Pathological Study of Ovaries and Uterine Tubes in Slaughtered Non-pregnant Cows in Sulaimani Province
A Thesis Submitted to the College of Veterinary Medicine at the University of Sulaimani in Partial Fulfillment of the requirements for the Degree of Master Science in veterinary medicine - Theeriogenology By Mardin Omer Mohammed (BVM&S & DVS) Supervised by Assist. Prof. Dr. Faraidoon Abdul Sattar Muhammad Amin (BVM& S; MVSc; PhD)
2015
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Acknowledgements First of all I am thankful to Great Allah for enabling me to carry out this work
I would like to express my deepest respect to the Presidency of Sulaimani University, and I wish to express my gratitude to Dr. Aumaid Umer Uthman, dean of College of Veterinary Medicine, University of Sulaimani. I would like to warmly thank my supervisor Dr. Faraidoon Abdul Sattar Muhammed for his invaluable advice, assistance and encouragement during the whole course of this study. My thanks are extended to Dr. Talib Ghaidan M. Ali, head of the department of Surgery &Theriogenology for his support and help during the period of this study. My special thanks go to Dr. Aree S. Maeruf, director of the Veterinary Directorate in Sulaimane, and support staff of Sulaimani slaughter house for their help in providing me with samples required for the research; without it this work was not able to be done. My thanks must also go to Dr. Karokh Hasan Salih for his kind help in the interpretation of the micromorphological part of this study. Finally, I wish to extend my sincere gratitude to all the staff of Veterinary Teaching Hospital at the College of Veterinary Medicine for their valuable support.
Mardin
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Examining Committee Certification
We certify that we have read this thesis entitled (Pathological study of ovaries and uterine tubes in slaughtered non- pregnant cows in Sulaimani) and have examined the student (Mardin Omer Mohammed) in its contents and that, in our opinion it meets the basic requirements toward the degree of Master of Science in Veterinary Medicine -Theriogenology.
Signature:
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Name: Abdul Sattar. F. Majeed.
Name: Dr.Talib Ghaidan M. Ali
Academic title: Professor
Academic title: Assis.professor
Date:
Date:
(Chairman)
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Signature:
Signature:
Name: Dr. Ali H. Hassan
Name: Dr. Faraidoon A. Muhammad
Academic title: Assis.professor
Academic title: Assis.professor
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Supervisor’sCertificate
I certify that this thesis (Pathological study of ovaries and uterine tubes in slaughtered non- pregnant cows in Sulaimani) was prepared under my supervision at the Department of Surgery and Theriogenology, College of Veterinary Medicine, University of Sulaimani, as a partial fulfillment of the requirements for the degree of Master of Science in Veterinary MedicineTheriogenology. Accordingly, I hereby recommended this thesis to be debated by an examining committee.
Signature: Supervisor: Dr. Faraidoon Abdul Sattar M. Amin Academic title: Assistant Professor. Date:
In view of the available recommendations, I forward this thesis for debate by the examining committee.
Signature: Head of postgraduate study Name: Dr. Faraidoon Abdul Sattar M. Amin Academic title: Assistant professor Date:
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Approved by the council of the College of Veterinary Medicine\ University of Sulaimani
Signature: Name: Dr. Aumaid Umer Uthman Academic title: Professor Date: Dean of the college of Veterinary Medicine and Surgery
Signature: Name: Dr.Talib Ghaidan M. Ali Academic title: Assistant professor Date: Head of the department of Surgery &Theriogenology
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Linguistic Evaluation Certification
I hereby certify that thesis titled” Pathological study of ovaries and uterine tubes in slaughtered non- pregnant cows in Sulaimani” prepared by (Mardin Omer Mohammed), has been read and checked and after indicating all the grammatical and spelling mistakes; the thesis was given again to the candidate to make the adequate corrections. After the second reading, I found that the candidate corrected the indicated mistakes. Therefore, I certify that this thesis is free from mistakes.
Signature: Name: Shilan Rashid Sharif Position: English Department, School of Language, Faculty of Humanities, University of Sulaimani
Date:
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Abstract
Abstract The current study was conducted to address the pathological conditions of ovaries and uterine tubes of cows slaughtered at the abattoir in Sulaimani, Kurdistan Region-Iraq. The pathologic conditions were objected to macroscopic and microscopic examination of 404 samples of female genitalia collected from slaughtered non-pregnant cows. Collection of female genitalia samples was conducted from February to September 2014 by visiting the Qaragol slaughterhouse twice a week. The organs were observed macroscopically for pathological abnormalities and stained tissues with Haematoxyline and eosin. They were examined under microscope for determination of the type of lesion present in the organ. Among the 404 genitalia samples collected from the non-pregnant animals, 206 (51%) were found without gross pathological abnormalities (with cyclic activity) and the remaining 198(49%) samples were found with gross pathological abnormalities of ovaries and uterine tubes. The ovaries exhibited the highest percentage of lesions 29.70% followed by the uterine tubes 19.30%.Detected ovarian lesions included follicular cyst 10.89%, cystic corpus luteum 5.44%, mild ovariobursal adhesions 4.45%, sever ovariobursal adhesion 0.25%, paraovarian cysts 3.22%, ovarian hypoplasia 1.98%, ovarian hemorrhage (hemorrhagic cystic corpus luteum) 1.48%, luteal cyst 1.24%, ovarian agenesis 0.50% and ovarian tumor (Gonadoblastoma) 0.25%. Histopathological examinations exhibited that the follicular cysts were lined by several layers of granulosa and theca cell, while the luteal cysts had follicular granulosa and the theca cells with marked luteinization of cytoplasm.
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Abstract
Microscopically, the ovarian hypoplasia showed lack of ovarian follicles and oocytes, while the cavities of paraovarian cysts were lined by a single layer of cuboidal epithelial cells, and the hemorrhagic cyst showed scattered hemorrhagic spots close to the lumen and luteinized of granulosa and theca cells layers of cystic wall. Histopathologically, the ovarian gonadoblastoma (Dysgenenticgonadoma) was characterized by dual population of germ cell tumor and sex-cord stromal tumor and this observation has not been recorded in Iraq previously. Detected lesions in the uterine tubes included salpingitis 9.15% , pyosalpinx 4.21%, hemosalpinx 1.49%, aplasia of the uterine tube 0.99%, uterine tube adhesion 0.74%, mesosalpinx cyst 0.74%, nodules on mesosalpinx 0.74%, segmental aplasia of the uterine tube 0.50%, occluded uterine tube 0.25%, accessory uterine tube (duplication of uterine tube) 0.25%, and presence of cysts on the uterine tube wall 0.25%. Histopathologically, salpingitis was characterized by erosion of the mucosal layer lining, while pyosalpinx showed a heavy inflammatory cell reaction composed of a mixture of neutrophils and lymphocysts. Hemosalpinx showed the stromal hemorrhage in the core of the villus like folds of epithelium. Cystic uterine tube, (paratubal paramesonephric cyst), revealed a single layer of tubal type ciliated columnar epithelium resting on fibrous tissue of the normal fallopian tube. It was concluded that ovarian and uterine tube abnormalities constitutes an percentage of 49%. Ovarian gonadoblastomas was firstly recorded in this study in Iraq.
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Contents
Contents Dedication……………………………………………………………………… …..ii Acknowledgements…………………………………………………...…………….iii Examining Committee Certification…………………………………………......…iv Supervisor, s Certificate…………………………………………………...…............v Approved by the council of the College of Veterinary Medicine……………...…...vi Linguistic Evaluation Certification………………………………………….....…..vii Abstract………………………………………………………………………...viii-ix Contents………………………………………………………………….………x-xv List of tables…………………………………………………………………..…...xvi List of figures………………………………………………………………...xvii-xix List of abbreviations…………………………………………………………..…....xx
Chapter one Introduction Introduction…………………………………………………………………..……1-2
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Contents
Chapter Two Review of Literatures 2.1 Female reproductive tract………………………………………………………..3 2.2. Estrous cycle in cow….……………………………………………………...….3 2.2.1. Phases of estrous cycle……………………………………………………..…4 2.2.1.1. Pro-oestrus phase……………………………………………………….......4 2.2.1.2. Oestrus phase………………………..……………………………………...4 2.2.1.3. Metestrus phase……………………………………………………………..5 2.2.1.4. Dioestrus phase…………………………………..…………………………5 2.3. Natural regulation of cyclical activity………………………………………..6-7 2.4. Ovaries………………………………………………………………..………8-9 2.4.1. Ovarian follicles………………………………………..……………….....9-10 2.4.2. Corpus luteum…………………………………………………..………..10-11 2.5. Uterine tube………………………………………………….......................12-14 2.6. Infertility and Sterility in cows………………………………………..…...15-16 2.6.1. Pathological abnormalities of varies……………………………………...…16 2.6.1.1. Ovarian congenital anomalies…………………………………………..…16 2.6.1.1.1. Ovarian agenesis ……………………………………………………..…16 2.6.1.1.2. Ovarian hypoplasia………………………………………………………17 xi
Contents
2.6.1.1.3. Freemartin……………………………………………………………….18 2.6.1.1.4. Hermaphrodite…………………………………………………………...18 2.6.1.2. Ovarian inflammatory conditions…………………………………………19 2.6.1.2.1. Oophoritis and perioophoritis…………………………………………...19 2.6.1.2.2. Ovarian abscess………………………………………...………………..20 2.6.1.2.3. Ovario-bursal adhesions…………………………..…………………20-22
[[[[
2.6.1.2.4. Ovarian Sclerosis…………………………………………......................22 2.6.1.2.5. Ovarian hemorrhage (Hemorrhagic cystic corpus luteum)…………..22-23 2.6.1.3. Ovarian functional disorders……………………………………………....23 2.6.1.3.1. Persistent corpus luteum……………………………………………...…23 2.6.1.3.2. Ovarian cysts…………………………………………………………….24 2.6.1.3.2.1. Follicular cysts……………………………………..………………….25 2.6.1.3.2.2. Luteal cysts……………………………………………….………..25-26 2.6.1.3.2.3. Cystic corpora lutea………………………………………….…….26-27 2.6.1.3.2.4. Pathophysiology of cystic ovarian disease…………………..…….27-28 2.6.1.3.3. Para ovarian cysts……………………………………………………..…30 2.6.1.3.4. Inactive ovaries……………………………………………………….....31 2.6.1.3.5. Ovarian tumor………………………………………………………..….32 2.6.2. Pathological abnormalities of uterine tubes………………………………....33 2.6.2.1. Congenital abnormalities of uterine tubes…………………………………34 xii
Contents
2.6.2.1.1. Aplasia (Agenesis) of the uterine tubes…………………………..……..34 2.6.2.1.2. Segmental aplasia of the uterine tube……………………………...…….34 2.6.2.1.3. Accessory uterine tubes………………………………...………………..34 2.6.2.2. Acquired tubal abnormalities……………………………………………...35 2.6.2.2.1. Salpingitis…………………………………………………………....35-36 2.6.2.2. Hydrosalpinx………………………………………………………..….36-37 2.6.2.2.3. Hemosalpinx…………………………………………………….…...37-38 2.6.2.2.4. Pyosalpinx………………………………………………………..…..38-39 2.6.2.2.5. Pachysalpinx………………………………………………………..…...39 2.6.2.2.6. Occluded uterine tube………………………………………………..….40 2.6.2.2.7. Cystic uterine tube………………………………….................................40
Chapter Three Materials and Methods 3.1Study abattoir samples……………………………………………….…………41 3.2. Requirements used in the study…………………………………..………..41-42 3.3. Examination of the non-pregnant genitalia…………………………………....43 3.3.1. Ovaries………………………………………………………..………….43-44 3.3.2. Uterine tubes…………………………………………………………….......45 3.4. Histopathological technique……………………………………………...……46 3.5. Haematoxylin (Harris) and Eosin…………………………………………...…47 xiii
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Chapter Four Result 4.1 Abattoir samples of cows genitalia………………………….............................48 4.2. Non-pregnant genitalia with gross pathological abnormalities……..……..49-50 4.3. Ovarian abnormalities…………………………………………………..……..52 4.3.1. Ovario bursal adhesion…………………………………………………..…..52 4.3.2. Para ovarian cysts……………………………………..……………………..53 4.3.3. Follicular cysts………………………..……………………………………..54 4.3.4. Luteal cysts………………………………………………...………………...55 4.3.5. Cystic corpus luteum…………………………..………………………...56-57 4.3.6. Ovarian agenesis………………………………………..…...........................58 4.3.7. Ovarian hypoplasia………………………………..……………………..58-60 4.3.8. Ovarian hemorrhage (Hemorrhagic cystic corpus luteum)……..………..61-62 4.3.9. Ovarian tumor (Gonadoblastoma)………………………………..……...62-64 4.4. Uterine tube abnormalities……………………………………………………65 4.4.1. Pyosalpinx………………………………………….……………………65-66 4.4.2. Aplasia of the uterine tube………………………………..…………………66 4.4.3. Segmental aplasia of the uterine tube………………………..………………67 4.4.4. Salpingitis……………………………………………………..................67-68 xiv
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4.4.5. Occludedd uterine tube…………………………………………..………68-69 4.4.6. Accessory uterine tube (Duplication of uterine tube)…………………..…...69 4.4.7. Uterine tube adhesion…………………………………..………………..70-71 4.4.8. Hemosalpinx…………………………………………………...……………71 4.4.9. Mesosalpinx cyst……………………………………………...……………..72 4.4.10. Nodules on mesosalpinx…………………………………………..……….73 4.4.11. Cyst on uterine tube wall……………………………………..………...73-74
Chapter Five Discussion 5.1.Discussion……………………………………………………...………………75 5.2. Pathological abnormalities of ovaries……………………………………...75-81 5.3. Pathological abnormalities of uterine tubes………………………………..82-86
Chapter Six Conclusions and Recommendation Conclusions………………………………………………………………..……….87 Recommendation………………………………………………………...…………88 References…………………………………………………………….………89-112 xv
List of Table
List of Table Table No.
Title of Table
Page No.
Table (3.1) Showing materials, solutions and stains used in the study……...……..42 Table (4.1) Distribution of the cow's genitalia according to the reproductive status in the Sulaimani abattoir………………..……...……………………..48 Table (4.2) Gross –pathological abnormalities of reproductive organs (ovaries and uterine tubes) of cow's genitalia in the Sulaimani abattoir………...…49 Table (4.3) Gross-pathological abnormalities of ovaries in cow's genitalia in the Sulaimani abattoir………………...…………………………………..50 Table (4.4) Gross-pathological abnormalities of uterine tubes in cow's genitalia in the Sulaimani abattoir……………………………..…………….........51
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List of Figures
List of Figures Figure No.
Figure Title
Page No.
