The document provides an overview of the digestive system from the mouth to the stomach. It discusses several key points: 1) The digestive system includes the mouth, pharynx, esophagus, stomach, intestines and anus. Along with associated glands and organs, it forms the alimentary system. 2) Gastrointestinal problems are commonly encountered in small and large animal practice and can be life-threatening, morbid, and costly. 3) The digestive system is directly exposed to the external environment and susceptible to pathogens from feed, water, and management practices like artificial feeding and confinement.

1. DIGESTIVE SYTEM
PART 1 (Mouth to Stomach)
PROF. V.O TAIWO
Modified by AJAADI, A.A.

2. INTRODUCTION
The Alimentary System includes the mouth, pharynx,
oesophagus, stomach, intestines and anus
With salivary glands, teeth, tonsils, liver, pancreas and
anal sacs, they make up the Digestive System
The alimentary system is directly or indirectly involved
in most diseases that affect the animal, and it is
accessible largely to routine clinical examination and
evaluation of the health status of an animal, including
endoscopy

3. Introduction contd
In both small and large animal practice, GIT
problems are among the most commonly
encountered conditions. Many of the conditions and
diseases are:
 Life-threatening
 Most often lead to morbidities and mortalities
 Cause great economic losses from
 Lower productivity, and
 Cost of treatment and control

4. BASIC REACTIONS OF THE SYSTEM TO INJURY
 Cellular degeneration/necrosis (resulting in vesicles, erosion,
ulcers, villous atrophy)
 Inflammation
 Proliferation of cells (reparative); may also lead to neoplasia
 Altered rate of secretion, absorption and/or motility

PREDISPOSING FACTORS
 Direct exposure to the environment (essentially “outside” the
body; mouth to anus)
 Management (artificial feeding and confinement which favour
pathogens)
 Entry of pathogenic organisms and toxins through feed and
water
 Relatively loose suspension of its segments in the abdominal
cavity

5. PROTECTIVE MECHANISMS
Fluid (water) intake (dilution factor, necessary for life)
Endogenous secretions (saliva, acid, bile, IgA)
Rhythmic contractions of wall and movement of villi
(propellation of ingesta towards exit points)
Rapid epithelial turnover (2-8 days for enterocytes
covering villi)
Local immune response (lymphocytes in Peyer’s
patches, lymph nodes, tonsils, IgA)

6. MOUTH AND ADNEXA
Developmental Abnormalities
 Cleft lip (Cheiloschisis)
 Affects upper lip (divided upper lip; fissure)
 Results from failure of fusion of the maxillary process and the medial
nasal process at or near the site known as the philtrum
 May occur alone or in association with cleft palate
 Cleft palate (Palatoschisis)
 A longitudinal fusion defect of varying lengths between the lateral
palatine shelves and the maxillary processes
 Results in an open cleft between the oral and nasal cavities
 Newborn animals often drip milk from their nostrils during nursing,
whereas older animals may develop respiratory infection and
pneumonia due to aspiration of food

7. Cleft lip (Cheiloschisis)

8. Cleft palate (Palatoschisis)

9. Traumatic Lesions
 The mucous membranes of the lips, oral cavity, gingiva, tongue, and
oropharynx are repeatedly subjected to varying degrees of trauma
 In herbivores, the coarse nature of pasturage and roughage, and
foreign objects that may be inadvertently ingested can cause
laceration or abrasions of the mucosa
 In dogs and cats, sharp bones, splinters thorns, needles, and string
may cause traumatic injury
 Burns of chemical, thermal, or electrical origin are seen
occasionally in the oral cavity, particularly in young puppies with
indiscriminate chewing habits

10. Inflammation of Structures in Oral Cavity
Gingivitis: This is the inflammation of the gingiva (gum)
 Results from opportunistic bacterial infections
following trauma, poor oral hygiene or various
immunodeficient states
 First manifestation of FIV infection and candidiasis
(thrush) in man
 Grossly, the inflamed gingiva bleeds easily,
erythematous and oedematous
 Histologically, inflammation confined to the gingival
connective tissue and is infiltrated by variable
numbers of neutrophils, lymphocytes, and plasma cells

11. Periodontitis or periodontal disease is the inflammation
of the tissues that surround teeth, including the gingival
sulcus, the epithelial attachment of the gingiva to the
teeth, the periodontitis ligament, and the alveolar bone of
the tooth socket.
 Occurs commonly in man, dogs and cats
 Begins as a gingivitis resulting from accumulation of
bacterial plaque on the tooth surfaces
 Plaques result from bacterial colonization of food
particles retained in the gingival sulcus surrounding
the tooth or the space between adjacent teeth

