Exam 2 Flashcards
(222 cards)
1
Q
Why is microbiota an essential part of life?
A
It allows us to digest food, promotes development, and prevents other bacteria from colonizing.
2
Q
How does microbiota contribute to disease?
A
When it overgrows due to an opportunity it creates disease.
3
Q
What is the function of the bacteria’s capsule?
A
Allows it to avoid phagocytosis.
4
Q
What is the function of the bacteria’s cell wall?
A
It is rigid and contains peptidoglycan which protects the bacteria from being phagocytized.
5
Q
What is the function of the bacteria’s cell membrane?
A
It is made of a lipid bilayer that control diffusion into and out of the cell.
6
Q
What is the function of pili?
A
It is made of F antigen and aids in adhesion.
7
Q
What is the function of flagella?
A
It is made of H antigen and used for movement.
8
Q
What are the two major spore-forming genera?
A
Bacillus and Clostridium
9
Q
What is the sporulation cycle?
A
Endospores are made to protect the genetic information when the environment isn’t suitable for the bacteria.
10
Q
What is the vegetative cycle?
A
Endospores become normal cells when the environment is suitable and begin replicating and dividing again.
11
Q
How does extracellular enzymes aid in immune system evasion?
A
Faciliate invasion and spread.
12
Q
What are endotoxins?
A
Toxins secreted when a cell is lysed and spreads.
Only secreted by gram negatives.
LPS
Less specific and potent.
13
Q
What are exotoxins?
A
Toxins secreted by bacteria when it is alive.
Secreted by both gram positives and gram negatives.
More specific and potent.
14
Q
What are molds?
A
Filamentous mycelium made of hyphae.
15
Q
What are yeast?
A
Unicellular, round to ovoid, and asexual.
16
Q
What is a dimorphic fungi?
A
Fungi that is a mold in one environment and yeast in another.
17
Q
What is the components of a fungal cell wall?
A
Chitin, glucans, and mannans.
18
Q
What is the function of the fungal cell wall?
A
Provides shape and rigidity, and protects from osmotic forces.
19
Q
What are the components of a fungal cell membrane?
A
Ergosterols.
20
Q
What is the function of the fungal cell membrane?
A
Regulates intake and secretion of solutes.
21
Q
What is SIRS?
A
Systemic inflammatory repsonse syndrome.
Excessive inflammatory reaction.
22
Q
What is sepsis?
A
SIRS caused by infection.
23
Q
What is shock?
A
Acute circulatory failure and persistent arterial hypotension despite volume resuscitation.
24
Q
What is MODS?
A
Multiple organ dysfunction.
Results in hypoperfusion and end organ dysfunction.
25
What is DIC?
Disseminated intravascular coagulation.
Results in microvascular thrombosis and bleeding out.
26
What is the morphology of Streptococcus spp.?
Gram-positive cocci.
Associated with abscess formation and suppurative inflammation.
Arranged in chains.
27
What is the morphology of Staphylococcus spp.?
Gram-positive cocci.
Associated with abscess formation and suppurative inflammation.
Arranged in clusters.
28
What is the morphology of Escherichia?
Gram-negative facultative anaerobic rod.
Causes intestinal disease.
29
Describe Mycoplasma haemofelis
Gram-negative bacteria that lack a cell wall.
Common in outdoor male cats.
Often subclinical, but can present with weakness, pallor, tachypnea, tachycardia, and collapse.
Causes feline infectious anemia that is cyclic.
30
What is the diagnostics for Mycoplasma haemofelis?
Clinical signs, bloodwork, and blood smear.
If found on a blood smear continue looking for another cause if it is an incidental finding.
31
What is the treatment for Mycoplasma haemofelis?
Doxycyline, enrofloxacin/pradofloacin, and supportive care.
32
How is Mycoplasma haemofelis transmitted?
Fleas and cat bite wounds.
33
Describe Ehrlichia canis
Causes canine monocytes ehrlichiosis.
Targets monocytes, macropahges, and some lymphocytes.
Can be an acute infection, persistent subclinical infection, or chronic infection leading to death.
34
What is the diagnositics of Ehrlichia canis?
Morulae in cells (rare), PCR, or ELISA (detects exposure not active infection).
