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Clinical Veterinary Science and One Health 23/24 > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

Differentiate staphylococcus and streptococcus lesions.

A

Staph – localised lesions, often peripheral. Skin infections and mastitis.

Strep – generalised lesions, tends to be deeper and spread more around the body. Strangles, mastitis and endocarditis

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2
Q

What are enterococcus infections?

A

Rarely pathogenic, found in intestine, can cause wound infections, type of streptococcus.

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3
Q

What are micrococcus infections?

A

Non-pathogenic, very small

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4
Q

What do actinomyces cause?

A

Localised lesions. Ororpharyngeal commensal (lumpy jaw)

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5
Q

What does truperella cause?

A

Generalised skin lesions. Skin necrosis, mastitis

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6
Q

What does dermatophilus cause?

A

Motile spores, very strange, highly evolved. Mud fever, rain scald

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7
Q

Why are staphylococcus and micrococcus found in the environment?

A

Very good at surviving due to peptidoglycan layer that can close up and protect them.

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8
Q

Where are staphylococcus found?

A

Upper respiratory tract and digestive tracts (animals lick themselves) in mucous membranes

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9
Q

Where are micrococcus found?

A

Mammary gland mucous membranes

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10
Q

How do staphylococcus species evade the immune system?

A

Form a clot of fibrin around themselves, which is why they do not spread around the body and hide from the immune system this way

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11
Q

Which species is important for wound infections?

A

Staphylococcus aureus.

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12
Q

How does staphylococcus aureus appear in an agar plate?

A

Yellow for human and animals
White in dogs

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13
Q

How do haemolytic species evade the immune system?

A

Breakdown RBCs and leukocytes

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14
Q

What is haemolysin-a?

A

Produced by staph aureus and breaks down red blood cells completely

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15
Q

What does haemolysin-b do?

A

Produced by staph aureus that partially breaks down RBCs, as it is a phospholipase that breaks down phospholipids and membranes.

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16
Q

What is the role of haemolysin-b in haemolysis?

A
  • Potent
  • Unique to animal strains
  • Partial red blood cell lysis, wide zone haemolysis and poorly defined
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17
Q

Name the 2 general types of disease associated with staphylococci.

A

Pyogenic/suppurative skin infections - dermatitis, pyoderma, abscesses

Systemic infections - septicaemia and/or deposition and localised damage

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18
Q

What is the reason behind pyogenic/suppurative skin infections?

A

This is because there is a big in rush of leukocytes that are being killed, creating pus.

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19
Q

What is greasy pig disease?

A

Staphylococcus hyicus. Gets under skin and crisps skin causing it to come off and suppurative layer of raw skin underneath.

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20
Q

How can staphylococcal infections be treated?

A

Resistance genes are common and widespread, such as MRSA. Physical treatment is wound drainage and disinfection, as this is close to the skin. Pus is protective so removing this you can get stuff in there.

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21
Q

List the main disease patterns of streptococcus.

A
  • Upper respiratory tract infections and lymphadenitis
  • Neonatal septicaemia infections
  • Secondary pneumonia
  • Urogenital tract infections
  • Mastitis
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22
Q

Name 3 streptococcus infections in pigs.

A

Streptococcus zooepidemicus - suppurative arthritis in piglets

Streptococcus porcinus - strangles-like disease in piglets.

Streptococcus suis - meningitis, endocarditis, arthritis

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23
Q

Name 4 streptococci infections in cattle.

A

Streptococcus uberis – commensal, most common, mild.

Streptococcus dysalactiae – commensal, less common, severe.

Streptococcus agalactiae – obligate, less common, zoonotic

Streptococcus zooepidemicus – least common, from horses

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24
Q

Name 3 streptococcal infections in horses.

A

Streptococcus pneumoniae – respiratory tract infection, pneumonia in foals, lower airway disease in adults.

