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WorksheetsPath - ID
Total questions: 115
Worksheet time: 3570secs
benefits only the human; no harm to the microorganism
Symbiosis
Mutualism
Commensalism
Pathogenicity
Opportunism
benefits the human and the microorganism
Symbiosis
Mutualism
Commensalism
Pathogenicity
Opportunism
benefits only the microorganisms no harm to the human
Symbiosis
Mutualism
Commensalism
Pathogenicity
Opportunism
benefits the microorganism; harms the human
Symbiosis
Mutualism
Commensalism
Pathogenicity
Opportunism
a situation in which benign microorganisms become pathogenic because of decreased human host resistance
Symbiosis
Mutualism
Commensalism
Pathogenicity
Opportunism
Period from initial exposure to the onset of the first symptoms; could last from hours to years.
Incubation period
Prodromal period
Invasion period
Convalescence
The occurrence of initial symptoms are often very mild with feelings of discomfort and tiredness.
Incubation period
Prodromal period
Invasion period
Convalescence
farther and affects other body tissues: SYMPTOMS
Incubation period
Prodromal period
Invasion period
Convalescence
Recovery occurs and symptoms decline, or the disease is fatal, or has a period of latency.
Incubation period
Prodromal period
Invasion period
Convalescence
Gram ________ bacteria have lipopolysaccharide in the outer membrane that is known as _________. ***
negative; endotoxin
negative; exotoxin
positive; endotoxin
positive; exotoxin
agents that can produce fever (exogenous or endogenous)
pyrogens
vectors
biofilms
Gram stain detects peptidoglycan --> gram ____ picks up stain ***
positive
negative
proteins released during bacterial growth
exotoxins
endotoxins
Released during lysis of bacteria
exotoxins
endotoxins
fever-producing: YES
exotoxins
endotoxins
toxicity (ability to cause disease): HIGH
exotoxins
endotoxins
Involves small mutations in the genes for HA or NA
antigenic drift
antigenic shift
mutation results in new strain (big change)
antigenic drift
antigenic shift
infects multiple species
Flu A
Flu B
only infects humans
Flu A
Flu B
binds host cell
HA-hemagglutinin
NA-neuraminidase
essential for release of new virions
HA-hemagglutinin
NA-neuraminidase
Gram stain detects peptidoglycan --> gram _____ does not pick up stain ***
positive
negative
are heavy; can land in mouth, nose or eyes of people nearby. Produced by coughing, sneezing or talking
droplets
aerosol
made of micro-droplets that are lighter and stay suspended in the air for longer than droplets. Produced during normal breathing.
droplets
aerosol
transfer microorganisms passively from a contaminated site to an individual
mechanical vector
biologic vector
transmit microbes through bites or stings
mechanical vector
biologic vector
Vectors are
direct contact
indirect contact
from mother to offspring
vertical transmission
horizontal transmission
Listeria, CMV, Toxoplasma
Microbes that cross placenta
Microbes that ascend birth canal
Microbes that pass through breast milk
group B strep, HIV, Candida
Microbes that cross placenta
Microbes that ascend birth canal
Microbes that pass through breast milk
Staph aureus
Microbes that cross placenta
Microbes that ascend birth canal
Microbes that pass through breast milk
Diseases with relatively high, but constant, rates of infection in a particular population
Endemic
Epidemic
Pandemic
Number of new infections in a particular population that greatly exceeds the number usually observed
Endemic
Epidemic
Pandemic
An epidemic that spreads over a large area such as a continent or worldwide
Endemic
Epidemic
Pandemic
Ability to spread from one individual to others and cause disease
Virulence
Communicability
Opportunistic
Vector
Agent that carries infectious microorganisms from an infected organism to uninfected ones
Virulence
Communicability
Opportunistic
Vector
Capacity of an organism to cause severe disease
Virulence
Communicability
Opportunistic
Vector
Normally not causing disease, but able to do so when an individual's immune system is suppressed
Virulence
Communicability
Opportunistic
Vector
Bacteria that grow in complex multicellular masses called ______ have some protection from host immune responses and antibiotics
pyrogens
vectors
biofilms
Bacteria that produce endotoxins are called _______ bacteria because they cause fever.
pyrogenic
biofilm
Occurs with hepatitis B and hepatitis C with a predisposition to cirrhosis and hepatocellular carcinoma.
Chronic active hepatitis
Fulminant hepatitis
Encephalopathy
-Is a complication of hepatitis B (with or without hepatitis D infection) or hepatitis C.
-Causes widespread hepatic necrosis.
-Is often fatal.
Chronic active hepatitis
Fulminant hepatitis
Encephalopathy
-Manifests as confusion, stupor, and coma.
