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− | # | + | {{review}} |
+ | |||
+ | {{toplink | ||
+ | |backcolour =BCED91 | ||
+ | |linkpage =Alimentary System - Pathology | ||
+ | |linktext =Alimentary System | ||
+ | |maplink = Alimentary System (Content Map) - Pathology | ||
+ | |pagetype =Pathology | ||
+ | }} | ||
+ | <br> | ||
+ | ==Introduction== | ||
+ | *Stomatitis - generalised inflammation throughout mouth. | ||
+ | |||
+ | *Glossitis - inflammation of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]. | ||
+ | |||
+ | *Pharyngitis - pharynx inflammation. | ||
+ | |||
+ | ==Functional Anatomy== | ||
+ | |||
+ | See anatomy and physiology [[Alimentary - Anatomy & Physiology#Oral Cavity|of the oral cavity]] | ||
+ | |||
+ | ==Defence Mechanisms== | ||
+ | ==Developmental Pathology== | ||
+ | [[Image:Cleft-palate.gif|right|thumb|125px|<small><center>A congenital cleft palate defect (Courtesy of Alun Williams (RVC))</center></small>]] | ||
+ | ===Cleft Palate=== | ||
+ | *The commonest structural defect is probably the various forms of cleft palate due to: | ||
+ | **failure of fusion and the ingrowths of the [[Skull and Facial Muscles - Anatomy & Physiology#Palatine Bone (os palatinum)|palatine]] shelves or | ||
+ | **[[Skull and Facial Muscles - Anatomy & Physiology#Frontal Bone (os frontale)|frontonasal]] and [[Skull and Facial Muscles - Anatomy & Physiology#Maxilla|maxillary]] processes. | ||
+ | |||
+ | ==Erosive & Ulcerative Pathology== | ||
+ | *"True ulcer" occurs when connective tissue under epithelium is exposed i.e. stratum germinativum is breached and then lesion takes much longer to heal. | ||
+ | ===[[Bovine Virus Diarrhoea Virus]]=== | ||
+ | *'''Mucosal Disease''': erosive condition produces small multiple, cleanly punched out lesion in mouth | ||
+ | *[[Neutrophils - WikiBlood|Neutrophils]] invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either: | ||
+ | ::#This lesion develops a granular base and becomes diphtheritic. | ||
+ | ::#If bacterial colonisation does not take place, healing occurs within fourteen days. | ||
+ | *Seen in most parts of mouth (or maybe on muzzle) e.g. dental pad, [[Cheeks - Anatomy & Physiology|cheeks]], sides of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] | ||
+ | *Lesions extend throughout gut with particularly big ulcers in small intestine over [[Peyer's Patches - Anatomy & Physiology|Peyers patches]]. Necrosis occurs in lymph nodes and [[Spleen - Anatomy & Physiology|spleen]] | ||
+ | |||
+ | ====<span id="BVDHistology">Histology</span>==== | ||
+ | *No vesicular stage, prickle cells die off from surface resulting in layer of necrotic debris over epithelial layer | ||
+ | *Infection penetrates inward through stratum germinativum. | ||
+ | *Epithelium does not recover as animal does not recover | ||
+ | |||
+ | ===[[Malignant Catarrhal Fever Virus]]=== | ||
+ | |||
+ | ==Vesicular Pathology== | ||
+ | ===Pathology=== | ||
+ | *Damage to [[prickle cell]]s ([[stratum spinosum]]). | ||
+ | *Appears as accumulation of fluid within epithelium, quickly erodes leaving hyperaemic [[stratum germinativum]]. | ||
+ | *Heals by proliferation of new cells, so long as infection does not continue. | ||
+ | ===Pathogenesis=== | ||
+ | May be caused by: | ||
+ | #Ingestion of hot food (corrosive liquids) | ||
+ | #Systemic viral diseases. e.g: | ||
+ | ##[[picornaviridae#Foot and Mouth Disease Virus|Foot and Mouth disease]] - ruminants and pigs | ||
+ | ##[[Vesicular stomatitis]] - horse, pigs, cattle | ||
+ | ##[[Vesicular exanthema]] - pigs | ||
+ | |||
+ | N.B. All are indistinguishable from FMD clinically. | ||
+ | |||
+ | ===[[Foot and Mouth Disease (FMDV)]]=== | ||
+ | |||
+ | ====Pathology==== | ||
+ | =====Gross===== | ||
+ | #Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]], may be other places | ||
+ | #Small vesicle coalesce to produce big ones -i.e. Bullae | ||
+ | #Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis | ||
+ | #Leave painful, hyperaemic epithelium | ||
+ | #Looks like "ulcer "with ragged edge but not a true ulcer as stratum germinativum retained and will rapidly heal completely in about 2 weeks unless becomes secondarily infected | ||
+ | |||
+ | =====Microscopic lesions===== | ||
+ | *Degeneration of prickle cells | ||