35
What is the treatment of ehrlichia canis?
Doxycycline and supportive care.
Tick prevention to prevent.
36
Describe Rickettsia rickettsii
Causes rickettsiosis.
Targets vascualr endothelial cells.
Clinical signs: vasculitis with wide range of signs (fever, depression, muscle and joint pain, edema, coughing, etc.).
Zoonotic.
37
What is the diagnostics of rickettsiosis?
Increasing antibody titer or PCR.
38
What is the treatment of rickettsiosis?
Doxycycline, tick prevention, and supportive care.
39
Describe Francisella tularensis
Non-spore forming, gram negative coccobacillus.
Targets macrophages.
Causes bacterial septicemia, fever, lethargy, and anorexia.
Common in outdoor cats with acute lymphadenopathy, malaise, and oral ulcers.
Zoonotic.
40
How is Francisella tularensis transmitted?
Aerosolized: dust or mowing over dead infected animals.
Direct contact/ingestion: contaminated water or touching animal.
Arthropods: ticks and deer flies.
41
Describe Type A Tularemia
Highly virulent.
Found in North America.
42
Describe Type B Tularemia
Less virulent.
Located in North America, Europe, and Asia.
43
What are the pathologic lesions found with Tularemia?
Miliary whtie foci of liver necrosis.
Palpable mesenteric lymph nodes.
Multifocal splenic necrosis.
44
What are the diagnostic appraoches with Tularemia?
Culture
4 fold increase in antibody titers.
PCR
Lymph node aspirate/biopsy.
45
What is the treatment for Tularemia?
Isolation, supportive care, tetracycliens, fluoroquinolones, streptomycin, and gentamicin.
46
Describe Bacillus anthracis
Causes anthrax.
Gram-positive, facultative anaerobic, encapsulated, spore-forming saprophyte.
Causes acute septicemia with high fatality and hemorrhagic lymphadentiis.
47
What are the forms of Anthrax?
Inhalation: mediastinal lymph node lesions.
Cutaneous: biting flies.
Ingestion: soil, water, feed/hay.
48
What are the common lesions of Anthrax?
Blackberry jam liver.
Hemorrhages
Bloody discharge
Failure of blood to clot.
Delayed or incomplete rigor mortis.
49
What are the diagnositic approaches to Anthrax?
Report if you suspect.
Blood sample from ear or tail.
Liver culture
PCR
50
What is the tripartite exotoxin of Anthrax?
Protective antigen: makes pore in cell.
Lethal factor: prevents cytokine release while promoting cytokine production, until the cell swells and bursts.
Edema factor: releases fluid causing edema.
51
Describe Corynebacterium pseduotuberculosis
Gram-positive, facultative intracellular coccobacilus.
Causes caseous lymphadenitis.
52
What are the two forms of caseous lymphadenitis?
External and Internal
53
Describe external form of CL
Peripheral lymph node abscess.
May mature and drain.
Sheep: caseous material.
Goats: pasty exudate.
Recurrence and scarring are common.
54
Describe internal form of CL
Internal organ involvement.
Most common in sheep.
Causes chronic weight loss and lung abscesses (cough, fever, and tachypnea).
55
What is the management of caseous lymphadentitis?
The best option is to cull before transmission to the herd takes place.
Could do intralesional and/or systemic antimicrobial off-label.
Drain the abscess and rinse with idodine.
Isolate from the herd.
56
Describe Anaplasma marginale
Gram-negative, small intracellular bacteria at margin of erythrocytes.
Causes bovine anaplasmosis.
Common in Bos indicus breeds and adult cattle.
Calves have maternal immunity, but if they are infected they are more than likely carriers.
Causes progressive anemia which is the extravascular destruction of infected and uninfected RBCs.
57
What are the signs for bovine anaplasmosis?
Weight loss, inappetence, breathlessness, loss of coordination, rapid bounding pulse, fever, pale MM, icterus, and sudden death.
58
What are the diagnostics of bovine anaplasmosis?
Clinical signs and cELISA test.
59
What is the treatment of bovine anaplasmosis.
Tetracycline or imidocarb and supportive care.
Can get veterinary feed directives or chlortetracycline to reduce clinical disease.
