Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The agent of human granulocytic ehrlichiosis (HGE) is a newly recognized tick-borne pathogen that resides within polymorphonuclear leukocytes. C3H/HeN mice can become infected with the agent of HGE (designated aoHGE) by syringe inoculation or tick-borne infection and develop transient neutropenia. They thereby partially mimic human disease and provide a model in which to study immunity to this microorganism. Mice vaccinated with lysates of purified aoHGE, or administered aoHGE antisera, were partially protected from both syringe- and tick-transmitted challenge with aoHGE. These data suggest that antibodies are sufficient to provide substantial, but not complete, immunity against aoHGE.
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PMID:Immunization against the agent of human granulocytic ehrlichiosis in a murine model. 939 47

Following intravenous inoculation with horse blood-infected with the agent of human granulocytic ehrlichiosis (HGE) from a human fatality, two rhesus macaques (Macaca mulatta) exhibited pyrexia and lethargy on days 4-12 postinfection (PI). Hematology revealed neutropenia, thrombocytopenia, and anemia, with ehrlichial morulae in monocytes and neutrophils on days 4-12. Blood was polymerase chain reaction (PCR)-positive on days 4-12 and bone marrow was PCR-positive on day 11. There was a minor increase in gamma-glutamyl transpeptidase on day 12 and serum interferon-gamma levels increased by day 18. Seroconversion occurred on day 20 PI to a titer of 100 by day 22. Western blot bands characteristic of HGE included 25-, 44-, 80-, 94-, 105-, and 125-kD bands. There was generalized lymphohistiocytic infiltration in the liver, spleen, lymph nodes, and other tissues. The liver had focal hepatocyte apoptosis. There was HGE DNA (by PCR) only in the spleen. Comparable findings were not observed in a monkey that received uninfected horse blood as a control. This animal model of human disease is important for further studies of HGE diagnosis, management, and pathogenesis.
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PMID:A simian model of human granulocytic ehrlichiosis. 1040 32

Anaplasma phagocytophilum is the recently designated name replacing three species of granulocytic bacteria, Ehrlichia phagocytophila, Ehrlichia equi and the agent of human granulocytic ehrlichiosis, after the recent reorganization of the families Rickettsiaceae and Anaplasmataceae in the order Rickettsiales. Tick-borne fever (TBF), which is caused by the prototype of A. phagocytophilum, was first described in 1932 in Scotland. A similar disease caused by a related granulocytic agent was first described in horses in the USA in 1969; this was followed by the description of two distinct granulocytic agents causing similar diseases in dogs in the USA in 1971 and 1982. Until the discovery of human granulocytic anaplasmosis (HGA) in the USA in 1994, these organisms were thought to be distinct species of bacteria infecting specific domestic animals and free-living reservoirs. It is now widely accepted that the agents affecting different animal hosts are variants of the same Gram-negative obligatory intracellular bacterium, which is transmitted by hard ticks belonging to the Ixodes persulcatus complex. One of its fascinating features is that it infects and actively grows in neutrophils by employing an array of mechanisms to subvert their bactericidal activity. It is also able to survive within an apparently immune host by employing a complex mechanism of antigenic variation. Ruminants with TBF and humans with HGA develop severe febrile reaction, bacteraemia and leukopenia due to neutropenia, lymphocytopenia and thrombocytopenia within a week of exposure to a tick bite. Because of the severe haematological disorders lasting for several days and other adverse effects on the host's immune functions, infected animals and humans are more susceptible to other infections.
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PMID:The natural history of Anaplasma phagocytophilum. 1981 78