MicrobiologyBytes

Today’s post is from guest blogger Alexis Bonari, freelance writer and blog junkie. She is currently a resident blogger at onlinedegrees.org, researching online degree programs. In her spare time, she enjoys square-foot gardening, swimming, and avoiding her laptop.

MicrobiologyBytes welcomes guest bloggers who would like to contribute occasional posts which conform to the style and content of this site. If you would like to be a guest blogger here, please email your post with a completed copyright release form to me at: alan.cann@gmail.com

Cystic fibrosis (CF), a hereditary chronic disease affecting pulmonary and digestive function in over 70,000 individuals worldwide, has proven difficult to analyze in terms of the relationships among lung function, patient age, and microbial colonization of the airways. In the first study of airway microbial colonies in CF patients ranging from neonates (9 months) to adults (72 years), younger patients have been recorded as having more diverse airway bacteria than their older counterparts. This could imply that more limited bacterial diversity and deteriorating airway health correlate.

The study, conducted at the University of California in San Francisco, analyzed deep-throat swab and expectorated sputum samples from 51 patients at the University’s pediatric and adult CF clinics. Analysis was performed using the PhyloChip microarray, which enabled control for variations in fragmentation, biotinylation, hybridization, washing, staining, and scanning; the resulting data were used to generate a phylogenetic distance matrix. Despite these and many other precautions taken, the study suggests that factors such as unmeasured antibiotic use, chest physical therapy, adherence, nutrition, and other potential variables might encourage more stringent inquiry into the subject of airway microbial diversity as a function of patient age. With the affirmation that bacterial community structure and composition are substantial factors in defining the functionality of microbial assemblage and host health status, future research has the potential to further explain pulmonary health in terms of airway microbiota diversity.

Airway Microbiota and Pathogen Abundance in Age-Stratified Cystic Fibrosis Patients. 2010 PLoS ONE 5(6): e11044. doi:10.1371/journal.pone.0011044
Bacterial communities in the airways of cystic fibrosis (CF) patients are, as in other ecological niches, influenced by autogenic and allogenic factors. However, our understanding of microbial colonization in younger versus older CF airways and the association with pulmonary function is rudimentary at best. Using a phylogenetic microarray, we examine the airway microbiota in age stratified CF patients ranging from neonates (9 months) to adults (72 years). From a cohort of clinically stable patients, we demonstrate that older CF patients who exhibit poorer pulmonary function possess more uneven, phylogenetically-clustered airway communities, compared to younger patients. Using longitudinal samples collected form a subset of these patients a pattern of initial bacterial community diversification was observed in younger patients compared with a progressive loss of diversity over time in older patients. We describe in detail the distinct bacterial community profiles associated with young and old CF patients with a particular focus on the differences between respective “early” and “late” colonizing organisms. Finally we assess the influence of Cystic Fibrosis Transmembrane Regulator (CFTR) mutation on bacterial abundance and identify genotype-specific communities involving members of the Pseudomonadaceae, Xanthomonadaceae, Moraxellaceae and Enterobacteriaceae amongst others. Data presented here provides insights into the CF airway microbiota, including initial diversification events in younger patients and establishment of specialized communities of pathogens associated with poor pulmonary function in older patient populations.

Related:

• Can the Common Cold Cure Cystic Fibrosis?
• Molecular basis for Pseudomonas aeruginosa persistent infections in CF patients
• Other Guest Bloggers

Today’s post is from guest blogger Melissa Tamura from Zen College Life, a directory of online degrees.

