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Infectious Diseases Exam 2
Terms in this set (100)
Core vaccines for horses?
West Nile Virus, WEE/EEE, Rabies, Tetanus
Top ddx for horses with respiratory problems, fever, inappetence?
Equine Influenza Virus, Equine Herpes virus, Equine Arteritis Virus, Streptococcus equi
Equine Influenza virus (what type of virus/family? Importance? How are they species specific/which strain most common in horses (& state did this likely originate in)? Subject to which types of genetic changes/explain them?
Enveloped ssRNA virus, family Orthomyxoviridae;
most frequent diagnosed cause of equine viral respiratory disease;
surface proteins (HA - hemaglutinin & NA - neuraminidase; H3N8 most common in horses & from Florida/Clade 1);
subject to antigenic drift (Ag drift - minor point mutation in HA protein in genome so develops into new strain & this is common; Ag shift - major gene reortment that results in new subtype & uncommon)
Equine Influenza virus - age group affected? Morbidity/mortality? Transmission? Pathology/where does this virus attack in the body/effects?
young horses (less than or = to 3 years of ages)
Morbidity 60-90%, mortality <1%
Commingled animals (spread through aerosolized respiratory secretions or direct nose/nose contact)
attacks respiratory epithelium (pseudo stratified columnar; in trachea & bronchi) so impairs mucociliary clearance system & potentiates secondary bacterial infection of lower respiratory tract
Most common type of equine influenza virus found in horses? (type? Strain? Sub lineage? Clade?)
Subtype A (like A2; H3N8), American sub lineage, Florida Strain, Clade 1
Clinical signs & incubation of horse with equine influenza virus
1-3 day incubation, shedding within 48 hours
Persistent (up to 5 days at 105 F) fever, anorexia, persistent dry/hacking cough, nasal discharge (initially serous, becomes mucopurulent), goes on 7-14 days cough 21 days
Diagnostic test options for equine influenza virus & when to sample
ELISA/viral isolation (nasopharyngeal swab for respiratory secretions; non cotton swab, store on ice to transport to lab), serology maybe (blood sample)
Take samples 24-48 hours after clinical signs develop (naive horses may show greater diagnostic value)
Strangles - another common name? Type of organism? How does it have its virulence? How contagious/transmission? Incubation?
Equine Distemper; Streptococcus equi spp. equi (G+ cocci - aerobic bacteria)
SeM protein for virulence (binding to respiratory epithelium)
Highly contagious (nasal discharge, fomite (tack, equipment, people) contamination, ingestion, inhalation)
Incubation 3-14 days, often young horses
Strangles clinical signs? Diagnostic tests?
Fever, depression, purulent nasal discharge, lymphadenopathy (submandibular, parotid, retropharyngeal leading to tracheal compression), respiratory distress, inappetance (likely due to the guttural pouch pus contacting the cranial nerves responsible for swallowing)
enlarged lymph nodes, endoscopy of upper respiratory tract & guttural pouches, culture (nasal wash/guttural pouch/abscess; requires 2-3 negative cultures to be considered -), PCR
Equine Herpesvirus - what type of virus/family? Commonness/where is the virus found & age horses typically affected? Strains/what systems they affect? Pathogenesis/where in the body does this virus target?
DsDNA enveloped viruses (Herpesviridae family), common worldwide & ubiquitous in environment
EHV1 - neuro too (changes form) & abortions in mares & respiratory signs
EHV4 - respiratory signs
affects local lymph nodes --> viremia (disseminates virus to distant organs) & virus targets vascular endothelium (vasculitis, hemorrhage, thrombosis, necrosis)
Equine Herpes Virus clinical signs? Diagnostic tests?
Upper respiratory tract infection (cough uncommon), FEVER, serous or purulent nasal discharge, ocular discharge sometimes, malaise, limb edema
Virus isolation/PCR (nasopharyngeal swab of respiratory secretions - tests for EHV1 but EHV4 cross reacts with it)
Is strep a normal part of horse flora?
