| Anaplasma phagocytophilum | |
|---|---|
 | |
| HumanHL60 cells containingAnaplasma phagocytophilum (indicated by arrows) which are basophilic intracytoplasmic inclusions when stained withWright-Giemsa stain | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Alphaproteobacteria |
| Subclass: | "Rickettsidae" |
| Order: | Rickettsiales |
| Family: | Ehrlichiaceae |
| Genus: | Anaplasma |
| Species: | A. phagocytophilum |
| Binomial name | |
| Anaplasma phagocytophilum (Foggie 1949) Dumler et al. 2001[1] | |
| Synonyms | |
Rickettsia phagocytophila ovis | |
Anaplasma phagocytophilum (formerlyEhrlichia phagocytophilum)[2] is aGram-negative bacterium that is unusual in itstropism toneutrophils. It causesanaplasmosis in sheep and cattle, also known astick-borne fever andpasture fever, and also causes thezoonotic diseasehuman granulocytic anaplasmosis.[3]
A. phagocytophilum is a Gram-negative,obligate bacterium of neutrophils. It causes humangranulocytic anaplasmosis, which is a tick-borne rickettsial disease. Because this bacterium invades neutrophils, it has a unique adaptation and pathogenetic mechanism.[4]
A. phagocytophilum is a small, obligate, intracellular bacterium with a Gram-negative cell wall. It is 0.2–1.0 μm and lacks a lipopolysaccharide biosynthetic machinery. The bacterium first resides in an earlyendosome, where it acquires nutrients for binary fission and grows into small groups called morulae. This bacterium prefers to grow within myeloid or granulocytic cells.[4]
Hosts includegoats,cattle,horses anddogs. Cattle infections had been suspected but were only first confirmed by Nieder et al. 2012.[5]
A. phagocytophilum causes human granulocyticanaplasmosis (HGA). This disease was first identified in 1990, although this pathogen was known to cause veterinary disease since 1932. Since 1990, incidence of HGA has increased, and it is now recognized in Europe. This disease was first identified due to a Wisconsin patient who died with a severe febrile illness two weeks after a tick bite. During the last stage of the infection, a group of small bacteria was seen within the neutrophils in the blood. Other symptoms include fever, headache, absence of skin rash,leucopenia,thrombocytopenia, and mild injury to the liver.[4]
The disease is multisystemic, but the most severe changes areanaemia andleukopenia. This organism causeslameness, which can be confused with symptoms ofLyme disease, another tick-borne illness. It is a vector-bornezoonotic disease whose morula can be visualized withinneutrophils (a type of white blood cell) from the peripheral blood and synovial fluid. It can causelethargy,ataxia,loss of appetite, and weak or painful limbs.[3]
A. phagocytophilum binds to fucosylated and sialylated scaffold proteins on neutrophil and granulocyte surfaces. Atype IV secretion apparatus is known to help in the transfer of molecules between the bacterium and the host. The most studied ligand is PSGL-1 (CD162). The bacterium adheres to PSGL-1 (CD162) through the 44-kDa major surface protein-2 (Msp2). After the bacterium enters the cell, the endosome stops maturation and does not accumulate markers of late endosomes orphagolysosomes. Because of this, the vacuole does not become acidified or fused tolysosomes.A. phagocytophilum then divides untilcell lysis or when the bacteria leave to infect other cells.[4]
This bacterium has the ability to affect neutrophils by altering their function. It can survive the first encounter with the host cell by detoxifyingsuperoxide produced byneutrophil phagocyte oxidase assembly. It also disrupts normal neutrophil function, such as endothelial cell adhesion, transmigration, motility, degranulation, respiratory burst, and phagocytosis.[4] It causes an increase in the secretion ofIL-8, a chemoattractant that increases the phagocytosis of neutrophils. The purpose of this is to increase bacterial dissemination into the neutrophil.[6]
These tests can be performed to determine anA. phagocytophilum infection:
Patients with HGA undergodoxycycline therapy, 100 mg twice daily until the patient's fever subsides for at least 3 days. This drug has been the most beneficial to those patients infected with the bacteria. Some othertetracycline drugs are also effective. In general, patients with symptoms of HGA and unexplained fever after a tick exposure should receive empiric doxycycline therapy while their diagnostic tests are pending, especially if they experienceleukopenia and/orthrombocytopenia.[7]
In animals, antibiotics such asoxytetracycline, sulphamethazine,sulphadimidine,doxycycline, andtrimethoprim-sulphonamides have been used.[3]