Bacteria (Caitlin's Half) Flashcards
(251 cards)
1
Q
Trueperella pyogenes affects what species?
A
Cattle and swine
2
Q
Is Trueperella pyogenes part of the normal flora? If so, where does it reside?
A
It is normal flora of skin and mucous membranes of upper respiratory, urogenital, and GI tract of cattle and swine
3
Q
What is the gram stain and morphology of Trueperella pyogenes?
A
Gram-positive rod
4
Q
How is Trueperella pyogenes primarily transmitted?
A
Endogenous infections primarily
Can be spread cow to cow by flies (exogenous)
5
Q
Clinical presentation of Trueperella pyogenes?
A
- Purulent infection of the lung, jointa, uterus, and SQ tissue of ruminants and swine
- Mastitis in cattle
- Septic arthritis in sow after farrowing
6
Q
How is Trueperella pyogenes treated?
A
- Incision of drainage in abscess if accessible
- Abx therapy should be initiated but often poor response due to poor penetration in presence of pus/bacteria encapsulation
7
Q
When clinical presentation of Mycobacterium avium-mycobacterium intracellularae complex (MAC) infection is seen, it is usually due to one of two factors:
A
- Immunocompromised host
- High infectious dose
8
Q
What species are affected by Mycobacterium bovis?
A
Cattle are the natural host
However, can also affect several other species
(humans, swine, primates, cats, dogs, sheep, goats, horse, deer, elk, other wildlife, etc.)
9
Q
Is Mycobacterium zoonotic?
A
YES
10
Q
What are the virulence factors of Mycobacterium?
A
- Lipid rich cell envelope
- Faculative intracellular pathogen of macrophages
- SLOW growing species - more virulent
11
Q
What is the gram-stain/morphology of Mycobacterium?
A
Acid Fast. stain required
Rod Shaped
12
Q
Where does Mycobacterium reside?
A
Within host (can survive for years - latent)
Can survive (NOT REPLICATE) in environment 4 days in summer and 28 in winter
13
Q
How is Mycobacterium bovis transmitted?
A
Infected animals are the source
Spread through exhaled respiratory droplets
Inhaled/ingested by macrophages in new host
14
Q
How are most cases of Mycobacterium bovis found?
A
At slaughter during routine inspections
15
Q
Clinical signs of Mycobacterium bovis?
A
Granuloma/tubercles on infected organs
If signs present, depend on organs involved (respiratory signs, weight loss, enlarged nodes)
There may be no clinical signs
16
Q
How is Mycobacterium bovis diagnoses?
A
- Caudal Fold Test
- Lesions and enlarged nodes (tuburcles) found at necropsy
17
Q
What is a caudal fold test?
A
Skin test measuring immune response to tuburculin of Mycobacterium bovis. Look for swelling at 72hrs. Positive test must then be confirmed by cervical test
18
Q
How is Mycobacterium bovis controlled?
A
Is a REPORTABLE disease
National TB Eradication Program
Quarantine herds
Positives slaughtered
Keep Closed herds or test before purchase and isolate after purchase
19
Q
Is Mycobacterium bovis zoonotic?
A
YES
20
Q
Mycobacterium bovis in deer (presentation and importance)
A
Susceptible
Pulmonary or disseminated dz
Put cattle in MI at risk
21
Q
Mycobacterium bovis in humans (presentation and transmission)
A
Very susceptible
Pulmonary or disseminated dz
Serious zoonotic problem where unpasteurized milk is consumed
22
Q
Is Mycobacterium bovis reportable?
A
YES
23
Q
Mycobacterium tuberculosis usually effects what species?
A
Humans are the natural host
(Other species also susceptible, lap animals like cats and dogs especially)
24
Q
1/3 of the world’s population is infected with this bacteria:
A
Mycobacterium tuberculosis
25
How is Mycobacterium tuberculosis transmitted?
Inhalation
26
How is Mycobacterium tuberculosis diagnosed?
PPD skin test
27
What is the treatment for Mycobacterium bovis?
There is no treatment
28
Describe the Mycobacterium tuberculosis vaccine:
BCG M. bovis based vaccine used for TB in people only
29
What is the treatment for Mycobacterium tuberculosis?
Dogs - long term anti-TB drugs
Humans - Abx
Cattle - would not treat
30
Mycobacterium leprae affects what species?
Humans
Armadillos
31
What is the main reservoir of Mycobacterium leprae?
Armadillos in southern US (TX;LA)
32
Mycobacterium avium Complex (MAC) usually affects what species?
Birds, swine, sheep, goats, dogs, and cats
RARE in horses
33
What is generally required for clinical disease associated with Mycobacterium avium Complex (MAC) to occur?
Host with immunocompromised state
High infectious dose
34
What are the usual symptoms of Mycobacterium avium Complex (MAC)?
Weight loss, LN enlargement, sometimes enteritis
35
Mycobacterium avium Complex (MAC) is commonly found in what group of humans?
AIDS patients
36
Mycobacterium avium Complex (MAC) is diagnosed using what tests?
Biopsy of lesions
PCR
Culture
Comparative cervical skin testing in cattle/swine
37
Describe the treatment for Mycobacterium avium Complex (MAC):
Abx in people and can be attempted in dogs
Other species treatment is not attempted
38
How is Mycobacterium avium Complex (MAC) controlled?
Routine disinfection and exclusion of wild bird from livestock buildings/feed areas
39
How is Mycobacterium avium Complex (MAC) transmitted?
Ingestion
40
What is a main reservoir of Mycobacterium avium Complex (MAC)?
Feces of many domestic and wild birds
41
What is a significant problem regarding Mycobacterium avium Complex (MAC) in livestock?
Interference with TB skin testing because can give a false positive for TB.
42
Do hosts infected by Mycobacterium avium Complex (MAC) usually show signs of diease?
No. Only hosts who are immunocompromised or exposed to very high infectious dose show signs
43
Mycobacterium avium ssp. paratuberculosis (MAP) is transmitted through what route?
Fecal-oral spread primarily
Often when animals exposed shortly after birth by ingestion of small amounts of manure, contaminated food/water, or organisms on udder or in milk
44
What species are primarily affected by Mycobacterium avium ssp. paratuberculosis (MAP)?
Ruminants
45
Mycobacterium avium ssp. paratuberculosis (MAP) is the causative agent of what major ruminant disease?
Johne's disease
46
Mycobacterium avium ssp. paratuberculosis (MAP) is _____ growing in vivo and in vitro, increasing virulence
Slow growing
47
Describe the clinical presentation of animals infected with Mycobacterium avium ssp. paratuberculosis (MAP):
Contagious, chonic enteritis, weight loss (emaciation)
48
Where does Mycobacterium avium ssp. paratuberculosis (MAP) reside?
Intestines of infected animals
LN and ilem affected by Johne's dz
49
Is Johne's disease reportable?
Yes in Georgia
50
How can Mycobacterium avium ssp. paratuberculosis (MAP) be controlled?
Eliminate infected animals
Keep closed herd
Keep birthing environment clean
Avoid manure contamination in feed and water
51
How is Johne's Disease diagnosed?
DNA based PCR
52
There is a ____ USDA Johne's Disease Herd Statud program for cattle
Voluntary
53
Describe the gram-stain and morphology of Nocardia:
Gram positive, partially acid fast
Filamentous
54
Where is Nocardia widely distributed?
Soil and water
55
Is Nocardia part of normal flora?
NO
56
Nocardia asteroides complex
Includes many species but species is rarely determined
57
Nocardia is a _________ intraceullar pathogen of ______
Facultative; macrophages
58
Virulence factors of Nocardia:
Cell wall lipids
Faculative intraceullular pathogen of macrophages
Inhibits phagosome fusion
59
How is Nocardia transmitted?
Contamination of wounds
Or by inhalation/ingestion (leads to more serious dz)
60
Nocardia asteroides has 3 forms of disease. What are they?
1. Localized skin form
2. Thoracic form
3. Septicemic form
61
Clinical disease in patients infected by Nocardia asteroides may reflect underlying _______?
Immunosuppression
62
Nocardia asteroides causes rare ____ respiratory and disseminated disease
respiratory
63
How is Nocardia asteroides diagnosed?
Cytologyical prep with gram stain of lesion - shows branching filaments
Culture/PCR confirmative
64
How is Nocardia asteroides treated?
