NEONATAL SEPTIC POLYARTHRITIS
“Joint-ill”
Etiology and Epidemiology
 Caused death in up to 1.5% of affected pigs
(occur within the first 2 days of life); cause
by various facultative and specific
pathogens that cause localized infections
that precede septicemia
 Streptococci (S. suis), Staphylococci,
Actinobacillus suis, Trueperella pyogenes,
E. coli, and occasionally P. multocida,
Erysipelotrhix rhusiopathiae or Haemophilus
spp
 Infection may be established due to
abrasion of skin of the carpi or coronary
bands when suckling pigs paddle with their
legs or dure to poor hygiene at tail docking,
ear notching, or castration; carless clipping
of needle teeth and if infection leads to
bacteremia, organisms can cross the
synovial membrane -> polyarthritis is
likely
 Can also gain entry to the circulatory
system via the tonsils or oropharynx or as
a result of an ascending omphalophlebitis
Clinical Signs and Lesions
 Lethargy and failure to suckle
 Piglet may dog sit
 Swollen, painful and warm joints (hock and
knee)
 Lameness in one or more limbs
 Severe cases – abscessation will burst out
from the joint
 Rare cases – early problem can contaminate
the end of the bone and affect the growth
plates; spontaneous fractures
 Meningitis – uncommon complication; seen
from 10-14 days of age
 Necropsy – cream or green pus in and
around swollen joints (elbows, carpi, stifles,
hocks), in the umbilical stalk, sometimes
over the meninges or the in the fissures
between the cerebrum and cerebellum
Diagnosis
 Clinical signs and bacterial culture
Treatment, Control and Prevention
 Antimicrobial therapy at early course of the
disease; Penicillins; Lincomycin,
Trimethoprim/Sulfonamide, Tylosin
 All-in/all-out flow of pigs; Improve hygiene
in the farrowing area; Identify and rectify
the route of entry of infection
 Teeth clipping – clipped singly with clean
sharp clippers or ground off
 Tail docking – use separate instruments from
those used to clip teeth; use thermocautery;
use iodine after docking
 Navels – dipped in iodine at birth
 Dry disinfectants in the farrowing pens; not
substitute to wash and disinfect or keep pen
clear of sow feces; do not allow sows to
spend more than 5 days in the farrowing
crate before farrowing
 Tonsillar penetration – long-acting penicillin
or amoxycillin; antibiotics either by
inclusion in the feed or top dressing onto the
feed
FOOT ROT
“Bush Foot”
Etiology
 Infection penetrating the soft tissues
between the claws; defect or penetration of
the wall of the hood or its bearing surface;
includes sole, heel and toe, fissures in the
wall and separation of the wall from the sole
at the white line
 Trauma bacterial infection; poor flocks;
lack of bedding
 Occurs in one foot only and more
commonly seen in the hind feet especially
the outer claws which are the larger ones
carrying more weight
 Affects sows and boars of all ages
Clinical Signs
  Lameness, painful swollen claw, cracks at
the sole-hoof junction or splitting of the hoof
itself
 Claw becomes enlarged and infection and
inflammation of the joint often develops
 Swelling is visible around the coronary band
which may form an abscess and burst to the
surface
Differential Diagnosis
 Erysipelas, Glasser’s disease, Leg weakness
or osteochondrosis, Mycoplasma arthritis,
Trauma
Diagnosis
 Clinical signs (painful swollen claw)
Treatment, Control and Prevention
 Antibiotic treatment – Oxytetracycline and
Amoxicillin
 Anti-inflammatory injections – Cortisone; if
the sow is not pregnant (phenylbutazone or
ketoprofen)
 Foot batch – 1% formalin (use in open air);
5% copper sulphate
 Walk the sows once through once each week
on 2-3 occasions – avoid if there are cracked
claws in the herd
LEG WEAKNESS SYNDROME
“Osteochondrosis, OCD”
Etiology and Epidemiology
 Defect in the development of cartilage of
growth plates or articular cartilage in
growing pigs
 Growth plates are more prone to fracture –
retained hypertrophic cartilage that focally
thicken and weaken the cartilage
 Developmental lesions have very high
prevalence in young pigs but mostly resolve
with age and development
 Seen in all the major breeds of purebred and
commercial hybrid pigs
 Clinical problems are not usually seen until
pigs are >4-8 months old
Clinical Signs and Lesions
Acute
 Separation or fracture of the bones at the
epiphyseal plate associated with sudden
movement
 Stiffness and shortened stride; Three-legged
lameness or an inability to stand
 Weight-bearing, shifting lameness – bilateral
lesions that affect multiple joints
 Crepitus or rubbing of the broken bones
together
 Sudden fractures in the knee and elbow
joints
 Fractures of the vertebrae in the spine –
during lactation and post weaning; dog
sitting position with the hind legs forward
 Hind muscles pulling away from their
attachment to the pelvis (apophyseolysis)
 Sow cannot pull the hind leg backwards; it
just slides forward
Chronic
 Gradual onset
 Abnormal leg conformation; gait with or
without stiffness and pain
 Abnormal gaits from pain in the joints or
abnormal movements in the hind legs from
the hips -> swaying motion
 Joints are inflamed, particularly in the hip,
knee, and elbow
Diagnosis
  Clinical signs
Diagnosis

Differential Diagnosis  Clinical signs

 Serum biochemistry, radiographs, bone
 Mycoplasma hyosynoviae, M. hyorhinis, biopsy
Bone fracture, Erysipelas
 Calcium, phosphorus, and vitamin D content
 OCD does not respond to antibiotics; M. of diet
hyosynoviae – lincomycin or tiamulin;
Erysipelas – penicillin; respond within 24-36
hours
Treatment, Control and Prevention

 Identify and address the underlying

Treatment, Control and Prevention deficiencies; Confinement for several weeks
after supplemental diet
 No specific treatment
 Limited movement until skeleton returns to
 Selecting against replacement pigs that are normal; complete recovery within months
lame or have poor conformation; providing with no or only minor limb and joint
adequate rations for growth of a strong deformities
skeleton; housing gilts in pens with ≥12 sq ft
per animal; promoting exercise on nonslip
floors
 “Hardening off” period for gilts – gilts at
<75 kg live weight; restricting their feed
intake to slow their growth rate; ≥1.1 sq m
per animals in pens with solid or partially
slatted floors; waiting to breed gilts until
they are 8-10 months old; housing gilts in
pens until they farrow

OSTEOMALACIA
Etiology

 Responsible for the downer sow syndrome

 Lack of calcification of bone -> weakness
of bone that can fracture with little trauma
 Inadequate dietary provision; physiological
abnormality of absorption and utilization of
calcium and phosphorus and during lactation

Clinical Signs

 Most typically seen in weaned gilts; sudden

onset lameness or collapse depending on the
bone or bones affected (spinal column
leading to broken backs)
 Dog sitting position, stiffness, sudden acute
lameness during lactation or post weaning,
fractures, pain, discomfort