What is bronchiectasis? The simplest way to explain it is, the airways have become widened and flabby, and the airway walls have become thick. Think of it this way; blow up a ballon over and over again, a million times. What happens? The ballon when deflated no longer holds it’s shape. The deflated balloon is flabby and has lost its elasticity. That is bronchiectasis. The lungs have lost their elasticity to pop back into shape or hold shape. These widened and misshapen air passages now become places that mucus holds up in, or gets stuck in. The stuck mucus becomes an additional breeding ground for infections. Those areas of damaged airways are permanently damaged, just as there is no way to fix that old ballon, there is no way to fix that damaged lung tissue.

Bronchiectasis can be acquired or bronchiectasis can be congenital. Acquired bronchiectasis is more common than congenital bronchiectasis. Acquired bronchiectasis affects adults and older children, usually as a result of a pneumonia, chemical exposure, chronic pulmonary aspiration, drug use, alcohol abuse, and as the result of another medical condition; such as Cystic Fibrosis, Primary Ciliary Dyskinesia, Alpha1, and a whole host of other medical conditions including Lupus and Rheumatoid Arthritis. Acquired bronchiectasis can develop in childhood, but often doesn’t affect the patient till adulthood. However bronchiectasis caused by an underlying medical condition such as CF or PCD can affect the patient in childhood. Congenital bronchiectasis effects infants and children, usually it’s the result how the lungs are developed in the fetal stage of development. Early detection and treatment of bronchiectasis and the patient’s underlying medical condition, that contributed to them acquiring bronchiectasis, is essential to the patient’s overall quality of life. Bronchiectasis can lead to serious issues like atelectasis, respiratory failure, and heart failure. The goal of treatment in bronchiectasis is to slow down the progression of bronchiectasis and prevent further lung tissue damage.

 Bronchiectasis is often sorted by medical professionals into two types; CF Bronchiectasis or Cystic Fibrosis Bronchiectasis and Non-CF Bronchiectasis or Non Cystic Fibrosis Bronchiectasis. Basically CF Bronchiectasis is bronchiectasis caused by cystic fibrosis. All other forms of bronchiectasis regardless of their underlying medical cause are thrown into the Non-CF Bronchiectasis group. There are concerns among clinicians that this practice may no longer be adequate as technologies and diagnostic tools for bronchiectasis have advanced. Non-CF Bronchiectasis is thought to be rare in the western world, but in the developing world, non-cf bronchiectasis is emerging cause of superlative lung disease in patients. Another issue with lumping all bronchiectasis cases not caused by CF together is that the basic treatment for non-cf bronchiectasis may not be appropriate for all bronchiectasis caused by other diseases. For instance in primary ciliary dyskinesia (PCD), use of corticosteroids unless the PCD patent also has asthma is discouraged. Whereas in chronic obstructive pulmonary disease (COPD) corticosteroids are a mainstay of treatment. It is theorized since PCD treatments mirror CF treatments that perhaps bronchiectasis caused by PCD should be grouped with CF Bronchiectasis or perhaps put in a new category such as PCD Bronchiectasis. Perhaps it is time for researchers to take a closer look at the two types or categories of Bronchiectasis to see if they are too loosely defined. This issue has big implications when it come to medication approval from the FDA. Medications deemed safe and effective for CF Bronchiectasis are often unavailable to the Non-CF Bronchiectasis patient population even though the drug may be beneficial to a certain subset of Non-CF Bronchiectasis patients; like for instance PCD Bronchiectasis patients.

Bronchiectasis is sorted into several subtypes based on anatomical/ microscopic appearance; basically based on their shape visible on a ct-scan. These subtypes are as follows; Cylindrical Bronchiectasis, Saccular or Varicose Bronchiectasis, and Cystic Bronchiectasis. A single patient can be found to have all three forms of these subtypes within their lungs. In cylindrical bronchiectasis, often the mildest form of bronchiectasis, the airways or bronchi are enlarged and cylindrical. In saccular or varicose bronchiectasis that airways or bronchi are irregular with areas of both dilatation and constriction. In cystic bronchiectasis, often the most severe form of bronchiectasis, the airways or bronchi are dilated and form clusters or cysts. Different types of bronchiectasis have similar symptoms, but vary in severity. Similarly, depending on the underlying disease causing the bronchiectasis, bronchiectasis affects different areas of the lungs. In cystic fibrosis, bronchiectasis mainly affects the upper lobes of the lungs; whereas in primary ciliary dyskinesia, bronchiectasis affects the lower lobes, the right middle lobe, and the left lingula.

