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Pathology II > EXAM 2 Infectious Diseases > Flashcards

EXAM 2 Infectious Diseases Flashcards

1
Q

Prions

A
  • modified host protein that are infectious in nature

- Cause spongiform encephalopathies

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2
Q

Viruses

A
  • Obligate intracellular organisms
  • Contain DNA or RNA
  • transient acute illnesses, chronic dz, life-long latent infections
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3
Q

Bacteria

A
  • Cell walls either G+/-

- intracellular, extracellular, or facultative intracellular growth

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4
Q

Fungi

A
  • eukaryotes
  • Mycoses - superficual infections of the skin, hair, nails, “tinea”
  • Invasion of SubQ tissue (granulomas), deep infections
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5
Q

Protazoa

A
  • Motile, single celled eukaryotes
  • Replicate intracellulary or extracell
  • Transmitted sexually, contaminated food/water, or by blood sucking insects
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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

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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

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8
Q

Skin

A

keratinized outer layer, Low pH, fatty acids

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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)

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10
Q

Urogenital tract as a physical barrier

A
  • frequent bladder flushing with urine

- Low vaginal pH

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11
Q

Resp tract as a physical barrier

A

bronchial epithelium ciliary activity, mucous layer, defensins, IgA, alveolar macrophages

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12
Q

Adhesion - a bacterial virulence

A

bacteria bind to host cell surface

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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)

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14
Q

Invasion - a bacterial virulence

A

bacteria produce proteins that either disrupt host cell membranes or stimulate their own endocytosis into host cells.

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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

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16
Q

Toxins - a bacterial virulence

A

toxins cause tissue damage.

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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)

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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

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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)
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20
Q

Liver damage

A

bacterial adhesions = tissue damage and fibrosis

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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

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22
Q

chronic inflammation and epithelial injury

A

may lead to malignancy - H pylori and gastric cancer

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23
Q

Chronic/latent infections

A

HSV
VZV
CMV (cytomegalovirus)

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24
Q

Chronic/productive infections

A

HBV
HIV
S. Pyrogenes
Diptheria

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25
Q

HSV

A
  • double stranded DNA
  • entry thru mucous membrane - viral mult - lysis of cells - vescicles - ulcers
  • Asymptomatic viral shedding is unique to HSV
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26
Q

VZV

A
  • Mucous membranes, skin, neurons are infected
  • Acute = chickenpox
  • Latent in dorsal root ganglia, reactivates - infects sensory nerves - carry virus to skin - shingles
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27
Q

CMV

A

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
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28
Q

Most common opportunistic viral pathogen in AIDS?

A

Cytomegalovirus

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29
Q

Sx of CMV

A
  • fever, lymphadenopathy, hepatosplenomegaly
  • Immunosuppressed - pneumonia, hepatitis
  • Cytomegalic inclusion disease - hemolytic anemia, jaundice, encephalitis
  • Infants - deafness, and mental retardation
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30
Q

HBV

A
  • 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
Q

S. Pyogenes

A
  • 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
Q

Diptheria

A
  • Toxin inhibits synthesis of protein in host cells
  • Pharyngitis, laryngitis, cutaneous
  • Transmission - aerosol or through skin exudates
33
Q

G - infections

A
  • neisserial (meningitis, gonorrheae)

- Pertussis

34
Q

2 neisserial virulence factors

A

antigenic variation and capsule preventing it from being protected

35
Q

Meningitis

A
  • oral to nasopharynx into blood and up to meninges. -Children younger than 2 especially.
  • Inhalation of respiratory droplets
36
Q

Gonorrheae

A
  • 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
Q

Pertussis

A
  • Whooping dough highly communicable
  • Deadly in infants
  • Attach to ciliated airway epithelium
  • Toxemic state - fever, prolonged cough
38
Q

