Cavity & Gingiva - Pathology

()Map ALIMENTARY SYSTEM (Map)

Introduction

• Stomatitis - generalised inflammation throughout mouth.

• Glossitis - inflammation of tongue.

• Pharyngitis - pharynx inflammation.

Functional Anatomy

See anatomy and physiology of the oral cavity

Developmental Pathology

A congenital cleft palate defect (Courtesy of Alun Williams (RVC))

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 Viral Diarrhoea / Mucosal disease

Small erosions of MDV/BVDV - vesicles are microscopic (Courtesy of Alun Williams (RVC))

Coalescing lesions of BVDV (Courtesy of Alun Williams (RVC))

• Erosive condition produces small multiple, cleanly punched out lesion in mouth.
• A major concern is that it can be confused with FMD (especially as it often occurs with clinical signs of salivation and depression).

• Two manifestations of disease with different severity, given different names but same condition and causal agent.

1. Mucosal Disease (MD)
2. Bovine Virus Diarrhoea (BVD).

Pathogenesis

• Caused by number of strains of Pestiviruses that are all closely related but produce two distinct syndromes.
• Two biotypes of virus cytopathic and non-cytopathic.

1. Bovine Viral Diarrhoea

• Often may sweep through a whole colony of young stock causing profuse diarrhoea (perhaps febrile) for a few days and then recover.
• Due to primary exposure to cytopathic strain of virus.

2. Mucosal Disease

• Presents as severe disease with lesions in mouth, profuse watery diarrhoea and always eventually results in death.
• It is the end result of an animal becoming infected in utero with non-cytopathic strain of virus. (cow may not show any signs).
• The foetus is tolerant of the virus and becomes persistently infected (if infected before 2nd month gestation).
• It is believed that later mutational events in the persistent non-cytopathic virus or subsequent infection with a cytopathic strain lead to establishment of a pathogenic infection. The animal thus develops severe disease and dies as it makes no immune response to cytopathic virus. It is found to be infected by two closely related strains of virus, one cytopathic and the other non-cytopathic.
• A dam infected by a cytopathic strain may produce a deformed foetus.
• Cerebellar hypoplasia, micro-opthalmia and other ocular abnormalities are common abnormalities.

Pathology

• Erosive lesions size of 5p piece develop in mouth, almost circular not ragged. Multiple. May coalesce and look more like FMD.
• Neutrophils invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:

1. This lesion develops a granular base and becomes diphtheritic.
2. 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.

Definitive diagnosis

• Viral antigen in blood 3-8 days post infection
  • (N.B Tolerant state exists when considering serology.)

Malignant catarrhal fever

Postgrad material... Postgraduate / Certificate_Material for WikiPath

• Caused by a gammaherpes virus.
• Cattle, deer and antelope
• Not all that common in UK.

Clinical

• Affects whole body but especially evident clinically in face and mouth.
• Sporadic and often seen in animals mixing with sheep(carriers).
• In parts of Africa see long outbreaks (diff serotypes) carried by Wildebeest.
• In deer produces very serious outbreaks, probably primarily sheep virus.

• Often youngish animal 6 months to 1 year.
  

  Sever Oculo-nasal Discharge of MCF (Courtesy of Alun Williams (RVC))
• Invariably fatal.
• Show fever and diarrhoea with severe oculo-nasal discharge.
• Not eating, dull with ulcers on muzzle may spread to rest of face with brown exudate.
• Ulcers also on tongue, dental pad, and cheeks that regularly become secondarily infected.
  

  Fissures on tongue (no vesicles) in MCF (Courtesy of Alun Williams (RVC))
• Skin becomes thickened and may peel.
• Conjunctivitis and corneal oedema / opacity (keratitis or "blue eye" - characteristic feature.)
• Often develop nervous signs.

• All lymph nodes become very enlarged.

Pathology

• Lymph nodes completely replaced by lymphoblasts - similar to lymphosarcoma; synonym lymphoma. (resembles lymphotropic herpes virus such as Epstein Barr)
• Also vasculitis with medial necrosis of blood vessels throughout body with infiltration of walls of vessels by lymphocytes.
• Ulcers are due to hypoxia of epithelium resulting from vascular lesions.

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:

1. Ingestion of hot food (corrosive liquids)
2. Systemic viral diseases. e.g:
   1. Foot and Mouth disease - ruminants and pigs
   2. Vesicular stomatitis - horse, pigs, cattle
   3. Vesicular exanthema - pigs

N.B. All are indistinguishable from FMD clinically.

Foot and Mouth disease

Introduction

• Affects all cloven hoofed animals, cattle, sheep and pigs and others.
• 1967 + 2001 major outbreaks in UK.
• Controlled by slaughter policy in UK.
• Still widespread in many parts of world especially S. America, far East.
• Very infectious virus - a picornavirus

Clinical

• Foot and Mouth disease is not a high fatal disease - approximately 5% mortality, usually young animals, older animals recover but stop giving milk yield - i.e. production losses are important factor.
• It is very debilitating and animals take weeks or months to recover.
• Economic impact as stops export of cattle and cattle products.
• Fairly easy to diagnose in classical form - difficult in sheep.
• Animals froth at mouth, usually in more than one animal (an individual animal alone may be dysphagic, or have oral pain from other causes).
• Lameness in a number of animals.
• Characteristic lesions in mouth that are short lived.
• Incubation from two days up to 3 weeks in sheep.

Pathology

Gross

1. Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of tongue, may be other places.
2. Small vesicle coalesce to produce big ones -i.e. Bullae.
3. Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis.
4. Leave painful, hyperaemic epithelium.
5. 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.

• Also produces cutaneous erosions in interdigital cleft, at coronet and bulbs of heals.
  • These feet lesions often take a long time to heal as secondary bacterial infections may ensue and produce true deep ulcerative dermatitis.
• Teats on animals that are suckling may also develop vesicles.

• Sheep develop very few vesicles in mouth but foot lesions can be dramatic - like a whole flock with foot rot. N.B. Can also be very mild!
• Coronets are very red with vesicles and erosions.

• Pigs have vesicles on snout, which are quickly traumatised to leave an eroded lesion - hard to look at pig’s tongue.
• Hoof lesions like other species; hoof may come off, known as "thimbling".
• Lesions will heal eventually but is very painful (often necessitates euthanasia)

Microscopic lesions

• Degeneration of prickle cells.
• Cells "balloon" as fill with fluid and then die to produce vesicle containing straw coloured or clear fluid.

Diagnosis

Definitive diagnosis.

N.B. Notifiable Disease.

• Inform MAFF (and police) as soon as suspect clinical diagnosis.
• MAFF will take specimens of fluid from vesicle. Suck out fluid with syringe.
• Skin that has sloughed off vesicle also good for diagnosis.
• If the above two are not available can use scraping of base of erosion.

• May see animals that have discoloration of tongue due to having had FMD. In these cases take scraping of retropharyngeal region, put scrapings in transport medium.

1. Atigen capture ELISA
2. PCR
3. Culture (need ph7 buffered transport media)
4. Antibody capture ELISA

• In foot and mouth disease usually use ELISA to provide quick diagnosis - especially if have vesicular fluid.

Swine Vesicular Disease

• Caused by Swine Vesicular Disease Virus.
• 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

Eosinophilic Inflammation

Eosinophilic granuloma

This is a complex of diseases affecting skin and oral cavity mainly of cat, which include:

1. Oral eosinophilic granuloma
2. Linear granuloma of skin
3. 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.

Immune Mediated Pathology

Autoimmune

• Occasionally see vesicles on the oral mucosa. associated with autoimmune diseases such as pemphigus vulgaris.

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

• Parapox virus infection.
• Quite a common zoonotic disease.
• In man lesion grows slowly over weeks. Heals but takes a long time, characteristically in angle of thumb and 1st finger.

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

Ring Zone Lesions of BPS - Calf (Courtesy of Alun Williams (RVC))

• 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.

Neoplastic

Squamous cell carcinoma

Oral squamous cell carcinoma. Courtesy of T. Scase

Metabolic Pathology

Uraemia

Lesions due to uraemia associated with pyelonephritis/chronic renal failure (Courtesy of Alun Williams (RVC))

• 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.

Learning Tools

Cavity and Gingiva Flashcards