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GRAM NEGATIVE INFECTIONS Flashcards

1
Q

MACCONKEY AGAR ONLY GROWS WHICH TYPE OF BACTERIA?

A

G-

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2
Q

WHAT DOES THE COLOR OF COLONIES IN THE MACCONKEY AGAR INDICATE?

A

PINK COLONIES INDICATE BACTERIA THAT ARE LACTOSE FERMENTERS

WHITE/COLORLESS COLONIES INDICATE NON-LACTOSE FERMENTING BACTERIA

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3
Q

MAIN USE OF THE MACCONKEY AGAR?

A

IT SELECTIVELY ISOLATES G- AND ENTERIC BACTERIA AND DIFFERENTIATES THEM BASED ON LACTOSE FERMENTATION

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4
Q

SOME MAJOR GROUPS OF G- BACTERIA?

A
  • AEROBIC BACILLI (i.e. RODS) (FREE LIVING; WATER, SOIL ETC)

- ENTERIC PATHOGENS (IN INTESTINES OF WARM-BLOODED ANIMALS; CAN BE LACTOSE FERMENTERS AND NON LACTOSE FERMENTERS)

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5
Q

EXAMPLES OF LACTOSE FERMENTING G- BACTERIA?

A

E. COLI

KLEBSIELLA PNEUMONIA

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6
Q

EXAMPLES OF NON-LACTOSE FERMENTING G- BACTERIA?

A

SALMONELLA ENTERICA
SHIGELLA SPP
PROTEUS MIRABILIS

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7
Q

DESCRIBE THE GROUP OF G- BACTERIA ‘AEROBIC BACILLI’?

A
  • LARGE, DIVERSE GROUP
  • NON-SPORE-FORMING BACTERIA
  • MOST AREN’T MEDICALLY IMPORTANT (BUT SOME ARE TRUE PATHOGENS AND SOME ARE OPPORTUNISTS)
  • ALL HAVE LIPOPOLYSACCHARIDE (LPS) OUTER MEMBRANE OF CELL WALL - ENDOTOXIN (LIPID A OF LPS)
  • DO NOT FERMENT CARBOHYDRATES
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8
Q

EXAMPLES OF G- AEROBIC BACILLI?

A

OPPORTUNISTIC PATHOGENS: PSEUDOMONAS AND BURKHOLDERIA
ZOONOTIC PATHOGENS: BRUCELLA AND FRANCISELLA
MAINLY HUMAN PATHOGENS: BORDETELLA AND LEGIONELLA

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9
Q

PSEUDOMONAS AERUGINOSA - DESCRIBE THE PATHOGEN + WHERE DOES IT RESIDE?

A
  • SMALL RODS WITH A SINGLE POLAR FLAGELLUM (G-, AEROBIC BACILLI GROUP)
  • FREE LIVING; COMMON INHABITANT OF SOIL AND WATER
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10
Q

PSEUDOMONAS AERUGINOSA IS AN INSTETINAL RESIDENT IN WHAT % OF HEALTHY PEOPLE?

A

10%

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11
Q

WHAT IS THE SPECIFIC SMELL AND COLOUR OF PSEUDOMONAS AERUGINOSA?

A
  • GRAPE-LIKE ODOR

- GREENSIH-BLUE WATER SOLUBLE PIGMENT (PIGMENT CALLED PYOCYANIN)

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12
Q

WHAT DOES PSEUDOMONAS AERUGINOSA EXHIBIT PARTICULAR RESISTANCE TO?

A

SOAPS, DYES, QUATERNARY AMMONIUM DISINFECTANTS, DRUGS, DRYING

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13
Q

WHAT DOES PSEUDOMONAS AERUGINOSA FREQUENTLY CONTAMINATE?

A

VENTILATORS, IV SOLUTIONS, ANESTHESIA EQUIPMENT

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14
Q

DESCRIBE WHAT KIND OF PATHOGEN PSEUDOMONAS AERUGINOSA IS; WHEN DOES IT AFFECT PEOPLE, WHAT KIND OF COMPLICATIONS DOES IT CAUSE?

