LISÄINFEKTIOIDEN AIHEUTTAMIA KUOLEMANTAPAUKSIA

Voiko Borrelioosiin/lisäinfektioihin kuolla?

Valvojat: Borrelioosiyhdistys, Bb, Jatta1001

Vastaa Viestiin
soijuv
Viestit: 3151
Liittynyt: Ke Tammi 21, 2009 14:16

LISÄINFEKTIOIDEN AIHEUTTAMIA KUOLEMANTAPAUKSIA

Viesti Kirjoittaja soijuv » Ma Syys 07, 2009 09:25

Punkkien/verta imevien hyönteisten välityksellä voi saada useita eri taudinaiheuttajia kuten ehrlichia, babesia, bartonella, mykoplasma jne. Myös ne voivat aiheuttaa kuolemantapauksia. Suomessa useita niistä ei tavata usein eikä niitä myöskään tutkita riittävästi. Matkailun lisääntyminen on joka tapauksessa merkittävästi lisännyt sairastumisriskiä.

Lukuisia tutkimuksia kuolemantapauksista:


Infections with Ehrlichia chaffeensis and Ehrlichia ewingii in persons coinfected with human immunodeficiency virus.
Paddock CD, Folk SM, Shore GM, Machado LJ, Huycke MM, Slater LN, Liddell AM, Buller RS, Storch GA, Monson TP, Rimland D, Sumner JW, Singleton J, Bloch KC, Tang YW, Standaert SM, Childs JE.
Clin Infect Dis. 2001 Nov 1;33(9):1586-94. Epub 2001 Sep 24. PMID: 11568857

The clinical course and laboratory evaluation of 21 patients coinfected with human immunodeficiency virus (HIV) and Ehrlichia chaffeensis or Ehrlichia ewingii are reviewed and summarized, including 13 cases of ehrlichiosis caused by E. chaffeensis, 4 caused by E. ewingii, and 4 caused by either E. chaffeensis or E. ewingii. Twenty patients were male, and the median CD4(+) T lymphocyte count was 137 cells/microL.

Exposures to infecting ticks were linked to recreational pursuits, occupations, and peridomestic activities. For 8 patients, a diagnosis of ehrlichiosis was not considered until > or =4 days after presentation. Severe manifestations occurred more frequently among patients infected with E. chaffeensis than they did among patients infected with E. ewingii, and all 6 deaths were caused by E. chaffeensis. Ehrlichiosis may be a life-threatening illness in HIV-infected persons, and the influence of multiple factors, including recent changes in the epidemiology and medical management of HIV infection, may increase the frequency with which ehrlichioses occur in this patient cohort.

Tissue diagnosis of Ehrlichia chaffeensis in patients with fatal ehrlichiosis by use of immunohistochemistry, in situ hybridization, and polymerase chain reaction.

Dawson JE, Paddock CD, Warner CK, Greer PW, Bartlett JH, Ewing SA, Munderloh UG, Zaki SR.
Am J Trop Med Hyg. 2001 Nov;65(5):603-9. PMID: 11716122

In the United States, human ehrlichiosis is a complex of emerging tick-borne diseases caused by 3 distinct Ehrlichia species: Ehrlichia chaffeensis, Ehrlichia ewingii, and the human granulocytotropic ehrlichiosis agent. Ehrlichioses are characterized by a mild to severe illness, and approximately 4% of cases are fatal. Because these obligate intracellular bacteria are difficult to resolve with routine histologic techniques, their distribution in tissues has not been well described. To facilitate the visualization and detection of ehrlichiae, immunohistochemistry (IHC), in situ hybridization (ISH), and polymerase chain reaction (PCR) assays were developed by use of tissues from 4 fatal cases of E. chaffeensis infection. Evidence of E. chaffeensis via IHC, ISH, and PCR was documented in all 4 cases. Abundant immunostaining and in situ nucleic acid hybridization were observed in spleen and lymph node from all 4 patients. Significantly, in 2 of these patients, serologic evidence of infection was absent. Use of IHC, ISH, and PCR to visualize and detect Ehrlichia in tissues can facilitate diagnosis of ehrlichial infections.

Severe Ehrlichia chaffeensis infection in a lung transplant recipient: a review of ehrlichiosis in the immunocompromised patient.
Safdar N, Love RB, Maki DG.
Emerg Infect Dis. 2002 Mar;8(3):320-3. PMID: 11927032

We describe a case of human ehrlichiosis in a lung transplant recipient and review published reports on ehrlichiosis in immunocompromised patients. Despite early therapy with doxycycline, our patient had unusually severe illness with features of thrombotic thrombocytopenic purpura. Of 23 reported cases of ehrlichiosis in immunocompromised patients, organ failure occurred in all patients and 6 (25%) died.

Rapidly Fatal Infection with Ehrlichia chaffeensis.
Martin GS, Christman BW, Standaert SM.
N Engl J Med. 1999 Sep 2;341(10):763-4. PMID: 10475799

Human ehrlichial infections are increasingly being recognized as common tick-borne diseases in the United States. Clinical characteristics of ehrlichiosis include fever, headache, and malaise with leukopenia, thrombocytopenia, and elevated levels of hepatic aminotransferases. In rare instances, infection may result in multiple organ failure and death, particularly in immunosuppressed patients. Despite the potential severity of disease, death is uncommon in normal human hosts. We report two cases of rapidly fatal Ehrlichia chaffeensis infection in patients who presented to our institution in early June.

Ehrlichia chaffeensis (Rickettsiales: Ehrlichieae) infection in Amblyomma americanum (Acari: Ixodidae) at Aberdeen Proving Ground, Maryland.
Stromdahl EY, Randolph MP, O'Brien JJ,Gutierrez AG.
J Med Entomol. May;37(3):349-56. 2000 PMID: 15535577

Human monocytic ehrlichiosis (HME) is a sometimes fatal, emerging tick-borne disease caused by the bacterium Ehrlichia chaffeensis.

Tissue diagnosis of Ehrlichia chaffeensis in patients with fatal ehrlichiosis by use of immunohistochemistry, in situ hybridization, and polymerase chain reaction.

