Infectious diseaes Kumar Flashcards

(326 cards)

1
Q

What is Human herpes virus (HHV)

what is it’s 8 types?

A

Large family of double stranded DNA viruses

❏ HHV‐1: HSV‐1‐Herpes simplex virus type 1 (most common in oral cavity)
❏ HHV‐2: HSV‐2‐Herpes simplex virus type 2
❏ HHV‐3: VZV‐Varicella zoster virus
❏ HHV‐4: EBV‐Epstein Barr virus
❏ HHV‐5: CMV‐Cytomegalovirus
❏ HHV‐6: Sixth disease/Roseola (commonly seen in children, spreads through saliva and respiratory droplets)
❏ HHV‐7: Roseola
❏ HHV‐8: KSHV‐Kaposi sarcoma‐associated herpesvirus

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2
Q

What is the Mode of infection of HHV?

A

Primary infection → Latency → Reactivationn → Recurrent infection

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3
Q

After the primary infection the HHV‐1/HSV1 stays in ————

A

Sensory ganglia

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4
Q

After the primary infection the HHV‐2/HSV2 stays in ————

A

Sensory ganglia

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5
Q

After the primary infection the HHV‐3/VZV stays in ————

A

Sensory ganglia (dorsal root ganglia)

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6
Q

After the primary infection the HHV‐4/EBV stays in ————

A

B‐Lymphocytes

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7
Q

After the primary infection the HHV‐5/CMV stays in ————

A

Myeloid cells, salivary gland cells, endothelium

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8
Q

After the primary infection the HHV‐6 stays in ————

A

CD4+ T‐Lymphocytes

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9
Q

After the primary infection the HHV‐7 stays in ————

A

CD4+ T‐Lymphocytes

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10
Q

After the primary infection the HHV‐8 stays in ————

A
  • *B‐lymphocytes (latency)**, **endothelial cells (Kaposi
    sarcoma) **
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11
Q

Herpes Simplex Virus

types

&

locations

A

Type 1‐ adapted to oral, facial, and ocular areas (more common in
oral cavity)
Type 2‐ adapted to genital area
❏ Other sites may also be affected
Herpetic whitlow (finger)
Herpes gladiatorum (wrestlers)
Herpes barbae (beard area)

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12
Q

Herpes Simplex Virus

primary infection

A

○ Acute/Primary Herpetic Gingivostomatitis
○ The easy way to remember where the ulcerations occur?
➢ gingiva and oral cavity

gingivo (=gingiva or fixed keratinized mucosa)

+
stoma (= the movable part of the oral cavity where the CT is
looser, including the labial and buccal mucosa, and the
tongue
).

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13
Q

Herpes Simplex Virus

Recurrent infection

A

two manifestations:

  1. Herpes labialis: occurs on the vermillion border
  2. Intra‐oral herpes: occurs ONLY on the fixed keratinized
    mucosa (mucosa that doesn’t move around) MEMORIZE
    THIS
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14
Q

What does it mean if a person has a primary infection?

A

 They don’t have antibodies

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15
Q

Who’s the typical group that will get primary herpetic gingivostomatitis?

A

 Children and young patients

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16
Q

What is this infectious disease?

Describe it

A

HSV‐1: Primary
Infection

it is a raised blister/papule on the
vermilion
The bottom arrow pointing to a mucosal
ulcer w/ tan pseudomembrane.

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17
Q

What is this infectious disease?

Describe it

A

HSV 1- Primary Herpetic
Gingivostomatitis

Ulcer with an erythematous halo (top two arrows). We
also have ulcerations that are irregular in shape on the gingiva
(bottom two arrows).

❏ Clinical Features:

  • Cervical lymphadenopathy
  • Chills
  • Fever
  • Nausea
  • Anorexia
  • Irritability
  • Sores in mouth
  • Ulcerations on fixed and movable mucosa
  • Variable number of lesions
  • Ulcers coalesce and form larger irregular ulcerations
  • Gingiva enlarged and painful
  • Resolution in 5‐7 days
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18
Q

What is this infectious diseease?

What is its pathogensis ?

A

HSV‐1: Primary
Infection

pathogensis

❏ Usually young age
❏ Often asymptomatic
❏ Symptomatic = Primary herpetic gingivostomatitis
❏ In adults is usually pharyngotonsillitis (back of throat)
❏ Spread through infected saliva or active lesions
❏ Incubation period = 3‐9 days

These photos represent

gingivostomatitis

multiple irregularly shaped
ulcers present on the fixed and movable mucosa, bilaterally

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19
Q

What is this infectious disease?

What probably this patient also have?

A

HSV1: primary herpetic gingivostomatitis

there are multiple irregularly shaped
ulcers present on the fixed and movable mucosa –> most likely
diagnosis is primary herpetic gingivostomatitis since the patient has
fever and malaise.

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20
Q

How is Primary HSV
(Herpes Simplex) diagnosed?

A

❏ Clinical diagnosis → based on putting all the features together
❏ Culture (may take 2 weeks) → not worth it
❏ Tissue biopsy → very invasive
❏ Cytologic smear (less invasive)
○ easiest bc you take a popsicle stick to scrape an ulceration
then you put those cells on a slide, you send it to a
pathologist after fixing the cells with some alcohol then you
can see the virally‐altered cells
❏ Serologic testing→ to look for antibodies 4‐8 days after they were
exposed.

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21
Q

HSV‐ Histopathology

A

❏ Molding
❏ Margination
❏ Multinucleation
❏ Also Tzanck cells

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22
Q

What is a
definitive diagnosis for HSV1 Herpes simplex

A

HSV‐ Cytology‐
Papanicolaou Stain
(PAP)

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23
Q

How to interpere HSV‐ Laboratory
Results based on IGg and IGm a

A

If you have positive IgM and negative IgG → that means it’s an acute
recent infection.
Then you have to wait 4‐6 weeks
If you do the serology then and get positive IgG and negative IgM → that means the person has the established infection.

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24
Q

What is the treatment of Primary Herpetic
Gingivostomatitis ?

