FEVER and RASH Lan-fang Tang Dept. Pediatric Pulmonology Email: [email protected] Pediatrics

FEVER and RASH

Lan-fang Tang

Dept. Pediatric Pulmonology

Email: [email protected]

Pediatrics

Rash appearance

Skin lesions evolve over time, but the characteristic

distribution and appearance provide important clues

to the diagnosis Macular or Maculopapular Rash

Diffuse Erythroderma

Urticarial Rash

Vesicular, Bullous, Pustular

Petechial-Purpuric

Erythema Nodosum

Differential Diagnosis of Fever and Rash

Macular or Maculopapular Rash -- virus:

Measles

Rubella

Roseola (HHV-6 or HHV-7)

Others: Erythema infectiosum (fifth disease,

parvovirus B19), Epstein-Barr virus,

Echoviruses, HBV, HIV


Macular or Maculopapular Rash--bacteria

Scarlet fever (group A streptococcus)

Others: Secondary syphilis, Leptospirosis,

Pseudomonas, Meningococcal infection (early),

Salmonella typhi (typhoid fever), Lyme disease

(erythema migrans), Mycoplasma pneumoniae

Measles

Etiology

Measles virus

genus Morbillivirus

family Paramyxoviridea

Only one serotype

Week vitality in vitro

Measles virus

Epidemiology

Source of infection

Route of transmission

Susceptible population

Source of infection

patients as the main source

infectivity from prodromal period to the

time of 5~10 days after the rash appears

respiratory secretions as the main media

Route of transmission

Direct respiratory transmission by droplet spray

Indirect transmission by contact with the

contaminated articles.

Susceptible population

Peak incidence: 8m~5yr

Pathogenesis

Virus inhalation incubation

Local proliferation

First viremia

Proliferation in endoreticular system

Second viremia prodromal

All parts of the body eruption

Clearance of virus convalescence

Clinical Manifestation

Typical measles

Incubation stage

Prodromal stage

Eruptive stage

Convalescent stage

Stage 1: Incubation stage

6~18 days

No symptoms or low fever, malaise

Stage 2: Prodromal stage (Catarrhal stage)

Lasts 3~4 days

Low-grade to moderate fever

Mucosal catarrh: conjunctivitis,

coryza

hacking cough

Stimson line: transverse line of inflammation along the eyelid margin

Koplik spots: a pathognomonic sign

Koplik spots

—a pathognomonic sign of measles

Appear 2-3 days after fever develops

Tend to occur over the buccal mucosa opposite

the lower molars

A grayish white dots(as small as grains of

sands) with slight reddish areola

Increase and disappear 1-2d after eruption

Stage 3: Eruptive stage

Lasts 3~4 days

Characterized by the eruption of the rash

The temperature rises abruptly as rash

develops (usually >40℃)

Exacerbated mucosal catarral symptoms:

cough, vomitting and diarrhea, anorexia,

a few rales on auscultation

The order of eruption

Usually starts on the upper lateral parts of the neck,

behind ears, along the hairline and on the posterior parts

of the cheek;

Spreads rapidly over entire face, neck, upper arms and the

upper parts of the chest within the first 24hr;

Over the back, abdomen, entire arm and thighs during the

succeeding 24hr;

Finally reaches the feet on the 2nd~3rd day.

The features of the rash

Faint macules initially

Pink maculopapular, 1-3mm in diameter

Sparse to confluent or even fused with each

other to form patches, but the normal skin can

be found.in between.

Begins to fade as the rash reaches the feet.

Stage 4: Convalescent stage

The symptoms resolve rapidly

The rash fades downwards in the same

sequence in which it appeared.

