allementry Flashcards
(164 cards)
1
Q
most important things to keep in mind about alimentary pathology
A
-normall mucosal and serosal surfaces should be smooth and shiny
-the quality and quantity of feces and vomit are good clinical signs of alimentary disfunction.
-anatomical location of organs and attachement
-need to know pathogens that affect different species and age groups and cause various
clinicopathological syndromes.
2
Q
small vs large intestinal diarrea
A
small: liquidy
large: hemmoragic or mucoid
3
Q
malfunction
A
-alterations in quallity and quantity of feces.
-diarrhea: increaed frequenxy and volume of discharged semisoild or fluid feces.
4
Q
erosive/ ulcertive stomatitis causes
A
non infectious:
- forgion bodies (foxtails)
-uremic stomatitis
-Lymphoplasmacytic stomatitis in cats - idiopathic condition. or with calcivurus in cats with FeLV.
infectious:
-BVD
-bovine papular stomatitis
-malignant catarrhal fever (MLC
-blyetongue
-IBR in neonatal calves
-feline calicivirus
5
Q
Uremic stomatitis
A
-Bucal and lingual erosions/ulcers often
occur adjacent to the openings of salivary ducts
-many causes, ammonia, uremic vasculitis and impaired microvascular perfusion, mechanical abrasions
6
Q
Lymphoplasmacytic stomatitis
A
Idiopathic condition
hypothetically associated
with presence of bacteria
or calicivirus in cats
infected with FeLV and/or
FIV.
7
Q
Proliferative (Parapox) stomatitis
A
-proliferative: bovine papular stomatitis: target lesion (looks like target) in oral, espohageal and ruminal mucosa.
-zoonosis are milkers nodules on humans fingers
8
Q
Contagious ecthyma (orf, infectious pustular
dermatitis) in sheep and goats
A
- Proliferative crusting dermatitis of mucocutaneous
junction (lips commissure, eyelids, anus), udder,
teats, and coronary bands - High morbidity and low mortality
- Economic importance due to weight loss
- Zoonosis (orf)
9
Q
Deep stomatitis (necrotizing)
A
- The end-stage of any forms of stomatitis when they are complicated by infection with Fusobacterium necrophorum that causes severe coagulation necrosis.
–Oral necrobacillosis (in calves which is
also laryngeal necrobacillosis)/
fibrinecrotis stomatits
-Actinobacillosis (“wooden tongue”)
caused by Actinobacillus lignieresii. Pyogranulomas resulting from infection with bacteria. inflammation and fibrosis-> wooden tongue.
-gangrenous stomatits (NOMA) human disease holes of mouth
o Eosinophilic stomatitis
- Oral eosinophilic granulomas or ulcers (“rodent ulcers”) occur frequently in cats
10
Q
actinobacillosis causes
A
-wooden tongue
-granulomatous disease in soft tissue of tongue, makes granuloma in tongue.
-neutrophils lead to pus, multinucleated macrophages
-leads to fibrosis so hard wooden tongue
11
Q
Gingival hyperplasia
A
o Simple overgrowth of gum tissue consisting of the fibrous submucosa lined by hyperplastic
gingival epithelium which is not driven by inflammatory process as in hyperplastic gingivitis.
Causes
* Idiopathic
* Breed predisposition
* Medications
12
Q
Eosinophilic granuloma
A
-cats see nodules on tongue and mouth, granuloma stimulated by immune reaction
13
Q
hyperplastic gingivitis
A
o Usually associated with periodontal disease and chronic irritation by plaque/tartar that initially
starts as inflammation (gingivitis) but can progress to severe hyperplastic gingivitis .
14
Q
Gingival epulis
A
-(gingival mass/tumor)
-Fibromatous epulis - a begin tumor of dental mesenchyme.
with lymphoplasmacytic hyperplastic gingivitis
15
Q
canine oral papillomatosis
A
It is a papillomavirus induced, transmissible and occurs in animals younger than 1 year.
o The lesions usually regress spontaneously and immunity is long-lasting.
16
Q
oral melanoma
A
-kiss of death, poor prognosis has metatisis.
-black, dark melanoma
-malignant tumor
17
Q
benign tumors of the mouth dog
A
-gingival hyperplasia
-firbomatous epulis
-locally invasive but begnin (acanthomatous ameloblastoma)
18
Q
malignant tumors oral masses in dogs
A
-melanoma: locally invasive with metastiatic
-squamous cell carcinoma: LN metastisis
-fibrisarcoma: LN metastisis
-osetosarcoma
19
Q
oral masses in cats mouth
A
-esonophilic granuloma: benign inflammatory always chronic.
-squamous cell carcinoma, firbosarcoma and lymphosarcoma: malignant, invasive, metastasis to LN.
20
Q
diff between granulomatous vs abscess
A
Granulomatous: Always chronic.
Are inflammatory processes with macrophages and fibrous tissue. Ex johnes disease.
Purulent or suppurative: can have acute or chronic and can lead to abscess. Abscess are formed by pyogenic bacteria.
-in abscess pyogenic bacteria are encapsulated by fibrous tissue.
21
Q
salivary glands lesions
A
o Rabies virus causes microscopic inflammation of the salivary glands. = sialoadenitis
-ranula: saliva filled cysts/ duct
- Salivary mucocele is a pseudocyst (cavity not lined by epithelium) filled with saliva.
- It occurs secondary to leakage of saliva into surrounding soft tissue and forming cavity surrounded by reactive connective tissue.
o Salivary gland adenocarcinoma
22
Q
megaesophagus
A
-is dilation of the esophagus because of bad/ uncoordinated peristalsis.
clinical signs: regurgitation after feeding, thin, aspiration pneumonia
causes:
-foreign bodies
-external pressure
-myasthenia gravis: either congenital or acquired due to autoimmune disease.
-lead poisoning
-due to persistent aortic arch
23
Q
muscular hypertrophy of esophagus
A
-due to obstruction
-idiopathic seen in horses and pigs
-if foreign body can lead to necrosis no basement membrane no scaffold so you get necrosis and fibrous scaring
24
Q
erosions and ulcers of esophagus (esophagitis)
A
-infectious erosive diseases
-BVD, stomatitis, foot & mouth
cats: calcicivirus
-reflux esophagitis
-improper use of stomach tubes
-foreign bodies
25
choke
o Choke is a clinical term referring to esophageal obstruction.
