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Micro Lec 2 Flashcards

Clinical micro (87 cards)

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1
Q

List 3 host defence mechanisms

A

Stomach acid pH 4
Bile salts
Mucosal defences

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2
Q

How does stomach acid pH act as a defence mechanism

A

It destroys 99.9% of ingested Enterobacteriaceae within 30 minutes

Patients with achlorhydria or taking antacids are vulnerable

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3
Q

How do bile salts act as a defence mechanism

A

They disrupt some bacterial cell surfaces, but enteric organisms are adapted to survive

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4
Q

How do mucosal defences act as a defence mechanism

A

IgA
Phagocytes
Digestive enzymes

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5
Q

How does gut motility act as a host defence mechanism

A

Peristalsis impedes attachments. Helps to clear pathogens. Diarrhoea especially.

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6
Q

how does commensal flora act as a host defence mechanism

A

Confers colonisation
Competition
Enterobacteriaceae produce bacteriocin
Changes to local pH
Production of H2S and fatty acids

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7
Q

Outline the features of commensal flora

A

10^6 organisms/ml small intestine fluid
Largely gram positive
10^11 organisms/g of faeces in the large intestine
Largely anaerobes
Highly competitive environment

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8
Q

What is gastrointestinal infection (gastroenteritis) characterised by

A

diarrhoea and/or vomiting, they often resolve over a few days and are self-limiting

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9
Q

Infections are extremely common in developing countries, outline the features of this infection

A

Can be more severe - e.g. malnutrition
Poor sanitation and access to clean water is a factor
Limited access to basic therapies - oral hydration therapy
5-6 million die each year

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10
Q

What is the large colon

A

the most abundant region of gut bacteria

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11
Q

What is acute gastroenteritis (or bacterial food poisoning)

A

The ingestion of food contaminated by bacteria or bacterial toxins

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12
Q

Outline the features of acute gastroenteritis

A

Bacteria have multiplied to reach infective dose before ingestion
Multiplication of bacteria within the gut (salmonella and shigella)
Ingestion of pre-formed bacterial toxin contaminated food (bacillus cereus)

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13
Q

How do outbreaks of gastroenteritis occur

A

Via ingestion of contaminated food or water, recreational contact with contaminated water or direct contact with animals

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14
Q

List the 4 common pathogens that cause food borne illness in the UK

A

E. coli
Campylobacter species; C. jejuni and C. coli
Salmonella enterica
Clostridium perfringens

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15
Q

List some rare bacterial pathogens causing food borne illness

A

Yersinia, Vibrio, Aeromonas and Piesiomonas species

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16
Q

List two non typical food borne illnesses

A

Shigella species
Vibrio cholerae

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17
Q

What bacterial pathogen is acquired following antibiotic therapy

A

Clostridium difficile

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18
Q

How are gastrointestinal infections typically diagnosed

A

by analysis of faecal specimen

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19
Q

What containment level are faecal specimens in the recovery of pathogens handled at

A

containment level 2 except if S. Typhi, S. Paratyphi A, B or C, Shiga toxin-producing E. coli 0157 or Shigella dysenteriae are suspected - Level 3

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20
Q

If processing is delayed, why must samples be refrigerated

A

because shigella is susceptible to pH changes and may not survive delayed processing

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21
Q

What 3 things should be noted if appears in stool samples

A

blood, mucus or parasites

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22
Q

What microscopy should be carried out on stool samples

A

gram stain of stool sample is of no value, immunofluorescence stain, e.g. cyrtosporidium. Parasite investigation - ova, cysts and parasites (OCP). Inoculate the plate directly or after dilution up to 1:4

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23
Q

Stool should be cultured using selective/differential media, what are some examples of these

A

Charcoal cefoperazone desoxycholate agar (CCDA) for Campylobacter
Xylose lysine desoxycholate agar (XLD) for Salmonella and Shigella
Cefixime , tellurite, sorbitol MacConkey agar (CT-SMAC) for STEC
Thiosulphate, citrate, bile sucrose agar (TCBS) for Vibrio

