Table 7.

Porcine models of orthopedic infections.

Model/Strain	Gender	Age/Weight	Microorganism/Concentration	Disease Model	Site of Inoculum	Timepoint	Aim of the Study	Results	Ref.
Domestic Landrace	na	12 weeks	S. aureus (haemolyticus). 2 × 108 CFU	Infectious bone diseases	Femur	16 days	To study the effect of gentamicin embedded in palacos bone cement.	The number of germ populations is reduced significantly by the antibiotic released in a microbiologically active concentration. The number of germs in control group remained at a high level	[222]
Yucatan mini swine	F	2–5 years, 68–95 kg	S. aureus ATCC strains 6538P, 25923, and 29213. 108–109 CFU	Chronic Mandibular Osteomyelitis	Mandible (5% sodium morrhuate as inducing agent)	8 weeks	To develop chronic mandibular osteomyelitis in miniature swine	Clinical evidence of mandibular osteomyelitis was developed in all mini swine by eight weeks post-infection. At this time, S. aureus was recovered from all six mini swine where bone wax had been used to seal the trephine hole, but not from the two PMMA animals	[131]
Large White	F	45.4 kg	S. aureus ATCC 29213. 107 CFU	Experimental osteomyelitis in a model of gunshot fracture	Tibia	14 days	To create a model of ballistic wounding in the proximal tibia of pigs	The incidence of osteomyelitis was significantly reduced thanks to treatment with antibiotics. The histological examination confirmed the diagnosis of osteomyelitis based on the presence of purulent material inside associated bone and osteonecrosis.	[220]
Large White × Pietrain male castrated	na	50–65 kg	S. aureus (field strain isolated from a human orthopaedic infection). 1.2 × 103 CFU	Orthopaedic implant–associated infection	Tibia	28 days	To create cDNA libraries that reflected changes in immune cell function after exposure to infection with Staph. aureus	7620 ESTs were clustered into 1029 clusters with an average of 3.6 sequences and 3846 singletons.	[223]
Yorkshire–Landrace crossbred	F	8 weeks, 20–25 kg	S. aureus strain S54F9 (clinical strain isolated from a chronic embolic porcine lung abscess). 2 × 109–2.5 × 109 CFU once (group 1 and 2) or twice (group 3 and 4) at 0 h and 12 h.	Non–traumatic osteomyelitis	Ear vein	6–12–24–48 h	To evaluate the pig as a model for the development of osteomyelitis following haematogenous spread of S. aureus	Disseminated micro abscesses within the lungs by 6 h were developed (but disappeared at 48 h). Within bones, lesions were localized in separate foci.	[142]
Yorkshire–Landrace crossbred	F	8–9 weeks, 15 kg;	S. aureus strain S54F9 (field strain isolated from a chronic embolic porcine lung abscess). 75, 7.5 × 102, 7.5 × 103, 7.5 × 104, 7.5 × 105 CFU	Acute haematogenous localized osteomyelitis	Brachial artery	5–15 days	To develop a porcine model for haematogenous localized osteomyelitis	Any lesion was not developed in low dose infection models. Pigs inoculated with 5000 and 50,000 CFU ⁄ kg BW only developed micro abscesses in bones of the infected legs. In trabecular osteonecrosis, bone lesions were evident.	[224]
Yorkshiree Landrace–cross pigs	F	12-weeks, 30 kg	S. aureus strains UAMS–1 (isolated from a case of human osteomyelitis), NCTC–8325–4 (isolated from a case of human sepsis) and S54F9 (isolated from a chronic embolic pulmonary abscess in a Danish slaughter pig). 3 × 105 CFU	Haematogenous osteomyelitis	Ear vein	11 or 15 days	To compare the infection potential of the porcine strain (S54F9) with two S. aureus strains of human origin (UAMS–1 and NCTC–8325–4) in this model and to examine the development of HO with a focus on pathology and the localization and microenvironment of S. aureus	In three, one, and none of the recipients of porcine and human strains, respectively, bone lesions were present. On the CT scans, the vascularized bone tissue was seen as foci of increased opacity.	[225]
Yorkshire–Landrace crossbred pigs	F	12 weeks, 30 kg	S. aureus S54F9. 3 × 105 CFU	Haematogenous osteomyelitis	Femoral artery	11–15 days	To describe a new intra–arterial inoculation technique in a porcine model of juvenile haematogenous osteomyelitis	Percutaneous catheterization is not an option due to the depth of the artery’s position. This model provides a reliable method for detecting lesions that discriminates the naturally occurring HO in long bones.	[150]
Specific pathogen–free	na	12 weeks, 30 kg	S. aureus S54F9. 1.5 × 107 CFU (pig no.1) 1.5 × 108 CFU (pig no.2)	Haematogenous osteomyelitis	Femoral condyle	6–8 days	To examine the histological bone changes of experimentally induced osteomyelitis in the porcine model	Lesions found in animals resemble those found in children suffering from haematogenous osteomyelitis	[226]
Danish Landrace	F	67–77 kg	S. aureus strain S54F9, (spa type t1333). 104 CFU	Implant–associated osteomyelitis	Tibia	5 days	To investigate cefuroxime penetration during implant–associated osteomyelitis	In the implant cavities, lesions referable to bone destruction were found; no alteration in adjacent areas was noted. Cefuroxime penetration into infected bone was incomplete.	[227]
Danish SPF Landrace	F	3–8 months	S. aureus strain S54F9 (spa–type t1333). Low dose (102 and 103 CFU) High dose (104 CFU)	Implant associated osteomyelitis	Tibia	5 days	To describe a novel porcine implant associated osteomyelitis model.	A significantly higher volume of bone lesion, number of neutrophils, concentration of acute–phase proteins in serum and enlargement of regional lymph nodes were induced by a high inoculum. Therefore, a threshold of 40 neutrophils for 10 high power fields was considered for the histopathological diagnosis of high–grade IAO.	[219]
Landrace SPF	F	35 kg	S. aureus S45F9. 104 CFU	Implant–associated osteomyelitis	Tibia	2–4–6 days	To elucidate how deep implant–associated osteomyelitis can go into the peri–implanted bone tissue within a week	On implants and from 25 µm to 6 mm into pathological bone area S. aureus bacteria were identified.	[228]

Abbreviations: na = not available.