ERUPTIVE DISEASES

PROF.DR. AYA VTRNEL

MEASLES
Measles virus is a RNA virus of the genus ;
MORBILLIVIRUS in the family PARA-
MYXOVIRIDAE
During the prodromal period , short time
after the rash appears= found in naso-
pharenx, blood, urine
Endemic throughout the world
Maximal dissemination; Occurs by droplet
spray during the prodromal period
MEASLES
Contagious from 1-2 days before onset of
symptoms to 4 days after apperance of the
rash.
Infants acquire immunity transplacentally
from mothers who have had measles or me-
asles immunization. This immunity is
usually complete for the first 4-6 months of
life.
Koplik spots
MEASLES
Essential lesion is found in the skin, in the
mucous membranes of the nasopharynx,
bronchi, intestinal tract, conjunctivae
Serous exudate and proliferation of mono-
nuclear and a few polymorphonuclear cells
occur around the capillaries.
Hyperplasia of lymphoid tissue usually
occurs particulary in the appendix.
MEASLES
CLINICAL MANIFESTATIONS : 3
clinical stages
1)Incubation period: 10- 12 days
2)Prodromal stage: 3-5 days(av: 4 days)
fever; subside rapidly within 2 days of rash.
Dry cough. Coryza. Conjuctivitis. Koplik
spots, patognomonic sign of measles
MEASLES
Consist of serous exudate, proliferation of
endothelial cells, grayish white dots have
slight reddish areola opposite to the molars
(rarely found within the mid partion of lo-
werlip, on the palate and on the lacrimal
caruncle.
MEASLES
3) Final stage: Rash starts as faint macules
on the upper parts of the neck, behind the
ears, along the hairline ,become maculopa-
pular as the rash spreads rapidly over the
entire face, neck, upper arms, upper part of
the chest in the first 24 hours.
Second day; spreads over the back, abdo-
men, arm and thigh It finally reaches the
feet on the 2nd.-3rd. days. It begins to fade
on the face.
MEASLES
In the severe cases the rash is confluent, the
skin is completely covered including the
palms and soles.
Often slightly hemorrhagic
As the rash fades BROWNY DESQUAMATION and
BROWNISH DISCOLORATION OCCUR.
Hemorrahagic type: BLACK MEASLES bleeding
may occur (mouth, nose, bowel)
Atypical measles : occurs in recipient of killed
measles virus vaccine
MEASLES
Rash appears firstly ; palms, wrists, soles,
ankles maculopapuler; vesicules, purpurical
hemorrhagic.
Koplic spots rarely occurs
Headache, severe abdominal pain, vomiting
myalgia, respiratory symptoms,
pneumoniae can occur.
MEASLES
DIAGNOSIS: Clinical picture.
Laboratory confirmation: rarely needed.
Prodrome: multinucleated giant cells can be
demonstrated in smears of nasal mucosa.
Abs: IgM detectable at least 1 month after
rash onset. Acute-convelascent sera 4 fold
increase
Virus culture
Leukopenia--- Lekocytosis
MEASLES
TREATMENT: No spesific antiviral thera-
py.
Supportive (antipyretics, bedrest, fluid inta-
ke)
Treatment with oral Vit A reduces morbidi-
ty and mortality in children with severe me-
asles in developing world.
6 mn-1 yr: 100.000 U PO
>1 yrs : 200.000 U PO
MEASLES
Hospitalized with measles and its
complications
Having risk factors:
Evidence of vit A def
Immundeficiency
mpaired intestinal absorbtion
Severe malnutrition
MEASLES
COMPLICATIONS:
Acute otitis media most common
Pneumonitis ; interstisiel primer pneumonia/
secondary bacterial
Encephalitis
Exacarbation of undelying tbc-SSPE after 7/10
years
Myocarditis-infrequate
Appandicitis
Laryngitis, tracheitis, bronchiolitis
MEASLES
PREVENTION : Vaccine license in 1963
(12-15 months/4-6 years)
Postexposure prophylaxia. Within 6 days of
exposure, Ig (0.25 ml /kg IM max 15 ml)
within 72 hrs VACCINE
RUBELLA
Rubella virus- RNA virus of genus Rubi-
virus in the family Togaviridae.
