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| − | [[Liver, Herpes Virus Infections]]
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| − |
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| − |
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| − |
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| − | ====[[Feline Infectious Peritonitis]]====
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| − |
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| − |
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| − | ===Bacterial===
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| − | *bacteria can enter the [[Liver - Anatomy & Physiology|liver]] through a variety of routes
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| − | **direct implantation
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| − | ***eg foreign body penetration from [[The Reticulum - Anatomy & Physiology|reticulum]]
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| − | **direct extension from disease in adjacent tissues of supportive [[Peritoneal Cavity Inflammatory - Pathology|peritonitis]]
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| − | **haematogenously
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| − | ***via the umbilical vein from an infected umbilicus
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| − | ***via the portal vein in the [[Alimentary - Anatomy & Physiology|alimentary tract]]
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| − | ***via the hepatic artery in bacteraemias and septicaemias
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| − | ***via the bile ducts
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| − | *the [[Liver - Anatomy & Physiology|liver]] may show microscopic evidence of involvement in a large variety of systemic infections
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| − | *these can be accompanied by jaundice
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| − | *the changes in the [[Liver - Anatomy & Physiology|liver]] are diffuse with many small areas of necrosis surrounded by [[Neutrophils - WikiBlood|neutrophils]] and [[Lymphocytes - WikiBlood|lymphocytes]]
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| − | **eg Salmonellosis or Listeriosis
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| − |
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| − | ====Hepatic abscessation====
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| − | *with supportive hepatitis
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| − | *especially common in cattle and sheep
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| − | =====Causes=====
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| − | *bacteria involved
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| − | **''Fusobacterium necrophorum'' 80% +
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| − | **''Arcanobacterium pyogenes''
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| − | **''Streptococcus''
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| − | **''Staphylococcus''
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| − | **''Bacteroides''
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| − | *spread from umbilicus in young animals
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| − | **omphalophlebitis (navel ill)
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| − | **usually mixed bacteria
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| − | ***''Actinomyces pyogenes''
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| − | ***''Staphylococci'' (predominates)
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| − | *haematogenously from other pyaemic source
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| − | **eg metritis or mastitis
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| − | **bacteria invade ruminal wall and enter portal circulation to [[Liver - Anatomy & Physiology|liver]]
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| − | *from rumenitis caused by overfeeding with grain
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| − | **erosion of ruminal epithelium due to acidosis
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| − |
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| − | =====Clinical Signs=====
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| − | *subclinical
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| − | *detected at exploratory laparotomy or sluaghter
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| − | *weight loss (most important)
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| − | *decreased weight gain or milk yields
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| − | *sporadic fever and anorexia
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| − | NB: animals can appear in good health as long as abscesses do not rupture
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| − |
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| − | =====Gross=====
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| − | *large
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| − | *pale greenish-yellow pus
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| − | *thick fibrous capsule
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| − | =====Sequelae=====
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| − | *variable
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| − | **resorption and healing
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| − | **abscess may extend into the heaptic vein
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| − | ***give rise to thrombosis in the caudal vena cava
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| − | ***possible pulmonary abscesses
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| − | ***endocarditis
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| − | **fibrous adhesion to adjacent viscera
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| − | ***if the abscess is near the surface
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| − | **epistaxis, sudden death
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| − |
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| − | NB: in many cases, abscesses are incidental findings at slaughter and result in condemnation of the affected [[Liver - Anatomy & Physiology|livers]]
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| − |
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| − | ====Bacillary necrosis====
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| − | *''Fusobacterium necrophorum''
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| − | *calves and lambs
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| − | *common in intensively reared beef cattle
