Patrick M. Meyer Sauteur

Risk factors for invasive reptile-associated salmonellosis in children.

Reptile-associated salmonellosis (RAS) in children has been reported primarily due to direct contact with turtles, but recently also due to indirect contact with more exotic reptiles, causing disease in infants. To evaluate risk factors for RAS, we reviewed the RAS cases published in the literature since 1965. A case was defined as a child ≤18 years of age with an epidemiological link by identification of Salmonella enterica in cultures from both the affected child and the exposed reptile. We identified a total of 177 otherwise healthy children (median age 1.0 years, range 2 days to 17.0 years). RAS manifested mainly with gastrointestinal disease, but 15% presented with invasive RAS, including septicemia, meningitis, and bone and joint infection. The children with invasive RAS were significantly younger than children with noninvasive disease (median age 0.17 and 2.0 years, p<0.0001). RAS is most frequently seen after exposure to turtles (42%). However, children with invasive RAS had been exposed more often (p≤0.001) to reptiles other than turtles, including iguanas, bearded dragons, snakes, chameleons, and geckos. Children exposed to those latter reptiles usually kept indoors were younger than children exposed to turtles mostly kept outdoors (p<0.0001). RAS in children is significantly associated with invasive disease at young age, in particular infants <6 months of age. Exposure to reptiles, other than turtles, kept indoors is associated with RAS at younger age and more invasive disease. This finding is helpful for recognizing or even preventing invasive RAS in young infants that are at highest risk.

Antibody Responses to Mycoplasma pneumoniae: Role in Pathogenesis and Diagnosis of Encephalitis?

1 Department of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Erasmus MC–Sophia Children’s Hospital, University Medical Center, Rotterdam, The Netherlands, 2 Laboratory of Pediatrics, Erasmus MC–Sophia Children’s Hospital, University Medical Center, Rotterdam, The Netherlands, 3 Division of Infectious Diseases and Hospital Epidemiology, University Children’s Hospital of Zurich, Zurich, Switzerland, 4 Children’s Research Center (CRC), University Children’s Hospital of Zurich, Zurich, Switzerland, 5 Department of Neurology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands, 6 Department of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands, 7 TU Dresden, Medical Faculty Carl Gustav Carus, Institute of Medical Microbiology and Hygiene, Dresden, Germany, 8 Erasmus University College, Erasmus University, Rotterdam, The Netherlands

Mycoplasma pneumoniae and mucositis – part of the Stevens‐Johnson syndrome spectrum

Background: Mycoplasma pneumoniae may induce mucosal inflammation, referred to as M. pneumoniae‐associated mucositis (MPAM). There is no generally accepted definition of MPAM, since there may be mucosal lesions only, or mucosal and minimal skin lesions.

Infection with and Carriage of Mycoplasma pneumoniae in Children.

“Atypical” pneumonia was described as a distinct and mild form of community-acquired pneumonia (CAP) already before Mycoplasma pneumoniae had been discovered and recognized as its cause. M. pneumoniae is detected in CAP patients most frequently among school-aged children from 5 to 15 years of age, with a decline after adolescence and tapering off in adulthood. Detection rates by polymerase chain reaction (PCR) or serology in children with CAP admitted to the hospital amount 4–39%. Although the infection is generally mild and self-limiting, patients of every age can develop severe or extrapulmonary disease. Recent studies indicate that high rates of healthy children carry M. pneumoniae in the upper respiratory tract and that current diagnostic PCR or serology cannot discriminate between M. pneumoniae infection and carriage. Further, symptoms and radiologic features are not specific for M. pneumoniae infection. Thus, patients may be unnecessarily treated with antimicrobials against M. pneumoniae. Macrolides are the first-line antibiotics for this entity in children younger than 8 years of age. Overall macrolides are extensively used worldwide, and this has led to the emergence of macrolide-resistant M. pneumoniae, which may be associated with severe clinical features and more extrapulmonary complications. This review focuses on the characteristics of M. pneumoniae infections in children, and exemplifies that simple clinical decision rules may help identifying children at high risk for CAP due to M. pneumoniae. This may aid physicians in prescribing appropriate first-line antibiotics, since current diagnostic tests for M. pneumoniae infection are not reliably predictive.

Mycoplasma pneumoniae triggering the Guillain-Barré syndrome: A case-control study.

