UTI Seminar:

2 main syndromes of UTI (can have symptom overlap)

1) Lower UTI: cystitis (bladder infection)
a. Dysuria (painful urination)
b. Frequency
c. Urgency
d. Cloudy/bloody urine (doesn’t necessarily indicate serious infection – just left over debris)
e. *NO FEVER
2) Upper UTI: pyelonephritis (kidney infection)
a. FEVER
b. Costovertebral angle pain +/- lower UTI symptoms
Risk Factors:
- Female, sexually active, diapgragm/spermicide use, pregnancy, ureteral reflux, surgeries, catheterizations, diseases/structural
anomalies affecting bladder function
- Gram – bacilli colonization of perineal/periurethral area:
o Increase epithelial cell receptivity for uropathogenic e. Coli
o Non secretor phenotype of soluble receptor compounds  fail to competitely inhibit adhesin-medieated
colonization
Organisms Causing UTI:
1) Enterobacteriaceae:
a. E.coli (80% uncomplicated infections
b. Klebsiella, proteus, etc
2) Staphylococcus saprophytiucus: (2nd most common in post-pubertal femals)
3) Enterococcus
4) Chlamydia trachomatis (uretritis w/o cystitis/upper tract infection)
Source:
1) Endogenous: normal GI flora colonizes perineal/periurethral areas  ascends into urinary tract
2) *Rare (except staph aureaus): hematogenous spread of bloodborne organisms  urinary tract
Mechanism: uropathogen adheres to epithelial cells of urinary tract mucous membranes  perineal/periurtheral colonization with
gram – bacteriia (esp “uropathogenic” e. Coli)

Investigations:
Urinanalysis:
- Cells: RBS (hematuria), WBC (pyuria)
- Nitrite: enterobacteriaceae can reduce nitrate  nitrite
- Gram stain
Mid Stream Urine: to avoid contamination by meatal and perineal flora on voiding
Significant bacteriuria: >108 CFU
- Urethral syndromes (dsyuria-pyruria syndrome): lower UTI symptoms with pyuria, but counts < 108 CFU (usually seen in
women)
- UTI’s in men, kids, catheterized pts  usually clinically significant without high counts for “significant bacteruria” (all the
studies for those numbers done on women)
Blood culture

Diarrhea:

Causes:
Bacteria Parasites Viruses
Enterobacteriaceae Entamoeba histolytica Rotavirus
- Salmonella, shigella, Giardia lamblia Norwalk
enterohemorrhagic e.coli (EHEC) Cryptosporidium Calicivirus, astovirus, adenovirus
- Yersinia, campylobacter, vibrio Cyclospora
cholerae Microspirida
Source: Exogenous: food, water, person-person, contaminated fomites
- Inoculum size varies with inherent virulence of pathogens & susceptibility to gastric acid
o Shigella: 101-2; Salmonella:106-9  therefore, shigella more likely to cause disease
Mech. Of disease:
First: adheres to intestinal mucosa & colonization, then..
- Enterotoxin: interfere with absorptive function of villus via increased cAMP
o V. Cholerae
o Eneterotoxigenic e. coli
- Aters absorptive surface of villus tip  not much inflamm cell infiltrate
o EHEC
o Cryptosporidium
o Giardia
o Norwalk, rotavirus
- Invade GI epithelium
o Salmoella
o Shigella
o Campylobacter
o Histolytica (inflammatory gastroenteritis)

Investigations:
- Stool for c & s
o Use selective media to enhance growth of pathogen and inhibit growth of normal flora
 Most pathogens need specific media to grow
o Enrichment media: allows detection of low numbers of pathogens

Prevention: SANITATION!!!
Intra-abdominal Sepsis:
Groups of bacteria causing intra-abdominal infections
- strict anaerobes: bacteroides fragilis
- enterobacteracea: e.coli
- enterococcus
Source: endogenous: anaerobes outnumber aerobes in GIT by 1000:1
- female genital tract  pelvic infections
- orophayngeal cavity  head/neck infections
Pathogenesis:
Breach colon wall  large numbers of bacteria contaminate periotneal cavity  immune system rapidly mobilizes phagoctyic cells
(*ecapsulated bactera like B.fragilis resistant to this)
- early predominance of facultative anaerobes, esp e. Coli
- as site becomes more anaerobic (O2 used up by bactera & vascularity decreases)  anaerobes predominate
- = synergy b/c aerobes & anaerobes
Abscess Formation: omentum & intestinal loops localize peritoneal spill gravity & lymphatic drainage

Investigations:
- Avoid contamination with indigenous flora  don’t send swabs (easily contaminated), abscess aspirate better
- Use anaerobic transport media

Clinical Clues to suggest anaerobes:

- LOCATION (abdominal, pelvic, head & neck infections)
- Foul smell
- Any condition that decreases blood supply to create anaerobic envt
- Failure to improve after antibiotics that don’t kill anaerobes
Pt. Managment: predicable to have mixed aerobic/anaerobic in intra-abdominal infections, gram stain showed many mixed
bacteria  inital mgment should cover polymicrobial infection