Classification

1. Gram positive bacteria arranged in chains of varying length
2. each cell is approximately 1 micrometre in diameter
3. non-motile
4. non-sporing
5. may be capsulate
6. most are facultatively anaerobes,but there are species that are strictly aerobic
7. Catalase negative
8. Classification depends on the type of haemolysis seen on the blood agar. Strains which have soluble haemolysins (streptolysins O and S) will produce a clear zone of haemolysis on fresh blood agar media. This is known as beta-haemolysis and the organism is classified as beta-haemolysis streptococci. Those that cause a narrow zone of partial clearing and green coloration are called alpha-haemolysis streptococci. Those that produce no obvious changes around the colonies on blood agar are called non-haemolytic or gamma-haemolytic

Streptococcus pyogenes

a) Pathogenesis

The most common route of entry of Streptococcus pyogenes is the upper respiratory tract,where the primary infection is established,usually in the throat

i) Structural Components

The virulence of Strep. pyogenes is closely related to the surface antigen,the M protein.The fimbriae on the surface of streptococci enable attachment to epithelial cells,contain M protein. Two other surface proteins,T and R protein,do not play any part in virulence but are useful in identification of infecting serotypes

ii) Extracellular products

These includes :-

• erythrogenic agents - erythrogenic toxins A,B and C are superantigens,T cell mitogens that induce lymphocytes to synthesize and release cytokines such as TNF,interleukin-1-beta,interleukin-6,with the subsequent production of fever,shock and tissue damage
• streptolysin O - a kind of haemolysin which lyse red blood cells by linking to bound cholesterol in the cell membrane,causing holes to form in this structure. It is also cytotoxic for other cells,including neutrophils,platelets and cardiac tissue. It is inactivated by oxygen. Streptococcus pyogenes produce this kind of haemolysin
• Streptolysin S - this haemolysin is not inactivated by oxygen and is responsible for the haemolysis produced on the surface of an aerobic blood agar plate
• streptokinase (fibrinolysin) - is protein in nature and is antigenic. Role is not clear but beacuse of its action in preventing the formation of an effective fibrin barrier,it may well influence the character of the lesions by interfering with the localization of the infection
• Deoxyribonuclease (DNAases) - at least four of these enzymes,designated types A,B (Streptococcus pyogenes),C and D and are all antigenic. They hydrolyse nucleic acids and nucleoproteins
• Hyaluronidase
• Nicotinamide adenine dinucleotidase (NADase) - antigenic
• Serum opacity factor (lipoproteinase)

b) Laboratory Diagnosis

1. examination of patient's sera for a rising titre of antibodies to one or more streptococcal antigens are the means of diagnosis
2. swabs are taken from patients or from suspected carriersas
3. microscopy is of little help in the diagnosis
4. using bacitracin sensitivity test as belta-haemolytic streplococci,being group A organism,are more sensitive than other groups to bacitracin but the test is not totally reliable as some non-group A strains may also be sensitive
5. antistreptolysin O (ASO) test is most common performed,and the anti-DNAase B test may also be useful

c) Epidemiology

Besides the acute case of sore throat and the nasal or saliva carrier,other dangerous sources of infection are patients with streptococcal otitis media,vulvovaginitis or infected skin lesions

d) Chemotherapy

Str.pyogenes is highly sensitive to a wide range of antibacterial drugs,including penicillin and erythromycin but strains resistant to sulphonamides and tetracyclines are common. Benzylpenicillin (penicillin G) or oral phenoxymethylpenicillin (penicillin V) are the drugs of choice. Treatment for 3 - 5 days will limit the effect of severe attacks of streptococcal infection and prevent suppurative complications such as otitis media,but studies have been shown that only if treatment is continued for 10 days will the streptococci be eliminated from the infected area. If the use of any other antimicrobial agent is contemplated,as in cases of hypersensitivity to penicillin,antimicrobial sensitivity testing must be done because of dangers of resistance to the drug

e) Clinical Infection

The most common and typical infection caused by Str.pyogenes is an acute sore throat. If the infecting streptococcus is capable of producing an erythrogenic toxin and the host has not developed antibodies to this toxin,the sore throat may be accompanied by a generalized punctate erythema or rash. This syndrome is called scarlet fever. Local extension of the infection from the throat may result rarely in such complications as peritonsillar abscess (quinsy),sinusitis,otitis media or mastoiditis.Puerperal sepsis or child-bed fever is traditionally associated with infection by Str.pyogenes. Besides local inflammation of uterine tissues,infection may spread to the adnexa (pelvic cellulitis or peritonitis). Wounds,burns and chronic skin lesions (eczema,psoriasis) may become infected with Str.pyogenes;these superficial infections may extend in the local tissues (cellulitis) or be carried by lymphatics to regional lymph glands (lymphadenitis) or get into the bloodstream and become generalized (septicaemia).

