Lyme disease pathophysiology: Difference between revisions
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Congenital transmission of Lyme disease can occur from an infected mother to [[fetus]] through the [[placenta]] during pregnancy, however prompt antibiotic treatment appears to prevent fetal harm.<ref>{{cite journal |author=Walsh CA, Mayer EW, Baxi LV |title=Lyme disease in pregnancy: case report and review of the literature |journal=Obstetrical & gynecological survey |volume=62 |issue=1 |pages=41-50 |year=2007 |pmid=17176487 |doi=10.1097/01.ogx.0000251024.43400.9a}}</ref> | Congenital transmission of Lyme disease can occur from an infected mother to [[fetus]] through the [[placenta]] during pregnancy, however prompt antibiotic treatment appears to prevent fetal harm.<ref>{{cite journal |author=Walsh CA, Mayer EW, Baxi LV |title=Lyme disease in pregnancy: case report and review of the literature |journal=Obstetrical & gynecological survey |volume=62 |issue=1 |pages=41-50 |year=2007 |pmid=17176487 |doi=10.1097/01.ogx.0000251024.43400.9a}}</ref> | ||
==Life cycle== | |||
{{see|Tick#Life cycle}} | |||
The life-cycle of ''B. burgdorferi'' is complex, requiring ticks, rodents, and deer at various points. Mice are the primary [[Vector (biology)|reservoir]] for the bacteria; [[tick|Ixodes ticks]] then transmit the ''B. burgdorferi'' [[infection]] to deer. | |||
Hard ticks have a variety of life histories with respect to optimizing their chance of contact with an appropriate host to ensure survival. The life stages of soft ticks are not readily distinguishable. The first life stage to come out of the egg, a six legged larva, takes a blood meal from a host, and molts to the first nymphal stage. Unlike hard ticks, many soft ticks go through multiple nymphal stages, gradually increasing in size until the final molt to the adult stage. | |||
The life cycle of the deer tick comprises three growth stages: the larva, nymph and adult. | |||
The life-cycle concept encompassing reservoirs and infections in multiple hosts has recently been expanded to encompass forms of the spirochete which differ from the motile corkscrew form, and these include cystic forms [[spheroplast|spheroplast-like]], straighted non-coiled bacillary forms which are immotile [[flagellin|due to flagellin mutations]] and granular forms [[Coccus|coccoid in profile]]. The model of Plasmodium species Malaria with multiple parasitic profiles demonstrable in various host insects and mammals is a hypothesized model for a similarly complex proposed Borrelia spirochete life cycle. | |||
<ref>Macdonald AB. "A life cycle for Borrelia spirochetes?" Med Hypotheses. 2006;67(4):810-8. PMID 16716532</ref> | |||
<ref>[http://www.lymeinfo.net/medical/LDAdverseConditions.pdf Lymeinfo.net - LDAdverseConditions]</ref> | |||
Whereas B. burgdoferi is most associated with [[deer tick]] and the white footed mouse,<ref>Wallis RC, Brown SE, Kloter KO, Main AJ Jr. Erythema chronicum migrans and lyme arthritis: field study of ticks. Am J Epidemiol. 1978 Oct;108(4):322-7.PMID 727201</ref> B. afzelii is most frequently detected in rodent-feeding vector ticks, B.garinii and B. valaisiana appear to be associated with birds. Both rodents and birds are competent reservoir hosts for Borrelia burgdorferi sensu stricto. The resistance of a genospecies of Lyme disease spirochetes to the bacteriolytic activities of the alternative immune complement pathway of various host species may determine its reservoir host association. | |||
===Ecology=== | ===Ecology=== | ||
Revision as of 19:04, 17 August 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Lyme disease is caused by Borrelia burgdorferi and is transmitted by tick named Ixodes scapularis. Ticks can attach to any part of the human body but are often found in hard-to-see areas such as the groin, armpits, and scalp. In most cases, the tick must be attached for 36 to 48 hours or more before the Lyme disease bacterium can be transmitted.
Pathophysiology
Transmission
Hard-bodied ticks of the genus Ixodes are the primary vectors of Lyme disease. The majority of infections are caused by ticks in the nymph stage, as adult ticks do not become infected through feeding.[1]
In Europe, the commonly known sheep tick, castor bean tick, or European castor bean tick (Ixodes ricinus) is the transmitter.
