tick-borne diseases – F.I.G.H.T for your health!

Mechanisms of Thrombocytopenia in Tick-Borne Diseases

Linda — Mon, 05 Jul 2010 23:46:01 +0000

Full article: http://www.ispub.com/ostia/index.php

Excerpt:

Thrombocytopenia is a common manifestation of all tick-borne diseases. Low platelet numbers contribute significantly towards the morbidity and mortality of infection. However, the pathogenesis of thrombocytopenia in many of the tick-borne diseases is poorly understood. Quantitative changes in platelet counts associated with infection may result from decreased marrow production, hypersplenism, consumption due to widespread endothelial damage or disseminated intravascular coagulation, as well as immune-mediated platelet destruction. Infection-induced thrombocytopenia may infrequently be associated with serious thrombosis. Direct infection of platelets by selected tick-borne pathogens also facilitates their dissemination within the host. This article reviews the mechanisms of thrombocytopenia associated with tick-borne infections, and discusses the therapeutic options available for managing this potentially fatal complication.

Conclusions

Thrombocytopenia due to tick-borne infection is likely to be of multifactorial etiology. In many of these infections, however, the actual mechanism of thrombocytopenia still remains unknown. Iatrogenic causes in some cases, such as drugs, should not be overlooked. Low platelet numbers in infected individuals may not only manifest with increased bleeding, but may herald more widespread life-threatening microthrombus formation. In addition to quantitative platelet disorders, qualitative defects may also be present. For example, inhibition of platelet migration has been induced by serum from E.canis-infected dogs, even before platelet numbers declined and before the appearance of specific humoral
antibodies (Kakoma et al 1978). The release of platelet factor 3, a phospholipid released from activated platelets that is necessary for the intrinsic conversion of prothrombin to thrombin, is also markedly decreased as a result of ehrlichial infection (Pierce et al 1977). Furthermore, platelet aggregation in ehrlichiosis can be prevented by autoantibodies directed against their surface glycoproteins (Lovering et al 1980; Harrus et al 1996).

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function. However, identification and correction of a specific tick-borne infection is only possible if the infection is considered in the differential diagnosis of thrombocytopenia. Rapid treatment of the underlying infection should result in normalization of platelet counts. Ehrlichia, bartonella and RMSF should also be excluded in cases presenting with a clinical picture resembling TTP, particularly in those patients that prove difficult to manage, and in regions where the incidence of tick-borne illness is high. The efficacy of platelet transfusions in many of the tick-borne diseases is unclear and anecdotal (Van Eeden et al 1985).

A clear and present danger: tick-borne diseases in Europe

Linda — Mon, 15 Mar 2010 04:23:30 +0000

Linda comments: How many of you have friends that live or have lived in Europe? Could they be suffering from tick-borne diseases?

Excerpt:

Ticks can transmit a variety of viruses, bacteria or parasites
that can cause serious infections or conditions in humans and
animals. While tick-borne diseases are becoming an increasing and
serious problem in Europe, tick-borne diseases are also
responsible for major depressions in livestock production and
mortality in sub-Saharan Africa, Latin America and Asia. This
review will focus on the most important circulating
tick-transmitted pathogens in Europe (Borrelia spp., Anaplasma
phagocytophilum, Babesia spp., tick-borne encephalitis virus,
Rickettsia spp. and Crimean-Congo hemorrhagic fever virus).

Persistence mechanisms in tick-borne diseases

Linda — Tue, 22 Dec 2009 07:10:40 +0000

The use of new, highly sensitive diagnostic methods has revealed persistent
infections to be a common feature of different tick-borne diseases, such as
babesiosis, anaplasmosis and heartwater. Antigenic variation can contribute to
disease persistence through the continual elaboration of new surface structures,
and we know in several instances how this is achieved.

Known or suspected mechanisms of persistence in babesial parasites include cytoadhesion and rapid
variation of the adhesive ligand in Babesia bovis and genetic diversity in
several merozoite stage proteins of different Babesia spp. In Anaplasma,
extensive variation in the pfam01617 gene family accompanies cycling of organism
levels in chronic infection. One result from the pioneering research at
Onderstepoort is the definition of a related polymorphic gene family that is
likely involved in immunity against heartwater disease. We are beginning to
understand the sizes of the antigenic repertoires and full definition is close,
with the possibility of applying simultaneous high-throughput sequencing to the
order of 1000 small genomes. We also, for the first time, can consider modifying
these genomes and looking at effects on persistence and virulence. However,
important biological questions remain unanswered; for example, why we are seeing
a new emerging Anaplasma infection of humans and is infection of endothelial
cells by Anaplasma significant to persistence in vivo.

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19967928&retmode=ref&cmd=prlinks
PMID: 19967928 [PubMed – in process]

Onderstepoort J Vet Res. 2009 Mar;76(1):53-8.

Persistence mechanisms in tick-borne diseases.

Barbet AF.

Department of Infectious Diseases & Pathology, College of Veterinary Medicine,
University of Florida, Gainesville, Florida, USA.

Maternal Lyme borreliosis and pregnancy outcome

Linda — Sun, 06 Dec 2009 04:37:45 +0000

Int J Infect Dis. 2009 Nov 17. [Epub ahead of print]

Lakos A, Solymosi N.

The Center for Tick-borne Diseases, Visegrádi 14, Budapest, H-1132, Hungary.

BACKGROUND: There is disagreement regarding whether Lyme borreliosis is associated with adverse pregnancy outcome.

METHODS: We performed a review of the data from 95 women with Lyme borreliosis during pregnancy, evaluated at the Center for Tick-borne Diseases, Budapest over the past 22 years.

RESULTS: Treatment was administered parenterally to 66 (69.5%) women and orally to 19 (20%). Infection remained untreated in 10 (10.5%) pregnancies.

Adverse outcomes were seen in 8/66 (12.1%) parentally treated women, 6/19 (31.6%) orally treated women, and 6/10 (60%) untreated women. In comparison to patients treated with antibiotics, untreated women had a significantly higher risk of adverse pregnancy outcome (odds ratio (OR) 7.61, p=0.004).

While mothers treated orally had an increased chance (OR 3.35) of having an adverse outcome compared to those treated parenterally, this difference was not statistically significant (p=0.052). Erythema migrans did not resolve by the end of the first antibiotic course in 17 patients.

Adverse pregnancy outcome was more frequent among these ‘slow responder’ mothers (OR 2.69), but this was not statistically significant (p=0.1425). Loss of the pregnancy (n=7) and cavernous hemangioma (n=4) were the most prevalent adverse outcomes in our series.
The other complications were heterogeneous.

CONCLUSION: Our results indicate that an untreated maternal Borrelia burgdorferi s.l. infection may be associated with an adverse outcome, although bacterial invasion of the fetus cannot be proven.

It appears that a specific syndrome representing ‘congenital Lyme borreliosis’ is unlikely.

PMID: 19926325 [PubMed – as supplied by publisher]