Gram Positive Bugs Flashcards
Why do gram + bacteria stain purple?
Because of the peptidoglycan cell wall, which is impermeable so it retains the blue stain.
Difference between the strep species hemolytic actions?
Beta: hemolyze fully
Alpha: incomplete hemolysis, turn green (viridans).
gamma: Don’t hemolyze at all
Differentiate between staph and strep presentation?
staph: cluster like grapes
strep: chains or diclocci (pair up), don’t clump like staph
What is associated with Corynebacterium Diptheriae?
gray pseudo membrane
How do you differentiate between gram + and - on a gram stain?
gram + = purple
gram - = red
Different structures of gram + and - bacteria?
bacillus= rod shaped coccus = sphere shaped spirillum = spiral streptococci -> cocci in chains staphylococci -> cocci in clusters
3 different staph species?
- staph aureus
- staph epidermis (foreign bodies - cath, prosthetic valve)
- staph saprophyticus (UTIs)
What does staph aureus look like on a gram stain?
It is bright yellow on sheep blood agar, and will coagulate positive with hydrogen peroxide (bubbles)
this differentiates it from the other 2 staph species that are negative coagulants.
What are the Streptococcus species?
Strep. pyogenes (group A) strep. agalactiae (group B) strep. pneumoniae (pneumococcus) -> GPdiplococci strep viridans Enterococcus (group D)
Why is strep pneumo so virulent?
Because it is encapsulated so when you have no spleen you are at high risk for strep pneumo infections (also why immunocompromised, children, and elderly are at risk). -> this doesn’t have lancefield antigens either
What are the lancefield antigens
differentiates between the different groups of streptococci species. All have specific antigens -> group A, B
Viridans (alpha hemo) and pneumo don’t have lancefield antigens
Where are common places for bacterial infections (staph and strep)?
skin (staph), soft tissue and bone
What are the 2 main classes of infection
local: face -> acne
generalized (systemic)
What is a localized infection?
the organism enters the body and reaches the target site of infection -> then adheres to or enters host cells and multiplies at site of infection. Infection spreads within site (resp. tract or intestines).
- the sxs of the illness appear
- organism doesn’t spread through the lymphatic system or reach the bloodstream. The infection subsides due to host defenses (immunity) -> the agent is eliminated from the body and the infected cells are replaced and pt is cured!!
Explain a generalized infection?
the organism enters the body and reaches the target site of initial infection. The organism then adheres to or enters the host cells and multiplies at initial site of infection. The infection spreads within the site and to other sites via tissues, lymphatic system, bloodstream (bacterimia, viremia) and possibly other routes.
- sxs of illness may appear
- organisms infect other organs, tissues and cells -> more spread via bloodstream
- sxs of illness become severe
- host defenses eliminate organisms leading to cure or disease continues, possibly leading to irreversible damage or death.
What are 2 common localized infections?
cellulitis, and erysipelas
What are some potentially lethal infections?
- necrotizing fasciitis (flesh eating)
- myonecrosis (gas gangrene or clostridial myonecrosis)
- pyomyositis (abscess from bacterial infection of skeletal muscles)
Common staph infections
gram positive
cocci, grape like clusters
most are harmless and reside normally on the skin and mucous membranes
MRSA: resistant to b-lactam antibiotics
What might MRSA be confused with?
a spider bite
How does coagulase differentiate the staph species?
coagulase + species (virulence) -> staph aureus (common nasal flora)
coagulase - species - staph epidermidis (universal skin flora)
How might staph present in an infection?
stye (cordeolum) boils, carbuncles, furuncles sinusitis hematogenous spread (IV -epid.) endocarditis pneumonia, emesis, impetigo, diarrhea, TSS, UTI, cystitis, osteomyelitis, SSSS
What are the cutaneous infections of S. aureus?
folliculitis (boils), furuncles, burns and wounds
What are deep infections of S. aureus?
osteomyelitis, abscesses, pneumonia, endocarditis, septicemia
What are the toxic mediated infections of S. aureus?
