what is community acquired pneumonia(CAP),what is the prevalence of (CAP) ,what are the risk factors and what are the causative agents ,what are the clinical presentations ,how to diagnose it,what are the needed investigations ,what is the management ,what are the procedures to decrease the incidence,
Pneumonia is an infection of the lungs. The air sacs in the lungs (called alveoli) fill up with pus and other fluid, which makes it hard for oxygen to reach the bloodstream.
Someone with pneumonia may have a fever, cough, or trouble breathing.
what is community acquired pneumonia(CAP),what is the prevalence of (CAP) ,what are the risk factors and what are the causative agents ,what are the clinical presentations ,how to diagnose it,what are the needed investigations ,what is the management ,what are the procedures to decrease the incidence,
Pneumonia is an infection of the lungs. The air sacs in the lungs (called alveoli) fill up with pus and other fluid, which makes it hard for oxygen to reach the bloodstream.
Someone with pneumonia may have a fever, cough, or trouble breathing.
Clinical presentation of active TB
Differential diagnosis of TB
Etiology
Transmission
Factors influencing transmission
Pathogenesis of Latent
TB Disease
Co-pathogenesis
Legionellosis is a respiratory disease caused by Legionella bacteria.
The term“legionellosis” may be used to refer to either Legionnaires’ disease or Pontiac fever.
https://www.cdc.gov/legionella/index.html
Clinical presentation of active TB
Differential diagnosis of TB
Etiology
Transmission
Factors influencing transmission
Pathogenesis of Latent
TB Disease
Co-pathogenesis
Legionellosis is a respiratory disease caused by Legionella bacteria.
The term“legionellosis” may be used to refer to either Legionnaires’ disease or Pontiac fever.
https://www.cdc.gov/legionella/index.html
Pneumonia is a leading cause of illness and death in Nepal, particularly among young children and the elderly. This PowerPoint presentation provides a comprehensive overview of pneumonia in Nepal, including the causes, symptoms, risk factors, and treatment options.
Through powerful images and personal stories, we showcase the impact of pneumonia on individuals, families, and communities in Nepal. We highlight the challenges of accessing healthcare in remote and impoverished areas, the lack of awareness and education about the disease, and the importance of early diagnosis and treatment.
The presentation provides detailed information about the various types of pneumonia and the risk factors associated with each. We also discuss the diagnostic procedures, including chest x-rays and blood tests, and the treatment options, such as antibiotics and oxygen therapy.
In addition, we explore the efforts being made to prevent and control pneumonia in Nepal. We highlight the importance of vaccination, particularly among children and high-risk groups, and the role of community-based interventions in improving access to healthcare and promoting healthy behaviors.
Through this PowerPoint presentation, we aim to raise awareness about pneumonia in Nepal and the importance of early diagnosis and treatment. We showcase the latest research and innovations in pneumonia prevention and treatment, and the importance of collaboration and partnership to address the disease.
We urge the audience to take action in the fight against pneumonia, whether it be through spreading awareness, supporting organizations working on the ground, or advocating for policy change. Let us come together to create a world where no one has to suffer from the devastating effects of pneumonia.
PNEUMONIA,
DEFINITION
Pneumonia is an infection of the pulmonary parenchyma.
To the pathologist, pneumonia is an infection of the alveoli ,distal airways, and interstitium of the lung that is manifested by increased weight of the lungs, replacement of normal lung’s sponginess by consolidation ,and alveoli filled with white blood cells ,red blood cells and fibrin .To the clinician, pneumonia is a constellation of symptoms and signs in combination with at least one opacity on CXR.
Epidemiology
Between 5 and 10 million cases of infectious pneumonia occur annually in the United States and result in more than 1 million hospitalizations.
Pneumonia is a leading cause of death worldwide, the sixth leading cause of death in the United States, and the most common lethal infectious disease.
Pneumonia is an inflammatory condition of the lung affecting primarily the small air sacs known as alveoli. Typically symptoms include some combination of productive or dry cough, chest pain, fever, and trouble breathing. Severity is variable.
