Hart C. Anthony, Shears Paul. Color Atlas of Medical Microbiology.pdf

Taxonomy and Overview of Human Pathogenic Bacteria 225

Table 3.9 Continued: Overview of the Medically Most Important Bacteria

226 3 General Bacteriology

Table 3.9 Continued: Overview of the Medically Most Important Bacteria

Section 10. Aerobic/microaerophilic, motile, helical/vibrioid Gram-negative rod bacteria

Taxonomy and Overview of Human Pathogenic Bacteria 227

Table 3.9 Continued: Overview of the Medically Most Important Bacteria

228 3 General Bacteriology

Table 3.9 Continued: Overview of the Medically Most Important Bacteria

Section 13. Mycoplasmas (bacteria without cell walls)

Nomenclature

The rules of bacterial nomenclature are set out in the International Code for the Nomenclature of Bacteria. A species is designated with two latinized names, the first of which characterizes the genus and the second the species. Family names always end in -aceae. Taxonomic names approved by the “International Committee of Systematic Bacteriology” are considered official and binding. In medical practice, short handles have become popular in many cases, for instance gonococci instead of Neisseria gonorrheae or pneumococci (or even “strep pneumos”) instead of Streptococcus pneumoniae.

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F. H. Kayser

Staphylococcus

Staphylococci are small spherical cells (1 lm) found in grapelike clusters. Staphylococci are nonmotile, catalase-producing bacteria. The genus Staphylococcus includes over 30 species and subspecies. Table 4.1 briefly summarizes the characteristics of those most important in the medical context. S. aureus (and E. coli) are among the most frequent causal organisms in human bacterial infections.

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Table 4.1 Overview of the Staphylococcus Species That Affect Humans Most Frequently

* CNS: coagulase-negative staphylococci

Staphylococcus Aureus

Morphology and culturing. Fig. 4.1a shows the appearance of Gram-stained S. aureus. This is a facultative anaerobe that is readily cultured on normal nutrient mediums at 37 8C. Colonies as in Fig. 4.1b develop after 24 hours of incubation. Hemolytic zones are frequently observed around the colonies.

Fine structure. The cell wall consists of a thick layer of murein. Linear teichoic acids and polysaccharides are covalently coupled to the murein polysaccharide (Fig. 3.10, p. 154). The lipoteichoic acids permeating the entire murein layer are anchored in the cell membrane. Teichoic and lipoteichoic acids can trigger activation of complement by the alternative pathway and stimulate macrophages to secrete cytokines. Cell wall-associated proteins are bound to the peptide components of the murein. Clumping factor, fibronec- tin-binding protein, and collagen-binding protein bind specifically to fibrinogen, fibronectin, and collagen, respectively, and are instrumental in adhesion to tissues and foreign bodies covered with the appropriate matrix protein. Protein A binds to the Fc portion of immunoglobulins (IgG). It is assumed that “false” binding of immunoglobulins by protein A prevents “correct” binding of opsonizing antibodies, thus hindering phagocytosis.

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Staphylococcus aureus

Fig. 4.1 a Gram staining of a pus preparation: Gram-positive cocci, some in grapelike clusters. Clinical diagnosis: furunculosis. b Culture on blood agar: convex colonies with yellowish pigment and porcelainlike surface.

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Extracellular toxins and enzymes. S. aureus secretes numerous enzymes and toxins that determine, together with the fine structures described above, the pathogenesis of the attendant infections. The most important are:

&Plasma coagulase is an enzyme that functions like thrombin to convert fibrinogen into fibrin. Tissue microcolonies surrounded by fibrin walls are difficult to phagocytose.

&a-toxin can have lethal CNS effects, damages membranes (resulting in, among other things, hemolysis), and is responsible for a form of dermonecrosis.

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&Leukocidin damages microphages and macrophages by degranulation.

&Exfoliatins are responsible for a form of epidermolysis.

&Food poisoning symptoms can be caused by eight serologically differentiated enterotoxins (A-E, H, G, and I). These proteins (MW: 35 kDa) are not inactivated by heating to 100 8C for 15–30 minutes. Staphylococcus enterotoxins are superantigens (see p. 72).

&Toxic shock syndrome toxin-1 (TSST-1) is produced by about 1% of Staphylococcus strains. TSST-1 is a superantigen that induces clonal expansion of many T lymphocyte types (about 10%), leading to massive production of cytokines, which then give rise to the clinical symptoms of toxic shock.

4Pathogenesis and clinical pictures. The pathogenesis and symptoms of

S. aureus infections take one of three distinct courses:

& Invasive infections. In this type of infection, the pathogens tend to remain in situ after penetrating through the derma or mucosa and to cause local infections characterized by purulence. Examples include furuncles (Fig. 4.2), carbuncles, wound infections, sinusitis, otitis media, and mastitis puerperalis.

Other kinds of invasive infection include postoperative or posttraumatic ostitis/osteomyelitis, endocarditis following heart surgery (especially valve replacement), postinfluenza pneumonia, and sepsis in immunocompromised patients. S. aureus and E. coli are responsible for approximately equal shares of nearly half of all cases of inpatient sepsis.