12. DENTAL CARIES (tooth decay, cavities)
This is a progressive destructive decalcification of the dental
enamel by the action of organic acids (esp. lactic acid)
followed by enzymic lysis of the exposed organic matrix
Common in cattle, swine, horses and sheep; rare in dogs
and cats
Caused mainly by the action of bacteria such as Strept.
aureus and Lactobacillus spp. on fermentable CHOs which
accumulate on the tooth surface
Results in the exposure of the periodontal pulp, pain and
refusal to eat
Seen grossly as large cavities inside the affected teeth
In horses, the condition usually leads to sinusitis in about
60-65% of cases

14. DENTAL CALCULUS (Tartar)
This is the presence of a composite calcified mass of
bacteria, fungi, food particles, desquamated epithelium
and leucocytes on the buccal and ligual surfaces of the
teeth
Results from stagnation of saliva, clinging of food
particles to teeth and the consumption of soft, sticky
food
Very common in human, dogs (old dogs) and cats and
occasionally in horses and sheep
Rare in other species
Plaques are carbonates in cattle; phosphates in horses

16. EPULIDES
 Epulides are benign tumour or tumour like masses present on
the gingival, arising from the periodontal ligament. They are
grossly similar to gingival hyperplasia and are more common
in dogs than cats.
 Epulides are slow-growing and firm masses on the gingiva
and are usually enveloped by intact epithelium.
 Four different types, including fibromatous, ossifying,
acanthomatous and giant cell epulides have been reported.
They can be differentiated histologically.

17. EPULIS….
Acanthomatous epulis reserves the potential to invade the bone, others including
fibromatous epulis are not invasive
 Oral cancers other than fibromatous and ossifying epulides that are attached to the
bone should be examined radiographically.
 Fibromatous epulis in dogs may be characterized by the following clinical signs;
gingival swelling excessive salivation, exophthalmos, weight loss, halitosis,
epistaxis, dysphagia, sanguineous oral discharge, cervical lymphadenopathy and
loose teeth.
 The fibromatous epulis is a firm growth found on epithelium-covered gingiva. It
may appear single or multiple near the teeth and its presence may hinder
mastication. It may be sessile or pedunculated.

18. EPULIS….
 Epulis of periodontal origin is characterized by dense cellular stroma which is
regularly associated with blood vessels and is made up of stellate cells and tightly
packed fibrillar collagen.
 Fibroblasts or fibrocytes that are observed in this condition are generally
elongated and spindle shape

19. FIBROMATOUS EPULIS

20. FIBROMATOUS EPULIS

21. Stomatitis
 Definition: Generally - Inflammation of the oral cavity
 The causes of stomatitis and oral ulceration include:
 a variety of bacteria, including fusobacteria and spirochetes;
 numerous viral agents, fungi (Candida albicans)
 certain parasites;
 several autoimmune disorders, including SLE, pemphigus vulgaris,
bullous pemphigoid,
 uremia;
 Vit C and Niacin deficiency
 Stomatitis is the general term used to describe the inflammation of the
various parts of the oral cavity, with each part having its own
terminology, viz: ginginvitis (gums), odontitis (teeth), periodotitis,
tonsillitis (tonsils) etc.
 Two main types
 Superficial stomatitis
 Deep stomatitis

22. SUPERFICIAL STOMATITIS
 Usually associated with the ingestion of caustic or toxic compounds which elicit
tissue destruction and inflammatory reaction
 Affects the superficial structures of the oral cavity
 Most common infectious causes of superficial stomatitis in animals are viruses
 Though the oral cavity contains a normal flora of microbionts, mainly
anaerobes (Actinomyces, Fusobacterium and Spirochaetes), the oral cavity is
quite resistant to microbial invasion
Defense mechanisms of anti-microbial invasion include
 Cornified stratified squamous epithelium
 Lysozymes present in saliva
 IgA in oral secretions
 Submucosal inflammatory cells and lymphoid tissue such as lymph nodes, and
tonsils in the buccal area
Factors such as systemic illness, stress and nutritional and hormonal
imbalances may alter the microbial population by altering the
amount, composition and pH of saliva

23. Depending on the cause, course and location of the
lesions, superficial stomatitis could be
Catarrhal
Vesicular
Erosive
Ulcerative

