Download Week 4: Fever and Infection Fever

Week 4: Fever and Infection
Fever
Fever/Pyrexia: A body temperature above the normal range.
Types of Fever
 Intermittent: Body temp. alternates between fever and normal at regular intervals
 Remittent: Body temp. always above normal but fluctuates in wide ranges
 Relapsing: Fluctuations occur between days. Ie: Week of fever followed by week of normal.
 Constant: Minimal fluctuation. Always above normal.
Stages of Fever
 Chill Phase: New temperature set point established. Heat production responses occur
o Chills
o Feeling Cold
o Vasoconstriction (Cold skin)
o Shivering
 Plateau Phase: Core temperature has reached the new set point.
 Flush/ Defervescent Stage: Threat eliminated. Heat reduction responses occur.
o Excessive Sweat
o Vasodilation (Hot, flushed skin)
Onset and Course of Fever
1. Pyrogens Production and Circulation
2. Hypothalamus Resets Core Temperature (↑)
3. Body produces Heat (Chill)
4. New core temperature is reached (Plateau)
5. Removal of cause (Pathogens); Pyrogen Production and Circulation stops
6. Hypothalamus Resets Core Temperature (↓)
7. Body releases Heat (Flush)
Infection
Infection: The invasion of a pathogen that damages the body.
Nosocomial Infection: Infection acquired from a medical environment. Improper aseptic technique or
presence of microbes (from other patients) may cause contamination.
Pathogenicity: Capacity to cause disease.
Virulence: Degree of pathogenicity based on invasive qualities, toxic qualities and ability to avoid host
defense. Those with strong virulence can cause disease in small quantities.
Onset and Course
 Incubation: Period where bacteria have made its way into the body but symptoms have not
occurred. The patient is now a reservoir and a carrier.
 Prodromal: Period of non specific symptoms. These symptoms are just a warning sign to the
patient that there is something off.
 Acute: Period of specific symptoms. Manifestations of the infection will localize at an area or be
systemic and affect the entire body. Leads to Recovery, Chronic Infection or Septicemia.
 Recovery: Symptoms, signs and defense mechanisms (immune system, inflammation, etc)
subside because the source of infection is gone.
 Chronic Infection: If the patient is not fully recovered from the infection and the source is still
present in the body. There may be mild symptoms with periods of acute infection.
 Death: Septicemia is the infection overwhelming the immune system and the entire body.
Pathogen is prevalent and circulates in the blood accessing all parts of the body.
Clinical Signs and Symptoms
Local
Inflammation Manifestations
Lymphadenopathy
Purulent Exudate (Bacterial)
Serous Exudate (Viral)
Systemic
Fever
Leukocytosis (Inflammation)
Elevated ESR (Inflammation)
Fatigue, weakness, anorexia
Headache, Arthralgia
Severe Systemic (Affect NS)
Confusion
Disorientation
Seizure
Loss of Consciousness
(Gould, 2006)
Diagnostic Tests for Infections
 Blood Test
o Leukocytosis (increase in WBC): bacterial infection
o Leukopenia (decrease in WBC): viral infection
o Neutrophil increase: Acute Infection
o Lymphocyte/monocyte increase: Chronic infection
o Antibody detection: Matches antibodies produced with specific pathogens
 Culture and Staining: Identify Type/ Characteristics of Invader through growth and appearance
 Radiologic Examination: Identify site of infection
Pathogens
Bacteria
Bacterial Components
 Cell Wall:
o Gram Positive: Thick peptidoglycan (sugar + amino acid) wall that can absorb Gram
stains well because of the amount of peptidoglycan
o Gram Negative: Cell wall with a small amount of peptidoglycan and a lot of
Lipopolysaccharide layer (contributes as an endotoxin). Cannot absorb Gram stains well.
 Cell Membrane: Controls movement of nutrients and may be involved in ATP synthesis
 Capsule/ Slime Layer: Outside cell wall. Protects against phagocytosis.
 Toxins
o Exotoxin: Mostly produced by Gram Positive Bacteria. Interferes with bodily functions
and are diffused into bodily fluids to get to other cells.
o Endotoxin: Released from Gram Negative Bacteria cell walls after death.
o Enzyme: Some bacterial enzyme are catalytic in nature and may destroy certain cells
and tissues by interfering with particular functions.
 Spores: Mostly Gram Positive Bacteria. Dormant form which is resistant to harsh conditions.
Areas of Attack by Drugs
 Cell Wall (Defenseless and Osmolysis)
 DNA Replication, RNA synthesis, Protein synthesis (Unable to carry out metabolic processes)
 Metabolic Processes (Enzyme Inhibition)
 Cell membrane (Leakage)
Bacteria that are similar to Viruses
Chlamydiae: obligate intracellular parasite. Causes inflammation in the pelvis which is sexually
transmitted. Bacteria are primitive and require a host because they do not contain proper machinery.
They exists in two forms:
 Elementary body (EB): infectious. The EB can bind onto a host cell and invade it.
 Reticular Body (RB): non infectious. Makes ATP and reproduce.
 EB invades a host cell. Becomes RB and starts reproduction. The collection of RB then transform
back into EB and is dispersed after lyses or exocytosis.
Rickettsiae: Obligate intracellular parasite. Causes fevers and attacks blood vessels.
Mycoplasma: Causes pneumonia. Smallest cellular microbe. Lacks Cell walls.
Viruses
Prion: protein that changes the shape of other proteins into its own.
Virion: Virus particle consisting of capsid (protein coat) and nucleic acid
Life Cycle
 Lytic: Active life cycle where viral particles incorporate their genetic information (DNA or RNA)
into the host cell and take over the machinery to make new virus particles.
 Lysogenic: Dormant life cycle. Viral genetic information is incorporated into host DNA.
Other Microbes
Fungi: Eukaryotic. Mycotic Infections are pathogenic by replication (take up space and nutrients).
Infections also grow at a slow rate. Systemic infections usually affect those that are immune suppressed
while superficial infections can happen to anyone.
Protozoa: Unicellular, eukaryotic microorganisms that lives in soil, water and animal hosts. They are
usually found in areas of bad hygiene and sanitation. Pathogenic Protozoa are usually parasitic. These
organisms can also go into a dormant state called a cyst to withstand harsh environments.
 Trichomoniasis: Trichomonas vaginalis can be sexually transmitted and causes inflammation.
 Malaria: Plasmodium. This protozoa is hemolytic. Infects the liver and blood.
 Amebiasis: Entamoeba histolytica invades the intestine. Proteolytic enzymes cause ulcers and
diarrhea (amebic dysentery). Can spread to bloodstream.
Multi Cellular Parasites
Helminthes (Parasitic Worms): Worms that are found in intestines (sometimes blood or elsewhere) and
feeds off host’s nutrients. Method of invasion is ingesting eggs or larvae. It is most common in areas
with low sanitation. There are three types of Helminthes which are: Roundworms (Nematodes), Flukes
(Trematodes) and Tapeworms (Cestodes). Drugs for this type of infection acts locally in the intestine or
systemic in muscles and organs. Drug resistance is not a problem.
 Complications
o Physical Obstructions
o Malabsorption
o Secondary Bacterial Infection
o Severe Fatigue (nutrient loss)
Resident Flora
Host/Resident Flora: Microorganisms that live inside the host and coexists with it.
Opportunistic Infection: Infection caused by host flora being transferred to another part of the body, an
imbalance of microbial populations or decreased immunity/immune response.
Flora Present
Skin
Nose, Pharynx
Mouth, Colon, Rectum
Vagina
Distal Urethra, Perineum
(Gould, 2006)
Flora Absent (Sterile)
Blood, Cerebrospinal Fluid
Lungs
Stomach
Uterus, Ovary, Fallopian Tube
Bladder, Kidney
Drugs for Infection
How Drug Resistance Forms: When a drug kills off bacteria, non resistant bacterial populations die off
and those that are resistant remain. With less competition for space and resources, these resistant
bacteria grow at a drastic rate. The bacterial population that was just eliminated is now replaced with a
drug resistant population
Superinfection: secondary infection that arises from killing off host flora and allowing pathogens to
grow rapidly because of lack of competition for nutrients and space
Selection of an Appropriate Antibiotic




