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VIRAL EXANTHEM General Objectives: To discuss the general spectrum of infectious diseases in children particularly common viral infections that produces exanthems or skin manifestations. Specific Objectives: To know common viral infections seen in children and discuss the following: Etiology Incidence Incubation period Transmission Pathogenesis Clinical manifestations Diagnosis Complications Management Prevention Prognosis MEASLES (Rubeola) acute communicable disease is characterized 3 stages: Incubation stage- approximately 10-12 days with few, if any signs or symptoms Prodromal stage- with an enanthem (Kopliks spot) on the buccal and pharyngeal mucosa, slight to moderate fever, mild conjunctivitis, coryza and an increasingly severe cough. Final stage- with a maculopapular rash erupting successively over the neck and face, body, arms and legs and accompanied by high fever ETIOLOGY - Measles is an RNA virus of the Family Paramyxoviridae, genus Morbilivirus One antigenic type During prodromal and short time after the rash appears the virus is found in the nasopharyngeal secretions, blood and urine It remained active for at least 34 hrs at room temperature INFECTIVITY EPIDEMIOLOGY PATHOLOGY - maximal dissemination of the virus via droplet spray during the prodromal period infected person becomes contagious by the 9yh-10th day after exposure (beginning of prodromal phase), in some instances as early as the 7th day isolation precaution should be maintained from the 7th day after exposure until 5 days after the rash has appeared Philippine statistics (DOH, 2001): 24,494 cases with rate of 31.4/100,000 population essential lesion of measles is found in the skin, mucous membrane of nasopharynx, bronchi, intestinal tract and conjunctivae. There usually hyperplasia of the lymphoid tissue particularly in the appendix with multinucleated giant cells (Warthin-Finkeldey reticuloendothelial cells) CLINICAL MANIFESTATIONS A. INCUBATION PERIOD: approximately 10-12 days if the first prodromal symptom is selected as the time of onset 14 days if the appearance of the rash is selected B. PRODROMAL PHASE: last 3-5 days, characterized with low to moderate grade fever, a hacking cough, coryza and conjunctivitis the 3 c’s nearly always preceed KOPLIK SPOTS – pathognomonic sign of measles by 2-3 days KOPLIK SPOTS: an enanthem or red mottling is usually present on the hard and the soft palates. This are slightly grayish white dots, usually as small as grains of snd, with slight, reddish areola, occasional hemorrhagic. Located opposite the lower molars but may spread irregularly over the rest of the buccal mucosa. They disappear within 12-18 hrs. C. Final stage/ appearance of rashes: temperature abruptly rises 40-40.5C 1 - uncomplicated cases: when rash appears on the leg and the feet within 2 days, symptoms subside rapidly. Macular rashes appears on the lateral side of the neck, behind the ears, along hairline and the posterior part of the cheek. 1st 24hrs: spread on the face neck, arms and upper part of the chest. Succeeding 24 hrs: back, abdomen entire arms and thighs 2nd-3rd day: feet and begins to fade on the face Rash is often slightly hemorrhagic, itching is generally slight As the rash fades, BRANNY DESQUAMATION and brownish discoloration occurs and then disappears within 7-10 days MODIFIED MEASLES v.s. ATYPICAL MEASLES Modified measles: Atypical measles: - occurs in partially immune host; young infants with partial protection from maternal antibodies and immunized children with partial vaccine failure short prodrome, less severe rash; Koplik spot; diagnosis should not be made in the absence of cough occurs in recipient of killed measles virus vaccine given until 1967 who came in contact with wild type measles vaccine; few, less severe cases in children given live attenuated measles vaccine sever headache, severe abdominal pain with vomiting, myalgia, pneumonia with pleural effusion and an atypical rash that first appears on the palms, wrist, soles and ankle and progresses into centripetal direction; maculopapular rashes can become vasicular later hemorrhagic. Koplik spots are rare. DIAGNOSIS: A. Clinical: characteristic clinical picture is the usual basis for diagnosis B. Laboratory: rarely needed a. Positive measles IgM antibody b. Significant increases in measles IgG antibody in paired acute and convalescent sera c. Isolation of measles virus from urine, blood and nasopharyngeal secretions COMPLICATIONS A. Otitis media B. Laryngitis, laryngotrachietis, laryngotracheobronchitis C. Pneumonia: most common complication and leading cause of death a. Primary