24. Catarrhal Stomatitis
 Usually involves the posterior fauces and may be associated with
mild ginginvitis
 It is a common non-specific lesion that often develops in the course
of debilitating diseases
Grossly
 Affected parts are hyperaemic, swollen and oedematous
 There may be hyperplasia of the lymphoid tissues of the soft palate,
tonsils and pharyngeal mucosae.
 The epithelium accumulates, producing a gray mucosal surface, and
there is excessive mucus production by palatine glands
Healing usually takes place if the cause is removed and the mucosa
returns to normal

25. Vesicular Stomatitides (sing. Stomatitis)
A group of superficial stomatitis characterized by the formation of
VESICLES and occur in most species of domestic animals
 The most common causes are different types of epitheliotropic viruses in
different species or group of species of domestic and laboratory animals and
man
 Generally, the vesicles develop as accumulation of fluids from ruptured
epithelial cells which had undergone ballooning and hydropic
degeneration due to viral invasion
 The fluid is usually found between epithelial cells and between the
epithelium and lamina propriae
 Vesicles may coalesce to form bullae and the subsequently raised
epithelium is easily rubbed off during chewing to leave raw eroded patches
(erosions) with bits of epithelium still adherent
 The transition from vesicles to erosion occurs rapidly so that in individual
animals, vesicles may not be seen
 Because the basal epithelium or basement membrane is intact, regeneration
and healing rapidly and completely take place

26. Some viral diseases in domestic animals characterized
by vesicular stomatitis
Foot and Mouth Disease (FMD)
 cattle, sheep, swine, guinea pigs and man
Vesicular Stomatitis
 swine, horses, sheep, guinea pig, mouse and man
Vesicular Exanthema
 swine

27. Foot & Mouth
Disease
Vesicular
Stomatitis
Swine Vesicular
Disease
Vesicular
Exanthema of
Swine
Clinical Signs
by Species
All vesicular diseases produce a fever with vesicles that progress to erosions in
the mouth, nares, muzzle, teats, and feet
Cattle
Oral & hoof lesions,
salivation, drooling,
lameness, abortions,
death in young
animals, "panters";
Disease Indicators
Vesicles in oral
cavity, mammary
glands, coronary
bands, interdigital
space
Not affected Not affected
Pigs
Severe hoof lesions,
hoof sloughing, snout
vesicles, less severe
oral lesions:
Amplifying Hosts
Same as cattle
Severe signs in
animals housed on
concrete; lameness,
salivation,
neurological signs,
younger more severe
Deeper lesions with
granulation tissue
formation on the feet
Sheep &
Goats
Mild signs if any;
Maintenance Hosts
Rarely show signs Not affected Not affected
Horses,
Donkeys,
Mules
Not affected
Most severe with
oral and coronary
band vesicles,
drooling, rub
mouths on objects,
lameness
Not affected Not affected

28. Foot and Mouth Disease (FMD; Aphthus fever)
28
It is a contagious viral disease of cloven footed animals
Caused by a Picorna virus of 7 distinct antigenic types (A,
O, C, SAT-1, SAT-2, SAT-3 and Asia-1)
Affects swine, cattle, sheep, goats, African buffalos
Transmission is by aerosol, contact, fomites
Characterized by ropy, stringy salivation; presence of
vesicles and erosions in oral mucosa, feet and teats
Tiger heart (necrotic streaks on myocardium) in neonates

29. Ropy, stringy saliva

30. 30
Vesicles on oral cavity

31. 31
Erosions

32. Ulcer on tongue
32

33. Rupture of vesicles leading to necrotic areas in feet
33

34. Ruptured vesicles on teats
34

35. Erosions on the ruminal mucosa

36. Tiger heart: Streaks of areas of degeneration
and necrosis in myocardium of neonates
36

37. Differential diagnoses
37
Vesicular stomatitis
Infectious bovine rhinotracheitis
Malignant catarrhal fever
Bovine viral diarrhea
Rinderpest

38. Vesicular Stomatitis in Swine
( P O R C I N E E N T E R O V I R U S I N F E C T I O N )

39. Virus
 Family Picornaviridae
 Genus Enterovirus
 Related to human enterovirus
 Unrelated to other porcine enteroviruses
 Survives for long periods in environment and in meat
products
Resistant to
 Temperatures up to 157 oF; pH ranging from 2.5-12
Aetiology

