Bacteriology and Mycology Flashcards

1
Q

Campylobacter

A

– Gram – rods
– Curved (“Vibrios”)
– Spiral when grouped
– Aerobes or microaerophilic
– 3-15% O2, 3-5% CO2
– Some grow optimally at 42°C
– Flagella
– Darting or corkscrew motility
– Wet mounts useful in diagnostics
* Hanging drop
– Commensals
– Obligate parasites
– Mucosa of GIT
– Glandular crypts of genital tract and GIT

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2
Q

Important Campylobacter

A

– C. jejuni
– Enteritis in many (including man)
* Abortion and hepatitis
– C. coli
– Similar to C. jejuni
– Organism seen commonly in pigs
– C. fetus subsp. venerealis
– Bovine venereal campylobacteriosis
* Endometritis, infertility and abortions
– C. fetus subsp. fetus
– Abortion in cattle and sheep
– L. intracellularis
– Proliferative enteritis in pigs

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3
Q

Campylobacter spp. (Parasitic properties)

A

– Attach
– Fibronectin binding proteins
– Pili (F antigens) ?
– Lipoproteins
– Flagella (H antigen) ?
* Colonisation
– LPS (O antigen) ?
– Invade
– Strain dependent (serovars)
– Capsule (S layer)
– Cause inflammation
– Enterotoxins
* Cholera Toxin and Heat Labile toxin
* Hypersecretory diarrhoea similar to ETEC
– Cytotoxins
* Shiga-like toxins – cell death and
haemorrhage similar to EHEC
– Endotoxins
– Intracellular survival
– C. jejuni can survive within macrophages
* Disease severity, duration of symptoms
and relapse

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4
Q

C. jejuni

A

– Found in the intestinal tract of normal and diseased
animals
– Causes mild to moderate febrile (fever), enteritis with diarrhoea in several animals including humans.
– Occasional cause of abortion in sheep and other species and vibrionic hepatitis in chickens
– Vibriosis = diseased caused by curved bacteria

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5
Q

C. jejuni (Host Factors)

A

– Young, pregnant and immunocompromised
– Superficial erosive colitis and ileitis
– Fluid loss
– Water, mucus and blood stained diarrhoea
– Extracellular immune arm important
– Local IgA to H antigen
– Intestinal immunity
– Colostrum in newborns important
– Humoral antibody (IgG and IgM) to surface antigens (mainly O antigens) important in systemic immunity
– Recovered can sometime still shed ?
– Commensal versus carrier ??
– Vaccine ??
– Care with antimicrobial therapy
– Worry about antimicrobial resistance
development
* Animal and public health
– Treat in severe cases ?

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6
Q

C. jejuni (Environmental Factors)

A

– Faecal-oral transmission
– Direct or indirect (exogenous)
– Stress and physiological status can facilitate
endogenous disease in carriers
* Reduce stress and improve
husbandry/nutrition
– Can be shed in milk and contaminate meat
during slaughter
* Zoonoses
– Close contact
– Reduce stocking density
– Poor hygiene
– Improve to control and prevent
– Survive in water
– Faecal contamination
– Treatment of water to control and prevent
* Chlorination
* Filtration

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7
Q

C. jejuni (Zoonoses)

A

– Self limiting diarrhoea in humans
– Various sequelae
* Guillain-Barre-Stohl Syndrome
– Severe neurological disease
– Acute immune-mediated
demyelination of peripheral nerves
– Follows infection with serotype O19
(20-40%)
– Genetic predisposition in the
individuals
– Illness often lasts months and in
some cases is associated with
permanent incapacitation or even
death
– Food safety issue in poultry, pigs and cattle

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8
Q

Path of C. jejuni

A

Ileum and large intestine –> susceptible animal –> attrated to and colonise mucus —> localise in glandular crypts –> invade intestinal epithelial cells –> mild (usually) to severe GIT illness –> Bacteraemia:

EITHER:
- Guillain-Barre syndrome (human)
- Abortion (sporadic to outbreak)

OR:
Recovery and shedding

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9
Q

C. fetus subsp. venerealis

A

– OBLIGATE PARASITE
– Bovine reproductive tract
* Preputial crypts of older bulls
* Vagina of carriers
– 1-2 years of carriage
– Endometritis, temporary infertility and occasional
abortion
– Serotype/subsp. intermedius also recognised
– Also known as serotype A-sub 1
* Serotype A-1 refers to subsp. veneralis
– S-layer