Surgical debridement with systemic abx
Treatment of thoracic and systemic forms minimally effective
65
Disease associated with Nocardia asteroides in dogs and cats usually presents as _______ and generalized ______ forms.
thoracic; systemic
66
Cats showing signs of Nocardia asteroides infection may be immunosuppressed with what diseases?
FeLV and FIV
67
What is a main characteristic of M. leprae clinical disease?
Granulomatous skin infections
68
Describe the gram-stain/morphology of Actinomyces:
Gram positive
Pleomorphic, filamentous branching, rod
69
Is Actinomyces part of normal flora?
YES - oropharynx, GI, and urogenital tract
70
How is Actinomyces transmitted?
Endogenous infection - trauma to oral mucous membranees
71
Actinomyces bovis is part of the normal flora of the mouth in what species?
Cattle
72
Actinomyces bovis causes actinomycosis, otherwise knows as what disease?
Lumpy jaw
73
"Lumpy Jaw" (actinomycosis) in cattle is granulomatous osteomyletitis of ___ and ____
Face and Jaw
74
'Lumpy Jaw" causes _____ to develop and drain
Fistulas
75
"Lumpy Jaw" (caused by Actinomyces bovis) can cause ______ problems and tooth loss
mastication (chewing)
76
How is Actinomycosis diagnosed?
Clinical signs
Cytology and culture of exudate
77
How is Actinomycosis treated?
Antibacterial therapy - primarily iodides +/- penicillin
Surgical Debridement
78
How can "Lumpy Jaw" be prevented?
Avoid feeding course, stemmy hay
Treat early
79
Actinomyces viscosus is present in the oral mucosa of what species?
Dog, cat, and humans
80
What bacterium is associated with periodontal disease?
Actinomyces viscosus
81
Describe the gram-stain/morphology of Dermatophilus congolensis?
Gramp-positive
Filamentous branching
Zoospores with railroad track appearance
82
Dermatophilus congolensis replicates only on _____?
animals
83
______ animals are the primary source of Dermatophilus congolensis infection
Carrier
84
Transmission of Dermatophilus congolensis ia favored by these three events:
1. Prolonged rainfall
2. Higher temperatures
3 Trauma to the skin
85
Epidemics of Dermatophilus congolensis can be seen during _____ seasons
Rainy
86
What bacterium can survive up to 3 years in crusts in the environment?
Dermatophilus congolensis
87
Dermatophilus congolensis is maintained in populations by?
carriers
88
Dermatophilus congolensis is transmitted how?
Direct contact
Contaminated fomites
Mechanically by flies or ticks
89
Soaking or trauma to the skin favors motile coccoid ________ growth, forming hyphal-like branches in the epithelium and invasion of hair follicles (associated with infection of Dermatophilus congolensis)
Zoospores
90
Dermatophilus congolensis organisms are eliminated from host as epithelium and _____ are shed.
Crusts
91
Dermatophilosis is a clinical disease associated with the infection of what bacteria?
Dermatophilus congolensis
92
Dermatophilosis is refered to as rain scald in ______ and called lumpy wool in _____?
Horses; sheep
93
Dermatophilosis affects what species?
Cattle, horses, sheep, and goats
(Infection is rare in pigs, dogs, cats, and humans)
94
Dermatophilosis (caused by D. congolensis is associated with what on the infected animal?
Purulent crusts and matted hair
The crusts are easily removed to reveal a moist, gray to pink surface
95
Dermatophilosis is treated by doing what?
Removing crusts by grooming (do not discard in environment)
Use iodine shampoo
96
Dermatophilosis can be prevented (or controlled) how?
Minimize exposure to rain
Flea Control
97
How is Dermatophilosis diagnosed?
Clinical signs
Stained, cytological prep of crusts
Culture
98
Clostridium gram-stain/morphology:
Gram-positive rods
99
Is Clostridium aerobic or anaerobic?
Anaerobic
100
Clostridial diseases are _______-based
Toxin
101
Clostridium produce ____?
Spores
102
Several species of Clostridium are found where?
Soil and intestine
103
Clostridium tetani is associated with what clinical disease?
Tetanus
104
Tetanus is due to _______ which enters the blood streat/lymphatics and is absorbed by ____ nerves..
