Skin Flashcards
Bacillus anthracis
* Pathogen category: G+ rods, aerobic, extracellular * Source: herbivores and their skin products * Virulence: endospore formation; capsule; exotoxin * Clinical: cutaneous anthrax form spores; respiratory anthrax if spores inhaled; eschar surrounded by edema * Immune response: Igs to opsonize the capsule * Treatment/Prevention: ciprofloxacin; alternative doxycycline; vaccine for military
Otherpathogens can do damage through their endospores(white powder in mailbox)
Bacillus anthracis, anthrax, is a Gram+rod that is an aerobic spore former. Spores, traditionally associated with infected animal products, may germinate bacteria that cause a cutaneousform of the disease notable for escharsurrounded by edema (from lethal and edema toxins, respectively). Ciprofloxacin would be an appropriate response to this and the pulmonary form.Exposure history is usually found with infected goat hairs, toxins with cutaneous lesion, edematous, eschar(kills of tissue), edema(adenylyl cyclase), and lethal. (shut down ribosome).
Bartonella henselae
* Pathogen category: G- rods, aerobic, intracellular * Source: zoonotic transmission from cat scratches or bites * Virulence: endotoxin * Clinical: cat scratch fever; bacillary angiomatosis (invade endothelial cells and trigger proliferation of blood vessels) in ICP * Immune response: cell mediated with CTLs * Treatment/Prevention: erythromycin or doxycycline; azithromycin alternative * Triggers localized lymphadenopathy (response in lymph nodes)
Bartonellacan be a genus of Gram-coccobacillusrodsrecognized under particular circumstances, e.g., arthropod vector exposure, as the pathogen can persist in RBCs. In contrast to a cat bite and Pasteurella, Bartonellahenselaeand cat-scratch fevertends to trigger a localized lymphadenopathy in immunologically intact individuals, where the organism is cleared. Not a local cellulitis patternthat is fought on the lymph nodes and can clear up on its own depending upon immunologic intactness with hematogenousspread to various areas and those with immunocomrpomisedinvades endothelial cells and response developing angioma(inflammatory response to the pathogen)
If there is free multiplication of Bartonellaorganisms, they can invade endothelial cells and trigger proliferation of blood vessels, leading to the appearance of bacillary angiomatosisin AIDS patients (treated by clarithromycin or azithromycin for 3 months or longer, Sanford Guide 2019).
Clostridium perfringens
* Pathogen category: G+ rod, anaerobe, extracellular * Source: soil * Virulence: endospore formation, enterotoxin, lecithinase (lead to cell death and gas production) that lyses cell membranes * Clinical: gas gangrene, self-limiting food poisioning * Immune response: antibodies formed to toxins * Treatment/Prevention: wound debridement, hyperbaric oxygen, penicillin
Clostridium perfringens:a colonic inhabitant seen in gas gangrene. Gas gangrene is a result of a number of toxins, with lecithinaseleading to cell death and gas production. Surgical debridement is essential, as is coverage for the anaerobic Gram positive rods, e.g., clindamycin and penicillin. In particular, the clindamycin with its anti-ribosomal function can help to decrease the toxin production. Crepitintissue and anaerobic smell, serosanginous,purulent flud. Gram postiiverods destroyed by enzymes that destroy cell membranes needed debridement.
Clostridium tetani
* Pathogen category: G+ rod, tennis racquet shaped, obligate anaerobe, extracellular * Source: soil * Virulence: endospore formation, tetanus toxin that inhibits glycine and GABA * Clinical: tetanus with spastic paralysis (blocks NT) * Immune response: antibodies to toxin * Treatment/Prevention: antitoxin, wound debridement, metronidazole, TDaP (toxoid vaccine); penicillin, doxycycline
Clostridium tetani, tetanus, does not lead to changes in skin appearance per se, but is well-known for the toxin tetanospasminthat blocks inhibitory neurotransmitters, leading to a seur
icparalysis. Immunoglobulin and tetanus toxoid (generated from a denatured toxin) are used depending on the extent of the wound. If actively infected, then penicillin, doxycycline, or metronidazole can be added as well following wound debridement (Sanford Guide 2019). Not releasing inhibitor glycine devleopingcontraction, spasmingdefinitive. Active infection no antibody response giving them passive immunization against toxin and heavy dose of gram positive coverage.
