Pathology and pathogenesis of human leptospirosis: a commented review.

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leptospirosis 98 Title: Revista do Instituto de Medicina Tropical de São PauloPathology and pathogenesis of human leptospirosis : a commented reviewThales De BritoAna Maria Gonçalves da SilvaPatrícia Antonia Estima Abreu1Universidade
leptospirosis 1045 penetrating mucous membranes or skin abrasions and disseminate through the hematogenic route. In humans, leptospirosis may cause a wide spectrum of symptoms. Most cases have a biphasic clinical presentation, which begins
leptospirosis 1892 the world[1]. It is a zoonosis associated with chronically infected carrier animals[2]. In humans, leptospirosis has a biphasic clinical presentation, which begins with the septicemic phase followed by immune manifestations[3].
leptospirosis 2210 hepatic, renal, pulmonary and skeletal muscles injury, is known as the Weil syndrome[4]-[7]. Many cases of leptospirosis exhibit a non-specific picture of a febrile disease, however the vascular manifestation of the disease
leptospirosis 2438 present as a hemorrhagic conjunctivitis[3],[8]. It has been estimated that the annual mortality rate of leptospirosis is 0.84 deaths per 100,000 people, globally[1].Pathogenic leptospires are widespread in nature and their
leptospirosis 3165 activities involving infected animals and contaminated soil and water are risk factors for developing leptospirosis [3],[9]. Humans are accidental hosts, and commonly exhibit urinary shedding of leptospires for short
leptospirosis 5674 septicemic phase of the disease, which lasts for the first eight days of fever[15]. Experimental studies of leptospirosis suggest that afterwards, leptospires find their way to the interstitium. This usually occurs either
leptospirosis 6809 active disease[11].Liver cell plate disarray is a major histopathologic finding in human autopsies of leptospirosis , receiving attention since the early pathologic studies of the disease during the first World War (1914
leptospirosis 6983 the disease during the first World War (1914 - 1918)[17],[18]. They are also present in experimental leptospirosis and are accompanied by antigen deposits over the cell membrane, as demonstrated by immunohistochemistry[19]
leptospirosis 7191 immunohistochemistry[19] and immunoelectron microscopy[20]. Liver cell disarray is absent in human biopsies of leptospirosis cases when studied by light microscopy[21],[22]. However, it must be remembered that since the biopsy
leptospirosis 7572 no longer present. In accordance with this, electron microscopy studies of human liver biopsies in leptospirosis show cellular junctions practically restored but with a few enlarged intercellular spaces[21],[23].
leptospirosis 8282 that can cause host cell membrane degradation[24],[25].CADHERINSOur previous autopsy work on human leptospirosis [26] has shown the importance of loss of E-cadherin membrane expression in the pathogenesis of liver
leptospirosis 8924 cytoskeleton, produces its fundamental roles in the organization and maintenance of the cell junction. In leptospirosis , the expression of E-cadherin in liver cells is diminished and/or absent in areas of the lobule, thus
leptospirosis 9158 the lack of a stable intercellular adhesion (Figures 1A and 1B). Human biopsy studies of the liver in leptospirosis demonstrate a robust recovery of E-cadherin expression in the liver, since, as noted earlier, biopsy
leptospirosis 9565 during the acute stage of the disease. The data corroborate, as previously noted (De Brito et al.)[5], leptospirosis as a disease of the cell membrane.Figure 1- Immunohistochemistry and histology analyses. A) Expression
leptospirosis 9795 in lobule of normal human liver; B) Areas of diminished and/or absent E-cadherin in liver in human leptospirosis ; C) Liver biopsy in human leptospirosis. Hepatic cells show slight variation in size and occasional
leptospirosis 9835 Areas of diminished and/or absent E-cadherin in liver in human leptospirosis; C) Liver biopsy in human leptospirosis . Hepatic cells show slight variation in size and occasional more marked hyaline cytoplasmatic change.
