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Bacti Final > Bacti Final Exam > Flashcards

Bacti Final Exam Flashcards

1
Q

What are the characteristics of Clostridium? (gram positive or negative, aerobic or anaerobic, etc)

A

-Gram positive
-rods/bacillus (short rods)
-Anaerobic
-Spore forming (anaerobic transmission)
-Toxin producing

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2
Q

Which clostridium species are histotoxic and which are neurotoxic?

A

-Histotoxic: C. perfringens (also enterotoxic), C. chauvoei, C. haemolyticum, C. novyi. C. septicum
-Neurotoxic: C. botulinum, C. tetani

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3
Q

Which species of Clostridium is both enterotoxic and histotoxic?

A

C. perfringens

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4
Q

Which species of Clostridium is the fastest replicating bacteria?

A

C. perfringens

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5
Q

How are the different subtypes of C. perfringens identified?

A

The type of toxin it produces (toxinotype A-E)

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6
Q

What are the virulence factors for C. perfringens?

A

-Alpha toxin: hydrolyzes the cell membranes
-Perfringolysin O: binds to cholesterol and forms pores resulting in cell death
-Glycosidases and lipases
-Sialidase: removes sialic acid residues from host cells
-capsule

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7
Q

What condition does C. perfringens cause? What are the symptoms of this condition?

A

Gas gangrene: necrotizing cellulitis and myonecrosis, edema, hemorrhage, gas production, toxemia

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8
Q

What are the virulence factors for C. chauvoei?

A

-Alpha toxin: pore forming hemolysin
-Beta toxin: DNAase
-Sialidase: removes sialic acid causing tissue disruption
-Chauveolysin: similar to perfringen toxin, binds cholesterol and causes cell death

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9
Q

What disease does C. chauvoei cause in cattle? Describe what the associated lesions look like.

A

Blackleg: muscles have a dark, emphysematous center with hemorrhage and edema around the outside

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10
Q

What are the symptoms of Blackleg?

A

High fever, lameness, anorexia, visible swelling of affected muscles, affected muscle will have rancid butter odor, sudden death

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11
Q

Where does C. chauvoei reside? How does it get there?

A

Resides in intestine, liver, and other tissues

Ingestion of contaminated feces and then spores travel to liver and other tissues or the bacteria enters externally through a wound (need germination of spores for disease to occur)

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12
Q

Describe the pathogenesis of C. chauvoei.

A

Spores in muscles -> decreased the O2 levels -> anoxia causes bruising and gadding of young cattle (exercise intolerance) germination -> toxin production

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13
Q

How can you diagnose a C. chauvoei infection?

A

-Fecal smear and gram stain
-PCR
-Culture at 37C

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14
Q

How do you treat a C. chauvoei infection? Is there a vaccine available?

A

-There is a vaccine
-Tx is usually unsuccessful, IV penicillin followed by IM

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15
Q

What is the main virulence factor of C. haemolyticum?

A

Phospholipase C

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16
Q

What disease does C. haemolyticum cause in ruminants? What are the symptoms?

A

-Redwater disease
-Clinical signs: hemoglobinuria, fever, pale/icteric MM, abortion, agalactia

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17
Q

Describe the pathogenesis of a C. haemolyticium infection.

A

Ingestion of spores -> travel to liver -> spore germination in liver -> vegetation growth and production of phospholipase C -> hemolytic crisis and rapid death

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18
Q

How do you treat a C. haemolytcum infection? Is there a vaccine available?

A

-Vaccine available in endemic areas
-Treat with broad spectrum abx such as tetracycline and blood transfusion if needed

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19
Q

What are the virulence factors of C. noyvi?

A

-Alpha toxin: breaks down cytoskeleton
-Beta and delta toxins: cell membrane damage

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20
Q

What disease does C. noyvi cause in rams? Describe its pathogenesis

A

-Bighead
-Fighting injury -> activation of spores -> edema in head and neck -> death

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21
Q

What disease does C. noyvi cause in ruminants?