Erysipelothrix rhusiopathiae
* Pathogen category: G+ rod, aerobic, extracellular * Source: animal (fish, rotting organic matter) handling with abraded skin * Virulence: capsule, neuraminidase * Clinical: erysipeloid local skin infection (painful subacute cellulitis with not much swelling and distinctive purplish tone); occasionally bacteremia and endocarditis * Immune response: phagocytosis if opsonized * Treatment/Prevention: penicillin
Erysipelothrixrhusiopathiaeis an aerobic G+ rod that can present from animal (farm animals, fish) exposure from handling with abraded skin. This generates a painful subacute cellulitis with not much swelling and a distinctive purplish tone.
Mycobacterium leprae
* Pathogen category: acid-fast bacillus, obligate aerobe, intracellular * Source: human reservoir (armadillos) * Virulence: acid-fast status with preference for lower temperatures * Clinical: leprosy (invades skin cells and nerves) * Immune response: granuloma formation effective * Treatment/Prevention: prolonged (24 month) multidrug therapy (clofazimine, dapsone, rifampin) * Tuberculoid leprosy- vigorous cell mediated response to the bacterium with Th1 cells; local numb patch * Lepromatous leprosy- weak cell mediated experiences with vigorous cell mediated immune response with more Th2 cells helping to down-regulate the CMI; infecting neurons so the immune system doesn’t want to go after it; more “classic” appearance of leprosy * Slow growth and long incubation period
Mycobacterium lepraeis an acid-fast bacterium (so slow-growing, aerobic) agent that causes leprosy. M.lepraeis not very infectious as it invades skin and nerves (e.g., thickened ulnarn. that can lead to ulnar palsy) as these mycobacteria proliferate in Schwann cells as well as macrophages. Prefers cooler environments of neurons and skin(skin deep and local nerves) happy and granulomatouslyrestraining it. Lepromatouspicture not good cell-mediated response due to its location in neurons utilizing IL10 and TH11 more skin infections from numb waxing skin human to human contamination with a slow cutaneous nasal spread taking months to years for contagious along with 2 years of clearance. Characterized by numbenessof the location trying to catch it before It turns bad.
If a patient experiences a vigorous cell-mediated response to the bacterium with Th1 cells, they will demonstrate tuberculoid leprosy.
A weak cell mediated immune response, with more Th2 cells helping to down-regulate the CMI, leads to the more classic lepromatousleprosy lack of TH1 activity.
That purely Th1 vs. Th2 pattern of response to leprosy is being challenged by a paradigm of additional Th17 and other Th cell types, with varying levels of Tregcells and TGF-beta being generated by the infection to account for the different patterns of leprosy expression.
The long incubation period, the slow growth, and the drug resistances leads to TB-like treatment patterns. Rifampin is used in conjunction with dapsone (interferes with folate synthesis pathway) and clofazimine (anti-DNA synthesis and with anti-inflammatory features;
Mycobacterium marinum
* Pathogen category: acid-fast bacillus, obligate aerobes, intracellular * Source: chronic exposure to water, fish * Virulence: acid fast status with preference for lower temperatures * Clinical: fish tank granulomas * Immune response: granuloma formation * Treatment/Prevention: surgical incision and subsequent 1-2 months of clarithromycin or rifampin+ehtambutol
Mycobacterium marinumis a slow growing pathogen associated with water and marine life exposures, such that with abraded skin, the mycobacterium can become established and in several week, enlarging papules may emerge that can persist and ulcerate. Histologically, these are granulomas.
Propionibacterium acnes
* Pathogen category: G+ rod, anaerobe, extracellular * Source: normal skin flora * Virulence: lipase can trigger inflammation secondary to sebum metabolism * Clinical: acne vulgaris (androgens and sebum production leads to folliculitis) * Immune response: inflammatory response with neutrophils * Treatment/Prevention: benzoyl peroxide (antibacterial, oxidizes- breaks down keratin, and anti-inflammatory) for topical effect, topical clindamycin or erythromycin (combination therapy), systemic doxycycline (antibiotic for G+); isotretinioin (decrease sebum production) * Open comedones- melanin in sebum can oxidize, blackheads; closed comedones- whiteheads
Propionibacterium acnesis an anaerobic Gram positive rod that is part of the normal flora, that under certain (hormonal) conditions, where androgens and sebum production are increased, can lead to a folliculitis. Thelipasethat is part of P. acnescan be triggered to create an inflammation from the sebum associated with the hair follicle, i.e., acne vulgaris.Open comedones, where the melanin in sebum can oxidize, are blackheads, in contrast to closed comedones, or whiteheads. Breaking down fatty acids, proliferation of bacteria itself develop inflamed pathogen and acne pathway.
