Respiratory symptoms often send folks scrambling to the doctor's office, seeking relief from their woes. When it comes to these symptoms, a whopping seventy percent of patients sporting a persistent cough end up with the diagnosis of acute bronchitis. But that's not all that can make you cough up a storm; pneumonia, cough-variant asthma, a heart that's seen better days (congestive heart failure), postnasal drip, rhinosinusitis, and even accidentally swallowing some of your own saliva can all be culprits.
For those who decide to consult their trusty primary care provider about their cough, here's a little crystal ball action: roughly 10% to 15% of them might be harboring pneumonia. The signs that might point to this not-so-welcome guest include being on the mature side (the odds are 4.6 times higher), feeling breathless (2.4 times more likely), running a fever (5.5 times the chance), having a racing heart (3.8 times more common), and last but not least, the doctor hearing something funky during a chest exam, like crackles (23.8 times the odds) or rhonchi (14.6 times more likely).
As you can see, the world of respiratory infections is quite a mixed bag, with different causes, treatments, and prognoses. Stick around, and we'll unpack it all in this chapter.
The Lowdown on Acute Bronchitis
Acute bronchitis, or AB for short, is a common affliction that tends to strike during the winter season. It's a viral party in your upper respiratory tract, so leave those antibiotics at the pharmacy. The incidence of AB hovers between 30 to 170 cases per 1000 individuals each year. The usual suspects behind this seasonal shindig are rhinoviruses, respiratory syncytial virus, influenza, parainfluenza, and adenovirus. These germs are like party crashers; they spread quickly through respiratory secretions or hitch a ride on shared surfaces.
AB is usually a "get well soon" kind of situation, lasting no more than 1 to 2 weeks. If you find yourself coughing up some gnarly-looking mucus (purulent sputum), don't jump to conclusions—it's more about your respiratory tract doing some spring cleaning than a bacterial invasion.
But, if your symptoms decide to outstay their welcome for over 2 weeks, it's time to play detective. It could be "atypical" bacteria like Bordetella pertussis or Mycoplasma pneumoniae causing trouble, or perhaps another diagnosis entirely, like postnasal drip syndrome, asthma, acid reflux, chronic bronchitis from smoking or other irritants, bronchiectasis, eosinophilic bronchitis, or the use of angiotensin-converting enzyme inhibitors.
Now, let's talk antibiotics. They're not the superhero in this story. Numerous trials and fancy meta-analyses have weighed in, and the verdict is clear: antibiotics don't offer much, if any, benefit in treating AB. In fact, they come with significant costs and potential side effects.
Overprescribing antibiotics for AB contributes to a bigger problem—antimicrobial resistance. In the United States alone, we're talking about over 2 million illnesses and 23,000 deaths related to antibiotic-resistant infections each year, costing more than a whopping $30 billion.
But wait, there's a caveat. Some AB cases do call for treatment, especially during documented B. pertussis (whooping cough) outbreaks or if you have underlying lung issues like chronic obstructive pulmonary disease, asthma, or a smoking habit. In such cases, second-generation macrolides like azithromycin or clarithromycin are the go-to choices.
Community-Acquired Pneumonia: A Persistent Threat
Pneumonia, the "captain of the men of death" as Sir William Osler put it, remains a formidable adversary despite our century-long journey of understanding its inner workings and treatment. It continues to hold its title as the leading infectious cause of death not only in the United States but worldwide.
Over the years, we've witnessed incremental victories in the battle against community-acquired pneumonia (CAP), thanks to medical breakthroughs. These milestones include antipneumococcal serum therapy (unveiled in 1895 and widely embraced by the 1920s), antibiotics (discovered in 1928 and widely used by the 1940s), and mechanical ventilation (revealed in 1952 and adopted in the 1960s). Pneumococcal vaccination, while beneficial, hasn't outshone these prior achievements significantly.
In the United States alone, approximately 4 million CAP cases emerge annually, translating to around 6 cases per 1000 people each year. Among these, 1 million necessitate hospitalization, resulting in 45,000 to 50,000 fatalities. The mortality rate for all hospitalized CAP patients can fluctuate from 2% to a staggering 30%, and those who find themselves in the intensive care unit (ICU) for initial care face an even bleaker prospect, with mortality rates as high as 40%. In stark contrast, outpatients generally fare better, with mortality rates ranging from less than 1% to 3%.
CAP is characterized by an abrupt lung infection, accompanied by a fresh infiltration on a chest X-ray or compatible findings during a lung examination. Typical CAP symptoms often include a mix of these features: fever or abnormally low body temperature, sweating, chills, pleurisy, and a new cough, with or without the production of sputum or changes in the color of respiratory secretions. If your cough isn't producing thick mucus, it might hint at "atypical" culprits like Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella species, or even Bordetella pertussis.
