Chapter 7: Viral Infections Flashcards
___ comes from the Greek word meaning “to creep or crawl”
herpes
___ are the only reservoir for HHV
humans
what are the 8 human herpes viruses (HHVs)?
- HSV-1 or HHV-1 - herpes simplex virus, type 1
- HSV-2 or HHV-2 - herpes simplex virus, type 2
- VZV or HHV-3 - varicella-zoster virus
- EBV or HHV-4 - epstein-barr virus
- CMV or HHV-5 - cytomegalovirus
- HHV-6
- HHV-7
- KSHV or HHV-8 - kaposi’s sarcoma herpesvirus
how does HSV-1 spread?
primarily through saliva or active perioral lesions
HSV-1 is best adapted to what locations?
above the waist
___ exposure has been the only condition to unequivocally induce HSV-1 lesions experimentally
UV light
in the case of HSV-1 symptomatic primary infections, ___ affects clinical presentation. how?
age
- younger = gingivostomatitis
- 18+ = pharyngotonsillitis
how does HSV-2 spread?
primarily through sexual contact
HSV-2 is best adapted to ___ locations
below the waist
clinical lesions produced by what herpes viruses are identical?
HSV-1 and HSV-2
in the initial exposure (aka primary infection) or HSV-2, is it primarily in old or young patients, and what percent are asymptomatic?
young, 80%
after initial HSV-2 exposure, the virus is taken up by ___ and transported to associated ___. which viral state does this describe?
- sensory nerves
- sensory ganglia
- at this point, the virus would be in the latent state
what is the most common site of HSV-2 latency?
trigeminal ganglion
what is the most common site of recurrence of HSV-1? what are other locations where recurrent lesions can occur?
- vermillion border and adjacent skin of the lips: herpes labialis, “cold sore”, “fever blisters”
- can also occur on the nose, chin, and cheek
___% of the US population have a history of herpes labialis
40%
HSV lesions appear as multiple, small, erythematous papules. describe them.
- papules form clusters of fluid-filled vesicles
- vesicles rupture and crust within 2 days
- heals without scarring in 7-10 days
- symptoms are most severe in the first 8 hours
the majority of people with HSV-1 or 2 will have how many outbreaks annually?
2
active viral replication of HSV-1 and 2 is complete within how many days?
2
what can result in the spreading of HSV-1 and 2 lesions?
mechanical rupture of intact vesicles releases the virus and can result in spreading of the lesions
recurrent intraoral herpes simplex lesions occur almost always on what type of tissue?
almost always on keratinized, bound mucosa (palate and attached gingiva)
describe the clinical presentation of recurrent intraoral herpes simplex lesions
- lesions begin as 1-3mm vesicles
- rapidly collapse to form a cluster or erythematous macules that coalesce and slightly enlarge
- damaged epithelium is lost
- central, yellowish area of ulceration
- heals in 7-10 days
primary HSV-1 infection is called ___
acute herpetic gingivostomatitis
what is the most common pattern of symptomatic primary HSV infection?
acute herpetic gingivostomatitis
most cases of acute herpetic gingivostomatitis occur before what age?
5
describe the clinical presentation of acute herpetic gingivostomatitis
- affected mucosa develops numerous pinhead vesicles
- both movable and attached oral mucosa can be affected
self-inoculation of fingers, eyes, and genitals can occur with ___
acute herpetic gingivostomatitis
what are the initial symptoms of pharyntotonsillitis (form primary herpes)
- sore throat
- fever
- headache
what is herpetic whitlow?
- aka herpetic paronychia
- less common presentation of HSV-1
- infection of the thumb or fingers
what is herpes gladiatorum?
- aka scrumpox
- less common presentation of HSV-1
- herpetic infection found in wrestlers or rugby players with contaminated abrasions
what is herpes barbae?
- less common presentation of HSV-1
- herpes over the bearded region of the face into minor injuries created by daily shaving
describe ocular involvement of HSV-1
- less common presentation of HSV-1
- leading infectious cause of blindness in the US
what is eczema herpeticum?
