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Susannah Mortimer/Mortimore my GGGG Grandmother Married Thomas O'Brien
Susannah Mortimore was sentenced to death at the 17 march 1788 Exeter Castle ( Devon) Assizes for the theft on 20 August 1787 of 2 sheep belonging to Elias Langdon at Moretonhampstead (Devon). She was reprieved several weeks later to 7 years transportation and remained in the county goal until 11 April 1788, when she was sent with several other women for embarkation on the "Lady Juliana" transport on the Thames, age given as 24. She was apparently the woman of this name whose conveyance from Southampton to Exeter (118 mile journey) for trial under a writ of Habeas Corpus cost the county 5 pounds 18 shillings.
In early August 1790, 8 weeks after landing at Sydney Cove, Mortimore was among 194 male and female convicts transferred to Norfolk Island. She brought with her a young child, Susannah, who had almost certainly been conceived on the voyage from England. Soon after arrival she formed a relationship with the 1st Fleet marine settler Thomas O'Brien on his 60 acre (24ha) farm (lot 86) on the west side of the Island. they were probably among a large number of couples married by Rev Richard Johnson on his November 1791 visit to the Island, with no record of the ceremonies surviving In September 1808 the family were among the settlers transferred to VDL, (Tasmania), where O'Brien was granted 100 acres (40.5 ha) in the New Town district.
Susannah died 31/12/1846 at Glenorchy and was buried at St Matthews church cemetery Glenorchy. The church still exists (1998) not as a church but as a meeting place for Aboriginals and Torres Strait Islanders. The headstone along with a number of other headstones are cemented in on the back wall of the church. When the headstone was cemented in they covered up the bottom name on the stone. the inscription reads " To The Memory of M~SUSANNAH O'BRIEN" who departed this life December 31 1846 Aged 86 years, Also, James O'Brien, Died December 21 1863 aged 63 also ? it can be assumed that the third person in the grave is Jame's wife Ann
As already described, Susannah came with her husband, Thomas, and eight children to Hobart Town in 1809. They were first class passengers. She helped her Husband fashion his farm from virgin bush at O'Briens Bridge ( Glenorchy). Susannah died in 1846 at the age of 86. The headstone, which once stood out in what is now the Centre of the main road, was placed at the rear of St Matthews Church, on the corner of Tolosa St and Main Road, Glenorchy.
Susannah was living with her daughter Margaret McDonald in the 1837 census
** SUSANNAH MORTIMORE age 24, tried Exeter, spring 1788, sentenced 7 years( Mutch index to " Lady Juliana" which arrived 3-6-1790) Left Plymouth 29-7-1789 arrived Sydney 3-6-1790.
Western Assize circuit goal book for 1774-1798 shows Susannah Mortimore convicted at Exeter Lent Assizes 1788 of stealing jointly with John Rice in August 1787 at Moreton, Hampstead, 2 sheep, property of Elias Langdon. Both she and Rice pleaded not guilty, were convicted to be hanged. Both sentences subsequently being commuted to 7 years transportation each.( Public records office, London - Assi 23/8 part 2)
Exeter Flying Post, Thursday 27-3-1788
"...J. Rice and Susannah Mortimore, for sheep stealing, all to receive sentence of death...hereby J. Rice and Susannah Mortimer, were reprieved;the others left for execution, Friday fortnight."
J. Rice died on the voyage to Australia aboard 2nd fleet ship " Neptune".
Susannah arrived Norfolk Island " Suprise" 7-8-1790 on rations. Had 9 chn and married Thomas O'Brien.
My GGG Grandfather
John was a convict, sentenced at Durham in April 1817 for larceny to seven years transportation. He came on the "Lady Castlereagh", arriving in Port Jackson on the 30th April 1818 the trip took 129 days, then the ship was chartered to transport the convicts on to Hobart at a rate of 2 pounds per convict , 39 disembarked at Port Jackson and 261 convicts went on to Hobart . This was the first ship to be fitted out with three distinct compartments, seperated by open iron railings. This seperated juveniles from hardened offenders, and allowed a freer flow of air.
John was a 24 year old waterman from Lincolshire, 5'6" tall, with flaxen hair, blue eyes, and a yellow complexion. His behaviour in the colony was good, with only two offences recorded against him, once for being absent from his lodgings at night and the second on December 1st 1826 after his freedom, for fighting and affray in Foulburn Street, for which he was bound over to keep the peace for three months.
John and Mary began their married life in Launceston, where their first three children were born, returning to Glenorchy in time for the birth of their fourth child in 1830, where John worked as a sawyer.
In 1838 John applied to the caveat board for the ratification of his title to 5 acres 6 perches of land in the parish of Glenorchy, part of the 60 acres originally granted to Thomas O'Brien. O'Brien had conveyed the land to Smith on 10 April 1823 just after his marriage to his daughter, Mary Ann O'Brien.
In 1839 John Smith of Glenorchy applied fo a grant of land in the Huon area, and a grant of 100 acres was made to him at Castle Forbes Bay in 1841. They moved there in time for the birth of Thomas in May of that year.
john bower convicted on 25th march 1826 at the warwick assize to life (transported to australia)
life for housebreaking. previous offence-breaking into a shop, stole wearing apparel(24 months sentence)
the ship woodford depart 5 august 1826 arrived hobart 22 november 1826
28th dec 1826 sent to mr. horton at ross Tasmania to help build "sumercoats" Mr Horton's residents
14th jan 1834 sent to campbell town
21st apr 1835 sent to new norfolk
28 jan 1839 cond. pardon no 1947
granted permission to marry joan hancock on 18 april 1836 at the Mance of St Davids Hobart
conduct in goal-bad
conduct in hulk-good
trade- jeweller
Became a storeman, Miller and a potter
Joan Handcock aged 18 sentanced to transportation to Australia on the ship William Bryan
28-3-1833 sentenced to 14 years at Somerset assize
transported for sealing solen goods as a farm hand
depart London 4 July 1833
arrive in hobart 23 oct 1833
12-11-1835 indifferent conduct-sent to wash tub until futher notice
30-5-1839 ticket of leave
28-10-1841 con. pardon no. 3429
sentanced to the Cascades Female Factory for convicts in Hobart
departed 9 oct 1840 london
arrival 17 jan 1841
female family founders database
December 1841 sent to work for Mr W T Mac Michael at Hobart
Married Frederick Ray 10 Jan 1842
My GGG grandmother Married to Thomas Smith (Fellows)
Sarah was aged about 3 or 4 when her father Joseph Ford was hanged for horse stealing when aged only 28 years!
(Sarah's birth/baptism registration not confirmed - 1815 or 1818 -
bap 31 May 1818 at St James the Great, Dursley in Gloucestershire)
Joseph was hanged on 1 Sep 1821 and was buried three days later on the 4 Sep 1821 under the Coaley Church Tower in Gloucester. 300 people attended his funeral.
(Joseph Ford was born 8 Jan 1793 at Coaley, married Sarah Workman 27 Apr 1812 at Dursley
Sarah's mother Sarah would have found life very hard with three or four young children to look after and no husband.
(Fourth child Edmund - details to be confirmed - an Edmund Ford buried Dursley 4 Mar 1821 aged 9 years.)
Within fifteen years Henry, Hannah and Sarah had all been charged with offences and gaoled - because of their second offences Henry and Sarah were transported for seven years to Van Dieman's Land.
Son Henry (b 1815c Coaley) was first imprisoned in 1831 aged 16 years and two years later in 1833 went on trial for receiving stolen goods.
In 1835 he was transported to Hobart arriving per 'George III' - according to records he drowned as the ship arrived at Hobart.
There is a book written of this disaster "An Imperial Disaster - The Wreck of George III" by Michael Roe.
(In 1846 Esk River in Tasmania, Bushrangers Henry Ford and Henry Smart, robbed people at gunpoint in their houses. While robbing Rev Browne's house, Chief Constable Midgely called in to see him and caught the two red handed - sentenced to death, but commuted to life. Perhaps our Henry Ford did not drown!)
Sarah and her sister Hannah were committed for trial on 9 Mar 1836 by J Wallington Esq. Their ages were given as 23 and 21.
They were charged with Larceny at the Lent Assizes in Gloucestershire on 29 Mar 1836 and are listed on the 'Register of all persons charged with an Indictable Offences'.
They were 'charged on the oaths of Maria Newth and others with having on the 6Jan last at Dursley, feloniously stolen a silk handkerchief, the property of William Rickards, one cotton apron the property of Charlotte Rickards and a cotton apron, the property of Mary Watts'.
Hannah was described as having brown hair, light grey eyes, round visage, fair complexion (much pickled?), cut on the forehead. She was 5ft 1/2in tall and worked as a servant. Her behaviour in goal was described as 'orderly'.
Sarah was described as having light brown hair, full dark eyes, round visage, fair complexion, a mole between her shoulders. She was 4ft 10 1/2in tall and also worked as a servant. Her behaviour in goal was described as 'indifferent'.
They received one month goal.
Hannah was aged 21 while Sarah was 19 - ages two years younger than on original charge sheet!
On the Register in the column headed Degree of Instruction - 'Imp' is written opposite each of the girls - meaning to be found.
Both girls were Discharged 31Mar1836.
Sarah re-offended and went to trial at the County Assizes on 10 Aug 1836. This time she was sentenced to 7 years transportation. Her conduct was described as Very Bad.
Sarah had been charged on 27 Jul 1836 and committed for trial by KB Copper Esq and F Needle Esq. Her age was 21 and from she came from Dursley.
She was 'charged on the oath of Mary Hawkins and another with having on the 26 Jul at Cheltenham, feloniously stolen one pair of shoes, one pair of stockings, one pound of sugar and other articles, the property of Geo. Hawkins'.
Sarah's Convict Indent - original page transcribed - Convict number 149.
Transported for Larceny - Goal Report Very Bad, convicted before, Single.
Stated this offence Stealing Beer Glasses…… having been in prison before, Single.
29Oct1838 …./Disobedience of orders, 10 days Solitary Imprisonment in a cell, then assigned in the Interior away from Town. (initials) MF.
Conditional Pardon No 950 15 Dec 1842 (in different handwriting)
Ship 'Platina' departed London 3May1837 arriving 22Oct1837 - assigned to Cascades Female Factory, aged 21.
Sarah's description -
Trade was Nurse & ….woman,
Height without shoes was 5ft
Age 21
Fair complexion, Round Head, Brown Hair, Oval Visage, High Forehead, Grey eyes, Medium Nose, Small mouth and chin.
The words Dersley(sic) and Gloster(sic) written to the side of her description.
Sarah (149) sought Permission to Marry 28Nov1839 to fellow William Foxall ('Lady Ripley' - Convict number 142). The letters EO are in Decision Column.
Further down the same page Sarah and William's details are re-entered.
This time the date is 17Jan1840 and next to the date 5Mar1840 a few lines of writing that is difficult to decipher - "… of the Clergy … … be satisfied with the evidence to proved the death of the … ….".
As there is no evidence of a marriage it appears that William Foxall died - no death registration found.
Sarah's first two children Elizabeth and Ellen - possibly twins - were born 6Mar1840 at New Norfolk in Tasmania. Ellen's life is well documented (she married John Alan Bower) but nil further known of Elizabeth.
Sarah Ford - Convict number 149 - ship 'Platina', Ticket of Leave on 31Dec1841? (p362 of 1841 Convict Muster). Worked for Rev Palmer.
Sarah Ticket of Leave dd 11Nov1841 - Details in Courier Newspaper 16Nov1841.
Sarah's second Permission to Marry application was dd 15Feb1842 - Thomas Smith Convict number 2544 ('Lord William Bentinck II). Approval for the marriage dd 5Mar1842.
The marriage took place at St Matthews Church, New Norfolk on 5 Apr 1842. Thomas Smith was aged 27, Sarah Ford 24. He signed his name, Sarah "X". The minister Chaplain W Garrard married them in the Parish Church according to the Rites and Ceremonies of the United Church of England and Ireland. The witnesses were William Dean who signed his name and Jane Dean "X".
Sarah spent possibly a year and a half in New Zealand!
She died 13 May 1892 in Down Street, Collingwood in Victoria Australia and is buried in Melbourne General Cemetery with her husband Thomas Smith who died 2 years later on 25 Jul 1894.
My GGG Grandfather Thomas Smith(fellows) married Sarah Ann Ford
From the Quarter Sessions Order Book June 1837.
> Thomas Smith late of the parish of Camborne in this county laborer
> was at this sessions indicted tried and convicted for feloniously
> stealing one piece of the current silver coin of the realm called a
> half crown of the value of two shillings and six pence two pieces of
> the current silver coin of the realm called shillings of the value of
> two shillings one piece of the current copper coin of the realm
> called a penny of the value of one penny and two pieces of the
> current copper coin of the realm called half pence of the value of
> one penny of the monies goods and chattels of Thomas Vincent from the
> person of Mary Anne Vincent the wife of the said Thomas Vincent
> against the form of the statute in that can made and provided.
> It is therefore ordered that for the said offence he the said Thomas
> Smith be transported to such parts beyond the seas as His Majesty
> with the advice of this Privy Council shall direct for the term of
> seven years.
> Tasmanian Convict Ships Records (ML Ref. CY1281,pg 355) Mitchell Library
> WHERE TRIED: Cornwall 2nd sessions
> WHEN TRIED: 27 June 1837
> AGE: 25yrs
> TRADE: Shoemaker, can cut
> SENTENCE: 7yrs
> NATIVE PLACE: Portsmouth
> HOW APPROPRIATED: Mr. Rd. Barker Macquarie Dist. T.L.
> CON 18/14 Tasmanian Archives
> Thomas Smith No. 7
> Trade....................................Shoemaker, can cut out
> Height (without shoes)..... 5' 41/4"
> Age....................................... 25
> Complexion........................ Dark
> Head.................................... Round
> Hair........................................Dark
> Whiskers............................. Jo?
> Visage...................................Long
> Forehead..............................High
> Eyebrows............................ Dark
> Eyes......................................Blue
> Nose.................................... Short
> Mouth....................................Medium
> Chin...................................... Long
> The Lord William Bentinck 11 arrived in Hobart on 26th Aug, 1838. It
> was a 564ton Bk built in Bristol in 1828. It was class A1, the master
> was William S Stockley and the surgeon was John Rankine. It sailed
> fom Portsmouth on 15th April, 1838. It
> sailed via the Cape and took 134 days. There were 320 males. 3 died.
> Quarter Sessions were Epiphany, Easter, Trinity, Michaelmas.
> Ref. Ns 489/1 St. Matthew's Church, New Norfolk-Marriages. Tasmania
> No. 57 1842 April 5
> Thomas Smith 27 Ld. William Bentinck Bachelor
> Sarah Ford 24 T.L./ Platina Spinster
> Signed: Tho. Smith
> Sarah Ford X her mark
> in the presence of William Dean
> Jane Dean X her mark.
> Born Isle of Wight. Lived in Tasmania ?yrs and in Victoria 26 yrs.
> (his death certificate)
> Death Notice- The Age Thursday July 26 1894
> SMITH On the 25th July at 4:30 a.m., at the residence of his
> daughter, Mrs Ruth Wood 23 Tait St North Fitzroy, Mr Thos Smith, late
> of Glenorchy, Tasmania, aged 78 years.
> Funeral Notice- Smith- the Friends of the late Mr Thomas Smith are
> respectfully invited to follow his remains to the place of
> internment, Melbourne General Cemetery. The funeral will leave the
> residence of his daughter Mrs woods, 23 Tait Street, North Fitzroy
> THIS DAY (Thursday) 26th inst at 2 o'clock.
According to the 1851 census, the ex-convict Thomas Smith lived at Nicholls Rivulet with his wife, son and daughter. Thomas Smith is listed in the 1851 Huon census (p.4). Funeral Notice- Smith- the Friends of the late Mr Thomas Smith are respectfully invited to follow his remains to the place of internment, Melbourne General Cemetery. The funeral will leave the residence of his daughter Mrs woods, 23 Tait Street, North Fitzroy THIS DAY (Thursday) 26th inst at 2 o'clock. He married Sarah Ann Ford, married 5 Apr 1842 in New Norfolk St Matthew, Tasmania, born 8 Jan 1815 in Dursley, Gloucestershire, (see note 32) died 13 May 1892 in Down Street, Collingwood, Victoria, Australia, (see note 33) buried 15 May 1892 in Melbourne General Cemetery, Victoria, Australia, (see note 34) occupation Nurse & Needle, Waits At. Sarah: The Platina arrived in Hobart on 22 Oct 1837. It was a 303ton Bk built in Sunderland in 1830. It was class A1, the Master was Robson Coltish and the surgeon, George Ellery Forman. It sailed from London on 3rd May , 1837, via the Cape and took 172 days. There were 116 females on board.
Greorge Porter my GGG Grand Uncle married to My GGG GrandAunt Susannah Mely Screech(o'Brien)
George Porter was born about 1768, in Middlesex, and when 20 was sentenced to death on 25 February 1789 during the Sessions at the Justice Hall, Old Bailey. His crime was stealing six silk handkerchiefs and a single leather slipper in the burglary of a shop near the corner of The Terrace and Cross Street, Islington, just north of the City of London. At 6 pm on 21 January he was seen breaking a pane of glass in a shop window, and snatching the items from a display. It was already dark, but he was caught running through Islington Churchyard after someone cried, "Stop Thief!" William Cook was also arrested, because he had been seen acting suspiciously with Porter earlier. He was acquitted at the trial with a solemn warning from the judge: "Your life is spared. I hope the fate of your unfortunate companion will be a warning to you." Witnesses identified both young men as Islington residents known to them by sight. Porter claimed in court to have innocently picked up the goods off the ground.
After Porter had spent seven months in the condemned cells, he was called to the bar of the Old Bailey with over a 100 other capital convicts in September 1787, and offered a pardon on condition of transportation for life. (William Rayner was also among the group.) He accepted, and on 10 November he was sent from Newgate to the transport, Scarborough. So he became a Second Fleeter, arriving at Sydney Cove on 28 June 1790. (See the chapter on the Rayners for more detail about the voyage of the Scarborough).
A year after landing, Porter was sent to Norfolk Island, where he worked quietly as a gardener, with James Warwick, and was still single when he was transferred to Van Diemen's Land on the City of Edinburgh in September 1808. Written alongside his name in the remarks column on the list of evacuees was recommended for a grant - a good character.The impression is that Porter was a fairly quiet sort of man, who kept out of trouble, and survived through the horrors of the Second Fleet and Norfolk Island by being as invisible as possible.
On 21 November 1808, a month after arriving in Hobart Town, he married Susannah Mortimore, (who went under the name of O'Brien), who had sailed with her family from Norfolk Island on the same ship as Porter. Perhaps he proposed to her on board? She was 18, and he was by now 40. They were married by the Rev'd Robert Knopwood, with Thomas O'Brien, Susannah's step-father, and Francis Barnes as witnesses. The couple both signed with an X. It was the 34th marriage to take place in Tasmania.
George farmed near New Norfolk, and for some years was a constable with the Hobart Town Police. In 1818 he was supplying wheat and meat to the government stores, and in 1819 held a grazing license at "Green Bottom", Broad Valley, Glenorchy. That year he was listed as farming 60 acres, of which 15 were in wheat, and 4 in beans and potatoes. He also had 5 cattle and 151 sheep. By then they had six children, and employed a government servant.
In the December 1821 Hobart Town Gazette the following advertisement appeared:
STRAYED, about three weeks ago, from the Black Snake, two Working Bullocks, branded G P on the near shoulder, one has a black mark with a star on the forehead, the other red colour with a white back - Whoever will give information where they are, to George Porter, the owner, as above, will receive 2 pounds for their trouble; but if found in any person's possession after this notice, they will be prosecuted agreeably to the Colonial regulations.
The first seven children were baptised by Bobby Knopwood, and George and Susannah's address was given as Hobart Town. The last two records give the address as Glenorchy, and George's occupation as farmer. But they were on their farm at Black Snake, Granton, long before 1825. In 1817 George was supplying the Government Stores, with 750 lbs of fresh meat, and 24 bushels of wheat. In 1828 a Return of Juvenile Population of the Black Snake, Van Diemen's Land, requiring Education lists the Porter family, boys and girls separately, with the comment "Parents of good character". They were Protestants. Both George Porter and William Mansfield claimed that the school was too far off for their children to attend.
George died on 8 September 1828, at the age of 60, leaving his wife responsible for a family of eight children. Susannah held them together on the farm, yet another remarkable pioneer woman. She died aged 45 on 7 May 1835, leaving her youngest child an orphan at only 6 years old. Perhaps her mother helped raise the children left behind.
