bacterial infections of the skin and soft tissue III Flashcards
clostridium- what are most infections of ?
- skin, soft tissue and food poisoning as well as antibiotic associated diarrhea/colitis
clostridium
type
features
where do they live
gram positive rod, SPORE-FORMING
- anaerobic
- spores are resilient and last years
- ubiquitous to soil, water, sewage and GI commensal
what are some virulence factors of clostridium
- hemolysin, neurotoxin, enterotoxin
Clostridium perfringens type what does it produce spores? toxins? what does it cause?
- gram pos, non-motile rod, anaerobic, beta hemolytic
- growth is associated with LARGE PRODUCTION OF HYDROGEN AND CARBON DIOXIDE
- rarely see spores
- makes lots of toxins A-E- mostly A
- causes GAS GANGRENE (CLOSTRIDIAL MYONECROSIS) AND GASTROENTERITIS
what toxins does c. perfringens produce and what do they do?
- alpha toxin- MOST IMPORTANT- phospholipase that hydrolyzes lecithin and sphingomyelin to disrupt cell membranes
- beta toxin- leads to loss of mucosa and formation of necrotic lesions that lead to necrotizing enteritis
- enterotoxin- binds small intestine altering its permeability
what type of soft tissue diseases does C perfringens cause?
- cellulitis
- fasciitis
- suppurative myositis
- myonecrosis (gas gangrene)
what is gas gangrene?
- it is a c. perfringens disease that are obtained by a surgical wound or a traumatic (war) wound via environment or GI
- surgery is usually during a colon surgery
- begins as wound infection and IS ACCOMPANIED BY GAS PRODUCTION (CREPITATIONS)
what is the progression of disease for gas gangrene
- starts of as cellulitis that turns in to myositis with PUS IN THE MUSCLE LAYER
- this progresses to muscle necrosis and systemic spread with high mortality
- CHARACTERISITIC RED/BROWN, FOUL SMELLING DISCHARGE
- ALPHA TOXINS THAT LEAD TO EDMA AND NECROSIS
- INCREASED VASCULAR PERMEABILITY OF TOXINS CAN LEAD TO DEATH WITHOUT BACTEREMIA-TOXIN INDUCED SHOCK
What can come up on an xray that would indicate that the infection was clostridium perfringens?
- there are clear spaces in the infected area that can be seen in an xray. it is a result of the gas production
how can c. perfringens be diagnosed? treatment?
- gas bubbles in xray
- gram pos rods in specimen WITHOUT LEUKOCYTES
- treat: surgical debridement with PCN or clindamycin and metronidazole
what is clostridium tetani?
- motile, spore forming, Gram pos rod
- STRICT ANAEROBE
- DRUMSTICK APPEARANCE =spores
- found in soil and GI
how does c. tetani enter the body?
- wound thru nail or splinter
- nonsterile technique
- ** key point- results from a wound that goes necrotic and provides great medium by which infection can occur locally and TETANOSPASMIN CAN ACT AND CAN MAKE ITS WAY TO THE CNS
What are the two toxins of c. tetani
A) tetanolysin- oxygen-liable hemolysin
B) TETANOSPASMIN- heat-liable neurotoxin**
tetanospasmin
- in c. tetani
- INACTIVATES PROTEINS THAT CONTROL RELEASE OF INHIBITORY NEUROTRANSMITTERS (GLYCINE AND GAMMA AMINOBUTARIC ACID) which causes unregulated excitation and SPASTIC PARALYSIS
- binding is irreversible but rapidly degraded in GI
what are the three generalized presentations of c. tetani
1) generalized- involve masseter muscles-lock jaw- sweat, back spasms, autonomic involvement
2) localized- disease just at infected musculature, head
3) neonatal- umbilical stump infected, 90% mortality
what is risus sardonicus
-caused by c. tetani
- sustained contraction of facial muscles
“sardonic smile”-abnormal, cynical like sustained grin
opsithotonic posturing
- spinal musculature curving and weirdness due to c. tetani infection
diagnosis and treatment of C. tetani
- diagnosis- cant really culture, so clinical pres is important, masseter, spasms
- treat- debride wound, metronidazole, HTIG-HUMAN TETANUS IMMUNOGLOBULIN VACCINATION (antibody that recognizes the toxin and kills it)
prevention for c. tetani
- childhood vaccination
- booster 10 yr
mycobacterium
type?
