Osd Viral Infections I And 2

Front 1

HIV Immunopathogeneis

Back 1

 Early: Acute phase HIV infection:
• Self-limiting illness within weeks (immunocompetent)
o CD4+ T cells return to near normal numbers
• High level of virus production, viremia and reduction of CD4+ T cells
o contagious
• Seroconversion: Production of Anti-HIV antibodies-not helpful
o Used for clinical screening for HIV infection
 Middle: Clinical latent period(10-20 years)
• A stage of relative containment of the virus
• Continue HIV replication
• Continue gradual CD4+ cell loss
• Asymptomatic, some may be persistent lymphadenopathy and minor opportunistic infections
 Final: crisis phase
• Break down of host defenses system
• Profound loss of CD4+ cells, full blown AIDS

Front 2

• HIV Transmission

Back 2

o Sexual Transmission
o Parenteral Transmission
 Can escape screening process
o Mother to infant transmission
 Usually occurs during delivery
• Mother can have C-section instead and baby can start anti-virals
o Body fluids such as semen and blood are usually the source of infection
o Saliva of AIDS patients contains HIV, but transmission of AIDS via saliva is rare

Front 3

Oral and Maxillofacial Lesions Strongly Associated with HIV Infection

Back 3

• Oral and Maxillofacial Lesions Strongly Associated with HIV Infection
o Candidiasis
o Oral Hairy Lerukoplakia
o Kaposi’s Sarcoma
o Non-Hodgkin’s lymphoma
o Periodontal Disease

Front 4

Candidiasis in HIV patients
-how common is it?
-caused by what virus?
-indication of?
-how to reduce frequency?

Back 4

o Oral candidiasis is the most common intraoral manifestation of HIV infection
o Most common: Candida albicans
o An indication of patients’ immune status:
 CD4 count low
o HAART significantly reduces the frequency

Front 5

• Oral Hairy Leukplakia
- most common
-causes?
-indicates?
-clinical:
-histopathology:
-how to detect: immunochem or insitu hybridization
-tx:

Back 5

o The most common EBV-related lesion in AIDS patients
 Causes epithelial hyperplasia + increase keratin
o Indicator of patient’s low immune status
o Clinical:
 Lateral tongue most common
• Faint or thickened white vertical streaks that do not rub off
• An indication of the patient’s immune status
o Histopathology:
 Hyperkeratosis and layer of “ballooning cells” in the upper spinous layer
 Histology is suggestive, but not specific
 Detect EBV by immunohistocehmistry or insitu hybridization
o Tx: Not needed

Front 6

• HIV-Associated Kaposi’s Sarcoma

most common?
compared to non HIV Kaposis?
type of tumor? caused by?
manfiests as?
what can be seen in the oral cavity?
requires a ___ for dx?
Therapy?

Back 6

o The most common malignancy in HIV patients
 Non-HIV associated in older/lower extremeties
 HIV-assoicated: younger, on trunk, mucous membranes and internal organs
o A malignant vascular tumor caused by HHV8/KSHV
 Vascular proliferation
o Manifest as multiple lesions of the skin. oral mucosa & viscera
o Oral cavity: palate, tongue & gingiva
 starts as purple macular lesions on skin and later develops into nodules
 Invade bone
o Biopsy is necessary
o HAART has significantly reduced KS prevalence

Front 7

• HIV-associated Non-Hodgkin’s Lymphoma

-how common is it?
-caused by?
-majority are what type?
-occur where?

Back 7

o The 2nd most common malignancy in HIV patients
o Caused by EBV (KSHV?)
o Majority are high grade B-cell lymphoma
o Usually occur in extranodal locations
 CNS is the most common location

Front 8

• HIV Periodontal Disease
-how many patterns?
-response to perio? progression? clinically looks similar to?
-3 types:

