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| + | *bacteria can enter the [[Liver - Anatomy & Physiology|liver]] through a variety of routes | ||
| + | **direct implantation | ||
| + | ***eg foreign body penetration from [[The Reticulum - Anatomy & Physiology|reticulum]] | ||
| + | **direct extension from disease in adjacent tissues of supportive [[Peritoneal Cavity Inflammatory - Pathology|peritonitis]] | ||
| + | **haematogenously | ||
| + | ***via the umbilical vein from an infected umbilicus | ||
| + | ***via the portal vein in the [[Alimentary - Anatomy & Physiology|alimentary tract]] | ||
| + | ***via the hepatic artery in bacteraemias and septicaemias | ||
| + | ***via the bile ducts | ||
| + | *the [[Liver - Anatomy & Physiology|liver]] may show microscopic evidence of involvement in a large variety of systemic infections | ||
| + | *these can be accompanied by jaundice | ||
| + | *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]] | ||
| + | **eg Salmonellosis or Listeriosis | ||
| + | </div> | ||
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| + | |||
| + | |||
| + | ====[[Hepatic Abscessation]]==== | ||
| + | |||
| + | |||
| + | ====Bacillary necrosis==== | ||
| + | *''Fusobacterium necrophorum'' | ||
| + | *calves and lambs | ||
| + | *common in intensively reared beef cattle | ||
| + | *occurs following an infected umbilicus in neonates and from rumenitis in adult cattle | ||
| + | |||
| + | =====Gross===== | ||
| + | *rounded pale multiple foci of coagulative necrosis throughout the [[Liver - Anatomy & Physiology|liver]] | ||
| + | *unsoftened, greyish-yellow patches | ||
| + | *ringed by a zone of hyperaemia | ||
| + | *foci coalesce in severe cases | ||
| + | *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 | ||
| + | *if animal survives, these lesions may soften develop into abscesses | ||
| + | |||
| + | =====Microscopically===== | ||
| + | *coagulative necrosis | ||
| + | *possible evidence of migrating flukes | ||
| + | *bacteria can be demonstrated in the periphery of the necrotic tissue, especially near its junction with viable tissue | ||
| + | *there is a rim of neutrophilic cells | ||
| + | |||
| + | ====Infectious Necrotic Hepatitis (Black Disease)==== | ||
| + | *''Clostridium novyi'' type B | ||
| + | *grazing animals | ||
| + | **mainly sheep, also cattle (and reported sometimes in horses and goats) | ||
| + | *organism is widely distributed within the soil and normally present in GIT and [[Liver - Anatomy & Physiology|liver]] of grazing animals on infected pastures | ||
| + | **worldwide | ||
| + | *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]] | ||
| + | *seasonal disease associated with Fasciola [[Liver - Anatomy & Physiology|liver]] flukes | ||
| + | **migrating immature [[Liver - Anatomy & Physiology|liver]] flukes precipitate the disease | ||
| + | **causes [[Liver - Anatomy & Physiology|liver]] damage which provides ideal anaerobic conditions for the activation and germination of spores | ||
| + | *''C. novyi'' produces three exotoxins | ||
| + | **alpha - a lethal toxin | ||
| + | **beta - a lecithinase which is both haemolytic and necrotising | ||
| + | **zeta - a haemolytic toxin | ||
| + | *acute toxaemia produced by organism | ||
| + | **affected animals are usually found dead because death is sudden due to the action of the powerful bacterial endotoxins | ||
| + | **not all animals will become sick - only when organism starts producing toxin | ||
| + | *post mortem changes occur rapidly | ||
| + | =====Clinical===== | ||
| + | *found dead/sudden death | ||
| + | **well conditioned sheep 2-4 years old | ||
| + | **lateral recumbency, few signs of struggle | ||
| + | **vaccination history (against Clostridium) | ||
| + | **no red urine or other bleeding | ||
| + | *IF seen alive | ||
| + | **severe depression | ||
| + | **not eating | ||
| + | **pyrexia | ||
| + | **hypothermia | ||
| + | **respiratory distress | ||
| + | **muffled heart sounds | ||
| + | |||
| + | =====Gross===== | ||
| + | *rapid decomposition of carcass | ||
| + | *extensive subcutaneous vessels engorged and haemorrhage causing dark colouration of the skin - hence the name ''''Black Disease'''' - and oedema | ||
| + | *blood stained fibrinous fluid in abdomen, thorax, and pericardium which clots on exposure to air | ||
| + | *tissues are autolysed | ||
| + | *[[Liver - Anatomy & Physiology|liver]] swollen and congested | ||
| + | *characteristic pale (greyish-yellow) foci (3cm diameter) of necrosis surrounded by a rim of haemorrhage where the bacteria have multiplied upon incision | ||
| + | *evidence of [[Liver - Anatomy & Physiology|liver]] fluke | ||
| + | *other organs show general signs of toxaemia | ||
| + | NB: Distinguish Black Disease from Red Water! The former will have several small areas of necrosis while the latter has one big lump | ||
| + | |||
| + | =====Microscopically===== | ||
| + | *coagulative necrosis | ||
| + | *possible evidence of migrating flukes | ||
| + | *demonstration of bacteria | ||
| + | **in the necrotic tissue | ||
| + | **especially near its junction with viable tissue | ||
| + | **rim of neutrophilic cells | ||
| + | =====Treatment===== | ||
| + | *rarely possible | ||
| + | *Penicillin or Oxytetracycline at very high doses | ||
| + | =====Prevention===== | ||
| + | *vaccination | ||
| + | **normally lasts up to 6 months | ||
| + | *[[Liver - Anatomy & Physiology|liver]] fluke control | ||
| + | *remove dead carcasses from pasture | ||
| + | |||
| + | ====Bacillary Haemoglobinuria (Red Water)==== | ||
| + | *''Clostridium haemolyticum'' AKA ''Clostridium novyi'' Type D | ||
| + | *cattle and sheep | ||
| + | *highly fatal | ||
| + | *similar pathogenesis to ''C. novyi'' | ||
| + | *beta toxin produced | ||
| + | **causes hepatic necrosis and intravascular haemolysis | ||
| + | *C. haemolyticum found in soil, poorly drained/wet pastures | ||
| + | *spores found routinely in [[Liver - Anatomy & Physiology|liver]] and GIT and faeces of grazing animals in affected pastures | ||
| + | *need disease in [[Liver - Anatomy & Physiology|liver]] casing anaerobic conditions to allow bacterial growth and toxin production | ||
| + | *normally associated with [[Liver - Anatomy & Physiology|Liver]] Fluke damage | ||
| + | *disease occurs in some areas and some farms - distribution is poorly understood | ||
| + | =====Clinical Signs===== | ||
| + | *found dead/sudden death | ||
| + | **lateral recumbency | ||
| + | **bloat | ||
| + | **little signs of struggle | ||
| + | **blood in nostrils, mouth, [[Rectum - Anatomy & Physiology|rectum]], [[Female Reprodcutive Tract -The Vagina/Vestibule - Anatomy & Physiology|vagina]] | ||
| + | *IF seen alive | ||
| + | **depressed, reluctant to move, pyrexia, respiratory distress | ||
| + | **red urine (haemoglobinuria) but not consistent | ||
| + | **pale mucous membranes/jaundice | ||
| + | **bloody froth in nostrils | ||
| + | |||
| + | =====Gross===== | ||
| + | *post mortem is confirmatory finding | ||
| + | *rapid decomposition of carcass | ||
| + | **organs decomposed | ||
| + | *subcutaneous hameorrhages, odema, emphysema | ||
| + | *blood stained abdominal and thoracic fluid, large quantity and pericardium | ||
| + | *animal is severely anaemic | ||
| + | *may be jaundiced | ||
| + | *red urine in [[Urinary Bladder - Anatomy & Physiology|bladder]], therefore haemoglobin in urine | ||
| + | *[[Urinary System - Anatomy & Physiology#Upper Urinary System|kidneys]] speckled with haemoglobin | ||
| + | *blood in lungs/trachea | ||
| + | *ischaemic hepatic infarct | ||
| + | **usually a single large necrotic focus in the [[Liver - Anatomy & Physiology|liver]] | ||
| + | **area of necrosis, sometimes partially liquefied centre, irregular outline with a hyperaemic edge | ||