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| − | *occurs following an infected umbilicus in neonates and from rumenitis in adult cattle
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| − |
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| − | =====Gross=====
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| − | *rounded pale multiple foci of coagulative necrosis throughout the [[Liver - Anatomy & Physiology|liver]]
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| − | *unsoftened, greyish-yellow patches
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| − | *ringed by a zone of hyperaemia
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| − | *foci coalesce in severe cases
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| − | *in adult animals, these lesions may have progressed to abscesses following lysis of the coagulated necrotic tissue and the formation of fibrous capsule around the damaged tissue
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| − | *if animal survives, these lesions may soften develop into abscesses
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| − |
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| − | =====Microscopically=====
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| − | *coagulative necrosis
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| − | *possible evidence of migrating flukes
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| − | *bacteria can be demonstrated in the periphery of the necrotic tissue, especially near its junction with viable tissue
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| − | *there is a rim of neutrophilic cells
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| − |
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| − | ====Infectious Necrotic Hepatitis (Black Disease)====
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| − | *''Clostridium novyi'' type B
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| − | *grazing animals
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| − | **mainly sheep, also cattle (and reported sometimes in horses and goats)
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| − | *organism is widely distributed within the soil and normally present in GIT and [[Liver - Anatomy & Physiology|liver]] of grazing animals on infected pastures
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| − | **worldwide
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| − | *it is ingested by the animal and spores are absorbed via the gut and travel to the [[Liver - Anatomy & Physiology|liver]] , where they lie dormant in [[Macrophages - WikiBlood|macrophages (Kupffer cells)]] - also found in [[Bone Marrow - Anatomy & Physiology|bone marrow]] and [[Spleen - Anatomy & Physiology|spleen]]
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| − | *seasonal disease associated with Fasciola [[Liver - Anatomy & Physiology|liver]] flukes
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| − | **migrating immature [[Liver - Anatomy & Physiology|liver]] flukes precipitate the disease
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| − | **causes [[Liver - Anatomy & Physiology|liver]] damage which provides ideal anaerobic conditions for the activation and germination of spores
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| − | *''C. novyi'' produces three exotoxins
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| − | **alpha - a lethal toxin
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| − | **beta - a lecithinase which is both haemolytic and necrotising
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| − | **zeta - a haemolytic toxin
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| − | *acute toxaemia produced by organism
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| − | **affected animals are usually found dead because death is sudden due to the action of the powerful bacterial endotoxins
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| − | **not all animals will become sick - only when organism starts producing toxin
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| − | *post mortem changes occur rapidly
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| − | =====Clinical=====
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| − | *found dead/sudden death
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| − | **well conditioned sheep 2-4 years old
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| − | **lateral recumbency, few signs of struggle
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| − | **vaccination history (against Clostridium)
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| − | **no red urine or other bleeding
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| − | *IF seen alive
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| − | **severe depression
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| − | **not eating
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| − | **pyrexia
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| − | **hypothermia
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| − | **respiratory distress
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| − | **muffled heart sounds
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| − |
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| − | =====Gross=====
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| − | *rapid decomposition of carcass
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| − | *extensive subcutaneous vessels engorged and haemorrhage causing dark colouration of the skin - hence the name ''''Black Disease'''' - and oedema
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| − | *blood stained fibrinous fluid in abdomen, thorax, and pericardium which clots on exposure to air
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| − | *tissues are autolysed
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| − | *[[Liver - Anatomy & Physiology|liver]] swollen and congested
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| − | *characteristic pale (greyish-yellow) foci (3cm diameter) of necrosis surrounded by a rim of haemorrhage where the bacteria have multiplied upon incision
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| − | *evidence of [[Liver - Anatomy & Physiology|liver]] fluke
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| − | *other organs show general signs of toxaemia
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| − | NB: Distinguish Black Disease from Red Water! The former will have several small areas of necrosis while the latter has one big lump
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| − |
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| − | =====Microscopically=====
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| − | *coagulative necrosis
