Bacteriology Flashcards
Identify Staphylococci in culture and in cytology of a sample ?
Staphylococcus is a gram positive coccus.
- Divides in all planes forming grape like clusters
- Well adapted to life on land, with a thick peptidoglycan outer membrane which provides them with environmental resistance
- Is a halophile
- Facultatively anaerobic
- Catalase positive
- Will grow in a saline environment = halotolerant
- The pathogenic staphylococci usually produce the enzyme coagulase
Order Bacillales – Family Staphylococaceae (essentially marine bacteria) – Genus Staphlococcus; Gemella
The members of the genus Staphylococus are non-motile, nonsporulating, gram positive cocci
Occurring in clumps
Identify potential sources of pathogenic staphylococci ?
Staphylococci are commensals on the skin and mucosa of all animals and people
Skin and mucosal microflora
- Can survive in dry environments eg clothing for up-to 3 months
- Pathogenic staphylococci are only a small part of the normal skin flora and oral – upper respiratory microflora, however, due to their ability to cause disease they are the most common cause of opportunistic infections in traumatic lesions of the skin and mucosae
They are common opportunistic pathogens of the skin and subcutaneous tissue
List the pathogenic staphylococci and the important diseases/s that each causes in animals ?
Pathogenic strains of staphlococci and the diseases they cause.
S. aureus
S. pseudintermedius
S.hyicus
Staphylococcus aureus – the golden grape cluster berry
S. Aureus is the most common of all the pathogenic staphylococci in animals causing pyogenic (production of pus) infections of the skin and related structures.
- usually initiated by traumatic wounds
- once established it may spread from these sites causing systemic infections, septic arthritis and osteomyelitis
- contagious with animal to animal, zoonotic transmission or even reverse zoonosis
MRSA = methicillin resistant staphylococci can be transmitted from animals to/from people
- Many published examples with MRSA in the nasopharynx of pigs resulting in mastitis in cattle
- Transmission = is by contact with either infected animals or with objects that have been in contact with infected animals (hand + hair clippers)
Osteomyelitis = inflammation of the bone or bone marrow
Staphylococcus pseudintermedius
S. pseudintermedius is a skin and mucosa commensal found in canids and is the most common cause of skin associated infections in dogs, cats and occasionally other animals/people.
- pyoderma, otitis externa (redness and swelling of the ear canal), MRSP
- difficult to distinguish within the laboratory from S. aureus
Staphlococcus Hyicus (Pig staphylococcus)
S.hyicus is the cause of exudative epidermitis or greasy pig disease
- may also affect poultry and rarely other animals
List the first line antibiotics that are effective against this genus and explain the importance of methicillin-resistant staphylococci ?
Amoxycillin potentiated with clavulanic acid = the antibiotic of choice
- Potentiated beta lactam drugs
- Most staphylococcus in companion animals is resistant to amoxycillin alone
- For skin infections cephalexin
- For livestock a procaine penicillin (long acting penicillin G), in horses a penicillin-gentamicin combination is used
Penicillin’s are highly synergistic with aminoglycosides and therefore in serious infections a combination of amoxicillin-gentamicin is often administered
Name and describe the function of important Staphylococcal toxins (6)?
To establish themselves pathogenic staphylococci produce a number of virulence factors dependant on their species and strain. (6)
Adhesins = binds to fibrin, fibronectin damaged tissue
Invasins Alpha and Beta toxins = hyaluronidase, protease, lipase enzymatic breakdown of DNA
Alpha toxin = porin toxin
Exfoliative toxin = Protease
breaks down desmoglein – 1 in the skin. Causes a bulla formation and skin sloughing
Superantigen = TSST-1 enterotoxin binds with MHC2 on antigen binding cells results in non specific T cell activation with subsequent release of cytokines
Immune system modulators = leukotoxin, protein A surface binding protein.
IgG binding protein at Fc region stimulates proliferation and apoptosis of some B lymphocytes microcolony formation.
Immune protection = catalase antioxidant and peroxidase respectively
- Review the cause, transmission, predisposing factors, pathogenesis, diagnosis and control of greesy pig disease ?
Staphylococcus hyicus is a contagious skin disease of predominantly piglets (greasy pig)
Cause = Staphylococcus hyicus
Transmission = This bacterium reaches high numbers in the sows vagina prior to partus and then colonises the skin and oral cavity of piglets during birth
Exudative dermatitis, it manifest as an explosive out break lasting for about 3 months. The affected pigs grow slowly and are susceptible to secondary infections.
Clinical signs = Crust formed by exudate and proliferating epidermal cells
- Skin starts by reddening, becomes brown and later develops a greasy texture
- Out breaks are frequent following weaning and may cause up-to a 15% mortality
Predisposing factors = The disease only manifests when there is trauma to the skin, biting, rough floors or straw bedding
- High infection rates with irritant skin mites
- Circovirus2 and parvovirus predispose the piglets hence it is more common to see in 1-5 week old piglets
Pathogenesis
- S. hyicus is a skin commensal proliferates on the skin in a humid warm environment.
- It will invade damaged skinproliferate and produce exotoxins
- Most important = exfoliative toxins (exhA, exhB, exhC and exhD) which destroys desmoglein 1 found in the intracellular cement of cells stratum spinosum and cleaves the cells.
- Elicits a severe inflammatory response within the skin
- Exudation of a protein rich fluid – which if severe enough can lead to weight loss and dehydration
- Pigs that die often have secondary bacterial infections especially of the kidneys and lungs
Diagnosis
Clinical signs (exudative dermatitis) and history piglets 1-5 weeks of age or at weaning
Control / prevention
- Chlorohexidine wash or novobiocin intramammary preparation with mineral oil sprayed directly onto the skin
- Topical antibiotics
- Prevent injury = upgrade surfaces, teeth clipping, tail-docking
- Iron injections
- Ensure cleanliness of farrowing crate and ensure disinfection between farrowing
- Treat for mange
- All in, all out policy
- autogenous vaccine of the sow 2-4 weeks prior to farrowing
Explain the predisposing factors and the clinical signs of Staphylococcus pseudintermedius infections in dogs?
Staphylococcus pseudintermedius is an unpigmented, coagulase positive Staphylococcus that is found in the skin and mucous membranes of dogs (all canids), and cats.
* Potentially zoonotic
* primary cause of skin infections and such as pyoderma as well as acute ear infections.
* clinical signs depend on the lesions depth and can be as mild as scaling to a papule and pustule formation, ulceration and exudation
* -deep pyodermas are the hardest of all skin infections to treat
* also affects other organs such as the bladder causing cystitis and bone causing osteomyelitis
Predisposing factors
Infection occurs when there is an overgrowth of mainly S.pseudintermedius
- Wet and moist areas have a higher number of bacteria and are more likely to become infected
- Any skin disease eg demodicosis causing itchiness that changes normal skin morphology from desert like to moist
- Immunosuppression
- Follicular hyperkeratosis, demodicosis or a foreign body
- It may occur secondarily to a superficial pyoderma (caused by allergy’s, seborrhoea, parasitic infections etc)
- German shepherds and Bull terriers have a genetic predisposition to disease
Pathogenesis
Deep pyoderma includes folliculitis, furunculosis, abscesses or cellulitis where there is an accumulation of pus within the dermis and subcutis
* Localised hair loss
* Pustules
* epidermal collarettes
* ulceration
* haemorrhagic bullae
* nodules
Distinguish between the staphylococci and streptococci using key morphological and biochemical features
Streptococci
* Gram positive, non-motile, non-spore forming, facultatively anaerobic cocci
* Form chains
* Catalase negative
* Tend to not develop resistance against antibiotics
* Beta-haemolysis (complete clearing of blood agar due to the destruction of red blood cells), some undergo alpha haemolysis P.Pneumonia greening on blood gar
* They are apart of the Lactic acid group (also includes Enterococcus, Lactobacillus)
Describe the Lancefield grouping scheme and how its works?
