Aerobic and Facultatively Anaerobic Gram-Positive Cocci

Enterococcus faecalis and Enterococcus faecium are gram-positive cocci that belong to the genus Enterococcus. They are facultatively anaerobic, meaning they can grow in the presence or absence of oxygen. They are also catalase-negative, meaning they do not produce the enzyme catalase that breaks down hydrogen peroxide. They are part of the normal flora of the human gastrointestinal tract, but they can also cause opportunistic infections in various sites of the body.

Enterococcus faecalis and Enterococcus faecium are among the most common causes of nosocomial infections, which are infections acquired in hospitals or other healthcare settings. They are responsible for about 10% of all bloodstream infections and 16% of all urinary tract infections in hospitalized patients. They can also cause peritonitis, endocarditis, wound infections, intra-abdominal abscesses, and meningitis. These infections are often difficult to treat because enterococci have intrinsic resistance to many antibiotics and can acquire additional resistance genes through horizontal gene transfer.

Enterococcus faecalis is more prevalent and more virulent than Enterococcus faecium. It accounts for about 80% of all enterococcal infections and has a higher mortality rate than Enterococcus faecium. However, Enterococcus faecium is more resistant to antibiotics and has emerged as a major cause of vancomycin-resistant enterococci (VRE) infections. VRE are strains of enterococci that are resistant to vancomycin, which is a last-resort antibiotic for treating serious gram-positive infections. VRE infections pose a serious threat to public health and require strict infection control measures to prevent their spread.

Enterococcus faecalis and Enterococcus faecium have relatively low virulence compared to other gram-positive pathogens such as Staphylococcus aureus or Streptococcus pyogenes. They do not produce many toxins or enzymes that damage host tissues or evade host defenses. However, they have several factors that contribute to their pathogenicity, such as adhesins, biofilm formation, aggregation substance, cytolysin, gelatinase, and enterococcal surface protein. These factors enable enterococci to adhere to host cells and surfaces, form protective communities, exchange genetic material, lyse host cells, degrade extracellular matrix, and evade phagocytosis.

Enterococcus faecalis and Enterococcus faecium are important pathogens that cause significant morbidity and mortality in hospitalized patients and immunocompromised individuals. They have a remarkable ability to adapt to different environments and acquire resistance to multiple antibiotics. Therefore, it is essential to understand their clinical features and virulence factors in order to prevent and treat their infections effectively.

Enterococcus faecalis and Enterococcus faecium are gram-positive cocci that belong to the genus Enterococcus. They are part of the normal flora of the human gastrointestinal tract, but they can also cause opportunistic infections in various sites of the body. The most common clinical manifestations of enterococcal infections are:

• Urinary tract infections (UTIs): Enterococci are responsible for about 10% of community-acquired UTIs and up to 30% of hospital-acquired UTIs. They can cause cystitis, pyelonephritis, prostatitis, and urethritis. They can also infect urinary catheters and cause biofilm formation. Enterococcal UTIs are often associated with underlying conditions such as diabetes mellitus, urinary obstruction, renal impairment, or immunosuppression.

• Peritonitis: Enterococci can cause peritonitis in patients with peritoneal dialysis or abdominal surgery. They can also cause spontaneous bacterial peritonitis in patients with liver cirrhosis or ascites. Peritonitis is a serious infection that can lead to septic shock and multiorgan failure.

• Bacteremia: Enterococci can enter the bloodstream from various sources such as the urinary tract, the gastrointestinal tract, the skin, or intravascular devices. They can cause persistent or recurrent bacteremia that is difficult to treat with antibiotics. Bacteremia can also result in metastatic infections such as endocarditis, osteomyelitis, or meningitis.

• Endocarditis: Enterococci are the third most common cause of infective endocarditis after streptococci and staphylococci. They can infect native or prosthetic heart valves and cause subacute or acute endocarditis. Endocarditis can lead to valvular damage, heart failure, embolic complications, or abscess formation.

Enterococcus faecalis is more prevalent and more virulent than Enterococcus faecium. However, Enterococcus faecium is more resistant to antibiotics and has emerged as a major nosocomial pathogen in recent years. Both species can exhibit intrinsic or acquired resistance to multiple classes of antibiotics, such as penicillins, aminoglycosides, glycopeptides, and linezolid. Therefore, enterococcal infections pose a significant challenge for clinical management and infection control.

