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Microbiology Flashcards

1
Q

Describe the key morphology and features of Helicobacter

A
  • Microaerophilic
  • Gram -ve
  • Vibrio/spiral
  • Motile
  • Urease positive
  • Oxidase positive
  • Catalase positive
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2
Q

On what type of media can Helicobacter be cultured?

A

Enriched

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3
Q

What tests are used to identify Helicobacter?

A
  • Blood antibody test
  • Stool antigen test
  • Carbon urea breath test
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4
Q

What diseases are caused by Helicobacter?

A
  • Chronic gastritis in ferrets
  • Found in gastric mucosa of dogs and cas
  • Human disease caused by H. pylori
  • Associated with gastritis in number of species
  • Considered low pathogenic significance, but possibly zoonotic
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5
Q

Describe the virulence factors

A
  • Secretes large amounts of urease
  • Metabolises urea to ammonia, neutralises gastric acid
  • ammonia toxic to epithelial cells, along with other secreted factors leads to stomach lining damage and ulcers
  • Survival in acidic stomach dependent on urease
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6
Q

Describe how Helicobacter pylori causes disease in humans

A
  • Drills into mucuous gel layer of stomach
  • Binds to membrane-associated lipids of epithelial cells
  • Secrete large amounts of urease
  • Urea metabolises urea to produce ammonia
  • Neutralises gastric acid, toxic to epithelial cells
  • Also produces protease, catalase, phospholipases
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7
Q

List the symptoms fo periodontal disease in companion animals

A
  • Purulent exudate around the tooth
  • Persisten bad breath
  • Gums that bleed easily
  • Sensitivity around the mouth
  • Pawing at the mouth
  • Gums that are inflamed, hyperpplastic or receding
  • Loose or missing teeth
  • Loss of appetite
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8
Q

What is gingivitis?

A

Inflammation of the gingiva

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9
Q

What can gingivitis be caused by?

A
  • Build up of plaque or calculus

- Inflammation from teh bacteria contained in plaque can lead to gingivitis

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10
Q

Explain how a healthy biofilm may shift towards a pathological biofilm

A
  • Intitial deposition and colonisation by pioneer species
  • Glycoproteins present
  • Confluent growth of biofilm with matrix
  • Pioneer species form micro colonies with polysaccharides, salivary proteins adn glycoproteins
  • Initially aerobic growth
  • Increased diversity and structure
  • Get mineral depositions
  • Accumulation of plaque is balance between deposition, growth and removal
  • Eh lowers as oxygen consumed, leads to anaerobic environment
  • Favours obligate anaerobes
  • Nutrition varies as flora changes
  • Many bacteria from subgingival plaque are proteolytic, can break down host proteins for nutrition
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11
Q

What bacteria are the first to colonise dental biofilm and why?

A
  • Streptococci
  • Actinomyces
  • Have adherence properties
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12
Q

Describe plaque

A
  • Sticky, colourless film of bacteria and sugars that constantly forms on teeth
  • Is main cause of cavities and gum disease
  • Can harden to tartar if not removed daily
  • Complex biofilm
  • Colonisation contributes to plaque development
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13
Q

Describe colonisation of the biofilm

A
  • Regimented pattern
  • Adhesion of initial colonisers (Streptococci, Actinomyces) to enamel salivary pellicle
  • Followed by secondary colonisation through interbacterial adhesion
  • Variety of adhesins and molecular interactions underlie these interactions
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14
Q

What is calculus?

A

Hardened plaque that cannot be removed by brushing

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15
Q

Explain how plaque can cause disease

A
  • Bacteria present in plaque can cause inflammation in gingiva, leading to gingivitis
  • Can lead to further inflammation and periodontitis
  • Bacterial toxins and body’s response to infection leads to breaking down of bone and connective tissue holding tooth in place
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16
Q

How can disease caused by plaque be avoided?

A
  • Regular teeth cleaning
  • Provide feed that will clean teeth i.e. dry, hard food
  • Check teeth regularly
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17
Q

What is the function of osteoclasts?

A

Bone resorption

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18
Q

How are osteoclasts formed?

A
  • originate from hematopoietic tissue
  • Form through fusion of precursor cells
  • Descended from stem ccells in bone marrow tha also give rise to monocytes
  • Precursor cells dervied from circulating monocytes in blood
  • Osteoclasts regulated by both microbial and host factors
  • Proliferation and macrophages, differentiation into pre-osteoclast, polarisation into mature osteoclast and tehn resorption
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19
Q

What pro-inflammatory cytokines are involved in stimulation of osteoclastic resorption?