Yes (Strep zooepidemicus, NOT STREP EQUI)
Equine Arteritis Virus - what type of virus? Clinical signs? Transmission (who usually carries it/what breed?)?
Respiratory disease (like EHV or flu), vasculitis, abortion, fever, conjunctivas, coughing, edema (sheath, limbs, pectorals, mammary), severe disease can cause death
Transmission via bodily fluids (aerosol, fomites, USUALLY VENEREAL/STD)
Usually carried in stallions, common in standardbreds
Equine Arteritis virus diagnostics?
Virus isolation (nasopharyngeal swab) or serology (blood; for venereal disease)
Most common sample to submit for equine respiratory disease?
List best diagnostic tests to perform for each:
equine influenza, equine viral arteritis virus, equine herpes virus, strangles
Flu & equine viral arteritis- virus isolation (nasopharyngeal swab)
Herpes - PCR
Strangles - endoscopy (upper respiratory tract), maybe culture
Treatment for equine influenza virus? (what should you NOT give?) Prevention?
Supportive/symptomatic (REST, NSAIDs if needed, monitor feed/water intake, isolation)
DON'T NEED ANTIBIOTICS
vaccination (decreases severity of infection but doesn't prevent infection, intended for high risk horses who travel/race/comingle)
Rhodococcus equi - geographic distribution? Causes mainly what in who? Zoonosis? Onset (how fast?)? What screening method to use for early ID?
pyogranulomatous pneumonia in foals (also extrapulmonary manifestations) but the most common form is
Zoonotic to immunocompromised individuals
most commonly insidious, chronic progression
Rhodococcus equi - clinical signs
Fever, lethargy, cough (NOT SNOTTY NOSED FOALS)
If more severe --> inappetence, tachypnea/tachycardia, flared nostrils, more coughing, increased respiratory effort
Extrapulmonary disorders --> immune mediated polysynovitis, ulcerative enterotyphlocolitis (abscesses), intra-abdominal lymphadenitis/abscessation, bone lesions/neuro signs
Rhodococcus equi - gram stain/morphology/growth appearance? Aerobe/anaerobe? Intra/extracelluar? Explain its replication. Where found?
G+ pleomorphic rod forming mucoid colonies (salmon colored)
Aerobic, facultative intracellular (primarily within macrophages & arrests phagosome maturation; replicates in phagolysosomes)
Mycolic acids, glycolipids, polysaccharides in cell envelopes
Found in soil (soil saprophyte; loves herbivore poop since thrives on VFAs; ubiquitous; survive long term)
Major virulence factors of Rhodococcus equi? How is this virulence transferred?
Ability to replicate w/in macrophages
(replicates within phagolysosomes & destroys phagosome maturation/prevents acidification)
Virulent isolates have 80 to 90 kb plasmid (transfered via conjugation) with a 21 kb pathogenicity island (encodes virulence associated protein A aka VapA)
VapA is necessary but not sufficient for disease (so if it's there, you will have disease, but it needs to be in combo with other things predisposing foal to disease)
Rhodococcus equi - diagnosis (gold standard?)? Limitations?
Culture from percutaneous tracheobronchial aspirate
(TBA) = GOLD STANDARD (culture will ID genus/species but NOT VIRULENCE STATUS aka presence of VapA gene; TBA is invasive, time consuming, & can be deadly in respiratory foals)
Also cytology (G+ pleomorphic rods & signs of septic inflammation; often seen within macrophages), thoracic imaging, serology (but maybe not useful for dx since just says if exposed, not necessarily infected)
PCR to find VapA/figure out virulence
(doesn't tell you whether organism live or dead, doesn't do antimicrobial susceptibility testing, isolate concurrent pathogens, or genotype; may get false + from contamination or false -; ~75% sensitivity of PCR of fecal samples)
Rhodococcus equi prevention/screening? Sensitivity/specificity of using ultrasonography?
