Infection by Schistosoma mansoni Sambon 1907 in the first four months of life of Biomphalaria straminea (Dunker, 1848) in Brazil.
(57/1021)
Compatibility between Schistosoma mansoni and Biomphalaria straminea when exposed to the parasite on the first four months of age was assessed for five parasitological aspects: indices of infection and mortality, duration of precercarial and cercarial periods, and rate of cercarial emission. Infections were made on molluscs from laboratory colonies, at the following ages: 8, 13, 18, 21, 53, 83 and 114 days. Two B. straminea colonies were used (Camorim, PE and Picos, PI), and one B. glabrata colony (Ressaca, MG) was used as control. The main results are as follows: (I) infection was significantly associated with mollusc age, being proportionally higher in sexually immature than in mature molluscs for the three colonies; (II) for B. straminea from Camorim, mortality did not differ significantly between infected and non-infected snails; for B. straminea from Picos significantly more deaths occurred among infected than among non-infected snails, while the opposite was observed for B. glabrata from Ressaca; (III) for the three colonies, the precercarial period was significantly shorter for immature molluscs than for mature ones; (IV) the duration of the cercarial period was extremely variable for the three colonies; (V) sexual maturity did not influence cercarial emission for the three colonies. (+info)
Short report: Schistosoma mansoni miracidia are killed by the defense system of an Argentine strain of Biomphalaria straminea.
(58/1021)
Biomphalaria straminea snails from Argentina fail to shed cercariae even if exposed to high doses of Schistosoma mansoni EC miracidia. Alternative explanations for this failure are that miracidia are unable to penetrate the snail's epithelium or that the miracidia are killed by the snail's defense system. To discriminate between these 2 possibilities, B. straminea snails were individually exposed to increasing doses of miracidia. Susceptible B. glabrata were used as controls. Exposed snails were fixed 12 hr after exposure, and histological sections of the whole specimens were examined. Miracidia were seen to penetrate the epithelium of B. straminea and B. glabrata at similar rates (14.7%), independent of the exposure level. Regardless of the miracidial dose, 94% of the penetrating miracidia appeared encapsulated by the B. straminea defense system, whereas in B. glabrata, only 42% of the miracidia underwent encapsulation. These results show that resistance of B. straminea to S. mansoni EC strain is due to an efficient defense system that destroys miracidia once they have penetrated. (+info)
Blood-sucking lice may disseminate Trypanosoma cruzi infection in baboons.
(59/1021)
Trypanosoma cruzi (Schyzotrypanum, Chagas, 1909), and Chagas disease are endemic in captive-reared baboons at the Southwest Foundation for Biomedical Research, San Antonio, Texas. We obtained PCR amplification products from DNA extracted from sucking lice collected from the hair and skin of T. cruzi-infected baboons, with specific nested sets of primers for the protozoan kinetoplast DNA, and nuclear DNA. These products were hybridized to their complementary internal sequences. Selected sequences were cloned and sequencing established the presence of T. cruzi nuclear DNA, and minicircle kDNA. Competitive PCR with a kDNA set of primers determined the quantity of approximately 23.9 +/- 18.2 T. cruzi per louse. This finding suggests that the louse may be a vector incidentally contributing to the dissemination of T. cruzi infection in the baboon colony. (+info)
Crohn's disease in Nottingham: a search for time-space clustering.
(60/1021)
All cases of Crohn's disease in the Nottingham area were ascertained and the date and place of domicile and work at the time of onset of symptoms noted. Applying the Knox and Pike and Smith tests for clustering of patients in time and space, no significant results were observed. Further analysis of differences in time-space clustering between a group of patients and matched controls is in hand. (+info)
Characterization of H5N1 influenza viruses that continue to circulate in geese in southeastern China.
(61/1021)
The H5N1 influenza virus, which killed humans and poultry in 1997, was a reassortant that possibly arose in one type of domestic poultry present in the live-poultry markets of Hong Kong. Given that all the precursors of H5N1/97 are still circulating in poultry in southern China, the reassortment event that generated H5N1 could be repeated. Because A/goose/Guangdong/1/96-like (H5N1; Go/Gd) viruses are the proposed donors of the hemagglutinin gene of the H5N1 virus, we investigated the continued circulation, host range, and transmissibility of Go/Gd-like viruses in poultry. The Go/Gd-like viruses caused weight loss and death in some mice inoculated with high virus doses. Transmission of Go/Gd-like H5N1 viruses to geese by contact with infected geese resulted in infection of all birds but limited signs of overt disease. In contrast, oral inoculation with high doses of Go/Gd-like viruses resulted in the deaths of up to 50% of infected geese. Transmission from infected geese to chickens occurred only by fecal contact, whereas transmission to quail occurred by either aerosol or fecal spread. This difference is probably explained by the higher susceptibility of quail to Go/Gd-like virus. The high degree of susceptibility of quail to Go/Gd (H5N1)-like viruses and the continued circulation of H6N1 and H9N2 viruses in quail support the hypothesis that quail were the host of origin of the H5N1/97 virus. The ease of transmission of Go/Gd (H5N1)-like viruses to land-based birds, especially quail, supports the wisdom of separating aquatic and land-based poultry in the markets in Hong Kong and the need for continued surveillance in the field and live-bird markets in which different types of poultry are in contact with one another. (+info)
Involvement of RNA2-encoded proteins in the specific transmission of Grapevine fanleaf virus by its nematode vector Xiphinema index.
(62/1021)
The nepovirus Grapevine fanleaf virus (GFLV) is specifically transmitted by the nematode Xiphinema index. To identify the RNA2-encoded proteins involved in X. index-mediated spread of GFLV, chimeric RNA2 constructs were engineered by replacing the 2A, 2B(MP), and/or 2C(CP) sequences of GFLV with their counterparts in Arabis mosaic virus (ArMV), a closely related nepovirus which is transmitted by Xiphinema diversicaudatum but not by X. index. Among the recombinant viruses obtained from transcripts of GFLV RNA1 and chimeric RNA2, only those which contained the 2C(CP) gene (504 aa) and 2B(MP) contiguous 9 C-terminal residues of GFLV were transmitted by X. index as efficiently as natural and synthetic wild-type GFLV, regardless of the origin of the 2A and 2B(MP) genes. As expected, ArMV was not transmitted probably because it is not retained by X. index. These results indicate that the determinants responsible for the specific spread of GFLV by X. index are located within the 513 C-terminal residues of the polyprotein encoded by RNA2. (+info)
Is Rhodnius robustus (Hemiptera: Reduviidae) responsible for Chagas disease transmission in Western Venezuela?
(63/1021)
We present evidence for the putative role of Rhodnius robustus as extradomestic vector of Chagas disease in Western Venezuela. First, we assessed the validity of this triatomine species by genetic characterization in relation with some other species of the prolixus group. Random amplified polymorphic DNA data showed a clear separation between this species and R. prolixus and indicated a probable genetic heterogeneity within R. robustus. Faeces and gut contents were microscopically examined in 54 of 137 R. robustus collected in palm trees. According to this morphological examination, 18% were positive for Trypanosoma cruzi, 11% harboured T. rangeli and 11% showed mixed infection. Five of the seven samples examined gave a polymerase chain reaction major band of 270 bp specific of T. cruzi. The hybridization probes showed that R. robustus may transmit clones 20 and 39 (or genetically related ones) in Venezuela. Such a transmission might occur when, in absence of domestic R. prolixus and attracted by artificial light, R. robustus enters houses and feeds on humans, or when people are bitten outdoors. The lack of bugs inside houses could mean that the insects leave houses after feeding, or die without reproducing there. (+info)
Introduction of West Nile virus in the Middle East by migrating white storks.
(64/1021)
West Nile virus (WNV) was isolated in a flock of 1,200 migrating white storks that landed in Eilat, a town in southern Israel, on August 26, 1998. Strong, hot westerly winds had forced the storks to fly under considerable physical stress before reaching the agricultural land surrounding the town. Most of the flock were fledglings, <1 year old, which had hatched in Europe. Thirteen dead or dying storks were collected 2 days after arrival and submitted to the laboratory for examination. Four WNV isolates were obtained from their brains. Out of 11 storks tested six days after arrival, three had WNV-neutralizing antibodies. Comparative analysis of full-length genomic sequences of a stork isolate and a 1999 flamingo isolate from the USA showed 28 nucleotide (nt) (0.25%) and 10 amino acid (0.3%) changes. Sequence analysis of the envelope gene of the stork isolate showed almost complete identity with isolates from Israeli domestic geese in 1998 and 1999 and from a nonmigrating, white-eyed gull in 1999. Since these storks were migrating southwards for the first time and had not flown over Israel, we assume that they had become infected with WNV at some point along their route of migration in Europe. (+info)