A
  • OPPORTUNISTIC PATHOGEN
  • COMMON CAUSE OF NOSOCOMIAL (HOSPITAL ACQUIRED) INFECTIONS IN HOSTS WITH BURNS, CYSTIC FIBROSIS
  • COMPLICATIONS: PNEUMONIA, UTI, ABSCESSES, OTITIS, CORNEAL DISEASE, ENDOCARDITIS, MENINGITIS, BRONCHOPNEUMONIA
  • MULTIDRUG RESISTANT!!!
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15
Q

% OF PATIENTS WITH CYSTIC FIBROSIS THAT GET INFECTED BY PSEUDOMONAS AERUGINOSA IN HOSPITALS?

A

60-70%

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16
Q

HOW MANY BURNS PATIENTS BECOME COLONISED WITH PSEUDOMONAS AERUGINOSA? WHY?

A

UP TO 1/3 OF BURN PATIENTS WHO RECEIVE SHOWER CART HYDROTHERAPY AS TREATMENT (MAINSTREAM TREATMENT) GET COLONISED BY P. AERUGINOSA
- TRANSMISSION CAUSED BY WATER OUTLETS!!!

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17
Q

P. AERUGINOSA IS A DOMINANT PATHOGEN IN PEOPLE WITH WHICH DISEASE?

A

CYSTIC FIBROSIS

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18
Q

PREVALENCE OF P. AERUGINOSA IN ADULTS WITH CYSTIC FIBROSIS?

A

31-47%

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19
Q

DESCRIBE THE PSEUDOMONAS AERUGINOSA VIRULENCE FACTORS?

A
  • BIOFILM FORMATION ABILITY AND COMPOSITION OF THE ECM OF BIOFILMS (EXOPOLYSACCHARIDES, PROTEINS AND EXTRACELLULAR DNA; AT LEAST 3 SECRETED POLYSACCHARIDES)
  • 3 MAIN QUORUM SENSING SYSTEMS
  • FLAGELLINS INCORPORATED WITHIN THE FLAGELLAR STRUCTURE
  • PYOVERDINE SIDEROPHORE AS AN IRON UPTAKE SYSTEM
  • LIPOPOLYSACCHARIDES (LPS) AND OUTER MEMBRANE PROTEINS (OMPs)
  • TYPE 4 PILI (T4P) USED FOR ADHESION, AGGREGATION, DNA UPTAKE
  • SECRETION SYSTEMS FOR TOXIN DWLIVERY
  • HIGHLY ADAPTIVE TO DIFFERENT ENVIRONMENTS
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20
Q

WHAT IS QUORUM SENSING?

A

Quorum sensing is the regulation of gene expression in response to fluctuations in cell-population density. !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Quorum sensing (QS) is a communication mechanism between bacteria that allows specific processes to be controlled, such as biofilm formation, virulence factor expression, production of secondary metabolites and stress adaptation mechanisms such as bacterial competition systems including secretion systems

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21
Q

A MAJOR CONTRIBUTOR TO PSEUDOMONAS AERUGINOSA GREAT ADAPTIVE CAPACITY IS?

A

ITS VERY LARGE GENOME (5-7 MB; mega bases)

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22
Q

MAIN SECRETION SYSTEMS USED BY PSEUDOMONAS AERUGINOSA?

A

TYPES III, VI AND II

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23
Q

BORDETELLA PERTUSSIS: TYPE OF BACTERIA, RESERVOIR AND TRANSMISSION?

A
  • VERY SMALL COCCOBACILLUS (G-; AEROBIC BACILLI GROUP)
  • RESERVOIR ARE APPARENTLY HEALTHY CARRIERS
  • TRANSMISSION BY DIRECT CONTACT OR INHALATION OF AEROSOLS
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24
Q

DESCRIBE THE DISEASE CAUSED BY BORDETELLA PERTUSSIS?

A
  • DISEASES: PERTUSSIS OR ‘WHOOPING COUGH’
  • COMMUNICABLE CHILDHOOD AFFLICTION
  • ACUTE RESPIRATORY SYNDROME
  • OFTEN SEVERE LIFE THREATENING COMPLICATIONS IN BABIES
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25
Q

WHICH CELLS DOES BORDETELLA PERTUSSIS ATTACH TO?

A
  • ATTACHED STRONGLY TO CILIATED (covered in microscopic projections that look like tiny hairs) RESPIRATORY EPITHELIAL CELLS
  • GENERALLY DOES NOT INVADE SUBMUCOSAL CELLS OR THE BLOODSTREAM
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26
Q

WHO USUALLY GETS PERTUSSIS?

