Please help me with my pneumonia.

I’m in my third week of a bad case of pneumonia. I’m a 62 year old
male. I smoked most of my life but haven’t for the last 8 years or so.
I have been treated by a doctor with two different kinds of
anti-biotics and am much better but there is still some fluid in my
lungs. The doctor considered tapping my lung (left one) to drain the
fluid but decided it wasn’t necessary.

My request for help is what self help can I do to help my body get rid
of the fluid in my lungs. I am doing the percussion on my lung area
several times each day. I do deep breathing exercises. I’m taking
Guaifenesin Rx to assist in breaking up the fluid. I occasionally have
a coughing spell and get a little bit of mucus up. The mucus is clear
but very sticky.

Any help or suggestions would be appreciated.

I assume that you know that you have pneumonia because you had
a chest X-ray… Some forms of pneumonia can cause fluid in the
pleural space, and some pneumonias may take a long time to resolve.
The antibiotic regimen might make a difference, as not all antibiotics
cover the different potential causes of pneumonia. Furthermore,
without knowing more of your health history, medications, etc. it is
pretty much next to impossible to give accurate or complete
information…

When I see someone who comes in with a history of “persistent
pneumonia,” I like to check to see the films, review any cultures or
lab and examine the patient for signs of heart failure, aspiration,
connective tissue diseases, etc. A history of iv drug abuse or
unprotected high-risk sex would make me wonder about PCP pneumonia in
HIV infection. If your CXR showed an infiltrate along with partial,
persistent collapse of a segment of lung, I’d worry about a bronchial
blockage. Even though you stopped smoking, your past smoking history
puts you at risk for bronchogenic carcinoma, which can do this.
Fungal infections or infections with atypical organisms might not
respond to whatever it was that you’ve been given. You see, it is a
complicated issue. If you’re not improving, talk to your doctor about
having an internist or pulmonary specialist look you over… Hope that
helps without being too frightening.

Drink plenty of fluids. One of the greatest dangers, especially with
elderly patients, is dehydration. Because of your age and the prolongation
of signs and symptoms of your disease, I strongly suggest that you have a
medical professional assess you daily. You should go in for an immediate
evaluation by a physician because of the prolongation of the signs and
symptoms of pneumonia. Also, I suggest that you take the Pneumovax
vaccination which will prevent and/or ameliorate not only pneumonia but
many other diseases and conditions. You should go to a hospital
immediately, if you have trouble breathing, have an altered mental status
(feel drowsiness alert),have low blood pressure, and/or have any other
significant disease . Again, because of your age, I believe that you
should have your pneumonia and your general health condition checked daily
until the signs and symptoms of pneumonia disappear. I am not a physician.
The morbidity and mortality associated with pneumonia is high for
individuals over 70 especially if associated disease or risk factor.

AIDS is not caused by drugs. There were drugs before 1980 in the
U.S., but no AIDS. AIDS is a syndrome– an immune problem in which
almost all of the afflicted person’s lymphocytes disappear. The idea
that this happened to chronic drug users in the US before 1980, but
that somehow nobody noticed, is so ludicrous that it deserves to go

Again, essentially all of the patient’s lymphocytes disappear in AIDS.
They are gone! Gone from the blood, gone from the lymph nodes. They
AIDS is real. AIDS is new. It is not caused by drugs. It
continues to kill a million people a year in Africa, and it is not
just a new name for the same old illnesses. AIDS has different
features from the traditional illnesses in Africa, which are obvious
enough that any bright teenage student should be able to grasp them
after a few minutes of not very involved discussion. The mystery is
why a very few adults, even now, don’t seem to get it.

I believe in Africa that AIDS was spread thru hetrosexual action.

Big question: Why is AIDS a “new” disease beginning about 1980?
Have not people had immune system problems throughout history?

Think of the new Ebola and Hanta virus outbreaks. Think of the
new strains of flu virus that sweep the Earth periodically. Where do
new viral diseases in humans come from? Animals.

HIV-2, which causes AIDS in West Africa, is basically the same
virus called SIV in monkeys. It’s just SIV that has been transferred
to humans, and now causes disease in them. It doesn’t hurt monkeys,
but it causes AIDS in baboons and macaques.

HIV-1, the main AIDS virus, and the one which causes almost all
the disease in Africa and America, is closest in structure to a virus
found in chimpanzees. It probably came from chimpanzies, sometime
before 1959, spreading slowly in humans at first because of slow human
movement in equatorial Africa before industrial development. Not
surprizingly, HIV-1 causes a very mild disease in chimps. They lose
the same cells in their immune systems that humans do, but only a few
chimps given HIV-1 have lost enough to become ill enough to be classed
as having AIDS. From what we can see, however, the process of
infection of HIV-1 in chimps, and HIV-2/SIV in baboons and macaques, is
identical. The same part of the immune system is destroyed.

The worldwide outbreak of AIDS is apparently related to the
Kinshasha highway, which connected the main AIDS regions in equatorial
Africa (endemic areas for chimps) with the coast. From there it spread
to France in the early to mid 1970’s. Starting in 1976, a French
Canadian homosexual airline steward who had been in France spread the
disease to many gay men on both coasts of the United States. HIV was
recovered from serum specimens stored from vaccine tests in gay men in
the US, starting in 1978. It wasn’t seen before then. The first AIDS
case in the US showed up in 1980, and a number of cases caused the
problem to be recognized in 1981. The maximal rate of silent HIV viral
infections in gay men, in transfusions, and in hemophilia products was
in 1982, all before the clinical disease itself (which takes at least
several years to incubate in most people) had shown up more than a few
hospital cases. There wasn’t a test for HIV until 1985, and by then
it was too late for hundreds of thousands of people in the US, who had
already been infected.

Influenza Disease Updates

Los Angeles, CA (US) – CORRECTION on quote “500 deaths due to influenza”
(posted within “Disease Updates – 1/6 to…” thread) —
Someone was quoted out of context in a TV interview, and this error was
picked up by every radio, print & TV news outlet – incorrect quote was
“500 deaths due to influenza”. Here is how it happened, with correction…
The CDC tracks nationally the proportion of deaths each week of the
influenza season – 10/1 thru 4/30 – that have an underlying cause of
pneumonia or influenza. Since influenza is usually a clinical diagnosis,
few cases are actually confirmed. However, during an outbreak one can
expect to see a rise in the death rate approx. 2 to 4 weeks after
influenza arrives.

According to the “P & I Index” (Pneumonia & Influenza), for 12/97 a
preliminary total of 11.7% (580/4900) deaths in Los Angeles County listed
pneumonia as a contributing or underlying cause. What was left out was the
12/96 total, 12.3% (617/5000) – indicating there hasn’t been an increase
IN DEATHS associated with pneumonia, and certainly not 500 deaths due to
influenza specifically.

This does not mean there hasn’t been an increase in cases, it just
means there was no increase in deaths.

The number of influenza cases did rise suddenly in mid- to late
December ’97, in southern CA, with numerous doctors & hospitals reporting
capacity crowds.

According to physicians, there appears to be TWO DISTINCT ILLNESSES –
one is clearly influenza (influenza A/Sydney – see 1/11 post for details),
the other hasn’t been identified but it doesn’t have typical “flu”
symptoms of high fever & muscle ache, it consists mostly of low fever and
chronic dry cough that lasts for weeks. (I would think doctors would know
bronchitis when they see it, this illness hasn’t been identified as
bronchitis.)

These illnesses appear to have spread from Los Angeles County, to
Orange, Riverside & San Bernardino Counties, with ancedotal reports of
extremely busy outpatient services.

CHILE – The Ministry of Health reported 33 cases of cholera, 12 confirmed,
which have occurred since the last week in December ’97. All occurred in
rural areas of northern Chile, near the border with Bolivia.

Nairobi, KENYA – An outbreak of Rift Valley fever – already believed to be
the cause of 300+ deaths – has killed another 21 people in northeast
Kenya, authorities said today.
Red Cross officials urged residents to burn all animal carcasses, one
source of the virus.

Another source has been mosquitos, after recent flooding scattered the
insects’ eggs.

Symptoms of Rift Valley fever include high fevers, headaches and vision
problems. In severe cases, fatal hemorrhaging from the nose & other
orifices can occur.

SOMALIA – In the region just across the border from Kenya, dozens of
people have also died recently from Rift Valley fever. Exact figures not
available yet.

HONG KONG – A 25-year old woman, who contracted influenza A/H5N1 before
the chicken slaughter here, became the sixth person to die from the
outbreak.

Her death, on Wednesday, wasn’t expected to change an official
assessment, made earlier this week, that the ‘bird flu’ has been stopped.

HONG KONG – It was learned late Wednesday that a woman, 34, who died on
Sunday from chronic lupus was also infected with the so-called ‘bird flu’,
influenza A/H5N1 virus. She had been hospitalized since Dec. 28, 1997. She
was the fifth confirmed death, out of 18 confirmed cases & 1 suspected
case.

A Deutsche Presse-Agentur article, quoting a Hong Kong Health Dept.
official, reported a sixth death as of yesterday. This death has not been
confirmed yet, currently labeled a “suspected case of”.

Montreal, QUEBEC (Canada) – An influenza outbreak has hit ice-storm
victims, many of whom have been forced to live in crowded emergency
shelters due to the weather and power outages.

