In a case now pending before the US District Court for the District of Columbia,1 the trial judge recently granted a preliminary injunction which purports to temporarily stop the Trump Administration from banning so-called “transgender” persons from serving in the Military.
But we will look at the real issue: Does the Judicial Branch of the federal government have constitutional authority to require the Legislative and Executive Branches of the federal government to permit transgender persons to serve in the Military?
· Article I, Section 8, clauses 11 – 13, delegate to Congress the powers to declare War, grant Letters of Marque and Reprisal, make rules concerning Captures on Land and Water; raise and support Armies; and to provide and maintain a Navy.
So! All the powers over the Military which have been delegated by the Constitution are vested in the Legislative and Executive Branches of the federal government.
The Judicial Branch has no role to play in the organizing and operation of the Military Forces.
Pursuant to Article I, Section 8, clauses 11-14, Congress alone has the delegated authority to decide who may serve in the Military. If Congress issues Rules banning transgender persons from serving, then it is the President’s job, as Commander in Chief, to enforce those rules.
The Judicial Branch of the federal government was created by Article III, US Constitution. That Article created the supreme Court, and authorized Congress to ordain and establish, from time to time, such inferior courts as needed. Pursuant to that authority, Congress has established 94 federal district courts (where most federal trials are conducted), and 13 US Circuit Courts of Appeals.
The US Military has its own court system which is not part of the Judicial Branch of the federal government. The military courts are “Article I Courts” created by Congress in the Uniform Code of Military Justice (UCMJ).2 They consist of trial courts where courts-martial are conducted; each Branch of Service has its own “Court of Criminal Appeals”; and the “US Court of Appeals for the Armed Forces” hears appeals from the Services’ Courts of Criminal Appeals.
And when military commanders need legal advice, they get it from their own Service lawyers (this is one of the duties of lawyers in the Judge Advocate Generals’ Corps).
The Judicial Branch of the federal government has no constitutional authority over the US Military.
But they would be wrong. In Federalist No. 80, Alexander Hamilton explains the jurisdiction of the courts created by Article III: In the 2nd, 3rd, 4th, and 13th paragraphs, he shows that the purpose of the language quoted just above is to authorize the Judicial Branch to enforce the Constitution – not re-write it; and to enforce constitutional federal laws – not re-write them.
Furthermore, in Federalist No. 81 (8th para), Hamilton addresses judicial encroachments on legislative authority, and reminds us that such encroachments need never be a problem because of the courts’ “total incapacity to support its usurpations by force”; and because Congress may protect the Country from usurping federal judges by impeaching, trying, convicting, and removing them from office.
Accordingly, when a power is vested by the Constitution in the Legislative or Executive Branches [the “political branches”] the federal courts [the “legal branch”] have traditionally refused to interfere.
Likewise, the power to determine who may serve in the Military has been delegated to the Legislative Branch of the federal government i.e., Congress. The Judicial Branch may not substitute its judgment for the Will of the Legislative Branch; and if it attempts to do so, Congress should employ the remedies suggested by Hamilton in Federalist No. 81.
An informed President who is a manly man will ignore ultra vires orders of the Judicial Branch.
Let us put the federal courts in their proper place! Congress and the President have the recognized power to refuse to go along with unconstitutional or ultra vires acts of the Judicial Branch; and their Oaths of office require them to do so. Congress also has the power to rid us of usurping federal judges via the impeachment process.
1 The US District Court for the District of Columbia was established by Congress pursuant to Art. III, §1, US Constitution.
2 Congress’ authority to create the Military Courts is derived from Art. I, §8, cl. 14, US Constitution.
4 I trust you see why Hamilton is viciously smeared. The relentless attacks on our Framers have a purpose: Take them down – and our Foundation is destroyed. Hamilton wrote most of The Federalist Papers, which Madison and Jefferson recognized as the best evidence of the genuine meaning of our Constitution. What effect do these constant attacks on Hamilton have on peoples’ respect for The Federalist Papers? Beware of false friends who undermine our Foundation; and of jealous men whose claim to fame is that they attack Hamilton.
Accordingly, Wyoming passed a delegate law earlier this year which purports to empower the WY Legislature to “immediately recall” any delegate who makes an “unauthorized vote” at the convention, and to charge with a felony any delegate who fails to follow the WY Legislature’s instructions on what he may do at the convention. The Texas delegate law purports to make “invalid” any “unauthorized vote” at the convention, and to empower the TX Legislature to recall any delegate who violates his instructions. But Tennessee takes the cake with its delegate law: Not only does the TN law purport to “void” votes cast at the convention by TN delegates which are outside the instructions or limits placed on the delegates by the TN Legislature – and then to prosecute such delegates for a felony; the TN law also asserts that if all TN delegates vote or “attempt to vote” outside the scope of the instructions or limits, TN’s previously filed applications for an Article V convention are to be treated as “having no effect at all”. Other States have passed similar laws.
Such laws are contrary to our Founding Principles and are based on false assumptions. Accordingly, they are unenforceable and ineffective.
The Declaration of Independence is the Fundamental Act of our Founding.3 It declares that all men are created equal; our rights are bestowed by God; our rights are unalienable; and the purpose of government is to secure the rights God gave us.
The Declaration is not “law” in the ordinary sense – it is higher than law, for it sets forth The Divine Standard which a Constitution – and the laws made pursuant to the Constitution – must meet.
It also declares that a People have the self-evident right to throw off their government and set up a new one. With that Principle firmly in mind, let’s look at our first amendments convention; and then, at State unfaithful delegate laws.
After our Revolution, we operated under our first Constitution, the Articles of Confederation. But there were defects in the Articles, so on Feb. 21, 1787, the Continental Congress called a convention to be held in Philadelphia “for the sole and express purpose of revising the Articles of Confederation”. The States also drafted instructions which purported to restrict delegates to proposing amendments.
Yet State unfaithful delegate laws claim a power to divest The Representatives of the People – and to criminally prosecute them for exercising – what the Fundamental Act of our Founding declares is a “self-evident” right”!
3. And what if the delegates make their proceedings secret?
The State Legislators who vote for unfaithful delegate laws assume they will be able to know what is going on every minute of every day of the convention.
But Madison’s Journal of the Federal Convention of 1787 (where our present Constitution was drafted) shows that on May 29, 1787, the delegates voted to make their proceedings secret.
If delegates to a convention today vote to make the proceedings secret, the States won’t know what is going on – and can’t stop it. And if delegates vote by secret ballot, the States would NEVER know who did what.
You might think that with cell phones & cameras, it’s impossible to have a secret meeting. But the American Legislative Exchange Council (ALEC), which “induces” State Legislators to push the COS application for an Article V convention, is experienced in conducting secret meetings with State Legislators. WATCH this 6.5 minute video of a Georgia TV crew which attempted to get into a meeting held at a Georgia hotel of ALEC and Georgia Legislators.
ALEC, which supports the COS application for an Article V convention, is funded by the Koch Brothers and other mega-corporations. The Koch Brothers spend vast sums on State politicians (e.g., Texas), to get their support for the COS application. Do the Kochs want an Article V convention so they can get a new Constitution which transforms us from a sovereign nation to a member state of the North American Union? And if there is a convention, will armed guards keep the press out? If delegates have been bought by the Kochs, will they tweet & text to the world what they are up to behind closed doors?
Americans have forgotten a Principle which is the basis of free government: That political power originates with The People. 4 The People create governments by means of constitutions. Since a government is the “creature” of its constitution, it can’t be superior to its Creator, The People.
Keeping that Principle firmly in mind, let’s look at Article V, US Constitution.
It provides that when two thirds of the State Legislatures (“mere creatures”) apply for it, Congress is to call a convention. At that point, it is out of the State Legislatures’ hands – the bell has tolled, and State Legislatures can’t un-ring it. Congress “calls” the convention (sets it up); but when it assembles, the delegates, as Sovereign Representatives of the People, are not answerable to State Legislatures (which are “mere creatures” of the State Constitution) or to Congress (which is a “mere creature” of the federal Constitution). The delegates actually have the power to eliminate the federal and state governments – and that is precisely what the proposed Constitution for the Newstates of America does.
Delegates to a federal convention called by the federal Congress, to perform the federal function of altering or replacing our federal Constitution, are performing a federal function, not a State function. The delegates don’t represent any government, federal or state. 5 They are supposed to represent The People; but in our corrupt time, they are more likely to represent the Koch Brothers (because they have the cash).
Dust off your copy of the federal Constitution we already have, read it and defend it. It filled all Europe with “wonder and veneration”. If you don’t do this, we will lose it.
1 The proposed Constitution for the Newstates of America creates a totalitarian dictatorship. The States are dissolved and replaced by regional governments answerable to the new national government. It is ratified by a national referendum [national popular vote] (Art. XII, §1). Other proposed Constitutions are also waiting in the wings for a convention.
3 Dr. Alan Keyes spoke of this on the radio some years ago; and I knew he had just handed me the Key to understanding our Constitution.
4 See Federalist No. 22, last para (Hamilton).
5 The term, “convention of states”, is a misnomer which gives the false impression that States control the convention. In Rob Natelson’s speech on Sep. 16, 2010, he said he will no longer call it a “constitutional convention”, but will henceforth say, “convention of states” (pg. 2).
This Chart illustrates who has the power to do what at an Article V convention.
Some are touting the federal Concealed Carry Reciprocity Act of 2017 (HR 38) as a bill which would expand our right to carry. But if you will walk with me for a few minutes, I’ll show you a better path to take.
Let us look at the applicable First Principles, to which I propose we return.
Our federal Constitution doesn’t delegate to the federal government any power over the Country at Large 2 to restrict our arms. Accordingly, all pretended federal laws, regulations, orders, opinions, or treaties which purport to do so are unconstitutional as outside the scope of powers delegated. They are also unconstitutional as in violation of the Second Amendment.
2. What does your State Constitution say about the right to keep and bear arms?
Each State has its own Constitution which addresses its State Militia and the right to be armed.
Now listen: No State may lawfully make any law which contradicts its State Constitution or which interferes with Congress’ power to “organize, arm, and discipline, the Militia”.
Accordingly, any State Statute which purports to require a permit before one may carry a gun is probably unconstitutional under that State’s Constitution; and is certainly unconstitutional under the federal Constitution because Congress may lawfully require able-bodied male Citizens to acquire firearms and ammo and report to their local Militia Unit for training!
Now let’s look at Title 18, US Code, Part I, Chapter 44, which HR 38 proposes to amend.
It sets up a complex federal regulatory scheme over firearms, every word of which is unconstitutional as outside the scope of powers delegated, and as in violation of the Second Amendment.
HERE it is, look through it (§§ 921-931).
to possess or carry a concealed handgun (other than a machinegun or “destructive device”) which has been shipped or transported in interstate or foreign commerce.
