Clostridia 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
Clostridium perfringens is an obligate pathogenic bacterium
F
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
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
Clostridium spread mostly with insecticides
F
Clostridium difficile can be treated with metronidazole
T
Enterotoxaemia of young animals foals and piglets
Clostridium difficile is seen in foal and piglets
T
Many Clostridium species have flagella
F
Only clostridium dificcile has peritrichous flagellae
je giafto troi metronitazoli :)
Clostridium species are only found in the subtropics
F
Clostridium can cause severe contagious diseases
F
Clostridium are obligate pathogens
F
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
Malignant oedema is generally endogenous in cattle
F
malignant odema = wound only
Black leg =swce sheep wound cattle endogenous
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
DDx : Blackleg
Malignant oedema is caused due to wound infection
T
Malignant oedema is only in ruminants
F
mainly horses also mammals and birds
Malignant oedema, one of the clinical signs is lameness/movement problems
T
Malignant oedema, attenuated vaccine for prevention
F
Anatoxin anaculture which are inactivated toxin and agent
Clostridium channel is the agent of malignant oedema
F
Clostridium septicum is an agent of malignant oedema
T
Clostridium histolyticum can cause malignant oedema
T
Agents of malignant oedema can be detected by bacterium culture
T
There are no vaccines for the prevention of malignant oedema
F
Malignant oedema occurs in ruminants and pigs
T
Mammals and birds
Malignant oedema is an acute fatal disease
T
Acute for sure 1-2days ip fatal yes because a lot of pathology
Malignant oedema can be treated with antibiotics
F
too late
Malignant oedema can occur in any warm-blooded animal
F
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
Strictly wound
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
Worldwide
The lesions of malignant oedema are mainly seen in the lungs
F
Blackleg is caused by Clostridium septicum
F
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
Generally attenuated vaccines are used for the prevention of blackleg
F
Anaculture or anatoxin vaccines are used for the prevention of blackleg
T
Blackleg occurs only in tropical and subtropical countries
F
Blackleg generally occurs in endemic
T
Endemic regions
Blackleg occurs most frequently in pigs
F
Blackleg is a gas gangrene disease
T
Blackleg is generally endogenous in sheep
F
Swce
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
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
Blackleg is caused by Clostridium chauvoei
T
Severe diarrhoea is the main clinical sign of blackleg
F
Blackleg occurs in cattle and sheep
T
If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is generally successful
F
Blackleg disease occurs only in ruminants
F
Rarely other species
Blackleg can usually be treated with antibiotics successfully
F
Blackleg in cattle is mainly endogenous between 6 months-3 years old
F
The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep
T
The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle
T
Blackleg has four toxins
T
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
swce
Blackleg in bovine is caused by wound infections
F
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
rennet = abomasum
Bradsot is caused by Clostridium chauvoei
F
Bradsot occurs mainly in tropical and subtropical countries
F
north europe kriada frozen potato and turnip
Soil contaminated frozen feed is a frequent predisposing factor of bradsot
T
Frozen food is a predisposing factor of bradsot
T
Bradsot occurs mainly late autumn and winter
T
Overeating can predispose the animals to bradsot
F
Thickening of and oedema in the stomach wall are typical lesions of bradsot
T
Aminoglycosides are successfully used for treatment in the case of bradsot
F
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
Bradsot is an acute disease resulting in sudden death in many cases
T
We can use anaculture strain vaccine against Bradsot
T
Bradsot causes oedema of the legs and necrosis
F
Post mortem lesions of bradsot can be seen in the stomach (rennet).
T
Köves disease is an indicator disease
T
Indicator of a primary disease theat caused ulceration haemorrhages on the git.
CSF is a predisposing factor of koves disease
T
Köves disease can be seen in pigs.
