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Pediatrics_Nelson. Children with shortened erythrocyte life span (e.g., sickle cell disease) may develop a transient aplastic crisis characterized by ineffective erythroid production typically lasting 7 to 10 days (see Chapter 150). Most children with parvovirus B19-induced transient aplastic crisis have multiple symptoms, including fever, lethargy, malaise, pallor, headache, gastrointestinal symptoms, and respiratory symptoms. The reticulocyte count is extremely low, and the hemoglobin level is lower than usual for the patient. Transient neutropenia and thrombocytopenia also commonly occur. Persistent parvovirus B19 infection may develop in children with immunodeficiency, causing severe anemia resulting from pure red blood cell aplasia. These children do not display the typical manifestations of erythema infectiosum.


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Pediatrics_Nelson. Hematologic abnormalities occur with parvovirus infection, including reticulocytopenia lasting 7 to 10 days, mild anemia, thrombocytopenia, lymphopenia, and neutropenia. Parvovirus B19 can be detected by PCR and by electron microscopy of erythroid precursors in the bone marrow. Serologic tests showing specific IgM antibody to parvovirus are diagnostic, demonstrating infection that probably occurred in the prior 2 to 4 months. The diagnosis of erythema infectiosum in children is established on the basis of the clinical findings of typical facial rash with absent or mild prodromal symptoms, followed by a reticulated rash over the body that waxes and wanes. The differential diagnosis includes measles, rubella, scarlet fever, enteroviral or adenoviral infection, infectious mononucleosis, scarlet fever, Kawasaki disease, systemic lupus erythematosus, serum sickness, and drug reaction.


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Pediatrics_Nelson. There is no specific therapy. Routine supportive care includes maintaining adequate hydration and antipyretics. Transfusions may be required for transient aplastic crisis. Intrauterine transfusion has been performed for hydrops fetalis associated with fetal parvovirus B19 infection. Intravenous immunoglobulin may be used for immunocompromised persons with severe anemia or chronic infection. The prognosis for erythema infectiosum is excellent. Fatalities associated with transient aplastic crisis are rare. Parvovirus B19 is not teratogenic, but in utero infection of fetal erythroid cells may result in fetal heart failure, hydrops fetalis, and fetal death. Of the approximately 50% of women of childbearing age susceptible to parvovirus B19 infection, 30% of exposed women develop infection, with 25% of exposed fetuses becoming infected and 10% of these culminating in fetal death.


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Pediatrics_Nelson. The greatest risk is to pregnant women. Effective control measures are limited. Exclusion of affected children from school is not recommended, because children generally are not infectiousby the time the rash is present. Good handwashing and hygieneare practical measures that should help reduce transmission.


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Pediatrics_Nelson. Chickenpox and zoster are caused by varicella-zoster virus (VZV), an enveloped, icosahedral, double-stranded DNA virus that is a member of the herpesvirus family. Humans are the only natural host. Chickenpox (varicella) is the manifestation of primary infection. VZV infects susceptible individuals via the conjunctivae or respiratory tract and replicates in the nasopharynx and upper respiratory tract. It disseminates by a primary viremia and infects regional lymph nodes, the liver, the spleen, and other organs. A secondary viremia follows, resulting in a cutaneous infection with the typical vesicular rash. After resolution of chickenpox, the virus persists in latent infection in the dorsal root ganglia cells. Zoster (shingles) is the manifestation of reactivated latent infection of endogenous VZV. Chickenpox is highly communicable in susceptible individuals, with a secondary attack rate of more than 90%. The period of communicability ranges from 2 days before to 7 days after the onset


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Pediatrics_Nelson. VZV. Chickenpox is highly communicable in susceptible individuals, with a secondary attack rate of more than 90%. The period of communicability ranges from 2 days before to 7 days after the onset of the rash, when all lesions are crusted.


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Pediatrics_Nelson. In the prevaccine era, the peak age of occurrence was 5 to 10 years, with peak seasonal infection in late winter and spring. In the postvaccine era, the incidence of varicella has declined in all age groups, with the peak incidence now in 10 to 14 year olds. Transmission is by direct contact, droplet, and air. Zoster is a recurrence of latent VZV and is transmitted by direct contact. Only 5% of cases of zoster occur in children younger than 15 years of age. The overall incidence of zoster (215 cases per 100,000 person-years) results in a cumulative lifetime incidence of approximately 10% to 20%, with 75% of cases occurring after 45 years of age. The incidence of zoster is increased in immunocompromised persons. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com The incubation period of varicella is generally 14 to 16 days, witha range of 10 to 21 days after exposure. Prodromal symptomsof fever, malaise, and anorexia may precede the rash by 1 day.The characteristic rash appears initially as small red papules thatrapidly progress to nonumbilicated, oval, “teardrop” vesicles onan erythematous base. The fluid progresses from clear to cloudy,and the vesicles ulcerate, crust, and heal. New crops appear for 3to 4 days, usually beginning on the trunk followed by the head,the face, and, less commonly, the extremities. There may be atotal of 100 to 500 lesions, with all forms of lesions being presentat the same time. Pruritus is universal and marked. Lesions maybe present on mucous membranes. Lymphadenopathy may begeneralized. The severity of the rash varies, as do systemic signsand fever, which generally abate after 3 to 4 days.


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Pediatrics_Nelson. The preeruption phase of zoster includes intense localized and constant pain and tenderness (acute neuritis) along a dermatome, accompanied by malaise and fever. In several days,the eruption of papules, which quickly vesiculate, occurs in thedermatome or in two adjacent dermatomes. Groups of lesions occur for 1 to 7 days and then progress to crusting and healing.Thoracic and lumbar regions are typically involved. Lesionsgenerally are unilateral and are accompanied by regionallymphadenopathy. In one third of patients, a few vesicles occuroutside of the primary dermatome. Any branch of cranial nerveV may be involved, which also may cause corneal and intraorallesions. Involvement of cranial nerve VII may result in facialparalysis and ear canal vesicles (Ramsay Hunt syndrome).Ophthalmic zoster may be associated with ipsilateral cerebralangiitis and stroke. Immunocompromised persons may haveunusually severe, painful herpes zoster that involves cutaneousand, rarely, visceral dissemination


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Pediatrics_Nelson. may be associated with ipsilateral cerebralangiitis and stroke. Immunocompromised persons may haveunusually severe, painful herpes zoster that involves cutaneousand, rarely, visceral dissemination (to liver, lungs, and centralnervous system). Postherpetic neuralgia, defined as pain persisting longer than 1 month, is uncommon in children.


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Pediatrics_Nelson. Laboratory testing confirmation for diagnosis is usuallyunnecessary. PCR is the current diagnostic method of choice,and genotyping to distinguish vaccine and wild-type strainsis available through the CDC. Detection of varicella-specificantigen in vesicular fluid by immunofluorescence using monoclonal antibodies or demonstration of a fourfold antibodyincrease of acute and convalescent sera is also diagnostic but not as sensitive as PCR.


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Pediatrics_Nelson. The diagnosis of varicella and zoster is based on the distinctive characteristics of the rash. Eczema herpeticum, or Kaposi varicelliform eruption, is a localized, vesicular eruption caused by HSV that develops on skin affected by underlying eczema or trauma. The differentiation between zoster and HSV infection may be difficult because HSV may cause eruption that appears to be in a dermatomal distribution. Coxsackievirus A infection has a vesiculopustular appearance, but lesions are usually localized to the extremities and oropharynx. A previously healthy patient with more than one recurrence probably has HSV infection, which can be confirmed by viral culture.


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Pediatrics_Nelson. Symptomatic therapy of varicella includes nonaspirin antipyretics, cool baths, and careful hygiene. Routine oral administration of acyclovir is not recommended in otherwise healthy children with varicella. The decision to use antiviral medications, the route, and duration of treatment depend on host factors and the risk for severe infection or complications. Early therapy with antivirals (especially within 24 hours of rash onset) in immunocompromised persons is effective in preventing severe complications, including pneumonia, encephalitis, and death from varicella. Acyclovir or valacyclovir may be considered in those at risk of severe varicella, such as unvaccinated persons older than 12 years; those with chronic cutaneous or pulmonary disease; receiving short-course, intermittent, or aerosolized corticosteroids; or receiving long-term salicylate therapy. The dose of acyclovir used for VZV infections is much higher than that for HSV.


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Pediatrics_Nelson. Antiviral treatment of zoster accelerates cutaneous healing, hastens the resolution of acute neuritis, and reduces the risk of postherpetic neuralgia. Oral famciclovir and valacyclovir have much greater oral bioavailability than acyclovir and are recommended for treatment of zoster in adults. Acyclovir is recommended for children and is an alternative therapy for adults. The necessity of concomitant oral corticosteroids for zoster is controversial.


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Pediatrics_Nelson. Secondary infection of skin lesions by streptococci or staphylococci is the most common complication. These infections may be mild, resembling impetigo, or life-threatening with toxic shock syndrome or necrotizing fasciitis. Pneumonia is uncommon in healthy children but occurs in 15% to 20% of healthy adults and immunocompromised persons. Myocarditis, pericarditis, orchitis, hepatitis, ulcerative gastritis, glomerulonephritis, and arthritis may complicate varicella. Reye syndrome may follow varicella; thus, salicylate use is contraindicated during varicella infection. Neurologic complications frequently include postinfectious encephalitis, cerebellar ataxia, nystagmus, and tremor. Less common neurologic complications include Guillain-Barre syndrome, transverse myelitis, cranial nerve palsies, optic neuritis, and hypothalamic syndrome.


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Pediatrics_Nelson. Primary varicella can be a fatal disease in immunocompromised persons as a result of visceral dissemination, encephalitis, hepatitis, and pneumonitis. The mortality rate approaches 15% in children with leukemia who do not receive prophylaxis or therapy for varicella (see Chapter 66). A severe form of neonatal varicella may develop in newborns of mothers with varicella (but not shingles) occurring 5 days before to 2 days after delivery. The fetus is exposed to a large inoculum of virus but is born before the maternal antibody response develops and can cross the placenta. These infants should be treated as soon as possible with varicellazoster immunoglobulin (VZIG) or intravenous immunoglobulin if VZIG is unavailable, to attempt to prevent or ameliorate the infection.


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Pediatrics_Nelson. Primary varicella usually resolves spontaneously. The mortality rate is much higher for persons older than 20 years of age and for immunocompromised persons. Zoster usually is self-limited, especially in children. Advanced age and severity of pain at presentation and at 1 month are predictors of prolonged pain. Scarring is more common with zoster because of involvement of the deeper layers of the skin. Children with chickenpox should not return to school until all vesicles have crusted. A hospitalized child with chickenpox should be isolated in a negative-pressure room to prevent transmission.