Neurotoxin; Motor
105
The neurotoxin associated with tetanus is?
Tetanospasmin
106
In tetanus, the neurotoxin binds _______ to inhibitory neurons in the CNS
Irreversibly
107
The binding of tetanospasmin (neurotoxin associated with tetanus) in the CNS results in _________ of the CNS and causes ______ paralysis (tonic contractions of muscles)
Excitation; Spastic
108
What species are most susceptable to Clostridium tetani?
Horses and humans
109
Susceptability to Tetanus Toxin from most to least (and most common source for each):
Horses and Humans (foot injuries most common source in horses)
Pig
Sheep/Goats (tail docking, castration)
Cattle (food injuries)
Dogs and cats - rare
Poultry - resistant
110
What species is resistant to tetanus toxin?
Poultry
111
Tetanus is also known as?
Lockjaw
112
Tetanus presents as:
Rigidity throughout body
Paralysis of breathing muscles
Stiff-legged gait
"Saw-horse" Stance
Still tail
Evental recumbancy
113
Diagnosis of tetanus:
Generally based on clinical signs +/- history of wound
114
Treatment of tetanus:
Admin. anti-toxin to neutralize any unbound, circulating toxin
115
Anti-Toxin
Give toxin antibodies to patient to stimulate passive immunity
116
Toxoid
Give inactivated/modified version of toxin to stimulate active immunity
117
______ immunization against tetanus in horses by administering toxoid, then boost when horse receives a wound.
Active
118
Clostridium botulinum causes what disease?
Botulism
119
Clostridium botulinum is found where in the environment?
Soil and aquatic sediment
120
What are the sources of intoxication of Clostridium botulinum contamination?
Animal and plant material contaminated with the toxin
121
What species are susceptible to Clostridium botulinum?
Chickens and ducks - most
Horses and cattle
Dogs, cats, pigs
Turkey buzzard/Vulture - least
122
Transmission of Clostridium botulinum is primarily through?
Ingestion of toxin
Wound contamination
123
______ motor paralysis results from Clostridium botulinum intoxication.
Flaccid
124
_______ of C. botulinum toxin affects speed and potency (more toxin = faster and increased lethality)
Quantity
125
C. botulinum neurotoxin irreversibly binds to the presynaptic portion of the peripheral cholinergic synapses of motor nerves, blocking ________ release
acetylcholine
126
What is the most potent neurotoxin known?
C. botulinum neurotoxin
127
Death caused by Botulism is usually due to _______ failure
respiratory
128
What is the most common form of Botulism Intoxication?
Ingestion of preformed toxin
129
What are the three forms of Botulism Intoxication?
1. Ingestion of preformed toxin
2. Wound botulism
3. Toxicoinfectious botulism
130
Toxicoinfectious botulism involves the ingestion of spores which germinate and vegetative bacteria release toxin in the gut. This is an __________ phenomenon.
Age-related: Occurs in human infants < 6 months and maybe in foals < 8 weeks
131
Botulism in birds and poultry can be characterized by what symptom?
"Limber neck" - flaccid neck of botulism
132
How do birds and poultry usually ingest botulism toxin?
Ingestion of toxin in decomposed vegetation, invertebrates (fish), or contaminated feed
133
Describe the clinical signs and outcome of botulism in birds:
Occurs 12-48 hrs after ingestion
Birds appear drowsy (droops head)
Eyelid, wing, and leg paralysis
Death by respiratory failure, predation, and drowning
134
How does Botulism usually occur in horses and ruminants?
Feedstuffs may be contaminated with carrion.
pH >. 5, moisture, and anaerobic conditions allow growth of C. botulinum in hay
Preformed toxin in forage or feed is absorbed from small intestine
May results from wound contamination with spores
135
Clinical signs of botulism in horses and ruminants?
Slowness to consume feed
Grain falling from between lips when eating
Decreased tongue and tail tone
Dysphagia (difficulty swallowing)
Drooling in cattle
Muscle weakness
Mydriasis (dilated pupil)
Bladder distention
Decreased gut motility (borborygmus)
136
What is Shaker Foal Syndrome?
