Exanthematous Viral Diseases

Measles/ Rubeola
Etiology

 Paramyxoviridae
Pathogenesis

 The measles virus enters the host via the respiratory mucosa or conjunctiva where it can replicate,
spread locally to lymphatic nodes and later disseminate into the bloodstream.
 The humoral immune system controls viral replication and confers antibody protection, whereas
the cell-mediated response eliminates infected cells.
 A transient immunosuppression occurs during measles virus infection, causing depressed
delayed-type hypersensitivity and T-cell counts, as well as an increased risk of bacterial
infections.
Clinical Manifestations
Incubation period: ranges between 7 and 21 days.
Prodrome
 fever (as high as 40.5°C [104.9°F]), malaise, conjunctivitis (palpebral, extending to lid margin),
coryza, and cough (brassy or barking)

Koplik spots
 are the pathognomonic enanthem of measles and develop during the prodrome.
 small, bright red macules that have a 1- to 2-mm blue-white speck within them and are typically
found on the buccal mucosa near the second molars

Exanthem
 consists of nonpruritic, erythematous macules and papules progressing in a cranial- to-caudal
direction.

Treatment
Supportive care

 focuses on antipyretics, fluids and managing complications related to bacterial superinfection,

respiratory compromise, and neurologic sequela
Hospitalized setting

 standard and airborne transmission precautions for 4 days after the rash onset
 IM IMMUNOGLOBULIN (0.55 mL/kg) as postexposure prophylaxis for rubella- susceptible
patients may decrease infection, viral shedding, and rate of viremia
 WHO recommends vitamin A should be administered to all children with measles regardless of
their country of residence.
 Ribavirin for children with severe disease or an immunocompromised state
Post exposure prophylaxis

 Given measles immunoglobulin if presenting within 6 days of exposure:

• infants younger than 1 year of age
• pregnant women,
• unimmunized
• Immunocompromised
 Measles immunoglobulin can be given either via an IM (0.5 mL/kg; maximum dose: 15 mL) or
IV route (400 mg/kg).
Healthy individuals

 (MMR) vaccine should be given to boost immunity if it can be administered within 72 hours of
measles exposure

Rubella
Etiology

 Togaviridae

Pathogenesis

 spread through direct or droplet contact from nasopharyngeal secretions.

 Infected individuals shed virus for 5 to 7 days before and up to 14 days after onset of rash
 Congenital rubella occurs when a nonimmunized, susceptible, pregnant woman is exposed to the
virus.
 Transplacental infection of the fetus occurs during the viremic stage.
 The risk is greatest to a fetus exposed to the virus in the first trimester.
 Congenitally infected infants may shed the virus through urine, blood, and nasopharyngeal
secretions for up to 12 months after birth, thus being a potential source of viral exposure to other
susceptible individuals.

Clinical Manifestations
Cutaneous lesions
 exanthem, occurring 14 to 17 days after exposure
 pruritic pink to red macules and papules that begin on the face, quickly progressing to involve
neck, trunk, and extremities
 Lesions on the trunk may coalesce, whereas those on the extremities often remain more discrete
 rash usually begins to disappear in 2 to 3 days and desquamation may follow resolution of the
rash.

Physical findings
 Lymphadenopathy
 arthritis of small and large joints with rubella infection.
 Joint symptoms often first appear as the rash fades and can last several weeks.
Congenital Rubella
  Neonatal manifestations of congenital infection include: growth retardation, interstitial
pneumonitis, radiolucent bone disease, hepatosplenomegaly, thrombocytopenia, dermal
erythropoiesis (“blueberry muffin lesions”)
 pruritic pink to red macules and papules that begin on the face, quickly progressing to involve
neck, trunk, and extremities

Treatment

PRIMARY UNCOMPLICATED RUBELLA

Supportive
 Standard and droplet precautions are recommended for patients with rubella for 7 days after rash
onset

NON PREGNANT
Rubella vaccine
 administration within 3 days of exposure
 IM IMMUNOGLOBULIN (0.55mL/kg) as postexposure prophylaxis for rubella- susceptible
patients may decrease infection, viral shedding, and rate of viremia

Neonates with congenital rubella syndrome

 supportive care
 contact isolation

Immunizations
 Rubella vaccine is typically administered (MMR) or (MMR and varicella) at 12 to 15 months of
age and again at 4 to 6 years of age.
 Infants of vaccinated breastfeeding mothers may become infected with rubella via breastmilk.

Roseola Infantum

Etiology
 Human herpesvirus-6

Pathogenesis
 The salivary glands are an important site of viral replication
 HHV-6 transmission occurs via shared saliva and can readily be detected in the saliva of adults
and children.
 In transplantation recipients, most cases of HHV-6 infection constitute reactivation of latent
infection; however, transmission of HHV-6 from the donor organ has been infrequently
described.
 The incubation period for HHV-6 infection is 5 to 15 days, with an average of 10 days.

