Exam 1 Flashcards
(110 cards)
1
Q
–Are bacteria euk or prok?
–how is genetic material stored? protected how? Another prok?
How much bigger is the euk?
A
prok.
- -large DNA molecule in an area of cyto called the nucleoid region.
- -cell membrane –cyanobacteria.,
- -10X
2
Q
Name the 3 groups of bacterial shapes and the subnames.
–2 cocci, chain of cocci and cluster of cocci are called?
which axis do rod bact divide on?
A
- -spherical (coccus plural: cocci) –rod (bacillus p: bacilli) –spiral
- -diplococci, streptococci, staphylococci
- -short axis.
3
Q
Some types not only have a cyto memb, cell wall, but also a ? What does this look like in stain?
Gram pos are considered blank because of the cell wall only while gram - are considered blank for having a double membrane.
Is the peptidoglycan thicker in gram +or gram -? which has techoic acids? LPS? porin?
A
–capsule–hollow surface.
- -monoderm and diderm.
- -gram pos –gram pos –gram neg –gram neg (because of outer membrane)
4
Q
Name the steps of gram stain and why do gram neg not stay purple?
What are the 4 external to the cell wall structures that we covered?
A
- -fixative, crystal violet, iodine, decolorization with alcohol and counter stain with safranin.
- -the peptidoglycan layer is thin in gram - and not as crosslinked, therefore the CV doesnt stay.
- —glycocalyx, fimbriae (pili), flagella, and capsules.
5
Q
What are flagella attached to? Fxn? Made of? Highly blank. Used for serotyping. Also called what? Name the 4 shapes on the bact that we covered.
Fimbriae are smaller and usually in higher numbers. Are they used for motility like flagella? Fxn MIGHT be blank
A
–cell wall. –motility –glycoproteins. –immunogenic –H antigens –monotrichous (one), lophotrichous (>2 on one end), peritrichous (all over), amphitricous (one on each end).
–NO –attachment to host cell.
6
Q
Capsule is like a “blank” covering. not easily seen on a gram stain, but can use 2 types of stain to see. Explain the 5 ways that they are used for virulence factors.
A
slime. –india ink or CuSO4.
- -disrupt phag, mediate attachment to mucous membranes, prevent desiccation of the cell, resist lysis by complement, inhibit lysis within phagolysosomes.
7
Q
Explain what a spore is. Ex. Steps to make them?
Sterilization kills/elims transmissable agents EXCEPT what? 5 forms of sterilization?
A
- -aka endospore: structure that some bacteria form. Resting stage that enables endure adverse conditions. Improved conditions–> transform into active bact. Anthrax, botulism, tetanus.
- -forespore engulfed in protoplast. Cortex forms. Spore coat forms. Spore is released.
- -heat, chemicals, irradiation, high pressure, filtration.
8
Q
What are the 2 forms of heat sterilization.
- -dry: explain process and why it works
- -moist: explain why it works
A
- -dry and moist
- -hot air-320 degree for 2 hrs or 340 for 1 hr. Destroys microorganisms by causing coag of proteins.
- -hot air laden with water vapor. Coag proteins aided by the water with high penetrating power.
9
Q
Explain incineration and when it is used.
Same but for gamma irradiation
A
- -temp of 1000C used for infected carcasses.
- gamma rays=electromagnetic radiation of a high freq (very short wavelength). IONIZING ray. Disposable plastic lab and surgical equip. NO glass or metal.
10
Q
Explain UV light and when it is used
Explain membrane filtration
A
- -electromagnetic radiation with wavelength shorter than visible light. NONE ionizing waves-poor penetration.. Biosafety cabinets.
- -filtering out bacteria for culture from heat sensitive fluids such as serum or tissue culture media.
11
Q
What are the 2 main categories of host defense. What is the body’s first line of defense? Can be split into 2. What conditions of the skin limit bact growth? What are 2 other defenses that the skin uses
A
- -body surfaces –defenses of tissues and blood
- -skin and mucosal surface. –nonspecific and specific induced defenses.
- -dry, acidic pH and low temp.
- -sloughing cells to remove bact. Resident microflora for competition to colonize.
12
Q
What is SALT? What do sebaceous glands make?
What are lactoferrin and lactoperoxidase?
A
- -skin associated lymphoid tissue
- -sebum: oily waxy matter. lubricates skin and hair.
- -found in mucin layer. Lactoferrin is bacteriostatic in tears, raw milk. tears. Protein that binds iron with high affinity. Bact must get iron, cant compete with lactoferrin. -Lactoperox is bactericidal. Milk, saliva, tears.
13
Q
What secretes the mucus for the mucous membrane? Explain the fxns of the mucus and what it contains
How does lysozyme work?
What do GALT and MALT produce? Why?
A
- -goblet cells –lubricant and physical barrier to trap bact. –SECRETORY IGA, lactoferrin, lactoperoxidase, lysozyme.
- -splits muramic linkage in bact cells (esp gram +) degrades bacterial peptidoglycan.
- -secretory antibody-prevents bacterial adherance to mucosal cells.
14
Q
Name the 5 cellular defenses of blood/tissue.
What forms inside of neutrophils and macrophages to kill bact?
When bacteria bind to macrophage receptors, what 3 main things are released from the macrophage?
A
- -transferrin, PMNS, monocytes, macrophages and complement.
- -phagosome and lysosome–> phagolysosome.
- -cytokines, chemokines, lipid mediators of inflamm.
15
Q
What are 4 abilities that bact have developed to survive inside of neut or macrophages.
A
–escape phagosome before it fuses with lysosome–prevent phag/lysosome fusion–prevent acidification of the vacuole or short circuiting the process of fusion itself –reduce effectiveness of the toxic compounds released into phagolysosome after fusion.
16
Q
What are the 4 requirements of koch’s postulate.
Virulence is the degree of what? Pathogenic capacity is determined by its what?
A
–org must always be found in animals with the dz but not in healthy–org must be isolated from ani with infect dz and grown in pure culture –org isolated in culture must initiate dz in re inoc into susceptible animals–org shouild be re isolated fromexperimentally infected animals.
–pathogenicity–virulence factors.
