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midterm 2 Flashcards

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1
Q

prevalence of UTIs

A

one of the most common reasons for visiting primary care physician

50% of women have one by 30

incidence decreases with age

about 25% of women will experience a second episode within 6 months of their first UTI = recurrent UTI

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2
Q

Bacteriuria

A

presence of bacteria in urine - does not mean infection

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3
Q

asymptomatic bacteriuria

A

presence of bacteria in urinary tract + absence of symptoms

usually clinically insignificant unless woman is pregnant or has undergone invasive procedure in urinary tract

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4
Q

normal mechanisms that maintain sterility of urine

A

adequate urine volume

free flow from kidneys through urinary meatus

complete bladder emptying

normal acidity of urine

peristaltic activity of ureters

increased intra-vesicular pressure preventing reflux

in males: antibacterial effect of zinc in prostatic fluid

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5
Q

how are UTIs classified

A

based on location:

  • upper: pyelonephritis
  • lower: cystitis + urethritis

based on condition of the urinary tract or patient:

  • uncomplicated
  • complicated

based on evolution:

  • acute
  • chronic (symptoms persist over time)
  • recurring (relapse or reinfection)
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6
Q

Cystitis

A

UTI confined to bladder

symptoms:
dysuria (painful peeing)
urinary frequency 
urinary urgency
supra-pubic pain 
hematuria ( blood in urine)
nocturia (peeing at night)
bladder tenesmus 
absence of vulvar/vaginal discharge or irritation

absence of symptoms or physical signs suggests inflammation at other sites in urinary tract

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7
Q

differential diagnosis (UTI)

A

acute lower UTI (cystitis)

acute urethritis ( chlamydia or gonorrhoeae)

vulvitis - contact dermititis, allergic rxn, yeast infection, HSV infection

vaginitis/ bacterial vaginosis

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8
Q

pyelonephritis

A

clinical diagnosis that implies a more invasive infection

Symptoms:

  • fever
  • flank pain
  • nausea
  • chills
  • malaise
  • headache

symptoms indicate: inflammation of the kidney and renal pelvis

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9
Q

prostatitis

A

inflammation/infection of prostate gland - acute or chronic

intrarenal /perinephric abscess: collection of pus in kidney or in the soft tissue surrounding the kidney

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10
Q

uncomplicated vs complicated UTIs

A

uncomplicated:

  • occurs in patients with normal genitourinary tracts
  • usually non- pregnant, premenopausal women of childbearing age

complicated:

  • structural or functional abnormality of the gentiourinary tract
  • pregnant women, elderly, men, children
  • chronic symptoms
  • comorbid illness or immuno-compromised
  • upper tract disease
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11
Q

complicated UTI infection definition

A

underlying abnormality that predisposes patient UTI or makes UTI more difficult to treat effectively

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12
Q

recurrent infections : relapse vs re-infection

A

relapse:
- recurrence of infection by the same organism after treatment ends (possibly resistance)

reinfection: recurrence of infection by a different organism after discontinuation of treatment

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13
Q

pathogenesis of UTIs

A

UTI usually due to patients own intestinal flora: ascending route of infection (organisms enter the urinary tract in a retrograde fashion via the urethra)

complicating factors (catheters, nephrostomy tubes, surgery, urinary stones) results in:

  • allows organisms to enter and persist in urinary tract
  • alter the typical spectrum of organisms
  • may have multiple etiologies
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14
Q

UTI Risk Factors

A
  1. aging (increased incidence of diabetes mellitus/risk of urinary stasis, incontinence, impaired immune response)
  2. female: short urethra, sex, contraceptives that alter normal flora, pregnancy
  3. male: prostatic hypertrophy, anal sex
  4. urinary tract obstruction: tumor or calculi, strictures
  5. impaired bladder innervation
  6. hematogenous spread
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15
Q

Etiology of UTIs

A

majority of UTIs are caused by single pathogen

enterobacterales are responsible for 90% of UTIs: gram neg bacilli, facultative anaerobes, common intestinal flora

E.coli is most commonly isolated (70%)

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16
Q

features of Uro-pathogenic E. coli

A

Adherence
- uropathogenic E.coli have P fimbria which bind to P blood group antigen present on uro-epithelial cells (99% of population)

hemolysins, colinin V: resistance to complement in serum

K antigen: assoc. with upper tract infections

Type 1 fimbria: interbacterial binding and biofilm formation

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17
Q

common characteristics of uro-pathogens + examples

A

proteus, morganella, providencia (classical UTI pathogens)

produce urease - increases urinary pH = crystal/ struvite stone formation = obstructs flow - provides matrix

formation of biofilms: colonization of catheters

highly motile, produce fimbria for attachment

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18
Q

staphylococcus saprophyticus

A

typically associated with younger, sexually active females

1-5% of cystitis

Lab ID: resistance to novobiocin

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19
Q

UTI diagnosis via rapid in-office lab testing

A

dipstick testing

looks for nitrites and leukocytes produced by infection

leukocyte detection is sensitive but not specific

nitrite is sensitive for gram negative but highly specific

RBC detection is not sensitive or specific

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20
Q

quantitative culture for UTI diagnosis

A

urine culture: significant bacteriuria defined as 10^5/ ml

can use SBA, MacConkey agar, chromogenic agars

lower numbers may be significant in children or catheter collected specimens

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21
Q

urine specimen collection

A

clean catch mid stream specimens:

  • most frequently used method
  • urethra cleaned prior to collection
  • first void urine allowed to pass to clear urethra
  • mid-stream collected in sterile container

collection bags (children):

  • used in young children
  • often contaminated
  • most meaningful result is a negative culture

indwelling catheters:

  • urine obtained by inserting needle into catheter or through diaphragm
  • preferable to obtain specimen from new catheter rather than old catheter

suprapubic aspiration/straight catheters:

  • invasive
  • specimen obtained directly from bladder
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22
Q

urine specimen transport

A

sent to and processed by lab ASAP

requires method of collection and time/date of collection on specimen

after 1-2hrs must be refrigerated

unless transported in boric acid tube urine not received in 24 hrs or not refrigerated will be rejected

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23
Q

antimicrobial therapy for UTIs

A

empiric therapy:

  • based on most probable pathogens
  • lower vs upper tract infection
  • local rates of resistance
  • acute infection vs relapse/re-infection

patient management is becoming more difficult due to increasing resistance to oral first line drugs

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24
Q

typical treatment regimes for UTIs

A 
uncomplicated cystitis:
- nitrofurantoin
- fosfomycin
- TMP/SMX (24% res)
pyelonephritis:
 - ciprofloxacin 
- beta lactam + aminoglycoside
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25
Q

common RTIs (bacteria)

