Pediatric emergency medicine trisk 583

Schistosomiasis— Sub-Saharan Africa
Katayama fever

Schistosoma—
Sub-Saharan Africa
swimmer’s itch
(freshwater),
digger’s itch
(saltwater)

High fever, urticaria,
eosinophilia
weeks after
contact with
freshwater in
endemic areas
Pruritic rash after
skin is penetrated
by schistosomal
cercaria

Laboratory findings include anemia, thrombocytopenia, hypoalbuminemia,
and hypergammaglobulinemia. Untreated visceral infection is nearly always
fatal. Diagnosis of the cutaneous form is through identification of leishmanial
organisms via Wright or Giemsa stain of tissue samples. Visceral disease is
diagnosed via bone marrow (iliac crest in children), spleen, or less commonly,
liver aspirations. Treatment is always indicated for the mucosal and visceral
cases. The drug of choice for visceral and mucosal disease is liposomal
amphotericin B. Miltefosine can be used to treat all three forms and is FDA
approved for patients ≥12 years old. Sodium stibogluconate, an antimonial, has
also been used in the treatment of leishmaniasis, but has multiple potential

adverse events including cardiotoxicity (EKG changes findings include STelevation or depression, T-wave inversion, and QT-interval prolongation),
hepatitis,
pancreatitis,
nephrotoxicity
with
proteinuria,
phlebitis,
myelosuppression, and optic atrophy. Treatment of localized cutaneous disease
depends on the type and characteristics of the lesion. Those that are rapidly selfhealing can remain untreated. Systemic treatment is recommended for large or
multiple cutaneous lesions. Diffuse cutaneous disease is resistant to treatment.
Expert consultation through the CDC Division of Parasitic Diseases and Malaria:
(404) 718-4745 or (770) 488-7100 is strongly suggested. Standard isolation
precautions are recommended.

Cutaneous Larva Migrans
CLM is caused by the larval form of canine and feline hookworms (Ancylostoma
species), found in fecal material in soil or sand. These nematodes can penetrate
intact skin; infection is most common in tropical regions, especially on beaches.
While most common in travelers returning from the Caribbean, Latin America,


Asia, and Africa, the infection is also seen in the southeastern United States.
Patients present with itchy papules at the entry site with a migratory, raised,
erythematous, serpiginous pattern as the larvae migrate. The feet and buttocks
most commonly are affected. The parasites enter the bloodstream and have a
maturation phase in the lungs. With a large inoculation, eosinophilic pneumonitis
(Löeffler syndrome) can be seen. Eosinophilia can also be seen with invasive
enteritis, but is not a feature of isolated CLM. The diagnosis is clinical; biopsy is
not recommended, but pathology may demonstrate an eosinophilic infiltrate.
Serologies and EIAs are not commercially available. While usually a self-limited

disease, albendazole or ivermectin can be used for treatment. Patients with
substantial eosinophilia should be monitored for manifestations of mast cell
degranulation after treatment, and some may require corticosteroids along with
antiparasitic therapy. Contact precautions are recommended for the incontinent
child.

Filariasis
Filariases are mosquito-borne infections caused by the nematodes (roundworms)
Wuchereria bancrofti, Brugia malayi, or Brugia timori ( e-Table 94.25 ). The
incubation period ranges from 3 to 12 months depending on the species. W.
bancrofti ’s clinical manifestations include acute adenolymphangitis (ADL),
hydrocele, lymphedema, elephantiasis, chyluria, and tropical pulmonary
eosinophilia (TPE). ADL is characterized by malaise, fever, chills, and enlarged
painful lymph nodes, usually in the lower limb. Hydrocele (unilaterally or
bilateral) is the most common chronic manifestation of W. bancrofti. Chronic
lymphedema may progress to elephantiasis and typically involves the lower
extremities. Edema usually becomes nonpitting with skin thickening and loss of
skin elasticity. Secondary bacterial and fungal infections are common. Chyluria
is seen when dilated lymphatics rupture and drain into the urinary excretory
system. It is typically recurrent and lasts for days to weeks. TPE is the result of
immune hyperresponsiveness to microfilaria in the lung. Patients with TPE
typically present with nocturnal coughing and wheezing and extreme peripheral
eosinophilia (counts >3,000 cells/mm3). If left untreated, TPE may progress to
chronic interstitial fibrosis and permanent lung damage. Brugian filariasis
(caused by both B. malayi and B. timori ) is very similar to Bancroftian filariasis,
except that hydroceles, genital manifestations, and chyluria are less common,
and that the elephantiasis is usually limited to the lower legs in Brugian
filariasis.