A
  • ❏ Supportive/Palliative Treatment
  • ❏ Fluids, nutrition, rest, avoid spreading to others
  • ❏ Avoid touching eyes, genitals
  • ❏ Possible referral to MD if infant is not drinking because of pain
  • ❏ Medications:
  1. Topical anesthetic (OTC vs Rx)
  2. Mucosal coating (OTC)
  3. Analgesic (OTC vs Rx)
  4. Antiviral (Rx)
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25
What are the medications used to treat Primary HSV?
**❏ OTC Magic Mouthwash Formulation:** helps the person to actually be able to eat bc they have so many ulcerations ○ 1 Part‐ Diphenhydramine/ Benadryl (anticholinergic) 12.5mg/5mL elixir ○ 1 Part‐ Lidocaine (topical anesthetic) ○ 1 Part‐ Magnesium hydroxide/ Maalox (mucosal coating agent) ○ Disp: 4 oz bottle ○ Label: Rinse with 5mL every 2 hours for 30 sec. then spit out **❏ Rx‐Topical Anesthetic** ○ Lidocaine 2% viscous solution\* (viscous lidocaine) ○ Disp: 100mL bottle ○ Label: Rinse with 10 mL for 2 minutes and spit out \*May diminish the gag reflex therefore better suited for older patients‐ shouldn’t be prescribed to kids. Remember serious sideeffects of seizures and methemoglobinemia in pediatric population. **❏ OTC Analgesic** ○ Acetaminophen (Tylenol) OR ibuprofen (NSAID) suspension/ tablets as directed for body weight ❏ **Rx Antivirals** ○ Generally only indicated for immunocompromised or dehydrated patients ○ Limited evidence for other cases‐ see Cochrane Oral Health Group Review\* (\*Amended recently) ○ Oral acyclovir suspension (Zovirax) is typically used ○ 15 mg/kg up to adult dose of 200mg ○ Rinse and swallow, 5 times a day for 5‐7 days
26
HSV-1 RECURRENT INFECTION
* §**Secondary herpes** * §Mild, self-limiting * §Vermilion border * §Intraorally on **fixed keratinized mucosa** * §7-10 days * **§Unilateral** * § Prevalence‐15‐45% * 90% of adults have the antibodies, but 15‐45% of them can get recurrent herpes. Most of us have the antibodies, but we never exhibited the primary infection or a recurrent infection***.** * **§ 1‐6 outbreaks a year**
27
**Reccurent HSV-1** Latency place is --------
**trigeminal ganglion**
28
What are the Stages of recurrent Hsv-1?
Prodrome►papules►vesicles►ulcer►crust►heals►no scar
29
What is this infectious disease? describe it
**recurrent Hsv-1/Recurrent herpes** It is raised (papule), so it’s in the middle stage
30
What are some of **triggers** of the Recurrent HSV?
* Old age, Allergy * UV light ,Trauma * Physical / emotional stress, Dental treatment * Fatigue, Respiratory illnesses * Heat, Fever * Cold, Menstruation * Pregnancy, Systemic Diseases * Malignancy
31
What is HSV‐ Recurrent Infection‐ Shedding ?
Asymptomatic shedding can occur in seropositive patients ❏ More common after surgical procedures and in immunocompromised patients ❏ We need to take Universal precautions
32
What is this infectious disease? describe it
Recurrent HSV-1 papule bc its raised
33
What is this infectious disease? describe it
Recurrent HSV-1 crust → later crust comes off and then you'll have epithelialization underneath
34
What is this infectious disease? describe it
Recurrent HSV-1 Vesicle stage (unilateral)
35
What is this infectious disease? describe it
Recurrent HSV-1 **Bilateral** \> THIS IS KEY -differential diagnosis with a Staph infection that occurs periorally with kids -\> impetigo
36
What is this infectious disease? describe it
Recurrent HSV-1 This is recurrent intraoral herpes. We have punctate (point‐like) ulcerations which sometimes have clusters of coalescing ulcers. That’s the words you wanna use Other features of the ulcers: ○ Erythematous border ○ Irregular shape ○ Fixed mucosa ○ Unilateral
37
What is this infectious disease? describe it
Recurrent HSV-1 Punctuate ulceration erythematous border, irregular shape, fixed mucosa, unilateral
38
What is this infectious disease? describe it
**Recurrent HSV-1** healing stage cause you might see this one day
39
How to diagnose Recurrent HSV?
**❏** **Clinical**‐ if you see punctate ulcers unilaterally on the palate, it is usually recurrent herpes simplex. ❏ Culture (may take 2 weeks) ‐ takes too long ❏ Tissue biopsy‐ if it wasn't typical **❏ Cytologic smear**‐ the ideal way if you want a definitive diagnosis
40
What is the Treatment Recurrent HSV-1?
_❏ **Depends on severity/frequency**_ _❏ **Preventive/suppressive vs episodic/abortive strategies** Two types of treatment:_ **Preventive/Suppressive: taking antivirals everyday to prevent an outbreak** **Episodic: taking antivirals here and there to abort the process; episodic: abortive. _❏ Drugs used:_** ❏ *Antiviral agents* ❏ *Antiviral‐steroid combination agents* **_❏ Avoid precipitating factors, like use sunscreens – avoid any triggers_**
41
e At which stage should the abortive/ episodic treatment be done to avoid the outbreak?
❏ the **prodrome**, prodrome treatment is abortive \*\*remember this!\*\*
42
RECURRENT HERPES LABIALIS-RX TOPICAL/SYSTEMIC AGENTS
Topical like Acyclovir or Acylovir + steroid combination There are many OTC topical medications
43
suppressive or preventative therapy of Recurrent HSV-1
: taking antivirals everyday to prevent those 6 outbreak/year. There is modest evidence that systemic **acyclovir or valacyclovir** prevents recurrent herpes labialis these drugs tend to only affect virally‐altered cells. They don’t affect the mammalian cells; they’re very safe.
44
Episodic/ Abortive therapy of reccurent HSV1
❏ Episodic‐Occurring, appearing, or changing at usually irregular intervals ❏ Abortive‐Tending to cut short the course of a disease ○ Medication has to be taken during Prodrome ○ When the patient feels a burning, itching, and tingling
45
What are Recurrent Herpes Labialis‐ FDA Approved Topical Treatments?
❏ Rx: **Acyclovir cream 5% (Zovirax)** Disp: 5g tube Label: dab on lesion every 2 hours for 4 days ❏ Rx: **Penciclovir cream 1% (Denavir)** Disp: 5g tube Label: dab on lesion every 2 hours for 4 days ❏ Rx: **Docosanal cream (Abreva) OTC** Disp: 2g tube Label: dab on lesion five times per day for 4 days **Acyclovir and Penciclovir should be taken during the prodrome stage** ❏ Rx: Acyclovir 5%/ hydrocortisone 1% cream (Xerese) Disp: 5g tube Label: dab on lesion 5 times a day for 5 days ❏ Rx: Acyclovir buccal tablets (Sitavig) 50mg Disp: 2 dose pack Label: apply to canine fossa within 1 hour of symptoms (single dose)
46
What are Recurrent Herpes Labialis‐ FDA Approved Systemic Antivirals ?
**❏ Rx: Valacyclovir 1g tablets** Disp: 4 tabs Label: 2 tabs stat PO, then again in 12 hours (ie 2 doses) *Given during prodrome.* **❏ Rx: Famciclovir 500mg tablets** Disp: 3 tabs Label: 3 tabs stat PO
47
What are other Topical Agents for treating Recurrent Herpes Labialis?
❏ Ice ❏ L‐lysine ❏ Bioflavonoids ❏ Evaporants ‐ Desiccants ❏ Emollients ❏ Bioadhesives (Zilactin‐benzyl alcohol, topical pain reliever) ❏ Wound‐healing modification/ occlusive agents
48
What is this infectious disease?
**Atypical recurrent HSV** **❏ Immunocompromised host** Atypical recurrent HSV can have this appearance on the movable mucosa too, not just fixed
49
What is this infectious disease?
**HSV Associated Erythema Multiforme** ❏ Skin immune reaction in response to infection ❏HSV implicated in trigger for erythema multiforme where you get target lesions and crusted ulcerations on the lip ❏ need to prescribe :antiviral prophylaxis
50
HHV3 What is it's primary infection and Secondary infection known as?
❏ Primary infection **○ Varicella/ Chicken pox** ❏ Secondary infection **○ Zoster/ Shingles** ○ May affect oral cavity/ face if reactivation along distribution of V1/2/3
51
What is this infectious disease? describe it
HHV3 Varicella (chickenpox) It is caused by Varicella Zoster Virus Infection a typical macular, papular, vesicular rash – it’s bilateral
52
What is this infectious disease?
**Herpes Zoster/ Shingles** * It is affecting the intraoral region * and the maxillary branch. * Picture on the far right looks like recurrent HSV (cluster of coalescing ulcers) * Looking at the picture on the left you can determine it is NOT a recurrent intraoral herpes **because we have vesicles that opened up and crusted over on** **the skin.** **VZV histopathology is the same as HSV.** **VZV remains latent in the dorsal root ganglion** travels down the sensory nerves to skin upon reactivation. ❏ The reactivation presents as **a painful rash in one or two adjacent dermatomes that does not cross the midline.** ❏ The rash is **maculopapular** and **develops into vesicles.** ❏ One complication of zoster is **post‐herpetic neuralgia**: pain that persists in the area where the rash once was present.
53
HHV‐4 Latency? and What are the EBV inducded diseases?
**Epstein‐Barr Virus Infection** Latency in **lymphocytes** §Infectious mononucleosis §Oral hairy leukoplakia §Nasopharyngeal carcinoma §EBV mucocutaneous ulceration §Burkitt lymphoma §Other lymphomas (Hodgkin, post transplant)
54
What is this infectious disease?
**Infectious mononucleosis** **Epstein‐Barr Virus/EBV‐induced disease** The virus spreads through saliva, which is why it's sometimes called "kissing disease." Mono occurs most often in teens and young adults. However, you can get it at any age. Symptoms of mono include: **Fever** **Sore throat** **Swollen lymph glands** * when you have salivary transfer, your lymph nodes get swollen * people feel fatigue and fever * they have tonsilitis * can lead to the secretion of white or gray‐ green tonsillar exudate * they can get petechiae on the palate too.
55
What is this disease? Which virus causes it describe it
**Oral hairy leukoplakia** Epstein‐Barr Virus induced disease ❏ Corrugated white keratotic lesion on the lateral tongue in HIV+ people
56
What is this diseases? Which virus is asscoaited with it?
**Nasopharyngeal carcinoma** ❏ Associated w/ HHV‐4 (EBV) ❏ You might be one of the first people to detect this cancer – the first sign is the swelling of the lymph nodes In this case, these are late stages of the disease. *this photo from google*
57
What is this infectious diasese?
**EBV mucocutaneous ulceration** Very rare *Photos from google*
58
Which disease has Stary sky pattern histopathology?
**Burkitt Lymphoma** *caused by **EBV***
59
What is this diasese? which viruse causes it
**Burkitt Lymphoma** Epstein‐Barr Virus Infection * Fast growing tumor discovered by Dr. Burkitt * **High grade lymphoma B** **cells**‐ Usually affects the jaws of children. * **It is the fastest growing tumor/cancer**. * There is _translocation of c‐myc_
60
**HHV5** is it symptomatics? where does the diseases predominantly found? Latency?
**Cytomegalovirus Infection** ❏ Usually **asymptomatic** ❏ Symptomatic infections are nonspecific: **chills, fever, sore throat** ❏ What’s interesting here: ❏ When the cells are affected, they form these owl eyes – they are **nuclear inclusions and cytoplasmic inclusions.** ❏ Disease states found predominantly in: * **○ pregnancy/neonates** (congenital infection) * **immunocompromised patients,** particularly **transplant and HIV+** **patients** **​** ❏ Latency in **myeloid cells, salivary gland cells and endothelium**
61
What is this infectious disease?
**HHV 5** **Cytomegalovirus Infection** Histopathology look like an owl eyes means the cells are affected- they are **nuclear inclusions and cytoplasmic inclusions.**
62
What is this infectious disease? Desercibe it
HHV 5 Cytomegalovirus Infection When a person is immunocompromised, particularly those who’ve had a transplant or HIV+ patients, only these people will present with ulcerations It's very hard to identify based on photo alone - it's very nonspecific
63
**HHV‐8** What is it? Assoicated with what? How it evolved? How it is treated?
**Kaposi sarcoma--associated herpesvirus (KSHV)** **❏ Vascular neoplasm of endothelium** ❏ Associated with **immunosuppression** ❏ Usually evolves through 3 stages: **○ Patch►plaque►nodular** * **More commonly seen in patients with HIV infection.** * **Treated** with _topical agents and chemotherapy._
64
What is this disease? Describe it
**Kaposi sarcoma** HHV 8 Kaposi sarcoma on the skin: \>1cm Different color, so this is called a **patch**. Erythematous patches present on multiple areas of the face.
65
Kaposi sarcoma Histopathology
Histopathology shows **malignant endothelial cells proliferating.** There are tiny spaces. Extravasation of RBCs can be seen
66
What is this disease?
**Kaposi Sarcoma (HHV‐8)** Right photo: we see Patch, slightly raised plaque stage ○ This is different from **hemangioma** because if you press on it, it doesn’t blanch (where all the blood goes away, and it looks white) Left photo: Nodular is when it becomes very exophytic You need to do a biopsy for this because it looks irregular.
67
what are the charcterstics of HUMAN PAPILLOMA VIRUS (HPV) ?
§Small, non-enveloped **icosahedral DNA virus** that infects **skin or mucosal cells of humans.** **§Circular DNA** §198 types established **§High and low risk types** ## Footnote **‐ HIGH risk = CANCER ‐ LOW risk = WARTS**
68
What can HPV Epithelial Lesions cause? | (3)
▪ **Benign**: neoplasms of squamous epithelium ▪ **Pre‐malignant**: epithelial dysplasia – can lead to cancer ▪ **Malignant**: squamous cell carcinoma – infiltration of epithelial cells
69
What are HPV types that cause **Non‐genital Benign** Involving the **Skin**?
**2 & 4**
70
What are HPV types that cause **Non‐genital Benign** Involving **Mucosa**?
**6 & 11**
71
What are HPV types that cause **Genital Benign Lesions**?
**6, 11, 16, 18** ***(condyloma – can be malignant)***
72
What are HPV types that cause **Malignant & Potentially Malignant Disorders**?
**16, 18**
73
What are Routes of Transmission for HPV?
▪ **Sexual/non‐sexual direct contact** ▪ **Salivary transfer** ▪ **Contaminated objects (fomite)** – not well established ▪ **Autoinoculation** – child puts finger into mouth ▪ **Perinatal/pre‐natal transmission**
74
What is HPV Pathogenesis and Incubation period?
Incubation period: **3 weeks – 2yrs** ▪ Basic Explanation: Basal epithelial cell infection ► Genome replicates ► DNA released into stratum corneum ▪ Detailed Explanation: 1. HPV accesses and infects cells of the epithelial basal layer through breaks in the skin or mucosa 2. The virus becomes incorporated in the genome of the infected cell 3. The site of HPV integration into the cellular genome is in the general region of known oncogenes 4. The virus replicates during keratinocyte differentiation in the spinous and granular cell layers 5. A portion of the HPV genome encodes proteins that are capable of inducing cell proliferation and transformation **(E6, E7)**
75
HPV Pathogenesis – High Risk ▪ Break in the skin ► HPV (dark dots) invades and infects basal cells ▪ HPV incorporates into DNA ► moves up epithelium as it matures ► releases Then 2 things happen 1. or 2.
1. Completely have infection go away or 2 .Stays and forms wart or affects maturation (becomes cancer, depending on strain)
76
**HPV Genome Organization**
▪ LCR: long control region ▪ P97: promoter protein ▪ E1‐E7: early region genes ▪ L1,L2: late region genes
77
What is the Molecular Mechanism of HPV?
``` **E6 = degrades p53 E7 = inactivates pRb** ``` ## Footnote 1. E2 = attachment location of Integrated HPV 2. transcription of E6 + E7 3. Binding of the viral E7 protein to pRb ► release of E2F and other proteins ► signals for the cell cycle to progress ▪ **As long as the E7 protein stays attached to pRb, uncontrolled cell proliferation will continue** HPV E6 protein is: ‐ A ubiquitin ligase ‐ contributes to oncogenesis by attaching ubiquitin molecules to p53 ► making p53 inactive and subject to proteasomal degradation ▪ **Normal function of p53 = to stop cell division + repair damaged DNA so that damaged cells do not reproduce (apoptosis)** ▪ _When p53 is inactive_, cells with changes in the DNA, such as integrated viral DNA, are not repaired ► destabilizes the cell ► increases the risk of malignant transformation
78
What is Persistence of HPV
▪ Low‐risk types: clear faster, less likely to become persistent ▪ High‐risk types: clear slowly, more likely to become persistent
79
What is the Prevalence of Oral (HPV)
Overall: 6.9% (CI 6.7‐8.3) ▪ Gender: **Men (10.1%) \> Women (3.6%) – women clear faster** ▪ Age: **bimodal distributio**n – 30‐34yo and 60‐64yo (she says 30‐34 but Dr. Kerr’s graph shows mid‐20s ▪ High Risk HPV (3.7%) \> Low risk HPV (3.1%) ▪ **HPV‐16 infection most prevalent** (1% or 2.13 million Americans) ▪ Based on NHANES study w/ oral rinse sampling and PCR
80
What are Risk Factors Associated w/ Prevalence of HPV?
▪ Ever had sex (7.6%) vs never had sex (0.9%) ▪ Male ▪ Increased number of sexual partners (vaginal or oral sex) ▪ Tobacco smoking ▪ HIV infection
81
Most prevelant HPV TYPE?
HPV 16 = most prevalent
82
What is the Prevalence in HIV + ?
**Ppl w/ HIV+ and low CD4 T‐cells lvl** = higher risk of HPV **HPV 16+ higher if CD4 \<200**
83
Compare between SCC in Squamous Cell Carcinoma caused by HPV vs Tobacco and Alcohol
**▪ HPV associated SCCa** ‐ Wild type TP53 ‐ Low pRb _‐ Increased p16_ **▪ Tobacco and Alcohol associated SCCa** _‐ \*Mutated TP53_ – mutated by carcinogens in tobacco and alcohol► cancer ‐ pRB overexpression ‐ Decrease p16
84
BENIGN ORAL LOW RISK HPV LESIONS (WARTS) How do they appear? Color? Size? Histologic?
§_Appear_ as **single or multiple exophytic papules, either sessile and flat or pedunculated and papillary.** §_Color_ depends upon degree of keratinization, ranging **from white to pink.** §_Size_ of papules **generally \<10mm in diameter.** §_Histologically_, lesions may have **koilocytes.**
85
What are the types of Benign Oral Low Risk HPV Lesion ? (5)
▪ Squamous papilloma ▪ Verruca vulgaris ▪ Condyloma acuminatum ▪ Focal epithelial hyperplasia ▪ Oral florid papillomatosis
86
**SQUAMOUS PAPILLOMA** _What is it?_ _Gender?_ _Age?_ _Location?_ _Apperance ?_ _Treatment?_
▪ **Benign proliferation of stratified squamous epithelium resulting** ► p*_apillary, verruciform, rugose (ridged or wrinkled) mass_* ▪ **HPV types 6 + 11** – Low risk ▪ **M = F** ▪ **Any age** (more common in 30‐50s) ▪ Any oral mucosal surface (palate most common) ▪ **Soft, painless, usually pedunculated, exophytic lesion w/ numerous finger‐like projections** ▪ **HPV DNA detected in only ~50%** ▪ \*\*should remove from mouth – but WOULD NOT submit for HPV typing
87
What is this infectious diease?
SQUAMOUS PAPILLOMA Benign Oral Low Risk HPV Lesion **HPV 6+11** “finger‐like projections
88
What is this infectious diease?
SQUAMOUS PAPILLOMA Benign Oral Low Risk HPV Lesion **HPV 6+11** “finger‐like projections - The projections are almost feathery - exophytic lesion
89
**Oral Verruca Vulgaris** What is it? Contagious? Age? Location? Apperance ?
▪ HPV **2**, and others (1,**4,6**,7,11,26,27,29,41,57,65,75‐77) ▪ Benign, HPV‐induced focal hyperplasia of stratified squamous epithelium ▪ **Contagious** – transmitted by direct contact ▪ **Any age** – frequently seen in children ▪ More common **Anterior** \> Posterior part of mouth ▪ **Soft, painless, usually pedunculated, exophytic lesions w/ numerous fingerlike projections** (similar to squamous papilloma) ‐ _How to tell the difference? Under microscope_
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What is this infectious disease?
***Oral Verruca Vulgaris*** HPV 2,4,6 Also “finger‐like projections” remember it's *contagious*
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**Condyloma Acuminatum (Venereal Wart)** What is it? Contagious? Transmission? Age? Location? Apperance ?
**HPV Types 6, 11** – _condyloma can turn cancerous_ ▪ Virually induced proliferation of stratified squamous epithelium – usually genital or anal mucosa ▪ **Contagious** – transmitted by direct contact ▪ Incubation period: 1‐3mo ▪ Considered **sexually transmitted disease** (if corroborated by history) ▪ **Oral lesions** – usually **anterior part of mouth** ▪ S**essile, pink, well‐demarcated, non‐tender exophytic mass ▪ Short, blunted surface projections ▪ Larger than papilloma or verruca vulgar** ## Footnote **▪ Characteristic clustering of multiple lesions**
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What is this infectious disease?
**Condyloma Acuminatum** (Venereal Wart) HPV 6,11 – can be cancerous Genital warts “short, blunt, clusters” Characteristic clustering of multiple lesions
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If you see Condyloma Acuminatum in a child, what is the next step?
-Since this is a sexually transmitted disease, we need to suspect sexcual child abuse and investigate further!
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**(Multifocal) Epithelial Hyperplasia/Heck's Disease** What is it? Appearance? Which communities or environment? Demographics age and gender? Histology?
▪ HPV Types **13, 32** and others (1,6,11,16,18,55) ▪ **HPV‐induced localized proliferation of oral squamous epithelium ▪ “Flat‐top papules”** ▪ Endemic in some **Inuit/Alaskan native + Native American** **communities**, **Puerto Rican communities** ▪ _Crowded situations, malnutrition_ ▪ Usually seen in children ▪ May be seen in HIV + individuals ▪ **M = F** ▪ Histology: **focal epithelial acanthos**
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What is this infectious disease?
(Multifocal) Epithelial Hyperplasia/**Heck's Disease** HPV 13,32 **“Flat‐top papules”**
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What is this infectious disease?
(Multifocal) Epithelial Hyperplasia/**Heck's Disease** HPV 13,32 **“Flat‐top papules”**
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**Oral Florid Papillomatosis** What is it? What are its types? What is clinical appearance?
IIt's benign HPV disease ▪ HIV infection ‐ Increased prevalence since advent of HAART therapy ‐ Multiple HPV types ▪ Down syndrome Oral Florid Characteristics: ‐ **Diffuse, multiple locations ‐ Papillary ‐ Bumpy and tall**
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What is this infectious disease?
**Oral Florid Papillomatosis** Very characteristic appearance - diffused, in multiple locations - papillary **"Multifocal, papillary lesions"** -if we biopsied these or had these removed for aesthetic regions, we’d see that the epithelium have become white, long, taller, and bumpy
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**Benign Oral HPV Lesions** HISTOPATHOLOGY
**§Acanthosis §Koilocytosis §Binucleated***and***multinucleated keratinocytes §Dyskeratosis §Mitosoid figures §Basilar hyperplasia**
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HPV is thought to cause --% of oropharyngeal cancers in the US
HPV is thought to cause **70%** of oropharyngeal cancers in the US That's why we want to know if high risk HPV– better prognosis
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**HPV Testing**
_▪ Pathologists order it_ ▪ Only do testing if pathologist sees cancer **No HPV testing on low‐risk HPV lesions (warts)** ▪ No medical indication for **low‐risk HPV testing** b/c ‐ infection **NOT** associated w/ disease progression ‐ no treatment or therapy change indicated when low‐risk HPV is ID’ed ▪ HPV testing using p16 surrogate on **oropharyngeal squamous cell carcinoma** **(SCC)**
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Management of Oral HPV Lesions Solitary Lesions
‐ Usually appear exophytic and papillary ‐ Excision is warranted ‐ Consider possible recurrence
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Management of Oral HPV Lesions ## Footnote **Multiple Lesions**
‐ Use high power evacuation to prevent transmission ‐ Treatment = controversial ‐ Excision/ablation vs Topical vs Intralesional therapy (or combo) ‐ Consider higher rate of recurrence
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HPV multiple lesions ## Footnote Excision/Ablation
Excision/Ablation ▪ Scalpel ▪ Carbon dioxide laser – be cautious, don’t know what is burned away ▪ Electrosurgery
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**HPV multiple lesions** Topical Therapy
▪ Podophyllin resin ▪ Imiquimod (extra‐oral use only) ▪ Cidofovir ▪ Interferon
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Topical Podophyllin for what is it used Is it FDA approved Safe or not Durging pregnancy?
