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Pathology of Streptococcal Infections

Dr Sampurna Roy MD          

 

                                                                                                                      

 

Streptococcal infections are caused by species of the genus streptococcus, which includes Streptococcus pyogenes (group A), S. agalactiae (Group B), S. faecalis (group D), S. pneumoniae (pneumococcus) and the viridans streptococci group.

Although streptococci elicit suppurative inflammatory responses, there are several nonsuppurative complications that reflect immune responses and deposition of immune complexes.

Streptococcal infections occur throughout the world, even where antibiotics are readily available.

As in the case of many infections, problems with streptococci are greatest among underprivileged populations for whom penicillin and other antibiotics are not readily available.

Streptococci become nonvirulent on desiccation, and indirect spread rarely occurs.

To acquire infection, an individual must usually be inoculated with millions of streptococci, spread by close contact with a carrier or with some one who has an active infection.

But of those colonized with streptococci, a few actually develop an overt infection.

Whether or not infection by a streptococcus becomes clinically apparent, patients are at risk from the late, "nonsuppurative", immune complications (Example: rheumatic heart disease, acute glomerulonephritis, and erythema nodosum ).

The streptococcus is gram-positive and is demonstrated in cultures, smears, and tissue sections.

The organisms are spherical and very small (less than 2 micrometer diameter), and the oil immersion lens must be used in searching for them in tissue sections.

Cultural, biochemical, and immunologic studies have identified many groups and subtypes of streptococci :

Group A beta-hemolytic streptococci (for example S. pyogenes) cause nasopharyngeal and cutaneous lesions, different strains infecting these sites.

Group B streptococci produce infections of the new born.

Group C, G, and other streptococci are responsible for respiratory infections.

Alfa (green) hemolytic streptococci (for instance S.viridans), are part of the flora of the mouth and cause about one-half of all bacterial endocarditis.

Group D streptococci (e.g. enterococci) are an important cause of infections of the urinary tract, endocarditis, postsurgical infections, septicemia, and other infections.

Pneumococci (Streptococcus pneumoniae) produce primary bacterial pneumonia, septicemia, meningitis,  and other infections.

Antigen and Exotoxins:

The capsule of the streptococcus is a polysaccharide that contains hyaluronic acid. 

The cell wall contains antiphagocytic “M protein” (closely linked to virulence), and lipoteichoic acid, which is required for recognition of and adhesion to the host epithelial cell membranes.

The structural backbone of the cell wall is a peptidoglycan that has pyrogenic properties and weak endotoxicity.

Group A streptococci produce several exotoxins, including erythrogenic toxins (pyrogenic exotoxins) and cytolytic toxins (streptolysins S and O).

Erythrogenic toxins cause the rash of scarlet fever (not directly but by enhancing acquired hypersensitivity to diverse streptococcal products).

Most, but not all, group A streptococci produce both streptolysin S and streptolysin O, which are not only "hemolysins" (lysing red blood cells), but also cytolytic (that is, they damage and lyse a broad spectrum of mammalian cells and cellular components).

The surface hemolysis on blood agar plates is largely caused by streptolysin S, which also lyses bacterial protoplasts (L-forms) and probably destroys neutrophils after they ingest group A streptococci.

This toxins influences T-lymphocytes to a much greater extent than B-lymphocytes and has antitumor activity.

Because streptolysin S is not immunogenic, its effect may be unimpeded even after repeated streptococcal infections.

By contrast, streptolysin O induces a persistently high antibody titer, an effect that provides a useful marker for the diagnosis and epidemiologic studies of group A streptococcal infections and the late nonsuppurative complications.

Streptolysin O also has cardiotoxic properties, possibly playing a role in acute rheumatic fever and rheumatic heart disease  .

Primary Streptococcal Infections: 

Infections of the Upper Respiratory Tract :

Infections of the upper respiratory tract are caused mainly by group A beta-hemolytic streptococcus and present as pharyngitis, pneumonia, and pulmonary abscesses.

The pharyngitis varies in intensity from mild lesions resembling the common cold, to more severe lesions that involve the epiglottis and the tonsillar crypts.

These lesions commonly produce vasodilatation, spreading edema, and an exudate composed mostly of neutrophils, often mixed with macrophages.

Streptococci may spread from the pharyngitis to the airways, especially if there is a peritonsillar or a retropharyngeal abscess.

Scarlet Fever:

Scarlet fever, which results from an acute pharyngitis or tonsillitis caused by group A streptococci, is characterized by a rash produced by the erythrogenic toxin.

The incubation period of 2 to 5 days is followed by chills and fever, fiery red pharyngeal mucosa, small crypt abscesses in enlarged tonsils, and a bright red tongue with edematous papillae ("raspberry tongue").

Erysipelas :

Erysipelas, caused chiefly by beta-hemolytic group A streptococci, is the classic cutaneous streptococcal infection.

It is common in warm climates, but is not often seen before the age of 20 years.