LIMITED (hyperimmune plasma (EXPENSIVE) only partially protective, at best, no vaccine available, etc)
Maybe can do PE, monitoring, &/or serology to look out for this in foals; maybe hematology (serum amyloid A, etc), radiography, ultrasonography (no good evidence for any except conflicting evidence for hematology)
For ultrasound --> Se is 89% & specificity 62%
Rhodococcus equi - 3 patterns of prevalence on farms? Morbidity/mortality %s?
Unaffected, sporadically affected, or endemic farms
Morbidity 5-20%, mortality 10-30%
Most common isolates of infectious endometritis in mares? Other isolates?
Opportunistics: Strep zooepidemicus, Escherichia coli
True venereal pathogens (spread via mating): Pseudomonas aeruginosa & Klebsiella pneumonia
Others: proteus, corynebacterium, taylorella equigenitalis (reportable), candida (normal commensal of GIT & vagina), Aspergillus, Mucor
Describe resistant vs. susceptible mares in terms of response to infectious endometritis
Resistant: intact uterine defenses & clear contaminants
Susceptible: compromised uterine defenses, can't clear contaminants, infection results
Common reasons for mare genital tract infections. Physical barriers to uterine contamination?
Breeding, parturition, anatomic defects, physiologic defects (like poor uterine clearance), non-hygienic exams, overwhelming inoculum
Physical barriers are vulvar seal, vestibulovaginal fold (remnant of hymen), & cervix
Diagnostics for infectious endometritis in mares
Uterine culture (quantify the plate growth; can see lots of different colony growths with different organisms, so this could mean contamination of the sample; in short, cultures are useless) in conjunction with cytology, biopsy, other clinical findings
Clinical signs of contagious equine metritis (CEM) in mares vs stallions. Causative agent (describe it & how to dx it)?
Mares: copious vaginal discharge 10-14 days post mating, hyperemia & edema (endometrium, cervix, vagina), return to estrus, infertility, fibrinosuppurative metritis
Taylorella equigenitalis (G- aerobic coccobacillus; hard to ID & grow so use chocolate Eugon agar & it's slow growing and often overgrown by contaminants)
Where are culture sites for mare & stallion for Taylorella equigenitalis?
Mare: clitoral fossa & sinuses, endometrium
Stallion: urethra fossa, urethra, preputial cavity, shaft of penis
Contagious Equine Metritis (Taylorella equigenitalis) transmission/implications?
Strict import regulations since highly contagious (recently in US)
Transmission via mating (natural cover) or fomites (breeding phantom, wash bucket, etc)
Equine Viral Arteritis - common names? Describe the causative agent. May also infect which other species? Remains infective at what temperatures? % stallions with persistent infections?
Epizootic cellulitis-pinkeye or Equine typhoid
Small enveloped RNA virus (family Arteriviridae), one of 3 most important equine viral respiratory pathogens (also affects llamas & alpacas)
Remains infective at refridgeration & freezing temperatures (can be transmitted in cooled semen & remain viable for years)
Up to 60% stallions persistently infected
Equine Viral Arteritis - reservoir host? Transmission? Diagnostics? Prevention?
Reservoir is stallion
Transmission is respiratory, venereal, fomites
Diagnostics virus isolation (ELISA) or paired titers
Prevention via vaccination (good immunity, specific procedures) or proper isolation procedures
Most important cause of equine abortion?
Equine Herpes Virus 1
Equine Herpes Virus 1 - transmission? Prevention?
Transmission is respiratory (not venereal) or via aborted tissues & fluids
Prevention via vaccinations & isolation/quarantine
Equine Herpes Virus 3 causes what condition (lesions? Consequences? How frequent is it?)?
Blisters on genitals that rupture so too painful to breed
Only get once in a breeding season
Differential diagnoses for sick fluffed bird?
Bacterial (G-, Chlamydia, Mycobacterial), viral (PDD, herpes), repro (male or female), heavy metal toxicity (lead or zinc), etc
Chlamydia psittaci -type of agent? Transmission? Commonness/species affected? Zoonosis? Clinical signs? Gross lesions? Dx? Length of treatment?