-Liver failure and death can occur
Chronic active hepatitis
Fulminant hepatitis
Encephalopathy
indicates there is an ongoing infection, acute or chronic
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Anti-HBc (IgM)
Indicates recovery and immunity from hepatitis B virus by natural infection or has been successfully vaccinated against hepatitis B
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Anti-HBc (IgM)
the person was infected with the virus and the virus particle was open to the immune system
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Anti-HBc (IgM)
*immunized individuals do not get exposure to
core proteins (HBeAg)
surface antigen (HBsAg)
*not measurable after vaccination
core proteins (HBeAg)
surface antigen (HBsAg)
-Appears at onset of symptoms in acute hepatitis B and persists for life.
-Indicates previous or ongoing infection in an undefined time frame.
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Anti-HBc (IgM)
-Indicates recent infection, 6 months or less
-Acute infection
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Anti-HBc (IgM)
viral surface antigen
HBsAg
Anti-HBs
HBeAg
Anti-HBc
antibody to the surface antigens
HBsAg
Anti-HBs
HBeAg
Anti-HBc
viral core protein
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Antibody to the viral core proteins
HBsAg
Anti-HBs
HBeAg
Anti-HBc
Fulminant hepatitis is most common in ***
Hepatitis A
Hepatitis B (with hep D infection)
Hepatitis B (w/o hep D infection)
Hepatitis C
Hepatitis E
Lesions can occur from scarring from cirrhosis common in
chronic Hep A
chronic Hep B
chronic Hep C
Hepatitis causing the most severe damage to hepatocytes
Hep A
Hep B
Hep C
Hep D
Hep E
Begins approximately 2 weeks after exposure; ends with the appearance of jaundice.
Incubation phase
Prodromal (preicteric) phase
Icteric phase
Recovery phase
Is highly transmissible at this phase
Incubation phase
Prodromal (preicteric) phase
Icteric phase
Recovery phase
Clinical manifestations: Fever, malaise, anorexia, and liver enlargement and tenderness; RUQ pain
Incubation phase
Prodromal (preicteric) phase
Icteric phase
Recovery phase
Is the actual phase of illness.
Incubation phase
Prodromal (preicteric) phase
Icteric phase
Recovery phase
Clinical manifestations: Jaundice and hyperbilirubinemia (itching); fatigue and abdominal pain, liver is enlarged smooth and tender.
Incubation phase
Prodromal (preicteric) phase
Icteric phase
Recovery phase
Prevented through vaccination
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D → through Hep B vaccine
Hepatitis E → vaccine only in China
-Is responsible for most cases of posttransfusion hepatitis.
-Is also implicated in infections related to IV drug use and human immunodeficiency viral (HIV) infection.
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
-Is transmitted through contact with infected blood, body fluids, and contaminated needles.
-Maternal transmission occurs if the mother is infected during the third trimester.
Hepatitis A
Hepatitis B
Hepatitis C
filamentous fungi grow as multinucleate, branching hyphae, forming a mycelium
molds
yeasts
grows as ovoid or spherical; single cells multiply by budding and division
molds
yeasts
Human-to-human-only with
dermatophytes
mycosis
strategy of fungi: they have ________ to adhere to receptors (typically toll-like receptors) ***
polysaccharides
pili
capsules
biofilms
most common fungal infection
Cryptococcus neoformans
Candida albicans
Capsule-resistance to phagocytosis
Cryptococcus neoformans
Candida albicans
Candida albicans: infection remains localized
immunocompetent
immunocompromised
Candida albicans: infection can become systemic
immunocompetent
immunocompromised
Transmitted by the tsetse fly
Trypanosomes
Leishmania spp.
Entamoeba Histolytica
Giardia lamblia
Transmitted by sand fleas
Trypanosomes
Leishmania spp.
Entamoeba Histolytica
Giardia lamblia
failure of at least two organs caused by a systemic inflammatory response after a severe illness or injury
bacteremia
sepsis
septic shock
a systemic response to inflammation, defined clinically by specific changes from baseline temperature, heart rate, respiratory rate, or WBC parameters
bacteremia
sepsis
septic shock
found in contaminated water or food and transmission is by ingestion
Trypanosomes
Leishmania spp.
Entamoeba Histolytica
Giardia lamblia
change their variable surface glycoproteins (VSG)
Trypanosomes
Leishmania spp.