60
How can Anaplasma marginale be transmitted?
Mechanical: fomites like reused needles.
Biological: ticks.
61
What are the mechanisms by which skin acts as an immunologic agent?
Keratinization, Langerhans cells, basement membrane, sebum, T cells, dermal dendritic cells, and commensal microbes.
62
What is the importance of identifying potential predisposing factors to any infection?
They have to be addressed when treating the infection.
63
What is the most common bacteiral isolate of canine pyoderma or canine bacterial folliculitis?
Staphylococcus pseudointermedius.
64
What are the predisposing factors to pyoderma?
Allergies, ectoparasites, dermatophytes, endocrinopathy (diabetes mellitus and Cushing's), trauma/foreign body, skin folds, and seborrhea.
65
Describe surface pyoderma
Affects the stratum corneum.
Presentation: hot spots.
Responds well to topical antimicrobials like chlorhexidine-containing shampoos.
66
Describe superficial pyoderma
Affects the epidermis and hair follicles.
Presentation: papules, pustules, epidermal collarettes, erythema, and crusting.
Treat with topicals unless it is too widespread then add systemic antimicrobials.
67
Describe deep pyoderma
Affects the epidermis, dermis, and subcutis.
Common in German Shepherds.
Treat with systemic and topical antimicrobials.
Usually needs extended therapies.
68
How are dermatophytes transmitted?
Direct contact, environmental, or fomties.
Arthroconidia are being transmitted not macroconidia.
69
Are dermatophytes zoonotic?
Yes
70
What skin layer is most affected by Dermatophytosis?
Stratum corneum of skin, hair, and claws.
71
What do dermatophytosis lesions look like?
Circles or rings.
72
Describe Wood's lamp diagnostics
Only detects Microsporum canis on and in hair.
Lots of false positives and negatives.
Used for screening.
73
Describe KOH prep diagnostics
Identifies ecto and endothrix.
Dissolves keratin to look for arthroconidia.
Macroconidia seen are contaminates.
74
Describe DTM culture
Take the sample and firmly press into the middle of the container.
If the media turns red in 5 days, it is dermatophytes.
If the media turns yellow, it is contaminates.
If it is yellow and then turns red, it is contaminates.
75
What is the treatment for dermatophytosis?
Miconazole-chlorhexidine shampoo and lime sulfur dips.
76
Describe Actinomyces
Commensal of oral and urogenital mucosa.
Can be a cutaneous or systemic infection that results in pyothorax, peritonitis, serositis, and discospondylitis.
Responds well to penicillins.
Good prognosis.
77
Describe Nocardia
Soil saprophyte which opportunistically causes infection.
Can have abscess to mycetoma-like lesion on limbs or trunk that can invade deeper and may disseminate.
Difficult to treat because it is resistant to a lot of antimicrobials.
Prognosis is guarded.
78
How do you tell the difference between actinomyces and nocardia?
Culture to tell.
79
What is mycetoma?
Chronic, subcutaneous lesion with granulomatous inflammtion, nodules, draining sinuses, and exudate-containing sulfur granules.
80
What is a sulfur granule?
Aggregate of microorganisms mixed with inflamamtory debris.
81
What are the common features associated with subcutaneous mycoses?
Chronic, granulomatous, saprophytic, trauma initiated, local, slow spread, and have poor therapy response.
82
What do oomycetes and zygomycetes result in?
Eosinophilic pyogranulomatous inflammation.
83
What is the etiologic agent of Rain Rot in horses?
Dermatophilus congolensis, which is a gram positive, filamentous branching rod.
84
What do the lesions of Rain Rot look like?
Paint brush lesions (exudative dermatitis) with easily removed hair matted with exudate.
85
What is the most common form of sporotrichosis in horses?
Lymphocutaneous.
86
Describe lymphocutaneous form of sporotrichosis.
Lymphangitis +/- open skin lesions.
Non-painful, non-pruritic nodules along lymphatics which may ulcer and become painful.
Common on distal limbs.
87
Describe lesions of equine pythiosis
Caused by phythiosis insidiosum.
Also caused swamp cancer.
Pruritic lesions on ventral abdomen and limbs containing kunkers which are irregular, yellowish concretions that form in tracts.
