Clostridium Flashcards by Benedicte Mæhlum

Most clostridia have low invasive capacity

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Spores of clostridia are generally very resistant against heat

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The habitat of clostridia is the gut and the soil

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Clostridia are obligate aerobic bacteria

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Clostridium perfringens is an obligate pathogenic bacterium

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Clostridium perfringens can produce main and auxillary toxins

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Extracellular enzymes and toxins are virulence factors of clostridia

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There are no vaccines for the prevention of diseases caused by clostridia

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There are no vaccines for the prevention of diseases caused by clostridia

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Clostridium bacteria is not in the environment, because it cannot tolerate oxygen

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Clostridium spreads usually rapid in a herd

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Clostridium spread mostly with insecticides

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Clostridium difficile can be treated with metronidazole

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Clostridium difficile is seen in foal and piglets

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Many Clostridium species have flagella

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Clostridium species are only found in the subtropics

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Clostridium can cause severe contagious diseases

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Clostridium are obligate pathogens

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Anaculture or anatoxin vaccines are used for the prevention of malignant oedema

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Cl. chauvoei is the agent of malignant oedema

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Lesions of malignant oedema are mainly seen in the large muscles

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Malignant oedema is generally a consequence of wound infection

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Malignant oedema is generally a consequence of wound infection

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Movement difficulties are frequently seen in the case of malignant oedema

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Clostridium novyi can cause malignant oedema

Malignant oedema can be diagnosed based on clinical signs

Malignant oedema is caused due to wound infection

Malignant oedema is only in ruminants

Malignant oedema, one of the clinical signs is lameness/movement problems

Malignant oedema, attenuated vaccine for prevention

Clostridium channel is the agent of malignant oedema

Malignant oedema is generally a consequence of a wound infection

Clostridium histolyticum can cause malignant oedema

Agents of malignant oedema can be detected by bacterium culture

There are no vaccines for the prevention of malignant oedema.

Malignant oedema occurs in ruminants and pigs

Malignant oedema is an acute fatal disease

Malignant oedema can be treated with antibiotics

Malignant oedema can occur in any warm-blooded animal.

Once an area is infected with gas gangrene re-occurrence is common

Malignant oedema cannot occur in swine

Malignant oedema usually develop following an endogenous infection

Malignant oedema is well treated with long-term antibiotics therapy

Malignant oedema can be treated with polymyxin

Malignant oedema can be well treated with antibiotics over a long period

Is gas gangrene (malignant oedema) a regional illness

The lesions of malignant oedema are mainly seen in the lungs

Blackleg is caused by Clostridium septicum

Lesions of blackleg are mainly seen on the claws

Lameness is a clinical sign of blackleg

Blackleg is a frequent disease in pigs

Generally attenuated vaccines are used for the prevention of blackleg

Anaculture or anatoxin vaccines are used for the prevention of blackleg

Blackleg occurs only in tropical and subtropical countries

Generally attenuated vaccines are used for the prevention of blackleg

Blackleg generally occurs in endemic form

Blackleg occurs most frequently in pigs

Blackleg is a gas gangrene disease

Blackleg is generally endogenous in sheep

Blackleg is generally endogenous in cattle

Movement disorders and lameness can be clinical signs of Blackleg

Clostridium chauvoei can produce acids and gas from carbohydrates

Blackleg occurs mainly in ruminants

Oedema is a typical clinical sign of blackleg

Live vaccines are used for the prevention of blackleg

Blackleg infects ovine through wounds

In Blackleg disease we use attenuated vaccine

In the case of sheep, blackleg is generally consequence of a wound infection

Oedema in the muscles is a typical clinical sign of blackleg

Attenuated vaccines are used for the prevention of blackleg

Blackleg is caused by Clostridium chauvoei

Severe diarrhoea is the main clinical sign of blackleg

Blackleg is caused by Clostridium septicum

Blackleg occurs in cattle and sheep.

Attenuated vaccines are used for the prevention of blackleg

Blackleg disease occurs only in ruminants

Blackleg can usually be treated with antibiotics successfully

Blackleg in cattle is mainly endogenous between 6 months-3 years old

The disease caused by Clostridium chauvoei occurs mainly in cattle and sheep

The disease caused by Clostridium chauvoei is primarily the result of endogenous infection in cattle.