So! Even though a State Constitution, such as that for Connecticut, 4 prohibits the State Legislature from making ANY laws restricting firearms (such as imposing requirements for registration, a permit, government issued photo ID), a Citizen of Connecticut who exercises his constitutionally recognized right to carry without registration or a permit or a government issued photo ID, wouldn’t qualify under HR 38 for concealed carry in another State.
To qualify for concealed carry in other States, the Citizen of Connecticut would need his State Legislature to pass a law [which is unconstitutional under the Connecticut and federal Constitutions], so that he could comply with an unconstitutional federal statute [HR 38], so that he could carry in other States which also would have to pass unconstitutional laws imposing permit requirements on those who carry concealed.
Do you see how a God-given right [self-defense] is thus converted into a privilege which is regulated, granted, or denied, by civil government?
HR 38 also provides that any person carrying a concealed handgun in a State under the reciprocity provisions may also carry concealed in the public parts of National Parks and certain other lands under federal control. Lest you think this a gain, consider that: (1) The Constitution doesn’t authorize the federal government to operate national parks and such like, and (2) the federal government has no lawful authority to impose registration requirements for carrying arms anywhere!
Read our Declaration of Independence and federal Constitution. Then you won’t fall for unconstitutional gimmicks like HR 38.
· by providing more classes for Citizens in arms training.
And please stop lobbying for unconstitutional federal legislation!
1 From the late Attorney Richard D. Fry’s email of Dec. 10, 2015 to US Senator Moran, a co-sponsor of SB 498, the Constitutional Concealed Carry Reciprocity Act of 2015. Richard, who was my Friend, sent me a copy of his letter.
2 Pursuant to Article I, § 8, next to last clause, Congress has general legislative powers over the District of Columbia, military bases, dock yards, mints, federal courthouses and post offices, and such other places needed for Congress to exercise its enumerated powers. The exercise of such powers by Congress over these small federal enclaves is restricted by the Bill of Rights – including the 2nd Amendment. So Congress is prohibited from making, for these federal enclaves, any laws which infringe the Right of The People to keep and bear Arms. Congress may properly require individuals visiting federal prisons, the psych ward of military hospitals, the mint, federal courthouses, and such like, to leave their arms in their vehicles. But Congress may not require Citizens to obtain and carry a permit or photo ID as a condition precedent to carrying a firearm.
3 The “Militia of the several States” were creatures of State Statutes – not of the federal government. Dr. Edwin Vieira’s short video shows how the State Militia were replaced by the federally controlled National Guard.
5 See A SERIOUS QUESTION FOR THE NRA, by Dr. Edwin Vieira, re revitalization of the Militia of the several States. Dr. Vieira’s mind is a delight.
Members of Congress also profit from ignoring our Constitution: By exercising the thousands of powers not delegated, they obtain endless opportunities to become rich, powerful, and “important”.
So, unless we turn over a new leaf, learn our Constitution and obey it, renounce unconstitutional federal programs and handouts, and demand that people in Congress also obey it; limiting their terms by an Amendment merely increases the turnover of politicians in Congress who ignore our Constitution – and to whom we must pay luxurious lifetime pensions.
1. The job of US Senator or Representative would be so boring, few would want to be reelected. After all, how many times can you revise the bankruptcy code (authorized by Art. I, § 8, cl. 4); fix the Standard of Weights and Measures (authorized by Art. I, §8, cl.5); and organize the Patent and Copyright Office (authorized by Art. I, §8, cl.8)?
2. There would be no opportunity to get rich while in Congress, build a power base, and have “prestige”. So the office would no longer attract those who go into politics for the sake of their own egos, pocketbooks, and depraved lust for power.
Take heed of this “unintended consequence” of a term limits amendment: As you decrease the powers of elected members of the US Senate and House by making them transient beings – you increase the powers of the “deep state”. With a term limits amendment, elected members of Congress would be like train cars passing in the night – the real power would be solidified in the nameless, faceless, un-elected bureaucrats who infest the Executive Branch and all its agencies.
1 The PEW Report shows what percentage of each State government’s revenue (for FY 2016) came from federal funds [click on “select a state” to see your State]. In addition to the funds paid by the federal government to the State governments; billions in additional funds are paid by the federal government into each State to local governments, non-governmental organizations, research grants, price supports, food stamps, rent subsidies, utility subsidies, free cell phones, Medicare, social security, etc., etc., etc. Yet the “balanced budget” amendment lobby blames the federal government for out of control spending! But it is the State and local governments, and the people in this Country, who have their hands out for every penny they can get from the federal government.
3 Unlike a “balanced budget” amendment, or the “regulation freedom” amendment, a term limits amendment is not one of the worst ideas since sin. But it doesn’t address the problem. We need to focus on the real problem, not on palliatives.
Don’t Fall for the National Popular Vote – Enforce the Electoral College!
Here are the Exhibits referenced in the video: Be a Berean and look at them!
George Mason’s comment on July 17, 1787 re election of chief Magistrate [from James Madison’s Journal of the Federal Convention of 1787].
George Washington’s letter of October 3, 1788 to Alexander Hamilton.
California’s Assembly Bill No. 60 (passed 2013) permitting illegal aliens to get drivers’ licenses.
California’s Assembly Bill No. 1461 (passed 2015) establishing “Motor Voter” procedures where, when one gets a drivers’ license, one is automatically registered to vote.
Gallup Poll showing declining support for a national popular vote.
The various voting numbers came from HERE.
Do you remember the public discussions which went on for years about the proposed equal rights amendment to our federal Constitution? That’s how it’s supposed to be before an amendment is ratified: The People get an opportunity to hear the arguments, discuss it among themselves and their state legislators, and reject amendments which are bad.
What if someone found a way to circumvent this pesky public discussion, and get an amendment ratified before The People found about it? And even before the state legislators who ratified it found out what they had done? And what if this amendment delegated massive new taxing powers to Congress?
Such a scheme has been developed by Compact for America (CFA). They present their already prepared compact legislation to state legislators as a “balanced budget amendment”; and urge them to get it passed by their state legislature.
Once three fourths of the States have passed CFA’s compact legislation, the new taxes amendment is thereby ratified.
The scheme was passed several years ago by state legislators in Alaska, Georgia, Mississippi, and North Dakota; was passed this year by Arizona Legislators as HB 2226 and signed by the Governor of Arizona on March 30, 2017; 2 and is now pending in Missouri as SB 13, in Oklahoma as HB 1434, and in Texas as SB 959. Arkansas rejected it a week or so ago.
Let’s look at the particulars of the compact legislation using the Arizona Bill as the example.
Section 1 of the Compact [page 2, line 16 of the pdf edition] allows Congress to spend as much as they take from us in taxes or add to the national debt! But that’s what Congress has been doing!
Sections 2 & 3 [page 2, lines 20-37] permit Congress to raise the debt whenever 26 States agree.
Section 4 [page 2, lines 38 et seq.] is a joke: Who believes Congress will impeach a President for refusing to “impound” an appropriation made by Congress?
CFA’s BBA is an actually a grant of MASSIVE new taxing powers to Congress.
The true purpose of the compact legislation is hidden behind promises such as, “cutting federal spending”, “balancing the budget”, and “scaring Congress”. The true purpose of the Compact is to delegate to Congress MASSIVE NEW TAXING POWERS. Specifically, it authorizes Congress to impose a national sales tax and a national value added tax (VAT).
Section 5 [page 3, lines 4-6] permits Congress, by a 2/3 vote of each House, to impose a new or increased “general revenue tax”.
There it is! All Congress needs to impose a national sales tax and/or a national VAT tax (in addition to the income tax) is a 2/3 vote in each House!
Section 5 also permits Congress, by a simple majority of each House, to impose a “new end user sales tax” which would replace the federal income tax. But nothing requires Congress to impose a “new end user sales tax” to replace the income tax.
It will be up to Congress to decide whether to impose a new national sales tax and/or VAT tax on top of the existing income tax (if they get 2/3 vote of each House); or whether to impose a new end user sales tax to replace the income tax (if they get only a simple majority in each House).
So! CFA’s version of a BBA is not about “balancing the budget”, or “scaring Congress”, or “reducing federal spending”. It’s about giving the federal government massive new taxing powers!
When State Legislatures pass compact legislation such as HB 2226, they are actually pre-ratifying the new Amendment to the US Constitution which grants these massive new taxing powers to Congress.
There it is: When State legislatures pass bills like HB 2226, they are thereby ratifying an amendment to the US Constitution which delegates massive new taxing powers to Congress.
When 38 States have passed legislation like HB 2226 – and when Congress approves it, 3 our Constitution is thereby AMENDED and Congress now has constitutional authority to impose a new national sales tax and a national VAT tax – even while keeping and increasing the income tax.
The provisions of the compact which deal with a convention – Articles V through VIII – are a smokescreen which obscures from state legislators the fact that when they pass legislation like HB 2226, they are pre-ratifying the amendment to our federal Constitution.
The convention is a formality – a free trip at taxpayers’ expense.
Don’t feed the beast by giving it massive new taxing powers. The solution is to downsize the federal government to its enumerated powers.
Our Constitution already limits federal spending to the enumerated powers – learn what those powers are, and enforce the Constitution we already have.
And use your heads! You who foolishly believe that a BBA [whether CFA’s version or another version] will force Congress to reduce spending, know this: a BBA is a mandate for Congress to increase taxes, among other horrors.
1 Legislators don’t read the bills they vote on. That’s why they have bill summaries. The Compact legislation filed in Arizona has two bill summaries: HERE and HERE. Can you find where Arizona Legislators were informed they would be pre-ratifying a new taxes amendment to the US Constitution if they passed the compact legislation?
2 Arizona Republican Legislators were warned over & over & over again; the Governor of Arizona was also warned. But they ignored the warnings, and are without excuse.
3 Pursuant to Article I, §10, last clause, US Constitution, CFA’s Compact is not effective unless Congress approves it. Will Congress approve a Compact Amendment which delegates massive new taxing powers to them?
If you come to this event, you will see why Mark Meckler, Michael Farris, COS operatives, and the con-con lobby don’t want you to hear what I say. I tell the TRUTH and prove it.


In California, up until December 15, 2014 when the U.S. Supreme Court ruled in Heien v. North Carolina, the general rule was that a traffic stop is illegal if based on a mistake of law, no matter how reasonable the officer’s mistaken belief in the law may have been.
Main Point: U.S. Supreme Court Changes California Law Concerning the Legality of a Traffic Stop Based on a Mistake of Law.
In other words, if a police officer believed it is illegal to turn a vehicle without using a turn signal, even if no other cars are affected by the turn, and makes a traffic stop for violating Vehicle Code § 22107, the traffic stop is improper and all evidence gained, i.e. drugs found in a car, are suppressed. People v. Carmona (2011) 195 Cal.App.4th 1385. The reason was because the search violated the Fourth Amendment. This was the state of law because courts want to deter officer mistakes of law. United States v. Song Ja Cha (9th Cir., 2010); People v. White (2003) 107 Cal. App. 4th 636, 644. Courts want officers to follow the law and do want to encourage ignorance of the law.
