Murray's Medical Microbiology - Staphylococcus and Gram-positive Cocci PDF
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This document provides information on the *Staphylococcus aureus* and other Gram-positive cocci bacteria, virulence factors, diseases, and clinical relevance. It includes details on the biology, epidemiology, diagnosis, treatment, and prevention of staphylococcal infections, along with tables summarizing key microorganisms and their associated diseases. The document also discusses structural components and the pathogenicity of these bacteria.
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Okay, here is the converted text into a structured Markdown format. I've done my best to retain the original information, formatting it into headings, lists, and tables where appropriate, and converting mathematical formulas into LaTeX format. # Staphylococcus and Gram-positive Cocci Related A 26-...
Okay, here is the converted text into a structured Markdown format. I've done my best to retain the original information, formatting it into headings, lists, and tables where appropriate, and converting mathematical formulas into LaTeX format. # Staphylococcus and Gram-positive Cocci Related A 26-year-old sailor visits the base doctor with large pus-filled lesions surrounded by erythema on both legs. An infection with *Staphylococcus aureus* is suspected. 1. What structural properties are unique to this species of *Staphylococcus*? 2. How do the cytotoxins produced by this microorganism produce the clinical manifestations observed in this individual? **Summaries of Clinically Significant Microorganisms** ## *STAPHYLOCOCCUS AUREUS* **Keywords**: Coagulase, cytotoxins, exfoliative toxins, enterotoxins, toxic shock syndrome toxin, MRSA. **Biology and Virulence** * Gram-positive, catalase-positive cocci arranged in clusters. * Species characterized by coagulase, protein A, and species-specific ribitol teichoic acid with N-acetylglucosamine residues ("polysaccharide A"). * Virulence factors include structural components that facilitate adherence to host and prevent phagocytosis, and a variety of toxins and hydrolytic enzymes (see Table 18.3). * Hospital and acquired infections with methicillin-resistant *Staphylococcus aureus* (MRSA) pose a significant worldwide problem. **Epidemiology** * Normal flora of human skin and mucous membranes. * Organisms can survive on dry services for extended periods (due to thickened peptidoglycan layer and lack of outer membrane). * Person-to-person transmission in close contact or exposure to fomites. * Risk factors include presence of a foreign body (e.g., splinters, sutures, prostheses, catheters), previous surgical procedures, and use of antibiotics that suppress normal microbiota . * Patients at risk for specific diseases are those with poor personal hygiene, intravascular catheters. * MRSA is now the most common cause of community acquired skin and soft tissue infections. **Diseases** * Diseases include toxin mediated food poisoning, toxic shock syndrome and scalded skin syndrome) pyogenic diseases (impetigo, folliculitis, furuncles, carbuncles, and wound infections), and other systemic diseases. **Diagnosis** * The microscope is useful for pyogenic infections, but not for blood infection for toxin mediated infections. * Staphylococci grow quickly in non-selective culture. * Selective media is used to recover *Staphylococcus aureus* in contaminated samples. * Nucleic acid applied for cribraging of patients with susceptible S. aureus and SARM. * S. aureus can be identified through biochemical tests **Treatment, Prevention, and Control** * Localized infection is treated by drainage; antibiotic systemic therapy is indicated. * Empirical treatment should be directed to SAMR strains. * Oral therapy consist on sulfamethoxazole, doxycycline or minocycline, clindamycin or linezolid; vancomicina is the drug of choice for the intravenous treatment * Treatment is symptomatic in food poisoning patients. * Proper cleaning prevent infection. * Proper hand washing and skin covering in medical staff. ## STAPHYLOCOCCUS COAGULASA NEGATIVO **Keywords**: Opportunistic, slime layer, subacute. **Biology and Virulence** * Gram-positive, catalase-positive, and coagulase-negative Cocci arranged in clusters. * Relatively avirulent, although the "slime" layer allows adherence to foreign bodies and protect it from phagocytosis and antibodies. **Epidemiology** * Normal flora in skin and mucous surfaces. * Microorganism can survive in dry surfaces during large periods. * Transmision through direct contact or contaminated fomites but most of the infections are from the patient´s organisms. * Patients are exposed to risk in the existence of an external