- aka kaposi’s varicelliform eruption
- less common presentation of HSV-1
- diffuse, life-threatening infection that can occur in patients with chronic skin conditions
how can newborns be infected with HSV, and what is the mortality rate without treatment?
- via an infected birth canal (usually HSV-2)
- 50% mortality rate without treatment
what are some histologic features of HSV?
- multinucleation
- ballooning degeneration
- acantholysis
- nuclear clearing
- nuclear enlargement
- tzanck cells
- free floating epithelial cells in an intraepithelial vesicle
what are some ways that HSV can be diagnosed?
- strong presumptive diagnosis from clinical presentation
- cytologic smear
- tissue biopsy
- serologic testing is positive 4-8 days after initial exposure
what is the general treatment of HSV?
antivirals, like acyclovir
what is the treatment for primary herpetic gingivostomatitis (HSV)?
- antivirals introduced early can reduce severity and frequency of recurrent infection
- antivirals introduced within 3 days can greatly accelerate clinical resolution
- once therapy is initiated, no new lesions develop
what is the primary varicella zoster (VZV) infection?
chickenpox represents the primary infection
how does VZV spread?
through air droplets or direct contact with active lesions
most cases of primary VZV infections occur in what age patients?
5-10
after initial VZV infection, where does the virus establish latency?
in dorsal spinal ganglia
what is shingles?
- reactivation VZV infection (single recurrence)
- occurs in 20% of patients
- prevalence increases with age
what are predisposing factors for reactivation of VZV?
- immunosuppression/immunosuppressive drugs
- radiation
- malignancies
- increasing age
- alcohol abuse
- emotional or physical stress
describe recurrent VZV oral lesions (shingles)
- occur with trigeminal nerve involvement
- present on movable or bound tissue (different from HSV)
- lesions tend to follow the path of the affected nerve and terminate at the midline; patient usually has accompanying skin lesions
- lesions are 1-4mm, white, opaque vesicles that rupture to form shallow ulcerations
describe ocular involvement of recurrent VZV (shingles)
- may cause significant morbidity (permanent blindness)
- if the tip of the nose is involved, it is a sign ocular infection may occur
- referral to ophthalmologist is mandatory if the patient experiences these lesions
what is ramsay hunt syndrome?
- cutaneous lesions of the external auditory canal as a result of recurrent VZV (shingles)
- involvement of ipsilateral face and auditory nerves
- facial paralysis
- hearing deficits
- vertigo
___ is the most common disease resulting from EBV exposure
infectious mononucleosis (kissing disease)
what are other lesions that demonstrate EBV?
- oral hairy leukoplakia
- lymphomas/lymphoproliferative disorders
- notably african’s burkitt’s lymphoma
- nasopharyngeal carcinoma
up to ___% of adults are infected with infectious mononucleosis
95%
how does infectious mononucleosis spread?
by intimate contact
how is infectious mononucleosis diagnosed?
presence of paul-bunnell heterophil antibodies
what is the treatment for infectious mononucleosis?
- most cases resove in 4-6 weeks
- NSAIDs can be given
- patients should avoid contact sports
- no steroids or antibiotics due to possible complications
- antivirals do not have clinical benefit
where can CMV reside?
in salivary gland cells, endothelium, macrophages, and lymphocytes
almost ___% of CMV infections are asymptomatic; of the ones that are symptomatic, what are the symptoms?
- 90%
- most common symptoms include fever, joint and muscle pain, shivering, etc.
CMV is common in patients with what disease?
AIDS
most individuals affected by CMV have ___
chronic mucosal ulcerations
what is the histology of CMV?
“owls eye” cell
enteroviruses are classified into what 3 categories?
- echoviruses
- coxsackievirus
- poliovirus
how many types of enteroviruses have been discovered up to this point? of those, how many cause symptomatic infections associated with rashes?