Obligate intracellular G- bacteria
Transmission via fecal oral or inhalation
Common (parrots, doves, pigeons)
Zoonotic & reporable
Clinical signs in birds - weight loss, depression, liver disease, chronic respiratory &/or ocular disease
Clinical signs in humans (especially immunocompromised) - headache, cold & flu like signs, pneumonia
Gross lesions - hepatomegaly, splenomegaly, airsacculitis (looks cloudy)
Dx via bloodwork (PCR; see elevated liver enzymes, leukocytosis, monocytosis)
Tx is LONG (6 weeks)
Polyoma - what type of infectious agent? Affects who/what age? Transmission? Incubation time? Clinical signs/path? Consequences? Prevention? Dx?
Neonatal parrots (7-50 days)
Transmission via feather dust, fecal oral, parental feeding of chicks, direct contact or fomites
Incubation is 7-14 days
Clinical signs - crop stasis, depression, anorexia, liver disease, hemorrhage, death
Survivors shed for weeks/months
Prevention - survivors can be sold as only bird or in home with only adult birds (separate exposed from unexposed), CLEAN EVERYTHING, feed birds separately, shut down all breeding for 6 months, maybe vaccine (controversial; 6 weeks of age)
Dx - PCR
Pacheco's Disease - causative agent/describe it. Clinical signs? Species affected? Transmission? Dx? Prevention? Duration of infection? Disease that can occur secondary to this?
Herpes virus (dsDNA; replicates in nucleus)
Clinical signs - acute death (
KILLS WITHIN 24 HOURS
) or chronic necrotizing hepatitis, depression, anorexia, lime green urates
Can affect all parrots
Transmission is fecal oral (intermittently shed in feces)
Dx via PCR (need at least 3 negatives)
Prevention via test & separate
HERPES IS FOR LIFE (& bird sheds the virus for life too)
Can get secondary papillomaviruses
Mycobacterium avium complex - infective agent species? Transmission? Incubation? Zoonosis? Diagnostics for other birds in the area (around the infected bird)?
Species - Avium, Intracellulare, Paratuberculosis
Transmission is fecal/oral or aerosol
Incubation is weeks/years
Maybe zoonotic (immunocompromised individuals)
exams, CBCs, fecal acid fast, & possibly mycobacterial PCR
Psittacine beak & feather disease - Causative agent (describe it)? Transmission? Who affected? diagnostic test? Lesions/clinical signs? Contagion?
Circovirus (ssDNA virus)
Transmission via fecal/oral, aerosol, fomites
Occurs in young old world birds
Dx via beak/feather PCR
Clinical signs/lesions - bursa & thymus necrosis (immunosuppression), usually die within a few days
SUPER CONTAGIOUS (long lived virus & hard to kill)
Ddx for thin weak bird?
Bacterial (Chlamydia, G- infection, Mycobacteria), viral (Psittacine bornavirus, Herpes (Pachecos)), toxin (lead/zinc), fungal (aspergillus), parasitic (sarcocystis or intestinal parasites), cancer
Proventricular Dilatation Disease - causative agent (describe it). Affects what parts of body? Birds affected? Transmission? Prevention? Dx (how many test - results does it take for the bird to be considered actually negative?)?
Psittacine Bornavirus (negative stranded neurotropic RNA virus)
Affects nerves of GIT, brain, & spine (FATAL)
Transmission via fecal/oral, maybe aerosol, egg transmission
Prevention - completely incubate hatched chicks, separate duties of care takers for adults & chicks, all new birds should be tested & +s housed separately
Dx via PCR/serology (intermittent shedders; need >3 - PCR tests to be considered -)
Ascaridia galli - common name? Host specificity Commonness? Life cycle/transmission? Prevention? Age of chicks infected? Clinical signs?