40. Morbidity/Mortality
Moderately contagious
Compared to foot-and-mouth
 Lower morbidity, less severe lesions
Mortality not generally a concern
 Low in adult pigs
 Up to 10% in piglets
No persistent infection
Animal develops protective antibody

41. Transmission
Contact
 Infected animals or faeces
Ingestion
 Contaminated meat scraps
Excretion of virus
 Nose, mouth, faeces
 Up to 48 hrs. before clinical signs seen
 Shed in feces for >3 months after infection

42. Clinical Signs
Vesicles and Erosions
 Snout

43. Vesicles and Erosions
 Feet
 Teat

44. Lesions of Vesicular
Stomatitis in Sheep

45. Differential Diagnosis
Foot-and-mouth disease
Vesicular exanthema of swine
Chemical or thermal burns

46. Erosive and Ulcerative Stomatitis
Both characterized by local epithelial defects of the oral
mucosa and nasolabium and are usually associated with
acute diffuse stomatitis and pharyngitis.
Erosive stomatitis is characterized by circumscribed areas
of loss of epithelium , leaving stratum germinativum and
basement membrane intact
Usually associated with acute inflammation of the
underlying lamina propria
Erosions may vary in size and shape
Erosions heal cleanly and completely, except when
secondarily infected, when they may become ulcers

47. Ulcerative stomatitis is a deeper lesion that extends into
the substantia propria, subsequent to a break in the
continuity or damage to the basement membrane
 Ulcers vary in size and shape, but generally, the edges
tends to be elevated and rugged
 The surface is raw, reddish to grayish, bleeding and
often contaminated
 When they heal, it is with scar tissue formation
The aetiologies of ulcerative stomatitis are in general
those of erosive stomatitis

48. However, a number of recognized syndromes and specific
diseases present with ulcerative changes. They include:
 Ulcerative stomatitis and glossitis in swine and cats
 Ureamic stomatitis (in dogs with chronic renal failure,
e.g. Leptospirosis)
 Rinderpest, MCF, MD (cattle)
 Bluetongue (sheep)
 Infectious bovine rhinotracheitis (IBR)
 Bovine papular stomatitis

49. DEEP STOMATITIS
Affect the deeper tissues and structures of the
oral cavity, including bones
The deep lesions arising from superficial lesions permit
the entry of pyogenic bacteria, often normal oral
flora, into the deeper tissues (submucosa, muscle, bone)
Purulent inflammation or cellulites may develop in
the lips, tongues, cheek, soft palate, tonsils, pharynx, jaw
bones
Abscesses may form and fistulate through the mucosa
or skin
Some of the most common deep stomatitides in
domestic animals are: Actinobacillosis,
Actinomycosis and Oral necrobacillosis

50. Actinobacillosis
Chronic
infectious
disease
a.k.a.
Wooden
tongue
Actinobacillus
lignieresii
Sporadic
Self
limiting
Gram
negative
coccobacilli
or
pleomorphic
rods
Actinobacillosis (Wooden tongue)

51. Epidemiology
Distribution: The disease in cattle is worldwide in
distribution and usually of sporadic occurrence
Found in areas with copper deficiency
Animal susceptibility: Cattle, buffaloes (mature and
of dairy breed are more susceptible), sheep and goats.
Predisposing factors : Oral mucosa injuries by fibrous
feed materials or by foreign bodies and during oral
manipulation by hand of owner or veterinarian

52. Mode of infection
 Source of infection: Pus or infected discharges are the
main source of infection
 Mode of transmission: The disease is transmitted by
ingestion of contaminated food and water with the
presence of oral mucosa injury (wounds or abrasions)
A. lignieresii is a Gram-negative coccobacillary
bacterium normal rumen inhabitant of sheep and cattle
It survives 4 to 5 days in forage

53. The characteristic lesion is a granuloma of the tongue,
with discharge of pus
Inability to eat or drink for several days
Drooling saliva
Painful and swollen tongue
Nodules and ulcers on the tongue
In later stages when the acute inflammation is replaced
by fibrous tissue, the tongue becomes shrunken and
immobile and there is considerable interference with
prehension

54. There is also cutaneous actinobacillosis with
granulomas occurring on atypical but visible areas
such as the external nares, cheeks, skin or eyelid, and
hind limbs
In sheep, tongue is not usually involved
Nodular lesions up to 8cm in diameter present on lower
jaw, face, nose, in the skin folds from lower jaw to
sternum
These lesions are superficial or deep, usually extend to
cranial or cervical lymph nodes, discharging viscid
yellow green pus containing granules through number
of openings (fistulation)