| + | |||
| + | =====Microscopically===== | ||
| + | *presence of Clostridia post mortem must be interpreted with great caution as they are common post mortem invaders | ||
| + | *FAT for organism | ||
| + | *identification of toxins | ||
| + | **need this for diagnosis | ||
| + | |||
| + | =====Treatment===== | ||
| + | *unlikely | ||
| + | *very high doses of penicillin or oxytetracycline | ||
| + | *blood transfusion | ||
| + | =====Prevention===== | ||
| + | *vaccination lasts up to 6 months | ||
| + | *[[Liver - Anatomy & Physiology|liver]] fluke control | ||
| + | *remove infected carcasses from pasture | ||
| + | NB: Distinguish Red Water from Black Disease! The former will have bleeding out of any orifice while the latter does not | ||
| + | |||
| + | ====Tyzzer's disease==== | ||
| + | *''Bacillus piliformis'' | ||
| + | *affects | ||
| + | **mostly laboratory rodents | ||
| + | **possibly foals 1-4 weeks of age | ||
| + | **young immune-compromised pups and kittens | ||
| + | *initial intestinal lesions can be hard to find at post mortem examination | ||
| + | |||
| + | [image from smythes' ppt] wheat sheaf | ||
| + | |||
| + | ====Leptospirosis==== | ||
| + | *''Leptospirosis icterohaemorrhagica'' - a septicaemic disease which affects the [[Liver - Anatomy & Physiology|liver]] | ||
| + | *puppies | ||
| + | *Leptospirosis is an important spirochaetal group of diseases causing disease in animals and humans (zoonotic) | ||
| + | *Transmission | ||
| + | **via urine of affected animals | ||
| + | **organisms can remain viable for weeks in damp conditions | ||
| + | *method of action | ||
| + | **cause anaemia via intravascular haemolysis | ||
| + | =====Clinical===== | ||
| + | *fever | ||
| + | *dehydration | ||
| + | *haemorrhaging from the mucous membranes of the body | ||
| + | =====Diagnosis===== | ||
| + | *dark field microscopy on fresh urine is best | ||
| + | =====Gross===== | ||
| + | *widespread hameorrhages | ||
| + | *icterus | ||
| + | *pale foci in the [[Liver - Anatomy & Physiology|liver]] (not always a constant finding) | ||
| + | *subcapsular and cortical renal haemorrhages | ||
| + | =====Microscopically===== | ||
| + | *foci of necrosis | ||
| + | *dissociation of hepatocytes form each other (similar to post mortem change) | ||
| + | *substantial haemosiderin in the Kuppfer cells (from the haemolysis) | ||
| + | *need to use a silver stain or immunofluorescence to demonstrate the organisms in tissues | ||
| + | |||
| + | ====Salmonellosis==== | ||
| + | *''Salmonella dublin'' | ||
| + | *calves | ||
| + | =====Clinical===== | ||
| + | *fever | ||
| + | *dehydration | ||
| + | *[[Diarrhoea|diarrhoea]] | ||
| + | =====Gross===== | ||
| + | *severe, often haemorrhagic, inflammation in the [[Ileum - Anatomy & Physiology|ileum]] | ||
| + | *'''paratyphoid nodules''' - pale foci of necrosis in the [[Liver - Anatomy & Physiology|liver]] | ||
| + | =====Microscopically===== | ||
| + | *foci of hepatocytic necrosis | ||
| + | *mixed mononuclear inflammatory cell infiltrate | ||
| + | NB: small foci of hepatocytic necrosis are often found as incidental lesions at post mortem examination | ||
| + | |||
| + | ====Other bacteria causing liver lesions==== | ||
| + | =====''Mycobacterium tuberculosis''===== | ||
| + | *in all species | ||
| + | *causes granulomas | ||
| + | |||
| + | =====''Actinobacillus equuli''===== | ||
| + | *foals | ||
| + | *bacteria from the septicaemia localise in the [[Liver - Anatomy & Physiology|liver]] and other tissues, including the [[Urinary System - Anatomy & Physiology#Upper Urinary System|kidney]] | ||
| + | |||
| + | =====''Nocardia species''===== | ||
| + | *dogs | ||
| + | *cause pyogranulomatous foci | ||
| + | |||
| + | |||
| + | |||
| + | |||
| + | |||
[[Category:Liver_-_Inflammatory_Pathology]] | [[Category:Liver_-_Inflammatory_Pathology]] | ||
