Myopathies Flashcards
You have a cow with no exercise intolerance, rhabdomyolysis, and no conduction problems. What does this make you think?
Inflammatory Muscle Disease
-Infectious or Immune Mediated
Different Large animal infectious myopathies
Bacterial: acute suppurative myositis, Actinobacillus, Clostridial disease
Parasitic: Trichinella, Sarcocystis
Viral: Influenza, Bluetongue, Foot and mouth
breakdown of muscle tissue with inflammation: heat, pain, swelling and systemic toxemia: fever
clinically see: CK, AST, Myoglobinemia, Myoglobinuria
Rhabdomyolysis
What will you see in an animal with rhabdomyolysis
Fever. Heat, Pain, Swelling
Clinical pathology: CK, AST, Myoglobinemia, Myoglobinuria
acute suppurative myositis in ruminants and swine is caused by
Corynebacterium pyogenes
acute suppurative myositis in horses is caused by
Streptococcus equi
Corynebacterium
Acute Suppurative Myositis can be ______ or _______
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
What causes Wooden tongue in cattle
Actinobacillus lignieresi
-Granulomatous or pyogranulomatous myositis
-Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species
Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species
Wooden Tongue
Actinobacillus lignieresi
Actinobacillus lignieresi
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
what causes pyogranulomas of sulfur granules composed of masses of gram negative rods
Granulomatous or pyogranulomatous myositis
-Small pyogranulomas in the tongue and soft tissues of the head and neck of cattle and other species
What are the bug basics of Clostridium
gram +
anaerobic
spore forming
bacilli
What causes black leg
Clostridium chauvoei
What is the pathogenesis of clostridial myositis (broad)
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
What is the difference from true blackleg vs false black leg
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
What kind of animals does Black leg typically infect
mostly cattle (and other ruminants)
Young stock: 6-12 months of age
rapidly growing animals on high plane of nutrition
Is blackleg contagious?
No- it is acute, non-contagious, infectious
What is the pathogenesis of Blackleg
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
What does the exotoxin of C. chauveoi cause locally at skeletal muscle
necrotizing myositis
When does blackleg typically occur
Summer and Fall (warm/wet months)
*environmental outbreaks with common injuries and soil excavation
*Epizootic outbreaks - flooding
What is the case fatality rate of Blackle g
100%
economic impact: death loss and prevent with vaccination
How is blackleg prevented
Vaccination protocols
What are the clinical signs of black leg in cattle *
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
What are the clinical signs of blackleg in sheep
clinical signs depend on the muscles affected
-discolored skin
-NO edema
- NO crepitus
*associated with wounds (as opposed to GI source)
What are the clinical signs of Blackleg in horses
not well described but
-pectoral edema
-stiff gate observed
How do you diagnose Blackleg *
CBC: inflammatory changes and bactermia
Muscle enzyme elevation
Need aspirate cytology**
often dead before you get samples
What is needed to diagnose blackleg *
CBC: inflammatory changes and bactermia
Muscle enzyme elevation
Need aspirate cytology**
often dead before you get samples
What is seen on necropsy of an animal with Blackleg
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
What clinical sign of Blackleg makes you need to rule out Anthrax in a cow
Clotting blood from nostrils and anus
With cattle or sheep with blackleg do you see a superficial wound
Sheep
muscle lesions are localized, less edema and emphysema, external wound
Where do you typically see the crepitant swellings of cattle with blackleg
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
What causes malignant edema
Clostridial wound infection (septicum* and novyi, sordelli and perfringens), many species, can be mixed
What kinds of animals does malignant edema typically affect
all ages and species
What causes Big head in rams
Clostridium novyi
In cattle, most malignant edema cases are caused by
Clostridium septicum
What organism is responsible for about 68% of myonecrosis cases in equids
Clostridium perfringens - 68%
C. septicum- 10%
What species does Clostridium sordelli cause malignant edema in?