Dawson JE, Paddock CD, Warner CK, Greer PW, Bartlett JH, Ewing SA, Munderloh UG, Zaki SR.
Am J Trop Med Hyg. Nov;65(5):603-9. 2001 PMID: 11716122

In the United States, human ehrlichiosis is a complex of emerging tick-borne diseases caused by 3 distinct Ehrlichia species: Ehrlichia chaffeensis, Ehrlichia ewingii, and the human granulocytotropic ehrlichiosis agent. Ehrlichioses are characterized by a mild to severe illness, and approximately 4% of cases are fatal.

Central nervous system manifestations of human ehrlichiosis.
Ratnasamy N, Everett ED, Roland WE, McDonald G, Caldwell CW.
Clin Infect Dis. 1996 Aug;23(2):314-9. PMID: 8842270

Since 1989, we have confirmed the diagnosis of human ehrlichiosis in 57 patients. Although routine radiological studies of the central nervous system (CNS) or analyses of cerebrospinal fluid (CSF) samples were not done for these patients, primary care physicians detected symptoms or signs that prompted them to perform such studies. CSF samples were examined for 15 of the 57 patients. Findings in eight of the 15 CSF samples were abnormal, and the most common abnormalities were lymphocytic pleocytosis and elevated protein levels. A search of the English-language literature revealed 21 additional cases in which CSF examinations were performed; in 13 of these cases, CSF findings were abnormal. The most common clinical finding that predicted CSF abnormalities was a change in mental status. A total of 14 patients underwent computerized tomographic studies, and none of these studies showed abnormalities. Four (19%) of the 21 patients with CNS manifestations of ehrlichiosis and abnormal CSF findings died.

Human ehrlichiosis: a newly recognized tick-borne disease.
Goldman DP, Artenstein AW, Bolan CD.
Am Fam Physician. Jul;46(1):199-208. 1992 PMID: 162163

Since then, more than 215 cases have been reported, including some fatalities. Ehrlichia species belong to the same family as the organism that causes Rocky Mountain spotted fever.

Ehrlichiosis mimicking thrombotic thrombocytopenic purpura. Case report and pathological correlation.

Marty AM, Dumler JS, Imes G, Brusman HP, Smrkovski LL, Frisman DM.
Hum Pathol. 1995 Aug;26(8 ):920-5. PMID: 7635455

Human ehrlichiosis is a tick-borne zoonosis caused by the newly described human hematotropic rickettsiae, Ehrlichia chaffeensis. The pathology and pathogenesis of human ehrlichiosis have not been adequately studied. Even with immunoperoxidase, the only previously known method to detect these organisms in tissue, ehrlichae are difficult or impossible to identify. This led many investigators to speculate that the pathogenesis of ehrlichiosis was not caused directly by the organism but could be caused by host-mediated injury. In this case study, a patient presented with rapidly progressive central nervous system symptoms and severe thrombocytopenia, prompting a presumptive diagnosis of thrombotic thrombocytopenic purpura (TTP). Despite corticosteroids, and later, antibiotics, the patient rapidly deteriorated and died.

Postmortem examination showed hemorrhages in multiple organs and mononuclear inclusions of infection with a monocytic ehrlichia. Other findings included widespread lymphohistiocytic perivascular infiltrates, focal hepatic necroses, interstitial pneumonitis, interstitial nephritis, mononuclear phagocyte invasion and proliferation in splenic, liver, and bone marrow, and hemophagocytosis. The diagnosis was proven by serology, immunohistology with both polyclonal and monoclonal anti E chaffeensis, and polymerase chain reaction on paraffin-embedded tissues using E chaffeensis-specific oligonucleotide primers. The presence of numerous ehrlichia with notable tissue and cellular injury but without a marked host response indicate that unlike other cases of documented human ehrlichiosis, this patient died after significant direct ehrlichia-mediated injury, and that immune mechanisms initiated after ehrlichiosis played little if any role in the pathogenesis.

Fatal seronegative human ehrlichiosis in a patient with human immunodeficiency virus disease.

Paddock C, Suchard D, Hadley WK, Kerschmann R, Grumbach K, Dawson J, Dumler JS, Anderson B, Sims K, Herndier B.
Abstr Gen Meet Am Soc Microbiol. 1993; 93: 110 (abstract no. D-87).

The first confirmed case of disease due to Ehrlichia chaffeensis occurring in a patient with human immunodeficiency virus type 1 (HIV-1) is reported. A 42 year-old Arkansas woman with HIV-1 disease (CD4 lymphocyte count = 64 cells per cmm) died of pulmonary hemorrhage approximately 2 weeks following acute onset of a febrile illness characterized by pancytopenia, particularly rapidly progressive thrombocytopenia, and elevated hepatic aminotransferase levels. Intracytoplasmic ehrlichial morulae were identified within mononuclear cells from a bone marrow biopsy obtained shortly prior to death.

At autopsy, ehrlichiae were identified by electron microscopy within bone marrow leukocytes and by an immunoperoxidase stain for Ehrlichia in leukocytes of the bone marrow, lung, spleen and lymph nodes. Distinct histopathological lesions included depletion and destruction of periarteriolar splenic lymphocytes with replacement by nodular histiocytic aggregates; focal lymph node necrosis; hemophagocytosis of erythrocytes in the bone marrow; and extensive alveolar hemorrhage within the lungs. Polymerase chain reaction techniques using probes to the 16S rRNA gene of E. chaffeensis revealed E. chaffeensis DNA in a sample of the patient's blood, although an antibody titer to Ehrlichia was absent by indirect fluorescent antibody testing. Given the potential for absence of a diagnostic serologic response, a high index of suspicion for human ehrlichiosis should be maintained in HIV-1 patients from endemic areas of E. chaffeensis who present acutely with fever and hematologic cytopenias.

Human babesiosis: an emerging tick-borne disease.
Kjemtrup AM, Conrad PA.
Int J Parasitol. Nov;30(12-13):1323-37. 2000 PMID: 11113258

This parasite is closely related to babesial parasites isolated from large wild ungulates in California. Like B. microti, WA1-type parasites cause mild to severe disease and the immunopathogenesis of these parasites is distinctly different from each other in experimental infections of hamsters and mice. A B. divergens-like parasite was also identified as the cause of a fatal human babesiosis case in Missouri.

