Week 22 Lecture Outline

Mycoplasma, Ureaplasma,
Orthomyxiviridiae,
Picornavirus, Enterovirus,
Rhinovirus
 Mycoplasma and Ureaplasma
• Class Mollicutes, family
Mycoplasmataceae, genera Mycoplasma
and Ureaplasma
• No true cell wall (but stain Gram (-)
– highly pleomorphic and susceptible to
external osmotic pressure
• Highly developed outer membrane
– contains sterols (cholesterol- like)
• maintain membrane integrity
– susceptible to agents like saponin, digitonin,
amphotericin B
 Mycoplasm/ Ureaplasm cont’d
• smallest known organisms (filterable)
that are capable of autonomous growth
– smallest known genome (580kb of DNA)
• divide by binary fission
• fastidious nutritional growth:
– blood serum and sterols, 36-380C
• facultative anaerobes
– except M. pneumoniae
– 1/3 of all species cause
haemadsorption and produce H2O2
 Mycoplasma and Ureaplasma
pathogenesis
• Role in disease is “not clearly defined”

• Attachment: adhesin P
– binds siliated glycoprotein receptors on:
• base of cilia
• epithelial and RBC cell surface
– cause ciliostasis
• then destruction of cilia and ciliated
epithelial cells
– decrease clearance of upper airways
» mechanical irritation and increased
bacterial colonization of lower
airways
» persistent cough
 Mycoplasm/ Ureaplasm pathogenesis cont’d

• M. pneumonia also binds to neuramic acid

– similar structure to glycolipids in human brain
neurological sequelae?
• M. pneumonia also is a superantigen
– inflammatory cells at site of infection causes
release of cytokines (TNF-alpha, IL-1, IL-6)
• that help clear bacteria and also are part of the
disease process
• produce H202 and inhibit host catalase
– initial cell disruption in respiratory tract and
damage to RBC membranes
• Incomplete immunity
 Mycoplasma and Ureoplasma epidemiology
• M. pneumonia:
– Worldwide distribution
• found in man, plants, soil, sewage, insects,
alligators/ turtles/ crocodiles, other animals
– No seasonality: epidemics every 4-8 years
– M/C 5- 15 y.o.a
• Spread via nasal secretions/ aerosolized
droplets
– close contact class mates/ family members
• M. hominis, M. genitalum, Ureaplasma
• infants/ girls colonized at birth but
transient
• Increased number of mycoplasma
associated genital infections iff sexually
active STD?
 M. pneumonia clinical syndrome
• Low grade fever, malaise,
H/A, can last> 2weeks
• Mild URI/ – symptoms similar to
RSV, Group A Strep
pharyngitis ect.

• persistent dry cough that

might become
• acute paroxsymal and simulate
tracheobronchitis whooping cough in
children
– compare pathogenesis
with B. pertussis
M. pneumonia clinical syndromes
• Prolonged, mild form of
• “Walking” pneumonia
pneumonia – M/C in teenagers, young
adults, military troops
– “Eaton’s agent”
• initial symptoms “non-
pneumonia
specific”
– H/A, malaise, low grade fever
– increase in severity over
a few days
• chest pain, dyspnea, non-
productive cough
paroxysmal
• CXR: patchy, unilateral,
lower lobe pneumonia
 M. pneumonia potential sequelae
• hypersensitivity syndrome (vasculitis)
• Erythema – characterized by many types of skin
multiforme and mucous membrane lesions
(macules, papules, vesicles, bullae,
bulls-eye lesions
• associated with many infections
(HSV), collagen disease, drug
sensitivities, allergies, and
pregnancy

• Stevens- • severe, sometimes fatal, bullous form of

erythema multiforme
Johnson
– acute onset of fever, bullae
syndrome
• ulcers of mucous membranes,
arthralgia
– pneumonia, prostration,
corneal perforation
Erythema multiforme
Erythema multiforme
Stevens Johnson syndrome
 M. pneumonia complications
• OM • Common, otalagia,
diminished acuity
etc.

• auto-immune
• haemolytic destruction of
anemia RBCs

• meningitis,
• auto- immune ???
pericarditis
 Ureaplasm urealyticum

• KI stones: produce urease

– induce crystallization in vitro and
experimentally
• Urethritis
– NGU, might be asymptomatic in women
but usually no progression to PID
• Pregnancy/ neonatal:
– low birth weight babies
 Mycoplasma hominis
• Urethritis
– NGU in men, can be asymptomatic in
women or can lead to pyelonephritis (flank
pain, fever, dysuria) or to PID (subsequent
infertility)

• Link to bacterial vaginosis STD?

