Re: are there protozoa in urine?

Greetings,
The following information was taken from an abstract from The American Society 
of Microbiologists.
Copyright © 2001, American Society for Microbiology
Clin Microbiol Rev. 2001 January; 14 (1): 150–164
DOI: 10.1128/CMR.14.1.150-164.2001


Drug Targets and Mechanisms of Resistance in the Anaerobic Protozoa
Peter Upcroft* and Jacqueline A. Upcroft


Queensland Institute of Medical Research and The Tropical Health Program, 
Australian Centre for International and Tropical Health and Nutrition, The 
University of Queensland, The Bancroft Centre, Brisbane, Queensland 4029, 
Australia 


* Corresponding author. Mailing address: Queensland Institute of Medical 
Research and The Tropical Health Program, Australian Centre for International 
and Tropical Health and Nutrition, The University of Queensland, The Bancroft 
Centre, Brisbane, Queensland 4029, Australia. Phone: 61-7-33620377. Fax: 61-7-
33620105. E-mail: peterU@qimr.edu.au.


The anaerobic protozoa Giardia duodenalis, Trichomonas vaginalis, and Entamoeba 
histolytica infect up to a billion people each year. G. duodenalis and E. 
histolytica are primarily pathogens of the intestinal tract, although E. 
histolytica can form abscesses and invade other organs, where it can be fatal 
if left untreated. T. vaginalis infection is a sexually transmitted infection 
causing vaginitis and acute inflammatory disease of the genital mucosa. T. 
vaginalis has also been reported in the urinary tract, fallopian tubes, and 
pelvis and can cause pneumonia, bronchitis, and oral lesions. Respiratory 
infections can be acquired perinatally. T. vaginalis infections have been 
associated with preterm delivery, low birth weight, and increased mortality as 
well as predisposing to human immunodeficiency virus infection, AIDS, and 
cervical cancer. All three organisms lack mitochondria and are susceptible to 
the nitroimidazole metronidazole because of similar low-redox-potential 
anaerobic metabolic pathways. Resistance to metronidazole and other drugs has 
been observed clinically and in the laboratory. Laboratory studies have 
identified the enzyme that activates metronidazole, pyruvate:ferredoxin 
oxidoreductase, to its nitroso form and distinct mechanisms of decreasing drug 
susceptibility that are induced in each organism. Although the nitroimidazoles 
have been the drug family of choice for treating the anaerobic protozoa, G. 
duodenalis is less susceptible to other antiparasitic drugs, such as 
furazolidone, albendazole, and quinacrine. Resistance has been demonstrated for 
each agent, and the mechanism of resistance has been investigated. 
Metronidazole resistance in T. vaginalis is well documented, and the principal 
mechanisms have been defined. Bypass metabolism, such as alternative 
oxidoreductases, have been discovered in both organisms. Aerobic versus 
anaerobic resistance in T. vaginalis is discussed. Mechanisms of metronidazole 
resistance in E. histolytica have recently been investigated using laboratory-
induced resistant isolates. Instead of downregulation of the 
pyruvate:ferredoxin oxidoreductase and ferredoxin pathway as seen in G. 
duodenalis and T. vaginalis, E. histolytica induces oxidative stress 
mechanisms, including superoxide dismutase and peroxiredoxin. The review 
examines the value of investigating both clinical and laboratory-induced 
syngeneic drug-resistant isolates and dissection of the complementary data 
obtained. Comparison of resistance mechanisms in anaerobic bacteria and the 
parasitic protozoa is discussed as well as the value of studies of the 
epidemiology of resistance.

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June Wingert
Associate Scientist