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Pediatrics_Nelson. Children with chickenpox should not return to school until all vesicles have crusted. A hospitalized child with chickenpox should be isolated in a negative-pressure room to prevent transmission. A live attenuated varicella vaccine—two doses for all children—is recommended. The first dose should be administered at age 12 to 15 months and the second dose at 4 to 6 years. Varicella vaccine is 85% effective in preventing any disease and 97% effective in preventing moderately severe and severe disease. Transmission of vaccine virus from a healthy vaccinated individual is rare but possible. Passive immunity can be provided by VZIG, which is indicated within 96 hours of exposure for susceptible individuals at increased risk for severe illness. Administration of VZIG does not eliminate the possibility of disease in recipients and prolongs the incubation period up to 28 days. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Nonbullous or crusted impetigo is caused most often by Staphylococcus aureus and occasionally by group A streptococcus. Itbegins as a single erythematous papulovesicle that progresses to one or many honey-colored, crusted lesions weeping serous drainage. Bullous impetigo accounts for approximately 10%of all impetigo. The skin lesions are thin-walled (0.5 to 3 cm)bullae with erythematous margins resembling second-degreeburns and are associated with S. aureus phage type 71. Impetigo most frequently occurs on the face, around the nares andmouth, and on the extremities. Fever is uncommon. The diagnosis usually is established by the clinical appearance alone.


Pediatrics_Nelson

Pediatrics_Nelson. Recommended treatment for nonbullous impetigo is topical 2% mupirocin or oral antistaphylococcal antibiotics. Extensive or disseminated lesions, bullous impetigo, lesions around the eyes, or lesions otherwise not amenable to topical therapy are best treated with oral antibiotics. Streptococcal impetigo is associated with increased risk of postinfectious glomerulonephritis but not acute rheumatic fever (see Chapter 163). Antibiotic treatment does not decrease the risk of postinfectious glomerulonephritis but decreases possible spread of nephritogenic strains to close contacts. Children with impetigo should remain out of school or day care until 24 hours of antibiotic therapy have been completed. Available @ StudentConsult.com


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Pediatrics_Nelson. Cellulitis is infection involving the subcutaneous tissues and the dermis and is usually caused by S. aureus or groupA streptococci. Cellulitis typically presents with indurated, warm, and erythematous macules with indistinct borders that expand rapidly. Additional manifestations commonly include fever, lymphangitis, and regional lymphadenitis. Erysipelasis a superficial variant of cellulitis usually caused by group A streptococcus that involves the dermis only. The rapidly advancing lesions are tender, bright red in appearance, and have sharp margins. The patients may appear toxic. Blood cultures are recommended for erysipelas. Empirical antibiotic treatment for cellulitis is recommended with a first-generation cephalosporin unless the local S. aureus methicillin-resistance rate is high, in which case alternatives include clindamycin or trimethoprim-sulfamethoxazole (although this agent has poor group A streptococcal activity). Many patients may be managed with oral antibiotics and


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Pediatrics_Nelson. in which case alternatives include clindamycin or trimethoprim-sulfamethoxazole (although this agent has poor group A streptococcal activity). Many patients may be managed with oral antibiotics and close follow-up; hospitalization and intravenous antibiotics are recommended for erysipelas and cellulitis of the face, hands, feet, or perineum; those with lymphangitis; and those not responding to outpatient therapy.


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Pediatrics_Nelson. Ecthyma usually is caused by group A streptococcus and may complicate impetigo. Initially it is characterized by a lesion with a rim of erythematous induration surrounding an eschar, which, if removed, reveals a shallow ulcer. Ecthyma gangrenosum is a serious skin infection occurring in immunocompromised persons due to hematogenous spread of septic emboli to the skin, classically caused by Pseudomonas aeruginosa, other gram-negative organisms, or occasionally Aspergillus. The lesions begin as purple macules that undergo central necrosis to become exquisitely tender, deep, punched-out ulcers 2 to 3 cm in diameter with a dark necrotic base, raised red edges, and sometimes a yellowish green exudate. Fever usually is present.


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Pediatrics_Nelson. Necrotizing fasciitis is the most extensive form of cellulitis and involves deeper subcutaneous tissues and fascial planes. It may progress to myonecrosis of the underlying muscle. Common causes include S. aureus and group A streptococcus alone or in combination with anaerobic organisms, such as Clostridium perfringens. Risk factors include underlying immunodeficiency, recent surgery or trauma, and varicella infection. Lesions progress rapidly with raised or sharply demarcated margins, although disease typically extends on a deeper plane beyond superficially evident lesions. Warning signs of necrotizing fasciitis include pain out of proportion to evident skin lesions, shock or toxic appearance, or crepitus due to subcutaneous gas formation by anaerobes. Necrotizing fasciitis is a surgical emergency, and early consultation with an experienced surgeon is recommended. Adjunctive tests such as magnetic resonance imaging can confirm the presence of gas in tissues, but obtaining imaging


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Pediatrics_Nelson. emergency, and early consultation with an experienced surgeon is recommended. Adjunctive tests such as magnetic resonance imaging can confirm the presence of gas in tissues, but obtaining imaging should not delay surgical consultation. Treatment includes rapid surgical debridement of all necrotic tissues and broad-spectrum intravenous antibiotics, such as clindamycin plus cefotaxime or ceftriaxone, with or without an aminoglycoside or vancomycin.


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Pediatrics_Nelson. Folliculitis refers to small, dome-shaped pustules or erythematous papules predominantly caused by S. aureus and located in hair follicles, with superficial, limited inflammatory reaction in the surrounding tissue. Furuncles (boils) are deeper hair follicle infections that manifest as nodules with intense surrounding inflammatory reaction. These occur most frequently on the neck, trunk, axillae, and buttocks. A carbuncle represents the deepest of hair follicle infections and is characterized by multiseptate, loculated abscesses. Boils and carbuncles frequently require incisional drainage. Superficial folliculitis can be treated with topical therapy, such as an antibacterial chlorhexidine wash or an antibacterial lotion or solution such as clindamycin 1%, applied twice a day for 7 to 10 days. Oral antibiotics are necessary for unresponsive cases, or for furuncles and carbuncles.


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Pediatrics_Nelson. P. aeruginosa folliculitis (hot tub folliculitis) presents as pruritic papules; pustules; or deeper, purple-red nodules predominantly on skin areas covered by a swimsuit after bathing in hot tubs. Folliculitis develops 8 to 48 hours after exposure, usually without associated systemic symptoms, and resolves in 1 to 2 weeks without treatment. Perianal dermatitis (perianal streptococcal disease) is caused by group A streptococcus and is characterized by well-demarcated, tender, marked perianal erythema extending 2 cm from the anus. Manifestations include anal pruritus and painful defecation, sometimes with blood-streaked stools. The differential diagnosis includes diaper dermatitis, candidiasis, pin-worm infection, and anal fissures. Treatment is oral penicillin or cefuroxime. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Cutaneous fungal infections are common in children (Table 98-1). The estimated lifetime risk of developing a dermatophytosis is 10% to 20%. Diagnosis is usually established by visual inspection and may be confirmed by potassium hydroxide (KOH) examination or fungal culture of skin scrapings from the margins of the lesion. Recommended tinea treatment is usually for 4 to 6 weeks and 2 weeks after resolution; topical antifungal creams (e.g., miconazole, clotrimazole, ketoconazole, tolnaftate) are appropriate for tinea corporis, tinea pedis, and tinea cruris, whereas tinea capitis requires oral treatment. The diagnosis of onychomycosis should be confirmed by KOH examination and fungal culture. Recommended treatment is terbinafine or itraconazole for at least 12 weeks. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Primary herpetic infections can occur after inoculation of the virus at any mucocutaneous site. Herpes simplex virus type 1 (HSV-1) is common in children and classically causes gingivostomatitis, whereas HSV-2 classically infects the genitalia as a sexually transmitted infection (see Chapter 116), though HSV-1 may cause approximately 30% of genital herpes, and Microsporum audouinii, Prepubertal infection of scalp, M. audouinii fluorescence: Griseofulvin; terbinafine, (ringworm) Trichophyton tonsurans, hair-shafts; black dot alopecia; blue-green with Wood itraconazole Microsporum canis T. tonsurans common in African lamp*; +KOH, culture Americans KOH, Potassium hydroxide. *Wood lamp examination uses an ultraviolet source in a completely darkened room. Trichophyton usually has no fluorescence. HSV-2 can cause gingivostomatitis. For the cutaneous manifestations of neonatal HSV infection, see Chapter 65.


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Pediatrics_Nelson. HSV-2 can cause gingivostomatitis. For the cutaneous manifestations of neonatal HSV infection, see Chapter 65. Herpes gingivostomatitis involves the gingivae and the vermilion border of the lips. Herpes labialis (cold sores or fever blisters) is limited to the vermilion border involving skin and mucous membranes. Clinical manifestations of primary HSV gingivostomatitis include typical oropharyngeal vesicular lesions with high fever, malaise, stinging mouth pain, drooling, fetid breath, and cervical lymphadenopathy.


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Pediatrics_Nelson. Herpetic skin lesions are quite painful and characteristically begin as erythematous papules that quickly progress tothe characteristically grouped, 2-to 4-mm, fluid-filled vesicles on an erythematous base. Removal of the vesicle roofreveals a small, sharply demarcated ulcer with a punched-outappearance. The characteristic grouped vesicles distinguishHSV from chickenpox (see Chapter 97). Within several days,the vesicles become pustular, rupture, and encrust. Diagnosisis made clinically, or with viral culture, fluorescent antibody staining, or polymerase chain reaction. Scarring is uncommon, but there may be residual hyperpigmentation. After primary infection, the virus remains latent in nerve dorsal rootganglia. About 20% to 40% of adults experience recurrentoral episodes of HSV labialis throughout life. Recurrencesoccur in roughly the same location and may be preceded byprodromal symptoms of tingling or burning without fever orlymphadenopathy.


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Pediatrics_Nelson. Viral paronychia (herpetic whitlow) is a painful, localized infection of a digit, usually of the distal pulp space, with erythematous and occasionally vesiculopustular eruption. It occurs in children who suck their thumbs, bite their nails, and those with herpetic gingivostomatitis. Herpes gladiatorum occurs in wrestlers and rugby players who acquire cutaneous herpes from close body contact with other players’ cutaneous infections. Cutaneous HSV infection in persons with an underlying skin disorder (e.g., atopic dermatitis) can result in eczema herpeticum (Kaposi varicelliform eruption), a disseminated cutaneous infection. There may be hundreds of herpetic vesicles over the body, usually concentrated in the areas of skin affected by the underlying disorder.


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Pediatrics_Nelson. Treatment with oral valacyclovir or famciclovir may shorten duration of disease for primary and recurrent infection. Prophylactic antiviral therapy may be warranted in those with frequent recurrences. Infants, persons with eczema, and persons with immunodeficiency are at increased risk for disseminated and severe HSV disease and should receive intravenous acyclovir therapy. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Warts are caused by the human papillomaviruses (HPVs),nonenveloped, double-stranded DNA viruses that infect skin and mucous membrane keratinocytes. More than 100 HPV serotypes have been identified, with different serotypes accounting for the variation in location and clinical presentations. There are 15 to 20 oncogenic (high-risk) types, including 16, 18, 31, 33, 35, 39, 45, 51, 52, and 58. HPV types 16 and 18 are associated with 70% of cases of cervical cancer as well as vulvar and vaginal cancers. Common nononcogenic (low-risk) types include 1, 2, 3, 6, 10, 11, 40, 42, 43, 44, and 54. Regardless of the infecting serotype, all warts are associated with hyperplasia of the epidermal cells.


