PPS UPEC PIDSP Rashes in Children Module (1).pdf

RASHES IN CHILDREN Rashes in Children 1.Viral Exanthems 2.Vesiculobullous Lesions 3. Purpura/Petechiae 4. Diffuse Erythemas with Desquamation 2 Rashes in Children Viral Exanthems MACULOPAPULAR RASH (red areas of the skin with small bumps) VESICULAR RASH (blisters/fluid-filled) 4 Rashes i...

RASHES IN CHILDREN Rashes in Children 1.Viral Exanthems 2.Vesiculobullous Lesions 3. Purpura/Petechiae 4. Diffuse Erythemas with Desquamation 2 Rashes in Children Viral Exanthems MACULOPAPULAR RASH (red areas of the skin with small bumps) VESICULAR RASH (blisters/fluid-filled) 4 Rashes in Children Maculopapular Rashes CHILDHOOD VIRAL DISEASES Medical history A mother presents a child with coryza, cough, conjunctivitis, fever. Patient also has a rash which began from the face to the chest. Tiny grayish white dots are seen on the buccal mucosa next to the 3rd molar. Rubeola (Measles) Virus PARAMYXOVIRUS (RNA) 7 Rashes in Children Measles: Disease Review > Highly contagious virus > Respiratory transmission2 > Incubation period: 10-12 days2 > Replication in nasopharynx and regional lymph nodes2 1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005) 2. Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health & Human Services CDC;7th Edition;2003;96-113 8 Rashes in Children Measles: Disease Review > Primary viremia 2-3 days after exposure2 > Secondary viremia 5-7 days after exposure with spread to tissues2 > Morbidity and mortality of measles are greatest in patients <5y/o and those >20 y/o 1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005) 2. Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health & Human Services CDC;7th Edition;2003;96-113 9 Rashes in Children Transmission and Immunity Transmission > Droplet infection > Direct contact > Period of communicability: 4 days before and after rashes appear Immunity > Long lasting > Passive immunity lasts for 5 – 6 months > Live attenuated vaccine confers lifelong immunity > Inactivated vaccine 6 – 18 months 1 0 Rashes in Children Pathogenesis Upper respiratory passage – nasopharynx or conjunctiva Epithelial cells infected and virus multiplies Extension to regional lymphoid tissue Primary viremia Multiplication in respiratory epithelium, RES, distant sites Secondary viremia Infection in skin and other sites Virus in blood, respiratory tract, skin and other organs Viremia, virus in organs 11 Rashes in Children Measles: Clinical Features Prodrome O > Stepwise increase in fever to >39.5 C or higher > Cough, coryza, conjunctivitis * Koplik spots – pathognomonic > 1 – 2 days before the rash > grayish white pinpoint dots ,red border, opposite lower molars > Transient Rash > 2-4 days after prodrome, 14 days after exposure > Maculopapular, becomes confluent > Begins on face and head > Persists 5-6 days > Fades in order of appearance > Leaves brawny desquamation Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health & Human Services CDC;7th Edition;2003;96-113 12 Rashes in Children Rash begins around hairline, on face and neck, behind ears Rash spreads downward to chest and abdomen Rash affects arms and legs last 13 Rashes in Children Measles manifestation on the skin Measles (rubeola) pharyngitis in an adult showing striking inflammation © Copyright American Academy of Pediatrics Rashes in Children © Copyright American Academy of Pediatrics Erythematous, maculopapular rash with areas of confluence Rashes in Children Measles: Diagnosis > Clinical picture > Isolation of measles virus from clinical specimens > Serology – IgG, IgM > Decreased WBC during prodrome and rash 16 Rashes in Children Common Complications Life-threatening : 1. Bronchopneumonia 2. Otitis media 3. Laryngotracheobronchitis 4. Diarrhea 5. Blindness 6. Flare up of existing TB 17 Rashes in Children Uncommon/Rare Complications Myocarditis /Pericarditis – rare ITP Mesenteric lymphadenitis Encephalitis – occurs during rashes, within 8 days from onset Convulsions, lethargy, irritability, coma 20 – 40% with brain damage Hemorrhagic/Black measles Subacute Sclerosing Panencephalitis (SSPE) 18 Rashes in Children Differential Diagnosis 1. Miliaria with acute URTI 2. Rubella 3. Roseola infantum 4. Allergic dermatitis 5. Infectious mononucleosis 19 Rashes in Children Inapparent Measles Infection > Subclinical form of measles > Individuals with passively acquired antibody: infants, recipients of blood products, some individuals who received the vaccine when exposed to Measles virus develop some symptoms > Does not shed the virus and does not transmit the infection to household contacts 20 Rashes in Children Atypical Measles > More severe type of measles > Due to circulating immune complexes that formed due to an abnormal immune response to the vaccine > Occurs in persons vaccinated with an Inactivated/Killed vaccine (1963-1967) exposed to natural virus 21 Rashes in Children Treatment and Prevention > Treatment No specific treatment Supportive measures – antipyretic, bed rest, fluids Vitamin A – reduces morbidity and mortality in children with severe measles in the developing world Antibiotics for complications > Prevention Live attenuated measles vaccine Immune globulin (Ig) 22 Rashes in Children Prevention > Isolation of patients: from 7th day after exposure until 5 days after the rash appeared > Measles vaccine: 9 months old > MMR vaccine: (2 doses): 12-15 months old, then 4-6y/o (minimum interval 4 weeks) * May be given to 9 months old > Post-exposure prophylaxis Passive immunization with Ig – within 6 days of exposure (<6 months old or those who are pregnant) Vaccine alone within 72 hours from exposure: exposed children 6 mos. of age or older 23 Rashes in Children Underutilization of Measles Vaccine The high measles disease burden, despite an increase in routine measles immunization coverage, is attributed mainly to the underutilization of measles vaccine These deaths are unacceptable because measles vaccine is safe, highly effective and cost-effective WHO/UNICEF Joint Report: Measles Mortality Reduction And Regional Strategic Plan 2003-2005 24 Rashes in Children Why do we need a 2nd dose of MMR? Eradication of measles cannot be achieved with a single-dose strategy alone A second dose of vaccine such as MMR is recommended by the WHO, to: Ensure individuals receive at least one dose Ensure immunity to individuals in whom no immunogenic response occurred with the first dose Restore immunity in those whose immunity has waned World Health Organization, Pan American Health Organization and CDC.MMWR 1997;46(RR-II) 25 Rashes in Children MEASLES OUTBREAK IN PH - Feb. 2019 > 12,7000 cases, 203 deaths ( 2-5 yo. ) > Mortality: 63% unvaccinated > NCR, Centarl Luzo, Calabarzon, Western Visayas, Central Visayas > Mindanao: Davao, Zamboanga, Taguig, Neg. Or “Vaccine confidence has also decreased in the Philippines following the dengue vaccine (Dengvaxia) issue. A recent study from the London School of Hygiene and Tropical Medicine documented that those believe “that vaccines are important, are safe and are effective” dropped from close to 100% in 2015 to 60-80% in 2018. This reveals a critical need to combat misinformation and improve public understanding of the critical importance and safety of vaccines.” 26 Roseola Infantum 27 Rashes in Children Roseola Infantum > 6th disease, Exanthem subitum > Etiology = Human herpesvirus 6 (most cases) = Human herpesvirus 7 = Echovirus 16 > Transmission > Probably acquired from saliva of healthy persons and enter the host through oral, nasal or conjunctival mucosa 28 Rashes in Children Roseola Infantum Children < 3 yrs. of age (esp. 6-15mos.) Peak incidence Mar – Apr Incubation period: 10 -16 days Fever – sudden onset, high grade subsides after 2 – 3 days With lysis of fever – rash appears on face and trunk disappears in 1 – 2 days 29 Rashes in Children Roseola Infantum Clinical manifestation > Prodrome period: rhinorrhea, pharyngeal inflammation, slight conjunctival redness, mild lymphadenopathy High-grade fever 3-5 days, may have febrile seizures > With defervescence :maculopapular rash Trunk, neck, face and proximal extremities for 1 – 3 days Diagnosis > Clinical picture > Rashes appear as fever disappears 30 Rashes in Children Roseola Infantum > PE – normal findings, child active, alert and playful Occasionally with full and tense anterior fontanel > Differential diagnosis 1. Measles 2. Meningitis > Treatment Symptomatic – antipyretics to lower temperature Sedatives or anticonvulsants for seizures 31 Rashes in Children Rose-pink, macular lesions of Roseola infantum 32 Rashes in Children Erythema Infectiosum > Fifth disease > Etiology Parvovirus B19 > Transmission Respiratory, blood transfusion 33 Rashes in Children Stages of Rash Erythematous and macular – “slapped cheek” appearance with circumoral pallor and sparing of nasal bridges Maculopapular rash + pruritus – lacey or reticular pattern Rash waxes and wanes in 1-3 weeks – rash recurrence due to heat, cold, exercise, stress 1. 2. 3. 34 Rashes in Children Erythema Infectiosum © MEDLibes Online Medical Library 35 Erythematous and macular ”slapped cheek” appearance Rashes in Children Complications 1. Arthropathy – arthritis/arthralgia 2. Transient aplastic crisis - arrest in production of red blood cells may occur in the following conditions: Sickle cell disease Thalassemia Hereditary spherocytosis Pyruvate kinase deficiency 3. Fetal infection: results in hydrops because of severe anemia cardiac failure, fetal death, and miscarriage 36 Rashes in Children Erythema Infectiosum Diagnosis > Clinical picture > Serology > PCR Treatment > Supportive 37 Rashes in Children Rubella Virus TOGAVIRUS (RNA) www.med.sc.edu:85/ mhunt/rub1.jpg; accessed in Aug 2005 38 Rashes in Children Rubella Virus: 3-day Measles Etiology Rubella virus belongs to Rubivirus genus of family Togaviridae Epidemiology Worldwide In RP, sporadic Highest attack rate in 5 – 9 yrs No sex difference Transmission Respiratory route – droplet infection Contact with infected individuals Contaminated linen and articles – nasopharyngeal secretion, stool or urine 39 Rashes in Children German Measles (Rubella) Reservoir Humans Transmission Respiratory – person-to-person Communicability 7 days before to 5-7 days after rash onset 40 Rashes in Children German Measles: Pathogenesis Respiratory transmission of the virus Replication in the nasopharynx and regional lymph nodes Viremia (5-7 days) Includes placenta and fetus 41 Rashes in Children Signs and Symptoms > Symptoms (if present) usually mild: inflammation of the lymph nodes maculopapular rash mild catarrhal symptoms > Adults may feel unwell with fever and loss of appetite > Approximately two-thirds of rubella cases not clinically evident © Copyright American Academy of Pediatrics www.vaccineinformation.org/photos/rubeaap001.jpg Accessed Aug 2005 Rubella rash (face) in a previously unimmunized young woman. Rashes in Children Clinical features Retroauricular, posterior cervical and post-occipital lymphadenopathy = most characteristic sign appear 24 hours before the rash appears up to the neck > Rash begins on the face and spreads quickly. > Evolution is so rapid that the rash may be fading on the face by the time it appears on the trunk 43 Rashes in Children Rash begins as red spots on the face Rash spreads quickly to trunk and extremities Rash is highly variable; often there is no rash 44 Rashes in Children Clinical Features Rash clears by the 3rd day, minimal desquamation Fever is low-grade or absent for 1-3 days Source: Centers for Disease Control and Prevention 45 © Copyright Dr. CW Leung, Department of Paediatrics and Adolescent Medicine, Princess Margaret Hospital, Hong Kong Rashes in Children Rubella rash © Copyright Dr. CW Leung, Department of Paediatrics and Adolescent Medicine, Princess Margaret Hospital, Hong Kong 46 Rashes in Children Rubella: Complications > Rare in childhood or adulthood > Arthritis or arthralgia in 2% of cases Mainly females > CNS complications (i.e., post-infectious encephalitis) occur in adults at a rate of 1/6000 cases > Congenital Rubella Syndrome (CRS) 47 Rashes in Children Congenital Rubella Syndrome > Up to 85% of infants affected if infection acquired in-utero during first trimester > Infection may affect all organs > May lead to fetal death or premature delivery > Severity of damage to fetus depends on gestational age Rubella in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health & Human Services CDC;7th Edition;2003;169-188 48 Rashes in Children Congenital Rubella Syndrome > Deafness > Cataracts > Heart defects > Microcephaly > Mental retardation > Bone alterations > Liver and spleen damage Infant with congenital rubella syndrome Source: Centers for Disease Control and Prevention Rubella in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health & Human Services CDC;7th Edition;2003;124-137 49 Rashes in Children CRS:Time of infection Time of infection Risk of congenital abnormalities Most common abnormalities 40–60% Multiple congenital defects and/or spontaneous abortion 9–12 weeks 30–35% Single defect e.g. congenital heart disease or deafness 12–16 weeks 10% Up to 8 weeks Single defect, usually deafness Mandell G, Douglas R, Bennett J eds. Principles and Practice of Infectious Diseases, third edition, 1990 50 Rashes in Children Treatment and Prevention Treatment = Symptomatic Prevention = Live vaccine Recommended in children from 1 yr of age * To protect children against measles, mumps and rubella * To eradicate measles , mumps and rubella from populations around the world 51 Rashes in Children German Measles Prevention MMR vaccine (2 doses): 12-15 months old 4-6 years old (minimum interval 4 weeks) Non-pregnant susceptible contacts of person with rubella should be vaccinated 52 Rashes in Children Adverse events of MMR vaccine Fever 6-12 days after vaccination Rash Encephalopathy and autism have not been shown to be causally associated with the MMR vaccine 53 Rashes in Children Epstein-Barr Virus > EBV is shed in oral secretions consistently x6 mos after acute infection and intermittently for life > It establishes lifelong latent infection after the primary illness > Immunosupression permits reactivation of latent EBV > EBV is also found in male and female genital secretions 54 Rashes in Children Epstein-Barr Virus > Childhood: inapparent infection (< 4y/o) > Incubation period: 30-50 days > Adolescent presentation: Triad: 1. Fatigue 2. Pharyngitis 3. Generalized lymphadenopathy > Infectious mononucleosis (IM): most common presentation in adolescents 55 Rashes in Children EBV: Pathogenesis Infects oral epithelial cells (pharyngitis) Intracellular replication and lysis Salivary glands Viremia (infection of B lymphocytes and entire lympho-reticular system including liver and spleen) 56 Rashes in Children Clinical features > Generalized lymphadenopathy > Splenomegaly > Hepatomegaly > Marked tonsillar enlargement, occasionally with exudates > Ampicillin rash – rash develops 5-10 days after giving Ampicillin or Amoxicillin to patients with EBV-associated IM 57 Rashes in Children Laboratory Tests > Leukocytosis with lymphocytosis > Atypical lymphocytes: CD8 T lymphocyte > Heterophile antibody tests > Specific EBV antibodies IgM VCA IgG VCA Anti EA antibodies Anti-EBNA – Last to develop in infectious mononucleosis Gradually appears 3-4 mos after the onset of illness and remain at low levels for life 58 Rashes in Children Laboratory Tests > IgM VCA - most valuable and specific serologic test for the diagnosis of acute EBV infection and sufficient to confirm diagnosis > Anti EBNA - last to develop in infectious mononucleosis, gradually appears 3-4 mos after the onset of illness and remains at low levels for life 59 Rashes in Children Treatment > Symptomatic treatment > Rest > High dose of acyclovir with or w/o corticosteroids decreases viral replication and oropharyngeal shedding during period of administration but does not reduce severity or duration of symptoms or alter eventual outcome 60 Rashes in Children Oncogenesis > Nasopharyngeal CA > Burkitt’s lymphoma > Hodgkin’s disease > Leiomyosarcoma (HIV) 61 Rashes in Children Fever with Vesiculobullous Lesions Coxsackie Virus > A non-polio enterovirus > Humans – only known reservoir > Mode of transmission Person-to-person by fecal-oral route, respiratory, vertically (transplacental, intrapartum or postnatal) 63 Rashes in Children Coxsackie Virus Hand, Foot and Mouth Disease (HFMD) > Most frequently caused by Coxsackie A16 > Oropharynx is inflamed and contains scattered vesicles on the tongue, buccal mucosa, posterior pharynx, palate, gingiva and/or lips that ulcerate, leaving shallow lesions with surrounding erythema > Same lesions occur on the hands, fingers, feet, buttocks and groin 1. 64 Rashes in Children Hand, Foot and Mouth Disease 65 Rashes in Children Lesions in the mouth 66 Rashes in Children Lesions on the hand(s) 67 Rashes in Children Lesions on the feet 68 Rashes in Children Coxsackie Virus Herpangina Characterized by fever, sore throat, dysphagia and characteristic lesion in the posterior pharynx Pleurodynia 2. 3. Acute sharp chest pain involving the intercostal muscles in between the ribs Myocarditis Hemorrhagic conjunctivitis Viral meningitis 4. 5. 6. 69 Rashes in Children Coxsackie Virus 70 Rashes in Children Coxsackie Virus Mystery Disease Kills 61 Children in Cambodia July 5, 2012 3:33 PM CDT 71 Rashes in Children Enterovirus 71 causing HFMD > Affects the lungs and brain > Meningitis, encephalitis, respiratory, cardiac complications 72 Rashes in Children Varicella-zoster virus 73 Rashes in Children Varicella-zoster virus infection > Public health concern > Highly communicable > Etiology:Varicella – Zoster virus 1.Varicella (chickenpox) – result of primary exposure 2. Zoster (Shingles) – affects skin and nerves due to reactivation of latent virus 74 Rashes in Children Varicella-zoster virus infection 75 Rashes in Children VZV or Chicken pox 76 Rashes in Children VZV or Chicken pox > Self-limiting > Causes severe complications Organ dissemination in adults and <1 yr. > Women of child-bearing age are immune Small percentage susceptible Chickenpox in 5/10,000 pregnancies Life-threatening to newborn 77 Rashes in Children VZV or Chicken pox > Fatal in persons with immune deficiency > With previous chickenpox Develop herpes zoster Reactivation of latent virus > Increased morbidity and mortality in newborns born to mothers who develop rash within 5 days before to 2 days after delivery 78 Rashes in