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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
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Systemic lupus erythematosus, or SLE is a multisystem autoimmune disease that occurs predominantly in African American women of childbearing age, who generally have more severe disease. There are several multi-ethnic global lupus registries ongoing to collect better information on the epidemiology of SLE worldwide [1]. The annual incidence of SLE is 3 cases /100,000 with prevalence rates reported up to 144/100,000 among the general population [1-2], 90% of SLE patients being female gender. African Americans and Hispanics as well as males with lupus, general ly have more severe diseases, particularly renal disease, with some studies also showing this association in Asians [1-2]. SLE is a thrombophilic state. Patients with SLE- related hypercoagulability can develop arterial and venous thrombosis as well as intrauterine fetal demise, such as miscarriages and stillbirths. Multiple mechanisms contribute to hypercoagulability in SLE, including lupus specific factors such as antiphospholipid antibodies. These antibodies also contribute to cardiovascular and cerebrovascular disease in lupus. The inflammation in SLE can increase certain procoagulant factors which can tip the balance towards thrombosis. In addition, platelet hyperfunction in SLE promotes thrombogenesis and is particularly important in premature cardiovascular disease management in women with lupus. Thrombogenesis in SLE is best explained by the multiple-hit theory in which several procoagulant or anticoagulant effects occur, which additively can attain the critical overall effect needed to generate a blood clot. Thus, when assessing lupus patients for thrombosis or intrauterine fetal demise, a larger laboratory work up is needed to define the coagulation abnormalities in order to fine tune the most effective anticoagulation regimen as well as determine length of treatment. This chapter will briefly review the clinical syndromes associated with thrombophilic lupus related antibodies, with an emphasis on pregnancy loss, cardiovascular disease and clotting, the multiple mechanisms for hypercoagulability in SLE, and discuss the complexity of this problem in this population.
The epidemiology of vascular thrombosis is well described in SLE and with several studies showing an increased risk for arterial and venous thrombosis. Arterial and venous thrombosis occurs in approximately 10% of SLE patients [3-7] with thrombosis being a major cause of death in patients with lupus [8]. Gender differences have been reported with male SLE patients having a higher prevalence of thrombosis and antiphospholipid antibody syndrome compared to women with lupus [9]. Thrombovascular events occur throughout the course of lupus disease with an increase risk over time [10-11]. Arterial vascular events occur more frequently in post- menopausal women with lupus and are associated with age, disease duration, smoking and mean dose of glucocorticoids [12]. Venous thrombosis is also associated with smoking in lupus [12]. Other risk factors for thrombosis in lupus include high disease activity, lupus nephritis /nephrotic syndrome, elevated homocysteine, and the presence of antiphospholipid antibodies [11, 13-16].
The factors which increase thrombosis risk also promote pregnancy loss in lupus. Patients with SLE have increased frequencies of intrauterine growth restriction and fetal demise (miscarriage and stillbirth) which can predate the diagnosis of lupus [17-18]. Pregnancy complications in SLE are fairly common with maternal hypertensive complications occurring in 10-20%, preterm births in 20% and fetal growth restriction occurring in about 28%, with an average drop in fetal growth weight to be 16% [18-19]. Fetal wastage is markedly increased in SLE with stillbirths occurring in 4-22% and miscarriage rates reported to range from approximately 10-46% [18-19]. The increased stillbirth rate in SLE is 4 fold greater than the general population [18]. Intrauterine demise and adverse fetal outcome in SLE are related in great part to lupus specific thrombophilic factors, which can cause placental infarctions, decidual vasculopathy, and lower placental weight [20-22]. Placental histopathological findings in SLE patients with lupus anticoagulant or anti-cardiolipin antibodies include extensive infarctions due to decidual vasculopathy (related to fibrinoid necrosis in the wall of decidual arterioles and thrombosis), syncytial knots, and perivillous fibrinoid change [20-22]. In addition, there is a decrease in vasculo-syncytial membranes,an increase in fibrosis and an increase in hypovascular villi all which can lead to fetal growth restriction or demise [20-22]. Pregnancy itself is a hypercoagulable state with fetal demise, thrombosis and pre-eclampsia being related to Factor V Leiden mutation, prothrombin gene mutation 20210A, and deficiencies of anti-thrombin III, protein C and protein S [23]. Thus, SLE specific thrombophilic factors are additive to the background of pregnancy related hypercoagulability (multiple hits), and this increases the occurrence of adverse fetal outcomes in lupus.
Lupus-specific thrombophilic factors contribute to premature cardiac disease and atherosclerosis in this population. These lupus specific factors can affect the endothelium resulting in premature arterial vascular disease contributing to the accelerated/premature atherosclerosis observed in SLE [24]. Atheroma formation is initiated when oxidized low density lipoprotein (LDL) is taken up by foam cells in vascular endothelium [24-25]. High density lipoprotein (HDL) and Apo-A1 are protective factors against atherosclerosis. β-2 glycoprotein-1 binding to oxidized LDL facilitates uptake by foam cells [26]. Patients with SLE have antibodies to LDL/ β-2 glycoprotein-1 complexes, HDL, and Apo –A1 [26-27]. Antibodies to HDL and Apo A-1 cross react with cardiolipin and prevent HDL and Apo-1 protection against atherosclerosis. Antibodies to oxidized LDL may cross react with β-2 glycoprotein-1 and may enhance uptake, thus promoting plaque formation [25-28]. Anticardiolipin antibody binding exposes immunogenic and normally hidden (or cryptic) epitopes on β-2 glycoprotein-1, which can bind to anti- β-2 glycoprotein-1 antibodies. These antibodies bind to adhered β-2 glycoprotein-1 on endothelial cells which causes endothelial activation and subsequent up regulation of inflammatory and procoagulant factors [24-26]. In addition, adhered β-2 glycoprotein-1 on oxidized LDL promotes LDL uptake by macrophages, thus facilitating plaque formation [24-26, 28]. During the acute phase response, HDL can be converted to pro-inflammatory molecules which promote LDL oxidation. Chronic inflammation can cause HDL dysfunction in SLE. HDL has been found to be pro-inflammatory in women with SLE and is termed pro-inflammatory HDL or piHDL [25-26, 28]. More than 85% patients with SLE and carotid plaques had piHDL vs. 40% in those without plaques [27]. Pro- inflammatory HDL is an independent risk factor for atherosclerosis in rheumatoid arthritis and antiphospholipid antibody syndrome [26, 28]. The prevalence of moderate to severe atherosclerosis in SLE at autopsy is 52% [29]. There is a higher prevalence of coronary artery disease in SLE than general population which is not predicted by traditional risk factors or increase in lupus activity alone [30-39]. Mortality studies show coronary artery disease (CAD) /myocardial infarction (MI) is a frequent cause of death in SLE and occurs in 11-48% of SLE patients [3, 30-35]. Death from CAD in SLE is disproportionately larger in late disease, with CAD/MI being the leading cause of death in SLE survivors. This accounts for the late peak in mortality in SLE [36-38]. Although there are a greater number of CAD risk factors (hypertension, diabetes mellitus, dyslipidemia, sedentary life style) in SLE patients than matched controls, the increased atherosclerosis in SLE is not fully attributed to these traditional risk factors [39-41]. Several other studies have reported an increased risk of cardiovascular disease in SLE. After controlling for age, sex, cholesterol, hypertension, diabetes mellitus, tobacco use the relative risk was 10.1 for non-fatal myocardial infarction [95%, CI 5.8-15.6] and 17.0 for death due to coronary artery disease (CI 8.1-29.7) [42]. Esdaile also reported a 7.5X increased risk for developing coronary artery disease in SLE [42]. Progression of coronary artery calcification has been associated with age, cholesterol and smoking [43]. In particular, premenopausal aged women with lupus seem to have premature CAD with >50X increase in MI in SLE women 35-44 years, and the risk of cardiovascular events being 8-9 X increased in middle age SLE women [44-45]. We have also reported an increased risk of myocardial infarction in premenopausal women with SLE [46]. Thus, myocardial infarctions occur in patients with SLE at younger age than the general population, and using traditional risk factors alone is inadequate for developing prevention and treatment programs in asymptomatic SLE patients [42, 44].
Cerebrovascular disease is increased in SLE with an increased risk of stroke reported to be 1.67, 3.2 and 7.9 X the general population [44, 47-48]. Age and hypertension are associated with progression of carotid intima media thickness and carotid artery plaque in SLE [43]. Male lupus patients tend to have a higher prevalence of strokes than females [49]. Antiphospholipid antibodies are established risk factors for ischemic stroke in lupus [50] and can increase cerebrovascular atherosclerotic disease [51].
Chronic Inflammation, which occurs in SLE, contributes to the development of thrombosis and accelerated atherosclerosis [52]. Inflammation and infections are known epidemiologic risk factors for venous thrombosis [53]. Inflammation can cause an acquired thrombophilia and subsequent thrombosis [54]. Inflammation activates the procoagulant arm of the coagulation system and inhibits anticoagulation and fibrinolysis [55].There is an association of lupus disease activity (i.e., inflammation) and elevated erythrocyte sedimentation rate and/or C-reactive protein levels with vascular thrombosis. [5, 6, 56-57]. In fact, complement activation which occurs in lupus can promote thrombosis by activating the coagulation cascade at multiple levels [58]. It is well established that venous thrombosis can occur with elevated levels of procoagulant factors 2, 8, 9 and 10, as well as with decreased levels of anticoagulant factors (antithrombin 3, protein S and protein S [54]. Coagulation factors that increase with inflammation include Von Willebrand factor, fibrinogen, Factor VII, and Factor VIII. Increases in high sensitivity C –reactive protein (HSCRP), fibrinogen and factor VIII are in seen in lupus anticoagulant-related thrombosis [59]. Additionally, fibrinogen increases with time in SLE patients which may partially explain the increased risk of thrombosis with increasing years of lupus disease [11, 60]. Lupus disease activity is associated with elevated procoagulant markers thrombin-anti thrombin complexes, prothrombin fragment 1+2, and soluble thrombomodulin, suggesting inflammatory mediated hypercoagulability [61]. Inflammatory cytokines promote endothelial damage, plaque formation and vascular smooth muscle hypertrophy [62]. Pro-inflammatory cytokines which activate endothelial and vascular smooth muscle cells include interleukin 1 (IL-1), interleukin 6 (IL-6), tumor necrosis factor (TNF) and vascular endothelial growth factor (VEGF), all of which are increased in active lupus, particularly lupus nephritis [62]. CD 40 ligand is increased in lymphocytes in SLE patients and CD40/CD40 ligand interactions can cause plaque rupture [62]. Other pro-inflammatory effects which promote atherosclerosis include chemokines and adhesion molecules. Inflammation induces thrombosis via endothelial cell dysfunction, tissue factor mediated activation of coagulation, platelet activation, impaired function of anticoagulants and suppressed fibrinolytic activity [55]. These effects all play a role in venous thrombosis in lupus.
Multiple mechanisms contribute to hypercoagulability in SLE and thrombosis is due to multiple hits to the clotting system (the multiple-hit theory). It has been shown that elevations of procoagulant factors in combination have an additive effect on thrombosis [63]. In lupus, this includes lupus-specific and non- specific thrombogenic factors. As discussed in the previous paragraph, inflammation can cause elevations of non- lupus related procoagulant factors. Other factors contributing to hypercoagulability in SLE includes hyperhomocysteinemia [16, 64-66], and elevated plasminogen activator inhibitor-1 ( PAI-1) which decreases fibrinolytic activity [16, 55], as well as deficiencies of anticoagulant factors such as protein C, protein S and tissue plasminogen activator (tPA)which activates the fibrinolytic system [17, 55]. Lupus-specific procoagulant factors include antiphospholipid antibodies. Other lupus- specific factors include antibodies to factor XII [67], prothrombin [68], and annexin V [69-71]. Antiphospholipid antibodies encompass anticardiolipin antibodies, lupus anticoagulant (LAC), anti- β-2 glycoprotein-1 antibodies and false positive rapid plasma reagin (RPR) tests. These antibodies are prevalent in SLE and are pathogenically involved in the thromboses, accelerated atherosclerosis and fetal demise seen in this population. The prevalence of antiphospholipid antibodies are common in SLE with anticardiolipin antibodies occurring in 17-86% (vs.1-6% in the general population), and LAC noted in 15-30% (vs. 1-4% in the general population) [72]. Antiphospholipid antibodies cause vascular thrombosis and fetal loss in SLE [6, 72-76]. The LAC has a much stronger association with venous thrombosis than anticardiolipin antibodies where the thrombosis risk is directly related to increasing titers of these antibodies, particularly IGG anticardiolipin antibody titers of medium to high titer [5, 72, 77-78]. Low titers or transient presence of these antibodies generally do not cause thrombosis [72, 77]. These antibodies bind to phospholipids and protein epitopes found in cardiolipin, annexin V, prothrombin and β-2 glycoprotein-1 [24]. The antiphospholipid antibodies that recognize epitopes on β-2 glycoprotein-1 also bind serine proteases involved in hemostasis and fibrinolysis and hence promote thrombosis [79].
The prothrombotic effect of these antibodies occur via multiple mechanisms including platelet activation, endothelial cell activation with resultant up regulation of adhesion molecules and production of thromboxane A2, and stimulation of monocytes to make tissue factor, all of which promote clotting and vasoconstriction [80-81]. Tissue factor activates the extrinsic coagulation system while tissue plasminogen activator (tPA) activates fibrinolysis. Tissue factor pathway inhibitor activity is reduced in SLE and this is associated with increased levels of tissue factor and subsequent hypercoagulability [82]. Antiphospholipid antibodies bind to components of the coagulation cascade and activate the coagulation system leading to a procoagulant state along with decreased fibrinolysis via reducing activity of tPA [79-81].