- Formation of strictures (if chronic), starvation and aspiration pneumonia: A foreign bodies lodged against the mucosa for longer than 2 days cause circumferential pressure necrosis of the esophageal mucosa (in part due to ischemia due to muscular constriction), which heals with fibrosis and cause strictures during healing
26
examination of ruminal contents
-dehydration= dry
-primary bloat= voluminous frothy
-urea toxicity= ammoniacidal odor and alkaline Ph
-organophophate toxicity=oder of cooked turnips
-grain overload=fermentative acidosis oder or ph less than 5
-lead toxicity= metalic lead, paint flakes or motor oil in rumen
27
bloat necropsy findings
-esophageal bloat line from pressure on thoracic inlet and jugular vein return is compromised.
-sinus hemorrhage
-cervical lymph node congestion: jugular vein compromised from bloat
-cranial congestion head and neck
-frothy ruminal contents
lymph edema in caudal portion
28
Bloat clinical signs and types
Primary (frothy) bloat: legume, frothy, due to diet.
* Secondary (free gas) bloat: caused by physical or functional defect in eructation of gas.
* Clinical signs of primary and secondary bloat are the same:
– Distended left paralumbar fossa and abdomen
– Increased respiratory and heart rates
– Decreased ruminal movements in late stages of disease
29
foreign bodies which can lead to bloat
* Trichobezoars (hair balls)
* Phytobezoars (plant balls)
* Nails and wire -> hardware disease
* Ingestion of lead plates from broken
batteries -> lead poisoning ->
polioencephalomalacia in cattle
-can lead to traumatic reticulitis which is firbinopurulent and constrictive pericarditus
30
Chemical rumenitis
* Sudden change to easily fermentable feed
* ↑ dissociated VFA
* Ruminal stasis
* Change in ruminal microflora
* ↑ [lactic acid]
* pH below 5
* Damaged epithelium -Superficial rumenitis
* Dehydration => acidosis => CV collapse
* Death due to dehydration and acidosis then circulatory collapse
31
Ruminal acidosis: Necropsy/Diagnosis
* Dehydrated carcass
* Grain/porridge-like, acidic watery content in rumen
* ↓ ruminal pH disappears after death (12 - 24hr)
* VENTRAL Ruminal mucosal epithelium is firmly attached
* Watery intestinal contents
* Microscopic confirmation of ‘chemical rumenitis’
– may be necessary in animals necropsied more than 12 hrs
after death
* Surviving animals may develop ruminal necrobacillosis
and if survive stellate scars (healed ruminal ulcers)
32
chemical rumenitis causes of death and sequencally
-death is due to: dehydration, acidosis, eventually circulatory collapse
-if survives leads to ruminal necrobacillosis from fusobacterium or truperella pyogens causing ruminal necrobacillosis or in liver can cause caval syndrome. which will lead to stelate scar in rumen.
-mycotic rumenitis from fungal infection in blood vessels.
-ruminal fibropapillomas
33
post mortem examination of abomasum and stomach
-open along greater curvature
-sample from bottom of crypts in the fundus
-examine for blood.
-look at worm count, tie off pylorys and cardia and collect and count worms for haemonchosis
34
gastric dialation causes
-volvus-> due to no eruptation can lead to rupture or death. in animals which cant eructation or vomiting.
-dog dilation and volvulus is always counter clockways, fatal disease.
-dogs predisposing are large breeds, obstruction of cardia or pylorus and repeated dialation.
-Both gastric and splenic
vein are compressed, resulting in a congested and edematous gastric wall (venous infarction
in later stages) and congested spleen, because the arterial blood supply remains patent longer
than venous drainage
35
gastric dilation cause of death and presisposing factors/ clinical
Predisposing factors:
* Hereditary predisposition – Large beeds
* Obstruction of the cardia that prevents eructation and emesis
* Obstruction of the pylorus that prevents passage of gastric contents
* Repeated episodes of gastric dilation, overfeeding,
Clinical consequences:
- Severe distention compromise respiration and cardiovascular function and electrolyte
balance
- Gastric rupture
Cause of death:
* Acid-base imbalance
* Increased intragastric pressure interferes with venous return from portal circulation
-decreased CO and shock
-pigs: gastric torsion is one of main causes of sudden death.
36
Gastric Dilation and Rupture
o Horses
- Acute gastric dilation and rupture in equids occurs most frequently as a terminal event in
small intestinal obstruction, ileus and displacement.
- It can also be a result of the rapid ingestion of fermentable feeds or grain, a situation
analogous to grain overload with lactic acidosis in cattle
o Gastric/abomasal dilation in other animals is usually secondary to ulcer, pyloric stenosis,
overeating, gastritis/abomesitis, vagal indigestion etc.
37
Ante-mortem or postmortem gastric rupture:
The only reliable indicator of ante-mortem rupture of the stomach is the presence of hemorrhage along the margins and evidence of acute
inflammation (e.g. fibrin strands).
38
abomasum displacement cattle
-usually dairy cattle after parturition
-causes: abomasal atony due to heavy grain feeding, hypocalcemia.
-clinical: anorexia, dehydration, ketonuria.
-l sided most common not fatal, R sided 10-15% may progress to volvulus and be fatal.
39
volvus
-intestinal infarction/ twisting, torsion, counter clock wise. on its mesenteric axis
-should always be hemmorage, necrosis.
-has to be transmural to be volvus all levels will be effected not just mucosa.
-torsion: a rotation of abomasum. colon or cecum along its long axis.
40
hemmoragic abomastitis (braxy)
-caused by clostridium septcum.
-with submucosal emphysema in lambs and calves.
-caused by ingested of frozen feeds.
-death due to an exotoxemia endotoxin in blood.
-braxy effects only abomasum
41
gastritis in dogs
-acute: , more common in dogs due to ingestion of spoiled foods, toxins. ect. non fatal and transcient.
-canine hemmoragic gastroenteritis (fatal) will have clinical hematemesis.
-chronic:
-esoniophilic gastroenteritis, hyperplastic gastritis, uremic gastritis, lymphoplasmacytic gastritis, parasites
42
canine hemmoragic gastroenteritis
-smaller breeds
-hematemesis due to superficial hemmorahic necrosis
-die due to dehyrdation and cardio collapse, DIC
-could also be parvoviral enteritis (stomach and colon are not affected)
43
eosinophilic gastroenterocolitis
-parasites-> hypersensitivity reaction. skin disease. or food allergy.
-diagnosis by endoscopic biopsy of stomach duo and colon ALL THREE EFFECTED
44
hyperplastic gastritis
-focal: antral hyperplastic gastritis
-in older and small breeds
-clinical signs of upper GI obstrucyion and vomiting
-other diagnosis: pyloric obstruction due to pyloris muscular hypertrophy. (interfers with food ingestion leads to vommiting and aspiration)
-diffuse: chronic giant hypertrophic gastropathy is rare. weight loss, hypoprotenemia.
45
uremic gastritis
-caused by chronic renal disease/ failure
-gross: congestion and edema with ulceration (sometimes)
-caused by renal failure then injury to capillaries within the lamina propria.
-microscopic mineralizaition of gastric mucosa.
-can lead to renal fibrosis, erosive glossitis or stomatitis, mineralization of intercostal mucosa, uremic pneumonitis.
46
pars esophagea ulceration horses
gastric ulcers
-horses, very common with high workload.
-stress and NSAIDS if they are used predisposing to ulceration.
-can get gastric ulcer with exsanguination which is hemorrhagic ulcer
-perforating abscess CHRONIC -> leads to fibrous scar.
-if given PPI to horses which are dehydrated will destroy kidneys
47
gastric ulcer
o An ulcer is a mucosal defect in which the entire epithelial thickness with the basement
membrane was lost.
o Penetration through the remaining tissue layers to the peritoneal cavity is termed a perforating
ulcer.
o Partial-thickness epithelial loss is termed an erosion
o Chronic ulcers differ from acute ulcers by the presence of an indurated rim caused by fibrosis
and epithelial hyperplasia
48
gastric ulcer signs
-vommiting
-anorexia
-abdominal pain
-anemia
-excanguination-> death
-peritonitis and septicema
49
gastric ulcer path
-imbalance between acid sectrtion and mucosal protection
-high HCL: could be mast cell tumors in dogs/ cats. or gastronoma in dogs.
-infection: helicobacter
-stress induced disturbance in BF (shock)
-NSAIDs depressing prostaglandin formation, decreasing HC03 and blood perfusion. directly toxic to vascular endothelium
-local trauma to mucosa, bile salts from dueodenum, lipid solvents such as alcohol.
50
gastric ulcer in pigs
-affecting pars esophagea
-from finley grown grain, ingredients in diet (whey), and stress
-mortality due to esanguination.
51
gastric ulcer in cattle
-subclinical to fatal
-in calves its mechanical irritation by roughage
-in dairy: heavy grain feeding (LA)leads to mycotic infection
-displacement of abomasum
-BVD and bovine leukosis
52
Mycotic rumenitis
-occurs secondary to the damage to the ruminal mucosa caused by
lactic acidosis or secondary to administration of antibiotics, which disturb the normal flora
and allow fungi (Aspergillus, Mucor etc) to proliferate.
- Ruminal lesions are generally red circular and well delineated, because they are caused by
infarction from thrombosis secondary to fungal vasculitis
53
Bots equine
-gasterophilus intestinalis and G. nasalis.
-not deworming properly
-if bots in stomach no significance
-larve lay eggs on horse very annoying
54
haemonchus contortus
-sheep and goats
-clinical signs (blood eaters blood loss), count worms in abomasum, severe anemia (pale mucus membranes), bottle jaw (hypoprotenemia), weight loss.
-haemonchus paeci affects calves
-barber pole worms, red look like candy canes, mucosa is thickened and edema and black.
55
ostertagia ostertagi
-o,ostertagi BOVINE
-o. circumcinta OVINE
-ingestion of larve, destroys glands in mucosa and destroys partial and cheif cells. (metaplasia as they are replaced by mucus cells) and hypoplasia.
-type I larve develop into adults summer or type II are dormant winter.
-clinical signs: inappetence, diarrhea, wasting, edema
-diagnosis: morocco leather abomasum. generalized edema from hypoprotenemia. proper worm count.
56
gastric / abomasul neoplasia
horses: squamous cell carcinoma of pars esophagia
cattle: lymphoma from BLV
dogs and cats: gastric adenocarcinoma is locally invasive and metastatic
57
Ileus
* Non-mechanical hypomotility resulting in a functional obstruction of the bowel
* Causes:
– Post-surgical - bowel manipulation
– Peritonitis
– Severe abdominal pain
– Electrolyte imbalances (especially hypokalemia)
* There are no gross lesions other than atonic dilation of the intestine.
58
intestinal strictures
causes:
-failure of regeneration
-postenterotony healing-> firbosis-> stricture
59
rectal stricutres
-causes:
-Recurrent rectal prolapse -> circumferential
necrosis -> fibrosis -> stricture, from high perastalis leads to constricting and circumferential necrosis.
-Salmonellosis -> thrombosis of hemorrhoidal artery -> necrosis -> circumferential fibrosis -> stricture.
salmonella causes erosive ulcerative enterocolotis.
60
Terminal or post-mortem invagination
versus antemortem intususeption
post mortom:
* easily reduced
* there is no vascular compromise (edema, congestion, hemorrhage)
* no fibrin or adhesions (peritoneal surfaces is smooth and glistening)
* no necrosis
61
hernias
o Internal herniations are displacements of intestine through a normal or pathologic foramen in the abdominal cavity
-horses: herniation through mesenteric tears and through the epiploic foramen
.o External hernias are formed when a hernial sac, formed by a pouch of parietal peritoneum,
penetrates outside the abdominal cavity. Types of external herniation include umbilical,
diaphragmatic, hiatal, inguinal,
62
Intestinal venous infarction
* Blood is pumped into the twisted segment but cannot drain due to occlusion of veins
* Transmural congestion, edema, hemorrhage, venous infarction
* Dark red intestine is distended with gas and hemorrhagic fluid
* Sharp line of demarcation between he affected and normal intestine
* During surgery, important to determine the viability of the bowel after reduction of a volvulus
* If reduction of a volvulus results in re-established circulation, reperfusion injury may occur.
63
cranial mesenteric artiritis and thrombosis leading to intermittend colic ? cause
Horses recover: not as distinct demarcations than a torsion. More multifocal, can be caused by strongyles vugaris. Confirm by cranial mesenteric artery with thrmbosis and firborisis. Thromb travel down to intestines cause intermittent colic.
64
intestinal lymphanigiectasia in dog
* Most common protein-losing enteropathy in
dogs, dialation of lymphatics
* Clinical signs:
– Diarrhea
– Steatorrhea
– Hypoproteinemia -> ascites
* Causes:
– Acquired (lymph vessel obstruction)
– Congenital (disorder of the lymphatic vessels
65
diarrhea
-increase in feces with fluid consistency or increased defecation or both
-leads to dehydration, lactic acid build up leads to acidosis. decreased perfusion, losing electrolytes, hypovolemia leads to hypovolemic shock. tissue isn't perfused properly.
66
Secretory diarrhea cause and morph
- will have normal intestines
-Enterotoxigenic E. coli (ETEC) infection of neonatal pigs, calves,
lambs, and humans causes secretory diarrhea. These bacteria are able to colonize the small intestinal enterocytes by way of their pilus antigens (fimbria)
-The bacteria produce
toxins that cause enterocytes to secrete water and electrolytes. The net result is diarrhea.
Because the enterocytes are not damaged, no lesions are observed, and absorption is
functional. Chyle is present in the mesenteric lymphatic vessels
- Or Osmotic diarrhea – Ruminal acidosis result in higher osmolarity of gastrointestinal
content, doesnt happen in young animals
67
diarrhea atrophy of villi
-malabsorptive diarrhea
R ota (not as bad)
C orona (fatal production animals)
M
P arvo (fatal)
-these cause, vilus damage and they contract small and shorter. Or they completely strip the vilus so there is no absorption. or they destroy the crypts.
68
Malabsorptive diarrhea and causes
- is caused by decreased absorptive surface usually a consequence of damage to absorptive enterocyte.
-villus atrophy
-The lost cells are replaced by the maturing cells migrating along the basement membrane from the crypt to the villus. The naked basement membrane stimulate contraction of the villi resulting in villous atrophy.
-when naked and blunted villi: Etiology: rotavirus, coronavirus, Cryptosporidium parvum
* Damage to undifferentiated crypt cells – loss of the undifferentiated epithelial cells in
the base of the crypts. FATAL, more severe.
~ Etiology: parvovirus, BVD virus
69
how to diagnose diarrhea post mortom
-dehydration
-perineal fecal staining
-abnormal water content in distal colon
70
Undifferentiated neonatal diarrhea
* Less than 3 wks in Po and Bo
* Variable degree of dehydration
* Yellow pasty to watery diarrhea
* Usually high morbidity
Necropsy:
* Usually marked dehydration
* Distended small intestines with watery contents which
are present also in the entire colon.
* Stomach may or may not be filled with milk
-secretory diarrhea you will have normal intestines.
71
Ulcerative enterocolitis causes and path
-(Salmonella, Brachyspira, Lawsonia, bovine coccidiosis,
Clostridium spp.).
-These microorganisms cause extensive necrosis of superficial
epithelium, lamina propria and/or blood vessels. The result is massive and acute
necrohemorrhagic or fibrinonecrotic enteritis.
-Absortive surface is lost (malabsorption)
and ulceration allows loss of interstitial and plasma fluids
72
Malfunctions of GIT
* Alterations in quantity and quality of feces (diarrhea)
– Constipation: decrease/absence of defecation
* Anorexia
* Vomiting
* Weight loss
* Dehydration and electrolyte imbalances
* Hypoproteinemia and anemia
* Septicemia, endotoxemia, enterotoxemia,
toxemia
73
GIT defense mechanisms
* Barriers:
– Biological: resident microbiological flora and fauna
– Chemical: Gastric pH, bile acids, enzymes
– Physical/Mechanical
* Static: epithelium and mucus
* Kinetic: peristalsis, vomiting, sloughing of epithelium
* Innate immunity:
– Cellular (macrophages, neutrophils)
– Humoral (defensins/cryptidins, lactoferrin)
* Acquired immunity:
– Cellular (lymphocytes)
– Humoral (antibodies)
74
Palatoschisis
cleft palate
-most common developmental abnormality of oral cavity
-leads to starvation (unable to suck), nasal regurgitation, and aspiration pneumonia.
75
* Brachygnathia superior
short maxillae
76
Brachygnathia inferior
short mandibles
77
Prognathism
long mandible
78
Agnathia
absence of mandible
79
Epitheliogenesis imperfecta
– absence of
epithelium of oral cavity and/or skin
80
Dental tartar
and periodontal
disease
* gingivitis and gingival recession
* loss of periodontal ligament and alveolar bone
* loosening and loss of tooth
* bacteremia/septicemia
Clin signs: pain, reluctance to masticate, halitosis
-the infection can spread to causing alveolar osetomyelitis and pupitis and result in apical abscess and bacteriemia.
81
Classification of stomatitides
Superficial stomatitis
* Vesicular stomatitis
* Erosive/ulcerative stomatitis
* Proliferative stomatitis
Deep stomatitis
* Necrobacillosis
* Actinobacilosis
* Eosinophilic granulomas and ulcers
82
vesicular stomatitis causes
-foot and mouth disease: picoronavirus
-vesicular stomatitis: rhabdovirus
- Swine Vesicular Disease – Enterovirus
-Federal authorities must be informed about suspected outbreaks of vesicular diseases
83
vesicular stomatitis of pigs and causes
Vesicular exanthema
of swine: calcivurus
-swine vesicular disease: enterovirus
84
FMD pathogenesis
-vesicles form Hydropic degeneration/ necrosis in stratified squamous epithelium
- Viral epithelial cytolysis creates microvesicles which coalesce to produce fluid filled vesicles and bullae
- due to mastication and abration the Vesicle rupture->Erosions -> healing
or
* Progress to ulceration
85
vesicular stomatitis clinical signs
* Fever
* Vesicular stomatitis (vesicles, bullae, erosions)
* Ptyalism (hypersalivation)
* Anorexia
* Lameness (if coronary bends affected)
86
foot and mouth disease lesions
-caused by picoronavirus (aphthocirus)
-lesions vesicles in mouth/ esophagus and heart
-ptyalism, lameness, anorexia
-erosive stomatitis
-erosive thelitis (on teats)
-erosive pododermatitis (on feet)
-ulcerative interdigital dermatitis
-vesicles on tongue or erosions
-healed lesions on tongue are round scars
* Due to mastication vesicles rupture -> erosions
-highly contagious with low mortality, CFIA reportable
87
Differential diagnosis for FMD
- Vesicular Stomatitis - Rhabdovirus
- Vesicular Exanthema - Calicivirus
- Swine Vesicular Disease – Enterovirus
- Final confirmatory diagnosis is based on demonstration of the particular virus
88
Erosive/ulcerative stomatitis causes
Ruminants
* Bovine viral diarrhea – complex
* Malignant catarrhal fever
* Bluetongue
* IBR systemic infection in neonatal caves (<1mo old)
* Peste des Petits Ruminants (PPR)
* Rinderpest (eradicated)
Cats: Calicivirus in cats
Primates: Herpesvirus
89
Bovine viral diarrhea
* Fetal infection
– Early embryonic death, mummification, or abortion
– Congenital fetal anomalies (90 – 150 days gestation):
cerebellar hypoplasia
– Persistently infected (PI) calves
* Mucosal Disease
* Severe (fulminant) acute BVD
-newborn calf: enamel hypoplasia, mucosal disease, lesions on tounge, feet. peyers patch necrosis.
90
segmental enamel hypoplasia
-dog: postnatal infection with canine distemper virus and damage to ameloblast cells of perminant teeth before eruption.
-calves: hypoplasia of decidous teeth can be caused by in utero infection of BVD
91
caries
-microbial destruction or necrosis of teeth. damaged enamel cannot be repaired or regenerated.
-happens in ruminants and horses
-consequence of infundibular impaction and infundibular necrosis
-buildup of dental plauques and tarter predispose to caries, gingivitis and tooth loss.
92
Bovine viral diarrhea (BVD) types of infections
-BVD virus likes epithelium and lymphoid tissues
-Classical BVD (subclinical, mild)
- High morbidity and no mortality
- Infection of immunocompetent, seronegative animal
-fever, lethargy, milk losses, upper GI erosions, get immunity
Fetal infection:
- Fetuses are infected transplacentally, if the above classical BVD infection occurs in pregnant immunocompetent seronegative (non-vaccinated) cows/heifers.
* Early embryonic death, mummification, or abortion
* Congenital fetal anomalies (infection between 90 – 150 days of gestation): cerebellar hypoplasia, enamel hypoplasia. m
-Persistently infected calf from 90-125 d gestation, if fetus survives t remains viremic for life and it is also immunotolerant for homologous
noncytopathic BVD viruses
Severe (fulminant) peracute BVD:
- Highly virulent strains of BVD virus can cause high morbidity and HIGH MORTALITY. same lesions as mucosal disease.
93
persistently infected calves with BVD
-infected 50-125 day gestation and survive.
-born viremic for life and is immunotolerant for homologous BVD viruses. ue to failure of the fetal immune system to recognize the
infecting viral antigen as ‘non-self’ or foreign (infection happened before immune system was developed – up to 4 mo of gestation.
- At birth, they are normal to weak and undersized.
- Over time they are usually unthrifty, smaller size, rough hair coat and more susceptible to
infectious diseases.
- PI calves are constantly viremic and shed virus all the time – THE MOST IMPORTANT SOURCE OF INFECTION.
- Almost all PI animals succumb to Mucosal Disease before 2 yr of age.
94
BVD diagnosis
– Gross and histopathology
– Immunohistochemistry of skin biopsies (large amounts
of viral load) in PI animals
-depends on form of the disease.
-rinderpest is eradicated in cattle but gross lesions are similar to musosal disease. but has inclusion bodies and syncytial cells which BVD doesnt have.
95
mucosal disease
- PI animals increased susceptibility to other common bovine infectious diseases.
- PI animals subsequently become infected with a closely related cytopathic BVD virus, or
noncytopathic virus that is causing persistent infection spontaneously develops recombination. The result is overwhelming infection and destruction of epithelial and lymphoid tissues that cannot be stopped by immune system of PI calves.
Clinical signs:
* Morbidity in a herd varies from 2% to 50%. All affected animals die (100% mortality).
* Anorexia, depression, pyrexia, profuse watery diarrhea with staining of the perineum
and tail, rumen atony, ptyalism, etc.
* Oral and interdigital erosions that may become ulcerations
96
PI BVD calves or mucosal disease diagnosis
* Differentiation between mucosal disease infecting PI animals and severe acute BVD infecting
immunocompetent animals is based on epidemiological observations and molecular characterization of BVD virus
97
Malignant catarrhal fever (MCF
* Ovine herpesvirus 2 or Caprine herpesvirus 2 cause cross infection with bison and deer. not contagious from direct contact.
* Sporadic, but high mortality
* Multiple organs
– Alimentary system: ulcers
- Skin: erosive dermatitis of muzzles, hooves.
– Respiratory system: nasal discharge, maybe trachitis and bronchitis.
– Urogenital system: renal infarction, hemmorage in bladder.
– Lymphoid tissue – lymphoid hyperplasia of LN (not in bison)
– Eye: Conjunctivitis,
diagnosis: – Histopathology is pathognomonic (lymphoblastic
arteritis) PCR for virus
98
pathogenesis of MCF
-vasculitis/ arteritis
-causes ischemia --> subsequent erosions/ulcerations.
Lymphoproliferation is the cause of enlarged lymph nodes
99
BVD vs MCF
* Differentiation of acute severe BVD and mucosal disease from MCF is sometimes difficult
* MCF usually affects one or more organ systems
(e.g. eye, kidney, bladder, respiratory)
* MCF typically produces lymphoid hyperplasia in cattle, whereas lymphoid depletion is present in BVD
100
bluetongue
-is an arthropode (Culicoides) born Orbivirus infection that causes widespread damage to endothelial cells resulting in hemorrhages and microvascular thrombosis followed by
ischemic necrosis characteristic for multisystemic gross changes.
-edema, congestion, hemorrhage and cyanosis of gums and tongue
-wild sheep/ ruminants, okanagon BC.
101
Alimentary IBR in neonatal calves
o Infectious bovine rhinotracheitis (IBR) virus can cause systemic infection in neonatal caves (up to 1 month), also called alimentary form of IBR
-Major lesions: Erosive stomatitis,
esophagitis, rumenitis and abomasitis; hepatic necrosis, mild rhinotracheitis
102
Erosive/ulcerative stomatitis cats
* Feline calicivirus
– Oral erosions
– Conjunctivitis
– Interstitial pneumonia
– Occasionally arthritis
103
Erosive/ulcerative stomatitis primates
Herpesvirus in primetes
* Herpesvirus B (Macacine herpesvirus 1)
– Mild stomatitis and conjunctivitis in macaques
– Fatal encephalomyelitis in humans
* Herpes simplex (Herpesvirus hominis type 1)
– Mild stomatitis is humans
– Fatal meningoencephalitis owl monkeys
104
Erosive/ulcerative stomatitis non infectious etiology
* Foreign bodies
– barley and foxtail awns
– porcupine quills
* Uremic stomatitis
105
Undifferentiated neonatal diarrhea diagnosis
* Causative agents are only transiently present in the
superficial layers of intestines; so, they are lost
during the early stages of autolysis
* Live untreated animals in the early phase of disease must be examined and sacrificed
* Modify regular necropsy procedure
– intestinal specimens are collected and fixed
within a few minutes after euthanasia
106
how to indentify types of diarrhea at necropsy
-normal vili means secratory caused by entero E-coli (less than 3 weeks old) or osmotic which must be more then 3 weeks old.
107
Enterotoxigenic E. coli (ETEC)
* ETEC affects piglets and calves (occ lambs)
* Pathogenesis:
– E. coli attach to surface enterocytes by a variety
fimbriae (e.g. F4 in piglets and F5 in calves)
– Produce enterotoxins (e.g. ST, LT) that induce secretion
Na and Cl into intestinal lumen so water is drawn into the intestinal lumen.
* Clinical signs:
– Diarrhea is voluminous, yellow to white, and watery
– Severe dehydration
– Diarrheic feces around perineum. FATAL, chyle present.
