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EPI PQ > MT3- Clostridium > Flashcards

MT3- Clostridium Flashcards

1
Q

Most clostridia have low invasive capacity

A

T

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2
Q

Spores of clostridia are generally very resistant against heat

A

T

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3
Q

The habitat of clostridia is the gut and the soil

A

T

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4
Q

Clostridia are obligate aerobic bacteria

A

F (obligate anaerobic)

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5
Q

Clostridium perfringens is an obligate pathogenic bacterium

A

F (obligate anaerobic)

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6
Q

Clostridium perfringens can produce main and auxillary toxins

A

T

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7
Q

Extracellular enzymes and toxins are virulence factors of clostridia

A

T

extracellular enzymes

toxins (can be converted to anatoxin)

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8
Q

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

A

F

(inactivated bacterium culture (anaculture)

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9
Q

Clostridium is anaerobe spore forming bacteria

A

T
?

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10
Q

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

A

F

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11
Q

Clostridium spreads usually rapid in a herd

A

F

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12
Q

Clostridium spread mostly with insecticides

A

F

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13
Q

Clostridium difficile can be treated with metronidazole

A

T

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14
Q

Clostridium difficile is seen in foal and piglets

A

T

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15
Q

Many Clostridium species have flagella

A

F

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16
Q

Clostridium species are only found in the subtropics

A

F (tropical and subtropical area)

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17
Q

Clostridium can cause severe contagious diseases

A

F

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18
Q

Clostridium are obligate pathogens

A

F (obligate anaerobic)

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19
Q

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

A

T

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20
Q

Cl. chauvoei is the agent of malignant oedema

A

F

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21
Q

Lesions of malignant oedema are mainly seen in the large muscles

A

T

  • oedema, swelling
  • wound infection
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22
Q

Malignant oedema is generally endogenous in cattle

A

F

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23
Q

Malignant oedema is generally a consequence of wound infection

A

T

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24
Q

Movement difficulties are frequently seen in the case of malignant oedema

A

T

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25
Q

Clostridium novyi can cause malignant oedema

A

T

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26
Q

Malignant oedema can be diagnosed based on clinical signs

A

F

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27
Q

Malignant oedema is caused due to wound infection

A

T

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28
Q

Malignant oedema is only in ruminants

A

F

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29
Q

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

A

T

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30
Q

Malignant oedema, attenuated vaccine for prevention

A

F

inactivated bacterium culture (anaculture)

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31
Q

Clostridium channel is the agent of malignant oedema

A

F

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32
Q

Attenuated vaccines are used for the prevention of malignant oedema

A

F

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33
Q

Clostridium septicum is an agent of malignant oedema

A

T

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34
Q

Malignant oedema is generally a consequence of a wound infection

A

T

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35
Q

Clostridium histolyticum can cause malignant oedema

A

T

-C. Septicum
-C. Novyi
- C. Histolyticum
- C. Sordelli

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36
Q

Agents of malignant oedema can be detected by bacterium culture

A

T

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37
Q

There are no vaccines for the prevention of malignant oedema.

A

F

inactivated bacterium culture (anaculture)

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38
Q

Malignant oedema occurs in ruminants and pigs

A

T

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39
Q

Malignant oedema is an acute fatal disease

A

T

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40
Q

Malignant oedema can be treated with antibiotics

A

F

difficult, limited (fast course, toxic effects)

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41
Q

Malignant oedema can occur in any warm-blooded animal.

A

T

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42
Q

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

A

T

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43
Q

Malignant oedema cannot occur in swine

A

F

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44
Q

Malignant oedema usually develop following an endogenous infection

A

F

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45
Q

Malignant oedema is well treated with long-term antibiotics therapy

A

F

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46
Q

Malignant oedema can be treated with polymyxin

A

F

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47
Q

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

A

F

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48
Q

Is gas gangrene (malignant oedema) a regional illness

A

F

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49
Q

The lesions of malignant oedema are mainly seen in the lungs

A

F

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50
Q

Blackleg is caused by Clostridium septicum

A

F. C. chauvoei

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51
Q

Lesions of blackleg are mainly seen on the claws

A

F

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52
Q

Lameness is a clinical sign of blackleg

A

T

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53
Q

Blackleg is a frequent disease in pigs

A

F - NOT FREQUENT

ruminants (sometimes pigs and other species)

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54
Q

Generally attenuated vaccines are used for the prevention of blackleg

A

F

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55
Q

Anaculture or anatoxin vaccines are used for the prevention of blackleg

A

T

  • anaculture, anatoxin
  • combined vaccines
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56
Q

