Ambler Prions Flashcards
BSA (blood sheep agar)
routine. most things GP, GN and candida grow here
MacConkey
For Gram negatives/enterics (bile tolerant).
Chocolate
lysed red cell media to release nutrients for picky (fastidious) organisms
Sabouraud
for dermatophytes and other fungi
Antibiotic Resistance
Decreased penetration to target
Gram negs. like P.aero has thick outer membrane (wall)
Alteration of target site
change in PBP by strep and staph so it is not recognized
Inactivation by enzyme
enzyme eats abx renderning ineffective. ‘ase’. ie penicillinase, carbapenimase
chromosomal - ie inducible by Enterobacter
plasmid – can be a moving target as non chromosomal
transposon – non chromosomal like plasmid. ‘jumping genes’
Beta-Lactam Resistance types
Penicillinase Cephalosporinase ESBL (Extended Spectrim Beta-lactamase) AMP-C Carbapenemase. ‘CRE’ has been in the news a lot recently.
Micro plate tests
Kirby Bauer
abx discs and read zone of clearing; CLSI has breakpoints for S, I or R
e-Test
graduated concentration of abx and read point
Urine
diagnosis of presumed UTI difficult.
Pyuria = >10wbc
Leukocyte esterase great at detecting very small WBC’s so despite decent sens/spec:75-96%/94-98%, it is not diagnostic
Nitrates – tells if nitrate splitting bacteria (ie Ecoli) is there. does not tell if problematic
Blood – not common in uti compared to non infectious causes
how about bacteria?
>100k only applies to enterobactericiae and only predicts persistant colonization or infection. Kass, MD in the 1950’s studied this extensively.
to comfortably dx UTI you need
1) symptoms. we only treat asymptomatic bacteria in the urine in the pregnant patient as it reduces pyelonephritis and preterm labor
2) pyuria (increase in wbc’s)
3) bacteria suggestive of infection. ie Staph epi = no.
again >100k suggest persistence and MAY mean infection that needs treatment.
Blood culture
major problem is it is usually collected through skin or through a catheter, both of which get colonized with bacteria.
pearls:
always try 2 separate sites of draw
if rigors/chills. Get 2 sets stat as rigors signify clearing of the bacteremia
if fever then q 15 min is fine
if thinking endocarditis or persistent bacteremia, showing persistence over time necessary.
Newer blood culture machines are better at culturing the ‘fastidious- (ie HACEK group).
Not many instances for holding blood cultures >5 days. Propionibacterium is one common exception
Fungal blood cultures very low yield except candida which grows on normal culture stuff.
Sputum
need deep specimen.
gingival scraping has 1012 anaerobic orgs.
again need inflammation (ie inc WBC’s)
Need to have a favorable ratio of wbc’s to respiratory epithelial cells. Bronchial epithelial cells more significant in indicating ‘deep’ specimen.
eg 4+ PMN’s and 0+ epithelial cells would be ideal.
thought that 104 -105 orgs needed for gram stain positivity.
Encapsulated
Worry for splenectomized patients
Typeable Haemophilus influenzae (ie type B) Strep pneumo Neisseria meningiditis Strep agalactiae (group B) Klebsiella Salmonella Capnocytophaga - means dog death. Splenectomy patient bitten by a dog that dies, think of this. Crytptococcus
Community Acquired Pneumonia
85% of bacterial cases: (also major causes of ear infections)
Strep pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Rest (atypicals)
Legionella pneumophila
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Respiratory viruses*
Haemophilus influenzae
small non motile gnr. needs factors ‘V’ and ‘X’ so chocolate agar better.
2nd most common CAP bacterial org.
common in smoker/copd patients
clinically nontypeable and type B strains have capsule
H. influ type B
kids = life threatening complication/disease of epiglottitis
fever, sore throat, leaning forward with mouth open and drooling.
medical emergency as they can lose airway fast.
Atypicals pneumonias
Legionella
Mycoplasma
Chlamydia
tend to treat with macrolides,
Mycoplasma pneumoniae
‘atypical’
cause of ‘walking pneumonia’ which is self limited. XRAY can look like they should be dead but they are ‘walking’ around.
cold agglutinins
can be a systemic disorder
extrapulmonary
Hemolysis, usually mild
skin: maculopapular rash or vesicular to SJS.
CNS: 0.1% of all pts and 7% hospitalized pts. aseptic menigitis, peripheral neuropathy, cranial nerve palsy, cerebellar ataxia, ADEM and transverse myelitis
cardiac: one of the more common presentations with rhythm abnormality, CHF
Rheum: raynauds, polyarthralgias and mylagias from immune-medicated mechanism but has been cultured from synovial fluid.
rare Glomeruloneprhitis
rare hepatitis and pancreatitis
Otitis media and bullous myrigitis
Legionella pneumophila
‘atypical’
syndrome of fever with temp/HR dissociation, H/A, myalgia, confusion, diarrhea, cough, inc LFT’s.