measles pneumonia b. Pneumonia secondary to bacterial infection ( H. influenza, Streptococcus pyogenes, Streptococcus pneumoniae) D. Encephalitis a. More common in measles than any other viral exanthems (0.5-1/1000 cases) b. Usually occurs 2-5 days after the rash c. Early occurrence is the result of direct viral invasion: later occurrence is predominantly demyelinating. E. Subacute a. b. c. d. e. F. G. H. I. J. K. Sclerosing Panencephalitis (SSPE)- DAWSON ENCEPHALITIS Rare degenerative CNS disease occurring years later (0.6-2.2/100,000 infection) Due to persistent measles virus Progressive behavioral and intellectual deterioration with seizures, mostly myoclonic jerks, motor incoordination, visual and speech impairment. Laboratory features: markedly elevated CSF globulin predominantly IgG, high serum measles antibody titers and high CSF measles antibody titers EEG: periodic suppression burst pattern Exacerbation of an underlying Mycobacterium tuberculosis infection. A temporary loss of hypersensitivity reaction to tuberculin occur 4-6 weeks (sate of anergy) Myocarditis Thrombocytopenic purpura Severe conjunctivitis which may lead to corneal ulcerations and blindness Dehydration Malnutrition TREATMENT: A. B. specific: none Non-specific a. Supportive measures 2 i. Antipyretics ii. Adequate nutrition and fluid intake b. Vitamin A supplementation: i. < 6months – 12mons: 100,000 iu ii. >12 months: 200,000 iu dose should be repeated the next day and 4 weeks later if with ophthalmologic evidence of vitamin a deficiency. c. Antimicrobial therapy: not routinely given except in the presence of complication like otitis media or pneumonia. SUPPORTIVE MANAGEMENT: A. isolation of hospitalized patients B. Care of exposed persons a. Active immunization: live measles vaccine given 72 hrs after exposure maybe protective in some cases b. Passive immunization: immunoglobulin may prevent or modify measles if given 6 days after exposure. c. Control measures: live measles vaccine immunization of infants 6-9 months and a second dose of at 12-15 months as MMR. A second dose of MMR given 4-6 years old. RUBELLA ( German Measles/ Three-day measles) - common communicable disease in childhood characterized by mild constitutional symptoms, a rash similar to mild rubeola, enlargement and tenderness of postoccipital, retroauricular and posterior cervical lymphnodes Rubella in early pregnancy may cause severe congenital anomalies ( Congenital Rubella Syndrome) - Rubella virus, an RNA virus under the family Togaviridae and genus Rubivirus ETIOLOGY: CLINICAL FORMS A. Postnatal Rubella a. Source: i. b. c. d. e. f. g. h. During clinical illness the virus is present in the nasopharyngeal secretions, blood, feces and urine of infected person including those with congenital rubella Mode of transmission: direct of droplet contact from nasopharyngeal secretions Period of communicability: i. The virus can be recovered from the nasopharynx 7 days before the exanthema and 7-8 days after its disappearance. Incubation period: 14-21 days Clinical Picture: i. Asymptomatic illness: account for 25-50% of cases ii. Symptomatic illness Manifestations: i. Adenitis: enlargement of retroauricular, postcervical and suboccipital lymph nodes at least 24 hrs before the rash ii. Forscheimer spots: discrete rose spots on the soft palte in 20% of patients before the rash iii. Rash: maculopapular rashes on the face, rapidly becoming generalized within 24 hrs, with minimal desquamation iv. Mild conjunctivitis with photophobia, mild pharyngitis, slight splenomegaly, polyarthralgia/ polyarthritis v. Fever is low grade or absent Diagnosis i. Clinical diagnosis is difficult because symptoms and rashes are similar to other viral infections ii. Laboratory diagnosis: 1. isolation of virus from nasal specimen, throat swab, blood, urine or CSF 2. Detection of antibodies a. Rubella-specific IGM: recent postnatal infection b. Rubella- specific IgG between acute and convalescent serum titters: fourfold increase—INFECTION Complications: rare i. Encephalitis ( 1/6000 cases) 3 ii. Purpura: thrombocytopenic or non-thrombocytopenic I. Treatment: supportive B. CONGENITAL RUBELLA a. Pathogenesis i. Transplacental infection of fetus with rubella virus occurs following primary maternal viremia ii. The time when rubella virus infection occurs during gestation is a critical factor that determines the risk of fetal infection and disease severity: Time of fetal infection 1st month of gestation 2nd month of gestation 3rd-4th month of gestation b. c. d. e. f. g. h. Risk of congenital defects >/= 50% 20-30% 5% Redbook 2003 Period of communicability: i. As long as virus shedding