Thrombosis and fetal loss in SLE share the same pathogenic pathways, and the mechanisms by which antiphospholipid antibodies cause fetal loss and thrombosis are complex and varied. They include target antigens in the coagulation, endothelial and immune systems summarized by Tripodi, et al, as follows [83]: 1.) inhibiting the protein C axis (targets- protein C, protein S, thrombomodulin, activated protein C ((APC) resistance, endothelial protein C receptor, 2.) increasing thrombin generation (targets- prothrombin, microparticles, tissue factor pathway inhibitor, protein Z, Factor XI, Factor XII, heparin cofactor II), 3.), disruption of the protective shield (target-annexin A5), 4.), decreasing fibrinolysis (targets-tPA, Annexin A2, β-2 glycoprotein-1 cleavage), 5.), altering complement levels (targets-C3, C5a, membrane attack complex, 6.) increasing platelet adhesion (target- Von Willebrand factor) and activation (targets-low density lipoprotein receptor 8, glycoprotein 1b, platelet factor 4, thromboxane A2, 7.) activation of endothelial cells (targets-Toll like receptor 4, tissue factor, prostacyclin, nitric oxide), 8.) activation of monocytes (target-tissue factor), 9.) activation of neutrophils (target-tissue factor), 10.) trophoblast activation (target-growth factor binding), 11.) angiogenesis (target- vascular endothelial growth factor, basic fibroblast growth factor), and 12.) increased atherosclerosis ( target-oxidized LDL) [83-84]. In fact, β-2 glycoprotein-1 binds to oxidized LDL to form atherogenic complexes as discussed above. These complexes have been detected in patients with autoimmune disease and promote macrophage uptake and subsequent atherosclerosis [85].
Laboratory diagnosis of hypercoagulability in lupus is complex and depends on where the patient is in the disease process. In general, more than basic tests are needed to cover the full range of possibly disrupted clotting mechanisms and this includes testing for lupus specific antiphospholipid antibodies and other hemostatic markers of coagulation. The lupus-specific antibodies include lupus anticoagulant, anticardiolipin antibodies, and anti β-2 glycoprotein-1 antibodies. These antiphospholipid antibodies are a heterogeneous group of antibodies identified by various laboratory tests all of which have some problems with standardization, specificity, interpretation and quality control [86-89]. The target antigens for these antibodies include prothrombin, negatively charged phospholipids (such as phosphatidic acid, phosphatidylinositol and phophatidyl serine), protein C, protein S, Annexin V, β-2 glycoprotein-1, thrombomodulin, factor XII, platelet adhesive receptor glycoprotein GP 1b ( which binds Von Willebrand factor) and other factors mentioned above [81, 86-90]. Anticardiolipin antibodies are directed against a protein known as β-2 glycoprotein-1, which binds anionic phospholipids [86-87]. Lupus anticoagulants encompass a heterogeneous group of antibodies that bind negatively charged phospholipids. The assay for LAC is a functional assay which measures the activity of these antibodies [84]. Anticardiolipin antibodies bind directly to cardiolipin as well as β-2 glycoprotein-1 bound to cardiolipin, and are generally detected by enzyme-linked immunosorbent assay or ELISA [69]. A subgroup of these anticardiolipin antibodies bind β-2 glycoprotein-1, and it is these anticardiolipin antibodies that are pathogenic for thrombosis. β-2 glycoprotein-1 is a glycoprotein found on many cells including endothelial cells, astrocytes, neurons, extravillous cytotrophoblasts, and syncytiotrophoblast cells of the placenta [84]. β-2 glycoprotein-1 has five domains of which domain V binds anionic phospholipids. Antibodies to domain I seem to be the most important domain related to thrombosis [84, 87]. The anti β-2 glycoprotein-1 antibodies are considered a “cofactor” for anticardiolipin antibody activity but are essentially a more specific assay for evaluation of clinically relevant prothrombotic antiphospholipid antibodies [87].
Detection of these antiphospholipid antibodies by current testing is problematic due to variable performance in different laboratories as well as difficulty of standardization [83, 86-87]. The recommended method for detecting lupus anticoagulant is a functional assay and involves a 3 step process: 1)
Along with the antiphospholipid antibodies discussed above which must be measured in patients with thrombosis or fetal loss in lupus patients with thrombosis or fetal loss, other hemostatic markers should be measured to better assess coagulation risk in SLE, i.e., a coagulation risk laboratory profile. This includes a broad panel of testing to include fibrinogen, factor VII, factor VIII, tPA, PAI-1, plasminogen activity, Von Willebrand factor activity and antigen, protein S activity, protein C activity homocysteine, and high sensitivity C-reactive protein or HSCRP [16]. It is also important to remember that estrogens and pregnancy can induce protein S deficiency and this may compound pregnancy and hormonal therapy management in lupus. Homocysteine has been associated with thrombosis in SLE, and should be measured in lupus patients as part of any hypercoagulable work up [16, 92-94]. Interestingly, rheological evaluation of SLE patients with and without thrombosis showed no association of blood viscosity and erythrocyte aggregation with thrombosis [95].
Congenital coagulation factors have been studied in in a limited fashion in SLE. The MTHFR 677 C>T polymorphism is associated with elevated homocysteine. This polymorphism was found to be homozygous form in 16.7% and heterozygous form in 83.3% of SLE patients tested and the homozygous form was increased in SLE patients vs. controls [57]. On the other hand, Factor V Leiden and Prothrombin G20210AS gene polymorphisms were not increased in SLE patients with thrombosis [64, 94]. These 2 gene polymorphisms are generally seen in Northern European Caucasian populations so it is not surprising that SLE populations, being more predominantly African American, would not show any increase of these gene types. The PROFILE cohort study by Kaiser, et al, assessed 33 single nucleotide polymorphisms (SNPs) in 1,361 predominantly Caucasian SLE patients and found that genetic risk factors for thrombosis in this cohort differed across ethnic groups, and there was an association of venous thrombosis and SNPs for these genes in whites for Factor V Leiden (OR=2.69, p=0.002), for MTHFR (OR=1.51, p=0.01), and for fibrinogen gamma (OR=1.49, p=0.02) [96]. Evaluation of functional polymorphisms of the coagulation Factor II gene, which is associated with elevated levels and activity of prothrombin and thrombosis, showed an association of one particular polymorphism (rs313516 G allele) with SLE susceptibility in African Americans and Caucasians [97]. Micro-RNAs are non-coding RNAs which function to control gene regulation post transcription by regulating mRNA translation or stability. One study assessing micro-RNAs in SLE showed that specific micro-RNAs resulted in increased tissue factor production and increased procoagulant activity [98]. There is limited data on PAI-1 promoter 4G/5G polymorphisms in SLE. Increased PAI-1 activity is associated with reduced endogenous fibrinolytic activity and is a risk factor for thrombosis. The 4G/4G genotype for PAI-1 promoter has the highest levels of PAI-1 activity and hence the highest risk for thrombosis. SLE patients with the4G/4G genotype were found to have increased carotid atherosclerosis [99]. In addition, SLE patients with PAI-1 4G/4G homozygosity were at increased risk for glomerular microthrombi [100]. An additional risk factor for the development of arterial thrombosis in antiphospholipid antibody syndrome is the presence of the 4G allele of the 4G/5G polymorphism of the PAI-1 gene [101].