body. * No geographic or seasonal limitations because of the ubiquity of the microorganisms. **Disease** * Diseases include subacute endocarditis, infection of foreign bodies as urinary tract. **Diagnosis** * Same as S. aureus infections. **Treatment, prevention and control** * The antibiotic choices are oxacillin or other penicillin resistance to penicillinase as vancomicyn in resistant strains of oxacilin. * Treatment requires body extraction. * Speedy treatment in endocarditis to prevent tissue damage. ## Table 18.1 Important Staphylococci | Microorganism | Origin History | | :------------------ | :------------------------------------------------------------------------ | | *Staphylococcus* | staphylé, grape bunch; coccus, grain or berry (grain in grape shape) | | *S. aureus* | aureus, golden (golden or yellow) | | *S. epidermidis* | epidermidis, external portion of the skin | | *S. lugdunensis* | Lugdunum, Latin name for Lyon, France. Where the microorganism was tested | | *S. saprophyticus* | sapros, putrid; phyton, plant (that develops on dead tissue) | (Image: A microscopic view of a Gram stain of Staphylococcus in a blood culture showing purple round cocci arranged in clusters.) ## Frequent Species of Staphylococcus and its diseases (Table 18.2) | Microorganismo | Diseases | | :---------------- | :------------------------------------------------------------ | | *Staphylococcus aureus* | Mediated by toxines (intoxication food borne, scalder skin and toxic schock) cutaneus diseases (carbuncle, folliculitis, furuncle, impetigo and infections on wounds) other ones (endocarditis, pneumonia, empiema, osteomielitis and septic arthritis.) | | *S. epidermidis* | Bacteriemia, endocarditis, surgery wounds, oportunistic catheters infections, shunts, and prótesis` | | *S. lugdunensis* | Endocarditis | | *S. saprophyticus*| Urinary tract infections | **Physiology and structure** **CAPSULE AND COAT OF LIME (POLYSACCHARIDES)** The outermost layer cell wall staphylococcal it is it covers himself of a capsule of polysaccharide. Has been identified several serotipos capsular of *S. aureus.* Serotipos 1 and 2 is associated to capsules very thick and colonies of aspect mucoide, but is rare that produce illness in people. On In contrast, the serotipos 5 and 8 are responsible of around 75% of the infections human. The capsule protects bacteria to inhibit it falto of these microorganisms for polymorphonuclear leukocytes (PMN). The majority of them staphylococcal produce a film biológica laxative *(*layer of silt or biopelícula) conformed for monosacáridos, proteinás y pequeños péptidos in a variable amount. Is extracelular substance unites to bacteria fabrics and external bodies, like catheters, grafts, valve prosthesis and articulations and derivations. This is properti is particularly important for survival coagulasa estafilocococosnegative because relatively avirulent. Sección 4 • Bacteriología **PEPTIDOGLYCAN AND ASSOCIATED ENZYMES** It is important to understand the structure of the cell wall of gram-positive bacteria, as it is the target of numerous important antibiotics. Peptidoglycan represents half of the cell wall by weight and is formed by layers of glycan chains constructed with 10 or 12 alternating subunits of N-acetylmuramic and N-acetylglucosamine acid. The oligopeptide side chains are attached to the N-acetylmuramic acid subunits and crosslinked by peptide bridges. Unlike what happens in gram-negative bacteria, the peptidoglycan layer in gram-positive microorganisms is composed of numerous cross-linked layers, which confers greater rigidity to the cell wall. The enzymes that catalyze the construction of the peptidoglycan layer are called penicillin binding proteins because they are the targets for penicillins and other ẞ-lactam antibiotics... Bacterial resistance to methicillin and related penicillins is mediated. By the acquisition of a gene (mecA and mecC) that encodes a novel penicillin-binding protein, PBP2a, which has low affinity for methicillin and related penicillins and cephalosporins. This information is important because MRSA strains, which were previously limited to hospital infections, currently appear in the community and are responsible for most staphylococcal infections. Although initially the nosocomial and community strains were different, hospital entrances and exits are commonplace, so no MRSA strain is found exclusively in either environment. Peptidoglycan has an endotoxin-like activity, as it stimulates the production of endogenous pyrogens, complement activation, and the formation of interleukin 1 (IL-1) by monocytes and PMN leukocyte aggregation (a process that gives rise to the formation of abscesses). **TEICHOIC ACIDS AND LIPO-TEICHOIC ACIDS** Teichoic acids are another prominent component of the cell wall. The teichoic acids are species-specific phosphorylated polymers that bind covalently to N-acetylmuramic acid residues in the peptidoglycan layer or through a lipophilic bond to the cytoplasmic membrane (lipo-teichoic acids). Although teichoic acids are poorly immunogenic, they stimulate a specific humoral response when bound to peptidoglycan. Initially antibody production was used as a marker for S. aureus infection, but this highly insensitive test has been abandoned in recent years. **ADHESION PROTEINS ON THE SURFACE** A large number of surface proteins have been identified in S. aureus that are virulence factors, since they adhere. to matrix proteins of the host bound to human tissues (e.g., fibronectin, fibrinogen, elastin, collagen). Most of these surface adhesion proteins are covalently bound to peptidoglycan in staphylococci and have been designated as proteins components of the microbial surface that recognize adhesive matrix molecules (MSCRAMM, microbial surface components recognizing adhesive matrix molecu- les). The nomenclature of individual proteins is confusing; for example, staphylococcal protein A binds to the Fc receptor of immunoglobulin (Ig) G1, IgG2 e IgG4; fibronectin-binding protein A binds to fibronectin, as its name indicates, and S. aureus surface protein has an undetermined function. The best characterized MSCRAMM proteins are staphylococcal protein A, fibronectin-binding proteins A and B, and aggregation factor proteins. Aggregation factor proteins (also called coagulase) bind to fibrinogen and convert it to insoluble fibrin, causing staphylococci to aggregate or form groups. All this can be a bit confusing, so it is important remember two facts: 1) S. aureus has several proteins on the bacterial surface that allow microorganisms to bind to host cells and establish infection, and 2) some of these proteins are unique to S. aureus and allow identify the microorganism. **CYTOPLASMATIC MEMBRANE** The cytoplasmic membrane is composed of a complex of proteins, lipids and a small amount of carbohydrates. It acts as an osmotic barrier for the cell and provides a support for cellular biosynthesis and respiratory enzymes. **PATHOGENESIS AND IMMUNITYI** The pathology of staphylococcal infections depends on the ability of bacteria to evade phagocytosis, produce surface proteins that mediate adherence of the bacteria to host tissues during colonization, and produce tissue destruction by elaborating specific toxins and hydrolytic enzymes. These properties (immunological evasion, adherence, tissue destruction) are common to most pathogenic microorganisms. **REGULATION OF VIRULENCE GENES** The expression of virulence factors and biofilm formation in staphylococci is under the complex control of the accessory gene regulator operon (agr, accessory gene regulator). This quorum sensing system regulates. (bacterial density) allows the expression of adhesion proteins and promotes tissue colonization and intracellular growth when bacterial density is low, and tissue invasion and the production of hydrolytic enzymes and toxins when density is high is high. The operon encodes a series of self of peptides (AIP1 to 4) that binds to cell surface receptors and regulate protein expression based on population density Innate immune regulation of bacterial virulence is mediated by apolipoprotein B, which is the main structural protein of low density and very low-density lipoproteins, which binds to AIR and suppress air signals. Therefore, 1 En presencia de anticuerpos específicos, Sin embargo, en presencia de anticuerpos específicos contra los estafilococos, el aumento de C3 se une a bacterias, lo que lleva a su fagocitosis. La capa de limo extracelular también interfiere con la fagocitosis de las bacterias. La capacidad de la proteína A de ligarse a las inmunoglobulinas evita de form eficaciala eliminación inmunitaria mediada por anticuerpos de *S. aureus*. La proteína A extracelular también puede unirse a los anticuerpos, formando inmunocomplejos con el consiguiente consumo del complemento. De este modo, en optimal conditions, bacterial density is maintained at low concentrations, providing the benefits of immune stimulation through colonization of staphylococci without sequelae of tissue invasion and destruction. **DEFENSES AGAINST INNATE IMMUNITY** Encapsulated staphylococci bind to opsonins (IgG, complement factor C3) in serum, but the capsule covers these opsonins and protects bacteria by inhibiting the phagocytosis of the germes parte of neutrophilic polymorphonuclears ## Factores de virulencia de Staphylococcus aureus (Tabla 18.3) | Factores de virulencia | Efectos biológicos | | :--------------------- | :---------------------------------------------------------- | | **COMPONENTES ESTRUCTURALES**| | | Cápsula | Inhibe la quimiotaxis y la fagocitosis | | Capa de limo | Ayuda a la adhesión a cuerpos extraños | | Péptidogluconos | Aporta estabilidad osmótica; estimula la producción | | Ácido teicoico | Elude la eliminación mediada por anticuerpos | | Proteína A | Inhibe la eliminación mediada por anticuerpos | | **TOXINAS** | | | Citotoxinas | Tóxicas para muchas células | | Toxinas exfoliativas | Proteasas de serina que interrumpen los puentes | | Enterotoxinas | Superantígenos (estimulan linfocitos) | | Toxina 1del SST | Superantígeno (estimula linfocitos) | | **ENZIMAS** | | | Coagulasa | Convierte el fibrinógeno en fibrina | | Hialuronidasa | Hidroliza los ácidos hialurónicos | | Fibrinolisina | Disuelve los coágulos de fibrina | | Lipasas | Hidrolizan los lípidos | | Nucleasas | Hidrolizan el ADN | ## Staphylococcal toxins S. Aureus produces an increased production of toxins that include five cytolytic toxins that damage the membrane Alpha, beta, delta gama Leucocidin two exfoliative toxins that differ one from the other. The cytotoxic toxins are also known as hemolisins, which don't constitute the correct name, the 4 first toxins are not exclusive from erithrocites, Leucocidin cannot lysate the cells La toxina alfa está codificada tanto en el cromosoma bac-teriano como en un plásmido, es un polipéptido de 33.000 Da producido por la mayoría de las cepas de *S. aureus* que causan enfermedad en el sr humano. La toxina alterna el músculo liso de os vasos sanguı́neos y es tóxica para muchas células, como los eritrocitos, los leucocitos, los hepatocitos y las plaquetas. Se une a la superficie celular, se agrega en un heptámero (7 moléculas de toxina) y forma poros de 1 a 2 nm, permitiendo un rápido flujo de salida de K+ y de entrada de Na+, Ca2+ y otras moléculas pequenas, lo que conduce a tumefacción por ósmosis y a lisis celular. Se cree que la toxina alfa es un mediador importante del dano tisular en la enfermedad estafilococćica. La toxina Beta es una proteina termoestable de 35000 Da producidad por la mayoria de las cepas de S. aureus, esta proteína presenta especificidad para la esfingomielina y la lisofosfatidilcolina, es toxica patra diversas celulas. ## TABLE 19.1 ESTREPTOCOCOS IMPORTANTES | Microorganismo | HISTORICAL ORIGIN | | :--------------- | :------------------------------------------------------------------------ | | Streptococus | Streptus, flexible, Coccus, grain or berry | | S. agalactiae | Agalactia. Needs milk. Initial strain origins mastistics bovina | | S. Anginosus | Anginosus Relatives a la angina | | S. constellatus | Constellatus | | S. disgalactiae | DYS Sick, hard;galactina relativos a the milk | | S. gallolytics | Gallatum Galato | | S. intermedius | Intermédius Intermédium Initially confused if would bacteria aerobical Aerobical | | S. Mitis | Mitis leve it was erroneosly thoughtthat produced low infections | | S. Mutans | Mutations Changing Coccus that can adoot a similar look | | S. pneumoniae | Preumón the lungs Cause pneumonia | | S. piágenes | Pus engender to Produce pus is associated to pus formation on wounds | | S. Salivarius | Salivarius saliva is present in saliva | | Enterococcus | Inteston cocous intestinales | ## TABLE 19.2 GRAM-POSITIVE NO CATALASA | Microorganismo | ILLNESS | | :--------------- | :------------------------------------------------------------------------ | | Abiotrópicos | Bacteriemia and cardiovascular infection in the central nervous system | | Aerococcus | Bacteriemia endocarditis urinary tract infetions | | Enterococcus | Bacteriemia endicarditis infection of damaged tissues | | Granulicatella | Bacteriemia in immunocomprimised | | Lactococus | Leuconostoc | Opotunistics Infections | | Pediococcus | Inmuno Suprimided | Los géneros streptococos y entereococos son un grupo for- mado por diversos cocos grampositivos que normalmente se disponen en parejas o en cadenas (a diferencia de los racimos formados por staphilococos) La mayoria de las especies son anaerobios facultutuvos y algunos crecen única- mente en una atmósfera enriquecida con dióxido de carbono (crecimiento capnofilico). Sus exigencias nutricionales son complejas, y su aislamiento requiere el uso de medios enriquecidos con sangre o suero. Son capaces de fermentar carbohidratos, proceso que produce ácido láctico, y son catalasa-negativos. El número de Cocos grampositivos, catalasa-negativos reconocidos como patógenos humanos sigue en aumento, Sin embargo, los géneros streptococos y enterococos son los que se aíslan conmás frecuencia y son las cepas responsables de la mayoria de las enfermedades en el ser humano. El resto de géneros