88
What is the most common ringworm in cattle?
Trichophyton verrucosum.
89
Describe the pathogenesis of Lumpy Jaw
Caused by actinomyces bovis
Initiated by oropharyngeal trauma.
Moves into bone and causes osteomyelitis and mycetomas of the mandible and maxilla.
90
What is the treatment of Lumpy Jaw?
sodium iodide administered IV with concurrent administration of oxytetracycline +/- surgical debridement to slow progression.
91
What etiologic agent causes exudative epidermitis/greasy pig disease?
Stahylococcus hyicus.
92
What is the typical signalment of Staphylococcus hyicus?
Pigs less than 8 weeks old.
93
How does greasy pig disease result in death in more severe cases?
Dehydration and protein loss.
94
What is the difference between exudative epidermitis and swine erysipelas lesions?
Exudative epidermitis causes brownish spots on head that enlarge, coalesce and spread posteriorly.
Where swine erysipelas causes diamond skin lesions.
95
What is the difference between exudative epidermitis and swine erysipelas lesions?
Exudative epidermitis causes brownish spots on head that enlarge, coalesce and spread posteriorly.
Where swine erysipelas causes diamond skin lesions.
96
How does breed play a role in canine interdigital furunculosis?
Short, bristle-haired breeds will have trauma caused by their hair.
97
How do you treat canine interdigital furunculosis?
Topical and systemic antimicrobials like deep pyoderma.
98
What two bacterial agents contribute to foot rot in ruminants?
Fusobacterium necrophorum and Dichelobacter nodosus.
99
Describe the lesions of ruminant foot rot
Located in the interdigital space and coronary band.
Will have erythema and swelling that progresses to pain, foul odor, and lameness.
In severe cases, systemic signs are possible.
100
What two bacterial agents are associated with foot abscess in sheep and cattle?
Fusobacterium and Trueperella.
101
What causes otitis?
Overgrowth of normal flora especially staphylococci and Malassezia.
102
What are some gram negative agents that can be isolated from otitis?
Pseudomonas aeruginosa, E. coli, proteus, and Pasteruella spp. (in cats).
103
Describe otitis externa
Involve the external ear canal: vertical and horizontal canals, and tympanic membrane.
Signs: pruritus, head shaking, erythematous canal, discharge, and aural hematomas.
104
Describe otitis media
Involves tymapnic bulla.
Signs: Horner's syndorme, facial nerve paralysis, and ruptured tymapnums.
105
Describe otitis interna
Involves the cochlea.
Signs: vestibular signs and hearing loss.
106
What is mastitis?
Inflammation of the mammary gland.
107
What causes mastitis?
Staphylococci, streptococci, and coliforms like E. coli and Klebsiella.
108
What are possible sources for contagious mastitis?
Fomites
109
What are posisble sources for environmental mastitis?
Bedding, teat dips, infusions, water, and flies.
110
Describe subclinical mastitis
Most common.
No visible signs but there will be production loss.
Diagnosed via California mastitis test.
111
Describe mild clinical mastitis
Visibly abnormal milk.
Localized udder inflammation.
112
Describe chronic masitis
Often subclincal but can have mild signs appear.
Udder atrohpy and fibrosis.
Hard to cure.
113
Why does etiologic diangosis matter when treating mastitis?
You need to treat the animal as well as what is spreading the infection.
114
Describe the upper respiratory tract
Conducts air, smell, and voclaization.
Has a similar microbiome to lungs.
Sampling techniques: nasal wash/swab or biopsy, and nasopharynx swabs/biopsies.
115
Describe lower respiratory tract
Conducts air and gas exchange.
Essential sterile.
Sampling techniques: transtracheal wash, bronchoalveolar lavage, lung aspirates, and percutaneous lung biopsies.
116
What are the protective mechanisms utilized in the respiratory tract?
Mucus, cilia, mucociliary elevator, coughing and sneezing, innate immune response, and alveolar macrophages.
117
What are some predisposing factors to ciliostasis?
Muzzle length, allergies, viruses, temperature extremes, smoke, and ammonia.
118
What immunoglobulin is produced with intranasal vaccinations?
IgA
119
What immunoglobulin is produced with parenteral or injectable vaccines?