A

pneumonia - community acquired, nosocomial

AECB (AE -COPD)

sinusitis
otitis media
pharyngitis - sore throat

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26
Q

RTI specimen

A

sputum

BAL/ bronchial washing
nasopharyngeal aspirates / swabs

endotracheal aspirates

sinus aspirates

typanocentesis - takes pain away right away = therapeutic + you get a specimen

throat swabs = diagnosis of group A strep

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27
Q

common bacterial RTI pathogens

A

strep pneumo
h. influenzae
moraxella catarrhalis
mycoplasma pneumoniae - no cell wall
chlamydia pneumoniae – atypical cell wall
legionella pneumophila - strict intracellular susceptibility doesnt match vitro and in vivo

s. aureus
B. pertussis
gram neg/ anaerobes
s. pyogenes - primarily pharyngitis

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28
Q

what is pneumonia

A

an inflammatory condition of the lung primarily affecting the alveoli

typical signs/symptoms:
fever, cough (productive or dry), chest pain, shortness of breath

severity of disease and mortality vary considerably

CAP, HAP, VAP

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29
Q

S. pneumoniae - RTI

A

most common cause of of bacterial RTI

sm. gram positive diplococci
alpha hemolytic, bile soluble, optochin sensitive
growth often enhanced in CO2 atmosphere

most are encapsulated- most important virulence factor

colonizes the nasopharynx in 5-10% of adults and 20-40% of children

incidence increases in winter months

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30
Q

predisposition to pneumococcal infection

A 
defective Ab formation
insufficient number of PMNs
day cares, military, prisons, shelters (close quarters)
chronic respiratory disease (COPD)
infancy and aging 
diabetes, alcoholism, liver diseases
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31
Q

S. pneumoniae virulence factors

A

capsule most important virulence factor

  • aids in escape from phagocytic cells
  • aids in adherence - essential for colonization

pneumolysin (hemolysin)

  • destroys ciliated epithelial cells
  • activates classical complement pathway
  • suppress oxidative burst by phagocytic cells

secretory IgA protease

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32
Q

vaccines for pneumococcus

A

pneumovax
- 23 different serotypes that account for 90% of invasive strains protection wanes with time and age

prevnar

  • conjugate vaccine
  • indicated for use in infants less than 2 years old and adults
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33
Q

conditions under which someone should get a pneumococcal vaccine

A 
advanced age
splenectomy 
HIV/AIDS
lymphoma 
myeloma 
alcoholism 
diabetes
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34
Q

antibiotic treatment of . pnumoniae

A 
penicillins
cephalosporins 
macrolides
fluoroquinolones
vancomycin
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35
Q

relationship between patient types, pulmonary function, and likely pathogens in COPD

A

as lung function goes down you get more gram negative infections and more complicated infections such as chronic bronchitis

also get more resistant bacteria

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36
Q

COPD

A

chronic obstructive pulmonary disease

characterized by breathlessness

umbrella term used to describe progressive lung diseases including:
emphysema
chronic bronchitis 
refractory (nonreversible) asthma 
some forms of brochiectasis
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37
Q

H. influenzae - RTIs

A

most common cause of AE- COPD

small gram negative bacilli

requires X and V factors for growth

will grow on chocolate agar (5% CO2)

may be encapsulated

type b (Hib) responsible or majority of invasive disease (meningitis, epiglottitis)

introduction of Hib vaccine - now we hardly see this

majority of mucosal disease due to non-encapsulated strains

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38
Q

haemophilus species

A

see notes for table with x factor v factor and catalase results

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39
Q

porphyrin test

A

determines and isolates X factor requirement

if it turns red = does not require x factor

no colour = requires exogenous source of X

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40
Q

treatment of H. influenzae RTIs

A

approx. 18% produce beta lactamase

1% have altered PBP

2nd and 3rd generation of cephalosporins effective

newer macrolides have reasonable activity

flouroqinolones very active , but contraindicated in children

amoxicillin-clavulualante very effective

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41
Q

moraxella catarrhalis -RTIs

A

sm. gram negative cocco-bacilli

otitis media, sinusitis, AECB

carriage rate = 50%

DNase +, asacchrolytic

90% of strains are resistant to ampicillin/amoxicillin

other than tmp/smx it will be susceptible to most oral antibiotics

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42
Q

Legionella pneumophila - RTI

A

gram neg bacilli
intracellular pathogen
common in environment
widespread spectrum of illness

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43
Q

culturing legionella

A

requires L-cysteine for growth

stimulated by 5% CO2

asaccharolytic

they are motile

fastidious, BCYE agar

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44
Q

best ways to ID legionella

A

Culture

urinary Ag - excrete legionella antigens in your urine

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45
Q

treatment of legionella

A

predictably susceptible to fluoroquinolones: cipro and levo

macrolides are excellent alternative

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46
Q

morphology and physiology of mycoplasma

A

smallest free-living bacteria

small genome size: require complex media for growth

facultative anaerobes except M. pneumoniae

lack a cell wall

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47
Q

clinical syndrome assoc with M. pneumoniae

A

tracheobronchitis:

  • 50% of infections
  • prolonged post-infectious cough

pneumonia:

  • approx 20-30% of infections
  • mild disease but long duration
  • most common cause of atypical pneumonia
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48
Q

antibiotics to treat atypical pathogens in RTIs

A

mycoplasma/chlamydia pneumoniae

not susceptible to cell wall active agents

highly susceptible to doxycycline, macrolides, and fluoroquinolones

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49
Q

bordetella pertussis -RTI

A 
causes pertussis 
sm. gram neg, cocci-bacilli
strictly aerobic, fastidious
requires growth on media containing charcoal, blood, or starch
BG or RL medium
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50
Q

classical course of pertussis disease

A

see notes

3 phases

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51
Q

lab diagnosis of pertussis RTI

A

naso-pharyngeal specimens are best yield

typically culture on BG agar and then do PCR

treatment = macrolides: azithromicin or clarithromicin

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52
Q

bacterial pharyngitis

A

caused by S. pyogenes
- gram +, catalse (-), beta haemolytic (grp A), PYR+, susceptible to TaxoA

treatment: pen/ amoxicillin

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53
Q

non-suppurative complications of bacterial pharyngitis (S. pyogenes)

A

rheutmatic heart disease
- treat patients to prevent this from happening

post-streptococcal glomerulonephritis:
- going to get this wether you you receive treatment or not ( don’t always get it)

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54
Q

arcanobacterium hemolyticum

A

pharyngitis in teens and young adults

  • rash similar to scarlet fever
  • invasive disease occurs but rare

usually doesn’t respond well to pen but disease is self limiting

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55
Q

culturing arcanobacterium hemolyticum

A

if doctor suspects this then incubate plate for 72hrs with CO2

usually weakly beta hemolytic - best seen on rabbit blood

anaerobically= slower growth

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56
Q

reasons for treating bacterial pharyngitis

A

only speeds up disease resolution by 18-24 horus so this is not why

eradication of the organism and stop the spread is a reason

most important reason is that it prevents complications - but you have 10 days to treat after onset so no need for empiric treatment

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57
Q

reasons to look for respiratory viruses

A

discontinuation of antibiotics

reduce unnecessary investigations

initiation of specific antiviral therapy

interventions = vaccine (flu)

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58
Q

how are viral RTIs transmitted?

A

droplet (not aerosol)
- tend to be enveloped

contact

sporadic cases
- outbreaks are common

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59
Q

specimen collection for viral RTIs

A

nasopharyngeal (NP) swab or aspirates
- need transport media (keeps nucleic acids stable) - does not support growth

bronchial alveolar lavages

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60
Q

what factors does viral RTI

A 
clinical illness
timing of collection (most important): preferably within 48hr
host factors
type of specimen
specimen transport 
diagnostic test
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61
Q

diagnostic methods for viral RTIs

A

EM - not good for diagnostics

culture + direct fluorescent antibody (DFA) - poor sensitivity

rapid antigen testing - poor sensitivity

molecular methods - high sensitivity + specificity (expensive)
- examples:
multiplex PCR and RT-PCR

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62
Q

Rhinovirus

A

most common viral RTI

number 1 cause of common cold

ssRNA+

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63
Q

coronavirus

A

2nd most common viral RTI

common cold (typically)

some strains linked t severe disease such as SARS

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64
Q

enterovirus

A

mild respiratory illness

aspectic meningitis
rash - hand, foot and mouth

EV-D68 = viral RTI linked to acute flaccid paralysis (similar to polio)

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65
Q

adenovirus

A

more than 60 types

spectrum of disease: RTIs, conjunctivitis (eye), hemorrhagic cystitis

types 40 and 41 cause GI illness

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66
Q

parainfluenza viruses

A

common cause of upper RIT in children

approx. 2% get croup:
inflammation of upper airway
narrowing subglotic region
barking cough

tends to go away on its own

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67
Q

respiratory syncytial virus (RSV)

A

most common cause of bronchiolitis in children

can also infect adults

severe infections can be fatal

antiviral = ribavirin for severe cases only

no vaccine YET

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68
Q

influenza virus

A

3 types: A, B, C (rare)
A and B cause seasonal pandemics

Flu A is the most important: causes more severe disease compared to B and has pandemic potential

sub typing based on hemagglutinin (HA) and neuraminidase (NA)

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69
Q

influenza symptoms

A

onset is abrupt
congestion/sneezing/sore throat = rare

cough = common (dry but severe)

headache
fever
fatigue/malaise - common/lasts for weeks

muscle pain - often severe

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70
Q

antiviral treatment for influenza

A

adamantanes = M2 channel inhibitor

neurominidase inhibitors:
oseltamivir or zanamivir

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71
Q

antiviral resistance

A

immunocompromised host:

  • virus shed for long periods of time
  • predisposes for development of resistance

amantidine is no longer an option bc mutations in the M2 channel amino acids = all fluA resistant
fluB doesn’t have M2 channel

resistance to neuraminidase inhibitors = mutations in surface proteins HA and NA

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72
Q

influenza vaccines

A

quadruvalent vaccine:
Flu A: pH1N1, H3N2
flu B: 2 lineages

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73
Q

antigenic drift

A

viral RNApol makes mistakes

mutations over time in surface glycoproteins (HA and NA)

mutations in vaccine-antibody epitope = mismatches

may lead to vaccine ineffectiveness

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74
Q

when do influenza pandemics arise?

A

no existing immunity

FluA becomes well adapted to human replication and spread

antigenic shift (result of genetic reassortments)

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75
Q

flu reservoirs

A

aquatic birds - direct transmission can occur but not common

only some flu strains are adapted to humans

pigs have receptors for both avian and human lineages = mixing species

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76
Q

antigenic shift

A

influenza has segmented genome (8 rna segments)

genetic reassortments between avian/swine/human flu

new viruses emerge with different HA and NA combinations

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77
Q

avian influenza A

A

poultry birds can also carry flu

transmission = direct contact with infected birds or objects contaminated but their feces

doesn’t have efficient human to human spread but they are usually fatal or very severe

example = H7H9
40% mortality but no sustained human-to-human transmission

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78
Q

CNS infections

A

life threatening - associated with mortality and morbidity

acute, sub-acute, chronic

clinical findings determined by anatomic sites, infecting pathogen, host response

vulnerability of CNS to effects of inflammation and edema mandates prompt diagnosis with appropriate therapy if consequences are going to be minimized

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79
Q

types of acute CNS infections

A

meningitis (bacteria/viral)

menigoencephephalitis (usually viral)

brain abscess

subdural empyema (pus)

epidural abscess

septic venous sinus thrombophlebitis

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80
Q

meningitis definition

A

an infection that causes inflammation of the membranes covering the brain and spinal cord

non-bacterial meningitis = aseptic meningitis

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81
Q

causes of meningitis

A

bacterial infections

viral infections

fungal infections

inflammatory diseases

cancer

trauma to head or spine

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82
Q

viral meningitis

A

generally benign, rarely fatal

enterovirus = 80% of cases

other viruses = mumps, EBV

HSV = rare but serious

most clear in 3-8 days

HSV/VZV - require systemic antivirals

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83
Q

causes of bacterial meningitis based on age range

A 
less than 3 months old:
grp B strep
L. monocytogenes
E.coli
S. pneumoniae

3 months -18yrs
N. meningitidis
S. pneumoniae
H. influenzae

18-50yrs
S. pneumoniae
N. meningitidis
H. influenzae

50+
S.pneumoniae
L. monocytogenes
gram neg bacilli

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84
Q

steps in meningococcal infection

A

nasopharyngeal colonization

invasion of epithelium

invasion of blood

further dissemination into cerebrospinal fluid

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85
Q

meningitis symptoms

A

see notes for bacterial vs bacteria + shared symptoms

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86
Q

goals for managing a patient with acute CNS infection

A

quickly recognize the acute CNS infection

initiate empiric therapy asap:
- ideal to get CSF before antimicrobials but if there is going to be any delay - initiate drugs

quickly ID causative organism - adjust management if needed

optimize management for complicating features

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87
Q

diagnostic test for meningitis

A

lumbar puncture:
collects CSF

spinal needle is inserted between the 3rd and 4th lumbar vertebrae

allows for the urgent distinction between viral and bacterial meningitis

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88
Q

typical CSF findings in viral vs bacterial meningitis

A

see notes

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89
Q

neisseria meningitidis

A

gram neg diplococci
polysaccharide capsule

13 sero-groups classified by their capsule - 5 accoutn for disease: A/B/C/Y/W-135