Figure 1. Neuro-endrocrine control of cyclical reproductive activity ……..………7 Figure 2. Endocrine sequence, types of cysts, and behavioral manifestations associated with cystic ovarian disease in cows……..……………..…...29 Figure 3. Measurement of cysts by Varnier caliper……..……………..…………..44 Figure 4. Injecting of uterine tube by colored fluid (Indian ink)……..….……….45 Figure 5. Mild ovario- bursal adhesion……..……………..………………...……52 Figure 6. Bilateral ovario-bursal adesion……..……………..……………..…..…52 Figure 7. Complete ovariobursal adhesion in the left ovary……..…………….…52 Figure 8. Single para-ovarian paramesonephric cyst in the right side……..……..53 Figure 9. Paraovarian paramesonephric cyst, the section show a single layer of tubal-type ciliated cuboidal epithelial c……..……………..…..………53 Figure 10.Follicular cyst in the right side isthin-walled and containing clear fluid...54 Figure 11. Follicular cyst with has several layers of follicular granulosa and theca cells cyst………………………………………..………………………54 Figure 12. Luteal cyst in the right ovary, thick walled and lutenized……..……….55 Figure 13. Luteal cyst; the section shows follicular granulosa side small and smooth surface and lack of ovarian follicle……..……………..…………….....55
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List of Figures Figure 14. Cystic corpus luteum……..……………..…………...…..……………..56 Figure 15. Two cystic corpra lutea……..……………..……………..……………..56 Figure 16. Cystic corpus luteum……..……………..……………..…………….....57 Figure 17. Cystic corpus luteum; zone of a thin layer of fibrous tissue between luteal cells and the cystic cavity……..……………..………....………57 Figure 18. Uterus unicornual and ovarian agenesis……..……………..…..………58 Figure 19. Showing the total ovarian hypoplasia in left side……..………..………59 Figure 20. Ovarian hypoplasia; the section shows lack of ovarian follicles…….....60 Figure 21. Ovarian hypoplasia; the section shows few inactive primordial ovaria follicles and related sex cords……..……………..……………….……60 Figure 22. Showing the haemorrhagic cyst. ……..……………..………….………61 Figure 23. Hemorrhagic cyst. The cystic lesion contains scattered spots of hemorrhage close to the lumen……..……………..…………...………62 Figure 24. Showing a single case of ovarian tumor (Gonadoblastoma) ………..…63 Figure 25 A tumor composed of round nests of small tubular formations……...…64 Figure 26. Ovarian gonadoblastoma dual population of cells, sex-cord stromal cells and germ cell tumor……..……………..………………………………64 Figure 27. Pyosalpinx of uterine tube, thicken wall accumulated pus in the luminal tube……………………………………………………………….…….65 Figure 28. Pyosalpinx show a heavy inflammatory cell composed of a mix of neutrophils and lymphocytes ……..……………..……………..………66 Figure 29. Uterus unicornus and aplasia of uterine tubes……..……………..……66 xviii
List of Figures Figure 30. Segmental aplasia considerable of the ampulla……..……………....…67 Figure 31. Chronic salpingitis, it shows ifiltration of monouclear……..……….…68 Figure 32. Occlusion of uterine tube……..……………..………..………..………69 Figure 33. Showing the duplication of uterine tube ……..………………..………69 Figure 34. Uterine tube adhesion, adhesion between mesosalpinx and perisalpingial tissues……..……………..……………..……………...……………….70 Figure 35. Hemosalpinx, swelling of uterine tube filled with bloody discharge..…71 Figure 36. Hemosalpinx, uterine tube with stromal hemorrhage in the core of villus……..……………..……………..……………..……………....71 Figure 37. Mesosalpinx cyst, which is 0.5-0.7 cm in diameter……..………..……72 Figure 38. Mesosalpinxcysts; describe the cyst, which is called paramesonephric cyst……..……………..……………..……………….…….…..………72 Figure 39. Nodule on mesosalpimx in the left part of genital tract……..…………73 Figure 40. Showing paratubal paramesonephric cyst in the right side……………73 Figure 41. Cystic on uterine tube, paratubal paramesonephric……..…….………74
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List of Abbreviations
List of Abbreviations CL
Corpus Luteum
COD
Cystic Ovarian Disease
DPX
Distrene- Plasticizec Xylene
FSH
Follicle Stimulating Hormone
GnRH
Gonadotropic Releasing Hormone
H&E
Haematoxyline (Harris) and Eosin
IGF-1
Insulin-like growth factor-1
LH
Luteinizing Hormone
LeicaYD Lica Geovid HD- Yards Model NEB
Negative Energy Balance
NBF
Neutral Buffered Formalin
PCL
Persistent Corpus Luteum
PGF2α
Prostaglandin F2 Alpha
PID
Pelvic inflammatory disease
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CHAPTER ONE
INTRODUCTION
Chapter One
Introduction
Chapter One Introduction Farm animals are one of the fundamental pillars of the economy of Kurdistan region in general, and cows in particular as an economical unit from which people of Kurdistan get great benefit. Thus reproductive problems among cows have a direct influence on the nutritional needs of the people as well as on the economic status of the region. Reproductive performance is vital to the continued existence of cattle and this determines production efficiency of an animal or herd. Generally cows are culled and sent to slaughterhouse either because they are uneconomic to maintain or because they have problems. Hence the slaughterhouses have been used as the preferred sources for studying the pathological lesions of female reproductive tracts. Genital organ disorders are important cause of infertility and sterility. Infertility among farm animals is one of the great economic problems (Zerihun, 2001). The basis for a successful cattle-breeding program is the efficient functioning of the entire reproductive system (Mwaanga et al., 2003). Infertility or sterility can be a complication of various infectious diseases that localize in the reproductive organs of cows with or without specific morphological defects (Kennedy and Miller, 1993). Delayed postpartum ovarian activity is a well-known drawback in cattle reproduction (Esslemont, 1991). One of the most prominent ovarian clinical disorder is ovarian dysfunction, this is an absolute ovarian inactivity with no functional structures on its surface beyond 60 days postpartum (Kalis and van de Wiel, 1980).According to Cetin et al., (2007) and Ali et al., (2009) associated with a lack of functional structures related to the sexual cycles on the ovaries leading to true anoestrus.
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Chapter One
Introduction
In various livestock farms, percentage of ovarian abnormalities can be different, depending on environment factors and nutritional deficiencies, diseases causing weight loss, various infectious agents, and environmental and climatic conditions (Mwaanga and Janoski, 2000). Abnormalities of uterine tubes of cows limit the transfer of male and female gametes may result in sterility or infertility. The gross abnormalities and lesions of the uterine tube like salpingitis, pyosalpinx, hydrosalpinx, occlusion, aplasia and other micro-lesion which are not palpable per rectum and could be responsible for reproduction failure in farm animals, and these tubular abnormalities may show repeat breeding of known or obscure etiology which requires to be confirmed by patency testing (Shivhare et al., 2012). In addition, most of the studies identifying fertility problems are not related to a specific clinical sign ( Katagiri & Takahashi, 2004; Givens, 2006). The present study is based on an investigation of percentage and the macroscopic features of ovarian and uterine tubes lesions in non-pregnant cows slaughtered at the abattoir of Sulaimani, Kurdistan region- Iraq. So the aim of this study is to determine: 1.
The frequency of macro and microscopic of different types of gross abnormalities of ovaries and uterine tubes in non-pregnant cows.
2.
Conducting histopathological feature of abnormalities of ovaries and uterine tubes in cow’s genitalia.
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CHAPTER TWO
REVIEW OF LITRETURE
Chapter Two
Literature Review
Chapter Two Literature Review 2.1 Female reproductive tract The parts that make up the reproductive system in cattle are two ovaries, two oviducts, two uterine horns, a uterine body, cervix, vagina andvulva. The cranial portions of the vagina arise from the primitive mullerian or paramesonephric ducts. The bladder lies below the reproductive tract and is connected at the urerthral opening located on the vaginal floor. The vulva,vestibule and the caudal portion of the vagina develop from the urogenital sinus.The rectum is located above the reproductive system (Roberts, 1986; Hafez and Hafez, 2000; Nebel, 2008).
2.2. Estrous cycle in cows Reproduction drives the production cycle in both beef and dairy enterprises and is of major economic consequence. Once puberty occurs in 7-18 months, the estrous cycles generally continue unabated unless pregnancy is established or nutritional conditions are limited severely (Youngquist and Threlfall, 2007).Over a period of time, many changes take place in the reproductive system in response to changing hormone levels. These changes in normal females repeated every 18 to 21 days. This regular repetitive cycle is called the estrous cycle. The average total time is about 21 days (Nebel, 2008).The terms of follicular phase(proestrus and estrus) and the luteal phase (metestrus and diestrus) occur in a cyclic and sequential manner (Bearden et al., 2004).The individuality of the animal may affect the cycle length (Robert, 1986).
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Chapter Two
Literature Review
2.2.1. Phases of estrous cycle 2.2.1.1. Pro-oestrus phase It is the phase immediately preceding oestrus. It is characterized by a marked increase in activity of the reproductive system by presence of various stage of follicular development with the regressed corpus luteum (Arthur et al., 2001), from day 19 until behavioral estrus occurs (Youngquist and Threlfall , 2007 ). Estrus begins with the regression of the corpus luteum of the previous cycle (in polycyclic specie) drop in the start of estrus (Bearden et al., 2004).The uterus enlarges very slightly; the endometrium becomes congested and oedematous, and its glands show evidence of vaginal mucosa becoming hyperemic; the number of cell layers of the epithelium starts to increase, and the superficial layers become cornified (Arthur et al., 2001).
2.2.1.2. Oestrous phase It is the period of time when the female acceptance of the male starts and their will stand for mating arises (0 day).The length of the period of estrus varies among cycle (Bearden et al., 2004). Onset and end of the phase are the only accurately measurable points in the estrus cycle. During estrus there is follicular growth with the presence of mature follicle with the absence of functional corpora lutea, the main ovarian hormones produced being oestrogens, the uterine, cervical and vaginal glands secrete increased amounts of mucus; the vaginal epithelium and endometrium become hyperemic; the cervix is relaxed. Ovulationoccurs during this phase of the cycle in all domestic species with the exception of the cow, where it occurs at about 12hours after the end of oestrus (Robert, 1986; Arthur et al., 2001).
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Chapter Two
Literature Review
The length of the period varies among species.Cows in hot environment have shorter periods of estrus (10 to 12 hours) than the average 18-hours period for cows in cool climate (Bearden et al., 2004). During this phase of the cycle estrogen levels are typically high while progesterone levels are low (Nebel, 2008).
2.2.1.3. Metoestrous phase It is the phase succeed ingoestrus, which lasts for about 3 days, and is characterized by the presence of corpus haemorrhagicum (Arthur et al., 2001). It is a phenomenon known as metestrous bleeding in cows which lasts (1-3) days. In this phase high estrogen concentrations increase the vascularity of the endometriumthis vascularity reaches peak in about 1 day after the end of estrus (Bearden et al.,2004).The granulosa cells of the ovulated follicle give rise to lutein cells which are responsible for the formation of the corpus luteum. Ovulation is spontaneous in cows and occurs on average 10.5 to 15.5 hours from the end of estrus phase (Robert, 1986).There is a reduction in the amount of secretion from the uterine, cervical and vaginal glands (Arthur et al., 2001).
2.2.1.4.Dioestrus phase The period of the corpus luteum is fully functional. It starts in about the 5th day of the cycle with an increase in blood concentration of progesterone and it ends with the regression of the corpus luteum on day 16 or 17 (Bearden et al., 2004). In 7 to 8 days after ovulation the corpus luteum has reached its maximum size of 2 to 2.5 cm (Robert, 1986). The uterine glands undergo hyperplasia and hypertrophy, the cervix becomes constricted and the secretions of the genital tract are scant and sticky; the vaginal mucosa becomes pale.The corpus luteum is fullyfunctional during this phase, and is secreting large amounts of progesterone (Arthur et al., 2001).
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Chapter Two
Literature Review
2.3. Endocrine control of cyclical activity Regulation of cyclical activity in the female is a complex process as in figure (1), with the development of new techniques, particularly those of hormone assays, and the application of new molecular biological techniques (Arthur et al., 2001). Physiological and the onset of puberty, as well as of no pubertal estrus, is influenced by several factors, including age, genotype, season, body score, nutrition, and social rearing environment(Youngquist and Threlfall, 2007). Utero-pituitary-ovarian relationships and the estrous cycle – the corpus luteum , follicle , and the placenta are the only three transitory endocrine glands (Robert ,1986).One component known to be an important influence is gonadotropic releasing hormone (GnRH).Changes in the rates of GnRH synthesis and release, as well as the rates of degradation of this hormone, are additional factors that modify its role in influencing gonadotropin release (Hafez and Hafez, 2000).There are two very important gonadotropins produced, stored and released from the pituitary gland, the first is follicles stimulating hormone, or FSH. As its name implies FSH stimulates the growth of small follicles. Luteinizing hormone or LH is the other gonadotropin. In addition to supporting progesterone production by the CL, LH can also stimulate estrogen production in large follicles. High levels of estrogen would bring the animal back into heat and make life difficult for a new embryo if she is pregnant. Thus, progesterone‟s regulation of FSH and LH is a very important aspect of maintaining the pregnancy (Nebel, 2008). Progestrone has a dominant role in regulating the estrous cycle and high concentration of progesterone inhibit release of FSH and LH through its negative feedback control of hypothalamus and anterior pituitary; and behavioral estrus(Bearden et al., 2004). At the end of estrus, ovulation occurs followed by corpus luteum formation resulting of progesterone secretion.
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Chapter Two
Literature Review
PGF2α has been reported by Hafez and Hafez, 2000; Bearden et al., 2004 to decrease blood flow through the corpus luteum, a possible factor in regression of the corpus luteum. According to Rajamahendran and Taylor (1990); Savio et al., (1990), follicular development occurs normally in a wave-like manner in normal cycling cattle.
Figure 1: Neuro-endrocrine control of cyclical reproductive activity (Lamming et al, 1979).
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Chapter Two
Literature Review
2.4. Ovaries The ovaries are considered to be the primary organs in a cow‟s reproductive tract. It performs both exocrine (egg release) and endocrine production of (steroidogenesis) hormones function (Banks, 1993; Bearden et al., 2004; Nebel, 2008).The ovaries contain thousands of ova. Theseareproduced by the embryo prior to birth. While thepotential to collect hundreds of ova from a cowexists, only one ovum is usually released duringeach estrous cycle ( Nebel, 2008).The ovaries are ovoid-shaped (Robert,1986) or almond shaped or flattened –shaped (Salisbury and Van Dernark, 1978).These are two oval bodies one on each side, Each ovary has two borders, two surfaces and two ends. The surfaces (lateral and medial) are convex and irregular in appearance situated slightly above to the middle of the pelvic inlet and are attached to the broad ligament by a fold of peritoneum called mesovarium. The size of ovary is highly variable from animal to animal. The average length of ovary in cows is 2-3 cm; with a width of 2cm, and its thickness is lcm. In ruminants, presence of rumen in left side perhaps restricts the blood supply to the left ovary, therefore, left ovary is less active than the right ovary (Kumar,2009, Amin, 2009).The shape and size are altered both with the species and stage of the estrous cycle (Bearden et al., 2004). Ovarian weight varies from 5 to 15 gm, per ovary with the average weight of both ovaries in cattle of all ages being 19.5gm (Robert, 1986).The ovary composed of the medulla and cortex, is surrounded by the superficial epithelium, commonly known as germinal epithelium, a single layer of cuboidal cells, was originally called the germinal epithelium because it was believed to be the origin of femal germ cells (oogonia). It is now known that germ cells do not arise from this epithelial layer (Bearden et al., 2004). The cortex contains follicles, corpora lutea, and stromal tissue with its blood vessels and lymphatics.
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Chapter Two
Literature Review
A dense layer of fibrous tissue, the tunica albuginea ovarii, is located between the outer cortex and the tunica albuginea (McEntee, 1990). The ovarian medulla consists of irregularly arranged fibroelastic connective tissue and extensive nervous and vascular systems that reach the ovary through the hilus (Hafez and Hafez, 2000). The medulla consists of large, tortuous blood vessels, lymph vessels, nerves and supporting connective tissue (Banks, 1993).The arterial supply of the ovary is derived from the ovarian branches of the utero-ovarian artery and the uterine artery, The arteries enter the hilus, the venous return is similar to the artery, lymph capillaries accompany blood vessels in both theca layers and in the corpus luteum (Wenger and Killian, 1991).The vascular pattern of the ovary changes with different hormonal states; and arterial blood flow to the ovary varies in proportion to luteal activity ( Nebel, 2008).
2.4.1. Ovarian follicles Ovarian follicles are fluid filled, blister like structures that contain developing oocytes or eggs. There are numerous follicles on each ovary which vary in size from barely visible to ones 18 to 20 mm in diameter (Nebel, 2008).The ovarian follicle protrude recognized as a smooth fluctuant structures on palpation that protrude from the ovary (Settergren, 1980). Over time, greater than 95% of the follicles on the ovary regress and die without ovulatinon and are replaced by new growing follicles (Matton et al., 1981; Nebel, 2008).In the studies of Adams et al., (1992) two waves of growth were demonstrated, with the first wave beginning on the third and fourth day, and the second starting on the 12th to 14th day of the cycle. In each cycle, either, two, three, or four waves of follicular growth can occur, with two waves being most common in adult cows (Youngquist and Threlfall, 2007).
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Three waves of follicular development in most oestrous cycles (Sirois and Fortune, 1988; Savio et al., 1990). McEntee, (1990) Classified the follicles according to their stage of development: primordial, primary, secondary, and vesicular. Robert, (1986); Roche et al.,(1992) divided the follicles into three categories according to the follicle diameter: small follicle where the diameter less than 5mm, medium follicles is 5 to 9 mm, and mature or dominate follicles where the diameter is approximately 10 to 25 mm. A primary follicle is a germ cell surrounded by single layer of follicular (granulose) cells; a potential ovum surrounded by two or more layers of granulose cells is a secondary follicle (Bearden et al., 2004). A vesicular (Graafian or tertiary) follicle has an antrum (cavity) formed by fluid collecting between the granulose cells and separating them (McEntee, 1990). Most notable feature was the regularity of the number of waves of follicular growth preposterouscycle, which probably reflected genetic or environmental influences. Follicular growth is under the influence of FSH, with normally one follicle obtaining dominance and subsequently ovulating. The dominance does not appear to be mediated by the effect of inhibin but probably by some yet unknown intra-ovarian mechanism which does not involve the suppression of FSH secretion (Arthur et al., 2001).