Blackleg occurs only in tropical and subtropical countries

A

F

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57
Q

Generally attenuated vaccines are used for the prevention of blackleg

A

F

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58
Q

Blackleg generally occurs in endemic form

A

T

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59
Q

Blackleg occurs most frequently in pigs

A

F

ruminants (sometimes pigs and other species)

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60
Q

Blackleg is a gas gangrene disease

A

T

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61
Q

Blackleg is generally endogenous in sheep

A

F

iatrogenic

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62
Q

Blackleg is generally endogenous in cattle

A

T

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63
Q

Movement disorders and lameness can be clinical signs of Blackleg

A

T

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64
Q

Clostridium chauvoei can produce acids and gas from carbohydrates

A

T

active carbohydrate fermentation (production of acid and gas)

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65
Q

Blackleg occurs mainly in ruminants

A

T

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66
Q

Oedema is a typical clinical sign of blackleg

A

T

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67
Q

Live vaccines are used for the prevention of blackleg

A

F

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68
Q

Blackleg infects ovine through wounds

A

T (sheep)

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69
Q

In Blackleg disease we use attenuated vaccine

A

F

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70
Q

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

A

T

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71
Q

Oedema in the muscles is a typical clinical sign of blackleg

A

T

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72
Q

Attenuated vaccines are used for the prevention of blackleg

A

F

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73
Q

Blackleg is caused by Clostridium chauvoei

A

T

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74
Q

Severe diarrhoea is the main clinical sign of blackleg

A

F

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75
Q

Blackleg is caused by Clostridium septicum

A

F

C. chauvoei

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76
Q

Blackleg occurs in cattle and sheep.

A

T

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77
Q

If antibiotics are applied after appearance of the clinical signs of blackleg, treatment is
generally successful

A

F

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78
Q

Attenuated vaccines are used for the prevention of blackleg

A

F

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79
Q

Blackleg disease occurs only in ruminants

A

F

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80
Q

Blackleg can usually be treated with antibiotics successfully

A

F

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81
Q

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

A

F

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82
Q

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

A

T

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83
Q

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

A

T

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84
Q

Blackleg has four toxins

A

T

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85
Q

Blackleg can be prevented by using vaccine

A

T

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86
Q

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

A

F

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87
Q

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

A

T

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88
Q

Blackleg in bovine is caused by wound infections

A

F

Soil infection: mainly on pastures of poor quality

-sheep: wound infection

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89
Q

Classical swine fever is a frequent predisposing factor of bradsot

A

F

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90
Q

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

A

T

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91
Q

Bradsot is caused by Clostridium chauvoei

A

F

C. septicum

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92
Q

Soil contaminated frozen feed is a frequent predisposing factor of bradsot

A

T

  • after driving the animals to winter pasture
  • frozen feed contaminated with soil (potato, turnip, grass)
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93
Q

Frozen food is a predisposing factor of bradsot

A

T

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94
Q

Bradsot occurs mainly late autumn and winter

A

T

late autumn, winter, frost

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95
Q

Overeating can predispose the animals to bradsot

A

F

after driving the animals to winter pasture

  • frozen feed contaminated with soil (potato, turnip, grass)
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96
Q

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

A

T (rennet)

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97
Q

Aminoglycosides are successfully used for treatment in the case of bradsot

A

F

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98
Q

Bradsot is mainly seen in late autumn and winter

A

T

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99
Q

Bradsot is mainly seen in late autumn and winter

A

T

late autumn, winter, frost

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100
Q

Bradsot is caused by Clostridium septicum

A

T

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101
Q

Severe pneumonia is a typical clinical sign of bradsot

A

F

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102
Q

Bradsot has a very fast course

A

T

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103
Q

Bradsot occurs only in suckling lambs

A

F

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104
Q

Bradsot is typically a chronic disease

A

F

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105
Q

Bradsot is common in the summer out on the pasture

A

F

late autumn, winter, frost

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106
Q

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

A

T

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107
Q

We can use anaculture strain vaccine against Bradsot

A

T, f ??

