Microbiology Flashcards
(95 cards)
1
Q
Name traits that increase an invaders chance of success
A
- high growth rates
- dispersal capability
- phenotypic plasticity
- genetic diversity
2
Q
Describe abiotic resistance as a barrier to invasion
A
- pH
- temperature
- salinity
3
Q
Describe biotic resistance as a barrier to invasion
A
- competition
- antagonism
- predation
4
Q
Describe the pathology of infection
A
- exposure
- adhesion
- invasion
- colonisation
- toxicity
- tissue damage and disease
5
Q
What is colonisation?
A
The establishment of a microorganism on or within a host, it may be short lived
6
Q
What is a pathogen?
A
Any microorganism that has the potential to cause disease
7
Q
What is virulence?
A
The likelihood of causing disease, opportunistic pathogen, accidental pathogen
8
Q
Name infections in the abdomen
A
- peritonitis (primary and secondary)
- oral infections
- oesophagitis
- gastritis, duodenitis
- hepatitis, liver abscess
- cholecystitis, cholangitis
- pancreatitis
- small bowel
- gastroenteritis, abscesses
- perineal abscesses
9
Q
Describe microbiological tests for enterobacteriaceae
A
- ferment glucose (and other CHO), this produces acid
- blood agar
- MacConkey agar, lactose fermenters turns it pink
- CED agar, cysteine lactose electrolyte deficient
- chromogenic agar
10
Q
Describe enterobacteriaceae
A
- 53 genera (26 cause human infection)
- gram negative
- non-spore forming
- grow on a variety of solid media
- ferment sugars
- facultative anaerobes mostly
- motile or non motile
- increasing resistance
11
Q
How can Enterobacteriaceae cause disease
A
- motility; flagella allows movement, shigella and klebsiella are not mobile
- colonisation factors; fimbriae
- endotoxin; cell wall component
- enterotoxin; eg. shiga toxin
12
Q
Describe classification of Enterobacteriaceae
A
- biochemical and antigenic characteristics
- DNA hybridisation has changed much of the classification
- many new genera discovered
- reclassification of many genera
13
Q
What is MALDI-TOF?
A
Mass spectrometry
14
Q
Describe the characteristics of MALDI-TOF
A
- identification quick
- accurate and effective
- low cost process
15
Q
Describe characteristics of gram stain, bacterial agglutination and metabolic tests
A
- give first orientations (gm +ve/-ve, morphology)
- determines where or not there is oxidase and catalase
16
Q
Describe characteristics of API test strips
A
- a prior knowledge of microorganism
- a lot of strips and reagents allow to identify bacteria
- each bacterial family have specific strips
17
Q
Describe the normal flora of the bowel
A
- mouth; strep viridans, Neisseria sp, anaerobes cadida sp, staphylococci
- stomach / duodenum (low pH); usually sterile, few cadida sp and staphylococci may survive
- jejunum; small numbers of coliforms and anaerobes
- colon; faecal flora, large numbers of coliforms, anaerobes and enterococcus faecalis
- bile ducts; usually sterile
18
Q
Describe anaerobes in the GI tract
A
- strict anaerobes; will not grow in the presence of oxygen
- c diff, bacteroides sp and anaerobic cocci
- present in large number in the large bowel
19
Q
Describe GI infection risk factors
A
- malnutrition (micronutrient) deficiency
- closed / semi closed communities
- exposure to contaminated food / water / travel
- winter congregating / summer floods
- age <5 not breastfeeding
- older age
20
Q
What is acid suppression a risk factor for?
A
- Yersinia enterocolitica, h pylori tolerant of acid
- c diff more common with acid suppression
- vibrio cholera, non-typhoidal slamonella., campylobacter jejuni, listeria, some e coli
21
Q
What is immunosuppression a risk factor for?
A
- salmonella, campylobacter, shigella shed for longer
- other organisms that are uncommon in immune competent
22
Q
Describe inoculum size
A
- median infecting dose required to cause disease in 50%
- low infectious doses make spread easier
- pH affects required dose
23
Q
What is diarrhoea?
