Infection-Exam 3 Flashcards
What are the four stages of infection?
- Invasion-intro of disease causing agents into body tissues (avoids immune system defense, triggers inflammatory response)
- Multiplication-period of rapid cell growth and division (occurs before immune system responds)
- Dissemination-local or disseminated presence of disease-causing agent
- Colonization-the presence of bacteria on body surface (like on the skin mouth, intestines or airway) without causing diseases in the person
Stage 1 of clinical infection: Incubation
Manifestations:
The incubation stage includes the time from exposure to an infectious agent until the onset of symptoms.
-Viral or bacterial particles replicate during the incubation stage.
Pathogen load:
Microorganisms have undergone initial colonization and begun multiplying, but are at insufficient numbers to cause symptoms; this period can last from several hours to years
Stage 2 of clinical infection: Prodromal
Manifestations:
The prodromal stage refers to the period after incubation and before the characteristic symptoms of infection occur.
-People can also transmit infections during the prodromal stage.
Pathogen load:
During this stage, the infectious agent continues replicating, which triggers the body’s immune response and mild, nonspecific symptoms.
Stage 3 of clinical infection: Invasion/Illness
Manifestations:
The pathogen is multiplying rapidly, invading farther and affecting the tissues at the site of initial colonization as well a other areas; the immune and inflammatory responses have been triggered; symptoms may be specifically related to the pathogen or the inflammatory response.
Pathogen load:
Signs and symptoms of disease are most obvious and severe. Number of pathogens is at its highest
Stage 4 of clinical infection: Decline
Manifestations: number of pathogen particles begins to decrease, and the signs and symptoms of illness begin to decline. However, during the decline period, patients may become susceptible to developing secondary infections because their immune systems have been weakened by the primary infection.
Pathogen load: pathogen particles begin to decrease and signs and symptoms begin to decline
Stage 5 of clinical infection: Convalescence
Manifestations: Removal of infectious agent and symptoms decline OR the disease may be fatal or may enter a latency phase with resolution of symptoms until reactivation at a later time.
Pathogen load: continue to decline and disappear
Bacteria
Structure:
•Unicellular and prokaryotes: no nucleus but have mitochondria so can produce energy
•Multiple shapes (spherical/cocci, rods/bacilli, spiral)
Pathogenic Properties:
- invasiveness: ability to invade tissues
- toxigenesis: can make exotoxins or endotoxins
Viruses
Structure:
•Smallest of the pathogens
•Capsid coating that protects the nucleic core
-least well developed
Pathogenic Properties: •Virus cannot replicate without a host!!!! •Binds to plasma membrane •Inserts into host cell •Matures •Buds and releases from plasma membrane
Fungi
Structure: eukaryotic microorganisms with thick, rigid cell walls and the capacity to form a variety of complex structures
Pathogenic Properties: •Highly opportunistic – T cells important to limit infection and produce cytokines for macrophage activation •Adapt to host environment •Change morphology, survive in macrophages, produce immunosuppressive cytokines •Tissue damage: •Direct – enzyme and toxin secretion •Indirect – inflammation -Opportunisitic
How are bacteria classified and how does the classification result in different clinical manifestations?
- Gram negative
- Gram positive
- Acid fast bacilli
- Aerobic
- Abnaerobic
- Facultative anerobes
Staph aureus: Bacteria
GRAM POSITIVE COCCI
FACULTATIVE ANAEROBIC
EXTRACELLULAR
COCCI
Etiology and/or Transmission:
S. aureus is most often spread to others by contaminated hand
•Common flora of skin and nasal passages
•Adheres via surface proteins to connective tissue and endothelium
•Resistant forms exist
•Community and hospital acquired strains
Manifestations:
These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo, and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning, and toxic shock syndrome (TSS)
Patho:
•Develop protective capsule, produce proteins that inhibit complement activation, resistant to intracellular oxidative lysis
E. Coli- Bacteria
GRAM NEGATIVE
FACULTATIVE ANAEROBIC
EXTRACELLULAR
CXD ASZ
Etiology and/or Transmission:
Transmission is via the fecal-oral route after consumption of contaminated, undercooked liquids, foods, and by person-to-person through fecal shedding.
•Various strains
•Commonly found in biofilm of foley catheters
•Resistant forms exist
Manifestations:
causes diarrhea, hemorrhagic colitis, and hemolytic-uremic syndrome (HUS) in humans.
Patho:
production of Shiga toxin that injures the intestine by sloughing off of intestinal mucosa cells and results in hemorrhagic diarrhea.