+ | *Cells "balloon" as fill with fluid and then die to produce vesicle containing straw coloured or clear fluid | ||
+ | |||
+ | ===[[Swine Vesicular Disease]]=== | ||
+ | *May produce vesicles in mouth that are indistinguishable from foot and mouth disease | ||
+ | *Swine vesicular disease produces sporadic large outbreaks | ||
+ | **Approximately 5% have lesions in mouth, foot lesions much more common | ||
+ | |||
+ | ===Vesicles in dogs=== | ||
+ | *Vesicles in mouth are often caused by hot food - especially in dogs. | ||
+ | *Can produce quite big vesicles, but will heal. | ||
+ | *No major problems associated with vesicles on [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] in dogs (except if due to drinking battery acid, but this also produces vomiting). | ||
+ | |||
+ | ==Catarrhal Stomatitis== | ||
+ | *Non-specific, general stomatitis | ||
+ | ===Pathology=== | ||
+ | *Starts as hyperaemia and oedema of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] or pharynx with mucoid exudate on surface. | ||
+ | *Lymphoid follicles on [[Soft Palate - Anatomy & Physiology|soft palate]] may enlarge and proliferate. | ||
+ | *Often see white spots due to epithelial hyperplasia and increased mucous secretion. | ||
+ | **(can be scraped off to leave ordinary mucosa underneath). | ||
+ | *May produce bad smell. | ||
+ | *Resolves normally if not secondarily infected. | ||
+ | |||
+ | ===Pathogenesis=== | ||
+ | *May be caused by: | ||
+ | **Low grade [[:Category:Streptococcus species|streptococcal]] infection | ||
+ | **Ingestion of toxins | ||
+ | **Result of other more systemic diseases | ||
+ | |||
+ | ==Granulomatous and pyogranulomatous Inflammation== | ||
+ | ==Eosinophilic Inflammation== | ||
+ | ===Eosinophilic granuloma=== | ||
+ | This is a complex of diseases affecting skin and [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]] mainly of cat, which include: | ||
+ | #Oral eosinophilic granuloma | ||
+ | #[[Linear granuloma]] of skin | ||
+ | #[[Eosinophilic plaque]] of skin | ||
+ | |||
+ | ====Clinical==== | ||
+ | *Any age, but usually young adults. | ||
+ | *Mainly affects [[Lips - Anatomy & Physiology|lips]], may also occasionally affect '''frenulum of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]'''. | ||
+ | *Sometimes called "rodent ulcer " | ||
+ | *Not neoplastic - it is an inflammatory disease but is '''progressive and destructive'''. | ||
+ | |||
+ | *May see small plaque or becomes very '''infiltrative'''. | ||
+ | *In worst cases may erode away whole nose. | ||
+ | |||
+ | ====Pathogenesis==== | ||
+ | *Histologically lots of eosinophils, polymorphs. | ||
+ | *Exaggerated eosinophilic response. | ||
+ | |||
+ | ==Necrotizing Inflammation== | ||
+ | ==Lymphocytic and plasmacytic Inflammation== | ||
+ | ==Immune Mediated Pathology== | ||
+ | ===Autoimmune=== | ||
+ | *Occasionally see vesicles on the oral mucosa. associated with autoimmune diseases such as [[pemphigus]] vulgaris. | ||
+ | |||
+ | ===Hypersensitivity=== | ||
+ | ==Proliferative Pathology== | ||
+ | ===Hyperplastic=== | ||
+ | ====Polychlorinated Napthalene Poisoning==== | ||
+ | *Polychlorinated biphenyl's (PCB's). | ||
+ | *Used in all sorts of things. | ||
+ | *Do not break down in environment and very toxic. | ||
+ | *Poisoning was classically seen as proliferative stomatitis when PCB used to lubricate feed pellet making machine. | ||
+ | *Vitamin A antagonist produces hyperkeratosis of mouth (like Vitamin A deficiency). | ||
+ | ===Papular=== | ||
+ | ====Orf==== | ||
+ | *[[Poxviridae|Pox]] infection | ||
+ | *Quite a common '''zoonotic''' disease | ||
+ | |||
+ | =====Clinical===== | ||
+ | *In sheep produces a proliferative nodule/papular mass on [[Lips - Anatomy & Physiology|lips]] | ||
+ | *In flocks in which it is endemic it is seen in lamb | ||
+ | *If flock is non-immune seen in ewes too but much worse in lambs (may spread to inside of mouth) | ||
+ | *Can spread to udder of ewe | ||
+ | |||
+ | =====Pathology===== | ||
+ | *Poxvirus infections produce local infection of [[prickle cells]] in epithelium with proliferation of cells and formation of papule followed by ulceration / necrosis and covered by necrotic epithelium | ||
+ | *Eventually scabs form and crust drops off | ||
