PQS - Clostridium Flashcards
Most clostridia have low invasive capacity
T
Spores of clostridia are generally very resistant against heat
T
The habitat of clostridia is the gut and the soil
T
Clostridia are obligate aerobic bacteria
F
obligate ANaerobic
Clostridium perfringens is an obligate pathogenic bacterium
F
facultative pathogens
Clostridium perfringens can produce main and auxillary toxins
T
Extracellular enzymes and toxins are virulence factors of clostridia
T
There are no vaccines for the prevention of diseases caused by clostridia
F
inactivated bacterium culture
Clostridium is anaerobe spore forming bacteria
T
Clostridium bacteria is not in the environment, because it cannot tolerate oxygen
F
Clostridium spreads usually rapid in a herd
F
No animal – to animal transmission
Clostridium spread mostly with insecticides
F
Clostridium difficile can be treated with metronidazole
T
Clostridium difficile is seen in foal and piglets
T
Many Clostridium species have flagella
F
Clostridium species are only found in the subtropics
F
tropical and subtropical area
Clostridium can cause severe contagious diseases
F
Clostridium are obligate pathogens
F
facultative pathogens
Anaculture or anatoxin vaccines are used for the prevention of malignant oedema
T
Cl. chauvoei is the agent of malignant oedema
F
Lesions of malignant oedema are mainly seen in the large muscles
T
- oedema, swelling
- wound infection
Malignant oedema is generally endogenous in cattle
F
Malignant oedema is generally a consequence of wound infection
T
Movement difficulties are frequently seen in the case of malignant oedema
T
Clostridium novyi can cause malignant oedema
T
Malignant oedema can be diagnosed based on clinical signs
F
Malignant oedema is caused due to wound infection
T
Malignant oedema is only in ruminants
F
Malignant oedema, one of the clinical signs is lameness/movement problems
T
Malignant oedema, attenuated vaccine for prevention
F
inactivated bacterium culture (anaculture)
Clostridium channel is the agent of malignant oedema
F
Attenuated vaccines are used for the prevention of malignant oedema
F
Clostridium septicum is an agent of malignant oedema
T
septicum, novyi, histolyticum and sordelli are causative agents
Malignant oedema is generally a consequence of a wound infection
T
Clostridium histolyticum can cause malignant oedema
T
-C. Septicum
-C. Novyi
- C. Histolyticum
- C. Sordelli
Agents of malignant oedema can be detected by bacterium culture
T
There are no vaccines for the prevention of malignant oedema.
F
inactivated bacterium culture (anaculture)
Malignant oedema occurs in ruminants and pigs
T
Malignant oedema is an acute fatal disease
T
Malignant oedema can be treated with antibiotics
F
difficult, limited (fast course, toxic effects)
Malignant oedema can occur in any warm-blooded animal.
T
Once an area is infected with gas gangrene re-occurrence is common
T
Malignant oedema cannot occur in swine
F
Malignant oedema usually develop following an endogenous infection
F
Malignant oedema is well treated with long-term antibiotics therapy
F
Malignant oedema can be treated with polymyxin
F
Malignant oedema can be well treated with antibiotics over a long period
F
Gas gangrene (malignant oedema) is a regional illness
F
The lesions of malignant oedema are mainly seen in the lungs
F
Blackleg is caused by Clostridium septicum
F.
C. chauvoei
Lesions of blackleg are mainly seen on the claws
F
Lameness is a clinical sign of blackleg
T
Blackleg is a frequent disease in pigs
F
Mainly seen in cattle and sheep, rarely in other species
Generally attenuated vaccines are used for the prevention of blackleg
F
Anaculture or anatoxin vaccines are used for the prevention of blackleg
T
- anaculture, anatoxin
- combined vaccines
Blackleg occurs only in tropical and subtropical countries
F
worldwide
Generally attenuated vaccines are used for the prevention of blackleg
F
Blackleg generally occurs in endemic form
T
Blackleg occurs most frequently in pigs
F
ruminants (sometimes pigs and other species)
Blackleg is a gas gangrene disease
T
Blackleg is generally endogenous in sheep
F
iatrogenic in sheep,endogenous in cattle
Blackleg is generally endogenous in cattle
T
Movement disorders and lameness can be clinical signs of Blackleg
T
Clostridium chauvoei can produce acids and gas from carbohydrates
T
active carbohydrate fermentation (production of acid and gas)
Blackleg occurs mainly in ruminants
T
Oedema is a typical clinical sign of blackleg
T
Live vaccines are used for the prevention of blackleg
F
Blackleg infects ovine through wounds
T
In Blackleg disease we use attenuated vaccine
F
In the case of sheep, blackleg is generally consequence of a wound infection
T
Oedema in the muscles is a typical clinical sign of blackleg
T
Attenuated vaccines are used for the prevention of blackleg
F
Blackleg is caused by Clostridium chauvoei
T
Severe diarrhoea is the main clinical sign of blackleg
F
Blackleg is caused by Clostridium septicum
F
C. chauvoei
Blackleg occurs in cattle and sheep.
