Gastroenterita transmisibil a porcului

Boal acut, contagioas, produs de un virus aparinnd familiei Coronaviridae, genul Coronavirus , caracterizat prin diaree profuz i vom, prin morbiditate i mortalitate mare la purceii sugari.

Etiologie: TGE virus (TGEV) genul Coronavirus,

stabil la congelare, sensibil la temperatura camerei , sensibil la radiaia solar sensibila la desinfectanti precum hipocloritul de sodiu i produi iodurai
Particulariti epidemiologice:
Receptivitate : susceptibili porcii indiferent de vrst, mortal la sugari De ce?: turnover enterocite mai mic dect la aduli la purcei nu se realizeaz reabsorbia fluidelor n intestinul gros spre deosebire de aduli

Factor de risc major: statusul imun Surse de infecie: adulii purttori i eliminatori n efective cu infecie endemic, vectori activi (pisica, cinele, psri), vectori mecanici(mute) Cale de contaminare: fecalo-oral Dinamica epidemiologic: epidemic sau endemic a) epidemic n efective fr anticorpi anti-coronavirusuri, mai iarna, morbiditate 100% la purceii 3 sptmni, mortalitatea descrete cu vrsta b) endemic: rata mortalitii pn la 10-20%.

Patogeneza
Incubaie: 18 ore - 3 zile Ingestie enterocite intestin subire enterocite replicare n enterocite liza enterocitelor eliberare n lumenul intestinal atrofia vilozitilor Criptele intestinale nu sunt afectate hiperplazie secretia continu Absorbia este defectuoas (liza enterocitelor + atrofia vilozitilor) malabsorbie crete osmolaritatea intestinal ( din cauza materialului nedigerat = maldigestie) scade activitatea enzimatic a mucoasei intestinale atracie fluide n lumenul intestinal fluid into the intestinal lumen. Malabsorbia i maldigestia induc creterea secreiei mucoasei intestinale diaree Exitus : deshidratare i acidoz metabolic.

Tabloul clinic
La subiecii descoperii imunologic: vom, diaree apoas, glbuie, cu resturi de lapte nedigerat, pierdere n greutate, deshidratare, , morbiditate i mortalitate ce tinde spre 100% la purcei mai mici de 2 sptmni. La purceii mai mari diaree steatoreic datorat maldigestiei. Purceii in vrst de peste 3 sptmni supravieuiesc dar sunt subdezvoltai Grsunii i porcii grai (GET epidemic) inapeten, diaree, agalaxie, sau uneori vom. GET endemic: asemntor clinic dar de gravitate redus fa de porcii seronegativi.

Tabloul lezional
Macroscopic: - deshidratare, tren posterior murdrit de fecale diareice, absena bolului fecal n intestinul gros - peretele intestinului subire este foarte subire, translucid, cu vasele mezenterice congestionate. - vasele limfatice mezenterice sunt lipsite de chil malabsorbia grsimilor - stomacul i intestinul subire pot conine coaguli de lapte sau fluid biliar. - la examinare cu lupa intestinul subire prezint atrofia vilozitilor Microscopic: - atrofia vilozitilor cu raportul cripte/viloziti 1/1 fa de 7/1 la porcii sntoi n jejun, rareori n ileon - reacie inflamatorie nesemnificativ, hiperplazia criptelor. - vilozitile prezint un epiteliu cu polaritate nuclear neregulat i fr epiteliu n perie - cnd leziunile formeaz insule se impune examinarea mai multor seciuni (dg.diferenial rotavirus)

Material patologic pentru confirmare: - materii fecale, segmente de mucoas afectat pstrate la 4oC - probe de snge ( n faza acut sau convalesceni) pt.serologie: VN, indirect ELISA i ELISA de competiie. - ELISA de blocare permite diferenierea ntre TGEV i PRCV

Diagnostic: 1) detecie antigen viral: IF, IHC 2) detecie acid nucleic: RT-PCR 3) detecie virus prin microscopie electronic: EM 4) izolarea i identificarea virusului:TC 5) creterea titrului anticorpilor fa de TGEV: serologie

Enterocitele la extremitatea vilozitii manifest puternic reacie imun fa de anticorpii anti-TGEV

Profilaxie
Achiziionarea de animale indemne, seronegative Carantin profilactic 2 4 sptmni i ex. Serologic nainte de introducere n efectiv. Respectarea normelor de biosecuritate. Limitarea/restricionare/ interzicerea traficului uman: acceptat cu respectarea normelor de filtru s-v.