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108
Q

Bradsot causes oedema of the legs and necrosis

A

F

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109
Q

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

A

T

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110
Q

Koves disease is an indicator disease

A

T

indicator (haemorrhages in the stomach, erosions)

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111
Q

CSF is a predisposing factor of koves disease

A

T

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112
Q

Koves disease can be seen in pigs

A

T

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113
Q

Koves disease is caused by Clostridium chavoei

A

F

C. septicum

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114
Q

Infectious necrotic hepatitis is mainly seen in pigs

A

F

sheep

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115
Q

Infectious necrotic hepatitis can be prevented by using anatoxin vaccines

A

T

(anaculture, anatoxin)

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116
Q

Liver fluke can predispose animals to infectious necrotic hepatitis

A

T

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117
Q

In sheep, Clostridium septicum causes necrotic liver infection

A

F

C. novyi B

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118
Q

Infectious necrotic hepatitis causes inflammation and necrotic nodules in the liver

A

T

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119
Q

There is no vaccine to prevent infectious necrotic hepatitis

A

F

vaccine (anaculture, anatoxin)

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120
Q

Infectious necrotic hepatitis is caused by Clostridium septicum

A

F

C. novyi B

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121
Q

Infectious necrotic hepatitis is mainly seen in suckling lambs

A

F

sheep 1-4 years (sometimes cattle, other)

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122
Q

Parasite infection is a frequent predisposing effect of infectious necrotic hepatitis

A

T

parasite infection (liver flukes)

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123
Q

Anatoxin vaccines can be used for the prevention of infectious necrotic hepatitis.

A

T

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124
Q

Focal necrosis in the liver is a typical post mortem lesion of infectious necrotic hepatitis.

A

T

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125
Q

Infectious necrotic hepatitis is caused by Clostridium novyi

A

T

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126
Q

Infectious necrotic hepatitis is spread by tick

A

F

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127
Q

Infectious necrotic hepatitis is caused by Clostridium novyi type B

A

T

127
Q

Infectious necrotic hepatitis is found worldwide

A

T

128
Q

Infectious necrotic hepatitis can be transmitted by liver flukes

A

T

129
Q

Infectious necrotic hepatitis occurs mostly in young sheep

A

F

sheep 1-4 year

130
Q

There is intravascular haemolysis in the case of bacillary haemoglobinuria

A

T

131
Q

Bacillary haemoglobinuria is caused by Clostridium haemolyticum

A

T

132
Q

There are no vaccines for the prevention of bacillary hemoglobinuria

A

F

vaccine (6-month-long protection)

133
Q

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

A

T

134
Q

Bacillary haemoglobinuria is mainly seen in cattle

A

T

cattle (sometimes sheep)

135
Q

Bacillary haemoglobinuria is caused by Clostridium septicum

A

F

C. haemolyticum

136
Q

Jaundice and anaemia are important clinical signs of bacillary hemoglobinuria

A

T

  • sudden onset
  • fever, depression
  • haemoglobinuri
  • jaundice
  • anaemia
  • increased heart and breath rate
137
Q

Red urine is a typical clinical sign of bacillary hemoglobinuria

A

T

138
Q

Bacillary hemoglobinuria is a slow, chronic disease

A

F

139
Q

Bacillary hemoglobinuria can frequently be seen in horses

A

F

cattle (sometimes sheep)

140
Q

Clostridium novyi is the causative agent of bacillary hemoglobinuria.

A

F

C. haemolyticum

141
Q

Bacillary hemoglobinuria causes severe haemorrhages

A

T

142
Q

Bacillary hemoglobinuria are caused by infection from the soil

A

T

habitat: gut, soil

143
Q

Lamb dysentery occurs in a week old animal

A

T

1–2-week-old lambs

144
Q

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

A

F

145
Q

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

A

F

146
Q

Lesions of lamb dysentery are generally seen in the large intestine

A

F

small intestine

147
Q

Lesions of lamb dysentery can be seen in the small intestine

A

T

148
Q

Lamb dysentery is caused by Clostridium perfringens

A

T

Clostridium perfringens B

149
Q

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

A

F

Prevention :
- improving hygiene
- ewes: penicillin
- vaccine: pregnant ewes are vaccinated twice, yearly booster

150
Q

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

A

F

Prevention :
- improving hygiene
- ewes: penicillin
- vaccine: pregnant ewes are vaccinated twice, yearly booster

