Hello, and welcome to the wonderful world of PIGS! Today, we will talk about piggy things likely to be on the NBE. Just do your best to retain this information until December 15th, and then you can delete it from your hard drive and overwrite it with Useful Information. NB: four handouts were given. If you were not here, you missed them. Sorry. Since only 13 people are here, that more than likely means YOU! :) THE CCT: CCT has five sections: History gathering: usually you don't get penalized for choosing things in this section. If you're unsure in this section it is probably ok to guess. Physical exam: do not auscult pigs, do not palpate their abdomens, do not rectal them. When in doubt, do a necropsy. Diagnostics: you're on your own at that point. Therapy: don't give antibiotics to growers near market weight or put abx in feed of pigs planned to go to market soon. Consider drug residues. Recommendations: preventive medicine always a good option Last year: question on atrophic rhinitis, year before question on trichinosis which is dumb b/c it is mainly a public health concern but not a veterinary medical concern. NEONATAL ENTERIC DISEASE - handout was given. colibacillosis- pigs under 7 days. noninflammatory. variable prevalence/morbidity clostridium pigs younger than under 7 days; ++++ inflammation. death or emaciation. rotavirus pigs at 7-21 days lasts 3-5 days. common TGE pigs under 7 day old , noninflammatory, lasts 5 days, high morbidity/mortality Coccidiosis pigs 7-14 days old, mild inflammation, 4-7 days most of the above target distal ileum, so submit that for histo and some fresh for antibody testing for TGE, or cecal contents for isolating antigen for rotavirus. Clostridia is tough to diagnose b/c secondary infxns overgrow quickly. environmental contamination important with clostridia and coccidia, hard to disinfect area. Colibaccilllosis and rotavirus most common and often found in combination together. e coli colibacillosis - yellow/white/watery/pasty diarrhea with milk curd in stomach. hypersecretory diarrhea modulated by cAMP. clostridia: bloody diarrhea peracute: death w/in 24 hrs acute: hyperemic bowel seen on necropsy w/emphysema under serosal surface subacute: pigs survive acute infxn, stunted in growth, dehydrated, fall behind littermates chronic: advanced stage of subacute, survive to weaning but do not grow due to damaged small intesting from inflammation rotavirus: often starts in nursery in older pigs and spreads to farrowing rooms. resistant in environment, contaminated surfaces are important in epidemiology. watery diarrhea due to malabsorption TGE: high high morbidity is a major feature - almost 100%; also near 100% mortality. adults also show clinical signs. classic sign is a vomiting sow. if hx includes vomiting sow, think TGE. watery diarrhea due to malabsorption coccidiosis - hard to control b/c resist disinfectant. sow is major source of coccidia and clostridia and TGE. carrier sows also important with rotavirus but with coccidia and clostridia you have to treat sows to control. treat sows with coccidiostats, sometimes piglets too. bloody diarrhea, necrotic enteritis prevention: many of these you vaccinate for - e. coli bacterin toxoid combined with clostridium perfringens type c toxoid. immunize sow 5 wks and 3 wks prior to farrowing to boost colostrol immunity. rotavirus/TGE vaccines not that useful due to strain variation; so often make autogenous preps taking infected material from farm and making crude oral vaccine and giving it to sows orally. "Feedback" of dead pigs' intestinal tracts to pregnant sows. Not good for long term control. For TGE you must STOP FARROWING in affected facilities. Keep them out of that room til it is disinfected. TGE is susceptible to most disinfectants. Also TGE a disease of cold weather, virus likes cold weather when it is outside the pig. Classic case may be feed truck visiting affected farm then nonaffected farm and transferring disease. Swine dysentery also worse in winter. Enteric disease of Growing pigs: one way to think of growing vs neonatal is think of primary site of fluid absorption. at about 4-6 wks of age, site switches from ileum to colon. in growers, diarrhea is a lower bowel disease. swine dysentery: caused by treponema hyodysenteria, a