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Large animal section: No. 13THE HEALTHY AND UNHEALTHY RUMEN WALL RUMEN MUCOSA Development of rumen papillae depends mainly on type of diet. Hyper- and parakeratosis does not develop in animals fed adequate levels of coarse roughage: approximately 15% Dystrophic lesions are reversible when adequate roughage is fed. Roughage removes keratinaceous debris and food particles from mucosal surface. Hyperkeratosis also occurs in calves deficient in Vit A.
1. Adequate roughage:
2. High concentrate rations:
Histology:
3. Barley containing rations = similar changes plus:
PM CHANGES Ruminal mucosa sloughs in few hours after death Separates from lamina propria in large grey patches.
PERSISTENT FIRM MUCOSAL ATTACHMENT = ABNORMAL
Note: acute acidosis = no adhesion.
SPECIFIC DISEASE CONDITIONS
Ruminal tympanyDistended rumen Marked erythema beneath rumen mucosa especially ventral sacs. Rumen could have ruptured. Dead several hours: Exfoliation of cornified epithelium Marked congestion of submucosa.
Traumatic reticuloperitonitis
Penetration of side of reticulum leads to suppurative inflammation of grooves between reticulum, omasum and abomasum, which may cause vagus indigestion (“vagus nerve paralysis”).
Vagus indigestionAbomasum may be distended and impacted with dry ingesta. Omasum can be very large & impacted with dehydrated ingesta. Rumen is distended with enough fluid to cause sloshing No ruminal fermentation or odor.
Rumenitis Inflammation of the rumen wall
Acidosis Cause : too high grain component in feed Early stage: copious amounts of porridge-like rumen contents which may visibly contain increased grain (finely ground). Rumenitis and low rumen pH (<5). May be slight, poorly defined bluish discoloration of ventral sac of rumen and in omasum visible through serosa. When epithelium is detached = hyperaemia of lamina propria in patches. Histology:
Note: remember acidosis may predispose to cerebrocortical necrosis (cerebral poliomalacia)
Necrobacillary rumenitisFusobacterium necrophorum Affects papillated areas of ventral sac and occasionally pillars. Inner surface: Early lesions = multiple irregular patches 2-15cm across Papillae are swollen, dark, slightly mushy and matted together by fibrinocellular inflammatory exudate. Affected papillae are necrotic Ulceration is delayed if there is ruminal atony or stasis. If animal recovers: Affected epithelium sloughs Ulcer contracts Epithelial regeneration starts at margins Regenerated epithelium is flat and white & papillae does not return completely A stellate scar often remains Perforation of omasal leaves is common. Histology:
Mycotic rumenitisInflammation extends to the serosa and is haemorrhagic. Can extend to peritoneum = haemorrhagic and fibrinous peritonitis.
Mucor, Rhizopus and Absidia spp.Fatal cases most of ventral sac, parts of reticulum and/or omasum are affectedMargins well demarcated by narrow zone of congestive swelling.Red to black, thickened to 1cm or more, firm and leathery.Acute fibrinohaemorrhagic peritonitis and in grooves bloodstained inflammatory oedema.Thrombosis as result of vasculitis = basis of this lesion.Inner surface rumen lesions are more haemorrhagic and more irregular in outline than in necrobacillosis.Necrotic epithelium is difficult to detach.Histology:
Parasitic diseases Conical flukes (Paramphistomum) = non-pathogenic adult parasites in rumen
NeoplasiaFibropapillomas = Bovine papilloma virus (BPV) 2 (rare) Squamous cell carcinoma in association with BPV 4 (rare)
(Courtesy of Jubb, Kennedy, Radostis, Gay & Hinchcliff. Compiled with help of Dr Thelma Meiring) For further information contact:
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