Bacteriology-1 PDF

07.02.2024 Bacteriology-1 Dogukan Ozbey, Lecturer Medical Faculty, Department of Medical Microbiology [email protected] ❑Prokaryotes ▪ Unicellular organism. ▪ Does not contain a nuclear membrane-enclosed nucleus and lack of any other membranebound organelles. ▪ Based upon molecular analysis,...

07.02.2024 Bacteriology-1 Dogukan Ozbey, Lecturer Medical Faculty, Department of Medical Microbiology [email protected] ❑Prokaryotes ▪ Unicellular organism. ▪ Does not contain a nuclear membrane-enclosed nucleus and lack of any other membranebound organelles. ▪ Based upon molecular analysis, prokaryotes are divided into two domains Bacteria and Archaea ▪ Flagellum provides structural backgrounds of chemotaxis. ▪ Plasmid is a small, extrachromosomal DNA molecule ▪ Cell Membrane Surrounds the cell's cytoplasm and regulates the flow of substances in and out of the cell. ▪ Cell Wall is outer covering of most cells that protects the bacterial cell and gives it shape ▪ Cytoplasm is a gel-like substance composed mainly of water that also contains enzymes, salts, cell components, and various organic molecules ▪ Ribosome is responsible for protein production ▪ Nucleoid is an area of the cytoplasm that contains the prokaryote's single DNA molecule. ❑Binary Fission ▪ Organisms in the domains of Archaea and Bacteria reproduce with binary fission. ▪ This form of asexual reproduction and cell division is also used by some organelles within eukaryotic organisms ▪ Binary fission results in the reproduction of a living prokaryotic cell (or organelle) by dividing the cell into two parts, each with the potential to grow to the size of the original. ❑Bacterial Growth Curve Lag Phase: Bacteria try to adapt to the environment. There is cellular activity but not growth. Log Phase: Cells are dividing by binary fission and doubling their numbers. Metabolic activity is high. Stationary Phase: Available nutriens depleted, waste products accumulated. Dividing and Dying cells are equal. Bacteria try to survive. Death Phase: Nutrients become less availabe. Number of dyings cells increase. ❑Koch’s Postulates Koch's postulates are four criteria designed to establish a causative relationship between a microbe and a disease. 1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms. 2. The microorganism must be isolated from a diseased organism and grown in pure culture. 3. The cultured microorganism should cause disease when introduced into a healthy organism. 4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent. ❑Diagnosis ❑ Acute Phase Reactants Acute phase reactants (APR) are inflammation markers that exhibit significant changes in serum concentration during inflammation. During the response to the inflammation plasma concentration of acute phase reactants may decrease (Negative acute phase reactants) or increase (Positive acute phase reactants) Positive Acute Phase Reactants: CRP, PCT, Serum Amyloid A, Complement Factors, Lectin, Fibrinogen, Ferritin, Haptoglobin... Negative Acute Phase Reactants: Albumin, Transferrin, Retinol-Binding Protein, Antithrombin, Complement 3 (C3) ❑Diagnostic Methods ▪ Culture Based Methods ▪ Non-Cultural Methods ✓ Microscope ✓ Biochemical Tests ✓ Immunological Methods ✓ Molecular Methods ❑Culture Methods ❖ Anaerobic Culture Kanamycin-Vancomycin (KV) Agar Phenylethyl Alcohol (PEA) Agar Thioglycolate Broth ❖ Aerobic Culture Blood Agar Chocolate Agar MacConkey or Eosin Methylene Blue Agar ❑ Microscopic Techniques Staining Peripheral Blood Smear ❑ Biochemical Tests Catalase Oxidase Urease Esculine Hydrolysis IMViC Triple Sugar-Iron Motility… Analytical Profile Index (API) Test ❑ Maldi-TOF MS Ionization technique that uses a laser (UV) energy It can be analyze biomolecules (DNA, proteins…) and various organic molecules Provides species-level diagnosis (25 minutes for 96 samples) ❑ Immunological/Serological Diagnostics Can be done by detecting bacterial antigens (Direct diagnosis) Legionella pneumophilia antigens can be detected from Urine sample Helicobacter pylori antigens can be detected from Stool sample Chlamydia trachomatis antigens can be detected from endocervical and urethral swab Haemophilus influenzae antigens can be detected from Body fluids Or can be done by detecting antibodies against bacterial antigens (Indirect diagnosis) ❑ Molecular Diagnostic Methods Molecular diagnostics is a collection of techniques used to analyze biological markers in the genome and proteome. In medicine the technique is used to diagnose and monitor disease, detect risk, and decide which therapies will work best for individual patients For microbiology; molecular diagnostics are used to identify microorganism or to determine specific strains of a microorganism Steps DNA/RNA extraction Nucleic Acid Amplification Electrophoresis Sequencing Types of Polymerase Chain Reaction (PCR) that used for nucleic acid amplification ❑Dental Infections Dental infections originate in the tooth or its supporting structures and can spread to the surrounding tissue. Dental infections were, historically, a common cause of death. Due to improved dental hygiene, modern dentistry, and antibiotics, dental infections are rarely life-threatening today. Periodontal infections first involve the gingival tissues causing gingivitis and, over time, periodontitis. ❑Dental Abscess A dental abscess is a build-up of pus in the teeth or gums caused by an infection. There are three types of dental abscess. Gingival abscess Periodontal abscess Periapical abscess It needs urgent treatment Without treatment, it can be life-threatening Common symptoms; ✓ Intense toothache or pain in gums ✓ Redness inside the mouth, or outside the mouth on the face or jaw ✓ Sensitivity to hot or cold food and drink in the affected area ✓ Bad taste in mouth ✓ Difficulty opening the mouth and chewing food ✓ Swollen face or jaw ✓ High temperature ❑Biofilm Formation Dental plaque is an example of a biofilm, which occurs naturally on the teeth structures The plaque biofilm is a tenacious microbial community embedded in an extracellular polysaccharide matrix ✓ Living and dead bacteria and their extracellular products ✓ Host compounds, mainly derived from the saliva. Biofilm infections are characterized by persisting and progressive pathology due primarily to the inflammatory response surrounding the biofilm Microorganisms universally attach to surfaces and produce extracellular polysaccharides, resulting in the formation of a biofilm. ❑Cavities It can be caused by cariogenic bacteria, that dissolves the hard tissues of the teeth (enamel, dentin and cementum). Streptococcus mutans, Streptococcus sobrinus and Lactobacillus Root cavities are caused by Lactobacillus acidophilus, Actinomyces spp., Nocardia spp., and Streptococcus mutans Comorbid diseases (SjS or DM) or medications (Antihistamines or antidepressants) are risk factors. Neutral pH: 7.0 Dentin: 6.5 Enamel: 5.5 ❑Biomineralization Enamel demineralization is the primary mechanism involved in the etiopathogenesis of caries When the oral microenvironment reaches low pH values the demineralization process is triggered When the microenvironment reaches pH values higher than 7.0 and there is an availability of calcium and phosphate ions, remineralization can occur Demineralization Remineralization ❑White Spot Lesions The white spot lesion is the first visual finding of enamel caries. The mineral content in the affected area is reduced, which in turn affects the translucent feature of the enamel, and the color of these areas appears more opaque white ❑Disclosing Solution Dental plaque disclosing solutions are dyes that color dental biofilm and dental plaque to make observation easier ❑Periodontal Diseases Gingivitis: Inflammation or infection of the gingiva ❑Periodontitis Periodontitis, also called gum disease, is a serious gum infection that damages the soft tissue and, without treatment, can destroy the bone that supports the teeth Periodontal disease can establish itself when the gums detach from the teeth as a result of an inflammatory response to plaque. Periodontitis can cause teeth to loosen or lead to tooth loss Periodontal infections are usually mixed, most often involving anaerobes such as Treponema denticola and Porphyromonas gingivalis Actinobacillus actinomycetemcomitans causes localized juvenile periodontitis ❑Acute Necrotizing Ulcerative Gingivitis (Vincent Gingivitis) It is an acute and painful infection of the tooth margins and gums that is caused by the symbiotic microorganisms, Prevotella intermedia, Bacillus fusiformis and Borrelia vincentii The main features are painful, swollen, bleeding gums; small, painful ulcers covering the gums and tooth margins; and characteristic fetid breath. ✓ Severe gum pain that characterizes ANUG distinguishes it from chronic periodontitis The ulcers may spread to the throat and tonsils The infection is readily treated by bed rest, the administration of penicillin or other antibiotics, and the use of antiseptic mouth rinses Treatment is removal of dead gum tissue and antibiotics (usually metronidazole) ❑Pericoronitis Pericoronitis is an inflammatory and infectious complication accompanying the clinical emergence of the third molars in the oral cavity It is caused by an accumulation of bacteria and debris beneath the operculum, or by mechanical trauma The microbial flora that develop at the site of eruption are contained within a periodontal pocket-like crevice Pericoronal infection is normally caused by a mixture of bacterial species present in the mouth, such as Streptococci and particularly various anaerobic species Prevotella, Veillonella, Bacteroides, Capnocytophaga can accompany ❑Dental Implant Infections A dental implant is one of the treatments to replace missing teeth. They can be used in the treatment of complete and partial edentulism. They can be prone to infection Dental implant infection is a condition that can be likened to gum disease. It causes inflammation and infection of the gums and bone tissue surrounding dental implants ✓ Local debridement ✓ Implant surface decontamination ✓ Anti-infective therapy (Antibiotics [Ornidazole, Metronidazole or Amoxicillin] or Antiseptics [Chlorhexidine]) ✓ If there is advanced bone loss, Removal of the implant itself. ❑Oro/Facial Gangrene Cancrum oris (Noma) is a devastating, non-contagious, bacterial infectious disease which destroys the soft and hard tissues of the oral and para-oral structures. The risk factors are poverty, malnutrition, poor oral hygiene, residential proximity to livestock in unsanitary environments, and infectious diseases, particularly Measles and those due to the Herpesviridae Acute Necrotizing Gingivitis and herpetic ulcers are considered the antecedent lesions Rapid progression of these precursor lesions to Noma requires infection with Fusobacterium necrophorum and Prevotella intermedia Enzymes and toxins (Dermonecrotic Toxin) are responsible for tissue destruction Early treatment with antibiotics and nutritional support may slow the spread of the disease. ❑Bad Breath (Halitosis) It can develop due to various reasons. Its persistence creates a major psychological disturbance in humans. Although the most common cause is poor oral hygiene, it can also be seen in people who pay attention to hygiene. Halitosis cases may not be caused by a single type, so two or more types of halitosis can be diagnosed at once. Being edentulous, periodontitis, crowns, fillings and brackets do not cause bad breath. Dense teeth, full dentures, gingivitis, excessively recessed tongue papillae, fistula, pericoronary infection, alcohol habit, containing alcohol mouthwashes, bacterial plaques can cause bad breath. ❑Bad Breath (Halitosis) Type 0 (Physiological bad breath): Bad breath that occurs in the morning and disappears by itself during the day Type 1 (Tongue smell): It is caused by volatile aromatic gases produced on the back of the tongue. Response to odor treatment can be obtained. Can be prevented with zinc or tongue cleaning Type 2 (Bad breath caused by throat-sinus): It is caused by any bacteria in the pharynx, tonsils, paranasal sinuses, nasal mucosa and surrounding tissues. May not be identified with Waters X-ray, should be supported by MRI or CT Type 3 (Bad breath caused by the digestive tract): There is a source of aromatic gas anywhere in the digestive tract and this gas reaches the mouth. If there is Helicobacter pylori gastritis in the stomach, there is a nitrite odor in the mouth. Type 4 (Breath odor): It may develop due to an infection in the lower respiratory tract. Even if there is no infection, volatile gases dissolved in the blood can create this odor. Diagnosed with blood gas biochemistry. Type 5 (Psychological bad breath): The patient's obsession with bad breath ❑Bloodstream infections Bloodstream infections are infectious diseases defined by the presence of viable microorganisms in the bloodstream Bacteremia: Bacteria are present in the bloodstream. Sepsis: Reproduction of a microorganism in the blood ❑Systemic Diseases Caused by Oral Infection Bacteremia was observed in 100% of the patients after dental extraction, in 70% after dental scaling, in 55% after third-molar surgery, in 20% after endodontic treatment, and in 55% after bilateral tonsillectomy Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed Metastatic infection Metastatic injury Metastatic inflammation ❑Systemic Diseases Caused by Oral Infection ▪ Metastatic infection from oral cavity via transient bacteremia Metastatic infection is defined as a deep, distal, or secondary infection, anatomically unrelated to the primary site infection ✓ Subacute infective endocarditis, acute bacterial myocarditis, brain abscess, cavernous sinus thrombosis, sinusitis, lung abscess/infection, Ludwig's angina, orbital cellulitis, skin ulcer, osteomyelitis, prosthetic joint infection ❑Systemic Diseases Caused by Oral Infection ▪ Metastatic injury from circulation of oral microbial toxins Some bacteria have the ability to produce diffusible proteins, or exotoxins, which include cytolytic enzymes and dimeric toxins ✓ Cerebral infarction, acute myocardial infarction, abnormal pregnancy outcome, persistent pyrexia, idiopathic trigeminal neuralgia, toxic shock syndrome, systemic granulocytic cell defects, chronic meningitis ❑Systemic Diseases Caused by Oral Infection ▪ Metastatic inflammation caused by immunological injury from oral organisms Soluble antigen may enter the bloodstream, react with circulating specific antibody, and form a macromolecular complex. These immunocomplexes may give rise to a variety of acute and chronic inflammatory reactions at the sites of deposition ✓ Behçet's syndrome, chronic urticaria, uveitis, inflammatory bowel disease, Crohn's disease ❑Gram Positive cocci Staphylococci Micrococci Enterococci Streptococci ❑Staphylococci Staphylococci are spherical cells about 1 μm in diameter arranged in irregular clusters Single cocci, pairs, tetrads, clusters and chains Gram positive, facultative anaerob, non-spore forming, non-motile Grow rapidly at 37°C, pigmentation (Gray-Golden Yellow) at room temperature (18-25°C) They are frequently isolated from the oral cavity. S. aureus, S. epidermidis, S. saphropyticus, S. lugdunensis Can be found in the saliva of healthy subjects older than 70 years. ❑Staphylococcus aureus They can be seen in clusters (multiple dividing zones) ✓ Clumping factor The habitat is the human skin, especially the anterior nares and the perineum. They are disseminated through air and dust and are always present in the hospital environment. Most strains are resistant to ß-lactam antibiotics Semi-synthetic penicillins (nafcillin, oxacillin, methicillin) cephalosporins, vancomycin, daptomycin, telavansin or linezolid ❑Staphylococcus aureus Toxins Super antigen Cytotoxins; Lyses cell Leukocidin (PVL); It causes lysis by opening pores in leukocyte membranes. Epidermolytic toxin; Exfoliation and splitting of epidermis Toxic Shock Syndrome Toxin; Shock, Rash or Desquamation Enterotoxin; Vomiting and Diarrhea Enzymes Exoenzymes Coagulase; Clots plasma (Fibrinogen→Fibrin) Catalase; Catalyzes the decomposition of hydrogen peroxide to water and oxygen Penicillinase; Breaks down ß-lactam drugs Protein A; Antiphagocytic Hyaluronidase; Connective tissue breakdown Lipase; Breaks lipids of cell membranes DNase; facilitates the spread of the pathogens in the tissue. ❑Staphylococcus aureus Cell surface components Capsule: It is found in more than 90% of S. aureus strains. Provides antiphagocytic properties. Peptidoglycan: Shows endotoxin-like activity. It provides IL-1 release and complement activation. It induces the production of antibodies that will opsonize. Teichoic acid: Provides complement activation. It plays a role in adhesion to mucosal cells. Adhesins: It is responsible for adhesion to skin and mucosal surfaces. It is associated with the adhesion of matrix molecules on the bacterial surface to host proteins. The main ones are clumping factor, fibronectin binding protein, collagen binding protein and protein A. Biofilm: Has a polysaccharide structure. It plays a role in the pathogenesis of foreign body infections. ❑Staphylococcus aureus Infections Skin and soft tissue infections ✓ Carbuncles, pustules, abscesses, conjunctivitis, mastitis and wound infections Bone and joint infections ✓ Osteomyelitis, Prosthetic joint infections… Toxin-related diseases ✓ Scalded skin syndrome, toxic shock syndrome, Food poisoning Bacteremia/sepsis Endocarditis Pericarditis Meningitis Lung infections ❑Staphylococcus aureus Folliculitis Furuncle Carbuncle Impetigo ❑Staphylococcus aureus Localized growth of toxin-producing strains of S. aureus, followed by release of the toxin into blood A diffuse, macular erythematous rash can be seen Multiple organ failure and shock Toxic Shock Syndrome ❑Staphylococcus aureus Staphylococcal scalded skin syndrome ❑Coagulase Negative Staphylococci Staphylococcus epidermidis: Skin Staphylococcus saprophyticus: GIS and Genital Tract Staphylococcus lugdunensis: Skin They can rapidly colonize on foreign bodies Biofilm ❑Staphylococcus epidermidis This species is found on the skin surface and is spread by contact. Grows as white colonies on blood agar. Being a normal commensal of the skin, this bacterium causes infection only when an opportunity arises. Can be treated with Vancomycin ❑Staphylococcus saphrophyticus This organism causes urinary tract infections It has the ability to colonize the periurethral skin and the mucosa. It can be differentiated from Staphylococcus epidermidis by the mannitol fermentation reaction ❑Staphylococcus lugdunensis S. lugdunensis may produce a bound coagulase, but unlike S. aureus, it does not produce a free coagulase ✓ Slide Coagulase (+), Tube Coagulase (-) Decarboxylates ornithine Pyrrolidonyl arylamidase-PYR (+) It can cause cardiovascular infections, empyema, osteomyelitis and prosthetic/native joints infections, skin and soft-tissue infections, central nervous system infections, peritonitis, endocephalitis, and urinary tract infections Treated with Penicillins ❑Micrococci Micrococci are catalase-positive organisms similar to Staphylococci. They are coagulase-negative and usually grow as white colonies on blood agar, although some species are brightly pigmented: pink, orange or yellow Micrococcus is generally thought to be a saprotrophic or commensal organism, though it can be an opportunistic pathogen, particularly in hosts with compromised immune systems It can be difficult to identify Micrococcus as the cause of an infection, since the organism is a normally present in skin microbiota ❑Streptococci Pyogenic Streptococci Streptococcus pyogenes Streptococcus agalactiae Streptococcus dysgalactiae Viridans Streptococci Streptococcus bovis Streptococcus anginosus Streptococcus mutans Streptococcus mitis Streptococcus sanguinis Streptococcus salivarus Streptococcus pneumoniae ❑Streptococci Residents of normal microbiota Non-Motile, Non-spore forming Facultative anaerobe They form a chain because they divide in one direction. Nutrient requirements are complex Predominant in dental plaques ❑Streptococci Lancefield Groups Lancefield grouping is a serological method for classifying streptococci into one of 20 groups (A to H and K to V) based on the presence of polysaccharide and teichoic acid antigens in the bacterial cell wall Some of these groups include human pathogens. Group A includes Streptococcus pyogenes (β hemolysis) Group B includes Streptococcus agalactiae (β hemolysis) Group D includes Enterecoccus species (α or γ hemolysis) ❑Streptococcus pyogenes The normal habitat of this species is the human upper respiratory tract and skin. Some strains produce mucoid colonies as a result of having a hyaluronic acid capsule (Resistance). ß-hemolytic colonies (Streptolysin O and S) Penicillin / Macrolide ❑Streptococcus pyogenes ❑ Toxins S. pyogenes produce biologically active substances Streptokinase: A proteolytic enzyme that lyses fibrin Hyaluronidase: Spreading factor. DNase: Destroys cellular DNA Haemolysins (Streptolysins and Leukocidins) Pyrogenic Exotoxins: Assocaited with severe diseases ❑Streptococcus pyogenes It is the most common cause of bacterial pharyngitis and tonsillitis, especially in children aged 5-15 years. S. pyogenes is an important cause of skin and soft tissue infections and pharyngitis and can cause many other suppurative infections tonsillitis and pharyngitis, necrotizing fasciitis (streptococcal gangrene), scarlet fever, mastoiditis and sinusitis, otitis media, wound infections, impetigo and erysipelas After an episode of infection, some people develop complications Rheumatic Fever (bacterial antigen-heart tissue) Glomerulonephritis (immune complexes) Erythema Nodosum Scarlet Fever Pharyngitis Impetigo Necrotizing fasciitis ❑Streptococcus agalactiae S. agalactiae is the only species that has the group B antigen. They form short chains in clinical specimens and longer chains after cultivation S. agalactiae has polysaccharide capsule (Antiphagocytic) It is the causative agent of neonatal meningitis and sepsis. Found in the human vagina and also can colonize in the lower GIT Babies acquire infection from the colonized mother during delivery. CAMP (+) Macrolide and Flourokinolon (R), Penicillin reduced susceptibility Ampicillin, Cephalosporin, Meropenem, Teicoplanin, Vancomycin ❑Streptococcus agalactiae ❑ Clinical Disease Early-Onset Neonatal Disease Bacteremia, Pneumoniae, Meningitis Clinical symptoms of group B streptococcal disease acquired in utero or at birth develop during the first week of life. Late-Onset Neonatal Disease Bacteremia with Meningitis Late-onset disease is acquired from an exogenous source and develops between 1 week and 3 months of age Infections in Pregnant Women Postpartum endometritis, wound infection, and urinary tract infections occur in women during and immediately after pregnancy Infections in Non-Pregnant Women and Men The most common presentations are bacteremia, pneumonia, bone and joint infections, and skin and soft-tissue infections. Underlying conditions ❑Viridans Streptococci Oral streptococci, which live principally in the oropharynx, are a mixed group of organisms with variable characteristics They typically show α-haemolysis on blood agar. They are easily killed with common disinfectants. Oral streptococci can be divided into four main species groups as follows: ✓ anginosus group ✓ mitis group ✓ mutans group ✓ salivarius group ❑mutans group S. mutans is naturally present in the human oral microbiota, along with at least 25 other species of oral streptococi Can contribute to oral diseases with S. sobrinus Differentiating is not necessary S. mutans is most prevalent on the pits and fissures, constituting 39% of the total streptococci in the oral cavity. Fewer S. mutans bacteria are found on the buccal surface Candida albicans supports biofilms formed by S. mutans. ❑Streptococcus mutans It is the primary organism involved in dental caries. Easily adheres to hard tissues Can eliminate many other bacteria by secreting Mutacin It can synthesize all the amino acids it needs by fermenting carbohydrates. It can lower the pH of the environment in which it grows up to 4 They synthesize large polysaccharides such as dextrans or levans from sucrose and contribute importantly to the genesis of dental caries. ❑Streptococcus sobrinus Enhances the formation of caries within teeth Biofilm from the mixture of sugar and plaque create a suitable environment for S. sobrinus to grow. S. sobrinus is also affiliated with early childhood caries, which are responsible for the majority of dental abscesses and toothaches in children ❑Streptococcus salivarus They can use urea by breaking it down into ammonia Can grow