Videomicroscopy of intralymphatic-dwelling<i>Brugia malayi</i>

Case, Todd; Witte, MH; Way, Dennis; Witte, Charles L.; Crandall, Catherine A.; Crandall, Richard B.

doi:10.1080/00034983.1992.11812690

Cited by 12 publications

(7 citation statements)

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“…The earliest clinically detectable abnormality in filariasis is hindlimb lymphatic dilatation and collateralization related to nests of live adult worms thrashing about inside hindlimb lymphatics. These lymphangiogenic events can not only be seen invasively (Case et al, 1992a) and imaged noninvasively (Witte et al, 1988), but also can be recreated in vitro. This early lymphatic abnormality has been used to screen for productive (microfilaremic) infection and also exploited to follow the efficacy of therapeutic intervention in patients in endemic areas such as northeastern Brazil (Amaral et al, 1994) and in Southern India (Suresh et al, 1997); 8) hydrops fetalis in the ovine fetus (Andres and Brace, 1990) by ligation and excision in utero of the fetal left thoracic, cervical, and brachycephalic lymph ducts dur-ing the last trimester of pregnancy in ewes simulates fetal hydrops and cystic hygroma of Turner syndrome; 9) congenital hereditary lymphedema occurs sporadically in dogs and several other species.…”

Section: Experimental Models Of Lymphvasculogenesismentioning

confidence: 99%

“…Magnetic resonance imaging and nuclear magnetic resonance spectroscopy can also be used to define and quantitate associated structural and biochemical matrix events to pinpoint the alterations that accompany and aggravate abnormal lymphatic growth and lymph stasis. With greater magnification, in vivo microscopy including videomicroscopy can provide other structural and functional details (Case et al, 1992a). From tissue sections, a quantitative cross-sectional index with immunohistochemical differentiation and laser capture microdissection is possible.…”

Section: Lymphvascular Phenotypingmentioning

confidence: 99%

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Lymphangiogenesis and lymphangiodysplasia: From molecular to clinical lymphology

Witte

Bernas

Martin

et al. 2001

Microscopy Res & Technique

188

136

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The lymph vascular system parallels the blood vasculature and as one of its key functions returns liquid and solutes to the bloodstream, including macromolecules that have escaped from blood capillaries and entered the interstitium. In conjunction with interspersed lymph nodes and lymphoid organs, the lymphatic vasculature also acts as a conduit for trafficking immune cell populations. Echoing the explosion of knowledge about blood vessel angiogenesis (properly termed "hemangiogenesis"), the past two decades have also witnessed a series of significant, yet less-noticed discoveries bearing on "lymphangiogenesis," along with delineation of the spectrum of lymphedema-angiodysplasia syndromes. Failure of lymph transport promotes a brawny proteinaceous edema of the affected limb, organ, or serous space that is disfiguring, disabling, and on occasion even life-threatening. Key members of the vascular endothelial growth factor (VEGF) and angiopoietin families of vascular growth factors (and their corresponding tyrosine kinase endothelial receptors) have been identified which preferentially influence lymphatic growth and, when manipulated in genetically engineered murine models, produce aberrant "lymphatic phenotypes." Moreover, mutations in VEGF receptor and forkhead family developmental genes have now been linked and implicated in the pathogenesis of two familial lymphedema-angiodysplasia syndromes. Thus, recent advances in "molecular lymphology" are elucidating the poorly understood development, physiology, and pathophysiology of the neglected lymphatic vasculature. In combination with fresh insights and refined tools in "clinical lymphology," these advances should lead not only to earlier detection and more rational classification of lymphatic disease but also to better therapeutic approaches, including designer drugs for lymphangiostimulation and lymphangioinhibition and gene therapy to modulate lymphatic growth.

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Section: Experimental Models Of Lymphvasculogenesismentioning

confidence: 99%

Section: Lymphvascular Phenotypingmentioning

confidence: 99%

Lymphangiogenesis and lymphangiodysplasia: From molecular to clinical lymphology

Witte

Bernas

Martin

et al. 2001

Microscopy Res & Technique

188

136

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“…The host-parasite interactions most often cited and studied in lymphatic filariasis are those dependent upon an active immune response involving antigen-specific [6][7][8][9] and antigen-nonspecific components. [10][11][12][13] In our description of the interaction of the lymphatic filarial parasite, B. pahangi, with its natural host, the dog, we have reported acute and chronic pathologic lesions, 1 pathogenesis, 1,10 and immunologic responses 6 that are nearly identical with those reported in human lymphatic filariasis. [2][3][4][5] In addition, we have reported on a strong familial association between amicrofilaremia and edema formation in its acute and chronic manifestation.…”

mentioning

confidence: 52%

Association of elevated lymph node cell release of histamine and tumor necrosis factor with genetic predisposition to limb edema formation in dogs infected with Brugia pahangi.

Orton

Weinstock

Hammerberg

1998

The American Journal of Tropical Medicine and Hygiene

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Brugia pahangi infection in the canine rear limb results in marked lymphatic duct and popliteal lymph node pathologic changes. Limb edema is variably associated with infection and does not correlate well with duct or node lesions. To understand the mechanisms of limb edema, lymph node cells were collected by sequential biopsy following infection and examined for production of inflammatory mediators. Lymph node cells from a litter of dogs selectively bred with a high incidence of edema formation (82%) demonstrated spontaneously released histamine and prostaglandin E2 levels higher than those of closely related nonedema-forming dogs (0-20%) and/or control dogs. These edema-forming dogs also showed elevated release of tumor necrosis factor-␣ when cells were cultured with Brugia antigen. Toluidine blue staining of infected lymph node sections revealed that the edema-forming dogs had higher numbers of mast cells than infected lymph nodes of nonedema-forming dogs.

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“…Videom icrography has con® rmed that adult B. malayi have the same rapid, whipping movements that enable W. bancrofti to be detected by ultrasound, at least in ferrets (Case et al, 1992b). This observation tends to rule out the possibility that the present failure to detect adult B. malayi is due to the sluggishness of their movem ents.…”

Section: Discussionmentioning

confidence: 88%

“…The choice of the other locations scanned with ultrasound was mainly in¯uenced by the results of experimental studies using histological (Ahm ed, 1966;Ash and Riley, 1970), lymphoscintigraphic (Case et al, 1992b) and videomicrographic techniques (Case et al, 1992b) and magnetic resonance (Case et al, 1992a). The responses seen in individuals with B. malayi micro® laraemias after treatment with DEC-forti® ed salt also offered clues about the possible location of the adult worms (Shenoy et al, 1998a); lymphnode tenderness and enlargem ent in the inguinal region and dilated, in¯amed lymph atic channels standing out as cords in the upper arm, seen in roughly half the subjects, were probably attributable to the adult worm s.…”

Section: Discussionmentioning

confidence: 99%

Apparent failure of ultrasonography to detect adult worms of Brugia malayi

Shenoy

John²,

Hameed³

et al. 2000

Annals of Tropical Medicine And Parasitology

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Adult worms of Wuchereria bancrofti, or rather their characteristic movements (the 'filarial dance'), can now be detected in the scrotal lymphatics of microfilaraemic males, using ultrasonography. This ability has been used to delineate the lymphatic pathology of bancroftian filariasis, guide the surgical removal of the adult worms and, most importantly, assess the macrofilaricidal effects of antifilarial drugs. In the present study, the first report of the use of ultrasonography in brugian filariasis, 22 men (aged 18-62 years) with 60-2972 (median = 370) Brugia malayi microfilariae/ml blood were subjected to ultrasonography using a linear, 7.5-MHz probe. In addition, four other men (aged 19-35 years), with W. bancrofti microfilaraemia [28-524 (median = 234) microfilariae/ml], were similarly examined. Adult worms were not detectable in any of the patients with B. malayi parasitaemia but were detected in the scrotal lymphatics of two of the four individuals with W. bancrofti infection. The reasons for the failure to detect adult B. malayi and the limitations of ultrasound as a screening tool are examined. The results highlight the differences between the two species that cause most lymphatic filariasis and the need for rapid development of tools that can be used for the control of brugian lymphatic filariasis.

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Videomicroscopy of intralymphatic-dwellingBrugia malayi

Cited by 12 publications

References 1 publication

Lymphangiogenesis and lymphangiodysplasia: From molecular to clinical lymphology

Lymphangiogenesis and lymphangiodysplasia: From molecular to clinical lymphology

Association of elevated lymph node cell release of histamine and tumor necrosis factor with genetic predisposition to limb edema formation in dogs infected with Brugia pahangi.

Apparent failure of ultrasonography to detect adult worms of Brugia malayi

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