Id Week 3

Front 1

Transfer of chromosomal genes by conjugation

Back 1

Requires conjugal plasmid integrated in the host cell chromosome
2. Transfer replication is initiated within the plasmid sequences but additional flanking chromosomal DNA is also conjugated to the recipient
3. The transferred DNA cannot be maintained as an autonomous plasmid so homologous recombination is required if the incoming DNA is to be maintained

Front 2

Mechanism of transformation

Back 2

1. Development of competence





2. DNA binds to the cell surface




3. DNA enters the recipient cell




4. DNA integrates into host chromosome by homologous recombination. Plasmid molecules can replicate extrachromosomally


Rare examples of capsule exchange among pneumococci
2. Most significant is acquisition of genes involved in resistance to antibiotics
a. Genes that encode antibiotic binding proteins (e. g. penicillin binding proteins)
b. Genes that encode enzymes that inactivate antibiotics (e.g. -lactamase)
c. Genes that encode exporters of antibiotics (e.g. tetracycline efflux)

Front 3

Toxin genes can be carried on bacteriophage,

Back 3

a. Diphtheria toxin in Corynebacterium diphtheriae
b. Streptococcal erythrogenic toxin
c. Botulinum toxin (Clostridium botulinum)
d. Cholera toxin (Vibrio cholerae)

Front 4

Bacterial culture plates

Back 4

A. Blood agar: grows nearly all bacteria
B. Chocolate agar: a few important pathogenic bacteria do not grow on blood agar, but grow on chocolate: H. influenzae, N. meningitidis
C. McConkey’s agar: chemicals that suppress growth of gram positive bacteria plus lactose plus a color indicator that goes red with falling pH; therefore, bacteria that ferment lactose produce red colonies.
D. CNA plate: blood agar that contains antibiotics to inhibit all gram negatives, so that gram positive colonies are more readily seen

Front 5

Gram stain

Back 5

A. Spread small amount of specimen on glass slide, allow to
dry, fix proteins to the glass by heating briefly over flame
B. Crystal violet (stains everything)
C. Iodine (fixes crystal violet in peptidoglycan, therefore holding
it in organisms with thick cell walls
D. Decolorize with ethanol or acetone (removes stain from
everything but cell wall)
E. Saffranin (everything that isn’t blue stains red)

Front 6

Kirby-Bauer antibiotic testing

Back 6

is a test which uses antibiotic-impregnated wafers to test whether particular bacteria are susceptible to specific antibiotics. A known quantity of bacteria are grown on agar plates in the presence of thin wafers containing relevant antibiotics. If the bacteria are susceptible to a particular antibiotic, an area of clearing surrounds the wafer where bacteria are not capable of growing (called a zone of inhibition).

The size of the zone and the rate of antibiotic diffusion are used to estimate the bacteria's sensitivity to that particular antibiotic. In general, larger zones correlate with smaller minimum inhibitory concentration (MIC) of antibiotic for that bacteria. This information can be used to choose appropriate antibiotics to combat a particular infection.

Front 7

A. Technique of obtaining blood

Back 7

1. Sterilize the skin well
2. Volume: sufficient to avoid false negatives
3. Dispense to two bottles: broth + essential nutrients + substances that adsorb antibiotics and block complement
4. One of these bottles is anaerobic: air replaced with N2 + CO2
5. One blood culture = single sample dispensed to two bottles
6. In adults, always get blood from two different sites
“two separate sticks,” (“two blood cultures”)

Front 8

B. Regarding aerobic and anaerobic bottles

Back 8

1. Most organisms grow in both; if only one bottle has growth:
a. may be an anaerobe (Clostridium, Bacteroides)
b. may be an obligate aerobe (Pseudomonas, Candida)
c. may just not be many organisms in the bloodstream
d. may be contaminant
C. These bottles placed in special incubator
1. Sensor recognizes CO2 (virtually all organisms
generate CO2 during active growth)
2. Constantly scanned
3. If sensor goes positive an alarm is sounded; this is a “critical value” which mandates direct notification of ordering MD

Front 9

Auramine to detect

Back 9

Mycobacteria

Front 10

Calcofluor white to

Back 10

Calcofluor white to detect fungi

Front 11

Fluorescent-labelled antibody to detect...