Enterococcus faecalis and Enterococcus faecium are relatively avirulent bacteria that cause infections, mainly in immunocompromised or debilitated patients. However, they have some virulence factors that enable them to adhere to host tissues, evade host defenses, and cause tissue damage.

One of the most important virulence factors of enterococci is their ability to form biofilms on various surfaces, such as catheters, heart valves, and prosthetic devices. Biofilms are complex communities of bacteria embedded in a matrix of extracellular polymeric substances (EPS) that protect them from antibiotics, host immune cells, and environmental stresses. Biofilm formation is mediated by several factors, such as surface proteins (e.g., Esp and Acm), polysaccharides (e.g., EPS and PIA), and quorum sensing molecules (e.g., AI-2 and FSAP).

Another virulence factor of enterococci is their resistance to multiple antibiotics, such as penicillins, aminoglycosides, glycopeptides, and daptomycin. This resistance is due to various mechanisms, such as altered cell wall synthesis (e.g., PBP5), modified target sites (e.g., 23S rRNA), efflux pumps (e.g., EmeA and EfmA), and enzymatic inactivation (e.g., beta-lactamases and aminoglycoside-modifying enzymes). Some enterococci also carry plasmids or transposons that encode resistance genes that can be transferred to other bacteria by horizontal gene transfer.

Enterococci also have some factors that help them adhere to host cells and tissues, such as pili, fimbriae, lipoteichoic acid, and collagen-binding proteins. These factors facilitate the colonization of the urinary tract, the gastrointestinal tract, the oral cavity, and the skin. They also enable the invasion of the bloodstream and the endocardium.

Enterococci can also produce some toxins and enzymes that cause tissue damage and inflammation. For example, enterococcal cytolysin is a hemolysin that lyses red blood cells and other cell types. It also induces the release of cytokines and chemokines that attract inflammatory cells. Enterococcal superoxide dismutase is an enzyme that detoxifies reactive oxygen species produced by host phagocytes. It also enhances the survival of enterococci in the presence of oxidative stress. Enterococcal gelatinase is a protease that degrades collagen and other extracellular matrix components. It also facilitates the dissemination of enterococci to deeper tissues.

These are some of the main virulence factors of Enterococcus faecalis and Enterococcus faecium that contribute to their pathogenicity. However, the expression and regulation of these factors may vary depending on the strain, the host, and the environmental conditions. Therefore, further studies are needed to understand the molecular mechanisms and interactions involved in enterococcal infections.

Staphylococcus aureus is a gram-positive coccus that forms clusters or pairs. It is a facultative anaerobe that can grow in the presence or absence of oxygen. It is also catalase-positive and coagulase-positive, meaning that it can produce enzymes that break down hydrogen peroxide and clot plasma, respectively.

Staphylococcus aureus is a common inhabitant of the human skin and mucous membranes, especially the anterior nares. It can also be found in the environment, such as on fomites or in food. However, it can also cause a variety of infections, ranging from superficial to invasive and from localized to systemic. Some of these infections are associated with specific strains of Staphylococcus aureus that carry certain virulence factors, such as toxins or antibiotic-resistance genes.

Staphylococcus aureus can be classified into two main types based on the presence or absence of a mobile genetic element called staphylococcal cassette chromosome mec (SCCmec). This element carries the gene for methicillin resistance (mecA), which confers resistance to beta-lactam antibiotics such as penicillin and methicillin. The strains that carry SCCmec are called methicillin-resistant Staphylococcus aureus (MRSA), while those that do not are called methicillin-susceptible Staphylococcus aureus (MSSA).

MRSA can be further divided into two subtypes based on their origin and epidemiology. Hospital-acquired MRSA (HA-MRSA) are strains that are acquired in healthcare settings, such as hospitals or nursing homes. They usually have multiple antibiotic-resistance genes and cause serious infections in patients with compromised immune systems or underlying conditions. Community-acquired MRSA (CA-MRSA) are strains that are acquired in the community, such as in schools or gyms. They usually have fewer antibiotic resistance genes but more virulence factors, such as Panton-Valentine leukocidin (PVL), which can cause necrotizing pneumonia or skin infections.