• Colonization increases with sexual

activity
Mycoplasmas and other diseases
• Mycoplasmas have been implicated as
causative or cofactors or opportunistic
pathogens in diseases like:
– Gulf War Illness, Chronic fatigue
syndrome/ Fibromyalgia, Sick building
syndrome, HIV/ AIDS, Rheumatoid
arthritis, amyotrophic lateral sclerosis,
Crohn’s disease, malignancies etc.
• find mycoplasma infections in blood of
infected people using PCR and
immunohistochemistry
 Mycoplasms diagnosis
• Culture: slow (1-4 days), insensitive,
some of the most difficult pathogenic
organisms to grow (fastidious growth)
– M. pneumonia mulberry shaped colonies
– M. hominis large “fried egg” colonies
– Ureaplasm needs urea, T (tiny) colonies
• Serology: M. pneumonia only
– ELISA, Complement fixation tests
• Cold agglutination
• PCR: gene for P1 adhesion protein
Mycoplasmas colonies
Mycoplasms treatment and control
• Treatment:
– no cell wall therefore, resistant to
penicillins, cephalosporins, vancomycin
but destroyed by doxycycline,
tetracycline (except ureaplasma),
erythromycin

• Control:
– safe sex, isolation of infected individual
is ineffective
Orthomyxoviridae introduction
• 3 types:
– 1) Influenzae A: epidemics, pandemics,
bird reservoirs (ducks, chickens)
– 2) Influenzae B: epidemics only, no
antigenic shift, no animal hosts, linked
more closely to GIT “stomach flu”
– 3) Influenzae C: no epidemics or
pandemics, minor URI only
• enveloped virus with hemagglutinin
and neuramidase spikes
• linear ssRNA genome in 8 segments:
– facilitates rearrangement
Influenzae virus
 Influenzae virus important proteins
• Haemagglutinin
– VAP binds sialic acid residues on epithelial cells
• epitope for neutralizing protective Abs
– haemagglutinates human, chicken, guinea pig RBCs

• Neuramidase
– cleaves sialic acid residues on mucosal surface to
prevent viral clumping and promote spread
• Matrix and nucleoprotein
– basis for labeling as Influenzae A, B, or C
• Strains labeled as: eg. A/HongKong/97(H5N1)
– first strain known to cross species barrier
from chicken to human (compare to H7N1)
Influenzae virus structure
 Influenzae epidemics and pandemics
• Epidemic antigenic drift
– in all types of virus, small mutations in H and N
Ags
• will re-infect individual with immunity to
previous strains iff multiply to significant levels
– every 2-3 years

• Pandemic antigenic shift

– only in Influenzae A, major recombinations
• reassortment of RNA segments and other
genetic changes new strain that can spread
through populations immune to previous
strains (every 10 years)
– (16 types of H, 9 types of N= 117 possible
combinations)
Influenzae virus genetic shift
• Also zoonoses:
– multiple virus
strains can affect
one animal (eg. pig)
and during
replication, shift
genetic material so
that a new strain is
formed that can be
spread to humans
 The challenge of a zoonoses!

From www.medicalecology.org/diseases/influenza/influenza.htm
 Influenzae epidemiology
Transmission:
– respiratory droplets
• can survive on counter top, blankets, glass (RT)
for 24 hours, dust: 2 weeks, glycerol saline and
seawater- several weeks at 400C, indefinitely if
freeze dried
– Destroy with heat >560C for 30 min., 20% ether,
phenols, detergents, soaps

• Increased spread with school children

– Increased risk of complications with
elderly, COPD/ smokers,
immunosuppressed, pregnant women, 6
months to <9 y.o.a.
• Flu season:
– winter months October-December only 4-6 wks.
 Influenzae virus pathogenesis
• Spread via small respiratory droplets
– talking, sneezing, coughing
– bind sialic acid residues on ciliated columnar
epithelial cells of URI
• destroy cells directly or via associated
inflammatory response (cytokines)
– spread to lower respiratory tract
» destroy bronchial/ alveolar epithelia
– damaged cells result in increased adherence/
infection of bacteria like S. aureus, S. pneumonia,
H. influenzae
• secondary complications like pneumonia
• limited viremia
– very rarely spread beyond lung
Influenzae attach to cilia
Influenzae pathogenesis
 Influenzae & immunity
• Th1 cell response and IFN are key in resolving
disease
– Ab mediated response (anti-HA Abs) protect
against re-infection from that particular
strain only
• Influenzae infection decreases macrophage and
T cell function
– hinder immune resolution
• Sx’s and duration of disease depends on:
– T cell response, IFN response (liberated from
damaged cells, responsible for classic flu
symptoms), level of epithelial tissue lost
 The “Flu”- The “Grippe”
• Influenzae A:
– Incubation period 1-4 days
• H/A , malaise for a few hours
– Abrupt onset of fever (38-410C for 1-5 days)
» non- productive cough, severe myalgia,
rhinorrhea, anorexia
– Children might have n/v and diarrhea
• rare in adults
– Persist for 3 days to 1 week, long
convalescence (cough, lassitude, malaise)
for 1-2 weeks