Branny desquamation and brownish

pigmentation occur and disappear within 7-

10days

Atypical measles

Mild measles (modified measles)

Severe measles

Measles without rash

Hemorrhagic measles (black measles)

Atypical measles syndrome

Atypical Measles

A laboratory confirmation is rarely needed

Leukopenia , with a relative lymphocytosis

Multinucleated giant cells in smear of nasal

mucosa (Warthin-Finkeldey cells)

Serum antibody(sIgM or double serum IgG)

Virus isolation or virus antigen/RNA detection

Laboratory examination

Complications

Pneumonia ( fatal giant cell (Hecht) pneumonia

in patients with impaired cell-mediated

immunity)

Laryngo-bronchitis

Myocarditis

Encephalitis

Reactive tuberculosis

Subacute sclerosing panencephalitis

Basis of diagnosis

Evidence of epidemiology

Koplik spots

The order and features of the rash

Branny desquamation and brownish

discoloration

Therapy

No specific antiviral therapy

Supportive treatment

antipyretics, bed rest,

maintenance of an adequate fluid intake

Management of complication

Vitamine A supplement

IVIG

Vitamin A and measles: evidence

Hyporetinemia is present in over 90% of measles

cases in Africa and 22-70% in USA.

There is an apparent inverse correlation between

retinol concentration and the severity of measles.

Oral Vitamin A supplement reduces the morbidity

and mortality of severe cases.

Indication for Vit A supplement

(American Academy of Pediatrics)

Hospitalized children 6mo~2yr of ages

Children >6mo with

immunodeficiency

ophthalmologic evidence of Vit A deficiency

impaired intestinal absorption

moderate to severe malnutrition

recent immigration from areas with a high

mortality from measles

Prevention

Isolation

Block the route of transmission

Vaccine

Post-exposure prophylaxis

Prevention: Isolation

Isolation precautions should be maintained from

the 7th day after exposure until 5 days after the

rash develops.

Until 10 days after the rash develops for severe

cases with pneumonia

Contact with susceptibility be isolated for 21

days (28days for passive immunity receiver)

Prevention: active immunization(Vaccine)

Measles attenuated vaccine , or Measles- Mumps-

Rubella vaccine(MMR)

Initial immunization: 8mo

A second immunization is recommended

routinely(7y).

Urgent vaccination for measles postexposure and

outbreak prophylaxis

Prevention: Passive immunization(post-exposure

prophylaxis)

Passive immunization with Ig within 5 days of

exposure is effective for the prevention and

attenuation of measles.

Susceptible children <12mo should receive Ig

(0.25ml/kg, <=15ml,IM)



Measles

Rubella





Rubella

also known as German measles and 3-day

measles;

congenital rubella syndrome (infection in

utero )

Etiology and epidemiology

a single-stranded, positive-sense RNA virus ( a

member of the togavirus family)

Humans as the only host

Spread either by oral droplet or transplacentally to

fetus causing congenital infection

Virus recovered from the nasopharynx 7d before

exanthem and 7-8 d after its disappearance.

Peak incidence in children 5~14 yr of age

Clinical manifestations

Incubation (14 to 21 d)

Prodromal phase

Mild catarrhal symptoms with shorter period

Low-grade fever (1~3d) with meager systemic

symptoms.

About 2/3 are subclinical.


The most characteristic sign ：

Enlarged post-occipital, retroauricular and

posterior cervical lymph nodes with tender.

Be evident 24h before rash and remain for 1

week or more


Exanthem more variable even no rash

first appear on face

rapid evolution, usually cover the entire body in 24 h

Usually clears by the 3rd day

Discrete maculopapules with large flushing, or

pinpoint appearance, or may be confluent on face

Mild itching and minimal desquamation


Enanthem in 20% patients

Just before rash

Discrete rose spots on the soft palate (Forchheimer

spots)

May coalesce into a red blush and extend over the

fauces

Slightly inflamed pharyngeal mucosa and conjunctivae

without photophobia


Congenital rubella (syndrome)

Affects virtually all organ systems

The most common manifestation is intrauterine growth

retardation

Other common findings: cataracts (microphthalmia,

myocarditis, PDA); “blueberry muffin” skin lesions;

hearing loss; meningoencephalitis.

Diagnosis

Apparent diagnosis based on clinical symptoms

and signs

Laboratory findings non-specific and generally do not

aid in diagnosis

confirmed by serology or virus culture

Congenital rubella: serum sIgM or virus culture

Prenatal diagnosis: cord blood sIgM or virus

culture from amniotic fluid

Treatment and prognosis

There is no specific antiviral therapy

Entirely supportive, and antipyretics

The prognosis is excellent, but congenital rubella

syndrome may have sequalae such as intrauterine

growth retardation, cataracts, deafness, and a

patent ductus arteriosus.

