Skin And Soft Tissue Infections PDF

MUSKLOSKELETAL BLOCK Skin and soft tissue infections prepared by dr. Heba M. Nageeb lecturer of microbiology dpt. ASWAN UNIVERSITY  Skin and soft tissue infection is caused by avariety of germs.symptoms varey from mild to serious.some cases need medical attention. Min...

MUSKLOSKELETAL BLOCK Skin and soft tissue infections prepared by dr. Heba M. Nageeb lecturer of microbiology dpt. ASWAN UNIVERSITY  Skin and soft tissue infection is caused by avariety of germs.symptoms varey from mild to serious.some cases need medical attention. Minor trauma that destroys the integrity and allows organisms access. Surface penetrated by ducts of pilosebaceous glands, sweat gland and hair follicles provide route of entry for microbes , esp. if ducts are obstructed. Fungi grow in moist warm areas,wearing sweaty or moist clothes is a risk factor for fungal infection Skin and soft tissue infection is classified according to the anatomical site from superficial to deep Modes of infection: Direct introduction of microbe into epithelium Circulating microbe Circulating toxin 1 Bacterial infections 2 Fungal infections 3 Viral infections The following are different type of skin infection: Bacterial skin infections: Boils (staphylococcus aureus) Impetigo (streptococcus pyogens& staphylococcus aureus ) Cellulitis(streptococcus pyogens) Necrotizing fasciitis (streptococcus pyogens) Anthrax (bacillus anthracis) Gas gangrene (clostridium perfringen) Burn infection (pseudomonas) Leprosy(mycobacterium leprea)  Staphylococcus aureus Natural habitat: Nostrils.skin Morphology: Gram positive cocci arranged in grape like clusters.non motile.non capsulted. Non spore forming. The commonest cause of localized suppurative lesions in humans. Biochemical reaction: catalase: positive Coagulase: positive DNAase : positive Oxidase: negative Ferment glucose, lactose ,sucrose,mannitol and prouce acid only. Diseases caused by Staph.aureus Focal suppuration and abscess formation: It is the characteristic infection of Staph.aureus that occurs due to coagulase which deposits fibrin around the lesions forming a wall which is reinforced by inflammatory cells. From any focus, organisms may spread via the lymphatics or blood to other parts of the body. 1. Superficial infections: e.g. folliculitis, carbuncles, boils and abscesses. 2. Deep seated lesions: e.g. osteomyelitis, broncho-pneumonia, empyema,endocarditis, meningitis. 3. Bacteraemia with multiple abscesses in tissues. 4. Outbreaks of hospital acquired wound infections commonly occur due to antibiotic resistant Staphylococci. Foreign bodies as sutures and intravenous catheters are predisposing factors to theses infections. 5. Septicaemia "sepsis" originates from any localized lesion, especially wound infection or as a result of intravenous drug abuse. Diseases caused by Staph.aureus Toxigenic diseases: : Toxic shock syndrome (TSS): * This is associated with TSST-1. * TSS was 1st described in menstruating women using tampons. The syndrome also occurs with wound or localized infections. It has onset of fever, vomiting, diarrhea, muscle pains and rash. Hypotension, heart failure and renal failure may occur in severe cases. Scaled skin syndrome "bullous exfoliation": * It is due to the exfoliative toxin A and B. The syndrome occurs in babies and young children. It is characterized by large areas of desquamation of the skin (heal without scaring) and generalized bullae formation. Staphylococcus treatment and drug resistance Staph. Aureus shows marked ability to develop resistance to antibiotics, therefore sensitivity testing is essential for the choice of proper antibiotic. 90%are resistant to penicillin due to production of b-lactamase which destroys the b-lactame ring in penicillin, those can be treated by mecithillin.  unfortunately 20% showed resistance to mecithilline, those are treated by vancomycin. Staph aureus with intermediate resistance(VISA)or complete resistance(VRSA)by increased cell wall synthesis and alteration of cell wall structure were reported.  