A
- > 3 unformed stool / day
- no other cause; exclude laxative use / abuse and other drugs / stimulants
- stools holds the shape of container
- departure from normal bowel habit
- use Bristol stool chart
24
Q
Describe dysentery
A
- inflammation of the intestine, particularly the colon, causing diarrhoea associated with blood and mucus
- examples include shigella, campylobacter
- generally associated with fever, abdominal pain and rectal tenesmus (sense of incomplete defaecation)
25
What can mimic appendicitis as it may invade mesenteric nodes?
Yersinia enterocolitica
26
Describe gastroenteritis
- an illness caused by eating food contaminated with micro-organisms, toxins, poisons etc
- bacteria
- usually have GI symptoms (diarrhoea, abdo pain, vomiting)
- large volume tends to be small bowel
- cholera causes large volume diarrhoea
- invasion of tissue +/- toxin production
27
Describe the history of gastroenteritis
- diarrhoea frequency, blood, mucous, time course
- other symptoms
- epidemiology (travel, contacts- human and animal)
- food history (time, type, storage, reheating, washing)
- contacts
- age of patient
- co morbidities
- medication history
28
What does shiga toxin do?
- binds to receptors found on renal cells, RBC and others
- inhibit protein synthesis
- causes cell death
29
Describe presentation of haemolytic ureamic syndrome
- abdo pain, fever, pallor, petechiae, obliguria
- bloody diarrhoea
- high white cells
- low platelets
- low Hb
- red cell fragments
- LDH >1.5 x normal
- may develop after diarrhoea stopped
30
Describe HUS investigation
- send stool culture samples; all patients with bloody faeces
- send U and E, FBC, film, LFT, clotting, urine (dipstick / micro), lactate dehydrogenase
31
Describe role of health protection unit
- you must notify Health protection unit of haemolytic ureamic syndrome or 0157
- contact tracing and investigation
- environmental health inspect food premises
- al lab confirmed cases are routinely reported to the local HPU
- advise on return to work for high risk groups (hospital staff, food handlers, nursery staff and children)
32
Describe enterotoxigenic e coli pathotypes
- produces heat labile and heat stable toxin
- heat stable toxin similar to cholera and Yersinia toxins
- travel related
33
Describe enteropathogenic e coli pathotypes
- attaching and effacing lesions. No toxin, not invasive
- synthesises, secretes and inserts its own receptor into cell membranes
- non breastfed children
- can be asymptomatic
34
Describe enteroinvasive e coli pathotypes
- watery diarrhoea, rare dysentery
- demonstrates invasion
- sereny test
35
Describe enteroaggregative e coli pathotypes
- travellers diarrhoea
- new kid on the block
- cytogenic, secretogenic, proinflammatory
36
Describe campylobacter species
- 16-48hrs incubation
- sporadic
- food; poultry (raw milk)
- small pathogen numbers
- invasive
- pain, blood, fever
- may be admitted
- food hygiene (raw poultry especially)
- macrolide
- less likely to spread person to person
- most common
37
Name the campylobacter human pathogenic strains (enteric)
- c jejuni subspecies
- c jejuni subspecies doylei
- campylobacter coli
- campylobacter upsaliensis
- campylobacter lari
- c fetus subspecies fetus
- campylobacter hyointestinalis
- campylobacter concisus
38
Describe salmonella enteritidis
- 12-48hr incubation
- food; poultry, meat, raw egg
- animal gut, multiplies in food
- toxin and invasion
- d and v, blood, fever
39
Describe typing salmonellae
- different antigens on the body
- call o antigen
- slide agglutination
- antigen agglutinates with the corresponding antibody
40
Describe serogrouping salmonellae
- >1500 different types affect humans
- a serogroup can help pinpoint source of infection
- useful for detecting outbreaks / contact tracing
- groups B,C and D are most common locally
41
Describe listeria monocytogenes - invasive
- 2 to 6 weeks
- immunosuppressed (particularly T cell)
- age >50
- pregnant
- meningitis / bacteraemia
42
Describe listeria monocytogenes - gastroenteritis
- 9 to 48 hours
- fever, muscle aches, diarrhoea
- pregnant women may have mild symptoms
- unpastreurised milk products, deli counter
43
Describe diagnosis of listeria monocytogenes
- easier from a sterile site
- gram positive rod (variable)
- cold enrichment
- culture; easier from sterile site, stool needs specific media
- molecular
44
Describe acute travellers diarrhoea
- 3 loose stool in 24 hr
- associated with self reported fever
- typically enterotoxigenic e coli
- also campylobacter, salmonella, shigella
- cruiseships; norovirus, rotavirus
- others; amoebic diarrhoea
45
Describe investigation for acute travellers diarrhoea
- stool culture
| - stool wet prep on recently passed stool for amoebic trophozoites
46
Describe treatment of acute travellers diarrhoea
- supportive; fluid rehydration (oral/IV)
- bloody diarrhoea with systemic upset may warrant treatment
- in those travelling a fluoroquinolone (ciprofloxacin) single dose can stop worsening
- antibiotic resistance; now very common especially in asia where a macrolide (azithromycin) may be more useful
47
Describe enteric fever
- typhoid or paratyphoid fever
- most common in those returning from indian subcontinent and SE asia
- often people visiting family or friends
- incubation 7-18 days
- caused by salmonella typhi or paratyphi
- lab precautions
48
Describe symptoms of enteric fever
- fever
- non specific
- headache
- constipation or diarrhoea
- dry cough
49
Describe complications of enteric fever
- GI bleeding
- GI perforation
- encephalopathy
- bone and joint infection
50
Describe management of enteric fever
- in hospital; isolate patient immediately if diagnosis considered
- vaccination incomplete protection against s typhi
- precaution; water, food and hand hygiene
- fever clearance time; azithromycin 4 days, ciprofloxacin <4 days, ceftriaxone 6 days
51
Describe pre hepatic (haemolytic) causes of fever and jaundice
- malaria
- HUS as complication of diarrhoeal illness
- sickle cell crisis triggered by infection
52
Describe hepatic causes of fever and jaundice
- hepatitis A and E
- leptospirosis - wells disease
- malaria
- enteric fever
- rickettsia
- viral haemorrhagic fever
53
Describe post hepatic causes of fever and jaundice
- ascending cholangitis
| - helminths
54
Describe investigations of fever and jaundice
- malaria blood film and rapid antigen
- blood film for red cell fragmentation
- FBC/UE/LFT/ coagulation
- blood cultures
- USS abdomen
- serological testing for viruses
55
Describe management and treatment for fever and jaundice
- appropriate isolation and infection control procedures
- supportive; may need dialysis if acute kidney injury
- if acute liver failure; hepatology / transplant unit
- directed to pathogen isolated
- discussion with infectious diseases
56
Describe amoebiasis
- entamoeba histoloytica, a protozoa
- faecal- oral spread strong association with poor sanitation
- asymptomatic carriage; shed cysts in stool chronically
- amoebic dysentery; abdominal pain, fever, bloody diarrhoea / colitis, toxic and unwell, abdominal tenderness, peritonism
57
Describe investigations of amoebiasis
- stool microscopy for trophozites or cysts
- AXR; toxic megacolon
- endoscopy or biopsy (not if evidence of toxic dilatation)
58
Describe amoebic liver abscess
- entamoeba histolytica
- incubation period 8-20 weeks
- most common in men
- subacute presentation over 2-4 weeks
- exclude hydatid disease before aspiration if from high risk country (middle east, central asia)
59
Describe presentation of amoebic liver abscess
- over 2-4 weeks
- fever, sweats
- upper abdominal pain
- sometimes history of GI upset (dysentery)
- hepatomegaly
- point tenderness over right lower ribs
60
Describe investigations of amoebic liver abscess
- abnormal LFTs
- CXR; raised right hemi-diaphragm
- USS/CT scan
- serology
- stool microscopy; often negative
61
Describe management of amoebic liver abscess
- metronidazole or tinidazole
- if pyogenic abscess a possibility then treat with appropriate antibiotics whilst awaiting diagnostic investigations
- need to clear the gut lumen of parasites; paramomycin . diloxanide
62
Describe giardiasis
- giardia intestinalis, flagellated protozoa
- invades duodenum and proximal jejunum
- faecal oral spread (contaminated water mostly)
- incubation usually around 7 days
63
Describe presentation of giardiasis
- watery, malodorous diarrhoea
- bloating, flatulence
- abdominal cramps
- weight loss
64
Describe investigations for giardiasis
