Jump to content

Human granulocytic anaplasmosis

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by 2015evolution7 (talk | contribs) at 14:43, 25 October 2015 (edited grammar and flow of article to make it little more visually pleasing). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Human granulocytic anaplasmosis
SpecialtyInfectious diseases Edit this on Wikidata

Human granulocytic anaplasmosis (HGA) (previously known as Human granulocytic ehrlichiosis, or HGE[1][2] ) is an infectious disease caused by Anaplasma phagocytophilum, an obligate intracellular bacterium that is typically transmitted to humans by at least three kinds of ticks, Ixodes scapularis, Ixodes pacificus, and Dermacentor variabilis. These ticks also transmit Lyme disease and other tick borne diseases.[3]

The bacteria infect white blood cells called neutrophils, causing changes in gene expression that prolong the life of these otherwise short-lived cells.[4]

First Diagnosis

The first outbreak of Human Granulocytic Anaplasmosis (HGA) in the United States was in a patient in early 1990 in Wisconsin. He was kept in the hospital in Minnesota for testing, and he had died after getting very sick after getting bitten by a tick.[5] He was tested for many things, and each result came back negative. The study was inconclusive for the time being. Over the next couple of years, many people within the same area of Wisconsin and Minnesota had come down with the same thing. These patients had many tests done and DNA sequencing was done, in attempt to figure out what this disease could be. It was discovered in 1994 that it was Human Granulocytic Ehrlichiosis (HGE), later to be known as HGA that caused these symptoms in humans.[6]

Ecology and epidemiology

A. phagocytophilum is transmitted to humans by Ixodes ticks. These ticks are found in the US, Europe, and Asia. In the US, I. scapularis is the tick vector in the East and Midwest states, and I. pacificus in the Pacific Northwest.[7] In Europe, the I. ricinus is the main tick vector, and I. persulcatus is the currently known tick vector in Asia.[5]

The major mammalian reservoir for A. phagocytophilum in the eastern United States is the white-footed mouse, Peromyscus leucopus. Although white-tailed deer and other small mammals[8] harbor A. phagocytophilum, evidence suggests that they are not a reservoir for the strains that cause HGA.[9] A tick that has a blood meal from and infected reservoir become infected themselves. If an infected tick then latches onto a human the disease is then transmitted to the human.

A tick that has a blood meal from an infected reservoir becomes infected themselves. If an infected tick then latches onto a human the disease is transmitted to the human host and A. phagocytophilum symptoms can arise.[6]

Anaplasma phagocytophilum shares its tick vector with other human pathogens, and about 10% of patients with HGA show serologic evidence of coinfection with Lyme disease, babesiosis, or tick-borne meningoencephalitis.[10]

Signs and symptoms

Signs and symptoms may include:

  • fever
  • severe headache
  • muscle aches (myalgia)
  • chills and shaking, similar to the symptoms of influenza
  • nausea
  • vomiting
  • loss of appetite
  • unintentional weight loss
  • abdominal pain
  • cough
  • diarrhea,
  • aching joints
  • sensitivity to light
  • weakness
  • fatigue
  • change in mental status (extreme confusion, memory loss, inability to comprehend environment- interaction, reading, etc.)
  • temporary loss of basic motor skills

Symptoms may be minor, as evidenced by surveillance studies in high-risk areas. Gastrointestinal tract symptoms occur in less than half of patients and a skin rash is seen in less than 10% of patients. It is also characterized by a low number of platelets, a low number of white blood cells, and elevated serum transaminase levels in the majority of infected patients.[11] Even though people of any age can get human anaplasmosis, it is usually more severe in the aging or immune-compromised. Some severe complications may include respiratory failure, kidney failure, and secondary infections.

Diagnosis

Clinically, HGA is essentially indistinguishable from Human monocytic ehrlichiosis, the infection caused by Ehrlichia chaffeensis, and other tick-borne illnesses such as Lyme disease may be suspected. As Ehrlichia serologies can be negative in the acute period, PCR is very useful for diagnosis.[12]

Treatment and Prevention

Doxycycline is the treatment of choice. If anaplasmosis is suspected, treatment should not be delayed while waiting for a definitive laboratory confirmation, as prompt doxycycline therapy has been shown to improve outcomes.[13] Presentation during early pregnancy can complicate treatment. Doxycycline compromises dental enamel during development.[14] Although rifampin is indicated for post-delivery pediatric and some doxycycline-allergic patients, it is teratogenic. Rifampin is contraindicated during conception and pregnancy.[15] Currently, there is no vaccine against human granulocytic anaplasmosis. Without antibiotic treatment very quickly, even before confirmed diagnosis, the patient can get extremely sick, eventually leading to death, much like the first patient that went undiagnosed. Most patients make a complete, predictable recovery, though some patients are intensively cared for, for many reasons. One reason for a patient needing intensive care is if the patient goes too long without seeing a doctor or being diagnosed. The majority of patients, though, make a 100% recovery with no residual damage.[5]

Terminology

Although the infectious agent is known to be from the Anaplasma genus, the term "human granulocytic ehrlichiosis" (HGE) is often used, reflecting the prior classification of the organism. E. phagocytophilum and E. equi were reclassified as Anaplasma phagocytophilum.