Streptococcus zooepidemicus – gastrointestinal infections and abortions, mastitis, naval infections, pneumonia in foals, lower airway disease in adults, lymphadenitis

Streptococcus equi – strangles

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25
Q

How are streptococcal infections treated and controlled?

A

Antibiotics – less resistance than staphylococcus

Disinfectants – milking machinery, stables, troughs. Pus is protective.

Vaccines

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26
Q

What is lumpy jaw?

A

Actinomyces bovis. Abscess in jaw bone – pyogranulomatous

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27
Q

How is lumpy jaw diagnosed?

A
  • Clinical signs
  • Sulphur granules in pus – 3-4mm, pale yellow
  • Club colonies of CaPO4 in histological sections
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28
Q

How is lumpy jaw treated?

A
  • Surgical removal if small
  • Drain abscess
  • Irrigate with iodine
  • Antibiotics orally or intravenously and iodides orally or intravenously
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29
Q

What are the conditions for truperella pyogenes?

A

Commensal. Aerobic and prefers raised CO2

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30
Q

How does truperella pyogenes appear on agar?

A

Haemolytic after 48h

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31
Q

Briefly describe the pathogenesis of truperella pyogenes.

A

Virulence determinants – haemolysin (skin necrosis) and protease activity (gelatinase).

Mixed infections, such as summer mastitis – fly bites on teats enables bacterial entry. Associated with streptococcus dysgalactiae infection.

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32
Q

How is truperella pyogenes treated?

A

Antibiotics systemically or intramammary

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33
Q

What type of bacteria is dermatophilus congolensis?

A

Obligate parasite of skin

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34
Q

What is the appearance of dermatophilus congolensis culture?

A

Fresh blood agar – aerobic, catalase +ve, haemolytic, rough, wrinkled, very adherent (72h)

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35
Q

What does dermatophilus congolensis cause?

A

Dermatitis in cattle, sheep, goats, horses

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36
Q

How is dermatophilus congolensis diagnosed?

A

Scabs – stain for filaments and spores, immunofluorescence

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37
Q

How is dermatophilus congolensis controlled?

A
  • Reduce ectoparasites – enter via bites
  • Keep dry
  • Keep environment clean
  • Remove scabs
  • Treat with iodine, penicillin, streptomycin
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38
Q

In general, how are staphylococcus and streptococcus infections treated?

A

Clean, drain, iodine. If you think systemic = antibiotics.

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39
Q

How are Enterobacteriaceae divided by genera?

A

Colonial morphology, biochemistry and DNA relatedness

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40
Q

How are Enterobacteriaceae divided by species?

A

Biochemistry and DNA relatedness

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41
Q

How are Enterobacteriaceae divided by strains?

A

Serotypes (antigens), biotypes (biochemistry), phagetypes (susceptibility to a panel of phage)

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42
Q

Which Enterobacteriaceae are very important disease causing genera?

A

Escherichia
Klebsiella
Proteus
Salmonella
Shigella
Yersinia

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43
Q

Which of the Enterobacteriaceae are zoonotic?

A

Salmonella
E.coli
Yersinia
Shigella

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44
Q

Which media are used for the isolation of Enterobacteriaceae?

A

Non specific = blood agar

Differential = MacConkey bile lactose agar, only bile tolerant can grow here

Selective = salmonella specific agar (XLD, BGA) and salmonella selective enrichment broth

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45
Q

How does MacConkeys bile lactose agar differentiate non-enterics from enterics?

A

Using bile and lactose. Lactose fermentation = acid = red. No fermentation = decarboxylation of amino acids = yellow

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46
Q

What are some general features of the Enterobacteriaceae family?

A
  • Grow in the presence of bile
  • Gram negative straight rods
  • Simple nutritional needs
  • Facultative anaerobes - anaerobically in gut, aerobically in environment
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47
Q

When serotyping E.coli, what are O antigens?

A

Sugar side chain of LPS. Greater than 170

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48
Q

When serotyping E.coli, what are H antigens?

A

Flagellar protein. Greater than 56

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49
Q

When serotyping E.coli, what are K antigens?