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24
Q

What are some examples of enrichment broths that can be used when recovering pathogens from stool

A

Selenite cysteine or Rappaport Vassiliadis broth for Salmonella
Alkaline peptone water for Vibrio

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25
Describe diarrhoea
Unusual frequency of bowel action (usually three time in a 24 hour period) Consistency of loose, watery, unformed faeces Associated symptoms include abdominal pain, cramps, nausea, malaise, vomiting, fever, dehydration
26
Describe dysentery
Inflammatory disorder of lower GIT Severe diarrhoea with blood and mucus in the faeces Additional symptoms of abdominal cramps and constitutional disturbance
27
List agars for cultivation of GIT pathogens
Culture - MacConkey agar Salmonella shigella agar - modified deoxycholate citrate agar (DCA) Xylose lysine desoxycholate (XLD)
28
What is MacConkey agar useful for
Determination of whether or not a pathogen is a lactose fermenter (e.g. E. coli) or a non-lactose fermenter (e.g. salmonella or shigella)
29
How does DCA agar present salmonella vs shigella
Salmonella Typhimurium appears in black single colonies compared to shigella sonnei which appears in yellow lighter colonies
30
How do pathogens present on XLD agar
Red colonies of salmonella (with black centtes due to hydrogen sulphide production) and yellow colonies of E. coli
31
How is campylobacter released
Campylobacter is excreted by a range of domestic and wild animals and bird: particularly associated with chickens
32
how is campylobacter spread
Is the leading cause of enteritis in the UK. Can have outbreaks but mostly sporadic infections. Is assocoated with BBQ's, undercooked chicken, cross -contaminated foods. Primarily C. jejuni (90%), rest by C. coli and C. lari
33
Outline the clinical features of campylobacter
Incubation = 2-5 days. Symptoms include: Initial diarrhoea can be severe but brief, fever, severe abdominal pain Blood and mucus in faeces Duration = 2-7 days Occasionally may be invasive Transient self-limiting bacteraemia Fulminant Garm negative sepsis Occasional sequelae Arthritis, bursitis, endocarditis and neonatal sepsis Guillain-Barré syndrome or Miller-Fisher syndrome
34
How can we confirm campylobacter
most commonly isolated species are thermophilic = grow at 37-43 degrees celsius, not 25 Charcoal, CCDA incubated microaerophiilic atmosphere, 42 degrees celsius, 48hr Colony appearance = characteristic grey, moist, metallic sheen. Oxidase positive Gram stain = confirmatory gram negative, 'gull wing'
35
Provide an example of how within one species there are a few subspecies and many serotypes of salmonella enterica
Salmonella enterica subspecies enterica serotype Enteritidis (note the use of italics) Abbreviated to Salmonella Enteritidis (S. Enteritidis) (note the use of italics)
36
Most S. enterica serotypes can cause what
gastroenteritis
37
What are serious systemic infections caused by
S. enterica serotypes Typhi or Paratyphi
38
Outline the features of salmonellae
-Members of the enterobacteriaceae - Facultatively anaerobic gram negative bacilli - Ubiquitous in animal populations, infection arises by consumption of food, animal or bird origin
39
What are the key salmonellae antigens
H - antigen; diphasic flagella (motile) O - antigens (LPS) Vi - antigen (virulence) polysaccharide of S. typhi
40
How is salmonella gastroenteritis acquired
by drinking water contaminated by animals, contact with infected individuals in. condition of extremely bad personal hygiene, foreign travel
41
What is salmonella gastroenteritis
non- typhoid salmonella
42
Outline the features of salmonella gastroenteritis
Incubation 12hr-3d Duration 2-7d Asymptomatic carriage can occur
43
What are teh typical presentations of salmonella gastroenteritis
diarrhoea, abdominal pain, nausea, vomiting, often fever
44
Describe occasional presentations of salmonella gastroenteritis