2.4.2. Corpus luteum Is a transient or temporary endocrine structure, which is formed from the remnant of follicle following ovulation (Smith and Mclntush, 1994). A solid body that forms rapidly from a mixture of thecal and granulosa cells, the corpus hemorrhagicum is replaced by the corpus luteum (Bearden et al., 2004). The CL may also have a fluid filled cavity but usually has a much thicker wall than a follicle graffianand thus a much denser texture. 10
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Corpus Luteum has yellow color in cows; while the outside of this structure is usually dark red in appearance. A cross section reveals a bright yellow to yelloworange interior (Nebel, 2008). Hemodynamic change to the luteal tissue can be attributed to changes in blood flow to the CL and seem to be important regulating CL function and lifespan (Fields et al., 1992). By the 48th hour after ovulation it has attained a diameter of about 1.4 cm. The CL attains its maximum size by the seventh to eighth day of dioestrus. The greatest dimension of the fully developed structure varies from 2.0 to 2.5cm; its weight also varies from 4.1 to 7.4g. Similar variations also occur in the weights of the CL of pregnancy, ranging from 3.9 to 7.5 g, the center of the yellow body is occupied by a cavity(Arthur et al., 2001) .Folds that penetrate the central cavity consist of a central core of stromal tissue and large blood vessel, which become distended. The size of the cavity varies; in the majority it is small, averaging 0.4 cm in diameter, but occasionally it is large, up to1cm or more. A mature corpus luteum with ovulation papilla could be readily palpated together with a mid-cycle follicle (Robert, 1986).The formation of the CL is initiated by a stimulus of pituitary LH (Dellman and Brown, 1976). The corpus luteum is made of two distinct steroidogenic cell types, both of which contribute significantly to the total progesterone secreted during luteal phase of estrous cycle; the small luteal cells secrete little progesterone stimulated by LH, while large luteal cells spontaneously secrete progesterone at a high rate (Hafez and Hafez, 2000). Luteal regression is caused by episodic release of PGF2α from the uterus that induced by oxytocin secreted by the corpus luteum (Arthur et al., 2001). When the corpus luteum regresses, it no longer produces progestins. It loses its color and converted to a small white scar on the surface of the ovary, which is called corpus albicans. The CL of the estrous cycle is known corpus luteum spurium (false yellow body) that is smaller than the corpus luteum of pregnancy known as corpus luteum vernum (Robert, 1986; Fields et al., 1992; Hafez and Hafez, 2000). 11
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During cyclic regression of the corpora lutea and the follicles, cellular hypertrophy and sclerosis occur in the walls of the arterial supply (Dellman and Brown, 1976).
2.5. Uterine tube The uterine tubes also called (oviduct) are pair of convoluted tubes. Each has a length of about 20-30 cm, and diameter about 2 to 3 mm in most farm species (Bearden et al., 2004; Kumar, 2009). Each uterine tube is divided into three parts which conduct the ova from each ovary to the respective horn of uterus and serve as site for fertilization of ova by spermatozoa (Salisbury and Van Dernark, 1978; Frandson and Spurgeon, 1992; Bearden et al., 2004).They are torturos, wiry and hard, feeling nearly cartilaginous when rolled between the fingers.They may be imbedded in fat of the mesosalpinx, a portion of the broad ligament supporting the uterine tube (Dellman and Brown, 1976; Roberts, 1986). The mammalian uterine tube is the physiologic site of sperm cell capacitation, gamete fertilization, and subsequent early embryonic development (Hunter, 1988). Secretory epithelial cells of the tube produce a wide array of glycoproteins, and this production is mediated by the steroidal milieu of the female's cycle (Oliphant et al., 1984; Wenger and Killian, 1991). Glycoproteins secreted in the tube bind to sperm cells, theoocyte, and the early embryo (Wenger and Killian, 1991; Boice et al., 1990).Contractile activity of the tube is stimulated by estrogens and inhibited by progestins (Bearden et al., 2004). Uterine tube is divided into three parts: fimbria are unattached except for one point at the upper pole of the ovary, infundibulum: it is a funnel-shaped structure located at the ovarian end , ampulla is the middle part of the tube & it forms the thin walled portion of
uterine tube the which contains numerous
mucosal-sub mucosal folds.
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The mucosal lining of the ampulla has from 20 to 40 longitudinal folds, which greatly increase the surface area of the lumen. The majority of the cells in the mucosa of the ampulla are ciliated, but some secretory cells are present. Action of the cilia aids movement of the ovum down the ampulla (McDonald, 1980; Hafez and Hafez., 2000; Bearden et al., 2004; Samuelson, 2007).The ampulla joins the isthmus at the ampullary-isthmic junction, the region where fertilization most likely occurs. The ampulla leads to the isthmus which has thicker muscular wall than that of the ampulla and fewer and less branched mucosa. It is the constricted portion of the fallopian tube which lies close to the uterus; isthmus is smaller than the ampulla, being 0.5 mm to 1 mm in diameter having a thicker smooth muscle layer than the ampulla and from 4 to 8 mucosal folds (Bearden et al., 2004). Uterotubal junction is a marked flexure at the transition of the isthmus with the elongated curving end of the uterine horn (McEntee, 1990; Hafez and Hafez., 2000; Bearden et al., 2004). Fertilized ova are transported from the site of fertilization to the uterus by light peristaltic muscular contraction, and by the cilia of the uterine tube that beat toward the uterus. The passage of spermatozoa to the ampulla is accounted for by muscular contractions of the uterine and tubal walls (Dellman and Brown, 1976).The uterine tubes of many species are internally lined by a simple columnar epithelium (Frandson and Spurgeon, 1992; Dellmann and Carithers, 1996). The epithelial cells are ciliated columnar cells, and nonciliated columnar cells exist within the epithelial lining, these cells are believed to be secretory and provide nutrition support for the gametes moving through this portion of the reproductive tract (Banks, 1993; Samuelson, 2007). Dellmann and Brown, (1976) reported that the epithelial cells of the uterine tube consist of columnar ciliated cell (non secretory cell) and non-ciliated columnar cell (Secretory cell) which exhibit marked changes during the estrous cycle; the secretory cells undergo periods of atrophy and hypertrophy during the estrous cycle. 13
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The wall of the uterine tube consists of three layer; mucosa, muscularis, and serosa. The mucosa is made of primary, secondary, and tertiary folds. The mucosa consists of a lamina epithelial and a lamina propria, the propria is continuous with the sub-mucosa in the female reproductive tract because the muscularis mucosa is absent. In the uterine tube the propria-submucosa consists of loose connective tissue with many plasma cells, mast cells and eosinophils. Tunica muscularis consists chiefly of circular smooth muscle bund, but isolated longitudinal and oblique bundles also occur (Hafez and Hafez, 2000). Tunica serosa is made of loose connective tissue. The connective tissue of the tunica serosal houses the immigrating and emigrating vasculature and autonomic innervations that serve the uterine tube (Samuelson, 2007). Arterial supply to the uterine tubes is derived from the utero-ovarian artery. Lymph vessels have capillary networks in the mucosal and serosal layers and drain into the lumbar lymph nodes, both myelinated and non myelinated nerve fibers are derived mainly from the sympathetic system (Dellmann and Brown, 1976). In the cow many ciliated and tall cell are seen at estrus. During the luteal phase the secretory cells become taller than the ciliated cells. During the estrous cycle the epithelial cell nuclei may migrate toward the cell apex (Hafez and Hafez, 2000; Bearden et al., 2004).
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2.6. Sterility and Infertility in Cows A healthy genital tract is essential to maintain the normal reproductive performance of the animals. Any defects in the genital tracts can harmfully hamper the reproductive efficacy (Alwan et al., 2001; Al-Fahad et al., 2004; Azwai et al., 2008a). Infertility in the cow can be attributed to a number of conditions affecting the tubular reproductive tract (Youngquist and Threlfall, 2007). Genital organ disorders are important cause of infertility and sterility (Hatipoglu et al., 2002a). Cattle are deemed infertile when they are neither normally fertile nor completely sterile; or infertility is the diminish or absent capacity to produce viable offspring (Robert, 1986). Osmanu, (1979) and Arthur et al., (2001) categories the causes of infertility and sterility into four broad groups: 1. Primary genital organs structural defects, which may relate to graffian follicle development and maturation, oestrus onset, ovulation, fertilization implantation, and development of the fetus and its membrane. 2. Infections, 3.Managemental and functional factors such as poor nutrition, inadequate herd management, 4.Hereditary and congenital factors, hormonal disturbances or environmental changes, makes the animal infertile, even if temporarily. According to Short (1990), anestrous is the main component of postpartum infertility in cattle production systems and can be related to deficient management associated with low feed levels during breeding seasons and suckling stimulus. Another factor causing an economic loss in the bovine production system is the presence of repeat breeder cow (Zemjanis, 1980; Bartlett, 1986; Bage, 1997). Abattoirs provide a good source for studying pathological of genital tract and prevalence of information and investigation of types of abnormalities that are severe enough to cause infertility and sterility (Kessy and Noekes, 1985; Dobson and Kamonpatana, 1986 and Fathalla et al., 2000).
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Numerous abattoir surveys of bovine genitalia have been conducted to investigate macroscopic and microscopic abnormalities (Shalash, 1958; Vale et al., 1981; Sharma et al., 1993; Ganorkar and Paikne, 1994; Ghora et al., 1996; Sujata, 2000; Tafit and Darahshiri, 2000). In Iraq there are few macroscopical and microscopical studies which include the
anatomical,
physiological,
and
pathological
abnormalities
affecting
buffaloscows buffalos reproductive tracts through an abattoir survey (Alwan et al., 1998; Alwan et al., 2001; Azawi etal., 2008a; Rahawy, 2009; Ali, 2009). Many studies were performed on these disorders, in many other countries in the world (Herenda, 1987; Fathalla et al.,2000; Chaudhari and Paul- Bokko., 2000; Hatipoglu et al., 2002a; Hatipoglu et al., 2002b; Kunbhar et al., 2003; Saxena et al., 2006; Ali et al., 2006; Nam and Aiumalmai, 2010; Simenewet al., 2011). Alwan et al. (1998) recorded the percentage of gross abnormalities of bovine genital tract in Iraq as 16% while Azawi et al. (2008a) observed it as 53.3%. In Sulaimani, Ali (2009) stated the in vitro and in vivo study of infertility of cows detected the abnormality as 21.75%.
2.6.1. Pathological abnormalities of ovaries The classification of ovarian pathologies has been done under the following four sub groups (Purohit, 2014):
2.6.1.1. Ovarian congenital anomalies 2.6.1.1.1. Ovarian agenesis A gensis complete absence of ovaries but less sever (MacLachlan, 1987). Agenesis of one or both ovaries rarely occurs in domestic mammals (McEntee, 1990).
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2.6.1.1.2. Ovarian hypoplasia Ovarian hypolasia is a condition of incomplete ovarian development, where in the affected ovary or part of the ovary completely lacks follicles, due to a germ cell deficiency. It occurs infrequently in certain breed of cattle (MacLachlan, 1987; Hafez and Hafez, 2000).This condition of the ovary is considered to be due to the failure of migration of primordial germ cells from the yolk sack to the developing gonad during embryonic stage (Venhoranta et al., 2013). Settergren (1964b) described three types of ovarian hypoplasia: total, partial, and transitional. In total hypoplasia the ovary was fusiform, had irregular longitudinal grooves on the surface; and it contained no follicles. With partial hypoplasia the uterine extremity of the ovary was affected most frequently and was small, wrinkled, and deficient in follicles. The ovary with transitional hypoplasia was small and had a smooth surface and a firm consistency, follicles and corpora lutea bulged from the surface in some cases. Deep longitudinal grooves were present in the ovarian hypoplasia, the surface epithelium in the grooves was tall columnar but varied between squamous and columnar on the rest of the ovary. In partial ovarian hypoplasia, cows exhibit varying degrees of functional impairment and infertility (Hafez and Hafez, 2000). Herenda (1987) recorded that the percentage of ovarian hypoplasia was
0.11%.While the percentage rate was recorded by Chaudhari and Paul-Bokko (2000) was 2.20% and Kunbhar et al., (2003) was 4.6% and Peng et al., (2011) stated the percentage of ovarian hypoplasia in echography characteristics of abnormal ovaries in infertile dairy cows as 21.6%.
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2.6.1.1.3. Freemartin A freemartin is an infertile female (born co-twin to a male) that is imperfectly developed and sterile probably due to influence of the male hormones of the twin during development in the uterus (Kastli and Hall, 1978). Freemartinism is distinct form of intersexuality which arises as a result of vascular anastmosis of the heterozygous fetuses in multiple pregnancies. In freemartins, the ovaries of the female fetus usually fail to develop, and remain small and rudimentary (Katragadda et al., 2013).
2.6.1.1.4. Hermaphrodite Hermaphrodite is an individual that has both male and female reproductive organs. A hermaphrodite animal has congenital anatomical variation that confuses the diagnosis of sex (Rama et al., 1976). In farm animal hermophrodtitism is most common in cattle, pigs, and goat, itcan be categorized into three groups: True hermaphroditism, male pseudohermaphroditism, female pseudohermaphroditism (Hafez and Hafez, 2000). True hermaphroditism is a bisexual manifestation in which both ovarian and testicular tissues are present (Narasimha et al., 1976).
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2.6.1.2. Ovarian inflammatory conditions 2.6.1.2.1. Oophoritis and perioophoritis Inflammation of the ovaries and surrounding structures is known as oophoritis and perioophoritis. The most common pathological condition of bovine ovary is perioophoritis, while oophoritis seems to be rare (Fathalla et al., 2000). The etiology of inflammatory conditions of the ovaries usually lies in the ovarian manipulations, although infections from the uterus and infectious diseases like Tubercullosis and Brucellosis might also be involved (Agarwal et al., 2005).Trauma caused by improper manipulations during palpation, forced attempts to enucleate corpus luteum or to manually rupture cystic ovaries is the most common cause of oophorits. Perioophoritis is usually chronic and often localized and seen as red fibrous and serosal tags attached to the surface of the ovary especially in heifers (Mittal et al., 2010). Severe bilateral inflammation causes sterility. In unilateral cases also, the prognosis is guarded. Whenever mesosalpinx or uterine tube is involved in the inflammatory process, severe oophoritis is comparatively rare in cattle in areas free of Tuberculosis and Brucellosis. It occasionally occurs in association with Brucellosis and Tuberculosis (Kennedy and Miller, 1993). Summers et al.,( 1974) observed that the percentage of mild, interstitial oophoritis of cattle in Australia was 73,7% ,while Parsonson et al., (1981) reported that cows infected with virus at the time of insemination developed multifocal necrosis and inflammatory cell foci in luteal tissue. Hatipoglu et al., (2002b) observed that the perioophoritis was 0.27%. Simenew et al.,(2011) in Ethiopia, observed percentage of 2.5% of major gross reproductive tract abnormalities in female cattle. Peng et al., (2011) in China reported that the percentage of one case of echnography characteristics of abnormal ovaries in infertile dairy cows. 19
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2.6.1.2.2. Ovarian Abscess The abscess usually develops subsequent to localization of an focus of infection following ovarian inflammatory disease. An ovarian abscess is silent clinically and can be diagnosed with precision only by transrectal ultrasonography (Kumar and Purohit, 2009). Ovarian abscesses in cattle are rare and may develop secondary to severe cases of postpartum metritis and pyometra. Actinomyces Pyogenes (Corynebacterium Pyogenes), which is the usual abscess-producing organism in the cow, was isolated from the exudates (Farin et al., 1989). The enucleation of a corpus luteum in a cow with pyometra occasionally results in the development of an ovarian abscess (McEntee, 1990). Couto and Megle (1959) found one ovarian abscess during the postmortem examination of 1300 bovine genitalia in a slaughterhouse survey.