T
If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is generally successful
F
Attenuated vaccines are used for the prevention of blackleg
F
Blackleg disease occurs only in ruminants
F
Blackleg can usually be treated with antibiotics successfully
F
Blackleg in cattle is mainly endogenous between 6 months-3 years old
F
Frequent in cattle between 2 months and 2 years
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
Causing by blackleg
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle.
T
Blackleg has four toxins
T
toxins: a, b, g, d
Blackleg can be prevented by using vaccine
T
We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei
F
Blackleg in cattle is mainly endogenous between 2 months-2 years old
T
Blackleg in bovine is caused by wound infections
F
Soil infection: mainly on pastures of poor quality
-sheep: wound infection
Classical swine fever is a frequent predisposing factor of bradsot
F
Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot
T
Bradsot is caused by Clostridium chauvoei
F
C. septicum
Soil contaminated frozen feed is a frequent predisposing factor of bradsot
T
- after driving the animals to winter pasture
- frozen feed contaminated with soil (potato, turnip, grass)
Frozen food is a predisposing factor of bradsot
T
Bradsot occurs mainly late autumn and winter
T
late autumn, winter, frost
Overeating can predispose the animals to bradsot
F
after driving the animals to winter pasture
- frozen feed contaminated with soil (potato, turnip, grass)
Thickening of and oedema in the stomach wall are typical lesions of bradsot
T (rennet)
Aminoglycosides are successfully used for treatment in the case of bradsot
F
Bradsot is mainly seen in late autumn and winter
T
Bradsot is mainly seen in late autumn and winter
T
late autumn, winter, frost
Bradsot is caused by Clostridium septicum
T
Severe pneumonia is a typical clinical sign of bradsot
F
Bradsot has a very fast course
T
Bradsot occurs only in suckling lambs
F
Bradsot is typically a chronic disease
F
Bradsot is common in the summer out on the pasture
F
late autumn, winter, frost
Bradsot is an acute disease resulting in sudden death in many cases
T
We can use anaculture strain vaccine against Bradsot
T, f ??
Bradsot causes oedema of the legs and necrosis
F
Post mortem lesions of bradsot can be seen in the stomach (rennet)
T
Koves disease is an indicator disease
T
indicator (haemorrhages in the stomach, erosions)
CSF is a predisposing factor of koves disease
T
Koves disease can be seen in pigs
T
Koves disease is caused by Clostridium chavoei
F
C. septicum
Infectious necrotic hepatitis is mainly seen in pigs
F
Sheep 1-4 years
Infectious necrotic hepatitis can be prevented by using anatoxin vaccines
T
(anaculture, anatoxin)
Liver fluke can predispose animals to infectious necrotic hepatitis
T
In sheep, Clostridium septicum causes necrotic liver infection
F
C. novyi B
Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver
T
There is no vaccine to prevent infectious necrotic hepatitis
F
vaccine (anaculture, anatoxin)
Infectious necrotic hepatitis is caused by Clostridium septicum
F
C. novyi B
Infectious necrotic hepatitis is mainly seen in suckling lambs
F
sheep 1-4 years (sometimes cattle, other)
Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis
T
parasite infection (liver flukes)
Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis.
T
Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis.
T
Infectious necrotic hepatitis is caused by Clostridium novyi
T
Infectious necrotic hepatitis is spread by tick
F
Infectious necrotic hepatitis is found worldwide
T
Infectious necrotic hepatitis can be transmitted by liver flukes
T
Infectious necrotic hepatitis occurs mostly in young sheep
F
sheep 1-4 year
There is intravascular haemolysis in the case of bacillary haemoglobinuria
T
Bacillary haemoglobinuria is caused by Clostridium haemolyticum
T
There are no vaccines for the prevention of bacillary hemoglobinuria
F
vaccine (6-month-long protection)
Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria
T
Bacillary haemoglobinuria is mainly seen in cattle
T
cattle, mainly beef cattle (sometimes sheep)
Bacillary haemoglobinuria is caused by Clostridium septicum
F
C. haemolyticum
Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria
T
- sudden onset
- fever, depression
- haemoglobinuri
- jaundice
- anaemia
- increased heart and breath rate
Red urine is a typical clinical sign of bacillary hemoglobinuria
T
Bacillary hemoglobinuria is a slow, chronic disease
F
Bacillary hemoglobinuria can frequently be seen in horses
F
cattle (sometimes sheep)
Clostridium novyi is the causative agent of bacillary hemoglobinuria.