Control
Elementul de baz : asigurarea prezenei IgA i excreia acesteia n laptele scroafelor pentru a transfera pasiv imunitatea la purcei. Stimularea secreiei de IgA de ctre limfocite se realizeaz cu eficien maxim prin prezentarea antigenului ctre celulele M din plcile Payer. Imunitatea activ postinfecie TGEV dureaz 6-18 luni Vaccinurile parenterale induc sinteza IgG i IgM: IgA este stabil n tractusul digestiv, m timp ce IgG i IgM sunt digerate. TGEV se transmite oral, celula int este enterocitul imperativ prezena IgA n lumenul intestinal

B254
Focar GET n efectiv liber de anticorpi debuteaz n maternitate. Izbucnirea trebuie controlat n sectorul de gestaie: dac gestaia a depit a 3-a lun, ftarea trebuie s se realizeze ntr-o zon liber de GET, purceii fiind crescui n primele 3 sptmni ntr-o zon liber de GET. Dac pn la ftere sunt mai mult de 3 sptmni, metoda "feed-back" GET endemic :flux all-in/all-out, maternitate n zon liber GET Administrare vaccin viu atenuat pt. booster rspuns imun scroafe anterior ftrii: IgA reduce morbiditatea i mortalitatea Expunerea multipl a scroafelor la PRCV genereaz titruri mari anti-TGEV IgA in lapte i protejeaz fa de infecia cu TGEV.

Management control and prevention

As soon as disease is suspected isolate those farrowing houses not infected, by using separate personnel boots and coveralls. This is particularly important in piglets under 14 days of age. The longer the disease can be kept away the more pigs will be reared and mortality reduced. If it is possible move sows that are within 3 weeks of farrowing from the farm before they become infected so that they could farrow down in an isolated building or outside in arks and escape disease. It is essential to develop immunity in the dry sows as soon as possible. There are two methods, either squeeze the piglets abdomen and collect the diarrhoea into a bowl or use sawdust or shavings in the areas where the piglets are scouring. Paper towels can also be used to soak up piglet faeces. This material is then mixed with a bucket of water and fed to the pregnant sows, (feed back). A further method is to collect the small intestines from a number of pigs that have died and macerate them in a food blending machine. The liquid provides a rich source of virus and this can if required be preserved by deep freezing. The disease should be spread as soon as possible across the whole farm. The object is to get a good immunity developed in the shortest possible period of time. It will take approximately 3 to 4 weeks to achieve this. Once the infected period is over ensure an all-in and all-out management system of the farrowing houses, weaner and finisher accommodation. Disinfection of pens between batches should be carried out using an iodine based disinfectant or one highly active against viruses This cleaning process is an important one to ensure the virus does not linger on the farm and become endemic. If your herd as become infected with TGE ask the question why and how? Look at all your prevention procedures and biosecurity as discussed in chapter 2. (Do this before you get TGE). Always provide boots and protective clothing for any one entering your farm. Provide disinfectant foot dips at all entrances. Keep starlings and migrating birds away from the farm by not exposing them to feed. Do not borrow equipment from another pig farm. Site all bins to the exterior of the unit and always have your own feeder pipes to your own feed bins. This is a high risk source for the spread of enteric diseases. Vaccination - live modified and killed vaccines are available in some countries. The results in the field are very variable. The objective is to maintain immunity in the colostrum. This can only be carried out by stimulating the gut of the sow to produce antibodies in the milk. Intra-muscular vaccines give a very poor response.