108
undifferentiated neonatal less than 3 week diarrhea causes etiology
-rotavirus: all (causes death to tips of villi)
-coronavirus: pigs, calves, causes mortality
-ETEC: pigs, calves sometimes lambs, causes mortalitu
-cryptosporidium: calves, lambs, foals
-isospora sius: pigs causes mortality
109
malabsorptive diarrhea
-rotavirus enteritis: in all farm species
-loss of villa epithelium from rotavirus damaging villi enterocytes at distal top 1/2 villus.
-moderate villus atrophy
-diagnosis: histopathy
110
Rotavirus Enteritis
o Rotaviruses cause malabsorptive diarrhea in calves, piglets, lambs and foals during the first few weeks of life
- Not fatal diarrhea; however, mortality occurs when there is a co-infection with other
pathogens (e.g. ETEC).
o Pathogenesis: rotavirus targets the most mature villus enterocytes (the distal ~1/2 of villus)
-moderate vilus atrophy
111
Coronavirus Enteritis path
* Malabsorptive diarrhea in calves and piglets
TGE (not as severe) in adult pigs
– <3wks high mortality
– >3wks transient diarrhea no mortality causes TGE.
* Pathogenesis:
– Targets all enterocytes on villi
– Severe villous atrophy
– ‘Naked adjacent villi’ adhere and fuse -> incomplete regeneration of villi
– If recovered may be a chronic ‘poor doers
112
Coronavirus Enteritis clinical and diagnosis
Clinical signs:
– Neonates may be severely dehydrated and weak
– Yellow watery diarrhea
– Very high morbidity and mortality (<3wks) in
susceptible herds
* Diagnosis:
– Preliminary diagnosis - subgross villous atrophy
– Histopathology - severe villous atrophy
– Immunohistochemistry
113
Porcine epidemic diarrhea PDE
* caused by Coronavirus different from TGE
* Clinical presentations similar for PED and TGE (SK still free)
– explosive epidemics of diarrhea and vomiting in all ages, with 90–95% mortality in suckling pigs
– severe atrophy of villi
– Rotaviruses and TGE virus -> negative so you know its PDE
114
Cryptosporidiosis
* Cryptosporidium parvum is a cause of malabsorptive
diarrhea in calves and occasionally in lambs and foals
-municipal water comtamination-> Zoonosis
* Pathogenesis:
– Cryptosporidia attach to surface epithelial cells
– Displace and damage the microvilli to 1/2.
– Loss of enterocytes
– Villous atrophy
* Clinical signs:
– Watery diarrhea
– Animal is dehydrated
– Usually non fatal,
115
Cryptosporidiosis at necropsy
* Necropsy:
– GI tract contain watery fluid
– Cryptosporidia may be observed in intestinal scrapings
stained with Giemsa or acid fast
* Diagnosis:
– Parasitology: Demonstration of large number of
oocytes in feces
– Histopathology: villous atrophy with large number of
Cryptosporidia
116
Isospora suis
* Porcine neonatal coccidiosis is malabsorptive diarrhea
* Affects 7-21 day old piglets (other species >3wk).
* Pathogenesis:
– Isospora replicates in enterocytes (distal/top 1/3 of villus)
– Infected cells slough
– Villous atrophy
– Very rare, infection is very severe and widespread necrosis
of enterocytes results in fibrinonecrotic enteritis which leads to ulcerative diarrhea.
117
Isospora suis
* Clinical signs:
* Clinical signs:
– Dehydration
– Yellow watery diarrhea
– High morbidity and low mortality
* Necropsy:
– Isospora (coccidial) organisms may be observed in
intestinal scrapings
* Diagnosis:
– Histopathology: villous atrophy with large number of
coccidial organisms
118
clostridial enteritis
-c. perfringes type C = necrohemmoragic enteritis small intestines.
-C. perfringens type D causes enterotoxemia and pulpy kidney in lambs with “overeating” or grain overload. Angiotoxin absorbed from intestines causes systemic endothelia damage (occ. with hemorrhages)
-clostridium difficile in piglets <1 wk causes mesocolon edema and typhocolotis.
119
Clostridium equine
-C. piliforme: causes equine liver, colon and heart lesions
-tyzzer disease
-C. difficile: hemorrhagic necrotizing enterocolitis in foals
120
eColi. 0157 people
-O157: H7 kills humans
(Shiga toxin–producing E. coli) of cattle does not cause disease in
livestock, but contaminated ground beef with this bacteria causes severe and potentially
fatal hemorrhagic colitis, thrombocytopenic purpura, and the hemolytic uremic syndrome
in people.
121
Edema disease
-caused by E.coli proliferates in intestines and produces
exotoxin (Stx2e) which is absorbed and causes systemic disease= Enterotoxemia
* Clinical signs:
– No diarrhea: for pigs older than 3 weeks
– Best pigs in the group (6 to 14 weeks of age)
– Sudden death
– Neurologic signs due to cerebral edema
– Morbidity is low (but may reach up to 35%)
– All affected animals die – mortality 100%
-brain, eyelids, wall of stomach edema, megocolonic edema
122
Edema disease pathogenesis
– Dietary changes
– E. coli (STEC) attachment and proliferation in intestines
– Production of exotoxin (Stx2e) which is absorbed and
causes enterotoxemia
– Vascular endothelial injury -> edema
* Necropsy: generalized edema
* Diagnosis:
– Histopathological demonstration of fibrinoid necrosis
of arterioles
– Bacterial culture of E. coli from intestinal content
123
Porcine postweaning diarrhea (PWD)
-Enterotoxigenic E. coli (of O149 serotype) causes enterotoxemia.
* Within a few weeks of weaning
* Clinical signs and necropsy findings are
manifested as two different conditions not
necessary affecting the same pigs:
– One is postweaning diarrhea with high morbidity and Variable mortality
– Second is mortality with signs of endotoxemiA
-diagnosis: necropsy, culture and virulence factors by PCR.
-lesions: fibrinous polyserositis (endotoxemia), fundic stomach infarction caused by septicemia.
124
Lawsonia enteritis
* Lawsonia intracellularis causes Proliferative enteropathy in pigs (foals, hamsters)
* Proliferative ileitis, intestinal adenomatosis, distal ileal HYPERTROPHY.
-could cause cerebriform (SI looks like brain), hemorrahagic, or fibrinonecrotic enteritis in distal SI. only cause of PROLIFERATIVE in pigs. corrugated ilium.
* Clinical sings:
– Diarrhea with or without blood
– Morbidity 10% to 15%; mortality is around 50%
– Recovered pigs are “poor-doers”
125
Lawsonia enteritis
* Necropsy
* Necropsy:
– Ileum and distal small intestines:
* Severe mucosal hyperplasia
* Variable degree of necrosis +/- hemorrhage.