A

Pseudoblackleg: spores get to liver causing hemolytic crisis and death

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22
Q

How do you diagnose a C. noyvi infection?

A

Gram stain liver lesions: large gram positive rods with spores at the ends

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23
Q

How do you treat a C. noyvi infection? Is there a vaccine available?

A

-Toxoid vaccine is effective
-No effective treatment

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24
Q

What condition is caused by C. botulinum? What is the main clinical sign?

A

Botulism, flaccid paralysis

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25
Q

What species does C. botulinum affect?

A

Ruminants, horses, minks, birds

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26
Q

How are the different subtypes of C. botulinum categorized? How many groups are there?

A

There are 7 types based on the type of botulinum toxin produced

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27
Q

How does an animal contract a C. botulinum infection?

A

-Ingestion of botulinum toxin from contaminated plant or animal material
-Ingestion of spores
-Wound contamination

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28
Q

Describe the pathogenesis of a C. botulinum infection.

A

Ingestion of toxin -> absorption into the blood -> toxin enters cholinergic nerve cells -> heavy chain of toxin forms a pore -> light chain hydrolyze the docking proteins -> inhibition of acetylcholine release -> flaccid paralysis

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29
Q

What can occur if C. botulinum affects the respiratory muscles?

A

Respiratory failure -> death

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30
Q

How can you diagnose a C. botulinum infection?

A

-Culture anaerobically on blood agar
-PCR

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31
Q

How do you treat a C. botulinum infection?

A

-Pump stomach
-Antitoxin tx
-Vaccination with toxoid
-Guanidine and aminopyridine to stimulate acetylcholine release (counteracts inhibitory effects of toxins)
-Germane to intensify neural impulses and effects of Ach

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32
Q

Describe the shape of C. tetani.

A

Drumstick or tennis racket shaped with spores on the end

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33
Q

What is the C. tetani toxin called and how is it released?

A

Tetanospasmin, it is released upon lysis of the clostridial cell

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34
Q

What condition is caused by C. botulinum? What are the clinical signs?

A

-Causes tetanus, main clinical sign is spastic paralysis
-Other clinical signs: fecal and urinary retention, high fever and sweating, death (~50% of cases)

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35
Q

Describe the pathogenesis of ascending tetanus.

A

spore is ingested -> spores germinate in anaerobic environment -> toxins are released and absorbed into bloodstream -> toxin binds to nearest cholinergic receptor -> endocytosis brings toxin into the cell -> toxins enter vesicles and travel retrograde up the axon into cell body -> light chain hydrolyzes docking proteins inhibiting the release of GABA messengers -> sustained clonic/tonic spasms

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36
Q

Describe the pathogenesis of descending tetanus.

A

pore is ingested -> spores germinate in anaerobic environment -> toxins are released and absorbed into bloodstream -> toxin ends up in CNS -> generalized tetanus

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37
Q

Which species are more prone to ascending tetanus and which are more prone to descending tetanus? Which type is more dangerous to the animal?

A

Species not prone to tetanus get the ascending type (dogs and cats)

Species more susceptible to tetanus get the descending type (humans and horses)

Ascending type is more severe

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38
Q

How do you diagnose a C. tetani infection?

A

-Culture wound exudate on blood agar and look for hemolysis and swarming motility
-PCR

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39
Q

How do you treat a C. tetani infection?

A

-Antitoxin injection
-Toxoid vaccination
-Sedatives and muscle relaxants
-Penicillin or metronidazole

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40
Q

What are the two AST test methods? Which one measures a zone of inhibition and which measures a minimum inhibitory concentration?

A

-Kirby Bauer: measures a zone of inhibition
-Broth microdilution: measures a minimum inhibitory concentration

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41
Q

How do you interpret a broth microdilution plate (how do you determine what the MIC is)?

A

The first concentration without a dot in the well is the MIC for that drug (if you see a dot that means there is bacterial growth)

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42
Q

The “rules” in the CLSI guidelines are based on what?

A

Rules are based on the expected serum concentration if the drug is given systemically

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43
Q

What are two reasons why you would get a no interpretation (NI) result for a drug on an AST?