spirochete. as far as diagnostics go, remember many intestinal spirochetes are normal flora and you need special staining to differentiate them. no ileal lesions, severe colonic lesions. complex epidemiology involving chronic carrier pig, and rats and mice also very important. first step is rodent control!! don't see this disease that much anymore b/c it is a dz of poor management and if you can't control this you probably are out of business from other problems as well. rare disease now. bloody stool is a cardinal sign. tx carbodox, Mecadox. salmonellosis: enteric form. mild ileal lesions, severe colonic lesions, enlarged ileocecal LN, occasionally other lesions. s. typhimurium or s. cholerasuis - the latter more associated with septicemic form. 35% of pneumonic lungs had salmonella in them in one study. cyanosis in ear margins, acute death, rapid autolysis are key signs. also this is only swine disease where isolation of infected animals is of benefit! B/c it has such a slow progression, isolating sick animals can reduce the challenge to remaining pigs. this goes to the enteric form, not the systemic form which is spread by nasal/oral secretions as opposed to fecal/oral. but it is difficult to tease out differences b/w these forms epidemiologically, so this isn't so useful. chronic carrier pig very important with salmonellosis. individual antibiotic treatment. hard to avoid thinking of depopulation, too. Porcine proliferative enteritis: different forms - intestinal adenomatosis "gardenhose gut" or hemorrhagic enteritis form, and necrotic enteritis. severe ileal lesions, occ colonic lesions. ileitis is another name for this disease (see article "Ileitis: Silent Killer" b/c it is insidious, doesn't really have dramatic clinical signs. 100 ppm of tylosin for control. (feed grade medication). not really practical to control economically until you are up to 3% death loss. almost every herd has this. "Lawsoni intracellularis" is the causative organism but the name keeps changing. It's an intracellular bacteria. The major epidemiological factor is stress: moving, mixing pigs, feed changes. when pigs were sold from here, they went to a farm with endemic ileitis and they got sick when they got there. control: change the feed. many abx have been used to control it as well. trichuriasis (trichuris suis): costly disease, but not common. no ileal lesions. moderate colonic lesions. usually secondary to other stressors, not primary disease. [icterus in pigs: eperythrozoonosis, an RBC parasite causing massive hemolysis] [dx that by doing a blood smear. the rickettsia are about 1 micron. control with arsenoic acid (??) and chlortetracycline or oxytetracycline. can't eliminate without eliminating mange and lice too.] [also bone up on Hog cholera, another great disease from the 60s.] most common cause of mortality in nursing pigs: sow crushing piglet. 2/3 of all pig deaths in farrowing room were crushing deaths. REPORTABLE DISEASES: expect a lot of questions on these. see handout for list of diseases! if you see vesicles, call the state no matter what it is. any species. not all of them are reportable but the differential at clinical level is impossible. Fowl Plague is H5N2 influenza according to Curtis, btw. :) Equine piroplasmosis is the same as babesiosis, texas fever; cattle tick fever, red fever are the names in cows. Hog Cholera, African Swine Fever, Foot and Mouth, Psuedorabies, TB - all reportable swine diseases (although TB is picked up at slaughter, not a clinical problem). Brucellosis kind of a nonentity in swine industry due to successful federal eradication program which has been pretty successful. feral pigs in barrier islands off georgia have brucellosis. viscerotropic velogenic newcastle disease - VVND: paramyxovirus like canine distemper virus Pseudorabies and Brucellosis both have extensive control programs. Highlights of hog cholera and african swine fever - both are exotic to the US. You can just read the handout. What's next? RESPIRATORY DISEASE: Atrophic Rhinitis: extremely common, widespread, high morbidity 2 forms: uncomplicated (bordetella bronchiseptica only, resolves on own by 6 wks) and progressive (b. bronchiseptica and pastuerella multocida type D aka PMD) difficult to control major impetus for SEW (segregated