ERUPTIVE DISEASES

PROF.DR. AYÇA VİTRİNEL

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 İmpaired 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 doesn’t 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 can’t 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 ß- 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 ß 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 ß 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 ºC 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 WİTH 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; PASTIA’S 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/m²/ 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

MENİNGOCOCCEMİA