My GGG GrandUncle Married my GGG GrandAunt Catherine O'brien
Alexander arrived in Tasmania as a convict on board the ship "Indefatigable"in 1812. He had been sentenced by court martial at Fort George, Upper Canada on the 28th August 1810 to transportation for life. On 13th December 1824 he wrote a memorial to the Lieutenant-Governor, Arthur, describing himself as free,but admitting that he came on the "Indefatigable" in 1812. He had been granted two town allotments in Launceston, and had built premises worth more than 1200 pounds ($2400). He had been a licensed innkeeper for 3 years, and held 300 acres (122ha) of land by purchase. This may have been at or near Longford, for he said that he intended to build a water mill "for the accommodation of the Norfolk Plains Settlers", Norfolk Plains is now Longford. Asserting that since his arrival he had "maintained a character unimpeachable for integrity and honesty of principal and conduct", he asked for a grant of land. Arthur authorized the grant of 200acres (81ha), which was taken up near Launceston (CSO1/92/2168.
On the 10th May 1827 this same Alexander Waddle wrote another petition to the Lieut-Governor. This time he admitted that he had arrived on the "Indefatigable as a convict . He said he had received a ticket-of-leave on arrival and had held it for seven years. On the 31 January 1820 he had received a conditional pardon, the condition being that he remained a district constable in the vicinity of Hobart Town for five years. He said he now possessed 250 head of cattle, 4 horses, three houses in Launceston and 700 acres (283ha) in the vicinity of Launceston, 200 of which had been granted. He was now a licensed publican. He now asked for a free pardon. A.W.H. Humphrey, a magistrate, attached a certificate of conduct. In this he stated that Waddle had deserted his wife some years before, that he was a licensed publican living with Catherine O'Brien by whom he had had several children, Mrs Waddle was now living with her family at Beresfords Creek about six miles (10km) from Hobart on the New Norfolk road. The petition was recommended by two well known men Edward Abbot and T.A. Lascelles. The letter stated that Waddle had been under his charge on the "Indefatigable" in 1812, but that he could not vouch for his conduct since Waddle had been living in Launceston. The next document in this file (CSO1/118/2968 is a deposition by Joseph Beresford to, whose sister Sarah, Waddle was married. He stated that she had married him about 8 years previously, had two children by her and had lived on a farm of 520 acres (210ha) which her father had settled upon her. He testified to Waddle's ill-treatment of his wife, and his association with Catherine O'Brien, the daughter of a Neighbour. He went to the North about 4 1/2 years before taking with him Catherine O'Brien and one of the children (one of his wifes).He (Beresford) had heard that Waddle kept an Inn and still lived with O'Brien, by whom he had five children, four of whom had not lived. He concluded " My father was a Marine and came out to New South Wales with Colonel Davey who used occasionally call at his house. I have heard Waddle say he would never have married my sister had he not expected to have got his emancipation by it thro' the interest my father had with Colonel Davey."
Arthur's first reaction to this and the petition was that very erroneous information must have been given to him on the previous occasion, otherwise he would never have authorized land to Waddle. He presumed that no grant had been made, and hoped it was not too late to have the land made available to his wife and children. "In the next place he is a most improper person to be allowed to keep a public house. After these observations it is scarcely necessary to add that he will get no free pardon from me." It appeared from the reference to the survey department that a grant deed for the 200 acres had not been issued, so that it could still be made available to Waddle's wife and family. Arthur therefore ordered that the Crown Solicitor should be asked the best way in which this might be done.
However, before the Crown Solicitor's opinion was received, the police magistrate in Launceston had enquiries made about Waddle and had discovered that in 1882 Waddle, then in Launceston had sent for his wife because of his "housekeeper's" ill treatment of his little boy. She had refused to go, Waddle explained that, after having lived unhappily with Sarah for some time they had agreed to separate, and had articles of separation drawn up by a lawyer in 1823. He had taken the eldest of their two children, the boy, to Launceston, and settled property on his wife. The little girl remained under Sarah's care and was sent to school at his expense. He had sent for the little girl when he heard that she was being miss-treated by Sarah, but she had refused to part with her. Since then he had heard that his wife was living with a man named Bannister, and this was confirmed by Magistrate Lascelles. Therefore, when the crown solicitor reported on 9th October 1827, that the land could either be granted direct to Sarah or to a third party as her trustee. Arthur wrote "I have since obtained positive information that the wife of Waddle is herself living in adultery - it is not therefore necessary that I should take any further interest in her behalf, and the grant may be issued according to the original intention"
Encouraged by this Waddle in 1829 made application for an additional grant. He stated he had lived on his grant near Launceston since 1825, and had kept an Inn about 1 1/2 miles (2 1/2 Km)from there. The Land Board recommended that he should be given an additional 300 acres (122 ha), and Arthur agreed to approve provided that the additional land adjoined his present holding so that he could superintend both personally. But circumstances made it necessary to locate the additional land elsewhere, and Arthur approved (CSO1/190/4509).
Alexander Waddle became a wealthy merchant and owned property all over Launceston, and well after he had set-up house with Catherine O'Brien he had a relationship with Mary Ann Porter. The children of this relationship were Sarah Ann B 6-3-1836, Alexander James B 25-10-1838, George
b1-4-1842 and twins Jessie and Mary B 27-7-1843, but died that year.
Alexander James married Elizabeth Bracey 8-4-1860 in Launceston. He was 21 and she was 18. The reg No of the certificate is 367.
They had eleven children, male b 26-12- 1859,Napoleon b 10-8-1861, Victoria b 1-8-1863, female
b 14-8-1865, Ada Elizabeth and Ada Alexandra 14-6-1869, Eva b 23-6-1871, Minnie b 7-11-1876,
Verbina Margaret Elizabeth b 27-7-1878, Charles Henry Warren b26-6-1881 and Alberto7-6-1883Burial:
9 December 1852, Cypress St Cemetery, Launceston, Tasmania
Cause of Death: Influenza
My GGG GrandUncle Married Agnes Theresa O'Brien
Thomas was born in Lusk a village in Co. Dublin circa 1795. He was convicted at Dublin County Court of highway robbery and sentenced to transportation for life.
Soon after Thomas' arrival in Port Jackson he was transferred to Hobart Town on the 'Elizabeth Henrietta'. On 11 Dec 1820 he married Agnes the daughter of Thomas O'Brien and Susannah Mortimore. In the 1820 and 1823 musters Thomas appears as the servant of Robert Hay but by 1825 he has a Ticket of Leave. In 1841
Thomas has a Conditional Pardon. In the 1842 Cencus the family are recorded as living on Woodburn Estate in the Parish of Richmond.
Thomas was born in the Lusk district of County Dublin, Ireland in 1792, and probably baptised that year on July 23. His parents may have been John Cruise and his wife Bridget. Sponsors may have been Christopher Devine and Mary Thelle.
Thomas Cruise was, in October 1816, convicted of highway robbery and sent out, on a life sentence, to Van Diemans Land. After languishing in a local prison for five months, he set out from Cork Harbour on March 9 1817. The convicts were herded aboard the 400-ton vessel, "Pilot" on that day and arrived at Port Jackson New South Wales on July 29 1817.
A physical description of Thomas, taken after landing, recorded that he was five feet seven inches in height and of a ruddy complexion. He had light brown hair and hazel eyes. One of 280 male prisoners sent on from Sydney to Hobart Town,on board the "Elizabeth Henrietta" on which embarkation tok place on the 11th August 1817, he arrived on Sept 14th 1817. They were escorted by Lt Robinson and 18 privates of the 48th regiment, another 80 convicts commanded by Lt Reevely and the 46th regiment were sent overland to Port Dalrymple.
On Dec 11th 1820 Thomas still in bondage, married Agnes O'Brien, a free woman, in Hobart. Both were 25 years of age, while the witnesses to the wedding were Mary Ann O'Brien, the brides sister, and Michael Robinson.
Thomas is recorded as holding a "Ticket of Leave" in 1841, (Conditional Pardon)
Thomas worked as a laborer or farmer in Tasmania all his Life. It is possible that he was employed for a time on Thomas O'Briens farm (his father in law). Thomas settled in the Richmond district and ended his days there, on August 5 1877, he was 85. Cause of death was given as chronic Bronchitis and dropsy.
Burial: 8 August 1877, Enfield, Tasmania
Cause of Death: Chronic Bronchitis and dropsy
Medical Information: Disease with watery fluid collecting in the body. Over-swollen state.
My GGG GrandUncle married My GGG GrandAunt Margaret O'Brien
William was born about 1803 in or near Glasgow. He had a brother James and his parents were probably poor Tennant farmers. The boys drifted into crime as a result of poverty which was probably caused by the landlord forcing the family off the farm.
On the 9th August 1821 William was tried in Glasgow for stealing a silver watch with a wind up key,at that time his aliases were O'Neil and Morgan, in 1822 he arrived before the sheriff of Edinborough , he stated he stole the watch from a married man in Glasgow, he was sentenced to 14 years transportation on the 6th January 1823.
On the 15/7/1823 he was embarked on the Justitia Hulk at Woolwich (Thames Estuary, near London) to await transportation to the colonies. He was transferred to the "Asia" and left Portsmouth on the 28/8/23, he arrived in Hobart Town on the 19/1/24 at this stage he was 21 years old with a height of 5 foot 7 inches or 170cm,with grey eyes,dark hair, and fair skin. On arrival in Tasmaniahe was assigned to Valentine Chapman. On 10 September he was found guilty of insolence, given 50 lashes and sent to the penitentary by Knopwood. On 26th march 1826 champion charged him with being absent from his masters premises without leave, and was returned to the prisoners barracks. On 26 April 1826, while still at the Barracks, he was charged with having engaged in an assult with some soldiers,but it was discharged, with no prosecution offered. On 21 september 1826, now assigned to Thomas Stace, he was charged with being absent from muster and church, and repremanded by Robert Knopwood, only to repeat the same offence the following March.
He married Margaret O'Brien on the 5/2/1827 in St Davids church Hobart (980), having petitioned for permission to marry on thd 23rd December 1826. Permission was granted on 20 January 1827. The Rev'd William Garrard, Chaplain took the service.
The next monthh he was in trouble again, he was still assigned to Mr Stace, but living in his own premises with his wife. He was charged on 17th April 1827, "with harboring James Ingle and Henry Phillips, assigned servants to Peter degraves, and Thomas Sprout, assigned servant to Thomas Stace, in his house in Davey Street at 10 o'clock on the night of 15th April, and keeping a disorderly house for the reception of lewd persons of both sexes. "He was returned to the Prisoners Barracks.
It was this occasion that led to Thomas Simpsonbeing charged "with being in the house Of William McDonald with Catherine Porter, aged 14 years". Catherine was the niece of Margaret McDonald, and Simpson was a convict, and they were married five months later when she was still only 14.