Children VZV or Chicken pox Transmission Respiratory (airborne) Direct contact with skin lesion Incubation period 14-16 days (10-21 days) Period of Communicability 1-2 days before to 4-5 days after onset of rashes Usually contagious until lesions dry with scab formation Clinical features Vesicular rash – characteristic feature and first manifestation 4 stages: 1. Incubation period 2. Prodromal phase 3. Appearance of varicella rash 4. Healing or crusting of vesicular rash 80 Rashes in Children Varicella or Chicken Pox Lesions 81 Rashes in Children Clinical features Symptom Fever Anorexia Headache Cough/Coryza Sore throat 82 % Occurrence in Infected person 80% 80% 77% 68% 50% Rashes in Children Varicella = Mild prodrome of fever, malaise for 1-2 days = Macules > vesicles in crops > crusted lesions (simultaneous presence of lesions in various stages of evolution is characteristic), mucous membrane also affected = Umbilication of lesions = Rashes appear first on head with highest concentration on the trunk (central/centripetal distribution) 83 Rashes in Children Varicella Macule Vesicle Time in days 84 Papule 2 Fluid-filled 4 Crusting 6 Rashes in Children Varicella or Chicken Pox skin lesions © Copyright American Academy of Pediatrics 8 5 Rashes in Children Varicella or Chicken pox = Asymptomatic course <5% = Immunocompromised Severe, progressive in 50% especially in leukemics Bulutong tubig (Chicken pox) 86 Rashes in Children Complications Skin = Most common = Bullous hemorrhagic, localized gangrene, necrotizing fascitis, purpura fulminans = Cellulitis = Scarring 87 Rashes in Children Complications Pneumonia = Rare in children, more in adults = Viral in etiology = Secondary infection may ensue 88 Rashes in Children Complications CNS = 75% of non-suppurative complications = 2 most common Encephalitis Reye Syndrome – 20% CFR Common in 5 – 14 yrs 1981 – 1990 in US – Among Reye Syndrome cases, 6% of hospitalization due to Varicella 89 Rashes in Children Complications Rare-induced by viral multiplication in organs Glomerulonephritis Endocarditis Hepatitis Gastritis Appendicitis Pancreatitis Orchitis Arthritis 90 Rashes in Children Congenital Varicella Infection = Clinical manifestations of congenital varicella infection following chickenpox in pregnancy = Perinatal transmission occurs in 26% of maternal infections (Drwal-Klein et al, Annals Pharmahother, 1993) Stage of Infection Sequelae 1st and 2nd Trimester Congenital varicella syndrome 2nd and 3rd Trimester Herpes zoster Perinatal Disseminated neonatal varicella Adapted from Miller E. et al Rev Med. Michiot 1993 91 Rashes in Children Neurologic Sequelae of Fetal VZV Infection Sequelae Manifestation Cutaneous manifestations Damage to Sensory e.g. zigzag (cicatricial) skin lesions, nerves hypopigmentation Microphthalmia Damage to optic Optic atrophy stalk and lens Cataracts vesicle Choriorerinitis Hypoplasia of upper/lower extremities Damage to cervical Motor/sensory deficits and lumbosacral Absent deep tendon reflexes cord Anisocoria Anal/vesical sphincter dysfunction Microcephaly Damage to Calcifications brain/encephalitis Hydrocephaly Aplasia of brain 92 Rashes in Children Maternal Antibody Development and Neonatal Varicella • Transfer of maternal antibody -8 93 -7 -6 • Period of risk for severe neonatal varicella • Antibody Responseo f newborn -5 -4 -3 -2 -1 0 1 2 3 4 5 6 7 Number of Days Relative to Delivery 8 Rashes in Children VZV or Chicken pox = Mortality rate low in Philippines = Morbidity and cost substantial = Anti-virals have minimal effect Should be given soon after onset = Prevention of illness alternative approach = Limited therapeutic measures Safe and effective vaccination to control varicella and complications 94 Rashes in Children Prevention of Varicella Vaccine developed in Japan 1974 by Prof. Takahashi Oka strain only strain considered suitable by WHO Initially for high-risk children in Japan 1987 1993 administered to healthy children Varicella vaccine 1-13 y/o = 2 doses (12months 4-6y/o or may give at 2 months interval for the 2 doses) >13 y/o = 2 doses (1 month apart) 95 Rashes in Children Prevention of Varicella Post-exposure prophylaxis = Varicella Zoster Immunoglobulin G: recommended for immunocompromised children, pregnant women and newborns exposed to maternal varicella within 96 hours after exposure = IVIG - if VZIG not available = Varicella vaccine for healthy children within 3 – 5 days of exposure 96 Rashes in Children Treatment of Varicella = Supportive therapy = Antiviral drugs: Acyclovir or Valacyclovir Not routinely recommended in healthy children Administer within 24 hours after rash onset * Indications: children >12 yrs without varicella vaccination; those with chronic skin or pulmonary disorders, on long term salicylate therapy,receiving corticosteroid therapy; those with other immunocompromised conditions 97 Rashes in Children VZV or Chicken pox Breakthrough Varicella = Varicella in vaccinated individuals = Following close exposure to VZV ( household or an outbreak in school), 1 of every 5 vaccinated children may develop breakthrough varicella = Rash is atypical, predominantly maculopapular, less commonly vesicular, illness is commonly mild with < 50 lesions and little or no fever Considered potentially infectious and should be isolated until lesions have crusted or if there are no vesicles present or until no new lesions are occurring 98 Rashes in Children Varicella vaccine Recommendation Susceptible persons at high risk of exposure or severe illness Teachers of young children Institutional settings Military Women of childbearing age International travelers Health care workers Family members of immunocompromised persons 99 Rashes in Children Herpes - Zoster 100 Rashes in Children Herpes – Zoster or Shingles = Reactivation of a latent VZV infection = Associated with aging, immunosuppression, intrauterine exposure, varicella at <18 mos. of age = Manifested as vesicular lesions clustered within one, or less commonly 2 adjacent dermatomes 101 Rashes in Children Common Sites for Shingles Front 102 Back Rashes in Children Complications * Post-herpetic neuralgia – late protracted pain, persisting for