Distributed worldwide and affects both
sexes equally
Peak incidence; 5-14 yr of age
During clinical illness: the virus is present
in nasopharyngeal secretions, blood, feces,
urine
RUBELLA
Virus has been recovered from the nasopha-
rynx 7 days before the exanthem and 7-8
days after its disappereance.
The risk for congenital defects and disease
is greatest with primary maternal infection
during the first trimester.
RUBELLA
CLINICAL MANIFESTATIONS :
Incubation period: 14-21 days, no prodro-
mal phase or milder, 2/3 of infections are
subclinical
Congenital rubella syndrome ophtalmolo-
gic, cardiac, auditory, neurologic anomalies
Most characteristical signs; retroauricular,
postcervical and postoccipital LAP ; appe-
ars 24 hr before and 1 wk after rash.
RUBELLA
Forsheimer spots : enantem appears in 20%
of patients just before the onset of the rash
on the soft palate
Exanthem begins on the face spreads quick-
ly. Discrete maculopapules. 2.day-pinpoint
appereance. Mild itching. Pharengeal
mucosa and the conjuctivativae are slightly
inflamed. Fever is low greade or absent. In
older girls and women polyarthritis may
occur
RUBELLA
Congenital RUBELLA
RUBELLA
DIAGNOSIS : Clinical symptoms. Physical
appearance. Serology : IgM (+) in the first
day. Virus culture :nasopharynx, blood.
TREATMENT: No spesific treatment, sup-
portive.
COMPLICATIONS: Encephalitis, trombo-
cytopenia, rubella panencephalitis,arthritis
RUBELLA
PREVENTION: Rubella vaccine
Especially important for girls to have immunity to
rubella before they reach childbearing age.
The susceptable pregnant woman exposed to
rubella for whom abortion is not an obtion Ig
should be administered in a dose of 0.55 ml/kg
which reduces the attack rate but doesnt eliminate
the risk of fetal infection.
Vaccine theoretically could prevent illness if
administered within 3 days of exposure.
ERYTHEMA INFECTIOSUM
(FIFTH DISEASE)
Parvovirus B 19 ( discovered in 1975) member of
Erythrovirus in the family Parvoviridae.
DNA virus
5-15 years
Late winter and spring
Transmission; respiratory route.
Beningn selflimited exanthematous illness of
childhood.
Incubation period 4-28 days (av :16-17 days)
Parvovirus B 19
ERYTHEMA INFECTIOSUM
Prodromal lesion phase ; mild, lowgrade fever ,
headache, URI signs.
RASH:
1st stage: erithematous facial flushing slapped
ceak
2nd stage: diffuse macular erthrema on the trunk
and proximal extremities
3rd stage: central clearing of macules (reticuler
apperance). Resolves without desqumation. Pro-
minent on extansor surface. Tends to wax over 1-3
wks
ERYTHEMA INFECTIOSUM
Recur with exposure to sunlight, heat,
exercise, stress
LAP, atypical papular, purpuric, vesicular
rashes are described.
DIAGNOSIS: clinical presentation
IgM detection: 6-8 wks
Virus cant be isolated by culture
ERYTHEMA INFECTIOSUM
TREATMENT: No spesific antiviral thera-
py.
COMPLICATIONS: Arthralgies, arthritis,
trompbocytopenic purpura, aseptic meningi-
tis.
 PAPULAR PURPURIC GLOVES and SOCKS
SYNDROME
Rare disease with a cutaneous involvement and with
lesions in the oral cavity by parvovirus B19
Affects children and young adults
Appears in both sexes in spring and summer
Edema and pruritus of hands and feet followed by a
purpura at the same site
Erythema and petechiae on the hard and soft palate
Small erosions in the oral mucosa and tongue
Commissural chelitis
Nonspesific urethritis can appear
PAPULAR PURPURIC GLOVES and
SOCKS SYNDROME

Diagnosis is made by the clinical dermatological

chracteristics and is confirmed by spesific serology
for Parvovirus B19 using ELISA or PCR
Supportive treatment
ROSEOLA INFANTUM (SIXTh
DISEASE)
Human Herpes Virus (HHV) type 6 was
discovered in 1986 ( etiologic agent for
most cases)
HHV 7 was discovered 1990 in few cases
HHV-6 and 7 belong to the - herpesvirus
subfamily of herpesviruses
Peak acquisition of primary HHV-6
infection 6-15 months of age ( occur
younger than 3 yr)
ROSEOLA INFANTUM
ROSEOLA INFANTUM
Higher incidense during spring and fall months
Incubation period, 5-15 days (av:10 days)
Most adults excrete HHV-6 and 7 in saliva and
may serve as primary sources for virus
transmission to children
Prodromal period is usually asymptomatic ;mild
URI signs
Mild cervical or less frequently occipital LAP may
be noted
Some chidren may have mild palpebral edema.
