A 20-year-old male Turkish immigrant to Norway suffering from severe chronic neurobrucellosis with spastic paraplegia and deafness is presented. The diagnosis was established by isolation of Brucella melitensis from cerebrospinal fluid (CSF) culture. Brucella antibody agglutination titers were high in serum and CSF. In spite of intensive, prolonged treatment with a combination of trimethoprim-sulfamethoxazole (TPM-SMZ), rifampicin and doxycycline, the course of the illness was characterized by relapses and severe neurological defects.
All 87 known cases of bacteraemia due to Streptococcus pyogenes (beta-haemolytic group A streptococci) occurring during the peak of a nationwide outbreak in Norway (population 4.2 million) between January and June 1988 were reviewed. Clinical features varied widely and appeared largely to be dependent on the patients' age. The case fatality rate ranged from 11% in the age group under 30 years to 44% in patients over 60 years. Clinical complications such as shock, severe renal or respiratory failure or serious local infection occurred particularly in 30-to 59-year old individuals. Shock was manifest in 32% of the patients and carried a 68% case fatality rate. Chronic heart disease in the elderly and pneumonia seemed to be associated with a fatal outcome. In the 25 patients (29%) who died the disease showed a fulminant course, 80% dying within 48 hours after admission. However, 56% of the patients had experienced symptoms for more than two days before admission, suggesting that early diagnosis and treatment might possibly have prevented the development of a serious disease. This study revealed a wide spectrum of clinical manifestations in bacteraemia cases in a unique epidemiological situation caused largely by a single serotype of Streptococcus pyogenes; 89% of the 27 preserved bacteraemia strains carried the M-1 antigen. The observations call attention to the ability of these organisms to cause fulminant clinical illness, indicating a probable increase in both invasiveness and toxicity of group A streptococci responsible for the epidemic.
The clinical and bacteriological features of septicemia caused by group G streptococci were analyzed in nine patients seen during a period of 28 months. Four of these patients had acute endocarditis with a high rate of serious neurological complications. The clinical response to antibiotic treatment was slow in the endocarditis patients despite sensitivity of the organism in vitro. Group G streptococcal septicemia can be a very serious condition associated with endocarditis of a destructive nature. Comparison with previous reports suggests that group G streptococcal infections are of increasing importance. The virulence of group G streptococci may be changing, resulting in more serious infections and complications. This series stresses the importance of prompt recognition of this infection and the need for aggressive management of these patients.
Recurrent group A streptococcal infection is a well-known phenomenon. It is well documented as a problem in pharyngotonsillitis and skin infections. This report describes a case of recurrent genital infection after puerperal sepsis caused by group A streptococci.
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