Inert foreign bodies (see p. 158 for examples) can be colonized by S. aureus. Colonization begins with specific binding of the staphylococci, by means of cell wall-associated adhesion proteins, to fibrinogen or fibronectin covering the foreign body, resulting in a biofilm that may function as a focus of infection.

Multiple Furuncles

Fig. 4.2 Furuncles in a patient with type 2 diabetes mellitus.

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&Toxicoses. Food poisoning results from ingestion of food contaminated with enterotoxins. The onset a few hours after ingestion takes the form of nausea, vomiting, and massive diarrhea.

&Mixed forms. Dermatitis exfoliativa (staphylococcal scalded skin syndrome, Ritter disease), pemphigus neonatorum, and bullous impetigo are caused by exfoliatin-producing strains that infect the skin surface. Toxic shock syndrome (TSS) is caused by strains that produce TSST-1. These strains can cause invasive infections, but may also only colonize mucosa. The main symptoms are hypotension, fever, and a scarlatiniform rash.

Diagnosis. This requires microscopic and culture-based pathogen identification. Differentiating S. aureus from the coagulase-negative species is achieved

by detection of the plasma coagulase and/or the clumping factor. The entero- 4 toxins and TSST-1 can be detected by means of immunological and molecular biological methods (special laboratories).

Plasma Coagulase and Clumping Factor Test

&To detect plasma coagulase, suspend several colonies in 0.5 ml of rabbit plasma, incubate the inoculated plasma for one, four, and 24 hours and record the levels of coagulation.

&For the clumping factor test, suspend colony material in a drop of rabbit plasma on a slide. Macroscopically visible clumping confirms the presence of the factor.

Therapy. Aside from surgical measures, therapy is based on administration of antibiotics. The agents of choice for severe infections are penicillinaseresistant penicillins, since 70–80% of all strains produce penicillinase. These penicillins are, however, ineffective against methicillin-resistant strains, and this resistance applies to all betalactams.

Epidemiology and prevention. S. aureus is a frequent colonizer of skin and mucosa. High carrier rates (up to 80%) are the rules among hospital patients and staff. The principle localization of colonization in these persons is the anterior nasal mucosa area, from where the bacteria can spread to hands or with dust into the air and be transmitted to susceptible persons.

S.aureus is frequently the causal pathogen in nosocomial infections (see p. 343f.). Certain strains are known to cause hospital epidemics. Identification of the epidemic strain requires differentiation of relevant infection isolates from other ubiquitous strains. Lysotyping (see p. 186) can be used for this purpose, although use of molecular methods to identify genomic DNA “fingerprints” is now becoming more common.

The most important preventive measure in hospitals is washing the hands thoroughly before medical and nursing procedures. Intranasal application of antibiotics (mupirocin) is a method of reducing bacterial counts in carriers.

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Coagulase-Negative Staphylococci (CNS)

CNS are an element in the normal flora of human skin and mucosa. They are classic opportunists that only cause infections given a certain host disposition.

& S. epidermidis. This is the pathogen most frequently encountered in CNS infections (70–80% of cases). CNS cause mainly foreign body infections. Examples of the foreign bodies involved are intravasal catheters, continuous ambulant peritoneal dialysis (CAPD) catheters, endoprostheses, metal plates and screws in osteosynthesis, cardiac pacemakers, artificial heart valves, and shunt valves. These infections frequently develop when foreign bodies in the

4macroorganism are covered by matrix proteins (e.g., fibrinogen, fibronectin) to which the staphylococci can bind using specific cell wall proteins. They then proliferate on the surface and produce a polymeric substance—the basis of the developing biofilm. The staphylococci within the biofilm are protected from antibiotics and the immune system to a great extent. Such biofilms can become infection foci from which the CNS enter the bloodstream and cause sepsislike illnesses. Removal of the foreign body is often necessary.

& S. saprophyticus is responsible for 10–20% of acute urinary tract infections, in particular dysuria in young women, and for a small proportion of cases of nonspecific urethritis in sexually active men.

Antibiotic treatment of CNS infections is often problematic due to the multiple resistance often encountered in these staphylococci, especially S. hemolyticus.

Streptococcus and Enterococcus

& Streptococci are Gram-positive, nonmotile, catalase-negative, facultatively anaerobic cocci that occur in chains or pairs. They are classified based on their hemolytic capacity (a-, b-, c-hemolysis) and the antigenicity of a carbohydrate occurring in their cell walls (Lancefield antigen).

b-hemolytic group A streptococci (S. pyogenes) cause infections of the upper respiratory tract and invasive infections of the skin and subcutaneous connective tissue. Depending on the status of the immune defenses and the genetic disposition, this may lead to scarlet fever and severe infections such as necrotizing fasciitis, sepsis, or septic shock. Sequelae such as acute rheumatic fever and glomerulonephritis have an autoimmune pathogenesis. The a-hemolytic pneumococci (S. pneumoniae) cause infections of the respiratory tract. Penicillins are the antibiotics of choice. Resistance to penicillins is