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300 at hospital feared
exposed to TB by intern
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KINGSTON (CP) - Health officials are tracking down
about 300 patients and staff at Kingston General Hospital
who may have been exposed to tuberculosis after an intern
tested positive for the disease Tuesday.
Officials are also searching the country for people
who
have been in contact with the Kingston doctor and
another doctor, in Edmonton, who was his classmate
at medical school and has also been diagnosed with TB.
Skin tests will show whether any have developed
signs of the disease.
"I don't think there's any real emergency," said
Dr. John
Hoey, an Ontario regional medical officer of health.
Any new infections are "pretty unlikely. We just
have to be careful," Hoey said.
Dr. Dick Zoutman, an infectious disease specialist
at the Kingston hospital, said the intern is no longer
working, but is being treated at home.
"We believe he has the active disease," Zoutman
said
yesterday, but added he is reasonably confident it
has not spread.
The doctor had access to few patients, Zoutman
said.
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"We are expecting there will be no other persons
who have come into contact with the bacteria."
Only about one in 10 people who test positive will
develop the disease, officials said.
The two men, whose identities have not been revealed,
graduated this spring from the University of Alberta medical school.
One remained in Edmonton.
It will likely take a year to identify, test and
re-test more than 1,000 people who have been exposed to the men,
officials say.
Tests are repeated at intervals to ensure results
are consistent.
Officials initially identified about 500 people
who were in-advertently exposed before the Edmonton doctor was diagnosed
July 21 with a highly infectious form of TB.
One of those was-the Kingston intern.
Meanwhile, the physician treating the Edmonton
doctor, who has been quarantined in a local hospital, played down
the significance of two medical students contracting the disease.
Dr. Michael Lee said this case is no different
from any of the others reported annually.
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Airline air not fresh
NEW YORK — The passenger cabin air in almost a quarter of commercial
airline flights flunks the ventilation industry's standard for freshness,
a study by Consumer Reports magazine showed.
The magazine reported in the August issue that
the Boeing 757, which recycles nearly half its ventilating air,
had some of the highest carbon dioxide levels in the study. Flights
on the Boeing 747-400
had, on average, the freshest air in the study.
Newer model airliners have recirculation systems
that use less
fuel to treat outside air, saving airlines money but reducing
the amount of fresh air in cabins. Older models use 100 per cent
fresh air, newer models provide ' half fresh air and half re-circulated
air.AP
G.M. July 21.1994
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Global epidemic of TB feared
'Hot zones' rife with incurable form of disease
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WASHINGTON (AP-Reuters) — "Hot zones" of untreatable
tuberculosis are emerging around the world
and threaten a global crisis, the World Health Organization
said yesterday.
A study of 50,000 patients in 35 countries found
that a
third of the countries have a form of TB resistant to
multiple drugs. Untreatable cases account for 2 per cent
to 14 per cent of the world total.
That number is low, but WHO said lethal tuberculosis
could spread rapidly because only one in 10 patients gets
medical care appropriate to curb drug resistance.
"Hot zones" in India, Russia, Latvia, Estonia,
the
Dominican Republic, Argentina and the Ivory Coast
have so much drug-resistant TB that it threatens to
overwhelm local health systems, said the study by
WHO and U.S. health officials.
"This study shows definitively,
and for the first time,
what we most feared but could not previously prove:
Our world again faces the spectre of incurable
tuberculosis," said Dr. Michael lseman, TB chief
at the National Jewish Medical and Research
Centre in Denver,who reviewed the study.
Drug-resistant TB "is on every continent,
probably in
every country," he said.
Tuberculosis kills an estimated
3 million people annually.
About one-third of the world's population is infected.
The world's top infectious killer
is spread through
coughing and sneezing and can be highly contagious. The average
patient infects 10 to 20 people
a year.
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In a cruel irony, the deadly new strains have emerged
as a result of improperly administered TB drug therapies that long
have been successful in battling the disease around the world. "This
is a creation of man, not nature," lseman said.
Researchers have found that when the standard TB
antibiotics aren't given in their full and proper doses, the TB
bacteria not only survive but mutate into forms resistant to one
or more of the drugs. The resistant disease then can be spread to
other people.
The WHO study found spots where resistance to a
single drug is alarmingly high. It reached 100 per cent of treated
but not cured TB patients in Ivanovo Oblast, Russia, about 290 kilometres
east of Moscow. These people can be treated
with other drugs, but they're in danger because
the TB germ must make just one more mutation to become multidrug
resistant and lethal.
"It is inexcusable that after declaring tuberculosis
a global health emergency four years ago, we are losing ground today,"
said ArataKochi, director of who's global TB program, told a news
conference yesterday.
"If tuberculosis were a new disease, the world
would spare no expense to fight it."
Tuberculosis is the most common serious infectious
disease in the world. About 7 million new cases occur each year.
The bacterium usually infects the lungs, which allows the disease
to be transmitted through the air, especially in crowded, closed
environments.
With Washington Postfiles.
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TB 'Trojan horse' inside us
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WASHINGTON (Reuter) - American researchers
said yesterday they have discovered how tuberculosis bacterium and
its cousin leprosy invade cells, which could open new avenues for
treating the two ancient plagues.
The bacteria hijack one component of the
immune system and use it like a Trojan horse to sneak into immune
cells known as macrophages, which they then destroy, the researchers
reported in the journal Science.
"This study helps us understand what's
special about this bacterium and what makes it such an effective
pathogen," said Eric Brown of Wash
ington University in St. Louis, who helped
write the report.
Scientists have known the tuberculosis
bacillus invades macrophages — the immune cells that eat invaders
like bacteria — but they did not know how it got in.
It's not like every time the macrophages and mycobacteria
see each other the macrophages say: 'Hey, I'll grab you and drag
you in'," said microbiolo-gist Jeff Scholey, who also worked
on the study.