Bacteraemia may arise in a few individuals Immunosuppression (eg malnutrition) or another underlying medical condition (eg inflammatory bowel disease) can be associated with more severe infection)
45
How can we confirm the presence of salmonella
Culture in: Selenite cysteine or Rappaport Vassiliadis broth overnight to enrich sample Not always necessary Xylose lysine desoxycholate (XLD) agar 24 h in air at 37C Red colonies with black centres Deoxycholate citrate agar (DCA) Chromogenic agar
46
What about salmonellas biochemical profile can help with conformation
Lactose negative Hydrogen sulphide producer Oxidase negative
47
Recovery and conformation of salmonella by
API 20E BioMerieux Used to differentiate members of the Enterobacteriaceae Profile generated can be used to confirm identity
48
What is MALDI-TOF
matrix-assisted laser desorption/ionisation - time of flight mass spectrometry. It allows for rapid identification. Bacterial protein 'molecular finger print' compared to database spectra
49
What happens once confirmed as S. enterica
- O somatic and H flagella antigen used to type salmonella - serovars - Polyvalent O antisera first used - If agglutinates with polyvalent use individual antisera - Repeat with H antisera
50
What is salmonella enteric (typhoid) fever
an invasive systemic infection e.g. S. typhi (typhoid) and S. Paratyphi A, B or C (paratyphoid)
51
Outline the features of salmonella enteric (typhoid) fever
- Is usually only carried by humans - transmitted by faecal contamination of food or water - Incubation 2 weeks
52
Outline the clinical features of salmonella enteric (typhoid) fever
- Septicaemia - High temp - Flu-like symptoms Diarrhoea not typical until late in disease course
53
What containment level are salmonella enteric fever samples manipulated at
level 3
54
What cultures should be taken in salmonella enteric fever
faecal culture alone is not sufficient (organism may not be present in stools), blood cultures should be taken. Other samples include bile, bone marrow or urine
55
Individuals may become chronic carriers on recovery, outline the features of this
organism principally reside in the biliary tract continue to be excreted in faeces and urine
56
Outline the features of Shigellae
- members of the enterobacteriaceae - facultatively anaerobic gram negative bacili - non-motile, non-encapsulated, no fimbriae - closely related to Escherichia - Humans are the only reservoir - Key antigens O antigen (LPS) - Shigella spp. are endemic in temperate and tropical climates - infection ranges from milk watery diarrhoea to dysentry; four species - Increasung prevalence of antimicrobvial resistant strains
57
Outline the features of S. dysenteriae
U ncommon, but cases associated with sub-saharan Africa and South Asia. Most severe form of infection
58
Outline the features of S. boydii
Uncommon
59
Outline the features of S. flexneri
typical of developing countries
60
outline the features of S. sonnei
predominant species in the UK
61
How does shigellosis present
Diarrhoea may be associated with efver and abdominal cramps
62
How is shigellosis transmitted
Directrly person to person. Via fingers, food, water or formites. Highly infective: infectious dose 10-100 organisms
63
What are shigellosis outbreaks associated with
overcrowding in prisons, schools, mental healthcare facilities; places with low hygeine standards and poor socio-economic conditions
64
Outline the features of S. dysenteriae
T- ype 1 causes the most sever disease - Classic bacillary dysentery = 'bloody flux' - UK cases are associated with foreign travel Cytotoxin; shiga toxin = destroys epithelial cells causing inflammatory diarrhoea = dysentry
65
How is shigella diagnosed
Sample processed soon after collection, as with salmonella growth on XLD, DCA
66
Outline the features of E. coli
- Major facultatively-anaerobic inhabitants of the human gut, so always in stool specimens - Difficult to identify specific roles in commensal flora, but may produce useful vitamins for host, and colicins may be protective - Many O and H serotypes - Most strains are harmless commensals - Recognition of some as pathogens since 1960s
