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Micro - Overview of Enteric Gram -ve Bacilli (i) (Enterobacteriaceae…
Micro - Overview of Enteric Gram -ve Bacilli (i)
Enterobacteriaceae
large family of gram -ve bacilli
ubiquitous: in normal intestinal flora, soil, water, vegetation
oropharyngeal colonisation in alcoholics + diabetics
E coli
Klebsiella (non-motile)
Proteus
Serratia
Enterobacter
cause 70% of GIT infections
most are motile thanks for peritrichous flagellae (all over surface)
Antigens on cell wall
K antigen: capsule
antiphagocytic
aids attachment to epithelial cells
H antigen: flagellae
O antigen side chains: LPS
virulence factors
adhesins (e.g. fimbriae, pili) aid host cell binding
toxins
LPS/endotoxin (esp Lipid A) = potent inducer of host immune response (overwhelming vasodilation, sepsis)
haemolysins of E Coi
capsule (poor immunogen)
plasmid exchange (transfers antimicrobial resistance)
grow on non-selective (agar) + selective (MacConkey - pink for E coli as it is a lactose fermentor) media
facultative aerobes
optimum temp = 35-37
multiply rapidly - fast growth
ID through biochemistry or MALDI-TOF
pseudomonas (oxidase +ve - purple on test)
can be tested for antimicrobial susceptibility
disk diffusion (multiple antibiotics on 1 disk)
MIC (more precise, 1 drug @ a time)
cause infections in community + health facilities in both immunocompetent + compromised patients
has be isolated from urine, blood, abdominal tissue + resp tract
E Coli
Coliform (in colon, hence faeces)
most strains are non-pathogenic in GIT
pathogenic strains have adhesins + exotoxins (shiva + heat labile toxin)
cause
UTIs
E Coli is the most common cause of these
originate in perianal area
travels to bladder via urethra
urethra shorter in females
often have type 1 fimbriae to aid attachment
certain serotypes more common in UTIs (1,2,4)
symptoms
suprapubic pain (indicates cystitis -> inflammed bladder)
flank pain (indicates pyelonephritis - > inflamed kidney)
do US to rule out abscess
longer Tx (10-14 days)
pyrexia
dysuria
polyuria (every 1-2 hrs)
urgency to pass urine now
nocturia (also in benign prostatic hypertrophy)
intra-abdo infections
cholecystitis (inflamm of gallbladder)
peritonitis (usually secondary)
liver/subphrenic abscess
appendicitis
cholangitis (inflamm of bile duct)
meningitis
often neonatal: acquired during birth, presents soon after delivery
post-traumatic/post-op
gastroenteritis
BSI
always secondary
intra-ab pathology
urinary tract sepsis
neonatal meningitis
specimen lab needs depends on infection type
Tx
depends on source + patient factors
NO TX FOR GASTROENTERITIS (supportive only - IV fluids)
70% amoxicillin-resistant
post-op/community-acquired infections: co-amoxiclav + cefuroxime (2GC)
lower UTI: trimethoprim/nitrofurantoin
increasing ESBL
enzyme in gram -ve organisms
spreads by contact (plasmids)
resistant to all beta-lactams (penicillins, 1st 2nd + 3rd gen cephalosporins, monobactams e.g. aztreonem) + sometimes to aminoglycosides + quinolones
susceptible to carbapenems
e.g. meropenem
broadest broad spectrum
last effective defence agains MDR gram -ve bacilli
CRE/CPE prevalent in many countries!
extra ESBL mutation
plasma-mediated acquisition of carbapenemase
v limited Tx options
isolation + hand hygiene NB