-staphylococcal scalded skin syndrome (SSSS), TSS, food poisoning
What are the most common skin and soft tissue infections of s. aureus? Who are they most common in?
Most common in immunocompetent host
- abscesses (cutaneous -> common)
- folliculitis
- mastitis
- wound infections
- infect. IV catheter sites
What are other common staph aureus infections? (more severe)
bacteremia, septicemia, endocarditis, pneumonia,
musculoskeletal: septic arthritis (injury)
Differentiate b/t the different associated MRSA’s
HA-MRSA: health care assod, occur in people that have been in hospitals. Usually assod with invasive procedures or devices
CA-MRSA: community associated among healthy people. Can begin as a painful skin boil. Spread by skin-skin contact, At risk pop: high school wrestlers, child care workers, and people who live in crowded conditions
Process of MRSA infection
generally start as small red areas that resemble spider bites, boils, pimples that can quickly develop into deep, painful abscess that require surgical draining (Really rapid -> in 24 hours will progress)
Sometimes will go deeper into tissue and cause life threatening infections in the bones, joints, blood stream, heart valves and lungs
Treatment process of MRSA
culture and sensitivity
- septra
or
-Doxy
If MRSA + -> what do you do to rid yourself of infection?
Bactroban -> ointment in nose qd
full body wash -Hibiclens: rule of 3: 3x a day for 3 days then 3 x a week for 3 weeks
Difference b/t strep cellulitis and staph cellulitis?
Group A strep cellulitis: follows an innocuous or unrecognized injury, inflammation is diffuse, spreading along tissue planes
Staph aureus: usually assod w/ wound or penetrating trauma, localized abscess become surrounded by cellulitis
Tx of cellulitis
Don’t use Keflex -> doesn’t cover MRSA
-now half of cellulitis infections are resistant to tx with kefex
-Current tx: clindamycin, doxycycline, Bactrim, Septra
What is the DOC of cellulitis
Bactrim
alt: clindamycin (sulfa allergy)
Vanco: MRSA
severe cellulitis: IV abx especially if pt has high fever and appears ill
- be aggressive with tx!
What is the admission criteria for cellulitis?
animal bite on pt’s face or hand
area of skin involvement >50% of limb or torso, or >10% of bod surface
-coexisting morbidity (diabetes, Heart failure, renal failure, edema)
-compromised host
-need for IV Abx
What is an abscess?
when the tissue in the area of cellulitis turns to pus under the surface of the skin, the collection of pus is called an abscess
-the pus is just dead, liquified tissue, billions of WBCs
- the most common bacteria in the abscess is staph aureus
- but many other bacteria can cause abscesses
-The organisms kill the local cells resulting in the release of cytokines which trigger an inflammatory response which draws large numbers of WBCS
-
What must abscesses be distinguished from?
empyemas -> these are accumulations of pus in a preexisting rather than a newly formed anatomical cavity
Clinical features of superficial, and deep seated infections?
superficial: skin and subcutaneous tissues -> infections of the hand
Infections of the head and neck: suppurative parotitis (acute infection of the parotid)
-Deep seated infections: hepatic abscess/ splenic abscess/ sub-phrenic abscess/ rectal abscess
When would you I and D?
What is other part of tx of this?
Only if you see that there is an obvious abscess
- should be drained + abx maybe
- if the abscess has a lot of cellulitis around it then an abx is probably needed.
- Antibiotics can’t penetrate w/o drainage so they need to be drained.
What is necrotizing fasciitis?
this is caused mostly from strep
- it is when the bacteria in a cellulitis or abscess starts spreading quickly between the fat layer and the muscle underneath
- necrotizing= living flesh to dead flesh
- fasciitis means the infection is spreading along space b/t fat and muscle
- the infection cuts off blood supply to the tissue above it and the tissue dies
- the bacteria may also enter the bloodstream.
Tx of necrotizing fasciitis
cut all the dead tissue out, and keep cutting until only living tissue is left.
- do this over and over again until the infection stops spreading.
- Antibiotics help but don’t cure the infection
- The open muscle needs to be tx like a burn with skin grafts
- empiric abx to cover anaerobes, gram -, streptococci, and staph aureus
- abx for min. of 3 weeks
What is myonecrosis?
Gas gangrene
- pure clostridium perfringens infection
- gas in gangrenous muscle group
- incubation hours to days
- local edema and pain accompanied by fever and tachycardia
- discharge is sero-sanguinous, dirty, and foul, crunchy upon palpation
Tx of myonecrosis
Pen G or chloramphenicol
- surgical removal of infected muscle
- watch out for diabetics
- consider hyperbaric chamber
What is pyomyositis
- mostly caused by staph aureus
- a purulent bacterial infection of skeletal muscles which results in pus-filled abscess.
- most common in tropical areas, temperate zones
- mainly a disease of children 2-5
Tx: must be drained surgically and abx given for min. of 3 weeks
What are the staph toxin disorders?
Gastroenteritis (food poisoning)
TSS
Toxic epidermal necrolysis (TEN)
- this started as rxn to drug -> SJS -> TEN
Staph scalded skin syndrome (SSSS)
SSSS
also known as Ritter disease:
causes by epidermolytic toxins produced by certain strains of staph. This toxin is distributed systemically and results in dissolution of keratinocyte attachments in only the upper layer of the epidermis.
- Usually affects newborns and children, adults less affected b/c of improved renal fxn allows for clearance of toxins from the body (w/ renal failure = more susceptible)
Staph epidermidis infections occur when?
Staph epidermidis is a major component of the skin flora.
- it is common in nosocomial infections: device/implant associated infections -> shunts, catheters, artificial heart valves, joints, pacemaker (anything foreign in the body)
(endocarditis)
Strep infections
30 species of bacteria
- gram + cocci in chains
subdivided by ability to lyse RBCS:
beta (complete lysis), alpha (partial lysis), gamma (no hemolysis)
What is erysipelas?
acute streptococcus infection of the upper dermis and superficial lymphatics.
Caused most by strep. pyogenes (group A Beta hemolytic )
-Rarely caused by beta hero of B, C, G group
- pathogen enters through a break in the skin and eventually spreads to the dermis and subcutaneous layer - can remain superficial or become systemic
General features and differences of cellulitis and erysipelas?
Varying degrees of skin or soft-tissue erythema, warmth, edema and pain
- associated fever and leukocytosis
- hx of trauma, abrasion, or skin ulceration
Cellulitis has an ill-defined border that merge smoothy with adjacent skin, usually pinkish to red
erysipelas: has an elevated and sharply demarcated border with a fiery-red appearance
Management of Cellulitis and erysipelas
local care: immobilization, elevation to reduce swelling, draw lines on areas to assess response to tx
- 2 weeks of abx therapy:
PCN or dicloxacillin
Impetigo
(pyoderma) -> superficial lesions that break and form highly contagious crust, often occurs in epidemics in school children, bug bites, poor hygiene, and crowded living situations
Differentiate between non-bullous and bullous impetigo?
Non bullous: strep Group A or it could be staph aureus
- see in pre-school and young school age, very thin walled vesicle on erythematous base, transient, yellowish-brain crusts (thick
Bullous (blister forming): staph aureus cause, all ages, bull: 1-2 cm, persist for 2-3 days, thin and flat, brownish crust, fluid filled
Predisposing factors to impetigo
malnutrition, diabetes, immuno-compromised status
complications of impetigo
strep infection (pink eye, meningitis, endocarditis)
- scarlet fever (strep pyogenes (group A): get strawberry tongue
- urtricaria
- erythema multiforme: usually follows an infection or drug exposure
Tx of impetigo
usually dx by presentation
- no cultures usually needed
- first soak affected area in warm water or use wet compress to help remove overlying scabs
- abx creams or ointments: bactroban AAA Fusidic acid cream AAA retapamulon ointment consider septra/bactrim if hx of MRSA
Common infections of strep progenies (group A beta hemolytic strep)
- cutaneous infections
- pharyngitis (sore throat)
- otitis media
- sinusitis
- pneumonia
- streptococcal TSS
Complications of GABHS:
rheumatic fever
glomerulonephritis
Describe the long term complications of Group A infections
rheumatic fever: follows overt or subclinical pharyngitis in children, extensive valve damage possible, arthritis, chorea, fever
acute glomerulonephritis: nephritis, increased BP, occasionally heart failure, can become chronic leading to kidney failure
Signs of strep throat?