More than 60 cases of what UPI reported as “potentially fatal flu” have
been recorded so far. Public health officials are administering flu
vaccines in an attempt to head-off a possible epidemic among the estimated
14,000 Quebec residents still in over 150 shelters as of late Saturday.

Hydro-Quebec power officials said most areas should have power by
Wednesday.

Quebecians should thank their lucky stars they aren’t in Ontario, which
may not be up to close-to-full power until at least NEXT weekend.

Beijing, CHINA – Victims of the earthquake in northern China need
medicine to combat (guess what?) influenza, bronchitis and pnuemonia,
according to the International Federation of Red Cross and Red Crescent
Societies (IFRC), the result of people sleeping in the open since the
destruction of their homes, with outside temperatures dropping as low as
27 Celsuis (thats MINUS 16.6 F)

The IFRC will also provide food because stocks in the province were low
following drought last summer.

Even basic drugs are unavailable because clinics have also been
destroyed.

The IFRC has launched an appeal to raise 1.7 million Swiss francs
(equal to $1.14 million US dollars) to provide this aid, which was
reported by Reuters this weekend.

Hawaii has one of the lowest heart disease death rates
for men in the world but it is still the number one
cause of death for men in Hawaii. About 40% of all
deaths in Hawaii are cardiovascular related. Don
Weisman of the American Heart Association in Hawaii
said the “Men and Heart Disease, An Atlas of Racial
and Ethnic Disparity in Mortality” [1] is not useful
in Hawaii because it fails to examine ethnic subgroups,
in particular within the asian american community.
Weisman said that Native Hawaiians and Filipinos
have a higher risk of heart disease in Hawaii than
other API subethnic groups where APIs make up 70 percent
of the state’s population. Cardiologist William Dang, Jr
also concludes that Hawaiians have a higher risk of
contacting Heart disease and point to Diabetes as
a related disease that factors into this phenomena.
The study only analyzed aggregate racial groups:
Caucasian, African Americans, Hispanics, and
Asian pacific Islanders.

Annual Death Rates for Men 35 years old and over
due to Heart disease for the state of Hawaii

DeathRate per 100,000

Race/ethnicity 1995 pop men in 1991-1995

all 284,131 482

American Indian/Alaskans 1,217 insufficent data

AsianPacificIslander 177,321 490

Black 5,595 338

Hispanic 15,882 397

White 99,998 476

[1]
Men and Heart Disease: An Atlas of Racial and Ethnic Disparities in Mortality was developed by the
Office for Social Environment and Health Research at West Virginia University* and the
Cardiovascular Health Branch at CDC to provide critical data on geographic, racial, and ethnic
inequalities in men’s heart disease death rates for the five major racial and ethnic groups.
http://www.cdc.gov/nccdphp/cvd/mensatlas/index.htm

Source # 1: Lyme Disease by Patricia Coyle of State University of NY

Chapter 23 Lyme Disease in Pregnancy
Genevieve Sicuranza and David Allen Baker
Lyme borreliosis became a reportable disease in the United States in 1982, and
in 1991 a national surveillance case definition was established. The Centers
for Disease Control in its June 1991 report indicated an eighteenfold increase
in the number of cases from 1982 through 1989(13,500). Lyme disease was first
described in 1977 in Old Lyme, Connecticut, as a juvenile-arthritis type
syndrome associated with tick bites.'(ref 12) Although cases are concentrated
in the northeastern, midwestern, and Pacific United States, Lyme disease has
now been reported from most states. It is clearly an international problem,
with a marked increase in infected and symptomatic people in Europe and Asia as
well. Due to the rising numbers of cases each year, there has been increasing
concern about the potential impact of Lyme disease on the pregnant woman and
her fetus.
Lyme disease is caused by a spirochete, Borrelia burgdorferi, classically
carried by the deer tick, hodes dammini.(ref10) Other vectors have been
identified in New Jersey and Texas (Amblyomma americanum). (ref 11) Although
the deer is the preferred host of the adult tick, almost any bird or domestic
animal can act as an intermediate host. It is known that the fetus is quite
vulnerable to the transplacental passage of the syphilis spirochete, Treponema
pallidum. Because the causative agent of Lyme disease is also a spirochete,
there is concern that B. burgdorferi might also affect the fetus. This chapter
reviews the available information pertaining to Lyme disease in pregnancy and
discusses the diagnosis and management in this selected population. (See Color
Plate 8.)

PREGNANCY
Maternal infection may involve transmission of the invading microorganism to
the fetus. This may have no adverse consequences or may produce a range of
sequela from minor transient problems to fetal death and abortion. Among the
spirochetal bacterial infections, syphilis is known to cause abortion,
stillbirth, and congenital abnormalities. Maternal relapsing fever and
leptospirosis have also been associated with an increased risk of fetal loss.