Back 11

Legionella, Pneumocystis, respiratory viruses

Front 12

Detection of specific microbial components, often by immunologic means (usually ELISA), and therefore
called antigen or toxin detection tests:

Back 12

Rapid influenza detection test
2. Rapid strep test: Group A polysaccharide
3. Legionella antigen sputum or urine
4. Clostridium difficile toxins A and B feces ELISA
5. Respiratory syncytial virus (RSV)
6. Histoplasma antigen in urine
7. Cryptococcal antigen in blood or CSF
8. Pneumococcus C polysaccharide in urine

Front 13

Molecular techniques, specifically PCR: amplify nucleic acid from a suspected organism

Back 13

Bordetella pertussis (bacterium is too hard to grow)
2. Mycobacteria
IMPORTANT DIGRESSION: on what kind of sample can you do PCR? For TB it identifies organisms once colonies have grown (3-5 weeks), but is not yet standardized to work on sputum. Clinicians mix that up and order sputum for PCR. Commercial labs do not care about validity of results – they simply wish to maximize revenues, and they will gladly do the test without regard to potential interpretability.
3. Herpes virus in CSF
4. HIV, hepatitis C, hepatitis B, etc.

Front 14

Indirect techniques
Detect antibody that emerges following infection

Back 14

1. St Louis encephalitis, West Nile Virus
2. Hepatitis A, B, C
3. Brucella
4. Some are much less reliable (e.g. Chlamydia, Mycoplasma, Borrelia [Lyme disease])
Major problems with these techniques. Day-to-day and lab- to-lab variability.
a. need to send ‘acute’ and ‘convalescent’ sera simultaneously, and noone ever does this
b. Extensive literature on unreliability. The literature agrees that there IS NO reliable antibody test for Chlamydia, labs do them and countless papers list this organism as a cause of pneumonia based on serologic diagnosis. Lyme disease is still problematic; need to send to CDC to get reliable results.

Front 15

Vibro species

Back 15

curved, gram - rod
oxidase +
single polar flagellum --> darting movement
somatic O and H antigens
TCBS agar

Front 16

Vibro cholerae epidemiology

Back 16

diarrhea epidemics,
water borne illness (through food too)
seasonal
loves warm temperatures
person-person is minimal
survives in food 14 days

Front 17

Vibro Cholerae pathogensis

Back 17

toxin mediated: 5B, 2A
non-invasive
B subunits bind GM1 ganglioside on intestinal surface
A gets into the cell --> adenylate cyclase -->Cl secretion --> watery diarrhea

Front 18

Vibro Cholerae disease

Back 18

18h-5d incubation
watery - rice -water diarrhea within hours dehydration and also vomiting;
no strains, tenesmus or abdominal pain
fever in <5%
1L/day loss!
death on day 1 can occur
renal failure-serious complication with mortality of 18%
seizures and fever are more common in children
pregnant women have worse prognosis; fetal loss of >50%

Front 19

Vibro Cholerae risks

Back 19

local intensinal immunity
# of bacteria ingested
gastric acidity
blood group O are at increased risk
H. pylori is associated
10^8 needed for healthy person
10^5 for sb on antacids

Front 20

Vibro Cholerae antibiotics

Back 20

not as important
Doxycycline (Alternative: trimethoprim-sulfamethoxazole, erythromycin, ciprofloxacin, azithromycin)
antimotility not reccomended
chemoprephylaxis not reccomended (increases resistance)

Front 21

Vibro Cholerae prevention

Back 21

safe water
boiled
no ideal vaccine
2 oral vaccines give temporary protection

Front 22

Vibro parahaemolyticus

Back 22

most common vibro in US
plankton blooms and warm temperatures cause rise in concentrations;
shellfish acquire it normally
if you eat raw fish - that's risky!!

causes watery diarrhea,
wound infection sepsis
explosive diarrhea, cramping, pain
fluid loss not as severe as cholerae

Front 23

Vibro vulnificus

Back 23

septicemia cause by ingesting uncooked seafood
necrotizing wound infection when contaminated with seawater
fever/chills --> hypotension --> cutaneous lesions

Rx: surgical debridement and antibiotices (tetracycline, quinolones, cephalosporines)

Risk: immunocompromised, cirrhosis, liver disease, Fe overload, chronic renal failure, diabetes, cancer HIV,

Front 24

Vibro alginolyticus

Back 24

marine flora, can cause cellulitis, otitis media/externa, can cause severe infection in immunocompromised

Front 25

Campylobacter

Back 25

comma shaped gram negative rods,
motile
non-spore forming
microaerophilic
main pathogenic species are C. jejuni and C. fetus
Jejuni grows best at 42 C !!! !
Jejuni is susceptible to freezing and drying; can survive in milk.. at 4C

worldwide zoonosis
common in GI of cattle, sheep, goats, rodents, fowl
most have life long carrier state
risk: homosexual men, HIV,
<1year 15-29 year olds in developed countries