This seems to change now. In the recent U.S. Supreme Court ruling in Heien, a North Carolina police officer stopped Nicholas Heien because his car had just one working rear brake light. The officers then found cocaine in Heien’s car and arrested him. He was then convicted of trafficking a controlled substance.
Heien had made a motion to suppress the cocaine, arguing that the North Carolina statute only required a car to be equipped with “a stop lamp,” not two. Therefore, Heien was not in violation of any law. The trial court denied his motion and Heien was then convicted. The trial court ruled that the mistake was reasonable, so there was no illegal stop.
Heien then appealed to the state appellate court and won. The state of North Carolina then appealed and lost, but appealed again with the case eventually made its way to the U.S. Supreme Court.
The U.S. Supreme Court then ruled in favor of North Carolina and against Heien. It ruled, in a nutshell, that a traffic stop based on a reasonable mistake of law does not violate the Fourth Amendment as long as the officer’s mistake of law is reasonable.
The big question then becomes what is a reasonable mistake of law? What standard should a court apply to determine if a mistake is reasonable? Moreover, does this mean the good faith exception applies to officer mistakes of law like when an officer, in good faith, executes a defective warrant and finds evidence of a crime?
The opinion in Heien gives us some indications of what is a reasonable mistake. Most importantly, there are indications in the North Carolina statute itself that all rear lights must be functional. Therefore, if the statute itself suggests all lights must be functioning, the officer’s mistakes was clearly reasonable.
The U.S. Supreme Court also seemed to set the bar high in determining what is a reasonable mistake, commenting that the test is objective and “not as forgiving” as when an officer asserts qualified immunity in a civil suit. Indeed, the U.S. Supreme Court noted that qualified immunity protects “all but the plainly incompetent or those who knowingly violate the law.” In other words, it is a forgiving standard in most situations.
Kagan even said that rulings for the prosecution on this ground, she predicted, will be “exceedingly rare.” We want this to be the standard in the future.
Curiously, North Carolina law does not provide for a “good faith exception” to the exclusionary rule, so the U.S. Supreme Court could not and did not rule on this applying to such a traffic stop and search. This is good, too, as we would never want a “good faith exception” to apply to the exclusionary rule.
In 2011 DUI Case Involving Drugs, the results of a Warrantless Blood Draw are Admissible If Officer Reasonably Relied on Then – Current Law Later Overruled.
Warrantless Blood Draw Allowed in DUI Case, Without Driver’s Consent – Does this Violate McNeely v. Missouri? Appeals Court Says No.
U.S. Supreme Court Rules Police May Not Draw Blood Without a Warrant When Suspect Refuses Breath or Blood Test.


text:
The genus Yersinia consists of 15 species (www.bacterio.cict.fr/xz/yersinia.html), and only three of them, Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica, are pathogenic to mammals, including humans. The Y. pseudotuberculosis-Y. pestis evolutionary linkage diverged from Y. enterocolitica between 41 and 186 million years ago, while Y. pestis diverged from Y. pseudotuberculosis within the last 1,500 to 20,000 years (1, 65). In accordance with this evolutionary cascade, wide genetic diversity exists between Y. pseudotuberculosis and Y. enterocolitica, while very close genetic similarity is found between Y. pseudotuberculosis and Y. pestis. Y. pseudotuberculosis causes only nonfatal gastrointestinal disease in mammalian hosts, including humans, and the disease is transmitted by the food-borne route. Y. pestis causes plague, which is one of the most deadly diseases (47). Three pandemics of plague have been recorded in human history and have claimed hundreds of thousands of lives (47). Plague is a typical enzootic disease (an infection of the animal population[s] in one or more confined natural foci without the need for external inputs), and epidemics of rodent plague are restricted in various enzootic plague foci especially in Asia, the Americas, and Africa (80). Compared to its progenitor Y. pseudotuberculosis, Y. pestis utilizes a radically different mechanism of transmission in rodent reservoirs that relies primarily upon biting by flea vectors. This review deals with how genetic changes (gene inactivation, loss, and acquisition) and remodeling of gene regulation encourage Y. pestis to switch from an enteric lifestyle to a mammalian blood-borne lifestyle that relies on vector-borne transmission.
Rodents and humans acquire Y. pestis by the bite of an infected flea, contact with infected tissues, or inhalation of respiratory droplets or aerosols, with manifestations of bubonic, septicemic, and pneumonic plague (47). After the flea bite, there is an initial subcutaneous and intradermal colonization, and then the bacteria migrate into the regional lymph nodes and inflammation, cellulitis, and occasionally large carbuncles develop around the bubo (bubonic plague) (60). Without timely effective treatment, the bacteria will rapidly escape from containment in the lymph node and spread systemically through the blood to various organs, causing fatal sepsis (septicemic plague) (82). An intracellular growth of Y. pestis in macrophages at early stages of infection is thought to allow this pathogen to proliferate and to synthesize virulence determinants, enabling the releasing bacteria to acquire the ability to eliminate the host immune response (39). In addition, secondary pneumonic plague could result from hematogenous spread from the bubo to the lung, presenting in patients as severe bronchopneumonia, cavitation, or consolidation with production of bloody or purulent sputum (82). Primary pneumonic plague could be caused directly by the inhalation of infectious droplets or aerosols, with symptoms including acute pneumonia, intra-alveolar hemorrhage and edema, profound lobular exudation, fibrin deposition, and bacillary aggregation (33). Both primary and secondary pneumonic plagues are highly contagious for close contacts by airborne transmission.
Animals, food, and the abiotic environment are Y. pseudotuberculosis reservoirs from which epizootic and human infection may arise, and the disease is mild and transmitted by the food-borne route. In humans, typical symptoms include fever and right-side abdominal pain. In rare cases the disease may cause skin complaints (erythema nodosum), joint stiffness and pain (reactive arthritis), or spread of bacteria to the blood (bacteremia).
Due to acute and systemic infection, the mortality rate of plague reaches 70 to 100% without treatment depending on routes of infection. Y. pestis has a limited ability to live in the environment, although there is evidence that Y. pestis can live in soil for up to 30 weeks (3). Maintenance of plague in enzootic plague foci is almost absolutely dependent upon cyclic transmission between fleas and mammals (80). Blocked fleas are important for transmission of plague (24). Blockage of fleas (heavy proliferation of bacteria in the adhesive biofilms in the proventriculus) makes them feel hungry and repeatedly attempt to feed, and the plague bacilli will be pumped into the host body during these futile feeding attempts (25). The development of heavy bacteremia (bacterial concentration reaching at least 106 CFU/ml) in hosts is necessary to reliably infect the fleas (38). Such a high level of bacteremia raises the risk of hosts' rapid death. Nevertheless, once some fleas achieve feeding prior to the host's death, they will seek alternative hosts, thereby increasing the likelihood of transmission to other individuals from the hosts (15).
Generally, it takes about 2 weeks for blockage to develop, which is not sufficient to explain the high rate of spread that typifies plague epidemics. Various species of rodent fleas are immediately infectious after biting a septicemic host and transmit bacteria efficiently for at least 4 days postinfection, and accordingly the mode of “early-phase transmission” by unblocked fleas has been proposed (14). Early-phase transmission helps explain not only the rapid spread that typifies plague epidemics but also previous inconsistencies between the rates of pathogen spread expected from the blocked fleas. It was suggested that mechanical transmission by unblocked fleas is significant during epidemics that represent the periods when Y. pestis can spread rapidly across landscapes but that transmission by blocked fleas is important primarily during interepizootic transmission (15). In addition, a combination of early-phase transmission and blocking probably helps to explain the observed high mortality rates of susceptible host populations, including humans during the Black Death (74).
The rodent reservoirs, the flea vectors, and Y. pestis constitute a well-balanced biocommunity in the plague foci. Y. pestis possesses potential to attack humans, and human infection usually occurs with the transmission of the pathogen from rodents. Although cases of human plague can be well controlled by timely antibiotic administration, plague still remains a significant concern for public health because it can be transmitted from person to person through respiratory droplets and used for bioterrorism and biological warfare (68).
Y. pestis has developed specialized strategies for virulence in hosts and transmission by fleas (Table 1), and many of these determinants are harbored in the genome of Y. pseudotuberculosis.
The major adhesin and invasin, YadA and Inv, respectively, specific for gastrointestinal infection are inactivated in Y. pestis (see below), but this pathogen still has additional proteins (Ail , YadBC , and YapE ) that account for bacterial colonization and dissemination during infection.
The ability to replicate in macrophages is conserved in Y. pestis and Y. pseudotuberculosis (53). RipABC (54), MgtCB (22), Ugd (22), Yfe (48), and Feo (48) have been shown to be required for the replication of Y. pestis in macrophages. Both MgtCB and Ugd are positively regulated by the PhoP-PhoQ two-component system (37) that is important for survival under conditions of macrophage-induced stress and virulence in Y. pestis (44).
The plasmid pCD1-borne type III secretion system (T3SS) is composed of a secretion machinery, a set of translocation proteins, a control system, and six Yop effector proteins (56). Through the T3SS, pathogenic yersiniae inject effectors into the cytosol of eukaryotic cells when docking at the surface of host cells, and the injected Yops mediate suppression of phagocytosis and the inflammatory reaction (56). Y. pestis utilizes T3SS to selectively destroy innate immune cells that represent the first line of host defense, thereby preventing adaptive responses and precipitating the fatal outcome of plague (40). Y. pestis still employs pH 6 antigen fimbriae to function as an antiphagocytic factor independent of Yops (27).
The Tc genes were first identified in the insect pathogen and encode a protein complex toxic to insects. Tc proteins in Y. pseudotuberculosis and Y. pestis are not insecticidal toxins but have evolved toxicity to mammalian cells (23).
Heavy proliferation of Y. pestis in the bloodstream is essential for its transmission by fleas. Resistance to complement-mediated lysis (serum resistance) is required for bacterial survival in mammalian blood. The Ail protein (4) and lipopolysaccharide (LPS) (50) promote serum resistance, which appears to be a conserved mechanism in pathogenic yersiniae.
In mammals, iron is bound to Fe3+-binding proteins and hemoproteins, and thus free iron is too rare to sustain bacterial growth. Iron acquisition is critical for the survival of pathogenic bacteria during infection. A wide array of iron acquisition systems have been characterized or annotated for Y. pestis (21), and at least two (Ybt and Yfe) of them were proven to be required for full virulence (5). Ybt, also known as the high-pathogenicity island (59), is essential to iron acquisition at the site of the flea bite and in the lymphatic system, while Yfe is likely used in the later stages of the disease, i.e., blood-borne systemic dissemination (5).
Lateral gene transfer directly introduces foreign DNA elements into the host genome, which will effectively alter the pathogenic characters of bacterial species (42). Y. pestis has acquired two unique virulence plasmids, pPCP1 and pMT1, through lateral gene transfer. pPCP1 encodes plasminogen activator (Pla), while pMT1 encodes murine toxin (Ymt) and F1 capsule (Table 1).
