To the Editors: A 52-day-old male infant was admitted because of pyrexia. Initial physical examination revealed no bulging anterior fontanel and no skin rash. The white blood cell count was 9300/mm3 with 59% neutrophils, and C-reactive protein was 0.02 mg/dL. Vomiting and seizure developed on the next day, and a tense anterior fontanel was found. Leukopenia (white blood cell count, 2200/mm3) with markedly elevated C-reactive protein (16.6 mg/dL) was associated. The findings of cerebrospinal fluid analysis were compatible with bacterial meningitis and Gram-negative diplococci were seen. Intravenous cefotaxime therapy (300 mg/kg/d, in 4 divided doses) was started immediately. Blood and cerebrospinal fluid cultures yielded Neisseria meningitidis, serogroup B, which had intermediate resistance to penicillin but was susceptible to cefotaxime by disk diffusion. The second cerebrospinal fluid culture showed no growth, and the fever subsided on the seventh admission day. Secondary fever with frequent seizure activity developed on the 10th day of intravenous cefotaxime therapy. Brain computed tomography and magnetic resonance imaging revealed left frontoparietotemporal subdural empyema and multiple brain infarctions. Purulent material was evacuated by burr hole and craniectomy, and the patient became afebrile soon after the procedure. The bacterial culture of drained fluid yielded no microorganism. The intravenous antimicrobial therapy was continued for a total of 19 days. Brain computed tomography obtained after discontinuation of antibiotics showed fibrotic change without residual subdural empyema. He was discharged from our hospital with mild hemiparesis. There was no significant neurologic sequela noted when he returned to our outpatient clinics 2 months after discharge. Meningococcal meningitis is infrequently encountered in early infancy, possibly because of protection of maternal antibodies.1 Subdural empyema is extremely rare as a complication of meningococcal meningitis.2,3 From a search of the English literature on MEDLINE, we believe that this is the second description of subdural empyema, caused by N. meningitidis. In 1982, Edwards and Baker4 described a 3-month-old infant in whom relapse of meningococcal meningitis was accompanied by a right-sided subdural empyema. Arango and Rathore5 reported 2 cases of neonatal meningococcal meningitis and reviewed 45 cases in the literature between 1916 and 1996. It is suggested that skin rash is not common in meningococcal meningitis of neonates and early infancy.1,5 No cutaneous lesion developed in our case throughout the course. The mode of transmission of meningococcal disease to young infants remains unclear. They might be infected while passing through the maternal genital tract or by an airborne route.6 Nathoo et al3 reviewed 699 cases of intracranial subdural empyema, and none was caused by N. meningitidis. The majority of cases of the patients younger than 5 years old were associated with meningitis. In another study of subdural collections of fluid in acute bacterial meningitis of children, Haemophilus influenzae accounted for 74.3% of subdural empyema cases. There were 6 cases of meningococcal meningitis with subdural fluid collection, but none of them was defined as subdural empyema.2 Surgical drainage (burr holes or craniotomy) is the standard treatment of subdural empyema. The best method should be individualized and based on patients’ neurologic status, general condition, and preoperative neuroimaging findings.7 Current data suggest that 2–3 weeks of antibiotic therapy might be enough for uncomplicated cases.6 Jui-Shan Ma, MD Section of Infectious Diseases Department of Pediatrics Show-Chwan Memorial Hospital Taiwan, Republic of China
Parvovirus B19 virus commonly causes subclinical infection, but it can prove fatal to the fetus during pregnancy and cause severe anemia in an adult with hemolytic diseases. We present the case of a woman with autoimmune hemolytic anemia who was diagnosed with parvovirus B19-induced transient aplastic crisis during her second trimester of pregnancy and faced the high risk of both fetal and maternal complications related to this specific viral infection. To the best of our knowledge, the experience of successful intravenous immunoglobulin treatment for B19 virus infection during pregnancy, as in our case, is limited.A 28-year-old and 20-week pregnant Chinese woman with genetically confirmed alpha-thalassemia trait was diagnosed with cold antibody autoimmune hemolytic anemia and suffered from transient aplastic crisis caused by B19 virus infection. She received intravenous immunoglobulin treatment to reduce the risk of hydrops fetalis. Her peripheral blood reticulocyte percentage recovered, but anemia persisted, so she underwent several courses of high dose intravenous dexamethasone for controlling her underlying hemolytic problem. Finally, her hemoglobin levels remained stable with no need of erythrocyte transfusion, and a healthy baby boy was naturally delivered.Parvovirus B19 virus infection should be considered when a sudden exacerbation of anemia occurs in a patient with hemolytic disease, and the possible fetal complications caused by maternal B19 virus infection during pregnancy should not be ignored. Close monitoring and adequate management can keep both mother and fetus safe.