MicrobiologyBytes welcomes guest bloggers who would like to contribute occasional posts which conform to the style and content of this site. If you would like to be a guest blogger here, please email your post with a completed copyright release form to me at: alan.cann@gmail.com

There’s no doubt that antibiotics have revolutionized medicine. Before antibiotics were available, any bacterial infection was potentially lethal. However, since their widespread use started in 1945, most bacterial infections are easily treated. Despite this good news, there are some surprising side effects of common antibiotics that are not publicized.
Antibiotics are compounds that kill or inhibit the growth of bacteria. However, antibiotics are not able to differentiate between ìbadî bacteria and ìgoodî bacteria. For example, at any given time, human bodies are awash in bacteria, and many of these bacteria are actually helpful to body systems.
It’s easy to understand, for example, one of the most common side effects of antibiotics: digestive upset. Many people complain of mild nausea or diarrhea when taking a course of antibiotics. This is due to the fact that the antibiotic, while killing the harmful bacteria, has also killed some of the necessary good bacteria that exists within the digestive tract. Overall, antibiotics are considered very safe despite these sometimes annoying side effects.
Yet as more synthetic, man-made antibiotics are created and placed on the market, there appear to be some unusual side effects that no one anticipated.
One of more surprising side effects of one antibiotic is possible tendon rupture or tendonitis. This painful side effect has been linked to Levaquin, an antibiotic first produced in 1996 and later refined in 2004. According available anecdotal information, some users have torn their Achilles tendon when on this antibiotic. However, potential harm is not limited to just that tendon. It may also cause injuries to other parts of the body, such as thumbs, biceps, shoulders and hands. Research into verifying this possible side effect is ongoing.
Another unusual side effect linked to an antibiotic is mood instability. Most often associated with such antibiotics clustered in the Fluoroquinolone family, patients have reported experiencing symptoms such as nervousness, agitation, anxiety, fears centered on distrust, and suicidal thoughts. These side effects are listed for such brand antibiotics as Cipro and Floxin. Because no one is quite sure why this is the case, further study is warranted.
Augmentin, another antibiotic, has been associated with unusual bruising or bleeding. While many people can tolerate this side effect and experience no lasting harm, people with blood disorders may not fare as well. Other cited side effects of Augmentin include vaginal discharge or irritation. This side effect is probably related to the antibiotic’s destruction of some of the good bacteria that live in the uro-genital area.
Perhaps one of the more disturbing possible effects of antibiotics involves children. The U.S. National Institutes of Health describes some lasting health effects for children under age two. It appears that some children who used antibiotics very early, may exhibit such lasting symptoms as eczema, wheezing, and other asthma related problems. In scientific studies, it appears that children, who have not had to use antibiotics before age two compared to those who have, show significantly less asthma-related symptoms. Obviously, children under two are sometimes more at risk to bacterial infection, and antibiotics are absolutely necessary. Medical research is studying this phenomenon to try and limit its effect.
For anyone who has had a serious bacterial infection, the quick recovery thanks to antibiotics can’t be underestimated. However, as in anything, people need to be aware of the types of medications that they take and the possible adverse side effects. Though most side effects are short lived and not harmful, medical literature suggests that this is not always the case.

Today’s post is from guest blogger Helen Fry, who is a student at the University of Leicester.

MicrobiologyBytes welcomes guest bloggers who would like to contribute occasional posts which conform to the style and content of this site. If you would like to be a guest blogger here, please email your post with a completed copyright release form to me at: alan.cann@gmail.com

A quick glance at the British National Formulary and it’s easy to see just how many antibiotics are licensed for use in the UK. What is more difficult to see is how many antiviral agents are available, and this is because there are much fewer. The only viral diseases with treatments listed in BNF 57 are HSV, VZV, HIV, RSV, viral hepatitis and influenza. Viruses are the most abundant ‘lifeforms’ on the planet and there is a huge diversity of viruses that cause disease in humans. Viral disease, although often milder than bacterial or eukaryotic disease, accounts for a major burden on the health service and is a considerable cause of morbidity and mortality. Some viral diseases cause very severe infections and are a heavy global issue, such as HIV and viral diarrhoea (a major cause of infant and childhood mortality in countries without safe drinking water). So if viruses are so abundant and are such a global health pest, why are there so few antiviral agents?

There are several reasons why this is the case. First there is the difficulty of researching viral disease. Most pathogenic bacteria can be cultured and investigated fairly easily, with some notable exceptions such as TB and Chlamydia trachomatis. Culturing and investigating viruses is a lot harder, as it requires cell culture methods, where the appropriate line of eukaryotic cells is grown up and infected with the virus. This means that the virus cannot be studied directly, as with a growing population of bacteria, and because they are so small they can only be visualised via electron microscopy (The impact of cell culture sensitivity on rapid viral diagnosis: a historical perspective). There are non-culture based detection methods, but these only confirm the presence of the virus, they do not allow it to be studied. Viruses do not release any compounds on their own, any proteins made are produced in the host cell, whereas bacteria release toxins and chemotactic agents, quorum sensing molecules and siderophores, to name a few. This makes them easier to study. The fact that viruses are harder to study means that less is generally known about them, and it is a lot harder to identify potential targets for antivirals. On the other hand, viruses have much smaller genomes (on the whole, with some obvious exceptions), meaning that the genomes can be sequenced easily (Role of Cell Culture for Virus Detection in the Age of Technology).

Once a virus has been fully characterised, despite the difficulties, it is still problematic to make useful antiviral agents, and even the ones licensed in the UK are often quite toxic. This is for several reasons. Since the most important part of the virus life cycle takes part inside host cells antivirals often have to penetrate the cell in order to be effective. This means that the drug has to be highly specific for virally infected cells or risk being toxic to healthy cells. The viruses use host cell machinery to replicate themselves, meaning that a drug targeted against this part of the cycle risks affecting genome replication in healthy cells unless a virus specific target can be identified. Bacteria are prokaryotes, which mean that their cells are highly different to ours and it is often a simple matter of identifying a difference between our cells and theirs, and finding a molecule that interacts with it, such as the beta-lactams and cell wall synthesis. Antivirals have similar issues to antiprotozoals, in that finding a compound active against the microbe is not that hard, the difficulty lies in finding one that does not interact with host processes and is therefore non-toxic.

Finally, however, it all comes down to money. Drug development is now a process that is left exclusively to pharmaceutical companies due to its prohibitive costs, and since they are primarily a business rather than a service, all activity undertaken by them will inevitably be profit driven, rather than need driven. Bringing a drug to market now costs several million US$ and taken over 10 years from target identification to phase IV clinical trials. It is therefore a huge investment, and the drug companies want to be as such as possible that their drug will make it to market and will make as much money as possible before the patent runs out. Since patents last for 20 years, a drug may only have 5 years to make back the money it took to develop before cheaper generics can be made. This has caused companies to focus on drugs that are least likely to fail trials due to toxicity and that will make the most money in a short amount of time. Therefore the focus has been on lifestyle drugs that people will take every day for years on end, such as statins and antihypertensives, that have a low risk of toxicity and are well established in doctors’ prescribing pads. HIV therapy has benefited from this, as HIV+ people will need to take their medication every day for the rest of their lives. This, along with the fact that HIV is a rapidly fatal disease without medication meaning that drug companies can charge almost what they like for them, has meant that the number of effective, less toxic antiretrovirals is increasing and is already fairly big in comparison to other viral illnesses. Drug companies will risk producing drugs that are more likely to be toxic if they can charge a large amount for them once approved. This is usually the case for life-threatening illnesses, explaining why chemotherapy for cancer costs so much (in the tens of thousands for a single cycle in some cases), but is quite good these days, at least for the common cancers.

The incentive of money can be seen with the influenza drugs. Not many people have the need for influenza antivirals, since there is a pretty good vaccine produced each year for those at risk, and those not in high risk groups do not tend to suffer from severe enough disease to warrant treatment with anything other than blankets and Lemsip. So why are there two good drugs sitting on the market when they are not needed? The answer lies with the government who, fearing an approaching flu pandemic (we are due for one) decided to stockpile the anti-influenza drugs before they were widely used and resistance developed.

The biggest burden of viral disease, as with most infectious diseases, lies in developing countries. They are the worst hit by the HIV pandemic, suffer outbreaks of haemorrhagic fevers, are plagued by water borne viral diarrhoeal diseases and various other viral nasties. However, since they for the most part do not have the capital to fund a national health service and the people cannot afford medications themselves, these countries and their endemic diseases have been largely ignored by the drug companies due to the lack of profit potential. This means that the countries worst affected by HIV are the ones who do not have access to effective antiretroviral therapy, and that children die in the thousands because of viral diarrhoea. Some drug companies are starting to research third world diseases, but progress is slow and funding is not the best. Since we in the west need medications we cannot boycott the companies, and allowing patents to be extended would only put more strain on the already overwrought NHS. However, there needs to be a shift in attitudes towards making the companies more responsible for the drugs they develop.