ROSEOLA INFANTUM
Clinical illness is generaly heralded by high
temparature.
Some children may become irritable and
anorexic.
Seizures may occur in 15% of children.
Rhinorrhea, sore throat, abdominal pain,
vomiting and diarrhea
Fever persists for 3-7 days ; resolves
abruptly
ROSEOLA INFANTUM
ROSEOLA INFANTUM
A rash appears within 12-24 hr of fever
resolution.
Rash . Rose colored, distinctive } on the trunk
to neck, face, prox extremities
1-3 days later the rash fades.
The characteristic enanthem ( Nagayama
spot) consist of the soft palate and the base of
the uvula
The enanthem may be present on the fourth
day in 2/3 of patients with roseola
ROSEOLA INFANTUM
DIAGNOSIS
Spesific test for HHV 6-7
Virus culture, PCR, Ag detection
TREATMENT
HHV-6 is inhibited by ganciclovir ( but not
acyclovir. Foscarnet.
SCARLET FEVER
Group A Hemolytic streptococcus is the
cause Pyrogenic (erythrogenic) exotoxins
(A,B,C) Responsible for the rash of scar-
let fever.
Infection may be spread by droplets, contact
with skin lesions, transmitted by food, milk
and water.
Incubation period: 1-7 days. (av: 3 days)
Group A Hemolytic
streptococcus
SCARLET FEVER
Onset in acute and is characterized by fever,
vomiting, headache, toxicity, pharangitis
and chills within 12-48 hrs the typical rash
appears.
Temperature increases abruptly, may peak
39,6 - 40 C on the 2nd day and gradually
returns to normal within 5-7 days in untrea-
ted patients.
SCARLET FEVER
The tonsils are hyperemic and edematous
and may be covered with a gray white exu-
date.
The tongue may be edematous and redde-
ned. During the early days of illness the
dorsum of the tongue has a white coat.
WHITE STRAWBERRY TONGUE
After several days the red tongue with
prominant papillae. RED STRAWBERRY
TONGUE
SCARLET FEVER
THE PALATE AND UVULA MAY BE REDDENED
AND COVERED WTH PETECHIA.
THE EXANTEM IS RED,PUNCTATIC OR FINELY
PAPULAR.
Appears initially in the axillers, groin and neck
and generalized within 24 hrs.
The area around the mouth is pale: CIRCUMORAL
PALLOR
Petechia may occur owing to capillary fragility
SCARLET FEVER
SCARLET FEVER
Area of hyperpigmentation on the antecubi-
tal fossae; PASTIAS SIGN
Small vesicular lesions in severe disease :
MILIARY SUDAMINA
Desquamation begins on the face over the trunk
hands and feet
Scarlet fever may follow infection of wounds,
burns or skin infection
STRAWBERRY TONGUES
SCARLET FEVER
DIAGNOSIS:
Throat culture
Current rapid Ag detection
WBC
ESR,CRP
ASO, antiDNA se B (+) (3-6 wks)
SCARLET FEVER
COMPLICATIONS :
Sinusitis
A.O.M.
Mastoiditis
Cervical adenitis
Retropharingeal abscess
Bronchopneumonia
Menengitis
Osteomyelitis
Septic arthritis
SCARLET FEVER
TREATMENT:Penicillin 10 days
Single IM inj of a long active benzathine
penicillin, erytromicin, clindamycin, first
generation cephalosporins
Successful treatment with shorter causes (5
days) of azithromycin or cefpodoxime has
been reported.
