Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
26 Cards in this Set
- Front
- Back
|
Is Lawsonia a new or ancient infection?
|
There's a new sheriff in town!
A new infectious problem –May have been known for a long time but is an increasing problem –May be an organism that has arisen in a new host –May be a previously unknown agent • Causative agent reported in 1985 • Koch’s postulates fulfilled in 1993 |
|
|
What is the gram staining and morphology of Lawsonia intracellularis?
What area does it inhabit? Does it share a trait with Listeria? |
• Gram negative, curved rod; single polar flagellum
• Obligate intracellular pathogen of the intestinal tract – Grows in the cytoplasm of infected cells – No evidence of actin polymerization (as seen in Listeria) – Extracellular bacteria have large similar sized electron dense bodies within the cytoplasm not seen in the intracellular form • Stored energy resources? |
|
|
What pathogen is Lawsonia intracellularis most similar to?
|
• Appears to be a very unique bacterium
– Not closely related to any pathogen discussed so far. – In the y-proteobacteria, distinct from all other known species – Originally “Campylobacter-like”but only has 30% identity with Campylobacter |
|
|
What are the two forms of Lawsonia intracellularis? What are their clinical signs? Which is associated with what age of pig?
|
–Chronic form -poor growth rate, diarrhea, stunting
• Porcine proliferative enteropathy(PPE) • porcine intestinal adenomatosis(PIA) in growing/finishing pigs –Acute form -bloody diarrhea, sudden death • proliferative hemorrhagic enteropathy(PHE) in finishing pigs and replacement gilts –Abortion associated with acute PHE in sows/gilts within six days of the onset of clinical signs |
|
|
What role does stress play in Lawsonia? Which type of disease form usually results?
|
• Role for stress? Acute form often presents
– when replacement breeding animals enter a herd – following movement of pigs. – following nutritional changes, feed antibiotic usage, changes in temperature – when there are fluctuations, pig density, pig age, facility design, sanitation, immune status, resistance, genetic susceptibility, outdoor raising |
|
|
What is the pathogenesis of Lawsonia intracellularis? How is it transmitted?
|
• Little is known about pathogenesis
–only recently cultured in vitro. Challenging to grow. –Characteristic hyperplastic proliferation of intestinal epithelia. • Nature of enterocyte proliferation – Cells at the bottom of intestinal crypts take over the entire crypt. – Results in • loss of mucus producing cells • expansion of mucosa, • disruption of structure of the villi • Likely fecal-oral transmission |
|
|
What is the only way that Lawsonia can be cultured?
In what species can Lawsonia be identified? What sort of clinical manifestations does it cause? |
In tissue culture
• L. intercellularis identified in many species • Emerging infection in horses –now a significant problem in the industry. –cause diarrhea, depression, fever, inappetance (anorexia), weight loss, edema (fluid swelling) on the abdomen or lower limbs, a poor hair coat, and intermittent colic due ... • Wet tail in hamsters |
|
|
What are the virulence factors of Lawsonia?
|
None clearly identified.
– Flagella • not seen intracellularly–may be required for penetration of mucus and then are lost after attachment – Adhesins and receptors • Has a T3SS secretion system • Animals make antibodies to components of the T3SS • T3SS may be crucial for intracellular development. – Decreased antigen exposure • Antibody decreases infection • Cells enter individually>>loss of microvilli, thickening and disruption of cell border – Entry dependent upon host cell metabolism – Lytictoxin (cytolysinor hemolysin) • Involved in escape from intracellular vacuoles – Empty vacuoles – Bacterial cells line up on apical side of host cell – Mitogenic toxin • Dividing host cells promote growth better than non-dividing cells • Immunosuppressive? – Chronic form • Decreased MHC expression on infected cells • No inflammation • No CD3+ cells, B cell infiltration observed – Acute form • More vigorous immune response, presence of IgM+ B cells • The bacteria more widely distributed – macrophages in the lamina propria, submucosa, tonsil and lymphatics infected • Possible Polymicrobial disease? |
|
|
How is Lawsonia diagnosed and controlled?
Is there a vaccine against Lawsonia? |
• Diagnosed via ELISA, PCR, microscopy of ileum.
• Prevention is best –vaccine available –replace stocks with ELISA-negative animals –antibiotics in feed |
|
|
Does Lawsonia have a vaccine? What are the goals of it?
