equine Flashcards
1
Q
What pathogen causes strangles?
A
Streptococcus equi equi
2
Q
What type of bacteria is Streptococcus equi equi?
A
Gram-positive cocci
3
Q
What are the clinical signs of strangles?
A
- Mucopurulent nasal discharge - Enlarged submandibular lymph nodes - Fever - Anorexia
4
Q
How can you confirm a diagnosis of strangles?
A
- Culture and sensitivity - qPCR - ELISA to test for Strep M protein-specific antibody (mostly just if you are suspicious of bastard strangles of purpura hemorrhagica)
5
Q
What are the four clinical presentations of strangles?
A
- Classic strangles (upper airway infection with submandibular and/or retropharyngeal abscesses) 2. Bastard strangles (internal abscesses) 3. Purpura hemorrhagica (vasculitis) 4. Immune-mediated myositis (cachexia)
6
Q
What are the two most common pathogens causing pneumonia in horses?
A
- Rhodococcus equi - Streptococcus equi zooepidemicus
7
Q
How would you determine the causative agent of pneumonia in a horse?
A
Do a transtracheal wash to determine the agent via Gram-stain, culture and sensitivity, and/or PCR
8
Q
What is the pathogenesis of Rhodococcus equi?
A
- Inhalation of pathogen 2. R. equi infects macrophages 3. Replicates inside macrophages (must have this virulence factor called VapA to do this) 4. Destroyed macrophages become pyogranulomas in the lung tissue
9
Q
True or False: Both foals and adult horses can get sick from Rhodococcus equi
A
False. Adults are essentially immune and only some foals exposed will get sick (we don’t really know why) but most infected foals are < 4 months old
10
Q
What type of pneumonia does Rhodococcus equi cause?
A
Pyogranulomatous
11
Q
What are the four clinical presentations of Rhodococcus equi?
A
- Chronic pyogranulomatous pneumonia (fever, tachypnea, increased effort) 2. Abdominal disease (enterocolitis, typhlitis, pot-bellied appearance) 3. Non-septic uveitis 4. Bone and joint disease (septic arthritis)
12
Q
What pathogen causes proliferative enteritis in horses?
A
Lawsonia intracellularis
13
Q
What are the clinical signs of proliferative enteritis in horses?
A
- Mild colic - Hypoproteinemia - Pot-bellied appearance - Depression - Weight loss
14
Q
What is the most common lesion of equine proliferative enteritis?
A
Thickened small intestine
15
Q
What pathogen causes potomac horse fever?
A
Neorickettsia risticii
16
Q
What are the symptoms of potomac horse fever?
A
- Liquid diarrhea - Acute enterocolitis - Fever - Laminitis (rare)
17
Q
Describe how horses become infected with potomac horse fever
A
- Neorickettsia risticii infects flukes 2. Flukes multiply inside snails 3. Horses drinking fresh water accidentally ingest snails or other infected aquatic insects
18
Q
Neorickettsia risticii has a preference for which anatomical site in the horse?
A
The intestinal wall, especially the large colon
19
Q
What is the best treatment for potomac fever?
A
Oxytetracycline
20
Q
What pathogen is most commonly associated with injection site abscesses/myositis?
A
Clostridium perfringens
21
Q
Which veterinary products have been associated with causing clostridium myositis when injected IM?
A
Flunixin meglumine and dexamethasone. This reaction causes a fever, local tissue necrosis, sloughing of skin, and eventually sepsis.
22
Q
What are the clinical signs of botulism in a horse?
A
- Weak tongue tone - Generalized muscle weakness - Inability to rise
23
Q
How does Clostridium botulinum cause paralysis?
A
The neurotoxin produced by clostridium botulinum binds at the neuromuscular junction where it prevents the release of acetylcholine
24
Q
What are the three ways horses can get infected with botulism?
A
- Ingestion of preformed toxin in feed (most common) 2. Toxicoinfectious botulism (called shaker foals and occurs when spores are ingested and toxin is released in digestive tract) 3. Wound botulism (rare - wound becomes contaminated and toxin is released in vivo)
25
What is the most sensitive species to botulism and tetanus?
