Prijevodi slavenskih književnosti ("Przekłady Literatur Słowiańskich") - poljski znanstveni časopis koji objavljuje Izdavačka kuća Šleskog sveučilišta na početku kao serijska publikacija  – pokrenuti su 2009. godine na Institutu za slavensku filologiju na Filološkom fakultetu Šleskog sveučilišta u Katowicama. Posvećeni su problematici književnog prijevoda s južnoslavenskih i zapadnoslavenskih jezika, promatranoj iz teorijske, književnopovijesne i kulturnopovijesne perspektive.

Od 2017. glavni urednik je doc. Leszek Małczak (docent na Institutu za slovensku filologiju Filozofskog fakulteta Šleskog sveučilišta), koji je zamijenio prof. Bożenu Tokarz (glavni urednik 2009-2016, osnivač) - redoviti profesor na Institutu za slovensku filologiju na Filozofskom fakultetu Šleskog sveučilišta.

Osnovne informacije
Časopis obuhvaća podjednako evidenciju prijevoda i njihovu recepciju, kao i znanstvene radove koje se odnose na:

1. osobitosti prijevoda na srodne, slavenske jezike srodnim jezicima specifici prijevoda u granicama srodnih jezika,

2. prenošenje jedne kulture u drugu posredstvom književnosti kao medija prijevoda jedne kulture na drugu posredstvom medija književnosti ,

3. ulogu prijevoda u komparatističkim istraživanjima.

Struktura
S obzirom na dvostrukost istraživanja, dokumentacijsko-sociološku komponentu (bibliografije prijevoda slavenskih književnosti na poljski jezik i poljske književnosti na slavenske jezike te njihova recepcija) i kritičko-intepretacijsku komponentu (koja služi teorijskom uopćavanju), pojedini su svesci izdavani u dva dijela.  Svaki se svezak sastoji od problemskog i bibliografskog dijela, koji se odnosi na prijevode poljske književnosti (na bugarski, hrvatski, češki, makedonski, srpski, slovački i slovenski) i prijevode slavenskih književnosti (bugarske, makedonske, hrvatske, češke, srpske, slovačke i slovenske) na poljski jezik. Bibliografski dio obuhvaća prijevode objavljene nakon 1990. godine (bibliografia koja se odnosi na ranija razdoblja bit će dopunjavana kasnije).  Cilj je publikacije, prve te vrste u slavističkome krugu (s iznimkom rusistike), utvrđivanje razlika, sličnosti i putova uzajamnoga dijaloga među slavenskim kulturama i stvaranje temelja za slavensku komparatistiku. Slavenski susjedi, unatoč srodnosti jezika, često su jedni drugima nepoznanica. Autori često uvode i treću, neslavensku kulturu, u krug svojih interesa, s obzirom na funkcioniranje slavenskih književnosti u međukulturnoj komunikaciji, koja je, pak, politički, društveno i umjetnički uvjetovana.

Svrha časopisa
Časopis "Prijevodi slavenskih književnosti" razvija se i zahvaljujući suradnji s poljskim znanstvenicima koji se bave znanošću o prevođenju (na sveučilištima u Bielsko-Bialoj, Gdanjsku, Krakovu, Lublinu, Poznanju, Szczecinu, Wrocławu) i s inozemnim znanstvenim centrima (u Bugarskoj, Hrvatskoj, Češkoj, Makedoniji, Srbiji, Slovačkoj i Sloveniji). Tekstovi objavljeni u časopisu prolaze recenziju, a časopis ima odjeka u cijeloj Poljskoj te izaziva zanimanje u sveučilišnim centrima u inozemstvu. Svaki je članak popraćen dvama sažetcima (na engleskome jeziku i na onome slavenskom jeziku čiju temu razmatra), abstraktom na engleskome jeziku i ključnim riječima na engleskome i odgovarajućem slavenskom jeziku.

Izvori

Vanjske poveznice
 Službena stranica časopisa
 Službena stranica Instituta za slavensku filologiju
 WorldCat
 VIAF

Stručni i znanstveni časopisi
Poljska
Slavistika
Prevoditelji

Przekłady Literatur Słowiańskich


Ctenitis, rod papratnica iz porodice rebračevki (Dryopteridaceae), kojemu pripada 144 priznatih vrsta iz tropske Amerike (preko 60), Indijskog oceana (39) i tropske Azije.

Vrste

 Ctenitis abyssi (Sehnem) Salino & P. O. Morais
 Ctenitis aciculata (Baker) Ching
 Ctenitis alteroblumei Holttum
 Ctenitis analamazaotrensis (Rakotondr.) Hennequin & Rouhan
 Ctenitis angusta Holttum
 Ctenitis anniesii (Rosenst.) Copel.
 Ctenitis apicalis (Baker) Ballard
 Ctenitis arthrothrix (Hook.) Tardieu
 Ctenitis aspidioides (C. Presl) Copel.
 Ctenitis atrorubens Holttum
 Ctenitis baulensis A. R. Sm.
 Ctenitis biformis (Mett. ex Kuhn) Tardieu
 Ctenitis bigarellae Schwartsb., Labiak & Salino
 Ctenitis bivestita (Mett.) Tardieu
 Ctenitis blepharochlamys (C. Chr.) Tardieu
 Ctenitis boholensis Holttum
 Ctenitis borbonica (Baker) Tardieu
 Ctenitis brevipetiolulata Li Bing Zhang & Yi F. Duan
 Ctenitis bullata A. R. Sm.
 Ctenitis bullescens Rouhan, Li Bing Zhang & Yi F. Duan
 Ctenitis bulusanica Holttum
 Ctenitis calcicola M. Kato
 Ctenitis cerea Li Bing Zhang & Yi F. Duan
 Ctenitis cheilanthina (C. Chr.) C. V. Morton
 Ctenitis chiapasensis (Christ) A. R. Sm.
 Ctenitis chiriquiana (C. Chr.) Lellinger
 Ctenitis christensenii R. S. Viveros & Salino
 Ctenitis cirrhosa (Schum.) Ching
 Ctenitis clathrata M. Kato
 Ctenitis comorensis Li Bing Zhang & Yi F. Duan
 Ctenitis coriacea M. Kato
 Ctenitis crinigera (C. Chr.) Hennequin & Rouhan
 Ctenitis crinita (Poir.) Ching
 Ctenitis croftii Holttum
 Ctenitis crystallina (Kunze) Proctor
 Ctenitis cumingii Holttum
 Ctenitis cyclochlamys (Fée) Holttum
 Ctenitis decaryana (C. Chr.) Hennequin & Rouhan
 Ctenitis decurrentipinnata (Ching) Tardieu & C. Chr.
 Ctenitis deflexa (Kaulf.) Copel.
 Ctenitis dentata Li Bing Zhang & Yi F. Duan
 Ctenitis desvauxii (Mett. ex Kuhn) Tardieu
 Ctenitis dianguiensis (W. M. Chu & H. G. Zhou) S. Y. Dong
 Ctenitis dingnanensis Ching
 Ctenitis distans (Brack.) Ching
 Ctenitis dolphinensis Proctor
 Ctenitis dumrongii Tagawa & K. Iwats.
 Ctenitis eatonii (Baker) Ching
 Ctenitis elata Holttum
 Ctenitis equestris (Kunze) Ching
 Ctenitis erinacea A. R. Sm.
 Ctenitis eriocaulis (Fée) Alston
 Ctenitis erythradenia Holttum
 Ctenitis exaggerata (Baker) Ching
 Ctenitis excelsa (Desv.) Proctor
 Ctenitis falciculata (Raddi) Ching
 Ctenitis fenestralis (C. Chr.) Copel.
 Ctenitis fibrillosa (Baker) Li Bing Zhang & Yi F. Duan
 Ctenitis fijiensis (Hook.) Copel.
 Ctenitis flexuosa (Fée) Copel.
 Ctenitis glandulosa R. S. Viveros & Salino
 Ctenitis grisebachii (Baker) Ching
 Ctenitis guidianensis H. G. Zhou & W. M. Chu
 Ctenitis harrisii Proctor
 Ctenitis hemsleyana (Baker ex Hemsl.) Copel.
 Ctenitis hirta (Sw.) Ching
 Ctenitis hispida (Kuhn) Li Bing Zhang & Yi F. Duan
 Ctenitis humida (Cordem.) Holttum
 Ctenitis humilis Holttum
 Ctenitis interjecta (C. Chr.) Ching
 Ctenitis iriomotensis (H. Itô) Nakaike
 Ctenitis jinfoshanensis Ching & Z. Y. Liu
 Ctenitis jouyana (Rakotondr.) Hennequin & Rouhan
 Ctenitis kinabaluensis Holttum
 Ctenitis kjellbergii (C. Chr. ex Kjellb. & C. Chr.) Ching
 Ctenitis koordersii Holttum
 Ctenitis laetevirens (Rosenst.) Salino & P. O. Morais
 Ctenitis lanceolata (Baker) A. R. Sm.
 Ctenitis latifrons (Brack.) Copel.
 Ctenitis leonii A. Rojas
 Ctenitis longivillosa Li Bing Zhang & Yi F. Duan
 Ctenitis lorencei Holttum
 Ctenitis madagascariensis Tardieu
 Ctenitis magna (Baker) Tardieu
 Ctenitis mannii (C. Hope) Ching
 Ctenitis marginalisora Li Bing Zhang & Yi F. Duan
 Ctenitis maritima (Cordem.) Tardieu
 Ctenitis mayottensis Li Bing Zhang & Yi F. Duan
 Ctenitis megalastriformis R. S. Viveros & Salino
 Ctenitis melanochlamys (Fée) Ching
 Ctenitis melanosticta (Kunze) Copel.
 Ctenitis meridionalis (Poir.) Ching
 Ctenitis mexicana A. R. Sm.
 Ctenitis microchlaena (Fée) Stolze
 Ctenitis microlepigera (Nakai) Ching
 Ctenitis minutiloba Holttum
 Ctenitis multilobata Li Bing Zhang, Yi F. Duan & Rouhan
 Ctenitis muluensis Holttum
 Ctenitis nemorosa (Willd.) Ching
 Ctenitis nervata (Fée) R. S. Viveros & Salino
 Ctenitis nigrovenia (Christ) Copel.
 Ctenitis oophylla (C. Chr.) Ching
 Ctenitis paleolata Copel.
 Ctenitis pallatangana (Hook.) Ching
 Ctenitis pallens (Brack.) M. G. Price
 Ctenitis paranaensis (C. Chr.) Lellinger
 Ctenitis parvula Proctor
 Ctenitis pauciflora (Kaulf. ex Spreng.) Holttum
 Ctenitis propinqua (J. Sm. ex C. Presl) Copel.
 Ctenitis pseudorhodolepis Ching & Chu H. Wang
 Ctenitis pulvinata (C. Chr.) Ching
 Ctenitis rapensis (E. D. Br.) Holttum
 Ctenitis refulgens (Klotzsch ex Mett.) Vareschi
 Ctenitis reunionensis Hennequin, Li Bing Zhang & Yi F. Duan
 Ctenitis salvinii (Baker) Stolze
 Ctenitis samoensis (C. Chr.) Holttum
 Ctenitis santae-clarae (C. Chr.) Ching
 Ctenitis sciaphila (Maxon) Ching
 Ctenitis seramensis Holttum
 Ctenitis setosa (C. Presl) Holttum
 Ctenitis sieberiana (Kaulf. ex Spreng.) Hennequin & Rouhan
 Ctenitis silvatica Holttum
 Ctenitis sinii (Ching) Ohwi
 Ctenitis sloanei (Poepp. ex Spreng.) C. V. Morton
 Ctenitis sparsa Li Bing Zhang & Yi F. Duan
 Ctenitis spekei (Baker) Li Bing Zhang & Yi F. Duan
 Ctenitis squamigera (Brack.) Copel.
 Ctenitis strigilosa (Davenp.) Copel.
 Ctenitis subconnexa (Christ) Holttum
 Ctenitis subcrenulata (Baker) Li Bing Zhang, Rouhan & Yi F. Duan
 Ctenitis subdryopteris (Christ) Lellinger
 Ctenitis subglandulosa (Hance) Ching
 Ctenitis submarginalis (Langsd. & Fisch.) Ching
 Ctenitis subobscura (Christ) Holttum
 Ctenitis sumbawensis Holttum
 Ctenitis tabacifera (Alderw.) Ching
 Ctenitis tardieu-blotiae Li Bing Zhang & Yi F. Duan
 Ctenitis thwaitesii Holttum
 Ctenitis truncicola (C. Chr.) Ching
 Ctenitis ursina A. R. Sm.
 Ctenitis velata (Kunze ex Mett.) R. M. Tryon & A. F. Tryon
 Ctenitis vellea (Willd.) Proctor
 Ctenitis vilis (Kunze) Ching
 Ctenitis warburii (C. Chr.) Tardieu

Izvori

Dryopteridoideae

Ctenitis


Liste der Baudenkmäler nach Stadtbezirken
In Regensburg gibt es über 1300 Baudenkmäler. Daher ist diese Liste in Teillisten für die einzelnen Stadtbezirke Regensburgs aufgeteilt, die zusätzlich noch in Ortsteile untergliedert sind. Zwischen den Denkmallisten der Stadtbezirke kann über eine nach den Nummern der Stadtbezirke sortierte Navigationsleiste gewechselt werden.

Siehe auch die Aufstellung  der Stadtbezirke mit Einwohnerzahl und kartographischer Übersicht!

In den Stadtbezirkslisten sind sowohl Einzelbauwerke als auch denkmalgeschützte Ensembles aufgeführt. Einen Überblick über alle Ensembles gibt die Liste der denkmalgeschützten Ensembles in Regensburg.

Veröffentlichungen
Die Liste der Baudenkmäler in Regensburg ist Bestandteil der Bayerischen Denkmalliste, die vom Bayerischen Landesamt für Denkmalpflege gepflegt wird.

Im ersten Teil dieser Reihe, welche die Baudenkmäler nach Regierungsbezirken geordnet darstellt, sind die Regensburger Teil des Bandes III über die Oberpfalz. Im dritten Teil, der für die Baudenkmäler jedes Landkreises und jeder Kreisfreien Stadt jeweils einen eigenen Band vorsieht, ist Regensburg noch nicht erschienen.

Anmerkungen

Literatur

Weblinks

 Straßenverzeichnis der Regensburger Wachten (PDF; 2,5 MB) bei der Stadt Regensburg
 Straßenverzeichnis der Regensburger Stadtbezirke (PDF; 2,6 MB) bei der Stadt Regensburg

Regensburg
Baudenkmaler Regensburg

Liste der Baudenkmäler in Regensburg


البيئة والتنمية  مجلة إقليمية تعنى بتغطية القضايا والمواضيع البيئية والتنموية. تصدر «البيئة والتنمية» باللغة العربية كل شهرين مرة واحدة، وتوزّع حوالى 38000 نسخة في 22 بلداً. نجحت «البيئة والتنمية» منذ انطلاقها عام 1996 بوضع البيئة على أجندة اهتمامات الحكومات في الشرق الأوسط، كما تمكنت من خلال أسلوبها الشيّق والسهل أن تجعل المواضيع البيئية المتخصصة مثار اهتمام القارئ العادي والمتخصص في آن.

نظّمت المجلة برامج توعية بيئية في المدارس منذ عام 1997 تحت عنوان «البيئة الأفضل تبدأ بك أنت» شارك فيها آلاف الطلاب. ونظّمت مسابقات بيئية، كما درّبت الأساتذة في التربية البيئية وساهمت في إنشاء أكثر من 500 نادٍ بيئي مدرسي.

في الذكرى العاشرة لتأسيسها عام 2006 عملت المجلة على تأسيس المنتدى العربي للبيئة والتنمية (أفد) كمنظمة إقليمية بيئية مستقلة ومنذ 1/1/2013 قدم صاحب الامتياز نجيب صعب المجلة بإيجار مجاني إلى المنتدى العربي للبيئة والتنمية.

المصادر

انظر أيضاً
 المنتدى العربي للبيئة والتنمية

وصلات خارجية
 الموقع الرسمي للمجلة

بيئة طبيعية
مجلات شهرية
مجلات عربية

مجلة البيئة والتنمية


In employment law, constructive dismissal, also called constructive discharge or constructive termination, occurs when an employee resigns as a result of the employer creating a hostile work environment. Since the resignation was not truly voluntary, it is, in effect, a termination. For example, when an employer places extraordinary and unreasonable work demands on an employee to obtain their resignation, this can constitute a constructive dismissal.

The exact legal consequences differ between different countries, but generally a constructive dismissal leads to the employee's obligations ending and the employee acquiring the right to make claims against the employer.

The employee may resign over a single serious incident or over a pattern of incidents. Generally, a party seeking relief must have resigned soon after an unreasonable situation was imposed.

United States law
In the United States, constructive discharge is a general term describing the involuntary resignation of an employee. There is no single federal or state law against constructive dismissal in general. From a legal standpoint, it occurs when an employee is forced to resign because of intolerable working conditions which violate employment legislation, such as:
 Family and Medical Leave Act of 1993 (FMLA)
 Equal Pay Act of 1963 (EPA)
 Change in schedules in order to force employee to quit (title 12)
 Americans with Disabilities Act of 1990 (ADA)
 Genetic Information Nondiscrimination Act of 2008 (GINA)
 Age Discrimination in Employment Act of 1967 (ADEA)
 Title VII of the Civil Rights Act of 1964 (Title VII)
 Any state employment law
 An employer showing favoritism to another employee without reason or explanation

The burden of proof in constructive dismissal cases lies with the employee.

The Equal Employment Opportunity Commission has provided a 3-part test to determine whether or not a constructive discharge has occurred: (1) a reasonable person in the complainant's position would have found the working conditions intolerable; (2) conduct that constituted discrimination against the complainant created the intolerable working conditions; and (3) the complainant's involuntary resignation resulted from the intolerable working conditions.

In California, the California Supreme Court defines constructive discharge as follows:

"In order to establish a constructive discharge, an employee must plead and prove, by the usual preponderance of the evidence standard, that the employer either intentionally created or knowingly permitted working conditions that were so intolerable or aggravated at the time of the employee's resignation that a reasonable employer would realize that a reasonable person in the employee's position would be compelled to resign."

Canadian law

Canadian courts recognize there are circumstances in which the employer, although not acting explicitly to terminate an individual's employment, alters the employment relationship's terms and conditions to such a degree that an employee is entitled to regard the employer's conduct as a termination, and claim wrongful dismissal, just as if they had been let go without any notice or termination pay in lieu of notice.

Constructive dismissal arises from the failure of the employer to live up to the essential obligations of the employment relationship, regardless of whether the employee signed a written employment contract. Employment law implies into employment relationships a common-law set of terms and conditions applicable to all employees. For example, once agreed upon, wages are implicitly locked in by the common-law of contract as an essential term of the employment relationship. In this regard, it is a constructive dismissal if an employer fails to pay an employee.

An employer's breach of the employment contract releases the employee from their obligation to perform under the contract, and thus allows them to treat themselves as dismissed without notice. Hence, a constructive dismissal always becomes a wrongful dismissal.

Changes to the employment relationship

Typically, the first way to claim constructive dismissal involves an employer making substantial changes to the employment contract, such as:

 a demotion;
 altering the employee's reporting structure, job description or working conditions;
 lowering an employee's compensation;
 changing hours of work;
 imposing a suspension or leave of absence; and
 relocating the employee's workplace.

In addition, failure on the part of an employer to provide employment standards (e.g. overtime pay, vacation pay, etc.), can result in a constructive dismissal.

Nevertheless, for an employee to have a successful case for constructive dismissal, the employer's breach must be fundamental. What is "fundamental" depends on the circumstances, and not all changes to the employment relationship give rise to a constructive dismissal. For example, administrative, i.e. non-disciplinary, suspensions might not amount to a constructive dismissal if imposed in good faith and justified by legitimate business reasons (i.e. lack of work). As well, a small reduction in salary, in tough times, and administered rationally, might not be a constructive dismissal.

Toxic work environments

An employee may also be able to claim a constructive dismissal based on an employer's conduct, rather than a change to a specific or implied term of the employment contract. Here, the second way to claim constructive dismissal examines whether the employer's (or employee of the employer) course of conduct, or even a single incident, demonstrates an intention to no longer be bound by the written or implied employment contract. An example of this kind of constructive dismissal is a "toxic work environment". In this regard, if a work environment is so poisoned that a reasonable person wouldn't be expected to return, then constructive dismissal is likely.

A toxic work environment is classically defined as  unjustified criticism as well as vague and unfounded accusations of poor performance, especially where authority and respect with co-workers had been seriously undermined and compromised. Another example of toxic work environment is where the employer fails to prevent workplace harassment.

UK law

In United Kingdom law, constructive dismissal is defined by the Employment Rights Act 1996 section 95(1)c:

 The circumstances in which an employee is entitled are defined in common law. The notion of constructive dismissal most often arises from a fundamental breach of the term of trust and confidence implied in all contracts of employment. In order to avoid such a breach "[a]n employer must not, without reasonable or proper cause, conduct himself in a manner calculated or likely to destroy or seriously damage the relationship of trust and confidence between the employer and the employee." Whilst a breach can be of the implied term of trust and confidence, a fundamental breach of any of the express or implied terms of a contract of employment is sufficient. The examples given on this page for actions by an employer likely to constitute grounds for constructive dismissal under Canadian law also almost certainly hold true under English law.

The Department of Trade and Industry states:

Following constructive dismissal, a claim for unfair dismissal and/or wrongful dismissal may arise.

Types of constructive dismissal

Although they tend to blend into one in a tribunal, strictly there are two types of constructive dismissal: statutory and common law.

At common law the requirement is acceptance of a repudiatory breach, which means the employer has indicated it no longer considers itself bound by an essential term of the contract, e.g. the requirement to pay wages or the requirement not to destroy the mutual bond of trust and confidence. It does not matter if the employer did not mean to repudiate the contract.

Under statute the requirement is employer's "conduct" allowing the employee to "terminate with or without notice"; as this can only happen with a repudiatory breach it amounts to the same thing.