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Pediatrics_Nelson. Warts occur at all ages. Common warts (verruca vulgaris),associated with HPV types 1 and 2, are the most common form (71%). They occur frequently in school-age children, with a prevalence of 4% to 20%. They are transmitted by direct contact or by fomites and have an incubation period of approximately 1 month before clinical presentation. The common wart is a painless, well-circumscribed, small (2to 5-mm) papule with a papillated or verrucous surface typically distributed on the fingers, toes, elbows, and knees. They also may be found on the nose, ears, and lips. Filiform warts are verrucous, exophytic, 2-mm papules that have a narrow or pedunculated base. Flat warts (verruca plana) are associated with HPV types 3 and 10 and are multiple, flat-topped 2to 4-mm papules clustered on the dorsal surface of the hands, on the soles of the feet (plantar warts), or on the face. Plantar warts may be painful because of the effect of pressure and friction on the lesions. Genital warts (condylomata


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Pediatrics_Nelson. surface of the hands, on the soles of the feet (plantar warts), or on the face. Plantar warts may be painful because of the effect of pressure and friction on the lesions. Genital warts (condylomata acuminata) are associated with the HPV types 6 and 11 (90%). They are flesh-colored, hyperpigmented, or erythematous lesions that are filiform, fungating, or plaquelike in appearance and involve multiple sites on the vulva, vagina, penis, or perineum. Genital warts are the most common sexually transmitted infection, with 1 million new cases annually.


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Pediatrics_Nelson. Warts typically are self-limited and resolve spontaneously over years without specific treatment. Treatment options are available for common and flat warts as well as condylomata acuminata. Topical preparations for common and flat warts disrupt infected epithelium (using salicylic acid, liquid nitrogen, or laser therapy) and result in the cure of approximately 75% of patients. Treatment of anogenital warts is complex, and specific treatments ( www.cdc.gov/std/hpv/default.htm ) may include topical podophyllotoxin or imiquimod. Additional treatment methods include laser ablation and immunotherapy with intralesional interferon; immunotherapy may result in significant toxicities.


Pediatrics_Nelson

Pediatrics_Nelson. The most serious consequence of HPV infection is cervical cancer (more than 12,000 new cases annually), vulvar, vaginal, penile, and anal cancers. A quadrivalent, recombinant HPV vaccine against serotypes 6, 11, 31, and 33 is recommended for all children at 11 to 12 years of age but may be given to children between 9 and 26 years of age. The three-dose regimen has 98% to 100% efficacy in preventing the precancerous dysplasia that precedes cervical cancer.


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Pediatrics_Nelson. Molluscum contagiosum virus, a poxvirus that replicates in host epithelial cells, produces discrete, small (2 to 4 mm), pearly flesh-colored or pink, nontender, dome-shaped papules with central umbilication. Papules occur most commonly in intertriginous regions, such as the axillae, groin, and neck. They rarely occur on the face or in the periocular region. The infection typically affects toddlers and young children and is acquired through direct contact with infected individuals. Spread occurs by autoinoculation. Infection with molluscum contagiosum may be complicated by a surrounding dermatitis. Severely immunocompromised persons or persons with extensive atopic dermatitis often have widespread lesions.


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Pediatrics_Nelson. Diagnosis is made clinically. Lesions are self-limited, resolvingover months to years, and usually no specific treatment is recommended. Available treatment options are limited to destructive modalities, such as cryotherapy with topical liquid nitrogen,vesicant therapy with topical 0.9% cantharidin, or removal bycurettage, and should be reserved for extensive disease. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Lymphoid tissue steadily enlarges until puberty and subsequently undergoes progressive atrophy. Lymph nodes aremost prominent in children 4 to 8 years of age. Normallymph node size is 10 mm in diameter, with the exceptions of15 mm for inguinal nodes, 5 mm for epitrochlear nodes, and2 mm for supraclavicular nodes, which are usually undetectable. Lymphadenopathy is enlargement of lymph nodes andoccurs in response to a wide variety of infectious, inflammatory, and malignant processes. Generalized lymphadenopathy is enlargement of two or more noncontiguous lymphnode groups, whereas regional lymphadenopathy involves one lymph node group only.


Pediatrics_Nelson

Pediatrics_Nelson. Lymphadenitis is acute or chronic inflammation of lymph nodes. Acute lymphadenitis usually results when bacteria and toxins from a site of acute inflammation are carried via lymph to regional nodes. Numerous infections cause lymphadenopathy and lymphadenitis (Tables 99-1 and 99-2). Causes of inguinal regional lymphadenopathy also include sexually transmitted infections (see Chapter 116). Regional lymphadenitis associated with a characteristic skin lesion at the site of inoculation defines various lymphocutaneous syndromes. Lymphangitis is an inflammation of subcutaneous lymphatic channels that presents as an acute bacterial infection, usually caused by Staphylococcus aureus and group A streptococci.


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Pediatrics_Nelson. Cervical lymphadenitis is the most common regional lymphadenitis among children and is associated most commonly with pharyngitis caused by group A streptococcus (see Chapter 103), respiratory viruses, and Epstein-Barr virus (EBV). Other common infectious causes of cervical lymphadenitis include Bartonella henselae (cat-scratch disease) and nontuberculous mycobacteria. EBV is the primary cause of infectious mononucleosis, a clinical syndrome characterized by fever, fatigue and malaise, cervical or generalized lymphadenopathy, tonsillitis, and pharyngitis. EBV, a member of the herpesvirus family, infects B lymphocytes and is spread by salivary secretions. After primary infection, EBV is maintained latently in multiple episomes in the cell nucleus of resting B lymphocytes and establishes lifelong infection that remains clinically inapparent. Most persons shed EBV intermittently, with approximately F. tularensis (ulceroglandular tularemia) B. henselae (cat-scratch disease)


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Pediatrics_Nelson. F. tularensis (ulceroglandular tularemia) B. henselae (cat-scratch disease) Y. pestis (plague) Nocardia (nocardiosis) Cutaneous diphtheria (Corynebacterium diphtherial) Cutaneous coccidioidomycosis (Coccidioides immitis) Cutaneous histoplasmosis (Histoplasma capsulatum) Cutaneous leishmaniasis Cutaneous sporotrichosis (S. schenckii) 20% of healthy individuals shedding EBV at any given time. Cytomegalovirus (CMV), Toxoplasma gondii, adenoviruses, hepatitis B virus, hepatitis C virus, and initial human immunodeficiency virus (HIV) infection, known as acute retroviral syndrome, can cause an infectious mononucleosis-like syndrome with lymphadenopathy.


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Pediatrics_Nelson. The cause of cat-scratch disease is B. henselae, a small, pleomorphic, gram-negative bacillus that stains with Warthin-Starry silver stain. B. henselae causes apparently asymptomatic bacteremia in cats, and kittens under 1 year of age are more likely to harbor the organism. B. henselae is transmitted to humans by bites and scratches, which may be minor. B. henselae also causes bacillary angiomatosis and peliosis hepatis in persons with HIV infection (see Chapter 125). Nontuberculous mycobacteria are ubiquitous in soil, vegetation, dust, and water. Mycobacterium species commonly causing lymphadenitis in children includes M. avium complex, M. scrofulaceum, and M. kansasii. M. tuberculosis uncommonly causes cervical lymphadenitis. Acute cervical lymphadenitis as a complication of group A streptococcal infection parallels the incidence of streptococcal pharyngitis (see Chapter 103). Many cases are caused by


Pediatrics_Nelson

Pediatrics_Nelson. Acute cervical lymphadenitis as a complication of group A streptococcal infection parallels the incidence of streptococcal pharyngitis (see Chapter 103). Many cases are caused by S. aureus. EBV and CMV are ubiquitous, with most infections occurring in young children, who may often be asymptomatic or only mildly symptomatic. Risk factors for other specific causes of lymphadenopathy may be indicated by past medical and surgical history; preceding trauma; exposure to animals; contact with persons infected with tuberculosis; sexual history; travel history; food and ingestion history, especially of undercooked meat or unpasteurized dairy products; and current medications.


Pediatrics_Nelson

Pediatrics_Nelson. The exact location and detailed measurement of the size, shape, characteristics, and number of involved nodes should be noted, including their consistency, mobility, tenderness, warmth, fluctuance, firmness, and adherence to adjacent tissues. Important findings include presence or absence of dental disease, oropharyngeal or skin lesions, ocular disease, other nodal enlargement, and any other signs of systemic illness, including hepatosplenomegaly and skin lesions. Acute cervical lymphadenopathy associated with pharyngitis is characterized by small and rubbery lymph nodes in the anterior cervical chain with minimal to moderate tenderness. Suppurative cervical lymphadenitis, frequently caused by S. aureus or group A streptococcus, shows erythema and warmth of the overlying skin with moderate to exquisite tenderness.


Pediatrics_Nelson

Pediatrics_Nelson. The characteristic triad of EBV infectious mononucleosis is fever, pharyngitis, and lymphadenopathy. The pharynx shows enlarged tonsils and exudate and, sometimes, anenanthem with pharyngeal petechiae. Lymphadenopathy ismost prominent in the anterior and posterior cervical andsubmandibular lymph nodes and less commonly involvesaxillary and inguinal lymph nodes. Other findings includesplenomegaly in 50% of cases, hepatomegaly in 10% to 20%, and maculopapular or urticarial rash in 5% to 15%. A diffuse,erythematous rash develops in approximately 80% of mononucleosis patients treated with amoxicillin. Compared with EBV infection, infectious mononucleosis-like illness caused by CMV has minimal pharyngitis and often more prominentsplenomegaly; it often presents with fever only. The mostcommon manifestation of toxoplasmosis is asymptomaticcervical lymphadenopathy, but approximately 10% of casesof acquired toxoplasmosis develop chronic posterior cervical lymphadenopathy and fatigue, usually


Pediatrics_Nelson

Pediatrics_Nelson. manifestation of toxoplasmosis is asymptomaticcervical lymphadenopathy, but approximately 10% of casesof acquired toxoplasmosis develop chronic posterior cervical lymphadenopathy and fatigue, usually without significantfever.


Pediatrics_Nelson

Pediatrics_Nelson. Cat-scratch disease typically presents with a cutaneous papule or conjunctival granuloma at the site of bacterial inoculation, followed by lymphadenopathy of thedraining regional nodes. The nodes are tender, with suppuration in approximately 10% of cases. Lymphadenopathy may persist 1 to 4 months. Less common features ofcat-scratch disease include erythema nodosum, osteolytic lesions, encephalitis, oculoglandular (Parinaud) syndrome,hepatic or splenic granulomas, endocarditis, polyneuritis,and transverse myelitis. Lymphadenitis caused by nontuberculous mycobacteria usually is unilateral in the cervical, submandibular, or preauricular nodes and is more common in toddlers. The nodes are relatively painless and firm initially, but gradually soften, rupture, and drain over time. The local reaction is circumscribed, and overlying skin may develop a violaceous discoloration without warmth. Fever and systemic symptoms are minimal or absent.


