Tag Archives: antibiotics

gallstones and mayonnaise

A few weeks ago we admitted Sylvia. She had been feeling unwell for a some days, with fever and episodes of uncontrollable shaking. What really alarmed her was when she turned yellow, and then developed abdominal pain and vomited a couple of times. Sylvia is forty eight, and had always been healthy. She rowed with the local club twice a week and kept her weight under control. For the past year or so she noticed that she got pains in her abdomen after eating fatty foods such as fish and chips, and now avoided foods like that. It was her son who noticed she was yellow – he then phoned Sylvia’s GP. The duty doctor came and confirmed that she was indeed jaundiced, feverish and unwell, and persuaded her that she needed to go to hospital.

these people look jaundiced - in fact they are not - the whites of their eyes are white - this image is copyrighted but Wiki thinks its ok to use it so I'm hoping its ok for me to do so
these people look jaundiced – in fact they are not – the whites of their eyes are white – this image is copyrighted but Wiki thinks its ok to use it so I’m hoping its ok for me to do so

We did all the usual things for someone with suspected biliary sepsis. Took blood cultures and routine blood tests. These tests confirmed she had elevated bilirubin and transaminases, increased alkaline phosphatase, as well as a high neutrophil count and CRP.  We gave her intravenous fluids, anti-emetics and antibiotics. We were able to get an ultrasound within a couple of hours. Ultrasound is really good at looking at the liver and biliary system in jaundiced patients – better than CT.

The ultrasound showed that Sylvia had a gallbladder full of gallstones and her common bile duct was dilated. It seemed likely that she had a stone blocking the flow of bile from the liver to the duodenum, and that the stagnant bile had become infected with bacteria causing ascending cholangitis and liver inflammation.

bile is made in the liver - it is stored in the gallbladder and squirted into the small intestine after a fatty meal, along with pancreatic secretions - Sylvia's gallstone was impacted in the sphincter of Oddi
bile is made in the liver – it is stored in the gallbladder and squirted into the small intestine after a fatty meal, along with pancreatic secretions – Sylvia’s gallstone was impacted in the sphincter of Oddi

The questions I want to answer this week are:

Why did Sylvia turn yellow?

What are gallstones made of and why do they form?

Why is there an increase in alkaline phosphatase in the bloodstream when the biliary system is obstructed?

The last of those questions is the hardest, but I will make some conjectures, and  hope that others who know more about it will correct me.

Jaundice is fairly straightforward. It is caused by the accumulation of bilirubin, which is a greenish-yellow colour. Bilirubin is made from haem, the central working part of myoglobin, but most bilirubin comes from the breakdown of haem in the haemoglobin from red blood cells.

So why is haemoglobin red? It is not only – or even mainly – the iron that makes haem red, but the porphorin ring that surrounds the iron. This large ring is made of four smaller pyrrole rings.

Pyrroles are often coloured – the dye indigo has two pyrrole rings and red acrylic paint often contains the dye pyrrole-red. Melanin, the pigment that gives skin and hair its colour is brown or black or red because it has a related structure – indole – a pyrrole stuck to a benzene ring. Without this pyrrole ring we would be like albinos, but without pink skin and eyes.  As we shall see, we would also produce beige poo and colourless urine.

this is a pyrrole - all pyrroles are highly coloured, and are in most of the things which make people the colour they are
this is a pyrrole – all pyrroles are highly coloured, and are in most of the things which make people the colour they are

Red blood cells last on average 120 days before they wear out and have to be recycled.  As we have five litres of blood and in each litre there is at least 120 grammes of haemoglobin, it means we have to make, and break down, five grammes a day.  About a teaspoonful.  This all happens inside macrophages in the spleen and liver, as they try to salvage useful parts of the red cells to make new things.

Macrophages are similar to neutrophils but slightly smarter.  Some are good at host defence: they come to the scene after the neutrophils have done their job, do the forensics, and find out what the germs are made of. They then tell the lymphocytes how to make antibodies to protect us in the future.