55. Postmortem findings
Granulomatous lesions containing pus in mouth
Hardening (induration) of the tongue, which may
protrude out of mouth
Cut surface presents multiple abscesses
Abscesses may be found in local lymph nodes
At histology, pyogranulomata and extensive fibrosis of
the tongue
other soft tissues of the oral cavity, neck, and regional
lymph nodes may be affected
Bony structures NOT affected

57. Neck
Oral
Leg
Udder
Chest
Tongu

58. Histology

59. Equine liver with Actinobacillus pyogranuloma

60. Differential diagnosis
 Actinomycosis: It involves both hard and soft tissues of
the oral cavity, head and neck
 Tuberculosis: especially the atypical form, differentiate
on basis of tuberculin test
 Abscess of throat region: contain single cavity and
discharge thin pus and readily heal after drainage

61. Actinomycosis (Lumpy jaw)
It is a chronic infectious debilitating disease of cattle
caused by Actinomyces bovis, a gram-positive organism
It is characterized by rarefying periostitis and formation
of bony cavities filled with pus, particularly in the
mandible and maxilla
It affects both soft and bony tissues of the oral cavity
and oropharynx
Presents with enlarged soft head bones (mandible and
maxillae

62. Grossly, the facio-maxillo-mandibulary bones are soft,
mis-shapen and may ulcerate
The head appears very big and droopy, while pus may
drain from fissures in the ulcerated bones
Soft tissues like the tongue, lymph nodes and
lymphatics are also affected
Microscopically, the lesions are similar to and must be
distinguished from those caused by Actinobacillus
lignieresii (staining characteristics of the organism)

63. Actinomycosis (Lumpy jaw) – ulcerated, fistulated mandible)

65. OESOPHAGUS
Disorders of the oesophagus can be categorized into one of
 Inflammation
 Degeneration
 Obstructive lesions
 Motility disorders
Oesophagitis: Inflammation of the oesophagus is infrequent
but, like that of the mouth, it generally results from
trauma produced by foreign objects, caustic chemicals,
infection or parasitism

66. Dog: Oesophageal perforation (rib piercing)

67. IBR: haemorrhagic, erosive and ulcerative oesophagitis

68. Reflux oesophagitis is a form of chemical oesophagitis
 Occurs when there is reflux of gastric acid and pepsin from the
stomach and bile salts and pancreatic enzymes from the
duodenum into the lower portion of the oesophagus
 The stratified squamous epithelium of the oesophageal mucosa is
not protected by a layer of mucus unlike the GIT mucosa;
Consequently it may be partially digested by these corrosive juices
Grossly, the affected portion is hyperemic or contains linear
erosions or ulcerations which may be covered by a
fibrinonecrotic plaque
At histology, there are areas of epithelial erosion and/or
ulceration with in-growth of fibroblastic connective tissue
and flattening and proliferation of the adjacent normal
epithelium in an attempt to re-epithelialize the denuded
surface

70. Oesophageal Stenosis or Stricture
 Sequel to extensive injury, chemical or traumatic, there is a
tendency to produce stenosis or stricture of the oesophagus
 Result from the formation of excessive scar tissue during
the healing process
 The contraction of scar tissue as it ages, causes localized
constriction of the lumen at the site of injury
 Injury from the swallowing of highly irritant or caustic
chemicals is a common cause
 Surgical procedures on the oesophagus may also lead to
contraction of scar tissue at the site of operation

71. Choke
This is complete or partial obstruction or impaction of the
oesophagus by foreign material
Common in cattle as the result of attempting to swallow
large, firm items of food such as beets, turnips, apples, or
small ears of corn without first reducing them to small pieces
Not common in horses
Dogs and cats become choked by sharp pieces of bone which
lodge usually in the thoracic oesophagus
In ruminants choke prevents eructation of gas, causing
ruminal tympanitis (2° bloat), which may be fatal
Without complication, choke can be relieved by the use of
stomach tube

73. Parasitic Oesophagitis
 In dogs, and related wild species, the spirurid nematode - Spirocerca
lupi penetrates the mucosa and submucosa of the lower oesophagus
and causes the formation of submucosal fibrous nodules as it
undergoes development at this site
 The smooth surfaced and sometimes coalescent nodules bulge into the
lumen as much as 0.5cm and usually there is a small fistula connecting
the parasite-inhabited center of the nodule to the lumen of the
oesophagus
 Interference with oesophageal function is minimal (unless a sarcoma is
formed) and the lesions are usually found incidentally postmortem
 Other parasites that invade the oesophagus include the nematode
Gongylonema spp. in ruminants and non-human primates, larvae of
the warble fly Hypoderma spp. in cattle and Sarcocystis spp. in
sheep, and, rarely, other species