2.6.1.2.3. Ovario-bursal adhesions Ovarian bursal adhesions involve the formation of fibrous tissue across the ovarian bursa which in severe cases obliterates its cavity (Acland, 2001). The condition results from adhesion between the mesoslpinx and mesoovarium, often including the fimbriae and ovary (Saxena et al., 2006). They usually follow inflammatory processes in and around the ovary (Arthur et al., 2001). The extent of the adhesions varies with specimens, showing fine-like strands in the depth of the bursa which do not involve the uterine tube to instances of complete envelopment of the ovary in a closely applied fibrous bursa (Azawi et al., 2008a; Mittal et al., 2010). Intermediate cases show that fibrous strands of varying thickness which connects the fimbriae or bursa to the ovary. Trauma from rough handling of the ovary and bursa by rectal manipulation or enucleation of the corpus luteum and descending infections are common causes of this condition (Jeevanajyothi and Sreemannarayana, 2003). 20
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Mild strand of fibrous tissues between the ovarian bursa and the ovary resulted from post-ovulation haemorrhage (Fathalla, et al., 2000). A large proportion of ovario- bursal adhesions resulted from ascending uterine infections (Robert, 1986; and Arthur et al., 2001). Where the ovarian bursa is completely adhered to the ovary and sometimes the fallopian tube; interference with ovulation, bursal and salphingeal occlusion may ensue. The latter predisposes to development of bursal cysts, hydrosalpinx and pyometra (Kennedy and Miller, 1993). The ovario- bursal adhesion affects fertility mainly by interfering with tubal motility and leads to irregular returns to estrus. In severe types, between 25 and 50% are bilateral and likely to interfere with ovulation or to impede sperm or egg transport through the uterine tube. Of the unilateral cases, the right side is more frequently involved (Arthur et al., 1996). Conception is unlikely to occur to ovulations from the affected side. Some cases may be preventing irrigation of uteri with large quantities of antiseptics; prompt attention to cases of dystocia can reduce the percentage by preventing puerperal metritis (Robert, 1986; Ali, 1989; Arthur et al., 2001; Ali, 2009). An percentage of (5.38%) of ovarian bursal adhesions in Canda was reported by Herenda (1978). Fathalla et al., (2000) observed that the percentage in Northern Jordan was 8%. While in Nigeria, the percentage of 2.20% was reported by Chaudhari and Paul-Bokko (2000) and in Pakistan, the percentage of 4.6% was recorded Kunbhar et al.,(2003).. Whereas, Ali et al. (2006) found the percentage of 7.27% of pathological studies on reproductive organs of cows in Pakistan and Simenew et al., (2011) observed the rate of 2.5%.
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In Mosul-Iraq, Alwan (1998), diagnoses that the percentage of ovariobursal adhesions was 3.4% of gross abnormalities affecting genital tract of Iraqi rumints, and the observation of lesion reported by Rahawy (2009) was 19.04% and 4.76% in sever and moderate ovariobursal adhesions, and Azawi et al. (2008a) recorded 6.4%, while in Sulaimani region the percentage of (4.19%) was reported by Ali (2009).
2.6.1.2.4. Ovarian Sclerosis Sclerosis means Hardening or indurations. It is also one of the common ovarian abnormalities noticed in the abattoir specimens (Peeva and Illeva, 2007). The ovaries appear very small and hard without any follicles. The etiology for ovarian sclerosis is poorly known. The pathogenesis of systemic sclerosis involves vascular, fibrotic, inflammatory, and immunologic processes and probably similar mechanisms might be involved. Ovarian tuberculosis as recorded for cows could be possible reason for induration of ovaries (Fathalla et al., 2000).
2.6.1.2.5. Ovarian hemorrhage (Hemorrhagic cystic corpus luteum) Ovarian hemorrhage was described as spontaneous in calves for unknown reasons (Stevens et al., 1995). Intrafollicular hemorrhage occurs frequently in atretic follicles in young calves but rarely in atretic follicles in cows. The amount of hemorrhage that occurs during ovulation varies in different species ( Kunbhar et al., 2003). In the cow a small blood-filled cavity in the corpus luteum will be present for only a few days following ovulation (McEntee, 1990).
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It was observed bilateral and their sizes were between 10- 15 cm. Hemorrhages on the ovarian surface may be attributed to the extension of perimetritis (Fathalla et al., 2000). The percentage of 3% that reported by (Kunbhar et al., 2003). In Iraq, the percentage rate of ovarian hemorrhage was (0.38%) that reported by Ali (2009).
2.6.1.3. Ovarian functional disorders 2.6.1.3.1. Persistent corpus luteum Occasionally the corpus luteum does not regress normally eventhough the animal is not pregnant (Lashari and Tasawar, 2012). This is considered a persistent corpus luteum (PCL). The PCL continues to produce progesterone to prevent further follicle development, estrus and ovulation. In the normal conditions the maintence of CL is the result of precise inter-action between pituitary and embryonic gonadotropins, as well as intraluteal autocrine and paracrine signals that modulate the endocrine function of luteal cells (Tomac et al., 2011). Maintance of CL in the absence of pregnancy may originate with pyometra and late embryonic mortality (Russo et al., 2010). Probably suspended under certain conditions and such animals continue to evidence anestrus in the presence or absence of uterine pathology (Peters and Lamming, 1986). The percentage of this condition in cows is known to vary from 2% to 11% (Lashari and Tasawar, 2012; Peters and Lamming, 1986). Previous studies utilized abattoir derived buffalo cows genitalia (Narsinha and Sreemannarayana, 1982; Azawi et al., 2008a), the percentage of the persistent CL was observed to vary between 0.19% to 9.12%. Similar percentage was recorded in more recent studies on abattoir derived buffalo genitalia (Purohit, 2014).
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2.6.1.3.2. Ovarian Cysts Cystic ovarian disease (COD) is a common and economically significant condition of dairy cattle (Johnson and Coates, 2004). It refers to a condition in which there is presence of fluid structures on the ovary more than 2.5 cm in diameter and persist at least 10 days in the absence of a corpus luteum (Roberts, 1986; Opsomer et al., 1997). Ovarian cysts arise from a failure of ovulation (Blowey and Weaver, 2003).Some cysts are incidental findings at post- mortem, others are associated with fertility disturbances. Intra ovarian cysts include anovulatory graffian follicles, cystic corpora lutea, and cystic rete ovarii and inclusion cysts (Maclachlan and Kennedy, 2002). Cyst formation is caused by an abnormal process such as genetic influences and production influence (Allrich, 2001). According to Laporte et al.(1994); Blowey and Weaver (2003); Sakaguchi et al., (2004), cysts are not incompatible with pregnancy, however, abattoir studies show a surprising number of pregnant cows with cysts. Stress, deficiencies, feeding for high milk yields and heredity are among the suggested causes. Many cysts resolve spontaneously, whilst other require treatment. Cystic ovaries are a common cause of infertility in cattle. It was first described in the early 1900‟s and is recognized as an important cause of reproductive loss in cattle. Each percentage of cyst formation increases the calving interval by 22-64 days (Johnson, 2008). It is characterized by nymphomania or anestrous behavior and it is known for many years Kingman, (1933) stated first described cystic ovaries. Ovarian cysts can be classified as follicular cysts, luteal cysts or cystic corpora lutea (Elmore, 1986). Being the result of anovulatory follicles, follicular and luteal cysts are true cysts associated with an abnormal condition in the animal while the cystic corpora lutea is considered non-pathological (Garverick, 1997).
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2.6.1.3.2.1. Follicular cysts Are thin-walled, varied in size from 2 to 4 cm. The cysts contained clear fluid (Hatipoglu et al., 2002b), may be single or multiple on one or both ovaries. High concentrations of estradiol are usually found in follicular cysts fluid than in fluid from luteal cyst and normal follicles (Odore et al., 1999; Hatipoglu et al., 2002b). Cows with follicular cysts continue to have follicular growth and turnover (Hamilton, 1995). Follicular wave emergence and FSH secretion are variable with differing cystic conditions. In cystic cows, follicular wave emergence is more variable than in normal cows (Kaneko, 2002). The microscopically, the membrane granulose is atrophied and represented by a layer of flat cells which line the inner wall of the cyst (McGavin and Zachary, 2007). The follicular cysts are lined by 1-3 layers of granulose cells in some cases, degeneration were seen in the granulose or partially luteinized, the theca interna is often thickened and may be partially luteinized, no ovum in cystic lumen in all cases (Kennedy et al., 1993; Jones et al., 1997; Hatipoglu et al., 2002b).
2.6.1.3.2.2. Luteal cysts Are thick-walled, usually occurring singly, that all the wall of follicular undergo luteinization, and affect one ovary and contain high concentrations of progesterone in their cystic fluid than follicular cysts and normal follicles (Ribadu et al., 1994). Luteal cysts develop when ovulation fails to occur and the theca undergoesluteinization (Schlafer, 2007). They are also often considered to be the later form of ovarian follicular cysts (Vanholder et al., 2006), and therefore the causes pertaining to follicular cysts can also be considered the original causes of luteal cysts. The luteal cyst occurs when the cells of the follicular cyst (granulosa and theca) become luteinized and start producing progesterone (Peter et al., 2009).
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Luteal cyst percentage increases with age and most often affects cows with high milk production (Foley, 1996). Anovulatory cyst occurs more frequently in cattle and swine than in other species of domestic animals (Kennedy et al., 1993). Microscopically, the granulose cells suffered from vasculization and luteinization forming granulosa lutein cells which appeared polyhedral with large vesicular nuclei and vascular cytoplasm. The cysts were surrounded by a fibrous connective capsule (McEntee, 1990). Luteal cysts are white creamy appearances; it is anovulatory cyst which is present in a single or multiple cysts (Sussan et al., 1998).
2.6.1.3.2.3. Cystic corpora lutea A cystic corpus luteum (CL) in a cow is defined as luteal tissue initiating from a corpus haemorrhagicum and containing fluid in a central cavity greater than 7 mm in diameter (Chuang et al., 2010). The terms for cystic CL can often be confused with those for luteal cysts, though the first is a normally functional structure and the latter a pathological condition. Because of this, the contemporary term „corpus luteum with a cavity has been suggested to replace theclassical term cystic corpus luteum (Chuang et al., 2010). Percentage of cystic CL ranges from 25.2% to 78.8% during diestrus and decreases with progression of the estrous cycle (Kahn, 2010). The diameter of cystic cavity in the center of corpora lutea varied considerably from about 0.5 to 3.2 cm (Fathalla et al., 2000). It has been reported that cystic corpus luteum develops following ovulation, was grossly undifferentiated from non cystic. A papillary projection, known as a “crown” is also apparent, and indicates the site of ovulation, when progesterone production is inefficient fertility may be negatively affected, therefore; there are no effects of the cystic corpora lutea on the reproductive function (McEntee, 1990). Microscopic examination shows that the cystic corpora lutea had a zone of fibrous connective tissue between the luteal tissue and the cystic cavity (Jonesetal., 1997; Hatipoglu et al., 2002b; McGavin and Zachary, 2007). 26
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Literature Review
The percentage rate of cystic ovaries of an abattoir study of gross reproductive abnormalities was 7% which was reported by Fathalla et al. (2000), and is higher than the percentage rate of cystic ovaries which was recorded by Chaudhari and Paul- Bokka, (2000) of the gross abnormalities of the genitalia in cows and was 3.35%. While in Indiana, astudy of dairy herds reported by Allrich, (2001) shows that the percentage of ovarian cysts was (39%), Hatipoglu et al., (2002b) reported 2.51% as percentage rate of cystic corpus lutea. Kunbhar et al., (2003) recorded the rate of 10.8% of follicular cysts and 7.7% of luteal cysts. In Pakistan, Ali et al., (2006) recorded one case of cystic corpus luteum 0.9% and follicular cysts three cases 2.72%. Simenew et al., (2011) reported 7.7% of cystic ovaries. In Iraq, the percentage rate of 72.7% of luteal cystic ovaries was observed by Majeed et al., (2004) and the percentage rate of cystic ovaries that was 2.67% of follicular cyst and 0.76% of luteal cyst that recorded by Ali (2009) in Sulaimani.
2.6.1.3.2.4. Pathophysiology of Cystic Ovarian Disease The etiology of COD is multifactorial and controversial ( Kesler and Garverick, 1982; Lopez-Diaz and Bosu, 1992; Woolums and Peter, 1994; Kaneko, 2002; Gumen and Wiltbank, 2002; Hampton, 2003; Peter, 2004). The basic pathophysiology of COD as showen in figure (2), involves a neuroendocrine dysfunction of the hypothalamic- pituitary- ovarian axis resulting in ovulation failure. The hypothalamus may be unresponsive to the positive feedback of estrogen from the dominant follicle resulting in a deficiency of GnRH and a subsequent inadequate or inappropriate timing of the LH surge resulting in ovulation failure. An ovulation may result from a pituitary deficiency where GnRH fails to induce adequate LH surge to induce ovulation or luteinization. The pituitary is often normal as exogenous, GnRH is able to induce a LH release, and however, the release pattern may be different in COD cows from normal cow. 27
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Literature Review
It is generally accepted that cystic follicles develop due to a dysfunction has amultifactoral etiology, in which genetic, phenotypic and environmental factors are involved ( Kesler and Garverick, 1982; Peter, 2004; Garverick, 1997). Many studies (Diskin et al., 2003; Lucy, 2003) have agreed that negative energy balance (NEB) in the postpartum period may affect COD at both levels of the hypothalamus- pituitary and the ovary- follicle through associated hormonal and metabolic changes. During NEB, circulating concentration of insulin-like growth factors and leptin which is a protein hormone secreted almost exclusively by adipocytes, are reduced ( Liefers et al., 2003; Vanholder et al., 2006). Zulu et al., (2002) show low concentration of IGF- 1 in early postpartum could contribute to an ovulation and subsequent development of cystic follicles.
28
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Literature Review
Figure 2: Endocrine sequence, types of cysts, and behavioral manifestations associated with cystic ovarian disease in cows. Inadequate secretion of LH results in ovulatory failure and formation of follicular or luteal cysts. Note that affected cows are either nymphomaniac or in anestrus (Hafez and Hafez, 2000).
29
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Literature Review
2.6.1.3.3. Par-ovarian cysts Parovarian cysts are cystic structures that do not occur in the ovaries themselves, but rather in the broad ligament close to the ovaries and the uterine tubes. Palpation or trasonography can be used to detect them, and they appear as “fluid-filled anechoic structures and are usually round or oval in shape, occur as a single cystic structure, and range from 1-5 cm in diameter (Peter et al., 2009). The walls of the cysts are characterized by a thin wall and have different sizes (Sussan and Asa, 1998). Histological appearances, the cavities of paraovarian cyst were lined by a single layer of cuboidal epithelium and the wall of cyst had smooth muscle fibers (Hatipoglu et al., 2002b). According to Gardner et al. (1948); Kennedy et al. (1993); Jones et al. (1997) cysts that are derived from mesonephric ducts are lined by low cuboidal non ciliated epithelium, and have distinct basement membrane and a muscular coat comprised of two layers. Cysts derived from mesonephric tubule are lined by cuboidal to low columnar, ciliated and non-ciliated epithelium, have a well- define basement membrane, and discernible muscular elements. Those derived from para mesonephric structure are lined by combination of ciliated and nonciliated epithelium; they have no basement membrane, and have thin muscular coat and cellswhich are larger with large nuclei in para mesonephric structure than cells in mesonephric structure. The percentage rate of paraovarian cysts recorded by Fathalla et al. (2000) was 2%, the percentage rate recorded by Chaudhari and Paul- Bokka, (2000) was 0.26%, while the condition of the disease recorded by Hatipoglu et al. (2002b); Kunbhar et al. (2003); Ali et al. (2003) and Simenew et al. (2011) in their studies were 0.72%, 15.4%,1.8% and 0.5% respectively. In Iraq, the condition recorded by Alwanet al. (1990) and Ali ( 2009) were 10.04%, 2.29% respectively.
30
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Literature Review
2.6.1.3.4 Inactive ovaries Inactive ovaries (true anestrous) are a condition in which the ovaries are quiescent without sings of cyclicity or cycle related ovarian structures. Macroscopically characterized by the ovaries, as possibly small, which are either flat or smooth or sometimes rounded if follicle are present ( Noakes, 1996; Amin, 2001). Robert (1986); Markusfeld (1987); Farin and Estill, 1993; Spain et al., (2007) demonstrated that the nutritional deficiency, particularly an energy deficit that leads to hormonal dysfunction like insufficient follicular stimulating hormone, is the primary mechanism causing inactive ovaries. The inactive ovaries can be attributed hypoplasia of hereditary (Butler and Smith, 1989). Mwaanga and Janowski, (2000) and Kinder et al., (1996) recorded that the percentage of inactive ovaries in cow can be different depending on environmental factors and nutritional conditions that resulted from poor pasture led to poor body condition which had an important role in increasing the percentage of inactive ovaries by suppressing release of gonadotropin hormones to cause folliculogenesis. Stevenson and Call (1988) mentioned that the reproductive performance is adversely affected by true an estrus, which causes prolonged intervals from calving to first estrous, first service and to conception. Microscopically, it is characterized by the lack of germinal cells, primordial follicles and absence of any stages of folliculogenesis (Amin, 2001).The percentage rate of 10.5% of inactive ovaries was reported by Fathalla, (2000). In SulaimaniIraq, Amin, (2001) recorded 22.26% of inactive ovaries of abattoir study of reproductive problems and the rate of percentage that was recorded by Ali, (2009) observed 3.81% in both ovaries.
31
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Literature Review
2.6.1.3.5. Ovarian tumor Ovarian tumors are assumed to arise from one of the three ovarian compartments: epithelium; germ cells, or ovarian stroma, including the sex cords (MacLachlan, 1987). The epithelial tumors are uncommon in most domestic animals, they may arise from the surface epithelium, the subsurface epithelial structures, or the rete ovarii (McEntee, 1990), and germ cell tumors are derived from the primitive germ cells of embryonic gonad (Talerman, 1994). The sex cordsstromal tumors are benign or malignant tumors that develop from the dividing cell population that would normally produce cells which support and surround the oocytes (Gerhenson and Wharton, 2013). The most common ovarian stromal tumors in cow are granulosa cell tumor which are ovarian stromal neoplasm developing in the soild granulose cells surrounding the ovum in the developing graafian follicle (Gerhenson and Wharton, 2013). Hatipoglu et al., (2002b) revealed that on the cut surface of cystic structures the size varied from ckick pea to walnut size, containing reddish-yellow colored fluid and sometimes with blood clot. Initially, estrogensecreting such tumors cause nymphomania. Advanced cases undergo luteinization, leading to anestrus or even masculinization. The incised uterine horn shows endometrial hyperplasia and mucometera (Blowey and Weaver, 2003). Microscopic examination shows cystic cavities lined by 3-4 layers of granulose cells; containing pink color fluid, in some sections, small rosette formation including pink color fluid like ovum referred to as Call-Exner bodies. In granulose cell tumor was accompanied by endometrial glandular hyperplasia, focal cervical squamous metaplasia and chronic vaginitis. The percentage rate of 0.06% of Ganulosa Cell tumor was revealed by Herenda, (1987) while Hatipoglu et al., (2002b) recorded 0.27% of Ganulosa Cell tumor.
32
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Literature Review
2.6.2. Pathological abnormalities of uterine tubes Abnormalities of the uterine tubes have been attributed as one of the most important causes of female infertility and sterility in all species of mammals (Alam, 1984; Lopez-Gatius ,1995). Tubal affections like endosalpingitis, pyosalpinx, hydro-salpinx, occlusion, aplasia and other micro-lesion which are not palpable per rectum and could be responsible for reproduction failure in farm animals has been reported by Khasatiya et al., (1999). According to the definition proposed by Zemjanis (1980), a repeat breeder cows refers to any cows that have failed to conceive after three or more services showing normal estrous cycles and no clinical pathologies. In repeat breeder cows, the cause of infertility might be either fertilization failure or early embryonic death Lamming & Darwash, (1998); Bage, (2002) as well as Ferreira et al., (2008) working only with repeat breeder cows, observed that these animals show some degree of oviduct occlusion. The percentage rate of uterine tube abnormalities in cows was recorded by Khasatiya et al., (1999) who recorded the fallopian tube patency testing as 16% in cow. Fathalla et al. (2000) mentioned that the oviductal lesions had 3.5%. Hatipoglu et al., (2002b); Kunbhar et al., (2003); Dorobantu, (2010); Shivhare et al., (2012) reported in their studies that the percentage of the disease was 0.81%, 60%, 9.27%, 25.2% respectively. In Iraq Amin, (2001); Ali, (2009) recorded the uterine tube abnormalities as 11.52%, 0.76%. A unilateral affection results in infertility, whereas a bilateral affection results in sterility. Ellington and Schlafer, (1993); Robert, (1986); Arthur et al. (2001); Shivhare et al. (2012) mentioned fallopian tube abnormalities to be classified into congenital and acquired.
33
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Literature Review
2.6.2.1. Congenital abnormalities of uterine tubes 2.6.2.1.1. Aplasia (Agenesis) of the uterine tubes Aplasia of the uterine tube is bilateral; where no parts of the tube is present. The reminder of the genital tract is normal indicating a segmental defect of the mullerian duct system (Kessy and Noakes, 1985). The uterine tubes rarely develop in bovine freemartins. Uterine tubes are present in femal pseudo hermaphrodite, occasionally present in true hermaphrodites (Robert, 1986; Shivhare et al., 2012). Kessy and Noakes, (1985) revealed 0.1%.
2.6.2.1.2. Segmental aplasia of the uterine tubes In this type of abnormalities the tube had a blind end near the uterotubal junction caused by the segmental aplasia. The whole length of the tube is distended (Dinc, 1990; Shivhare et al., 2012). Bilateral segmental evidenced hydrosalpinx (Duchateauand whitemore, 1978; Kessy and Noakes, 1985; Robert, 1986; Shivhareet al., 2012).The percentage rate of segmental aplasia of the uterine tube was 0.05%of (Kessy and Noakes, 1985).
2.6.2.1.3. Accessory uterine tubes There is duplication of the uterine tube, namely; the normal and the accessory one, patent with two distinct uterotubaljunctios, the accessory tube is macroscopiaclly normal (Kessy and Noakes, 1985; Mstroianni, 1999; Shivhare et al., 2012).The percentage rate of accessory uterine tube was 0.05% of (Kessy and Noakes, 1985). In Iraq recorded 1 case 0.2% of double uterine tubes by (Azawi et al., 2008a).
34
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Literature Review
2.6.2.2. Acquired tubal abnormalities 2.6.2.2.1. Salpingitis Salpingitis is inflammation of the uterine tubes which may be for some infectious cause (Ohashi et al., 1984). Grossly the salpinx were enlarged and thickened but did not reveal any changes in consistency (Shivhare et al., 2012). Tafti and Darahshiri, (2000) revealed the macroscopic lesions consisted of edematous appearance and thickening of oviduct, in some cases, adhesions between mesosalpinx and perisalpingial tissues and accumulation of yellowish green pus within oviductal lumen were observed. Hatipoglu et al., (2002b) diagnosed tuberculosis which was characterized with severe thickening of oviduct and 1-2 mm nodules scattered on the mucosal surface. In human being the term pelvic inflammatory disease (PID) or diseases of the femal upper genital tract include disease like salpingitis, oophoritis, myometritis, parametritis and infection in the pelvic peritoneum. In contrast, salpingitis only refers to infection and inflammation of the fallopian tubes in animals (Singh, 2009). Numerous studies have shown that the salpingitis and its squeals are the most infectious agents enter the uterine tube via the uterus (Runnel et al., 1965; McEntee, 1990). Salpingitis may also occur after rectal palpation of ovarium and oviduct (Ellington and Schlafer, 1993). Histopathologically, salpingitis was classified as acute cases where occlusion of the lumen occurs early as a result of swelling of the mucous folds, accumulations of pus occur. And the loss of cilia and focal desquamation of epithelium on the tips of some folds with leucocytic infiltration takes place ( Khasatiya et al., 1999). Salpingitis is characterized by degeneration and desqumation of the mucosal epithelium and lymphocytic-plasmaytic infiltrates with increase of connective tissue in the laminapropria. In the case of purulent salpingitis the lumen of oviduct was filled with extensive neutrophils accumulation and desquamated epithelial cells. 35
Chapter Two
Literature Review
Sever neutrophil accumulations and scattered lymphocytic- plasmacytic infiltrates throughout oviductal wall, and sometimes necrosis were also detected. In the salpingitistuberculosa, granuloma consist of necrotic centre surrounded by epitheloid and Langhan,s type giant cells and zone of mononuclear cells were observed in the lamina propria. Degeneration and desquamation in the lamina epithelialis were also seen (Kennedy, 1993; Hatipoglu et al., 2002b). The percentage rate of salpingitis in cows reported by many workers Hernda (1987) Chaudhari and Paul-Bokko( 2000) Fathalla et al.( 2000) Hatipoglu et al. (2002b) Kunbhar et al.( 2003) Simmenew et al.( 2011) Shivhare et al.( 2012) were 0.68%, 0.54%, 3%, 0.45%, 23%, 1.1%, 3.2% respectively. In Iraq, the observation of salpingitis was recorded by Amin, (2001) as 10.54% and the rate diagnosed by Azawi, (2008a) was 1.2%.
2.6.2.2.2 Hydrosalpinx It means distention of the tubal lumen due to accumulation of watery fluid. It occurs in association with congenital anomalies or acquired of the oviduct (Kennedy, 1993; McEntee, 1990; Mastroianni, 1999). The exact etiology of the condition is still not established although extension of inflammatory exudates from the uterus or blockage responsible for development of hydrosalpinx (Patra et al., 2012) and congenital serous secretions as another possible etiology (Ellington and Schlafer, 1993). Mastroianni, (1999) believed that the condition was the result of inflammation around the oviduct. Hydrosalpinx was accompanied with cystic bursa ovarica, paraovarian cyst and segmental aplasia of uterus ( Hatipoglu et al., 2002b). The accumulated fluid creates a hostile environment that will prevent implantation of an embryo. A hydrosalpinx does not have healthy cilia, hence, embryos that find their way into the uterine tube become trapped and may implant there, resulting infertility in unilateral condition and sterility under bilateral conditions (Shivhare et al., 2012). Miller and Campbell, (1978) claimed that hydrosalpinx result in oviductal obstruction. 36
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Literature Review
If the condition is unilateral, the fertility of the affected animal is maintained to some extent. If it bilateral, complete sterility occur ( Patra et al., 2012).Grossly, the uterine tubes were found distended of the uterine tube from the uterotubal junction to the infundibulum, which was firmly adherent to the ovarian surface ( Kessy and Noakes, 1985). Elongated and tortuous forming manycoils or straight in the mesosalpinx, the ampullary region was more affected ( Ohashi et al., 1984; Khasatiya et al., 1999). Histologically, the wall was thin, translucent, and distended with large amount of clear fluid (Shivhare et al., 2012). Mucosal atrophy and dilation of oviduct lumen and muscularis layer reveals hyalinization. Degeneration and desquamation of the epithelial lining (Hatipoglu et al., 2002b). Kennedy, (1985) elucidate histopathological lesions as an extensive multilocular cyst formation in the mucosa, with obliteration of the lumen, and in some chronically inflamed oviduct, mononuclear cell infiltrations of the substantial propria. The lamina propria which forms the framework of the folds was absent (Kessy and Noakes, 1985). The percentage rate of 0.05% of hydrosalpinx observed by Kessy and Noakes,(1985), Herenda, (1987) recorded 0.22%, Chaudhari and Paul-Bokk, (2000) on the other hand , reported 0.75%. Fathalla et al. (2000) diagnosed 3.5% of hydrosalpinx. Kunbhar et al., (2003) reported 10%, Simenew et al., (2011) recorded 0.9%, Shivhare et al., (2012) revealed 1.6% of hydrosalpinx. In Iraq, Amin, (2001) observed 0.88% of hydrosalpinx in Sulaimani district. Azawi et al, (2008a) recorded 4% and Naoman et al., (2009) reported 6.92%.
2.6.2.2.3. Hemosalpinx It refers to the present of bleeding in the uterine tube. A hemosalpinxis usually followed bilateral hematoma of the ovaries or tubal carcinoma. Furthermore, if blood flow is obstructed and gets backed up it may lead to a hematosalpinx (Fathalla et al., 2000). Hemosalpinx is characterized by thickening the wall of uterine tube due to filling with bloody discharge (Azawi et al., 2008a). 37
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Literature Review
Microscopic examination, Fibrin strands containing chorionic villi may appear as a multiple linear branching structural, large vessels filled erythrocytes separated by bands of connective tissue have been reportedby Hatipogluet al.,( 2002b). The percentage of hemosalpinx was recorded by Herenda, (1987), Fathalla et al.(2000) as 0.06%, 2% respectively.In Iraq, the diagnosis of hemosalpinx revealed by Ali, (1989), Azawi et al.( 2008a) was 0.91%, 0.7% respectively.
2.6.2.2.4. Pyosalpinx A pyosalpinx refers to accumulation of pus (suppurative exudates) in the lumen of uterine tube, when both tubes are affected with the accumulation of pus inside, the term used is pyosalpinges, the accumulated pus escape in the peritoneum and consequent peritonitis (Shivhare et al., 2012). Adhesions between the border of the mesosalpinx and neighboring structures would appear to be more commonly met with in pyosalpinx than in hydrosalpinx (Khasatiya et al., 1999). Kennedy, (1985); Roberts, (1986) and Shivhare et al.( 2012) mentioned that the pyosalpinx is less common than hydrosalpinx and follows metritis or sever uterine infection. Infections may have their origins from the prolonged salpingitis (Azawi et al., 2008a). Pyosalpinx is a consequence of pelvic inflammatory diseases (PID). Infection may start from vagina, and progress up to the cervix, uterus, and to one or both uterine tubes if not treated early (Shivhare et al., 2012). The common microbes isolated include Arcanobacterium pyogenes, E. coli and Staphylococcus arueus(Azawi et al., 2008b). According to McGavin and Zachary (2007), pyosalpinx has similar pathologic events to salpingits but is more sever, as suppurative exudates accumulates and scaring cause obstruction of lumen of tubes. Histologically, majority of pyosalpinx revealed moderate to marked infiltration of neutrophils, mononuclear cells, lymphocytes, plasma cells and hoisting mucosal and muscularis layer ( Tsianos et al., 2011). 38
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Literature Review
McEntee (1990) and Khasatiya et al., (1999) described the pathological changes of pyosalpinx as the fusion of mucosal folds, or the formation of granulation tissue, adhesion of the folds and cyst formation some of the area of surviving epithelium may undergo squamous metaplasia, bursal adhesions frequently accompany pyosalpinx. The percentage rates of pyosalpinx of 26.2%, 0.2%,0.8% were reported by Kunbhar et al.( 2003), Simenew et al.( 2011), Shivhare et al.(2012) respectively. In Iraq the observation of pyosalpinx of 0.09%, 2.69%, 2.2%, were reported by Amin, (2001) Naoman et al.( 2009), Azawi et al.( 2008b) respectively.
2.6.2.2.5. Pachysalpinx Pachysalpinx is an affection characterized by the enlargement of the whole length of uterine tube which are kinked and distorted with shape and outline (Shivhare et al., 2012). Kavani et al, (1986) in a study on repeat breeding associated with uterine tubes affections in cows and buffaloes found that salpingitis and pyosalpingitis causes atrophy-denudation of mucosal folds and moderates to massive fibrosis of tubular wall with multiple sub mucosal cyst formation inampullary region of the oviducts. Further more, they found multi-locular intramuscular cyst formation by the fusion of adjacent folds and denuded epithelial linings due to salpingitis and resultant tubal blockage.Histologically, The central lumen is completely filled with aconnective tissue mass and the distinct tubal mucosal folds are absent (Kessy and Noakes,1985) and the percentage rate of pachysalpinx recorded was 0.15% by (Kessy and Noakes,1985).
39
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Literature Review
2.6.2.2.6. Occlusion of uterine tubes The condition refers to tubes which were macroscopically normal but the lumen was completely obstructed and the tunica mucosa was replaced by a mass of proliferative connective tissue with extensive cellular infiltration (Kessy and Noakes, 1985). Vala et al., (2011) founded that the occlusion hinders the normal passage of gametes thus resulting in infertility. In the study of Azawi et al., (2008a) confirmed that the occlusions of the uterine tubes in buffalo occurred near the uterotubal junction or in the end part of isthmus. According to Kessy and Noakes (1985), occlusion could be a result of stenosis of the uterine tubes or blockage of the lumen of tubes. The percentage rate of occlusion of uterine tubes reported by Kessy and Noakes (1985), Chaudhari and Paul- Bokko (2000) and Shivhare et al., (2012) was 12.4%, 1. %, 15.2% respectively. In Iraq, the rate recorded by Ali, (1989) was 8.61% and the rate reported by Alwan, (1990) was 4.2% in cows and Azawi et al., (2008a) observed 1.5% in buffalo.