leptospirosis 10006 occasional more marked hyaline cytoplasmatic change. Portal space is unremarkable; D) Human liver biopsy in leptospirosis showing areas of dense reticulin framework. Variations of size and shape of liver cells is more evident
leptospirosis 10212 more evident with reticulin staining; E) VE-cadherin in normal human lung; F) VE-cadherin in lung in leptospirosis . Marked intra-alveolar hemorrhage. Dilated and discontinuous capillary walls with irregular stainingLeptospirosis
leptospirosis 11749 VE-cadherin is mediated by adhesins, proteins and lipoproteins, which have been identified in sera from leptospirosis patients[27],[28].Martinez-Lopez et al.[29] demonstrated that pathogenic strains of Leptospira did not cause
leptospirosis 13239 pulmonary failure.Figure 2– Immunohistochemistry and histology analyses. A) VE-cadherin in lung in human leptospirosis . Small openings in the alveolar lining. Areas of intra-alveolar hemorrhage; B) Low view of VE-cadherin
leptospirosis 13373 the alveolar lining. Areas of intra-alveolar hemorrhage; B) Low view of VE-cadherin in human lung in leptospirosis . Intra-alveolar hemorrhage and diminished and/or absent staining of capillary walls; C) Normal expression
leptospirosis 13652 VE-cadherin expression is diminished and/or absent in focal areas of glomerular capillaries in human leptospirosis A recent study by Sato and Coburn[33] showed that the most important finding seen in L. interrogans was
leptospirosis 14349 of the endothelial cells of the microcirculation involved in the altered vascular permeability seen in leptospirosis . The immunohistochemical detection of endothelial transmembrane glycoproteins by CD34[34], which also
leptospirosis 14865 expression of vascular intercellular adhesion molecules and Toll-like receptor was found in the lungs of leptospirosis cases[35].Recently, glycocalyx, another important component of the endothelium, was found to be damaged
leptospirosis 15026 important component of the endothelium, was found to be damaged in a study of acute kidney injury in human leptospirosis [36]. Glycocalyx has antiadhesive and anticoagulant properties that are essential for the endothelium
leptospirosis 15190 properties that are essential for the endothelium to maintain the barrier function. In this study, leptospirosis was found to be associated with higher levels of intercellular adhesion molecules, particularly ICAM-1
leptospirosis 15409 and syndecan-1[36].Taking the above data together, we suggest that the endothelial cell is injured in leptospirosis , and this includes not only the main important lesion at the adherens junction but also alterations
leptospirosis 15589 adherens junction but also alterations of the cell membrane, leading to altered permeability.The lung in leptospirosis showed a surprising amount of preservation of the immunohistochemical phenotype for cells of the alveolar
leptospirosis 16618 broad approach to the pathogenesis of aspects of the disease does not apply to muscular lesions in leptospirosis , the most severely involved skeletal muscles are those of the calf, pectoral muscles may also be, although
leptospirosis 20493 sarcoplasm[39]. However, it is necessary to note that in this instance, we are dealing with patients with leptospirosis , and the immune serum can also recognize the microorganism antigens which, as previously demonstrated[38],
leptospirosis 20711 demonstrated[38], may be present in the muscle.LIVER IN LEPTOSPIROSISIt is well known that the most severe form of leptospirosis , the Weil’s disease, is mainly characterized by hemorrhage, hepatic and renal manifestations[3]. Jaundice
leptospirosis 20908 manifestations[3]. Jaundice is an important manifestation of hepatic dysfunction, but its mechanism in leptospirosis remains not completely elucidated. Serum biochemical studies have demonstrated that the concentrations
leptospirosis 21124 of transaminases and to a lesser degree of alkaline phosphatase, are moderately increased in human leptospirosis . Jaundice is mainly due to increased conjugated bilirubin and disturbances of bile excretion with intrahepatic
leptospirosis 21360 cholestasis, which appeared at the time to be its main cause.Previous observations in patients recovering from leptospirosis , therefore out of the hemorrhagic phase of the disease, showed a non-specific hepatocellular damage affecting
leptospirosis 22620 hepatocytes in the experimental disease, sometimes close to the cell junctions[11].Therefore, cholestasis in leptospirosis was interpreted, at the time, as the result of disturbances to the bile secretory apparatus, which comprises
leptospirosis 23326 the altered cell membrane[23].Recent report from Miyhara et al.[41] in a hamster model of experimental leptospirosis proposes the destruction of the hepatocytic intercellular junction directly by leptospire intercellular migration,
