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Flashcards in Gram Positive Bugs Deck (88):

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
hematogenous spread (IV -epid.)
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)
-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


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

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)
Toxic epidermal necrolysis (TEN)
- this started as rxn to drug -> SJS -> TEN

Staph scalded skin syndrome (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)



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



(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
- streptococcal TSS

Complications of GABHS:
rheumatic fever


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)

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)


*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)

-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

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



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