Staphylococcus aureus can cause three main types of infections: suppurative, disseminated, and toxin-mediated. Suppurative infections are characterized by the formation of pus due to inflammation and tissue damage. Examples of suppurative infections include impetigo, folliculitis, furuncles, carbuncles, wounds, and abscesses. Disseminated infections are characterized by the spread of bacteria from the primary site of infection to other organs or tissues via the bloodstream. Examples of disseminated infections include bacteremia, endocarditis, pneumonia, empyema, osteomyelitis, and septic arthritis. Toxin-mediated infections are characterized by the production of toxins by the bacteria that cause specific symptoms or syndromes. Examples of toxin-mediated infections include toxic shock syndrome, scalded skin syndrome, and food poisoning.

Staphylococcus aureus has several virulence factors that enable it to adhere to host cells, evade host defenses, damage host tissues, and produce toxins. Some of these virulence factors are:

• Peptidoglycan: a thick layer of polysaccharide and peptide chains that surrounds the bacterial cell wall and provides structural support and protection from osmotic lysis.

• Capsule: a loose layer of polysaccharide that covers the peptidoglycan layer and prevents phagocytosis by host immune cells.

• Protein A: a surface protein that binds to the Fc region of immunoglobulin G (IgG) antibodies and inhibits opsonization and complement activation.

• Toxins: various substances that can cause cytotoxicity, exfoliation, enterotoxicity, superantigenicity, or leukocytosis. Some examples of toxins are alpha-toxin (hemolysin), beta-toxin (sphingomyelinase), gamma-toxin (leukocidin), delta-toxin (detergent-like peptide), exfoliative toxins (serine proteases), enterotoxins (heat-stable peptides), toxic shock syndrome toxin-1 (TSST-1) (superantigen), and Panton-Valentine leukocidin (PVL) (leukocidin).

• Hydrolytic enzymes: various enzymes that can degrade host tissues or molecules and facilitate bacterial invasion or dissemination. Some examples of hydrolytic enzymes are coagulase (clots plasma), staphylokinase (dissolves clots), lipase (hydrolyzes fats), nuclease (degrades DNA), hyaluronidase (breaks down hyaluronic acid), and protease (degrades proteins).

Staphylococcus aureus is a versatile and adaptable pathogen that can cause a wide range of infections in humans. It can also acquire new virulence factors or antibiotic-resistance genes through horizontal gene transfer or mutation. Therefore, it poses a significant challenge for clinical diagnosis and treatment.

Suppurative infections are infections that produce pus, a thick fluid that contains dead cells, bacteria, and inflammatory substances. Staphylococcus aureus is a common cause of suppurative infections of the skin and other tissues. Some of the suppurative infections caused by Staphylococcus aureus are:

• Boils. These are pockets of pus that develop in a hair follicle or oil gland. The skin over the infected area usually becomes red and swollen. If a boil breaks open, it will probably drain pus. Boils occur most often under the arms or around the groin or buttocks.

• Impetigo. This is a contagious, often painful rash that can be caused by staph bacteria. Impetigo usually has large blisters that may ooze fluid and develop a honey-colored crust.

• Cellulitis. This is an infection of the deeper layers of the skin. It causes redness and swelling on the surface of your skin. Sores or areas of oozing discharge may develop, too.

• Staphylococcal scalded skin syndrome. This is a rare condition that affects mostly babies and children. It is caused by toxins produced by the staph bacteria that make the skin peel off. It includes a fever, a rash, and sometimes blisters. When the blisters break, the top layer of skin comes off. This leaves a red, raw surface that looks like a burn.

• Wound infections. These are infections that occur in cuts, scrapes, surgical incisions, or other injuries to the skin. They can cause pain, swelling, redness, warmth, and pus drainage from the wound site.

Suppurative infections caused by Staphylococcus aureus can be serious and sometimes life-threatening if they spread to deeper tissues or the bloodstream. They can also lead to complications such as abscesses (collections of pus), osteomyelitis (bone infection), endocarditis (heart valve infection), pneumonia (lung infection), septic arthritis (joint infection), and toxic shock syndrome (a severe reaction to bacterial toxins).

Suppurative infections caused by Staphylococcus aureus are diagnosed by examining the appearance of the skin or by identifying the bacteria in a sample of the infected material. Treatment usually involves antibiotics and cleaning of the infected area. However, some strains of Staphylococcus aureus are resistant to common antibiotics and may require more potent or different types of drugs. To prevent suppurative infections caused by Staphylococcus aureus, it is important to practice good hygiene, avoid sharing personal items, cover wounds with clean bandages, and wash hands frequently.