Horses
26
How can you prevent botulism?
Vaccination
27
What are the clinical signs of tetanus in a horse?
- Stiff gait and neck - Dysphagia - Protruding third eyelid
28
What two exotoxins are responsible for the clinical signs of tetanus? What lesions does each toxin cause?
1. Tetanolysin (causes local tissue damage) 2. Tetanospasmin (causes neurological signs)
29
True or False: Vaccination is highly effective in preventing tetanus
True
30
What pathogen causes "pigeon fever" or "dryland distemper"?
Corynebacterium pseudotuberculosis
31
What does pigeon fever cause?
Abscesses (especially in the pectoral region). You have to wait for them to be mature and then drain them, but be careful because the pus is contaminated and can be infectious so use proper biosecurity
32
What are the three clinical presentations of pigeon fever?
1. External abscesses (91% of cases). Pectoral region and ventral midline of the abdomen are the most common 2. Internal abscesses (8% of cases) 3. Ulcerative lymphangitis (1% of cases):
33
Practice case: A 5-year-old Thoroughbred gelding presents with sudden onset of colic and profuse liquid diarrhea. Upon examination, the horse appears depressed, with increased heart and respiratory rates. Abdominal palpation reveals generalized discomfort. What is the likely bacterial agent?
Neorickettsia risticii (Potomac horse fever)
34
Practice case: A 4-year-old Appaloosa mare presents with multiple subcutaneous abscesses and ulcerative lesions on the neck, shoulders, and flanks. The horse appears systemically well but has evidence of localized swelling, pain, and purulent discharge from the affected areas. What is the likely bacterial agent?
Corynebacterium pseudotuberculosis (Pigeon fever)
35
Practice case: A 7-year-old Warmblood mare presents with acute onset of spasms, starting with stiffness and rigidity of the facial muscles and progressing to involve the entire body. The horse has difficulty swallowing and breathing, and there is evidence of third eyelid protrusion. What is the likely bacterial agent?
Clostridium tetani (tetanus)
36
Practice case: A 6-month-old Thoroughbred weanling presents with acute onset of colic, characterized by rolling, pawing, and stretching out. Upon physical examination, the foal is febrile and dehydrated. The initial bloodwork shows hypoproteinemia. What is the likely bacterial agent?
Lawsonia intracellularis (equine proliferative enteropathy)
37
Practice case: A 3-month-old Paint filly presents with chronic weight loss, coughing, and respiratory distress. The foal has evidence of submandibular lymphadenopathy and bilateral nasal discharge. Thoracic ultrasound reveals evidence of abscessation and consolidation in the lungs. What is the likely bacterial agent?
Rhodococcus equi (pneumonia) This could also be Streptococcus equi equi, but since the filly is so young, R. equi is a better diagnosis.
38
Practice case: A 3-year-old Quarter Horse mare develops progressive muscle weakness, starting in the hind limbs and progressing to involve the entire body. The horse is unable to stand and shows signs of respiratory distress. There is no evidence of trauma or neurological disease. What is the likely bacterial agent?
Clostridium botulinum (botulism)
39
Practice case: A 2-year-old Arabian filly presents with acute onset of fever, mucopurulent nasal discharge, and enlarged submandibular lymph nodes. There is evidence of difficulty swallowing, and the horse coughs intermittently. Nasal endoscopy reveals mucopurulent discharge and ulceration of the pharynx. What is the likely bacterial agent?
Streptococcus equi equi
40
Practice case: A 2-week-old Thoroughbred foal presents with progressive respiratory distress, including increased respiratory rate, flared nostrils, and audible respiratory effort. The foal appears lethargic and weak. Auscultation reveals bilateral wheezing and crackles. What is the likely bacterial agent?
Rhodococcus equi (pneumonia)
41
Practice case: A 7-year-old Morgan horse is found dead in a new pasture with no previous signs of illness. Upon necropsy, there is evidence of severe enterocolitis with hemorrhage and necrosis of the intestinal mucosa. What is the likely bacterial agent?
Neorickettsia risticii (Potomac horse fever) This sounds like it could also be Rhodococcus equi until you remember that only foals can get R. equi. Also, be suspicious of a suddenly ill horse on a new pasture... maybe there is some standing water somewhere that the owner didn't know about!
42
Practice case: A 10-year-old Warmblood mare presents with chronic weight loss, diarrhea, and intermittent colic. The horse has a dull hair coat, cellulitis, and evidence of dehydration. The owner remarks that there is no free-standing water in the pasture. What is the likely bacterial agent?
Corynebacterium pseudotuberculosis (pigeon fever) No standing water in the pasture makes Neorickettsia risticii unlikely.
43
Practice case: A 5-month-old Paint weanling presents with a history of mild colic, depression, and weight loss. The owner remarks that she has a "pot-bellied" appearance. Upon abdominal ultrasound you see a markedly thickened small intestine. What is the likely bacterial agent?
Lawsonia intracellularis (equine proliferative enteropathy)
44
Practice case: A 9-year-old Morgan horse presents with a history of fever and swollen neck after an intramuscular injection of dexamethasone. What is the likely bacterial agent?
Likely Clostridium perfringens although other Clostridia spp. could cause it too
45
Pathologic findings of Lawsonia intracellularis
Marked thickening of the intestinal mucosa, the surface has an irregular and corrugated appearance. SEVERE hyperplasia of crypts
46
A 6-month old weaning presents with marked weight loss, depression, mild colic for the last two weeks. They have neutrophilia and hypoproteinemia with a markedly thickened intestine.... what is the likely diagnosis?
Proliferative enteritis caused by lawsonia intraceullularis
47
How would you confirm a diagnosis of lawsonia intracellularis
1) Signalment/ clinical sings 2) hypoproteinemia 3) thickened small intestine PLUS PCR or Serology.
48
Clinical signs of lawsonia intracellularis
Depression, anorexia, weight loss, colic
49
What is the epidemiology of
50
List four clinical signs of Strangles
-Purulent nasal discharge -Swollen mandibular lymph node -Fever -Anorexia
51
Bacterial classification of Streptococcus equi subsp equi
-Gram positive equi
52
Causative agent of Strangles
-Streptococcus equi subsp equi
53
Why is Strangles such a concern for herds of horses?
-Highly contagious and can affect all ages
54
What are the three diagnostic methods we can use to confirm a Strangles diagnosis?
-Culture and sensitivity of a deep nasopharyngeal swab or wash -qPCR -Strep M protein-specific antibody ELISa
55
What clinical presentations of Strangles is the Strep M protein-specific antibody ELISA most useful?
-Bastard Strangles -Purpura hemorrhagica
56
What are the 4 clinical presentations of strangles?
1. Classic strangles (upper respiratory strangles with submandibular +/- retropharyngeal abscesses) 2. Bastard strangles (internal abscesses) 3. Purpura hemorrhagica (vasculitis) 4. Immune-mediated myositis
57
How long is shedding usually in cases of Starngles?
-Shedding continues for 2-3 weeks after clinical recovery
58
Why are long-term subclinical carriers of Strangles important in terms of disease management?
-Act as a source of infection for new horses particularly in the herd
59
Where in long-term silent carriers of Strangles, is the causative agent found?
-Guttural pouch chondroids or epyema
60
Describe the control strategy for Strangles on-farm
-Segregate horses and dedicate staff and supplies to three areas: +Red: All horses showing one or more clinical signs +Yellow: Healthy horses that had direct or indirect contact with red horses +Green: Healthy horses that did not have direct or indirect contact -No movement in or out -Frequent disinfection
61
How often should you monitor rectal temperature of yellow and green zone horses (Strangles)? What should you do if one becomes febrile?
-Twice a day -Move any febrile horse into the red zone
62
Describe the process of identifying persistent shedders of Strangles?
-At 3 weeks following clinical recovery, perform a guttural pouch endoscopy to visualize the guttural pouch and to collect lavage for culture and PCR
63
If a horse tests persistently negative for Strangles, then what should you do in terms of biosecurity?
-Move them into the green area
64
If you want to identify horses that are subclinical or persistent carriers, what is the most sensitive diagnostic?
