Filariasis pathophysiology: Difference between revisions
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====Life cycle of filariasis nematodes==== | ====Life cycle of filariasis nematodes==== | ||
In order to understand how filariasis could occur, it is important to know the [[Life cycle|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.<ref name="Mansonellosis">CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017 </ref><ref name="Loiasis">CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017 </ref><ref name="Onchocerciasis">CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017 </ref> | In order to understand how filariasis could occur, it is important to know the [[Life cycle|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.<ref name="Mansonellosis">CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_b_malayi.html Accessed on June 27, 2017 </ref><ref name="Loiasis">CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017 </ref><ref name="Onchocerciasis">CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017 </ref> | ||
{| class="wikitable" | {| class="wikitable" | ||
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* Coquillettidia.as C. juxtamansonia | * Coquillettidia.as C. juxtamansonia | ||
| rowspan="2" | | | rowspan="2" | | ||
* | * Infected [[mosquito]] bite introduces the third stage larva onto the [[skin]] and then enters to the [[blood]] through the wound. | ||
* The larvae develop to adult which reside in the '''[[lymphatic vessels]]'''. | * The larvae develop to adult which reside in the '''[[lymphatic vessels]]'''. | ||
* Adult worm produce sheathed microfiliae that migrate to [[lymph]] and [[blood]]. They have '''nocturnal periodicity'''. | * Adult worm produce sheathed microfiliae that migrate to [[lymph]] and [[blood]]. They have '''nocturnal periodicity'''. | ||
* Another [[mosquito]] ingests the microfiliae. | * Another [[mosquito]] ingests the microfiliae. | ||
* The microfilariae lose their sheaths and work their way through the wall of the proventriculus and [[cardiac]] portion of the [[midgut]] to reach the | * The microfilariae lose their sheaths and work their way through the wall of the proventriculus and [[cardiac]] portion of the [[midgut]] to reach the thoracic [[muscles]]. | ||
* Microfiliae mature inside the | * Microfiliae mature inside the mosquito till third stage larvae. | ||
* In another bite to a host [[skin]] the mosquito introduces the larvae onto the | * In another bite to a host [[skin]] the mosquito introduces the larvae onto the skin. | ||
| rowspan="2" |[[Image:W bancrofti LifeCycle.gif|350 px|center]] | | rowspan="2" |[[Image:W bancrofti LifeCycle.gif|350 px|center]] | ||
| rowspan="2" | | | rowspan="2" | | ||
* The difference between the | * The difference between the nematodes causing lymphatic filariasis is in the shape and size of the worm. | ||
* The | * The Brugia worms are similar to the W. bancrofti but smaller. | ||
|- | |- | ||
|[[Brugia timori]] and [[Brugia malayi]] | |[[Brugia timori]] and [[Brugia malayi]] | ||
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* Infected fly bite introduces the third stage larva onto the [[skin]] and then enters to the [[blood]] through the [[wound]]. | * Infected fly bite introduces the third stage larva onto the [[skin]] and then enters to the [[blood]] through the [[wound]]. | ||
* The larvae develop to adult which reside in the '''[[subcutaneous tissue]]'''. | * The larvae develop to adult which reside in the '''[[subcutaneous tissue]]'''. | ||
* | * Loa Loa adult worm produce sheathed microfilariae that are found in the blood during day and in the [[lungs]] during the non circulating phase. They have '''diurnal periodicity'''. | ||
* Another fly ingests the | * Another fly ingests the microfiliae. | ||
* After | * After ingestion, the microfilariae lose their sheaths and migrate from the fly's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]]. | ||
* Microfilariae mature inside the fly till third stage larvae. | * Microfilariae mature inside the fly till third stage larvae. | ||
* The third-stage infective larvae migrate to the fly's proboscis and in another bite the cycle restarts. | * The third-stage infective larvae migrate to the fly's proboscis and in another bite the cycle restarts. | ||
| rowspan="4" |[[Image:L loa LifeCycle.gif|350 px|center]] | | rowspan="4" |[[Image:L loa LifeCycle.gif|350 px|center]] | ||
| rowspan="4" | | | rowspan="4" | | ||