Roundworm; host specific (so not zoonotic); common
Simple & direct life cycle (bird to bird via ingestion of infective larvae in poop; eggs in poop & infective after 10-12 days & mature in 28-30 days post ingestion)
Prevent by cleaning litter/wood chips (clean the poop up)
<12 week old chicks (since takes several weeks for eggs to hatch into infective larvae in poop)
Non-specific clinical signs (unthrifty, inactivity, wing drooping, depressed appetite, retarded growth, maybe death, low weight with large #s in GIT)
Coccidiosis in poultry - what is the causative agent? Host specificity? Clinical signs/seen when? Transmission/life cycle/PPP/pathogenesis? Prevention?
HOST SPECIFIC (so means not zoonotic)
Cecal infections & blood in ceca and poop (seen at 3-8 weeks)
Fecal-oral (sporulation in soil or litter in poop in 1-2 days, PPP=6 days; Eimeria breaks enterocyte; path via lysing of epithelial cells by merozoites)
Prevention if very high or freezing temperatures (EIMERIA LOVES 72 DEGREES F WITH 20% MOISTURE)
Most important ectoparasite of caged layers and breeding chickens?
Northern fowl mite (Ornithonyssus sylviarum)
Ornithonyssus sylviarum - location? Pathology? Transmission? Clinical signs? Prevention? Zoonosis?
Remain on birds or in nests
Female mites lay only 2-5 eggs (mite can go through 1 month without blood meal) --> mites at 200,000/bird cause death via blood loss
Transmission via bird to bird, intro of infected birds, or wild birds
Heavy infestations --> blackened feathers/dark patches around vent, anemia, decreased egg production/growth rate/carcass quality, anorexia
Prevention via DON'T INTRODUCE NEW BIRDS OR INFECTED BIRDS WITHOUT QUARANTINE/TREATMENT
Not technically zoonotic (doesn't readily live on skin & hair of humans, but can blood feed & then leave)
Which backyard poultry diseases have the most seroprevelance/are we most worried about?
Mycoplasma gallisepticum & synoviae, Infectious Bronchitis, Newcastle disease
Most pathogenic avian mycoplasma?
Mycoplasma gallisepticum - strains vary how? Virulence factors? Clinical signs? Worst in who/what can occur secondarily? Transmission?
Strain variability - range of host susceptibility, virulence, clinical signs, immune response
Virulence factors - integral membrane surface proteins (adhesins; attaches to host cells/stays in place to allow colonization & infection) & factors involved in Ag variation/immune invasion
Upper respiratory tract clinical signs (asymptomatic, nasal discharge, coughing, tracheal rales, conjunctivitis, perirorbital/eyelid edema, slowly progressive chronic respiratory disease)
Worse in young birds in winter (secondary invader is E. coli)
Transmission via aerosols (main route of horizontal transmission), direct/indirect fomites (can survive for days in chicken litter), vertical transmission (into eggs, mainly noncommercial sources)
Mycoplasma gallisepticum - diagnostic tests? Zoonosis?
Clinical signs (presumptive dx), culture (difficult & Gram "not"),
(plate agglutination, hemagglutination inhibition, ELISA)
Mycoplasma synoviae (poultry) - clinical signs?
Lameness, swollen leg joints & footpads
Infectious bronchitis (poultry) - causative agent? Clinical signs (& what age group?)? Consequences? Pathogenesis? Transmission? Incubation period? Secondary infection?
Infectious bronchitis virus (coronavirus)
Respiratory signs (& also maybe renal, GIT, & repro signs) like gasping & nasal exudate in young chicks, misshapen eggs (leathery wavy things)
Acute/highly contagious so severe $$$ consequences in poultry industry (low performance & death)
Primarily replicates in respiratory tract --> viremia within 1-2 days of infection & distributes throughout body (even to oviducts)
Transmission via aerosol (
respiratory droplets are main source of virus
, incubation 48 hours), contaminated fecal material
Secondary E. coli infection
Newcastle disease - causative agent (describe its forms; common name?)? Clinical signs/pathology?