VARICELLA (CHICKENPOX)
Primary infection of VARICELLA ZOSTER
VIRUS (VZV). HUMAN HERPES VIRIDAE
Lifelong latent infection of sensory ganglion
neurons reactivation of the latent infection
HERPES ZOSTER (SHINGLES)
Mild illness in childhood
Occurs in winter-spring
Within hauseholds of with a case of varicella
transmission of VZV to susceptible individuals
occurs at a rate of 80-90%
VARICELLA VIRUS
VARICELLA
Contagious from 24-48 hr before the rash
appears and until the vesicles are crusted (3-
7 days after onset rash)
Susceptible children may also acquire
varicella after close direct contact with
adults who have HZ.
Transmitted respiratory secretions, fluid of
skin lesions by airborne spread/through
direct contact
VARICELLA
Incubation period: 10-21 days ( mean 15
days)
Virus replicated in the resp tract primary
(subclinical) viremia, widespread cutenous
lesions occur during second viremia
Prodromal symptom: fever, malasia, ano-
rexia, headache, abdominal pain (24-48 hr
before the rash)
VARICELLA
Varicella lesions appears on the scalp, face
or trunk
Prurutic erythamatous macules clear
fluid vesicles (24-48 hr) clouding and
umblication.
While initial lesions are crusting new
crops form on the trunk and then the extre-
mites.
VARICELLA
Ulcerative lesions oropharenx and vagi-
na, eyelids and conjuctivae
Average number of varicella lesions 30
(10-1500)
VARYING STAGES OF DEVELOPMENT (MACULE,
PAPULE, VESICLE).
PRESENT AT THE SAME TIME.
VARICELLA
VARICELLA
Progresivve varicella: visceral organ invol-
vement, coagulopathy, severe hemorhage,.
Highest in children with congenital cellular
immune deficiency.
High dose CST, HIV, malignancy etc...
VARICELLA
DIAGNOSIS : Laboratory evaluation is not
necessary
Leukopenia (first 72 hr) lymphositosis
Liver function tests are usually elevated
Tissue culture method ( virus isolation) (7-
10 days)
VZV IgG Ab tests ; determine the immune
status of individuals whose clinical history
of varicella, is unknown.
VARICELLA
TREATMENT : Antiviral treatment modifies
the course: ACYCLOVIR : is not
recommended routinely for uncomplicated
cases
Oral therapy: 20 mg/kg/dose (max: 800 mg)
x4 dose 5 days
Children older than 12 yrs,receiving aerosol
steroids,having chronic cutaneous disease
IV therapy: severe disease and
immunocomprimised patients: 500 mg/m/
every 8 hrs 7 days
 VARICELLA
COMPLICATIONS : Mild varicella hepatitis
Mild trombocytopenia
Purpura, hemorrhagic vesicles, hematuria, GI
bleeding rare
Nephritis, NS, HUS, arthritis, myocarditis,
pericarditis, pancreatitis, orchitis
Secondary bacterial infections (AGBHS, S.aureus)
5%
Encephalitis and cerebellar ataxia; 5yr, 20 yr 2-
6 days after onset
Pneumonia: very rare in children
VARICELLA
PREVENTION : Vaccine : postexposure
within 3 days.
VZIG: postexposure prophylaxis for
immunocomprimised children. Pregnant
women. Newborn exposed to maternal
varicella, whose mothers develop varicella ,
5 days before to 2 days after delivery
Hand Foot Mouth Disease
Viral illness that usually affects infants and children
younger than 5 years old
Caused by viruses that belong to enterovirus genus
Coxsackievirus A16 is the most common cause
Incubation period 3-7 days
Usually starts with a fever, poor appetite, malaise
and sore throat
1-2 days after fever starts painful sores usually
develop in the mouth ( herpangina) ulcers
Skin rash usually on the palms of the hands and
soles of the feet,also may appear on the knees,
elbows,buttocs or genital area
 Hand Foot Mouth Disease
Spread from person to person by direct
contact
Viruses are found in the nose and throat
secretions, fluid in blisters and stool of
infected persons
May be spread when infected pensons touch
objects and surfaces that are then touched by
others.
 Hand Foot Mouth Disease

Infected persons are most contagious during

the first week of the of the illness
Samples from the throat or stool may be
collected for the diagnosis
No spesific treatment
MENNGOCOCCEMA