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Microbiology 3 Flashcards

1
Q

What are the major phyla making up the gut flora?

A
  • Firmicutes
  • Bacteroides
  • Proteobacteria
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2
Q

Describe Firmicutes

A
  • Majority Gram +ve
  • Some form endospores
  • Mollicutes (Mycoplasmas) lack cell walls altogether
  • Some sub groups have porous pseudo outer membrane casuign Gram -ve staining
  • Found in various environments
  • Commensals and pathogens
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3
Q

List the important Gram +ve Firmicutes

A
  • Listeria
  • Staphylococcus
  • Enterococcus
  • Lactobacillus
  • Streptococcus
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4
Q

List the important Gram +ve endospore forming Firmicutes

A
  • Clostridium

- Bacillus

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5
Q

Describe Bacteroides

A
  • Composed of 3 large classes of bacteria
  • Bacteroidales, Bacteroides, Porphyromonas
  • Widely distributed in environment
  • Rarely pathogenic
  • Some evidence for opportunistic infection by Bacteroides (abundant in faeces)
  • Bacteroides, Porphyromonas Gram -ve
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6
Q

Describe Proteobacteria

A
  • All Gram -ve
  • Includes commensals and pathogens
  • Defined by rRNA sequences
  • Diversity of forms
  • Either facultative or obligate anaerobes
  • Heterotrophic (numerous exceptions)
  • Divided into 5 sections: alpha, beta, gamma, delta, epsilon
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7
Q

Give an example of alpha Proteobacteria

A

Rickettsia

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8
Q

Give examples of beta Proteobacteria

A
  • Neissericeae

- Burkholderia

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9
Q

What are the families within gamma Proteobacteria?

A
  • Psuedomonadaceae
  • Enterobacteriaceae
  • Vibrionaeceae
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10
Q

Give an example of Psuedomonadaceae

A

Pseudomonas

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11
Q

Give examples of Enterobacteriaceae

A
  • Escherichia
  • Salmonella
  • Proteus
  • Klebsiella
  • Yersinia
  • Enterobacter
  • Shigella
  • Citrobacter
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12
Q

Give an example of Vibrionaceae

A

Vibrio

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13
Q

Give an example of delta Proteobacteria

A

Myxobacteria

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14
Q

Give an example of epsilon proteobacteria

A
  • Helicobacter

- Campylobacter

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15
Q

Describe Alphaproteobacteria

A
  • Symbionts of plants and animals
  • Important group, contains pathogens (Rickettsiaceae)
  • Minute Gram -ve, obligate intracellular pathogens
  • Not GI
  • Rickettsia rickettsii = rocky mountain spotted fever in US, vector bourn (ticks)
  • Rickettsia typhi - rodent vectors
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16
Q

Describe Betaproteobacteria

A
  • Aerobic or facultative
  • Several groups
  • highly versatile in degradation capacities
  • Range from plant pathogens, environmental organisms to pathogenic species
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17
Q

Describe Gammaproteobacteria

A
  • 3 important groups
  • Important pathogens
  • Not all are GI importance
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18
Q

Describe Epsilonproteobacteria

A
  • Contains Vibrio pathogens Helicobacter and Campylobacter

- Microaerophilic

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19
Q

Describe Actinobacteria

A
  • Contains Mycobacteria (acid fast) and Bifidobacterium (Gram +ve)
  • Corynebacterium
  • Range of organisms, some cause disease, some healthy commensals
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20
Q

Describe the genus Bacteroides

A
  • Gram -ve
  • Rod
  • Anaerobic
  • Non-endospore
  • Variable motility between species
  • Novel membrane sphingolipids and mesodiaminopimelic acid in peptidoglycan layer
  • Major component of GI flora
  • Complex molecules to simpler ones in host intestine
  • Simple sugars when available, main source of energy is polysaccharide from plant sources
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21
Q

Describe the genus Lactobacillus

A
  • Gram +ve
  • Facultative anaerobe/microaerophilic
  • Firmicutes
  • Lactose and other sugars to lactic acid
  • Common and benign
  • Mucosa of reproductive and GIT
  • makes environment acidic, inhibitis growht of someharmful bacteria
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22
Q