To the Editor: Choi et al. (1) conducted a study on sequence analysis of a partial rompB gene amplified from sera of humans who were seropositive for spotted fever group (SFG) and typhus group rickettsioses. They write, These finding suggested that several kinds of rickettsial diseases, including boutonneuse fever, rickettsialpox, R. felis infection, and Japanese spotted fever… are occurring in Korea.
These claims propagate some errors and may lead to an inadequate conclusion. First, rompB is conserved in Rickettsia spp. and consists of 4,968 bp with respect to the published sequence of the R. conorii strain Seven (2,3). Fournier et al. (4) amplified 4,682 bp of rompB and showed a high degree of nucleotide sequence similarity (99.2%) between R. africae and R. sibirica, R. pakeri, and R. slovaca. Choi et al. amplified ≈420 bp of rompB (position 3562–4077) for sequence analysis. This segment is located in a highly conserved region of the gene, which may decrease the ability to differentiate particular species from other SFG rickettsiae. This study cannot prove the existence of specific SFG rickettsioses until the results are confirmed further by, for example, isolating these SFG rickettsiae from humans, animals, or ticks in South Korea. Recently, the authors analyzed nucleotide sequences of 267-bp amplicons of rompB (position 4762–4496) obtained from patient sera and found that R. conorii could not be differentiated from R. sibirica (5). This finding also supports our concerns.
Second, although partial rompB nucleotide sequence analysis of rickettsiae obtained from 1 patient's serum showed 98.87% similarity with R. conorii strain Seven, the finding does not indicate boutonneuse fever is occurring in South Korea because high similarities (98.6%–99.8%) are found among 4 subspecies of R. conorii. Multilocus sequence typing can help differentiate among these subspecies (6).
This study provided a model to amplify SFG rickettsial DNA from sera of patients, and it will be helpful in surveillance of these diseases. However, the results should be interpreted more carefully in the context of clinical and epidemiologic data and combined with different gene sequence analyses to obtain a reliable and specific diagnosis.
Infected cephalohematoma associated with meningitis is rare in neonatal period. Herein we reported a case and the causative microorganism is Klebsiella pneumoniae. With intravenous ceftriaxone therapy and surgical drainage of the infected cephalohematoma, he was successfully treated and no sequel was reported. Early diagnosis of the association of meningitis is important and leads to a good prognosis. The reported cases of infected cephalohematoma with concurrent meningitis in literature are also reviewed.
Japanese Spotted Fever in KoreaJang and colleagues in 2004 claimed their study to be the first documentation of spotted fever group (SFG) rickettsiosis in Korea and indicated that Japanese spotted fever (JSF) was prevalent in Korea from 1992 to 1993 (1).I believe that some drawbacks exist in their study design and have drawn them to a premature and inadequate conclusion.This study was focused on Korean patients with acute febrile illness from December 1992 to November 1993.The diagnosis was made on the basis of indirect immunofluorescence assay in which only Rickettsia japonica and Orientia tsutsugamushi were used as rickettsial antigens.Overall, 676 (19.88%) out of 3,401 patients were found to have polyvalent antibody at a 1:40 serum dilution against R. japonica.In another study by the same group with the same study design, 546 (16.24%), 482 (14.34%), and 269 (8%) out of 3,362 patients were seropositive at the level of 1:40 dilution against R. akari, R. conorii, and R. sibirica, respectively (2).Because these serum samples of both studies were obtained from the same population from 1992 to 1993, there is significant overlapping in populations who were seropositive to individual SFG rickettsial antigens, obviously.However, the authors did not consider the effect of crossreactions between R. japonica and other SFG and typhus group rickettsiae.They did not analyze the antibody titers of other rickettsial antigens except O. tsutsugamushi in this study.In a recent study, the authors further demonstrated the existence of several SFG rickettsiae in sera of Korean patients by using a PCR-based amplification method (3).They collected 200 serum samples with immunoglobulin M titers of 1:40 to 1:160 against SFG rickettsial antigens from 1993 to 1999.Only one among them showed a sequence homologous to that of the partial rickettsial outer membrane protein B gene (rompB) of R. japonica.The significant discrepancy between results of serology and molecular methods may be caused by inadequate cutoff values and cross-reactions.It is reasonable that a significant part of these 676 seropositive patients should not be ascribed to JSF and further confirmatory tests are necessary.In other words, they have overestimated the seroprevalence of JSF in Korea and the epidemiological analysis which they made accordingly is inadequate.Though Paddock et al. have mentioned the concept, we would like to emphasize again that the serological tests are only group-specific and cannot be used to ascribe etiology to a specific pathogen of SFG rickettsiae (4).