- stool microscopy for cysts (often difficult), in developed world PCR tests
- OGD for duodenal biopsy (rarely necessary)
65
Describe treatment of giardiasis
- metronidazole or tinidazole
66
Describe the parasites of helminth infections
- in the gut
- in the tissue
- often associated with eosinophilia
- often diagnosed by the adult worm passed or the eggs in stool
- helminths; nematodes (round worms), intestinal roundworms, tissue roundworms (filariasis )
- trematodes (flukes)
- cestodes (tapeworms); intestinal, larval
67
Describe the lifecycle of helminth infections
- egg ingested
- hatch in small intestine
- invade gut wall into venous system and via liver and heart reach lungs
- break into alveoli
- ascend tracheobronchial tree then swallowed and in the gut develop into adult worm where they start to produce eggs
68
Describe Chagas disease
- trypanasoma cruzi - American trypanosmiasis
- transmitted by the kissing bug (triatome)
- causes parasympathetic denervation affecting the colon and or oesophagus
- megaoesophagus
69
Define antimicrobials
A wider term that includes all agents that act against microorganisms, namely bacteria, fungi, viruses and protozoa
70
Define anti-bacterials
Act only on bacteria. Broadly defined, this term encompasses all compounds that act against bacteria, including antibiotics. today the term is sometimes used for different types of disinfectants that are not used as medicine, such as alcohol or triclosan
71
Define antibiotics
Produced naturally by microorganisms and kill or inhibit the growth of other microorganisms.
72
Define antimicrobial stewardship
Defined as an organisational or healthcare system wide approach to promoting and monitoring judicious use of antimicrobials to preserve their future effectiveness
73
Name the hepatitis viruses
- hepatitis A
- hepatitis B
- hepatitis C
- hepatitis D
- hepatitis E
74
Describe transmission of hepatitis A virus
- faecal-oral spread
- poor hygiene / overcrowding
- some cases imported
- some clusters, gay men and people who inject drugs
- importance has declined in uk
- virus presents in faeces and to a lesser extent urine
- no carrier state, no chronic hepatitis
75
Describe hepatitis A tests
- lab confirmation of acute infection
- clotted blood for serology (gold top vacutainer), same sample for all causes of viral hepatitis
- hepatitis A IgM
- IgM usually detectable by the onset of illness
76
Describe control of hepatitis A
- hygiene
- vaccine prophylaxis
- vaccine gives long term protection but needs 10 days to take effect
77
Describe hepatitis E
- more common in tropics
- clinically like hep A
- has become more common than hep A in UK
- faecal-oral transmission like hep A in tropics
- evidence of chronic infection in pigs
- cases acquired in UK are thought to be zoonoses
- tropical genotypes associated with severe disease in pregnant women
- no vaccine available
- some immunocompromised humans can get chronic infection
- cases acquired in tropics are thought to be caught through person to person transmission
78
Describe hepatitis D virus
- only found with hepatitis B virus
- parasite of a parasite
- exacerbates hepatitis B virus infection
- co-infection or superinfection
- rare in Scotland
- clinical significance is that it exacerbates hepatitis B
79
Describe hepatitis B virus transmission
- sex
- mother to child
- blood to blood
- chronic infection more likely to result if first exposure is in childhood
80
Name people at higher than average risk in UK of hepatitis B virus
- people born in areas of intermediate / high prevalence
- multiple sexual partners
- people who inject rugs
- children of infected mothers
81
Describe lab confirmation of hepatitis B virus
- hepatitis B surface antigen (HBsAg) present in blood of all infectious individuals
- present for more than 6 months in chronic infection
- hepatitis B e antigen (HBeAg) usually also present in highly infectious individuals
- hep B virus DNA always also present in high titre (amount) in highly infectious individuals
- hep B DNA tests also used to predict risk of chronic liver disease and monitor therapy
- hep B IgM most likely to be present in recently infected cases
- anti-HBs present in immunity
82
Describe control of hepatitis B