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10
Q

C. fetus subsp. venerealis (Factors)

A

Parasitic properties
– Obligate parasite bovine reproductive tract
– Surface array proteins (S layer)
* Repetitive array of proteins on the outer cell wall
– Antiphagocytic, inhibits complement and
provides antigenic variation

Host factors
– Asymptomatic infections common
* Preputial crypts in bulls > 5 years old protect
organisms and result in prolonged carrier
state.
– More common in beef herds
* Natural mating
– Immunity and immune response important
* Humoral as it is extracellular in nature
– Immune status of the herd dictates clinical signs
* Acute (no previous exposure), chronic
infection (if local vaginal antibodies
produced)

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11
Q

C. fetus subsp. venerealis (Immunity)

A

– Protective immune responses develop between 6-12 weeks after infection
– Recovery is antibody mediated
* Immobilsation and opsonisation of the
bacteria
Uterus response
– IgG1 predominant Ig in uterus and is derived
from serum
– IgG1 immobilises and opsonises the bacteria
– Once engulfed by phagocytic cells it is rapidly
destroyed
– Bacteria are gradually eliminated from uterus
and fallopian tubes within 6 months
– Vaginal response
– Locally produced IgA is the predominant Ig in
the vagina
– IgA immobilises but does not opsonise
bacteria.
– IgA binding blocks the opsonising function of
IgG
* This my account for the persistence
of bacteria in the cervix and vagina
for up to 2 years
– Incidence of carrier cows that retain infection from one gestation to the next is
low, it is often enough to permit disease to persist in large beef herds.
– There is a period of convalescent immunity
following recovery in which they are protected
from re-infection
– However, cows eventually become susceptible
to re-infection

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12
Q

C. fetus subsp. venerealis (vaccination)

A

– Bivalent killed vaccine containing the two serotypes;
veneralis and intermedius
– Has a preventive effect
– Immunity lasts <12 months
– May also be of assistance in treatment and cure
of carriers ?
* IgG1 ✓

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13
Q

Pathogenesis of Bovine venereal campylobacteriosis

A

Preputial cavity
Venereal infection
Infection of vagina, cervix and uterus
endometreosis
THE EITHER:
1. sporatic abortion
2. Infertility (extended cycles and repeat breeding)
3. Development of immunity (IgA or IgG1)

IgA –> Vagina Cervix –> carrier 1-2 years
IgG1 –> Uterus —> Resistance to reinfection

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14
Q

C. fetus subsp. venerealis (Control and prevention)

A

– Good husbandry
– The use of young bulls that have tested negative
– Culture and antibody !!
– PCR useful
– Breed virgin heifers to young negative tested bulls
– Replacement heifers or cows
– Culture/PCR and antibody tested negative
before entering the breeding herd
– If endemic
– Annual vaccination
* Immunity is short-lived
* Boosters in bulls and cows 1 month prior
to joining
– Cull bulls
– Rest the herd for a breeding season
* Eliminating the bacteria
– Use of Artificial Insemination (AI) (with semen
treated with antimicrobials) can eliminate the
organism

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15
Q

Order Spirochaetales

A

– Slender, flexible and helically coiled
– Motile by rapid rotation around long axis and by flexing
– Anaerobes, microaerophilic or aerobes
– Differentiations based on morphology and antigenic
properties rather than biochemical tests
– Gram negative but stains poorly
– Darkfield and silver stains work best

– 4 pathogenic genera
– Brachyspira (formerly Serpulina)
– B. hyodysenteriae → swine dysentery
– Borrelia
– B. anserina → avian spirochaetosis
– B. burgdorferi → Lyme disease
– B. theileri → tick spirochaetosis in cattle
– Leptospira
– Leptospira serovar Hardjo → abortion and
agalactica in cattle
– Leptospira serovar Pomona → abortion and
stillbirth in pigs
– Leptospira serovar Icterohaemorrhagiae →
mild disease in rodents, fulminant (sudden and
severe) leptospirosis in various incidental hosts
including humans tick spirochaetosis in cattle
– Treponema
– T. pallidum → syphilis in humans