75. NEOPLASMS OF THE OESOPHAGUS
 Papillomas of the oral cavity, pharynx, oesophagus and rumen of
cattle are caused by bovine papillomavirus type 4
 The virus is related to but distinct from bovine papillomavirus types
3 and 6, which cause fibro-papillomas of the skin
 Two causative factors have been implicated
 the bovine papillomavirus - 4
 chronic poisoning resulting from ingestion of bracken fern
(Pteridium aquilinum)
 Osteosarcoma and fibrosarcoma of the oesophagus of dogs have
been associated with long-standing lesions of Spirocerca lupi
 Metastasis of tumours to the oesophagus is rare as tumours of adjacent
structures (lymph nodes or thyroid) usually do not invade the
esophagus

76. FORESTOMACHS OF RUMINANTS
(Rumen, Reticulum and Omasum)
The rumen, reticulum, and omasum are called
forestomachs
They have no secretory function comparable to that of
true stomach in monograstrics
The abomasum of ruminants functions as the true
(glandular) stomach where enzymatic breakdown of
ingesta occurs
The rumen, reticulum and omasum are lined by keratinized
stratified squamous epithelium
They function as large fermentation and absorption
chambers where symbiotic bacteria and protozoa digest large
quantities of plant material

77. Ruminant Stomach
Anatomy:
 Reticulum
 Rumen
 Omasum
 Abomasum

80. Compound stomach Simple stomach
4 compartments No compartments
Long digestive system Short digestive system
Prominent microbial digestion Enzymatic digestion
Can synthesize protein Can not synthesize protein
More utilization of fibers Fiber utilization not significant
No need to provide good protein Need to provide good protein
Syntheses of Vit. B No synthesis of vitamin b
pH 4.7 pH 3.2-4
Duration of digestion 4-7 days Duration of digestion is 12- 24
hours
Propionic acid is the source of Glucose is the source of energy

81. Rumen
 First part of the “stomach”
 composes 80% of ruminant
stomach in mature bovine
animals and 30% in young
animals
 Papillae lining
 Storage , Soaking , Physical
mixing and breakdown
 Fermentation
 Breaks down fibrous feeds
into VFAs

82. Reticulum
Second compartment of
stomach
 It has honey comb-like
structure
Help open and close rumen
Make up 5% of the
“stomach”

83. Omasum
 “Many plies”
 No enzymes from walls
 Reduce particle size
 Absorb some water
 Composes 7-8% of bovine
“stomach”
 Absorbs mostly water

84. Abomasum
 the “true” stomach
 Fourth compartment
of the stomach
 True digestion occurs
here
 Composes 7-8% of
stomach in mature
animals and 70% in
young animals
 Enzymes activity
breaks down the feed

85. The fermentation action of ruminal microbial flora
produces volatile faty acids (acetic, proprionic and
butyric acids), gases (CO2 and methane), energy, and
water
The relative proportions of these and other by-products of
ruminal fermentation vary considerably with the type and
composition of the diet
The composition of the ruminal flora is influenced by diet
and the type and amounts of fermentation by-products
produced as well as the resulting pH
In cattle and sheep, the normal pH of the rumen ranges
from 5.5 to 7.5
Deviations from this range can alter the composition of the
ruminal flora, which in turn can adversely affect ruminal
function and the health of the animal

86. RUMINAL TYMPANITES (BLOAT)
 Tympanitis of the rumen, or bloat, consists of the
accumulation of excessive quantities of gas in the lumen of
the organ, distending it to life-threatening proportions.
The gas, which is usually flammable, consists largely of
methane, carbondioxide, carbon monoxide, and smaller
amounts of others gases, including the poisonous
dihydrogen sulfide (H2S). These gases are the common
products of microbiological fermentation of carbohydrates
and proteins and result from the action of many kinds of
Gram-negative saprophytic bacteria and protozoa
present on ingested plant material. The production of these
gaseous metabolic byproducts is normal and goes on
continuously, but normally the gas is expelled in the form of
frequent belchings or eructations through the oesophagus
and mouth.