Streptococcus pyogens Gram positive cocci arranged in chains. Non motile, non spore forming and some are capsulated. Group A beta heamolytic streptococci. They are facultative anaerobes, on blood agar they produce beta heamolysis. They are catalase negative. Pathogenisis &virulence factors: Through adhesion ,invasion of tissues ,escaping phagocytosis and by production of enzymes and toxins. Pyrogenic exotoxins (erythrogenic toxins): These are heat labile toxins produced by group A streptococci These toxins are produced by streptococci lysogenized by a bacteriophage carrying the gene for the toxin. They include: Pyrogenic exotoxin A (erythrogenic toxin); It has the same mode of action as TSST of Staph. aureus. It is a superantigen that causes the release of a large amount of cytokines from helper T cells and macrophages. It is associated with streptococcal toxic shock syndrome (STSS) and scarlet fever. Pyrogenic exotoxin B; is a protease that rapidly destroys tissues and is produced in large amounts by the strains of Str. pyogenes that cause necrotizihg fasciitis. These strains are referred to as "flesh eating bacteria". Pyrogenic exotoxin C: it contributes to STSS. Diseases Caused by Str. pyogenes: Pyogenic local infections: Pyoderma (impetigo): A local infection of the skin characterized by formation of blisters which break leaving a denuded surface covered with pus or crusts. It is usually caused by M types 49, 57 and 59-61 and may be followed by acute glomerulonephritis. Invasive diseases: These are diffuse rapidly spreading infections that involve the lymphatics with minimal local suppuration. From the lymphatics the infection can extend to the blood stream.  Erysipelas: It is a skin infection characterized by redness, oedema and a rapidly advancing margin, often on the face or the legs.  Soft tissue sepsis: Wound infection, cellulites, necrotizing fasciitis and lymphadenitis. Any of these conditions may be complicated by streptococcal septicaemia.  Acute bacterial endocarditis: The organism reaches the heart valve through the blood stream as a complication of any of the primary lesions mentioned above. The presence of a deformed or rheumatically affected valve encourages the condition. Diseases Caused by Str. pyogenes: Toxigenic diseases:  streptococcus toxic shock syndrome: Str. pyogenes may cause fulminant invasive infections with toxic shock syndrome manifestations i.e. shock, bacteraemia, respiratory and multiorgan failure. Infection follows minor trauma and presents with soft tissue infections including necrotizing fasciaitis (progressive subcutaneous tissue infection, destruction of fascia and fat and myositis). Such severe infections are associated with group A streptococci of the M type 1, 3, 12 & 28 that produce pyrogenic exotoxin A and B. Death occurs in about 30% of patients.  Scarlet fever: It is a disease of children characterized by sore throat and an erythematous rash. It occurs due to infection with a streptococcal strain that produces erythrogenic toxin in susceptible individuals (i.e. have no antitoxin).. Post-streptococcal immunologic diseases:  Acute glomerulonephritis (AGN): This sometimes develops 3 weeks after throat or skin infection with a nephrogenic strain of streptococci (M types 2, 4, 12, 49 and 59-61). This disease is characterized by edema, urea nitrogen retention; high blood pressure and low serum complement levels. Blood, albumin and granular casts are present in urine. The condition is due to antigen antibody complex deposition on the glomerular basement membrane (type III hypersensitivity reaction). The majority of patients recover completely. However, few may die or pass to chronic glomerulonephritis and renal failure.  Bacillus anthracis Morphology: Gram positive rectangular large organisms arranged in chains. They are capsulated in vivo; when stained with polychrome methylene blue, the capsule appears as pink rim around the blue bacillus (MacFadyean reaction). They form spores in vitro. The spores are central, ovoid and are not stained with gram. They appear pink when stained with the acid fast spore stain. Cultural Characters: Aerobes, grow on nutrient agar at 37°C. Pathogenesis and Virulence: The virulence of the organism is due to the polypeptide capsulewhich is anti- phagocytic and toxin production.  Pseudomonas aeuroginosa This organism is widely distributed in nature and commonly present in moist environment in hospitals. Morphology: gram negative bacilli , non spore forming, non capsulted and motile by polar flagella. Culture characters: obligate aerobic. can grow on any simple media producing colonies with distinctive sweet grape odor. on nutrient agar they cause greenish discoloration due to formation of diffusible pigment pyocianine(blue) and pyoverdin( greenish yellow). Biochemical reaction :oxidase positive. Pathogenesis: P.aeuroginosa is invasive and toxigenic.can attach and colonize mucous membrane and skin.Invade locally and produce systemic disease due to several virulence factors: Pilli Adhesins, glycocalyx :attachment Exotoxin A:prevent host protein synthesis. Lypopolysacharides endotoxin Enzymes(elastase,protease and phospholipase) It represents a major cause of nosocomial infection due to: Their ability to grow in aqueous environment that favors its presence in environment containing anesthesia and respiratory equipments and IV fluid. Their remarkable ability to withstand disinfectants. The presence of compromised patients in hospitals.  