SANJEEV K. SWAMI
HISTORY OF PRESENT ILLNESS
The patient, a 2-year-old girl, was well until 1 month prior to admission, when she began to experience intermittent periods of abdominal pain. The pain was dull and diffused throughout the entire abdomen. It did not awaken her at night. One week prior to admission, the patient experienced mucousy, nonbloody diarrhea twice per day. URI symptoms developed 2 days prior to admission. A sibling had a “cold.” The patient’s family brought her to the primary medical doctor with complaints of fever and worsening abdominal pain. A three-pound weight loss history was elicited. There was a strong history of pica, specifically geophagy. The family has two cats and a new puppy.
History is significant for breath-holding spells (none recently) with an extensive work-up that included a normal EEG, a normal Holter monitor, and a normal ECG. Per her parents, growth was always “a concern.” No other information was available with regard to her growth. She had no history of surgery and no drug allergies; her immunizations were up-to-date, and there was no significant family medical history.
T 37.8°C; HR 120 bpm; RR 20/min; BP 92/62 mmHg
In general, the patient was an alert but pale child. The neck was supple. There was no prominent cervical adenopathy, and the trachea was midline. The lung fields were clear, and the cardiac examination was unremarkable, with no murmurs, rubs, or gallops. Abdominal examination revealed a soft and nontender abdomen with good bowel sounds, a palpable spleen tip, and a liver edge that was about 2 cm below the right costal margin. The patient was a Tanner I female, and the rectal examination revealed good tone, no tenderness on examination, no fissures, no masses, and a small amount of stool in the vault. Neurologic examination was normal.
Complete blood count revealed a white blood count of 39 800/mm3 with 1% band forms, 18% segmented neutrophils, 53% eosinophils, 17% lymphocytes, 3% basophils, the hemoglobin was 7.8 g/dL; hematocrit, 29.4% (MCV of 52.7 fL, MCHC of 29.7 pg, RDW of 19.5%), and platelets of 1 000 000/mm3. Erythrocyte sedimentation rate was 20 mm/h.
COURSE OF ILLNESS
Chest and abdominal radiographs were normal, stool for ova and parasites as well as culture were pending. Serum immunoglobulins were elevated. Anti-A and anti-B isohemagglutinins were markedly elevated (A = 1:16,000, B = 1:512). ELISA was pending. The patient was discharged home after a normal ophthalmologic examination with outpatient follow-up to monitor the eosinophilia.
DISCUSSION CASE 7-6
Diseases that are transmitted from animals to humans are called zoonoses. The presence of pets in more than 50% of homes in the United States, and the acquisition of zoonoses via fecal-oral or direct contact puts children at higher risk for these infections. While this patient had a history of abdominal pain and diarrhea, the most important pieces of history were the family’s pets and the patient’s history of geophagia. Zoonotic diseases that are transmitted via the fecal-oral route and cause gastroenteritis in children include salmonellosis (Salmonella sp., approximately 5 million cases per year), campylobacteriosis (C jejuni), cryptosporidiosis (Cryptosporidium parvum), giardiasis (Giardia sp. found in 8% of children in US day care centers), dog tapeworm (Dipylidium caninum), and visceral larval migrans.
The clinical history along with laboratory abnormalities supported a diagnosis of visceral larva migrans.
INCIDENCE, EPIDEMIOLOGY, AND LIFE CYCLE
Visceral larva migrans or toxocariasis is caused by infection with dog ascarid (Toxocara canis) or cat ascarid (Toxocara cati). The reservoir for latent infection is usually female dogs. Toxocara eggs are passed in the feces of infected animals and require several weeks, depending on environmental conditions, to embryonate and become infective (Figure 7-6). Shedding rates vary from 13% to 75% for dogs and 21% to 55% for cats. Areas that usually harbor infectious ova include playgrounds and sandboxes where children might play. The disease in humans is primarily seen in children younger than 6 years, especially those with geophagus pica, who ingest soil that contain the larvae.
FIGURE 7-6. Lifecycle of Toxocara canis and Toxocara cati. (Courtesy of the Centers for Disease Control and Prevention, Division of Parasitic Diseases and Malaria—DPDx website: http://www.dpd.cdc.gov/dpdx/Default.htm.)
In the United States, children in kindergarten have been found to have antibody prevalence rates as high as 23% and a diagnosis of the disease is made in 3000 to 4000 patients per year. There are regional and socioeconomic variations with highest rates reported in the South and areas with higher rates of poverty.
The clinical spectrum of Toxocara infections varies from asymptomatic to primarily visceral to primarily ocular manifestations. Infectious eggs are ingested followed by penetration of gastric mucosa, incorporation into the portal circulatory system, and then spread into the systemic circulation. Damage from these traveling larvae and the marked eosinophilic response cause the clinical manifestations which can include fever, hepatosplenomegaly, abdominal pain, irritability, malaise, and pruritic rash. Pulmonary involvement can be seen in up to 86% of infected children and can be severe; it is often confused with asthma exacerbations, and visceral larva migrans may be an independent risk factor for asthma. Ocular complaints can occur alone and the subsequent strabismus, failing vision, uveitis, or endophthalmitis occur secondary to the local inflammatory response to the infection. The myocardium and central nervous system are also rarely affected.
The age of the child, history of contact with dogs, and geophagus are all important historical clues to the diagnosis. Definitive diagnosis with biopsy of affected tissue is rarely warranted, and the yield is low. Additional clues include elevated serum gamma-globulins, a high white cell count with eosinophilia, and elevated titers of anti-A or anti-B isohemagglutinin (seen in 50% of patients). Serology is the laboratory test of choice and a titer of greater than 1:32 has good sensitivity and specificity.
Treatment is controversial, and many children will improve without any specific therapy. Albendazole (10 mg/kg/day divided twice daily) has been used in the past but may lead to a more robust inflammatory response. Because of this, some experts recommend treatment with corticosteroids in addition to antiparasitic therapy if treatment is started. Prevention of repeat infection is crucial, and any affected pets should be treated promptly.
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