Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fluids, Respiratory, Muscles > Myopathies > Flashcards

Myopathies Flashcards

1
Q

You have a cow with no exercise intolerance, rhabdomyolysis, and no conduction problems. What does this make you think?

A

Inflammatory Muscle Disease
-Infectious or Immune Mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Different Large animal infectious myopathies

A

Bacterial: acute suppurative myositis, Actinobacillus, Clostridial disease

Parasitic: Trichinella, Sarcocystis

Viral: Influenza, Bluetongue, Foot and mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

breakdown of muscle tissue with inflammation: heat, pain, swelling and systemic toxemia: fever
clinically see: CK, AST, Myoglobinemia, Myoglobinuria

A

Rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What will you see in an animal with rhabdomyolysis

A

Fever. Heat, Pain, Swelling

Clinical pathology: CK, AST, Myoglobinemia, Myoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

acute suppurative myositis in ruminants and swine is caused by

A

Corynebacterium pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

acute suppurative myositis in horses is caused by

A

Streptococcus equi
Corynebacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Suppurative Myositis can be ______ or _______

A

1) Abscesses in skeletal muscle: invasion of muscle following wound contamination and manifestation of septicemia
or
2) Diffuse interstitial myositis: phlegmon with exudate extending along fascial planes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes Wooden tongue in cattle

A

Actinobacillus lignieresi
-Granulomatous or pyogranulomatous myositis
-Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species

A

Wooden Tongue
Actinobacillus lignieresi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Actinobacillus lignieresi

A

Causes Wooden Tongue
Granulomatous or pyogranulomatous myositis
-Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species

*Extensive proliferation of connective tissue which causes the tongue to be enlarged, hard and partially immobilized
*Pyogranulomas contain small “sulfur granules” composed of masses of gram negative rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes pyogranulomas of sulfur granules composed of masses of gram negative rods

A

Granulomatous or pyogranulomatous myositis
-Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the bug basics of Clostridium

A

gram +
anaerobic
spore forming
bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes black leg

A

Clostridium chauvoei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathogenesis of clostridial myositis (broad)

A

neurotoxins produced locally in the lesion that can cause death when absorbed into the blood stream as well as production of exotoxins that result in extensive local edema and necrosis by gangrene

*rapidly fatal infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference from true blackleg vs false black leg

A

True: Myositis associated with Clostridium chauoei, primarily seen in cattle (and other ruminants) and most commonly young stock

False: is associated with other or mixed infections of clostridial species and is more accurately classified as Malignant edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of animals does Black leg typically infect

A

mostly cattle (and other ruminants)

Young stock: 6-12 months of age

rapidly growing animals on high plane of nutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Is blackleg contagious?

A

No- it is acute, non-contagious, infectious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the pathogenesis of Blackleg

A

1) Tissue damage through trauma/ bruising
2) Tissue hypoxia/ ischemia
3) Favorable microenvironment fro vegetative growth
4) Bacterial proliferation (unvaccinated animals)
5) Exotoxin production
6) Tissue necrosis and systemic illness
7) Spores disseminated to tissues via bloodstream and remains latent
or
1) Bacteria in GI tract of normal animals
2) fecal contamination of soil and spores ubiquitously present
3) Spores are absorbed from the intestinal tract: contaminated feed, damaged mucosa (eg eruption of teeth)
4) Spores disseminated to tissues via the bloodstream and remains latent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the exotoxin of C. chauveoi cause locally at skeletal muscle

A

necrotizing myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When does blackleg typically occur

A

Summer and Fall (warm/wet months)

*environmental outbreaks with common injuries and soil excavation
*Epizootic outbreaks - flooding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the case fatality rate of Blackle g

A

100%
economic impact: death loss and prevent with vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is blackleg prevented

A

Vaccination protocols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical signs of black leg in cattle *

A

Systemic phase: depression, anorexia, rumen stasis, fever, tachycardia (death in 12-36 hours)

Acute phase: lesion is swollen/ stiff, hot, and severely painful

Latter stages: lesion becomes cold, non-painful, edema and emphysema present, skin may be discolored or died out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the clinical signs of blackleg in sheep

A

clinical signs depend on the muscles affected

-discolored skin
-NO edema
- NO crepitus

*associated with wounds (as opposed to GI source)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the clinical signs of Blackleg in horses

A

not well described but
-pectoral edema
-stiff gate observed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you diagnose Blackleg *

A

CBC: inflammatory changes and bactermia
Muscle enzyme elevation
Need aspirate cytology**

often dead before you get samples

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is needed to diagnose blackleg *

