Lähettäjä: Soijuv Lähetetty: 23.1.2006 9:01
Tutkimuksen mukaan sellaisilla henkilöillä, jotka ovat ensin sairastaneet ehrlichioosin ja saavat sen jälkeen borrelioosin, on alhainen Th1 -vaste. Tämä saattaa vaikeuttaa borrelioosista ja muista taudeista paranemista.
Clin Exp Immunol. 2006 Feb;143(2):322-8.
Reduced number of interleukin-12 secreting cells in patients with Lyme borreliosis previously exposed to Anaplasma phagocytophilum.
Jarefors S, Karlsson M, Forsberg P, Eliasson I, Ernerudh J, Ekerfelt C.
Division of Clinical Immunology, Faculty of Health Sciences, University of Linkoping, Sweden.
Summary Lyme borreliosis and human granulocytic ehrlichiosis are tick-borne diseases caused by Borrelia burgdorferi and Anaplasma phagocytophilum, respectively. Infection with A. phagocytophilum has been observed to induce immunosuppression and animal studies suggest that the bacteria might also have prolonged inhibitory effects on immune cells. The aim of this study was to investigate the cytokine secretion in patients exposed previously to A. phagocytophilum and currently infected with B. burgdorferi compared with patients infected with B. burgdorferi and seronegative for A. phagocytophilum. Eight patients with erythema migrans and antibodies against A. phagocytophilum, 15 patients with erythema migrans and negative A. phagocytophilum serology and 15 non-exposed healthy individuals were included in the study. Blood mononuclear cells were stimulated with Borrelia-antigen and the number of cytokine [interleukin (IL)-4, IL-5, IL-12, IL-13 and interferon (IFN)-I(3)]-secreting cells was detected by enzyme-linked immunospot (ELISPOT).
This study shows that patients with a previous exposure to A. phagocytophilum and a current infection with B.burgdorferi have a lower number of Borrelia-specific cells secreting IL-12 compared to Ap seronegative patients infected with B. burgdorferi (P < 0.001), indicating impairment in the ability to mount strong Th1-responses. We suggest that this mirrors a reduced Th1 response caused by A. phagocytophilum which could influence the outcome of the Borrelia infection and, speculatively, may also have implications in other conditions.
PMID: 16412057 [PubMed - in process]
EHRLICHIOOSI + BORRELIOOSI
Valvojat: Jatta1001, Borrelioosiyhdistys, Bb
EHRLICHIOOSI + BORRELIOOSI
Viimeksi muokannut Bb, Pe Maalis 06, 2009 21:57. Yhteensä muokattu 2 kertaa.
Lähettäjä: Soijuv Lähetetty: 28.1.2006 10:07
Ehrlichioosi + borrelioosi 60-vuotiaalla naisella joka oli ollut 3 viikkoa aiemmin vaeltamassa Itävallassa ja Sloveniassa.
Ehlichioosia ei ole juurikaan raportoitu Saksasta, mutta sen mahdollisuus tulee ottaa huomioon erityisesti silloin kun henkilöllä esiintyy kuumetta, leukopeniaa, trompostyopeniaa ja kohonneita maksa-arvoja. Hoito: doksisykliiniä 200mg 3 viikon ajan.
Neljässä päivässä laboratoriotestit normalisoituivat. Maksa-arvot olivat normaalit kuukauden kuluttua. Borrelia vasta-aineet (IgM) sen sijaan oli koholla vielä vuodenkin kuluttua!
Borrelia burgdorferi and Anaplasma phagocytophilum Coinfection
Micha Loebermann,* Volker Fingerle,? Matthias Lademann,* Carlos Fritzsche,* and Emil C. Reisinger*Comments
http://www.cdc.gov/ncidod/EID/vol12no02 ... .htm#email
*University of Rostock Medical School, Rostock, Germany; and ?Ludwig-Maximilian-Universität München, Munich, Germany
Suggested citation for this article
To the Editor: In central Europe, Anaplasma phagocytophilum and Borrelia burgdorferi are transmitted by the hard tick Ixodes ricinus (1). Acute human granulocytic ehrlichiosis (HGE) caused by A. phagocytophilum has rarely been documented in Europe (2). Typical symptoms include fever, headache, myalgia, leukopenia, thrombocytopenia, and abnormal liver function test results. The serologic prevalence ranges from 1.9% to 14% in Germany (1), while clinically apparent infections of HGE have not been reported.
