Ehrlichioosia käsittelevä artikkeli:
Current management of human granulocytic anaplasmosis, human monocytic ehrlichiosis and Ehrlichia ewingii ehrlichiosis
Expert Review of Anti-infective Therapy
August 2009, Vol. 7, No. 6, Pages 709-722 , DOI 10.1586/eri.09.44
Rachael J Thomas, J Stephen Dumler and Jason A Carlyon?
Anaplasma phagocytophilum, Ehrlichia chaffeensis and Ehrlichia ewingii are emerging tick-borne pathogens and are the causative agents of human granulocytic anaplasmosis, human monocytic ehrlichiosis and E. ewingii ehrlichiosis, respectively. Collectively, these are referred to as human ehrlichioses. These obligate intracellular bacterial pathogens of the family Anaplasmataceae are transmitted by Ixodes spp. or Amblyomma americanum ticks and infect peripherally circulating leukocytes to cause infections that range in clinical spectra from asymptomatic seroconversion to mild, severe or, in rare instances, fatal disease. This review describes: the ecology of each pathogen; the epidemiology, clinical signs and symptoms of the human diseases that each causes; the choice methods for diagnosing and treating human ehrlichioses; recommendations for patient management; and is concluded with suggestions for potential future research.
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23-vuotias mies oli saanut punkinpureman välityksellä kolme eri taudinaiheuttajaa elimistöönsä; borreliabakteeri, ehrlichia, babesia.
Se vaikeutti taudinkuvaa, hoitoa ja diagnostiikkaa. (USA 2009)
Severe, Concurrent Lyme Disease, Babesiosis and Ehrlichiosis in a Healthy 23 Year-Old Connecticut Resident
M. Villanueva, B. Behjatnia, J. I. Meek
http://www.cdc.gov/ncidod/osr/site/eip/ ... D_2002.pdf
Waterbury Hospital, Waterbury, CT, Connecticut Emerging Infections Program, New Haven, CT
Background: Lyme disease (LD), babesiosis, and human granulocytic ehrlichiosis (HGE) are emergent zoonotic diseases affecting residents in the Northeastern and Midwestern United States. The etiologic agents of each disease are perpetuated in a natural cycle between vertebrate reservoir hosts and the tick vector, Ixodes scapularis. The geographical and ecological over-lap between HGE, LD and babesiosis suggests the potential for co-transmission, co-infection and co-morbidity. We describe the case of a Connecticut resident simultaneously infected with all three agents.
Case Report: A previously healthy, 23 year-old male presented to an emergency department (ED) after five days of headache, fever, sweats, myalgia, and fatigue. He recalled a tick bite about one week earlier. He was given the diagnosis of LD and treated with clarithromycin. Approximately two weeks later, the symptoms returned and he presented to our ED. Laboratory evaluation revealed leukopenia, thrombocytopenia, and a hematocrit of 41%. Liver function tests, and erythrocyte sedimentation rate were normal. LD serologies were sent. On evaluation, he was found to have tonsillar, cervical, and inguinal lymphadenopathy and splenomegaly that was confirmed by abdominal CT scan. Five days later, the patient returned to the ED with acute left upper quadrant pain, and persistent fevers. Hematocrit was 29%. Repeat abdominal CT scan demonstrated increased splenomegaly and new left flank and pelvic fluid. The patient was admitted to the surgical intensive care unit with the presumed diagnosis of splenic rupture. Laboratory data were significant for leukopenia, thrombocytopenia, elevated LDH and AST, and decreased haptoglobin. The hospital course was remarkable for persistent high-grade fevers to 104.6° F. Lymph node biopsy showed follicular lymphoid hyperplasia and no evidence for malignancy. A peripheral smear showed intraerythrocytic ring forms 54 consistent with Babesia. The patient was treated with clindamycin and quinine with rapid defervescence. LD serologies from the previous ED visit were positive on both ELISA and Western Blot. After completing a course of clindamycin and quinine, the patient was started on a course of doxycycline. Serum samples were sent for HGE and Babesia microti serology. Indirect fluorescent antibody staining methods revealed an HGE titer of 1:4096 and a B. microti titer of 1:640. HGE-specific ELISA was confirmatory. Nine months later, repeat testing demonstrated a >4-fold decrease in antibody titer to both HGE and B. microti.
Conclusion: This patient had concurrent infection with three I. scapularis-borne diseases. The unexpected severity of illness in this otherwise healthy host can in part be attributed to the delay in diagnosis resulting from an atypical presentation and the possible immunosuppressive effects resulting from the interplay of the three diseases.