See also

References

  1. ^ Malik A, Jameel M, Ali S, Mir S (2005). "Human granulocytic anaplasmosis affecting the myocardium". J Gen Intern Med. 20 (10): 958. doi:10.1111/j.1525-1497.2005.00218.x. PMC 1490240. PMID 16191146.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ Human Anaplasmosis Basics - Minnesota Dept. of Health
  3. ^ http://www.bioone.org/doi/abs/10.1603/0022-2585%282003%29040%5B0534%3ADOBBEC%5D2.0.CO%3B2
  4. ^ PMID: Lee HC, Kioi M, Han J, Puri RK, Goodman JL (September 2008). "Anaplasma phagocytophilum-induced gene expression in both human neutrophils and HL-60 cells". Genomics. 92 (3): 144–51. doi:10.1016/j.ygeno.2008.05.005. PMID 18603403.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ a b c Bakken, Johan S.; Dumler, J. Stephen (2006-10-01). "Clinical Diagnosis and Treatment of Human Granulocytotropic Anaplasmosis". Annals of the New York Academy of Sciences. 1078 (1): 236–247. doi:10.1196/annals.1374.042. ISSN 1749-6632.
  6. ^ a b "Human Granulocytic Anaplasmosis and Anaplasma phagocytophilum - Volume 11, Number 12—December 2005 - Emerging Infectious Disease journal - CDC". wwwnc.cdc.gov. Retrieved 2015-10-21.
  7. ^ Dumler JS, Madigan JE, Pusterla N, Bakken JS (July 2007). "Ehrlichioses in humans: epidemiology, clinical presentation, diagnosis, and treatment". Clinical Infectious Diseases. 45 (Suppl 1): S45–51. doi:10.1086/518146. PMID 17582569.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ "Diagnosis and Management of Tickborne Rickettsial Diseases: Rocky Mountain Spotted Fever, Ehrlichioses, and Anaplasmosis --- United States A Practical Guide for Physicians and Other Health-Care and Public Health Professionals". www.cdc.gov. Retrieved 2015-10-21.
  9. ^ Massung RF, Courtney JW, Hiratzka SL, Pitzer VE, Smith G, Dryden RL (October 2005). "Anaplasma phagocytophilum in white-tailed deer". Emerging Infectious Diseases. 11 (10): 1604–6. doi:10.3201/eid1110.041329. PMID 16318705.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Dumler JS, Choi KS, Garcia-Garcia JC, et al. (December 2005). "Human granulocytic anaplasmosis and Anaplasma phagocytophilum". Emerging Infectious Diseases. 11 (12): 1828–34. doi:10.3201/eid1112.050898. PMC 3367650. PMID 16485466.
  11. ^ Murray, Patrick R.; Rosenthal, Ken S.; Pfaller, Michael A. Medical Microbiology, Fifth Edition. United States: Elsevier Mosby, 2005
  12. ^ Prince LK, Shah AA, Martinez LJ, Moran KA (August 2007). "Ehrlichiosis: making the diagnosis in the acute setting". Southern Medical Journal. 100 (8): 825–8. doi:10.1097/smj.0b013e31804aa1ad. PMID 17713310.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Hamburg BJ, Storch GA, Micek ST, Kollef MH (March 2008). "The importance of early treatment with doxycycline in human ehrlichiosis". Medicine. 87 (2): 53–60. doi:10.1097/MD.0b013e318168da1d. PMID 18344803.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Muffly T, McCormick TC, Cook C, Wall J (2008). "Human granulocytic ehrlichiosis complicating early pregnancy". Infect Dis Obstet Gynecol. 2008: 359172. doi:10.1155/2008/359172. PMC 2396214. PMID 18509484.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  15. ^ Krause PJ, Corrow CL, Bakken JS (September 2003). "Successful treatment of human granulocytic ehrlichiosis in children using rifampin". Pediatrics. 112 (3 Pt 1): e252–3. doi:10.1542/peds.112.3.e252. PMID 12949322.{{cite journal}}: CS1 maint: multiple names: authors list (link)
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Human_granulocytic_anaplasmosis&oldid=687426436"