A

Capsular polysaccharide. Greater than 80

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50
Q

When serotyping E.coli, what are F antigens?

A

Fimbrial protein

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51
Q

What do Enterobacteriaceae all commonly cause?

A

All can cause wound infections and UTIs and diarrhoea in neonates.

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52
Q

What does enterotoxigenic E.coli (ETEC) produce?

A

Toxins that cause diarrhoea

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53
Q

What does verotoxigenic E.coli (VTEC) produce?

A

Toxins that cause kidney failure in humans.

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54
Q

What do attaching and effacing E.coli (AEEC) do in the body?

A

Attaching and destroy the intestinal wall

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55
Q

What do enteroinvasive E.coli (EIEC) do in the body?

A

Invade the body, cause sepsis, deposit around the body

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56
Q

How are Enterobacteriaceae infections treated?

A
  • Supportive – fluids. Diarrhoea is self-limiting (clients don’t like this = probiotics and supplements)
  • Good husbandry
  • Antibiotics not used to treat, disease self-limiting
  • Unless there are signs of sepsis
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57
Q

What are the properties of campylobacter?

A
  • Microaerophilic – 5% O2
  • Thermophiles (40-43˚C) in birds and non-thermophiles (37 ˚C) in mammals
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58
Q

How do campylobacter affect different animals?

A
  • Normal inhabitants of gut and/or reproductive tract of animals, not humans
  • Frequent apparently asymptomatic carriage in non-human species
  • Commensal in birds and gets into the muscle
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59
Q

What does campylobacter cause in humans?

A

Campylobacter in humans causes to shed whole gut lining and pass it out = profuse bloody diarrhoea with bits of your intestine

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60
Q

What is the typical infectious dose of campylobacter?

A

Infectious dose = 500 bacteria

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61
Q

What is campylobacter fetus venerealis?

A

Carried by bone. STD in cows. Can be avoided be screening by AI.

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62
Q

What is campylobacter fetus fetus?

A

Lives in sheep gut and causes abortions. From gut to late term placenta, causing a late explosive abortion.

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63
Q

Name the 2 strict anaerobes.

A

Dichelobacter
Clostridium

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64
Q

What is the oxidation-reduction potential (Eh)?

A

Anaerobe survival < -100mV

Healthy tissue +120mV to +240mV

Damaged tissue -150mV to -250mV

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65
Q

What are the characteristics of clostridium?

A
  • Strict anaerobes
  • Gram positive rods
  • Spore formers
  • Endogenous gut commensal and soil survivors
  • Ingestion or deep wound entry
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66
Q

How does clostridium tetani cause damage to the body?

A

Tetanolysin – aids necrosis

Tetanospasmin – neurotoxin

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67
Q

What species does descending tetanus occur in?

A

Horses
Humans

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68
Q

What species does ascending tetanus occur in?

A

Ruminants
Pigs
Dogs
Cats

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69
Q

How are wounded and vaccinated horses treated for tetanus?

A

Clean wound, boost vaccine (toxoid)

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70
Q

How are wounded and unvaccinated horses treated for tetanus?

A

Clean wound, antibiotics (not aminoglycosides), anti-toxin or vaccine

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71
Q

How are clinically affected horses treated for tetanus?

A

Clean wound (if still open), antibiotics (not aminoglycosides), anti-toxin, tranquilisers and artificial respiration

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72
Q

How does clostridium botulinum cause disease?

A

Ingested toxin > absorption in gut or toxin produced in wound > blood > peripheral nerves > 3-17 days incubation > flaccid paralysis and/or death.

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73
Q

How is clostridium botulinum prevented?

A

Cook food
Avoid spoiled food
Vaccination

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74
Q

How is clostridium botulinum treated?

A

Anti-toxin
Purge gut
Artificial respiration

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75
Q

What are some of the diseases from invasive toxigenic clostridia?

