Viral Infections

Part 1
By: PGI Nicolle Ann Ruiz Pancho
MEASLES
Etiology Transmission
• Measles virus is a single-stranded, • Respiratory tract or Conjunctivae
lipid-enveloped RNA virus in the • Large droplets or small-droplet
family Paramyxoviridae and genus aerosols
Morbillivirus
• Infectious: 3 days before to up to
• Humans are the only hosts
4-6 days after the onset of rash
• 2 most important structural
proteins in terms of induction of
immunity: hemagglutinin (H)
protein and the fusion (F) protein
Pathology
• Necrosis of the respiratory tract
epithelium and an accompanying
lymphocytic infiltrate.
• small-vessel vasculitis on the skin
and on the oral mucous
membranes.
• Histology of the rash and exanthem
reveals intracellular edema and
dyskeratosis
• Epidermal syncytial giant cells
(Warthin-Finkeldey giant cells )
Pathogenesis
• Prodrome: Fever, Malaise, Conjunctivitis, Cough, Coryza
• Exanthem: Erythematous macules and papules begin on the
face and spread cephalocaudally and centrifugally (by the 3 rd
day, the whole body is involved).
• Enanthem: Koplik spots (occur in prodromal period)
• Recovery: Clinical improvement begins within 2 days of
appearance of the rash. The rash tends to fade after 3-4 days
and will last around 6-7 days.
Pathogenesis

8-12 days 1-4 days 1-7 days

They first appear as discrete red lesions with
bluish white spots in the center on the inner
aspects of the cheeks at the level of the
premolars.
pathognomonic sign of measles
Symptoms increase in intensity for 2-4 days
until the 1st day of the rash.
The rash begins on the forehead (around the
hairline), behind the ears, and on the upper
neck as a red maculopapular eruption. It
thenspreads downward to the torso and
extremities, reaching the palms and soles in
up to 50% of cases.
The exanthem frequently becomes confluent
on the face and upper trunk
Laboratory findings
• The diagnosis of measles is almost
always based on clinical and
epidemiologic findings.
• Laboratory findings in the acute phase
include reduction in the total white
blood cell count, with lymphocytes
decreased more than neutrophils.
• In measles not complicated by
bacterial infection, the erythrocyte
sedimentation rate and C-reactive
protein level are normals
Diagnosis
• Serologic confirmation is most
conveniently made by identification
of immunoglobulin (Ig) M antibody
in serum. IgM antibody appears 1-2
days after the onset ofthe rash and
remains detectable for about 1 mo.
• Serologic confirmation may also be
made by demonstration of a 4-fold
rise in IgG antibodies in acute and
convalescent specimens collected 2-
4 wk apart
DDx
• Rubella
• Adenovirus infection
• enterovirus infection
• Epstein-Barr virus infection
• Exanthem subitum (in infants)
• Erythema infectiosum (in older children)
may also be confused with measles.
• Mycoplasma pneumoniae and group A
streptococcus may also produce rashes
similar to that of measles.
• Kawasaki syndrome
Complications
• Morbidity and mortality from
measles are greatest in patients
younger than 5 yr of age (especially
<1 yr of age) and older than 20 yr of
age.
• Pneumonia is the most common
cause of death in measles
• Acute otitis media is the most
common complication of measles
• Encephalitis (subacute, hemorrhagic,
subsclerosing panencephalitis)
Treatment
• Management of measles is
supportive
• Antiviral therapy is not effective
• Hydration, oxygenation, and
comfort are goals of therapy
• Antipyretics
• for comfort and fever control are
usefu
Prevention
• Vaccine
• Monovalent or combined
• Current recommendations
include a 1st dose at 12-15 mo
of age, followed by a 2nd dose at
4-6 yr of age.
Post exposure
prophylaxis
• vaccine is effective in prevention or
modification of measles if given
within 72 hr of exposure.
• Immune globulin may be given up to
6 days after exposure to prevent or
modify infection.