Streptococci
Lancefield grouping scheme
Latex agglutination test
Beta-haemolytic streptococci can be grouped into Lancefield types based on antibodies to carbohydrates/antigens (C-substance) in the streptococcal outer membrane.
(Group D)
* Requires antigen detection test = latex agglutination test is used
* Clumping of the blue latex particles indicates that agglutination antibodies have attached to the outer membrane of a homologous antigen (+ve).
List of potential diseases
- s. agalactiae bovine mastitis
- S. equi equi strangles
- S. equi zooepidemicus pyogenic infections and endometritis
- S. suis pyogenic infections + septicaemia + meningoencephalitis
- S. cani
- S. iniae fish septaceamia
- S. uberis mastitis
BE ABLE TO IDENTIFY POTENTIAL SOURCES OF PATHOGENIC STREPTOCOCCI AND ENTEROCOCCI ?
Streptococci
Streptococci are normal flora or the skin and mucous membranes of the mouth, nose and throat as well as external genitalia.
Some pathogenic streptococci have specific niches on the body. For example, Streptococcus equi subsp. equi, the agent of strangles, is found in the nasal cavity or guttural pouch of carrier horses, and Streptococcus uberis is a commensal within the teat canal of cows.
Under ideal conditions i.e. kept moist in mucus secretions, streptococci can last 7 to 9 weeks in the environment.
Enterococci are commensals within the intestinal tract.
LIST AND DESCRIBE THE FUNCTION OF IMPORTANT STREPTOCOCCAL VIRULENCE FACTORS ?
Streptococci cause pyogenic (pus causing) infections of the skin, udder, ear, upper and lower respiratory tract.
- Lipotechoic acid LTA,
Adhesin attached to the cell membrane acts in adhesion molecule and stimulates inflammation - Hyaluronidase, streptokinases
Invasin causing connective tissue break - Superantigen non specific T-cell mitogens
By interacting with a large number of T cell receptors causing activation (outside of the antigen recognition site) causing massive cytokine release and shock - M protein
Immune modulator = blocks complement binding, antiphagocytic and can mimic host cell surface proteins resulting in autoimmunity. - Streptolysin S leukocidins (kills leucocytes).
- Hyaluronic acid capsule
Immune system modulators = acts as a poor antigen in host connective tissue and allows micro colony formation.
LIST THE ANTIBIOTICS THAT ARE EFFECTIVE AGAINST THE STREP FAMILY ?
Streptococci treatment
Use either penicillin or amoxycillin to treat streptococcal infections
- Most effective especially early on in the disease is penicillin
- For oral therapy amoxicillin is effective
- Lipid soluble trimethoprim sulphonamides may work better for animals with long standing infections and abscesses which are not easily accessible (lincosamides and macrolides)
Note = High risk that these animals may develop toxic shock syndrome
Enterococcus is much more prone to antibiotic resistance
Review the cause, transmission and predisposing factors of strangles in horses?
One of the most commonly diagnosed and important contagious bacterial diseases of horses in Australia
Cause = Streptococcus equi equi
- This is a notifiable disease Victoria only (the disease is endemic in Australia)
Transmission = directly through inhalation of sneezed bacteria; or nasal abscess contact
- Possible transmission through contaminated stables, equipment or water (fomites)
- Highly contagious
Predisposing factors
- Communal drinking sources
- Population density
- mobility
Describe the pathogenesis and clinical signs of strangles in horses ?
Strangles
Pathogenesis
Within three hours of transmission it attaches to the tonsillar crypt and follicular cells of the soft palate through surface lipotechoic acids and SEM binding proteins.
SEE produces a capsule and SEM protein
- this works by actively binding fibrinogen and IgG which inhibits deposition of C3b on the bacterial cell surface. This results in a antiphagocytic action.
SEE then divides and spreads to other lymph nodes (mandibular and retropharyngeal). The dividing bacteria stimulate an inflammatory response resulting in fever and abscessation of the lymph nodes.
Rupture of the retropharyngeal abscesses can lead to bronchopneumonia or guttural pouch empyema (pockets of pus).
Guttural pouch empyema may result in persistent carrier horses.
Clinical signs
- first sign pyrexia (fever), this is when the horse becomes infectious to other horses (18days)
- purulent nasal discharge
- lymph nodes of the head and neck will develop abscesses
- the abscesses once ripe will rupture either to the outside or leading to the purulent nasal discharge.
- marked swelling of the neck causing breathing difficulties hence the name strangles
Shedding of bacteria lasts 2-3 weeks
Describe the very serious concerns which surround strangles ?
The possible complications of strangles
- Persistently infected horses / guttural pouch empyema
- the bacteria may decimate in the blood stream and lodge in other tissues of the body causing metastatic abscessation.
- this condition requires long term antibiotic therapy and often results in death
- bastard strangles - Type three hypersensitivity
Three to four weeks after infection with SEE may trigger an immune complex reaction.
- usually in horses with high titres
- pupura haemorrhagica (swelling of the blood vessels, head, legs and underbelly).
- hypersensitised horses produce high quantities of IgA which results in generalised vasculitis leading to oedema and haemorrhages.
- fatal if left untreated
Describe how you would go about diagnosing and treating a case of strangles ?
Strangles
Diagnosis
- qPCR (quantitative)
- bacterial culture of nasal swabs or abscess exudates are used to diagnose clinical cases.
- Serology is used to determine exposure with high titres found in carrier horses
Detection of carrier animals
- Infection occurs through abscessed retropharyngeal rupture and drainage into the guttural pouches
- 50% have a chronic cough
- Pus in guttural pouch if not drained will dry into chondroids (dry and hard).
- There is reluctance to scope guttural pouches so most cases of guttural pouch empyema are carried out using nasal fluids.
Control
- Quarantine horses that are known to be infected for a minimum period of 21 days
- twice daily rectal temperature check of unaffected horses / pyrexia precedes shedding
- Horses inContact with those infected moved to an orange zone, no known contact green zone
(take rectal temperatures to determine infection twice daily)
- Avoid movement off property
- Warm compresses to the abscess will assist with their ripening, once ripened can be lanced
- Antibiotics are controversial as they may extend the time required to heal and prevent the build up of immunity
- Treat sick horses last eg fomites
- Clean disinfect stables and equipment
- Can vaccinate unaffected horses
Describe the transmission and predisposing factors of Streptococcus suis infections in pigs ?
Streptococcus suis
Transmission
- Carried on the tonsils of pigs and external genitalia of sows
- Usually by droplets of the oral and respiratory secretions of carrier pigs or birth
- Flies and humans may mechanically transmit the disease to neighbouring pig houses/farms
Predisposing factors
- Disease in pigs is usually precipitated by stress ie weaning, mixing of age groups, overcrowding
- Other infections may increase susceptibility
Describe the pathogenesis, diagnosis and control of Streptococcus suis in pigs ?
Streptococcus suis in pigs
Pathogenesis
The only difference discovered between virulent strains and non-virulent strains is that virulent strains may survive within the phagolysosome of macrophages.
