Pediatric emergency medicine trisk 580

The diagnosis is made primarily via CT scanning or MRI demonstrating calcified, hypodense or ring-enhancing
larval cysts. Antibody assays detecting IgG to T. solium in the CSF and serum are the confirmatory diagnostic tests
available via the CDC and multiple commercial laboratories. Serum serologies are more sensitive than CSF
serologies.
Neurocysticercosis treatment has to be individualized on the basis of the number and viability of cysts present
on neuroimaging and where they are located. Calcified, or nonviable cysts, only require symptomatic treatment
and anticonvulsant therapy in children with seizures. Parenchymal cysts without enhancement typically respond to
antihelminthic treatment: albendazole (15 mg/kg/day, max 1,200 mg, in two doses for 14 days). Praziquantel (50
mg/kg/day in 3 doses × 9–13 days) should be considered for patients with >2 viable cysts. Albendazole is better
tolerated than praziquantel, is indicated for children of all ages, and does not interact with most antiepileptic
medications. One large meta-analysis found that antihelminthic treatment was associated with decreased seizure
frequency and more rapid radiographic resolution of granulomas that form around cysts. Coadministration of
corticosteroids for the initial 2 to 3 days of treatment is recommended if extensive CNS involvement is suspected,
but is not associated with improved neurologic outcomes. Clinicians should be aware that patients may have
paradoxical worsening during therapy, as most of the CNS effects of neurocysticercosis are immune mediated and
often worsen as the host inflammatory response is activated. Anticonvulsant therapy is recommended until
resolution of neurologic symptoms and patient has been seizure free for 2 years. Surgical excision is generally
recommended for intraventricular and ocular cysts. Standard precautions should be observed.

Rabies
Rabies is an almost uniformly fatal zoonotic infection caused by a rhabdovirus. While most commonly spread to
humans from dogs internationally (more than 95% of cases occur in Africa and Asia), the majority of U.S. cases
are caused by exposure to bats and wild carnivores (raccoons, skunks, foxes, coyotes). Among domesticated
animals, cats are reported as rabid three times more commonly than dogs. The incubation period is longer for bites
on the distal extremities than on the trunk or face. The two major clinical syndromes are furious and paralytic
rabies; each lasts approximately 2 to 10 days. Furious rabies consists of hyperesthesia at the bite site, agitation,
confusion, hallucinations, aerophobia, and hydrophobia; in the absence of an exposure history, early symptoms can
be difficult to differentiate from psychiatric illness. Paralytic rabies (approximately 30% of all cases) begins with
paresis of the muscles surrounding the bite site and progress to generalized paralysis. This form often is
underreported. There are a few case reports of rabies survivors (protocol available at www.mcw.edu/rabies ), but
treatment generally is supportive; contact precautions should be used. Pre-exposure prophylaxis with the rabies

vaccine is recommended for veterinarians and others at risk for bites from wild or domesticated animals. PEP
indications are summarized in
e-Table 94.21 and include both the rabies vaccine and receipt of rabies
immunoglobulin (RIG).
The diagnosis is clinical, with culture or PCR of stool or pharyngeal swabs serving as confirmatory tests.
Treatment is supportive. Contact precautions are recommended.

African Trypanosomiasis
African trypanosomiasis (“African sleeping sickness”) is a protozoal infection transmitted through the bite of the
tsetse fly. Wild animals serve as the reservoir for Trypanosoma brucei rhodesiense (East African trypanosomiasis),
whereas humans are the most important reservoir for Trypanosoma brucei gambiense (West African
trypanosomiasis). Clinical manifestations vary by subspecies. An erythematous swelling or chancre at the site of
the fly bite, intermittent high fevers, retrobulbar headache, posterior cervical adenopathy (Winterbottom sign),
myalgia, and myocarditis can be preceded by the meningoencephalitis. Chronic meningoencephalitis is associated
with behavioral changes, delusions, and the somnolence that result in the illness name. Laboratory findings include
anemia, thrombocytopenia, transaminitis, and, rarely, disseminated intravascular coagulation. During the acute
phase, trypomastigotes are often detectable on blood smears of buffy coats or aspirates of lymph nodes. Serologies
are not available for East African trypanosomiasis. Early treatment is essential because the prognosis is poor once
CNS involvement has occurred. In the absence of CNS disease, pentamidine is used for West African and suramin
for East African trypanosomiasis. CNS involvement requires use of eflornithine for West African and melarsoprol
for East African trypanosomiasis. Drugs for trypanosomiasis are difficult to obtain in the United States and care
should be coordinated via the CDC Drug Service: (404) 639-3670. Standard precautions are recommended.

