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Bacteriology/ Mycology > Histiotoxic/ Enteropathogenic Clostridia > Flashcards

Histiotoxic/ Enteropathogenic Clostridia Flashcards

1
Q

What do the endotoxins of histiotoxic clostridia produce? What is the effects of this? Where are they typically present in the body/ where can they be found in the environment?

A
  • Exotoxins induce local tissue necrosis and systemic effects LETHAL.
  • They are present in tissue as latent spores (muscle and liver).
  • Endospores are widely distributed in the environment and persist for
    long periods in soil.
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2
Q

How does histotoxic clostridia cause endogenous infections? What is the steps? What about exogenous infections?

A
  • Endogenous:
    Spores in intestinal lumen -> tissue (phagocytes) ->Tissue injury (reduced oxygen) -> Spore germination -> vegetative bacteria -> exotoxins production -> Necrosis and Toxaemia
  • Exogenous infections Infected wounds
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3
Q
A
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4
Q

What is egg yolk agar? What characteristics does it support? What can be seen if the bacteria plated is specific for this characteristic?

A

Egg Yolk Agar is a differential and enriched medium used in the isolation and presumptive differentiation of different species based on their lecithinase activity. Lecithin is a normal component of the egg yolk
Such an opaque halo, surrounding the colony when grown on the egg yolk agar medium indicates positive lecithinase activity of the test organism.

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5
Q

What is seen in this image? What bacteria likely causes these lesions?

A
  • Necropsy: Necrosis of muscles/ dark discoloration, emphysema usually in larger muscles of the body. Clostridium produces gas. You can also see edematous fluid that’s hemorrhagic.
    This is C. chauvoei, causing black leg in cattle.
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6
Q

What are the 4 clostridia that can cause malignant edema?

A

Malignant edema can be caused by 4 clostridium:
◦ Clostridium perfringens Type A
◦ Clostridium novyi
◦ Clostridium chauvoei
◦ Clostridium sordellii
- Also CL Septicum

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7
Q

A farmer accidentally punctured the skin with a fork trying to get the cow up. What is likely causing the pathology in these images? What is another name for this condition?

A

Cause is likely one of the 5 clostridia that causes malignant edema. These are signs of malignant edema

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8
Q

What can you see in this image? What is the likely cause?

A

Braxy, Clostridium septicemia-> hemorrhagic, abomasum -> ulcerated

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9
Q

What can be seen in the stomach and liver of cattle with C. Novyi? What is the name of the disease? What is it associated with? What animals is it a

A
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10
Q

How does fasicola hepatica enhance the experience of C. Novyi?

A

◦ When the liver parasites are there it creates and anaerobic environment -> this allows the spores of clostridium to start to reproduce since the environment is now favorable.

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11
Q

What is occurring in these images? What is a way to remember these lesions? What can be seen in both the liver and stomach?

A

A.) Full stomach and gas bubbles in the liver.
B.) The liver uniformly infiltrated with gas bubbles, presenting a spongy appearance on the cut surface, probably the most distinguishing feature of sudden death in sows caused by clostridium Novyi

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12
Q

What is a key findings in patients with Clostridium Haemolyticum?

A
  • Jaundice/ icteric (yellow color or pale of gum and sclera)
  • Pinpoint red blood spots ( petechia)
    Dark purple/ red port wine colored urine (hemoglobinuria) and dark colored feces ( melena)
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13
Q

What is seen in this images? What is likely the cause?

A

Left: Jaundice/ icterus
Right: Open urinary bladder showing dark red urine in lumen.
Clostridium haemolyticum
Bacillary haemoglobinuria

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14
Q

What is the cause of jaundice and hemaglobinuria in cases infected with C. Haemolyticum?

A

Clostridium haemolyticum- Bacillary haemoglobinuria
* High numbers of RBC are being destroyed in body. The hemoglobin cannot be metabolized/ eliminated, if kidney starts excreting hemoglobin, it will cause dark, hematuria. You can see yellow discoloration of MM/ pinpoint red blood spots ( petechia)
* Melena
* Port wine urine.