Clinical signs
- Serotype one Polyarthritis and meningitis in 10-14 day old piglets
- Serotype two is more common and results pneumonia and sepsis in weaned and grower pigs (serotype two is zoonotic)
- Sporadic and sudden, explosive out-breaks which may also stop suddenly
Diagnosis
- History, clinical signs
- Isolation and serotyping of the infectious agent
- Evaluation of microscopic lesions
Control
- Animals respond well to penicillin treatment
Describe the pathogenesis and clinical signs of Streptococcus canis ?
Streptococcus canis
Streptococcus canis is a normal commensal in the mucosa of dogs.
- Produces a unique M protein that is antiphagocytic and causes a variety of localised infections including abortions, vaginitis, cystitis and bronchopneumonia
- It may decimate from the site of infection to the rest of the body to cause septicaemia
- In dogs it is frequently identified in infections of the external ear and skin
Rare strains of S. canis are infected with a bacteriophage DNA that encodes for superantigens – which cause the development of streptococcal toxic shock syndrome
- fluroquinolones may regulate expression of this gene
Review the cause, transmission, predisposing factors, pathogenesis, diagnosis and control of Streptococcus iniae infections in fish ?
Streptococcal sepsis in fish Streptococcus iniae
The most important bacterial infection of farmed tropical freshwater and marine fish
Fish usually become infected through cannabilism of affected fish
* High water temperatures increase the risk of disease + stressed fish
Pathology
* Bacterial septicaemia and meningoencephalitis resulting in the loss of orientation, lethargy, anorexia, ulcers, exophthalmia and erratic swimming
* New outbreaks within naïve populations of fish may result in a 50% mortality
* Zoonotic sepsis toxic shock n fisherman
Streptolysin S like toxin
The prime toxin responsible for cell destruction in numerous tissues
Beta haemolytic, dose not group in the Lancefield grouping scheme and is CAMP positive
Control
Control measures may include reducing the feed to decrease bacteria ingestion, reducing water temperature and decreasing of the stocking density
- Many farmed species are vaccinated by bath immersion or by intraperitoneal injection affording 6 months of protection
(must contain the serotype on farm to be affective). - Susceptible to penicillin antibiotics
Define mastitis and explain the importance of mastitis to the dairy industry
Mastitis
Is defined as inflammation of the mammary gland usually in response to a bacterial infection. Other infectious causes include fungal, algal or viral.
It may manifest as peracute (severe short duration), acute, subacute (inbetween) or chronic
Or subclinical (no clinical signs)
The importance of mastitis to the dairy industry
- loss in milk production
- increase in discarded downgraded milk
- early culling of cows (need to replace sooner)
- treatment expenses
- reduction of breed performance
- Painful to the cow may prevent suckling of young
- antibiotic/pathogenic residues may cause diarrhoea in the calf.
-The presence of bacteria in milk is a public health risk, as it may result in disease in people
Explain how the bacteria infect the udder and overcome udder defences ?
Bacteria usually infect the udder by the teat canal. The teat is an invagination of the skin and is lined with squamous cell epithelium.
A healthy udder
* During milking the teat lining is continually sloughed off and replaced
* This process flushes out the bacteria trapped in cells during milking
- the narrow canal is surrounded by a thick muscular layer known as the teat sphincter which serves to exclude bacteria.
(musculoelastic layer = Rosette of Furstenburg)
Reason for disease
- During the dry period the udder becomes more susceptible to infection with the keratin plug being the main line of defence.
- during milking the teat may evaginate allowing bacteria in
- bacteria may be propelled within the teat canal by vaccum fluctuations of the milking machine
- to long of a vacuum by the milking machine can result in congestion and oedema allowing the entry of bacteria
Once the bacteria have breached the teat defences as little as 100 bacterial cells can result in mastitis.
Why is lactoferrin important in defence of the udder in dairy cows ?
Lactoferrin
Lactoferrin in milk bind iron making it unavailable to bacteria.
It also binds to LPS (Gram negative bacterium) causing peroxide formation and damage to the bacterial cell membrane.
Lactoferrin also protects cell membranes from viral attack and will oxidise RNA.
However bacteria in high numbers can overcome lactoferrin
What factors could predispose to mastitis ?
Factors which predispose to mastitis
Any activity that leads to teat damage and loss of its ability to act as a barrier will allow the entry colonisation and invasion of pathogens
- udder anatomy and physiology
- stage of lactation (udder oedema early lactation in heifers)
- milkers
- milking equipment
- environment (faecal contamination muddy)
- teat damage by injury or viruses
What factors could predispose to mastitis ?
Factors which predispose to mastitis
Any activity that leads to teat damage and loss of its ability to act as a barrier will allow the entry colonisation and invasion of pathogens
- udder anatomy and physiology
- stage of lactation (udder oedema early lactation in heifers)
- milkers
- milking equipment
- environment (faecal contamination muddy)
- teat damage by injury or viruses
List the more common causes of mastitis and explain their origin and how they reach the mammary cells ?
The common causes of mastitis
Infection of the mammary gland can be either via the haematogenous route or more commonly ascending from the teat canal.
Haematogenous or lymphatic spread
- Mycobacterium bovis
- Brucella abortus
- the above bacteria often become trapped in the mammary lymph nodes and are decimated from there (both are notifiable)
- Leptospirosis flabby udder
Bacteria that enter the teat canal and are spread within the herd are described as contagious
- Staphylococcus aureus
- Escherichia coli and Streptococcus uberis (faecal contamination) usually affect single animals.
- Streptococcus dysgalactiae
- Pseudomonas aeruginosa only results in disease after the cow has been repeatedly treated with antibiotics
- Trueperella pyogenes + Cornybacterium pseudotuberculosis (abscess and severe mastitis)
Describe blue bag its’ cause, transmission and pathology ?
Blue bag is mastitis in sheep
Cause. Staphylococcus. aureus and Mannhemia haemolytica
Transmission =
The infection usually occurs shortly after birth or at weaning.
Lambs/kids will spread the infection between mothers as they carry the bacteria in their oral cavities. Once a ewe is infected she may boot her lamb due to pain who will then attempt to suckle another ewe.
What are the four most common causes of mastitis in South Australian dairy herds ?
Describe the cause, transmission, pathogenesis and clinical signs of postpartum dysgalactia syndrome (PPDS) in sows ?
Postpartum dysgalactia syndrome (PPDS)
Cause = Escherichia coli / Klebsiella species
Transmission = sows being maintained in faecal rich environment
Pathogenesis
Endotoxin from these bacteria stimulate macrophages to release inflammatory cytokines which reduce the production of prolactin. This causes a loss in milk production even within unaffected teats.
Clinical signs
- suckling pigs decrease in size, restless and cry alot
- sow may lay on cool grand to reduce the heat in her mammary
- sow will avoid suckling due to pain
- sow will pant a lot and become restless
Diagnose the causes of mastitis and interpret antimicrobial susceptibility tests?
Diagnoses of mastitis and interpretation
Once mastitis is suspected
Screening test
1. Collect a milk sample into a strip cup and observe for clotting, unusual colour, consistency and odour
2. Milking machines / robotic milkers have in line conductivity test
- increased conductivity is due to increased sodium and chloride ions with decreased potassium ions and lactose indicating mastitis.
3. Rapid test
Detect the enzyme lactate dehydrogenase (LDH). This enzyme acts as a marker of mammary cell changes as they are released by lysosomes when the mammary cells are damaged.