2.6.2.2.7. Cystic uterine tube
The condition is characterized by the enlargement of the uterine tube with the serosal surface covered with multiple nodules (Shivhare et al., 2012). Histologically, the normal tubal lumen is replaced by multilocular cysts, multiple intraepithelial cysts in the infundibulum and ampulla, a single mucosal cyst which caused partial occlusion of the tube (Kessy and Noakes, 1985).The percentage rate of cystic uterine tube recorded by Kessy and Noakes, (1985) was 0.25% and the rate of 4.6% was reported by Kunbhar et al. (2003).
40
CHAPTER THREE
Materials and Methods
Chapter Three
Materials and Methods
Chapter Three Materials and Methods 3.1. Abattoir samples The study was conducted on 404 samples of non-pregnant cow'sgenitalia which were collected on two days of week from anew slaughterhouse in “Qaragol” district in Sulaimani province. The data collection was carried out from February to the end of September 2014. These samples were collected randomly from different breeds, the age of the animals was from 2- 5 years and no information regarding the identity and history of the animals were included in this study. The samples were transported in a cool box to laboratory of Veterinary Teaching Hospital at the College of Veterinary Medicine in the University of Sulaimani within three hours of the collection for gross pathological examination. The pregnant genitalia were excluded and all non-pregnant genitalia were examined visually for gross morphological or pathological abnormalities.
3.2. Materials and instruments used in the study 1. Surgical gloves 2. Scalpel 3. Forceps 4. Scissors 5. Plastic container 6. Sterile disposable syringe 5, 10, 20 ml 7. Plastic bags 8. Transportation 9. Ruler 41
Chapter Three
Materials and Methods
Table (3.1) Materials, solution and stain used in the study
No.
Materials, solution
Company
and stain 1.
Vernier caliper
(WORKZONE Battery 1.55 V, LR44)
2.
Digital camera
(Sony 10.1 mega pixels)
3.
Rotary microtome
(Computerized Micrtome (Leica) YD -335, china)
4.
Microscope
(Olympus)
5.
Water bath
(Grant OLS.Cambridge, England)
6.
Formalin
35-40%(BDHchemical Ltd. Poole, England)
7.
Indian Ink
KMmo4( Dollar)
8.
Methylene blue
9.
Absolute ethyl alcohol 100% Scharlab S.L., Spain
10.
Acid alcohol
0.5-1%, Carolina Biological Com.
11.
Fresh egg albumin
Ratio 1:1, Mouzlo Dot com.
Central Drug House (P) Ltd, India
glycerin 12.
Hematoxylin and
Abbey color com.
eosin stain 13.
Paraffin wax
Melting point 56 -58C(kun lun-china)
14.
Thymol crystals
15.
Xylene
Jiangxi Baicao Pharmaceutical Co.,Ltd. (china) Klean-Strip GXY24Xylol Xylene, 1-Gallon
42
Chapter Three
Materials and Methods
3.3. Examination of the non-pregnant genitalia During the routine method of slaughter cow eachnon-pregnant reproductive tract was removed immediately and examined within 3 hours after slaughter. All ovaries and uterine tubes were carefully examined for any gross abnormalities. During gross examination, these genital organs were thoroughly examined visually and manually for the presence of various pathological abnormalities such as color, consistency, shape, size, cyst and tumors.
3.3.1. Ovaries The ovary was the first part of the genitalia to be examined and the observations were recorded. The cycle ovarian activity was assessed by the presence or absence of a current corpus luteum in either ovaries and stages of follicular growth, therefore the phases of estrous cycle was determined, following Koujan, (1974); Chaudhari and Paul- Bokko, (2000), these include, proestrous phase (prese--nce of various stage of follicular development with the regressed corpus luteum), estrus phase (presence of mature follicle), metestrus phase (presence of corpus heamorragicum) and diestrus phase (presence of corpus luteum). Each ovary of non-pregnant genitalia was carefully examined externally and internally for the presence of different types of gross pathological abnormalities like tumor, cysts, inflammatory conditions, hemorrhage and other visible changes; thenthe data were recorded in percentage as well as photographed. The size of the largest follicle and cysts on the ovary was measured using electronic Vernier caliper as in figure (3). 43
Chapter Three
Materials and Methods
Figure 3: Measurement of largest follicle cysts by Vernier caliper
Ovaries with follicles greater than 2.5 cm in diameter were considered cystic, based on the appearance the cysts were classified into follicular and luteinized cysts. Follicular cysts were more tense, thin-walled follicles while luteinized cysts were presented as thick-walled follicles. The ovarian bursa were examined carefully for the presence of adhesions. The severity of the adhesions ranged from the mild strands of connective tissues between the ovarian bursa and the ovary to severe adhesions were completely embedded in fibrous tissues. Tissue samples from affected part of ovaries (sections of approximately 1 cubic centimeter in length) are fixed in a plastic container that contains 10% buffered formalin for histopathological examination which contains (100 ml of 40% formalin in 4g sodium phosphate monobasic, 6.5g sodium phosphate dibasic and 900 ml D.W).
44
Chapter Three
Materials and Methods
3.3.2. Uterine Tubes The uterine tubal patency assessment was carried out
according to the
method of Dawson, (1958) by injecting colored fluid (Indian ink) at their junction with the uterine horns of both right and left sides of tubes, free flow of stain from the other side (fimbriated end) was considered indicative of non-obstructed tubes as in figure (4).
Figure. 4 Injecting of uterine tube by colored fluid (Indian ink) The uterine tube was classified and ranked ( Ferreira et al., 2008) according to its patency (patent; partially patent; occluded). Uterine tubes were opened by midline incision and examined for inflammation, presence of pus and other changes were recorded and tissue samples were fixed in a plastic container which contains 10% buffered formalin for histopathological examination.
45
Chapter Three
Materials and Methods
3.4. Histopathological Technique Tissue samples of ovary and uterine tube were removed from affected part with approximately (1cubic cm in size) sample was obtained, and the process was made as follows: 1.
Fixation: The tissue was fixed in 10% Neutral Buffered Formalin (NBF) about 5 days.
2.
Dehydration of tissue was performed by transferring them through graded alcohol (70%, 90%, 90%, 100%, and 100%) which was made (1hour) for exchange and the first step was (70%) over night.
3.
Clearing: The tissue was placed into an equal volume of alcohol and xylene for 2hrs, followed by 2 stages of xylene 1 hour for each one.
4.
Embedding: The tissue was embedded in melted paraffin (56-58 c) mixed with equal volume of xylene for 2 hrs, followed by 2 exchange of paraffin, 1 hour for each step.
5.
Blocking: The specimens were hold horizontally into paraffin wax and made into blocks.
6.
Sectioning: The blocks were cut by using rotary microtome (Computerized Micrtome (Leica) YD -335, china) into sections (4-6µm) thickness, and then each slide was transferred into water bath (Grant OLS.Cambridge, England) fixed at point (50-53℃).
Each slide will be fixed on glass slide which contains a light smear of mixture which consists of egg albumin and glycerin at ratio (1:1) added to a few amount of thymol crystals which play a role in preventing the growth of fungi then the slides were stored in a clean place to dry according to Carleton (1967) and Luna, (1968). The samples were examined under a light microscope (Olympus).
46
Chapter Three
Materials and Methods
3.5. Haematoxylin (Harris) and Eosin staining 1. Deparaffinizing the section was performed by 2 exchange of xylene for 30 minutes for first step then by the xylene for 15 minutes at room temperature. 2. Hydration through graded alcohol (100%, 90%, and 70%) was made 2 minutes for each exchange. 3. The sections were dipped in water. 4. The sections were stained with Harris Haematoxylin for 3 minutes. 5. Washed well in running tap water for 7 min. 6. The section was dipped in distill water for 5 minutes. 7. Differentiate in acid alcohol and lift immediately. 8. Washed well in tap water and put in Scotts water for 5 minutes. 9. Washed in tape water. 10. Stained in eosin for 15 minutes. 11. Dehydration through graded alcohol (70%, 90%, and 100%) was made 2 minutes for each exchange. 12. Clearing by using xylene 3 exchange 30 minutes for each one and dry. 13. Mounting by using Distrene- plasticizer xylene (DPX) and covering slides modified from (Luna, 1968).
47
CHAPTER FOUR
RESULTS
Chapter Four
Results
Chapter Four RESULTS 4.1. Abattoir samples A total of 404 non-pregnant genital tracts of cows were obtained from Sulaimani abattoir in Qaragol and examined at the veterinary teaching hospital of the Sulaimani from Sulaimani abattoir, Qaragol. Table (4.1) shows the distribution of these genitalia according to the reproductive status. Table (4.1): Distribution of the cow's genitalia according to the reproductive status in the Sulaimani abattoir.
Reproductive status
Number examined
Percentage %
206
51
198
49
404
100
Non-pregnant genitalia without gross pathological abnormalities(with cyclic activity)
Non-pregnant
genitaliawith
gross
pathological abnormalities of ovaries and uterine tubes
Total
48
Chapter Four
Results
4.2. Non-pregnant genitalia with gross pathological abnormalities Out of 198 non-pregnant genitalia with gross pathological abnormalities were subdivided as gross abnormalities of ovaries and uterine tubes as in table (4.2). It was found that 120 (60.6%) ovaries were affected and 78 (39.4%) of uterine tubes had different types of abnormalities.
Table (4.2) Grosspathologicalabnormalities of reproductive organs (Ovaries and Uterine tubes) ofcow’sgenitalia in the Sulaimani abattoir. Percentage Percentage Reproductive
Right
Left
Both
Total
Organs
SideNo.
SideNo.
sideNo.
No.
Ovaries
Uterine tube
Total
%
%
n=198
n= 404
64
51
5
120
60.60
29.70
21
15
42
78
39.40
19.30
85
66
47
198
100.0
49
49
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Table (4.3) Gross-pathological abnormalities of ovaries in cow's genitalia in the Sulaimani. Percentage of
Percentageto
Percentage
ovarian
the total
%
abnormalities
abnormalities
n= 120
n=198
18
15.00
9.09
4.45
1
1
0.83
0.51
0.25
Pathological
R-side
L-side
abnormalities
No.
No.
Mild-ovariobursal
9
adhesions
7
Both side No.
2
Total No.
n= 404
Sever- ovario bursal adhesion Parovarian cysts
7
6
13
10.83
6.56
3.22
Follicular cysts
24
20
44
36.67
22.22
10.89
Luteal cysts
4
1
5
4.17
2.53
1.24
Cystic corpus
13
8
22
18.33
11.11
5.44
2
2
1.67
1.00
0.50
5
8
6.67
4.04
1.98
6
5.00
3.03
1.48
1
0.83
0.51
0.25
120
100
60.60
29.70
luteum Ovarian agenesis Ovarian
3
1
Hypoplasia Ovarianhemorr hage
3
1
2
(Hemorrhagic cystic corpus luteum) Ovarian tumor
1
(Gonadoblastoma) Total
64
51
5
50
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Table (4.4) Gross-pathological abnormalities of uterine tube in cow's genitalia in the Sulaimani abattoir.
Pathological Abnormalities
R-
L-
Both
side side side
Total Percentage No.
No. No.
No.
n= 78
Percentage
Percentage
tothe total
%
abnormalities
n= 404
n= 198 Pyosalpinx
3
3
Aplasia of the
1
uterine tube Segmental aplasia
11
17
21.79
8.60
4.21
3
4
5.13
2.02
0.99
1
1
2
2.56
1.01
0.50
of the uterine tube Salpingitis
5
5
37
47.44
18.69
9.15
Occluded uterine
1
1
1.28
0.51
0.25
1.28
1.51
0.25
3
3.85
1.52
0.74
6
7.69
3.00
1.48
27
tube Accessory uterine tube (Duplication of uterine tube) Uterine tube adhesion
1 2
1 1
Hemosalpinx
2
Mesosalpinx cyst
2
1
3
3.85
1.52
0.74
2
1
3
3.85
1.52
0.74
1
1.28
0.51
0.25
78
100
39.40
19.30
Nodules on mesosalpinx Cyst on uterine tube wall
Total
4
1
21
15
42
51
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4.3. Ovarianabnormalities 4.3.1. Ovariobursal adhesion It was observed in19 cases (4.70 %), 17 cases were unilateral 9 of which were on the right and 8 on the left sides of the ovary and 2 cases were bilateral as in figure (6). In 18 unilateral adhesions slight strands connecting the ovaries with the ovarian bursa as in figure (5), one unilateral sever adhesion on left side completely enveloped the ovary as in figure (7).
Figure 5: Mild ovario- bursal adhesion.
Figure 6: Bilateral ovario-bursal adesion.
Figure 7: Complete ovariobursal adhesion in the left ovary.
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Chapter Four
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4.3.2. Para ovarian cysts (Paramesonephric cyst) Thirteen specimens (3.22 %) showed par-ovarian cyst, 7 were on the right side and 6 on the left side. The size of paraovarian cysts ranged from 2mm to 5mm in diameter. Fluctuating, spherical, oval shapes and were attached to the surface of ovary, mesovarian ligament or to the mesosalpinx as in figure (8). Histopathologically explained in figure (9)
shows a single layer of tubal-type
ciliated cuboidal epithelial cells resting on a thin layer of fibrous tissue.
Figure 8: Single para ovarian paramesonephric cyst side in the right side, attached to the mesosalpinx.
Ciliated cuboidal epithelial cells
Figure 9: Paraovarian paramesonephric cyst, the section shows a single layer of tubal-type ciliated cuboidal epithelial cells resting on a thin layer of fibrous tissue (H&E, 400X). 53
Chapter Four
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4.3.3. Follicular cysts Follicular cysts were found in 44 cases (10.89%) unilaterally, which were 24 on the right and 20 on the left side of the ovary. Grossly, the follicular cysts varied in size from 2.5 to 4 cm, and the cysts contained clear fluid, and were thin walled. Most of the cysts appear as spherical mass bulging from the surface of the ovary as in figure (10). Microscopic examination revealed in figure (11) that several layers of follicular granulosa and theca cells line the cyst which gradually blend with normal ovarian stroma. The lumen contains an esinophilic proteinaceous secretion and lacks ovum.
Figure10: Follicular cyst showing in the right side is thin-walled and contain clear fluid.
Non-lutenized granulosa and theca cells of follicular cyst
Figure11: Follicular cyst of with several layers of follicular granulosa and theca cells line the cyst which gradually blend with normal ovarian stroma. The lumen contains an esinophilic proteinaceous secretion (H&E, 100X). 54
Chapter Four
Results
4.3.4. Luteal cysts Luteal cysts were observed in 5 cases (1.24%) Cysts were 4 on the right and 1 on the left side, and were characterized by thick- wall, lutenized and became opaque with fleshy like consistency as in figure (12). On histopathological examination, follicular granulosa and theca cells with marked lutenization of cytoplasm as in figure (13).
Figure 12: Luteal cyst in the right ovary, thick-walled and lutenized.
Luteni zed granul osa and theca cells
Figure 13: Luteal cyst; the section shows follicular granulosa and theca cells with marked lutenization of cytoplasm (H&E, 400X). 55
Chapter Four
Results
4.3.5. Cystic corpus luteum These cysts were 22 cases (5.44%), were 13 on the right side and 8 on the left side unilaterally and 1 case bilaterally, the cystic corpora lutea had an average diameter from 1.5cm to 3.5cm.The diameter of cystic cavity in the center of corpora lutea varied considerably from about 0.5 to 2.2 cm. The conspicuous cavity contained a brownish fluid and the diameter of cavity is 1.7cm in some case as in figure (14). One case had two cystic corpus luteum as figure (15). In figure (16) and (17) microscopically showed a zone of a thin layer of fibrous tissue between luteal cells and the cystic cavity.
Figure 14: Cystic corpus luteum. The diameter of cavity is 1.7cm.
Figure 15: Two cystic corpora lutea. 56
Chapter Four
Results
Lumen of cyst
Figure 16: Cystic corpus luteum, (H&E, 100X).
Cavity of cyst
Luteinized cells
Thin layer of fibrous tissue separates luteinized cells from lumen
Figure 17: Cystic corpus luteum, Zone of a thin layer of fibrous tissue between luteal cells and the cystic cavity (H&E, 400X). 57
Chapter Four
Results
4.3.6. Ovarian agenesis The agenesis was recorded in two cases (0.50%) which were found on the left side of the ovary associated with uterus unicornus of the genital tract as in fig (18).
