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1338                                       CHAPTER 14



  VetBooks.ir  efficiency of the innate immune system, subsequent   is not balanced by the compensatory anti-inflam-
                                                          matory response  syndrome.  Uncontrolled  SIRS  or
           to the lack of absorption of complement and other
           factors. Sepsis occurs in foals when the bacterial
                                                          dysfunction and death. The major factors that con-
           challenge exceeds the host immune response, due to   sepsis rapidly leads to a syndrome of multiorgan
           either  the magnitude  or  pathogenicity  of  bacterial   tribute to this include circulatory collapse, from
           challenge, or a reduced host response.         endothelial dysfunction and myocardial suppression,
             The most common route of entry for bacteria into   and coagulation dysfunction with the formation of
           the foal’s circulation is via the intestinal tract. The   microthrombi in the blood vessels within various
           enterocytes designed to allow pinocytosis of immu-  tissues.  The  most  common  bacteria  implicated  in
           noglobulin are non-specific and can rapidly trans-  neonatal sepsis are all environmental pathogens and
           port bacteria in addition to immune factors directly   include  E.  coli,  Enterobacter  spp.,  Staphylococcus  spp.,
           into the circulation. Other routes of pathogen entry   Streptococcus  spp.,  Actinobacillus  spp.,  Klebsiella  spp.,
           include the respiratory tract, the placenta in utero and   Pasteurella spp., Salmonella spp., Clostridium spp. and
           the umbilicus. Following invasion of the pathogen a   Enterococcus  spp. In many foals, sepsis is caused by
           cascade of events is initiated, which is responsible for   mixed infections.
           most of the clinical signs seen with SIRS and sepsis.
           Pathogen associated molecular patterns (PAMPs),  Clinical presentation
           present on bacteria, activate both the innate and   Clinical signs are variable. They may range from sub-
           adaptive immune systems. Leucocytes and other   tle, non-specific and insidious in onset to acute and
           inflammatory cells release cytokines that cause fur-  fulminant. They may include: less frequent feeding
           ther upregulation of the immune system. The cas-  or complete anorexia; lethargy and increasing peri-
           cade initiates a wide variety of effector organs and   ods of recumbency; increased heart and respiratory
           tissue types including the coagulation system, endo-  rates; increased respiratory effort; respiratory dis-
           crine system and endothelial cells.            tress; raised or subnormal temperature; congestion
             In a well-balanced immune response, activation   and petechiation of mucous membranes; coronary
           of the inflammatory cascade causes removal of the   band hyperaemia (Fig. 14.5); altered  mental status
           bacterial pathogen from the circulation and a return   such as depression and seizures; diarrhoea; colic
           to normal homeostasis. However, in many situa-  and abdominal distension; uveitis with ocular pain
           tions, the immune response becomes excessive and   (Fig. 14.6); hypovolaemia; bone or joint infections




           14.5                                           14.6




















           Fig. 14.5  Distinct hyperaemia of the coronary band   Fig. 14.6  A septic uveitis of the left eye of a foal with
           can be an indication of sepsis.                septicaemia. Note the marked miosis of the pupil.
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