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16
Q

Leptospira

A

– Strict aerobe
– Grow best at 30°C
– Morphologically and physiologically similar
– Thin spiral organisms
– Occur in many animal species and humans
– Considerable heterogeneity amongst the genus
– Serological (antigenic) classification has been used for many years

– The organism is excreted in the urine (leptospiruria) as it tends to colonise in the kidney tubules

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17
Q

Leptospirosis

A

– In the incidental (dead-end) host
– Acute and subacute disease
– Severe to moderate disease
– Septicaemia and endotoxaemia
* Haemorrhages and fever
– Nephritis, hepatitis, agalactica and meningitis
– In the reservoir host
– Chronic or subclinical disease
* Abortion, stillbirth, infertility, nephritis and
inflamed iris (iridocyclitis)
– Obligate parasites
– Disease ➔ Localisation and proliferation

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18
Q

Leptospirosis factors

A

Parasitic properties
– Haemolysins
* Cytotoxin
– Endotoxins
* Gram negative LPS cell wall
* Low potency
– LPS may mediate adherence of neutrophils to endothelial cells and platelets
* Role in thrombocytopaenia
– LPS is immunogenic and responsible for serovar specificity
– Glycoprotein cytotoxins ?

Environmental factors
– Host adaptive
– Survives in the environment for up to 6 weeks
(not a saprophyte as it doesn’t replicate)
* Prefers warm, moist, neutral or slightly
alkaline pH
– Contaminated water is an important infectious
source

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19
Q

Leptospirosis pathogenesis

A

– Entry via mucous membranes or damaged skin
– Pass into circulation via lymphatic
– Disease results from systemic infection and
localisation
– Disease spectrum depends on the serovar and the
host infected

– Incidental host → acute disease
      * Damage to endothelium of small blood vessels 
        and leakage of blood and leptospires into 
        tissue
     * Host develops a marked antibody response 
        and there is rapid elimination of the pathogen
    * Or overwhelming infection can lead to death

– Reservoir host → chronic disease
* Passes into the kidney and resides in the
lumen of the proximal convoluted tubules
and shed in urine
* Weak antibody response which facilitates
persistent infection (months or years)
* Venereal transmission possible

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20
Q

Leptospirosis Immunity and Vaccination

A

– Protective antibody is serovar specific
– Agglutination and/or opsonisation
– Persistent infection may result from inability of
antibody to reach sites of infection in the
absence of inflammation
* More often related to reservoir host-
adapted poor antigenicity
– Vaccination (bacterin) is used for most prevalent
serovars in a species/region.
– Immunity lasts 12 months, therefore need
annual booster
– Passive acquired antibody is protective
(usually for the first 6 months)
– Can reduce the incidence of shedding,
particularly when vaccinated young animals
(reservoir host)
– Incidental host can be fully protective

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21
Q

Leptospirosis zoonosis

A

– Occupational zoonosis of dairy farmers and abattoir
workers
– Headache, fever, muscle pains and
conjunctivitis
– Vaccination of herd can reduce shedding and
zoonotic risk
– Dairy design can also reduce risk
– Wear protective equipment
– Disinfect the dairy and improved dairy hygiene

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22
Q

Leptospirosis (Control and Prevention)

A

– Ideally elimination of carriers
– Reduce environmental contamination
– Vaccination may help reducing shedding in reserve host
– Vaccinating dogs is effective (protects against
some serovars)
– Antimicrobial therapy not advisable in cattle or pigs
– Often not curative, can still culture the
organism from urine samples
– Companion animals and man use doxycycline
– Can be lengthy up to one month
– Deal with urine waste
– Disinfecting and clean the dairy regularly
– Water treatment and security
– Pest control
– Rodents can be reservoir or incidental hosts
and mechanical vectors
– Dairy design and farmer education
– Most cases in young dairy farmers 20-24 yrs

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23
Q

Genus Mycoplasma

A

– Class Mollicutes
– Obligate extracellular parasites of animals
and plants
– Smallest and simplest free living
– NO CELL WALL
– Cannot synthesis peptidoglycans
– Cytoplasm bound by a cytoplasmic
membrane
– VERY FRAGILE
* Do not survive long outside the host
* Susceptible to heat, desiccation,
disinfectants and detergents
– Resistant to antibiotics that interfere with cell
wall synthesis
* Penicillin 
– PLEOMORPHIC
– Filamentous, spherical, hollow rings and pear
shape