* Unlike | * Unlike Loa Loa filaria, Mansonella streptocerca , Mansonella ozzardi and Onchocerca volvolus produce '''unsheathed non-periodic microfilariae'''. | ||
* Mansonela streptocerca adults residue in the | * Mansonela streptocerca adults residue in the dermis. | ||
* Onchocerca volvulus adults residue mainly in the | * Onchocerca volvulus adults residue mainly in the subcutaneous nodules. Their microfilariae can be found in the peripheral [[blood]], [[urine]], and [[sputum]] but are typically found in the [[skin]] and in the [[Lymphatic|lymphatics]] of connective tissue. | ||
|- | |- | ||
|[[Mansonella streptocerca]] | |[[Mansonella streptocerca]] | ||
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* Blackfly (genus Simulium) | * Blackfly (genus Simulium) | ||
| | | | ||
* Infected | * Infected midge bite introduces the third stage larva onto the skin and then enters to the blood through the wound. | ||
* The larvae develop to adult which reside in the different | * The larvae develop to adult which reside in the different body cavities like [[peritoneal cavity]], [[pleural cavity]], and less frequently in the [[pericardium]]. | ||
* Adult | * Adult worm produce unsheathed subperiodic microfilariae that reaches the [[blood stream]]. | ||
* Another midge ingests microfilariae during a [[blood]] meal. | * Another midge ingests microfilariae during a [[blood]] meal. | ||
* After [[ingestion]], the microfilariae migrate from the midge's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]]. | * After [[ingestion]], the microfilariae migrate from the midge's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]]. | ||
* Microfiliae mature inside the midge till third stage larvae. | * Microfiliae mature inside the midge till third stage larvae. | ||
* The third-stage infective larvae migrate to the midge's proboscis and in another | * The third-stage infective larvae migrate to the midge's proboscis and in another bite the cycle restarts. | ||
|[[Image:M perstans LifeCycle.gif|350 px|center]] | |[[Image:M perstans LifeCycle.gif|350 px|center]] | ||
| | | |
Revision as of 15:12, 27 July 2017
Filariasis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Filariasis pathophysiology On the Web |
American Roentgen Ray Society Images of Filariasis pathophysiology |
Risk calculators and risk factors for Filariasis pathophysiology |
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 individual skin introducing these larvae into the skin. The larvae then enter the patient 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 tend to mature in a six to twelve months process to be 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
- Pathogenesis of developing lymphedema and its progression to elephantiasis has been controversial to understand as host related or worm related. A study conducted to completely understand the pathogenesis of the disease showed that some factors have an obvious impact in development of the filariasis clinical manifestations. These factors include the following:[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 |
---|---|
Immune response of the host |
|
Secondary bacterial infections |
|
Wolbachia bacteria |
|
Genetics
- Studies have been held to detect the genetic predisposition probability in patients developing lymphedema.[3]
- It is found that patients who develop primary lymphedema has a mutation in gene of the vascular endothelial growth factor receptor 3 (VEGFR-3). This will lead to dysfunction of the endothelial cells and impairment lymphangiogenesis.[7]
- Mutation in the forkhead transcription factor (FOXC2) also leads to hereditary lymphedema and forms impaired protein.
- The last two genetic mutations increase the possibility of filarial lymphedema to be genetically related and increase the risk of disease occurrence among the same family members.
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][9][10][11]
Type of filariasis | Causative nematode | Vectors | Life cycle | Illustrative image | Distinctive features |
---|---|---|---|---|---|
Lymphatic filariasis | Wuchereria bancrofti |
|
| ||
Brugia timori and Brugia malayi |
| ||||
Subcutaneous filariasis | Loa loa filaria |
|
|
| |
Mansonella streptocerca |
| ||||
Mansonella ozzardi |
| ||||
Onchocerca volvulus |
| ||||
Serous cavity filariasis | Mansonella perstans |
|
|
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
- ↑ 9.0 9.1 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