Dengue type 2 outbreak in the south of the State of Bahia, Brazil: laboratorial and epidemiological studies

Nogueira, Rita Maria Ribeiro; Miagostovich, Marize Pereira; Schatzmayr, Hermann G.; Moraes, Gerusa C.; Cardoso, Floriene M. A.; Ferreira, Janete; Cerqueira, Vera; Pereira, Manuel

doi:10.1590/s0036-46651995000600006

Cited by 13 publications

(12 citation statements)

References 9 publications

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“…An increase in DHF was observed in 2003, when 23 796 dengue cases were reported, including 291 DHF cases and 20 deaths. This scenario was also observed in 2005 with 22 817 cases reported, including 195 DHF cases and 20 deaths (13)(14)(15)(16).…”

Section: Dengue Viruses In Other Brazilian Statesmentioning

confidence: 67%

Dengue viruses in Brazil, 1986-2006

Nogueira¹,

Araújo²,

Schatzmayr³

2007

Rev Panam Salud Publica

104

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A total of 4,243,049 dengue cases have been reported in Brazil between 1981 and 2006, including 5,817 cases of dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) and a total of 338 fatal cases. Although all Brazilian regions have been affected, the Northeast and Southeast regions have registered the highest number of notifications. DENV-1 and DENV-4 were isolated for the first time in the Amazon region of Brazil in 1981 and 1982. The disease became a nationwide public health problem following outbreaks of DENV-1 and DENV-2 in the state of Rio de Janeiro in 1986 and 1990, respectively. The introduction of DENV-3 in 2000, also in the state of Rio de Janeiro, led to a severe epidemic with 288 245 reported dengue cases, including 91 deaths. Virus strains that were typed during the 2002 epidemic show that DENV-3 has displaced other dengue virus serotypes and entered new areas, a finding that warrants closer evaluation. Unusual clinical symptoms, including central nervous system involvement, have been observed in dengue patients in at least three regions of the country.

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Section: Dengue Viruses In Other Brazilian Statesmentioning

confidence: 67%

Dengue viruses in Brazil, 1986-2006

Nogueira¹,

Araújo²,

Schatzmayr³

2007

Rev Panam Salud Publica

104

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“…Indeed, erroneous clinical diagnoses of ''rubella'' and of certain other acute febrile illnesses have persisted for months during epidemics that later were rec- ognized as dengue. 9,[24][25][26][27] An activated system of dengue surveillance in sentry hospitals may provide sufficient sensitivity to serve as the basis for rapid initiation of interventions in response to outbreaks. It may be that a sudden increase in the incidence of dengue-like disease can usefully signal a dengue epidemic, even where laboratory capabilities are lacking.…”

Section: Discussionmentioning

confidence: 99%

Vector densities that potentiate dengue outbreaks in a Brazilian city.

Pontes¹,

Freeman²,

Oliveira-Lima³

et al. 2000

The American Journal of Tropical Medicine and Hygiene

127

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Abstract. To identify the critical vector density that potentiates dengue outbreaks in an endemic site and to identify obstacles to anti-dengue activities, we correlated a series of dengue outbreaks in a Brazilian city with the intensity of its anti-vector source-reduction activities. The proportion of houses infested by vector mosquitoes correlated inversely with intensity of anti-mosquito interventions, and the vector population developed independently of rainfall. Local periods of drought promoted vector abundance in two ways: residents stored water in which vector mosquitoes could breed, and cholera outbreaks due to contaminated water diverted local health workers from routine anti-vector activities. One dengue outbreak became apparent to authorities more than two months after it commenced but would have been identified almost immediately had dengue-like disease in indicator hospitals been monitored. Active surveillance, therefore, offers a window of opportunity for promptly executed anti-dengue interventions. Source-reduction measures that suppress vector infestations to less than 1% of houses effectively avert outbreaks of dengue.

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“…The DENV-2 used in these experiments, isolated from a patient serum during an outbreak of the virus in the state of Rio de Janeiro in 1995, 12 was kindly provided by the Flaviviruses Laboratory of Fiocruz, Rio de Janeiro, Brazil. The virus, a non-mouse-adapted sample, was propagated in Aedes albopictus mosquito cell line monolayers (C6/36), with L-15 medium (Sigma, St Louis, MO, USA) supplemented with 1% non-essential amino acids, 10% tryptose phosphate broth and 10% fetal bovine serum, and maintained at 281C for 15 days.…”

Section: Materials and Methods Virusmentioning

confidence: 99%

“…The virus, a non-mouse-adapted sample, was propagated in Aedes albopictus mosquito cell line monolayers (C6/36), with L-15 medium (Sigma, St Louis, MO, USA) supplemented with 1% non-essential amino acids, 10% tryptose phosphate broth and 10% fetal bovine serum, and maintained at 281C for 15 days. Virus was identified by indirect immunofluorescence technique, using a type-specific DENV-2 monoclonal (3H5) antibody as described elsewhere, 12 and further tittered in C6/36 cells by Reed and Muench method (1938).…”

Section: Materials and Methods Virusmentioning

confidence: 99%

Hepatic damage associated with dengue-2 virus replication in liver cells of BALB/c mice

Paes

Lenzi

Nogueira

et al. 2009

Laboratory Investigation

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One difficulty in studying dengue virus (DENV) is the lack of an experimental model that reproduces the human disease. In a previous work, we have shown that BALB/c mice intraperitoneally inoculated with a DENV-2 isolate presented viremia and mild focal areas of liver injuries. In this study, mice were inoculated by the intravenous route and presented extensive damage areas in the liver tissue, which were evaluated by histopathological and ultrastructural analysis. Hepatic injury was noted mainly around the central vein and portal tracts. Damages consist of hepatocyte injury, including steatosis, swelling and necrosis. Further, erythrophagocytosis, intercellular edema and vascular damages were evident, including hemorrhage, which is characteristic of the dengue-induced hepatitis in human liver. Hepatic lesions were already noted 2 days post infection (p.i.), although effects were more extensive after the seventh day p.i. An increase in alanine aminotransferase and aspartate aminotransferase serum levels was detected 7 and 14 days p.i., respectively, and had correlation to hepatic lesions. Alterations caused by the DENV infection were self-limiting, with a remarkable reduction of all liver damages 49 days p.i. Virus antigens were detected in hepatocytes, Kupffer cells and vascular endothelium, suggesting virus replication in these cells. In situ hybridization, using a probe that anneals in the virus negative RNA strand, showed positive reaction in hepatocytes and vascular endothelium cells of infected mice, thus confirming virus replication in such cells. In general, results revealed that this mouse model reproduces some histopathological effects observed in humans and supports previous findings indicating virus replication in the hepatic tissue.

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Dengue type 2 outbreak in the south of the State of Bahia, Brazil: laboratorial and epidemiological studies

Cited by 13 publications

References 9 publications

Dengue viruses in Brazil, 1986-2006

Dengue viruses in Brazil, 1986-2006

Vector densities that potentiate dengue outbreaks in a Brazilian city.

Hepatic damage associated with dengue-2 virus replication in liver cells of BALB/c mice

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