Describe the genus Clostridia

A
  • Gram +ve
  • Rod
  • Obligate anaerobes
  • Can produce endospores
  • Pathogenic
  • Botulinum, dificile, perfringes, tetani all important species
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23
Q

Describe the genus Streptococci

A
  • Gram +ve
  • Coccoid
  • Firmicutes phylum
  • May be commensal or pathogenic
  • Lots of species
  • Distinguish by haemolysis, serology and biochemical testing
  • Grow in chains or pairs
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24
Q

Describe Enterococcus faecalis

A
  • Gram +ve
  • Non-motile
  • Commensal
  • Facultatitve anaerobe
  • Catalase -ve
  • Gamma haemolytic
  • Niche gastrointestinal tracts of mammals
  • May be opportunistic pathogen
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25
Q

Describe the genus Bifidobacterium

A
  • Gram +ve
  • Non-motile
  • May appear branched
  • Anaerobe
  • GIT of mammals
  • Ferment carbohydrates/oligosaccharides
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26
Q

Describe how restriction enzymes function

A
  • Sequence specific
  • Recognise and bind to specific DNA sequences
  • Once bound to recognition sequence, cut sugar-phosphate backbones of DNA strands
  • Some leave overhanging sticky ends
  • Sticky ends can be reattached by ligase enzyme
  • Catalyses chemiccal reaction that rejoins sugar-phosphate bonds
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27
Q

Describe the process of DNA sequencing

A
  • New DNA strand synthesis using existing strand as template
  • Add nucleotides in 5’ to 3’ direction
  • 5’ carbon of incoming deoxynucleotide (dNTP) joined to 3’ carbon at end of chain
  • Hydroxyl groups in each position form ester linkages with central phosphate
  • Nucleotide chain elongates
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28
Q

Describe Sanger’s method of DNA sequencing

A
  • dideoxynucleotides (didNTP) incorporate into chain by forming phosphodiester linkage at 5’ end
  • Lack 3’ hydroxyle group needed to form linkage with incoming nucleotide
  • Addition of didNTP stops elongation
  • To sequence DNA 4 reactions needed to give information about each nucleotide
  • Each reaction contains template DNA, short primer, DNA polymerase, 4dNTPS (one radioactively labelled) and one type of didNTP (A, C, T, G)
  • Same as normal process, but when didNTP added to chain by polymerase synthesis is terminated generating DNA strand of certain size
  • Put through gel electrophoresis
  • Read bottom to top, knowing the terminator lane give sequence of nucleotides in tempate DNA
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29
Q

Outline cycle sequencing

A
  • Based on Sanger method
  • Fragments produced in same way
  • Each didNTP emits light of characteristic wavelength
  • Record as coloured band on simulated gel image
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30
Q

What is point mutation?

A

A base replaced by a different base

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31
Q

What is a silent mutation?

A

ONe that does not change the peptide sequence i.e. has no effect

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32
Q

What is a mis-sense mutation?

A

One that changes a codon to code for a different amino acid

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33
Q

What is a non-sense mutation?

A

One that changes a codon to stop truncate peptides, usually negative

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34
Q

What is the effect of a mutation in the coding region?

A
  • May have no effect if silent mutation
  • May prevent synthesis of the protein (non-sense)
  • May alter the protein in structure or ability to function (non-sense mutation)
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35
Q

What is the effect, on gene expressiong, of a mutation in the regulatory region of a sequence?

A
  • Can impact on promotor or enhancer sequences, termination signals, splice donor and acceptor sites and ribosome binding sites
  • Initiation of transcription controlled by short sequence elements called promotors
  • Genes include information that tells RNA polymerase where to start and stop
  • May prevent protein being expressed or may increase expression
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36
Q

What are somatic mutations?

A
  • Those only affecting one cell and those created from the mutated cell
  • Cannot be passed onto offspring as does not affect the cells that create gametes
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37
Q

What are germ line mutations?