Guillain‐Barré syndrome (GBS) is an acute postinfectious immune‐mediated polyneuropathy. Although preceding respiratory tract infections with Mycoplasma pneumoniae have been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear. We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against galactocerebroside (GalC), which cross‐reacted with the isolate. This case prompted us to unravel the role of M. pneumoniae in GBS in a case‐control study.

Mycoplasma pneumoniae intrathecal antibody responses in Bickerstaff brain stem encephalitis.

The pathogenesis of Mycoplasma pneumoniae encephalitis is not established. We report, for the first time, the case of a patient with severe Bickerstaff brain stem encephalitis in whom we detected intrathecal production of M. pneumoniae-specific antibodies, contrasting the findings in another patient with less severe encephalitis in whom we detected intrathecal M. pneumoniae DNA but no specific antibodies. Our observations suggest that intrathecal M. pneumoniae-specific antibody responses may contribute to a more severe course of M. pneumoniae encephalitis.

Survey of macrolide-resistant Mycoplasma pneumoniae in children with community-acquired pneumonia in Switzerland.

Mycoplasma pneumoniae is a leading cause of communityacquired pneumonia (CAP) in children and macrolides are recommended for this entity [1]. Extensive macrolide use led to the rapid, worldwide emergence of macrolide-resistant M. pneumoniae (MRMP) [2] with rates of over 90% in Asia (China, 2012 [3]) and up to 26% in Europe (Italy, 2010 [4]). The first two cases of MRMP in Switzerland were reported in adults in 2012 [5]. We aimed to assess the presence of MRMP in children with CAP.

Severe childhood Guillain‐Barré syndrome associated with Mycoplasma pneumoniae infection: a case series

We report seven children with recent Mycoplasma pneumoniae infection and severe Guillain‐Barré syndrome (GBS) that presented to two European medical centres from 1992 to 2012. Severe GBS was defined as the occurrence of respiratory failure, central nervous system (CNS) involvement, or death. Five children had GBS, one Bickerstaff brain stem encephalitis (BBE), and one acute‐onset chronic inflammatory demyelinating polyneuropathy (A‐CIDP). The five patients with severe GBS were derived from an original cohort of 66 children with GBS. In this cohort, 17 children (26%) had a severe form of GBS and 47% of patients with M. pneumoniae infection presented with severe GBS. Of the seven patients in this case series, five were mechanically ventilated and four had CNS involvement (two were comatose). Most patients presented with non‐specific clinical symptoms (nuchal rigidity and ataxia) and showed a rapidly progressive disease course (71%). Antibodies against M. pneumoniae were detected in all patients and were found to be intrathecally synthesised in two cases (GBS and BBE), which proves intrathecal infection. One patient died and only two patients recovered completely. These cases illustrate that M. pneumoniae infection in children can be followed by severe and complicated forms of GBS. Non‐specific clinical features of GBS in such patients may predispose a potentially life‐threatening delay in diagnosis.

Neuroinvasive Mycoplasma pneumoniae infection without intrathecal antibody response.

The pathogenesis of extrapulmonary Mycoplasma pneumoniae-associated neurologic disease is unclear. We present a case of acute meningoencephalitis in a 15-year-old girl with central nervous system invasion of the bacterium but without intrathecal antibody synthesis. Our observations suggest that in this setting M. pneumoniae infection can be self-limiting and mild despite invasion of the central nervous system.

Intrathecal antibody responses to GalC in Guillain-Barré syndrome triggered by Mycoplasma pneumoniae

Mycoplasma pneumoniae (Mp) triggers Guillain-Barré syndrome (GBS) and elicits anti-galactocerebroside (GalC) antibodies. Specifically anti-GalC IgG is associated with Mp-GBS, possibly because of its better ability to cross the blood-nerve barrier (BNB). We here investigated CSF for the presence of anti-GalC in GBS. Intrathecal anti-GalC was found in 46% of Mp-GBS patients (n=6/13), in contrast to 16% of GBS controls (n=4/25) and 0% of non-GBS controls (n=0/7). The antibodies most likely originated from increased BNB permeability and/or intrathecal synthesis. Intrathecal anti-GalC IgG was specifically associated with Mp-GBS, further supporting that anti-GalC IgG contributes to the pathogenesis of GBS.