Although platelet hyperfunction plays an important role in thrombosis in SLE, it has not been well studied in this population. There is some evidence that platelet activation occurs in SLE and is associated with thrombosis [102-105]. Platelet hyperfunction and platelet activation can be induced by inflammation or antiphospholipid antibodies [106-108]. Antiphospholipid antibodies have been shown to bind to β-2 glycoprotein-1 -phospholipid complexes on activated platelet membranes. Sticky platelet syndrome or hyperfunctioning platelets is a well described autosomal dominant disorder associated with arterial and venous thrombosis and characterized by hyperaggregable platelets in response to adenosine diphosphate (ADP), epinephrine or both [109-111]. Hyperaggregable platelets have been described in other conditions including diabetes, unstable angina, atrial fibrillation, thrombotic strokes, migraine headaches, retinal artery occlusions, pre-eclampsia, arterial thromboembolism, nephrotic syndrome and patients in intensive care units [109-111]. This suggests that platelet aggregation is a response to stress or epinephrine [109-111]. In women with recurrent miscarriages, sticky platelet syndrome was found in 21% [112]. Enhanced platelet aggregation was noted in non-lupus patients with venous thromboembolism [113]. It is logical to assume that SLE patients would have activated platelets and platelet hyperfunction due to stress, inflammation and antiphospholipid antibody mediated activation. Few studies have assessed platelet function in SLE. Platelet activation markers CD 62 and CD 63 are increased in patients with primary antiphospholipid antibody syndrome, suggesting platelet activation plays an important role in thrombosis mediated by antiphospholipid antibodies [114].
Platelet hypofunction can also occur in SLE and has also not been well studied. Platelet hypofunction is usually the result of platelet dense granule deficiency and can result in bleeding and bruising disorders. Prolonged bleeding times suggesting platelet hypofunction have been described lupus patients who had LAC [117]. Our study (Dhar, et al) showed that the patients who had bleeding problems had platelet dense granule deficiency as measured by electron microscopy [16].
Selecting SLE patients for a coagulation assessment is well established for those with a thrombosis or fetal loss but is not well defined for those who are at risk but have not yet had an event. Thus, patients who have had an event should clearly be selected for a coagulation work up. The guidelines for this are the Sydney Clinical Criteria for antiphospholipid antibody syndrome [118]. This includes any 1.) vascular ( arterial, venous or small vessel) thrombosis except for superficial thrombosis, 2.) Pregnancy morbidity (one or more unexplained deaths of a morphologically normal fetus at or beyond 10 weeks of gestation, one or more premature births of a morphologically normal neonate at or before 34 weeks gestation due to severe pre-eclampsia, eclampsia or severe placental insufficiency, or three or more unexplained consecutive spontaneous abortions before the 10th week of gestation excluding anatomic or hormonal abnormalities or maternal/paternal chromosomal causes [118]. However, medical management should advance towards prevention of thrombosis and adverse fetal outcomes and one should evaluate high risk clinical settings as reason enough for a thrombophilic risk assessment. These would include pregnancy, pre-estrogen hormone therapy, pre-tamoxifen therapy, pre-organ transplant, pre- vascular procedure (such as coronary artery stenting), pulmonary hypertension, nephrotic syndrome, and chronic inflammatory setting, etc. In other words, one should assess the risk of thrombosis in the clinical situation and assess the multiple hits on that background. If the clinical setting is high risk for thrombophilia, one should do the coagulation profile discussed above along with genetics and platelet function studies. Then once this information is obtained, one should assess the number and degree of procoagulant hits and determines a treatment plan. This allows fine tuning of treatment while minimizing bleeding risk. Treatment strategies should be tailored to minimize bleeding complications, reduce recurrence of thrombosis, reduce intrauterine fetal demise, and simplify monitoring. Another complicating issue for thrombophilia management is that SLE patients frequently have mixed disorders with both prothrombotic and bleeding tendencies. Thus, when ordering a laboratory work up, an extensive battery of tests is needed to most accurately define the coagulation status. Unfortunately, since these factor abnormalities are independent of each other for the most part, there is no way to truncate the testing to an algorithm. However, as much information as possible should be obtained to determine the procoagulant and anticoagulant factors that would increase the risk for thrombosis and decide on optimal treatment.
For those SLE patients with hypercoagulability who have not had a thrombosis, treatment options for hypercoagulability in lupus consist of thromboprophylaxis for acute high risk situations, chronic prophylaxis for thrombosis prevention, and full dose anticoagulation therapy. Thromboprophylaxis for patients without any history of thrombosis and presence of antiphospholipid antibodies is controversial. However, evaluating thrombosis risk by assessing the multiple hits with a full thrombophilia profile would provide more support for deciding on intensity and type of thromboprophylactic treatment. High risk settings for which acute/short term thromboprophylaxis is indicated for antiphospholipid antibody positive patients would include surgery, ovarian stimulation or other short term hormonal therapy, pregnancy, vascular procedures, lupus flares, infections, and prolonged immobilization [119]. In pregnant SLE patients positive for lupus anticoagulant, it is recommended that low dose molecular weight or unfractionated heparin be used during pregnancy since neiher cross the placenta [19]. It is not recommended to treat thrombophilia in pregnant SLE patients who are positive for anti cardiolipin antibodies or lupus anticoagulant with corticosteroids since only anticoagulation has been shown to be of proven benefit in preventing thrombosis and fetal loss [19]. Corticosteroids have no benefit in preventing thrombotic complications in this setting and should only be used if any active lupus disease is present [19]. In addition, there is no role for prophylactic corticosteroids in patients who have no active lupus disease. Corticosteroids are relatively safe to use during pregnancy from a fetal standpoint, since the placenta metabolizes 90 % of non-flourinated corticosteroids. However, corticosteroids increase maternal complications such as hypertension and gestational diabetes [19]. Appropriate settings for chronic thromboprophylaxis would include those patients with persistent medium to high titers of anticardiolipin antibodies, those with triple antiphospholipid antibody positivity (+LAC, +anticardiolipin antibody, and +anti β-2 glycoprotein-1 antibody), and those with multiple hits on a background of high risk clinical settings such as, long term hormonal therapy, nephrotic syndrome, cardiovascular disease, and history of obstetric antiphospholipid antibody related events [119]. Both platelet function and the balance of procoagulant and anticoagulant factors should be assessed. Low dose aspirin therapy for prophylaxis is recommended by the Task Force at the 13th International congress on Antiphospholipid Antibodies for these aforementioned situations along with lifestyle changes and is commonly accepted as standard treatment by many [120-121]. In SLE patients with antiphospholipid antibodies, the task force recommends both low dose aspirin and hydroxychloroquine [120]. In pregnant SLE patients with antiphospholipid antibodies only and no previous history of pregnancy loss, low dose aspirin is recommended [122]. If platelet hyperfunction is present, low dose aspirin is indicated. If hyperhomocysteinemia is present, folic acid and B complex should be used to lower homocysteine levels to below 10 µmoles/liter. However, if other high risk situations are identified in which thrombosis is likely, such as very low protein S activity, then anticoagulation with warfarin or low molecular weight heparin is indicated.
For those SLE patients with antiphospholipid antibodies and hypercoagulablity who have had an arterial or venous thrombosis full dose anticoagulation is recommended with unfractionated or low molecular weight heparin (e.g., enoxaparin, dalteparin), fondaparinux (a synthetic of the minimal anti thrombin binding sequence of heparin), vitamin K antagonists (e.g., warfarin), direct thrombin inhibitors (e.g., dabigatran), or direct factor Xa inhibitors (e.g., rivaroxaban) [83, 123]. For acute arterial or venous thrombosis, treatment consists of an initial course of unfractionated or low molecular weight heparin followed by indefinite long term treatment with warfarin to keep the international normalized ration or INR between 2.0-3.0, heparin- type drugs, or more recently, one of the newer thrombin or factor Xa inhibitors. For arterial thrombosis (stroke, myocardial infarction), addition of antiplatelet agents (low dose aspirin, clopidogrel 75 mg) may be helpful, particularly if platelet hyperfunction is present [16, 83]. The disadvantage of using warfarin is the difficulty of maintaining the correct therapeutic INR range and frequency of INR testing that must be done, which is inconvenient to the patient. The disadvantage of the heparin- type drugs is that the patient must administer self-injections daily. The heparin- type drugs do have one advantage in that coagulation lab monitoring is unnecessary. The newer thrombin or factor Xa inhibitor drugs have the dual advantage of being an oral medication and not requiring laboratory anticoagulation monitoring. For catastrophic antiphospholipid antibody syndrome, which has a high mortality rate, treatment with plasma exchange, high dose corticosteroids, intavenous immunoglobulins and anticoagulation is recommended [124].
SLE pregnancies should be considered high risk and must be managed in a multidisciplinary setting to address three problem areas: hypertensive pregnancy complications, lupus disease activity and thrombophilia [19]. Pregnancy is a hypercoagulable state which is worsened by the inflammation of active lupus disease. Pregnancy outcomes are worse with active lupus, particularly nephritis and active central nervous system (CNS) disease. Thus, it is recommended that patients with SLE have planned pregnancies and not attempt conception until the disease has been in remission for the preceeding 6 months [19]. Pregnancies that occur during active lupus or in patients with a history of severe major organ involvement such as nephritis or CNS disease are higher risk for poor fetal outcomes and maternal complication [19].Patients with mild disease generally have good pregnancy outcomes. For those pregnant SLE patients with no prior pregnancy loss or previous vascular thrombosis who have anti phospholipid antibodies, it is recommended that prophylaxis with low dose aspirin be used [125]. However if there are multiple hits such as triple antiphospholipid antibody positivity, low dose aspirin along with prophylactic doses of unfractionated or low molecular weight heparin be used [125-126]. Pregnancy- induced protein S deficiency can occur in these patients and when present should be treated with full dose anticoagulation with of unfractionated or low molecular weight heparin to prevent pregnancy loss. For pregnant SLE patients with antiphospholipid antibodies, other hypercoagulability factors, and a previous pregnancy loss or vascular thrombosis, treatment with full dose of unfractionated or low molecular weight heparin along with dose aspirin is recommended [127-128]. Generally anticoagulation is interrupted briefly during the delivery period and resumed and continued post- partum until the protein S levels return to normal and the other coagulation parameters correct. For antiphospholipid antibody persistence post-partum, continued treatment with daily aspirin is often used. Although these treatments for pregnant SLE patients are generally accepted, there is a lack of definitive data from clinical trials to support these accepted regimens [83].
Other adjuvant treatments summarized by Mehudi [81] for antiphosphoipid antibodies in SLE include: 1.) statins (which decrease antiphospholipid antibody mediated thrombosis and inflammation, 2.)Ritxuamib (which depletes CD 20 B lymphocyte cells involved in antiphospholipid antibodyl mediated disease), 3.) Hydroxychloroquine (which inhibit platelet aggregation of antiphospholipid- activated platelets by binding to GPIIbIIIa and by binding β-2 glycoprotein-1 or to target cells), 4.) Specific GPIIbIIIa inhibitors (e.g,abciximb) which bind and inactivate GPiia IIIb which is upregulated on antiphospholipid antibody activated platelets, 5.) inhibitors of tissue factor up regulation seen in antiphopholipid antibody activated endothelial cells (e.g., ACE inhibitors), 6.) anti TNF therapy to block high TNF levels seen in antiphospholipid antibody positive patients, 7.) blockage of receptors for β-2 glycoprotein-1 or antiphospholipid antibodies on target cells [81].
It is clear that thrombophilia assessment and management is complex in SLE. The balance of procoagulant factors, anticoagulant factors and platelet function determine the overall hypercoagulability risk. Simply testing for antiphospholipid antibodies alone is inadequate for determining thrombophilia status and risk in SLE. Extended coagulation profile testing along with genetic evaluation of procoagulant markers and measurements of platelet function provide more clear and precise information to develop a thrombotic or fetal loss risk assessment in SLE. This allows for fine tuning of prophylactic or full dose anticoagulation treatment and may help determine intensity and length of treatment. The overall benefit of this extended testing is to improve selection of patients to treat, improve management of anticoagulation therapy, reduce re-thrombosis and fetal loss risk, and minimize treatment complications. Further research is needed to better elucidate the multiple mechanisms behind hypercoagulability in lupus with thrombotic risk stratification and subsequent development of more definitive treatment recommendations.
Zoonoses are diseases transmitted by its natural way between man and animals pose a serious health risk. Principally, the zoonoses transmission is accomplished through close contact with domestic animals, especially dogs and cats, with whom we share more than 60 parasitic species [1]. Of about more than 370 parasite species, 40 of them are classified as zoonotic. According to the WHO data [2, 3], more than 2 billion people are affected by parasitic zoonoses. This is happening not only within developing but also in the industrialised countries, including Slovakia.
\nZoonotic diseases are mainly transmitted through the soil or water. Primarily, they are represented by endoparasites such as protozoa and nematodes [4, 5]. In all of these diseases caused by endoparasites, the most likely route of man infection is oral transmission followed by the contact with infected humans and animals (wild, stray, and domestic), with contaminated food, soil, water, or infected environment. The main sources of the infected environment are faeces from infected animals living in close vicinity with the man. Though the contact with an animal is more intense in the rural than in the urban ecosystems, the likelihood of animal diseases spread is greater between stray animals or in animals without veterinary control.
\nThe prevalence of intestinal parasitic diseases in Slovakia is due to its geographical location and relatively low good hygiene conditions. However, it may be easily dispensable in socially disadvantaged groups of people. Primarily, these diseases occur in the population of marginalised communities, which as a consequence of various factors are distinct by socio-economic exclusion. In Slovakia, according to the performed studies and governmentally released strategy papers, the group most at risk and living in poverty, which is socially excluded and discriminated, is represented by the Roma people. They are a very specific and the most numerous marginalised group in Slovakia [6]. The Roma population is the population with the progressive age structure, that is, with a high proportion of the younger population and with a low proportion of the population over the age of 60. Life expectancy, which is considered to be a fundamental indicator of the population’s health status is within the Roma’s men 55.3 and Roma’s women 59.5 years, respectively. WHO specified the same numbers for the life expectancies in developing countries. The health status of Roma citizens is much worse when compared with the general (major) population. Particularly, there is a high risk of diseases linked with low hygiene standards. The most affected group are children, who are often exposed to the environmental and anthropogenic risks. Among of aformentioned parasitoses, the soil- and man-transmitted nematodes are the most important. They are represented by ascariasis (
The objective of this chapter is to investigate: (i) the incidence of nematodes in domestic animals; (ii) contamination of the environment with nematodes; and (iii) the occurrence of the most important nematode infections spread in major populations and population living under low hygienic standard conditions in the Slovak Republic territory.