Babesiosis in Wisconsin: a potentially fatal disease.
Herwaldt BL, Springs FE, Roberts PP, Eberhard ML, Case K, Persing DH, Agger WA.
Am J Trop Med Hyg. Aug;53(2):146-51. 1995 PMID: 7677215

Three cases (30% of 10) we now report were fatal and occurred in elderly patients (65-75 years old) who died after complicated hospital courses? Medical personnel should be knowledgeable about this zoonosis, which is not limited to the northeastern United States, and is potentially serious, sometimes fatal.

Human Babesiosis in New York State: Review of 139 Hospitalized Cases and Analysis of Prognostic Factors.
Dennis J. White, PhD; John Talarico, DO; Hwa-Gan Chang, MS; Guthrie S. Birkhead, MD, MPH; Tracey Heimberger, MD; Dale L. Morse, MD, MS
Arch Intern Med. 1998;158:2149-2154.

Babesiosis infections are infrequent, occur in limited geographic locations, and range from asymptomatic infection to severe illness and death. The most common signs and symptoms on admission were nonspecific symptoms of fatigue/malaise/weakness (91.2%), fever (90.6%), shaking chills (76.6%), diaphoresis (69.2%), and nausea/anorexia (57.3%) (Table 2). Clinical findings on physical examination included temperature higher than 38°C (55.8%), heart murmur (20.1%), hepatomegaly (14.4%), and splenomegaly (10.8%). Only 6 patients (4.3%) had jaundice listed. A review of medical records indicated that 51.8% had a history of chronic disease, 11.9% had a history of Lyme disease, and 11.7% had undergone splenectomies. No patient had evidence of human immunodeficiency virus infection. More than one third (37.5%) of the patients reported having a tick bite within 30 days prior to their hospitalization.

Fifty-four hospitalized patients (38.8%) had some type of complication (Table 4). Congestive heart failure (n=15, 10.9%) and acute respiratory distress syndrome (n=11, 8.0%) were the most common complications. Nine patients died during hospitalization, for a fatality rate of 6.5%. The death certificate analysis identified 29 patients who died from 1982-1995.

Concurrent Babesiosis and Ehrlichiosis in an Elderly Host.
Muhammad Z. Javed, MD; Manjul Srivastava, MD; Shengle Zhang, MD; Mathew Kandathil, MD
Mayo Clin Proc. 2001 May;76(5):563-5. PMID: 11357805

An 85-year-old man, actively infected with Babesia microti and Ehrlichia chaffeensis, presented with fatigue and thrombocytopenia. He developed rhabdomyolysis and multiple organ failure, which led to death 6 days after initial presentation. To our knowledge, concurrent acute disease due to these 2 organisms has not been reported previously, although serologic studies have shown that some patients acquire both infections in life.

Babesosis--difficulty of diagnosis.
Cichocka A, Skotarczak B.
Wiad Parazytol.;47(3):527-33. 2001 PMID: 16894770

Clinical manifestation varied widely from asymptomatic infection to a serve rapidly fatal disease.

Babesiosis.
Krause PJ.
Med Clin North Am. Mar;86(2):361-73. 2002 PMID: 11982307

Those at greatest risk of fatal disease include individuals older than age 50 years; asplenic individuals; and immunocompromised individuals as a result of immunosuppressive drugs, malignancy, or HIV infection.

Vacation souvenirs: inoculation pathologies (cutaneous larva migrans, cutaneous leishmaniases, Lyme disease, rickettsioses).
Tas S.
Rev Med Brux. Sep;21(4):A257-65. 2000 PMID: 11068477

If untreated this infection may expose to chronic debilitating rheumatologic, cardiac and neurological complications. Rickettsiosis, especially boutonneuse fever, are a potentially fatal multisystemic infectious diseases transmitted through the bite of a dog tick.

A Fatal Case of Babesiosis in Missouri: Identification of Another Piroplasm That Infects Humans
Barbara L. Herwaldt, MD, MPH; David H. Persing, MD, PhD; Eric A. Precigout, PhD; W. L. Goff, PhD; Dane A. Mathiesen, BS; Philip W. Taylor, MD; M. L. Eberhard, PhD; and Andre F. Gorenflot, PhD
Ann Intern Med. 1996 Apr 1;124(7):643-50.

A 73-year-old man who had had a splenectomy and had a fatal case of babesiosis.

Although MO1 is probably distinct from B. divergens, the two share morphologic, antigenic, and genetic characteristics; MO1 probably represents a Babesia species not previously recognized to have infected humans. Medical personnel should be aware that patients in the United States can have life-threatening babesiosis even though they are seronegative to B. microti and WA1 antigen.

Babesia microti, human babesiosis, and Borrelia burgdorferi in Connecticut.

Anderson JF, Mintz ED, Gadbaw JJ, Magnarelli LA.
J Clin Microbiol. Dec;29(12):2779-83. 1991 PMID: 1757548

Two patients died with active infections, and one patient died from chronic obstructive pulmonary disease soon after treatment with clindamycin and quinine.

A fatal case of human babesiosis in Portugal: molecular and phylogenetic analysis.

Centeno-Lima S, do Rosário V, Parreira R, Maia AJ, Freudenthal AM, Nijhof AM, Jongejan F.
Trop Med Int Health. 2003 Aug;8(8 ):760-4. PMID: 12869099

We report the first case of human babesiosis in Portugal. A 66-year-old splenectomized man was admitted to a Lisbon hospital after 1 week of fever, abdominal pain, anorexia and nausea. A high parasitaemia (30%) of Babesia parasites was found in Giemsa-stained blood smears and, despite treatment, the patient died several weeks later of renal failure. Ethylenediaminetetraacetic acid blood samples were processed for polymerase chain reaction (PCR) and reverse line blot hybridization to confirm and characterize the Babesia infection. The amplified PCR product was cloned and subsequently sequenced. Molecular analysis showed that the infection was caused by Babesia divergens and that other blood parasites were not involved. Phylogenetic analysis showed that the 18 S ribosomal RNA gene sequence was similar to three other European isolates of B. divergens. In view of the high risk for splenectomized individuals, strict measures should be taken to avoid tick bites.