Pla is essential for bubonic and primary pneumonic plague (but not primary and secondary septicemic forms), since it specifically promotes Y. pestis dissemination from peripheral infection routes (34, 61). At 37°C but not 26°C, Y. pestis expresses a capsule-like antigen, called F1 antigen. F1 provides Y. pestis the ability to block phagocytosis by a mechanism different from those of T3SS and pH 6 antigen (13). Ymt does not play a role in mouse infection (57) but shows phospholipase D activity and is required for survival of Y. pestis in fleas (26). It was thought that intracellular phospholipase D activity appeared to protect Y. pestis from a cytotoxic digestion product of plasma in the flea gut (26).
Unexpectedly, only two chromosomal regions seem to be specific to Y. pestis (76) (Table 1). They are located in two different genomic islands probably acquired through lateral gene transfer (45). These two Y. pestis-specific chromosomal regions deserve more attention to investigation of their roles in virulence and/or transmission by fleas. However, it has been argued that analysis of more bacterial strains could further reduce the number of Y. pestis-specific chromosomal genes, perhaps to zero (7, 45).
About 13% of Y. pseudotuberculosis genes no longer function (inactivated or absent) in Y. pestis CO92 (45). Genome decay (gene loss and inactivation) appears to be closely linked to flea-borne transmission and increased virulence of Y. pestis (Table 1).
yadA and inv encode the major adhesin and invasin, respectively, in Y. pseudotuberculosis and enable this enteropathogen to specifically adhere to surfaces of host intestines and invade lining epithelial cells. Both of them are inactivated in Y. pestis (30). Urease plays its role in using urea as a source of nitrogen. Production of urease by the ure operon is necessary for oral transmission of Y. pseudotuberculosis, but it is inactivated in Y. pestis due to the mutation causing a premature stop codon in ureD (33). Since Y. pestis spends its life almost exclusively in a flea-host-flea cycle, the organism can lose with impunity the function of urease needed for survival in natural environments.
Y. pestis expresses rough LPS lacking the O antigen, due to the inactivation of several genes in the O-antigen gene cluster (52). Y. pseudotuberculosis produces a rough LPS at 37°C but not at 26°C, and a variable number of LPS genes are seen to be defective when various biovars of Y. pestis are compared (64). Expression of rough LPS is essential for Pla activity and virulence in Y. pestis (32). A pathogenic advantage of rough LPS in Y. pestis is that it enables efficient Pla-mediated bacterial dissemination to cause systemic disease.
For the blocked fleas, Y. pestis synthesizes an attached biofilm in the flea proventriculus and in its midgut posteriorly (25). Three distinct operons, hmsHFRS, hmsT, and hmsP, are involved in the synthesis of bacterial extracellular matrix, which is the primary component of Yersinia biofilm (28). Y. pseudotuberculosis contains all of these hms genes, which are 99% identical to the Y. pestis homologues (9). In addition to Hms, several other proteins (GmhA, SpeAC, and YrbH) involved in biofilm formation by Y. pestis are harbored in Y. pseudotuberculosis (Table 1).
Only a small number of Y. pseudotuberculosis strains are able to form biofilm on Caenorhabditis elegans, and none of them has the ability to form adhesive biofilms in fleas (17). The transcriptional regulator RcsA (69) and the glycosyl hydrolase NghA (16) have been shown to inhibit Yersinia biofilm formation, but both of them are functional in Y. pseudotuberculosis but inactivated in Y. pestis (16, 69). Expression of functional RcsA or NghA in Y. pestis strongly represses biofilm formation and abolishes flea blockage (16). Therefore, Y. pestis has evolved the changes in regulatory functions on biofilm development to ensure stable biofilm formation in the flea proventriculus and to result in efficient arthropod-borne transmission.
Hexa-acylated LPS observed in many gram-negative pathogens is able to activate TLR4 signaling and to further stimulate the host innate immune response (55). The acyltransferase LpxL is required for addition of the secondary acyl chains to the tetra-acylated precursor (55). The lpxL gene is absent from Y. pestis, leading this pathogen to produce tetra-acylated LPS that inhibits TLR4 activation, which allows this pathogen to evade the protective inflammatory response and establish fatal infection (41).
Five additional Y. pseudotuberculosis-specific chromosomal loci (R1, R3, ORF2, ORF3, and ORF4) required for its survival, optimal growth, or virulence are absent from Y. pestis (51) (Table 1). ORF3 and ORF4, with unknown function, are essential for the viability of Y. pseudotuberculosis, while ORF2 (a putative pseudouridylate synthase involved in RNA stability) and R3 (a genomic region composed mostly of genes of unknown functions) are necessary for its optimal growth in a chemically defined medium (51). Deletion of R1 (a genomic region responsible for the methionine salvage pathway) alters the mutant's virulence, suggesting that the availability of free methionine is severely restricted in vivo (51).
Virulence determinants are tightly and coordinately regulated during infection. Virulence-related regulators can sense host signals, e.g., changes in temperature, and then differentially regulate not only virulence genes but other large sets of genes required for adaptation to the host niche (84). A number of virulence-required regulators have been characterized in Y. pestis and Y. pseudotuberculosis (Table 1), indicating that remodeling of gene regulation contributes to the indicated differences between these two pathogens (Fig. 1).
Remodeling of gene regulation in Y. pestis and Y. pseudotuberculosis. Transcription regulators listed here bind to cis-acting DNA sequences within the promoters of their target genes and either activate or repress transcription initiation of these targets. Some regulators (e.g., CRP) can function as either activators or repressors according to the target promoters. Shown also is autoregulation of some regulators (e.g., RovA).
The global transcriptional regulators cyclic AMP receptor protein (CRP) (49, 79) and RovA (8, 73) are conserved and required for virulence in the three pathogenic Yersinia species. In addition, the Y. pestis CRP is 98.6% identical to the Escherichia coli one with the same length, and CRPs from these two bacteria share an identical consensus box sequence (TGTGA-N6-TCACA) that represents the conserved signals for CRP recognition of promoter DNA (79). Through regulator-promoter DNA interaction in Y. pestis, CRP activates two laterally acquired plasmid genes, pla and pst (30, 79), while RovA upregulates a genomic region, YPO2272 to YPO2281 (8). The prophage YPO2272 to YPO2281 is acquired by the Y. pestis ancestor, and its genome forms an unstable episome in biovars Antiqua and Medievalis whereas it is stably integrated in biovar Orientalis (12, 36). The acquisition of this prophage does not correlate with flea transmission but contributes to virulence in mice (12). These “newly” acquired virulence genes have evolved to integrate themselves into the “ancestral” Yersinia regulatory cascade. The plague pathogen integrates laterally acquired genes to coordinate virulence factor expression within global gene regulatory networks to maintain homeostasis through the infectious life cycle.
The pMT1-borne F1 antigen locus is transcribed as two operons (caf1M-caf1A-caf1 and caf1R) with opposite directions. Caf1R is a positive transcriptional activator responsible for the regulation of capsule formation (29). Thus, the newly acquired caf genes constitute a self-controlling regulatory cascade. According to our microarray expression data, CRP activated caf1R whereas it repressed the caf1M-caf1A-caf1 operon (79), and the nucleoid-associated protein Fis stimulates all the caf genes (unpublished data). Whether these two caf operons are controlled by the host's regulators still needs to be elucidated.
As mentioned above, Y. pestis has evolved the genetic inactivation of inhibitory functions (RcsA or NghA) on biofilm formation, which greatly contributes to efficient flea-borne transmission. RovA and VirF positively control inv and yadA, respectively, while reductive inactivation of these two targets has occurred in Y. pestis (see above). However, the upstream regulators RovA and VirF still function to regulate other virulence genes in Y. pestis, and both of them are required for virulence of Y. pestis (8, 19). The established target of the activator RovA is PsaABC (pH 6 antigen) (8), while VirF stimulates several components (YpkA-YopJ, LcrG/V/D-YopB/D, VirC, YopH, and YopE) of T3SS (77), which appears to be conserved between Y. pestis and Y. pseudotuberculosis.
Y. pseudotuberculosis harbors a set of functional or structural determinants including adhesion/invasin, T3SS, pH 6 antigen, Tc proteins, iron uptake systems, and enzymes for biofilm formation. Thereby, it has the potential to attack mammals to cause systemic infection and to be transmitted by fleas. At a certain stage of history, the change of natural environment might have led to the dramatic increase of population size or to behaviors of a certain rodent, probably the woodchuck (70). This change in animal reservoir might trigger the speciation of Y. pestis from Y. pseudotuberculosis as a directional positive selection (Darwinian selection). Y. pseudotuberculosis is found widely in the environment and is a common cause of animal infections. The bacteria can invade individual rodents suffering from cold, hunger, or illness due to drastic in-species competition or a harsh environment and then are sucked into the bodies of fleas through flea biting.
Y. pseudotuberculosis or ancestral Y. pestis shares a niche with other organisms in rodents and fleas, which might allow the random occurrence of lateral gene transfer. At the same time, gene loss or inactivation occurs randomly as well. Beneficial events of genetic variations would be stabilized by vertical inheritance under Darwinian selection. The positive and directional selection promotes the acquisition of novel virulence determinants as well as the decay of redundant or deleterious functions, which would stimulate the emergence of Y. pestis. In addition, remodeling of gene regulation enables the coordinated regulation of existent and newly acquired virulence markers. The Darwinian selective advantages contribute to the demonstrated differences between Y. pestis and Y. pseudotuberculosis and favor an ordered buildup of specific combinations of virulence determinants enabling the establishment and transmission of Y. pestis as a new clone from Y. pseudotuberculosis.
Y. pestis has been historically divided into three biovars, namely, Antiqua, Medievalis, and Orientalis, and they are thought to be linked with the first to third plague pandemics, respectively. Each biovar has unique genes, a different profile of inactivated genes, and a distinct genome structure according to the relevant sequenced genomes. In addition to the above three classical biovars, another distinct group of strains, called biovar Microtus (83), are avirulent in primates and some large rodent species and are thought to be the intermediate evolutionary clade between Y. pseudotuberculosis and Y. pestis (36, 72, 81). Compared to other types of Y. pestis, biovar Microtus strains have a unique genomic profile of gene loss and pseudogene distribution (36, 72, 81, 83). The specific loss of genes or gene functions documented for this group of strains is thought to be responsible for the human attenuation of these strains, providing candidates for further hypothesis-driven investigations of virulence microevolution of Y. pestis.