88. Pathogenesis of Bloat
 Pathologic bloating can result from any interference with
 normal eructations
 production of gas in quantities that exceed the capacity of
oesophageal eructations
 The mechanisms that limit the amount of gas that can be
discharged via the oesophagus in a given period of time is
unknown
 However, eructation is an active reverse peristalsis of the
oesophagus, under the control of the autonomic nervous
system
 The amount of gas produced depends upon the rate of bacterial
fermentation, and this is enhanced when fresh succulent green
legumes, such as clover and alfalfa are ingested

89. Theories of Pathogenesis of Bloat
One theory regarding its pathogenesis is that the green
succelent materials are very soft and hence lack the
required mechanical irritation that the initiation of
expulsive ruminal contractions requires.
Another theory is that the gases arising from the
fermentation of fresh green legumes include sufficient
amounts of toxic H2S that suppress the function of local
nervous structures
 It has not been confirmed that considerable amounts of the
gas is absorbed, or that if H2S is absorbed, it has such a toxic
effect

90. Types of Bloat
Primary (Frothy) bloat
It is the most common form of tympanites in cattle
Arise from consumption of fresh wet leguminous plants
Gas is dispersed in form of small foamy bubbles in viscous
ruminal fluid with low surface tension
The gas entrapped in the frothy fluid is not easily expelled by
eructation and therefore progressively accumulates, causing
massive distention of the rumen
Also, if the fluid enters the oesophagus, it stimulates the
swallowing reflex which in turn prevents normal eructation
This type of bloat is acute, occurring suddenly and often
causing death in a matter of hours

91. FROTHY BLOAT IN CATTLE
 Bloat, or rumen tympany, is the abnormal gas distension of the rumen and reticulum. These
stomachs are located on the left hand side of the animal between the ribcage and the pelvis
and distension results in an abnormal shape to the abdomen especially when viewed from
behind. Gas is normally produced by fermentation of stomach contents through the action of
rumenal microbes (stomach bacteria) and is eliminated by eructation (belching). This gas
layer generally sits above the solid and fluid rumen contents and is belched out periodically.
Problems arise when the gas layer is trapped in a stable froth or foam which prevents it from
being belched out.
 Frothy/pasture bloat is usually associated with feeding of lush, immature pasture such as
clover, lucerne and rapidly growing legumes which are low in fibre but high in water, protein
and sugars which can result in a higher rate of rumen gas production. Bloat can occur within
one hour of grazing especially if cattle are hungry and gorge and can be a cause of sudden
death in cattle. Such cases may be confused with Clostridial diseases which also cause sudden
death and rapid carcase degradation. Animals that have died from bloat are usually found partly
on their backs with legs distended in the air and bloody discharge from body orifices. The
anterior regions of the carcase may be very congested due to huge pressure changes and the
oesophagus (gullet) may have a “bloat line” (red thoracic portion and pale abdominal portion).
Distension of the rumen may decline steadily after death and may not be observable after 12
hours so prompt post mortem examination is advisable.
 Huge increases in intra-rumenal pressure results in blood being prevented from returning to
the heart and interferes with breathing so animals asphyxiate. Other signs in addition to
abdominal distension include kicking at the abdomen, bellowing, increased frequency of lying
down and getting up, respiratory distress, excessive salivation, tongue protrusion and
vomiting in extremely severe cases.

92. SECONDARY (FREE GAS) BLOAT
This is a less common form of tympanites
Results from physical obstruction(or obturation) of the
oesophageal or pharyngeal passageways
Choke, resulting from foreign bodies, is a mechanical cause
of such obstruction
Strictures may have the same effect but are rare
Other causes include pressure upon the oesophagus by
tumours, abscesses, swollen lymph nodes, and other
enlargements
Except in the case of a completely obstructing choke, this
form of bloating arises more gradually and often is chronic
or intermittent depending upon the cause

93. Sequellae of Bloat
Forward displacement of the diaphragm, which
severely limits the respiratory capacity
The increased pressure within the rumen causes it to
expand and thereby compress the abdominal
viscera and occlude the caudal vena cava
This shunts blood from the caudal to the cephalic
parts of the body
These mechanisms result in anoxia, which is the
immediate cause of death when it occurs
If the excessive pressure is relieved by surgical
(trocharization) or other forms of intervention
(stomach tube), the above effects promptly subside