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15
Q

What are the immunological aspects of histotoxic clostridia?

A
  • Circulating antibody to toxins and cellular components determines resistance
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16
Q

What are the types of Laboratory diagnostics that can be preformed for Histotoxic clostridia? What are the requisites?

A

Laboratory Diagnosis

  • Immunofluorescence of infected tissue smears
    * Sporulated gram positive rods
  • Isolation requisites:
    * Strict anaerobic conditions
    * Culture medium rich in cysteine and water-soluble vitamins
  • Detection in tissue or identification in culture can be done by molecular methods (PCR)
    * Flagellin and other genes 16S-23S DNA spacer regions
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17
Q

What are the treatment options available for Histotoxic Clostridia? Is treatment usually effective?

A
  • Treatment is often disappointing
  • Intravenous penicillin (but it is hard to catch infection early)
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18
Q

What are control measures/ preventative measures in place for farms exposed to histotoxic clostridia?

A
  • Cattle are vaccinated at 3-6 months (usually combined vaccine)
    * Vaccination should precede exposure by at least 2 weeks
    * Pregnant ewes are vaccinated 3 weeks prior to parturition
    * Lambs may require vaccination during their first year
    * Change of pasture is advisable when cases are first observed
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19
Q

What are the enteropathogenic / enterotoxaemia producing clostridia? Where do they live? What effects does the toxins produce?

A
  • Clostridium present and replicate in GI tract
  • Clostridium produce toxins
  • Toxins can produce local and generalized effects/damage
  • Produce disease only in defined circumstances
  • Clostridium perfringens type A, B, C, D, and E.
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20
Q

What are the factors that predispose animals to the development of enterotoxemias associated with C. Perfringens in sheep

A
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21
Q

What kind of tissue destruction is caused by enterotoxemia A? What Diseases are caused by this bacteria?

A
  • Tissue destruction
  • Membrane active toxins and connective tissue toxins Diseases
  • Outbreaks of gastritis and hemolytic diseases of ruminants
  • Yellow lamb diseases
  • Hemorrhagic enteritis in cattle, horses and infant alpacas
  • Necrotic enteritis in poultry
  • Canine hemorrhagic gastroenteritis
  • Food poisoning in humans
  • Antibiotic-associated diarrheas
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22
Q

What is important toxins for Enterotoxemia Type A?

A

α-TOXIN, perfringlolysin O and enterotoxins are important!!!

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23
Q

What is seen in these images? In chickens, what can be seen as a coinfection of this bacteria?

A
24
Q

What is seen in this image?

A
  • Necrosis seen on the abomasum of this calf
25
Q

What is seen in this image?

A
  • Necrotic enteritis, ( hemorrhagic necrosis) in chickens.
26
Q

What is enterotoxemia (Type B)? What condition does it cause? Why?

A
  • Old world diseases (Europe and some regions in Asia) * Causes lamb dysentery in newborn lambs
  • Absence of microbial competition in the neonatal intestine
  • Low proteolytic activity in the neonatal intestine
27
Q

Why is there low proteolytic activity in infants?

A

‣ Why are proteolytic enzymes low in young infants? This is because the colostrum would be degraded if they had more proteolytic activity, and they would not get the same nutrients/ antibodies.

28
Q

For enterotoxemia (type B) what is the principle factor producing hemorrhagic enteritis in the small intestine? What is it susceptible to?

A
  • β-toxin is the principal factor producing hemorrhagic enteritis in
    small intestine
  • SUSCEPTIBLE TO TRYPSIN!!!
29
Q

What are the signs of enterotoxemia type B? What is the prognosis? Is this a chronic condition?

A
  • Signs include depression, anorexia, abdominal pain, and diarrhea
  • Course is rapid
  • Mortality rates approaching 100%
30
Q
A
  • 20 sheep present -> presented with HGE and distended abdomens. They died pretty quickly. You can see hemorrhagic large and small intestine. ( Left)
  • Right image: you can see pericardial sac -> dilated with fluid and fibrin
31
Q

What is enterotoxemia type C? Who does it effect? Why? What is the principle virulence factor?