Lentogenic is slow/avirulent form, mesogenic is medium/sometimes virulent, velogenic is FAST & VIRULENT (called Exotic Newcastle Disease aka END; can be viscerotropic or neurotropic)
Clinical signs are widely varying based on viral virulence & tropism and host immune status
1. Viscerotropic velogenic form causes hemorrhagic necrosis, gasping, rales, edema of head/neck, conjunctivitis, ocular discharge, anemia, GI signs, greenish diarrhea (GI form can be very virulent w/ acute high mortality)
2. Neurotropic velogenic form causes necrosis of glial cells, neuronal degeneration, perivascular cuffing, & hypertrophy of endothelial cells --> causes respiratory destress & NEURO SIGNS (wing & leg paralysis, torticolis, muscle spasms)
Newcastle disease - transmission? Shedding when/how long? Where can this virus hang out? Prevention? Diagnosis? Zoonosis?
Inhalation or ingestion (virus shed in all secretions, shedding starts 2-3 days after exposure, shed for weeks), mechanical transfer (feed, water, fomites)
Virus stable in environment (carcass of infected bird, wild birds asymptomatic & there are asymptomatic carriers)
Prevention via litter management; vaccine only for lentogenic form, NOT for velogenic form (the one that actually kills birds)
Dx via virus isolation (embryonated egg), ELISA, HI, real time PCR
Zoonotic (self limiting conjunctivitis)
Bumblefoot - condition name? Causative agents? lesions/clinical signs?
Plantar pododermatitis (Staph aureus, coliforms, others)
Penetrating wound/pressure necrosis
Lameness, swelling, heat, hard pus filled abscesses, black scabs
Marek's disease - causative agent (describe it & the lesions it creates). Pathogenesis/age of birds affected?
Gallid herpesvirus 2 (viral tumor producing disease; contagious lymphoproliferative disease of chickens)
Clinical signs depend on where tumor is: cutaneous, ocular, visceral, neural (usually paralysis of wings & limbs due to peripheral nerve involvement, Classical Marek's disease) forms
Pathogenesis (visceral form) - 6-12 week old birds, diffuse infiltration of internal organs w/ neoplastic lymphoid cells (liver, spleen, kidneys, brain, spine, death)
Pathogenesis (neural form) - Range paralysis; commonly birds <14 weeks old, lymphomatous lesions/lymphoid tumors (peripheral nerves often affected via demyelination; nerves 2-3x normal size), occurs 2 weeks-months post infection
Marek's disease - transmission/shed when/how?
Virus shed 2-3 weeks post infection, lifetime shedders (follicle cells/chicken dander for several months; most susceptible in first few weeks of life)
Transmission via inhalation, direct & indirect contact (NO EGG TRANSMISSION)
General ways to prevent diseases in backyard poultry?
Litter management, all in all out (don't add new additions unless tested & quarantines), don't commingle with other birds, know disease status of egg/chick supplier, control pests (other birds, rats, etc), restrict visitors & promote cleanliness
Causative agent of ovine interdigital dermatitis
Causative agent(s) of ovine footrot/contagious footrot of sheep
& maybe Fusobacterium necrophorum & maybe Spirochetes & Truperella pyogenes
Causative agent of strawberry footrot?
What environmental/weather factors predispose ruminants to footrot & why?
Damp wet weather (these pathogens are found in the environment; if skin in tact, it's okay but if disruption in skin like trauma or wet weather then these pathogens enter the hoof/skin)
Causative agent of contagious ovine dermatitis?
Fusobacterium necrophorum in sheep - prognosis? What happens/clinical signs? What part of body involved? Describe this organism. Virulence factors. Natural habitat?
