MS you wrote,

   And to make it simple I have given you my best advice
and see no reason to modify it. But if you go further down
I will share my personal experience.

      snip of my old tags

   You shouldn't have symptoms all year unless as I did for so many
years you are ignoring dietary sensitivities.  Shortly before I came
up with the virual illness that ended in my case of chronic post-virual
fatigue syndrome aka cfids. I was informed that I was allegic to cows
milk and I gave it up though it took me 6 months.  After the illnesses
and in the midst of cfids I had a terrible time with wheat allegies and
apparent yeast allegies.  A kindly and well informed
allegist-immunologist
got me on a rotation diet.  That helped my rhinitis terrifically and let
me isolate the foods that caused the problems that were keeping me awake
all night.

   I make no diagnosis especially since #1, I am only a nurse, and #2 I
have
never done a physical on you or even read your chart.  I never came
close to
using the expensive chemicals you have at your disposal.  My last UR
problem
seems to have been an exhaberation of allergies which I treated with
staying
warm, breathing warm air, and doubling the frequency at which I take my
generic loratidine 10 mg. usually one in the AM.  I keep forgetting the
value of warm air but I was having a lot of coughing and sneezing and
having
to go to the market, put on a dust mask,  It warmed up the air I was
(re)breathing
and my nasal congestion diminished and my cough went away in about 5
blocks.

   This is only my personal experience.  I think you might consider
seeking
advice from a knowlegable specialist in allergy, if you don't continue
to
improve or rather continue as ill as you have been.

   later
   bliss -- C O C O A  Powered ...

--    
bobbie sellers - a retired nurse in San Francisco
         bliss at california dot com

But you'll accept advice from anonymous strangers on the internet?

I'm still looking for that data...

As I stated, the severe symptoms of cold...malaise, feve, stuffy nose, etc,
last usually less than 10 days.  However, a post viral cough can last for
several weeks:
http://www.clevelandclinicmeded.com/diseasemanagement/pulmonary/cough/cough.htm:

Acute Cough:
Acute cough has been defined as one with a duration of less than 3 weeks at
presentation.1 In general, acute cough usually results from respiratory
infections, of which the common cold is the most frequent. Some authors have
proposed a category of subacute cough, with a duration of 3 to 8 weeks.
Postinfectious cough due to irritation of cough receptors accounts for the
bulk of these cases. However, there are no case series assessing the
relative frequency of causes in either the acute or subacute categories.

The most common causes of acute cough are listed in Table 1. In the presence
of a compatible history and examination, further diagnostic testing is not
usually necessary. The mainstay of treatment includes nonspecific
antitussive therapy. Under-recognized causes for acute or subacute cough
include pertussis and mycoplasma infection. Rarely, life-threatening illness
may present primarily with acute cough. Examples include pulmonary embolus,
cardiogenic pulmonary edema, and pneumonia.

     Table 1:
     Acute Cough
     Etiology Recommended Treatment Comments
     Viral rhinosinusitis Antitussives, decongestants, first-generation
antihistamines, ibuprofen Difficult to distinguish from acute sinusitis.
Neuraminidase antagonists may be helpful if started earlier.
     Acute bronchitis Antitussives Antibiotics not routinely indicated
     Acute sinusitis Antibiotics, decongestants, first-generation
antihistamines Treatment duration 2-3 weeks
     Allergic/
     irritant rhinitis  Irritant avoidance; nonsedating antihistamines
Nasal corticosteroids useful for maintenance therapy
     Acute exacerbation
     of COPD Beta-agonist/anticholinergic MDIs with spacer, antibiotics,
systemic corticosteroids
     Pertussis Macrolides (if started within 8 days of symptom onset);
TMP-SMX (if macrolide allergy) Diagnosis is difficult (serologic or
nasopharyngeal culture)
     Mycoplasma Macrolides; alternatively, tetracyclines
     COPD=chronic obstructive pulmonary disease; MDIs=metered dose
inhalers;
     TMP-SMX=trimethoprim-sulfamethoxazole

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Tamiflu and a couple medication are available for the flu.  They have been
shown to shorten the duration and lessen the severity of the flu.  Tamiflu
has some efficacy in prophylaxis in high-risk populations with potential for
exposure to the flu.