T
Köves disease is caused by Clostridium chavoei
F
Infectious necrotic hepatitis is mainly seen in pigs
F
Infectious necrotic hepatitis can be prevented by using anatoxin vaccines
T
Liver fluke can predispose animals to infectious necrotic hepatitis
T
In sheep, Clostridium septicum causes necrotic liver infection
F
Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver
T
There is no vaccine to prevent infectious necrotic hepatitis
F
Infectious necrotic hepatitis is caused by Clostridium septicum
F
Infectious necrotic hepatitis is mainly seen in suckling lambs
F
Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis
T
Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis
T
Anatoxin vaccines can be used for the prevention 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 caused by Clostridium novyi type B
T
Infectious necrotic hepatitis is found worldwide
T
Infectious necrotic hepatitis can be transmitted by liver flukes
F
Infectious necrotic hepatitis occurs mostly in ** young sheep**
F
Mainly sheep also cattle
1-4 years old? is this young
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
Phospholipidase C is a virulence factor of the agent of bacillary hemoglobinuria
T
Bacillary haemoglobinuria is mainly seen in cattle
T
Black disease SC
Bac haemo CS
Bacillary haemoglobinuria is caused by Clostridium septicum
F
Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria
T
Red urine is a typical clinical sign of bacillary hemoglobinuria
T
Bacillary haemoglobinuria is a slow, chronic disease
F
sudden onset all histolytic clostridia and (enterotoxaemic clostridia?)
Bacillary hemoglobinuria can frequently be seen in horses
F
Clostridium novyi is the causative agent of bacillary hemoglobinuria
F
Bacillary hemoglobinuria causes severe haemorrhages
T
Bacillary hemoglobinuria are caused by infection from the soil
T
mainly endogenous but also infection from the soil
Lamb dysentery occurs in a week old animal
T
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
Lesions of lamb dysentery can be seen in the small intestine
T
Lamb dysentery is caused by Clostridium perfringens B
T
Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery
F
Ewes
Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery
F
Pregnant ewes have to be vaccinated in order to prevent lamb dysentery
T
Haemorrhagic diarrhoea is a clinical sign of lamb dysentery
T
Lamb dysentery can be seen in lambs around weaning
F
Lamb dysentery is found in 3-4-week-old lambs.
F
Pathological lesions of Lamb dysentery starts in the colon
F
We can culture the pathogen of Lamb dysentery from the intestines
T
Lamb dysentery is caused by Clostridium dysenteriae
F
Lamb dysentery can be seen in lambs after weaning
F
There is no vaccine for the prevention of lamb dysentery
F
Lamb dysentery occurs in 2-6 weeks old lambs
F
For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine
T
lamb dysentery no bacterium isolation from the gut but microscopy culture is okay
Pathological symptoms of lamb dysentery can be found in the large intestines
F
Lamb dysentery can be prevented by vaccinating pregnant ewes
T
Lamb dysentery can be successfully treated with penicillin when clinical signs appear
F
Lamb dysentery occurs in a week-old animal
T
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 the disease
T
Infection of lamb by secretion in the milk
F
Lamb dysentery occurs in 1-2 weeks old lambs
T
Struck is caused by Clostridium perfringens C.
T
Overeating is a predisposing factor of struck
T
Struck can be seen mainly in lambs younger than 2 weeks
F
Struck is an acute disease in horses
F
Struck is a zoonotic disease
F
Struck is a slow disease of older sheep
F
Fast course sudden onset
Struck is a worldwide common disease with great economic impact
F
Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life
T
2-4d so 1st week
The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine
F
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
Pig enterotoxaemia can be prevented by vaccinating the pregnant sows
T
Pig enterotoxaemia is caused by Clostridium perfringens C
T
Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics immediately
F
Too late
Penicillins to sows
Lesions of pig enterotoxaemia can be seen in the small intestine
T
Pig enterotoxaemia is more frequent in the litter of young than old sows
T
Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets
T
Pig enterotoxaemia can be generally seen in weaned piglets
F
Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia
T
Clostridium enterotoxaemia of piglets is caused by C. perfringens
T
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
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
direct detection
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
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
Pig enterotoxaemia can cause a high mortality
T
Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut
T
Epidi en na evris c.perfringes C pou kami jalla disease??