red, beefy tonsils that are covered in exudate, strawberry tongue, petechiae
Differential: mono
Beta hemolytic group B strep
normal flora in lower GIT, female genital tract
-pathogenicity: neonatal meningitis and sepsis and pneumonia
meningitis in babies: won’t eat, crabby -> fever, vomiting: Emergency
Strep pneumoniae (pneumococcus)
gram + cocci in pairs:
pneumonia, otitis media, sinusitis, meningitis
Prevention: vaccination (capsular antigens)
immunization!!!
sxs of strep pneumonaie pneumonia -> shaking, chills, rust colored sputum, consolidation in lungs
Otitis media
presence of a middle ear infection
acute otitis media: occurrence of bacterial infection w/in the middle ear cavity
otitis media w/ effusion: presence of non purulent fluid w/in middle ear cavity -> have bulging, taut, inflexible TM (have effusion: add decongestant to abx -> drain better)
*OM: is 2nd most common clinical problem in childhood after URI
Epidemiology of otitis media
peak incidence in 1st 2 years
Acute otitis media facts
more common in boys
- lower socioeconomic status (smoking)
- seasonal disease (peak in Jan, Feb)
- corresponds to rhinovirus, RSV, influenza seasons ( secondary infection to virus, don’t get good drainage from initial infection, immunity down)
RFs for acute otitis media
young age, bottle feeding, drinking a bottle in bed, parental hx, sibling hx, second hand smoke, daycare
etiology of acute otitis media
suppurative infection of middle ear cavity, common bacterial pathogens achieve access through blocked eustachian tube (infection, pharyngitis, pr hypertrophied adenoids)
- air trapping -> neg. pressure -> bacterial reflux
bacterial reflux + obstructed flow = effusion
organisms that cause otitis media
strep. pneumo H. influenza Moraxella catarrhalis Group A strep staph aureus pseudomonas aeruginosa RSV assoc. w/ acute otitis media
Signs and sxs of otitis media
sxs are often nonspecific:
fever, irritability, poor feeding, otalgia, otorrhea, signs of common cold
What will you see on the physical exam if pt has otitis media?
erythematic, opaque (not translucent, bulging TM w/ loss of anatomic landmarks including a dull/absent light reflex
otoscopy: decreased tympanic membrane motility (pulled tight)
Complications of otitis media
hearing loss, acute mastoiditis, chronic perforation of TM, tympanosclerosis, cholesteatoma, chronic suppurative OM, cholesterol granuloma: blue drum syndrome, facial nerve paralysis
even worse:
intracranial complications, bacterial meningitis, epidural abscess, brain abscess, subdural empyema, otitic hydrocephalus, lateral sinus thrombosis
Tx guidelines for otitis media
infants 102) observation period is an option
tx of otitis media
amoxicillin for 10-14 days or augmentin
+
auralgan (analgesic/adjunct for ear pain -> drops) TID
2nd line tx for otitis media
cefzil (2nd gen cephalosporin) 6 months to 12 years
pediazole (erythro/sulfisoxazole)
bactrim
*used as secondary agents if the pt is allergic to pcn or primary abx has failed after 10 days and sxs persist
Streptococci viridans
alpha or gamma hemolytic
-common oral/pharyngeal flora (bind to teeth, cavities)
infections: endocarditis, bacteremia, and septic shock
Group D streptococci (enterococcus)
- UTI
- endocarditis
- intraabdominal infections (abscesses)
- biliary tract infections
- wound infections
*resistant to vanco and ampicillin, even becoming resistant to aminoglycosides
Dx of streptococcal infections
- culture
- ASO titers/streptozyme (body will develop abs to strep -> streptolysin O)
- rapid Group A strep tests
- gram stains
antistreptolysin O (ASO) titer is a blood test to measure abs against streptolysin O, a substance produced by group A streptococcus bacteria
DOC for streptococcal infections
S. pyogenes: PCN (low incidence of resistant organisms
S. pneumoniae: increased PCN resistance
Erythromycin for both in PCN allergic pt
Ampicillin for enterococcus
What is anthrax?