Clostridium perfringens (Cl. welchii) Large Gram-positive bacilli. capsulated & non-motile. Spores are central or sub terminal. Anaerobic.Present in soil & intestinal tract of humans and animals. On Blood agar: target hemolysis (Double zone of hemolysis) : Outer Alpha toxin- Alpha hemolysis; Inner-Delta Toxin- Beta hemolysis. Glucose ,Lactose and Maltose Fermented with Acid & Gas production. Stormy fermentation of lactose in litmus milk; the acid coagulates casein-acid clot. Nagler’s Reaction:Done to detect the lecithinase activity of alpha toxin. Characteristics opalescence in egg yolk media is produced around colonies in +v test due to breakdown of lipoprotein complex in the medium. Clinical disease: Disease due to release of toxin after sporulation. Soft tissue infection:cellulitis, fasciitis ,myonscrosis( gas gangrene). Food poisoning. The toxins of Cl. perfringens alpha toxin (phospholipase C, lecithinase) is the most important toxin: Lyses RBCs, platelets, leucocytes and endothelial cells. Increased vascular permeability with massive hemolysis and bleeding &tissue destruction. Hepatic toxicity and myocardial dysfunction Theta toxin is responsible for necrotic lesions in necrotizing enterocolitis. Enterotoxin is heat labile toxin produced in colon → food poisoning.  extracellular enzymes:DNAase, hyaluronidase, a collagenase are also produced fungal skin infections: Superficial mycosis (tinea versicolor) Superficial chronic skin infection.Affect outermost layer of skin and hair. It has primarily cosmetic symptoms. manifests as hypo-or hyper pigmented skin patches, usually on the trunk of the body, caused by Malassezia furfur. It is diagnosed by KOH mount of skin scales that show the fungus as short curved septate hyphae and budding yeast-like cells (spaghetti and meat balls). It is treated by topical miconazole.  cutaneous mycosis (dermatophytes) Dermatophytes include Trichophylon ,Microsporum,Epidermophyton floccosum.  Infection is from man to man by direct contact or from animals. The clinical form of the disease is named according to the site infected. the skin scales are put in a drop of 10-20% KOH mount solution shows the presence of hyphae or spores. For the isolation of dermatophytes, the medium used is Sabouraud's dexstrose (SDA) agar. To inhibit bacterial contaminants, antibiotics are added as chloramphenicol. Also actidione is added as an inhibitor for contaminating moulds to the media  sub cutaneous mycosis (Madura foot) It is a subcutaneous disease characterized by swelling, abscess formation and drainage through sinus tracts. Granules (0.5 -2 mm in width) and variable species specific colors are found in the exudates. It is caused by filamentous fungi living in soil.The most common fungal causes is Madurella mycetomatis, enters the body via wounds; usually occurs in rural area in agricultural workers in the tropics. Laboratory diagnosis is important to identify the causing agent wether it is bacterial actinomycotic which can be treated by antibiotics or fungal eumycotic which is resistant and need surgical interference.  Sporotrichosis It is caused by the dimorphic fungus Sporothrix schenckii which is present in soil, vegetations, hay, or decaying material. Trauma to the skin commonly thorn prick in the hands leads to direct inoculation of the fungus The organism converts to the yeast form in the body. The clinical picture evolves as the organisms spread along lymphatics draining the primary inoculation site. Clinical manifestations: Sporotrichosis is chronic subcutaneous disease. After inoculation, a papule develops at the site within days to weeks. ulcerates, but remains only mildly tender  Candidiases (Moniliases) This term refers to infections caused by different Candida species the commonest of them is Candida albicans which is a part of normal flora of the skin, mucous membranes, and gastrointestinal tract. Predisposing factors to Candida infections are: Extremes of age,Chronic debilitating diseases e.g. diabetes mellitus,Nutritional disorders,Excessive moisture,Pregnancy or Long-term antibiotic and steroid usage. Superficial candidiasis involves nails, skin folds, or groin region,appers as clearly defined patch of red itchy skin.  