F
C. haemolyticum
Bacillary hemoglobinuria causes severe haemorrhages
T
Bacillary hemoglobinuria are caused by infection from the soil
T
habitat: gut, soil
Lamb dysentery occurs in a week old animal
T
1–2-week-old lambs
Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery
F
Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery
F
Lesions of lamb dysentery are generally seen in the large intestine
F
In the small intestine
Lesions of lamb dysentery can be seen in the small intestine
T
Lamb dysentery is caused by Clostridium perfringens
T
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
pregnant ewes are vaccinated
Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery
F
Prevention :
- improving hygiene
- ewes: penicillin
- vaccine: pregnant ewes are vaccinated twice, yearly booster
Pregnant ewes have to be vaccinated in order to prevent lamb dysentery
T
pregnant ewes are vaccinated twice, yearly booster
Haemorrhagic diarrhoea is a clinical sign of lamb dysentery
T
Lamb dysentery can be seen in lambs around weaning
F
1–2-week-old lambs
Lamb dysentery is found in 3-4-week-old lambs
F
1–2-week-old lambs
Pathological lesions of Lamb dysentery starts in the colon
F
Small intestine
We can culture the pathogen of Lamb dysentery from the intestines
T
Lamb dysentery is caused by Clostridium dysenteriae
F
C. perfringens B
Lamb dysentery can be seen in lambs after weaning
F
1–2-week-old lambs
There is no vaccine for the prevention of lamb dysentery
F
Vaccine: pregnant ewes are vaccinated twice, yearly booster
Lamb dysentery occurs in 2-6 weeks old lambs
F
1–2-week-old lambs
For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine
T
Pathological symptoms of lamb dysentery can be found in the large intestines
F
small intestine
Lamb dysentery can be prevented by vaccinating pregnant ewes
T
pregnant ewes are vaccinated twice, yearly booster
Lamb dysentery can be successfully treated with penicillin when clinical signs appear
F
treatment is generally not possible
Lamb dysentery occurs in a week-old animal.
T
1–2-week-old lambs
Lamb dysentery can be diagnosed by culturing the bacteria
T
Newborn lambs have to be vaccinated in order to prevent lamb dysentery.
F
Toxoid vaccines can be used in the prevention of lamb dysentery
T
Infection of lamb dysentery by secretion in the milk
F
Lamb dysentery occurs in 1-2 weeks old lambs.
T
Struck is caused by Clostridium perfringens
T
Clostridium perfringens C
Overeating is a predisposing factor of struck
T
- overeating
- high protein and carbohydrate content
- change of the diet
Struck can be seen mainly in lambs younger than 2 weeks
F
In grower, adult sheep
Struck is an acute disease in horses
F
Struck is a zoonotic disease
F
Struck is a slow disease of older sheep
F
very fast course
Struck is a worldwide common disease with great economic impact
F
it is worldwide, but not great economic impact
Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life
F
2–4-day-old piglets
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine
F
small intestine, jejunum
Maternal protection is important in the case of Infectious necrotic enteritis of piglets
T
There is no vaccination for the prevention of Infectious necrotic enteritis of piglets
F
vaccination of pregnant sows
Pig enterotoxaemia can be prevented by vaccinating the pregnant sows.
T
PIG ENTEROTOXAEMIA (INFECTIOUS NECROTIC ENTERITIS OF PIGLETS)
Pig enterotoxaemia is caused by Clostridium perfringens C
T
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics
immediately
F
Fast course ,no time for treatment
Lesions of pig enterotoxaemia can be seen in the small intestine
T
Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets
T
Pig enterotoxaemia is more frequent in the litter of young than old sows
T
Older sows give protection through colostrum
Pig enterotoxaemia can be generally seen in weaned piglets
F
2–4-day-old piglets
Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia
T
Clostridium enterotoxaemia of piglets is caused by C. perfringens
T
C. perfringens C
Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows
T
Clostridium perfringens C causes infectious necrotic enteritis of piglets
T
Infectious necrotic enteritis of piglets occurs in piglets after weaning
F
The lesions of infectious necrotic enteritis of piglets can be seen generally in the small intestine
T
Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows
T
Necrotic enteritis of piglets is seen in piglets around weaning
F
Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin
T
Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets
F
detection of the agent
Pig enterotoxaemia causes abdominal contractions in sows
F
Mesenteric lymph node is congested in case of pig enterotoxaemia
F
Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut
T
Enteritis in piglets are caused by Clostridium perfringens D
F
Clostridium perfringens D causes pulpy kidney disease
Enteritis in piglets can be avoided by anatoxin vaccination
T
Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology
F
Pig enterotoxaemia is caused by β-toxin production in 1st week of life
T
a and b toxin (b toxin is trypsin sensitive)
Pig enterotoxaemia can cause a high mortality
T.