While Streptococcus pneumoniae is still a prevalent cause of CAP, its incidence has dwindled, thanks in part to pneumococcal vaccination. However, "atypical" pathogens are garnering recognition as both outpatient and inpatient CAP instigators, warranting the use of empirical antibiotics in all cases. Yet, identifying the exact cause of CAP often proves elusive in clinical practice. Surprisingly, pathogen identification succeeds in less than 10% of hospital-admitted CAP cases, according to one review of over 17,000 cases. Recent studies utilizing specialized tests like broad-range polymerase chain reaction (PCR) assays have upped the microbiologic diagnosis rate to 38% to 87%, with viruses emerging as the most frequently detected culprits, found in roughly one-third of cases. The high rate of culture-negative CAP can be attributed to various factors, including prior antibiotic use, difficulty in producing suitable sputum samples, viral origins, or as-yet-unidentified emerging pathogens.
To unearth less common pneumonia causes such as Mycobacterium tuberculosis, Coxiella burnetii, and endemic fungi (Coccidioides species, Histoplasma capsulatum, and Blastomyces dermatitidis), epidemiological clues can provide valuable insights.
Diagnosing CAP hinges on the presence of localized pulmonary findings, either through lung auscultation or chest radiography. The latter is crucial for ruling out complications like pleural effusions and potentially hinting at the responsible pathogen (e.g., lymphadenopathy) or alternative diagnoses (e.g., lung mass, lung abscess). However, radiographic patterns don't reliably differentiate specific pathogens, particularly among the elderly and immunocompromised patients who may present unusual or no infiltrates despite having CAP. Post-pneumonia, tobacco smokers and individuals over 65 should undergo follow-up chest radiography within 3 to 6 months to exclude underlying malignancies.
Determining when patients should undergo an extensive microbiologic evaluation for the causative agent remains somewhat tricky. It's typically recommended for immunocompromised patients, those admitted to the hospital or ICU, or those who haven't responded to recent treatment. Hospitalized patients should have at least blood cultures and sputum Gram stain and culture. ICU-bound patients require additional diagnostic testing, including Legionella and pneumococcus urinary antigen tests and multiplex PCR testing, if available. If the etiologic agent remains elusive or the patient's condition deteriorates, individuals with severe pneumonia may undergo bronchoalveolar lavage, which can be sent for bacterial, fungal, mycobacterial, and viral testing.
Several risk-stratification methods have been developed and validated to pinpoint patients with low mortality risk, making home therapy a cost-effective option compared to inpatient stays. The CURB65 risk score is a user-friendly tool based on five simple criteria, including confusion, elevated blood urea nitrogen, rapid respiratory rate, low blood pressure, and age over 65. The higher the CURB65 score, the greater the risk of death or ICU admission.
Another risk assessment method, the pneumonia severity index, takes into account demographic factors (with age playing the biggest role) and key physical and laboratory findings. Notably, aside from arterial oxygenation measurement, all lab tests are at the discretion of the healthcare provider. Patients in risk class I or II can typically receive home care safely, while risk class III patients may still be candidates for home care but warrant close observation. Risk classes IV and V usually require hospital admission. CAP patients with unexplained or severe hypoxemia should be hospitalized, with clinical judgment ultimately outweighing clinical prediction rules.
When it comes to pharmacotherapy principles for CAP, there are a few crucial points to remember: First, once the diagnosis is confirmed, delaying antibiotic administration is associated with higher mortality rates. Second, all CAP patients should receive coverage for "atypical" pathogens. And third, prior antibiotic exposure should influence empirical antibiotic selection. Clinicians should also be on the lookout for specific environmental exposures that might suggest an uncommon pathogen.
A snapshot of the Infectious Diseases Society of America (IDSA) and American Thoracic Society combined recommendations is provided for easy reference. Once the responsible organism is identified, antibiotics should be adjusted to target that specific pathogen with minimal spectrum overlap and cost. Treatment typically lasts 5 to 7 days, though some pathogens like Staphylococcus aureus, Legionella species, and Pseudomonas aeruginosa may require a longer duration. The IDSA guidelines advocate transitioning patients from intravenous to oral therapy when they're clinically improving, hemodynamically stable, and able to take oral medications. Antibiotics can be discontinued once patients have maintained clinical stability for 48 hours, defined by normal body temperature, heart rate, respiratory rate, blood pressure, and oxygen saturation on room air. Unlike clinical improvement, chest radiography doesn't dictate treatment duration as pneumonia resolution often lags behind clinical recovery.
For most patients, pneumonia symptoms start improving within 3 to 5 days of initiating treatment. When pneumonia doesn't resolve, it could be due to factors like an atypical pathogen not covered by standard therapy (e.g., Mycobacterium tuberculosis, Coccidioidomycosis), antibiotic-resistant organisms, loculated infections like empyema, underlying malignancies, or noninfect