The goal of treatment is removal of symptomatic warts to induce wart-free periods. Treatment modalities involve destruction of infected epithelium; patient-applied therapies include podofilox or imiquimod, and provider-applied therapies include cryotherapy with liquid nitrogen or cryoprobe, topical podophyllin resin, and trichloroacetic acid or bichloracetic acid. An alternative is surgical removal.
Intralesional interferon and laser surgery also have been effective. Factors that may influence selection of treatment include wart number, size, anatomic sites, wart morphology, patient preference, treatment cost, convenience, adverse effects, and provider experience. Recurrences after treatment are common and are frequently asymptomatic.
Pubic lice, or pediculosis pubis, are caused by infestation with Phthirus pubis, the pubic crab louse. The louse is predominantly sexually transmitted and lives out its life cycle on pubic hair, where it causes characteristic, intense pruritus (see Table 116-4). Diagnosis can be made clinically; lice are visible to the naked eye. Erythematous papules and egg cases (nits) are not seen before puberty. Treatment consists of education regarding personal and environmental hygiene and the application of an appropriate pediculicide, such as permethrin 1% cream or pyrethrins with piperonyl butoxide. Bedding and clothing should be decontaminated (machine washed and machine dried using the heat cycle or dry cleaned) or removed from body contact for at least 72 hours.
Acute hematogenous osteomyelitis is the most common manifestation of osteomyelitis in children and evolves secondary to bacteremia. Subacute osteomyelitis usually follows local inoculation by penetrating trauma and is not associated with systemic symptoms, and chronic osteomyelitis results from an untreated or inadequately treated (usually subacute) osteomyelitis.
In children beyond the newborn period and without hemoglobinopathies, bone infections occur almost exclusively in the metaphysis of long bones due to sluggish blood flow through tortuous vascular loops unique to this site. Preceding nonpenetrating trauma is often reported and may lead to local bone injury that predisposes to infection. Bone infections in children with sickle cell disease occur in the diaphyseal portion of the long bones, probably as a consequence of antecedent focal infarction. In children younger than 12 to 18 months of age, capillaries perforate the epiphyseal growth plate, permitting spread of infection across the epiphysis leading to suppurative arthritis, whereas in older children, infection is contained in the metaphysis because these vessels no longer cross the epiphyseal plate (Figs. 117-1AB).
Staphylococcus aureus is responsible for more than 80% of acute skeletal infections. Other common causes include Group A streptococcus and Streptococcus pneumoniae. Neisseria meningitidis, Mycobacterium tuberculosis, Bartonella henselae, Actinomyces spp., and anaerobes are less common causes. Group B streptococcus and enteric gram-negatives are other major causes in neonates. Sickle cell disease and other hemoglobinopathies predispose to osteomyelitis caused by Salmonella and S. aureus. Pasteurella multocida osteomyelitis may