appear intracellular in gram stain

catalase +

oxidase +

grows on chocolate and blood agar

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90
Q

clinical presentations of meningitis

A

fever + headache (flu like symptoms)

stiff neck

nausea

altered mental status

seizures

up to 40% fatality

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91
Q

clinical presentations of meningococcemia

A

rash

vascular damage

DIC

multi-organ failure

shock

death can occur in under 24hrs

fatality rate = 3-10%

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92
Q

transmission of meningitis

A

humans only

asymptomatic pharyngeal carriage can occur in 10-30% of the population

transmission by saliva, most often by aerosol effect (coughing, sneezing), kissing

incubation period varries between 2-10days

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93
Q

prevention of meningitis caused by N. meningitidis

A

monovalent serogroup C

quadrivalent serogroups: A/C/Y/W-135

monovalent serogroup B

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94
Q

listeria monocytogenes

A

gram postive

CAMP+

catalase +

tumbling motility at 25 degrees

umbrella motility in semi-soft agar

beta hemolytic

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95
Q

clinical manifestations of L. monocytogenes

A

meningitis

abortion

perinatal septicemia:

  • infant dies shortly after birth
  • symptoms = disturbance of respiratory, circulatory, central nervous system
  • if infant survives = meningitis or permanent mental deficiency

others = influenza like/ GI

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96
Q

L. monocytogenes virulence

A

listeriolysin O = most significant virulence factor

responsible for beta hemolysis on RBCs

destruction of phagocytic

aids in escape from the phagosome

present in all strains

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97
Q

management of meningitis

A

if possible obtain CSF before antibiotic treatment

in adults 3rd gen cephalosporin and vancomycin are empirically given

ampicillin added if patient is at risk for L. monocytogenes (50+)

steroids often added concomitantly

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98
Q

C. Difficile

A

anaerobic, spore forming, gram positive rod

major cause of nosocomial infectious diarrhea

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99
Q

pathogenesis: C diff colonization

A

see notea

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100
Q

C. diff pathogenesis: disruption of microflora

A

antibiotic exposure disrupts flora = selection for c. diff

c diff colonizes and then starts to produce toxins

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101
Q

C.difficile toxins

A

without the toxins they are unable to produce disease

paloc pathogenecity locus: 2 toxins = TcdA and TcdB

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102
Q

inflammation caused by C. diff

A

inflammation of the colon = colitis

neutrophil infiltration
intestinal damage
impaired permeability
fluid secretion

overall result = diarrhea and inflammation

103
Q

C. difficile associated disease (CDAD)

A 
spectrum of disease:
asymptomatic (colonization)
antibiotic assoc, diarrhea (AAD)
psuedomembranous colitis (PMC)
toxic megacolon (rare)
104
Q

lab diagnosis of C.diff (pathogenic)

A
  1. detection of C. diff
    - do an EIA for C. diff by looking for glutamatedehydrogenase (GDH) common to all c. diff

then:

  1. detection of toxins:
    - cell culture cytotoxicity neutralization assay (CCCNA)
    - EIA for toixin
    - nucleic acid amp test (PCR)
105
Q

toxin enzyme immunoassays

A

toxin B alone or toxin A and B

never do just toxin A bc it is sometimes deficient

sometimes do this in combination with GDH

106
Q

management and prevention of C. difficile

A

barrier precauaitons and envrionmental cleaning in hospitals

stop unnecessary antimicrobial use

107
Q

new approaches to treating C.diff

A

biotherapuetics - microflora restoration

fecal transplants: repopulation had successes in clinical trials

108
Q

indications of viral gastroenteritis

A

incubation period is longer than toxigenic disease

no warning signs of bacterial infection like high fever, bloody diarrhea, sever abdominal pain

vomiting is often prominent

duration: entire illness is usually over in 24-72 hours

no epidemiological clues to suggest alternative diagnosis

109
Q

common viruses associated with gastroenteritis

A

caliciviruses

adenoviruses (40and 41)

astroviruses

rotavirus

Hep a and E

110
Q

caliciviruses

A

4 genera, 2 cause human disease:
norovirus = most common cause of actue viral gastroenteritis in adults

saporovirus = rare cause of human disease

clinical presentaiton: projectile vommiting/ explosive diarrhoea

111
Q

epidemiology of norovirus

A

highly infectious - low infectious dose (1-10 partcicles)

transmission = fecal-oral or contact/fomites

viral shedding

112
Q

detection of norovirus

A

real time RT-PCR

sequencing for genotyping

113
Q

rotavirus

A

looks like a wheel
non-enveloped
3 capsids: outer, inner, intermediate

7 groups: A-C cause human disease

detected by RT-PCR or EIA from stool

114
Q

transmission of rotavirus

A

low infectious dose: 10-100

by age 3 majority of children have been infected

transmission = fecal-oral, food/waterborne

115
Q

clinical features of Rotavirus in children

A

low grade fever

vomiting for 2-4 days

explosive, non-bloody diarrhea

hospitalized for dehydration
- treat with IV fluids + electrolytes

116
Q

epidemiology of rotavirus

A

25-65% of severe gastroenteritis is in children

6% of deaths among children under the age fo 5

117
Q

current rotavirus vaccines

A

rotarix: IV and monovalent

RotaTeq: oral and pentavalent

118
Q

enteric adenoviruses

A

linear DNA, non-enveloped

serogroup F, serotypes 40 and 41 cause gastroenteritis

119
Q

enteric adenoviruses vs noro/rotavirus

A

longer incubation period: 3-10 days

less fever and dehydration

more prolonged sickness

more likely to infect children than adults (like rota)

diarrhea +, no vomiting

transmission = fecal-oral

detected by RT-PCR or EIA testing on stool

120
Q

astrovirus

A

ssRNA +, non-enveloped

infections mainly in childhood

decal oral spread, low infectious dose

similar to rotavirus but less vomiting, fever, and nausea

detected by RT PCR

121
Q

waterborne vs bloodborne hepatitis

A

see notes

122
Q

hepatitis A

A

in developing countries: usually contracted in childhood

developed countries: adutls who travel to endemic countries or out breaks in food/water

usually self limiting

no chronic disease

risk of symptoms increases with age

123
Q

hepatitis A symptoms

A

fatigue
nausea/vomiting
abdominal pain

jaundice (yellow skin and eyes)

dark amber urine

124
Q

diagnosis of HAV

A

serology

early in disease HAV is excreted in stool so pcr is possible

diagnosis usually made by serology: IgM = acute infection vs IgG = immunity

125
Q

prevention of hep A

A

natural infection confers life long immunity

vaccination: HAV or can get HAV and HBV

126
Q

diagnosis of viral gastroenteritis

A

EM- nope

culture of enteric adenoviruses is possible but not sensitive (noro cant be cultured)

antigen detection (EIA) - sensitivity = only 60%

molecular testing - much more sensitive

serology = not typical for GI viruses except for HAV

127
Q

prevention of gastroenteritis

A

hand washing
removal of source of infection

decontamination of environment (bleach)

vaccines

128
Q

neisseria classification

A

see notes

129
Q

N. gonorrhoeae

A

aerobic gram negative diplococci (Ox+, Cat+, superoxol+)

often appear intracellular on gram stain

fastidious
- grow on TM media (chocolate agar with antibiotics)

