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__NOTOC__
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{{Filariasis}}
{{Filariasis}}
{{CMG}} {{AE}} {{KD}} {{AEL}}  
{{CMG}}; {{AE}} {{KD}}, {{AEL}}  
 
==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 [[Wound|skin wound]] and spread to the different sites such as [[lymphatic vessels]], [[Subcutaneous tissue|subcutaneous tissues]] or the [[Serous cavity|serous cavities]]. At these sites, the larvae matures in a six to twelve months period into the adult [[Filaria|filariae]] which can live up to fifteen years. [[Reproduction]] takes place between the [[male]] and [[female]] adult [[Worm|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 [[Mosquitoes|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 [[Antigen|worm antigens]], release of [[Wolbachia]] [[bacteria]] from the [[worm]] and the [[genetic predisposition]].


==Overview==
==Pathophysiology==
==Pathophysiology==
Generally, filariasis infection occurs when a larva carrying mosquito bites individual skin introducing these larvae onto the skin. The larvae then enter the patient blood through the skin wound and spread to the different sites of infection either lymphatic vessels, subcutaneous tissues or the serous cavities. At those different 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 those microfilariae lose their sheath within two weeks to be larvae that enter the human body when the human is bitten by a mosquito and the cycle restarts again.<ref name="pmid21803313">{{cite journal| author=Chandy A, Thakur AS, Singh MP, Manigauha A| title=A review of neglected tropical diseases: filariasis. | journal=Asian Pac J Trop Med | year= 2011 | volume= 4 | issue= 7 | pages= 581-6 | pmid=21803313 | doi=10.1016/S1995-7645(11)60150-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21803313  }} </ref>
===Pathogenesis===
The pathogenesis of [[lymphedema]] and its progression to [[elephantiasis]] is controversial. Factors involved in the clinical manifestations of filariasis include:<ref name="pmid21803313">{{cite journal| author=Chandy A, Thakur AS, Singh MP, Manigauha A| title=A review of neglected tropical diseases: filariasis. | journal=Asian Pac J Trop Med | year= 2011 | volume= 4 | issue= 7 | pages= 581-6 | pmid=21803313 | doi=10.1016/S1995-7645(11)60150-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21803313  }} </ref><ref name="pmid12041732">{{cite journal| author=Taylor MJ| title=A new insight into the pathogenesis of filarial disease. | journal=Curr Mol Med | year= 2002 | volume= 2 | issue= 3 | pages= 299-302 | pmid=12041732 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12041732  }} </ref><ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref><ref name="pmid23053393">{{cite journal| author=Babu S, Nutman TB| title=Immunopathogenesis of lymphatic filarial disease. | journal=Semin Immunopathol | year= 2012 | volume= 34 | issue= 6 | pages= 847-61 | pmid=23053393 | doi=10.1007/s00281-012-0346-4 | pmc=3498535 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23053393  }} </ref><ref name="pmid11741630">{{cite journal| author=Cross HF, Haarbrink M, Egerton G, Yazdanbakhsh M, Taylor MJ| title=Severe reactions to filarial chemotherapy and release of Wolbachia endosymbionts into blood. | journal=Lancet | year= 2001 | volume= 358 | issue= 9296 | pages= 1873-5 | pmid=11741630 | doi=10.1016/S0140-6736(01)06899-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11741630  }} </ref><ref name="pmid8337737">{{cite journal| author=Kar SK, Mania J, Kar PK| title=Humoral immune response during filarial fever in Bancroftian filariasis. | journal=Trans R Soc Trop Med Hyg | year= 1993 | volume= 87 | issue= 2 | pages= 230-3 | pmid=8337737 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8337737  }}</ref>
*[[Immune response]] of the [[patient]]
*The number of [[filarial]] and [[bacterial infection]]
*The accumulation of the [[Antigen|worm antigen]] in the [[lymphatic vessels]]
*The release of [[Wolbachia]] [[bacteria]] following death of the [[worm]]
 
{| class="wikitable"
!Factor
!Role in pathogenesis
|-
|[[Immune response]] of the host
|
* There is a strong correlation between the host [[immune response]] and [[lymphoedema|lymphedema]] development. 
* Patients with [[lymphedema]] mount a higher immune response when compared to those with [[Microfilaria diurnal|microfilariae]] just circulating in the [[blood]].
* It is believed that the role of the [[Immune system|immune response]] in the development of the lymphedema leads to [[inflammation]] and [[obstruction]] of the [[lymphatic vessels]].
* [[Infection]] by filariasis induces [[cell mediated immunity]] in response to the filarial [[antigens]]. 
* This leads to the production of [[cytokines]] and [[interleukins]]. 
* High levels of [[immunoglobulins]] ([[Immunoglobulin G|IgG]]1,2,3) have been detected in [[patients]] with [[lymphedema]] which increases the evidence of the role of the immune response in pathogenesis of the disease.
|-
|[[Bacterial infections|Secondary bacterial infections]]
|
* Adenolymphangitis is a result of the [[inflammation]] induced by the [[filarial infection]] and the [[immune response]].
* It is believed that it worsens the disease and leads to [[morbidity]].
* It affects the [[lower limbs]] resulting in [[cord]] like lesion of the [[lymphatic vessels]] and worsening of the filariasis.
|-
|Wolbachia [[bacteria]]
|
* [[Nematodes|The round worms]] causing filariasis are carriers of a kind of [[bacteria]] called [[Wolbachia]] that is released after the death of the [[Worm|worms]].
* There is a correlation between [[Wolbachia]] [[bacteria]] and the [[inflammatory]] reactions in cases of filariasis especially in the phase of treatment by [[chemotherapy]] that ends with [[lymphedema]].
* Immunologically, [[serum]] [[antibodies]] released against Wolbachia [[Protein|surface protein]] may also play a role in the development of the [[lymphedema]].
|}


