Oral microbiology Flashcards

1
Q

What are the main features of the mouth as a habitat that are relevant for bacteria?

A
  1. Teeth
  2. Mucosal surfaces
  3. Saliva
  4. Gingival crevice fluid
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2
Q

True/false: plaque is found on the teeth of both healthy and diseased animals.

A

True

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3
Q

What makes teeth a good place for bacteria to colonise?

A
  • Non-shedding surface
  • Number of surfaces/crevices/ridges
  • Bacteria can accumulate in a biofilm
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4
Q

What features of the oral mucosa are relevant for bacteria if they try and colonise?

A
  • Stratified, non-keratinised epithelium with layers that can be worn off and replaced
  • Non-sterile: has a population of commensal bacteria that can stop others colonising
  • Houses immune cells in the tissue; if damaged can initiate inflammation
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5
Q

What features of saliva are relevant for bacteria trying to colonise the mouth?

A
  • Washes mouth to help physically remove material
  • Has a buffering capacity
  • Contains antimicrobial factors important to control microorganisms
  • Provides a source of nutrition for microbes, can help aggregation of bacteria
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6
Q

What features of the gingival crevice fluid are relevant for bacteria trying to colonise the oral cavity?

A
  • GCF: serum-like fluid
  • Increased production of GCF e.g. during infection can lead to localised rise in pH, changing the type of bacteria that can grow
  • Contains a variety of enzymes e.g. collagenase, elastase, trypsin
  • GCF has antimicrobial properties: IgG and sometimes leucocytes
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7
Q

Give some non-specific antimicrobial factors in the oral cavity

A
  • Saliva flow
  • Mucins and agglutinin
  • Sloughing of surface epithelial cells

All the above physically remove microorganisms

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8
Q

Give some innate (general) antimicrobial defenses in the oral cavity and describe their modes of action

A
  • Lysozymes cause bacterial cell lysis
  • Lactoferrins sequester iron, block some viral receptors and have anti-bacterial and anti-yeast activity
  • Sialoperoxidase inhibits glycolysis
  • Antimicrobial peptides disrupt the microbial membranes of bacteria or yeast
  • Neutrophils patrol tissue and engulf pathogens
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9
Q

Give some adaptive (specific) immune defenses in the oral cavity

A
  • Serum antibodies (sIgA) prevent/disrupt adhesion, reducing the capacity of bacteria to colonise
  • Complement binds to and promotes phagocytosis of pathogens. Also activates neutrophils.
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10
Q

List the clinical signs of periodontal disease

A
  • Problems picking up food
  • Bleeding/red gums/blood in water bowl or on toys
  • Loose teeth
  • Halitosis
  • Unusual noises when eating
  • Chewing on one side of the mouth
  • (If advanced) sneezing/nasal discharge
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11
Q

Explain the causes and mechanisms of gingivitis development in companion animals

A
  1. Plaque develops, changing the micro-environment
  2. This allow anaerobes to establish
  3. Mineral deposition can occur
  4. Sub-gingival deposits and growth will trigger inflammation
  5. Bacteria also secrete enzymes, weakening the tissue and causing more damage
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12
Q

Plaque

A

a biofilm that builds up on teeth

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13
Q

Calculus

A

a.k.a. tartar

calcified dental plaque

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14
Q

Briefly describe, using this diagram, how plaque develops

A
  1. Glycoproteins enable pioneer (aerobic) species to establish.
  2. Bacteria in a biofilm contribute to each others’ metabolism, allowing complex plaque to develop
  3. As bacterial growth/plaque builds up, the environment becomes one of reduced oxygen –> eventually anaerobic bacteria can establish
  4. Plaque formation is not uniform: some sites are more at risk - gingival sulchus vs. smooth surfaces
  5. Mineralised phosphates are deposited around the bacteria (sub- or supra-gingivally) forming calculus
  6. Periodontal pathogens cause tissue to secrete cytokines, which leads to activation of odontoclasts which resorb bone and enamel
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15
Q

How is calculus formed?

