Neonatal D+ Pathogenesis Flashcards by Rebecca Williamson

how does cryptosporidium affect the GI cells

infects SI cells
endocytic vauole under luminal membrane
absorptive function disrupted = nutrients pass into colon like rota, corona
cell mediated immune response follows

How well did you know this?

Not at all

Perfectly

what kind of D+ does crypto cause

maldigestion and malabsorption: encased in endocytic vacuole under the luminal membrane of enterocytes -
- presence triggers immune response = cytokine release = villus blunting = inflammatory changes

How well did you know this?

Not at all

Perfectly

what parts of the intestine are hit hardest with crypto

jejunum and ileum but lesions can go into duodenum and aborad into colon

How well did you know this?

Not at all

Perfectly

common enteric zoonosis of veterinarians

cryptosporidiosis

How well did you know this?

Not at all

Perfectly

what are the 2 causes of inflammatory D+

clostridial enteritis (clostridium perfringens)
salmonellosis (>2000 serotypes)

How well did you know this?

Not at all

Perfectly

what age and species can get clostridial and salmonella D+

any age, any animal

How well did you know this?

Not at all

Perfectly

coccidiosis (eimeria and isospora spp) cause disease in ruminants, camelids, and swine, but is rarely seen in what species?

foals

How well did you know this?

Not at all

Perfectly

T/F: clostridium perfringens is a bacteria that is considered part of normal flora

true

How well did you know this?

Not at all

Perfectly

if clostridium perfringens is normal gut flora why is it bad?

present in GI tract of all verts
one of earliest members of neonatal gut flora
problem: some genotypes and strains are really pathogenic
type C and D are super pathogenic

How well did you know this?

Not at all

Perfectly

under what conditions does C. perfringens proliferate in?

conditions of high starch, sugar or protein content in the SI

How well did you know this?

Not at all

Perfectly

“overeating disease”

C. perfringens

How well did you know this?

Not at all

Perfectly

T/F: Salmonella are opportunists

true: they like attacking a weakened host

How well did you know this?

Not at all

Perfectly

what is overeating disease?

C perfringens
if host overeats rich diet, high starch/sugar/protein causes overgrowth of C. perfringens pathologic strains
this results in exotoxin production and severe disease

How well did you know this?

Not at all

Perfectly

T/F: pathologic strains of salmonella prefer young animals

False: have no preference for age and species, but can be devastating for the neonate

How well did you know this?

Not at all

Perfectly

clostridial basics

gram + rod
“vegetative form” growing rods release potent lethal exotoxins

How well did you know this?

Not at all

Perfectly

what are exotoxins?

antigens in effective vaccines (toxoids)

How well did you know this?

Not at all

Perfectly

T/F: clostridium is a spore former

true: persists in the environment!!

How well did you know this?

Not at all

Perfectly

T/F: clostridium is found in all warm blooded verts’ GI tracts

true

How well did you know this?

Not at all

Perfectly

gram +, spore forming, generates very lethal exotoxins

clostridium

How well did you know this?

Not at all

Perfectly

how do we prevent clostridiosis?

vaccines! treatment expensive, case fatality risk high, vaccines are effective

How well did you know this?

Not at all

Perfectly

what are the vaccines for clostridium?

toxoids that induce antibody that neutralizes the exotoxins

How well did you know this?

Not at all

Perfectly

what triggers proliferation of pathogenic strains of C. perf?

ingestion of lots of spores (teat contamination from dam)
ingestion of lots of starch/sugar/protein (like ingesting large volumes of milk, grain, lush grass etc)

these substances act as substrate for intraluminal proliferation of C. perf = exotoxins harm host tissue = inflammation, necrosis of gut wall

sources of vegetative/rod form of clostridium

feed and water, feces, environmental surfaces, fomites like feeding bottles

C. perfringens type C is

colorful: cranberry (bloody) contents and cranberry crap. critters crash
die in hours

C. perfringens type C

- classic culprit of clostridial enteritis - makes toxins (alpha toxin/phospholipase, beta toxin) that kills enterocytes and cause intraluminal hemorrhage - protein losing enteropathy! - becoming hypovolemic from losing blood into the GI tract peracute death often a classic clinical sign

what is the ideal spot for C. perfringens type C?

intestine of the newborn: - anaerobic environment - not much competitive microflora established yet - warm - lots of nutrients/milk

where can lesions of C. perfringens type C be found?

small intestine, colon or both

how is C. perfringens Type D different?

