細菌性心筋炎を伴った僧帽弁狭窄症の猫の1例

誌名誌名 The journal of veterinary medical science

ISSNISSN 09167250

巻/号巻/号 6911

掲載ページ掲載ページ p. 1171-1174

発行年月発行年月 2007年11月

農林水産省 農林水産技術会議事務局筑波産学連携支援センターTsukuba Business-Academia Cooperation Support Center, Agriculture, Forestry and Fisheries Research CouncilSecretariat

NOTE lnternal Medicine

Mitral Stenosis with Bacterial Myocarditis in a Cat

Aya MATSUU1)， Teppei KANDAl)， Akihiko SUGIYAMA2)， Toshiyuki MURASE3) and Yoshiaki HlKASA1

)

I)Departments of Veterinary Internal Medicine， 2JLaboratory Veterinary Medicine and 3JVeterinary Microbiology， Faculηof Agriculture， Tottori University， Koyama-Minami 4-101， Tottori 680-8553， Japan

(ReαlV巴d30 March 2007/Accepted 10 July 2007)

ABSTRACf. An eleven-year-old female Japanese mongrel cat was referred to the Tottori University Veterinary Teaching Hospital for assessment of acute p訂 esisand dyspnea. Two-dimensional echocardiography showed a hydropericardium. The mitral valve leaflets were thickened， the separation of the right and left leaflets was not complet巴. Treatments with intravenous f1uids of lactate Ringer solu-tion， furosemide， urokinase， antibiotics were initiated， but did not improve the respiratory failure. The cat died 10 days later. From pathological and microbiological exarninations， this was an unusual case diagnosed as acquired mitral stenosis associated with congenital malformation of the mitral valve complex， and accompanied by secondary infectious myocarditis with Streptococcus canis. KEY WORDS: mitral stenosis， myocarditis， Streptococcus canis.

An el巴ven-year-old，4.0 kg female Japanese mongrel cat

was referred to出eTottori University Veterinary Teaching

Hospital for assessment of acute paresis. The history given

by the owner was that the cat had sudden paresis and dysp-nea three weeks before. The p訂巴sisresolved by the next

day; however，出edyspnea had progressed. On the day of

adrnission， the cat presented paresis again. The cat was subjected to a complete c¥inical evaluation

under oxygen inhalation. S巴veredyspn巴aand lethargy were

observed. The femoral pulse was faint and the hind limbs

felt cold. The respiration and heart rates were remarkably

high， 180 breaths/rnin and 200 beats/rnin， respectively. C佐

diac auscultation revealed tachycardia with slight murrnur. Full complete blood counts and serum biochemistry tests

were performed. Leukocytosis (18，200 counts/μl)， slight

increases in blood urea ni位ogen(40.7 mg/dl)， creatine (1.3

mg/dl) and alanine arninotransferase (407 U/l)， and a great elevation in creatine phosphokinase (> 40，000 U/l)， were

found. Serum cardiac仕oponin1 was also high， at 0.8 ng/ml (reference range: 0.03-0.16 ng/ml [9]). From these find-

ings， some myocardial cellular damage was suspected.

Slight abnorrnalities were also seen in the blood coagulation

profiles， incJuding the platelet counts (120，000/，μ1)， pro-

thrombin time (10.6 sec)， and activated partial thromboplas-tin time (27.9 sec). Both feline leukemia virus antigen and

feline immunodeficiency virus antibody tests were negative.

Thoracic radiographs revealed a rounded cardiac silhou-

ette with elevated pleural parenchymal density， suggesting the presence of pulmonary edema. Two-dim巴nsional

echocardiography showed a pericardial effusion， and 250 ml of effusion fluid was removed by pericardiocentesis. The

specific gravity of the effusion fluid was 1.018 and the cytology detected a moderate amount of segmented neutro-

phils. B-mode echocardiography revealed a greatly

* CORRESPONDENCE TO: MATSUU， A.， Department of Veterinary Intemal Medicine， Faculty of Agriculture， Tottori University， Koyama-Minami 4ー¥01，Tottori 680-8553， Japan. e-mail: matsuu@muses.tottori-u.ac.jp

J. Vet. Med. Sci. 69(11)・1l71-1174，2007

enlarged left atrium (AO:LA ratio=I:2.1). The presence of

thromboembolism was not demonstrated in any of the car-

diac chambers. An echodense mass was detected on the ori-

gin of the left mitral leaflets (Fig. 1). The mitral valve leaflets were thickened and白巴 separationof the right and left leaflets was not compl巴te，with dorning of the ant巴riormitral valve leaflet into the left ventricle during diastole.

