SSTI Disease Types PDF

SSTI disease types Pyoderma: localized skin infection with vesicles progressing to pustules; no evidence of systemic disease Erysipelas: localized skin infection with pain, inflammation, lymph node enlargement and systemic symptoms Cellulitis: infection of the skin that involves the su...

SSTI disease types Pyoderma: localized skin infection with vesicles progressing to pustules; no evidence of systemic disease Erysipelas: localized skin infection with pain, inflammation, lymph node enlargement and systemic symptoms Cellulitis: infection of the skin that involves the subcutaneous tissues Necrotizing fasciitis: deep infection of skin that involves destruction of muscle and fat layers Streptococcal toxic shock syndrome: multiorgan systemic infection resembling staphylococcal toxic shock syndrome; however, most patients with bacteremia and evidence of fasciitis. 16  Necrotizing fasciitis Necrotizing fasciitis: deep infection of skin that involves destruction of muscle and fat layers. In picture: patient in excruciating pain localized to the leg below the knee. Extensive necrotizing fasciitis was present on surgical exploration. The patient died despite aggressive surgical and medical management. 17  Pathogenesis Virulence determined by ability to avoid phagocytosis (mediated primarily by capsule, M and M-like proteins, C5a peptidase), adhere to and invade host cells (M protein, lipoteichoic acid, F protein), and produce toxins (streptococcal pyrogenic exotoxins, streptolysin S, streptolysin O, streptokinase, DNases). M protein, a protein anchored in the cytoplasmic membrane and protrudes above the cell surface, is the major type-specific protein associated with virulent strains. The epidemiologic classification of S. pyogenes is based on sequence analysis of the emm gene that encodes the M proteins. Pharyngitis and soft-tissue infections typically caused by strains with different M proteins. 18  Staphylococci Staphylococcus refers to the fact that these gram-positive cocci grow in a pattern resembling a cluster of grapes; however, organisms in clinical specimens may also appear as single cells, pairs, or short chains. Most staphylococci are 0.5 to 1.5 µm in diameter, nonmotile, and able to grow in a variety of conditions—aerobically, and anaerobically, in the presence of a high concentration of salt (e.g., 10% sodium chloride) and at temperatures ranging from 18°C to 40°C. wikipedia 19  Staphylococcus aureus S. aureus colonies can have a yellow or gold color because of the carotenoid pigments that form during their growth, hence the species name “aureus”. Catalase-positive, facultative anaerobe, gram- positive cocci arranged in clusters, mannitol fermenting, coagulase positive. The “aureus” was a gold coin of ancient Rome http://www.microbiologyinpictures.com/bacteria- 20 photos/staphylococcus-epidermidis-photos/staph-epidermidis-tsa.html Gram stain  Characteristics of disease Diseases include toxin-mediated diseases (food poisoning, toxic shock syndrome, scalded skin syndrome), pyogenic diseases (impetigo, folliculitis, furuncles, carbuncles, wound infections), and other systemic diseases (e.g. bacteremia and endocarditis). Scalded skin syndrome (Ritter disease): caused by the bacterial toxin; disseminated desquamation of epithelium (skin peeling) in infants; blisters with no organisms or leukocytes. primarily of neonates and young children, with a mortality rate of less than 5%. 21  Pathogenesis Virulence factors include structural components that facilitate adherence to host tissues and avoid phagocytosis, and a variety of toxins (cytotoxins, exfoliative toxins, enterotoxins, and toxic shock syndrome toxin-1) and enzymes that could hydrolyze host tissue components and aid in the spread of the bacteria (e.g. coagulase, lipases, nuclease etc). Exfoliative toxin (responsible for scalded skin syndrome) A, the enterotoxins, and TSST-1 belong to a class of polypeptides known as superantigens. These toxins bind to class II major histocompatibility complex (MHC II) molecules on macrophages, which, in turn, interact with the variable regions of the β subunit of specific T-cell receptors (VβTCR). This results in a massive release of cytokines by both macrophages and T cells, causing hypotension and shock, and fever. 