Pneumonia is usually caused by infection with viruses or bacteria and less commonly by other microorganisms, certain medications and conditions such as autoimmune diseases. Risk factors include cystic fibrosis, chronic obstructive pulmonary disease (COPD), asthma, diabetes, heart failure, a history of smoking, a poor ability to cough such as following a stroke, and a weak immune system. Diagnosis is often based on the symptoms and physical examination. Chest X-ray, blood tests, and culture of the sputum may help confirm the diagnosis. The disease may be classified by where it was acquired with community, hospital, or health care associated pneumonia.
Vaccines to prevent certain types of pneumonia are available. Other methods of prevention include handwashing and not smoking. Treatment depends on the underlying cause. Pneumonia believed to be due to bacteria is treated with antibiotics. If the pneumonia is severe, the affected person is generally hospitalized. Oxygen therapy may be used if oxygen levels are low.
Pneumonia affects approximately 450 million people globally (7% of the population) and results in about four million deaths per year. Pneumonia was regarded by William Osler in the 19th century as "the captain of the men of death". With the introduction of antibiotics and vaccines in the 20th century, survival improved. Nevertheless, in developing countries, and among the very old, the very young, and the chronically ill, pneumonia remains a leading cause of death. Pneumonia often shortens suffering among those already close to death and has thus been called "the old man's friend"
This slide presents some Gynecologic diseases and disorders in females and their proper management. It is a third-year course for those wishing to major PA or Nursing.
This PowerPoint presentation was compiled and prepared by Platon S. Plakar, Jr a student majoring in Physician Assistant at Cuttington University. This presentation provides a brief understanding of Syphilis, an infectious disease condition that affects people exposed to sexual contact.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
3. INTRODUCTION
• Pneumonia is an infection of the pulmonary parenchyma.
• It is frequently categorized based on the site of acquisition.
• Community-acquired Pneumonia (CAP) refers to an acute infection of the
pulmonary parenchyma acquired outside of the hospital.
• Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma
acquired in hospital settings and encompasses both hospital-acquired
pneumonia (HAP) and ventilator-associated pneumonia (VAP).
– HAP refers to pneumonia acquired ≥48 hours after hospital admission.
– VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.
4. EPIDEMIOLOGY
• CAP is one of the most common and morbid conditions encountered in clinical
practice
• CAP results in more than 1.2 million hospitalizations and more than 55,000 deaths
annually.
• CAP is the second most common cause of hospitalization and the most common
infectious cause of death
• Usually, 80% of the affected patients are treated as outpatients and 20% as
inpatients.
• The mortality rate among outpatients is usu- ally <5%, whereas among hospitalized
patients the rate can range from ~12% to 40%
• 18% of hospitalized CAP patients are readmitted within 1 month of discharge.
5. RISK FACTORS
• Combination of risk factors below are additive in terms of risk.
• Older age: risk of CAP increases with age.
• Chronic comorbidities: The comorbidity that places patients at highest risk for
CAP hospitalization is chronic obstructive pulmonary disease (COPD).
• Impaired airway protection – Conditions that increase risk of macroaspiration of
stomach contents and/or microaspiration of upper airway secretions predispose
to CAP, such as alteration in consciousness (eg, due to stroke, seizure,
anesthesia, drug or alcohol use) or dysphagia due to esophageal lesions or
dysmotility.
6. RISK FACTORS
• Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and
opioid use are key modifiable behavioral risk factors for CAP
• Other lifestyle factors – Other factors that have been associated with an
increased risk of CAP include crowded living conditions (eg, prisons, homeless
shelters), residence in low-income settings, and exposure to environmental
toxins (eg, solvents, paints, or gasoline)
• Viral respiratory tract infection – Viral respiratory tract infections can lead to
primary viral pneumonias and also predispose to secondary bacterial pneumonia.