Common symptoms in bronchiectasis, no mater the type or subtype are; persistent cough, productive cough with increased sputum, frequent respiratory infections, tiredness, shortness of breath, chest pain, weight loss, decreased lung function, and or hemoptysis (bloody sputum.) Symptoms may also vary based on the patient’s underlying medical condition that contributed to them acquiring bronchiectasis. A bronchiectasis patent who’s underlying medical condition is Crohn’s may also present with abdominal pain and diarrhea. Nontuberculosis Mycobacterium patients may have fever, chills, and night sweats along with the more common symptoms of bronchiectasis. The symptoms of bronchiectasis may be transient (come and go), symptoms may also develop and change over time as well. Due to the transient nature of the symptoms of bronchiectasis, the disease oftentimes progresses unnoticed for huge periods of time.

The treatment goals for bronchiectasis are to slow down and or to stop the progression of airway damage caused by bronchiectasis. This is achieved by controlling symptoms and prompt treatment of infections. Treatment usually includes keeping immunizations up to date, smoking cessation, chest physiotherapy, bronchodilators, corticosteroids, oxygen therapy, increasing hydration, diet, exercise, inhaled antibiotics, oral antibiotics, mucolytics, pulmonary rehabilitation, and surgery to resect portions of localized bronchiectasis. However in cases such as CF and PCD resections of localized bronchiectasis are not recommended anymore, because they have proven not to be an effective treatment of bronchiectasis in CF and PCD. In cases of severe bronchiectasis exacerbations, patients are often hospitalized and given IV antibiotic therapy. In PCD, bronchiectasis exacerbations are oftentimes treated with IV antibiotics whether the patient is hospitalized or not. Advances in treatment and access to treatment have allowed PCD patients to start and complete their entire IV antibiotic therapy in the comfort of their own home. One final note on bronchiectasis as it relates to the PCD patient; in end stage PCD, where lung transplants are needed, transplants are often the result of respiratory failure due to bronchiectasis.

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 The human body has a natural filter for dust, bacteria, and debris. That filter consists of mucus and cilia, which protect human tissue and makes sure that dust, bacteria, and debris do not reach certain tissues or organs of the human body. The cilia in the respiratory system traps the larger pieces of the dust, bacteria, and debris and moves those pieces out of the respiratory system via cough or sneezing. The smaller pieces of the dust, bacteria, and debris is trapped in the mucus; the cilia then help to transport the debris filled mucus out of the respiratory system via cough or sneezing. Mucus production in the respiratory system is completely normal. Our respiratory system can not function without mucus. Mucus also helps to keep the respiratory tissue moist and in proper working order. Mucus often changes in color, viscosity, and volume due to a number of reasons including bacterial infections, viral infections, types of trapped debris, and even because of inflammation. It is theorized that the human body naturally produces between ten and one hundred milliliters of mucus a day. Mucus that is expelled from the respiratory system is oftentimes referred to as sputum.

Sputum can give important information about the status of a patient’s health. People do not often notice the everyday natural sputum. It is only when sputum is overproduced or hyper-secreted, when their respiratory system is irritated or inflamed, or when their sputum has changed in color and viscosity that a person is bothered by their mucus. Hyper-secretions happen during the body’s normal immune system process and is a good sign that tells you that your immune system is working. Changes in color and viscosity also give us a clue that the body’s normal immune responses are working. From a viscosity stand point thick mucus can be laden with dust and debris as well as bacteria, so it is not always an indication of a contagious illness in the patient. Whereas thin, slippery mucus is laden with viruses; and is often your most contagious mucus from the respiratory system.