cell wall?
what are some important characteristics about mycobacterium
- gram pos rod
- acid fast
- aerobic
- cell wall is LIPID RICH
- NONSPORE FORMING
- STAIN BRIGHT PINK- FROM MYCOLIC ACID IN THE CELL WALL (FATTY ACID)
- CONTAINS LAM-LIPOARABINOMANNAN (LIKE LPS)- proinflammatory cell wall
what is important to note about mycobacterium and its resistance? what about it’s growth rate?
- it is resistant to many cleaning detergents, antibiotics, immune responses, and disinfectants
- slow growing therefore slow disease process
what is important to note about the disease process when it comes to mycobacteria
- it is slow and follows a chronic course that leads to granuloma formation
- there are no endo or exotoxins
what type of immunity helps to kill mycobacteria?
CELL MEDIATED
what is Mycobacteria tuberculosis
- caused by mycobacteria
- slow growing
- NONPIGMENTED OR TAN COLONIES
- usually obtained via inhalation of droplets
what can result from a long-term mycobacteria tuberculosis infection?
- you can get upper lumbar and lower thoracic vertebrae problems via hematogenous spread from the respiratory tract - potts disease, tuberculus vertebral osteomyelitis and skeletal TB
how is m tuberculosis osteo probs diagnosed
- travel hx
- back pain and GIBBUS DEFORMITY
- radiographic evidence
- positive PPD
- aspirate or biopsies of spinal lesions
pathogenesis of m. tuberculosis
- infect and live in macrophages so the macrophages cant kill them
- macrophage secretes IL-12 and TNF-alpha in response
- T cells differentiate intoTH1 AND PRODUCE IFN-GAMMA
- MACROPHAGE INCREASES KILLING POTENTIAL IN RESPONSE TO IFN-GAMMA
- mycobacteria resti the effects so the immune system , like T cells, compensates by surrounding macrophages to form a granuloma over time
treatment and prevention of m tuberculosis
- treat- resistance due to lipid rich cell wall =challenge!
I-REP: isoniazid, rifampin, ethambutol, pyrazinamide
-combo of four given over SIX TO 9 MONTHS
Prevention: vaccine for kids, prophylaxis with isoniazid
what is mycobacterium leprae
- obligate intracellular parasite
- no growth on lab media
- human and armadillo reservoirs
- causes leprosy
- slow disease course with granulomas
- no endo or exo toxins
what does m. leprae target? what’s its cell wall like
- schwann cells and macrophages
- cell wall- proinflammatory, PHENOLIC GLYCOLIPID
Transmission of m. leprae
-nasal secretions
what are the stages of m. leprae
- 2 stages
a) tuberculoid (th1)- paucibacillary- containing few bacilli - cell mediated so gets rid of it
b) lepromatous (th2)- HENSEN’S DISEASE- multibacillary, chronic disease of the skin and dermal macrophages as well as peripheral nerves (schwann cells)
- humoral or antibody mediated so does not get rid of it
presentation of tuberculoid leprosy vs lepromatous leprosy skin lesions- histopathology- infectivity- immune response- immunoglobulin levels- erythema noduosum-
skin lesions- few hypopigment plaques with flat centers and raised boarders, peripheral nerve involvement ////many erythmatous macules, extensive tissue destruction, diffuse nerve involvement
histopathology-few or no acid fast rods/// numerous
infectivity- low/// high
immune response- th1///th2
immunoglobulin levels-normal///hi
erythema noduosum: absent/// usually present (inflammation of fat cells)
diagnosis of m. leprae
- diagnosis- mostly clinical observation
LEPROMIN TEST- inject inactivated m. leprae and see if there is a delayed response (lepromatous leprosy) and no reaction with tuberculoid leprosy
-CULTURE IS IMPOSSIBLE
- you can confirm lepromatous with nose or ear smear
- tuberculoid you do a skin biopsy
treatment of m leprae
- tuberculoid- sulones (dapsone) and rifampin for SIX MONTHS
-lepromatous- dapsone, rifampin, clofazimine for 12 months
-
what are nocardiosis and actinomycosis
- actinobacteria
- cause cutaneous skin infections and bronchopulmonary disease that bring cough, dyspnea and fever
- thought to be fungi because HAVE FILAMENTS THAT LOOK LIKE HYPHAE
Nocardia
type
stain
special feature
- gram pos rod but most appear gram neg with intracellular gram pos beads
- WEAKLY ACID FAST- CELL WALL STRUCTURE IS SIMILAR TO MYCOBACTERIA WITH BRANCHED CHAIN FATTY ACIDS IN CELL WALL
- have BRACHED FILAMENTS THAT RESEMBLE HYPAHE
- slow growing
- HAVE AERIAL HYPHAE THAT GROW UPWARD- look hairy
what is mycetoma?
