2 Etiology and Pathogenesis

Transcript

A warm welcome to you all,

In the last sessions, we have seen the types and incidence of uterine infections as well as, the clinical signs and various degrees of effection of these uterine infections. In this session, I am going to deal with the Etiology and Pathogenesis of Endometritis. This is one of the important features, we have to know before attempting any treatment or prevention. In that way, this Aetio[1]pathogenesis is very important in the Endometritis lesson. If you see the causative factors, Endometriosis is a multifactorial disease, so only it is having importance. Determining its causative risk factors has great potential as a source of information, that must be considered for the treatment and prevention of endometritis. The major causative risk factors for the incidence of uterine infections are Extrinsic factors as well as Intrinsic factors.

The Extrinsic factors include the calving season as well as the environment and nutrition, as far as the season is concerned, we all know that the rainy season is more vulnerable for most of the infections, the general health status of the animal will be decreasing during the rainy season, a lot of endemic diseases are coming into being during this rainy season. And the environment, if it is having endemic infectious agents then it is also a problem for this utility infections.

Nutrition’s very very very very important:

The Negative energy balance usually happens during the postpartum period,

The Protein deficiency or excess,

Vitamin deficiency especially A, B, C, and E,

Mineral deficiency especially Selenium.

Then comes the Intrinsic factors:

Dystocia and Retention of the placenta (ROP) is a very important thing. How do you handle the animal during the parturient period, is very important and is one of the Intrinsic factors: Inappropriate and indiscriminate handling of the uterine environment during Dystocia and manual removal of retained placenta, is one of the predisposing factors for uterine infections. The Incidence of twinning, how twinning is going to affect or cause the endometritis, because of Dystocia and Retention of the placenta, there are more incidences of chances for dystopia during twinning in case of cattle.

Metabolic disorders: this is again going to be linked with nutrition, Hypocalcemia, Ketosis, all these conditions will pave the way for the entry of uterine pathogens.

After parturition, the anatomical barriers of the vulva, vagina, and cervix are breached, introducing bacteria into the uterus, including pathogens, along with the bacteria that is normally found in the uterine environment and this is one of the reasons, the breaching of the genital tract for the incidence or occurrence of endometritis.

What are the important pathogens that are going to affect or cause endometritis? The uterine disease is commonly caused by Escherichia coli (E-coli), Arcanobacterium pyogenes, Fusobacterium necrophorum, and Prevotella species.

The most prevalent pathogens are E-coli and Arcanobacterium pyogenes.

E-coli infections appear to precede and pave the way for other infections, in that way E-coli is a very very important pathogen in the cause of endometritis.

Arcanobacterium pyogenes, Fusobacterium necrophorum, and Prevotella species act synergistically and increase the risk of clinical endometritis and its severity. The uterine immune response to the microbes leads to the influx of neutrophils from the peripheral circulation into the endometrium and uterine lumen.

The presence of pathogenic bacteria in the uterine lumen and the associated inflammation of the endometrium, preclude the successful development and implantation of the embryo. so these animals cannot conceive while they are affected.

Normal implantation process: we should know about the normal implantation process, what is happening to the normal implantation, before going into the pathology.

Normally a blastocyst will elongate, and it will slowly get a position with the uterine endometrium, and it gets added so that it will end up in the implantation, it’s a normal process blastocyst elongation> opposition> as well as addition.

In the case of endometriosis, especially sub-clinical endometritis, there is a secretion of Mucin 1(Muc 1), the expression of Mucin 1(Muc1), increases in the bovine endometrium in response to the subclinical infection.

It is an epithelial cell glycosylated transmembrane protein, that has a role in microbial defense, it is appearing as a role of defense mechanism.

But this Muc 1, is an anti-adhesion factor that prevents the conceptus from attachment and implantation. So, this is how it is going to affect.

In the normal implantation, we can see the blastocyst coming and attaching to the receptors in the uterine endometrium and it is going for the normal implantation.

In the case of Sub-clinical uterine infection, what happens? A layer of Muc 1, is going to appear between the receptors as well as the blastocyst, this will prevent the implantation of the blastocyst and blastocyst will be lost. There will be early embryonic mortality and conception will not occur and impaired implantation will lead to conception failure.

The next important factor is the Endotoxin:

As a part of the pathogenesis of uterine inflammation, the bacteria or the pathogens will be having bacterial endotoxins that are called the Lipopolysaccharides (LPS). These are the components of the outer cell wall of the gram-negative and gram-positive bacteria that are highly immunostimulatory.

The peripheral plasma of animals with E-coli infection of the endometrium have higher concentrations of LPS.

What happens? It is going to affect the Hypothalamus, the Ovary, the Follicle, as well as the Corpus Luteum. Here the LPS from the bacteria can attack the Hypothalamus and it can interfere with the pre-ovulatory sequence of endocrine events via suppression of GnRH and LH pulsatility and thus the ovulation is going to be affected.

The LPS from the bacteria can act at the follicular level, it will reduce follicular growth and it can also inhibit or suppress the protection of our synthesis of Oestradiol from the granulosa cell. Again, the LPS can attack the corpus luteum level also, the luteal phase of the animal will be prolonged, in the case of animals with endometritis or sub-clinical endometriosis. why? It can suppress the PGF2 Alpha and accumulate PGE, in that way the luteal phase/luteolysis is affected and most of the time it will be having a prolonged luteal phase, and these are the problems how the LPS will affect the endocrine system.

And again, the Cytokines, the inflammatory products: These are the immune or inflammatory challenges that can affect reproduction at the level of the hypothalamus, pituitary gland, and gonads. How these Cytokines affect the theca and granulosa cells and production of androstenedione and oestradiol, respectively. In that way, the entire inflammation can affect the endocrine system.

In the case of Chronic Inflammation, the consequences are a little bit more actually. The chronic inflammation of endometrium may lead to conception failure due to-

• chronic scarring of the endometrium.
• obstruction of the uterine fallopian tube and over bursal addition will lead to complete sterility of the animal also.

In this session, we have seen in detail about the Etiology and Pathogenesis of Endometritis as well as clinical endometritis.

See you all in the next session

Thank you!