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| − | *possible evidence of migrating flukes
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| − | *demonstration of bacteria
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| − | **in the necrotic tissue
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| − | **especially near its junction with viable tissue
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| − | **rim of neutrophilic cells
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| − | =====Treatment=====
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| − | *rarely possible
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| − | *Penicillin or Oxytetracycline at very high doses
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| − | =====Prevention=====
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| − | *vaccination
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| − | **normally lasts up to 6 months
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| − | *[[Liver - Anatomy & Physiology|liver]] fluke control
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| − | *remove dead carcasses from pasture
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| − |
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| − | ====Bacillary Haemoglobinuria (Red Water)====
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| − | *''Clostridium haemolyticum'' AKA ''Clostridium novyi'' Type D
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| − | *cattle and sheep
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| − | *highly fatal
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| − | *similar pathogenesis to ''C. novyi''
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| − | *beta toxin produced
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| − | **causes hepatic necrosis and intravascular haemolysis
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| − | *C. haemolyticum found in soil, poorly drained/wet pastures
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| − | *spores found routinely in [[Liver - Anatomy & Physiology|liver]] and GIT and faeces of grazing animals in affected pastures
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| − | *need disease in [[Liver - Anatomy & Physiology|liver]] casing anaerobic conditions to allow bacterial growth and toxin production
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| − | *normally associated with [[Liver - Anatomy & Physiology|Liver]] Fluke damage
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| − | *disease occurs in some areas and some farms - distribution is poorly understood
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| − | =====Clinical Signs=====
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| − | *found dead/sudden death
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| − | **lateral recumbency
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| − | **bloat
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| − | **little signs of struggle
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| − | **blood in nostrils, mouth, [[Rectum - Anatomy & Physiology|rectum]], [[Female Reprodcutive Tract -The Vagina/Vestibule - Anatomy & Physiology|vagina]]
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| − | *IF seen alive
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| − | **depressed, reluctant to move, pyrexia, respiratory distress
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| − | **red urine (haemoglobinuria) but not consistent
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| − | **pale mucous membranes/jaundice
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| − | **bloody froth in nostrils
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| − |
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| − | =====Gross=====
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| − | *post mortem is confirmatory finding
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| − | *rapid decomposition of carcass
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| − | **organs decomposed
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| − | *subcutaneous hameorrhages, odema, emphysema
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| − | *blood stained abdominal and thoracic fluid, large quantity and pericardium
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| − | *animal is severely anaemic
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| − | *may be jaundiced
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| − | *red urine in [[Urinary Bladder - Anatomy & Physiology|bladder]], therefore haemoglobin in urine
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| − | *[[Urinary System - Anatomy & Physiology#Upper Urinary System|kidneys]] speckled with haemoglobin
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| − | *blood in lungs/trachea
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| − | *ischaemic hepatic infarct
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| − | **usually a single large necrotic focus in the [[Liver - Anatomy & Physiology|liver]]
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| − | **area of necrosis, sometimes partially liquefied centre, irregular outline with a hyperaemic edge
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| − |
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| − | =====Microscopically=====
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| − | *presence of Clostridia post mortem must be interpreted with great caution as they are common post mortem invaders
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| − | *FAT for organism
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| − | *identification of toxins
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| − | **need this for diagnosis
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| − |
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| − | =====Treatment=====
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| − | *unlikely
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| − | *very high doses of penicillin or oxytetracycline
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| − | *blood transfusion
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| − | =====Prevention=====
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| − | *vaccination lasts up to 6 months
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| − | *[[Liver - Anatomy & Physiology|liver]] fluke control
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| − | *remove infected carcasses from pasture
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| − | NB: Distinguish Red Water from Black Disease! The former will have bleeding out of any orifice while the latter does not
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| − |