Y. pestis strains in North and South America are clonally derived from a biovar Orientalis strain due to the third pandemic of human plague in the early 20th century and thus genetically restricted (2). In China, Mongolia, and the former Soviet Union, there are large areas of enzootic plague foci containing genetically diverse strains (2). Y. pestis isolates from these plague foci can be classified into many different genotypes (also known as genomovars) (2, 10, 36, 72, 81). Accumulation of genetic variations promotes the diversification of Y. pestis, while distribution of Y. pestis genotypes is plague focus specific (36, 81). The parallel expansion of plague foci as well as the directional diversification of Y. pestis within these foci is likely subject to the action of the complex of interactions between the environment, the hosts, and the pathogen (81). For a specific plague focus, Y. pestis genotypes can be assigned into major and minor genomovars (36). Strains of major genomovars represent the dominant populations in a specific plague focus, and they are generally isolated from the main reservoirs/vectors and distributed throughout the focus. In contrast, the strains of minor ones account for a very small portion of the tested stains from the specific plague focus and are distributed sporadically in a focus or along the border of neighboring foci. Notably, major and minor genomovars make sense in combination with the concept of a specific plague focus. The major genomovar in one plague focus might be the minor one in the others.
In summary, adaptive microevolution likely promotes diversification of Y. pestis (different major and minor genomovars) within enzootic foci; major genotypes would play a crucial role in the maintenance of plague in enzootic foci, whereas minor ones (likely representing evolutionary dead ends) would make little contribution to the well-balanced interactions between environment, hosts, and Y. pestis (36, 81). This speculation still needs further evidence to show phenotypic effects of gene loss/gain during microevolution of Y. pestis.
The driving forces of molecular evolution involve two aspects, namely, “genetic drift” and “natural [or Darwinian] selection.” Genetic drift promotes the accumulation of neutral, random changes in a gene pool, and thus it affects only genotypic frequencies within a population and has no phenotypic causes. Darwinian selection makes alleles more or less widespread in a population due to their effects on fitness advantages; therefore, it influences both phenotype and genotype components in a population. Darwinian selection impels the creation of adaptations, while genetic drift does not. Classical Darwinian evolution refers to the specific selection and fixation of small allelic variants (point mutations) that confer positive evolutionary advantage. It is becoming more and more evident that accumulation of large genomic changes (gene loss/acquisition) can alter the phenotypes in “quantum leaps” during the evolution of bacterial pathogenesis (43). Herein, selection and fixation of inactivation, loss, and acquisition of functional genes are all thought to be under the framework of Darwinian adaptive evolution.
Although evolved from the mildly pathogenic bacterium Y. pseudotuberculosis, Y. pestis is a highly virulent pathogen and has switched from an enteric lifestyle to a mammalian blood-borne one. For it to become a more virulent pathogen, at least three adaptive evolution mechanisms were involved to gain more pathogenic phenotypes: (i) the horizontal acquisition of genes encoding specific virulence determinants (“gain-of-function” mechanism), (ii) an appropriate functional inactivation or loss of preexisting genetic materials (“loss-of-function” mechanism), and (iii) laterally acquired virulence genes either with or without their own specific regulators, which evolve to being integrated into the host's regulatory cascades to coordinate expression of virulence factors within global gene regulatory networks for maintaining homeostasis through the infectious life cycle (“regulation-remodeling” mechanism). Genetic variations occur randomly, yet only those beneficial to mammalian blood-borne infection or vector-borne transmission of Y. pestis would be stabilized by vertical inheritance under Darwinian selection. Darwinian adaptive evolution (rather than neutral genetic drift) would induce Y. pestis to evolve from Y. pseudotuberculosis to a newly emerged pathogen that is not only able to parasitize insects in part of its life cycle but also highly virulent to rodents and humans, causing pandemics of a systemic and often fatal disease.
Comparison of available genome sequences of Y. pestis and Y. pseudotuberculosis enables us to find genetic differences in minute detail. Subsequent hypothesis-directed studies have presented a wealth of experimental evidence that promotes our understanding of the positive evolution of virulence during speciation of Y. pestis, whereas phenotypic characterization of intraspecific microevolution of Y. pestis and its link to expansion of enzootic plague foci is lacking.
Tightly regulated virulence genes are important components of the global gene regulation network, which is a three-dimensional architecture involving various regulators and structural genes. Y. pestis has evolved extremely complex signaling and regulatory pathways that are activated during different stages of infection. Global comparative analysis of gene regulation (84) in Y. pestis and Y. pseudotuberculosis would bring a dynamic and complete picture of virulence and host adaption in Y. pestis.
The insertion sequence (IS) elements constitute about 3% of the whole genome in Y. pestis (67). Due to IS-mediated homologous recombination, the genome structures of different Y. pestis strains are markedly different, although their genome contents and sequences show high similarity (67). There are no reported data for the IS-mediated recombination event that is experimentally linked to the virulence evolution of Y. pestis.
An evolutionary “source-sink” model was recently proposed to detect genetic adaptation of bacterial pathogens, with which the evolution of bacterial pathogens can be seen from the angle of continuous switching between permanent (source) and transient (sink) habitats (66). Virulence habitats are marginal sink habitats for some pathogens, and virulence-enhancing genetic adaptation is mostly transient in nature. The adaptation to harsh, or “sink,” environments is the supply of beneficial mutations via migration from a “source” population. Experimental evidence to support the source-sink model for Y. pestis needs to be characterized and would provide a conceptual framework for understanding the population dynamics and molecular mechanisms of virulence evolution.
Related work in our laboratory has been supported by grants from the National Science Foundation of China for Distinguished Young Scholars (30525025), the State Key Development Program for Basic Research of China (2009CB522604 and 2009CB522601), the National Natural Science Foundation of China (30771179 and 30600353), and the Beijing Natural Science Foundation (5072040).
Ayyadurai, S., L. Houhamdi, H. Lepidi, C. Nappez, D. Raoult, and M. Drancourt. 2008. Long-term persistence of virulent Yersinia pestis in soil. Microbiology 154:2865-2871.
Bearden, S. W., and R. D. Perry. 1999. The Yfe system of Yersinia pestis transports iron and manganese and is required for full virulence of plague. Mol. Microbiol. 32:403-414.
Bearden, S. W., C. Sexton, J. Pare, J. M. Fowler, C. G. Arvidson, L. Yerman, R. E. Viola, and R. R. Brubaker. 2009. Attenuated enzootic (pestoides) isolates of Yersinia pestis express active aspartase. Microbiology 155:198-209.
Brubaker, R. R. 2005. Influence of Na+, dicarboxylic amino acids, and pH in modulating the low-calcium response of Yersinia pestis. Infect. Immun. 73:4743-4752.
Cathelyn, J. S., S. D. Crosby, W. W. Lathem, W. E. Goldman, and V. L. Miller. 2006. RovA, a global regulator of Yersinia pestis, specifically required for bubonic plague. Proc. Natl. Acad. Sci. USA 103:13514-13519.
Cui, Y., Y. Li, O. Gorge, M. E. Platonov, Y. Yan, Z. Guo, C. Pourcel, S. V. Dentovskaya, S. V. Balakhonov, X. Wang, Y. Song, A. P. Anisimov, G. Vergnaud, and R. Yang. 2008. Insight into microevolution of Yersinia pestis by clustered regularly interspaced short palindromic repeats. PLoS ONE. 3:e2652.
Darby, C., S. L. Ananth, L. Tan, and B. J. Hinnebusch. 2005. Identification of gmhA, a Yersinia pestis gene required for flea blockage, by using a Caenorhabditis elegans biofilm system. Infect. Immun. 73:7236-7242.
Derbise, A., V. Chenal-Francisque, F. Pouillot, C. Fayolle, M. C. Prevost, C. Medigue, B. J. Hinnebusch, and E. Carniel. 2007. A horizontally acquired filamentous phage contributes to the pathogenicity of the plague bacillus. Mol. Microbiol. 63:1145-1157.
Eisen, R. J., S. W. Bearden, A. P. Wilder, J. A. Montenieri, M. F. Antolin, and K. L. Gage. 2006. Early-phase transmission of Yersinia pestis by unblocked fleas as a mechanism explaining rapidly spreading plague epizootics. Proc. Natl. Acad. Sci. USA 103:15380-15385.
Eisen, R. J., and K. L. Gage. 2008. Adaptive strategies of Yersinia pestis to persist during inter-epizootic and epizootic periods. Vet. Res. 40:1.
Erickson, D. L., C. O. Jarrett, J. A. Callison, E. R. Fischer, and B. J. Hinnebusch. 2008. Loss of a biofilm-inhibiting glycosyl hydrolase during the emergence of Yersinia pestis. J. Bacteriol. 190:8163-8170.
Erickson, D. L., C. O. Jarrett, B. W. Wren, and B. J. Hinnebusch. 2006. Serotype differences and lack of biofilm formation characterize Yersinia pseudotuberculosis infection of the Xenopsylla cheopis flea vector of Yersinia pestis. J. Bacteriol. 188:1113-1119.
Felek, S., M. B. Lawrenz, and E. S. Krukonis. 2008. The Yersinia pestis autotransporter YapC mediates host cell binding, autoaggregation and biofilm formation. Microbiology 154:1802-1812.
Flashner, Y., E. Mamroud, A. Tidhar, R. Ber, M. Aftalion, D. Gur, S. Lazar, A. Zvi, T. Bino, N. Ariel, B. Velan, A. Shafferman, and S. Cohen. 2004. Generation of Yersinia pestis attenuated strains by signature-tagged mutagenesis in search of novel vaccine candidates. Infect. Immun. 72:908-915.
Forman, S., C. R. Wulff, T. Myers-Morales, C. Cowan, R. D. Perry, and S. C. Straley. 2008. yadBC of Yersinia pestis, a new virulence determinant for bubonic plague. Infect. Immun. 76:578-587.
Gao, H., D. Zhou, Y. Li, Z. Guo, Y. Han, Y. Song, J. Zhai, Z. Du, X. Wang, J. Lu, and R. Yang. 2008. The iron-responsive Fur regulon in Yersinia pestis. J. Bacteriol. 190:3063-3075.
Grabenstein, J. P., H. S. Fukuto, L. E. Palmer, and J. B. Bliska. 2006. Characterization of phagosome trafficking and identification of PhoP-regulated genes important for survival of Yersinia pestis in macrophages. Infect. Immun. 74:3727-3741.
Hares, M. C., S. J. Hinchliffe, P. C. Strong, I. Eleftherianos, A. J. Dowling, R. H. Ffrench-Constant, and N. Waterfield. 2008. The Yersinia pseudotuberculosis and Yersinia pestis toxin complex is active against cultured mammalian cells. Microbiology 154:3503-3517.
Hinnebusch, B. J. 2003. Transmission factors: Yersinia pestis genes required to infect the flea vector of plague. Adv. Exp. Med. Biol. 529:55-62.
Hinnebusch, B. J., and D. L. Erickson. 2008. Yersinia pestis biofilm in the flea vector and its role in the transmission of plague. Curr. Top. Microbiol. Immunol. 322:229-248.
Hinnebusch, B. J., A. E. Rudolph, P. Cherepanov, J. E. Dixon, T. G. Schwan, and A. Forsberg. 2002. Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector. Science 296:733-735.
Huang, X. Z., and L. E. Lindler. 2004. The pH 6 antigen is an antiphagocytic factor produced by Yersinia pestis independent of Yersinia outer proteins and capsule antigen. Infect. Immun. 72:7212-7219.
Jarrett, C. O., E. Deak, K. E. Isherwood, P. C. Oyston, E. R. Fischer, A. R. Whitney, S. D. Kobayashi, F. R. DeLeo, and B. J. Hinnebusch. 2004. Transmission of Yersinia pestis from an infectious biofilm in the flea vector. J. Infect. Dis. 190:783-792.
Karlyshev, A. V., E. E. Galyov, V. M. Abramov, and V. P. Zav'yalov. 1992. Caf1R gene and its role in the regulation of capsule formation of Y. pestis. FEBS Lett. 305:37-40.
Kim, T. J., S. Chauhan, V. L. Motin, E. B. Goh, M. M. Igo, and G. M. Young. 2007. Direct transcriptional control of the plasminogen activator gene of Yersinia pestis by the cyclic AMP receptor protein. J. Bacteriol. 189:8890-8900.
Kolodziejek, A. M., D. J. Sinclair, K. S. Seo, D. R. Schnider, C. F. Deobald, H. N. Rohde, A. K. Viall, S. S. Minnich, C. J. Hovde, S. A. Minnich, and G. A. Bohach. 2007. Phenotypic characterization of OmpX, an Ail homologue of Yersinia pestis KIM. Microbiology 153:2941-2951.
Kukkonen, M., M. Suomalainen, P. Kyllonen, K. Lahteenmaki, H. Lang, R. Virkola, I. M. Helander, O. Holst, and T. K. Korhonen. 2004. Lack of O-antigen is essential for plasminogen activation by Yersinia pestis and Salmonella enterica. Mol. Microbiol. 51:215-225.
Lathem, W. W., P. A. Price, V. L. Miller, and W. E. Goldman. 2007. A plasminogen-activating protease specifically controls the development of primary pneumonic plague. Science 315:509-513.
Lawrenz, M. B., J. D. Lenz, and V. L. Miller. 2009. A novel autotransporter adhesin is required for efficient colonization during bubonic plague. Infect. Immun. 77:317-326.
Li, Y., E. Dai, Y. Cui, M. Li, Y. Zhang, M. Wu, D. Zhou, Z. Guo, X. Dai, B. Cui, Z. Qi, Z. Wang, H. Wang, X. Dong, Z. Song, J. Zhai, Y. Song, and R. Yang. 2008. Different region analysis for genotyping Yersinia pestis isolates from China. PLoS ONE. 3:e2166.
Li, Y. L., H. Gao, L. Qin, B. Li, Y. P. Han, Z. B. Guo, Y. J. Song, J. H. Zhai, Z. M. Du, X. Y. Wang, D. S. Zhou, and R. F. Yang. 2008. Identification and characterization of PhoP regulon members in Yersinia pestis biovar Microtus. BMC Genomics 9:143.
Lorange, E. A., B. L. Race, F. Sebbane, and B. J. Hinnebusch. 2005. Poor vector competence of fleas and the evolution of hypervirulence in Yersinia pestis. J. Infect. Dis. 191:1907-1912.
Ochman, H., J. G. Lawrence, and E. A. Groisman. 2000. Lateral gene transfer and the nature of bacterial innovation. Nature 405:299-304.
Patel, C. N., B. W. Wortham, J. L. Lines, J. D. Fetherston, R. D. Perry, and M. A. Oliveira. 2006. Polyamines are essential for the formation of plague biofilm. J. Bacteriol. 188:2355-2363.
Perry, R. D., and J. D. Fetherston. 1997. Yersinia pestis—etiologic agent of plague. Clin. Microbiol. Rev. 10:35-66.
Perry, R. D., I. Mier, Jr., and J. D. Fetherston. 2007. Roles of the Yfe and Feo transporters of Yersinia pestis in iron uptake and intracellular growth. Biometals 20:699-703.
Porat, R., W. R. McCabe, and R. R. Brubaker. 1995. Lipopolysaccharide associated resistance to killing of yersiniae by complement. J. Endotoxin Res. 2:91-97.
Pouillot, F., C. Fayolle, and E. Carniel. 2008. Characterization of chromosomal regions conserved in Yersinia pseudotuberculosis and lost by Yersinia pestis. Infect. Immun. 76:4592-4599.
Prior, J. L., J. Parkhill, P. G. Hitchen, K. L. Mungall, K. Stevens, H. R. Morris, A. J. Reason, P. C. Oyston, A. Dell, B. W. Wren, and R. W. Titball. 2001. The failure of different strains of Yersinia pestis to produce lipopolysaccharide O-antigen under different growth conditions is due to mutations in the O-antigen gene cluster. FEMS Microbiol. Lett. 197:229-233.
Pujol, C., J. P. Grabenstein, R. D. Perry, and J. B. Bliska. 2005. Replication of Yersinia pestis in interferon gamma-activated macrophages requires ripA, a gene encoded in the pigmentation locus. Proc. Natl. Acad. Sci. USA 102:12909-12914.
Ramamurthi, K. S., and O. Schneewind. 2002. Type iii protein secretion in yersinia species. Annu. Rev. Cell Dev. Biol. 18:107-133.
Robinson, V. L., P. C. Oyston, and R. W. Titball. 2005. A dam mutant of Yersinia pestis is attenuated and induces protection against plague. FEMS Microbiol. Lett. 252:251-256.
Schubert, S., A. Rakin, and J. Heesemann. 2004. The Yersinia high-pathogenicity island (HPI): evolutionary and functional aspects. Int. J. Med. Microbiol. 294:83-94.
Sebbane, F., D. Gardner, D. Long, B. B. Gowen, and B. J. Hinnebusch. 2005. Kinetics of disease progression and host response in a rat model of bubonic plague. Am. J. Pathol. 166:1427-1439.
Sebbane, F., C. O. Jarrett, D. Gardner, D. Long, and B. J. Hinnebusch. 2006. Role of the Yersinia pestis plasminogen activator in the incidence of distinct septicemic and bubonic forms of flea-borne plague. Proc. Natl. Acad. Sci. USA 103:5526-5530.
Sha, J., S. L. Agar, W. B. Baze, J. P. Olano, A. A. Fadl, T. E. Erova, S. Wang, S. M. Foltz, G. Suarez, V. L. Motin, S. Chauhan, G. R. Klimpel, J. W. Peterson, and A. K. Chopra. 2008. Braun lipoprotein (Lpp) contributes to virulence of yersiniae: potential role of Lpp in inducing bubonic and pneumonic plague. Infect. Immun. 76:1390-1409.
Skurnik, M., and J. A. Bengoechea. 2003. The biosynthesis and biological role of lipopolysaccharide O-antigens of pathogenic Yersiniae. Carbohydr. Res. 338:2521-2529.
Skurnik, M., A. Peippo, and E. Ervela. 2000. Characterization of the O-antigen gene clusters of Yersinia pseudotuberculosis and the cryptic O-antigen gene cluster of Yersinia pestis shows that the plague bacillus is most closely related to and has evolved from Y. pseudotuberculosis serotype O:1b. Mol. Microbiol. 37:316-330.
Sokurenko, E. V., R. Gomulkiewicz, and D. E. Dykhuizen. 2006. Source-sink dynamics of virulence evolution. Nat. Rev. Microbiol. 4:548-555.
Song, Y., Z. Tong, J. Wang, L. Wang, Z. Guo, Y. Han, J. Zhang, D. Pei, D. Zhou, H. Qin, X. Pang, J. Zhai, M. Li, B. Cui, Z. Qi, L. Jin, R. Dai, F. Chen, S. Li, C. Ye, Z. Du, W. Lin, J. Yu, H. Yang, P. Huang, and R. Yang. 2004. Complete genome sequence of Yersinia pestis strain 91001, an isolate avirulent to humans. DNA Res. 11:179-197.
Stenseth, N. C., B. B. Atshabar, M. Begon, S. R. Belmain, E. Bertherat, E. Carniel, K. L. Gage, H. Leirs, and L. Rahalison. 2008. Plague: past, present, and future. PLoS Med. 5(1):e3.
Sun, Y. C., B. J. Hinnebusch, and C. Darby. 2008. Experimental evidence for negative selection in the evolution of a Yersinia pestis pseudogene. Proc. Natl. Acad. Sci. USA 105:8097-8101.
Tan, L., and C. Darby. 2006. Yersinia pestis YrbH is a multifunctional protein required for both 3-deoxy-D-manno-oct-2-ulosonic acid biosynthesis and biofilm formation. Mol. Microbiol. 61:861-870.
Tong, Z., D. Zhou, Y. Song, L. Zhang, D. Pei, Y. Han, X. Pang, M. Li, B. Cui, J. Wang, Z. Guo, Z. Qi, L. Jin, J. Zhai, Z. Du, X. Wang, J. Yu, P. Huang, H. Yang, and R. Yang. 2005. Pseudogene accumulation might promote the adaptive microevolution of Yersinia pestis. J. Med. Microbiol. 54:259-268.
Tran, H. J., A. K. Heroven, L. Winkler, T. Spreter, B. Beatrix, and P. Dersch. 2005. Analysis of RovA, a transcriptional regulator of Yersinia pseudotuberculosis virulence that acts through antirepression and direct transcriptional activation. J. Biol. Chem. 280:42423-42432.
Twigg, G. 2003. The Black Death and DNA. Lancet Infect. Dis. 3:11.
Viola, R. E., L. Yerman, J. M. Fowler, C. G. Arvidson, and R. R. Brubaker. 2008. A missense mutation causes aspartase deficiency in Yersinia pestis. Microbiology 154:1271-1280.
Wang, X., Y. Han, Y. Li, Z. Guo, Y. Song, Y. Tan, Z. Du, A. Rakin, D. Zhou, and R. Yang. 2007. Yersinia genome diversity disclosed by Yersinia pestis genome-wide DNA microarray. Can. J. Microbiol. 53:1211-1221.
Wattiau, P., and G. R. Cornelis. 1994. Identification of DNA sequences recognized by VirF, the transcriptional activator of the Yersinia yop regulon. J. Bacteriol. 176:3878-3884.
Williams, K., P. C. Oyston, N. Dorrell, S. Li, R. W. Titball, and B. W. Wren. 2000. Investigation into the role of the serine protease HtrA in Yersinia pestis pathogenesis. FEMS Microbiol. Lett. 186:281-286.
Zhan, L., Y. Han, L. Yang, J. Geng, Y. Li, H. Gao, Z. Guo, W. Fan, G. Li, L. Zhang, C. Qin, D. Zhou, and R. Yang. 2008. The cyclic AMP receptor protein, CRP, is required for both virulence and expression of the minimal CRP regulon in Yersinia pestis biovar microtus. Infect. Immun. 76:5028-5037.
Zhou, D., Y. Han, Y. Song, P. Huang, and R. Yang. 2004. Comparative and evolutionary genomics of Yersinia pestis. Microbes Infect. 6:1226-1234.