Prevention

Live rubella vaccine recommended as MMR for

children( initial at 12-15m and second 4-6y)

It is important for girls to have immunity before

they reach childbearing age



Measles

Rubella





Etiology

Roseola was first established as a distinct illness

at the turn of 20th century;

No causative pathogens were consistently

identified until recent 10 years;

It appears now that primary infection of human

herpesvirus type 6 (HHV-6) and less frequently

HHV-7 causes the majority of the cases of roseola.

Epidemiology

Primary HHV-6 infection occurs early in life with

peak acquisition from 6-15 months of age.

Rarely report contact with other infected children

and outbreak uncommon.

Most adults excrete HHV-6 and HHV-7 in saliva

and may serve as primary sources for virus

transmission.

HHV-6 can be transmitted in utero.

Cinical manifestations

Incubation period: 5-10d

Prodromal period:

Usually asymptomatic

Mild URT signs

Mild cervical lymphadenopathy


Clinical illness heralded by high fever

37.9~40.0 with an average of 39℃

Persists for 3-5 days and then resolves rather abruptly

(crisis). Occasionally fever diminish over 24-36h gradually

(lysis).

May be irritable and anorexia but most behave normally

Seizures in 5~10%

Infrequent : rhinorrhea, sore throat, abdominal pain,

vomiting and diarrhea.


Eruption and fever

A rash appears within 12~24 hours of fever

resolution

Eruption during defervescence or within a

few hours of fever resolution


Characteristic rash

Rose colored rash ( discrete, small (2~5mm),slightly

raised pink lesions)

appears trunk , neck, behind ears, face and proximal

extremities

No pruritic, no vesicles

Fade in 1~3 days

Treatment and prevention

There is no specific therapy

HHV-6 is inhibited by ganciclovir but the

benign nature preclude consideration of

antiviral therapy.

Excellent prognosis in majority

no guidelines for prevention of roseola.

Varicella

Etiology

Chickenpox (varicella) is the manifestation of

primary infection of varicella-zoster virus (VZV).

Zoster (shingles) is the manifestation of reactivated

latent infection of endogenous VZV.

Clinical manifestation

Incubation period: 10~21d

Subclinical varicella is rare

Prodromal symptoms

Usually moderate fever

malaise, headache, anorexia and occasionally

mild abdominal pain

precede the rash by 24~48h


The characteristic rash

initially as small red papules

rapidly progress to nonumbilicated, oval, "teardrop" vesicles on an erythematous base.

The fluid progresses from clear to cloudy, and the vesicles ulcerate, crust, and heal.

New crops appear for 3 to 4 days, usually beginning on the trunk followed by the head, the face, and, less commonly, the extremities.


Pruritus, mucous membrane lesions,

lymphadenopathy

Hypopigmentation or hyperpigmentation persists

for days to weeks in some

Scarring unusual unless secondarily infected


Progressive varicella

usually in immunocompromised children

Neonatal chickenpox

delivery within 1 week before or after the onset of maternal varicella frequently results in severe varicella in neonates

Congenital varicella

when pregnant women (especially between 8-20 weeks) contract chickenpox, 25%of the fetuses may become infected.

Complication

Complications are common

secondary infection of skin lesions by streptococci

or staphylococci, Thrombocytopenia and

hemorrhagic lesions or bleeding, pneumonia ,

myocarditis, pericarditis, orchitis, hepatitis,

ulcerative gastritis, glomerulonephritis, and

arthritis , Reye syndrome, encephalitis, cerebellar

ataxia, nystagmus, and tremor

Therapy

Symptomatic therapy

Antivirals (acyclovir, famciclovir, or valacyclovir )

are effective in preventing severe complications

the routine oral administration of acyclovir is not

recommended in otherwise healthy children because of

the marginal therapeutic benefit, the lack of difference in

complications, and the cost of acyclovir treatment.

Thank you!

Email: [email protected]

Documents

FEVER and RASH Lan-fang Tang Dept. Pediatric Pulmonology Email: [email protected] Pediatrics