A

Ones that affect every cell in an organism and are passed onto offspring

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38
Q

Give the key types of infections of the oral cavity

A
  • Endogenous (usually bacterial and fungal)
  • Exogenous (usually viral)
  • Number of viral diseases
  • Bacterial oral infection usually opportunistic and preceeded by trauma
  • Mycotic oral infection uncommon
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39
Q

Outline the key types of infections in the oesophagus

A
  • No defined flora or pathogens but viral infections occur
  • Rapid passage of material through oesophagus
  • Tough stratified epithelium, infection uncommon
  • Some viral infections cause ulcers
  • Most notable BVDB and mucosal disease
  • Newcastle disease in poultry
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40
Q

Outline key infections of the stomach

A
  • Hostile to organisms

- Helicobacter

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41
Q

Outline key features of small and large intestinal infections

A
  • Affect all domestic animals
  • Effective vaccinations against many viral pathogens
  • Close confinement increases risk of contracting disease
  • Stress can increase growth of pathogens in intestine
  • Major clinical manifestation is vomiting or diarrhoea
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42
Q

Describe the group Enterobacteriaceae

A
  • E. coli, Salmonella serotypes
  • Inhabit intestinal tract of animals and man
  • Gram -ve rods
  • Growth on enriched media
  • Oxidase negative
  • Tolerate bile salts
  • Mostly non-haemolytic
  • Pathogens: E. coli (also commensal), Salmonella enterica, Yersinia species
  • Opportunistic pathogens: Proteus spp, Enterobacter spp, Klebsiella spp.
  • All look roughly the same on cultures
  • Differentiation by growth characteristics and biochemistry
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43
Q

How can Proteus spp. be distinguished on media?

A

Unusual swarming pattern (ripples on a pond)

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44
Q

What tests can be used to distinguish between members of the Enterobacteriaceae group?

A
  • Culture characteristics
  • Motility at 30degreesC
  • Lactose fermentation
  • IMViC tests
  • Hydrogen sulphide production
  • Lysine decarboxylase
  • Urease activity
  • Can combine tests in XLD for example
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45
Q

Describe Escherichia coli

A
  • Opportunistic infections
  • Possess virulence factors which allow them to cause disease
  • 3 main groups of pathogenic E coli
  • ETEC, AEEC, EAggEC
  • AEEC also has subgroups EPEC and STEC/EHEC
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46
Q

Describe ETEC (name, virulence factor, pathology, disease examples)

A
  • Enterotoxigenic E coli
  • Characteristic fimbrail adhesins
  • LT and ST pig associated, Sta calves and pigs, STb pigs
  • Cause secretory diarrhoea
  • Increase Cl- and HCO3- secretion and inhibit Na+ absorption
  • Less water absorption
  • Mechanism of each toxin differs slightly
  • Diarrhoea in neonatal piglets, calves, lambs, post-weaning diarrhoea in pigs, diarrhoea in pups
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47
Q

Describe EPEC in general

A
  • Enteropathogenic
  • Atypical and typical types
  • No enterotoxins
  • Different virulence factors for typical and atypical
  • Both cause attaching and effacing lesions, determined by locus of enterocyte effacement (LEE)
  • Intimate adherence to enterocytes and effacement of microvilli
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48
Q

Describe atypical EPEC (virulence factor, disease examples)

A
  • Outer membrane protein intimin
  • Wide range of diseases
  • Slight changes or haemorrhagic diarrhoea in calves, pigs and dogs
  • Lambs and kids occasionally affected
  • Major cause of diarrhoea in neonatal and weanling rabbits
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49
Q

Describe typical EPEC (virulence factors, disease examples)

A
  • Intimin (OMP) and EPEC adherence factor (EAF)
  • Uncommon pathogens in intestinal tract of animals
  • Causes human infantile diarrhoea in developing countries
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50
Q

What does STEC stand for and what are the 2 subgroups?