This is most pronounced for influenza virus infection
7. ETIOLOGY
• Typical bacteria:
–S. pneumoniae (most common bacterial cause),
–Haemophilus influenzae,
–Moraxella catarrhalis,
–Staphylococcus aureus,
–Group A streptococci,
–Aerobic gram-negative bacteria (eg, Enterobacteriaceae such
as Klebsiella spp or Escherichia coli),
–Microaerophilic bacteria and anaerobes (associated with aspiration)
8. ETIOLOGY
• Atypical bacteria: ("atypical" refers to the intrinsic resistance
of these organisms to beta-lactams and their inability to be
visualized on Gram stain or cultured using traditional
techniques)
–Legionella spp
–Mycoplasma pneumoniae
–Chlamydia pneumonia
–Chlamydia psittaci
–Coxiella burnetii
9. ETIOLOGY
• Respiratory viruses:
– Influenza A and B viruses
– Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
– Other coronaviruses
– Rhinoviruses
– Parainfluenza viruses
– Adenoviruses
– Respiratory syncytial virus
– Human metapneumovirus
– Human bocaviruses
10. ETIOLOGY
• Certain epidemiologic exposures also raise the likelihood of infection with a
particular pathogen
• Alcohol use disorder: Streptococcus pneumoniae, oral anaerobes, Klebsiella
pneumoniae, Acinetobacter species, Mycobacterium tuberculosis
• Aspiration: Gram-negative enteric pathogens, oral anaerobes
• COPD and/or smoking: Haemophilus influenzae, Pseudomonas
aeruginosa, Legionellaspecies, S. pneumoniae, Moraxella catarrhalis, Chlamydia
pneumoniae
11. ETIOLOGY
• Lung abscess: CA-MRSA, oral anaerobes, endemic fungal pneumonia, M. tuberculosis,
atypical mycobacteria
• Exposure to bat or bird droppings: Histoplasma capsulatum
• Exposure to birds: Chlamydia psittaci (if poultry: avian influenza)
• Exposure to rabbits: francisella tularensis
• Exposure to farm animals or parturient cats: Coxiella burnetti (Q fever)
• HIV infection: Pneumocystis jirovecii,
• Hotel or cruise ship: Legionella species
• Structural lung disease: P. aeruginosa, Burkholderia cepacia, S. aureus
• Bioterrorism: Bacillus anthracis (anthrax), Yersinia pestis(plague), Francisella tularensis
(tularemia)
• Injection drug use: S. aureus, anaerobes
12. PATHOPHYSIOLOGY
• Pneumonia results from the proliferation of microbial pathogens at the alveolar level
and the host’s response to those pathogens.
• Respiratory pathogens are transmitted from person to person via droplets or less
commonly via aerosol inhalation
• Microorganisms needs to colonize the oropharynx and then gain entry to the lower
respiratory tract.
• Microorganisms gain access to the lower respiratory tract in several ways.
– The most common is by aspiration from the oropharynx.
• Small-volume aspiration occurs frequently during sleep (especially in the elderly) and in
patients with decreased levels of consciousness(stroke, alcoholics).
– Rarely, access to the lower respiratory tract occurs via hematogenous spread
– or by contiguous extension from an infected pleural or mediastinal space.
13. PATHOPHYSIOLOGY
• To gain access to the lower respiratory tract, it must overcome the body
mechanical factors.
• These mechanics factors are a part of our body’s respiratory defense mechanism
– The hairs and turbinates of the nares capture larger inhaled particles before they reach the
lower respiratory tract.
– The branching architecture of the tracheobronchial tree traps microbes on the airway
lining, where mucociliary clearance and local antibacterial factors either clear or kill
the potential pathogen.
– The gag and cough reflexes offer critical protection from aspiration.
– the normal flora adhering to mucosal cells of the oropharynx, prevents pathogenic
bacteria from binding and thereby decreases the risk of pneumonia
14. PATHOPHYSIOLOGY
• When these barriers are overcome or when microorganisms are small enough,
they’ll then be inhaled to the alveolar level.
– resident alveolar macrophages are extremely efficient at clearing and killing
pathogens
– Alveolar macrophages are assisted by proteins that are produced by the alveolar
epithelial cells (e.g., surfactant proteins A and D)
• These proteins have intrinsic opsonizing properties or antibacterial or antiviral activity.