Clinical Manifestations

 The rash appears around days 3 to 5, as fever subsides

 Typically small rose-pink or red raised spots (2–5 mm in diameter) that blanch (turn white) when
touched
 Some spots may be surrounded by a lighter halo of pale skin
 Mainly affects trunk and rarely spreads to nvolve the neck, face, arms and legs
  Similar spots occur on soft palate and uvula (Nagayama spots)
 Non-itchy, painless and does not blister
 May fade within a few hours or persist for as long as two days
 The rash usually peaks within 3 days and begins to disappear in 4 to 5 days in the order that it
appeared

Treatment

 There is no specific treatment for roseola.

 The disease is usually mild and self- limiting.
 Rest, maintaining fluid intake and paracetamol for fever is all that is usually required.
 No treatment is necessary for the rash, as it does not itch or hurt and fades spontaneously.

Erythema Infectiosum (Fifth disease)

Etiology
 Parvovirus B19

Pathogenesis
 The virus infects and lyses erythroid progenitor cells.
 The blood group P antigen (globoside) is a receptor of parvovirus
 B19 infection may lead to transient aplastic crisis.
 When parvovirus infects the erythroblasts in a developing fetus with
 decreased red cell survival, the result may be hemolysis and anemia.

Clinical Manifestations
 begins with nonspecific symptoms such as headache, coryza, and low-grade fever approximately
2 days before the onset of the rash.
 characteristic rash begins with confluent, erythematous, edematous plaques on the malar
eminences, the “slapped cheeks”
 As the facial rash fades over 1 to 4 days, pink to erythematous macules or papules appear on the
trunk, neck, and extensor surfaces of the extremities.
• These lesions have some central fading, giving them a lacy or reticulated appearance

Treatment
 No specific treatment
 Supportive therapy for the relief of fatigue, malaise, pruritus, and arthralgia may be needed

Kawasaki Disease

Etiology
 acute febrile illness with inflammation of small- and medium- sized blood vessels (coronary
arteries)
 occur in children younger than 5 years of age with a peak incidence between 1 to 2 years.
  The disease is very uncommon in those over 14 years old and in adults.
 Cause is unknown

Clinical Manifestations

 Rash may be morbilliform (measles-like), maculopapular (red patches and bumps), erythematous
(red skin) or target-like.
 redness within the mouth or on the pharynx, strawberry tongue, red or cracked lips.
 Redness of the bulbar conjunctivae (whites of the eyes) without exudate or stickiness.
 Including firm swelling of the hands and feet, sometimes including the fingers and toes, with
redness of the palms and soles.
 Periungual desquamation (peeling of skin around the fingernails) may occur during the
convalescent stage of the illness.
 swollen lymph glands can occur, often on one side of the neck.
 One lymph gland of at least 1.5cm in length is considered diagnostically enlarged.
Treatment

 Usually children are treated with antipyretic and analgesic medication (e.g. paracetamol) until the
5th day of fever is reached
 Once the diagnosis of Kawasaki disease is made a single large dose of intravenous
immunoglobulin (IVIG)
 IVIG is most effective when given between the 5th and 10th days of illness. Low dose oral
aspirin is also usually commenced at this time.

Pityriasis Rosea
Etiology

 Herpesviruses 7
Pathogenesis

 establishes persistent infection in salivary glands, and transmission is likely through saliva
 Latent virus can be activated in vitro from peripheral blood mononuclear cells, and its DNA can
be found in CD4+ T cells. HHV-7 can downregulate expression of CD4 and major
histocompatibility complex class I, which may play a role in establishment of latency or
pathogenesis.

Clinical Manifestations

 the rash sometimes follows a few days after an upper respiratory viral infection (cough, cold, sore
throat or similar).
 appearance of herald patch, a single plaque that appears 1–20 days before the generalized rash of
pityriasis rosea. It is an oval pink or red plaque 2–5 cm in diameter, with a scale trailing just
inside the edge of the lesion like a collaret
  A few days after the appearance of the herald patch, more scaly patches (flat lesions) or plaques
(thickened lesions) appear on the chest and back.
 Plaques that usually follow the relaxed skin tension lines or cleavage lines (Langer lines) on both
sides of the upper trunk.
 The rash has been described as looking like a fir tree. It does not involve the face, scalp, palms or
soles.
Treatment

 Bathe or shower with plain water and bath oil, aqueous cream, or another soap substitute.
 Apply moisturizing creams to dry skin
 Expose skin to sunlight cautiously (without burning)
 A 7-day course of high-dose aciclovir
A 2-week course of oral erythromycin
Topical steroid cream or ointment; this may reduce the itch while waiting for the rash to resolve.
 Phototherapy for extensive or persistent cases