Staphylococcus aureus can also cause serious infections that spread through the bloodstream and affect distant organs. This condition is called bacteremia or staphylococcal sepsis. Bacteremia can occur when the bacteria enter the bloodstream through a wound, an intravenous catheter, a surgical site, or a medical device. Bacteremia can also result from a localized infection, such as pneumonia, endocarditis, or osteomyelitis.

Bacteremia can lead to complications such as metastatic abscesses, which are pockets of pus that form in various organs, such as the lungs, liver, spleen, kidneys, or brain. Bacteremia can also cause endocarditis, which is an infection of the inner lining of the heart or the heart valves. Endocarditis can damage the heart and lead to heart failure or stroke. Another complication of bacteremia is osteomyelitis, which is an infection of the bone or bone marrow. Osteomyelitis can cause bone pain, swelling, and fractures.

The symptoms of bacteremia and its complications may include fever, chills, low blood pressure, rapid heart rate, confusion, shortness of breath, chest pain, joint pain, and skin lesions. The diagnosis of bacteremia is based on blood cultures that identify the bacteria and their susceptibility to antibiotics. The treatment of bacteremia and its complications involves intravenous antibiotics for several weeks and sometimes surgery to remove infected tissue or devices.

Bacteremia caused by Staphylococcus aureus is a serious and potentially life-threatening infection that requires prompt diagnosis and treatment. It can be prevented by following good hygiene practices, such as washing hands frequently, cleaning wounds properly, and avoiding sharing personal items. It can also be prevented by using sterile techniques when inserting or handling intravenous catheters or medical devices and by removing them as soon as possible.

Staphylococcus aureus can produce various toxins that can cause different types of infections in humans. These toxins can damage the host cells and tissues, interfere with the immune system, or trigger inflammatory responses. Some of the toxin-mediated infections caused by S. aureus are:

• Toxic shock syndrome (TSS): This is a rare but life-threatening condition that occurs when S. aureus toxins, especially toxic shock syndrome toxin-1 (TSST-1), enter the bloodstream and cause a systemic inflammatory response. TSS can affect multiple organs and lead to fever, rash, hypotension, organ failure, and death.

• Scalded skin syndrome (SSS): This is a condition that affects mostly infants and children and is caused by exfoliative toxins (ETs) produced by some strains of S. aureus. ETs cause the separation of the epidermis from the dermis, resulting in blisters, peeling skin, and a red, raw surface that resembles a burn.

• Food poisoning: This is a common type of gastroenteritis that occurs when S. aureus toxins, especially enterotoxins, contaminate food and are ingested by humans. Enterotoxins stimulate the vomiting center in the brain and cause nausea, vomiting, diarrhea, dehydration, and low blood pressure. Symptoms usually appear within hours of eating the contaminated food and last for a short time.

Other toxin-mediated infections caused by S. aureus include staphylococcal pneumonia, which is associated with Panton-Valentine leukocidin (PVL), a toxin that destroys white blood cells, and staphylococcal skin infections, such as impetigo and furuncles, which are caused by cytotoxins that lyse host cells. Toxin-mediated infections caused by S. aureus are often difficult to treat because antibiotics do not neutralize the toxins. Therefore, novel therapeutic strategies that target the toxins or their effects are needed.

Coagulase-negative Staphylococcus (CoNS) are a group of Gram-positive cocci that are distinguished from Staphylococcus aureus by their inability to produce the enzyme coagulase, which clots plasma. CoNS are part of the normal flora of the skin and mucous membranes of humans and animals, and they rarely cause disease in healthy individuals. However, they can become opportunistic pathogens in immunocompromised patients or those with indwelling medical devices, such as catheters, shunts, prosthetic valves, or joints. CoNS can cause infections such as wound infections, urinary tract infections, bacteremia, endocarditis, and meningitis. Cons are also a common cause of contamination of blood cultures and other clinical specimens.

The most clinically significant species of CoNS are Staphylococcus epidermidis and Staphylococcus saprophyticus. S. epidermidis is the most prevalent species on the skin and the most common cause of CoNS infections, especially in hospitalized patients with intravascular catheters or prosthetic devices. S. epidermidis can form biofilms on the surfaces of these devices, which protect them from host defenses and antimicrobial agents. S. saprophyticus is a common cause of urinary tract infections in young women, especially sexually active ones. S. saprophyticus produces high concentrations of urease, which hydrolyzes urea to ammonia and increases the pH of urine, facilitating bacterial growth and stone formation.