Ingestion of preformed and toxicoinfectious form of C. botulinum toxin occurring in foals
Weakness is predominant finding
Drooling milk, lying down a lot, sleepy/dull appearance, unsteady gait, toe scuffling, muscle tremor
Other clinical signs same as in adult
137
Is botulism in dogs and cats common or rare? Details of intoxication?
Rare, but usually associated with carrion ingestion
Symptoms same as in other mammals
138
Hos is botulism diagnosed?
Often diagnosis of exclusion after routine lab work is normal
Toxin ID by ELISA in lab can give definitive diagnosis
139
Describe the treatment for botulism:
Administer antitoxin to ruminants and horses. The antitoxin ties up circulating toxin but has no effect on bound toxin.
Recovery is by growth of new presynaptic nerve endings.
Rest! Muscular activity consumes acetylcholine and worsens symptoms.
140
Botulism can be prevented by:
Proper storage of feedstuffs
Prevent access to carrion
Preventative vaccine in horses
Heating foods to boiling to destroy toxin
141
What is carrion (a common source of botulism)?
The decaying flesh of dead animals
142
Infant botulism is caused by what form of botulism?
Toxicoinfectious - is seen in babies < 6 months
Toxin usually ingested in honey or corn syrup which vegetate and produce the toxin in the intestine
143
Clostridium haemolyticum is found where?
Spores are found in soil
NOT part of normal flora
144
Clostridium haemolyticum causes what disease?
Redwater Disease - characterized by red/coffee colored urine (hemoglobinuria) from lysis of RBCs
145
C. haemolyticum is associated with the presence of _________.
Liver Flukes
146
What must occur for C. haemolyticum to grow and cause disease?
The liver is damaged by liver flukes causing anaerobic conditions, allowing the spores to germninate and produce a hemolytic-necrotoxin toxin.
147
Intoxication of Clostridium haemolyticum involves the toxin (phospholipase C) _____ RBCs and causing intravascular hemolysis and capillary damage.
Lysing
148
Redwater disease caused by C. haemolyticum is primarily seen in what species?
Cattle and sheep
149
Redwater disease increases during what seasons due to the increased presence of liver flukes?
Summer and Fall
150
Clinical signs of C. haemolyticum intoxication (Redwater Dz) include:
Hemoglobinuria
Fever
Anemia
Death due to destruction of RBCs and associated anoxia
151
C. haemolyticum intoxication (Redwater Dz) is treated how?
Treatment is often ineffective if animal severely affected.
Penicillin, anti-toxin, and supportive care can be tried.
152
C. haemolyticum intoxication is diagnoses through what means?
Necropsy:
Demonstration of Fluorescent Antibody (FA) of organisms in the live
PCR of organisms from liver and blood
153
C. haemolyticum intoxication (Redwater Dz) is diagnosed through what means?
Necropsy:
Demonstration of Fluorescent Antibody (FA) of organisms in the live
PCR of organisms from liver and blood
154
Redwater disease can be prevented by giving what?
A multivalent (mult. strains/species) bacterin (whole killed/modified bacteria) for affected regions
155
What is the gram-stain/morphology of Clostridium perfringens?
Gram-positive, toxin producing, anaerobic, gas-producing, spore-forming rod
156
Clostridium perfringens is ubiquitous in ____ and _____.
Soil; Water
157
The types of Clostridium perfringens (A, B, C, D) is based on what?
The type of toxin they make
158
Are the types of Clostridium perfringens part of normal flora? If so, where do they reside?
Yes - found in normal flora of the intestines of many animals and people
159
Clostridium perfringens causes serious _____ disease with toxemia, _____ infections, and mastitis
enteric; wound
160
C. perfringens Type A possess an ____ toxin (phospholipase) which hydrolyzes host cell membranes, especially ____, ____, and____.
Alpha
RBCs, WBCs, and platelets
161
C. perfringens Type A possesses an ______ which causes necrosis of the intestinal wall
enterotoxin
162
How is C. perfringens Type A transmitted?
Ingestion
Wound Contamination
163
Characteristics of clinical disease due to C. perfringens Type A include:
Necrotic, hemorrhagic enteritis in many species (ADULT horses, cows, foals, pigs, dogs, poultry)
Food poisoning in people
Wound infection in animals and humans leading to gas gangrene
164
Diagnosis of C. perfringens Type A intoxication is done by?
