enterobacteriae: gram negative rods Flashcards
name the lactose fermenter gram negative rods
escherichia coli
klebsiella spp.
name the non lactose fermenter gram negative rods
shigella spp.
proteus spp.
salmonella spp.
name the 2 groups of salmonella
enteric (typhoid) fever group: s. typhi, s. paratyphi
acute gastroenteritis group:
s. typhimurium, s. enteritidis
name the bactera of shigella spp.
sh. dysenteriae, sh. boydii, sh. flexneri, sh. sonnei
how to differentiate between lactose fermenters and non-lactose fermenters
lactose fermenters show pink/red colonies (produce acid)
non lactose fermenters show yellow/pale colourless colonies
enterobacteriae culture medium
macconkey agar:
contains bile salts the inhibit the growth of unwanted bacteria
enterobacteriae are oxidase __
negative
gram negative cocci are oxidase positive
escherichia coli: character
oxidase negative lactose fermenting gram negative rods
normal gut flora
escherichia coli: virulence factors
exotoxins produced by certain strains
EPEC, ETEC, EHEC, EIEC
escherichia coli: clinical presentations
urinary tract infections
neonatal infections (meningitis, septicaemia)
sepsis associated with the gut (either due to GIT lining damage or due to blockage that prevents bacterial drainage)
nocosomial disease
diarrhoeal disease:
- e. coli (enteropathogenic e. coli): infantile gastroenteritis
- etec (enterotoxigenic e. coli): diarrhoeal disease in developing world and travellers
- eiec (enteroinvasive e. coli): invades colonic wall, produces similar disease to shigella dysentry
- ehec (verocytotoxin producing/ enterohaemorrhagic e. coli): causes haemorrhagic colitis with bloody diarrhoea, complicated by renal failure
what does epec cause
infantile gastroenteritis
what does etec cause
adult diarrhoeal disease
what does eiec cause
invades colonic wall, produces similar disease to shigella dystentry
what does ehec cause
haemorrhagic colitic with bloody diarrhoea, complicated by renal failure
shigatoxins produced by ehec lead to haemolytic uraemic syndrome
escherichia coli: diagnosis
difficult: virulent strains closely resemble normal e. coli strains
PCR: detect genes encoding specific toxins serology: impt e. coli serotype O157H7 surface antigens urine microscopy (UTI must contain white blood cells)
important e. coli serotype
O157 H7
o represents the somatic bacterial cell wall antigen, h represents the flagellar antigen
klebsiella spp.: character
oxidase negative lactose fermenter gram negative rod
normal gut flora
klebsiella spp.: clinical presentations
urinary tract infection
friedlander’s pneumonia (severe form of community-acquired pneumonia with abscess formation)
nocosomial infections
community acquired liver abscess
frequently seen in alcoholics/ diabetic patients
enterobacteriae is a common cause of __
nocosomial infections
explain why enterobacteriae is a common cause of nocosomial infections
- due to git surgery - release of bacteria, causing wound infections, peritonitis, abdominal and pelvic abscesses
- due to neurosurgery or head trauma that causes meningitis
- due to prolonged hospitalisation as broad spectrum antibiotic used select for survival of resistant strains of coliforms
enterobacteriae treatment
most strains produce beta lactamases: ceftriaxone co-amoxiclav/piptazo ciprofloxacin aminoglycosides like gentamicin and amikacin (requires therapeutic drug monitoring)
shigella spp.: character
oxidase negative non lactose fermenting gram negative rods
NOT normal flora
shigella spp.: transmission
faecal-oral transmission, flies
shigella spp.: clinical presentations
sh. dysenteriae: dysentery (intestinal inflammation) that leads to blood stained mucopurulent stools, may be complicated by HUS from shiga toxin)
sh. sonnei: common cause of mild diarrhoeal disease (outbreaks in institutions)
proteus spp.: character
oxidase negative non lactose fermenting
normal gut flora
swarms on surface of blood agar in waves
proteus spp.: clinical presentations
urinary tract infections
renal calculi/stones: urease produced breaks down urea to ammonia and carbon dioxise, alkalinsation of urine results in stone formation
enteritic (typhoid) fever group: character
s. typhi, s. paratyphi
oxidase negative non-lactose fermenting gram negative cocci
NOT normal flora
enteritic (typhoid) fever group: transmission
faecal-oral transmission
enteritic (typhoid) fever group: clinical presentation
initial invasion of ileal mucosa & multiplication within mesenteric lymph nodes; entry into bloodstream and replication within macrophages of many organs (incubation period 10-14days)
second invasion of bloodstream resulting in clinical symptoms (fever, anorexia, epistaxis, cough, headache, abdominal pain, constopation or diarrhoea, bradycardia, enlarged liver and spleen, rose spots)
excretion of infected bile by gall blader into gut creates second invasion of gut wall, resulting in inflammation caused typhoid ulcers of ileal patches (can cause haemorrhage and intestinal perforations)
*some individuals become chronic carriers even after recovery due to chronicall infected gall bladder
enteritic (typhoid) fever group: diagnosis
culture: blood (early), urine/stool (later)
serology: widal’s test (not reliable)
enteritic (typhoid) fever group: prevention
vaccination- Ty 21a oral, Vi injectable
detect and treat carriers
clean food and water, proper sewage disposal
acute gastroenteritis group: character
s. typhimurium, s. enteritidis
oxidase negative non-lactose fermenting gram negative rods
NOT normal flora, usually originates in animal faeces
acute gastroenteritis group: transmission
contaminated food by animal faeces
acute gastroenteritis group: clinical presentations
salmonella food poisoning (diarrhoea, vomitting, abdominal pain, fever) that is usually self limiting
invasive infections after spread through blood; atheromatous plaques in arteries, osteomyelitis, meningitis
in HIV and SLE patients, any food poisoning salmonella may produce a disseminated invasive infection
acute gastroenteritis group: diagnosis
culture: stool, blood
enteric (typhoid) fever group: explain ileal perforation
it targets m cells on the epithelial lining; m cells phagocytose the salmonella bacteria, and spit them out through onto the peyer’s patches which is part of the submucosal layer
necrosis of the epithelial layer results in ileal perforation; secondary infection of the peritoneum
enteric (typhoid) fever group: main effectors
macrophages; phagocytose the salmonella bacteria and can travel to different sites of the body to cause systemic effects
acute gastroenteritis group: mechanism of inflammation and diarrhoea
main effectors: neutrophils that induce inflammation of the colon
as immune cells travel through the mucosa to the site of infection, they damage the mucosa and cause git dysfunction; excessive loss of water hence diarrhoea
mechanism of ehec
e. coli travels to the epithelial cells and release shiga toxins that cause injury to the intestinal epithelium + the underlying blood vessels -> results in inflammation
^fluids and blood leak into the intestine; bloody diarrhoea
haemorrhagic uremic syndrome
after. e.coli releases shiga toxins into the bloodstream that travel to the kidneys and damage the glomerular endothelial cells through apoptosis
holes in the endothelium allow proteins and blood to enter the urine - bloody urine, proteinuria
platelets clot the holes formed and there are less platelets in the blood; thrombocytopenia
rbcs try to squeeze through these clots and microangiopathic hemolysis occurs - forms schistocytes; number of rbcs reduce and there is anemia
clots can block blood supply to the kidney and cause ischemia, non functional kidneys prevent filtration and there is uraemia