IgG
120
What procedures or factors predispose an animal to sinusitis?
Dental disease, upper respiratory viral infections, trauma, nasal tumors, and dehorning.
121
What bacterial and/or fungal agents are responsible for sinusitis in dogs?
Bordetella bronchispetica, Aspregillus fumigatus,a nd Rhinosporidium seeberi.
122
What bacterial and/or fungal agents are responsible for sinusitis in cats?
Cryptococcus neoformans, Mycoplasma spp., and Chlamydophila spp.
123
What bacterial and/or fungal agents cause sinusitis in horses?
Streptococcus spp., Aspergillus spp., and Phycomycetes.
124
Described canine fungal rhinosinusitis
Caused by Aspergillus spp.
Common in dolichocephalic breeds.
Causes epistaxis, nasal pain, ulceration, sanguineopuruluent nasal discharge, and destruction of turbinates.
125
How do you diagnose canine fungal rhinosinusitis?
Clinical signs, rhinoscopy and biopsy, cultures, and radiographs.
126
How do you treat canine fungal rhinosinusitis?
Under general anesthesia you debride the area dn give topical infusions of itraconazole.
127
What are the common signs of cryptococcosis?
Nasal form: granulomatous lesions and masses, sneezing, nasal discharge, and ulcerative lesions.
CNS form: sudden blindness, seizures, behavioral changes, and granulomatous encephalomyelitis.
Cutaneous: alopecia and non-prurutic, non painful dermal or subcutis nodule(s).
Systemic: hematogenous dissemination to CNS, eye, joints, lymph nodes, kidneys, etc.
128
How do you diagnose cryptococcosis?
Clinical signs, CT/MRI, PCR, cytology or histology, or latex agglutiantion test.
129
What is the treatment for cryptococcosis?
Excision and debulking.
Polyenes and azoles.
130
What is the difference of prognosis for dogs and cats with cryptococcosis?
Dogs: guarded because it disseminates offten = multifocal CNS signs.
Cats: good because it is nasal = pneumonia or extended to ocular and CNS tissue.
131
What is the pathogenesis of Cryptococcus neoformans?
Inhale encapsulated yeast from enviornment.
Capsulation in vivo evades phagocytosis.
Infects nasal mucosa.
Mild disease or expansive granulomas +/- mengoencephalitis and pneumonia.
132
What is a possible cuase of polypoid nasal granulomas?
Rhinosporidosis.
133
What are the probably bacterial etiologies for pneumonia in dogs and cats?
Bordetella bronchiseptica, staphylococcus spp., streptococcus spp., E. coli, Pasteruella spp., Klebsiella spp., proteus spp., pseudomonas aeruginosa, and Mycoplasma spp.
134
Describe cranioventral bacterial pneumonia
Bacteria from oral cavity and pharynx enter via airways and settle into right middle lung lobe.
135
Describe Bordetella bronchiseptica
Gram negative coccobacillus.
136
What role do shelters play in the spread of Bordetella bronchiseptica?
It spreads easily through co-mingled dogs, so those that aren't vaccinated at the shelter have a higher risk of getting it and spreading it to others.
137
What does Bordetella's tracheal cytotoxin do?
Paralyzes cilia by targeting their mitochondria.
138
What does Bordetella's adenylyl cyclase do?
Blocks phagocytosis of macrophage/neutrophil.
139
What does Bordetella's adhesins do?
Adhere it to the upper respiratory eptihelial cells.
140
What is the treatment for infectious tracheobronchitis?
Cough suppressants if needed.
Give doxycycline for 7-10 days if they have fever, lethargy, and mucopurulent nasal discharge.
141
What is the treatment for Bordetella pneumonia?
Empirical doxycycline while waiting on culture.
Supportive care and hospitalizaiton.
142
What other disease is caused by Bordetella bronchiseptica?
Atrophic rhinitis in swine.
143
What is atrophic rhinitis?
Damage of osteoblasts of nasal turbinates resulting in regenerative turbinate atrophy in young pigs.
144
What are the 4 etiologies that can cause fungal pneumonia in dogs and cats?
Histoplasma capsulatum.
Blastomyces dermtitidis.