▪ Topical cytotoxic agent which arrests mitosis ▪ Genital warts and other papillomas ▪ Not FDA approved for oral warts ▪ Serious adverse reaction if absorbed systemically ▪ Pregnancy category X
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Topical Imiquimod
▪ Induces cytokines + chemokines w/ resutlant anti‐virl (HPV) effects Not FDA approved for oral warts
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HPV vaccine
**Newest is Gardsail 9** against many types for both men and women ▪ 2 doses recommended for boys/girls age 11‐12 and 6mo later ▪ Recommended for everyone \<26yo (MAX) ▪ NOT recommended for 26+yo unless risk for new infections (less benefit since most already exposed) ▪ Virus like particles (VLP) of L1 capsid protein present in vaccine Results of Vaccination ▪ Drops in infections w/ HPV types that cause most HPV cancers + genital warts in teen girls, young adult women ▪ Among vaccinated women – cervical precancers dropped by 40%
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What precentge of people will be infected with HPV in their lifetime?
▪ 80% ppl will be infected in lifetime so better take the vaccine early!
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**Oral Molluscum Contagiosum** _Which viruse causes it?_ _Clinical Appaerance?_ _Who get affected?_ _Histopathology?_ Treatment?
▪ **Poxvirus** ▪ Presents as: ‐ pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug involving skin, lips, buccal mucosa, and palate ▪ Florid cases seen in immunocompromised persons ▪ Children, young adults ▪ Histopathology characterized by: ‐ Large intracytoplasmic inclusion bodies – “Henderson‐Paterson bodies” ‐ Kids can have 6‐9mo and will go away
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What is this infectious disease?
**Oral Molluscum Contagiosum** *multiple pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug*
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**Measles** Which viruse causes it? How does it spread? Symptoms? Clinical charcterstics? location?
**▪ Paramyxovirus** ▪ Spread through _respiratory droplets_ ▪ **Symptoms**: runny nose, red/watery eyes, cough, fever, rash, desquamation of skin ▪ \***Characterized by Koplik’s spots** ‐ Pathognomonic for measles ‐ Discrete, bluish white punctate mucosal macules ‐ Surrounded by rim of erythema ‐ Represent foci of epithelial necrosis ‐ Often precedes skin manifestations **▪ Most common location for Koplok’s spots:** _Buccal mucosa_ ‐ Lesions may resemble _“grains of salt sprinkled on erythematous background”_
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What is this infectious disease?
**Measles** **\*Characterized by Koplik’s spots** salts/grains
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Enterovirus‐Coxsackie Virus What diseases can it cause ? (3) Who do they effect? How they are treated?
**-Herpangina**‐soft palate, red macules ► fragile vesicles (back of throat) ‐ **Hand, foot, and mouth disease** – oral lesions more in anterior regions (aphthous‐like), hand/foot (vesicles) ‐ **Acute lymphonodular pharyngitis** – nodules on the soft palate ▪ Usually seen in children ▪ Self‐limiting
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What is this infectious disease?
**_Hand, foot, and mouth disease_** caused by **Coxsackie Virus** affect children contagious The condition is spread by direct contact with saliva or mucus.
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What is this infectious disease?
**Herpangina** casued by **_Coxsackie Virus_** *red macules and vesciles on the soft palate* a sudden viral illness in children. It causes small blisterlike bumps or sores (ulcers) in the mouth
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What is this infectious disease
**Acute lymphonodular pharyngitis** Caused by **Coxsackie Virus** *Affects children* Nodules on the soft palate. -distinctive, raised, micronodular lesions occur primarily in the pharynx and related structures and regressed without ulceration.
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**Rubella (German Measles)** Which viruse causes it? How does it spread? Symptoms? Clinical signs? Assosited with what syndrome? Is there a vaccine? How it is diagnosed?
**▪ Family: Togavirus; Genus: Rubivirus** **▪ Respiratory droplets** **Symptoms:** ‐ Fever, headache, malaise, coryza (runny nose), anorexia, pharyngitis, lymphadenopathy ▪ Rash – **maculopapular w/ desquamation** * *▪ Forchheimer sign** * *▪ Palatal petechiae** ▪ **Congenital rubella syndrome** – pandemics in past ▪ Vaccine: **MMR** – so we barely see this anymore ▪ Diagnosis**: by serology**
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What is this infectious disease?
Rubella caused by Family: Togavirus; Genus: Rubivirus ``` Forchheimer sign (left) Palatal petechiae (right) ``` | (German Measles)
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What is the **Most common opportunistic fungal pathogen/ infection?**
**Candida Species** ● Over 200 species exist ● At least 15 distinct Candida species cause human disease
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Mucosal/Oral infections, which are generally non‐invasive are caused primarily by --------
**Candida albicans**
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\>90% of invasive disease is caused by 5 most common species, which are?
‐ C. albicans ‐ C. glabrata ‐ C. tropicalis ‐ C. parapsilosis ‐ C. krusei
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Candida Species have what kind of symbiosis with humans?
● **Commensalism**: ‐ “long‐term biological interaction (symbiosis) in which members of one species gain benefits while those of the other species neither benefit nor are harmed” ● \>50% of humans carry candida without harmful effects
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**What is Candida Species‐ Disease State**
* Becomes an “infection” called **candidiasis** when environment changes and encourages growth * ● Defect in cell‐mediated immune response * ‐ Ranges from mild superficial mucosal infection ►(can be) fatal disseminated disease (usually with people with HIV and transplants)
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What causes Candida Infection?
● A disrupted balance of the normal mucosal flora ● Impaired barrier functions ● Immunosuppression such as: ‐ Use of broad‐spectrum antibiotic ‐ Leukemia ‐ HIV ‐ Cancer chemotherapy ‐ Diabetes ‐ Xerostomia (what we deal with, candidiasis can persist here)
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Normally Candida is in the commensal state and once you reach a certain level where the fungal burden has increased, you increase the c‐FOS pathway ‐ This is when the organism forms -----; once these are formed, you see invasion into the------- cells.
Normally it is in the commensal state and once you reach a certain level where the fungal burden has increased, you increase the c‐FOS pathway ‐ This is when the organism forms **hyphae**; once these are formed, you see invasion into the **epithelial** cells.
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**Pathogenesis‐ Key Features**
**● Commensalism** * **Fungus is tolerated** (threshold not reached) * I**mmune cells are not activated** **● Pathogenicity** * _Fungal burden is increased_ and **hyphae** form * Immune cells are recruited by cytokines, chemokines * Neutrophils are recruited and kill fungus * Dendritic cells present antigen to T‐cells * T‐cells also decrease fungal burden (IL‐22, IL‐17) * Innate and acquired clear fungus to levels below threshold
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How does Candida overcome host defenses? 6
1. **Dimorphism** (can be _spore_ and a _hyphae_‐ 2 forms) 2. **Phenotypic switching** (change shape) 3. **Adhesins/Invasins** (aid in attachment) 4. **Molecular mimicry of mammalian integrins** (helps to be avoided by the immune system) 5. **Secretion of hydrolytic enzymes** (aids in invasion) 6. **Phospholipase B contributes to degradation of host tissue** (aids in degradation to gain entry)
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Dimorphism of Candida Two forms?
SPORES‐ when they are in this form, they do NOT invade HYPHAE‐ when they begin their invasion
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Crosstalk: Candida ------- play an important role in the continuous interchange that regulates the balance between saprophytism and parasitism
Crosstalk: Candida **glycans** play an important role in the continuous interchange that regulates the balance between saprophytism and parasitism
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TYPES OF CANDIDIASIS INFECTION
**● Superficial and localized‐more common (mild disease)** ‐ Intertrigo §Paronychia/Onychomycosis ‐ “Diaper Rash” ‐ Vulvovaginitis ‐ Esophageal Candidiasis §Oral Candidiasis (Candidosis) **● Invasive, disseminated and deep infection‐rare (moderate‐severe)** ‐ Affects blood (candidemia‐hospitalized), heart, brain, eyes, bones)
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What is this infectious disease?
**Intertrigo** a type of candidiasis
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What is this infectious disease?
**“Diaper Rash”** a type of candidiasis
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What is this infectious disease?
**Vulvovaginitis** a type of candidiasis
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What is this infectious disease?
**Esophageal Candidiasis** a type of candidiasis
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What is this infectious disease?
**Oral candidiasis** a type of candidiasis
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What is this infectious disease?
**Onychomycosis** a type of candidiasis
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Which Candida is the most common species with what kind of Candidal Sepsis and Disseminated Candidiasis ?
**C. albicans** * **Candidal sepsis** means that you have the fungal moving around in your body * **Life‐threatening event** in individual with severely deficient cell * mediated immunity * Most commonly involves urinary tract infection (women/men 4:1) * _Very rare_
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_Oral Candidiasis_ facts
● 30‐50% of people carry organism without infection (called candida carriage) ● Rate of carriage increases with age and risk factors ● 70‐80% of oral isolates are Candida albicans
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**What are the Predisposing Factors for Oral Candidiasis ?** Local and general
**Local** * denture wearing * smoking * atopic consitituion * steroid inhalation * hyperkeratosis * imblance of the oral microflora * quality and qunatity of saliva\ **General** * immunosupressive disease * impaired health status * immunosupressive drugs * endocrine disorders * hematinic deficiencies
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**Pseudomembranous Candidiasis** Also known as? Key feature? Symptoms? In which patients it is seen?
● “**Thrush**” ● KEY FEATURE: **Wipeable** _white plaques that resemble curdled milk_ ● Underlying mucosa is **erythematous** ● Asymptomatic usually ● Mild symptoms: burning, dysgeusia ● Seen in patients with: **HIV, broad‐spectrum antibiotics, leukemia, infants**
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What is this infectious disease?
**PSEUDOMEMBRANOUS CANDIDIASIS** *UNCONTROLLED DIABETIC* When you wipe away these plaques, you might see some Erythematous areas that causes some of the symptoms that the patient feels -This is **MILD DISEASE**
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What is this infectious disease?
* *Pseudomembranous Candidiasis‐** * Uncontrolled HIV* ● This can be mistaken with materia alba (this is just food) ‐ Should ask patient if they just ate ● This is **MODERATE DISEASE**
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What is this infectious disease?
**Pseudomembranous Candidiasis** *Topical Corticosteroid Use* Can be brought about from steroid use **(steroid inhaler example)** ‐ If you don’t rinse your mouth after using steroids, this can happen ■ _A proliferation of hyphae_
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What is this infectious disease?
