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Med Micro Exam IV Flashcards

1
Q

Most common cause of UTI

A

bacteria

E.coli are responsible for 80% of community acquired infections and 40% of nosocomial infections

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2
Q

What is the entry of UTI

A

Entry from the urethra to the bladder

Through the catheter to the bladder in nosocomial 

More serious spread urethra (urethritis)  → bladder (cystitis)  → ureters (urethritis) → kidney (pyelonephritis)  → blood (sepsis)
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3
Q

Neurological conditions of UTI

A

Interrupt urine flow

i. Multiples sclerosis
ii. Paraplegia
iii. Spinafida

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4
Q

other conditions of UTI

A
  1. tumors, bladder stones, pregnancy, prostate problems
  2. sexual intercourse
  3. women- female anatomy, 14% increased risk
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5
Q

characteristics of e.coli

A

gram negative

ii. Facultative anaerobe
iii. Common intestinal microbe

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6
Q

Virulenece factors of E.coli

A
  1. Peritrichous
2.	Uropathogenic  E.coli 
Differentiated by
a.	O – LPS antigen 
b.	H – flagella antigen 
c.	K – capsule antigen
  1. P fimbriae
    a. Polyneuphritis – associated pili
    b. Attachment to urethra and bladder epithelium
    c. 10 different genes associated
  2. Capsule
    a. Attachement
    b. Resist phagocytosis
  3. Hemolysin
    a. Lysis triggers cell damage which leads to inflammation and kidney damage
  4. Siderophores
    a. If it enters the blood, competes for iron binding
  5. LPS
    a. If it enters the blood , it can cause endotoxemia
  6. Exotoxin
    a. Shigatoxin toxins
    b. Heat stable toxins
  7. Antigenic phase variation
    a. Occurs in capsule, flagella, and pili genes
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7
Q

Defenses against UTI

A

i. Few microbes
1. Commonly skin and vaginal microbes contaminate the urethra
ii. Main defense
1. Urine flow (flushing action)
iii. Other defenses
1. Urine is acidic
2. Chemicals
3. Mucus membrane

iv. Superficial infection
1. Colonization in mucus membrane area
2. Leads to an inflammatory response
a. Recruitment of immune cells
3. Can get IgG and IgA

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8
Q

UTI symptoms

A

i. Asymptomatic
1. Usually in elderly and catheterized
ii. Acute disease
1. Rapid onset of S and S
a. Frequent, urgent need to urinate
b. Painful, burning
c. Cloudy urine
i. Bacteria ( bacteriuria)
ii. WBS (pyuria)

iii. Polyneuphritis
1. Upper UTI
2. 75% caused by E.coli
a. Often lead to sepsis
3. Signs and Symptoms
a. UTI and S&S + fever
b. Tender in back
c. Inflammation in kidneys
i. Can lead to kidney damage and hypertension ( increase in blood pressure)

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9
Q

Diagnosis of UTI

A

Urinalysis

i. Genital track infections have pyuria but no bacteriuria
ii. Midstream
1. Immediate testing to prevent overgrowth
iii. If catheterized patient
1. Any bacteria is significant
iv. Look at bacteria number per ml and diversity
1. 105/ mL single species
v. Pyuria
1. WBC count
2. > 10 WBCs/ mL
vi. Kirby Bauer test
1. Determine susceptibility
vii. Pyelonephritis
1. Blood culture
2. Gram stain from blood and urine
3. Urine is positive for leukocyte esterase (enzyme from neutrophils)

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10
Q

Treatment for UTI

A

a. An uncomplicated case of UTI/ cystitis
i. 40% of patients resolve within a month
ii. Oral antibiotic
1. One dose or three day dose
a. A best guess or from Kirby Bauer results
2. Sulfa drugs
3. drug resistant strains
a. fluoroquinolones
b. ampicillin
4. drink lots of fluids
a. increase flushing
i. cranberry juice because of decreased pH and it changes the membrane, shape, fimbriae, of E. coli in vitro
iii. symptomatic and asymptomatic patients are treated
1. all are treated because of the risk of kidney infection
iv. follow up analysis of urine
1. at least two days later
2. urinalysis, culture, or culture of the blood
3. complicated UTI
a. pyelonephritis
i. at least one kidney infected
ii. iv antibiotics that are broad spectrum (cephalosporin)
iii. usually for greater than 10 days
4. catheter patient
a. catheter is removed, if possible

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11
Q

Defenses of the genital tract

A

i. Mucus membrane
ii. IgA present prevents attachment of some microbes
iii. No flushing action
iv. Microbiota
v. Estrogen

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12
Q

Microbiota of males and females

A
  1. Males
    a. Considered sterile except around the urethra
  2. Females
    a. Lactobacillus, Streptococcus, anaerobes, some gram negative bacteria, 10-25% of women have yeast Candida albicans
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13
Q

Transmission of sti’s

A

i. Usually very direct
ii. Fomites can be involved if it is a quick infection
iii. The microbes don’t survive long outside of the host
iv. Easier to control spread

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14
Q

Risk factors of STI

A

i. Increased sexual activity of any sort
ii. Increased partners
iii. Open wounds
iv. Uncircumcision in males

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15
Q

Chlamydia caused by ?

A

i. Chlamydia trachomatis
1. Bacteria, serotypes D-K are STI
2. Obligate intracellular parasites

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16
Q

Chlamydia entry to body

A
  1. Enters the body through abrasions in mucosa and infect columnar epithelial cells
    a. Elementary body attaches to the epithelial cell
    i. Receptor is unknown
    ii. Enters through endocytosis
    b. After entry, differentiation into reticulate body ( RB form) this form with replicate in cells
    i. RB form goes through binary fission in cells > more EB
    c. Differentiate into EBs
    d. EDs released by lysis > pathogenesis ( also due to inflammatory response)
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17
Q

Urethritis

A

a. Caused by Chlamydia and Neisseria gonorrhoeae
b. If untreated leads to epididymitis
1. Epididymitis
2. Uterine tube scaring which leads to sterility

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18
Q

Disgnosis of Urethritis

A

i. Requires urethra/ vaginal swab analysis
ii. Culture in cells
iii. Stain inclusion bodies with iodine ( glycogen)
iv. Antigen detection (immunofluorescence)
v. DNA detection (PCR) more sensitive and more expensive

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19
Q

Treatment of Urethritis

A

i. Doxycycline
1. Inhibits tRNA entry/ translation
2. Greater uptake in prokaryotes
3. Penetrate cells well
a. Intracellular
4. Treat gonorrhea patients as well
a. Common co-infection

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20
Q

PID

A

Pelvic Inflammatory Disease

i. Caused by Chlamydia and N. gonorrhea

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21
Q

Transmission of PID

A

ii. Microbe binds to sperm cells and transported into uterine tubes

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22
Q

Treatment of PID

A
  1. Doxycycline and Cephalosporin
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23
Q

Gonorrhea antigenic variation is due to what?

A

several virulenece factors

24
Q

Antigentic variation of Gonorrhea

A

i. Due to multiple genes and recombination
ii. Regulated by different environmental ques
1. Changes in iron concentration
iii. Leads to evasion of immunity
iv. Virulence factors
1. Pili- inhibit phagocytosis
2. Por- facilitate invasion of epithelial cells
a. Interfere with neutrophil degranulation, phagolysosome fusion and complement
3. Opa- binds to CD4 ( helper T cells)
a. Prevent activation and proliferation
4. Los
5. Rmp proteins
a. Inhibit complement
b. Prevents anti-Por antibody from biding
6. IgA protease
a. No capsule
i. N. gonorrhea

25
Attachment of Gnorrhea microbe
vi. Attachment non-ciliated epithelium on urethral or vaginal mucosa 1. Pili, opa, LOS 2. Endocytosis initiated by Opa a. Replication within vacuoles 3. Exocytosis a. Into the underlining tissue, sub-mucosa
26
Immune response to Gonnorrhea
1. Low levels of serum and secretory Ig (IgA) a. Antigenic variation b. IgA protease c. Rmp proteins d. Can get repeated infection e. Chronic inflammation (LDS and CW) and fibrosis
27
Diagnosis of Gonorrhea
sis 1. Symptomatic men a. Gram negative diplococci in discharge 2. Asymptomatic women a. Gram-stain isn’t diagnostic ( complication microbiota in women ) 3. MH and 5% cos and lysed RBCs i. Heating at 56C b. V- inhibits CW , kills G+ c. C kills G- not Neisseria d. N- kills fungi e. Rapid antigen detection is becoming more common
28
Treatment Gonorrhea
a. Neisseria produces penicillinase b. Cephalosporin i. Ceftriaxone ii. Broad spectrum iii. Resistant to b-lactamase c. Doxycycline i. Treat Chlamydia d. Treat partners e. Infants i. Antibacterial drops ii. Drops have erythromycin or tetracycline iii. No vaccine
29
Prevent of Gonorrhea
condom usage
30
Trichomoniasis
a. Most curable STI in US i. 7.4 million new cases a year b. Found in urethra and vagina, motile c. Common co-infection with Neisseria and Chlamydia d. STI e. Can transfer through fomites like toilet seats
31
Diagnosis of Trichomoniasis
i. Based on microscopy of discharge, urine/semen ii. Metronidazole 1. Anti- protozoans and anaerobes
32
9. Genital Warts and Cervical Cancer entry
b. Enters through breaks in mucosa i. Infects stratifying basal epithelial cells ii. Requires dividing cell 1. Infect nucleus- uses host cell machinery iii. Enters via receptor mediated endocytosis iv. Oncogenic proteins E5-7 1. Drive epithelial cell division v. Virus is released as cells are sloughed off vi. No good culturing system vii. Virus may go latent 1. 4-20 years
33
Diagnosis of Warts
1. Pap smears: routine annual exam 2. Early diagnosis is key 3. PCR detection a. Episomal from bacteria b. Integrated from malignant
34
Treatment of Warts
1. Warts a. Imiquimod i. Gel that increases IFN production b. Cancerous lesions or pre- cancerous i. Surgical removal 2. HPV Vaccine a. Gardasil HPV 18, 18, 6, and 11 b. Subunit vaccine of capsid protein c. Empty capsid shells are the immunogen i. Non-infectious host antigenic d. Recommended for girls 11-26 years old
35
Gi defenses
i. pH 1.2-3 b. 10^11 bacterial cells/ g, > 100 billion i. (more than 40% of the mass)
36
Gastritis
i. Inflammation of the stomach lining ii. S+S abdominal pain, upset stomach, nausea, bloating, decreased appetite, weight loss, vomiting ( with blood) iii. Helicobacter pylori infection 1. Increased risk- excessive alcohol consumption, non-steroidal anti-inflammatory drugs (NSAIDS), some surgeries
37
e. Helicobacter pylori
i. Peritoneal cavity ii. Urea >(urease) > ammonia and CO2 iii. Pathogenesis 1. Fecal-oral transmission of the microbe 2. H. pylori penetrates the mucus layer a. Cell shape and flagella help in the penetration layer b. Attachment via adhesions c. Replication
38
Urease in GI
1. Increased pH 2. Neutralize stomach acid 3. Ammonia, protease, phospholipase a. Results in damage of epithelium 4. Mucus layer thins which leads to inflammation and then gastritis 5. Continual inflammation and damage lead to ulceration 6. Gastrin increases gastric acid production by parietal cells a. Increased gastrin leads to increased acidity b. Decreased gastrin leads to neutral pH , hypochlorhydia and achlorhydia
39
Peptic ulcers
i. About 80% of infected individuals are asymptomatic | ii. Only about 10-15 % will develop ulcers or caner remaining develop gastritis
40
Therapy of Peptic ulcers