Acute Lyme borreliosis in Europe is associated with erythema migrans (3), recognized in up to 90% of patients (4). Erythema migrans may be accompanied by systemic symptoms such as fever, fatigue, myalgia, arthralgia, headache, or stiff neck (3,4). In southern Germany, an incidence of 111 per 100,000 inhabitants has been reported (4).
A 60-year-old woman from northern Germany was admitted with temperature of <40°C, headache, myalgia, and generalized weakness that had begun 6 days earlier. She had noticed an erythema migrans on her right thigh 4 days before she sought treatment. At admission, a tender, 5 × 8 cm rash and a central papule were seen, but without central clearing. The clinical examination was otherwise normal. Three weeks earlier she had been on a trekking tour in Austria and Slovenia but had not been aware of any tick bites.
The leukocyte count was 3,030/μL (normal 4,000?9,000), with 65% neutrophils, 24% lymphocytes, 10% monocytes, and 1% lymphoid cells. The following results were observed: platelets 127,000/μL (normal 150,000?450,000), aspartate aminotransferase 108 U/L (normal <31), alanine aminotransferase 154 U/L (normal <34), gamma-glutamyl transferase 98 U/L (normal <38 ), lactate dehydrogenase 317 U/L (normal <247), alkaline phosphatase 314 U/L (normal <237), direct bilirubin 4.7 μmol/L (normal <3.4), C-reactive protein 132 mg/L (normal <5), and neopterin 30 nmol/L (normal <10). All other routine laboratory parameters were normal.
May-Grünwald-Giemsa (Fluke, Neu Ulm, Germany)?stained whole-blood smears did not show Anaplasma initially and during follow-up. On admission serum antibody tests were negative for A. phagocytophilum, B. burgdorferi, hepatitis A, B, and C, human herpes virus 6, herpes simplex virus 1 and 2, Epstein-Barr virus, cytomegalovirus, and tickborne encephalitis virus.
Because Lyme borreliosis and possible HGE were suspected, the patient was treated with oral doxycycline 200 mg once daily for 3 weeks. Within 4 days after initiation of treatment, the patient recovered completely; thrombocytes and leukocytes had normalized. Liver enzyme levels were still elevated but had normalized at a follow-up examination 28 days later.
Four days after the initial examination, results for Borrelia-specific immunoglobulin M (IgM) antibodies were positive, while results for IgG antibodies remained negative (Table). Four weeks after the onset of symptoms, a test for A. phagocytophilum?specific IgM antibodies was positive and IgG was negative thereafter (Table). An initial EDTA blood sample that was stored frozen and examined retrospectively as well as follow-up EDTA blood samples were negative for A. phagocytophilum in a polymerase chain reaction (PCR) assay.
One year after initial examination, results for Borrelia-specific IgM antibodies were positive and results for A. phagocytophilum-specific antibodies were negative (Table). Although HGE has not been reported in Germany, a coinfection with B. burgdorferi and A. phagocytophilum should be considered in patients with erythema migrans and atypical changes for Lyme borreliosis such as fever, leukopenia, thrombocytopenia, and elevated liver function test results.
The patient had traveled to an area where both tickborne pathogens, A. phagocytophilum and B. burgdorferi, were endemic. Erythema migrans and antibody follow up suggested Lyme borreliosis. High fever, leukopenia, thrombocytopenia, and elevated liver enzyme levels indicated HGE. Anaplasma PCR was negative, possibly because blood samples were tested retrospectively after 3 months of storage at ?20°C. However, a commercially available indirect fluorescent antibody assay was able to demonstrate seroconversion of HGE-specific IgM antibodies 1 month after the initial onset of symptoms. According to manufacturer's information, specificity ranged from 97.5% to 100%; sensitivity was 71.4% at 60 days after A. phagocytophilum infection. A. phagocytophilum IgG antibodies were not detected during follow-up, likely because of prompt treatment with doxycycline.
Wormser et al. (5) suggested that Borrelia-specific antibodies might indicate false-positive results in patients with HGE infection. Our case, however, meets criteria of a newly acquired infection with B. burgdorferi sensu lato, with an erythema migrans and seroconversion of Borrelia-specific IgM antibodies.
References
1. Fingerle V, Goodman JL, Johnson RC, Kurtti TJ, Munderloh UG, Wilske B. Human granulocytic ehrlichiosis in southern Germany: Increased seroprevalence in high-risk groups. J Clin Microbiol. 1997;35:3244?7.
2. Lotric-Furlan S, Petrovec M, Avsic-Zupanc T, Nicholson WL, Sumner JW, Childs JE, et al. Prospective assessment of the etiology of acute febrile illness after a tick bite in Slovenia. Clin Infect Dis. 2001;33:503?10.
3. Weber K, Neupert U, Büchner SA. Erythema migrans and early signs and symptoms. In: Weber K, Burgdorfer W, editors. Aspects of Lyme borreliosis. Berlin: Springer; 1993. p.105?22.
4. Huppertz HI, Böhme M, Standaert SM, Karch H, Plotkin SA. Incidence of Lyme borreliosis in the Würzburg region of Germany. Eur J Clin Microbiol Infect Dis. 1999;18:697?703.
5. Wormser GP, Horowitz HW, Dumer JS, Schwartz I, Aguero-Rosenfeld M. False-positive Lyme disease serology in human granulocytic ehrlichiosis. Lancet. 1996;347:981?2.
Table. Results of serologic tests at diagnosis and during follow-up*
Time (d) after onset of symptoms
Anaplasma (Ehrlichia) phagocytophilum (IFA)?
Borrelia burgdorferi (ELISA)?
Borrelia burgdorferi (Immunoblot)§
IgM
IgG
IgM
IgG
IgM
IgG
6
Negative (<1:20)
Negative (<1:32)
Negative
Negative
Negative
Negative
10
ND
ND
Positive
Negative
ND
ND
28
Positive (1:40)
Negative (1:32)
Positive
Negative
Positive
Negative
107
Positive (1:20)
Negative (<1:32)
Positive
Negative
Positive
Negative
380
Negative (<1:20)
Negative (<1:32)
Equivocal
Negative
Positive
Negative
*Symptoms (fever, headache, myalgia) started 6 days before presentation. IFA, immunofluorescent assay; ELISA, enzyme-linked immunosorbent assay; Ig, immunoglobulin; ND, not done.
?Genzyme Virotech, Germany. Positive titers: IgM >1:20, IgG >1:64.
?Behring, Germany.
§In-house Immunoblot, Max von Pettenkofer-Institut, Munich, Germany.
Ehrlichioosi + borrelioosi 60-vuotiaalla naisella joka oli ollut 3 viikkoa aiemmin vaeltamassa Itävallassa ja Sloveniassa.
Ehlichioosia ei ole juurikaan raportoitu Saksasta, mutta sen mahdollisuus tulee ottaa huomioon erityisesti silloin kun henkilöllä esiintyy kuumetta, leukopeniaa, trompostyopeniaa ja kohonneita maksa-arvoja. Hoito: doksisykliiniä 200mg 3 viikon ajan.
Neljässä päivässä laboratoriotestit normalisoituivat. Maksa-arvot olivat normaalit kuukauden kuluttua. Borrelia vasta-aineet (IgM) sen sijaan oli koholla vielä vuodenkin kuluttua!
Borrelia burgdorferi and Anaplasma phagocytophilum Coinfection
Micha Loebermann,* Volker Fingerle,? Matthias Lademann,* Carlos Fritzsche,* and Emil C. Reisinger*Comments
http://www.cdc.gov/ncidod/EID/vol12no02 ... .htm#email
*University of Rostock Medical School, Rostock, Germany; and ?Ludwig-Maximilian-Universität München, Munich, Germany
Suggested citation for this article
To the Editor: In central Europe, Anaplasma phagocytophilum and Borrelia burgdorferi are transmitted by the hard tick Ixodes ricinus (1). Acute human granulocytic ehrlichiosis (HGE) caused by A. phagocytophilum has rarely been documented in Europe (2). Typical symptoms include fever, headache, myalgia, leukopenia, thrombocytopenia, and abnormal liver function test results. The serologic prevalence ranges from 1.9% to 14% in Germany (1), while clinically apparent infections of HGE have not been reported.
Acute Lyme borreliosis in Europe is associated with erythema migrans (3), recognized in up to 90% of patients (4). Erythema migrans may be accompanied by systemic symptoms such as fever, fatigue, myalgia, arthralgia, headache, or stiff neck (3,4). In southern Germany, an incidence of 111 per 100,000 inhabitants has been reported (4).
A 60-year-old woman from northern Germany was admitted with temperature of <40°C, headache, myalgia, and generalized weakness that had begun 6 days earlier. She had noticed an erythema migrans on her right thigh 4 days before she sought treatment. At admission, a tender, 5 × 8 cm rash and a central papule were seen, but without central clearing. The clinical examination was otherwise normal. Three weeks earlier she had been on a trekking tour in Austria and Slovenia but had not been aware of any tick bites.