A

IL-1

IL-6

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20
Q

Describe bone resorption in periodontal disease

A
  • Due to osteoclasts
  • Use hydrolytic enzymes to break down bone
  • Digest organic portion of bone
  • Activity regulated by PTH and calcitonin
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21
Q

Describe the function of osteoclasts in periodontal disease caused by trauma from occlusion in absence of inflammation

A
  • Changes caused by trauma vary from increased compression and tension of periodontal ligament, increased osteoclasis of bone
  • Triggered and resorption of bone and tooth structure occurs
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22
Q

Describe the function of osteoclasts in periodontal disease caused by trauma from occlusion in presence of inflammation

A
  • Aggravates bone destruction caused by inflammation
  • As advancing inflammatory front approaches alveolar bone, osteoclastic bone resorption commences
  • Prevents bacterial invasion of bone
  • Leads to tooth mobility and loss
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23
Q

List systemic disorders that may cause periodontal disease

A
  • Age
  • Systemic disease
  • Hormones
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24
Q

Explain how age can lead to periodontal disease

A

Increase in age leads to decreased osteoblasts but no decrease in osteoclasts so more loss then remodelling occus

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25
Q

Explain how systemic disease can lead to periodontal disease

A

Immunocompromised state inducing disease

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26
Q

Explain how hormones can lead to periodontal disease

A

PTH, calcitonin, growth hormone, corticosteroids impede healing

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27
Q

What diseases predispose cats to periodontal disease in cats and why?

A
  • FIV
  • FeLV
  • Cause immunosuppression
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28
Q

What are the stages of periodontal disease?

A

Stages 1-4

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29
Q

Describe stage 1 of periodontal disease

A
  • Build up of tartar
  • Some swelling of the gums
  • No bone loss
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30
Q

Describe stage 2 of periodontal disease

A
  • GUms swollen
  • Early attachment loss
  • Sulcus deepened by disease
  • Not much else visible
  • However up to 25% bone loss
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31
Q

Describe stage 3 of periodontal disease

A
  • Moderate attachment loss
  • Deepening pocket
  • Still not many visible changes (swelling, redness, potential bleeding)
  • Significant bone loss taking place blow gum line
  • Teeth may be loose or may fall out
  • Extraaction may be necessary
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32
Q

Describe stage 4 of periodontal disease

A
  • Severe attachment loss
  • Significant visible changes (bleeding, loose teeth, calculus visible, gingivitis)
  • Significant bone loss
  • Horizontal bone loss most likely
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33
Q

What does FORL stand for?

A

Feline odontoclastic resorptive lesion

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34
Q

What is feline odontoclastic resorptive lesion?

A
  • Usually occurs where gum meets tooth on lower premolars
  • May drool, bleed or have difficulty eating
  • Often erodes sensitive dentine, causes cat to show pain with jaw spasms when FORL is touched
  • 4 classes
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35
Q

Describe class 1 FORL

A
  • Enamel defect noted
  • Chipped tooth appearance
  • Minimally sensitive
  • Has not entered dentine
  • Therapy iinvolved cleaning, polishing and daily tooth brushing with fluoride paste
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36
Q

Describe class 2 FORL

A
  • Lesions penetrate enamel and dentine

- Radiographs essential to asses whether lesions have entered pulp

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37
Q

Describe class 3 FORL

A
  • Lesions entered pulp

- Tooth must be extracted

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38
Q

Describe class 4 FORL

A
  • Crown eroded or fractured
  • Gum tissue grows over root fragments, leaves painful lesion that bleeds when probed
  • Crown amputation or extraction of fragments needed
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39
Q

List the non-specific antimicrobial factors and their functions in the oral cavity

A
  • Saliva flow: physical removal
  • Mucin/agglutinins: physical removal
  • Lysosyme-proteases-anion system: cell lysis
  • Lactoferrin: iron sequestration
  • Apo-lactoferrin: cell killing
  • Sialoperoxidase system: inhibit glycolysis
  • Histidine rich peptides: antibacterial activity and shown to kill Candida
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40
Q

List the specific antimicrobial factors and their functions in the oral cavity

A
  • Intra epithelial lymphocytes: sentinels to penetrating bacteria
  • Langerhans cells sIgA: prevents adhesion
  • IgG, IgA, IgM: prevent adhesion, opsonisation, complement activators
  • Complement: activates neutrophils
  • PMNs/macrophages: phagocytosis
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41
Q

List factors affecting microbial growth in the oral cavity

A
  • Temperature
  • pH
  • Redox Eh
  • Antibiotics
  • Nutrients (endogenous and exogenous nutrition)
42
Q