– Once engulfed by the macrophage, the pathogens—even if they are not killed—are
eliminated via either the mucociliary elevator or the lymphatics and no longer
represent an infectious challenge.
• Only when the capacity of the alveolar macrophages to ingest or kill the
microorganisms is exceeded does clinical pneumonia become manifest
15. PATHOPHYSIOLOGY
• In that situation, the alveolar macrophages initiate the inflammatory response to
bolster lower respiratory tract defenses.
• The host inflammatory response, rather than proliferation of microorganisms,
triggers the clinical syndrome of pneumonia.
• The release of inflammatory mediators, such as interleukin 1 and tumor necrosis
factor, results in fever.
• Chemokines, such as interleukin 8 and granulocyte colony-stimulating factor,
stimulate the release of neutrophils and their attraction to the lung, producing both
peripheral leukocytosis and increased purulent secretions.
•
16. PATHOPHYSIOLOGY
• Inflammatory mediators released by macrophages and newly recruited
neutrophils create an alveolar capillary leak.
• The leak causes the alveolar to fill with fluid and patient becomes hypoxemic
because gas exchanged is impaired.
• Erythrocytes can cross the alveolar capillary leak
• Decreased compliance due to capillary leak, hypoxemia, increased respiratory
drive, increased secretions, and occasionally infection-related bronchospasm all
lead to dyspnea.
17. PATHOLOGY
• Pneumonia evolves through a series of pathologic changes.
• Edema phase-with the presence of a proteinaceous exudate—and often of
bacteria—in the alveoli.
• Red hepatization phase: presence of erythrocytes in the cellular intra-alveolar
exudate
• Gray hepatization phase: no new erythrocytes are extravasating, and those
already present have been lysed and degraded. The neutrophil is the
predominant cell, fibrin deposition is abundant, and bacteria have disappeared.
This phase corresponds with successful containment of the infection and
improvement in gas exchange.
• Resolution phase: the macrophage reappears as the dominant cell type in the
alveolar space, and the debris of neutrophils, bacteria, and fibrin has been
cleared, as has the inflammatory response.
18. CLINICAL MANIFESTATIONS: SYMPTOMS
• The patient is frequently febrile with tachycardia or may have a
diagnosis.
• Identification of an unexpected pathogen allows narrowing history of chills and/or
sweats.
• Cough may be either nonproductive or productive of mucoid, purulent, or blood-
tinged sputum.
• Depending on the severity, the patient may be able to speak in full sentences or
may be very short of breath.
• If the pleura is involved, the patient may experience chest pain.
• Up to 20% of patients may have GI symptoms such as nausea, vomiting, and/or
diarrhea.
• Elderly may present with only confusion.
19. CLINICAL MANIFESTATIONS: SIGNS
• An increased respiratory rate (tachypnea) and use of accessory muscles of
respiration are common.
• Palpation may reveal increased or decreased tactile fremitus, and the
percussion note can vary from dull to flat, reflecting underlying
consolidated lung and pleural fluid, respectively.
• Crackles, bronchial breath sounds, and a possible pleural friction rub may
be heard on auscultation.
• Severely ill patients may have septic shock and evidence of organ failure.
20. DIAGNOSIS
• When confronted with possible CAP, the physician must ask two questions:
– Is this Pneumonia? And if so, what is the likely etiology?
– The first can be answered by clinical and radiographic methods
– The last required the aid of laboratory techniques
• The diagnosis of CAP generally requires the demonstration of an infiltrate on
chest imaging in a patient with a clinically compatible syndrome (eg, fever,
dyspnea, cough, and sputum production)
• However, this combination of findings is nonspecific and is shared among many
cardiopulmonary disorders. Thus, remaining attentive to the possibility of an
alternate diagnosis as a patient's course evolves is important to care.
21. DIAGNOSIS
• Clinical Diagnosis:
– A careful history is needed to differentiate blw Pneumonia and other differentials.