Figure 18: uterus unicornus and ovarian agenesis.
4.3.7. Ovarian hypoplasia This study revealed 8 cases (1.98%) of l ovarian hypoplasia. 3 cases were in the right side and 5 cases in the left side of the ovary was found small and had a smooth surface and a firm consistency as in figure (19). The histopathological, sections figure (20) showed lack of ovarian follicles and oocytes, which instead are replaced by bands fibrovascular stroma.There are, however, few primoridal follicles and figure (21) section show few inactive primordial ovarian follicles and related sex cords,which indicate arrest of embryologic development of the ovary.
58
Chapter Four
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Figure 19: Showing the total ovarian hypoplasia in left side small, smooth surface and lack of ovarian follicles.
59
Chapter Four
Results
Figure 20: Ovarian hypoplasia, the section shows lack of ovarian follicles and oocytes, which instead are replaced by bands of fibro vascular stroma.There are, however, few primoridal follicles (H&E,100X).
Primitive sex cords
Figure 21: Ovarian hypoplasia. The section shows few inactive primordial ovarian follicles and related sex cords, which indicate arrest of embryologic development of the ovary (H&E, 400X). 60
Chapter Four
Results
4.3.8. Ovarian hemorrhage (Hemorrhagic cystic corpus luteum) It was observed in 6 specimens (1.48%), 3 cases unilaterally in the right side and 1in the left side and 2 cases in bilaterally of the ovary, the cysts had a thick highly vascular wall associated with enlargement of the ovary without follicles or CL. In cut section, brownish material occupied the antral cavity as in figure (22). Microscopically figure (23) the cystic lesion contains scattered spots of hemorrhage close to the lumen, the wall of the cyst is lined by numerous layers of luteneized granulosa and theca cells, with a thin rim of fibrous tissue separating it from the lumen.
Figure 22: Showing the haemorrhagic cyst.
61
Chapter Four
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Spots of hemorrhage
Lutenized granulosa and theca cells
Figure 23: Hemorrhagic cyst. The cystic lesion contains scattered spots of hemorrhage close to the lumen. The wall of the cyst is lined by numerous layers of lutienzed granulose and theca cells (H&E, 100X).
4.3.9. Ovarian tumor (Gonadoblastoma) Only single case of ovarian tumors (Ovarian gonadoblastoma) was observed (0.25%) in the right side of the ovary. Basing on the gross and microscopic features was considered benign tumor which had spherical, firm, 10 cm mass as in figure (24). The histopathological sections figure (26) also showed dual population of cells sex-cord stromal cells form micro-follicular formations in form of tubules lined by an outer layer of small cells resting on a thick layer of basement membrane and reveal calcification, and aggregates of larger cells with vesicular nuclei (germ cell tumor component), figure (25) showed a tumor composed of round nests of small tubular formations. Dark blue spots represent calcifications.
62
Chapter Four
Results
Figure 24: Showing a single case of ovarian tumor (Gonadoblastoma), had spherical, firm, 10 cm mass.
63
Chapter Four
Results
calcification
Figure 25: A tumor composed of round nests of sl tubular formations. Dark blue spots represent calcification ( H&E 100X).
Microfollicles composed of sex cord stromal cells
calcifications
Germ cell tumor cells
Figure 26: Ovarian Gonadoblastoma, dual population of cells, sex-cord stromal cells forming micro-follicular formations in form of tubules lined by an outer layer of small cells resting on a thick layer of basement membrane, and aggregates of larger cells with vesicular nuclei (germ cell tumor component) (H&E, 400X).
64
Chapter Four
Results
4.4. Uterine tube abnormalities 4.4.1. Pyosalpinx 17 cases (4.21%) of pyosalpinx were observed; 6 cases were unilateral, 3 in the right side and 3 in the left side of uterine tube and 11 bilaterally as in figure (27), was found thicken wall accumulated pus in the luminal tube following incision. Microscopically, with figure (28) show a heavy inflammatory cell composed of of neutrophils associated with a notable degree of tissue edema.
Figure 27: Pyosalpinx of uterine tube, thicken wall accumulated pus in the luminal tube.
65
Chapter Four
Results
Collection of neutrophils and red blood cells in the lumen of uterine tube
Figure 28: Pyosalpinx shows a heavy inflammatory cell composed of neutrophils associated with a notable degree of tissue edema (H&E, 400X).
4.4.2. Aplasia of the uterine tube This study revealed 4 (0.99%) cases of uterine tube, 1of them was in the right side and 3 in the left side, as in figure (29).
Figure 29: Uterus unicornus and aplasia of uterine tubes
66
Chapter Four
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4.4.3. Segmental aplasia of the uterine tube Two cases (0.50%) of segmental tubal aplasia figure (30) were observed accounting for 0.5% of the total non-pregnant genitalia involved in the current study and for 1.01% of the total gross pathological abnormalities recorded Table (4.4)
Figure (30): Segmental aplasia in the ampulla of right side of the uterine tube.
4.4.4. Salpingitis Salpingitis was found in 37 cases (9.15%), were 10 cases observed unilaterial and 27cases bilaterally, grossly consisted of swelling and thickening of uterine tube. Histopathologic examination showed in figure (31) there is denudation of mucosa resulting from inflammatory cell infiltrate of lamina propria composed of chronic inflammatory cells in form of lymphocytes.
67
Chapter Four
Results
Lymphocytes infiltrating soft tissue of uterine tube
Figure
31:
Chronic salpingitis, it
shows
infiltration
of mononuclear
inflammatorycells mainly lymphocytes within the lamina propria (H&E, 400X).
4.4.5.Occludedd uterine tube Occluded uterine tube revealed (1)case (0.25%), was characterized by partial patency upon insufflations with colored fluid to the tubal in the right side as in figure (33), is characterized by presence of a single cyst on uterine tube.
68
Chapter Four
Results
Fibrous obliteration of lumen
Figure 32: Occlusion of the uterine tube, longitudinalsection shows obliteration of lumen by fibrous tissue which lack epithelial lining. (H&E,100X).
4.4.6. Accessory uterine tube (Duplication of uterine tube) In this study one case (0.25%) of partial duplication of uterine tube was observed, which was about 6cm from the uterotubal junction and extended distally for a distance of 4cm that was found in right side of tracts as in figure (34).
Figure 33: Showing the duplication of uterine tube
69
Chapter Four
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4.4.7. Uterine tube adhesion Three cases (0.74%) of uterine tube adhesion were found, which were 2 in the right side and 1 in left side of tube which revealed adhesion between mesosalpinx and perisalpingial tissues, as in figure (35).
Figure 34: Uterine tube adhesion, adhesion between mesosalpinx and perisalpingial tissues.
70
Chapter Four
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4.4.8. Hemosalpinx Hemosalpinx was found in 6 cases (1.49%), 2 of them were unilaterally and 4 bilaterally, characterized by swelling of uterine tube filled with bloody discharge as in figure (36). The histopathologically section, in figure (37) shows the uterine tube with stromal hemorrhage in the core of the villus like folds of epithelium.
Figure 35: Hemosalpinx; swelling of uterine tube filled with bloody discharge
Stromal hemorrhage in soft tissue of uterine tube
Figure (36) shows the uterine tube with stromal hemorrhage in the core of the villus like folds of epithelium. 71
Chapter Four
Results
4.4.9. Mesosalpinx cyst Three cases (0.74%) of mesosalpinx cysts were found on mesosalpinx, 2 were on the right side and 1 on the left side of mesosalpinx as in figure (38). The diameter of these cysts were generally 0.5- 0.7 cm. Microscopically , figure (39) describes themesosalpinx cyst, which is called paramesonephric cyst and is a remnant of paramesonephric (Mullerian)duct system.
Figure 37: Mesosalpinx cyst, which is 0.5-0.7 cm in diameter.
Figure 38: Mesosalpinx cyst; describes the cyst, which is called paramesonephric cyst and is a remnant of paramesonephric (Mullerian) duct system (H&E, 100X).
72
Chapter Four
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4.4.10. Nodules on mesosalpinx Presence of 3 specimens (0.74%) the nodules on mesosalpinx, were found 2 on the right side and 1on the left side of mesosalpinx as in figure (40).
Figure 39: Nodule on mesosalpimx in the left part of genital tract.
4.4.11. Cyst on uterine tube wall (paratubal paramesonephric cyst) One case (0.25%) of cyst related to the wall of uterine tube as in figure (41). Microscopic examination, figure (42) revealed paratubal paramesonephric cyst (also called Hydatic of Morgangni), showed single layer of tubal type ciliated columnar epithelium resting on fibrous tissue of the normal uterine tube.
Figure 40: Showing the cyst on uterine tube wall in the right side. 73
Chapter Four
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Normal uterine tube epitheliu m
Ciliated columnar epithelial cells
Figure 41: Cystic on uterine tube, paratubal paramesonephric cyst also called (Hydatid of Morgangni), single layer of tubal type ciliated columnar epithelium resting on fibroustissue of the normal fallopian tube (H&E, 400X).
74
CHAPTER FIVE
Discussion
Discussion
Chapter Five
Chapter Five Discussion Pathological abnormalities of the genitalia play an important role in animal breeding either by causing infertility or sterility, and thus reproductive problems among cows have a direct influence on the nutritional needs of people as well as on the economic status of the region.Many cows with reproductive problems and low milk production have been sold or sent to slaughterhouses, so the present abattoir study has provided useful information on the types and prevalence of gross pathological abnormalities of ovaries and uterine tubes of cows in Sulaimani region. About 198 genitalia 49% showed one or more abnormalities as in table (4.1).These results are lower than the results mentioned by Kunbhar et al. (2003); Azawi et al.(2008a) which were 65%, 53.3%, and higher than the results reported by Chaudhari and Paul- Bokko, (2000); Fathalla et al. (2000); Hatipoglu et al. (2002b); Simenew et al. (2011) which are 13.57%, 13.5%, o.81%, 22.3% respectively. This variation may be attributed to that the percentage of gross abnormalities and lesions of reproductive tracts appear to vary from country to country, from population of animal to another population of animal , from year to year and from breed to breed ( Herenda, 1987; Alwan et al., 1990; Hatipoglu et al., 2002).
5.1. Pathological abnormalities of ovaries The total percentage of ovarian abnormalities 29.70% from the total reproductive tracts is higher than the results of other studies by Fathalla et al.(2000); Durgut et al. (2003) ; Ali, (2009) and Simenew et al. (2011) which were 10.5%, 23.84%, 4.5%, 3.81% respectively, and lower than the observation mentioned by Kunbhar et al. (2003) which was 49.2%.These variations between the 75
Discussion
Chapter Five
percentage are due to many factors such as hereditary origin, high milk production, high nutritional deficiency and inadequate energy intake, sample size, geographical variation and season indicated by Robert (1986). He also mentioned the factors such as twinning, dystocia, retained placenta, metabolic disorder and age of cow, which play a role in post partum uterine infections which contribute to variations of percentage of lesions. Hussain (1989) and Lewis (1997) reported that lack of sanitary precautions in artificial breeding of cows might predispose to variety of specific and nonspecific microorganisms. The percentage of total of ovarian bursal adhesions reached 4.70 %. The lesions ranged from slight connective tissue strand to sever extensive lesions and this is in agreement with Arthur ( 2001). The majority of the cases are found in the right ovary. The result was higher than the result of Chaudhari and Paul- Bokko, (2000); and Simenew et al., (2011) which were 2.9%, 2.5% respectively, while lower than the result mentioned by Fathalla et al. (2000); Ali, (2006) which were 8%,7.27%, and nearly resemble of Kunbhar et al. (2003) which was 4.6%. In Iraq, lower than this result was reported by Azawi et al. (2008a) and Rahawy, (2009) which were 6.4%, 19.04% respectively, and higher than the result of Alwan, (1998) was 3.4% and nearly resemble with Ali, (2009) which was 4.19%. In this study, the most cases of adhesions associated with the other pathological conditions which are in agreement with Bondurant, (1999); Fathalla et al. (2000). They mentioned that extreme adhesions have probably resulted from complications of parturition that include retained fetal membranes and endometritis; mild adhesions could result from non-infectious conditions such as physical trauma as a result of rough manipulation.
76
Discussion
Chapter Five
Enucleation of cyst may also result in the formation of these adhesions. Localized abdominal infections such as omphalophlebitis and peritonitis are also suggested to cause this condition (Noakes et al., 2002). Paraovarian cysts in the present study reached 3.22% from the total reproductive tracts, and the percentage is higher than the results reported by Chaudhari and Paul- Bokko, (2000);
Fathalla et al. (2000); Hatipoglu et
al.,(2002b); Ali, (2006) and Simenew et al. (2011) which were 0.26%, 2%, 0.72%, 1.81%, 0.5% respectively and lower than the rate reported by Kunbhar et al. (2003) which was 15.4%. In Iraq, this rate is higher than the value of Ali et al., (2003); and Ali, (2009) which were 1.8%, 2.29% respectively and lower than the rate of Alwan, (1990) and Azawi et al. (2008a) which were 10.04%, 4.4% respectively. This result is in agreement with Morris et al. (1999) which is observed on mesovarian and mesosalpinx. They are grossly as visible as translucent vesicles on the broad ligament and 2mm to 5mm. Their presence is very seldom of pathological consequence unless they impinge on the uterine tube. All paraovarian cysts are benign,with no negative effects on reproduction and fertility (Arthur et al., 2001; Peter et al., 2009). It is one of the congenital anomalies correlated to mesosalpinx and does not interfere or affect the uterine tube (Arthur et al., 2001). On histopathological examination of paraovarian cysts in this study agreed with Hatipogluet al. (2002b), which showed a single layer of tubal-type ciliated cuboidal epithelial cells resting on a thin layer of fibrous tissue. Cystic ovarian diseases are important causes of infertility in cows by causing nymphomania and anoestrus. Cystic follicles are observed during this study having diameters exceeding 2.5 to 4cm in size containing variable quantities of fluid in their antrum. The right ovary is more affected, and cystic ovaries are structures which usually persist on the ovary in the absence of a corpus luteum, and the total 77
Discussion
Chapter Five
percentage of follicle cysts reached 10.89%, the rate of the percentage was lower than of Herenda, (1987) which was 14.9% and nearly resembled the result of Kunbhar et al. (2003) which was 10.8%. The prevalence in the present study is higher than that of other previous reports recorded by Ellwisky, (1976); Alam, (1984); Fathalla et al. (2000); Chaudhari and Paul- Bokko, (2000); Hatipoglu et al. (2002b); Ali et al. (2006); Simenew et al., (2011) which were 2.2%, 4.5%, 7%, 3.35%, 1.88%, 2.72% and 3.3% respectively. In Iraq, the rate was higher than the observation reported by Ali, (2004); Azawi et al. (2008a); Ali, (2009) which were 2.67%, 1.5%, 2.67% respectively, Variations in the percentage are the result of many factors such as breed, age, level of milk production, feeding, management and exercise (Noakes et al., 2002). In dairy cattle cystic ovaries prolongs the postpartum interval to first estrous and conception (Kesler and Garverick, 1982). It is speculated that hormonal dysfunction such as insufficient luteinizing hormone prior to the time of ovulation, is the primary mechanism. Microscopical finding in this study demonstrated several layers of follicular granulosa and theca cells lining the cyst which gradually blend with normal ovarian stroma. The lumen contains an esinophilic proteinaceous secretion and lack of ovum, and this is in agreement with Miller and Campbell, (1978); Ali et al. (2006); Hatipoglu et al. (2002b). Another type of cystic ovarian disease observed in this study is luteal cyst. Its percentage reaches 1.24% the right side is more affected, which is thick- walled and lutenized and became opaque with fleshy like consistency. They represent anovulatory follicles, this rate of percentage was lower than the rate reported by Durgut et al. (2003); Kunbhar et al. (2003) which were 10.7%, 7.7% respectively. In Iraq, it was higher than the result reported by Azawi, et al. (2008a); Ali, (2009) which were 0.2%, 0.76%, and was lower than the result observed by Majeed et al., (2004) which was 72.7%. Histopathological of luteal cyst showed follicular granulosa and theca cells with marked lutenization of cytoplasm, this is in 78
Discussion
Chapter Five
agreement with Ali et al. (2006); Fathalla et al.(2000) and also mentioned that the luteinized ovarian cysts were experimentally induced by testosterone injections. The most common lesion in the ovary was cystic corpus luteum which reached 5.44%. The corpora lutea had an average diameter from 1.5cm to 3.2 to 3.5cm, the conspicuous cavity contained a brownish fluid in some case, and one case had two cystic corpus luteum, the right side is more affected. This result is higher than previous results observed by Fathalla et al. (2000) and Hatipoglu et al. (2002b); which were 2%, 1.2% respectively.In Iraq, the rate in present study is lower than Azawi et al. (2008a) which is 0.18%.The difference might be due to breed species variation and hormonal imbalance (Ali et al., 2006). Because cystic corpora lutea are found in cows that are normally cycling or pregnant, they are considered to be a normal stage or variation of CL development (Kahn, 2010). Cystic corpora lutea arise as a consequence of premature closure of the ovulation site hence forming a central cavity (Jones et al., 1997). They have no effects on the cow's fertility (McEntee, 1990; Acland, 2001). Cystic CL occur spontaneously, when follicles become luteinized without ovulation (Pineda and Dooley, 2003). Microscopic examination on this study shows the zone of a thin layer of fibrous tissue between luteal cells and the cystic cavity that is in agreement with Hatipoglu et al. (2002b) and McEntee, (1990). Congenital lesions of the ovaries are rare. Ovarian agenesis can affect one or both ovaries and the associated tubular genitalia may be absent or underdeveloped (Arthur et al., 2001). The percentage observed in present study is0.50%, which is associated with uterus unicornuas of the genital tract,while Fincher (1946) reported three cases accompanied by an infantile genital tract and an absence of cyclical behavior. However there is no report in recent study. The ovarian hypoplasia is recorded as 1.98% in the present study. This value is higher than the finding of Herenda ( 1987) which is 0.11% while lower than the 79
Discussion
Chapter Five
findings of Chaudhari and Paul-Bokko, ( 2000); Kunbhar et al.,( 2003) and Peng et al.( 2011) which are 2.20% and 4.6%, 21.6% respectively. This variation in ovarian hypoplasia may be due to hereditary characters and other environmental factors such as body condition and the percentage of gonadal hypoplasia can be reduced by using only animals (both male and female) with normally developed sexual organs as breeding stock.(Herenda, 1987; Bearden et al., 2004). According to Settergren (1964a)the total ovarian hypoplasia accompanied by small, smooth surface and lack of ovarian follicle, and Hafez and Hafez(2000) described the common manifestations of cows with hypoplastic ovaries are failure of
estrous
cycles
andpoorly
developed
secondary
sex
characteristics.