In North America, the black-legged tick or deer tick (Ixodes scapularis) has been identified as the key to the disease's spread on the east coast. Unfortunately, only about 20% of persons infected with Lyme disease by the deer tick are aware of having had any tick bite,[2] making early detection difficult in the absence of a rash. Another possible vector is the lone star tick (Amblyomma americanum), which is found throughout the southeastern U.S. as far west as Texas, and increasingly in northeastern states as well. These tick bites usually go unnoticed due to the small size of the tick in its nymphal stage, as well as tick secretions that prevent the host from feeling any itch or pain from the bite.
On the west coast, the primary vector is the western black-legged tick (Ixodes pacificus).[3] It was once thought to be a vector, although recent studies demonstrate that this tick species is not a competent vector of Borrelia burgdorferi sensu lato.[4]
While Lyme spirochetes have been found in insects other than ticks,[5] reports of actual infectious transmission appear to be rare.[6] Sexual transmission has been anecdotally reported; Lyme spirochetes have been found in semen[7] and breast milk,[8] however transmission of the spirochete by these routes is not known to occur.[9]
Congenital transmission of Lyme disease can occur from an infected mother to fetus through the placenta during pregnancy, however prompt antibiotic treatment appears to prevent fetal harm.[10]
Life cycle
The life-cycle of B. burgdorferi is complex, requiring ticks, rodents, and deer at various points. Mice are the primary reservoir for the bacteria; Ixodes ticks then transmit the B. burgdorferi infection to deer.
Hard ticks have a variety of life histories with respect to optimizing their chance of contact with an appropriate host to ensure survival. The life stages of soft ticks are not readily distinguishable. The first life stage to come out of the egg, a six legged larva, takes a blood meal from a host, and molts to the first nymphal stage. Unlike hard ticks, many soft ticks go through multiple nymphal stages, gradually increasing in size until the final molt to the adult stage.
The life cycle of the deer tick comprises three growth stages: the larva, nymph and adult.
The life-cycle concept encompassing reservoirs and infections in multiple hosts has recently been expanded to encompass forms of the spirochete which differ from the motile corkscrew form, and these include cystic forms spheroplast-like, straighted non-coiled bacillary forms which are immotile due to flagellin mutations and granular forms coccoid in profile. The model of Plasmodium species Malaria with multiple parasitic profiles demonstrable in various host insects and mammals is a hypothesized model for a similarly complex proposed Borrelia spirochete life cycle. [11] [12]
Whereas B. burgdoferi is most associated with deer tick and the white footed mouse,[13] B. afzelii is most frequently detected in rodent-feeding vector ticks, B.garinii and B. valaisiana appear to be associated with birds. Both rodents and birds are competent reservoir hosts for Borrelia burgdorferi sensu stricto. The resistance of a genospecies of Lyme disease spirochetes to the bacteriolytic activities of the alternative immune complement pathway of various host species may determine its reservoir host association.
Ecology
Urbanization and other anthropogenic factors can be implicated in the spread of the Lyme disease into the human population. In many areas, expansion of suburban neighborhoods has led to the gradual deforestation of surrounding wooded areas and increasing "border" contact between humans and tick-dense areas. Human expansion has also resulted in a gradual reduction of the predators that normally hunt deer as well as mice, chipmunks and other small rodents -- the primary reservoirs for Lyme disease. As a consequence of increased human contact with host and vector, the likelihood of transmission to Lyme residents has greatly increased.[14][15] Researchers are also investigating possible links between global warming and the spread of vector-borne diseases including Lyme disease.[16]
The deer tick (Ixodes scapularis, the primary vector in the northeastern U.S.) has a two-year life cycle, first progressing from larva to nymph, and then from nymph to adult. The tick feeds only once at each stage. In the fall, large acorn forests attract deer as well as mice, chipmunks and other small rodents infected with B. burgdorferi. During the following spring, the ticks lay their eggs. The rodent population then "booms." Tick eggs hatch into larvae, which feed on the rodents; thus the larvae acquire infection from the rodents. (Note: At this stage, it is proposed that tick infestation may be controlled using acaricides (miticide).