Among animals, borreliae have been associated with bovine abortion. Whether
Lyme disease affects the pregnancy or the fetus has been a subject of several
studies. In 1985, Schlessinger (ref 8) documented transplacental transmission
of B. burgdorferi for the first time. The infant involved showed congenital
heart anomalies. An autopsy revealed numerous spirochetes in the spleen, kidney
and bone marrow. The chorionic villi had histologic evidence of involvement
with increased numbers of Hofbauer cells. The mother in question had been
infected during the first trimester and had not received treatment. The Centers
for Disease Control conducted a retrospective study on 19 women with Lyme
disease. (ref 5) There were five poor outcomes:
prematurity. cortical blindness, fetal demise, syndactyly, and rash. No
association was noted between a poor outcome and the trimester in which
infection occurred, or whether treatment was given. A second study conducted by
the Centers for Disease Control (ref 5) involved a prospective analysis of 17
females infected during the first trimester. In this small prospective study,
one infant was born with syndactyly and there was one spontaneous loss at 13
weeks. All the other pregnancies resulted in normal infants.
From 1986 through 1987, Nadal et a (ref 17) surveyed over 1000 mothers at
deliveries where anti-B burgdorferi antibody titers were obtained. ** see
note below
Of these 1000 mothers, 12 had elevated titers, but only one mother was
symptomatic with Lyme disease during her first trimester. Her child was born
with a ventricular-septal cardiac defect (VSD). None of the children born to
mothers with a positive titer had detectable antibodies. Of the 12 mothers with
positive titers, 8 delivered at term, 2 were preterm and 2 were postterm. Seven
infants had problems in the newborn period: there were two cases of
hyperbilirubinemia and one case each of hypotonia; (attributed to medication),
microcephaly, supra-ventricular extrasystoles, VSD, and small for gestational
age when examined between 9 and I7 months of age; however, only the child with
the VSD remained abnormal.

MacDonald published two papers regarding
Lyme disease in pregnancy. He described four cases of fetal borreliosis found
while prospectively studying abortuses.(ref 4) His findings included one term
stillbirth and three second-trimester losses. One of the second-trimester
losses was complicated by toxemia and another by systemic lupus erythematous.
B. burgdorferi was cultured from the fetal liver in each case. From the term
stillbirth, spirochetes were found in the liver, heart, adrenal, brain, kidney,
meninges, and subarachnoid. Three of the cases had identifiable cardiac
malformations:
atrial-septal defect, VSD, and coarctation of the aorta. He questioned whether
or not B. burgdorferi could be a cause of fetal demise, congenital heart
defect, or fetal loss after toxemia. In l989, MacDonald described several other
cases. One was a 25-year-old black woman at term in labor who delivered a male
fetus who was small for gestational age with multiple anomalies including VSD
in addition to central nervous system (CNS) anomalies. B. burgdorferi was
identified in the fetal autopsy. Another was a term intrauterine
growth-retarded infant who succumbed to a large VSD and absence of the left
hemidiaphragm. This autopsy also found spirochetes in tissue. MacDonald also
reports several second-trimester losses, with and without anomalies, that at
autopsy revealed B. burgdorfen. In the same article, MacDonald refers to a
retrospective study of 10 sudden infant deaths; he reported that 2 had
spirochetes consistent with B. burgdorferi in the brain. No other laboratory,
however, has confirmed this high report of spirochetal invasion of the fetal
and placental tissue.
In contrast to these reports of MacDonald, (ref 3,4) the Fourth International
Conference on Lyme Borreliosis held in Stockholm in June of 1990 concluded that
there is little risk to the fetus.(ref 9) The symposium examined a large
retrospective study in which there was no increased rate of congenital
malformations in infants with seropositive mothers. The symposium referred to a
study in which there were six pregnant women with Lyme disease, all of whom had
healthy infants. Another study, which surveyed pediatric neurologists in areas
highly endemic for Lyme disease, failed to discover any (??!!) records of
neurologic cases that could be attributed to Lyme disease.
In a series of 143 pregnant women from Wisconsin, titers for B. burgdorferi
exposure were examined and correlated with pregnancy outcome. In the group, the
incidence of first-trimester spontaneous abortions was no greater for
seropositive women than for seronegative women.

DIAGNOSIS
According to the Centers for Disease Control (ref 5) a diagnosis of Lyme
disease in pregnancy can be made with certainty if erythema migrans (EM) is
present or if there is the new onset of typical neurologic, cardiac, or joint
involvement in a pregnant woman accompanied by laboratory confirmation of
infection (typically diagnostic antibody levels or a significant rise in acute
versus convalescent antibody levels; isolation of spirochetes from a clinical
sample is also acceptable). In reality, however, patients in whom there is a
reasonable
clinical suspicion for Lyme disease warrant treatment.