+ | *Scabs - very infectious ( N.B.if touch -> catch it) | ||
+ | |||
+ | ====Bovine Papular stomatitis==== | ||
+ | [[Image:BPS.gif|right|thumb|125px|<small><center>Ring Zone Lesions of BPS - Calf (Courtesy of Alun Williams (RVC))</center></small>]] | ||
+ | *Parapox virus | ||
+ | *Very similar disease to orf but seen in cattle and generally milder condition. | ||
+ | *'''Must be differentiated from [[#Foot and Mouth disease|Foot and Mouth Disease]] and [[#Bovine Viral Diarrhoea / Mucosal disease|Mucosal Disease.]]''' | ||
+ | *Sporadic, in cattle, less than 1 year old. | ||
+ | *Develop papules on the muzzle, external nares and in the [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]]; the [[Oesophagus - Anatomy & Physiology|oesophagus]] and [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]] may also be affected. | ||
+ | *Usually heals spontaneously. | ||
+ | =====Pathogenesis===== | ||
+ | *The early lesions are round areas of intense congestion up to 1.5 cm in diameter. | ||
+ | *The centre becomes necrotic and slightly depressed. | ||
+ | *Slow peripheral extension of this lesion gives a classical ring zone formation with concentric rings of | ||
+ | **yellow (necrosis), | ||
+ | **grey (epithelial hyperplasia) | ||
+ | **red (congestion). | ||
+ | =====Histology===== | ||
+ | *There are focal areas of hydropic degeneration in the stratum spinosum | ||
+ | *Large eosinophilic intracytoplasmic inclusion | ||
+ | *Epidermis is markedly thickened. | ||
+ | *The superficial layers of the epithelium become necrotic and slough. | ||
+ | *''Vesicle formation is not a feature of this disease.'' | ||
+ | |||
+ | ====Papilloma==== | ||
+ | |||
+ | ===Neoplastic=== | ||
+ | ====Squamous cell carcinoma==== | ||
+ | [[Image:oral squamous cell carcinoma.jpg|right|thumb|125px|<small><center>'''Oral squamous cell carcinoma'''. Courtesy of T. Scase</center></small>]] | ||
+ | |||
+ | ==Degenerative Pathology== | ||
+ | ==Metabolic Pathology== | ||
+ | ===Uraemia=== | ||
+ | [[Image:uraemia.gif|right|thumb|125px|<small><center>Lesions due to uraemia associated with pyelonephritis/chronic renal failure (Courtesy of Alun Williams (RVC))</center></small>]] | ||
+ | *In terminal renal failure animal may present with painful ulcers in mouth, which become secondarily infected with Fusiformis. | ||
+ | **High concentrations of toxic materials in the blood results in degeneration of small arterioles. | ||
+ | *In the mouth, this damage to the blood supply can cause epithelial necrosis. | ||
+ | *Usually seen as erosions along the ventrolateral borders of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] and on the [[Cheeks - Anatomy & Physiology|cheeks]], especially opposite the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]]. | ||
+ | *In some cases there may be more extensive necrosis which may involve subepithelial tissue | ||
+ | **for example, the tip of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] may slough. | ||
+ | *Most commonly seen in dog sometimes in cat. | ||
+ | |||
+ | ==Nutritional Pathology== | ||
+ | ===Nicotinic Acid Deficiency=== | ||
+ | *May also cause epithelial necrosis and sloughing. | ||
+ | |||
+ | ==Traumatic Pathology== | ||
+ | ===Ulcers Following Trauma=== | ||
+ | *Any animal that is exposed to coarse feed or sharp things in food can suffer from ulcers in mouth. | ||
+ | *They often become secondarily infected with production of metastatic infection that may result in large abscess on point of jaw. | ||
+ | **i.e. trauma on [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] may lead to secondary infection that may lead to abscess in drainage lymph node. | ||
+ | |||
+ | *Deep ulcers may occur as a result of trauma in any species. | ||
+ | *These readily become secondarily infected by [[Fusiformis]]. | ||
+ | *Produces a fibrin-covered ulcer. | ||
+ | *Responds to antibiotics, but may leave a defect or scar in mucosa. | ||
+ | |||
+ | ==Vascular Pathology== | ||
+ | ==Learning Tools== | ||
+ | ::[[Alimentary Flashcards - Pathology#Cavity and Gingiva Flashcards|Cavity and Gingiva Flashcards]] |
Revision as of 10:57, 17 May 2010
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
|
Introduction
- Stomatitis - generalised inflammation throughout mouth.