Somatic cell counts
These can either be collected on individual cows or on the bulk tank.
- detect sloughed epithelial cells, secretory udder cells or leucocytes
- high numbers indicate a case of mastitis
Direct somatic cell counts
- microscopy
- automated cell counter (Fossomatic gold standard)
If the somatic cell count is greater than >400,000/ml the milk will be discarded.
Bacterial cultures and identification of individual milk samples is carried out if SCC > 2*105/ml milk.
Explain the principles of mastitis Treatment ?
The principals of mastitis control
Acute mastitis = fever reddened and swollen mammary
Peracute mastitis = high fever, purple udder, inability to rise
- pathogen based treatment
- generally acute infections with gram negative bacteria will self cure so need to treat with antibiotics
Peracute mastitis = high fever, purple udder, unable to rise
Chronic mastitis = more than 100 days in duration
Poor prognosis cows with >3 episodes or a SCC >250,000 cells/ml in consecutive lactations should be culled
Cases of subclinical mastitis are usually treated via dry cow therapy. By using a long acting intramammary antibiotic injected into each quarter at the end of lactation to eliminated persistent infections.
Dry cow therapy is where the majority of antibiotic are used on farm as there is no long a withholding issue. To reduce this do not treat cows with less than <1 Mastitis episode over milking and low SCC prior to dry off
Describe the bacteria within the genera Acinomycetota ?
What is the purpose of Mycolic acids ?
Genera Acinomycetota
This genera contains pathogens including Actinobaculum, Actinomyces and Corynebacterium and trueperella.
- These are gram positive pleomorphic rods or filaments
- Tend to be intracellular pathogens (intracytoplasmic niche in phagocytic cells)
- Non-motile
- Facultative anaerobes
Are known to cause a pyogranulomatous infection in soft tissues
Mycolic acids
* All contain an outer cell membrane rich in mycolic acids (this makes them more resistant to intravesical destruction.
Describe the cause, route of transmission, target cells and virulence factor of Corynebacterium pseudotuberculosis ?
Corynebacterium. pseudotuberculosis
Caseous lymphadenitis sheep and goats
ulcerative lymphangitis in cattle and horses
Also known as cheesy gland
The source = the mucosa
Transmission =
* shearing, food, or trauma or coughing of sheep with abscesses
* enters through wounds
Target cells = neutrophils and macrophages
Virulence factor = Phospholipase D
Results in hydrolysis of sphingomyelin causing cell destruction and bacterial spread. Kills macrophages haemolysin and bacterial icterus
Describe the cause, pathology and clinical signs of cheesy gland ?
Cheesy gland = Corynebacterium
Pathology
C.pseudotuberculosis enters via wounds causing an expanding non painful lesions at the regional lymph node. From here it may spread via blood or the lymphatic system and causes abscessation of internal lymph nodes or organs (visceral or internal form).
The slow developing abscesses contain concentric rings of inspissated pus and fibrous tissue giving an onion like appearance.
Phospholipase D
Results in hydrolysis of sphingomyelin causing cell destruction and bacterial spread. Kills macrophages haemolysin and bacterial icterus
Clinical signs
Abscessation of regional lymph nodes and internal organs
Slow developing – laminated abscesses “onion skin”
* This disease results in carcass trimming and downgrading.
* In wool sheep it decreases clean fleece yield
* Internal abscesses in the lungs can cause chronic weight loss (thin ewe syndrome) even death
* One of the most important causes of weight loss in sheep
* The incidence of abscesses steadily increases with age
* High fever, anorexia, anaemia and cellulitis at the infection site
Pus is usually cream to slightly green or red tinged and does not have a bad smell.
Describe the route of transmission, target cells and virulence factor of Trueperealla pyogenes?
Truepearella. pyogenes
Skin abscessation and internal organs
The most common cause of abscesses in cattle and pigs.
Transmission = wounds ticks, food, wires and feet
Target cells = neutrophils
Pyolysin
A haemolysin cholesterol dependant porin, often found together with obligate anaerobes
Describe the pathogenesis and clinical signs of Trueperealla. pyogenes?
Trueperealla pyogenes
The most common cause of abscesses in cattle and pigs
Pathology
Skin abscessation and internal organs - brain, lungs and join
- Watery to creamy consistency, colour grey-green, foul odour
Pyolysin
A haemolysin cholesterol dependant porin, often found together with obligate anaerobes
Clinical signs
* Sitting lamb disease where the tail has been docked too short.
* Cattle with micro-damage to the lumbar vertebrae through excessive riding
What could result in the rare condition of pituitary abscess syndrome ?
Trueperealla. pygenes
An unusual condition is pituitary abscess syndrome
where the purulent exudate and necrosis will develop in the pituitary fossa and adjacent organs in sheep – potentially secondary to ear infections or head butting.
Clinical signs
- Head pressing bulging eyes, abnormal stance and recumbency
- Lesions are often unilateral and result in cranial nerve malfunction
- Diagnose through the presence of bacteria and neutrophils in the spinal fluid
What is the cause, transmission route and virulence factor of lumpy jaw ?
Actinomyces. bovis
Actinomyces is an obligate anaerobe that is a commensal of the oral cavity of cattle
Source = oral mucosa
Transmission = Periodontitis due to coarse feed or entrapment of grass awns, wounds in the mouth. Associated with a change in teeth.
Cholesterol dependent pyolysin
Elicits the splendore Hoepli phenomenon a protective inflammatory derived layer.
Describe the pathogenesis and clinical signs of lumpy jaw ?
Lumpy jaw = Actinomyces. bovis
Pathogenesis
It causes a slowly progressive granulomatous disease of the jaws of 2-5 year old cattle known as lump jaw.
* Lumpy jaw – usually soft tissues and bones of the face. Can gravitate into the lungs.
* Initially cause soft tissue inflammation and then penetrate into the bony tissue
* Slowly developing, grey, watery, large splendore-Hoepli bodies
Clinical signs
* Infection of the bone causes a chronic inflammatory response characterised by the presence of yellow granules known as Splendore hoepli bodies “sulphur granules” and pus
* Distruction and remodelling of the bone results in an enlargement of the affected bone and facial distortion
* The bone takes on a honey comb appearance and is easily fractured
Cholesterol dependent pyolysin
Elicits the splendore Hoepli phenomenon a protective inflammatory derived layer.
Describe the source, route of transmission and virulence factor of Actinobacillus lignieresii ?
Actinobacillus ligniersii Wooden tongue
Gram negative bacillus rod
Source = oral mucosa commensal
Transmission = lesions follow damage to the mucous membranes
Cholesterol dependent pyolysin
Elicits the splendore Hoepli phenomenon a protective inflammatory derived layer.
Pathogenesis
Wooden tongue – soft tissues of the head.
Identify and manage cattle suffering from contagious pyelonephritis ?
Bacterial infections of the urinary tract are most common in multiparous, post parturient cows (about 83 days post partum).
The disease is sporadic and its prevalence low
Cause = Corynebacterium. Renal, C. cystitidis and C.pilosum
These bacteria are commensals of the vagina and prepuce and can be spread from cow to cow via urine droplets.
Predisposing factors = Anatomical defects (IE trauma due to partus), high protein diet increasing urine PH is conducive to tcolonisation and proliferation of bacteria.
Pathogenesis
The bacteria once infecting the bladder move up the urinary tract and usually produce the enzyme urease.
- Urease allows the bacteria to utilise urea as an energy source
- Majority of damage is associated with the cellular response.