CARDIAC INFECTIONS


Chagas Disease
Chagas disease, an infection caused by the protozoan parasite T. cruzi, is seen in Mexico and central and South
America. The parasite is transmitted through feces of infected triatomine insects (kissing bugs) after a blood meal.
The global prevalence is 8 to 10 million. The common initial presentation is a painless red nodule known as a

chagoma that develops at the site of initial inoculation. Most develop low-grade fever, generalized
lymphadenopathy, and malaise. Rare acute presentations include myocarditis, hepatosplenomegaly, edema, and
meningoencephalitis. While most cases resolve over 1 to 3 months, in approximately 20% of patients, serious
sequelae such as dilated cardiomyopathy, megaesophagus, and megacolon may occur years to decades after the
initial infection. Cardiac manifestations include pericardial effusion which can lead to tamponade physiology, left
ventricular aneurysms, abnormal diastolic function, contractile anomalies, and characteristic EKG findings (right
bundle branch block, left anterior block, AV block, sinus bradycardia, and ST segment, T- and Q-wave
abnormalities). Mortality is due to ventricular arrhythmias, complete heart block, congestive heart failure, or
emboli. Diagnosis is made via Giemsa staining of blood specimens or by direct wet mount prep. Serologies,
available via the CDC, are used to diagnose chronic Chagas. Treatment is with antitrypanosomal medications such
as benznidazole (for 30 to 90 days) or nifurtimox (for 90 to 120 days). The latter can be obtained from the CDC
under a compassionate use protocol: (404) 718-4745. Expert consultation is strongly recommended. Travelers
should avoid contact with the triatomine bug by utilizing insecticide and bed netting and avoiding habitation in
buildings constructed of mud, palm thatch, or adobe brick. Standard precautions are recommended.

RESPIRATORY TRACT INFECTIONS
The most common respiratory infections in returned travelers will be simple viral infections. However, knowledge
of the region of travel can alert clinicians to either common viruses with different seasonality in other hemispheres
(e.g., influenza virus in the middle of the calendar year in subequatorial nations) or for pathogens more common in
other settings. The latter includes tuberculosis (described earlier in the chapter), some vaccine-preventable diseases
more common in developing nations (e.g., diphtheria), and emerging infections, such as the coronaviruses causing
Severe Acute Respiratory Syndrome (SARS) and Middle Eastern Respiratory Syndrome (MERS), which were first
reported in Asia and the Middle East, respectively.

Coronaviruses (SARS, MERS)
Coronaviruses are common causes of mild upper respiratory tract infections, and are known to cause lower
respiratory tract disease, primarily in young or immunocompromised children. In 2002, SARS caused a febrile
illness associated with ARDS and a mortality rate that exceeded 50% in older adults. Disease severity was milder
in young children. Laboratory findings included leukopenia, elevated LDH, and elevated creatinine kinase. In
2012, MERS was first described in a Saudi Arabian man who died of ARDS. Symptoms include fever, chills,

myalgias, and a minority of patients develop diarrhea. Acute kidney injury and multiorgan failure can be seen.
Treatment is supportive. Contact and droplet precautions should be used.

Diphtheria
Diphtheria, a bacterial infection caused by an exotoxin-producing gram-positive bacillus, Corynebacterium
diphtheriae, remains an important disease in resource-poor countries and has experienced resurgence in recent
years in Russia, Haiti, and other countries. Diphtheria is spread via contact with respiratory secretions (airborne,
droplet, or direct contact) or skin lesions. Infection may lead to an asymptomatic carrier state, respiratory disease,
or cutaneous disease. Faucial (nasopharyngeal) diphtheria is the most common form of the disease and is
characterized by the gradual onset of a moderate fever, malaise, and pharyngitis in 80% with a gray-white
pseudomembrane usually covering one or both tonsils. A characteristic odor is usually present. Extensive
membranous pharyngitis may ensue, causing significant swelling of the tonsils, uvula, anterior neck, and regional
lymph nodes causing a “bull neck” appearance. Stridor can be seen with laryngeal involvement. Fever, if present at
all, usually is low grade. Severe complications are seen in approximately 10% of patients and include myocarditis
with arrhythmias or heart failure, or neuritis of the palatal, bulbar, or skeletal muscles. Baseline EKGs should be
obtained in a patient with suspected diphtheria. Cutaneous diphtheria is now more common than nasopharyngeal
disease in the West, with recent resurgence seen in homeless persons in the United States. Chronic, painless
nonhealing scaly rashes with well-demarcated borders or ulcers with a gray membrane appearance characterize
skin involvement.


The diagnosis is made clinically and confirmed by culture. The laboratory should be notified that diphtheria is
suspected, as the organism has specific culture requirements (cysteine-tellurite blood agar or modified Tinsdale
agar). Treatment involves administration of IV equine antitoxin (after tests for sensitivity to horse serum are
performed, as allergic reactions can be seen in up to 20% of patients) and antibiotics. Antibiotic treatment with
erythromycin (oral or parenteral) or penicillin G IM or IV for 14 days will stop toxin production and prevent
dissemination. Cutaneous lesions should be thoroughly washed with soap and water and treated with antimicrobial
treatment as discussed above. Household contacts and providers, irrespective of their immunization status, should
receive nasopharyngeal cultures and be offered PEP with either oral erythromycin or intramuscular penicillin G.
Persons receiving PEP also should be offered a booster dose of a diphtheria-containing vaccine. Droplet

precautions are recommended for all patients and carriers with pharyngeal diphtheria until nasopharyngeal cultures
collected 24 hours after completing antimicrobial treatment are negative.