130
Q

epidemiology of N. gonorrhoeae

A 
risk factors :
less than 25 yrs
street youth/homeless
new sexual partners (more than 2/year)
non-barrier contraception
131
Q

clinical manifestations of N. gonorrhoeae

A 
acute urethritis/cervicitis 
ano-rectal gonorrhea
pharyngeal gonorrhea
pelvic inflammaotry disease (PID)
septic arthritis
132
Q

transmission/epidemiology of N. gonorrhoeae

A

risk of transmission of GC from infected woman to male =1/5

risk of transmission from male to female =1/2

perinatal transmission occurs during vaginal delivery and typically involves the eyes

risk during anal sex is high too

133
Q

virulence factors associated with N. gonorrhoea

A

pili:

  • adherence to mucosal surfaces
  • inhibit killing by neutrophils

outer membrane:

  • proteins (OMPs) facilitate invasion of epithelial cells
  • lipooligosaccharides possess endotoxin activity, results in ciliary death
134
Q

pathogenesis of N. gonorrhoeae

A

primarily infects columnar or cuboidal epithelium - found in cervix

attachment mediated by pili and OMPs

epithelial cells penetrated within 20-24hrs

vigorous neutrophil response follows with sloughing of epithelium and exudation of pus (neutrophils)

infection may spread - proximal genital tract, blood stream and joints

135
Q

culture/diagnosis of gonorrhoea

A

does not grow on SBA
for culture used to take urethral of cervical swabs

now we use PCR

  • vaginal swabs
  • voided urine for males
136
Q

sensitivity vs specificity

A

sensitivity = the percentage of sick people who are correctly identified as being sick

specificity = the percentage of healthy people who are correctly identified as negative for disease

137
Q

positive vs negative predictive value

A

positive: proportion of patients with positive test results who are correctly diagnosed. its value is dependent on the the prevalence of the disease
negative: proportion of patients with negative test results who are correctly diagnosed

138
Q

antimicrobial resistance treatment options for gonorrhoea

A

plasmid mediated beta lactamases

tetracycline resistance is common

fluoroquinolone resistance common

current recomendation: 800 mg cefixime or 250mg ceftriaxone intramuscular

139
Q

chlamydia classification

A

c. trachomatis
c. pneumoniae
c. psittaci

biphasic life cycle (notes)

140
Q

chalmydia infections

A

urethritis in men:

  • incubation period = 7-21 days
  • 25% of men are asymptomatic

cervicitis in women:
- 80% are asymptomatic + have normal cervical exam -this makes control of PID complicated

urethritis in women

141
Q

laboratory diagnosis of chlamydia

A

antigen detection

immuno-fluorescence

cell culture

PCR(male urine, vaginal swab)

142
Q

treatment of chlamydia

A

1st line: 1g azithromycin (single dose)

2nd line: 100mg BID doxycycline (10 days)

143
Q

haemophilus ducreyi

A

cause chancroid ulcers/ bubos (STI)

morphology:

  • intracellular or extracellular
  • pleomorphic cocco bacilli or short rods
  • gram variable
  • bipolar staining
  • arranged in parallel chains
144
Q

cultural characteristics and growth requirements of haemophilus ducreyi

A

fastidious organism
grows slowly on chocolate agar
use of two medias is optimal
gonococcal agar or mueller hinton based medium

145
Q

treatment of haemophilus ducreyi (chanchroid)

A

1g azithromyci (single dose) or 250 mg ceftriaxone intramuscular

146
Q

molluscum contagiosum diagnosis

A

clinical appearance:

  • dome shaped with dimpled center
  • smooth waxy or pearly surface
  • core = curd like (cheese/waxy)

electron microscopy (insensitive)

PCR in reference labs only

147
Q

symptoms of molluscum contagiosum

A

not painful but sometimes itchy

scratching can cause irritation + scarring

secondary bacterial infections

shaving = bleeding risk+spread

148
Q

molluscum contagiosum transmission

A

contact:

  • affects skin/mucosal membranes
  • sexual or scratching/touching skin

indirect = fomites such as clothes or towels

149
Q

molluscum contagiosum treatment

A

chemical or surgical removal

150
Q

herpes simplex virus (HSV)

A

HSV-1 +HSV-2= enveloped, icosahedral capsid, dsDNA

two important enzymes: thymidine kinase and DNA polymerase

151
Q

HSV epidemiology

A

HSV2 = second most common sti

HSV1 causes cold sores - 80% of the population

40% of genital herpes is caused by HSV-1

most people dont know theyve been infected bc primary infections are usually asymptomatic

first symptoms = usually reactivation

152
Q

HSV spectrum of disease

A

encephalitis
ocular infections
muco-cutaneous lesions

153
Q

HSV latency and reactivation

A

primary infection = local replication and viral entry into neurons - migration along the axons to ganglia = latency

replication (triggered by stress or immunosuppression) - migration to epidermis = reactivation

154
Q

reactivation of HSV-1 vs HSV-2

A

HSV-2: reactivation is frequent
- asymptomatic shedding on 28% of days

HSV-1: reactivation is less frequent, less than once a year
- asymptomatic shedding occurs less frequently

155
Q

acyclovir mechanism of action

A

it is a pro-drug that blocks viral DNA polymerase by acting as a nucleotide analogue

requires phosphorylation by viral thymidine kinase - then gets phosphorylated by host enzymes

156
Q

acyclovir resistance

A

less frequent in immunocompetent hosts

resistance mechanism = thymidine kinase mutats (95%)
viral DNApol (5%)
157
Q

alternative treatments for HSV

A 
cidofivir = phosphorylated nucleotide analog (doesn't need TK)
foscamet = pyrophosphate analog (blocks viral DNApol)
158
Q

diagnosis of HSV

A

molecular testing: RT-PCR or other NAAT

159
Q

human papilloma virus (HPV)

A

non-enveloped, dsDNA circular
most common sti (80% of adults)

cannot be grown in culture
-pap test are best for ID

160
Q

high risk vs low risk HPV strains and what they cause

A

high risk: 16 and 18 - cause cancer - low or high grade pap smear abnormalities

low risk: 6 and 11 - cause anogential warts and recurrent respiratory papillomatosis

161
Q

respiratory papillomatosis

A

benign warts in the upper airway
- may cause obstruction
surgical removal

caused by hp 6 and 11

childhood - normally aquired at birth

adult - oral intercourse

162
Q

how to treat genital warts

A

treatment is usually for aesthetic reasons
- clearnence rate = 30-90%

available treatments:
- podophyllin resin
- trichloroacetic acid (TCA)
cryotherapy

163
Q

HPV acquisition

A

hpv is acquired shortly after onset of sexual intercourse

coninfection with multiple strains is common

38% of females get hpv after one year of being sexually active

164
Q

HPV infection

A

individual episodes last between 4-20 months

for most people = transient infection (nothing happens)

body’s immune system eliminates hpv infection

for infections that clear, reappearance of same type is common

165
Q

why are only some HPV strains oncogenic?

A

high risk strains integrate into the host DNA as linear - disrupts E2 (transcriptional repressor) = increase in expression of E6andE7

drives cell growth = cancer

166
Q

development of cervical cancer from HPV infection

A

hpv infects basal layer cells

hpv replicates and infects squamous epithelial cells = squamous intraepithelial lesion

abnormalities arise as E6/E7 are produced

proceeds to invasive cancer

167
Q

detection of the development of cervical cancer

A

do a primary screen (pap test)

detection of patients with cervical cell abnormalities = atypical squamous cells of unknown significance (ASCUS)

do follow up

168
Q

HPV prevention

A

vaccines

gardasil = types 16,18, 6, 11

ceravix = 16 and 18 only

169
Q

epidemiology of bacterial GI infections

A

developed countries:

  • waterborne/foodborne outbreaks
  • overall burden not well established
  • attack reate: 1-3 illnesses per child/year

developing countries:

  • major cause of morbidity and mortality in children
  • 10/18 illnesses/child/year
  • 4-6 million deaths/year (asia, latin America, africa)
170
Q

ID of bacterial GI based on incubation periods

A

really short time span (hours): toxin mediated

really long time (2-8 days): E. coli 0157

171
Q

lab diagnosis/ appropriate specimens

A

1g of feces contains approx. 10^11 bacteria therefore selective media must be used

most bugs present in 3 days so if stool is from patient admitted to hospital more than 3 days ago sample is rejected

formed stool should also be rejected

on requiest use TCBS agar for virbio

routine agars: XLD, Campy, MacConkey, sorbitol MacConkey, chromogenic

172
Q

camplyobacter

A

gram neg, highly motile, spiral rod
C. jejuni & C. coli

thermophillic (25-44)

microaerophilic

isolation on blood/charcoal containing agar + antibiotics

C. fetus occasionally associated with disease

173
Q

campylobacter infection

A

incubation period: usually 2-4 days
infective dose= large

prodrome of fever, myalgia

diarrhoea (occasionally bloody) - abdominal pain and malaise

usually self limiting, resolves within 7 days - only treat if bacteremic or immunosuppressed

occasionally assoc. with guillain barre syndrome

174
Q

salmonella species

A

only 2 species: s. enterica (most relevant) and s. bongori

over 2000 serovars such as S. typhimurium

175
Q

salmonella antigenic structure

A

kauffmann-white antigenic scheme: agglutination reactions with specific antisera against salmonella antigens

O antigens:
- O polysaccharide of LPS

H antigens:
- flagellar antigens (protein)

Vi antigens (S.typhi only)
- capsular polysaccharide
176
Q

salmonella gastroenteritis

A

incubation period depends on dose (infectious dose = 1million+)

symptoms (within 48-72hrs)

  • nasuea/vomiting
  • diarrhoea
  • abdominal pain
  • myalgia + headache
  • fever

duration = 2-7days

usually self limiting

only fatal in elderly/immunocompromised

177
Q

salmonella enteric fever

A

caused by S. typhi

incubation period = 10-14 days

bacteraemic illness:

  • myalgia and headache
  • fever
  • splenomegaly
  • abdominal pain
  • leukopenia
  • rose spots/ rash

blood, bone marrow, stool and urine cultures are positive

potential consequence: intestinal hemorrhage and perforation

178
Q

isolation of salmonella

A

pre-enrichment broths:
-selenite or tetrathionate

selective and differential media
-XLD, HE. SS agar, Bismuth-sulfite agar

179
Q

XLD

A

selective and differential medium designed for the isolation of gram negative enteric pathogens from clinical specimens

contains xylose, lysin, sodium desoxycholate, sodium thiosulfate, and ferric ammonium citrate

180
Q

prinicple of XLD selection

A

all enterics ferment glucose except shigella

salmonella rapidly uses xylose and the decarboxylates lysine (mimics the shigella rxn) - reverts to alkaline conditions

(lactose and sucrose are added in excess to prevent lactose fermenters from doing same thing)

production of hydrogen sulfide under alkaline conditions results in black colonies (salmonella)

181
Q

E.coli 0157 infection

A

incubation period = 3-9 days
infectious dose= 10 bugs

diarrhoea: mild to grossly bloody (haemorrhagic colitis)

severe abdominal cramping

HUS in up to 10% of cases:
-anemia, thrombocytopenia, kidney damage

significant mortality (1-5%)

182
Q

shiga-like toxin on E.coli 0157

A

a distinguishing virulence factor

subunit toxin:
A: inhibits protein synthesis by acting on ribosomes
B: binds glycolipid receptor in mammalian cells (renal endothelium)

183
Q

E.coli 0157

A

virtually all 0157 stains do not ferment sorbitol (most non-0157 strains do)
- use a sorbitol-MacConkey agar where lactose is replaced with sorbitol

0157 strains are beta-gluconidase neg

latex agglutination to confirm 0157 strains

ID is important bc:

  • antibiotics/antimotility agents are a risk factor for HUS
  • want to know if you’re dealing with an outbreak
184
Q

shigella species

A

S.dysenteriae (grp A)
S. flexneri (grpB)
S boydii (grpC)
S. sonnei (grpD)

tests:
Urea -
motility -
TSI K/A - no gas
all ferment mannitol except  s.dysenteriae
185
Q

clinical significance of shigella

A

shigellosis or bacillary dysentery

infectious dose = low
fecal-oral route (may be person to person)

2-4day incubation

fever, cramping, abdominal pain, watery diarrhea

may be followed by frequent scan stools with blood, mucous, and pus (invasion of intestinal muscosa)

disease severity depends on infecting species

186
Q

shigella antigenic structure and virulence factors

A

A, B, C, D grouping is based on O antigen serotyping
- similar O antigen to E.coli so need to ID as shigella first

shiga toxin = virulence factor
- produced by dysenteriae and in smaller amounts from S. felxneri and S.sonnei