A

BABIES YOUNGER THAN 1 YEAR OLD

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27
Q

DESCRIBE THE PERTUSSIS TOXIN?

A
  • A/B TYPE
  • LARGE MULTI-UNIT PROTEIN ASSOCIATED WITH SEVERE PERTUSSIS DISEASE
  • THE TOXIN IS BOTH SECRETED INTO THE EXTRACELLULAR FLUID AND CELL BOUND
  • SOME COMPONENTS OF THE CELL BOUND TOXIN FUNCTION AS ADHESINS AND APPEAR TO BIND THE BACTERIA TO HOST CELLS
  • ANOTHER COMPONENT HAS ENZYMATIC ACTIVITY THAT INHIBITS SIGNALLING IN MAMMALIAN CELLS ENABLING EARLY COLONISATION OF CILIATED CELLS
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28
Q

BORDETELLA PERTUSSIS VIRULENCE FACTORS?

A
  • PERTUSSIS TOXIN
  • ADDITIONAL TOXINS PLAYING A ROLE IN RESISTANCE TO PHAGOCYTOSIS
  • KILLING CILIATED EPITHELIAL CELLS
  • FIMBRIAE
  • LIPOPOLYSACCHARIDE (LPS)
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29
Q

SINCE WHEN HAS THE PERTUSSIS VACCINE BEEN AVAILABLE?

A

1950s

30
Q

CURRENT AVAILABLE PERTUSSIS VACCINES AND GUIDANCE?

A

Two kinds of vaccines used today help protect against whooping cough, both of which also protect against other diseases:

Diphtheria, tetanus, and pertussis (DTaP) vaccines
Tetanus, diphtheria, and pertussis (Tdap) vaccines
Babies and children younger than 7 years old receive DTaP, while older children and adults receive Tdap.

CDC recommends whooping cough vaccination for all babies and children, preteens and teens, and pregnant women. Adults who have never received a dose of Tdap should also get vaccinated against pertussis.

31
Q

DESCRIBE THE PATHOGEN LEGIONELLA PNEUMOPHILIA:

A
  • SMALL
  • WATERBORNE
  • UNENCAPSULATED
  • NONMOTILE
  • AEROBIC
  • G- (‘AEROBIC BACCILI GROUP)
32
Q

LEGIONELLA PNEUMOPHILIA IS NUTRITIONALLY FASTIDIOUS AND IT REQUIRES:

A

L-CYSTEINE (AMINO ACID NATURALLY PRESENT IN HUMANS) AND FERRIC SALTS (FROM IRON)

33
Q

WHERE CAN LEGIONELLA PNEUMOPHILIA COMMONLY BE FOUND?

A

NATURAL WATER SYSTEMS, SOILS, ENGINEERED STRUCTURES USING WATER (COOLING TOWERS, AIR CONDITIONING SYSTEMS, WATER SYSTEMS, HUMIDIFIERS…)

34
Q

LEGIONELLA PNEUMOPHILIA NAME ORIGIN?

A

NAMED AFTER A 1976 EPIDEMIC OF PNEUMONIA AFFECTING 200 AMERICA LEGION MEMBERS ATTENDING A CONVENTION IN PHILADELPHIA AND KILLED 29

35
Q

DISEASES CAUSED BY LEGIONELLA PNEUMOPHILIA?

A
  • LEGIONNAIRES DISEASE (PNEUMONIA)

- PONTIAC FEVER (MILDER VERSION OF DISEASE)

36
Q

SYMPTOMS OF DISEASE CAUSED BY LEGIONELLA PNEUMOPHILIA?

A

FEVER, HEADACHES, COUGH, MUSCLE PAIN

37
Q

SO FAR, HOW MANY OUTBREAKS OF LEGIONELLOSIS HAVE BEEN REPORTED IN PEER-REVIEWED ARTICLES?

A

AT LEAST 150

38
Q

RISK FACTORS FOR LEGIONELLA P.?

A
  • 5O+
  • SMOKERS
  • IMPAIRED IMMUNE SYSTEM
39
Q

OUTBREAK OF LEGIONELLA IN SPAIN?