22  Epidemiology Ubiquitously present as normal flora on human skin and mucosal surfaces. Organisms can survive on dry surfaces for long periods (because of thickened peptidoglycan layer and absence of outer membrane). Person-to-person spread through direct contact or exposure to contaminated objects (e.g., bed linens, clothing). Risk factors include presence of a foreign body (e.g., splinter, suture, prosthesis, catheter), previous surgical procedure, and use of antibiotics that suppress the normal microbial flora. Hospital- and community-acquired infections with MRSA (Methicillin-resistant S. aureus) are a significant worldwide problem. 23  Pseudomonas aeruginosa Small, gram-negative rods typically arranged in pairs, obligate aerobe, glucose oxidizer, simple nutritional needs, with mucoid polysaccharide capsule. These bacteria tend to thrive in moist environments. P. aeruginosa grows rapidly and has flat colonies with a spreading border, β-hemolysis, a green pigmentation caused by the production of the blue (pyocyanin) and yellow-green (pyoverdin) pigments, and a characteristic sweet, grapelike odor. Gram stain Colony On blood agar http://www.pseudomonas.com/acknowledgements24  Characteristics of P. aeruginosa Appear mucoid (appears like mucus) due to the abundance of a polysaccharide capsule. Gram stain of Pseudomonas aeruginosa surrounded by mucoid capsular material in cystic fibrosis patient. 25  Antibiotic Resistance: inherently resistant to many antibiotics and can mutate to even more resistant strains during therapy. The mutation of porin proteins constitutes the major mechanism of resistance because penetration of antibiotics into the pseudomonad cell is primarily through pores (formed by porins) in the outer membrane. It can also produce a number of different β-lactamases. An opportunistic pathogen present in a variety of environments. Ubiquitous in nature and moist environmental hospital sites (e.g., flowers, sinks, toilets, mechanical ventilation, and dialysis equipment). Pseudomonas has minimal nutritional requirements, tolerates a wide range of temperatures (4° C to 42° C), and is resistant to many antibiotics and disinfectants. 26  Pseudomonas diseases P. aeruginosa can cause a variety of primary skin infections. The most recognized are infections of burn wounds. Colonization of a burn wound, followed by localized vascular damage, tissue necrosis, and ultimately bacteremia, is common in patients with severe burns. The moist surface of the burn and inability of neutrophils to penetrate into the wounds predispose patients to such infections. 27  Folliculitis is another common infection caused by Pseudomonas, resulting from immersion in contaminated water (e.g., hot tubs, whirlpools, swimming pools). Secondary infections with Pseudomonas also occur in people who have acne or who depilate their legs. Folliculitis is an inflammation of the hair follicles, which are the small pouches in the skin from which hairs grow, that can be caused by an infection. 28  P. aeruginosa can cause fingernail infections in people whose hands are frequently exposed to water or frequent “nail salons”. http://www.nailsmag.com/article/114307/a-day-in-the-life-of-a- nail-expert-pseudomonas P. aeruginosa is also the most common cause of osteochondritis (inflammation of bone and cartilage) of the foot after a penetrating injury (e.g. associated with stepping on a nail). Diseases also include infections of the respiratory tract, urinary tract, ears and eyes, as well as bacteremia and endocarditis. 29  Pathogenesis P. aeruginosa has many virulence factors, including adhesins, toxins, and enzymes. The delivery system used by Pseudomonas, the type III secretion system, is particularly effective in injecting toxins into the host cell. 30 https://people.biochem.umass.edu/heuck/research.html  Treatment and control Hard to treat because (1) the bacteria are typically resistant to most antibiotics and (2) the infected patient with compromised host defenses cannot augment the antibiotic activity. Effective infection-control practices should concentrate on preventing the contamination of sterile equipment, such as mechanical ventilation equipment and dialysis machines, and the cross-contamination of patients by medical personnel. The inappropriate use of broad-spectrum antibiotics should also be avoided because such use can suppress the normal microbial flora and permit the overgrowth of resistant strains of Pseudomonas. 31