• Influenzae B:
– similar course but milder and GI symptoms
are more likely
 Clinical features of Influenza A

Cunha BA. 2004. Influenza: historical aspects of epidemics and

pandemics.
 Influenzae complications
• Young children • OM, croup, bronchiolitis,
secondary bacterial
pneumonia

• Encephalopathy • rare
– 2-3 weeks after recovery,
M/C self-limiting

• Reye’s syndrome • acute encephalopathy

and LV dysfunction in
children, also can follow
varicella and other
• Guillain Barre infections, link to ASA
syndrome • polyneuritis
 Influenza lab diagnosis
• Usually symptomology and
community history of outbreak is
enough for diagnosis
• Cell culture:
– non specific CPE in monkey KI cells or
Madin-Darby canine KI cells
• Haemadsorption of guinea pig RBCs, or CFT
• Virus isolation:
– from nasal secretions
• detect with direct ELISA etc.
 Influenzae treatment
• NEVER give aspirin
• Amantadine/ Rimantadine
– inhibit replication of Influenzae virus A
• useful iff given within 1-2 days of onset of
symptoms (side-effects and decrease duration
by only 1 day--same as Vitamin C and
Echinacea, EHB- NF formulas, Echinaseal- St.
Frances etc. etc.)
• Zanamivir/ Oseltamivir
– neuramidase inhibitors
Influenzae control

• Reduce contact
with infected
individuals
– (contagious 1 day
before onset of
symptoms and 3-4 days
after)

• Wash hands, avoid

elective
hospitalization of
elderly
 Influenza control

• Vaccine against “strain of the year”--2002/ 2003

– trivalent A/NewCaledonia/20/99-like(H1N1), A/Moscow/10/99-
like (H3N2), and B/HongKong/330/01-like virus
• grown in allantoic cavity of embryonated chicken eggs
purified formalin inactivatedextract with ether-
• parenteral injection NOT for people with egg allergy
– protect up to 70% people for 1 year, based on previous years
strains, ineffective against new strains as well as other viruses
(RSV, rhinovirus) natural immunity is longer
» Politics?, business?, fear mongering? etc.
 The consequences of vaccinating for viruses
that constantly change
• Jefferson T. et al., 2005. Efficacy and effectiveness of influenza vaccines
in elderly people: a systematic review. Lancet 366(9492):1165-74.
• BACKGROUND: Influenza vaccination of elderly individuals is
recommended worldwide. Our aim was to review the evidence of
efficacy and effectiveness of influenza vaccines in individuals aged 65
years or older.
• FINDINGS: In homes for elderly individuals (with good vaccine match
and high viral circulation) the effectiveness of vaccines against
influenza-like illness was 23% (95% CI 6-36) and non-significant against
influenza (RR 1.04, 0.43-2.51). In elderly individuals living in the
community, vaccines were not significantly effective against influenza
(RR 0.19, 0.02-2.01), influenza-like illness (RR 1.05, 0.58-1.89), or
pneumonia (RR 0.88, 0.64-1.20).
• INTERPRETATION: In long-term care facilities, where vaccination is
most effective against complications, the aims of the vaccination
campaign are fulfilled, at least in part. However, according to reliable
evidence the usefulness of vaccines in the community is modest.
Vitamin D and epidemic influenza

From Cannell et al., 2006. Epidemic influenza and

Vitamin D. Epidemiol Infect. 134(6):1129-40.
 B) Prevention
Support physical terrain
• 1) Supplements cont’d

• Vitamin D:
– Functions:
• Optimize bone health
• Local cell growth regulator
– it is now recognized that
many tissues, including
colon, breast and
prostate, have the
enzymatic machinery to
produce 1,25(OH)2D.AA
• Innate immunity:
– Increase anti-microbial
peptide release
• Adaptive immunity
– Balance immune
cytokines
– Dosage:?
• At least 1000-1500 IU bid
 Picornaviridae
• One of the largest families of viruses
– includes enteroviruses (HAV, Coxsackie virus,
polio virus, echo virus) and rhinovirus
• small (pico) mRNA- like genome
– enough to infect cell
– icosahedral naked capsid virus resistant to
environment:
– Enterovirus stable at pH 3- pH 9,
detergents, heat, mild sewage treatment,
food to 600C
» Rhinovirus labile at acidic pH,
optimal growth is 330C
• viruses replicate in cytoplasm
– damage is directly due to viral
cytopathology NOT immunopathology
Polio virus
 Enterovirus pathogenesis
• Rarely cause gastrointestinal disease but fecal-
oral spread, attach to and replicate in intestinal
cells
– infections are M/C’ly asymptomatic but can range
from cold-like symptoms to paralytic disease
• Difference in tissue tropism affects
pathogenesis:
• Echo/ Coxsackie viruses relatively wide tropism
– relatively wide range of disease
• Polio virus narrow tissue tropism
– anterior horn cells of spinal cord, dorsal root
ganglion, skeletal muscle, B lymphoid cells; cross BBB
directly or via retrograde transport up skeletal muscle
nerves
• Cause direct cytolytic damage (except HAV)
 Enterovirus pathogenesis cont’d

• stomach acid, protease and bile do

NOT kill virus
– heat, chlorine, UV light and
formaldehyde do
 Enterovirus course of disease
• Entry
– nasopharynx, upper respiratory tract,
intestine
• First replication
– mucosa/ lymphoid tissue of tonsils/
pharynx or lymphoid cells of Peyer’s
patches
• primary viremia
– fever, generalized symptoms
• Second replication
– after 48 hours of well-being
• iff tissues carry specific receptors
– other signs and symptoms occur 2’ary viremia
Enterovirus course of disease
• Immune protection is from Abs:
– sIgA
• prevent establishment of infection
– humoral Abs block viremia
• prevent spread
– CMI
• resolution and some pathogenesis
(disease is less severe in children)not
protective
• Viruses detected in oropharynx 1-3
days before symptoms start and shed
from intestine for up to 30 days
 Enterovirus epidemiology
• Ubiquitous in children
– only found in humans and primates
• Fecal- oral spread
– hands, sewage, waste landfills water
sources shellfish humans
• Coxsackie and echo virus also can be
spread by aerosolized droplets
respiratory disease
– Increased spread with crowding (schools,
daycare), poor sanitation, unvaccinated
• Polio used to be a “middle class”
disease
– good hygiene delayed the response until
older
• more severe symptoms
Enterovirus prevention
Enterovirus clinical syndromes

• Different possible outcomes

depending on
– viral serotype, infecting dose, tissue
tropism, site of entry, age/ gender/ state of
health, pregnancy

• 1-35 day incubation

– shortest if affect oral or respiratory sites
 Polio outcomes
• Most common (90%)
• 1) Asymptomatic – virus limited to
oropharynx and GIT

• non-specific febrile
• 2) Abortive
illness 5% of
people
– fever, headache,
vomiting, malaise,
sore throat 3-4
days after
exposure
 Polio outcomes
• Symptoms of
• 3) Non-paralytic abortive
poliomyelitis poliomyelitis as well
– (aseptic as
meningitis) – headache, nuchal
rigidity, back pain,
muscle spasms/
rigidity
• 1-2% of people
– M/C’ly complete,
rapid recovery in
10 days
 Paralytic polio
• 4) paralytic • Onset: 3-4 days after non- paralytic
polio symptoms have subsided
– 0.1- 2% of people initially infected
• Spinal
paralytic • asymmetric flaccid paralysis in one or
more limbs, no sensory loss
– progressive over several days
• complete recovery (6 months--2
yrs.) or residual paralysis or
death
– also from attenuated virus
becoming virulent
• affect cranial nerves or medullary
• Bulbar respiratory center
– affect muscles of pharynx, vocal cords,
respiration, 75% mortality
 Increased risk of paralytic polio

