Bacti Final Exam Flashcards
What are the characteristics of Clostridium? (gram positive or negative, aerobic or anaerobic, etc)
-Gram positive
-rods/bacillus (short rods)
-Anaerobic
-Spore forming (anaerobic transmission)
-Toxin producing
Which clostridium species are histotoxic and which are neurotoxic?
-Histotoxic: C. perfringens (also enterotoxic), C. chauvoei, C. haemolyticum, C. novyi. C. septicum
-Neurotoxic: C. botulinum, C. tetani
Which species of Clostridium is both enterotoxic and histotoxic?
C. perfringens
Which species of Clostridium is the fastest replicating bacteria?
C. perfringens
How are the different subtypes of C. perfringens identified?
The type of toxin it produces (toxinotype A-E)
What are the virulence factors for C. perfringens?
-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
What condition does C. perfringens cause? What are the symptoms of this condition?
Gas gangrene: necrotizing cellulitis and myonecrosis, edema, hemorrhage, gas production, toxemia
What are the virulence factors for C. chauvoei?
-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
What disease does C. chauvoei cause in cattle? Describe what the associated lesions look like.
Blackleg: muscles have a dark, emphysematous center with hemorrhage and edema around the outside
What are the symptoms of Blackleg?
High fever, lameness, anorexia, visible swelling of affected muscles, affected muscle will have rancid butter odor, sudden death
Where does C. chauvoei reside? How does it get there?
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)
Describe the pathogenesis of C. chauvoei.
Spores in muscles -> decreased the O2 levels -> anoxia causes bruising and gadding of young cattle (exercise intolerance) germination -> toxin production
How can you diagnose a C. chauvoei infection?
-Fecal smear and gram stain
-PCR
-Culture at 37C
How do you treat a C. chauvoei infection? Is there a vaccine available?
-There is a vaccine
-Tx is usually unsuccessful, IV penicillin followed by IM
What is the main virulence factor of C. haemolyticum?
Phospholipase C
What disease does C. haemolyticum cause in ruminants? What are the symptoms?
-Redwater disease
-Clinical signs: hemoglobinuria, fever, pale/icteric MM, abortion, agalactia
Describe the pathogenesis of a C. haemolyticium infection.
Ingestion of spores -> travel to liver -> spore germination in liver -> vegetation growth and production of phospholipase C -> hemolytic crisis and rapid death
How do you treat a C. haemolytcum infection? Is there a vaccine available?
-Vaccine available in endemic areas
-Treat with broad spectrum abx such as tetracycline and blood transfusion if needed
What are the virulence factors of C. noyvi?
-Alpha toxin: breaks down cytoskeleton
-Beta and delta toxins: cell membrane damage
What disease does C. noyvi cause in rams? Describe its pathogenesis
-Bighead
-Fighting injury -> activation of spores -> edema in head and neck -> death
What disease does C. noyvi cause in ruminants?
Pseudoblackleg: spores get to liver causing hemolytic crisis and death
How do you diagnose a C. noyvi infection?
Gram stain liver lesions: large gram positive rods with spores at the ends
How do you treat a C. noyvi infection? Is there a vaccine available?
-Toxoid vaccine is effective
-No effective treatment
What condition is caused by C. botulinum? What is the main clinical sign?
Botulism, flaccid paralysis
What species does C. botulinum affect?
Ruminants, horses, minks, birds
How are the different subtypes of C. botulinum categorized? How many groups are there?
There are 7 types based on the type of botulinum toxin produced
How does an animal contract a C. botulinum infection?
-Ingestion of botulinum toxin from contaminated plant or animal material
-Ingestion of spores
-Wound contamination
Describe the pathogenesis of a C. botulinum infection.
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
What can occur if C. botulinum affects the respiratory muscles?
Respiratory failure -> death
How can you diagnose a C. botulinum infection?
-Culture anaerobically on blood agar
-PCR
How do you treat a C. botulinum infection?
-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
Describe the shape of C. tetani.
Drumstick or tennis racket shaped with spores on the end
What is the C. tetani toxin called and how is it released?
Tetanospasmin, it is released upon lysis of the clostridial cell
What condition is caused by C. botulinum? What are the clinical signs?
-Causes tetanus, main clinical sign is spastic paralysis
-Other clinical signs: fecal and urinary retention, high fever and sweating, death (~50% of cases)
Describe the pathogenesis of ascending tetanus.
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
Describe the pathogenesis of descending tetanus.
pore is ingested -> spores germinate in anaerobic environment -> toxins are released and absorbed into bloodstream -> toxin ends up in CNS -> generalized tetanus
Which species are more prone to ascending tetanus and which are more prone to descending tetanus? Which type is more dangerous to the animal?
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
How do you diagnose a C. tetani infection?
-Culture wound exudate on blood agar and look for hemolysis and swarming motility
-PCR
How do you treat a C. tetani infection?
-Antitoxin injection
-Toxoid vaccination
-Sedatives and muscle relaxants
-Penicillin or metronidazole
What are the two AST test methods? Which one measures a zone of inhibition and which measures a minimum inhibitory concentration?
-Kirby Bauer: measures a zone of inhibition
-Broth microdilution: measures a minimum inhibitory concentration
How do you interpret a broth microdilution plate (how do you determine what the MIC is)?
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)
The “rules” in the CLSI guidelines are based on what?
Rules are based on the expected serum concentration if the drug is given systemically
What are two reasons why you would get a no interpretation (NI) result for a drug on an AST?
-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)
Why is the drug with the lowest MIC not always the best drug to use?
Each drug is evaluated at different concentrations and have different rules so you cannot compare their MIC values to each other
What is the mechanism of resistance for MRSA? What drugs is it resistant to?
-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
In general, what are the AST rules for topical drugs?
There are no rules for topical drugs, they are established based on expected serum concentrations if the drug is given systemically
In general, what are the AST rules for drugs to be used in birds?
-No rules for birds
-Enrofloxacin is illegal for use in birds
What pathogen(s) is/are most likely to cause equine mastitis?
Staph spp
Describe the distribution of equine mastitis.
usually unilateral
What pathogen(s) is/are most likely to cause canine or feline mastitis?
E. coli, staph, and strep
What factors are associated with mastitis in canines and felines?
-Ascending infection
-Trauma
-Unsanitary environment
What is the difference between clinical and subclinical mastitis in dairy cows?
-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
When testing for mastitis, what cell type are you testing for? What number indicates mastitis is present?
Testing for somatic cells, >200,000 cells/ml indicates mastitis
What is the difference between contagious and environmental mastitis?
-Contagious mastitis can spread from cow to cow
-Environmental mastitis is contracted through the environment
What are the 3 bacteria that cause contagious mastitis in cows?
-Staph aureus
-Strep agalactiae
-Mycoplasma spp
What are 4 species of bacteria that cause environmental mastitis in cows?
-E. coli
-Enterococcus spp
-Coagulase neg staph
-Strep uberis
What should you do if you culture a milk sample for mastitis and grow 3 or more species of bacteria for an individual cow?
Collect a new sample
How should you manage cows with contagious mastitis?
-Milk infected cows last
-Cull infected cows
-Maintain a closed herd
-Proper milking technique and maintenance of milking equipment
How should you manage cases of environmental mastitis?
-There is a vaccine to prevent E. coli mastitis
-Sanitation, clean up the environment
-Treat individual cows as needed
Describe the structure of Staph aureus.
Gram positive cocci, forms grape-like clusters
What results would you expect to see if growing S. aureus on blood agar and mannitol salt agar plates?
-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)
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?
-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
Describe the structure of Strep agalactiae.
Gram positive cocci, can be single cocci, pairs, or long chains
What Lancefield group is S. agalactiae in?
B
What is the CAMP test? What result would indicate the presence of S. agalactiae?
-It tests for hemolytic synergism
-Look for an “arrow” of enhanced hemolysis, if present, it indicates the bacteria is S. agalactiae
What test can you run to differentiate staph and strep species?
Catalase test: strep is neg (no bubbles) and staph is positive (bubbles)
Exception: staph aureus is catalase neg
Describe the structure of mycoplasma.
-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
Describe how you would culture mycoplasma and what you would expect to see on the plate.
-Requires special media with a source of sterols and has to incubate for 3-4 weeks
-Forms small colonies with fried egg appearance
Describe the structure of E. coli. What type of mastitis does it (and other bacteria with the same characteristics) cause?
Gram negative motile rods, causes coliform mastitis
How is mastitis from E. coli transmitted?
-Fecal contamination of environment
-Contaminated sawdust and bedding
-Rainfall and high humidity increase the risk of contamination
What part of the E. coli bacteria causes damage to the mammary glands?
endotoxin
Describe the characteristics of Listeria bacteria.
-Gram positive rods
-Facultative anaerobe
-Facultative intracellular
-Grows from 4-45C
Is Listeria zoonotic?
Yes
What are the 2 pathogenic species of Listeria and what species does each infect?
-L. monocytogenes: ruminants, dogs, cats, horses, pigs, birds, humans
-L. ivanovii: sheep and cattle
Why is silage a common place for Listeria to grow?
It needs to be stored anaerobically
Besides silage, where else can Listeria be found?
-Decaying vegetation
-Excreted in feces and milk during stress
-Water (forms biofilms in troughs)
-Sewage
-Contaminated produce (responsible for a few food recalls)
How does Listeria enter its host?
Ingestion of contaminated silage, water, vegetation, food, etc
How does Listeria multiply within the host?
-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
How does Listeria spread within the host?
-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
Is Listeria an intracellular or extracellular pathogen?
Both, found extracellularly in the blood and lymph and intracellularly in phagocytic cells (facultative intracellular)
Where are the 2 predilection sites for Listeria? Which form of bacteremia is more common in ruminants?
-Neural tissue and placenta
-Neural target is more common in ruminants (causes circling)
What animals can get uveitis or conjunctivitis from Listeria? How does this happen?
Sheep and cattle get it from burying their head in contaminated silage when eating
When in the pregnancy does Listeria normally cause abortions?
Usually last trimester (8 or 9 months)
How is Listeriosis diagnosed grossly? How about histologically?
-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
What conditions are required to culture Listeria?
Blood agar plate at 25C. Will see tumbling motility
Is serology useful in diagnosing Listeria?
No
How do you prevent Listeria? Is there a vaccine?
-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
Is listeria more or less common in small animals compared to large? How do they contract it and what are their clinical signs?
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
How can humans contract Listeria? Which individuals are most at risk of severe illness?
-Handling infected fetuses or eating contaminated deli meat
-Life threatening in neonates, elderly people, and immunosuppressed people
Describe the characteristics of Bacillus. Where are they found?
-Gram positive rods, facultative anaerobes
-Ubiquitous
What are the 2 pathogenic Bacillus species of interest? What does each one cause?
Bacillus anthracis and Bacillus cereus
Which species mentioned above is zoonotic? Which is used as a bioterrorism agent?
B. anthracis is zoonotic and used as a bioterrorism agent
How can you identify Bacillus anthracis under a microscope?
They are rods with square ends, often form chains
How does B. anthracis enter the host?
Infective spores are ingested, inhaled, or entered through the skin
How does B. anthracis evade host defenses?
Capsule encoded by pX02 plasmid (This is the target of the Sterne vaccine)
How does B. anthracis multiply and spread within the host?
Spores germinate and multiply within macrophage. Bacteria escape from phagolysosome and macrophages to enter bloodstream
What toxin does B. anthracis produce?
edema toxin
What are the clinical signs of B. anthracis?
-Terminal bacteremia
-Gelatinous edema
-Widespread hemorrhages
-Black, engorged, friable spleen
-Absence of rigor mortis
How is B. anthracis transmitted from one host to another?
Spores form in decomposing carcasses and use “sit and wait” tactic, new host will come by and ingest spores
Which species are most susceptible to an anthrax infection? Which species are resistant?
Cattle and sheep and susceptible
Swine, dogs, rabbits, and chickens are resistant
What are the clinical signs of anthrax in ruminants?
fever, agalactia, abortion, hematuria, hemorrhage, regional edema, sudden death
What are the clinical signs of anthrax in horses?
colic, diarrhea, edema around site of entry
What are the clinical signs of anthrax in swine?
settles in pharyngeal tissues, edema at site of entry
What are the clinical signs of anthrax in carnivores?
settles in pharyngeal tissues, edema at site of entry
What are the 3 types of B. anthracis that affects humans? Which is the most common?
-Cutaneous anthrax: most common
-Pulmonary anthrax (wool sorter’s disease)
-Gastrointestinal anthrax: rare
How do you diagnose B. anthracis? Is it a reportable disease?
-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
How do you treat and prevent anthrax? Is there a vaccine?
-Vaccinate with Sterne strain (no capsule)
-Burn or bury infected carcasses
-Treat exposed animals with appropriate abx
What diseases does Bacillus cereus cause in bovine?
rare mastitis, causes necrosis of entire infected quadrant
What diseases does Bacillus cereus cause in dogs and cats?
rarely causes food poisoning
What diseases does Bacillus cereus cause in humans?
food borne diarrheal illness
How does B. cereus enter the host?
Opportunistic infection
How does B. cereus evade host defenses?
Capsule formation
What lesions does Bacillus licheniformis cause?
-Necrotizing placentitis
-Fetal multifocal suppurative bronchopneumonia
Describe the characteristics of Leptospira.
Gram negative spirochete aerobes
Where do leptospira live? How are they killed?
-They live in moist, warm environments
-Killed by drying, freezing, detergents, soaps, and acidic environments
Is Leptospirosis zoonotic?
yes
How is lepto transmitted? Can humans contract lepto directly from companion animals?
-Contact with urine or water contaminated with infected urine
-Humans rarely contract lepto directly from infected animals
What are the virulence factors for leptospira?
-Antigenic variation
-Motility, ability to penetrate mucosa and skin
-Hemolysin: induces apoptosis of endothelial cells, hepatocytes, and other cells
What people are most at risk for getting a lepto infection?
People with at risk jobs: farmers, vets, zookeepers, slaughterhouse workers
Recreational risks: campers, swimmers, triathletes
What is the role of maintenance/reservoir hosts in the spread and transmission of lepto? What are some animals who serve as maintenance hosts?
-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
What is the role of maintenance/reservoir hosts in the spread and transmission of lepto?
They are a source of environmental contamination
Explain the pathogenesis of lepto.
lepto enters the bloodstream and disseminates to various tissues. Where the bacteria ends up determines the clinical signs
How do the clinical signs of lepto differ between maintenance hosts and incidental hosts?
-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
What lepto serotype infects adult cattle? What are the clinical signs?
Serotype L. hardjo-bovis
Clinical signs: reproductive loss, decreased production (milk drop syndrome)
What lepto serotype infects calves? What are the clinical signs?
Serotype L. pomona
Clinical signs: fever, icterus, hemolysis, liver and/or renal compromise
What lepto serotype infects swine? What are the clinical signs?
L. pomona is most common but also L. bratislava and L. icterohemorrhage
Clinical signs: reproductive loss
What lepto serotype infects horses? What are the clinical signs?
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
What lepto serotype infects dogs? What are the clinical signs?