Pediatrics_Nelson

Pediatrics_Nelson. Initial laboratory tests of regional lymphadenopathy include a complete blood count and inflammatory markers. Infectious mononucleosis is characterized by lymphocytosis with atypical lymphocytes; thrombocytopenia and elevated hepatic enzymes are common. Cultures of infected skin lesions and tonsillar exudates should be obtained. Isolation of group A streptococci from the oropharynx suggests, but does not confirm, streptococcal cervical lymphadenitis. A blood culture should be obtained from children with systemic signs and symptoms of bacteremia. Serologic testing for EBV and for B. henselae should be obtained if there are appropriate findings. The most reliable test for diagnosis of acute EBV infection is the IgM antiviral capsid antigen (Fig. 99-1). Heterophil antibody is also diagnostic but is not reliably positive in children younger than 4 years with infectious mononucleosis.


Pediatrics_Nelson

Pediatrics_Nelson. Extended diagnostic workup for lymphadenopathy is guided by the specific risk factors in the history and physical examination findings. Chest radiograph, throat culture, antistreptolysin O titer, and serologic tests for CMV, toxoplasmosis, syphilis, tularemia, Brucella, histoplasmosis, and coccidioidomycosis may be indicated. Genital tract evaluation and specimens should be obtained with regional inguinal lymphadenopathy (see Chapter 116). Screening for tuberculosis can be performed using the standard tuberculin skin test or an interferon gamma release assay; both may be positive with atypical mycobacterial infection.


Pediatrics_Nelson

Pediatrics_Nelson. Aspiration is indicated for acutely inflamed, fluctuant cervical lymph nodes, especially those larger than 3 cm in diameter or not responding to antibiotic treatment. Ultrasound orcomputed tomography may help in establishing the extent oflymphadenopathy and defining whether the mass is solid, cystic, or suppurative with abscess formation. Pus from fluctuantlesions should be examined by Gram and acid-fast stains andcultured for aerobic and anaerobic bacteria and mycobacteria. Biopsy should be performed if lymphoma is suspectedbecause of firm, matted, nontender nodes and other systemicfindings.


Pediatrics_Nelson

Pediatrics_Nelson. If the diagnosis remains uncertain and lymphadenopathy persists despite empirical antibiotic therapy for presumed S. aureus and group A streptococcus, excisional biopsy of the entire node should be performed, if possible. This is curative for nontuberculous mycobacterial lymphadenitis. Biopsy material should be submitted for histopathology as well as Gram, acid-fast, Giemsa, periodic acid-Schiff, Warthin-Starry silver (B. henselae), and methenamine silver stains. Cultures for aerobic and anaerobic bacteria, mycobacteria, and fungi should be performed. 1:320 1:160 1:80 1:40


Pediatrics_Nelson

Pediatrics_Nelson. 1:320 1:160 1:80 1:40 Figure 99-1 The development of antibodies to vari-1:20 ous Epstein-Barr virus antigens in patients with infectious mononucleosis. The titers are geometric mean values expressed as reciprocals of the serum dilution. The IgM 1:10 response to viral capsid antigen (VCA) is divided because of the significant differences noted according to the age of the patient. (From Jenson HB, Ench Y: Epstein-Barr virus. In Rose NR, Hamilton RG, Detrick B: Manual of Clinical Laboratory Immunology, ed 7, Washington DC, 2006, American Society for Microbiology Press, p 640.)


Pediatrics_Nelson

Pediatrics_Nelson. Noninfectious causes of cervical swelling and/or lymphadenopathy include congenital and acquired cysts, Kawasakidisease, sarcoidosis, benign neoplasms, and malignancies.The differential diagnosis for generalized lymphadenopathy includes juvenile idiopathic arthritis; systemic lupuserythematosus; and serum sickness and other adverse drugreactions, especially with phenytoin and other antiepileptic medications, allopurinol, isoniazid, antithyroid medications, and pyrimethamine. Leukemia, lymphoma, and occasionally neuroblastoma may have lymph nodes that areusually painless, uninflamed, matted, and firm (see Chapters 155 and 156). A syndrome of periodic fever, aphthous stomatitis, pharyngitis, and adenitis is an occasional cause of recurrent fever and cervical lymphadenitis (seeChapter 103).


Pediatrics_Nelson

Pediatrics_Nelson. Management of lymphadenopathy and lymphadenitis depends on patient age, associated findings, node size and location, and severity of the acute systemic symptoms. In children most cases of cervical lymphadenopathy, without other signs of acute inflammation, require no specific therapy and usually regress within 2 to 3 weeks. Progression to lymphadenitis or development of generalized lymphadenopathy requires further evaluation. The specific treatment of cervical lymphadenitis dependson the underlying etiology. Empirical treatment targeting


Pediatrics_Nelson

Pediatrics_Nelson. The specific treatment of cervical lymphadenitis dependson the underlying etiology. Empirical treatment targeting S. aureus and group A streptococcus includes a penicillinase-resistant penicillin (e.g., oxacillin) or first-generationcephalosporin (e.g., cefazolin). For patients with hypersensitivity to β-lactam antibiotics, or if community-acquired methicillin-resistant S. aureus is suspected, clindamycin is appropriate.Response to empirical antibiotic therapy for suppurative cervical lymphadenitis obviates the need for further evaluation.Absence of a clinical response within 48 to 72 hours is an indication for further laboratory evaluation and possible excisionalbiopsy and culture.


Pediatrics_Nelson

Pediatrics_Nelson. There is no specific treatment for infectious mononucleosis. Cat-scratch disease usually does not require treatment because the lymphadenopathy resolves in 2 to 4 months without sequelae. Azithromycin may hasten resolution and reduces node size at 30 days but no benefit is evident at 90 days. Aspiration is indicated for suppurative nodes. The recommended treatment of cervical lymphadenitis caused by nontuberculous mycobacteria is complete surgical excision. Antimycobacterial drugs are necessary only if there is recurrence or inability to excise infected nodes completely, or if M. tuberculosis is identified, which requires 6 months of antituberculous chemotherapy (see Chapter 124). Most acute infections caused by S. aureus and group A streptococcus respond to treatment and have an excellent prognosis. Complications such as abscess formation, cellulitis, andbacteremia may occur. Abscess formation is treated with incision and drainage in conjunction with appropriate antibiotictherapy.


Pediatrics_Nelson

Pediatrics_Nelson. Infectious mononucleosis usually resolves in 2 to 4 weeks,but fatigue and malaise may wax and wane for several weeks tomonths. EBV also is associated with numerous complicationsduring the acute illness. Neurologic complications includeseizures, aseptic meningitis syndrome, Bell palsy, transversemyelitis, encephalitis, and Guillain-Barre syndrome. Hematologic complications include Coombs-positive hemolytic anemia, antibody-mediated thrombocytopenia, hemophagocyticsyndrome, and, rarely, aplastic anemia. Corticosteroids havebeen used for respiratory compromise resulting from tonsillar hypertrophy, which responds rapidly, and for thrombocytopenia, hemolytic anemia, and neurologic complications.Splenic rupture is very rare. X-linked lymphoproliferative disease, which results from a mutation of the SH2D1A gene located in the Xq25 region, manifests as fulminant infectiousmononucleosis with primary EBV infection and progresses tomalignant lymphoproliferative disease or dysgammaglobulinemia.


Pediatrics_Nelson

Pediatrics_Nelson. EBV infection, as with other herpesviruses, persists for life, but no symptoms are attributed to intermittent reactivation in immunocompetent hosts. EBV is causally associated with nasopharyngeal carcinoma; Burkitt lymphoma; Hodgkin disease; leiomyosarcoma in immunocompromised persons; and EBV lymphoproliferative disease, especially in posttransplant patients and in those with acquired immunodeficiency syndrome (AIDS). Lymphadenitis caused by nontuberculous mycobacteria has an excellent prognosis. Surgical excision of cervical lymphadenitis caused by nontuberculous mycobacteria is curative in >97% of cases. The incidence of suppurative regional lymphadenitis reflects the incidence of predisposing conditions, such as dental disease, streptococcal pharyngitis, otitis media, impetigo, and other infections involving the face and scalp. There are no guidelines to prevent lymphadenitis caused by nontuberculous mycobacteria.


Pediatrics_Nelson

Pediatrics_Nelson. Meningitis, inflammation of the leptomeninges, can be caused by bacteria, viruses, or, rarely, fungi. The term aseptic meningitis refers principally to viral meningitis, but meningitis with negative cerebrospinal fluid (CSF) bacterial cultures may be seen with other infectious organisms (Lyme disease, syphilis, tuberculosis), parameningeal infections (brain abscess, epidural abscess, venous sinus empyema), chemical exposure (nonsteroidal anti-inflammatory drugs, intravenous immunoglobulin), autoimmune disorders, and other diseases.


Pediatrics_Nelson

Pediatrics_Nelson. The organisms commonly causing bacterial meningitis (Table 100-1) before the availability of current conjugate vaccines were Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis. In the United States, the rates of H. influenzae type b and S. pneumoniae meningitis have declined substantially after the introduction of targeted vaccines. The bacteria causing neonatal meningitis are the same as those causing neonatal sepsis (see Chapter 65). Staphylococcal meningitis occurs primarily after neurosurgery or penetrating head trauma. Partially treated meningitis refers to bacterial meningitis complicated by antibiotic treatment before the lumbar puncture, which may result in negative CSF cultures, although other CSF findings suggestive of bacterial infection persist. The etiology can sometimes be confirmed by polymerase chain reaction of the CSF.


Pediatrics_Nelson

Pediatrics_Nelson. Viral meningitis is caused principally by enteroviruses andparechoviruses. Fecal excretion and transmission are continuous and persist for several weeks. Enteroviruses, parechoviruses, and arboviruses (St. Louis, LaCrosse, West Nile,California encephalitis viruses) are the principal causes ofmeningoencephalitis (see Chapter 101). Other viruses thatcause meningitis include herpes simplex virus, Epstein-Barrvirus, cytomegalovirus, lymphocytic choriomeningitis virus,and human immunodeficiency virus (HIV). Mumps virus isa common cause of viral meningitis in unvaccinated children.Less frequent causes of meningitis include Borrelia burgdorferi (Lyme disease), Bartonella henselae (cat-scratch disease),Mycobacterium tuberculosis, Toxoplasma, fungi (Cryptococcus, Histoplasma, Blastomycosis, and Coccidioides), and parasites(Angiostrongylus cantonensis, Naegleria fowleri, and Acanthamoeba).


Pediatrics_Nelson

Pediatrics_Nelson. Histoplasma, Blastomycosis, and Coccidioides), and parasites(Angiostrongylus cantonensis, Naegleria fowleri, and Acanthamoeba). The incidence of bacterial meningitis is highest among children under 1 year of age. Extremely high rates are found in Native Americans, Alaskan Natives, and Australian aboriginals, suggesting that genetic factors play a role in susceptibility. Other risk factors include acquired or congenital immunodeficiencies, hemoglobinopathies such as sickle cell disease, functional or anatomic asplenia, and crowding such as occurs in some households, day care centers, or college and military dormitories. A CSF leak (fistula), resulting from congenital anomaly or following a basilar skull fracture, increases the risk of meningitis, especially that caused by S. pneumoniae.