The possible role of ticks as vectors of leptospirae.
Burgdorfer W.
Exp Parasitol. 1956 Nov;5(6):571-9. PMID: 13375683

Transmission of Leptospira pomona by the argasid tick, Ornithodoros turicata, and the persistance of this organism in its tissues.

Scrub typhus and tropical rickettsioses.
Watt G, Parola P.
Curr Opin Infect Dis. 2003 Oct;16(5):429-36. PMID: 14501995

Department of Retrovirology, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand.

Recent developments in molecular taxonomic methods have led to a reclassification of rickettsial diseases. The agent responsible for scrub typhus (Orientia tsutsugamushi ) has been removed from the genus Rickettsia and a bewildering array of new rickettsial pathogens have been described. An update of recent research findings is therefore particularly timely for the nonspecialist physician. An estimated one billion people are at risk for scrub typhus and an estimated one million cases occur annually. The disease appears to be re-emerging in Japan, with seasonal transmission. O. tsutsugamushi has evolved a variety of mechanisms to remain viable in its intracellular habitat. Slowing the release of intracellular calcium inhibits apoptosis of macrophages. Subsets of chemokine genes are induced in infected cells, some in response to transcription factor activator protein 1. Cardiac involvement is uncommon and clinical complications are predominantly pulmonary. Serious pneumonitis occurred in 22% of Chinese patients.

Dual infections with leptospirosis have been reported. Standardized diagnostic tests are being developed and attempts to improve treatment of women and children are being made. Of the numerous tick-borne rickettsioses identified in recent years, African tick-bite fever appears to be of particular importance to travellers. The newly described flea-borne spotted fever caused by Rickettsia felis may be global in distribution. Rash and fever in a returning traveler could be rickettsial and presumptive doxycycline treatment can be curative. Recent research findings raise more questions than answers and should stimulate much needed research.

Clinical Features Symptoms include fever, headache, chills, muscle aches, vomiting, jaundice, anemia, and sometimes a rash. The incubation period usually is 7 days, with a range of 2-29 days. If not treated, the patient could develop kidney damage, meningitis, liver failure, and respiratory distress. In rare cases, death occurs.

Infective Endocarditis due to Bartonella spp. and Coxiella burnetii.
Experience at a Cardiology Hospital in São Paulo, Brazil
Ann. N.Y. Acad. Sci. 1078: 215?222 (2006). doi: 10.1196/annals.1374.123

A total of 61 patients with endocarditis diagnosis were evaluated, 17 (27%) were culture-negative. Two have had IgG titer greater than 800 (≥3,200) against Bartonella spp. and one against C. burnetii (phase I and II≥6,400).

Those with Bartonella-induced endocarditis had a fatal disease.

Necropsy showed calcifications and extensive destruction of the valve tissue, which is diffusely infiltrated with mononuclear inflammatory cells predominantly by foamy macrophages. The patient with C. burnetii endocarditis received specific antibiotic therapy. Reports of infective endocartitis due to Bartonella spp. and C. burnetii in Brazil reveal the importance of investigating the infectious agents in culture-negative endocarditis.

Fatal meningitis and encephalitis due to Bartonella henselae bacteria.
Gerber JE, Johnson JE, Scott MA, Madhusudhan KT.
J Forensic Sci. 2002 May;47(3):640-4. PMID: 12051353

Bacterial infection due to Bartonella henselae commonly develops in children and young adults following cat/dog contacts and/or cat/dog scratches. Regional lymphadenopathy is its most common clinical expression. However, encephalitis and Parinaud's syndrome (oculoglandular syndrome) have also been reported as has systemic illness. A review of the international literature in all languages revealed no fatal complications in immunocompetent hosts. A four-year-old white child with no underlying illness began to have seizure-like activity. She was taken to a local hospital and subsequently transferred to a medical center. The child was treated aggressively for seizures and fever of unknown origin. However, her condition rapidly declined and she died without a specific diagnosis.

At autopsy there was marked cerebral edema with no gross evidence of acute meningitis. Microscopic exams revealed multiple granulomatous lesions as well as a meningitis and encephalitis. A variety of cultures and stains were negative for acid fast and fungal organisms. Warthin-Starry stains of involved tissue including brain and liver revealed pleomorphic rod shaped bacilli consistent with Bartonella henselae. Analysis of brain tissue with polymerase chain reaction (PCR) and Southern blot for the deoxyribonucleic acid (DNA) was definitive for DNA of Bartonella henselae bacteria.

Diagnosis of 22 new cases of Bartonella endocarditis.
Raoult D; Fournier PE; Drancourt M; Marrie TJ; Etienne J; Cosserat J; Cacoub P; Poinsignon Y; Leclercq P; Sefton AM
Ann Intern Med 1996 Oct 15;125(8 ):646-52. PMID- 8849149

22 patients had definite endocarditis. Five were infected with B. quintana, 4 with B. henselae, and 13 with an undetermined Bartonella species. These cases were compared with the 11 previously reported cases. Of the patients with the newly reported cases, 19 had valvular surgery and 6 died.

Outcome and treatment of Bartonella endocarditis.
Raoult D; Fournier PE; Vandenesch F; Mainardi JL; Eykyn SJ; Nash J; James E; Benoit-Lemercier C; Marrie TJ
Arch Intern Med 2003 Jan 27;163(2):226-30.

Endocarditis caused by Bartonella species is a potentially lethal infection characterized by a subacute evolution and severe valvular lesions. We performed a retrospective study on 101 patients who were diagnosed in our laboratory as having Bartonella endocarditis between January 1, 1995, and April 30, 2001. Bartonella infection was diagnosed using immunofluorescence with a 1:800 cutoff, polymerase chain reaction amplification of DNA, and/or culture findings of Bartonella species from whole blood, serum, and/or valvular biopsy specimens. A standardized questionnaire was completed by investigators for each patient. Twelve of the 101 patients died and 2 relapsed.

Tick-borne infections. What starts as a tiny bite may have a serious outcome.

Middleton DB.
Postgrad Med Apr; 95(5):131-9 1994.