Coccidioides immits
Cryptococcus neoformans
145
Why is it ill advised to attmpt to culture respiratory mycoses in clinic?
They spread through inhalation, so they are very hazardous.
146
Describe granulomatous disease
Lots of neutrophils
147
Describe Histoplasma capsulatum
Located in Missouri, Ohio, and Mississippi River valley.
Morphology: yeast in macrophages.
Bird droppings and bat guano promote frequency.
Signs: weight loss, fever, +/- cough, icterus, pale MM, anemia of chronic disease, and diarrhea in dogs.
Dissemination: GI tract, liver, spleen, eye, and bone marrow.
History: cats (respiratory disease and icterus) and dogs (GI disease).
148
Describe Blastomyces dermatitidis
Located on the east coast and Oregon and Washington area.
Large, broad-based, and thick-walled.
Proximity to water promotes frequency.
Signs: chronic disease (persistent cough, depressed mentation, fever, and weight loss.
Dissemiantion: lymph nodes, skin, eyes, and bones.
149
Describe Coccidioides immits.
Located in the southwest states.
Very large, round, double-walled spherules with internal endospores.
Outbreaks seen with earthquakes, dust storms, and farming.
Signs; cough, fever, anorexia, lameness, draining skin lesions, and ocular infections.
Dissemination: lymph nodes, bone, and skin.
150
What are the diagnostics of pulmonary mycoses?
Identify organism: aspirate, biopsy, or impression smears.
Culture: at lab bc it is hazardous.
Antigen testing on urine, serum, and CSF.
151
Explain relevance of equine guttural pouch anatomy.
Large diverticula off Eustachian tube with a cartilaginous flap acting as a gate, so just about anything can get in.
Cranial nerves and arteries pass through it.
152
What cranial nerves pass through the guttural pouch?
Facial, glossopharyngeal, vagus, accessory, hypoglossal, pharyngeal plexus, cranial laryngeal, and mandibular.
153
What arteries pass through the guttural pouch?
External carotid, internal carotid, and maxillary.
154
How does guttural pouch mycosis result in severe epistaxis?
Fungal plaques form over internal carotid artery and eat through the membrane causing it to bleed profusely.
155
Describe Streptococcus abscess formation.
It enters tonsillar crypts and spreads to lymph nodes.
Lymph nodes abscess and drain into the guttural pouch. Describes
156
Describe Strangles
Affects horses, donkeys, and mules.
High morbidity, low mortality.
Presentation: depression, anorexia, fever, lymph node enlargement, and mucopurulent nasal discharge.
Lesions: lymph nodes with abscesses and retropharyngeal nodes may drain into guttural pouches.
157
What sequelae can occur after acute strangles?
Guttural pouch empyema (pus), purpura hemorrhagica (type 3 hypersensitivity), bastard strangles (dissemination to tissues), immune mediate myositis, and suppurative, necrotic bornchopneumonia.
158
Is antibiotics recommended with Strangles?
No because it will prolong the infection and the animal won't develop an immune response which makes things worse later.
Prolongs because it doesn't allow the abscesses to mature and drain.
159
What is the most common cause of equine shipping fever (pneumonia)?
Streptococcus equi zooepidemicus.
160
Describe Rhodococcus equi.
5-10 week old foals.
Causes foal pneumonia - bronchopneumonia or embolic pneumonia.
Presentation: respiratory signs, extrapulmonary signs, and rarely elevated, ulcerated foci of granulomatous colitis and lymphadenitis.
161
What does VapA protien do?
Protects bacteria from being phagocytized by macrophages and promotes proliferation.
162
What does IFN-gamma do?
Activates macrophages and functional T cells, so if it doesn't work like with R. equi, the infection can't be cleared.
163
What role does the mare play in R. equi transmission?
She passes it in her feces, so when the newborn comes out and ingests the mare's feces it becomes infeceted.
164
What are the extrapulmonary signs associated with R. equi?
Uveitis, diarrhea, and synovitis.
165
What screening methods reduce the clinical occurrence of R. equi?
Daily temperatures, biweekly fibrinogen tests, and thoracic ultrasounds.
166
Describe Fusobacterium necrophorum
Gram negative anaerobic rod/filament.