gram positive spore forming bacterium Bacillus anthracis (special capsule to avoid phagocytosis)
- anthrax spores are easily found in nature, and can be produced in the lab, can last a long time in the environment
- anthrax has been used before as bioterrorism agent
- can be released into powders, sprays, food and water
- primarily disease of herbivores which are infected by ingesting spores in the soil
- natural transmission to humans by contact with infected animals or contaminated animal products
epidemiology of anthrax
reservoir: herbivores (cattle, goats, sheep), capable of surviving in enviro for prolonged periods
Transmission: contact, ingestion, or inhalation of infective spores
sources of infection: contaminated hides, wool, hair, bone, meat, or other animal products
Clinical features of anthrax
incubation period: 1-7 days (1-60 days)
- clinical syndromes: cutaneous ulcer, respiratory, gi, oropharyngeal
- inhalation anthrax= main threat
spores may germinate up to 60 days after exposure
- bronchopneumonia not a component -> hemorrhagic lymphadenitis and mediastinitis
- hard to early dx
Cutaneous anthrax
stays local, necrotic center
inhalation anthrax epidemiology and clinical sxs
epidemiology: sudden appearance of multiple cases of severe flu illnesses with fulminant course and high mortality
non-specific prodrome of flu-like sxs
- possible brief interim improvement
- abrupt onset of resp failure and hemodynamic collapse 2-4 days after initial sxs, possible accompanied by thoracic edema and widened mediastinum on CxR (from bleeding)
Diagnostic studies, microbe and pathology of inhalation anthrax
dx studies: chest radiograph w/ widened mediastinum, periph blood smear w/ gm + bacilli on unspun smear
Micro: blood culture growth of large gm + bacilli with preliminary identification of Bacillus sp.
patho: hemorrhagic medistinitis (death), hemorrhagic thoracic lymphadenitis, hemorrhagic meningitis
prophylaxis anthrax control
prophylaxis:
pre-exposure: vaccine (not available?)
post exposure: cipro or other quinolone or doxy (vaccine if available)
CDC isolation: standard
contact isolation if cutaneous lesions present
treatment of anthrax
prophylaxis: cipro or doxy x 60 days
tx for cutaneous: cipro or doxy x 60 days
tx for inhalation: cipro or doxy plus
vanco, imipenem (initial rx= IV then switch to PO for total 60 days)
same tx for children and pregos
Diphtheria
gram + rod
- acute bacterial respiratory infxn caused by Corynebacterium diphtheria
- may involve any mucous membrane: will see gray pseudomembrane
- classified based on site of infection (laryngeal, cutaneous, ocular, genital)
- very rare in 1st world countries
Most common complications of diphtheria
myocarditis and neuritis
- death occurs in 5-10% from respiratory disease
symptoms and findings of Diphtheria
sxs: sore throat, malaise, cervical lymphadenopathy, and low grade fever
- earliest pharyngeal finding is mild erythema, which can progress to isolated spots of gray and white exudate. In 1/3 of pts - elaboration of toxin induces formation of coalescing pseudomembrane. This membrane adheres tightly to underlying tissue and bleeds with scraping but doesn’t scrape off.
Tx of diphtheria
abxs: erythro or PCN G
diphtheria antitoxin for severe cases
- careful airway management
-serial electrocardiograms and cardiac enzymes
- neuro status should also be monitored carefully