187
Q

yersinia enterocolitica

A

infection can mimic appendicitis

virulence = result of tissue invasiveness by the organism

main pathogenic strains from swine but also get it from:
beef, lamb, seafoods, veg milk, cake, vaccum packaged meet

grown on MacConkey agar

188
Q

vibrio, aeromonas and plesiomonas: similarities and differences compared to enterobacteriaceae

A

similarities:

  • gram negative
  • facultative anaerobes
  • fermentative bacilli

differences:

  • polar flagella
  • oxidase positive

the three used to be vibrionaceae:
- primarily found in water sources + cause GI disease

189
Q

morphology and physiology of vibrio

A

shaped like commas

v.cholerae, v. parahaemolyticus, V. vulnificus = significant

broad temp/pH range

grow on MacConkey and TCBS

V.cholerae grow without salt, most other vibrios are halophilic

190
Q

taxonomy of vibrio cholerae

A

over 200 serogroups based on somatic O antigen
O1 and 0139 = epidemic cholera
O1 subdivded into El Tor and classical

some O1 strains dont produce cholera enterotoxin

191
Q

pathogenesis of V. cholerae

A

incubation period: 2-3 days

high infectious dose > 10^8 CFU
- lower if you have reduced stomach acid

abrupt onset of vomiting and life threatening diarrhea (15-20L a day)

as more fluid s lost, feces streaked stool changes to rice water stool

192
Q

encephalitis

A

inflammation of the brain itself

meningitis symptoms + mental status changes

seizures, decreased consciousness, confusion, hallucination

193
Q

indications of viral CNS infection

A

gram stain does not show bacteria

WBCs are less than 300 and mainly lymphocytes

occasionally increased RBCs (HSV)

normal to mid-high protein

normal glucose

194
Q

etiology of viral CNS infections

A

enterovirus
HSV 1 and 2
arboviruses
rabies

195
Q

enterovirus epidemiology

A

RTIs
myocarditis, exanthems (rash), acute flaccid paralysis

causes 30-50% of viral meningitis = aseptic meningitis

people at risk: anyone

seasonal outbreaks are common

196
Q

enterovirus aseptic meningitis

A

usually RTI symptoms

sometimes vomiting

severe headaches

photophobia

no longterm sequelae

will go away on its own

197
Q

diagnosis, treatment, prevention of enterovirus CNS infection

A

diagnosis

  • clinical suspicion: RTI, meningitis, photophobia
  • CSF profile (high WBC (lymphocytic), mod-high protein)
  • CSF rt-pcr

prevention: no vaccine available

treatment: supportive as needed
- antivirals are no longer available/effective

198
Q

HSV - encephalitis epidemiology

A

most common cause of sporadic viral encephalitis in north america

no seasonal distribution

high morbidity/mortality without treatment

199
Q

pathogenesis of HSV encephalitis

A

rare to occur from primary infection

often a reactivation from latency

200
Q

clinical manifestations of HSV encephalitis

A

fever/headache

progressive neurological symptoms

mental status changes are frequent (temporal lobe)

seizures = common

long term neurological sequelae are possible

immunodeficiency can lead to systemic spread = often fatal

201
Q

diagnosis of HSV encephalitis

A

clinical suspicion (mental status changes)

CSF profile (high wbc, mod/high protein, high rbc)

CSF pcr for hsv 1/2

diagnostic imagaing (MRI or CT) - temporal lobe involvement

202
Q

prevention and treatment fo HSV encephalitis

A

no vaccines

treat empirically with acyclovir

203
Q

rabies virus epidemiology

A

common in developing countries but rare in north america

204
Q

rabies virus transmission

A

transmission through saliva of infected animals

reservoir in north america = bats, skunks, raccoons and foxes

infected animals show no fear of humans and are agitated
bat bites often go unnoticed
rare form domestic pets

205
Q

pathogenesis of rabies virus

A

rabies is neurotropic = affinity for nerve cells/tissue

has a long incubation descending on the location of the bite - will infect other things on the way to the brain

206
Q

clinical manifestations of rabies

A 
fever 
agitation 
hydrophobia = fear of water 
painful spasms - infecting muscles on way to brain
excessive saliva
207
Q

lab diagnosis of rabies virus

A

clinical suspicion with exposure history

CSF profile not helpful

post-mortem exam of the animal or human is best

post-mortem on CSF/saliva/tissue

DFA on neck skin biopsies - specifically need the skin with hair follicles

208
Q

treatment and prevention of rabies virus infection

A

prevention = vaccine
- only covered for people at risk (vets)

treatment = rabies immunoglobulin and vaccine

  • was cute/bite with soap and water then add Ig directly to opening
  • administer vaccine at same time
209
Q

arboviruses

A

transmitted through vectors

-insect that can transmit an infection - transmits from one infect animal to another

210
Q

zika virus

A

association with microcephaly

211
Q

arboviruses that cause encephalitis

A

west nile virus (WNV)
Japanese encephalitis virus
eastern equine encephalitis virus
la crosse virus

212
Q

clinical manifestations of arboviruses

A

most are asymptomatic
mild, non-specific viral syndrome
meningoencephalitis (fever, headache, seizures)

severity varies with virus and host

longer term neurological sequelae are possible

213
Q

epidemiology of arboviruses

A

seasonal bc of mosquitos

geographically distributed - need vector and reservoir

214
Q

transmission cycles of arboviruses

A

epidemic cycle

endemic cycle

enzoonotic cycles

and all of these cycles can overlap

215
Q

epidemic transmission cycle of arboviruses

A

reservoir = humans (high level of viremia)

vector readily transmits virus between humans

examples: dengue, yellow fever, chickungunya

216
Q

enzootic transmission of arboviruses

A

reservoir = vertebrae host (has virus without showing symptoms)

vector = mosquito

humans are incidental hosts (there is no human to human spread and low viremia)

example = west nile virus

217
Q

epizooic cycle (rural cycle)

A

virus amplification in animal (gets visibly sick)

possible spillover into humans

218
Q

diagnosis, treatment, and prevention of arboviruses

A

diagnosis:

  • clinical suspicion: exposure/travel
  • CSF profile: high wbc (lymphocytic, mod-high protein
  • pcr on CSF + serology

treatment: supportive

prevention: no vaccine for most
but have things like: nets, insect repellent, clothing

219
Q

CA-MRSA

A

serious community acquired infections

necrotizing skin and soft tissue infections

several clonal groups/PVL positve

treat with: TMP/SMX, doxycycline, and clindamycin

220
Q

definition of MRSA

A

novel PBP

PBP-2a has reduced affinity for beta-lactam agents- can perform essential functions for other pbp

encoded on the mecA gene - acquired via transposition but is now chromosomal

221
Q

homogenous vs heterogeneous expression

A

homogenous - all bugs have the resistance

heterogenous - see a haze after about 24hrs around the disk because the resistant organisms start to move in