Other species of CoNS that have been associated with human infections include Staphylococcus lugdunensis, Staphylococcus haemolyticus, Staphylococcus hominins, Staphylococcus capitis, Staphylococcus warneri, and Staphylococcus simulans. These species are less frequently isolated and have variable clinical significance.

CoNS have relatively low virulence compared to S. aureus, but they possess some common virulence factors that contribute to their pathogenicity. These include a thick peptidoglycan layer that provides resistance to lysozyme and phagocytosis, a loose polysaccharide slime layer that facilitates adherence and biofilm formation, and various enzymes that degrade host tissues or immune components, such as lipases, proteases, nucleases, and hemolysins. CoNS can also acquire resistance to multiple antibiotics through plasmids or chromosomal mutations, making them difficult to treat. The most common resistance mechanisms are the production of beta-lactamases that inactivate penicillins and cephalosporins and the expression of altered penicillin-binding proteins (PBPs) that reduce the affinity of methicillin and other beta-lactam antibiotics. CoNS that are resistant to methicillin are called methicillin-resistant CoNS (MRCoNS), and they are usually resistant to other classes of antibiotics as well.

CoNS infections are diagnosed by isolating and identifying the bacteria from clinical specimens using conventional microbiological methods or molecular techniques. The identification of CoNS is based on their Gram stain morphology, catalase test (positive), coagulase test (negative), and other biochemical tests that differentiate them from each other and from S. aureus. The susceptibility testing of CoNS is performed by disk diffusion or broth dilution methods to determine the minimum inhibitory concentration (MIC) of various antibiotics.

The treatment of CoNS infections depends on the type and severity of the infection, the susceptibility pattern of the isolate, and the patient`s condition and comorbidities. The general principles of treatment include removing or replacing the infected device if possible, draining any abscesses or collections of pus, and administering appropriate antimicrobial therapy based on culture and sensitivity results. The choice of antibiotics should cover both Gram-positive and Gram-negative bacteria until the final identification and susceptibility testing of CoNS is available. The duration of therapy varies depending on the site and extent of infection, but it is usually longer than for S. aureus infections due to the presence of biofilms and resistance mechanisms.

CoNS infections can be prevented by following standard infection control measures in health care settings, such as hand hygiene, aseptic technique, proper disinfection and sterilization of equipment and instruments, and judicious use of antibiotics. In addition, patients with indwelling devices should be educated about the signs and symptoms of infection and instructed to seek medical attention promptly if they develop any.

Streptococcus pyogenes (group A) is a gram-positive coccus that grows in chains and forms beta-hemolytic colonies on blood agar. It is also known as the causative agent of strep throat, scarlet fever, rheumatic fever, and other infections. It is one of the most common human pathogens and can cause a wide range of diseases, ranging from mild to severe and potentially life-threatening.

Streptococcus pyogenes (group A) has several virulence factors that enable it to adhere to host tissues, evade the immune system, and damage host cells. Some of these factors are:

• Capsule: a polysaccharide layer that surrounds the bacterial cell and prevents phagocytosis by neutrophils and macrophages.

• M protein: a surface protein that binds to fibrinogen and prevents opsonization by complement and antibodies. It also helps the bacteria to adhere to epithelial cells and resist phagocytosis. There are more than 80 serotypes of M protein, which vary in antigenicity and tissue tropism.

• M-like protein: a surface protein that binds to immunoglobulin G (IgG) and interferes with its function. It also helps the bacteria to adhere to keratinocytes and resist phagocytosis.

• F protein: a surface protein that binds to fibronectin and facilitates the invasion of epithelial cells and endothelial cells.

• Pyrogenic exotoxins: a group of toxins that act as superantigens and stimulate the release of cytokines from T cells and macrophages. They are responsible for the rash of scarlet fever, the shock-like syndrome, and the tissue necrosis seen in some infections. There are at least 12 types of pyrogenic exotoxins, which vary in antigenicity and toxicity.

• Streptolysin S and O: two hemolysins that lyse red blood cells, white blood cells, platelets, and other cells. Streptolysin S is oxygen-stable and contributes to beta-hemolysis on blood agar. Streptolysin O is oxygen-labile and induces the production of antibodies that can be detected by the antistreptolysin O (ASO) test.

• Streptokinase: an enzyme that activates plasminogen and converts it to plasmin, which degrades fibrin clots and facilitates the spread of bacteria in tissues.

• Deoxyribonuclease: an enzyme that degrades DNA and reduces the viscosity of pus.