Relation to unfair dismissal
A common mistake is to assume that constructive dismissal is exactly the same as unfair treatment of an employee – it can sometimes be that treatment that can be considered generally evenhanded nevertheless makes life so difficult that the employee is in essence forced to resign (e.g., a fair constructive dismissal might be a unilateral change of contract justified by a bigger benefit to the business than the inconvenience to the employee), but the Employment Appeal Tribunal doubts that it will be very often that the employer can breach ERA96 s98(4) whilst being fair.

A constructive dismissal occurs when the employer's repudiatory breach causes the employee to accept that the contract has been terminated, by resigning. The fairness of it would have to be looked at separately under a statutory claim for unfair dismissal.

The problems for the employer are that constructive dismissal is a contractual claim, which can be made in a tribunal for up to £25,000 or in court without limit, and, by dismissing constructively, it by definition misses out on the correct procedure meaning that even if the reason was fair, the decision was probably not, and so an unfair dismissal usually arises, creating a statutory claim alongside the contractual claim.

The court can look behind the lack of, or different, stated reason given by the employee at the time of resignation to establish that a cover story was in fact a resignation caused by fundamental breach.

Typical causes
The person causing the dismissal does not need the authority to dismiss, as long as they acted in the course of employment.

Grounds
Constructive dismissal is typically caused by:-

unilateral contract changes by the employer such as:
 deliberate cuts in pay or status (even temporary),
 persistent delayed wages,
 refusal of holiday,
 withdrawal of car,
 suspension without pay (or even on full pay),
 dramatic changes to duties, hours or location (beyond reasonable daily travelling distance), or
 breach of contract in the form of bullying, e.g.:
 ignoring complaints,
 persistent unwanted amorous advances,
 bullying and swearing,
 verbal abuse (typically referring to gender, size or incompetence),
 singling out for no pay rise,
 criticising in front of subordinates,
 lack of support (e.g. forcing to do two peoples' jobs),
 failure to notify a woman on maternity leave of a vacancy which she would have applied for if she had been made aware of it,
 refusal to confirm continuity on TUPE transfer,
 revealing secret complaints in a reference (even ones required by a regulator), or
breaches such as:
 behaviour which is arbitrary, capricious, inequitable, intolerable or outside good industrial practice,
 conduct that undermined trust and confidence (i.e. offering an incentive to resign to avoid performance managing capability),
 refusal to look for an alternative role due to workplace stress,
 disproportionate disciplinary penalty,
 employer tricks employee into resigning.

Flexibility and mobility clauses
A flexibility clause does not allow the employer to change a type of job as it is implied that the flexibility is to operate within the original job.

A mobility clause is subject to the implied term of mutual trust which prevents the employer from sending an employee to the other side of the country without adequate notice or from doing anything which makes it impossible for the employee to keep his side of the bargain.

Insufficient grounds
There is no right to automatic pay rises. Nor is a smoking ban a breach.

Compensation
The employee's conduct is irrelevant to liability, although it can affect quantum; in other words it cannot get the employer off the hook, but could reduce compensation if he helped bring about his own downfall.

Timing
The conduct by the employer could be:

 a one-off repudiatory or fundamental breach of contract,
 a series of acts or omissions which amount to a repudiatory or fundamental breach of contract, or
 a 'last straw' act or omission which, although in itself not a repudiatory or fundamental breach of contract can when taken in the context of earlier breaches amount to conduct which is a repudiatory or fundamental breach of contract.

Note: unreasonable conduct will not suffice to establish constructive dismissal claim since a repudiatory or fundamental breach of contract must be established.

Employee must resign quickly
The employee has to resign within a reasonable time of the trigger, which is the one-off outrage or the last straw. The employee could work under protest while he or she finds a new job.

Waiver

If the employer alleges that the employee waived a breach by not resigning, each breach needs to be looked at to see if it was waived separately, but even if a breach was waived, the last straw revives it for the purpose of determining whether overall there was a repudiation.

Affirmation

If the employer alleges that the employee has affirmed a breach by not resigning, the employee could point out that no consideration was paid for it and so no contract change has been accepted. Acceptance of a replacement job would prove affirmation.

An employee who stays on for a year after refusing to sign a new contract does not necessarily accept it.

Last straw

The last straw does not have to be similar to the earlier string of events or even unreasonable or blameworthy – it need only be related to the obligation of trust and confidence and enough that when added to the earlier events the totality is a repudiation.

Notice period

Although the employer's breach must be serious enough to entitle the employee to resign without notice, the employee is entitled to give notice if they prefer, so that they could enjoy the benefit of wages during the notice period.

To prevent the employer alleging that the resignation was caused by a job offer, the employee should resign first and then seek a new job during the notice period.

During the notice period, the employer could make the employee redundant or summarily dismiss them, if it has the grounds to do so fairly.  Otherwise, the reason for termination will be resignation and not dismissal, since the employee cannot serve a counternotice.

Notes

Termination of employment
Labour law
Ethically disputed working conditions
Corporate crime

Constructive dismissal


Melioidosis is an infectious disease caused by a gram-negative bacterium called Burkholderia pseudomallei.  Most people exposed to B. pseudomallei experience no symptoms; however, those who do experience symptoms have signs and symptoms that range from mild, such as fever and skin changes, to severe with pneumonia, abscesses, and septic shock that could cause death. Approximately 10% of people with melioidosis develop symptoms that last longer than two months, termed "chronic melioidosis".

Humans are infected with B. pseudomallei by contact with contaminated soil or water. The bacteria enter the body through wounds, inhalation, or ingestion. Person-to-person or animal-to-human transmission is extremely rare. The infection is constantly present in Southeast Asia particularly in northeast Thailand and northern Australia. In temperate countries such as Europe and the United States, melioidosis cases are usually imported from countries where melioidosis is endemic. The signs and symptoms of melioidosis resemble tuberculosis and misdiagnosis is common. Diagnosis is usually confirmed by the growth of B. pseudomallei from an infected person's blood or other bodily fluid such as pus, sputum, and urine. Those with melioidosis are treated first with an "intensive phase" course of intravenous antibiotics (most commonly ceftazidime) followed by a several-month treatment course of co-trimoxazole. In countries with the advanced healthcare system, approximately 10% of people with melioidosis die from the disease. In less developed countries, the death rate could reach 40%.

Efforts to prevent melioidosis include: wearing protective gear while handling contaminated water or soil, practising hand hygiene, drinking boiled water, and avoiding direct contact with soil, water, or heavy rain. There is little evidence in supporting the use of melioidosis prophylaxis in humans. The antibiotic co-trimoxazole is used as a preventative only for individuals at high risk for getting the disease after being exposed to the bacteria in laboratory settings. One study conducted in 2018 determined that the drug could be useful in preventing melioidosis in high-risk renal failure patients undergoing haemodialysis. There is no approved vaccine for melioidosis.

Approximately 165,000 people are infected by melioidosis per year, resulting in about 89,000 deaths, based on a mathematical model published in 2016. Diabetes is a major risk factor for melioidosis; over half of melioidosis cases are in people with diabetes. Increased rainfall and severe weather events such as thunderstorms are associated with an increased number of melioidosis cases in endemic areas.

Signs and symptoms

Acute

Most people exposed to B. pseudomallei experience no symptoms. The mean incubation period of acute melioidosis is 9 days (range 1–21 days). Nevertheless, symptoms of melioidosis can appear in 24 hours for those who experienced near drowning in water. Those affected present with symptoms of sepsis (predominantly fever) with or without pneumonia, or localised abscess or other focus of infection. The presence of non-specific signs and symptoms has caused melioidosis to be nicknamed "the great mimicker".

Diabetes mellitus is one of the most important risk factors in developing melioidosis. The disease should be considered in anyone who has spent time in endemic areas who develops a fever, pneumonia, or abscesses in their liver, spleen, prostate, or parotid gland. The clinical manifestation of the disease can range from simple skin changes such as abscesses or ulcerations to severe organ problems. The commonest organs affected are liver, spleen, lungs, prostate, and kidneys. Among the most common features are bacteremia (in 40 to 60% of cases), pneumonia (50%), and septic shock (20%).
People with only pneumonia may have a prominent cough with sputum and shortness of breath. However, those with septic shock together with pneumonia may have minimal coughing. Results of a chest X-ray can range from diffuse nodular infiltrates in those with septic shock to progressive consolidation located most commonly in the upper lobes for those with pneumonia only. Pleural effusion and empyema are more common for melioidosis affecting lower lobes of the lungs. In 10% of cases, people develop secondary pneumonia caused by other bacteria after the primary infection. In northern Australia, 60% of the infected children presented with only skin lesions, while 20% presented with pneumonia.

Depending on the course of infection, other severe manifestations develop. Approximately 1 to 5% of those infected develop inflammation of the brain and brain covering or brain abscess; 14 to 28% develop pyelonephritis, kidney abscess or prostatic abscesses; 0 to 30% develop neck or salivary gland abscesses; 10 to 33% develop liver, spleen, or paraintestinal abscesses; and 4 to 14% develop septic arthritis and osteomyelitis.  Rare manifestations include lymph node disease resembling tuberculosis, mediastinal masses, pericardial effusion, mycotic aneurysm, and inflammation of the pancreas. In Australia, up to 20% of infected males develop prostatic abscess which may manifests clinically as pain during urination, difficulty in passing urine, and urinary retention requiring catheterisation. Rectal examination may find enlarged prostate. In Thailand, 30% of the infected children develop parotid abscesses. Encephalomyelitis not only happens in those with risk factors, but can also occur in healthy people without risk factors. Those with melioidosis encephomyelitis tend to have normal computed tomography (CT) scans but increased T2 signal by magnetic resonance imaging (MRI), extending to the brain stem and spinal cord. Clinical signs include: unilateral upper motor neuron limb weakness, cerebellar signs, and cranial nerve palsies (VI, VII nerve palsies and bulbar palsy). Some cases presented with flaccid paralysis alone. In northern Australia, all melioidosis with encephalomyelitis cases had elevated white cells in the cerebrospinal fluid (CSF), mostly mononuclear cells with elevated CSF protein.

Chronic
Chronic melioidosis is usually defined by symptoms lasting greater than two months and occurs in about 10% of patients. Clinical presentations include fever, weight loss, productive cough with or without bloody sputum which may mimic tuberculosis. Additionally, long-standing abscesses at multiple body sites may also present. Tuberculosis should be considered for lymph nodes enlargement at the root of the lung. Additionally, pneumonia caused by melioidosis rarely causes scarring and calcification of the lungs, unlike tuberculosis.

Latent
The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the "Vietnam time-bomb". Initially, it was thought that the longest period between presumed exposure and clinical presentation is 62 years in a prisoner of war in Burma-Thailand-Malaysia. However, subsequent genotyping of the bacteria isolate from the Vietnam veteran showed that the isolate may not come from Southeast Asia, but from South America. This reinstates another report that put the longest latency period for melioidosis as 29 years. Patients with latent melioidosis may be symptom-free for decades. Less than 5% of all melioidosis cases have activation after a period of latency. Various comorbidities such as diabetes, renal failure, and alcoholism can predispose to reactivation of melioidosis.