Before laboratory testing: use broad spectrum (if patient’s condition is serious)
After laboratory testing: use narrow spectrum. Less effect on host flora, less side effects
Limit to one drug: Antagonism may decrease effectiveness and promote resistance
Host Factors
o Suppressed immune response: use of bactericidals and prophylactics
o Infection past the Blood Brain Barrier: many drugs cannot bypass the barrier
o Injury/Inflammation: Lower circulation and become acidic or anaerobic.
o Excessive pus formation (hematoma): may impede drugs getting to target
o Intracellular: Drugs have a harder time getting to the pathogen
o Age: young/old can’t metabolize or excrete drugs as well. Doses are decreased.
o Pregnancy: some antibiotics cross the placenta
o Allergies to Certain Drugs
o Health Status
o Genetics: some people lack enzymes to metabolize certain antibiotics
Antibacterial







Penicillin: Inhibits cell wall synthesis. Bacteria die from osmolysis.
Cephalosporin: Inhibits cell wall synthesis. Bacteria die from osmolysis.
Macrolide: Binds to Ribosomes. Inhibits protein/enzyme synthesis.
Tetracycline: Binds to Ribosomes. Inhibits protein/enzyme synthesis.
Aminoglycoside: Inhibits protein/enzyme synthesis.
Fluoroquinolones: Binds to topoisomerase IV and DNA gyrase
Sulfonamides: Inhibits folic acid (required for rapid cell growth). Do not give to pregnant women
Antifungal/Antiprotozoal



Azole: Ergosterol synthesis inhibitor. Fungi die from leaking cell membranes
Superficial Antifungal Drugs: Method of action depends on the type. Safer than systemic drugs
Metronidazole: Disrupts nucleic acid synthesis.
References
Adams, M., Holland, L. N., & Urban, C. Q. (2011). Pharmacology for nurses: a pathophysiologic approach
(3rd ed., pp. 479 – 494, 508-509, 512-517, 522). Upper Saddle River, N.J.: Pearson Education.
Gould, B. E., & Buttle, G. (2006). Study guide for pathophysiology for the health professions (3rd ed., pp
79-97). Philadelphia: Saunders/Elsevier.
Kozier, B., Berman, A., Berke, K., Bouchal, S., & Hirst, S. (2004). Fundamentals of nursing--the nature of
nursing practice in Canada, (Canadian edition. Pp 711-712). Toronto: Pearson Education Canada.