Culture
PCR toxin ID
165
What is the treatment for C. perfringens Type A intoxication?
Antibiotics for wound infection
Supportive treatment for diarrhea
166
How is C. perfringens Type A intoxication prevented?
Toxoid available for cows
167
C. perfringens Type C most commonly associated with diarrhea in ______ animals.
Neonatal (foals, ruminants, and piglets)
168
Pathogenic features of C. perfringens Type C:
Produces multiple toxins which cause hemorrhagic necrosis of intestine
Immaturity of GI tract may allow overgrowth of C. perfringens Type C (related to most common type in neonatal animals)
169
Acute necrotic enteritis (bloody diarrhea) and abdominal pain in foals, piglets, lambs, kids, and calves is due to the overgrowth of what bacteria?
C. perfringens Type C
170
C. perfringens Type C intoxication can be diagnosed using what means?
Culture
PCR for toxin ID
171
C. perfringens Type C is treated how?
Antibiotics
Supportive care
172
C. perfringens Type D in low numbers is part of the ___________ of __________.
Normal flora; ruminants
173
High ____ diet and ______ results in proliferation of C. perfringens Type D in sm. intestine and release of many toxins
Grain; stress
174
Toxins produce in the intestine by C. perfringens Type D results in increased cell _________. The toxin is absorbed and effects of toxin are _______.
Permeability; Systemic
175
C. perfringens Type D leads to what two diseases?
"Over eating disease"
"Pulpy kidney disease"
176
Clinical disease associated with C. perfringens Type D is characterized by what symptoms?
Rapid onset of ataxia
Convulsions
Coma
May see diarrhea and sudden death
177
C. perfringens Type D can be diagnosed using what methods?
Culture to identify organism
Elisa/PCR to ID toxin type
178
What is the treatment of C. perfringens Type D usually unsuccessful?
Clinical course too rapid
179
How is C. perfringens Type D managed?
Vaccination with Type D toxoid or bacterin.
Adjust feeding practices (i.e. reduce concentrate in diet)
180
Match types of C. perfringens (A, C, D) with common host:
C. perfringens Type A - ADULT horses, cows, pigs, dogs, and poultry (can be seen in foals) - A for Adult
C. perfringens Type C - Neonatal animals (foals, ruminants, piglets) - C for "crib" for babies
C. perfringens Type D - Ruminants
181
Clostridium chauvoei spores are found where?
In soil and intestinal tract of normal ruminants (esp. cattle, but also seen in sheep)
182
Clostridium chauvoei vegetative bacteria produce a group of toxins that increase capillary permeability and cause emphysematous necrotic _______ and systemic _______.
Myositis; toxemia
183
Risk factors for Clostridium chauvoei are?
Rapidly growing animal on high plane of nutrition (well fed cattle)
184
Clinical disease of Clostridium chauvoei is known as?
Blackleg
185
Manifestation of Blackleg (clinical dz associated with Clostridium chauvoei) is characterized by the sudden onset of what symptoms?
Muscle inflammation with necrosis
186
What are the steps of Blackleg transmission?
1. Ingestion of spores in soil or endogenous in intestine
2. Spores enter blood/lymph from intestinal tract
3. Spores seed muscle
4. Unknown stimulus triggers germination of spore
5. Fever, lameness, or rapid/sudden death without signs
187
Blackleg is associated with what clinical symptoms?
Acute lameness and stiff gait but skin is normal (no wound)
- or -
Necrotic muscle (gangrenous)
Often lesion confined to part of the limb, sometimes mult. lesions
188
How is C. chauvoei diagnosed?
Sporulated gram-positive rods can be found in muscle
PCR of muscle tissue
FA test for organisms in tissue can provide definitive dx
189
Is treatment of C. chauvoei successful?
No.
190
How can Blackleg associated with C. chauvoei be prevented?
Vaccination with bacterin
191
Clostridium septicum is found where?
In soil and the GI tract
192
How does Clostridium septicum enter the body?
Enters muscle via wounds (shearing, tail docking, lambing, castrations, etc.)