Cause

Bacteria

Melioidosis is caused by gram-negative, motile, saprophytic bacteria named Burkholderia pseudomallei. The bacteria are usually opportunistic, facultative intracellular pathogens. It is also aerobic and oxidase test positive. A granule at the centre of the bacterium makes it resemble a "safety pin" when Gram stained. The bacteria emit a strong soil smell after 24 to 48 hours of growth in culture, however smelling for the identification of the bacteria is not recommended for routine laboratory practice. One of the factors causing B. pseudomallei resistance to various kinds of antibiotics is because of its production of a glycocalyx polysaccharide capsule.  It is generally resistant to gentamicin and colistin but sensitive to co-amoxiclav. B. pseudomallei is a biosafety level 3 pathogen which requires specialized laboratory handling. In humans and animals, another similar organism named Burkholderia mallei is the causative agent of the disease glanders. B. pseudomallei can be differentiated from another closely related, but less pathogenic species B. thailandensis by its ability to assimilate arabinose. B. pseudomallei is highly adaptable to various host environments ranging from inside mycorrhizal fungi spores to amoeba. Its adaptability may give it a survival advantage in the human body.

The genome of B. pseudomallei consists of two replicons: chromosome 1 encodes housekeeping functions of the bacteria such as cell wall synthesis, mobility, and metabolism; chromosome 2 encodes functions that allow the bacteria to adapt to various environments. Horizontal gene transfer has resulted in highly variable genomes in B. pseudomallei. Australia has been suggested as the origin for B. pseudomallei because of the high genetic variability of the bacteria found in this region. Bacteria that was introduced to Central and South America in the 17th to 19th centuries seem to have a common ancestor from Africa. B. mallei is a clone of B. pseudomallei that has lost substantial portions of its genome as it adapted to live exclusively in mammals. This makes the B. mallei genome much smaller than B. pseudomallei.

Transmission
B. pseudomallei is normally found in soil and surface water, and is most abundant at soil depths of 10 to 90 cm. It has been found in soils, ponds, streams, pools, stagnant water, and rice paddy fields. B. pseudomallei can survive in nutrient-poor conditions such as distilled water, desert soil, and nutrient-depleted soil for more than 16 years. It can also survive in antiseptic and detergent solutions, acidic environments (pH 4.5 for 70 days), and in environments at temperatures ranging from 24 °C (75.2 °F) to 32 °C (89.6 °F). However, the bacteria may be killed by the presence of ultraviolet light.

Bacteria can enter the body through wounds, inhalation, and ingestion of contaminated soil or water. Person-to-person transmission is extremely rare. Melioidosis is a recognised disease in animals including pigs, cats, dogs, goats, sheep, horses and others. Cattle, water buffalo, and crocodiles are considered to be relatively resistant to melioidosis despite their constant exposure to mud. Birds are also considered resistant to melioidosis although several cases had been reported in Australia and aquatic birds. Transmission from animals to humans is rare.

Inadequate chlorination of water supply has been associated with B. pseudomallei outbreak in Northern and Western Australia. The were also several cases of where bacteria have also been found in unchlorinated water supply in rural Thailand. Based on the whole genome sequencing of the bacteria, the variety of the bacteria B. pseudomallei in Papua New Guinea is narrow due to limited movements of the indigenous people. This findings supports the hypothesis that humans play an important role in bacterial dispersal.

Pathogenesis

B. pseudomallei has the ability to infect various types of cells and to evade human immune responses. Bacteria first enter at a break in the skin or mucous membrane and replicate in the epithelial cells. From there, they use flagellar motility to spread and infect various cell types. In the bloodstream, the bacteria can infect both phagocytes and non-phagocytes. B. pseudomallei use their flagella to move near host cells, then attach to the cells using various adhesion proteins, including the type IV pilus protein PilA as well as adhesion proteins BoaA and BoaB. Additionally, adhesion of the bacteria partially depends on the presence of the host protein Protease-activated receptor-1 which is present on the surface of endothelial cells, platelets, and monocytes. Once bound, the bacteria enter host cells through endocytosis, ending up inside an endocytic vesicle. As the vesicle acidifies, B. pseudomallei uses its Type 3 secretion system (T3SS) to inject effector proteins into the host cell, disrupting the vesicle and allowing the bacteria to escape into the host cytoplasm. Within the host cytoplasm, the bacteria evade being killed by the host autophagy using various T3SS effector proteins. The bacteria replicate in the host cytoplasm.

Inside the host cell, the bacteria move by inducing the polymerization of the host actin behind them, propelling the bacteria forward. This actin-mediated motility is accomplished with the autotransporter BimA which interacts with actin at the tail-end of the bacterium. The bacteria that has BimABm allele has higher possibility of causing neurological melioidosis, thus higher chance of death and residual disability to the host when compared to the bacteria that has BimABp variant. Propelled by actin, the bacteria push against the host membrane, creating protrusions that extend into neighbouring cells. These protrusions cause neighboring cells to fuse, leading to the formation of multinucleated giant cells (MNGCs). When MNGCs lyse, they form plaques (a central clear area with a ring of fused cells) that provide shelter for the bacteria for further replication or latent infection. This same process in infected neurons can allow bacteria to travel through nerve roots in the spinal cord and brain, leading to inflammation of the brain and spinal cord. In addition to spreading from cell to cell, the bacteria can also spread through the bloodstream, causing sepsis. The bacteria can survive in antigen-presenting cells and dendritic cells. Thus, these cells act as vehicles that transport the bacteria into the lymphatic system, causing widespread dissemination of the bacteria in the human body.

While B. pseudomallei can survive in phagocytic cells, these cells can kill B. pseudomallei by several mechanisms. Macrophages activated by interferon gamma (IFN) have improved the killing of B. pseudomallei via the production of inducible nitric oxide synthase. Acidification of the endosome and degradation of the bacteria is also possible, however, the bacterial capsule and LPS makes B. pseudomallei resistant to lysosomal degradation. Once B. pseudomallei escapes into the host cytosol it can be recognized by pattern recognition receptors such as NOD-like receptors, triggering the formation of the inflammasome and activation of caspase 1, which induces death of the host cell by pyroptosis and further activation of the immune system. Several systemic host defenses also contribute to the immune response. B. pseudomallei triggers both the complement system and coagulation cascade, however the thick bacterial capsule prevent the action of the complement membrane attack complex.

Additional elements of the immune system are activated by the host toll-like receptors such as TLR2, TLR4, and TLR5 that recognize the conserved pieces of the bacteria such as LPS and flagella. This activation results in the production of cytokines such as Interleukin 1 beta (IL-1β) and Interleukin 18 (IL-18). IL-18 increases IFN production through natural killer cells while IL-1beta reduces the IFN production. These immune molecules drive the recruitment of other immune cells such as neutrophils, dendritic cells, B cells, and T cells to the site of infection. T cells seem to be particularly important for controlling B. pseudomallei; T cell numbers are increased in survivors, and low T cell numbers are associated with a high risk of death from melioidosis. Despite this, HIV infection is not a risk factor for melioidosis. Although macrophages show deregulated cytokine responses in individuals with HIV infection, bacterial internalization and intracellular killing are still effective. People infected with B. pseudomallei may develop antibodies against the bacteria, and people that live in endemic areas tend to have antibodies in their blood that recognize B. pseudomallei. However, the effectiveness of these antibodies at preventing melioidosis is unclear.

B. pseudomallei can remain latent in the human body for up to 29 years until it is reactivated during human immunosuppression or stress response. However, the site of bacteria during latent infection and the mechanism by which they avoid immune recognition for years are both unclear. Amongst mechanisms suggested are: residing in the nucleus of the cell to prevent being digested, entering a stage of slower growth, antibiotic resistance, and genetic adaption to the host environment. Granulomas (containing neutrophils, macrophages, lymphocytes, and multinucleated giant cells) formed at the infection site in melioidosis have been associated with latent infection in humans.

Diagnosis

Culture
Bacterial culture has 60% sensitivity in diagnosing melioidosis. B. pseudomallei is never part of human flora. Therefore, any growth of the bacteria is diagnostic of melioidosis. Other samples such as throat, rectal swabs, pus from abscesses, and sputum can also be used for culture. However, culture from CSF is difficult because in one case series, only 29% of the neuromelioidosis cases are culture positive. When bacteria do not grow from people strongly suspected of having melioidosis, repeated cultures should be taken as subsequent cultures can become positive. B. pseudomallei can be grown on any blood agar, MacConkey agar, and agar containing antibiotics such as Ashdown's medium (containing gentamicin), and Ashdown's broth (containing colistin) for better isolation of B. pseudomallei from other types of bacteria. Agar plates for melioidosis should be incubated at 37 °C (98.6 °F) in air  and inspected daily for four days. On the agar plates, B. pseudomallei forms creamy, non-haemolytic, colonies after 2 days of incubation. After 4 days of incubation, colonies appear dry and wrinkled. Colonies of B. pseudomallei that are grown on Francis medium (a modification of Ashdown medium with gentamicin concentration increased to 8 mg/L and neutral red indicator replaced with 0.2% bromocresol purple) are yellow. For laboratories located outside endemic areas, Burkholderia cepacia selective agar can be used if Ashdown's medium is not available. It is important not misinterpret the bacterial growth as Pseudomonas or Bacillus spp. Other biochemical screening tools can also be used for detecting B. pseudomallei, including the API 20NE or 20E biochemical kit combined with Gram stain, oxidase test, typical growth characteristics, and resistance to certain antibiotics of the bacteria. API 20NE biochemical kit is 99% sensitive in identifying B. pseudomallei.

Molecular methods such as 16S rDNA sequencing, multiplex polymerase chain reaction (PCR), and real-time PCR can also be used to identify B. pseudomallei in culture. Other bacterial genes such as fliC genes encoding flagellin, rpsU gene encoding for ribosomal protein, and TTS genes encoding Type III secretion systems has also been employed for detection. Another method of gene detection namely multiple cross displacement amplification for the bacterial TTS1 gene detection produces results within an hour.

Hematological and biochemical tests
General blood tests in people with melioidosis show low white blood cell counts (indicates infection), raised liver enzymes, increased bilirubin levels (indicates liver dysfunction), and raised urea and creatinine levels (indicates kidney dysfunction). Low blood glucose and acidosis predicts a poorer prognosis in those with melioidosis. However, other tests such as C-reactive protein and procalcitonin levels are not reliable in predicting the severity of melioidosis infection.

Serological tests
Serological tests such as indirect haemagglutination assay (IHA) have been used to detect the presence of antibodies against B. pseudomallei. However, different groups of people have widely different levels of antibodies, so interpretation of these tests depends on location. In Australia, less than 5% of people have B. pseudomallei antibodies, so the presence of even relatively low amounts of antibody is unusual and could suggest melioidosis. In Thailand, many people have antibodies against B. pseudomallei so the diagnosis of melioidosis should not be reliant entirely on the serological tests done in endemic areas. Indirect immunofluorescent test (IFAT) uses either B. pseudomallei or B. thailandensis antigens to look for the total number of antibodies in human serum. Using IFAT is labour intensive and is not used in large scale investigations.