f) Non-Suppurative Complications

i) Rheumatic Fever

• An attack of rheumatic fever is related to antecedent streptococcal throat infection occurring 1 - 5 weeks earlier. Diagnosis may be difficult since throat swabs may or may not yield growth of Str.pyogenes,thus,the most important investigations are serological. Two samples of serum must be assayed to check for a rising titre of antibody to Str.pyogenes. Titres become detectable in the 2nd week after the onset if infection and are maximal by the 6th week and thereafter decrease. Penicillin prophylaxis after a primary attack of rheumatic fever will reduce substantially the risk of a second attack by preventing further streptococcal infection of the throat. However,prevention of primary attacks is virtually impossible and penicillin treatment of streptococcal sore throats plays little or no part

ii) Acute Glomerulonephritis

• almost always produced by Group A streptococci but group C streptococci may also be involved
• acute glomerulonephritis is produced by a much narrower range as compared to rheumatic fever which can be caused by a wide range of serotypes of Str.pyrogenes
• Acute Glomerulonephritis following streptococcal throat infection occurs at the colder times of the year and mostly in children and younger adults
• flies of the genus Hippelates is of important vectors of streptococci in hot humid weather
• post-streptococcal glomerulonephritis arises because components of the glomerular basement membrane are immunologically similar to the cell membranes of nephritogenic belta-haemolytic streptococcus

Other Streptococci

a) Group B Streptococci

• major streptococcal pathogens in neonates and young infants
• infections in the neonate is can be an 'early-onset' infection,which occurs soon after birth or the 'late-onset',which occurs several days to several weeks after birth
• for early-onset,neonates may be ill at birth or develop acute and fulminating illness a few hours or a day or two later. Neonates may be lethargic,cyanosed and apnoeic and when septicaemia progresses,shock ensues and death will occur if treatment is not quicklyu instituted. Meningitis AND pulmonary infection may be asociated
• early rupture of the membranes,prolonged labour,prematurity,low birth weight and heavy colonization of the mother's genital tract by Group B streptococci lead to infection
• purulent meningitis is the most common Group B streptococci infection for late-onset. There is usually no history of obstetric complications and seldom does the mother have genital tract colonization by Group B streptococci
• late-onset infection can be prevented or decreased by standard aseptic nursing procedures whereas early onset infection is more difficult to prevent
• swabbing the mother's genital tract during pregnancy is not helpful because carriage can be intermittent and isolation of the organism during pregnancy does not indicate that it will be present during labour. Moreover,administration of antibiotics to women who are psoitive during pregnancy has little effect on the carriage of Group B streptococci
• Group B Streptococci can produce other infections in infants including septic arthritis,osteomyelitis,conjunctivitis,sinusitis,otitis media,endocarditis,peritonitis and omphalitis

b) Group C Streptococci

• consists of four species Str.equi,Str.equisimilis,Str,dysgalactiae,Str.zooepidemicus
• human and animal pathogens
• cause epidemic sore throat usually assoicated with unpasteurized milk

c) Group G streptococci

• resemble those of group A and C in their pathogenic properties and in the types of infections produced
• cause sore throat,sometimes after ingestion of contaminated food and pneumonia
• erysipelas and cellulitis may be caused as well as bone and joint infection

d) Group D Streptococci and Enterococci

• is a separate entity in terms of its biochemical,serological and pathogenic profiles,thus classified as Enterococcus species
• less sensitive to penicillin
• Species include E.faecalis,E.faccium,E.avium,E.durans
• some species cause nosocomial infection and may cause sporadic outbreaks
• the non-enterococcal group D strains which include Str.bovis,Str.equinus remain sensitive to penicillin
• the normal habitats of Enterococci and Group D Streptococci are the intestine and vagina and the diseases associated include :- urinary tract infections,infective endocarditis,biliary tract infections,suppurative abdominal lesions and peritonitis

e) Group R Streptococci

• a well established cause of septicaemia and meningitis in pigs,can infect people in contact with contaminated pork or infected pigs,causing septicaemia,meningitis and respiratory tract infection

f) Viridans Streptococci

• also known as the Oral Streptococci
• produce partial alpha haemolysis when grown on blood agar but some are non-haemolytic and produce no change in blood
• the normal habitat of most species is the mouth but they are not evenly distributed there
• involves in dental caries an in more serious non-oral conditions such as infective endocarditis,septicaemia,deep-seated abscesses
• bacteria,a susceptible host and a cariogenic diet are the three essentials for the production of caries
• dietary sucrose is an important contributor to caries production and restriction of this reduces the substrate for the activities of the plaque bacteria
• as for infective endocarditis,various factors predispose to endocarditis. Minute platelet thrombi adhere to the roughend epithelium and organisms may grow in the thrombi and produce fragile vegetations from which emboli can break off. Infected vegetations consist of bacteria enmeshedin fibrin and platelets. Fibrosis can occur in the valve and this surrounds and further protects the bacteria
• for laboratory diagnosis,blood culture can be performed as soon as infective endocarditis is suspected before antibiotic therapy is started
• a combination of benzylpenicillin and gentamicin is generally used for treatment and if staphylococci are thought to be involved flucloxacillin should be added


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