Zhou, D., Y. Han, Y. Song, Z. Tong, J. Wang, Z. Guo, D. Pei, X. Pang, J. Zhai, M. Li, B. Cui, Z. Qi, L. Jin, R. Dai, Z. Du, J. Bao, X. Zhang, J. Yu, P. Huang, and R. Yang. 2004. DNA microarray analysis of genome dynamics in Yersinia pestis: insights into bacterial genome microevolution and niche adaptation. J. Bacteriol. 186:5138-5146.
Zhou, D., Y. Han, and R. Yang. 2006. Molecular and physiological insights into plague transmission, virulence and etiology. Microbes Infect. 8:273-284.
Zhou, D., Z. Tong, Y. Song, Y. Han, D. Pei, X. Pang, J. Zhai, M. Li, B. Cui, Z. Qi, L. Jin, R. Dai, Z. Du, J. Wang, Z. Guo, J. Wang, P. Huang, and R. Yang. 2004. Genetics of metabolic variations between Yersinia pestis biovars and the proposal of a new biovar, microtus. J. Bacteriol. 186:5147-5152.
Zhou, D., and R. Yang. 2006. Global analysis of gene transcription regulation in prokaryotes. Cell. Mol. Life Sci. 63:2260-2290.

matches: V. V. V. V. V. V. V. V. V. V. V.


text:
26 In the sixth month the angel Gabriel was sent by God to a town in Galilee called Nazareth, 27 to a virgin betrothed to a man named Joseph, of the House of David; and the virgin's name was Mary. 28 He went in and said to her, “Rejoice, you who enjoy God's favor! The Lord is with you.” 29 She was deeply disturbed by these words and asked herself what this greeting could mean, 30 but the angel said to her, “Mary, do not be afraid; you have won God's favor. 31 Look! You are to conceive in your womb and bear a son, and you must name Him Jesus. 32 He will be great and will be called Son of the Most High. The Lord God will give Him the throne of His ancestor David; 33 He will rule over the House of Jacob for ever and His reign will have no end.” 34 Mary said to the angel, “But how can this come about, since I have no knowledge of man?” 35 The angel answered, 'The Holy Spirit will come upon you, and the power of the Most High will cover you with its shadow. And so the child will be holy and will be called Son of God. 36 And I tell you this too: your cousin Elizabeth also, in her old age, has conceived a son, and she whom people called barren is now in her sixth month, 37 for nothing is impossible with God.” 38 Mary said, “You see before you the Lord's servant; let it happen to me as you have said.” And the angel left her.
- In the sixth month: do my eyes see the angels whom God sends to visit me?
- Do not be afraid: do our worries arise from our fears and anxieties or do they come from our perception of some mystery hanging over us and involving us personally?
- Nothing is impossible with God: Generating is the work of God; accepting is the task of humanity. Do I make it possible for it to be a life that comes from the Spirit of God?
v. 26-27. In the sixth month the angel Gabriel was sent by God to a town in Galilee called Nazareth, to a virgin betrothed to a man named Joseph of the House of David; and the virgin’s name was Mary.
In the sixth month: This is a precise moment for those who have read the previous page of the Gospel, the meeting of the angel Gabriel with Zechariah in the temple. But for Mary, unbeknownst to her, this sixth month is her “today”. As it was for her so it is for us. There is a unique today, the time of invitation to enter into the plan for us. This today is not an isolated time; it is connected to the times of others, each unique and unrepeatable, a today to be set alongside the other todays until such time as the Word of God is fulfilled. The way of grace is very linear. The subject is God. The term of reference: a virgin. The intermediary: the angel Gabriel. Everything is named: the city is called Nazareth; the virgin: Mary; the man to whom she is betrothed: Joseph. Everything has a precise historical setting. The sixth month is that of Elizabeth’s pregnancy. The virgin is the betrothed bride. Joseph is of the House of David. God does not come haphazardly; He comes within what is already in existence, drawn by people who have names.
v. 28. He went in and said to her, “Rejoice, you who enjoy God’s favor! The Lord is with you.”.
The words of the Gospel, “He went in”, may be understood in two ways: he went into her house or he went into her being. So, did Mary see the angel or not? She saw him and heard him. This is true since all that was said will be accomplished. With which eyes did she see him? The physical eyes or the spiritual ones? The mystery of a person’s encounter with God cannot be explained. It happens and that’s all. It is an encounter that leaves a sign, and herein lies the greatness of the event. She who is full of grace has only the eyes of the spirit, thus for her there is only one way of seeing, spiritually, that transparent look of the pure heart that can look upon God and not die.
v. 29. She was deeply disturbed by these words and asked herself what this greeting could mean.
Mary being disturbed is quite legitimate. The way she sees herself, even though she is full of grace, does not allow her to distance herself from others, and so she is not aware of being full of grace. For her it is natural to be what she is, faithful to doing good always and everywhere, faithful to that interior attraction that raises her on high.
v. 30. The angel said to her: “Mary, do not be afraid; you have won God’s favor.
Mary’s fear is the amazement of all little ones who are surprised at being the object of attention from someone important. And if this someone is God, how great then is that fear? So great that one feels one’s utter smallness and that one has everything from the free gift of love.
v. 31. You are to conceive in your womb and bear a son, and you must name Him Jesus.
The divine plan is revealed: to conceive and bring this to light and to name Him. The Savior is already there, in the words of the angel. How wonderful! Centuries and centuries of waiting are fulfilled in these two syllables: Jesus.
v. 32-33. He will be great and will be called the Son of the Most High. The Lord God will give Him the throne of His ancestor David; He will rule over the House of Jacob forever and His reign will have no end.
When the Lord approaches a person to call that person to participate in His thoughts of redemption, He does so completely. What remains still obscure is the manner of human cooperation, because the person remains free to put into practice the fulfillment of God’s thought. The point of departure is an “unforeseen” son. The destination is the Son of the Most High, who will sit on the throne of David and will reign forever. The means for accomplishing this is your person. Now it is up to you to become the protagonist.
Mary asks of the angel the “how” of the fulfilment of the will of God. She does not doubt God; she knows that the Word pronounced by God is always possible. The “how” is what concerns her, to what she is being called to be. She is certain that her desire and intention of not “knowing man” will continue, because God does not cancel the plans of his children, drawn up by their most authentic desires. She knows that her plan will fit into the plan just heard. But she does not know how it will happen. And so she simply asks to do exactly what has been asked of her.
The angel explains. Mary will simply have to accept, because it will be the Spirit who will descend on her, it will be the Most High who will overshadow her, and the Holy One will be born.
vv. 36-37. And I tell you this too: your cousin Elizabeth also, in her old age, has conceived a son, and she whom people called barren is now in her sixth month, for nothing is impossible with God.
The experience of Elizabeth told by the angel to Mary is an occasion to connect with history. Mary must have already known of Elizabeth, because both were preparing the way for the fulfillment of promise made to Israel: John the voice, Jesus the spouse. It is the same plan.
v. 38. Mary said, “You see before you the Lord’s servant; let it happen to me as you have said.” And the angel left her.
Mary’s reply is essential: Here I am. Her concentration on the Word announced to her is so great that she can only feel that she is a “servant”, a useful instrument in the realization of the will of the Father. Let it happen to me… this is nothing like a passive yes, it is a yes that is aware of the greatness of her involvement, a yes so deep that it brings forth the face of God in human features.
Ecce ancilla Domini; fiat mihi secundum verbum tuum! Behold… This word is essential and full of life. No words are better suited to humankind than this being present, awake, holding one’s breath so as not to lose anything of what the mystery is sharing of Himself. Let it happen… God’s choice is worthy of acceptance, but requires the deep silence of one’s whole being, let it happen to me… Mary knows that she is not the protagonist, but the servant of the divine will; she belongs to the group of servants that Jesus will call friends: a servant does not know what his master does, but friends do know. Whatsoever I have heard from my Father I have revealed to you. The shadow of the Spirit that covers the tent of the presence on such a beautiful creature for her availability, will whisper the mysterious secrets of the Eternal. And the times that go on tracing new ways of grace will come to their peak when the Son of God will see the light of an infinitely small space for his power, the space of limitation and contingency. Mary, first cradle of the ineffable Word, first embrace of the coming light, has no other treasure than her humility, a hollow that receives the fullness, smallness that is called infinite, limited love that demands the embrace of the infinite.
for I rejoice in Your deliverance.
but those who were tottering are now braced with strength.
He raises up the strength of his Anointed.
Lord, let the gentle breeze of silence, the breeze of grace, carry away all the voices and sounds that gradually take my heart away from my own existence. May the luminous trail of Your passing by intoxicate the air I usually breathe with your perfume so that I may seek no one but You. And when the ruminated syllables of scripture, together with the events that form the memory of our encounter, will become the fiber of my flesh, the world will see You again, will see Your face in the physical features that I shall give to You. The limits of my being will tell of the prodigies of Your power, unless I try uselessly to flee or avoid them, but I shall love them as the precision of my human uniqueness. I shall then come to think Your words, speak Your words, fulfill Your words, because, by not fleeing from myself, I shall have met you where You are: in the depths of my limited being, in my inner self and in my essential silence, where love given brings forth love gift and creates bridges of communion.

matches: v. v. v. v. v. v. v.


text:
A. Gay Jenson Farms Co. v. Cargill, Inc.
Blasius Industries, Inc. v. Atlas Corp.
Brascan Ltd. v. Edper Equities Ltd.
Carlton Investments v. TLC Beatrice International Holdings, Inc.
Cookies Food Products, Inc. v. Lakes Warehouse Distributing, Inc.
Elkind v. Liggett & Myers, Inc.
Fletcher v. A.J. Industries, Inc.
Gagliardi v. TriFoods International, Inc.
Graham v. Allis-Chalmers Manufacturing Co.
Hariton v. Arco Electronics, Inc.
Jennings v. Pittsburgh Mercantile Co.
Kahn v. Lynch Communications Systems, Inc.
Omnicare, Inc. v. NCS Healthcare, Inc.
Paramount Communications Inc. v. QVC Network Inc.
Rosenfeld v. Fairchild Engine & Airplane Corp.
Schnell v. Chris-Craft Industries, Inc.
Securities and Exchange Commission v. Texas Gulf Sulphur Co.
Smith v. Atlantic Properties, Inc.
State ex rel. Hayes Oyster Co. v. Keypoint Oyster Co.
Unocal Corporation v. Mesa Petroleum Co.
Waltuch v. Conticommodity Services, Inc.
Zetlin v. Hanson Holdings, Inc.

matches: v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v. v.


On March 20, 2014, the United States Court of Appeals for the Eighth Circuit issued a mandate (Doc. 180) in this case affirming in part and reversing in part this Court's previous judgments, and remanding the matter for proceedings consistent with the Eighth Circuit's opinion.