- Initially Haematuria (presence of blood in urine)
- Fever, anorexic and urinate frequently
- Colic
- Polydipsia and polyuria
Diagnosis
Based upon the clinical picture and confirmed by blood chemistry (high urea and creatinine levels)
Carry out urine examination and culture.
Treatment = penicillin or potentiated sulphonamides for Corynebacterium infections
Compare the epidemiology of the porcine cystitis-pyrelonephritis complex with opportunistic infections of the urinary tract in pigs?
Actinobaculum. suis
- Frequent urination with blood-stained urine
- Confirm diagnosis through culture
Describe the morphology of the Cornebacteriales ?
Corynebacteriales = Rattles, Dermatophilosis and Nocardiosis
All bacteria within the order Corynebacteriales have an outer membrane rich in fatty acids and tend to be environmentally resistant.
Nocardia and Dermatophilus – produce bacterial spores further enhancing their environmental survival.
Prescotella equi the agent of rattles
Characteristic of genera Corynebacterialles
- Soil inhabitants (few exceptions)
- Gram positive rods
Describe the epidemiology, transmission and virulence factor of Prescottella equi ?
Prescottella equi Epidemiology
Prescottella equi is the cause of chronic bronchopneumonia and typhlocolitis in 1-6 month old foals. (peak 6-12 weeks of age in foals).
This is a non-spore forming bacterium which forms rods in culture and a coccus in the host. Prescotella equi is an opportunistic pathogen in other animals/humans and can infect any tissue (especially the skin and RS)
Epidemiology
- Soil saprophyte prefers to grow in warm soils, that are high in manure (containing volatile fatty acids).
- Can be found in the manure of all herbivores
- Equine virulent strains (carry in a plasmid genes that encode for VAPA protein) have a preference for horse manure
- Grows in the large intestine of foals (<12weeks of age)
- More common in horse breeding facilities where Prescottella equi has time to build up over many years.
Infection = inhalation of dust particles by foals
Usually infected when antibodies obtained from colostrum is declining
VapA
Reduces lysosome maturation and prevents acidification of the phagolysome.
Describe the pathology and clinical signs of Prescottella equi ?
Prescottella equi
Pathology
Once inhaled the bacterium will enter the alveolar macrophages and stimulate an inflammatory reaction.
- This leads to a multifocal pyogranulomatous inflammation
- Bacteria coughed up from the lung are swallowed and result in typhlocolitis
Macrophages are not effective, the bacterium can survive and multiply in the phagocytic vesicle by preventing its maturation with virulence factor VAPA
Virulence factors VAP
- Are produced by equine strains of P.equi in the phagocytic vesicle when the temperature is greater than 34 degrees.
- VapA reduces lysosome maturation and prevents acidification of the phagolysome.
Clinical signs
The early stages of disease are difficult to detect. Affected foals develop a low grade cough and wheeze, fever.
- Often appear bright and suckle well until critically ill
- Days later respiratory rate increases
- Diarrhoea in 50% of foals
How would you go about making a diagnosis and treating a case of Prescottella equi?
Prescottella equi
Diagnosis
- Thoracic ultrasound examination every two weeks until two months of age
- Age of animal and clinical signs
- Presence of opaque densities in a radiograph of the lungs
- Conformation by the presence of intracellular bacteria and alveolar macrophages on TTWW cytology
- Transtracheal wash and culture of P.equi
- PCR to detect ChoE and vapA genes
Control
- Foals with lung abscesses <10cm2 in total may recover even without antibiotics
- Target foals with large lung abscesses
- Very few antibiotics able to penetrate cells as well as abscesses
- Control is based on rotation of foaling and foal camps, sunlight exposure and regular removal of faeces
- Potential use of firing where foals are fed a live virulent strain at 2,7 and 14 days of age to stimulate immunity (natural epidemiological cycle of P.equi)
The most effective treatment is prolonged oral with a combination of macrolide (erythromycin, clarithromycin) and rifampin. These combinations need to be used for at lesat one week post cure.
It is possible to utilise immune stimulants to increase the production of cytokines such as IL-6 and interferon gamma. (hyperimmune plasma)
No vaccine is commercially available as of yet
Describe the pathology, diagnosis and treatment of Nocardiosis ?
Nocardiosis - granulomas which rupture
This is a rare disease in animals;
Gram positive, filamentous, branching bacteria produce spores in their aerial filaments or hyphae.
Common soil microbe that will infect animals usually via skin wounds.
Pathogenesis
- Able to survive within phagocytes as the mycolic acids in their cell walls inhibit phagosome-lysosome fusion.
- Induce localised granulomas that rupture draining a viscous pus which is often red tinged, containing microcolonies of Nocardia
- Splendore hoepli bodies (sulphur granules)
- Common infection of the udder in cattle
- In cats and dogs lesions of the skin, mouth and thorax
- Nocardial abortions may occur in horses and pigs
- Zoonotic cutaneous, eye and pulmonary infections in people.
Cytology
- can acid stain
- will grow on Sabourad’s agar
- Dermatophilosis will not acids stain or grow on Sabourad’s agar.
Describe the characteristics and transmission and epidemiology of Dermatophilus congolensis infections ?
Describe Dermatophilosis in animals – Dermatophilus congolensis infections
Dermatophilus congolensis, is an exudative to proliferative pustular dermatitis which is chracterised by scab formation.
- Usually affects cattle, sheep and horses + zoonotic occasionally affecting humans
- More prevalent in tropical areas with high rainfall (rain scald)
- This disease results in damage to hides, decreased productivity IE drop in milk production, and rarely death.
Epidemiology
Infection occurs via the skin either by direct contact with an infected animal or indirectly from plants/insects, ectoparasites.
- Wet skin and lesions are attractive to flys
- Trauma (constant wetting, bites portal of entry)
- Prolonged wetting of the skin such as that which occurs during the rainy season results in emulsification of the protective sebum layer and maceration of the stratum corneum of the skin facilitating the spread of disease.
Describe the how animals become infected and the pathogenesis Dermatophilus congolensis infections ?
Dermatophilus congolensis
Infection
The resistant endospore form, when in contact with water will lose its outer layer and become a zoospore (flagella) that can attach to the skin. Once attached it germinates to produce branching filaments. These produce parallel rows (typical morphology of endospores).
- Zoospores are chemotactic to CO2 that diffuses through the skin
Pathology
Alternating layers of exudate and thick laminated crust
After germinating the branching filaments of D.congolensis invade the living cell layers of the epidermis and sheaths of hair and wool follicles.
- Extensive proliferation of the organism occurs
- They stimulate kertinisation of the epidermis and induce an acute inflammation reaction, that is characterised by the accumulation of an exudate rich in neutrophils beneath the invaded part of the epidermis
- The organisms do not penetrate the layer of exudate
- The new epidermis is forming under the exudate is invaded from the side
- Once enough skin is infected it forms a thick laminated crust composed of alternating layers of para and orthokeratotoc hyperkeratosis and exudate
Alternating layers of hyperkeratosis and exudate
Immunity is primarily cellular
Describe the clinical signs of Dermatophilus congolensis infections ?
Dermatophilus congolensis
Clinical signs
- Vary in severity
- Mild cases may only be detected on palpation of the hair coat and fleece
- Acute – chronic cases localised to widespread lesions
- Exudative to proliferative epidermitis
- Subsequent formation of scabs and crusts
- Under the scabs hair tends to matt or break leaving detached raw areas
- Strawberry fotrot, lumpy wool in sheep, localised and generalised lesions
Describe how you would go about diagnosing and treating an outbreak of Dermatophilus congolensis ?