• Immunocompetent children should
receive 0.25 mL/kg intramuscularly,
and immunocompromised children
should receive 0.5 mL/ kg (maximum
dose in both cases is 15 mL/kg).
RUBELLA
German measles or 3 day measles
Mild, often exanthematous disease of infants and children
Its major clinical significance is transplacental infection and fetal damage as part of the
congenital rubella syndrome (CRS).
Etiology Epidemiology
• Family Togaviridae • Most common in preschool-age
• The only species of the genus and school-age children
Rubivirus.
• Sensitive to heat, ultraviolet
light, and extremes of pH
• Relatively stable at cold
temperatures.
• Humans are the only known
host.
Pathogenesis
• Following infection, the virus replicates in the respiratory epithelium
and then spreads to regional lymph nodes
• 10-17 days after infection: Viremia ensues
• 10 days after infection: Viral shedding from the nasopharynx begins
may be detected up to 2 weeks following onset of the rash.
• The period of highest communicability is from 5 days before to 6 days
after the appearance of the rash.
Pathogenesis
• Maternal infection during the 1st 8 weeks of gestation results in the
most severe and widespread defects
• Risk for congenital defects has been estimated at 90% for maternal
infection before 11 weeks of gestation
• Defects occurring after 16 wk of gestation are uncommon, even if
fetal infection occurs
Clinical manifestations
• Incubation period of 14-21 days
• Prodrome consisting of low-grade fever, sore throat, red eyes with or without
eye pain, headache, malaise, anorexia, and lymphadenopathy begins.
Suboccipital, postauricular, and anterior cervical lymph nodes are most
prominent
• In children, the first manifestation of rubella is usually the rash,
- It begins on the face and neck as small, irregular pink macules that coalesce, and it
spreads centrifugally to involve the torso and extremities
- Forchheimer spots - About the time of onset of the rash, examination of the
oropharynx may reveal tiny, rose-colored lesions or petechial hemorrhages on the soft
palate.
- Usually lasts up to 3 days
Laboratory findings Diagnoses
• Leukopenia • The most common diagnostic
• Neutropenia test is rubella immunoglobulin
(Ig) M enzyme immunosorbent
• Mild thrombocytopenia assay.
Congenital rubella syndrome
• Nerve deafness is the single most common finding among infants
• Intrauterine growth restriction
• Retinal findings described as salt-and-pepper retinopathy
- most common ocular abnormality but have little early effect on vision.
• Unilateral or bilateral cataracts are the most serious eye finding
• Patent ductus arteriosus is the most frequently reported cardiac
defect
Treatment
• no specific treatment available for
either acquired rubella or CRS.
• Postnatal rubella is generally a
mild illness that requires no care
beyond antipyretics and
analgesics.
• CRS is more complex and requires
pediatric, cardiac, audiologic,
ophthalmologic, and neurologic
evaluation
Prevention
• Vaccination
• Usually administered in combination with
measles and mumps (MMR) or also with
varicella (MMRV) in a 2 dose regimen at
12-15 mo and 4-6 yr of age.
• Vaccine should not be administered to
severely immunocompromised patients
(e.g., transplant recipients) and pregnant
women
• Patients with HIV infection who are not
severely immunocompromised may benefit
from vaccination.
• Fever is not a contraindication
MUMPS
Mumps is an acute self-limited infection that was once commonplace
It is characterized by fever, bilateral or unilateral parotid swelling and tenderness,
and the frequent occurrence of meningoencephalitis and orchitis.
Etiology
• Family Paramyxoviridae
• Genus Rubulavirus.
• Single-stranded pleomorphic
RNA
• Humans are the only natural
host
Epidemiology
• In the prevaccine era, mumps
occurred primarily in young
children between the ages of 5
and 9 yr and in epidemics about
every 4 yr.
Transmission
• Mumps is spread from person to person by respiratory droplets.