– The findings on physical examination are less than ideal therefore chest radiography is often
needed
• Etiologic Diagnosis:
– Cannot solely be determined on the basis of clinical presentation.
– Except for CAP patients admitted to the ICU, no data exist to show that treatment directed at a
specific pathogen is superior to empirical therapy.
– The benefit of establishing a microbial etiologic diagnosis can be questioned in the light of the
cost of diagnostic testing.
– However a number of reasons can be advanced for attempting an etiologic diagnosis
• Identification of an unexpected pathogen
• Pathogens associated with Public safety implications: M. tuberculosis, Influenza virus
• Follow trends of resistance accurately to guide empiric therapeutic regimens
22. DIAGNOSIS: TEST
• Gram stain and culture of sputum: main purpose of gram stain is to
ensure the sputum is suitable for culture.
• Gram stain may also identify certain pathogens by their characteristic
appearance.
• Many patients may not be able to produce an expectorated sputum
sample.
• Dehydration may cause inability to produce sputum.
• Others may have started antibiotics that can interfere with culture
results.
• Other stains and cultures may be used for specific organism
23. DIAGNOSIS: TEST
• Chest radiography: obtain CXR in all patients with suspected CAP to
evaluate for an infiltrate and to help exclude conditions that may mimic
CAP.
• Patients who present very early with CAP may have negative findings on
chest radiography.
– In these patients, repeat chest radiography within 24 hours may be
beneficial.
• Obtain a posteroanterior and lateral chest radiographs.
• Radiographic appearance alone cannot reliably differentiate among
etiologies.
• Radiographic findings consistent with the diagnosis of CAP include lobar
consolidations, interstitial infiltrates, and/or cavitations.
25. DIAGNOSIS: TEST
• Blood cultures: The yield from blood cultures, even when
samples are collected before antibiotic therapy, is
disappointingly low.
• Only 5-14%, of cultures of blood from patients hospitalized
with CAP are positive, and most frequently isolated pathogen
is S. Pneumoniae.
• Because of low yield, blood cultures are no longer considered
de rigueur for all hospitalized CAP patients
26. DIAGNOSIS
• Urinary antigen test: Two commercially available tests detect
pneumococcal and Legionella antigen in urine.
• Both tests can detect antigen even after the initiation of
appropriate antibiotic therapy.
• Polymerase chain reaction: PCR which amplify a microorganism’s
DNA or RNA are available for a number of pathogens.
• PCR of nasopharyngeal swabs, have become the standard for
diagnosis of respiratory viral infection.
• It is not cost effective
27. DIAGNOSIS: TESTS
• Biomarkers: A few substances can serve as markers of severe
inflammation.
• The two most commonly in use are C-reactive protein (CRP) and pro-
calcitonin (PCT).
• Levels of these acute-phase reactants increase in the presence of an
inflammatory response, particularly to bacterial pathogens.
• CRP may be of use in the identification of worsening disease or
treatment failure.
• PCT may play a role in distinguishing bacterial from viral infection,
determining the need for antibacterial therapy, or deciding when to
discontinue treatment.
28. MANAGEMENT
• For patients with a working diagnosis of CAP, the next steps
in management are
–defining the severity of illness and
–determining the most appropriate site of care (ICU, Inpatient,
Outpatient).
• To accomplish this, we use severity scores.
• The most used severity scores the are the Pneumonia Severity
Index (PSI) and CURB-65.
29. MANGEMENT: PSI SCORING
• To determine the PSI, points are given for 20 variables, including
age, coexisting illness, and abnormal physical and laboratory
findings.
• Based on the resulting score, patients are assigned to one of five
classes with the following mortality rates:
– class 1: 0.1% mortality
– class 2: 0.6% mortality
– class 3: 2.8% mortality
– class 4: 8.2% mortality
– class 5: 29.2%. mortality
– Determination of the PSI is often impractical in a busy emergency-
department setting because of the number of variables.
