Ambler Bacteria Flashcards
Gram Stain
Hans Christian Gram, 1884
tells if bacteria are Gram ‘POS’ or ‘NEG’.
Gram Positives
Staphylococcus Enterococcus/Streptococcus Bacillus Clostridium Listeria Corynebacterium(Diphtheroids)
generalizations about spores
In a crux:
Bacillus and clostridium sporalate
Staph, Strep, Listeria and corynebacterium do not spore
My mnemonic: Spores, get Back in the Closet. Bacillus and Clostridium.
What GP has endotoxin?
Listeria has eNdotoxin where most GP do not
Staphylococcus
Gram Positive, catalase +, coagulase + cocci seen in Clusters.
Defenses –protein A, coagulase, hemolysins, leukocidins, penicillinase, beta-lactamases
- hyaluronidase, staphylokinase, lipase
Exotoxins
staphylococcus coagulase tests
COAGulase POS = aureus COAGulase NEG = rest, including epidermidis lugdenensis saprophyticus
Staphylococcus aureus general actions
Can infect head to toes and pretty much everything in-between
Really NEVER considered a contaminant.
Has a extracellular vesicles that carry beta lactamase into the surroundings
ie. There is a mixed abscess with ampicillin sensitive E.coli and MRSA. Some beta lactamase inhibitor needs to be included in the treatment.
Staph aureus toxins
Enterotoxin is heat stable
TSST-1: superantigen
Coagulase
Cytolytic toxin (α toxin); pore forming toxin
Panton-Valentine leukocidin (PVL); (β toxin); pore forming toxin
seen in CA-MRSA
Exfoliatins: skin exfoliating toxin (scalded skin)
staph aureus symptoms/ rx
purulent symptoms
- Boils
- septic arthritis/osteomyelitis
- Endocarditis
- Necrotizing pneumonia (salmon tinged sputum)
- intestinal
treatment is source control if possible
boils may only need I&D but many treat with abx as well.
bacteremia always treated with IV ABx
MRSA (Meth R Staph aureus)
MRSA almost universally put in Contact Isolation where MSSA is not.
Penicillin introduced to public 1941 (1942)
Methicillin 1958 (1960)
SCC MEC gene
CA-MRSA late 1990’s causes recurrent boils
Vancomycin 1958 (2002)
Linezolid 2000 (2001)
Daptomycin 2003 (2005)
VRSA
vanco resistant staph aureus
13 cases in US (first Detroit 2002). MI, PA, NY, DE
usually a history of recurrent MRSA and VRE skin/wound colonization with repeated vancomycin use (think dialyisis)
VAN-A gene from Enterococcus
VISA
vanco intermediate staph aureus
reduced vanco suceptibility
1997 Japan
Heteroresistance? Mixed MRSA with some VISA as well
mechanism is thickened cell wall
May confer some decrease daptomycin susceptibilities
Staphylococcus epidermidis
Indwelling foreign device
Usually more resistant than S.aureus = more methicillin R.
Vancomycin usually empiric choice
Treatment usually involves removal of foreign body.
Not typically as ‘virulent’ and not usually as purulent (no abscesses).
#1 cause of contaminated blood cultures
Staphylococcus saprophyticus
“Honeymoon cystitis” in women
Cause of UTI
Not resistant so PCN ok.
Enterococci
Historically Group D Strep so on micro reports, you may see strep species (gpc chains) that miraculously changes to enterococcus.
Clinically relevant are : faecalis and faecium
PYR + (pyrrolidonyl-arylamidase)
Highly resistant to many antibiotics
faecalis is usually less, highly resistant.
faecium is usually more, highly resistant
enterococci hemolysis
Usually gamma hemolysis
Can be alpha – especially some VRE
VRE (vancomycin resistant enterococci)
- Difficult to treat
- Seen in highly abx experienced patients
- Must refer to culture sensitivity but depending on the infection and site
- -linezolid
- -daptomycin
- -tetracyclines (for non-severe infections and not really urine)
- -nitrofurantoin (for urine only)
VRE
First described Europe 1980’s. felt to be from a food additive avoparcin.
Meta-analysis of 1614 enterococcal bloodstream infections had 42% VRE which has higher mortality.
