Clinical, Parasitologic, And Immunologic Observations Of Patients With Hydrocele And Elephantiasis In An Area With Endemic Lymphatic Filariasis

Addiss, David G.; Dimock, Kathleen A.; Eberhard, Mark L.; Lammie, Patrick J.

doi:10.1093/infdis/171.3.755

Cited by 64 publications

(46 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Antifilarial IgG levels were standardized against a calibrated reference sample generously provided by Dr. Eric Ottesen (formerly of the National Institutes of Health, Bethesda, MD) as previously described. 8,21 IgE assays were performed without prior absorption of IgG. In previous studies of specimens from Haiti, we found no evidence that antifilarial IgG4 interfered with detection of antifilarial IgE.…”

Section: Methodsmentioning

confidence: 64%

“…Assays for antigen-and parasite-specific immunoglobulins were quantified by enzyme-linked immunosorbent assay as previously described. 8,20 Briefly, assays to detect antibody responses to adult filarial antigen (Bpa) were performed using biotinylated monoclonal antibodies (Zymed Laboratories, San Francisco, CA) specific for IgG1, IgG2, IgG3, IgG4, and IgE. Antifilarial IgG levels were standardized against a calibrated reference sample generously provided by Dr. Eric Ottesen (formerly of the National Institutes of Health, Bethesda, MD) as previously described.…”

Section: Methodsmentioning

confidence: 99%

“…7 Third, in many filaria-endemic settings, the prevalence of microfilaremia and antigenemia is significantly lower among persons with lymphedema than among age-matched controls without overt disease, suggesting a possible relationship between heightened antifilarial immunity and disease development. 2,8 According to this model of disease development, parasite antigen stimulation of T cells may be associated with increased local inflammatory responses that promote lymphatic damage, ultimately triggering a cascade of responses that lead to pathology.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis.

Baird¹,

Charles²,

Streit³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. Both secondary infections and antifilarial immunity are thought to play roles in the development and progression of lymphedema. To investigate this issue, immune responses to a panel of bacterial, fungal, and parasite antigens were examined for women with lymphedema and elephantiasis (n ϭ 28) and for women with no clinical evidence of lymphatic dysfunction who were either microfilaremic (Mfϩ, n ϭ 23) or microfilaria-and filarial antigennegative (AgϪ, n ϭ 24). The prevalence and intensity of delayed-type hypersensitivity (DTH) responses was similar for most recall antigens; for individual antigens, lymphedema patients were significantly more likely to be reactive only to Proteus. Lymphedema patients with a history of three or more attacks of adenolymphangitis in the last 18 months showed increased DTH reactivity to Trichophyton. Proliferative responses to fungal and bacterial antigens were similar for all three groups; however, antigen-negative women, independent of disease status, mounted greater responses to filarial antigen. In contrast, lymphedema patients had higher levels of antifilarial specific IgG1, IgG2, and IgG3 and higher IgG responses to streptolysin O than either AgϪ or Mfϩ women. In persons with lymphatic filariasis, immune reactivity is influenced by disease status as well as infection status.

show abstract

Section: Methodsmentioning

confidence: 64%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis.

Baird¹,

Charles²,

Streit³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

show abstract

“…They also do not account for more recently suggested sources of the observed heterogeneity, including acquired immunity, 10,11 maternally-derived immune tolerance, 12,13 and adult-worm induced or immune-mediated pathology. 14,15 Recent work has indicated that one factor that may systematically explain differences in age-patterns of infection and disease between endemic communities in filariasis is parasite transmission intensity. For example, Michael and Bundy used a mathematical modeling approach to demonstrate that variations in community transmission intensity may, via the generation of exposure-driven acquisition of herd immunity, shape the observed age-patterns of infection (microfilaremia) in endemic communities.…”

Section: Introductionmentioning

confidence: 99%

Bancroftian filariasis infection, disease, and specific antibody response patterns in a high and a low endemicity community in East Africa.