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| − | ====Tyzzer's disease====
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| − | *''Bacillus piliformis''
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| − | *affects
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| − | **mostly laboratory rodents
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| − | **possibly foals 1-4 weeks of age
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| − | **young immune-compromised pups and kittens
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| − | *initial intestinal lesions can be hard to find at post mortem examination
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| − |
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| − | [image from smythes' ppt] wheat sheaf
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| − |
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| − | ====Leptospirosis====
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| − | *''Leptospirosis icterohaemorrhagica'' - a septicaemic disease which affects the [[Liver - Anatomy & Physiology|liver]]
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| − | *puppies
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| − | *Leptospirosis is an important spirochaetal group of diseases causing disease in animals and humans (zoonotic)
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| − | *Transmission
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| − | **via urine of affected animals
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| − | **organisms can remain viable for weeks in damp conditions
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| − | *method of action
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| − | **cause anaemia via intravascular haemolysis
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| − | =====Clinical=====
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| − | *fever
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| − | *dehydration
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| − | *haemorrhaging from the mucous membranes of the body
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| − | =====Diagnosis=====
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| − | *dark field microscopy on fresh urine is best
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| − | =====Gross=====
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| − | *widespread hameorrhages
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| − | *icterus
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| − | *pale foci in the [[Liver - Anatomy & Physiology|liver]] (not always a constant finding)
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| − | *subcapsular and cortical renal haemorrhages
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| − | =====Microscopically=====
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| − | *foci of necrosis
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| − | *dissociation of hepatocytes form each other (similar to post mortem change)
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| − | *substantial haemosiderin in the Kuppfer cells (from the haemolysis)
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| − | *need to use a silver stain or immunofluorescence to demonstrate the organisms in tissues
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| − |
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| − | ====Salmonellosis====
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| − | *''Salmonella dublin''
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| − | *calves
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| − | =====Clinical=====
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| − | *fever
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| − | *dehydration
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| − | *[[Diarrhoea|diarrhoea]]
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| − | =====Gross=====
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| − | *severe, often haemorrhagic, inflammation in the [[Ileum - Anatomy & Physiology|ileum]]
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| − | *'''paratyphoid nodules''' - pale foci of necrosis in the [[Liver - Anatomy & Physiology|liver]]
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| − | =====Microscopically=====
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| − | *foci of hepatocytic necrosis
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| − | *mixed mononuclear inflammatory cell infiltrate
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| − | NB: small foci of hepatocytic necrosis are often found as incidental lesions at post mortem examination
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| − |
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| − | ====Other bacteria causing liver lesions====
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| − | =====''Mycobacterium tuberculosis''=====
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| − | *in all species
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| − | *causes granulomas
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| − |
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| − | =====''Actinobacillus equuli''=====
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| − | *foals
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| − | *bacteria from the septicaemia localise in the [[Liver - Anatomy & Physiology|liver]] and other tissues, including the [[Urinary System - Anatomy & Physiology#Upper Urinary System|kidney]]
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| − |
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| − | =====''Nocardia species''=====
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| − | *dogs
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| − | *cause pyogranulomatous foci
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| − |
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| − | ===Parasitic===
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| − | Many parasites pass through the [[Liver - Anatomy & Physiology|liver]] as part of their life cycle within the host
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| − |
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| − | Some migrate further to other organs while others remain in [[Liver - Anatomy & Physiology|liver]] tissue, especially the bile ducts
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| − |
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| − | Most migrating parasites escape the [[Liver - Anatomy & Physiology|liver]] but occasionally some may die and provoke a granulomatous reaction that may calicfy later
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| − |