– Facultative anaerobes and microaerophilic
– Even when given required nutrition supplements and optimal conditions, they grow SLOWLY
- require COMPLEX media for culture
– Some are impossible to grow in the lab
– PCR and serology are useful diagnostic
aids

“fried egg apperance”

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24
Q

Mycoplasma

A

No cell wall
Motile
– Commensal
– Host specific

– Chronic disease
* Respiratory
* Urogenital (including mammary
gland)
* Serosal surfaces (joints, peritoneum, pleura)
– Anaemia
* Parasites of erythrocytes

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25
Mycoplasma epidemiology and properties
– Very fragile – easily inactivated – Most spread by close contact – Contagious – Aerosols * Piggeries, poultry sheds – Vertical transmission * Auto-immune disease
26
Mycoplasma key points
– Host and environmental factors may predispose to disease caused by mycoplasmas – Stress (eg. transport and overcrowding – Husbandry practices – Age (eg. young most susceptible) – Immunity – Concurrent disease – Mycoplasmas often exacerbate disease initiated by other pathogens and vice versa – This is particularly true in the respiratory tract.
27
What is the most signif disease of cattle worldwide?
M. mycoides subsp. mycoides small colony type Contagious bovine pleuropneumonia
28
M. hyopneumoniae (Enzootic pneumonia of pigs (EPP))
– Obligate parasite of the respiratory tract of pigs – Upper and lungs – Associated with cilia and causes ciliostasis and extensive loss of cilia – The continuous nature of pig production ensures a self perpetuating cycle of infections from older to younger pigs – Recovered pigs protected against re-infection – Breakdown in EPP-free herds usually occurs following the introduction of infected animals, although windborne transmission is also suspected – Wild boars ?
29
M. gallisepticum
– Respiratory tract of chickens, turkeys and other birds – Nasal sinuses and tracheas – Reproductive tract – Causes respiratory disease – Many factors influence the onset and severity of disease – Subclinical to severe in complicated disease – Exacerbated by: * Concurrent infections (ILT and E. coli) * Environmental factors which lower the resistance in the bird Sinusitis – Immune birds may remain carriers and can transmit the disease horizontally (aerosols) or vertically (egg) Live attenuated vaccine
30
M. haemofelis
– Haemophilic mycoplasma - cats * Diagnosis by DiffQuik of blood smears – Short rods or cocci which stain deep purple – Associated with RBC – Intravascular haemolysis resulting in anaemia and ill-thrift – Feline Infectious Anaemia – Fleas play a role as vectors – Ectoparasite control is important !!!
31
Mycoplasma Prevention, control and treatment
vaccination live attenuation eradicate through serological tsting and culling Pathogen free herds and flocks – General management factors can help reduce severity and spread – Stress, stocking density, nutrition and concurrent disease – Can’t use penicillin (no cell wall), drug of choice is tetracycline (not reliant on cell wall synthesis for its activity) – Water medication in pigs and poultry common when endemic to control spread – Ectoparasite control for the haemophilic mycoplasma important
32
Coxiella burnetii
– Obligate intracellular parasite – Small pleomorphic rods – Non motile endotoxins From cattle, sheep and goats - relativly resistant in the environment
33
Q Fever
Transmission – Shed in birth fluid of cattle, sheep and goats – Found in milk, urine and faeces – Aerosol and ingestion result in human infections Prevention and control – Occupation hazard – Protective clothing and masks – Vaccine available for humans – single shot * Live attenuate vaccine grown in eggs * YOU ALL SHOULD BE VACCINATED AGAINST THIS – Preventative tick treatment of pets and livestock – Prophylactic treatment of pregnant or lactating animals ?? * Minimise exposure ?? * Infectious dose may be as low as 1 cell per humans ?? Treatment – Long term tetracyclines – Acidic intracellular environment reduces antimicrobial efficiency ?
34
Genus : Bacillus
– Large Gram + rods – Facultative anaerobes – Catalase + – Endospore forming – Aerobic condition – Centrally located – Free – living in the environment – Saprophyte – 2 species of importance – B. cereus * Acute mastitis and food poisoning in humans – B. anthracis * Anthrax
35
Exotoxin complex