What is its relationship with antibiotic use? |
• Attenuated live vaccine – put in water/feed
• Goals –To reduce overall in-feed and water medication use –To improve clinical control of disease in both high value replacement gilts and finishing pigs. Vaccine decreases shedding, increases serum antibody. Vaccine decreases antibiotic use |
|
|
Who gets infected by Bartonella? How is it transmitted? Is it zoonotic?
|
Multiple bacterial species make up Bartonella. They use and arthropod vector and mammalian reservoir hosts.
They are zoonotic. Transmitted by the vector and/or reservoir. Can cause dz in accidental host. |
|
|
What is the morphology of Bartonella species? What is their gram staining?
What protein is required for its growth? |
Gram neg, short pleiomorphic bacillus/coccobacillus.
Fastidious, aerobic, slow-growing. Hemin must be present. Catalase, oxidase, ureease and nitrate reductase negative. (this is a very negative bacteria). Blood-borne, intracellular organism |
|
|
What is carrion's disease?
|
human syndrome associated with Bartonella infection: acute dz - fever, life threatening anemia. chronic dz - vascular proliferative disease.
Other human dz: trench fever (fever, lymphadenopathy); cat scratch fever |
|
|
How does Bartonella present clinically in cats?
|
Some strains can cause persistent infection for months to years.
May also cause lymphadenopathy, gingivitis, stomatitis, renal and urinary tract abnormalities. Uveitis - ocular production of Bartonella IgG in aqueous humor. |
|
|
What does Bartonella hensalae infection result in, in cats?
Which antibody corresponds with control of this infection? |
Bacteremia. Infects and persists in endothelial cells.
IgM's and IgG are detected both at around 14 days post-infection, but IgM doesn't effect the bacteria, IgG controls it. |
|
|
What are the virulence factors of Bartonella?
|
Type 4 secretion system. Mediates adhesion and intracellular transfer of DNA or proteins to target cells. Bartonella has multiple T4SSs.
TRW mediates adhesion to RBC VirB mediates adhesion to endothelial cells. |
|
|
How does Bartonella target red blood cells?
|
By firm adherence - bacteria must be internalized and replicated in RBCs - an adaptation to transport by blood-sucking arthropods.
TRW - T4SS mediating adherence to RBC |
|
|
What host cell does Bartonella target?
|
Endothelial cells.
|
|
|
What is the host immune response to Bartonella mediated by?
Is there cross protection? |
In humans, TH1.
In cats, TH2. No cross protection among Bartonella species. Cats can be simultaneously infected with multiple genotypes and species, but antibodies do prevent reinfection with the homologous strain. |
|
|
Why is Bartonella henselae more prevalent in feral cats?
Why is there geographic distribution? |
More fleas.
Fleas are geographic, they like hot and humid conditions. |
|
|
How is Bartonella Henselae transmitted?
|
Among cats - clearly associated with fleas, and fleas only. And then only by cat flea feces entering the flea bite site with scratching or grooming. Neither flea saliva, nor ingestion of the flea do it.
To humans: cat scratches, not clearly associated with fleas, though flea feces in the environment can act as a source of human infection. |
|
|
How is Bartonella diagnosed?
Are the species cross reactive? |
Isolation, real-time PCR, RFLP and PcR, ELISA, western blot. Positive titer >64
High level of cross reactivity among Bartonella species make differentiation difficult. Cross-reactivity seen with other bacteria (chlamydia) |
|
|
How do veterinarians and vet techs get Bartonella?
|
years of exposure. More years of practice, more likelihood of being seropositive.
|
|
|
How is Bartonella treated?
|
Very sensitive to antibiotics in vitro, but not in vivo.
For serious infections in humans, critical to use two antibiotics. No clear evidence antibiotic treatment will clear bacteremia or prevent carrier state in cats. |
|
|
How do you control Bartonella?
|
Flea control and spay and neuter.
IMPORTANT. |
|
|
Is there a Bartonella vaccine?
Will declawing help the spread of Bartonella? How could spaying/neutering reduce the prevalence of Bartonella in the cat population? |
No vaccine.
Control the arthropod vector on dogs and cats, most important control. B. henselae not transmitted by milk - no evidence of cat to cat transmission without the vectors. Declawing doesn't reduce transmission to humans. Neutering may decrease incidence of recurrent bacteremia in cats because bacterial multiplication may be directly or indirectly under hormonal influence. Reactivation of bacteremia higher in estrous cats than non-estrous. |