On May 4, 1994, Petitioner Andrew Sasser was convicted of capital murder and sentenced to death for the July 12, 1993 homicide of Jo Ann Kennedy. See Sasser v. State, 902 S.W.2d 773 (Ark. 1995). The murder occurred while Kennedy worked as a clerk at an E-Z Mart convenience store in Garland City, Arkansas. Id. at 774-75. Following a direct appeal, and Sasser's effort to obtain Arkansas state court postconviction relief pursuant to Arkansas Rule of Criminal Procedure 37, Sasser sought federal relief through a writ of habeas corpus. (Doc. 3). The Court dismissed the petition but granted a certificate of appealability with respect to several issues. (Docs. 30 and 34). During Sasser's first appeal to the Eighth Circuit, and following the Supreme Court's decision in Atkins v. Virginia,  the Eighth Circuit remanded for a determination of whether Sasser was ineligible for the death penalty because of intellectual disability, but retained jurisdiction over the bulk of Sasser's case. After reviewing the Atkins issue twice, the Eighth Circuit issued its opinion and mandate remanding to this Court and giving rise to these proceedings. The Eighth Circuit affirmed dismissal of many of Sasser's claims, but reversed with respect to Sasser's Atkins claim and four of his claims of ineffective assistance of counsel at the sentencing phase of Sasser's trial. The Eighth Circuit vacated the Court's denial of relief on those four claims and the Court's finding that Sasser is not intellectually disabled under Atkins.
The four claims to be considered on remand are that Sasser's trial counsel was unconstitutionally ineffective when he failed to: “1. Prepare for the sentencing phase of the trial; 2. Obtain a timely psychological evaluation of Sasser; 3. Meaningfully consult with a mental health professional; and 4. Object when the prosecutor misconstrued the mitigating evidence that the defense had presented concerning Sasser's mental impairment and lessened culpability or to rebut the argument.” Sasser v. Hobbs (Sasser II), 735 F.3d 833, 851 (8th Cir. 2013) (brackets and quotation omitted). The Eighth Circuit directed the Court to conduct a hearing on the four ineffective assistance of counsel claims to determine whether they are procedurally defaulted claims, and if so, whether they should be excused. Id. at 853, 855; see also Sasser v. Hobbs, 743 F.3d 1151, 1151 (8th Cir. 2014) (denying rehearing) (“It should be clear the district court, on remand, must consider whether Andrew Sasser's state postconviction counsel failed to raise the four potentially meritorious ineffectiveness claims.” (quotation and brackets omitted)). The Eighth Circuit also directed the Court to make a new Atkins finding using the appropriate standard. Sasser II, 735 F.3d at 855. The Court's Atkins finding is addressed by a separate opinion.
A hearing was set, and the Court's scheduling order directed the parties that the Court was to hear evidence regarding Sasser's four surviving ineffective assistance claims. (Doc. 217). The Court also directed the parties to submit prehearing briefs with proposed findings of fact and conclusions of law. In February 2016, the Court held a four-day hearing and heard testimony from the following individuals in the following order: Charles Potter (“trial counsel”), Jacquelyn Carter, Rupert Purifoy, Steve Jackson, Leroy Brown, Deborah Sallings (“postconviction counsel”), Joseph Cummings, Dr. Ann Thomas, Dana Harrison, Mark Bezy, Betty Perry, Margie Sasser Kemp, Artha Sasser, H.B. Sasser, James Blackburn, Ph.D., Pamela Blake, M.D., Dale Watson, Ph.D., Leslie Lebowitz, Ph.D., and Richard Burr. Following the hearing, the Court invited posthearing briefing.
A federal court may consider a petition for writ of habeas corpus from a person serving a state court sentence that violates the Constitution or a federal law or treaty. 28 U.S.C. § 2254(a). A state court sentence may violate the Sixth Amendment to the Constitution if the petitioner was deprived of the right to effective assistance of counsel at trial and sentencing, which occurs when counsel's performance is deficient (“counsel made errors so serious that counsel was not functioning as the ‘counsel' guaranteed the defendant by the Sixth Amendment”) and the performance prejudiced the defense (“counsel's errors were so serious as to deprive the defendant of a fair trial, a trial whose result is reliable”). Strickland v. Washington, 466 U.S. 668, 687 (1984).
Before a federal court may grant a petition, the petitioner must first have exhausted state court remedies, “unless the state remedies are ineffectual or non-existent.” Sasser II, 735 F.3d 833, 842 (citing 28 U.S.C. § 2254(b)(1)). The exhaustion requirement protects a state court's interest in correcting its own constitutional violations, and is grounded in principles of comity. Coleman v. Thompson, 501 U.S. 722, 731 (1991). Where state court remedies have been exhausted, a federal court cannot grant a petition for a writ of habeas corpus unless the state's decision “was contrary to, or involved an unreasonable application of, clearly established Federal law, as determined by the Supreme Court of the United States; or … was based on an unreasonable determination of the facts in light of the evidence presented in the State court proceeding.” 28 U.S.C. § 2254(d).
Where a claim has not been exhausted, that new claim must be presented and exhausted in state court proceedings before a federal court can grant a petition. Rhines v. Weber, 544 U.S. 269, 274 (2005). Dismissal of the entire petition without prejudice is generally required in such instances. In limited circumstances where there has been good cause for a petitioner's failure to exhaust a claim in state court, a federal court may stay its proceedings and hold the matter in abeyance until the new claim is exhausted, or allow the petitioner to amend his petition and omit the new claim. Id. at 277, 278.
Where a claim has been raised but defaulted during state proceedings due to the petitioner's failure to abide by a state's procedural requirements, although it is technically exhausted (because a state remedy is no longer available to the petitioner), the same need for comity exists that undergirds the exhaustion requirement. Coleman, 501 U.S. at 732. When there has been a procedural default, there is typically an independent and adequate state ground barring federal habeas relief, unless a petitioner can show cause to excuse the default and prejudice to himself if the default is not excused. See Id. at 745-47.
where (1) the claim of ineffective assistance of trial counsel was a substantial claim; (2) the cause consisted of there being no counsel or only ineffective counsel during the state collateral review proceeding; (3) the state collateral review proceeding was the initial review proceeding in respect to the ineffective-assistance-of-trial-counsel claim; and (4) state law requires that an ineffective assistance of trial claim be raised in an initial-review collateral proceeding.
Trevino v. Thaler, 569 U.S. 413, 423 (2013) (citing Martinez v. Ryan, 566 U.S. 1, 14, 17-18 (2012)) (quotations and punctuation omitted). Because there is no meaningful distinction between a state that denies permission to raise ineffective assistance claims on direct appeal and one that, “as a matter of procedural design and systemic operation, ” technically allows but effectively denies a meaningful opportunity to raise ineffective assistance claims on direct appeal, the Supreme Court has expanded the narrow exception to cover states in the second category. Id., at 429. In this case, Arkansas falls into the latter category. Sasser II, 735 F.3d at 853 (“For these reasons, we conclude Arkansas did not ‘as a systematic matter' afford Sasser ‘meaningful review of a claim of ineffective assistance of trial counsel' on direct appeal.” (citation omitted)).
The four ineffective assistance claims before this Court on remand may provide grounds for habeas relief if (1) they were exhausted in state court, and the state court's decision was contrary to or unreasonably applied clearly established federal law, or was based on an unreasonable determination of the facts based on the evidence in the state court proceeding; or (2) they were procedurally defaulted in state court proceedings, but the default was due to postconviction counsel's ineffective assistance and that ineffective assistance would prejudice the petitioner.
As an initial matter, the Court will address Sasser's fourth claim identified by the Eighth Circuit-that trial counsel was unconstitutionally ineffective when he failed to object when the prosecutor misconstrued the mitigating evidence that the defense had presented concerning Sasser's mental impairment and lessened culpability or to rebut the argument. Sasser has presented no argument or evidence concerning this claim. Because “[t]he law favors an adversarial presentation of issues in order to conserve judicial resources and to ensure that cases are resolved in the context of an actual dispute, ” Sasser's failure to present argument or evidence concerning this claim results in abandonment. Malone v. Vasquez, 138 F.3d 711, 716 (8th Cir. 1998). This leaves only three claims that must be analyzed-Sasser's claims that his trial counsel was unconstitutionally ineffective when he failed to: (1) prepare for the sentencing phase of the trial; (2) obtain a timely psychological evaluation of Sasser; and (3) meaningfully consult with a mental health professional. Sasser II, 735 F.3d at 851.
The first issue the Court must resolve is whether these three claims are claims that Sasser exhausted before the state court, or if they are new or procedurally defaulted claims and susceptible to a Martinez/Trevino analysis. Claims are the same when they have the same factual and legal premises, and are new when new factual allegations fundamentally alter the legal claim already considered. See Vasquez v. Hillery, 474 U.S. 254, 260 (1986) (holding supplemental evidence did not fundamentally alter legal claim).
The Court is cognizant that a determination that a claim is new might in a similar case require the Court to follow the stay and abeyance process identified in Rhines. See Sasser v. Hobbs, 745 F.3d 896, 899 (8th Cir. 2014) (Colloton, J., dissenting from denial of rehearing en banc).
However, if no state court remedy is available for the unexhausted claim-that is, if resort to the state courts would be futile-then the exhaustion requirement in § 2254(b) is satisfied, but the failure to exhaust ‘provides an independent and adequate state-law ground for the conviction and sentence, and thus prevents federal habeas corpus review of the defaulted claim unless the petitioner can demonstrate cause and prejudice for the default' (or actual innocence, which is not an issue in this case).
Armstrong v. Iowa, 418 F.3d 924, 926 (8th Cir. 2005) (quoting Gray v. Netherland, 518 U.S. 152, 162 (1996). That is, if there is no state remedy, new claims are treated as procedurally defaulted. To the extent any of these three ineffective assistance claims is new, Arkansas has no available state court remedy to exhaust the claim. See, e.g., Ward v. State, 455 S.W.3d 830, 832, 835 (Ark. 2015) (“This court will recall a mandate and reopen a case only in extraordinary circumstances.” … “As we have held, recalling the mandate is an extremely narrow remedy reserved for unique situations; to enlarge it to allow typical claims of ineffective assistance of counsel would alter the nature of the relief entirely.”) Therefore, any claim that is new, or any claim that was otherwise procedurally defaulted, may be excused under Martinez and Trevino and the matter need not be stayed pending exhaustion in state proceedings.
Determining whether any of Sasser's three ineffective assistance claims was exhausted or procedurally defaulted requires the Court to compare those claims to the claims Sasser made in the state court proceedings. This analysis is complicated by the parties' competing arguments that the other party is judicially estopped from asserting the position now taken with respect to whether these claims were exhausted or procedurally defaulted. Judicial estoppel “generally prevents a party from prevailing in one phase of a case on an argument and then relying on a contradictory argument to prevail in another phase.” New Hampshire v. Maine, 532 U.S. 742, 749 (2001) (quoting Pegram v. Herdrich, 530 U.S. 211, 227 n.8 (2000)). It is employed to protect the integrity of the judicial process. Stallings v. Hussman Corp., 447 F.3d 1041, 1047 (8th Cir. 2006). The Court will address the judicial estoppel arguments first.