- about 60
- 30
what are the three enteroviruses that are important to oral health care professionals, and what subgroup of enteroviruses are they produced by?
- herpangina
- hand-foot-and-mouth disease
- acute lymphonodular pharyngitis
- all three are produced by the coxsackievirus
what is the incubation period for enterovirus?
4-7 days
___ and ___ promote the spread of enteroviruses
crowding and poor hygiene
what is the major path of transmission of enteroviruses?
fecal-oral route
during the acute phase, enterovirus can be transmitted via ___ or ___
saliva or respiratory droplets
what does infection to one enterovirus strain confer?
immunity to other enteroviruses
nearly half of reported cases of enterovirus infection occur in what age patient?
infants younger than 1 year
85% of all reported cases occur in patients younger than 20
what is the annual incidence of enterovirus in the US?
between 10-15 million symptomatic infections
how does herpangina present clinically?
- skin rash
- 2-6 oral lesions in the posterior mouth
- soft palate, tonsillar pillars
- begin as red macules and form fragile vesicles that rapidly ulcerate
- ulcerations are 3mm in diameter
- resolve within 10 days
what are symptoms of herpangina?
sore throat, fever, and dypshagia
with hand-foot-and-mouth disease, skin rash and oral lesions are associated with ___
flu-like symptoms
what lesions are almost always present with hand-foot-and-mouth disease?
hand and oral lesions
describe the oral lesions present with hand-foot-and-mouth disease
- arise first and without prodrome
- resemble those of herpangina, but larger and more numerous
- up to 30 lesions, up to 1cm in diameter
- affect buccal mucosa, labial mucosa, and tongue most commonly
describe the cutaneous lesions associated with hand-foot-and-mouth disease
- borders of palms and soles
- ventral surfaces and sides of fingers and toes
- erythematous macules that develop central vesicles
- heal without crusting
acute lymphonodular pharyngitis is characterized by what 3 symptoms?
sore throat, fever, mild headache
how does acute lymphonodular pharyngitis present clinically? when does it resolve?
- 1-5 yellow to dark pink nodules on the soft apalte or tonsillar pillars
- represent hyperplastic lymphoid aggregates
- resolves within 10 days without vesiculation or ulceration
the diagnosis of enteroviruses can be made from ___ manifestations, and the infection is ___
- clinical manifestations
- self-limiting
rubeola (measles) is caused by ___
a paramyxovirus
is there a vaccine for rubeola (measles)?
yes, it has been available since 1963 and is 95% effective (probably don’t need to know these specifics)
most cases of rubeola (measles) arise in what season?
winter
how does rubeola (measles) spread?
through respiratory droplets
the incubation period for rubeola is ___
10-12 days
rubeola is infectious how long before symptoms and how longer after the rash appears? what is responsible for the rash?
- 2 days before symptoms
- 4 days after rash appears
- vasculitis is responsible for the rash
rubeola is associated with significant ___
lymphoid hyperplasia
which disease lasts 9 days, with 3 stages that are 3 days each?
rubeola
termed nine-day measles
what is the first stage of rubeola?
- 3 C’s + fever
- cyroza, conjunctivitis, cough
- koplik’s spots
describe koplik’s spots
- multiple areas of mucosal erythema with numerous, small, blue-white macules (“grains of salt” on a red background)
- pathognomonic
- represent foci of epithelial necrosis
describe the second stage of rubeola
- fever continues
- koplik’s spots fade
- maculopapular and erythematous (morbilliform) rash begins
- face first
- downward spread from trunk extremities
- blanches on pressure
describe the 3rd stage of rubeola
- fever ends
- rash fades in similar downward progression
- replaced by brown pigmentary staining
rubella is caused by ___
togavirus
what is the greatest importance of rubella?
capacity to induce birth defects (congenital rubella syndrome)
what is the incubation time of rubella?
2-3 weeks
when are patients infected with rubella contagious?
from 1 week before rash to 5 days after its development
what are the vaccine contraindications for the rubella vaccine?