Clindomycin- gram positive and anaerobic specialization coverage,
Benzoylperoxide (benzoic acid) is antibacterial, oxidizing (so breaking down keratin), and anti-inflammatory. A topical antibiotic, such as clindamycin or erythromycin, can be used as combination therapy. Doxycycline is a typical oral antibiotics for acne treatment Gram positive coverage (Sanford Guide 2019).Isotretinoin is an agent that decreases sebum production and regulates epidermal cell proliferation for severe acne.
Staphylococcus aureus
* Common cause of osteomyelitis- slow blood flow, vertebrae most commonly affected in adults; hemotogenous spread from single pathogen but extending to skin lesion is usually polymicrobial (blood culture before initiating treatment). While we think of slowed blood flow in the metaphysis of long bones as the most common process in children, vertebrae will be the most commonly affected in adults. Those infections that arise from hematogenous spread are more likely to be from a single pathogen, whereas osteomyelitis extending from a skin lesion (like decubiti) could be polymicrobial. As a result, blood (or if need be, bone) cultures are helpful before initiating treatment. Due to direct innoculation from broken leg, or hematogenous spread as the bone blood flow is slow meaning that it takes a long time for the bacteria to increase in amount meaning it takes a long time for the antibiotics to get to it and clear. Periosteum usually generative cells but reactive affect with bulging under the periosteum * Endocarditis- adheres to the valves and destroys tissue. a major concern with respect to endocarditis (Establishment of infection on the mitral valve, activating the surface and develop a vegetative plug can get large developing a mix of fibrin, platelets, and spraying the mixture throughout the blood stream creating surface features of thromboemboli on the surface) ). e.g., why oral streptococci may be a problem following dental procedures, although recent American Heart Association guideline modifications have limited the recommended circumstances for antibiotic prophylaxis, e.g., to those with prosthetic heart valves. * Pathogen category: G+ coccus, aerobic, extracellular, in clusters * Source: nasal carriage, skin, nosocomial * Virulence: multiple exotoxins, coagulase (generate the fibrin crust), hemolysins (breakdown blood, easy food source), TSST superantigen, enterotoxin, PVL (leucocidin), Protein A (grabs Fc part of Igs * Clinical: boils, rapid onset food poisoning, osteomyelitis, infectious arthritis, endocarditis, toxic shock * Immune response: opsonize with complement or IgG, then phagocytosis with neutrophils * Treatment/Prevention: MRSA-type drugs (community or hospital acquired- distinction from gene origin of the altered transpeptidase) * TSST-1 (toxic shock syndrome toxin 1)- responsible for desquamation in TSS o Superantigen stimulation can lead to TSS and presentation of erythema and desquamation * Scalded skin syndrome- exfoliative toxin targets the cell junctions in the epidermis; hemotogenous spread that gives the appearance of that bulla
Staphylococcus epidermidis
* Pathogen category: G+ coccus, aerobic, extracellular, in clusters * Source: normal flora skin * Virulence: glycocalyx, forms biofilm like adhesions * Clinical: bacteremia/sepsis/endocarditis from infected catheters/needles/artificial valves * Immune response: opsonize with complement, then phagocytosis with neutrophils * Treatment/Prevention: typically MRSA-type drugs; no long term immunity * Coagulase negative
S. epidermidisis a Gram positive , coagulase-negative cocci that forms in clusters, like other staphs, and is the most common skin bacterium. It is known as a biofilm-forming organism, thereby leading to infection in the context of indwelling prosthetic surfaces. Catalase negative, coagulase negatives, epidermal colonizers. Don’t produce toxins but produce biofilm particularly on artifficalsurfaces(prosthesis, valve, pacemaker)- staph. Aureus if right away, or several weeks later smoldering pathogenic is s. epidermidis creating biofilm in structure
herpes simplex (HSV-1, -2)
* Pathogen category: enveloped ds linear DNA virus * Source: human reservoirs * Virulence: infectivity through contact * Clinical: herpes; usually local but can be widespread * Immune response: cell mediated for clearance of epidermis, control in sensory neuron * Treatment/Prevention: avoidance; acyclovir, valacyclovir
human herpesvirus 6, 7 (HHV-6,7; roseola)
* Pathogen category: enveloped ds linear DNA virus * Source: human reservoir * Virulence: infectivity through respiration * Clinical: roseola (high temp-convulsion, rash, lack of resp findings) * Immune response: cell mediated for clearance * Treatment/Prevention: symptomatic treatment (short lived) * Replicates in WBC and salivary cells * Fever from infection of CD4 cells and trigger cytokines (TNF and IL-1) * Latent in bone marrow cells
Herpes virus: HHV-6: roseolainfantum: high temperature (may trigger convulsions), and subsequent rash in childhood, with lack of accompanying respiratory findings, as the virus first replicates in WBCs and salivary cells. The high fever can stem from its infection of CD4 cells and trigger cytokines such as TNFα and IL-1 to cause symptoms in the primary infection. Not surprising, given that it is a herpesvirus, it can remain latent in bone marrow cells (and so potentially reactivate in immunocompromised individuals). For most is a childhood response, cell-mediates response or have such a low level that it wont perk back up. Don’t always hide out in neurons (EBV- hide out in lymphocytes)
human herpesvirus 8 (HHV-8; Kaposi sarcoma)
* Pathogen category: enveloped ds linear DNA * Source: human reservoirs * Virulence: infectivity through saliva * Clinical: Kaposi sarcoma (vascular tumor with purple coloring from RBC collections); associated with low CD4 counts * Immune response: cell mediated * Treatment/Prevention: antiretroviral therapy
Herpesvirus: HHV-8: Kaposi sarcoma (KSHV, Kaposi sarcoma human herpes virus), a vascular tumor with its purple coloring from RBC collections, that may proliferate internally as well as on the skin. Many of the standard immunologic factors triggered by HIV infection, e.g., fibroblast growth factors, can stimulate this proliferation, and ongoing loss of CTLs and NK cell activitywith AIDS can lead to the tumors of spindle cells with presumably endothelial/mesenchymal origin.
Rare illness in older mediaterraneanpeople from low CD4minimizing coverage and immunity. More widespread and subclinical and with AIDS targettingCD4 counts rather than supressionleading to proliferating getting endothelial smooth muscle tumors on the skin and within internal organs. Prevelantin the 80s and AIDS defining condition.
human papilloma virus (HPV)
* Pathogen category: undeveloped ss DNA * Source: human reservoir * Virulence: “low profile” invasion of basal epithelial cells * Clinical: warts, gential warts, cervical cancer; keratinized verricous lesions * Immune response: cell mediated clearance * Treatment/Prevention: removal (cryotherapy or calicylate application); vaccine for genital wat/cervical cancer strains (16 and 18)
Papillomavirusesare nonenvelopedDNA viruses. Wartscan take a variety of forms, depending on the genotype of papilloma virus, and may trigger cervical cancer as the high risk strains can integrate into the host genome. The currently available 9-valent Gardasil®vaccine covers types 6, 11 (genital warts) and 16, 18 (cervical cancer), in addition to five other strains associated with cervical cancer.
Warts are familiar as keratinized verrucous lesions. Human papillomavirus(HPV) targets basal epithelial cells, and replicates its genome in low numbers. As infected cells progress through the layers, viral genes keep the epithelial cells proliferating, so that both more viral DNA and now viral proteins are synthesized, creating the familiar warty patterns seen in this slide. Anogenitalwarts can develop into cervical cancer with a couple strains as it slowly circualtesin basal layer are oncogenic and insert themselvesinto genome of basal cell (16 &18) not a targettedinsertion and can cause cancer
molluscum contagiosum
* Pathogen category: enveloped ds linear DNA * Source: human reservoir * Virulence: infectivity through contact (sexual contact in adults); inclusion bodies of collected viral material * Clinical: mollscum contagiosum (widespread in ICP); wart like tumor (unbilicated) * Immune response: cell mediated for clearance; reinfection can occur * Treatment/Prevention: spontaneous clearance
Molluscumcontagiosumforms a distinctive wart-like tumor that is slightly cratered. (umbilicated) These may need to be removed, as they can persist for months. The virus is spread by close contact, and is preferentially controlled by cell-mediated (as vs. humoral) immunity. proliferate in cytoplasm leading leftover viral particles (not virions and shed)-the inclusion bodies are collected of viral materials, typically capsid proteins. Low CD4 counts. can scrape them out to get the wholething if surgical needed particularly common in children with contact by hands as the spread.
parvovirus B-19 (fifth disease, erythema infectiosum
* Pathogen category: unenveloped ss linear DNA * Source: human reservoir * Virulence: infectivity through respiration * Clinical: fifth disease (erythema infectiosum) (antigen-antibody complex formed and infection of erythrocyte precursor cells) * Immune response: cell ediated for clearance * Treatment/Prevention: self-limiting; IgG protection after infection * More impacting if there is a RBC condition (sickle cell, chemo)
Parvoviruses (unenvelopedvirus)are unusual in that they are ss DNA. The “slapped cheek” rash of fifth disease(erythemainfectiosum) from parvovirus B19 and subsequent confluent rash (and occasional joint pain) stems from the immune response to the infection and generation of antigen-antibody immune complexes, and infection of erythrocyte precursor cells, e.g., an aplastic anemia crisis seen in sickle cell anemia patients with viral cytopathic destruction of those cells. No vaccine is available. Looks to settle down in bone marrow and attacks erythroblasts thorughhemategnousspread, which can produce humoral antibody resposnenot letting it get to the bone marrow, rash and joint bone depending upon where complexes settle. Common in children, can develop slight anemia. However, someone with sickle cell, or chemo reactivated and can really impact these particular populations.
Smallpox
* Pathogen category: enveloped ds linear DNA; double-membrane capsule, DNA dependent RNA polymerase; replicated in cytoplasm * Source: human reservoir * Virulence: infectivity through close contact when rash is present * Clinical: smallpox (following asymptomatic viremia and a febrile prodrome of fever and malaise pt generates maculopapular rash) * Immune response: cell mediated and neutralizing antibodies * Treatment/Prevention: vaccine (live-virus), vaccine for military, officially extinct in 1980 (bioterroism) Mortality- viral cytopathic damage (necrosis, inflammation and hemorrhage) Monkeypox in Midwest in 2003 Virus-8) varicella-zoster (VZV)
Thepoxvirusesare large, complex viruses, containing an unusual disk-shaped, double-membraned capsule, and a DNA-dependent RNA polymerase, as the virus replicates in the cytoplasm, (not the nucleus, which the herpesviruses do). Replicate more in cytoplasm than nucelus, phase where there is an epithelial presnce.
Although officially eliminated in 1977 (there was a lab case in 1978), smallpoxremains as a possible bioterrorismthreat. Following an asymptomatic viremia and a febrile prodromeof fever and malaise, the patient generated a maculopapular rash that becamevesicular, then pustular, before crusting and leaving scars. Mortality was associated with viral cytopathic damage, and hence, necrosis, inflammation, and hemorrhageleading to scarring if more deep seeded than chicken pox.
There was an outbreak of the related monkeypoxvirus in 2003 in the upper Midwest following importation of exotic rodents from Ghana (monkeypoxis on the NYS notifiable conditions list as a result).; there isan ongoing outbreakin Nigeria with over 300impacted to date, postural pox virus.
Varicella-Zoster (VZV)
* Pathogen category: enveloped ds linear DNA virus * Source: human reservoir * Virulence: infectivity through aerosol * Clinical: chicken pox (reticuloendothelial system spread, vesicules/pustules), zoster (shingles ( Zoster(shingles): a dermatome-dependent reactivation of the virus, with a vaccine recommended for older adults. In distribution of trigeminal nerve can cause problems into rapidly proliferative epithelial disease), dermatome dependent reactivation) * Immune response: cell mediated for clearance in epidermis, control in sensory neuron * Treatment/Prevention: live vaccine; acyclovir, valacyclovir if needed; varicella-zoster immune globulin (VZIG) as needed for ICP prophylaxis following exposure
VZV(varicella-zoster virus) is another herpesvirus, withasimilar latency pattern and skin eruption. The respiratory spread of VZV along with carriage by the reticuloendothelialsystem helps to generate the systemic illness of chickenpox, with vesiculesand pustules at different stages of development. A live attenuated vaccine helps to decrease the severity of the illness, and decrease the likelihood of zoster.