The leukocyte count was 3,030/μL (normal 4,000?9,000), with 65% neutrophils, 24% lymphocytes, 10% monocytes, and 1% lymphoid cells. The following results were observed: platelets 127,000/μL (normal 150,000?450,000), aspartate aminotransferase 108 U/L (normal <31), alanine aminotransferase 154 U/L (normal <34), gamma-glutamyl transferase 98 U/L (normal <38 ), lactate dehydrogenase 317 U/L (normal <247), alkaline phosphatase 314 U/L (normal <237), direct bilirubin 4.7 μmol/L (normal <3.4), C-reactive protein 132 mg/L (normal <5), and neopterin 30 nmol/L (normal <10). All other routine laboratory parameters were normal.
May-Grünwald-Giemsa (Fluke, Neu Ulm, Germany)?stained whole-blood smears did not show Anaplasma initially and during follow-up. On admission serum antibody tests were negative for A. phagocytophilum, B. burgdorferi, hepatitis A, B, and C, human herpes virus 6, herpes simplex virus 1 and 2, Epstein-Barr virus, cytomegalovirus, and tickborne encephalitis virus.
Because Lyme borreliosis and possible HGE were suspected, the patient was treated with oral doxycycline 200 mg once daily for 3 weeks. Within 4 days after initiation of treatment, the patient recovered completely; thrombocytes and leukocytes had normalized. Liver enzyme levels were still elevated but had normalized at a follow-up examination 28 days later.
Four days after the initial examination, results for Borrelia-specific immunoglobulin M (IgM) antibodies were positive, while results for IgG antibodies remained negative (Table). Four weeks after the onset of symptoms, a test for A. phagocytophilum?specific IgM antibodies was positive and IgG was negative thereafter (Table). An initial EDTA blood sample that was stored frozen and examined retrospectively as well as follow-up EDTA blood samples were negative for A. phagocytophilum in a polymerase chain reaction (PCR) assay.
One year after initial examination, results for Borrelia-specific IgM antibodies were positive and results for A. phagocytophilum-specific antibodies were negative (Table). Although HGE has not been reported in Germany, a coinfection with B. burgdorferi and A. phagocytophilum should be considered in patients with erythema migrans and atypical changes for Lyme borreliosis such as fever, leukopenia, thrombocytopenia, and elevated liver function test results.
The patient had traveled to an area where both tickborne pathogens, A. phagocytophilum and B. burgdorferi, were endemic. Erythema migrans and antibody follow up suggested Lyme borreliosis. High fever, leukopenia, thrombocytopenia, and elevated liver enzyme levels indicated HGE. Anaplasma PCR was negative, possibly because blood samples were tested retrospectively after 3 months of storage at ?20°C. However, a commercially available indirect fluorescent antibody assay was able to demonstrate seroconversion of HGE-specific IgM antibodies 1 month after the initial onset of symptoms. According to manufacturer's information, specificity ranged from 97.5% to 100%; sensitivity was 71.4% at 60 days after A. phagocytophilum infection. A. phagocytophilum IgG antibodies were not detected during follow-up, likely because of prompt treatment with doxycycline.
Wormser et al. (5) suggested that Borrelia-specific antibodies might indicate false-positive results in patients with HGE infection. Our case, however, meets criteria of a newly acquired infection with B. burgdorferi sensu lato, with an erythema migrans and seroconversion of Borrelia-specific IgM antibodies.
References
1. Fingerle V, Goodman JL, Johnson RC, Kurtti TJ, Munderloh UG, Wilske B. Human granulocytic ehrlichiosis in southern Germany: Increased seroprevalence in high-risk groups. J Clin Microbiol. 1997;35:3244?7.
2. Lotric-Furlan S, Petrovec M, Avsic-Zupanc T, Nicholson WL, Sumner JW, Childs JE, et al. Prospective assessment of the etiology of acute febrile illness after a tick bite in Slovenia. Clin Infect Dis. 2001;33:503?10.
3. Weber K, Neupert U, Büchner SA. Erythema migrans and early signs and symptoms. In: Weber K, Burgdorfer W, editors. Aspects of Lyme borreliosis. Berlin: Springer; 1993. p.105?22.
4. Huppertz HI, Böhme M, Standaert SM, Karch H, Plotkin SA. Incidence of Lyme borreliosis in the Würzburg region of Germany. Eur J Clin Microbiol Infect Dis. 1999;18:697?703.
5. Wormser GP, Horowitz HW, Dumer JS, Schwartz I, Aguero-Rosenfeld M. False-positive Lyme disease serology in human granulocytic ehrlichiosis. Lancet. 1996;347:981?2.
Table. Results of serologic tests at diagnosis and during follow-up*
Time (d) after onset of symptoms
Anaplasma (Ehrlichia) phagocytophilum (IFA)?