- enteric proliferation occurs but doesn't manifest as an enteric disease - exotoxin is epsilon toxin: doesn't act on mucosa of the gut - exotoxin absorbed and acts on DISTANT organs

C. perfringens type D is

different: acts differently and acts on Distant organs: doesn't act on the mucosa of the gut! acts on Distant organs causes endothelial cell Death eDeeeema of multiple tissues and organs results DEAD SMALL RUMINANTS

what pathogenesis results from exotoxin?

C. perfringens type D - endothelial cell death, is absorbed and acts on distant organs - edema of multiple tissues and organs results - causes vasculitis!

describe C. perfringens type D pathogenesis

1. doesnt act on mucosa of gut but enteric proliferation does occur 2. exotoxin (epsilon) absorbed from gut 3. toxin increases vascular permeability in a variety of distant organs 4. edema results

Dead sheep and goats

type D clostridial enteritis

how are clostridial type D animals found

often dead or terminal

what species are affected by C. perfringens type D?

small ruminants: DEAD sheep and goats

how does C. perfringens Type D manifest in small ruminants

- edema of brain = terminal opisthotonus and convulsions - edema in pericardial sac (effusion) and chest/abdomen (effusion) - mobilize so much glycogen in stress response that they develop glucosuria - so much glucose in lumen of neophrons: kidneys may undergo autolysis = PULPY KIDNEY

pulpy kidney

CLOSTRIDIUM PERFRINGENS TYPE D

what is the pathogenesis of pulpy kidney disease?

- small ruminants, clostridium perfringens type D - mobilize so much glycogen in stress response that glucose builds up = glucosuria - so much glucose in nephron lumens = kidneys undergo autolysis = pulpy kidney

how does C. perfringens type D cause edema?

triggers endothelial cell death throughout the body

histology of brain from C. perfringens type D

perivascular edema; also found in other organs

a sheep presents acutely terminal with opisthotonus and convulsions. the producer had just recently turned them out to pasture after a storm. what is your immediate differential

clostridium type D (overeating disease)

what type of D+ does salmonella cause?

inflammatory

what bacteria contains LPS that will cause endotoxic shock and massive inflammation?

salmonella: LPS endotoxin

salmonella causes an enterocolitis. what does this mean?

small intestine, cecum, and large intestine can be affected

pathogenesis of salmonella

pathogenic strains INVADE the gut wall - triggers massive inflammatory response! - as a gram (-) bacteria, salmonella sheds LPS during division or death: amplifies inflammation and triggers endotoxic shock! - causes an ENTEROCOLITIS: small intestine, cecum and large intestine can be affected

is LPS an endotoxin or exotoxin?

endotoxin!!

we associate bloody D+ with what

salmonellosis, type C clostridial enteritis, coccidiosis

T/F: salmonellosis is a protein-losing enteropathy

true

what kind of damage does salmonella wreck on the GI

- protein-losing enteropathy: severe inflammation causes exudation of WBC, proteins and fluid into the gut lumen - blood and fibrin in stool = evidence of bad gut wall inflammation

blood and fibrin in the stool is a key factor in IDing what bacteria? what caused those?

salmonellosis! is a PLE, blood and fibrin are indicators of significant gut wall inflammation = "inflammatory pathogens" suspected

you see a dairy calf that has yellow, stringy and bloody diarrhea. what are you suspecting? why?

salmonellosis: blood and fibrin indicate severe gut wall inflammation