Bacterial diseases Flashcards
Types of toxicity of Clostridial diseases (3) - depending in kind of tissue damage
1 Enterotoxic
2 Histotoxic
3 Neurotoxic
What Clostridium types are related to enterotoxin diseases?
- Clostridium perfringes
- Clostridioides difficile
Clasification in general of Clostridial bacteria
Anaerobic
Gram (+)
Sporulated rods
Which is the only Clostridial bacteria that is Gram -
Clostridium piliforme
For most of all Clostridium diseases infection is needed, except for __________, that ingestion of the toxin will cause the disease
Botulism
What is the purpose of sporulation in this type of bacteria?
That can pass in between hosts in a vegetative form and is resistant to a los of adversities in the environment
How many toxotypes are identified in the family of Clostridium perfringes ?
7
A,B,C,D,E,F,G,
Which serotypes of C. Perfringens are the most commonly associated with enteric disease in horses (foals)?
Type A, B and C
What are the main toxins identified in Clostridial enteric diseases ?
CPA - alpha
CPB - beta
ETX - epsilon
ITX - iota
CPE - enterotoxin
NeTB
NetF
Which toxins does C. perfringes type A and B the codify?
Type B : CPA, CPB and ETX
Type C: CPA, CPB2, PFG, TPEL
Why is believed that foals are more susceptible to C. Dif?
Because colostrum has calostral trypsin inhibitors that protects the toxins from degradation by trypsin in the stomach
Describe the pathogenesis of Clostridium perfringens
- Spores ingested from feces or soil, 2. Trypsin inhibitors prevents lysis of CPB, 3. Bacterial colonization in intestinal mucosa, 4. CPB toxin damage endothelial cells and create cell pores
How does CPB toxin cause cell death?
- Create cell pores (Ca+, Na+ and Cl- in the cell and K+ escapes the cell)
- Endothelia damage : vascular damage, thrombosis and necrosis
Typical gross pathologic lesions in C. perfringens
Ulcerative enteritis (diffuse or multifocal)
Orange pseudomembrane
Endotoxemia lesions
Histophatological findings in C. perfringens
Hemorrhagic and necrotizing enteritis/colitis
Best diagnosis tools for C. perfringens
ELISA - CPBtoxin
PCR - bacteria but bacteria may not be always present
NetF toxin how does it affect the cells and which toxin type has been isolated?
Type A
B - pore forming
What are the principal toxins generated by Clostridioides difficile?
TcdA - toxin A
TcdB - toxin B
CDT - ADP ribosylating binary toxin
Pathogenesis of Clostridioides difficile?
Ingestions of spores, germinate in the intestines, toxin production
How does the main toxins of C. difficile, cause damage?
TcdA - Binds to multiple carbs receptors
TcdB - Not known yet
CDT - Cytoskeletal alterations, induce apoptosis, change intracellular signaling by GTPase inactivation
Typical histopathological lesions of C. difficile?
Volano-ulcers -focal disruptions of the mucosa with release of neutrophils, fibrin and debris
Which other Clostridium types other than difficile and perfringens have been related to enteric diseases ?
Paeniclostridium sordelli
In Clostridial gas gangrene, which bacteria are involved?
C. perfringens type A (most common)
C. septicum
C. chauvoei
C. novyi
C. ramosum
C. sporogenes
C. fallax
P. sordelli
What is the pathogenesis of gas gangrene?
- Contamination of wounds, parturition, vaccination or trauma, 2. less REDOX potential, metabolite decomposing protein and acid pH, 3. promote germination of spores and toxins
What similar disease exist in cows?
Blackleg (Clostridial myositis) due to C. Chauvoei
Does gas gangrene can presented without history of wound or trauma?
Yes, it can be patent in muscle or heart
Mechanism of action of toxins in how they cause damage?
Enzymes:
- Collagenases
- DNAses
- Hyaluronidases
- Neuroaminidases
Clinical signs of gas gangrene?
Muscle tremors, tissues swollen, red, hot and painful, skin will turn dark, crepitation
How to diagnose gas gangrene?
Isolation of bacteria in subcutaneous exudate, fluorescent antibody test, IHC, anaerobic culture
Which disease is caused by Clostridium piliforme?
Tyzzer´s disease
Characteristics of C. piliforme
Obligate intracellular and Gram -
Which population is mainly affected?
Foals <45 days old
Due to coprophagia <5 weeks
Foals born in March-April
Pathogenesis of Tyzzer´s disease
Ingestion of spores, spores colonization of ileum, cecum and/or colon, direct damage to enterocyte, absorbed blood, liver portal circulation and will be reach liver
Main organs affected in Tyzzer´s disease
- Liver
- Heart
- Intestines
Characteristics of histophatology findings for Tyzzer´s disease
Filament of bacteria seen in hepatocytes, visualized with GIEMSA or silver stains
Which bacteria cause infectious necrotic hepatitis ?
Clostridium novyi
How many toxinotypes have been identified in C. novyi?
4
A,B,C,D, and B is the one related to the disease
Which genes can encode C. novyi type B that make it trigger the disease?
TcnA - alpha - main virulence factor
TcnB - beta toxins
Pathogenesis of C. novyi ?
Ingestion of the spores, reach intestines and is absorbed, get to the liver, keeps latent in Kupffer cells and geminate in anaerobic environments
How does TcnA toxin affects the cell?
Has a monoglycosyl transferase activity that inactivates GTP-binding proteins in endothelial cells and cause cytoskeletal disruption and increased vascular permeability
How does TcnB toxin affects the cell?
Indice direct hepatic necrosis but usually no as fatal as toxin a
Gross important pathological findings in C. novyi?
In horses necrosis is focal and ruminant is multifocal, gas in parenchyma
Histopathological lesions for C. novyi?
Stain positive to Okajima stain
Multiple hemorrhage affecting other organs
Diagnosis for infectious necrotic hepatitis?
Hx of previous cases
Cl Sx
Liver biopsy
PCR frozen samples
No culture due to strict intracellular
