**4.5.4 Prostaglandins**

The luteolytic effect of prostaglandins has been used to treat RBCs. In this case, treatment aims to achieve better heat detection and to increase the number of cows in heat. Numerous protocols are used in cow, e.g. two PGF2alpha injections apart 11 days and insemination 80 hours later. Intravenous PGF2alpha (0,2 ml cloprostenol) has also been reported in RBCs at AI time. However, the most frequent use of this hormone has been combined with other

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substances, serving as a pretreatment and with the ultimate goal of improving the reproductive management.

#### **4.6 Reproductive management improvement**

Treatments are being used recently for fixed-timed artificial insemination, without heat detection. These protocols allow the treatment of cows with silent heats or ovulation problems. Ovsynch is a protocol based on the administration of GnRH, PGF2alpha and GnRH (Pursley et al., 1995) to schedule the insemination time.

It is also essential to improve all aspects related to heat detection, since it has been demonstrated that estrus detection mistakes involve very significant losses in reproduction and production cattle. Therefore, it could be interesting to implement different methods for estrus detection as Kamar or Bovine Heat-beacon devices and pedometers.

#### **5. References**


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**19** 

 *Poland* 

and Katarzyna Dudek

 *National Veterinary Research Institute, Department of Cattle and Sheep Diseases,* 

**Bovine Respiratory Syndrome (BRD)** 

Dariusz Bednarek, Monika Szymańska-Czerwińska

**Etiopathogenesis, Diagnosis and Control** 

Bovine respiratory disease (BRD) complex is a major disease, classically in the indoor calves and feedlot young cattle. The etiopathogenesis of BRD is multifactorial and complex. In this complex etiology an equivalent role plays both the infectious agents as well as the environmental factors which are called also as environmental stressors (inappropriate livestock management like mistakes in animal nutrition, transport, handling, veterinary interventions etc.) (tab. 1). The most significant pathogens which are involved in the etiopathogenesis of BRD, i.e. suitable species of viruses such as (bovine respiratory syncytial virus (BRSV), parainfluenza virus type 3 (PI3V), bovine herpes virus type 1 (BHV1), bovine viral diarrhea virus (BVDV), are usually associated with concurrent bacterial infections represented by: *Mannheimia haemolytica*, *Pasteurella multocida, Histophilus somni* and others (tab. 1) (Jared et al., 2010a, Kita et al., 1994, Klimentowski et al., 1995) and also mycoplasmal factors such as: *Mycoplasma bovis*, *Mycoplasma bovirhinis*, *Mycoplasma dispar*, *Ureaplasma diversum* and even *Mycoplasma canis* (Szymańska et al., 2010). Among bacteria *M. haemolytica* and *P. multocida* have been traditionally considered as the most common bacterial infectious factors in the BRD etiology (Fulton et al.; Reggiardo et al., 2005). On the other hand the one of the most often isolated mycoplasmal factors from BRD cases is *Mycoplasma bovis*. Its adaptative ability to a host organism increases owing to different versions of the same *vsp* gene family which encode particular adhesive factors of the mycoplasma, i.e. variable surface proteins (Vsps; Razin et al., 1998). The variability of *vsp* gene based on DNA transposition (Lysnyansky, 1996). Therefore the high Vsp variation determines the phenotypic variability of the antigen (Rosengarten et al., 1994) which further increases the virulence of the pathogen. *M. bovis* possess the ability to immunomodulate host defence against infection (Razin et al., 1998), for example inducing a synthesis of proinflammatory agents, i.e. TNF-α and nitric oxide (Jungi, et al., 1996) or stimulation of some acute phase protein production, such as haptoglobulin and serum amyloid A, which represent one of the most important components of acute phase response for cattle (Dudek, 2010). It is known that *M. bovis* acts as a stimulant on major subsets of T-lymphocytes (Vanden Bush, 2003). In contrast, some data show inhibitory properties of the pathogen which come down to its suppressive effect on lymphocytes (Vanden Bush & Rosenbusch, 2002; Thomas et al., 1990)

**1. Introduction** 

**1.1 Etiopathogenesis** 