A
  • IN MURCIA, SPAIN IN 2001
  • 800 SUSPECTED CASES
  • SOURCE: COOLING TOWERS AT A CITY HOSPITAL
40
Q

LEGIONELLA PNEUMOPHILIA: VIRULENCE FACTORS?

A
  • FORMS BIOFILMS WHICH PROVIDE ADDITIONAL PROTECTION FROM ENVIRONMENTAL STRESSES SUCH AS DISINFECTION
  • CAN INVADE AND SURVIVE INTRACELLULARLY IN VARIOUS PROTOZOANS
  • HAS FLAGELLA, FIMBRIAE, TYPES II AND IV SECRETION SYSTEMS AND IRON ACQUISITION MECHANISMS
  • RESIST KILLING BY PHAGOCYTES THROUGH THE TYPE IV SECRETION SYSTEM WHICH HELPS IT ESTABLISH A REPLICATIVE NICHE KNOWN AS THE ‘LEGIONELLA-CONTAINING VACUOLE’
  • FOLLOWING HOST CELL LYSIS, THE RELEASED BACTERIA INFECT OTHER HOST CELLS, BEGINNING A NEW CYCLE OF INFECTION
41
Q

HOW DOES L. PNEUMOPHILIA RESIST KILLING BY PHAGOCYTES?

A

RESIST KILLING BY PHAGOCYTES THROUGH THE TYPE IV SECRETION SYSTEM WHICH HELPS IT ESTABLISH A REPLICATIVE NICHE KNOWN AS THE ‘LEGIONELLA-CONTAINING VACUOLE’

42
Q

WHICH SECRETION SYSTEM TYPES DOES L. PNEUMOPHILIA CONTAIN?

A

II AND IV

43
Q

DESCRIBE THE GROUP OF G- BACTERIA ‘ENTERIC PATHOGENS’?

A
  • TYPICALLY EXIST IN THE INTESTINES OF ANIMALS AND HUMANS (ESP LARGE BOWEL)
  • ENTERIC BACTERIA CAN EITHER BE: HARMLESS (SUCH AS GUT FLORA OR MICROBIOTA), PATHOGENIC (THEY ALWAYS CAUSE DISEASE) OR OPPORTUNISTIC
  • LARGE FAMILY SMALL, NON SPORE FORMING G- RODS
  • MANY MEMBERS INHABIT SOIL, WATER, DECAYING MATTER….
  • MOST FREQUENT CAUSE OF DIARRHOEA THROUGH ENTEROTOXINS
  • FACULTATIVE ANAEROBES, GROW BEST IN AIR
  • ALL FERMENT GLUCOSE, REDUCE NITRATES TO NITRITES
  • ALL ARE OXIDASE NEGATIVE AND CATALASE POSITIVE
44
Q

WHICH INDIVIDUALS ARE MOST SUSCEPTIBLE TO OPPORTUNISTIC INFECTIONS?

A
  • VERY YOUNG OR ELDERLY
  • PREGNANT WOMEN
  • IMMUNOCOMPROMISED PATIENTS (E.G. CHEMOTHERAPY, AIDS)
  • RECOVERING FROM SURGERY
  • HAD A BREACH OF PROTECTIVE BARRIERS (SEVERE WOUND OR BURN)
45
Q

ALONG WITH PSEUDOMONAS SP., ENTERIC PATHOGENS ACCOUNT FOR WHAT % OF NOSOCOMIAL (HOSPITAL ACQUIRED) INFECTIONS?

A

ALMOST 50%

46
Q

ALL ENTERIC G- PATHOGENS FERMENT WHAT?

A

GLUCOSE

47
Q

DESCRIBE THE FUNCTIONING OF E. COLI IN HUMANS IN NORMAL CONDITIONS?

A
  • E.COLI IS A MEMBER OF THE NORMAL INTESTINAL BACTERIAL MICROFLORA IN HUMANS, OTHER WARM-BLOODED ANIMALS AND REPTILES
  • A HARMLESS COMMENSAL IN THE MUCOUS LAYER OF THE CECUM AND COLON
  • A MOTILE BACILLUS, G-, AND A FAST LACTOSE FERMENTER
48
Q

HOW ARE PATHOGENIC E. COLI STRAINS CATEGORISED?