Blackleg has four toxins

Blackleg can be prevented by using vaccine

We use neomycin and polymyxin to treat disease caused by Clostridium chauvoei

Blackleg in cattle is mainly endogenous between 2 months-2 years old

Blackleg in bovine is caused by wound infections

Oedema in the wall of the abomasum and duodenum are postmortem lesions of bradsot

Bradsot is caused by Clostridium chauvoei

Soil contaminated frozen feed is a frequent predisposing factor of bradsot

Frozen food is a predisposing factor of bradsot

Bradsot occurs mainly late autumn and winter

Overeating can predispose the animals to bradsot

Thickening of and oedema in the stomach wall are typical lesions of bradsot

Aminoglycosides are successfully used for treatment in the case of bradsot

Bradsot is mainly seen in late autumn and winter

Severe pneumonia is a typical clinical sign of bradsot

Bradsot has a very fast course

Bradsot occurs only in suckling lambs

Bradsot is typically a chronic disease

Bradsot is common in the summer out on the pasture

Bradsot is an acute disease resulting in sudden death in many cases

We can use anaculture strain vaccine against Bradsot

Bradsot causes oedema of the legs and necrosis

Post mortem lesions of bradsot can be seen in the stomach (rennet)

Koves disease is an indicator disease

CSF is a predisposing factor of koves disease

Koves disease can be seen in pigs

Koves disease is caused by Clostridium chavoei

Infectious necrotic hepatitis is mainly seen in pigs

Infectious necrotic hepatitis can be prevented by using anatoxin vaccines

Liver fluke can predispose animals to infectious necrotic hepatitis

In sheep, Clostridium septicum causes necrotic liver infection

Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver

There is no vaccine to prevent infectious necrotic hepatitis

Infectious necrotic hepatitis is caused by Clostridium septicum

Infectious necrotic hepatitis is mainly seen in suckling lambs

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

Infectious necrotic hepatitis is caused by Clostridium septicum

Infectious necrotic hepatitis is caused by Clostridium novyi

Infectious necrotic hepatitis is spread by tick

Infectious necrotic hepatitis is caused by Clostridium novyi type B

Infectious necrotic hepatitis can be transmitted by liver flukes

Infectious necrotic hepatitis occurs mostly in young sheep

There is intravascular haemolysis in the case of bacillary haemoglobinuria

Bacillary haemoglobinuria is caused by Clostridium haemolyticum

There are no vaccines for the prevention of bacillary hemoglobinuria

Phospholipase C is a virulence factor of the agent of bacillary hemoglobinuria

Bacillary haemoglobinuria is mainly seen in cattle

Bacillary haemoglobinuria is caused by Clostridium septicum

Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria

Red urine is a typical clinical sign of bacillary hemoglobinuria

Bacillary hemoglobinuria is a slow, chronic disease

Bacillary hemoglobinuria can frequently be seen in horses

Clostridium novyi is the causative agent of bacillary hemoglobinuria.

Bacillary hemoglobinuria causes severe haemorrhages

Bacillary hemoglobinuria are caused by infection from the soil

Lamb dysentery occurs in a week old animal

Isolation of the agent from the gut gives aetiologic diagnosis of lamb dysentery

Isolation of Cl. perfringens from the gut confirms the diagnosis of lamb dysentery

Lesions of lamb dysentery are generally seen in the large intestine

Lesions of lamb dysentery can be seen in the small intestine

Lamb dysentery is caused by Clostridium perfringens

Lambs have to be vaccinated with anatoxin vaccine in order to prevent lamb dysentery

Lambs have to be vaccinated with attenuated vaccine in order to prevent lamb dysentery

Pregnant ewes have to be vaccinated in order to prevent lamb dysentery

Haemorrhagic diarrhoea is a clinical sign of lamb dysentery

Lamb dysentery can be seen in lambs around weaning

Lamb dysentery is found in 3-4-week-old lambs

Pathological lesions of Lamb dysentery starts in the colon

We can culture the pathogen of Lamb dysentery from the intestines

Lamb dysentery is caused by Clostridium dysenteriae

Lamb dysentery can be seen in lambs after weaning

There is no vaccine for the prevention of lamb dysentery

Lamb dysentery occurs in 2-6 weeks old lambs

For diagnosis of lamb dysentery, the pathogen should be cultured from the intestine

Pathological symptoms of lamb dysentery can be found in the large intestines

Lamb dysentery can be prevented by vaccinating pregnant ewes

Lamb dysentery can be successfully treated with penicillin when clinical signs appear

Lamb dysentery occurs in a week-old animal.