Dermatophilus congolensis
Diagnosis
The diseases is suspected when there is an outbreak of proliferative dermatitis (exudative lesions and skin crusts) in more than one species of animal during the wet season.
- Confirm diagnosis examination of biopsy material from lesions
- Smears prepared from affected skin (gram stain, Giemsa, CAMs quick). Examine for the presence of branched filaments that are transversely and longitudinally septate
- DOSE not stain acid fast
- Small B haemolytic colonies
- Concave base of freshly removed scabs
Control of Dermatophilosis
Cattle are rarely treated as in most cases symptoms are limited and will heal when conditions become dryer
Sheep
- Isolate from infected sheep
- Cull chronically affected sheep
- Avoidance of excessively wet pastures
- Tick and fly control
- Good dip tank management (drain regularly)
- Carry out shearing and dipping during dry times of the year
- No vaccine
- High value animals may be treated with oxytetracycline
Horses
Since the condition in horses is unsightly and possible zoonotic treatment is carried out
- Emollients or gentle bathing of crusts with warm water and soap wil add in the removal of thick crust. (daily chlorhexidine , benzoyl peroxide)ghg
- Severe lesions treated with antibiotics penicillin / streptomycin
- Keep animal equipment clean and dry
Describe the morphology of the mycobacterium ?
Pathogenic members of mycobacterium and related genera are known to cause chronic garnulomatous lesions in people and animals.
- Thick mycolic acid layer covering the peptidoglycan layer in the outer membrane
- Resistant to desiccation and improves their survivability in the host (especially the monocyte macrophage)
- Slow to replicate (slowest being Mycobacterium avium every 12 hours)
- Facultative intracellular parasites (survive cytoplasm and phago-lysosome)
- Chronic insidious (presence only revealed late in the disease process)
- Poor antigenicity of the cell wall
Effective immunity is predominantly cell mediated.
A special acid fast stain known as the Ziehl Neelsen stain will stain them a deep red. (other bacteria stain blue, green of the counter stain)
Why is it not possible to gram stain the mycobacterium ?
Mycobacterium
- Thick walls rich in mycolic acids are impermeable to the usual method of gram staining (gram positive beaded rods if visible)
- Able to resist acid degradation in the phago-lysosome within macrophages
- Gram positive
- Rarely take up the gram or Romanoski type stains. The stain must be heated to render the wall permeable to stains like other bacteria.
- Resist a strong acid decolouristaion.
A special acid fast stain known as the Ziehl Neelsen stain will stain them a deep red. (other bacteria stain blue, green of the counter stain)
Describe the general transmission, virulence factor and pathogenesis of mycobacterium species ?
Mcobacterium
Transmission = Enter into the body either through inhalation, ingestion or percutaneously.
The local phagocytic cells (receptor dependant) phagocytose the mycobacterium. Being receptor dependant (antibody dependant killing is not induced). This allows mycobacteria to survive and divide in phagocytic cells.
To kill mycobacteria requires activated macrophages ie those primed by interferon Y produced by differentiated TH1 cells by the respiratory burst or phagosome acidification, phagosome – lysosome fusion. This is augmented by cytotoxic T cells that lyse infected macrophage releasing the bacteria and thus making them accessible to the immune system.
Amycolic acid
In the cell wall known as trehalose dimycolate (TDM) or “cord factor” is thought to assist in protecting the bacteria from phagocytic killing, especially the action of gamma interferon.
The infected macrophages recruit other macrophages to the site of infection ensuring a predominantly granulomatous inflammation.
As more cells are recruited they re-organise into discrete granulomas or tubercules. These granulomas typically consist of a central area of necrosis, sometimes with minerlisation surrounded by giant, epitheloid cells, lymphocyts and fibroblasts encased in a collagen layer.
Describe the epidemiology and transmission of Mycobacterium tuberculosis variant bovis?
Mycobacterium bovis
Epidemiology
In many countries including Australia bovine tuberculosis is a notifiable disease. This is not just because it is a chronic debilitating desease but also because the agent is zoonotic
- Affects the lymphohematogenous system
- Primary lesions common in the lower respiratory tract
- People = dead end host
- absent in Australia
Bovids such as cattle and buffaloes are the primary maintenance hosts, the bacterium is able to infect a wide range of animals including humans, dogs, badgers and possums.
Transmission = inhalation and ingestion h
Describe the pathology and clinical signs of mycobacterium tuberculosis bovis ?
Mycobacterium bovis
Pathology
Transmission = inhalation or ingestion
The bacteria are then ingested by macrophages and transported to the nearest lymph node. Inflammation at the site of entry and the regional lymph node is know as primary complex.
If the animal has incomplete immunity the lesion/s will enlarge slowly eventually resulting in significant tissue damage and clinical disease. Bacteria may remain viable in thses lesions and reactivate years later where they may disseminate through out the body and cause numerous small areas of necrosis and ultimately the clinical presentation of disease.
Clinical signs
- Gradual weight loss
- Persistent cough (lung infection)
- Especially noticeable on exercise or when the animal gets up after a period of rest
- Enlarged lymph nodes
- M.bovis usually results in lesions of the lung and associated lymph nodes however any organ may be affected.
Describe how you would go about diagnosing and treating a outbreak of mycobacteria tuberculosis bovis ?
Mycobacteria tuberculosis bovis
Diagnosis
Confirming the diagnosis of Bovine tuberculosis is critical as a positive result often ends in the animal being killed.
- Based on the presence of a specific immune response
Intradermal tuberculin
Test where an infected animal will show a localised area of inflammation 2-3 days after a purified protein derivative (PPD) suspension of the bacteria has been injected into the skin.
-48-72hours
-Neck caudal fold of the skin
-Type 4 hypersensitivity response (can utilise calipers)
-Animals in the late stage of tuberculosis may become insensitive to the intradermal test
-Late stage = ELISA measurable antibodies and clinically thin, enlarged superficial lymph nodes, cough)
Positive animals are slaughtered and examined for any granulomatous lesions. Particular attention is paid to the lymph nodes of the head, thorax and udder.
Lesions are collected and submitted for organism detection by culture and qPCR.
-Radioisotope broths are used to speed up the process (extremely slow growing may take upto 2 months)
-typical granulomatous response numerous giant, epitheloid and a central area of necrosis that may contain areas of minerlisation.
Control
Australia has been declared free of the disease by WOAH.
- Routine surveillance completed at the abattoir by meat inspectors
- “stamping out”
- Strict importation regulations, permits
Describe the cause, transmission of Johne’s disease in ruminants and alpacas ?
Johne’s disease
Epidemiology
Mycobacterium avium ssp. Paratuberculosis (Mptb) is the agent of paratuberculosis or Johne’s disease.
A slowly progressive granulomatous disease of the intestine that affects predominantly ruminants (zoonotic). Since it is a very slow developing disease it may not be recognised within a herd for many years.
The disease caused by sheep strains of Mptb are endemic in many states of Australia, less common are the cattle strains of MpTB.
Transmission = usually to calves in utero (26%), and other young animals within the first few weeks of life. (faecal oral route, maternal milk)
Repeated exposure to the agent is required for infection.
Describe the cause, pathology and clinical signs of Johne’s disease ?
Johne’s disease (Mycobacterium avium sp. Paratuberculosis)
Pathology
Oral infection with this slow-growing mycobacteria results in phagocytosis by macrpphages in the lymphoid tissue of the small intestine.