Tick-borne illnesses are being reported increasingly often. Unlike Rocky Mountain spotted fever and ehrlichiosis can kill and so must be recognized and treated promptly. These diseases require clinical diagnosis, because laboratory confirmation with antibody tests takes too long. Other diseases (eg, babesiosis, tularemia) are encountered occasionally and can also be fatal but are treatable with antibiotics.

Assessment of maternal mortality in Tanzania.

Walraven GE, Mkanje RJ, van Roosmalen J, van Dongen PW, Dolmans WM.
Br J Obstet Gynaecol. May; 101(5):414-7. 1994. PMID: 8018613

Relapsing fever or Borrelia infection was an indirect cause of death common to the region and particularly hazardous to pregnant women.

Mortality in high risk patients with tick-borne relapsing fever analysed by the Borrelia-index.
Melkert PW.
East Afr Med J. Nov; 68(11):875-9. 1991. PMID: 1800081

Causes of death were septicaemia (3x), severe spirochaetemia in a neonate (1x), and successive relapses in complicated cases without adequate treatment (2x).

Fatal-Jarisch Herxheimer reaction in a case of relapsing fever misdiagnosed as lobar pneumonia.

Melkert PW.
Trop Geogr Med. Jan; 39(1):92-3. 1987. PMID: 3603698

A fatal Jarisch-Herxheimer reaction developed after treatment with high doses of penicillin in a case of lobar pneumonia caused by Borrelia duttoni?. Treatment may have contributed to the death of this patient.

Clinical diagnosis and treatment of human granulocytotropic anaplasmosis.

Bakken JS, Dumler JS.
Ann NY Acad Sci. 2006 Oct;1078:236-47. PMID: 17114714

Tick-borne rickettsiae in the genera Ehrlichia and Anaplasma are intracellular bacteria that infect wild and domestic mammals and, more recently, man. The increased desire of humans for recreational activities outdoors has increased the exposure to potential human pathogens that previously cycled almost exclusively within natural, nonhuman enzootic hosts. Anaplasma phagocytophilum causes an acute, nonspecific febrile illness of humans previously known as human granulocytotropic ehrlichiosis (HGE) and now called human granulocytotropic anaplasmosis (HGA).
However, delayed diagnosis in older and immunocompromised patients may place those individuals at risk for an adverse outcome, including death. Thus, prompt institution of antibiotic therapy is advocated for any patient who is suspected to have HGA and for all patients who have confirmed HGA.

Fatal pancarditis associated with human granulocytic Ehrlichiosis in a 44-year-old man.

Jahangir A, Kolbert C, Edwards W, Mitchell P, Dumler JS, Persing DH.
Clin Infect Dis. Dec; 27(6):1424-7. 1998. PMID: 9868655

We describe a case of fatal pancarditis during the course of human granulocytic ehrlichiosis (HGE) in a 44-year-old outdoor worker who was previously treated for presumptive Lyme disease.

Human granulocytic ehrlichiosis in Connecticut: report of a fatal case.

Hardalo CJ, Quagliarello V, Dumler JS.
Clin Infect Dis. Oct; 21(4):910-4. 1995. PMID: 8645839

We report a case of granulocytic ehrlichiosis in a 71-year-old man who presented with an acute febrile illness and subsequently developed multisystem organ dysfunction and sudden severe anemia with thrombocytopenia requiring intensive care, mechanical ventilation, hemodialysis, and transfusions?.This, to our knowledge, represents to first documented case of human granulocytic ehrlichiosis to occur outside the Upper Midwest.

Human granulocytic ehrlichiosis in the upper Midwest United States. A new species emerging?

Bakken JS, Dumler JS, Chen SM, Eckman MR, Van Etta LL, Walker DH.
JAMA. Jul 20; 272(3):212-8. 1994. PMID: 8022040

Two of the 12 patients died.

Is Human Granulocytic Ehrlichiosis (HGE) another Lyme Disease? A Comparison of Clinical, Laboratory, and Epidemiologic Features.
J. Stephen Dumler, M.D.

HGE has been diagnosed in about 100 patients so far - 4 have died.

Rocky Mountain spotted fever from an unexpected tick vector in Arizona.
Demma LJ, Traeger MS, Nicholson WL, Paddock CD, Blau DM,Eremeeva ME, Dasch GA, Levin ML, Singleton J Jr, Zaki SR, Cheek JE, Swerdlow DL, McQuiston JH.
N Engl J MedAug 11;353(6):587-94 . 2005 PMID: 16093467

A total of 16 patients with Rocky Mountain spotted fever infection (11 with confirmed and 5 with probable infection) were identified. Of these patients, 13 (81 percent) were children 12 years of age or younger, 15 (94 percent) were hospitalized, and 2 (12 percent) died. Dense populations of Rhipicephalus sanguineus ticks were found on dogs and in the yards of patients' homesites

Hidden mortality attributable to Rocky Mountain spotted fever: immunohistochemical detection of fatal, serologically unconfirmed disease.

Paddock CD, Greer PW, Ferebee TL, Singleton J Jr, McKechnie DB, Treadwell TA, Krebs JW, Clarke MJ, Holman RC, Olson JG, Childs JE, Zaki SR.
J Infect Dis Jun;179(6):1469-76. 1999.

Rocky Mountain spotted fever (RMSF) is the most severe tickborne infection in the United States and is a nationally notifiable disease. Since 1981, the annual case-fatality ratio for RMSF has been determined from laboratory-confirmed cases reported to the Centers for Disease Control and Prevention (CDC). Herein, a description is given of patients with fatal, serologically unconfirmed RMSF for whom a diagnosis of RMSF was established by immunohistochemical (IHC) staining of tissues obtained at autopsy.

During 1996-1997, acute-phase serum and tissue samples from patients with fatal disease compatible with RMSF were tested at the CDC. As determined by indirect immunofluorescence assay, no patient serum demonstrated IgG or IgM antibodies reactive with Rickettsia rickettsii at a diagnostic titer (i.e., >/=64); however, IHC staining confirmed diagnosis of RMSF in all patients. Polymerase chain reaction validated the IHC findings for 2 patients for whom appropriate samples were available for testing. These findings suggest that dependence on serologic assays and limited use of IHC staining for confirmation of fatal RMSF results in underestimates of mortality and of case-fatality ratios for this disease.