– *Protective antigen (PA)* channel forming protein * Required for activity of other toxins – *Oedema factor (EF)* calmodulin-dependent adenylate cyclase * Increase cAMP → electrolytic and fluid loss – *Lethal factor (LF)* metalloprotease cleaves MAPK (mitogen activated protein kinase) * Disruption of signalling pathways of macrophages * Massive IL-1 release from macrophages * Inflammatory cascade – LF together with PA form lethal toxin – EF together with PA form oedema toxin
36
Anthrax host factors
Acute septicaemia vaccination is effective in preventing disease
37
Anthrax zoonosis
– Transmission to human – Ingestion * Intestinal – Inhalation * Pulmonary – Contact * Cutaneous form – Spores germinate  Toxin  Disease – Pulmonary and Intestinal form most serious * 95% and 50% mortality respectively
38
Anthrax enviro factors
Saprophytes - soil - anthrax belt - endospores highly resistant - formed when CO2 pressure drops *dead animals = environmental contamination --> burn them – Spores brought to the surface – Flood, industrial effluent from rending plants, tanniers, carpet mills or wherever carcasses are salvaged can be a source of contamination – Spores germinate and bacteria multiple when exposed to high temperatures, moist conditions and when there is a lack of other soil-living bacteria – Alkaline soil – Heavy rain following drought – Decaying vegetative matter * Spore survival, germination and sporulation * Increase environmental contamination * Increases likelihood of an outbreak
39
Anthrax path
Inhilation Ingestion of spores scratches or wounds invade mucous membranes/ skin through breaks *germinate in host
40
Anthrax control and prevention ?
– Disease occurs when and where ?? – “Anthrax belt” – Ideal soil condition – Warm humid/wet weather – Recent floods * Watering holes – Drought – Stalky feed – Windy ?? – HOW DO YOU CONTROL and PREVENT IT?? – In the anthrax belt !! * Vaccination ?? * Penicillin prophylaxis ?? * Timing ?? – Heavy rains after a period of drought  – Supplement feed in drought – Removing soil ?? – Infected animals and material should be burned (source of contamination) * Stop environmental seeding
41
Clostridial disease
Neurotoxic (paralysis or stiffness) Histotoxic (local disease) Enterotoxic (GI disease) Invasive
42
Neurotoxic Clostridia
– C. tetani → tetanus – C. botulinum → botulism
43
Clostridium tetani (tetanus)
spores found in soil cross strain protection
44
Tetanus toxins
unable to inhibit muscle contraction specific neurotoxin for neurones toxi destroyed in intestine
45
Tetanus pathogenesis
Local infection of wound by spores ↓ Other bacteria and necrosis lowers redox potential allowing germination and growth ↓ Exotoxin produced and either binds to local nerve endings or enters circulation and binds to nerve endings distant from site of replication ↓ Toxin internalised and transported up the axon to the cell body ↓ Cleavage event and translocation to hydrolyse ‘docking’ proteins of inhibitory synapses ↓ Block of GABA and glycine release ↓ Tetanic spasm due to failure to control muscular contraction ↓ Respiratory paralysis and death
46
Tetanus factors (HPE)
*Host* – Bruising * Germination and toxin production – Horses most susceptible * Then pigs, ruminants and carnivores *Environment* – Invasions of spores through wounds * Nail wounds to foot * Tail docking * Castration *Immunity* – Toxoid made from the neurotoxin * Inactivated toxin * Antibodies against the toxin – Passive acquire antibodies protective – Anti-toxin can be use but will not remove bound toxin
47
Tetanus control, prevention and treatment
Treatment – Sensitive to penicillin but unlikely to be affective * Necrotic tissue  – Anti-toxin treatment in early cases Preventions – Vaccination and minimise chance of abrasions or wounds * Vaccinate mother to increase passive transfer * Vaccinate prior to castration or tail docking * Good procedures and clean yards help. Control – Usually sporadic cases – Environmental and minimising host factors
48
Clostridium botulinum
– Spores very resistant and essentially ubiquitous – Germinates when environment suits – Toxin ingestion – Intoxication – Environment or the animal source – Toxin can be inactivated by heat – Toxico-infectious
49
Botulinum toxins
7/8 neurotoxic – Protection against one type DOES NOT confer protection against the others – Not all types of botulinum toxin produce intoxication in all species – INACTIVE PROTOXIN is release on cell lysis – Requires activation by enzymes
50
Botulism