A

-There is no rule for that host-bug-drug scenario
(Ex: there are very few drugs that have had sensitivity tests done in camels, but you can extrapolate data from related species)

-The concentrations tested in lab do not align with the interpretation guidelines
(Ex: the rules say the concentration range is 2-20 but the concentrations on your plate only go from 8-20)

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44
Q

Why is the drug with the lowest MIC not always the best drug to use?

A

Each drug is evaluated at different concentrations and have different rules so you cannot compare their MIC values to each other

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45
Q

What is the mechanism of resistance for MRSA? What drugs is it resistant to?

A

-Resistant to Oxacillin and Penicillin… therefore resistant to all beta lactams
-MRSA has the MecA gene which codes for an altered PBP target protein that beta lactams cannot bind to

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46
Q

In general, what are the AST rules for topical drugs?

A

There are no rules for topical drugs, they are established based on expected serum concentrations if the drug is given systemically

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47
Q

In general, what are the AST rules for drugs to be used in birds?

A

-No rules for birds
-Enrofloxacin is illegal for use in birds

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48
Q

What pathogen(s) is/are most likely to cause equine mastitis?

A

Staph spp

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49
Q

Describe the distribution of equine mastitis.

A

usually unilateral

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50
Q

What pathogen(s) is/are most likely to cause canine or feline mastitis?

A

E. coli, staph, and strep

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51
Q

What factors are associated with mastitis in canines and felines?

A

-Ascending infection
-Trauma
-Unsanitary environment

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52
Q

What is the difference between clinical and subclinical mastitis in dairy cows?

A

-Clinical: visible changes to milk and udder, and decreased production
-Subclinical: no visible changes to milk or udder, may or may not have decreased production

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53
Q

When testing for mastitis, what cell type are you testing for? What number indicates mastitis is present?

A

Testing for somatic cells, >200,000 cells/ml indicates mastitis

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54
Q

What is the difference between contagious and environmental mastitis?

A

-Contagious mastitis can spread from cow to cow
-Environmental mastitis is contracted through the environment

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55
Q

What are the 3 bacteria that cause contagious mastitis in cows?

A

-Staph aureus
-Strep agalactiae
-Mycoplasma spp

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56
Q

What are 4 species of bacteria that cause environmental mastitis in cows?

A

-E. coli
-Enterococcus spp
-Coagulase neg staph
-Strep uberis

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57
Q

What should you do if you culture a milk sample for mastitis and grow 3 or more species of bacteria for an individual cow?

A

Collect a new sample

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58
Q

How should you manage cows with contagious mastitis?

A

-Milk infected cows last
-Cull infected cows
-Maintain a closed herd
-Proper milking technique and maintenance of milking equipment

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59
Q

How should you manage cases of environmental mastitis?

A

-There is a vaccine to prevent E. coli mastitis
-Sanitation, clean up the environment
-Treat individual cows as needed

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60
Q

Describe the structure of Staph aureus.

A

Gram positive cocci, forms grape-like clusters

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61
Q

What results would you expect to see if growing S. aureus on blood agar and mannitol salt agar plates?

A

-Beta hemolysis on blood agar plate
-All staph will grow on mannitol salt agar but strep will not
-Most staph do not ferment mannitol (it stays pink), but staph aureus does ferment it (it turns yellow)

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62
Q

Is S. aureus coagulase positive or negative? What would we expect to see visually with this result, and what does it tell us about the organism’s pathogenicity?

A

-Coagulase positive, would expect a clump at the bottom of the tube
-Coagulase positive are generally the only species of staph that are pathogenic, coagulase negative are usually commensals and do not cause infections

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63
Q

Describe the structure of Strep agalactiae.

A

Gram positive cocci, can be single cocci, pairs, or long chains

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64
Q

What Lancefield group is S. agalactiae in?

A

B

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65
Q

What is the CAMP test? What result would indicate the presence of S. agalactiae?