- pregnancy
- immunodeficiency
- acute febrile illnesses
- allergy to vaccine components
how long does rubella last? what are the symptoms?
- 3 days
- mild symptoms
arthritis is the most common complaint of ___
rubella
what are the oral lesions of rubella?
- forchhemier’s sign
- 20%
- small, discrete, dark-red papules on the palate
describe congenital rubella syndrome
- frequency of transmission from infected mother during first trimester is 80%
- triad: deafness (80%), heart disease, cataracts
the rubella vaccine is ___ preventative
95%
mumps is also called ___
epidemic parotitis
mumps are a disease of ___
exocrine glands
salivary glands are best known sites of involvement
in mumps, the involved glands exhibit ___ and ___
edema and lymphocytic infiltration
what is the incubation period of mumps?
2-4 weeks
when are mumps cantagious?
from 1 day before clinical appearance to 2 weeks after resolution
30% of mumps infections are ___
subclinical
with the onset of mumps, there will be a nonspecific ___ followed by significant ___ changes. what are the changes?
- prodrome
- salivary gland
- discomfort and swelling
- saliva stimulation increases pain
25% of postpubertal males with mumps will experiencee ___, characterized as swelling of the testicles (up to 4x the size), followed by atrophy
epididymorchitis
25% of first-trimester women with ___ will experience spontaneous abortions
mumps
what is the treatment of mumps?
- palliative treatment
- 99% decrease since MMR vaccine
when were the first cases of HIV/AIDS in the US documented?
1981
where is the HIV virus found?
in bodily fluids
what are the most frequent routes of transmission of HIV/AIDS?
- sexual contact
- parenteral exposure to blood
- transmission from mother to fetus
what is the target cell of HIV/AIDS?
- CD4+ helper T lymphocyte
- when T-helper cells are destroyed, immune function is lost
what are the 3 stages of HIV/AIDS?
- acute self-limited viral syndrome
- asymptomatic period
- final symptomatic period
what are the 5 oral manifestations most strongly associated with HIV infection?
- oral hairy leukoplakia (EBV)
- candidiasis
- non-hodgkins lymphoma
- kaposi’s sarcoma (HHV-8)
- periodontal disease
oral candidiasis is present in ___ of HIV patients and ___ of AIDS patients
- 1/3
- 90%
what is the treatment for oral candidiasis associated with HIV/AIDS?
- treatment is difficult - skip nystatin and prescribe topical clotrimazole
- systemic fluconazole is given if:
- patient is not on HAART
- patients CD4+ count is <50
- patient has a high viral load
- there is esophageal involvement
oral hairy leukoplakia present in HIV/AIDS patients is a sign of what?
severe immune depression and advanced disease
oral hairy leukoplakia rarely occurs in any other form of immune suppression other than ___
HIV/AIDS
its presence in the absence of known immunosuppresion mandates HIV testing
___ is the most common EBV-related lesion in AIDS patients
oral hairy leukoplakia
how does oral hairy leukoplakia in HIV/AIDS patients present clinically? how is it diagnosed? what is the treatment?
- white mucosal plaque that does not rub off, usually occurs on the lateral border of the tongue
- clinical diagnosis can be made
- no treatment necessary
___ is present in up to 20% of AIDS patients and is characterized by multifocal neoplasm of vascular endothelial cell origin
kaposi’s sarcoma (HHV-8)
with kaposi’s sarcoma in HIV/AIDS patients, the ___ may represent the predominant reservoir of the infectious virus
oral cavity
___% of HIV/AIDS patients with kaposi’s sarcoma have oral lesions
70%
in 20% of HIV/AIDS patients, where is the primary site of involvement of kaposi’s sarcoma?
the oral cavity
what 3 areas of the oral cavity are commonly affected by kaposi’s sarcoma?
hard palate, gingiva, and tongue
how is kaposi’s sarcoma in HIV/AIDS patients diagnosed?
biopsy is required
up to ___% of HIV-infected patients will have non-hodgkins lymphoma
5%
how does non-hodgkin’s lymphoma in the HIV/AIDS patient present?
high-grade and aggressive disease
what is non-hodgkin’s lymphoma in the HIV/AIDS patient associated with?
widespread involvement and short survival times
a large number of non-hodgkin’s lymphoma in the HIV/AIDS patient cases have a relationship with what other virus?