A

Redwater and black disease
Bighead – head butting rams
Gas gangrene
Mild malignant oedema
Braxy – ingested form of clostridium septicum
Blackleg

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76
Q

Name 3 genuses of the pasteurellaceae family.

A

Pasteurellaceae multocida
Mannheimia haemolytica
Haemophilus

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77
Q

What are the characteristics of pasteurellaceae?

A
  • Very small gram negative rods – coccobacilli
  • Non-motile
  • Facultative anaerobes – aerobic and anaerobic so energetically expensive
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78
Q

What is the pathogenesis of pasteurellaceae multocida?

A
  • Poor environmental survivor
  • Most are commensals of the mammalian naso-oropharynx
  • Exogenous or endogenous
79
Q

What are the diseases of Pasteurellaceae multocida in cattle?

A

Shipping fever, haemorrhagic septicaemia, mastitis

80
Q

What are the diseases of Pasteurellaceae multocida in pigs?

A

Shipping fever, atrophic rhinitis

81
Q

What are the diseases of Pasteurellaceae multocida in sheep, rabbits adn birds?

A

Sheep – mastitis

Rabbits – snuffles

Birds – fowl cholera

82
Q

How is Pasteurellaceae multocida treated and prevented?

A
  • Antibiotics
  • Vaccines – but need serotype specific/which LPS it has
83
Q

What are the diseases associated with Mannheimia haemolytica in species?

A

Cattle – shipping fever

Sheep – shipping fever and mastitis (bluebag)

Lambs – septicaemia

84
Q

What are the characteristics of haemophilus?

A
  • Very small gram negative rods – coccobacilli pleomorphic
  • Facultative anaerobes
  • Strict pathogens
85
Q

What are the nutritional requirements of haemophilus?

A

X (haemin) and/or V (NAD) factor so are host reliant, limiting where they live

86
Q

Where do haemophilus infect?

A

Commensals of the upper respiratory tract, the GI and urogenital tracts

87
Q

Where does haemohilus infect in humans and primates?

A

Haemophilus influenzae: respiratory tract, joints, brain

88
Q

Where does haemophilus infect in cattle

A

Haemophilus/histophilus somnus: respiratory, joints, genital tract, brain

89
Q

Name the species of haemophilus that affects pigs and how.

A

Haemophilus parasuis

Young pigs – serous surfaces and brain
Older pigs – respiratory and joints

90
Q

Name the species of haemophilus that affects poultry and where it infects.

A

Haemophilus paragallinarum

Respiratory

91
Q

How is haemophilus treated and prevented against?

A
  • Antibiotics
  • Some vaccines – species specific
  • Better husbandry and keeping animals in better conditions
92
Q

What are the characteristics of bordatella?

A
  • Very small gram negative coccobacilli
  • Motile
  • Aerobes – not fermentative
  • Obligate parasites
93
Q

Where does bordetella infect and in which species?

A

Upper RT commensals in dogs, pigs, cats, horses, rodents

94
Q

Name the 3 diseases associated with bordatella.

A

Bordetella pertussis/parapertussis: whooping cough in humans

Bordetella bronchiseptica: atrophic rhinitis and bronchopneumonia in pigs, kennel cough/bronchopneumonia in dogs

Bordetella avium: rhinotracheitis in poultry

95
Q

Why do moraxella have lots of fimbria?

A

Good at attaching and sticking. To hide from immune system

96
Q

Where are moraxella found?

A

Mucosal surfaces

97
Q

What are the signs of moraxella?

A
  • Wet face due to inflamed and blocked tear ducts
  • Thickening of bovine cornea
98
Q

Why is there thickening of the bovine cornea in response to moraxella bovis/bovine keratoconjunctivitis?

A

Body produces neutrophils in response to infection, that move to the site of infection. Phagocytosis or explode, releasing protease and enzymes to break down bacteria, but this also breaks down corneal epithelium.

99
Q

Where are mollicutes found?

A

In plasmas. Pathogens of the upper respiratory tract, GI tract and genital tract

100
Q

What are the characteristics of mollicutes?

