Download Aseptic Bacterial Arthritis Dr Abdul

Aseptic Bacterial Arthritis
Dr Abdul-Hadi Abbass Abd
SUMMARY
Arthritic inflammation in man and animals can result from a great
variety of causes, and the causative stimuli of many types of arthritis are
unknown such as rheumatoid arthritis or imperfectly understood such as
reactive arthritis associated with microbial infections.
In conclusion: The sequence of events that is responsible for the
inflammatory reactions observed in these experimental models has not
been defined.
The recommendations are continuing in these studies in regarding solve
this chronic health problem.
Dr Abdul-Hadi Abbass Abd
‫التهـــاب المفاصاللجرثومي العقيم‬
‫الدكتور عبدالهادي عباس عبد‬
‫الخالصــــة‬
‫ان التهاب المفاصل في االنسان والحيوان تكون نتيجة لعوامل واسباب عديدة والكثير من‬
‫هذه االسباب والعوامل غير معروفة كما في الروماتيزم والتهاب المفاصل المتفاعل ‪Reactive‬‬
‫المرتبط باالصابات الجرثومية‪ .‬ان فهم التهاب المفاصل وخصائص البكتريا التي تكون اساسا‬
‫لدراسات تجريبية اللتهاب المفاصل المزمن قد توصلنا الى معرفة االسباب التي تؤدي الى‬
‫التهاب المفاصل‪.‬‬
‫لقد كانت دراسة وتحليل المشاهدات والتغيرات المصاحبة اللتهاب المفاصل الجرثومي‬
‫المتفاعل على الحيوانات المختبرية لم تصل الى تكوين صورة واضحة عن السبب اللتهاب‬
‫المفاصل لحد االن‪.‬‬
‫ألهدف من هذه الدراسة هو لتوضيح ومعرفة الشواهد واالسباب التي تصاحب التفاعالت‬
‫المرضي ة التي تسببها البكتريا في التهاب المفاصل‪ .‬اضافة الى ذلك مالحظة النظام المناعي‬
‫المتكون اثناء التهاب المفاصل للحيوانات المختبرية التجريبية المستعملة في دراسة هذه الظاهرة‬
‫ودورها في تكوين المرض‪.‬‬
‫‪Dr Abdul-Hadi Abbass Abd‬‬
INTRODUCTION
The term arthritis (acute and chronic form) refers to any inflammatory
reaction occurring in a joint.
Chronic arthritis is one of the most challenging of modern medical problems.
Theoretically, chronic inflammation might occur from a continuous stimulus,
which can result from the perpetual supply of antigen in the circulation or
persisting antigen in the joints. It is known that arthritic syndromes can be caused
by many mechanisms including various infections and types of trauma and in some
cases the etiology is uncertain, as in rheumatoid arthritis (RA) in humans [1].
Types of Arthritis
The clinical, pathological and serological features of Rheumatoid arthritis
compared with other types of arthritis are shown in Table 1.
1. Rheumatoid arthritis.
RA causes aches and pains in connective tissues near or around the joints for about one
per cent of the adult population. RA is characterized by a constellation of histological
changes. It is a broad spectrum of chronic destructive inflammatory disease involving
synovial articulating joint [ 2]Many potential causative agents of RA have been proposed
including viruses and persistent bacterial cell debris[ 3]. However, RA etiology is still
undetermined.
The clinical, pathological and serological features of RA compared with other
Dr Abdul-Hadi Abbass Abd
Table (1) . Comparison of Rhematoid arthritis with other types of arthritis
Rheumatoid Adjuvant Collagen Streptococcal
arthritis
arthritis arthritis
arthritis
ClinicalFeatures
Spontaneous
Persistent or recurrent distribution
Peripheral.
Spinal
Extra-articular Involvement
Uveitis
Nodules
Genital lesions
Sjŏgren's syndrome
Pathological Features
Mononuclear cell,
Infiltrative synovitis
PannusPeriostitis or bony ankylosis
+
+
+
-
-
-
+
Serologic Features
Rheumatoid factor
Anti-Type II collagen antibodies
types of arthritis are showed in Table 1. The large joints such as knee, ankle, elbow, and
wrist are involved [4]. If RA is severe, the fluid is transformed to thick, characteristic
pus. The normal knee joint Figure 1 was comparing with the synovial displays patchy
acute, nonspecific alterations, along with increased vascular permeability and infiltration
by inflammatory cells, especially polymorphonuclear leukocytes. The histopathology of
RA involves hypertrophy of the synovial lining surface and grossly, the synovial appears
edematous, inflamed and protrudes into the joint space as slender villous projections[5].
2. Infectious or septic arthritis.
Septic arthritis is an infection in the joint (synovial) fluid and joint tissues. The
infection usually reaches the joints though the bloodstream, although some joints
Dr Abdul-Hadi Abbass Abd
may become infected due to an injection, surgery, or injury. Different bacteria and
viruses can infect a joint and usually are associated with a person's age. The
following types of infectious organisms have been associated with septic arthritis.
This type of arthritis is caused by microorganisms such as bacteria, Mycoplasmas,
viruses. These microorganisms infect the joint directly [6]. β-hemolytic
streptococci have been reported as causing between 3% and 30% of cases of
human septic arthritis [7]. S. pyogenes and group G streptococci [8].were isolated
from arthritic joints. Other bacteria are also isolated from rheumatic patients, such
as Brucella[9], E. coli[10]. A number of investigators reported that Mycoplasma
arthritidisinduced chronic relapse arthritis in rats, pigs, mice and turkeys. Viruses
can cause disease in any of several ways, ranging from acute short- term infections
to those that progress with age and last perhaps a life-time.
3. Non-infectious (aseptic or reactive) arthritis.
Reactive arthritis is an acute, non-purulent arthropathy that develops as a result of an
infection elsewhere in the patient. The variety of organisms associated with reactive
arthritis is considerable, ranging from several Salmonella and Shigella species which
cause enteric infection associated with arthritis [2], to Clostridium perfringens which is
reported in higher numbers in colons of RA patients compared with normal colon.
Some investigators found that Campylobacter jejune enteric infection correlated with
reactive arthritis [11]. Arthritis may also be related to genital tract infections caused by
other pathogens, such as Chlamydia and gonococci [12]. Intraperitoneal and intravenous
injection of live Yersinia enterocolitica induced arthritis in Lewis rats[13]. An
experimental mouse model of Yesinia infection was created to induce reactive arthritis
[14]. Reactive arthritis generally does not require that the initiating organisms be viable
and bacterial cell wall fragments have been used extensively in experimental model.
The ability of a cellular component of S. pyogenes initiates and sustains a chronic
inflammatory process. Other researcher’s induced chronic arthritis in rabbits with S.
Dr Abdul-Hadi Abbass Abd
pyogenes cell wall components inoculated intraarticularly [15]. The clinical, pathological
and serological features of streptococcal arthritis compared with RA and other human and
animal models of arthritis (Table 1).
Reactive arthritis is associated with the persistence of bacterial antigen in the joint
tissue after the symptoms have disappeared. The symptoms then reappear after a minor
stimulus[16]. Histological changes in an acute exudative streptococcal arthritis in guinea
pig and rat were followed by erosive synovitis with pannus formation and destruction of
the margins of the articular cartilage and subchondral bone[17]. Streptococcal fragments
have the ability to stimulate a number of immune responses that have not been precisely
defined. Similarities exist between streptococcal arthritis and human RA:
1- The incidence of cell wall-induced disease is greater in females than males in
Sprague-Dawley rats [18].
2- Genetic factors play a key role in disease induction [19]
3- The disease is complementing dependent, and the immune cells of cell wall-treated
rats are IL-2 deficient [20].
4- Clinical disease is remittent and relapsing [21].
Study of the streptococcal fragments model of arthritis will be of interest in
elucidating general mechanisms of arthritis that may be applicable in man.
4
4. Collagen arthritis.
This type of arthritis is induced by injection of emulsified type II collagen with
either incomplete or complete Freund's adjuvant [22], and is presumed to involve the
generation of an autoreactive immune response against the joint. The latent period of
collagen arthritis is 2 weeks after injection of collagen, after which the disease develops
in 40% of rats [23]. The characteristics of collagen arthritis in animals are synovial
hyperplasia, infiltration of the subsynovial tissue with inflammatory exudation of cells
into the joint space, marginal erosion, periostitis, and destruction of the cartilage surface
Dr Abdul-Hadi Abbass Abd
[24].
The role of cellular and humoral immunity in collagen II-induced arthritis in rats
was studied [25]. Collagen-induced arthritis was associated with the elevation of
Urokinase and tissue-type Plasminogen Activator in animals but it was not related to
lymphocyte proliferation reactivity. Collagen arthritis in an animal model was used to
study the immunogenetic and pathogenetic aspects of development of autoimmune
arthritis. This study was developed in two different ways:
Firstly, T cells mediated activation of macrophages and fibroblasts in the joint
leading to destructive delayed-type hypersensitivity, and secondly, formation of immune
complexes in the joints, consisting of anti-collagen autoantibodies and rheumatoid factors
[26]. Furthermore, the immune response to collagen may be regulated by genes closely
associated with the major histocompatibility complex [27].
5. Adjuvant arthritis.
Adjuvant arthritis in the rat can be induced by a single injection of a dispersion of
certain dried, heat-killed microorganisms such as Mycobacterium, Corynebacteria,
Streptococci, or their cell wall components in a suitable oily vehicle. It is known
that Nocardia and Corynebacterium rubrum [28],can replace Mycobacterium for
adjuvant arthritis production. [29],have reported that cell walls from Streptomyces
fradiae, S. lavenulae,L. plantarum and Staphylococcus aureus were able to
produce adjuvant arthritis. The cell walls of S. aureus and streptococci showed that
in water-in-oil emulsion were arthritogenic in female Lewis rats [30]. Following
the injection of Freund's adjuvant consisting of whole heat-treated acid-fast bacilli,
mineral oil and an emulsifying agent, arthritis is produced. This occurred without
any added tissue homogenate or other bacteria. Following a latent period of 2 to 3
weeks arthritis and periarthritis develops which involves most of the joints and
Dr Abdul-Hadi Abbass Abd
extremities [2]. The clinical symptoms of adjuvant arthritis are redness, edema,
deformity of limbs and tail[31]. Clinical, pathological and serological features
compared with RA are listed in Table 1.
Humoral and cellular immunity have been extensively studied in adjuvant
polyarthritis [27]. Unlike RA, there is little or no increase in immunoglobulin
synthesis by affected tissues, and rheumatoid factor is absent [32]. The major
cellular components are rapidly proliferating cells, presumably macrophages,
arising from the bone marrow and resembling those of a delayed hypersensitivity
reaction. However, it is likely that the pathogenic cells are T lymphocytes, for two
reasons.
Firstly, treatment with anti-thymocyte serum or monoclonal anti-T cell antibodies
in vivo hinders the development of adjuvant arthritis [33].
Secondly, arthritis has been passively transferred with concanavalin A (Con A)
activated T cell blasts derived from rats with adjuvant arthritis[34], although it has
not been possible to determine the specificity of these pathogenic T cells.
However, Mycobacterium-reactive T cell clones have been isolated from rats
immunized with Mycobacterium and one of these clones, the A2b clone, has been
reported to induce arthritis in naive recipients and interestingly, to protect the rats
from adjuvant arthritis[35],[36]reported that the epitope of mycobacterium) cell
wall recognized by the A2b T cell clone was located on the 65kd heat shock
protein.
Dr Abdul-Hadi Abbass Abd
Figure 1: Anatomy of Knee Joint
Dr Abdul-Hadi Abbass Abd
References
[1] Jacobs C., D. Young, S. Tyler, G. Callis, S. Gillis, and P.J. Conlon. 1987.
111 vivo treatment with IL-1 reduces the severity and duration of antigeninduced arthritis in rats. J. Immunol. 141:2967-2974.
[2] Bennett J.C. 1981. The etiology of rheumatoid arthritis in:W.N. Kelley, E.D.
Harris, S. Ruddy, C.B. Sledge (ed.), Textbook of Rheumatology p. 887-895.
W.B. Saunders, Philadelphia.
[3] Pritchard D.G., R.L. Settine, and J.C. Bennett. 1980. Sensitive
mass spectrometric procedure for the detection of bacterial cell
wall components in rheumatoid joints. Arth.Rheum. 23:608-610.
[4]Zvaifler
N.J.
1973.
The
immunopathology
of
joint
inflammation in rheumatoid arthritis. Adv. Immunol. 16:265-336.
[5] Campbell I.K., M.R. Rich, R.J. Bischof and J.A. Hamilton.2000. The colonystimulating factors and collagen induced arthritis: Exacerbation of disease by
M-CSF and G-CSF and requirement for endogenous M-CSF. Journal of
Leukocyte Biology. 68:144-150.
[6] Reese R.E., and R.G. Douglas. 1983. Practical approach to infectious disease.
Brown L. & Co. Boston USA.
[7] Rosenthal J., G.G. Bole, and W. Robinson. 1980. Acute non-gonococcal
infectious arthritis. Evaluation of risk factors, therapy and outcome.Arthritis
Rheum. 23:887-889.