Ed

A "primer" on common respiratory viruses:
http://web.uct.ac.za/depts/mmi/jmoodie/vires2.html#RHINOVIRUSES

Clinical Picture
PARA-INFLUENZA Types 1, 2, 3 and 4
All can cause minor infections in children and adults.
Types 1, 2 and 3 may be associated with more severe lower respiratory tract
disease in children. For instance, in an American series of cases, 30% of
acute laryngo-tracheo-bronchitis (LTB) cases yielded para-influenza viruses.
Type 1 is especially associated with LTB, sometimes also type 2.
Paraflu's have also been isolated from patients with pneumonia.

The virus grows locally in the respiratory tract lining of the URT and it
may then spread down into the lungs.
IgA type antibodies are induced. These are present in the respiratory
secretions and seem to be more important than the IgG antibodies in the
serum with regard to protection.
However, IgA antibodies do not cross the placenta and babies thus have no
maternal protection against this type of infection. Primary infections with
para-influenza viruses usually occur in the first year or years of life.
Re-infection usually causes only minor infection of the URT - one of the
causes of a common cold in children and adults.

Diagnosis
In cell cultures, the para-influenza viruses produce a recognisable
cytopathic effect, and haemadsorption is also used to detect their presence.

Each virus type has specific antigens by which they can be "typed", and
there are also a few minor subtypes.

Treatment
No specific treatment is available. Killed virus vaccines have been tried
but are of limited value in an infection which is so widespread and usually
of trivial significance.

----------------------------------------------------------------------------
----

Respiratory Syncytial virus - (RSV)
This is an unusual but very important member the Paramyxovirus group:
while it resembles the other members morphologically, no haemagglutinin or
neuraminidase or haemolytic properties have been detected, and there is no
antigenic similarity to other members. In cell cultures it readily induces
many large syncytia with cytoplasmic inclusions - hence its name.

Clinical
RSV was first isolated from chimpanzees with colds, and it was soon found to
cause colds in man as well. (Chimps were probably infected by their human
handlers.) However, it was also found to be associated with severe pulmonary
infections in infants - especially Bronchiolitis. RSV is the prime cause of
Bronchiolitis.

In Britain, RSV is the single major pathogen in respiratory infections of
childhood. The figures from Newcastle by Gardner are startling:

 under 1 year of age:
 78% of Bronchiolitis
 38% of LTB
 36% of Pneumonia
 35% of Bronchitis
 12% of minor respiratory illness,
were all caused by RSV.

RSV causes a fairly localised infection of the respiratory tract, and
infants have no maternal passive protection.
Re-infections do occur but seem only to produce fairly minor URT illness.

----------------------------------------------------------------------------
----
Vaccine
Because of its apparent importance, an attempt was made at vaccinating
infants. However, when the RS epidemic arrived, the vaccinated children
suffered more severe reactions than unvaccinated children. Somehow the
killed virus vaccine had unfortunately sensitised these children and
exposure to the live virus then induced a type of allergic reaction. This
drew attention to the possibility that RS viruses may in fact cause much of
its lung damage by immune mechanisms. Because of the importance of RSV in
childhood infections, intensive efforts to make a vaccine have continued,
especially along the lines of sub-unit vaccines (parts of virions) avoiding
those antigens which seem responsible for hypersensitisation. However, no
vaccine is as yet in general use.

----------------------------------------------------------------------------
----

RHINOVIRUSES
(Common Cold virus)

Over 100 serotypes of this Picorna virus family are responsible for about
50% of common colds.

Clinical
An inhalational infection of the URT. Incubation period is short: 1 to 3
days followed by headache, sore throat, fullness in the nose. Then there is
a profuse watery discharge from the nose which gradually thickens and
becomes mucopurulent and decreases in volume. The infection resolves in
about a week. Following a rhinovirus cold, there is a short period of
immunity to all colds but prolonged immunity to the specific serotype
causing the recent infection.