A

-It tests for hemolytic synergism
-Look for an “arrow” of enhanced hemolysis, if present, it indicates the bacteria is S. agalactiae

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66
Q

What test can you run to differentiate staph and strep species?

A

Catalase test: strep is neg (no bubbles) and staph is positive (bubbles)

Exception: staph aureus is catalase neg

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67
Q

Describe the structure of mycoplasma.

A

-Very small, no cell wall, unable to gram stain, unaffected by abx that target cell wall synthesis
-Mycoplasma mastitis infections are usually very severe, affect multiple quarters, and sometimes go systemic

68
Q

Describe how you would culture mycoplasma and what you would expect to see on the plate.

A

-Requires special media with a source of sterols and has to incubate for 3-4 weeks
-Forms small colonies with fried egg appearance

69
Q

Describe the structure of E. coli. What type of mastitis does it (and other bacteria with the same characteristics) cause?

A

Gram negative motile rods, causes coliform mastitis

70
Q

How is mastitis from E. coli transmitted?

A

-Fecal contamination of environment
-Contaminated sawdust and bedding
-Rainfall and high humidity increase the risk of contamination

71
Q

What part of the E. coli bacteria causes damage to the mammary glands?

A

endotoxin

72
Q

Describe the characteristics of Listeria bacteria.

A

-Gram positive rods
-Facultative anaerobe
-Facultative intracellular
-Grows from 4-45C

73
Q

Is Listeria zoonotic?

A

Yes

74
Q

What are the 2 pathogenic species of Listeria and what species does each infect?

A

-L. monocytogenes: ruminants, dogs, cats, horses, pigs, birds, humans
-L. ivanovii: sheep and cattle

75
Q

Why is silage a common place for Listeria to grow?

A

It needs to be stored anaerobically

76
Q

Besides silage, where else can Listeria be found?

A

-Decaying vegetation
-Excreted in feces and milk during stress
-Water (forms biofilms in troughs)
-Sewage
-Contaminated produce (responsible for a few food recalls)

77
Q

How does Listeria enter its host?

A

Ingestion of contaminated silage, water, vegetation, food, etc

78
Q

How does Listeria multiply within the host?

A

-Invades phagocytic and non-phagocytic cells, internalins help bacteria adhere to host cell membranes
-Listeriolysin destroys membranes of phagocytic vacuoles so listeria can get into cytoplasm

79
Q

How does Listeria spread within the host?

A

-Transfers cell to cell without exposure to humoral defense mechanisms
-Hijacks actin filaments of host cell to induce formation of pseudopod like projections
-Cell bursts when overloaded with too many bacteria, bacteria are released into blood and lymph

80
Q

Is Listeria an intracellular or extracellular pathogen?

A

Both, found extracellularly in the blood and lymph and intracellularly in phagocytic cells (facultative intracellular)

81
Q

Where are the 2 predilection sites for Listeria? Which form of bacteremia is more common in ruminants?

A

-Neural tissue and placenta
-Neural target is more common in ruminants (causes circling)

82
Q

What animals can get uveitis or conjunctivitis from Listeria? How does this happen?

A

Sheep and cattle get it from burying their head in contaminated silage when eating

83
Q

When in the pregnancy does Listeria normally cause abortions?

A

Usually last trimester (8 or 9 months)

84
Q

How is Listeriosis diagnosed grossly? How about histologically?

A

-Grossly: fetus is autolyzed and has hepatitis, the placenta has exudate between the cotyledons
-Histologically: fetus has suppurative hepatitis (evidence of septicemia), placenta also has suppurative placentitis

85
Q

What conditions are required to culture Listeria?

A

Blood agar plate at 25C. Will see tumbling motility

86
Q

Is serology useful in diagnosing Listeria?

A

No

87
Q

How do you prevent Listeria? Is there a vaccine?

A

-Do not feed poor quality silage to pregnant ruminants
-Segregate aborting animals
-Remove aborted tissues from the environment
-Aborting animals are usually resistant to the infection and are able to conceive the following year
-No vaccine available

88
Q

Is listeria more or less common in small animals compared to large? How do they contract it and what are their clinical signs?