94. Pathology of Bloat
Animals that die of frothy bloat have marked forward
displacement of the diaphragm that compresses their lungs
into the anterior portion of the thorax
Abdominal viscera appear pale due to compression of blood
vessels by the distended rumen
Presence of bloat line in distal 3rd of oesophagus
Rumen will contain small bubbles of entrapped gas
Except for the character of the ruminal contents, animals that die
of secondary bloat have similar signs, but in addition may
have some form of obstructive lesion involving the pharynx
or oesophagus
Sheep, as well as cattle, are susceptible to bloating, but because
of their more conservative eating habits, are less commonly
affected

95. RUMINALACIDOSIS, INFLAMMATION
(RUMENITIS, RETICULITIS, OMASITIS)
 These conditions represent successive stages of a syndrome
often associated with an abrupt change of diet from a low
energy ration to one containing large quantities of highly
fermentable carbohydrates in the form of grains, beets,
turnips, bread, brewery byproducts, or apples
 Occurs most often in high production beef and dairy cattle
operations, but sheep and goats are also susceptible
 Frothy bloat may occur concurrently with this disorder
 Often an extension of stomatitis and oesophagitis (e.g. in some
viral infections)
 The most important and specific form of inflammation here is
that due to grain overload (synonyms ruminal lactic acidosis,
engorgement toxaemia, rumen overload)

96. Grain Overload (Ruminal Acidosis)
It is seen mainly in intensive beef and dairy production and
occurs when the animals have sudden access to a higher level
of carbohydrates
Primary bloat may co-exist
Pathogenesis: Sudden changes to a much higher carbohydrate
diet promotes growth of gram positive bacteria (Streptococci
and Lactobacilli) leading to the production of excess lactic and
volatile fatty acids and a rumen pH less than 4.5
The acids damage the ruminal mucosa and attract large
quantity of fluid from the circulation, leading to
dehydration, acidosis, rumen atony and toxaemia
Death may occur in 24 hours or disease may become
subclinical and yet have significant sequelae.

97. Gross Lesions: These are nonspecific, but rumen pH below 5 is
helpful; Hyperaemia, erosion and ulceration of mucosa are
common features
Histology: Presence of vesicles and neutrophilic infiltration of
the epithelium of ruminal papillae
Sequelae:
 Necrobacillary rumenitis: Caused by Fusobacterium
necrophorum and produces ulcers and stellate scar tissue in
forestomachs. Bacteraemia leads to liver abscesses, vena caval
syndrome etc.
 Polioencephalomalacia: Proliferation of thiaminase
producing bacteria in the acidic rumen has been linked to some
cases of polioencephalomalacia.
 Laminitis - inflammation of the soft portions of the hoof
 Renal cortical necrosis

98.  Mycotic rumenitis: Aetiology includes Rhizopus spp,
Mucor spp and Absidia spp. This is a more severe
complication and could also be secondary to any other
damage to the forestomachs and to prolonged antibiotic
treatment, especially in calves
 Gross: Well-demarcated, often circular, areas of
haemorrhagic infarction covered with a fibrinohaemorrhagic
exudate. Lesion may be present also in liver.
 Histopathology: Acute inflammation with haemorrhage,
oedema, coagulative necrosis and presence of numerous
non-septate branching hyphae, vasculitis and thrombosis

102. TRAUMATIC RETICULITIS/PERITONITIS
(Hardware Disease)
 Cattle kept in farm yards, stables, or at other sites close to human
mechanical habitation are prone to swallowing metallic objects such
as nails, screws, and pieces of wire that have been carelessly left in
their feeding areas
 Most of these foreign bodies almost always remain in the reticulum,
being retained there by the baffle-like folds of its mucosal lining
 Those that penetrate the wall are gradually forced through it by the
recurrent peristaltic contractions of the organ, especially during
preganancy and labour
 While migration of the foreign body in any direction is possible, the
vast majority move antero-ventrally, passing through the diaphragm
into the pericardium and heart muscle, carrying ingesta and
contaminating bacteria with them, causing a condition known as
traumatic pericarditis (hardware disease)

103. Hardware Disease

106. ABOMASUM AND STOMACH
Gastric Dilatation and Torsion
Abomasal Displacement
Abomasal Impaction
GASTRITIS/ABOMASITIS
 Catarrhal
 Haemorrhagic
 Ulcerative
Causes of gastric Ulcers
Neoplasms

107. Equine stomach

108. Bovine stomach

109. Gastric Ulcers
Horse: Gastric ulcer (endoscopy)

110. END OF PART I