Simonsen

Meyrowitsch²,

Jaoko³

et al. 2002

Am J Trop Med Hyg

View full text Add to dashboard Cite

Abstract. Bancroftian filariasis infection, disease and specific antibody response patterns in a high and a low endemicity community in East Africa were analyzed and compared to assess the relationship between these parameters and community transmission intensity. Overall prevalences of microfilaremia and circulating filarial antigenemia were 24.9% and 52.2% in the high and 2.7% and 16.5% in the low endemicity community, respectively. A positive history of acute attacks of adenolymphangitis was given by 12.2% and 7.1% of the populations, 4.0% and 0.9% of the adult (Ն 20 years old) individuals presented with limb lymphedema, and 25.3% and 5.3% of the adult males had hydrocele, in the high and the low endemicity community, respectively. Both infection and disease appeared earlier and reached much higher levels in the high than in the low endemicity community. The observed overall and age-specific infection and disease patterns in the two communities were in agreement with the view that these are primarily shaped by transmission intensity. No statistically significant relationships between infection status of fathers and mothers and that of their children were observed in any of the communities for either microfilaremia or for circulating filarial antigenemia. The overall levels (prevalence and geometric mean intensity) of filarial-specific IgG1, IgG2, IgG4, and IgE were significantly higher in the high endemicity community than in the low endemicity community. Surprisingly, the opposite pattern was found for IgG3. Community transmission intensity thus appears to be an important determinant of observed inter-community variation in infection, disease, and host response patterns in Bancroftian filariasis.

show abstract

“…There is also increasing consensus that progression from this stage to symptomatic disease may occur along different pathways for the two most common manifestations of chronic disease, namely lymphodema and hydrocele. 32 For lymphodema, the available evidence suggests that pathogenesis could involve three possible mechanisms. The first is that disease develops as a natural sequel to worminduced physical damage to the lymphatics, which eventually becomes sufficient to reduce the flow of lymph fluid.…”

mentioning

confidence: 99%

Epifil: a dynamic model of infection and disease in lymphatic filariasis.

Chan

Srividya²,

Norman³

et al. 1998

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. The lack of a quantitative framework that describes the dynamic relationships between infection and morbidity has constrained efforts aimed at the community-level control of lymphatic filariasis. In this paper, we describe the development and validation of EPIFIL, a dynamic model of filariasis infection intensity and chronic disease. Infection dynamics are modeled using the well established immigration-death formulation, incorporating the acquisition of immunity to infective larvae over time. The dynamics of disease (lymphodema and hydrocele) are modeled as a catalytic function of a variety of factors, including worm load and the impact of immunopathological responses. The model was parameterized using age-stratified data collected from a Bancroftian filariasis endemic area in Pondicherry in southern India. The fitted parameters suggest that a relatively simple model including only acquired immunity to infection and irreversible progression to disease can satisfactorily explain the observed infection and disease patterns. Disease progression is assumed to be a consequence of worm induced damage and to occur at a high rate for hydrocele and a low rate for lymphodema. This suggests that immunopathology involvement may not be a necessary component of observed age-disease profiles. These findings support a central role for worm burden in the initiation and progression of chronic filarial disease.Lymphatic filariasis continues to be a significant source of chronic morbidity in the developing world, with more than 120 million people currently thought to be infected with either Wuchereria bancrofti or Brugia malayi, the major lymph-dwelling filariae of humans. 1,2 Despite the considerable advances in intervention options, 3 attempts to control the infection have met with variable success, partially because of inadequate understanding of the epidemiology of transmission and disease. 4,5 This gap in epidemiologic understanding stems from the intricate relationships between infection, immunity and the development of filarial disease. [3][4][5][6][7] This situation may also reflect the lack of a quantitative framework to assist understanding of the long-term effects and costs of intervention. 8 Such mathematical frameworks have played an important role in improving understanding of the epidemiology and control of other helminthiases, including intestinal nematodiases, 9-11 onchocerciasis, 12 and schistosomiasis. 13 Simple epidemiologic models, based on the catalytic models devised by Muench, 14 have been in existence for filariasis since the 1960s.15-17 These models have provided useful insights into the dynamics of filariasis in human populations, including improving the understanding of the roles of host immunity and parasite biology in the epidemiology of infection. Less work exists on the modelling of filarial disease, 5,6,18 despite the importance of morbidity models in improving understanding of the health impacts of parasite control and thus the ability to rationally evaluate different control options in s...

show abstract

Clinical, Parasitologic, And Immunologic Observations Of Patients With Hydrocele And Elephantiasis In An Area With Endemic Lymphatic Filariasis

Cited by 64 publications

References 9 publications

Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis.

Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis.

Bancroftian filariasis infection, disease, and specific antibody response patterns in a high and a low endemicity community in East Africa.

Epifil: a dynamic model of infection and disease in lymphatic filariasis.

Contact Info

Product

Resources

About