167
What syndromes in production animals does Fusobacterium necrophorum cause?
Necrotic rhinitis, calf diphtheria, ruminant foot rot, and liver abscesses in cattle.
168
What are the signs of calf diphteria?
Anorexia, dspyena, swelling, and cough.
Fibirnonecrotic inflammation of the larynx with possible secondary aspiration pneumonia.
169
How can you prevent calf diphtheria?
Better hygeine, viral vaccines, and avoid rough feed.
170
What bacterial agent is associated with atrophic rhintis?
Bordetella bronchiseptica.
171
What agents are associated with progressive atrophic rhinitis?
Bordetlla bronchiseptica and Pasteurella multocida.
172
What is bovine respiratory disease complex?
combination of a number of pathogens and stressors causing disease
173
Waht bacterial agents are associated with BRD?
Mannheimia haemolytica, Pasteruella mutlocida, Bibersteinia trehalosi, Histophilus somni, Mycoplasma spp., and Trueperella pyogenes.
174
What is the BRD reservoir?
Oropharyngeal, nasopharyngeal, and tonsillar.
175
Describe Mannheimia haemolytica
Gram negative coccobacilli or short rods.
Ruminant disease
Causes severe pneumonia and pleuropneumonia in ruminants, mastitis in ewes, and septicemia in lambs < 2 months of age.
176
Describe Pasteurella multocida
Gram negative coccobacilli or short rods.
Affects ruminants, pigs, dogs, cats, rabbits, birds, and humans.
Causes suppurative bronchopneumonia in ruminants, pigs, dogs, and cats, atrophic rhinitis in pigs, snuffles in rabbits, fowl cholera in birds, and bite wound contamination in humans, dogs, and cats.
177
Describe Bibersteinia trehalosi
Ruminant only.
Gram-negative coccobacili or short rod.
Causes septicemia in lambs > 2 months of get, pneumonia in bighorn sheep, and sporadic pneumonia in cattle.
178
Describe Histophilus somni
Gram negative coccobacilli or short rods.
causes bronchopneumonia or fibrinous pneumonia, CNS disease, myocarditis, or synovitis.
179
Describe Mycoplasma bovis
Very spherical to filamenotus cells with no cell wall.
Caseus coalescing caseous foci of necrosis sin lungs, otitis media, and fibrous polyarthritis.
180
Describe Trueperella pyogenes
Gram positive coccobacillus.
Affects all domestic species.
Causes abscesses, pneumonia, metritis, and mastitis.
181
Describe Enzootic pneumonia
In preweaning dairy calves < 4 months of age.
Pasteurella multocida is most commonly found.
182
Describe shipping fever
Post-weaning beef calves from 6-18 months.
Acute: Mannheimia haemolytica.
Chronic: mycoplasma bovis and trueperella pyogens.
183
What are the signs for acute shipping fever?
Nasal discharge, dyspnea, cough, depression, anorexia, abnormal lung sounds, and fever.
Cranioventral bronchopneumonia, firbinous pneumonia, or pleuropnumonia.
184
What are the signs for chronic shipping fever?
Weight loss or lack of gain, letharyg, anorexia, and chronic respiratory signs.
Cranioventral fibrosis and abscesses.
185
How can you prevent enzootic pneumonia?
Reduce stresses and predisposing factors via adequate colostrum, immunized dams,good hygiene, appropriate air flow, adequate diet, and avoidance of older cattle.
186
How can you prevent shipping fever?
Control stresosrs, pre-conditioning programs, vaccinations, avoid co-mingling and eliminate persistently infected BVDV cattle.
187
What are the preconditioning programs?
Anthelmintics, vaccinations, nutrition, and spacing fo stressful events/procedures with shipping.
188
What agent is responsibel for cotnagious bovine pleuropneumonia?
Mycoplasma myocides mycoides (small colony).
189
What agent is responsible for enzootic pneumonia of pigs?
Mycoplasma hyopneumoniae.
190
What agent is responsible for chronic repsiratory disease in birds?
Mycoplasma gallisepticum.
191
What agent is responsible for pneumonia in dogs?
Mycoplasma cynos.
192
What agent is responsible for chronic sinusitis in cats?