Lamb dysentery can be diagnosed by culturing the bacteria

Newborn lambs have to be vaccinated in order to prevent lamb dysentery.

Toxoid vaccines can be used in the prevention of the disease

Infection of lamb by secretion in the milk

Lamb dysentery occurs in 1-2 weeks old lambs.

Struck is caused by Clostridium perfringens

Overeating is a predisposing factor of struck

Struck can be seen mainly in lambs younger than 2 weeks

Struck is an acute disease in horses

Struck is a zoonotic disease

Struck is a slow disease of older sheep

Struck is a worldwide common disease with great economic impact

Infectious necrotic enteritis of piglets occurs in the first 1-2 weeks of life

The lesions of Infectious necrotic enteritis of piglets can be seen typically in the large intestine

Maternal protection is important in the case of Infectious necrotic enteritis of piglets

There is no vaccination for the prevention of Infectious necrotic enteritis of piglets

Pig enterotoxaemia can be prevented by vaccinating the pregnant sows.

Pig enterotoxaemia is caused by Clostridium perfringens C

Lesions of pig enterotoxaemia can be seen in the small intestine

Lesions of pig enterotoxaemia can be seen in the large intestine

Pig enterotoxaemia can be generally seen in weaned piglets

Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia

Clostridium enterotoxaemia of piglets is caused by C. perfringens

Clostridium enterotoxaemia of piglets is more frequent in the case of first farrowing Sows

Clostridium perfringens C causes infectious necrotic enteritis of piglets

Infectious necrotic enteritis of piglets occurs in piglets after weaning

The lesions of infectious necrotic enteritis of piglets can be seen generally in the small intestine

Infectious necrotic enteritis of piglets can be prevented by vaccinating the pregnant sows

Necrotic enteritis of piglets is seen in piglets around weaning

Necrotic enteritis of piglets can be prevented by vaccination the sow with anatoxin

Pig enterotoxaemia has to be diagnosed by detecting antibodies in the piglets

Pig enterotoxaemia causes abdominal contractions in sows

Mesenteric lymph node is congested in case of pig enterotoxaemia

Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut

Enteritis in piglets are caused by Clostridium perfringens D

Enteritis in piglets can be avoided by anatoxin vaccination

Enteritis in piglets cannot be diagnosed by post-mortem, only by bacteriology

Pig enterotoxaemia is caused by β-toxin production in 1st week of life

Pig enterotoxaemia can cause a high mortality

Necrotic enteritis of piglets cannot be diagnosed by isolating the agent from the gut

Enterotoxaemia is mainly seen in piglets after weaning

Pig enterotoxaemia is not present in Europe

Pig enterotoxaemia cannot be prevented by using vaccines

Pulpy kidney disease is caused by Clostridium perf. D

Overeating is a predisposing factor to pulpy kidney disease

The toxin of the agent of pulpy kidney disease is sensitive to trypsin

Pulpy kidney disease is caused by Clostridium perfringens D

Pulpy Kidney Diseases is caused by Clostridium chauvoei.

Pulpy kidney disease generally occurs in 1-2week old lambs

Pulpy kidney disease can occur at any age

Pulpy kidney disease of suckling lambs can be prevented by vaccinating pregnant ewes

Sudden change the diet is a predisposing factor to pulpy kidney disease

The toxin damages the endothelial cells in the case of pulpy kidney disease

Neurological signs are typical in the case of pulpy kidney disease

Isolation of the agent is necessary to the diagnosis of pulpy kidney disease

Pulpy kidney disease is typically seen in lambs below 2 weeks of age

Inactivated vaccines are used for the prevention of pulpy kidney disease

Pulpy kidney disease is seen in piglets in the first week of life

Pulpy kidney disease is a worldwide common disease.

Enterotoxaemia of sheep is also called pulpy kidney disease.

Pulpy kidney disease is caused by Clostridium perfringens D.

Cattle are not susceptible to this disease

Vaccination are possible against pulpy kidney disease

Coccidiosis is a predisposing factor of ulcerative enteritis in poultry

Ulcerative enteritis of chicken is caused by Clostridium colinum.Ulcerative enteritis of chicken is caused by Clostridium colinum.