Van-A, Van-B, Van-C genes
transposon. Frightened, Promiscuous bacteria!!!
(see VRSA)
Streptococci
Different classification systems have been developed.
Rebecca Lancefield classified group A-V(no I/J) and was based on the C carbohydrate on wall
We use hemolysis as well to characterize today
catalase (-) unlike staph or other aerobes/facultative anaerobes
streptococcus by hemolysis
alpha: green pneumoniae, viridans
Beta: pyogenes, agalactiae
gamma: enterococcus
Streptococcus pyogenes (symptoms, etc.)
Group A Pharyngitis (main cause of ‘strep throat’) --Red, purulent tonsils --Fever --Lymph nodes (ant cerv)
Skin infection
- -Folliculitis
- -Cellulitis
- -Impetigo (usually Staph)
- -Necrotizing disease
Scarlet fever = fever/rash
Associated with rheumatic fever Can cause Toxic shock syndrome “M” proteins (>70types) are virulence factors Cause of post strep glomerulonephritis Rapidly progressing
S. pyogenes: antibody mediated
Rheumatic Fever
- pharyngitis 2-4 weeks prior
Acute PSRPGN (post strep rapidly progressing glomerulonephritis) - skin infection or pharyngitis
Acute Rheumatic Fever
Major:
Migratory Arthritis (several joints in quick succession, each lasting days- 1 wk)
Carditis ( peri, epi, myo and dendo) and valvulitis (mitral stenosis as late complication)
CNS (Sydenham chorea)= St. Vitus dance
Erythema marginatum- rash
Subcutaneous nodules
Minor: Arthralgias Fever Acute phase reactant elevation Prolonged PR interval
Tx: symptomatic ie anti-inflammatories. Not proven to dec risk of rheumatic heart disease.
Abx even with negative throat culture – for stopping transmission
PCN for years to life
Streptococcus agalactiae
Group B
Know this causes neonatal sepsis so pregnant moms get a screening culture antepartum
Can cause occult and sporadic disease in adults including bacteremia, SSTI, pneumonia and sepsis
esp DM
PCN DOC. Some clindamycin resistance so not reliable
Group F = milleri group
another beta strep
PUS formers including abdomen, head and neck and brain abscesses! Think of CIA – sneaky fellows. Strep constellatus Strep intermedius Strep anginosus
Viridans Strep
GI flora teeth to colon
A very large group of bacteria.
Subacute endocarditis esp post teeth cleaning
PCN DOC
pattern, remember to treat strep with:
penicillin
Streptococcus pneumoniae
1 bacterial cause of Community Acquired Pneumonia (20-60%), Otitis Media (29-40%) and meningitis (61%)
CAPSULE with >90 serotypes that are pathogenic.
- Polysaccharide vaccine = 23 serotypes
- Conjugated vaccine = 13 serotypes
Gram positive DIPLOCOCCI
Pneumococcal treatment
ceftriaxone for serious infection (meningitis, bacteremia, pneumonia)
PCN still considered most potent abx
resistance starting to be a concern so with serious infection, the addition to the above with vancomycin, daptomycin, linezolid warranted prior to culture susceptibilities
Bacillus and Clostridium
Spore Formers
Bacillus are more aerobic and clostridium anaerobic.
Clostridium look like ‘tennis rackets’
Bacillus look like ‘box cars’(anthrax)
Bacillus anthracis
Anthrax
- Respiratory
- –Widened mediastinum
- GI
- Meningitis
- Cutaneous most common
Potent eXotoxin
Tx: severe - antitoxin (MAB or IG), cipro, meropenum
– Less severe, pcn, clindamycin, doxy
Bacillus cereus
Boards: refried rice or penetrating eye trauma
Food poisoning via heat stable enterotoxin that causes nausea/vomiting and limited diarrhea.
Clostridium botulinum
Making doctors a lot of money…….
Neurotoxin that blocks release of Ach from presynaptic terminals -> flaccid muscles
Infants should not ingest natural honey prior to 6 months due to inability of GI immune system to neutralize spores. ->floppy baby
Adults usually ingest from bad canned/smoked foods.
Antitoxin and vent support.
Clostridium tetani
Vaccine with Primary series and boosters q 10yrs.
