BACKGROUND: Illicit sexual behavior by commercial sex workers (CSW) may have a disproportionate impact on the reproductive health of a woman that often leads to cervicitis. This study aimed at examining the cytopathology, patterns, prevalence and burden of cervicitis in CSW in Enugu metropolis, Nigeria. METHODS: Cervical smear was collected from the endocervix of about one hundred and eighteen (n=118) CSWs between November, 2014 and February, 2015 using the liquid-based cytology (LBC) method. Smears were processed and stained by the modified Papanicolaou method. Leftover samples were tested for sexually transmitted diseases, especially N. gonorrhea, and C. trachomatis using ligase chain reaction and nucleic acid amplification test. A randomized sampling design was used for data collection. RESULTS: Cytopathological examination of cervicitis in CSWs showed a moderate infection, and moderately severe to chronic inflammatory cells. The epidemiological study revealed that acute cervicitis are predominant 7(5.9%) and 2(1.7%) are chronic cervicitis. The prevalence of CSWs living with cervicitis in Enugu, Nigeria (7.6%), is significantly affected by age and working duration as CSWs. Also, Chlamydia trachomatis is the solely associated pathogen implicated in cervicitis group (n=9). Candidiasis infection (n=12) and T. vaginalis (n=3) are observed in non-cervicitis group (n=109) while the association between C. trachomatis and cervicitis infection is statistically significant (P= 0.0221). CONCLUSIONS: Acute cervicitis was prevalent with a preponderance of 4:1 in CSWs in Enugu, Nigeria. C. trachomatis infection was the most prevalent etiologic agent of cervicitis in this study. Further molecular study of LBC smears from CSWs using PCR is strongly recommended.

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Following the intraperitoneal inoculation of 200 Wistar rats (96 males, 96 females and 8 controls) aged 2 to4 months with graded-doses of saline and peptone water broth cultures of Staphylococcus aureus, Staphylococcus xylosus and Staphylococcus lentus isolates obtained from urinary tract infection (UTI) in Enugu, Nigeria and typed down to species using API® Staph typing kit, the rats were observed for 72 h and were euthanized. The liver, kidney and bladder were harvested and processed histologically. Out of the 96 rats (48 males and 48 females) inoculated with peptone water broth cultures of S. aureus 834, S. xylosus 837, S. aureus 856 and S. lentus 853 strains, 12 (12.5%) died, with 8 (66.7%) from S. xylosus 837 and 4 (33.3%) from S. aureus 856 but no death from S. aureus 834 and S. lentus 853. More males 6(75%) died from S. xylosus 837 than females 2 (25%) while more females 4 (100%) died from S. aureus 856 than males 0 (0%). No death occurred from inoculation of another 96 rats with saline broth culture of the test strains. Evidence of necrosis of the liver parenchyma with infiltration of the inflammatory cells around the pericentral areas upon S. aureus inoculation was observed. S. xylosus and S. lentus showed no histological damage to the liver. In the kidney, S. aureus produced tubular casts, erosions and glomerular oedema. S. xylosus and S. lentus produced tubular casts, glomerular distortions and oedema. The bladder showed mild effect on the musculature with S. aureus and none for S. xylosus and S. lentus, respectively.

an increased clonal proliferation of one or more myeloid lineages [1,2]. According to the World Health Organization (WHO), the classical myeloproliferative neoplasm can be divided into two major groups namely the Philadelphia chromosome positive group which includes chronic myeloid leukemia (CML) and the Philadelphia chromosome negative groups which includes Essential Thrombocythemia (ET), Polycythemia Vera (PV) and Primary Myelofibrosis (PMF) [3]. Due to an underlying clonal proliferation, patients with myeloproliferative neoplasms suffer complications including thrombosis and haemorrhage. Over time, patients develop progressive bone marrow failure and may also transform to acute myeloid leukemia. Studies identified three main mechanisms of pathophysiology which include (i) Somatic driver mutations that stimulate activation of various tyrosine kinase pathways, (ii) Cooperating driver mutations in myeloid genes and, (iii) Uncommon genetic factors that initiate different clinical neoplastic phenotypes [4]. Oncogenes in Myeloproliferative Neoplasms Underlying myeloproliferative neoplasms are abnormalities in various genes involved the tyrosine kinase signaling pathways [5]. These may include: