Bacterial Diseases (Chapter 74)

Strep Toxic Shock syndrome - How is the diagnosis made - Initial treatment, other options

Diagnosis and differential diagnosis Published criteria require isolation of group A streptococci from a sterile site for a "definite" diagnosis, combined with hypotension and clinical or laboratory abnormalities in two or more organ systems (see Table 74.8). Serum creatinine often rises early in the course, and creatine phosphokinase is elevated in the setting of necrotizing fasciitis or myonecrosis. The white blood cell count may be increased or normal with a substantial left shift33. Although staphylococcal and streptococcal TSSs share some common features, major differences exist (see Table 74.9). Treatment Most cases require intensive supportive therapy. Hypotension should be treated with aggressive intravenous fluid and vasopressors. Clindamycin inhibits the production of bacterial toxins and is a component of first-line antimicrobial treatment (together with penicillin); linezolid also blocks toxin production, and administration of IVIg to neutralize toxins may be of benefit33a. Early surgical intervention (e.g. drainage, debridement, fasciotomy, amputation) is crucial for necrotizing soft tissue infections and can be life-saving11.

Pitted Keratolysis - What is it? - Occurs most commonly in what part of the world, risk factors - Most common organisms? other culprits? - Ddx and treatment

Introduction Pitted keratolysis is a non-inflammatory bacterial infection of palmoplantar skin. Epidemiology and pathogenesis Pitted keratolysis occurs worldwide in temperate and tropical climates. Hyperhidrosis, prolonged occlusion, and increased skin surface pH are predisposing factors. Most infections are caused by Kytococcus sedentarius (formerly Micrococcus sedentarius), but other bacteria such as Dermatophilus congolensis, Corynebacterium, and Actinomyces spp. have been implicated. K. sedentarius produces two serine proteases (K1 and K2) that degrade keratin in the stratum corneum. Sulfur-containing compounds released by the bacteria lead to a characteristic associated malodor. Clinical features Small (1-7 mm), crater-like depressions are present within the stratum corneum on weight-bearing regions of the soles (Fig. 74.20) and rarely the palms. These pits may coalesce into large craters or rings of craters. There is usually no associated erythema, and the condition often goes unnoticed by the patient. Hyperhidrosis and malodor are common associated findings. Pathology Well-defined "pits" extend approximately two-thirds of the way into the stratum corneum. Gram, PAS, and Gomori methenamine silver stains reveal bacteria in the walls and at the bottom of the craters. No inflammation is observed. The diagnosis of pitted keratolysis is usually clinical. There is no fluorescence on examination with a Wood's light. The differential diagnosis includes plantar warts, tinea pedis, palmoplantar punctate keratoderma, pits of basal cell nevus syndrome, Darier disease, and circumscribed palmoplantar hypokeratosis. Treatment Topical benzoyl peroxide, erythromycin, clindamycin, mupirocin, tetracycline, and azole antifungals have all been reported to lead to a rapid resolution of pitted keratolysis. Aluminum chloride 20% solution or (in recalcitrant cases) botulinum toxin can be used to treat the associated hyperhidrosis

Scarlet Fever - Typically seen in whom? Causative organism? - Pathogenesis - clinical presentation

Introduction Primarily a disease of children, scarlet fever was often fatal in the pre-antibiotic era. The erythematous exanthem and enanthem are due to toxins produced by group A β-hemolytic streptococci. Epidemiology and pathogenesis Scarlet fever is caused by streptococcal pyrogenic exotoxins (SPEs) types A, B, and C (also referred to as erythrogenic toxins), which are produced by group A streptococci and lead to immune activation. The majority of cases occur between 1 and 10 years of age; by the age of 10 years, 80% of the population has developed anti-SPE antibodies that prevent development of the eruption. Scarlet fever usually follows tonsillitis or pharyngitis and is most common during the late fall, winter, and spring in temperate climates. However, it occasionally develops as a complication of wound ("surgical scarlet fever"), post-burn, pelvic, or puerperal infections28. Clinical features Scarlet fever is typically preceded by the sudden onset of a sore throat, headache, malaise, chills, anorexia, nausea, and high fevers. Patients, especially young children, may experience vomiting, abdominal pain, and seizures. The eruption begins 12-48 hours later as blanchable erythema on the neck, chest, and axillae. There is subsequent generalization (usually within 12 hours) and development of tiny superimposed papules with a sandpaper-like texture ("sunburn with goose pimples"). Pastia's lines (linear petechial streaks) are seen in the axillary, antecubital, and inguinal areas. The cheeks are flushed with circumoral pallor. The throat is red and edematous, developing an exudate after 3-4 days; palatal petechiae and tender cervical adenopathy are often evident. The tongue is initially white with bright red papillae, but later becomes beefy red ("strawberry tongue"). Desquamation occurs after 7-10 days, most prominently on the hands and feet (Fig. 74.8), and can last for 2-6 weeks. Possible complications of scarlet fever and the underlying streptococcal infection include otitis, mastoiditis, sinusitis, pneumonia, myocarditis, meningitis, arthritis, hepatitis, acute glomerulonephritis, and rheumatic fever23.

Staph Scalded - Pathophysiology - Most commonly seen in whom, what about adults? - How is the pathophys different from bullous impetigo?

Introduction Staphylococcal scalded skin syndrome (SSSS) is caused by hematogenous dissemination of the same exfoliative toxins that lead to bullous impetigo when produced locally. Cleavage of the epidermis through the granular layer results in the formation of tender, flaccid bullae21. Epidemiology SSSS is primarily a disease of infants and young children, who have decreased renal toxin clearance (especially neonates) and/or a lack of toxin-neutralizing antibodies. Occasionally, adults with chronic renal insufficiency or immune suppression are affected. Outbreaks occurring in neonatal nurseries are usually secondary to asymptomatic carriage of a toxigenic strain of S. aureus by healthcare workers or parents. A male predominance exists, with a 2 : 1 male : female ratio in sporadic cases and 4 : 1 in epidemics. Pathogenesis Most cases of SSSS are caused by phage group II strains (e.g. types 55, 71) of S. aureus, which can be methicillin-sensitive or resistant and produce exfoliative (also known as epidermolytic) toxins (ETs). ETA (chromosomally encoded) and ETB (plasmid encoded) are serine proteases that bind and cleave desmoglein 1 (Dsg1). This causes splitting of the desmosomes, which leads to disruption of the epidermal granular layer and bulla formation. Desmoglein 1 is targeted by autoantibodies in pemphigus foliaceus, which has identical histologic features to SSSS. In contrast to bullous impetigo, where the effects of the ETs are limited to the site(s) of infection, in SSSS the toxin diffuses from a focus of infection and (in the absence of specific antitoxin antibody) spreads hematogenously to produce widespread effects. In children, the infectious focus is usually in the nasopharynx or conjunctivae, whereas staphylococcal pneumonia or bacteremia may be present in adults23

Empiric treatment of cutaneous strep and staph

Strep - Dicloxacillin 500 mg PO four times a day • First generation cephalosporin (see below) • Nafcillin or oxacillin 1-2 g IV four times a day, if severe • First-generation cephalosporin, e.g. cephalexin 250-500 mg PO three or four times a day • Dicloxacillin 250-500 mg PO four times a day MRSA • Doxycycline 100 mg PO two times a day* • Trimethoprim-sulfamethoxazole 1 or 2 double-strength tablets PO twice a day* • Clindamycin 300-450 mg PO four times a day Other oral options • Minocycline* • Linezolid† or tedezolid† • Delafloxacin† Intravenous options for severe disease • Vancomycin (first line) • Daptomycin • Telavancin, oritavancin, or albavancin • Teicoplanin‡ • Ceftaroline or ceftobiprole‡ Penicillin allergy • Clindamycin (see above) • Clarithromycin 250 mg PO two times a day

More Neck Fasc - What is nec Fasc of the groin called

Clinical features Infection begins with an area of exquisite tenderness, erythema, warmth, and swelling that does not respond to antibiotics. The skin appears shiny and tense. Initially, severe pain may be out of proportion to skin findings. The disease progresses at an alarming rate, with the skin changing from red and purple to a characteristic gray-blue color in ill-defined patches within 36 hours of onset (Fig. 74.16). Violaceous discoloration and/or hemorrhagic bullae may develop. Necrosis of the superficial fascia and fat produces a thin, watery, malodorous fluid. The area may later become anesthetic as cutaneous nerves are destroyed. The subcutaneous tissues may feel hard and "woody" on palpation. Patients can become extremely toxic, with fever, chills, malaise, leukocytosis, tachycardia, and shock. The most common site of involvement is the extremities, although the trunk is often affected in children. When necrotizing fasciitis involves the perineum and genitalia, it is referred to as Fournier gangrene, which is typically a polymicrobial infection11,54,56. Pathology Gangrene of the subcutaneous tissues, with spread along fascial planes, is followed by involvement of the overlying skin. Fibrinoid necrosis is present in the media of vessels passing through the destroyed fascia, and fibrin thrombi are evident. The epidermis, dermis, and skin appendages in the area of gangrene undergo coagulation necrosis. Infiltration with neutrophils and mononuclear cells as well as numerous bacteria occurs in upper layers of the dermis.

strep toxic shock

Clinical features Streptococcal TSS is defined as a group A streptococcal infection with an early onset of shock and organ failure (see Table 74.8). The most common initial symptom is severe local pain in an extremity. Although 50% of patients display signs of a soft tissue infection (e.g. swelling, tenderness, erythema), some present with only pain and no obvious physical findings. The development of a violaceous hue, bullae, or necrosis points to a deeper infection, such as necrotizing fasciitis or myositis, and portends a worse outcome. The disease may begin insidiously with nonspecific flu-like symptoms, such as fever, chills, myalgias, and diarrhea. CNS symptoms (e.g. confusion, altered consciousness) are commonly seen. A generalized blanching macular erythema is observed much less often than in staphylococcal TSS, but blistering is more likely to occur. Desquamation on the hands and feet eventually appears in 20% of patients. Shock and multi-organ failure usually develop 48-72 hours after the onset of symptoms. Complications of streptococcal TSS can include renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome. The mortality rate for streptococcal TSS ranges from 30% to 60%. Pathology Biopsy specimens from skin lesions may show spongiosis, necrotic keratinocytes, subepidermal blister formation, and a neutrophilic and/ or lymphocytic perivascular infiltrate in the dermis

More Bartonellosis - clinical features - Key pathologic finding - treatment

Clinical features The onset of Oroya fever is often sudden, with dyspnea, weakness, pallor, tachycardia, fever, thirst, anorexia, arthralgias, and headache. A precipitous drop in the erythrocyte count may occur secondary to massive hemolysis, and hyperbilirubinemia and hemoglobinuria can result. After the initial septicemia, a variable degree of immunodeficiency ensues. During this phase, a third of patients develop secondary bacterial infections; when death occurs, it is often secondary to an enteropathic bacterial infection, especially Salmonella enterica. Lymphadenopathy, splenomegaly, and megaloblastic hyperplasia of the bone marrow are seen in severe cases. Patients with Oroya fever usually require 8-10 weeks for full recovery. Most patients who recover from Oroya fever develop cutaneous nodules during or after their convalescent period, but verruga peruana can also appear in previously asymptomatic individuals. Bright red papules and nodules measuring 2 mm to several centimeters in diameter appear within small erythematous patches. Lesions may be sessile or pedunculated and are usually located on the head and extremities.Hemorrhage, ulceration, and secondary bacterial infection can occur. In the absence of complications, lesions usually heal without scarring but may recur. Pathology The histologic features of verruga peruana vary and can resemble those of a pyogenic granuloma or Kaposi sarcoma. Masses of intracytoplasmic Bartonella organisms (Rocha-Lima inclusions) are present within swollen endothelial cells as well as in red blood cells; the bacilli are also found extracellularly. Thrombosis and occlusion of vessels occurs. Diagnosis and differential diagnosis The presence of organisms within red blood cells or within the cytoplasm of endothelial cells is diagnostic. B. bacilliformis can be isolated from blood cultures; immunologic testing (e.g. ELISA, immunoblot) and PCR-based assays for blood or tissue samples are also available101. The differential diagnosis of verruga peruana includes multiple pyogenic granulomas, bacillary angiomatosis, warts, molluscum contagiosum, and yaws. Treatment Table 74.14 outlines the treatment recommendations for bartonellosis. • Chloramphenicol* plus β-lactam antibiotic • Quinolone (norfloxacin, ciprofloxacin) [>6 years of age, non-pregnant] Amoxicillin-clavulanate or ceftriaxone (first-line in children and pregnant women) • Trimethoprim- sulfamethoxazole • Macrolide • Doxycycline

More Staph Scalded Skin - Clinical Features - Mortality rate for kids and adults - What is seen on histology - Ddx

Clinical features There is often a prodrome of malaise, fever, irritability, and tenderness of the skin. The patient may have purulent rhinorrhea or conjunctivitis as a manifestation of the underlying staphylococcal infection. Erythema typically first appears on the head (accompanied by variable facial edema) and in intertriginous sites, often with generalization within 48 hours. The skin subsequently develops a wrinkled appearance owing to the formation of flaccid, sterile bullae within the superficial epidermis (Fig. 74.6). The Nikolsky sign is positive. Classically, the flexural areas are the first to exfoliate, leaving behind moist skin and thin, varnishlike crusting. Patients also demonstrate characteristic periorificial (e.g. perioral, periocular) crusting and radial fissuring (see Figs 34.17 & 81.16). Intraoral lesions do not occur. Scaling and desquamation continue for the next 3-5 days, followed by re-epithelialization without scarring. With proper treatment, SSSS resolves in 1-2 weeks, usually without sequelae. The mortality rate is ≤4% for children but may approach 60% in adults21. Pathology Histologic examination shows a sharply demarcated zone of cleavage at or below the stratum granulosum. There are usually no inflammatory cells in the bullae. The upper dermis also lacks an inflammatory infiltrate, and no organisms are seen on Gram stain of biopsy specimens. Diagnosis and differential diagnosis SSSS is generally a clinical diagnosis. Although cultures taken from intact bullae are negative, S. aureus may be cultured from the conjunctiva, nasopharynx, perianal area, or pyogenic foci on the skin. Blood cultures are almost always negative in children but may be positive in adults. The leukocyte count can be elevated or normal. Examination of frozen sections is occasionally helpful in confirming the level of the split in the bullae. Slide latex agglutination, double immunodiffusion, or enzyme-linked immunosorbent assay (ELISA) tests can identify the toxins responsible for SSSS. The differential diagnosis may include a drug reaction, a viral exanthem, sunburn, Kawasaki disease, extensive bullous impetigo, toxic shock syndrome, graft-versus-host disease (GVHD), and pemphigus foliaceus. Differentiation from toxic epidermal necrolysis (TEN) is outlined in Table 74.7 and Fig. 81.16.

Clostridial skin infections - clostridia are what type of bacteria? where can they be found? - What are the toxics produced by perfringens? - What should prompt clinical suspicion for clostridia infection? - Treatment

Clostridia are spore-forming Gram-positive rods that are ubiquitous soil saprophytes and part of the normal intestinal flora. Clostridium perfringens, the most frequent cause of trauma-associated gas gangrene, is an obligate anaerobe and thus proliferates in hypoxic or ischemic tissue. Clostridium septicum is much more aerotolerant, requires a smaller infective dose, and is associated with spontaneous gas gangrene in patients with neutropenia or gastrointestinal malignancy11. C. perfringens produces two membrane-active toxins, alpha and theta (perfringolysin O), which have synergistic effects. Alpha toxin possesses biologic activity akin to phospholipase C and sphingomyelinase, while theta toxin disrupts endothelial cell integrity, impairs recruitment of phagocytes, and induces intravascular platelet aggregation, leading to reduced arteriolar blood flow. Impaired oxygen delivery then results in tissue hypoxia and anaerobic glycolysis of muscle tissues. Production of hydrogen sulfide and CO2 accounts for the characteristic "gas" gangrene visualized on radiographic imaging. Local progression results in myonecrosis, whereas shock and multi-organ failure can occur when the toxins enter the systemic circulation. The majority of cases of anaerobic cellulitis (a necrotizing subcutaneous infection) and myonecrosis (gas gangrene) are caused by clostridia. These diseases are compared and their treatment outlined in Table 74.11. Soft tissue crepitus, evidence of gas on plain films, or a foul-smelling brownish discharge ("dirty dishwater") should prompt the clinician to suspect a clostridial infection, especially following trauma or surgery in patients with diabetes mellitus and peripheral vascular disease58 Treatment is Clinda + Zosyn

Cornybacterium skin infections - are what type of bacteria? Erythrasma - causative organisms - clinical presentation - clinical exam finding? Why - Ddx? Treatment?

Corynebacteria are Gram-positive rods that account for nearly half of the cutaneous flora. A warm, moist local environment represents a risk factor for infection of the skin with non-diphtherial corynebacteria Erythrasma Erythrasma is a superficial and often chronic skin infection caused by excessive proliferation of Corynebacterium minutissimum within the stratum corneum. The organism's growth is favored by moist, occluded intertriginous areas, including the groin, axillae, intergluteal fold, inframammary region, umbilicus, and web spaces between the toes. Other predisposing factors include a warm humid climate, poor hygiene, hyperhidrosis, obesity, diabetes mellitus, advanced age and immunosuppression. Whether the associated scale precedes and promotes development of erythrasma or results from bacterial overgrowth is a matter of debate. Lesions are pink to red, well-defined patches that are covered with fine scales and have associated wrinkling. With time, the red color fades to brown (Fig. 74.19A,C). The condition is asymptomatic or mildly pruritic. Interdigital erythrasma is the most common bacterial infection of the foot and the most frequent form of erythrasma. It presents as asymptomatic, chronic maceration with fissuring or scaling of interspaces. A "disciform" variant can occur in a more widespread distribution outside the usual intertriginous locations (Fig. 74.19D); this is occasionally the presenting manifestation of type 2 diabetes mellitus. Progression of erythrasma to cellulitis or bacteremia in immunocompromised patients has occasionally been reported. When lesions are illuminated with a Wood's lamp, bright coral-red fluorescence appears as a result of porphyrin produced by the bacteria (Fig. 74.19B). Gram staining of the scale demonstrates Gram-positive filaments and rods, and corynebacteria can be cultured on Tissue Culture Medium 199. The differential diagnosis of intertriginous erythrasma includes tinea, seborrheic dermatitis and cutaneous candidiasis, while interdigital erythrasma needs to be distinguished from tinea pedis and complex toe web infections60. Topical therapies include 20% aluminum chloride, clindamycin, erythromycin, mupirocin, fusidic acid, azole antifungals, and Whitfield ointment (salicylic and benzoic acids). Oral erythromycin, tetracyclines, or single-dose clarithromycin can be used for widespread or recalcitrant cases. Use of antibacterial soaps may help to prevent recurrences

Cutaneous Diptheria - caused by what organisms - does vaccination agains diptheria prevent cutaneous disease - clinical presentation - Diagnosis and treatment

Cutaneous Diphtheria Cutaneous diphtheria can be caused by both toxigenic (i.e. capable of producing systemic disease) and non-toxigenic strains of Corynebacterium diphtheriae and Corynebacterium ulcerans. It is endemic in some tropical countries and in several urban poor populations, e.g. in Vancouver, Latvia, Russia, and Ukraine63a,64, where it is spread by personto-person contact in a highly contagious manner. C. ulcerans can also be transmitted by domestic animals, including cats and dogs. Development of cutaneous diphtheria in non-endemic regions is typically related to travel, and recent European outbreaks have occurred in refugees from East Africa and Syria64a. For children living in endemic regions, cutaneous diphtheria represents a form of immunization, as toxin is absorbed slowly from skin lesions and induces high levels of antibodies. In addition to children,elderly and immunocompromised individuals are most commonly affected, with predisposing factors including poor hygiene, injection drug use, and skin trauma. Vaccination against diphtheria does not necessarily prevent cutaneous disease. Cutaneous diphtheria most commonly presents as an ulcer (ecthyma diphthericum) with a punched-out appearance and variable gray "pseudomembranous" eschar (Fig. 74.22). Acral sites are favored, and a pustule or crusted dermatitis may also be observed. Lesions are commonly co-infected with S. aureus or Str. pyogenes. Local lymphadenopathy and toxin-mediated complications, such as myocarditis and polyneuritis, are rare. Gram stain of ulcer exudate and culture on specialized media can establish the diagnosis. Toxigenicity can be assessed utilizing a modified Elek immunoprecipitation test, a rapid enzyme immunoassay, or PCR-based methods. Treatment includes a 10-day course of oral antibiotics, with erythromycin and penicillin representing first-line agents; additional measures include thorough cleansing of the wound site, application of a topical antibiotic, and (for toxigenic strains) intravenous diphtheria antitoxin. Contacts should be screened and asymptomatic carriers treated

Cutaneous malacoplakia - what is it - most commonly seen in whom and caused by what organism - what area is most commonly affected, clinical presentation - key histopath finding and stains for it - treatment

Cutaneous malacoplakia is a rare chronic infectious condition that is characterized by granulomatous inflammation with distinctive macrophages that are unable to phagocytose and kill bacteria effectively. It occurs primarily in immunocompromised hosts, including solid organ (especially kidney) transplant recipients, HIV-infected individuals, and children with primary immunodeficiencies111. Malacoplakia is most commonly due to E. coli, although Pseudomonas, Proteus, Klebsiella, Staphylococcus, Shigella, Enterococcus, Rhodococcus, and Mycobacterium spp. have also been implicated. Malacoplakia most often affects the genitourinary tract. Cutaneous lesions usually involve the perianal region and can present as ulcerations, abscesses with multiple draining sinuses, yellow-to-pink soft papules, and erythematous indurated nodules. Histologic examination of involved tissue shows highly characteristic findings. Michaelis-Gutmann bodies are intracytoplasmic laminated concretions that represent accumulations of calcified, iron-containing phagolysosomes; they stain with PAS, von Kossa, Perls', and Giemsa stains. Von Hansemann cells are large macrophages that contain Michaelis-Gutmann bodies and stain positively for CD68, lysozyme, and alpha-1 antitrypsin. The histopathologic differential diagnosis may include sarcoidosis, infectious granulomas, Langerhans cell histiocytosis, granular cell tumor, and fibrous histiocytoma. The treatment of malacoplakia is difficult. Localized disease may be amenable to surgical excision. Prolonged courses of antibiotics, including quinolones, TMP-SMX and clofazimine, have been used successfully. Ascorbic acid and bethanechol chloride have been employed to increase intracellular cGMP and improve macrophage function. In severe cases, reducing the dosage of immunosuppressive therapy (if possible) may be of benefit1

More Nec Fasc - Diagnosis - Empiric antibacterial treatment

Diagnosis and differential diagnosis Early in the disease course, it is often difficult to differentiate necrotizing fasciitis from cellulitis. The presence of severe pain or anesthesia suggests a deeper component, and an MRI can delineate the depth of tissue involvement. Other clues that suggest necrotizing fasciitis rather than cellulitis include rapidly spreading tense edema, hemorrhagic bulla formation, grayish discoloration, foul-smelling discharge and an elevated creatine phosphokinase level. Fig. 74.17 outlines an algorithm for assessing and treating suspected necrotizing fasciitis. Conditions that can mimic necrotizing fasciitis include trauma with hematoma formation, clostridial myonecrosis, pyomyositis, phlebitis, bursitis, and arthritis. Treatment Extensive surgical debridement (fasciotomy) is the mainstay of effective treatment. On occasion, amputation is necessary. Empiric therapy should be initiated with broad-spectrum coverage against streptococci, staphylococci (including MRSA), Gram-negative bacilli and anaerobes - e.g. vancomycin, linezolid, or daptomycin combined with piperacillin/ tazobactam or a carbapenem11. In a patient with true penicillin allergy, empiric therapy with ciprofloxacin plus metronidazole or clindamycin can be used. Coverage of Pseudomonas spp. is particularly important for neutropenic patients. Once the microbial etiology has been determined, antibiotic coverage can be narrowed appropriately. Hyperbaric oxygen therapy remains controversial, though it may be beneficial for a subset of patients with anaerobic Gram-negative necrotizing fasciitis; however, surgery and antimicrobial therapy should never be postponed. Although IVIg may be useful for patients with severe group A streptococcal infections, a recent randomized placebo-controlled trial failed to show benefit of IVIg administration in intensive care unit patients with necrotizing soft tissue infections56a. Nutritional support is crucial for enhancing postoperative wound healing, and, eventually, reconstructive surgery is often necessary11

ESKAPE Pathogens - importance - organisms

Enterococcus faecium Staphylococcus aureus Klebsiella pneumoniae Acinetobacter baumannii Pseudomonas aeruginosa Enterobacter speciesswab Pathogens with increased antibiotic resistance due to over exposure of antibiotics

Green Nail Syndrome - caused by infection with what? underling pathophys - diagnosis is usually made how? - ddx - Treatment options

Green Nail Syndrome In green nail syndrome (chloronychia), the nail develops green-black to green-blue discoloration due to pyocyanin, a blue-green pigment produced by P. aeruginosa (Fig. 74.25). Predisposing factors include frequent or prolonged exposure to water, excessive use of detergents and soaps, nail trauma and other causes of onycholysis (see Ch. 71). The diagnosis of green nail syndrome is usually clinical; if necessary, it can be confirmed by Gram stain and culture of exudate and nail fragments. The differential diagnosis includes a subungual hematoma, melanocytic nevus, melanoma, and Aspergillus infection. Treatment involves avoidance of predisposing factors, clipping the nail, and topical application of 2% sodium hypochlorite (household bleach diluted 1:4; see Ch. 71), a quinolone, or aminoglycoside (e.g. tobramycin) solution for 1-4 months87. In refractory cases, removal of the affected nail may be required88.

Botryomycosis - what is it, how does it get its name, most often caused by what? - associated risk factor - clinical features

Introduction Botryomycosis was named for its characteristic groups of granules that resemble grapes. It is a rare, chronic, purulent and granulomatous bacterial infection that primarily affects the skin and is most often caused by S. aureus. Epidemiology and pathogenesis Botryomycosis is found worldwide, and over two-thirds of patients have only skin involvement. The disease affects all ages and has a slight male predominance (male : female ratio, 3 : 2). Although most often due to infection with S. aureus, it can also be caused by Pseudomonas, Proteus, Moraxella, Serratia, and Corynebacteria spp. Defects of cellular immunity, particularly low T-lymphocyte counts, have been associated with the development of botryomycosis49. Clinical features Botryomycosis presents as cutaneous and subcutaneous nodules, ulcers, or verrucous plaques. Multiple sinuses and fistulas may discharge purulent fluid or yellow granules composed of bacterial masses. Most patients have localized involvement of an extremity following trauma; disseminated cutaneous disease is rare50. The lesions may be pruritic or tender, and they may affect the underlying muscle or bone. Systemic symptoms are infrequent. Visceral botryomycosis, most often affecting the lungs, has been reported primarily in immunocompromised patients or following surgery49

Cat Scratch Fever - Caused by what bacteria - Characterized by what? - what causes the transmission among cats? - clinical features

Introduction Cat scratch disease (CSD) is caused by infection with Bartonella henselae. In immunocompetent hosts, it is a benign, self-limited illness characterized by tender regional lymphadenitis that lasts for weeks to months. Over 90% of patients report a recent scratch and/or bite from a cat. Epidemiology and pathogenesis Approximately 12 500 cases of CSD are diagnosed annually in the US101a. CSD occurs worldwide and has a predilection for younger persons (median age 15 years). Both sexes are equally affected. In the US, CSD is most common during the fall and winter. Transmission of infection among cats occurs via a flea vector, Ctenocephalides felis. Although flea-vectored transmission to humans has not been documented, it could explain some cases in which there is no history of exposure to cats. Clinical features CSD is a common cause of persistent lymphadenopathy (longer than 3-4 weeks) in children and adolescents. Lymphadenopathy usually presents 2-4 weeks after a scratch and can last 2-6 months, or even longer if fibrosis occurs. A single, large (1-10 cm), tender, mobile lymph node, with erythema and swelling of the overlying skin, is most often noted in the axilla. Suppuration occurs in only 10-25% of patients. A skin lesion (e.g. a red papule or crusted pustule) develops at the inoculation site in two-thirds of patients. Although most patients are otherwise well, the lymphadenopathy can be accompanied by fevers, malaise, fatigue, weakness, and headaches. Additional manifestations such as encephalopathy, hepatic granulomas, osteomyelitis, and pulmonary involvement develop in up to 15% of patients. The oculoglandular syndrome of Parinaud - unilateral conjunctivitis and ipsilateral preauricular lymphadenopathy - occurs in ~5% of individuals with CSD. Immunosuppressed patients (e.g. those with HIV infection) are prone to a more severe and complicated disease course

Cutaneous Anthrax - what type of bacteria - how does it cause infection in humans? - How do most human infections occur? What % of anthrax cases are cutaneous? - Bacillus anthracus produces what to toxins?

Introduction and epidemiology The name Bacillus anthracis is derived from the Greek word for coal, anthrakis, reflecting the black, coal-like eschars. B. anthracis is an aerobic, sporulating, Gram-positive rod measuring 1-1.5 × 3-5 microns. The bacterium causes disease in humans via three routes: inhalation, ingestion, and cutaneous inoculation. While the latter produces the least severe form of anthrax, it accounts for ~95% of infections. Anthrax is primarily a disease of animals (e.g. sheep, cows, horses, goats) that is endemic in parts of western Asia and Africa. Most human cases are due to occupational exposure to infected animals or their carcasses, including hides and wool ("woolsorter's disease")67. Two thousand cases are reported annually worldwide, with <10 per year in the US. History The fifth and sixth plagues of Egypt that are described in the book of Exodus are thought to have been anthrax. B. anthracis was the first bacterium proven to be the etiologic agent of a specific disease, independently demonstrated by Dr Robert Koch and Dr Louis Pasteur. Anthrax was first used as a biologic weapon during World War I. Accidental release of anthrax from a biologic weapons complex in the Soviet Union in 1979 resulted in 68 fatalities. In 2001, anthrax spores were sent through the US mail as a terrorist weapon, resulting in 22 cases of inhalational or cutaneous anthrax and 5 fatalities Anthrax spores are environmentally hardy and can survive for decades in the soil. Full virulence requires the presence of an antiphagocytic capsule and three toxin components (protective antigen, lethal factor, and edema factor) that combine to form both lethal toxin and edema toxin. Edema toxin impairs neutrophil function and affects water homeostasis, leading to edema; lethal toxin causes release of TNF-α and IL-1β

More actinomycosis - what to look for on histology - treatment of choice

Pathology An intense neutrophilic infiltrate is followed by the development of granulomatous inflammation with giant cells. Histiocytes, plasma cells, and epithelioid cells can be seen at the periphery of the abscess, while characteristic granules representing microcolonies of Actinomyces are seen centrally. Histologically these "sulfur granules" have a basophilic center and acidophilic periphery; they measure up to 28 microns in diameter. Diagnosis and differential diagnosis Careful microscopic examination of purulent material should be performed to detect the sulfur granules that are characteristic of actinomycosis (or actinomycotic mycetoma). They are composed of Gram-positive, branching filaments that fragment into diphtheroid forms and coccobacilli; acid-fast staining is negative. Cervicofacial actinomycosis may resemble symbiotic anaerobic (e.g. Eikenella corrodens) and aerobic bacterial infections, tuberculosis (scrofuloderma), dimorphic fungal infections, dental sinus tracts, and even neoplasms. Treatment The drug of choice for actinomycosis is penicillin G or ampicillin. Deep-seated, chronic infections should be treated with 2-6 weeks of intravenous therapy followed by 3-12 months of oral penicillin. For acute infections, 2-3 weeks of oral penicillin plus incision and drainage and surgical excision of sinus tracts is sufficient. Doxycycline, erythromycin, and clindamycin are acceptable alternatives for penicillin-allergic patients. Imipenem has been shown to be effective in treatment-resistant cases. In order to avoid relapse, therapy should be extended beyond the resolution of symptoms

Plague - caused by what organism - transmitted by what? - where does this occur in the use - what are the three forms of disease - treatment

Plague is an acute bacterial infection caused by Yersinia pestis, a Gram-negative, rounded, bipolar bacillus transmitted by fleas and rodents (Fig. 74.32). The highest incidence of Y. pestis infection is in Southeast Asia. In the US, most human infections occur in two regions: (1) northern New Mexico, northern Arizona and southern Colorado; and (2) California, southern Oregon, and far western Nevada. Plague also occurs in Africa, South America, and other regions of Asia. Three clinical forms of plague are recognized - bubonic, septicemic, and pneumonic. The symptoms of bubonic plague are variable. Constitutional symptoms may be lacking or severe. In approximately 10% of patients, the inoculation wound develops into a pustule or ulcer. This is followed by painful regional lymphadenopathy (bubo); suppuration and discharge from the lymph nodes may occur. In septicemic plague, vesicles, carbuncles, petechiae, and purpura may be seen. Necrotic lesions and hemorrhage from the nasopharynx or gastrointestinal tract have also been described. In pneumonic plague, the patient develops acute pneumonitis. Apathy, delirium, coma, and seizures occur in seriously ill patients. Bubonic plague may simulate tularemia, rat-bite fever, sporotrichosis, tuberculosis, streptococcal ecthyma, syphilis, or lymphogranuloma venereum. Septicemic plague must be differentiated from typhus, typhoid fever, tularemia, malaria, and other bacteremias. Untreated bubonic plague has a 40-60% fatality rate, while untreated septicemic or pneumonic plague is nearly always fatal. Streptomycin and other aminoglycosides (e.g. gentamicin) are first-line treatments for plague. Doxycycline and quinolones may be used when oral therapy is acceptable. Chloramphenicol (which attains high concentrations in the cerebrospinal fluid) is the drug of choice for plague meningitis or endophthalmitis. Postexposure prophylaxis with doxycycline or ciprofloxacin, if taken within 6 days, is extremely effective in preventing disease. Live whole cell-based vaccines are utilized for prevention of plague in some parts of the world (e.g. the former Soviet Union), but they have poor safety profiles. There are ongoing efforts to develop a safe and effective Y. pestis vaccin

Rat bite fever - caused by infection with what? - clinical presentation, what is one hallmark of disease? - treatment

Rat-bite fever in North America is most often due to infection with Streptobacillus moniliformis, while infection with Spirillum minus is more common in Asia, where it is known as sodoku. Infection results in an acute illness characterized by fever, arthritis, and a rash. While the disorder is usually caused by a bite (rat-bite fever), it can also occur from close contact with rodents or ingestion of contaminated food, water, or raw milk (Haverhill fever). Although the incidence of rat-bite fever is highest in urban areas with poor sanitation where there is a large population of rats, it can also occur from exposure to pet rats or laboratory rats. Approximately half of cases are in children123. Erythema, edema, abscess formation, ulceration, and secondary infection may develop at the site of the bite. Regional lymphadenopathy is common. Paroxysms of fever interspersed with afebrile periods as well as headaches, nausea, vomiting, and myalgias may occur. In infants and children, weight loss and diarrhea can be significant. One of the hallmarks of the disease is a migratory polyarthritis that occurs in 50% of patients and may mimic rheumatoid arthritis. At 2 to 4 days following the onset of fever and arthritis, most patients with rat-bite fever develop an acrally distributed eruption involving the palms and soles. Morbilliform macules and papules, petechiae, vesicles, pustules, and crusts may be seen. Rat-bite fever can be diagnosed by culturing Streptobacillus moniliformis from blood, synovial fluid or abscess aspirates, which requires special media and conditions; Spirillum minus does not grow in culture. PCR-based assays may also be utilized. The triad of fever, arthritis/arthralgias, and a rash can be caused by a variety of infectious diseases, including viral infections (e.g. enteroviruses, EBV, parvovirus B19), Rocky Mountain spotted fever, acute or chronic meningococcemia, acute rheumatic fever, and secondary syphilis. Non-infectious causes include Still disease, systemic lupus erythematosus, serum sickness-like drug reactions, and Sweet, Schnitzler, and periodic fever syndromes. Penicillin is the drug of choice for rat-bite fever and is usually administered for a week, although patients with septicemia may require up to 6 weeks of parenteral therapy. Ceftriaxone, tetracyclines, and streptomycin represent additional options; erythromycin and clindamycin have also been used, but studies of their efficacy are lacking. Although most infections resolve spontaneously within 2 weeks, 10-15% of untreated cases are fatal

Treatment of SSSS - What antibiotics - which antibiotic should not be used alone?

Treatment Patients with severe, generalized forms of SSSS require hospitalization and parenteral antibiotics. Oral treatment with a β-lactamase-resistant antibiotic (e.g. dicloxacillin, cephalexin) for a minimum of 1 week is usually sufficient for milder disease, although SSSS is occasionally caused by MRSA. Clindamycin administration may help to reduce bacterial toxin production, but up to 50% of strains implicated in SSSS are clindamycin resistant, so monotherapy with this agent is not recommended21a. Identification and decolonization of S. aureus carriers (see Folliculitis section above) are important, especially in hospital-acquired cases

Abcesses, Furuncles, Carbuncles - Most common organism - risk factors - Treatment, when are antibiotics warrented

Abscesses and furuncles (boils) are collections of pus that are "walled-off" from the surrounding tissues. Whereas an abscess can occur anywhere in or on the body, a furuncle, by definition, involves a hair follicle. A contiguous collection of furuncles is termed a carbuncle. Epidemiology and pathogenesis Furuncles most often occur in adolescents and young adults. S. aureus is usually the causative organism, although anaerobic bacteria are occasionally cultured from recurrent furuncles in the anogenital region. Predisposing factors include chronic S. aureus carriage, close personal contact with affected individuals (e.g. households, athletic activities), diabetes mellitus, obesity, poor hygiene, immunodeficiency syndromes (e.g. chronic granulomatous disease, hyperimmunoglobulin E syndrome), and hereditary sensory and autonomic neuropathy due to defects in nerve growth factor β or its high-affinity receptor For simple furuncles, warm compresses may promote maturation, drainage, and resolution. Larger or deeper fluctuant lesions typically require incision and drainage. Systemic antibiotic therapy is recommended (in conjunction with incision and drainage if possible) in the following situations: (1) furuncles around the nose, in the external auditory canal, or in other locations where drainage is difficult (e.g. elsewhere on the face, hands, genitalia); (2) severe or extensive disease (e.g. multiple sites); (3) lesions with surrounding cellulitis/phlebitis or associated with signs/symptoms of systemic illness; (4) lesions not responding to local care; and (5) patients with concerning comorbidities or immunosuppression10,11. Given the high proportion of furuncles that are caused by MRSA, empiric coverage with antibiotics such as doxycycline, trimethoprim-sulfamethoxazole (TMP-SMX), or (depending on local resistance patterns) clindamycin should be considered (see Table 74.3 and below). Recent large controlled studies found that administration of a systemic antibiotic (TMP-SMX or clindamycin) following incision and drainage of a solitary, uncomplicated cutaneous abscess increases the cure rate (~80-85%, vs ~70% with placebo) and decreases the likelihood of recurrence11a,11b. However, this benefit must be weighed against the potential for antibiotic side effects. Patients with recurrent furunculosis may benefit from eradication of S. aureus from the nares, axillae, and perineum (see Bacterial folliculitis above).

Acrodermatitis chronica atrophicans - a cutaneous manifestation of what? - more common where? onset timing? - clinical appearance

Acrodermatitis chronica atrophicans (ACA) is a cutaneous manifestation of chronic Lyme disease. First described in Europe in 1883 by Buchwald as "idiopathic atrophy", it is most commonly due to an infection with B. afzelii, although it has also been associated with B. burgdorferi and B. garinii. As a result, it is extremely rare in the US but is seen in up to 10% of patients with Lyme disease in Europe. ACA occurs 6 months to 8 years after the initial infection, predominantly in women 40-70 years of age, and appears to be associated with long-term persistence of Borrelia organisms in the skin. It is a biphasic disorder consisting of an early, easily treatable, inflammatory stage and a late, treatment-resistant, atrophic stage. Initially, erythematous to violaceous plaques and nodules develop on the acral portion of the extremities, often insidiously. The skin is frequently doughy and swollen. This early stage follows a waxing and waning course for weeks to years. In the late stage, the skin has a glistening ("cigarette-paper") appearance with prominent blood vessels (Fig. 74.34). Fibrous nodules may form on extensor surfaces (ulnar or tibial bands). Hypopigmentation, hyperpigmentation, pain, pruritus, hyperesthesia, paresthesias, and scaling may also be present. Rarely, the condition may be complicated by the development of basal cell or squamous cell carcinoma131. In biopsy specimens of early lesions, a dermal perivascular lymphocytic infiltrate with plasma cells, telangiectatic endothelial-lined spaces, and mild epidermal atrophy are seen. Histologic examination of late lesions shows an atrophic epidermis and an interstitial lymphocytic infiltrate with plasma cells and occasional histiocytes and mast cells. The dermis may be attenuated, with periadnexal fibrosis. The differential diagnosis may include eczematous dermatitis (e.g. due to stasis), cold injury, atrophy secondary to chronic use of potent topical corticosteroids, severe photodamage, and, in the case of fibrotic lesions, scars, morphea, and fibromatoses

Bartonella - what kind of bacteria - name three species and the diseases they cause

Bartonella are small, pleomorphic, facultative intracellular Gram-negative bacilli closely related to Brucella species. Although there are >30 known species of Bartonella, B. henselae (cat scratch disease), B. quintana (trench fever), and B. bacilliformis (Carrion disease) represent the three major human pathogens. Both B. henselae and B. quintana also cause bacillary angiomatosis and endocarditis. Depending on factors such as the immune status of the infected individual, a particular Bartonella species can cause either acute or chronic infection and manifestations ranging from vascular proliferation to suppuration

Brucellosis - what is it? Cause, what type of bacteria - Most common what world wide, what are the endemic regions - How does infection occur, usually seen in who in the US - symptoms, cutaneous findings - Treatment

Brucellosis is a chronic granulomatous disease caused by Brucella, a genus of Gram-negative coccobacilli. It is the most common zoonosis worldwide, with >500 000 cases annually. Endemic regions include the Middle East, Mediterranean basin, Central Asia, and Indian subcontinent. Transmission occurs through the consumption of contaminated unpasteurized milk products (commonly raw goat's milk and cheese), direct contact with infected animal parts, or inhalation of aerosolized particles. Infection is rare in the US (~100 cases per year) and is primarily an occupational disease of farmers, laboratory personnel, butchers, and veterinarians. Children tend to have a more benign course, with fewer complications and better response to treatment105. Brucellosis demonstrates substantial clinical variability (Fig. 74.30). The acute form is characterized by nonspecific signs and symptoms such as fever, malaise, headache, diaphoresis, arthralgias, myalgias, back pain, lymphadenopathy, and hepatosplenomegaly. Patients with chronic brucellosis are afebrile but experience arthralgias, headaches, myalgias, diaphoresis, cyclic depression, sexual impotence, spondylitis, episcleritis, and uveitis. Malodorous perspiration is highly characteristic. Skin lesions occur in <10% of patients, most often presenting as a disseminated eruption of violaceous papulonodules. Other cutaneous manifestations of brucellosis include erythema nodosum-like lesions, extensive purpura, and morbilliform eruptions106. Endocarditis represents the major cause of death105. Acute brucellosis may mimic mononucleosis, influenza, malaria, typhoid fever, typhus, tularemia, tuberculosis, or sarcoidosis. The chronic form can be confused with rheumatologic, neurologic, or psychosomatic conditions. Multidrug regimens are recommended for brucellosis, with six weeks of doxycycline plus streptomycin, gentamicin, or rifampin representing a first-line treatment regimen; quinolones and TMP-SMX are other possible components of combination therapy. There is some concern regarding the use of rifampin in areas with a high prevalence of tuberculosis, as resistance may develop

Cellulitis - What are the four cardinal signs of inflammation

Clinical features Cellulitis is often preceded by systemic symptoms such as fever, chills, and malaise. The affected area displays all four of the cardinal signs of inflammation: rubor (erythema), calor (warmth), dolor (pain), and tumor (swelling). The borders are usually ill-defined and non-palpable. In severe infections, vesicles, bullae, pustules or necrotic tissue may be present (Fig. 74.11). Ascending lymphangitis and regional lymph node involvement may occur. In children, cellulitis most often affects the head and neck, whereas in adults it tends to involve the extremities. Cellulitis due to injection drug use typically affects the upper extremities, the usual sites of drug injection. Complications are uncommon but may include acute glomerulonephritis (if caused by a nephritogenic strain of streptococcus), lymphadenitis, subacute bacterial endocarditis, and recurrences related to disrupted lymphatic damage. Pathology A mild or moderate inflammatory infiltrate composed of lymphocytes and neutrophils can be seen throughout the dermis, often extending into the subcutaneous fat (Fig. 74.12). Additional findings include edema, which occasionally leads to subepidermal bullae, and dilation of lymphatics and small blood vessels. With special stains, the causative organism may be identified. Diagnosis and differential diagnosis The diagnosis of cellulitis is usually clinical (Fig. 74.13). The leukocyte count is often normal or only slightly elevated. Blood cultures are almost always negative in immunocompetent hosts. An exception is H. influenzae cellulitis, where there is usually an increased leukocyte count with a left shift and positive blood cultures. Atypical organisms are more common in children and immunocompromised patients, and needle aspiration or skin biopsy may help to identify the infectious etiology. The differential diagnosis of lower extremity cellulitis includes deep vein thrombosis and inflammatory diseases such as stasis dermatitis, superficial thrombophlebitis, lipodermatosclerosis, and other forms of panniculitis. While superficial thrombophlebitis often presents with redness and tenderness, the absence of a fever and the presence of a palpable cord aid in the diagnosis. Misdiagnosis of lipodermatosclerosis as cellulitis often leads to unnecessary hospitalizations. Additional causes of "pseudocellulitis" are listed in Table 74.10 and illustrated in

More Bacillary angiomatosis - Clinical appearance - what stain can identify bartonella on histo

Clinical features Cutaneous lesions of bacillary angiomatosis may present as superficial angiomatous papules and nodules, violaceous lichenoid plaques, or deep subcutaneous nodules. The papules and nodules resemble pyogenic granulomas (Fig. 74.29A) and may be smooth-surfaced, pedunculated, or surrounded by a collarette of scale. These lesions may display central umbilication, crusting, or ulceration. Subcutaneous nodules are often several centimeters in diameter and skin-colored; overlying erosions or ulcerations may develop. Less commonly, bacillary angiomatosis presents as a cellulitic erythematous plaque that can involve the underlying bone. The host immune status largely determines the number and distribution of the lesions. Immunocompetent patients may have a single lesion at the site of inoculation, whereas the entire cutaneous surface can be affected in those who are severely immunocompromised. Extracutaneous bacillary angiomatosis may occur with or without cutaneous disease and can affect any organ. Bacillary peliosis hepatis caused by B. henselae (but not B. quintana) presents with nausea, vomiting, diarrhea, abdominal pain, hepatosplenomegaly, and elevated Histologically, a dermal proliferation of vessels with plump endothelial cells is evident and scattered neutrophils are present in the accompanying infiltrate. Bacilli (in this case Bartonella henselae) are identified with the Warthin-Starry stain (inset).

More TSS - clinical Features - Two causative organisms? Which is worse? - Histology

Clinical features TSS is characterized by the sudden onset of high fever with myalgias, vomiting, diarrhea, headache, and pharyngitis. Rapid progression to hypotensive shock can occur, but the clinical spectrum ranges from relatively mild to fulminant fatal disease. The dermatologic manifestations are more extensive and predictable in staphylococcal TSS than in streptococcal TSS (Table 74.9). Patients usually develop diffuse erythema or a scarlatiniform exanthem that starts on the trunk and spreads to the extremities (Fig. 74.7). Additional findings include erythema and edema of the palms, soles, and oral mucosa as well as a strawberry tongue, hyperemia of the conjunctivae, and (with diseaseprogression) generalized non-pitting edema. Desquamation of the hands and feet occurs 1-3 weeks after the onset of symptoms. After recovery, Beau's lines and nail shedding can be seen. In severe cases, telogen effluvium may occur. With proper treatment, the majority of patients completely recover. However, complications include decreased renal function, prolonged weakness and fatigue, protracted myalgias, vocal cord paralysis, upper extremity paresthesias, carpaltunnel syndrome, arthralgias, amenorrhea, and gangrene25. Pathology Biopsy specimens of the eruption show an infiltrate of neutrophils and lymphocytes in the superficial dermis. Papillary dermal edema as well as epidermal spongiosis and exocytosis may be noted. Hair follicles and eccrine sweat glands display similar findings.

Even more cutaneous anthrax - diagnosis can be made how? - DDx - Treatment

Diagnosis and differential diagnosis Gram staining of exudate or touch preparations can aid in rapid diagnosis. The organism grows in culture within 6-24 hours; however, antibiotic administration for more than 24 hours prevents the recovery of pathogens in culture. Laboratory personnel must be alerted to the possibility of anthrax to ensure that the Bacillus isolate is not assumed to be B. cereus and that further speciation is performed. Definitive diagnosis of anthrax requires specific testing such as detection of lethal factor, PCR-based analysis, and immunohistochemical staining. Serologic assays can become positive as early as 10 days after onset of symptoms, with peak titers at 40 days. The differential diagnosis includes cutaneous infection with Bacillus megaterium, a brown recluse spider bite, the eschar of several rickettsial diseases, cellulitis, ecthyma gangrenosum, orf, milker's nodule, opportunistic bacterial and fungal infections, and entities in the ulceroglandular category (e.g. tularemia; see below)72. Treatment Without antibiotic treatment, mortality from cutaneous anthrax may be as high as 20% (usually from septicemia), but that number falls to almost zero with proper antimicrobial therapy. Although antibiotics do not alter the evolution of the cutaneous lesions (which are toxin-mediated), the likelihood of systemic illness is reduced. When cutaneous anthrax is associated with a concomitant inhalational exposure, the Centers for Disease Control and Prevention (CDC) recommend antibiotic therapy for at least 60 days, compared to a 7-10-day course for a purely cutaneous exposure to an animal-based source69. Quinolones (e.g. ciprofloxacin, levofloxacin, moxifloxacin) and doxycycline are first-line agents, with clindamycin and (if susceptible) penicillin or amoxicillin as alternatives69. An anthrax vaccine, consisting of an inactivated cell-free filtrate of a non-encapsulated, attenuated strain of B. anthracis, is available. The recommended five-dose pre-exposure series includes administration at 0, 1, 6, 12, and 18 months, followed by yearly boosters. For post-exposure prophylaxis, the vaccine can be given in three doses at 0, 2, and 4 weeks together with antimicrobial treatment. Raxibacumab is a recombinant human immunoglobulin monoclonal antibody targeting the B. anthracis protective antigen. Either raxibacumab or polyclonal anthrax immune globulin may be administered as a single intravenous infusion (in conjunction with antibiotics) for the treatment and post-exposure prophylaxis of inhalational anthrax

Normal Skin Bacteria - what 4 phyla make up the majority of normal skin bacteria

Four phyla - Actinobacteria, Firmicutes, Bacteroidetes and Proteobacteria - account for the vast majority of skin bacteria (Fig. 74.1)1. Together these organisms help prevent skin infections by providing ecologic competition with pathogenic microorganisms and by hydrolyzing lipids of sebum to produce free fatty acids, which are toxic to many pathogenic bacteria.

HI Cellulitis - What type of bacteria is HI - Typically occurs when and favors what areas - First line therapy

Haemophilus influenzae is a Gram-negative coccobacillus that can cause facial cellulitis with a violaceous hue in infants and young children (usually 6-24 months of age) following an upper respiratory tract infection. It favors the buccal and periorbital areas and is often associated with high fevers, an increased leukocyte count with a left shift, and positive blood cultures. If diagnosis is delayed, systemic spread may lead to meningitis. Routine vaccination of children against H. influenzae type b has greatly reduced the incidence of this form of cellulitis42. First-line therapy for severe H. influenzae infections is a third-generation cephalosporin; selection of empiric antibiotic therapy for cellulitis is discussed above.

Glanders - cause, what animals are typically infected - how does infection occur, how does damage to the skin occur? - what are the four forms of disease? - when should glanders be suspected?

Glanders is principally a disease of horses, mules, and donkeys that is caused by Burkholderia mallei (formerly Pseudomonas mallei), a nonmotile, strictly aerobic, non-pigment-producing, Gram-negative bacillus. Glanders is endemic in Africa, Asia, the Middle East, and Central and South America. Human disease is rare, occurring chiefly in those with direct contact with infected animals, such as veterinarians, animal caretakers, abattoir workers, and laboratory personnel. Tissue damage results from production of exotoxins, including pyocyanin (interferes with electron transfer), lecithinase (causes cell lysis), collagenase, lipase, and hemolysin. Glanders has four clinical forms - septicemic, localized, pulmonary, and chronic. Acute septicemic glanders is characterized by malaise, anorexia, chills, fever, diarrhea, and joint pains. Patients may have flushing, cyanosis, a disseminated pustular eruption, cellulitis, lymphangitis, erythroderma, and/or jaundice. Multi-organ failure ensues, and the mortality rate is ~50% (>90% without treatment). In the localized form, a nodule, pustule, or vesicle surrounded by hemorrhagic edema appears at the inoculation site after approximately 1 to 5 days. The superficial portion of the lesion sloughs, producing an ulcer with a gray-brown base. Glanders may also involve the nose and cause ulceration or perforation of the nasal septum or palate. Chronic glanders features malaise, myalgias, and often fevers. Painful subcutaneous and intramuscular abscesses may appear at any site and can ulcerate, drain, or extend into joints, periosteum, and bone. Multiple subcutaneous and intramuscular nodules ("farcy buds") appear along the draining lymphatics, and the term "farcy pipes" refers to the firm cords that result from lymphatic involvement. Glanders should be considered when localized cutaneous abscesses and secondary lesions appear in the path of lymphatic drainage (see Table 77.17). Accurate diagnosis can be made with serologic testing or PCR-based methods. For localized disease, a 60- to 150-day course of oral amoxicillin/clavulanate, doxycycline, or TMP-SMX can be prescribed; the regimens recommended for melioidosis represent another option (see below). Alternatives include ciprofloxacin, streptomycin, and gentamicin108. Cutaneous manifestations may include cellulitis, subcutaneous abscesses, granulomatous lesions, ecthyma gangrenosum, purpura, pustules, and urticaria. Bacterial culture represents the standard for diagnosis of melioidosis, but the sensitivity is as low as 60%. Recently developed multiplex PCR-based assays are more sensitive as well as species-specific108a. Both complement-fixing and agglutinating antibodies appear within 4 to 6 weeks after infection. Treatment of melioidosis is difficult, and susceptibility testing should be performed. Current guidelines recommend an initial intensive phase with intravenous administration of ceftazidime or a carbapenem for at least 10-14 days, followed by an eradication phase with oral TMP-SMX or amoxicillin/clavulanate for ≥3 months109. Of note, B. pseudomallei has shown resistance to quinolones, macrolides, and aminoglycosides. Melioidosis-associated sepsis has a mortality rate of 50-90%; however, intensive supportive care lowers this to ~20%. Melioidosis has a relapse rate of ~10%, and B. pseudomallei can remain latent in the body for several decades109. Because B. mallei and B. pseudomallei represent potential agents of bioterrorism, attempts are being made to develop vaccines for these infections

Bartonellosis - What is it? caused by what bacteria? - clinical forms - transmitted by what? occurs where

Introduction Bartonellosis is a potentially life-threatening biphasic infection caused by Bartonella bacilliformis. Two distinct clinical forms may occur independently or sequentially: (1) Oroya fever, an acute febrile disease with associated hemolytic anemia; and (2) verruga peruana (Peruvian wart), a chronic disease characterized by cutaneous vascular lesions. History The biphasic nature of bartonellosis was first described in 1540 by Miguel de Steta. In 1885, a Peruvian medical student, Daniel Carrion, died of complications of Oroya fever after inoculating himself with blood derived from a lesion of verruga peruana, proving a common causality for the two disease states100. Epidemiology and pathogenesis The disease is transmitted by the bite of female Phlebotomine sand flies (Lutzomyia verrucarum). It occurs in mountain valleys of Peru, Ecuador and southwestern Colombia, where the vector resides. There is no racial, gender, or age predilection, but the disease tends to be milder in children than in adults. The incubation period varies between 3 and 14 weeks.

Pseudomonas aeruginosa - what type of bacteria

Pseudomonas aeruginosa is a ubiquitous Gram-negative, strictly aerobic, motile bacillus. It is widely distributed in the soil and on plants, growing especially well in aqueous environments. This organism has relatively low virulence and usually requires a local anatomic or immunologic defect to cause disease. Primary cutaneous infection with P. aeruginosa can occur in otherwise healthy individuals in areas exposed to high levels of moisture in conjunction with skin barrier disruption; these infections have a very good prognosis86. In contrast, cutaneous manifestations of Pseudomonas sepsis in immunocompromised individuals are associated with a grave prognosis

More Bacillary angiomatosis - diagnosis - Treatment

Warthin-Starry silver stain demonstrates bacilli within areas of necrosis. Diagnosis and differential diagnosis For patients who present with regional adenopathy and a history of a recent cat scratch, the diagnosis is usually made clinically. A sensitive and specific assay for B. henselae antibodies is available, and antibody titers are usually high during the first few weeks after the onset of lymphadenopathy; PCR-based testing can also be performed. Culture is difficult and not routinely recommended103. Other causes of lymphadenopathy such as infections (bacterial, fungal or viral), reactive hyperplasia, drug reactions, or malignancy can be excluded by fine-needle aspiration histology or biopsy and culture of lymph node tissue. Treatment - Doxycycline plus gentamicin • Doxycycline plus rifampin • Azithromycin plus gentamicin

Yaws - cause, occurs where in the world - clinical presentation?

Yaws is a three-stage infection caused by T. pallidum subspecies pertenue and represents the most common and severe endemic treponematosis. It occurs in warm, humid, tropical climates, most often in Africa, Asia, South and Central America, and the Pacific islands. In 2012, the WHO announced a new strategy plan to eradicate yaws by 2020133,133a,135. Yaws most commonly involves the lower extremities of children <15 years of age (Fig. 74.35). A "mother yaw", the main lesion of the primary stage, occurs at the site of inoculation within 10 days to 3 months (mean, 21 days). It begins as an erythematous, infiltrated, painless papule that over time enlarges peripherally to become 1-5 cm in diameter, then ulcerates and develops an amber-yellow crust. The lesion is rich in treponemes and eventually heals spontaneously over 3 to 6 months. "Daughter yaws", the lesions of secondary yaws, are smaller and more widespread than the primary lesion. They usually occur adjacent to body orifices, such as the nose and mouth, and can expand or ulcerate. Both types of lesions are highly infectious. Only 10% of patients progress to the final stage, during which abscesses form, become necrotic, and ulcerate. The ulcers may coalesce into serpiginous tracts, which heal with significant scarring and produce crippling deformities. Yaws can also cause various forms of periostitis, dactylitis and osteitis, with the latter potentially leading to curvature of the tibia ("saber shins"). Histologic examination of early yaws lesions demonstrates spongiosis, acanthosis, and papillomatosis. A moderate to dense dermal inflammatory infiltrate composed mostly of plasma cells and lymphocytes can be seen. Silver stains easily identify treponemes in specimens. Clinically, the skin lesions of yaws can resemble venereal syphilis, eczema, psoriasis, verrucae, calluses, scabies, tungiasis, sarcoidosis, and vitamin deficiencies

Blistering Distal Dactylitis - what is it? - most commonly seen in whom? most common organism? - ddx - Treatment

Blistering distal dactylitis is a localized infection of the volar fat pad of a finger or, less often, a toe, with occasional involvement of the nail fold or more proximal portion of the digit. Darkening of the skin is often observed for several days to a week before blister formation. The infection most commonly occurs in children aged 2-16 years. Group A Streptococcus spp. or S. aureus are usually the causative organisms. Inoculation may follow local skin trauma or autoinoculation from nose picking18. The differential diagnosis includes herpetic whitlow, a thermal or chemical burn, acute paronychia, bullous impetigo, and frictional bullae. Drainage and a 10-day course of an oral anti-staphylococcal antibiotic are recommended. Although topical therapy with mupirocin has been described, systemic therapy can prevent development of new sites of infection as well as local extension.

More Cutaneous Anthrax - clinical features - how do spores look on histo?

Clinical features The clinical features of cutaneous anthrax are outlined in Table 74.1271. Additional key points include the following: • The lack of pain despite a necrotic eschar helps to differentiate cutaneous anthrax from the bite of a brown recluse spider. • A pustular primary lesion is unlikely to be cutaneous anthrax, although "cloudy" vesicles may form a "pearly wreath" around the eschar. The term "malignant pustule", which is often attributed to anthrax, is therefore a misnomer. • Vesicles may discharge serosanguineous fluid containing numerous organisms, which are evident on Gram stain. • Lymphangitis and painful lymphadenopathy with systemic symptoms (fever, malaise, headache) occur rarely. • Antibiotic therapy does not alter the progression from vesicle to ulcer to eschar, as the process is toxin-mediated. • Multiple lesions, when present, tend to cluster in the same area of the body. Pathology Spongiosis, papillary dermal edema, and a superficial and deep inflammatory infiltrate with abundant neutrophils are observed. Substantial hemorrhage is often evident, and the inflammatory infiltrate may involve nerves. Extensive ulceration and coagulative necrosis can be seen in older lesions. Elongated Gram-positive bacilli are present, often in small clusters. Spores grow readily on all routine culture media at 37°C, with a "jointed bamboo-rod" cellular appearance and a unique "curled-hair" colonial morphology.

Ddx of TSS Treatment of TSS

Diagnosis and differential diagnosis A high index of suspicion is required in order to make a timely diagnosis. Table 74.8 outlines the case definition of TSS. The possibility of streptococcal TSS (see Table 74.9 and below) should also be considered. TSS can have clinical overlap with Kawasaki disease, scarlet fever, SSSS, early TEN, Rocky Mountain spotted fever, and leptospirosis. Treatment Severe cases of TSS require intensive monitoring and supportive therapy. Hypotension can be treated with intravenous fluids and vasopressor agents. Foreign bodies (e.g. surgical mesh, nasal packing, tampons) should be removed and abscesses drained. Beta-lactamaseresistant antibiotics are used to eradicate the toxin-producing staphylococci; MRSA is responsible for only a small proportion of TSS cases24. Some advocate using antibiotics that suppress protein (and thereby toxin) production, such as clindamycin, and administration of intravenous immunoglobulin (IVIg) may help to neutralize the toxin26. In severe cases of shock unresponsive to antibiotics, low-dose corticosteroids have been used27.

Impetigo - two types, which type is more common? - two biggest causes - Most commonly occurs in whom? how contagious?

Impetigo is a common, contagious, superficial skin infection that can present in non-bullous and bullous forms (Fig. 74.2). The most common pathogen in both non-bullous and bullous impetigo is Staphylococcus aureus. Group A β-hemolytic Streptococcus (Streptococcus pyogenes) represents another important cause of non-bullous impetigo. Overall, non-bullous impetigo accounts for approximately 70% of cases. Table 74.1 compares the clinical characteristics and complications of bullous and non-bullous impetigo. Most commonly occurs in children under 6. Is highly contagious, more common in summer months.

Bacillary angiomatosis - Caused by what - what is the most predominant feature of this condition and who does it most commonly occur in? - possible underlying pathophysiology

Introduction Bacillary angiomatosis is caused by infection with B. henselae or B. quintana. Vascular proliferation is the predominant feature of this condition, which most often affects HIV-infected individuals. History The disorder was first described in 1983 as subcutaneous vascular proliferations in individuals with AIDS. Electron microscopy and Warthin-Starry-stained sections of the lesions revealed small bacilli. In 1989, LeBoit and colleagues coined the name "bacillary angiomatosis" and proposed histologic criteria for the disorder. In the early 1990s, Rochalimaea quintana and R. henselae (subsequently reclassified in the genus Bartonella) were recognized as the causes of bacillary angiomatosis (see Table 74.14). Epidemiology and pathogenesis Bacillary angiomatosis is an uncommon disease that is most often seen in HIV-infected patients when their CD4+ count is <200 cells/mcl (see Ch. 78). Fortunately, with the advent of effective antiretroviral therapy (ART), the prevalence of bacillary angiomatosis has decreased substantially. The associated vascular proliferation may reflect aberrant vascular endothelial growth factor (VEGF) signaling in endothelial cells104. Only 20% of patients with bacillary angiomatosis due to B. henselae report a preceding cat scratch or bite, compared to 90% of those with CSD.

More Botryomycosis - Most distinctive histologic feature - diagnosis is made how - ddx - treatment

Pathology Biopsy specimens reveal a chronic inflammatory reaction with fibrosis and foreign body giant cells. The most distinctive feature is 1-3 mm granular bodies (grains) that represent bacteria, cells, and debris (Fig. 74.15). Grains have basophilic centers and a homogeneous, eosinophilic, hyaline periphery thought to be secondary to a host immunoglobulin response (Splendore-Hoeppli phenomenon). The granules stain with PAS, Gram, and Giemsa. Diagnosis and differential diagnosis When botryomycosis is suspected, both bacterial and fungal cultures should be obtained and a skin biopsy performed for histopathologic examination as well as culture. Microscopic examination (fresh mount or 20% KOH) shows coarsely lobulated granules with club-like projections. Gram staining of crushed granules usually displays masses of staphylococci. The differential diagnosis of cutaneous botryomycosis includes mycetoma, actinomycosis, a ruptured epidermoid cyst, a staphylococcal abscess, orf, tuberculosis, and dimorphic fungal or atypical mycobacterial infections. Treatment Botryomycosis is typically treated surgically with debridement or excision in conjunction with antibiotic therapy. If possible, reducing immunosuppression may be of benefit. Ablation with the CO2 laser could be considered when surgical excision is not feasible

Tularemia - caused by what bacteria and what are its characteristics - what are the main reserviors - what are the types of the disease, which is the most common - treatment

Tularemia is a bacterial infection caused by Francisella tularensis, a Gram-negative, non-motile coccobacillus. First described in 1911 as a plague-like illness, there were 1739 cases reported in the US from 2005 to 2015114. Skin or mucous membranes are the portal of entry for infections associated with tick or deer fly bites and exposure to the organism via abrasions. Inhaled or ingested organisms rarely cause the disease, and person-to-person transmission does not occur. Rabbits, hares, and ticks are the main reservoirs for F. tularensis. Although infected rabbits and their carcasses are classically described as the main sources of infection, deer flies and (especially in the US) ticks are more significant vectors. Tularemia occurs in six clinical forms according to the mode of transmission - ulceroglandular, glandular, oculoglandular, oropharyngeal/gastrointestinal, typhoidal/septicemic, and pneumonic Ulceroglandular tularemia is the most common form and is characterized by lymphadenopathy and an erythematous, indurated, punched-out ulcer at the site of cutaneous exposure that may last for several weeks. The lymph nodes can become fluctuant and suppurate. Occasionally, ulceration or lymphadenopathy occurs in isolation. Other rare cutaneous manifestations include buboes, a morbilliform or vesicular eruption, erythema nodosum, and erythema multiforme. Because of concern regarding the potential use of F. tularensis as a biologic weapon, tularemia is a reportable disease in the US. Diagnostic methods include direct fluorescent antibody (DFA) testing (available in designated reference laboratories), immunohistochemical staining of tissue samples, and PCR-based assays115. Attempts to culture F. tularensis are usually not made due to its high infectivity, risk to laboratory workers, and inability to grow on most media. The differential diagnosis of ulceroglandular tularemia includes other ulceroglandular entities (e.g. bubonic plague, tuberculous chancre, rat-bite fever, glanders), anthrax, soft tissue infections (i.e. Staphylococcus, Streptococcus, Pasteurella multocida), and infectious causes of a sporotrichoid pattern (see Ch. 77). Treatment recommendations include a 10-day course of streptomycin (the classic first-line agent), gentamicin, or ciprofloxacin; a 14-21-day course of doxycycline is another option that results in a higher risk of relapse due to this agent's bacteriostatic rather than bactericidal nature116. A Jarisch-Herxheimer-like reaction may occur following the initiation of therapy. The previously utilized live attenuated tularemia vaccine is no longer available, and there are ongoing efforts to develop a safe and effective vaccine.

Ecthyma - What is it? - presentation and how does it heal? - causative organism - clinical presentation - diagnosis is made how

Ecthyma Ecthyma is a deep form of non-bullous impetigo characterized by extension into the dermis to produce a shallow ulcer that heals with scarring (Fig. 74.5). It can be caused by a primary infection with Str. pyogenes or streptococcal superinfection of a pre-existing ulceration or excoriated insect bite. Outbreaks of ecthyma have occurred among infantry units where skin trauma, poor hygiene, and crowded living conditions facilitate disease spread19. Table 74.6 summarizes the clinical aspects and treatment of ecthyma. • Fewer than 10 lesions are typically seen, most commonly on the lower extremities • An initial vesiculopustule enlarges (0.5-3 cm in diameter) over the course of several days, and develops a hemorrhagic crust • The ulcer has a "punched-out" appearance and a purulent, necrotic base • Lesions are slow to heal and produce scarring • Clinical appearance • Culture of moist, purulent base; skin biopsy with deep-tissue Gram stain and culture occasionally required

Ecthyma Gangrenosum - develops when? - clinical presentation - Key histologic finding? - Treatment

Ecthyma Gangrenosum P. aeruginosa septicemia occurs primarily in patients who are immunocompromised, with severe neutropenia representing a major predisposing factor. Fever, hypotension, and alterations in consciousness often develop, and ecthyma gangrenosum is an occasional cutaneous manifestation. Lesions are usually few in number and begin as erythematous or purpuric macules, most commonly located in the anogenital area or on the extremities. They then evolve into hemorrhagic vesicles or bullae, which rupture and become necrotic ulcers with a central black eschar. The surrounding tissue is erythematous and tender (Fig. 74.28). Of note, a localized anogenital form of ecthyma gangrenosum can also occur in immunocompromised patients (including premature infants96) and may not be associated with identifiable bacteremia. Histologic examination shows a necrotizing hemorrhagic vasculitis, and Gram-negative rods can be seen in the medial and adventitial walls of deeper vessels.(BLUEISH HAZE) The intima is characteristically spared. Multiple lesions, prolonged neutropenia, and a delay in antibiotic treatment portend a poor prognosis. Once the diagnosis is suspected, biopsy and tissue culture of a skin lesion (as well as blood and urine cultures) should be performed, followed by prompt initiation of intravenous therapy with an aminoglycoside and an antipseudomonal penicillin86. Clinically identical lesions can result from septic emboli due to other organisms, including Pseudomonas stutzeri, E. coli, Aeromonas hydrophila, Burkholderia cepacia, Citrobacter freundii, Stenotrophomonas maltophilia, Candida, Fusarium, Aspergillus, and other saprophytic fungi97. Disseminated HSV may have a similar appearance.

Endemic syphilis - cause -

Endemic syphilis is caused by an infection with T. pallidum subspecies endemicum. Most cases are seen in the arid, warm climates of North Africa and the Arabian Peninsula as well as in Southeast Asia. Children <15 years of age are most commonly affected. In contrast to yaws and pinta, a primary lesion is rarely noticed. It usually consists of an inconspicuous small papule or ulcer in the oropharynx or on the nipples of breastfeeding women. Secondary endemic syphilis may present with findings similar to venereal syphilis, such as patches on mucous membranes, split papules, angular stomatitis, non-pruritic papular skin eruptions, and generalized lymphadenopathy. Condylomata lata are also frequently present. During the secondary stage, some patients experience osteoperiostitis of the long bones, which can cause nocturnal leg pain. Six months to several years after inoculation, some patients develop the tertiary stage of endemic syphilis. Gumma formation may lead to gross mutilation of the skin, mucous membranes, muscle, cartilage, and bone. Without treatment, disfiguring lesions of the palate and nasal septum may occur, leading to difficulty in articulation and swallowing. The eyes and bones can also be severely affected in late-stage endemic syphilis. The histologic picture closely resembles that of venereal syphilis. In the early stages, biopsy specimens demonstrate a perivascular dermal infiltrate of mostly plasma cells and lymphocytes. Oral lesions may resemble venereal syphilis, aphthosis, perlèche, vitamin deficiencies, and primary herpes simplex viral infection. The mutilating nasopharyngeal lesions of endemic syphilis can be mistaken for tertiary venereal syphilis, leprosy, rhinoscleroma, mucocutaneous leishmaniasis, paracoccidioidomycosis, and tuberculosis

Erysipeloid - Caused by what organism? bacteria characteristics? - Most commonly seen in whom? - how many types, clinical features - ddx - treatment of choice?

Erysipeloid is an acute cutaneous infection caused by Erysipelothrix rhusiopathiae (formerly insidiosa), a Gram-positive, non-motile, smooth or curved bacillus. It is caused by traumatic inoculation of the organism into the skin, which most often occurs in fishermen or persons who prepare meat, poultry, or fish. There are two types of erysipeloid, localized and generalized, and they usually occur within 1 week of inoculation. The localized form is characterized by an erythematous to violaceous area of non-suppurative cellulitis (Fig. 74.23), which can be pruritic or painful. Hemorrhagic vesicles may develop. Although the classic finding is involvement of the finger webs with sparing of the terminal phalanges, other sites may be affected. Constitutional symptoms are unusual in localized erysipeloid, which is typically a self-limited condition. However, the generalized form presents with fever and arthralgias in addition to widespread cutaneous lesions. The latter range from perifollicular papules to erythematous plaques to macular purpura and necrosis. Complications can include endocarditis, septic arthritis, and cerebral and other visceral abscesses. The organism is often difficult to culture, and PCR-based assays can help to establish the diagnosis74. Erysipelas, cellulitis, spider bites, and fixed drug eruptions may simulate localized erysipeloid (see Table 74.10). Most patients with untreated localized disease recover spontaneously. Penicillin is the drug of choice; erythromycin, cephalosporins, clindamycin, linezolid, and quinolones are alternatives75. The best means of prevention is using gloves when preparing fish or meat.

Impetigo Treatment? Can you develop post strep glomerulonephritis? is that impacted by treatment?

For healthy patients with a few superficial lesions and no systemic symptoms, topical mupirocin, retapamulin, or fusidic acid (not available in the US) are often equally (if not more) effective than oral antibiotics. However, S. aureus can develop resistance to each of these agents3a,4. Treatment should also include cleansing the affected area and removing crusts, which can be facilitated by wet dressings. The extent of skin involvement, the presence of complications (e.g. cellulitis, lymphangitis, bacteremia), comorbid conditions (e.g. atopic dermatitis, varicella), the patient's immune status, and local drug resistance patterns (e.g. the prevalence of community-associated methicillin-resistant S. aureus [CA-MRSA]) should be considered when deciding whether topical, oral, or intravenous therapy is the most appropriate treatment (Table 74.3). The risk of developing post-streptococcal glomerulonephritis following streptococcal impetigo is not affected by treatment and is greater with certain subtypes of Str. pyogenes (see Table 74.1)2,5,6. In contrast to pharyngitis, a link between streptococcal pyoderma and acute rheumatic fever has not been established. Methods for "decolonizing" the nares and skin of patients with recurrent staphylococcal impetigo are discussed in the folliculitis section below.

Impetigo histology impetigo Ddx

In non-bullous impetigo, small neutrophilic vesiculopustules are present within the epidermis. Spongiosis frequently underlies the pustule. The upper dermis contains an intense infiltrate of neutrophils and lymphocytes. Gram-positive cocci are present within the vesiculopustules. In bullous impetigo, there is cleavage of the upper epidermis, typically within the granular layer. Acantholysis mimicking pemphigus foliaceus may be observed. Relatively few inflammatory cells are present within the blister cavity, and a neutrophilic infiltrate is often found in the upper dermis. Gram-positive cocci may be evident. ddx: • Insect bites • Eczematous dermatoses • Herpes simplex viral infection • Candidiasis • Inflammatory tinea corporis/faciei • Varicella • Scabies • Pediculosis • Pemphigus foliaceus

Toxic Shock Syndrome - Pathophysiology

In the early 1980s, there was an outbreak of TSS in young women using highly absorbent tampons ("menstrual" TSS). The incidence of menstrual TSS then declined substantially following changes in tampon manufacturing and use, and by the early 2000s it accounted for approximately half of TSS cases24. TSS can also occur in patients who have undergone surgical procedures. In addition, it may develop in association with cutaneous pyodermas, postpartum infections, abscesses, burns, and infections associated with nasal packing or insulin pump infusion sites. Non-menstrual TSS affects both sexes equally. TSS is due to infection or colonization with strains of S. aureus that produce toxic shock syndrome toxin-1 (TSST-1). This toxin is thought to act as a "superantigen" that binds to major histocompatibility complex (MHC) class II molecules of antigen-presenting cells (APCs) and the Vβ region of T-cell receptors in a non-antigen-specific manner, which leads to massive release of cytokines and chemokines as well as clonal T-cell expansion (see section on Streptococcal TSS)23. Recent investigations implicate invariant natural killer T cells, mucosa-associated invariant T (MAIT) cells, and interleukin-17A-producing effector memory T cells in this hyperinflammatory "cytokine storm" response to bacterial superantigens23a,23b. Of note, the neonatal TSS-like exanthematous disease (see Ch. 10) occurs during the first week of life due to colonization with TSST-1-producing S. aureus (usually methicillin-resistant) and has a relatively mild course due to the immature, relatively anergic state of T cells in newborns.

Actinomycosis - Cause, what is it, reservoir for disease - most important predisposing factor - presentation

Introduction Actinomycosis is a subacute or chronic bacterial infection characterized by suppurating abscesses, granulomatous inflammation, and sinus formation. Actinomyces israelii, an anaerobic or microaerophilic Grampositive, non-acid-fast actinomycete, is the most common causative organism. Cervicofacial (accounting for two-thirds of infections), pulmonary/thoracic, gastrointestinal, and pelvic forms exist. Epidemiology and pathogenesis Actinomycosis is seen worldwide, and men are affected three times more often than women. Humans are the only known reservoir for Actinomyces spp. A. israelii is part of the normal flora of the oral cavity and is also found in the gastrointestinal tract and female genital tract. The most important predisposing factor is trauma, especially dental procedures. Actinomyces spp. are not considered particularly pathogenic, and their virulence is enhanced by co-infection with other organisms. In actinomycotic mycetoma, species of Actinomyces other than A. israelii are usually responsible for the formation of sulfur granules (see Ch. 77). Clinical features In patients with cervicofacial actinomycosis ("lumpy jaw"), there is usually a history of poor dental hygiene, dental disease, or a previous orofacial injury or procedure. An initial bluish swelling in the mandibular area progresses to brawny erythematous nodules, which gradually increase in size and form fistulous abscesses (Fig. 74.36). These eventually drain purulent material with characteristic yellow "sulfur granules" that represent clumps of bacteria. Multiple sinus tracts, fever, pain, and leukocytosis may develop. Lymphadenopathy is usually absent. Pulmonary actinomycosis (15-20% of patients) occurs after bacteria gain access to the lung through the aspiration of infected oral material. Pulmonary cavities are usually seen at the bases of the lungs. Extension to the pleura and chest wall may occur, and pleurocutaneous fistulas can develop. Gastrointestinal actinomycosis is usually preceded by trauma or inflammatory disease but may occur spontaneously. Granulomatous lesions involving the bowel can eventually extend to the abdominal wall, producing a brawny, erythematous mass with draining sinus tracts. Pelvic actinomycosis is more common in women and is often associated with intrauterine contraceptive devices. Actinomycosis may also involve the central nervous, musculoskeletal, and other organ systems.

Cellulitis - Most common organisms

Introduction Cellulitis is an infection of the deep dermis and subcutaneous tissue that manifests as areas of erythema, swelling, warmth, and tenderness. Epidemiology and pathogenesis Cellulitis in immunocompetent adults is most often caused by group A streptococci or S. aureus, and the latter organism is the most frequent etiology in children. Although H. influenzae was once a common cause of cellulitis in pediatric patients, it is now rare due to routine vaccination against H. influenzae type b42. A mixture of Gram-positive cocci and Gram-negative aerobes and anaerobes is often implicated in cellulitis surrounding diabetic and decubitus ulcers43. Bacteria typically gain access to the dermis via a break in the skin barrier in immunocompetent individuals, but a bloodborne route is common in immunocompromised patients. Lymphedema, alcoholism, diabetes mellitus, injection drug use, and peripheral vascular disease are all risk factors for cellulitis. Recurrent bouts of cellulitis may result from damage to the lymphatic system, e.g. via prior lymph node dissection, saphenous vein harvest, or cellulitis.

Erysipelas - Major causative organism? - affects what layers of the skin - Other possible causative agents? - Most commonly affected area

Introduction Erysipelas is a superficial variant of cellulitis caused primarily by group A streptococci that affects the dermis with prominent lymphatic involvement; in contrast, classic cellulitis is centered in the deep dermis and subcutaneous tissues34. Epidemiology and pathogenesis Erysipelas is usually a disease of the very young, the aged, the debilitated, and those with lymphedema or chronic cutaneous ulcers. Women outnumber men, but boys are more commonly affected than girls in the pediatric age group. Erysipelas is usually caused by group A streptococci; groups G, B, C, and D streptococci are occasionally implicated. S. aureus, Pneumococcus spp., Klebsiella pneumoniae, Yersinia enterocolitica, and Haemophilus influenzae type b can also cause an erysipelaslike infection35. Clinical features Although erysipelas classically affects the face, the lower extremity is the most common location. After an incubation period of 2 to 5 days, there is an abrupt onset of fever, chills, malaise, and nausea. A few hours to a day later, a sharply marginated erythematous plaque with a ridge-like border develops and progressively enlarges. It is clearly demarcated from the surrounding skin (Fig. 74.10A,B), hot, tense, and indurated with non-pitting edema. The affected area is painful to palpation and may burn. Regional lymphadenopathy is usually present, with or without lymphangitis. Pustules, vesicles, bullae, and small areas of hemorrhagic necrosis may also form. Complications of erysipelas are uncommon and usually occur in patients with underlying disease When the infection resolves, desquamation and postinflammatory pigmentary changes may ensue.

Necrotizing Fasciitis - What is it, what are the subtypes - Risk factors, Mortality rate - Most common cause in kids, how about adults

Introduction Necrotizing fasciitis is characterized by rapidly progressive necrosis of subcutaneous fat and fascia, which can be life-threatening without prompt recognition, aggressive surgical intervention, and immediate antibiotic therapy. It is classified into two major subtypes: (1) type 1, a polymicrobial infection including at least one anaerobe in addition to facultative anaerobes; and (2) type 2, a monomicrobial infection, most often with group A Streptococcus. Some authors also distinguish type 3 due to Gram-negative marine organisms (e.g. Vibrio and Aeromonas spp.) and type 4 due to fungi (e.g. post trauma or in immunocompromised patients). Epidemiology and pathogenesis Approximately 700-1200 cases of necrotizing fasciitis are reported each year in the US. Risk factors include diabetes mellitus, immunosuppression, cardiac or peripheral vascular disease, renal failure, and bevacizumab therapy52, but it can also occur in young, previously healthy individuals. Necrotizing fasciitis may follow penetrating or blunt injury or develop in the absence of preceding trauma. Other predisposing factors include injection drug use, recent surgery, varicella, and decubitus or ischemic ulcers. Mortality rates range from 20% to 60%. Higher mortality is associated with female sex, older age, malnutrition, greater extent of infection, delay to first debridement, an elevated serum creatinine or lactic acid level, disease due to group A streptococci, and a greater degree of organ dysfunction at the time of admission to hospital. Diabetes mellitus can also result in higher mortality, particularly if renal dysfunction or peripheral arterial disease is also present53. In children, necrotizing fasciitis is most commonly caused by group A streptococci. In adults, it often follows trauma or surgery and is due to a polymicrobial infection with bacteria such as streptococci, S. aureus, Escherichia coli, Bacteroides, and Clostridium spp. Uncommon pathogens include V. vulnificus (associated with sea water injuries; see below), Aeromonas hydrophila (associated with fresh water injuries), Pseudomonas aeruginosa, and H. influenzae type b54. Opportunistic fungal infections, including zygomycosis, can cause necrotizing fasciitis in immunocompromised patients

Nocardiosis - what kind of bacteria - how is the disease acquired - what are the three major forms of disease?

Introduction Nocardiosis is caused by various species of Nocardia, a filamentous, Gram-positive, acid-fast organism. Nocardia is recognized as an opportunistic pathogen in immunocompromised individuals, causing disseminated or systemic disease; in contrast, cutaneous nocardiosis commonly occurs in immunocompetent hosts. Epidemiology and pathogenesis Nocardiosis has a worldwide distribution and affects all age groups. Men are affected three times more often than women, and children may be more prone to developing lymphocutaneous disease. Nocardia spp. are ubiquitous in the soil. Localized trauma (e.g. puncture wounds), occupational exposures (e.g. farmers, gardeners), and immunodeficiency are risk factors for contracting nocardiosis. Clinical features The three major forms of primary cutaneous nocardiosis are: (1) mycetoma (see Ch. 77); (2) lymphocutaneous nocardiosis; and (3) superficial cutaneous nocardiosis. In addition, approximately 10% of patients with pulmonary-systemic nocardiosis develop secondary skin lesions. In immunosuppressed patients, lesions may present as widely disseminated subcutaneous nodules138. Table 74.18 details the various clinical presentations of Nocardia infection.

Strep Toxic Shock syndrome - Causative agent - toxin involved

Introduction Streptococcal TSS is a rapidly progressive, life-threatening illness caused by infection with toxin-producing group A and rarely group G streptococci29a. Epidemiology and pathogenesis Streptococcal TSS mainly affects healthy individuals between 20 and 50 years of age but can also occur in children (mean age, 4-5 years)29b. A disruption of the cutaneous barrier usually serves as the portal of bacterial entry. In contrast to the occult infections that predominate in staphylococcal TSS, many cases are associated with invasive soft tissue infections (e.g. necrotizing fasciitis) with virulent (e.g. M types 1 and 3) strains of group A streptococci, and the majority of patients are bacteremic30. Toxins that have been implicated include SPEs A, B, and C as well as the more potent streptococcal mitogenic exotoxin Z (SMEZ)30a. Streptolysin O may also act synergistically with SPE-A. Similar to staphylococcal TSS, the clinical manifestations of streptococcal TSS result from massive cytokine release due to superantigen activity of bacterial exotoxins30a. Superantigens bind directly (without intracellular processing) to MHC class II molecules on APCs (outside the antigen-presenting groove) and the Vβ region of the T-cell receptor (Fig. 74.9), thereby stimulating T cells in a relatively nonspecific manner. A given superantigen-T-cell interaction may lead to the activation of 5-30% of the entire circulating T-cell population, compared to ~0.01% for conventional antigens. This leads to production of huge amounts of cytokines, especially tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-6; there is also upregulation of Toll-like receptors (TLRs) 2 and 4, which augments deleterious effects of endotoxin from Gram-negative bacteria (e.g. those colonizing the gut) as well as streptococci, resulting in further elaboration of proinflammatory mediators. As a consequence, patients develop clinical manifestations such as fever, erythematous eruptions, vomiting, hypotension, and tissue injury in multiple organ systems23. The use of nonsteroidal anti-inflammatory drugs (NSAIDs), which lessen fever and other signs of infection, might delay the diagnosis and treatment of a streptococcal soft tissue infection, allowing TSS to occur31.

Leptospirosis - type of bacteria - transmission, two forms of disease - cutaneous findings - treatment

Leptospirosis is a worldwide zoonosis caused by spirochetes in the genus Leptospira. It is transmitted via contact of non-intact skin or mucous membranes with urine or other body fluids (with the exception of saliva) from infected mammals (e.g. rodents, dogs, livestock, wild animals), either directly or from drinking or swimming in contaminated water. Veterinarians, farmers, slaughterhouse or sewer workers, and recreational water sport participants are most often affected. Leptospirosis occurs in an anicteric form (~90% of cases) and a more severe icteric form (~10% of cases). After an incubation period of 7-12 days, an initial "septicemic" stage of fevers, chills, and myalgias lasting 3-7 days is followed by an "immune" stage (during which serologic tests are positive) that can result in meningitis, uveitis, and renal, hepatic, and/or pulmonary dysfunction. Cutaneous manifestations include erythematous macules, papules, patches, and/or plaques in a widespread distribution or (especially with L. interrogans serovar Autumnalis) localized to the shins, as well as petechiae and purpura secondary to vascular involvement. Although most cases of leptospirosis are selflimited, antibiotics may decrease the duration of illness and reduce shedding of organisms in the urine. Oral doxycycline, amoxicillin, or azithromycin and (for more severe disease) intravenous penicillin or third-generation cephalosporins have been used

Listeriosis - what type of bacteria - commonly found in what animals? humans are usually infected how? - what types of disease usually develope from infection - treatment of choice

Listeriosis Listeria monocytogenes is a motile Gram-positive bacillus that is ubiquitous in the environment (e.g. soil, water, vegetation) and represents a common veterinary pathogen, especially in sheep and cattle. In humans, infection is usually acquired by eating contaminated food and primarily affects the elderly, pregnant women, and immunocompromised individuals (e.g. those with HIV infection or receiving immunosuppressive medications). These patients most often develop meningitis or a gastrointestinal illness accompanied by fever, myalgias, and bacteremia. Neonatal septicemia and meningitis due to vertical transmission can also occur and may be associated with disseminated skin lesions ranging from pustules and occasionally vesicles to petechiae and purpura to granulomatous papules and nodules. In addition, veterinarians and farmers who assist animals in parturition may acquire primary cutaneous listeriosis, which typically presents with pustular or papular lesions on the arms and hands. In otherwise healthy individuals, primary cutaneous listeriosis may be self-limited. The first-line treatment for listeriosis is ampicillin, and TMP-SMX represents an alternative; L. monocytogenes is resistant to cephalosporins

Lyme Disease - Cause, vector - typically how long does the tick need to be attached for significant risk of transmission?

Lyme disease is a multisystem disorder with prominent skin findings that is caused by Borrelia species of spirochetes. Although found worldwide, it has a particularly high incidence in North America and Europe, representing the most common tick-borne disease in the US. Lyme disease can occur year-round, but most cases present in the summer. If diagnosed in its early stages, it is a completely curable illness. The species of Ixodes tick vector differs depending on the geographic region, e.g. I. pacificus in the western US, I. scapularis (also called I. dammini) in the eastern US and Great Lakes region, I. ricinus in Europe, and I. persulcatus in Asia. B. burgdorferi is the predominant etiologic organism in the US, whereas B. garinii and B. afzelii are the predominant causes of Lyme disease in Europe127. This may explain the occurrence of borrelial lymphocytoma and acrodermatitis chronica atrophicans in Europe but not the US. Once the spirochete is in the midgut of the tick vector after feeding on an infected host (e.g. whitetailed deer), it produces outer surface protein C (OspC), which enables it to traverse the midgut epithelium, enter the hemocoel, and make its way to the salivary glands. B. burgdorferi is ultimately transmitted to humans via the tick's saliva. The rate of transmission is extremely low during the first 48 hours of tick attachment128. Chapter 19 describes the clinical features and treatment of Lyme disease, in particular erythema migrans (see Fig. 74.14), and Table 74.17 outlines the extracutaneous manifestations of Lyme disease. The next sections discuss borrelial lymphocytoma and acrodermatitis chronica atrophicans.

Borelia lymphocytoma - what is it? cause - occurs during what stage of lyme disease? - presentation

Lymphocytoma is a benign, reactive form of lymphoid hyperplasia that can be attributed to various stimuli, including Borrelia infection. Borrelial lymphocytoma usually appears during the early disseminated stage of Lyme disease (see Ch. 19). Because it is caused by B. afzelii and B. garinii, neither of which is found in North America, borrelial lymphocytoma is virtually never seen in those who have not traveled outside of the US. However, it occurs in approximately 1% of patients with Lyme disease in Europe. The formation of a lymphocytoma following a tick bite was first reported in 1950, but it was not until 1986 that Borrelia was cultured from such a lesion. A firm, bluish-red, occasionally tender nodule or plaque appears most commonly on the earlobes in children and the nipple/areola in adults, less often developing on the genitalia, trunk, or extremities. It may be associated with regional lymphadenopathy. Histologically, the epidermis is normal and separated from the dermal infiltrate by a Grenz zone. The dense dermal infiltrate of lymphocytes forms a pattern that closely resembles the architecture of a lymphoid follicle. The histologic differential diagnosis includes an arthropod bite reaction and cutaneous lymphoma, with the presence of Bcl-2 protein within follicular cells and monoclonality by PCR favoring the latter (see Ch. 119). Of note, B. burgdorferi-associated B-cell lymphomas have rarely been described129. Borrelial lymphocytoma responds to the antibiotics used for Lyme disease

Impetigo Pathogenesis, bullous and non-bullous - for bullous, what toxin is responsible, where is the split, and what is the target

Non-bullous impetigo is usually caused by S. aureus or (less often in temperate climates) Str. pyogenes. Infection typically occurs at sites of scratching (e.g. insect bites, atopic dermatitis), minor trauma (e.g. an abrasion, laceration, or burn) or other skin infections (e.g. varicella). Disruption of the skin barrier allows bacteria to invade and adhere. Bullous impetigo results from the local production of exfoliative toxins (ETA, ETB) by phage group II S. aureus at the site(s) of cutaneous infection; systemic elaboration of the same toxins is the cause of staphylococcal scalded skin syndrome (SSSS; see below). In both diseases, blister formation is mediated by exfoliative toxin binding to the desmosomal protein desmoglein 1 and cleaving its extracellular domain, thus leading to acantholysis within the epidermal granular layer. S. aureus can be cultured from fluid within the blisters of bullous impetigo, but not those of SSSS. Compared to non-bullous impetigo, the BitesTESbullous form is more likely to develop on clinically intact skin, especially in intertriginous sites.

Otitis externa and malignant ottitis externa - bacterial cause and clinical presentation - Treatment

Otitis Externa and Malignant Otitis Externa P. aeruginosa colonizes 1-2% of normal ear canals. However, acute pseudomonal infection can result in otitis externa ("swimmer's ear"). In this condition, the external auditory canal is swollen and macerated with a green, purulent discharge. The tympanic membrane is uninvolved, and manipulation of the pinna results in extreme pain. An exudative dermatitis of the external ear and retroauricular area may also be present. Treatment includes removal of canal debris, antibiotic eardrops (preferably those that cover S. aureus co-infection), and possibly the instillation of a cotton wick. Oral therapy is only occasionally required91. Malignant otitis externa is a severe variant that is seen most often in elderly diabetic patients and those with HIV infection or other immunodeficiencies. Manifestations include severe pain, persistent drainage, and the development of granulation tissue at the junction of the osseous and cartilaginous portions of the auditory canal. Local lymphadenopathy and parotid swelling may be present. Deeper invasion can result in osteomyelitis of the skull, nerve palsies, mastoiditis, sepsis, and sigmoid sinus thrombosis. Treatment includes extended courses of intravenous antipseudomonal penicillins or cephalosporins as well as oral ciprofloxacin; surgical intervention may be required92. Auricular chondritis secondary to Pseudomonas spp. has also been associated with piercing of the cartilaginous portion of the pinna93

More Cat Scratch Fever - Diagnosis - what stain can be used - Treatment

Pathology Affected lymph nodes display central necrosis surrounded by histiocytic and epithelioid cells with an inner palisading layer. Giant cells with a peripheral zone of lymphoid cells are also evident. The primary skin lesion can show similar changes, albeit less well developed. The Warthin-Starry silver stain demonstrates bacilli within areas of necrosis. Diagnosis and differential diagnosis For patients who present with regional adenopathy and a history of a recent cat scratch, the diagnosis is usually made clinically. A sensitive and specific assay for B. henselae antibodies is available, and antibody titers are usually high during the first few weeks after the onset of lymphadenopathy; PCR-based testing can also be performed. Culture is difficult and not routinely recommended103. Other causes of lymphadenopathy such as infections (bacterial, fungal or viral), reactive hyperplasia, drug reactions, or malignancy can be excluded by fine-needle aspiration histology or biopsy and culture of lymph node tissue. Treatment • Supportive care (analgesics) • Needle aspiration of painful suppurative lymph nodes • Azithromycin (antibiotic treatment is optional) • Clarithromycin • Rifampin

Erysipelas - Histology - Ddx - Treatment of choice

Pathology Biopsy specimens reveal diffuse edema and a neutrophilic infiltrate in the dermis. Dilation of the lymphatics, foci of suppurative necrosis, and dermal-epidermal separation are often seen. There is no primary necrotizing vasculitis, thrombosis, or leukocytoclasis. Diagnosis and differential diagnosis Diagnosis is based primarily on clinical findings. Laboratory evaluation shows an elevated leukocyte count with a left shift. Blood cultures are positive in only ~5% of cases. Although cultures from pustules or bullae may be helpful, the sensitivity of cultures of skin biopsy specimens is low, especially in immunocompetent hosts. Anti-DNase B and ASO titers are useful indicators of the streptococcal etiology. Direct immunofluorescence and latex agglutination tests can be used to detect streptococci within skin specimens. The differential diagnosis of erysipelas includes other forms of cellulitis and soft tissue infections (e.g. erysipeloid, necrotizing fasciitis) as well as inflammatory causes of "pseudocellulitis" (Table 74.10). Treatment A 10- to 14-day course of penicillin is the treatment of choice for erysipelas caused by streptococci. Although macrolides (e.g. erythromycin) may be used in penicillin-allergic patients, some strains of Str. pyogenes are macrolide-resistant. Erysipelas may recur in patients with abnormal local circulation (e.g. lymphedema), and penicillin prophylaxis is occasionally required36. The development of an effective vaccine against Streptococcus spp. could dramatically change the epidemiology of the infections caused by this microorganism

More Scarlet Fever - ddx and diagnosis - Treatment of choice, secondary treatment

Pathology Biopsy specimens reveal engorged capillaries and dilated lymphatics, most prominent around hair follicles. Dermal edema, perivascular neutrophilic infiltrates and small areas of hemorrhage represent additional findings. Spongiosis and parakeratosis are seen during the desquamative stage. Diagnosis and differential diagnosis Clinical diagnosis is usually not difficult. There is almost always an elevated leukocyte count with a left shift. Eosinophilia of 10-20% is often seen after 2-3 weeks of convalescence. Hemolytic anemia can occur, and mild albuminuria and hematuria may be present early in the disease. Nasal and/or throat cultures grow group A streptococci. Detection of antistreptolysin O (ASO) and anti-DNase B antibodies can also be useful in confirming the streptococcal infection. The differential diagnosis of scarlet fever may include a drug eruption, a viral exanthem, TSS, early SSSS, Kawasaki disease, and recurrent toxin-mediated perineal erythema. Infection with Arcanobacterium haemolyticum, a Gram-positive rod, can result in pharyngitis and a scarlatiniform exanthem in adolescents and young adults29. Treatment As with other group A streptococcal infections, penicillin (or amoxicillin) is the drug of choice; a 10-14-day course is usually sufficient. A clinical response can be expected within 24-48 hours. Antibiotic treatment as long as 10 days after the onset of symptoms will prevent the development of rheumatic fever. In penicillin-allergic patients, a first-generation cephalosporin (if no history of an immediate-type reaction), clindamycin, or a macrolide can be used; of note, some strains of group A streptococci are resistant to macrolides.

More Narcoiosis - treatment of choice?

Pathology Histologically, an intense neutrophilic infiltrate with abscess formation is seen. Sulfur granules are observed in Nocardia mycetoma but are absent in other forms of cutaneous nocardiosis. Organisms are not visible in routinely stained sections but appear as branching filaments on Gram stain. Nocardia also stains with methenamine silver and acidfast stains. Diagnosis and differential diagnosis Nocardia grows easily on all common laboratory media. However, the laboratory should be notified if Nocardia is suspected, because its growth is slow and specimens must be held for up to 2 weeks. Nocardiosis should be suspected in patients with sporotrichoid lesions or trauma-associated superficial cutaneous infections that do not respond to routine treatment. It should also be considered in patients at risk for opportunistic infections. Treatment Sulfonamides are the drugs of choice for nocardiosis. Minocycline is an effective alternative for sulfonamide-allergic patients, and linezolid may be added in resistant cases. For subcutaneous abscesses, surgical treatment is often required. Local forms of nocardiosis should be treated for 6-12 weeks, whereas immunocompromised patients and those with disseminated disease require 3-12 months of antimicrobial therapy

Perianal group A streptococcal infection - Clinical presentation, what other areas can be involved - Most commonly affects who? - Ddx - Treatment

Perianal group A streptococcal infection presents as sharply demarcated, bright erythema extending 1-3 cm around the anal verge (Fig. 74.10C); similar findings can extend from the vaginal introitus onto the vulva in girls and, less often, around the urethral meatus in boys. Patients may complain of pruritus or irritation; painful defecation or dysuria; and blood-streaked stools, soiling of undergarments due to anal leakage, or vaginal discharge. Systemic symptoms are generally absent. Children ages 2-7 years, especially boys (for perianal disease), are most commonly affected39a. Perineal infection may be preceded by symptomatic pharyngitis and is frequently associated with a positive pharyngeal culture for Str. pyogenes even in asymptomatic patients; patients often have family members with a recent streptococcal infection39a. Assessment for perineal streptococcal infection should be performed in children with an outbreak of guttate psoriasis39b. Other causes of perineal erythema or pruritus include contact dermatitis (irritant or allergic), S. aureus infection40, candidiasis, seborrheic dermatitis, pinworm infestation, inflammatory bowel disease, lichen sclerosus, child abuse, and the early phase of Kawasaki disease. Perineal streptococcal infection can be diagnosed with skin culture or group A streptococcal rapid testing, although the latter is less specific. In a randomized controlled study, a 7-day course of cefuroxime was found to be more effective than a 10-day course of penicillin in the treatment of perianal streptococcal disease

Pinta - cause - clinical appearance can mimic what dermatologic diseases?

Pinta affects the skin exclusively and is caused by an infection with T. carateum. The disease is found only in the western hemisphere (Central and South America) in semiarid, warm climates. All ages are equally affected. The primary lesions occur 7 days to 2 months after inoculation, most often on the lower extremities. They begin as tiny macules or papules surrounded by an erythematous halo. Over a period of months, they develop into poorly defined, erythematous, infiltrated plaques that measure 10-12 cm in diameter. Secondary lesions ("pintids") start as small, scaly papules, subsequently enlarging and coalescing into psoriasiform plaques. They are initially red but later become slate-blue, brown, gray, and black. The primary and secondary lesions are highly infectious. Tertiary pinta is characterized by symmetric depigmented, vitiligo-like lesions, which may be atrophic or hyperkeratotic and are not considered to be infectious. Biopsy specimens of primary and secondary lesions reveal moderate acanthosis, slight spongiosis, and a superficial dermal inflammatory infiltrate consisting of lymphocytes, plasma cells, and neutrophils around dilated blood vessels. Some lesions show lichenoid changes, with hyperkeratosis, hypergranulosis, and vacuolar degeneration of the basal layer. The depigmented lesions of late pinta have epidermal atrophy and a complete absence of melanin. Except for longstanding, late depigmented lesions, treponemes can be visualized in biopsy specimens with silver stains. Early pinta is difficult to differentiate from venereal syphilis, yaws, and endemic syphilis. The early lesions can also be confused with eczema, psoriasis, leprosy, lichen planus, lupus erythematosus, and tinea corporis. The lesions of late pinta are frequently mistaken for vitiligo

Pseudomonal Folliculitis - aka - underlying cause - treatment

Pseudomonal Folliculitis Pseudomonal folliculitis ("hot tub folliculitis") is associated with the use of whirlpools, hot tubs, and (less often) swimming pools with low chlorine levels; transmission from fomites such as nylon bath towels and rubber gloves has also been reported. Erythematous, edematous perifollicular papules and papulopustules arise 8-48 hours after exposure and resolve spontaneously in 7-14 days (see Ch. 38). The lesions frequently occur in sites covered by bathing suits, and the face and neck are usually spared. Associated symptoms (which do not reflect systemic spread of P. aeruginosa) may include pruritus, painful eyes, earaches, a sore throat, headache, fever, painful swollen breasts, malaise, rhinorrhea, nausea, vomiting, and abdominal pain. The diagnosis can be confirmed by isolation of P. aeruginosa, especially serotype O-11, from lesions. The differential diagnosis includes other forms of folliculitis (e.g. due to S. aureus) and papular urticaria. Treatment is generally not indicated in immunocompetent hosts, as it is usually a self-limited process. Warm compresses with 2% acetic acid and application of topical polymyxin B or gentamicin may be of benefit. In the case of widespread eruptions, recurrences, an immunosuppressed host, or associated systemic symptoms, an oral quinolone can be used9

what is Pseudomonal Pyoderma, clinical features What is blastomycosis pyoderma, clinical features, key histofinding Treatment of both

Pseudomonal Pyoderma and Blastomycosis-like Pyoderma Pseudomonal pyoderma is a superficial infection of the skin with P. aeruginosa. Features include a blue-green purulence, a "grape juice-like" or "mousy" odor, and a moth-eaten appearance of the skin. The borders are often macerated and eroded (Fig. 74.26). Pseudomonal pyoderma can complicate burns, decubitus ulcers, and other chronic cutaneous ulcers. Pseudomonal pyoderma often plays a role in Gram-negative toe web infections and in "infectious eczematoid dermatitis" on the hands and feet or in the anogenital region89. Blastomycosis-like pyoderma is a rare condition that presents as large verrucous plaques with multiple pustules and elevated borders. Histologic examination reveals pseudoepitheliomatous hyperplasia with intraepidermal abscesses; fungi are not seen, and fungal cultures are negative. This condition usually occurs in immunocompromised patients, and other bacteria (e.g. S. aureus) have also been implicated. Treatment of these conditions includes systemic antipseudomonal antibiotics, topical antimicrobial and drying agents, and debridement of the hyperkeratotic rim in web space infections. Additional treatment options for blastomycosis-like pyoderma include acitretin, surgical excision, electrodesiccation and curettage, and ablative laser therapy90

Pseudomonas hot foot syndrome - Cause and clinical presentation - ddx - Treatment

Pseudomonas Hot-Foot Syndrome Pseudomonas hot-foot syndrome occurs after swimming or wading in pool water that contains high concentrations of P. aeruginosa. The soles may be diffusely erythematous, and extremely painful, red-to-purple, 1-2 cm nodules develop on weight-bearing surfaces (Fig. 74.27); palmar involvement occasionally occurs. Systemic symptoms are uncommon. Histologic examination of the nodules shows perivascular and perieccrine neutrophilic infiltrates with microabscess formation. The condition is self-limiting and requires only symptomatic treatment. Idiopathic palmoplantar hidradenitis (see Ch. 39) has identical clinical features and may be pathogenically related to pseudomonas hot-foot syndrome. Additional diagnostic considerations may include pernio, symmetric lividities, and erythema nodosum95

Pyomyositis - What is it? - most common causative organism, other organims - occurs where, predisposing factors, clinical presentation - diagnosis, treatment

Pyomyositis Pyomyositis is a primary bacterial infection of the skeletal muscles that is most commonly caused by S. aureus. Other reported etiologies include: Str. pyogenes, Str. pneumoniae, Escherichia coli, Yersinia enterocolitica, and H. influenzae as well as mycobacteria and fungi; polymicrobial infections can also occur in immunocompromised patients45-47. Once referred to as tropical myositis, it also occurs in temperate climates. Predisposing factors include trauma, diabetes mellitus, HIV infection, injection drug use, and other forms of immunosuppression. Patients often present with a 1-2-week history of low-grade fevers, myalgias, and progressive firmness, pain, and enlargement of a deep soft tissue mass. Palpation of the affected area reveals "woody" induration. Muscle abscess formation occurs during the second stage of disease, and septicemia may follow. MRI is the diagnostic modality of choice for the early disease; ultrasound-guided aspiration may be helpful later in the course. Treatment of staphylococcal pyomyositis includes incision and drainage as well as appropriate intravenous antibiotics until clinical improvement is noted, followed by oral therapy for a total of ≥3 weeks48.