193
Clostridium septicum toxins produced at wound site cause _________ _________ which is gangrenous myonecrosis with edema and systemic toxemia
Malignant Edema
194
What is systemic toxemia?
Rapid shock-like syndrome
195
Can be seen in all domestic animals, but typically _______ cases affecting random, individual animals under the right circumstances
Sporadic
196
T/F? Malignant Edema can also be caused by other clostridium species?
True.
197
Malignant Edema caused by C. septicum is diagnosed how?
Clinical signs
Culture/PCR of muscle
FA on muscle for Clostridial organisms
198
How is Malignant Edema treated?
Antibiotics
Drainage
Supportive care
199
How can Malignant Edema caused by C. septicum be controlled/prevented?
Good hygiene!
Multivalent Clostridial bacterin or toxoid for ruminants for prevention
200
T/F? An injection given IM can cause Malignant Edema given the right circumstances.
True.
201
Where can Clostridium difficile be found?
Large intestine of normal and clinically affected animals
202
Where are the spores of Clostridium difficile found?
In the environment where animals are housed
203
Clostridium difficile can cause hemorrhagic _______.
enterocolitis
204
What species are affected by Clostridium difficile?
Foals, horses, dogs, cats, and humans
205
What bacterial infection is often associated with long-term antibiotic use due to changes in normal flora and resulting in increased numbers of this bacteria?
Clostridium difficile
206
Clostridium difficile may respond to what drug commonly used to treat diarrhea?
Metronidazole
207
All Clostridium species do these two things:
Produce toxins
Form spores
208
What is the gram-stain/morphology of Bacillus?
Gram-positive, spore-forming, rod (often chains)
209
What are the spore forming bacteria?
All Clostridium species
Bacillus
210
What is the most important pathogen in Bacillus genus?
Bacillus anthracis (anthrax agent)
211
B. anthracis spores are found worldwide in _____ and persist for _____.
Soil; years
212
What form of Bacillus anthracis grows poorly in soil?
Vegetative form
213
When do outbreaks of B. anthracis always occur?
In summer (temp. > 60F)
214
What are the environmental risk factors for B. anthracis?
1. Summer (temps >60F)
2. Heavy rain following drought or dry summer
3. Livestock usually infected by ingesting spores while grazing
215
Where are the virulence determinants encoded for B. anthracis?
On two plasmids. Virulent bacteria carry both plasmids.
216
What does each of the two virulent determining plasmids in B. anthracis carry?
One encodes a capsule - resists phagocytosis
One encodes toxins (A-B Toxin)
217
What species are most commonly affected by B. anthracis?
Cattle, sheep, goats, horses, cats, dogs, swine, and humans
218
Is B. anthracis part of the normal flora?
No.
219
The toxin associated with B. anthracis is a 3 component toxin. What are the 3 components?
1. EF - edema factor
2. PA - protective antigen
3. LF - lethal factor
**All encoded on a plasmid**
220
T/F. The toxin components associated with B. anthracis (EF, PA, LF) are harmful as individuals.
FALSE.
Individually, the components are harmless.
221
In _____ combinations, edema toxin (PA and EF) and lethal toxin (PA and LF) are formed and called A-B toxins
binary
222
Which toxin component is the cell binding component?
PA - protective antigen
223
__________ is a protease which inhibits Mitogen Activated Protein Kinases (MAPK) perturbing host signaling (host cells die)
Lethal toxin
224
How is B. anthracis transmitted?
Ingestion of spores (in soil, in contaminated foodstuffs, or water)
Cutaneous (spores enter through skin abrasions)
Inhalation of spores (minor route in animals but rapidly fatal)
225
What is the most common route of transmission for B. anthracis?
Ingestion of spores (esp. grazing cattle)
226
Forms of Clinical Disease: Anthrax
Peracute (found dead)
Acute
Intestinal Form
Chronic
227
What are the characteristics of clinical disease, Anthrax, peracute form?
Sudden death in cattle, sheep, goats
228
What are the characteristics of clinical disease, Anthrax, Acute form?
Fever, mucosal hemorrhages in cattle, sheep, goats, and horses.
Diarrhea, edema of the tongue and throat, bleeding from body openings because of clotting disruption
229
What are the characteristics of clinical disease, Anthrax, intestinal form?