leptospirosis 24030 leptospiral infection, based on a previous electron microscopy study of the liver in a hamster experimental model of leptospirosis [42].The mechanism of jaundice proposed by Miyhara et al.[41] is supported by the electron microscopy
leptospirosis 24392 experimental disease[11].However, despite the electron microscopy findings showing that human and experimental leptospirosis is non-specific and differs only in degree from findings associated with viral hepatitis[23], they show
leptospirosis 24594 hepatitis[23], they show the importance of altered hepatocyte transport and chiefly the excretion of bile in leptospirosis . Most likely, both mechanisms are at work in the pathogenesis of jaundice in leptospirosis, but the
leptospirosis 24685 bile in leptospirosis. Most likely, both mechanisms are at work in the pathogenesis of jaundice in leptospirosis , but the mechanism suggested by Miyhara et al.[41] has strong experimental support and is in accordance
leptospirosis 24808 mechanism suggested by Miyhara et al.[41] has strong experimental support and is in accordance with leptospirosis being a disease with important cell membrane damage.A biopsy study of the liver in leptospirosis during
leptospirosis 24905 with leptospirosis being a disease with important cell membrane damage.A biopsy study of the liver in leptospirosis during recovery[21] showed that the liver architecture is preserved but infrequent mitotic figures are
leptospirosis 25446 variations in size and shape. This shows the importance of a previous general hepatocyte injury in leptospirosis , which cannot be neglected when the pathogenesis of jaundice is discussed.KIDNEY IN LEPTOSPIROSISThe
leptospirosis 25596 pathogenesis of jaundice is discussed.KIDNEY IN LEPTOSPIROSISThe kidney is a common target organ in leptospirosis , and tubule-interstitial nephritis is the most common clinical and pathological manifestation. Clinically, non-oliguric
leptospirosis 25824 Clinically, non-oliguric acute kidney injury with hypokalemia, sodium and magnesium wasting frequently occurs in human leptospirosis . Immunohistochemical exams in autopsy material[43] confirmed a primary lesion of the proximal convoluted
leptospirosis 27097 far unknown[45]. These glomerular alterations might be related to the proteinuria observed in a few leptospirosis patients[46]. Mesangial cell hypertrophy, also focally detected, is a non-specific reactive manifestation
leptospirosis 27428 manifestations such as leptomeningitis and myocarditis are expected during the disease. Myocarditis in leptospirosis was reported initially by Arean in 1957 in 61.5% of the hearts studied[47]. Our data[48] found myocarditis
leptospirosis 27880 the heart in our cases, which might be clinically relevant.Vascular injury is present in the heart in leptospirosis and usually characterized by segmental lesions in on the walls of the coronary artery and their branches. Deposits
leptospirosis 28562 seen by us both in humans and in experimental animals[48].Another interesting vascular lesion seen in leptospirosis is aortitis, found in 57.8% of cases[48]. First described by Arean[49], it resembles syphilitic aortitis
leptospirosis 28921 extension of adventitial inflammation.Therefore, we suggest that the most common and important lesion in leptospirosis is the vascular damage, which affects the endothelial cell as a whole. Moreover, the altered adhesion
leptospirosis 29894 on hepatocytes from human autopsies showed a definite presence of the enzyme in the cell membrane in leptospirosis . Lipase is probably secreted by leptospires during cell adhesion and is probably important in the pathogenesis
leptospirosis 30337 cadherin expression might corroborate suggestions that cell membrane damage is the primary lesion in leptospirosis , which is mediated by unknown factors, among them glycol and/or lipoproteins of the leptospiral surface.
leptospirosis 31480 as an important factor in the mechanism of the disease.CONCLUSIONSIn summary, the primary lesion in leptospirosis seems to be the cell membrane damage mediated by unknown factors, possibly leptospiral proteins and/or
leptospirosis 31888 dysfunctions. Understanding the molecular mechanisms involved in the pathogenesis and pathology of leptospirosis is of utmost importance for prognostic and therapeutic applications
meningitis 27353 MANIFESTATIONS OF LEPTOSPIROSISLeptospirosis is a septicemic disease and manifestations such as lepto meningitis and myocarditis are expected during the disease. Myocarditis in leptospirosis was reported initially
syphilis 28693 found in 57.8% of cases[48]. First described by Arean[49], it resembles syphilitic aortitis but, unlike syphilis , the vasa vasorum fail to show obstructive vasculitis and there are no changes in the aortic media other than
viral hepatitis 24479 experimental leptospirosis is non-specific and differs only in degree from findings associated with viral hepatitis [23], they show the importance of altered hepatocyte transport and chiefly the excretion of bile in leptospirosis.

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