Discuss the mouth as a unique habitat

A
  • Range of surfaces
  • Each with different community of organisms
  • Conditions change rapidly
  • Teeth, specialised mucosal surfaces, saliva and gingival crevice fluid
43
Q

Describe teeth in terms of oral microbiology

A
  • Non-shedding surface for colonisation
  • Accumulation of bacteria
  • Number of different surfaces
  • Clean but not sterile
  • Plaque found in health and disease
  • Biofilm with own microenvironment
  • Gingival sulcus critical environment
44
Q

Describe the mucosal surfaces in terms of oral microbiology

A
  • Not sterile
  • Barrier to deep infection
  • House immune cells in tissue
  • If damaged can intiate inflammation
  • Organisms gain nutrition from saliva and other things in mouth
  • Plenty of commensals present
45
Q

Describe the saliva in terms of oral microbiology

A
  • buffering capacity against acids produce by sugar breakdown
  • Anti-microbial factors important in control of bacterial and fungal colonisation
  • Washes mouth
  • Proteins adn glycoproteins (mucin) source of nutrition, involved in aggregation of bacteria
  • Normal pH range favourable to many bacteria
46
Q

Describe the gingival crevice fluid in terms of oral microbiology

A
  • Serum componetns can reach mouth by flow of serum like fluid through junction of epithelium of gingivae
  • Increased production of GCF during infection can lead to small localised rise in pH
  • Can promote growth of some putative periodontal pathogens
  • Contains many components for defence - IgG (predominant immunoglobulin) and leucocytes
  • Also has collagenase, elastase and trypsin which can contribute to tissue destruction
47
Q

Describe redox and bacteria in terms of oral microbiology

A
  • Anaerobiosis not rigid
  • Anaerobes require reduced conditions for their normal metabolism
  • Oxygen only one of many components contributing to Eh of a habitat
  • Oxygens inhibitory action attributed to ability to raise redox potential
  • Even if oxygen completely excluded some anaerobes can not grow if redox too high for other reason
48
Q

Describe oral flora development

A
  • High species diversity in oral cavity
  • Many obligate anaerobes
  • Some fastidious nutrition
  • Acquisition increases with age
  • Development can be allogenic or autogenic
  • Bacteria similar at genus level between species of different diets
  • Some difference at species level
49
Q

What is allogenic development?

A

Due to factors of non microbial origin (e.g. tooth eruption, addition of dentures, diet change)

50
Q

What is autogenic development?

A

Due to changes in microbiology (development of food chains, low redox environments)

51
Q

List factors affecting adherence

A
  • Chewing
  • Natural flow of saliva
  • Some salivary components aid aggregation
  • Desquamation
  • Biofilms aid adhesion
  • Stagnant blind spots in mouth
  • Bacterial factors e.g. fimbriae
52
Q

Describe floral distribution in the oral cavity

A
  • Plaque formation not uniform
  • Depends on degree of protection from oral removal forces and gradients of biological factors from the host
  • Distinct sites such as gingival crevive, smooth surfaces, pits and fissures
  • Colonisation of areas depends on characteristics of bacteria
53
Q

What bacteria are normally found in the saliva of dogs?

A
  • Actinomyces
  • Streptococcus
  • Granulicatella
54
Q

What bacteria are found in the plaque of dogs?

A
  • Porphymonas
  • Actinomyces
  • Neisseria
55
Q

Describe Actinomyces

A
  • Gram +ve
  • Slow growth
  • Facultative anaerobes
  • Rod shaped
  • Colonise mucous membranes
  • Opportunistic pathogen, oral cavity infections
  • Colonies form branched networks of hyphae
  • In rare cases can cause Actinomycosis
  • Also found in environment incl soil and range of species
56
Q

Describe Streptococcus

A
  • Gram +ve
  • Fastidious, require range enriched media
  • Small range of haemolytic activities
  • Facultative anaerobes
  • Linked to a number of infections (different species)
  • In human dental disease linked to periodontitis
  • Found in animals different species between differen host animals
  • Different species of Streptococci involved in many disease
57
Q

Describe Porphyromonas

A
  • Gram -ve
  • Non spore forming
  • Anaerobic
  • Rod shaped
  • Produces porpyrin pigments (dark brown/black)
  • Periodontal disease in humans, some non human primates and beagles
  • Oral infections for peritonitis P. gingivalis can not be trasnferred between cats and dogs and humans
  • Not zoonotic, species differences
58
Q

Describe Neisseria

A
  • Gram -ve
  • Diplococci
  • Human medially important
  • Catalase and oxidase positive
  • Species differentiation by sugar fermentation
59
Q

Describe how periodontal disease occurs

A
  • Organisms accumulate
  • Activate inflammatory cells
  • Cells trapped at site of inflammation
  • Transform into clast cells
  • Odontoclastic activity leads to degradation of tooth enamel
  • Drives chronic tooth decay
60
Q

Why may a wound contain components of oral microbiology?