months to years after the rash has healed 103 Rashes in Children Diagnosis = Clinical = Direct fluorescence assay, PCR =Tzanck smear = Serology 104 Rashes in Children Treatment Self-limiting, supportive therapy Antiviral drugs: Acyclovir or Valacyclovir Not recommended routinely for healthy children Should be started within 72 hrs Indications: immunocompromised; with complications like pneumonia, severe hepatitis, thrombocytopenia or encephalitis 105 Rashes in Children Prevention = New formulation VZV vaccine (Zostavax) for persons > 60 y/o – to prevent reactivation of herpes zoster and decrease the frequency of herpetic neuralgia = Not indicated for the treatment of zoster or post-herpetic neuralgia = Risk for developing subsequent herpes zoster is lower after VZV vaccine than after natural Varicella infection among immunocompromised children and healthy vaccinees 106 Rashes in Children Herpes Simplex Virus = Manifested as a primary infection or as a reactivation HSV type 1 – commonly seen in skin and mucous membranes above the waist HSV type 2 – seen in the genitals and in neonates = HSV establishes latent infection in regional sensory ganglion neurons, but periodically can reactivate and cause recurrent infection 107 Rashes in Children Herpes Simplex Virus = Symptomatic recurrent infections tend to be less severe and of shorter duration than first infections = Asymptomatic recurrent infections are common = Recurrent infections are contagious and can transmit the disease to susceptible individuals 108 Rashes in Children Pathogenesis Viral infection begins at the cutaneous portal of entry (oral cavity, genital mucosa, ocular conjunctiva, breaks in keratinized epithelia) virus replicates locally spreads to neural tissue where replication also occurs 109 Rashes in Children Herpes Simplex Virus = Primary infection – occurs in individuals who have not been infected previously with either HSV 1 or HSV2 = No pre-existing immunity, infections can be severe 110 Rashes in Children Herpes Simplex Virus = Non-primary 1st infection – occurs in individuals previously infected with one HSV type who become infected for the 1st time with the other HSV type =Because immunity to one HSV type provides some cross protection against disease caused by the other HSV type, non primary 1st infections tend to be less severe than true primary infections 111 Rashes in Children 112 Rashes in Children Herpes Simplex Virus Acute herpetic gingivostomatitis 1. Pain in mouth, salivation, fetor oris, refusal to eat and fever HSV 1 – most common cause of stomatitis Dendritic keratitis 2. Eye involvement is unique to HSV Presence of herpetic vesicles on the lids Steroids will worsen it 113 Rashes in Children Eye involvement unique to HSV 114 Rashes in Children Herpes Simplex Virus 3. Genital herpes 4. Eczema herpeticum 5. Herpes labialis - fever blisters or cold sores 6. Herpetic whitlow Due to HSV2, transmitted by sexual activity Most serious manifestation of traumatic herpes, results from widespread infection of the eczematous skin with HSV Most common recurrent HSV 1 infection Occurs on the vermilion border of the lips Painful, erythematous, swollen lesion that occurs on the terminal phalanx 115 Rashes in Children most common Herpes lesions: found on shaft of penis (male), vagina, vulva, cervix (female) and around anus 116 Rashes in Children Herpes lesions 117 Rashes in Children Herpes Simplex Virus CNS infection 7. HSV1 – most common cause of fatal sporadic encephalitis Fever, altered consciousness, headaches, personality changes, seizures, dysphasias and focal neurologic signs Most common cause of recurrent aseptic meningitis 118 Rashes in Children Diagnosis CSF PCR – the only practical test to diagnose HSV encephalitis beyond the neonatal period, with sensitivity and specificity >95% Brain MRI Tzanck smear 119 Rashes in Children Treatment Acyclovir – parenteral is recommended treatment for neonatal HSV infection Given to all neonates w/HSV disease 60 mg/kg/day in 3 divided doses 14 days for SEM; 21 days for CNS or disseminated disease Foscarnet Drug of choice for acyclovir-resistant HSV Topical Acyclovir For oral or genital herpes Decreases the period of viral shedding but with little effect on symptoms 120 Rashes in Children Fever with Purpura/ Petechiae Meningococcal infection Etiology Neisseria meningitidis Gram (-) diplococcus Commensal colonies of nasopharynx Micrograph of Neisseria meningitidis 122 Rashes in Children Acute Meningococcemia > Initially mimics viral illness with pharyngitis, fever, myalgia, weakness, vomiting and headache > Maculopapular rash- petechia/purpura progresses rapidly to septic shock in a few hours (hypotension, DIC, acidosis, adrenal hemorrhage, renal failure, myocardial failure, and coma) 123 Rashes in Children Petechia/purpura of Meningococcemia 124 Rashes in Children Extensive purpuric lesion of Meningococcemia 125 Rashes in Children Meningococcal Invasive infection Meningitis (stiff neck, high fever, headache, petechial rash) Bacteremia/sepsis (meningococcemia) Pneumonia Pericarditis Arthritis 1. 2. 3. 4. 5. 126 Rashes in Children Meningococcal meningitis > Headache, > Photophobia, > Lethargy, > Vomiting > Nuchal rigidity > Other signs of meningeal irritation 127 Rashes in Children Incubation Period 1-10 days, usually 2-4 days 128 Rashes in Children Mode of Transmission = Person to person via aerosolized respiratory droplets or oral secretion from asymptomatic carriers or individuals with invasive disease = May also be spread by inanimate objects contaminated with saliva (e.g. cigarettes, food utensils, water bottle) = Human – only known reservoir of Neisseria meningitidis 129 Rashes in Children Period of Communicability ● Cases remain infective as long as meningococci are present in oral secretions or until 24 hours after initiation of effective antibiotic treatment 130 Rashes in Children Meningococcal meningitis Remember: 5-10% of adults are asymptomatic nasopharyngeal carriers of strain of Neiserria meningitidis, most of which are not pathogenic 131 Rashes in Children Diagnosis Isolation of meningococci from CSF and blood by culture Latex agglutination of CSF 132 Rashes