– Colon affected in 20-25%
* Diagnosis:
– Pathognomonic necropsy and histopathological
lesions
– Demonstration of Lawsonia by PCR
126
sudden death with anemia (pale carcass pigs) causes
-gastric ulcer (exsanguination)
-lawsonia intercellularis: which causes hemorrahagic iletits
-cranial mesenteric tosion
127
Swine dysentery
*caused by Brachyspira hyodysenteriae affects weaner pigs LARGE INTESTINE
* Clinical signs:
– Morbidity 90%, mortality up to 30%
– Dehydration
– Diarrhea with specific smell; feces contains blood, mucus, and fibrin.
* Necropsy:
– Mucohemorrhagic to fibrinonecrotic typhlocolitis!!!
-use PCR AND histopathy with silver staining need both. not just PCR.
128
salmonellosis pigs, horses, cows
-peracute= septicemia
-acute enteric salmonellosis =(firbrino, necrotis enteritis)
-acute= enteric salmonellosis: caused by bacterial toxins that cause thrombosis of mucosal venules, all
of which result in severe inflammation, necrosis and ulceration of enteric mucosa.
- Clinical signs:
* Malodorous diarrhea; feces contains mucus, fibrin, and occasionally blood
* Severe dehydration
-chronic= button ulcers, - Cecal and colonic erosion/ulcerations are the most common lesions
o Carrier state: Some recovered animals become carriers and shed the organism in their feces,
particularly after stress
-need histo of lesions and bacterial culture
129
septicemia
-septicemia is widespread damage to endothelium leading to edema, pretichiation, fibrinous exudate.
130
salmonellosis septecemia foals
-osetomyelitis with sequestrum
-acute=necrotis enteritis
-peracute septicemia
131
BVD complex
-Mucosal Disease and Fulminant BVD
– Fibrinonecrotic ulceration of ileum over lymphoid
necrosis in Peyer’s patch
– Fibrinonecrotic colitis.
* MCF – hemorrhagic enteritis in deer
132
coccidiosis
-* Lesions:
– Necrohemorrhagic typhlocolitis in cattle
-o Lesions vary from proliferative in sheep and goats to hemorrhagic and necrotic in cattle.
– Proliferative enteritis in sheep (nodules)
– In piglets - villous atrophy
* Clinical signs:
– Diarrhea (hemorrhagic in Bo) and weight loss
– ‘Nervous coccidiosis’ in Bo
133
jejunal hemorrage syndrome
* Sporadic but fatal disease of dairy cattle
* Intraluminal-intramural hemorrhage of the small intestine with obstruction and death
* Regional necrohemorrhagic jenjunitis
* Clostridium perfringens type A - suspected
-dark, clotted blood in the feces; variable and multifocal distention of the
small intestine; small intestinal ileus; and necrohemorrhagic jejunitis.
134
Winter dysentery
-nonfatal seasonal diarrhea of adult dairy cows
* Coronavirus – suspected (BRDC, calf diarrhea...)
* Clinical signs:
– Morbidity ~100%, no (or very low) mortality.
-decrease milk production, leads to herd immunity
135
cattle diseases of enteritis older than 3 weeks
-acute: salmonellosis, BVD, coccidiosis, jejunal hemorrage syndrome, winter dysentery
-chronic: johnes disease (mostly dairy) leads to emaciation
136
johnes disease
-caused by Mycobacterium avium ssp. paratuberculosis
* In cattle (older than 2yr): persistent diarrhea, emaciation, and hypoproteinemia
* In sheep and goats
– Same as cattle but no diarrhea
path: Lesions in the lamina propria of the intestines and lymph nodes are cause by severe infiltration of macrophages as part of granulomatous inflammation
* Necropsy:
– Granulomatous enteritis
– Granulomatous lymphadenitis
-acid fast positive bacteria
137
diarrhea in horses up to 6 months
-rotavirus
-coronavirus (rare)
-cryptosporidium
138
Potomac horse fever
-caused by Neorickettsia risticii – (ingestion of aquatic insects with infected trematodes?)
* Clinical signs:
– Fever, depression, dehydration
– Diarrhea (range from cow-like feces to watery)
– 30% mortality without treatment
– Abortion in pregnant mares
139
Potomac horse fever necropsy
– Severe congestion, petechiae, and edema in the
cecum and colon.
– Superficial necrotizing enterotyphlocolitis.
* Diagnosis:
– Clinical and pathological signs
– PCR for Neorickettsia risticii
140
colitis X horses
* Rapidly progressing and fatal diarrhea with sudden onset and shock
* Cause: stress, exhaustion and Clostridial infections
* Clinical signs
– Acute diarrhea, severe dehydration, shock and death
* Necropsy:
– Severe cecal and colonic mucosal edema, congestion,
and hemorrhage (LI only)
– Endotoxic shock and disseminated intravascular
coagulopathy
* Diagnosis: rule out the others
141
NSAIDs toxicity horses
* Oral NSAIDs can cause necrotizing colitis of right dorsal colon
* Direct damage to endothelium of colonic
vasculature and inhibition of prostaglandin
resulting in ischemic necrosis
-ulceration of pars esophagea.
142
Equine granulomatous enteritis
* Clinical signs: wasting and hypoalbuminemia, < 5yr
* Necropsy:
– Diffuse or segmental mucosal noncaseating
granulomatous enteritis or small and sometimes large intestines
– Lymph nodes may be enlarged due to granulomatous lymphadenitis
(looks like johnes disease but in horses)
differential dg: proliferative enteritis.
143
Rhodococcus equi enterocolitis
* Necropsy:
– Enteric: Multifocal pyogranulomatous ulcerative
enterotyphlocolitis and pyogranulomatous
lymphadenitis
– Pulmonary: Pyogranulomas in lungs of foals under 6 months
– Reproductive: Placentitis and abortion
* Diagnosis:
– Gross and histopathology lesions
– Bacteriology 52
144
Feline panleukopenia
– Lymphoid depletion, thymic involution and suppression of bone marrow
– Fibrinonecrotic enteritis
– Hemorrhagic lymphadenopathy (lympholysis)
– In utero infection causes congenital cerebellar hypoplasia in cats but not dogs
-crypts are gone.
Clinical signs: dehydration, depression, diarrhea, vomiting and death (due to shock)
145
Canine parvovirus enteritis and path
* Puppies 3 to 8 weeks of age:
– Myocarditis –> death or undetected
– at 5 mos die unexpectedly or heart-failure because of myocardial scarring
* Puppies 8 weeks or older:
– firbinonecrotic enteritis
– No cerebellar hypoplasia
– Die from shock within 24 hours
path: Virus causes necrosis of crypt epithelial cells. Surviving epithelial cells
changes to squamoid to cover the surface of the denuded crypts and denuded villous basement membrane. Because the villous basement membrane is exposed villous fusion
occurs, resulting in lack of a scaffold for enterocyte replacement (once the crypts recover) and in permanent villous distortion and atrophy.