Back 8

o 3 atypical patterns (not specific, but strongly associated with HIV)
o No response to conventional perio Tx. Rapid progression.
 Though similar to marginal gingivitis
o Linear gingival erythema
 Linear band of erythema involving the free gingival margin
o Necrotizing ulcerative gingivitis/stomatitis
 Ulceration/necrosis of one or more interdental papillae without loss of periodontal attachment
 Loss of tissue  oral bacteria access to soft tissues
o Necrotizing ulcerative periodontitis
 Gingival ulceration/necrosis associated(2) with rapid progression loss of periodontal attachment
 Multiple isolated defects often are seen in contrast with the diffuse pattern associated with typical chronic periodontitis
• Punched out isolated lesions of bone loss
• Depp isolated pockets of bone loss in mandibular anteriors

Front 9

Other Oral and Maxillofacial Lesions Associated with HIV Infection

Back 9

Diffuse Infiltrative Lymphocytosis Syndrome
Human Papillomavirus
Aphthous Ulcerations
Molluscum Contagiosum
Oral Squamous Cell Carcinoma
Mycobacteria
Histoplasmosis
HSV and EBV

Front 10

Diffuse Infiltrative Lymphocytosis Syndrome

-clinical sx
-type of disease?
-affects what area? looks like?
-develop risk for?
-dx?

Back 10

 CD8 lymphocytosis(CD4 decreasing) and lymphadenopathy
 HIV-associated salivary gland disease
• Salivary gland enlargement, particularly parotid gland caused by CD8 lymphocytic infiltrate
o Looks like mumps
• High risk to develop B-cell lymphoma. Patients need to be monitored.
 Biopsy

Front 11

o Human Papillomavirus
- clinical manifesation
- HAART has what affect?
- Normal vs. HIV
-normal do occur in

Back 11

 Verruca vulgaris (common wart) and oral squamous papilloma
• Multiple exophytic on papillary nodules
 HAART treated patients show increased prevalence of HPV-related lesion
 More exaggerated in HIV patients
• Surface corrugated and covered with keratin
• Lesions merge together(usually single isolated)never happens in normal patient

Front 12

o Aphthous Ulcerations “canker sore”

-type of disease?
-HIV patients see?
-HIV patients usually develop what form?
-which resembles and looks like?
-how do you tell the difference

Back 12

 Autoimmune disease
• Can also occur in under stress
 HIV patients have increased frequency to develop all forms of aphthous ulcer (minor, major and herpetiform)
 In contrast to normal patients, most HIV patients develop major or herpetiform variants
• Herpetiform: resembles herpetic ulcer, cluster of small pinheadlesions
• Normal-heals in 2 weeks
 Vs. herpetic form
• Herpetic ulcer stats w/ a vesicle, aphthous doesn’t not though
• Aphthous Ulcerations attack moveable mucosa(lips, tongue) , herpetic form affects bone bound(palate, gingival) mucosa-not keratin!

Front 13

o Molluscum Contagiosum
-type of infection? caused by?
-Clinical
-in children presents as?
-in HIV patients presents as?

Back 13

 Infection of the skin caused by poxvirus
• Only on skin
 Clinical:
• Oral lesions have been reported, but rare
• Small dome-shaped papules with a central depression crater
 Usually affects children as 1 small nodule and self limiting.
 HIV+ patients:
• Hundred of lesions, occasionally large size
• Little tendency to undergo spontaneous resolution thus needing treatment

Front 14

o Molluscum Contagiosum
-type of infection? caused by?
-Clinical
-in children presents as?
-in HIV patients presents as?

Back 14

 Infection of the skin caused by poxvirus
• Only on skin
 Clinical:
• Oral lesions have been reported, but rare
• Small dome-shaped papules with a central depression crater
 Usually affects children as 1 small nodule and self limiting.
 HIV+ patients:
• Hundred of lesions, occasionally large size
• Little tendency to undergo spontaneous resolution thus needing treatment

Front 15

o Oral Squamous Cell Carcinoma

Back 15

 Tumor has the same risk factor in HIV patients as in normal population, but tends to occur at younger age which it normally doesnt

Front 16

Other oral maxillo-facial lesions

Back 16

o Mycobacteria
o Histoplasmosis
o HSV and EBV

Front 17

Treatment for HIV

Back 17

 Low fidelity of RT used to form DNA
• Transition from RNA DNA allows more chance for mutation
 Produce large proteins which need to get spliced to become functional proteins

Treatment via:
Cocktail: inhibitors for reverse transcriptase, protease(1 large protein spliced into small ones), integration

Front 18

 HAART
cocktail of?
effect?
kills virus?