Erysipelas is an erythematous swelling of the skin that usually begins on the face and spreads rapidly.

The map-like area of brawny erythema has a sharp, well-demarcated, serpiginous border.

A diffuse, edematous, acute inflammatory reaction in the dermis and epidermis extends into the subcutaneous tissues.

The inflammatory infiltrate (mostly neutrophils) is more intense around vessels and adnexae of the skin.

Cutaneous microabscesses and small foci of necrosis are  not uncommon.

Impetigo:

Impetigo, another infection of skin that may be caused by streptococci, has increasingly been reported as a cause of post-streptococcal complications in children.

Streptococcal and staphylococcal impetigo have similar lesions, including folliculitis, pyoderma, wound infection, lymphatic spread, and sepsis.

Streptococcal impetigo more often induces lymphangitis  (red streaks along the draining lymphatics) than does staphylococcal impetigo, and less frequently causes focal tissue necrosis or abscesses.

Apthous Ulcers :

Recurrent aphthous ulcers of the lip (chancres) have been associated with and may be caused by Streptococcus sanguis in those who are susceptible.

Puerperal Sepsis :

Puerperal sepsis, a result of infection by group A streptococci from the contaminated hands of attendants at delivery, was formerly common but with the acceptance of the "germ theory" of disease and improved hygiene, is now rare in the developed countries.

Group B streptococcus is an important neonatal pathogen, causing pneumonia, sepsis, and meningitis.

Infants acquire the infection from their mothers during delivery, and mortality rates are high (50% or more) if the onset on infection is within 10 days of delivery.

Secondary Streptococcal Infections:

Streptococcal septicemia:

Streptococcal septicemia with group A streptococci may spread from the nasopharynx to the systemic circulation and seed the lungs, meninges, or heart valves.

Streptococcal septicemia can develop quickly, may be life-threatening, and is a particular hazard for splenectomized patients or those with abnormal splenic function.

Pneumococcal pneumonia and meningitis:

Pneumococcal pneumonia and meningitis result from infection with S. pneumoniae (the pneumococcus), an organism that is responsible for 80% of all bacterial pneumonias.

 

Pneumococci also spread from the nasopharynx through  the systemic circulation and seed the meninges.

 

Some patients develop meningitis from primary pneumococcal pneumonia.

 

For example, in most parts of Africa, a meningitis is more commonly caused by the pneumococcus than by the meningococcus.

 

The histologic features of pneumococcal meningitis resemble those described for meningococcal meningitis.    

 

Meningococcal Infection

Bacterial Endocarditis:    

Infective Endocarditis

Bacterial endocarditis is a complication of streptococcal septicemia in which the organisms spread from a site of local infection through the circulation to colonize heart valves.

The alpha-hemolytic streptococci are a leading cause of subacute bacterial endocarditis , where as Streptococcus pneumoniae frequently produces acute bacterial endocarditis.

Endocarditis caused by group A streptococci is rare.

Group D streptococci (including enterococci) also cause endocarditis, but infection of the valves with group A streptococci is rare.

Nonsuppurative Complications:

Rheumatic Fever :

Rheumatic fever is an acute, recurrent, systemic inflammatory process that usually follows a pharyngeal infection by group A streptococci.

Rheumatic fever probably results from a reaction between antibodies to streptococcal antigens and tissue antigens that takes place in many sites, but it is particularly dangerous in the heart.

The disease is characterized by pancarditis, migratory polyarthritis of large joints, erythema marginatum of the skin, subcutaneous nodules, and chorea (a neurologic disorder with involuntary, purposeless movements). 

Acute Glomerulonephritis :

Acute glomerulonephritis is an immune complex-mediated disease that is caused only by certain nephritogenic strains of group A streptococci.

There is a latent period between the infection and the onset of nephritis during which the titer of antibodies (Example:  Antistreptolysin-O) increases.

Granular deposits in the glomeruli contain immunoglobulin and complement, a reflection of antigen-antibody complexes. 

Erythema Nodosum :

Erythema nodosum is an inflammatory reaction of the subcutaneous adipose tissue (panniculitis) that is sometimes associated with infections, including those with group A streptococci. 

The connective tissue septa of the fat are widened by edema and an exudate of fibrin and neutrophils.

Later the inflammatory infiltrate contains lymphocytes, histiocytes, giant cells and occasional eosinophils.

 

Further reading

Streptococcus pyogenes aortic aneurysm infection: forgotten but not gone.

Histopathology of Streptococcus Mitis/Oralis Endophthalmitis after Intravitreal Injection with Bevacizumab: A Report of 7 Patients.

Macrolide resistant Streptococcus pneumoniae in Charoenkrung Pracharak Hospital, Thailand.

A rare case of Streptococcus agalactiae mycotic aneurysm and review of the literature.

Viridans group streptococcal infections among children with cancer and the importance of emerging antibiotic resistance.

 

 

 

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)


 

 

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