• Virus appears in the saliva from up to 7 days before to as long as 7 days after onset
of parotid swelling
• The period of maximum infectiousness is 1-2 days before to 5 days after onset of
parotid swelling. Viral shedding before onset of symptoms and in asymptomatic
infected individuals impairs
Pathology and Pathogenesis
• Mumps virus targets the salivary glands, central nervous system
(CNS), pancreas, testes, and, to a lesser extent, thyroid, ovaries, heart,
kidneys, liver, and joint synovia
• initial viral replication occurs in the epithelium of the upper
respiratory tract. Infection spreads to the adjacent lymph nodes by
the lymphatic drainage, and viremia ensues, s
• Mumps virus causes necrosis of infected cells and is associated with a
lymphocytic inflammatory infiltrate.
Clinical manifestation
• incubation period for mumps ranges from 12-25 days but is usually
16-18 days.
• The typical patient presents with a prodrome lasting 1-2 days and
consisting of fever, headache, vomiting, and achiness.
• Parotitis then appears and may be unilateral initially but becomes
bilateral in approximately 70% of cases. parotid swelling peaks in
approximately 3 days and then gradually subsides over 7 days.
DIAGNOSIS
• Diagnosis could be made on the basis of a history of exposure to
mumps infection, an appropriate incubation period, and development
of typical clinical findings.
• Confirmation of the presence of parotitis could be made with
demonstration of an elevated serum amylase value.
• Leukopenia with a relative lymphocytosis was a common finding.
Today
• specific diagnosis of mumps should be confirmed or ruled out by
virologic or serologic means
Differential Diagnosis Complication
• Viruses that cause parotitis include • Most common complications of
parainfluenza 1 and parainfluenza 3 mumps are meningitis, with or
viruses, influenza A virus,
cytomegalovirus, Epstein-Barr virus, without encephalitis, and
enteroviruses, lymphocytic gonadal involvement.
choriomeningitis virus, and HIV
• Maternal infection with mumps
during the 1st trimester of
• Purulent parotitis, usually caused by pregnancy results in increased
Staphylococcus aureus, is unilateral, is
extremely tender, is associated with an fetal wastage
elevated white blood cell count, and may
involve purulent drainage from the
Stensen duct.
Treatment Prevention
• No specific antiviral therapy is • Immunization with the live
available for mumps. mumps vaccine is the primary
Management should be aimed at mode of prevention
reducing the pain associated
with meningitis or orchitis
• Given as part of the MMR 2
• Maintaining adequate hydration. dose vaccine schedule, at 12-15
• Antipyretics may be given for mo of age for the 1st dose and
fever. 4-6 yr of age for the 2nd dose
POLIOVIRUSES
Spread from the intestinal tract to the central nervous system where they cause
aseptic meningitis and poliomyelitis, or polio.
The polioviruses are extremely hardy and can retain infectivity for several days at
room temperature.
Epidemiology
• The most devastating result of
poliovirus infection is paralysis
• Paralytic poliomyelitis occurred
primarily in adolescents.
• Poor sanitation and crowding
have permitted the continued
transmission of poliovirus
Transmission
• Humans are the only known
reservoir for the polioviruses
• Spread by the fecal-oral route.
• Poliovirus has been isolated
from feces for longer than 2 wk
before paralysis to several weeks
after the onset of symptoms.
Pathogenesis
• The primary site of replication is in the M cells lining the mucosa of
the small intestine.
• Regional lymph nodes are infected, and primary viremia occurs after
2-3 days
• Exact mechanism of entry into the CNS is not known. However, once
entry is gained the virus may traverse neural pathways.
• Poliovirus primarily infects motor neuron cells in the spinal cord (the
anterior horn cells) and the medulla oblongata (the cranial nerve
nuclei).
• Infants acquire immunity transplacentally from their mothers.
Transplacental immunity disappears at a variable rate during the 1st 4-
6 mo of life.
• Active immunity after natural infection is probably lifelong
Clinical Manifestation
• Incubation period of poliovirus from contact to initial clinical
symptoms is usually considered to be 8-12 days, with a range of 5-35
days.