Back 18

• Reverse transcriptase inhibitor
• Potease inhibitor
• Integrase inhibitors
• CCR5 inhibitors: CCR5 is a co-receptor for HIV-1 (predominant)infection
o PPL resistance to HIv hace CCR5 gene mutation(coreceptor for HIV-1)
 Survival times are increasing; clinically significant reconstitution of the immune system
 The treatment does not kill cells infected by the virus, but can drive HIV to undetectable levels in many patients
• Cannot eliminate HIV
• Patients still eventually enter chrisis stage
 Prevention of initial infection is still the best defense

Front 19

• HHV types

Back 19

o HSV1,2
o Varicella-zoster virus(HHV3)
o EBV-HHV4
o CMV-HHV5
o HHV6/7
o HHV8/Kaposis sarcoma herpes virus(HHV8/KSHV)

Front 20

• HSV1 vs. HSV2

Back 20

 1 is waist up
 2 is waist down/sexually transmitted

Front 21

• Primary herpes
-majority of patients have?
-clinicial symptoms?
-treatment?
• Secondary herpes
-occurs when
-clinical manifestion
-systemic sx?
-location?
-treatment?

Back 21

• Primary herpes
o Majority of patients have subclinical infection
o Vesiculoulcerative eruption on skin or mucosa in symptomatic patients
 Eruptions may spread
 Systemic effects: fever
o Resolve by itself in immunocompetent patients
• Secondary herpes
- Immunocompromised
o Vesiculoulceartive eruptions on epithelium innovated by the nerve-localized
o milder primary: No systemic symptom in normal patients
o Localized to nerve and self-limiting

Front 22

• Primary Herpetic gingivostomatitis

-transmission?
-most common patients?
-clinical manfiestion?

Back 22

o Transmission:
 physical contact with infected individuals
o Most patients are children
o Clinical: Vesiculoerosive eruptions (not limited to bone-bound mucosa- all sites of oral mucosa)
 Numerous pin-head vesicles, which quickly ulcerate and merge
 Gingiva is always involved, extremely erythematous
 May involve vermillion and perioral tissue as well as tongue and lymph nodes
o Systemic symptoms:
 fever, malaise, headache, cervical lymphadenopathy-fairly mild
o Heal in a week, as virus migrate to the trigeminal ganglion (latency)

Front 23

• 2nd or Recurrent Herpes Simplex Infections
-caused by?
- symptoms prior to flare up?
- clinical manifestation?
- compared to angular chelitis?
-immunocompetent vs. immunodeficient patients

Back 23

o Reactivation:
 breakdown in focal immunosurveilance
o Prodromal(distinct tingling prior to flare up) symptoms in the site where lesions will appear
o Vesiculoerosive process: clusters of pin-head vesicles that rupture quickly
 Oral cavity: limited to mucosa that is bound to bone (hard palate & gingiva)
 Vermillion and the surrounding skin: Herpes labialis
 No systemic symptom, self-limiting
o Vs. Angular chelitis
 Angular chelitis never remits spontatneously, and doesn’t start as vesicles
o Immunocompetent patients
 Self limiting and no systemic
o Immunodeficient patients
 Atypical presentation
• Not restricted to gingiva and palate
• Large, chronic and destructive
 Predispose to bacteria infection, and CMV co-infection
 Not self-limiting-destructive

Front 24

• Herpetic Whitlow
-type of infection?
-clinical?
-lasts?
-caused by?