EBV
what are the 3 atypical patterns of periodontal disease associated with HIV?
- linear gingival erythema
- necrotizing ulcerative gingivitis
- necrotizing ulcerative periodontitis
describe linear gingival erythema associated with periodontal disease in the HIV patient
- linear gingival erythema diagnosis is reserved for gingivitis that doesn’t respond to improved plaque control and has a greater degree of erythema than would be expected
- distinguishes from marginal gingivitis
describe necrotizing ulcerative gingivitis associated with periodontal disease in the HIV patient
ulceration and necrosis of interdental papillae with no attachment loss
describe necrotizing ulcerative periodontitis associated with periodontal disease in the HIV patient
ulceration and necrosis with rapidly progressing attachment loss
what is the treatment for linear gingival erythema associated with periodontal disease in the HIV patient?
systemic antifungals
what is the treatment for NUG and NUP associated with periodontal disease in the HIV patient?
debridement, antimicrobials, immediate follow up, long term maintenance
___ can occur if periodontal disease in the HIV/AIDS patient is left untreated
necrotizing stomatitis
___ altered the course of the HIV/AIDS epidemic
highly active antiretroviral therapy (HAART)
how has the risk of seroconversion after exposure to HIV-contaminated blood been altered as a result of HAART?
- percutaneous exposure = 0.3%
- mucous membrane exposure = 0.09%
- non-intact skin exposure = lower than 0.09%
in addition to HAART, the risk of seroconversion after exposure to HIV-contaminated blood is reduced by 75% via ___
prophylaxis with antiretrovirals
must take within 24 hours and for 4 weeks
HSV-1
younger patient, so this is gingivostomatitis
HSV-1
older patient, so this is pharyngotonsilitis
acute herpetic gingivostomatitis
90% from HSV-1
acute herpetic gingivostomatitis
90% from HSV-1
acute herpetic gingivostomatitis
pharyngotonstilitis
can be HSV-1 or 2
recurrent herpes simplex
recurrent intraoral herpes simplex
recurrent intraoral herpes simplex
recurrent intraoral herpes simplex
HSV-1 - herpetic whitlow
HSV-1 - herpes gladiatorum aka scrumpox
HSV-1 - herpes barbae
HSV-1 - eczema herpeticum aka kaposi’s varicelliform
VZV - chicken pox
VZV - chicken pox
VZV - shingles
ramsay hunt syndrome (VZV)
characterized by cutaneous lesions of the external auditory canal, involvement of ipsilateral face and auditory nerves, and facial paralysis, hearing deficits, and vertigo
VZV herpes zoster oral lesions
VZV herpes zoster oral lesions
VZV - herpes zoster oral lesions
infectious mononucleosis (EBV)
cytomegalovirus
notice the “owl eyes” cells
herpangina (coxsackie virus, enterovirus)
hand foot and mouth disease
Rubeola - characterized by koplik’s spots
Rubeola
rubella
rubella - characterized by forchheimer’s sign
mumps aka epidemic parotitis
HIV+
HIV-associated candidiasis
HIV+
HIV-associated oral hairy leukoplakia
HIV+
HIV-associated kaposi’s sarcoma (HHV-8)
HIV+
HIV-associated kaposi’s sarcoma (HHV-8)
HIV+
HIV-associated kaposi’s sarcoma (HHV-8)
HIV+
HIV-associated kaposi’s sarcoma (HHV-8)
HIV+
HIV-associated kaposi’s sarcoma (HHV-8)