146
Coronavirus in carnivores
* Canine coronavirus -> transient nonfatal diarrhea in puppies
– villar epithelium necrosis/sloughing -> villus atrophy and sloughing.
* Feline coronavirus -> mild diarrhea in kittens
– villus atrophy
– Some cats (~10%) cannot clear infection -> mutation of virus -> FIP virus
147
Histiocytic ulcerative colitis (boxer colitis)
The cause is unknown
* Boxers and French bulldog younger than 2 yrs
* Clinical signs:
– Soft feces, but no diarrhea
– Mucus and blood present in feces
– Proctoscopy: raised ulcerative nodular mucosa.
* Diagnosis
– Biopsy and histopathology
148
Inflammatory bowel disease (Ca & Fe)
* Lymphoplasmacytic enteritis.
* Unknown cause
– Dietary antigens?
* Malabsorption and chronic protein-losing enteropathy
* Diagnosis: biopsy -> histopathology
149
Exocrine Pancreatic Atrophy
* Autoimmune pancreatitis in some young dogs
* Clinical signs:
– maldigestion secondary to exocrine pancreatic insufficiency
– rapid weight loss despite of an avid appetite, vomiting, diarrhea.
*Necropsy/laparoscopy: pancreas is small with small islands of normal exocrine pancreas
150
acute pancreatitis (necrosis)
-more common dogs> cats
* Clinical signs:
– vomiting, diarrhea, anorexia, and abdominal tenderness
– systemic effects secondary to the release of inflammatory mediators and activated enzymes from the damaged pancreas may result in shock and DIC.
-gross: * Edema, hyperemia, hemorrhage of the pancreatic parenchyma
151
Acute Pancreatic Necrosis pathogenesis
Pathogenesis: autodigestion as a consequence of
release of activated pancreatic enzymes into the
pancreatic parenchyma and adjacent tissue
Causes:
– Idiopathic: dietary indiscretion
–Obstruction of the duct
–Direct injury to acinar cells
-saponification of fat on necropsy
152
Chronic Pancreatitis
* Fibrosis, inflammation and parenchymal atrophy
* It results from repeated episodes of acute pancreatic necrosis and pancreatitis
* Necropsy/laparoscopy
– distorted, shrunken, nodular pancreas
* Exocrine pancreatic insufficiency - rare
153
pancreatin adenocarcinoma
-Exocrine pancreases disease: poor prognosis. Painful
-can infultrate to duodenum and abomasum.
154
hemoperitoneum
-ascites from:
– Hypoproteinemia
– Disrupted lymphatic outflow
– Increased venous hydrostatic pressure
– Uroperitoneum
* Peritoneal exudate – fibrinous peritonitis
-causes: dogs bleeding hemangiosarcoma
155
Peritonitis
-always excaudate from damage to endo cells.
* Bacteria
* Viral- FIP
* Parasitic migration – S. equinus
* Organ rupture and perforation
* Sterile (bileperitonitis)
* Egg peritonitis in birds
* Diagnosis: Cytological examination in vivo and bacterial culture
156
Causes of porcine polyserositis
-anything that causes septicemia
* Haemophilus parasuis
* Streptococcus suis type II (zoonotic)
* Actinobacillus suis
* Septicemic E. coli
* Septicemic Salmonellosis
o Mycoplasma hyorhinis – this is the only non-fatal cause
157
Feline infectious peritonitis
* FIP is a fatal disease of cats
* Cause is a mutated enteric feline coronavirus
* Pathogenesis:
– Wet - strong humoral and weak cell-mediated immunity
– Dry - partial cell-mediated immunity
– Strong cell-mediated immunity – resistant or carrier.
morph diagnosis: multifocal pyogranulomatous menigitis in brain
-multifocal and coalesing pyogranulomatous pluritis
158
feline infectious peritonitis clinical
* 6-24 mos and older than 13 yrs
* Effusive FIP
– distention of the abdomen
* Non-effusive FIP
– vague illness, chronic fever
– organ system failure
* 40% with ocular lesions (NB-examine eyes!!!)
* 50% intra-abdominal involvement = kidney, liver, spleen,
-nodules on intestines,
159
Feline infectious peritonitis
* Necrospy
– ‘Wet form’ or ‘effusive’ -> fibrinous polyserositis
– ‘Dry form’ or ‘noneffusive’ -> pyogranulomas in
various organs (e.g. kidney, liver, lungs, meninges )
– Both forms can be present in the same animal
* Diagnosis:
– Postmortem diagnosis – gross, histo and IHC
– Clinical diagnosis of effusive FIP is easier than of non-
effusive form – clinical pathology is essential for antemortem diagnosis of FIP
160
primary neoplasia in peroteneal cavity
* Primary
–Lipomas in horses
–Mesothelioma in primates
* Secondary
–Hemangiosarcoma
161
SEPTICEMIA / ENDOTOXEMIA leads to
* Peripheral congestion (vasodilation) of skin and organs
* Petechiation (endothelial damage and DIC) could be renal
* Pulmonary edema and congestion
(endothelial leakage and vasodilation)
* Mild fibrinous polyserositis and polyarthritis
(endothelial leakage/damage)
* Enlarged spleen and lymph nodes (activation of macrophages).
162
septicemia pathogenesis
-Disorder of endo cells and cytokine secretion. -Endo cells will start to have cytokine storm which effects multiple systemic reactions and animal dies from cardio collapse from endo damage and vasodialation or septic shock.
-or secondary is failure of passive transfer (colostrum)--> immunodeficent animal born hypogammaglobulemic
163
Morphologic lesions of septic shock (septicemia)
* Mild fibrinous polyserositis, polyarthritis, meningitis
from endothelial damage and leakage of fibrinogen
* Congested skin & organs from vasodilation;
* Diffuse pulmonary edema & congestion from
vasodilation, endothelial activation/damager/
leakage and terminal CV compromise (ARDS)
* Generalized petechiation from endothelial damage and DIC
* Enlarged meaty spleen and lymph nodes from
activation and mobilization of residual tissue macrophages
164
Anthrax
* Acute febrile fatal septicemia in herbivours
* Etiology: Bacillus anthracis
* Pathogenesis
– Portal of entry: ingestion, inhalation, cutaneous wounds
– Organisms produce a variety of lethal toxins
– Acute septicemia high vascular permeability
-post morum: thick oozing blood, splenomegaly (blackberry jam spleen), lymphanomegaly, serosal hemmorage