Mycoplasma felis
193
What country is contagious bvoine pleuropneumonia a disease in?
Africa
194
What agent is associated with bovine tuberculosis?
Mycobacterium bovis.
195
What is a tubercle?
Fibrous capsuel that forms around macrophages that is surrounded by lymphocytes, granulocytes, and other cells when the mycobacteria proliferate and cause hypersensitivity reaction.
196
What do you do if the cudal fold PPD test is positive at 72 hour?
Report
State vet needs to perform cervical fold test.
197
What do you do if the comparative cervical test is positive for Mycobacterium bovis?
Remove animal from herd and do necropsy.
198
What do you do if the comparitive cervical test is positive for mycobacterium avium?
The animal is fine and can stay with herd.
199
What is the most common source for zoonosis of bovine tuberculosis?
Through ingestion of contaminated milk.
200
Describe Actinobacillus pleuropneumoniae
Causes porcine pleuropneumonia.
Affects pigs 2-6 months of age.
Signs: sudden death, severe respiratory distress, fever, and lethargy - peracute, slowed growth rates, concurrent infections, and pleurisy - chronic, and severe fibrinonecrotic and hemorrhagic pneumonia with fibrinous pleuritis that is bilateral.
201
What is peracute porcine pleuropneumonia?
Outbreak in naive herd.
202
What s chronic porcine pleuropneumonia?
Disease established in herd.
203
Describe Psittacosis
Caused by chlamydia psittaci.
Zoonotic and reportable.
204
What is blepharospasm?
Squinting or twitching of eye.
205
What is conjunctivitis?
Inflammation of conjunctiva.
206
What is chemosis?
Edema of eyelids.
Most seen with allergies.
207
What is keratitis?
Corneal inflammation.
208
What is uveitis?
Inflammation of uvea.
209
What is chorioretinitis?
Inflammation of choroid and retina. Fundic exam will be very red and vessels will be prominent.
210
What is corneal ulceration?
Cloudiness over the pupil.
211
What is descemetocoeles?
Deep ulceration on descemet's membrane of the corena.
Looks like skin tag on eye.
Eye is close to rupturing.
212
What are soem etiological agents that cause ocular infections in dogs?
Rickettsial disease, Lepto, Histplasma capsulatum, canine distemper, and canine adenovirus 1.
213
What are soem etiological agents that cause ocular infections in cats?
Chlamydia felis, mycoplasma felis, histplasma capsulatum, cryptococcus spp., FIP, feline herpesvirus01, FIV, and FeLV.
214
What are some etiological agents that cause ocular infections in horses?
Lepto, Aspergillus spp., Fusarium spp., equine viral arteritis, adenovirus, and equine influenza.
215
What are some etioloigcal agents that cause ocular infections in cattle?
Moraxella bovis, Moraxella bovoculi, IBR viurs, and malignant catarrhal fever.
216
What are 3 common differntials for keratoconjunctivitis in cattle?
Also called pinkeye.
IBR, parasitic, foreign bodies.
217
What is the treatment for keratoconjunctivitis?
Oxytet: IM/SC, florfenicol, and tulathromycin.
Subconjunctival penicillin injections.
Eye patch, sew eyelids togther, or suture thrid eyelid over the ulcer.
218
How do you prevent pinkeye in cattle?
Shade access, isoalte infected aniamls, gloves and protective clothing, keep grass low, fly control, and moraxella bovis vaccine.
219
Describe the Moraxella bovis vaccine
Adhesins specific.
Effectiveness is highly variable.
Helps reduce the incidence and virulence of infection.
220
Describe the life cycle of Chlamydia felis
The infectious form (elementary body) enters the cell via endocytosis and is converted to metabolically active and non-infectious reticulate body.
These bodies multiply within membrane-bound vacuoles inside the host cell - latent phase.
Once complete, reticulate bodies revert back to elementary bodies and stimulate lysis and move on to infect other cells.
221
What are the signs of feline conjunctivitis?
Serous nasal discharge, chemosis, blepharospasm, and conjunctival hyperemia.
Can be both eyes or just one.
Infection may persist subclinically.
222
What are some differentials for feline conjunctivitis?
Feline herpesvirus-1
Mycoplasma felis
Feline calicivirus.
