Infectious Diseases of the Musculoskeletal System Flashcards
describe routes of transmission of CAEV
- most common route is from dam to kid through colostrum/milk and close contact
- but can also possibly utilize horizontal transfer via respiratory secretions on fomites
describe the pathophysiology of CAEV-associated polysynovitis/arthritis
immune complexes formed by non-neutralizing antibodies plus virus-infected macrophages result in arthritis, encephalitis, pneumonia, mastitis, and weight loss
describe specific ages at which arthritis and encephalitis caused by CAEV occur
most (70-80%) of goats are asymptomatic, but if they develop symptoms
encephalitis is more common in kids (<6months)
arthritis is more common in goats >6 months
describe testing (2) and management (4)
practices utilized to reduce transmission of CAEV within a herd
testing can be done ins 2 ways:
1. serology: serological monitoring 2x/year, but this is challenging as animals can shed the virus PRIOR to seroconversion
- PCR is less commonly utilized (usually only in big diagnostic labs), but can test milk, blood, and joint fluid/synovium
management:
1. pasteurize milk/colostrum before feeding to kids
2. restrict pooling of colostrum on surfaces
3. separate/cull any affected animals
4. quarantine new animals and test twice at at least a 60d interval
state the gram stain characteristics, typical morphology, typical residence location, and how transmission of disease caused by this species occurs: actinomyces spp. (A. bovis)
-gram positive, pleiomorphic filamentous branching rod
-normal flora of oropharynx, GI tract, and urogenital tract
-transmission of disease: since these are endogenous bacteria, disease is caused by trauma to oral mucous membranes, allowing opportunistic infection that is usually locally invasive and rarely disseminates
describe the pathogenesis and main clinical presentation of lumpy jaw in various hosts and aspects of diagnosis/disease control and prevention
pathogenesis: A. bovis are normal flora of mouth of cattle, if there is trauma to oral mucosal membranes due to sharp pieces of feed or a foreign body (or teeth eruption), this can cause actinomycosis (Lumpy Jaw), or pyogranulomatous osteomyelitis and soft tissue infection of the face and jaw
aspects of disease: initially painless, hard boney swelling that enlarges slowly, becomes painful and open to the outside, and drains; can cause difficulty chewing or tooth loss and may expand into soft tissue; more common in beef breeds and not contagious
diagnosis: clinical signs most commonly, can also cytology and culture
treatment: must catch early!
-surgical debridement
-antibacterial therapy (iodides +/- penicillin)
prevention: avoid feeding course stemmy hay (environmental factor of disease)
state the gram stain characteristics, typical morphology, typical residence location, and how transmission of disease caused by this species occurs: clostridium spp.
-gram positive, anaerobic rods
- several species commonly found in soil and intestines
-diseases are toxin based (histiotoxic, neurotoxic, or enterotoxic)
-clostridia can produce spores: dormant and resistant bacterial forms that preserve the genetic material during times of extreme environmental stress
describe the pathogenesis and main clinical presentation of black leg in various hosts and aspects of diagnosis/disease control and prevention
pathogenesis: Clostridium chauvoei spores are present in the soil and the intestinal tract of normal ruminants (cattle esp); these spores enter the blood/lymph from the intestinal tract and seed in muscle, quiescent until any local anoxic condition that causes bruising triggers germination of spores and leads to toxin production, resulting in Blackleg
risk factors: rapidly growing animal on high plane of nutrition (nice pasture, spring)
clinical disease: called Blackleg, sudden onset of muscle inflammation and necrosis, usually multiple cattle are affected
-fever, lameness, rapid death or sudden death without signs (hallmark of clostridia spp.), postmortem will see necrotic, edematous, emphysematous muscle
diagnosis: sporulated gram positive rods can be found in the muscle postmortem via PCR or fluorescent antibody tests; culture is not often done bc bacteria are anaerobic
treatment: antibiotics (penicillin) often not successfull
prevention: vaccination!! is key!!
describe the pathogenesis and main clinical presentation of malignant edema in various hosts and aspects of diagnosis/disease control and prevention
pathogenesis: Clostridium septicum organsims/spores are found in soil and GI tract and enter the muscle via wounds (shearing, tail docking, lambing, castrations, IM INJECTION); histiotoxic toxins produced at site cause host muscle cell death and malignant edema
disease: malignant edema: gangrenous myoncerosis with edema, subcutaneous emphysema, and systemic toxemia (rapid shock-like syndrome);
-acute onset fever, pain over affected area
-malignant edema can also be caused by other clostridia species!
spread: can affect ALL domestic animals, typically in sporadic cases affecting individual animals
diagnosis: clinical signs, culture/PCR of muscle or fluorescent antibody test on muscle tissue
treatment: antibiotics, incision and drainage of wound (expose bacteria to air) and supportive care
control: good hygiene, multivalent clostridial bacterin or toxoid vaccine for ruminants!