A
  • Neonatal calves, foals, piglets and lambs worldwide
  • Absence of established normal intestinal flora
  • Causes hemorrhagic enteritis
  • β-toxin is the principal virulence factor
  • Protease inhibitors in colostrum favors its action
32
Q

What favors the action of B-toxin in young calves, foals ect?

A
  • β-toxin is the principal virulence factor
  • Protease inhibitors in colostrum favors its action
33
Q

What are the clinical signs of enterotoxemia type C? Is the prognosis good? Is this a chronic condition?

A
  • Signs include depression, anorexia, abdominal pain,
    and diarrhea (Causes HGE)
  • Course is rapid and mortality ~100%
34
Q

What is seen in these images?

A
35
Q

What is struck? What is this caused by? What is the characteristic seen that can give you an indication of the cause?

A

Enterotoxemia (Type C )
* “Struck” in older sheep (Europe)
* Often rapidly fatal toxemia-bacteremia
* Alpha, beta and perfringolysin O toxins * Beta toxin plays the main role
* Impression that the animal has been struck by lightning!!!!!

36
Q

What is Enterotoxemia type D? Who does it affect? What does it cause? What is a typical cause?

A

Enterotoxemia (Type D)
* Enterotoxemia in older lambs (<1 year) and sometimes in goats
and calves
* Overeating diseases * Pulpy kidney disease
* Diseases often follows upsets in the gut flora
* Abrupt change to a rich diet
* Gorging on energy-rich diet
* Intestinal hypo-motility, a consequence of overeating

37
Q

What is the primary virulence factor for Enterotoxemia Type D? What is this toxin activated by? What affects does it have to the patient?

A
  • Epsilon toxin
  • Increases intestinal permeability, causes vascular damages, fluid losses, edema
  • Has effects in CNS
  • Encephalomalacia
    Predilection for older animals!!
  • Activated by trypsin
38
Q

What is seen in this image? What is the likely cause?

A
39
Q

What signs are seen in sheep with pulpy kidney? What can be seen in post mortem exam? What is a characteristic finding?

A

Pulpy kidney in sheep causes acute deaths with few or no symptoms, and a mostly negative post mortem except for the rapid breakdown of the kidney tissue (insert) - Glycosuria is one of the few finding
- Toxin makes kidneys very soft.

40
Q

What signs can be seen in patients with enterotoxemia type D that has caused encephalomalecia?

A
  • Clinical Signs:
    ◦ Opisthotonos, encephalomalacia, ulcerative fibronecrotic ileitis.
41
Q

What are the immunological aspects associated with enterotoxemia type D? What is important for control of the disease?

A

Immunological Aspects
* Immunity is antibody-mediated and correlates with anti-toxin
levels * Passive and active immunization is important in control of
diseases

42
Q

What are strategies/ characteristics that can aid laboratory diagnosis? What can you see in the lab?

A
  • If sample obtained from contaminated tissue (intestine) the spores will
    survive heating at 80°C for 15 min
  • Laboratory Diagnosis
  • Non-motile and produces a polysaccharide capsule in tissue
  • Spores are rarely demonstrated in exudates
  • Isolation in BA in anaerobic environments
43
Q

What can you see on blood agar when plating for C. perfringens? Is it proteolytic? Does it have an odor? Is it hemolytic? What do the colonies look like?

A
44
Q

If you were to take the same blood agar plate with C.Perfringens, what would you see if it is examined with transmitted light?

A
45
Q

What are the laboratory diagnostic features of enterotoxin D?

A
  • Diagnostic features include:
  • Alpha toxin-associated hemolytic activity (Hot-cold lysis)
  • Positive CAMP test with S. agalactiae
  • Alpha toxin of C. perfringens
  • In cases of enterotoxemia
  • Giemsa, Gram stains reveal Gram-positive rods * Molecular diagnosis (PCR) * Injection of toxins from small intestine in mice * Serology
  • ELISA (Cpe)
46
Q

When looking at sample isolations of c. perfringens, what would you see that is called stormy milk?