Rocky Mountain Spotted Fever, Panama
Dora Estripeaut; María Gabriela Aramburú; Xavier Sáez-Llorens; Herbert A. Thompson; Gregory A. Dasch; Christopher D. Paddock; Sherif Zaki; Marina E. Eremeeva
Emerg Infect Dis. 2007;13(11):1763-1765. ©2007 Centers for Disease Control and Prevention (CDC)

We describe a fatal pediatric case of Rocky Mountain spotted fever in Panama, the first, to our knowledge, since the 1950s. Diagnosis was established by immunohistochemistry, PCR, and isolation of Rickettsia rickettsii from postmortem tissues. Molecular typing demonstrated strong relatedness of the isolate to strains of R. rickettsii from Central and South America.

Family cluster of Rocky Mountain spotted fever.
Jones TF, Craig AS, Paddock CD, McKechnie DB, Childs JE, Zaki SR, Schaffner W.
Clin Infect Dis Apr;28(4):853-9. 1999. PMID: 10825050

Soon after a patient from Tennessee died of Rocky Mountain spotted fever (RMSF), several family members developed symptoms suggestive of the disease and were treated presumptively for RMSF.

Fifty-four persons visiting the index patient's home were interviewed; serum samples were collected from 35. Three additional cases of RMSF were confirmed, all of which occurred in first-degree relatives. Time spent at the family home and going into the surrounding woods were significantly associated with developing antibodies to Rickettsia rickettsii. Ticks were collected and examined for rickettsiae by polymerase chain reaction analysis. Because hyperendemic foci and family clusters of RMSF can occur, when a case is suspected clinicians should be vigilant for signs and symptoms consistent with R. rickettsii infection in other persons who may have been similarly exposed.

Rocky Mountain spotted fever in the United States, 1997-2002.
Chapman AS, Murphy SM, Demma LJ, Holman RC, Curns AT, McQuiston JH, Krebs JW, Swerdlow DL.
Vector Borne Zoonotic Dis. Summer;6(2):170-8. 2006 PMID: 16796514

Rocky Mountain spotted fever (RMSF) is the most commonly reported fatal tick-borne disease in the United States.

Rocky Mountain Spotted Fever caused by blood transfusion.
Wells GM, Woodward TE, Fiset P, Hornick RB.
JAMA. 1978 Jun 30;239(26):2763-5 PMID: 418193

Transfusion of 500 ml of blood, contributed by a donor three days before the onset of Rocky Mountain spotted fever and refrigerated for nine days, caused this disease in the recipient.

The blood donor died of Rocky Mountain spotted fever after six days; rickettsia were identified in various tissues by immunofluorescence techniques.

The recipient of the blood became mildly ill and recovered fully; specific antibiotic treatment was initiated on the fourth day of illness. Diagnosis of Rocky Mountain spotted fever was confirmed in the recipient by positive serologic reactions and isolation of Rickettsia rickettsii from blood after inoculation in animals and tissue culture.

National surveillance for Rocky Mountain spotted fever, 1981-1992: epidemiologic summary and evaluation of risk factors for fatal outcome.

Dalton MJ, Clarke MJ, Holman RC, Krebs JW, Fishbein DB, Olson JG, Childs JE.
Am J Trop Med Hyg. May;52(5):405-13. 1995 PMID: 7771606

The case-fatality ratio was 4.0%.

Physician knowledge of the diagnosis and management of Rocky Mountain spotted fever: Mississippi, 2002.

O'Reilly M, Paddock C, Elchos B, Goddard J, Childs J, Currie M.
Ann N Y Acad Sci. Jun;990:295-301. 2003 PMID: 12860642

RMSF has a high case fatality rate among untreated individuals, and the median time from onset of symptoms to death is only eight days, making early recognition and treatment of RMSF crucial.

Rocky Mountain spotted fever in an endemic area in Minas Gerais, Brazil.

de Lemos ER, Machado RD, Coura JR.
Mem Inst Oswaldo Cruz. Oct-Dec;89(4):497-501. 1994 PMID: 8524052

In order to obtain information on tick-borne rickettsiosis, a study was performed in the County of Santa Cruz do Escalvado, State of Minas Gerais, Brazil, where a fatal clinical case confirmed by specific immunofluorescence had been reported.

Natural Infection of the Tick, Amblyomma Cajennense, with Rickettsia Rickettsii in Panama.

Enid C. de Rodaniche.
Am. J. Trop. Med. Hyg., 2(4), 1953, pp. 696-699

The occurrence of Rocky Mountain spotted fever on the Isthmus of Panama was established for the first time in 1950 when a highly virulent strain of Rickettsia rickettsii was isolated by the author from the blood of a 26 year old Panamanian farmer who died February 8 of that year, shortly after admission to the hospital. The patient evidently had contracted his infection near the town of Ollas Arriba about seven miles north of Capira in the Province of Panama.
Since then similarly virulent strains of R. rickettsii have been isolated from two additional cases, hospitalized in May 1950 and February 1951, both male, aged 13 and 26 years respectively, who were employed in agricultural work on farms located in the same area as the previous case. The 13-year old boy died. The 26-year old man survived after a severe and protracted illness. His blood showed complement-fixing antibodies against Rocky Mountain spotted fever antigen in high titer during convalescence.

Fatal spotted fever rickettsiosis, Kenya.
Rutherford JS, Macaluso KR, Smith N, Zaki SR, Paddock CD, Davis J, Peterson N, Azad AF, Rosenberg R.
Emerg Infect Dis. May;10(5):910-3 2004 PMID: 15200829

We report a fatal case of rickettsiosis in a woman from the United States living in Kenya, who had a history of tick exposure.

Mediterranean spotted fever in Portugal: risk factors for fatal outcome in 105 hospitalized patients.

de Sousa R, Nobrega SD, Bacellar F, Torgal J.
Ann N Y Acad Sci. Jun;990:285-94. 2003 PMID: 12860641

Although recognized as a benign acute disease and treated mainly with ambulatory procedures, some cases are severe and fatalities have increased in the last few years. In 1997, MSF mortality became more evident in Beja, a Portuguese southern district, with a case fatality rate of 32.3% in hospitalized patients.