Wliiiam sent a petition to Lieutenant Govenor Arthur in May 1827 :-
"The humble Memorial of William McDonald, respectfully sheweth:- That your excellency's memoralist arrived in the colony (per ship Asia) sentence 14 years Transportation now in the penitentiary.
The object of your memorialist's petition is to solicit that your Excellencymay be pleased to order an investigation into your memorialist'sconduct and if found satisfactory - your memorialist prays for the indulgence of being allowed to be out of the penitentiary and live with his wife and one child. Your memorialist flatters himself his conduct will bear scrutiny from this inspection and hopes your Excellency will condescend to take his case into your humane consideration".
After reports were considered on previous conduct and from his employer , the petition was refused.
The next month, on 11 June 1827, he was absent from his muster at one o'clock in nthe prisoners Barracks, and sent to the chain gang for one week. On 7th August 1827, still at the barracks, he was out after hours at 12 minutes past eight, and was reprimanded.
On the 6th November1827, while working in the stablesand lumberyard, he had in his possession a bundle of hay believed to be stolen, back he went to the barracks. On the 14th December 1827 he was absent from his gang or an hour and a half during the afternoon without leave and went back to the chain gang for a week.
He then went to work for the Post Office as a postman, on 24th September 1828 he was charged with
" having taken a horse, the property of some person unknown, for the purpose of riding to New Norfolk with his mail bags insted of walking". For this he was sent to the chain gang for two months, and it was recommended that he not be employed again in such a situation. He seems to have been a rogue and a larrikan.
On 2nd March 1829 and 23rd June 1829 he was in trouble for being drunk in the police Barracks, for which he spent ten days on the treadmill, for being drunk and neglecting his duty at the lumber yard, he was gien 25 lashes, and then for being drunk in the Barracks again another two weeks on the treadwheel.
Things became more serious when on the 5th January 1830 he was charged with stealing a watch belonging to Robert Cox of Elizabeth Town, New Norfolk. He was remanded for further examination and had a detainer lodged at the goal against him being confined and fully committed on another charge. It is not clear what these other charges were, although the press reported that he was convicted for stealing a pair of leather fronts worth two shillings (20cents), the property of William Clarke, a shoemaker, on 9th May ( Hobart Courier 9/1/1830) He was sentenced to twelve months hard labour.
on 14th January 1831 he was charged with stealing from the person of Robert Parkinson on thr 13th Jan two promissory notes worth five pounds each, and two more worth one pound each. He was committed for trial and sentenced to 14 years transportation.
on 6th March 1833, still in the prisoners barracks, he was found near Austin's Ferry on 20th February without a pass and was sentenced to Port Arthur for the remainde of his sentence, in irons. Clearly the authorities were out of patience with him.
On 3rd March 1836, having completed hid time in port Arthur, he was charged with not reporting himself in proper time at his establishment, and as forwarded to his station in custody. The 1837 census shows him living at Newtown with his wife Margaret and six children, all under 14 years of age. The last notation on his record was that he was sentenced to life in prison, or transportation, on the 1st January 1843, but there is no report in the press of any trial.
It must have been a very odd marriage, William was often incarcerated, and therefore away from home. But they still managed to have eight children between October 1826, before they were married, and 1845. There are some long gaps, in particular between 1833 and 1840, the time he was in Port Arthur.
It seems likley that William disappeared from the scene in 1843 after he was sentenced to life in prison, and may well be the man of that name who died at Port Arthur on 4th May 1861 from disease of the Brain, (839), aged 52. the father of Emma Jesse must be in doubt and the logical conclusion is that she was fathered by Thomas cridge, but that is only conjecture.
Margaret moved to Victoria with Thomas Cridge and they were married in St James's Melbourne in 1853, (6286). Their daughter Ceila must have been born around that time, although her birt was not registered. At least some of Margarets older children crossed the strait with her. She was then 46 and Thomas was 33.
Thomas Cridge came on the scene in1844 when he was mustered at Glenorchy.
On the 17/6/1851 William was granted an absolute pardon on the condition that he did not return to England or remain in Van Dieman's Land.
This is an attempt to translate from the original notes from a photocopy of his prison record .
337 Donald Wm Mc Asia 1824 (ship and arrival date)
Edinbro Jan 7-6 1823 = 14 (place, date and sentence)
March 1 1826. Champion / Absent from his master without leave no prov returned to public works
April 20 1826. Public works/ Engaged in an ? with some soldiers yesterday dis.s no pros.r
Sept 21 1826. absent from Muster and Church on Sunday last reported (rev R.K)
March 3 1827. (Thomas) stace/ Absent from Church Muster last Sunday reported (-HH-)
April 17 1827. Stace/ Harbour & at Ingle & Henry Phillips assigned servant to Thomas Stace in his McDonalds House in Davey Street at 10 o'clock of 15th April & keeping a disorderly house for the reception of lewd persons of both sexes prisoner barracks/arv. (see notes on Thomas Simpson )
Sept10 1825. Young / insolence accorded 50 lashes & penitentiary (Rev RK. GI. AG & 18 prisoners)
June 11 1827.Prisoner Barracks /absent from muster yesterday at one O'clock at the prison Barracks, chain gang one week (prison sentence)
August 1 1827. Public Works / Out after hours last night at 1/2 past 8 O'clock reported ( T A S) could be Thomas A Stace.
Dec 14 1827. Prisoner Barracks /Absent from his gang for an hour and a half yesterday afternoon without leave, chain gang 7 days (prison sentence)
Nov 6 1827. Stables Lumber yard/ having in his possession a bundle of hay believed to be stolen & unable to satisfactorily account for it - prisoner barracks (T A S )
Sept 24 1828. Collicott/ Drunk and absent from his lodgings at 9 O'Clock last night 7 days tread wheel (& upside)
Nov 17 1828. Theft at the Post Office /charged with having taken a horse the property of some person unknown for the purpose of riding to New Norfolk with his mail bags instead of walking - 2 months chain gang, and recommended not to be employed again at the Post Office.
March 2 1829. Prison Barracks/ Intoxicated in the prison barracks on Sunday night last tread wheel
10 days ( prison sentence)
May 7 1829.Prison Barracks / drunk and neglecting his duty at the lumber yard 25 lashes (Prison sentence )
June 23 1829. Committed for trial for stealing a hat and two pieces of leather in R Clarkes, D W/house ( J Spode)
June 1 1829. Prison barracks / Intoxicated last night in the prisoners barracks tread wheel ? days (prison sentence)
Jan 5 1830. Public works/ Stealing a watch of the goods and chattels of Robert Cox of Elizabeth Town New Norfolk. Remanded for further examination and a detainer lodged at the goal against him, he being confined and fully committed upon another charge ( C P M)
Jan 14 1831. public works/ Stealing from the person of Robert Parkinson on the 13th of this month at Hobart Town two promissory notes for the payment of Five Pound each value five pound each, and two other promissory notes value one pound each the property of said Robert Parkinson, committed for trial (committed)
March 6 1833. public works/ found near Austins Ferry on 20th February with a ?? . to be removed to Port Arthur for the remainder of his sentence in irons /A P M , L I S.
March 30 1836 public works/ not reporting himself in proper time at this establishment, to be forwarded to his station in custody/ p.s/ supply v.p. 176
17-3-1834 P T Office 29-4-1834
? April 1836.............. to leave barracks when ordered to be ? counted............to be sent to Port Arthur to work at his trade for 6 months he being a sawyer. ps/Aug 3 1837 having a fishing line in his possession 14 days chain gang/ Port Arthur. March 2 1837 fighting (3 weeks chain gang/Port Arthur. April 3 1837 ? suspicion of pilfering vegetables, 2 months Port Arthur. April 3 1838 ? leave to R C Murray.......... from work very disorderly.......... afterwards to be ......... Port Arthur.......of s?. 1?-10-38 .......22-10-38 tl/ in a public house after hours............ days., 24-10-42.............to be sent ............. 26-2-43........ at the supreme court Hobartown 1st June 1843........... life... to be sent to Port Arthur for 3 years conduct
17-6-51 grant of absolute pardon available everywhere save the United Kingdom and the Island of Van Diemans Land.
My GGG GrandUncle Married My GGG GrandAunt Margaret O'Brien 2nd Marrage
Thomas was a convict, tried at the Somerset Quarter sessions on 2nd July 1838 for stealing wearing apparel from Thomas Rollins. He had a previous coniction for stealing a shirt. His sentence was transportation for 15 years. Thomas was a native of Somerset, aged 18, single, standing 5'5" (165cm) tall, with a pale complexion, brown hair hazel eyes, a small flat nose, and a scart on the left side of his mouth.
He arrived on the "Gilmore" on 22nd June 1839. For about 4 years he was assigned to J H Wedge, the surveyor and explorer, but a series of infringements led to him being returned to the Government on 9th October 1843. His ticket of leave came soon after, and he was working at Glenorchy, where he presumably met Margaret McDonald. Three minor offences against the Police Act and the Weights and Measures Act for which he was fined 1845 and 1847 suggest that he was engaged in some sort of shopkeeping or commerce.
In the 1856 Electoral role Thomas is listed as storekeeper, freehold Lt. Bourke St Melbourne. He is also listed as a farmer deep Creek, freeholder, Bacchus Marsh, Div.
Also, 1855 & 1876 Thomas Cridge, Hay & Corn Dealer, 11 Little Bourke St Melbourne Directories


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2018 - 19 Women's Water Polo News
Sasson Named Coach of the YearDecember 03, 2018After leading San Diego Mesa College to another PCAC water polo conference championship, head coach Emma Sasson was
Espinoza Earns Player of the YearDecember 01, 2018Sophomore center Imperia Espinoza was honored as the 2018 PCAC Player of the Year.
Breaking News: Mesa women's water polo wins back-to-back conference titlesNovember 04, 2018The women's water polo has done it again, back-to-back conference champions!
Olympians poised for title runOctober 29, 2018Heading into the 2018 campaign, the San Diego Mesa women's water polo team had more questions than answers on how they would defend the Pacific Coast Conference title.
2018 WOMEN'S WATER POLO IN-SEASON UPDATEOctober 08, 2018Women's water polo head coach Emma Sasson provides us with an in-season update on the 2018 campaign.
Race wide open for WWP titleOctober 05, 2018With half the season in the books, the race for the Pacific Coast Athletic Conference women's water polo title is very tight. The next three weeks will determine what program can call themselves champions of the PCAC.
