ReviewFEMS immunology and medical microbiology2012
The biological basis of severe outcomes in Anaplasma phagocytophilum infection.
Review in FEMS immunology and medical microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 85 citations in OpenAlex.
- Trial
- Trends in Anaplasmosis Over the Past Decade: A Review of Clinical Features, Laboratory Data, and Outcomes.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026Article
- Comparative evaluation of oxytetracycline and an herbal formulation in the treatment of bovine anaplasmosis.Tropical animal health and production · 2026Article
- A roll of the dice: pathogen-host interaction and the evolution of disease susceptibility.Parasitology · 2026Review
- Generation of Population-Level Diversity inPathogens (Basel, Switzerland) · 2025Article
- Molecular surveillance of zoonotic pathogens from wild rodents in the Republic of Korea.PLoS neglected tropical diseases · 2024Article
- Aptamer selection against cell extracts containing the zoonotic obligate intracellular bacterium, Anaplasma phagocytophilum.Scientific reports · 2024Article
- Molecular surveillance and genetic diversity of Anaplasma spp. in cattle (Bos taurus) and goat (Capra aegagrus hircus) from Hainan island/province, China.BMC veterinary research · 2023Article
- Anaplasma phagocytophilum Ats-1 enhances exosome secretion through Syntenin-1.BMC microbiology · 2023Article
- Development of a Syndromic Molecular Diagnostic Assay for Tick-Borne Pathogens Using Barcoded Magnetic Bead Technology.Microbiology spectrum · 2023Article
- Article
- The Biological and Ecological Features of Northbound Migratory Birds, Ticks, and Tick-Borne Microorganisms in the African-Western Palearctic.Microorganisms · 2023Review
- Immune evasion strategies of major tick-transmitted bacterial pathogens.Trends in microbiology · 2023Review
- Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023Review
- Human granulocytic anaplasmosis complicated by hemophagocytic syndrome and coinfection.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2022Article
- Human Granulocytic Anaplasmosis-A Systematic Review of Published Cases.Microorganisms · 2022Review
- Parasitic and Vector-Borne Infections in HIV-Positive Patients in Slovakia-Evidence of an Unexpectedly High Occurrence ofPathogens (Basel, Switzerland) · 2021Article
- Epidemiological and Clinicopathological Features ofFrontiers in veterinary science · 2021Review
- Immunization against Anaplasma phagocytophilum Adhesin Binding Domains Confers Protection against Infection in the Mouse Model.Infection and immunity · 2020Article
- Molecular detection of pathogens in ticks associated with domestic animals from the Colombian Caribbean region.Experimental & applied acarology · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Anaplasma phagocytophilum causes granulocytic anaplasmosis, an acute disease in humans that is also often subclinical. However, 36% are hospitalized, 7% need intensive care, and the case fatality rate is 0.6%. The biological basis for severe disease is not understood. Despite A. phagocytophilum's mechanisms to subvert neutrophil antimicrobial responses, whether these mechanisms lead to disease is unclear. In animals, inflammatory lesions track with IFNγ and IL-10 expression and infection of Ifng(-/-) mice leads to increased pathogen load but inhibition of inflammation. Suppression of STAT signaling in horses impacts IL-10 and IFN-γ expression, and also suppresses disease severity. Similar inhibition of inflammation with infection of NKT-deficient mice suggests that innate immune responses are key for disease. With severe disease, tissues can demonstrate hemophagocytosis, and measures of macrophage activation/hemophagocytic syndromes (MAS/HPS) support the concept of human granulocytic anaplasmosis as an immunopathologic disease. MAS/HPS are related to defective cytotoxic lymphocytes that ordinarily diminish inflammation. Pilot studies in mice show cytotoxic lymphocyte activation with A. phagocytophilum infection, yet suppression of cytotoxic responses from both NKT and CD8 cells, consistent with the development of MAS/HPS. Whether severity relates to microbial factors or genetically determined diversity in human immune and inflammatory response needs more investigation.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.