Streptococci are gram +ve cocci that form chains of different lengths.. Streptococci are facultative anaerobes and require the addition of blood or serum to culture media. Streptococci are a group of bacteria which can cause pyogenic infections in many animal species.. Strephtococci have translucent and non motile greyish colonies. It does not use catalase and is sensitive to bile salts so therefore does not grow on MacConckey agar. Generally streptococci does not grow on simple media and generally survive poorly in the environment.

There are 3 laboratory procedures that are used for differentiating streptococcu. Type of haemolysis, lancefield grouping and biochemical testing. On sheep or ox blood agar, beta haemolussi refers to complete haemolysis indicated by clear zones around colonies. Alpha haemoloysi is partial haemolusis indicated by a greenish zone around the colonies.
Lancefield grouping is a serological methos based on group specific c substance in the cell wall. Pyogenic streptococci is associated with abscess formation, suppurative conditions and septicaemias. Beta haemolytic streptococci are normally  more pathogenic.

Streptococci are often commensals on mucosus membranes and many streptococci infections are opportunistic. Infections might be primary (strangles) or secondary like in streptococcal pneumonia following viral infection. Strangles (s.equi), porcine steptoccal meningitis and bovine streptococcal mastitis are important specific infections. Strangles is an important contagious disease in young horses caused by s.equi. it involved the upper respiratory tract with abscessation of regional lymph nodes. Streptococcus suis recognized to cause huge losses in the pig industry with meningitis, arthritis, septicaemia and bronchopneumonia in pigs of all ages. Streptococci agalactiae, s.dysgalactiae, and s.uberis are the principal pathogens involved in streptococcal mastitis. The difference between these is the type of haemolyssi produced on blood agar in adwards medium, id with lancefield groups and results of CAMP test. S.agalactiae is the only one that produces a beta hemolossi. And gives a positive CAMP test.

Adherence to epithelium, causing cytotaxis and adherence factors bind to extracellylar matrix proteins, just like staphylococcus. They produce inhibit hemotaxis (anti chemotaxis). Anti opsonic and anti phagocytic factors makes capsules, haemolsis streptococci are very haemolytic that act on white cells to inhibit phagolysis. M protein in unique to stephtococci. Can also produce superantigens that give toxic shock syndrome. Streptococci produce a range of DNA degrading enzymes like DNAase, and is therefore good at spreading in tissue.


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Non specific host defence- bacteria overcome it & how specific interact.

The non specific immune system consists of barriers like skin and mucous membranes. The immune system is non specific meaning it will react the same way weather it’s the first or second time its being attacked. The non specific immune system can have phagocytic cells, NK, complement (lyse/opsonise bacteria) or iron binding protein ( starve bacteria for iron).the innate immune system will slow down the phatogen. If the bacteria gets past this system the adaptive immune system will take over. The adaptive immune system is a slower response, but is pore precise. The main difference is that adaptive has antibodies T & B cells. The adaptive immune system have developed a memory : eg LPS has different O side chains and adaptive can develop ab against each type of O chain.

The skin epithelium and the epithelium lining the gastrointestinal tract, uritogenital tract and respiratory tract are part of the protective barrier of the innate immune system, some also secretes mucous that prevents the bacteria living on the surface. The epithelial lining provides a tight junction and mount a non specific chemical attach like the acidic environment of the stomach. If there is a hole in the epithelium so that the pathogens get through the barrier there are macrophages patrolling the lining. They have many receptors on their surfaces that recognise common pathoges (lipopolysaccharides/ liptoeichoic acids – found in the bacterial walls). When the mø’s recognises the pathogen they engulf them called phagocytosis. Once inside the lysosome(containting many different substaces like Nitric oxide, hydrogen peroxide, Lacroferrin can deprive bacteria of nutrients (iorn & B12) etc) will help destroy the pathogen. Once the mø’s are activated they secrete chemicals called cytokines that recruite other pahgocytes to the site if infection. These might cause inflammation that bring other effector cells to help fight the infectionand not allowing the pathogens to get into the bloods stream. Another aspect of the innate immune system is the activation of the complement cascade (enzyme cascade). There are 3 main outcomes of the complement. 1) more inflammatory cells are signalled to come to the site of infection. 2) the pathogens are opsonised (pathogen surface is coated with protein- making them easier to recognise) for the  phagocytes to engulf and destroy the pathogen. 3) pathogens are directly killed.