A

Small animals: less common, contracted by ingesting contaminated meat or meat byproducts (clinical signs: v+/d+ and fever)

Large animals: more common, contracted from eating silage

89
Q

How can humans contract Listeria? Which individuals are most at risk of severe illness?

A

-Handling infected fetuses or eating contaminated deli meat
-Life threatening in neonates, elderly people, and immunosuppressed people

90
Q

Describe the characteristics of Bacillus. Where are they found?

A

-Gram positive rods, facultative anaerobes
-Ubiquitous

91
Q

What are the 2 pathogenic Bacillus species of interest? What does each one cause?

A

Bacillus anthracis and Bacillus cereus

92
Q

Which species mentioned above is zoonotic? Which is used as a bioterrorism agent?

A

B. anthracis is zoonotic and used as a bioterrorism agent

93
Q

How can you identify Bacillus anthracis under a microscope?

A

They are rods with square ends, often form chains

94
Q

How does B. anthracis enter the host?

A

Infective spores are ingested, inhaled, or entered through the skin

95
Q

How does B. anthracis evade host defenses?

A

Capsule encoded by pX02 plasmid (This is the target of the Sterne vaccine)

96
Q

How does B. anthracis multiply and spread within the host?

A

Spores germinate and multiply within macrophage. Bacteria escape from phagolysosome and macrophages to enter bloodstream

97
Q

What toxin does B. anthracis produce?

A

edema toxin

98
Q

What are the clinical signs of B. anthracis?

A

-Terminal bacteremia
-Gelatinous edema
-Widespread hemorrhages
-Black, engorged, friable spleen
-Absence of rigor mortis

99
Q

How is B. anthracis transmitted from one host to another?

A

Spores form in decomposing carcasses and use “sit and wait” tactic, new host will come by and ingest spores

100
Q

Which species are most susceptible to an anthrax infection? Which species are resistant?

A

Cattle and sheep and susceptible

Swine, dogs, rabbits, and chickens are resistant

101
Q

What are the clinical signs of anthrax in ruminants?

A

fever, agalactia, abortion, hematuria, hemorrhage, regional edema, sudden death

102
Q

What are the clinical signs of anthrax in horses?

A

colic, diarrhea, edema around site of entry

103
Q

What are the clinical signs of anthrax in swine?

A

settles in pharyngeal tissues, edema at site of entry

104
Q

What are the clinical signs of anthrax in carnivores?

A

settles in pharyngeal tissues, edema at site of entry

105
Q

What are the 3 types of B. anthracis that affects humans? Which is the most common?

A

-Cutaneous anthrax: most common
-Pulmonary anthrax (wool sorter’s disease)
-Gastrointestinal anthrax: rare

106
Q

How do you diagnose B. anthracis? Is it a reportable disease?

A

-Anthrax is suspected when there is sudden death, unclotted blood from orifices, and delayed rigor mortis
-Gram stain can be done on uncoagulated blood, look for rods with square ends
-DO NOT open carcass in the field!! It will release spores that can be ingested by other animals and make them sick
-Anthrax is a reportable disease

107
Q

How do you treat and prevent anthrax? Is there a vaccine?

A

-Vaccinate with Sterne strain (no capsule)
-Burn or bury infected carcasses
-Treat exposed animals with appropriate abx

108
Q

What diseases does Bacillus cereus cause in bovine?

A

rare mastitis, causes necrosis of entire infected quadrant

109
Q

What diseases does Bacillus cereus cause in dogs and cats?

A

rarely causes food poisoning

110
Q

What diseases does Bacillus cereus cause in humans?

A

food borne diarrheal illness

111
Q

How does B. cereus enter the host?

A

Opportunistic infection

112
Q

How does B. cereus evade host defenses?

A

Capsule formation

113
Q

What lesions does Bacillus licheniformis cause?

A

-Necrotizing placentitis
-Fetal multifocal suppurative bronchopneumonia

114
Q

Describe the characteristics of Leptospira.