Top two causes of death world wide

A
  1. HIV

2. TB

39
Q

Mycobacterium

A
  • 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
Q

Secondary TB

A
  • occurs in previously exposed host - more severe

- Ghon complexes in apex of lung - granulomatous lesion

41
Q

Malaria basic facts

A
  • fecal oral route, occupy intestines or blood

- plasmodium falciparum transmitted by female anopheles mosquitos

42
Q

Malaria life cycle

A

-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
Q

Malaria pathogenicity

A
  • 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
Q

Malarial resistance

A
  • 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
Q

Transmission and dissemination of microbes

A
  • per-person, person-animal, insects
  • Release microbes from the body like skin shedding, coughing, sneezing,
  • STIs
  • nosocomial
46
Q

Microorganisms cause damage

A
  • changes in cellular metabolism/proliferation - transformation
  • release toxins that kill cells, releasing enzymes that degrade tissue components, damaging blood vessels, causing ischemic necrosis
47
Q

Tissue Tropism

A

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
Q

ways microbes evade innate and adaptive immunity

A
  • 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
Q

Mechanisms of viral injury

A
  • direct cytopathic effects (reduce host macros), produce degradatiev enzyme and toxic proteins
  • Anti viral immune response
  • Transformation of infected cells
50
Q

Decreased recognition by T cells

A

microbes alter MHC expression and impair antigen presentation; compromise lymphocyte functions

51
Q

acute/transient cells viral infections

A
  • measles
  • poliovirus
  • viral hemorrhagic fever
52
Q

Poliovirus

A
  • fecal-oral
  • gastrointestinal –> BBB –> CNS
  • skeletal muscle –> neural pathway –> CNS. effects brain stem = pyelonephritis
  • 1/100 develop Sx
53
Q

Viral Hemorrhagic fever

A

-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
Q

Transforming Virus

A

EBV

55
Q

EBV Patho

A
  • 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
Q

EBV Outcome

A
  • 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
Q

Mono caused by EBV

A

naso/oro –> B cells –> lymphoid tissues –> infectious mono - benign, self limited dz with fever, fatigue, sore throat, lymphocytosis, lymphadenopathy, splenomegaly, hep, and rash

58
Q

G+ Bacterial infection

A
  • staphylococcal

- Group A/B streptococcal

59
Q

Staph infections

A
  • 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
Q

Group A streptococcal

A

-most dangerous member is S. pyrogenes, which causes scarlet fever. Immune system recognizes via complement and use opsonization/type specific antibody. -Phagocytosis

61
Q

Group B streptococcal

A

infection of the fetus, neonatal sepsis

62
Q

Spirochetes

A

Syphillis

Lyme

63
Q

Syphilis

A

T. pallidium, sexual/transplacental transmission

64
Q

Syphilis primary

A

primary: 3 weeks after contact, chancre in inguinal region will heal without therapy

65
Q

Syphilis secondary

A

secondary: 2-10 weeks later, spread and proliferation of spirochetes in mucocutaneous tissues. lymphadenopathy, mild fever, malaise, weight loss

66
Q

Syphilis tertiary

A

tertiary: 5 year latent period, cardiovascular, aortic valve insufficient, neurosyphillis, or benign with necrotic rubbery masses in bone, skin, and oral mucosa

67
Q

Lyme dz

A
  • 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
Q

Lyme dz stages

A

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
Q

Fungal infections

A

candidiasis

Aspergillosis

70
Q

Candidiasis

A
  • normal flora of skin, mouth, and GI.
  • Can cause superficial infection in healthy and visceral infections in neutropenic.
  • chronic mucocutaneous candidiases in AIDS
71
Q

Candidiasis virulence factors

A

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
Q

Asperigillosis

A
  • air borne spores: causes allergy in healthy, and pneumonia in immunocompromised.
  • Neutropenia is major risk factor
  • Tends to invade blood vessels - thrombosis
73
Q

Asperigillosis virulence factors

A
  • adhesions to albumin, surfactant and ECM proteins

- ONLY MICROBE that has antioxidant defenses such as mannitol and catalases

Pathology II (10 decks)

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