Pathology of Viral Infections, Equine Grass Sickness, and Intestinal Displacements

List the defense mechanisms of the alimentary system (I am so sorry for how long this flashcard is)

Saliva

Gastric pH

Paneth cells - make antimicrobial peptites and proteins

Intestinal proteolytic enzymes

Intestinal biotransforming and metabolic enzymes

Extra-intestinal secretions from liver and pancreas

Mucus

Vomiting

High rate of epithelial turnover

Increased peristalsis

Shedding of receptor-laden ALP and catalase-containing vesicles from microvilli

Resident commensal bacteria and protozoa

Phagocytes (zack’s fav!)

Innate lymphoid cells

Kupffer cells

Adaptive immune system

Secreted immunoglobulins

Describe the GI immunity system with mucosal associated lymphoid tissue (MALT)

M cell in the mucosa overlying MALT takes up an antigen and presets it to macrophages and dendritic cells

These cells migrate to MALT/Peyer’s patch

Then through lymphatic vessel to mesenteric lymph nodes

Here antigens are presented to T-cells and they are activated, then B-cells are stimulated to proliferate and differentiate

Antibodies are produced and secreted through the intestinal epithelium

Describe the pathogenesis of canine and feline parvoviral infections

Oronasal exposure

Viral uptake in tonsil epithelium and Peyer’s patches

Infection of lymphocytes and viral replication

Systemic dissemination

Final target = crypt enterocytes in small intestine

The virus replicates in and causes necrosis of rapidly dividing cells

→ Lymphoid tissue necroses = immunosuppression; crypt enterocyte necrosis

What are the clinical signs?

Pyrexia

Depression

Inappetence

Vomiting

Diarrhea

Dehydration

Anemia

List the key histological features of parvoviral enteritis

Necrosis of crypt epithelial cells

Dilation of crypts with necrotic cells

Intranuclear viral inclusions (only detectable in early phase)

Atrophy of villi

Necrosis of lymphoid tissue in Peyer’s patches

Epithelial regeneration (in late phase)

What coronaviruses infect pigs?

Porcine epidemic diarrhea virus (PEDV)

Transmissible gastroenteritis virus (TGEV)

What age pigs are infected with coronaviruses?

Any age can be affected but most severe in piglets

Up to 100% mortality in piglets

What part of the body is affected by these?

Target enterocytes of vulvus tips → blunting and fusion of villi in the small intestine

What coronaviruses affect cattle?

Bovine coronavirus (BCoV)

How does bovine coronavirus affect cows of different ages?

Calves: diarrhea, lesions in SI and colon

Adult cattle: winter dysentery - high morbidity but low mortality → blood-tinged diarrhea, drop in milk prod, lesions mostly in colon

What are the clinical signs of equine coronavirus?

Fever

Acute colic

Anorexia

Acute neruological signs (head pressing, aimless circling, depression/lethargy) with sever hyperammonemia

Describe the histopathology associated with equine coronavirus

Necrotizing enteritis with marked villous attenuation (attenuation meaning thinning/flattening of villi)

Epithelial cell necrosis at tips of villi

Neutrophilic and fibrinous exudation

Crypt necrosis

Microthrombosis and hemorrhage

How does rotavirus affect the body?

Significant infection is limited to enterocytes of SI

Causes villous atrophy and fusion

Also associated with co-infections of other pathogens

Major cause of diarrhea in foals

Differentiate equine adenovirus (EAdv)-1 and EAdv-2

EAdv-1: upper respiratory tract infections in young foals

EAdv-2: GI tract infections

What are the effects of EAdv-2 on the GI tract?

Necrosis and ulceration in distal esophagus and non-glandular gastric mucosa

Intestinal lumen soft to semi-fluid ingesta

Typical adenovirus inclusions (intranuclear) in SI

Villous atrophy in SI

What part of the body does equine grass sickness affect?

Autonomic NS

• Postganglionic sympathetic and parasympathetic neurons

• Prevertebral and paravertebral ganglia

• Cranial nerve nuclei of the brainstem

What causes it?

Not completely sure

• Oxidative stress

• Fungal toxins

• Changes in weather

• Exposure to C. botulinum type C?

What are the risk factors for equine grass sickness?

Strong association with grazing, recent move to new pasture

Higher incidences in 2-7 year olds

Seasonal peak between spring and early summer

Cooler dryer weather and irregular ground frost

What are the symptoms?

Dull, patchy sweating

Episodes of colic

Reflux of gastric content from nostrils

What happens in acute/subacute equine grass sickness?

Attempts to swallow painful → reverse peristalsis in esophagus

Swallowing avoided → drooling

Stomach distended with pale tan mucinous fluid

Gastric rupture

LI impacted with dry components (surface of contents blackened by small amount of blood)

What happens during the chronic form (>7 day duration)?

Markedly reduced alimentary contents in stomach due to inappentance

Hypertrophy of intestinal musculature

Define dilatation

Widening or enlargement of an opening or hollow structure beyond its usual size

Define volvulus

Twisting of an intestinal segment on its mesenteric axis

Define torsion

Rotation of a tubular organ along its long axis

What are the consequences of GDV in the dog? Think both in the GI tract and circulatory system

Vascular stretching and compression

Decreased venous drainage congestion, hypoxia

Hemorrhagic infarction of the gastric wall

Possible hemoabdomen

Acid-base and electrolyte imbalance

Decreased portal venous return

Pancreatic ischemia

Release of myocardial depressant factor

Cardiovascular collapse and circulatory shock

What causes primary gastric dilatation in the horse?

Excess fermentable carbohydrates

Sudden access to lush pastures with rapid intake of large amounts of food

Excess water intake

What causes secondary dilatation in the horse?

Intestinal obstruction or colic with ileal paralysis

Manifestation of acute equine grass sickness

What happens to a horse with torsion of an intestine?

Compression of vessels - veins more susceptable to so blood still pumped in but the twisted segment cannon drain

Edema → congestion → hemorrhage → necrosis

Stasis of contents with toxemia and possible bacteremia resulting from necrosis of the affected segment

Besides torsion, how else do horse’s intestines sometimes get strangled?

Intestinal loop herniation through the epiploic foramen

Strangulation by pedunculated lipomas that become wrapped around the intestine