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| − | The following are types of parasites causing [[Liver - Anatomy & Physiology|liver]] lesions:
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| − |
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| − | ====Nematodes====
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| − | *these cause damage during migration through the [[Liver - Anatomy & Physiology|liver]]
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| − | =====Ascaris suum=====
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| − | *Ascariasis
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| − | *''''milk spot' liver'''
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| − | *pigs
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| − | *common incidental finding at post mortem examination
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| − | *affected [[Liver - Anatomy & Physiology|livers]] are condemned at meat inspection
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| − | ======Gross======
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| − | *initial haemorrhagic tracts through the [[Liver - Anatomy & Physiology|liver]] attributed to the migration of ascarid larvae
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| − | *later stages show fibrosis of these tracts as poorly defined, diffuse, white spots on the capsular surface
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| − | ======Microscopically======
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| − | *initial haemorrhage and necrosis of parenchyma along the tracts
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| − | *later repair by fibrous tissue at foci
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| − | *inflammatory cell response contains many [[Eosinophils - WikiBlood|eosinophils]], as well as [[Lymphocytes - WikiBlood|lymphocytes]] and [[Macrophages - WikiBlood|macrophages]]
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| − |
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| − | =====Strongyles=====
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| − | *horses
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| − | *it is common to find fibrous tags incidentally on the [[Liver - Anatomy & Physiology|liver]] surface and adjacent diaphragm
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| − | *these are remnants of fibrous repair following the egress of the parasites from the [[Liver - Anatomy & Physiology|liver]]
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| − |
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| − | ====Cestodes====
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| − | *tapeworms
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| − | *have both intermediate and final hosts in their life cycle
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| − | *main expression in the UK are the encysted forms that utilise the [[Liver - Anatomy & Physiology|liver]] and other organs in intermediate hosts
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| − | =====Taenia hydatigena=====
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| − | *the most important species
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| − | *final host
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| − | **dog
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| − | **alimentary tract
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| − | *intermediate host
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| − | **ruminant, horse, or pig
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| − | *life cycle is completed when the carnivore eats the tissues of the intermediate host containing the cysts
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| − | *the intermediate stage - Cysticercus tennuicollis
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| − | **fluid filled cysts on the surface of the [[Liver - Anatomy & Physiology|liver]] and in the [[Peritoneal cavity - Anatomy & Physiology|peritoneal cavity]]
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| − | NB: other Taenia species have muscle and brain as preferred sites in the intermediate hosts
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| − |
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| − | Some can infect humans - zoonoses
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| − |
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| − | =====Echinococcus granulosus=====
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| − | *Hydatid Disease
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| − | *final host
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| − | **dog, fox, and other canids
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| − | *intermediate host
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| − | **sheep most commonly affected
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| − | **ox and horses
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| − | NB: can also affect man - zoonosis
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| − | *'''hydatids''' - the cyst form
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| − | **develops from the ova
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| − | **occur in the lung and [[Liver - Anatomy & Physiology|liver]]
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| − | **cysts are usually multiple
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| − | **5-10cm in diameter
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| − | **contain a clear fluid with numerous scolices or '''"hydatid sand"'''
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| − | **the small calcified lesions that are sometimes present in the [[Liver - Anatomy & Physiology|liver]] of sheep may represent degenerate hydatid cysts
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| − | **can be very prevalent in some geographical areas
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| − |
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| − | ====Trematodes====
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| − | *flukes are important pathogens of the [[Liver - Anatomy & Physiology|liver]]
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| − | *Fascioliasis is among the most important parasitic conditions of sheep and cattle and is common
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| − | =====Fasciola hepatica=====
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| − | *common [[Liver - Anatomy & Physiology|liver]] fluke
| |
| − | *intermediate host
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| − | **aquatic snails
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| − | **therefore infestation is more common in damp or poorly drained pastures
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| − | *final host