A

Clotting of milk followed by gaseous disruption
Proteins of milk are digested and produces gas.
Can see bubbles on surface.

47
Q

What are treatment methods for enterotoxemia D?

A
  • Most causes of enterotoxemia are too acute for
    successful treatment
  • Antitoxin of appropriate type may be given to sick
    animals and those at risk
  • Protection last for 2-3 weeks
48
Q

What are control methods for enterotoxemia D? Are antibiotic treatments usually effective?

A
  • Active immunization of dams with two injections of
    bacterin-toxoid combinations
  • Prior to parturition ensures nursling passive protection for first
    week
  • Ensuring against overeating is a worthwhile preventive
    measure
  • Antibiotic treatment can be use in some cases * Rarely successful due to acute presentations!!!
49
Q

What are the characteristics of C. dificile? What does it cause in humans? what can be seen in other animals?

A

Clostridium difficile
* Gram-positive, motile, encapsulated, spore-forming anaerobic rod
* Significant cause of diarrheal diseases in humans
* Antibiotic-associated diarrhea
* Pseudomembranous colitis
* Isolated from symptomatic and asymptomatic dogs, cats and horses

Typhilitis in hamsters. - inflammation of cecum
Colon main organ affected

50
Q

What is Toxin A in C. Difficile? How does it affect the host cell?

A

Toxin A (Tox A or TcdA)
* ENTEROTOXIN * Breakdown of cytoskeletal components of the affected
cell * Disruption of the tight junctions between intestinal
epithelial cells
* RESULTS IN CELL DEATH * Stimulates influx of polymorphonuclear cells
* Synthesis of prostaglandins
* RESULTS in secretion of chloride ions and water (Diar

51
Q

What is the pathogenesis of C. Difficile?

A
  • trigger event -> Normal flora disrupted (C.diff takes advantage)-> adheres to lg intestine, produces toxins, causes epithelial cell death -> intense inflammatory response. ( fluid + electrolyte secretion, diarrhea w/ or w/o blood.
52
Q

What is seen in these images?

A
53
Q

What is seen in these images? What is this presentation classic for? In the 2nd image, what is the black arrow indicating?

A

Image 1: position of fibrin and necrotic tissue is classic for c.diff.
Image 2: Characteristic plaque seen ( black arrow) overlying intact intestinal mucosa) H& E stain

54
Q

What are the immunological aspects of C. Difficile? What are potential lab diagnostics that can be preformed?

A

Immunologic Aspects
* Antitoxin
* Orally administered antitoxin (bovine) is protective for humans

Laboratory Diagnosis
* Molecular diagnosis (PCR) and Immunological based tests
from feces samples
* Can be isolated by using selective medium
* Cycloserine, cefoxitin, and fructose agar (CCFA)

55
Q

What are the treatment and control methods for C. Difficile infections? Are there any antibiotics that are functional?

A
  • Diarrhea associated C. difficile responds rapidly to
    metronidazole
  • Resistance exists (Alternative antibiotic: vancomycin)
  • No vaccines available
  • In humans: probiotics can be useful in preventing the diseases * In hospitals
  • Hand washing by health care personnel is a very efficient
    mechanism for curtailing spread
  • Disinfectants are not effective against the spore
56
Q

What are other species of veterinary interest? What can they cause>

A
  • C. piliforme
    * Acute fatal diarrheal diseases of laboratory mice with focal liver necrosis (Tyzzer’s diseases)
    * Also in foals rabbits, hares, gerbils, rats, hamsters, muskrats, dogs, cats, snow leopards, and rhesus monkeys
    * High mortality events
  • C. sordellii
    * Fatal myositis and hepatic diseases in ruminants and horses
  • C. colinum
    * Causes quail disease, ulcerative enteritis and necrotizing hepatitis of several species of fowl
  • C. spiroforme
    * Juvenile enteritis (mucoid enteritis) in rabbits
    * Antibiotic induced enteritis in rabbits

Bacteriology/ Mycology (19 decks)

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