Entamoeba Histolytica
Giardia lamblia
Survive intracellularly
Trypanosoma
Leishmania
Entamoeba Histolytica
Giardia lamblia
Switching Variant Surface Glycoprotein Gene Expression in Trypanosomes
gene conversion
telomere exchange
transcriptional switch
In Sepsis, Microbes Enter the Bloodstream Directly and/or Indirectly: microbes enter the bloodstream from a site of localized infection
direct
indirect
In Sepsis, Microbes Enter the Bloodstream Directly and/or Indirectly: microbes release toxic substances directly into the bloodstream
direct
indirect
Enzyme used to generate complementary DNA (cDNA) from an RNA template, a process termed reverse transcription; used by retroviruses to replicate their genomes
Reverse transcriptase
Integrase
Enzyme that integrates (forms covalent links between) its DNA into the host DNA
Reverse transcriptase
Integrase
envelope proteins
gp41
gp120
CD4
CCR5
gp160
the spike
gp41
gp120
CD4
CCR5
gp160
converts single-stranded viral RNA into double-stranded DNA
Reverse transcriptase
Integrase
inserts viral DNA into the infected cell's DNA, where it may remain dormant
Reverse transcriptase
Integrase
encodes a protein that is modified by viral protease to generate smaller matrix (e.g., p17) and capsid proteins (e.g., p24)
gag gene
env gene
encodes a glycoprotein that is processed by cellular protease (furin) into the TM and SU proteins
gag gene
env gene
replication and release of new virions triggers apoptotic cell death of the infected cell; infected cells also become a target for killing by CD8+ T-cytotoxic cell
Infected cell death
Neighboring uninfected cell death
release of death ligands (e.g., Fas ligand [FasL], TNF) initiates apoptosis in neighboring uninfected Th cells
Infected cell death
Neighboring uninfected cell death
Viral replication and T-cell destruction continue in the lymph nodes, although the individual is generally asymptomatic.
Period of Clinical Latency
Disease Progression
Initial Phase of Infection
As the disease progresses, the person may develop constitutional symptoms—a variety of symptoms of acute viral infection that do not involve opportunistic infections or malignancies.
Period of Clinical Latency
Disease Progression
Initial Phase of Infection
When the number of CD4+ cells is critically suppressed, the person becomes susceptible to a variety of opportunistic infections and cancers.
Period of Clinical Latency
Disease Progression
Initial Phase of Infection
Antibodies against HIV-1 are not yet detectable (window period)
Initial Phase of Infection
Latent Phase of Infection
Disease Progression
Viral products, including p24 antigen, viral RNA, and infectious virus, may be detectable in the blood a few weeks after infection
Initial Phase of Infection
Latent Phase of Infection
Disease Progression
Most antibodies produced against envelope proteins in the early phase are absorbed onto viral particles in the blood and are not detectable by most routine assays.
Initial Phase of Infection
Latent Phase of Infection
Disease Progression
Antibody levels against p24 and other viral proteins, as well as HIV-specific CTLs, generally increase and then remain constant until the development of AIDS.
Initial Phase of Infection
Latent Phase of Infection
Disease Progression
As the immune system becomes severely depressed and excess viral antigen is released into the blood, measurable antibody levels decrease.
Initial Phase of Infection
Latent Phase of Infection
Disease Progression
Inhibitors of the enzyme reverse transcriptase
NRTIs
NNRTIs
PIs
Entry/Fusion Inhibitors
Inhibitors of non-nucleoside reverse transcriptase inhibitors
NRTIs
NNRTIs
PIs
Entry/Fusion Inhibitors
Inhibitors of the viral protease
NRTIs
NNRTIs
PIs
Entry/Fusion Inhibitors
prevent attachment of the virus to the target cell or prevent fusion between HIV and the cell membrane
NRTIs
NNRTIs
PIs
Entry/Fusion Inhibitors
Inhibitors of the viral integrase enzyme
Entry/Fusion Inhibitors
INSTIs
Pharmacokinetic enhancers
-Administered with some PIs and INSTIs
-Affect intestinal transport proteins and liver enzyme that would normally break down some antiretroviral drugs, thus allowing smaller doses to be used
Entry/Fusion Inhibitors
INSTIs
Pharmacokinetic enhancers
Which of the following is indicative of autoimmune hepatitis? [Riggs prac quiz]
Positive ANA result
elevated ALT levels
HBsAG positive
HBsAG negative
HBsAg is a measure of: [Riggs prac quiz]
a history of infection (time line non-specific)
immunization
resolved infection
Acute infection
A 45-year-old woman was diagnosed 6 months ago with acute hepatitis B infection. She is unaware of how she contracted the virus. She takes no medications and since the diagnosis, she has started taking a multivitamin and has started exercising. She now has the following serologies: HBsAg negative; anti-HBsAg positive; HBeAg negative; anti-HBcAg positive. Which of the following is the correct diagnosis? [Riggs' prac quiz]
Susceptible to infection
Chronic active infection with high infectivity
Resolved acute infection
Immune due to vaccination
low systemic vascular resistance, normal or elevated cardiac output, body temperature instability, elevated blood cytokine levels, possible manifestations of infection and of organ dysfunction
bacteremia
sepsis
septic shock
presence of viable bacteria in the blood
bacteremia
sepsis
septic shock
life-threatening organ dysfunction caused by a dysregulated host response to infection
bacteremia
sepsis
septic shock
sepsis that is complicated by persistent hypotension refractory to fluid therapy
bacteremia
sepsis
septic shock