A
  • Shiga Toxin producing E coli
  • EHEC
  • Strains of E coli producing oedema disease
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51
Q

Describe EHEC (virulence factors, pathology caused, diseases)

A
  • Intimin adhesin, STx toxins (affect endothelial cells)
  • Attaching and effacing lesions
  • Intimate adherence to enterocytes and effacement of microvilli
  • Rare cause of haemorrhagic diarrhoea in calves
  • Cattle asymptomatic carriers
  • Other domestic animals may be reservoirs
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52
Q

Describe strains of E coli producing oedema disease (virulence factors, pathology caused, disease)

A
  • F18 fimbriae adhesin
  • STx2e toxin
  • Alpha haemolysin also present
  • STx2e damages vascular endotehlium in target tissues = localised oedema
  • Oedema disease in recently weaned pigs
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53
Q

Describe EAggEC

A
  • Enteroaggregative
  • Typical and atypical subgroups
  • Both cause histopathological lesions charaterised by “stacked brick” formation of epithelial cells
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54
Q

Describe atypical EAggEC (virulence factors, pathology caused, disease)

A
  • No adhesins or enterotoxins identified
  • Histopathological lesions characterised by stacked brick appearance of epithelial cells
  • Frequently subclinical, occasionally associated with diarrhoea in animals
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55
Q

Describe typical EAggEC (virulence factors, pathology caused, disease)

A
  • Aggregative adherence fimbriae, EAST1 toxin, plasmid encoded toxin
  • Histopathological lesions characterised by “stacked brick” formation of epithelial cells
  • Diarrhoea in humans
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56
Q

Describe Salmonella

A
  • 2 species
  • S. bongori and S. enterica
  • S. enterica has number of subspecies: Typhimurium, Enteritidis, Gallinarium, Pullorum
  • Some host specific, others non-host specific
  • Over 2400 serotypes
  • O and H antigens
  • Invades gut lining
57
Q

List sources of Salmonella infection

A
  • Water
  • Soil
  • Animal feed
  • Raw meat
  • Eggs
  • Offal
  • Plant material
58
Q

Describe enteric Salmonellosis

A
  • Acute disease, can affect most farm animals
  • Restricted to intestine and its mucosa
  • Fever
  • Depression
  • Anorexia
  • Profuse foul smelling diarrhoea
  • Severely affected animals may become recumbent
  • When endemic, milder signs may occur due to acquired immunity
  • Inflammatory disease
59
Q

How does Salmonella cause its pathology?

A
  • Attachment and invasion damages enterocyte
  • Penetration of mucosal barrier leads to inflammation and fluid secretion
  • Neutrophils attracted to site increasing inflammation
  • Infection of macrophages
60
Q

Explain how Salmonella is detected

A
  • Enrichment in selenite broth
  • Inoculation onto MacConkey or XLD
  • Confirm suspect colonies with serotyping
61
Q

Describe Campylobacter

A
  • Many commensals in GIT of warm blooded animals
  • Number of species in genus
  • Most common jejuni, coli, lari
  • C. fetus in abortion
  • In humans jejuni and coli
  • Commensal of poultry, cattle adn sheep
  • Unclear in young pups
  • Most common infection
  • Not as severe as EHEC or Salmonella
  • Contaminates meat and eggs of poultry
  • Causes inflammation, tissue damage, secretion and fluid release, inflammatory diarrhoea
  • Sporadic infection not outbreaks
62
Q

Describe Campylobacter jejuni

A
  • Gram -ve
  • Vibrio (coccoid under stress)
  • Flagellated, motile
  • Non-fermentative, oxidase positive, variable catalase reaction
  • Microaerophilic
  • Optimum range 37-42degreesC
  • Nutrient or isolation media using Campylobacter selective medium
  • Adapted optimally in poultry, can grow in mammals
63
Q

How is Campylobacter cultured or typed?

A
  • Neck swabs from birds, caecal contents, faecal swabs
  • Culture at 37-42degreesC
  • Selective or enrichment medium
  • Smear with dilute carbol fuchsin or Gram
  • Look for vibrio shape
  • Identification by specieation (biochem, specific PCR), subtyping, MLST, serotyping
64
Q

What can be used to distinguish between Campylobacter species?

A
  • Colonial morphology
  • Biochemistry
  • Growth temp
  • Serology
65
Q

What can be used for differentiation within Campylobacter species?

