Gardnerella vaginalis bacteria

Gardnerella vaginalis bacteria

Running Head: Gardnerella vaginalis bacteria 1


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GardnerellaVaginalisis a facultative anaerobic bacterium which belongs to the genusGardnerellaand G. vaginalisisthe only species in this genus. This organism is microscopic in sizemeasuring about 1-1.5µm in diameter, it is non-motile and non-sporeforming Coccobacilli. G.Vaginalisduring the process of its growth grows as circular, small, gray andconvex colonies when cultured on chocolate and HBT agar (1). Thisbacterium was originally discovered and named by Dukes and Garner in1955 however it was once referred to as HaemophilusVaginalisand later classified as Corynebacteriumvaginalis(1) .

Itcauses an infection that affects the genital tract of females usuallybecoming more virulent in association with several other anaerobicbacteria. This disease is called Gardnerella vaginalis and alsoreferred to as the bacterial vaginosis (13). It is the most commoncausative agent of abnormal vaginal discharge and odor which arise asa result of change in the types of bacteria located in the vagina.The infection is mainly transmitted sexually with the most essentialrisk factors facilitating its spread, for example having a sexualrelationship with a new partner, multiple sex partners, use of theintrauterine contraceptive device (IUD) and vaginal douching.


Theclinical significance of bacterial vaginosis isbroughtabout by the disruption of the normal vaginal microflora by G.vaginalis bacteria. Acidic environment in the vagina is caused byresident facultative anaerobic lactobacillus population, but it isdisrupted usually by the G.vaginalis(16).Upon the invasion of these anaerobic bacteria in the vaginal tract,antibiotics prescription helps to re-establish the equilibrium of thenormal vaginal bacteria thus restoring the balance (1). G.Vaginalisisis usually not considered as the leading cause of bacterial vaginosisbut it brings about the change of microbial ecology linked with theovergrowth of several bacterial species.

Sourceorganism and details of the original description and taxonomy

Thebacteria classification has been controversial from the time it wasdiscovered by two leading scientists Gardner and Dukes. Gram stainidentification and affiliation of its genus has yielded unsuccessfulleads to the understanding of G. Vaginalis. Dukes and Gardner firstdescribed the organism to be the main causative agent of nonspecificvaginitis, a disease which affects the majority of women (2). Thisbacterium was first identified as G.Vaginalisafter a series of taxonomic studies was done, which established thatit was unrelated to bacteria belonging to other genera such as thosebelonging to Corynebacterium and Haemophilus.

Theorganism gram-variable reaction has been elucidated through chemicaland electron microscopy analyses. There existed controversy for along time concerning the etiology of bacterial Vaginosis (14).However, this controversy was resolved by studies usingstandardization of criteria for clinical and laboratory diagnosis andalso by use of highly improved media and methods for the isolationand identification of bacteria in vaginal fluids (15).

Thescientist who made the discovery in 1955, Gardner and Dukes, firstnamed the organism Haemophilus Vaginalis because it possessedgram-negative features and it was isolated with much success on bloodagar and would not be isolated from any other media. The bacteriawere considered the leading cause of the vaginal discharge. After awhile the genus Haemophilus was believed to be inappropriate for theclassification of the organism (3). Because the bacteria lacked therequirements for X and V factors which are essential for theacceptable growth of Heamophilus species and also the absence of theability to retain the crystal violet dye in the gram reaction coupledwith the presence of some Corynebacterium-like features indicatedthat the bacteria should be placed in the genus Corynebacterium, thisprompted the scientist Zinnemann and Turner to name itCorynebacterium Vaginale.

In1980 there were two major taxonomic studies conducted and publishedexamining the data derived from several biochemical methods, electronmicroscopy and DNA-DNA hybridization. The result of this studiesindicated that the ‘Haemophilus Vaginalis’ develops a goodtaxospecies which revealed little or no similarities to eithergram-negative or gram-positive genera. This therefore, led to theclassification of this organism to the genus Gardnerella by Greenwoodand Picket which received an extensive supports (20).

Thisbacteria is linked to vaginal syndrome, initially it was referred toas non-specific vaginitis due to its characteristic absence ofrecognized agents of vaginitis like the Candidaspeciesand Trichomonasvaginalis(3). Gardner maintained that the term nonspecific should cover onlythe conditions without assignable etiology and that G. Vaginalisvaginitis is appropriately define he supportedthis claim untilhis death in 1982 (3). The change of the name bacterial vaginosis wasaccepted because the vaginitis conditions indicated there is aninflammatory reaction of the vaginal epithelium, normally absent (3).This same condition has been given several names, more than 15different names.

Taxonomyand cellular morphology of this bacteria

G.vaginalis is classified under the seven taxa it belongs to thekingdom bacteria, categorized into the phylum actinobacteria andplaced under the class actinobacteria in the order Bifidobacterialeswithin the family of Bifidobacteriaceae (4). Its generic and specificepithet is Gardnerella and Vaginalis, therefore its binomial name isGardnerellaVaginalis.

Thisbacterium has cells with the shape resembling pleomorphic rods, whichare gram negative to gram-variable, small in size and are not motile.They do not possess an endospore, typical capsule or flagella. Thevaginal fluid smears during gram reaction of G. Vaginalis showsvariation from negative to positive (17). Its cellular morphologywhen it is being prepared in papanicolaou may be seen in areas notcrowded located in the peripheral regions of the epithelial cells.Their staining reactions and morphology is significantly affected byphysiological state of the bacteria (4). The coccobacilli of G.vaginalis both small and longer forms normally are found occurring ina 24 hour cultures on blood agar.

Theymeasure about 0.4 by 1.0 to 1.5µm on average dimensions. Usuallythey are not elongated to form filaments but the cells can grow up to2 to 3 in length. When cultured on vaginalis agar, several short rodsare observed with gram negative state and its cells were moreclumped, pleomorphic and beaded on medium inoculated with starch, orany other fermentable compound (4). On the other hand, these cellsare predominantly gram positive when cultured on patient’s bloodspecimen in 48 hours (4) this is the case during its earlyexponential growth phase where the organism is partially orcompletely gram positive.

Majorityof the investigators described that G. Vaginalis resembled coryneformbacteria (18). The cells exhibit palisade and angular arrangements asa result of snapping when the cells are undergoing division (4). Whencultured on sodium phosphate or fermentable compound, metaphosphategranules form. The resulting granules turn reddish purple whenstained with alkaline methylene blue or stain gram positive. Itbecomes beta-hemolytic when grown in cultures containing rabbit orhuman blood and not on agar inoculated with sheep blood (4).Hemolysis of G. vaginalis is significantly improved by anaerobicincubation.

Clinicalsignificance of this bacteria and parthenogenesis

G.vaginalis bacteria exhibit clinical significance indirectly in theprocess of colonizing the vaginal tract. It causes an infection invaginal regions of female victims causing a disease called bacterialvaginosis (5). This disease is brought about by the change of type ofnormal vaginal bacteria located in the vagina region which causes noinfection. Bacteria that are in the family Lactobacillus are themajority of harmless bacteria in the vagina and are responsible forthe production of chemicals that keeps the vaginal tract partiallyacidic (19). Upon the invasion of vagina by the G. vaginalis, theLactobacillus bacteria are then replaced by other strains of bacteriausually occurring at lower concentrations in the vagina. Thosestrains of bacteria occur at low concentration that cannot illicitany harm in the vaginal tract, but upon the colonization by G.vaginalis these harmful strains of bacteria multiply rapidly to reachunprecedented level where it causes bacterial vaginosis.

Mostscientists have yet to establish the reason facilitating this suddenchange of vaginal microbial population. The overgrowth of thesuppressed bacterial population causes infection which gives rise tobacterial vaginosis disease (25). According to many studiesconducted, it is found out that G.vaginalisand other facultative anaerobic gram-variable strain of bacteriatogether disrupts the vaginal microflora. Therefore, G. vaginalis isnot considered the direct cause of bacterial vaginosis but instead itinterferes with the balance of microbial ecology leading to theovergrowth of harmful bacteria which causes the infection (23).

Theentry of these bacteria to the vagina is associated with factors suchas having multiple sex partners, vaginal douching, having sexualrelations with new partner among others. However, under some rarecases, bacterial vaginosis can develop in women who have never hadvaginal intercourse. Also this disease normally occurs in pregnantwomen who may lead to postpartum uterine infections premature labourand delivery (5).

Majorityof women infected do not exhibit any symptoms. But others experiencerare vaginal discharge usually white or yellow in color and fishy’odor (5). These symptoms can be bothersome during and afterintercourse. The discharge seen in bacterial vaginosis is differentthan the discharge seen in the vaginal yeast infections, which isthicker and cheesy. Bacterial vaginosis normally does not causeconsiderable irritation of the vulva or pain during sexual activity(21).

Virulencefactor of the bacteria

Bacterialvaginosis is considered one of the unique diseases and occurs due tovariation in the composition of vaginal microflora. This is oftenindicated by the significant decrease in the number and prevalence ofhydrogen peroxide- producing lactobacilli and consequent rise in theconcentration of G. Vaginalis and other resident anaerobic bacteria(30). Despite the disease being widely prevalent, little progress hasbeen made to understand the factors that predispose the bacterialvaginosis and pathophysiology (6). G. vaginalis is categorized intoeight unique biotypes based on the activity of β-galactosidase andlipase and hydrolysis of hippurate (6).

Severalstudies have been carried out to correlate these biotypes with thepathogenicity of G. vaginalis (7). It is established that thepresence of clue cells in the vaginal discharge of infected women,shows that the adherence mechanism of the bacteria play an importantrole in its pathogenesis (27). This provides the basis forcolonization and initiates the process of pathogenesis. In addition,the development of biofilm in the vagina often has been found toboost the ability of bacteria to resist lactic acid and hydrogenperoxide consequently facilitating colonization despite the presenceof lactobacilli. This makes up predisposing factors causing thevirulence of G. vaginalis (7). The reproductive tract tissue can bedamaged by the bacterial phospholipase C through both indirect anddirect mechanisms. When the placental tissues are destroyed by thebacterial phospholipase C, premature labor is stimulated which resultto complications such as low-birth weight of the infants, pre-termbirth, and post-operative cellulites in women with bacterialvaginosis and post-partum endometritis (28).

Ithas not been established yet whether G. vaginalis produce protease.Protease are associated to enzymatically degrade the tissue proteinswhich leads to the release of amino acids that may facilitate thegrowth of G. vaginalis and the other types of bacterial strains inthe vagina (7). There are several biotypes that have been isolatedfrom both the women infected with bacterial vaginosis and normalwomen, in all these cases there is a significant variation offrequency of results (29). According to one study, G. vaginalisisolates from the infected victims showed that it has better biofilmformation and adherence when compared with the isolates derived fromthe healthy women. As researchers have found out that the sialidaseactivity positively correlates to the biotypes 5 and 8 (7).

Theprocess of biotyping acts as an effective marker system which isimportant for the epidemiological studies of bacterial vaginosis. Inessence these studies on the frequency of isolation of differentbiotypes of G. vaginalis from cases of both the symptomatic and womeninfected with bacterial vaginosis, go along to help the best treatingoptions for the disease. It helps in the development of probioticsthat are used in the treatment of the different biotypes usuallyisolated from infected and symptomatic women (26). The recent studies carried out in this this area shows that the virulence factorsexpressed by the G. vaginalis are not whatsoever related to all typesof biotypes but it only applies to the few biotypes (7). To ascertainproper relationships between biotypes and virulence factors of the G.vaginalis requires studies with a bigger sample size (7).

Isolationand identification

Thevaginal smears are collected from the infected patients it is takento the laboratory for identification (8). To avoid the disruption ofthe bacterial cells, the vaginal smears are carried to the laboratoryusing Stuart’s transport medium and grown on schaedler andchocolate agar (35). The agar containing chocolate is incubated in 7%Carbon (IV) oxide for about 48 hours and schaedler plates are kept inan anaerobic environment for close to 48 hours. After culturing thevaginal smears, different tests for identification is done usingclear beta-hemolysis and colonial morphology (37). Theseidentification tests is carried out with a negative catalase test,typical cell morphology and diffuse edges on human bloodbilayer-Tween agar in the Gram stain. Through this procedure it isfound out that the suspected colonies of G. vaginalis is identifiedwith an accuracy of 90% to 98% (39).

Treatmentand antibiotic resistant

Womeninfected by bacterial vaginosis can be treated though it is notguarantee that the disease is completely suppressed. The disease istreated using antibiotics such as metronidazole or clindamycin (9).It can be applied as vaginal gel or cream and may also be taken bymouth. The Center for Disease Control and Prevention (CDC) advocatesoral medication for the infected pregnant women because oral intakeis safer and effective compared to vaginal creams or gels (9).Metronidazole which is taken 500 mg twice daily for a week is bestchoice of treatment.

Despitethe drugs being effective in most cases, certain strains of G.vaginalis has been found to resist antibiotics (32). On the otherhand, avoiding the factors that can predispose one to an infection isappropriate way to prevent the disease. The best manner to preventthis bacterial vaginosis disease is by avoiding sexual relation withmultiple partners in addition one should avoid sexual relation withnew partners

Thehabitat, niche, physiology of the organism

G.Vaginal natural habitat is the vagina in majority of women having nosigns of bacterial vaginosis infection. For the infected women, it is100% possibility to find the bacteria in the vaginal tract (10). Thebacteria are found attached to the vaginal epithelium where it issuspended in the vaginal fluids referred to as biofilm. Biofilmoffers a favorable environment for the G. vaginalis growth andsurvival (39).

Beingfacultative anaerobic bacteria, G. Vaginalis bacteria is highlyadapted to survive in this vaginal region lacking oxygen. Vaginaltract at most times experience low amount of oxygen, it is onlyduring urination and sexual activity when it is fully aerated andthus the vaginal tract enjoys plenty amount of oxygen count (40).When oxygen is available, G. vaginalis can also survive, because thebacteria utilize aerobic means of respiration. But when the oxygencount drops below the recommended concentration, the bacteria usesanaerobic mode of respiration and thus G. vaginalis bacteria is ableto produce the required energy to sustain its metabolic needs.Therefore, it has appropriate physiological adaptation to survive inthis habitat (10).


Dueto the inefficacy of treatment reported in the treatment of bacterialvaginosis infections using antibiotics, new exploration are underwayto improve the success of antibiotic treatment. In the recentexperimental therapies, researchers aim to understand the complexityof the disease and the best way to eliminate the collection ofopportunistic bacterial strains causing the disease (11). New studiesare targeting to understand biofilms that is resident habitat for G.vaginalis. It has been found that extracellular DNA in the biofilm isan integral part for its function. In the event this DNA isenzymatically disrupted, the function of biofilm is inhibited.Consequently, the residing G. vaginalis in the Biofilm is liberatedand can be easily targeted (12). Once it is liberated the bacteria isseparated into supernatant fractions and in effect increase exposureto antibiotics such as metronidazole.

Toundertake the disruption of the extracellular DNA, the researchershave found DNase effective to enzymatically digest Extracellular DNA.However, there is a need for further investigation to ascertain thepotential for use of DNase to increase antibiotic efficiency (36).This is because careful research must be undertaken to access thepossibility of side effects when administered with the normaltherapies and in the process lower the chances of recurrence,associated morbidities and chronic infection.


1.Cavera V, Volski A, Chikindas M. 2015. The Natural AntimicrobialSubtilosin A Synergizes with Lauramide Arginine Ethyl Ester (LAE),ε-Poly-l-lysine (Polylysine), Clindamycin Phosphate andMetronidazole, Against the Vaginal Pathogen Gardnerella vaginalis.Probiotics &amp Antimicro. Prot. 7:164-171.

2.Dyas A, Wise R. 1982. Gardnerella vaginalis and non-specificvaginitis. European Journal of Clinical Microbiology 1:201-203.


4.Turovskiy Y, Cheryian T, Algburi A, Wirawan R, Takhistov P, Sinko P,Chikindas M. 2012. Susceptibility of Gardnerella vaginalis Biofilmsto Natural Antimicrobials Subtilosin, ε -Poly-L-Lysine, andLauramide Arginine Ethyl Ester. Infectious Diseases in Obstetrics andGynecology 2012:1-9.

5.Balsdon M. 1982. Gardnerella vaginalis and its clinical syndrome.European Journal of Clinical Microbiology 1:288-293.

6.Gibbs, R. S., M. H. Weiner, K. Walmer, and P. J. St. Clair. 1987.Microbiologic and serologic studies of Gardnerella vaginalis inintra-amniotic infection. Obstet. Gynecol. 70:187-190.

7.Villegas H, Arias F, Flores E, Casanova G, Karchmer S. 1997.Ultrastructural Characteristics of Gardnerella vaginalis Infection inthe Heterosexual Couple. Syst Biol Reprod Med 39:147-153.

8.Boustouller, Y. L., A. P. Johnson, and D. Taylor-Robinson. 1987. Pilion Gardnerella vaginalis studied by electronmicros- copy. J. Med.Microbiol. 23:327-329.

9.Boustouller, Y. L., and A. P. Johnson. 1986. Resistance ofGardnerella vaginalis to bactericidal activity of human serum.Genitourin. Med. 62:380-383.

10.Bannatyne, R.M., J.Jackowski, R.Cheung,andK. Biers. 1987.Susceptibility of Gardnerella vaginalis to metronidazole, itsbioactive metabolites, and tinidazole. Am. J. Clin. Pathol.87:640-641.


13.Yamamoto, T., X. Zhou, C. J. Williams, A. Hochwalt, and L. J. Forney.2009. Bacterial populations in the vaginas of healthy adolescentwomen. J. Pediatr. Adolesc. Gynecol. 22:11-18.

14.Thorsen, P., I. P. Jensen, B. Jeune, N. Ebbesen, M. Arpi, A.Bremmelgaard, and B. R. Moller. 1998. Few microorganisms associatedwith bacterial vaginosis may constitute the pathologic core: apopulation-based microbiologic study among 3596 pregnant women. Am.J. Obstet. Gynecol. 178:580-587.

15.Sobel, J. D. 2000. Bacterial vaginosis. Annu. Rev. Med. 51:349-356.

16.O`Brien, R. F. 2005. Bacterial vaginosis: many questions—anyanswers? Curr. Opin. Pediatr. 17:473-479.

17.Hill, G. B. 1993. The microbiology of bacterial vaginosis. Am. J.Obstet. Gynecol. 169:450-454.

18.Hawes, S. E., S. L. Hillier, J. Benedetti, C. E. Stevens, L. A.Koutsky, P. Wolner-Hanssen, and K. K. Holmes. 1996. Hydrogenperoxide-producing lactobacilli and acquisition of vaginalinfections. J. Infect. Dis. 174:1058-1063.

19.Agarwal M, Dixon R. 2001. A study to detect Gardnerella vaginalis DNAin interstitial cystitis. BJU International 88:868-870.

20.Gutman, R. E., J. F. Peipert, S. Weitzen, and J. Blume. 2005.Evaluation of clinical methods for diagnosing bacterial vaginosis.Obstet. Gynecol. 105:551-556.

21.Forsum, U., E. Holst, P. G. Larsson, A. Vasquez, T. Jakobsson, and I.Mattsby-Baltzer. 2005. Bacterial vaginosis—a microbiological andimmunological enigma. APMIS 113:81-90.

22.Ferris, D. G., M. S. Litaker, L. Woodward, D. Mathis, and J.Hendrich. 1995. Treatment of bacterial vaginosis: a comparison oforal metronidazole, metronidazole vaginal gel, and clindamycinvaginal cream. J. Fam. Pract. 41:443-449.

23.Eschenbach, D. A., P. R. Davick, B. L. Williams, S. J. Klebanoff, K.Young-Smith, C. M. Critchlow, and K. K. Holmes. 1989. Prevalence ofhydrogen peroxide-producing Lactobacillus species in normal women andwomen with bacterial vaginosis. J. Clin. Microbiol. 27:251-256.

24.Centers for Disease Control and Prevention. 2006. Sexuallytransmitted disease treatment guidelines, 2006. MMWR Recommend. Rep.55(RR11):1-94.

25.Catlin, B. W. 1992. Gardnerella vaginalis: characteristics, clinicalconsiderations, and controversies. Clin. Microbiol. Rev. 5:213-237.

26. Amsel, R., P. A. Totten, C. A. Spiegel, K. C. Chen, D. Eschenbach,and K. K. Holmes. 1983. Nonspecific vaginitis. Diagnostic criteriaand microbial and epidemiologic associations. Am. J. Med. 74:14-22.

27.Alvarez-Olmos, M. I., M. M. Barousse, L. Rajan, B. J. Van Der Pol, D.Fortenberry, D. Orr, and P. L. Fidel, Jr. 2004. Vaginal lactobacilliin adolescents: presence and relationship to local and systemicimmunity, and to bacterial vaginosis. Sex. Transm. Dis. 31:393-400.

28.Bhat G, Kotigadde S, Udayalaxmi J. 2011. Biotypes and virulencefactors of Gardnerella vaginalis isolated from cases of bacterialvaginosis. Indian Journal of Medical Microbiology 29:165.

29.Alderete J. 1988. Alternating Phenotypic Expression of Two Glasses ofTrichomonas vaginalis Surface Markers. Clinical Infectious Diseases10:S408-S412.

30.Heimler I, Aroutcheva A, Simoes J, Faro S. 2000. Characteristics ofgardnerella vaginalis strains isolated from patients with bacterialvaginosis. International Journal of Gynecology &amp Obstetrics70:A109.

31.Jolly J. 1983. Minimal criteria for the identification of Gardnerellavaginalis isolated from the vagina. Journal of Clinical Pathology36:476-478.

32.Hodge T, Levy C, Smith M. 1995. Disk Space Infection Due toGardnerella vaginalis. Clinical Infectious Diseases 21:443-445.

33.Chetty R. 1992. Well differentiated (benign) papillary mesotheliomaof the tunica vaginalis. Journal of Clinical Pathology 45:1029-1030.

34. Balsdon M. 1982. Gardnerella vaginalis and its clinical syndrome.European Journal of Clinical Microbiology 1:288-293.

35.Greenwood J. 1981. Gardnerella vaginalis (Haemophilus vaginalis,Corynebacterium vaginale). Clinical Microbiology Newsletter 3:23-25.

36.VAN ESBROECK M, VANDAMME P, FALSEN E, VANCANNEYT M, MOORE E, POT B,GAVINI F, KERSTERS K, GOOSSENS H. 1996. Polyphasic Approach to theClassification and Identification of Gardnerella vaginalis andUnidentified Gardnerella vaginalis-Like Coryneforms Present inBacterial Vaginosis. International Journal of Systematic Bacteriology46:675-682.

37.Catlin B. 1992. Gardnerella vaginalis: characteristics, clinicalconsiderations, and controversies. Clinical Microbiology Reviews5:213.

38.Algburi A, Volski A, Chikindas M. 2015. Natural antimicrobialssubtilosin and lauramide arginine ethyl ester synergize withconventional antibiotics clindamycin and metronidazole againstbiofilms of Gardnerella vaginalis but not against biofilms of healthyvaginal lactobacilli. Pathogens and Disease 73:ftv018-ftv018.

39.Pybus V, Onderdonk A. 1997. Evidence for a Commensal, SymbioticRelationship between Gardnerella vaginalis and Prevotella biviaInvolving Ammonia: Potential Significance for Bacterial Vaginosis.Journal of Infectious Diseases 175:406-413.

40.Noll K. 2010. The safe, natural antimicrobial peptide subtilosin forcontrol of bacterial vaginosis.