Not uncommon to get worse before better
Resistant to cephalosporins lest we forget the Legionnaires convention in Philadelphia.
respiratory FQ or macrolide.
ie levofloxacin or azithromycin
Endocarditis
Most common are streptococcus (viridans) sub acute, S. aureus usually acute, S. epidermidis usually foreign body
boards like the HACEK group – fastidious GNB (5-10% cases)
Haemophilus aphrophilus Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae
Left sided lesions (mitral and aortic valves) = septic emboli to organs
Right sided lesions (ie venous/catheters, tricuspid valve) = septic pulmonary emboli
Endocarditis prevention
From AHA guidelines. (Other society guidelines will differ and thus controversial)
need prophylactic antibiotics for
previous history of endocarditis
prosthetic heart valve
non-corrected congenital cyanotic heart disease
cardiac transplant with valvular disease
Immunocompromised Host
We are talking about no neutrophils.
Antimicrobials are really only protection
Guidelines available but in essence, with fever, we need to cover Pseudomonas.
Neutropenic Fever
defined as:
fever ≥38.3(101) or ≥38(100.4) over 1 hr
management
cultures including blood, sputum if able, urine.
start empiric anti-pseudomonal abx
Gram positive coverage if line suggested as possible source. (cover MRSA/MRSE)
imaging as needed
isolation only if a reason is known
if after 4-7 days with fever, without source, add antifungal.
Fever of Unknown Origin
goes against the dogma of testing confirms your suspicion. Here we are loosening the net and casting it out to see what we catch.
2003-2005 Netherlands Connective Tissue –> 22% Infection -> 16% Malignancy -> 7% Miscellaneous -> 4% No diagnosis -> 51%!!!
despite no diagnosis, most adults had good prognosis.
min workup: but guided by history and symptoms
blood cultures, erythrocyte sedimentation rate or C-reactive protein, serum lactate dehydrogenase, HIV antibody test and viral load, rheumatoid factor, heterophile antibody test, creatine phosphokinase, antinuclear antibodies,tuberculin skin testor interferon-gamma release assay, serum protein electrophoresis, and computed tomography scan of abdomen and chest
Pasteurella multocida
small GNCB
cat and also dog bites (80% cat bites/5%dog bites get infected).
found as usual flora in respirator tract/mouth
even though Bartonella usually associated with cat scratch, Pasteurella also with cat scratch or cat/dog licks.
purulent and with cats, tenosynovitis common as well as joint/bone infections
Beta-lactamase producer
Bartonella henselae
causative agent of ‘cat scratch disease’.
usually self limited. can cause a purulence at site of innoculation.
causes enlarged, tender lymph nodes 1-3 weeks after scratch.
In AIDS, causes bacillary angiomatosis
can be few to hundreds of lesions
papules or nodules which are red, globular and non-blanching, with a vascular appearance
purplish nodules sufficiently similar toKaposi’s sarcomathat abiopsymay be required to verify which of the two it is
a purplish lichenoid plaque
a subcutaneous nodule which may have ulceration, similar to a bacterialabscess
(Obligate) Anaerobes
most numerous organisms in GI tract
estimated to outnumber facultative anaerobes 1000:1
Bacteroides fragilis group number one by #s
treatment is mainly some combination drugs with beta-lactamase inhibitors or metronidazole. Clindamycin losing some activity but still pretty good.
Clinically see in GI infections/abscess
They STINK!
spore forming anaerobes
clostridium
non spore forming anaerobes
propionibacterium
lactobacillus
bifidobacterium
actinomyces
Ludwig’s Angina
special condition of anaerobic infections
infection of sublingual and submandibular spaces especially with base of tongue swelling
starts with dental infection 50-90% of the time
Lemiere’s Syndrome
special condition of anaerobic infections
Fusobacterium necrophorum
post compartment of lateral pharyngeal space with suppurative thrombopglebitis of IJ vein. shows right sided septic emboli to lung
Prion disease aka Creutzfeldt-Jakob
abnormal protein formation that is hard to break down. It ‘replicates’.
adult patient who presents with dementia, an atypical movement disorder, or late-onset psychiatric disease, especially if the rate of disease progression is accelerated or if it is accompanied or preceded by other neurologic signs or symptoms
Disease is suggested but not confirmed with testing the CSF for 14-3-3 protein. also tau protein and brain specific enolase. New test amplifies prion activity called real-time quaking-induced conversion (RT-QUIC) looks promising.
Death within 6-12 months. 1.5 years with vCJD
types and frequency of prion disease
Sporadic (90%) – no history of exposure to PrPSc nor genetic mutation.
Creutzfeldt-Jakob (sCJD)
Sporadic Fatal Insomnia (sFI)
variable protease sensitive prinopathy (VPSPr)
Familial (10%) – presence of mutant PrPc gene (thus a PrPSc
Familial Creutzfeldt-Jakob (fCJD)
Fatal Familial Insomnia (FFI)
Gerstmann-Strӓussler-Scheinker disease (GSS)
Acquired – exposure to PrPSc through food or medical/surgical procedures
Variant CJD (vCJD) – related to Bovine Spongiform Encephalopathy (BSE) “mad cow”. Also Chronic Wasting Disease (CWD) in elk and deer. Endemic in CO, WY, NE. also seen in SD, NM, WI, MI, KS, OK, MN, MT and Canada.
Kuru in Papua New Guinea.
MIC’s
min inhibitory concentration to stop bugs from growing.
in the lab, they culture is subjected to different concentrations of antibiotics. We then look at what concentration stops the growth of the culture. This is the MIC (minimum inhibitory concentration).