Related:

• MicrobiologyBytes: Antivirals
• GSK to provide cheap drugs to the developing world
• Targeting inside-out phosphatidylserine as a therapeutic strategy for virus diseases

Today’s post is from guest blogger Sarah Scrafford, who regularly writes on the topic of ultrasound technician salary. She invites your questions, comments and freelancing job inquiries at her email address: sarah.scrafford25@gmail.com.

MicrobiologyBytes welcomes guest bloggers who would like to contribute occasional posts which conform to the style and content of this site. If you would like to be a guest blogger here, please email your post with a completed copyright release form to me at: alan.cann@gmail.com

It’s a common enough practice to pop antibiotics the moment you’re down with something as harmless as a common cold, but that’s exactly what you’re not supposed to do. An antibiotic will not help relieve your cold or its symptoms because it is caused by a virus, not bacteria. And antibiotics are not effective in fighting viral infections. There’s so much we don’t know about these drugs that can both save lives and threaten them at the same time. So here’s some detailed information about antibiotics, information we must all be familiar with and aware of:

• Antibiotics don’t work against viruses: They are only effective against some bacterial, parasitic and fungal infections. So don’t just pop them in your mouth because they’re lying around the house; instead, consult your medical practitioner and take only the medication that he/she prescribes.
• They contribute to the formation of germs that are resistant to antibiotics: When we misuse antibiotics, especially for illnesses that are not caused by bacteria, it leads to the formation of new strains of bacteria that are immune to the antibiotic you’ve just had. So a new antibiotic has to be invented to take care of this bacteria and the infections it could cause, and when this is misused too, the cycle keeps repeating itself. When more and more antibiotics are used, it leads to the development of many more bacteria that are antibiotic-resistant. As a result, illnesses last longer and you have to spend more on visits to the doctor and newer forms of treatment and medicines.
• You must take them as prescribed: Just because your symptoms have eased or your infection cured, it doesn’t mean you can stop taking your prescribed antibiotics. You need to take them exactly as prescribed, sticking to the times of day and the number of days religiously. A whole course is necessary to kill off all the bacteria that are responsible for causing your illness.
• Don’t use antibiotics without a prescription: First of all, they may not be effective in treating your illness. And worse, when you take antibiotics that are not right for the infection you have, you’re leaving yourself prone to developing new strains of bacteria that become resistant to this particular antibiotic and similar others. So when you become ill with a disease that is curable with the help of this antibiotic, it’s going to be an absolutely useless course of treatment because of the resistance developed by the bacteria. Besides, they also kill the good bacteria that are in your stomach and are needed for a variety of bodily functions like digestion and others.

Antibiotics are not a magical cure to any illness that you have. It’s always good to remember that prevention is better than cure; so maintain good hygiene by keeping yourself and your surroundings clean and by washing your hands regularly to keep illness at bay.

Related:

• MicrobiologyBytes: Antibiotics
• Antibiotics, your gut, and you
• Resistance to Widely-Used Antibiotics among Inhabitants of Remote South American Villages

Today’s post is from regular guest blogger:

Ed Rybicki, Department of Molecular and Cell Biology, University of Cape Town, South Africa.

Now that the dust has begun to settle after the launch of Merck’s much-hyped Gardasil genital papillomavirus vaccine – discussed in MicrobiologyBytes here and here – people are turning again to looking at the natural history of the virus.

With some serious surprises…

There is a wonderfully-titled paper in the December issue of Journal of Virology describing a novel virus isolated from an Australian marsupial, which looks like a natural chimaera resulting from recombination between a cutaneous papillomavirus and a polyomavirus (A Novel Virus Detected in Papillomas and Carcinomas of the Endangered Western Barred Bandicoot (Perameles bougainville) Exhibits Genomic Features of both the Papillomaviridae and Polyomaviridae), from a collaborative group drawn from Murdoch University in Perth, WA, and the University of Leuven in Belgium.

They set out to look for papillomaviruses in lesions of a progressively debilitating cutaneous and mucocutaneous papillomatosis and carcinomatosis syndrome observed in captive and wild populations of the western barred bandicoot, using the relatively new technique of multiply-primed isothermal rolling-circle DNA amplification (RCA) – adapted from a natural phage replication process similar to that described here previously. It was a reasonable assumption that papillomaviruses were involved, given the type of lesions and the fact that papillomavirus sequences had previously been amplified out of other cutaneous lesions of marsupials – however, use of RCA would allow amplification of any circular DNA genome, given the non-specific nature of the technique which could show up “escapes” from even broad-spectrum degenerate primer PCR DNA amplifications. What they found was at first non-controversial: RCA products from lesions from several animals gave a ~7.5 kDa genomic DNA band after digestion with BamHI or SalI, typical of a papillomavirus; however, sequencing of the cloned DNA revealed that although the genomes did in fact contain the characteristic L1 and L2 structural protein ORFs of a papillomavirus, they also had the large-T and small-t antigen regulatory protein-coding ORFs typical of a polyomavirus – and on the opposite strand to the structural protein genes, also typical of polyomaviruses:

The natural assumption in this case would be that they had cloned an artifact of template-swapping in the RCA reaction: however, a number of checks using PCR with specific primers and sequencing of DNA from other animals confirmed the result. The newly-designated bandicoot papillomatosis carcinomatosis virus type 1 (BPCV1) DNA was subsequently found in 94.7% of fresh lesion tissue extracts, and 100% of bandicoots withe papillomatosis and carcinomatosis syndrome screened by skin swabbing, indicating it is almost certainly the causative agent.

This is a landmark finding in virology: the two families of viruses, while both classed as DNA tumour viruses, are very different indeed, and while it is possible they have a common origin, it is evolutionarily very distant indeed, given that the two groups have been cospeciating with their hosts over geological aeons. They both have circular dsDSNA genomes, and similar-looking particle morphology, but neither their structural nor their regulatory proteins have any discernible homology to one another – which means it is conceptually as likely to find a viable recombinant between them as it is to successfully cross a crocodile and a tortoise.

The authors explore a number of options in explaining just how such a tortodile or crocoise came to be, and appear to give equal credence to the possibilities of simple recombination between a papillomavirus and a polyomavirus, and that the virus is a descendant of the last common ancestor of the two groups of viruses. Their own analysis of phylogenetic relationships, however, places the putative L1 protein firmly among the beta- and gamma-papillomaviruses, which are viruses isolated from humans and associated with the condition of epidermodysplasia verruciformis in immunosuppressed people, and cutaneous lesions respectively. This indicates to me that an already-evolved cutaneous papillomavirus recombined with an as yet undiscovered representative of the family Polyomaviridae, to give a new and unexpectedly viable chimaeric offspring that has persisted in its unique biological niche.

What this result opens up is the possibility that there is a lot more of this going on than we knew about – and that techniques like RCA may be the key to unlocking a completely unsuspected world of virus diversity.

I have recently been participating in a to-and-fro evolutionary discussion in the columns of a local weekly newspaper, in the course of which one protagonist stoutly proclaimed that evolution was hokum because “like only begats like” [sic]. I would show him this virus as an example of what rubbish that statement is – if only he could understand it.

If you would like to be a guest blogger on MicrobiologyBytes, click the Guests tab above.

Today’s post is from regular guest blogger:

Ed Rybicki, Department of Molecular and Cell Biology, University of Cape Town, South Africa.