A
  • Mineralised phosphates are deposited around the bacteria. This can occur sub- or supra-gingivally
  • The contact between pathogens and tissue can cause the tissue to secrete cytokines which activate odontoclasts, leading to bone resorption
  • Once formed, calculus takes a lot of force to remove
  • Dental products may contain compounds to reduce mineralisation
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16
Q

Describe how dental caries (decay) arises

A
  • Occurs due to increased acids causing local mineralisation
  • The change to the environment (e.g. reduced pH) can lead to altered cell activity
  • Example: Feline Odontoclastic Resorptive Lesions
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17
Q

Describe the formation of Feline Odontoclastic Resorptive Lesions

A
  1. Chronic accumulation of microorganisms leads to endothelial and eptihelial cytokine production
  2. Initiation and stimulation of odontoclastic activity
  3. Stem cells are attracted to the sulchus area by cytokines
  4. Instead of forming macrophages, stem cells become clast cells
  5. Clast cells dissolve in mineralised tissue, forming a multinucleated giant. They dissolve tooth tissue, leading to bone and enamel resorption.
18
Q

List some bacteria commonly found in the oral cavity

A
  • Streptococcus sp.
  • Actinomyces sp.
  • Neisseria sp.
  • Fusobacterium sp.
  • Porphyromonas sp.
19
Q

Name and describe a yeast organism commonly found in the oral cavity

A
  • Candida sp
  • Normal component of oral microflora
  • When normal control mechanisms fail, can overgrow leading to pseudomembranous candidiasis (oral thrush). Thrush can also happen on other mucosal surfaces.
20
Q

Give the causative agent, route of infection, pathology and treatment for lumpy jaw (actinomycosis)

A

Cause: Actinomyces bovis

Pathology: Mucosal commensal that invades tissues through breaks in the lining of the mouth (rough forage, sharp teeth)

  • Tumour like swellings slowly develop.
  • These are immovable and hard swellings on the upper/lower jawbones around central molar level.
  • They consist of honeycombed thin bone filled with pus. Advanced cases can show pus discharge/gritty yellow granules in this.

Treatment is tetracyclines/iodine therapy or PTS

21
Q

Describe the causative agent and pathology of Wooden tongue (a.k.a. timber tongue)

A

Cause: Actinobacillus lignierseii

  • Commensal of mucous membranes, invades tissue through breaks in the lining of the mouth

Pathology: sudden onset with tongye becoming hard, swollen and painful.

  • There is then chronic pyogranulomatous inflammation of soft tissue
  • Infection is limited in most cases to soft tissue of tongue and lymph nodes of head
22
Q

Describe infections of Fusobacterium necrophorum

A
  • This is an obligate anaerobe found in the alimentary tract of animals, humans, and the respiratory tract of cattle
  • Infections involve mucous membranes and underlying oral cavity tissues. To invade, pathogen needs to breach epidermis via an injury.
  • Infection is self-limiting
  • Commonly seen in calves, pigs, sometimes goats.
  • Clinical signs include reducing/stopping drinking
23
Q

List some common viral infections of the oral cavity

A
  • Feline immunodeficiency virus (FIV)
  • Papillomavirus
  • Feline calcivirus
  • Foot and mouth disease
24
Q

Describe the transmission and clinical signs of FIV

A

Transmission: primarily by deep bite wounds though saliva of infected cats

Clinical signs:

  • Lethargy
  • Anorexia
  • Fever
  • Lymphadenopathy
  • Leaves cats vulnerable to secondary infections including FAIDS
25
Q

Describe the pathology and treatment of canine papillomavirus

A
  • Causes benign tumours of epithelial lining of mouth and throat. In severe cases, oesophagus may be affected.
  • Incubation period = 1 month, recovery = 2-3 months.
  • Once removed, immune to further infections.

Treatment

  • Tumours usually removed surgically for diagnostic purposes, but will disappear spontaneously on their own
  • Medication can be given to relieve pain and reduce inflammation
26
Q

Vesicle

A

Circumscribed epidermal elevations in the skin containing clear fluid. Usually less than 5mm in diameter.

27
Q

Bulla

A

Vesicle with a diameter over 5mm

28
Q

Erosion

A

partial loss of the epidermis that does not penetrated beneath the basal lamina zone

29
Q

Ulcer

A

loss of epidermis, dermis and sometimes deeper tissue

30
Q

Name some common vesicular diseases caused by viruses

A
  • Foot and mouth disease (FMD)
  • Swine vesicular disease (SVD)
  • Vesicular stomatitis (VS)
  • Vesicular exanthema (VE)
31
Q

Describe the clinical signs of FMD

A

Clinical signs

Cows

  • Fever
  • Loss of appetite
  • Marked milk drop
  • Profuse salivation
  • Foot and oral lesions; Vesicles on tongue and gums; smacking of lips causes rupture
  • Ruptured vesicles form large denuded ulcerative lesions
  • Secondary bacterial infection can lead to mucoprurulent nasal discharge
  • Pregnant cows may abort (due to high fever; virus doesn’t cross placenta)

Pigs

  • First sign often lameness; severe and painful foot lesions
  • Large vesicles that quickly rupture on snout

Other animals

  • Mild clinical signs characterised by foot lesions and lameness
32
Q

Describe the epidemiology and transmission of FMD

A
  • Respiratory infections/aerosols. Can spread for miles in airstreams
  • Ingestion of contaminated food/direct inoculation
  • Transmitted by animals and contaminated items/people
  • Short incubation period; virus can be excreted up to 4 days before clinical signs appear
  • Can have carriers where the virus persists in the pharynx
33
Q

Describe the diagnosis of FMD

A
  • Lab diagnosis essential
  • Samples from vesicular fluid/epithelial tissue at edge of vesicle, blood/serum, pharyngeal fluid
  • Detection of FMD antigen by ELISA/PCR detection of viral nucleic acid
  • FMD is notifiable
34
Q

Describe the clinical signs, diagnosis and control of swine vesicular disease virus

A

Clinical signs

  • Lesions on the coronary bands; less commonly snout, lips, tongue
  • Main sign is lameness

Diagnosis

  • ELISA/virus isolation needed to distinguish from other vesicular diseases

Control

  • Susceptible and in-contract animals are culled
35
Q
A
36
Q

Describe the causes and clinical signs of cat flu caused by FCV

A

Cats present with upper respiratory tract disease.

2 main causes: Feline calcivirus (FCV) and Feline herpes virus (FHV)

Clinical signs

  • Conjunctivitis
  • Rhinitis
  • Tracheitis
  • Pneumonia
  • Vesiculation/ulceration of oral epithelium
  • Fever
  • Lethargy
  • Anorexia
  • Stiff gait
37
Q

Describe the causes and clinical signs of cat flu caused by FHV

A

Cats present with upper respiratory tract disease.

2 main causes: Feline calcivirus (FCV) and Feline herpes virus (FHV)

Clinical signs

  • Sneezing
  • Nasal discharge
  • Dehydration
  • Anorexia
  • Pyrexia
  • Ocular signs including chemosis, keratoconjunctivitis, corneal ulceration
38
Q

Describe the treatment and control for cat flu caused by FCV or FHV

A

Treatment

  • Supportive nursing
  • Fluid therapy
  • Broad spectrum antibiotics to prevent secondary infection

Prevention

  • Inactivated/attenuated vaccines
  • Quarantine for hospitalised cases
39
Q

Feline Viral Rhinotracheitis

A
  • Acute disease similar to FCV
  • Clinical signs include profuse frothy salivation
40
Q

Why are disease notifiable?

A
  • Significant morbidity/mortality in animals
  • Potential to affect trade in animal products
  • Zoonotic
41
Q

Name some notifiable vesicular diseases

A
  • Foot and mouth disease (FMD)
  • Swine vesicular disease (SVD)
  • Vesicular stomatitis (VS)