Women's water polo defeats tough Orange Coast College team 16 – 14September 10, 2018After dropping the first two matches against Golden West College and Sierra College, the Mesa women's water polo team bounced back with an impressive win over Orange Coast College 16 - 14.
SD Mesa College 2018 Women's Water Polo PreviewSeptember 05, 2018Head coach Emma Sasson previews the upcoming 2018 women's water polo season.

subset: commoncrawl


text:
Check this document in the use of house design to combat Malaria:
Malaria is a mosquito-borne infectious disease affecting humans and other animals caused by parasitic protozoans(a group of single-celled microorganisms) belonging to the Plasmodium type.[2] Malaria causes symptoms that typically include fever, feeling tired, vomiting, and headaches. In severe cases it can cause yellow skin, seizures, coma, or death.[1] Symptoms usually begin ten to fifteen days after being bitten. If not properly treated, people may have recurrences of the disease months later.[2] In those who have recently survived an infection, reinfection usually causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria.[1]
The disease is most commonly transmitted by an infected female Anopheles mosquito. The mosquito bite introduces the parasites from the mosquito's saliva into a person's blood.[2] The parasites travel to the liver where they mature and reproduce. Five species of Plasmodium can infect and be spread by humans.[1] Most deaths are caused by P. falciparum because P. vivax, P. ovale, and P. malariae generally cause a milder form of malaria.[2][1]The species P. knowlesi rarely causes disease in humans.[2] Malaria is typically diagnosed by the microscopic examination of blood using blood films, or with antigen-based rapid diagnostic tests.[1] Methods that use the polymerase chain reaction to detect the parasite's DNA have been developed, but are not widely used in areas where malaria is common due to their cost and complexity.[5]
The risk of disease can be reduced by preventing mosquito bites through the use of mosquito nets and insect repellents, or with mosquito control measures such as spraying insecticides and draining standing water.[1] Several medications are available to prevent malaria in travellers to areas where the disease is common. Occasional doses of the combination medication sulfadoxine/pyrimethamine are recommended in infants and after the first trimesterof pregnancy in areas with high rates of malaria. Despite a need, no effective vaccine exists, although efforts to develop one are ongoing.[2] The recommended treatment for malaria is a combination of antimalarial medicationsthat includes an artemisinin.[2][1] The second medication may be either mefloquine, lumefantrine, or sulfadoxine/pyrimethamine.[6] Quinine along with doxycycline may be used if an artemisinin is not available.[6] It is recommended that in areas where the disease is common, malaria is confirmed if possible before treatment is started due to concerns of increasing drug resistance. Resistance among the parasites has developed to several antimalarial medications; for example, chloroquine-resistant P. falciparum has spread to most malarial areas, and resistance to artemisinin has become a problem in some parts of Southeast Asia.[2]
The disease is widespread in the tropical and subtropical regions that exist in a broad band around the equator.[1]This includes much of Sub-Saharan Africa, Asia, and Latin America.[2] In 2015, there were 296 million cases of malaria worldwide resulting in an estimated 731,000 deaths.[3][4] Approximately 90% of both cases and deaths occurred in Africa.[7] Rates of disease have decreased from 2000 to 2015 by 37%,[7] but increased from 2014 during which there were 198 million cases.[8] Malaria is commonly associated with poverty and has a major negative effect on economic development.[9][10] In Africa, it is estimated to result in losses of US$12 billion a year due to increased healthcare costs, lost ability to work, and negative effects on tourism.[11]
- 1Signs and symptoms
- 2Cause
- 3Pathophysiology
- 4Diagnosis
- 5Prevention
- 6Treatment
- 7Prognosis
- 8Epidemiology
- 9History
- 10Society and culture
- 11Research
- 12Other animals
- 13References
- 14Further reading
- 15External links
Signs and symptoms
The signs and symptoms of malaria typically begin 8–25 days following infection;[12] however, symptoms may occur later in those who have taken antimalarial medications as prevention.[5] Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms,[13] and can resemble other conditions such as sepsis, gastroenteritis, and viral diseases.[5] The presentation may include headache, fever, shivering, joint pain, vomiting, hemolytic anemia, jaundice, hemoglobin in the urine, retinal damage, and convulsions.[14]
The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days (tertian fever) in P. vivax and P. ovale infections, and every three days (quartan fever) for P. malariae. P. falciparum infection can cause recurrent fever every 36–48 hours, or a less pronounced and almost continuous fever.[15]
Severe malaria is usually caused by P. falciparum (often referred to as falciparum malaria). Symptoms of falciparum malaria arise 9–30 days after infection.[13] Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing, nystagmus, conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus, seizures, or coma.[13]
Malaria has several serious complications. Among these is the development of respiratory distress, which occurs in up to 25% of adults and 40% of children with severe P. falciparum malaria. Possible causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and severe anaemia. Although rare in young children with severe malaria, acute respiratory distress syndrome occurs in 5–25% of adults and up to 29% of pregnant women.[16] Coinfection of HIV with malaria increases mortality.[17] Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.[13]
Infection with P. falciparum may result in cerebral malaria, a form of severe malaria that involves encephalopathy. It is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever.[18] Enlarged spleen, enlarged liver or both of these, severe headache, low blood sugar, and hemoglobin in the urine with renal failure may occur.[13] Complications may include spontaneous bleeding, coagulopathy, and shock.[19]
Malaria in pregnant women is an important cause of stillbirths, infant mortality, abortion and low birth weight,[20] particularly in P. falciparum infection, but also with P. vivax.[21]
Malaria parasites belong to the genus Plasmodium (phylum Apicomplexa). In humans, malaria is caused by P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi.[22][23] Among those infected, P. falciparum is the most common species identified (~75%) followed by P. vivax (~20%).[5] Although P. falciparum traditionally accounts for the majority of deaths,[24] recent evidence suggests that P. vivax malaria is associated with potentially life-threatening conditions about as often as with a diagnosis of P. falciparum infection.[25] P. vivax proportionally is more common outside Africa.[26] There have been documented human infections with several species of Plasmodium from higher apes; however, except for P. knowlesi—a zoonotic species that causes malaria in macaques[23]—these are mostly of limited public health importance.[27]
Global warming is likely to affect malaria transmission, but the severity and geographic distribution of such effects is uncertain.[28][29]
Life cycle
In the life cycle of Plasmodium, a female Anopheles mosquito (the definitive host) transmits a motile infective form (called the sporozoite) to a vertebrate host such as a human (the secondary host), thus acting as a transmission vector. A sporozoite travels through the blood vessels to liver cells (hepatocytes), where it reproduces asexually (tissue schizogony), producing thousands of merozoites. These infect new red blood cells and initiate a series of asexual multiplication cycles (blood schizogony) that produce 8 to 24 new infective merozoites, at which point the cells burst and the infective cycle begins anew.[30]
Other merozoites develop into immature gametocytes, which are the precursors of male and female gametes. When a fertilized mosquito bites an infected person, gametocytes are taken up with the blood and mature in the mosquito gut. The male and female gametocytes fuse and form an ookinete—a fertilized, motile zygote. Ookinetes develop into new sporozoites that migrate to the insect's salivary glands, ready to infect a new vertebrate host. The sporozoites are injected into the skin, in the saliva, when the mosquito takes a subsequent blood meal.[31]
Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar and do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They usually start searching for a meal at dusk and will continue throughout the night until taking a meal.[32] Malaria parasites can also be transmitted by blood transfusions, although this is rare.[33]
Recurrent malaria
Symptoms of malaria can recur after varying symptom-free periods. Depending upon the cause, recurrence can be classified as either recrudescence, relapse, or reinfection. Recrudescence is when symptoms return after a symptom-free period. It is caused by parasites surviving in the blood as a result of inadequate or ineffective treatment.[34] Relapse is when symptoms reappear after the parasites have been eliminated from blood but persist as dormant hypnozoites in liver cells. Relapse commonly occurs between 8–24 weeks and is commonly seen with P. vivax and P. ovale infections.[5] P. vivax malaria cases in temperate areas often involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite.[35] Reinfection means the parasite that caused the past infection was eliminated from the body but a new parasite was introduced. Reinfection cannot readily be distinguished from recrudescence, although recurrence of infection within two weeks of treatment for the initial infection is typically attributed to treatment failure.[36] People may develop some immunity when exposed to frequent infections.[37]
Malaria infection develops via two phases: one that involves the liver (exoerythrocytic phase), and one that involves red blood cells, or erythrocytes (erythrocytic phase). When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver where they infect hepatocytes, multiplying asexually and asymptomatically for a period of 8–30 days.[38]
After a potential dormant period in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells to begin the erythrocytic stage of the life cycle.[38]The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.[39]
Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their host cells to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.[38]
Some P. vivax sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead, produce hypnozoites that remain dormant for periods ranging from several months (7–10 months is typical) to several years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in P. vivax infections,[35] although their existence in P. ovale is uncertain.[40]
The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.[41] The blockage of the microvasculature causes symptoms such as in placental malaria.[42] Sequestered red blood cells can breach the blood–brain barrier and cause cerebral malaria.[43]
Genetic resistance
According to a 2005 review, due to the high levels of mortality and morbidity caused by malaria—especially the P. falciparumspecies—it has placed the greatest selective pressure on the human genome in recent history. Several genetic factors provide some resistance to it including sickle cell trait, thalassaemia traits, glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy antigens on red blood cells.[44][45]
The impact of sickle cell trait on malaria immunity illustrates some evolutionary trade-offs that have occurred because of endemic malaria. Sickle cell trait causes a change in the hemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow capillaries; however, when the modified hemoglobin S molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together forming strands that cause the cell to sickle or distort into a curved shape. In these strands the molecule is not as effective in taking or releasing oxygen, and the cell is not flexible enough to circulate freely. In the early stages of malaria, the parasite can cause infected red cells to sickle, and so they are removed from circulation sooner. This reduces the frequency with which malaria parasites complete their life cycle in the cell. Individuals who are homozygous (with two copies of the abnormal hemoglobin beta allele) have sickle-cell anaemia, while those who are heterozygous (with one abnormal allele and one normal allele) experience resistance to malaria without severe anemia. Although the shorter life expectancy for those with the homozygous condition would tend to disfavor the trait's survival, the trait is preserved in malaria-prone regions because of the benefits provided by the heterozygous form.[45][46]
Liver dysfunction
