EXAM 2 Infectious Diseases Flashcards
(73 cards)
1
Q
Prions
A
- modified host protein that are infectious in nature
- Cause spongiform encephalopathies
2
Q
Viruses
A
- Obligate intracellular organisms
- Contain DNA or RNA
- transient acute illnesses, chronic dz, life-long latent infections
3
Q
Bacteria
A
- Cell walls either G+/-
- intracellular, extracellular, or facultative intracellular growth
4
Q
Fungi
A
- eukaryotes
- Mycoses - superficual infections of the skin, hair, nails, “tinea”
- Invasion of SubQ tissue (granulomas), deep infections
5
Q
Protazoa
A
- Motile, single celled eukaryotes
- Replicate intracellulary or extracell
- Transmitted sexually, contaminated food/water, or by blood sucking insects
6
Q
Helminthes
A
- Life cycles involves humans and intermediary hosts
- Adult works produce eggs or larvae that are passed in stool. Adults are not passed in stool
7
Q
Ectoparasites
A
- insects or arthropods that attach to, and live on the skin
- Might directly cause injury or be vectors for other pathogens
8
Q
Skin
A
keratinized outer layer, Low pH, fatty acids
9
Q
GI tract as a physical barrier
A
gastric acids, pancreatic bile, lytic enzymes, mucous layer, defensins (peptides active against microbes), IgA (always in mucous)
10
Q
Urogenital tract as a physical barrier
A
- frequent bladder flushing with urine
- Low vaginal pH
11
Q
Resp tract as a physical barrier
A
bronchial epithelium ciliary activity, mucous layer, defensins, IgA, alveolar macrophages
12
Q
Adhesion - a bacterial virulence
A
bacteria bind to host cell surface
13
Q
Colonization - a bacterial virulence
A
bacteria produce special proteins that allow them to colonize parts of the body. (H. Pylori is able to survive in the stomach by producing urease)
14
Q
Invasion - a bacterial virulence
A
bacteria produce proteins that either disrupt host cell membranes or stimulate their own endocytosis into host cells.
15
Q
Immune response Inhibitors - a bacterial virulence
A
Many bacteria produce factors that inhibit the hosts immune system defenses. Such as binding to antibodies
16
Q
Toxins - a bacterial virulence
A
toxins cause tissue damage.
17
Q
Endotoxin
A
cell wall component like lipid A elicit inflammatory response - cell recruitment and cytokine production, which tells the hypothalamus to release PGs, increase temperature (pyrogenic response)
18
Q
Exotoxin
A
bacteria produced exotoxin, which is released then engulfed by host cell. Part of the exotoxin will inhibit protein synthesis and the other part will be released from the host cell
19
Q
Granulomatous response by host
A
- granuloma - organized collection of macrophages
- May contain additional cells that give clues to their cause
- Form in response to antigens that are resistant to our “first responders” like neutrophils and eosiniphils. May by non necrotizing or caseating (necrotic) (M. tuberculosis granulomas in lungs)
20
Q
Liver damage
A
bacterial adhesions = tissue damage and fibrosis
21
Q
Antibodies against bacterial antigens
A
May cross react with host molecules, or form immune complexes that lodge in vascular beds such as the glomerulus
22
Q
chronic inflammation and epithelial injury
A
may lead to malignancy - H pylori and gastric cancer
23
Q
Chronic/latent infections
A
HSV
VZV
CMV (cytomegalovirus)
24
Q
Chronic/productive infections
A
HBV
HIV
S. Pyrogenes
Diptheria
25
HSV
- double stranded DNA
- entry thru mucous membrane - viral mult - lysis of cells - vescicles - ulcers
- **Asymptomatic viral shedding is unique to HSV**
26
VZV
- Mucous membranes, skin, neurons are infected
- Acute = chickenpox
- Latent in dorsal root ganglia, reactivates - infects sensory nerves - carry virus to skin - shingles
27
CMV
cytomegalovirus
- Carries in breast milk, respiratory drops, saliva
- Transmission - Transplacental, venereal, fecal/oral, tranfusion, organ transplant
- infect dendritic cells and cause severe immunosuppression
- Virus remains latent in leukocyte
28
Most common opportunistic viral pathogen in AIDS?