Pediatrics_Nelson

Pediatrics_Nelson. Enteroviruses and parechoviruses cause meningitis with peaks during summer and fall in temperate climates. These infections are more prevalent among low socioeconomic groups, young children, and immunocompromised persons. The prevalence of arboviral meningitis is determined by geographic distribution and seasonal activity of the arthropod (mosquito) vectors. In the United States, most arboviral infections occur during the summer and fall. Available @ StudentConsult.com Preceding upper respiratory tract symptoms are common. Rapid onset is typical of S. pneumoniae and N. meningitidis.Indications of meningeal inflammation include headache, irritability, nausea, nuchal rigidity, lethargy, photophobia, and vomiting. Fever usually is present. Kernig and Brudzinski types a, b, c, d, e, f, and nontypable


Pediatrics_Nelson

Pediatrics_Nelson. Table 100-2 Cerebrospinal Fluid (CSF) Findings in Various Central Nervous System Disorders CONDITION PRESSURE LEUKOCYTES (/µL) PROTEIN (mg/dL) GLUCOSE (mg/dL) COMMENTS Normal 50–180 mm H2O <4; 60%–70% lymphocytes, 30%–40% monocytes, 1%–3% neutrophils 20–45 >50% of serum glucose HSV, Herpes simplex virus; IGRA, interferon gamma release assay for tuberculosis; PCR, polymerase chain reaction; PMNs, polymorphonuclear leukocytes; TST, tuberculin skin test.


Pediatrics_Nelson

Pediatrics_Nelson. HSV, Herpes simplex virus; IGRA, interferon gamma release assay for tuberculosis; PCR, polymerase chain reaction; PMNs, polymorphonuclear leukocytes; TST, tuberculin skin test. signs of meningeal irritation are often positive in children older than 12 months. In young infants, signs of meningeal inflammation may be minimal with only irritability, restlessness, depressed mental status, and poor feeding present. Focal neurologic signs, seizures, arthralgia, myalgia, petechial or purpuric lesions, sepsis, shock, and coma may occur. Symptoms of increased intracranial pressure include headache, diplopia, and vomiting; a bulging fontanelle may be present in infants. Ptosis, sixth nerve palsy, anisocoria, bradycardia with hypertension, and apnea are signs of increased intracranial pressure with brain herniation. Papilledema is uncommon, unless there is occlusion of the venous sinuses, subdural empyema, or brain abscess.


Pediatrics_Nelson

Pediatrics_Nelson. If bacterial meningitis is suspected, a lumbar puncture shouldbe performed unless there is evidence of cardiovascular instability or of increased intracranial pressure (because of the risk ofherniation), other than a bulging fontanelle. Routine CSF examination includes a white blood cell count, differential, proteinand glucose levels, and Gram stain (Table 100-2). CSF should be cultured for bacteria and, when appropriate, fungi, viruses, andmycobacteria. The polymerase chain reaction is used to diagnose enteroviruses, parechoviruses, and herpes simplex virus;it is more sensitive and rapid than viral culture. Peripheral leukocytosis is common, and blood cultures are positive in 90%of cases of bacterial meningitis. An electroencephalogram mayconfirm an encephalitis component (see Chapter 101).


Pediatrics_Nelson

Pediatrics_Nelson. Many disorders may show signs of meningeal irritation and increased intracranial pressure, including the infectious causes of meningitis or encephalitis, hemorrhage, rheumatic diseases, and malignancies. Seizures are associated with meningitis, encephalitis, and intracranial abscess or can be the sequelae of brain edema, cerebral infarction or hemorrhage, or vasculitis. Treatment of bacterial meningitis focuses on sterilization of the CSF by antibiotics (Table 100–3) and maintenance of (0–28 days) ceftriaxone plus gentamicin ampicillin with or Ceftazidime plus without gentamicin ampicillin adequate cerebral and systemic perfusion. Due to increasing S. pneumoniae resistance to penicillin and cephalosporins, empirical cefotaxime (or ceftriaxone) plus vancomycin should be administered until antibiotic susceptibility testing is available. Cefotaxime or ceftriaxone are also adequate to treat


Pediatrics_Nelson

Pediatrics_Nelson. N. meningitidis and H. influenzae. For infants younger than 2 months of age, ampicillin is added to cover the possibility of Listeria monocytogenes. Duration of treatment is 5 to 7 days for N. meningitidis, 7 to 10 days for H. influenzae, and 10 to 14 days for S. pneumoniae. Dexamethasone (0.6 to 0.8 mg/kg daily in two to three divided doses for 2 days), as adjunctive therapy initiated just before or concurrently with the first dose of antibiotics, significantly diminishes the incidence of hearing loss and neurologic deficits resulting from H. influenzae meningitis. Adjuvant steroids do not appear to decrease mortality or hospital stay in studies in the developed world. Supportive therapy involves treatment of dehydration, shock, disseminated intravascular coagulation, syndrome of inappropriate antidiuretic hormone (SIADH), seizures, increased intracranial pressure, apnea, arrhythmias, and coma. Adequate cerebral perfusion must be maintained in the presence of cerebral edema.


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com SIADH may complicate meningitis and necessitates monitoring of urine output and fluid administration. Computed tomography or magnetic resonance imaging commonly detects subdural effusions with S. pneumoniae and H. influenzae meningitis. Most effusions are sterile and asymptomatic and do not necessitate drainage unless associated with increased intracranial pressure or focal neurologic signs. Persistent fever is common during treatment but also may be related to infective treatment or immune complex-mediated pericardial or joint effusions, thrombophlebitis, drug fever, or nosocomial infection. A repeat lumbar puncture after 48 hours of therapy should be considered for those whose condition has not improved or has worsened and for those who received adjunct steroids, which can interfere with the ability to monitor clinical response. Even with appropriate antibiotic therapy, the mortality rate for bacterial meningitis in children is significant: 25% for


Pediatrics_Nelson

Pediatrics_Nelson. Even with appropriate antibiotic therapy, the mortality rate for bacterial meningitis in children is significant: 25% for S. pneumoniae, 15% for N. meningitidis, and 8% for H. influenzae. Of survivors, 35% have sequelae, particularly after pneumococcal infection, including deafness, seizures, learning disabilities, blindness, paresis, ataxia, or hydrocephalus. All patients with meningitis should have a hearing evaluation before discharge and at follow-up. Poor prognosis is associated with young age, long duration of illness before effective antibiotic therapy, seizures, coma at presentation, shock, low or absent CSF white blood cell count in the presence of visible bacteria on CSF Gram stain, and immunocompromised status. Rarely relapse may occur 3 to 14 days after treatment, possibly from parameningeal foci or resistant organisms. Recurrence may indicate an underlying immunologic or anatomic defect that predisposes the patient to meningitis.


Pediatrics_Nelson

Pediatrics_Nelson. Routine immunizations against H. influenzae and S. pneumoniae are recommended for children beginning at 2 months of age. Quadrivalent vaccines against N. meningitidis (serotypes A, C, Y, and W-135) are recommended for adolescents, college freshmen, military personnel, and travelers to highly endemic areas (see Chapter 94), and are licensed down to 2 years of age. Chemoprophylaxis with rifampin, ciprofloxacin, or ceftriaxone to eradicate the carrier state and decrease transmission is recommended both for index cases with N. meningitidis or H. influenzae and for their close contacts.


Pediatrics_Nelson

Pediatrics_Nelson. H. influenzae and for their close contacts. Encephalitis is an inflammatory process of the brain parenchyma leading to cerebral dysfunction. It is usually an acute process but may be a postinfectious encephalomyelitis, a chronic degenerative disease, or a slow viral infection. Encephalitis may be diffuse or localized. Organisms cause encephalitis by one of two mechanisms: (1) direct infection of the brain parenchyma or (2) an apparent immune-mediated response in the central nervous system that usually begins several days after the appearance of extraneural manifestations of the infection.


Pediatrics_Nelson

Pediatrics_Nelson. Viruses are the principal causes of acute infectious encephalitis (Table 101-1). The most common viral causes of encephalitis in the United States are the enteroviruses, arboviruses, and herpesviruses. Human immunodeficiency virus (HIV) is an important cause of subacute encephalitis in children and adolescents and may present as an acute febrile illness but, more commonly, is insidious in onset (see Chapter 125). Enterovirus and parechovirus +++ Herpes simplex viruses (HSV 1, 6, 7) ++ Arthropod-borne viruses (especially West Nile ++ virus, St. Louis, California, LaCrosse, and equine encephalitis viruses) Epstein-Barr virus + Adenovirus + Human immunodeficiency virus + Borrelia burgdorferi (Lyme disease) + Bartonella henselae (cat-scratch disease) + Mycoplasma pneumoniae + Rickettsia rickettsii +


Pediatrics_Nelson

Pediatrics_Nelson. Adapted from Willoughby RE Jr, Long SS: Encephalitis, meningoencephalitis, acute disseminated encephalomyelitis, and acute necrotizing encephalopathy. In Long SS, Pickering LK, Prober CG : Principles and Practice of Pediatric Infectious Diseases, revised reprint, ed 3, Philadelphia, 2008, Saunders. Other causes of subacute encephalitis include measles, slow viruses (e.g., JC virus), and prion-associated diseases (e.g., Creutzfeldt-Jakob disease). Encephalitis also may result from metabolic, toxic, and neoplastic disorders. Acute disseminated encephalomyelitis (ADEM) is the abrupt development of multiple neurologic signs related to an inflammatory, demyelinating disorder of the brain and spinal cord. ADEM follows childhood viral infections (such as measles and chickenpox) or vaccinations and resembles multiple sclerosis clinically.


Pediatrics_Nelson

Pediatrics_Nelson. Arboviral and enteroviral encephalitides characteristically appear in clusters or epidemics that occur from midsummer to early fall, although sporadic cases of enteroviral encephalitis occur throughout the year. Herpesviruses and other infectious agents account for additional sporadic cases throughout the year.


Pediatrics_Nelson

Pediatrics_Nelson. Arboviruses tend to be limited to certain geographic areas, reflecting the reservoir and mosquito vector. St. Louis encephalitis virus is present throughout the United Statesin birds. California encephalitis virus, common in the Midwest, is carried by rodents and spread by mosquitoes. Easternequine encephalitis virus is limited to the East Coast in birds.Western equine encephalitis virus is present throughout theMidwest and West in birds. West Nile virus infection occurs worldwide and causes outbreaks of summer encephalitis inNorth America. The principal vector for West Nile virus isthe Culex pipiens mosquito, but the organism can be isolatedin nature from a wide variety of Culex and Aedes species.A broad range of birds serves as the major reservoir for WestNile virus. Acute infectious encephalitis usually is preceded by a prodrome of several days of nonspecific symptoms such as sore


Pediatrics_Nelson

Pediatrics_Nelson. Acute infectious encephalitis usually is preceded by a prodrome of several days of nonspecific symptoms such as sore Available @ StudentConsult.com throat, fever, headache, and abdominal complaints followed by the characteristic symptoms of progressive lethargy, behavioral changes, and neurologic deficits. Seizures are common at presentation. Children with encephalitis also may have a maculopapular rash and severe complications such as fulminant coma, transverse myelitis, anterior horn cell disease, or peripheral neuropathy. West Nile encephalitis produces a broad spectrum of illness from asymptomatic infection to death. Severity of disease increases with advancing age. Most children are asymptomatic. Typical symptoms include mild, nonspecific extraneurologic illness characterized by fever, rash, arthralgias, lymphadenopathy, gastrointestinal complaints, and conjunctivitis.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis is established presumptively by the presenceof characteristic neurologic signs, typical epidemiology findings, and evidence of infection by cerebrospinal fluid (CSF)analysis, electroencephalogram (EEG), and brain imagingtechniques. Encephalitis may result from infections withbacteria, Mycoplasma, Rickettsia, fungi, and parasites andfrom many noninfectious diseases, including metabolic diseases (encephalopathy), such as Reye syndrome, hypoglycemia, collagen vascular disorders, drugs, hypertension, andmalignancies.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of viral encephalitis is supported by examination of the CSF, which typically shows a lymphocytic pleocytosis, slight elevation in protein content, and normal glucose level. The CSF occasionally may be normal. Extreme elevations of protein and reductions of glucose suggest tuberculosis, cryptococcal infection, or meningeal carcinomatosis. The EEG is the definitive test and shows diffuse, slow wave activity, although focal changes may be present. Neuroimaging studies may be normal or may show diffuse cerebral swelling of the parenchyma or focal abnormalities. A temporal lobe focus on EEG or brain imaging is the characteristic feature of herpes simplex virus (HSV) infection.


Pediatrics_Nelson

Pediatrics_Nelson. Serologic studies should be obtained for arboviruses (including West Nile virus, if indicated by the patient risk factors), Epstein-Barr virus, Mycoplasma pneumoniae, cat-scratch disease, and Lyme disease. Additional serologic testing for less common pathogens should be performed as indicated by the travel, social, or medical history. In most cases of viral encephalitis, the virus is difficult to isolate from the CSF. Polymerase chain reaction tests for HSV, enteroviruses, West Nile virus, and other viruses are available and should be sent. Viral cultures of stool and a nasopharyngeal swab may also be obtained. Even with extensive testing and the use of polymerase chain reaction assays, the cause of encephalitis remains undetermined in one third of cases.


Pediatrics_Nelson

Pediatrics_Nelson. Brain biopsy is seldom performed but may be useful in patients with focal neurologic findings. It may be appropriate for patients with severe encephalopathy who show no clinical improvement if the diagnosis remains obscure. Rabies encephalitis and prion-related diseases (Creutzfeldt-Jakob disease and kuru) may be routinely diagnosed by culture or pathologic examination of brain biopsy tissue. Brain biopsy may be helpful to identify arbovirus and enterovirus infections, tuberculosis, fungal infections, and noninfectious illnesses, particularly primary central nervous system vasculopathies and malignancies.


Pediatrics_Nelson

Pediatrics_Nelson. With the exception of HSV, varicella-zoster virus, cytomegalovirus, and HIV, there is no specific therapy for viral encephalitis. Management is supportive and frequently requires intensive care unit admission to facilitate aggressive therapy for seizures, timely detection of electrolyte abnormalities, and, when necessary, airway monitoring and protection or reduction of increased intracranial pressure and maintenance of adequate cerebral perfusion pressure. Intravenous acyclovir is the treatment of choice for HSV andvaricella-zoster virus infections. Cytomegalovirus infection is treated with ganciclovir. HIV infections may be treated with a combination of antiretroviral agents. M. pneumoniae infections may be treated with doxycycline, erythromycin, azithromycin, or clarithromycin, although the clinical value of treatingencephalitis associated with mycoplasmal disease is uncertain.


Pediatrics_Nelson

Pediatrics_Nelson. ADEM has been treated with high-dose intravenous corticosteroids, but it is unclear whether the improved outcome with corticosteroids reflects milder cases recognized by magnetic resonance imaging, fewer cases of ADEM caused by measles (which causes severe ADEM), or improved supportive care.


Pediatrics_Nelson

Pediatrics_Nelson. Among survivors, symptoms usually resolve over several days to 2 to 3 weeks. Although most patients with epidemic forms of infectious encephalitis (St. Louis, California, West Nile, and enterovirus infections) in the United States recover without sequelae, severe cases leading to death or substantial neurologic sequelae can occur with virtually any of these neurotropic viruses. About two thirds of patients recover fully before being discharged from the hospital. The remainder show clinically significant residua, including paresis or spasticity, cognitive impairment, weakness, ataxia, and recurrent seizures. Most patients with neurologic sequelae of infectious encephalitis at the time of hospital discharge gradually recover some or all of their function. The overall mortality for infectious encephalitis is approximately 5%.


Pediatrics_Nelson

Pediatrics_Nelson. Disease caused by HSV, Eastern equine encephalitis, or M. pneumoniae is associated with a worse prognosis. The prognosis may be worse for encephalitis in children younger than 1 year of age or with coma. Rabies, with very rare exceptions, is fatal. Relapses of ADEM occur in 14%, usually within 1 year with the same or new clinical signs. Recurrences of ADEM may represent onset of multiple sclerosis in childhood.


Pediatrics_Nelson

Pediatrics_Nelson. Relapses of ADEM occur in 14%, usually within 1 year with the same or new clinical signs. Recurrences of ADEM may represent onset of multiple sclerosis in childhood. The best prevention for arboviral encephalitis is to avoid mos-quito-borne or tick-borne exposures and to remove ticks carefully (see Chapter 122). There are no vaccines in use in the United States for the prevention of arboviral infection or for enteroviruses except for poliomyelitis. There are no specific preventive measures for HSV encephalitis except for cesarean section for mothers with active genital lesions (see Chapter 65). Rabies can be prevented by preexposure or postexposure vaccination. Influenza encephalitis can be prevented by use of influenza vaccination. Reye syndrome can be prevented by avoiding use of aspirin or aspirin-containing compounds for children with fever as well as use of varicella and influenza vaccines.


Pediatrics_Nelson

Pediatrics_Nelson. The common cold is a viral infection with prominent symptoms of rhinorrhea and nasal obstruction, absent or mild fever, and no systemic manifestations. It is often referred to as rhinitis but usually involves the sinus mucosa and is more correctly termed rhinosinusitis. The viruses primarily associated with colds are rhinoviruses and, less commonly, coronaviruses. Other viruses that cause common cold symptoms include respiratory syncytial virus and, less commonly, influenza, parainfluenza, and adenoviruses. Viral infection of nasal epithelium causes an acute inflammatory response with mucosal infiltration by inflammatory cells and release of cytokines. The inflammatory response is partly responsible for many of the symptoms.


Pediatrics_Nelson

Pediatrics_Nelson. Colds occur throughout the year with peak incidence from early fall through late spring, reflecting the seasonal prevalence of viral pathogens and confined habitation during colder months. Young children have an average of 6 to 7 colds each year, and 10% to 15% of children have at least 12 colds each year. The annual number of colds decreases with age, to two to three colds each year by adulthood. Children in out-of-home day care during the first year of life have 50% more colds than children cared for at home only. This difference diminishes during subsequent years in day care. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Common cold symptoms typically develop 1 to 3 days after viral infection and include nasal obstruction, rhinorrhea, sore or scratchy throat, and occasional nonproductive cough. Colds usually persist about 1 week, although 10% last 2 weeks. There is often a change in the color or consistency of nasal secretions, which is not indicative of sinusitis or bacterial superinfection. Examination of the nasal mucosa may reveal swollen, erythematous nasal turbinates. Laboratory studies often are not helpful. A nasal smear for eosinophils may be useful in the evaluation for allergic rhinitis (see Chapter 79).


Pediatrics_Nelson

Pediatrics_Nelson. Laboratory studies often are not helpful. A nasal smear for eosinophils may be useful in the evaluation for allergic rhinitis (see Chapter 79). The differential diagnosis of the common cold includes allergic rhinitis, foreign body (especially with unilateral nasal discharge), sinusitis, pertussis, and streptococcal nasopharyngitis. Allergic rhinitis is characterized by absence of fever, eosinophils in the nasal discharge, and other manifestations, such as allergic shiners, nasal polyps, a transverse crease on the nasal bridge, and pale, edematous, nasal turbinate mucosa. Rare causes of rhinorrhea are choanal atresia or stenosis, cerebrospinal fluid fistula, diphtheria, tumor, congenital syphilis (with snuffles), nasopharyngeal malignancy, and Wegener granulomatosis.


Pediatrics_Nelson

Pediatrics_Nelson. There is no specific therapy for the common cold. Antibacterial therapy is not beneficial. Management consists of symptomatic therapies. Antihistamines, decongestants, and combination antihistamine-decongestants are not recommended for children younger than 6 years of age because of adverse effects and lack of benefits. Low-grade fever is seen with colds, particularly in the first few days of illness and can be treated with antipyretic medications. Cough suppressants and expectorants have not been shown to be beneficial. Vitamin C and inhalation of warm, humidified air are no more effective than placebo. The benefit of zinc lozenges or sprays has been inconsistent.


Pediatrics_Nelson

Pediatrics_Nelson. Otitis media is the most common complication and occursin 5% to 20% of children with a cold (see Chapter 105). Othercomplications include bacterial sinusitis, which should beconsidered if rhinorrhea or daytime cough persists without improvement for at least 10 to 14 days or if severe signsof sinus involvement develop, such as fever, facial pain, orfacial swelling (see Chapter 104). Colds may lead to exacerbation of asthma and may result in inappropriate antibiotic treatment. There are no proven methods for prevention of colds other than good hand washing and avoiding contact with infected persons. No significant effect of vitamin C or Echinacea for prevention of the common cold has been confirmed.


Pediatrics_Nelson

Pediatrics_Nelson. Many infectious agents can cause pharyngitis (Table 103-1).Group A streptococci (Streptococcus pyogenes) are gram-positive, nonmotile cocci that are facultative anaerobes. Onsheep blood agar, the colonies are small (1 to 2 mm in diameter)and have a surrounding zone of β (clear) hemolysis. Other bacterial organisms less often associated with pharyngitis include group C streptococcus (also β-hemolytic), Arcanobacterium haemolyticum (β-hemolytic, gram-positive rod), and Francisella tularensis (gram-negative coccobacillus and cause of tularemia). Chlamydophila pneumoniae, strain TWAR, is associated with lower respiratory disease but also causes sore throat.Mycoplasma pneumoniae is associated with atypical pneumoniaand may cause mild pharyngitis without distinguishing clinical manifestations. Other bacteria, including Staphylococcus aureus, Haemophilus influenzae, and Streptococcus pneumoniae,are cultured frequently from the throats of children with pharyngitis, but their role in causing


Pediatrics_Nelson

Pediatrics_Nelson. Other bacteria, including Staphylococcus aureus, Haemophilus influenzae, and Streptococcus pneumoniae,are cultured frequently from the throats of children with pharyngitis, but their role in causing pharyngitis is unclear.


Pediatrics_Nelson

Pediatrics_Nelson. Many viruses cause acute pharyngitis. Some viruses, such as adenoviruses, are more likely than others to cause pharyngitis as a prominent symptom, whereas other viruses, such as rhinoviruses, are more likely to cause pharyngitis as a minor part of an illness that primarily features other symptoms, such as rhinorrhea or cough. Epstein-Barr virus, enteroviruses (herpangina), herpes simplex virus, and primary human immunodeficiency virus (HIV) infection also produce pharyngitis.


Pediatrics_Nelson

Pediatrics_Nelson. Sore throat is the primary symptom in approximately one third of upper respiratory tract illnesses. Streptococcal pharyngitis is relatively uncommon before 2 to 3 years of age, but the incidence increases in young school-age children and then declines in late adolescence and adulthood. Streptococcal pharyngitis occurs throughout the year in temperate climates, with a peak during the winter and early spring. The illness often spreads to siblings and classmates. Viral infections generally spread via close contact with an infected person and peak during winter and spring. Available @ StudentConsult.com Pharyngeal inflammation causes cough, sore throat, dysphagia, and fever. If involvement of the tonsils is prominent, the term tonsillitis or tonsillopharyngitis is often used. Adapted from Hayden GF, Hendley JO, Gwaltney JM Jr: Management of the ambulatory patient with a sore throat, Curr Clin Top Infect Dis 9:62–75, 1988.


Pediatrics_Nelson

Pediatrics_Nelson. Adapted from Hayden GF, Hendley JO, Gwaltney JM Jr: Management of the ambulatory patient with a sore throat, Curr Clin Top Infect Dis 9:62–75, 1988. The onset of streptococcal pharyngitis is often rapid and associated with prominent sore throat and moderate to high fever. Headache, nausea, vomiting, and abdominal pain are frequent. In a typical, florid case, the pharynx is distinctly red. The tonsils are enlarged and covered with a yellow, blood-tinged exudate. There may be petechiae or doughnut-shapedlesions on the soft palate and posterior pharynx. The uvula may be red, stippled, and swollen. Anterior cervical lymph nodes are enlarged and tender to touch. Many children, however, present with only mild pharyngeal erythema without tonsillar exudate or cervical lymphadenitis. Conjunctivitis, cough, coryza, hoarseness, or ulcerations suggest a viral etiology. The diagnosis of streptococcal pharyngitis cannot be made on clinical features alone.


Pediatrics_Nelson

Pediatrics_Nelson. In addition to sore throat and fever, some patients exhibit the stigmata of scarlet fever: circumoral pallor, strawberry tongue, and a fine diffuse erythematous macular-papular rash that has the feeling of goose flesh. The tongue initially has a white coating, but red and edematous lingual papillae later project through this coating, producing a white strawberry tongue. When the white coating peels off, the resulting red strawberry tongue is beefy red with prominent papillae. Patients infected with A. haemoyticum may present with similar findings. Compared with classic streptococcal pharyngitis, the onset of viral pharyngitis is typically more gradual, and symptoms more often include rhinorrhea, cough, and diarrhea. Many upper respiratory tract infections present with symptoms of rhinorrhea and nasal obstruction, whereas systemic symptoms and signs, such as myalgia and fever, are absent or mild.


Pediatrics_Nelson

Pediatrics_Nelson. Gingivostomatitis is characteristic of herpes simplex virus-1 (see Chapter 65). Herpangina is an enteroviral infection with sudden onset of high fever, vomiting, headache, malaise, myalgia, backache, conjunctivitis, poor intake, drooling, sore throat,and dysphagia. The oral lesions of herpangina may be nonspecific, but classically there are one or more small, tender, papular,or pinpoint vesicular lesions on an erythematous base scatteredover the soft palate, uvula, and tongue. These vesicles enlargefrom 1 to 2 mm to 3 to 4 mm over 3 to 4 days, rupture, and produce small, punched-out ulcers that persist for several days. The principal challenge is to distinguish pharyngitis caused by group A streptococcus from pharyngitis caused by nonstreptococcal (usually viral) organisms. A rapid streptococcal antigen test, a throat culture, or both are often performed to improve diagnostic precision and to identify children most likely to benefit from antibiotic therapy of streptococcal disease.


Pediatrics_Nelson

Pediatrics_Nelson. Many rapid diagnostic techniques for streptococcal pharyngitis are available with excellent specificity of 95% to 99%. The sensitivity of these rapid tests varies, however, and negative rapid tests should be confirmed by a throat culture. Throat culture is the diagnostic gold standard for establishing the presence of streptococcal pharyngitis. False-positive cultures can occur if other organisms are incorrectly identified as group A streptococcus. As many as 20% of positive cultures in children during winter months reflect streptococcal carriers and not acute pharyngitis. The predictive values of white blood cell count and differential, erythrocyte sedimentation rate, and C-reactive protein arenot sufficient to distinguish streptococcal from nonstreptococcal pharyngitis, and these tests are not routinely recommended.The white blood cell count in patients with infectious mononucleosis usually shows a predominance of atypical lymphocytes. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com The differential diagnosis of infectious pharyngitis includes other local infections of the oral cavity, retropharyngeal abscesses (S. aureus, streptococci, anaerobes), diphtheria (if unimmunized), peritonsillar abscesses (with quinsy sore throat or unilateral tonsil swelling caused by streptococci, anaerobes, or, rarely, S. aureus), and epiglottitis. In addition neutropenic mucositis (leukemia, aplastic anemia), thrush (candidiasis secondary to T-cell immune deficiency), autoimmune ulceration (systemic lupus erythematosus, Behçet disease), and Kawasaki disease may cause pharyngitis. Pharyngitis is often a prominent feature of Epstein-Barr virus-associated mononucleosis (see Chapter 99).


Pediatrics_Nelson

Pediatrics_Nelson. Vincent infection or trench mouth is a fulminant form of acute necrotizing ulcerative gingivitis with synergistic infection with certain spirochetal organisms, notably Treponema vincentii, with anaerobic Selenomonas and Fusobacterium. Vincent angina refers to a virulent form of anaerobic pharyngitis; gray pseudomembranes are found on the tonsils. Lemierre syndrome is acute pharyngitis complicated by thrombosis of the internal jugular vein and septic emboli (most often to the lungs). It occurs primarily in adolescents and is caused by Fusobacterium necrophorum.


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Pediatrics_Nelson. Ludwig angina is a mixed anaerobic bacterial cellulitis of the submandibular and sublingual regions. Although often applied to any infection of the sublingual or submandibular region, the term originally was reserved for a rapidly spreading bilateral cellulitis of the sublingual and submandibular spaces. It typically is due to spreading from a periapical abscess of the second or third mandibular molar. It also has been associated with tongue piercing. A propensity for rapid spread, glottic and lingual swelling, and consequent airway obstruction makes prompt intervention imperative.


Pediatrics_Nelson

Pediatrics_Nelson. A syndrome of periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis is a rare cause of recurrent fever in children. Recurring nonspecific pharyngitis is accompanied by fever and painful solitary vesicular lesions in the mouth. The fevers begin at a young age (usually <5 years). Episodes last approximately 5 days, with a mean of 28 days between episodes. Episodes are shorter with oral prednisone and unresponsive to nonsteroidal anti-inflammatory drugs or antibiotics. The syndrome resolves in some but persists in other children. Long-term sequelae do not develop.


Pediatrics_Nelson

Pediatrics_Nelson. Even if untreated, most episodes of streptococcal pharyngitis resolve uneventfully over a few days. Early antimicrobial therapy accelerates clinical recovery by 12 to 24 hours. The major benefit of antimicrobial therapy is prevention of acute rheumatic fever (see Chapter 146). Because the latent (incubation) period of acute rheumatic fever is relatively long (1 to 3 weeks), treatment instituted within 9 days of illness is virtually 100% successful in preventing rheumatic fever. Treatment begun more than 9 days after the onset of illness, although less than 100% successful, has some preventive value. Antibiotic therapy should be started promptly in children with a positive rapid test for group A streptococcus, scarlet fever, symptomatic pharyngitis whose sibling has documented streptococcal pharyngitis, a past history of rheumatic fever or a recent family history of rheumatic fever, or symptomatic pharyngitis and living in an area experiencing an epidemic of acute rheumatic fever or


Pediatrics_Nelson

Pediatrics_Nelson. pharyngitis, a past history of rheumatic fever or a recent family history of rheumatic fever, or symptomatic pharyngitis and living in an area experiencing an epidemic of acute rheumatic fever or poststreptococcal glomerulonephritis.


Pediatrics_Nelson

Pediatrics_Nelson. A variety of antimicrobial agents can be used to treat streptococcal pharyngitis (Table 103-2). Cephalosporins have superior pharyngeal bacterial eradication rates compared to Oral penicillin V (2–3 times daily for 10 days) 10 mg/kg/dose, maximum dose 250 mg/dose Intramuscular benzathine penicillin G (single dose) For children ≤27 kg: 600,000 U For larger children and adults: 1.2 million U For persons allergic to penicillin Cephalexin 20 mg/kg/dose BID, maximum dose 500 mg/dose × 10 days Cefadroxil 30 mg/kg OD maximum, maximum dose 1 g × 10 days Clindamycin 7 mg/kg/dose TID, maximum dose 300 mg/dose × 10 days For persons allergic to β-lactams Erythromycin ethyl succinate: 40–50 mg/kg/day (max 1 g/day) in 3–4 doses for 10 days Erythromycin estolate: 20–40 mg/kg/day in 2–4 doses (max 1 g/day) for 10 days Azithromycin, children: 12 mg/kg orally once daily for 5 days (to maximum adult dose); adults: 500 mg orally on day 1, then 250 mg orally on days 2–5


Pediatrics_Nelson

Pediatrics_Nelson. Azithromycin, children: 12 mg/kg orally once daily for 5 days (to maximum adult dose); adults: 500 mg orally on day 1, then 250 mg orally on days 2–5 BID, Twice daily; OD, once daily; TID, three times daily. penicillin. One proposed explanation is that staphylococci or anaerobes in the pharynx produce β-lactamase, which inactivates penicillin and reduces its efficacy. Another possible explanation is that cephalosporins are more effective in eradicating streptococcal carriage. Children with recurrent throat culture episodes of group A streptococcal pharyngitis pose a particular problem. An alternative antibiotic may be chosen to treat β-lactamase producing flora, which may be responsible for the recurrences. Either amoxicillin-clavulanate or clindamycin is an effective regimen for eliminating streptococcal carriage.


Pediatrics_Nelson

Pediatrics_Nelson. Specific antiviral therapy is unavailable for most cases of viral pharyngitis. Patients with primary herpetic gingivostomatitis benefit from early treatment with oral acyclovir. Pharyngitis caused by streptococci or respiratory viruses usually resolves completely. The complications of group A streptococcal pharyngitis include local suppurative complications, such as parapharyngeal abscess and other infections of the deep fascial spaces of the neck, and nonsuppurative complications, such as acute rheumatic fever and acute postinfectious glomerulonephritis. Viral respiratory tract infections, including infections caused by influenza A, adenoviruses, parainfluenza type 3, and rhinoviruses, may predispose to bacterial middle ear infections. Antimicrobial prophylaxis with daily oral penicillin V prevents recurrent streptococcal infections and is recommended only to prevent recurrences of rheumatic fever.


Pediatrics_Nelson

Pediatrics_Nelson. Antimicrobial prophylaxis with daily oral penicillin V prevents recurrent streptococcal infections and is recommended only to prevent recurrences of rheumatic fever. Sinusitis is a suppurative infection of the paranasal sinuses and often complicates the common cold and allergic rhinitis. The maxillary and ethmoid sinuses are present at birth, but only the ethmoidal sinuses are pneumatized. The maxillary sinuses become pneumatized at 4 years of age. Frontal sinuses begin to develop at 7 years of age and are not completely developed until adolescence. The sphenoid sinuses are present by 5 years of age. The ostia draining the sinuses are narrow (1 to 3 mm) and drain into the middle meatus in the ostiomeatal complex. The mucociliary system maintains the sinuses as normally sterile.


