Re: [SPAM] Re: Tendon issues with Fluoroquinolones

January 8, 2008

Toni,

I agree with . It may be coincidental that you are finding

other sites of inflammation in a dogs body. We do, however, see ACL

tears secondary to chronic corticosteroid usage and to immunne mediated

joint disease. I would suggest searching medline or google for

references to this idea. You might find some support. On that note,

in reference to the flouroquinolone issue, I did some searching and

found two articles, and then included a third unrelated one that was of

interest about post-op rehab. This quinolone issue might very well be

real in vet med, but I did not find anything solid to substantiate

discontinuing the use of then in at least small animals, other than

immature animals. Also attached is a PDF file describing

Fluoroquinolone induced tendinopathy.

Thanks,

Mark B. Parchman, DVM, DACVS, CVA

The effects of enrofloxacin on canine tendon cells and chondrocytes

proliferation in vitro. S Lim , M Hossain , J Park , S Choi , G Kim

Vet Res Commun. 2007 Nov 20; : 18027099

Enrofloxacin, a fluoroquinolone antibiotic has been used widely in

humans and domestic animals, including dogs, because of its

broad-spectrum activity and relative safety. The side effects of

fluoroquinolone, induced tendinopathy, tendonitis, spontaneous tendon

rupture and cartilage damage, remain incompletely understood. In the

present study, we investigated the in vitro effects of enrofloxacin on

cell proliferation and induction of apoptosis in canine Achilles tendon

cells and chondrocytes. Cell growth and proliferation after treating

with enrofloxacin for 2-6 days was quantified by a colorimetric

2,3-bis{2-methoxy-4-nitro-5-sulfophenyl}-2H-tetrazolium-5-carboxyanilide

inner salt (XTT) assay. The results showed that enrofloxacin could

inhibit the proliferation of canine tendon cells and chondrocytes at

increasing concentrations (10-200 mug/ml). The inhibition of

proliferation of canine tendon cells and chondrocytes after exposure to

enrofloxacin were associated with induction of apoptosis, as evidenced

by the typical nuclear apoptotic condensed nuclei found using Hoechst

33258 staining. It was demonstrated that canine tendon cells and

chondrocytes treated with 200 mug/ml enrofloxacin for 4 days exhibited

apoptotic features and fragmentation of DNA. Enrofloxacin also

increased the apoptosis of canine tendon cells and chondrocytes in a

dose and time-dependent manner. The results indicate that enrofloxacin

inhibits cell proliferation, induces apoptosis and DNA fragmentation,

which might explain enrofloxacin-induced tendinopathy and cartilage

damage.

Characterization of Fluoroquinolone-Induced Achilles Tendon Toxicity

in Rats: Comparison of Toxicities of 10 Fluoroquinolones and Effects of

Anti-Inflammatory Compounds YOKO KASHIDA AND MICHIYUKI KATO

Drug Safety Research Laboratory, Daiichi Pharmaceutical Co. Ltd.,

1-16-13, Kitakasai, Edogawa, Tokyo 134, Japan

Fluoroquinolone antibacterial agents have been reported to induce

tendon lesions in juvenile rats. In the present study, we characterized

fluoroquinolone-induced Achilles tendon lesions by comparing the

effects of 10 fluoroquinolones and examining the potential of one of

these antimicrobial agents, pefloxacin, to induce tendon lesions when

coadministered with one of nine anti-inflammatory compounds. Among the

10 fluoroquinolones tested, fleroxacin and pefloxacin were the most

toxic, inducing lesions at a dose of 100 mg/kg of body weight or more,

while lomefloxacin, levofloxacin, and ofloxacin or sparfloxacin and

enoxacin induced lesions at 300 mg/kg or more and 900 mg/kg,

respectively. In contrast, norfloxacin, ciprofloxacin, and tosufloxacin

had no effect even at the high dose of 900 mg/kg. The severity of the

Achilles tendon lesions appeared to correlate with the structure of the

substituent at the seventh position. Furthermore, pefloxacin-induced

tendon lesions were inhibited by coadministration with dexamethasone

and N-nitro-L-arginine methyl ester. Phenidone

(1-phenyl-3-pyrazolidinone) and

2-(12-hydroxydodeca-5,10-diynyl)3,5,6-trimethyl-1,4-benzoquinone

(AA861) also decreased the incidence of tendon lesions. In contrast,

catalase, dimethyl sulfoxide, indomethacin, pyrilamine, and cimetidine

did not modify these tendon lesions. These results suggest that nitric

oxide and 5-lipoxigenase products partly mediate

fluoroquinolone-induced tendon lesions.

