Streptococcus Questions and Answers

Answer: A

Correct answer: Rheumatic fever

Rheumatic fever is the autoimmune sequel to streptococcal pharyngitis: antibody raised against the M protein and the cell wall carbohydrate cross-reacts with myocardium and cardiac valves, producing carditis, arthritis and chorea weeks after the throat infection has settled. Scarlet fever is a toxin-mediated feature of the acute illness, not an autoimmune complication.

Answer: C

Correct answer: The morphological characteristics resemble that of S. pyogenes

This is the least accurate statement. Enterococci appear as gram-positive cocci in pairs and short chains and are usually non-haemolytic or alpha-haemolytic, whereas S. pyogenes forms long chains and is beta-haemolytic. The other three are correct: enterococci are facultative, grow in 6.5 per cent salt, and are among the commonest causes of hospital-acquired infection.

Answer: A

Correct answer: Enterococcus faecalis

E. faecalis is a normal inhabitant of the human large intestine, which is the origin of its name and of most of the infections it causes - urinary tract infection, intra-abdominal sepsis and endocarditis all follow escape from the bowel. S. mutans belongs to the mouth, and the other two to the skin.

Answer: A

Correct answer: Endotoxins

Endotoxin is lipopolysaccharide, a component of the gram-negative outer membrane, and S. pyogenes is gram-positive and has none. Its virulence rests on the M protein, which resists phagocytosis and is the principal antigen; the streptolysins, which lyse cells; and enzymes such as streptokinase and hyaluronidase, which spread the infection through tissue.

Answer: B

Correct answer: Enterococcus faecalis

Enterococci are among the leading causes of infective endocarditis, and they characteristically settle on valves already damaged by rheumatic or degenerative disease. They reach the bloodstream from the bowel or the urinary tract, which is why enterococcal bacteraemia in a patient with valve disease is taken seriously and treated as endocarditis until proved otherwise.

Answer: B

Correct answer: Aminoglycoside with penicillin

Enterococci are only inhibited by penicillin, not killed, and aminoglycosides alone cannot cross the cell wall in sufficient quantity. Given together the penicillin damages the wall enough for the aminoglycoside to enter, and the combination is bactericidal - a genuine synergy, and the reason endocarditis is treated with two drugs rather than one. Cephalosporins are inactive against enterococci altogether.

Answer: A

Correct answer: Enterococcus faecium

Vancomycin resistance is far commoner in E. faecium than in E. faecalis, and vancomycin-resistant E. faecium is one of the principal hospital-acquired resistance problems. The resistance comes from van gene clusters that replace the terminal D-alanine of the cell wall precursor, so vancomycin can no longer bind.

Answer: D

Correct answer: None of the above

All three statements are correct, so there is no exception. Micrococcus colonies are smaller than staphylococcal ones and often pigmented, the genus is widely distributed in the environment and on skin, and both genera are catalase positive - which is what separates them from the streptococci rather than from each other.

Answer: C

Correct answer: Streptococcus pyogens (A)

S. pyogenes is regarded as a pathogen rather than a commensal: asymptomatic throat carriage occurs, particularly in children, but it is not part of the established normal flora and its presence is significant. The other three are genuine commensals - S. aureus in the anterior nares, S. agalactiae in the genital and gastrointestinal tracts, E. faecalis in the bowel.

Answer: D

Correct answer: Found only in the oral cavities as commensals

Viridans streptococci are commensals of the mouth but also of the pharynx, the gastrointestinal tract and the female genital tract, so “only in the oral cavities” is too narrow. The other three statements hold: most are alpha-haemolytic, they are the principal agents of dental caries, and they carry no Lancefield group antigen.