151
Q

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

A

T

pregnant ewes are vaccinated twice, yearly booster

152
Q

Haemorrhagic diarrhoea is a clinical sign of lamb dysentery

A

T

153
Q

Lamb dysentery can be seen in lambs around weaning

A

F

1–2-week-old lambs

154
Q

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

A

F

1–2-week-old lambs

155
Q

Pathological lesions of Lamb dysentery starts in the colon

A

F

small intestine

156
Q

We can culture the pathogen of Lamb dysentery from the intestines

A

T

157
Q

Lamb dysentery is caused by Clostridium dysenteriae

A

F

C. perfringens B

158
Q

Lamb dysentery can be seen in lambs after weaning

A

F

1–2-week-old lambs

159
Q

There is no vaccine for the prevention of lamb dysentery

A

F

Vaccine: pregnant ewes are vaccinated twice, yearly booster

160
Q

Lamb dysentery occurs in 2-6 weeks old lambs

A

F

1–2-week-old lambs

161
Q

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

A

T

162
Q

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

A

F

small intestine

163
Q

Lamb dysentery can be prevented by vaccinating pregnant ewes

A

T

pregnant ewes are vaccinated twice, yearly booster

164
Q

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

A

F

165
Q

Lamb dysentery occurs in a week-old animal.

A

T

1–2-week-old lambs

166
Q

Lamb dysentery can be diagnosed by culturing the bacteria

A

T

167
Q

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

A

F

168
Q

Toxoid vaccines can be used in the prevention of the disease

A

T

169
Q

Infection of lamb by secretion in the milk

A

F

170
Q

Lamb dysentery occurs in 1-2 weeks old lambs.

A

T

171
Q

Struck is caused by Clostridium perfringens

A

T
Clostridium perfringens C

172
Q

Overeating is a predisposing factor of struck

A

T

  • overeating
  • high protein and carbohydrate content
  • change of the diet
173
Q

Struck can be seen mainly in lambs younger than 2 weeks

A

F

174
Q

Struck is an acute disease in horses

A

F

175
Q

Struck is a zoonotic disease

A

F

176
Q

Struck is a slow disease of older sheep

A

F

177
Q

Struck is a worldwide common disease with great economic impact

A

F

it is worldwide, but not great economic impact

178
Q

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

A

F

2–4-day-old piglets

179
Q

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

A

F

small intestine

180
Q

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

A

T, F??

181
Q

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

A

F

vaccination of pregnant sows

182
Q

Pig enterotoxaemia can be prevented by vaccinating the pregnant sows.

A

T

PIG ENTEROTOXAEMIA (INFECTIOUS NECROTIC ENTERITIS OF PIGLETS)

183
Q

Pig enterotoxaemia is caused by Clostridium perfringens C

A

T

184
Q

Pigs showing clinical signs of enterotoxaemia have to be treated with antibiotics
immediately

A

F

185
Q

Lesions of pig enterotoxaemia can be seen in the small intestine

A

T

186
Q

Lesions of pig enterotoxaemia can be seen in the large intestine

A

F

186
Q

Clostridium Enterotoxaemia of Piglets occurs in 2-4 days old piglets

A

T

187
Q

Pig enterotoxaemia is more frequent in the litter of young than old sows

A

T

188
Q

Pig enterotoxaemia can be generally seen in weaned piglets

A

F

2–4-day-old piglets

189
Q

Necrosis of gut epithelium is a postmortem lesion of pig enterotoxaemia

A

T

190
Q

Clostridium enterotoxaemia of piglets is caused by C. perfringens

A

T

C. perfringens C

191
Q

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

A

T

192
Q

Clostridium perfringens C causes infectious necrotic enteritis of piglets

A

T

193
Q

Infectious necrotic enteritis of piglets occurs in piglets after weaning

A

F

194
Q

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

A

T

195
Q

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

A

T

196
Q

Necrotic enteritis of piglets is seen in piglets around weaning

A

F

197
Q

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

A

T

198
Q

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

A

F

detection of the agent

199
Q

Pig enterotoxaemia causes abdominal contractions in sows

A

F

200
Q

Mesenteric lymph node is congested in case of pig enterotoxaemia

A

F

201
Q

Clostridium enterotoxaemia can be cultured from mesenteric lymph nodes or gut

A

T

202
Q

Enteritis in piglets are caused by Clostridium perfringens D

A

F

Clostridium perfringens C

203
Q

Enteritis in piglets can be avoided by anatoxin vaccination

A

T

204
Q

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

A

F

205
Q

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

A

T

a and b toxin (b toxin is trypsin sensitive)

206
Q

Pig enterotoxaemia can cause a high mortality

A

T. (20-100%)

207
Q

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

A

F

208
Q

Enterotoxaemia is mainly seen in piglets after weaning

A

F

209
Q

Pig enterotoxaemia is not present in Europe

A

F (worldwide)

210
Q

Pig enterotoxaemia cannot be prevented by using vaccines

A

F

vaccination of pregnant sows

211
Q

Pulpy kidney disease is caused by Clostridium perf. D

A

T

212
Q

Overeating is a predisposing factor to pulpy kidney disease

A

T

  • overaating
  • sudden change of the diet
213
Q

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

A

F

214
Q

Pulpy kidney disease is caused by Clostridium perfringens D

A

T

215
Q

Pulpy Kidney Diseases is caused by Clostridium chauvoei.

A

F

Clostridium perfringens D

216
Q

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

A

F

  • most frequent in 6-12-month-old lambs, kids
  • sometimes 1-2 months old
217
Q

Pulpy kidney disease can occur at any age

A

F

  • most frequent in 6-12-month-old lambs, kids
  • sometimes 1-2 months old
218
Q

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

A

F

219
Q

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

A

T

  • overeating
  • sudden change of the diet
220
Q

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

A

T

221
Q

Neurological signs are typical in the case of pulpy kidney disease

A

T

  • neurological signs
  • abdominal pain
  • diarrhoea
  • glucosuria
222
Q

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

A

F

223
Q

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

A

F

  • most frequent in 6-12-month-old lambs, kids
  • sometimes 1-2 months old
224
Q

Inactivated vaccines are used for the prevention of pulpy kidney disease

A

T

225
Q

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

A

F

  • most frequent in 6-12-month-old lambs, kids
  • sometimes 1-2 months old
226
Q

Pulpy kidney disease is a worldwide common disease.

A

T

227
Q

Enterotoxaemia of sheep is also called pulpy kidney disease.

A

T

228
Q

Pulpy kidney disease is caused by Clostridium perfringens D.

A

T

229
Q

Cattle are not susceptible to this disease

A

T
???idk

230
Q

Vaccination are possible against pulpy kidney disease

A

T

231
Q

Coccidiosis is a predisposing factor of ulcerative enteritis in poultry

A

T

Predisposing factor:
- coccidiosis
- infectious bursitis
- chicken anaemia
- overcrowding
- nutritional problems
- old litter

232
Q

Ulcerative enteritis of chicken is caused by Clostridium colinum.

A

T

233
Q

Ulcerative enteritis is frequently seen in day old chicken

A

F (4–12-week-old chicken)

234
Q

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

A

T

235
Q

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

A

T

236
Q

Clostridium perfringens is the causative agent of ulcerative enteritis in poultry

A

F

ENTEROTOXAEMIA DISEASES

237
Q

Ulcerative enteritis of poultry is generally prevented with vaccination.

A

F

  • hygiene
  • optimal management
  • elimination of predisposing factors
238
Q

Lesions of ulcerative enteritis are mostly seen in the small intestines

A

T

239
Q

Ulcerative enteritis is a common disease in large scale farms

A

T

240
Q

Prevention of coccidiosis can help lower the incidence of ulcerative enteritis

A

T

241
Q

Coccidiosis is a predisposing factor of necrotic enteritis of chicken

A

T

predisposing factors:
- coccidiosis, mycotoxicosis
- feed: wheat, fishmeal
- poorly digestible feed
- alteration of the intestinal flora
- damage of the mucosa

242
Q

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

A

T

243
Q

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

A

F

small intestine: jejunum and ileum

244
Q

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

A

F

245
Q

Necrotic enteritis mostly occurs in chicken

A

T

246
Q

Waterfowl are not susceptible to necrotic enteritis

A

F

247
Q

Necrotic enteritis occurs in 1-3 weeks of age

A

F

broiler 2–5-week-old
turkey 7–12-week-old

248
Q

Tyzzer’s disease is caused by Clostridium piliforme

A

T

249
Q

Gangrenous dermatitis is caused by Clostridium septicum and Clostridium perfringens A

A

T

  • C. septicum
  • C. perfringens A
  • Staphylococcus aureus
  • facultative pathogenic bacteria
250
Q

Gangrenous dermatitis is caused by obligate pathogens

A

F

251
Q

Gangrenous dermatitis causes muscle oedema

A

T

  • muscles: oedema, reddish, crepitation
252
Q

Vaccines are the primary way of prevention of gangrenous dermatitis

A

F

  • antibiotics p.o.
  • elimination of predisposing effects
253
Q

Flaccid paralysis is a frequent clinical sign of tetanus

A

F

254
Q

The agent of tetanus is strictly anaerobic

A

T

255
Q

The agent of tetanus can enter the host through wounds

A

T

predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria

256
Q

Tetanus is only seen in horse

A

F

  • horse, sheep
  • cattle
  • swine, dog
257
Q

Over-eating can predispose animals to Tetanus

A

F

predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria

258
Q

The agent of Tetanus needs oxygen to replicate

A

F

anaerobic conditions

259
Q

Anatoxin vaccines are available for the prevention of tetanus

A

T

260
Q

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

A

F

261
Q

Spasms are typical clinical signs of tetanus

A

T

horse, sheep:
* spasms, stiffness, tonic contractions
* lockjaw, „saw-horse”
* ears stand up, third eyelid, nares are wide