Treatment
No specific treatment but numerous symptomatic treatments are available.

Complications
A cold may temporarily upset the mucosal cilia and predisposes to secondary
invaders especially bacterial infections, eg. sinusitis (pneumococcus,
haemophilus, etc) and bronchitis and possibly pneumonia. These may require
antibiotic treatment.

Epidemiology
An infected person is infectious in the first two days of coryza. Colds are
readily acquired from breathing room air from a room crowded with coldy
people. Wet cold weather per s? does not cause colds, but may predispose to
infection from other persons. Colds are ubiquitous around the world except
in very isolated communities.

Prevention
The enormous diversity of cold-causing viruses essentially rules out a
vaccine. Vitamin C and bacterial vaccines are unproven.

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ADENOVIRUSES
Virus
Ds DNA, Non-enveloped 70nm capsid shell with protruding penton-fibres.
See electron micrograph
Most adenoviruses grow easily in cell culture, and give rise to large
intranuclear inclusions.

1. Group Common Antigen
Shared by all adenoviruses, eg.a single complement fixation test can detect
a rise in antibody to any adeno infection also, a single immunofluorescent
reagent can be made which will react with all adenoviruses.

2. Type Specific Antigen
Can identify a specific type by neutralisation of infectivity or
haemagglutination. 47 Serotypes are grouped into about 6 larger groups
(labelled A ....... to F).

Clinical
Adenoviruses cause infections of man (many animals have their own
adenoviruses) and are spread by droplet, fomites and ingestion. They infect
the mucous membranes of the eye, respiratory and gastro intestinal tract,
occasionally urinary tract. Local lymph nodes often involved (enlarged and
tender). Infections are usually self-limiting.
Syndromes

1. Asymptomatic Infection
Adenoviruses may be present in healthy persons, eg. in stools of children,
and may also cause persistent silent infection of the tonsils.

2. Acute pharyngitis with fever
Adenoviruses are a common cause of an acute sore throat.

3. Pharyngoconjunctivical fever
Adenoviruses may cause an acute conjunctivitis together with a shore throat
and fever.

4. Acute follicular conjunctivitis
This is a non-purulent contagious inflammation with pearly, translucent
lymphoid hyperplasia.

5. Epidemic kerato-conjunctivitis (shipyard eye)
Mild trauma to the eye may facilitate a damaging adeno infection of cornea
(spread by multi- shared towels).

6. Pneumonia (and pneumonitis in children)
In some cases there may be a severe destructive pneumonia (and death) caused
by an adenovirus infection following measles or other predisposing factors,
eg. artificial airway.

7. Acute respiratory disease (ARD)
Is an epidemic form of acute pneumonic disease characteristically appearing
in military camps. Has been prevented by enteric capsulation of a live
vaccine strain which bypasses the respiratory tract and sets up a silent
infection in the gut, giving protection against acute respiratory infection.

8. Diarrhoea
In young children many adenoviruses may cause a generalised infection -
upper and lower respiratory tract infection with fever and diarrhoea. Quite
separately, some adenos (40/41) have been specifically associated with
causing acute gastroenteritis in children, which may lead to dehydration and
death.

9. Mesenteric Adenitis
Children may present with abdominal pain due to enlarged tender adenovirus
infected mesenteric lymph nodes. Occasionally an enlarged node may
invaginate the bowel wall and be gripped by peristaltic waves, leading to
intussusception of the bowel.

10. Immunocompromised host
In transplant patients, AIDS or other immunocompromised patients,
adenoviruses may cause a variety of infections - renal, disseminated, or a
haemorrhagic cystitis.

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PARAMYXOVIRUSES
General Properties of the Paramyxoviruses
The whole important group of Paramyxoviruses is fairly homogeneous.