Some bacteria have a capsule (made of polysaccharides) that will protect the bacteria from phagocytosis. Without help phagocytes find it hard to deal with capsulated bacteria.



Acquired immune system: the main focus is to amplify and focus the activity of the components of the innate immune response. Making complement and phagocytes more efficient. Memory is very important to have a quicker response the next time it encounter the bacteria with a more amplified response. Dendritic cells engulf bacteria and break down the pathogens to present them on the surface of the cell. This leads to activation and proliferation and differential of lymphocytes.  T cells provide stimulus that allows B cells to prolifereate and then differentiate into lymphoblasts. This again helps macrophage activation.

Many intracellular bacterial pathogens can survive and grow inside the macrophages. Macrophages needs to be activated by TH1 cells to deal with the pathogens. When mø’s are activated they are cleared by all bacteria that might live inside them (mycobacteria).

How bacteria cause disease?

Bacteria have to be able to colonize host at mucosal surfaces and adherer to host. The pathogen needs to get nutrients and counter act host defence. This is done by contact/entry, conisation and replication, before transmitting to new host. To adhere avidly to host cells and tissues some bacteria have developed special pili that allow attachment (so they are not flushed away- eg. Urinary tract). Adhesion is hard for the bacteria and it often needs a virus  first to kill the cilia (cant bind to cilia) for then to attack as a secondary bacterial infection. The pili attach to mucous( where they replicate at high rate that beats out rate they are flushed) or bind to chards or surface proteins or extracellular matrix proteins. The bacteria needs to bind to the host tissues and resist defences. This is done by two ways extracellular vs intracellular mechanisms.

Extracellular consist of 1) adhestion, 2) anti phagocytic factors like a capsule that often consist of polysaccharides. This capsule will resist complement cascade and is often non immunogenic because if might have host components. The capsule might have surface proteins or toxins that prevents it from being phagocytosed. Exotoxis are toxic proteins that affect phagocytes, chemotaxis and degranulation. 3) nutrient acquisition systems like iron & infecton. Iron is needed for the  bacteria to grow. If there are low Fe in the environment the bacteria can starve and therefore they have special adaptive systems to overcome this. Sidephores are made that have higher affinity for Fe and capture Fe from lactoferrin. Or TF or LF binding protein that bind lactoferrin or transferring to the surface of itself for then to pull Fe off and into the bacteria.

Intracellular pathogens invade cells, modify intracellular environment, counter intracellular defences and aquire nutrients. Some will evade the system by getting inside and living inside the macrophages. This is beneficial because macrophages are long lived (compared to neutrophils), mobile and have a rich nutrient supply. Once inside the macrophage they escape the phagosome. Some inhibit phagolysosome fusion and coxiella is even able to live inside the phagolysosome. C5a is a peptidase, a protein that interrupts the complement cascade. Some bacteria also produce different proteins that kill neutrophils. M protein on the surface of the capsule of the bacteria is very variable and will  avade the host even when they have mounted a humoral response (memory) because it might infect with a different M type strain thereby evading the memory antibodies.

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Microbiology Fungi


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Canine Eye (fluid)

Function of eye = conversion of light energy to electrical energy and carried to brain by CN2 optic nerve. Eye is 3 layered wall which holds fluid and lens.

The eye has 3 chambers = A. aqueous chamber (aqueous humor fluid), split into anterior chamber (btw iris and cornea) and posterior (btw lens and iris).  B. vitreous chamber – posterior to lens, filled with vitreous humor.  C. Outer fibrous layer includes sclera and cornea.