• C5a peptidase: an enzyme that cleaves C5a, a chemotactic factor for neutrophils, and impairs the recruitment of these cells to the site of infection.

Streptococcus pyogenes (group A) can be classified into different types based on their M protein serotype, their pyrogenic exotoxin profile, or their emm gene sequence. These types have different epidemiological patterns, clinical manifestations, and susceptibility to antibiotics. For example, types 1, 3, 12, 28, and 49 are associated with invasive disease and necrotizing fasciitis; types 1, 3, 4, 6, 12, 18, 19, 22, 24, 27, 29, and 49 are associated with rheumatic fever; types 1-4 are associated with scarlet fever; types 1-3 are associated with toxic shock–like syndrome; types 1-3 are resistant to erythromycin; types 4-6 are resistant to tetracycline.

Streptococcus pyogenes (group A) can be diagnosed by culture, rapid antigen detection tests (RADTs), polymerase chain reaction (PCR), or serological tests. Culture is considered the gold standard for diagnosis, but it takes up to 48 hours to obtain results. RADTs are faster but less sensitive than culture. PCR is highly sensitive and specific but requires specialized equipment and expertise. Serological tests can detect antibodies against streptococcal antigens such as ASO or anti-DNase B, but they are not useful for acute diagnosis as they reflect past exposure rather than current infection.

Streptococcus pyogenes (group A) can be treated with antibiotics such as penicillin or cephalosporins. Antibiotic therapy can reduce the duration of symptoms, prevent complications such as rheumatic fever or glomerulonephritis, and reduce the transmission of bacteria to others. However, antibiotic resistance is an emerging problem among some strains of Streptococcus pyogenes (group A), and alternative agents such as macrolides or clindamycin may be needed in some cases. In addition to antibiotics, supportive care such as analgesics, antipyretics, hydration, and rest may be needed for symptomatic relief.

Streptococcus pyogenes (group A) can be prevented by good hygiene practices such as washing hands frequently, covering coughs and sneezes, avoiding sharing utensils or personal items with infected people, and staying home when sick. Vaccination against Streptococcus pyogenes (group A) is not currently available, but several candidates are under development. These vaccines aim to elicit protective immunity against common M protein serotypes or other antigens such as pyrogenic exotoxins or C5a peptidase.

Streptococcus pyogenes (group A) is a versatile pathogen that can cause a variety of diseases in humans. It has evolved multiple mechanisms to evade host defenses and damage host tissues. It can be classified into different types based on its molecular characteristics and clinical features. It can be diagnosed by various methods, but culture remains the gold standard. It can be treated with antibiotics, but resistance is a growing concern. It can be prevented by hygiene measures, but vaccination is still a future goal.

Nonsuppurative infections are those that do not involve the formation of pus or abscesses. They are usually caused by the immune response to the bacteria or their toxins rather than by the direct invasion of the tissues. Streptococcus pyogenes (group A) can cause two major types of nonsuppurative infections: rheumatic fever and glomerulonephritis.

Rheumatic fever

Rheumatic fever is a systemic inflammatory disease that can affect the heart, joints, skin, and nervous system. It occurs as a delayed complication of untreated or inadequately treated streptococcal pharyngitis (sore throat). The exact mechanism of rheumatic fever is not fully understood, but it is believed to involve cross-reactivity between streptococcal antigens and human tissues, resulting in autoimmune damage.

The most common manifestation of rheumatic fever is carditis or inflammation of the heart valves. This can lead to valvular stenosis or regurgitation, which can impair the function of the heart and cause heart failure. Other manifestations include arthritis, which affects multiple joints and causes pain and swelling; erythema marginatum, which is a rash with red edges and clear centers that appears on the trunk and limbs; subcutaneous nodules, which are firm and painless lumps under the skin; and Sydenham`s chorea, which is a neurological disorder characterized by involuntary movements of the face, limbs, and trunk.

The diagnosis of rheumatic fever is based on clinical criteria known as the Jones criteria, which include evidence of a preceding streptococcal infection and the presence of two major or one major and two minor manifestations. The major manifestations are carditis, arthritis, erythema marginatum, subcutaneous nodules, and Sydenham`s chorea. The minor manifestations are fever, arthralgia, elevated acute phase reactants (such as erythrocyte sedimentation rate and C-reactive protein), prolonged PR interval on electrocardiogram, and previous history of rheumatic fever.