Morphology
Generally fairly similar to influenza: roughly spherical sometimes
filamentous, easily distorted. A bit larger than influenza virus -
100-300nm. Composed of inner helical nucleocapsid containing protein/RNA,
contained within a membranous envelope studded with "spikes" of:
Haemagglutinin (Haemadsorption) and Neuraminidase (Haemolysis)

Antigens
Antigenically distinct from influenza virus. Within the paramyxovirus group
there is considerable overlapping, eg:
Parainfluenza 1, 2, 3 and mumps. Exposure of an adult to any one of these
viruses often induces a rise in serum antibodies to the others. Thus,
interpretation of serum antibody levels in this group of viral infections
may be difficult.

As in influenza vrus, there are two major antigens:
1. The haemagglutinin, present in the envelope of the intact virion (this is
sometimes called the "V" antigen);
2. On breaking open the virion, or rupturing of infected cells before virion
assembly, a "soluble" virus antigen is released, which is thought to be the
protein component of the nucleocapsid. This is sometimes called the "S"
antigen.

Infection induces antibodies to these two major antigens, amongst others.
The antigens are fairly stable. In contrast to influenza virus, there is no
antigenic drift or epidemics of infection

Primary infections
usually occur in (early) childhood, with some resultant degree of protection
against developing clinical disease later on in life. However, re-infections
do occur in adulthood, but disease is subclinical or very minor.

Spread
The human paramyxoviruses are essentially diseases of man only, and are
spread by droplets from the nose and mouth to fairly close contacts. Many of
them are fairly highly infectious and go around the community in epidemics -
often seasonal, eg. Winter coughs and colds. Fomites might also assist
spread.

----------------------------------------------------------------------------
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Laboratory Diagnosis
1. Viral Detection
Isolation of a paramyxovirus from a patient is strong evidence for a cause
of a respiratory infection. All the Paramyxoviruses are to be found in the
respiratory tract secretions - and this is the best material to send to the
laboratory. The paramyxoviruses are unstable and do not survive well outside
cells.

a) Direct Examination
Viral antigens or viral infected cells in the secretions may be directly and
rapidly detected by immunofluorescence or ELISA tests.

b) Culture
Primary Monkey kidney cells will support replication of all the
Paramyxoviruses and many of the other respiratory viruses.

An intriguing property of most Paramyxo's is their ability to induce cell
fusion. Neighbouring cells join up to form large multinucleate syncytia or
giant cells. Viral fusion to cell for penetration follows proteolytic
cleavage of fusion protein on virion surface.
One of the first discovered members of the Paramyxo group - probably a mouse
virus - called Sendai , is used as a cell fusing agent in experimental work
on cells. The Sendai virus is first inactivated by UV (which damages the
nucleic acid) so that the virus will not grow and interfere with the
experiment. The inactivated virus still induces cell fusion - even across
species, eg. heterokaryons of murine and human cells.

Multinucleated giant cells can sometimes be seen in lung sections from
children dying with Paramyxovirus infection in the lung. Not all Paramyxos
do this readily, and haemadsorption is usually used to detect Paramyxovirus
infection in culture cells.

Once isolated, a haemadsorbing virus can be further typed using standard
specific antisera in various laboratory procedures:

 a.. haemadsorption inhibition;
 b.. neutralisation; and
 c.. fluorescent antibody.
2. Serological Diagnosis
Antibody determinations in acute and convalescent blood specimens by
complement fixation, Elisa or haemagglutination inhibition may sometimes be
helpful in arriving at a specific diagnosis.
Respiratory syncytial virus and measles virus infections are fairly
clearcut.
Mumps and Para influenza viruses seem to share a group common antigen, and
serological interpretation may be difficult.

----------------------------------------------------------------------------
----

----- Original Message -----
From: " MS" <ms@nospam.com>
Newsgroups: sci.med
Sent: Thursday, October 21, 2004 10:07 PM
Subject: Re: Can a cold last a month?

possible

from

it

nose

prominent

Rhinoviruses

that

in

cannot

of

they?