Mortality = 20-100%
Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut
F
Enterotoxaemia is mainly seen in piglets after weaning
F
Pig enterotoxaemia is not present in Europe
F
worldwide
Pig enterotoxaemia cannot be prevented by using vaccines
F
vaccination of pregnant sows
Pulpy kidney disease is caused by Clostridium perf. D
T
Overeating is a predisposing factor to pulpy kidney disease
T
- overaating
- sudden change of the diet
The toxin of the agent of pulpy kidney disease is sensitive to trypsin
F
activated by trypsin
Pulpy kidney disease is caused by Clostridium perfringens D
T
Pulpy Kidney Diseases is caused by Clostridium chauvoei.
F
Clostridium perfringens D
Pulpy kidney disease generally occurs in 1-2 week old lambs
F
most frequent in 6-12-month-old lambs, but sometimes 1-2 months old
Pulpy kidney disease can occur at any age
F
- most frequent in 6-12-month-old lambs, kids
- sometimes 1-2 months old
Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes
F
Sudden change the diet is a predisposing factor to pulpy kidney disease
T
- overeating
- sudden change of the diet
The toxin damages the endothelial cells in the case of pulpy kidney disease
T
Neurological signs are typical in the case of pulpy kidney disease
T
- neurological signs
- abdominal pain
- diarrhoea
- glucosuria
Isolation of the agent is necessary to the diagnosis of pulpy kidney disease
F
Pulpy kidney disease is typically seen in lambs below 2 weeks of age
F
- most frequent in 6-12-month-old lambs, kids
- sometimes 1-2 months old
Inactivated vaccines are used for the prevention of pulpy kidney disease
T
Pulpy kidney disease is seen in piglets in the first week of life
F
- most frequent in 6-12-month-old lambs, kids
- sometimes 1-2 months old
Pulpy kidney disease is a worldwide common disease.
T
Enterotoxaemia of sheep is also called pulpy kidney disease.
T
Pulpy kidney disease is caused by Clostridium perfringens D.
T
Cattle are not susceptible to pulpy kidney disease
T
Sheep an goat
Vaccination are possible against pulpy kidney disease
T
Coccidiosis is a predisposing factor of ulcerative enteritis in poultry
T
Predisposing factor:
- coccidiosis
- infectious bursitis
- chicken anaemia
- overcrowding
- nutritional problems
- old litter
Ulcerative enteritis of chicken is caused by Clostridium colinum.
T
Ulcerative enteritis is frequently seen in day old chicken
F
4–12-week-old chicken and 3–8-week-old turkey
Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of ulcerative enteritis of chicken
T
Ulcerative enteritis can occur in 4-12-week-old chickens
T
Clostridium perfringens is the causative agent of ulcerative enteritis in poultry
F
It is C. colinum
Ulcerative enteritis of poultry is generally prevented with vaccination.
F
With hygiene, optimal management and elimination of predisposing factors
Lesions of ulcerative enteritis are mostly seen in the small intestines
F
Ulcerative enteritis is a common disease in large scale farms
T
Prevention of coccidiosis can help lower the incidence of ulcerative enteritis
T
Coccidiosis is a predisposing factor of necrotic enteritis of chicken
T
predisposing factors:
- coccidiosis, mycotoxicosis
- feed: wheat, fishmeal
- poorly digestible feed
- alteration of the intestinal flora
- damage of the mucosa
Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken
T
Lesions of necrotic enteritis of chicken are typically occur in the large intestine
F
small intestine - jejunum and ileum
Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis
F
Necrotic enteritis mostly occurs in chicken
T
Waterfowl are not susceptible to necrotic enteritis
F
seen in chickens, turkeys and ducks worldwide
Necrotic enteritis occurs in 1-3 weeks of age
F
In broiler 2–5-week-old, and turkey 7–12-week-old
Tyzzer’s disease is caused by Clostridium piliforme
T
Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A
T
- C. septicum
- C. perfringens A
- Staphylococcus aureus
- facultative pathogenic bacteria
Gangrenous dermatitis is caused by obligate pathogens
F
facultative pathogens
Gangrenous dermatitis causes muscle oedema
T
- muscles: oedema, reddish, crepitation
Vaccines are the primary way of prevention of gangrenous dermatitis
F
No vaccines are available
Flaccid paralysis is a frequent clinical sign of tetanus
F
The agent of tetanus is strictly anaerobic
T
The agent of tetanus can enter the host through wounds
T
Tetanus is only seen in horse
F
horse, sheep, cattle, swine, dog
Over-eating can predispose animals to Tetanus
F
predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria
The agent of Tetanus needs oxygen to replicate
F
cannot survive in the presence of oxygen !!