– FLACCID paralysis of skeletal muscle – Respiratory paralysis and death
51
Botulism pathogenesis
Organism multiplies under suitable conditions in feed ↓ Toxin released by lysis of cells ↓ Toxin ingested, activated by trypsin cleavage and absorbed (resistant to gastrointestinal conditions) ↓ Toxin binds to gangliosides at the neuromuscular junction ↓ Active component enters nerve and blocks acetylcholine release ↓ Flaccid paralysis due to inability to initiate muscle contraction ↓ Respiratory paralysis and death
52
Botulism factors
Host - shaker foal syndrome - GI environment Immunity - anti toxin can be used bu won't remove boud toxin Environment - related to poor quality feed pica in cattle ingestion of exposed rotting aquatic veg material (waterfowl)
53
Control, prevention and treatment of botulism
– Freshly made feed – Clean feed troughs – Cook thoroughly – Place feed away for contaminated area – Discourage waterfowl from feeding near waterways with exposed decaying material – Exclusion zone, netting, sirens ?? – Maintain nutritional balance in diet – Prevents pica – Vaccination – Remove dead carcasses – MANAGE THE ENVIRONMENT and the ANIMAL to reduce the chance of bacterial proliferation and toxin ingestion – Difficult especially with wildlife – Difficult to control environment and animal habits – Treatment → Specific antitoxin if seen early
54
Histotoxic disease
– C. novyi type A → malignant oedema – C. novyi type B → Blacks disease – C. chauvoei → Black leg
55
Clostridium novyi
– Motile, very fastidious anaerobe – 3 types based on toxins produced – A and B are pathogenic – Type A → malignant oedema “big head” – Gas gangrene – Young rams fighting and head butting – Alpha, Gamma, Delta and Epsilon toxins – Type B → Black disease – Infectious necrotic hepatitis – Alpha, beta, zeta and eta toxins – Alpha toxin is phage mediated – Lethal and increases capillary permeability and causes oedema. – Vaccination ✓
56
C. chauvoei
– Malignant oedema = Blackleg – Rancid odour and gas bubbles – Form short chains or occur singly – Produce a range of toxins with systemic and local effects (alpha to delta)
57
Blackleg pathogenesis
Ingested and replicates in the intestine ↓ Spores lodge in muscle, presumably reaching there via the circulation ↓ Muscle damage (eg. bruising particularly in young animals on a high plane of nutrition) allows germination and replication ↓ Toxins cause local damage but also enter circulation ↓ Lameness, fever, depression and eventually death
58
Blackleg control and prevention
– Minimise muscle damage – Avoid overtly high nutritional feed – Especially young animals – Bacterin (not just toxoid) necessary to produce protective antibody as antibody needed against cell wall as well as toxins – Some antigenic variation between isolates from different geographic regions which may necessitate a local derived vaccine strain
59
Enterotoxaemia
-C. perfringens types A, B, C – Dysentery/enteritis – C. perfringens type D – “Pulpy kidney” – C. perfringens type E – “Enterotoxaemia” in calves and lambs
60
C. perfringens
– Non-motile – Types A – E based on possession of four major lethal toxins (alpha, beta, epsilon and Iota) – Also can cause malignant oedema
61
C. perfringens toxins
*Alpha (a)* – Phospholipase C which splits lecithin-protein complexes in cell membranes – Types A - E *Beta (b)* – Causes inflammation of intestine and loss of mucosa – Causes damage only in the presence of trypsin inhibitors as is destroyed by trypsin – Type B and C *Epsilon (e)* – Activated by trypsin and pepsin and also by the exotoxins Kappa and Lambda – Lethal systemic affects – Type B and D *Iota (i)* – Activated by cleavage – Composed of two components – Type E
62
Pulpy kidney
– Overeating, sudden change in diet or continued feeding on rich feed a post mortem change due to rapid autolysis
63
C. perfringens enteritis
– Immunity – Toxoids prepared from types C and D induce protection against types A-D – Protection depends on the neutralisation of the toxin * Antibody – Prevention of enteric disease = antibody in the intestinal lumen * Colostrum
64
Important Pseudomonas and Burkholderia
*P. aerguinosa* – Variety of opportunistic diseases * Skin, ears, mastitis and others – Many host species *P. fluorescens* – Tail/fin rot and septicaemia – Occasionally seen in other species *B. mallei* – Glanders * Skin and respiratory disease * Equidae, Carnivores *B. pseudomallei* – Melioidosis * Chronic suppurative lesions * Many species