67
List E. coli culture characteristics
Usually motile Ferment lactose Produce acid and gas from lactose and other carbohydrates Yellow colonies on CLED, pink/red colonies on MAC, pink colonies on DCA Except Shiga toxin-producing strains (E. coli O157) Produce indole
68
List the four E. coli pathotypes
Enterotoxigenic E.coli (ETEC) Enteropathogenic E. coli (EPEC) Enteroaggregative E. coli (EAEC) Enteroinvasive E. coli (EIEC) Shiga toxin-produciong E. coli (STEC) Diffusely adherent E.coli (DAEC)
69
Outline the features of ETEC
Most common, childhood diarrhoea (but rare in the west) and travellers diarrhoea
70
Outline the features of EPEC
Infantile enteritis, especially in low income countries
71
Outline the features of EAEC
chronic, persistent diarrhoea
72
Outline the features of EIEC
Resembles shigella dysentry, developing countries
73
Outline the features of STEC
Includes enterohaemmorrhagic (EHEC), also known as verocytotoxigenic E. coli (VTEC)
74
Outline the features of DAEC
Recently recognised; watery diarrhoea
75
E.coli strains
pg 43
76
Outline the features of shiga toxin producing E. coli (STEC)
most common strains in developed countries. STEC (VTEC) Verocytotoxin (VT) is similar to the shiga toxin (ST) of S. dysenteriae Over 300 serotypes recognised E. coli O157:H7 is the most common Varies in severity; mild to bloody diarrhoea to haemolytic uremic syndrome (HUS)
77
Outline features of STEC (2)
Occurs in any age group but most common in children under 5yr Outbreaks have occurred in nursing homes, open farms.
78
What is STEC associated with
Contaminated cooked meat Ground beef, beef burgers Drinking unpasteurized milk or juice and contaminated water The disease can be transmitted from person to person Low infective
79
Outline the features of haemorrhagic colitis
Incubation. 1-5 days Severe abdominal cramps begin suddenly along with watery diarrhoea Becomes bloody within 1-3 days - Haemorrhagic colitis - blood diarrhoea 'like red poster paint' The diarrhoea usually lasts 1-8 days fever is usuallyt absent or mild
80
About 2-7% of people develop a sever compliucation. of haemorrhagic colitis; haemolytic uremic syndrome (HUS)
- more likely to occur in children younger than 5 years and in older people - May occur 2-14 days after onset of diarrhoea in children Even with HUS and its complications, haemorrhagic colitis may cause death in older people
81
Outline the features of HUS
Toxins damage the lining of the large intestine Abnormal premature destruction of red blood cells Damaged red blood cells clog the filtering system in the kidneys Some people develop complications
82
Toxin damage the lining of the large intestine
if absorbed into the bloodstream, can also affect other organs such as the kidney
83
Abnormal premature destruction of red cells
Anaemia caused by the destrution of red blood cells (haemolytic aneamia) Low platelt count (thrombocytopenia)
84
Damaged red blood cells clog the flitering system in the kidneys
sudden kidney failure
85
Some people develop complications
Nerve or brain damage such as seizures or strokes
86
STEC lab diagnosis
Sorbitol MacConkey Agar (SMAC) Lactose switched for sorbitol in MAC Cefixime and tellurite increase selectivity (CT- SMAC) BCIG improves specificity E. coli O157 are pale translucent colonies Incubated 37C in air for 24 h Serology to confirm – O157 LPS-specific antisera
87
Treatment for gastrointestinal infections
Supportive measures Drinking sufficient fluids Pain relief for abdominal cramps Anti-diarrhoeal agents may exacerbate HUS by delaying clearance from bowel Antibiotics are not given; May prolong carriage With E. coli STEC may increase the risk of developing HUS Some antibiotics stimulate SOS response in organisms resulting in more toxin production Overuse has induced development of resistance Antibiotics are given for; Enteric fevers, severe cases of salmonellae and shigellosis
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