Rickettsia helvetica: an emerging tick-borne pathogen in Hungary and Europe.

Sreter T, Sreterne Lancz Z, Szell Z, Egyed L.
Orv Hetil. 2005 Dec 11;146(50):2547-52. PMID: 16440500

Rickettsia helvetica belonging to spotted fever group rickettsiae was recently detected by polymerase chain reaction followed by sequencing in European sheep ticks (Ixodes ricinus) from Hungary. Current knowledge on these rickettsiae and the clinical and diagnostic aspects of R. helvetica infection is summarized. In acute cases, R. helvetica is generally responsible for flu-like symptoms. Nevertheless, recent data indicate that in chronic cases, these rickettsiae can be responsible for perimyocarditis resulting sudden cardiac death and might play a role in the pathogenesis of aortic valve disease.
Viimeksi muokannut soijuv, Ma Syys 07, 2009 09:34. Yhteensä muokattu 1 kertaa.

soijuv
Viestit: 3151
Liittynyt: Ke Tammi 21, 2009 14:16

Viesti Kirjoittaja soijuv » Ma Syys 07, 2009 09:28

Puutiaisaivokuumeen aiheuttamia kuolemantapauksia:

Fatal case of deer tick virus encephalitis.
[Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, P.H.S.]
Tavakoli NP, Wang H, Dupuis M, Hull R, Ebel GD, Gilmore EJ, Faust PL
N Engl J Med 2009 May 14; 360(20):2099-107.

Deer tick virus is related to Powassan virus, a tickborne encephalitis virus. A 62-year-old man presented with a meningoencephalitis syndrome and eventually died. Analyses of tissue samples obtained during surgery and at autopsy revealed a widespread necrotizing meningoencephalitis. Nucleic acid was extracted from formalin-fixed tissue, and the presence of deer tick virus was verified on a flavivirus-specific polymerase-chain-reaction (PCR) assay, followed by sequence confirmation. Immunohistochemical analysis with antisera specific for deer tick virus identified numerous immunoreactive neurons, with prominent involvement of large neurons in the brain stem, cerebellum, basal ganglia, thalamus, and spinal cord. This case demonstrates that deer tick virus can be a cause of fatal encephalitis.



Specific clinical and epidemiological features of tick-borne encephalitis in Western Siberia.
Poponnikova TV.
Int J Med Microbiol. May;296 Suppl 40:59-62. Epub Mar 9. 2006 PMID: 16524768

Severe progression and fatal outcomes of the disease have been recorded in all age groups.


Monitoring of tick-borne encephalitis virus populations and etiological structure of morbidity over 60 years.
Pogodina VV.
Vopr Virusol. May-Jun;50(3):7-13. 2005 PMID: 16078427

The Siberian and Far Eastern subtypes in the area of joint circulation were found to cause the whole spectrum of infection manifestations from unapparent to severe focal forms with a fatal outcome.

The Golden Agers and Tick-borne encephalitis. Conference report and position paper of the International Scientific Working Group on Tick-borne encephalitis.
Kunze U, Baumhackl U, Bretschneider R, Chmelik V, Grubeck-Loebenstein B, Haglund M, Heinz F, Kaiser R, Kimmig P, Kunz C, Kunze M, Mickiene A, Misic-Majerus L, Randolph S, Rieke B, Stefanoff P, Suss J, Wimmer R.
Wien Med Wochenschr.Jun;155(11-12):289-94. 2005 PMID: 16035390

The incidence of the disease is increasing with age, also the clinical course is more severe, they suffer significantly more sequelae, need a longer rehabilitation and have a higher case fatality.

Tick-borne encephalitis with hemorrhagic syndrome, Novosibirsk region, Russia, 1999.
Ternovoi VA, Kurzhukov GP, Sokolov YV, Ivanov GY, Ivanisenko VA, Loktev AV, Ryder RW, Netesov SV, Loktev VB.
Emerg Infect Dis. Jun;9(6):743-6. 2003 PMID: 12781020
Eight fatal cases of tick-borne encephalitis with an unusual hemorrhagic syndrome were identified in 1999 in the Novosibirsk Region, Russia.


The location of the infecting tick bite and the severity of the course of tick-borne encephalitis.
Okulova NM, Chunikhin SP, Vavilova VE, Maiorova AD.
Med Parazitol (Mosk). Sep-Oct;(5):78-85. 1989 PMID: 2615717
?fatal outcomes are most frequent in case of the bites in the axilla, arms (14-16%), head and neck (11.2%), and less frequent in case of the bites in the lower limbs (5.9%) and groin (0).


Tick-borne encephalitis: possibly a fatal disease in its acute stage. PCR amplification of TBE RNA from postmortem brain tissue.
Tomazic J, Poljak M, Popovic P, Maticic M, Beovic B, Avsic-Zupanc T, Lotric S, Jereb M, Pikelj F, Gale N.
Infection. Jan-Feb;25(1):41-3. 1997 PMID: 9039538
Tick-borne encephalitis has occurred regularly in Europe since it was first diagnosed in 1931 by Schneider. The mortality rate of patients with this disease is 1-2%. Death usually occurs in the acute stage of illness. A case report of a 28-year-old patient from Slovenia, who died shortly after the onset of tick-borne encephalitis, is described. The clinical course of disease, results of serological tests, neuropathological findings and polymerase chain reaction amplification of parts of viral genome from postmortem brain tissues are presented.

Repeated case of tick-borne encephalitis with a fatal outcome.
Shasaitov ShSh, Chartorizhskii NA, Smekalov VP.
Sov Med. Jun;(6):146. 1978 PMID: 675340

soijuv
Viestit: 3151
Liittynyt: Ke Tammi 21, 2009 14:16

Viesti Kirjoittaja soijuv » Ma Syys 07, 2009 10:14

"Autismi johtuu näkemykseni mukaan aivotulehduksesta jonka aiheuttajana on esim. bartonella tai mykoplasma. Bartonella aiheuttaa todennäköisesti myös krooniseen borrelioosiin liittyvät kuolemantapaukset. Kroonista borrelioosia sairastavat sairastavat useimmiten lisäinfektiona myös mykoplasmaa."

New Data Supporting the Link Between Autism and Lyme Disease

The LIA foundation plans to release new data at the Lyme-Autism Connection conference this weekend linking Autism and Lyme disease. It's time that parents and doctors start looking outside the box as to why these children are so sick

Corona, CA (PRWEB) June 20, 2007 -- News reports indicate a staggering number of Lyme disease cases going unreported. With autism rates rising each year, doctors are examining this new connection.

With new CDC numbers showing one of the largest populations of Lyme disease sufferers being boys from the age of 5-14, this rings of déjà vu to parents of children with autism. Young boys are the largest category of victims of autism as well as Lyme disease, which is caused by a bacteria called Borrelia Burgdorferi. Interestingly, the symptoms of chronic Lyme disease when affecting the central nervous system are literally the same symptoms as autism spectrum disorder.

The LIA Foundation will hold its first conference this week in Irvine, CA, in which new data will be released supporting this connection. "It's time that parents and doctors start looking outside the box as to why these children are so sick," comments co-founder of the LIA Foundation, Tami Duncan. "At this conference, we have presenters who will show that this connection is real."

"The increasing incidence of autism spectrum disorder (560,000 in the US) is a serious threat to our children and in most cases the cause is still unknown. Some clinicians and parents have noted chronic infections, including tick-borne infections; including Lyme disease and the immune reactions to these infections are sometimes associated with autistic symptoms and autistic spectrum disorder. This meeting will review the data regarding this observation and possible explanations of this association with a goal to help reduce any preventable cases of autism spectrum disorder," states Robert Bransfield, M.D. of Red Bank, NJ.

Doctors are beginning to support this link. Joseph Burrascano, M.D., the Vice President of ILADS (International Lyme and Associated Disease Society) states his position on Lyme disease and Autism. "It is my contention that Autism is an inflammatory encephalitis cause by a pathogen such as Bartonella or Mycoplasma. I share the view that Bartonella is a major infection that may eclipse Borrelia Burgdorferi as the ultimate cause of the morbidity in chronic Lyme disease. Mycoplasma too is a major concern of mine- in reviewing my 7000+ cases, those patients who were relentlessly chronic, all at one point or another in their illness, were positive for Mycoplasma." In fact, one speaker at the conference, Professor Garth Nicholson of the Institute for Molecular Medicine has found that 58% of children with Autism spectrum disorder are also harboring multiple-infections, specifically Mycoplasma. "Since these chronic infections like Borrelia, Mycoplasma and Bartonella are known to suppress the immune system, it is not a stretch to assume that when the child was injected with obscene amounts of mercury, that his fate of having an autism diagnosis, would become reality," Duncan states.

Proof is on the way, with data to be released at the Lyme-Autism Connection Conference this weekend and studies in progress, parents and doctors can be sure to hear more about this in the coming months.

Conference information is available online at www.liafoundation.org . It is going to be held at the Hyatt Regency in Irvine, CA, June 22 - 24th. Registration is available at the door.

About Autism
Autism is a disorder that currently affects 1 out of 150 children. Boys are the majority of those affected. The numbers of autism cases spiked in the mid-late 90's and continues to remain high. The exact cause of autism is still unknown, however, many theories exist. Most children do improve with some sort of bio-medical intervention.
About Lyme disease

Lyme disease is generally caused by a tick bite in which the tick transmits a bacteria called Borrelia Burgdorferi. Symptoms of Lyme disease include, achy joints, confusion, slurring words or word retrieval problems, brain fog, sensitivity to light and sound. Lyme disease in its late stage can be fatal, causing MS like symptoms and debilitating its victims. Treatment for Lyme disease consists of antibiotic therapy.

About the LIA Foundation
The foundation was started in September 2006 by parents of children with autism and Lyme disease. Kathy Blanco of Beaverton, OR and Tami Duncan of Corona, CA are the founders. The foundations' goals are to educate families and physicians on the link between Lyme and autism, bring physicians together to form a consensus for testing and treatment

soijuv
Viestit: 3151
Liittynyt: Ke Tammi 21, 2009 14:16

Viesti Kirjoittaja soijuv » Ma Syys 07, 2009 10:27

Borrelioosia sairastavilla on erityisesti USA:ssa usein lisäinfektiona ehrlichioosi. Aiemmin terve 50-vuotias nainen sai kuumetta, ihomuutoksia ja voimakkaan verenvuodon. Hän menehtyi viiden päivän kuluttua. Aiheuttajaksi paljastui Anaplasma phagocytophilum. Taudinaiheuttajaa esiintyy samoilla seuduilla kuin borrelioosia esim. USA:ssa ja Euroopassa. Tauti leviää esim. punkkien välityksellä. Taudin oireet ovat useimmiten lieviä ja antibioottihoito, doksisykliini, on tehokasta useissa tapauksissa.

Nosocomial Transmission of Human Granulocytic Anaplasmosis?
Peter J. Krause, MD; Gary P. Wormser, MD


JAMA. 2008;300(19):2308-2309.

In this issue of JAMA, Zhang and colleagues describe a possible nosocomial outbreak of human granulocytic anaplasmosis (HGA) in China.1 The clinical presentation of the index case, a previously healthy 50-year-old woman who developed a febrile illness with rash and massive bleeding and who died 5 days later, is consistent with many infectious etiologies including viral hemorrhagic fever (VHF) for which she was given ribavirin.2 Laboratory studies in 9 subsequent cases in family members and health care workers who had contact with the patient, however, suggested that her disease was HGA.

Human granulocytic anaplasmosis is an emerging tick-borne infectious disease caused by Anaplasma phagocytophilum that occurs in Lyme disease?endemic areas in the United States and sporadically in Europe. Clinical manifestations of HGA are usually mild to moderate and most patients promptly respond to treatment with doxycycline, which neither the index patient . . .

Author Affiliations: Department of Epidemiology and Public Health, Yale School of Medicine, New Haven, Connecticut (Dr Krause), and the Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla, New York (Dr Wormser).

Full article:

http://jama.ama-assn.org/cgi/content/short/300/19/2308

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