Antigen detect tests allow rapid detection of melioidosis. Examples of antigen detection tests are: latex agglutination test and ELISA. Latex agglutination uses antibodies coated on latex beads to detect B. pseudomallei antigens in solid or liquid media, although not all the assays can detect different species of Burkholderia. Latex agglutination is useful in screening for suspected B. pseudomallei colonies. IgG and IgM ELISAs has been used to detect lipopolysaccharide (LPS) antigens of B. pseudomallei, but plagued with low sensitivity. Commercial ELISA kits for melioidosis no longer available in the market due to low sensitivity to human antibodies detection. Nevertheless, antigen detection tests may be useful in severely ill patients because the bacterial load is high enough for detection. Other methods of antigen detection such as direct immunofluorescence, antibody-sandwich ELISAs, and lateral flow immunoassays using monoclonal antibody.

Microscopy
By microscopy, B. pseudomallei is seen as gram-negative and rod-shaped, with a bipolar staining similar in appearance to a safety pin. Bacteria can sometimes be seen directly in clinical samples from infected people; however, identification by light microscopy is neither specific nor sensitive. Immunofluorescence microscopy is highly specific for detecting bacteria directly from clinical specimens, but has less than 50% sensitivity.

Imaging
Various imaging modalities can also help with the diagnosis of melioidosis. In acute melioidosis with the spreading of the bacteria through the bloodstream, the chest X-ray shows multifocal nodular lesions. It may also show merging nodules or cavitations. For those with acute melioidosis without the spread to the bloodstream, chest x-ray most commonly shows upper lobe consolidation or cavitations. In chronic melioidosis, the slowly progressing of upper lobe consolidation of the lungs resembles tuberculosis. For abscesses located in other parts of the body apart from the lungs, especially in the liver and spleen, CT scan has higher sensitivity when compared with an ultrasound scan. In liver and splenic abscesses, an ultrasound scan shows "target-like" lesions while CT scan shows "honeycomb sign" (abscess with loculations separated by thin septa) in liver abscesses. For melioidosis involving the brain, MRI have higher sensitivity than a CT scan in diagnosing the lesion. MRI shows ring-enhancing lesions for brain melioidosis.

Prevention
Melioidosis is a notifiable disease in Australia which enables the country to monitor disease burden and contain outbreaks. On the other hand, melioidosis is only a notifiable condition in Thailand since June 2016.  However, until recently, the official notification system in Thailand has significantly underestimated the incidence of culture-positive melioidosis and its mortality. Nevertheless, Australia also embarked on awareness campaigns to increase the community's understanding of the disease. In the United Kingdom, where reporting by laboratories is mandatory, 41.3% of cases imported since 2010 were not notified. In the United States, lab workers can handle clinical specimens of B. pseudomallei under BSL-2 conditions, while mass production of such organisms requires BSL-3 precautions. On the other hand, in other endemic areas where the B. pseudomallei samples were handled less stringently, there has been no confirmed laboratory-acquired infection reported. This phenomenon may show that the risk of infection with B. pseudomallei is less than a typical biohazard type 3 agent. There are also several cases of hospital-acquired infection of melioidosis. Therefore, healthcare providers are recommended to practice hand hygiene and universal precautions.

Large-scale water chlorination has been successful at reducing B. pseudomallei in the water in Australia. In middle to low-income countries, water should be boiled before consumption. In high income countries, water could be treated with ultraviolet light for those at risk of contracting melioidosis. Those who are at high risk of contact with the bacteria should wear protective gear (such as boots and gloves) during work. Those staying in endemic areas should avoid direct contact with soil, and outdoor exposure to heavy rain or dust clouds. Bottled water or boiled water are preferred as drinking water. A study conducted from 2014 to 2018, however showed no significant differences on whether behavioural changes can reduce the risk of contracting melioidosis. Modification of behavioural changes or more frequent interventions may be needed to ensure a definite reduction in risk of getting melioidosis.

Antibiotic prophylaxis
Administering cotrimoxazole three times a week throughout a wet season for dialysis patients has no obvious benefit of preventing melioidosis. Besides, high cost and side effects of this drug limits its use to only those with high risk of getting melioidosis. After exposure to B. pseudomallei (particularly following a laboratory accident, penetrating injuries, exposure of mouth and eyes to contaminated materials or aerosols), treatment with antibiotics is only given when in highly selected individuals after weighing the risk of adverse effects of the drugs against the benefits from contracting melioidosis. Cotrimoxazole can be used in this context. Alternatively, co-amoxiclav and doxycycline can be used for those who are intolerant to co-trimoxazole. Low-risk individuals would receive frequent monitoring instead.

Vaccination

Several vaccine candidates have been tested in animal models. Nevertheless, no vaccine candidates have been tried in humans. Major hurdles of the vaccines are limited efficacy in animal models, establishing the best method of vaccine administration in humans and logistical and financial issues in establishing human trials in endemic areas.

Treatment
The treatment of melioidosis is divided into two stages: an intravenous intensive phase and an eradication phase to prevent recurrence. The choice of antibiotics depends upon the susceptibility of the bacteria to various antibiotics. B. pesudomallei are generally susceptible to ceftazidime, meropenem, imipenem, and co-amoxiclav. These drugs generally kill bacteria. B. pseudomallei is also susceptible to doyxcycline, chloramphenicol, and co-trimoxazole. These drugs generally inhibit the growth of the bacteria. However, the bacteria are resistant to penicillin, ampicillin, 1st and 2nd generation cephalosporin, gentamicin, streptomycin, tobramycin, macrolides, and polymyxins. On the other hand, 86% of the B. pseudomallei isolates from the region of Sarawak, Malaysia are susceptible to gentamicin and this has not been found elsewhere in other parts of the world.

Prior to 1989, the standard treatment for acute melioidosis was a three-drug combination of chloramphenicol, co-trimoxazole and doxycycline; this regimen is associated with a mortality rate of 80% and is no longer used unless no other alternatives are available.  All three drugs are bacteriostatic (they stop the bacterium from growing, but do not kill it) and the action of co-trimoxazole antagonizes both chloramphenicol and doxycycline.

Intensive phase
Intravenous ceftazidime is the current drug of choice for treatment of acute melioidosis and should be administered for at least 10 to 14 days. Meropenem, imipenem and the cefoperazone-sulbactam combination (Sulperazone) are also effective. Intravenous amoxicillin-clavulanate (co-amoxiclav) may be used if none of the above four drugs is available; co-amoxiclav prevents death from melioidosis as well as ceftazidime. Co-amoxiclav is also used if patient has allergy towards sulfonamide, unable to tolerate co-trimaxazole, in pregnant patients or in children. High dose of co-amoxiclav (20 mg/kg for amoxicillin and 5 mg/kg for clavulanate) is recommended to prevent treatment failures. Intravenous antibiotics are given for a minimum of 10 to 14 days. The median fever clearance time in melioidosis is 9 days. The treatment duration is in accordance with Darwin melioidosis treatment guidelines where there is low rate of recrudescence and relapse.

Meropenem is the preferred antibiotic therapy for neurological melioidosis and those with septic shock admitted into intensive care units. Co-trimoxazole is recommended in addition to ceftazidime for neurological melioidosis, osteomyelitis, septic arthritis, skin and gastrointestinal infection, and deeply seated abscess. For deep-seated infections such as abscesses of internal organs, osteomyelitis, septic arthritis, and neurological melioidosis, the duration of antibiotics given should be longer (up to 4 to 8 weeks). The time taken for the fever to be resolved can be more than 10 days in those with deep-seated infection. According to the 2020 Revised Royal Darwin Hospital Guideline, the dosage for intravenous ceftazidime is 2g 6-hourly in adults (50 mg/kg up to 2g in children less than 15 years old). The dosage for meropenem is 1g 8-hourly in adults (25 mg/kg up to 1g in children). Acquired resistance to ceftazidime, carbapenems, and co-amoxiclav is rare in the intensive phase but resistance to cotrimoxazole during eradication therapy is technically difficult to assess. There are no differences between using cefoperazone/sulbactam or ceftazidime to treat melioidosis as both shows similar death rates and disease progression following treatment. However, data are lacking to recommend cefoperazone/sulbactam usage. For those with kidney impairment, the dosage of ceftazidime, meropenem, and co-trimoxazole should be lowered. Once the clinical condition improved, meropenem can be switched back to ceftazidime.

Eradication phase
Following the treatment of the acute disease, eradication treatment with co-trimoxazole is the drug of choice and should be used for 3 months (12 weeks) as all-cause mortality was lower in 12 weeks group when compared to those receiving treatment for 20 weeks. For those with neurological melioidosis and osteomyelitis, drugs should be given for more than 6 months. Co-amoxiclav and doxycycline are drugs of second choice. Co-trimoxazole should not be used in those with glucose-6-phosphate dehydrogenase deficiency as it can cause haemolytic anemia. However, in Thailand, usage of co-trimoxazole does not accompany G6PD screening. Other side effects such as rash, hyperkalemia, renal dysfunction, and gastrointestinal symptoms should prompt the reduction of co-trimoxazole doses. Chloramphenicol is no longer routinely recommended for this purpose. Co-amoxiclav is an alternative for patients unable to take co-trimoxazole and doxycycline (e.g. pregnant women and children under the age of 12), but is not as effective and has a higher relapse rate. Single-agent treatment with fluoroquinolone (e.g., ciprofloxacin) or doxycycline for the oral eradication phase is ineffective.

In Australia, co-trimoxazole is used with children and pregnant mothers after the first 12 weeks of pregnancy. Meanwhile, in Thailand, co-amoxiclav is the drug of choice for children and pregnant women. B. pseudomallei rarely acquires resistance when co-amoxiclav is used. The dosing regimen for co-trimoxazole (trimethoprim/sulfamethoxazole) in eradication phase is 6/30 mg/kg, up to maximum 240/1200 mg in children, 240/1200 mg in adults weighing 40 to 60 kg, and 320/1600 mg in adults weighing more than 60 kg, taken orally every 12 hours. In both Thailand and Australia, co-trimoxazole is taken together with folic acid (0.1 mg/kg up to 5 mg in children). There are also cases where melioidosis is successfully treated with co-trimoxazole for 3 months without going through intensive therapy provided that there is only skin manifestations without the involvement of internal organs or sepsis. Resistance to cotrimoxazole is rare in Asia. Besides that, it is difficult to determine the resistance reliably because resistance to cotrimoxazole is defined when minimum inhibitory concentration (MIC) of more than 4 mg/L is required to completely inhibit the growth of 80% of the bacteria (80% inhibition point). Interpretation of 80% inhibition point is subjective and prone to human error. In 2021, European Committee on Antimicrobial Susceptibility Testing (EUCAST) released a new guideline on interpreting the susceptibility of B pseudomallei towards various antibiotics on disc susceptibility testing. The new guideline includes "S" for susceptible organism, "I" for susceptible organism only after increased exposure (when dosage or concentration of the drug increases) and "R" for resistant organism.

Surgery
Surgical drainage is indicated for single, large abscesses in the liver, muscle, and prostate. However, for multiple abscesses in the liver, spleen, and kidney, surgical drainage may not be possible or necessary. For septic arthritis, arthrotomy washout and drainage are required. Surgical debridement may be necessary. For those with mycotic aneurysm, urgent surgery is required for prosthetic vascular grafts. Lifelong therapy with co-trimoxazole may be needed for those with prosthetic vascular grafts according to a review of case reports in 2005. Other abscesses rarely need to be drained because most resolve with antibiotic treatment. Prostate abscess may require routine imaging. Antibiotics treatment for prostatic abscess may be enough except for abscesses more than 10 to 15 mm where surgical drainage is required.

Others
Several immunomodulating therapies are suggested to boost the human body immune function against the bacteria because the pathogenesis of melioidosis is thought to be contributed by defects in neutrophils. The Royal Darwin Hospital 2014 guidelines recommended granulocyte colony-stimulating factor (G-CSF) as immunomodulating therapy for those with septic shock at 300 ug daily as soon as the bacteriological laboratory flag the culture as possibly Burkholderia pseudomallei. The main contraindication of starting (G-CSF) is a heart event. The G-CSF is continued for ten days depends on clinical response or a contraindication develops such as white cell count greater than >50,000 X106/litre.

Anti-PDI (programmed cell death) agents could be useful in melioidosis treatment especially for those with septic shock. This is because Burkholderia pseudomallei bacteria increases the expression of PDI-1 that regulates and inhibits the formation of T-cells that are essential for fighting against melioidosis.

Prognosis
In well-resourced settings, where the disease can be detected and treated early, the risk of death is 10%. In resource-poor settings, the risk of death from the disease is more than 40%.

Recurrent melioidosis can occur either due to re-infection or relapse after the completion of eradication therapy. Re-infection is due to a new strain of B. pseudomallei bacteria. Meanwhile, relapse is due to failure to clear infections after the eradication therapy. Recurrent melioidosis is rare since 2014 due to improved antibiotic therapy and prolongation of the intensive phase of therapy as evident in Darwin Prospective Melioidosis Study. On the other hand, recrudescence are those who present with symptoms during the eradication therapy. Recrudescence rates may be improved by ensuring adherence to a full course of eradication therapy e.g. by reducing self-discharge against medical advice.

Underlying medical conditions such as diabetes mellitus, chronic kidney disease, and cancer can worsen the long-term survival and disability of those who recover from infection. One of the complications of melioidosis is encephalomyelitis. It can cause quadriparesis (muscle weakness in all the limbs), partial flaccid paraparesis (muscle weakness of both legs), or foot drop. For those with previous melioidosis-associated bone and joint infections, complications such as sinus tract infection, bone and joint deformities with limited range of motion can occur.

Epidemiology

Melioidosis is an understudied disease that remains endemic in developing countries. In 2015, the International Melioidosis Society was formed to raise awareness of the disease. In 2016, a statistical model was developed which predicted that the number is 165,000 cases per year with 138,000 of those occurring in East and South Asia and the Pacific. In approximately half of those cases (54% or 89,000), people will die.  Under-reporting is a common problem as only 1,300 cases were reported worldwide since 2010, which is less than 1% of the projected incidence based on the modelling. Lack of laboratory diagnostic capabilities and lack of disease awareness amongst health care providers also causes under diagnosis. Even if bacterial cultures show positive result for B. pesudomallei, they can be discarded as contaminants especially in laboratories in non-endemic areas. In 2015, it was estimated that the yearly disability-adjusted life year (DALY) was 84.3 per 100,000 people. As of 2022, melioidosis is not included in the WHO list of neglected tropical diseases.

Geography
Melioidosis is endemic in parts  of southeast Asia (including Thailand, Laos, Singapore, Brunei, Malaysia, Myanmar and Vietnam), southern China, Taiwan northern Australia. India, and South America. Since 1991, a total of 583 cases were reported in India. Most Indian cases are located in Karnataka and Tamil Nadu. Fifty-one cases of melioidosis were reported in Bangladesh from 1961–2017. Nonetheless, lack of awareness and resources gives rise to under diagnosis of the disease in the country. The true burden of melioidosis in Africa and Middle East remain unknown due to low amount of data. Several melioidosis cases were reported over the years. Although 24 African countries and three Middle Eastern countries predicted to be endemic with melioidosis, however not a single case was reported from these specific countries. In the United States, two historical cases (1950 and 1971) and four recent cases (2010, 2011, 2013, 2020) have been reported amongst people that did not travel overseas. Despite extensive investigations, the source of melioidosis was never confirmed. One possible explanation is that importation of medicinal plant products or exotic reptiles could have resulted in the introduction of melioidosis in the United States. In 2021, there was a melioidosis outbreak in several states in the United States due to usage of contaminated aromatherapy spray imported from India. There are also cases of infection through imported tropical fishes in home aquariums.
In Europe, more than half of the melioidosis cases are imported from Thailand.

Age, risk factors
Melioidosis is found in all age groups. For Australia and Thailand, the median age of infection is at 50 years; 5 to 10% of the patients are under 15 years. The single most important risk factor for developing melioidosis is diabetes mellitus, followed by hazardous alcohol use, chronic kidney disease, and chronic lung disease. More than 50% of people with melioidosis have diabetes; diabetics have a 12-fold increased risk of contracting melioidosis. Diabetes decreases the ability of macrophages to fight the bacteria and reduced the T helper cell production. Excessive release of Tumor necrosis factor alpha and Interleukin 12 by mononuclear cells increases the risk of septic shock. Other risk factors include thalassaemia, occupational exposure (e.g. rice paddy farmers), recreational exposure to soil, water, being male, age greater than 45 years, and prolonged steroid use/immunosuppression. However, 8% of children and 20% of adults with melioidosis have no risk factors.  HIV infection does not appear to predispose to melioidosis, although several other co-infections have been reported. Infant cases have been reported possibly due to mother-to-child transmission, community-acquired infection, or healthcare-associated infection. Those who are well may also be infected with B. pseudomallei. For example, 25% of children started producing antibodies against B. pseudomallei between 6 months to 4 years of staying in endemic areas although they did not experience any melioidosis symptoms; suggesting they were exposed to it over this time. This means that many people without symptoms will test positive in serology tests in endemic areas. In Thailand, the seropositivity rate exceeds 50%, while in Australia the seropositivity rate is only 5%. The disease is clearly associated with increased rainfall, with the number of cases rising following increased precipitation. Severe rainfall increases the concentration of the bacteria in the topsoil, thus increasing thus of transmitting the bacteria through the air. A recent CDC Advisory indicated that the recent detection of the organism in the environment in Mississippi following the occurrence of two indigenous cases of melioidosis, confirms that parts of the southern USA should now be regarded as melioidosis-endemic.

History
Pathologist Alfred Whitmore and his assistant Krishnaswami first reported melioidosis among beggars and morphine addicts at autopsy in Rangoon, present-day Myanmar, in a report published in 1912. Whitmore was able to grow the organism in culture and its showed similarity with B. mallei, another bacteria that was known causing glanders in animals. Therefore, he named the new organism Bacillus pseudomallei. He did no further work on the organism. Arthur Conan Doyle may have read Whitmore's report before writing a short story that involved the fictitious tropical disease "Tapanuli fever" in a Sherlock Holmes story titled "The Adventure of the Dying Detective" published in 1913. In the same year, melioidosis outbreak occurred inside the Institute for Medical Research (IMR), Kuala Lumpur, Malaya after its laboratory animals such as guinea pigs and rabbits were infected. William Fletcher and Ambrose Thomas Stanton, doctors who worked at the IMR, were the next ones to study the organism. They were unable identify the organism that caused the outbreak. It was only in 1917, when Fletcher isolated an organism similar to Whitmore's bacillus from a Tamil rubber estate worker, the presence of the new species of bacteria was confirmed. The term "melioidosis" was first coined in 1921. The name melioidosis is derived from the Greek melis (μηλις) meaning "a distemper of asses" with the suffixes -oid meaning  "similar to" and -osis meaning "a condition", that is, a condition similar to glanders. B pseudomallei is similar in clinical presentation and genome make-up with B. mallei but is distinguished from it due to epidemiological and zoonotic characteristics.

The first human case of melioidosis in South Asia was reported in Sri Lanka in 1927. In 1932, Thomas and Fletcher collected 83 cases of melioidosis from literature. In this case series, there were only two survivals. Since then, more case series of melioidosis were reported. Thomas and Fletcher also pioneered the use of serological methods in diagnosing the disease. Thomas and Fletcher incorrectly believed that melioidosis infection came from human contact with rodents. However, observations on the disease noted that humans usually got it after exposure to mud or contaminated water. Besides, the organism was never grown from rats. This led to a search of the bacteria in the environment. In 1936, the first animal (pig) case of melioidosis in Africa was reported in Madagascar. In 1937, water was first identified as the habitat of B. pseudomallei. The first case of Australian melioidosis was described in an outbreak in sheep in 1949 at North Queensland. This was followed by the first case of human melioidosis at Townsville in 1950. Initially, the discovery of melioidosis in Australia had led to a debate on when and how the disease spread from Southeast Asia to a new distant environment. However, this hypothesis was later disproved in 2017 when whole genome sequencing of B. pseudomallei over 30 countries collected over 79 years suggested Australia as the early reservoir for melioidosis. In 1955, first case of local human melioidosis was reported in Thailand. During the Vietnam War from 1967 to 1973, 343 American soldiers were reported with melioidosis, with about 50 cases transmitted through inhalation. An outbreak of melioidosis at the Paris Zoo in the 1970s (known as L'affaire du jardin des plantes) was thought to have originated from an imported panda or horses from Iran. It is unclear how imported melioidosis is able to persist in a completely new environment. Eventually, the outbreak terminated by itself after a period of time. It was only during the 1980s, Infectious Disease Association of Thailand started took notice of this disease. First conference on melioidosis was held in 1985 in Thailand. It was during this meeting that collaboration between Sappasitprasong Hospital, Thailand, and Wellcome-Mahido-Oxford Tropical Medicine Research Programme was established. Such collaboration made Thailand a world leader in clinical and epidemiology research on melioidosis.

In 1989, several studies conducted in Thailand demonstrated ceftazidime as an effective antibiotic against melioidosis. Ceftazidime had been shown to reduce the risk of death of melioidosis from 74% to 37%. In 1990, a non-virulent 'arabinose-positive B. pseudomallei' was found by Vanaporn Wuthiekanun. The organism was later reclassified into a new species called B. thailandensis. This species has become a useful tool in the laboratory for the studies of the pathogenesis of B. pseudomallei. B. pseudomallei was previously classified as part of the genus Pseudomonas. In 1992, the pathogen was formally named B. pseudomallei. In 1994, First International Symposium on melioidosis was held in Kuala Lumpur where 80 delegates attended. Papers were presented and later published as a book. Subsequent congresses were held in Thailand, Australia, and Singapore once every three years. In 2002, B. pseudomallei was classified as a "Category B agent". In 2004, the complete genome of B. pseudomallei was published. In 2012, B pseudomallei was classified as a "Tier 1 select agent" by the U.S. Centers for Disease Control. In 2014, co-trimoxazole was established as the only oral eradication therapy rather than combination therapy of co-trimoxazole with doxycycline. In 2016, a statistical model was developed to predict the occurrence of global melioidosis per year.