-Guttural pouch endoscopy with guttural pouch lavage submitted for PCR and culture
65
Typical clinical presentation of Rhodococcus equi
-Young horse (,4 months) with fever, depression, tachypnea and dyspnea (pneumonia)
66
Bacterial classification for Rhodococcus equi
-Gram positive, pleomorphic, facultative intracellular bacterium
67
What is the difference between virulent and avirulent Rhodococcus equi?
-Virulent strains carry a plasmid that encodes virulence proteins, including VapA
68
Where is Rhodococcus equi commonly found?
-Found in soil and in the GIT
69
List three risk factors associated with Rhodococcus equi
-Large acreage -Large numbers of mares and foals -Having a population of transient mares and foals -Dusty environment
70
VapA
-Virulence factor which facilitates uptake and intra-macrophage replication
71
Describe the pathogenesis of Rhodococcus equi
1) Rhodococcus equi is ingested or inhaled 2) Inflammatory response induced 3) R. equi infects macrophages 4) R. equi replicates withing macrophages 5) R. equi destroys macrophages 6) Formation of pyogranulomatous lesions
72
True or false. All young foals are highly susceptible to R. equi, while adults are essentially resistant
-False. Not all foals are susceptible
73
What are the four clinical presentations of R. equi?
1. Chronic pyogranulomatous pneumonia (most common) 2. Abdominal disease (enterocolitis and typhlitis, pot-bellied appearance, weight loss) 3. Non-septic polysynovitis and/or uveitis 4. Bone and joint disease
74
What category of antimicrobials do we most commonly use against R. equi?
-Macrolides
75
Typical clinical presentation of a horse with Lawsonia intracellularis
-Young, weanling (4 to 7 months) horse with marked weight loss, depression and colic
76
What are key bloodwork signs of Lawsonia intracellularis infection? (2)
-Neutrophilia - Hypoproteinemia/hypoalbuminemia
77
In a foal/horse with a Lawsonia intracellularis infection, what would we expect to see on abdominal ultrasound?
-Markedly thickened small intestine
78
Bacterial classification of Lawsonia intracellularis
-Obligate intracellular, curved, gram-negative bacteria
79
Key diagnostic factors to confirm a Lawsonia intracellularis infection
1) Signalment and clinical signs 2) Hypoproteinemia 3) Thickened small intestine 4*) PCR and/or serology (best if there are clinical signs)
80
Describe the epidemiology of Lawsonia intracellularis in horses
-Sporadic outbreaks, typically localized to specific farms
81
Post-mortem, what do the intestinal lesions of Lawsonia intracellularis infection look like grossly?
-Marked thickening of the intestinal mucosa, with a corrugated appearance
82
Two clinical presentations of Lawsonia intracellularis
1. Chronic infection 2. Acute necrotizing enteritis (rapid mortality)
83
Typical clinical presentation of Potomac Horse Fever
-Horse in Alberta between late July and early October grazing near freshwater develops a fever, anorexia, depression and diarrhea
84
Causative agent of Potomac Horse Fever
-Neorickettsia risticii
85
How do confirm the presence of Potomac Horse Fever?
-PCR on feces or whole blood
86
Bacterial classification of Neorickettsia risticii
-Obligate intracellular, gram-negative cocci
87
Life cycle of Neorickettsia risticii
1) Infects trematodes in fresh water 2) Trematodes infect snails 3) Trematodes release from snails and infect water insects 4) Horse ingests insects carrying N. risticii or flukes infected with N. risticii
88
Describe the pathogenesis of N. risticii
1) Ingestion of N. risticii 2) Infection of blood monocytes and colonic epithelial cells, mast cells and macrophages 3) Diarrhea and bacteremia
89
Key clinical signs of N. risticii infection
-Acute onset of depression and anorexia -Diarrhea within 24-48 hours (60% of cases) -In severe cases, toxemia and laminitis
90
Main treatment option for N. risticii
-Oxytetracycline
91
Typical presentation of Clostridial myositis
-Horse that was given an injection, typically flunixin (can be dexamethasone) in the neck (or other muscle) that develops swelling and inflammation at the site of infection, along with depression and a fever
92
Most common causative agent of Clostridial myositis in horses?