Myobacterium Tuberculosis- Bacteria
WEAK GRAM POSITIVE
AEROBIC
EXTRACELLULAR
RODS
Etiology and/or Transmission:
**Survives and grows within MACROPHAGES and
phagolysosomes
•Develop a capsule that prevents phagocytosis
•Induce anergy, suppresses host response
Manifestations:
cough, cough blood, night sweats, fatigue, fever
Patho:
•Forms granuloma»_space; tubercle»_space; caseates
» collagen scar»_space; immune response»_space; dormant
Candida Albicans- Fungus
Etiology and/or Transmission: •Part of normal microbiome •transmitted by direct or indirect contact with contaminated people or objects. •Opportunistic •Antibiotics change normal flora •Immunocompromised •Cell wall adhesion molecules – adhere to medical devices **troublesome on devices
Manifestations:
lesions in most areas of skin, mucous membranes, thrush, vaginal infection
Patho:
any disruption in the host environment or under conditions of immune dysfunction, C. albicans can proliferate and invade virtually any site in the host; can form biofilms
Coronavirus- Virus
Etiology and/or Transmission: •Identified initially in the 1960s •100s of strains •Prior severe strains SARS (2002- 2004) and MERS (2012 – localized outbreaks) •Transmitted via droplet
Manifestations:
Mild to moderate URI symptoms
Patho:
Once inside the body, the virus binds to host receptors and enters host cells through endocytosis or membrane fusion. S1 and S2 proteins bind host cell receptor and fusion of viral and host cellular membranes
Influenza
Etiology and/or Transmission:
•Family of RNA viruses with different types
(A, B and C)
Manifestations:
Symptoms: fever, ache and fatigue from
release of pro-inflammatory cytokines and
chemokines (TNF and interferon) produced
by viral cells
Patho:
is a result of lung inflammation and compromise caused by direct viral infection of the respiratory epithelium, combined with the effects of lung inflammation caused by immune responses recruited to handle the spreading virus
Herpes:
Simplex
Etiology and/or Transmission: •HSV1: Oral infection via saliva contact -Infection of epithelia cells -Virus moves along axon of dorsal root ganglion •HSV2: Genital with mucous membrane contact
Manifestations:
Fever, swollen lymph nodes, headaches, tiredness, lack of appetite, blistering sores (mouth and genital), pain during urination (genital), itching
•Activates with fatigue, fever and stress
Patho:
-last 10-14 days
virus then lays dormant in the periaxonal sheath of the sensory nerves of either the trigeminal, cervical, lumbosacral, or autonomic ganglia. Once reactivated, the virus goes to sensory nerves and leads to vesicular clusters
Herpes:
Varicella (chicken pox)/Herpes Zoster (shingles)
Etiology and/or Transmission:
A person is not infectious before the blisters appear or after the rash has crusted over. For disseminated zoster, transmission occurs through airborne and droplet transmission, in addition to contact with fluid in the blisters of the rash.
Manifestations:
•Appears as vesicles along dermatomes
Patho:
the virus spreads to the lymph nodes, the liver, and the lungs. This process known as primary viremia. As the incubation period progresses, the virus makes its way to the skin via both CD4+ and CD8+ T cells, initiating secondary viremia. As the infection progresses, small skin vesicles filled with pus and infected cell particles form on the skin surface.
-Exposure causes the production of host immunoglobulin G, M, and A
-Herpes zoster or shingles is reactivation of latent infection
Measles: Rubeola (aka Classic Measles)
Etiology and/or Transmission:
•RNA paramyxovirus spread via upper respiratory tract
Manifestations:
Maculopapular rash, head, trunk and extremities, Koplik spots, cough, coryza (head cold), conjunctivitis, characteristic rash
Patho:
The measles virus is transmitted via the respiratory route and replicates in the nasopharynx and regional lymph nodes within 2 to 3 days after exposure
-caused by a paramyxovirus
-Amplifies in local lymphatic tissues and disseminates
-no symptoms for 5 days so can easily spread
Measles: Rubella (aka German Measles-3 day)
Etiology and/or Transmission:
•RNA virus that is enveloped spread via upper respiratory tract
Manifestations:
•Maculopapular rash, head, trunk and extremities (last about 3 days)
-fever with postauricular lymphadenopathy
•1st trimester pregnancy – congenital rubella syndrome!!!!
•Sensorineural deafness
•Retinopathy, cataracts
•Congenital heart disease, PA stenosis
*RASH STARTS FROM FACE TO THE REST OF THE BODY
Patho:
Rubella virus multiplies in cells of the respiratory system; this is followed by viremic spread to target organs. Congenital infection is transmitted transplacentally.
Australia and Southern Africa
HIV
Etiology and/or Transmission:
– blood born pathogen
•IV drug use, blood and blood products, sexual encounters, mother to baby
Manifestations:
Common symptoms: fever, lymphadenopathy, pharyngitis, rash, myalgias, diarrhea, headache, N/V, hepatosplenomegaly, weight loss, thrush
Patho:
•Virus binds with CD4 cells
•Viral RNA is injected into cell cytoplasm
•Viral RNA is uncoated (capsid removed)
•Enzyme reverse transcriptase is used to make DNA from viral RNA
•Viral DNA travels to cell nucleus and integrates with host DNA
•Transcription and translation result in new viral protein production
•Virus buds through cell membrane and infects more cells
What are the mechanisms of antibiotic resistance?
- inactivate the antibiotic (beta-lactam antibiotic resistance)
- modification or alteration of the antibiotic target binding site so antibiotic has no binding site
- alteration of metabolic pathway-bypasses the activity of the antibiotic
- preventing antibiotic accumulation- leads to low amounts of antibiotic in intracellular fluid
Communicability
the time during which an infectious agent may be transferred directly or indirectly (infectious period)
Infectivity
the ability to produce or transmit infection (contagious period)
Immunogenicity
the ability of a foreign substance, such as an antigen, to provoke an immune response in the body
Toxigenicity
the ability of a microorganism to produce a toxin that contributes to the development of disease
Pathogenicity
the ability of an organism to cause disease (i.e., harm the host)
Virulence
the degree of pathology caused by the organism; it is usually correlated with the ability of the pathogen to multiply within the host but may
be affected by other factors
Portal of entry
the way a pathogen enters a susceptible host
Outbreak***
a greater-than-anticipated increase in the number of endemic cases. It can also be a single case in a new area. If it’s not quickly controlled, an outbreak can become an epidemic
Endemic***
a disease or condition regularly found among particular people or in a certain area