early weaning) source of infection is sow. signalment: sneezing grower and finisher pigs. crooked snouts more prevalent in summer (lag: transmisison higher in late winter and in spring) pigs are infected prior to 21 d of age and dz runs its course. bordetella toxin inhibits osteoblasts, PMD secretes toxin that stimulates osteoclasts, so you get extensive nasal bone remodelling. oftentimes, though, it's more like pig outgrows its snout, soft tissues push it aside. crooked nose isn't best way to evaluate for this disease, best way is slaughter check. signs: sneezing +/- unilateral bloody nasal d/c; tear stained faces (r/o dust - every pig has tears; atrophic rhinitis - some pigs have tears), wrynose, waxing/waning signs losses - poor growth rate due to PMD hepatotoxin, higher rate of pneumonia lesions - turbinate atrophy, wrynose all sows in most herds are carriers; pigs exposed by 3 wks, there is a pilus we can vaccinate against for b.bronchiseptica to prevent colonization. dx: gross lesions, but not specific control: correct mgmt deficiencies, vaccine is good if properly managed - use a killed or live-avirulent on the sows (bacterin or pilus antigen) then save the toxoid to give to the pigs, b/c toxoid won't be interfered with by maternal antibodies in colostrum. antibiotics ineffective or impractical. DON"T give abx. prevention is by segregated early weaning aka SEW but that info is too new for the boards, so consider cleaning up the sow heard via vaccine and culling if it comes up on boards. you can get aggressive with vaccination, using live avirulent vax at birth, that might be an option on the exam. multiple vaccinations of sows. very common disease. Enzootic Pneumonia - the biggest pneumonia of growing swine. generally pneumonia is in growers not baby pigs. very common, high morbidity, low mortality. slow spread. chronic bronchopneumonia, slow spread. get infected when with sow but takes 6 wks to develop. affecteds usually do recover. often complicated by pasteurella type A. don't really look sick. just cough a lot. etiology: mycoplasma hyopneumoniae - hard to culture, hard to dx via lab sig: >6 wks of age, chronic dry hacking cough, slow spread lab: blood test useful for herd status, not individual pig status. signs: dry nonproductive cough in pigs >6 wks, dyspnea only in severely affected animals. losses: poor growth rate, 3.3% per 10% lung involvment. lesions: lobular bronchopneumonia (A-V lobes). acutely, interlobular edema w/moist raised lobules, chronically there are dry, depressed lobules. fibrinous pleuropneumonia suggests pasteurella complication. sows are chronic carriers, spread by direct contact in grow/finish; bacteria disrupt normal fxn of mucociliary elevator, lesions may be totally gone in 8-16 wks. dx based on signs, gross lesions. blood test useful for herd status only. control: vaccination to reduce clinical signs. vaccinate at weaning and in nursery to control losses. on CCT suggest aggressive vaccination. strategic medication in nursery to reduce challenge - lincomycin in feed, pulse dosing is effective. abx not used to tx active cases. prevention: SEW, all-in all-out flow, eradication without depopulation is possible. Porcine Pleuropneumonia aka APP actinobacillus pleuropneumonia common but inapparent until animals are stressed high mortality in naive animals rapid course and progression in acute cases easy dx acute cases are "train wrecks." dramatic outbreak. etiology: actinobacillus pleuropneumonia - several serotypes w/poor crossprotection so no vaccine. makes a couple of toxins which cause awful tissue damage. sig: sudden death in growing pigs, not preceeded by poor growth rate; history of commingling pigs. often dead pigs are best looking ones b/c no hx of APP. death 6-12 hrs postinfection! lots of dyspnea, breathing hard, pyrexia, depression, reluctance to move, recumbency, congested or cyanotic skin. usually no cough. so right there is a big contrast w/enzootic pneumonia. losses: dead pigs, medication costs lesions: fibrinous pleuropneumonia, prominent interlobular edema, clearly demarcated areas of pleuropneumonia involving diaphragmatic lung lobe -- actually an abscess in chronic case, grape to grapefruit sized. the pathology could mimic pasteurella type a. sows are chronic