• 1) strenuous physical activity

• 2) pregnant women in 3rd trimester
• 3) infection within 1 month of injection
with adjuvant or heavy metal containing
vaccine
• 4) previous tonsillectomy
Iron lung
 Post polio syndrome (PPS)
• Deterioration of affected muscles (or previously non-
affected muscles) later on in life (10- 40 years later)
without presence of virus
• Symptoms:
– new muscle weakness that gradually worsens
• decreased muscular endurance, myalgia, arthralgia,
cachexia, severe fatigue, somnolence, nocturia, sleep
apnea, CFS/ fibromyalgia
– rare dysphagia and dyspnea
• Causes?:
– unusual stress placed on surviving motor neurons (must
compensate for loss of neurons from original polio), compounded
by aging process- loss of motor neurons, persistence of
polio virus in the CNS (latent infection?)
 Coxsackie/ Echovirus virus clinical
syndromes
• M/C’ ly asymptomatic but can cause a polio- like
syndrome
– Coxsackie A usually vesicular lesions
– Coxsackie B myocarditis, pleurodynia , pancreatitis
• Herpangina:
– Coxsackie A and echovirus (not HSV)
• fever, sore throat, anorexia, vomiting, dysphagia
– multiple, small (1-2mm) vesicular, ulcerated
lesions on soft palate and uvula and tonsillar
pillars
» no external skin lesions unlike hand-foot-
mouth ds.
» self-limiting--symptomatic treatment only
– M/C in young children
Herpangina
 Coxsackie A syndromes
• Caused by Coxsackie A16
• Hand-foot-mouth – mild febrile disease with
disease vesicular lesions on
hands, foot, tongue
• M/C in young children (1-10
y.o.a.) in summer months,
in clusters

• Acute hemorrhagic
• caused by Coxsackie A24 or
conjunctivitis
enterovirus 70
(pharyngoconjunctival
– extremely contagious
fever, epidemic
• 24 hr incubation, 1-2 week
keratoconjunctivitis)
resolution, fever, sore
throat, conjunctivitis,
pseudomembrane ?
Hand-foot-mouth lesions
Acute hemorrhagic conjunctivitis
Acute hemorrhagic conjunctivitis
 Coxsackie B syndromes
• Pleurodynia • “devil’s grip” severe
(Bornholm’s pleuritic chest pain
disease) unilateral intercostal myalgia
 “stitch-like pain”
– abdominal pain/ vomiting,
sudden fever
• usually self limiting after 4 days but
can relapse

• Myocarditis • M/C in adult males

– mistaken for MI
/ • chest pain, dyspnea, fever
pericarditis – children
• sudden unexplained heart
failure
• tachycardia, cardiomegaly,
hepatomegaly, cyanosis
Coxsackie B, entero and echo virus syndromes
• IDDM
– possible link iff Coxsackie B infects
pancreas and destroys Islets of
Langerhans
• Aseptic meningitis
– sudden onset of H/A, fever, nuchal rigidity
• skin rash if enterovirus etiology
– M/C uneventful recovery unless
meningoencephalitis
– biggest risk for severe damage is children
<1 y.o.a
– #1 cause is echo virus
• also cause of neonatal encephalitis & neonatal fulminant
hepatitis
 Enteroviruses lab diagnosis
• Culture:
– can isolate polio/ echo/ coxsackie virus
from throat and stool during infection
• CPEs on monkey KI tissue culture
• Serology:
– 4X increase titer of IgM Abs
• Other:
– ELISA, RT-PCR in CSF/ other fluids
• CSF for aseptic meningitis:
– lymphocytosis, normal/ low glucose,
normal/ slightly elevated proteins
Treatment for enterovirus
• Allopathic treatment:
– anti-viral pleconaril,
corticosteroids
• Naturopathic treatment:
– Increase sIgA (mushroom
beta-glucans, selective
probiotic strains, l-
glutamine, glutathione)
– Increase NK cell activity
(astragalus, codonopsis,
engystol)
– Antivirals (eg. allium
sativum, usnea, baptista,
isatis)
– TAM: Wind heat
– Homeopathy: Mezereum,
Urtica etc.
 Enterovirus Treatment/ Prevention/ Control
• Prevention: good hygiene
• Control: polio vaccine “triumphs of modern
medicine”- WHO- eradicate poliomyelitis by
2005
– Two types:
• 1) IPV (Jonas Salk-1956) inactivated virus,
safer, given to babies, parenteral
• 2) OPV (Albert Sabin-1962) live attenuated
virus
– replicate in oropharynx and GIT but not neuronal
cells, shed in feces therefore, mass immunization,
oral
» more risks--active disease to
immunocompromised, revert to virulent form
» “more like natural infection”
– Schedule: 2, 4, 15 months, 4-6 years
 Rhinovirus introduction and epidemiology
• Most common cause (>50%) of the common cold
(coryza) and URI (also by Coxsackie A21 and echovirus
11/ 20)
– spread via aerosolized nasal droplets, fomites, hands
(#1)
• only symptomatic in about 50% of people infected
– highest rate of infection in infants <2 y.o.a.
• resistant to drying and detergents
– can’t grow in acid of stomach (unlike enteroviruses)
and also grow best at 330C (cooler in nasal mucosa)
• gradual antigenic drift (like Influenzae A)
• < winter (rainy season in tropics)
– “deliberate exposure of “volunteers” to wet and cold
does not cause colds”
Cough & sneeze etiquette
Cough & sneeze etiquette
Rhinovirus structure
 Rhinovirus pathogenesis and
immunity
• Infection by as little as 1 infectious
particle
• peak illness: 500-1000 infectious particles per ml
– bind ICAM-1 receptor
• member of Ig superfamily on epithelial
cells, fibroblasts, LDL?
– up-regulated during infection
– enter via nose/ mouth/ eyes
• cause URI (including throat)
– most replication is in the nose
 Rhinovirus pathogenesis and
immunity
• Symptoms:
– relative to amount of viral shedding,
• rhinorrhea due to bradykinin and histamine
release