Ulcerative enteritis is frequently seen in day old chicken

Ulcers sometimes covered with pseudomembranes are frequent post mortem lesions of ulcerative enteritis of chicken

Ulcerative enteritis can occur in 4-12-week-old chickens

Clostridium perfringens is the causative agent of ulcerative enteritis in poultry

Ulcerative enteritis of poultry is generally prevented with vaccination.

Lesions of ulcerative enteritis are mostly seen in the small intestines

Prevention of coccidiosis can help lower the incidence of ulcerative enteritis

Coccidiosis is a predisposing factor of necrotic enteritis of chicken

Foamy, brownish-red faeces is a clinical sign of necrotic enteritis of chicken

Lesions of necrotic enteritis of chicken are typically occur in the large intestine

Day-old chickens are widely vaccinated in order to prevent of necrotic enteritis

Necrotic enteritis mostly occurs in chicken

Waterfowl are not susceptible to necrotic enteritis

Necrotic enteritis occurs in 1-3 weeks of age

Tyzzer’s disease is caused by Clostridium piliforme

Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A

Gangrenous dermatitis is caused by obligate pathogens

Gangrenous dermatitis causes muscle oedema

Vaccines are the primary way of prevention of gangrenous dermatitis

Flaccid paralysis is a frequent clinical sign of tetanus

The agent of tetanus is strictly anaerobic

The agent of tetanus can enter the host through wounds

Tetanus is only seen in horse

Over-eating can predispose animals to Tetanus

The agent of Tetanus needs oxygen to replicate

Anatoxin vaccines are available for the prevention of tetanus

Haemorrhages under the serous membranes and enlargement of parenchymal organs are typical postmortem lesions of tetanus

Spasms are typical clinical signs of tetanus

Tetanus is a zoonosis

Toxoid vaccines can be used for the prevention of tetanus.

Dogs are resistant to tetanus

The clinical signs of tetanus are inducible

Tetanus toxin cleaves synaptobrevin

For tetanus we use vaccines which contain toxoid

Tetanus cannot be prevented with vaccination.

Tetanus is caused by Clostridium tetani

The agent of tetanus causes septicaemia.

Tetanus can be diagnosed on the basis of post mortem lesions

Clostridium tetani produced endotoxin

C. tetani needs anaerobic conditions for propagation

Dogs are susceptible to tetanus

Tetanus can be prevented with vaccines containing inactivated bacteria

Tetanus can cause spasms

Horses are resistant to tetanus

Tetanus can only develop after deep wounds

Wounds can predispose to tetanus

The paralysis usually starts at the place of the wound

Clostridium tetani toxin is produced in the feed

Horses are most sensitive to tetanus

Tetanus can be prevented by anatoxin vaccination

Tetanus causes rigid paralysis

There is no vaccine for tetanus

Dogs have high resistance to tetanus

The toxin of clostridium botulinum causes flaccid paralysis

Clostridium botulinum generally causes wound infection

Focal necrosis in the liver is a typical post mortem lesion of Botulism

The toxin of Clostridium botulinum has irreversible effect

Botulism can be seen as a result of a wound infection

Flaccid paralysis is the main clinical sign of botulism

Birds are resistant to botulism

Necrotic foci in the liver are typical post mortem lesions of botulism

Generally wounds predispose animals to botulism

The agent of botulism generally produces toxin at the site of entry

Botulism is diagnosed on the basis of the typical post mortem lesions

Clostridium botulinum can produce toxins outside the hosts.

No characteristic post mortem lesions can be seen in the case of botulism

Botulism doesn’t occur in Europe

Clostridium botulinum cannot tolerate air at all

Botulism usually develops following a wound infection

Clostridium botulinum propagates in rotten materials.

In Hungary, botulism is seen most commonly in birds

In Hungary, botulism occurs in winter and early spring.

Botulism is eradicated in Europe

Clostridium botulinum can produce toxin, some of which are activated by proteases

Botulism is seen mainly during summer

Spasms are the typical clinical sign of botulism

Paralysis is the main sign of botulism

Toxins of botulism are produced generally in the food.

Botulism happen generally through wound infection

Animals are mostly sensitive to C and D types of Clostridium botulinum.

Clostridium Flashcards

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