Color changes in mucus are what tend to bother people, not always the patient though, the most about mucus. Mainly due to the myth that green or yellow mucus is always contagious. No one is really sure how the myth got started. But that myth permeates the medical field to this very day, and is constantly passed around; even in medical books that medical students study from. The color of mucus/sputum can range from clear to black. Mucus that is clear, white, grey, frothy, and or any combination of those and that is overly abundant in volume typically happens at the beginning of a viral infection and is the most contagious of the colors of mucus. Red and black mucus, which can be frothy and prevalent or not, indicates the presence of blood. Blood in the mucus can happen at the beginning of a bacterial infection, indicating an infection is brewing. But bloody mucus can also be signs of a serious infection like NTM (nontuberculosis mycobacterium), PA (pseudomonas), TB (tuberculosis), and even cancer. Typically expelling streaks of blood or expelling less than 4 tablespoons of blood in a single day can be handled at your next appointment. Or you can even ring your physician’s office to inform them of the change in your mucus which contains blood. However expelling more than a cup full of blood, in a single day, in your mucus requires immediate medical intervention; so ring 911, don’t wait. Green and yellow mucus are typically bacterial infections and a natural part of the immune system’s inflammation response; the mucus is typically not contagious at this point. This is because of the body’s immune process; the presence of white blood cells, the presence of cell debris, and the very low viral load present in the mucus at this point. Green and yellow mucus is usually not an indication that bacteria have taken over, however it does signal the infection is bacterial and needs antibiotics. A strong indicator that stronger antibiotics maybe necessary to clear a bacterial infection is how dark the green mucus is.

Mucus secretion and mucus clearance are extremely important in maintaining a healthy respiratory system. In PCD where airway clearance is already hindered by non-working or partially-working cilia the other half of the body’s natural defense against dust, bacteria, and debris, mucus is also compromised. The body’s natural response to clear out stuck mucus is to secret even more mucus. That leads to a constant cycle of hyper-secretion of mucus which becomes stuck, so the body make even more mucus in its attempt to clear the already stuck mucus. This leads to mucus becoming thick and sticky. That stuck mucus hangs out in the respiratory system for extraordinarily long periods of time. That extra time lows trapped dust, bacteria, and debris to become infections. Bacteria and organisms that are usually harmless to people, because their systems can clear those bacteria and organism, can become trapped so long in a PCD patient’s respiratory system that those bacteria and organisms take up residence and cause illness in the PCD patient. These infections can become chronic, lead to overall decline in respiratory function, and eventually lead to respiratory failure.

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***For the purposes of this topic we will be focusing solely on NTM pulmonary disease in regards to the PCD patient. Please keep in mind that many medical conditions can contribute to the acquisition of NTM pulmonary disease and affect it’s disease path. This topic is not meant to be an all encompassing article on NTM, nor does it replace or is it intended to replace medical advice from your physician. If you believe that you may have an NTM pulmonary disease, please seek the advice of a licensed physician or licensed Infectious Disease Specialist.***

NTM pulmonary disease, or Nontuberculosis mycobacterial lung disease, is caused by inhaling naturally occurring mycobacteria which are found in the environment; most notably water and soil. People are exposed to NTMs every single day, everywhere they go, and they do not get sick from it. Those who develop NTM pulmonary disease are people who have other health issues like preexisting or prior lung disease, and or a weakened immune system. NTM is also called atypical TB or atypical tuberculosis, EM or environmental mycobacteria, environmental tuberculosis, MOTT or mycobacteria other than tuberculosis, and MAC or mycobacterium avium complex; MAC is actually just one of the 170, known to date, species of NTM. Typically the species of NTM that cause moderate to severe pulmonary disease in pulmonary patients are mycobacteria avium complex also known as M. avium complex or MAC, MAI also known as M. intracellulare, mycobacteria abscessus also known as M. abscessus, and mycobacteria kansasii also known as M. kansasii. MAC, MAI, and M. kansasii are the most common NTM species to cause pulmonary disease; where as M. abscessus is the least common and the most difficult of the four species of NTM that cause pulmonary disease to treat. Once a person develops a NTM pulmonary disease they are not considered to be contagious even when showing signs of illness, because current research has shown that NTMs can not be passed from person to person. NTMs if caught early are treatable; though treatment is often very expensive, and can last two to three years in length. If left untreated, the pulmonary disease will worsen causing structural damage and worsening lung function. It’s extremely important to note that due to NTM species’ resistance to antibiotics; treatment of a NTM pulmonary disease should only be considered if there is solid scientific evidence that the NTM is causing illness to the patient.

NTMs can be divided into two classes; slow growing NTMs and rapid growing NTMs. Slow growing NTMs require more than fourteen days of incubation for mature growth. The most common slow growing NTMs that cause pulmonary disease are MAC, MAI, and M. kansasii. M. kansasii is the easiest of the three to treat; often being able to be treated with only three antibiotics. Whereas MAC and MAI can be stubborn and require three to five antibiotics, for up to eighteen months, to achieve effective treatment. Pulmonary disease from slow growing NTMs progresses slowly and has a overall better chance of successful treatment; which increases the chance of preventing pulmonary structural defects in the patient. Rapid growing NTMs can mature in just seven days of incubation. The common rapid growing NTM that causes pulmonary disease is M. abscessus. Rapid growing NTMs are often the most difficult and most stubborn of the NTMs to treat, because they can form biofilms and they can interact with protozoans; to protect themselves from antibiotics. M. abscessus usually requires lengthy treatment with three to five antibiotics for two to three years, chemotherapy in patients that can withstand it, tissue resection of the diseased lung tissue, and or any combination of the aforementioned treatments. M. abscessus is notoriously difficult to treat with antibiotic therapy alone. Pulmonary disease from rapid growing NTMs can progress very fast and have a poorer chance of successful treatment; which increases the likelihood of permanent pulmonary structural defects.

Not all persons with NTM pulmonary disease will have symptoms of disease; especially in the early stages of the disease. As the disease progresses, the more likely the person is to exhibit symptoms. Common symptoms seen with NTM pulmonary disease are; chronic fatigue, chronic cough, chest pain, wheezing, malaise, coughing up bloody mucus, night sweats, fever, reoccurring lung infections, shortness of breath, unexplained weight loss, and or unexplained loss of appetite. Unfortunately because there are no typical clinical features of NTM pulmonary disease diagnosis is often delayed, even for years.

Once successful treatment has been achieved the treatment and monitoring of NTM pulmonary disease shifts to preventing reinfection of the NTM species or infection with a different NTM species. A person with a past history of NTM pulmonary disease has about a seventy five percent chance of relapse of their NTM pulmonary disease and or acquiring a new NTM pulmonary disease with a different NTM species. There are steps to help prevent a relapse or reinfection they are as follows; switching to bottled spring water, limiting showering in enclosed spaces or shower stalls, turn up the temperature on home water heaters, avoid public hot tubs and public swimming pools, avoid private hot tubs and private swimming pools that are not properly chemically maintained, avoid home and public sprinklers, and boil all water that is used for cooking or drinking. However boiling water to get rid of NTMs can actually aerosolize the NTMs so use caution when doing so. Indoor air quality can also affect exposure to NTMs.