262
Q

Tetanus is a zoonosis

A

F

263
Q

Toxoid vaccines can be used for the prevention of tetanus.

A

T

264
Q

Dogs are resistant to tetanus

A

F

265
Q

The clinical signs of tetanus are inducible

A

T

266
Q

Tetanus toxin cleaves synaptobrevin

A

T

267
Q

For tetanus we use vaccines which contain toxoid

A

T

268
Q

Tetanus cannot be prevented with vaccination.

A

F

269
Q

Tetanus is caused by Clostridium tetani

A

T

270
Q

The agent of tetanus causes septicaemia.

A

F

271
Q

Tetanus can be diagnosed on the basis of post mortem lesions

A

F

272
Q

Clostridium tetani produced endotoxin

A

F

273
Q

C. tetani needs anaerobic conditions for propagation

A

T

274
Q

Dogs are susceptible to tetanus

A

T

275
Q

Tetanus can be prevented with vaccines containing inactivated bacteria

A

F

276
Q

Tetanus can cause spasms

A

T

277
Q

Horses are resistant to tetanus

A

F

278
Q

Tetanus can only develop after deep wounds

A

F

279
Q

Wounds can predispose to tetanus

A

T

predisposing factor:
- wounds
- anaerobic condition
- synergetic effect of other bacteria

280
Q

The paralysis usually starts at the place of the wound

A

F

281
Q

Clostridium tetani toxin is produced in the feed

A

F

282
Q

Horses are most sensitive to tetanus

A

T

283
Q

Tetanus can be prevented by anatoxin vaccination

A

T

284
Q

Tetanus causes rigid paralysis

A

T

285
Q

There is no vaccine for tetanus

A

F

anatoxin vaccination

286
Q

Clostridium tetani produces neurotoxins

A

T

287
Q

Dogs have high resistance to tetanus

A

T

288
Q

The toxin of clostridium botulinum causes flaccid paralysis

A

T

289
Q

Clostridium botulinum generally causes wound infection

A

F

290
Q

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

A

F

291
Q

The toxin of Clostridium botulinum has irreversible effect

A

T

292
Q

Botulism can be seen as a result of a wound infection

A

F

293
Q

Flaccid paralysis is the main clinical sign of botulism

A

T

294
Q

Birds are resistant to botulism

A

F

  • birds
  • horse
  • mink
295
Q

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

A

F

Pathology:
* not characteristic
* hyperaemic organs
* oedema in the lungs

296
Q

Generally wounds predispose animals to botulism

A

F

297
Q

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

A

F

298
Q

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

A

F

299
Q

Clostridium botulinum can produce toxins outside the hosts.

A

T

300
Q

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

A

T

Pathology
* not characteristic
* hyperaemic organs
* oedema in the lungs

301
Q

Botulism doesn’t occur in Europe

A

F

worldwide – warmer climate

302
Q

Clostridium botulinum cannot tolerate air at all

A

T

anaerobic bacterium, meaning it cannot survive in the presence of oxygen. Exposure to air can inhibit its growth and toxin production.

303
Q

Botulism usually develops following a wound infection

A

F

304
Q

Clostridium botulinum propagates in rotten materials.

A

T

305
Q

In Hungary, botulism is seen most commonly in birds

A

T

306
Q

Clostridium botulinum spores are extremely resistant to heat

A

T

307
Q

In Hungary, botulism occurs in winter and early spring.

A

F

worldwide – warmer climate

308
Q

Botulism is eradicated in Europe

A

F

worldwide – warmer climate

309
Q

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

A

T

310
Q

Botulism is seen mainly during summer

A

T

worldwide – warmer climate

311
Q

Spasms are the typical clinical sign of botulism

A

F

312
Q

Paralysis is the main sign of botulism

A

T

313
Q

Toxins of botulism are produced generally in the food.

A

T

314
Q

Botulism happen generally through wound infection

A

F

315
Q

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

A

T

EPI PQ (81 decks)

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