30. MANGEMENT: CURB-65
• The CURB-65 criteria include five variables:
• Confusion: (C);
• Urea: >7 mmol/L (U);
• Respiratory rate: ≥30/min (R);
• Blood pressure: systolic ≤90 mmHg or diastolic ≤60 mmHg (B);
• Age ≥65 years.
–If the patient gets a single variable, it accounts for 1 point.
–The total score is thus 5 points meaning the patient has all 5 criteria.
31. MANGEMENT: CURB-65
• Patients with a score of 0, can be treated outside the hospital
(Outpatient).
• With a score of 1 or 2, the patient should be hospitalized on the
ward or ER(Inpatient) but does not need ICU admission.
–Unless the score is entirely or in part attributable to an age of ≥65
years, in such cases, hospitalization may not be necessary.
• Among patients with scores of ≥3, these patients require
hospitalization specifically ICU admission.
–mortality rates are 22%.
32. TREATMENT
• Initial antibiotic treatment:
– Since the etiology of CAP is rarely known at the outset of treatment, initial
therapy is usually empirical, designed to cover the most likely pathogens
• In all cases, empiric antibiotic treatment should be initiated as expeditiously
as possible.
• Empiric therapy coverage includes both typical and atypical organisms.
• Once the etiologic agent(s) and their susceptibilities are known after culture,
therapy may be altered to target the specific pathogen(s).
• a 5-day course is sufficient for otherwise uncomplicated CAP.
• A longer course may be required for patients with bacteremia, metastatic
infection, or infection with a virulent pathogen such as P. aeruginosa or CA-
MRSA.
33. EMPIRICAL ANTIBIOTIC TREATMENT
• Outpatients (CURB score of 0):
• 1. previously healthy and has not taken antibiotics in the past three months:
– Macrolide (clarithromycin 500mg PO bid) or Azithromycin 500mg po once,
then 250mg qd) or
– Doxycycline 100mg po bid
• 2. Comorbidities or antibiotics in past 3 months: select an alternative from a
different class
– A respiratory fluoroquinolone [moxifloxacin (400 mg PO qd), gemifloxacin
(320 mg PO qd), levofloxacin (750 mg PO qd)] or
– A β-lactam [preferred: high-dose amoxicillin (1 g tid) or amoxicillin/
clavulanate (2 g bid); alternatives: ceftriaxone (1–2 g IV qd), cefpodoxime (200
mg PO bid), or cefuroxime (500 mg PO bid)] plus a macrolide
34. EMPIRICAL ANTIBIOTIC TREATMENT
• Inpatients (Non-ICU) CURB score: 1 or 2:
–A respiratory fluoroquinolone [e.g., moxifloxacin (400 mg PO or IV
qd) or levofloxacin (750 mg PO or IV qd)]
–A β-lactam [e.g., ceftriaxone (1–2 g IV qd), ampicillin (1–2 g IV
q4–6h), cefotaxime (1–2 g IV q8h), ertapenem (1 g IV qd)] plus a
macrolide
[e.g., oral clarithromycin or azithromycin or IV azithromycin (1 g
once, then 500 mg qd)]
35. EMPIRICAL ANTIBIOTIC TREATMENT
• Inpatients (ICU) CURB score ≥3 :
–A β-lactam [e.g., ceftriaxone (2 g IV qd), ampicillin-
sulbactam (2 g IV q8h), or cefotaxime (1–2 g IV q8h)] plus
either azithromycin or a respiratory fluoroquinolone
36. MANAGEMENT: ADJUNCTIVE THERAPY
•In addition to appropriate antimicrobial therapy,
certain adjunctive measures should be used.
–Adequate hydration
–oxygen therapy for hypoxemia
–vasopressors, and
–assisted ventilation when necessary are critical to
successful treatment.
37. MANAGEMENT: FAILURE TO IMPROVE
• Patients slow to respond to therapy should be reevaluated (careful
reassessment and laboratory studies/procedures) at about day three (3)
(sooner if their condition is worsening rather than simply not improving),
and several possible scenarios should be considered.