The treatment of rheumatic fever consists of antibiotics to eradicate streptococcal infection, anti-inflammatory drugs to reduce inflammation and pain, and prophylaxis to prevent recurrent episodes. Prophylaxis involves long-term administration of penicillin or other antibiotics to prevent reinfection with streptococcus. Patients with rheumatic heart disease may also require surgery to repair or replace damaged valves.

Glomerulonephritis

Glomerulonephritis is an inflammation of the glomeruli, which are the filtering units of the kidneys. It can occur as a complication of streptococcal skin infections (such as impetigo) or pharyngitis. The mechanism of glomerulonephritis is also not fully understood, but it is thought to involve immune complex deposition in the glomeruli, leading to complement activation and inflammation.

The main clinical features of glomerulonephritis are hematuria (blood in urine), proteinuria (protein in urine), edema (swelling), hypertension (high blood pressure), and reduced renal function. The diagnosis is based on urinalysis, blood tests, and renal biopsy. The treatment consists of supportive measures such as fluid restriction, diuretics, antihypertensives, and dialysis if needed. Antibiotics are not effective in treating glomerulonephritis, but they may be given to prevent secondary infections. Most cases of glomerulonephritis resolve spontaneously within weeks or months, but some may progress to chronic kidney disease or end-stage renal disease.

Streptococcus agalactiae, also known as group B streptococcus (GBS), is a gram-positive coccus that can form chains or pairs. It is a facultative anaerobe, meaning it can grow with or without oxygen. It is also beta-hemolytic, meaning it can break down red blood cells and produce a clear zone on blood agar plates.

GBS is a common bacterium that colonizes the gastrointestinal and genital tracts of healthy adults, usually without causing any symptoms. However, it can cause serious infections in certain populations, such as newborns, pregnant individuals, and adults with chronic conditions such as diabetes.

GBS is the leading cause of neonatal sepsis, meningitis, and pneumonia in the United States. It can be transmitted from mother to baby during labor and delivery or after birth through contact with contaminated surfaces or hands. GBS can also cause infections in pregnant individuals, such as urinary tract infections, chorioamnionitis (infection of the membranes and fluid surrounding the fetus), postpartum endometritis (infection of the uterus after delivery), and bacteremia (bacteria in the blood).

In nonpregnant adults, GBS can cause bacteremia without a focus (bacteria in the blood without an identifiable source), sepsis (a life-threatening response to infection), soft tissue infections (such as cellulitis, abscesses, and necrotizing fasciitis), and other focal infections (such as endocarditis, osteomyelitis, arthritis, and meningitis). The risk factors for invasive GBS disease in adults include advanced age, diabetes mellitus, immunosuppression, malignancy, liver disease, renal disease, and alcohol abuse.

GBS has a polysaccharide capsule that helps it evade phagocytosis (ingestion by immune cells) and complement-mediated killing (destruction by proteins in the blood). It also produces various virulence factors that enable it to adhere to host cells, invade tissues, damage cells and tissues, and resist antibiotics. Some of these virulence factors include surface proteins (such as C5a peptidase, alpha C protein, Rib protein), toxins (such as hemolysins, CAMP factor), enzymes (such as hyaluronidase, sialidase), and biofilm formation.

The diagnosis of GBS infection is based on the isolation and identification of the bacterium from clinical specimens, such as blood, cerebrospinal fluid, urine, or wound swabs. The identification of GBS can be made by using biochemical tests (such as catalase test, hippurate hydrolysis test), serological tests (such as latex agglutination test for group B antigen), molecular tests (such as polymerase chain reaction for specific genes), or mass spectrometry (such as matrix-assisted laser desorption/ionization time-of-flight mass spectrometry).

The treatment of GBS infection depends on the type and severity of the infection, the susceptibility of the bacterium to antibiotics, and the presence of any allergies or contraindications. The most commonly used antibiotics for GBS infection are penicillins (such as penicillin G or ampicillin) or cephalosporins (such as ceftriaxone or cefotaxime). For patients who are allergic to penicillins or cephalosporins, alternative antibiotics include vancomycin or clindamycin. However, some strains of GBS may be resistant to clindamycin or erythromycin due to macrolide-lincosamide-streptogramin B resistance genes.

The prevention of GBS infection in newborns is achieved by screening pregnant individuals for vaginal and rectal colonization with GBS at 35 to 37 weeks of gestation and administering intrapartum antibiotic prophylaxis to those who are colonized or have other risk factors. The recommended antibiotics for intrapartum prophylaxis are penicillin G or ampicillin. For patients who are allergic to penicillins or cephalosporins, alternative antibiotics include cefazolin or clindamycin.