Pediatrics_Nelson

Pediatrics_Nelson. Obstruction to mucociliary flow, such as mucosal edemaresulting from the common cold, impedes sinus drainage andpredisposes to bacterial proliferation. In 90% of children withacute sinusitis, the bacterial causes are Streptococcus pneumoniae, nontypable Haemophilus influenzae, Moraxella catarrhalis,Staphylococcus aureus, and group A streptococcus. Anaerobesemerge as important pathogens in subacute and chronic sinusitis. Indwelling nasogastric and nasotracheal tubes predisposeto nosocomial sinusitis, which may be caused by gram-negativebacteria (Klebsiella or Pseudomonas). Antibiotic therapy predisposes to infection with antibiotic-resistant organisms. Sinusitis in neutropenic and immunocompromised persons may becaused by Aspergillus or the Zygomycetes (e.g., Mucor, Rhizopus).


Pediatrics_Nelson

Pediatrics_Nelson. The true incidence of sinusitis is unknown. The common cold is the major predisposing factor for developing sinusitis at allages. Other risk factors include allergy, cystic fibrosis, immunodeficiency, human immunodeficiency virus (HIV) infection,nasogastric or nasotracheal intubation, immotile cilia syndrome,nasal polyps, and nasal foreign body. Sinusitis also is a frequent problem in immunocompromised children after organtransplantation. Available @ StudentConsult.com Clinical manifestations most commonly include persistent, mucopurulent, unilateral or bilateral rhinorrhea, nasal stuffiness, and cough, especially at night. Less common symptoms include a nasal quality to the voice, halitosis, facial swelling, facial tenderness and pain, and headache. Sinusitis may exacerbate asthma. Culture of the nasal mucosa is not useful. Sinus aspirate culture is the most accurate diagnostic method but is not practical or necessary in immunocompetent patients.


Pediatrics_Nelson

Pediatrics_Nelson. Culture of the nasal mucosa is not useful. Sinus aspirate culture is the most accurate diagnostic method but is not practical or necessary in immunocompetent patients. Plain x-ray and computed tomography may reveal sinus clouding, mucosal thickening, or an air-fluid level. Abnormal radiographic findings do not differentiate infection from allergic disease; computed tomography and magnetic resonance imaging often show abnormalities, including air-fluid levels, in the sinuses of asymptomatic persons. Conversely normal radiographs have high negative predictive value for bacterial sinusitis. The diagnosis usually is based on history and physical findings for longer than 10 to 14 days without improvement or increased severity of symptoms compared to the common cold.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis usually is based on history and physical findings for longer than 10 to 14 days without improvement or increased severity of symptoms compared to the common cold. Amoxicillin-clavulanate for 10 to 14 days is recommended as first-line therapy of sinusitis in children. High-dose therapy is recommended for children at increased risk for resistant bacteria (antibiotic treatment in the preceding 1 to 3 months, day care attendance, age <2 years, high rates of antimicrobial resistance locally). Levofloxacin is recommended for children with type I hypersensitivity to penicillins. Clindamycin plus a third generation cephalosporin (cefixime, cefpodoxime) is recommended for children with non-type I hypersensitivity.


Pediatrics_Nelson

Pediatrics_Nelson. Complications include orbital cellulitis, epidural or subdural empyema, brain abscess, dural sinus thrombosis, osteomyelitis of the outer or inner table of the frontal sinus (Pott puffy tumor), and meningitis. These all should be managed with sinus drainage and broad-spectrum parenteral antibiotics. Sinusitis also may exacerbate bronchoconstriction in asthmatic patients.


Pediatrics_Nelson

Pediatrics_Nelson. Orbital cellulitis is a serious complication of sinusitisthat follows bacterial spread into the orbit through the wallof the infected sinus. It typically begins as ethmoid sinusitisand spreads through the lamina papyracea, a thin, bony platethat separates the medial orbit and the ethmoid sinus. Orbitalinvolvement can lead to subperiosteal abscess, ophthalmoplegia, cavernous sinus thrombosis, and vision loss. Manifestations of orbital cellulitis include orbital pain, proptosis,chemosis, ophthalmoplegia and limited extraocular muscle motion, diplopia, and reduced visual acuity. Infection of the orbit must be differentiated from that of the preseptal (anterior to the palpebral fascia) or periorbital space. Preseptal (periorbital) cellulitis usually occurs in children younger than 3 years of age; these children do not have proptosis or ophthalmoplegia. Periorbital cellulitis may be associated with a skin lesion or trauma and usually is caused by S. aureus or group A streptococcus.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of orbital cellulitis is confirmed by a computed tomography scan of the orbit, which determines the extent of orbital infection and the need for surgical drainage. Disorders to be considered in the differential diagnosis are zygomycosis (mucormycosis), aspergillosis, rhabdomyosarcoma, neuroblastoma, Wegener granulomatosis, inflammatory pseudotumor of the orbit, and trichinosis. Therapy for orbital cellulitis involves broad-spectrum parenteral antibiotics, such as vancomycin and ceftriaxone. More than half of children with acute bacterial sinusitis recover without any antimicrobial therapy. Fever and nasal discharge should improve dramatically within 48 hours of initiating treatment. Persistent symptoms suggest another etiology. The best means of prevention are good hand washing to minimize acquisition of colds and management of allergic rhinitis.


Pediatrics_Nelson

Pediatrics_Nelson. The best means of prevention are good hand washing to minimize acquisition of colds and management of allergic rhinitis. Otitis media (OM) is a suppurative infection of the middle ear cavity. Bacteria gain access to the middle ear when the normal patency of the eustachian tube is blocked by upper airway infection or hypertrophied adenoids. Air trapped in the middle ear is resorbed, creating negative pressure in this cavity and facilitating reflux of nasopharyngeal bacteria. Obstructed flow of secretions from the middle ear to the pharynx combined with bacterial reflux leads to infected middle ear effusion.


Pediatrics_Nelson

Pediatrics_Nelson. Both bacteria and viruses can cause OM. The common bacterial pathogens are Streptococcus pneumoniae, nontypable Haemophilus influenzae, Moraxella catarrhalis, and, less frequently, group A streptococcus. S. pneumoniae that is relatively resistant to penicillin (minimal inhibitory concentration 0.1 to 1 μg/mL) or highly resistant to penicillin (minimal inhibitory concentration ≥2 μg/mL) is isolated with increasing frequency from young children, particularly those who attend day care or have received antibiotics recently. Viruses, including rhinoviruses, influenza, and respiratory syncytial virus, are recovered alone or as co-pathogens in 20% to 25% of patients.


Pediatrics_Nelson

Pediatrics_Nelson. Diseases of the middle ear account for approximately one third of office visits to pediatricians. The peak incidence of acute OM is between 6 and 15 months of life. By the first birthday, 62% of children experience at least one episode. Few first episodes occur after 18 months of age. OM is more common in boys and in patients of lower socioeconomic status. There is increased incidence of OM in Native Americans and Alaskan Natives and in certain high-risk populations, such as children with human immunodeficiency virus (HIV), cleft palate, and trisomy 21. In most of the United States, OM is a seasonal disease with a distinct peak in January and February, which corresponds to the rhinovirus, respiratory syncytial virus, and influenza seasons. The major risk factors for acute OM are young age, lack of breastfeeding, passive exposure to tobacco smoke, and increased exposure to infectious agents (day care).


Pediatrics_Nelson

Pediatrics_Nelson. As defined by the presence of six or more acute OM episodes in the first 6 years of life, at least 12% of children in the general population have recurrent OM and would be considered otitis-prone. Craniofacial anomalies and immunodeficiencies often are associated with recurrent OM; most children with recurrent acute OM are otherwise healthy. Available @ StudentConsult.com In infants, the most frequent symptoms of acute OM are nonspecific and include fever, irritability, and poor feeding. Inolder children and adolescents, acute OM usually is associatedwith fever and otalgia (acute ear pain). Acute OM also may present with otorrhea (ear drainage) after spontaneous ruptureof the tympanic membrane. Signs of a common cold, whichpredisposes to acute OM, are often present (see Chapter 102).A bulging tympanic membrane, air fluid level, or visualizationof purulent material by otoscopy are reliable signs of infection(Table 105-1).


Pediatrics_Nelson

Pediatrics_Nelson. Examination of the ears is essential for diagnosis and should be part of the physical examination of any child with fever. The hallmark of OM is the presence of effusion in the middle ear cavity (see Table 105-1). The presence of an effusion does not define its nature or potentially infectious etiology, but it does define the need for appropriate diagnosis and therapy.


Pediatrics_Nelson

Pediatrics_Nelson. Pneumatic otoscopy, using an attachment to a hermetically sealed otoscope, allows evaluation of ventilation of the middle ear and is a standard for clinical diagnosis. The tympanic membrane of the normal, air-filled middle ear has much greater compliance than if the middle ear is fluid-filled. With acute OM, the tympanic membrane is characterized by hyperemia, or red color rather than the normal pearly gray color, but it can be pink, white, or yellow with a full to bulging position and with poor or absent mobility to negative and positive pressure. The light reflex is lost, and the middle ear structures are obscured and difficult to distinguish. A hole in the tympanic membrane or purulent drainage confirms perforation. Occasionally bullae are present on the lateral aspect of the tympanic membrane, which characteristically are associated with severe ear pain.


Pediatrics_Nelson

Pediatrics_Nelson. Routine laboratory studies, including complete blood count and erythrocyte sedimentation rate, are not useful in the evaluation of OM. Tympanometry provides objective acoustic measurements of the tympanic membrane-middle ear system by reflection or absorption of sound energy from the external A diagnosis of AOM requires: History of acute onset of signs and symptoms Presence of middle ear effusion Signs and symptoms of middle ear inflammation The definition of AOM includes all of the following: Recent, usually abrupt, onset of signs and symptoms of middle ear inflammation and middle ear effusion The presence of middle ear effusion that is indicated by any of the following: Bulging of the tympanic membrane Limited or absent mobility of the tympanic membrane Air-fluid level behind the tympanic membrane Otorrhea Signs or symptoms of middle ear inflammation as indicated by either:


Pediatrics_Nelson

Pediatrics_Nelson. Signs or symptoms of middle ear inflammation as indicated by either: Distinct erythema of the tympanic membrane Distinct otalgia (discomfort clearly referable to the ear that results in interference with or precludes normal activity or sleep) ear duct as pressure in the duct is varied. Measurements of the resulting tympanogram correlate well with the presence or absence of middle ear effusion. Instruments using acoustic reflectometry are available for office and home use. Use of reflectometry as a screening test for acute OM should be followed by examination with pneumatic otoscopy when abnormal reflectometry is identified. Bacteria recovered from the nasopharynx do not correlate with bacteria isolated by tympanocentesis. Tympanocentesis and middle ear exudate culture are not always necessary, but they are required for accurate identification of bacterial pathogens and may be useful in neonates, immunocompromised patients, and patients not responding to therapy.