Histopathologically in present study shows few inactive primordial ovarian follicles and related sex cords,which indicate arrest of embryologic development of the ovary that is in agreement with McEntee (1990) that the number of primordial follicles varied considerably from one area of the cortex to another in normal ovaries. The percentage of ovarian hemorrhage reaches 1.48 % this result is higher than the percentage observed by( Fathalla et al.,2000) whichwas 0.5%, while the result is less than the result reported by (Kunbhar et al., 2003) whichwas 3.0%. In Iraq, the percentage rate in present study is higher than the resultreported by Ali (2009) which was 0.38%.Irland et al. (1980) and Fathalla et al. (2000) mentioned that the condition is different from corpora hemorrhgia of recent ovulation as a blood-filles crater-like depression and the swelling was grossly visible, the ovarian surface felt smooth and fluctuating on digital manipulation. Bearden et al. (2004) described that the result of bleeding during the process of ovulation or physical trauma resulting from manipulation of the ovaries through the reproductive examination. According to McEntee (1990) mentioned that the relationship may
80
Chapter Five
Discussion
exist between the level of milk production and the tendency toward fatal hemorrhage with the most severe hemorrhage occurring in the highest producers. Microscopically, the result agreed with McEntee, 1990 and Ali, 2009which represented by the hemorrhagic cyst, that contains scattered spots of hemorrhage closeto the lumen. The wall of the cyst is lined by numerous layers of lutienzed granulose and theca cells. The percentage rate of ovarian Gonadoblastomas reach 0.25% from the total gross abnormalities, and it is less than the results found by Macmillian et al. (1984) which were observed in two casesof two immature heifers.This observationhas not been reported previously by Iraqi researchers. Ovarian Gonadoblastoma (dysgeneticgondoma) is a benign tumor, and is a mixture of germ cell tumor and sex-cord stromal tumor, which occur more commonly in human. It usually occurs in individuals with abnormal sexual development and indeterminate gonads (Kennedy and Miller, 1993;Donald, 2002).The basic pattern of gonadoblastoma may be altered by three processes: hyalinization, calcification and overgrowth by neoplastic germ cell element (Donald, 2002). Histopathological study of this condition agreed with Donald ( 2002) whomrevealed thatthe lesion of thistumor composed of round nests of small tubular formations and it is characterized bydual populations of sexcord stromal cells forming microfollicular formation in the form of tubules lined by an outer layer of small cells resting on a thick layer of basement membrane, and aggregates of larger cells with vesicular nuclei germ cell surrounded by ovarian stroma. Calcification is prominent.Theyoccur in all age groups but their percentage increase with age. Majority of the cases reported are unilateral and benign in nature (Jones et al., 1997). In the mare and the cow where the tumors are frequently reported and effects extensively studied, active steroid secretion has been documented, and progesterone, oestrogen, testosterone, and inhibin are secreted by the tumor to varying degrees (Jones et al.,1997; Maclahlan and Kennedy, 2002). The pathophysiology of gonadoblastomas is gonadal differentiation starts during of 81
Discussion
Chapter Five
gestation and depends on sex chromosome of fetus, errors in this complex multistep process of sexual differentiation may cause dysgentic gonads (Donald, 2002).
5.2. Pathological abnormalities of uterine tube Ahmad et al., (2003) claimed that in order to reach a precise result about percentages of the abnormality of uterine tube (congenital or acquired), gross examination, injection of dye into the uterine tube for detection of obstructions, and histopathological studies are important for obtaining correct results on uterine tube disorders. Diseases of the uterine tubes are represented by pyosalpinx which are characterized by dilation of the oviduct due to a thick yellowish fluid. The percentage of the condition reaches 4.21% from the total reproductive tracts, and the result is lower than the rate of Kunbhar et al. (2003) which was 26.2% and higher than the rates of Simenew et al.( 2011) and Shivhare et al.( 2012) which were 0.2%, 0.8% respectively. In Iraq, the rate of percentage in present study is higher than reported by several workers (Amin, 2001; Azawi et al.,2008b; Naoman et al.,2009) which were (0.09%; 2.2%,2.69%) respectively. The result is agree with McGavin and Zachary (2007) that pyosalpinx has similar pathologic events to salpingitis, but it is more sever, as suppurative exudates accumulates and scaring cause obstraction of lumen of tubes. Pyosalpinx occurs following ascending uterine infections and this agree with the suggestion of Robert (1986) and Kennedy and Miller (1993). Actinomyces pyogences, E.coli and Staphylococcus aureusare the most common causes of pyosalpinx in cattle (McEntee, 1990; Azawi et al., 2008b; Naoman et al., 2009). Microscopic appearance of pyosalpinx in present study is in agreement with McEntee (1990) that a heavy inflammatory cell reaction is composed of a mix of neutrophils and lymphocytes associated with a notable degree of tissue edema. 82
Chapter Five
Discussion
Aplasia of the uterine tube, in this study is revealed as 0.99% and in three cases it was unilaterally, represented by uterus unicornuas which was associated with incomplete development of the genital tract of cow's genitalia, this value in present study was nearly in agreement with the value of Kessy and Noakes( 1985) which was 0.1%. Heinze, (1964) reported a case of ovarian and tubal agenesis in a calf, while in present study the aplasia of uterine tube is associated with cases of ovarian agenesis which are associated with uterus unicornuas of cows, genitalia. In this study, segmental aplasia of the uterine tube reaches 0.50% which were identified unilaterally . This rate of percentage is higher than the finding by Kessy and Noakes, (1985) which was (0.05%), the tube had blind sac near the ampulla region, while Tanabe and Almquist, (1967) recorded two cases of congenital malformation of uterine tubes in heifers that they had a total absence of both infundibulum. Salpingitis have an percentage of 9.15%, which were observed more bilaterally than unilaterally, grossly consisted of edematous appearance and thickening of oviduct. The percentage rate of salpingitis in cows, in present study was higher than 0.68%, 0.54%,3%,0.45%, 1.1% and 3.2% as reported by Hernda (1987), Chaudhari and Paul-Bokko (2000), Fathalla et al.( 2000), Hatipoglu et al.(2002b),Simmenewet al.( 2011) and Shivhare et al.( 2012) respectively, and lower than 23% as reported by Kunbhar et al.(2003). In Iraq, the observation of salpingitis was lower than the recorded by Amin, (2001) which was 10.54% and higher than the rate diagnosed by Azawi, (2008a) which was 1.2%. In this study, along with salpingitis adhesions, mesosalpingitis with adhesions were also found; this is agreement with Ali (1989) that referred thesalpingitis was associated with ovaroburasl adhesion, and I also agree with Ali (1989) that the salpingitis is very frequently associated with pathological conditions in the ovary, the most common lesion is that of retained and cystic corpus luteum, so in this study in most cases of salpingitis associated with ovarian cysts such as follicular cyst and cystic corpus 83
Discussion
Chapter Five
luteum. The change of mesosalpingitis and adhesions with perisalpingial tissue may cause infertility by restriction the oviductal movements (Hatipoglu et al., 2002b). Salpingitis was the most common lesion developed as sequels to an obstetrical problems (Herschler and Lawrwnce, 1984). McEntee,(1990) stated that cows failed to conceive had chronic suppurative salpingitis orendometritis. Histopathologic examination, chronic salpingitis which is in agreement with Hatipoglu et al.(2002b) showed erosion of lining mucosal layer caused by inflammation and explained the chronic salpingitis, and there is denudation of mucosa resulting from inflammatory cell infiltrate of lamina propria composed of chronic inflammatory cells in form of lymphocytes. Kessy and Noakes, (1985) mentioned that the salpingitis in cows is characterized by masses of connective tissue with extensive cellular infiltration replacing the mucosa and resulting in a complete obstruction of the lumen. Occludedd uterine tube revealed 0.25% that were identified in this survey by attempted tubal insufflations would not have been detected on rectal palpation, this condition is characterized by presence of a single cyst on uterine tube which caused partial occlusion. Even close visual inspection did not reveal pathological signs of thickening or enlargement. The percentage being lower than the percentage recorded by several authors ( Kessy and Noakes, 1985 ; Chaudhari and PaulBokko, 2000; Shivhare et al., 2012) were12.4%, 1.%, 15.2% respectively. In Iraq, the rate of percentage in this study is lower than the rate recorded by Ali, (1989) which was 8.61% and the rate reported by Alwan, (1990) which was (4.2%) and Azawiet al. (2008a) observed 1.5%. Beck and Boots, (1974) and Azawi et al. (2008a) described that uterine horn of cows is confluent with isthmus, it is thus more likely to allow the ascending of infection from the uterus to the tube; persistent chronic or acute of infection can result in salpingitis with subsequent occlusion of the uterine tube.Microscopically in this study, shows obliteration of lumen by fibrous tissue which lack epithelial lining, while the section in complete occlusion that described by Kessy and Noakes 84
(1985) that the lumen was
Discussion
Chapter Five
completely obstructed and and the tunica mucosa had been replaced by a mass of proliferative connective tissue with extensive cellular infiltrations. Accessory uterine tube (Duplication of uterine tube) in this study observed (0.25%).There is duplication of the uterine tube observed the normal and the accessory one; the recorded rate in this study was slightly higher than that reported by Kessy and Noakes (1985) which was 0.05% while similar with Azawi et al. (2008a) in Iraq was 0.2%. This is agreement with McEntee (1990) that the accessory of uterine tube is never unite with the principal funnel; they end blindly at uterotubal junction. Uterine tube adhesion revealed 0.74% which represented by adhesion between mesosalpinx and perisalpingial tissues. This percentage was higher than that reported by Hatipoglu et al., (2002b) which was 0.09%, They, furthermore, mentioned that this pathological lesion was accompanied by adhesions between ovary and periovaial tissue and purulent salpingitis. In Iraq, the rate of the present study was lower than what was reported by Azawi et al., (2008a) which was 1.7%. The percentage ofhemosalpinx in this study recorded 1.48%it is higher than thepercentage of Herenda (1987) which was 0.06% while it is lower than the percentage reported by Fathalla et al.(2000) which was (2%). Hemosalpinx is characterized by thickening the wall of uterine tube due to filling with bloody discharge, which is in agreement with Azawi et al. (2008a). In Iraq the percentage of present study is higher than the percentage of (Ali, 1989; Azawi et al., 2008a) which were 0.91% and 0.7% respectively. The histopathologically section, is in agreement with Azawiet al., (2008a) which showed the uterine tube with stromal hemorrhage in the core of the villus like folds of epithelium. Nodules on mesosalpinx revealed 0.74%. Feng et al., (2013) mentioned in a woman case report that the simultaneous osseous metaplasia nodules of thesubmucosaand mesosalpinx after first trimester abortion that result in vaginalbleeding and
85
Discussion
Chapter Five
infertility. McEntee, (1990) described that nodules are found occasionally in the mesosalpinx of queen, bitch, cow, and mare, relatively few of the nodules are large enough to be recognized readily on gross examination. Mesosalpinx cyst showed an percentage 0.74%. The cysts found on mesosalpinx were (0.5-0.7) cm in diameter. Microscopically, present study describes a cystcalled paramesonephric cyst which is a remnant of paramesonephric (Mullerian)duct system.Schlarfer and Miller, (2007) state that these cysts do not appear to have any effect on fertility but cyst formation may be associated with hormonal dysfunction, and Tsumura et al., (1982) reported that cyst formation in the uterine tube was most frequently seen in the fimbriae in cows and in the mesosalpinx in sows, and they also describe that the sex hormones and oviductal constrictions might cause oviduct cysts. In Turkey, a study reported by Sevimil et al.,(2012) observed that oviduct cyst depend on the value of high oestrogen concentration during oestrous phase of the sexual cycle in water buffalo. Cyst on uterine tube wall reveals 0.25% of cyst related to the wall of uterine tube. The percentage of present study is similar of the percentage observed by Kessy and Noakes (1985) whichis 0.25%and is lower than the value of 16.5%, and 4.6%which
is reported by
Tsumura et al.(1982) and Kunbhar et al.( 2003)
respectively. The result agrees with McEcntee (1990),who states that these cysts are so close to or adjacent to the uterine tube, in these cases, a differential diagnosis can be established by injecting India ink into the lumen of the tube. He, furthermore, mentions that a large cyst may compress the tube, so that increased pressure is necessary for passage of the ink around the cyst. Kessy and Noakes (1985) that a single mucosal cyst which caused partial occlusion of the tube.Microscopic examination, that was paratubal paramesonephric cyst also called Hydatid of Morgangni,showed single layer of tubal type ciliated columnar epithelium resting on fibrous tissue of the normal uterine tube this is agreement with McEntee, (1990).
86
CHAPTER SIX
Conclusions and
Recommendation
Chapter Six
Conclusions and Recommendation
Conclusions and Recommendation Conclusions 1. The ovarian tumor (Ovarian Gonadoblastoma or dysgenetic Gonadoma) is the pathological abnormality of ovary that has not been reported previously in cows in Iraq. 2. The total percentage of gross pathological abnormalities of ovaries and uterin tubes in slaughtered non-pregnant cows in Sulaimani reached to 49 %. 3. The follicular cystic ovaries are the most common pathological abnormalities of ovaries in Slaughtered non-pregnant cows in Sulaimani region. 4. Salpingitis is the most common pathological abnormality of uterine tubes in slaughtered non-pregnant cows in Sulaimani region.
87
Chapter Six
Conclusions and Recommendation
Recommendation 1. Further research is required to determine the effects of diseases of ovaries and uterine tubes on the cow's fertility.
2. Field animal health workers should be encouraged to carry out routine on-farm clinical investigations of reproductive defects. This will help in timely institution of treatment and control measures where possible or hasting the culling of cows that are not economically viable to maintain.
3. Increasing the awareness and hygienic routine particularly of responsibility of cow farmers, veterinarians at the time of calving and considerable attention should be given to sanitation, prior to, during and after calving,
4. Infusing with antibiotics and mucolytics intra uterine by pressuring inflation, may sometimes be beneficial for the tubal patency.
5. Conducting the microbiological studies of ovarian, uterine tube and uterine abnormalities in cows.
6. Conducting the histopathological studies of uterine abnormalities in cows.
88
References
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