<2 years symptoms and then asymptomatic for children of underdeveloped countries
(difference due to exposure ages-immunity rather than different strains)

not all infections cause disease
dose, strain and immunity play role

C. jejuni multiplies in bile-rich place, (jejunum) and causes diffuse bloody edematoius exudative enteritis, non-specific colitis (confused with Crohn's) and occasional bacteremia



2mio infections US/year
C. jejuni most commonly isolated from diarrheal pt in US

Front 26

Campylobacter (virulence, clinical)

Back 26

flagellae (one on each side)
cytolethal distending toxin
high MW plasmid: enhance invasivenes
PEB1 antigen: immunodominant, an adhesin and vaccine antigen

Jejuni: some O antigens have sialic-acid structures similar to gangliosides (role in Guillan Barre)

C. fetus: S-layer protein with capsule (role in bacteremic disease)

Front 27

campylobacter jejuni clinical

Back 27

acute enteritis: fever, loose stools and bloody diarrhea,
abdominal cramps, frequent self-limited, symptoms resolve within a week

acute colitis (confused with crohns)
fever, cramps, tenesmus, bloody diarrhea, ill appearing, toxic

pseudoappendicitis: fever, RLQ pain without diarrhea

Bacteremia:
in <1%, underdiag

Guillan-Barre Syndrome
20-50% of GB cases follow C.jejuni
some strains are overrepresented O19 O41

reactive arthritis:
carriers in HLA-B27 histocompat.
a preceding C. jejuni infection may be mild

Front 28

C. fetus

Back 28

diarrhea: same as jejuni
bacteremia: relapsing fever chills and myalgias
vascular infections: endocarditis..
CNS infections, meningoencephalitis worse in neonates

Front 29

campylobacter therapy

Back 29

fluid replacement, don't wait with antibiotics!! do presumptive therapy:
macrolides, tetracyclines, quinolones, aminoglycosides, clindamycin, ampicillin, imipenem

Front 30

C. fetus vs C. jejuni

Back 30

C. jejuni: avian, food animals, all ages healthy 32-42 C, feces, acute gastritis/colitis/pseudoappendicitis/GuillanB/reactive arthitis

C. fetus:
cattle, sheep, immunocompromised, 25-37C, BLOOD, meningitis...

Front 31

Helicobacter species

Back 31

motile, lives in mucous layer of gastric duodenal and esophageal epithelium
each mammal has a different fan (stomach is favourite neiche)

H. pylori most common humans (hepaticus, bilis and rappini are less common)

Front 32

H. pylori

Back 32

motile! rapid corkscrew, microaerophilic, major BCHS is production of UREASE - also CATALASE +
urease hydrolizes urea to make ammonia and then a basic medium!

50% of world has this, humans can have more than just one strain;
cagA pathogenicity island: CagA+ proteins are important signal molecules that interfere with cell cycle and cytoskeletal configuration;
human adaptation to favor persistance of colonization; cagA gene is associated with gastric cancers and duodenal ulcers

vacA encodes vacuolating cytotoxin, S1 genotype of vacA is strongly associatied with cagA +
VacA is immunosuppressive: down T-cells

fecal-oral ; oral-oral
cluster in large families

overlies gastric type but not intestinal type mucosa
lamina has lymphocytes, monos and plasma cells and neutrophils
all induced by H.pylori: not a secondary colonizer

H. pylori downregulates pro-inflammatory cytokine production

gastritis, peptic ulcer dieases, increased risk with cag+, remitting relapse course in the face of presistent infections; eradication of the infection is associated with a reduced rate of relapse;

gastric cancer: atrophic gastritis; MALT (from B cells)

Tx: omeoprazole + amoxicillin or ranitidine bismuth and clarithromycin

Front 33

Atrophic gastritis

Back 33

Atrophic gastritis (also known as Type A Gastritis) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems, vitamin B12 deficiency, and megaloblastic anemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin.

Front 34

Haemophilus influenzae type b

Back 34

encapsulated (one of a -f)
can penetrate artificial tissue layers of pharynx, go to blood stream, circulate and settle in choroid plexus causing meningitis

major cause of meningitis in young until vaccine - protein conjugate capsular polysaccharide

Front 35

unencapsulated Haemophilus influenzae causes?

