Search

The introduction of a G1P[8] rotavirus vaccine in Recife, Brazil, caused a decrease in rotavirus detection from 27% (March-May, 2006) to 5.0% (March-May, 2007), with all strains becoming G2, against which less protection had been predicted.

Norovirus has captured increasing attention as an agent of childhood diarrhoea. However, it is not known whether norovirus causes as severe diarrhoea as rotavirus, particularly among children in developing countries. In a 1-year study conducted between May 2004 and April 2005 in Recife, Brazil, norovirus was detected by ELISA in 34/233 (15%) diarrhoeal children less than 5 years of age. The severity of clinical illness, as indicated by the presence of dehydration, the requirement for hospitalization, and the duration of hospital stay, was similar between children with norovirus and rotavirus infection. These data underscore the importance of norovirus as a cause of severe diarrhoea in children.

We identified 21 rotaviruses in 129 patients with diarrhea in a Brazilian city with high rotavirus vaccine coverage. All rotaviruses were genotype P[4]G2 with 1 mixed infection with P[NT]G9. Although virus predominance could have occurred randomly, the vaccine may be less protective against P[4]G2. Prospective surveillance is urgently needed.

In 2006, Brazil will initiate universal immunization of its 4-million infants with a live attenuated serotype G1P[8] human rotavirus vaccine. In anticipation of the national immunization program, this study was undertaken to characterize rotavirus strains circulating among children in Recife, one of the largest cities in the northeast region of Brazil. Group A rotaviruses were detected in 102 (35%) of 290 faecal specimens collected from children under 5 years of age who presented with acute diarrhoea during a 1-year period between May 2004 and April 2005. In addition to the globally common G1P[8] serotype that accounted for 49% of strains, emerging rotavirus serotypes G8P[6] and G9P[8] represented 2% and 29% of strains, respectively. Following cell culture adaptation, RNA-RNA hybridization demonstrated that two Brazilian G8P[6] rotavirus strains shared a high level of genomic RNA homology with Malawian G8P[6] strains, and a Brazilian G9P[8] strain was related most closely to a G9P[8] strain from India. The results suggest that certain rotavirus strains have a much wider global circulation than generally appreciated. Continued global spread of such strains might challenge the efficacy of current rotavirus vaccines.

Acute respiratory infections (ARI) are one of the most important causes of death in children. Human metapneumovirus (HMPV), a virus first described in 2001, has now been detected in almost all continents. HMPV causes bronchiolitis and pneumonia with a clinical spectrum similar to respiratory syncytial virus (RSV). We describe the incidence of HMPV and RSV during two consecutive seasons with a high incidence of ARI in Aracaju, Brazil. HMPV was responsible for 24% of cases of bronchiolitis in the 1st season (April-May 2002) but was not found in the 2nd year (April-May 2003). RSV was recovered from 61 (55%) children with ARI in 2002 and from 72 (68%) in 2003. Children with RSV bronchiolitis in 2002 had more hypoxia but less wheezing than in 2003. The incidence of HMPV and RSV genotypes causing bronchiolitis varied between the years. Long-term prospective studies are required to better describe the epidemiology of these viruses in children., (Copyright 2004 Liverpool School of Tropical Medicine)

We describe the epidemiologic and clinical characteristics of 111 children attending clinics and hospitals in Aracaju, northeast Brazil, with acute respiratory infections attributable to human metapneumovirus (HMPV), respiratory syncytial virus (RSV), or both in May and June 2002. Fifty-three (48%) children were infected with RSV alone, 19 (17%) with HMPV alone, and 8 (7%) had RSV/HMPV co-infections.