\nTotally, 1237 dog faecal samples were collected and examined for the presence of parasite developmental stages. Dog faeces have been collected from around the dwellings, public places, or taken directly by the owners from backyards. After the collections, faecal samples were stored at 4°C and transferred to the laboratory for parasitological examination, which was performed within 24–48 h.
\nFlotation method with the sucrose flotation solution with specific density of 1.27 was used for coprological examination, where 3 g of faecal sample mixed with water was centrifuged for 5 min at 1200 rpm (Eppendorf 5804, Germany). After pouring out the supernatant, the sucrose flotation solution was added into the test tube. The sediment was then stirred and centrifuged again. After 5 min of sedimentation the test tube was refilled with flotation solution again. Than the top of tube was covered with cover glass to detect the eggs trapped in formed meniscus formed. All samples were further examined under the light microscope at 20× and 40× magnification (Leica Microsystems, DM 5000B light microscope, Germany).
\nIn order to identify the presence of parasites in the environment, totally 539 soil samples were collected within the vicinity of human settlements and around the kennels and dog pens. The sand samples were surveyed according to the Kazacos [7]. Briefly, 100 g of pooled sand sample, 100 ml of water, and 0.5 ml of Tween 40 were mixed and decanted for 10 min. Subsequently, the samples were sieved and replenished with 1000 ml of water. After 1 h sedimentation, the soil samples were centrifuged (Eppendorf 5804, Germany) and then floated with sucrose flotation solution (specific density of 1.3). Samples were examined under the light microscope at 20× and 40× magnification (Leica Microsystems, DM 5000B light microscope, Germany).
\nTotally, 1571 children’s stool samples were collected into the plastic containers. After an informed consent was signed by parents or legal guardians stool containers with unique identifiers were handed out together with the instruction regarding its return. Stool samples (up to 5–15 g of morning stool) were stored in refrigerator without any preservation at 4°C and transferred to the laboratory for examination that was performed within 24–48 h. Samples were examined with commercially available kit (Paraprep L, Mondial, France). Briefly, for each stool sample, 2 ml of ethyl acetate solution and 0.5 g of stool sample were added to 6 ml of 10% formalin in a mixing chamber. The chamber was then connected through filter with a conical collection chamber. Mixed content was incubated for 24 h at room temperature and the tube was centrifuged at 1000 rpm for 1 min (Eppendorf 5804, Germany). The entire samples volumes were collected into the collection chambers.
\nThe supernatant was discarded and the sediment placed on microscope slides and covered with coverslip. The entire area was examined at 20× and 40× magnifications with Leica DM 5000B light microscope (Leica Microsystems, Germany).
\nStatistical significances were determined using Student t-test, ANOVA, and Dunnett Multiple Comparison test at the levels of significance 0.05, 0.01, and 0.001 (Statistica 6.0, USA) [8].
\nAll together, 1237 faeces samples from free living spaces and grass areas were collected within selected urban and rural ecosystems in the Slovak Republic territory for parasitological examinations. Endoparasites were found in 38.56% of all examined samples (Table 1). The most frequent were eggs from the family Ancylostomatidae (20.94%) and
Ecosystems | \nNegative | \nPositive | \nNumber of samples | \nPrevalence (%) | \n
---|---|---|---|---|
Urban | \n580 | \n198 | \n778 | \n25.45 | \n
Rural | \n133 | \n89 | \n222 | \n40.09** | \n
Low hygienic standard | \n46 | \n191 | \n237 | \n80.59*** | \n
Prevalence of parasitic developmental stages in dog faeces.
Significance at the level P < 0.01.
Significance at the level P < 0.001.
Significance at the level P < 0.05.
\n | Negative (n = 1237) | \nPositive (n = 1237) | \nPrevalence (%) | \n
---|---|---|---|
1060 | \n177 | \n14.31 | \n|
1168 | \n69 | \n5.58 | \n|
1137 | \n100 | \n8.08 | \n|
Ancylostomatidae | \n978 | \n259 | \n20.94 | \n
1145 | \n92 | \n7.44 | \n|
1191 | \n46 | \n3.72 | \n|
1232 | \n5 | \n0.40 | \n|
Strongyloid eggs | \n1220 | \n17 | \n1.37 | \n
Occurrence of nematode eggs/larvae in dog faeces.
n, number of examined samples.
Among of 1237 examined faecal specimens, 778 were collected within the urban ecosystem. Samples were collected randomly from the public spaces in seven cities of the Slovak Republic and examined microscopically. In summary, 25.45% of all samples were positive for the occurrence of parasitic nematodes (Table 1). Eggs, found in the excrements, were from the family Ancylostomatidae (8.61%),
\n | Negative (n = 778) | \nPositive (n = 778) | \nPrevalence (%) | \n
---|---|---|---|
715 | \n63 | \n8.10 | \n|
745 | \n33 | \n4.24 | \n|
Ancylostomatidae family | \n711 | \n67 | \n8.61 | \n
748 | \n30 | \n3.86 | \n|
765 | \n13 | \n1.67 | \n|
Strongyloid eggs | \n764 | \n14 | \n1.80 | \n
Nematode eggs/larvae occurrence in dog faeces collected within urban ecosystem.
n, number of examined samples.
In 146 of positive faecal samples, a simple endoparasitic infection was the most common. Mixed infections with multiple intestinal parasites were detected in 52 cases. The most frequent was
Totally, 222 canine faeces samples were collected and coprologically examined from the rural ecosystem. Samples came from both, the public spaces and private land within numerous villages located in Slovakia.
\nThe presence of parasitic intestinal developmental stages was confirmed in 40.09% of collected samples (Table 1), where 12 species of nematodes were detected. The most prevalent were the eggs of
\n | Negative (n = 222) | \nPositive (n = 222) | \nPrevalence (%) | \n
---|---|---|---|
179 | \n43 | \n19.37 | \n|
221 | \n1 | \n0.45 | \n|
Ancylostomatidae family | \n185 | \n37 | \n16.67 | \n
204 | \n18 | \n8.11 | \n|
209 | \n13 | \n5.86 | \n|
206 | \n3 | \n1.44 | \n|
Strongyloid eggs | \n1220 | \n17 | \n1.37 | \n
Nematode eggs/larvae occurrence in dog faeces collected in rural ecosystem.
n, number of examined samples.
