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ORIGINAL ARTICLE |
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Year : 2012 | Volume
: 9
| Issue : 1 | Page : 2-5 |
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Inflammatory cervical smears and infection in Kano, Northern Nigeria
Ochicha Ochicha1, Aminu Z Mohammed1, Zakari Mohammed2, Sani A Malami1, Hamisu Takalmawa3
1 Department of Pathology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria 2 Department of Obstetrics and Gynecology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria 3 Department of Medical Microbiology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria
Date of Web Publication | 10-Oct-2012 |
Correspondence Address: Ochicha Ochicha Department of Pathology, Bayero University, Kano Nigeria
 Source of Support: Bayero University Research Committee, Conflict of Interest: None  | Check |
DOI: 10.4103/0331-8540.102100
Background : Inflammation is commonly present in cervical smears for screening of pre-malignant lesions. This study was done to identify microbial pathogens responsible for the inflammation. Materials and Methods : This was a prospective study of cervical smears and endocervical swabs from patients at the gynecology, postnatal, and general outpatient clinics of Aminu Kano Teaching Hospital over a 4-month period. Results : A total of 421 women between the ages of 17 and 80 years were recruited for the study, but most (95%) were premenopausal (< 50 years). Two hundred and thirteen (50.6%) of the smears were inflammatory as evidenced by prominent neutrophilic infiltrate, but only 127 (30%) of the study patients had infection as demonstrated by microbial growth on culture and positive Chlamydia antigen test. Seventy-eight (61%) of the 127 cervical infections occurred among the 213 patients with inflamed smears. The remaining 39% (49 cases) of cervical infections occurred in patients with non-inflammatory smears. Chlamydia and candida were the most frequent microbes accounting for 68.5% of all cervical infections. Thirty-nine (8.7%) of all smears were dysplastic with low grade dysplasia comprising the overwhelming majority - 35 cases. Conclusion : As in most published studies, cervical inflammation did not correlate with infection as infection also commonly occurs in patients without inflammatory smears. This renders patient management problematic for gynecologists. Further research is, therefore, required to clarify the microbial and non-microbial causes of cervico-vaginal inflammation. Keywords: Cervical smears, inflammation, infection, Nigeria
How to cite this article: Ochicha O, Mohammed AZ, Mohammed Z, Malami SA, Takalmawa H. Inflammatory cervical smears and infection in Kano, Northern Nigeria. Niger J Basic Clin Sci 2012;9:2-5 |
How to cite this URL: Ochicha O, Mohammed AZ, Mohammed Z, Malami SA, Takalmawa H. Inflammatory cervical smears and infection in Kano, Northern Nigeria. Niger J Basic Clin Sci [serial online] 2012 [cited 2023 Jun 8];9:2-5. Available from: https://www.njbcs.net/text.asp?2012/9/1/2/102100 |
Introduction | |  |
Although screening for dysplasia in order to prevent the development of cancer is the major reason for the widespread use of cervical smears, most studies document inflammation as the most frequent diagnosis. [1],[2],[3] The inflammation is not usually associated with dysplasia, [1],[3],[4] and its severity varies from negligible mild neutrophilic infiltrate to severe purulent exudates.
Quite disturbingly, some of the patients with cytologically severe inflammation are clinically asymptomatic being detected during routine smear screening. The long term adverse consequences of such simmering sub-clinical inflammation on female reproductive health are quite obvious - STI transmission, sub-fertility, infertility, ectopic pregnancy and miscarriages, not to mention the disruptive social impact on family and relationships.
Worse still, chronic cervical inflammation is a known predisposing factor in the progression of dysplasia to cancer. [3],[4],[5] It is, therefore, imperative that the microbial culprits of this cervical inflammation be identified and eradicated, hence the relevance of this study.
Although a variety of microbes (viruses, parasites, fungi, and bacteria) and non-microbial causes have been implicated in cervical inflammation, bacteria are by far the major pathogens. [6],[7],[8],[9],[10] By virtue of their peculiar diagnostic features, most of the non-bacterial pathogens can be microscopically identified during cytological examination of cervical smears. The different bacterial pathogens can, however, only be properly identified and eradicated after microscopy, culture, and sensitivity tests, hence the bacteriological emphasis of this study.
Interestingly, some studies suggest a disconnect between cervical inflammation and infection i.e. infection occurring with or without inflammation. [6],[11] It would be useful to characterize the relationship between cervical inflammation and infection in our locality, with a view to ascertain the occurrence and pattern of microbial infections, particularly as microbial pathogens are known to differ among different populations. Such data should be of immense value to the management of patients with inflammatory smears, not just in Kano but possibly the entire Sahelian West Africa.
Materials and Methods | |  |
This 4-month prospective study of 421 patients was approved by the ethical committee of Aminu Kano Teaching Hospital where the research was carried out. Two cervical smears and 2 endocervical swabs were collected from each of the 421 women at gynecology, antenatal, postnatal, and general outpatient clinics of the hospital.
Postnatal smears were all taken from women after 6 weeks puerperium when the female genitalia is expected to have returned to its normal pre-gestational state.
Cervical smears were stained with the usual stain and then microscopically examined by the study pathologists. One of the endocervical swabs from each patient was gram stained for microscopy and was cultured on blood, chocolate, MacConkay, Sabaroud, and Mycoplasma agars. The blood agar plates were incubated anaerobically with Oxoid gas packs.
All culture plates were examined after 24 hours, and biochemical tests were performed on positive cultures to identify microbial genus and species. Sensitivity tests were also carried out using sensitivity discs from Ablek Biologicals. The second endocervical swab from each patient was for Chlamydial antigen test using Diaspot kit.
Results | |  |
A total of 421 cervical smears and endocervical swabs were collected from the study patients. One hundred and fifty six (34.7%) of these patients were postnatal, 145 (32.3%) gynecological, 53 (11.8%) antenatal, and 95 (21.1%) for routine asymptomatic screening. Although their age range was broad (17 to 80 years), most patients (95%) were premenopausal (≤ 50 years).
Two hundred and thirteen (50.6%) of the smears were inflammatory as evidenced by prominent neutrophilic infiltrate, but only 127 (30%) of the study patients had demonstrable infections as evidenced by microbial growth on culture and positive Chlamydia antigen test [Table 1].
Seventy-eight (61%) of the 127 cervical infections occurred among the 213 patients with inflammatory smears. The remaining 39% (41 cases) of cervical infections occurred in patients with non-inflammatory smears. Overall, infection was demonstrated in only 37% (78 cases) of the 213 inflammatory smears.
All together, there were 76 pathogenic growths on microbial culture, and 61 swabs were positive for Chlamydia antigen test, with 10 of the positive Chlamydial infections being associated with other microbial growths on culture. Chlamydia and candida were the most frequent microbes accounting for 68.5% of all cervical infections [Table 2].
Thirty-nine (8.7%) of cervical smears were dysplastic with low grade dysplasia comprising the overwhelming majority (35 cases) and high grade dysplasia accounting for just 4 cases.
Discussion | |  |
About half (50.6%) of the 421 smears in this study were inflammatory as evidenced by prominent neutrophilic infiltrate; but only 18% (76 cases) of the accompanying endocervical swabs yielded pathogenic growths on culture.
Chlamydia infection as determined by antigen test kit was demonstrated in 14.6% (61 cases) of microbial infections. Ten of these Chlamydia cases also had microbial growth on culture, so the Chlamydia test only yielded additional 51 cases totaling 127 patients with microbial infections. This amounts to 30% of the total 421 patient population - a far cry from the 50.6% (213 cases) with inflammatory cervical smears.
Thus, there appears to be an obvious disconnect between inflammation in cervical smears and microbial infection as inflammation does not appear to correlate with microbial growth. This disconnect is accentuated by the observation that more than a third (39%) of microbial infections occurred in women whose cervical smears were deemed non-inflammatory.
Our findings were broadly similar to several published studies around the world, which found no correlation between cervical infection and inflammatory cervical smears [11],[12],[13],[14],[15] as significant proportion of infection also occurred in patients with non-inflammatory smears.
In a British Medical Journal commentary, Mali and Josh (1993) postulated that infection in patients without inflammation could be due to recent infection, in which inflammatory response was not yet fully developed. [14] This is particularly likely because some of the smears deemed non-inflammatory actually had scanty neutrophilic infiltrate.
Cervical infection in published reports varied from 29% to 48% of patients with inflammatory smears. [11],[12],[13],[14],[15] In this study, only 37% of patients with inflammatory smears had demonstrable evidence of infection - bacteria (including Chlamydia) and Candida. In other words, most women with inflamed cervical smears had no evidence of infection.
This absence of demonstrable infection in many women with inflammatory smears has so far defied explanation. One remote possibility is that viruses or some other yet to be identified pathogen may be responsible. This is particularly likely as unusual pathogens like cytomegalovirus and Human T-lymphotropic virus have occasionally been implicated as etiological factors in some studies. [15],[16]
Cytologically, apart from the 38 cases of dysplasia (9.3%) usually due to human papilloma virus (HPV), no cytopathic changes indicative of viral infections were present in the cervical smears. However, more sensitive molecular diagnostic techniques like nucleic acid hybridization for viruses were not undertaken in this appraisal.
Another possible explanation is that inflammation in cervical smears is indicative of vaginal infection rather than cervical.
The ectocervix, from which smears are mostly taken, is directly continuous with the vagina and bathed with vaginal fluid.
By virtue of the fact that the vagina directly communicates with the exterior via the introitus, and is the receptacle for the penis during STI transmission, it (vagina) is quite vulnerable to infection.
This vaginal inflammation hypothesis is supported by the observation that neutrophilic infiltrates in cervical smears are often not accompanied by reactive changes in cervical epithelial cells (squamous and endocervical), indicative of cellular injury.
Furthermore, although acute inflammation with neutrophilic infiltrate is common in cervical smears, such neutrophilic infiltrates are relatively uncommon in histological sections of the cervix. Histologically, cervical inflammation is usually of the chronic variety with lymphocytic rather than neutrophilic infiltrate.
A comparative study by Vural et al, (1995) in Sweden similarly demonstrated that cytological inflammation of the cervix did not correlate with histopathology. [17] Thus, high vaginal swabs rather than the endocervical might prove to be more useful in evaluating inflammatory cervical smears. But, a study of both vaginal and endocervical swabs by Tibaldi et al, (2009) [18] failed to demonstrate infection in nearly half of symptomatic women.
Perhaps because inflammation in cervical smears does not appear to have any clinical significance, the newer liquid based cytology (LBC) deliberately dispenses with inflammatory cells to enhance clarity in the cytological evaluation of epithelial cells for dysplasia.
But, this extreme of removing leukocytes from LBC cervical smears deprives the pathologist of useful information that might be relevant for evaluating cervical smears. For instance, the presence or absence of inflammation sometimes aids the distinction of atypical squamous cells of undetermined significance (ASCUS) from marked reactive cellular change in the 2001 Bethesda diagnostic classification.
With regards to the microbial profile of cervical infections, Chlamydia trachomatis, Candida sp., and Escherichia More Details coli were the most frequent pathogens in this review. This is somewhat at variance with published studies from the Europe and United States where Chlamydia Trachomatis and Neisseira gonorrhea appear to be major culprits. [19],[20],[21],[22] Significantly, gonorrhea was conspicuously absent from this review.
Thus, the significance of inflammation in cervical smears remains problematic, particularly for gynecologists who have to decide whether or not to investigate and treat patients with inflamed smears. This problem is compounded by the observation that cervical inflammation often persists even after antibiotic treatment. [21],[22]
More studies are, therefore, required to further define the infectious and non-infectious causes of cervico-vaginal inflammation with a view to enhancing patient management.
Acknowledgement | |  |
We are immensely grateful to Bayero University Research Committee for funding this project and to Medical Lab. Scientists Mallam Sani Abubakar and Hajiya Amina Mohammed for their technical support.
References | |  |
1. | Mohammed AZ, Galadanci HS, Ochicha O, Omale AE, Jido TA. Cytopathological findings on cervical smears in Aminu Kano Teaching Hospital, Kano. J Med Women Assoc 2003;1:51-3.  |
2. | Okeke TA, Okafor U, Akpala CO. Epidemiological studies of a cervical cancer programme population. Sahel Med J 1999;2:30-3.  |
3. | Varghese C, Amma NS, Chitrathara K, Dhakad N, Rani P, Malathy L, et al. Risk factors for cervical dysplasia in Kerala India. Bull World Health Organ 1999;77:281-3.  [PUBMED] |
4. | Verteramo R, Pierangeli A, Mancini E, Calzolari E, Bucci M, Osborn J, et al. Human Papillomaviruses and genital co-infections in gynaecological outpatients. BMC Infect Dis 2009;9:16.  [PUBMED] |
5. | Misra JS, Das V, Srivastava AN, Singh U. Role of different aetiological factors in progression of cervical intra-epithelial neoplasia. Diagn Cytopathol 2006;34:682-5.  |
6. | Paavonen J, Critchlow CW, DeRouen T, Stevens CE. Aetiology of cervical inflammation. Am J Obst Gynecol 1986;154:556-64.  |
7. | Borisov I, Shopova E, Mainkhard K. The aetiology of cervicitis in women. Akush Ginekol (Sofia) 1999;38:23-5.  |
8. | Kovacs GT, Westcott M, Rusden J, Asche V. Microbiological profile of the cervix in 1000 sexually active women. Aust NZ J Obstet Gynaecol 1988;28:216-20.  |
9. | Lefèvre JC, Averous S, Bauriaud R, Blanc C, Bertrand MA, Lareng MB, et al. Lower genital tract infections in women: Comparison of clinical and epidemiologic findings with microbiology. Sex Transm Dis 1988;15:110-3.  |
10. | Marrazo JM. Mucopurlent cervicitis: No longer ignored, but still misunderstood. Infec Dis Clin North Am 2005;19:333-49.  |
11. | Ayres de Campos D, Nogueira A, Magalhaes F, Bayer P. Inflammatory cervical smears in cervicovaginal cytology. A finding meaning infection? Acta Med Port 1997;10:637-41.  |
12. | Bertolino JG, Rangel JE, Blake RL Jr, Silverstein D, Ingram E. Inflammation on the cervical Papanicolaou smear: The predictive value for infection in asymptomatic women. Fam Med 1992;24:447-52.  |
13. | Parsons WL, Godwin M, Robbins C, Butler R. Prevalence of cervical pathogens in women with and without inflammatory changes on smear testing. BMJ 1993;306:1173-4.  |
14. | Mali BN, Joshi JV. Interpreting inflammatory changes in cervical smears. BMJ 1993;307:383.  |
15. | McGalie CE, McBride HA, McCluggage WG. Cytomegalovirus infection of the cervix: Morphological observations in five cases of a possibly under-recognised condition. J Clin Pathol 2004;57:691-4.  |
16. | Zunt JR, Dezzutti CS, Montano SM, Thomas KK, Alarcón JO, Quijano E, et al. Cervical shedding of human T cell lymphotropic virus type I is associated with cervicitis. J Infect Dis 2002;186:1669-72.  |
17. | Vural G, Platz-Christensen JJ, Hagmar B, Jonassen F, Warleby B, Anderson E. Inflammatory signs in wet smear and Pap-smear compared with the histopathology of the female genital tract. Acta Obstet Gynecol Scand 1995;74:451-4.  |
18. | Tibaldi C, Cappello N, Latino MA, Masuelli G, Marini S, Benedetto C. Vaginal and endocervical microorganisms in symptomatic and asymptomatic non-pregnant females. Clin Microbiol Infect 2009;15:670-9.  |
19. | Borisov I, Shopova E, Mainhard K. Problems in diagnosis and treatment of cervicitis. Akush Ginecol 1999;38:60-3.  |
20. | Eckert LO, Koutsky LA, Kiviat NB, Krone MR, Stevens CE, Eschenbach DA. The inflammatory papanicolaou smear: What does it mean? Obstet Gynecol 1995;86:360-6.  |
21. | Marrazo JM, Martin DH. Management of women with cervicitis. Clin Infect Dis 2007;44:S102-10.  |
22. | Workowski KA, Berman SM. CDC Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55:41-5.  |
[Table 1], [Table 2]
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