Redness/ulcers in interdigital area (hoof NOT involved) & you see immune response to overcome bacteria and its toxins; DON'T REALLY SEE MUCH LAMENESS
Resolves in ~1 week
G- pleomorphic rods/filaments, non spore forming, obligate anaerobe
Virulence factors - LPS (endotoxin) & cytotoxin (leukotoxin)
Natural habitat - mucus membranes & GIT
Dichelobacter nodosus - clinical signs/lesions? Describe this pathogen & its natural habitat. Virulence factors?
Ulcers/redness/moistness/nastiness in skin around hoof & hoof/foot (super contagious) with invasion of hoof sole; undermining & separation of hard horn especially in rear hooves & IT STINKS & VERY VERY LAME
G- obligate anaerobe, non spore forming
Natural habitat - primary pathogen of epidermal tissues of hoof region, survives a few days in mud
Virulence factors -
(fimbriae is major virulence factor & highly immunogenic so stimulates a major immune response), exotoxin (extracellular protease & elastase), LPS (endotoxin)
Dichelobacter nodosus - discuss virulent vs. benign strain in terms of virulence factors
Adhesions - fimbria, love interdigital epidermis
Exotoxin - extracellular proteases & elastases, damage interdigital epidermis, keratolytic, separates horn & lamina
Benign vs virulent strains may have none, all, or a mix of these virulence factors
Pathogenesis of Dichelobacter nodosus - what happens/where does the bacteria come from?
1. Disruption of normal skin (like from environmental moisture --> maceration of interdigital skin & sand/stones can cause mechanical skin damage)
2. Colonization of wound (F. necrophorum in environment, D. noodles from subclinical, acute, & chronically infected contaminated sheep
3. Development of anaerobic conditions (vascular breakdown, inflammation, O2 utilization by anaerobes)
4. Separation of horn from underlying lamina virulent strains
Dermatophilus congolensis - causes what condition? Describe the causative agent. Sources/habitats/what is the primary source of infection? What predisposes sheep to this infection?
G+ rod or filament, aerobe
Natural habitat is skin or crusts in environment for 42 months, chronically infected carrier animals are reservoirs & primary sources of infections
Moisture/rain predisposes sheep to this infection
Pathogenesis of Dermatophilus congolensis
Moisture in environment facilitates development of motile zoospores & zoospores enter tissues
Filaments/hyphae allow for penetration/transmission/spreading/inflammation
Becomes cyclic & self perpetuating
List diseases/conditions caused by Dermatophilus congolensis
Strawberry footrot, greasy heel, rain scald, rain rot, lumpy wool
Describe diagnostics for foot infections. Prevention of all foot problems? Can any be eradicated?
Clinical signs, culture (interpretation difficult, contamination can be caused by commensals from environment), scabs/crusts for D. congolensis (G+ with railroad track appearance)
Prevent via prioritizing foot/skin health (foot baths, minimize skin trauma) & vaccination, or selective culling for D. nodosus
Can eradicate Dichelobacter nodosus
Causative agent of interdigital dermatitis in cattle?
Causative agents of bovine interdigital necrobacillosis?
Fusobacterium necrophorum & Prevotella melaninogenica & Truperella pyogenes
Causative agents of bovine footrot?
Fusobacterium necrophorum & Prevotella melaninogenica & Truperella pyogenes
Causative agents of bovine digital dermatitis?
Fusobacterium necrophorum, Prevotella melaninogenica & Spirochetes
Causative agents of papillomatous digital dermatitis in cattle?
Fusobacterium necrophorum, Prevotella melaninogenica & Spirochetes
Causative agents of hairy heel warts in cattle?
Fusobacterium necrophorum, Prevotella melaninogenica & Spirochetes
Causative agents of strawberry foot in cattle?
Fusobacterium necrophorum, Prevotella melaninogenica & Spirochetes
Clinical signs of Dichelobacter nodosus in cattle?
Mild soft tissue swelling w/ only slight or no lameness
Fusobacterium necrophorum in cattle - natural habitat?
Mucus membranes, mouth, GIT
Pathogenesis of F. necrophorum in cattle. virulence factors?