[8] Trenkner S.W., Braunstein, M.D. Lynn, and R.W. Ike. 1987. Group G
streptococcal arthritis and bowel disease: a rare enteropathic arthropathy.
Gastrointest.Radiol. 12:265-267.
[9] Al-Rawi Z.S., N. Al-Khateeb, and S.J. Khalifa. 1987. Brucella arthritis among
Dr Abdul-Hadi Abbass Abd
Iraqi patients. Br. J. Rheum. 26:24-27.
[10] Bayer A.S., D.C.Norman, and I.K. Blomquist.1988.Comparative efficacy of
ciprofloxacin and ceftriaxone in experimental arthritis caused by Escherichia
coli. Rev. Infect. Dis. 10:184-188.
[11] Skirrow M.B. 1977. Campylobacter enteritis a 'new' disease.Br. Med. J. 2:911.
[12] Keat , A. 1983 . Reiter’s syndrome and reactive arthritis in perspective. N. Engl.
J. Med. 309:1606-1615.
[13] Hill, J.L. and D.T.Y. Yu. 1987. Development of an experimental animal model
for reactive arthritis induced by Yersinia enterocolitica infection. Infect. Immun.
55: 721-726.
[14] Yong Z., J.L. Hill, T. Hirofuji, M. Mander, and D.T.Y. Yu. 1988. An
experimental mouse model of yersinia -induced reactive arthritis. Microbial
Pathogenesis 4:305-310.
[15] Schwab J.B., J.B. Allen, S. K. Anderle. F. G. Dalldorf. R. Eisenberg, and W.J.
Cromartie. 1982. Relationship of complement of experimental arthritis induced
in rats with Streptococcal cell walls. Immunol. 66:255-261.
[16]
Stimpson
S.A.,
Cromartie
Esser
W.J.,
R.E.,
Carter
and
P.B.,
Sartor
Schwab
R.B.,
J.H.
1 9 8 7 . Lipopolysaccharide induced recurrence of arthritis in rat joints pre
viously
injured
by
peptidoglycan -polysaccharide. J. Exp. Med.
165:1688-1702.
[17]Cromartie
W.J.
1981.
Arthropathic
properties
of
peptidoglycan-
polysaccharide complexes of microbial origin.In: Deicher H., C.I. Schulz (ed.),
Arthritis Models and Mechanisms p. 24-50. Springer-Verlag, Berlin
Heidelberg.
[18] Wilder R.L., J.B. Allen, and C. Hansen. 1987. Thymus -dependent
Dr Abdul-Hadi Abbass Abd
and -independent regulation of Ia antigen expression in situ by cells in the
synovium of rats with streptococcal cell wall-induced arthritis.
Differences in site and intensity of expression in euthymic, athymic, and
cyclosporin in a treated LEW and F344 rats. J. Clin. Invest. 79:1160-1171.
[19] Abu Kheir W., J.C. Gevrey, H. Yamaguchi, B. Isaac, and D. Cox. 2005. A
WAVE2-Abi1 complex mediates CSF-1-induced F-actin-rich membrane
protrusions and migration in macrophages.118:5369-5379.
[20]Stimpson S.A., F.G. Dalldorf, I.G. Otterness, and J.H. Schwab. 1988.
Excerbation of arthritis by ILl in rat j o i n t s p r e v i o u s l y i n j u r e d b y
p e p t i d o g l y c a n polysaccharide. J. Immunol. 140:2964-2969.
[21]Irvine K.M., M.R. Andrews, M.A. Fernandez-Rojo, K. Schroder, C.J.Burns, S.
Su, A.F. Wilks, R.G. Parton, D.A. Hume, and M.J. Sweet.2009. Colonystimulating factor-1(CSF-1) delivers a proatherogenic signal to human
macrophages.85:278-288.
[22]Shoen R.T., H. Mahlman, D.E. Trentham, L. Perry, M.I. Greene, and
J.R. David. 1982. Autoimmunity induced by type II collagen-coupled spleen
cells. J. Immunol. 128:717-725.
[23]Trentham D.E., G.M. Kammer, W.J. McCune, J.R. David. 1981.
Au t o i mmu n i t y t o c o l l a g e n . A s h a r e d f e a t u r e o f psoriatic and
rheumatoid arthritis.Arthritis Rheum. 24:1363-1369.
[24]Terato K., R. Hashida, K. Miyamoto, T. Morimoto, Y. Kato, S. Kobayashi, T.
Tajima, S. Otake, H. Hori and Y.
Nagai. 1982.
