The key idea of ketone body metabolism is to convert free fatty acids into more water-soluble substrates that are easier to transport and to metabolize. Utilization of ketone bodies in the brain, muscle and other tissues is quite straightforward. Thiolase then cleaves acetoacetyl-CoA to two molecules of acetyl-CoA, which enter the TCA cycle. ISBN: 0009-8981), the rate of decarboxylation is enhanced by unfractionated serum proteins.
The first step of the pathway shown here is catalyzed by the enzyme cytochrome P450 type 2E1. This enzyme can also metabolize ethanol and is transcriptionally induced by both acetone and ethanol. At higher than physiological plasma concentrations, acetone acts like a general anesthetic, as do many organic solvents (e.g. Accordingly, acetone has been proposed to be responsible for the effectiveness of the ketogenic diet in epilepsy. ISBN: 0065-2598, and it remains in use in a significant number of patients, particularly children, who dona€™t respond to antiepileptic drugs. The ketogenic diet restricts carbohydrates and protein, and it supplies most calories as triacylglycerol, much of which is then converted to ketone bodies. ISBN: 0013-9580, the GABAA receptor antagonist pentylenetetrazole was used to induce epileptic seizures. The ketogenic diet does not work in all patients, and it seems desirable to increase its effectiveness. Amino acids Proteins DIET Range of normal plasma glucose Gluconeogenesis Body protein Protein synthesis Glucose pool Amino acid pool Figure 22-2 (3 of 4) Amino Acid Metabolism Amino acids are used for building needed body proteins. Fasted-State Metabolism Figure 22-7 Liver glycogen stores Energy production Free fatty acids Glycerol Amino acids Ketone bodies Glucose Adipose lipids become free fatty acids and glycerol that enter blood. Fasted-State Metabolism Figure 22-7 (1 of 4) Liver glycogen stores Free fatty acids Ketone bodies Glucose 1 Energy production Liver glycogen becomes glucose.
Fasted-State Metabolism Figure 22-7 (2 of 4) Liver glycogen stores Free fatty acids Glycerol Ketone bodies Glucose Adipose lipids become free fatty acids and glycerol that enter blood. Fasted-State Metabolism Figure 22-7 (3 of 4) Liver glycogen stores Free fatty acids Glycerol Amino acids Ketone bodies Glucose Adipose lipids become free fatty acids and glycerol that enter blood. Fasted-State Metabolism Figure 22-7 (4 of 4) Liver glycogen stores Energy production Free fatty acids Glycerol Amino acids Ketone bodies Glucose Adipose lipids become free fatty acids and glycerol that enter blood. Intestinal lipid droplets can also be visualized by supplementing the normal laboratory diet of C. Intricate metabolic networks tightly coordinate the flow of sugars and fats through synthesis, storage, and breakdown pathways. In general, cells break down carbohydrates, amino acids and fats to generate ATP, the universal energy resource of cells (Salway, 2004).
Inhibition of fat-5, fat-6, and fat-7 genes encoding delta-9 fatty acid desaturation enzymes is associated with reduced fat levels. Mammalian delta-9 stearoyl-CoA desaturase-1 (SCD-1) has emerged as a therapeutic target for obesity and metabolic disorders. Further conservation of function for sbp-1 has emerged from studies in which sbp-1 stimulated transcription of mammalian SREBP targets in a human cell line. Several other NHRs, whose mechanisms of function are unknown, are also required for wild type intestinal fat deposits (Ashrafi et al., 2003). O-linked N-acetylglucosamine (O-GlcNAc) is thought to function as a dynamic posttranslational modification of many proteins (Lindsley and Rutter, 2004; Love and Hanover, 2005). Signaling cascades through insulin, transforming growth factor (TGF-β) and cyclic nucleotide regulated pathways control whether C. Classical neurotransmitters have dramatic effects on fat regulation in nemotodes and in mammals. The provocative hypothesis that bbs-1 and tub-1 form a neuroendocrine axis with kat-1 is based on the synergistic rather than additive fat content of double mutants as assessed by Nile Red fluorescence. Our understanding of body fat regulation as a homeostatic, organismal process has flourished in the past decade. Similarly, compensatory mechanisms that operate at organismal level to maintain energy homeostasis are just being elucidated.