at 10-45°C It can be found on the tongue, saliva and Deciduous teeth. May cause infective endocarditis when bacteremia ❑Streptococcus mitis Streptococcus mitis, previously known as Streptococcus mitior, is a mesophilic α-hemolytic species of Streptococcus that inhabits the human mouth It is most commonly found in the throat, nasopharynx, and mouth It can cause infective endocarditis, brain abscesses, sepsis, pneumonia, and peritonitis In children with leukemia or lymphoma, it can cause meningitis ❑Streptococcus sanguinis (sanguis) May delay cavities caused by Streptococcus mutans or other bacteria They can coexist in biofilms. There is a competitive relationship between each other. S. sanguinis may gain entrance to the bloodstream when opportunity presents (dental cleanings and surgeries) and colonize the heart valves, particularly the mitral and aortic valves, where it is the most common cause of subacute bacterial endocarditis May require short-term antibiotic use before and after surgery. ❑Streptococcus pneumoniae Gram-positive cocci in pairs (diplococci) or short chains, cells are often capsulate, fastidious, α-haemolytic on blood agar. Draughtsman colonies after 2 days of incubation Since they are lack of catalase enzyme, they need exogenous source of catalase to grow (H2O2) S. pneumoniae causes several common diseases, such as pneumonia and meningitis in adults and otitis media and sinusitis in children. Can colonize oropharynx and nasopharynx Vaccine is available Penicillin is the first choice, Vancomycin+Ceftriaxone is used for emphric therapy ❑Streptococcus pneumoniae ❑Virulence factors Peptidoglican layer (binds to NAMA and NAGA) and teichoic acid (binds to plasma membrane lipids) of cell wall Capsule: Antiphagocytic. Only capsulated strains are infectious Adhesins: Attaches to epitelial surfaces IgA Protease: Destroys secretory IgA (sIgA) Pneumolysin: Lysis of epithelial and phagocytic cells ❑Streptococcus pneumoniae ❑Clinical Outcomes Pneumonia Pneumococcal pneumonia develops when the bacteria multiply in the alveolar spaces. Most patients have a productive cough with blood-tinged sputum, and they commonly have chest pain Meningitis S. pneumoniae can spread into the central nervous system after bacteremia, infections of the ear or sinuses, or head trauma that causes a communication between the subarachnoid space and the nasopharynx. Otitis Media The disease is usually preceded by a viral infection of the upper respiratory tract, after which polymorphonuclear neutrophils infiltrate and obstruct the sinuses and ear canal Bacteremia Bacteria are generally not present in the blood of patients with sinusitis or otitis media. Endocarditis can occur in patients with both normal or previously damaged heart valves. Destruction of valve tissue is common. ❑Enterococci (Enterococcus faecalis and Enterococcus faecium) The enterococci are gram-positive cocci, typically arranged in pairs and short chains. The cocci grow both aerobically and anaerobically in a broad temperature range (10° C to 45° C), in a wide pH range (4.6 to 9.9), and in the presence of high concentrations of sodium chloride (NaCl) and bile salts. Glucose is fermented with L-lactic acid as the predominant end product Usually non-hemolytic Antibiotic-resistant strains has become a serious problem in hospitalized patients. VanA, VanB / VanC Daptomycin, Linezolid, Streptogramins, Tigecycline Differential diagnosis can be made with "arabinose fermentation« E. faecalis (-), E. faecium (+) ❑Oral Cavity Infections of Enterococci Enterococcus faecalis is part of microbiota in the oral cavity, but also it has a relation with different oral diseases Enterococcus faecalis causes several infections in the oral cavity as an opportunistic pathogen, such as marginal periodontitis, root canal infections, primary endodontic infections, persistent/secondary infections, dental caries, peri-implantitis, periradicular abscesses and oral mucosal lesions It is commonly found in root canal failures and root-filled tooth treatment failure. They participate in mixed infections with other bacteria in the necrotic root canal