The prevention of GBS infection in adults is mainly based on the management of underlying conditions that increase the risk of invasive disease. There is currently no vaccine available for GBS infection in humans. However, several vaccine candidates are under development that targets different components of the GBS capsule or surface proteins.

Viridans streptococci are a heterogeneous group of gram-positive cocci that are part of the normal flora of the oral cavity, respiratory tract, gastrointestinal tract, and urogenital tract. They are named viridian (green) because they produce a green pigment on blood agar due to their partial hemolysis. They are classified into five groups based on their phenotypic and genetic characteristics: Streptococcus anginosus group, Streptococcus mitis group, Streptococcus mutans group, Streptococcus salivarius group, and Streptococcus bovis group.

Viridans streptococci are generally considered to be low-virulence organisms that cause opportunistic infections in immunocompromised or debilitated hosts or in patients with predisposing factors such as dental caries, periodontal disease, trauma, surgery, or indwelling devices. The most common clinical manifestations of viridans streptococci infections are:

• Abscess formation: Viridans streptococci can cause abscesses in various sites such as the brain, liver, spleen, lung, kidney, and subcutaneous tissue. The abscesses are usually polymicrobial and contain anaerobic bacteria as well. The Streptococcus anginosus group is particularly associated with abscess formation.

• Septicemia: Viridans streptococci can cause septicemia in neutropenic patients who have hematological malignancies or who receive chemotherapy. Septicemia can be associated with shock, disseminated intravascular coagulation (DIC), and multiple organ failure. The Streptococcus mitis group is the most common cause of septicemia in this setting.

• Subacute endocarditis: Viridans streptococci are the most common cause of subacute infective endocarditis, which is a chronic infection of the heart valves that develop over weeks to months. The infection usually occurs in patients who have preexisting valvular abnormalities such as rheumatic heart disease or congenital heart defects. The infection can lead to valvular damage, embolic complications, and heart failure. The Streptococcus mutans group and the Streptococcus sanguinis group are the most common causes of subacute endocarditis.

• Odontogenic infections: Viridans streptococci can cause infections of the oral cavity and its adjacent structures, such as the sinuses, jawbones, and facial soft tissues. The infections can result from dental caries, periodontal disease, trauma, or dental procedures. The infections can range from mild gingivitis to severe necrotizing fasciitis. The Streptococcus mutans group and the Streptococcus salivarius group are the most common causes of odontogenic infections.

• Dental caries: Viridans streptococci are the main etiological agents of dental caries, which are localized demineralization and destruction of the tooth enamel and dentin. The caries are caused by the production of organic acids from dietary sugars by the bacteria. The acids dissolve the tooth mineral and create cavities. The Streptococcus mutans group is the most important cause of dental caries.

Viridans streptococci have relatively low virulence factors compared to other gram-positive cocci. They do not produce capsules, toxins, or hemolysins. Their main virulence factors are their ability to adhere to host surfaces such as teeth and heart valves by producing extracellular polysaccharides and surface proteins; their ability to form biofilms that protect them from host defenses and antibiotics; and their ability to resist phagocytosis by producing hydrogen peroxide and catalase.

The diagnosis of viridans streptococci infections is based on the isolation and identification of the bacteria from clinical specimens such as blood cultures, pus cultures, or tissue biopsies. The identification is done by using biochemical tests, serological tests, or molecular methods such as PCR or sequencing. The treatment of viridans streptococci infections depends on the type and severity of the infection, the susceptibility of the bacteria to antibiotics, and the presence of any underlying conditions or complications. The treatment usually involves a combination of surgical drainage or debridement and antibiotic therapy. The antibiotic therapy should be guided by the results of antimicrobial susceptibility testing because viridans streptococci can exhibit variable resistance to different classes of antibiotics such as penicillins, cephalosporins, macrolides, fluoroquinolones, and vancomycin.

Viridans streptococci infections can be prevented by maintaining good oral hygiene; avoiding dental caries and periodontal disease; avoiding trauma or surgery that can introduce bacteria into the bloodstream; using prophylactic antibiotics before dental procedures or other invasive procedures in patients who have a high risk of endocarditis; and using appropriate infection control measures in health care settings to prevent nosocomial transmission.

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