A
  • Serology

- Molecular analysis (ribosome sequence analysis, MLST, whole genome based comparisons)

66
Q

Describe Spirochetes

A
  • Spiral motile bacteria
  • Endoflagella
  • Gram -ve
  • many zoonoic
  • 3 important genera: Leptospira, Borellia, Brachyspira
67
Q

Describe the respiration of Leptospira, Borellia, Brachyspira

A
  • Leptospira: anaerobic
  • Borellia: microaerophilic
  • Brachyspira: anaerobic
68
Q

What are the important species of Brachyspira?

A
  • Hyodysenteriae
  • Innocens
  • Pilosicoli
  • Intermedia
  • Alvinipulli
69
Q

Describe the growth of Brachyspira

A
  • Strict anaerobe
  • Does not form discrete colonies
  • 42degreesC for at least 3 days (slow)
  • B. hyodysenteriae is haemolytic
70
Q

What can be used to differentiation between Brachyspira

A
  • Pattern of haemolysis
  • Indole test
  • Hippurate test
71
Q

How is Brachyspira diagnosed?

A
  • Sleective media (blood agar with selective antibiotics)
  • Stained faecal smear for spirochaetes
  • Silver stain faecal mear
  • PCR tests
72
Q

Describe the pathogenesis of Brachyspira

A
  • Motility in gastric mucus essential
  • Haemolytic activity correlates with virulence
  • Proteases
  • Mucosal disruption leas to cell shedding and oedema
73
Q

What are the virus protein functions?

A
  • Genome protection, delivery, replication and spread

- Host interaction

74
Q

Explain the role of virus proteins in genome protection, delivery, replication and spread

A
  • Structural (genome protection)
  • Entry and uncoating
  • replication of genome (polymerase and/or accessory factors)
  • Reguation of virus gene expression
  • Assembly, genome packaging, exit from cell
75
Q

Explain the role of virus proteins in host interaction

A
  • Determine type of host infected and tissues affected
  • Persistence (in environment and host)
  • Evasion of host immunity and intracellular defences
  • Manipulation of intracellular environment to support virus replication (host shut off, cell cycling)
  • Pathogenesis, tumorigenesis
76
Q

What is the basic process of viral replication?

A
  • Receptor binding
  • Entry
  • Uncoating of viral nucleic acid
  • Genome transcription
  • mRNA translation
  • Replication of nucleic acid
  • Assembly of new virus particles
  • Release by cytolysis or budding
  • Genome affects exact steps in replication
77
Q

Explain the role of polymerase enzymes in viral replication

A
  • Replicate viral genetic material to produce mRNA and genomic nucleic acid
  • Can be provided by cell ro virus depending on genome type
  • If not provided by cell, virus must supply polymerase (many RNA viruses)
  • Most DNA viruses replicate in nucleus
  • Most RNA viruses replicate in cytoplasm
78
Q

Describe replication of +ssRNA

A
  • Viruses encoved RNA polymerase translated directly from viral genome i.e. acts as mRNA
  • Can act directly as mRNA, genome directly infectious
  • RNA translated to produce single polyprotein
  • Protein cleaved by viral proteases
  • Genome replicated by viral polymerase
79
Q

What is unusual about the replication of Coronavirus and Arterivirus?

A
  • +ssRNA
  • More complex
  • Produce nested mRNAs via negative strand intermediate
80
Q

DEscribe replication of -ssRNA

A
  • RNA polymerase contained within adn encoded by virus
  • Replication of genome via synthesis of complimentary RNA strand
  • Transcription then translation
  • Cannot act directly as mRNA
  • Virions contain (and genome encodes for) RNA dependent RNA polymerase
  • generates +ve mRNA
  • Genome replicated by same RNA polymerase, via +ve sense intermediate
  • Replicate in cytoplasm
81
Q

What is unusual about the replication of Bunyaviridae and Orthomyxoviridae?

A
  • -vessRNA

- Replicate in nucleus

82
Q

Describe the replication of retroviruses

A
  • Viral RNA reverse transcribed
  • Uses reverse transcriptase (RNA-dependent DNA polymerase)
  • Converts genome ot complimentary DNA (cDNA)
  • Integrates into chromosome of host cell by viral integrase enzyme
  • Integrated DNA termed proviral DNA
  • Integrated DNA then produces RNA and protein using normal cell machinery
  • Integration into host genoome permanent
  • Can disrupt normal activity and lead to tumour formation
83
Q

Describe the replication of dsDNA

A
  • Replicate in host cell nucleus
  • transcription of DNA viruses by cellular (DNA-dependent) RNA polymerase
  • Encode own DNA polymerases so can control replication of genome independently of cellular DNA replication
84
Q

Describe the replication of ssDNA

A
  • Requires dsDNA intermediate
  • Active host DNA polymrase needed to replicate genome (produce dsDNA)
  • Use host RNA polymerases to produce mRNA
  • Can infect only dividing cells where DNA polymerase is active
  • E.g. intestinal, bone marrow, cardiac, neural cells
85
Q

Describe viral gene expression

A
  • Some regulate expression very tightly
  • Can go for long periods with little viral gene expression
  • latency important featuer of some viruses
  • Helps explain patterns of disease
  • Intermittent, delyaed
  • Only expressed when conditions optimal for virus
86
Q

Outline post-translational modification of viral proteins

A
  • Viral proteins may also be modified by other host systems e.g. glycosylation
  • Can prevent antibody binding to virus
87
Q

Outline different ways in which viruses are adapted to compensate for limited genome size

A
  • Larger viruses able to encode larger number of proteins
  • Own polymerases, regulatory proteins etc
  • Smaller can only code for limited number of proteins
  • Can maximise encoding potential by number of strategies
  • Overlapping genes (different reading frames), production of polyproteins, multiple splicing to produce RNAs
88
Q

What are the methods of genetic variation in viruses?

A
  • Spontaneous mutation

- Gene trasnfer between viruses or cell via recombination or reassortment

89
Q

Describe spontaneous mutation in viruses

A
  • Mistakes made during genome replication
  • RNA viruses higher rate of mutation
  • Enzymes cannot proof read
  • Very high replication rate of some RNA viruses means very large numbers of mutant viruses
  • Virus population exists as a quasispecies
90
Q

Describe gene transfer between viruses or cell

A
  • Transfer of genetic information between 2 usually related viruses which have infected the same cell
  • Produces hybrid genomes
  • Entire genes/gene sequences derived from another virus
  • Via recombination or reassortment (segmented viruses)
91
Q

Describe recombination in viral genetics

A
  • Relatively uncommon
  • Between viruses with related DNA/RNA sequence or between virus and host nucleic acid
  • Can lead to viruses acquiring host sequences
92
Q

Describe gene reassortment in viral genetics

A
  • Occurs with segmented genomes
  • Simple exchange of genes when 2 different viruses infect cell (influenza, rotavirus)
  • Frequency of viable recombinants higher than for random mutations
  • Emergence of successful variants
  • Extends gene pool of virus
  • Produces daughter strain with combination of parent genes
  • Rapid mutation of virus circulation
93
Q

Describe the consequences of viral mutation

A
  • Lethal mutation
  • Silent muation
  • Growth advantage/disadvantage
  • May be better at survival and spread
  • Different antigens (vaccines!)
  • Virulence altered (clinical consequences)
  • Altered host range
  • Drug resistance
94
Q

Describe mycobacteria in terms of their Gram staining

A
  • Do not stain with Gram stain
  • Cytochemically Gram +ve
  • Lipid and mycolic acid content of walls prevents uptake of Gram stain dyes
  • Acid fast
95
Q

What stain is used to visualise mycobacteria?

A
  • Ziehl-Neelson

- Stain red

96
Q

How does Ziehl-Neelson stain work?

