Filariasis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2], Ahmed Elsaiey, MBBCH [3]
Overview
Filariasis infection occurs when a larva carrying mosquito bites an individual, introducing these larvae into the skin. The larvae then enters the patient's blood through the skin wound and spread to the different sites such as lymphatic vessels, subcutaneous tissues or the serous cavities. At these sites, the larvae matures in a six to twelve months period into the adult filariae which can live up to fifteen years. Reproduction takes place between the male and female adult worms producing microfilariae which are premature organisms with sheath that circulate the blood in case they are settled in the lymphatic vessels. During another blood meal, the mosquito takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the human body. When a human is bitten by a mosquito, the cycle restarts again. Pathogenesis of the disease depends on number of factors including immune response of the patient, the number of secondary bacterial infections, the accumulation of the worm antigens, release of Wolbachia bacteria from the worm and the genetic predisposition.
Pathophysiology
Pathogenesis
The pathogenesis of lymphedema and its progression to elephantiasis is controversial. Factors involved in the clinical manifestations of filariasis include:[1][2][3][4][5][6]
- Immune response of the patient
- The number of filarial and bacterial infection
- The accumulation of the worm antigen in the lymphatic vessels
- The release of Wolbachia bacteria following death of the worm
Factor | Role in pathogenesis |
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Immune response of the host |
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Secondary bacterial infections |
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Wolbachia bacteria |
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Genetics
- A mutation in the vascular endothelial growth factor receptor 3 (VEGFR-3) is associated with development of primary lymphedema secondary to dysfunction of the endothelial cells and impaired lymphangiogenesis.[3][7]
- Mutation in the forkhead transcription factor (FOXC2) also leads to hereditary lymphedema.
Life cycle of filariasis nematodes
In order to understand how filariasis could occur, it is important to know the life cycles of different nematodes causing filariasis. Through this table the important steps in the worms life cycle is discussed as well as the vectors responsible for disease transmission.[8][9][10][11]
Type of filariasis | Causative nematode | Vectors | Life Cycle |
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Lymphatic filariasis | Wuchereria bancrofti | ||
Brugia timori and Brugia malayi |
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Subcutaneous filariasis | Loa loa filaria |
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Mansonella streptocerca |
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Mansonella ozzardi |
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Onchocerca volvulus |
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Serous cavity filariasis | Mansonella perstans |
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Microscopic pathology
This video gives a brief explanation on the possible histopathological findings of soft tissue sample of case of filariasis: {{#ev:youtube|67zC7mXigpY}}
References
- ↑ Chandy A, Thakur AS, Singh MP, Manigauha A (2011). "A review of neglected tropical diseases: filariasis". Asian Pac J Trop Med. 4 (7): 581–6. doi:10.1016/S1995-7645(11)60150-8. PMID 21803313.
- ↑ Taylor MJ (2002). "A new insight into the pathogenesis of filarial disease". Curr Mol Med. 2 (3): 299–302. PMID 12041732.
- ↑ 3.0 3.1 Lammie PJ, Cuenco KT, Punkosdy GA (2002). "The pathogenesis of filarial lymphedema: is it the worm or is it the host?". Ann N Y Acad Sci. 979: 131–42, discussion 188-96. PMID 12543723.
- ↑ Babu S, Nutman TB (2012). "Immunopathogenesis of lymphatic filarial disease". Semin Immunopathol. 34 (6): 847–61. doi:10.1007/s00281-012-0346-4. PMC 3498535. PMID 23053393.
- ↑ Cross HF, Haarbrink M, Egerton G, Yazdanbakhsh M, Taylor MJ (2001). "Severe reactions to filarial chemotherapy and release of Wolbachia endosymbionts into blood". Lancet. 358 (9296): 1873–5. doi:10.1016/S0140-6736(01)06899-4. PMID 11741630.
- ↑ Kar SK, Mania J, Kar PK (1993). "Humoral immune response during filarial fever in Bancroftian filariasis". Trans R Soc Trop Med Hyg. 87 (2): 230–3. PMID 8337737.
- ↑ Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA; et al. (2000). "Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema". Nat Genet. 25 (2): 153–9. doi:10.1038/75997. PMID 10835628.
- ↑ CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017
- ↑ CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017
- ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017
- ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017