Diagnosis is mainly clinical and confirmed by detection of gram positive budding yeast yeast cells in Gram stained film or KOH mount of the lesion. viral skin infections: Herpes simplex type 1 Chicken box (varicella) Shingles( herpes zoster) Measles Rubella (German measles) Hand ,foot &mouth disease. Genital wart (human papilloma virus)  Herpesvirus (HSV) 1 Double stranded enveloped DNA viruses with icosahedral symmetry. HSV 1 is present in the saliva and transmitted by droplets or by contact with secretions containing the virus. Pathogenesis: Virus initially infects the mucoepithelial cells and replicate in them causing disease at the site of infection and then establish latent infection of ganglia of the innervating neurons. The infection may be primary or recurrent (latent). Primary infection: * Most 1ry infections are asymptomatic.HSV 1 occurs in children 2-4 years. * The virus multiplies locally in the mucous membrane or abraded skin (HSV can not penetrate intact skin) causing: * Vesicular lesions are formed which may change to shallow ulcers. Scabs are formed and lesions heal without scarring. Latent infection: From the primary lesions the virus travels through the nerves to the trigeminal ganglia (HSV-1) causing acute infection that subsides and the virus persists latent for life time of the host. Recurrent infection: * The recurrent attacks are common and occur following specific stimuli such as exposure to excess sunlight, fever, menstruation or emotional stress. * The virus migrates down the neurons (so that recurrence occurs at the same site as the primary lesion) and replicates in the skin causing: Asymptomatic virus shedding or Vesicular lesions which are less severe, more localized and of shorter duration than the 1ry episodes because of the nature of the spread and existence of memory immune response Diseases caused by HSV 1: 1. In persons with normal immunity, primary infections are usually localized including: Acute herpetic gingivostomatitis, mostly in children 1-3 years old. Keratoconjunctivitis that may be complicated by corneal ulcers, opacities and blindness. Skin infections, herpetic whitlow in fingers & eczema herpeticum (in children). 2. The most common form of recurrence is herpes labials (fever blisters/ cold sores, herpes febrilis) that manifest as clusters of localized vesicles at the mucocutaneous junction of the lips or nose. Recurrences occur at the same site. 3. In immunocompromized patients e.g. AIDS or transplant patients disseminated infections as pneumonia are common  VARICELLA-ZOSTER VIRUS (VZV) Both diseases are caused by the same virus.  Varicella (chickenpox / primary infection): Mode of infection: Air borne and contact with lesions. It is a highly contagious disease of children which occurs in epidemics. Incubation period: 14-21 days. Virus multiplies in the mucosa of the respiratory tract then it spreads via the blood and lymphatics to the reticulo-endothelial system (1ry viremia). 2ry viremia occurs after 11-13 days and spread the virus throughout the body and skin causing typical rash: Starts on the trunk and spreads to the limbs and face Evolves from papules to vesicles, pustules and finally crusts. All stages of rash present at the same time. Lesions heal without scar formation Recovery is the rule with life long immunity. After recovery the virus becomes latent in the dorsal root ganglia and zoster can occur despite this immunity to varicella. Zoster (shingles, reactivation of latent virus): It results from reactivation of latent VZV later in life at times of reduced cell mediated immunity or local trauma. VZV latent in sensory ganglia travels down sensory nerves leading to severe pain in the area of skin or mucous supplied by the affected nerves. Pain is followed by appearance of crop of vesicles which is usually unilateral affecting the trunk, head and neck. A chronic pain syndrome called post herpetic neuralgia occurs in 30% of patients older than 65 years in whom herpes zoster develops. Shingles( herpes zoster) Chicken box (varicella)  Measles It is acute highly communicable viral disease that affects children cauesd by measels virus the virus belongs to Paramyxoviridae. it is -ve sense ssRNA enveloped viruses