Other macrophages are good at clearing up the mess, breaking down dead tissue and making things neat and clean.  The spleen and liver macrophages that deal with old red cells are the latter kind. When they take red cells apart, they separate haem from globin, and then take the iron out of the haem.  Next, the porphorin ring is broken to form bilirubin – its molecule of linked pyrrole rings looks like four beach huts in a row.

haem is broken down by the enzyme haem oxygenase to form bilirubin
haem is broken down by the enzyme haem oxygenase to form bilirubin

The bilirubin is then thrown away (I don’t know why it can’t be re-used).  It attaches to albumin and becomes water soluble after conjugating in the liver with a sugary molecule called glucuronate.  The conjugated bilirubin is then transported into the biliary system, stored in the gallbladder, and squirted into the duodenum when we eat fatty food.  In the bowel, it is converted to urobilinogen, which makes poo brown.  Some is reabsorbed and excreted in urine, which makes urine yellow.Slide2

Sylvia had noticed that her poo had changed colour – it had become putty-coloured – and her urine had become much darker. That is because conjugated bilirubin was not getting into her intestines and instead some had leaked into her bloodstream and was appearing in her urine. The whites of her eyes and skin had become yellow because of the very high level of conjugated bilirubin in her blood.

Now to the gallstones.  In Western countries they are most commonly made of cholesterol.  I have already talked about the importance of cholesterol in keeping cell membranes rigid and non-leaky.  Cholesterol is made in large amounts by the liver and transported to other cells gift-wrapped as LDL cholesterol.  It is also used to make bile salts.  It only needs a minor modification of the basic chemical structure of cholesterol to make bile salts – the main component in bile which makes it work – the main function of bile salts is to help us digest dietary fat.

structure of cholesterol
structure of cholesterol

Bile salts are detergents.  Just like washing-up liquid, they emulsify fats, breaking large fat globules into smaller micelles which do not stick to each other, or anything else. Cholesterol is essentially very insoluble in water, or hydrophobic.  When an organic acid group is added – to make bile salts – it gains a hydrophilic or water-attracting group. This is just like soap – a long lipid chain with an organic acid group at the end.  The hydrophobic lipid part is embedded in the tiny fat globule and the hydrophilic groups stick outside in the watery medium of the intestinal contents.

bile acids are a minor modification of cholesterol - hydrophilic OH  and COOH  groups are added to make it into a detergent
bile acids are a minor modification of cholesterol – hydrophilic OH and COOH groups are added to make it into a detergent

As well as bile salts, the liver secretes phospholipids into bile – principally phosphatidylcholine. This, with cholesterol, is the main stuff cell membranes are made of.  It is also an emulsifying agent, and is used extensively in the food industry to keep fats in suspension.

So, when we eat fat, the small intestine detects it and releases the hormone cholecystokinin (CCK).  This causes the gallbladder to contract to send bile into the duodenum, and also makes the pancreas release enzymes, including lipase.  CCK also has some very interesting effects on our brains, making us feel less hungry, and curiously, opposing the effects of opiate drugs.  The bile and pancreatic secretions are both delivered into the duodenum through the same tube – see diagram. The detergent bile salts, emulsifying phospholipid and pancreatic lipase are designed to work together to digest fat.

the hydrophilic parts of cholesterol are all on one side of the molecule - this allow it to act as a detergent - it works well to disperse fat into small globules so that pancreatic lipase can work on it and break it down to fatty acids and monoglyceride
the hydrophilic parts of cholesterol are all on one side of the molecule – this allow it to act as a detergent – it works well to disperse fat into small globules so that pancreatic lipase can work on it and break it down to fatty acids and monoglyceride

The bile breaks it up into tiny globules and the lipase breaks triglyceride into fatty acids and monoglyceride. These are transported across the intestinal mucosal cell membrane and then the triglyceride is put back together again. Seems a daft system, but it clearly works. The triglyceride is taken away from the intestine not in the portal blood, like most other substances absorbed by the gut, but in the lymphatic system in the form of chylomicrons – small fatty globules covered by a layer of phospholipid. The chylomicrons travel up the lymphatic vessels to emerge into the circulation just below our left clavicle. This means that it avoids passing straight away through the liver. If blood is taken soon after a fatty meal and centrifuged, it will have a milky appearance because of the large amount of chylomicrons.

So why do gallstones form? As well as bile salts, unmodified cholesterol is also secreted into bile. It is only kept soluble by the bile salts and phospholipid – the ratio of cholesterol to bile salts and phospholipid is therefore important. When it goes wrong, cholesterol precipitates out and forms solid stones like those that caused all Sylvia’s recent problems – a bit like when I try to make mayonnaise and it curdles – the fat becomes un-emulsified and separates out.