65
Pseudomonas aeruginosa Features
– Colony morphology * Blue-green * Beaten copper appearance – Odour * Old socks – Saprophyte – Soil – Freshwater – Marine * Absolute require for MOISTURE (biofilm) * Minimal nutrient requirement – Isolated from skin, mucous membranes and intestine – Reflects exposure and TRANSIENT colonisation – Environmental organism – Resistant to chemical * DISINFECTANTS * ANTIMICROBIALS *unpredictable antimicrobial sensitivity*
66
Diseases associated with P. aeruginosa
Opportunistic Fleece rot Corneal ulcers
67
Parasitic properties of P. aeruginosa
Adhesions Slime layer Capsule polysacceride siderophores pigment - blue-reen - fluorescent green yellow
68
EXOTOXINS of P. aeruginosa
– Causing tissue damage, oedema and haemorrhage Exotoxin A
69
P. aeruginosa host factors
– Stress – Changes in feed – Antimicrobial usage – Concurrent disease * Allergies – Immunosuppression burns Breeds obesity floppy ears
70
P. aeruginosa enviro factors
needs moisture aquatic enviro and moist soils biofilms - rocks - feedig, water troughs and dips
71
Pathogenesis and epidemiology P. aeruginosa infection
Enviro organism | Opportunistic PAth | compromised individual | infection | disease
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Control and prevention P. aeruginosa (fleece rot)
FLEECE ROT – Plunge dipping  Pour-on ✓ – Shearing prior to rainy season * Shearing wounds  * Saturated rain post-shearing  * After March in winter rainfall districts  – Susceptibility greatest when 4-6 months of wool – Shearing timing and genetics ? * Low wax content, irregular fibre size and wrinkling  OTITIS EXTERNA – Floppy ears !! – Dry out ears or limit swims – Clean ears * Cotton swabs – Hairy ears ?? – Allergies ?? – Foreign bodies / wounds – Ear mites
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Burkholderia mallei
Obligate parasite respitory and skin nasal cutaneous facultative intracellular parasite - saphroyte killed by chilling and freeezing Pathology - nasal discahrge - nodules - inhailation - skin abrasion - zoonotic * host fitness important
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Burkholderia mallei Prevention and control
Endemic - ELIZA cull pos isolate cases quarantine and test imports - at least 2 weeks
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Order Chlamydiales
Chlamyda – C. trachomatis → genital, ocular and respiratory pathogen of humans – C. suis → enteritis and conjunctivitis in pigs – C. muriadum → pneumonia in mice Chlamydophila – C. pneumoniae → pneumonia in humans, ocular, respiratory and urogenital tract disease in Koala and possible respiratory disease in horses – C. psittaci → systemic disease in birds and zoonotic
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Chlamydiosis pathogenesis
local necrosis chronic inflam immune-mediated damage persistant and latent infections Suppression but not elimination
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Chlamydiosis Immunity
– Antibody against the Major Outer Membrane Protein (MOMP) is thought to play some role in protective immunity – MOMPS are adhesins and are distinct in different species and serovars – Useful diagnostic - killed vaccines used in sheep and cats
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C. pneumoniae
– TWAR, Koala, Equine – TWAR causes pneumonia in humans
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C. psittaci
Wild bird resovior - parrots wild birds --> parrots – Shed in discharge * Ocular * Nasal * Faecal – Resistant in environmental condition Zoonotic Gardening close contact with bird secretions Treated by antibiotics Control: Biosecurity and wild game meat PPE when gardening
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Moraxella
– M. ovis → pinkeye sheep – M. equi → pinkeye horse – Non haemolytic – M. catarrhalis → pinkeye and respiratory disease in humans – M. bovis → PINKEYE – Mucous membrane – Carriers – Nasopharynx – Conjunctiva – Vagina – Highly contagious – Avoid predisposing factors * Minimise risk of irritants – Fly repellents – Shelter – Irrigation of yards – Clovers rather than tall stalky grass
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Important Brucella
B. arbortus → Cattle (horses) – abortion / orchitis B. melitensis → Goats and sheep – abortion / orchitis / arthritis B. ovis☺* → Sheep – abortion / epididymitis B. suis* → Pigs (cattle) – abortion / orchitis / arthritis / spondylitis ▪Transmission ▪Ingestion (milk)* ▪Venereal ▪Exposure to mucosal surfaces ▪Abortion / Parturition / Vaginal discharge ZOONOTIC Test and cull bulls