It should not have escaped the eye of the interested bystander that there has been a most unfortunate and premature end to a HIV vaccine trial recently – and that something that had been tested as “safe” and “immunogenic” in Phase I and II trials went on to not only to not show any efficacy at all, but may actually have increased susceptibility in recipients to HIV-1 infection. The so-called STEP trial in North and South America, the Caribbean and Australia, and the Phambili trial in South Africa, were “Phase IIB” or international test-of-concept trials in at-risk populations of the efficacy of Merck & Co. Inc. Adenovirus 5-based vectors (MRKAd5) encoding subtype B-derived Gag, Pol and Nef proteins. The outcome was about as gloomy as could possibly have been predicted, and was nothing like what researchers expected from preliminary primate testing.
The trials – more formally designated as “HVTN 502 and HVTN 503 HIV Vaccine Clinical Trials” by the HIV Vaccine Trials Network – were testing a mixture of three replication-defective Adenovirus 5 vectors, containing gag, pol and nef genes respectively, aimed at stimulating mainly CD8+ T-cell responses. There had earlier been some disagreement in the research community about the ethics of trialling a subtype B-specific vaccine in a subtype C-dominated epidemic region – and in a population known to have a high incidence of high titres of antibodies against Ad5, which is after all a common cold virus. However, regulatory bodies were in no doubt that the trials were appropriate, and standard Phase I and II trial results were non-contentious, leaving the way clear for the present exercise.

The study was designed as a randomized, double-blind, placebo-controlled Phase IIB clinical trial, sponsored by Merck and the National Institute of Allergy and Infectious Diseases (NIAID), which enrolled HIV-negative volunteers between 18 and 45 years of age at high risk of HIV infection. Participants were randomly assigned to receive three injections of either the study or a placebo vaccine. Some 3000 participants were planned for each of the two trials; HVTN 502 was closed while 503 was still recruiting, when the Data and Safety Monitoring Board (DSMB) of the STEP trial (HVTN 502) – an independent committee providing oversight of the study – decided on September 18th that “… the trial as originally designed should be discontinued because the trial would not meet its efficacy endpoints”, as there was no evidence for protection. In fact, of people with low anti-adenovirus titres at enrollment who had received one vaccine/placebo dose, 24 of 741 vaccinees became HIV+, while among placebo-vaccinated people, 21 of 762 became infected. Among two-dose trialists, the figures were 19 HIV infections in 672 vaccinated volunteers, and 11 HIV infections among the 691 placebo recipients. This led to the discontinuing of the Phambili trial in South Africa as well, given no additional expectation of success.

And inevitably, things got worse: among male volunteers with high levels of antibodies against Ad5, 21 of 392 vaccinees became infected, but only 9 of 386 in the placebo group. Thus, it could be that pre-existing immunity to the vector virus actually increases susceptibility to HIV infection: one mechanism that has been proposed is that the secondary response to the Ad5 transiently boosts production of CD4+ T-cells – the preferred host cells of HIV.

The upshot of all this is that researchers worldwide are taking a hard look at Adenovirus-based HIV vaccines, even those which do not naturally occur in humans, and to which there should be no immunity: for example the Vaccine Research Center at the NIH has another Adenovirus-vectored candidate about to enter clinical trial, which may yet be delayed as the results of the STEP and Phambili trials are analysed in minute detail. The STEP volunteers are to be informed what they were inoculated with, and all Phambili volunteers have been advised to report back to the clinics for counselling. From the Merck site:

The Phambili DSMB also recommended that Phambili volunteers be told whether they received the vaccine or placebo, be strongly encouraged to return to study sites for protocol-related tests, and be counseled about the possibility that those who received the vaccine might have an increased susceptibility to HIV infections. STEP volunteers will also be counseled about this possibility, and discussions are underway to define the details of continued follow-up for STEP volunteers, including when STEP volunteers will be unblinded. Detailed analyses of the available data are being conducted, including analyses to better understand if there may be an increased susceptibility to HIV infection among those volunteers who received the vaccine.

Inevitably, there has also been political fallout in South Africa: the Minister of Health, Manto Tshabalala-Msimang, announced a moratorium last week on HIV vaccine trials, which could affect the home-grown vaccines due for trial next year.

This is not the only bad news recently on the HIV vaccine front: there seems to be evidence that another hitherto-promising HIV vaccine vector, the adeno-associated viruses (AAVs) may help to exhaust memory T-cells, by over-stimulating them with continuously-produced antigen.