PSEUDOMEMBRANOUS CANDIDIASIS **Severe dry mouth** **This is severe disease** we would want to use **systemic treatments/ intervention**
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**Erythematous Candidiasis** what are its _Clinical finding?_ _Subtypes?_
● **Clinical Findings:** * Red macules or patches * Can be due to multiple things **● Subtypes:** ‐ **Atrophic Candidiasis** (acute‐feels like mouth has been scalded) ‐ **Median Rhomboid Glossitis** (asymptomatic) ‐ **Denture Stomatitis** (asymptomatic) ■ HAS THE SHAPE OF THE DENTURE ‐ **Chronic multifocal (**asymptomatic) ■ THIS HAS BEEN THERE FOR A LONG TIME
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What is this infectious disease?
**ATROPHIC CANDIDIASIS** ● Erythematous on any mucosal surface **● “Bald Tongue”** ● Typically, painful ● (Chronic multifocal, looks familiar) ***a subtype of Erythematous Candidiasis***
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What is this infectious disease?
**Median Rhomboid Glossitis** *a subtype of Erythematous Candidiasis* ● “**Central Papillary Atrophy”** ● _Well‐demarcated erythematous zone_ ● **Loss of papillae on midline posterior dorsal tongue** ● Usually, **asymptomatic** ● “**Kissing” palatal lesion** ‐ Because the tongue and the palate are in contact with each other ● Can have **a diamond shape**
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What is this infectious disease
**Denture Stomatitis** ● _Chronic atrophic candidiasis_ ● **Erythema** in _denture bearing areas of maxilla_ ● **Petechiae** may be noted ● Usually, **asymptomatic** ● _Consider denture care/fit/allergy/inadequate curing of acrylic_ ● This can occur if the patient NEVER takes off their denture ● **Inflammatory papillary hyperplasia** is associated with condition ● **Treatment**‐**Nystatin** applied to intaglio surface of denture and wear denture and patient to remove denture at night *a subtype of Erythematous Candidiasis*
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What is this infectious disease?
*a subtype of Erythematous Candidiasis*
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What is this infectious disease
**Angular Cheilitis** ● **Erythema**, _fissuring and scaling at angles of mouth_ and _commissures of mouth_ ● ***Loss of vertical dimension*** ● ***Pooling of saliva*** ● _May be mixed bacterial/fungal infection_ ● _Differential diagnosis_ can be **Vit B Deficiency** *a subtype of Erythematous Candidiasis*
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What is Hyperplastic Candidiasis?
● a Rare and controversial form of candidiasis ● Candidiasis superimposed on pre‐existing leukoplakic lesion ● White plaque which cannot be removed by scraping (NOT WIPEABLE) ● **Increased frequency of epithelial dysplasia** ● MUST **BIOPSY** then diagnose as hyperplastic candidiasis **if you see fungi post biopsy**
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What is this infectious disease?
**HYPERPLASTIC CANDIDIASIS**
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What is **Chronic Mucocutaneous Candidiasis**?
● Group of rare disorders with immunologic pathogenesis ● Clinical: Severe infection of mucosal surfaces, nails and skin ● Oral‐ lesions‐thick white plaques that do not rub off but may see other forms
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**Chronic Mucocutaneous Candidiasis** May be associated with **endocrine abnormalities (APECED**); what does **APECED** stands with?
‐ **A**: autoimmune ‐ **PE**: polyendocrinopathy ‐ **C**: candidiasis ‐ **E**: ectodermal ‐ **D**: dystrophy **Chronic Mucocutaneous Candidiasis** is also genetic associted with **AIRE** gene
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Chronic Mucocutaneous Candidiasis is at increased risk of what?
● Increased risk of **squamous cell carcinoma**
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What is this infectious disease?
**Chronic Mucocutaneous Candidiasis** Severe infection of mucosal surfaces, nails, and skin
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What is this infectious disease?
Mucocutaneous Candidiasis APECED Autoimmune Polyendocrinopathy Candidiasis Ectodermal Dystrophy Syndrome Biopsy of the tonuge revealed SCC
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How is Oral Candidiasis Diagnosed?
● Clinical signs ● Therapeutic diagnosis ● Cytologic smear: scrape cells and look at them under the microscope and stained with PAS stain ● Periodic Acid Schiff Stain (PAS stain) ● KOH float §Biopsy (esp. hyperplastic candidiasis) ● Culture
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What are Antifungal Drug Classes? *3*
● **Polyene‐Nystatin, Amphotericin B** (not absorbed; used for deep fungal infections) ● **Imidazole‐Clotrimazole, Ketoconazole** (GI absorption) ● **Triazole‐Fluconazole, Itraconazole, Posaconazole, Echinocandins**
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What is the treatment of mild Candiadisis Disease?
* **Clotrimazole troches**, 10 mg 5 times daily or * **miconazole mucoadhesive buccal 50 mg tablet** applied to the mucosal surface over the canine fossa once daily for 7–14 days * Alternatives for mild disease include **nystatin suspension (100 000 u/mL) 4–6 mL** swished for \>1min then swallow **4 times daily.**
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What is treatment of moderate to severe Candiadisis Disease?
* **Oral fluconazole, 100–200mg daily for 7–14 days** ● For **fluconazole‐refractory disease:** ‐ **Itraconazole suspension 200 mg once daily OR posaconazole** su**spension 400 mg twice daily for 3 days then 400 mg once dail**y, for up to **28 days**, are recommended *_Alternatives for fluconazole‐refractory disease include:_* ‐ **Voriconazole, 200 mg twice daily**, OR **AmB deoxycholate oral suspension, 100 mg/mL 4 times daily**(strong recommendation; moderate‐quality evidence). ‐ **Intravenous echinocandin** (caspofungin: 70‐mg loading dose, then 50 mg daily; micafungin: 100 mg daily; or anidulafungin: 200‐mg loading dose, then 100 mg daily) (weak recommendation; moderate‐quality evidence). § **Intravenous Amphotericin B** deoxycholate, 0.3 mg/kg daily, are other alternatives for refractory disease (weak recommendation; moderate‐quality evidence).
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What is Chronic Suppressive Therapy?
**this is when you keep the fungal infection under control for a long time** Usually **unnecessary in immunocompetent patients** ● For patients who have recurrent infections: ‐ **For HIV‐infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections** (strong recommendation; high‐quality evidence). ‐ **Fluconazole, 100 mg 3 times weekly, is recommended** (strong recommendation; high‐quality evidence). ● **Clotrimazole 10mg troches 1 week out of every month?** (no evidence
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What is Denture Stomatitis Treatment?
YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION antifungal medication (1) Topical Antifungal Agents ‐ Rx. Clotrimazole cream 1% vs OR ‐ Rx. Nystatin‐Triamcinolone Acetonide ointment or cream (why? To keep the inflammation down) ■ Disp: 15g tube ■ Label: apply to angles of mouth after meals and before bedtime (2) Denture adjustment, reline, remake YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION
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What are other ways to manage denture stomoatitis ?
● **Bleach‐**1 part bleach to 10 parts water (not for dentures with metallic clasps) ● **Polident** (NYU Carries Polident) ● **Microwave**? ( could be risky, careful not to ruin the denture) CLEANSERS FOR REMOVABLE PROSTHESIS- you have to use this everynight to avoid denture stomoatits **_NYU Carries Polident_** Formulation: **sodium bicarbonate, citric acid, potassium monopersulfate**, sodium carbonate, sodium carbonate peroxide, TAED, sodium benzoate, PEG‐180, sodium lauryl sulfate, VP/VA copolymer, flavor, cellulose gum, FD&C blue 2, blue 1 lake, yellow 5, yellow 5
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What is the Most common systemic fungal infection in US?
Histoplasmosis
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What causes **Histoplasmosis**? what is its mode of pathogensis ?
**● Histoplasma capsulatum** ● **Dimorphic** (yeast at body temperature and mold in soil)
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**Histoplasmosis** is endemic where who can get infected by it? How does is spread?
● Endemic in **fertile river valleys** ‐ Seen in people who spend **a lot of time outside; near Ohio and Mississippi rivers** ● Bird and bat excrement ● Airborne spores enter lungs through inhalation ● Macrophage ingests fungusà**T‐lymphocyte immunity** ● Antibodies develop several weeks later ● **Macrophages may confine fungus** (express disease later)
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Histoplasmosis‐ Clinical Features
● **Most** cases produce **no symptoms or only mild symptoms** ● Acute‐Self‐limited lung infection (similar to influenza; the flu) ● Chronic‐Lung infection similar to tuberculosis ● Disseminated‐Extrapulmonary spread in immunocompromised (spreads from the lungs) **● Tongue, palate, buccal mucosa ● Solitary ulcer with firm rolled borders** ● **Clinically appear indistinguishable from malignancy (squamous cell carcinoma)**
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How is **Histoplasmosis** Diagnosed? How about its histology?
● Histopathology (H&E and special stain‐GMS) ● Culture ● Serology as for histology ● **Epithelioid macrophages containing histoplasma capsulatum** (white arrows) ● Lymphocytes ● Plasma cells
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What is the infectious disease?
**Histoplasmosis** ● This can be squamous cell carcinoma, shanker, ulcers ‐ Differentials for non healing ulcerations on the lateral tongue ● The white area is called the *pseudomembrane*
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what is the treatment for **Histoplasmosis**? acute chronic Disseminated
● **Acute**‐Supportive (analgesics and antipyretics) ● **Chronic**‐IV lipid preparation of amphotericin B or itraconazole ● **Disseminated**‐Lipid preparation of amphotericin B (2 weeks or more) followed by daily itraconazole for 6‐18 months
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**Blastomycosis** _What is it?_ _What causes it?_ _What is its mode of pathogenesis?_
● _Uncommon_ **fungal infection** ● **Blastomyces dermatitidis** ● **Dimorphic**
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Which regions can **Blastomycosis** happen?
● **Eastern half of US** which extends _farther north_ ● _Seen in the wild_
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How does **Blastomycosis** spread? Is there any gender prediclation?
● Airborne spores enter lungs through inhalation ● **M**\>F
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Acute Blastomycosis resembles ----------
● **Acute**‐ Resembles pneumonia
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ChronicBlastomycosis resembles ----------
Chronic Resembles **tuberculosis**
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What are the clinical features of **Blastomycosis**?
● Skin lesions‐extrapulmonary dissemination from lungs ● Oral lesions‐extrapulmonary dissemination or local inoculation ● Skin lesions ● Granular(rough looking) erythematous plaques which may become verrucous(wart‐like) or ulcerated ● Oral lesions ‐ Erythematous or white ‐ Intact surface or ulceration with rolled borders ‐ Painful ‐ Ddx‐Squamous cell carcinoma
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What is this infectious disease?
**Blastomycosis**
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How to diagonse **Blastomycosis**?
● **Histopathology** (Granulomatous inflammation , Broad based budding , Double refractile cell wall) ● Cytology ● KOH ● Culture from sputum (3‐4 weeks) ● DNA probe (where you actively look for the DNA of the blastomycosis)
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How to treat Blastomycosis?