A
  • Very small – 0.2um diameter
  • Some are obligate pathogens and some are commensals/opportunistic pathogens
  • Pleomorphic
101
Q

What does having no rigid cell wall allow mollicutes to do?

A

Very highly evolved and can squeeze between cells

102
Q

Why can mollicutes fuse with host cells?

A

Can fuse with host cells and survive intracellularly due to eukaryote like cell membrane - sterols in plasma membrane instead of hopanoids.

103
Q

What affect do mollicutes have in the body?

A

Cytotoxic and inhibits ciliation in the respiratory tract

104
Q

What are the characteristics of mycobacteria?

A
  • Opportunistic/obligate pathogens or saprophytes
  • Aerobic, gram positive rods
105
Q

Why do mycobacteria clump in tissue?

A

They are waxy

106
Q

What protects mycobacteria from the immune system?

A

High lipid content from cell wall, which slows growth and protects them from the immune system. Means they are very slow developing diseases

107
Q

What is required to get through lipid content of cell wall in Ziehl-Neelsen staining of mycobacteria?

A

Heat required to drive carbol fuchsin through

108
Q

What are mycobacteria de-stained with in Zeihl-Neelsen staining?

A

Alcohol-acid or just acid. Just acid not enough to de-stain waxy bacteria.

Pathogens = acid-alcohol fast
Saprophytes = acid-fast (less wax, less protected from immune system)

109
Q

Name the mycobacteria species causing clinical TB and the main species they affect.

A

M.tuberculosis – humans, primates

M.bovis – cattle (not birds)

M.avium complex – poultry, most avian species (not psittacines)

M.microti – voles

M.marinum – fish

110
Q

How does a granulomatous tubercle form in TB infections?

A

Infected macrophage surrounded by T cells > caseous necrosis and calcification > surrounded by fibroblasts > granuloma > walled off from the rest of the body due to calcium deposition > tubercle grows and risk of shedding and spread increases or subclinical

111
Q

How does mycobacterium tuberculosis cause TB?

A

Inhalation > lesions in lung and local lymph nodes

112
Q

How is mycobacterium avium spread?

A

Faecal-oral spread so found in gut instead in poultry

113
Q

What is the incubation period of mycobacterium avium?

114
Q

What are the clinical signs of mycobacterium avium?

A

Lesions in intestine, liver, spleen, bone marrow

Weak, listless, lame, wing droop

115
Q

What is the treatment and prevention for TB and the issue with this?

A

Antibiotics for 3-4 years and vaccination

Done in humans, not cattle

116
Q

What is the bacterium and species affected of Johne’s disease?

A

Ruminants

M.avium subspecies paratuberculosis

117
Q

How is Johne’s disease spread?

A

Faecal-oral spread – exposed in 1st year of life by close contact.
Environment – survives months in faeces.

118
Q

Where is Johne’s disease found in the body?

A

Live in macrophages – ileum, colon, local lymph nodes closest to gut

119
Q

What is the pathogenesis of Johne’s disease?

A
  1. Granulomatous lesions in a few months
  2. Spread and progression down gut
  3. Clinical after 1-2 years
  4. Chronic enteritis: diarrhoea in cattle and sheep > wasting
  5. Death in 2-3 years
120
Q

How can paratuberculosis be controlled?

A
  • Johnin test - 75% false positives
  • Rectal smear - ZN stain, 75% false positives
  • Immunological assays and PCR
  • Culture
  • Rabbit control (not feasible)
121
Q

What are the 3 groups in which the corynebacterium diptheroids are classified?

A

C.renale – affects kidneys

C.pseudotuberculosis

Rhodococcus equi – infects horses

122
Q

When diagnosing corynebacteria, what is seen in light micrscopy?

A
  • Gram positive rods, non-motile, non-sporing
  • Pleomorphic
  • Cell patterns can be palisades/club shaped or clumped together in odd shapes
123
Q

How are corynebacteria diagnosed with culture?