- Glossitis - inflammation of tongue.
- Pharyngitis - pharynx inflammation.
Functional Anatomy
See anatomy and physiology of the oral cavity
Defence Mechanisms
Developmental Pathology
Cleft Palate
- The commonest structural defect is probably the various forms of cleft palate due to:
- failure of fusion and the ingrowths of the palatine shelves or
- frontonasal and maxillary processes.
Erosive & Ulcerative Pathology
- "True ulcer" occurs when connective tissue under epithelium is exposed i.e. stratum germinativum is breached and then lesion takes much longer to heal.
Bovine Virus Diarrhoea Virus
- Mucosal Disease: erosive condition produces small multiple, cleanly punched out lesion in mouth
- Neutrophils invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:
- This lesion develops a granular base and becomes diphtheritic.
- If bacterial colonisation does not take place, healing occurs within fourteen days.
- Seen in most parts of mouth (or maybe on muzzle) e.g. dental pad, cheeks, sides of tongue
- Lesions extend throughout gut with particularly big ulcers in small intestine over Peyers patches. Necrosis occurs in lymph nodes and spleen
Histology
- No vesicular stage, prickle cells die off from surface resulting in layer of necrotic debris over epithelial layer
- Infection penetrates inward through stratum germinativum.
- Epithelium does not recover as animal does not recover
Malignant Catarrhal Fever Virus
Vesicular Pathology
Pathology
- Damage to prickle cells (stratum spinosum).
- Appears as accumulation of fluid within epithelium, quickly erodes leaving hyperaemic stratum germinativum.
- Heals by proliferation of new cells, so long as infection does not continue.
Pathogenesis
May be caused by:
- Ingestion of hot food (corrosive liquids)
- Systemic viral diseases. e.g:
- Foot and Mouth disease - ruminants and pigs
- Vesicular stomatitis - horse, pigs, cattle
- Vesicular exanthema - pigs
N.B. All are indistinguishable from FMD clinically.
Foot and Mouth Disease (FMDV)
Pathology
Gross
- Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of tongue, may be other places
- Small vesicle coalesce to produce big ones -i.e. Bullae
- Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis
- Leave painful, hyperaemic epithelium
- Looks like "ulcer "with ragged edge but not a true ulcer as stratum germinativum retained and will rapidly heal completely in about 2 weeks unless becomes secondarily infected
Microscopic lesions
- Degeneration of prickle cells
- Cells "balloon" as fill with fluid and then die to produce vesicle containing straw coloured or clear fluid
Swine Vesicular Disease
- May produce vesicles in mouth that are indistinguishable from foot and mouth disease
- Swine vesicular disease produces sporadic large outbreaks
- Approximately 5% have lesions in mouth, foot lesions much more common
Vesicles in dogs
- Vesicles in mouth are often caused by hot food - especially in dogs.
- Can produce quite big vesicles, but will heal.
- No major problems associated with vesicles on tongue in dogs (except if due to drinking battery acid, but this also produces vomiting).
Catarrhal Stomatitis
- Non-specific, general stomatitis
Pathology
- Starts as hyperaemia and oedema of tongue or pharynx with mucoid exudate on surface.
- Lymphoid follicles on soft palate may enlarge and proliferate.
- Often see white spots due to epithelial hyperplasia and increased mucous secretion.
- (can be scraped off to leave ordinary mucosa underneath).
- May produce bad smell.
- Resolves normally if not secondarily infected.
Pathogenesis
- May be caused by:
- Low grade streptococcal infection
- Ingestion of toxins
- Result of other more systemic diseases
Granulomatous and pyogranulomatous Inflammation
Eosinophilic Inflammation
Eosinophilic granuloma
This is a complex of diseases affecting skin and oral cavity mainly of cat, which include:
- Oral eosinophilic granuloma
- Linear granuloma of skin
- Eosinophilic plaque of skin
Clinical
- Any age, but usually young adults.
- Mainly affects lips, may also occasionally affect frenulum of tongue.
- Sometimes called "rodent ulcer "
- Not neoplastic - it is an inflammatory disease but is progressive and destructive.
- May see small plaque or becomes very infiltrative.
- In worst cases may erode away whole nose.
Pathogenesis
- Histologically lots of eosinophils, polymorphs.
- Exaggerated eosinophilic response.
Necrotizing Inflammation
Lymphocytic and plasmacytic Inflammation
Immune Mediated Pathology
Autoimmune
- Occasionally see vesicles on the oral mucosa. associated with autoimmune diseases such as pemphigus vulgaris.
Hypersensitivity
Proliferative Pathology
Hyperplastic
Polychlorinated Napthalene Poisoning
- Polychlorinated biphenyl's (PCB's).
- Used in all sorts of things.
- Do not break down in environment and very toxic.
- Poisoning was classically seen as proliferative stomatitis when PCB used to lubricate feed pellet making machine.
- Vitamin A antagonist produces hyperkeratosis of mouth (like Vitamin A deficiency).
Papular
Orf
- Pox infection
- Quite a common zoonotic disease
Clinical
- In sheep produces a proliferative nodule/papular mass on lips
- In flocks in which it is endemic it is seen in lamb
- If flock is non-immune seen in ewes too but much worse in lambs (may spread to inside of mouth)
- Can spread to udder of ewe
Pathology
- Poxvirus infections produce local infection of prickle cells in epithelium with proliferation of cells and formation of papule followed by ulceration / necrosis and covered by necrotic epithelium
- Eventually scabs form and crust drops off
- Scabs - very infectious ( N.B.if touch -> catch it)
Bovine Papular stomatitis
- Parapox virus
- Very similar disease to orf but seen in cattle and generally milder condition.
- Must be differentiated from Foot and Mouth Disease and Mucosal Disease.
- Sporadic, in cattle, less than 1 year old.
- Develop papules on the muzzle, external nares and in the oral cavity; the oesophagus and forestomachs may also be affected.
- Usually heals spontaneously.
Pathogenesis
- The early lesions are round areas of intense congestion up to 1.5 cm in diameter.
- The centre becomes necrotic and slightly depressed.
- Slow peripheral extension of this lesion gives a classical ring zone formation with concentric rings of
- yellow (necrosis),
- grey (epithelial hyperplasia)
- red (congestion).
Histology
- There are focal areas of hydropic degeneration in the stratum spinosum
- Large eosinophilic intracytoplasmic inclusion
- Epidermis is markedly thickened.
- The superficial layers of the epithelium become necrotic and slough.
- Vesicle formation is not a feature of this disease.
Papilloma
Neoplastic
Squamous cell carcinoma
Degenerative Pathology
Metabolic Pathology
Uraemia
- In terminal renal failure animal may present with painful ulcers in mouth, which become secondarily infected with Fusiformis.
- High concentrations of toxic materials in the blood results in degeneration of small arterioles.
- In the mouth, this damage to the blood supply can cause epithelial necrosis.
- Usually seen as erosions along the ventrolateral borders of the tongue and on the cheeks, especially opposite the teeth.
- In some cases there may be more extensive necrosis which may involve subepithelial tissue
- for example, the tip of the tongue may slough.
- Most commonly seen in dog sometimes in cat.
Nutritional Pathology
Nicotinic Acid Deficiency
- May also cause epithelial necrosis and sloughing.
Traumatic Pathology
Ulcers Following Trauma
- Any animal that is exposed to coarse feed or sharp things in food can suffer from ulcers in mouth.
- They often become secondarily infected with production of metastatic infection that may result in large abscess on point of jaw.
- i.e. trauma on tongue may lead to secondary infection that may lead to abscess in drainage lymph node.
- Deep ulcers may occur as a result of trauma in any species.
- These readily become secondarily infected by Fusiformis.
- Produces a fibrin-covered ulcer.
- Responds to antibiotics, but may leave a defect or scar in mucosa.