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Effects of Aging on Parasite Biomass, Inflammation, Endothelial Activation, Microvascular Dysfunction and Disease Severity in Plasmodium knowlesi and Plasmodium falciparum Malaria.

Abstract In populations pauci-immune to malaria, risk of severe malaria increases with age. This is particularly apparent in Plasmodium knowlesi malaria. However, pathophysiological mechanisms underlying knowlesi malaria, and of the age-related increase in risk of severe malaria in general, are poorly understood.
PMID
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Authors

Mayor MeshTerms

Aging

Plasmodium knowlesi

Keywords

Plasmodium knowlesi

aging

endothelial activation

malaria

pathogenesis

Journal Title the journal of infectious diseases
Publication Year Start




PMID- 28863470
OWN - NLM
STAT- MEDLINE
DA  - 20170902
DCOM- 20170907
LR  - 20170907
IS  - 1537-6613 (Electronic)
IS  - 0022-1899 (Linking)
VI  - 215
IP  - 12
DP  - 2017 Jun 15
TI  - Effects of Aging on Parasite Biomass, Inflammation, Endothelial Activation,
      Microvascular Dysfunction and Disease Severity in Plasmodium knowlesi and
      Plasmodium falciparum Malaria.
PG  - 1908-1917
LID - 10.1093/infdis/jix193 [doi]
AB  - Background: In populations pauci-immune to malaria, risk of severe malaria
      increases with age. This is particularly apparent in Plasmodium knowlesi malaria.
      However, pathophysiological mechanisms underlying knowlesi malaria, and of the
      age-related increase in risk of severe malaria in general, are poorly understood.
      Methods: In Malaysian patients aged >/=12 years with severe (n = 47) and
      nonsevere (n = 99) knowlesi malaria, severe (n = 21) and nonsevere (n = 109)
      falciparum malaria, and healthy controls (n = 50), we measured parasite biomass, 
      systemic inflammation (interleukin 6 [IL-6]), endothelial activation
      (angiopoietin-2), and microvascular function, and evaluated the effects of age.
      Results: Plasmodium knowlesi parasitemia correlated with age (Spearman's
      correlation coefficient [rs] = 0.36; P < .0001). In knowlesi malaria, IL-6,
      angiopoietin-2, and microvascular dysfunction were increased in severe compared
      to nonsevere disease, and all correlated with age, independent of parasitemia. In
      falciparum malaria, angiopoietin-2 increased with age, independent of parasite
      biomass (histidine-rich protein 2 [HRP2]). Independent risk factors for severe
      malaria included parasitemia and angiopoietin-2 in knowlesi malaria, and HRP2,
      angiopoietin-2, and microvascular dysfunction in falciparum malaria. Conclusions:
      Parasite biomass, endothelial activation, and microvascular dysfunction are
      associated with severe disease in knowlesi malaria and likely contribute to
      pathogenesis. The association of each of these processes with aging may account
      for the greater severity of malaria observed in older adults in low-endemic
      regions.
FAU - Barber, Bridget E
AU  - Barber BE
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
AD  - Infectious Diseases Society, Sabah-Menzies School of Health Research Clinical
      Research Unit, Queen Elizabeth Hospital.
FAU - Grigg, Matthew J
AU  - Grigg MJ
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
AD  - Infectious Diseases Society, Sabah-Menzies School of Health Research Clinical
      Research Unit, Queen Elizabeth Hospital.
FAU - William, Timothy
AU  - William T
AD  - Infectious Diseases Society, Sabah-Menzies School of Health Research Clinical
      Research Unit, Queen Elizabeth Hospital.
AD  - Jesselton Medical Centre, Kota Kinabalu, Sabah, Malaysia.
FAU - Piera, Kim A
AU  - Piera KA
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
FAU - Boyle, Michelle J
AU  - Boyle MJ
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
AD  - Centre for Biomedical Research, Burnet Institute, Melbourne, Victoria, Australia.
FAU - Yeo, Tsin W
AU  - Yeo TW
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
AD  - Infectious Diseases Society, Sabah-Menzies School of Health Research Clinical
      Research Unit, Queen Elizabeth Hospital.
AD  - Lee Kong Chian School of Medicine, Nanyang Technological University.
AD  - Institute of Infectious Disease and Epidemiology, Tan Tock Seng Hospital,
      Singapore.
FAU - Anstey, Nicholas M
AU  - Anstey NM
AD  - Global and Tropical Health Division, Menzies School of Health Research and
      Charles Darwin University, Northern Territory, Australia.
AD  - Infectious Diseases Society, Sabah-Menzies School of Health Research Clinical
      Research Unit, Queen Elizabeth Hospital.
LA  - eng
PT  - Journal Article
PT  - Observational Study
PL  - United States
TA  - J Infect Dis
JT  - The Journal of infectious diseases
JID - 0413675
SB  - AIM
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - *Aging
MH  - Biomass
MH  - Case-Control Studies
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Malaria/*parasitology
MH  - Malaria, Falciparum/*parasitology
MH  - Malaysia
MH  - Male
MH  - Middle Aged
MH  - Parasitemia/*parasitology
MH  - *Plasmodium knowlesi
MH  - Prospective Studies
MH  - Severity of Illness Index
MH  - Statistics, Nonparametric
MH  - Young Adult
OTO - NOTNLM
OT  - Plasmodium knowlesi
OT  - aging
OT  - endothelial activation
OT  - malaria
OT  - pathogenesis
EDAT- 2017/09/03 06:00
MHDA- 2017/09/08 06:00
CRDT- 2017/09/03 06:00
PHST- 2017/01/23 [received]
PHST- 2017/04/15 [accepted]
AID - 3870664 [pii]
AID - 10.1093/infdis/jix193 [doi]
PST - ppublish
SO  - J Infect Dis. 2017 Jun 15;215(12):1908-1917. doi: 10.1093/infdis/jix193.