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Foodborne disease outbreaks of chemical etiology in the United States, 1970-1974.

In the United States between 1970 and 1974 there was an increase each year both in the absolute number of foodborne diseases outbreaks of chemical etiology reported to the Center for Disease Control and in the proportion of these outbreaks in the total reported foodborne disease outbreaks. Nearly half (48.9%) of these foodborne disease outbreaks of chemical origin were caused by toxic fish or shellfish. Of the rest, 16.5% were caused by poisonous mushrooms, 10.9% by heavy metal poisoning, 7.2% by excessive use in food of monosodium glutamate (the etiologic agent of Chinese Restaurant Syndrome) and 16.5% by miscellaneous chemicals. Practices that contributed to the occurrence of these outbreaks included the inadvertent selection for consumption of toxic fish, shellfish, or mushrooms, storage of fish at improper temperatures, storage of acidic liquids in metal containers, and addition of excessive amounts of monosodium glutamate to foods. Commercially-processed foods were responsible for outbreaks of scombroid fish poisoning, shellfish poisoning, and heavy metal poisoning. Because outbreaks of chemical etiology due to contaminated commercial products do occur, prompt recognition and reporting of outbreaks to public health personnel are essential so that epidemiologic investigations can be conducted and effective control measures promptly initiated.

Animals

Incorporating Epidemiological Data into the Genomic Analysis of Partially Sampled Infectious Disease Outbreaks.

Pathogen genomic data are increasingly being used to investigate transmission dynamics in infectious disease outbreaks. Combining genomic data with epidemiological data should substantially increase our understanding of outbreaks, but this is highly challenging when the outbreak under study is only partially sampled, so that both genomic and epidemiological data are missing for intermediate links in the transmission chains. Here, we present a new dynamic programming algorithm to perform this task efficiently. We implement this methodology into the well-established TransPhylo framework to reconstruct partially sampled outbreaks using a combination of genomic and epidemiological data. We use simulated datasets to show that including epidemiological data can improve the accuracy of the inferred transmission links compared with inference based on genomic data only. This also allows us to estimate parameters specific to the epidemiological data (such as transmission rates between particular groups), which would otherwise not be possible. We then apply these methods to two real-world examples. First, we use genomic data from an outbreak of tuberculosis in Argentina, for which data was also available on the HIV status of sampled individuals, in order to investigate the role of HIV coinfection in the spread of this tuberculosis outbreak. Second, we use genomic and geographical data from the 2003 epidemic of avian influenza H7N7 in the Netherlands to reconstruct its spatial epidemiology. In both cases, we show that incorporating epidemiological data into the genomic analysis allows us to investigate the role of epidemiological properties in the spread of infectious diseases.

Humans

Tomato bacterial wilt disease outbreaks are accompanied by an increase in soil antibiotic resistance.

The presence of soil-borne disease obstacles and antibiotic resistance genes (ARGs) in soil leads to serious economic losses and health risks to humans. One area in need of attention is the evolution of ARGs as pathogenic soil gradually develops, which introduces uncertainty to the dynamic ability of conventional farming models to predict ARGs. Here, we investigated variations in tomato bacterial wilt disease accompanied by the resistome by metagenomic analysis in soils over 13 seasons of monoculture. The results showed that the abundance and diversity of ARGs and mobile genetic elements (MGEs) exhibited a significant and positive correlation with R. solanacearum. Furthermore, the binning approach indicated that fluoroquinolone (qepA), tetracycline (tetA), multidrug resistance genes (MDR, mdtA, acrB, mexB, mexE), and β-lactamases (ampC, blaGOB) carried by the pathogen itself were responsible for the increase in overall soil ARGs. The relationships between pathogens and related ARGs that might underlie the breakdown of soil ARGs were further studied in R. solanacearum invasion pot experiments. This study revealed the dynamics of soil ARGs as soil-borne diseases develop, indicating that these ecological trends can be anticipated. Overall, this study enhances our understanding of the factors driving ARGs in disease-causing soils.

Soil Microbiology

Computer simulation of Gumboro disease outbreak. II. Results obtained with models G-1 and G-2.