• Immunity:
– IFN limits progression of disease and also
adds to symptoms, increase ICAM expression
• only transient: >80 serotypes, sIGa protects
for only 18 months, CMI is not important
 The common cold- coryza
• Symptoms:
– URI/ sneezing
• rhinorrhea (clear, watery purulent/ mucoid
iff secondary bacterial infection)
– nasal obstruction--mild sore throat, H/A, malaise, low
grade fever, chills, myalgia
– often have sinusitis and OM
• Lab diagnosis:
– usually not necessary characteristic Ss
and Sxs
• Culture:
– Characteristic CPE in human diploid
fibroblast cells at 330C and acid labile
 Common cold treatment
• “Resolve in 48 hrs. with aggressive
treatment with decongestants, analgesics,
nasal vasoconstrictors and ABCs
– iff left untreated, will resolve in 2 days!!”
• hand- washing/ disinfect contaminated
surfaces
• Naturopathic:
– No sugar/ much fluids/ onions/ garlic,
probiotics, Pleo-Not, Oscillinum, Immune
matrix, Vitamin C, Zinc losenges, Yin Ciao/
Zong Gan Ling/ Jade Windscreen,
hydrotherapy with aromatic oils/
homeopathy/ TLC/ chicken soup/
lomatium dissectium, Cold-Fx etc.
 Chicken soup and the common cold
• Chicken soup “The Jewish penicillin”
– inhibits neutrophil chemotaxis in vitro
• theoretically diminish WBC response that
leads to cough and runny nose and nasal
congestion
– fluids
• help replenish electrolyte imbalance and
dehydration (from vomiting/ diarrhea)
– decrease symptoms of malaise
– Calories/ protein
• easy to digest, nutritional, support
immunity
 Zinc and the common cold
• Important for immune system (IFN), decrease
inflammation, decrease viral attachment to nasal
mucosa, inhibit viral replication, Zn fingers and Ab
synthesis and many other fxns.
• Zinc acetate/ zinc citrate/ zinc gluconate
– inconclusive results: 12 trials since 1984- 6 with
benefit, 6 without (formulations that contain sugar/
fructose as sweeteners decrease effect, need 40-80 mg )
– Better if sucked (not swallowed) & small frequent
doses (q2-3h)
• supplement with copper if long term (15 Zn: 1
Cu), long term high doses can suppress immune
system, decrease HDL
 Allopathic Rx’s
• Nasal vasoconstrictors
– rebound congestion with symptoms worse
• INF
– long term use can have side effects
• Decongestant:
– phenylpropanolamine increased risk of stroke in young
women
• Anti-histamine:
– diphenyhydramine (Benadryl/ Nytol) “greater impact on
ability to drive than 0.1% alcohol” do NOT give to elderly
• Pain relievers (ASA, acetaminophen, ibuprofen)
– reduce body’s immune response increase viral spread
• ABCs
– useless against primary infection
• flu and cold are caused by viruses NOT bacteria
 Quote of the day
• “Here in this body are the sacred
rivers: here are the sun and moon as
well as all the pilgrimage places…I
have not yet encountered another
temple as blissful as my own body”

– Saraha
 Quote of the day

• "Sit down before fact as a little

child,
• be prepared to give up every
preconceived notion,
• follow humbly wherever and to
whatever abysses nature leads,
• or you shall learn nothing."
• Thomas Henry Huxley