At this point I can see at least three possible causes of Susie’s illness:

* Covid vax shedding,

* A bad and lingering case of the flu or

*Walking pneumonia

*I also think there is a fourth cause that I am seeing and many are missing. Permanent damage from covid/shedding that flares up when your system is stressed.

….

I started poking around the internet at about the same time Wolfie did. At the time I was not aware that “Influenza A(H1N1)pdm09 [2009 Swine Flu] and A(H3N2) were the predominant viruses reported the week… ending January 11, 2025” – CDC

THE FLU

H3N2 Flu Symptoms

No matter what strain of influenza is circulating each year, you need to know what to expect from the flu. H3N2 virus infection usually lasts between five and seven days but can cause a severe cough that lasts up to three weeks. Whether it is caused by H3N2 influenza A or another strain, typical flu symptoms include: …

H3N2 is one subtype of the influenza A virus that often causes significant illness. Flu seasons are often more severe when H3N2 is the dominant strain causing illness.

So one possibility is a lingering flu. However it should not be hanging around for months.

……

WALKING PNEUMONIA

What is walking pneumonia? — Mayo Clinic

“Walking pneumonia” is an informal term for a common bacterial condition. It produces milder symptoms that appear more gradually than in other types of more serious pneumonia. Symptoms usually appear within two to three weeks of becoming infected and can continue for weeks. A cough could continue for months….

With walking pneumonia, you may feel like you have a cold. But symptoms are usually mild, so you likely won’t need bed rest or a hospital stay. You may not feel the need to stay home from work or school. So you may be out walking around. That’s how the illness got its name…

So a second possibility is an opportunistic bacterial infection that invades a weakened system.

…..

VACCINE SHEDDING

I am going to quote our resident expert, PAVACA on this.

[QUOTE]

PAVACA(@pavaca)  January 28, 2025 12:53 … #1404674

WOLF MOON —

Endless Thank You’s for today’s post. I don’t think this was an easy one to write.

I will weigh in with my thoughts:

IMO, our good DePat was a “sitting duck”, in some ways, for what I firmly believe was being terribly negatively affected by COVID-19 “vaccine” shedding.
— She was, for the last 18 months or so (perhaps longer), the caregiver for her late mother (who herself passed away from cardiac complications from the Moderna modRNA COVID-19 “vaccine” doses that she had taken);
— During this period, and after her mother’s death, DePat took over the household work and responsibilities that her mother had done (cleaning, cooking, shopping, etc.)
Because of the above, IMO, there’s a good chance that her natural immune system was getting hammered on a regular basis.

— She also had to keep up a demanding professional schedule as a vocal soloist in her choir. This also meant doing daily vocal practice at home.
— She lived with other COVID-19 “vaccinated” members of her family (father and at least one brother.)
Because of the above,since there is a 99.999% likelihood that the other members of the choir were also COVID-19 “vaccinated”, she was potentially exposed to COVID-19 “vaccine” shedding on multiple occasions.

That leaves what happened to her on / around 17 November 2024 at choir rehearsal. This is the rehearsal where DePat was beside a choir member who had just been “boosted” with COVID-19 “vaccine” shot #4.

Many of the symptoms that DePat described about her condition after 17 November match those found in the Appendix 1. List of Adverse Events of Special Interest section of this report about BNT162b2, given to the FDA on 30 April 2021: https://phmpt.org/wp-content/uploads/2021/11/5.3.6-postmarketing-experience.pdf
For examples: Chronic Fatigue Syndrome (page 2 of the Appendix 1.); Cough (page 3); Inflammation (page 5).

But I will posit that there’s something else in play here: the LIPID NANOPARTICLES in the modRNA COVID-19 “vaccines” — the chemical compounds that carry the “payload” of the modRNA to every cell in the “vaccinated” person’s body — and are ALSO carried by the EXOSOMES in the “vaccinated” person’s body to places like the SKIN and onto the BREATH.

These LNPs are TOXIC and DANGEROUS. They were formulated so that the “vaccinated” person’s body either doesn’t recognize and destroy them; or, that the “vaccinated” person’s body DOES recognize them but can’t eliminate them.