A
  • Cell wall lipids bind to carbol fuchsin

- Not removed by acid-alcohol decolouriser

97
Q

Describe teh growth rate of pathogenic mycobacteria

A
  • Most slow growing
  • Colonies take a few weeks
  • Saphrophytes grow quickly
98
Q

Describe the general growth requirements of pathogenic species of Mycobacteria

A
  • Complex

- Egg-enriched media

99
Q

Describe the cultural and growth requirements of M. tuberculosis

A
  • 3-8 weeks
  • 37degreesC
  • Aerobic
  • Colonies rough, buff and difficult to break apart
  • Enhanced growth with glycerol
  • Pyruvate has no effect on growth rate
100
Q

Describe the growth requirements of M. bovis

A
  • 3-8 weeks
  • 37degreesC
  • Aerobic
  • Colonies cream coloured, raised central roughness, break apart easily
  • Growth inhibited with glycerol
  • Enhanced growth with pyruvate
101
Q

Describe the growth of M. avium

A
  • 2-6 weeks
  • 37-43degreesC
  • Aerobic
  • Colonies sticky, off-white, break apart easily
  • Enhanced with glycerol
  • No effect with pyruvate
102
Q

Describe the pigments produced by some mycobacteria

A
  • Some produce carotenoid pigments
  • Non-chromogens produce colonies with no carotenoid pigments (M. avium)
  • Photochormogens = non-pigmented colonies that become pigmented when exposed to light
  • Scotochromogens produce pigments when cultured in dark/light
103
Q

What disease is caused by M. tuberculosis?

A

TB in humans and captive primates

104
Q

What disease is caused by M. bovis?

A

TB in cattle

105
Q

What disease is caused by M. avium?

A

TB in most avian species excpet Psittacines

106
Q

What are the clinical characteristics of Johne’s disease

A
  • Diarrhoea (intermittent becoming permanent and profuse)

- Weight loss (without loss of appetite)

107
Q

Where does M. avium reside during infection?

A
  • In macrophages
  • Granuloma formation
  • Intracellular pathogen (more difficult for immune system)
108
Q

What is the public health risk with Johne’s disease?

A
  • Milk transmission

- Non-pasteurised can carry infection (also true for cheese)

109
Q

What is the outcome of Johne’s disease in cattle?

A
  • No treatment

- Slaughtered

110
Q

Describe Clostridia

A
  • Large
  • Gram +ve
  • Rods
  • Endospores
  • Anaerobic
  • Catalase and oxidase negative
  • Motile
  • Enriched media required for growth
  • Diverse forms of disease in many animal species
111
Q

Where are clostridia normally found?

A
  • Soil
  • Alimetnary tracts of animals
  • Faeces
112
Q

What are the 4 pathogenic groups of clostridia?

A
  • Neurotoxic
  • Histotoxic
  • Enteropathogenic
  • Enterotoxaemic
113
Q

What types of C. perfringens are most important in domestic animals?

A
  • Have types A-E

- A, B, C and D most important

114
Q

What does C. perfringens look like on blood agar?

A
  • Surrounded by zones of double haemolysis
  • Ring of complete haemolysis in centre around colony
  • Aroudn first ring, second ring of incomplete haemolysis
115
Q

What is the egg yolk antigen toxin media test with C. perfringens called?

A

Nagler reaction

116
Q

Describe the Nagler reaction

A
  • C. perfringens
  • Identifies alpha toxin
  • Antitoxin specific to alpha toxin applied to half of egg yolk plate
  • C. perfringens streaked across place, incubated at 37degreesC for 24 hours
  • Organisms grows on both halves, activity only on half of plate (where no antitoxin)
117
Q

What divides the groups of C. perfringens and what are the types?

A
  • The significant and minor toxins they use

- Types A-E

118
Q

What are the major and minor toxins of type A C. perfringens?

A
  • Major: alpha

- Minor: NetB toxin

119
Q

What are the major and minor toxins of type B C. perfringens?

A
  • Major: Alpha, beta

- Minor: epsilon (protoxin, needs to be activated by proteolytic enzymes)

120
Q

What are the toxins of type C C. perfringens?

A

Alpha, beta and enterotoxin

121
Q

What are the toxins of type D C. perfringens?

A

Alpha, epsilon (both major)

122
Q

What are the toxins of type E C. perfringens?

A

Alpha and zeta (both major)

123
Q

What do the enterotoxins beta, epsilon and zeta toxins do?