222
Q

detection of MRSA

A

muller hinton agar with salt and oxicillin

or chromogenic agar with cefoitin (better at inducing mrsa)

223
Q

risk factors for CA-MRSA

A 
younger age groups (us)
IV drug users
lower economic status 
MSM
crowded conditions
224
Q

factors that cause spread of CA-MRSA

A

-skin to skin contact
-cuts and abrasions
-shared contaminated items/surfaces
-poor hygiene
crowded living conditions

225
Q

clinical manifestations of CA-MRSA

A

halmark = pus

boils or draining pimples

sores that won’t heal

red areas of the skin that feel warm

systemic infections

226
Q

MRSA genetics

A

MecA gene complex is carried on specific integrated genetic element = staphylococcal cassette chromosome (SCC)

5 types of SCC-mec

HA-MRSA mec has types 1,2,3

CA-MRSA strains have type 4 (don’t carry multiple resistance genes) - usually only resistant to beta lactams and erythromycin

227
Q

panton-valentine leucocidin (PVL) toxin

A

cytotoxin present in less than 5% of MRSA

rare in HA

capable of destroying WBC

severe tissue damage and associated with necrotic skin lesions

severe necrotizing pneumonia

228
Q

vancomycin resistant enterococci (VRE)

A

intrinsic glycopeptide resistance in gallinarum and casselifavus but chromosomal

faeciuma and faecalis have transferable resistnance

229
Q

ID of enterococcus

A

motility
E. faecium/faecalis = non.motile
gallinarurm = motile (mostly)

pigment:
E.casselifavus = yellow pigment (not visible on plate)

glucopyranoside
gallinarium/casselifavus = +
faecium/faecalis = -

230
Q

CRE

A

carbapenem resistant enterobacterales

KPC = K. pneumoniae cabapenemase (first discovered in kp but exists in other organisms)

NDM = bad one

231
Q

modified carbapenem inactivation method mCIM

A

fill tubes with broth
inoculate with bug of interest

put in merepenem disks - incubate

inoculate pate with susceptible E.coli strain

takes the disks out and put them on the plate

if the organism produced a carbapenemase then the disks will not work against e coli

232
Q

classifications of SSTIs

A

related to the depth fo the infection

uncomplicated = superficial wound

complicated = deep wound

233
Q

cellulitis

A

acute

infection of dermis and epidermidis

inflammation but little/no necrosis or edema

lymphatic involvement

fever, chills, leukocytosis

bacteremia (30% of cases)

s.aueus and strep pyogenes

234
Q

bugs that infect surgical wounds

A 
s. aureus
enterococci
coag neg staph
e.coli
p. aeruginosa
235
Q

bacteria that infect traumatic woulds

A

S.aureus and enterobacterales

streptococci/clostridia

vibrio vulnificus (salt water wounds)

236
Q

vibrio vulneificus

A

infection results when skin lacerations or abrasions come in direct contact with seawater

infections begin with swelling, redness, and intense pain around the infected site

develop and progress to tissue necrosis in a rapid process

50% require surgical intervention

237
Q

bacteria that infect burns

A 
s.aureus
enterobacter clocacae
coag-neg
staphylococci
p.eruginosa 
e.coli
enterococcus spp
238
Q

bacteria that infect bites

A 
pasteurella maltocida
capnocytophaga canimorsus
eikenlla corrodens 
peptostreptococci
alpha and beta strep
239
Q

staph enzymes

A

coagulase:
fibrin coagulum
sets up localized infection

hylauronidase:
hydrolyzes hyaluronic acids in the intracellular matrix of connective tissue - facilitates spread of s.aureus through tissues

240
Q

staph toxin: exfoliative toxin

A

exfoliative toxin genes are carried on plasmids

mechanism of action is unknown

leads to disturbance of the adherence of cells in the stratum granulosum layer of the epidermis

neutralizing antibodies develop after infection, protecting older children and adults

241
Q

staphylococcal scalded skin syndrome

A

abrubt onset of a localized peri-oral erythema (redness and inflammation around the mouth) - covers entire body in 2 days

large bullae or cutaneous blisters form - then sequamation of the epithelium

caused by exfoliative toxin

242
Q

toxic shock toxin

A

responsible for toxic shock syndrome

this is a super antigen - causes massive polyclonal t ell stimulation

usually associated with s.aureus and occasionally in coagulase negative staph

243
Q

toxic shock syndrome

A

initially described in women on their periods or ppl with localized staph infections

systemic absorption TssT-1

TSS produces fever, blood vessel dilation, and a sunburn-like rash

cytokine stimulation: hypotension and multi-organ failure

fatality rate =15%

244
Q

S.pyogenes (SSTIs)

A

cellulitis
toxic shock
necrotizing fasciitis

245
Q

pasteurella multocida

A

sm. fastidious gram negative rod

facultative anaerobe

catalase/oxidase +

MacConkey rarely supports growth

characteristic odor

intrinsically resistant to oral cephalosporins

50% of infections caused by dog bite wounds

246
Q

capnocytophaga

A

capno = co2 loving

gram neg
dogs and cats
oxidase/catalase +

serious disease in asplenic and immuno compromised

247
Q

cat bites

A

serological diagnostics

pasteurella/capnocytophaga

bartonella henselae

aerobic, fastidious gram negative cocco-bacilli

hemin dependent:

  • cat scratch fever
  • endocarditis

rarely cultured

248
Q

eikenella

A

e. corrodens

small gram neg rod

catalse - / oxidase +

no growth on MacConkey

no acid on TSI slant

bleach odour

human bites

clenched fist injuries

249
Q

rat bites

A

streptobacillus monoliformis

rat bit fever

pleomorphic facultative gram negative rod

catalase/oxidase -

biochemically inert

250
Q

bone infections

A

osteomyelitis = inflammation of the bone caused by an infecting organism

remain localized or may spread from bone to marrow to cortex, periosteum and then soft tissue surroundings

251
Q

3 ways organisms may reach the bone

A

skin wound communicating with bone - open fracture

direct spread form neighbouring soft tissue infection

indirectly via the blood stream

252
Q

septic arthritis

A

infection of joint spaces

hematogenous or contiguous

caused by s. aureus, step, gram negative bacilli

253
Q

osteomyelitis

A

infection of the bone

hematogenous or contiguous

s.aureus, s.pyogenes
CNS H influenzae, gram neg bacilli

254
Q

diabetic foot infection

A

cellulitis - deep soft tissue infection and then osteomyeltis

risk factors:

  • vascular disease
  • peripheral neuropathy
  • poor foot care

clinical microbiology (2 decks)

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