All of this bad news looks, at first sight, to be a major body-blow to efforts to develop viable HIV vaccines. However, this is exactly what clinical trials are for: to test vaccines, for safety, immunogenicity, and efficacy. It is actually encouraging in a perverse sense that the trials work as they should – even though the first two HIV vaccines that have made it as far as efficacy trials are both abject failures. Lessons from the AIDSVAX debacle were that large trials can be done for an HIV vaccine; that HIV infection is a reasonable endpoint for a HIV vaccine trial; that HIV gp120 is not a good vaccine candidate. While it is still too early to be specific, lessons from this trial may be that immunogenicity / efficacy results from monkeys may not be a good predictor of human results, and that Ad5 is not a good HIV vaccine vector in pre-immune populations.

So the search goes on: the longest, most expensive vaccine development exercise in human history, with no clear end in sight.

If you would like to be a guest blogger on MicrobiologyBytes, click the Guests tab above.

Related:

• HIV vaccines – bad news, good news
• The emergence of HIV/AIDS in the Americas and beyond
• How does HIV cause AIDS?

Today’s post is from regular guest blogger:

Ed Rybicki, Department of Molecular and Cell Biology, University of Cape Town, South Africa.

I inadvertently became a published literary critic a little while ago. A long-time English Department colleague asked me for some help interpreting the collected works of possibly the most important modern poet from South Africa, and I quickly got caught up in some of the more interesting poetry I have ever read:

Douglas Livingstone was South Africa’s most important poet of the late twentieth century. He was also a practicing scientist who received a PhD for his work as a parasitologist for the CSIR in Durban, testing water purity levels along the Natal coast. Did Livingstone use poetry to reflect on his work as a scientist? Did his findings as a scientist influence his poetry? The self-reflection on the motivation for and results of a life of science come as he starts off on his early morning routine of driving along the coast to collect water for testing:

… coffee, toast, the rush for the lab
in the dark to gather up paraphernalia
load the station wagon and off again
for the river: man as hunter, Ahab
again, and Nomad, more prosaically
the quarry is microscopic Escherichias,
salmonellas, staphylococci, ascarid eggs,
coliphages, abject in the face of men,
a turning to an urge to heal the earth, its waters,
first the detection of ills which becomes
life-long non-progressive
find & measure the ills first, others
can heal with statute, exhortation,
engineering, first and for a lifetime detect. [RF: 473]

He then muses on the vision the microscope gives into the nature of life:

… Miraculous
cheek that prying probe, like some damned
gods voyeuristic telescope:
cilia spun from spirochaetes,
chloropasts from bacteria.

Billion year-old invaders
the silent mitochondria
propel our mobile towers, shared cells
sparking, colonized by vandals:
a fifth column of DNA
in interstellar sequences,
bland in their promiscuity. [RF, 287]

Heady stuff…deep thinker, Dr Livingstone. And in tune with modern microbiological thinking at a time when many biologists wondered if it were true. But he also had fun – and this is the one I printed out to stick up on the wall of the lab:

THE PASSIONATE BACTERIOLOGIST TO HIS LOVE

Come live with me & be my love
Up in the lab… first floor, above:
Where, shrouded in hygienic white.
We’ll potter through the febrile night.

Up here amid the test-tube racks
The centrifuge, the power- pack
I’ll show you botulinous meat
Mutations of a Spirochaete.

Entamoeba’s selfish mission
(Delighting in asexual fission):
And, just to elevate your hair
Some droppings from the Old Grey Mare.
Bacilli with a sunset hue
Will form a little chain for you.
And cocci on a culture plate
Will make your giddy heart gyrate.
You’ll see some eggs infected by
A Virus from a bloodshot eye;
For your delight, my lover doll,
I’ll flourish spleens in alcohol.
With dawn the roosters start to crow:
We’ll make a little fungus grow.
If you dig culture, little dove.
Why, come upstairs and be my love.

There’s obviously some culture in microbiology… B-)

If you would like to be a guest blogger on MicrobiologyBytes, click the Guests tab above.