• infections with wild-type virus may follow 1 of several courses
• Inapparent infection, which occurs in 90-95% of cases and causes no disease
and no sequelae
• Abortive poliomyelitis
• Nonparalytic poliomyelitis
• Paralytic poliomyelitis – appears 3-8 days after the initial symptoms.
Abortive Poliomyelitis
• Nonspecific influenza-like syndrome occurs 1-2 wk after infection.

• Fever, malaise, anorexia, and headache are prominent features,there

may be sore throat and abdominal or muscular pain. Vomitingoccurs
irregularly. The illness is short lived, lasting up to 2-3 days
• physical examination may be normal or may reveal nonspecific
pharyngitis, abdominal or muscular tenderness, and weakness.
• Recovery is complete, and no neurologic signs or sequelae develop.
Non Paralytic Polimyelitis
• More intense headache, nausea, and vomiting, soreness
• Fleeting paralysis ofthe bladder and constipation.
• 2 phases: 1st phase (minor illness) and the 2nd phase (CNS disease or
major illness). Nuchal rigidity and spinal rigidity are the basis for the
diagnosis of nonparalytic poliomyelitis during the second phase.
• Physical examination reveals nuchal-spinal signs and changes in
superficial and deep reflexes
• Sensory defects do not occur in poliomyelitis.
Paraylytic Poliomyelitis
Spinal Paralytic
Severe muscle pain is present, and
sensory and motor phenomena (e.g.,
paresthesia, hyperesthesia, fasciculations,
and spasms) may develop.
distribution of paralysis is characteristically
spotty. Single muscles,
multiple muscles, or groups of muscles may be
involved in any pattern.
Within 1-2 days, asymmetric flaccid paralysis
or paresis occurs.
Involvement of one leg is most common,
followed by involvement of
one arm
Bulbar
may occur as a clinical entity
without apparent
involvement of the spinal cord
Clinical findings seen with bulbar
poliomyelitis with respiratory
difficulty (other than paralysis of
extraocular, facial, and masticatory
muscles) include:
 nasal twang to the voice or cry
 inability to swallow smoothly
 accumulated pharyngeal
Secretions
 absence of effective coughing
 nasal regurgitation of saliva and
fluids
 irregularities in rate, depth, and
rhythm of respiration
 paralysis of 1 or both vocal cords
 the rope sign
Polioencephalitis
Seizures, coma, and spastic
paralysis with increased reflexes
may be observed
Hypoxia and
hypercapnia caused by inadequate
ventilation due to respiratory
insufficiency
may produce disorientation without
true encephalitis (Paralytic
poliomyelitis with ventilatory
insufficiency)
Diagnosis
• should be considered in any
unimmunized or incompletely
immunized child with paralytic
disease
• confirmed by isolation and
identification of poliovirus in the
stool
• high in the stool in the 1st wk after
the onset of paralysis
• 2 stool specimens should be
collected 24-48 hr apart
Treatment
• There is no specific antiviral
treatment for poliomyelitis.
• The management is supportive
and aimed at limiting
progression of disease
• Analgesics, sedatives, an attractive
diet
Complications
• Post polio syndrome - After an
interval of 30-40 yr, as many as
30-40% of persons who survived
paralytic poliomyelitis in
childhood may experience
muscle pain, exacerbation of
existing weakness or
development of new weakness
or paralysis
Prevention
• Vaccination is the only effective
method of preventing
poliomyelitis.
• inactivated polio vaccine (IPV)
and the live attenuated OPV
have established efficacy
• All children should receive 4
doses of IPV, at 2 mo, 4 mo, 6-18
mo, and 4-6 yr of age
Enteroviruses
Agents that produce a broad range of illnesses.
The genus name reflects the importance of the gastrointestinal tract as the primary
site of invasion and replication and the source for transmission.
Epidemiology
• young age, male sex, exposure
to children, poor hygiene,
overcrowding, and low
socioeconomic
• >25% of symptomatic infections
occur in children younger than 1
yr of age.