Adult ticks may also transmit disease to humans. After feeding, female adult ticks lay their eggs on the ground, and the cycle is complete. On the west coast, Lyme disease is spread by the western black-legged tick (Ixodes pacificus), which has a different life cycle.
The risk of acquiring Lyme disease does not depend on the existence of a local deer population, as is commonly assumed. New research suggests that eliminating deer from smaller areas (less than 2.5 hectares or 6.2 acres) may in fact lead to an increase in tick density and the rise of "tick-borne disease hotspots".[17]
References
- ↑ "Lyme Disease Transmission". Lyme Disease. CDC. 2005-12-07. Retrieved 2007-08-21.
- ↑ Wormser G, Masters E, Nowakowski J; et al. (2005). "Prospective clinical evaluation of patients from missouri and New York with erythema migrans-like skin lesions". Clin Infect Dis. 41 (7): 958–65. PMID 16142659.
- ↑ Clark K (2004). "Borrelia species in host-seeking ticks and small mammals in northern Florida" (PDF). J Clin Microbiol. 42 (11): 5076–86. PMID 15528699.
- ↑ Ledin K, Zeidner N, Ribeiro J; et al. (2005). "Borreliacidal activity of saliva of the tick Amblyomma americanum". Med Vet Entomol. 19 (1): 90–95. PMID 15752182.
- ↑ Magnarelli L, Anderson J (1988). "Ticks and biting insects infected with the etiologic agent of Lyme disease, Borrelia burgdorferi" (PDF). J Clin Microbiol. 26 (8): 1482–6. PMID 3170711.
- ↑ Luger S (1990). "Lyme disease transmitted by a biting fly". N Engl J Med. 322 (24): 1752. PMID 2342543.
- ↑ Bach G (2001). "Recovery of Lyme spirochetes by PCR in semen samples of previously diagnosed Lyme disease patients.". 14th International Scientific Conference on Lyme Disease.
- ↑ Schmidt B, Aberer E, Stockenhuber C; et al. (1995). "Detection of Borrelia burgdorferi DNA by polymerase chain reaction in the urine and breast milk of patients with Lyme borreliosis". Diagn Microbiol Infect Dis. 21 (3): 121–8. PMID 7648832.
- ↑ Steere AC (2003-02-01). "Lyme Disease: Questions and Answers" (PDF). Massachusetts General Hospital / Harvard Medical School. Retrieved 2007-03-22.
- ↑ Walsh CA, Mayer EW, Baxi LV (2007). "Lyme disease in pregnancy: case report and review of the literature". Obstetrical & gynecological survey. 62 (1): 41–50. doi:10.1097/01.ogx.0000251024.43400.9a. PMID 17176487.
- ↑ Macdonald AB. "A life cycle for Borrelia spirochetes?" Med Hypotheses. 2006;67(4):810-8. PMID 16716532
- ↑ Lymeinfo.net - LDAdverseConditions
- ↑ Wallis RC, Brown SE, Kloter KO, Main AJ Jr. Erythema chronicum migrans and lyme arthritis: field study of ticks. Am J Epidemiol. 1978 Oct;108(4):322-7.PMID 727201
- ↑ LoGiudice K, Ostfeld R, Schmidt K, Keesing F (2003). "The ecology of infectious disease: effects of host diversity and community composition on Lyme disease risk". Proc Natl Acad Sci U S A. 100 (2): 567–71. PMID 12525705.
- ↑ Patz J, Daszak P, Tabor G; et al. (2004). "Unhealthy landscapes: Policy recommendations on land use change and infectious disease emergence". Environ Health Perspect. 112 (10): 1092–8. PMID 15238283.
- ↑ Khasnis AA, Nettleman MD (2005). "Global warming and infectious disease". Arch. Med. Res. 36 (6): 689–96. doi:10.1016/j.arcmed.2005.03.041. PMID 16216650.
- ↑ Perkins SE, Cattadori IM, Tagliapietra V, Rizzoli AP, Hudson PJ (2006). "Localized deer absence leads to tick amplification". Ecology. 87 (8): 1981–6. PMID 16937637.