Tick-Transmitted Infectious Diseases in the United States

Walker, David H.

doi:10.1146/annurev.publhealth.19.1.237

Cited by 97 publications

(78 citation statements)

References 91 publications

(96 reference statements)

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“…Although mosquitoes surpass ticks as vectors of public health importance, ticks transmit the greatest variety of microbial pathogens of any arthropod vector including established, emerging, and resurging infectious agents (Walker 1998, Childs and Paddock 2003, Jongejan and Uilenberg 2004, Telford and Goethert 2004, Dennis and Piesman 2005, Ginsberg and Stafford 2005, Hanincová et al 2006, Walker 2005. The hard-bodied tick Ixodes scapularis transmits causative agents of Lyme disease, human babesiosis, and human granulocytic anaplasmosis (Krause 2002, Steere et al 2004, Dumler et al 2007.…”

mentioning

confidence: 99%

Dermatologic Changes Induced by RepeatedIxodes scapularisBites and Implications for Prevention of Tick-Borne Infection

Krause

Grant‐Kels

Tahan

et al. 2009

Vector-Borne and Zoonotic Diseases

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Previous studies in rodents and people have demonstrated that repeated tick exposure is associated with reduced Borrelia burgdorferi transmission but the mechanism of prevention remains unclear. We examined the acute histopathologic reactions to initial and repeated Ixodes scapularis bites in BALB/c mice and in people. Skin biopsies of BALB/c mice infested for the first time by I. scapularis nymphs revealed vascular dilatation and an accumulation of inflammatory cells adjacent to the bite site but absent at the site of tick attachment. Such changes would enhance tick-borne pathogen transmission. Mice reexposed to I. scapularis nymphs experienced a decrease in vascular dilatation and a marked increase in inflammatory cells at the site of tick attachment. Skin biopsies of people with attached I. scapularis nymphs revealed similar histologic patterns. These results indicate that cellular changes at the tick-dermal interface following I. scapularis attachment are likely to allow for successful transmission of tick-borne pathogens in non-tick-immune hosts and to inhibit tick-borne pathogen transmission in hosts that have developed tick immunity.

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confidence: 99%

Dermatologic Changes Induced by RepeatedIxodes scapularisBites and Implications for Prevention of Tick-Borne Infection

Krause

Grant‐Kels

Tahan

et al. 2009

Vector-Borne and Zoonotic Diseases

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“…Rickettsiae are obligate, intracellular parasites and causative agents of severe bacterial diseases of humans, including epidemic typhus and Rocky Mountain spotted fever, caused, respectively, by Rickettsia prowazekii and R. rickettsii. These bacteria are transmitted to their mammalian hosts by arthropod vectors such as ticks, fleas, lice, and mites and grow within the cytoplasm (and occasionally the nucleus) of eukaryotic cells (37,62). Rickettsiae exhibit a tropism for the endothelium and invade vascular endothelial cells as a major target.…”

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confidence: 99%

“…These bacteria are transmitted to their mammalian hosts by arthropod vectors such as ticks, fleas, lice, and mites and grow within the cytoplasm (and occasionally the nucleus) of eukaryotic cells (37,62). Rickettsiae exhibit a tropism for the endothelium and invade vascular endothelial cells as a major target.…”

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confidence: 99%

Rickettsia rickettsiiInfection of Cultured Human Endothelial Cells Induces Heme Oxygenase 1 Expression

et al. 2002

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Existing evidence suggests that oxidative insults and antioxidant defense mechanisms play a critical role in the host cell response during infection of endothelial cells by Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever. Heme oxygenase (HO), a rate-limiting enzyme in the pathway for heme catabolism, protects against oxidant damage in a variety of stress situations. Here, we report on the expression of the inducible and constitutive HO isozymes, HO-1 and HO-2, during R. rickettsii infection of endothelial cells. Steady-state levels for HO-1 mRNA were increased two-to threefold, as early as 4 h postinfection, whereas HO-2 mRNA was not affected. Induction of HO-1 mRNA was dependent on the dose of infection and occurred in a time-dependent manner, reaching maximal levels at 4 to 7 h. The increase in HO-1 mRNA occurred at the level of trancription as it was blocked by the transcriptional inhibitors, actinomycin D and ␣-amanitin. Rickettsiae are obligate, intracellular parasites and causative agents of severe bacterial diseases of humans, including epidemic typhus and Rocky Mountain spotted fever, caused, respectively, by Rickettsia prowazekii and R. rickettsii. These bacteria are transmitted to their mammalian hosts by arthropod vectors such as ticks, fleas, lice, and mites and grow within the cytoplasm (and occasionally the nucleus) of eukaryotic cells (37,62). Rickettsiae exhibit a tropism for the endothelium and invade vascular endothelial cells as a major target. The proliferation of organisms in capillary endothelium and associated cytopathic effects of infection contribute to increased vascular permeability (57). Studies have suggested that the host endothelial cells actively respond to intracellular infection by altering the expression of several proteins, including tissue factor (50, 56), plasminogen activator inhibitor 1 (13, 44), E-selectin (12, 49), interleukin-1 (IL-1), 51). Ultrastructural studies have shown that infected endothelial cells sustain severe damage at late stages of infection, as indicated by dilatation of the rough endoplasmic reticulum and outer nuclear envelope, loss of osmoregulatory control, and cell lysis (45,46).The mechanisms of cell injury induced by R. rickettsii remain largely unknown. Based on the striking architectural changes in the cytoskeleton of infected cells, it was speculated that reactive oxygen species may be one of the major causes of cell injury by R. rickettsii. Subsequent biochemical analysis confirmed the accumulation of intracellular peroxides and superoxide radicals (42, 47), detection of higher amounts of extracellular hydrogen peroxide in the culture medium of infected cells (21), and reduction in levels of intracellular thiols (48). Further, the activities of three important enzymes of the cellular antioxidant system, namely, glucose-6-phosphate dehydrogenase, catalase, and glutathione peroxidase, were downregulated, while that of superoxide dismutase was increased in endothelial cells exposed to R. rickettsii (11,42). ␣-Lipoic acid...

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“…In several countries, ticks are important public health hazards, since these arthropods are vectors of several bacterial, viral and protozoan tick-borne diseases (Walker, 1998).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological action of tick saliva upon haemostasis and the neutralization ability of sera from repeatedly infested hosts

et al. 2009

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S U M M A R YTicks are blood-feeding arthropods widely distributed in the world and vectors of several diseases. As haematophagy demands evasion strategies and repeatedly infested hosts develop protective immune responses, we investigated the mechanisms of the Rhipicephalus (Boophilus) microplus saliva anti-haemostatic activity and the possible relationship between the acquired natural anti-tick host resistance and anti-haemostatic action. For this purpose, we studied the effects of R. microplus saliva on different pathways of haemostasis and tested whether repeated infested bovine sera (RIBS) are able to abolish salivary anti-haemostatic activities. R. microplus saliva (i) displays inhibitory activity upon collagen-induced platelet aggregation ; (ii) inhibits the induction of endothelial pro-coagulant state ; and (iii) reduces thrombogenesis in vivo. RIBS were shown to be able to partially block the delay of coagulation and the anti-thrombotic effect of saliva, and to totally abolish the modulation of endothelium activation. Conversely, RIBS has no effect on the inhibition of platelet aggregation. These results show, for the first time, the neutralization ability of sera from acquired resistance hosts against tick antihaemostatics. Moreover, this is the first report of a haematophagous parasite able to modulate endothelial cell procoagulant state, and addresses the presence of anti-platelet and anti-thrombotic activity in R. microplus saliva.

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Tick-Transmitted Infectious Diseases in the United States

Cited by 97 publications

References 91 publications

Dermatologic Changes Induced by RepeatedIxodes scapularisBites and Implications for Prevention of Tick-Borne Infection

Dermatologic Changes Induced by RepeatedIxodes scapularisBites and Implications for Prevention of Tick-Borne Infection

Rickettsia rickettsiiInfection of Cultured Human Endothelial Cells Induces Heme Oxygenase 1 Expression

Pharmacological action of tick saliva upon haemostasis and the neutralization ability of sera from repeatedly infested hosts

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