[back] Chickenpox

Bringing Chickenpox to the Boil

by Hilary Butler

[Chapter 48] From One Prick to Another

[pdf version]

This appeared in VRAN Newsletter Fall 2008

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.

In 2001, a headline¹ 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 paper3 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.”

Many countries have recently been bombarded with stories⁸ about chickenpox resulting in death or serious bacterial infection.

The New Zealand Herald article cited above talked about a 14-year-old student, Luchan Li, who “died of heart failure as a result of a blood infection, also known as septic shock. The illness was possibly connected to a case of chickenpox Luchan had two weeks earlier, but no one knows for certain.”

At the same time, the Daily Mail in England ran a very emotive article about a little girl called Isobel: “Within days, the virus had taken hold of her body, leading to toxic shock syndrome – a rare type of blood poisoning caused by bacteria – and necrotising fasciitis, a bacterial infection that rapidly eats away at the flesh.”

Isobel’s mother said that “íf she’d had a big dose of antibiotics at the start, none of this would have happened.” Just maybe Isobel didn’t have enough vitamin C to operate her leucocyte system to get rid of the bacteria. And did Isobel’s mother use the English version of acetaminophen? The second child in the article, Christopher, who died from chickenpox, was given that drug.

Group A streptococcus also causes scarlet fever, and rheumatic fever, which in most developed countries, started declining in 1850⁹, well before antibiotics were marketed. As a marker of group A streptococcus severity, scarlet fever has exhibited at least four cycles of varying severity followed by remission, believed to have been due largely to virulence variation. A very good article¹⁰ on the web states, “…reports of fatal infection with invasive strep A bacteria have been increasingly recognized in the United States since 1987. Researchers do not know why the new strain of strep A is on the increase or why it targets certain otherwise healthy people.”  Older textbooks and papers all mention the need to be careful when GAS infections follow chickenpox. For thirty years after the introduction of penicillin, there were no reports of serious GAS complications after chickenpox. But those years follow hard on the heels of the “conquest” of rickets, which up to the 1930s had affected nearly 50% of wealthy parents’ children in London. There are still some alive who remember the blackstrap molasses and cod liver oil morning routines of the times. Both “malnutrition” and “bad” nutrition can result in infections becoming far more serious.

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.”

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.”

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.)

I could bombard you with article after article showing not only that fever in infections is beneficial, but also that when you use paracetamol products, you increase the likelihood of dying and you increase the likelihood of complications.

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 corner 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. They²¹ 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.

Doctors²² will say that the resurgence of streptococcal infections “highlights the wisdom of recommending widespread use of the varicella vaccine to prevent this kind of infection”. Why worry about GAS, when a vaccine will prevent both chickenpox and GAS. On the surface, this looks logical.

Get smart with your computer, and the whole thing can crash. That analogy applies to the processes of fighting infections. So the next time you read a historical novel where the family is relieved to see the break out of a fevered sweat, you will have an idea why. The anecdote of the old wives wins out yet again. Everyone knew that to beat the sickness lottery, a big sweat was usually a plus. Now we know why.  A big sweat is part of the beneficial natural defense your skin immune system uses to fight any bacterial flora on/in the skin, such as group A streptococcus.

A big sweat shows that the immune system is working properly. A fever and a sweat in any infection, if you do not have heart or lung disease,²³ is the right thing²⁴ to allow to happen.

TLC,²⁵ drinks, maybe cool cloths to the wrists and face, and a gentle breeze from a slow fan is all that is needed.

5 Borregaard, N. et al. 2005. “Neutrophils and keratinocytes in innate immunity – cooperative actions to provide antimicrobial defense at the right time and place.” J Leukoc Biol, 77(4): 439–43, April. Epub 2004, December 6. Review. PMID: 15582983.

6 Braff, M.H. et al. 2005. “Keratinocyte production of cathelicidin provides direct activity against bacterial skin pathogens.” Infect Immun, 74(10): 6771–81, October. PMID: 16177355.

12 Dorschner, R.A. et al. 2001. “Cutaneous injury induces the release of cathelicidin anti-microbial peptides active against group A streptococcus.” J Invest Dermatol, 117(1):91–7. PMID: 11442754. http://www.nature.com/jid/journal/v117/n1/pdf/5601121a.pdf (Pox from chickenpox qualifi es as cutaneous injury.)

13 Roberts. N.J. Jr. 1991. “Impact of temperature elevation on immunologic defenses.” Rev Infect Dis, 13(3): 462–72, May–June. Review. PMID: 1866550.

23 Shann, F. 1995. “Paracetamol: use in children.” Australian Prescriber, 18: 233–4. http://www.australianprescriber.com/magazine/18/2/33/5/.  Accessed 6 December 2007.

24 Eichenwalk, H.F. 2003. “Fever and antipyresis.” Bulletin of the World Health Organization, 81(5). http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0042-96862003000500012 . Accessed 6 December 2007.

25 TLC = Tender loving care.