Back 24

o HSV infection involving the finger(s)
o May be primary or secondary
o Vesiculoerosive eruptions
 Vesicles which become ulcerated
o Very painful and can last from 4-6 weeks
o Before the universal use of examination gloves, herpetic whitlow was not uncommon in dental practitioners in physical contact with infected individuals

Front 25

• Oral Herpes Simplex Infection
Primary vs. 2ndary DDH
Diagnosis:
Tests used:

Back 25

 EM:
• resembles primary herpes
o but no gingival involved(mucosa/lips)
• major forms can have skin involvement but usually just oral
 ANUG:
• adjacent gingival affected, no tongue or lip,,
• interdental papillae become necrotic
• No systemic effects
• Herpes has systemic effects and papillae not affected
o 2nd DDH:
 Apthous ulcers: all forms occur on mobile mucosa, no vesicle, usually one lesion
 Traumatic ulcers: multiple vs. single lesion, no vesicles
o Dx: clinical symptoms
 Cytologic smear or biopsy
• Histopathology:
o Acantholysis and intraepithelial vesicles
 Fluid accumulation in epithelium  intraepithelial vesicles
 Acantholysis: epithelieal cells fall apart and detatch from each other forming Tzanck cells
o Tzanck cells(non specific to herpes): free floating epithelial cells. In case of herpes simplex infection, cells exhibit cytopathologic effect by virus infection (multinucleation, nuclear margination of chromatin)
o Culture, serology (for primary-patient never seen herpes b4) etc-scrape vesicles

Front 26

• Herpetic Whitlow
-type of infection?
-clinical?
-lasts?
-caused by?

Back 26

o HSV infection involving the finger(s)
o May be primary or secondary
o Vesiculoerosive eruptions
 Vesicles which become ulcerated
o Very painful and can last from 4-6 weeks
o Before the universal use of examination gloves, herpetic whitlow was not uncommon in dental practitioners in physical contact with infected individuals

Front 27

• Oral Herpes Simplex Infection
Primary vs. 2ndary DDH
Diagnosis:
Tests used:

Back 27

o Primary DDH: erythema multiforme, and acute necrotizing ulcerative gingivitis
 EM:
• resembles primary herpes
o but no gingival involved(mucosa/lips)
• major forms can have skin involvement but usually just oral
 ANUG:
• adjacent gingival affected
o no tongue or lips
• interdental papillae become necrotic
• No systemic effects
• Herpes has systemic effects and papillae not affected
o 2nd DDH:
 Apthous ulcers: all forms occur on mobile mucosa, no vesicle, usually one lesion
 Traumatic ulcers: multiple vs. single lesion, no vesicles
o Dx: clinical symptoms
 Cytologic smear or biopsy
• Histopathology:
o Acantholysis and intraepithelial vesicles
 Fluid accumulation in epithelium  intraepithelial vesicles
 Acantholysis: epithelieal cells fall apart and detatch from each other forming Tzanck cells
o Tzanck cells(non specific to herpes): free floating epithelial cells. In case of herpes simplex infection, cells exhibit cytopathologic effect by virus infection (multinucleation, nuclear margination of chromatin)
o Culture, serology (for primary-patient never seen herpes b4) etc-scrape vesicles

Front 28

• Oral Herpes Simplex Infection
treatment timing:
treatment

Back 28

o Tx:
 Timing is everything: ideally within 48 hours from the onset of the symptom
o Primary:
 supportive therapy w/o antiviral agents (acyclovir and analogs)
o Secondary:
 Normal patients: usually not required. Prophylactic Tx reserve for problematic cases
 Immunodeficient patients: always need antiviral treatment

Front 29

• Oral Herpes Simplex Infection
treatment timing:
treatment

Back 29

o Tx:
 Timing is everything: ideally within 48 hours from the onset of the symptom
o Primary:
 supportive therapy w/o antiviral agents (acyclovir and analogs)
o Secondary:
 Normal patients: usually not required. Prophylactic Tx reserve for problematic cases
 Immunodeficient patients: always need antiviral treatment
o Tx:
 Timing is everything: ideally within 48 hours from the onset of the symptom
o Primary:
 supportive therapy w/o antiviral agents (acyclovir and analogs)
o Secondary:
 Normal patients: usually not required. Prophylactic Tx reserve for problematic cases
 Immunodeficient patients: always need antiviral treatment
o Can treat patients with prodromal sx to prevent vesicles