A

CBC: inflammatory changes and bactermia
Muscle enzyme elevation
Need aspirate cytology**

often dead before you get samples

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is seen on necropsy of an animal with Blackleg

A

Cattle:
1) Recumbent with affected leg up
2) Bloating and putrefaction
3) Clotting blood from nostrils and anus (Rule out Anthrax)
4) Dark hemorrhagic muscle (red to black)
5) No superficial wound

Sheep
1) Muscle lesions localized
2) Less edema and emphysema
3) External wound
4) Involvement of fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What clinical sign of Blackleg makes you need to rule out Anthrax in a cow

A

Clotting blood from nostrils and anus

30
Q

With cattle or sheep with blackleg do you see a superficial wound

A

Sheep
muscle lesions are localized, less edema and emphysema, external wound

31
Q

Where do you typically see the crepitant swellings of cattle with blackleg

A

thighs, rump, back, and shoulders
major lesions in underlying muscles
small lesions may be present in other muscles
yellow gelatinous exudate. blood and gas bubbles

32
Q

What causes malignant edema

A

Clostridial wound infection (septicum* and novyi, sordelli and perfringens), many species, can be mixed

33
Q

What kinds of animals does malignant edema typically affect

A

all ages and species

34
Q

What causes Big head in rams

A

Clostridium novyi

35
Q

In cattle, most malignant edema cases are caused by

A

Clostridium septicum

36
Q

What organism is responsible for about 68% of myonecrosis cases in equids

A

Clostridium perfringens - 68%
C. septicum- 10%

37
Q

What species does Clostridium sordelli cause malignant edema in?

A

Cattle and sheep

38
Q

What are the different clostridium pathogens that cause malignant edema

A

C. septicum- cattle (10% myonecrosis of equids)
C. sordelli- cattle and sheep
C. novyi- big head in rams
C. perfringens- 68% myonecrosis in equids

39
Q

How does malignant edema infection occur *

A

1) Wounds
-Trauma
-Umbilical cord
-Surgical site
-IM or perivascular injections (even with asepctic technique, dormant spores of C. perfringens have been found in normal muscle)

2) Induced anaerobic environment

40
Q

How can malignant edema occur after aspectic technique of IM or perivascular injections

A

dormant spores of C. perfringens have been found in normal muscle)

41
Q

What might lead to a ruminant outbreak of malignant edema

A

shearing and tail docking
after parturition due to vaginal laceration, castration, and after fighting between males

42
Q

Why might a horse have IM injection for colic treatment be at risk for malignant edema

A

certain drugs that are irritating like Banamine (Flunixin meglumine, supplements, and anthelmintics) can induce muscle necrosis
why we dont have IM neck injections in horses

43
Q

What are the clinical signs of malignant edema

A

Acute (within 6-48 hours)
Local site- early stage
-Soft doughy swelling
-Marked local erythema
-Severe pain with palpation
-Emphysema (Not C. noyvi)

Later stages: tense swelling, dark coloration, cool

Systemic signs:
-high fever
-depression
-weakness or lameness/stiffness (depending on location)
-IMHA (horses)
*Death within 24-48 hours after onset of clinical signs

44
Q

What clinical sign is not present with C. novyi infection

A

emphysema

45
Q

What might occur in horses after systemic malignant edema infection

A

Immune mediated hemolytic anemia
*generally delayed (days)

46
Q

What are the clinical signs of pigs with malignant edema (fill in later after clarifying)

A

-Restricted to Axilla, neck and limbs

*No emphysema
*No edema??? idk she is wild

47
Q

rams with swollen head which first occurs under the eyes and then spreads under SC and along the neck

A

Big Head

48
Q

What can cause the red line on the gums of horses

A

Toxic line
a) Endotoxemia
b) Exotoxemia

49
Q

How do you diagnose Malignant edema

A

Antemortem: presumptive, ultrasound, aspirate and gram stain, culture and PCR

Postmortem: sample quickly (overgrowth), muscle0 impression smears, histology, culture, IHC, Fluorescent antibody to ID C. chavoei

50
Q

What are your differential diagnoses for malignant edema

A

Anthrax
Bacillary Hemoglobinuria
Lightning strike
toxicity
other causes of sudden death

51
Q

What are the necropsy findings of malignant edema

A

Tissue changes occur rapidly after death
gangrene of skin and muscle around lesion
local blood stained edema
varies from serum like to gelatinous deposit
emphysema but not with C. novyi
Foul, putrid odor (C. perfringens or C. sordelli)