Now, here’s the thing:
It’s now DIFFICULT to find complete MSDS Safety Sheets for the ALC-0159 or for the ALC-0315 lipid nanoparticles used in the Pfizer-BioNTech modRNA COVID-19 “vaccines.” One used to be able to see complete MSDS Safety Sheets on these compounds. Not now. In fact, Yours Truly has found multiple chemical company supplier websites stating that “customers must call for further information”; and, even “this information is not available to the general public. It is only available to the FDA.”

For example, the MSDS Safety Sheet information for ALC-0159 and for ALC-0315 by Cayman Chemical now has THIS for Section 4 of the MSDS for EACH of these compounds (below is for ALC-0159; for ALC-0315 it is the same):

HOWEVER, Yours Truly downloaded the MSDS for BOTH ALC-1059 AND for ALC-0315 back in 2023, BEFORE this 2024 revision was done. Here’s the Section 4 for ALC-0159 FROM 2022 (the Section 4 for ALC-0315 from 2022 is the same);

What I’m getting at here is that, IMO, our good DePat WAS COVID-19 “vaccine” shed upon by that choir member in November 2024; that she immediately began to have “Long COVID”-type effects from it; that the modRNA that was shed on DePat from the COVID-19 “booster shot” that the choir had just had ALSO contained the lipid nanoparticles ALC-0159 and ALC-0315, which then also shed onto DePat; and that a cascade of negative effects took over.

Below is a paper that describes the pro-inflammatory effects of the LPNs in the modRNA COVID-19 “vaccines”;

https://pmc.ncbi.nlm.nih.gov/articles/PMC9047613/
“Pro-inflammatory concerns with lipid nanoparticles”
Seyed Moein Moghimi, Dmitri Simberg
28 April 2022

May our good DePat rest in eternal Peace.

[END QUOTE]

…..

I want to take a look at this paper PAVACA pointed to because I think it is KEY:

Pro-inflammatory concerns with lipid nanoparticles”

The development of ionizable cationic lipids has been a pivotal factor in the clinical success of lipid nanoparticle (LNP)-RNAi (Onpattro) and the two LNP-mRNA vaccines against SARS-CoV-2 (Pfizer-BioNTech and Moderna).1,2 The ionizable cationic lipids demonstrate improved efficacy and safety compared with the permanently charged cationic lipids.1,2 
However, acute side effects such as pain, swelling, fever, and systemic inflammatory responses have been reported in many human subjects receiving LNP-mRNA vaccines.
Although these vaccines use N1-methyl-pseudouridine-modified RNA (which is poorly recognizable by the Toll-like receptors 7/8), it is not clear how these vaccines elicit reactogenicity, but this presumably indicates that LNPs have intrinsic adjuvant activity.3 Infusion-related adverse effects have been noted in up to 19% of patients receiving Onpattro….

….Considering the rare episodes of human anaphylactic reactions following LNP-mRNA vaccine administration,6 we cannot disregard a role for a subset of monocytes and dendritic cells in orchestrating these responses. Extensive studies are now needed to map the interactions between ionizable cationic lipids and intracellular pattern-recognition receptors and unravel integrated and multifaceted mechanisms by which these lipids induce inflammasome activation. Such information would be valuable for identification and tailoring of lipid-based adjuvant and delivery systems and for generating diversified portfolios of vaccine components and platforms to provide immunity in specific target tissues….
The success of LNP-based vaccines has prompted a surge in overenthusiastic research focused on the broader application of LNP-based nanomedicines.2 Considering the pro-inflammatory nature of the currently available ionizable cationic lipids,4,5 notably their undesirable immune cascade initiated through the IL-1β release, and of other cationic lipids,7 the potential application of LNPs for systemic administration must be viewed cautiously. This is important, particularly when targeting biological barriers such as the blood-brain barrier with intravenously administered LNPs for the intended delivery of nucleic acid medicine to brain parenchymal cells to combat neurological diseases and disorders, which could initiate severe inflammatory reactions in the brain either directly or through monocyte recruitment...

DEFINING TERMS

Reactogenicity

Reactogenicity represents the physical manifestation of the inflammatory response to vaccination, and can include injection-site pain, redness, swelling or induration at the injection site, as well as systemic symptoms, such as fever, myalgia, or headache.

Anaphylaxis

 Anaphylaxis is a severe, life-threatening allergic reaction. It can happen seconds or minutes after you’ve been exposed to something you’re allergic to.

Systemic Inflammatory Response Syndrome

Systemic inflammatory response syndrome (SIRS) is an exaggerated defense response of the body to a noxious stressor (infection, trauma, surgery, acute inflammation, ischemia or reperfusion, or malignancy, to name a few) to localize and then eliminate the endogenous or exogenous source of the insult….Even though the purpose is defensive, the dysregulated cytokine storm can cause a massive inflammatory cascade leading to reversible or irreversible end-organ dysfunction and even death.

Mast Cell Activation Syndrome (MCAS)

Mast Cell Activation Syndrome (MCAS) happens with repeated symptoms of anaphylaxis – allergic symptoms such as hives, swelling, low blood pressure, difficulty breathing and severe diarrhea….

……

Gudthots added another piece of the puzzle.

[QUOTE]

Gudthots  Reply to  Gail Combs
 January 25, 2025 17:59 …. #1402668
An interview of a doctor that learned of Mast Cell Activation due to her daughter’s suffering of the condition. Goes into details of what is going wrong in the condition. I choose to suspend my reaction to one of her lines of work in order to learn more about this condition.

[I cut out the intro of what this doctor’s background is. GC]

Or macrophage activation syndrome.
Side note: Pepcid worked against CV as a histamine receptor blocker.

[PEPCID® is a histamine-2 blocker (H2 blocker) with the active ingredient famotidine –GC]

Reactive macrophage activation syndrome in a patient with parvovirus B19 infection, lymphocytic lichenoid vasculitis, urticaria and angioedema

Introduction

A 47-year-old woman had a history of episodic acute intermittent angioedema and urticaria with moderate pruritus for one month. She was on 10 mg of loratadine daily. She had a fever of 39°C, arthralgia, fatigue, and angioedema of the upper respiratory tract. Laboratory results are shown in Table 1. She had elevated IgE (206 kU/L). The immunoassay for C1-esterase inhibitor was normal. She was treated with H1- and H2-blocking antihistamines, and methylprednisolone intravenously (1 mg/kg/day). Culture results and viral titers were negative except for a high positive titer of specific IgG antibody to parvovirus B19 of 11.1 (positive titer >1). On the third week of hospitalization, she deteriorated rapidly and developed a macular rash on the trunk and extremities with generalised lymphadenpathy, liver dysfunction and disseminated intravascular coagulopathy (DIC) (Figure 1). A skin biopsy specimen was compatible with lymphocytic lichenoid vasculitis. An inflammatory pattern centered on the basal layer of the epidermis and upper dermis in a dense band-like distribution. Direct immunofluorescence showed no IgG, IgA, IgM, C3, C1q and fibrinogen deposits. A bone marrow aspirate showed hemophagocytosis (Figure 2). Parvovirus B19 DNA was detected by the polymerase chain reaction (PCR) in bone marrow (Figure 3). Macrophage activation syndrome was confirmed. The patient was treated with methylprednisolone 250 mg/day intravenously and intravenous immunoglobulin (IVIG) 0.55 g/kg BW/day for five consecutive days, followed by methylprednisolone 1 mg/kg daily. Fresh frozen plasma and enoxaparin were administered. Two days after treatment, she improved. Monthly infusions of IVIG were continued for 6 months. Corticosteroids were tapered gradually to 8 mg of methylprednisolone daily. On periodic follow-up, the patient was quite well without episodes of angioedema and no new skin lesions were seen. Our patient met all criteria for reactive macrophage activation syndrome (rMAS) outlined by Imashuku.

[UNQUOTE]

………

Useful definitions before we dive into a couple of papers on this subject:

Presynaptic Neuron – an overview | ScienceDirect Topics

As a convention, the neuron transmitting or generating a spike and incident onto a synapse is referred as the presynaptic neuron, whereas the neuron receiving the spike from the synapse is referred to as the postsynaptic neuron.

Hematopoiesis 

Hematopoiesis is the process through which the body manufactures blood cells…. Hematopoiesis is the production of all of the cellular components of blood and blood plasma. It occurs within the hematopoietic system, which includes organs and tissues such as the bone marrow, liver, and spleen.

Refractory chronic urticaria

Urticaria is a mast-cell-driven disease characterized by the development of transient pruritic wheals [hives] with or without associated angioedema [sudden swelling of the deep layers of the skin and subcutaneous tissues]… Chronic urticaria (CU) is defined by the presence of recurrent urticaria, angioedema, or both, for a period of 6 weeks or longer..

And now another paper:

Antihistamine: New Advancement in H1&H2 Receptor used for Pregnancy

ABSTRACT

…This study shows that H1 antihistamine therapy alone is not statistically better to combined H2 and H1 antihistamine therapy for the treatment of chronic urticaria symptoms. Histamine has been one of the biological amines most extensively studied in medicine. It encourages the contraction of smooth muscles and the release of stomach acid, enhances vascular permeability, functions as a neurotransmitter, and has a range of actions in the control of the immune system, allergies, inflammation, haematopoiesis, and cell division. Histamine works by attaching to the H1, H2, H3, and H4 receptors. H3 and H4 receptors are predominantly presynaptic and haematopoietic, respectively, whereas H1 and H2 receptors are widely dispersed. Human H1- and H2-histamine receptors were cloned and described in the early 1990s, followed a few years later by human H3- and H4-histamine receptors. The main treatment for chronic urticaria is second-generation non-sedating non-impairing H1 antihistamines. Then, the H1 antihistamines permitted dosage is raised by a factor of up to four…

SO THERE ARE NOT TWO BUT FOUR HISTAMINE RECEPTORS.
Back to the paper:

INTRODUCTION

Histamine decarboxylase, an enzyme, creates histamine, a substance that occurs naturally in the body, entirely from l-histamine. It is expressed in cells all throughout the body, including basophils, mast cells, neurons in the central nervous system, and parietal cells in the stomach mucosa [1]. Histamine is a low-molecular-weight amine [2].

Histamine has a significant biological function in maintaining human health by acting on four different types of receptors. Cell proliferation and differentiation, haematopoiesis, embryonic development, regeneration, and wound healing are all impacted by it. In Histamine is produced by the mammalian central nervous system, neurons that only contain cell bodies in the posterior hypothalamic tuberomamillary nucleus, and axons that deliver histamine to the frontal and temporal cortexes and other regions of the brain. [3,4]. With the identification of certain histamine receptors, we have learned a lot more about the effects of histamine in the past ten years. Now, it is known that histamine binds to four distinct binding sites (H 1 -, H 2 -, H 3 -, and H 4 -receptors)[5,6,7]. Sneezing, nasal obstruction, itching, and rhinorrhoea are the primary early allergic response symptoms caused by activation of the H 1 -receptor by histamine binding. Leukotrienes, prostaglandins [8, 9], and other cytokines are also produced in greater amounts when H 1 receptors are activated, which also occurs before the late phase of an allergic reaction [10,11]. Several physiological and pathological processes, including skin allergies, “septic inflammation, and various neutral transmission and digestion [15, 16]. The histamine receptors found in the skin are partially blocked by H1 antihistamines. The purpose of this clinical trial was to determine whether a combination therapy using H1 (hydroxyzine) and H2 (cimetidine) antihistamines is more effective than H1 antihistamines alone in treating patients with refractory chronic idiopathic urticaria [20,21]. Histidine decarboxylase, an enzyme, catalyses a reaction in which the amino acid LHistidine is decarboxylated to produce histamine (HDC). Mast cells, Histamine are produced in large numbers by basophiles, enterochromaffin-like cells of the stomach mucosa, and histaminergic neurones. These cells also store histamine within the cells in specialised storage granules.

First-generation antihistamines, often referred to as sedating antihistamines, were the initial group of these medications to be developed. Examples include diphenhydramine, chlorpheniramine, and promethazine.

Second-generation or non-sedating antihistamines were developed to address the shortcomings of first-generation antihistamines. These medications, including cetirizine, fexofenadine, and loratadine, are more selective for the H1 receptor and exhibit a lower capacity to cross the blood-brain barrier, leading to fewer side effects in the central nervous system (CNS)…

H2-receptor antagonists (H2RAs)

Histamine H2-receptor antagonists for urticaria

H2RAs are used clinically in the treatment of acid-related gastrointestinal conditions, such as peptic ulcer disease, gastrooesophageal reflux, and dyspepsia…

Medications contained in this group include cimetidine, famotidine, ranitidine, roxatidine, lafutidine, and nizatidine, most of which are available as oral preparations….

There is still a degree of uncertainty as to the precise mode of action of H2RAs. Histamine is a potent mediator of immediate hypersensitivity reactions. Fifteen per cent of the histamine receptors in the skin are H2-receptors, and it is acknowledged that human skin mast cells, which store histamine also express H2-receptors (Lippert 2004). The H2RAs are reversible structural analogs (a chemical compound with a slightly altered chemical structure) of histamine that cause a decrease in the tonic activation rate of the receptor. Thus, these agents act as inverse agonists (agents that bind to the same receptor binding-site as an agonist for that receptor and reverse the activity of receptors) with a functional antagonism of histamine activity, hence, reducing the histamine activity on the receptor sites. In this way they may be able to block histamine release and curtail, or even prevent, symptoms of urticaria from occurring. It has also been suggested that one of these H2RAs, cimetidine, has an immunomodulator function (Nielsen 1996) and may have a role to play in chronic autoimmune urticaria….

>>>>>>>>>>>>>>>>>>>>>>>>>

GAIL COMBS THE LAB RAT

I have been taking daily for at least a week:

20 mg Loratadine (double dose H1 Antihistamine)

400 mg Cimetidine (double dose H2 Antihistamine)

888 mg Fenbendazole

24 mg of Ivermectin

2 multi -vitamins (Women + 50)

1500 Vitamin C

400IU Vitamin E

K2 (90mcg) + D3 (5000 IU)

Vitamin B complex.

B 12 under the tongue helps for a short while.

1000 mg NAC

60,000 units Serrapetase (acts as an anti-inflammatory)

10 mg Melatonin (Sleep aid)

240 m6 Magnesium Glycinate (for muscle spasms + sleep)

100 mg CoQ 10

A Brazil nut for selenium, green tea & nettle leaf tea (a natural anti histamine)

For arthritis which has flared up:

Glucosamine Hcl (1500 mg) + Chondroitin (200 mg) + Hyauluronic acid (6.6 mg) + MSM (750 mg) + Boron (5 mg)

I am not taking Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) such as Ibuprofen, Naproxen or Aspirin because they tear up my stomach. However when I do take them, they help.

>>>>>>>>>>>>>>>>>>>>

When I took ‘goat spit’ and Moxidectin the improvement was quick.

Moxidectin and Ivermectin Inhibit SARS-CoV-2 Replication

This time I am getting only a slight improvement from the Ivermectin.

My next step is to head to the medical clinic where I will probably be given Prednisone (a cortisone) and an antibiotic to take care of any infection in my lungs.

MY CONCLUSION

I have had allergies for years and I am pretty good at telling the difference between an illness and an allergy. I am seeing zero indication of an illness.

A very good allergist once told me to think of my allergies as a bucket that you are filling up. You can get away with chocolate. You can get away with strawberries and even cantaloupe. BUT put them all together and you get hives.

What I am wondering is if we are seeing permanent alterations in our bodies, or just a higher load of toxins like spike shedding and perhaps crap that has been sprayed in the air.

And that brings me to the last bit of information H/T to the video from Gudthots.

 What the bleep can I eat?!

This has lists of food for those with specific food intolerance including histamine. This is a second listing: Foods High in Histamine

I SURE HOPE SO!