The intestinal wall becomes thickened due to the proliferation of large numbers of epitheloid cells and will resemble the gyri of the brain.
- Spreads haematogenously
- Diffuse granulomatous inflammatory response occurs in the distal intestine (ileum)
- Intestinal lymphatics and associated lymph nodes
- Incubation 15-18 months
- Intestinal wall thickening and poor nutrient absorption
Clinical signs
The progressive granulation of the intestinal mucosa gradually leads to
- Malabsorption
- Diarrhoea
- Hypoproteinaemia
- Emaciation and death
- Bottle jaw
- Extremely hungry
- Lymphagiectasia (epitheloid cells block the lymphatics becoming twisted and having a glassy appearance.)
Only one in 20 infected animals will show clinical evidence of disease.
Describe how you would diagnose and treat an out break of Johne’s disease ?
Johne’s disease (Mycobacterium avium sp, Paratuberculosis)
Diagnosis
Due to its long incubation period and non-specific clinical signs, the disease in live animals can be difficult to diagnose.
Since animals shed bacteria prior to the development of clinical signs and maintain appetite diagnosis must be made early
- Farm history
- Presence of emaciation and diarrhoea in older animals (>2 tooth)
- Abattoir surveillance
- Acid fast staining of rectal swabs and serology to screen animals (pink cocci)
- Preclinical stage = ELISA tend to be positive just prior to clinical signs (herd test)
- Clinical stage = Pooled culture of faeces qPCR by a certified laboratory (ion chelating agent known as mycobactin J) can take 2-3 months to culture
Describe the control of Johne’s disease
This is a notifiable disease in Australia states and territories and control is based upon the disease status of the state and whether the individual farm is accredited free.
Johne’s disease is a category 1 restricted matter and under the biosecurity act.
- Quality assurance program SheepMAP, goatMAP, alpacaMAP
- Vaccination is possible Gudiars bacterin vaccine for endemic farms
- All positive animals should be culled
Describe the morphology and common sources of the enterobacteriales ?
Morphology of the Enterobacterioles or coliforms
Coliforms especially E.coli are amongst the most common group of bacteria identified in Veterinary diagnostic laboratories.
- Gram negative
- Non spore forming
- Mostly motile
- Oxidase negative
- Facultative anaerobic
- Rod or coccobacilli
- collectively known as coliforms
The most pathogenic members of this enormous order are Escherichia coli and Salmonella enterica.
Escherichia coli, Salmonella species, Yersinia and Klebsiella spp and Proteus sp.
All members of this family have an endotoxin as part of their cell wall and therefore the potential to cause endotoxaemia.
The natural habitats of the enterobacteriales
Most pathogenic members are found in the gastrointestinal tracts of animals where they reside as intestinal commensals.
Describe the characteristics we can use to differentiate between E.coli and Salmonella?
E.coli vrs Salmonella
E.coli
MacConkey agar = which contains bile salts and crystal violet is one agar designed to selectively allow the growth of the class E.coli a lactose fermenter on agar.
- Produces indole
- XLD yellow colonies
Salmonella enterica
- Non lactose fermenter on MacConkey agar
- XLD reduces iron salts to hydrogen sulphide (black colonies)
- Dose not produce indole
- Citrate positive
Isolation on xylose-lysine-deoxycholate (XLD) Salmonella
In addition various typing schemes are used and include
- Serotyping antigens; flagella H antigen, Capsule K antigen, O antigen outermembrane polysaccharide chain. (only smooth colony types of Escherichia coli on MacMonkey agar – thick outer membrane can be serotyped)
- Biotyping – arrays of biochemical and phenotypic test
- Phage typing
- Genotyping – shigatoxin specific genes for virulence factors
- Genetic fingerprinting
Describe the most common ways in which animals become infected with the enterobacterioles ?
Describe the general pathogenesis of the enterobacterioles
Diseases caused by the enterobacteriales fall into three categories
- Enteric disease with diarrhoea
- Septicaemia
- Localised pyogenic infections
Since these bacteria are ubiquitous disease only occurs when the predisposing factors associated with the animal host, environment or agent occur.
Host factors
- Age neonate, genetic F4 piglets, immunity
- Stress, nutrition or concurrent infections
Environmental factors
- Chilling eg temperature
- Overcrowding and faecal rich soils, increases the exposure to pathogens
Agent factors
- Only those members that are able to adhere to the intestinal tract and produce toxins or invade the host will cause disease.
There is a balancing act
Transmission = faecal oral route
Occasionally the respiratory, urogenital or wounds may act as ports of entry.
Umbilicus in a neonatal animal where entry via this route leads to a localised infection which spreads to the rest of the body via blood vessels (haematogenous).
Describe the pathogenesis of septicaemia resulting from gammaproteobacteriaceae?
Describe the pathogenesis of septicaemia?
Members of the gammaproteobacteriaceae all have liposaccharide (LPS) as a component of their outer cell membrane. The pathogens have factors that allow them to attach, invade, overcome the host’s immune defences and multiple within the host.
Animals who have not received sufficient maternal antibodies or have not developed a strong adaptive immunity are prone to these infections.
Septicaemia when it develops is usually a endotoxemia as once the bacteria have proliferated they die, and release their LPS which set of the systemic inflammation cascade.
Describe the pathology and clinical signs of colibacillosis and colisepticaemia ?
Describe the Escherichia coli infections “colibacillosis”
Escherichia coli is the cause of colibacillosis (diarrhoea or septicaemia) in neonatal calves, lambs piglets, pups and chicks.
In some instances also cause opportunistic infections such as environmental mastitis cows, urinary tract infections and ear infections dogs.
Colisepticaemia
Watery mouth in lambs (Colisepticaemia)
Colisepticaemia is caused by virulent strains of E.coli and is more common in neonatal animals who have not received sufficient maternal or passive immunity.
Pathology
Prominent clinical signs noted in neonatal lambs between 12-72 hours of age that are suffering from colisepticaemia.
Transmission = E.coli ingestion
- These lambs are usually born in dirty camps, come from multiple births and have failed to obtain sufficient colostrum.
- The ingested E.coli proliferate in the intestine releasing endotoxins which result in intestinal hypomotility
- The endotoxins can then be taken up systemically
Clinical signs
- Dull
- Wet mouth excessive salivation
- Eyes appear puffy
- The abdomen is often distened
Watery mouth is diagnosed by culturing E.coli from a whole blood sample.
Treatment = fluids, glucose, anti-inflammatory drugs and a bacteriostatic antibiotics early in disease may be successful.
Describe the enteritits types ETEC, EPEC and STEC caused by the Escherichia coli strains ?
Enteritits caused by Escherichia coli strains
Enteritis in the neonatal animal occurs in animals that have failed to receive maternal immunity and is caused by different pathogenic strains of E.coli
- Enterotoxigenic E.coli (ETEC) – most common
- fimbrial antigens F4, F5,F^ and F41 and heat labile toxins LT
- exotoxin educes upregulation of membrane pumps leading to hypersecretion of ions followed by water
- white scours - Enteopathogenic E.coli (EPEC)
- more severe / lesser known / some animals develop dysentery
- intimin type three secretion system
- stimulate actin reorganisation = pedestrals - Enterohaemorrhagic or shigatoxin producing E.coli (STEC)
- STEC = enterohemorrhagic shigatoxin
- A portion attaches to ribosome 28 removing an adenine residue preventing it from interacting with elongation factor halting protein synthesis = cell death
Describe the pathology of E.coli (ETEC) ?