Borrelia burgdorferi (ELISA)?
Borrelia burgdorferi (Immunoblot)§
IgM
IgG
IgM
IgG
IgM
IgG
6
Negative (<1:20)
Negative (<1:32)
Negative
Negative
Negative
Negative
10
ND
ND
Positive
Negative
ND
ND
28
Positive (1:40)
Negative (1:32)
Positive
Negative
Positive
Negative
107
Positive (1:20)
Negative (<1:32)
Positive
Negative
Positive
Negative
380
Negative (<1:20)
Negative (<1:32)
Equivocal
Negative
Positive
Negative
*Symptoms (fever, headache, myalgia) started 6 days before presentation. IFA, immunofluorescent assay; ELISA, enzyme-linked immunosorbent assay; Ig, immunoglobulin; ND, not done.
?Genzyme Virotech, Germany. Positive titers: IgM >1:20, IgG >1:64.
?Behring, Germany.
§In-house Immunoblot, Max von Pettenkofer-Institut, Munich, Germany.
Viimeksi muokannut Bb, Pe Maalis 06, 2009 21:59. Yhteensä muokattu 1 kertaa.
Lähettäjä: Soijuv Lähetetty: 30.1.2006 10:21
Yhteisinfektiolla vaikutus sairauden vaikeusasteeseen, johtuen suuremmasta taudinaiheuttajien määrästä + ehrlichian kyvystä muuttaa immuunivastetta:
Infect Immun. 2001 May;69(5):3359-71.
Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis alters murine immune responses, pathogen burden, and severity of Lyme arthritis.
Thomas V, Anguita J, Barthold SW, Fikrig E.
Section of Rheumatology, Department of Internal Medicine, Yale University
School of Medicine, New Haven, Connecticut 06520, USA.
Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively.
We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with B. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera.
During dual infection, IFN-gamma receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.
PMID: 11292759 [PubMed - indexed for MEDLINE]
Yhteisinfektiolla vaikutus sairauden vaikeusasteeseen, johtuen suuremmasta taudinaiheuttajien määrästä + ehrlichian kyvystä muuttaa immuunivastetta:
Infect Immun. 2001 May;69(5):3359-71.
Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis alters murine immune responses, pathogen burden, and severity of Lyme arthritis.
Thomas V, Anguita J, Barthold SW, Fikrig E.
Section of Rheumatology, Department of Internal Medicine, Yale University
School of Medicine, New Haven, Connecticut 06520, USA.
Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively.
We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with B. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera.
During dual infection, IFN-gamma receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.
PMID: 11292759 [PubMed - indexed for MEDLINE]
Viimeksi muokannut Bb, Pe Maalis 06, 2009 22:01. Yhteensä muokattu 2 kertaa.
Lähettäjä: Soijuv Lähetetty: 30.1.2006 10:21
Yhteisinfektiolla vaikutus sairauden vaikeusasteeseen, johtuen suuremmasta taudinaiheuttajien määrästä + ehrlichian kyvystä muuttaa immuunivastetta:
Infect Immun. 2001 May;69(5):3359-71.
Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis alters murine immune responses, pathogen burden, and severity of Lyme arthritis.
Thomas V, Anguita J, Barthold SW, Fikrig E.
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively.
We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with B. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera.
During dual infection, IFN-gamma receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.
PMID: 11292759 [PubMed - indexed for MEDLINE]
Yhteisinfektiolla vaikutus sairauden vaikeusasteeseen, johtuen suuremmasta taudinaiheuttajien määrästä + ehrlichian kyvystä muuttaa immuunivastetta:
Infect Immun. 2001 May;69(5):3359-71.
Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis alters murine immune responses, pathogen burden, and severity of Lyme arthritis.
Thomas V, Anguita J, Barthold SW, Fikrig E.
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne illnesses caused by Borrelia burgdorferi and the agent of HGE, respectively.
We investigated the influence of dual infection with B. burgdorferi and the HGE agent on the course of murine Lyme arthritis and granulocytic ehrlichiosis. Coinfection resulted in increased levels of both pathogens and more severe Lyme arthritis compared with those in mice infected with B. burgdorferi alone. The increase in bacterial burden during dual infection was associated with enhanced acquisition of both organisms by larval ticks that were allowed to engorge upon infected mice. Coinfection also resulted in diminished interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha levels and elevated IL-6 levels in murine sera.