A

Gram negative spirochete aerobes

115
Q

Where do leptospira live? How are they killed?

A

-They live in moist, warm environments
-Killed by drying, freezing, detergents, soaps, and acidic environments

116
Q

Is Leptospirosis zoonotic?

A

yes

117
Q

How is lepto transmitted? Can humans contract lepto directly from companion animals?

A

-Contact with urine or water contaminated with infected urine
-Humans rarely contract lepto directly from infected animals

118
Q

What are the virulence factors for leptospira?

A

-Antigenic variation
-Motility, ability to penetrate mucosa and skin
-Hemolysin: induces apoptosis of endothelial cells, hepatocytes, and other cells

119
Q

What people are most at risk for getting a lepto infection?

A

People with at risk jobs: farmers, vets, zookeepers, slaughterhouse workers

Recreational risks: campers, swimmers, triathletes

120
Q

What is the role of maintenance/reservoir hosts in the spread and transmission of lepto? What are some animals who serve as maintenance hosts?

A

-Maintenance hosts do not show clinical signs but are infected and can shed lepto in their urine for months to years
-Maintenance hosts include raccoons, rats, skunk, possums

121
Q

What is the role of maintenance/reservoir hosts in the spread and transmission of lepto?

A

They are a source of environmental contamination

122
Q

Explain the pathogenesis of lepto.

A

lepto enters the bloodstream and disseminates to various tissues. Where the bacteria ends up determines the clinical signs

123
Q

How do the clinical signs of lepto differ between maintenance hosts and incidental hosts?

A

-Maintenance hosts: infection is usually subclinical, long term shedding, and have lower titers
-Incidental hosts: can have subclinical or clinical infection, short term shedding, and have higher titers

124
Q

What lepto serotype infects adult cattle? What are the clinical signs?

A

Serotype L. hardjo-bovis

Clinical signs: reproductive loss, decreased production (milk drop syndrome)

125
Q

What lepto serotype infects calves? What are the clinical signs?

A

Serotype L. pomona

Clinical signs: fever, icterus, hemolysis, liver and/or renal compromise

126
Q

What lepto serotype infects swine? What are the clinical signs?

A

L. pomona is most common but also L. bratislava and L. icterohemorrhage

Clinical signs: reproductive loss

127
Q

What lepto serotype infects horses? What are the clinical signs?

A

L. pomona is most common but also L. bratislava and L. grippotyphosa

Clinical signs: recurrent uveitis, abortion, stillbirth, perinatal death, acute renal failure, hepatic disease in foals

128
Q

What lepto serotype infects dogs? What are the clinical signs?

A

L. canicola, icterohemorrhage, grippotyphosa, pomona, and bratislava (basically all of the ones we have talked about)

Clinical signs: acute hepatic disease and/or acute kidney injury (most common), bleeding disorders, fever, vasculitis, uveitis, systemic disease from dissemination

129
Q

How can lepto be diagnosed?

A

Serology test (MAT or ELISA) in combination with antigen detection (PCR of urine or blood) is recommended

130
Q

How do you interpret a microscopic agglutination test (MAT) for lepto?

A

4x increase in titer of 1-3 weeks indicates a positive infection

131
Q

How can you prevent and control lepto?

A

-Avoid exposure of pets and people to standing water and rodents/wildlife
-Clean and disinfect environment
-Vaccines available for cattle, swine, and dogs

132
Q

What points should you be sure to tell a client when educating them about lepto?

A

-Avoid handling animal urine
-Segregate infected animals
-Use proper PPE when working with infected animals or urine
-Clean and disinfect environment as needed

133
Q

Describe the characteristics of Brucella.

A

-Gram negative coccobacillus
-Capnophilic- loves CO2
-Slow growing

134
Q

Is Brucella zoonotic?

A

Yes

135
Q

What risk factors make a person more at risk for contracting Brucella?

A

-Working with animals (vet, slaughterhouse, butcher, lab workers)
-Consuming unpasteurized dairy products
-Hunters of feral swine, elk, bison, caribou, deer

136
Q

What species of Brucella is considered to be eradicated from the US?