1. The cornea – transparent area of eye, where light enters eye.  Collagen fibers are very regularly arranged within bundles to give direct transmission of light and no reflection.  Light passed to retina unaltered.  Water balance essential and strictly monitored by epithelium and if damaged becomes opaque.

2. Sclera – posterior portion of eyeball made of dense white fibrous CT.  collagen fibers are irregularly arranged into bundles, scatters light so appears white.  Function = protect inner layers, point of insertion of inter ocular muscles.  Sclera and cornea meet at limbus (junction).

Cornea – Does not contain blood vessels.  Nutrients for its cells permeate the substantia propria (bulk thickness of cornea) from vessels in the limbus or are carried to its surface in the lacrimal fluid and aqueous humor (from ciliary body). 

Lacrimal apparatus brings about production of tears and protection of cornea.

2 glands, 1. Lacrimal (dorsolateral wall of orbit).  2. 3rd eyelid gland (at base). Drains via puncta lacrimalia (adjacent to caruncle) and feed into lacrimal sac. Nasolacrimal duct drains into nasal cavity.

Tear film nourishes outer cornea.  Middle layer is aqueous layer and 2/3 of this is from lacrimal gland.

Aqueous humor: clear and watery.  maintains shape of eyeball – ocular pressure and distention of anterior chamber.  drainage = production to maintain constant intraocular pressure.

The aqueous humor is secreted into the posterior chamber by the cillary body, (non pigmented epithelium). It flows through the narrow cleft between front of the lens and the back of the iris to escape through the pupil into the anterior chamber and then drain out of the eye via the trabecular meshwork (iridocorneal = drainage angle or filtration angle) = goes to venous sinuses in sclera.

(From here, it drains into Schlemm’s canal by one of two ways: directly, via aqueous vein to the episcleral vein, or indirectly, via collector channels to the episcleral vein by intrascleral plexus and eventually into the veins of the orbit.)

The aquous humor is continually produced by cillary processes and rate of the production must equal rate of aqueous humour drainage.

Dorso corneal angle: where the base of the iris attaches to the peripheral cornea and sclera; the site of aqueous drainage from the anterior chamber. Iridocorneal meshwork.

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Canine tongue

Extends from oral cavity into oropharynx.  Muscular organ.  Covered with stratified squamous epithelium (heavier keratinized). 

Covered with papillae types: 1. Filiform – soft protective.  Fungiform, foliate and vallate give taste in tongue. 

Tip of tongue is apex and most caudal is called root that attaches to hyoid apparatus.

Palatoglossal folds = side of tongue and join palate at top = entry into oropharynx. 

Frenulum – attaches at midline to floor of mouth (rostral end of base of tongue).  Either side of frenulum is sublingual caruncles – forming opening to some salivary ducts. 

Extrinsic muscles = 1. Geniohyoideus – from mandible (incisive area) and runs to hyoid apparatus to draw tongue rostrally.
2. Genioglossus – arises at incisive area of mandible and fans into tongue body.  Pulls apex of tongue caudally, draws body rostrally and dorsum of tongue ventrally.
3. Hyoglossus – arises from basihyoid bone and runs into tongue (lateral genioglossus).  Draws tongue caudally.
4. Styloglossus – arises at stylohyoid and runs lateral to hyoglossus and draws tongue caudally and dorsally (base of tongue).
5. Mylohyoideus – transverse sling that runs from side to side of mandible.  Supports extrinsic muscles of tongue. 

Development = from 4 swellings on floor of pharynx. 

Lateral swellings – body and apex, 1st and 2nd arches.  Gives general sensation by CN5 and taste sensation by cranial nerve 7.
Proximal swelling – root of tongue sensation via CN9 and CN10.

Median swelling – tongue innervated by CN12 and all motor function through this nerve. 

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Topographical relationships of the canine heart

The coronary groove is external and about 1/3 down from greater vessel (division btw atria and ventricles).  Usually covered by fat and carries coronary vessels. 
Auricles determine L from R and groves reflect internal septa.  Auricle surface is on the L (bc both auricles can be seen).  Auricles are blind extensions of atria.  L auricle receives blood from pulmonary vein.
Pulmonary trunk on L side disrupts coronary groove and pulmonary trunk is deep to aorta.  Auricle surface has both R and L ventricles on it but L interventricular groove helps differentiate it.
Cranial to interventricular groove is R ventricle and caudal to the groove is LV. L interventricular groove does not bisect heart evenly bc L ventricular wall is thicker.
Apex of heart is made of LV mostly and RV makes up cranial margins of heart.  LV makes of apex on caudal margins of heart. 
R side is mostly made up of RV but caudally you find interventricular groove (subsinosal groove) which separates cranial RV and caudal LV.  R side has caudal vena cava and cranial vena cava (brings blood from abdomen and into RA). 
On external surface of left side, the L coronary artery divides the caudal margin of pulmonary trunk and L auricle into the circumflex and paraconal branches. 
Paraconal goes down paraconal groove (L interventricular).
Circumflex goes down R side and runs down subsinuosal groove.
L circumflex supplies most of heart in ruminant (left side more important). 
Heart located in middle mediastinum and from rib 3-6 and extends to 2nd to 5th intercostal space.  Apex is in 6th intercostal cartilage. 
Heart is surrounded by pericardium (fluid) and included in medisatinum. 
Caudal border is met my diaphragm and attached via phrenicopericardial ligament (sternopericardial in ruminants). 
Cranially is thoracic inlet with vessels. 

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Equine larynx

Suspensory apparatus for tongue and larynx that is attached to skull at synovial joint and forms base of the larynx.
The bones are: tympanohyoid, stylohyoid, epihyoid, ceratohyoid, basihyoid, thyrohyoid. 
Horse has huge stylohyoid – visble in gutteral pouch.  Basihyoid has lingual process in tongue.
Larynx is series of 4 types of main cartilages: 1. epiglottis (rests on cd part of soft palate, points rostrally).  Epiglottis is made of elastic cartilage, moving passively with pharynx/larynx.  Hyoepiglottic ligament attaches epiglottis to baseihyoid.  2. Thyroid cartilage – major part of larynx and made of lamina on either side of floor.  Made of hyaline cartilage and less mobile than epiglottis.  Thyrohyoid ligament attaches thyroid to hyoid apparatus and thyrohyoid bone (also attached to epiglottis).  3. Cricoid cartilage – most caudal, made of hyaline cartilage, most stable.  Cricotracheal ligament attaches it to trachea and cricothyroid ligament to attach to thyroid.  4. Arytenoid cartilage on either side of midline, forming dorsal part of larynx.  Two articulating with cricoid.  Vocal ligament attaches vocal process to thyroid cartilage.  Mixed hyaline and elastic cartilage.  Vestibular ligament attaches arytenoid to thyroid. 
Caudal to larynx is trachea.  There are several mucous membrane folds within larynx.  Arytenoepiglottic fold – from epiglottis to arytenoid to form entrance to larynxVestibular fold – elevation in larynx wall, lining rostrally.  Vocal fold – elevation in larynx wall, lining caudally.
Floor of larynx also has ventral recess. 
Additus laryngis – opening of larynx and opens into laryngeal vestibule.  Consists of arytenoepiglottic fold, epiglottis, arytenoid cartilage, rimaglottis. 
Vagus nerve gives rise to Cranial larnygeal nerve that supplies additus and glottis.
Recurrent laryngeal nerve supplies structures caudal to glottis.
Dorsal cricoarytenoideus rotates arytenoid to abduct folds and tenses vocal folds (opening rima glottis).  Lateral cricoarytenoideus – rotates arytenoids to adduct folds to midline – closes rima glottis.  Both innervated by recurrent laryngeal n.
Cuneiform process of arytenoid is incorporated into epiglottis, rather than arytenoid.  Has both vestibular and vocal folds. 
Larynx is fixed in nasopharynx which makes horse obligate nasal breathers. 

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