Infected cephalohematoma associated with meningitis is rare in neonatal period. Herein we report a neonate with huge infected cephalohematoma associated with meningitis, which was caused by Escherichia coli. With intravenous antibiotic therapy and surgical drainage of the infected cephalohematoma, he became afebrile soon. Intravenous ceftriaxone therapy was continued for 21 days and no sequela was reported. It is suggested that meningitis should be considered in neonates with infected cephalohematoma.
To the Editor: Moran et al. write, In areas with a high prevalence of [community acquired methicillin-resistant Staphylococcus aureus], empiric treatment for skin and soft tissue infections (SSTIs) with β-lactam agents such as cephalexin may no longer be appropriate. Oral agents such as clindamycin or trimethoprim/sulfamethoxazole and rifampin should be considered in CA-MRSA (1). However, some studies have had different results. Lee et al. reported that 31 (84%) of 37 Texas children with SSTIs showed clinical improvement after incision and drainage, even though they received an ineffective antimicrobial agent that was not changed after the susceptibility results became available (2). These researchers also reviewed some reports with similar experience in the United States and further suggested that incision and drainage without adjunctive antimicrobial therapy were effective in immunocompetent children for SSTIs <5 cm in diameter.
To the Editors: An 8-year-old girl was admitted because of bacteremia and polyarthritis. Her blood and synovial fluid cultures yielded methicillin-resistant Staphylococcus aureus (MRSA). A 7-day course of intravenous vancomycin was prescribed during hospitalization and oral linezolid therapy (30 mg/kg/d in 3 divided doses) was continued for 3 weeks as outpatient antimicrobial therapy. Linear brownish discoloration over both incisors appeared 1 week after initiating linezolid therapy. It was not removable by dental cleaning. Dark brownish discoloration of the tongue developed 2 weeks after initiating linezolid therapy. Sparing of such discoloration was found in a small area over the tongue tip. Discoloration of the tongue and teeth persisted for 3 and 4 weeks, respectively. Aside from the discoloration, the girl tolerated linezolid therapy well. Finally, she had an uneventful recovery from MRSA bacteremia and polyarthritis. Vancomycin historically has been the treatment of choice for MRSA infections, but adverse effects, the need for intravenous access, and growing resistance limit its use. Oral formulation of linezolid provides a definite economic advantage over vancomycin, allowing earlier hospital discharge and reduced cost of outpatient care.1 Linezolid is believed to be useful and well-tolerated in the step-down therapy for pediatric patients with osteoarticular infections caused by MRSA and in those patients with intolerance to glycopeptides.2 Few adverse effects have been reported during linezolid therpay, such as gastrointestinal effects, myelosuppression, skin eruptions, and elevated liver enzymes.2,3 There are only 2 searchable case reports of linezolid-related tooth or tongue discoloration in the current English literature. Matson and Miller4 have reported an immunocompromised 11-year-old girl with tooth discoloration after receiving a 28-day course of linezolid. The discoloration was present on the enamel of her lower anterior teeth and was superficial and reversible with dental cleaning. Amir et al5 have reported a 65-year-old kidney transplant recipient experienced tongue discoloration after receiving a 14-day course of linezolid. The discoloration resolved 6 months after the discontinuation of linezolid. We believe this is the first case report of both teeth and tongue discoloration of linezolid therapy. This phenomenon seems to happen not only to immunocompromised but also to immunocompetent patients, such as the girl in this report. The discoloration can involve teeth and tongue simultaneously and is reversible after discontinuation of linezolid therapy. The discoloration lasted longer for teeth than for tongue and such discoloration was unremovable in this patient. Further studies are still need to establish the mechanism of such discoloration. However, we present this case to increase clinicians' awareness of the adverse event. Jui-Shan Ma, MD Show-Chwan Memorial Hospital Changhua, Taiwan
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