Parasitic monoinfection was detected in 58 samples. The most common was
In addition to the examination within standard urban and rural environment, the occurrence of parasitic eggs was determined in dog faces from areas with low environmental hygiene. Such locations in our region are represented by Roma settlements. Totally, 237 samples of dog faeces from four areas with low environmental hygiene were examined.
\nAbout 80.59% of canine faeces collected around houses were found to be positive for parasitic developmental stages (Table 1) and 13 different nematode species were identified. The most common findings were the eggs from the family Ancylostomatidae (65.40%). Despite the fact that the dogs are not host of
\n | Negative (n = 222) \n | \nPositive (n = 222) \n | \nPrevalence \n % | \n
---|---|---|---|
166 | \n71 | \n29.96 | \n|
202 | \n35 | \n15.77 | \n|
Ascaris spp. | \n137 | \n100 | \n42.19 | \n
82 | \n155 | \n65.40 | \n|
193 | \n44 | \n18.57 | \n|
217 | \n20 | \n8.44 | \n|
235 | \n2 | \n0.84 | \n
Nematode eggs/larvae occurrence in dog faeces collected in localities with low hygienic standard.
n, number of examined samples.
Unlike in the urban and rural ecosystems, only 45 dogs living in areas with low hygiene environment have monoinfections. Multiple co-infections have been confirmed in 146 dogs. Two nematode species were detected in 48 samples and represented primarily by the eggs of the family Ancylostomatidae and
The above average occurrence of nematode eggs and larvae in dog faeces poses high risk for environmental contamination. Therefore, their prevalence in the soil was monitored and its effect on population living in the affected areas was analysed.
\nTotally 539 samples of soil samples from cities in the Slovak Republic were examined to study the risk of environmental contamination. The presence of nematodes was confirmed in 14.47% of all samples. The representation for particular species was as follows: Ancylostomatidae family (7.79%),
In the cities, we focused primarily on the collection of samples from children’s sandpits and public spaces. Together 497 samples were examined and the overall incidence of nematodes in urban environment was 9.86%. The most frequent eggs were of
\n | Sandpits (n = 497) % (p) | \nUnfenced (n = 341) % (p) | \nFenced (n = 156) % (p) | \n
---|---|---|---|
4.43 (22) | \n5.28 (18) | \n3.21 (5) | \n|
0.80 (4) | \n1.17 (4) | \n0 | \n|
Ancylostomatidae family | \n3.62 (18) | \n4.69 (16) | \n1.28 (2) | \n
0.20 (1) | \n0.29 (1) | \n0 | \n|
Nematode eggs occurrence in sandpits.
n, number of examined samples.
During the sandpits analysis, we sorted them as fenced and unfenced. The unfenced sandpits were found to be contaminated more than fenced. This finding was notable and statistically significant. In comparison with fenced sandpits (4.49%), the prevalence in unfenced sandpits was 12.32% (Table 6). The most frequent were the eggs of
In rural environment, the soil samples were collected from parks, public spaces, and/or from private yards and gardens. In general, significantly higher incidence of parasitic eggs and larvae was found in soil samples collected from rural areas. Up to 44.44% of all examined samples were positive for the occurrence of Ancylostomatidae
\n | Rural (n = 18) % (p) | \nRural with low hygienic standard (n = 24) % (p) | \n
---|---|---|
16.67 (3) | \n58.33 (14) | \n|
5.56 (1) | \n41.67 (10) | \n|
0 | \n79.17 (19) | \n|
Ancylostomatidae family | \n27.78 (5) | \n79.17 (19) | \n
5.56 (1) | \n41.67 (10) | \n|
0 | \n8.33 (2) | \n|
Nematode eggs occurrence in rural environment and from localities with low hygienic standard.
Significance at the level P < 0.01.
Significance at the level P < 0.001.
n, number of examined samples; p, number of positive samples.
Significance at the level P < 0.05.
The highest soil contamination was found in the areas with low environmental hygiene where up to 87.5% of the soil samples contained nematode eggs or larvae at various developmental stages (Table 7). The difference, when compared with rural and urban environment, was statistically significant. The soil collected from these sites was contaminated heavily with eggs of Ancylostomatidae family,
The differences between the urban, rural and/or with low environmental hygiene examined sites were also compared according to the number of eggs detected per 100 g soil. Soil and sand samples in the urban ecosystem contained 1–10 eggs per 100 g sample. Typically, 1–20 eggs per 100 g sample were found in soil samples from the rural ecosystem. Soil samples collected in low-hygiene areas comprised of 10–1000 eggs per 100 g sample. Moreover, soil samples analysed at these sites contained in general up to 100–200
Parasitic nematodal disease incidence in the human population in correlation with environmental contamination and domestic animals was evaluated. Disease monitoring was focused on the most vulnerable children population divided into two groups. First one was represented by kids living satisfactory hygiene condition. Second one was represented by so-called marginalised group living in poor hygienic condition with limited access to the clean water. The living conditions in such settlements are often inadequate and the residents usually live in wooden or brick shacks that often lack basic infrastructural support. Under such conditions, the living space is often shared with a great number of dogs without appropriate veterinary care. As soon as the informed consent was signed by all participants, 1571 randomly selected stool samples from the major and minor (marginalised) population were collected and examined in collaboration with paediatricians and pertinent laboratories. The overall parasitic infections prevalence in children was 12.99%. The most dominant species were
\n | Total (n= 1571) % (p) | \nMarginalised Roma population (n = 720) % (p) | \nMajor non-Roma population (n = 851) % (p) | \n
---|---|---|---|
12.03 (189) | \n25.56 (184) | \n0.59 (5) | \n|
2.99 (47) | \n6.53 (47) | \n0 | \n|
Nematodes occurrence in children according the division to Roma or non-Roma population.
Significance at the level P < 0.01.
Significance at the level P < 0.001.
n, number of examined samples; p, number of positive samples.
Significance at the level P < 0.05.
All examined children were divided into groups according to the environment where they live. The first group consisted of 851 children from the major population and came from the environment with standard hygiene conditions. The second, marginalised group consisted of 720 children who lived in an environment with low environmental hygiene.
\nAmong of all 851 children who belong to the major population and lived in satisfactory hygiene conditions, only 5 kids were infected with
A single parasitic monoinfection was observed in 170 children. Co-infection with two nematode species was found in 32 children. The most common infections were of
The incidence of nematodes in children at different ages was also examined. Based on the age, children were divided into three groups: Group 1: Newborn (0–2 years), Group 2: Preschool age (3–5 years), and Group 3: School age (6–18 years). The overall rejection rate between all participants due to incomplete data analysis or non-compliance was 15%.
\nIn children from the marginalised group, the overall parasitic prevalence ranged from 14.17 to 29.66%. The least infected were kids under the age of 2. The most positive stool samples were found in preschool children and kids attending primary school. In opposite to the marginalised group, the overall disease prevalence in children living within major population did not exceed 1% (Table 9).
\n\n | Marginalised Roma population % (n/p) | \nMajor non-Roma population % (n/p) | \n
---|---|---|
Newborn | \n14.17 (127/18) | \n0.94 (106/1) | \n
Preschool age | \n29.66 (236/70) | \n0.63 (315/2) | \n
School attending | \n28.10 (331/93) | \n0.48 (420/2) | \n
Nematodes occurrence in children according to age.
n, number of examined samples; p, number of positive samples.