During dual infection, IFN-gamma receptor expression on macrophages was also reduced, implying a decrease in phagocyte activation. These results suggest that coinfection of mice with B. burgdorferi and the HGE agent modulates host immune responses, resulting in increased bacterial burden, Lyme arthritis, and pathogen transmission to the vector.
PMID: 11292759 [PubMed - indexed for MEDLINE]
Viimeksi muokannut Bb, Pe Maalis 06, 2009 22:02. Yhteensä muokattu 1 kertaa.
Lähettäjä: Soijuv Lähetetty: 5.4.2006 11:42
Ehrlichioosi saattaa aiheuttaa erilaisia keskushermosto-oireita. Hoito: Ensisijaisesti doksisykliiniä. Riittävästä hoidon pituudesta ja annoskoosta ei ole olemassa riittavästi tutkimuksia. Ehrlichioosi saattaa esiintyä yhdessä borrelioosin kanssa ja hoito saattaa sen vuoksi olla normaalia pidempi.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Curr Treat Options Neurol. 2006 May;8(3):179-84.
Ehrlichia infection of the central nervous system.
Hongo I, Bloch KC.
Division of Infectious Diseases, Vanderbilt University School of Medicine, A-2200 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232, USA. igen.hongo@vanderbilt.edu.
Ehrlichiosis in the United States is caused by three closely related bacterial species (Ehrlichia chaffeensis, Ehrlichia ewingii, and Anaplasma phagocytophilum), all transmitted through tick bite. Although there is variation with respect to geography and tick vector, the clinical manifestations are similar, and treatment of these infections is identical.
Ehrlichiosis can present with a spectrum of neurologic manifestations, ranging in severity from headache to meningoencephalitis. Treatment is straightforward if the diagnosis is suspected, but antibiotic therapy should not be delayed pending laboratory confirmation. Doxycycline, the treatment of choice for adults and children with suspected ehrlichiosis, has high bioavailability and can be administered orally in most cases. Therapy is typically continued at least 3 days after the last documented fever.
Although there have been no studies specifically evaluating duration or dosing of doxycycline for Ehrlichia meningoencephalitis, anecdotal reports suggest 100 mg doxycycline administered twice daily is effective, despite limited penetration into the cerebrospinal fluid. Because doxycycline interacts with CYP3A4 enzymes, there is potential for drug interactions with a number of medications.
In endemic areas, documentation of coinfection with Borrelia burgdorferi, the etiologic agent of Lyme disease, may require prolonging the duration of doxycycline therapy.
PMID: 16569376 [PubMed - in process]
Ehrlichioosi saattaa aiheuttaa erilaisia keskushermosto-oireita. Hoito: Ensisijaisesti doksisykliiniä. Riittävästä hoidon pituudesta ja annoskoosta ei ole olemassa riittavästi tutkimuksia. Ehrlichioosi saattaa esiintyä yhdessä borrelioosin kanssa ja hoito saattaa sen vuoksi olla normaalia pidempi.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Curr Treat Options Neurol. 2006 May;8(3):179-84.
Ehrlichia infection of the central nervous system.
Hongo I, Bloch KC.
Division of Infectious Diseases, Vanderbilt University School of Medicine, A-2200 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232, USA. igen.hongo@vanderbilt.edu.
Ehrlichiosis in the United States is caused by three closely related bacterial species (Ehrlichia chaffeensis, Ehrlichia ewingii, and Anaplasma phagocytophilum), all transmitted through tick bite. Although there is variation with respect to geography and tick vector, the clinical manifestations are similar, and treatment of these infections is identical.
Ehrlichiosis can present with a spectrum of neurologic manifestations, ranging in severity from headache to meningoencephalitis. Treatment is straightforward if the diagnosis is suspected, but antibiotic therapy should not be delayed pending laboratory confirmation. Doxycycline, the treatment of choice for adults and children with suspected ehrlichiosis, has high bioavailability and can be administered orally in most cases. Therapy is typically continued at least 3 days after the last documented fever.
Although there have been no studies specifically evaluating duration or dosing of doxycycline for Ehrlichia meningoencephalitis, anecdotal reports suggest 100 mg doxycycline administered twice daily is effective, despite limited penetration into the cerebrospinal fluid. Because doxycycline interacts with CYP3A4 enzymes, there is potential for drug interactions with a number of medications.
In endemic areas, documentation of coinfection with Borrelia burgdorferi, the etiologic agent of Lyme disease, may require prolonging the duration of doxycycline therapy.
PMID: 16569376 [PubMed - in process]
Viimeksi muokannut Bb, Pe Maalis 06, 2009 22:03. Yhteensä muokattu 1 kertaa.