17
Q
What are the 5 main ways that pathogens cause dz?
A
–adhesion to host cell surfaces.-produce special proteins that allow colonization of parts–produce proteins that either disrupt host cell membranes or stim endocutosis into host cells (invasion) –produce virulence factors taht inhibit the host’s immune systems defenses (immune response inhibitors) –virulence factors that are proteins made by bact that poison host cells/cause tissue damage (toxins).
18
Q
What is the ex of bact that can penetrate gut epi? Explain the 3 routes.
A
- -salmonella typhimurium
- enter through M cells (apoptosis of M cell) and infects macrophages and eli cells –invade gut epi by adherence of their fimbriae to the luminal epi. –dendritic cells protrude dendrites betwen epi cells. open tight jxns, dendrites protrude between cells–> can be inffeccted.
19
Q
What are the 2 main categories of virulance factors that a bact can have?
Promote colonization and survival: What do bacteria use as the best mechanism for adherence? Explaon
A
- -factors that promote bacterial colonization/invasion –factors that cause damage to host.
- -pili/fimbriae–tip of pilus aheres to host cell.
20
Q
Promote colonization and survival:what are adhesins? What are invasins?
–whtat cover the surface of bact and protect it from host’s response like complement or phags?
A
- -cell surface proteins that mediate tighter binding of bact to host cell. Imp for adherence.
- -bacterial surface proteins that provoke phagocytic ingestion of the bacteria by host cells even if the cell is not phag, are called invasins,
- -capsule.
21
Q
How do siderophores help bacteria survive.
A
–they are low MW cmpds that chelate iron with ^^affinity. Excreted into medium by bact. Iron/siderophore complex taken up by receptors on bact surface. Iron=essential for bact growht.
22
Q
Many strategies have evolved for bact to avoid the immune system.
Ex: mycobact tuberculosis causes reduced interleukin 2=what is this an ex of?
–Some bacteria hide in cells and then what?
What special method of immune evasion do shigella and listeria use?
A
- -bact targets the cells of the immune system that specifically reacts against them. Prevents immune response.
- -multiply inside of cells and then invade the body when they are greater in number.
- -escape vacuole and use cellular machinery to propel from cell to cell.
23
Q
Some bact can use several mechanisms to evade being killed within a phagolysosome. What does catalase do?
Where can spores be found.
how does anthrax infect?
A
- -deactivates products generated by phagofcytes. H2o2 and O2 is converted to water and O2.
- -soil borne.
- -blowflies transfer spores onto vegetation–> eaten–> flourishes in mucosa–> septic–> death.
24
Q
What are exotoxins and what do they do?
What are endotoxins and what do they do?
A
- -toxin excreted from microorg–> destroys cells/disrupts normal cellular metab. Ex. clost botulinum, corynebacterium diptheriae.
- -part of outer memb of gram neg bact. Mainly released when bact are lyse. Trigger phags to release cytokines that prod local or systemic symptoms.
25
What are the 3 strategies bact use against phags.
how do they inhib phagocytosis?
--directly, bact make exotoxins, endotoxins or use direct cytopathic effects. what are 3 indirect straitegies used.
- -inhibit chemotaxis, inhib phagocytosis, kill phag, colonization of phag.
- -dont present anything to grip onto.
--immunes complexes (Antigen/Ab) to activate macrophages --anti-host antibody (cross reacts to host tissue). --cell-mediated immunity.
26
- C. botulinum make at least 7 neurotoxins. How are they transferred? Move to blood and do what?
- Cl. tetani germinate and produce toxins where? 3-21 days, what toxins block NTs (glycine and GABA). 2 ways to spread?
- -ingestion of toxins. --invade peripheral nerves))> block release of Ach. Animals are aware and fell pain.
- -deep tissues with low oxygen tension. --tetanospasmin,
- -ascending tetanus-peripheral nerves -descending tetanus-hematogenous through lymph.
27
What organism makes diphtheria toxin, alpha-toxin, cholera toxin and toxic shock?
--what are super antigens. Most imp cytokine secreted?
What is an antibiotic induced infection?
- -C. diptheria, S. aureus, V. cholera, S. aureus.
- -overstim T cells by binding the MHC molecule and the t cell recep. Over prod of cytokines--> shock/multiple organ failure.
- -TNF-alpha.
- -tx with them causes massive death of commensal organisms and pathogenic bact like C diff can proliferate quickly and occupy.
28
Cl. perfringens Type D produces what toxins? Describe
--virulent foot rot is caused by an anaerobe called: blank. Explain
- -alpha and epsilon--overeating dz (pulpy kidney dz) in sheep--> enterotox. Damages kidneys. Neural signs. no fever/vomiting. Kidenys are swollen and soft.
- -bacteroides nodusus. pili used for virulence. MHC susceptibility. Hoof from soil. Prtease dissolves keratin and horn separates from foot.
29
what is LPS. what is it made of? When LPS activates macrophages, what 3 things occur.
- -gram neg bact cell membrane part. lipd A is the endotoxic portion. oligosacc core that has an O plysacc antigen attached.
- -cytokine release that cause: complement, PG and leukotriene release, coag cascade that all end up in endo damage and multi organ fail
30
Actinomyces bovis is an opportunistic invader of deep tissue. usually intro by a foreign body. What occurs?
Mycobacterium bovis cause granulomatous lesions called what? How does this organism get in the body/what occurs?
- -neut, mac and plasma cells surround and breakdown CT. Fibrous masses are often observed with exudate.
- -inhaled/ingested. Neut and macrophages engulf. Block phagolysossome. Escapes it and replicates within host cells. Necrotic tissue--> epi surround and wall off. CT encompasses and impairs organ fxn.
31
M. paratuberculosis is the agent of what dz. How does it get in the boyd/what happens.
--Johne's dz--ingest infected feces. Young and suckling often. Mac ingest but no phagolysosomal fusion. Thick intestinal wall, emaciation with normal app. Swelling of LN, dry/rough coat. Bottlw jaw and diarrhea.
32
What shape are enterobacteriaceae? Aerobe/anaerobe? Spore forming? Motile/ Capsules? Exo or endotoxins?