in Children Treatment Penicillin G – drug of choice, given for 5-7 days Other antibiotics: Ceftriaxone Cefotaxime Chloramphenicol Vancomycin 133 Rashes in Children Complications Gangrene of extremities Adrenal hemorrhage Endophthalmitis Arthritis Endocarditis Pericarditis Myocarditis Pneumonia Lung abscess Peritonitis Renal infarcts Deafness – most common neurologic sequela 134 Rashes in Children Control of further spread = Minimum period of isolation of patient: until 24 hours after initiation of appropriate antibiotic therapy = Protection of contacts of a case: close contacts of the patient should be identified for antibiotic prophylaxis: Rifampicin Ceftriaxone Ciprofloxacin 135 Rashes in Children Definition of ‘close contact’ = Any member of patient’s household or other individuals who had intimate contact with the patient’s saliva or oral/nasal secretion = Health care workers who have intimate contact with the patient’s oral/nasal secretion (through unprotected mouth-to-mouth resuscitation, intubation or suctioning) 136 Rashes in Children Preventive measure To prevent additional cases: 1. Refer close contacts to health care provider for appropriate chemoprophylaxis 2. Admit contacts with signs and symptoms of illness and refer them to their health care provider should they experience symptoms compatible with invasive meningococcal disease 3. Practice good hygiene and handwashing 137 Rashes in Children Preventive measure To prevent additional cases: 4. Avoid sharing food, beverages, cigarettes or eating utensils 5. Consider immunization in certain circumstances: Meningococcal conjugate vaccine Meningococcal polysaccharide vaccine 138 Rashes in Children Recommended Chemoprophylaxis AGE OF INFANTS, CHILDREN AND ADULTS DOSE DURATION < 1 month 5 mg/kg orally q 12 h 2 days > 1 month 10 mg/kg orally q 12 h 2 days < 15 years old 125 mg IM Single dose > 15 years old 250 mg IM Single dose 20 mg/kg orally Single dose 10 mg/kg Single dose RIFAMPICIN CEFTRIAXONE CIPROFLOXACIN 1 month AZITHROMYCIN 139 Rashes in Children Dengue Infection Etiology Dengue virus 1, 2, 3, 4 Mode of transmission Day-biting female mosquito: Aedes aegypti and Aedes albopticus 140 Rashes in Children Dengue Infection 141 Rashes in Children Increasing Global Burden of Dengue 142 Rashes in Children Dengue in the Philippines First DHF cases identified in Manila, 1953/1954/1956 Subsequent outbreaks observed in the 1960s and subsequently at 5-year intervals Nationwide endemicity Over 200,000 cases in 2013 1 Bravo L et al PLoS Negl Trop Dis 2014;8(11):e3027 2 Carlos CCet al. Am J Trop Med Hyg 2005 Aug;73(2):435–40 143 Dengue cases continue to increase, with highest ever recorded in 2013 Rashes in Children Dengue: Rapidly spreading, vector-borne, viral disease > Dengue is the most rapidly spreading mosquito-borne viral disease in the world > The dengue virus is a member of the genus Flavivirus in the family Flaviviridae A genus that also includes yellow fever, Japanese encephalitis, Zika and West Nile encephalitis > The mosquito vector Aedes aegypti, is found mainly in tropical and sub-tropical regions > Dengue is a febrile illness that affects people of all ages > Leading cause of illness and death in the tropics and subtropics 144 Rashes in Children Dengue mosquito vectors Aedes aegypti = Yellow fever mosquito = Has bright silvery lyre-shaped dorsal pattern and white banded legs = Sneaky biter = High preference for taking blood meals from humans and to lesser extent from domestic mammals, which makes it a very capable vector of dengue viruses Main dengue vector worldwide 145 Rashes in Children Transmission of Dengue infection Female Aedes Aegypti mosquito acquires dengue virus by biting infected human during viremic phase (4 to 5 days, up to 12 days) Extrinsic incubation period in the mosquito Mosquito transmits virus to man during every feeding Clinical manifestations in man 146 (2 to 15 days after the bite) Rashes in Children Dengue Transmission 147 Rashes in Children Dengue Transmission 148 Rashes in Children Dengue Transmission 149 Rashes in Children Dengue Transmission 150 Rashes in Children Dengue Transmission 151 Rashes in Children Dengue Transmission 152 Rashes in Children Dengue Transmission 153 Rashes in Children Clinical manifestation Incubation = 3-14 days after the bite of an infected mosquito, with an average of 4-7 days Symptoms Sudden onset of high fever (39O to 40O) Maculopapular rash (appear 2-5 days after onset of fever) Severe headache Myalgia Arthralgia Retro-orbital pain Prostration Malaise Nausea 154 Rashes in Children Dengue infection Dengue infection results in a spectrum of disease WHO Dengue guidelines for Diagnosis, Treatment, Prevention and Control, 2009. 155 Rashes in Children Dengue Classification WHO has provided 2 sets of guidelines for Dengue classification 1 WHO, 1997, Clinical diagnosis 2 WHO, 2009, Dengue Guidelines for diagnosis, treatment, prevention and control 156 Rashes in Children Dengue Fever (DF) Non specific signs and symptoms Headache Conjunctivitis Eye pain Sore throat Cough Anorexia Nausea Vomiting Abdominal pain Myalgia/arthralgia Flushed skin Lymphadenopathy hepatomegaly 157 Rashes in Children Rash in DF and DHF = Varies with virus strain = More often seen in upper and lower extremities = Unusual character of rash = Flushing or erythematous mottling coincides with fever maculopaular (2nd – 6th day) May start in trunk face extremities (2-3 days) = Petechiae or rashes seen during or after defervescence on lower legs = Pruritus and desquamation 158 Rashes in Children Character of Rash in DHF 159 Rashes in Children Character of Rash in DHF 160 Rashes in Children Diagnostic Tests = Sensitivity of diagnostic tests for dengue is influenced by the duration of the illness1 = Serotyping of the dengue virus is possible2 The SIMPLEXATM Dengue RT-PCR assay has been used to serotype diverse strains in the field 1 Simmons, 2012, N Engl J Med 2 Boaz, 2014, Tials Vaccinol 161 Rashes in Children Dengue diagnosis VIRUS ISOLATION Hemagglutination Inhibition (HI) Plaque Reduction Neutralization test IgM and IgG ELISA Rapid tests: Dot blot, Immunoblot, Dipstick, Immunochromatography Mosquito