Anatoxin vaccines are available for the prevention of tetanus
T
Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus
F
No gross lesions
Spasms are typical clinical signs of tetanus
T
horse, sheep:
* spasms, stiffness, tonic contractions
* lockjaw, „saw-horse”
* ears stand up, third eyelid, nares are wide
Tetanus is a zoonosis
F
Toxoid vaccines can be used for the prevention of tetanus.
T
Dogs are resistant to tetanus
F
The clinical signs of tetanus are inducible
T
= capable of being induced
Tetanus toxin cleaves synaptobrevin
T
For tetanus we use vaccines which contain toxoid
T
Tetanus cannot be prevented with vaccination.
F
Tetanus is caused by Clostridium tetani
T
The agent of tetanus causes septicaemia.
F
Tetanus can be diagnosed on the basis of post mortem lesions
F
Clostridium tetani produced endotoxin
F
C. tetani needs anaerobic conditions for propagation
T
Dogs are susceptible to tetanus
T
Tetanus can be prevented with vaccines containing inactivated bacteria
F
Tetanus can cause spasms
T
Horses are resistant to tetanus
F
Tetanus can only develop after deep wounds
F
Wounds can predispose to tetanus
T
predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria
The paralysis usually starts at the place of the wound
F
Spasms begin at the site of entry, in the LOCAL form
Clostridium tetani toxin is produced in the feed
F
Horses are most sensitive to tetanus
T
Tetanus can be prevented by anatoxin vaccination
T
Tetanus causes rigid paralysis
T
Causing spastic or rigid muscle paralysis
There is no vaccine for tetanus
F
anatoxin vaccination
Clostridium tetani produces neurotoxins
T
Dogs have high resistance to tetanus
T
Tetanus is a relatively uncommon disease in dogs and cats because of their natural resistance to the toxin
The toxin of clostridium botulinum causes flaccid paralysis
T
Clostridium botulinum generally causes wound infection
F
Focal necrosis in the liver is a typical post mortem lesion of Botulism
F
Pathological lesions are not characteristic
The toxin of Clostridium botulinum has irreversible effect
T
Botulism can be seen as a result of a wound infection
F
Flaccid paralysis is the main clinical sign of botulism
T
Birds are resistant to botulism
F
Most frequent = mink, fox, duck, geese, pheasant
Necrotic foci in the liver are typical post mortem lesions of botulism
F
Pathology:
* not characteristic
* hyperaemic organs
* oedema in the lungs
Generally wounds predispose animals to botulism
F
The agent of botulism generally produces toxin at the site of entry
F
Botulism is diagnosed on the basis of the typical post mortem lesions
F
Clostridium botulinum can produce toxins outside the hosts.
T
No characteristic post mortem lesions can be seen in the case of botulism
T
Pathology
* not characteristic
* hyperaemic organs
* oedema in the lungs
Botulism doesn’t occur in Europe
F
worldwide – warmer climate
Clostridium botulinum cannot tolerate air at all
T
anaerobic bacterium, meaning it cannot survive in the presence of oxygen. Exposure to air can inhibit its growth and toxin production
Botulism usually develops following a wound infection
F
Clostridium botulinum propagates in rotten materials.
T
In Hungary, botulism is seen most commonly in birds
T
Clostridium botulinum spores are extremely resistant to heat
T
In Hungary, botulism occurs in winter and early spring.
F
worldwide – warmer climate
Botulism is eradicated in Europe
F
worldwide – warmer climate
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
Botulism is seen mainly during summer
T
worldwide – warmer climate
Spasms are the typical clinical sign of botulism
F
Paralysis is the main sign of botulism
T
Toxins of botulism are produced generally in the food.
T
Botulism happen generally through wound infection
F
Animals are mostly sensitive to C and D types of Clostridium botulinum.
T
A, B, E, F = Humans
Lesions of pig enterotoxaemia can be seen in the large intestine
F
Jejunum
Infectious necrotic hepatitis is caused by Clostridium novyi type B
T
