Swine Neurology

a. ubiquitous: cultured from vagina of normal sows
survives in environment: dust, feces, biofilms; also spread by flies
**mostly a nursery dz (5-6 wks of age)**
**risk factors**: crowding, co-mingling, PRRS virus
b. clinical dz can occur w/o other agents, but PRRS, PCV-2, & pseudorabies --> ↑ morbidity & mortality
**bacteria enter thru crypts of tonsils**
MP carry bacteria --> mandibular lymph nodes --> systemic (CSF, meninges, brain, lungs, joints)

a. pigs that die acutely have fibrinous meningitis
often rapid onset: may appear normal w/in hr. of death
any serosal membrane may be affected: polyserositis, polyarthritis, myocarditis, endocarditis, pericarditis, bronchopneumonia
**lesions indistinguishable from those of Haemophilus parasuis**
b. pigs often appear scruffy & malnourished
**CNS signs: opisthotonus, nystagmus, paddling, +/- convulsions

a. culture: gold standard
b. β-lactam ABs (mostly still sensitive, definitively sensitive to ceftiofur)
c. commercial, autogenous vaccines marginally effective
elimination of PRRS: very difficult
strategic AB use in water, feed, & parenterally

a. can see in nursery & grow/finish pigs
b. same as Strep suis
c. culture: gold standard
d. β-lactam ABs
tx difficult when PRRS, PCV-2, or influenza also active

F-18 or F-4 strains of E. coli
α-hemolytic & produces Shiga-like enterotoxin
toxins produced in SI after attachment to brush border: receptor for fimbrial Ag must be present on brush border cells: genetically determined
toxin damages small arteries & arterioles --> localized edema in several organs (colon, SI, eyelids, brain)
acute & typically fatal

a. not seen in baby pigs while nursing: lactogenic protection & absorbed Abs
changes in gut environment assoc. w/ weaning favor enteropathogenic E. coli
buildings become contaminated & colonized
co-mingling of pigs may ↑ risk of clinical dz
change from milk to corn/soy ration
survives in biofilms & fecal contaminated trucks
b. clinical signs, hx, gross lesions
labs can ID both F-18 & F-4 adhesion Ag & specific toxin
**histopath: typical vascular lesions, brain stem malacia
ddx: S. suis, H. parasuis

a. unrewarding once signs appear
b. may prevent in non-affected pigs
sanitation & biosecurity: dry rooms before filling
**oral inoculums w/ non-toxin producing strains of F-18 (autogenous oral vaccine)

a. sodium ion toxicosis d/t water deprivation of at least 48 hrs
b. most common in nursery, can also occur in grow/finish

a. usually high morbidity & mortality in affected groups
refusal to eat, commotion/squealing at water source
**CNS signs begin w/in hours after resumption of water availability: “dog sitting” w/ convulsions common
b. **hx of water deprivation
**histopath (pathognomonic): cerebral perivascular cuffing by eosinophils
dog sitting --> convulsions

What neuro dz is consistent with this clinical appearance?

What neuro dz might you suspect in this pig?

What neuro dz might you suspect based on these lesions?

What neuro dz might you suspect based on these lesions?

What neuro dz might you suspect based on these lesions?

What neuro dz might you suspect based on these lesions?