state the gram stain characteristics, typical morphology, typical residence location, and how transmission of disease caused by this species occurs: borrelia spp.
gram NEGATIVE spirochetes; require host or tick vector for survival since they are NOT free living in the environment
transmission of disease: B. burgdorferi is the causative agent; sticks to tick gut via OspA protein, and other Osp proteins = attach to mammalian host collagen; capable of antigenic variation of the surface patterns of these Osp proteins interferes with antibody clearance
describe the pathogenesis and main clinical presentation of lyme disease in various hosts and aspects of diagnosis/disease control and prevention
pathogenesis: reservoir hosts (mice, birds, chipmunks, deer) are fed on by the larvae and nymphs of deer ticks (Ixodes); then the nymphs and adult ticks bite domestic animals and humans; spirochetes migrate to the tick salivary glands and then are secreted into saliva and therefore the host, BUT tick must be attached for 36-48 hours for transmission to occur; the spirochetes bind in the dermis layer and then spread systematically
lyme disease: 95% of exposed, serologically positive, dogs are asymptomatic/subclinical
-if clinical signs occur, primary manifestation is arthritis
-one or more joints may be swollen, hot, and painful due to the host’s inflammatory response (shifting leg lameness)
-lameness typically occurs 2-5 months post bite
-chronic disease primarily includes recurring polyarthritis, nephritis, arrythmias, seizures, and aggression
diagnosis: hella hard!
need: history of exposure, clinical signs, positive serology, and response to treatment to even call it lyme disease
-SNAP test can discriminate infection (C6 peptide antibodies) from vaccine (no C6 peptide)
treatment: long term (>30d) antibiotic (doxycycline) is often effective if administered early
prevention: remove attached ticks, tick control (lawn mowed and prevention), +/- vaccination
give 4 members of class eimerionia and 2 classes of adeleorina (apicomplexan parasites) that are important in vet med; describe their life cycles and preferred cells
eimeriorina
1. eimeriidae: direct LC, intestinal cells, host specific
2. cryptosporidiae: direct LC, intestinal cells, less specificity
3. sarcocytsiidae: tissue cyst forming; indirect LC (asexual in intermediate host and sexual in final host: includes neospora sp., sarcocystic sp., and toxoplasma spp.
- adelorina
-hepatozoon sp.: indirect LC; sexual stage in ticks
describe neospora caninum; give taxonomy: protozoan or nematode
general life cycle features: direct vs. indirect, what is infective stage, where is parasite in host
clinical importance: presentation and severity, zoonotic concerns
basic diagnosis and management:
morphological vs. molecular, treatment or prevention available?
taxonomy: tissue-cyst forming coccidian with worldwide distribution
life cycle: indirect; transplacental/congenital (vertical) spread common in dogs and cattle
-direct host: canids, sexual stage in intestinal epithelium
-intermediate host: most mammals (cattle, ungulates), asexual stage in tissue cysts
clinical importance:
-NOT zoonotic
-causes infectious inflammatory myopathy in dogs, leading to meningoencephalitis, polymyositis, polyradiculoneuritis (incoordination/paresis of hind limbs and rigid paralysis)
-major cause of abortion in cattle at 5-6 months of gestation
diagnosis:
-serology, ID or PCR in biopsy, aspirate, CSF, blood
prevention: NO raw meats! cull or bulk milk test
treatment: clindamycin +/- sulfa drugs
describe sarcocystis neurona; give taxonomy: protozoan or nematode
general life cycle features: direct vs. indirect, what is infective stage, where is parasite in host
clinical importance: zoonotic concerns, presentation and severity
taxonomy: tissue forming coccidian and causative agent of EPM
life cycle: indirect
-direct host: opposum (seen in western hemisphere only!), sexual stage in intestinal epithelium
indirect host: variety of mammals, asexual stage in tissue cysts
aberrant host: horses (get fucked up EPM style)
not zoonotic? we hope
presentation: 3 As
1. asymmetry
2. atrophy
3. ataxia
describe toxoplasma gondii; give taxonomy: protozoan or nematode
general life cycle features: direct vs. indirect, what is infective stage, where is parasite in host
clinical importance: presentation and severity, zoonotic concerns
basic diagnosis and management:
morphological vs. molecular, treatment or prevention available?
taxonomy: ZOONOTIC tissue forming coccidian with worldwide distribution
life cycle: indirect
direct host: felids only; asexual and sexual reproduction in enterocytes
indirect host: So. Many.
clinical presentation: major cause of abortion in small ruminants, significant morbidity in marsupials, ocular disease in humans, congenitally infected kittens may be clinical