• Breastfeeding reduces the risk
for infection
Transmission
• Humans are the only known
reservoir for human
enteroviruses
• Primarily spread person to
person, by the fecal-oral and
respiratory routes,
• spread via airborne transmission
• types causing acute hemorrhagic
conjunctivitis
Clinical Manifestations
• Nonspecific febrile illnesses
• are the most common symptomatic manifestations, especially in infants and
young children.
• fever of 38.5-40°C (101-104°F)
• Duration of illness is usually 4-7 days but can range from 1 day to >1 wk.
• Serotypes commonly associated with rashes are echoviruses 9, 11, 16, and
25; coxsackie A viruses 2, 4, 6, 9, and 16; coxsackie B viruses 3-5; and
enterovirus 71
Clinical Manifestations
• Hand-foot-and-mouth disease
• one of the more distinctive rash syndromes, is most frequently caused by
coxsackievirus A16
• mild illness, with or without low-grade fever.
• The oropharynx is inflamed and contains scattered vesicles on the tongue,
buccal mucosa, posterior pharynx, palate, gingiva, and/or lips
• Vesicles resolve in about 1 wk
Clinical Manifestations
• Herpangina
• characterized by sudden onset of fever, sore throat, dysphagia, and lesions in
the posterior pharynx.
• Characteristic lesions, present on the anterior tonsillar pillars, soft palate,
uvula, tonsils, posterior pharyngeal wall, and, occasionally, the posterior
buccal surfaces
• Fever generally lasts 1-4 days, and resolution of symptoms occurs in 3-7 days
• coxsackie A viruses are implicated most often.
Clinical Manifestations
• Viral meningitis (Coxsackie B viruses 2-5; echoviruses 4, 6, 7, 9, 11,
13, 16, and 30; and enteroviruses 70 and 71)
• Enteroviruses are the most common causes in mumps-immunized
populations, accounting for up to 90% or more of cases.
• Common in infants, especially in those younger than 3 mo of age
• irritability, malaise, headache, photophobia, nausea, emesis,
anorexia, lethargy, hypotonia, rash, cough, rhinorrhea, pharyngitis,
diarrhea, and/or myalgia.
• Usually resolve within 1 wk. The prognosis for most children is good.
Treatment
• In the absence of a proven
antiviral agent for enterovirus
infections, supportive care is the
mainstay of treatment.
Prevention
• The first line of defense is
hygiene, such as handwashing,
to prevent fecal-oral and
respiratory spread within
families, schools, and
institutional settings
• Chlorination of drinking water
and swimming pools may be
important.
PARVOVIRUSES
They are common infectious agents of a variety of animal species, including
mammals, birds, and insects.
Parvovirues B19 and HBoV are the only 2 parvoviruses known to be pathogenic in humans.
Erythema infectiosum
• The most common manifestation of parvovirus B19
• Also known as fifth disease, which is a benign, self-limited exanthematous illness of
childhood.
• incubation period is 4-28 days
• Headache, and symptoms of mild upper respiratory tract infection
• Hallmark of erythema infectiosum is the characteristic rash, which occurs in 3 stages
• The initial stage - an erythematous facial flushing often described as a “slapped-cheek” appearance
• Second stage - rash spreads rapidly or concurrently to the trunk and proximal extremities as a
diffuse macular erythema
• Third stage - Central clearing of macular lesions occurs promptly, giving the rash a lacy, reticulated
appearance
• Rash tends to be more prominent on extensor surfaces, sparing the palms and soles
Diagnosis
• The diagnosis of erythema
infectiosum is usually based on
clinical presentation of the
typical rash and rarely requires
virologic confirmation.
Prevention
• Children with erythema
infectiosum are not likely to be
infectious
• Isolation and exclusion from
school or child care are
unnecessary and ineffective after
diagnosis.
HERPES SIMPLEX VIRUS
The 2 closely related herpes simplex viruses HSV type 1 and HSV type 2 (HSV-2), cause a variety of illnesses,
depending on the anatomic site
Common infections involve the skin, eye, oral cavity, and genital tract.
Infections tend to be mild and self-limiting, except in the immunocompromised patient and newborn infant
Epidemiology
• Type 1 (HSV-1) causes most
cases of oral, skin, and cerebral
disease.
• Type 2 (HSV-2) causes most (80–
85%) genital and congenital
infections.
Transmission
• Direct contact with infected
secretions.
• The source of primary infection
is usually an asymptomatic
excreter
• Recurrences may be
spontaneous or induced by
external events (eg, fever,
menstruation, or sunlight) or
immunosuppression.
Clinical Manifestations - Oropharnygeal
• Herpes gingivostomatitis
• involves the gingivae and the vermilion border of the lips.
• Herpes labialis (cold sores or fever blisters) is limited to the vermilion border involving skin
and mucous membranes.
• typical oropharyngeal vesicular lesions with high fever, malaise, stinging mouth pain,
drooling, fetid breath, and cervical lymphadenopathy
• Herpetic skin lesions
• painful and characteristically begin as erythematous papules
• progress to the characteristically grouped, 2- to 4-mm, fluid-filled vesicles on an
erythematous base.
• Removal of the vesicle roof reveals a small, sharply demarcated ulcer with a punched-out
appearance.
• The characteristic grouped vesicles distinguish HSV from chickenpox
Clinical Manifestations – Oropharyngeal
• Viral paronychia (herpetic whitlow)
• painful, localized infection of a digit, usually of the distal pulp space, with
erythematous and occasionally vesiculopustular eruption.
• It occurs in children who suck their thumbs, bite their nails, and those with
herpetic gingivostomatitis
• Herpes gladiatorum
• occurs in wrestlers and rugby players who acquire cutaneous herpes from
close body contact with other
• Eczema herpeticum (Kaposi varicelliform eruption)
• Cutaneous HSV infection in persons underlying skin disorder (e.g., atopic
dermatitis)
Clinical Manifestations – Genital
• Infection may result from genital-genital transmission (usually HSV-2)
or oral-genital transmission (usually HSV-1)
• Periodic viral shedding
• Increases the risk for acquiring HIV infection.
• Genital infections caused by HSV-1 and HSV-2 are indistinguishable,
but HSV-1 causes significantly fewer subsequent episodes of recurrent
infection
Classic Primary Genital Herpes
• Short period of local burning and tenderness
before vesicles develop on genital mucosal surfaces
and keratinized surface
• Mucosal ulcers produce shallow, tender ulcers
covered with a yellowish gray exudate and
surrounded by an erythematous border.
• Vesicles on keratinized epithelium progress to the
pustular stage and then crusting.
Recurrent Genital Herpes
• Usually less severe and of shorter duration than
the primary infection.
• Some patients experience a sensory prodrome with
pain,burning, and tingling at the site where vesicles
subsequently develop.
Clinical Manifestations – Occular Infections
• May involve the conjunctiva, cornea, or retina
• May be primary or recurrent.
• Corneal and Retinal infections are rare.
• Conjunctivitis or keratoconjunctivitis
• unilateral and is often associated with blepharitis and tender preauricular
lymphadenopathy.
• conjunctiva appears edematous
• rarely purulent discharge.
• Vesicular lesions may be seen on the lid margins and periorbital skin. Patients
typically have
• Untreated infection generally resolves in 2-3 wk.
Clinical Manifestations – CNS
• CSF:
• moderate number of mononuclear cells & polymorphonuclear leukocytes
• a mildly elevated protein concentration,
• normal or slightly decreased glucose concentration
• moderate number of erythrocytes.
• HSV is also a cause of Aseptic Meningitis and is the most common
cause of Recurrent Aseptic Meningitis (Mollaret meningitis).
Clinical Manifestations – CNS
• It is an acute necrotizing infection generally involving the frontal
and/or temporal cortex and the limbic system
• If beyond the neonatal period, is almost always caused by HSV-1.
