6. Viral Infection II Flashcards
What is the most common clinical presentation for patients that develop symptoms from primary herpes?
Primary herpetic gingivostomatitis
What population does primary herpetic gingivostomatitis tend to affect?
Children
What are the clinical presentations of gingivostomatitis?
Vesiculo-ulcerative eruptions (not limited to bone-bound mucosa)
numerous pin head vesicles which quickly ulcerate and merge
gingiva is always involved, extremely erythematous
May involve vermillion and perioral tissue
Older pts develop vesicles in pharynx and mimics pharyngostonsillitis
What are the systemic symptoms of primary herpetic gingivostomatitis?
fever
malaise
headache
cervical lymphadenopathy
How does primary herpetic gingivostomatitis resolve?
Heals in a week as virus migrates to trigeminal ganglion (latnecy)
What allows a secondary/recurrent HSV to occur?
A breakdown in local immunosurveillance allows the virus to reactivate
What kind of symptoms occur at the site where secondary HSV lesions will appear?
Prodromal symptoms (pain or tingling)
S/S of 2nd HSV infection
Vesiculo-ulcerative process
clusters of pin head vesicles that rupture quickly
In oral cavity, limited to mucosa that is bound to bone (hard palate and gingiva)
Vermillion and surrounding skin can have lesions (esp commissure area): herpes labialis
No systemic symptoms
How does secondary HSV infection resolve?
Selt-limited
How does secondary HSV infection affect immunodeficient pts?
Atypical presentation
lesions not limited to bound muscoa (will see on tongue)
vesicles are bigger, chronic and destructive
Presdisposes pt to bacteria infection andusually con-infected with CMV
What is herpetic whitlow?
infection of the finger by the HSV
S/S of herpetic whitlow
Vesiculo-ulcerative eruptions
very painful and lasts for 4-6 weeks
Do herpetic whitlow lesions occur in primary or secondary infection?
both
What population was once often affected by herpetic whitlow?
dentists before use of gloves
What are other conditoins that must be listed as a DDH when thinking about primary oral HSV infection? What differentiates each condition from primary HSV?
Erythema multiforme
- spares gingiva whereas gingivostomatitis always involves gingiva
Acute necrotizing ulcerative gingivitis
- no vesicles whereas gingivostomatitis has vesicles
- do not involve other mucosa whereas gingivostomatitis can involve palate, tongue, etc
What are other conditions that must be considered for an secondary oral HSV infection? How do they differ from secondary oral HSV?
Apthous ulcers
- movable ulcers
- non-keratinized mucosa
- no vesicles
Traumatic ulcers
- one single large lesion whereas HSV tends to be multiple small vesicles
- no vesicles
Dx for oral HSV infection
Clinical symptoms unless for atypical or immunocompromised pts
Culture is difficult for herpes
Serology only works for primary HSV infection
Cytology smear or biopsy:
- Ballooning degeneration
- acantholysis
- Tzanck cells
- intraepithelial vesicles
- Cytopathologic effects on virus infection
- herpes infection causes keratinocytes to fuse resulting in below features
- multinucleation
- margination of chromatin
Tx for oral HSV infection
Ideal treat within 48 hours fro monset of symptoms
Normal pts don;t need any antiviral drugs. Just supportive treatment
Immunodeficient pts always need antiviral treatment
Primary
- supportive therapy w/o antiviral agents
Secondary
- Normal pts usually dont need tx
- prophylactic Tx is reserved for problematic cases
What are the general clinical features of varicella-zoster virus?
Vesiculoulcerative eruption on skin and mucosa
Self-limiting in immunocompetent patients
What are the two classifications of varical-zoster virus infections?
Primary infection = Varicella (chickenpox)
Secondary/recurrent infection = Herpes zoster (shingles)
How does chickenpox differ in adults vs children?
adults usually suffer from severe symptom and may develop complications
how is chickenpox transmitted?
Inhalation of contaminated droplets, readily spread from child to child
Pts are very contagious, readily spread from child to child
Clinical features of varicella?