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| − | **cattle and sheep
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| − | *can cause severe haemorrhagic [[Liver - Anatomy & Physiology|liver]] damage
| |
| − | *death in heavy infestations in sheep during migratory phase (1 month) through the [[Liver - Anatomy & Physiology|liver]] tissue
| |
| − | *recovered animals will have scarred [[Liver - Anatomy & Physiology|livers]]
| |
| − | *more commonly associated with chronic bile duct inflammation - cholangitis [need link to below]
| |
| − | **the adults live in the bile ducts
| |
| − | '''Acute Fascioliasis'''
| |
| − | *acute disease associated with immature fluke migration through the [[Liver - Anatomy & Physiology|liver]]
| |
| − | *occurs in late autumn and winter
| |
| − | *severity of outbreaks depend on a number of epidemiological factors
| |
| − | *the [[Liver - Anatomy & Physiology|liver]] of animals which die of this disease will be
| |
| − | **enlarged
| |
| − | **haemorrhagic
| |
| − | **honeycombed with the tracts of migrating flukes
| |
| − | ***tracts become filled with blood and degenerate hepatocytes later infiltrated with [[Eosinophils - WikiBlood|eosinophils]], [[Lymphocytes - WikiBlood|lymphocytes]] and replaced by fibrosis
| |
| − | **surface is covered with a fibrinous peritonitis, especially the ventral lobe
| |
| − | **subcapsular haemorrhages are frequent
| |
| − | **rupture into the abdomen is not an uncommon finding
| |
| − | '''Chronic Fascioliasis'''
| |
| − | ======Gross======
| |
| − | *[[Liver - Anatomy & Physiology|liver]] is reduced in size, unevenly
| |
| − | **left lobe is most severely affected with atrophy of the extremities
| |
| − | *hypertrophy may occur in some cases
| |
| − | **dorsal lobe
| |
| − | **this changes size and distorts shape of [[Liver - Anatomy & Physiology|liver]]
| |
| − | *the surface will be uneven with areas of fibrous tissue replacing the cells damaged by the migrating flukes
| |
| − | *bile ducts
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| − | **prominent thick protruding white bile ducts on the '''visceral surface''' spreading from the hilus to the left lobe
| |
| − | **the bile ducts are dilated, black, and calcified on '''cut surface'''
| |
| − | **numerous adult flukes can be expressed from the bile ducts
| |
| − | **chronic cholangitis
| |
| − | **''''pipe stem'''' appearance in cattle because bile ducts are very much thickened and often calcified
| |
| − | *bile
| |
| − | **dark brown, thick, and gritty in consistency
| |
| − | NB: the fibrosis which occurs in the chronic stage is realted only partly to the healing of the migratory tracts and the rest may be related to the development of immunity and rechallenge
| |
| − |
| |
| − | ======Microscopically======
| |
| − | *reactive hyperplasia of the bile ducts
| |
| − | *substantial inflammatory cell infiltrate and peripheral fibrosis
| |
| − | *calcification of the chronically damaged tissue
| |
| − |
| |
| − | ===Protozoal===
| |
| − | ====Toxoplasmosis====
| |
| − | *''Toxoplasma gondii''
| |
| − | *broad host range
| |
| − | *characterised by widespread necrosis in many organs
| |
| − | *[[Liver - Anatomy & Physiology|liver]] lesions
| |
| − | **appear as disseminated foci of necrosis with little or no inflammatory reactions
| |
| − | **white or yellow foci are visible on the surface
| |
| − |
| |
| − | == Peliosis hepatica ==
| |
| − |
| |
| − | *Dogs and cats
| |
| − | *Vasculoproliferative disorder – cystic, blood filled spaces in the [[Liver - Anatomy & Physiology|liver]] , surrounded by fibromyxoid matrix containing inflammatory cells and dilated capillaries.
| |
| − | *Spaces may merge with hepatic sinuosoids.
| |
| − | *May be associated with Bartonella henselae infection.
| |
| − | *Natural host is the cat
| |
| − | *Transmitted between cats by fleas
| |
| − | *Cause of cat-scratch fever and bacillary angiomatosis in humans
| |
| − |
| |
| − | == Lobular dissecting hepatitis ==
| |
| − |
| |
| − | *Rare cause of chronic [[Liver - Anatomy & Physiology|liver]] failure in young dogs
| |
| − | *Less than 5yrs of age
| |
| − | *Standard poodle overrepresented
| |
| − | *Gross findings:
| |
| − | **Micronodular microhepatica, ascites, numerous portosystemic shunts
| |
| − | *Histology:
| |
| − | **Hepatic architecture disrupted by collagen and reticulin fibres separating the hepatic lobules into small clusters and individual cells
| |
| − | **Hepatocytes mutlifocally swollen, lightly eosinophilic, some binucleated.
| |
| − | **Variable nodular regeneration.
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| − | **Scattered necrotic cells and occasional foci of inflammation.
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| − | *Cu2+ accumulation not a consistent finding.
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| − | *Aetiology – possibly a specific reaction pattern in neonatal/juvenile [[Liver - Anatomy & Physiology|liver]] .
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| − | *Differentials:
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| − | **Copper toxicity
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| − | **Copper storage disease
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| − | **Aflatoxin
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| − | **Infectious diseases such as Leptospria spp. and CAV-1.
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| − |
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| − | == Hepatitis in cats ==
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| − |
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| − | *2 main types
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| − | **cholangiohepatitis
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| − | ***cholangitis
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| − | ***periportal hepatocellular necrosis
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| − | ***neutrophils in the portal areas
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| − | ***acute or chronic.
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| − | ***Usually male, pure bred
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| − | *** Cats more ill than lymphocytic portal hepatitis.
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| − | ***Higher ALT and serum bilirubin levels.
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| − | **Lymphocytic portal hepatitis
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| − | ***infiltration of portal areas with lymphocytes and plasma cells
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| − | ***no cholangitis
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| − | ***no periportal hepatocellular necrosis.
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| | [[Category:Liver_-_Pathology]] | | [[Category:Liver_-_Pathology]] |