carriers, stress causes shedding, naive pigs then acutely infected. spread only by direct contact. APP is dynamic antigenically. dx on hx, signs, lesions; culture lesions to determine serotype but hard bug to grow (like mycoplasma). serology for herd dx only. tx: high levels injectable abx to save pigs, antihistamines to tx dyspnea (eh); bacterins poorly effective prevent: do not commingle growing pigs!!!!!!!!!!!!!!!! SEW will prevent infection - wean at 16 days avoid stress, overcrowding, drafts depopulation can be considered but replacement stock are often carriers. for boards, focus on not commingling and avoiding stress for prevention. also know that abx tx won't work unless started very early. Pasteurella - similar to APP. main considerations with pasteurellosis are ruleouts and different abx sensitivities. APP kind of a hot button b/c if you characterize a herd as having it, this has negative connotations, whereas pasteurella does not so you must know which it is. Pneumonias are generally again diseases of growing pigs. Vaccine for mycoplasma is quite effective, very worthwhile control measure. as far as control for pasteurella, can't come up with much. Antibiotic tx is difficult, oxytet and ampicillin or ceftiofur are ok to try. similar prevention measures to APP. all in all out, decreased density, don't commingle. lots of bacterins out there, probably don't do that much good. Swine Influenza: H1N1 type A influenza virus. a new one is out too H3N2 causing many problems but won't be on boards. issue with flu is that people are carriers so people can bring it into the herd. that's unique among respiratory diseases of swine. infected peopel are reservoir for it. high morbidity, very rapid bonfire like spread. all over within 2 wks. low mortality but we do want to control it b/c pigs do not grow while they are sick and its a big loss. rapid onset, signs w/in 12 hrs of exposure. fever, depression, anorexia, dyspnea after exercise, moist cough is very consistent sign with flu. lesions with flu - diffuse or lobular consolidation of a-v lung lobes, emphysema, pharyngeal edema or hyperemia, airways filled with mucus and fibrin. viral pneumonia lesions are very diffuse. flu viruses spread a lot during winter months because virus survives in environment - fomites are important. dx flu on serology, histopath - but the dz is over by the time the results rae in. use abx to control secondary infxn (feed grade abx) but mainly just ride it out. effective vaccines exist. vaccines are very effective at preventing - can give to sows and get long lived immunity from colostral antibody through early stages of life. IFA on lung 2-3 days post infection, viral isolation from nasal swabs. control: do not move nursery pigs to affected areas for 2 wks post outbreak, do not move pigs during acute disease. commercial vax is good prevention. Systemic Disease: strep suis, haemophilus suis, blood infections, etc - we'll try to cover this. PRRS - porcine respiratory and reproductive stress? a bad problem. not sure how much to talk about it. typical PRRS outbreak in naive herd: first thing is sows off feed in farrowing rooms, then early farrowings - cardinal sign of PRRS - farrowing at 112 or earlier (normal is 114 or 115 days) plus pyrexia, off feed. PRRS is a highly infectious virus, some think it takes one particle to infect an animal, but it spreads slowly d/t variation in how immunity is developed. some develop it fast, others do not. it's an arterivirus. like EVA (equine viral arteritis). neat thing with prrs is progression of clinical signs in classic outbreaks. then weak pigs, stillborn pigs, then mummified pigs. sows in various stages of gestation respond differently. late gestation - pigs born alive, but weak. sows infected earlier - like a week or two - born dead, stillborn. sows infected still earlier, in midgestation, produce mummified fetuses. ossification normally occurs at about 50 days gestation. mummified fetuses mean pregnancy was affected after 50 days gestation, might be useful to know for the boards. hopefully that isn't too complicated as far as progression goes. other unique thing is the slow development of neutralizing antibody and therefore animals remain viremic for up to five montsh. that becomes a challenge for control