Candida albicans
* Pathogen category: yeast * Source: normal skin flora * Virulence: cell wall * Clinical: local infection (thrush, vaginitis) spread with ICP or antibiotic-induced decrease of bacterial flora * Immune response: delayed type hypersensitivity; lost with ICP * Treatment/Prevention: thrush- clotriamzole troche, nystatin suspension; fluconazole for oral therapy; capsofungin if serious systemic illness * Usually in areas of high friction (intertrigo; like armpits)
Therecan be a variety of fungal infections on the skin as well. For example, Candidaalbicansis a fungus in yeast form. As a member of the normal flora, it will present itself pathogenically if there is some alteration with the host, e.g., skin infections occurring with either moisture or damaged skin, or with decreased immunity. Pseudohyphae- fungi are into absorption for a living protonasealybreak through and ejoyinga little bit of a mealin the armpit (oral fluera- inhaled steroids for asthma). Yeast infection if antibiotics and lost nromalfluoro.
dermatophytes (e.g., Trichophyton, Microsporum, Epidermophyton)
* Pathogen category: mold * Source: nor normal flora; may be from animals, soils, other people, fomites (wet surfaces) * Virulence: keratin focus (keratinase to break down food); requires contact and some skin disruption (maceration) * Clinical: tinea (pedis, corporis, capitis, unguium) * Immune response: delayed type hypersensitivity * Treatment/Prevention: terbinafine cream (tinea corporis); oral terbinafine * Concern of id reaction(generalized pruritic rash) from circulating fungal antigens
Dermatophytesare fungi which are characterized by itching, scaling skin that can become inflamed. The three main genera of Epidermophyton, Microsporum, andTrichophytonlive off the keratinin the superficial epidermis, by producing a keratinaseto break down the food. Generally speaking, terbinafine or one of the azole drugs, both of which interfere with ergosterol synthesis, will be useful for treatment (Sanford Guide 2019).One possible concern is an “id reaction” (a generalized pruritic rash) from circulating fungal antigens that can occur with dermatophyte infections.
Can be located on head, body, jock-itch, athletes foot.
Thedifferent names of the tinea infection reflect the different sites of infection. There is also the issue, though, of differing treatments of the fungus depending on the site. For example, tinea corporisand tinea crurisare more amenable to topical treatments. Fungus is mycelimand where growing tips of hyphae is where battle is being fought with the edge of it being where we need to focus. Involving the hair takes longer need it to grow out to clear it,nails are worse because of slow growth and need for constant anti-fungal
- Tineapedis: moistened, cracked skin among the toes.
- Tineacorporis: the edge of the ringwormis the site of active growth.
- Tinea capitis(scalp ringworm): hair shafts can become invaded by hyphae.
- Tineaunguium(onychomycosis): must continue treatment for months to treat all of the infected nail.
Malassezia (Pityrosporum) furfur
* Pathogen category: dimorphic fungus * Source: commensal on skin * Virulence: cell wall * Clinical: tinea (pityriasis) versicolor (hyper or hypopigmented lesions); disease within stratum corneum; usually oily moist skin (young adults in the tropics) * Immune response: delayed type hypersensitivity * Treatment/Prevention: topical terbinafine or ketoconazole; can do suppressive oral fluconazole with occasional dose
Ina slightly different pattern, pityriasis(tinea)versicoloris caused by the resident dermatophyteMalesseziafurfurthat lead to hypo-or hyperpigmentedlesions with oily moist skin, e.g., younger adults in the tropics. Although the infection is in the stratum corneum, the fungal metabolites may generate either tyrosinase inhibitors (hypopigmentation, typically more noticeable) or may stimulate more melanosomes(hyperpigmentation).
KOH prep will dissolve keratinbut not chitin of the cell walls of the fungus, warmer stickier climates than dry cooler climates
Sporothrix schenckii
* Pathogen category: dimorphic fungus * Source: soil; plant matter * Virulence: cell wall * Clinical: sporotrichosis, with dermal penetration and lymphatic travel * Immune response: delayed type hypersensitivity * Treatment/Prevention: protective gear while gardening, oral itraconazole
Sporothrixschenckiiis a widespread environmental fungus that grows on plants. Typically, it is traumaticallyintroduced, e.g., through a rose thorn prick, and the infection will spread along a series of nodules as it infects the local lymphatics. An azole drug, e.g., itraconazole, is taken for 3-6 months in order to clear the deep-seated infection. Environmental mold once introducedto skin goes into yeast mode fought is granulomatous slow patches or battles along the arm (alcoholic- macrophage weaker less granules gardner-introduction to plants) several months of azole therapy
folliculitis
infection/inflammation of follicles.