PCD increases the risk or vulnerability to NTMs, and having PCD with Bronchiectasis considerably increases the chances of contracting a NTM pulmonary disease. NTMs enter the lungs through the environment, and most people can clear the NTMs with the help of the cilia. In PCD where ciliary function is oftentimes limited or nonexistent NTMs can hang out in the lungs for huge amounts of time; which is what puts PCD patients at greater risks from NTMs. Due to the nature and disease progression seen in PCD; NTM pulmonary disease can and is often missed due to Bronchiectasis, pseudomonas, and lung cavitation due to pneumonia or other organisms often seen in PCD patients. According to current research the most common NTM pulmonary disease in PCD is MAC. Only about thirteen percent of PCD patients end up with M. abscessus pulmonary disease. Treatment of NTM in PCD patients is extremely important when considering that end stage PCD, in advanced PCD cases, leads to lung transplantation. If a lung transplant patient has a prior history of NTM lung disease it is important to retreat the patient for NTM pulmonary disease after transplantation. The goal of retreatment is to prevent any NTMs that have colonized in the body or are just hiding out elsewhere in the body from infecting the new lungs. Lung transplant patients with NTM pulmonary disease have a higher mortality rate than lung transplant patients without prior NTM pulmonary disease. Relapse rates for NTM pulmonary disease in PCD patients is as high as eighty percent according to some researchers. One final and interesting note on NTM pulmonary disease, that has specific implications in PCD, is study observations have revealed that women may be more susceptible to NTM pulmonary disease, because of the practice among women to cough quietly and covertly. The suppressing of the clearance of mucus for privacy sake appears to directly correlate to increase risks in NTMs and other organisms.

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 What is Ototoxicity? Ototoxicity is basically ear poisoning. The damage in ototoxicity occurs to the inner ear specifically the cochlea or auditory nerve, and oftentimes the vestibular system. Ototoxicity is caused by pharmaceutical drug therapy a majority of the time; including the use prescription medications, over the counter medications, and even supplements. Ototoxicity causes hearing loss and balance disorders; which can cause serious social, communication, and educational issues. The risks of developing ototoxicity is dependent on several factors including use of other ototoxic drugs at the same time, which ototoxic drug is being used, how long the ototoxic drug is being used, and several other factors including but not limited to kidney function. Ototoxicity seems to occur more frequently in adults than children, but those numbers are skewed based on unreliable reporting of ototoxicity instances and the inability of some children to accurately describe their situation to their caregivers and their physicians. Some patients are more susceptible to ototoxicity based on prior frequent usage of ototoxic drugs, their unique genetic factors, and their need to use more than one ototoxic drug at a time based on their unique overall health picture. Furthermore; ototoxicity caused by antibiotics can be and more than likely is permanent, whereas ototoxicity caused by drugs other than antibiotics can be and is most likely temporary.

The term cochleotoxicity can be used to describe the damage done to the auditory system by ototoxic drugs. The damage done to the cochlea can cause complete deafness, hearing loss in the high-frequency range, or hearing loss in any of the ranges in between. Inconsistencies in the data reported regarding coch;leotoxicity make it virtually impossible to pinpoint actual frequency of cochleotoxicity associated with specific drugs. However; “the relationship between cochleotoxicity and drug administration parameters such as dosage, duration of treatment, and serum concentration is highly variable (Barza & Lauermann, 1978; Fausti et al., 1992b; Fausti et al., 1993; Schentag, 1980).” Basically, a physician should not rely solely on lab work and dosage scales to predict a particular patient’s risk for ototoxicity. Hearing screenings and assessments remain the only reliable method for detecting cochleotoxicity. Hearing screenings should be conducted prior to the start of an ototoxic drug to establish a patient’s baseline, and continued hearing screenings should be conducted simultaneously during treatment with an ototoxic drug; at least every three months during treatment. Additionally; it should be noted the ototoxic drugs should not be used as ear drops because the ototoxic drug might diffuse into the inner ear when the tympanic membrane of the inner ear is perforated which increases the risk of ototoxicity.

The term vestibulototoxicity can be used to describe the damage done to the vestibular system by ototoxic drugs. Many physicians do not understand the risk of injuries to the vestibular system from ototoxicity, nor do they seem to appreciate the devastating effects of ototoxicity injuries to the vestibular system. Symptoms of vestibulototoxicity can include disequilibrium, oscillopsia (the perception that viewed stationary objects or surroundings move in harmony with head movement), vertigo, difficulties walking in low light, difficulties walking in darkness, and many other symptoms. Each of these symptoms is related to balance. Simply put; the mind is confused with the direction of motion or lack of motion, and therefore the patient has difficulty seeing and processing images. That is what often leads the patient to describe the feeling of dizziness and wooziness. If the symptoms of vestibulototoxicity appear severe, they will most likely not dimmish over time, but instead will most likely be permanent. The onset of vestibulototoxicity can be sudden or gradual depending on the damage that was done by the ototoxic drug. Additionally, asking the patient to contact their physician at the onset of symptoms is not helpful in monitoring for vestibulototoxicity; as patients do not seem to recognize the exact onset of symptoms with regards to vestibulototoxicity.