-Clostridium perfringens
93
What are two ways you could confirm a diagnosis of clostridial myositis?
-Ultrasound examination -Culture and sensitivity and cytology of aspirate
94
What can happen to the muscle region affected by clostridial myositis?
-Local tissue necrosis and sloughing of the skin
95
Can clostridial myositis result in systemic signs?
-Yes. Can cause severe sepsis and multiorgan dysfunction
96
Typical presentation of a horse with botulism
-Horse with acute onsey of dysphagia, ataxia, delayed neurological responses, muscle trembling and weakness
97
Main way to detect botulism toxin
-Can use serum, feces, GI content or suspected feed material and perform a toxin test
98
What are three important routes of infection for botulism in horses?
1. Forage poisoning (most common) -- Contaminated feed 2. Toxicoinfectious botulism (shaker foal) 3. Wound botulism (rare)
99
True or false. Horse and cattle are the most sensitive species to Botulism.
-False. Horses are
100
What is the best way to prevent botulism in horses?
-Vaccination
101
Typical clinical presentation of tetanus in horses
-Horses that is unable to eat or drink, very stiff neck and gait, sawhorse stance, protruding third eyelid, raised tailhead, and easily startled by noise
102
What are the two main exotoxins Clostridium tetani produces to induce its effects?
-Tetanolysin which damages local tissue -Tetanospasmin which is responsible for neurological signs via retrograde axonal transport in the CNS
103
Typical presentation of Dryland Distemper or Corynebacterium pseudotuberculosis infection
-Horse in hot, dry conditions, and presents with a reluctance to move and swelling of muscle bodies like the pectorals
104
Bacterial classification of Corynebacterium pseudotuberculosis
-Gram positive, pleomorphic, rod-shaped, intracellular, facultative anaerobe
105
How do we treat Corynebacterium pseudotuberculosis in horses?
-Wait for abscess to mature -Establish drainage and lavage
106
Transmission of Corynebacterium pseudotuberculosis
-Unknown likely contact between infected insects and wounds/abrasions
107
Three clinical presentations of Corynebacterium pseudotuberculosis
1. External abscesses (91% of cases) (pecs and ventral midline most common) 2. Internal abscesses (8%) (filtering organs) 3. Ulcerative lymphangitis
108
What type of bacteria is Streptococcus equi equi?
gram positive cocci
109
How can you confirm a diagnoses of strangles?
-culture and sensitivity -qPCR -ELISA to test for Strep M protein-specific antibody
110
What are the 4 types of clinical presentations of strangles?
1. classic strangles: upper airway infection with submandibular and/or retropharyngeal abscesses 2. bastard strangles: internal abscesses 3. Purpura hemorrhagica: vasculitis 4. immune-mediated myositis: they lose muscle mass
111
Explain silent shedders with strangles:
In most of the cases nasal shedding of pathogen will occur for 2-3 weeks after clinical recovery. In some cases the nasal shedding will go on for even longer like ~6 weeks after clinical recovery. In rare cases horses will become long term subclinical carriers for years and even though they have fully recovered they will continue to be infectious through intermittent shedding.
112
Outline what you can do to control a strangles outbreak:
Segregate horses into 3 groups -Red: horses showing 1 or more clinical signs -Yellow: healthy horses that had contact with red group horses -Green: healthy horses that have not come into contact with a sick animal *monitor rectal temp of green and yellow horses 2x a day for fevers as horses will show fevers before they start shedding virus so you can catch them early and isolate them *3 weeks following clinical recovery, screen for persistent shedders with endoscopy and guttural pouch lavage. If endoscopy not available then nasopharygneal washes for culture and PCR
113
What are the 2 most common pathogens causing pneumonia in horses?