Synonyms
Pseudoglanders
Whitmore's disease (after Captain Alfred Whitmore, who first described the disease)
Nightcliff gardener's disease (Nightcliff is a suburb of Darwin, Australia where melioidosis is endemic)
Paddy-field disease
Morphia injector's septicaemia

Biological warfare
Interest in melioidosis has been expressed because it has the potential to be developed as a biological weapon. Another similar bacterium, Burkholderia mallei was used by the Germans in World War I to infect livestock shipped to Allied countries. Deliberate infection of human prisoners of war and animals using B. mallei were carried out in China's Pingfang District by the Japanese during World War II. The Soviet Union reportedly used B. mallei during the Soviet–Afghan War in 1982 and 1984. B. pseudomallei, like B. mallei, was studied by both the US and Soviet Union as a potential biological warfare agent, but never weaponized. Other countries such as Iran, Iraq, North Korea, and Syria may have investigated the properties of B. pseudomallei for biological weapons. The bacterium is readily available in the environment. It can also be aerosolized and transmitted via inhalation. However, the B. pseudomallei has never been used in biological warfare. The actual risk of the deliberate release of B. pseudomallei or B. mallei is unknown.

References

External links

 Resource Center for melioidosis

 Burkholderia pseudomallei genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID

Bacterium-related cutaneous conditions
Biological weapons

Melioidosis


Site Finder was a wildcard DNS record for all .com and .net unregistered domain names, run by .com and .net top-level domain operator VeriSign between 15 September 2003 and 4 October 2003.

Site Finder
All Internet users who accessed any unregistered domains in the .com and .net domain space were redirected to a VeriSign web portal with information about VeriSign products and links to "partner" sites. This gave VeriSign the advantage of receiving greater revenue from advertising and from users wishing to register these domain names. It had the effect of capturing the web traffic for several million mistyped or experimental web accesses per day, and meant that VeriSign effectively owned all possible .com and .net domains that had not been bought by others, and could use them as an advertising platform.

VeriSign described the change as an attempt to improve the Web browsing experience for the naive user, without mentioning any use of the domain name system other than by browsers. VeriSign's critics saw this claim as disingenuous. The change led to a dramatic increase in the amount of Internet traffic arriving at verisign.com. According to the web traffic measurement company Alexa, in the year prior to the change verisign.com was around the 2,500th most popular website. In the weeks following the change, the site came into the top 20 most popular sites, and reached the top 10 in the aftermath of the change and surrounding controversy.

Issues and controversy
There was a storm of controversy among network operators and competing domain registrars, particularly on the influential NANOG and ICANN mailing lists, some of whom asserted:
 that the redirection was contrary to the proper operation of the DNS, ICANN policy, and the Internet architecture in general;
 that VeriSign breached its trust with the Internet community by using technical architecture for marketing purposes;
 that the redirection broke various RFCs and disrupted existing Internet services, such as email relay and filtering (spam filters were not able to detect the validity of domain names);
 that the redirection amounted to typosquatting where the unregistered domain being resolved is a spelling mistake for a famous registered domain;
 that VeriSign abused its technical control over the .com and .net domains by exerting a de facto monopoly control;
 that VeriSign may have been in breach of its contracts for running the .com and .net domains;
 that the Site Finder service assumed that all DNS traffic was caused by Web clients, ignoring the fact that DNS is used by other applications such as networked printers, FTP software, and dedicated communications applications. If users of these applications accidentally entered a wrong host name, instead of a meaningful "host not found" error they would get a "request timed out" error, making it look like the server existed but is not responding. No statement by VeriSign in support of Site Finder even acknowledged the existence of DNS traffic not caused by Web clients, although they published implementation details which mentioned this traffic.
 that Site Finder contained an end-user license agreement which stated that the user accepts the terms by using the service—but since mistyping an address automatically caused the service to be used, users could not refuse to accept the terms.

Others were concerned that the Site Finder service was written entirely in English and therefore was not accessible by non-English speakers.

The Internet Architecture Board composed a document detailing many of the technical arguments against registry-level wildcards; this was used by ICANN as part of its supporting arguments for its action.

Fallout
A number of workarounds were developed to locally disable the effects of Site Finder on a per-network basis. Most notably, the Internet Systems Consortium announced that it had produced a version of the BIND DNS software that could be configured by Internet service providers to filter out wildcard DNS from certain domains; this software was deployed by a number of ISPs.

On October 4, 2003, as a result of a strong letter from ICANN, VeriSign disabled Site Finder. However, VeriSign has made public statements that suggest that they may be considering whether they will change this decision in the future. On February 27, 2004, VeriSign filed a lawsuit against ICANN, claiming that ICANN had overstepped its authority. The claim regarded not only Site Finder, but also VeriSign's much-criticised Wait Listing Service. The claim was dismissed in August 2004; parts of the lawsuit continued, and culminated in a March 1, 2006 settlement between VeriSign and ICANN which included "a new registry agreement relating to the operation of the .COM registry."

On July 9, 2004, the ICANN Security and Stability Advisory Committee (SSAC) handed down its findings after an investigation on Site Finder. It found that the service should not be deployed before ICANN and/or appropriate engineering communities were offered the opportunity to review a proposed implementation, and that domain name registries that provide a service to third parties should phase out wildcard records if they are used.

References

External links

 VeriSign's announcement to NANOG of their wildcard DNS changes
 ICANN Advisory Concerning Demand to Remove VeriSign's Wildcard of 3 October 2003
 Slashdot discussion regarding Site Finder
 Internet Software Consortium announcement of "delegation-only" feature that can be used to ignore gTLD wildcards

 Washington Post (27.02.2004): Suit Challenges Powers of Key Internet Authority
 Findings of ICANN SSAC on Site Finder service (PDF)

Domain Name System

Site Finder


Warrnambool (Maar: Peetoop or Wheringkernitch or Warrnambool) is a city on the south-western coast of Victoria, Australia. At the 2021 census, Warrnambool had a population of 35,743. Situated on the Princes Highway, Warrnambool (Allansford) marks the western end of the Great Ocean Road and the southern end of the Hopkins Highway.

History

Origin of name
The name "Warrnambool" originated from Mount Warrnambool, a scoria cone volcano 25 kilometres northeast of the town. Warrnambool (or Warrnoobul) was the title of both the volcano and the clan of Aboriginal Australian people who lived there. In the local language, the prefix Warnn- designated home or hut, while the meaning of the suffix -ambool is now unknown. William Fowler Pickering, the colonial government surveyor who in 1845 was tasked with the initial planning of the township, chose to name the town Warrnambool. The traditional Indigenous owners of the land today are the Dhauwurd Wurrung people, also known as the Gunditjmara.

Aboriginal Australians
Aboriginal Australians have been occupying the site of Warrnambool for at least the last 35,000 years. The vicinity around the Merri River was inhabited by people known as the Merrigundidj, part of the larger Gunditjmara nation. They spoke a language called Bi:gwurrung, which was a dialect of the Dhauwurd Wurrung language. These people constructed large stone and timber weirs called yereroc across various waterways in the region in order to facilitate the trapping of eels. The area at the mouth of the Hopkins River was known as Moyjil. At the beginning of British colonisation of the region in 1841, there were approximately 400 Aboriginal people living around the coastal parts of the Merri River including a number of Koroitgundidj people residing in a village at what is now known as Tower Hill. There are several Maar placenames for locations in the area including: 'Kunang' referring to a waterhole on present-day Koroit Street which was a celebrated place for kangaroos to drink, 'Wirkneung' referring to the site of Warrnambool cemetery, 'Puurkar' referring to the Western Hill area of Warrnambool, and 'Peetoop' which is one of the names for the area meaning 'small sandpiper'.

European maritime exploration
A popular legend is that the first Europeans to visit the region were Cristóvão de Mendonça and his crew who surveyed the coastline nearby and were marooned near the site of the present town as early as the 16th century, based on the unverified reports of local whalers' discovery of the wreck of a mahogany ship. The ship's provenance has been variously attributed to France, China, Spain and Portugal. There is no physical evidence to suggest that it ever existed.

The first documented European exploration of the area occurred under Lieutenant James Grant, a Scottish explorer who sailed the  along the coast in December 1800 and named several features. This was followed by that of the English navigator Matthew Flinders in the , and the French explorer Nicholas Baudin, who recorded coastal landmarks, in 1802. The area was frequented by whalers early in the 19th century.

British settlement
British settlement of the land in the region began in 1838 when Captain Alexander Campbell, a whaler based at nearby Port Fairy, took possession of 4,000 acres around the mouth of the Merri River. He set up a farm there and built his main hut where Warrnambool now stands. The township was planned and surveyed in 1845, with the first allotments being sold in 1847. A Post Office opened on 1 January 1849.

During the Victorian Gold Rush, Warrnambool became an important port and grew quickly in the 1850s, benefiting from the private ownership of nearby Port Fairy. It was gazetted as a municipality in 1855, and became a borough in 1863. Warrnambool was declared a town in 1883, and a city in 1918. Post Offices opened at Warrnambool South in 1937 (closed 1973), Warrnambool East in 1946, and Warrnambool North in 1947 (closed 1975).

Climate

Warrnambool has a mild Mediterranean climate (Csb) that closely borders the oceanic climate (Cfb), and is characterised by mild, dry, very swingy summers and cool, rainy winters with frequent cloud cover. Annual and especially winter rainfall is much higher than in Melbourne due to its westerly exposure.

During the heatwave in southeastern Australia, Warrnambool recorded a maximum temperature of  on 7 February 2009.

Cityscape
The original City of Warrnambool was a 4x8 grid, with boundaries of Lava Street (north), Japan Street (east), Merri Street (south) and Henna Street (west). In the nineteenth century, it was intended that Fairy Street – with its proximity to the Warrnambool Railway Station – would be the main street of Warrnambool. However, Liebig Street has since become the main street of the central business district (CBD). The Warrnambool CBD is particularly notable for its number of roundabouts.

Outside the CBD, the Warrnambool Botanic Gardens feature wide curving paths, rare trees, a lily pond with ducks, a fernery, a band rotunda, and was designed by notable landscape architect, William Guilfoyle.

Eleven suburbs surround the CBD of Warrnambool: North, South, East and West Warrnambool, Brierly, Sherwood Park, Merrivale, Dennington, Woodford, Bushfield and Allansford, though only the four latter are recognised as localities of the city.

Culture

Wunta Fiesta, a festival held in Warrnambool over the first weekend of February annually, is one of south-west Victoria's major community festivals. It incorporates a wide range of entertainment (mostly music) for all ages.

The Flagstaff Hill Maritime Museum is in Warrnambool built on Flagstaff Hill that also holds the original lighthouses and Warrnambool Garrison. Its most prized item in its collection is the Minton peacock salvaged from the Loch Ard.
Flagstaff Hill Maritime Village is built around the original lighthouses and now operates as a heritage attraction and museum of shipwreck and maritime trade artefacts.

The Lady Bay Lighthouse complex is on the Victorian heritage register due to its significance as an example of early colonial development. There has been a flagstaff on top of Flagstaff Hill since 1848, and the current lighthouses were moved to the site in 1878. They still operate as navigation aids for the channel into Warrnambool harbour.