● Most cases **asymptomatic** ● **Itraconazole** (mild to moderate disease) ● **Systemic amphotericin B** (severe cases) ● There is a connection with people taking TNF‐alpha inhibitors
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Paracoccidio Mycosis What is it? What causes it?
A deep fungal infecion causes by: Paracoccidioidomycosis brasiliensis
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Which regions Paracoccidio Mycosis happen?
● South American blastomycosis
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Paracoccidio Mycosis is seen in the soil around ------- (name of an animal)
**nine‐ringed armadillos**
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**Paracoccidio Mycosis** what gender is more common ? which workers are more affected?
● More common in **males** ● _Agriculture workers_
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**Paracoccidio Mycosis** presents intially as which infection?
Pulmonary infection
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What is infectious disease?
**Paracoccidio Mycosis** *looks like the three tail in **Naruto** lol*
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what are the clinical presentation of **Paracoccidioidomycosis**?
●affects the Alveolar mucosa, gingiva and palate lesions with “Mulberry‐like” ulceration (little bumps around it) ● Looks like **strawberry gingivitis** (differential diagnosis)
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what is this infection disease ?
**Paracoccidioidomycosis** looks like strawberry gingiva but it is not
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How is **Paracoccidioidomycosis** diagnosed?
● Histopathology (- Granulomatous inflammation, Epithelioid macrophages and multinucleated giant cells,GMS or PAS, Multiple daughter buds) ● Culture ● KOH
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How is Paracoccidioidomycosis treated?
● **Trimethoprim/ sulfamethoxazole** (mild‐moderate) ● **IV Amphotericin B** (severe disease)
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What is **Coccidiomycosis**?
deep fungal infection that present as Pulmonary infection
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**Coccidiomycosis** is known as -------
**Valley Fever**
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What are the two types of Coccidiomycosis ?
* Coccidioides immitis * Coccidioides posadasii
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What is the mode of _pathogenesis_ of **Coccidiomycosis?**
**Dimorphic organism** (spores and hyphae)
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**Coccidioidomycosis** **symptoms?** What is the Clinical Features? how does the oral and skin lesions appear?
● Most cases are **asymptomatic** ~60% ● **Flulike** ● *Fatigue, cough, chest pain, myalgia, headache* ● May see a **hypersensitivity reaction** (_valley fever)_ ‐ When you are over responding; immune system is over reacting ● **Chronic**‐_mimics tuberculosis_ ● **Disseminated**‐ \<1% of cases
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**Coccidioidomycosis** What is the Clinical Features? how does the oral and skin lesions appear?
● Oral lesions **ulcerated granulomatous nodules** ● Skin lesions: **papules**(slightly raised), **abscesses**, **verrucous**(patchy), **plaques**, **granulomatous nodules**
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What is this infectious disease?
**Coccidioidomycosis**
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How is Coccidioidomycosis diagnosed?
● Histopathology ( Round spherules with numerous endospores , Granulomatous inflammation, Suppurative neutrophils infiltrate, Special Stains used: GMS, PAS) ● Culture ● In situ hybridization (ISH) ● Cytology‐ scraping ulcers then stained with GMS ● Serology‐ check for antibodies ● Skin testing (limited value)
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How is Coccidioidomycosis treated?
● **Mild symptoms**‐ no treatment usually ● **Amphotericin B** (‐ Immunosuppressed ‐ Severe pulmonary infection ‐ Disseminated disease ‐ Pregnant patients ‐ Life‐threatening situation ) ● **Itraconazole** or **fluconazole** (fewer side effects and complications)
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Cryptococcus How common is it? What causes it?
●Uncommon ● Cryptococcus neoformans ● Incidence increased due to AIDS epidemic in 1990s ● Pulmonary infection ● Meningitis
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Cryptococcus is seen in --------------
pigeon excrement (poo)
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Cryptococcus can cause what kind of infections?
● Pulmonary infection ● Meningitis ( after it spreads from the lungs to the brain. )
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What are the Clinical Features of **Cryptococcus**?
**Lung infection often asymptomatic** ● Flulike illness ● Dissemination *‐ Meninges ‐ Skin ‐ Bone ‐ Prostate ‐ Oral‐papillary/granular erythematous plaques*
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How is **Cryptococcus** diagnosed?
● Biopsy ● Culture ● Serology Note: Histopathologically they appear as Granulomatous inflammation (epithelioid histiocytes trying to confide the infection) ● Yeast are surrounded by a clear halo (capsule)
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How is **Cryptococcus** treated?
● Mild case: ***Fluconazole or Itraconazole*** ● Cryptococcal meningitis: ***amphotericin B + other antifungals***
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**Mucormycosis** is caused by what?
* **Infections** caused by **molds** belonging to the order **Mucorales** * _Grow in natural state on_ **decaying organic materials** (saprobic‐ recycling) * **Spores** may be _liberated into air and inhaled by humans_
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Mucormycosis can affect people with what underlying conditions?
‐ Insulin dependent diabetics ‐ Bone marrow transplant recipients ‐ AIDS ‐ Patients receiving systemic corticosteroids ‐ Neutropenic patients (no white blood cells)
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What are the Clinical Features of Mucormycosis?
● Rhinocerebral form ● Nasal obstruction ● Bloody nasal discharge ● Facial pain ● Facial paralysis ● Facial swelling/cellulitis ● Visual disturbances ● Into cranial vault‐blindness, lethargy, seizures ● Oral swelling/ulceration of the maxillary alveolar process/palate as a result of sinus involvement ● Black and necrotic ulcer (eschar) ● Massive tissue destruction
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What is this infectious disease?
Mucormycosis‐ arrow refers to **ESCHAR**‐ always look for this and extreme-Black and necrotic ulcer ( we can see massive tissues destruction
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What is this infectious disease?
Mucormycosis‐ CT Sinus opacificatio ● First thing to do is to find out more about this lesion, how did this patient get this lesion?
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Mucormycosis‐ Histopathology has a sepcial shape?
● Non‐septate hyphae with **90degrees branching** ● You see necrosis of tissue in the area because this attacks the blood vessels
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How is **Mucormycosis** diagnosed?
● Histopathology ● Culture
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How is **Mucormycosis** treated?
● Surgical debridement (massive tissue destruction) ● High doses of lipid formation of amphotericin B ● Control underlying disease (main one) ● Prosthetic obturation of palatal defects
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What is **Aspergillosis** *and* what causes it?
* Saprobic (in an environment rich of oxygen) * it caused by Aspergillus flavus and Aspergillus fumigatus
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Where is **Aspergillosis** typically seen? how it is spread?
● Seen in **hospitals** and **construction sights** ●caused by _Aspergillus flavus_ and _Aspergillus fumigatus_ **● Spores** *are* **inhaled**
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Aspergillosis‐ Clinical Features Two types noninvasive and invasive
● **Noninvasive** ‐ Allergic fungal sinusitis ‐ Aspergilloma (fungus ball, mycetoma [‐oma: like a tumour made of aspergillus]) ● **Invasive** ‐ Localized (possibly after tissue damage in oral cavity) ‐ Disseminated ‐immunocompromised
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Which infectious disease has fruting body in its histopathology?
**Aspergillosis** Histopathology includes: ●Branching septate hyphae ● Acute angle branching **● “Fruiting body**
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How is Aspergillosis diagnosed?
● Histopathology ● Culture
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what is this infectious disease?
***Aspergillosis*** arrow points toward a violaceous‐ purple colour
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How is Aspergillosis treated?
● Aspergilloma‐**debridement** ● Allergic fungal sinusitis‐**debridement and corticosteroid drugs** ● Localized invasive‐**debridement & voriconazole and amphotericin B** ● Disseminated invasive‐**consider poor prognosis even with treatment**
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What are Oral Manifestations of Bacterial Infections?
Caries (streptococcus mutans) ‐ Gingivitis/Periodontitis ‐ Necrotizing Periodontal Diseases ‐ Noma (Cancrum Oris) Impetigo ‐ Erysipelas ‐ Streptococcal Tonsillitis and Pharyngitis Scarlet Fever ‐ Diphtheria ‐ Syphilis ‐ Gonorrhea ‐ Tuberculosis Leprosy Actinomycosis ‐ Cat Scratch Disease ‐ Bacillary Angioma
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What is **Necrotizing Periodontal Diseases?**
Bacterial infection which presents with a spectrum of lesions ‐ Vary depending upon the localization of lesion and predisposing factors
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Necrotizing Periodontal Diseases include 4 types,what are they? What do they mean?
‐ Includes: **o Necrotizing gingivitis (NG):**rapidly destructive, non-communicable microbial disease of the gingiva **o Necrotizing periodontitis (NP)**:apidly progressing disease process that results in the destruction of the periodontium o **Necrotizing stomatitis (NS):**When the bacterial infection extends further to OTHER parts of the mouth o **NOMA** (extension to skin of face) ▪ Extreme disfigurement due to bacterial infection extending onto the skin of the face
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Necrotizing Periodontal Diseases name has changed how?
‐ The term "**acute**" has not been included since 1999 (ANUG=old name) o As the infections are ALWAYS acute ‐ The term "**ulcerative**" removed in 2017 World Workshop proposed classification "Necrotizing Periodontal Disease (NPD)" is term proposed in 2017 World Workshop for NG, NP and NS o There is ALWAYS ulceration as a result of necrosis
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what are the Clinical Features of Necrotizing Periodontal Diseases?
‐ **Ulceration with necrosis of interdental papillae** o Results in a **"punched out" crater‐like appearance of the papilla** **‐ Gray pseudomembrane** o Dead tissue **‐ EXTREMELY Painful** **‐ Fetid odor** _‐ Spontaneous hemorrhage Fever, lymphadenopathy, malaise_
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Which population affected by Necrotizing Periodontal Diseases?
**Young and middle‐aged adults** Prevalence \<0.1%
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What is this infectious disease?
**Necrotizing Gingivitis (NG)** o No periodontitis features o SIMILAR APPEARANCE to *_gonorrhea_* ▪ Distinguishing characteristic of NG **– Fetid Odor**
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What is this infectious disease?
**Necrotizing Periodontitis (NP)** o Bone loss of the periodontium seen
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What are the risk factors of Necrotizing Periodontal Diseases?
Many related factors (Multifactorial etiology): o Psychological stress o Immunosuppression o Smoking o Local trauma o Poor nutritional status o Poor oral hygiene o Inadequate sleep