===Pathogenesis===
===Genetics===
*Factors affecting the pathogenesis of filariasis:
*A mutation in the [[Vascular endothelial growth factor|vascular endothelial growth factor receptor 3 (VEGFR-3)]] is associated with development of [[primary lymphedema]] secondary to [[dysfunction]] of the [[endothelial cells]] and [[impairment|impaired]] [[lymphangiogenesis]].<ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref><ref name="pmid10835628">{{cite journal| author=Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA et al.| title=Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema. | journal=Nat Genet | year= 2000 | volume= 25 | issue= 2 | pages= 153-9 | pmid=10835628 | doi=10.1038/75997 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10835628  }} </ref>
**Immune response of the patient
*Mutation in the [[FOXC2|forkhead transcription factor (FOXC2)]] also leads to [[hereditary lymphedema]].  
**Insect bite extent
**The number of filarial and bacterial infection
**The accumulation of the worm antigen in the lymphatic vessels.


===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>


{| class="wikitable"
{| class="wikitable"
Line 20: Line 51:
!Causative nematode
!Causative nematode
!Vectors
!Vectors
!Life cycle
!Life Cycle
!Illustrative image
!Comments
|-
|-
| rowspan="2" |Lymphatic filariasis
| rowspan="2" |Lymphatic filariasis
|[[Wuchereria bancrofti]] 
|[[Wuchereria bancrofti]] 
|
|
* Culex as C. pipiens
* Culex as ''C. pipiens''
* Aedes as A. aegypti
* [[Aedes]] as ''A. aegypti''
*  [[Anopheles]] as A. arabinensis
*  [[Anopheles]] as ''A. arabinensis''
* Coquillettidia.as C. juxtamansonia
* Coquillettidia.as ''C. juxtamansonia''
| rowspan="2" |
| rowspan="2" |[[Image:W bancrofti LifeCycle.gif|500px|thumb|center|Source: https://www.cdc.gov/]]
* 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'''.
* Adult worm produce sheathed microfiliae that migrate to lymph and blood. They have '''nocturnal periodicity'''.
* 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 thoracic muscles
* Microfiliae grow up inside the mosquito till third stage larvae.
* 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" |
* The difference between the nematodes causing lymphatic filariasis is in the shape and size of the worm.
* The Brugia worms are similar to the W. bancrofti but smaller.  
|-  
|-  
|[[Brugia timori]] and [[Brugia malayi]]
|[[Brugia timori]] and [[Brugia malayi]]
Line 53: Line 71:
|
|
* Chrysops  
* Chrysops  
* C. silacea
* ''C. silacea''
* C. dimidiata
* ''C. dimidiata''
| rowspan="4" |
| rowspan="4" |[[Image:L loa LifeCycle.gif|500px|center|thumb|Source: https://www.cdc.gov/]]
* 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'''.
* 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 microfiliae.
* After ingestion, the microfilariae lose their sheaths and migrate from the fly's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]].
* Microfiliae grow up 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.
| rowspan="4" |[[Image:L loa LifeCycle.gif|350 px|center]]
| rowspan="4" |
* Unlike Loa Loa filaria, Mansonella streptocerca , Mansonella ozzardi and Onchocerca volvolus produce '''unsheathed non-periodic microfilariae'''.
* Mansonela streptocerca adults residue in the dermis.
* 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|''Mansonella streptocerca'']]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
|-
|-
|[[Mansonella ozzardi]]
|[[Mansonella ozzardi|''Mansonella ozzardi'']]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
Line 81: Line 87:
* Blackfly (genus Simulium)
* Blackfly (genus Simulium)
|-
|-
|Serous cavity filariasis
|[[Serous cavity|Serous cavity filariasis]]
|[[Mansonella perstans]]
|[[Mansonella perstans]]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
* Blackfly (genus Simulium)  
* Blackfly (genus Simulium)  
|
|[[Image:M perstans LifeCycle.gif|500px|center|thumb|Source: https://www.cdc.gov/]]
* 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 body cavities like [[peritoneal cavity]], [[pleural cavity]], and less frequently in the [[pericardium]].
* Adult worm produce unsheathed subperiodic microfilariae that reaches the blood stream.
* 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]].
* Microfiliae grow up inside the midge till third stage larvae.
* 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]]
|
|}
|}
Life cycles of the roundworms causing filariasis:
 
===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==
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Latest revision as of 21:46, 29 July 2020

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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]

Factor Role in pathogenesis
Immune response of the host
Secondary bacterial infections
Wolbachia bacteria

Genetics

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
Lymphatic filariasis Wuchereria bancrofti 
  • Culex as C. pipiens
  • Aedes as A. aegypti
  • Anopheles as A. arabinensis
  • Coquillettidia.as C. juxtamansonia
Source: https://www.cdc.gov/
Brugia timori and Brugia malayi
  • Mansonia
  • Aedes
Subcutaneous filariasis Loa loa filaria
  • Chrysops
  • C. silacea
  • C. dimidiata
Source: https://www.cdc.gov/
Mansonella streptocerca
  • Midge (genus Culicoides)
Mansonella ozzardi
  • Midge (genus Culicoides)
Onchocerca volvulus
  • Blackfly (genus Simulium)
Serous cavity filariasis Mansonella perstans
  • Midge (genus Culicoides)
  • Blackfly (genus Simulium)
Source: https://www.cdc.gov/

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

  1. ↑ 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.
  2. ↑ Taylor MJ (2002). "A new insight into the pathogenesis of filarial disease". Curr Mol Med. 2 (3): 299–302. PMID 12041732.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017
  9. ↑ CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017
  10. ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017
  11. ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017

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