Hot tub- folliculitis: Pseudomonasaeruginosais a pathogen that will show up in a number of contexts, given its minimal environmental requirements and large set of virulence factors. Particualrlyin immune compromised individuals that are not resistant to toxins.
As a mild infection in someone who has intact skin and immune system, Pseudomonasaeuroginosacan infect hot tubs if there is insufficient chlorine.
Furuncles (boil)
abscess formation that occurs from worsening folliculitis o Treatment- incision and drainage of the lesion o Antibiotics for lesions > 5cm, multiple lesions, and/or presence of a fever Definition
Carbuncles
cluster of furuncles
Impetigo
intraepidermal infection caused by strep or staph o Honey-crusted non-bullous lesions if strep; bullous generated by exotoxin if staph o Treatment- topical mupirocin or oral sulfra drugs or clindamycin (covers MSSA and MRSA)
Impetigois an intraepidermalinfection caused by strep or staph. The lesions may be more “honey crust” (non-bullous) if strep, and more bullous(generated by exotoxin) if staph-derived. Treatment, in either case, could be topical mupirocin (a bacteriostaticagent), or oral sulfa drugs or clindamycin could cover both MSSA or MRSA (2019 Sanford Guide). Direct skin innoculationfrom colonizingflora pick the nose and scratch the face staph. Colonize the nares can get staph or strep. Superficial spreading infection bactrabadan.
Cellulitis
subcutaneous tissue infection (staph/strep) o Treatment- depends on out/inpatient status and comorbidities; systemic antibodies
erysipelas
- involves superficial lymphatics (red raised edges); another form of cellulitis. . Red demarcation on the face, limbs, due to involvement of lymphatics not fat layer leading to a raiseddred edge
Endocarditis
- major concern of bacteremia; prophylaxis antibiotics for oral procedures if prosthetic valves o Vegetations- aggregation of platelets and fibrin seen on the higher pressured left side; can spray through the bloodstream o Fever and murmur, can be several weeks before these appear o IV drug users will have it on their tricuspid valve o Splinter hemorrhages (small clots) and Osler nodes (localized vasculitis from immune complex deposition) reflect the widespread, blood-borne nature of the infection. Swelling from hermmorhagesgetting caught in the skin chain wave lesions of maculesor antigen-antibody complex creating oslernodes are due to the showeirngeffect off of the valve. Common in IV drug users as staph. Enters the body and immunocompromised individuals.
Symptoms: fever (sepsis), chest pain, PE sounds of murmur
Endocarditisis a major sequela from many hematogenousillnesses. History (IV drug use, prosthetic valve), and physical may suggest certain pathogens on the differential diagnosis. Feverand a murmurwill be consistent findings in most patients in endocarditis.Depending on the rate or progressionof the condition, there can be several weeks before these symptoms appear. Destructive pathogens- staph. Aureus or biofilmerscause endocarditis creating giant tarp like effect. For IV drug users tricuspid valve is the most common from venous seeding rather than arterial. Most endocarditis is on the left side given how its stronger and better connects with arteries.
Necrotizing fasciitis
strep with toxin production to account for the cleavage of tissue planes requiring aggressive surgical debridement o Antibiotics will cover most.
Necrotizing fasciitisoften involves streptococci with toxin production to account for the “cleavage” of tissue planes, requiring aggressive surgical debridement.Diabetes due to neutrophilcompromise start off as small dark spot (more painful than surface indicateds, purculatingdeeply toxin destroyed sheets of fascia and must do more and more debridement.
Antibiotic coverage will vary on the organisms involved, whether strep, Clostridium, or polymicrobial(penicillin for strep or clostridia vs. the broad coverage of a carbepenenmsuch as meropenem or imipenem, or vancomycin or daptomycin if MRSA may be included; Sanford Guide 2019).
Pasteurella multocida
o Pathogen category: G- coccobacillus, aerobic, extracellular o Source: zoonotic transmission from bites o Virulence: capsule o Clinical: cellulitis (cat and dog bites; quick onset) o Immune response: strong inflammation response, eventually Igs o Treatment/Prevention: amoxicillin+clavulanic acid
Pasteurella multocida, a Gram-rod, is the typical major contaminant of cat and dog bites, and the basis of a quick-onset (less than 24 hour) cellulitis. Augmentin®(amoxicillin + clavulanic acid) works well, as the organism is resistant to many broad spectrum antibiotics.Cellulitiisshowing up with different innocultionexposure from different animals with different rapidity depending upon bite.