In some parts of the world, gallstones are made from bile pigment – bilirubin. This can be due to increased red blood cell breakdown resulting from abnormalities such as sickle cell disease, but it’s also common in East Asia, for reasons which are not clear.  A good, comprehensive analysis of why gallstones of all types form can be found at:

http://gastro.ucsd.edu/fellowship/materials/Documents/Gallstones/pathogenesis%20gallstones.pdf

Now the alkaline phosphatase. Bile is alkaline.  Alkaline phosphatase is an enzyme that removes phosphate groups in alkaline conditions.  When bile flow is blocked – by stones, as in Sylvia’s case, or for any other reason – the liver makes much more alkaline phosphatase, some of which appears in the blood.  Bones use a similar alkaline phosphatase to rearrange phosphate groups to make hydroxyapatite – the hard stuff bone is made from.  Most of the alkaline phosphatase normally in our blood is the bone sort.

There is plenty of information about whether alkaline phosphatase is from bone or liver, but very little I can find that suggests why the liver should make this enzyme when the biliary system is blocked.  I think a clue here is that neutrophils also have alkaline phosphatase in their granules, which help kill bacteria.  This is in addition to the myeloperoxidase and esterase mentioned in earlier posts.  Why should a phosphatase be damaging to bacteria?  The answer may well involve techoic acid, an important reinforcing molecule in some gram-positive bacteria.

cartoon of gram positive bacterial cell wall - techoic acid is thought to inhibit the action of lysozyme and protect the peptidoglycan from being broken down - techoic acid contains phosphate groups which may be removed by alkaline phosphatase
cartoon of gram positive bacterial cell wall – techoic acid is thought to inhibit the action of lysozyme and protect the peptidoglycan from being broken down – techoic acid contains phosphate groups which may be removed by alkaline phosphatase

In these microbes, techoic acid strengthens the peptidoglycan cell wall and inhibits the action of lysozyme, yet another enzyme made by neutrophils.  Lysozyme is designed to break some of the sugar-sugar bonds in peptidoglycan – so getting rid of the techoic acid would surely be helpful.  We know that alkaline phosphatase is effective in breaking up techoic acid – see, for instance:

http://jb.asm.org/content/102/3/747.short

Maybe the liver is producing this anti-bacterial enzyme to help prevent infection when the flow of bile slows down.  Unfortunately, this won’t work with gram negative organisms such as E.coli because they don’t make techoic acid – and it was a gram negative bacterium we grew from Sylvia’s blood culture – the germ that was causing her ascending cholangitis.

Soon after she came in, Sylvia had an ERCP – an endoscopic retrograde cholangio-pancreatoscopy.  The endoscopist managed to remove the impacted gallstone from her ampulla of Vater, and she quickly recovered.  A week later she had her gallbladder removed, including the stones, and now is quite well – she can even eat fish and chips.

Now to the food link: mayonnaise.

French mayonnaise - made with olive oil and mustard
French mayonnaise – made with olive oil and mustard

This is an emulsion of lipid, such as olive oil, in an aqueous (watery) medium – vinegar or lemon juice.  The emulsifying agent is raw egg yolk, which – just like bile – contains lots of phospholipid – phophatidylcholine and is also rich in cholesterol.  In France, mustard is also added.  Mustard seed contains mucilage, a gooey stuff that some plants produce made of sugar polymers. (Thanks again to Harold McGee). These also act as emulsifiers and further thicken the mayonnaise, and give it a better taste. When I make cheese sauce, I use a sugar polymer (flour) to achieve a stable emulsion between butter and milk – no doubt the phospholipid in the milk helps too.  It seems likely that in the small intestine, the mucus from the stomach, a similar gloopy sugar polymer, probably has a similar effect to mustard seed mucilage to help with fat emulsification.

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back pain and blue cheese

These are lambs kidneys - not eaten much in the UK but muched loved in France - rognons de veau
these are lambs kidneys – not eaten much in the UK but much loved in France – rognons de veau

Kirsty was admitted this morning. She is twenty eight  and had been unwell for the last two days. The first thing she noticed was a nasty burning pain when she passed urine. Almost as soon as she had finished peeing she needed to go again. Kirsty went to the doctor yesterday and was prescribed antibiotic tablets. She took one dose and was immediately sick. Then she developed pain in her back, on the left side, under her lower ribs. It started gradually but became almost unbearable. Then she started to feel feverish and shivery. Not ordinary shivery, but uncontrollably shivery – and then she vomited again and again. Her new husband, Sam, drove her up to the emergency department at nine thirty this morning. Their two year old daughter, Ellie, was in the back of the car. In the emergency department Ellie was sitting on Sam’s knee, looking very unconcerned when we talked to Kirsty, who was lying on the trolley.