Disruption of normal skin, colonization of wound, development of anaerobic conditions
Surface virulence factors are
, flagellum, fimbria or pilus, or
(LPS, hemaglutinin, hamolysins, dermotoxins); also has secreted exotoxins like leukotoxin (virulence correlated to amount)
Do we have Brucella abortus and B. suis in Texas?
YES (in wildlife; commercial herds are free of it...for now)
Why is there a national Brucellosis eradication program in place? (most important reason?)
ZOONOTIC DISEASE (main reason), reduce abortions/disease in cattle, pasteurization of milk (humans mostly get Brucella meletensis from small ruminants & it get destroyed in pasteurization process)
Cattle testing program for Brucellosis in TX performed when?
Change of ownership (livestock markets, special sales, private treaty sales) & passive slaughter surveillance
Main species affected (aka reservoirs) by Brucella abortus, B. melitensis, B. suis, canis, ovis
Brucella abortus - CATTLE, BISON, ELK, somewhat camels & yaks
B. melitensis - SMALL RUMINANTS, also camels, alpacas, llamas
B. suis - PIGS, also cattle & caribou & dogs
B. canis - DOGS
B. ovis - SHEEP
Which form(s) of Brucella are most zoonotic to humans? (& how infected?)
B. melitensis >> B. suis >> B. abortus > B. canis
Aerosol (esp. hunters with B. suis while harvesting wild hogs; ingesting contaminated meat or milk, direct contact)
Describe card test for Brucellosis. Describe 2 types of vaccines for Brucella.
Card test (serological test) looks for Abs to O Ag (on LPS) & agglutinates if +
Strain 19 vaccine (smooth strain; has O Ag present) is used worldwide except in US & it interferes with card test
RB51 vaccine (rough strain; lacks O Ag) used in US & doesn't interfere with card test
Diagnostics for Brucella?
Card test (screening since cross reactions with O Ag of other G- bacteria possible so get lots of false +s; low PPV & high NPV so high sensitivity & low specificity) + CULTURE (gold standard; confirmatory test; tells species & biovar; high PPV & low NPV)
List some types of serological tests
Agglutination (like card test), AGID, ELISA, CFT, FP
Prevalence of Brucella in TX. How does this affect PPV & NPV?
LOW prevalence so means PPV very low & NPV quite high
Is the card test a good test for Brucellosis? Explain
Depends on outcome we are looking for
Yes - if using it as a screening test & we are testing in series (with a test with a higher specificity like a culture as a confirmatory test)
No - if you're looking for true +s (because there are so many false +s)
Brucella prefers to attack what types of tissues? What samples should we take to test for Brucellosis?
Repro tissues like testes, uterus, placenta, etc
Test repro tissues, lymph nodes, blood samples
Describe pathogenesis of Brucella abortus
Ingestion (repro tissues like placenta, etc) by mature susceptible bovid --> lymph nodes --> carried by macrophages to blood (bacteremia) --> uterus, mammary gland, spleen, lymph nodes, testes --> abortion, shed in milk, shed at parturition, shed in semen
How could cow get Brucella suis?
Clinical signs of Brucella canis in dogs?
Diskospondylitis, synovitis, osteomyelitis, polyarthritis, meningoencephalitis, glomerulopathy, anterior uveitis, enlarged prostate, enlarged spleen, orthitis, epididymitis, infertility, abortions
What form (smooth or rough) of Brucella are B. abortus, B. suis, B. meletensis, & B. canis? What do smooth/rough forms mean?
B. abortus, meletensis, suis are smooth (express O side chain of LPS)
B. canis are rough (means doesn't express O side chain on surface)
Diagnostic testing for Brucellosis in dogs?
Serology (IFA, slide agglutination, AGID)
Types of Brucella that dogs can get?
B. canis & B. suis (from boar hunting)
This set is often in folders with...
Infectious Diseases Exam 1
Infectious Diseases - Fish, Reptile, & Amphibian P…
Exotic bird/Poultry Diseases
Infectious Diseases Exam 3
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