Hantavirus
Hantaviruses are members of the Bunyaviridae family and are spread by infected rodents. Two different syndromes
have been reported: hemorrhagic fever with renal syndrome (HFRS) and Hantavirus cardiopulmonary syndrome.
The clinical features of HFRS include fever, hemorrhage, hypotension, and renal failure. The clinical features of
Hantavirus cardiopulmonary syndrome consist of a 2- to 8-day prodrome, and a febrile phase associated with
diffuse interstitial edema with respiratory compromise developing within 72 hours. Patients may develop chills,
headaches, vomiting, myalgia, and diarrhea. Symptoms typically seen with upper respiratory tract infections are
notably absent, except for cough. Laboratory findings include a neutrophilic leukocytosis with bandemia,
thrombocytopenia, and increased hemoglobin. Renal manifestations include proteinuria and hematuria. The
diagnosis is serologic. Treatment is supportive. Mortality rates approaching 40% have been reported for
Hantavirus cardiopulmonary syndrome, whereas death from HFRS is rare. Standard precautions are recommended;
it has not been associated with healthcare transmission or person-to-person infection.

Lymphadenopathy
The differential diagnosis for lymphadenopathy in the returned traveler is broad, and should include both
pathogens endemic to the region of travel as well as infectious agents with a global distribution. Most returned
travelers with infectious adenopathy will have viral etiologies, similar to the epidemiology in children who have
not traveled. However, there are some systemic diseases for which the initial manifestations may be
lymphadenopathy or lymphadenitis. These are summarized below. Filarial diseases, which cause lymphedema, are
discussed separately later in the chapter.

Measles
Measles is caused by a paramyxovirus that is transmitted by droplet and airborne routes. It is one of the most
contagious infectious diseases. Approximately 1 million children per year develop measles globally, with an
estimated 120,000 deaths, primarily in children less than 5 years of age who live in tropical regions. In recent
years, more cases have been seen in industrialized countries due to un- or undervaccinated children. The
incubation period is 8 to 12 days. Transmission is directly from respiratory secretions and cases are infectious only

during the early stages of illness. Children present with fever, upper respiratory tract symptoms, nonpurulent
conjunctivitis, and an erythematous blanchable rash that begins on the head and moves in a cephalocaudal manner.
The presentation can mimic that of Kawasaki disease. Oral lesions (Koplik spots) are transient and not seen in all
children. Acute complications include pneumonitis and meningoencephalitis, and the dreaded delayed
complication is subacute sclerosing panencephalitis (SSPE), associated with irreversible neurocognitive decline
years–decades after the initial infection. The diagnosis is primarily clinical, with confirmatory serologies available.
Treatment is supportive. In developing nations, the use of vitamin A daily for 2 days has been associated with
reductions in morbidity and mortality. Any child with suspected measles should be placed in a negative-pressure
room and airborne precautions taken by providers for 4 days after the onset of rash. Exposed susceptible patients
should be placed on airborne precautions from day 5 after the first exposure until 3 weeks after the last exposure.

Mumps
Mumps is caused by a paramyxovirus transmitted by infected respiratory tract secretions. Humans are the only
known natural host. Mumps occurs worldwide (peaking in the winter), although there has been a significant
reduction in the number of cases in the United States since the introduction of the mumps vaccine in 1977. In
2018, over 2,200 cases were reported in the United States. Approximately 20% are asymptomatic. The incubation


period is approximately 2 weeks; children then develop a nonspecific prodrome of myalgia, low-grade fever, and
headache. Subsequently, there is a swelling of the salivary glands (primarily parotid glands). However, multiorgan
involvement (epididymitis, prostatitis, oophoritis, mastitis, myocarditis, hearing impairment, hepatitis, pancreatitis,
thyroiditis, and arthritis) can be seen. Diagnosis is made clinically, with confirmatory laboratory PCR and serology
testing available. Treatment is supportive. The infectious period is from 3 days prior to onset of symptoms to the
4th day of active disease. Standard and droplet precautions are recommended.

Brucella
Brucellosis is a systemic infection caused by the bacteria in the genus Brucella, small gram-negative aerobic
bacilli. Brucella is a zoonotic infection of livestock that is most common in the Mediterranean region, Indian
subcontinent, and Latin America. Brucella can be transmitted via inhalation of aerosols, mucosal or skin contact,
or ingestion of unpasteurized dairy products, raw meat, liver, or bone marrow. Symptoms include fever, night

sweats, malaise, anorexia, headache, abdominal pain, and myalgia. Complications include meningitis, arthritis,
osteomyelitis, and endocarditis. Diagnosis is made by isolation of the organism from the blood and acute and
convalescent titers; the laboratory should be instructed that Brucella is suspected, as cultures need to be incubated
for a minimum of 4 weeks. Treatment of children consists of combination therapy with TMP-SMZ and rifampin
for at least 4 to 6 weeks. Adolescent and adult patients are preferably treated with either doxycycline or TMP-SMZ
and rifampin; an aminoglycoside should be added for the first 14 days of therapy in cases of suspected meningitis,
endocarditis, and osteomyelitis. Rifampin monotherapy is not recommended for concern for selecting for antibiotic
resistance. Standard precautions can be used.