"They do it, but they don't always
do it to maximum efficiency." Brown and Scholey said the key
lies in another aspect of the immune system,
known as complement
Complement is a protein complex that helps
call in the macrophages and other immune cells when an invader is
detected.
Once its job is done, complement breaks
down into its components, which indude a protein known as C2a.
"This C2a, once it is released, it
floats around in the serum and it was believed for the longest time
it was non-functional," Scholey said. Instead. "the mycobacteria-
have learned, or adapted, to use it." Tuberculosis and other
mycobacter
ia like the one that causes leprosy and
one that causes avian tuberculosis can grab on to the C2a, which
attracts the attention of the macrophages.
"They think.- 'Okay, this is a bacteria
that is flagged for us to ingest and kill But what happens is the
mycobacterium has adapted other ways to circum vent that killing
mechanism," Scholey said.
Once inside the macrophage, the mycobacterium
thrives, eventually kill ing its host and causing disease be it
tuberculosis, leprosy or avian tubercu-losis.
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TUBERCULOSIS UPDATE
(Text of a presentation to the ORCS-MTYR seminar
Respiratory Update '92, November 6, 1992)
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Jean Barton
Historical Background
At the end of the seventies, it
seemed that
we were on the verge of the story: "Once upon a time
there was tuberculosis". The last chapter was near
, a happy ending in view and then a new twist. The unexpected drama
with the advent of HIV infection cou
ld not have been foreseen. Tuberculosis, the
plague of mankind, was discovered by prehistoric
anthropologists to be found in skeletal remains
from between 5,000 and 3,000 years B.C.
It was in the age of Pericles when
the Greeks
began to think as doctors and Phthisiology was
born - the study of the wasting disease of the
lungs. But it was not until the 19th century that
tuberculosis occupied centre stage. With the Industrial
Revolution the epidemic reached its climax. The progress
in the study of tuberculosis was methodical, logical and
rational. Pulmonary signs and symptoms became a
study, contagiousness was recognized and the
discovery of the bacillus responsible for the disease
was discovered.
At the beginning of the 20th century when the disease
was widely propagated, Sanatoria became part of the history of this
disease.During this period 70% of the
patients who initially benefitted from Sanatoria care were dead within
a ten (10) year period due to reactivation.
Pneuinothorax was a common procedure before the
arrival of antibiotics and with the aid of Strepiomycin in 1944, resectional
surgery replaced surgical collapse.
In 1952 isoniazid came on the market.
At this time,
treatment was for at least two (2) years using the
combination of streptomycin, isoniazid and P. A. S.
(paraamino salicylic acid), bedrest and often resectional surgery.
In 1974 the long awaited rifampin was made available to us at the
chest clinic level. Rifampin had been used for several years in
the Sanatorium
while it was under study for efficacy and side effects.
There were very few research papers available to us at
the time -only lots of rumours about the "new wonder
drug", that made possible the discharge of
many
patients from Sanatoria who could not achieve
sputum conversion with the drugs INH, PAS
and streptomycin.
The need for three (3) months or more in a
Sanatorium was no longer necessary.
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Shorter sputum conversion time meant
less disruption of income and family life. Treatment in the
mid '70s consisted of isoniazid and rifampin for 12-18
months and streptomycin and PAS seemed to be on
their way out. As our success rate increased, the trea
treatment time decreased, but the word "cure" was s
till not part of our vocabulary. We continued to follow
people for years.
In the late 1970s I first became aware of the problem
of
drug resistance and the need for patient
compliance was stressed. By this time
ethambutol was available at chest clinics and
multiple drug therapy and close monitoring by chest clinic
staff reduced the possibility of drug resistance. These
problems were just surfacing in the mid 70's in the
inner cores of the larger cities in the United
States. By 1980- 1981 all former Sanatoria wards were closed, many
converted to rehabilitation centres or chronic care facilities.
Chest clinics in Ontario were no longer viewed as necessary and
in 1982 the management of tuberculosis was returned to the family
physician and consultants.
As the morbidity and mortality rates fell in the
1960s and 1970s, we had medical students and many general practitioners
who had never seen an active case of tuberculosis and when they
did, many were happy to refer their patients to a chest clinic.
The busy general practice, I was told by many, did not have the
knowledge to deal with the variety of problems often associated
with tuberculosis, nor the time for recall and monitoring.
In the 1980s in the collective memory
the disease had disappeared and tuberculosis seemed on its way to
history books, like smallpox. Funds that should have been spent
on screening and treatment among high risk groups were diverted
elsewhere. The armistice was declared before the battle was won.
The apathy that I have watched set
in troubles me. I see and hear of numerous diagnosis errors and
treatment delays, sometimes leading to irreparable damage and occasionally
death. It is my hope that with what I share with you today, you
too will play a role in disrupting lhe apathy.
Continued on page 5
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Back to top
Ozone more deadly than first though,
U.S. study says
Tno Los Angeles Times LOS ANGELES —
New air pollution studies have concluded that ozone has acute health
effects at lower concentration: than previously thought and the
National Clean Air standard may no longer protect even healthy individuals.
Among the health effects at ozone levels near the
current standard were persistent reductions in lung capacity, aggravation
of respiratory diseases such as asthma, and increased hospital admissions
at times when ozone concentrations are at or near the Clean Air
Act standard. In addition, separate animal toxicology studies point
to the premature aging of lungs, structure damage and a weakened
ability to resist respiratory infections. It has long been known
that high levels of ozone — the principal component of smog — are
unhealthy for everyone. But, the new studies indicate low concentrations
decrease breathing ability even in athletes, especially when involved
in heavy exercise.
Published in the Ottawa, "Citizen" the week of
August 5th
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