The authors conducted a computer simulation with their Models G-1 and G-2 for Gumboro disease ten times in each of the following initial conditions: (1) size of population, 50, 100, and 1,000 chickens; (2) age of housing, 1, 7, 14, and 21 days; (3) nine levels of parentally conferred immunity in one-day-old chicks; (4) four levels of virus contamination; and (5) three steps of coefficient for aggravating morbid status. Every simulation was operated up to the age when all the birds of a flock turned to be insusceptible so as to yield the daily numbers of chickens (1) susceptible, (2) diseased, (3) immunized, and (4) removed, and (5) the accumulation of diseased chickens. The innate resistance, parentally conferred immunity, virus contamination, and morbid status were expressed in such values that they could be compared with one another. As a result, Model G-2 produced a more realistic epizootic pattern than Model G-1, but both models concealed the effect of differences in size of population and in age of housing. Notwithstanding the incompleteness of the models, the computer simulation gave valuable information for a further advancement in this series of studies.

Animals

Interspecies Exchange of Mobile Genetic Elements During a Plant Disease Outbreak.

Outbreak sequencing provides insight into the origin and evolutionary processes acting on emerging pathogens. Sequencing a historic multihost outbreak of Ralstonia spp. in Martinique shows the outbreak was caused by two lineages that diverged at separate times from mainland populations. One lineage (Ralstonia pseudosolanacearum I-18) was originally introduced from Asia to South America, where it became well established prior to its dissemination to Martinique, where it retains a signature of specialization on solanaceous hosts. The novel lineage first identified during the outbreak (Ralstonia solanacearum IIB-4NPB) arose from a mainland population endemic to the Americas prior to its arrival in Martinique, where host-range expansion was observed. In contrast to minor changes in secreted effector protein repertoires, the emergent R. solanacearum IIB-4NPB acquired a novel integrative and conjugative element (ICERsoRUN1145). After identifying all Ralstonia spp. ICEs and mapping their spatial and phylogenetic distribution among Ralstonia spp. sampled during the outbreak, we found closely related ICEs circulating in mainland populations of R. pseudosolanacearum, indicating likely exchange between introduced and endemic Ralstonia spp. The family of ICEs in Ralstonia (ICERs) has a conserved bipartite structure and display a striking pattern of functional specialization in each cargo gene insertion hotspot: the first hotspot is a target for metabolic gene acquisition, and the second is a target for defense element acquisition. This work provides unparalleled phylogenetic and spatial resolution of an unusual outbreak and highlights the role of horizontal transfer in shaping the ecological success of an emerging pathogen.

Plant Diseases

Infection rates and outbreaks of disease due to Babesia argentina in unvaccinated cattle on 5 beef properties in south-eastern Queensland.

Serums from unvaccinated groups in 5 herds of beef-cattle in South-East Queensland were tested for antibodies to Babesia argentina at intervals while the cattle were increasing in age from about 6 months. An indirect fluorescent antibody test was used. Infection rates, indicating the proportions of the groups that had been exposed to tick-transmitted infection were 49.2, 56.9 and 69.1% for cattle aged approximately 6, 12 and 18 months, respectively. The degree to which cattle were infested with the vector, Boophilus microplus, was estimated. There appeared to be a strong correlation between infection rate and tick incidence. Four serologically negative animals died of either confirmed or suspected babesiosis during the sampling period. Sickness was observed in 5 others. The serological status of 57 changes from negative to positive without symptoms being observed, indicating relatively low mortality and morbidity rates in the enzootic situation studied.

Animals

An outbreak of disease in pigeons associated with a herpesvirus.

An outbreak of disease in young pigeons associated with a herpesvirus is reported. The clinical history, macroscopic and microscopic appearance of lesions and virus isolation are described. Most affected birds showed lesions in the upper alimentary tract epithelium as well as in skin, nasal mucosa and salivary glands. Lesions in liver, spleen and pancreas were uncommon. A herpesvirus capable of producing CPE on tissue culture and lesions on chorioallantoic membrane of developing chicken embryos was isolated and described. Inoculation of experimental pigeons with the virus failed to reproduce the disease.

Animals

Assessment of multiple probiotic strains that protect Montipora capitata coral from infection by Vibrio coralliilyticus.