with helical symmetry.Their genome is not segmented. They are genetically stable. Transmission: Droplet transmission. Direct contact or use of contaminated articles. Infection occurs by droplets. Primary multiplication occurs in the respiratory mucosa from where it passes to the regional lymph nodes and the recticulo-endothelial system to cause viremia, then localizes in the skin and mucous membrane. Clinical manifestations: Incubation period is 10 days. Prodromal phase: fever which lasts for 4 days associated with conjunctivitis, cough and "koplik´s spots" in the mouth (bluish-white ulcerations of the buccal mucosa opposite the lower molars). Rash phase: As the fever subsides the maculopapular rash appears all over the body. The rash is caused primarily due to the action of cytotoxic T cells attacking virus infected vascular endothelial cells of the skin. One attack of measles is followed by long lasting immunity. Diagnosis: Is usually clinical. Prophylaxis: Immunization using living attenuated vaccine given I.M at the age of 15 months. Another dose is recommended at 4-6 years (Now MMR is used).  RUBELLA (German measles) Rubella virus belongs to Togavirus family; however, it is not transmitted by arthropods. It is a +ss icosahedral enveloped RNA virus. Postnatal rubella Airborne transmission from the upper respiratory tract secretions of active cases. It affects neonates, children and adults. IP is 2-3 weeks. Pathogenesis: Initial replication of the virus occurs in the nasopharynx and local lymph nodes, and then spreads via blood to internal organs and skin. Clinical features: Fever. Pharyngitis. Enlargement of cervical lymph nodes. -Macular rash on the face and trunk (the rash is due to Ag-Ab mediated vasculitis).Polyarthritis occur in adult women due to immune complexes. The disease is mild and self limited (3 days measles).one attack is followed by solid immunity. Congenital rubella syndrome  Trans-placental transmission to the fetus. The mother contract infection via respiratory droplets. The child is liable to be born with congenital anomalies (especially if infection occurred during the first trimester of pregnancy) as: Congenital heart disease. CNS anomalies as nerve deafness, blindness, meningiocephalitis and mental retardation. hepatosplenomegaly.  Children infected in utero can continue to excrete the virus for up to 18 months after birth. The virus is found in pharyngeal secretions and other body fluids. They can be a source of infection to pregnant women.  Diagnosis: Diagnosis of postnatal rubella is mainly clinical. Infection during pregnancy needs laboratory confirmation (to consider therapeutic abortion) as follow: A. In the mother: 1. Serology: Detection of rubella IgM in a single serum sample or detection of a rising titer of rubella IgG in paired serum samples separated by 10 days by ELISA is diagnostic of recent rubella infection. 2. Virus isolation: Isolation of virus from amniotic fluids indicates definite fetal infection. Rubella infection during pregnancy is an indication for therapeutic abortion especially during the 1st trimester. B. In the newborn: 1. Serology: Detection of rubella IgM in the newborn serum by ELISA is diagnostic of infection in utero since IgM do not cross the placenta, so its presence indicates that its must has been synthesized by the fetus in utero. 2. Virus isolation from newborn specimens.  Prophylaxis: A living attenuated rubella vaccine is effective & gives immunity for 10 years. It is available:  in combination with measles and mumps vaccines (MMR) which is given to children at the age of 15 months and a booster dose at 4-6 years. As a single vaccine which is recommended for unimmunized young adult women if they are not pregnant and they should use contraception for the next 3 months.  Molluscum contagiosum Human warts (benign skin nodules) usually on arms, face and genitalia. caused by Molluscum contagiosum virus. Transmitted by close contact and sexually. It's common in children and immunosuppressed people. Diagnosis is clinical. Prevention of HPV infection: 1. Avoid contact with cases. 2. HPV quadrivalent recombinant vaccine: Composed of HPV L1 proteins of types 6, 11, 16 and 18. Administered by I.M. injection in 3 doses. The second and third doses are given 2 and 6 months after the first dose. It is recommended for females from 9-12 years (before sexual activity). A catch-up vaccination is recommended at 13-26 years. It protects against cancer cervix and anogenital warts