culture smear microscopy no isolation
Pig enterotoxaemia is not present in Europe
F
Pig enterotoxaemia cannot be prevented by using vaccines
F
Pulpy kidney disease is caused by Clostridium perf. D
T
Overeating is a predisposing factor to pulpy kidney disease
T
The toxin of the agent of pulpy kidney disease is sensitive to trypsin
T
D(α, ε=trypsin act)
Pulpy Kidney Diseases is caused by Clostridium chauvoei
F
Pulpy kidney disease generally occurs in 1-2week old lambs
F
Pulpy kidney disease can occur at any age
F
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
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
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
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
Pulpy kidney disease is a worldwide common disease
T
Enterotoxaemia of sheep is also called pulpy kidney disease
T
Cattle are not susceptible to this disease
T
Vaccination are possible against pulpy kidney disease
T
Coccidiosis is a predisposing factor of ulcerative enteritis in poultry
T
Ulcerative enteritis of chicken is caused by Clostridium colinum
T
Ulcerative enteritis is frequently seen in day old chicken
F
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
do not confuse with Necrotic enteritis of Chicken caused by C. perfringes A
Broiler 2-5w, turkeys 7-12w
Clostridium perfringens is the causative agent of ulcerative enteritis in poultry
F
Ulcerative enteritis of poultry is generally prevented with vaccination
F
Lesions of ulcerative enteritis are mostly seen in the small intestines
T
First small intestine then upper large intestine
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
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
jejunum and ileum =SI
Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis
F
Necrotic enteritis mostly occurs in chicken
T
Thus the name necrotic enteritis of chicken
Also turkeys
Waterfowl are not susceptible to necrotic enteritis
F
They are
Necrotic enteritis occurs in 1-3 weeks of age
F
Tyzzer’s disease is caused by Clostridium piliforme
T
Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A
T
Gangrenous dermatitis is caused by obligate pathogens
F
Gangrenous dermatitis causes muscle oedema
T
Vaccines are the primary way of prevention of gangrenous dermatitis
F
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
Over-eating can predispose animals to Tetanus
F
The agent of Tetanus needs oxygen to replicate
F
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
Spasms are typical clinical signs of tetanus
T
Tetanus is a zoonosis
F
xoid vaccines can be used for the prevention of tetanus
T
Dogs are resistant to tetanus
F
The clinical signs of tetanus are inducible
T
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
The bacterium never enters the bloodstream. Only the toxins released after the autolysis of the vegetative bacterium. Necrotic anaerobic conditions at entry site initiate spore germination.
Tetanus can be diagnosed on the basis of post mortem lesions
F
Clostridium tetani produced endotoxin
F
Endotoxins= membrane compounds of gram negative bacteria
Exotoxins = are proteinoid substances released
C. tetani needs anaerobic conditions for propagation
T
Dogs are susceptible to tetanus
T
Tetanus can be prevented with vaccines containing inactivated bacteria
F
inactivated toxoid = Anatoxin
Tetanus can cause spasms
T
Horses are resistant to tetanus
F
Tetanus can only develop after deep wounds
F
Not deep only, even navel infection, teeth of foals, and ear tagging
Wounds can predispose to tetanus
T
The paralysis usually starts at the place of the wound
F
Spasms begin from the head
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
There is no vaccine for tetanus
F
Dogs have high resistance to tetanus
T
have natural resistance to the toxin
Clostridium tetani produces neurotoxins
T
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
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
Necrotic foci in the liver are typical post mortem lesions of botulism
F
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
Botulism doesn’t occur in Europe
F
Clostridium botulinum cannot tolerate air at all
T
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
warmer climate summer
Botulism is eradicated in Europe
F
Clostridium botulinum can produce toxin, some of which are activated by proteases
T
Botulism is seen mainly during summer
T
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
Animals are mostly sensitive to C and D types of Clostridium botulinum
T
