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Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Alphaproteobacteria
Order: Rickettsiales
Family: Anaplasmataceae


Genus: Ehrlichia
Species: Ehrlichia canis
Ehrlichia chaffeensis
Ehrlichia ewingii

Ehrlichia is a genus of rickettsiales bacteria that is transmitted to vertebrates by ticks. This disease is considered zoonotic, because the main reservoir for the disease is animals.

Ehrlichia are obligately intracellular pathogens and are transported between cells through the host cell filopodia during initial stages of infection, whereas, in the final stages of infection the pathogen ruptures the host cell membrane.[2]


The genus Ehrlichia is named after a German microbiologist Paul Ehrlich.The first ehrlichial disease was first recognized in South Africa during the 19th century. Its tick-borne nature was determined in 1900. The organism itself was demonstrated 1925 when it was recognized to be a rickettsia. It was initially named Rickettsia ruminantium, and is currently named Ehrlichia ruminantium. In 1945 a "infection and treatment" method for livestock was developed. This is still the only commercially available "vaccine" against the disease, which is not a true vaccine, but intentional exposure to the disease with monitoring and antibiotic treatment if needed. In 1985 the organism was first propagated reliably in tissue culture. A new species of Ehrlichia was discovered inside the deer tick Ixodes scapularis. This newly found organism has only been isolated from deer ticks in Wisconsin and Minnesota in the USA. The species is known as Ehrlichia Wisconsin HM543746.


Ehrlichia have evolved greatly since they first emerged. The evolution in their genome has taken many different pathways, some of which have led to an increase in fitness and survival.

The Ehrlichia genome contains many different variants of genes that encode outer membrane proteins.[3] These genes have gone through intense modification over long periods of time.[4] Truncation is the most common modification that may result in a change in protein structure. Truncation can alter protein translation and provide antigenic variants to the organism.[4] These truncated genes could have been the result of a fusion event of two short open reading frames or by a fission event.[4] After the gene has been truncated and duplicated, the resulting protein's structure may be different than the original.[4] This has a profound effect on the fitness of an organism. The survival of Ehrlichia depends greatly on the immune response of its host. With a higher range of outer-membrane proteins, the parasite can evade the immune system of the host more effectively and establish persistent infection.

The most pronounced evidence of evolution in the genome size of Erhlichia is the presence of tandem repeats.[3] These repeats vary highly among individuals and species. Over time, individuals may expand or contract parts of their genes and alleles which adds genetic variation and may sometimes affect phenotype.[3]

Ehrlichia and their closely related species Anaplasma show extreme diversity in the structure and content of their genomes.[5] This diversity is direct result of rare clones with extreme genomes that emerged by chance after repeated bottleneck events, and this diversity persists because of the lack of selective constraints on rapid growth inside the host tissue.[5]

Ehrlichia ruminantium[edit]

The evolutionary changes in the outer membrane proteins have led to the emergence of new strains which can infect a larger variety of hosts. Heartwater, caused by Ehrlichia ruminantium, is a prevalent tick borne disease of livestock in Africa and the Caribbean but also threatens the American mainland.[3] Three strains have arose from this species due to evolutionary change in their genomes. When sequencing their genomes, there were many active genomic modifications such as high substitution rates, truncated genes, and the presence of pseudogenes and tandem repeats.[3] When analyzing substitution rates between the three strains in 888 orthologous coding DNA sequences, it was observed that there were only 3 coding DNA sequences that were biased towards non-synonymous substitutions that affect phenotype.[3] In contrast, 181 coding DNA sequences were biased towards synonymous substitutions which do not affect phenotype.[3] This indicates there was a selection pressure to maintain protein function, and this selection acted against the non-synonymous mutations.

Ehrlichia canis[edit]

Ehrlichia canis are small, obligate intracelllar, tick transmitted, gram-negative, α-proteobacterium.[6] This species is responsible for the globally distributed canine monocytic ehrlichiosis.[6] Ehrlichia canis also show evolution in their complex membrane structures and immune evasion strategies.[6] These evolutionary features are derived traits that do not show up in the previous lineages which may indicate that these features may have contributed to a fitness advantage that kept this lineage going.[6] Unique glycoproteins and major outer membrane proteins can be expressed variously using 25 different genes.[6] The glycoproteins are important targets of the host immune response, attachment to the host cell, and other features in the immune response.[6] The more outer-membrane protein genes that can be expressed, the higher the chance the organism can avoid being recognized by the host's immune system.

There is also the presence of reductive evolution in the Ehrlichia canis. The genome has had a severe loss of metabolic pathway enzymes compared to its ancestors.[7] Natural selection may not be the reason for small genomes.[7] Reductive evolution in obligate intracellar pathogens is usually the direct result of genetic drift in small populations, low recombination rates, and high mutation rates.[7] The host metabolic pathway enzymes take control of the functions lost due to reductive evolution, and this contributes to the Ehrlichia's need for a host.

See also[edit]


  1. ^ Garrity, George (2005). Bergey's Manual of Systematic Bacteriology. Springer. ISBN 0-387-24145-0. 
  2. ^ Thomas S, Popov VL, Walker DH (2010) Exit Mechanisms of the Intracellular Bacterium Ehrlichia. PLoS ONE 5(12): e15775.
  3. ^ a b c d e f g Frutos, Roger. 2007. Ehrlichia ruminantium: genomic and evolutionary features. Trends in Parasitology. 23: 414-419. doi:10.1016/
  4. ^ a b c d Andersson, Siv. 2007. Intracellular pathogens go extreme: genome evolution in the Rickettsiales. Trends in Genetics. 23: 511-520.
  5. ^ a b C. Dale, N. Moran. Molecular interactions between bacterial symbionts and their hosts Cell, 126 (2006), pp. 453–465
  6. ^ a b c d e f Mavromatis, K. 2006. The Genome of the Obligately Intracellular Bacterium Ehrlichia canis Reveals Themes of Complex Membrane Structure and Immune Evasion Strategies. Journal of Bacteriology. 4015-4023.
  7. ^ a b c Moran, N. A. 1996. Accelerated evolution and Muller's rachet in endosymbiotic bacteria. Proc. Natl. Acad. Sci. USA 93:2873-2878

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