Morbidity in schistosomiasis: an update.
ABSTRACT Schistosomiasis is an important poverty-related health problem and more than 200 million people are infected. This review summarizes papers from April 2003 to June 2004 with a focus on schistosomiasis morbidity and the various factors that affect the level of morbidity in endemic populations. The aim is to provide an update on the current state of knowledge and, hopefully, thereby stimulate continued research interest in this important area.
Research into the immune responses associated with severe morbidity has provided new insights into the mechanisms of immune regulation as well as the role of genetic predisposition to periportal fibrosis. Malaria and schistosomiasis are co-endemic and co-infection with malaria may increase the level of morbidity in hepatosplenic schistosomiasis, and alter the host immune response towards schistosome antigens. Schistosome infections may render the host more susceptible to human immunodeficiency virus infection by either interfering with immune responses or increasing the risk of transmission due to genital lesions. An important advance in schistosomiasis research, and parasite genomics, is the recent availability of two major Schistosoma mansoni and Schistosoma japonicum DNA bioinformatic resources.
Significant advances have been achieved in our understanding of the epidemiology, immunology and genetics of schistosomiasis, and the various factors that may influence morbidity. However, good research is vital for sustainable disease control, and continued progress requires a critical mass of researchers with a range of expertise from basic parasite biology to public-health interventions. It is therefore important to strengthen research capacity in endemic countries.
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ABSTRACT: Lechiguana is a disease of cattle caused by an interaction between Dermatobia hominis warble and the bacteria Manheimia granulomatis. It is characterized by subcutaneous swellings that grow rapidly and result in death after 3 to 8 months. The objective of this paper was to investigate some vascular and fibrogenic changes of the disease at different lesion stages by histochemical and immunohistochemical techniques. A peculiar histopathological aspect observed during a proliferative phase (before treatment) was the intense vasculitis, described as degenerative and fibro-proliferative, expressed by the oncogene p53, possibly caused by the presence of bacteria in close contact with enthotelial cells, along with dense accumulations of lymphoid cells around venules. The synthesis of collagen fibers during the development of Lechiguana lesions assume a structural aspect of star arrangement with fiber radiation centers that gradually interconnect to design the Extracellular Matrix (ECM) framework, seen by Confocal Laser Scanning Microscopy (CSLM). Angiogenesis was the most characteristic finding in both proliferative and regressive stages as seen by the immunohistochemical expression of cytoskeleton proteins and von Willebrand (Factor VIII-Related Antigen). Additionally, in all tissues samples, active ECM elements like Metalloproteinases (MMPs), Tissue Inhibitors Metalloproteinases (TIMP) and Fibronectin (FN) were mainly associated to vessels structures. The extraordinary regression of exuberant granulation tissue after treatment is undoubtedly associated to the maintenance of the vascular components observed during the regressive phase.Veterinary Research Communications 01/2015; 39(1). DOI:10.1007/s11259-015-9627-4 · 1.36 Impact Factor
Article: Schistosomes versus platelets.[Show abstract] [Hide abstract]
ABSTRACT: Schistosomes are parasitic platyhelminths that currently infect >200million people and cause the chronic debilitating disease schistosomiasis. While these large intravascular parasites can disturb blood flow, they do not appear to activate platelets and provoke thrombus formation. Host-interactive tegumental molecules have been proposed to be important in this regard. For example, tegumental apyrase, SmATPDase1 can degrade the platelet-activating molecule ADP in the extracellular environment. The parasites themselves can produce prostaglandins (or may induce prostaglandin production by host cells) which could inhibit platelet aggregation. Additional tegumental proteins have been proposed to impede the coagulation cascade and to promote fibrinolysis. Platelets have been shown to be directly toxic to schistosomes. Platelets recovered from infected rats are able to kill larval parasites in culture and platelets obtained at later times post-infection are generally better at killing. Even platelets from uninfected rats can rapidly kill larval schistosomes if first exposed to a variety of activators (such as: serum from infected rats, the IgE fraction of that serum, C-reactive protein, cytokines (TNFα or TNFβ)). Passive transfer of stimulated platelets can protect rats against a challenge schistosome infection. Cytokines (TNFα, TNFβ, IFNγ or IL-6) have been shown to similarly promote normal human platelet killing of schistosomes in vitro. Platelet antimicrobial effector molecules (e.g. platelet microbicidal proteins) may mediate such killing. While platelets can be protective against schistosomes following infection of humans and mice, platelet numbers decline (but not so in the non-permissive rat host) and coagulopathy becomes more apparent as schistosome-induced pathology increases.Thrombosis Research 10/2014; DOI:10.1016/j.thromres.2014.09.032 · 2.43 Impact Factor
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ABSTRACT: Schistosoma haematobium eggs can induce lesions in the urinary and genital tract epithelia, as eggs pass through or get trapped in the tissue. Local inflammatory reactions induced by S. haematobium eggs might affect the ability of bacteria to establish mucosal super-infection foci. S. haematobium infection and asymptomatic bacteriuria can both portray haematuria, proteinuria and leukocyturia. This shared set of proxy diagnostic markers could fuel routine misdiagnosis in S. haematobium endemic areas. Furthermore, S. haematobium infected individuals might be at a higher risk of contracting bacterial urinary tract infections, which could manifest either as symptomatic or asymptomatic bacteriuria. The aim of the current study was to explore whether schistosomal lesions are susceptible to super-infection by bacteria measured as asymptomatic bacteriuria. S. haematobium infection was determined by microscopy of urine samples. Furthermore, urine samples were tested with dipslides for asymptomatic bacteriuria and with dipsticks for haematuria, proteinuria and leukocytes. We found no association between asymptomatic bacteriuria and S. haematobium infection in a sample of 1040 female primary and high school students from a schistosomiasis endemic area in KwaZulu-Natal, South Africa. Furthermore, it was demonstrated that asymptomatic bacteriuria is not a bias for use of micro-haematuria as a proxy diagnostic measure for S. haematobium infection in this population.Acta Tropica 01/2015; 144:19-23. DOI:10.1016/j.actatropica.2015.01.008 · 2.52 Impact Factor