A

BASED ON ELEMENTS THAT CAN ELICIT AN IMMUNE RESPONSE IN ANIMALS, NAMELY:
O ANTIGEN: PART OF THE LPS
K ANTIGEN: CAPSULE
H ANTIGEN: FLAGELLA

49
Q

E.COLI O157:H7 STRAIN?

A
  • ONE OF THE HUNDREDS OF E. COLI STRAINS
  • MOST COMMON STRAIN TO CAUSE DISEASE IN PEOPLE
  • PRODUCES A POWERFUL TOXIN (SHIGA TOXIN) THAT CAN CAUSE SEVERE ILLNESS
  • FIRST RECOGNISED AS A CAUSE OF ILLNESS IN 1982
  • MOST INFECTIONS HAVE COME FROM THE CONSUMPTION OF UNCOOKED MEAT
50
Q

WHAT ARE THE MAIN E. COLI STRAINS OR PATHOTYPES (BASED ON THE VIRULENCE FACTORS AND HOST SYMPTOMS)?

A

ENTEROTOXIGENIC (ETEC), ENTEROINVASIVE (EIEC), ENTEROAGGREGATIVE (EAEC), UROPATHOGENIC (UPEC), NEONATAL MEMNINGITIS (NMEC), ENTEROPATHOGENIC (EPEC) AND ENTEROHEMORRHAGIC (EHEC) E. COLI

51
Q

DESCRIBE THE ENTEROTOXIGENIC E.COLI? (ETEC)

A
  • THE MOST COMMON CAUSE OF TRAVELLERS’ DIARRHOEA
  • CAN HAVE FATAL CONSEQUENCES FOR CHILDREN UNDER 5 YEARS OF AGE
  • IMPORTANT IN THE FARMING INDUSTRY, AS POST-WEANING PIGLETS ARE HIGHLY SUSCEPTIBLE TO INFECTION
  • PREVALENCE HIGHER WERE HYGIENE STANDARDS ARE LOWER
  • CAUSES SEVERE DIARRHOEA DUE TO HEAT-LABILE TOXIN AND HEAT-STABLE TOXIN - STIMULATE SECRETION AND FLUID LOSS
  • HAS FIMBRIAE
52
Q

WHICH STRAIN OF E. COLI IS THE MOST COMMON CAUSE OF TRAVELLERS’ DIARRHOEA?

A

ENTEROTOXIGENIC E. COLI (ETEC)

53
Q

OTHER NAME FOR THE ENTEROINVASIVE (EIEC) STRAIN OF E. COLI?

A

SHIGELLA

54
Q

WHAT DOES SHIGELLA (ENTEROINVASIVE E. COLI; EIEC) CAUSE?

A

INFLAMMATORY DISEASE OF THE LARGE INTESTINE AND SOMETIMES BLOODY DIARRHOEA

55
Q

DESCRIBE THE ENTEROINVASIVE (EIEC) STRAIN OF E. COLI?

A
  • HIGHLY INFECTIOUS BACTERIA ALSO KNOWN AS SHIGELLA
  • CAUSES INFLAMMATORY DISEASE OF THE COLON AND SOMETIMES BLOODY DIARRHOEA
  • INCLUDES OBLIGATE INTRACELLUALR BACTERIA THAT HAVE NEITHER FLAGELLA NOR ADHERENCE FACTORS
  • VIRULENCE IS LARGELY DUE TO A 220 kb PLASMID THAT ENCODES A TYPE 3 SECRETION SYSTEM THAT IS REQUIRED FOR INVASION, CELL SURVIVAL AND APOPTOSIS OF MACROPHAGES
56
Q

DESCRIBE THE ENTEROAGGREGATIVE (EAEC) STRAIN OF E. COLI?

A
  • THE 2ND MOST COMMON CAUSE OF TRAVELLERS’ DIARRHOEA AFTER ETEC IN BOTH DEVELOPED AND DEVELOPING COUNTRIES
  • BECOMING COMMONLY RECOGNISED AS A CAUSE OF ENDEMIC AND EPIDEMIC DIARRHOEA WORLDWIDE
  • DIARRHOEA CAUSED BY EAEC OFTEN WATERY, BUT IT CAN BE ACCOMPANIED BY MUCUS OR BLOOD
  • PRODUCES ENTEROTOXINS AND CYTOTOXINS
  • COLONISATION CAN OCCUR IN THE MUCOSA OF BOTH THE SMALL AND LARGE BOWELS, WHICH CAN LEAD TO MILD INFLAMMATION IN THE COLON
  • THE ASSOCIATION OF THIS STRAIN WITH DISEASE NOT ENTIRELY CLEAR
57
Q

UROPATHOGENIC E. COLI (UPEC) ACCOUNTS FOR WHAT % OF ALL UTIs?

A

ROUGHLY 80%

58
Q

DESCRIBE THE UROPATHOGENIC STRAIN OF E. COLI (UPEC)?

A
  • INFECTIONS ACCOUNT FOR 80% OF ALL UTIs
  • CAUSES CYSTITIS IN THE BLADDER AND ACUTE PYELONEPHRITIS IN THE KIDNEYS
  • MOVES FROM THE INTESTINAL TRACT TO ESTABLISH AN INFECTION IN THE URINARY TRACT
  • ASCENDS THE URINARY TRACT FROM THE URETHRA TO THE BLADDER AND KIDNEYS
  • VIRULENCE FACTORS: MULTIPLE PILI AND FIMBRIAE, FLAGELLA, SECRETED TOXINS, MULTIPLE IRON ACQUISITION SYSTEMS AND POLYSACCHARIDE CAPSULE
59
Q

WHAT IS THE MAIN DETERMINANT OF PATHOGENICITY OF UROPATHOGENIC E.COLI?

A

THE ABILITY TO ADHERE TO HOST EPITHELIAL CELLS IN THE URINARY TRACT AGAINST THE URINE FLOW

60
Q

DESCRIBE THE NEONATAL MENINGITIS STRAIN OF E. COLI (NMEC)?

A
  • CAN CROSS THE BLOOD-BRAIN BARRIER INTO THE CENTRAL NERVOUS SYSTEM, CAUSING MENINGITIS
  • A COMMON INHABITANT OF THE GI TRACT
  • THE MOST FREQUENT CAUSE OF G- ASSOCIATED MENINGITIS IN NEWBORNS
  • FATALITY RATES APPROACH 40% AND SURVIVORS ARE USUALLY BURDENED WITH SEVERE NEUROLOGICAL SEQUELAE
  • COMPLEX PATHOGENESIS
61
Q

WHAT IS THE MOST FREQUENT CAUSE OF G- ASSOCIATED MENINGITIS IN NEWBORNS?

A

NEONATAL MENINGITIS E. COLI (NMEC)

62
Q

FATILITY RATES OF NEONATAL MENINGITIS E. COLI?

A

ALMOST 40%

63
Q

DESCRIBE THE ENTEROPATHOGENIC (EPEC) STRAIN OF E. COLI?

A
  • A MAJOR CAUSE OD POTENTIALLY FATAL DIARRHOEA IN INFANTS IN DEVELOPING COUNTRIES
  • FORMS ATTACHING AND EFFACING (A/E) LESIONS ON INTESTINAL EPITHELIAL CELLS
  • THE ATTACHING BACTERIA EFFACE THE MICROVILLI AND SUBVERT HOST CELL ACTIN TO FORM DISTINCT PEDESTALS BENEATH THE SITE OF ATTACHMENT (BRUSH BORDER DESTRUCTION) —> MECHANISM DRIVEN BY A PROTEIN CALLED TIR
  • THIS PHENOTYPE IS CAUSED BY GENES ENCODED ON A PLACE KNOWN AS THE ‘LOCUS OF ENTEROCYTE EFFACEMENT’; LEE
  • LEE ENCODES A TYPE 3 SS THAT TRANSLOCATES BACTERIAL EFFECTOR PROTEINS INTO THE HOST CELL CYTOPLASM
  • 7 EFFECTORS ARE ENCODED BY LEE, BUT THERE ARE SEVERAL NON-LEE ENCODED (Nle) EFFECTORS IN ADDITION TO THESE
64
Q

WHAT ARE BACTERIAL EFFECTOR PROTEINS?

A

PROTEINS SECRETED BY PATHOGENIC BACTERIA INTO THE CELLS OF THEIR HOSTS, USUALLY USING A T3, T4 OR T6SS. EFFECTORS PROTEINS ARE USUALLY CRITICAL FOR VIRULENCE

65
Q

DESCRIBE THE ENTEROHEMORRHAGIC STRAIN OF E. COLI (EHEC)?