Many genuses were coverd in the enterobacteriaceae section: escherichia, enterobacter, klebsiella, citrobacter, proteus, providencia, morganella, shigella.
--Rod --facultative anaerobe --NO --some --some --exotoxins: some are enterotoxins because they affect the GI.
33
E.coli-gram? Rod. Motile. Flagella? (What type) Fimbria? Capsule? What kind of hemolysis? Ferment lactose? Grows green on EMB.
E Coli is ubiquitous: can be split into 2 groups.
What are the 4 types of pathogenic E. coli.
gram neg. peritrichous flagella and fimbria. Often has mucoid capsule. ALhpa and beta hemo. Yes.
- -pathogenic and non-pathogenic.
- -etnerotoxic, enterotoxemia, local invasive, septicemic form.
34
In enteric colibacillosis from enterotoxic, After E. coli prolif in the lumen of SI, what happens.
In enterotoxemic colibacillosis, E coli localizes in SI, then what
--enterotoxin is prod, fluid secretion--> diarrhea. No absorption necessary.
--produces toxin, absorbed, action of toxin elsewhere.
35
In locally invasive colibacillos, what occurs? Enterotoxigenic?
Septicemic colibacillosis can be in 2 forms. How does it occur?
--local invasion/destr of int epi by E coli--> lam proprioa. Invade and prolif in cells. Mechanism unknown. --no. no bacteremia.
--bacteremia or extraintestinal E coli with endotoxin mediated damage to cells. +/- diarrhea. Resp tract or intestine and lives in blood/tissues. Immuno supp birds ^ risk.
36
Not only do certain strains of E coli have exotoxins, they all have endotoxins. These are less tox than exo, but name the symptoms.
The exo toxins are called enterotoxins for being in the int. What cascade occurs?
What are the 5 main sp that get Ecoli
- -pyrogenic, leukopenia, hypotension, complement, intravasc coag and death.
- -adenylate cyclase--> cAMP--> hypersec of water and Cl into gut lumen--> fluid loss.
--cattle, dogs, poultry, pigs, humans
37
2 forms of E coli seen in cattle? Age? Symptoms
--importance of colustrum to fend of e coli in neonates. How much % BW should be ingested in the first 12 hrs? Repeat 18-20 hrs later.
- -septicemic--4-5 days--Usually no scouring or fever because septicemia is too overhwelming.
- -Enteric (enterotoxic)-- 0-2 weeks (up to 4)--Excess fluid in intestines--diarhea-mucus.
--5%.
38
E Coli can also be associated with what in the udders if poor sanitation? Symps>
E coli is commonly found in what infections of dog and cats? Also what inf in bitches? 1% of abortions in mares.
--mastitis. --high fever, low/no milk.
- -UTI
- -pyometra.
39
E coli in pigs is called? Age? Symptoms? Dx? Diffs?
- -neonatal colibacillosis/piglet scours.
- -1-12 days. --diarrhea, dehydration, HIGH mortality. --culture from sm and large int--> pure growth. -transmissable gastroenteritis, starvation, C. perfringens.
40
Pigs can get E Coli 1 week after weaning called what? Associated with what? How does it work? Symptoms?
How to control E coli in pigs
- -edema dz/post weaning colibacillosis/ E coli enterotox.
- -dietary changes. --Sm int colonized by E coli that produce toxin. Hemolysis and have pili antigens. Toxin causes arterial degen and increased vasc perm.
- -staggering gait, muscle tremors, spasms, edema of eyelids and SQ edema.
- -good sanitation, disperse farrowing, VACC WITH PILI ANTIGEN, electrolytes, determine antibiotic sens before tx.
41
E Coli in poultry colisepticaemia/colibacillosis: what are the 3 type of infection seen and what are the 3 main forms?
In neonatal, how old? If they live, what symptoms/
--acute septicemia, sub acute polyserositis and chronic granulomatous inflamm. --neonatal,
respiratory and enteric.
--2 days of hatching. High mortality. Yolk sac infection from fecal contam of shell. Shrunken eggs
--darkened lungs, enlarged spleen, fibrinous pericarditis, pleuritis, peritonitis, air sacculitis, inflamm of naval.
42
In respiratory colisepticaemia-where does the E coli infect? Where do the lesions form. What happens.
What 2 things of the airways become compromised in resp form?
- -bloodstream through resp. --tracheitis, bronchitis, pneumonia, air sacculitis, pericarditis, peritonitis.
- -air sacs thicken. Fibrinous pericarditis.
- -cilia and goblet cells.
43
Enteric colisepticaemia occurs due to what? Main lesian is usually what? Internal lesions are similar to resp form.
This form of E Coli can also cause other infections within the abdomen. NAme a few
- -sequel to something that has already damaged the GI. --liver congestion.
- -egg peritonitis (peritoneal cavity), inflamm of ovaries, salpingitis.
44
Septic Ecoli infections can also cause what inf?
Name a few other inf/dzs caused in poultry from e coli.
Most vaccines fagainst enterotoxigenic ecoli are antiblank? Give to preg females to be in milk/colostrum.
- -synovitis/arthritis.
- -cellulitis, air sac dz, yolk sac inf, swollen head syndrome, panopthalmitis, coligranuloma,
- -antifimbrial
45
Human E coli is usually from? In infants. Causes? UTIs as well.
What is the form of E Coli that was first described as a human form? Symptoms?
How does bact get in the meat or milk?
- -raw hamburger/raw milk. Diarrhea.
- -O157:H7 --hemorrhagic colitis, hemolytic uremia syndrome, thrombotic thrombocytopenic purpura, renal failure, bloody diarrhea, vomition, abdominal cramps.
- -can live intestines of healthy cows--can contam in slaughter. Live on cows udders/equipment.
46
2-7% of humans end up with what end problem from infection? 2% die
Ecoli in lambs cause what symptoms in milk and what in severe? Which lambs are the most vulnerable? Abortion/sterility in grown females.
Next genus in enterobacteriaceae is enterobacter. Lactose fermenter? Hemolysis? Opportunistic in which hosts? Which 2 are important species and what are they associated with?
- -Hemolytic uremia syndrome--> kidney failure.