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Which infectious diseases was known by Trench mouth?
**Necrotizing Periodontal Diseases** o During WW1, soldiers that were fighting in the trenches were under extreme stress o they commonly developed necrotizing periodontal diseases
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What are the Constant bacterial species found in Necrotizing Periodontal Diseases? Will we be able to use microbiological testing to form a diagnosis?
**o Treponema spp.** **o Selenomonas spp.** **o Fusobacterium spp.** **o Prevotella intermedia** o \*Also always present in healthy gingiva ▪ so, No, Microbiological testing is NOT used to form a diagnosis
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What is the Treatment of Necrotizing Periodontal Diseases?
**o Removal of bacteria (scaling)** **o Chlorhexidine rinse** **o Antibiotics (fever or signs of systemic illness)** ▪ Metronidazole ▪ Penicillin **o Oral hygiene instruction** **o Supportive therapy** ▪ Rest ▪ Fluids ▪ Soft nutritious diet **o Predisposing (Immunosuppressive)factors** ▪ Smoking ▪ HIV?
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NOMA is also called as ------------
**cancrum oris**
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What is NOMA? Where it is seen?
‐ **Rapidly progressive opportunistic infection caused by many bacteria** o More commonly seen in other parts of the world o Seen in the US in immunocompromised patients ▪ HIV ‐ WHO estimates the global yearly incidence = 140,000
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Which bacteria involved in **NOMA**?
**‐ Polymicrobial etiology** ‐ Normal flora become pathogenic during immunocompromised states ***‐ Key bacteria:*** o **Fusobacterium necrophorum** **o Prevotella intermedium** ‐ Other common bacteria: **o Actinomyces pyogenes** o Bacillus cereus o Bacteroides fragilis o Fusobacterium nucleatum o Prevotella melaninogenica
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What are the Predisposing Factors of NOMA?
‐ Previous necrotizing periodontal disease Poverty ‐ Malnutrition or dehydration ‐ Poor oral hygiene ‐ Poor sanitation ‐ Unsafe drinking water ‐ Proximity to unkempt livestock ‐ Recent illness Malignancy ‐ Immunodeficiency disorder, including AIDS
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What is this infectious disease?
**NOMA** This is an aid patient Figure 2: Extension of infection onto the face ‐ Figure 3: Lost bone and gingiva ‐ Figure 4 & 5 Bone destruction
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NOMA can affect who?
Children Adults with debilitating disease
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What are the clinical features of NOMA?
Gingiva (NG) ► Adjacent tissue (necrotizing stomatitis) + Non‐ contiguous tissue (trauma) ► Blue black discoloration of skin ‐ Spreads through muscle, bone (osteomyelitis) **‐ Other features:** _o Fetid odor_ ▪ Due to tissue necrosis _o Pain o Fever o Malaise_ o Tachycardia o Increased respiratory rate o Anemia o Leukocytosis o Regional lymphadenopat
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What is this infectious disease?
NOMA Development of NOMA from day 1 to day 15
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What is the treatment of Noma?
o **Antibiotics** ▪ Penicillin ▪ Metronidazole **o Local wound care** _▪ Conservative debridement_ to avoid iatrogenic tissue damage **o Consider nutrition, hydration and electrolyte imbalances** **o May cause significant morbidity**
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What is this infectious disease?
**Impetigo** ‐ “Cornflakes glued to Surface" Appearance o Little papules that can form little vesicles around the mouth o Vesicles burst open and dry up around the skin of the mouth ‐ Bilateral
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What causes Impetigo?
‐ Caused by: o Staphylococcus aureus o Streptococcal pyogenes _Damaged skin allows infection to enter_ **Usually affects kids**
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What is **Impetigo** Differential Diagnosis
**o Recurrent Herpes Labialis** ▪ Resemblance to initial impetigo stages when still unilateral **o Perioral Dermatitis** ▪ Triggered by cosmetics and other substances on the skin **o Exfoliative Cheilitis (chapped lips)**
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How is Impetigo diagnosed and treated?
Diagnosis: o Presumptive from clinical features _‐ Treatment:_ **o Topical mupirocin** **o Systemic antibiotics**
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What is this infectious disease?
**Erysipelas** Superficial skin infection in immunosuppressed adults ‐ Group A beta‐hemolytic streptococci ‐ Painful ‐ Bright‐red, well‐circumscribed, swollen, indurated (firm) ‐ Warm to touch ‐ Systemic manifestations: o High fever o Swollen lymph nodes Diagnosis: Cultures not useful ‐ Treatment: **o Penicillin ‐ Complications without treatment**
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What is differential diagnosis for _Erysipelas_?
**o Systemic Lupus Erythematosus (SLE)** ▪ Due to sparing of nasolabial folds ▪ Butterfly rash in SLE resembles erysipelas **o Cellulitis (dental infection induced):** ▪ Tooth infection burrowing through the tissues rather than forming an abscess **o Actinomycosis**
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What is Syphilis? What causes it/
* Chronic infection * caused by *_spirochete_* **Treponema pallidum**
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What are the three stages of Syphillis?
Three stages 1. o Primary (**chancre**) 2. o Secondary (**rash**) 3. o Tertiary (**gumma**)
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What is this infectious disease?
_Primary Syphilis_ **Chancre** at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
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What is this infectious disease?
**Primary Syphilis** _Chancre_ at site of inoculation (3 – 90 days later) ‐ Papule ► Ulceration ‐ Most chancres occur in genital area (4% oral
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What is Differential Diagnosis for Primary Syphilis (Chancre)? 3
1. **SCC** 2. **Fungal Ulcer** 3. **Trumatic Ulcer**
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What is this infectious disease?
Secondary Syphilis ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks **‐ Diffuse maculopapular (flat, raised) rash** o May involve oral cavity ‐ **Mucous patches** **o Most common on tongue and lip** _‐ Condylomata lata_ o **Resembles viral papillomas** ‐ Systemic symptoms
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What is this infectious disease?
Secondary Syphilis ( Rash) here we see **muscus patches** (right) and **Condylomata lata** (left) ‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection ‐ Resolve in 3‐12 weeks ‐ Diffuse maculopapular (flat, raised) rash **o May involve oral cavity ‐ Mucous patches** **o Most common on tongue and lip** **‐ Condylomata lata** **o Resembles viral papillomas** ‐ Systemic symptoms
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What is this infectious disease?
**Tertiary Syphilis** **Gumma** ‐ **Latent** period for **1 ‐ 30 years** **‐ 30% of patients develop tertiary syphilis** ‐ Serious complications develop: * Vascular system * Central nervous system * Ocular lesions What is "Gumma"? * o Granulomatous inflammation with tissue destruction * o Common on palate and tongue * o Causes a hole in the palate
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Differential Diagnosis for teritiary syphillis "Gumma"
Differential Diagnosis: 1. ▪ T‐cell Lymphoma 2. ▪ Cocaine abuse 3. ▪ Granulomatosis 4. ▪ Polyangiitis 5. ▪ Mucor
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**Congenital Syphilis** is associated with what Triad?
‐ Pathognomonic features in **Hutchinson triad**: **o 1. Hutchinson teeth** **o 2. Ocular interstitial keratitis** **o 3. Eighth nerve deafness** ‐ Other Features: o High arched palate o Saddle nose o Frontal bossing **Clinical changes secondary to fetal infection**
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What is this infectious disease?
**Congenital Syphilis** ‐ Hutchinson Incisors (left image) ‐ Mulberry molars (right image) - not part of the triad
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**Syphilis** Histopathology stage 1 and 2
Not specific ‐ Stage 1 and 2 similar o Ulceration o Hyperplasia (Stage 2) o Exocytosis of neutrophils into epithelium Intense Iymphoplasmacytic inflammatory infiltrate in superficial stroma and around deeper vascular channels (blood vessels)
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Syphilis Histopathology Stage 3
Stage 3 o Granulomatous inflammation o Ulceration may be present ‐ Special stain "**Warthin Starry"**, highlights _**corkscrew spirochetes** ‐_ **Immunohistochemical stain**
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How is Syphilis diagnosed?
**o Biopsy with histopathology** **o Dark field examination of a smear of active lesion** o Serologic screening lab tests * ▪ Venereal Disease Research Lab (VDRL), RPR (non‐ specific and not highly sensitive) * ▪ Fluorescent Treponemal Antibody Absorption (FTA‐ ABS), TPHA, TPPA, MHA‐TP (specific and sensitive)
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How is **Syphilis** Treated?
_o Single dose of parenteral long_‐ acting **benzathine penicillin G** (primary, secondary, early latent) o **Intramuscular penicillin** weekly for three weeks (late latent and tertiary
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What is this infectious disease?
**Secondary Syphilis** Mucous Patch
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What is **Gonorrhea**? What causes it?
‐ a Sexually transmitted (F\>M) caused by **‐ Neisseria gonorrhoeae**
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How **Gonorrhea** affects the body? what complications can arrise?
‐ Genital area usually‐**purulent discharge** ‐ **Systemic bacteremia** (myalgia, arthralgia, polyarthritis, dermatitis) ‐ **Pelvic inflammatory disease** in women (affects pregnancies) ‐ **Gonococcal ophthalmia neonatorum** (infection of infant's eyes)
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What are the Clinical Features of **Gonorrhea?**
‐ Oral lesions ‐ **similar to aphthous** o Very rare _‐ Tonsils edematous and erythematous_ ‐ May **simulate necrotizing gingivitis (NG)** but _fetor oris not present_
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What is this **infectious disease**?
**Gonorrhea** looks like necrotizing gingivitis (NG) but fetor oris not present
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How is **Gonorrhea** diagnosed?
**‐ Gram stain** **‐ Culture of** _endocervical swab_ ‐ **Nucleic acid amplification tests** (NAATs)‐_detect DNA, RNA_
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How is **Gonorrhea** treated?
Many cases of resistance with antibiotics §Cephalosporins *Adults with gonorrhea are treated with antibiotics. Due to emerging strains of drug-resistant Neisseria gonorrhoeae, the Centers for Disease Control and Prevention recommends that uncomplicated gonorrhea be treated with the antibiotic ceftriaxone* — given as an injection — with oral azithromycin (Zithromax)
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**Gonorrhea** can have coinfection with what other infectious bacteria?
**Chlamydia trachomatis**
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Chlamydia trachomatis can trigger which autoimmune disease
**Reactive arthritis (reiter)** _o Can’t see, Can’t Pee, Can’t Climb a Tree_ ▪ _Causes_: **● Conjunctivitis ● Urethritis ● Arthritis** **Remember: Chlamydia trachomatis** coininfect with Neisseria **gonorrhoeae**
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What is **Tuberculosis**? What causes it? How does it spread?
- _Chronic granulomatous infectious disease_ - Caused by **Mycobacterium tuberculosis** §Direct person-to-person spread through **airborne droplets**
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**Primary TB**
_affects previously unexposed, lungs - They breathe in the organisms that someone is coughing out_ 1st: C_hronic inflammatory reaction_ ► Next, **a fibrocalcific nodule** (_Ghon focus)_ forms at initial site of infection
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What are the chance active disease if you get infected with Primary TB
Only **5%-10%** infections lead to active disease i
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**“Secondary TB” reactivation**
* Leads to **disseminated TB** (miliary TB) * True, active TB
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What is this infectious disease?
‐ Tuberculosis
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What is this infectious disease?
‐ Tuberculosis
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What are the causes of **secondary** **Tuberculosis**?
* Immunosuppressive medications * Diabetes * Old age * Crowded living conditions * AIDS
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Tuberculosis Clinical Features **Primary TB**
Usually asymptomatic
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Tuberculosis Clinical Features **SecondaryTB**
o Typically see lung lesions (productive cough) o _Fever, malaise, anorexia, night sweats_
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Tuberculosis Clinical Features **Extrapulmonary TB**
* Lymphatics * Skin * Skeletal system * CNS * Kidney * GI tract * **Oral cavity (uncommon)**
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**Tuberculosis** CLINICAL FEATURES OF ORAL LESIONS
§Ulceration (tongue ulceration most common) §Mucosal granularity §Diffuse inflammation §Non-healing extraction socket
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What is this infectious disease?
**Miliary TB** compared to miliary seeds
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What is this infectious disease?
TB Ulceration (tongue ulceration most common)
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What is this infectious disease?
**Primary Oral TB** tongue ulceration
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What is this infectious disease?
Primary Oral TB Oral Primary TB clinical manifestation is very rare TB is directly in the **_epithelial cells._** Person coughs ⇒ organism enters broken skin somewhere in the oral mucosa ⇒directly causing TB in the mouth -this person would NOT have any issues in their lungs **-**primary TB = infection went directly into their mucosa from another person
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What is the Differential Diagnosis of **_non‐healing ulcer?_**
**o TB o Deep fungal infections o Traumatic ulcer o SCC o Major Aphthous ulcer**
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What is the histological features of Tuberculosis
**Granulomas** * o Epithelioid histiocytes * o Multinucleated giant cells * ▪ \* Langhans giant cells * ● Nuclei along the periphery * o Central caseous necrosis
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TB staining
Special stain Epithelioid o Ziehl‐Neelson or AFB o Consider scarcity of organisms **o MAY NOT VISUALIZE ORGANISMS WITH STAIN** **_▪ NEGATIVE RESULT DOES NOT RULE OUT TB INFECTION_**
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How is Tuberculosis treated?
**§Multiagent therapy for active infection to prevent mutation and resistance** §8 week course §Pyrazinamide §Isoniazid §Rifampin §Ethambutol **§Followed by 16 week course** §Isoniazid §Rifampin **‐ Chemoprophylaxis** ‐ For positive PPD but no active infection **‐ BCG vaccine** o Not used in US due to controversy regarding effectiveness
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How is Tuberculosis diagnosed ?
o TB‐Test **§Delayed type hypersensitivity (Type 4)** §Checks if developed an immune response to TB §**PPD (purified protein derivative)** *(what they inject under the skin)* §**T cells** are attracted by immune system to the skin site §**Lymphokines** induce _hard raised area with clear margins_ §Need to check 48-72 hours later (measure area)
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What is Non‐Tuberculosis Mycobacterial Infection
Scrofula
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What causes scrofula?
**Mycobacterium bovis** **Infected milk** leads to **scrofula** **RARE** today _as milk is pasteurized_
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What are the clinical features of scrofula?
o Enlargement of oropharyngeal lymphoid tissues and cervical nodes o Significant caseous necrosis may occur and cause sinus tracts to skin
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What is this infectious disease?
**Scrofula**
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**Leprosy** is also known as ---------
**Hansen disease**
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What causes **Leprosy**?
**Mycobacterium leprae**
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What are the two types of **Leprosy**?
**1. Tuberculoid leprosy** ▪ High immune reaction ▪ Oral manifestations are **RARE** **2. Lepromatous leprosy** ▪ Reduced cell‐mediated response
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Leporsy prevelance & in which regions it is usually found?
**EXTREMELY RARE** o 80% of cases occur in: ▪ Brazil ▪ India ▪ Indonesia ▪ Madagascar ▪ Myanmar ▪ Nepal ▪ Nigeria
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What are the clinical features of Leporsy ?
Clinical features: **o Leonine facies** ▪ Appearance of a lion **● Loss of eyebrows** ● **Scarring (fibrosis)** from infection prevents hair growth o **\* Oral Manifestations seen in areas of mouth with lower** temperatures: ▪ Hard/soft palate ▪ Maxillary gingiva ▪ Tongue ## Footnote **Oral‐enlarging papules ► ulcer ► necrosis**
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What is this infectious disease?
Leprosy
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What is this infectious disease?
**LEPROSY** _Clinical features_ * *§Bone destruction** ( hole in the palate) * *§Nodular** will become **nectortic** and then **destruction** will follow
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**LEPROSY** How is it diagnosed?
**Diagnosis:** o Clinical presentation o Acid fast stain Histopahology No well‐formed granulomas o Lepromatous leprosy diffuse presentation
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How is Leprosy treated?
§Rifampicin, clofazimine, dapsone
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What is **Actinomycoses**?
‐ Infection caused by filamentous branching gram positive anaerobic bacteria ‐ Normal component of oral flora
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What causes **Actinomycoses**?
‐ Associated Bacteria: **o Actinomyces israelii o Actinomyces viscosus** ‐ Normal component of oral flora -gram positive anaerobic bacteria
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What are the clinical features of **Actinomycoses**?
can be Acute or chronic ‐ **Hard indurated swelling** o Result of injury / trauma ▪ Tooth extraction o Erythematous o Formation of **external sinus** ▪ Drains into the skin **‐ "Sulfur granules"** o May be present in suppuration o Indurated area of fibrosis
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Which locations **Actinomycoses** affect?
**‐ 55% in cervicofacial area** ‐ Hard indurated swelling o Result of injury / trauma/tooth extraction o Erythematous **‐ Area overlying angle of mandible** o Formation of external sinus ▪ Drains into the skin ‐ Other locations include: **o Abdomen o Pelvis o Lungs**
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What is this infectious disease?
**Actinomycoses** it's an external Sinus
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How does Actinomycoses infection spread?
‐ **Enters tissue through an area of prior trauma** o Soft tissue injury o Periodontal pocket o Non‐vital tooth o Extraction socket o Infected tonsil ‐ **Direct extension through soft tissue to the surface**
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What is "Sulfur granules" Where it is found? In which infection? color?
colonies of bacteria (o Actinomyces israelii o Actinomyces viscosus) found in suppuration (pus) which means Suppuration (pus) is dead tissue, bacteria, dead white blood cells, and other products of tissue breakdown.. Sulfur granules found in Actinomycoses yellow in color
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Differential Diagnosis to Actinomycoses
o Erysipelas
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What are other presentations of Actinomycoses?
‐ Tongue ‐ Tonsillar crypts ‐ Salivary gland involvement ‐ Osteomyelitis ‐ Periapical inflammatory lesions
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what is the histology of Actinomycoses and stain used?
‐ Colony of actinomycotic organisms surrounded by neutrophils ‐ Grocott‐Gomori methenamine silver stain (GMS) In this histo slide, we see: \* Sulfur Granule o 1. Collection of actinomycoses israelii organisms o 2. MANY neutrophils surround the periphery o BOTH are requirements for a TRUE diagnosis of actinomycoses
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‐ Actinomycoses o Diagnosis
* **Culture** * o \< 50% of cases are positive * ▪ Due to various types of bacteria in the culture * **Presumptive diagnosis from biopsy** **in this histology: GMS stain was used** o Correlates with top H&E histopathology o Filamentous branches are the actinomycotic organisms
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How is Actinomycoses treated?
* \* **Prolonged high dose antibiotics for _cervicofacial actinomycosis_** * Due to the fibrosis that occurs * Early cases 5‐6 weeks * Deep‐seated infections up to 12 months * **Abscess drainage** * **Sinus tract excision** * **Penicillin**
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What is Cat‐Scratch Disease?
‐ Infectious disease which is seen in _lymph nodes_
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What causes Cat‐Scratch Disease ?
‐ Causative organism: o Bartonella henselae ‐ Previous contact with a cat (scratch or saliva)
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What are the age of the patients that usually get Cat‐Scratch Disease ?
‐ 80% in patients **_younger than 21_**
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----- is the most COMMON cause of regional lymphadenopathy in children | (22,000 cases annually)
Cat Scratch Disease
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What are the clinical features of Cat Scratch Disease ?
‐ Initial **scratch** ‐ **Papule** at _inoculation site_ (3‐14 days later) **‐ Papule ► erythematous ► vesicular ►crusted** ‐ **Healing** (1‐3 weeks) ‐ **Lymph node enlargement** with _fever and malaise_
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What are the Differential Diagnoses: of Cat Scratch Disease ?
**‐ o Swellings in the lymph node** **o Unilateral swellings of the neck**
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How is Cat‐Scratch Disease diagnosed ?
‐ **Clinical features:** o Presence of a cat ▪ Presumptive diagnosis can be made ‐ Serology (antibody detection) ‐ Histopathology (biopsy) (Stellate suppurative necrosis surrounded by a band of histiocytes and neutrophils) and the use of Immunohistochemistry and Warthin‐Starry silver stain to identify the organism Left o Histiocytes on the periphery o Stellate necrosis in the center ‐ Middle Immunohistochemistry o Antibodies allow for visualization of Bartonella henselae (red little dots) ‐ Right : Warthin‐Starry silver stain o Silver stain allows for visualization of Bartonella henselae (black areas)
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How is Cat‐Scratch Disease treated?
o **Self‐limiting (resolves within 4 months)** o Local heat o Analgesics o Mechanical removal of suppuration (aspiration) o May use antibiotics for severe cases ▪ Azithromycin
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What is this infectious disease?
Cat‐Scratch Disease