Bringing Chickenpox to the Boil

Bringing Chickenpox to the Boil

by Hilary Butler

Avid readers of dramatic novels from yesteryear will recall stories from the days when fevered patients were watched over by family, and the oldies in the group just “knew” that a proper fever would “break” with a sweat. When that happened, they knew that the prognosis would be good. Of course, such sentiments today would be greeted with alarm, or scepticism, by those who consider illness should never be endured.

Isn’t that why acetaminophen (in all their different brand names) is reached for, at the first sign of a fever?

In 2001, a headline

1 made me look twice. “Sweat has the power to fight off disease.” We were told that sweat contains a versatile antibiotic that may be on the front line against disease-causing bacteria and that: “The researchers said dermcidin probably plays a key role in the innate immune responses of the skin”.  A news roundup from the British Medical Journal told us2 that dermcidin killed escherichia coli, enterococcus faecalis, staphylococcus aureus and Candida albicans. It was active at high salt concentrations and the acidity range of human sweat. In concentrations of 1–10 μg/ml, it killed all of the staph aureus colonies in only four hours. Unsurprisingly, the scientists didn’t know how dermcidin worked.

Up until the late 1990s the skin was simply thought to be a “barrier” with no active participation in the immune system. The original 2001 paper

3 said that during some inflammatory skin disorders and wound healing, skin cells functioning within a salty sweat with a pH of 4–6.8, produced many effective pharmacologically active substances, such as immunoglobulin A, interleukin 1, 6 and 8, tumour necrosis factor, transforming growth factor β receptor, epidermal growth factor, and a prolactin-inducible protein.

As time has gone on, other researchers have taken a closer look at skin, and have found that the neutrophil,

4 which is the professional phagocyte of fundamental importance for defence against micro-organisms, provides instant help, not only in microbial infection,5 but to the growth factors when the skin is broken and there is a risk of infection. Another article6 says that mast cells, macrophages and skin cells produce antimicrobial peptides. These are called cathelicidin, which disrupts bacterial cell walls, modifies the host cells inflammation, and provides additional immune defence. At the heart of this all, is our friendly neutrophil:

“These studies clearly illuminate the importance of neutrophil recruitment in cutaneous defense against bacterial infection. … Recent advances in understanding of innate immune defense systems have suggested that these ancient evolutionary immune mechanisms may be important to human disease yet previously underappreciated.” (Underlining mine)

The article looked at whether just skin and mast cells were involved, or whether neutrophils were also important. Using mice, they found that mice with few neutrophils developed much worse tissue death (necrosis) and had 3,000 times the amount of bacteria on the skin than mice with active neutrophils. The skin cells worked hard and could produce some cathelicidin on their own, but didn’t have the killing power of the skin cells plus neutrophils. The article’s conclusion said that life-threatening necrotizing skin and soft-tissue infections can develop in patients with depressed neutrophils, but that numerous examples exist of patients with increased frequency of skin infections who have no

“demonstrable defect 7 in leukocyte recruitment or function.”

Properly fed, healthy children, whose parents know what to do, and what not to do, will rarely get any complications to chickenpox. As was the case for our children, well-managed chickenpox should not even lead to any scarring. So let’s ask some questions here, with chickenpox in mind. What is the function of fever?

Here’s a really simple statement11 from twenty years ago: “… elevated body temperature enhances the infl ammatory response and function of the immune system at the same time that it reduces the replication of microbes and tumor cells.”

 

 

 

 

Not so simple is this sentence.

 

“Fever also appears to be a prominent component of cytokine therapy and attends the use of several biologic response modifiers.”

Fever switches on the chemical messengers and processes which call on the body immune system to respond and “modify” or deal with the infection.

If fever is a key to an immune-system process, without a fever, how effective is the body going to be in fi ghting viruses, or bacteria? With viruses like chickenpox, which are known to have an affinity with

 

group A streptococcus,

which can infect the pox rash and so have access to the body, what do we want the immune system to do? It’s pretty obvious isn’t it?

We

 

want

to allow the body temperature to rise to the level it needs so that all the on-switches can be thrown.

We

 

want

the body to send out all those little chemical messengers which get the antiviral side of things going.

We

 

want the messengers to call the neutrophils to join the skin cells in producing cathelicidin, and to work with the whole array of anti-viral and antibacterial components12 in “sweat” to stop group A streptococcus

in its tracks.

As a 1991 article13 says: “… temperature elevation … enhances the processes involved in initial antigen recognition and support for immunological specifi c response to challenge.

We want the body to recognize the virus, ring the bell and sound the red alert (fever) to fight, don’t we? Why, then, turn the fever off with acetaminophen products? Doesn’t that defy logic?

Another article14 of that era said: “There is considerable in-vitro evidence that a variety of human immunological defences function better at febrile temperatures than at normal ones … Studies have clearly shown that fever helps laboratory animals to survive an infection whereas antipyresis15 increases mortality.”

A 1998 article16 said: “The elevation of body temperature by a few degrees may improve the efficiency of macrophages in killing invading bacteria, whereas it impairs the replication of many microorganisms, giving the immune system an adaptive advantage. There is a simultaneous switch from the burning of glucose, an excellent substrate for bacterial growth, to metabolism based on proteolysis and lipolysis. The host organism is anorectic (doesn’t want to eat) minimizing the availability of glucose, and somnolent, reducing the demand by muscles for energy substrate. During the febrile response, the liver produced proteins known as acute phase reactants … the net effect … is to give the host organism an adaptive advantage over the invader.” (Underlining mine.)

Treating fevers is dicing with more severe infection, and a greater likelihood of death, because fever is a key immune response to get the immune system working properly.

You mess with fever, and you mess with lots of things. It stands to reason. Do you need to know what the medical profession does not yet know about fever in its totality, to see that?

 

Back to chickenpox. Tucked away in a small co

 

rner of the New Zealand Herald in 2001 was a warning:17 “GPs warned over chickenpox drug.” Doctors were warned about treating chickenpox with ibuprofen to reduce fever because of a higher rate of necrotizing fasciitis18. There was no mention of paracetamol in the warning, yet, since both perform the same function, there is reason to argue that paracetamol might do the same as ibuprofen. In USA, the link between the use of non-steroidal anti-infl ammatories and chickenpox reached the ears of doctors,19,20

but not, it seems, the public.

There was a flurry of articles suggesting it was dangerous to use anti-febrile drugs with chickenpox; there was also an article by a group of doctors, who in defiance of all logic and known immunological impacts of drugs used to reduce fever, decided that there was no association. They

 

21

decreed that when parents used drugs to “treat high fever and severe illness”, drug use was merely the identifying factor of who was at high risk for secondary bacterial infection! That interesting little word “coincidental” again.

… I see the increase in these infections as evidence of a total lack of common sense about how to prevent complications. I see the association between nonsteroidal anti-febrile drugs and GAS as a predictable outcome of the loss of home nursing skills and handed-down generational wisdom. I see the increase in secondary bacterial infections as something which can stem from parental lack of understanding that messing around with fever, and using symptom-suppressing/immune-suppressing drugs can restrict the ability of the immune system to fi ght the virus. It also reduces the ability of the leucocyte system of neutrophils, macrophages and phagocytes to fight bacterial toxins from secondary bacterial infections.

As pointed out in Chapter 70, if you don’t have enough vitamin C in your system, then the neutrophils won’t be recognized by the macrophages, and you might be in big trouble, because if that happens, the result could be toxic shock/sepsis taking hold very quickly. Even if you have enough vitamin C, if the amount of GAS toxin is such that the glucose transporters (which are part of the vitamin C shuttle service which takes ascorbate from A to B) are blocked, that can result in a GAS infection which threatens to run out of control. The quickest way to restore the immune function in a case of sepsis is by giving vitamin C intravenously. The body can fight sepsis by itself, but it’s a bit more of a lottery as to whether it will succeed if it doesn’t have the tools to do the job.

BOOK: From One Prick to Another

 

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