Lyme disease pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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]
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.[11][12] Researchers are also investigating possible links between global warming and the spread of vector-borne diseases including Lyme disease.[13]
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".[14]
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.
- ↑ 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.