• Nonspecific findings: fever, headache, nuchal rigidity
• Findings more indicative of HSV encephalitis: anosmia, memory loss,
peculiar behavior, expressive aphasia and other changes in speech,
hallucinations, and focal seizures
Clinical Manifestations – In Immuno
compromised patients
• Severe, life-threatening HSV infections
• At risk: neonates, severely malnourished, those with primary or
secondary immunodeficiency diseases, including AIDS, and those
receiving some immunosuppressive regimens, particularly for cancer
and organ transplantation
Mucocutaneous infections: Disseminated infection Other HSV infections

• Most common: mucositis and • Sepsis-like presentation, with • Tracheobronchitis

esophagitis; result in lesions liver and adrenal involvement • Pneumonitis
that slowly enlarge, ulcerate, • Disseminated intravascular • Anogenital infections
become necrotic coagulopathy
• Shock.
Clinical Manifestations – Perinatal Infections
• Maybe acquired: in utero, during the birth process, or during the
neonatal period.
• Most cases of from maternal infection and transmission during
passage through an infected birth canal
• Never asymptomatic
Clinical Manifestations – Perinatal Infections
• Intrauterine infection
• Symptoms preset at delivery
• Skin vesicles or scarring
• Eye findings including chorioretinitis and keratoconjunctivitis
• Microcephaly or hydranencephaly
Clinical Manifestations – Perinatal Infections
• Infected during delivery or the postpartum period present with 1 of
the following:
1. Disease localized to the skin, eyes, or mouth – at 5 to 11 days
2. Encephalitis with or without skin, eye, and mouth disease – at 8 to 17 days
3. Disseminated infection involving multiple organs, including the brain, lungs,
liver, heart, adrenals, and skin – at 5 to 11 days of life.
Diagnosis
• Confirmed by laboratory test,
preferably isolation of virus or
viral DNA detection by
polymerase chain reaction (PCR)
• Virus culture remains the gold
standard for diagnosing HSV
infections.
• The highest yield comes from
rupturing a suspected herpetic
vesicle
Treatment
• Acyclovir, valacyclovir, and famciclovir.
• All 3 are available in oral form, but only
acyclovir is available in a suspension and
intravenous formulation.
• All 3 drugs have exceptional safety
profiles and are safe to use in pediatric
patients.
• Patients with genital herpes also require
counseling to address psychosocial issues,
including possible stigma, and to help
them understand the natural history and
management of this chronic infection.
Prognosis
• Most HSV infections are self-
limiting, last from a few days (for
recurrent infections) to 2-3 wk
(for primary infections), and heal
without scarring.
• Recurrent ocular herpes can lead
to corneal scarring and
blindness.
Prevention
• Handwashing
• Use of gloves by health care
workers
• Correct and consistent use of
condoms.
• Male circumcision is associated
with a reduced risk of acquiring
genital HSV infection condoms
• Health education
VARICELLA ZOSTER VIRUS
Chickenpox and zoster are caused by varicella-zoster virus (VZV), an enveloped,
icosahedral, double-stranded DNA. virus that is a member of the herpesvirus family.
Humans are the only natural host.
Epidemiology
• In the prevaccine era, the peak
age of occurrence was 5 to
10years
• Most children are infected by 15
yr of age, with fewer than 5% of
adults remaining susceptible
Transmission
• Chicken pox is transmitted via
direct contact, droplet, and air
• Zoster is a recurrence of latent
VZV and is transmitted by direct
contact.
Pathogenesis
• infects susceptible individuals via the conjunctivae or respiratory tract
• replicates in the nasopharynx and upper respiratory tract.
• It disseminates by a primary viremia and infects regional lymph
nodes, the liver, the spleen, and other organs.
• A secondary viremia follows, resulting in a cutaneous infection with
the typical vesicular rash
• After resolution of chickenpox, the virus persists in latent infection in
the dorsal root ganglia cells.