TREATMENT
According to the Centers for Disease Control, any pregnant woman with the
diagnosis of Lyme disease, or the suspicion of it, should be treated.(ref 5)
The diagnosis should be a clinical one and not based on serology because
serologic conversion may occur too late in the disease process. The problems
with current antibody assays, and the problem of seronegativity, are addressed
in Chapters 14 and 25. In the Centers for Disease Control study, 3 of
13 patients treated had abnormal fetal outcomes (23%), as did 2 of the 6
patients who were not treated (33%). According to their study, the time of the
disease in relation to poor outcome and whether the patient was treated were
not significant. The Centers for Disease Control admitted that none of these
adverse outcomes was documented to be a direct sequela of Lyme disease. These
adverse outcomes are only possible associations of Borrelia burgdorferi
maternal infection (Table 23-1).

Table 23-1 Adverse pregnancy outcomes with possible association to Lyme disease
Congenital anomlies (especially heart, great vessels)
Congenital cortical blindness
Miscarriage
Small for gestational age
Stillbirth
Toxemia

According to Mikkelsen and Palle, (ref 6) to avoid a potential adverse effect
on the fetus, the mother should be treated aggressively. Treatment is guided by
the clinical manifestations of the disease (Table 23-2).

Table 23-2
Treatment of Lyme disease during pregnancy
Disease stage Antibiotic regimen
Uncomplicated erythema migrans after first trimester:
Amoxicillin 500 mg P0 tid-qid x 21-30 days
Erythromycin 250 mg P0 qid x 21-30 days
[Newer macrolides such as Azithromycin may prove to he superior to
erythromycin]
Avoid tetracyclines, probenecid

Disseminated or late disease; first trimester infection
Intravenous antibiotics for 2-4 weeks
Ceftriaxone 2g
Penicillin G 20 million U qd

Lyme disease limited to the skin can probably be treated with amoxicillin or
erythromycin (see Chapter 18 for a different approach). Probenecid should not
be used, and the tetracyclines should be avoided. Disseminated disease, and
infections in the first trimester, should be treated with parenteral
antibiotics (ceftriaxone or penicillin – ref 6).

In 1987, Mikkelsen and Palle (ref 6) reported the case of a 29-year-old woman
who during her 24th week was bitten by a tick. She developed EM without any
systemic manifestations, with a positive antibody titer. She was treated with
penicillin for 10
days and subsequntly delivered a term baby. Histologic study of the placenta
was negative, and the antibody titer in cord and maternal blood was not
elevated.

SUMMARY
A body of evidence (ref 3 and 4) suggests that the causative agent of Lyme
disease, B. burgdorfen, can cross the placenta and infect the fetus. There are
also several reports that suggest that this may be associated with a poor fetal
outcome. However, the majority of studies have not been able to identify B.
burgdorferi as a direct cause of spontaneous abortions, congenital anomalies,
or neurologic sequelae in infants.
It is essential to realize that in the pregnant woman Lyme disease is a
clinical diagnosis regardless of her serologic status. Because the precise risk
to the fetus from an infected pregnant female is not yet clear, it is important
to be aggressive in the diagnosis and management of Lyme disease. This is
important not only for the fetus, but also for the mother. The mother is
certainly at risk for serious and potentially debilitating manifestations of
Lyme disease including arthritis, carditis, and neurologic problems.
In conclusion, Lyme disease in pregnancy is a clinical diagnosis irrespective
of serologic status.

The diagnosis must be made promptly, and treatment must be instituted in the
interest of maternal, in addition to fetal, welfare.

REFERENCES
1. Centers for Disease Control, MMWR 40(25):417, 1991.
2. Dlesk A et al: Lyme seropositivity and pregnancy outcome in the absence
of symptoms of Lyme disease, Arthritis Rheum 32(suppl):S46, 1989.
3. MacDonald AB: Human fetal borreliosis, toxemia of pregnancy, and fetal
death, Zentralbi Bakieriol Mikrobiol Hyg
[A] 263:189, 1986.
4. MacDonald AB: Gestational Lyme borreliosis, Rheum Dis Clin North Am
15(4):657, 1989.
5. Markowitt LE et al: Lyme disease during pregnancy. JAMA
255(24):3394, 1986.
6. Mikketsen AL, Palle C: Lyme disease during pregnancy. Acta Obstet
Gynecol Scand 66:477, 1987.
7. Nadal D et al: Infants born to mothers with antibodies against Borellia
burgdorferi at delivery, Eur J Pedjair
148:426, 1989.
8. Schlessinger PA et al: Maternal-fetal transmission of Lyme disease
spirochete Borrelia burgdoDferi, Ann Intern Med
103:67, 1985.
9. Sigal LH: Summary of the Fourth International Symposium on Lyme
Borreliosis, Arthritis Rheum 34(3):367, 1991.
10. Steere AG: Lyme disease, N Engi J Med 321:586, 1989.
11. Steere AC, Malawista SE: Cases of Lyme disease in the United States:
locations correlated with distribution of Ixodes dammini, Ann Intern Med
91:730, 1979.
12. Steere AC et al: The clinical spectrum and treatment of Lyme disease,
Yale J Biol Med 57:453, 1984.

My father has diabetes..am not sure wat type but he takes 2 insulin shots a day…anyway,he got a sore on the bottom of his foot…the doctor performed some surgery..now they say hes contracted mercer blood disease.i cannot find anything about this blood disease.can someone help me to learn about this disease?

As far as I can tell from a web search, “Mercer” is a common misinterpretation of MRSA, methicillin resistant Staphylococcus aureus.  This is an antibiotic resistant strain of a bacterium normally found on the skin that often infects wounds or causes boils.

These infections are not usually serious in healthy people, but they can become quite serious in people who can’t fight off infections easily, because antibiotics are not effective against them. Diabetics are prone to infections, especially in the lower legs and feet.

Your best bet is to talk to your father’s doctor to get accurate information about his medical problems. Your father may need to give his doctor formal permission to discuss his problems with you.

The great French writer Marcel Proust (1871-1922) embodied
contradictions. His prose was among the most graceful of his age. Yet
Proust understood inconsistencies, including those in medicine. The son
of a distinguished French physician, Proust once wrote that medicine is
¡°a compendium of the successive and contradictory mistakes of medical
practitioners ¡­¡±

A century later, a pair of Arizona-based physicians finds singular merit
in Proust¡¯s observations on contradictions. Dr. John Polacheck, an
internist, and Dr. Eduardo Vega, a pathologist, struggle with a modern
medical incongruity: Can an infectious disease be simultaneously
chronic and acute?

The distinction between an acute and a chronic infection is usually
self-evident. Acute infections generally have an abrupt onset and a
rapid progression. Examples are: strep throat, pneumococcal pneumonia,
and bacterial meningitis. If successful, their response to treatment is
usually relatively rapid also. By contrast, chronic infections
generally have an insidious onset and a gradual progression. Examples
are: tuberculosis, AIDS, and Lyme disease. Moreover, their response to
treatment is most often gradual.

Furthermore, the body responds quite differently to an acute or a
chronic infection. The pathologic response to an acute infection is
with white blood cells that are specialized to fight bacteria:
polymorphonuclear (PMN) cells, commonly referred to as pus cells. On
the other hand, the body uses very different types of white blood cells
to fight chronic infections: lymphocytes and monocytes. A pathologist
can readily distinguish acute cells from chronic ones when examining
tissue under the microscope.

Chronic vs. acute: It should be an ¡°either/or¡± situation. Webster¡¯s
Third Edition Dictionary goes as far as defining ¡°acute¡± as the opposite
of ¡°chronic.¡± But could there be a disease that simultaneously
manifests signs of both? A contradiction incarnate?

Drs. Polacheck and Vega have focused their attention on the prostate, a
mere walnut-sized pelvic gland located between a man¡¯s bladder and his
penis. When infected acutely, a true acute illness, properly called
¡°acute¡± prostatitis, occurs. Acute prostatitis has an acute clinical
course and demonstrates an acute pathologic picture. However, that is
not the prostate illness which has puzzled these two physicians. The
mysterious illness which is the subject of this story is the so-called
¡°chronic¡± prostatitis.

¡°Chronic¡± prostatitis is a true medical malady!!! It is quite common and
afflicts young and old men alike. The symptoms can be quite minimal or
they can become most severe and even disabling. Often, the severity
fluctuates ¨C a patient will have good periods alternating with bad ones.
The scourge can last for decades. It is a most ill-defined disease
medically. ¡°Prostatitis¡± means simply that the prostate is inflamed.
Often, there is pain, varying widely from mild irritation to searing
pain that prevents one from sitting down, urinating properly, or even
experiencing normal sexual pleasure. Yet this disorder has received
precious little attention. Its more ominous cousin, prostate cancer,
overshadows prostatitis and siphons off large amounts of the available
clinical and research funds. Scant little is actually known. In a
recent urology book devoted entirely to the prostate, only ten pages out
of 312 were dedicated to prostatitis. And yet, as Dr. Charles Brendler,
chief urologist with the University of Chicago medical school, said, he
cannot find normal prostate tissue in patients over forty years of age.

Embracing the concept that the study of a disease begins with pathology,
Drs. Polacheck and Vega examined the rudiments of so-called ¡°chronic¡±
prostatitis. ¡°Something wasn¡¯t fitting right,¡± said Polacheck. ¡°We
needed a fresh approach to its pathology.¡± As a diagnostic tool, they
used the fluid called Expressed Prostatic Secretion (EPS). It is a
clear, goopy fluid that comes out of the tip of the penis when the
prostate receives a vigorous massage (done by a physician with a finger
in the rectum). Dr. Polacheck provided EPS samples (from Prostatitis
Center, Tucson, Arizona patients) to Dr. Vega, who examined them
microsopically, using the same methods as those for PAP smear for women.
The clinical findings for all of these patients are most consistent
with so-called ¡°chronic¡± prostatitis. In fact, Dr. Polacheck exclaimed,
¡°these patients are the most chronic of the chronic!¡±

When Dr. Vega examined the EPS from these patients under the microscope,
he observed that the fluid was teeming with clumps of white blood cells.
Furthermore, when he looked at the details of the cells, he found
predominately PMNs, acute-inflammatory (pus) cells. Drs. Polacheck and
Vega decided to call these clumps ¡°Prostatic Acute-Inflammatory
Aggregates (PAAs). What a surprise to find acute-inflammatory cells
under the microscope in a disease which manifests itself chronically.
Thus, Drs. Polacheck and Vega have found a disease which is most
¡°chronic¡± in its clinical presentation, yet most ¡°acute¡± in its
pathological picture!!! They are unaware of any other such
chronic-acute disease.

Meningitis is an infection of the fluid of a person’s spinal cord and
the fluid that
surrounds the brain. People sometimes refer to it as spinal meningitis.
Meningitis is
usually caused by a viral or bacterial infection. Knowing whether
meningitis is caused
by a virus or bacterium is important because the severity of illness and
the treatment
differ. Viral meningitis is generally less severe and resolves without
specific treatment,
while bacterial meningitis can be quite severe and may result in brain
damage, hearing
loss, or learning disability. For bacterial meningitis, it is also
important to know which
type of bacteria is causing the meningitis because antibiotics can
prevent some types
from spreading and infecting other people. Before the 1990s, Haemophilus
influenzae
type b (Hib) was the leading cause of bacterial meningitis, but new
vaccines being given
to all children as part of their routine immunizations have reduced the
occurrence of
invasive disease due to H. influenzae. Today, Streptococcus pneumoniae
and
Neisseria meningitidis are the leading causes of bacterial meningitis.

What are the signs and symptoms of meningitis?

High fever, headache, and stiff neck are common symptoms of meningitis
in anyone
over the age of 2 years. These symptoms can develop over several hours,
or they may
take 1 to 2 days. Other symptoms may include nausea, vomiting,
discomfort looking
into bright lights, confusion, and sleepiness. In newborns and small
infants, the classic
symptoms of fever, headache, and neck stiffness may be absent or
difficult to detect,
and the infant may only appear slow or inactive, or be irritable, have
vomiting, or be
feeding poorly. As the disease progresses, patients of any age may have
seizures.

How is meningitis diagnosed?

Early diagnosis and treatment are very important. If symptoms occur, the
patient should
see a doctor immediately. The diagnosis is usually made by growing
bacteria from a
sample of spinal fluid. The spinal fluid is obtained by performing a
spinal tap, in which a
needle is inserted into an area in the lower back where fluid in the
spinal canal is readily
accessible. Identification of the type of bacteria responsible is
important for selection of
correct antibiotics.

Can meningitis be treated?

Bacterial meningitis can be treated with a number of effective
antibiotics. It is important,
however, that treatment be started early in the course of the disease.
Appropriate
antibiotic treatment of most common types of bacterial meningitis should
reduce the risk
of dying from meningitis to below 15%, although the risk is higher among
the elderly.

Is meningitis contagious?

Yes, some forms are bacterial meningitis are contagious. The bacteria
are spread
through the exchange of respiratory and throat secretions (i.e.,
coughing, kissing).
Fortunately, none of the bacteria that cause meningitis are as
contagious as things like
the common cold or the flu, and they are not spread by casual contact or
by simply
breathing the air where a person with meningitis has been.
However, sometimes the bacteria that cause meningitis have spread to
other people
who have had close or prolonged contact with a patient with meningitis
caused by
Neisseria meningitidis (also called meningococcal meningitis) or Hib.
People in the
same household or day-care center, or anyone with direct contact with a
patient’s oral
secretions (such as a boyfriend or girlfriend) would be considered at
increased risk of
acquiring the infection. People who qualify as close contacts of a
person with meningitis
caused by N. meningitidis should receive antibiotics to prevent them
from getting the
disease. Antibiotics for contacts of a person with Hib meningitis
disease are no longer
recommended if all contacts 4 years of age or younger are fully
vaccinated against Hib
disease (see below).