Rhodococcus equi and Streptococcus equi zooepidemicus
114
What is the pathogenesis of Rhodococcus equi:
1. inhalation of pathogen 2. R. equi infects macrophages 3. replicates inside macrophages (must have this virulence factor called VapA to do this) 4. destroyed macrophages become pyogranulomas in the lung tissue
115
True or false: Both foals and adult horses can get sick from Rhodococcus equi
False, adults are essentially immune and only some foals exposed will get sick (we don't really know why) but most infected foals are < 4 months old
116
What are the 4 clinical presentations of Rhodococcus equi:
1. chronic pyogranulomatous pneumonia (most common) 2. abdominal disease 3. non septic uveitis 4. bone and joint disease
117
What is the most common sign of equine proliferative enteritis?
thickened small intestine
118
What pathogen causes Potomac horse fever?
Neorickettsia risticii
119
Describe how horses become infected with potomac fever:
1. Neorickettsia risticii infects flukes 2. those flukes multiply inside snails 3. horses drinking fresh water accidentally ingest snails or other infected aquatic insects
120
Describe the pathogenesis of Potomac horse fever:
1. after ingestion, N. risticii infects blood monocytes 2. i dunno what happens next they basically have a predilection for attacking the intestinal wall and cause diarrhea
121
What veterinary product is associated (although rarely) with causing Clostridium myositis when injected IM?
Flunixin meglumine
122
If you suspect botulism what is the gold standard way you can prove your diagnoses?
confusing but you inoculate mice with it and see if they get botulism????
123
How does Clostridium botulinum cause paralysis?
The neurotoxin produced by clostridium botulinum binds at the neuromuscular junction where it prevents the release of acetylcholine
124
What are the 3 ways horses can get infected with botulism?
1. Forage poisoning (most common): ingestion of the preformed toxin in feed 2. Toxicoinfectious botulism: called shaker foals, occurs when spores are ingested and toxin is released in digestive tract 3. Wound botulism (rare): wound becomes contaminated and toxin is released in vivo
125
How can you prevent botulsim?
theres a vaccine
126
What 2 exotoxins are responsible for the clinical signs of tetanus?
1. Tetanolysin- causes local tissue damage 2. Tetanospasmin- causes neurological signs
127
True or false: vaccination is highly effective in preventing tetanus
true
128
What pathogen causes what is known as "pigeon fever" or "dryland distemper"?
Crynebacterium pseudotuberculosis
129
What are the 3 clinical presentations of pigeon fever?
1. external abscesses 2. internal abscesses 3. ulcerative lymphangitis
130
What is the causative agent of strangles in horses?
Streptococcus equi ssp equi
## Footnote
Highly contagious and causes upper airway infection with abscesses.
131
What are the clinical signs of classic strangles?
Purulent nasal discharge, swollen mandibular lymph nodes, fever, anorexia
## Footnote
Typical presentation following the introduction of a new horse to a herd.
132
What diagnostic tests can be used for strangles?
* C+S (culture and sensitivity)
* qPCR
* Strep M protein-specific Ab ELISA
## Footnote
These tests help confirm the diagnosis and guide treatment.
133
What distinguishes classic strangles from bastard strangles?
Classic strangles involves upper airway infection, while bastard strangles involves internal abscesses
## Footnote
Both can result from Streptococcus equi ssp equi infection.
134
What is purpura hemorrhagica?
Vasculitis characterized by hot, swollen legs
## Footnote
Can occur as a complication of strangles.
135
What is the significance of silent carriers in strangles?
Nasal shedding can continue for weeks after recovery, posing a risk for outbreaks
## Footnote
Some horses may remain infectious for years.
136
What is the main pathogen associated with pneumonia in foals?
Rhodococcus equi
## Footnote
It is a facultative intracellular bacterium that can cause severe respiratory disease.
137
What are the risk factors for R. equi pneumonia?
* Large acreage
* High number of mares and foals
* Dusty environments
## Footnote
These factors contribute to the prevalence of the disease.
138
What are common clinical findings in foals with R. equi pneumonia?
Fever, tachypnea, increased respiratory effort
## Footnote
These signs indicate the need for further diagnostic evaluation.
139
What is the role of PCR in diagnosing equine proliferative enteritis (EPE)?
PCR on feces can confirm the diagnosis of EPE caused by Lawsonia intracellularis
## Footnote
It's specific but may yield false negatives.