Liver dysfunction as a result of malaria is uncommon and usually only occurs in those with another liver condition such as viral hepatitis or chronic liver disease. The syndrome is sometimes called malarial hepatitis.[47] While it has been considered a rare occurrence, malarial hepatopathy has seen an increase, particularly in Southeast Asia and India. Liver compromise in people with malaria correlates with a greater likelihood of complications and death.[47]
Owing to the non-specific nature of the presentation of symptoms, diagnosis of malaria in non-endemic areas requires a high degree of suspicion, which might be elicited by any of the following: recent travel history, enlarged spleen, fever, low number of platelets in the blood, and higher-than-normal levels of bilirubin in the blood combined with a normal level of white blood cells.[5]Reports in 2016 and 2017 from countries were malaria is common suggest high levels of over diagnosis due to insufficient or inaccurate laboratory testing.[48][49][50]
Malaria is usually confirmed by the microscopic examination of blood films or by antigen-based rapid diagnostic tests(RDT).[51][52] In some areas, RDTs need to be able to distinguish whether the malaria symptoms are caused by Plasmodium falciparum or by other species of parasites since treatment strategies could differ for non-P. falciparum infections.[53]Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010.[54] Despite its widespread usage, diagnosis by microscopy suffers from two main drawbacks: many settings (especially rural) are not equipped to perform the test, and the accuracy of the results depends on both the skill of the person examining the blood film and the levels of the parasite in the blood. The sensitivity of blood films ranges from 75–90% in optimum conditions, to as low as 50%. Commercially available RDTs are often more accurate than blood films at predicting the presence of malaria parasites, but they are widely variable in diagnostic sensitivity and specificity depending on manufacturer, and are unable to tell how many parasites are present.[54]
In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell person who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become common to use only a history of fever as the indication to treat for malaria—thus the common teaching "fever equals malaria unless proven otherwise". A drawback of this practice is overdiagnosis of malaria and mismanagement of non-malarial fever, which wastes limited resources, erodes confidence in the health care system, and contributes to drug resistance.[55] Although polymerase chain reaction-based tests have been developed, they are not widely used in areas where malaria is common as of 2012, due to their complexity.[5]
Malaria is classified into either "severe" or "uncomplicated" by the World Health Organization (WHO).[5] It is deemed severe when any of the following criteria are present, otherwise it is considered uncomplicated.[56]
- Decreased consciousness
- Significant weakness such that the person is unable to walk
- Inability to feed
- Two or more convulsions
- Low blood pressure (less than 70 mmHg in adults and 50 mmHg in children)
- Breathing problems
- Circulatory shock
- Kidney failure or hemoglobin in the urine
- Bleeding problems, or hemoglobin less than 50 g/L (5 g/dL)
- Pulmonary oedema
- Blood glucose less than 2.2 mmol/L (40 mg/dL)
- Acidosis or lactate levels of greater than 5 mmol/L
- A parasite level in the blood of greater than 100,000 per microlitre (µL) in low-intensity transmission areas, or 250,000 per µL in high-intensity transmission areas
Cerebral malaria is defined as a severe P. falciparum-malaria presenting with neurological symptoms, including coma (with a Glasgow coma scale less than 11, or a Blantyre coma scale greater than 3), or with a coma that lasts longer than 30 minutes after a seizure.[57]
Various types of malaria have been called by the names below:[58]
|algid malaria
|Plasmodium falciparum
|severe malaria affecting the cardiovascular system and causing chills and circulatory shock
|bilious malaria
|Plasmodium falciparum
|severe malaria affecting the liver and causing vomiting and jaundice
|cerebral malaria
|Plasmodium falciparum
|severe malaria affecting the cerebrum
|congenital malaria
|various plasmodia
|plasmodium introduced from the mother via the fetal circulation
|falciparum malaria, Plasmodium falciparummalaria, pernicious malaria
|Plasmodium falciparum
|ovale malaria, Plasmodium ovale malaria
|Plasmodium ovale
|quartan malaria, malariae malaria, Plasmodium malariae malaria
|Plasmodium malariae
|paroxysms every fourth day (quartan), counting the day of occurrence as the first day
|quotidian malaria
|Plasmodium falciparum, Plasmodium vivax
|paroxysms daily (quotidian)
|tertian malaria
|Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax
|paroxysms every third day (tertian), counting the day of occurrence as the first
|transfusion malaria
|various plasmodia
|plasmodium introduced by blood transfusion, needle sharing, or needlestick injury
|vivax malaria, Plasmodium vivax malaria
|Plasmodium vivax
Methods used to prevent malaria include medications, mosquito elimination and the prevention of bites. There is no vaccine for malaria. The presence of malaria in an area requires a combination of high human population density, high anopheles mosquito population density and high rates of transmission from humans to mosquitoes and from mosquitoes to humans. If any of these is lowered sufficiently, the parasite will eventually disappear from that area, as happened in North America, Europe and parts of the Middle East. However, unless the parasite is eliminated from the whole world, it could become re-established if conditions revert to a combination that favors the parasite's reproduction. Furthermore, the cost per person of eliminating anopheles mosquitoes rises with decreasing population density, making it economically unfeasible in some areas.[59]
Prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the initial costs required are out of reach of many of the world's poorest people. There is a wide difference in the costs of control (i.e. maintenance of low endemicity) and elimination programs between countries. For example, in China—whose government in 2010 announced a strategy to pursue malaria elimination in the Chinese provinces—the required investment is a small proportion of public expenditure on health. In contrast, a similar program in Tanzania would cost an estimated one-fifth of the public health budget.[60]
In areas where malaria is common, children under five years old often have anemia which is sometimes due to malaria. Giving children with anemia in these areas preventive antimalarial medication improves red blood cell levels slightly but did not affect the risk of death or need for hospitalization.[61]
Mosquito control
Vector control refers to methods used to decrease malaria by reducing the levels of transmission by mosquitoes. For individual protection, the most effective insect repellents are based on DEET or picaridin.[62] Insecticide-treated mosquito nets (ITNs) and indoor residual spraying (IRS) have been shown to be highly effective in preventing malaria among children in areas where malaria is common.[63][64] Prompt treatment of confirmed cases with artemisinin-based combination therapies (ACTs) may also reduce transmission.[65]
Mosquito nets help keep mosquitoes away from people and reduce infection rates and transmission of malaria. Nets are not a perfect barrier and are often treated with an insecticide designed to kill the mosquito before it has time to find a way past the net. Insecticide-treated nets are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net.[66] Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa.[67] About 13% of households in Sub-Saharan countries owned ITNs in 2007[68]and 31% of African households were estimated to own at least one ITN in 2008. In 2000, 1.7 million (1.8%) African children living in areas of the world where malaria is common were protected by an ITN. That number increased to 20.3 million (18.5%) African children using ITNs in 2007, leaving 89.6 million children unprotected[69] and to 68% African children using mosquito nets in 2015.[70] Most nets are impregnated with pyrethroids, a class of insecticides with low toxicity. They are most effective when used from dusk to dawn.[71] It is recommended to hang a large "bed net" above the center of a bed and either tuck the edges under the mattress or make sure it is large enough such that it touches the ground.[72]
Indoor residual spraying is the spraying of insecticides on the walls inside a home. After feeding, many mosquitoes rest on a nearby surface while digesting the bloodmeal, so if the walls of houses have been coated with insecticides, the resting mosquitoes can be killed before they can bite another person and transfer the malaria parasite.[73] As of 2006, the World Health Organization recommends 12 insecticides in IRS operations, including DDT and the pyrethroids cyfluthrin and deltamethrin.[74] This public health use of small amounts of DDT is permitted under the Stockholm Convention, which prohibits its agricultural use.[75] One problem with all forms of IRS is insecticide resistance. Mosquitoes affected by IRS tend to rest and live indoors, and due to the irritation caused by spraying, their descendants tend to rest and live outdoors, meaning that they are less affected by the IRS.[76]
There are a number of other methods to reduce mosquito bites and slow the spread of malaria. Efforts to decrease mosquito larva by decreasing the availability of open water in which they develop or by adding substances to decrease their development is effective in some locations.[77] Electronic mosquito repellent devices which make very high-frequency sounds that are supposed to keep female mosquitoes away, do not have supporting evidence.[78]
Other methods
Community participation and health education strategies promoting awareness of malaria and the importance of control measures have been successfully used to reduce the incidence of malaria in some areas of the developing world.[79] Recognizing the disease in the early stages can prevent the disease from becoming fatal. Education can also inform people to cover over areas of stagnant, still water, such as water tanks that are ideal breeding grounds for the parasite and mosquito, thus cutting down the risk of the transmission between people. This is generally used in urban areas where there are large centers of population in a confined space and transmission would be most likely in these areas.[80] Intermittent preventive therapy is another intervention that has been used successfully to control malaria in pregnant women and infants,[81] and in preschool children where transmission is seasonal.[82]
There are a number of drugs that can help prevent or interrupt malaria in travelers to places where infection is common. Many of these drugs are also used in treatment. Chloroquine may be used where chloroquine-resistant parasites are not common.[83] In places where Plasmodium is resistant to one or more medications, three medications—mefloquine (Lariam), doxycycline (available generically), or the combination of atovaquone and proguanil hydrochloride (Malarone)—are frequently used when prophylaxis is needed.[83] Doxycycline and the atovaquone plus proguanil combination are the best tolerated; mefloquine is associated with death, suicide, and neurological and psychiatric symptoms.[83]
The protective effect does not begin immediately, and people visiting areas where malaria exists usually start taking the drugs one to two weeks before arriving and continue taking them for four weeks after leaving (except for atovaquone/proguanil, which only needs to be started two days before and continued for seven days afterward).[84] The use of preventative drugs is often not practical for those who live in areas where malaria exists, and their use is usually only in pregnant women and short-term visitors. This is due to the cost of the drugs, side effects from long-term use, and the difficulty in obtaining anti-malarial drugs outside of wealthy nations.[85]During pregnancy, medication to prevent malaria has been found to improve the weight of the baby at birth and decrease the risk of anemia in the mother.[86] The use of preventative drugs where malaria-bearing mosquitoes are present may encourage the development of partial resistance.[87]
Malaria is treated with antimalarial medications; the ones used depends on the type and severity of the disease. While medications against fever are commonly used, their effects on outcomes are not clear.[88]
Simple or uncomplicated malaria may be treated with oral medications. The most effective treatment for P. falciparum infection is the use of artemisinins in combination with other antimalarials (known as artemisinin-combination therapy, or ACT), which decreases resistance to any single drug component.[89] These additional antimalarials include: amodiaquine, lumefantrine, mefloquine or sulfadoxine/pyrimethamine.[90] Another recommended combination is dihydroartemisinin and piperaquine.[91][92]ACT is about 90% effective when used to treat uncomplicated malaria.[67] To treat malaria during pregnancy, the WHO recommends the use of quinine plus clindamycin early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters).[93] In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia.[94][95] Infection with P. vivax, P. ovale or P. malariae usually do not require hospitalization. Treatment of P. vivax requires both treatment of blood stages (with chloroquine or ACT) and clearance of liver forms with primaquine.[96] Treatment with tafenoquine prevents relapses after confirmed P. vivax malaria.[97]
Severe and complicated malaria are almost always caused by infection with P. falciparum. The other species usually cause only febrile disease.[98] Severe and complicated malaria are medical emergencies since mortality rates are high (10% to 50%).[99] Cerebral malaria is the form of severe and complicated malaria with the worst neurological symptoms.[100]Recommended treatment for severe malaria is the intravenous use of antimalarial drugs. For severe malaria, parenteralartesunate was superior to quinine in both children and adults.[101] In another systematic review, artemisinin derivatives (artemether and arteether) were as efficacious as quinine in the treatment of cerebral malaria in children.[102] Treatment of severe malaria involves supportive measures that are best done in a critical care unit. This includes the management of high fevers and the seizures that may result from it. It also includes monitoring for poor breathing effort, low blood sugar, and low blood potassium.[24]
Drug resistance poses a growing problem in 21st-century malaria treatment.[103] Resistance is now common against all classes of antimalarial drugs apart from artemisinins. Treatment of resistant strains became increasingly dependent on this class of drugs. The cost of artemisinins limits their use in the developing world.[104]Malaria strains found on the Cambodia–Thailand border are resistant to combination therapies that include artemisinins, and may, therefore, be untreatable.[105]Exposure of the parasite population to artemisinin monotherapies in subtherapeutic doses for over 30 years and the availability of substandard artemisinins likely drove the selection of the resistant phenotype.[106] Resistance to artemisinin has been detected in Cambodia, Myanmar, Thailand, and Vietnam,[107] and there has been emerging resistance in Laos.[108][109]
When properly treated, people with malaria can usually expect a complete recovery.[110] However, severe malaria can progress extremely rapidly and cause death within hours or days.[111] In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment.[5] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria.[112] Chronicinfection without severe disease can occur in an immune-deficiency syndrome associated with a decreased responsiveness to Salmonella bacteria and the Epstein–Barr virus.[113]
During childhood, malaria causes anemia during a period of rapid brain development, and also direct brain damage resulting from cerebral malaria.[112] Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders, and epilepsy.[114] Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups.[112]
The WHO estimates that in 2015 there were 214 million new cases of malaria resulting in 438,000 deaths.[116] Others have estimated the number of cases at between 350 and 550 million for falciparum malaria[117] The majority of cases (65%) occur in children under 15 years old.[118] About 125 million pregnant women are at risk of infection each year; in Sub-Saharan Africa, maternal malaria is associated with up to 200,000 estimated infant deaths yearly.[20] There are about 10,000 malaria cases per year in Western Europe, and 1300–1500 in the United States.[16] About 900 people died from the disease in Europe between 1993 and 2003.[62] Both the global incidence of disease and resulting mortality have declined in recent years. According to the WHO and UNICEF, deaths attributable to malaria in 2015 were reduced by 60%[70] from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies.[67] In 2012, there were 207 million cases of malaria. That year, the disease is estimated to have killed between 473,000 and 789,000 people, many of whom were children in Africa.[2] Efforts at decreasing the disease in Africa since the turn of millennium have been partially effective, with rates of the disease dropping by an estimated forty percent on the continent.[119]
Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; in Sub-Saharan Africa, 85–90% of malaria fatalities occur.[120] An estimate for 2009 reported that countries with the highest death rate per 100,000 of population were Ivory Coast (86.15), Angola (56.93) and Burkina Faso (50.66).[121] A 2010 estimate indicated the deadliest countries per population were Burkina Faso, Mozambique and Mali.[118] The Malaria Atlas Project aims to map global endemic levels of malaria, providing a means with which to determine the global spatial limits of the disease and to assess disease burden.[122][123] This effort led to the publication of a map of P. falciparum endemicity in 2010.[124] As of 2010, about 100 countries have endemic malaria.[125][126] Every year, 125 million international travellers visit these countries, and more than 30,000 contract the disease.[62]
The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other.[127] Malaria is prevalent in tropical and subtropical regions because of rainfall, consistent high temperatures and high humidity, along with stagnant waters in which mosquito larvae readily mature, providing them with the environment they need for continuous breeding.[128] In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall.[129] Malaria is more common in rural areas than in cities. For example, several cities in the Greater Mekong Subregion of Southeast Asia are essentially malaria-free, but the disease is prevalent in many rural regions, including along international borders and forest fringes.[130] In contrast, malaria in Africa is present in both rural and urban areas, though the risk is lower in the larger cities.[131]
Although the parasite responsible for P. falciparum malaria has been in existence for 50,000–100,000 years, the population size of the parasite did not increase until about 10,000 years ago, concurrently with advances in agriculture[132] and the development of human settlements. Close relatives of the human malaria parasites remain common in chimpanzees. Some evidence suggests that the P. falciparum malaria may have originated in gorillas.[133]
References to the unique periodic fevers of malaria are found throughout recorded history.[134] Hippocrates described periodic fevers, labelling them tertian, quartan, subtertian and quotidian.[135] The Roman Columella associated the disease with insects from swamps.[135] Malaria may have contributed to the decline of the Roman Empire,[136] and was so pervasive in Rome that it was known as the "Roman fever".[137] Several regions in ancient Rome were considered at-risk for the disease because of the favourable conditions present for malaria vectors. This included areas such as southern Italy, the island of Sardinia, the Pontine Marshes, the lower regions of coastal Etruria and the city of Rome along the Tiber River. The presence of stagnant water in these places was preferred by mosquitoes for breeding grounds. Irrigated gardens, swamp-like grounds, runoff from agriculture, and drainage problems from road construction led to the increase of standing water.[138]
Additional educational resources
Willcox ML, Bodeker G, Rasoanaivo P. Traditional medicinal plants and malaria. Boca Raton: CRC, 2004—book contains detailed systematic reviews and guidelines for further studies in malaria control
The Research Initiative on Traditional Antimalarial Methods (www.who.int/tdr/publications/publications/ritam.htm)—features a report of the inaugural meeting of RITAM
World Health Organization Essential Drugs and Medicine Policy (www.who.int/medicines/organization/trm/orgtrmmain.shtml)—details WHO Traditional Medicine Strategy 2002-5


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Brentford travel to the Hawthorns on Monday night, looking to break their duck of three straight defeats in the Championship. Thomas Frank's side have a daunting prospect ahead of them. They have only managed to gain four points away from Griffin Park this season and West Brom have made their stadium one of the most difficult places to play in the Championship this season.
After conceding another three goals against Sheffield United on Tuesday, the need to improve defensively is pressing.
"They are a threat going forward, they create chances and play some great football, they're the best attacking team in the league we will have to have a big focus on defending," Frank said of Monday's hosts.
The Bees have only won one league game since Frank replaced Dean Smith in October, although some would claim they have been unfortunate. They have often showed promise in games in their passing combinations and movement, but their lack of concentration at the back has let them down repeatedly in key moments. They have lost six games by a solitary goal under the Dane.
Frank said: "Losing by one shows we're doing something right, but there's things we don't do well enough, that is conceding goals and game management, it's too big a pattern we concede too quickly after scoring or conceding."
As part of the preparation for Monday night, the Brentford head coach took the opportunity to add an extra training session on Friday afternoon, focusing on those who have not received the most first team minutes.
Frank also reiterated that new standards and new methods were being implemented in the two sessions: "We have some issues and areas we need to improve, obviously the defensive side of the game, we're conceding too many avoidable goals."
Their opponents on Monday have only lost at home twice all season and come into the game on the back of three consecutive wins as they look to get back into the automatic promotion spots.
Whereas the bottom half of the table encapsulates the unpredictability and competitiveness of the Championship, as Brentford — who are currently 18th in the league — find themselves ten points from the play-off positions, but will be fearful of the fact they are also only four points clear of the relegation zone.
"We are in a spell," Frank acknowledged. "And the only way out of it is hard work, toughness and togetherness from players, staff, fans and administration."
Featured Photographer/Darren Barnard


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KIX Blow New Jersey's Fuse
October 9, 2018, a year ago
Celebrating the 30th anniversary of their biggest album, Blow My Fuse (which was recently reissued as Fuse 30 Reblown with bonus tracks), Kix made a stop at the Starland Ballroom in NJ on October 7th. Back in action since 2004, the lineup is 4/5ths original: singer Steve Whiteman, Ronnie Younkins and Brian Forsythe on guitars, Jimmy Chalfant on drums, with Funny Money bassist Mark Schenker in place of Donnie Purnell. Having seen Kix many times over the years I have yet to see a bad show, and you'd never know Whiteman is 62. The guy still dances around full of energy, and has a lot of fun with the crowd during "Cold Blood" (asking the girls, and guys, who likes to suck dick).
Aside from the said album's hits, "Get It While Its Hot", "No Ring Around Rosie", and "She Dropped Me The Bomb" are often in the setlist. Deep cuts like "Piece Of The Pie" and "Boomerang" are ok, better live, and "Dirty Boys" works the best. The boys also bookended the show with two new songs ("Love Me With Your Top Down" and "Wheels In Motion") from the latest album Rock Your Face Off, Midnight Dynamite title track (still a great headbanger), and Hot Wire singles "Girl Money" and "Same Jane". "The Itch" the only song from their earlier years and the debut in 1981 was also played. Yes, Kix have been around that long. One of the few glam/hair metal names still bringing it like they did in the '80s.
Kix aren't for kids, they are for hard rockers.


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Water Warriors
By Anne Burke
Published Jul 1, 2006 12:00 AM
Copyright ©Diana Koenigsberg
YORAM COHEN LOOKS UP FROM THE PHONE. He's wearing an expression that says, "Wait 'til you hear this." Cohen is the director of the Water Technology Research Center at UCLA and one of the world's foremost experts on reverse-osmosis membrane desalination. He's talking to a developer who called looking for advice about installing a desalination plant at a housing tract in the San Joaquin Valley. Cohen finishes the conversation and chuckles.
"He wants to know if we're on top of our game!" One might ask if Kobe or Tiger is on top of his game. Cohen and his colleagues have put together the academic world's leading R&D program in reverse-osmosis, or "RO" membrane desalination — a process invented at UCLA nearly half a century ago.
RO desalination is the state-of-the-art technology for turning seawater and brackish water into fresh drinking water. But the process is still too problematic to be practical and economical for the parched masses. If we're going to meet the needs of a thirsty planet, we'll look to scientists like the 53-year-old Cohen (photo above) to help do it.
Freshwater Falloff
"Water, water, everywhere, nor any drop to drink," is as apt today as when Samuel Taylor Coleridge wrote "The Rime of the Ancient Mariner" in the 18th century. Seventy percent of the world's surface is covered in water, but only a tiny percentage of that is freshwater. Due to overconsumption, pollution and climate change, supplies of this most precious of natural resources are dwindling at an alarming rate.
Today, about 20 percent of the world's population lacks access to safe drinking water, according to the United Nations Environment Programme. More than 2.2 million people die each year from diseases associated with poor water and sanitary conditions, the UN reports. At any one time, half of the world's hospital beds are occupied by people suffering from waterborne diseases.
If present consumption patterns continue, two out of three people will live in water-stressed conditions by the year 2025, according to the UN's World Meteorological Organization. We can laugh at the chestnut attributed to Mark Twain — "Whiskey is for drinking, water is for fighting over" — but not at former World Bank Vice President Ismail Serageldin's unsettling prediction that the next world war will be fought not over oil or ideology, but water.
- The Road to Car-Free Commutes
- A Fine Balance
- Great Escapes
- CicLAvia: Heart of L.A. Takes Cyclists Back to UCLA's Origins
- Beyond the Library Walls


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Plainwell: Free mental health film
PLAINWELL—'The film "Resilience: The Biology of Stress and the Science of Hope" will be shown at the old Plainwell High School auditorium Thursday, May 10, from 6 to 8 p.m. The screening is designed as a childhood and youth mental health awareness event. The hour-long documentary presents a movement among some pediatrics, education, and social welfare professionals to combat the effects stress has on brain development in children. For more information on the film screening and to register for the free event, contact Becky Huberty at email@example.com or Amy Embury at email@example.com.


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Fish is one of the favorite seafood at home and most of the times it is the fish curry with pulao, as they are tangy in flavor & quick to make. The authentic Nellore Fish Curry recipe is quite popular in Andhra Telangana Regions. Even there are many restaurants that enlisted as Andhra Chepala Pulusu. Explore the exclusive taste of Traditional Andhra spices seeped into juicy fish pieces.
Nellore fish curry with special additions of tamarind extract and curry leaves gives incredible savor to your taste buds. Try out the recipe with detailed step by step recipe video.
Nutri facts about Nellore Fish curry
Fish is a rich source of omega-3 fatty acids, which is essential for the development of the brain and eyes.
They are high in many nutrients that most people aren't getting enough of. This includes high-quality protein, iodine, and various vitamins and minerals.
Fish May Lower Your Risk of Heart Attacks and Strokes
Omega-3 fatty acids can be beneficial against depression, both on their own and when taken with antidepressant medications.
Easy Nellore Fish Curry Recipe
- 20 Mins
- Persons: 3
- Difficulty: Easy
- Ingredients
- Coriander seeds: 2 tbsp
- Fenugreek: 1 tbsp
- Oil: 1/2 cup
- Mustard seeds: 1 tsp
- Onion: 3, chopped into half
- Tomatoes: 1 cup
- Curry leaves: few
- Red chilli powder: 5 tsp
- Turmeric powder: 1/2 tsp
- Salt: 2 tsp (use rock salt)
- Mix Well
- Tamarind: small lemon size
- Butter: 1 tbsp
- Brinjal: 3 medium size
- Raw mango: 1
- Making Procedure
- Soak tamarind water in little water for 15 minutes and extract juice from it and keep aside.
- Heat a kadai and add coriander seeds, fenugreek seeds and dry roast them for a minute or until color changed then add to blender.
- Make smooth powder from them and keep it aside.
- Take the same pan and heat oil in it, add mustard seeds, onions, and tomatoes and curry leaves to it and fry well by stirring regularly. Fry for 2 minutes.
- Then add red chilli powder, turmeric powder, coriander methi powder that prepared earlier and salt as per your taste and mix well.
- Add juice that extracted from tamarind to pan and mix well. Sauté it for 2 minutes.
- Now add fish pieces, dipping the fish pieces into curry gently, close the lid and simmer for 20 mins.
- You can add brinjal cutting in the middle vertically, (please refer the video to make sure) and butter 1 tsp and simmer for 15 mins.
- Check the pieces are cooked completely if not simmer for few more minutes. Add raw mango pieces to it.
- Close the lid and cook for 10 mins. if you feel more spicy adjust salt accordingly.
- Turn of the flame and serve hot with any flavored rice or steamed rice.
Mango should be added in the last
Adding brinjal is optional you can skip it if you don't like.
Use coriander leaf for garnishing and squeeze some lime some juice on top to finish it off.


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Sterile Processing Technician* – Not Currently Hiring
On the Job Training Available!
Casey Dental is not currently hiring for this position, but feel free to post your résumé so that we will have you on file if a position becomes available.
- Cleaning and sterilizing instruments
- Sterilizing dental operatories after patient care
- Maintain daily, weekly, and monthly equipment servicing in accordance with Casey Dental policy and update appropriate logs for maintenance and repairs
- Strong communication and organizational skills
- Must be a team-player
- Must have the ability to multi-task effectively
- Applicants must be self-motivated
- Must excel in task prioritization
*Training Available
Full-time benefits: Medical, Dental, and Vision Insurance. Paid time off. Optional FSA and 401k
Job Type: Full-time


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Accessibility Instructions
Accessible Entrance to Tapestry Opera Offices and Ernest Balmer Studio:
- Enter the Artscape Studio Building through either 15 Case Goods Lane (best level access for wheelchairs) or 60 Distillery Lane (Parking Lot side of building, but unfortunate slight bump at the door)
- Take elevator to 3rd floor.
- Turn right immediately as you exit elevator and proceed across a short pedestrian bridge connecting the 15 Case Good Lanes building to the 9 Trinity Street building. At the end of the short bridge turn left (only way to go).
- Then follow the hallway (and signage) right and then left towards Tapestry Opera. (Although the hall zig zags after the pedestrian bridge, it is an easy navigation as there is only a single hallway route to follow.)


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You started as a droplet inside a shell,
Warm, languid, liquid.
Now that safe harbour,
Has turned you into a sea.
To create you, every wonderful thing I've thought,
Every ray of light I've ever seen,
Was harnessed in that single drop.
To nourish…to divide,
Cell by cell
Pouring forward from me,
Toward my ultimate worth.
I didn't know it,
But until that point,
My world had been flat.
You helped me peek over the edge,
We looked into an unfolding universe,
Then you jumped with me!
A galaxy of light and giggles
Radiated through me,
To get to you.
Spirit and Soul,
Light and Hope.
You are so much more
Than an extension
Of my heart or limb.
I am, because of you.
You are, because of me.
Forever bundled in love,
I get to be your Mother.
© 2012


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Most Humble Players of UAAP Women's Volleyball of 2014Humblest UAAP Players, inside and outside the court. From a point-of-view of a Psychology Student.
The Top Ten
Alyssa, hands down! The only thing she does when she scores is either she points where the ball fell (to emphasize) or simply jump happily and celebrate a point with her teammates. And whether she creates a point or an error, she'll smile and recognize it anyway.
Her smile, whether she commits an error or she scores, it's just adorable. She's indeed one of the most humble players of this generation's women's volleyball.
Alyssa, when she is angry her face is always smiling;;;like an angel in the sky;;;go baldo I puts in a way mo;!
I love the way she played and lead her teamates
Shes so humble and adorable
Ara Galang is Ara Galang. I just love this player. Inside and outside the court, she stays humble. Not to mention that she's a great player. She rarely reacts whenever she scores, but when she does, you'll surely love it.
Not only she is dangerous inside the court but also silent and very humble person..
True star of the 76 team, but you would never hear her say it. hopefully will never adopt her former captains attitude (taunting, trash talk, complete lack of humility, etc. etc. etc. )
Yna Papa may be criticized for being inconsistent. But even so, she does not rant back not even once on all these destructive criticisms and bashes. She just held her head high, do what she do best and delivers at the right time
Yna Louise Papa is an adorable setter with just the right amount of swag. She has this great leadership in her which her team mates look up to. Very humble and unassuming.
Recently crowned as the Best Setter for the 11th season of Shakey's V-League. Go and add her on Facebook, she'll gladly accept you.
What she lacks in height, she makes up with heart. She plays behind the shadow of Gyselle Sy for the longest of time, yet won the best setter award (SVL) when she played as first setter for the first time. had she bragged about it? Not at all. Her passion when she plays is all over the place. She is gracious in defeat and humble in victory. #Team captain
This girl is approachable. I love her attitude, inside the court but outside it, you can actually hug her when you see her.
Beast Mode Don't Care. This girl surely has a lot of haters because of her court attitude. But who cares? We love her. True volleyball fans love her. If you don't, you're surely not a true volleyball fan. Oh, did I mention that she's also an epitome of a true captain?
She's one of the underrated setters in this season. I love how she belongs to the players who are just silent on court, those who don't show any facial expressions.
The "Silent Assassin" of the Lady Bulldogs. She rarely reacts whenever she scores, like Ara Galang, and when she does, her smile just melts the hearts of everyone.
She really is very humble. I can't find another player like Mina Aganon who just simply gives a straight face despite a very strong spike.
This girl is so cute. Her smile on court is something.
Denden can easily be mistaken for 'maldita' or 'snob' on and off court. I think it's her eyebrows and her eyes. But then she's really humble. Very underrated libero when, in fact, she's one of the best in her age.
I love her especially when she's on tough position doing aerial toss, best setter what can I say but stay on the other side without saying anything.. humble person
A friend once told me, "Si Kim Fajardo, nakita ko! Grabe sobrang bait and approachable." I actually agree to her. Kim made a fansign for my friend and gladly poses for the picture.
The Contenders
I actually had a chance to chat with her on her legit Facebook account and she's really nice. She kept on thanking me for supporting her and her team. Just by that, I can tell that she's a humble player. Not all players will give their time chatting with you on social networking sites.
Related ListsMost Beautiful UAAP Women's Volleyball Players Best Female UAAP Volleyball Player Best Female Volleyball Rookie Performance In the UAAP Top Ten Most Humble Male Singers and Groups Top Ten Most Humble Celebrities
List Stats
5 years, 200 days old