Are there vaccines against meningitis?

Yes, there are vaccines against Hib and against some strains of N.
meningitidis and
many types of Streptococcus pneumoniae. The vaccines against Hib are
very safe and
highly effective.

There is also a vaccine that protects against four strains of N.
meningitidis, but it is not
routinely used in the United States and is not effective in children
under 18 months of
age. The vaccine against N. meningitidis is sometimes used to control
outbreaks of
some types of meningococcal meningitis in the United States. Meningitis
cases should
be reported to state or local health departments to assure follow-up of
close contacts
and recognize outbreaks. Although large epidemics of meningococcal
meningitis do not
occur in the United States, some countries experience large, periodic
epidemics.
Overseas travelers should check to see if meningococcal vaccine is
recommended for
their destination. Travelers should receive the vaccine at least 1 week
before departure,
if possible. Information on areas for which meningococcal vaccine is
recommended can
be obtained by calling the Centers for Disease Control and Prevention at
(404)-332-4565.

A vaccine to prevent meningitis due to S. pneumoniae (also called
pneumococcal
meningitis) can also prevent other forms of infection due to S.
pneumoniae. The
pneumococcal vaccine is not effective in children under 2 years of age
but is
recommended for all persons over 65 years of age and younger persons
with certain
chronic medical problems.

We should probably consider that not having people die on a planet with
a population of (then) 15B is probably not a good idea. But having
healthy people is better than perpetually sick people. In addition to
eliminating the causes of genetic disease, other genetic flaws
will be eliminated as well. Like homosexuality, nearsightedness,
deafness, etc.

But we should consider whether we want to end genetic propensity toward
getting some cancers, etc, because it’s those diseases that help keep
the population explosion in-check, at least partially.

If the World can get down to a birthrate of around 2 per thousand (some
places, Africa for instance, have rates in the teens) then allowing
cures for all disease might be acceptable, we won’t need a disease-borne
attrition rate.

The planet can support 15 billion people – IF the people using stone-age
agricultural techniques are required to start doing things better.

GE can also get more YEILD from food crops … get ’em to grow in crappy,
salty soil too.

Actually, genetic engineering can make us more biologically efficient too
– more calories extracted from ever gram of food, more muscle energy from
every calorie burned. Ought to knock-back the impact figure a bit.

Also, people who don’t die – or at least can plan on living 500 or 1000
years – can adopt a more RELAXED lifestyle. You wouldn’t have to try and
squeeze everything into a short span. You wouldn’t need to produce 15
children every 20 years either in hopes that one or two might survive.

Also, in return for the aging fix, perhaps it would not be unreasonable to
demand a FECUNDITY fix as payment … greatly reducing (though not eliminating)
the rate at which it’s possible to reproduce. Two or three kids per century seems
acceptable … there will be losses due to accidents and such …..

Does anyone have any experience with either of these two meds ?

Procrit is used to treat anemia (and from the labs you posted, you’re
not anemic). Sensipar is used for patients on dialysis with
hyperparathyrodism caused by the dialysis. These drugs do not treat
kidney disease, but complications of kidney disease/failure.

The drugs used to treat/slow the progress of kidney disease are: ACE
inhibitors, ARBs (both ACE inhibitors and ARBs are hypotensive agents
that have protective properties on the kidneys, even in the absence of
high blood pressure), corticosteroids and fish oil (for certain kidney
diseases). Some diseases, like FSGS, show almost no response to any
treatment, but ACE inhibitors or ARBs are tried anyway, while others,
like diabetic nephropathy, repsond well to ACE inhibitor/ARB therapy.
IgA Nephropathy repsonds well to fish oil, but most other kidney
diseases show no change.

You need another doctor who knows what they are doing because the lab
ranges quoted here are what every doctor I’ve seen has gone by for the last
12 years. Believe me if your hematocrit were below normal you would feel
it. You’d be lucky to drag your ass out of bed each day and be able to stay
awake. I can only wish for an 11.5. I haven’t been able to get at or above
10.2 in over 2 months and I’ve been using procrit for 6 months now.

The reference ranges from the lab used for this panel may show
he is very slightly out of range, but with a history of poorly
controlled diabetes and enlarged prostate, I’m guessing that there’s no
mystery to these results and most certainly no anemia or kidney failure
(or at least no failure so severe as to require Procrit or Sensipar).

Unfortunately for the OP, the best to forestall future kidney problems
is through the tedious work of tight glucose control, and not throwing
handfuls of expensive pills down the throat.