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We Need a Cure for Bacterial Vaginosis, One of the Great Enigmas in Women’s Health

Source: Lenka Vodstrcil & Catriona Bradshaw via The Conversation

Few have heard of bacterial vaginosis (BV) although it’s a relatively common condition. It affects at least 12% of Australian women, 30% of American women and up to 50% in parts of Africa.

Symptoms include a watery, milky discharge and fishy odour coming from the vagina.

Women with BV are more likely to get sexually transmitted infections (STIs) – such as chlamydia, gonorrhoea and herpes – and to transmit or acquire HIV. They are more likely to develop pelvic inflammatory disease, a painful condition that can result in infertility.

Pregnant women with BV are more likely to suffer miscarriages and deliver premature and low birth-weight babies.

Studies have shown women’s self-esteem, sexual relationships and quality of life suffer significantly from this infection. Women have reported BV symptoms make them feel embarrassed, “dirty” and concerned others may be able to detect their odour.

Many women with BV symptoms think they are experiencing thrush, and commonly report being treated for this. But BV doesn’t cause itching and there is often a noticeable fishy odour. Improper treatment for this condition leads to persistent symptoms, frustration and distress.

Why BV is hard to treat

Bacterial vaginosis is caused by groups of bacteria. This makes it different from other genital infections, such as chlamydia and gonorrhoea, where one bacterium is responsible.

While the cause of BV remains the subject of ongoing research, we do know there is a marked disruption of the vaginal bacterial community in women with BV compared to those with a healthy vaginal state.

BV is associated with a decreased number of good bacteria, known as lactobacilli, and an increase in bad bacteria. Lactobacilli dominate the healthy vagina, fighting bad bacteria and other other disease-causing agents.

Latest research into the bacterial profile of the vagina has suggested that as well as this imbalance, women with BV have a bacterial biofilm on their vaginal wall.

This is a kind of network and scaffolding of bacteria that cause cells to stick to each other. The biofilm blocks the body’s defence mechanisms and protects bacteria against antibiotics which have difficulty penetrating the biofilm.

Current treatment guidelines include seven days of either oral antibiotic tablets or the insertion of a vaginal antibiotic cream for seven nights.

These antibiotics have 80% to 90% cure rates one month after treatment. But more than half of treated women get BV back again within six months.

No other treatment approaches (longer antibiotic regimens, combinations of different antibiotics or supplementing antibiotics with probiotics to try and restore the healthy vaginal bacterial balance) have resulted in a sustained, long-term cure.

This is likely due to the bugs causing BV persisting after treatment or because women are being reinfected by their partners.

Sexual transmission

Trials between 1985 and 1997, where males were treated alongside their female partners, didn’t consistently reduce BV recurrence rates. These trials have since been shown as flawed and inconclusive.

Now there is mounting evidence to suggest sex is strongly linked with the acquisition of BV and its recurrence in treated women.

Studies have found women with male sexual partners who didn’t use condoms were consistently more likely to have BV. And women who have been treated and then re-exposed to the same partner were more likely to get their BV back.

Studies exploring bacterial communities on the penis have found BV-linked bugs under the foreskin and at the end of the urine tube. These were more common in men whose partners had BV than in those whose partners didn’t.

In African trials, female partners of circumcised males were found to have less BV than those of uncircumcised males.

Despite men not having associated symptoms, the data support the hypothesis that in treated women, sex with an untreated partner may be re-introducing the BV bugs responsible for high recurrence rates.

Other studies have shown women with female sexual partners were more likely to develop BV if they had more partners or a partner with BV.

We need a cure

The current state of BV treatment is unacceptable. Despite mounting evidence of sexual transmission, treatment of male and female partners of women with BV is not recommended by international guidelines, based on the trials two decades ago.

There are few conditions where doctors know that more than 50% of patients will be back with symptoms within six months. This characteristic of BV highlights the importance of finding the cause of high reinfection rates.

Failure to find a single organism responsible for BV and the difficulty in establishing whether BV is sexually transmitted have all been significant barriers to making progress with a cure.

A number of treatment strategies must be explored, include conducting well-designed clinical trials of partner treatment to see if eradicating the bacteria from women and their partners simultaneously (as we do routinely for STIs such as chlamydia) improves the cure rate.

It is quite possible that no single strategy will eliminate BV in all women and that combinations of approaches may be needed; including using antibiotics with biofilm-disrupting agents and partner treatment.

Drugs that disrupt biofilm are highly experimental, but will also be subject to clinical trials over the next few years and may prove essential in the fight to eradicate BV.

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Low or High Dose Oral Isotretinoin for Acne?

By Dr Vivienne Miller, GP and Fellow, The Royal Australian College of General Practitioners

Oral isotretinoin may be used in continuous twice weekly low dose (suppressive) or higher daily dose (curative).1

When used in high dose daily (usually for between four to eight months), Oral isotretinoin results in permanent reduction in acne in approximately 80% of cases.2 This mode of use is indicated particularly in patients who have scarring acne, especially when cystic and severe, those who have not adequately responded to oral antibiotics, the combined pill and topical treatments and those who are distressed by their skin.2,3 It should be remembered that younger adolescents and teenagers typically develop worse acne as they get older, but most people find their skin improves in their twenties onwards. Approximately 10% of women and 5% of men have ongoing “adult” acne4 and both suppressive and curative oral isotretinoin treatment is of benefit in this group too.

High dose oral isotretinoin is associated with symptoms such as dry skin, peeling, cheilitis, sometimes dry eyes, and in more severe cases of acne, skin redness and cystic flares.2,3 Low dose oral isotretinoin has far fewer side-effects. Any use of oral isotretinoin mandates exclusion of pregnancy before prescription and effective contraception during treatment, due to risk of serious birth deformities. Liver function tests and serum fasting lipids should be investigated prior to commencing oral isotretinoin and six weeks after treatment. This is ensure idiosyncratic hepatitis does not occur and that lipids are not dangerously raised before treatment begins.2 Care should also be taken before prescribing to patients who have diabetes, significant depression and alcohol problems.2

 

1. Akman, A. et al Treatment of acne with intermittent and conventional isotretinoin: a randomized, controlled multicenter study, Arch Dermatol Res. 2007 Dec; 299(10): 467–473.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2094720/

2. Sullivan, J. Oral isotretinoin  Aust Prescriber 2005;28:59-61. 1 June 2005
http://www.australianprescriber.com/magazine/28/3/59/61

3. See, J. Drug treatment of acne. Aust Prescriber 2012;35:180-2,  3 December 2012
http://www.australianprescriber.com/magazine/35/6/180/2

4. Rao, J.  Acne vulgaris, Medscape 11 Dec 2015
http://emedicine.medscape.com/article/1069804-overview#a7

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CREST Syndrome: Raynaud’s Disease vs Raynaud’s Syndrome

By Dr Vivienne Miller, GP and Fellow, The Royal Australian College of General Practitioners

Janet was a fifty-five year old music teacher and she had come to see the doctor the previous winter. At this time, she had noticed that in cold weather, early in the morning on the way to school, her fingers felt numb and were pale. She had not noticed this before, although she remembered having chilblains on her fingers and toes as a teenager. When she was questioned during that consult she told her GP that she had no problem putting her hands into the freezer to remove frozen foods and that her fingers went back to normal after she warmed them up; she had not noted any particular colour change. Janet was on no medications and had no medical problems, especially not arthritis. There was no family history of autoimmune conditions.

Janet returned almost a year later in late autumn. This time she was noticing similar symptoms to the year before, but her fingers felt stiff and this was affecting her ability to play musical instruments at times. She had no pain in her joints.

On examination, Janet had early sclerodactyly, telangiectasia of the nail cuticles and the skin on the ends of her fingers looked pale. She did not complain of any respiratory or swallowing problems and was otherwise well.

Janet has enough criteria to diagnose CREST Syndrome. This is an autoimmune connective tissue disease and stands for Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly and Telangiectasia. It is considered to be a more limited and milder form of systemic scleroderma and predominantly affects the hands (calcinosis around the joints of the fingers, telangiectasia, dermal thickening and oedema of the skin over the fingers and wrist joints resulting in contractures of the finger joints) and the oesophagus (distal hypomotility and reflux oesophagitis)  and is associated in approximately 10% of cases with a late presentation (many years after diagnosis) of pulmonary hypertension and, independently of this, bibasilar pulmonary fibrosis.1 The diagnosis is suggested clinically and typically, anti-nuclear antibodies and auto-antibodies to centromere proteins are positive (anti-Scl 70 antibodies carry a poorer prognosis and suggest systemic involvement).1 CREST syndrome is more common in middle aged women and in people of Indigenous African origin.

The pathology underlying CREST syndrome is that there is increased collagen deposition, fibrosis, a perivascular mononuclear cell infiltrate and vascular abnormalities (thrombosis, endothelial cell dysfunction, vasospasm) involving capillaries especially, most notably in the fingers. This is best seen as initially oedema (along with stiffness and arthralgia which lasts months to a year or so), then induration, with tightening and redness of the skin (lasting years) and finally atrophy of the digits.

The changes occurring in the hands in people with either Raynaud’s disease or the syndrome are initially pallor, numbness and burning discomfort, then cyanosis and discomfort and then redness and recovery after minutes to hours. The changes may involve the ears and nose and are typically related to exposure to cold or stress.2 The difference between Raynaud’s disease (also known as primary Raynaud’s) and Raynaud’s syndrome, or phenomenon (also known as secondary Raynaud’s) is that the former is not associated with any other symptoms or signs and is of excellent prognosis. Raynaud’s syndrome is associated with other conditions, classically connective tissue diseases, carpal tunnel compression, recurrent severe vibration, Buerger’s disease (accelerated arteriosclerosis associated strongly with cigarette smoking and affecting the extremeties especially). Raynaud’s syndrome is more difficult to manage than Raynaud’s disease and may result in ulceration and infection of the distal extremities from the calcinosis or ischaemia.2

Other associations of CREST syndrome and scleroderma include Sicca syndrome, primary biliary cirrhosis, glomerulonephritis (this may be rapidly progressive), myocardial fibrosis (usually focal) and an increased risk of cancer (especially in the lung).2

Other investigations include kidney function testing, respiratory function testing, if symptoms of dysmotility are present, a barium swallow and if myocardial disease or pulmonary hypertension is suspected, a cardiac echo. It should be noted that CREST syndrome carries a high risk of depression.

The management of the CREST syndrome includes physical means of preventing cold to the extremities, such as gloves and warming devices. Calcium antagonists increase blood supply to the extremities and are a first line management for Raynaud’s phenomenon. The management of oesophageal dysmotility may include antacids, mechanical means of reducing reflux (tipping the head of the bed, not lying down after eating); surgery is uncommonly indicated. Painful or ulcerated calcinosis may respond to debridement or excision. Intralesional steroid injections, oral colchicine and minomycin have all had some degree of success against calcinosis, but prevention of the lesions is currently not possible.

 

1. Yoon, J. & Elston, D. CREST Syndrome, Medscape, 15th Oct 2015
http://emedicine.medscape.com/article/1064663-overview

2. Mayo Clinic, Raynaud’s Disease, 4 March 2015
http://www.mayoclinic.org/diseases-conditions/raynauds-disease/basics/causes/con-20022916

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Zika Virus: What GPs Need to Know

By Dr Vivienne Miller, GP and Fellow, The Royal Australian College of General Practitioners

Zika virus is a flavivirus similar to Dengue fever and transmitted (mainly) though the Aedes aegypti mosquito, which is endemic in Northern Queensland, localised areas in Central Queensland and (Aedes albopictus) in the Torres Strait.  Appropriate mosquito vectors are currently not elsewhere in Australia.

Infection with the virus is asymptomatic in four out of five cases and is considered to be a mild febrile illness when symptoms occur. The incubation is three to twelve days. Symptoms and signs include fever (37.8 to 38.5°C), arthralgia, retro-orbital headache, diffuse maculopapular rash, conjunctivitis and post-viral fatigue.

The differential diagnosis is broad and includes malaria, rickettsial diseases, some bacteria, Dengue fever and many other viruses. Both acute (IgM) and convalescent (IgG) serum should be taken. Non-steroidal anti-inflammatories should be avoided until Dengue haemorrhagic fever has been excluded (these medications are contraindicated in pregnant women).

There is currently limited data about Zika virus and its complications in pregnancy. It has been associated with congenital abnormalities, notably, microcephaly, and other adverse fetal outcomes. These effects are assumed to occur at any gestation, but breastfeeding is safe.  Ideally, women considering pregnancy should not travel to countries in which there is a Zika virus outbreak. These include Central and South America, Samoa and Tonga. Islands comprising Micronesia and other more Western Pacific islands (including Fiji), have mosquito vectors present and have also been known in the recent past to have circulated Zika virus.

Summary of Recommendations for Clinicians and Public Health Practitioners

  • Zika virus infection should be considered in patients with acute fever, rash, arthralgia or conjunctivitis, who have travelled in the two weeks prior to onset of illness to areas with current or recent outbreaks or transmission; refer to the Department of Health Webpage: http://www.health.gov.au/internet/main/publishing.nsf/Content/ohp-zika-health-practitioners.htm
  • All travellers should take steps to avoid mosquito bites in order to prevent Zika virus infection and other mosquito-borne diseases such as dengue, malaria and chikungunya;
  • Until more is known about Zika virus transmission in pregnancy and the association with adverse fetal outcomes, pregnant women are advised to consider postponing travel to any area where Zika virus transmission is ongoing;
    • Pregnant women who do decide to travel to one of these areas are advised to consult with a doctor first and strictly follow mosquito bite prevention measures during their trip;
    • Women trying to become pregnant are advised to consult with a doctor before travelling and strictly follow mosquito bite prevention measures;
  • Zika virus infection is notifiable in Australia as a Flavivirus (unspecified) infection and should be notified to state and territory health departments;
  • In north Queensland and parts of central Queensland where mosquito vectors are present, clinicians should immediately report clinically suspected cases of Zika virus to local public health units, as they do for suspected cases of Dengue. Public health Authorities will take action to mitigate the risk of local transmission.

 

Australian Government Department of Health, Zika Virus – Information for Clinicians and Public Health Professionals, January 29th 2016
http://www.health.gov.au/internet/main/publishing.nsf/Content/ohp-zika-health-practitioners.htm

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98% of Women in Somalia have Undergone Female Genital Mutilation

Source: Cassie Werber at Quartz

The practice of female genital mutilation is more widespread, and affects many more women and girls, than previously thought, according to a new report from Unicef.

In the most-affected country, Somalia, 98% of the female population aged between 15 and 49 had undergone the procedure, the United Nations children’s fund says. Its report was released to mark International Day of Zero Tolerance for Female Genital Mutilation (FGM), which falls on Feb 6. As the Guardian notes, the initiation rite is often performed on girls as young as five, even if their parents don’t consent… Read More>>

Benson3

In 2015, Dr Jill Benson AM spoke about the FGM/C at the Healthed Women’s & Children’s Health Updates. To watch part of her talk, click here.

 

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Invasive Measurement of Blood Glucose No Longer Necessary

Source: Tohuku University via Medical Xpress

A group of researchers, led by Prof. Yuji Matsuura of Tohoku University’s Graduate School of Biomedical Engineering, has developed a method of measuring blood glucose using far infrared light, which is both harmless and non-invasive.

Diabetes patients traditionally monitor their daily blood glucose levels by using a conventional meter which requires blood sampling from the finger tips. The discomfort of pain and risk of infection can sometimes be a source of great stress and concern.

To address that, other researchers have proposed and developed non-invasive methods for glucose measurement using near infrared light. This method works on the premise that near infrared light of some specific wavelengths are selectively absorbed by glucose in the blood… Read More>>

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Researchers Connect Sleep Loss to Higher Rates of Illness

Source: Sleep via Medical Xpress

In 2009, Carnegie Mellon University’s Sheldon Cohen found for the first time that insufficient sleep is associated with a greater likelihood of catching a cold. To do this, Cohen, who has spent years exploring psychological factors contributing to illness, assessed participants self-reported sleep duration and efficiency levels and then exposed them to a common cold virus.

Now, Cohen, the Robert E. Doherty University Professor of Psychology in the Dietrich College of Humanities and Social Sciences, and researchers from UC San Francisco and the University of Pittsburgh Medical Center have confirmed that insufficient sleep is connected to an increased chance of getting sick. Published in the journal Sleep, the researchers used objective sleep measures to show that people who sleep six hours a night or less are more than four times more likely to catch a cold, compared to those who sleep more than seven hours in a night.

Aric Prather, assistant professor of psychiatry at UCSF and lead author of the study, said that the findings add to growing evidence emphasizing how important sleep is for health.

“It goes beyond feeling groggy or irritable,” Prather said. “Not getting enough sleep affects your physical health.”

Cohen’s lab is renowned for using the common cold virus to safely test how various factors affect the body’s ability to fight off disease. Prather approached Cohen about the possibility of investigating sleep and susceptibility to colds using data collected in a recent study in which participants wore sensors to get objective, accurate sleep measures… Read More>>

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‘BPA-Free’ Plastic Accelerates Embryonic Development, Disrupts Reproductive System

Source: Endocrinology via Medical Xpress

Companies advertise “BPA-free” as a safer version of plastic products ranging from water bottles to sippy cups to toys. Many manufacturers stopped using Bisphenol A to strengthen plastic after animal studies linked it to early puberty and a rise in breast and prostate cancers.

Yet new UCLA research demonstrates that BPS (Bisphenol S), a common replacement for BPA, speeds up embryonic development and disrupts the reproductive system.

Reported in the Feb. 1 edition of the journal Endocrinology, the animal study is the first to examine the effects of BPA and BPS on key brain cells and genes that control the growth and function of organs involved in reproduction.

“Our study shows that making plastic products with BPA alternatives does not necessarily leave them safer,” explained senior author Nancy Wayne, a reproductive endocrinologist and a professor of physiology at the David Geffen School of Medicine at UCLA… Read More>>

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Improvised Naloxone Nasal Sprays Lack Evidence of Absorption and Effect

Source: Addiction via Medical Xpress

Naloxone hydrochloride is a medication that can reverse the effects of an opioid overdose. First responders (peers, family, police, etc.) may prefer nasal sprays to injectable naloxone, which has led to widespread use of improvised naloxone kits with atomisers for nasal delivery of the drug. On 18 November 2015, the US Food and Drug Administration (FDA) approved a nasal naloxone product to replace those improvised kits.

In a debate paper published online by the scientific journal Addiction, top researchers at the National Addiction Centre at King’s College London criticise the extensive use of improvised nasal naloxone kits without testing and without regulatory approval. Improvised nasal naloxone kits were first introduced in the early 2000s in the absence of licensed non-injectable products, and today they continue to be used in the US (where improvised kits are still in circulation in the community) and also in an increasing number of countries where nasal Narcan has not yet been approved.

The authors point out that there isn’t enough information available on improvised nasal naloxone kits to warrant this level of acceptance. Improvised nasal kits consist of standard naloxone syringes (developed and licensed for injection), to which a nasal atomizer is attached. The formulation is not concentrated, as naloxone syringes are only commercially available in concentrations of up to 1mg/ml… Read More>>

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The Deadly Flea

By Peter Paisley, PhD, History of Medicine, UNSW

flea

Above is the most celebrated insect illustration – the flea, from Robert Hooke’s Micrographia (1665): a classic of microscopy, it is reproduced in many historical studies.  1665 was the year of the “great plague” in London, but the flea aroused no suspicion then as an agent of bubonic plague spread – nor did it, until the 1890s.  It is now common knowledge, purveyed by specialist and popularising works alike, that fleas transmit plague from rats or other infected species to humans.  But far from commonly known and sparsely mentioned, are the investigations which elucidated the flea’s role in epidemic plague.

In Asia, outbreaks of plague have probably continued regularly since the fourteenth century “Black Death”.  Sylvatic animal reservoirs of infection exist, for instance in gerbils, whose underground habitats serve to perpetuate the disease.  (The same is true of ground squirrels in California, where sporadic human plague cases continue to occur.) Even major Asian epidemics were unlikely to excite much European interest, until spread into Hong Kong and India in the late nineteenth century generated huge volumes of literature from plague commissions sent from many European countries.  When India and Hong Kong were engulfed, they were seen as extensions of Europe, so a third “world pandemic” was now announced.  Prolific sea trade threatened Europe itself, for the first time in over two centuries.  It was known that rat deaths coincided with human plague, but nobody causally connected the two until the 1890s.  It now seems obvious that fleas jumping from sick rats to healthy humans are likely plague vectors: but experiments showing this were ignored – worse, denounced by the “scientific” establishment, especially in England.

