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Management of Abnormal Vaginal Discharge in Pregnancy

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Sanusi Mohammed Ibrahim, Mohammed Bukar and Bala Mohammed Audu

Reviewed: February 19th, 2016 Published: June 29th, 2016

DOI: 10.5772/62599

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Abnormal vaginal discharge in a pregnant woman causes discomfort and increases risk of complications. Management of such patient is difficult as the physician will need to distinguish leucorrhoea of pregnancy from pathological vaginal discharge and also to decide on the drugs to prescribe that are not contraindicated in pregnancy.


  • Vaginal discharge
  • Pregnancy
  • Antibiotic treatment
  • Maiduguri
  • Nigeria

1. Introduction

Most pregnant women have vaginal discharges that are either physiologic or pathologic. The challenge to the clinician is to separate the vaginal infections with potentially serious input for pregnancy from annoying but not serious secretions, irritation and pruritus [1]. Infectious vaginitis is usually caused by yeast, such as Trichomonas vaginalis, bacterial vaginosis, gonorrhoea, Chlamydia trachomatis, Mycoplasma, Group B streptococcus or herpes [1]. Normal vaginal secretions consist of water, electrolytes, epithelial cells, microbial organisms, fatty acid and carbohydrate compounds [1, 2].The concentration of anaerobic bacteria is usually five times than that of aerobic organisms. The most prevalent organisms in the vagina are lactobacilli, Streptococci, Staphylococcus epidermidis, Gadnerella vaginalis and Escherichia coli. Anaerobic species that are frequently isolated include Peptostreptococci, anaerobic lactobacilli and bacteroides [3].

Vaginal pH, glycogen content and amount of secretion influence the quantity and type of organisms present in the vagina. Lactobacilli restrict the growth of other organisms by producing lactic acid, thus maintaining a low pH. These organisms also produce hydrogen peroxide, which is toxic to anaerobes. The normal vaginal bacterial population assists in inhibiting the growth of pathologic vaginal organisms. If the normal vaginal ecosystem is altered, there is a greater chance of proliferation of pathogenic organisms. The challenge of treating vaginitis in pregnancy is the necessity of making accurate diagnosis and treating correctly [2]. True infections (some of which can have dangerous effect on gestation) must be separated and distinguished from the exaggeration of physiologic discharge by pregnancy. Infection with bacterial vaginosis, Chlamydia trichomonas or Group B Streptococcus has been associated with septic abortion, premature rupture of membranes and premature delivery [2, 4].


2. Management of common causes of abnormal vaginal discharge in pregnancy

2.1. Vulvovaginal candidiasis

Vulvovaginal candidiasis (VVC) is a common cause of vaginal discharge worldwide [5, 6]. It is estimated that approximately 75% of women will experience an episode of VVC [7]. Candidiasis is caused by the fungus, Candida species. Candida species include Candida albicans, Candida tropicalis, Candida pseudotropicalis, Candida krusei and Candida stellaloidea. Other strains are torulopsis, glabrata and rhodotromla. C. albicans accounts for 60–80% of vaginal fungal infection [57], Candida glabrata accounts for 20% and C. tropicalis accounts for 6–23% [5]. Predisposing factors to VVC include pregnancy, diabetes mellitus, immunosuppressive therapy (cytotoxic drugs, steroids, etc.), antibiotics, oral contraceptives, immunodeficient conditions (HIV, cancer, chronic illness) and tight fitting and nylon undergarments [5]. Heat and moisture favour the growth of Candida species [8]. VVC can be sexually transmitted, and several studies reported an association between candidiasis and orogenital sex [7, 9].

C. albicans can be identified by culture from the vagina during pregnancy in approximately 25% of women [10]. While the prevalence of VVC in pregnancy in Zabrze of Poland is 42% [11], few studies in Africa reported the prevalence of 65% [12], 42% [13] and 23% [14] in Benin City of Nigeria, Addis Ababa of Ethiopia and Papua of New Guinea, respectively. Similarly, studies in India reported incidences ranging from 45% to 61% [15, 16].

Most patients with VVC will complain of vaginal discharge [5]. Dyspareunia, vulval pruritus and burning are the main symptoms [17]. Patients commonly complain of pruritus and burning after intercourse or upon urination. Erythema and oedema of the labia majora and minora and rashes on the perineum and thighs may be seen on physical examination, and a whitish, thick and curd-like vaginal discharge is usually present [17]. Recurrence requiring repeated treatment during pregnancy is likely [18].

The diagnosis is made on both clinical examination and laboratory identification of Candida by positive wet-mount test or potassium hydroxide (KOH) preparation [17]. In the wet-mount test, the spores and Candida are seen when vaginal discharge or scrapings from vulval lesions are mixed with normal saline and viewed under high-power magnifications. The presence of yeast blastospores or pseudohyphae can be detected in approximately 30–50% of patients with symptomatic VVC [17]. The addition of 10% KOH to the solution lyses white blood cells, red blood cells and vaginal epithelial cells, making the alkali-resistant branching budding hyphae of Candida easier to see[17]. Because vaginal pH usually remains normal in VVC, positive results from these two tests in combination with a normal vaginal pH are helpful in confirming the diagnosis. Most studies demonstrate that most of vaginal isolates are C. albicans [17]. Therefore, fungal cultures have not been used by most clinicians as part of the initial evaluation [17].

Various drug formulations are effective in treating both uncomplicated and complicated infections [10]. Both intravaginal and oral agents are available [10, 19]. Uncomplicated VVC includes sporadic or infrequent VVC, mild-to-moderate VVC, VVC with likely infecting agent being C. albicans, and non-immunocompromised patient. Complicated VVC is recurrent candidal infection or severe infection or non-albicans candidiasis (C. tropicalis, C. glabrata, etc.), VVC in uncontrolled diabetes mellitus, VVC with associated immunosuppression, VVC with debilitation or VVC in pregnancy [10]. Women who have four or more candidal infections during a year are classified as having complicated disease [9]. Intravaginal agents used in the treatment of VVC are 5 g of 2% butoconazole cream intravaginally for 3 days or 5 g (sustained-release) once; 5 g of 1% clotrimazole cream for 7–14 days or 100 mg tablet intravaginally for 7 days; 5 g of 2% miconazole cream intravaginally for 7 days or 100 mg suppository intravaginally for 7 days or 200 mg suppository for 3 days or 1200 mg suppository once; Nystatin 100,000 U tablet intravaginally for 14 days; 5 g of 6.5% tioconazole ointment intravaginally once; 5 g of 0.4% terconazole cream intravaginally for 7 days or 0.8% cream 5 g intravaginally for 3 days or 80 mg suppository intravaginally for 3 days. Oral agent is fluconazole 150 mg oral tablet once.

Prolonged local intravaginal therapy regimens and addition of oral fluconazole may be required to treat non-albicans VVC [7]. Fluconazole, 100–200 mg weekly for 6 months, is also the drug for prevention of recurrent VVC, whereas 600 mg boric acid gelatine capsule intravaginally daily for 2 weeks is useful in the management of non-albicans recurrent VVC [7].

2.2. Anaerobic bacterial infection and bacterial vaginosis

Vaginal flora of a normal asymptomatic reproductive-aged woman includes multiple aerobic or facultative species as well as obligate anaerobic species [9]. Of these, anaerobes are predominant and outnumber aerobic species approximately 10–1 [20]. These anaerobes include gram-negative organisms such as Prevotella, Bacteroides, Fusobacterium species, and Veillonella species and gram-positive bacilli such as Propionibacterium species, Eubacterium species and Bifidobacterium species [9, 20]. These anaerobic bacteria cause non-specific vaginitis [5].

Bacterial vaginosis is characterised by a shift from normal vaginal population of lactobacilli to anaerobes such as G. vaginalis, Prevotella, Bacteroides and Mobiluncus species and other bacteria such as Mycoplasma and Ureaplasma species [20]. It is one of the most frequent conditions encountered in reproductive health clinics throughout the world [20]. The condition had been previously called Haemophilus vaginalis vaginitis, non-specific vaginitis and G. vaginalis vaginitis [5, 21].

Bacterial vaginosis has been strongly associated with poor pregnancy outcomes such as preterm delivery and low birth weight infants, and several studies have now established the associations between bacterial vaginosis, human immunodeficiency virus and puerperal sepsis [20, 22].

Bacterial vaginosis appears to be particularly common in Sub-Saharan Africa where several studies have reported high prevalence rates, ranging from 20–49% among women presenting to STD clinics with vaginal discharge to 21–52% among pregnant women attending antenatal clinic [20]. These are very much higher than the rates reported from industrialised countries with 13% in the United Kingdom [23], 11% in London [20] and 15–30% in the United States [24].

Bacterial vaginosis usually occurs in sexually active patients. Some of the other risk factors include multiple sexual partners, low socioeconomic status, lesbians, presence of intrauterine device and prior STD [5]. It is still debatable whether it is sexually transmitted; however, supporting this is the recovery of G. vaginalis in the urethral of male partners [5].

Bacterial vaginosis is characterised by a malodorous, profuse, thin, homogenous yellow, white or grey discharge that is adherent to the anterior and lateral vaginal walls. Typically, the patient may complain of a fishy odour during or shortly after coitus and also during menses. The alkaline nature of blood or semen (pH > 7) brings about a transient increase in the vaginal pH, and this causes the release of amines, which the patient perceives as fishy odour. This typical discharge may be found on examination in some patients who in fact have not complained of a vaginal discharge [25]. The fishy smell of the discharge is the main problem and is often responsible for sexual disharmony between partners. Vulvitis and pruritus are very minimal or totally absent. Nearly half of patients with BV have no symptoms. Obstetric complications include premature rupture of foetal membranes, late miscarriage and postpartum endometritis, whereas pelvic inflammatory disease, post-hysterectomy cuff infection and postabortal sepsis are some of the gynaecological complications [25].

Diagnosis of BV can be based on the Amsel’s clinical criteria or the microbiological Nugent’s scoring technique [26, 27]. In Amsel’s criteria, three of the following are required to diagnose BV: (1) homogenous vaginal discharge; (2) vaginal pH greater than 4.5; (3) positive Whiff test and (4) presence of clue cells on microscopy. The Nugent’s method relies on the identification of categories of vaginal microflora based on quantitative assessment of a vaginal gram-stained smear. The Nugent’s method has been extensively validated in industrialised countries where assessment of vaginal microflora is an important step in understanding the pattern of flora association with BV. Culture is the least accurate in making a diagnosis of BV as there is overgrowth of many vaginal organisms in this condition [5]. Though virtually, all patients with BV have G. vaginalis isolated on culture, it must also be noted that the organism can also be cultured in 40–50% of women with normal flora [5].

In pregnancy, BV should be treated with metronidazole 250 mg three times a day (alternatives; metronidazole 2 g single dose, clindamycin 300 mg twice a day; or metronidazole gel) [5]. The standard treatment of BV in non-pregnant women is oral metronidazole 500 mg twice daily for 7 days; clindamycin cream 2% on applicator ful (5 g) intravaginally at bedtime for 7 days or metronidazole gel one applicator ful (5 g) intravaginally once or twice a day for 5 days [5, 10, 28].

2.3. Trichomoniasis

Trichomoniasis is the commonest sexually transmitted disease worldwide [5]. It was originally thought to be innocuous but has now been found to be associated with preterm labour, premature rupture of membranes, increased perinatal loss and pelvic inflammatory disease (PID) [5, 29]. T. vaginalis can be identified during perinatal examination in as many as 20% of women [29].

T. vaginitis is caused by the trichomonas organism, which is a small, flagellated, motile and anaerobic protozoan. The particular trichomonad responsible for vaginitis is T. vaginalis, which is the type found in the vagina. Other trichomonads, which include Trichomonas buccalis found in the mouth and Trichomonas hominis found in the anal canal and rectum, are known but do not cause vaginal discharge because they cannot survive in the vagina. T. vaginalis has been demonstrated in the male urethra and prostate gland.

T. vaginalis is usually transmitted sexually. The organism may survive for several hours in urine, wet towels and even on toilet seats. The possibility of transmission by these routes had been suggested but not completely proven [5]. Incubation period is 4–20 days with an average of 7 days. Males are usually asymptomatic, but they can easily infect treated female.

The prevalence of trichomoniasis in pregnancy has been found to be 7.5–19% [14, 30]. A prevalence of 10.1% has been reported from the Gambia, West Africa [20].

The vaginal discharge of trichomoniasis is malodorous, frothy and profuse, thin creamy or slightly greenish and may cause itching. The classic yellow–green discharge is found in 20–50% of patients [5]; more often, the discharge is grey or white. The patient may also complain of dyspareunia, postcoital bleeding, pruritus vulvae, frequency of micturition and dysuria. Characteristically, vulvitis is minimal or absent compared with candidiasis. On speculum exam, apart from the discharge, a cervical erosion may be seen, and in severe cases, multiple, small punctuate haemorrhages and swollen papillae may be found on the cervix (“straw berry” cervix) and vagina [17].

The vaginal pH is usually 5–5.5 in trichomonas infection [17]. Applying litmus to the unlubricated speculum after it has been withdrawn from the vagina easily tests the pH. A saline wet mount of the swab taken from the vagina or cervix will show motile flagellated protozoa and leucocytes. Wet mount alone detects 64% infection in asymptomatic women, 75% of those with clinical vaginitis and 80% of those with characteristic symptoms [5]. The use of culture (Feinberg-Whittington or Diamond culture) gives a sensitivity of 86–97% [5]. Pap smear has a detection rate of about 50–86% [5]. Monoclonal antibody staining is also used. It is sensitive and is reported to detect 77% of those missed on wet mount [5].

Metronidazole is effective in eradicating T. vaginalis administered orally in a single 2 g dose [5, 10]. Ootrimazole, which is both a fungicide and trichomonacide, can be used intravaginally usually in pregnancy in the same dosage regime as in candidiasis [5]. In persistent infection, it is best to treat the patient and her male sexual partner simultaneously.

2.4. Gonorrhoea and chlamydial infection

Chlamydia and gonorrhoea can both cause vaginal discharge in pregnancy and a major cause of morbidity among women in developing countries [31]. Both infections have been associated with pregnancy-related complications [32]. These two conditions are prevalent worldwide particularly in Africa [20]. They are a major cause of acute pelvic inflammatory disease, infertility and adverse pregnancy outcomes [20].

The prevalence of Chlamydia and gonorrhoea among pregnant women in Africa, in several studies, is between 6–13% [4, 33] and 2–8% [4, 34], respectively. According to the WHO, globally new cases of C. trachomatis infection have been estimated as 92 million, including 19 million in Sub-Saharan Africa [3537]. In Maiduguri, North-eastern Nigeria, Amin et al. reported a prevalence of 9% [38].

Chlamydia is characteristically asymptomatic [39, 40]. About one-third of patients may have symptoms including mucopurulent vaginal discharge [5]. The role of Chlamydia in infertility is well documented [3942]. Tubal pathology in Chlamydia infection is the cause of infertility in 10–30% of couples in developed countries and in up to 85% in developing countries [36, 37, 43, 44]. The main cause of tubal pathology is PID. Several different methods to diagnose chlamydial infection are available. Great studies have been performed in the areas of reliable methods of diagnosis [40, 45]. Chlamydia culture is considered as the gold standard because it has near 100% specificity [40, 45]. Because only viable infectious chlamydial elementary bodies are detected by culture, this is the method of choice for medico-legal issues. The disadvantages of culture include its low sensitivity and is that it depends on the laboratory inter-personal experience [46]. Non-culture methods include enzyme immunoassay (EIA), direct fluorescent staining with monoclonal antibodies (DFA), nucleic acid amplification tests (NAATs) and nucleic acid hybridisation techniques. In the management of chlamydial infection, both the patient and her infected sexual partner must be treated. It is, therefore, important to screen the sexual partners and treat those who are infected. With the advent of single-dose therapy, patients are now diagnosed and treated with the highest convenience and reliability [47]. Antimicrobial groups effective against C. trachomatis include the tetracyclines, macrolides, quinolones and penicillins [47].

Most women with gonorrhoea are asymptomatic [48]. When symptoms occur, they are localised to the lower genitourinary tract and include vaginal discharge, urinary frequency or dysuria and rectal discomfort. The incubation period is only 3–5 days [48]. The vulva, vagina, cervix and urethra may be inflamed and may itch or burn. Specimens of discharge from the cervix, urethra and anus should be taken for culture from the symptomatic patients. A stain of purulent urethra exudates may demonstrate gram-negative diplococci in leucocytes. Similar findings in a purulent cervical discharge are less conclusively diagnostic of Neisseria gonorrhoea. Gram-negative diplococci that are oxidase positive and obtained from selective media (Thayer-Martin or Transgrow) usually signify N. gonorrhoea. Carbohydrate fermentation tests may be performed, but in addition to being time consuming and expensive, they occasionally yield other species of Neisseria. Therefore, cultures are reported as presumptive for N. gonorrhoea. In addition, other techniques for detecting gonorrhoea include EIA for cervical swab or urine specimens, DNA probes for endocervical swabs and NAATs for endocervical swabs, liquid Papanicolaou specimens, vaginal swabs and urine specimens. Any patient with gonorrhoea must be suspected of having other STDs and managed accordingly. Treatment should cover N. gonorrhoea, C. trachomatis and incubating syphilis. Dual therapy has contributed greatly to the declining prevalence of Chlamydia infection. Therefore, if chlamydial infection is not ruled out, doxycycline (for non-pregnant women) should be added to ceftriaxone or azithromycin.


3. Outcome of study on abnormal vaginal discharge among pregnant women conducted in Maiduguri, Borno State in North-eastern Nigeria

3.1. Goal and objectives

The general objective of the study is to detect the clinical features associated with abnormal vaginal discharge and antibiotic sensitivity pattern of the causative microorganisms in pregnant women to improve the early diagnosis and prompt treatment. The specific objectives were as follows:

  1. To determine the prevalence of abnormal vaginal discharge as a presenting complaint in pregnancy

  2. To determine the frequency of bacterial causes of abnormal vaginal discharge in pregnancy and symptoms associated with it

  3. To evaluate the sensitivity of microbial isolates from the vaginal discharge to antibiotics

3.2. Methodology

Borno State lies between latitude 10° and 14° north and longitude 14° and 45° east. It is located in the north-eastern part of Nigeria. Maiduguri is the capital city. The University of Maiduguri Teaching Hospital (UMTH) is a tertiary health institution and is the only functional teaching hospital in the north-eastern zone of Nigeria. The 2006 Nigerian provisional census puts the population of Borno State at 4,151,193 with 1,990,036 females [49].

It was a cross-sectional analytical study. The study population consisted of pregnant women presenting to the antenatal clinic with complaint of abnormal vaginal discharge while pregnant women without complaints of abnormal vaginal discharge attending the antenatal clinic of the hospital served as controls. A sample size of 800, consisting of 400 cases and 400 controls, was obtained using Taylor’s and Kish’s formulas [50]. Information on sexual and reproductive risk factors and symptoms was obtained. Vaginal examination was performed, and discharge was assessed. Endocervical and high vaginal swabs were collected and immediately processed in accordance with microbiological standard. Infection with Candida species was diagnosed by microscopy of a saline mount, which showed a highly refractile, round or oval budding yeast cells, and gram-stained smear of material from the vagina showed gram-positive pseudohyphae with budding yeast cells; T. vaginalis was diagnosed by microscopy of a saline mount for actively motile, spear-shaped flagellates, whereas bacterial vaginosis was diagnosed using Amsel’s criteria [26]. N. gonorrhoea was identified by typical colonial morphology, reactions to gram stain, positive oxidase test and sugar fermentation. The antibiotic sensitivity of isolates was tested by the agar diffusion method on chocolate agar plates using oxoid multi discs with standard antibiotic concentration.

The computer program SPSS V 20.0 (2010) Inc., Illinois, United States was used to analyse the results; the association between organisms and studied variables was compared using chi-square (χ2) and Fisher’s exact tests while P value <0.05 was considered significant at 95% confidence level.

3.3. Results

During the period of study, 1280 pregnant women were seen at the antenatal booking clinic among which 800 satisfied the inclusion criteria. Four hundred of the pregnant women complained of abnormal vaginal discharge (cases), whereas 400 had no complaint of vaginal discharge, giving a prevalence of abnormal vaginal discharge in pregnancy of 31.5%.

Table 1 shows the clinical features associated with vaginal discharge in the study group. Vulval pruritus was present in 266 patients, and 200 (75%) of them complained of vaginal discharge, whereas 66 (25%) were in the control group. There was a significant association between pruritus and vaginal discharge (χ2 = 1.011, P < 0.001). As much as 63% of those without itching were in the control group. Dysuria showed statistically significant association with vaginal discharge (χ2 = 44.008, P < 0.000) with 74 (83%) of the 89 patients who complained of dysuria having vaginal discharge. There was no statistically significant association between dyspareunia and vaginal discharge (χ2 = 2.082, P = 0.149). The only patient that had vulval wart complained of vaginal discharge, there was, however, no statistically significant association between vulval warts and abnormal vaginal discharge.

Figure 1.

(Findings from culture of ECS/HVS from pregnant women with abnormal vaginal discharge (N=400)) shows outcome of culture and microscopy from vaginal discharge specimens collected from women with complaint of vaginal discharge. The prevalence of positive culture was 77% (308) among the cases and 21.3% (85) among the control group. Of the 400 patients with abnormal vaginal discharge, the commonest microorganism found was C. albicans, 160 (40%), whereas N. gonorrhoea infection was the least, 1(0.2%). E. coli was isolated in 20 (5%), T. vaginalis in 7 (1.8%), Staphylococcus aureus in 36 (9%), Klebsiella species in 8 (2%), G. vaginalis in 68 (17%) and Streptococcus species in 8 (2%) of the pregnant women. Samples from 92 (23%) patients had negative culture.

Feature Case Control Total
1. Vulval itching Yes 200 (75 %) 66 (25 %) 266
No 200 (37 %) 334 (63 %) 534
x 2 = 1.011, P < 0.001
2. Dysuria Yes 74 (83 %) 15 (17 %) 89
No 326 (46 %) 385 (54 %) 711
x 2 = 44.008, P = 0.000
3. Dyspareunia Yes 25 (61 %) 16 (39 %) 41
No 375 (49 %) 384 (51 %) 759
x 2 = 2.082, P = 0.149
4. LATa Yes 24 (60 %) 16 (40 %) 40
No 376(49 %) 384 (51 %) 760
x 2 = 1.684, P = 0.194
5. Vulval warts Yes 1 (100 %) 0 (0 %) 1
No 399 (49.9 %) 400 (50.1 %) 799
x 2 = 1.001, P = 0.317

Table 1.

Clinical features associated with vaginal discharge in the study group (N = 800).

aLower abdominal tenderness.

Table 2 shows the association between the bacterial isolates and their antibiotic sensitivity patterns. G. vaginalis was sensitive to augmentin and ofloxacin in 64% of cases. Streptococcus sp. was most sensitive to augmentin and erythromycin in 92% (12/13) and 84% (11/13) of cases, respectively. N. gonorrhoea was sensitive to augmentin and ofloxacin in 100% of cases but was 100% resistant to other antibiotics. E. coli was sensitive to cefuroxime and gentamicin in 62% and 65% of cases, respectively. Most of the microbial isolates were resistant to ampicillin and norbactam. Only augmentin had greater than 60% sensitivity rate to all the isolated microorganisms.

Antibiotics S. aureus Klebsiella sp. E. coli G. vaginalis Streptococcus sp. N. Gonorrhoea
Amoxicillin 16.9 10.5 14.2 35.9 0 0
Augmentina 86 61.5 75 64 92 100
Ofloxacin 75 55 12.5 64 25 100
Ciprofloxacin 64 51 25 9.2 22.5 0
Erythromycin 45 1.2 25 72 84 0
Cefuroxime 50 50 62 26 50 0
Gentamicin 61 64 65 21 30 0
Ampicillin 25 45.5 0 7.2 0 0
Norbactam 17.5 25 4.2 0 0 0

Table 2.

Antibiotic sensitivity rate (%) of isolated bacteria.

aAmoxicillin-clavulanic acid.


4. Conclusion

Vaginal discharge in pregnancy is common, but distinguishing abnormal vaginal discharge from normal leucorrhoea of pregnancy is challenging. Since findings have showed that the trio of vaginal candidiasis, trichomoniasis and bacterial vaginosis are common causes of abnormal vaginal discharge in pregnancy; efforts must be made to exclude these conditions in pregnant patients presenting with vaginal discharge so that appropriate treatment can be instituted timely. Finally, gonococcal infection must also be excluded since though it is less prevalent than others, it is a major cause of morbidity in women in developing countries.


  1. 1. Witkin SS, Inglis SR, Polaneczky M. Detection of Chlamydia trachomatis and Trichomonas vaginalis by polymerase chain reaction in introital specimens from pregnant women. Am J Obstet Gynecol 1996; 175:165–167.
  2. 2. Goldstein MS. Vaginitis. In: Chekry & Merkatz’s complications of pregnancy. 5th edition. Edited by Wayne RC. Lippincott, Williams & Wilkins (Philadelphia) 2000: 47–54.
  3. 3. Mayaud P, Mabey D. Approaches to the control of sexually transmitted infections in developing countries: old problems and modern challenges. Sex Transm Infect 2004;80:174–182.
  4. 4. Sexton J, Garnett G, Rottingen JA. Meta analysis and meta regression in interpreting study variability in the impact of sexually transmitted disease on susceptibility to HIV infection. Sex Transm Dis 2005; 32:351–357.
  5. 5. Agboola A. Vaginal discharge. In: Textbook of obstetrics and gynaecology for medical students. 2ndedition. Edited by Agboola A. Heinemann Educational Books Ibadan, Nigeria 2006:70–77.
  6. 6. Kwawukume EY, Acquaah-Arhin R. Vulvovaginitis. In: Comprehensive gynaecology in the tropics. Edited by Kwawukume EY, Emuveyan EE. Graphic Packaging Ltd., Accra, Ghana 2005: 72–79.
  7. 7. Sobel JD. Treatment of complicated Candida vaginitis, comparison of single and sequential dose of fluconazole. Am J Obstet Gynecol 2001; 185:363.
  8. 8. Tricia EM, David LB. Benign disorders of the vulva and vagina. In: Current obstetrics and gynaecology diagnosis and treatment. 9thedition. Edited by Alan HD, Lauren N. Lange Medical Books, McGraw-Hill, NY 2003:651–670.
  9. 9. Bradshaw CS, Morton AN, Garland SM, et al. Higher-risk behavioural practices associated with bacterial vaginosis compared with Vaginal candidiasis. Obstet Gynecol 2005; 106:105.
  10. 10. Workowski KA, Berman SM, Centre for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines. MMWR 2006; 55 (RR-11):1.
  11. 11. Kazmierczak W, Wnek M, Kaminski K. Frequency of vaginal infections in pregnant women in the Department of Perinatology and Gynaecology in Zabrze. Ginekol Pol 2004;75: 932–936.
  12. 12. Akende J, Abhitimen P, Okonofua F. Prevalence of asymptomatic genital infection among pregnant women in Benin City, Nigeria. Afr J Reprod Health 2002; 6: 93–97.
  13. 13. Marai W. Lower genital tract infections among pregnant women: a review. East Afr Med J 2001; 78: 581–585.
  14. 14. Klufio CA. Prevalence of vaginal infections with bacterial vaginosis, Trichomonas vaginalis and Candida albicans among pregnant women at the Port Moresby General Hospital Antenatal Clinic. PNG Med J 1995; 38: 163–171.
  15. 15. Puri KJ, Mdan A, Benjal K. Evaluation of causes of vaginal discharge in relation to pregnancy status. Indian J Dermatol Venereol Leport [semal online] 2003; 69:129–130.
  16. 16. Sobel JD. Vulvovaginal candidiasis. In: Sexually transmitted diseases. 3rd edition. Edited by Holwes KK, Mardh PA, Sparling PF, et al. Mc Graw Hill, New York 1999: 629–639.
  17. 17. Omnia MS, Robert WH. Vulvovaginitis 2005. Retrieved from Updated 20 July 2005, accessed 11 November 2010.
  18. 18. Sobel JD. Vulvovaginal candidosis. Lancet 2007; 369:1961.
  19. 19. Bornstein J, Lakovsky Y, Lavi I. The classic approach to diagnosis of Vulvovaginitis: a critical analysis. Infect D Obstet Gynecol 2001; 9:105[PMID: 11495550].
  20. 20. Edward D, Linda M, Maarten S. Bacterial vaginosis, vaginal flora patterns and vaginal discharge syndrome in the Gambia, West Africa. BMC Infectious Disease 2005; 12.DOI: 10.1186/1471-2334-5-12. Retrieved
  21. 21. Joharah MA. Patients with vaginal discharge: a survey in a University Primary Care Clinic in Riyadh City. Ann Saudi Med 2000; 20:3–4.
  22. 22. Schmid G, Markowitz L, Koumans E. Bacterial vaginosis and HIV infection. Sex Transm Infect 2000; 76: 3–4.
  23. 23. Morris MC, Rogers PA, Kinghorn GR. Is bacterial vaginosis a sexually transmitted infection? Sex Transm Infect 2001; 77: 63–68.
  24. 24. Holzman C, Leventhal JM, Qlu H. Factors linked to bacterial vaginosis in non-pregnant women. Am J Public Health 2001; 91: 1664–1670.
  25. 25. Edmonds DK. Benign disease of the vagina, cervix and ovary. In: Dewhurst’s textbook of Obstetrics and Gynaecology. 7th edition. Edited by Edmonds DK. Blackwell Publishing, Oxford, UK 2007: 606–613.
  26. 26. Amsel R, Totten PA, Spiegel CA, Chen KC, Eschenback D, Holmes KK. Non-specific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983; 74:14–22. Retrieved from
  27. 27. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of Gram stain interpretation. J Clin Microbiol 1991; 29: 297–301. Retrieved from
  28. 28. American College of Obstetricians and Gynaecologists. Assessment of risk factors for preterm birth. Practice Bulletin 31, 2001.
  29. 29. Wendel KA, Workowski KA. Trichomoniasis: challenges to appropriate management. Clin Infect Dis 2007; 44:S123.
  30. 30. Fernandez LO. Prevalence of Candida albicans and Trichomonas vaginalis in pregnant women in Havana city by an immunologic latex agglutination test. Med Gen Med 2004; 6: 50.
  31. 31. Maria R, Johanne S, Manonmany V. Chlamydia and gonorrhoea in pregnant Botswana women: time to discard the syndromic approach? BMC Infect Dis 2007; 7:27.
  32. 32. Botswana Ministry of Health. Management of STI: reference manual for health workers. Gaborone, 2005.
  33. 33. Wessel HF. Genital infections among ANC attendees in Cape Verde. Afr J Reprod Health 1998; 2: 32–40.
  34. 34. Stum AW. Pregnant women as a reservoir of undetected sexually transmitted disease in rural South Africa: implications for disease control. Am J Public Health 1998; 88: 1243–1245.
  35. 35. World Health Organization. Global prevalence and incidence of selected curable sexually transmitted infections - overview and estimates. WHO, Geneva 2001: 1–48.
  36. 36. Family Health International. Preserving fertility. Network 2003; 23: 3–23.
  37. 37. Okonofua FE. Female and male infertility in Nigeria. PhD Thesis. Karolinska Institute, Stockholm 2005.
  38. 38. Amin JD, Zaria LT, El-Nafaty AU, Mai AM. Genital Chlamydia trachomatis infection in women in a Nigerian hospital. Genitourin Med 1997; 73: 146–147.
  39. 39. Land JA, Evers JL. Chlamydial infection and subfertility. Best Pract Res Obstet Gynecol 2002; 16: 901–912.
  40. 40. Manavi K. A review on infection with Chlamydia trachomatis. Best practice and research. Clin Obstet Gynecol 2006; 20: 941–951.
  41. 41. Valentine A. Tubal damage in infertile women: prediction using Chlamydia serology. Hum Reprod 2003; 18: 1845–1847.
  42. 42. Thomas K, Simms I. Chlamydia trachomatis in subfertile women undergoing uterine instrumentation. Human Reprod 2002; 17: 1431–1432.
  43. 43. Okonofua F. Infertility and women’s reproductive health in Africa (editorial). Afr J Reprod Health 1999; 3: 7–9.
  44. 44. Omo-Aghoja LA, Okonofua FE, Onemu SO, Larsen U, Bergstrom S. Association of Chlamydia trachomatis serology with tubal infertility in Nigerian women. J Obstet Gynecol Res 2007; 33: 688–695.
  45. 45. Ostergaard L. Microbiological aspects of the diagnosis of Chlamydia trachomatis. Best practice and research. Clin Obstet Gynecol 2002; 16: 789–799.
  46. 46. Macmillan S, McKenzie H, Flett G, et al. Which women should be tested for Chlamydia trachomatis? Br J Obstet Gynecol 2000; 107: 1088–1093.
  47. 47. Manavi K. A review on infection with Chlamydia trachomatis. Best practice &research. Clin Obstet Gynaecol 2006; 20(6): 941–951.
  48. 48. Centres for Disease Control and Prevention. Sexually transmitted diseases, treatment guidelines. MMWR Rep 2002; 51(RR-6): 1.
  49. 49. Federal Government of Nigeria. Report on 2006 census final results. Federal Government Printer Abuja 2009; 96: B39.
  50. 50. Kish L. Survey sampling. J Royal Statist Soc 1969; 132(2): 272–274.

Written By

Sanusi Mohammed Ibrahim, Mohammed Bukar and Bala Mohammed Audu

Reviewed: February 19th, 2016 Published: June 29th, 2016