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Flashcards in Microbiology Deck (100):

Describe the key morphology and features of Helicobacter

- Microaerophilic
- Gram -ve
- Vibrio/spiral
- Motile
- Urease positive
- Oxidase positive
- Catalase positive


On what type of media can Helicobacter be cultured?



What tests are used to identify Helicobacter?

- Blood antibody test
- Stool antigen test
- Carbon urea breath test


What diseases are caused by Helicobacter?

- 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


Describe the virulence factors

- 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


Describe how Helicobacter pylori causes disease in humans

- 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


List the symptoms fo periodontal disease in companion animals

- 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


What is gingivitis?

Inflammation of the gingiva


What can gingivitis be caused by?

- Build up of plaque or calculus
- Inflammation from teh bacteria contained in plaque can lead to gingivitis


Explain how a healthy biofilm may shift towards a pathological biofilm

- 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


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

- Streptococci
- Actinomyces
- Have adherence properties


Describe plaque

- 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


Describe colonisation of the biofilm

- 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


What is calculus?

Hardened plaque that cannot be removed by brushing


Explain how plaque can cause disease

- 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


How can disease caused by plaque be avoided?

- Regular teeth cleaning
- Provide feed that will clean teeth i.e. dry, hard food
- Check teeth regularly


What is the function of osteoclasts?

Bone resorption


How are osteoclasts formed?

- 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


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



Describe bone resorption in periodontal disease

- Due to osteoclasts
- Use hydrolytic enzymes to break down bone
- Digest organic portion of bone
- Activity regulated by PTH and calcitonin


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

- 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


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

- 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


List systemic disorders that may cause periodontal disease

- Age
- Systemic disease
- Hormones


Explain how age can lead to periodontal disease

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


Explain how systemic disease can lead to periodontal disease

Immunocompromised state inducing disease


Explain how hormones can lead to periodontal disease

PTH, calcitonin, growth hormone, corticosteroids impede healing


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

- FeLV
- Cause immunosuppression


What are the stages of periodontal disease?

Stages 1-4


Describe stage 1 of periodontal disease

- Build up of tartar
- Some swelling of the gums
- No bone loss


Describe stage 2 of periodontal disease

- GUms swollen
- Early attachment loss
- Sulcus deepened by disease
- Not much else visible
- However up to 25% bone loss


Describe stage 3 of periodontal disease

- 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


Describe stage 4 of periodontal disease

- Severe attachment loss
- Significant visible changes (bleeding, loose teeth, calculus visible, gingivitis)
- Significant bone loss
- Horizontal bone loss most likely


What does FORL stand for?

Feline odontoclastic resorptive lesion


What is feline odontoclastic resorptive lesion?

- 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


Describe class 1 FORL

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


Describe class 2 FORL

- Lesions penetrate enamel and dentine
- Radiographs essential to asses whether lesions have entered pulp


Describe class 3 FORL

- Lesions entered pulp
- Tooth must be extracted


Describe class 4 FORL

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


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

- 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


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

- 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


List factors affecting microbial growth in the oral cavity

- Temperature
- pH
- Redox Eh
- Antibiotics
- Nutrients (endogenous and exogenous nutrition)


Discuss the mouth as a unique habitat

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


Describe teeth in terms of oral microbiology

- 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


Describe the mucosal surfaces in terms of oral microbiology

- 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


Describe the saliva in terms of oral microbiology

- 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


Describe the gingival crevice fluid in terms of oral microbiology

- 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


Describe redox and bacteria in terms of oral microbiology

- 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


Describe oral flora development

- 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


What is allogenic development?

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


What is autogenic development?

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


List factors affecting adherence

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


Describe floral distribution in the oral cavity

- 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


What bacteria are normally found in the saliva of dogs?

- Actinomyces
- Streptococcus
- Granulicatella


What bacteria are found in the plaque of dogs?

- Porphymonas
- Actinomyces
- Neisseria


Describe Actinomyces

- 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


Describe Streptococcus

- 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


Describe Porphyromonas

- 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


Describe Neisseria

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


Describe how periodontal disease occurs

- 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


Why may a wound contain components of oral microbiology?

- Wound may be from a bite
- Or from licking the wound (this may also introduce faecal material into the wound)


Describe the development of a cat bite abscess

- 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


What is the difference between abscesses and emphysemas?

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


Describe oral mycological infections

- 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


Discuss the oral mucosa as a route for disease

- 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


What is lumpy jaw caused by?

Actinomyces bovis


Describe how Lumpy Jaw occurs

- Invades tissues through breaks in lining of mouth
- Damage due to rough forage or sharp teeth


What are the signs of Lumpy Jaw?

- 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


How is Lumpy Jaw treated?

- Iodine therapy
- Tetracyclines


What is Wooden Tongue caused by?

- Actinobacillus lignieresii
- Gram -ve, facultative anaerobe


How does Wooden Tongue occur?

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


What are the signs of Wooden Tongue?

- 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


List some of the important oral viral infections

- Fleinne immunodeficiency virus
- Papillomavirus (dogs)
- Feline calicivirus


Define vesicle

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


Define bulla

A vesicle greater than 5mm in diameter


Define erosion

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


Define ulcer

Loss of epidermins and dermis, sometimes deeper tissue


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

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

May also be:
- Vesicular exanthema
- Chemical or physical
- Photosensitisation
- Autoimmune


What is the causative pathogen of foot and mouth disease?

Piconaviridae (Apthovirus genus)


What farm animals are susceptible to foot and mouth disease?

- Cattle, sheep/goats, pigs
- Horses resistant


Describe the epidemiology of foot and mouth disease

- 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


What are the 7 serotypes of foot and mouth disease

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


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

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


Describe the clinical signs of foot and mouth disease in cattle

- 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)


What are the clinical signs of FMDV in pigs?

- 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)


How is FMDV diagnosed?

- 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


How can FMDV be controlled?

- Notifiable
- Exposed and affected animals culled
- Rigid enforcement of quarantine and restriction of movement
- In endemic countries inactivated vaccines used


What is the causative pathogen of swine vesicular disease?

- Enterovirus
- Part of Picornaviridae family
- Non-enveloped
- +ve ssRNA


Describe the epidemiology of SVD

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


What are the clinical signs of SVD?

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


How is SVD diagnosed?

- ELISA or virus isolation to distinguish from other vesicular diseases
- Laboratory diagnosis essential


How is SVD controlled in the UK?

- Diseased, other susceptible and in contact animals culled
- Vaccine development unlikely


What farm animals are susceptible to SVD?



Describe the causative pathogen of vesicular stomatitis virus

- Rhabdoviridae
- Single stranded
- -ve RNA
- non segmental genome
- Rod shaped, enveloped


Describe the epidemiology of vesicular stomatitis

- 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


Describe the pathogenesis of vesicular stomatitis

- 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


Describe the clinical signs of vesicular stomatitis

- 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


Describe how vesicular stomatitis is diagnosed

- 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)


Describe the control of vesicular stomatitis

- Vaccines available but generally not used
- Movement restriction and quarantine for 30 days post last case


How is vesicular stomatitis treated?

- Try to minimise secondary infection
- No specific treatment
- Insect proof buildings, avoidance of insects


What farm animals are susceptible to vesicular stomatitis?

Cattle, pigs, horses