- minimise exposure; safe blood, safe sex, needle exchange, prevention of needlesticks, screening of pregnant women
- two pre-exposure vaccination strategies in use in UK
- post-exposure prophylaxis, vaccine, plus HBIG (hyperimmune Hep B immunoglobulin)
83
Describe hepatitis C virus transmission
- similar to hepatitis B
- no vaccine available
- infection results in chronic infection in about 75% of cases
- natural history does not seem to be dependent on age at time of infection
84
Describe the natural history of chronic infection
- six months of infection defines chronic
- in hep B; spontaneous cure not uncommon, even after many years of infection
- in hep c; once chronic infection established, spontaneous cure is not seen
- time from infection to cirrhosis; typically >20 years
- time from infection to hepatocellular carcinoma; typically >30 years
85
Describe hepatitis c virus control
- no vaccine
| - minimise exposure
86
Describe management of chronic viral hepatitis
- antivirals; increasing number, twelve for HCV, six for HBV
- vaccination
- infection control
- alcohol decrease
- hepatocellular carcinoma awareness / screening
87
Name drugs used in chronic HBV therapy
- adefovir
- entecavir
- tenofovir
- laminivudine
- telbivudine
- inteferon alfa
88
Describe who to treat in terms of chronic infection of hepatitis
- chronic infection; HCV RNA present and genotype known, HBsAg and hep B DNA present
- risk of complications; evidence of inflammation / fibrosis sought, especially in hep B, non-invasive tests of fibrosis eg. fibroscan good at identifying cirrhosis, biopsy less used than it was, biochemical evidence of inflammation
- fit for treatment; established cirrhosis more difficult to treat, but cirrhotic patients are treated as a priority, liver cancer at presentation is a contraindication, HIV co-infection more difficult to treat, and stabilising HIV may be a more urgent issue if both infections diagnosed at the same time
- patients may have other priorities
89
Describe when to treat chronic hepatitis
- Hep B; raised ALT and high HBV DNA
- trial data in children lags behind that in adults
- when patient ready
- when clinical priority
- chronic hep C is treated right away, if there is a waiting list, treat those with advanced fibrosis or cirrhosis first
90
Describe interferon alfa
- human protein
- part of immune response to viral infection
- made by drug companies by genetic engineering
- given by injection as PEGylated interferon (peginterferon)
- complex mode of action, including as immune-adjuvant
- many side effects, so used less and less
- side effects; flu like symptoms, autoimmune disease, psychosis
91
Describe the adverse effects of peginterferon
- common; flu-like symptoms, chills, sore muscles, malaise etc
- less common but more severe; thyroid disease, autoimmune disease, psychiatris disease
92
Describe therapy for chronic hepatitis B
- option 1; suppressive antiviral drug, eg. entecavir, tenofovir, safer, increasing range available, suppression not cure, resistance can develop
- option 2; peginterferon alone, sustained cure possible from a few months of therapy, side effects, injections, only minority gain benefit
93
Describe aims / benefits of chronic hepatitis B therapy
- virological; reduction in HBV DNA (suppression), loss of HBeAg (more enduring suppression, loss of HBsAG (cure)
- improved liver biochemistry
- improved histopathology
- reduced infectivity
- reduced progression to cirrhosis and primary hepatocellular carcinoma
- reduce mortality
94
Describe aims / benefits / limitations of chronic hepatitis C therapy
- response defined by loss of HCV RNA in blood sustained to 6 months after end of therapy, virological cure, known as sustained virological response or SVR, relapse after SVR is rare, reinfection can occur
- after SVR patients have; improved liver biochemistry, improved histopathology, reduced infectivity, reduced mortality, reduced incidence of primary liver cancer
95
Describe the principles of HCV therapy
- choice of antiviral regime based on; genotype of virus and viral load
- genotype of patients interferon response genes
- stage of disease
- past treatment experience, genotypic resistance info
likelihood of side-effects
- cost effectiveness considerations