Back 35

second most common cause of pneumonia (1st is pneumococcus),
most influenza infections due to this less virulent type;
most common cause of acute exacerbation bronchitis (ppl with chronic underlying lung disease), most common or second for acute bacterial sinusitis and otitis media;

Front 36

pathogenesis of Haemophilus

Back 36

nontypable H. influenza (most common) colonize pharynx. it does not generate toxins, but lipooligosaccharide stimulates a strong immunologic response;
when it's carried to other places it doesn't belong: bronchi, alveoli, sinuses, eustachian tube, this organism causes inflammation = disease

Front 37

Brazilian haemorrhagic fever

Back 37

special virulent plasmid of the Haemophilus influenzae, biogroup aegyptius;

Front 38

Haemophilus ducreyi

Back 38

causes chanceroid, a venereal ulcer that looks enough like syphilitic chancre to warrent it's name

Front 39

Moraxella catarrhalis

Back 39

less virulent than non-typable Haemophilus influenzae; causes many of the same diseases with less severity;
never cultured from blood and only rarely causes meningitis

Front 40

ID Haemophilus

Back 40

gram -
fine, coccobacilli
Pili - for attachment
LOS - shorter
LPS - damages tissues and stimulates inflammation;
outer membrane proteins determined by PAGE (polyacrylamide gel electrophoresis) -- some are unique others shared, antibody may play role in immunity

capsule:
-as with pneumococci, basis for serotyping
-major contributor: type b
type b: PRP - polyribosyl ribitol phosphate used by HIB (haemophilus influenza type b)
-non-encapsulated are "non-typable"

Front 41

Haemophilus growth

Back 41

"blood loving" now we can use growth factors, before the we had to add blood to make them grow;

X-factor: hemin; must lyse RBC to release it as in chocolate agar (made by heating blood)

V-factor: NAD; diffuses from RBC; may be destroyed by enzymes of sheep blood and is routinely added back to chocolate agar

H influenza grows only on chocolate agar; H. parainfluenza needs only factor V and grows on choc.

all grow better with CO2; some require it (sputum samples better set up in a candle jar)

H. ducreyi grows well in enriched Mueller-Hinton agar + 5% sheep blood + CO2 5-10% + high humitdity

Front 42

products of Haemophilus

Back 42

no recognized exotoxins;
LOS causes inflammation and damages tissues

Front 43

Pathogenesis of Hemophilus

Back 43

encapsulated:
type b: nasopharynx colonies --> penetrate epithelial layers --> hematognous spread to cause meningitis / lymphatic / veins
high phagocytosis resistance
proliferate and cause intense inflammation; LOS triggers complement and damages tissues (like pneumococcus)
HITB meets all definitions of virulence

non-typable NTHI
not invasive like HITB
in most kids
25% healthy adults; 50% with chronic bronchitis;
proliferates especially in damaged tissues; also in middle ear/sinus --> stimulates vigerous inflammation;

H. parainfluenzae - like NTHI but less violent

Front 44

diseases caused by HITB

Back 44

haemophilus influenzea type b;

Meningitis
Cellulitis
Epiglotitis
Bacteremia
Septic arthritis

Front 45

diseases by NTHI

Back 45

non-typable haemophilus influenzae

otitis media (S.pneumoniae > H. influenzae (NT) >> Moraxella catarrhalis)
sinusitis
acute purulent tracheobronchitis
pneumonia
meningiti
puerperal fever and sepsis of newborn: biotype IV

Front 46

diseases of H. parainfluenzae

Back 46

sinusitis, bronchitis, (rare pneumonia)
endocarditis

Front 47

diseases of H. influenzae biogroupaegyptius

Back 47

Brazilian hemorrhagic fever

Front 48

H. ducreyi

Back 48

chancroid, painful shaggy, inflamed-looking venereal ulcer

striking enlargement of local lymph nodes

Front 49

what do you do with HITB?

Back 49

antibody to PRP capsule opsonizes for phagocytosis and is bactericidal; antibodies to lipooligosaccharide and outer membrane proteins are also bacteriocidal;

Front 50

prevention of Haemophilus?

Back 50

vaccination: HITB
PRP is a poor antigen for <2 yrs
protein-conjugated vaccine highly effective when given in series of 3 to kids under 6yrs

NTHI : outer membrane proteins are studied; antibodies are aquired after infection;

Front 51

Moraxella catarrhalis

Back 51

common in nasopharynx
less virulent version of NTHI;
otitis media (after haemophilus)
sinusitis
tracheobronchitis and pneumonia only in ppl with chronic lung disease

outer membrane gets antibodies made to it

majority make beta-lactamase

no vaccine yet

Front 52

anaerobes

Back 52

Clostridium tetani - tonic paralysis
Clostridium botulinum - falcid paralysis (cans and honey)
Clostritium perfringens - gas gangrene
Clostridium difficile - nosocomial diarrhea
Bacteroides
peptostreptococcus - brain lung and vagina abscesses
Actinomycosis - mass like - misdiagnosed as cancer

Front 53

Vibro epiemiology

Back 53

water borne, warm temperatures,
fecal-oral,

Front 54

cholera pathology

Back 54

A and B subunit toxin
A - transport
B - adenylate cyclase --> Cl excretion --> watery rice water diarrhea;
stools are infective

Front 55

V. cholerae risks

Back 55

stomach acid, blood group O is more infectable, H. Pylori,

Front 56

V. cholerae Tx

Back 56

rehydration
Doxyacycline
not antimotility
not prophylactic antibiotic

Front 57

most common vibro in US?

Back 57

parahaemolyticus

plankton, shellfish

Front 58

V. parahaemophilus

Back 58

Halophilic (salt-loving)
Japan- diarrhea
conc in shell fish

Front 59

V. parahaemophilus

Back 59

watery diarrhea or dysentery (bloody diarrhea)

wound --> sepsis maybe

24 h explosive diarrhea

fluid loss not as severe

not toxin mediated

Front 60

Vibro vulnificus

Back 60

part of normal marine flora, all oysters at Chesapeake Bay,
25% fatality!

systemic illness, septicemia, shock
wound contaminated in sea / eating uncooked seafood

pain necrotizing ulcers, heamorrhagic bullae

Front 61

campylobacter

Back 61

comma, gram -, motile, non-spore,
microaerophilic
pathogenic: jejuni + fetus

Jejuni: grows better at 42 C
susceptible to freezing and drying, but can survive in foods at 4C for weeks

2 polar flagella

infection from chicken GI / milk

2 mio / year US
more severe in <1 and 15-29

not all infections cause disease - dose/host/age...

Front 62

C jejuni diseases + virulence

Back 62

virulence:
bipolar flagellae;
cytolethal toxin
plasmid for invasiveness
PEB1antigen or adhesin



bloody edematous enteritis, or non-specific colitis (confused with Crohn's)
pseudoappendicitis
reactive arthritis
occasional bacteremia

jejuni: Gullian Barre after the infection due to antibody mimickry;

Front 63

C. fetus trick

Back 63

S-layer protein makes up a capsule resistant to phago

Front 64

C. fetus diseases

Back 64

bacteremia,
diarrhea
vascular infection
CNS - rare

immunocompromised are at risk; also aortic valve

Tx with antibiotics much longer then C. jejuni

Front 65

helicobacter

Back 65

H. pylori
slow grower
makes urease!!! ammonium for stomach acid

cagA pathogenicity island: growth factor assoc with stomach cancer + duodenal ulcers

vacA encodes vacuolating cyotoxin, immunosuppressive; vacA + means most likely cagA +

H.pylori clusters in families

on gastric mucosa, not intestinal

Front 66

"low dose pathogens" for diarrhea

Back 66

Shigella spp 10-100
Shigatoxin-producing E. coli 0157:H7 (10-100)
Giardia and C. parvum (30-100)
Norwalk virus

person to person spread

Front 67

intermediate dose cause for diarrhea

Back 67

Salmonella
Campylobacter

needs thousands

Front 68

high dose cause for diarrhea

Back 68

Vibro cholerae
enterotoxigenic E.coli (travellers 1)

needs 10^6-10^8

Front 69

EPEC

Back 69

entero-pathogenic
leading cause of diarrhea in infants of developing countries; attaching and effacing the intestinal wall --> loss of microvilli; breast feeding is protective - anti-adhesive factor;

no enterotoxin

Front 70

ETEC

Back 70

Enterotoxigenic like cholera;
travellers diarrhea
watery stools
one or two or both enterotoxins: LT(camp) ST(cgmp)
LT: composite B - binding + A - activates the adenylate cyclase

not bloody / mucous / WBC / pus

preventions is good choice of beverages, Bi-subsalicylate

Front 71

EIEC

Back 71

Enteroinvasive
bloody, mucous, secretory diarrhea
similar to shigellosis
5-6% travellers diarrea
not common otherwise

Front 72

EHEC

Back 72

=STEC
hemorrhagic diarrhea;
bloody, NO FEVER;
from food: beef, GI of cattle, petting zoos,
0157:H7
shiga toxin
HUS

Front 73

EAEC

Back 73

Enteroaggregative

brick wall aggregating; developing countries; second most common cause of travelers diarrhea