purposes. having a hard time concentrating due to chatterboxes behind me, sorry. REPRO Porcine Parvovirus: virus, immunity to which is long lived. who shows clinical signs? young'uns. old sows have immunity. once pig has gone through it, immune for life. only gilts show signs. if you see abortions and mummified fetuses among youngest sows, think parvovirus. usually we see mummies. Lepto causes more abortions. not so many mummies. Lepto immunity is short lived. we can have animals be susceptible again in six months, need to vaccinate semiannually to prevent. lepto/parvo vax is cheap, routine to vax for these at weaning every time. every animal. lepto is spread in surface waters, often via contaminated urine. if sows are confined indoors and there is good rodent control, risk is low. Brucellosis is another repro disease we do not see much of anymoer - reportable and zoonotic. brucella suis - sort of a classic disease. seen in subtropics mainly. if herd in LA, AR, TX and repro failure is occuring, try to r/o brucellosis. morbidity low, under 30% but can reach 80% in acute outbreak, abortion at 70 days or earlier, infertility. persistent metritis is associated with brucella, unlike parvo/lepto. aborted tissues spread infection so if sows are free ranging they can pick it up. dx via serology. Lots of blood testing for brucellosis is going on. it's required for health certificates for interstate movement (unless going to slaughter; only for breeding stock is this testing required). brucellosis negative herds are called "validated" for pigs, "certified" for cows. TB in cows "accredited" TB free herds. Pseudorabies free pig herds are "certified." Porcine enzootic cystitis: eubacterium suis - vaginal d/c, infertility, anorexia, UTI. sows housed in wet environment, poor hygeine. requires abx therapy, sanitation, hygeine. SYSTEMIC DISEASE eperythrozoonosis also can cause repro failure enterovirus can cause abortion outbreaks. any systemic/septicemic dz can cause abortion - actinobacillus suis, salmonellosis, strep suis, erisypelas... Actinobacillus suis - early colonizer, affects very young pigs. toxoplasma gondii - can be an entity in swine herds. don't forget that. good obscure board question deal. Strep. suis: meningitis, arhtritis, polyserositis, endocarditis and pneumonia persists in TONSIL in carrier pig up to 17 mos - important. exacerbated by PRRS. pigs are infected by day 5 of life. NOT eliminated with SEW procedures. survives in environment, esp in cold. transmitted by respiratory route or wounds. big serovar differences, poor crossprotection b/w them, so no good commercial vaccine. need autogenous vax. third most important cause of URI disease. dx on signs - CNS signs in nursery pigs - depression**, incoordination, paralysis, paddling, head tilt, tremors, convulsions in advanced cases. "fading pigs" 1-3 wks of age may be seen but more often streps wreak havoc within a week or two of entering nursery. lesions: septicemia, polyserositis, cerebral edema, suppurative meningitis, turbid CSF, arhtritis in nursing pigs- swollen joints. submit whole head without removing brain b/c will get contaminant overgrowth otherwise. use amies culture for sample collection. control: pcn or amp, compound with dexamethasone to control cerebral edema. TMS in water is ok. improve management and reduce stress, avoid overcrowding, this is key. avoid thermal stress - keep warm enough! nursery pigs most common stress is too cold. avoid age spread of over 2 wks within one room. vaccinate with autogenous vax prefarrowing; vax at 10-14 days, at weaning - but hard to control with vaccine. real control is elimination of stress. monitor temperature in rooms. eradicate prrs! blah blah about temperature and environmental control. everyone is getting antsy. a massive group up and left. also people are chattering away. Haemophilus parasuis - Glasser's disease. bacteria associated with polyserositis. colonize nasal cavity then gets into bloodstream. similar to s. suis in many way. parasuis doesn't cause meningitis though. signs fever, depression, swollen joints, abnormal gait, tremors, lameness. CNS signs point more to strep, though. tx pcn, amp, vax as for s.suis, same prevention techniques, avoid stress, etc. CNS SIGNS: noninfectious cause of CNS