Lähettäjä: Soijuv Lähetetty: 5.4.2006 11:57
Ehrlichioosin hoitoon käytetään yleisesti Doksisykliiniä. Tutkimuksen mukaan se ei näyttänyt olevan kovin tehokas eläinten Ehrlichioosin hoidossa. Eläimillä havaittiin plasmasytoosia, joka vaurioittaa munuaisia.
J Clin Microbiol. 1994 Jul;32(7):1644-9.
Reisolation of Ehrlichia canis from blood and tissues of dogs after
doxycycline treatment.
Iqbal Z, Rikihisa Y.
Department of Veterinary Pathobiology, Ohio State University, Columbus
43210.
We present evidence that supports the carrier status of dogs experimentally infected with Ehrlichia canis after treatment with doxycycline. Canine ehrlichiosis was induced in five dogs by intravenous inoculation with E. canis-infected DH82 cells. All animals developed mild clinical signs of transient fever, body weight loss, thrombocytopenia, and increased gamma globulin levels in plasma. An indirect fluorescent-antibody test (IFA) revealed that all dogs had seroconverted (titer, 5,120) by day 10 postinoculation (p.i.). E. canis was reisolated from blood samples collected at intervals throughout the 2-month period p.i. Doxycycline was administered orally once daily at 10 mg/kg of body weight per day for 1 week starting at 2 months p.i. Following treatment, gamma globulin levels in plasma were decreased. At necropsy on days 54 to 59 after the start of treatment, spleen, liver, kidney, and lymph nodes were collected for E. canis culture and histopathologic examination. Although the dogs did not show significant clinical signs during or after treatment with the antibiotic, E. canis was reisolated from the blood and tissue samples of three of five dogs. A 16-fold reduction in IFA titer was noted in two dogs which were negative for E. canis reisolation at day 49 after the start of treatment, whereas a zero- to fourfold reduction in IFA titer was seen in the remaining three dogs.
Western immunoblot reactions to higher-molecular-size E. canis antigens in the sera of two dogs which were negative for E. canis on blood culture decreased, whereas they remained continuously high or only transiently decreased for the duration of the study for antigens in the sera of three dogs from which E. canis was reisolated.
Histopathologically, prominentplasmacytosis in the kidney cortex was present in three dogs from which E. canis was reisolated, whereas the kidney cortices of two dogs had moderate to minor plasmacytosis.
These findings pose questions regarding the efficacy, dosage and duration of doxycycline treatment in dogs with E. canis infection. In addition, it was shown that IFA and Western immunoblotting may aid in assessing the efficacy of antibiotic therapy when definitive reisolation procedures are not readily available.
PMID: 7929751 [PubMed - indexed for MEDLINE]
Ehrlichioosin hoitoon käytetään yleisesti Doksisykliiniä. Tutkimuksen mukaan se ei näyttänyt olevan kovin tehokas eläinten Ehrlichioosin hoidossa. Eläimillä havaittiin plasmasytoosia, joka vaurioittaa munuaisia.
J Clin Microbiol. 1994 Jul;32(7):1644-9.
Reisolation of Ehrlichia canis from blood and tissues of dogs after
doxycycline treatment.
Iqbal Z, Rikihisa Y.
Department of Veterinary Pathobiology, Ohio State University, Columbus
43210.
We present evidence that supports the carrier status of dogs experimentally infected with Ehrlichia canis after treatment with doxycycline. Canine ehrlichiosis was induced in five dogs by intravenous inoculation with E. canis-infected DH82 cells. All animals developed mild clinical signs of transient fever, body weight loss, thrombocytopenia, and increased gamma globulin levels in plasma. An indirect fluorescent-antibody test (IFA) revealed that all dogs had seroconverted (titer, 5,120) by day 10 postinoculation (p.i.). E. canis was reisolated from blood samples collected at intervals throughout the 2-month period p.i. Doxycycline was administered orally once daily at 10 mg/kg of body weight per day for 1 week starting at 2 months p.i. Following treatment, gamma globulin levels in plasma were decreased. At necropsy on days 54 to 59 after the start of treatment, spleen, liver, kidney, and lymph nodes were collected for E. canis culture and histopathologic examination. Although the dogs did not show significant clinical signs during or after treatment with the antibiotic, E. canis was reisolated from the blood and tissue samples of three of five dogs. A 16-fold reduction in IFA titer was noted in two dogs which were negative for E. canis reisolation at day 49 after the start of treatment, whereas a zero- to fourfold reduction in IFA titer was seen in the remaining three dogs.