A

Dry and crumbly, white-cream-yellow, non-haemolytic, very small, grows very slowly (need 48-72h).

124
Q

What are the exceptions to corynebacteria culturing?

A

C.pseudotuberculosis – waxy flakes, haemolytic

Rhodococcus equi – 24h = shiny colonies, longer than 24h = mucoid and pink tinge

125
Q

Name 3 infections associated with the corynebacteria renale group.

A

C.renale – most frequent and important

C.cystidis – less frequent but widespread and severe

C.pilosum – rare

126
Q

How is caseous lymphadenitis caused by cirynebacteria pseudotuberculosis?

A

Inhaled/ingested/wound entry > local lymph nodes > local inflammation > invades macrophages > local superficial or mesenteric/thoracic lymph nodes > inflammation, necrosis and pus

127
Q

What happens if there is possible rupture of caseous lymphadenitis?

A

Green odourless pus > emaciation and death

128
Q

Where does rickettsia invade?

A

Capillary endothelial cells – multiply in cytoplasm

129
Q

Where does ehrlichia and anaplasma invade?

A

Damage red blood cells – haemolytic anaemia

Invade immune cells – multiply in vacuoles

130
Q

How is ehrlichia and anaplasma transmitted?

A

Transmitted to blood sucking arthropod vectors

131
Q

How are rickettsial infections treated and prevented?

A
  • Antibiotics (oxytetracycline) for 2-3 weeks
  • Blood transfusion (if blood heavily infected)
  • Vector control
  • Susceptible to detergents
  • Some vaccines available
132
Q

Where does chamydiaceae infect in the body?

A

Mucus membrane associated – respiratory, gastrointestinal, conjunctival, urinogenital

133
Q

What can a more systemic chlamydiaceae infection cause?

A

Arthritis
Encephalomyelitis

134
Q

Is chlamydiaceae zoonotic?

135
Q

What are elementary and reticulate bodies of chlamydiaceae?

A

EB – infectious form, resistant wall and metabolically active. 0.2-0.3um

RB – intracellular form, active and reproductive form, 0.5-1um

136
Q

What is the lifecycle of chlamydiaceae?

A
  1. EB attaches to host cell
  2. EB stimulates uptake by endocytosis, lives in endosome
  3. EB converts to RB, wall softens, rehydrates
  4. RB undergoes binary fission, formation of inclusion body in host cell
  5. RBs condense to EBs once all the nutrients in the host cell are gone
  6. Cell lysis releases EBs – 30-60 hours
137
Q

How does avian chlamydiosis develop?

A

Inhalation of EBs > acute systemic disease > ocular/nasal discharge, green bloody diarrhoea

138
Q

What is the pathogenesis of avian chlamydiosis?

A
  • High mortality
  • Or subclinical carriers – gut/visceral organ dissociation
  • Stress on the immune system causes EBs to be shed in faeces
139
Q

How are chlamydial infections diagnosed?

A
  • ID bacteria in lesion smear - Giemsa for inclusion bodies
  • PCR
  • Serology on paired sera from several birds
  • Isolation: Tissue culture, embryonated eggs
140
Q

How are chlamydial infections treated and prevented?

A
  • Antibiotics for 2-3 weeks
  • Detergents – sensitive due to high lipid content
  • Vaccines for feline and avian chlamydiosis
141
Q

Which antibiotics cannot be used to treat chlamydial infections?

A

Penicillin – affects bacterial cell wall but unable to lyse it due to intracellular nature

142
Q

Which chlamydiosis infection is a regulated disease?

A

Avian
35-45 days quarantine and antibiotics in feed

143
Q

Describe the spores of coxiella burnetiid.

A

Tough, sunlight resistant

144
Q

How do coxiella burnetiid spores survive in cattle, sheep and goats?

A

Inhaled/ingested. Macrophages in oropharynx require acidic pH for germination of spore bacteria survive in phagolysosome

145
Q

What does coxiella burnetiid cause in cattle, sheep and goats?

A

Bacteria travel in macrophages via blood

Gut/udder = mild infection, if it goes to placenta = abortion

146
Q

How is coxiella burnetiid controlled?

A
  • Can’t eradicate – reservoirs, resistant spores
  • Screen herds serologically and pasteurise milk – screening with serology of full tanks of milk
  • Treat with antibiotics or cull
147
Q

What are the characteristics of spirochaetes?

A
  • Slender Gram negative spiral cells
  • Motile due to flagella
  • Most saprophytic, some commensal, few pathogenic
148
Q

What are the genuses of spirochaetes?

A

Borrelia - Lyme disease and syphilis (rabbits)

Brachyspira

Leptospira

149
Q

How are spirochaetes diagnosed?

A
  • Serology – rising titre
  • Organisms in lesion material
  • Silver based stains – for fine spirochaetes
  • Negative staining and dark field microscopy
  • PCR – best
150
Q

Which brachyspira species are non-pathogenic in pig guts?

A

B. innocens
B. intermedius
B. murdochii

151
Q

What does brachyspira pilosicoli cause in pigs?

A

Porcine intestinal spirochaetosis

152
Q

What does brachyspira hyodysenteriae cause in pigs?

A

Swine dysentery

153
Q

How does swine dysentery spread?

A

Faecal-oral spread

154
Q

What are the reservoirs of infection of swine dysentery?

A
  • Clinical cases + carriers (3 months)
  • Wild rodents
  • Environment (3 days in moist faeces)
155
Q

Describe the different severities of swine dysentery.

A
  • Asymptomatic
  • Acute – mild, diarrhoea, drop in condition
  • Severe – mucohaemorrhagic colitis (50% fatality)
  • Chronic – dehydration, acidosis, emaciation
156
Q

How is swine dysentery treated and controlled?

A

Antibiotics in feed/water

Control – eliminate carriers, control rodents, clean environment

157
Q

What are the characteristics of borrelia?

A

Microaerophilic
Mostly blood parasites

158
Q

What are the reservoirs and hosts of borrelia burgorferi?

A

Wild rodent and tick reservoir

Humans, dogs, horses, cattle (sheep?)

159
Q

What are the 3 stages of borreliosis/lyme disease?

A

Skin rash/bulls eye rash

Systemic problems: fever, fatigue, stiff joints, arthritis, nervous system disorders

Chronic problems: arthritis, neurological, cardiac

160
Q

What is the presentation of borreliosis in horses?

A

Laminitis
In-utero infection

161
Q

What is the presentation of borreliosis in cattle?

A

In-utero infection

162
Q

What is the presentation of borreliosis in dogs?

A

Renal problems

163
Q

How is borreliosis controlled?

A
  • Aggressive antibiotic treatment – no resistance
  • Tick control
  • Vaccine – dogs (USA
164
Q

What are the important hosts of leptospira?

A

Humans, dogs, cattle, pigs

165
Q

Why is leptospira a good reason for barrier nursing puppies?

A

Dogs can pass to humans via wounds

166
Q

How is leptospira spread?

A

Replicates in rat host and associated with rat urine and stagnant water.

167
Q

Why does vaccinating against leptospira not work via herd immunity?

A

Dogs pass this to other dogs

168
Q

Describe the development of acute/visceral leptospirosis.

A

Enters via mucous membranes/skin cuts > spleen, liver, kidneys > haemorrhagic jaundice > possible death

169
Q

What are the clinical signs of acute leptospirosis?

A

Fever
Diarrhoea
Depression
Anorexia
Haemolytic anaemia
Haemorrhagic jaundice

170
Q

How does the immune system react to leptospira?

A

Immune response of IgM. Multiplies in the kidneys as antibodies can’t get through to nephron so stays there. IgG response can kick in and clear from the kidneys because it is smaller.

171
Q

Why does leptospira cuase nephritis and kidney failure?