Front 30

• Varicella-zoster virus

clinical
classification

Back 30

o Clinical:
 Vesiculoerosive eruption on skin and mucosa
 Self-limiting in immunocompetent patients
o Classification
 Varicella (Chickenpox): primary infection
 Herpes zoster (shingles): recurrent infection

Front 31

• Varicella(Chicken pox)
-common in?
-transmission?
-clinical?
-why should you try to get it as a child

Back 31

o Common in children. Adult patients usually suffer from severe symptom and may develop complications
o Transmission:
 Inhalation of contaminated droplets, or direct contact (rare)
 Patients are very contagious, readily spread from child to child
o Clinical: rash +systemic symptoms (fever, malaise)
 Generalized eruption of vesicles
• Start as skin rash, progress to vesicles and pustules that rupture and crusted
• For about a week, a mixture of lesions at various stages of development and resolution is present
• Minor oral involvement
o Try to get it as a child… as in adults you see many complications

Front 32

• Herpes zoster (shingles)
-occurs mostly in?
-compared to HSV
-Clinical:

Back 32

o Mostly in the elderly and the immunocompromised
 Reactivation of VZV is not as common as HSV
o Clinical:
 Predromal: pain or paresthesia in the affected dermatome
 Develop unilateral vesicular rash along the nerve distribution and terminate at the midline
• Coalescence of the vesicles followed by crusting, occurs quickly
o Trigeminal ganglia-can affect any branch
 Oral lesions
• Both movable and bound mucosa, terminate at the midline
• Skin overlying the affected quadrant is affected-dermatome-doesn’t cross midline
 Ocular involvement may result in blindness

Front 33

• Varicella-zoster virus

clinical
classification

Back 33

o Clinical:
 Vesiculoerosive eruption on skin and mucosa
 Self-limiting in immunocompetent patients
o Classification
 Varicella (Chickenpox): primary infection
 Herpes zoster (shingles): recurrent infection

Front 34

• Varicella(Chicken pox)
-common in?
-transmission?
-clinical?
-why should you try to get it as a child

Back 34

o Common in children. Adult patients usually suffer from severe symptom and may develop complications
o Transmission:
 Inhalation of contaminated droplets, or direct contact (rare)
 Patients are very contagious, readily spread from child to child
o Clinical: rash +systemic symptoms (fever, malaise)
 Generalized eruption of vesicles
• Start as skin rash, progress to vesicles and pustules that rupture and crusted
• For about a week, a mixture of lesions at various stages of development and resolution is present
• Minor oral involvement
o Try to get it as a child… as in adults you see many complications

Front 35

• Herpes zoster (shingles)
-occurs mostly in?
-compared to HSV
-Clinical:

Back 35

o Mostly in the elderly and the immunocompromised
 Reactivation of VZV is not as common as HSV
o Clinical:
 Predromal: pain or paresthesia in the affected dermatome
 Develop unilateral vesicular rash along the nerve distribution and terminate at the midline
• Coalescence of the vesicles followed by crusting, occurs quickly
o Trigeminal ganglia-can affect any branch
 Oral lesions
• Both movable and bound mucosa, terminate at the midline
• Skin overlying the affected quadrant is affected-dermatome-doesn’t cross midline
 Ocular involvement may result in blindness

Front 36

• Varicella-zoster Virus
- pain?
-histopath?
-clinical presentation?
-tx?

Back 36

o Postherpetic neuralgia: 15%
o Uncommon in young patients, Most resolve in 1 year
o Histopathology: same as HSV-clinically distinct though
o Dx: Clinical presentation
 Unilateral lesions along dermatomes of the peripheral nerves
 If presentation is atypical, lab tests are required
• Immunocompromised patients: wide spread and chronic lesions with severe complications(doesn’t follow midline rules)
o Tx: Normal patients: symptomatic and supportive treatment
 Immunocompromised patients: Treated with acyclovir and analogs
o Vaccines available (not 100%)

Front 37

• Epstein-Barr Virus diseases?