Rash + systemic symptoms (fever + malaise)
Generalized eruption of vesicles
Start as skin rash, progress to vesicles and pustules that rupture and ulcer
For about a week, a mixture of lesions at various stages of development and resolution is present
Oral invovlement is common but minor
Varicella Dx
Based on clinical presentation
Varicella complications
Secondary skin infections, encephalitis, pneumonia
infection during pregnancy may result in spontaneous abortion or congenital defects
Most common in adults
Prevention is the best Tx, get vaccinated
What populatin does herpes zoster (shingles) affect?
elderly and immunocompromised
S/S of shingles
Prodromal: pain or paresthesia in the affected dermatome
Develop unilateral rash along the nerve distribution and terminate at the midline (coalescence of the vesicles followed by crusting)
Vesicles develop in one dermatome - waistline = common location
Postherpetic neuralgia (15%) - resolves in a year and uncomon in young pts
Trigeminal ganglia presence:
- Oral lesions
- both movable and bound mucosa, terminate at the midline
- skin overlying the affected quadrant is affected
- Ocular involvement may result in blindness
Herpes Sozter Dx
Clinical presentation
Unilateral lesions along dermatome of the peripheral nerves
Lab tests are req’d for atypical presentation:
- Immunocompromised pts wide spread and chornic lesions that cross the midline with severe complications
- histopathology is the same as HSV
Tx for Zoster
normal patients only need symptomatic and supportive treatment
immunocompromised pts need antivirals (acyclovir and analogs)
Vaccine for shingles is available and recommended for elderly but not 100% effective
What diseases are caused by EBV?
Infectious mononucleosis
Oral hairy leukoplakia
Lymphoproliferative disorders (NHL, African Burkitt lymphoma)
Nasopharyngeal carcinoma
Chronic fatigue syndrome
How is CMV transmitted?
Exchange of body fluid
organ transplant
S/S of CMV infection in normal pts
almost everyone is infected by CMV
asymptomative in healthy individuals
S/S of CMV in immunocompromised pts
Affects many organs
Oral manifestations:
- chronic oral ulcer: often co-infect with HSV
- CMV sialadenitis (salivary gland enlargement)
CMV Dx
Clinical + lab test
Histopathology:
- CMV infected cells are HUGE
- Cells have owl eye presentation
- Cells contain intranuclear and cytoplasmic inclusions
Tx for CMV
Only necessary for immunocompromised pts
Which enterovirus causes head and neck conditions?
Coxsackie virus
How is coxsackie virus transmitted?
Inhalation of resp droplets
Fecal-oral route
Population most affected by coxsackie?
Children
3 diseases caused by coxsackie
Herpangina
Hand,foot, mouth dz
Acute lymphonodular pharyngitis
Dx for coxsackie infection?
Clinically
Specific lab tests are available
S/S of herpangina
sore throat
dysphagia
mild flu-like symptom
small number of vesicles develop in oropharynx area
vesicles ulcerate very quickly
self-limiting process with recovery in 1 week
S/S of hand-foot-mouth disease
skin rash (eruption of small vesicles on the hands and the feet, including fingers and toes)
oral lesions (oral vesicles and uclers on any mucosa)
flu-like smyptom
S/S of acute lymphnodular pharyngitis
No vesicles or ulcers
Low number of yellow nodules develop in oropharynx area (nodules caused by lymphoid hyperplasia)
sore throat
flu like symptoms
Usually recover in 1 week without Tx
How are rubeola, rubella and mumps transmitted?
respiratory droplets, highly contagious
S/S of rubeola infectoin (measles)
Koplik’s spots (clusters of tiny white papules; preceed the skin rash and are pathognomonic)
Skin rash: spread from face to trunk and extremities
Rash fades and followed by desquamation
pt feels very sick
Self limiting but can be complicated by significant morbidity and mortality
Rubeola (measles) Dx
clinical and confirm with lab tests such as serology
Rubella (german measles) S/S
Similar to measles but milder and shorter
Skin rash all over body that fades in ~3 days
low fever
mild symptoms (pt doesnt feel sick)
What is congenital rubela syndrome?
Rubella infects fetus and induces birth defects
What happens to most fetus that contract a rubella infection?
spontaneous abortion
How to prevent congenital rubella syndrome
80% transmission from mother to child in first trimester
Check mother’s immunity to ensure she’s immune bc vaccine does not provide lifetime protection
Rubella Dx
Clinicaland confirmed by lab tests
What structure does mumps attack?
Excorine glands esp salivary glands (parotid gland = #1 target)
S/S of parotid gland infection by mumps
Swelling
pain
discomfort
mostly bilateral
What population often only has salivary gland involvement in mumps infection?
Children
What occurs in mumps infection of postpubertal males?
Epididymis and testis involvement (epididymo-orchitis)
Swelling, pain, atrophy on affected testes
Permanent sterility is rare
Tx for mumps?
self limited dz
control symptoms with pain meds
Oophoritis?
Ovary affected by mumps
Mastitis?
Breast affected by mumps
What does the MMR vaccine protect from?
Measles (98%)
Mumps (95%)
Rubella (protection doesnt last as long as other two)