“I think you have a serious kidney infection” I said, “and we’d better admit you and give you intravenous antibiotics”.

Kirsty was not looking well. She was pale, sweaty, febrile and a bit blotchy with wet hair stuck to her face.  She was clutching her painful back with one hand and holding a vomit bowl with the other. She was happy to come in and be looked after. So was Sam. Ellie did not look so sure.

its really important to take blood cultures before giving antibiotics - otherwise it will be difficult to find out the germs responsible for infection
its really important to take blood cultures before giving antibiotics – otherwise it will be difficult to find out the germs responsible for infection

We took a blood sample and blood cultures, gave her intravenous morphine, paracetamol, gentamicin, co-amoxyclav and cyclizine (an antiemetic). She had pyelonephritis – a bacterial infection of her kidney.

Young women get urinary tract infections much more commonly than young men. It’s to do with anatomy. The female urethra is very short, and germs can quite easily travel up to the bladder and then up the ureters to the kidney. Men get urine infections when they are older and have enlarged prostate glands.

Then they cannot empty their bladders completely and the stagnant urine is more likely to become infected. I was taught that urine is normally sterile in healthy people. It seems this is not the case. All of us have bacteria in our urine in small numbers – if you are interested read: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744036/ 

We use urine dipstick testing a lot on the acute medical unit. In theory it should be able to tell us which of our patients have a significant urinary tract infection. In practise it is not quite as useful as it should be. Kirsty’s urine tested positive for nitrites and leukocytes. In young women this is a good test, but we knew she had a urinary tract infection anyway. In elderly women, the tests are often positive even if a serious infection is not evident – perhaps because of the innocent commensal bacteria which are present.

Slide02

How do urine dipsticks work? The test for leukocytes is leukocyte esterase. In infected urine, the leukocytes are polymorphonuclear leukocytes, or neutrophils. I talked earlier (phlegm and horseradish) about how neutrophils, when they get excited by the presence of germs, make the enzyme myeloperoxidase which generates bleach. Esterase is another enzyme neutrophils make which breaks down peptide bonds, and specifically is useful in breaking down the peptidoglycan in bacterial cell walls. I guess its like getting stains out of clothes. Bleach works fine, but the proteolytic enzymes in washing powder can help too.

So what about nitrites? Bacteria like Eschericia coli, which are a common cause of urine infections are known as facultative anaerobes. This means that they can use oxygen to “burn” carbohydrates, protein and fats. But they can also use other “electron acceptors” to do this such as nitrate. Mammalian cells can only use oxygen. When I say mammalian cells, what I mean is mitochondria in mammalian cells – these small structures in our cells are responsible for all the energy generation from glucose, fats and protein. Think what happens when you eat a slice of toast. The amylase in our saliva starts to break down the starch in the toast to form glucose, a process which is finished by amylase in pancreatic secretions. This yields glucose, which is absorbed into the bloodstream. Glucose can be made into energy by the Kreb’s cycle, or citric acid cycle mainly happens in mitochondria. This is a complicated process, but essentially it means that glucose is turned into carbon dioxide and protons and electrons:

The mitochondria don’t get much energy from the Kreb’s cycle, but rely on the protons and electrons produced to make energy by combining them with oxygen. This happens in the electron transport chain:

Bacteria are more versatile than mammalian cells and can get energy out of these protons and electrons, even if oxygen is not available, by using nitrate instead of oxygen:

To do this they need to have the enzyme nitrate reductase. Human cells do not have nitrate reductase, so if nitrate is being turned into nitrite there must be bacteria present. So, if urine contains significant amounts of nitrite, the only way it can get there is if bacteria are using nitrate to “breathe” – a tell-tale sign that infection is present. The reason E.coli is called a facultative anaerobe is that it can survive by making energy if oxygen is present and also when it is not, by using molecules such as nitrate to “breathe”.

our mitochondria can only use oxygen to get energy from electrons and protons derived from glucose - some bacteria have nitrate reductase which can use nitrate as an electron acceptor - nitrite is a by-product- and appears in infected urine as an indicator of infection
our mitochondria can only use oxygen to get energy from electrons and protons derived from glucose – some bacteria have nitrate reductase which can use nitrate as an electron acceptor – nitrite is a by-product- and appears in infected urine as an indicator of infection

When I saw Kirsty later in the afternoon she was much better. The pain had not gone, but was eased by the morphine. Her temperature had come down, and she had stopped vomiting. Her infection was coming under control.

Both gentamicin and co-amoxyclav are very effective in treating urinary tract infections. They are both rapidly excreted by the kidneys and achieve much higher concentrations in the urine than in the bloodstream. Gentamicin has a half-life of about 2 hours in patients with normal renal function. So, lets say we give a person 250mg of gentamicin intravenously. The blood volume is about 5 litres, so the immediate concentration will be 50mg/litre of gentamicin. In two hours about 100ml of urine will be made, and half of the gentamicin previously given intravenously will be in that urine. That is 125mg in 100mls or 1250mg/litre – more than twenty times the concentration in blood. Amoxycillin has a half-life of more like one hour, so achieves even higher urine concentration in comparison to blood.

What do gentamicin and co-amoxyclav do? They are antibiotics that work in quite different ways.

Gentamicin is an aminoglycoside. That means it is a sugar with amine groups. Here is the structure – just three sugars with lots of NH2 groups:

gentamicin is a relatively small molecule with three sugar groups and lots of amine groups (in red) - an aminoglycoside
gentamicin is a relatively small molecule with three sugar groups and lots of amine groups (in red) – an aminoglycoside

It gets into the bacteria and binds strongly to its ribosomes. These are the really important and clever machines in bacteria which make proteins from DNA. Mammalian cells also have ribosomes to make our proteins – but they are not at all the same. They work in the same way but over the past 2 billion years have changed with evolution so they are a different shape and are larger than bacterial ribosomes. Gentamicin does not interfere with mammalian ribosomes. For an antibiotic to be useful it has to damage bacteria but not human cells. Luckily, ribosomes are so different between bacteria and mammalian cells that some chemicals such as gentamicin will selectively bind only to bacterial ribosomes.

mitochondrion - it has all the stuff inside that a bacterium has, but without a tough cell wall
mitochondrion – it has all the stuff inside that a bacterium has, but without a tough cell wall – redrawn from wikipedia – author kevinsong

Other antibiotics such as tetracyclines, macrolides (erythromycin and clarithromycin), chloramphenicol and clindamycin also work by interfering with bacterial ribosomal function. A bacterium with damaged ribosomes has major problems – it cannot make new proteins. That means it cannot divide and make new bacteria. It will be immobilised and suffer a slow and painful death. (Not really, I don’t think bacteria don’t feel pain – but then I don’t have evidence for that). If it is a bacterium which makes a protein toxin, such as staphylococcus causing toxic shock syndrome, turning off protein production with a ribosomal poison such as clindamycin is a good idea – rather than causing bacterial cell wall damage and leakage of more toxin with penicillin therapy.

Gentamicin can cause problems if it is given over prolonged periods, because it can accumulate and cause damage to ears and kidneys. The damage to hearing is probably due to damage to mitochondria. More specifically damage to mitochondrial ribosomes. We only gave Kirsty one dose of gentamicin – problems with this drug usually happen when patients with impaired renal function are given aminoglycosides for several days, or when aminoglycosides are given with other drugs such as vancomycin which can impair renal function.

Mitochondria are thought to derive originally from bacteria. Once upon a time, a long time ago there was a cell that survived well enough by getting energy from glycolysis – turning glucose into pyruvate. This cell did not need any oxygen. It scraped a living producing at most 2 ATP molecules per glucose molecule. Then it had a conversation with a bacterium which said “Hi doll, I could take that pyruvate you make and turn it into another 28 ATP molecules by combining it with oxygen – how about it?” Maybe this conversation happened at the time oxygen had begun to appear in the atmosphere (see great oxygenation event in last week’s blog). “With your looks and my talent we could do Broadway together”. This is technically known as endosymbiosis, where one type of cell engulfs another to work together to their mutual benefit. The result is eukaryotic cells – the cells we are made of. Our cells contain mitochondria that derive from bacteria. They can make lots of energy from glucose and oxygen. The bacteria are looked after and nurtured inside the cells which engulfed them. Like bacteria, these mitochondria have their own ribosomes, that, not surprisingly, are similar to the ribosomes of bacteria that are causing Kirsty’s pyelonephritis. Too much gentamicin can damage mitochondrial ribosomes and cause hearing loss – see:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1376819/pdf/9443888.pdf