Western immunoblot reactions to higher-molecular-size E. canis antigens in the sera of two dogs which were negative for E. canis on blood culture decreased, whereas they remained continuously high or only transiently decreased for the duration of the study for antigens in the sera of three dogs from which E. canis was reisolated.
Histopathologically, prominentplasmacytosis in the kidney cortex was present in three dogs from which E. canis was reisolated, whereas the kidney cortices of two dogs had moderate to minor plasmacytosis.
These findings pose questions regarding the efficacy, dosage and duration of doxycycline treatment in dogs with E. canis infection. In addition, it was shown that IFA and Western immunoblotting may aid in assessing the efficacy of antibiotic therapy when definitive reisolation procedures are not readily available.
PMID: 7929751 [PubMed - indexed for MEDLINE]
Viimeksi muokannut Bb, Pe Maalis 06, 2009 22:05. Yhteensä muokattu 1 kertaa.
Lähettäjä: Soijuv Lähetetty: 18.5.2006 10:44
23-vuotiaalla serbialaisella ilmeni kuumetta, päänsärkyä, oksentelua, yleistä heikkoutta jne. Häneltä löytyi ehrlichioosi.
Vojnosanit Pregl. 2006 Apr;63(4):403-8.
[Human ehrlichiosis]
[Article in Serbian]
Dokic M, Curcic P, Nozic D, Lako B, Begovic V, Rajic-Dimitrijevic R, Hristovic D.
Vojnomedicinska akademija, Klinika za infektivne i tropske bolesti, Beograd. milomirdj@yahoo.com
BACKGROUND: Human ehrlichiosis is a newly recognized disease. It is a tick-borne disease caused by several bacterial species of the genhus Erlichia. These are small gram-negative pleomorphic cocci, that are obligatory intracellular bacteria. Tick Ixodes is the principle vector in Europe, and Amblyomma amenicanum in the United States. Bacterial organisms replicate in a tick, and are transmited from infected cells in a vector to the blood cells of animals or humans. Human ehrlichiosis is a name for a group of diseases caused by different species of Ehrlichia. One of them is the disease named human monocytic ehrlichiosis, caused by Ehrlichia chaffeensis, and the other is a human granulocytic ehrlichiosis caused by Anaplasma phagocytophilia.
CASE REPORT: We reported a 23-year-old patient admitted for the clinical treatment with the symptoms of high febrility (above 40 degrees C), headache, vomiting, general weakness and exhaustion, but without data on a tick bite. The patient was treated with trimetoprim-sulfamethoxazole for a week when Ehrlichia chaffeensis was confirmed by the immunofluoroscence test, and the therapy contimed with doxacyclin.
CONCLUSION: Human ehrlichiosis is also present in our country, so this disease should be considered everyday, especially in infectology practice.
PMID: 16683411 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
23-vuotiaalla serbialaisella ilmeni kuumetta, päänsärkyä, oksentelua, yleistä heikkoutta jne. Häneltä löytyi ehrlichioosi.
Vojnosanit Pregl. 2006 Apr;63(4):403-8.
[Human ehrlichiosis]
[Article in Serbian]
Dokic M, Curcic P, Nozic D, Lako B, Begovic V, Rajic-Dimitrijevic R, Hristovic D.
Vojnomedicinska akademija, Klinika za infektivne i tropske bolesti, Beograd. milomirdj@yahoo.com
BACKGROUND: Human ehrlichiosis is a newly recognized disease. It is a tick-borne disease caused by several bacterial species of the genhus Erlichia. These are small gram-negative pleomorphic cocci, that are obligatory intracellular bacteria. Tick Ixodes is the principle vector in Europe, and Amblyomma amenicanum in the United States. Bacterial organisms replicate in a tick, and are transmited from infected cells in a vector to the blood cells of animals or humans. Human ehrlichiosis is a name for a group of diseases caused by different species of Ehrlichia. One of them is the disease named human monocytic ehrlichiosis, caused by Ehrlichia chaffeensis, and the other is a human granulocytic ehrlichiosis caused by Anaplasma phagocytophilia.
CASE REPORT: We reported a 23-year-old patient admitted for the clinical treatment with the symptoms of high febrility (above 40 degrees C), headache, vomiting, general weakness and exhaustion, but without data on a tick bite. The patient was treated with trimetoprim-sulfamethoxazole for a week when Ehrlichia chaffeensis was confirmed by the immunofluoroscence test, and the therapy contimed with doxacyclin.
CONCLUSION: Human ehrlichiosis is also present in our country, so this disease should be considered everyday, especially in infectology practice.
PMID: 16683411 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum