Bacterial Diseases

Chapter 21 Bacterial Diseases



Thomas A. Brown, MD, Sonali J. Shah




Insider’s Guide to Bacterial Diseases for the USMLE Step 1


There is no better way to say it: the USMLE loves bacterial diseases! This is one of the highest-yield subjects on the examination, so you must know it well! Our book has divided microbiology into two chapters, but you should note that the breakdown of the examination is not likely to be evenly distributed among bacteria, viruses, fungi, and parasites. Bacterial diseases are tested far more commonly than the other three types, but recently, fungal diseases have been heavily represented on many students’ forms. Fungal diseases are discussed more in Chapter 22.


As you may know, microbiology is not inherently difficult, but it does take time to learn. The most effective way to study for microbiology on the USMLE is to introduce yourself to this material early on, preferably during your microbiology class in medical school. This is one subject for which multiple resources may be quite helpful to you. For those of you seeking to combine your medical school education with boards studying, we recommend using Clinical Microbiology Made Ridiculously Simple and Microcards when you first begin learning the material. Pull the highest-yield facts from these already high-yield materials and write them into First Aid. You can then study from your annotated copy of First Aid and the cases in this book once your focus shifts entirely to boards.


How should you be expected to know which facts are the most important to learn for boards? That is why you purchased this book! As always, we will be pointing this information out along the way. However, you should keep in mind that the USMLE will expect you to know the major diseases and toxins associated with each and every medically important bacterial species. The Step 1 places heavy emphasis on the mechanisms of various bacterial toxins as well as the associated characteristics of individual bacterial species that can be helpful in identifying and differentiating among them in the laboratory.



Basic Concepts



1 What makes an organism gram-positive or gram-negative?


Both gram-positive and gram-negative organisms have an internal cell membrane and cell walls made of peptidoglycan. However, gram-negative bacteria have much thinner cell walls and, in addition, have an outer membrane outside the cell wall. Gram-positive organisms have techoic acid in their cell walls, and gram-negative organisms have lipopolysaccharide (endotoxin) (Fig. 21-1).


image

Figure 21-1 Structure of the cell wall in gram-positive and gram-negative bacteria. A, Gram-positive bacteria have a thick peptidoglycan layer that contains teichoic and lipoteichoic acids. B, Gram-negative bacteria have a thin peptidoglycan layer that is connected by lipoproteins to an outer membrane. LPS, lipopolysaccharide.


(From Rosenthal K, Tan J: Rapid Review Microbiology and Immunology, 2nd ed. Philadelphia, Mosby, 2007.)



2 Why are gram-negative infections more likely to produce bacterial sepsis?


The outer membrane of gram-negative organisms (see previous question) contains lipid A, an endotoxin that is part of the lipopolysaccharide in the cell wall of gram-negative bacteria. Lipid A gets released upon bacterial death and has potent proinflammatory effects.



3 Describe the mechanism by which lipid A causes toxicity?


Lipid A activates macrophages to secrete interleukin 1 (IL-1) and tumor necrosis factor (TNF), both of which are referred to as acute-phase cytokines. Lipid A also stimulates the release of nitric oxide (NO) from endothelial cells. Large amounts of lipid A may lead to shock and intravascular coagulation via this stimulatory effect (Fig. 21-2).


image

Figure 21-2 Mechanism by which lipid A causes toxicity.


(From Brown TA, Brown D: USMLE Step 1 Secrets. Philadelphia, Hanley & Belfus, 2004.)



4 What are exotoxins?


Exotoxins are proteins released by both gram-positive and gram-negative bacteria during their normal life cycle. Exotoxins released into food can cause poisoning, as in Bacillus cereus and Staphylococcus aureus food poisoning. Pyrogenic exotoxins released by S. aureus and Streptococcus pyogenes can cause rash, fever, and toxic shock syndrome. Enterotoxins act on the gastrointestinal system, whereas neurotoxins act on nerves or motor end plates. For example, infectious diarrhea is caused by enterotoxins released by Vibrio cholerae, Escherichia coli, Campylobacter jejuni, and Shigella dysenteriae.



5 What is a capsule and what purpose does it serve?


Certain species of bacteria produce a slippery outermost covering called a capsule. This covering consists of high-molecular-weight polysaccharides, which help the bacteria to evade phagocytosis by neutrophils and macrophages. Note that Bacillus anthracis has a proteinaceous capsule which consists of D-glutamic acid. The capsule is not essential for growth and serves only in a protective capacity. The most common medically relevant encapsulated organisms are Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae type b, Pseudomonas aeruginosa, Neisseria meningitidis, and Cryptococcus neoformans (a fungus).


Remember that Some Killers Have Perfectly Nasty Capsules. This mnemonic will help you recall the encapsulated organisms that are important to know for boards.


Note: In the Quellung reaction, which tests for the presence of encapsulated bacteria, encapsulated bacteria will swell when exposed to specific antibodies. The latex agglutination assay and India ink stain are two other methods for detecting capsular presence.




Step 1 Secret


Although the Quellung reaction and several other techniques in this book may be clinically outdated, you should remember that many of the physicians who author boards questions will have relied upon this technology during the course of their careers and will thus expect you to know the names and basic principles behind these tests. As a general rule, you should focus on learning the techniques listed in this book and in First Aid. You are not expected to know complex or cutting-edge technologies that are not mentioned in your USMLE study resources.



6 What sort of individuals are susceptible to infection by encapsulated bacteria?


Because the spleen normally sequesters encapsulated bacteria, patients who have undergone splenectomy are at a greater risk for incurring infection by encapsulated bacteria.



7 Identify the Gram stain and the morphology of the organisms in Table 21-1



Table 21-1 Bacterial Images


















Image Gram Stain and Morphology
imageGram stain of a sputum sample infected with Streptococcus pneumoniae. Gram-positive cocci in pairs: S. pneumoniae
imageExpectorated sputum with gram-negative rods in a patient with Klebsiella pneumoniae pneumonia. Gram-positive cocci (staining purple in a color image) in chains: Staphylococcus aureus
imageSputum smear, stained with Gram stain, shows many neutrophils and intracellular gram-negative diplococci, suggestive of Neisseria meningitidis infection (oil immersion).
 Gram-negative cocci (staining pink in a color image) in pairs: Neisseria spp.
image Gram-negative rods: many possibilities

Klebsiella pneumoniae image from Mandell GL, Bennett JE, Dolin R: Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th ed. Philadelphia, Churchill Livingstone, 2009. Images of Streptococcus pneumoniae, Neisseria meningitidis, and gram-negative rods from McPherson RA, Pincus MR: Henry’s Clinical Diagnosis and Management by Laboratory Methods, 22nd ed. Philadelphia, WB Saunders, 2011.



8 Cover the two columns on the right in Tables 21-2 through 21-9 to test your knowledge of the properties of the clinically relevant bacteria listed in the left column



Table 21-2 Gram-Positive Cocci







































Organism Associated Disease(s) Pearls to Remember
Staphylococcus aureus Cellulitis
Acute endocarditis (in previously normal valve)
Osteomyelitis
Pneumonia
Carbuncles/furuncles
Stye (hordeolum)		 Toxin-mediated diseases:
Staphylococcal toxic shock
Scalded skin syndrome
Staphylococcal gastroenteritis
Note: Like all staphylococcal species, S. aureus is catalase-positive—but it also is coagulase-positive.
Staphylococcus epidermidis Prosthetic valve endocarditis Normal skin flora
Novobiocin-sensitive
Staphylococcus saprophyticus Cystitis in young women
Second most common cause of UTI (behind E. coli)		 Novobiocin-resistant
Streptococcus agalactiae (group B streptococci) Neonatal pneumonia, meningitis, sepsis
Chorioamnionitis		 Normal vaginal flora
β-Hemolysis
Bacitracin-resistant
Streptococcus pneumoniae Pneumonia
Meningitis
Sinusitis
Otitis media		 Bile-soluble
Optochin-sensitive
α-Hemolysis
See Case 21-1 for more details
Streptococcus pyogenes (group A streptococci) Pharyngitis
Impetigo
Erysipelas
Cellulitis
Necrotizing fasciitis
Rheumatic fever
Poststreptococcal glomerulonephritis		 Remains largely sensitive to penicillin
β-Hemolysis
Bacitracin-sensitive
Enterococcus spp. UTI
Bacteremia/sepsis
Endocarditis
Abdominal abscess		 Part of normal bowel flora that causes disease when host is immunocompromised or gastrointestinal tract has been breached
α- or γ-Hemolysis
Viridans streptococci Dental caries (S. mutans)
Subacute bacterial endocarditis (S. sanguis)		 Normal oral flora
α-Hemolysis
Optochin-resistant

UTI, urinary tract infection.


Table 21-3 Gram-Positive Bacilli



















Organism Associated Disease(s) Pearls to Remember
Bacillus anthracis Cutaneous anthrax (most common form)
Pulmonary anthrax		 Painless black eschars with cutaneous anthrax
Wool-sorters at risk for pulmonary anthrax (“wool-sorter’s disease)
Spore-forming
Corynebacterium spp. Diphtheria
Granulomatous lymphadenitis
Pneumonitis
Pharyngitis
Skin infections
Endocarditis		 Normal skin flora
Pseudomembrane or esophageal web
Toxin causes disease and is encoded by β-prophage
Metachromatic granules
ADP ribosylation of EF-2
Listeria monocytogenes Listeriosis Perinatal/neonatal infections
Immunocompromised persons at risk
Raw milk and dairy products

ADP, adenosine diphosphate; EF-2, elongation factor.


Table 21-4 Gram-Negative Cocci















Organism Associated Disease(s) Pearls to Remember
Neisseria meningitidis (meningococcus) Meningitis
Septicemia
Waterhouse-Friderichsen syndrome		 Has a capsule
Purpuric nonblanching rash
Vaccine available
See Case 21-8
Neisseria gonorrhoeae
(gonococcus)		 Infects superficial mucosal surfaces lined with columnar epithelium:
Urethra: urethritis (gonorrhea)
Vagina: vulvovaginitis in young girls
Rectum: proctitis
Conjunctiva: ophthalmia neonatorum		 No vaccine
Main cause of infectious arthritis in sexually active persons
Prepubescent vaginal epithelium is columnar because not yet acted on by estrogen to become squamous

Table 21-5 Enteric Gram-Negative Rods



























Organism Associated Disease(s) Pearls to Remember
Campylobacter jejuni Enteritis Present in animal feces
Escherichia coli Enteritis
UTI
Meningitis
Peritonitis
Mastitis
Septicemia
Gram-negative pneumonia
HUS		 Normal gut flora
E. coli O157:H7—a particularly virulent pathologic strain associated with HUS
See Case 21-2
Salmonella spp. Food-borne illness
Typhoid fever (Salmonella typhi)		 Osteomyelitis in patients with sickle cell anemia
Shigella spp. Shigellosis (bacterial dysentery) Bloody diarrhea
Fecal oral route of transmission
Low inoculum required
Toxin-mediated
Helicobacter pylori Peptic ulcer disease
Gastritis
Duodenitis
Gastric cancer
Mucosa-associated lymphoid tissue (MALT) lymphoma		 Positive urea breath test due to presence of enzyme urease
Lives in stomach but common in duodenal ulcers
Triple treatment: amoxicillin, clarithromycin, and proton pump inhibitor

HUS, hemolytic uremic syndrome; UTI, urinary tract infection.


Table 21-6 Other Gram-Negative Rods







































Organism Associated Disease(s) Pearls to Remember
Bordetella pertussis Pertussis (whooping cough) Highly contagious; spread by coughing and nasal drops
Brucella spp. Brucellosis (also called “undulant fever”) Transmitted via contaminated or unpasteurized milk
Francisella tularensis Tularemia (“rabbit fever”) Reservoir in rabbits; transmitted by tick
Symptoms/signs similar to those of plague
Culture, drainage contraindicated owing to high virulence
Haemophilus influenzae Meningitis (type b)
Bacteremia
Cellulitis
Pneumonia
Sinusitis		 Type b encapsulated and more virulent
Vaccine available for type b strain
Pseudomonas aeruginosa Pneumonia in cardiac failure patients
External otitis
Osteomyeltis in diabetics
Endocarditis
UTI
Hot tub folliculitis		 Think Pseudomonas infection in burn patients and intravenous drug users
Can cause black skin lesions
Cultures make blue-green pigment
Has endotoxin A
Resistant to many antibiotics
Legionella pneumophila Legionnaire’s disease
Pontiac fever		 Legionnaire’s disease: acute pneumonia with multisystem involvement; from water source, so no person-to-person spread
Pontiac fever: similar to flu
Yersinia pestis Bubonic plague Transmitted by fleas from rodents to humans
Black buboes
Yersinia enterocolitica Enterocolitis Pseudoappendicitis
Seen in nursery schools

Table 21-7 Anaerobes























Organism Associated Disease(s) Pearls to Remember
Clostridium perfringens Anaerobic cellulitis
Gas gangrene (myonecrosis)
Food poisoning		 Crepitus is associated with gas gangrene
Alpha toxin (lecithinase)
Clostridium tetani Tetanus Exotoxin that causes spastic paralysis by blocking glycine release from Renshaw cells in spinal cord
Vaccine is available
Clostridium botulinum Botulinism Food poisoning that causes flaccid paralysis
Preformed toxin prevents release of ACh
Classic scenario from consumption of dented canned goods or honey
Clostridium difficile Pseudomembranous colitis Caused by antibiotic use, especially clindamycin or ampicillin
Treat with metronidazole or oral vancomycin

ACh, acetylcholine.


Table 21-8 Spirochetes























Organism Associated Disease(s) Pearls to Remember
Borrelia burgdorferi Lyme disease See Case 21-5
Borrelia recurrentis Relapsing fever Organism switches surface proteins to evade immune response, leading to intermittent fevers
Treponema pallidum Syphilis See Case 21-4
Leptospira interrogans Leptospirosis Transmitted by water that is contaminated by animal urine through cracks in the skin, eyes, or mucous membranes

Table 21-9 Intracellular Organisms



































Organism Associated Disease(s) Pearls to Remember
Mycoplasma pneumoniae Atypical (“walking”) pneumonia No cell wall
Treat with macrolides
Blood shows IgM “cold agglutinins”
Chest radiograph demonstrates diffuse interstitial infiltrates; radiographic changes often more extensive than expected from patient’s symptoms
Chlamydia trachomatis Urethritis
Pelvic inflammatory disease
Blindness
Lymphogranuloma venereum
Neonatal conjunctivitis		 See Case 21-7
Treat neonates with erythromycin eye drops for conjunctivitis
Chlamydia psittaci Psittacosis (flu-like syndrome) Transmitted from bird droppings via aerosol
Chlamydia pneumoniae Atypical pneumonia Transmitted via aerosols
Mycobacterium tuberculosis Tuberculosis See Case 21-6
Mycobacterium leprae Leprosy (Hansen’s disease) Tuberculoid form: milder with few organisms in lesions
Lepromatous form: severe with many organisms in lesions
Grows in cool temperatures, so affects distal sites
Treat with dapsone
Rickettsia rickettsii Rocky Mountain spotted fever Rash that starts on palms and soles and migrates centrally (centripetal migration)
Weil-Felix test results positive for rickettsial diseases


Basic concepts in antibacterial pharmacology



1 What are the β-lactam antibiotics and what is their mechanism of action?


The β-lactam antibiotics include the penicillins, cephalosporins, and carbapenems (imipenem, meropenem). By virtue of their β-lactam chemical moiety, they all inhibit bacterial cell wall synthesis. Resistance to these antibiotics is mediated by bacterially synthesized β-lactamase enzymes that destroy the β-lactam ring (Fig. 21-3).


image

Figure 21-3 General structure of penicillins and cephalosporins.


(From Rosenthal K, Tan J: Rapid Review Microbiology and Immunology, 2nd ed. Philadelphia, Mosby, 2007.)



2 Why are clavulanic acid and sulbactam added to some penicillins?


These agents inhibit β-lactamase, thereby reducing resistance of bacterial species to the penicillins.



3 What is the antibacterial spectrum of the various subclasses of penicillins and cephalosporins (Table 21-10)?


About 10% of people receiving penicillin will have a hypersensitivity reaction. Approximately 10% to 20% of people with a penicillin allergy will also have a hypersensitivity reaction to cephalosporins. There is no cross-reactivity between penicillins and aztreonam.


Table 21-10 β-Lactams











































Drug Class Examples Coverage
Natural penicillins Penicillin V (oral)
Penicillin G (intravenous)
Benzathine penicillin		 Mostly gram-positive
Extended-spectrum penicillins Ampicillin
Amoxicillin (oral)		 Gram-positive and increased gram-negative
Antistaphylococcal penicillins Dicloxacillin
Cloxacillin		 Staphylococcus aureus
Antipseudomonal penicillins Ticaracillin
Piperacillin		 Increasing gram-negative coverage, including Pseudomonas
Penicillin plus beta-lactamase inhibitor Ampicillin-sulbactam (Unasyn)
Amoxicillin–clavulanic acid (Augmentin)
Piperacillin-tazobactam (Zosyn)		 β-Lactam–resistant bacteria
First-generation cephalosporins Cephalexin
Cefotetan
Cefazolin		 Mostly gram-positive
Second-generation cephalosporins Cefuroxime
Cefaclor
Cefoxitin		 Mostly gram-positive
Third-generation cephalosporins Ceftazidime
Ceftriaxone		 Penetrates the blood-brain barrier
Ceftazidime covers Pseudomonas
Aztreonam Aztreonam Gram-negative rods

Notice that the first-generation cephalosporins are similar in spectrum to the natural penicillins, and that the third-generation cephalosporins are similar in spectrum to the extended-spectrum penicillins. Knowing this general pattern helps in understanding selection of antimicrobial therapy.



4 What is the antibacterial spectrum of the fluoroquinolones and what is their mechanism of action?


This class has a broad spectrum of activity, including both gram-positive and gram-negative organisms. They also cover Pseudomonas, making them fairly similar in spectrum to the antipseudomonal penicillins. These antibiotics work by inhibiting bacterial DNA synthesis by inhibiting the bacterial topoisomerase (DNA gyrase) protein.



5 What is the spectrum and mechanism of action of the macrolides?


These antibiotics have good gram-positive coverage, and several members of this class are effective against intracellular organisms. They work by inhibiting bacterial protein synthesis.



6 What is special about the tetracyclines?


These drugs are the most important agents for the treatment of intracellular organisms. They also work by inhibiting bacterial protein synthesis.



7 What are the mechanism of action and spectrum of the aminoglycosides?


These are irreversible inhibitors of protein synthesis that are generally only effective against gram-negative rods. However, they may be used in combination with penicillins for enterococcal endocarditis (a gram-positive organism).



8 How does chloramphenicol work and why is it not used more often?


This antibiotic also inhibits protein synthesis, but because of the risk of aplastic anemia it is not commonly used in industrialized nations.



9 Why is trimethoprim commonly given in combination with sulfamethoxazole, as TMP-SMX?


Because these agents inhibit folic acid synthesis at different steps, their combination is synergistic.



10 Cover the two columns on the right of Table 21-11 and describe the mechanism of action and mechanism of bacterial resistance for the antimicrobial agents listed in the left column



Table 21-11 Mechanisms of Drug Action/Resistance



























































Drug Class Mechanism of Action Mechanism of Resistance
Penicillin, cephalosporin, aztreonam Inhibit transpeptidase and stimulation of autolysins Formation of β-lactamases that break the β-lactam ring
Vancomycin Inhibits cell wall synthesis by binding D-alanine D-Alanine replaced with D-lactate
Tetracyclines Bind to the 30S subunit of the bacterial ribosome, inhibiting protein synthesis Decreased transport into the cell and increased transport out of the cell
Aminoglycosides Impairs proper assembly of the ribosome, causing the 30S subunit to misread the genetic code Acetylation, adenylation, or phosphorylation
Clindamycin Binds 50S subunit to prevent peptide bond formation  
Chloramphenicol Reversibly inhibits protein synthesis by binding to the 50S subunit Acetylation
Linezolid Binds to 50S subunit to prevent protein synthesis  
Macrolides Bind to 50S subunit of ribosome, inhibiting translocation Methylation
Fluoroquinolones Inhibit DNA gyrase, preventing DNA replication  
Trimethoprim Inhibits folic acid synthesis by inhibiting dihydrofolate reductase  
Sulfonamides Inhibit folic acid synthesis by being a structural analog (competitive inhibitor) of PABA, a precursor of folic acid in bacteria Modifications of PABA enzyme and increased synthesis of PABA
Metronidazole Converts to a toxic metabolite that prevents cell wall synthesis  
Polymyxins Interact with phospholipids to disrupt the bacterial cell wall  

PABA, para-aminobenzoic acid.



11 Cover the right column in Table 21-12 and describe the adverse effects for each of the antimicrobial agents listed in the left column



Table 21-12 Adverse Drug Effects




































Drug Adverse Effects
β-Lactams Hypersensitivity
Diarrhea
Cephalosporins have 10-20% cross-reactivity in penicillin-allergic patients
Tetracyclines Gastrointestinal upset
Discolors teeth in children
Toxicity in patients with renal impairment
Photosensitivity
Affects bone growth in children
Aminoglycosides Nephrotoxicity and ototoxicity
Macrolides Gastrointestinal distress
Acute cholestatic hepatitis
Prolonged QT interval
Fluoroquinolones Damages cartilage in young children
Tendon rupture in adults
Chloramphenicol Aplastic anemia
Gray baby syndrome
Trimethoprim Mimics folic acid deficiency (megaloblastic anemia, leukopenia, granulocytopenia)
Sulfonamides Allergic reactions
Hemolysis in glucose 6-phosphate deficiency
Photosensitivity
Vancomycin Nephrotoxicity and ototoxicity
Thrombophlebitis
Red man syndrome (prevented by antihistamines)
Metronidazole Disulfiram-like reaction with concurrent alcohol intake
Metallic taste


Step 1 Secret


The list of antibiotics to know for Step 1 is quite extensive, and students often wonder how in depth their knowledge must be to learn this subject for boards. Our best guess is that you should expect anywhere from one to three questions on antibiotics. First Aid has a great review of this topic, but there is still quite a bit of information in these pages. If you can learn it all, great! If you find yourself short on time, go for the highest-yield points. For each antibiotic you should therefore learn this information in the following order:



image Mechanism of action and mode of resistance


image Unique side effects and toxicity symptoms: Note that we said you should learn the unique side effects of each drug. Boards will not test you on the fact that certain antibiotics can cause occasional gastrointestinal (GI) upset or headache. These symptoms are characteristic of too many drugs to make for good test questions. Focus on the toxicities listed in Table 21-12.


image Clinical uses: Note that you should know the general uses for each drug (e.g., vancomycin is used for gram-positive organisms only, aminoglycosides for serious gram-negative infections, aztreonam for gram-negative rods, metronidazole and clindamycin for anaerobes) but you do not necessarily need to learn the individual organisms affected by every antibiotic. We do not mean to imply that this material is not important for your clinical years or fair game for boards, but it is less likely to be tested than the previous two points. However, you should be sure to know which drugs can be used for select bacterial species—namely, Pseudomonas, methicillin-resistant Staphylococcus aureus (MRSA), and Enterococcus.




Case 21-1


A 64-year-old man is evaluated for a 3-day history of productive cough, fever, and chills. He describes his phlegm as “rust colored” and notes that his ribs hurt when he takes a deep breath. On examination, the patient is febrile with a temperature of 101.5° F and an O2 saturation of 89%. Crackles are heard in the right lower posterior lung field. Laboratory workup reveals a significant leukocytosis. Chest x-ray study and sputum culture are pending.



1 What is the most likely diagnosis?


The combination of fever, chills, pleuritic chest pain, hypoxemia, and productive cough is very suggestive of pneumonia. Furthermore, the rust-colored sputum suggests streptococcal pneumonia.




Step 1 Secret


Gram-positive diplococci and rust-colored sputum are common buzzwords for Streptococcus pneumoniae. Salmon-colored sputum, on the other hand, is associated with Staphylococcus aureus. You should know the buzzwords associated with various microorganisms. We will draw attention to these buzzwords throughout the microbiology chapters.



2 What defense mechanisms prevent pneumonia in the healthy individual?


The respiratory tract has many defenses in place to prevent access to the lungs by potential pathogens. The nasal hairs, mucosa, and dynamics of airflow all act early to prevent inhalation of microorganisms. The epiglottis and cough reflex both act to prevent particulate matter from traveling into the deeper airways. The respiratory tract is lined with mucus until the terminal bronchioles are reached. This mucus is propelled upward by the ciliated epithelium, eliminating foreign material as expectorant. The last line of defense is in and around the alveolar complex and is composed of macrophages, neutrophils, immunoglobulin, and complement. These components will become hyperactive during an infectious process because many of their triggers are foreign antigens.


Note: Any state that alters the level of consciousness (anesthesia, seizure, intoxication, sedation, and neurologic disorders such as coma) predisposes to aspiration pneumonia due to suppression of the cough reflex. The organisms causing this type of infection are usually anaerobes from the mouth or refluxed gastric contents.

Related posts:

  1. Bleeding Disorders
  2. Gastroenterology
  3. Rheumatology
  4. Clinical Anatomy

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Apr 7, 2017 | Posted by in NURSING | Comments Off on Bacterial Diseases

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