Acute pericarditis of toxoplasmic origin

82

Letters to the editor

seems to illustrate the possibility of airborne transmission for rotavirus and subsequent respiratory illnesses, including laryngitis. U n f o r t u n a t e l y , rotavirus was not detected in throat swabs, but the Virus concentration m a y have been too low for the E L I S A system, or the nasopharyngeal sample m a y have been taken too late. Even if the possibility of an u n k n o w n or undetected agent causing acute laryngitis simultaneously to rotavirus infection cannot be ruled out, it appears reasonable to suppose that rotavirus caused the manifestations observed. (This work was supported by a grant from Consiglio Nazionale delle Richerche, Progetto Finalizzato ' C o n t r o l l o malaltie da infezione.)

I V Clinica Pediatrica UniversitY. ' L a Sapienza '--Centro C N R . Virus Respiratori, Rome, Italy

Giovanni Nigro and Mario Midulla

References L McCormack JG. Clinical features of rotavirus gastroenteritis. J Infection 1982; 4: 167-I 74. 2. Lewis HM, Parry JV, Davies HA, Parry RP, Mott A, Dourmashkin RR, Sanderson PJ, Tyrrell DAJ, Valman HB. A year's experience of the rotavirus syndrome and its association with respiratory illness. Arch Dis Child 1979; 54, 339-3463- Gurwith M, Wenman W, Hinde D, Feltham S, Greenberg H. A prospective study of rotavirus infection in infants and young children. J Infect Dis I98I; 144: 218-224. 4. Foster SO, Palmer EL, Gary GW, Martin ML, Herrmann KL, Beasley P, Sampson J. Gastroenteritis due to rotavirus in an isolated Pacificisland group: an epidemic of 3439 cases. ff Infect Dis 198o; I4I : 32-39.

Acute pericarditis of toxoplasmic origin Sir, Acute toxoplasmic pericarditis is considered a rare disease but we would like to report a case of acute toxoplasmic pericarditis in a y o u n g adult differing from previously reported cases by the absence of development of pericardial effusion. A 35-year-old non-alcoholic m a n was a d m i t t e d to the hospital because of chest pain. F o r seven days he complained of malaise, catarrhal s y m p t o m s and sweats. T h e day before admission he experienced precordial pain w i t h o u t dyspnoea, nausea or vomiting. Physical examination showed a patient in good health and apyrexia w i t h o u t any abnormality except for the presence of a pericardial friction r u b ; there was no sign of congestive cardiac failure; nor was there hepatosplenomegaly. A n electrocardiogram (ECG) disclosed sinus r h y t h m with Slight S T segment elevation in leads Vs, V 6. O n the following days the elevated S T - s e g m e n t r e t u r n e d to base line b u t with T - w a v e inversion in leads D u , Di1 l, aVF, V 5, V 6. X - r a y of the chest was normal. An echocardiogram showed no pericardial effusion and normal left ventricular wall motion. L a b o r a t o r y studies revealed a leukocyte count of IO'9 x io9/1 (74 per cent neutrophils, two per cent eosinophils, I4 per cent lymphocytes and IO per cent monocytes). E r y t h r o c y t e sedimentation rate was 27 m m an hour.

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Letters to the editor

Liver function tests were diffusely perturbed : serum glutamic oxalic transaminase (SGOT) 71 iu/l (N 3-32 iu/l), serum glutamic pyruvic transaminase (SGPT)

72 iu/l

(n o-29

iu/l),

lactic

dehydrogenase

(LDH)

448 iu/l

(N

5~240 iu/l), gammaglutamyl transferase (r GT) I IO iu/l (N o-45 iu/l), alkaline phosphatase(314 iu/l (N 65-240 iu/l), creatine phosphokinase (CPK) 230 iu/l (N less than IOO iu/l) and CPK MB 16 iu/l (N less than 15 iu/l). Significant

negative

laboratory

results

included

rheumatoid

factor,

cold

agglutinins, antistreptolysin 0 and Coxsackie A and B titres. Indirect fluorescent antibody test for Toxoplasma gondii performed on admission revealed no IgG, and IgM less than 128, with increasing titre in the convalescent

serum drawn

IO days later:

IgG 31 iu, IgM:

4000. A thallium

myocardial scintigram was normal. The patient was first treated with antipyreties. After serological confirmation of the diagnosis, a course of trimethoprim (80 mg) with sulfamethoxazole continued for four weeks.

(400 mg) four

times

daily

was started

and

ECG changesand biochemical abnormalities eventually returned to normal. Acute toxoplasmic pericarditis is exceptional. Only eleven caseshave been reported in the literature, ten occurring in adults and one in a child.l+ Leak1 observed two cases in his series but these patients had chronic

toxoplasmosis. In all casesthe diagnosis was supported by serological findings. Our patient differed from previously described cases by the absence of development

of pericardial

effusion.

In almost all other casesthe pericardial effusion was haemorrhagic. Abnormal liver function tests observed in our patient seem to be related to hepatic involvement; there was no suggestion of cardiac necrosis. We suggest that acquired toxoplasmosis is included in the differential diagnosis of acute

pericarditis of unknown origin, even without development of pericardial effusion, Dept of Medicine and Microbiology, Brugmann University Hospital, Brussels, Belgium

I.

F. Collart Y. Ghpzinski E. Cogan and J. Schmerber

References Leak D, Meghji M. Toxoplasmic infection in cardiac disease.AmJ

Cardiol1979;

43:

841-

849.

2. Grappe JM, Berthier

G, Melon

C. Pkkardite

et toxoplasmose.

Strasbuurg

M 1965; I%:

48*489.

3. Hakkila J, Frick HM, Halonon PI. Pericarditis and myocarditis caused by toxoplasma: report of a case and review of the literature. Am Heart J 1958; 55: 758-765. 4. Mirada A, Rub&+Prat J, Cerda E, Foz M. Pericarditis associated with acquired toxoplasmoSis in a child.

Cardiology

1976; 61: 303-306.