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
How can lepto be diagnosed?
Serology test (MAT or ELISA) in combination with antigen detection (PCR of urine or blood) is recommended
How do you interpret a microscopic agglutination test (MAT) for lepto?
4x increase in titer of 1-3 weeks indicates a positive infection
How can you prevent and control lepto?
-Avoid exposure of pets and people to standing water and rodents/wildlife
-Clean and disinfect environment
-Vaccines available for cattle, swine, and dogs
What points should you be sure to tell a client when educating them about lepto?
-Avoid handling animal urine
-Segregate infected animals
-Use proper PPE when working with infected animals or urine
-Clean and disinfect environment as needed
Describe the characteristics of Brucella.
-Gram negative coccobacillus
-Capnophilic- loves CO2
-Slow growing
Is Brucella zoonotic?
Yes
What risk factors make a person more at risk for contracting Brucella?
-Working with animals (vet, slaughterhouse, butcher, lab workers)
-Consuming unpasteurized dairy products
-Hunters of feral swine, elk, bison, caribou, deer
What species of Brucella is considered to be eradicated from the US?
B. melitensis
Which species of Brucella are reportable diseases?
B. abortus, B.melitensis (eradicated), B. suis, and B. ovis
What animal species are affected by B. abortus?
cattle (elk and buffalo are reservoirs)
What animal species are affected by B. ovis?
sheep
What animal species are affected by B. suis?
swine
What animal species are affected by B. canis?
dogs
How does Brucella enter the host? Where does it live inside the host?
-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
How does Brucella evade the host defenses?
Facultative intracellular pathogen (survives and multiplies within phagocytic cells to avoid/inhibit phagolysosomal fusion)
What is Bang’s disease and what does it cause? What species of Brucella causes it?
-Caused by B. abortus
-Abortion occurs usually in the third trimester
-First calf heifers and new herd additions are exposed, infected, and abort
What is a key histopathologic finding you will see in placentitis due to B. abortus?
Bronchopneumonia in the fetus
You will NOT see septicemia in the fetus like is present with listeria
What are the clinical signs of B. canis?
Late term abortion, lesion on external male genital tract (epididymitis, periorchitis, prostatitis), or discospondylitis
What is poll evil and what species of Brucella cause it?
-Caused by B. abortus and B. suis
-Inflammation and thickening of bursal wall that may rupture and cause a fistula
How can you diagnose Brucella?
-PCR
-Serology: serum agglutination test for IgG and IgM
-Milk ring test (agglutination test): detects the presence of Ab in milk
How do you treat Brucella in large animals and dogs?
-Large animals: cull
-Dogs: euthanasia or long term abx (and must spay/neuter since the bacteria lives in the repro tissues)
Is there a vaccine for Brucella?
B. abortus strain RB51 vaccine available
Describe the characteristics of Chlamydia.
-Obligate intracellular pathogen
-Gram negative
-Coccobacillus
How many genus of chlamydia are there?
One: Chlamydia
What animal species does C. psittaci affect?
birds
What animal species does C. felis affect?
cats
What animal species does C. abortus affect?
cattle, sheep, goats
What animal species does C. pecorum affect?
cattle and sheep
What animal species does C. caviae affect?
guinea pig
Which species of Chlamydia are reportable diseases?
C. abortus and C. psittaci
How does Chlamydia multiply and spread?
-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
What are the clinical signs of C. psittici?
Nasal and ocular discharge
Conjunctivitis
How can a human contract C. psittici?
Transmitted from inhalation or aerosol from infected droppings or feathers
What are the clinical signs for C. felis?
Conjunctivitis, occasional rhinitis
How is C. felis diagnosed?
-PCR or cytology
-Culture is NOT effective because it is an obligate intracellular organism
What are the clinical signs of C. abortus?
Enzootic abortion of ewes (late term)
What are the clinical signs of C. caviae?
conjunctivitis in guinea pigs