signs == salt toxicity/water deprivation! do not forget this. the thing that goes with it is the pigs are off feed. theywon't eat if they're not getting water. over several days they will lose weight d/t anorexia. they will be depressed. you won't see other prominent signs. when you turn water back on you have to do it slowly to avoid cerebral edema or you get CNS signs. so the CNS signs occur after the water is turned back on, not originally! steroids will prevent the cerebral edema. used to use dmso, but that isn't convenient and is an extremely extralabel use. could hose them down with it though, or osmething. baptize them in dmso? :) no, don't suggest that on the CCT. but remember about salt toxicity/water deprivation. you might want to delve into the clin path of salt toxicity...diagnostics aren't that great. history is more important. you introduce water slowly but pigs go nuts for the water so it is hard to control their intake and it breaks your heart to see it really, trying to ration water in that situation is impossible because pig in charge will get all the water and die, and then so on. just turn water on and give them dexamethasone. extralabel drugs - may or may not come up on boards but the veterinary feed directive coalition paper on the slide says for feed grade meds, extralabel use is strictly prohibited under any circumstances. don't ever screw that up. that could be on the boards. feed grade meds can only be used as per label. Banned drugs in swine: pen-strep combo dimetridizole/ipronidazole - coccidiostats for turkeys nitrofurazone/furazolidine (except topical) - effective against coliforms chloramphenicol Edema Disease - E. Coli infxn of growers or nursery pigs - caused by enterotoxigenic e.coli like neonatal enteritis, but has different toxin. different strain. toxin is absorbed and causes vascular leakage, cerebral edema, and CNS signs associated with that. so there's another DDx for CNS signs. also called post-weaning scours. typically best pigs affected. dogsitting is the cardinal sign of water deprivation and also seen with edema disease. also head pressing. lesions with edema disease - edema of eyelids, stomach wall, intestine, mesentery. encephalomalacia microscopically. common under conditions of excellent mgmt and nutrition. high protein feed may predispose. other encephalitides: pseudorabies also causes CNS signs; but these are always in 7-10 day old pigs, never younger or older. what you see with these is they go down on their sides and paddle w/in 12-24 hrs of infection. they die. high morbidity in naive herds more than one pig in litter affected. hypoglycemia - good cause of CNS signs, typically pigs about a week old. low morbidity. always you would have lactation failure in the sow. more than one pig probably affected. also ear infection - maybe an oddball cause of CNS signs, head tilt, incoordination. Mulberry heart disease can cause CNS signs - d/t vitamin e deficiency. give selenium to sows prefarrowing (injection) Chemical toxicoses - arsenic, lead, mercury, insecticides (organophosphates - tx atropine) Dr. P is having random brain firings. PRRS is the cause of some really big economic losses. E. coli is also big. Ileitis is prevalent but not that costly. VACCINE USE: almost everyone uses lepto/parvo, lot use erysipelas/rhinitis. those four are the main ones everyone uses. e.coli, atrophic rhinitis, TGE, clostridia, pseudorabies, salmonella cholerasuis, PRRS, swine influenza, mycoplasma, and rotavirus are also vaccinated against. in PA you need official permission to use pseudorabies vaccine. see herd health vaccination handout. parvo/lepto done brior to breeding, in farrowing crate to control dz in baby pigs vaccinate sows, except tough cases of rhinitis you could vax pigs with live avirulent bordetella culture from day 1. WORMING STUFF prevalence of swine parasites - 70% of farms have ascarids, 45% have whips, nodular worms in adults, lungworms not a big deal. treat breeding stock at farrowing; there is a periparturient rise in parasite problems b/c sow will tone down immune system in late gestation, something to do wtih preserving the pregnancy. so periparturient rise in worm population in sow occurs -so worm them just prior to farrowing. OTHER TIDBITS PRCV - porcine respiratory