AIDS
slim disease

Front 74

Shigella and diarrhea

Back 74

500 000 cases in US / year
S. sonnei
invasive. small bowl multiplication;
watery diarrhea and high fever, later colitis and findings change to urgency, tenesmus and dysentery\

complications: Reiter's syndrome (S. flexneri) or HUS

Front 75

small volume bloody

Back 75

must be in colon

Front 76

salmonella diarrhea

Back 76

<1year and 15-29 are most common
<3mo and >65 --> must give antibiotics because 50% get septic

Front 77

Campylobacter jejuni diarrhea

Back 77

like shigellosis with dysentery
fever
chicken
most common cause of diarrhea
best 42C
Guillan Barree (40%)

Tx: azithromycin (Z-pac)

Front 78

Aeromonas species diarrhea

Back 78

water associated
tropical
diarrhea and dysentery

Front 79

Plesimonas shigelloides

Back 79

travellers diarrhea
seafood

Front 80

Clostridium difficile

Back 80

antibiotic-associated Colitis/diarrhea
1) hospitalization
2) antibiotics
3) exogenously aquired with cytotoigenic C. difficile

vancomycin

case: elderly, diffuse colonic diarrhea, picked up at hospital, pseudomembrane formation

resistant to fluoroquinolones and makes more severe disease

Front 81

Cholera

Back 81

Vibro cholerae; profuse, watery;
TCBS medium with high salt conc
10% body wt loss = mortality sets in
dehydration

Front 82

Non-cholera vibrios

Back 82

seafood
fecal WBC, bloody
-Staph aureus - vomiting
-Clostridium perfringens - no vomiting, longer incubation
-Bacillus cereus - can be like S. aureus (2-7h incubation) or like C. perfringens (8-14h) - two toxin choices

= all food poisoning NO FEVER!

Front 83

Dx diarrhea: recent travel to developing country

Back 83

ETEC, EAEC, other

Front 84

Dx: recent antimicrobial Tx - diarrhea

Back 84

rule out Clostridium difficile colitis

Front 85

Dx: homosexual male; diarrhea

Back 85

herpes virus
chlamydia trachomatis (LGV - lymphogranuloma venerum)
Treponema pallidum
Neisseria gonorrhoea
AIDS (Cryptosporydium, Microsporidia, Cyclospora, herpes viruses, mycobacterum avium-intracellulate)
bacterial enteropathogens

Front 86

Dx: diarrhea day care centers

Back 86

increased occurance of low dose enteropathogens

Front 87

Dx: sporadic versus multiple cases
diarrhea

Back 87

multiple cases - outbreak - an incubation period may be constructed

Front 88

Dx: diarreha with vomiting

Back 88

multiple cases develop 2-7 h after eating a meal, staphylococcal or Bacillus cereus food poisoning is likely

Front 89

Dysentery Dx

Back 89

Shigella
Campylobacter
Salmonella
Shigatoxin-producing E. coli
Clostridium dificile,
Aeromonase,
E. histolytica

Front 90

persistant diarrhea

Back 90

>14days
parasitic is likely (Giardia, Cryptosporidium, Cyclospora);
disaccaridase deficiency, enteroaggreagativ E. coli, occasional Shigella, Salmonella, Campylobacter, Yersinia, Brainerd diarreha, post infectious IBS, sprue syndromes and in developing countries malnutrition, Zn or Vit A deficinecy

Front 91

UTI diagnostic problems

Back 91

a) can't get a sample from a healthy woman without contamination of the perineal bacteria.
b) if the infection is confined to the urethra, a midstream sample might wash out bacteria, leaving very small numbers of bacteria, overlapping with culture results from patient with uninfected urine. (dilute them ?)

Front 92

what cells can be found in urine with UTI

Back 92

WBC number is greatly increased

but: midstream urine eliminates the inflammatory cells in women whose infection is confined to urethra (1/3 of cases!)

Front 93

casts that contain WBC prove that

Back 93

an infection involves renal tubules

Front 94

Tx duration for bladder infection vs kidney or prostate

Back 94

bladder: few days,
vs: 2-4 weeks

Front 95

UTI include

Back 95

a) most infections of kidney, called pyelonephritis (xcept when S. aureus spreads here hematogenously)
b) bladder, called cystitis

Front 96

urethritis

Back 96

reserved for STD (gonococcus, Chlamydia or Ureaplasma) even though most of the UTI are confined to the urethra

Front 97

UTI in men

Back 97

infection often recurs because of persistent infection in the prostate, which may or may not be called prostatitis