A

Multiply at the kidneys for 3-6 months until IgG response clears them from kidneys

172
Q

What are the accidental hosts of leptospira?

A

Humans, cattle, pigs

173
Q

How is leptospira controlled?

A
  • Rodent control
  • Fence off ponds
  • Screen replacement stock
  • Eliminate carrier animals with high dose antibiotics
  • Vaccines
  • Penicillin/streptomycin within 1-4 days
174
Q

What are the characteristics of bacillus?

A
  • Spore formers
  • Large Gram positive rods
  • Aerobic/facultatively anaerobic
  • Ubiquitous and saprophytic
175
Q

What does bacillus licheniformis cause?

A

Abortion in cattle and sheep

176
Q

What does bacillus cereus cause?

A

Mastitis in cattle - spore forming
Food poisoning in humans - can germinate in rice

177
Q

What are the characteristics of bacillus anthracis?

A
  • Obligate pathogen – cattle, sheep, goats, horses, pigs/carnivores
  • Often fatal
  • Zoonotic infection – notifiable disease
  • Very resistant spores
  • Easily treatable with antibiotics
178
Q

How is the poly-D-glutamic acid capsule a virulence determinant of bacillus anthracis?

A

Allows it to resist antibodies, complement, phagocytes

179
Q

How is protective antigen a virulence determinant of bacillus anthracis?

A

Allows it to binds to target cell, cleaved by host serum protease

180
Q

What does oedema factor in bacillus anthracis cause?

A

Causes oedema and prevents leucocyte activity

181
Q

What does lethal factor in bacillus anthracis cause?

A

Increases vascular permeability and kills macrophages

182
Q

What is the pathogenesis of cutaneous anthrax?

A

Spores enter wounds, germinate, multiply and release toxins

183
Q

What is the result of cutaneous anthrax?

A

Painless lesion and very dark crust, as a result of local oedema and haemorrhage

184
Q

Where do animals ingest spores for septicaemic anthrax?

A

Horses and ruminants from soil
Pigs and carnivores from protein supplements and carcasses

185
Q

What are the effects of the toxins released by septicaemic anthrax?

A
  • Oedematous focus – GIT or RT
  • Bacteria spread to lymphatics causing local LN inflammation
  • Bacteria spread to blood causing enlarged spleen
  • Very rapid, uncontrolled bacterial multiplication in blood
186
Q

What is the pathogenesis of septicaemic anthrax?

A
  1. Bacteria use up oxygen
  2. Speticaemia and toaxaemia
  3. Capillary thrombosis and haemorrhgaing
  4. Fluid loss from bv and pulmonary oedema
  5. Circulatory collapse and extreme hypoxia
  6. Death
187
Q

What are the clinical signs before death of septicaemic anthrax?

A
  • Greatly increased respiratory and heart rates
  • Fever
  • Very dark tar-like blood oozes from all body orifices
188
Q

What are the clinical signs of septicaemic anthrax after death?

A
  • Dark blood around orifices
  • Incomplete rigor mortis
189
Q

What is the incubation period of septicaemic anthrax?

190
Q

What is the pathogenesis of septicaemic anthrax in infected ruminants?

A

Peracute. Rapid onset of signs, death in 1-2 hours

191
Q

What is the pathogenesis of septicaemic anthrax in infected humans and horses?

A

Acute. Slightly slower onset of signs, death in 24 hours.

192
Q

What is the pathogenesis of septicaemic anthrax in infected pigs and carnivores?

A

Subacute. Oedema of face, throat, neck. Acute is rare and involved invasion of blood.

193
Q

What actions are taken if there are at risk animals and further suspect cases of anthrax in living animals?

A
  • Cull
  • Treat with antibiotics (penicillin/tetracycline)
  • Treat with antitoxin – doesn’t treat just have a carrier animal that is no longer susceptible to toxins, source of spread
  • Vaccinate

Clinical Veterinary Science and One Health 23/24 (36 decks)

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