Narrow jet stream into the left v巴ntricleduring diastole was found by color flow-doppl巴rechocardiography. Regur-

gitant rnitral flow during systole was also found (Fig. 2). M-

mode measurement revealed a marked hyposystole of the

left ventricle (FS: 6.8%). Based on these findings， mitral stenosis was strongly suspected. Treatments with intrave-

nous fluids of lactate Ringer solution， furosernide (1 mglkg IVevery 12 hr， and 2.5 mglkg in intravenous fluids)， uroki-nase (6，000 U IV over 60 rnin)， antibiotics (ofloxacine， 5

mglkg SC)， wer巴initiated，but did not improve the respira-tion failure. On the next day， the same volume of effusion was detected again by pericardiocentesis with echocardio-

Fig. 1. Two-dimensional echocardiogram showing the right parastemaI long axis view. There is an enlarged left atrial (LA) The mitral valves (MV) are thickened， and an echodense mass was located at the origin of the left mitralleaf (arrow).

1172 A. MATSUU ET AL

Fig. 2. (A) Color flow-doppler echocardiography recording narrow J巴tstream into the left ventricle (L V) during diastole DOlT】ingof the anterior mitral valve leaflet into the left ven-tricIe was also found (抑制). (8) Color flow-doppler echocardiography recording regurgitate mitral flow during systol巴.

graphy. Continuous treatments were recommended， but the owner declined this. Th巴 catwas discharged and died 10 days lat巴r.

Necropsy was performed within a few hours of出edea出.

The lungs were diffus巴lycongested and edematous， and par-tial emphysema was observed. The left atrium was severely enlarged. The left ventricular free wall side papillary mus-cle was extremely hyper仕ophied，and the chordae tendineae W巴renot observed adjac巴ntωthernitral valve. Both mitral valve leaflets were thicken巴d，white-colored and smooth on their surfaces， and they were fused to each other， producing an oval and stenosed orifice (Fig. 2). Yellow-to white-col-ored foci， varying in sizes (2 to 5 mm)， were founded in the myocardium (Fig. 2)， lung， and parenchyma of the liver that were especially prominent in marginal areas (Data not

shown). Histological exarninations of the ventricular and papillary

myocardium rev巴aledthe characteristics of myocarditis，

which were accompanied by randomly distributed multifo-cal areas of necrosis surrounded by inflammatory infiltrates

Fig. 3. Gross appearance of th巴heart.The left ventricular free wall side papillary muscIe (PM) was extremely hypertro-phied. Chordae tendineae were not observed. Both mitral valve leaflets (arrow) were thickened

chiefly consisting of neutrophils. In the necrotic regions， multiple Gram-positive cocci were observed， suggesting that the myocarditis was of bacterial etiology. The myocar-dium surrounding the focal n巴crosiswas mildly atrophied and partially disorganized， howev巴r，fibrosis was extremely rnild (Fig. 3). The rnitral valve apparatus was fibrous and thickened， and accompanied by mild mucus production and collagenous proliferation. Bacterial multiplication and inflammatory infiltrations were absent in the rnitral valve apparatus. Directjunctions between the mitral valve and the papillary muscl巴swere observed (Data not shown). Obvi-ous structures of the chordae tendineae were not present (Fig.4). In other organs including the lungs， liver， kidneys， and spleen， there were severe suppurative inflammations characterized by bacterial multiplications and inflammatory infiltrations with neutrophils， macrophages， lymphocytes， and plasma cells. These findings indicated that this case had generalized bacterernia. Centrilobular congestion was also found in the liver. Atrophy， fatty degeneration， and coagu-lative n巴crosiswere found in related hepatocytes.

Heart specimens w巴resubjected to bacteriological exam-inations. Aerobic culture on heart infusion agar plates with 5 percent sheep erythrocytes yielded a heavy growth of beta-hemolytic colonies in pure culture. These colonies wer巴 identifiedas Streptococcus species by their positive Gram staining， the absence of catalase， and the absence of tolerance of 6.5 percent sodium chloride. The Lancefield

group was detected from the isolate by slide agglutination t巴stfor the identification of s汀巴ptococcalgroup with com-mercial rabbit antisera (Denka-Seiken， Tokyo， Japan)， and was found to be group G. PCR amplification was carri巴dout using species-specific primers to the sodAint gene of Streptococcus canis [4]. Th巴 isolatewas positive for the sodAint gene， with a specific amplicon of 363 bp (data not shown).

This case had severe left ventricular heart failure includ-

MITRAL STENOSIS， STREPTOCOCCUS CANIS 1173

Fig.4. (A) Microscopic finding of focal necrosis in the left ventral myocardium. H&E stain x 40. Bar = 500μm. (B) Higher magnification of the focal necrosis in出巴 leftv巴ntralmyocardium. The focal necrosis was infiltrated by neutro-phils， and multiple cocci were observed. H&E stain x 400. Bar = 50μm

ing left atrial enlargement， pulmonary， and pericardial effu-sion， and these were suspected to be caused by mitral stenosis. Characteristic echocardiography findings of this cat， including thicken巴dmitral valve， poor leaf¥et separation were similar to those reported in cats with mitral stenosis [10]， and diastolic doming of anterior mitral valve which was found in over half of mitral stenosis dogs [6] were also detected. Although diastolic mitral filling velocity was not determined， color f1ow-doppler echocardiography showed narrow jet stream into the left ventricle during diastole. Mitral valvular stenosis would obstruct ventricular filing and limit cardiac output.

In cats， mitral stenosis is an巴xtremelyrar巴 cardiacdis-ease， and may occur as a congenital or acquired condition. Only fiv巴catsof mitral stenosis have been report巴dto date. They were two cats with congenital supravalvular mitral stenosis [2， 10]， one cat with hypertrophic cardiomyopathy [12]， and two cats of secondary acquired lesions related to congenital dysplasia of the mitral valve complex [10]. In our case，出emacroscopic changes in the mitral valve com-

Fig. 5. Microscopic findings of a direct junction of the mitral valve and papillary muscle. Obvious chordae tendineae struc-ture was not present. H&E stain x 30. Bar = 500μm.

plex-thickened mitral valve leaflets and hyp巴rtrophiedpap-illary muscles resulting in absence of chordae tendineae-are compatible with the anatomicallesions previously described in malformation of the mitral valve complex in cats [8]. These anatomic abnormalities would reduce leaflet mobility and advanc巴 thedynamic outflow tract obstruction or increase systolic valvular regitation secondly as same as two

cats previously reported [10]. Additionally， bacterial myocarditis caused by S. canis

was present in our case. S. canis is a beta-hemolytic Lance-field group G streptococcus isolated as commensal f10ra from the skin and mucosa of dogs [3]. S. canis has been iso-lat巴dfrom a variety of animals， including dogs， cats， rats， mice， foxes， and raccoon dogs [3，5， 7， 13]. In cats， this pathogen has been report巴dto cause arthritis [5]， contagious lymphadenitis， pharyngitis， and submandibular edema [5， l3]. Streptococcci， especially S. canis， have b巴enreport巴dto be the most common cause of infectious endocarditis， and are lik巴Iyto infect the mitral valve in dogs [11]. This is the first reported case of S. canis myocarditis with focal necro-sis in a cat. In human beings， chronic rheumatic endocardi-tis infected with group A beta-hemolytic Streptococcus is the most f白quentetiology of acquired mi汀alstenosis， and fusions of the valve commissures， with or without thicken-ing of the leaflets and chordae tendineae， are characteristic findings [1]. However， no endocarditis was recognized in the cat described in this report. In addition， there was no evidence from the histological findings to support the pres-ence of an immune-m巴diatedphenomenon. The random，

multifocal distribution and intramyocardial location of the lesions suggested that the organisms were of hematogenous origin. Indeed， as other organs had severe suppurative lesions infected with Gram-positive streptococci， general-ized hematosepsis with this organism was support巴d

The size and degree of fibroplasia of the myocardial lesions may be consistent with出巴durationof the inflamma-

1174 A. MATSUU ET AL.

tion. The myocardial lesions might hav巴 aggravatedheart

function， but these lesions seemed to be comparatively newer出anthe ventrallesions. There was only a mild fibro-

plastic component in th巴circumferentialmyocardium of the

focal necrosis in this cas巴， sugg巴stingthat th巴hypertrophied

papillary muscle and absenc巴ofchordae tendineae were not

due to a result of出emyocarditis. In addition， there wer巴no

inflammatory infiltrations of出ejunctions of出epapillary

muscles and mitral valve 1巴aflets.From these features， this

case was diagnosted as acquired mitral stenosis associated

with mitral valve complex malformation， and accompanied by secondary infectious myocarditis with S. canis.

In a previous report， nine of 15 dogs with mitral stenosis

W巴reeuthanatized or died by 2.5 y巴紅sof age [6]. However，

two cats with mitral stenosis related to mitral valve complex

malformation reported previously [10] and a cat in the

present report， all were over 10 years old. In cats， mitral stenosis associated with mitral valve dysplasia may develop

subclinically until the terminal stage. In our case， the bacte-rial infection， which might be resulted from aging or less resistant to infect， developed acutely and contribut巴dto the

d巴teriorationin this cat' s condition.

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