The Warrnambool foreshore is a popular swimming area, and is adjacent to the Lake Pertobe parklands. A number of caravan parks are also located in the area.

Baritone Robert Nicholson recorded the song Back to Warrnambool in 1924.

Warrnambool is the setting and filming location of the 2015 film Oddball, starring Shane Jacobson.

Warrnambool's Bathing History

Warrnambool has a rich history when it comes to outdoor bathing. The city has been a popular destination for beachgoers for over a century, with the first public bathing area built in 1876 on the south end of Gilles Street, and was later moved to the current location with the advent of the railway. The sea baths were filled with water drawn from Lady Bay, initially by windmill and later by gas pump.

Over the years, Warrnambool' s outdoor bathing facilities evolved, with the introduction of new amenities and features. In 1881, the sought after Hot Sea Baths opened, and people travelled to Warrnambool to receive the benefits of bathing- noting their 'wonderful creative powers', and a 'tonic for the feeble'.

Today, Warrnambool continues to be a popular destination for bathing, with world class facilities available for locals and tourists alike. The Deep Blue Hot Springs, offer two bathing experiences and although no longer using salt water drawn from the sea, their Indoor Bath House and Outdoor Bathing Sanctuary offers naturally warm geothermal water, drawn from the Dilwyn Aquifer, 850 meters below earths surface.

Media
Warrnambool is served by one daily newspaper, The Standard, which is owned by Australian Community Media. The local commercial radio stations are 94.5 3YB and 95.3 Coast FM, both owned by Ace Radio. There is also a community radio channel, 3WAY FM. The ABC also owns a radio station, ABC South West Victoria, which is based in Warrnambool.

Warrnambool is also served by local transmission of free-to-air television networks ABC, SBS, Prime7, Southern Cross and WIN.

Out of those networks, WIN Television produces the only local television news bulletin, WIN News, which uses resources from their Ballarat and Warrnambool newsrooms.

Sport

Warrnambool is home to the Grand Annual Sprintcar Classic, a race which attracts Australian and international drivers on the Australia Day long weekend, especially because of its position in the motorsport calendar.

The city is also the finishing point of the Melbourne to Warrnambool Classic cycle race. It is the longest one-day bicycle endurance race in the world, held every October since 1895 to be the world's second oldest bike race.

Warrnambool has a horse racing club, the Warrnambool Racing Club, which schedules around twenty race meetings a year including the Warrnambool Cup and Grand Annual Steeple three-day meeting in the first week of May. The Woodford Racing Club also holds one meeting at Warrnambool racecourse. The Grand Annual steeplechase has 33 jumps, more than any other horse race and is one of the longest steeplechases in the world.

The Warrnambool Greyhound Racing Club holds regular greyhound racing meetings on most Thursdays. The Greyhound version of the Warrnambool Cup is held on the first Wednesday of May.  The club also holds the Seaside Festival over the Christmas and New Year period providing great entertainment and value for money for both kids and kids at heart. The club is located centrally in the Warrnambool Showgrounds Precinct on Koroit Street and opened on 27 July 1978.

Warrnambool is home to the Premier Speedway, a  dirt track oval speedway located approximately 5 km east of the town. As well as hosting various Victorian state championships, Premier Speedway has hosted Australian championships for Sprintcars, Super Sedans and Street Stocks. Premier Speedway has also regularly hosted rounds of the World Series Sprintcars, being one of only five tracks to host a round of every series run since its inception in 1987. Since 1973 the speedway has been home to the Grand Annual Sprintcar Classic, the biggest single sprint car racing meeting in Australia, and on occasion has outdrawn the famed Knoxville Nationals in the United States for number of competitors entered, as better known drivers enter both races. The Classic is traditionally run the weekend before the national title meeting. The speedway has hosted the Classic / Australian Championship double on six occasions - 1979, 1986, 1994, 1999, 2003 and 2011, with Sydney's 10 time Australian Champion Garry Rush the only driver to win the double at Warrnambool in 1986 when he won his 6th Classic and a week later his 7th national title.

Gunditjmara Bulls and North Warrnambool Warriors play rugby league in NRL Victoria.

From 1 to 3 September 2008, the city hosted, along with Melbourne, the 2008 Australian Football International Cup, featuring 14 nations from around the world playing Australian rules football. The sport is highly popular in Warrnambool which has a competitive local league and is the origin of many high-profile AFL players. The city has three Australian Rules football teams playing in the Hampden Football League (North Warrnambool, South Warrnambool and Warrnambool), and many more in the Warrnambool District Football League

Golfers play either on the 18 hole course at the Warrnambool Golf Club a public access course ranked in Australia's top 100 courses, or at the 9 hole course at the Deakin University Warrnambool campus.(Deakin course not playable)

Economy

Warrnambool attracts many visitors each year, and is a comprehensive regional service centre. The town's tourism benefits from the views from the Great Ocean Road, and its nearby beaches, some of which are used for surfing. In the winter months, Southern Right whales can be seen in the waters near the city at the Logan's Beach nursery, and boats make whale-watching tours.

The mainstay of the economy is agriculture and its support industry – particularly dairy farming and associated milk processing. Other major industries and services include retail, education, health, meat processing, clothing manufacture and construction. The Fletcher Jones and Staff Pty Ltd clothing factory opened in 1948 and was closed in 2005.

Demographics

15.1% of Warrnambool residents were born outside Australia, which is significantly less than the Australian average of 33.1%. 89.1% speak only English at home and 2.0% are Indigenous.

Governance

The Local Government is the Warrnambool City Council.

At the state level, Warrnambool was within the electoral district of Warrnambool until it was abolished in 2002. Since then, Warrnambool has been in the South-West Coast electorate. This was held by former Premier Denis Napthine of the Liberal Party until his retirement in 2015, the resulting by-election electing Roma Britnell, also of the Liberal Party.

At the federal level, Warrnambool is the largest town in the division of Wannon, which has been a safe Liberal seat since 1955. However, Warrnambool booths typically receive a much stronger Labor vote than the rural areas that surround it. The seat was held by former Prime Minister Malcolm Fraser for 28 years, before being held by former Speaker of the lower house David Hawker for 27 years.

Education

Primary
There are many primary schools in Warrnambool, including:
Warrnambool Primary School
Warrnambool East Primary School
Warrnambool West Primary School
 Merrivale Primary School
 Allansford and District Primary School
 Grassmere Primary School
 Woodford Primary School
 Our Lady Help of Christians Primary School (Catholic)
 St Joseph's Primary School (Catholic)
 St Pius X Primary School (Catholic)
 St John's Primary School, Dennington (Catholic)
 Kings College (primary and secondary)
 Merri River School (formally Warrnambool Special Development School) (primary and secondary)

Secondary
Warrnambool has two public high schools:

 Brauer College
Warrnambool College

In addition, there is:

 Emmanuel College, a Catholic school
 King's College, a private Presbyterian school

Tertiary
The city's only university facilities are at the Deakin University Warrnambool campus. The South West Institute of TAFE and SEAL both provide vocational education.

Environment

Logan's Beach on the eastern side of the city is recognised as a nursery site for the southern right whale Eubalaena australis, and many tourists have been attracted to opportunities for land-based observations. Most years one, two or three adult female whales arrive between late May and August, giving birth within days of their arrival. The young whale calf is then reared at the site, usually departing with its parent by mid to late September. Besides the southern right whale, the coastline is also visited by Australian fur seals, little penguins and common dolphins. During the winter and early spring albatross cruise along the coastline and can be sighted from Thunder Point, a popular coastal lookout in the town.

Middle Island has a colony of  Australian little penguins (Eudyptula novaehollandiae). Fox predation reduced numbers significantly. In 2005 only four penguins were remaining in the colony. Warrnambool City Council introduced a world first program using Maremma dogs to guard the penguins. This program has supported the re-establishment of a colony of over one-hundred penguins in 2009. By 2015 the population had reached almost two-hundred. The film Oddball tells the story of the dogs saving the penguins.

Transport

Warrnambool is situated on the Princes Highway between Port Fairy to the west and Terang to the east as well as at the south-western terminus of the Hopkins Highway. The Great Ocean Road terminates 13 km east of Warrnambool, near Allansford.

Rail services operate to Melbourne and Geelong. V/Line passenger train services call at Warrnambool's two stations, Warrnambool in the city and Sherwood Park in the city's outer east, seven days a week. A daily container freight service is being run by Pacific National for local container handler Westvic.

Local buses under the Transit South West brand cover Warrnambool's city and suburbs and extend to the nearby towns of Port Fairy and Koroit. V/Line coaches connect Warrnambool with Mount Gambier, Ballarat, Ararat, Casterton and the Great Ocean Road to Geelong.

Health
There are two main hospitals in Warrnambool:

Warrnambool Base Hospital, run by South West Healthcare, founded in 1854 as Warrnambool Hospital & Benevolent Asylum, with further name changes and mergers over the years, including a name change to Warrnambool and District Base Hospital in 1925 and Stage 1 of a  redevelopment opened in 2011 as Warrnambool Base Hospital.

St John of God Warrnambool Hospital, a private hospital established in  1939 by the Sisters of St John of God and run by St John of God Health Care

Notable people
 Airbourne, hard rock band
 Tom Ballard (b. 1989), comedian
 Ben Barber (b. 1984), actor
 Smoky Dawson (1913–2008), country music performer (born in Collingwood, raised in Warrnambool)
 Alex Dyson (b. 1988), radio presenter
 Sir John Eccles (1903–1997), Nobel Prize winner in physiology or medicine, 1963
 Brian Fitzpatrick (1905–1965), Australian economic historian
 Danielle Green, Member of Victorian Parliament was raised and educated in Warrnambool
 Dave Hughes (b. 1970), comedian
 Paul Jennings (b. 1943), children's author – (resides in Warrnambool)
 Sally Walker, Law Professor, Vice-Chancellor and President of Deakin University
 Axle Whitehead (b. 1980), musician and TV personality

Sportspeople
 Jonathan Brown (b. 1981), Leon Cameron (b. 1972), Paul Couch (1964–2016), Simon Hogan (b. 1988), Jordan Lewis (b. 1986), Brent Moloney (b. 1984), Noel Mugavin (b. 1956), Kevin Neale (b. 1945), Matt Maguire (b. 1984), Billie Smedts (b. 1992), Wayne Schwass (b. 1968), Michael Turner (b. 1954), Sam Dwyer (b. 1986), Martin Gleeson (b. 1994), John Burns (b. 1949) Australian rules football players
 Marc Leishman (b. 1983), golfer
 Christian Ryan (b. 1977), Olympic Silver Medallist, rowing 2000
 Nathan Sobey (b. 1990), basketball player
 Tim Ludeman, cricket player

Sister cities

 Miura, Kanagawa, Japan
 Changchun, Jilin Province, P.R.China
 Knoxville, Iowa, United States of America

See also
 ABC South West Victoria
 Mahogany Ship
 Warrnambool Airport
 Warrnambool V/Line rail service

References

External links

 Warrnambool City Council official website
 Warrnambool Tourism Association official website

 Warrnambool – Official state tourism website.

Towns in Victoria (state)
City of Warrnambool
Cities in Victoria (state)
Coastal cities in Australia
Port cities in Victoria (state)

Warrnambool