NUR 239 Lecture Notes - Lecture 15: Respiratory Tract, Human Microbiota, Superinfection
21 May 2018
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Patho Exam 2
• Colonization – the presence and growth of microorganisms, no tissue injury or immune response
is produced; have the organism on you but you’re not actually infected
• Empiric Treatment – Treatment which begins after samples are collected but before lab results
provide definitive results (usually antibiotics to treat infections)
• Opportunistic Infection – Infection caused by microorganisms that flourishes because the host’s
deficient immune system. Often the infection is caused by normal flora that would be non-
pathogenic in a healthy host. (imbalance of power)
• Superinfection – “on top of”, an second infection related to a change in the normal flora from
antibiotic use (c. diff after taking antibiotics)
Mechanisms of Transmission:
• Portal of entry (regardless of the mechanism of entry, the transmission of the MO is directly
related to the number of MO absorbed by the host – porth p. 306)
• Penetration – disruption of the host’s barrier defense system (skin, mucous membrane)
• Direct contact – physical contact with an infected person, vertical transmissions, congenital
infections, contact with a contaminated inanimate object (fomites)
• Ingestion – oral cavity/GI tract, often associated with food/water
• Inhalation – multiple protective layers/respiratory tract (aerosolized, droplets)
Clinical Presentation:
• Symptomatology/Clinical Presentation: collection of signs & symptoms expressed by the host
during disease course
• Site of Infection: Inflammation of an anatomic location is designated by adding the suffix –itis to
the name of the involved tissue; determined by type of pathogen, portal of entry, and competence
of the host’s immunologic defense system
• Nonspecific: Fever, myalgia, lethargy
Overview of Microorganisms:
• Normal flora outside of its niche can be a pathologic problem (E.coli in the GI tract = normal
flora, E. coli in the urinary bladder = UTI)
o E. coli is supposed to be inside of the GI tract but when it goes outside of the GI tract and
into the urinary bladder, you can get a UTI
• Classifications
o Bacteria – one-celled organism
▪ Aerobic vs Anaerobic
• Gram Positive = staphylococcus (skin), streptococcus (upper respiratory
tract), enterococcus (GI tract)
• Gram Negative = All GI: E. coli, klebsiella, pseudomonas, Enterobacter
• Pathogens
o Relatively rare, disease producing MOs (pathogens) cause infectious disease
o Normal flora (normally present in the host) but are outside of their niche (endogenous)
o Pathogens from the environment (outside the host) = exogenous
o Severity of the disease depends on:
▪ MOs characteristics
• Virulence = the MOs disease producing potential
• Drug-resistance = ability to live in the presence of antibiotics
o Host’s immune system (immunocompetence) = host’s ability to protect itself from a
MO because of a strong immune system (we want this!!!)
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o Infectivity/Invasiveness of the MOs
▪ Infectivity = MOs ability to defeat the host’s immune system
▪ Invasiveness = MOs ability to invade the host and multiply/replicate
o Community acquired vs Hospital acquired MOs
▪ Community acquired (CA) = usually less virulence/pathogenic MO, often gram +
(staph, strep).
• Recent increase in CA MRSA
▪ Hospital acquired (HA) = typically very virulent/pathogenic and may be resistant
to treatment
• Gram Negative microorganisms
• Transmissibility – how MOs can spread →International travel contributes to increasing the
sources of infections
Clinical Manifestations
1. Acute Infection:
o Incubation Stage: Active replication of MO, no symptoms in host, variable time period
(influenced by host’s characteristics)
o Prodromal Stage: Initial appearance of symptoms is usually generalized (just not feeling
well/tired)
o Acute Stage: Max. impact of infectious process, rapid growth of MO, toxic by-products
of MO, immune/inflammatory processes engaged, symptoms are more
pronounced/specific
o Convalescent Stage: Containment, elimination of MO, repair
o Resolution: Total elimination of MO
2. Chronic Infectious Diseases:
o Longer & irregular course
o No convalescent/resolution stages
3. Subclinical Infections
o Subclinical (subacute) stage: infection without symptoms (progress from infection to
resolution with a clinical appearance of the disease), Infectious disease – long prodromal
stage (AIDS), fulminant illness (abrupt onset of symptoms, may progress to death quickly
(Ebola)
Superinfections - a second infection resulting from treatment of a primary infection, especially by a
different MO.
o Examples: the overgrowth of endogenous C. difficile which occurs following treatment
with a broad-spectrum ABX.
Opportunistic Infections – Infections caused by MOs that usually do not cause infections but due to
suppress immune/inflammatory responses or disruption in normal flora, MOs cause infections. Examples
are herpes, candida (yeast)
o Signs and symptoms of an infection are very similar to inflammation: redness, swelling,
pain, loss of function, fever, leukocytosis
- Drug Therapy
o Lab Studies: Serology Testing- tests for antibody titers- is not as sensitive as a culture but
can be help for diseases such as Hep B diagnosis
▪ CBC with differential, Urinalysis- dipstick/microscopic (If we don’t know what’s
wrong with someone we’ll give them CBC or Urinalysis test)
o Culture & Sensitivity Tests: Culture (type of bacteria) and Sensitivity (what ABX to use)
(C & S) – growing MO and determining what ABX will work best to treat.
▪ Important to obtain a sample before starting ABX
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▪ Susceptibility: vulnerability of the bacteria to the effects of an antibiotic, tests
determine which drugs are likely to be effective against the organism
• Susceptible (S) or resistant (R) to the tested drugs
Patterns of Antibiotic Resistance
1. MOs that can survive and multiply despite ABX therapy.
2. This is becoming a major public health concern and results in the use of more toxin and
expensive drugs, causes prolonged illnesses and hospitalizations, and increased mortality rates
3. Mechanisms used:
4. Make enzymes that deactivate ABX
5. MOs hide/change their identity (ABX don’t recognize or can’t connect)
1. Modifying target site, so ABX cannot recognize MOs
2. Change cell wall to prevent ABX penetration
o Efflux – pump ABX out of cell
o Mechanisms of acquired resistance
1. Genetic mutations – transfers ABX resistance copies to the next generation of MOs
2. Gene transfer - transferring genetic material between MOs – spreads resistance to MOs that
haven’t been exposed to the ABX yet
3. Natural selection – Survival of the fittest
o ABX resistance increases with:
o Overuse/Widespread use of broad-spectrum ABX (kills pathogens + normal flora and
allows overgrowth of weaker MOs and resistant MOs) = Superinfection
o Interruption or inadequate use of ABX treatment regimens – stopping ABX early
o MRSA, VRE and all gram + MOs have developed some resistant strains (MRSA, PCN
resistant strep, VRE – all serious Public Health Threats)
o Gram Negative are more resistant naturally, especially pseudomonas and serratia – may
cause sepsis and septic shock
o Hospitals have more resistant MOs hanging out, and some regions have been found to
have greater risks than others (variation by regions)
Penicillins
- Prototype: Ampicillin
- PK: Rapidly excreted by kidneys, unchanged, Half-life is 1-2 hours
- Characterized by beta-lactam ring → many MO produce beta-lactamase enzyme which makes
them resistant to PCN
- Bactericidal Action, Broad-Spectrum, Inhibits cell wall synthesis
o Used for Gram + MOs, but there are a lot of resistant MOs
o Used for respiratory, GI, GU infections, skin & soft tissue, respiratory infections &
prophylaxis of infective endocarditis (before dental procedures)
o AE: Check for allergic reactions
- PCN G (IM, IV) and PCN V (PO)
o Penicillinase resistant: methicillin which is used mainly for staph infections (not effective
for MRSA)
o Ampicillins: broad-spectrum that is used for Gram + and – and are often used for ear
infections and sinusitis
o Extended Spectrum: Carbenicillin- used for Gram – especially pseudomonas
o Combination:
▪ Extends the spectrum of the antibacterial activity for PCN & Beta-Lactamase
inhibitor combo
• Augmentin = Amoxicilin + Clavulanate
• Unasyn = Ampicillin + Sulbactam
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Ingestion oral cavity/gi tract, often associated with food/water. Inhalation multiple protective layers/respiratory tract (aerosolized, droplets) Mo because of a strong immune system (we want this!!!) Infectivity = mos ability to defeat the host"s immune system. Superinfections - a second infection resulting from treatment of a primary infection, especially by a different mo: examples: the overgrowth of endogenous c. difficile which occurs following treatment with a broad-spectrum abx. Opportunistic infections infections caused by mos that usually do not cause infections but due to suppress immune/inflammatory responses or disruption in normal flora, mos cause infections. Examples are herpes, candida (yeast: signs and symptoms of an infection are very similar to inflammation: redness, swelling, pain, loss of function, fever, leukocytosis. Mos that can survive and multiply despite abx therapy. This is becoming a major public health concern and results in the use of more toxin and expensive drugs, causes prolonged illnesses and hospitalizations, and increased mortality rates.