52
Q

How do you treat Clostridial myonecrosis

A

EMERGENCY

-Antibiotics: Penicillin, Oxytetracycline, Metronidazole (Not in food animals)
-Anti-inflammatories
-Surgical debridement (fasciotomy, myotomy)
-Supportive care

53
Q

What antibiotics do you use to treat clostridial myonecrosis

A

Penicillin, Oxytetracycline (stops exotoxin production) , Metronidazole (Not in food animals)

54
Q

What is the most common antecedent condition in Equine Clostridial Myonecrosis

A

Colic
within 6-72 hours after soft tissue injection
most occur in the cervical musculature
survival rate of 73%

55
Q

How can colic lead to equine clostridial myonecrosis

A

within 6-72 hours after soft tissue injection
most occur in the cervical musculature
survival rate of 73%

56
Q

How will you detect the IMHA seen with Equine Clostridial myonecrosis

A

CBC: Severe regenerative anemia, intravascular hemolysis, RBC agglutination

Positive Direct Coombs test

Reticulocytes

57
Q

How do you control and prevent malignant edema

A

Vaccines
Injection and procedure technique
burn and bury dead

in outbreak, vaccinate all unaffected cattle, treat with penicillin, move cattle to unaffected pasture, constant surveillance recommended

58
Q

What do you do with animals that died of black leg *

A

burn or deep burial to minimize soil contamination *

59
Q

Immune mediated myositis in horses can develop secondary to

A

S. equi infection (Strangles)

60
Q

What are the clinical signs of immune mediated myositis secondary to S. equi infection

A

markedly firm swollen, painful epaxial and gluteal muscles

61
Q

Myositis associated with S. equi * **

A

1) Muscle infarctions- severe manifestation of purpura hemorrhagica (prognosis is guarded, even with aggressive therapy
2) Rhabdomyolysis with acute myonecrosis- horses with clinically evident strangles will be stiff and recument, evelations in CK and AST
3) Rhabdomyolysis with progressive atrophy- concurrent signs of strangles is variable

*Pathogenesis is likely immune mediated
*Necessitates euthanasia within 24-48 hours

62
Q

What is purpura hemorrhagica in horses *

A

aseptic necrotizing vasculitis caused by deposition of immune complexes associated with previous S. equi infection or exposure
*characterized primarily by edema and petechial or ecchymotic hemorrhages
can occur secondary to other antigen, not just S. equi

63
Q

What are the two types of myopathy seen after horses infected with S. equi

A

1) Muscle infarction (purpura hemorrhagica)
2) Rhabdomyolysis with progressive atrophy

64
Q

What are the clinical signs of muscle infarction in horses

A

likely from immune complex deposition and vaccination
manifestation of purpura hemorrhagica
Signs:
-Severe vasculopathy with infarctions to skeletal muscle, skin, GI tract, and lungs
-Muscle stiffness and lameness
-May see abdominal pain and sc swelling

CK elevations
SeM protein titer can exceed 1:6400

65
Q

How do you treat muscle infarction in horses

A

aggressive corticosteroid therapy and antibodies

prognosis is still guarded

66
Q

What are the theories of why you get rhabdomyolysis with atrophy in horses after S. equi infection

A

1) high level of inflammatory cytokines secondary to nonspecific T cell stimulation from super antigens associated with S. equi
2) Cross reactivity of SEM protein and myosin protein in muscle

*Produces exotoxins within the skeletal muscle, leading to muscle necrosis

67
Q

What are the clinical signs of rhabdomyolysis with atrophy in horses

A

mailaise
firm swelling and pain with eventual rapidly progressing atrophy of epaxial and gluteal muscle
-+/- signs of active strangles infection

68
Q

How do you diagnose rhabdomyolysis with atrophy in horses

A

muscle biopsy
-chronic active rhabdomyolysis with regeneration
-macrophage infiltration
-atrophy of fast fibers
-lymphocytic vasculitis
-fibrosis surrounding blood vessels

69
Q

How do you treat rhabdomyolysis with atrophy in horses

A

corticosteroids
if concurrent infection: antibiotics

prognosis is fair, with therapy- muscle mass may return to normal (better than the muscle infarction form)

70
Q

What are your other differentials if a horse has rhabdomyolysis with atrophy

A

-seaosnal pasture myopathy/ MADD
-storage disease (polysaccharide or glycogen branching enzyme deficiency)
-Vitamin E responsive myopathies (equine motor neuron disease)
-Spinal cord lesion
-Other infectious- lyme disease

71
Q
A

Fluids, Respiratory, Muscles (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions