Infectious diseases Flashcards
1
Q
Where does the majority of the bodys normal flora exist
A
Large intestine >10 to the power of 14
2
Q
Where are the other sites of the bodys flora
A
Skin
Oral cavity
3
Q
What type of bugs occupy the skins normal flora
A
Majority are obligate anaerobes
4
Q
What are the 4 types of common flora
A
- bacteria (i.e. prokaryotic cells)
- fungi (e.g. yeast Candida albicans and malassezia furfur)
- viruses (e.g. herpes group)
- possibly parasites (e.g. intestinal amoebae)
5
Q
Why is the skin not an ideal environment for many microbes
A
- resident microbial flora
- dryness
- acid pH (~5.5)
6
Q
What type of environemnt in the body fo flora microbes predominate?
A
High humidity/ nutrient rich areas
7
Q
What microbiral flora is found in the upper intestinal tract
A
Enterococcus faecelias
8
Q
What anaerobes are predominantly found in the mouth
A
Porphyromonas, Prevotella and Peptostreptococcus genera
9
Q
What antibiotics are anaerobes in the mouth susceptible to
A
are susceptible to amoxycillin/clavulanic acid (coamoxyclav) combinations.
10
Q
What abx are good for bite wounds and why
A
Augmentin (anaerobes in mouth are sensitive to this)
11
Q
Is candida albicans a common skin commensal?
What circumstances allow it to colonise?
A
No
Excess hydration (i.e nappy rash) can allow to it transiently colonise
12
Q
What is an important difference between gram positive and gram negative cell walls.
A
Gram positive has a thick cell wall with NO outer membrane.
Gram negative has a thin cell wall with an outer membrane
13
Q
What are the 3 important features of the outer membrane of the gram negative cell wall
A
LPS (lipopholysaccaride which is made up of the following)
- lipid A classical endotoxin responsible for toxicity
- polysaccharide core
- terminal repeating units of ‘O’ somatic antigenic side chains, both important taxonomically
14
Q
What is the function of the gram negative outer membrane
A
- Prevents leakage of periplasmic proteins
- Protects the cell (in enteric bacteria) from bile salts and hydrolytic enzymes of host environment
- Proteinaceous pores (porins) -> allow passage of LMW solutes (large antibiotic molecules penetrate it slowly)
- may act as a barrier to the entry of antimicrobials, as most antibiotics are not lipid soluble, so can’t get through OM
15
Q
What does the cell wall of gram positive bacteria consist of
A
- Peptidoglycan containing strands of tecihoic acid, proteins and CHO (depending on the species)
- Not protected by an outer membrane (therefore susceptible to degradation by lysozyme)
16
Q
How does the cell wall of mycobacteria differ from both gram positive and gram negative bacteria
A
contains large amounts of lipid , responsible for intracellular survival, adjuvant effect and survival in presence of acid
17
Q
What happens when Gram negative LPS is injected intravenously
A
- produce arteriolar dilatation
- activate complement through the alternate pathway
- injure endothelial cell membrane
18
Q
Under optimal conditions how fast can bacteria divide
A
10 to the power of 8 progeny in less than 24 hours
19
Q
How do bacteria divide and how often
A
Binary fission every 10-20 minutes in vitro
20
Q
What conditions do aerobic bacteria divide in
A
need air (i.e. oxygen as the hydrogen acceptor) to grow and divide
21
Q
What conditions do anaerobic bacteria divide in
A
Only grow in the abscence of O2
22
Q
What happens to obligate anaerobes exposed to oxygen
A
sensitive to oxygen, gets killed after brief exposure
23
Q
What conditions do facultative anaerobes grow in
A
Anaerobe or aerobically
24
Q
What conditions do microaerophilic microbes grow in
A
grow best under slightly reduced oxygen levels
25
What 3 ways are genes transferred between cells
Transformation
Transduction
Conjugation
26
Explain how transformation works and which bacteria is is common in
- recipient cell takes up DNA released from donor cell
- common in pneumococci, meningococci
27
Explain how transduction works and which bacteria it is common in
DNA transferred from donor cell to recipient via a virus (bacteriophage) vector
- common in staph
28
Explain how conjugation works and which bacteria it is common in
transfer always from donor to recipient via the fertility (F) factor, typically a plasmid or transposons (movable
segments of DNA)
29
What is a plasmid
Extra-chromosomal fragment of DNA
usually circular
30
5 reasons why plasmids are important
1. may be a/w virulence
2. are important in the transfer of drug resistance
3. readily transmissible between related and unrelated bacterial strains
4. often carry genes responsible for virulence and antibiotic resistance (e.g. resistance or R plasmids)
5. whole or parts of plasmids may incorporate into chromosomal DNA
31
4 facts about genes for antibiotic resistance
1. are often found in plasmids
2. may be incorporated into cosmids
3. often occur in circular DNA molecules
4. are useful markers in recombinant DNA technology
32
What are the 2 types of toxins in bacteria
Endotoxin
Exotoxin
33
Which are more potent, endotoxins or exotoxins and why
exotoxins, they have a more specific site of action
34
Where do exotoxins produce their effect
Locally (may be severe eg gas gangrene)
OR distant from site of entry e.g Tetatnus
35
Which bacteria secrete exotoxins (be specific)
- Corynebacterium diphtheria
- clostridium difficile
- staph. aureus )staph enterotoxins)
- pseudomonas aeruginosa (one of the few gram negatives to excrete a significant exotoxin)
- tetanus toxins
36
Are exotoxins proteins or lipids
Proteins
37
Are endotoxins proteins or lipids
Lipids
Lipid A portion of LPS!
38
When are exotoxins secreted
During growth of may gram positive bacteria
39
Are exotoxins immunogenic
Yes, the invoke an adaptive immune response. Stimulate the production of antibodies which provide a good measure of immunity.
40
What bugs are endotoxins typically found in
Gram negative, e.g E.coli and pseudomonas
41
What normally causes shock in patients with gram negative septicaemia
1. bacterial endotoxins
2. bacterial LPS
3. products of complement activation
42
Are endotoxins more inflammatory or immunogenic
inflammatory
Initiate a series of events, promote cytokines and TNF with subsequent vascular endothelial damage
43
How do exotoxins differ from endotoxins
- Convertible into toxoids
- Cell wall associated
44
List the 5 ways that tissue responds to inflammation
1. Exudative inflammation
2. Necrotising inflammation
3. Granulomata's infalammtion
4. Interstitial mononuclear
5. Cytopathic-cytoproliferative
45
What causes exudative inflammation
Pyogenic infection
* by extracellular G+ve cocci and G-ve rod
* secondary to increased vascular permeability & leukotaxis of neutrophils attracted by bacterial peptides
* sizes of exudative lesions vary from small abscesses to entire lobe of lung
46
What causes necrotising inflammation
1. uncontrolled viral infection, e.g. fulminant HBV infection,
2. secreted bacterial toxins (e.g. those of clostridium perfringes)
3. contact-mediated cytolysis of host cells by protozoa (e.g. Entamoeba histolytica)
47
What causes granulomatos inflammation
intracellular organisms
48
What causes interstitial mononuclear inflammation
viruses, intracellular bacteria, spirochetes, intracellular parasites, helminthes
- includes mostly lymphocytes, e.g. chancre of primary syphilis, or macrophages (e.g. granulomas of mycobacteria),
depending on the characteristics of the organism and the host
Chronic inflammation
49
What is cytopathic-cytoproliferative infections characterised by and what might they show
- characterized by virus-mediated damage to individual host cells in the absence of host inflammatory response
- may show
a. inclusion bodies, e.g. CMV
b. polykaryons, e.g. measles viruses
c. Blisters, e.g herpes
d. Warty changes, e.g. papillomaviruses
50
Describe the shape staph aureus
Gram positive cocci, grapelike clusters
51
Common sites for staph aureus infection
skin, pharyngitis, pneumonia, endocarditis
major cause of infection in persons with severe burns and surgical wounds
52
Virulence factors associated with staph aureus
- surface proteins,involved in adherence to host cells
- enzymes that degrade host proteins (coagulase)
- toxins that lyse host cells and cause
a. scalded skin syndrome (toxins)
b. food poisoning (enterotoxins)
c. shock (endotoxin and toxic shock syndrome toxin ! which is a superantigen)
53
What type of infection does staph aureus cause (i.e type of effect on tissue)
pyogenic
54
What antibiotic is the only reliable emperiic treatment for MRSA, + what other abx may be useful for some strains
Vancomycin
Fusidic acid
55
Abx of choice for SA septicemia when MRSA is not an issue
Flucloxacillin
56
What antibitiocs are used for MSSA
- Cefalexin
- Augmentin
- Flucloxacillin
- Cefuroxime
57
What do strep looks like
gram positive cocci in pairs or chains
58
How are strep classified
According to their surface antigens
59
What does S. pneumoniae cause
major cause of community acquired pneumonia and causes adult bacterial meningitis
60
What does S pyogenes cause
produces pharyngitis, Scarlet fever, impetigo, rheumatic fever, glomerulonephritis
61
What does S agalactiae cause
causes neonatal sepsis and UTI
62
What does enterococcus faecalis and S viridians cause
endocarditiis
63
What does S mutans cause
dental caries
64
list 5 streptococcal virulence factos
1. Rodlike surface M-proteins and a polysaccharide capsule that prevent bacteria from being phagocytosed
2. A pneumolysin that lyses host cells and waste host complement
3. Exotoxins that produce the rash in scarlet fever
4. proteases that degrade chemotactic peptides and immunoglobulins
5. lactic acid that demineralises tooth enamel
65
2 side effects of streptococcus pneumonia
- blood shunting through affected lung
- Does NOT commonly cause residual fibrosis in affected area of lung
66
Does pneumococcal pneumonia cause necrosis and explain why
Pneumococcal pneumonia causes inflammation without significant lung necrosis BECAUSE
Pneumococci include chemotaxis, but elaborate no major toxins
67
What organism causes lobar pneumonia, who does it affect and does it leave functional abnormalities
Strep pneumoniae
On resolution leaves a few functional abnormalities
Disease of healthy young adults
68
What is strep pneumonias main virulance factor and what impact does this have
Capsule
Allows bacteria to escape phagocystosis (therefore bacteremia is common)
69
What type of bacteria is Nesiseria gonorrhea
encapsulated, G-ve diplococcus
70
What infections does Neisseria gonorrhea cause
- urethritis, pharyngitis, or proctitis
- may cause urethral strictures and chronic infections of the epididymis, prostate and seminal vesicles
- may infect the fallopian tubes (salpingitis) ! tubo-ovarian abscesses and scars, sterility, and ectopic pregnancy
71
How does N gonorrhea cause disease
binds to host epithelial cells via pili, which show antigenic variation based on intragenomic recombination and on
recombination after incorporation of exogenous DNA from lysed gonococci
72
Which organism is developing increasing resistance to vancomyinc
Eneterococcus faecilias
73
What is becoming an increasingly important nosocomial pathogen
Eneterococcus faecilias
74
E coli is a major causative agent of what 3 things
1. haemorrhagic colitis
2. bacteraemic episodes in the early stages of peritonitis
3. osteomyelitis of IV drug abusers
75
Where is pseudonomas widely distributed
Hospitals
Burns units
76
Is pseudonomas readily contained by host defences
yes
77
important pathogen following faecal leakage during colonic surgery
Gram negative anaerobes
78
Important pathogens in lung abscesses following aspiration
Gram negative anaerobes
79
Frequently associated with oxygen tolerant microbes
Gram negative anaerobes
80
What type of organism is PJP
unicellular protozan (fungus)
81
Who gets PCP
Immunocompromsied people
82
When does PCP attach in HIV patients
CD4 <200
83
Are antibodies to PCP helpful
No
84
What type of infection does PCP cause?
infection causes a diffuse or patchy pneumonia, which alveolar spaces filled with a foamy stuff ! mainly proliferating
parasites and cell debris
85
What type of inflammatory reaction is seen and not seen in PCP
mainly fluid and protein with perhaps hyaline membranes, but few cells
granulomatous reaction is not seen
86
Who carries Hydatid disease
Sheep/dogs in autralasia
zoonosis
87
How do humans become infected with Hydatid disease
- tape worm segments (proglottids) containing eggs (ova) are in the dog’s faeces
- Human disease results from ingestion or inhalation of ova of the tapeworm (Echinococcu granulosus) which resides in the dog intestine
88
How do dogs become infected with Hydatid
Dogs, but NOT humans, become infected by eating sheep offal (e.g. liver, lungs) containing hydatid cysts
89
How do you treat Hydatid disease
the only really effective treatment of hydatid disease in humans, is surgical removal of cysts
Chemotherapy (e.g. mebendaole type drugs) is generally ineffectively
90
What infections are typically associated with lymph nodes
1. toxoplasmosis
2. secondary syphilis
3. pulmonary tuberculosis in childhood
91
how is HIV trasmitted
Blood
92
What does HIV show tropism to
CD4 bearing cells
93
Why cant a vaccine be made for HIV
Genetic variation between isolates
94
What is hookworm disease
Hookwroms live in small intestine of humans, where they are attached to the mucosa
they suck blood and large numbers feeding in such a manner can produce a microcytic, hypochromic anaemia, esp. in
malnourished hosts
95
What is the important hookworm in south east asia
Ankylostoma duodenale
96
How do humans become infected with hook worms
- Eggs containing developing larvae are shed in the faeces
- in the soil, these develop into free-living juveniles which after some weeks develop into filariform larvae which invade man
by penetrating the exposed skin, usually on the feet
- after migration via the blood to the lungs, these larvae break into the alveolar spaces to migrate to the glottis and are
swallowed
- upon arriving in the small intestine, they develop into adults
- larval passage through the lungs can induce a mild transient atypical broncho-pneumonia accompanied by eosinophilia