Revision as of 14:02, 7 June 2010
Hepatitis, Bacterial
- bacteria can enter the liver through a variety of routes
- direct implantation
- eg foreign body penetration from reticulum
- direct extension from disease in adjacent tissues of supportive peritonitis
- haematogenously
- via the umbilical vein from an infected umbilicus
- via the portal vein in the alimentary tract
- via the hepatic artery in bacteraemias and septicaemias
- via the bile ducts
- direct implantation
- the liver may show microscopic evidence of involvement in a large variety of systemic infections
- these can be accompanied by jaundice
- the changes in the liver are diffuse with many small areas of necrosis surrounded by neutrophils and lymphocytes
- eg Salmonellosis or Listeriosis
Hepatic Abscessation
Bacillary necrosis
- Fusobacterium necrophorum
- calves and lambs
- common in intensively reared beef cattle
- occurs following an infected umbilicus in neonates and from rumenitis in adult cattle
Gross
- rounded pale multiple foci of coagulative necrosis throughout the liver
- unsoftened, greyish-yellow patches
- ringed by a zone of hyperaemia
- foci coalesce in severe cases
- 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
- if animal survives, these lesions may soften develop into abscesses
Microscopically
- coagulative necrosis
- possible evidence of migrating flukes
- bacteria can be demonstrated in the periphery of the necrotic tissue, especially near its junction with viable tissue
- there is a rim of neutrophilic cells
Infectious Necrotic Hepatitis (Black Disease)
- Clostridium novyi type B
- grazing animals
- mainly sheep, also cattle (and reported sometimes in horses and goats)
- organism is widely distributed within the soil and normally present in GIT and liver of grazing animals on infected pastures
- worldwide
- it is ingested by the animal and spores are absorbed via the gut and travel to the liver , where they lie dormant in macrophages (Kupffer cells) - also found in bone marrow and spleen
- seasonal disease associated with Fasciola liver flukes
- C. novyi produces three exotoxins
- alpha - a lethal toxin
- beta - a lecithinase which is both haemolytic and necrotising
- zeta - a haemolytic toxin
- acute toxaemia produced by organism
- affected animals are usually found dead because death is sudden due to the action of the powerful bacterial endotoxins
- not all animals will become sick - only when organism starts producing toxin
- post mortem changes occur rapidly
Clinical
- found dead/sudden death
- well conditioned sheep 2-4 years old
- lateral recumbency, few signs of struggle
- vaccination history (against Clostridium)
- no red urine or other bleeding
- IF seen alive
- severe depression
- not eating
- pyrexia
- hypothermia
- respiratory distress
- muffled heart sounds
Gross
- rapid decomposition of carcass
- extensive subcutaneous vessels engorged and haemorrhage causing dark colouration of the skin - hence the name 'Black Disease' - and oedema
- blood stained fibrinous fluid in abdomen, thorax, and pericardium which clots on exposure to air
- tissues are autolysed
- liver swollen and congested
- characteristic pale (greyish-yellow) foci (3cm diameter) of necrosis surrounded by a rim of haemorrhage where the bacteria have multiplied upon incision
- evidence of liver fluke
- other organs show general signs of toxaemia
NB: Distinguish Black Disease from Red Water! The former will have several small areas of necrosis while the latter has one big lump
Microscopically
- coagulative necrosis
- possible evidence of migrating flukes
- demonstration of bacteria
- in the necrotic tissue
- especially near its junction with viable tissue
- rim of neutrophilic cells
Treatment
- rarely possible
- Penicillin or Oxytetracycline at very high doses
Prevention
- vaccination
- normally lasts up to 6 months
- liver fluke control