Usually from skin trauma with environmental exposure.
Releases an eXotoxin called tetanospasmin that acts on inhibitory Renshaw cell interneurons preventing the release of GABA and glycine, both inhibitory substrates
When to give tetanus shot vs. immunoglobulin
shot if unknown vaccination history or less than 3 doses previous or more than 10 years since last one
TIG if dirty wound and unknown vaccination history/
Black Tar Heroin
Clostridium spores documented infections
necroziting disease or specific toxin disorder esp in skin poppers
- Botulism
- Tetanus
- C. sordellii also in wounds
(by the way, not common but this is in the literature for sepsis post medically induced abortion and less so spontaneous abortion. also seen post normal childbirth.)
Clostridium difficile (C diff)
CDC data: 500k infections in US 2011 and 29k died within 30 days. Incidence rising and now considered most common HAI.
Risk is Antibiotics!, even what we treat with but obviously less so a risk.
Symptoms range from watery diarrhea +/- mucous to full blown septic colitis and death.
Contact isolation due to spore formation, shedding and inadvertent contamination
Spores
(C Diff!)
this is the infectious problem. Found in hospital rooms on EVERYTHING (including curtains).
Patient shedding with every bowel movement and probably gasseous explosions.
put the toilet seat down to flush
spores can survive 5 months. may be dormant in colon with normal neighborhood of flora.
Patient considered infective if stool conforms to the vessel to which it is contained. Therefore contact isolation.
C diff treatment
Vancomycin IV does not penetrate across colonic mucosa and oral does not really get absorbed.
Probiotics are popular with some possible benefit and little risk it appears.
Newest and greatest is Fecal Microbiota Transplantation.
Really not new but re-discovered recently.
Either it goes down from above or more commonly introduced by rectal endoscope or enema.
Clostridium perfringens
Gas gangrene
Three classes
- Cellulitis/wound: causes crepitus
- Myonecrosis: CK elevation due to muscle dmg
- Diarrhea: hemorrhagic necrosis of jejunum
Tx: HBO (hyperbaric O2), PCN+clinda?+IVIG?, Emergent Surgery
Corynebacterium
Most are commensal flora and not pathogenic
Also reported as diphtheroids
Corynebacteium diphtheriae
‘pseudomembranes’ composed of fibrin, wbc, necrotic epithelial cells
Warn micro of specimen as it requires special culture techniques
– Potassium tellurite agar and Loeffler’s coagulated blood serum media.
– TREAT 1st!
Antitoxin, PCN or erythro, and vaccinate as natural immunity may not occur.
Listeria monocytogenes
Endotoxin GPR. Facultative intracellular org.
Grows in cold temperatures such as fridge
Tropism for CNS esp in young or old/immunocompromised
– also blood, amniotic fluid/placenta
3rd most common cause of neonatal meningitis.
Ampicillin 1st line. Sulfa/tmp also works
Mycobacterium
acid fast staining. also weakly gram positive.
Grow on Löwenstein-Jensen media
Most are very slow growing (weeks) except Runyon Grp IV which are fast (ie 5 days)
Classified by Runyon group or Staining
Actinomycetes
bacteria that act like fungi
– filamentous
– water and soil organisms
Nocardia and Actinomyces
Nocardia
Beaded, weakly GPR and weakly acid fast (but…acid fast:think mycobacterium) no sulfur granules can present like sporothrix (fungus) can disseminate including CNS infections/brain abscesses as well as pulmonary including infiltrative, nodular and cavities. (can mimic TB). N. asteroides N. brasiliensis many other species TX: Sulfa/TMP
Actinomyces
Beaded GPR SULFUR granules Causes cervicfacial, abdominal infections that act like tumors. also thoracic can look like TB or cancer *** Historically pelvic disease associated with IUD’s.*** A. israelli others Tx: PCN
Propionibacterium acnes
anaerobic slow growing gram positive rod; normal human skin and mucosal surface flora.
- Acne in teens
- surgical wounds
- Invasive deep infections with implantable devices
becoming a real problem esp with orthopedic devices UE>LE
Painful but not necessarily inflammatory on an aspiration of a suspected joint.
Tx: PCN, Clindamycin. TCN for those acne sufferers.
