Bacterial infections of the skin, muscle and blood stream Flashcards
Streptococci
Gram positive coci chains, Gram variable as culture ages and cells die.
- beta strep- nonhemolytic (pyogenic strep)
Group A strep (strep pyogenes)- can be in upper skin layers or it can go deep, infection can send toxin to another area, causing pathology
- common infection in the throat- pharyngitis, common bacterial infection, 1-4 weeks or more after infection, organism in throat, sometimes anus, 2-10% of population may be carriers, spread by DIRECT CONTACT or AERSOLS
- Scarlet fever is strep throat with a deep red color rash, have cheeks, temples, buccal mucosa, with a “strawberry tongue-PUNCTATE HEMORRHAGE on palates, sandpaper rash on trunk arms legs due to toxin.
- Toxic Shock-liek syndrome- progressive infection with bacteremia, shock, diarrhea, rash, renal impairment, respiratory failure and multiple organ system involvement, caused by the toxin–vascular compromise, desquamation of skin,
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group A strep toxin
Pyrogenic exotoxin- (SPE-streptococcal pyrogenic exotoxin)) stimlates cytokine release causing multiple effects. makes a red rash on skin- scarlet fever. Minority of strains carry this toxin
Impetigo
Gropu A strep infectin of skin, starts as insect bite or minor abrasion, may co-infect with Staph auresu,, lesions are small vesicles with erythema that become pustular and later crusted.
complication is glomerulonephritis 2-4 weeks after skin infection
is at the stratum corneum level
can form full thickness ulcer of the skin called ecthyma
Less common cause is Corynebacterium diptheria- most cmmon in tropics and occastionally in american indians, rarely fatal
Post streptococcal sequelae- acute rheumatic fever
infalmmatory disease, fever, carditis, subcutaneous nodules, migratory polyarthritis, hear valve damage,
-mumurs, cardiac enlargment, repeat infections lead to progressive damage.
Staph aureus
Gram + cocci in clusters, thick cell wall, often intracellulary in granulocytes,
- grows on blood agar in aerobic conditions, white colony, somteimes yellowsh but usually beta hemolytic.
- usually everywhere but only causes problems if it gets into wounds.
- Positive for production of CATALASE AND COAGULASE
- some strains can produce extracellular biologically active substances- hemolysins, hyaluronidase
- ## birulence is relatively low normally 10-5 or 10-6 organisms needed howevere in the presence of a suture only need 10^2 organisms will initiate infection-deeper
MAJOR CAUSE OF WOUND INFECTION- two sources from or nosocomial strains spread by health care workers practicing poor hygiene.
DEEP TISSUE INFECTION- can move to bone, joints, liver, lungs, other tissue, can cause acute endocarditis microabscesses and vegetations
BONE- common agent of acute and chronic osteomyelitis
THERAPY
resistance issues- most are currently resistant to penicillin G. so treatment of choice is Methicillin. many strains now resistant to methicillin (MRSA)
Coagulase in infection
not a toxin but plays role in pathogenesis, staphy coated with fibrin are resistant to phagocytosis, Fibrin deposition in the area of stpah infections helps locailize the lesion
ALPHA TOXIN
major cytotxoin fpr staph aureus, chromosomally encoded low molecular weight protein, causes necrosis or death in experimental animals, cuases certain mammalian cell membranes to leak through pores formed by toxin- causes RBC’s to lyse
Panton Valnetine Leukocidin
PVL- cytotoxin for staph aureus- lyses neutrophils and relesase enzymes that damage host cells
- associated with severe pneymonia, severe skin infections, common in community aquired methicillin resistant strains.
Faruncle
boils develop in hair follicles, infection at base of eyelash gives rise to stye can spread causing adjacent abscess known as a carbuncle. this happens on the back of the neck.
Chronic staph disease
chronic granulomatous disease- genetic disorder, immune cells unable to kill some types of bacteria or fungi, leads to recurrent or chornic infections, often discovered in early childhood, milder forms diagnosed during teen years
associated with diabetes.
Bullous impetigo
caused by strains of s. aureus that produce exfoliatin, large blisters in superficial layers of skin, these blisters contain many staph organisms.
Chornic furunculosis
chronic boils- delayed hypersensitivity to staph products, are responsible for much of the inflammation and necrosis that develops.
Scalded skin syndrome
Caused by Staph Exfoliatin toxins. Toxin is absorbed into the blood stream with erythema and intraepidermal desquamation at remotes sites
– No s. Aureus can be isolated from desquamation site.
Exofoliatins
- produced by some strains of staph only, exotoxin leads to intercellular splitting of the epidermis. between the stratum spinosum and stratum granulosum by disruption of the intercellular junctions.
- toxins produced at site of infection, but won’t be able to find it at the remote sites of the body
Toxic Shock syndrome
high fever, vomiting, diarrhea, sore through, muscle pain, shock within renal 48 hours, renal and hepatic damage
Skin rash followed by desquamation at a deepr level than scalded skin syndrome, strawberry toungue.
- caused by the pyrogenic exotoxin Toxic shock syndrome toxin-1 TSST-1. body absorbs the toxin at a local site and stimulates the release of cytokines and a direct toxic effect on endothelial cells.
- action is similar to group A strep (strawberry toungue) stimulates enhanced T-lympohcyte responses by direct interaction with surface receptors on T-cell, the resultant release of cytokines can have widespread effects.
-Mechanism of action. - women carry s. aureus in vaginal flora and 20% produce TSST-1 combination of mensturation and high absorbancy tampon usage provided conditions for production of the toxin which is then abosrbed. - can occur in non menstruation as well.
Ricketsial rashes
infected by insect bite, and starts out with localized infection followed by a systemic infection.
Pathogenesis- they infect the vascular ENDOthelium, RBC’s leak from breaks in vessels and result in rash with petechial lesions. same process occurs in organs and can cause the systemic symptoms.
Louse-borne typhus fever
caused by Rickettsia Prowazekii- disease of war and upheaval, epidemics in refugees, passed by lice. louse becomes infected feeding on an infected person. The louse will die of the infection but not before it feeds on others. the louse defecates when it feeds and deposits the organisms near bite wound
- typhus fever rash after 10 days.
- compromised circulation can lead to gangrene infection due to infection induced vascular injury
Diagnosis- culture needs to have tissure or eggs, not routine
PCR IS BEST-
- do an immuno assays for antibody production after infection(used for epidemiology and presumptive diagnosis after acute phase)
Primary classic lyme disease
Causitive agent- borrelia burgdorferi- spirochete shaped.
Initial tick bite- spirochete enters skin- 3-30 days later at the site of the bite you will see:
- erythema chronicum migrans (ECM) which has a slowly expanding red ring,
-biopsy shows that the leading edge has the organisms,
-this will disappear within weeks
Constittuinoal symptoms will last for months with fever, muscle and joint pains, and meningeal irritation.
- will demonstrate a small nymph stage of tick in-situ with early erythema migrans
organism can get into joint and stay there this is the place you can get the organism.
Acceptable diagnositic tests
- EIA for antibody plus western blot
- rarely use a PCR of joint fluid. .
- EIA is used for screening
- western blot is a follow up for confirming which is a more specific tests, not all will give multiple bands especially early in the disease so you may need to do a follow up western blot.
