 4 mm, firm yellow granules which represent bacterial colonies. They drain in pus from multiple sinuses in infected sites but are also found in healthy mouths in tonsillar crypts, plaque, calculus, necrotic pulps.
  • The disease occurs when the bacteria penetrate deeper tissues.
101
Q

Diagnosis of actinomycosis…

A
  • Culture (positive in only 50% of cases) or by finding typical colonies in inflammatory lesions.
  • Each actinomycosis species is identified by fluorescein-isothiocyanate species specific conjugate antisera.
  • Histology: acute suppurative inflammation with colonies which consist of central basophilic mycelium with peripheral radiating eosinophilic filaments (“ray fungus”)
  • Colonies are surrounded by suppurative necrosis, numerous white blood cells including pmn’s, foamy macrophages, occasional giant cells, granulation tissue and fibrosis.
102
Q

Clinical presentation of actinomycosis…

A
  • 60% of all cases are cervicofacial.
  • Portals of entry are deep soft tissue trauma, caries/P.A.P., and tooth extractions.
  • Classical presentation: several woody (fibrotic) circumscribed swellings which eventually break down, forming a central softer abscess and discharging yellow fluid with sulfur granules via sinus tracts.
  • Initially, soft tissue is involved more often than bone, but osteomyelitis may develop. Radiographs may show ill-defined areas of radiolucency (sometimes with a reactive opaque component).
  • Necrotic pulp –> periapical infection –> alveolar abscess –> skeletal muscle –> draining sinuses on the surface of the skin or mucosa
  • When soft tissue overlying the infected mandible is involved, it is known as “lumpy jaw”
  • An acute (non-fibrotic) form of the disease sometimes occurs as localized abscesses
103
Q

Treatment of actinomycosis

A

Surgical drainage and antibiotics (primarily penicillin) for long periods.

104
Q

Etiology of Candidiasis

A

• Candida is the genus. C. albicans is the species which most often causes oral disease.
• It is an oral commensal.
• C. albicans is a yeast-like fungus which invades epithelium in hyphae or pseudohyphae form, inducing
proliferative reaction and plaque.
• Local predisposing factors: smoking, dentures, xerostomia, broad spectrum antibiotics.
• Systemic predisposing factors: cell mediated immune deficiency, HIV, other debilitating diseases, iron
deficiency, steroids, extremes of age.
• When organisms become pathogenic, they become intracellular parasites and (some authorities claim)
cause epithelial dysplasia.

105
Q

Classifications of Candidiasis

A

• White removable plaques (pseudomembranous)
• chronic white adherent plaques (hyperplastic)
- Candidal leukoplakia
- Chronic mucocutaneous candidiasis
• Red macules (“erythematous/atrophic”)
- Multiple acute red macules
- Multiple chronic red macules with or without removable white plaques (“Chronic multifocal”)
- Denture stomatitis
• Other distinctive clinical presentations
- Median rhomboid glossitis (central papillary atrophy of tongue)
- Angular cheilitis/cheilosis/stomatitis (Perleche)

106
Q

Candidiasis classification: white removable plaques (pseudomembranous candidiasis i.e. “thrush”)

A
  • Removable, soft, creamy, slightly raised, white or blue-white flecks or confluent plaques. Underlying mucosa may appear normal, red, or ulcerated, and may bleed slightly
  • Usually asymptomatic, but sometimes there is mild burning sensation and a bad taste
  • It is seen in association with other forms of candidiasis
  • Acute onset when induced by broad-spectrum antibotics
  • Chronic (slow onset, long standing) in debilitating conditions
107
Q

Chronic white adherent plaques (“chronic hyperplastic candidiasis”)

A

White, tough, adherent plaques seen in candidal leukoplakia and in chronic mucocutaneous candidiasis

108
Q

Candidal leukoplakia

A
  • In candidal leukoplakia, the adherent white plaques are surrounded by erythema and/or are speckled.
  • This form occurs most at the commissures, dorsal surface of the tongue, and palate.
  • Such lesions may have increased frequency of dysplasia.
  • It is not known whether the organism produces dysplasia or secondarily infects previously altered epithelium.
109
Q

Chronic mucocutaneous candidiasis

A
  • Oral chronic white adherent plaques (chronic hyperplastic candidiasis) are accompanied by candidiasis of nails, skin, and other mucosae.
  • There are several types some of which are inherited.
  • Oral candidiasis is prominent in Familial CMC (AR), Diffuse CMC, and APECS.
110
Q

What is autoimmune polyendocrine candidiasis syndrome (Candidiasis endocrinopathy syndrome)?

A 
• Transmitted on an autosomal recessive basis
• Autoimmune endocrinopathies include:
    - Thyroiditis
    - Hypoparathyroidism
    - Addison's disease
    - Diabetes mellitis
    - Ovarian pathology
• There is chronic mucocutaneous candidiasis of the mucosae, skin, and nails.
• Other stigmata include:
    - Enamel hypoplasia
    - Pernicious anemia
    - Achlorhydria
    - Malabsorption
    - Eye lesions
111
Q

Candidiasis classification: Multiple acute red macules (“erythematous/atrophic)

A
  • Antibiotic sore mouth is due to broad spectrum antibiotics
  • Similar lesions occur following loss of the removable white plaques (seen in thrush)
  • Mucosa is red, edematous, and may be sore (burning)
  • When the tongue is affected, there is loss of lingual papillae.
112
Q

Candidiasis classification: multiple chronic red macules (“Chronic multifocal)

A
  • May present with or without removable white plaques
  • Red lesions on the dorsal tongue (central papillary atrophy), palate and angles of the mouth
  • Burning sensation
  • This occurs in HIV and may occur in xerostomia, other debilitating conditions such as diabetes mellitus and with immunosuppressive agents including steroids.
113
Q

What is denture stomatitis?

A
  • “Denture sore mouth” is usually classified as another example of “erythematous or atrophic” candidiasis.
  • Fiery red palate is sharply outlined by the shape of the denture. Pain or burning sensation is noted at times.
  • The tight-fitting denture blocks access of saliva to that area. Organisms may produce enzymes which provoke inflammation and/or cause hypersensitivity. Other possible factors include denture trauma, poor oral hygiene, and systemic factors.
  • Usually smears from the denture fitting surface are positive for hyphae, but those from mucosa are not.
  • This condition is often seen with thrush flecks, angular cheilosis, or palatal hyperplasia.
  • It may be treated with Nystatin cream applied to the mucosa and the fitting surface of the denture
114
Q

Median rhomboid glossitis (central papillary atrophy of the tongue)

A
  • Clinically, there is a smooth area in the midline of the dorsal surface of the tongue, immediately anterior to the sulcus terminalis. The area may be red or pink and slightly sore. It is depapillated but in some (hyperplastic) cases there is a lobulated elevation.
  • Historically, it was believed to be a developmental defect (failure of tuberculum impar to fuse with lateral processes of the tongue).
  • It occurs alone, or as part of chronic multifocal candidiasis.
  • Histologically, there is loss of lingual papillae but there is also extensive acanthosis with long anastomosing rete ridges.
  • Hyphae are usually seen in the superficial layers of the epithelium.
115
Q

Angular cheilitis

A

• Also known as cheilosis/stomatitis (Perleche)
• Erythema & fissures at corners of mouth which appear wrinkled and macerated; they do not extend onto the mucosa. They ulcerate and crust. The area feels dry and burning
• Seen with all other forms of candidiasis, particularly chronic multifocal candidiasis, but often occurs alone.
• Other etiologic factors include:
- Other microorganisms (Staphylococcus aureus, etc.)
- Overclosure
- Dietary deficiencies, e.g. riboflavin
- Debilitating diseases

116
Q

What is cheilocandidiasis?

A

Circumoral fissuring and discoloration occur in people with severe lip-sucking habits.

117
Q

Candidiasis variants in HIV include…

A
  • White removable (Pseudomembranous)
  • Multiple chronic red macules (chronic multifocal)
  • Chronic white adherent (Chronic hyperplastic)
  • Angular cheilitis
118
Q

Compare non-HIV candidiasis vs HIV candidiasis…

A
  • Compared with non-HIV cases, HIV candidiasis is more often multifocal, chronic, and resistant to treatment.
  • Histology shows that hyphae evoke only a weak inflammatory cell reaction.
119
Q

Treatment for candidiasis includes…

A
  • Nystatin and clotrimazole are topical agents.
  • Peridex (chlorhexidine) mouthrinse.
  • Fluconazole and itraconazole are used systemically as tablets and/or intravenously
  • Treat underlying cause
120
Q

Diagnosis for candidiasis includes…

A
  • Exfoliative cytology
  • Tissue sections
  • Culture
121
Q

Discuss exfoliative cytology in the diagnosis for candidiasis

A 
• Pseudohyphae (elongated yeast cells) or hyphae (2m diam)
• Stained smears
   - Magenta with PAS
   - Black with silver-based stains
• KOH
   - 10-20% KOH lyses epithelial cells
   - Yeasts & hyphae more resistant
   - Disadvantages
          • No permanent record
          • Organisms stain less intensely than with PAS
122
Q

Discuss tissue sections in the diagnosis for candidiasis

A
  • Pseudohyphae (elongated yeast cells) or hyphae (2u diameter) within thick perakeratin
  • They stain black with silver-based stains or magenta with PAS
  • Neutrophil microabscesses associated with the organisms
  • Elongated rete ridges
  • CIC’s in superficial lamina propria
123
Q

Discuss culture in the diagnosis of candidiasis…

A
  • Colonies grow on Sabouraud’s agar in 2-3 days of incubation at room temperature
  • Immunofluorescent techniques may be needed if colonies fail to grow.
124
Q

Most are secondary to pulmonary disease…

A

Deep fungal infections of the mouth

125
Q

Endemic pathogenic fungi cause…

A
  • Such as Histoplasmosis capsulatum

* Intense chronic inflammation and granulomas in normal hosts

126
Q

Opportunistic fungi in immunosuppressed hosts cause…

A
  • Life-threatening invasive infections
  • Tissue necrosis, hemorrhage, and vascular occlusion with little or no inflammatory response.
  • Macrophages stuffed with organisms. NO GRANULOMAS (unlike pathogenic fungi)
127
Q

Histoplasmosis capsulatum infection

A
  • Infection by inhalation of soil particles contaminated by bird droppings
  • It is a pathogenic fungus which occasionally causes isolated pulmonary disease in previously healthy people, especially along the Ohio and Mississippi rivers and in the Caribbean.
  • Disseminated disease in immunosuppressed individuals.
  • Oral lesions are secondary to pulmonary or disseminated disease.
  • Oral lesions are typically ulcerated, often irregular, mucosal enlargements with ill-defined margins.
128
Q

Zygomycosis (Mycormycosis)

A

• Occurs in people with advanced systemic diseases (such as diabetes mellitis)
• Inhalation of spores rarely causes disease in healthy people
• Opportunistic infection caused by fungi of class Zygomycetes, order Mucorales
- Including genera Absidia, Mucor, Rhizomucor, and Rhizopus
• In bread molds and decaying vegetation
• Hyphae invade walls of blood vessels, causing thrombi and necrosis

129
Q

Diagnosis of deep fungal infections…

A
  • Best diagnosed by culture
  • Morphology of stained organisms in tissue sections using PAS or silver stains is also useful.
  • There are serologic tests for antibodies and antigens.
130
Q

Zygomycetes disease course…

A 
Zygomycetes (especially Mucor)
Aspergillus & Cryptococcus
--> Susceptible host
--> Maxillary "sinusitis"
--> Vessel blockage or compression
--> Black necrotic tissue
--> Palatal perforation (often fatal)
131
Q

Palatal perforation may be due to…

A 
• Malignancies
   - Salivary gland malignancies
   - Extranodal T cell lymphoma
   - Squamous cell carcinoma
   - Melanoma
• Wegener granulomatosis
• Infections
   - Zygomycosis (murcormycosis)
   - Gummas of tertiary syphilis
   - Leprosy
• Cocaine use
• NSM rarely causes perforation

Oral Pathology (9 decks)

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