140
What are the typical clinical signs of equine proliferative enteritis?
* Poor body condition
* Weight loss
* Depression
## Footnote
Often accompanied by hypoproteinemia and thickened intestines on ultrasound.
141
What is Potomac Horse Fever caused by?
Neorickettsia risticii
## Footnote
It is an obligate intracellular bacterium associated with severe enterocolitis.
142
What is a common clinical presentation of Potomac Horse Fever?
Fever, lethargy, liquid diarrhea
## Footnote
Typically occurs during late summer to early fall near freshwater sources.
143
What is the main treatment for Potomac Horse Fever?
Oxytetracycline
## Footnote
Administered early can lead to dramatic improvement of clinical signs.
144
What can cause injection site myositis in horses?
Clostridium perfringens
## Footnote
Often associated with IM injections of certain medications.
145
What are the clinical signs of botulism in horses?
* Difficulty swallowing
* Weakness
* Dilated pupils
## Footnote
Caused by neurotoxin from Clostridium botulinum.
146
What are the three routes of infection for botulism?
* Forage poisoning
* Toxicoinfectious botulism
* Wound botulism
## Footnote
Each route has different mechanisms of transmission and clinical presentation.
147
What is the pathogenesis of tetanus?
Tetanus is caused by tetanospasmin toxin which leads to spastic paralysis
## Footnote
It binds to peripheral nerve terminals and affects inhibitory interneurons.
148
What are the key clinical signs of tetanus?
* Rigidity of facial muscles
* Protruding third eyelid
* Stiff gait
## Footnote
Characteristic signs include trismus and elevated tail head.
149
What is dysphagia?
Difficulty in swallowing
## Footnote
Common clinical sign in various medical conditions.
150
What are the clinical signs of tetanus?
Stiff gait, elevated tail head
## Footnote
Indicative of neurological involvement in tetanus.
151
What are the two exotoxins responsible for clinical signs in tetanus?
* Tetanolysin
* Tetanospasmin
## Footnote
Tetanolysin causes local tissue damage, while tetanospasmin leads to spastic paralysis.
152
What is the role of Tetanolysin?
Responsible for local tissue damage favoring anaerobic infection
## Footnote
It helps in the proliferation of bacteria.
153
What is the role of Tetanospasmin?
Responsible for neurologic signs and causes spastic paralysis
## Footnote
It diffuses locally and binds irreversibly to presynaptic inhibitory interneurons.
154
What species are most susceptible to tetanus?
Horses
## Footnote
Vaccination is highly effective in preventing tetanus in horses.
155
What is the causative agent of 'Pigeon Fever'?
Corynebacterium pseudotuberculosis
## Footnote
It is a pleomorphic, rod-shaped, intracellular, facultative anaerobe.
156
Where is Corynebacterium pseudotuberculosis most commonly reported in North America?
Southwestern USA
## Footnote
First cases reported from southern Alberta in summer 2013.
157
What are the common clinical presentations of abscesses caused by Corynebacterium pseudotuberculosis?
* External abscesses (91% of cases)
* Internal abscesses (8% of cases)
* Ulcerative lymphangitis (1% of cases)
## Footnote
External abscesses are most common, while internal abscesses carry higher mortality.
158
What is the mortality rate of internal abscesses without treatment?
100%
## Footnote
Mortality is 30-40% with treatment.
159
What is the treatment approach for abscesses caused by Corynebacterium pseudotuberculosis?
Wait for the abscess to mature, establish drainage, and implement strict biosecurity control
## Footnote
Environmental contamination from draining pus must be managed.
160
Fill in the blank: The bacteria causing abscesses are phagocytosed after entry into the host but continue to replicate due to _______.
Intracellular survival
## Footnote
This is key to the formation of abscesses.
161
What is the characteristic of ulcerative lymphangitis?
Severe cellulitis with involvement of lymphatics in one or more limbs
## Footnote
Early medical therapy is required for successful treatment.
162
True or False: The pathogenesis of Corynebacterium pseudotuberculosis infection is fully understood.
False
## Footnote
Abrasions, wounds, and insects are thought to play a role but are not fully understood.