Coral disease outbreaks threaten reef ecosystems, often leading to widespread mortality and declines in coral cover. Outbreaks of tissue loss diseases like acute Montipora white syndrome (aMWS) have impacted coral populations that include the Hawaiian rice coral (Montipora capitata). Multiple strains of Vibrio coralliilyticus are known pathogens, and strain OCN008 has been demonstrated as an etiological agent of aMWS in Hawai'i. Recent work has demonstrated that probiotic bacterial strains can be used to directly treat or prevent transmission (prophylaxis) of coral diseases. Based on their production of zones of inhibition and isolation from disease-resistant corals, Pseudoalteromonas ardens R96, Pseudoalteromonas obscura P94, strain Y97 (the genomic similarity to Pseudoalteromonas piscicida is presented), Pseudoalteromonas umbrosa B95, and Vibrio tetraodonis subsp. pristinus OCN044 were assessed for their ability to impair V. coralliilyticus OCN008 infection of M. capitata during laboratory infection trials. Individual inoculation of each of the five aforementioned strains on M. capitata fragments for 48 h prior to V. coralliilyticus OCN008 inoculation resulted in up to a 93.75% reduction in mortality. These results indicate that strains of Pseudoalteromonas and Vibrio can act as prophylactics to prevent M. capitata mortality from V. coralliilyticus OCN008 infection and provide tools to improve disease resilience for Pacific corals.IMPORTANCECoral disease outbreaks are a growing threat to the continued health of coral reefs, which are already vulnerable ecosystems. Strains of the bacterium Vibrio coralliilyticus are known to infect various coral species worldwide, predominantly causing tissue loss and death of the coral animal. Previous research has indicated that constituents from healthy coral microbiomes can act as probiotics to treat or prevent coral infections, and the discovery of effective probiotics is important in the effort to further develop mitigation tools for disease outbreaks. This work provides a demonstration of probiotic species that can protect coral from tissue loss infections by a strain of Vibrio coralliilyticus and is an example of probiotics developed for coral species in Hawai'i. This work provides new tools for probiotic-based coral protection and evidence for this research as a viable avenue to protect coral in their native environments.

Animals

An infectious bursal disease virus outbreak in 14- and 15-week-old chickens.

Infectious bursal disease virus (IBDV) observed in a flock of 14- and 15-week-old chickens was typical of the acute symptomatic IBDV infections more common in younger birds. High flock morbidity was indicated by a marked decrease in feed consumption, although deaths were not excessive. At necropsy, affected birds had small hemorrhages in thigh muscles, creamy-yellow-colored bursae of Fabricius with prominent longitudinal striations, and swollen mottled kidneys. Histopathologic examination revealed bursal lesions typical of IBDV infection. One of six sera from necropsied birds was positive for antibody to IBDV in the agar-gel precipitin (AGP) test, and one week later all 35 samples tested were positive. Bursae were homogenized and found to contain IBDV as evidenced by precipitation, with antibody to IBDV, in the AGP test.

Age Factors

1974 outbreak of Legionnaires' Disease diagnosed in 1977. Clinical and epidemiological features.

An illness characterized by high fever and pneumonia struck 2.9% of a group of the Independent Order of Odd Fellows attending a convention held in Philadelphia, in September, 1974. The convention headquarters was the hotel where the American Legion met in July, 1976. The epidemiological, clinical, and laboratory characteristics of the illness were nearly identical to those of the disease in American legionnaires in 1976. Illness was significantly associated with attendance at one convention activity held on Monday morning, Sept. 16, 1974, in the grand ballroom of the hotel. A serological survey in February and March, 1977, showed that people who had attended the convention and became ill were more likely to have raised indirect fluorescent antibody titres than persons who had attended and remained well. The illness seen in Odd Fellows members in September, 1974, was caused by the legionnaire's disease organism.

Aged

Influenza vaccination with live-attenuated and inactivated virus-vaccines during an outbreak of disease.

Immunization procedures with live attenuated and inactivated vaccines were carried out on a group of young recruits at the beginning of an outbreak of infection due to an A/Victoria/3/75-related virus strain, which occurred in February 1977 in a military camp. A retrospective investigation on protection from clinical influenza was then performed in order to investigate whether immunization with live virus vaccines, administered at the beginning of an epidemic, could provide early protection from the disease. In the course of the two weeks following vaccination, laboratory-confirmed clinical influenza cases occurred in 4 subjects among the 110 volunteers of the control group which received placebo, and in 8, 7 and 4 subjects respectively of the 3 groups of about 125 individuals, each of which received one of the following vaccine preparations: (a), live attenuated A/Victoria/3/75 influenza virus oral vaccine, grown on chick embryo kidney culture; (b), live attenuated nasal vaccine, a recombinant of A/Puerto Rico/8/34 with A/Victoria/3/75 virus; and (c), inactivated A/Victoria/3/75 virus intramuscular vaccine. These data do not support the hypothesis that, during an epidemic of infection, early protection from clinical influenza can be achieved through immunization with live attenuated or inactivated influenza virus vaccines, in spite of the high immunizing capability of the vaccine preparations.

Adolescent