- Enterotoxigenic E.coli (ETEC) Enterotoxigenic
ST and LT - Guanylate cyclase and ADenylate cyclase
Pathology
ST and LT - Guanylate cyclase and Adenylate cyclase
E.coli strains with the fimbrial antigens: F4,F5,F6 and F41 adhere to the brush border of the intestinal cells and produce a heat stable (ST) or heat labile (LT) toxins.
These toxins are internalised in the cells and adhere to guanylate cyclase and adenyl cyclase receptors respectively increasing the production of cyclic guanosine.
Monophosphate (cGMP) and cyclic adenosine phosphate (cAMP).
Both affect the ion channels within the cell membrane by increasing ion loss and reducing ion intake.
- Intestinal lumen high osmolality than the cells causing water loss into the intestinal lumen by osmosis
- Acts as a water pump drawing water from the interstitium through the intestinal epithelium and into the intestinal lumen across a water gradient
This results in dehydration and metabolic acidosis in untreated animals can lead to death.
There is no structural damage of the intestinal cells.
Clinical signs
- Whitish watery diarrhoea (white scours)
- Severe dehydration
Describe the pathogenesis of EPEC in piglets
E.col (EPEC) Enteropathogenic
EPEC is a lesser known cause of diarrhoea in calves, piglets and pups. Since the colon is usually more severely affected, some animals will develop dysentery. It can even be a common infection in children.
It affects neonatal and animals up-to 2 months of age.
This group of pathogens produce an adhesion protein known as intimin (Type three secretion system) that adhere tightly with the enterocytes and stimulate and stimulate actin reorganistaion of the enterocyte cytoskeleton to form pedestrals.
These pedestrals improve the contact of the bacterium with the cell.
- Decreases absorptive surface
- Interferes with ionic exchange
- Bacterium presence stimulates an inflammatory response
- While most of the intestinal tract is affected the colon has the most severe lesions
Most strain of EPEC will produce shigatoxin – however its affect is more important in people.
Describe the pathology of Enterohaemorrhagic or shigatoxin E.coli (STEC)
E.coli and shigatoxin pathology
Zoonotic – once common in children who visited petting zoos
EHEC strains produce intimin leading to the typical attaching and effacing lesions as well as shigatoxin.
STx1 and STx2 both shigatoxins have the same mode of action.
After attachment E.coli produces shigatoxin, an A-B toxin (B toxin = porin) that is taken up by the cell via endocytosis.
The vesicle moves to the endoplasmic reticulum, where the A portion moves out of the vesicle and attaches to ribosome 28s.
Shigatoxin removes an adenine residue from the ribosome, preventing it from interacting with ELONGATION factor.
This halts protein manufacture and the cell dies.
Describe the cause, transmission, pathology and clinical signs of Oedema disease in pigs ?
Oedema disease in pigs (shigatoxin)
Oedema disease is a sporadic, global disease in commercial piggeries caused by shigatoxin ST2e-producing strains of E.coli
Pathology
The ST2e associated damage of the arterioles results in widespread oedema. The piglets have swelling.
Odema is present in the greater curvature of the stomach, between the mucosa and the muscle layers. Jelly like areas of oedema may be present in the mesocolon, larnx and the kidney capsule.
Clinical signs
- 30% of the best piglets
- Outbreak by deaths in some and nervous signs in others
- CS usually appear 10 days after weaning
- Swellin eyelids, snout and ears
- Brain odema results in apparent blindness
- Head pressing and incoordination
- Lay down with paddling movements
Diagnosis
- Clinical signs
- Culture beta haemolytic E.coli that contains genes coding for F18 and ST2e
- ST2e detection in the intestines and bloodstream
- Use only fresh carcases for toxin identification
Treatment =
- Water medication with ampicillin, teracyclines , neomycin or potentiated sulphonamides
- Limit disease by adding zinc oxide to the diet
- Restrict feed intake and increase the roughage
- Depopulate, sanitise and repopulate after three weeks
Describe uropathogenic E.coli (UPEC) in dogs ?
Uropathogenic E.coli (UPEC) in dogs.
Female dogs are susceptible to infections with uropathogenic E.coli.
Intestinal commensal E.coli colonises the vaginal and periurthral tissue and moves up the urethra to the bladder (ascending infection).
Pathology
P fimbriae and fusiform vessicles
These bacteria have special adherence fimbriae, P fimbriae that attach to the bladder epithelium of dogs.
- Forming biofilms
- The biofilms protect the bacteria against flush out and antibiotic destruction.
- Fusiform vesicles (assist the bladder in stretching and returning to its normal size), these same vesicles assist in the internalisation of E.coli into cells.
- E.coli in these vesicles rapidly multiply and persist in the bladder epithelium.
- Stimulate inflammatory response
Clinical signs
- Cystitis
- Increase in bladder cell turnover
Uropathogenic strains produce haemolysins and thus are beta- haemolytic on blood agar.
E.col has a further adaptation to beta-lactam antibiotics- some strains are not killed but produce cross walls and daughter cells. These become elongated forming long filaments.
Describe the the clinical signs of salmonellosis and the three different carrier types ?
Salmonella - salmonellosis
In mammals and birds, salmonella enterica and occasionally salmonellae of reptile origin are responsible for salmonellosis.
Salmonellosis is characterised clinically by
- septicaemia, acute enteritis, chronic enteritis
- extraintestinal infections such as abortion or joint ill
Although the disease affects all animals it is particularly prevalent in stressed animals kept in high densities. (intensive farming)
In salmonella there are 3 types of carrier states
1 Active carriers; individuals infected and actively shedding in stool. Animals still shed salmonellae for a period following recovery.
2 Latent carriers; individuals are infected with salmonella but the bacteria is inactive. During periods of stress the bacteria may activate and start shedding. (intestinal lymphatic tissue)
3 Passive carriers; The uninfected individuals pass the bacteria intact through the intestines. They will not shed once removed from the source of bacteria.
Humans, animals and their environment which includes food sources are linked
The intricate web of salmonellae dissemination and faecal oral transmission
The environment
- Although the bacteria colonises and multiples in the intestinal tract, it can survive for several weeks in a dry environment, and even months in a moist environment. (ultra violet light and heating at 60 for 90mins will destroy the bacteria)
Describe the pathogenesis of Salmonella ?
Pathogenesis of salmonella
Macropinosome
Transmission = faecal oral route
Incubation period = 4 days
Salmonella uses fimbriae to colonise the small and large intestine and ‘M cells’.
Salmonella uses a molecular syringe to inject proteins into the cell.
Type 3 secretory system
These proteins effect a rearrangement of the cell actin proteins so that projections engulf the the bacterium in a macropinosome.
Macropinosome (vacuole excess extracellular fluid).
- These vacuoles are less subject to fusion with lysosomes (not phagocytic)
- They survive in the vacuole by delaying maturation, and making their outer membrane more resistant to attack.
- Bacteria can divide within these vacuoles
The vacuolated bacteria eventually move to the basement membrane end of the cell where they are released into the interstitium where they are engulfed in the same way by macrophages, dendritics cells and neutrophils.
Clinical signs
Necrotising fibrinous enteritis
- Serotypes causing an enteritis also initiate a secretory diarrhoea using shigatoxins and stimulate intestinal inflammation with the migration of neutrophils into the intestinal lumen.
- More sever enteritis than E.coli
- Lesions most severe in the lower ileum and the large intestine
- Thrombi in blood vessels