inoculation (intrathoracic) Toxorhynchites splendens Mosquito cell culture C6/36 (Aedes albopictus) Anti-dengue Ig Molecular techniques Polymerase chain reaction(PCR) NS1 antigen detection Fever Viremi a 0 2 4 6 Manifestations: Shock Hemorrhage Encephalitis Liver injury 8 10 12 14 16 Days after infection 162 Rashes in Children Management of Dengue Infection > Early and effective replacement of lost plasma with plasma expanders or fluids and electrolyte solutions favorable outcome > Issues on other forms of treatment 163 Rashes in Children Despite decades of research, there is no Dengue specific treatment available Current treatment methods include 1 Acetaminophen for fever and pain Oral or intravenous fluid management Careful monitoring of patients during the critical phase around defervescence is vital 1 for the early detection and effective management of severe dengue In patients with severe dengue, management includes 1 Admission to a hospital with access to intensive care facilities and blood transfusion Management of patients’ body fluid volume Antiviral treatments are being investigated, but the field of dengue drug research is 1,2 still relatively new 164 1 WHO, 2009, Dengue Guidelines for diagnosis, treatment, prevention and control 2 WHO, Antiviral Research and Development Against Dengue Virus Rashes in Children Dengue Control and Prevention Reduce risk for further transmission Vector Control WHO promotes the strategic approach known as Integrated Vector Management (IVM) to control mosquito vectors, including those of dengue Vector transmission is reduced through the use or combination of these three methods: Environmental management Chemical control Biological control 165 Rashes in Children Dengue Control and Prevention Reduce risk for further transmission Individual and household protection Self-initiative for course reduction in homes and community. See “Environmental management” Clothing that minimizes skin exposure during daylight hours when mosquitoes are most active affords some protection from the bites of dengue vectors Repellents may be applied to exposed skin or to clothing (in strict accordance with label instructions). 166 Rashes in Children Health Teaching Posters 167 Rashes in Children Dengue Control and Prevention Personal Protection Clothing Wear full sleeves clothes , long dresses Screen Bednets Mosquito repellant Contain N, N-diethyl-mtoterosamide (DEET) applied to exposed skin can prevent mosquito bites Avoid DEET at concentration > 30% OFF lotion has 28.5% DEET In tropical countries, frequent application because of perspiration Care when treating small children, not applied to hands or face Clothing can be treated with DEET or permethrine Mosquito coils and electric vapor prevents mosquito bites 168 Rashes in Children Dengue Control and Prevention Apart from vector and environmental control Vaccine now available (?) Indicated for Children 9 years up to 45 old with medical history or laboratory confirmation of previous dengue infection Given subcutaneously for 3 doses: 0, 6, 12 months Effective against 4 serotypes of dengue virus 1 6 Rashes in Children Chikungunya > Chikungunya is an alphavirus of the family Togaviridae. “Chikungunya” = Means “to become contorted” or “that which bends up” > Translated from Bantu language – Tanzania and Mozambique > Described the stooped appearance of sufferers with joint pains. 170 Rashes in Children Chikungunya > Spread by mosquitoes: Aedes aegypti, Aedes albopticus > Causes fever and severe joint pains Muscle pain, headache, nausea, fatigue and rashes > Shares some clinical signs with Dengue and can be misdiagnosed in areas where Dengue is common 171 Rashes in Children Chikungunya 172 Rashes in Children Clinical features CLINICAL FEATURES CHIKUNGUNYA DENGUE Fever (Temp 38.9 C) Myalgia Arthralgias Headaches Rash Bleeding dyscrasia Shock Leukopenia Neutropenia Lymphopenia Thrombocytopenia +++ + +++ ++ ++ +/++ + +++ + ++ ++ +/++a + ++ +/+++ +++ ++ +++ Note: The mean frequencies of symptoms were determined from studies where the 2 diseases were directly compared among patients symbols indicate the % of patients exhibiting each feature. +++:70-100%, ++: 40-69%, +: 10-39%, +/-: <10%, -: 0% a - Headache was often retroorbital 173 Clin Infect Dis. (2009) 49 (6) 942-948 Rashes in Children Symptoms > Joint pains or arthritis – may be debilitating that may last for weeks or months. > The prolonged joint pain associated with Chikungunya is not typical in Dengue > Maculopapular rash precedes disappearance of fever; petechial rash is not common > Neurological, heart and GI complications have been reported but rare and is seen in older people 174 Rashes in Children Incubation Period > 2-12 days but is usually 3-7 days > Chikungunya virus infection is thought to confer lifelong immunity. > Fatalities related to Chikungunya are rare 175 Rashes in Children Diagnosis Serology (ELISA): IgM and IgG anti-chikungunya antibodies IgM antibody levels are highest 3-5 weeks after the onset of illness and persist for about two months. Should be done after 5 days of illness Chikungunya PCR - best done during the first four days of illness 176 Rashes in Children Treatment > No specific antiviral treatment > Symptomatic: rest, fluids For fever and joint pains: Ibuprofen, Naproxen, Acetaminophen or Paracetamol. > Aspirin should be avoided 177 Rashes in Children Prevention > No vaccine > Modify or remove natural and artificial water-filled container habitats that support breeding of mosquitoes. > During outbreaks, insecticide may be sprayed to kill flying mosquitoes > Clothing that minimize exposure to day biting mosquitoes is encouraged. 178 Rashes in Children Prevention Repellents can be applied to exposed skin or clothing: contain DEET, IR 3535 (Ethyl butylacetylaminopropionate) or Picaridin For those who sleep during daytime, insecticide treated nets should be used Mosquito coils or other insecticide vaporizers may reduce indoor biting. 