coronavirus - causes inapparent disease. TGE is also a coronavirus so the serologic tests cross react. + can be due to PRCV or TGE. CMV causes rhinitis in pigs. kind of obscure but pops up on boards now and then. Erysipelas: zoonotic b/c if you get bacteria in open wound you get local cellulitis/bacterial thing going on "farmer's hand" or something like that. signalment is unvaccinated finishers, unvaccinated pigs. not seen unless there is a situationw here they stopped vaccinating. they then have outbreaks. usually late grower/finishers - 4-5-6 mos of age. morbidity low, sporadic. mortality is low if you treat affecteds, tx is effective. signs are very distinct - pyrexia 106 F (not 106.5, always 106). animal lying against pen wall, won't get up, depressed. some hyperemic areas of skin, skin painful to touch - squeal when touched. signs basically pathognomonic - hyperemia, anorexia, lameness, lethargy. no lesions in acute dz - diamond skin lesion seen in subacutely infected animals due to capillary thrombosis - capillary supplies rhomboid shaped area. losses - acute daeth. chronic lesions endocarditis and arthritis. organism harbored in tonsil and other lymphoid organs of 30-50% of healthy swine, so you will see it if not vaccinated. survives in soil for decades. caused by erysipelothrix somethingopathia :). dx on signs and lesions primarily. no samples to lab for this. two large doses pcn, fix'em right up. used to use antitoxin, probably not available anymore. funny thing is that it's easy to give your first does of PCN, hard to catch'em for second dose. vax is routine prevention. NB PRRS may also have diamond skin lesions associated with it as will anything causes capillary thrombosis. Greasy Pig - staph hyicus - for some reason we see more greasy pigs farrowed by gilts as opposed to sows; something with immunity there. a greasy pig is covered with scabs. they will grow out of it, develop immunity gradually and get over it. can tx with injections of abx and can also treat pennmates b/c does spread horizontally to a degree. spray them with nolvasan to prevent spread. won't fix affecteds but prevents the spread. inject with pcn/ampicillin to tx. some staphs have beta lactamase, don't forget those. ddx skin: swine pox - poxvirus - uniformly sized round lesions about 1 cm in diameter on ventral skin of abdomen. pityriasis rosea - may mimic pox. cause unknown. it is a skin dz. irregularly sized round lesions distributed over more than just the ventral abdomen - also sides, and head and neck. ruleouts include ringworm. ringworm more lichenified type of lesion, though. pityriasis is more red, scabby. both spread kind of concentrically with raised border of lesions. septicemic dz - mycoplasma arthritis polyserositis - m. hyosynovia et al. that bug causes exclusively polyarthritis, that might help you out... systemic salmonellosis - s. cholerasuis, always. enteric can also be typhimurium but systemic only cholerasuis. 6-24 wks age growers, low morbidity/mortality. 5-10% of herd would be severe. not always scours. lethargic, toxemic. multiple organ involvement. pneumonia, hepatitis, all sorts of things. cyanosis, red/purple ears/belly. splenomegaly, hepatomegaly, lymphadenopathy. ddx splenomegaly hog cholera, african swine fever, other sepsis. swine paratyphoid is the liver lesion caused by s. cholerasuis- pathognomonic. source - infected shedding pigs, contaminated feces. nasal secretions also important source. bug doesn't live in environment with no organic substrate - needs something like manure, so sanitation is helpful. culture of tissues diagnostic; also can culture from tonsils. neomycin/oxytet in feed reduces duration; any injectable helpful for individuals. isolate affecteds! avoid stress, overcrowding, poor nutrition, poor nutrition, and poor nutrition. avoid poor nutrition. avirulent live vax available. live vacx in swine - salmonella and bordetella pretty much only ones. MLV PRRS exists. also pseudorabies. all else killed. one problem area if farmer gets no response to psuedorabies vax - look at vax handling. with live vax, must be careful about using disinfectants in syringe and stuff. parakeratosis - Zn deficiency, hyperkeratization of skin. Gastric Ulcers we could discuss, good board material we're all done!