- mycetoma is caused by nocardia infection
- chronic infection of the skin, underlying tissues and sometimes bones/viscera
- tropics
- slowly progressive and PAINLESS
- usually starts with minor injury- FOOT IS THE MOST COMMON SITE
- CAUSES SINUS TRACT FORMATION
what forms of disease can nocardia present with?
- 1) cellulits and subcutaneous abscesses like mycetoma
2) lymphocutaneous diease- starts as cutaneous and spreads to lymph nodes forming chronic granulomas and ulcers
3) 1/3 get meningitis
diagnosis of nocardia
- hx- indicates direct exposure from environment via gardening, farming***
-directly examine branched. filamentous gram pos weakly acid fast organism
culture
biospy
treatment of nocardia
-tetramethoprim and sulfamethoxazole
actinomyces israellii
What do they look like
where do they colonize
when do they infect
- FILAMENTOUS bacteria that look like fungi
- anaerobe
- colonizes mucosa of upper respiratory tract and GI and female genital tract
- opportunistic pathogen- breach in barrier LIKE IN DENTAL WORK
what is the infection of actinomyctes israelli like
- pyogenic abscesses connected with sinus tracts
- abscesses have sulfur granules that look like grains of sand- yellow/orange
treatment of a. israellii
- PCN
what is cervicofacial actinomycosis
- nodules on face around jaw
- usually dental- poor hygiene or surgery
- abdominal, pelvic and chest wall involvement sometimes seen
- result of a. israelli
diagnosis and treatment of actinomycosis
- direct examination of draining material and culture with biopsy - has a gram stain and filaments
- colonies appear5-7 days but two weeks may be needed
treat: PCN
how do you distinguish actinomycetes israelli from nocardia
nocardia is acid fast and actinomycets are not
actinommyocis vs nocardiosis
clinical pattern- lump with draining sinuses (mouth)//// sporotrichoid cellulitis and myocetoma
site- cervicofacial, thorax,ab, pelvis/// extremities
source- endogenous/// environment
most common causative agent - actinomyces israelli////nocardia brasilensis
acne vulgaris -what are the four key elements?
1) follicular epidermal hyperproliferation
2) excess sebum
3) inflammation
4) presence and activity of PROPRIONIBACTERIUM ACNES
What kind of bacteria are acne vulgaris? what does it do?
- small, anaerobic , gram positive rod
- causes an inflammatory response
treatment of acne vulgaris?
- topical with benoyle peroxide and antibiotics like erythromysin and clindamycin
- followed by oral- doxycycline and isotretenoin
gingivitis and periodontitis -what clinical pres are they
- gingivitis - inflammation of gingiva
- periodontitis- chronic inflammatory disease that includes gingivitis along with loss of connective tissue and bone support for the teeth
what can periodontitis cause
CAD, preterm birth, and chronic kidney disease
what is gingivitis and periodontitis caused by
- dental plaque that is a biofilm on enamel of teeth that many microbes bind on that causes inflammatory response in gingival tissues or the bone supporting teeth
- POLYMICROBIAL AND ANAEORBIC
- common bacteria: poryphyomonas gingivalis and treponema denticola
what are dental caries and what is the main causative agent
- cavities
- streptococcus mutans
what is the cause of the underlying disease in caries?
- acid products made during the interaction of strepto mutans with multiple species of biofilm are the cause