179 Rashes in Children Diffuse erythema with Desquamation Scarlet Fever > Causative agent > Group A Beta-hemolytic Streptococcus “Streptococcus pyogenes” > MC cause: URTI(pharyngitis),SKIN(Impetigo, pyoderma) Humans: natural reservoir > Exanthem = Finely papular erythematous, “sand-paper” rash on trunk and extremities with circum-oral pallor = Presence of Pastia’s lines (petechiae that develop in the folds of joints) = Rash fades on pressure and always leads to desquamation 181 Rashes in Children Scarlet Fever Rash Pastia’s Line 182 Rashes in Children Scarlet Fever Rash 183 Rashes in Children Scarlet Fever 184 Rashes in Children Scarlet Fever > Enanthem = Tonsillopharyngeal congestion = Palatal petechiae = Strawberry tongue (swollen red and mottled appearance that eventually peels) 185 Rashes in Children Strawberry tongue 186 Rashes in Children Tonsillopharyngeal erythema with tonsillar exudates 187 Rashes in Children Treatment and Diagnosis Diagnosis Throat swab culture, ASO Treatment Penicillin for 10 days 188 Rashes in Children Staphylococcal Scalded Skin Syndrome = Ritter disease = Child <5 yo with abrupt onset of generalized diffuse, tender erythema > blisters and erosions form within 24-48 hrs > exfoliation = (+) Nikolsky sign – areas of epidermis separate in response to gentle shear force = Characteristic facies (periorificial scaling and superficial erosions) = Entire skin heals without scarring within 14 days 189 Rashes in Children Staphylococcal scalded skin syndrome 190 Rashes in Children Staphylococcal scalded skin syndrome 191 Rashes in Children Staphylococcal Scalded Skin Syndrome = Causative agent Staphylococcus aureus, producing toxins (exfoliative toxin A and B) = Mc cause of pyogenic infections in the skin, soft tissues = Bacteremia- osteomyelitis, endocarditis, empyema, soft tissue abscesses, pneumonia = Toxin-mediated diseases - food poisoning, SSS, TSS Toxin released by focus of infection Nasopharynx, umbilicus, conjunctivae, blood, superficial abrasion, urinary tract = Diagnosis 192 Blood culture Intact bullae are sterile Rashes in Children Treatment Anti-staphylococcal antibiotics (e.g. Oxacillin) Local skin care Dry exfoliating lesion – petrolatum/emollients Weeping, crusted lesion – NSS compress for 15 mins every 1-2 hrs Symptomatic and supportive measures 193 Rashes in Children Toxic Shock Syndrome 194 Rashes in Children Toxic Shock Syndrome Major criteria Minor criteria Exclusionary criteria 1. 2. 3. 195 Rashes in Children Major Criteria ALL REQUIRED 1. Acute fever; temperature >38.8OC 2. Hypotension 3. Rash (erythroderma with late desquamation) – sunburn like or scarlatiniform 196 Rashes in Children Minor Criteria ANY THREE (3) 1. Mucous membrane inflammation (conjunctivae, vagina, pharynx, strawberry tongue) 2.Vomiting, diarrhea 3. Liver abnormalities 4. Renal abnormalities 5. Muscle abnormalities 6. CNS abnormalities 7. Thrombocytopenia 197 Rashes in Children Risk Factors 1. Use of tampons and other vaginal devices 2. Nasal packing 3. Wound infections 4. Sinusitis, tracheitis, pneumonia, empyema 5. Abscesses, burns 6. Osteomyelitis 7. Primary bacteremia 198 Rashes in Children Staphylococcal Toxic Shock Syndrome Etiology: S. aureus producing Toxic Shock Syndrome Toxin (TSST-1) and other enterotoxins 199 Rashes in Children Complications Acute respiratory distress Myocardial dysfunction Renal failure 1. 2. 3. 200 Rashes in Children Outcome Recovery in 7-10 days Desquamation of palms and soles Hair and nail loss in 1 – 2 months 201 Rashes in Children Diagnosis No specific laboratory test Involvement of several organ systems 202 Rashes in Children Differential Diagnosis Kawasaki Disease Streptococcal Toxic Shock Syndrome Scarlet fever Measles Leptospirosis Toxic Epidermal Necrolysis (TEN) 203 Rashes in Children Treatment Anti-staphylococcal antibiotics, e.g. Oxacillin, Nafcillin, first generation Cephalosporin, Vancomycin, Clindamycin Fluid replacement Drainage of vagina or of focally infected sites 204 Rashes in Children Prevention Avoid using tampons Drainage of abscesses Early institution of appropriate systemic antimicrobial therapy 205 Rashes in Children Kawasaki Disease Mucocutaneous lymph node syndrome or infantile polyarteritis nodosa Acute multisystemic vasculitis of infants and children Age of predilection: <5 y.o. Etiology Unknown 206 Rashes in Children Diagnostic Criteria Fever lasting for at least 5 days Presence of at least 4 of the following 5 signs: 1. 2. 207 Bilateral bulbar conjunctival infection, generally non-purulent Changes in mucosa of oropharynx, including injected pharynx, dry fissured lips, strawberry tongue Rashes in Children Bilateral bulbar conjunctival infection Changes in mucosa of oropharynx 208 Rashes in Children Diagnostic Criteria 3. 209 Changes of the peripheral extremities such as edema and/or erythema of hands or feet in the acute phase; or periungual desquamation in the subacute phase Rashes in Children Changes of the peripheral extremities 210 Rashes in Children Diagnostic Criteria 4. 5. 211 Rash - primarily truncal; polymorphous, erythematous rash but non-vesicular; can be maculopapular, morbilliform (measles-like rash), or scarlatiniform Cervical adenopathy, >1.5 cm, usually unilateral lymphadenopathy; illness not explained by other known disease process Rashes in Children Polymorphous erythematous rash 212 Rashes in Children Cervical adenopathy 213 Rashes in Children Kawasaki Disease Cardiac involvement – most important manifestation/sequelae Myocarditis, coronary artery aneurysm (25% of untreated patients) 214 Rashes in Children Diagnosis Clinical Laboratory findings: Normal to elevated WBC with predominance of neutrophils and immature forms Elevated ESR, CRP Platelet count is normal in the 1st week of illness, increases by 2nd-3rd week 2D Echo: most useful test to monitor potential development of coronary artery abnormalities 215 Rashes in Children Treatment IVIG – reduces the prevalence of coronary arterydisease from 20-25% to 2-4%; should be given within 10 days of the onset of fever Aspirin – used for its anti-inflammatory and antithrombotic activity 216 Rashes in Children Non-infectious causes of Fever and Rash Connective tissue disease Malignancies Drug Reactions 217 Rashes in Children Children are not things to be moulded, but are people to be unfolded. 218 Rashes in Children Thank you 219 Rashes in Children