Cattle and sheep
What are the different clostridium pathogens that cause malignant edema
C. septicum- cattle (10% myonecrosis of equids)
C. sordelli- cattle and sheep
C. novyi- big head in rams
C. perfringens- 68% myonecrosis in equids
How does malignant edema infection occur *
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
How can malignant edema occur after aspectic technique of IM or perivascular injections
dormant spores of C. perfringens have been found in normal muscle)
What might lead to a ruminant outbreak of malignant edema
shearing and tail docking
after parturition due to vaginal laceration, castration, and after fighting between males
Why might a horse have IM injection for colic treatment be at risk for malignant edema
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
What are the clinical signs of malignant edema
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
What clinical sign is not present with C. novyi infection
emphysema
What might occur in horses after systemic malignant edema infection
Immune mediated hemolytic anemia
*generally delayed (days)
What are the clinical signs of pigs with malignant edema (fill in later after clarifying)
-Restricted to Axilla, neck and limbs
*No emphysema
*No edema??? idk she is wild
rams with swollen head which first occurs under the eyes and then spreads under SC and along the neck
Big Head
What can cause the red line on the gums of horses
Toxic line
a) Endotoxemia
b) Exotoxemia
How do you diagnose Malignant edema
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
What are your differential diagnoses for malignant edema
Anthrax
Bacillary Hemoglobinuria
Lightning strike
toxicity
other causes of sudden death
What are the necropsy findings of malignant edema
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)
How do you treat Clostridial myonecrosis
EMERGENCY
-Antibiotics: Penicillin, Oxytetracycline, Metronidazole (Not in food animals)
-Anti-inflammatories
-Surgical debridement (fasciotomy, myotomy)
-Supportive care
What antibiotics do you use to treat clostridial myonecrosis
Penicillin, Oxytetracycline (stops exotoxin production) , Metronidazole (Not in food animals)
What is the most common antecedent condition in Equine Clostridial Myonecrosis
Colic
within 6-72 hours after soft tissue injection
most occur in the cervical musculature
survival rate of 73%
How can colic lead to equine clostridial myonecrosis
within 6-72 hours after soft tissue injection
most occur in the cervical musculature
survival rate of 73%
How will you detect the IMHA seen with Equine Clostridial myonecrosis
CBC: Severe regenerative anemia, intravascular hemolysis, RBC agglutination
Positive Direct Coombs test
Reticulocytes
How do you control and prevent malignant edema
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
What do you do with animals that died of black leg *
burn or deep burial to minimize soil contamination *
Immune mediated myositis in horses can develop secondary to
S. equi infection (Strangles)
What are the clinical signs of immune mediated myositis secondary to S. equi infection
markedly firm swollen, painful epaxial and gluteal muscles
Myositis associated with S. equi * **
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
What is purpura hemorrhagica in horses *
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
What are the two types of myopathy seen after horses infected with S. equi
1) Muscle infarction (purpura hemorrhagica)
2) Rhabdomyolysis with progressive atrophy
What are the clinical signs of muscle infarction in horses
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
How do you treat muscle infarction in horses
aggressive corticosteroid therapy and antibodies
prognosis is still guarded
What are the theories of why you get rhabdomyolysis with atrophy in horses after S. equi infection
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
What are the clinical signs of rhabdomyolysis with atrophy in horses
mailaise
firm swelling and pain with eventual rapidly progressing atrophy of epaxial and gluteal muscle
-+/- signs of active strangles infection
How do you diagnose rhabdomyolysis with atrophy in horses
muscle biopsy
-chronic active rhabdomyolysis with regeneration
-macrophage infiltration
-atrophy of fast fibers
-lymphocytic vasculitis
-fibrosis surrounding blood vessels
How do you treat rhabdomyolysis with atrophy in horses
corticosteroids
if concurrent infection: antibiotics
prognosis is fair, with therapy- muscle mass may return to normal (better than the muscle infarction form)
What are your other differentials if a horse has rhabdomyolysis with atrophy
-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