PCD or Primary Ciliary Dyskinesia where prompt treatment of infection reduces the risks of progression of the damage done to the body by PCD, puts the PCD patient at higher risk of instances of ototoxicity. Also the likelihood of a patient with PCD culturing rare or unusual infections in their lungs, ears, or sinuses such as pseudomonas aeruginosa, enterobacter species, and nontuberculosis mycobacterial lung infections also increases the risk of ototoxicity to a patient with PCD. This is due to the fact that these types of infections require the use of an antibiotic from the aminoglycoside family. Antibiotics in the aminoglycoside family include gentamicin, tobramycin, streptomycin, amikacin, netilmicin, neomycin, dihydrostreptomycin, kanamycin, ribostamycin, and vancomycin. “Aminoglycosides are among the most efficacious antibiotics used to treat serious Gram-negative infections (Forge and Schacht, 2000).” Approximately ten percent of people taking aminoglycoside antibiotics experience ototoxicity, although up to thirty-three percent has also been reported in adult patients; again these numbers are most likely skewed due to unreliable reporting of instances involving ototoxicity and aminoglycosides. However; aminoglycosides are well known for their potential to cause permanent hearing loss, tinnitus, temporary increase of hearing followed by gradual decrease in hearing loss, permanent vestibular loss, permanent vestibular sensitivity, and or vision issues. Hearing loss onset due to ototoxic drugs can occur after the very first dose, after a few days or weeks, or even several months after completing aminoglycoside therapy. Aminoglycosides given intravenously (by IV) increases the risk of ototoxicity for any patient, not just PCD patients. Whereas aminoglycosides administered by inhaling them using a nebulizer reduces the risk of ototoxicity for any patient, again, not just PCD patients. Furthermore, recent studies indicate that infections that cause systemic inflammation greatly increases the risks of aminoglycoside induced cochleotoxicity. Researchers hope to include that knowledge in future models that are used to predict comorbidity factors and their risks of predisposing a patient to ototoxic drug induced hearing loss. Unfortunately antibiotics from the aminoglycoside family are a necessary evil in the effort to treat infections in PCD and slow the progression of PCD.

The signs and symptoms of ototoxicity are often dizziness, uncoordinated movements, oscillating or bouncing vision, tinnitus or ringing in the ears, an unsteady gait, vertigo, and bilateral or unilateral hearing loss. If you notice any of these symptoms call your physician right away, don’t wait! You and your physician may need to discuss discontinuing the ototoxic drug, lowering the dosage of the ototoxic drug, finding an alternative drug, discuss the benefits of continuing treatment with the ototoxic drug, as well as whether the risks of the ototoxic drug outweigh the benefits of the ototoxic drug in your unique health circumstances. It should also be noted here that you should not discontinue the ototoxic drug, at the first sign of symptoms of ototoxicity, without first discussing the situation with your physician.

The prevention of ototoxicity must be the focal point of managing treatment with an ototoxic drug, as most hearing loss is permanent when the ototoxic drug is an antibiotic. There are no treatments for ototoxicity. Instead efforts and current research projects are aimed at helping the patient cope with the side effects of ototoxicity, and minimizing the risks of potential ototoxicity from offending drugs while maintaining the ototoxic drug’s therapeutic qualities. The American Academy of Audiology recommends ototoxic monitoring to allow for possible prevention and detection of ototoxicity, as well as the rehabilitation of hearing loss through the use of cochlear implants or hearing aids. Physical therapy may help patients regain some balance and walking abilities, or at the very, least help the patient learn to compensate by learning to use adaptive mechanisms.

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