MRSA macrolide resistance - Three causes - If an organism comes back resistant to erythromycin, it will have inducible resistance to what other drug?

Resistance to macrolides (e.g. erythromycin) in staphylococci may result from: (1) active drug efflux via a pump encoded by the msrA/msrB gene (frequent in MRSA isolates); (2) synthesis of macrolide-inactivating enzymes; or (3) modification of the bacterial ribosome by the erythromycin ribosomal methylase encoded by erm genes, which produces cross-resistance to clindamycin16. Erythromycin stimulates expression of erm, which leads to clinically relevant resistance. If initial sensitivity testing shows resistance to erythromycin and susceptibility to clindamycin, resistance to clindamycin will still develop if erm is present, since bacterial variants with constitutive expression of this gene commonly arise and are selected for during clindamycin therapy. This "inducible resistance" can be assessed with the D-test (double-disk diffusion)

Rhinoscleroma - what is it? caused by what organism - endemic to what areas - how is it acquired - key histopath findings - treatment

Rhinoscleroma Rhinoscleroma is a slowly progressive, chronic granulomatous infection involving the nose and upper respiratory tract. It is caused by Klebsiella rhinoscleromatis, a short, immotile Gram-negative coccobacillus that is a subspecies of Klebsiella pneumoniae. Endemic foci exist in Central Europe, Egypt, India, Indonesia, Mexico, Central America, and tropical Africa117. Rhinoscleroma is acquired via inhalation of contaminated droplets. Deficiencies of cellular, but not humoral, immunity cause ineffective phagocytosis by macrophages, giving rise to large, vacuolated, non-lipidized histiocytes with intracellular bacteria (Mikulicz cells)118. clinical Features: Stage one: rhinitic/ catarrhal/atrophic • Nonspecific rhinitis • Purulent rhinorrhea and crusting • Nasal obstruction Stage two: granulomatous/infiltrative/ hypertrophic • Granulomatous nodules form in the nose, pharynx, and larynx • Dysphonia, anosmia, and anesthesia of soft palate may occur • Epistaxis, deformity of the nose, destruction of the nasal cartilage (Hebra nose) Stage three: sclerotic/ cicatricial • Nodules replaced by fibrous tissues with resultant extensive scarring and stenosis often requiring surgical intervention (e.g. tracheotomy, reconstruction of the airway) Treatment • Antimicrobial therapy for 6 months or until nasal biopsy is negative; tetracycline is first-line therapy along with surgical correction of obstructed airway • Rifampin and ciprofloxacin are alternative antibiotics • Sclerotic lesions respond to ciprofloxacin • Bacterial superinfection is common, requiring treatment with clindamycin or a third-generation cephalosporin

Bacterial Folliculitis - Most common agent - what about gram negative and pseudomonas? - Treatment - How can you decolonize staph?

S. aureus is the most common infectious cause of folliculitis (see Ch. 38). Gram-negative folliculitis occasionally develops in acne vulgaris patients treated with prolonged courses of oral antibiotics. In addition, pseudomonal folliculitis can result from the use of improperly chlorinated hot tubs and whirlpools. Treatment: Superficial staphylococcal folliculitis can be treated with antibacterial washes that contain chlorhexidine or sodium hypochlorite. Topical antibiotics such as mupirocin or clindamycin may also be used for 7-10 days to treat localized lesions. When staphylococcal folliculitis is widespread or recurrent, oral β-lactam antibiotics (e.g. a β-lactamase-resistant penicillin or first-generation cephalosporin), tetracyclines, or (depending on local resistance patterns) macrolides can be prescribed (see Table 74.3). Although pseudomonal folliculitis is often self-limited, ciprofloxacin is an option for more severe cases. In patients with recurrent staphylococcal folliculitis and their close contacts, application of mupirocin 2% ointment twice daily to the nares for 5-10 days can be used to eradicate nasal carriage of S. aureus; methods to decolonize the skin (e.g. axillae, perineum/groin, submammary area) include topical mupirocin, washes containing chlorhexidine or triclosan (OTC product banned in the US), and dilute sodium hypochlorite baths (e.g. 0.5 cup household bleach [6-8.25% sodium hypochlorite] in a full standard bathtub). Elimination of bacterial contamination of potential fomites such as keyboards, toys, and sports equipment (e.g. shoulder pads, wrestling mats) should also be considered, e.g. by using ethanol- or sodium hypochlorite-based disinfectants.

Salmonellosis - What are the two types of salmonella. How is each acquired - what are some cutaneos manifestations of non-typhoidal salmonella - Treatment

Salmonellosis refers to the spectrum of infections caused by Gramnegative aerobic bacilli in the genus Salmonella. Enteric fever due to S. typhi is known as typhoid fever, and a similar clinical syndrome of enteric fever produced by non-typhoidal strains such as S. paratyphi is referred to as paratyphoid fever. S. typhi is spread via direct contact with persons who have typhoid fever or are chronic carriers. In contrast, non-typhoidal Salmonella is most commonly acquired from inadequately cooked poultry or eggs as well as other contaminated food products or water, resulting in gastroenteritis. Typhoid fever is characterized by fever, headache, malaise, myalgias, cough, sore throat, nausea, vomiting, diarrhea, and constipation. The characteristic cutaneous sign, "rose spots", are pink, blanching, slightly elevated papules that measure 2-8 mm and are usually found on the anterior trunk in groups of 5-15 lesions. They occur in up to 30% of patients with typhoid fever and less often in non-typhoidal enteric fever. Rose spots often occur in crops during the second to fourth weeks of the illness, and Salmonella spp. can usually be cultured from these lesions. Other cutaneous manifestations of salmonellosis include erythema multiforme, Sweet syndrome, hemorrhagic bullae, pustular dermatitis, and a generalized erythematous eruption known as erythema typhosum. A history of travel to endemic areas (e.g. Southeast Asia, South America), persistence of fevers, and positive cultures aid in distinguishing typhoid fever from influenza and other viral infections. Culture of Salmonella spp. from the bone marrow is the most sensitive diagnostic procedure but is rarely used in clinical practice. Blood cultures are less sensitive and PCR-based detection is limited by the low concentrations of microbial DNA in clinical samples121. Since the late 1980s, S. typhi has developed resistance to all the drugs that were then used as first-line treatments (chloramphenicol, TMP-SMX, and ampicillin). Current treatment options include quinolones for susceptible strains (with resistance most common in South Asia), ceftriaxone, and azithromycin. Third-generation cephalosporins are the treatment of choice in children

Strep Intertrigo - usually affects who? - clinical presentation - Treatment of choice

Streptococcal Intertrigo Intertrigo caused by group A streptococci is an under-recognized entity that usually affects infants and young children37. Infants are particularly vulnerable due to irritation and friction in moist, deep skin folds of the neck, axillae, antecubital and popliteal fossae, and inguinal region. Sharply demarcated, intensely erythematous patches or thin plaques are observed in an intertriginous site, often accompanied by a foul odor. In contrast to intertriginous candidiasis, satellite lesions are uncommon. Affected children occasionally exhibit irritability, low-grade fevers, and Str. pyogenes bacteremia. In genetically predisposed children, cutaneous streptococcal infection may trigger psoriasis30a,38. Bacterial culture can confirm the diagnosis, which should be considered when simple intertrigo fails to respond to barrier creams and other measures to reduce friction and minimize moisture. A 10-day course of oral penicillin or amoxicillin is usually effective

MRSA Pathogenesis - what gives methicillin resistance? - two types

The cause of methicillin resistance is the production of an altered penicillin-binding protein 2a (PBP2a) that has decreased affinity for β-lactam antibiotics, which interfere with bacterial cell wall synthesis by binding to PBPs. PBP2a is the protein product of the mecA gene, which is located within a specific mobile genetic element called the staphylococcal cassette chromosome mec (SCCmec). Acquisition of different SCCmec elements by S. aureus led to the emergence of HA-MRSA (usually SCCmec types I-III) and CA-MRSA (usually SCCmec types IV and V) strains; methicillin-resistant coagulasenegative staphylococci are thought to represent a reservoir of SCCmec for CA-MRSA. Many CA-MRSA strains also encode virulence factors such as Panton-Valentine leukocidin (PVL), a pore-forming cytotoxin that can cause destruction of leukocytes and tissue necrosis. As a reflection of their distinct SCCmec elements, CA-MRSA and HA-MRSA have different patterns of antibiotic resistance. CA-MRSA is typically susceptible to multiple non-β-lactam antibiotics, whereas HA-MRSA is usually resistant to several antimicrobial classes, including aminoglycosides, macrolides, and clindamycin. However, some isolates of the USA300 clone, which currently causes most CA-MRSA skin infections in the US, have developed resistance to macrolides, clindamycin, tetracycline (less often doxycycline), quinolones, and mupirocin15.

Vibrio Vulnificus - infection typically occurs after exposure to what? - skin findings?

The genus Vibrio constitutes a group of Gram-negative anaerobic bacteria, among which V. vulnificus is the most common cause of cutaneous disease. V. vulnificus infections occur most commonly in men over 40 years of age who have chronic liver disease, diabetes mellitus, or immunosuppression plus a history of exposure to warm seawater or raw/undercooked seafood. Additional risk factors are listed in Table 74.16. The clinical presentation of V. vulnificus septicemia includes fever, chills, nausea, vomiting, diarrhea, abdominal cramps, and hypotension. Skin lesions develop in 75% of these patients, with progression from erythematous and purpuric macules to vesicles and hemorrhagic bullae (Fig. 74.33) and then to necrotic ulcers in a manner reminiscent of purpura fulminans. Wounds acquired in or contaminated by seawater can also lead to Vibrio cellulitis that is erythematous, edematous, and painful, typically with rapid evolution to hemorrhagic bullae.

Cellulitis treatment - Antibiotics of choice

Treatment Treatment of cellulitis is typically targeted against group A streptococci and S. aureus. For uncomplicated cases, a 10-day course of an oral antibiotic that covers these organisms (e.g. dicloxacillin, cephalexin, or clindamycin) is appropriate. Hospitalization and parenteral antibiotics may be necessary for patients who are seriously ill, have facial involvement, or fail to respond to oral therapy. If MRSA is suspected, e.g. when there is cellulitis in association with an abscess, agents such as clindamycin, TMP-SMX or doxycycline should be used (see Table 74.5); if group A streptococcal infection is also a possibility, the latter agents should be combined with a β-lactam. Diabetic or decubitus ulcers complicated by cellulitis require broad-spectrum coverage, such as piperacillin/tazobactam or, in penicillin-allergic patients, metronidazole plus ciprofloxacin. Adjunctive measures include immobilization and elevation of an affected extremity and the application of wet dressings to areas with bullae or exudate. If signs and symptoms do not improve after 36-48 hours of treatment, cultures and susceptibilities should be obtained and antibiotics adjusted accordingly. NSAIDs may mask the signs and symptoms of deeper necrotizing infections and should be avoided when treating cellulitis. Prophylactic low-dose penicillin has been shown to decrease the risk of recurrent lower extremity cellulitis; however the protective effects diminish upon discontinuation of therapy44. The clinical features and treatment of other types of cellulitis (e.g. Erysipelothrix rhusiopathiae, Vibrio vulnificus) are discussed below.

Trichomycosis - what is it? - Clinical presentation - woods lamp exam - ddx - Treatment

Trichomycosis is a superficial corynebacterial infection that results in concretions on the shafts of axillary and less often pubic hairs; occasionally scalp hairs in infants are affected. The hair shafts develop adherent yellow, red, or black nodules or cylindrical sheaths that can be seen with the naked eye (Fig. 74.21). Dermoscopic examination enhances identification of these flame-like concretions. There is a characteristic odor, and the sweat occasionally takes on a red color and stains clothing. However, like pitted keratolysis, the condition frequently goes unnoticed. Wood's lamp examination reveals a pale yellow fluorescence, and Gram staining of the concretions shows Gram-positive rods. The differential diagnosis includes white piedra, black piedra, nits, and hair casts (see Ch. 77). Shaving the affected hair provides an instant cure, and use of antimicrobial cleansers can prevent recurrences. Additional treatment options include benzoyl peroxide and topical erythromycin or clindamycin59.

Non venerial treponematoses - refers to what diseases that have what cause? - transmission - treatment of yaws?

Yaws, pinta, and endemic syphilis (bejel) are caused by organisms that are morphologically and antigenically identical to the causative organism of venereal syphilis, Treponema pallidum (see Ch. 82). All three diseases have chronic relapsing courses with major dermatologic manifestations. The primary route of transmission is person-to-person via skin, mucous membrane, or possibly fomite contact. With the exception of pinta, children are most often affected. The diagnosis of yaws, pinta, and endemic syphilis is based primarily upon clinical features. The same serologic assays used for venereal syphilis can be used to diagnose the endemic treponematoses, but a positive test does not differentiate among the four diseases. Treponemal tests (e.g. TPHA, FTA-ABS, MHA-TP) are specific for treponemal infections (see Ch. 82) and may remain positive for life, regardless of treatment. The non-treponemal tests (e.g. VDRL, RPR) may indicate a current or recent infection, or a biologic false-positive result (in 1-3% of the population). The vast majority of false-positive sera have antibody titers of <1 : 4. The quantitative non-treponemal tests are particularly useful in the evaluation of patients following therapy; a fourfold decrease in antibody titers indicates successful treatment, while a fourfold rise indicates reinfection or relapse. Diagnosis can also be made through darkfield examination of exudates from lesions. For over 50 years the primary treatment for patients with endemic treponematoses was benzathine penicillin, given as a single intramuscular dose of 1.2 million units in individuals ≥10 years of age and 0.6 million units in children <10 years of age. More recently, a single high dose of oral azithromycin (30 mg/kg, maximum 2 g) was shown to be non-inferior to benzathine penicillin for the treatment of yaws. Due to the ease of administration and safe use in patients with penicillin allergy, azithromycin is now recommended as the first-line treatment for yaws by the WHO, with goals of mass treatment and disease eradication (see below)133,133a. Surveillance for treatment failure and resistance is ongoing, considering the development of azithromycin resistance by venereal syphilis134. To date, no formal trials have studied azithromycin efficacy for pinta and endemic syphilis.