Cytomegalovirus
29
Sx of CMV
- fever, lymphadenopathy, hepatosplenomegaly
- Immunosuppressed - pneumonia, hepatitis
- Cytomegalic inclusion disease - hemolytic anemia, jaundice, encephalitis
- Infants - deafness, and mental retardation
30
HBV
- covalently closed circular DNA
- IV drug use, transfuction, perinatally, sexually
- Infects hepatocytes, immune response causes cellular injury
- lymphocytic inflammation, apoptotic hepatocytes, progressive destruction of the liver, cirrhosis, hepatocellular carcinoma
31
S. Pyogenes
- Hyaluronidase in the cell wall is the most virulent factor
- Evades immune response via molecular mimicry
- Protein F - mediates adhesion to fibronectin
- Protein M - prevents phagocytosis by binding to fibrinogen and complement proteins
- Streptokinase - cleaves plasminogen to activate plasmin, dissolving clots
32
Diptheria
- Toxin inhibits synthesis of protein in host cells
- Pharyngitis, laryngitis, cutaneous
- Transmission - aerosol or through skin exudates
33
G - infections
- neisserial (meningitis, gonorrheae)
| - Pertussis
34
2 neisserial virulence factors
antigenic variation and capsule preventing it from being protected
35
Meningitis
- oral to nasopharynx into blood and up to meninges. -Children younger than 2 especially.
- Inhalation of respiratory droplets
36
Gonorrheae
- Acquired through sexual contact.
- Microbes engulfed by polymorphonuclear leukocyte are secreted in PMN righ exudate
- 2nd most common STI in US
- Females are asymptomatic
- males have symptomatic urethritis
37
Pertussis
- Whooping dough highly communicable
- Deadly in infants
- Attach to ciliated airway epithelium
- Toxemic state - fever, prolonged cough
38
Top two causes of death world wide
1. HIV
| 2. TB
39
Mycobacterium
- TB
- Multi-drug resistant, infection only represents the presence of organism, does not mean clinical dz
- Does NOT secrete toxins
- Virulence depends on properties of the cell wall.
- Bacterial dissemination to lymph node - dendritic cell presents bacterial antigen - T cell priming - triggers expansion of antigen-specific T cells - recruited to lung - granulomas containing TB
40
Secondary TB
- occurs in previously exposed host - more severe
| - Ghon complexes in apex of lung - granulomatous lesion
41
Malaria basic facts
- fecal oral route, occupy intestines or blood
| - plasmodium falciparum transmitted by female anopheles mosquitos
42
Malaria life cycle
-1/2 human, 1/2 mosquito
-sporozoite goes to liver, mitotic division
ruptures liver. goes to RBC , mosquito bites and takes, gametocytes from blood
43
Malaria pathogenicity
- Infects erythrocytes of any age
- RBCs clump together or adhere to small vessel endothelium - vascular occlusion - ischemia causes the manifestation of cerebral malaria
- Induce high levels of cytokines (TNF, INF) - suppress red cell production, cause fever, and stimulate NO production
- Antigenic variation to continuously modify surface proteins
44
Malarial resistance
- sickle celled anemia -
- carrier protected because there are no normal RBCs for the spirochetes to use
- shape cant hold them and are lysed quickly
45
Transmission and dissemination of microbes
- per-person, person-animal, insects
- Release microbes from the body like skin shedding, coughing, sneezing,
- STIs
- nosocomial
46
Microorganisms cause damage
- changes in cellular metabolism/proliferation - transformation
- release toxins that kill cells, releasing enzymes that degrade tissue components, damaging blood vessels, causing ischemic necrosis
47
Tissue Tropism
the cells and tissues of a host which support growth of a particular virus or bacteria. Some bacteria and viruses have a broad tissue tropism and can infect many types of cells and tissues. Other viruses may infect primarily a single tissue
48
ways microbes evade innate and adaptive immunity
- Modulation of surface structure to avoid recognition
- Inhibition of phagocytosis
- Inhibition of phagosome-lysosome fusion
- Escape from phagosome
- Modulations in signal transduction, gene expression, cell death
- Viral cytokines or soluble receptor homologs
- Inhibition of antigen presentation
- Hide from immune surveillance; viral latency
49
Mechanisms of viral injury
- direct cytopathic effects (reduce host macros), produce degradatiev enzyme and toxic proteins
- Anti viral immune response
- Transformation of infected cells
50
Decreased recognition by T cells
microbes alter MHC expression and impair antigen presentation; compromise lymphocyte functions
51
acute/transient cells viral infections
- measles
- poliovirus
- viral hemorrhagic fever
52
Poliovirus
- fecal-oral
- gastrointestinal --> BBB --> CNS
- skeletal muscle --> neural pathway --> CNS. effects brain stem = pyelonephritis
- 1/100 develop Sx
53
Viral Hemorrhagic fever
-transmission through infected insects or animal
caused by enveloped RNA viruses
-Infect endothelial cells, macrophages, and dendritic
-Sx: fever, HA, myalgia, neutropenia, hemodynamic deterioration, shock
54
Transforming Virus
EBV
55
EBV Patho
- oral cavity - enters B cell nucleus - viral replication - proliferation of B cells
- Uses different glycoproteins to infect epithelial cells and naiive B cells
- Priming of naiive T cells by antigen presenting cells
- In circulation - B cell lytic replication, shedding
56
EBV Outcome
- normal immune fx - asymptomatic or leads to mono
- immunodeficient - B cell blast, uncontrolled proliferation of infected cell leading to B cell neoplasms like nasopharyngeal carcinoma and hodgkin
57
Mono caused by EBV
naso/oro --> B cells --> lymphoid tissues --> infectious mono - benign, self limited dz with fever, fatigue, sore throat, lymphocytosis, lymphadenopathy, splenomegaly, hep, and rash
58
G+ Bacterial infection
- staphylococcal
| - Group A/B streptococcal
59
Staph infections
- G+. surface proteins cause adherence and evasion of the host immune system. Super antigen - toxic shock syndrome
- Cell wall anchored protein adhesions
- stimulates inflamm
- Immune invasion to B cells and iron acquisition
- Sx: resp infection, toxic shock, food poisoning, endocarditis, skin infections, osteomyelitis
60
Group A streptococcal
-most dangerous member is S. pyrogenes, which causes scarlet fever. Immune system recognizes via complement and use opsonization/type specific antibody. -Phagocytosis
61
Group B streptococcal
infection of the fetus, neonatal sepsis
62
Spirochetes
Syphillis
| Lyme
63
Syphilis
T. pallidium, sexual/transplacental transmission
64
Syphilis primary
primary: 3 weeks after contact, chancre in inguinal region will heal without therapy
65
Syphilis secondary
secondary: 2-10 weeks later, spread and proliferation of spirochetes in mucocutaneous tissues. lymphadenopathy, mild fever, malaise, weight loss
66
Syphilis tertiary
tertiary: 5 year latent period, cardiovascular, aortic valve insufficient, neurosyphillis, or benign with necrotic rubbery masses in bone, skin, and oral mucosa
67
Lyme dz
- B. burgforfi transmitted from rodents by ticks. Antigenic variation is virulence factor.
- Bacterium does NOT produce toxin, the pathology is due to the hosts immune response
68
Lyme dz stages
stage 1: spirochetes multiply at site of tick bite -erythema
stage 2: spirochetes spread hematogenously - arrythmias, joint pain
stage 3: Chronic arthritis - **can resemble SLE but no butterfly rash or photosensitivity**
69
Fungal infections
candidiasis
| Aspergillosis
70
Candidiasis
- normal flora of skin, mouth, and GI.
- Can cause superficial infection in healthy and visceral infections in neutropenic.
- chronic mucocutaneous candidiases in AIDS
71
Candidiasis virulence factors
adhesions that mediate binding to host cells, enzymes that help with invasiveness, catalases that help with intracellular survival by resisting phagocyte oxidative killing, ability to grow as biofilms
72
Asperigillosis
- air borne spores: causes allergy in healthy, and pneumonia in immunocompromised.
- Neutropenia is major risk factor
- Tends to invade blood vessels - thrombosis
73
Asperigillosis virulence factors
- adhesions to albumin, surfactant and ECM proteins
| - ONLY MICROBE that has antioxidant defenses such as mannitol and catalases