A
  • Beta: lethal, necrotising
  • Epsilon: increases intestinal and capillary permeability, lethal
  • Zeta: dermonecrotic, lethal
124
Q

What are teh virulence factors shared by all enteric strains of E. coli?

A
  • Pili (fimbriae)

- TTSS (type three secretion systems)

125
Q

Define adhesin

A
  • Cell surface components or appendages of bacteria that facilitate adhesion or adherence to other cells or surfaces
  • Type of virulence factor
126
Q

Define toxin

A
  • A poison of plant or animal origin, especially produced by or derived from microorganisms and acting as an antigen in the body
127
Q

Describe intimins

A
  • Type of adhesin
  • EPEC, EHEC
  • Formation of attaching and effacing lesions
  • On bacterial cell surface
  • Bind to receptor Tir (translocated intimin receptor)
128
Q

How is Tir introduced into eukaryotic cells?

A
  • Translocated intimin receptor
  • By E. coli TSS with 25 other bacterial proteins
  • Inserted into plasma membrane of host cell
129
Q

Describe fimbrial adhesins

A
  • ETEC
  • Attachment to mucosal surfaces in SI and LUT
  • Facilitates colonisation by diminishing expulsive effects of peristalsis and flushing effect of urine
  • Formerly known as pili
  • Significant: K88, K99, 987P, F41
  • Pigs: K88, K99
  • F41 in calves
  • K99 in lambs
130
Q

Describe LT enterotoxin

A
  • Heat labile
  • K88 adhesins
  • Lead to hypersecretion of fluid into intestine
  • Stimulate adenylate cyclase activity
131
Q

Describe STa enterotoxin

A
  • Pigs, sheep, humans, cattle
  • ETEC
  • Increases guanylate cyclase activity in enterocytes
  • Intracellular guanosinemonophosphate stimualte fluid and electrolyte secretion into SI
  • Inhibits fluid absorption from intestine
132
Q

Describe STb enterotoxin

A
  • Causes secretion of chloride and bicarbonate ions
  • Inhibits absorption of sodium ions
  • Differs from STa and LT1
133
Q

Describe Shiga toxins

A
  • STEC
  • Letahl for cultured veo cells
  • Heat labile
  • STEC colonises intestinesand damages enterocytes
  • Absorbed into blood stream, deleterious effect on endothelial cells (CNS in pigs)
  • Inhibits protein synthesis in eukaryotic cells
  • Vascular damage and ST2E is oedema disease of pigs
134
Q

Describe cytotoxic necrotising factor 1

A
  • CNF1
  • Encoded chromosomally
  • Exact role uncertain
  • Extraintestinal E coli infections
135
Q

Describe cytotoxic necrotising factor 1

A
  • CNF2
  • Extraintestinal E coli infections
  • Encoded by transmissible plasmid known as Vir
  • Exact role uncertain
136
Q

Describe SEPEC (virulence factors, pathology, disease)

A
  • Septicaemia
  • Adhesins differnt for each host
  • Fimbrial adhesins in many, CS31A surface antigen in calves
  • Produce toxins CNF and CDT
  • Hypogammaglobulinaemia
  • Capsular antigens smooth LPS and other OMPs contribute to resistance to circulating antibody
  • Septicaemia in some domestic animals
  • Occasionally fatal pneumonia in horses, dogs and cats
137
Q

Describe UPEC (virulence, pathology, disease)

A
  • Uropathogenic
  • Adhesins: type 1, P and S fimbriae
  • Toxins: alpha haemolysin and CNF1
  • Adhere to bladder epithelium, iron scavenging mechanisms
  • UTI, pyometra in dogs
138
Q

Describe opportunistic E coli infections (virulence, pathology, disease)

A
  • Strains causing localised infection
  • Adhesins not identified
  • Endotoxin
  • Opportunistic infection by environmental E. coli, host factors predispose to infection
  • Mastitis, omphalitis, other localised infections
139
Q

Explain how E. coli can be both a pathogen and a commensal

A
  • Commensal does not carry TTSS (needed for invasion)
  • Depends on which strain is where, may be commensal in one system and pathogenic in another
  • Host species specificity
  • Commensal in one species, pathogenic to another

GI (31 decks)

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