Back 37

o Diseases caused by EBV
 Infectious mononucleosis
 Oral hairy leukoplakia: AIDS patients
 Lymphoproliferative disorders (African Burkitt lymphoma)
 Nasopharyngeal carcinoma
 Chronic fatigue syndrome

Front 38

• Cytomegalovirus
-common?
-transmission?
immunocomrpomised patients?
histpathology?

Back 38

o Transmission:
 exchange of body fluid, organ transplant
 Infection ubiquitous, most subclinical
o Immunocompromised patients: affects many organs
 Oral manifestation:
• Chronic oral ulcer: often co-infect with HSV
• Cytomegaloviral sialadenitis
o Histopathology:
 CMV infected cells are massively enlarged. They contain intranuclear and cytoplasmic inclusions and exhibit “owl eye” alteration
 Attacks salivary gland too

Front 39

Enteroviruses
-type of virus?
-transmitted?
-3 diseases?
-tx?

Back 39

o Transmission:
 Inhalation of respiratory droplets and fecal-oral route
 Most common in schoolchildren during outbreak
o 3 diseases are discussed here. All three are self-limiting.
 Herpangina
 Hand, foot, and mouth Disease
 Acute lymphonodular pharyngitis
o Usually diagnose can be made clinically. Specific lab tests are available.

Front 40

• Herpangina
sx:
clincal:
tx?

Back 40

o sx Sore throat, dysphagia and mild flu-like symptom
 Clinical:
A small number of vesicles develop in oropharynx area
 The vesicles ulcerate quickly.
o Don’t need anti-viral meds

Front 41

• Hand, Foot, and Mouth Disease
-sx?
-clinical?
tx

Back 41

o Clinical: Skin rash, oral lesions and flu-like symptoms
 Skin rash: eruption of small vesicles on the palms of the hand and the feet
 Oral lesions: Oral vesicles and ulcers on any oral mucosa
o TX: self limiting

Front 42

• Acute Lymphonodular Pharyngitis

clinical:
nodules caused by?
treatment?

Back 42

o Clinical: sore throat and flue-like symptom(similar to strept pharyingitis)
 Low number of yellow nodules develop in oropharynx area
 No vesiculation or ulceration
o Nodules are caused by lymphoid hyperplasia
o Tx: self limiting

Front 43

MMR vaccine protects

Back 43

 Measles 98%
 Mumps 95%
 Rubella - not liftime 100%, only 100% if you get the disease

Front 44

• Rubeola (Measles)
-transmission
-clinical:
-dx
-tx

Back 44

o Transmission: respiratory droplets, highly contagious
o Clinical: Systemic symptoms and high fever
 Koplik’s spots: clusters of tiny white papules with an erythematous areola on buccal mucosa. The proceed the skin rash and are pathognomonic.
 Skin rash: spread from face to trunk and extremities
• Rash fades and are follow by desquamation
o Dx: clinical and confirm by serology
o Self-limiting but can be complicated by significant morbidity and mortality

Front 45

• Rubella (German Measles)
transmission?
clinical?
effects during pregnancy?
Dx?

Back 45

o Transmission: respiratory droplets
o Clinical:
 Most subclinical
 Symptomatic patients develop skin rash that fades in a few days. Symptoms are generally very mild.
 Milder measles-no systemic effects
o Congenital rubella syndrome: infection induce birth defects in the developing fetus
 Frequency of transmission from an infected mother to the fetus is greater than 80% in the first trimester
 Immunity in pregnant women need to be confirmed since vaccine does not provide life time protection
o Dx: (clinical and) confirmed by lab tests

Front 46

• Mumps
-transmission?
-clinical?

Back 46

o Transmission: respiratory droplets
o 30% subclinical, symptomatic patients develop lesions in major salivary glands
 Most patients develop swelling and pain in parotid glands. Other major salivary glands also can be involved
 Primarily parotid
o Also infect other exocrine glands, but usually not severe
 Males: Orchitis(testis): the 2nd most common finding in mumps, occurs in 25% of postpubertal males
• Sterilize males
 Females: Oophoritis(ovaries) and mastitis(breast): less common
• Can cause spontaneous abortion
o Dx: clinical and lab tests