Front 98

Host defenses against UTI

Back 98

1) urethra is a mechanical barrier. less effective in females bc it's short; and bc it terminates in the vaginal introitus which may be colonized.
2) irrigation by urine: bacteria washed out
3) phagocytic activity of epithelial cells: a) not professional phagocytes but b) ingest bacteria and appear to contain their growth; c) shed into urine and voided
4) complete emptying. For bladder cells to ingest, must come into close contact. Normal residual urine volume in young adult <1ml; at and of voiding urine spreads out in a thin sheet over bladder mucosa
5) "urine antibacterial?" DO NOT BELIEVE IT
6) Tamm-Horsfall protein contains mannose and may block sites on bacterial pili or fimbriae
7) Ureterovesical valve prevents ascent of infection from bladder; efficacy compromised by infection
8) Local antibody production terminates pyelonephritis (infection in kidney); probably not operative in bladder.

Front 99

Virulence factors

Back 99

Bacterial pili (fimbriae) attach to receptors on mammalian cells
a) indirect identification
b) mannose sensitive binding inhibited by mannose; most strains causing cystitis have these receptors and adhere more avidly to bladder cells than other E.coli. Also called type I pili.
c)mannose resistant binding not inhibited by mannose; called type II pili or P pili (P stands for pyelonephritis)
d)most pyelonephritis is caused by E. coli strains with P pili which adhere to globoseries glycolipic receptors on human cells that resemble P antigen on RBC
2) make hemolysin
3) resist bactericidal effect of serum: pyelonephritis strains
4) Capsule: pyelonephritis strains
5) Urease, produced by Proteus, Provedencia, Morganella alkalinizes urine. Causing precipitation of magnesium ammonium phosphate (called struvite) stones

Front 100

Host factors associated with high risk for UTI

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Introduction of bacteria (sex, catheters),

Obstruction (preventing of complete emptying of bladder allows small number of organisms to persist: they proliferate and lead to UTI; anatomic - tight foreskin - duplicate ureters, horseshoe kidneys... enlarged prostate in older men, stones - adhesins,)

altered physiology (pregnancy)

diabetes

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Urinalysis

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UA
normal : some WBC <3000 WBC/ml
(reports are like "<5 per field")

men: very sensitive and specific for diagnosing UTI; more complicated in women because of issue of urethral infection and reliance on midstream specimen

extreme dehydration or decline in urine for any other reason can cause pyuria (increased WBC in urine) in the absence of infection; also vasculitis, other kinds of inflammation can too;

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microscopic bacteriuria

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reliable and easy to see bacteria in uncentrifuged infected urine using high power lens; however, what labs repost as "moderate bactiera" in UA is not reliable

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Bacteriuria by culture

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1) normally urine is sterile
2) specimen likely to be contaminated during voiding (especially young children, women or circumcised men)
3) bacteria may proliferate if urine stands around
4) used to accept > 10^5 cfu/ml midstream urine as definition of infection (significant bacteriuria")
a) consistant with observation that bacteria causing UTI will grow to 10^6/ml as urine remains in bladder
b)this number present in urine of men or women with UTI cystitis (infection of bladder) or pyelonephritis
c)women with bacterial infection of urethrea (urethritis) have pyuria and bacteriuria in first few drops of urine
d) when we culture "midstream urine" we wash out the infected area; no surprise that there may be no pyuria and only 100-10000cfu/bacteria/ml
5) because of d) textbooks state that midstream urine with >100 bac/ml in women with symptoms = UTI.
6) from 2 and 3 : positive culture without abnomal urinalysis is highly suspect and should not be used
7) diagnosis of asymentric bacteruria and the literature that goes with it is supect bc urinalysis have generally not been done

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1) acute uncomplicated UTI in young women: Clinical syndromes

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symptoms of urethritis or cystitis: dysuria, frequency, urgency, without fever, flank pain. 1/3: infection may be confined to urethra, which is why midstream urinalysis and urine culture may be non-informative
1) bacteria: 80% E.coli; 10-15% Staphylococcus saprophyticus; proteus and klebsiella cause the rest (finding staph aureus in urine means bacteremia, and should be taken very seriously, especially in absence of indwelling urinary catheter)
2) increased risk: sexual intercourse, diaphragm/spermacide use, failure to void after intercourse, history of recent infection
3)controversy over need and length of lab evaluation and Tx
4)Dysuria may be symptom of vaginitis; great majoruty of women with vaginitis have vaginal discharge and this symptom is not with women with cystitis
5) Tx: Trimethoprim/sulfapethoxazole officialy reccomended 3 day Rx. but 25% E. coli are resistant - nitrofurantoin for 5 days;

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Clinical of Acute uncomplicated pyelonephritis in young women

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1) fever, flank pain, nausea, vomiting, frequency +/- dysuria
2) Lab support: WBC in urine (if not must have broad range of possibilities from appendicitis to vertebral osteomyelitis;) note that rarely, an abscess adjacent to ureter may lead to all these symptoms PLUS pyuria without bacteriuria
WBC casts in urine. cast (as in plaster cast) in shape of tubule proves that infection involves kidney
blood cultures should be obtained(+ in 20%)
3) E.coli = 80% pyelonephritis strains have virulence factors that distinguish them from those causing cystitis
4) controversy over hospitalization; my preference, especially because of increasing problems with antibiotic resistance is to hospitalize unless patient is tolerating infection very well
5) antibiotic: a) initial: 3rd generation cephalosporin, aminoglycoside (gentamycin, amikacin) or quinolone. first dose parenterally bc vomiting may occur
b) after lab results, continue oral antibiotic or change to class with oral form
c)select easily tolerated, less expensive
d)if no improvement within 48 h, evaluate for a complication (abscess, (-diabetics), obstructing stone)
e) Tx for 14 days

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Clinical of acute uncomplicated UTI in older women

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nearly all same as younger

risk include: increased risk of vaginal colonization and increased post voiding residual

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Clinical of recurrent UTI in women

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1) usually no anatomic or functional UTI abnormalities
2) voiding after intercourse greatly reduces bacterial inoculum and greatly reduces risk of infection
3) if that fails: antibiotic prophylaxis daily or 3x/week or after intercourse (nitrofurantoin does not change bowel flora and rate of resistance is low)
4) self diag and Tx is reccomended by some experts
5) older women: maybe due to post-void residual or lack of estrogen associated with menopause; (can also be managed similarily, topical vaginal estrogen therapy)

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Clinical UTI young adult man

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1) <50yrs uncommon
2) risk: homosexuality, lack of circumcision, ? sexual partner with vaginal E. coli colony by an E.coli with virulence
3) associations: enlarged prostate and obstruction of outflow (more residual volume detracts from the important protective mechanism of phagocytic activity of bladder epithelilal cells) and UT intrumentation
4) cysitis (may be confused with uretritis = STD) must do urinalysis and urine culture, probably best to do first few drops then midstream separately
5) no fever, cholls , flank pain to indicate complicated infection, may treat with 7-day course of fluoroquinolone or other antibiotic based on culture
6) if symptoms of pyelonephritis are present or infection happens again, urology evaluation is advisted

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Complicated UTI

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infection that involves kidney, recur, cause serious complications

a) recurrent (except sexually active)
b) pregnancy
c) older men
d) symptoms of pyelonephritis
e) known anatomic abnormality
f) hospital-aquired
g) delayed response to Tx
h) proteus or other urese producer
i) diabetes

micro: broader range of bacteria & fungi
urine cultures must be done to define micro
therapy: antibiotic + correction of underlying anatomic functional or metabolic abnormality

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UTI form indwelling catheter

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1) bypasses the host defenses, it's a question of time until it will get infected
4wk - all are infected
2) bacteria from pt own colonic flora enter bladder (at insertion time, through catheter lumen, along catheter/mucosal surface)
3)preventing has not worked (periurethral washes, topical antibiotics, antimicrobial impregnated catheters, bad antiseptics, unless catheter will only be present for a few days, it's proven that prophylactic antibodies simply select for resistance)
4) pyuria in all cases shows that it's a cubclinical infection not "colonization"
5_ alternatives: external collection devices, intermittent catheterization
6) should catheters be changed? must if obstructed, otherwise if infected changing catheter reduces rate of recurrence; once catheter removed, the urine should be cultured several days later
7) symptomatic UTI associated with indwelling catheter: duration of therapy unclear. 1-4wk

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Bacterial prostatitis

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infection in prostate from instrumentation, catheter!

serves as nidus (nest) causing recurrent UIT

prostate-blood barrier prevents antibiotic penetration; requires prolonged Tx, shorter courses followed by recurrent UTI, obviously due to the sam organism

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Asymptomatic bacteriuria

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1) major problem with this diagnostic entity is that the urine culture may simply be erroneous
2) hard to know if literature is based on pt who have bacteriuria or simply those who provide urine samples that have become contaminated during voiding
3) help to avoid problem if you use urinalysis along with urine culture
4) only group with consequence: pregnant (repeat study, give very special instructions on how to get the sample)