PCR tests were used to assign genomovar status to 39 non-cystic fibrosis (non-CF) and 11 CF Burkholderia cepacia complex isolates from patients in hospitals in Recife, Brazil. Non-CF isolates were assigned to genomovar IIIA (71.8%), genomovar I (15.4%), B. vietnamiensis (7.7%), and B. multivorans (5.1%). CF isolates were assigned to genomovar IIIA (18.2%), B. vietnamiensis (18.2%), and genomovar I (9.1%). Six CF isolates sharing recA PCR-restriction fragment length polymorphism (RFLP) and randomly amplified polymorphic DNA (RAPD) patterns could not be assigned to a genomovar. 16S rDNA sequence obtained from these isolates indicated a closest relationship to B. anthina, but the recA sequence was equally divergent from several genomovars. PCR screening indicated the presence of cblA in only two isolates, whereas the B. cepacia epidemic strain marker was found in 22 of 28 genomovar IIIA isolates. A type III secretion gene was detected in all but genomovar I isolates. RAPD and PCR-RFLP assays, targeting both recA and fliC, indicated a large amount of genetic variability among the isolates, with many novel patterns being observed. Nine genomovar IIIA isolates from different non-CF patients and clinical sources had identical genotypes, indicating the presence of a common clone.

Although oral rehydration therapy greatly reduces mortality from diarrhoeal diseases, it has little effect on stool frequency. However, there is mounting evidence that zinc is an effective adjunct to the treatment of diarrhoea, although few studies have examined its efficacy in Latin America. This study assessed the efficacy of zinc supplementation in children with acute diarrhoea in Brazil. The study was a double-blind, placebo-controlled, randomised, clinical trial in children <5 years of age attending emergency services in Sergipe, Brazil. Subjects received zinc or vitamin C as placebo. There was a marked reduction in the duration of the diarrhoea (1.1 vs 2.6 days) and of watery stools in the zinc-supplemented group. The efficacy of zinc was independent of the presence of viral enteropathogens in the stools. It is concluded that, similar to studies in India and Bangladesh, zinc could be an important adjunct for treating acute diarrhoea in Brazilian children.

The tuberculin test (PPD) is used frequently in the diagnosis of tuberculosis. PPD, however, relies on an intact cell-mediated immunity and infected children often have false negative results. This study assessed whether a single oral zinc supplement modifies the PPD induration size and its association with nutritional status in Brazilian children. Ninety-eight children below 15 years of age who had been exposed to adults with smear-positive pulmonary TB in 1998 were tested by PPD in 1998 and 2000. Children were randomised in 2000 to receive a single oral dose of zinc sulphate or a placebo at the time of administering the PPD. Forty-three (44%) children were PPD-positive in 1998 and 54 (55%) in 2000. A higher proportion of children were classified as PPD-positive in 2000 in the zinc-supplemented group (57.1%) than in the placebo group (53.1%). PPD indurations were larger in children receiving zinc (mean 18.5 and 15.5 mm in the zinc and placebo groups, respectively) (p < 0.03). Mean induration sizes in 2000 were larger in zinc-supplemented children, regardless of their nutritional status. Our study demonstrates that zinc increases the PPD induration size in children irrespective of nutritional state. Zinc supplementation could work by correcting asymptomatic or marginal zinc deficiencies or as a non-specific booster of immunological mechanisms (whether or not there is a deficiency).

From a collection of cefotaxime-resistant Klebsiella pneumoniae isolated from neonatal blood culture specimens in a maternity hospital in Aracaju, Brazil, two isolates (strains KPBRZ-842 and -843, indistinguishable by pulsed-field gel electrophoresis) were found to produce beta-lactamases with isoelectric points (pI) of 5.4 and 8.2, respectively. Using a gel overlay method, cefotaxime hydrolysis was shown to be associated with the pI 8.2 protein. Nucleotide sequencing of the gene encoding the pI 8.2 beta-lactamase revealed a bla(SHV-ESBL)-type gene differing from the gene encoding SHV-1 by three silent point mutations, and a fourth that resulted in an amino acid substitution, aspartate for glycine, at position 156. This novel SHV-type extended-spectrum beta-lactamase is designated SHV-27.