Skin Infections/Skin Wounds Flashcards
Staphylococcal Diseases
S/S of multiple diseases, common Causative Agent, and Epidemiology
Folliculitis: inflammation, causes red bumps (pimples)
Furuncles: a single boil that has progressed past folliculitis
Carbuncle: a worse version of furuncle, large area of redness, swelling, pain, draining pus, cluster of furuncles
Causative Agent: Staphylococcus Aureus (turns bright yellow on MSA plate)
Epidemiology: S. Aureus found on almost everyone
people with boils shed large number, and they survive well in environment
Staphylococcal Scalded Skin Syndrome (SSSS)
S/S: begins with redness of skin, malaise, irritability, and fever —> 48 hrs later there is redness, skin wrinkles, large peels of it, and fluid filled blisters develop
Causative Agent: Staphylococcus Aureus
5% of strains produce a toxin called exfoliatin: destroys material that binds outer layers of epidermis, fluid loss leads to increase of other infections
Treatment: antibiotics and dead skin removal
Streptococcal Impetigo
Streptococcal Infection, most common type of pyoderma (pus producing skin infection), characterized by pus production resulting from infection of insect bite, burn, scrape, or other wound
S/S: superficial skin infection w/inflammation, thin-walled blisters, lymph nodes enlarge
Causative Agent: Streptococcus pyogenes or more rarer Staphylococcus Aureus
Lyme Disease
first recognized in the 70s, most common vector borne disease in US
Causative Agent: Spirochete
S/S: three stages, individual patients may by asymptomatic in one or more:
1) Early Localized Infection: erythema migraines (dizziness), circular skin rash, follows few days or weeks after tick bite; nearby lymph nodes enlarge + flulike symptoms
2) Early Disseminated Infection: 2-8 weeks later, nervous system affected, electrical conduction in heart impaired (heart doesn’t function properly and really bad muscle pain); dizzy spells, fainting, paralysis of face (looks like you’ve had a stroke)
3) Later Persistent Infection: 6 months after skin rash, joint pain, swelling appear, slowly disappear over years (chronic nervous system impairments may occur)
Lyme Disease
Causative Agent: Borrelia Burgdorferi
large, Gram NEGative micrroaerophilic spirochete
vector borne: you get it from a tick bite, and because of that it’s not contagious
Pathogenesis: spirochetes introduced into skin by bite of infected tick, migrate in an outward circular fashion, LPS causes inflammatory reaction on skin (bulls eye)
Epidemiology: the bacteria’s life is intertwined with the tick life cycle; the ticks are beige and hard to see, most people don’t feel it and it’s a deer tick, usually bites people in their Nymph phase
Measles
S/S: fever, runny nose, and swollen weepy eyes; fine red rash appears after a few days and lasts around a week; often secondary infections are what people worry about,
measles increases risk of miscarriage/premature labor/low birth weight
Causative Agent: it’s a virus from the paramyxovirus family- it’s an enveloped single stranded RNA virus; hemagglutinin (attachment)
Pathogenesis: acquired via respiratory route; spreads to lymphatic tissues; rash results from cell-mediated immune response to lymphatic tissues —> Koplik spots of mucous membranes identifying feature (diagnostic feature), and suppresses immunity
Epidemiology: humans only natural host, now there’s a vaccination but measles still comes back every once in awhile
Treatment: attenuated vaccine (altered vaccine that won’t cause disease) for prevention
Varicella (chickenpox!)
S/S: fever, headache, malaise, rash
childhood: begins as small red spots (macules), little bumps (papules), and then small blisters (vesicles)
they occur anywhere, but mainly head + chest + back, and the lesions are pruritic (itchy) —> scratching can lead to secondary infection S. aureus or S. pyogenes
More severe in adults around 20% end up developing pneumonia
reactivation of latent virus later in life produces shingles: reoccurence of chicken pox hies in nerves, then when they become active they follow the nerves (hurts like crazy and can hide for 30 years before becoming active again)
Pseudonyms Wounds
CA + S/S
CA: Pseudomonas aeruginosa (Gram NEGative rod);
they are an opportunistic pathogen and they like to grow in places with moisture soap, water, contact solution, water on veggies, and they grow in QUATS (disinfectant)
S/S: chills, fever, skin lesions, shock (you really won’t know for a bit that you have it, but eventually people turn green because they produce pyosin which is what makes them green
Tetanus (clostridium infection)
CA + S/S + Toxin+ Pathogenesis + Treatment/Prevention
CA: Clostridium Tetani (Gram POSitive rod–> drum stick morphology) it’s anaerobic (doesn’t have catalase or superoxide dismutase), and it forms endospores
S/S: also known as lockjaw, initially difficulty swallowing, jaw muscle contractions; muscles contract too much so they tighten you to death because you can’t breathe properly and you might drown on your own liquid
Pathogenesis: not invasive (germinates but doesn’t get into the cell itself), colonization localized to wound
Toxin: it’s an endotoxin tetanospasm (A-B mediated toxin) and it inhibits relaxation of muscles, which makes most of your muscles contract at the same time and so you become locked in place and unable to move
Treatment/Prevention: once you get it you can receive a human tetanus immune globulin (TIG) injection: antibodies bind to free toxin molecules and provide passive immunity and maybe some muscle relaxants; people usually get a vaccination with tetanus toxoid (DPT shots = diphtheria, pertussis, and tetanus); other treatment could include being in a hyperbaric chamber which forces oxygen in you, and this works because the bacteria is anaerobic which means it will kill the endospores
Clostridual Myonecrosis (Gas Gangrene)
CA + S/S
CA: Clostridium Perfringens (Gram POSitive Rod, same for all clostridium)
S/S: severe pain, swelling, and thin bloody or brownish fluid leaks (this is because the gas gets so pressurized that your skin can’t hold the liquid) from wound; may look frothy (gas bubbles, which are huge and BLACK)
Clostridual Myonecrosis (Gas Gangrene)
Toxin + Treatment/Prevention
Toxin: this is an alpha toxin (a-toxin) which is an enzyme that destroy lecithin in host cell membranes, resulting in cell lysis; carriers collagenase and hyaluronidase which break down host tissues (this means it breaks down proteins that hold together cell membranes and liquify it)
Arteriosclerosis or diabetes (poor oxygenation of tissue) and cancer are predisposing factors
Treatment: prompt disposal of all dead and infected tissue, antibiotics, and hyperbaric chamber!
no antiserum for alpha toxin, DPT shots don’t help because tetanus has a different toxin