Histological,
immunological and biochemical studies on type II collagen-induced
arthritis in rats. Biomed. Res. 3:495-498.
[25]Cook, A.D., E.L. Braine, I.K. Campbell, and J.A. Hamilton. 2002. Differing
roles for urokinase and tissue-type plasminogen activator in collagen-induced
arthritis. Am.J. Pathol. 160: 917-926.
Dr Abdul-Hadi Abbass Abd
[26] Holmdahl R., M.E. Andersson, T.J. Goldschmidt, L. Jansson, M. Karlsson,
V. Malmstrom, and J. Mo. 1989. Collagen induced arthritis as an
experimental model for rheumatoid arthritis. AMPIS 97:575-584.
[27] Huang JC, Vestberg M, Minguela A, Holmdahl R, Ward ES: Analysis of
autoreactive T cells associated with murine collagen-induced arthritis
using peptide-MHC multimers. Int Immunol 2004, 16:283-293.
[28] Paronetto F.1970. Adjuvant arthritis induced by C o r y n e b a c t e r i u m
r u b r u m . Proc. Soc. Exp. Biol. Med.133:296-298.
[29] Koga T., K. Kakimoto, T. Hirofuji, S. Kotani, H. Ohkuni, K. Watanabe, N.
Okada, H. Okada, A. Sumiyoshi, and K. Saisho. 1985. Acute joint
inflammation in mice after s y s t e m i c i n j e c t i o n o f t h e c e l l w a l l ,
its
peptidoglycan, and chemically defined peptidoglycan subunits from
various bacteria. Infect. Immun. 50:2734.
[29] Koga T., K. Maeda, K. Onoue, K. Kato, and S. Kotani. 1979. Chemical
structure required for immunoadjuvant and arthritogenic activities of cell wall
peptidoglycans. Mol. Immunol. 16:153-162.
[30] Kohashi 0. A. Kaora, 0. Atsushi, S. Kotani, and I. Azuma.1 9 8 2 . N e w
m o d e l o f a s y n t h e t i c a d j u v a n t N - acetylmuramyl - L- alanyl- Disoglutamine induced arthritis, clinical and histological studies in
athymic nude and euthymic rats. Lab. Invest. 47:27-36.
[30] Kohashi 0. C.M. Pearson, Y. Watanabe, S. Kotani, and T. K o g a .
1976.
Structural
requirements
for
arthritogenicity of
peptidoglycans from Staphylococcus aureusand Lactobacillus plantarum
and anologoussynthetic compounds. J. Immunol. 116:1635-1639.
[31] Wood F.D., C.M. Pearson, and A. Tanaka. 1969. Capacity of mycobacterium
wax D and its subfracticns to induce adjuvant arthrit is in rats. Int. Arch. Allergy
Dr Abdul-Hadi Abbass Abd
Appl. Immunol. 35:456-467.
[32]
Jasin
H.E.,
T.D.
Cooke,
and
E.R.
Hurdet
al.1973.
Immunological models used for the study of rheumatoid arthritis. Fed. Proc.
32:147-152.
[33] Larsson P., R. Holmdahl, L. Dencker, and L. Klareskog. 1989. I n v i v o
t r e a t m e n t w i t h a n t i - C D 8 a n d a n t i - C D 5 monoclonal antibodies
alters induced tolerance to adjuvant arthritis. J. Cell Biochem. 40:49-56.
[34] Taurog J.D., G.P. Sandberg, and M.L. Mahowald. 1983. The cellular
basis of adjuvant arthritis. Enhancement of cell mediated passive transfer
by concanavalin A a n d b y i m m u n o s u p p r e s s i v e p r e t r e a t m e n t o f
t h e recipient. Cell Immunol. 75:271-282.
[35] Holoshitz J., A. Mattitau, and I.R. Cohen. 1984. Arthritis induced in rats by
cloned T lymphocytes responsive to Mycobacterium but not to collagen type II.
J. Clin. Invest. 73:211-215.
[36] van der Zee R., W. van Eden, R.H. Meloen, A. Noordzij, and J.D.A. van
Embden. 1989. Efficient mapping and characterization zation of a T cell epitope by
simultaneous sythesis of multiple peptides. Eur. J. Immunol. 19:4347
[ 3 7 ] . U t s i n g e r P.D., N.J.Z v a i f l e r , and G.E.E r l i c h . 1985. R h e u m a t o i d
Arthritis, Lippincott. Philadelphia, USA.
Dr Abdul-Hadi Abbass Abd