• Scenario I:
– The patient may have a non-infectious condition that is mimicking pneumonia.
– These conditions include pulmonary edema, pulmonary embolism, lung
carcinoma, radiation pneumonitis, hypersensitivity pneumonitis, and connective
tissue disease involving the lungs.
38. MANAGEMENT: FAILURE TO IMPROVE
• Scenario II: If the patient truly has CAP and empirical treatment is aimed at
the correct pathogen, lack of response may be explained in a number of
ways.
– The pathogen may be resistant to the drug selected,
– or a sequestered focus (e.g., lung abscess or empyema) may be blocking access
of the antibiotic(s) to the pathogen.
– The patient may be getting either the wrong drug or
– The patient may be getting the correct drug at the wrong dose or frequency of
administration.
– Another possibility is that CAP is the correct diagnosis but an unsuspected
pathogen (e.g., CA-MRSA, M. tuberculosis, or a fungus) is the cause
39. COMPLICATIONS
• Complications of severe CAP include
– respiratory failure,
– shock and
– multiorgan failure,
– coagulopathy, and
– exacerbation of comorbid illnesses.
40. FOLLOW-UP
• Fever and leukocytosis usually resolve within 2–4 days in otherwise healthy
patients with CAP, but physical findings may persist longer.
• Chest radiographic abnormalities are slowest to resolve (4–12 weeks), with
the speed of clearance depending on the patient’s age and underlying lung
disease.
• Patients may be discharged from the hospital once their clinical conditions,
including comorbidities, are stable.
• For a hospitalized patient, a follow-up chest radiograph ~4–6 weeks later is
recommended.
•
41. PROGNOSIS
• The prognosis of CAP depends on the patient’s age, comorbidities, and site
of treatment (inpatient or outpatient).
• Young patients without comorbidity do well and usually recover fully after
~2 weeks.
• Older patients and those with comorbid conditions can take several weeks
longer to recover fully.
• The overall mortality rate for the outpatient group is <5%.
• For patients requiring hospitalization, the overall mortality rate ranges from
2 to 40%, depending on the category of patient and the processes of care,
particularly the administration of appropriate antibiotics as soon as possible.
42. PREVENTION
• Vaccination is the main preventive method.
• A pneumococcal polysaccharide vaccine (PPSV23) and a protein conjugate
pneumococcal vaccine (PCV13) are available in the United States.
• The influenza vaccine is available in an inactivated or recombinant form.
Editor's Notes
Microaerophile: requires environment containing very little free oxygen.
The frequency and importance of atypical pathogens have significant implications for therapy. They are intrinsically resistant to all β-lactam agents and must be treated with a macrolide, a fluoroquinolone, or a tetracycline. In the ~10–15% of CAP cases that are polymicrobial, the etiology usually includes a combina- tion of typical and atypical pathogens.
So if your preload is high and your afterload is low, your heart will have an easier time pumping blood throughout your body and keeping up with demand.
Anaerobes play a significant role only when an episode of aspiration has occurred days to weeks before presentation for pneumonia. The com- bination of an unprotected airway (e.g., in patients with alcohol or drug overdose or a seizure disorder) and significant gingivitis constitutes the major risk factor. Anaerobic pneumonias are often complicated by abscess formation and by significant empyemas or parapneumonic effusions.
So if your preload is high and your afterload is low, your heart will have an easier time pumping blood throughout your body and keeping up with demand.
code for a protein aggregate that is essential for breaking down the bacterial signaling molecules that dampen the macrophage response.
Fluoroquinolones are active against a wide range of aerobic gram-positive and gram-negative organisms. The fluoroquinolones are believed to act by inhibition of type II DNA topoisomerases (gyrases) that are required for synthesis of bacterial mRNAs (transcription) and DNA replication. The common side effects of the fluoroquinolones are gastrointestinal disturbances, headaches, skin rash and allergic reactions. Less common but more severe side effects include QT prolongation, seizures, hallucinations, tendon rupture, angioedema and photosensitivity.
Nalidaxic acid
Cipro
Gemi- moxi-