A

B. melitensis

137
Q

Which species of Brucella are reportable diseases?

A

B. abortus, B.melitensis (eradicated), B. suis, and B. ovis

138
Q

What animal species are affected by B. abortus?

A

cattle (elk and buffalo are reservoirs)

139
Q

What animal species are affected by B. ovis?

A

sheep

140
Q

What animal species are affected by B. suis?

A

swine

141
Q

What animal species are affected by B. canis?

A

dogs

142
Q

How does Brucella enter the host? Where does it live inside the host?

A

-Ingestion of contaminated fetus or placenta, or consuming infected milk
-Can also be transmitted through infected semen
-Enters host through MM but travels to macrophages or regional LN
-Spreads through blood to other organs such as placenta and male repro tract, the presence of erythritol (sugar) stimulates growth of the bacteria

143
Q

How does Brucella evade the host defenses?

A

Facultative intracellular pathogen (survives and multiplies within phagocytic cells to avoid/inhibit phagolysosomal fusion)

144
Q

What is Bang’s disease and what does it cause? What species of Brucella causes it?

A

-Caused by B. abortus
-Abortion occurs usually in the third trimester
-First calf heifers and new herd additions are exposed, infected, and abort

145
Q

What is a key histopathologic finding you will see in placentitis due to B. abortus?

A

Bronchopneumonia in the fetus

You will NOT see septicemia in the fetus like is present with listeria

146
Q

What are the clinical signs of B. canis?

A

Late term abortion, lesion on external male genital tract (epididymitis, periorchitis, prostatitis), or discospondylitis

147
Q

What is poll evil and what species of Brucella cause it?

A

-Caused by B. abortus and B. suis
-Inflammation and thickening of bursal wall that may rupture and cause a fistula

148
Q

How can you diagnose Brucella?

A

-PCR
-Serology: serum agglutination test for IgG and IgM
-Milk ring test (agglutination test): detects the presence of Ab in milk

149
Q

How do you treat Brucella in large animals and dogs?

A

-Large animals: cull
-Dogs: euthanasia or long term abx (and must spay/neuter since the bacteria lives in the repro tissues)

150
Q

Is there a vaccine for Brucella?

A

B. abortus strain RB51 vaccine available

151
Q

Describe the characteristics of Chlamydia.

A

-Obligate intracellular pathogen
-Gram negative
-Coccobacillus

152
Q

How many genus of chlamydia are there?

A

One: Chlamydia

153
Q

What animal species does C. psittaci affect?

A

birds

154
Q

What animal species does C. felis affect?

A

cats

155
Q

What animal species does C. abortus affect?

A

cattle, sheep, goats

156
Q

What animal species does C. pecorum affect?

A

cattle and sheep

157
Q

What animal species does C. caviae affect?

A

guinea pig

158
Q

Which species of Chlamydia are reportable diseases?

A

C. abortus and C. psittaci

159
Q

How does Chlamydia multiply and spread?

A

-Infectious elementary bodies initiate the infection
-Elementary bodies reorganize into reticulate bodies once in the cytoplasm
-Reticulate bodies replicate
-Reticulate bodies revert back to elementary bodies
-Host cell ruptures and releases the elementary bodies, infection spreads

160
Q

What are the clinical signs of C. psittici?

A

Nasal and ocular discharge
Conjunctivitis

161
Q

How can a human contract C. psittici?

A

Transmitted from inhalation or aerosol from infected droppings or feathers

162
Q

What are the clinical signs for C. felis?

A

Conjunctivitis, occasional rhinitis

163
Q

How is C. felis diagnosed?

A

-PCR or cytology
-Culture is NOT effective because it is an obligate intracellular organism

164
Q

What are the clinical signs of C. abortus?

A

Enzootic abortion of ewes (late term)

165
Q

What are the clinical signs of C. caviae?

A

conjunctivitis in guinea pigs

Bacti Final (1 decks)

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