- remove dead carcasses from pasture
Bacillary Haemoglobinuria (Red Water)
- Clostridium haemolyticum AKA Clostridium novyi Type D
- cattle and sheep
- highly fatal
- similar pathogenesis to C. novyi
- beta toxin produced
- causes hepatic necrosis and intravascular haemolysis
- C. haemolyticum found in soil, poorly drained/wet pastures
- spores found routinely in liver and GIT and faeces of grazing animals in affected pastures
- need disease in liver casing anaerobic conditions to allow bacterial growth and toxin production
- normally associated with Liver Fluke damage
- disease occurs in some areas and some farms - distribution is poorly understood
Clinical Signs
- found dead/sudden death
- IF seen alive
- depressed, reluctant to move, pyrexia, respiratory distress
- red urine (haemoglobinuria) but not consistent
- pale mucous membranes/jaundice
- bloody froth in nostrils
Gross
- post mortem is confirmatory finding
- rapid decomposition of carcass
- organs decomposed
- subcutaneous hameorrhages, odema, emphysema
- blood stained abdominal and thoracic fluid, large quantity and pericardium
- animal is severely anaemic
- may be jaundiced
- red urine in bladder, therefore haemoglobin in urine
- kidneys speckled with haemoglobin
- blood in lungs/trachea
- ischaemic hepatic infarct
- usually a single large necrotic focus in the liver
- area of necrosis, sometimes partially liquefied centre, irregular outline with a hyperaemic edge
Microscopically
- presence of Clostridia post mortem must be interpreted with great caution as they are common post mortem invaders
- FAT for organism
- identification of toxins
- need this for diagnosis
Treatment
- unlikely
- very high doses of penicillin or oxytetracycline
- blood transfusion
Prevention
- vaccination lasts up to 6 months
- liver fluke control
- remove infected carcasses from pasture
NB: Distinguish Red Water from Black Disease! The former will have bleeding out of any orifice while the latter does not
Tyzzer's disease
- Bacillus piliformis
- affects
- mostly laboratory rodents
- possibly foals 1-4 weeks of age
- young immune-compromised pups and kittens
- initial intestinal lesions can be hard to find at post mortem examination
[image from smythes' ppt] wheat sheaf
Leptospirosis
- Leptospirosis icterohaemorrhagica - a septicaemic disease which affects the liver
- puppies
- Leptospirosis is an important spirochaetal group of diseases causing disease in animals and humans (zoonotic)
- Transmission
- via urine of affected animals
- organisms can remain viable for weeks in damp conditions
- method of action
- cause anaemia via intravascular haemolysis
Clinical
- fever
- dehydration
- haemorrhaging from the mucous membranes of the body
Diagnosis
- dark field microscopy on fresh urine is best
Gross
- widespread hameorrhages
- icterus
- pale foci in the liver (not always a constant finding)
- subcapsular and cortical renal haemorrhages
Microscopically
- foci of necrosis
- dissociation of hepatocytes form each other (similar to post mortem change)
- substantial haemosiderin in the Kuppfer cells (from the haemolysis)
- need to use a silver stain or immunofluorescence to demonstrate the organisms in tissues
Salmonellosis
- Salmonella dublin
- calves
Clinical
- fever
- dehydration
- diarrhoea
Gross
- severe, often haemorrhagic, inflammation in the ileum
- paratyphoid nodules - pale foci of necrosis in the liver
Microscopically
- foci of hepatocytic necrosis
- mixed mononuclear inflammatory cell infiltrate
NB: small foci of hepatocytic necrosis are often found as incidental lesions at post mortem examination
Other bacteria causing liver lesions
Mycobacterium tuberculosis
- in all species
- causes granulomas
Actinobacillus equuli
Nocardia species
- dogs
- cause pyogranulomatous foci
Pages in category "Hepatitis, Bacterial"
The following 8 pages are in this category, out of 8 total.