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Foot rot
– Foot rot is contagious – Prevention and control ✓ – Parasitic properties – Variation in breed susceptibility – Spread occurs in warm, wet condition ◼ D. nodosus survive away from the host for less than a week or two – Formalin or zinc sulphate footbaths – Foot paring/trimming segregation, quarantine
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Pasteurellaceae
– Actinobacillus – Haemophilus – Avibacterium – Mannheimia – Pasteurella – Most are commensals – Extensive taxonomic change – Haemophilus / Avibacterium – Pasteurella / Mannheimia
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Actinobacillus
– A. lignieresii → ‘wooden tongue’ in cattle – A. equuli → ‘sleepy foal disease’ – A. pleuropneumoniae → pneumonia in pigs and horses – A. suis→ septicaemia in young pigs EXOTOXINS
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A. lignieresii
– “Wooden tongue – Endogenous origin * Commensal of the oral cavity – Special initiating circumstances are required * Wounds in the mouth * Rough feed * Foreign body injuries – Avoid these circumstance = prevention – Produce small grey-white granules in pus – “Club colonies”
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Actinobacillus pleuropneumoniae
– Serious, obligate parasite of pigs – Fibrinohaemorrhagic pneumonia – Lung lesions covered with pleuritic adhesions *prevention through eradication* – Predominantly a pathogen of pigs < 6 months of age – Geographical localisation of serovars – Recently introduced animal – Spread of infection is facilitated under intensive conditions. – Autumn/winter – Stress (poor ventilation, cold) and concurrent infection increase severity of disease. – Strict biosecurity to reduce introduction and spread in non- endemic herds – Quarantine (cases and in-coming) – Screening new breeding stocks etc.. – All-in/All-out✓
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Pasteurella and Mannheimia
– 19 recognised species – P. multocida ✓ – M. haemolytica ✓ – Septicaemia – cattle (haemorrhagic septicaemia), pigs, birds (fowl cholera) and rabbits – Bronchopneumonia – cattle, sheep, goats, horses, pigs and rabbits (usually secondary to respiratory virus and/or Mycoplasma infection) – Rhinitis – piglets and rabbits – Wound infections – Other occasional opportunistic infections – Prevention and control – Environmental and husbandry – Stress minimisation – Avoid overcrowding – Health management and concurrent disease – Host and environmental factors
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Mannheimia haemolytica
“Shipping fever complex” in cattle and sheep
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Salmonella
– S. Abortus-equi → abortion and septicaemia in horses – S. Abortus-ovis → abortion and septicaemia in sheep – S. Choleraesuis → pigs – S. Dublin → Cattle – S. Gallinarium and S. Pullorum → poultry – S. Typhi → humans – Faecal contamination of feed/pasture – Ingestion of Salmonella (dose received is critical) – Excreted in faeces and survives in the environment – Carriers !!! – High stocking rates and other stresses predispose to disease both by lowering host resistance and increasing environmental contamination – Test, detect carriers and eliminating ✓ – Biosecurity ✓ – Both humoral and cell mediated immunity ✓ – Test and cull positive
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Genus Yersinia
– Y. pestis → Bubonic plaque in humans – Y. pseudotuberculosis → Systemic disease in mammals and birds, enteritis in lambs and calves – Localised inflammation and water loss = enteritis Hosts: fleas, rats – Control and prevent – Minimise faecal contamination – Wild reservoirs and carriers
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Enterobacteriaceae
– O antigen – Somatic H, K and F antigens E.coli S.enteritis Y.psuedotuberculosis
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E. coli key points
– Lactose fermenter – Pili, Flagella, Capsule and O-antigen – Toxins – Nature of pathogenesis – What type of toxins? – Is the bacteria invasive or not? – Host and environmental factors – Hygiene, age, other predisposing factors – Concentration – Control and prevention – Treatment of infections ?? – Based on pathogenesis – Invasive and cytotoxic versus non-invasive and cytotonic