At the present, it is necessary to create conditions for the co-existence of humans and animals. Man, in the course of domestication, incorporated various animal species into its environment. However, these animals can transfer and can be a source of many viral, bacterial, fungal, and parasitic diseases [9, 10, 11]. From this point of view, regarding the spread of parasitic diseases, a significant role is played by domestic animals. Especially, by the dogs and cats which share its living environment with humans. Thus, this co-habitation may represent an important source of contamination by parasites [12, 13, 14].
\nParasitic status of house held dogs, as well as the other domestic animals, is affected by several factors such as the ecosystem type, breeding, wildlife, dogs use, age, and quality of veterinary care. In an urban ecosystem, the primary roles of the dog (hunting and protection) are diminishing, but its positive psychosocial and emotional influence on humans is on the rise. The town’s infrastructure with flats and apartments impacts the ways how dogs are kept and share their living space with owners. Dogs in cities are in close contact with humans and became part of households. In some cases, the owner takes exaggerated care of their pets what leads to some kind of anthropomorphosis of domestic animals that occasionally could become family members’ substitute [15, 16].
\nOn the other side, such close contact can contribute to the contamination of the nearby human environment. For example, human toxocarosis is traditionally identified as a parasitic disease transmitted by contaminated soil. However, several studies have pointed out on the possibility of transfer through direct contact with the infected animal’s fur. For instance, Wolfe and Wright [17] detected the eggs of
In rural ecosystems, the dogs have less companion function and are predominantly kept to guard properties. Usually, the animals do not have access to the interior spaces and are kept loosely on the yards or in the kennels. Under such conditions and in the case of infection, they can spread parasitic germs in surrounding territories. We found that in most municipalities there is no appropriate veterinary care, which may result in insufficient attention to the animal health. Additionally, this is probably also related with poor public health awareness and overall ignorance of the parasitic diseases spread associated with domestic animals. From various reasons, the dog health care very often does not include the prevention against parasitic diseases spread. Especially, in the animals that have no clinical symptoms, a visit to a local veterinarian is not necessary. Another phenomenon is free movement of dogs in villages what is the result of poorly maintained fences and also the owner’s negligence. This leads to the spread of parasites into larger areas. The possibility of wandering and close uncontrolled contact with wildlife increases the probability of parasitic infections occurrence in domestic animals. Free living animals that are not under veterinary supervision may be an important source of infection. Many studies have confirmed that there is a higher parasitic of parasites in the population of dogs living in a rural ecosystem than in an urban ecosystem. Fok et al. [23] compared the occurrence of helminths in rural and urban dogs. A higher incidence of helminths was found in rural dogs (56%) when compared with cities (44%). Similar statistically significant difference in domestic animal parasitoses prevalence in the rural and urban ecosystem was reported also by Dubná et al. [24]. The total prevalence of parasites in municipalities around city Prague was 41.7%; meanwhile in the urban ecosystem, it was only 17.60%. Moreover, in a rural ecosystem, the authors found higher prevalence for all 13 detected species. Work of Habluetzel et al. [25] showed that 48.4% of dogs from the rural ecosystem had
Among the other important factors affecting the occurrence of parasites within human population is socio-economic status and environmental hygiene quality. In the developing countries, the domestic animals health care is not addressed properly. It is affected by unsatisfactory financial income in large proportion of the population, as well as with low level of health awareness and poor veterinary care. In Nigeria, Ugbomoiko et al. [28] detected 68%, predominantly of
Increase in the number of dogs over the time in the cities with very limited access to green areas leads to the accumulation of excrement/faces in public spaces. The pollution of public spaces occurs despite the existence of laws (differs from country to country) regulating the conditions for housing and breeding the animals. For instance, in Slovakia, it is Act No. 282/2002 [32] and paragraph 6, which instructs the owners how to remove biological waste from the environment. The goal of law is to eliminate both factors: the negative aesthetic effect and removal of the endoparasites, which are released into the environment. In particular, dogs and cats are often infected with
Mizgajska-Wiktor and Jarosz (2007) performed a 5-year epidemiological monitoring for parasitic soil contamination in the city of Poznan and its surroundings. Interestingly, there was higher soil contamination within the city (19.8%) than in its rural area (15.6%). Gawor et al. [36] studied the epidemiology of soil contamination and the probability of reinfection in children diagnosed with toxocarosis. After the examination of soil around the households of sick children, it was found that
An extensive attention should also be focused on the endoparasitic contamination of children’s playgrounds where if not properly fenced the dogs and cats can litter. Children who have not yet developed their hygienic habits and are in direct contact with sand or may have geophagia are at the most risk. Ferre and Dorchies [37] detected
Our results confirmed that the occurrence of endoparasites at children’s playgrounds is also affected by the level of protection against house held or free living animals. Jansen et al. [39] confirmed that fenced sandpits reduced the occurrence of parasitic developmental stages in comparison to the unprotected. This finding was endorsed by the study of Blaszkowska et al. [40] who carried out a survey on parasitic contamination in Lodz (Poland). Fenced sandpits and playgrounds, which were part of schools or kindergartens, contained only 1.4% geohelminths eggs. Meanwhile up to 15.7% of soil samples were found to be positive in unfenced playgrounds. The clear influence of fencing on the reduction of sand and soil contamination has also been confirmed by Dubná et al. [24] and Avcioglu and Balkaya [41].
\nAs we mentioned earlier, younger population is most vulnerable to the nematode infections. Our results show that the total prevalence of nematodes within population with low hygiene standards was 27.64%, while only a small number of infections (0.59%) were observed within major population.
Despite the temperate climatic conditions, nematode infections are still a threat to the public health. The counter measures against diseases spread should be engaged at several levels. Those are represented by appropriate sanitation, disruption of natural parasitic life cycles, soil decontamination, and improvement in hygiene standards. This all should be accomplished through the following actions:
Perform compulsory surveys regarding the epidemiology, the presence of intermediate, and definitive hosts and soil contamination.
Approaches such as geographical information systems (GIS) including spatial and environmental analysis should be considered and utilised to reveal biogeographical properties for particular parasitic diseases spread.
Scrutinise the cultural and social habits from the rural and urban areas and examine the sanitary conditions and hygiene in affected areas.
Implement appropriate control strategies, for the urban and rural settings, to protect farmers and pet owners.
Increase public awareness about parasitic diseases spread via community centres, local governmental authorities, veterinary and health care services.
This work was supported by the grants VEGA no. 2/0125/17 (0.5) and APVV-18-0351 (0.5). We declare that we have no conflict of interest, and we have no financial or personal relationships with other people or organisations that could inappropriately influence our work. The proposal was reviewed and approved by the Ethical Commission of Institute of Parasitology SAS in Košice. Children’s parents, legal representatives, agreed with all investigations and signed the informed consent prior to examinations and hospitalisations. We would like to thank people (students, postdocs, and colleagues) who allowed us to gather data needed for elaboration of this chapter.
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