occurs in nasopharyngeal secretions and urine; can last for 1 year or in more in a small number of patients Clinical features: i. Intrauterine growth retatardation: most common manifestation ii. Ophthalmologic manifestations: cataract, retinopathy, congenital glaucoma iii. Cardiac anomalies: PDA, peripheral pulmonary artery stenosis iv. Auditory: sensorinueral deafness v. Neurologic anomalies: behavioral disorders, meningoencephalitis, mental retardation vi. “Blueberry muffin” skin lesions vii. Hepatomegaly viii. Persistent infection that may lead to pneumonia, hepatitis, bone luscencies, thrombocytopenic purpura and anemia Diagnosis: i. Isolation of virus from nasopharyngeal secretions, urine, CSF and any tissue/organ in the body ii. Presence of specific rubella IgM antibodies in a newborn Treatment: supportive Isolation of patient i. Droplet precaution in addition to standard precautions are recommended for 7 days after the onset of rash ii. Contact isolation is recommended in congenital rubella until at least 1 year old Care of exposed persons: i. Pregnant: tested for rubella antibody. If (+) rubella specific IgG antibody- likely IMMUNE. If (-) test is repeated 2-3 weeks and then again, 6 weeks later, to note for seroconversion which will indicative of infection Control measures i. Use of immunoglobulin for post exposure prophylaxis of rubella in early pregnancy is not routine, but may be considered. ii. Live rubella vaccine had not found to prevent infection after exposure but theoretically can prevent the illness if given within 3 days after exposure iii. MMR vaccine: 12-15 months (1st dose); 4-6 years old (2nd dose) ERYTHEMA INFECTIOUSUM (Fifth Disease) benign, self-limiting exanthematous lesions in childhood it is fifth in the classification ( rubella, measles, scarlet fever and Filatov-Dukes disease- atypical scarlet fever) ETIOLOGY: Parvo virus B19; small DNA contating virus under the family Parvoviridae CLINICAL MANIFESTATION: hallmark of EI is the characteristic rash but indistinguishable in the 3 stages Prodromal phase: mild, low grade fever, headache and mild AURI. The rash during this stage erythematous facial flushing“slapped- cheek” appearance Second stage: rashes spread rapidly to the trunk and proximal extremities as a diffuse macular erythema 3rd stage: central clearing of macular lesions giving a lacy reticulated appearance Palms and soles are spared and rashes more prominent on extensor surface DIAGNOSIS: 4 A. B. Laboratory: a. Not routinely done b. Virus cannot be isolated Based on clinical observation of the rash TREATMENT: no specific antiviral treatment ROSEOLA INFANTUM (Exanthem subitum or Sixth disease) ETIOLOGY: EPIDEMIOLOGY: - INCIDENCE: - Human herpes virus 6: common Human herpes virus 7 and Echo virus 16: less frequent HHV 6/7: beta- heper virus under subfamily of herpes virus Double stranded DNA 6-15 months: peak of roseola which also correspond to peak age of acquisition of HHV 6 infection Can develop in children year round Mode of transmission: most adults excrete the virus in saliva and may serve as the primary source of virus transmission in children Saliva of healthy persons and enter the host oral, nasal and conjunctival mucosa less then 3 years old: 95% with peak at 6-15 months. Transplacental antibodies likely to protect most infants until 6 months. MANIFESTATIONS: Prodromal period: asymptomatic but may include mild upper respiratory signs ( rhinorrhea, slight pharyngeal irritations, mild conjuctival redness) Mild cervical or less frequent occipital lymphaenopathy High grade fever ( 37.9-40C) CHILDREN BEHAVE NORMALLY DESPITE HIGH TEMPERATURE NAGAYAMA SPOTS: seen in asian children, ulcers at the uvulopalatoglossal junction. Fever persist for 3-5 days and resolved abruptly RASHES: appears 12-24 hrs after resolution of fever Rose colored Discrete, non-pruritic, small (2-5mm), slightly raised pink lesion on the trunk and spread neck, face, and proximal extremities- CENTRIFUGAL 1-3 days rashes fades DIAGNOSIS based mainly on age, history and clinical findings to differentiate with other potentially serious viral exanthems laboratory: serology, virus culture, antigen detection and PCR D/Dx: - - Rubella: mild prodromal period (+) prominent occipital and postauricular lymphadenopathy Low grade fever which coincides with the exanthema More extensive rashes (+) exposure to person with Rubella Measles: exanthems at the height of fever 3Cs (+) Koplik spot TREATMENT: - SUPPORTIVE HHV 6: gancyclovir VARICELLA - disease spectrum encompasses: - primary infection (varicella/chicken pox), - latent infection ( latent infection on sensory ganglia) - recurrent infection (herpes zoster/ shingles) ETIOLOGY - Varicella-zoster virus: neurotropic human herpesvirus Alpha-herpes virus; double stranded DNA EPIDENMIOLOGY 5 PATHOGENESIS - - contagious from 24-48 hours before the rash appears and until the vesicles are crusted, usually 3-7 days after onset of rash “ Breakthrough varicella”: mild manifestation; varicella among immunized children Hepes zoster: due to reactivation of latent VZV; uncommon in childhood (~45 year old) transmission via respiratory secretions and in the fluid of skin lesions either by airborne spread of through direct contact Primary Infection (VARICELLA): respiratory inoculation of the virus IP: 10-21 days- the virus replicate in the respiratory tract followed by brief subclinical viremia Second viremic phase: wide spread cutaneous lesions Latent infection: VZV establishes in the sensory ganglia cells in all individual who experienced primary infection Herpes zoster infection: subsequent reactivation of latent virus Vesicular rashes that usually located dermatomal in distribution – posterior nerve roots, more frequently on the trunk (dorsal root0, shoulder, arms and neck (second to fourth cervical ganglia) CLINICAL MANIFESTATION A. VARICELLA (PRIMARY INFECTION) begins 14-16 days after exposure fever, malaise, anorexia, headache, mild abdominal pain- 24-48 hrs before the appearance of rashes starts to appear on the scalp, face, trunk erythematous pruritic macule popular stage vesicle with clear filled fluidlesions become cloudy and umbilicated 24-48 hrs crusting. While other lesions are crusting, new crops form on the trunk and extremities simultaneous presence of lesions on various stages of evolution is the characteristic picture of varicella crusting (“celestial map”) Rash distribution is predominantly central that goes distally (difference from small pox – rashes starts at the face and distal extremities) B. BREAKTHROUGH VARICELLA vaccination of varicella vaccine can prevent 95% of having a typical varicella and 70-90% preventing all disease varicella in a child vaccinated more than 42 days before onset of rash and is due to wild type VZV rash occurring within first 2 weeks of vaccination is most commonly wild type VZV. Rash occurring 2-6 weeks after vaccination could be due to either wild or vaccine strains Rash: atypical, maculopapular, vesicles are uncommon. C. NEONATAL VARICELLA birth within 1 week before or after the onset of maternal varicella frequently result in the newborn developing varicella which maybe severe if there was 1 week or greater interval between maternal varicella and parturition, it is likely that the newborn received sufficient transplacental antibody to VZV to ameliorate neonatal infection if less than 1 week, the newborn will be unlikely to have protective VZV antibody and neonatal varicella may be exceptionally severe. D. CONGENITAL VARICELLA SYNDROME Embryopathy: affects the skin, eye, brain and limbs 2% of fetuses affected if mother had varicella on the first 20 weeks of pregnancy 6-12 weeks: maximum interruption on limb development 16-20 weeks: affects the eye and brain development CICATRIX: characteristic cutaneous lesion; zigzag scarring pften dermatomal in distribution Shortened and malformed extremities, cataract, extensive aplasia of the entire brain Stigmata of VZV infection A. Damage to sensory nerves cicatricial skin lesion hypopigmentation B. Damage to optic stalk and lens vesicle microphthalmia cataract chorioretinitis optic atropy 6 C. D. E. Damage Damage - to brain and encephalitis microcephaly hydrocephalus calcifications aplasia of brain to cervical and lumbosacral cord hypolpasia of extremities motor and sensory deficit absent deep tendon reflex anisocoria horner’s syndrome anal/urinary sphincter dysfunction Herpes zoster: vesicular lesion clustered within one or less common 2 adjacent dermatome i. Children: less common. Less painful, low grade fever 1. Complete resolution within 1-2 weeks ii. 2nd episode is common. 3rd is rare DIAGNOSIS b. c. COMPLICATIONS d. e. f. g. h. i. j. determination of VZ antibody titer demonstration of VZ virus by electron microscopic examination of vesicular fluid not common in children secondary bacterial infection encephalitis or meningitis pneumonia Reye syndrome ( associated with aspirin administration) Congenital varicella Glomerulonephritis TREATMENT: k. l. SPECIFIC: none except those who are immunocompromised, >12 year old, with chronic skin disease, persons using long term salicylate and those person under treatment of corticosteroids Acyclovir: 15-30 mkday IV in 3 divided dose or 200-400 tablet orally every 4hrs minus the midnight dose for 5 days. 7