A
  • FIRST DESCRIPTION OF AN EHEC STRAIN OF E. COLI WAS E. COLI O157:H7 IN 1982; 4 PATIENTS WITH BLOODY DIARRHOEA, LINKED TO UNDERCOOKED HAMBURGERS AT A FAST-FOOD CHAIN
  • CATTLE RESERVOIR!!!!!!
  • TRANSMISSION TO HUMANS USUALLY OCCURS THROUGH CONTAMINATED FOOD AND WATER
  • HIGHLY INFECTIOUS A/E PATHOGEN LIKE EPEC
  • COLONISES THE DISTAL ILEUM AND LARGE BOWEL IN HUMANS
  • CAUSES HEMORRHAGIC COLITIS (BLOODY DIARRHOEA)
  • FURTHER COMPLICATIONS CAN LEAD TO POTENTIALLY FATAL HAEMOLYTIC URAEMIC SYNDROME (HUS)
  • ASYMPTOMATIC IN CATTLE WHERE IT COLONISES THE RECTO-ANAL JUNCTION
66
Q

WHICH PART OF THE HUMAN AND CATTLE GI TRACT DOES ENTEROHEMORRHAGIC (EHEC) STRAIN OF E. COLI COLONISE?

A

HUMANS: DISTAL ILEUM AND LARGE BOWEL
CATTLE: RECTO-ANAL JUNCTION

67
Q

WHICH PATHOTYPE OF E. COLI MIGHT LEAD TO THE POTENTIALLY FATAL HAEMOLYTIC URAEMIC SYNDROME (HUS)?

A

ENTEROHEMORRHAGIC E. COLI (EHEC), WHICH INCLUDES THE E.COLI O157:H7

68
Q

EXAMPLES OF WHAT HAVE THE OUTBREAKS OF ENETEROHEMORRHAGIC E. COLI (EHEC) BEEN LINKED WITH?

A
  • UNDERCOOKED OR RAW HAMBURGER MEAT
  • SPINACH, LETTUCE, SPROUTS
  • UNPASTEURIZED MILK
  • UNPASTEURIZED APPLE JUICE OR APPLE CIDER
  • SALAMI
  • WELL WATER OR SURFACE WATER AREAS FREQUENTLY VISITED BY ANIMALS
  • ANIMALS AT PETTING ZOOS AND DAY CARE CENTRES
69
Q

DESCRIBE THE EHEC O157:H7 VIRULENCE FACTORS?

A
  • INJECTS AROUND TWICE AS MANY EFFECTORS INTO HOST CELLS AS EPEC, MOST OF WHICH ARE REDUNDANT
  • CONTAINS O157 PLASMID (pO157) WHICH ENCODES SEVERAL VIRULENCE FACTORS RELATED TO ADHERENCE AND ACIDIC RESISTANCE
  • LEE AND NON-LEE EFFECTOR PROTEINS
  • MAIN VIRULENCE FACTOR: SHIGA TOXIN!!!
70
Q

HOW IS SHIGA TOXIN RELEASED AND HOW DOES THIS AFFECT TREATMENT OPTIONS?

A
  • LACKS A SECRETORY MECHANISM AND IS RELEASED THROUGH LAMBDOID PHAGE-MEDIATED LYSIS IN RESPONSE TO DNA DAMAGE AND THE SOS RESPONSE
  • ANTIBIOTIC THERAPY SHOULD THEREFORE BE DISCOURAGED AS THE TOXIN WOULD BE RELEASED
71
Q

WHAT IS LEE; LOCUS OF ENETEROCYTE EFFACEMENT?

A

The locus of enterocyte effacement (LEE) is a 35.6 kb pathogenicity island inserted in the genome of some bacteria such as enteropathogenic Escherichia coli, enterohemorrhagic E.coli, Citrobacter rodentium, and Escherichia albertii. LEE comprises the genes responsible for causing attaching and effacing lesions, a characteristic lesion that involves intimate adherence of bacteria to enterocytes, a signaling cascade leading to brush border and microvilli destruction, and loss of ions, causing severe diarrhea

INF (40 decks)

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