iii. Triple therapy 1. Proton pump inhibitor – decrease stomach acid 2. Clarithromycin- macrolible: inhibits protein synthesis 3. Amoxicillin if allergic to beta lactams, metronidazole
41
Treatment of peptic ulcers
iv. Pro-biotics | 1. Lactobacillus and Bifidobacterium
42
Defenses of CNS
i. Brain – barrier ii. Meninges- membranes, physical barrier iii. Cerebral spinal fluid (CSF), protects against physical shock. 1. Nutrient rich fluid 2. Immunoprivileged site iv. Blood brain barrier
43
Why are infection of NS rare?
i. Disruption of barriers 1. Trauma 2. Surgery ( head, neck surgery ) 3. Chronic inflammation ii. Infection of barrier cells or microbe-triggered transport through barrier cell 1. Streptococcus pneumoniae iii. Most common route of infection 1. Blood/lymph leads to CNS iv. Less commonly 1. Microbes from the PNS to CNS a. Rabies virus, herpes virus, HSV and V7Z ( chicken pox), tetanus toxin
44
Diagnosis of CNS
b. Encephalitis, meningitis
45
Fungal mennigitis
a. Inhalation to lungs to internalized by alveolar macrophages to blood/lymph to CNS
46
Capsules of F. mennigits
b. Capsule – 5 capsules i. Only produced in the host 1. Low glucose, 5% CO2, low Fe 2+ ii. Inhibit phagocytosis iii. Binds C3 and inhibits opsonization iv. Interferes with antigen presentation 1. CMI and IG v. Some capsule antigens are shed into blood and systemically suppress immune responses
47
Melanin
i. In CW ii. Protect against phagocytosis iii. Contributes to neurotropism iv. Inhibits radical formation, protect against antimicrobial peptides v. Protects against temp changes and iron reduction vi. Clearance is due to 1. T cell response is essential a. Capsule is not antigenic i. Neutralizing IG
48
S&S of F. menningitis
Signs and Symptoms 1. Severity depends on immune status 2. Fever, headache, dizziness, visual disturbances, abnormal mental status, seizures 3. 10- 15% develop skin lesions
49
Treatment of F. mennigits
1. Amphotericin B and Flucytosine for two weeks a. A binds to ergosterol and created ion channel b. Same toxicity because it can bind cholesterol c. F pyrimidine analog ( DNA synthesis) – 2 weeks d. Followed by 8 weeks with Fluconazole i. Inhibits cytochrome p450 and membrane synthesis e. AIDS patient – lifelong therapy f. Non AIDS patients have 26% relapse rate g. Follow up with spinal tap
50
Rabies virus attachment
i. G protein binds to nicotinic acetylcholine receptors 1. Rec-mediated endocytosis ii. Fusion of envelope with endosome membrane iii. Uncoating in cytoplasm iv. Biosynthesis 1. Viral RdrRP transcribe +ssRNAs which leads to translated by host ribosome 2. RdRp – ssRNA to full length +ssRNA (intermediate) to –ssRNA v. Assembly0 1. Release by budding a. Very little cell damage
51
Rabies transmission
1. Zoonotic infections a. Infects all warm-blooded animals 2. Transmitted through saliva during bite a. Limited replication in striated muscle cells b. Enters peripheral nerves i. Retrograde axonal transport to CNS 200mm/day vii. Incubation
52
Incubation of Rabies V.
1. 10 days to 6 months 2. Spread to brain a. Rabies encephalitis 3. Spread to highly enevated tissues a. Salivary glands b. Como leads to death 4. Little immunity a. Early- no IG or CMI b. Late- begin to detect neutralizing Ig (serum and CSF) c. Incubation period i. 4 days to 6 years ii. Wound severity iii. Amount of virus iv. CNS proximity v. Immune status of host
53
S&S of Rabies
2 – 14 days leads to coma and then death i. Approx. 100% mortality e. Diagnosis
54
Diagnosis of Rabies
i. Neurological symptoms and history of bite wound ii. Confirm by RNA or virus antigen detection iii. PCR and Immunofluorescence 1. Skin / brain biopsy 2. Corneal smear
55
Preventtiion of Rabies
f. Live recombinant virus | i. Wildlife management

Medical Micro (3 decks)

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