A
  • Wound may be from a bite

- Or from licking the wound (this may also introduce faecal material into the wound)

61
Q

Describe the development of a cat bite abscess

A
  • Cat bites, introduces oral microflora deep into tissue
  • Anaerobic organisms (malodorous) grow, may be haemorrhagic
  • Leads to a collection of pus form by tissue destruction in an inflamed area of localised infection
  • Defnsive reaction of tissue to prevent spread of infectious material
  • Attracts WBCs and increases regional blood flow
  • Wall formed by adjacent healthy cells in attempt to contain infection
  • Barrier can prevent immune cells attacking bacteria in pus
62
Q

What is the difference between abscesses and emphysemas?

A

Abscess is accumulation of pus in newly formed anatomical cavity rather than a pre-existing one

63
Q

Describe oral mycological infections

A
  • Fungi and yeast
  • C. albicans, C. tropicalis
  • Candidiasis mainly disease of keratinised epithelium
  • Immunosuppressed or where other chronic oral disease
  • WHite pseudomembranous covering greyish plaques with some ulceration
  • Candidiasis recognised by budding yeasts with pseudo hyphae or true hyphae in cytology
64
Q

Discuss the oral mucosa as a route for disease

A
  • Through damage of mucosa
  • Can lead to number of nfections from commensals of oral cavity
  • E.g. lumpy jaw, wooden tongue
  • Damage to mucosa in mouth can lead to infection due to microorganisms that normally reside in mouth
65
Q

What is lumpy jaw caused by?

A

Actinomyces bovis

66
Q

Describe how Lumpy Jaw occurs

A
  • Invades tissues through breaks in lining of mouth

- Damage due to rough forage or sharp teeth

67
Q

What are the signs of Lumpy Jaw?

A
  • Tumour like swellings slowly develop
  • Immovable hard swellings on upper and lower jawbones of catle, central molar level (mostly)
  • Advanced before external signs visible
  • Lumps consist of honeycombed masses of thin bone filled with yellow pus
  • Advanced can develop and discharge small amounts of sticky pus containing gritty yellow granules
68
Q

How is Lumpy Jaw treated?

A
  • Iodine therapy

- Tetracyclines

69
Q

What is Wooden Tongue caused by?

A
  • Actinobacillus lignieresii

- Gram -ve, facultative anaerobe

70
Q

How does Wooden Tongue occur?

A
  • A. lignieresii is commensal of mucous membranes
  • Invasion through breaks in lining of mouth
  • Abrasion through rough feed
71
Q

What are the signs of Wooden Tongue?

A
  • Tongue very hard, swollen and painful
  • Chronic pyogranulomatous inflammation of soft tissue
  • Infection limited in most cases to soft tissue of tongue and lymph nodes of head
  • Sudden onset
72
Q

List some of the important oral viral infections

A
  • Fleinne immunodeficiency virus
  • Papillomavirus (dogs)
  • Feline calicivirus
73
Q

Define vesicle

A

Circumscribe epidermal elevations in skin containing clear fluid, less than 5mm in diameter

74
Q

Define bulla

A

A vesicle greater than 5mm in diameter

75
Q

Define erosion

A

Partial loss of peidermis that does not penetrate beneath the basa laminar zone

76
Q

Define ulcer

A

Loss of epidermins and dermis, sometimes deeper tissue

77
Q

Name the common vesicular diseases caused by viruses affecting domestic and small animals

A
  • Foot-and-mouth disease
  • Swine vesicular disease
  • Vesicular stomatitis

May also be:

  • Vesicular exanthema
  • Chemical or physical
  • Photosensitisation
  • Autoimmune
78
Q

What is the causative pathogen of foot and mouth disease?

A

Piconaviridae (Apthovirus genus)

79
Q

What farm animals are susceptible to foot and mouth disease?

A
  • Cattle, sheep/goats, pigs

- Horses resistant

80
Q

Describe the epidemiology of foot and mouth disease

A
  • Extremely infectious
  • Rapid replication cycle, high virus yield
  • In resp tract, spread by breathing
  • Stable virus
  • Short incubation period
  • Wide host range
  • Many methods of transmission
  • Virus excreted up to 4 days pre clinical signs, mild clinical picture in some hosts
  • 7 serotypes
81
Q

What are the 7 serotypes of foot and mouth disease

A

O, A, C, ASIA1, SAT1, SAT2, SAT3

82
Q

What are teh methods of transmission for footh and mouth disease?

A
  • Animal to animal
  • Contaminated items
  • People
  • Windborne
  • Predominantly by respiratory infection
  • Ingestion of contaminated food or direct inoculation also effective
83
Q

Describe the clinical signs of foot and mouth disease in cattle

A
  • Incubaton 2-8 days
  • Fever, loss of appetite, marked drop in milk production
  • Profuse salivation, drooling, vesicles develop on tongue and gums
  • Also on teats and coronary band of feet (lameness)
  • Smacking of lips (oral veselces rupture)
  • Ruptured vesicles = large denuded ulcerative lesions
  • Secondary bacterial infection = mucupurulent nasal discharges
  • Abortion (but not transplancental infection, is due to fever)
84
Q

What are the clinical signs of FMDV in pigs?

A
  • Lameness first
  • Foot lesions may be severe, pig may not stand
  • Large vesicles rupturing quicky on snout
  • Shed more than catle (flumes of cirus produced by pigs)
85
Q

How is FMDV diagnosed?

A
  • Laboratory diagnosis essential
  • Samples of vesicular fluid, epithelial tissue from edge of vesicle, blood in anticoagulant, serum and pharyngeal fluid
  • Detection of FMDV antigen n tissue and fluid samples by ELISA
  • Pharyngeal fluid from convalescing animals
  • PCR for detection of viral nucleic acid
86
Q

How can FMDV be controlled?

A
  • Notifiable
  • Exposed and affected animals culled
  • Rigid enforcement of quarantine and restriction of movement
  • In endemic countries inactivated vaccines used
87
Q

What is the causative pathogen of swine vesicular disease?

A
  • Enterovirus
  • Part of Picornaviridae family
  • Non-enveloped
  • +ve ssRNA
88
Q

Describe the epidemiology of SVD

A
  • Similar to other vesicular viruses
  • Notifiable
  • Pigs natural host
  • Milder disease, febrile illness
  • Regular outbreaks in southern EU, occasional in UK
89
Q

What are the clinical signs of SVD?

A
  • Lesions on coronary bands
  • Less commonly on snout, lips, tongue
  • Main symtom lameness
  • Mostly oral lesions in cattle, foot lesions in swine
90
Q

How is SVD diagnosed?

A
  • ELISA or virus isolation to distinguish from other vesicular diseases
  • Laboratory diagnosis essential
91
Q

How is SVD controlled in the UK?

A
  • Diseased, other susceptible and in contact animals culled

- Vaccine development unlikely

92
Q

What farm animals are susceptible to SVD?

A

Pigs

93
Q

Describe the causative pathogen of vesicular stomatitis virus

A
  • Rhabdoviridae
  • Single stranded
  • -ve RNA
  • non segmental genome
  • Rod shaped, enveloped
94
Q

Describe the epidemiology of vesicular stomatitis

A
  • Endemic Central America, South Ameria, USSA
  • Enters through breaks in mucosa nad skin
  • Minor abrasions and arthropod bites
  • Transmission by sand flies
  • Virus isolated from mosquitoes, midges, black flies, house flies and mites
95
Q

Describe the pathogenesis of vesicular stomatitis

A
  • Enters through abrasions or insects
  • Vesicles develop at site of infection
  • Spread occurs locally by extension of primary lesion e.g. entire epithelium of tongue or teat sloughed off
  • Vesicular fluid contains high titres of infectious virus
    0 Incubation period 1-5 days
96
Q

Describe the clinical signs of vesicular stomatitis

A
  • Fever, excessive salivation (first sign in cattle, horses)
  • Lameness (first sign in pigs)
  • Vesicles, blisters on oral mucous membrane, lots of saliva
  • Vesicular lesions on tongue, oral mucosa, teat, coronary bands
  • Tongue lesions more pronounced in horses
  • Vesicular lesions most common on snout and coronary bands
  • Heal within 7-10 days
97
Q

Describe how vesicular stomatitis is diagnosed

A
  • EM of vesicular fluid (detection of virus)
  • Immunofluorescent antibody staining of vesicle tissue (detection of viral antibody)
  • Demonstration of rise in antibody titre by ELISA (serology)
98
Q

Describe the control of vesicular stomatitis

A
  • Vaccines available but generally not used

- Movement restriction and quarantine for 30 days post last case

99
Q

How is vesicular stomatitis treated?

A
  • Try to minimise secondary infection
  • No specific treatment
  • Insect proof buildings, avoidance of insects
100
Q

What farm animals are susceptible to vesicular stomatitis?

A

Cattle, pigs, horses

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