Kinematic gait analysis of the hind limb after tibial plateau levelling

osteotomy and cranial tibial wedge osteotomy in ten dogs.

J Y Lee , G Kim , J-H Kim , S H Choi

J Vet Med A Physiol Pathol Clin Med. 2007 Dec ;54 (10):579-84 18045343

This study identifies and compares the kinematic gait changes occurring

in tibial plateau levelling osteotomy (TPLO) and cranial tibial wedge

osteotomy (CTWO) limbs after transection of the cranial cruciate

ligament (CrCL). Ten, healthy, adult beagle dogs were assigned to TPLO

(five dogs) and CTWO (five dogs) groups. Hind limb kinematics were

assessed, while dogs were trotted at speeds ranging from 2.0 to 2.3

m/s. The animals were evaluated preoperatively (prior to TPLO and CTWO

surgery) and at both 8 and 12 weeks after surgery. Two-dimensional

evaluation was synchronized to obtain the three-dimensional coordinates

using the APAS motion analysis software. Gait patterns were assessed by

measuring stifle, tibiotarsal joint angles and stifle joints angular

velocity. Stifle and tibiotarsal joint functions were not affected by

TPLO surgery, but stifle and tibiotarsal joint angles were changed,

following CTWO surgery, compared with their preoperative values. The

angular velocity patterns of CTWO were characterized by increased

stifle joint extension velocity from the middle to end swing phase and

decrease in the peak velocities (flexion) during swing phase. None of

these changes was observed in the stance phase after the CTWO surgery.

These kinematic results showed that dogs that underwent a CTWO

procedure were more likely to have significantly hyperextended gait

patterns of the swing phase postoperatively than the dogs that had a

TPLO procedure for repair of a ruptured CrCL.

Toni Lynch wrote:

Dear ,

This info was given to me by my

collegue who is a board vet pathologist and teaches at uni. This was

the result of her correlation of the literature and I did not find

anything in it to discredit the info. Perhaps it was not as well

researched as I had assumed but it was quite extensive. As for my

findings - they are real. There are definitely a number of the cruciate

dogs I see with other sites of inflammation. I never looked for

inflammation anywhere else in the body before reading this info from my

collegue and would only address the biomechanics (with success).

However I have found it interesting to note other findings , regard

the dog as a whole and attempt to address them as part of the whole

animal.

Dr Toni Lynch

BVSc Hons GDAnimal Chiro

-----

Original Message -----

From:

Freedman

To:

VetRehab

Sent:

Tuesday, January 08, 2008 12:18 PM

Subject:

Re: Tendon issues with Fluoroquinolones

Toni

I'm not sure where you got your

info' but it isn't correct-cruciate dz isn't a result of inflamm-we

don't see as many acute tears in humans because of dog's comformation

and activity, as well as an associated collagen degenration and loads.

The inflammation is not pre-existing-it's been there as part of

the inflamm repsonse to the ligamentous pathology, not the opposite.

Also, meniscal injury contributes to this as well.

Freedman VMD CCRT

-----

Original Message -----

From:

Toni Lynch

To:

VetRehab

Sent:

Monday, January 07, 2008 7:30 PM

Subject:

Re: Tendon issues with Fluoroquinolones

Dear Laurie,

I am not sure how to approach

this but when I studied the pathophysiology of cruciate repairs, my

looking up the pathology evidence indicated that usually they were

secondary tears - not primary as in people. Also there was inflammation

and degenerative changes present usually prior to tearing. Can any

others add to this?

This being the case I have paid

attention to cruciate injury in dogs and have often found there other

sites of pain/inflammation in the body concurrently- most commonly the

GIT. If some other condition did exist in the body that was recognized

and was prescribed either NSAIDs or abios- this may be important.

However would it indicate the medication is the issue or the

preexisting inflammation? This angle may need to be considered in the

questions asked.

Dr Toni Lynch

BVSc Hons GDAnimal Chiro

-----

Original Message -----

From:

Dr. Laurie McCauley

To:

VetRehab

Sent:

Monday, January 07, 2008 1:20 AM

Subject:

RE: Tendon issues with Fluoroquinolones

Hi All,

If we come

up with a survey, Clean run may be willing to put it up on their

website. Clean run is “the” magazine company for agility people. This

way we could reach a large percentage of canine athlete owners.

I am not a

researcher so I would need some help. What I was thinking was to ask

people:

Has your

athlete torn his or her cruciate?

Was your

athlete on any medication just prior to or when this happened?

If yes, was

an antibiotic or NSAID? (this way people will not freak out thinking

ab’s are going to cause cruciate damage?????)

If your dog

has torn their cruciate and was on or recently on an antibiotic, which

antibiotic (list 10 or more)

Maybe a

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