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The Pediatric Infectous Disease Journal® Newsletter: May 2009

Nelson, John D. M.D.; McCracken, George H. Jr. M.D.

The Pediatric Infectious Disease Journal: May 2009 - Volume 28 - Issue 5 - p A5
doi: 10.1097/01.inf.0000350905.10912.ea
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In the March 2009 Newsletter we mentioned 5 cases of invasive Haemophilus influenzae type b (Hib) infections that occurred in 2008 in Minnesota. On March 18, 2009 the Centers for Disease Control and Prevention (CDC) in Atlanta, GA reported that there had been an additional 5 cases reported from Philadelphia, PA with two deaths. All of the Philadelphia cases occurred since October 2008 and were unvaccinated or under-vaccinated. These 10 cases are vivid reminders of the severity of invasive Hib diseases and the importance of complete immunization against this organism. Since December 2007 there has been a nationwide shortage of Hib vaccine resulting in under-immunization of an unknown number of infants and children. The CDC and American Academy of Pediatrics have strongly recommended that the primary series of 3 doses be given at 2 month intervals in infancy as a means to reduce nasopharyngeal colonization and invasive disease. The booster dose at 12 to 15 months should be deferred except in high risk patients. The shortage is unfortunate because it is the booster dose that ensures systemic immunity and reduces the likelihood of colonization in early childhood.

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In a 2 week period in mid March of this year we encountered 4 interesting cases of bacterial meningitis. The first was a 2 month old infant who had preseptal cellulitis and sepsis. The CSF contained 2100 WBC/μL and a protein of 236 mg/dl and blood and CSF cultures grew MRSA. A cranial MRI revealed multiple small orbital abscesses and a transverse sinus thrombosis. He had surgical drainage of the orbit and will receive at least 4–6 weeks of vancomycin and rifampin therapy. Optimal management of MRSA meningitis is uncertain. The second patient was a 23 month old, fully immunized male who developed influenza A infection and otitis media. Because of the infant's somnolence his pediatrician performed a lumbar puncture that revealed 3900 WBC/μL, a glucose value of 0 mg/dl and very many Gram-positive cocci in pairs, the last two being poor prognostic findings. The blood and CSF cultures grew Streptococcus pneumoniae, serotype 7 that was susceptible to penicillin and cefotaxime. Despite prompt therapy he developed cerebral and cellebellar infarcts. The third patient was a 1 year old girl with acute lymphocytic leukemia receiving intense chemotherapy. She developed fever during neutropenia and a central venous catheter culture yielded small Gram-positive rods thought at first to be a catheter infection. The organism was identified as Listeria monocytogenes, at which time we were consulted and advised a second blood culture and a lumbar puncture. The CSF had 600 WBCs, mostly neutrophils and Gram-positive rods were seen on stained smear. The blood and CSF cultures grew Listeria and the patient was treated with ampicillin and gentamicin for 8 days and ampicillin alone for an additional 6 days. We have seen very few cases of Listeria meningitis beyond the neonatal period, but this is one of the settings (immunosuppresion) in which it can occur. The fourth case was a 2 week old male who had failed to regain his birth weight, but otherwise seemed well. His pediatrician did a urine culture that grew Citrobacter species; this observation prompted him to order a cranial CT scan that revealed multiple abscesses. The CSF was abnormal and both it and material from one of the abscesses grew C. kooseri on culture. This is a classic presentation except the usual pathogen is C diversus.

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Because acute mastoiditis was commonly seen in the pre-antibiotic period it was assumed that untreated otitis media was the predisposing event. This does not appear to be the only explanation as shown in an excellent retrospective cohort study using the United Kingdom General Practice research database (Pediatrics 2009;123:424). There were 2,622,348 children between the ages of 3 months and 15 years enrolled from 1990 through December 2006. Mastoiditis was noted in 854 patients, giving an approximate incidence of 1.2 cases per 10,000 child-years that was stable during the study period. Only one-third of children had preceding otitis media and the incidence of mastoiditis was only two-fold higher in those with untreated otitis media (3.8 per 10,000) than in those with treated disease (1.8 per 10,000). The authors calculated that a UK practitioner would need to treat 4831 otitis media episodes to prevent one child from developing mastoiditis. We identified 57 cases of acute mastoiditis at Children's Medical Center Dallas in a 17 year period from 1983 through 1999 (Pediatr Infect Dis J 2001;20:376). Almost 40% of the Dallas patients had no history of previous episodes of otitis media. Both studies show that many patients with acute mastoiditis have no clearly defined predisposing condition for which antibiotics were prescribed.

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Arbor Pharmaceuticals Inc has recently introduced Xylarex®, an oral solution of xylitol for prevention of recurrent acute otitis media (AOM) in children. According to the manufacturer 1 teaspoon is to be administered by syringe 3 times daily as part of a normal diet following meals or snacks. The premise for its use comes from a study by Uhari and coworkers (Pediatrics 1998;102:879) in which children who received xylitol-containing gum, syrup or lozenge 5 times daily for 2 to 3 months had one-third fewer episodes of AOM and antibiotic prescriptions than did those given placebo. These authors showed that the same total daily amount of xylitol given in 3 divided doses for 3 months was ineffective during the respiratory infection season in preventing recurrent episodes of AOM (Pediatr Infect Dis J 2007;26:423). Will Xylarex® work? We are skeptical because for the product to be effective the parent must inject it slowly into the mouth over 5 minutes 3 times daily for many weeks. We doubt that the target age group of infants and young children will tolerate this, not to mention the frustration of parents in trying to accomplish this feat.

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The word “coccidioidomycosis” triggers thoughts of the San Joaquin Valley in the minds of many physicians, but the geographic spread in the U.S. is considerably greater than the southern California area: Arizona, Utah, Nevada, New Mexico, and western Texas. The diagnosis of coccidioidal disease in California increased greatly in the 2000–2007 period (MMWR 2009;58:105). The reasons are not clear but speculations center around environmental and climate changes, soil disturbance by construction activities, and increased numbers of immunocompromised persons among other things. Diagnosis of coccidioidal pneumonia is difficult because the signs and symptoms mimic viral pneumonias and the disease spontaneously remits in most patients. In 2006 there was a report from Tucson, Arizona that coccidioidomycosis accounted for 29% of 55 patients who were evaluated for community acquired pneumonia (Emerg Infect Dis 2006;12:1958). That experience was not a fluke occurrence according to a similar report from the Mayo Clinic in Scottsdale, Arizona (Emerg Infect Dis 2009;15:397). Investigators evaluated patients 18 years of age and older for community acquired pneumonia with paired acute and convalescent serologic tests for Coccidioides anitibodies and found positive results in 17%. Similar studies in children would be interesting to pursue. Coccidioides risk areas are popular tourist destinations and the incubation period is 2 weeks to as long as a month. Bear that in mind when evaluating patients with acute pneumonia.

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Plasmodium knowlesi may be joining P. vivax, p. falciparum, P. ovale and P. malariae as a cause of malaria in humans (MMWR 2009;58:229). P. knowlesi is a simian species, so it is not surprising that human cases of infection with this species have been reported from Singapore, Thailand, Burma, Malaysia and the Philippines. A recent case diagnosed in New York was acquired in the Philippines. Simian species are susceptible to chloroquine and other antimalarials.

© 2009 Lippincott Williams & Wilkins, Inc.