Texas Outbreak Research Articles

Characterization of recent H5 subtype avian influenza viruses from US poultry

In the US, the isolation of H5 subtype avian influenza (AI) viruses has been uncommon in commercial chickens and turkeys, although sporadic isolations have been made from the live bird markets or its supply chain since 1986. In 2002, two different outbreaks of H5 AI occurred in commercial chicken or turkey operations. The first occurred in Texas and was identified as a H5N3 subtype AI virus. The second outbreak was caused by a H5N2 virus isolated from a turkey farm in California. In this study we analyzed recent H5 subtype AI viruses from different avian species and different sources in the US. Most recent H5 subtype isolates shared a high sequence identity and phylogenetically assorted into a separate clade from the Pennsylvania/83 lineage isolates. However, no established lineage was found within this clade and the recent H5 subtype isolates seemed to be the result of separate introductions from the wild bird reservoir. The Texas H5N3 isolate shared the lowest homology with the other recent isolates in the haemagglutinin gene and had a unique haemagglutinin cleavage site sequence of REKR/G (other recent isolates have the typical avirulent motif, RETR/G). Furthermore, this isolate had a 28 amino acid deletion in the stalk region of the neuraminidase protein, a common characteristic of chicken adapted influenza viruses, and may indicate that this virus had actually been circulating in poultry for an extended period of time before it was isolated. In agreement with genetic evidence, the Texas H5N3 isolate replicated better than other H5 isolates in experimentally infected chickens. The outbreak in Texas with a more chicken-adapted H5N3 virus underscores the importance of ongoing surveillance and control efforts regarding the H5 subtype AI virus in the US.

Automated Ribotyping Differentiates Vibrio parahaemolyticus O3:K6 Strains Associated with a Texas Outbreak from Other Clinical Strains

Automated ribotyping with a Qualicon Riboprinter was used to determine whether clinical isolates of Vibrio parahaemolyticus O3:K6 recovered during two U.S. outbreaks of oyster-associated gastroenteritis in 1998 were related to each other and to a previously identified highly virulent Asian clone of this serotype. The patterns produced using the restriction enzymes Eco RI and Pst I suggest that the outbreak in the Northeastern United States was caused by a single strain closely related to the Asian clone. In contrast, it appears that multiple strains were involved in the Texas outbreak and that the predominant type was genetically distinct from the Northeastern and Asian clone.

Lack of serologic evidence for an association between Cache Valley Virus infection and anencephaly and other neural tube defects in Texas.

We tested the hypothesis that Cache Valley Virus (CVV), an endemic North American bunyavirus, may be involved in the pathogenesis of human neural tube defects. This investigation followed a 1990 and 1991 south Texas outbreak of neural tube defects with a high prevalence of anencephaly and the demonstration in 1987 that in utero infection by CVV was the cause of outbreaks of central nervous system and musculoskeletal defects in North American ruminants. Sera from 74 women who gave birth to infants with neural tube defects in south Texas from 1993 through early 1995 were tested for CVV neutralizing antibody. All tested sera did not neutralize CVV. These data suggest that CVV is not involved in the induction of human neural tube defects during nonepidemic periods but do not preclude CVV involvement during epidemics. Other endemic bunyaviruses may still be involved in the pathogenesis of neural tube defects or other congenital central nervous system or musculoskeletal malformations.

Effect of host size on virulence of Taura Virus to the marine shrimp Penaeus vannamei (Crustacea:Penaeidae)