We also gave Kirsty co-amoxyclav.

the basic penicillin molecule - the central beta lactam is in the pink circle
the basic penicillin molecule – the central beta lactam is in the pink circle

This is a combination of amoxicillin and clavulanic acid. Amoxycillin is a penicillin. Originally discovered by Alexander Fleming, the original penicillin, benzylpenicillin, has been modified by pharmaceutical companies to be more effective. Unlike benzylpenicillin, amoxycillin is rapidly absorbed by the stomach. It is also effective against gram negative organisms such as E.coli. Penicillins have a beta lactam group. This structure makes it difficult for bacteria to make a vital component of their cell wall – peptidoglycan.  This is a tough polymer made of special sugars and short peptide chains. The beta-lactam group in penicillins is the right shape to get stuck in the cell wall building enzymes and prevent cell walls being made. Our cells do not have cell walls – they just have thin, delicate plasma membranes made of phospholipid and cholesterol. Similarly, although mitochondria are similar to bacteria, they also do not have cell walls. Mammalian cells and their mitochondria are very cosseted and protected in a 5-star luxury apartment with all mod-cons.  They are looked after in a temperature-controlled environment. Oxygen is supplied free and waste carbon dioxide and other unwanted substances taken away continually. Acidity is tightly controlled – pH between 7.35 and 7.45, osmolarity not too high or low. The poor bacterium, in contrast, has to tolerate acid, alkali, high and low osmolarity and a whole host of chemical insults as well as having to find its own food. And then there is the danger of being chased by an angry green neutrophil. No wonder it feels happier with a thick, tough cell wall to protect it. The clavulanic acid is to inactivate beta lactamase – an enzyme some wily bacteria have started making to destroy beta lactam antibiotics. No doubt the bacteria will soon be making betalactamaseinhibitorase enzymes.

There are other ways to selectively attack bacteria without harming human cells. All cells need folate to manufacture nucleic acids. We get our folate from diet – particularly green, leafy vegetables (folate is related to the word foliage). Bacteria do not, in general, have a healthy diet. They instead make the large folate molecule themselves from much smaller molecules. Trimethoprim and sulphonamides prevent bacteria from making folate causing them to suffer and die a “thymineless death” (look it up in Wiki).

Fluoroquinolones such as ciprofloxacin are some of the newer antibiotics which have come into clinical use since I qualified. They were hailed as the new wonder drug, but we now use them relatively rarely because they particularly seem to promote C.difficile infections in frail, elderly people. They work by inhibiting DNA gyrase and Topoisomerase IV. I hope the illustrations will explain how they work:

bacterial DNA is circular
bacterial DNA is circular
DNA helicase pulls the DNA strands apart so that they can be replicated to make more DNA  when the bacterium divides - but it causes a problem, the DNA becomes supercoiled
DNA helicase pulls the DNA strands apart so that they can be replicated to make more DNA when the bacterium divides – but it causes a problem, the DNA becomes supercoiled
DNA gyrase sorts out this problem - cutting the DNA strand and rejoining it having removed the twist
DNA gyrase sorts out this problem – cutting the DNA strand and rejoining it having removed the twist – fluoroquinolones such as ciprofloxacin stop this enzyme working
having replicated the DNA - the two circular strands are interlinked!
having replicated the DNA – the two circular strands are interlinked!
but topoisomerase IV comes to the rescue and chops the chain and rejoins it to separate the circular strands
but topoisomerase IV comes to the rescue and chops the chain and rejoins it to separate the circular strands- fluoroquinolones also inhibit this enzyme
all sorted
all sorted

The food link this week is blue cheese.

blue stilton
blue stilton – the blue bits are penicillum mould

The reason it is blue is because of the growth of the mould penicillium, which is a grey/greenish blue colour.  The spores are blue, not the fungus itself.

volkornbrot past its sell by date - the blue mould is penicillium - not sure what the yellow stuff is - any ideas anyone?
volkornbrot past its sell by date – the blue mould is penicillium – not sure what the yellow stuff is – any ideas anyone?

The mould in Roquefort and Stilton is P. roquefortii, a close relative of P. notatum (now known as P. chrysogenum), the penicillium mould that Alexander Fleming found inhibiting the growth of staphylococci.

I’ll be in France next week so the next post will be in 2 weeks’ time