- -transitory scouring, sickness
- -per acute toxemia, septic lameness, diarrhea
- -first 2 days.
- -YES --NO --immunocomp --cloacae-bacterimia in humans --aerogenes-mastitis and uterine infections in mares.
47
Next genus in enterobacteriaceae is Klebsiella. Species? OPPORTUNISITIC. Capsule? Associated with what dzs?
Next genus in enterobacteriaceae is citrobacter: naturally found where therefore indicator of what? OPPORTUNISTIC. NON PATHOGENIC. Lactose fermenter? Mistaken for? Causes what dz?
--pneumoniae --yes (large) --mastitis in cattle, cervicitis and metritis (wall of uterus) in mares, UTIs. Pneumo in humans, cystitis in dogs.
--soil, pollution --YES BUT DELAYED SO MISTAKEN FOR SALMONELLA. --UTI, some others.
48
Next genus in enterobacteriaceae is proteus. lactose fermenter? Genus contains how many sp? MOTILE. Hemolysis? What does the agar plate look like? Most frequent sp in animals? Commonly cuase what inf in dogs and cats? Appear similar to what on diff media. Is this enteric?
--NOOO. 4. NO. Swarming over surface. --proteus mirabilis. --UTIs. --salmonella.--no
49
Next genus in enterobacteriaceae is providencia. Similar to which other sp in biochem rxns. Lactose fermenter? What infections? Enteric?
Next genus in enterobacteriaceae is Morganella. Similar to which other sp in biochem rxns. Lactose fermenter? Sp? OPPORTUNISTIC. Where can it be found/what inf are caused? Enteric?
--proteus.--NOO --rare in animals. Diarrhea in humans --nO.
--proteus --NOO --morganii --in intestinal tract of humans and animals --wound and UTIs. --NO.
50
Next genus in enterobacteriaceae is Shigella. Only affects what sp? Name some common types. Closely related to what other sp?
Next genus in enterobacteriaceae is salmonella. Gram? Aerobic or anaerobic?
- -humans and NHPs --dysenteriae, flexneri, boydii, sonnei. --escherichia.
- -gram negative --facultative aerobic.
51
What are the 3 epidemiological classes of salmonella grouped as
What are the 2 species of salmonella
--those infecting humans (typhi, parathypi A-C) --those for particular sp of verts (gallinarum-poultry, dublin-cattle/humans, abortus equi-horses, abortus ovis-sheep, choleraesuis-swine/humans) --no particular host preference (PARATYPHOIDS)
--bongori and enterica (6 subspeciies).
52
Approx 2500 serotypes of salonella. due to 67 what antigen grouips? and numerous what antigens? Names based on 3 things
-what media are most commonly used to iD salmonella?
- -O or H antigens
- -dz syndrome or animal --place found or antigenic formular.
- -mcconkey (most common), brilliant green, XLD or XLT4.
53
what biochem tests can be used to serotype salmonella?
Name the 3 main antigenic structures used to serotype salmonella enterica/
What are the 4 kinds of antigen
- -TSI-blank/pink or commerical id systems.
| - -O-somatic antigen-surface-heat stable --H-flagellar antigen- 2 phases-heat labile. --Vi-capsular antigen.
54
What occurs in salmonella HO variation?
S-R variation?
Loss of H antigen/flagella. HO to O. Turns into mutant non motile. Rare and irreversible. The genetic material for the enzyme that synthesize H is lost/altered
--change from smooth to rough form (all bact.) Gradual loss of O-exposed core polysacc. Rough--> non spec agglut. Low virulence. Good for vac. No cahnge in H.
55
What occurs in the O and V-W variation.
***What is phase variation.
- -causes quantitative antigenic changes of O antigen. --quantitative antigenic change of Vi antigen. O and H stay unchanged.
- the H antigen exists in 2 phases. Change during multiplication. Some salm are nonmotile/monophasic.
56
pathogenesis of salm-ingestion. Colonization of where? invades mucosa. Inflamm--> cytokines, PG, enterotoxins. Increased adenylate cyclase--> increased what? Causes what?
Human serotype Typhi. enters GI and then what? Can stay where for years? Have vacc against this.
--lower intestine. --cAMP --fluid prod and diarrhea.
- -enters lymphatic system, disseminates throughout body by blood stream.
- -gall bladder or bile ducts.
57
Salmonellosis in poultry: name the 2 host specific and there are many paratyphoid salmonellas.
S. pullorum AKA what? is a reduced incidence in the US> What are the symptoms in young and old and how does infeciton spread
--gallinarum and pullorum--both non motile.
==white bacillary diarrhea/pullorum dz.
--young: mortality. depressed/huddle under heat. anorexic. white fecal pasting from vents. white nodes in lungs. necrotic lesions in liver/spleen. adult: symptomless carriers.
--ovaries/eggs. Chicks hatch and are infected. Feces of chicks contam environment.
58
The other host specific in poultry is gallinarum AKA? Similar cycle of inf to pullorum. Symtoms?Affects what age the most? Acute outbreaks with high to chornic infections. NONE IN THE US.
How can poultry get non host specific paratyphoid?
fowl thyphoid. greenish yellow diarrhea, discoloration of comb and wattles. growing/adults>young.
--comtam feed.
59
2 main salmonellas in cattle? which is host adapted or not.
S. dublin affects adults how? Excreted in feces, which is bad why?
s typhimurium usually occurs in what age? infection cycle alike to dublin, but not many CHRONIC carriers. symptoms calves vs adults? lesions?
- -S. dublin (host specific) and S typhimurium (non host specific)
- -symptomless carriers --can survive in feces for 2-4 months and contom env.
- -2-6 wk old --fever, diarrhea,--low milk prod, fever. feces with blood. death in 1-5 days, abortions.
- -arthritis, pneumonia, encephalities.
60
paratyphoid salm in cattle?
--what are the two main types of host adapted salm in pigs? Which one is most common in the US? symptoms? what about the other one?
What salm of cattle is can affect pigs?
Many non host adapted in pigs.
- -yes. humans can get from eating.
- -S coleraesuis-most common-necrotic enteritis.from ingestion
- -S. typisuis-not as common, alike to coleraesuis. diarrhea, emaciation, lesions of LN and int, sepsis.
- -S typhhimurium.
61
- -What are the 4 most common serotypes of salm in horses? young more suscep. Initiation of dz is often caused by? Symptoms?
- -many types of salm in dogs. often in feces of normal dogs. symptoms?
Typimurium (also in cattle and pigs), enteritidis, newport, heidelberg. --stress like sx, NG tubes, other illnesses. --fever, colicky pains, diarrhea.
--intermittent diarrhea. puppies more suscept wtith very rare septicemia.
62
- -many types of salm in cats. kittens more suscept. symptoms?
- -many types of salm in sheep including what non host specific type> symptoms? in preg animals?
--can be carriers without symptoms. acute or subacture enteritis with or without septicemia. intermittent diarrhea, vomiting.
- -typhimurium. --fever, scouring, blood in feces. in acute=watery putrid diarrhea. high mortality. scouring of greenish/yellowish paint like material.
- -preg=die before abortion. fetus and placent=^^comtam.
63
wild animals that have high case of salm and give to humans (3)? Where do birds get salm? what kind? most comon birds?
General Tx for salm?
The family pasteurellaceae have many genuses! What 3 do we cover?
- -turtles, iguanas, frogs.
- -contam env. s typhimurium. --canaries. homing pigeons.
- -antibiotics for acute salm after antimicrobial suscept testing.
--pasteurella, mannheimia, gallibacterium
64
Pasteurellaceae pastuerella: size/ gram? non acid fast. shape? capsule? aeriobic/anaerobic? MOtile/ spores? grows on? around bile salts? Ferments what? catalase/oxidase? Colornies look/smell like?
very small-gram neg. rod or coccobacilli (pleomorphic). capsules in virulent form. --aerobic OR facultative anaerobe. --non motile.-- no spores. --blood agar (attacks CHO weakly). no/scantily on bile salts. --sucrose, therefore NO GROWTH ON MAC. --pos catalos/oxidase -round, gray, mucoid. thick hyaluronic acid capsule. fruity/sweet odor.
65
what is interesting about pasteurella staining on wrights? How are the different serotypes of P multocida identified. Most common letter of capsule type?
--P multocida survive in blood for 3 weeks and carcasses for 18 months. Main wild animal carcasses? Transmission?
bipolar staining
- -numbered and lettered capsular polysaccs (A-E) and cell wall lipopolysaccs/proteins (1-16).
- -A.
- -skunks, raccoons and wild fowl.
- -airborne droplets, contam water and food.
66
P multocida is norm in mammals, but what happens if the animal's immune is suppressed?
Unlike mammals, P mult in birds=? Whos more suscept turkeys or chickens?
- -secondary invader--> pneumonic pasteurellosis.
| - -acute/chronic dz. All birds get it but --turkeys>>chickens, pigeons, waterfowl
67
P mult in ruminant bovids (cattle, camels, goats, sheep) can cause what? What are the sysmtoms and where can it be found? Remember BIPOLAR ORGANISMS.
- -hemorrhagic septicemia --high fever, dysentary,edema of the throat, neck and brisket. high mort-die within 24 hrs or pneumo if living. blood stained fluid accum, wide spread petechial hemorrhages, enlarged LN.
- -rainy, tropical/subtrop regions. europe, italy. none in n america.
68
Tx for p mult in calttle? disinfecteant?
| P mult in birds is called??? symptoms? pet birds often get it from?
- -antibiotic tx: peniccilin and tetracycline. Vac availble: modified live.
- -0.5% phenol.
- -fowl cholera. swelling, edema of wttles, lameness due to arthritis of survives. serofibrinous pericarditis. high mort. vacc avail
- -cats mouth-bites. prompt tx or fatal septicemia.
69
Older or younger birds more suscept to fowl cholera? How is it transfered from bird to bird? How do the lungs look? BIPOLAR ORGANISMS. Egg transmission? How do you deal with carcasses? Tx?
- -older
- -excretions from mouth, nose, conjunctiva.
- -consolidated, hemorrhagic, peritonitis.
- -NO. --pick up and destroy. dispose by burying and burning. carcasses can have orgnaisms for 18 months.
- -keep from wild animals. BacterinS and live vaccs. bacterins-severe rxns sometimes. each bird injected. live in drinking water for 6-8 weeks. repeat. Sulfa and antibiotics will lower mort. CU++and Mg straings of vacc.
70
what is p mult called in rabbits? symptoms? transmitted how? tx?
- -snuffles and septicemia.
- -snuffles=mild resp inf, rhinitis, conjuenctivisit, oneumo, otitis media, mucopurulent exudate, blocked nasal passages, difficulty breathing. --septicemia-fever, purulent nasal discharge, breathing diff, consolidated lungs, fibrinous deposit on pleura, emaciated.
- -aerosol, contact with fomites. mORE withage.
- -no vacc, antibiotics
71
what is p mult in pigs called? symptoms? age? Control/Tx?
--dogs and cats?
Humans? Tx?
- -atrophic rhinitis. sneezing, excessive lacrimation, occasional epistaxis, turbinate bone destruction, deform snout, demonecotic toxins.
- -3-8 weeks. --sulphonamides, tylosin, tetracycline. vacc wtih bordatella.
- -normal flora.
- -accidental hosts from bites. P canis from dogs. P mult from cats. --penicillin, sulfonamides, tetra.
72
Next pasteurellaceae family genus is mannheimia. what does this cause in what sp? Symptoms?
--what generally stops m haemolytica in the lungs? what does the org produce to cause damage.
- -mannhemia haemolytica in CATTLE AND SHEEP.
- -cattle-acute fibrinous pleuropneumo in cattle (shipping fever). abscesses/penumo of lungs. both: worse under stress and multiplies in nasopharyns and lungs.
- -sheep-septicemia
- -macrophages phag, but too many escape macrophages. --leukotoxins (exotoxin) that kill macrophages, hemolysis, neuraminidase, proteolyric enzymes.
73
how do you dx m haemolytica> tx?
Next pasteurellaceae family genus is galliacterium. Poorly understood. Found in many lesions of chickens. 2 types? Gram? shape? motile? Capsule? hemo? colonies?
--ver small pink colonies on Mac. Indirect hemagglutination test, narrow zone of hemolysis. --antibiotics labelled for tx (ceftiofus, oxytetra), vaccs.
--anatis and genomospeciess. --gram negative coccobacillus. non motile, yes capsule. beta hemp. grayish round semi transparent colonies.
74
Symtoms of gallibacterium anatis? What age?
- -low egg prod. affect repro tract. ovaryian attrophy, he moor, fillicles are fucked. nonfxnal oviduct. peritonitis, large kidneys.
- -22-34 weeks. 40 weeks in brooilers.
75
BORDATELLA: gram? shape? aerobic? motile? ox? catalase? hemo? COMMENSAL. Tropism for?
Name the 4 types we are covering.
- -gram neg pleomorphic coccbacilli. Aerobic OBLIGATE. motile or non motile. ox and catalase pos. hemolytic except avian strains.
- -ciliated epi
- -pertussis-humans, parapertussis-sheep, bronchiseptica-dogs and pigs mainly, avium-birds.
76
Name the 4 bordatella toxins and how they work.
- -demonecrotic toxin (diff from p mult one). Heat labile toxin-sm m of peripheral BVs, arterial constriction, ischemia. Intracell-lysis of bact--> release
- -tracheal cytotoxin-ciliated resp epi. Destruction. Exotoxin-released
- -LPS-endo-fever, completment
- -adenylate cyclase-(not avium) inhibs phag and phaglysosomal fusion.
77
Bordatella pertussis in humans. Motile? Symptoms? Toxin doeswhat? Vacc made of what? Tx? Transmission?
NON MOTILE. --paroxysmla cough. Mucus prod and vomition. --paralyzes cilia--> cough. Blockage of airways. --killed toxin-highly effective --erythromycin --aerosol droplets.
78
bordatella parapertusis is a lot like pertussis, but what/ found in?
bordatella bronchiseptica. motile? bipolar? not only catalase and ox pos, but also what pos. does what to litmus milk.
what 3 sp is it found in?
--milder --sheep.
- -motile. yes, bipolar. urease pos. alkalinizes.
- -atrophic rhinitis of swine (often at same time as p multi)--kennel cough in dogs (often 2*)-=cats.
79
what are the 3 vaccs in dogs for bord? what is the main toxin in bord in pigs? What does teh toxin of p mult act on? bord?
injectable--2 does at 4 mos. --intranasal-2 weeks. local immunity. --oral
- -demonecrotix toxin--atrophy of nasal turbinates and sever bronchopneumo
- -osteoclasts==increase activity to destruct--osteoblast-impaiirs osteogenesis. ALSO attaches to cilia and causes cilial stasis.
80
bord in cats causes? --vacc in pigs?
4.)bordatella avium resembles bronchiseptica but WHATS THE BIG DIFF.
HIGHLY contagious. high or low morbid/mortality? Causes rhinotracheitis. Also called what in turkeys? spread how? symptoms?
- -mild URI
- -pigs at 7 days old and repeated.
- -urease neg. --high morbid, low motat.
- -turkey coryza. --direct contact by aerosols and env sources
- -submax swelling, URI, frothy discharge from eyes, lacrimation, sneezing, mucus, cough, tracheal collapse.
81
COntrol and tx of bord avium?
FRANCISELLA TULARENSIS-- name both strains, what they ar elike and what is suscept.
- -live vaccs/cleaning --killed with disinfectant and broad spect antibiotics and polyymyxin. NOT PENICILLIN.
- -type A-highly virulent-rabbits, cats, some dogs.
- -type B-less virulent-muskrats and beavers.
82
How is francisella tularensis spread?
| Lesions associated? What tox is resp for lesions? Symptoms?
- -deer fly and tick
- -granulomatous lesion in visceral organs--> necorsis and suppuration of LNs. Bite of tick--> ulcer and LN swelling in 3-10 days. Small abscess in organs and LN.
- -endotoxin.
- -also, systemic or typhoidal--> GI. fever, chills, malaise, headache, skin lesions, 5-10% death.
83
Yersinia- gram? Name the 3 main ones covered and what they affect. All 3 can adapt to a wide range of what?
Yersinia pestis:
bipolar? --Aerobic? Ferment lactose? Small colonies on what kind of agar? TSI=alkaline slant and acid butt. Motile? Pos or neg for citrate, urease and indole? Facultatively intracelllar in what?
- -gram neg. --enterocolitica-foorborne in children, pseudotuberculosis-animals, occasionally humans, pestis-rodents. --temps (4-37)
- YES. --yes --NO FERMENTATION--mackonkey
- -no motility --negative for all three. -macrophages.
84
What does yersinia pestis cause? dz in what animals. Carnivorous animals show symptoms? What domestic animals are more susceptible, even though this is NOT A DZ OF DOMESTIC ANIMALS. 3 forms humans get? How?
- -plague --wild rodents.
- -nope.
- -cats --bubonic, septicemic, pneumonic plague.
- -bite of infected flea, handling infected tissues, airborne droplets from human or househould pets.
85
What are bubos and what are they characteristic of?
though cats would have more symptoms with plague what about dogs?
rest of the world has vax, no longer in US. --Tx? Decontam?
- -massively swollen LN--yersinia pestis.
- -only fever and recovery.
- -7 days antibiotics. --sunlight, heat, cant survive long. bleach- 30 min.
86
Yersinia pseudotuberculosis is primarily in which animals, rarely in humans. Symptoms?
--Yersinia entercolitica-From what? INfects what sp? Symtoms?
- -rodents, turkeys, goats, swine, cattle, sheep, wild birds, deer. --acute mesenteric lymphadenitis and fever in humans, fatal sept in animals and urinary tract disturbances in cats
- -foodborne--wild and domestic animals, cold blooded animals, pigs, healthy catlle, swine. Humans=mild and severe GI issues. msesnteric lymph gland inflame. Terminal ileitis. common in young children-day cares.
87
HAEMOPHILUS: gram? shape? motile? sporess? aerobic/anaerobic? capsules?
Most sp requre one or both of what factors for growth?
- -gram neg --coccbacillary rods/pleomorphic/sometimes long filaments. --non motile --no spores --aerobic and facultatively anaerobic --capsules present
- -X factor (haemin) and V factor (co enzyme 1 of nicotinamide adenine dunucleotide (NAD+).
88
Where is haemophilus usually found? What sp? potential pathogens. Modes of infection?
--9 Species exist. Which one causes GLASSER'S DZ? What are the symptoms in what sp?
- -commensal in mucus membranes of upper GI, resp, and genital tract. Humans and animals. --inhalation and fomite.
- -haemophilus parasuis
- -fibrinous inflamm of serous memb, lesions on pericardium, pleura, peritoneum, joints. fever, resp/abd distress, lameness, paralytic and convulsive signs. --YOUNG pigs in wearning, transport, management stress.
89
haemophilus parasuis causes fibrinous deposits called what?
NEXT GENUS: histophilus somni. Causes what in cattle? How does the infection occur and what symptoms happen?
Does it need X or V factors?
- -polyserositis.
- -infectious thromboembolic meningoencephalitis --colonizes nasal cav, gets into blood--> bacteremia. Cerebral thrombus. Adheres to vasc endo cells--> damage. Expose subendo collagen--> thrombus. LOCALIZES IN CNS. RESP DISTRESS--> pneumo. Fever, staggering, knuckling of fetlocks, stiffness, paralysis, death. Arthritis.
-NONE
90
What if a preg cow gets histophilus somni?
--what does brain look like in TEME?
Stress makes it worse.
Are vax avail for histophilus somni? Tx?
Avibacterium. What type do we cover? X or V factors?
- -repro failure, endometritis, late abortion, mastitis.
- -hemorrhagic areas, firing thrombi in BVs of brain and meninges. Congestion and hemorrhage
- -yes! bacterins. --penicillin and tetracyclines
- avibacterium paragallinarum
- -BOTH X AND V.
91
avibacterium paragallinarum are BIPOLAR. Symptoms?
| How does resp distress occur?
- -nasal discharge, resp distress, sneezing, edema of the face, drop in egg prod. high mort, swollen wattles, mucus in nasal passages-watery to mucoid. Fibrinous sinusitis--> 2* infection.
- -clotted blood, mucus and fibrin flake into the trachea and cause. Death due to suff.
92
how is avibact grown? vacc avail? tx?
NEXT: Pseudomonacdaceae pseudomonas. Ubiquitous. Found where? gram? Aerobic? Shape? Motile? Spores? HIGHLY resistant to disinfectants. Makes many pigments.
- -on chocolate agar from tracheal swab/exudate-
- yes! bacterins.
- -tetracyclines, neomycin, erythromycin.
--aquatic habitats and in soil. --gram neg --obligate aerobic. --motile with one or more flagella. --NO spores.
93
What pseudomonas is in animals? Normal in healthy animals/humans. Opportunistic. Where does it live? What does it released that destructs the tissues? Causes hemorrhagic pneumo ins what animals? Vacc available? Tx?
pseudomonas aeruginosa. --water faucets, humidifiers, jacuzzies, etc.
- -proteolyric enzymes.
- -mink and chinchillas --yes, for minks/chinchillas=bacterin. --highly resistant to antibiotics, do susceptibility test. Usually combo of gentamicin/tobramycin with carbenicillin/ticaricillin. NOT PENECILLIN. Phenols work.
94
Next: burkholderia mallei causes what dz? What sp? What forms in each sp? What sp are resistant? More suscept=felids or canids?
--where is it still found?
--Glander's dz. --donkeys=acute, horses=fatal chronic, mules=intermediate, seldom in humans, canids, felids. Sheep, cattle, swine, birds=resistant. Cats>>dogs (from eating the meat)
--certain parts of asia, africe, middle east. test and slaughter programs have eradicated most.
95
symptoms of glanders in humans?
3 forms of glanders? Explain. Often happen together
Transmission?
- -nodular eruption on face, legs, arms, nasal mucosa, pyemia, metastatic pneumo.
- -nasal-catarrhal discharge --pulm-nasal septum nodules, granulamotous pneumo/lesions and ulcers, fever, death --skin=thick lymph channels.
- -resp, contact with exudates, contam food/water, eating meat that is infected (esp zoos and circuses)
96
Make sure to diff glanders with what dz in horses? biggest different in tests? Also diff from epizootic lymphangitis. Cutaneous nodules, but mallein neg.
What is the mallein test like?
What is the other type that is a lot like burkholderia mallei? Animals that were resistant are not to this type. Symptoms? Infected how?
Tx for both?
- -strangles=strep equi equi=mallein test neg while glanders will be pos.
- -intrapalpebral-delayed hypersense test. Pos will develop sever purulent conjunctivitis in 6-12 hrs.
- -burkholderia pseudomallei=pseudoglanders
- -small caseous nodules, abscesses in organs and SQ.
- -ingestion, inhalation, through wounds/abrasions
- -no vaccs, tx is prolonged and often unsuccesful.
97
NEXT: MORAXELLA. What are the forms in sp of interest? Gram? Aerobe? Motile/ Ferment CHO? X or V factors? hemolytic? Causes what symptoms in bovines. MOST COMMON DZ OF CATTLE.
- -m. bovis (conjunctiva of cattle) (dont need to know m boevrei of goats, m canis, m ovis (sheep)).
- -gram neg, obligate aerobe, non motile rods, DOES NOT ferment CHO. NO X OR V. Beta hemolysis on BAP. --infectious bovine keratoconjunctivitis (pinkeye), keratitis, corneal opacity, ulcertaion. lacrimation. VERY CONTAGIOUS
98
How does moraxella bovis attach to eye? What causes the inflamm response? TransmissioN? Susceptibility differences among cows? Vacc? Tx?
- -fimbriae aid in the attachment to corneal epi. --enzymes break dwon the jxns between corneal epi. --house flies and stable flies, direct contact, fomites. --highest in summer, less eye pigment=higher chance. Higher solar radiation=higher change, dairy breeds<
99
NEXT: Campylobacter: ZOONOTIC. Diarrhea in humans, esp kids. Foundn where in humans and animals? Gram? shape? Aerobic/anaerobic? Name the 3 of importance and what sp it affects and basic symptoms
- -repro and alimentary tracts
- -gram neg --curved, S shapes, spiral, corkscrew. microaerophilic/obligate anaerobe.
- -C fetus venerealis-CATTLE-embryonic death
- -C fetus fetus-sheep cattle-abortion
- -C jejuni-wide range of animals-bacterial gastroenteritis.
100
How are c fetus venerealis and c fetus fetus transmitted. --venerealis reservoir is where on cattle? SYmptoms? Where does it replicate?
- -venerealis--veneral and fetus=oral.
- -prepuceal crypts of male and vagina. --infert, metritis, salpingitis, failure to implant, early embronic death, abortion.
- -cervicovaginal jxn and then into uterus in progestational period to replicate at both places.
101
C fetus venerealis-if calf born, does it live? Sheds from uterus for a very long time. Infects human? Older or younger bulls more suscept? Cows can rid of it in 5 mos, but bulls is lifelong. Control how?
- -dies within a few hrs (endotoxins). NO NOT IN HUMANS. --older-lifelong. In crypts of prepuce.
- -treat semen and uterus with streptomycin and penicillin. Oil adjuvented killed vaccines.
102
C fetus fetus is found in what sp? Tranmistted how? Causes abortion when? Pathogenesis is similar to venerealis. INvades uteruss--> fetus
After ingestion--> bacteremia. Where does the organism LOCALIZE. Causes? If a ewe aborts, does it get immunity? Human symptoms?
- cattle, sheep, goats, humans.
- -ingestion --later half of gestation.
- placenta--> placentitis--> abortion.
- -yes for about a year
- -rare in humans, but premies, termination of preg,
103
C fetus fetus specimans to test? Vacc? Tx?
C. jejuni (and C. coli) are widely distrib in what sp mainly, but also what sp? Causes what? From what sp would a human get it
- -fetal stomach contents, placenta, etc.
- -oil/alum adjuvanted bacterins, polyvalent. --penicillin and streptomycin. tetracyclines in feed/water.
- -wild birds. --int tract of wild/domestic dogs, cats, cattle, poultry, sheep, pigs, minks, ferrets. and rarely humans
- -abortion in sheep, enteritis in humans.
- -any domesticated sp
104
Main symptom of C jejuni in pigs, lambs, mink, ferrets, cats, dogs, huamns?
In chickens, where does c jejuni colonize? Causes what symptoms in chickens? Vacc for poultry?
Symptoms in bovine?
- -diarrhea.
- -lower intestines/cecal region/no attachment, but remains in crypts.
- -causes infectious hepatitis, poor egg prod and lesions of liver.
- -NO VACC. --mastitis and unpasteurized milk will cause GI issues in humans.
105
campylocater is leading cause of what worldwide?
NEXT: VIBRIO: gram? aerobic/anaerobe? shape? motile? found where? domestic animals/ Humans?
V cholerae causes what? Vacc?
bacterial diarrhea.
--gram neg--anaerobe --straight/curved rods, motile and polar flagella. --sea/fresh water in aquatic animals. --none in domestic animals --5 sp cause diarrhea in humans.
--potent enterotoxin in small int--> colera in humans. Vacc of killed whole cell vacc.
106
NEXT: Lawsonia intracellularis is an obligate intracell bact. NON FLAGELLATED. Gram? many hosts! name the main ones. Main name for dz in pigs? Symptoms?
Pathogical findings in the gut?
- -pigs, NHPs, hamsters, rabbits, rats, guinea pigs, foals, shepp, etc etc.
- -proliferative enteritis
- -intermittent diarrhea, retarded growth, severy dysentery, wasting dz, death.
- -thickened and flaccid gut wall of ileum and spiral colon. Surface thrown into fold. Prolif of epi. Bact in cyto of epi. Can live env for 2 weeks. Irreg villi/crypt.
107
L intracell has been found in 2 other sp other than pigs. Tx? Vacc>
NEXT: Actinobacillus are found in farm animals. Mucus membrane commensals in waht 2 parts of body? Cant survive in env for too long,
Main 2 sp? Symptoms of each?
- -horses and dogs.
- -no approved antibiotics. Judicious use is ok.
- -modified live vaccs.
- -upper resp and oral cav.
- -A. ligneieresii-pyogranulomatous-inflamm of soft tissue, induration of tongue
- -A. equuli-septic polyarthritis, neonatal septicemia.
108
Gram? Shape? motile? ox? Aerobe? anaerobe? Mack or BAP? Granules. Worldwide. Involved with soft tisue.
A. lignieresii-main host sp? Normal flora where in cows? Describe pathogenesis
- -gram neg, short rods. NON MOTILE. Ox pos, facultative anaerobe. --mackonkey.
- -cattle
- -buccal membranes and upper GI of cattle.
- -enter via wounds in buccal epi usually with penetrance of foreign material. Phags cause granulomas--> wooden tongue. Abscess, ulcerate, fail to hear. Pus with granules. Likes soft tissues.
109
Symptoms of wooden tongue
Tx? Vacc?
Next; A. equuli: pathogen of what animals. LIves where normally? COlornies look like? In culture makes the liquid feel like what/
drool saliva, tongue protrudes, ulcers, unable to eat/drink--> fatal if untreated.
- -responds to antibiotics like sufonamids with penicilin/streptomycin. Sodium iodide parentally or potassium iodide orally. NO VACCS.
- -foals--> fatal.
- -intestines and tonsils of horses of all ages
- -sticky smooth colonies. non hemolytic.
- -viscous.
110
Symptoms of A. equuli in older horses vs foals? Older=opportunistic
Tx? Vacc? Test joint fluid/blood/cervical fluid.
- -older=septicimia, nephritis, abortion, fever, dysphagia, liver, lungs.
- -foals from utero through umbilicus, ingestion, inhalation. --> diarrhea, pneumo, polyarthritis=sleepy foal dz/joint ill. many deaths.
- -streptomycin=effective
- -vacc not widely practiced, but giving to mare seems to help foal via colostrum.
