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Bergey's

Microbiology

Fluorescence microscopy

Bacti pathogenesis

Clinical Microbiology
gnr GPR GNC
Clinical bacteria GPC microscope

The genus Enterococcus.

Enterococcus faecalis
Enterococcus faecalis in blood culture.

Enlargement, 1400x730

Enterococcus faecium

Enterococcus faecium
- Gram-positive, VRE, Vancomycin Resistant Entercoccus. SEM x33,370

More Enterococcus EM images from Dennis Kunkel:

96453b / 96539e / 96540e

"The enterococci have become the second most common bacterium isolated from nosocomial urinary and wound infections, and the third most common cause of nosocomial bacteremia. Each year in the U.S., in fact, enterococci account for approximately 110,000 urinary tract infections, 40,000 wound infections, 25,000 cases of nosocomial bacteremia, and 1100 cases of endocarditis. Furthermore, the enterococci are among the most antibiotic resistant of all bacteria, with some isolates resistant to all known antibiotics." Dr Gary Kaiser
cat.cc.md.us/courses/bio141/labmanua/lab14/l14index.html


Dear Enterococcus research site;

Two questions: 1) Is Enterococcus a genus completely separate from Streptococcus? In the past it was called S. faecalis or Group D Streptococcus.

2) Bergey's Manual of Determinative Bacteriology has stated that the some enterococci posses polar flagella. Is this correct?

1) Yes, Enterococcus became a separate genus in 1984. See: Chapter 18 in Manual of Clinical Microbiology, ASM Press, 7th Ed. 1999; Int J Syst Bacteriol, 1984, 34:31-34

2) Motility has been reported for two species (see: Manual of Clinical Microbiology). E. casseliflavus and E. gallinarum can show motility in some cases. All other enterococci are not motile, especially not the most common species faecalis and faecium.

Were these two species ever considered as taxonomically or phylogenetically related to the Streptococci?

Yes, they belonged to the genus streptococcus before 1984.The problem is as follows: much of the work has been done at a time when Enterococcus was still part of the Streptococcus genus, and when the two species mentioned were still considered variants of other species of Enterococcus / Streptococcus. However, there are several papers that talk about flagella in streptococcus (enterococcus ?). Work in more recent times has been published in Russian or the exact species has not been identified. Considering that Bergey states that they may have flagella, and since this is the usual form of bacterial motility, it is safe to say that some isolates of E. gallinarum or E. casseliflavus can have flagella.

Were these two species ever found in human clinical specimens? If so what was the nature of their pathogenicity or lack thereof?

Yes, but not very often. (e.g. 8 of 632 enterococcal isolates were E. gallinarum or E. casseliflavus in one study done in the US) There is not much known about it (pathogenicity). Most studies look only at antibiotic resistance. There are only very few virulence factors known for the major players, E. faecalis and E. faecium. In general, the bacteria are very resistant to harsh environments and they inhabit many different ecological niches, including humans.

If you don't have access to the journals, you can do searches and view abstracts on MedLine http://www.ncbi.nlm.nih.gov/PubMedOld/medline.html

Information courtesy of the Enterococcus research website.

http://w3.ouhsc.edu/enterococcus/

Enterococcus images

http://w3.ouhsc.edu/enterococcus/images.asp


Endocarditis is a significant consideration for Enterococcus sp. and Streptococcus sp. and other species of clinical bacteria as well.
Endocarditis, endo- inside. -card- heart. -itis, inflammation. Bacterial infective endocarditis is the inflammation of the lining of the interior of the heart, particularly the aortic and mitral valves, caused by bacteria.. Chronically over time localized inflammatory reaction causes the heart valves to become hardened or stenotic and they may not be able to function effectively. Due to the fluid dynamics involved in blood flow through the heart, white blood cells cannot adhere to the heart valve surfaces because of their large size. Fluid turbulence has much less of an effect on bacteria which are much smaller in physical size. The bacteria are able to adhere to the valve surfaces which in effect are a safe haven from white blood cells which would phagocytize the bacteria in slower moving, less turbulent areas of the blood circulatory system. As bacteria multiply they are sloughed off from foci within the heart causing a constant or recurring low level bacteremia. Bacteria which fail to maintain adherence are returned to the slower moving areas where they are eaten by white blood cells, particularly neutrophils and to some extent monocytes.
Paradoxically, when bacteria cause endocarditis, it is a general indication of a lack of virulence factors for the type of organism involved. This is because the more virulent bacteria have antigenic determinant sites which induce a strong production of antibodies from lymphocytes. Antibodies are much smaller than bacteria in physical size. The antibodies can attach to the bacterial antigenic sites in even the most turbulent areas of the heart and by any of several different methods of action, cause their destruction. Less virulent bacteria do not elicit strong production of antibodies and are able to live in relative safety on heart valve surfaces.
When bacteria are detected in a sample of blood, physicians have the responsibility of deciding whether those bacteria may represent an acute threat, as for example a Salmonella bacteremia, a chronic threat, as for example a bacterial infective endocarditis caused by a less virulent Streptococcus sp., or merely a contaminant such as Propionibacterium acnes. This is one reason why a sequence of several samples has to be taken and examined. If enterococci are found in several serial samples, the finding is significant and there may be a high level of resistance to antimicrobial therapy.

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