Our periodic correspondent Dan Fleshler is a New York-based writer, media strategist and longtime type 1. This content is created for Diabetes Mine, a consumer health blog focused on the diabetes community. The content is not medically reviewed and doesn't adhere to Healthline's editorial guidelines.
Please note that we are unable to respond back directly to your questions or provide medical advice. Today, our D'Mine columnist and correspondent Wil Dubois takes a real close look at an essential component of our health that most of us never think about.
The article we published about "going Paleo with diabetes" in 2013 has been one of our most-searched posts for the past three years. If we had a dollar for every time "What the heck??" was uttered in managing diabetes, we'd probably have enough funds to find the cure ourselves! As the fastest growing consumer health information site a€” with 65 million monthly visitors a€” Healthlinea€™s mission is to be your most trusted ally in your pursuit of health and well-being. The information contained within this article covers a range of topics written to fully educate pet owners about kennel cough in dogs (a disease otherwise known as canine infectioustracheobronchitis, canine cough, canine croup, canine parainfluenza and canine Bordetella infection). This scheme gives an overview of organ relationships and pathways; note that the reactions are not stoichiometrically balanced.
The catalytic activity of serum is greater when ketogenesis has been induced, suggesting the existence of a specific enzyme activity. In animal experiments, acetone has greater antiepileptic potency than the two other ketone bodies and, as illustrated here, also than the metabolites formed in its own breakdown. Injection of acetone raises the dosage of pentylenetetrazole necessary to trigger seizures. About this Chapter Appetite and satiety Energy balance Metabolism Homeostatic control of metabolism Regulation.
Obesity arises when energy intake, principally stored as triglycerides, exceeds energy expenditure (Flier, 2004; Spiegelman and Flier, 2001). Thus, genes that encode the molecular components of this system may underlie obesity and related disorders. Moreover, developmental programs that underlie fat storage capacity are fundamental to understanding fat regulation. Some of the reported phenotypes may be indirect consequences of global alterations in fat levels and membrane composition. This discrepancy may be explained by the observation that loss of function mutations in fat-6 or fat-7 cause compensatory transcriptional responses in the remaining delta-9 desaturase genes.
Thus, nhr-49 responds to nutrient signals and functions as a regulatory node of metabolic gene expression. Thus, AMPK is a major target of therapeutic intervention for metabolic syndromes such as type II diabetes. This suggests that fat storage capacity of intestinal cells is distinct from developmental program of these cells as enterocytes.
GFP-reporter fusions for each of these genes are exclusively expressed along the apical membrane of intestinal epithelia.
The synergistic nature of the excess fat accumulation in tub-1;kat-1 double mutants suggests that defects in neuronal tub-1 are normally compensated by kat-1 mediated fat oxidation in non-neuronal tissues.
Mutations in human ortholog of bbs genes including bbs-1 underlie Bardet-Biedl syndrome, a pleiotropic syndrome associated with obesity (Beales, 2005). Together, these findings suggest that tub-1 and bbs-1 function in the same fat regulatory pathway. Pumping stimulatory effects of serotonin are abrogated by mutations in each of two serotonergic receptors ser-1 and ser-7 (Hobson et al., 2006). In other cases, such as tub-1 mutants, animals display wild-type pumping rates despite increased fat levels.
Both of which will support, guide, and inspire you toward the best possible health outcomes for you and your family. The information presented is detailed (but still easy to understand) because we areaiming to educate owners thoroughly about the disease, including its transmission, treatmentand prevention, and provide owners with enough information that they might be better informed and able to troubleshoot problems with their own pets.
The resulting acetyl-CoA is turned into acetoacetate along the pathway detailed in the next slide. It does this at lower concentrations than its metabolite acetol, indicating greater anticonvulsant potency.
Muscles also use fatty acids and break down their proteins to amino acids that enter the blood.


Obesity is a complex trait influenced by diet, developmental stage, age, physical activity and genes (Brockmann and Bevova, 2002; Friedman, 2003).
The basis for this paradoxical result is not yet clear but likely reflects compensatory and homeostatic mechanisms. Additionally, sbp-1 regulates expression of elo-5 and elo-6, two fatty acid elongation enzymes required for synthesis of monomethyl branched chain fatty acids (Kniazeva et al., 2004). Thus, this pathway responds to environmental conditions and function as a central regulator of C. Many human BBS genes, which are implicated in ciliogenesis and intraflagellar transport (IFT), have C.
Additionally, serotonin, dopamine and glutamate signaling pathways are implicated in different foraging strategies of C. Sad to say, highly skilled guides through the wilderness of dietary options are hard to find. The subsequent reduction of acetoacetate to I?-hydroxybutyrate allows the liver to dispose of some of the surplus hydrogen that accumulates during I?-oxidation. An important common target for anesthetics and antiepileptic drugs is the GABAA receptor, which is one of the two major inhibitory neurotransmitter receptors in the central nervous system.*Considering the very high concentrations of ketone bodies in diabetic coma, one might assume that acetone contributes to the causation of unconsciousness in this condition. SCD-1 deficiency promotes β-oxidation pathways and decreases lipogenesis in liver and skeletal muscle. This suggests that down-regulation of mitochondrial β-oxidation underlies excess fat levels of nhr-49 inactivation. In Drosophila melanogaster and mammals, the TSC tumor suppressor complex provides a mechanism of cross talk between the insulin and TOR signaling pathways.
Animals that have experienced starvation will pump faster when re-exposed to food than well-fed animals. Similar to mammalian PPARα nhr-49 also regulates expression of fatty acid desaturation and lipid binding proteins.
3e) My dog hasn't been near another dog in months - how could he get kennel cough?3f) Can vaccines cause kennel cough?4) Symptoms of kennel cough - what does kennel cough do to your dog? This section discusses the diagnostic modalitiesused by veterinarians in order to test animals for the various causes of coughs and respiratory illness.It contains information on findings that might be expected in animals with kennelcough and the pitfalls that might be encountered with the testing procedures.
The infectious aerosolised droplets of fluid are so small that, when the next dog inhales them, they are capable of penetrating deeply into the nasal passages, throat, trachea and even the smallest air passages of the lungs.Once inhaled, the infectious organisms invade and replicate within the cells lining these airway passages, damaging these cells in the process and causing local infection and inflammation of the airways.
This results in symptomsof coughing and sneezing and in the production of watery nose, throat and airway discharges. The coughing, sneezingand watery discharges all shed replicated infectious disease particles into the environment and, consequently, the disease spreads and infects new hosts.
Such inadvertent consumption of infectious disease particles can occur if your pet eats or drinks out of (apparently clean) feeding dishes and water bowls that have been contaminated by a sick dog's respiratory secretions (e.g. It is for this reason (the riskof catching infectious diseases) that owners should be very careful about letting dogs eat and drink from the same unwashed feeding dishes, water troughs and standing water sources (pools, puddles etc.) as other animals.
They might even sneezeor cough on those hands and clothes, coating them with infectious aerosols. The hands and clothes may appear visibly clean to the person, but still contain hundreds of organisms that are infectious to other animals (e.g.
Infected animals spread virus particles onto their own fur through licking their bodies (infectious respiratory secretions are transferred onto the coat in this way). 3b) What environmental and husbandry conditions predispose to kennel cough transmission?Given that kennel cough is most commonly transmitted via the air (through infectious, aerosolizedrespiratory fluids being ejected into the air via coughing and sneezing), it follows thatmost dog to dog infections will occur when large numbers of dogs are placed in enclosed conditions in close proximity to each other. The closer the dogs are to each other, location-wise, the more likely it is that infection from a sick dog will spread to others: the virus-laden aerosolised particles will have less distance to travel in order to find a new host. Author's note: it is possible for dogs with kennel cough to infect animals that are locatedin other rooms or locations.
This can occur if animal handlers do not exercise appropriate levels of hygiene when handling other dogs (e.g. It can also occur in open-air settings if air-currents are in such a direction as to be able to blow infectious aerosols from one group of dogs to another group of dogs further downwind.
Firstly, infectious aerosolized droplets attach to dust particles in the air, where they can remain infectiousfor longer periods of time (dust protects fragile viruses from heat and drying out) and be easily inhaled by animals. Secondly, dusty conditions irritate and abrade the airways of animals, leading to airway lining damage - this results in inflammation and irritation of the airways, thereby worsening the signs of kennel cough. The damaged areas also provide a nice place for secondary bacteria to invade and grow and produce bigger infections. High air humidity:High air humidity levels do not irritate the airways as badly as dry air conditions do, but they do increase the risks of airborne infectious disease transmission because respiratory bacteria and virusestend to survive longer (hang around longer) in wet, humid environments and the infectiousaerosols are less likely to evaporate very quickly in wet conditions (thus they remain in the air longer and havemore opportunity to be breathed in). It is possible for a human (owner) to be contaminated by a dog with kennel cough and to spread the disease on to another animal via unwashed hands and clothes. Another possibility is that your dog was notexposed to a dog with kennel cough recently, but ages ago, and developed a 'latent' virus infection at that time, which has, only now, decided to reactivate. Adenoviruses and herpesvirusesare two viruses that are known to 'go dormant' in the body for long periods of time.
Following infection with these viruses, some of the organisms will go dormant and hide out in the animal's cells for months to years, producing no signs of infection.
Similarly, the kennel cough bacteria: Bordetellabronchiseptica, can survive in the airways of animals for long periods of timewithout causing any symptoms. Similar to the latent virus situation, Bordetella canreactivate in periods of high stress or immune suppression and go on to produce clinicalsymptoms of kennel cough, regardless of recent exposure to a dog. Kennel cough vaccines, particularly the live intranasal parainfluenza 2, Bordetella and adenovirusvaccines, can be associated with mild to moderate upper respiratory disease symptoms(watery eye and nose discharges, sneezing, fever and coughing). These symptoms are usually self limiting(they usually abate in 4-7 days) and, in normal animals, they are generally neither severe nor life threatening.
Owners tend to get concerned about the signs because they are concerned about vaccine failure and believe that the vaccine has not worked. The information contained in each genesequence can be used by the cell as a template or set of instructions by which that cell is able to manufacture certain important proteins and molecules vital to cellular function,replication and survival.
Every cell in the body has the same DNA (every cell therefore contains every gene in the body), but not every gene contained in thefull DNA sequence is switched on (activated) in every cell.
The insulingene is only switched on in pancreatic cells and the cells of the pancreas use the informationcontained in the sequence to enable them to make insulin for the body.
The DNA and RNA (RiboNucleic Acid) sequences contained within the adenoviruses (DNA) and parainfluenzaviruses (RNA) play a similar role in the functioning of the virus organisms to the role that DNA plays in our own cells.
Similar to human DNA, viral DNA and RNA is basically just a strand of protein molecules arranged in various combinations (genes) that code for certain proteins and molecules vital tovirus function, replication and survival. The virus has specific surface proteins, called attachment proteins, that allow itto recognize, bind to and access certain cell types.
For example, in canine cough, the cells that the virus prefers to invade are the cells of the upper respiratory tract and mucous membranes (conjunctiva of the eye and lining of the mouth and nose). When a kennel cough virus attaches to the right kind of cell, one of two things may happen: 1) the virus outer membrane fuses with the cell membrane (in the case of paramyxovirus), resulting in the virus capsid and RNA being released into the cytoplasm of the cell OR2) the cell membrane reaches outwards, surrounding the adenovirus or parainfluenza 2 virus inside a 'bubble' of cell membrane (the process is termed endocytosis). This bubble gets released into the cell's cytoplasm where the virus fuses with it, resulting in the release of the viral RNA or DNA into the cytoplasm.
As mentioned above, the nucleus is the region of the cell that contains the cell's DNA - all of the gene sequences that code for the production of all of the proteins, sugars and fats that make the cell function normally (e.g.
The viral DNA or RNA enters the nucleus of the cell and makes use of the enzymes that the cell nucleus contains (and that the virus itself lacks), which enable the DNA of the cell to replicate prior to cell division. Using these borrowed enzymes, the virus replicates hundreds of copies of identical viral DNA or RNA sequences. The new DNA or RNA copies get packaged into the newly-created capsids, along with the other viral elements and surface proteins that the cell body has produced and, viola, hundreds of new viruses are made. In the case of canine adenovirus, the cell dies as a result of this infection and bursts, releasing all of the newly-formed viruses into the respiratory tract, where they can then go and infect other cells.
This cell membrane becomes the newviral envelope of the parainfluenza virus and contains all of the viral surface proteins required to attach to and invade other dog cells (these surface proteins weresecreted onto the dog cell membrane surface during their creation, in preparation forthe moment of budding). The cell dies as a result of the destruction of its cell membrane by the many evacuating viruses.This repeated process of virus invasion and cell destruction is what causes disease in the animal.
In the case of kennel cough, because the virus needs to make use of the cells of the upper respiratory tract(nasal passages, throat, pharynx, trachea, bronchi), this is where the cell damage occurs: consequently, most of the clinical signs seen relate to these organs.
They are capable of replicating on their own, without making use of a cell, and they exert theirdamaging effects on cells, not by way of intracellular reproduction (like viruses do),but by the production of toxic byproducts that they release into their general environment.
In this way, Bordetella is able to withstand the air currents present within the respiratory tract (even coughs and sneezes)and not be blown away from its target cells. 2) Ciliary spasm toxin: Bordetella releases a toxin that stops the small 'hairs'(termed cilia) lining the respiratory tract from moving. These hairs act to moveinfectious particles and debris (mucus etc.) upwards along the trachea to thethroat, ready to be coughed out.
By preventing them from working, Bordetella reducesthe ability of the lungs to clear out primary and secondary infectious disease organisms.


Old tissues are replaced by new ones.Normally the bone and cartilage breakdown rate = the bone and cartilage regeneration rate.
Bordetella bronchiseptica is capable of suppressing this bone and cartilageregeneration rate such that the overall result is an eroding and softening of the bone andcartilage of the trachea and nasal passages. Over time, this eroding and softening can lead to lossof cartilage and bone in the upper respiratory tract and warping of structures such as the trachea and bronchi (if they lose their rigid structure, they can start to collapseas the animal breathes in and out, resulting in airway obstructive signs). Bordetella, on the other hand, likes to grow in conditions of high oxygenation and thus it is perfectlysuited to inhabit the respiratory tract.
In the case of many Staphylococcus species, the attachmentmechanism is not via small fingers, but, instead, via a sticky, slimy coating that glues the bacteriato the target cells. In this way, these organisms are able to withstand the air currents present within the respiratory tract (even coughs and sneezes)and not be blown away from their target cells.
These chemicals create vast regions of cell destruction, open ulcers and tissue inflammation and more places (e.g. Pseudomonas aeruginosa in particular, is noteworthy:this bacteria produces many cell-destroying toxins and causes severe necrosis (rotting)and ulceration of the respiratory tract tissues. 4) Chemicals that call-in inflammatory cells: Many bacteria (particularly the pus-making bacteria such as Streptococcus, Staphylococcus) release chemicals thatact as powerful messages, calling white blood cells into an area of infection (thisis all pus is - bacteria and white blood cells mixed together). Although these white blood cellsare doing the right thing (coming in to kill bacterial invaders), their effects on thelungs and respiratory tract can be very damaging. White blood cells kill bacteriain many ways, one of which is by 'exploding' near the bacteria and releasing nasty chemicalsinto the environment that break down the bugs. Unfortunately, these chemicals alsoerode the cells and tissues of the respiratory tract, creating further damage and inflammation.
In addition to this, too many white cells (too much 'pus') in the airways can blockthe airways, resulting in an animal that is having trouble breathing past all the junk. This isparticularly the case if the ciliary clearance mechanisms of the lungs are not working (not helpingto clear the excess pus from the airways). Similar to Bordetella, these organisms are able to evadethe body's immune system defenses and the many antibiotic types that are unable to penetrate inside ofcells. As with Bordetella, these intracellular bacteria are able to hide out within the body's cells until the antibiotics have stopped and then reemerge to create disease signs all over again. Bacteria with this property are able to avoid immune system destruction for longer periods and, therefore,have extra time in which to create more damage and replicate more copies. 8) Coagulases: Some bacteria, including Staphylococcus species, produce chemicals calledcoagulases that facilitate the clotting of plasma proteins (which leak into inflamedrespiratory tissues from the blood stream) into a firm, white protein matte or mesh called fibrin.
Fibrin is useful for bacterial survival because the bacteria can hide out in it, thereby avoiding the white blood cells of the immune system that are out to eat them. Fibrin protects the bacteria from the white blood cells because the white cells are too largeto get through the mesh of fibrin protein: it is as though the bacteria have protected themselvesinside a 'fence' of protein that the white cells can't access. Similarly, carbon dioxide (a waste product of cell metabolism) is able toleave the body through the same route: diffusing from the blood into the airways for exhalation.
Ulceration of the lining of respiratory tract results, leading to severe irritation and inflammation of the affected regions (trachea, throat and lining of the nose).
Animals with severe pneumonia can even die from a lack of oxygenation, though this is rare with the kennel cough condition. These animalswill be very unwell, with increased respiratory rates, a soft, wet-sounding coughand often fever and inappetence. These are all signs of an animal with severe lung disease and respiratory compromise: these animals need urgent veterinary attention!
In the vast majority of cases, the antibiotics and other therapeutics prescribed bythe veterinarian will have their desired effect: the kennel cough infection will go away and the dog will be fine. In a small minority of patients, however, the kennel cough infection will seem to keep coming back again. The animals will seem to respond to the antibiotics prescribed (although, sometimes they may not even respond to these), the cough will seem to settle down and then, within weeks to months of the antibiotics coming off, the symptoms will return again (especially the characteristic harsh, dry cough).
Well, there are many reasons why the symptoms of kennel cough may keep on returningwithin the one animal.
If you are treating a condition correctly and the animal is not respondingto the treatment given, it is time to re-evaluate the diagnosis. There are many conditionsthat can mimic the symptoms of kennel cough, including other tracheal diseases (e.g. Some of these conditions can even be complicatedby secondary bacterial infections, such that they, like kennel cough, will seem to respond favorably (but transiently) to antibiotic therapies.
They remain there safely, in hiding, until the antibiotics have stopped whereupon they then re-emerge as a renewed infection. If recurrent infection is thought to be the issue,it is important for your vet to get a culture of the airways (culturing one of the known intracellularbacterial types may be highly supportive of this diagnosis). Pseudomonas) are very difficult to kill and highly resistantto a wide variety of antibiotic types: they will keep coming back if the therapy isinsufficient. If resistant infection could be an issue, it is important for yourvet to perform a culture and sensitivity test on the animal's airways (see section 5c). The vet takes a sample of fluid from the trachea or bronchi of the animal and sends the sample to a lab, not only to determine the species of bacteria responsible for the recurrent infection, but also to determine the antibiotics that the bacteria is sensitive and resistant to. Generally, the reappearance of latent virusesis not a big factor in recurrent kennel cough infections (it is a huge issue withrecurrent herpesvirus cat-flu infections in felines). Preventionof recurring latent virus infections involves determining the source of stress or immune suppressionand removing it (if possible).
5) The animal has some form of immune suppression and keeps getting infections:Antibiotics can only really go a small way towards eradicating infection from an airwayor any other part of the body. When we give an animal antibiotics, we are hoping thatthe antibiotics will kill as many of the bugs as possible, holding the infection at bayso that the immune system (white blood cells, antibodies etc.) has time to respond andfinish the job (clearing all of the infection). Consequently, as soon as the antibiotics are stopped, the infection will returnin a big way. Alternatively, because immune suppressed animals are at risk of catching infections in general, even if your antibiotics do do the job and wipe out all of the infectiousorganisms this time, there is every chance that the animal will very soon get a whole new infection from the next virus or bacterial invader that comes along. 6) Environmental factors are still playing a role:Kennel cough is a multifactorial disease with infectious, environmental and host elementsall playing a role in the severity and presentation of clinical symptoms. For example, bacterial infections such as Bordetellosis have theability to penetrate deeply into the cartilage of the airways, damaging and weakeningtheir structures.
Animals with this secondary airway disease(collapsing trachea, dynamic airway disease) will have persistent airway problems and a long term chronic cough. Diagnosis of secondary mechanical airway issues can be madeon the basis of chest radiographs and endoscopy (a camera inserted down the trachea underanaesthetic) - see section 5.
4e) Can animals show little or no signs of kennel cough and yet carry and transmit the infection?
Theseand other factors all interact to determine if an animal will display disease signs ornot and, if so, how severe those disease signs will be.
For example, low numbers (a low dose) of a very virulent, highly-aggressive organism be enough to create disease signs. Animals that have been previously vaccinated against kennel cough and which have good immunity towards the disease will often only get very mild disease symptoms or show no clinical signs at all whenexposed to a primary kennel cough virus or bacteria. All you might get is a low fever, a few days (around about a week) of occasional coughing and sneezing and perhaps some watery eye and nasaldischarges. The signs could be so subtle (a couple of coughs a day) that owners do not even know their pet has the disease.Similarly, animals infected with a very low dose of kennel cough organisms or infected with very weak strains of kennel cough organisms may also permit these infectious agents to replicate briefly within their respiratory tracts (ready to pass on to other pets), but only show minimal signs ofinfection themselves. Most animals of normal vaccine status that encounter kennel cough organismsin their environment will show no signs or only develop mild signs of disease. They make up a much larger proportion of animals than those that go on to get the full-blown signs of kennel cough.
The trouble is that we only recognizethose animals with the moderate to severe signs - we don't recognize the mildly affectedanimals as readily and so their true prevalence goes unidentified.
Vaccination may go a big way towards stopping the animalfrom showing severe clinical signs of disease, but it can not 100% stop the viruses and bacteriafrom growing and replicating in and shedding from that dog's airways during the period of clinical infection and for variable periods of time after the clinical signshave resolved.
This is the main way in which kennel cough still manages to be passed from dog to dog in high-vaccination-rate facilities such as dog clubs, breeding facilities and boarding kennels.
Because these animals (I'll term them 'mildly clinical') show minimal symptoms of infection (maybea subtle watery nasal discharge, an occasional cough etc.) the operators of the dog facilities do not recognise the infection and do not think to isolate these animals from the other dogs. Therefore, when new dogs enter the facility, whose vaccination statusis not optimum or whose levels of stress make their immune responses suboptimal, theyare likely to encounter the primary viruses and bacteria being shed by the mildly clinicalanimals and consequently, they catch the disease.



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