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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Existing mathematical models of trypanosomiasis epidemiology and epizootiology are extended by including some relevant biology of the disease vector, the tsetse fly. Rickettsia-like organisms, or RLO, are a vertically transmitted symbiont of tsetse, which confer an increased susceptibility to trypanosomiasis infection. Tsetse populations are also limited by density-dependent starvation. Modelling leads to the prediction of a stable dimorphism with a fraction of tsetse possessing RLO. The equilibrium prevalence of trypanosomiasis in the vertebrate hosts is no longer in RLO models determined simply by such traditional parameters as vectorial capacity. Only the RLO-positive tsetse carry infection, and their number is itself regulated by trypanosomiasis prevalence. The result of a naive model is that controlling tsetse numbers does not decrease prevalence until all tsetse are RLO-positive. However, under the density-dependent starvation model derived in this paper, the relative mortality of RLO-positive flies is greater at lower tsetse numbers. This tips the balance towards lower equilibrium prevalence of trypanosomiasis as tsetse numbers are decreased. The presence of RLO also gives rise to long-term oscillations in trypanosomiasis prevalence in humans and animals. However, when another mechanism that can also cause periodic epizootics (of shorter periodicity) is included, namely host immunity, the two epizootic processes combine to produce periodic epizootics (and therefore epidemics) at a single frequency. There are two decaying modes, one in which the tsetse population size quickly reaches equilibrium in a few weeks, and a second very slowly decaying mode in which host immunity and RLO effects interact. The equilibrium reached is shown to be asymptotically stable. In view of the seeming importance of RLO in trypanosomiasis epidemiology, it is important that field biologists enable RLO models to be validated by measuring the proportion of tsetse with RLO, in conjunction with vector density and trypanosomiasis prevalence and incidence in tsetse and vertebrate hosts.
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PMID:Modelling trypanosomiasis prevalence and periodic epidemics and epizootics. 130 61

Transmission of vector-borne diseases depends largely on the ability of the insect vector to become infected with the parasite. In tsetse flies, newly emerged or teneral flies are considered the most likely to develop a mature, infective trypanosome infection. This was confirmed during experimental infections where laboratory-reared Glossina morsitans morsitans Westwood (Diptera: Glossinidae) were infected with Trypanosoma congolense or T. brucei brucei. The ability of mature adult tsetse flies to become infected with trypanosomes was significantly lower than that of newly emerged flies for both parasites. However, the nutritional status of the tsetse at the time of the infective bloodmeal affected its ability to acquire either a T. congolense or T. b. brucei infection. Indeed, an extreme period of starvation (3-4 days for teneral flies, 7 days for adult flies) lowers the developmental barrier for a trypanosome infection, especially at the midgut level of the tsetse fly. Adult G. m. morsitans became at least as susceptible as newly emerged flies to infection with T. congolense. Moreover, the susceptibility of adult flies, starved for 7 days, to an infection with T. b. brucei was also significantly increased, but only at the level of maturation of an established midgut infection to a salivary gland infection. The outcome of these experimental infections clearly suggests that, under natural conditions, nutritional stress in adult tsetse flies could contribute substantially to the epidemiology of tsetse-transmitted trypanosomiasis.
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PMID:The effect of starvation on the susceptibility of teneral and non-teneral tsetse flies to trypanosome infection. 1719 50

Tsetse-transmitted trypanosomiasis poses a serious threat to human and animal health in sub-Saharan Africa. The majority of tsetse flies (Glossina spp.) in a natural population will not develop a mature infection of either Trypanosoma congolense or Trypanosoma brucei sp. because of refractoriness, a phenomenon that is affected by different factors, including the tsetse fly's immune defence. Starvation of tsetse flies significantly increases their susceptibility to the establishment of a trypanosome infection. This paper reports the effects of nutritional stress (starvation) on (a) uninduced baseline levels of gene expression of the antimicrobial peptides attacin, defensin and cecropin in the tsetse fly, and (b) levels of expression induced in response to bacterial (Escherichia coli) or trypanosomal challenge. In newly emerged, unfed tsetse flies, starvation significantly lowers baseline levels of antimicrobial peptide gene expression, especially for attacin and cecropin. In response to trypanosome challenge, only non-starved older flies showed a significant increase in antimicrobial peptide gene expression within 5 days of ingestion of a trypanosome-containing bloodmeal, especially with T. brucei bloodstream forms. These data suggest that a decreased expression of immune genes in newly hatched flies or a lack of immune responsiveness to trypanosomes in older flies, both occurring as a result of fly starvation, may be among the factors contributing to the increased susceptibility of nutritionally stressed tsetse flies to trypanosome infection.
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PMID:Nutritional stress affects the tsetse fly's immune gene expression. 1971 50

African trypanosomes, parasites that cause human sleeping sickness, undergo a density-dependent differentiation in the bloodstream of their mammalian hosts. This process is driven by a released parasite-derived factor that causes parasites to accumulate in G1 and become quiescent. This is accompanied by morphological transformation to 'stumpy' forms that are adapted to survival and further development when taken up in the blood meal of tsetse flies, the vector for trypanosomiasis. Although the soluble signal driving differentiation to stumpy forms is unidentified, a recent genome-wide RNAi screen identified many of the intracellular signalling and effector molecules required for the response to this signal. These resemble components of nutritional starvation and quiescence pathways in other eukaryotes, suggesting that parasite development shares similarities with the adaptive quiescence of organisms such as yeasts and Dictyostelium in response to nutritional starvation and stress. Here, the trypanosome signalling pathway is discussed in the context of these conserved pathways and the possible contributions of opposing 'slender retainer' and 'stumpy inducer' arms described. As evolutionarily highly divergent eukaryotes, the organisation and conservation of this developmental pathway can provide insight into the developmental cycle of other protozoan parasites, as well as the adaptive and programmed developmental responses of all eukaryotic cells.
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PMID:Assembling the components of the quorum sensing pathway in African trypanosomes. 2563 May 52

Trypanosomosis is a significant disease affecting wild animals throughout the globe. The literature pertaining to wild life trypanosomosis in India is very much scanty. Therefore, an effort was made to compile all the available literatureabout prevalence of trypanosomosis in wild animals, its clinico-pathology, diagnosis, treatment and control from Indian perspective. Reports suggest that the clinical disease and outbreaks in Indian wildlife occurs more commonly among captive than the free-living wild animals. Though the clinical symptoms showed by affected animals are same as described everywhere, however carnivorism of affected meat was found to be the striking feature in many feline and canine wild life outbreaks from India. Draught, starvation and concurrent diseases often compromise the trypano-tolerant status leading to flared up trypanosomosis in free-living wild animals. The cumulative effect of any of these factors produces severe physiological and somatic stress which in turn leads to immunosupression. Stress is the underlying cause that compromises the trypanotolerance in wild animals.
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PMID:Trypanosomosis of wild animals with emphasis on Indian scenario. 3101 93