Gastroenteritis
More common in swine, dogs, and cats
230
What are the characteristics of clinical disease, Anthrax, chronic form?
Pharyngeal edema, tonsillar involvement, dysphagia
May see hemorrhaging of mouth and through
More common in swine, dogs, and cats
231
T/F? Dogs and cats are highly susceptible to anthrax.
FALSE.
Dogs and cats are relatively resistant. If seen, usually associated with outbreaks in farm animals.
232
What form of transmission of anthrax is seen in 95% of cases in people? What are the clinical symptoms?
Cutaneous - entry via skin wound.
Solitary, initially painless, necrotizing, hemorrhagic, ulcerous
233
What form of anthrax transmission is NOT common in animals?
Cutaneous anthrax
234
Clinical signs of inhaled anthrax in humans:
Pulmonary - due to inhalation of spores.
Severe lung edema.
Almost always fatal.
Very rare.
235
What clinical symptom most commonly associated with ingested anthrax in humans?
Intestinal - gastroenteritis
236
Diagnosis of Anthrax?
Hallmark signs:
Absence of rigor mortis
Dark, tarry blood at orifices which do not clot
237
You find a group of cattle suddenly dead on your farm. You suspect they have died of anthrax. What do you do?
1. Seek advice from regulatory vets (state and federal) regarding disposal and disinfection
2. Infected carcasses and contaminated bedding and soil should be burned or possibly buried 6ft deep.
3. Care must be taken to avoid human exposure during clean up. Wear proper PPE.
238
A neighbor is concerned about your suspicion that your cattle died from anthrax and tells you to ask the local vet for a necropsy to determine whether or not it was actually anthrax.
What do you tell your friend?
If anthrax is suspected, NEVER perform a necropsy.
The vegetative B. anthracis will die in an unopened carcass. If exposed to air, the bacteria can sporulate and you risk personal exposure and further environmental contamination.
239
Since you cannot perform a necropsy on the cows that died of suspected anthrax, how would the diagnosis be confirmed?
Blood can be collected aseptically from an ear vein, and a PCR can detect the presence of the organism in the blood and tissues.
240
Describe anthrax treatment:
Isolate affected animals
Quarantine premises for 3-4 weeks from last case
Antibiotics (penicillin or oxytetracycline for sick animals in early stages)
Supportive care
241
ESCutaneous form of anthrax in humans responds well to what?
Antibiotics
242
Is anthrax a reportable disease?
YES!
243
B. anthracis is a _______ _______. This is a bio-agent with potential to cause a severe threat to public health and safety.
Select agent
244
How can anthrax be prevented?
Vaccination with a plasmid-cured (lacks plasmid) non-enacpsulated live-attenuated vaccine (Sterne-strain) to livestock provides good protection.
245
For prevention of anthrax in humans, what could be done?
Administer a subunit vaccine (PA adsorbed to alum) to at risk personnel (military, researchers, etc.)
246
Which bacteria are zoonotic?
(9)
1. Staphylococcus aureus
2. Streptococcus suis
3. Streptococcus equi ssp. zooepidemicus
4. Listeria monocytogenes
5. Rhodococcus equi
6. Erysipelothrix rhusiopathiae
7. Mycobacterium bovis (humans - erysepeloid)
Mycobacterium avium complex (humans w/ AIDS)
Mycobacterium leprae (leprosy)
247
Is every bacteria on test 2 Gram Positive?
All but one! Mycobacterium bovis is stained with Acid fast stain, so not declared pos/neg.
248
Which bacteria are rod shaped? (8)
LECTMACB
1. Listeria
2. Erysipelothrix
3. Corynebacterium
4. Trueperella
5. Mycobacterium
6. Actinomyces
7. Clostridium
8. Bacillus
249
Which bacteria are cocci? (Coccus in name)
SSER
1. Staphylococcus
2. Streptococcus
3. Enterococcus
4. Rhodococcus
250
Which bacteria are filamentous? (3)
NAD
1. Nocardia
2. Actinomyces
3. Dermatophilus
251
What characteristics do streptococcus and staphylococcus share?
1. Normal flora causes dz
2. Common cause of mastitis in cattle
3. Similar morphology
4. Neutrophil infiltration typical of lesions