DAO Diseases of Aquatic Organisms Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsSpecials DAO 30:45-51 (1997) - doi:10.3354/dao030045 Effect of host size on virulence of Taura Virus to the marine shrimp Penaeus vannamei (Crustacea: Penaeidae) Lotz JM Taura Disease (Taura Syndrome), caused by Taura Virus (Taura Syndrome Virus), is the most important disease of the farmed penaeid shrimp Penaeus vannamei in the Western Hemisphere. One possible tactic to offset Taura Virus-induced mortalities is for culturists to use larger shrimp for stocking ponds. This study consisted of 4 experiments designed to test the hypothesis that P. vannamei becomes more tolerant of Taura Virus infections as it becomes larger. Experiments were done in either 100 l glass aquaria or 4000 l cylindrical fiberglass tanks. All shrimp used in experiments were Specific-Pathogen-Free Penaeus vannamei derived from the United States Marine Shrimp Farming Program Population 1. The Taura Virus in all experiments originated from infected farm-reared shrimp collected during a 1995 Taura Virus outbreak in Texas, USA. Experimental shrimp were inoculated with virus either per os by allowing shrimp to feed on triturated infected shrimp tissue or intramuscularly by injection of a cell-free suspension of infected shrimp tissue into the abdominal musculature. In the 4 experiments 9 to 14 d survival ranged from 0 to nearly 60%. Analysis of each of the 4 experiments by logistic regression revealed a consistent trend for larger shrimp to be more likely to succumb to infection; however, the effect was only statistically significant in 2 of the 4 experiments. The results of the experiments failed to support the hypothesis that P. vannamei increases its tolerance to Taura Virus as it increases in size from 1 to 30 g. Taura Virus · TSV · Host-size effects · Penaeus vannamei · Shrimp disease · Route of exposure · Disease resistance Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in DAO Vol. 30, No. 1. Publication date: July 24, 1997 Print ISSN:0177-5103; Online ISSN:1616-1580 Copyright © 1997 Inter-Research.

Measles Vaccination in Infants-Reply

<h3>In Reply.—</h3> The decision to recommend measles vaccination for migrant children as young as 6 months of age during the Texas outbreak was reached after careful consideration of (1) the impact of measles in children aged 6 to 11 months; (2) the risk of measles to children of this age in the migrant population; (3) the potential consequences of vaccinating children this young; and (4) alternative means of measles prophylaxis. Measles can be particularly severe in children younger than 1 year. Infants have consistently had the highest mortality rates and the highest death-to-case ratios.^1-3Thus, it is important to protect them when they are at high risk of exposure to measles. At the time of the outbreak, Texas was experiencing its most severe measles outbreak in three years. The outbreak began among children seen at migrant health clinics. Many cases occurred in infants who had a high frequency of

Experimental Infection of Birds with Epidemic Venezuelan Encephalitis Virus

Sixty-three birds representing 13 species were inoculated with a strain of epidemic Venezuelan encephalitis (VE) virus from the 1971 Texas outbreak. More than 95% of the birds became infected. Mortality which could be attributed to infection with VE virus was very low. Viremia persisted 2-6 days. Peak viremia levels ranged from 10(3.2) to 10(8.2) suckling mouse intracranial 50% lethal doses per milliliter (SMICLD50/ml). Blood virus levels were highest in juvenile Louisiana Herones, adult Robins and adult Mockingbirds and were lowest in juvenile Common Egrets. Most bird species had blood virus levels about 10(5) SMICLD50/ml (high vector infection potential) for 2-3 days. Neutralizing antibody response was more uniform and frequent in herons (95%) than in passerines (56%). The role of birds in the epidemiology of Venezuelan is discussed.

Exotic Newcastle Disease Eradication Program in the United States

Exotic Newcastle disease was first diagnosed in two unrelated cases in the United States: in August 1970 in a pet-shop bird in New York City; and in chickens in El Paso County, Texas. The virus was later isolated in Massachusetts, New Mexico, Florida, California, Connecticut, Puerto Rico, Illinois, Arizona, Georgia, and Colorado. The probable source in most outbreaks was imported pet birds, especially psittacine and mynah birds. Secondary outbreaks in domestic poultry, spread from primary introductions via imported birds, occurred in California and are suspected to have occurred in Florida. Outbreaks in Texas, New Mexico, and Arizona were probably caused by virus transported via infected or exposed game chickens or on the clothing of Mexican day laborers. Federal and state quarantines have been placed on infected areas to combat spread. On March 14, 1972, the Secretary of Agriculture declared an emergency because of the threat posed to the entire U.S. poultry industry by exotic Newcastle disease. In a program to eradicate the disease, 9,677,457 birds in 910 flocks had been destroyed in California, Florida, Arizona, Colorado, and Texas by December 31, 1972, with indemnity payments of $18,610,071 from federal funds and $259,400 from state funds. In addition, a federally sponsored vaccination program was carried out in the quarantined area in California. Exotic Newcastle disease in the United States is part of a worldwide pandemic beginning in 1967 in all major poultry-producing and bird-growing countries.

A malaria outbreak in Texas, 1970.

A malaria outbreak in Texas, 1970.