A Japanese physician working in Formosa, Ogata Masanori, demonstrated in 1897 that fleas harboured plague bacilli.  The implications for transmission to man were obvious, and should have been further examined immediately.  That was not the case, and only one established researcher paid attention. Paul-Louis Simond, working for the Pasteur Institute, in 1897 took over a post in Bombay vacated by Alexandre Yersin (co-discoverer of the plague bacillus in 1894 in Hong Kong), and worked on plague vaccines.  The following year he moved to Karachi, and while there, he demonstrated that plague from sick rats transferred to healthy rats in adjacent cages.  The most likely mechanism was the flea, which Simond was convinced was the responsible agent.  It was an obvious conclusion, given Ogata’s observations: but exact transmission details were yet to be demonstrated, so the flea theory, however persuasive, was still “only a hypothesis”.  In 1901, the British Plague Commission in India dismissed Simond’s work, thus:

“It will have become manifest that the process of induction by which Dr. Simond endeavours to establish the proposition that suctorial insects play an important part in the transference of plague from sick to healthy animals is so weak as to be hardly deserving of consideration.”

This was metaphysics, not biology – the key term being “induction”: Simond offered a hypothesis, but suspect French speculation transgressed English methodological Holy Writ, fortified by Newton’s dislike of hypotheses and firmly consolidated by Whewell and Mill in the 19th century.  Induction, not hypothesis and deduction, was to be practised (and this orthodoxy demanded that evidence was to be ignored, as necessary).

Meantime, plague was spreading round the world – and it was on its way to Sydney.  The Australian and Tasmanian Intercolonial Plague Conference, meeting in Melbourne in April 1900, declared that,

“The danger threatening Australia is more terrible than war.”

Busy port cities all over the world were vulnerable.  When plague reached Sydney in 1900, John Ashburton Thompson, president of the NSW Board of Health, accepted the logic of flea transmission.  Some human cases displayed signs of flea bites in the lower limbs: as Thompson said:

“I am unable to imagine any plausible explanation ……. which does not include some means of communication between them and the plague-rats which is complete in itself, endowed with locomotive powers, attracted to man by instinct, and more likely to reach this than any other part of the body.  These requirements betoken an insect, and the insect which best meets them appears to me to be the flea.”

plague poster

A poster from Sydney, 1905

Thompson managed the outbreak on that basis, but could not prevent politicians from evicting residents of the Rocks area of Sydney, demolishing their houses, and incarcerating so-called “contacts” in quarantine at North Head – measures whose validity were denied by Thompson.  When a second outbreak occurred in 1902, Thompson got his way, cutting out such senseless measures – thereby saving a large amount of human distress and public money.  A landmark had been passed – twice – namely, management of bubonic plague on what are now recognised as correct measures.  But the rest of the world seems to have paid no attention.

In terms of laboratory investigation, the jigsaw piece missing from Simond’s work had been supplied well before 1900, by a young member of the Indian Medical Service, William Glen Liston.  Liston’s elegant work involved placing fleas from plague infected rats in tubes sealed with muslin, through which they could bite but not escape: healthy rats were infected by their bites.  He also demonstrated that fleas from plague stricken rats had blocked digestive tracts, clogged by proliferating bacilli.  Hence, when they bit, instead of sucking blood, they regurgitated plague bacteria into the skin of healthy victims.  Astonishingly, the various Indian Plague Commissions ignored his research.  He went unrecognised until 1971, when the American Vetinary Epidemiological Society posthumously awarded him its Golden Headed Cane for his pioneering studies: the citation reads,

“On the basis of his work, plague control became possible, thus saving countless millions from this dread disease.”

Thompson, in 1900, was unaware of Liston’s work, but – convinced that Simond was right – he was first in the world to put the correct theory into public health practice.    It was, of course, not possible to take wholesale measures against fleas.  Rat-catching gangs were paid to hunt down the rodents: but, as Thompson saw, building regulations designed to exclude rats from human habitation were prophylactic, so he instituted appropriate regulations.  Likely places where rats might gain entry via openings for pipes – kitchens, bathrooms and lavatories – were required to have thick cement floors, something which persists to this day in our planning laws.

Sporadic outbreaks continued in Australia until 1921, when the last couple of cases occurred in South Australia.  In 1900, a Sydney diarist noted “extraordinary devices to prevent [rats] from leaving the ships”.  I assume this refers to discs on mooring lines, which, from the diary, seem to have been new at the time, at any rate in Sydney.  I’ve been unable to discover whether these were invented here: perhaps a reader can enlighten me.

 

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