Lymphatic filariasis may be diagnosed via microscopic detection of
microfilaria on blood smears obtained at night. In addition, adult worms or
microfilaria may be detected with skin biopsy, and ultrasonography can
sometimes be used to detect adult worms. Nocturnal microfilaria of W. bancrofti
and B. malayi may be provoked to enter the bloodstream during the day with a
one-time dose of diethylcarbamazine citrate (DEC). Blood examination should
be performed 30 to 60 minutes after administration of DEC. PCR and
immunologic testing are also available. The drug of choice for lymphatic
filariasis is DEC (2 mg/kg/dose three times daily after food for 12 days; there is
no maximum adult dose). Ivermectin (150 μg/kg; there is no maximum adult
dose) is effective against the microfilaria of W. bancrofti but has no effect on the
adult worm. Consequently, combination therapy with DEC-ivermectin or
ivermectin-albendazole is needed for suppression of microfilaremia. TPE is
treated with DEC for 12 to 21 days. DEC is no longer commercially available in
the United States but can be obtained through the CDC (404-718-4745).
Paradoxical worsening, including encephalopathy, can occur during treatment,
especially in patients with high organism burdens. Standard precautions exist for
isolation of patients with lymphatic filariasis. There is no human-to-human
transmission of microfilaria and adult worms with the exception of transfusion
with infected blood.
Onchocerciasis (river blindness) is caused by Onchocerca volvulus and
transmitted by Simulium blackflies. Approximately 18 million people worldwide
are infected, over 500,000 have severe visual disability. Clinical manifestations
may be dermatologic or ocular. Skin manifestations present as a pruritic rash
with multiple papules that may resolve spontaneously or continue to spread.
Painless, firm, mobile granulomas may develop in subcutaneous tissue, but
rarely cause morbidity. Ocular lesions involve both the anterior and posterior
segments. Anterior segment lesions result from an acute inflammatory reaction
around microfilariae and are reversible with therapy. Posterior segment lesions
involve the optic nerve and chorioretinitis and may result in blindness. Diagnosis

can be made clinically. Laboratory confirmation may be sought via PCR or
microscopic examination of skin snips for microfilariae. The diagnosis is
primarily clinical, as microfilariae may not be present in patients with
lymphedema. Treatment is with ivermectin in a single dose of 150 μg/kg (there
is no maximum adult dose). DEC can cause adverse ophthalmic reactions and is
contraindicated in onchocerciasis. Standard precautions should be used.

SEXUALLY TRANSMITTED INFECTIONS


STIs are the most commonly reported infections in the United States and
represent an important pediatric problem, particularly during infancy or
adolescence. This chapter focuses on HIV, syphilis, HSV outside the neonatal
period, and neonatal chlamydia and gonorrheal infections and nongenital
gonorrheal infections. STIs causing pelvic inflammatory disease and cervicitis
are covered elsewhere (Chapter 92 Gynecology Emergencies ) and management
of STIs in the abused child is discussed in Chapter 87 Child Abuse/Assault . In
these children, the most common pathogens are Trichomonas, C. trachomatis,
and Neisseria gonorrhea, and one study in sexually abused girls found that 8%
of girls had one or more STIs. As many adolescents with one STI can be infected
with more than one pathogen, identification of one STI should prompt diagnostic
evaluation for others. The manifestations, diagnosis, and treatment of common
STIs are described in Table 94.22 .

Chlamydia, Neonatal
C. trachomatis can cause a number of syndromes in infants: conjunctivitis,
trachoma, and pneumonia. Chlamydia is the most common STI in the United
States, and adolescent females comprise the most at-risk group. Vertical
transmission occurs in up to 50% of infants born to infected mothers. Chlamydia
conjunctivitis is characterized by a serous, slightly purulent eye discharge that

can be first noticed within 5 days to several weeks after delivery. There is
conjunctival injection and lid edema. The drainage typically lasts 1 to 2 weeks.
Approximately 30% of children with neonatal chlamydia conjunctivitis also will
have chlamydial pneumonia. Chlamydia conjunctivitis and trachoma are not
prevented by erythromycin that is given in the immediate newborn period to
prevent ophthalmia neonatorum (see below). Trachoma is a sequela of chronic
chlamydial eye infection and is characterized by corneal neovascularization
which can result in blindness. While rare in the United States, trachoma is the
leading infectious cause of blindness globally, estimated to impact up to 80
million persons. C. trachomatis pneumonia occurs most commonly from 2
weeks to 5 months after birth and is characterized by an afebrile illness with
repetitive, paroxysmal cough similar to pertussis. In contrast to pertussis,
leukemoid reactions are rare, but eosinophilia can be seen. Upper respiratory
tract symptoms are common from chlamydial colonization of the nasopharynx.
Radiographic findings may include hyperinflation and patchy interstitial
infiltrates. The diagnosis is made on the basis of direct fluorescent antibody
(DFA) testing, the only FDA-approved test for the detection of C. trachomatis
from nasopharyngeal and conjunctival specimens. The treatment of chlamydia