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Term 3/4 Flash Cards > Micro - UTIs, HIV, AIDS > Flashcards

Micro - UTIs, HIV, AIDS Flashcards

1
Q

UTI facts

A

Ascending more common than descending (S. aureus)

More commonly found in:

  • Women - d/t shorter urethra
  • Children <2 (only show fever and different. urination patterns)
  • Older adults
  • Pregnant women (smooth muscle relaxation, urethral dilation, greater chance to progress to pyelonephritis). Untreated → premature or low birth wt. Give abx to prevent fetus from being colonized w/Grp B Strep

Recurrence - 3+ in 1 year (w/same microbe or new infection, different strain)

Risk factors - female, sex, diaphragm w/spermicide (kills Lactobacillus), hx of recurrent infection, catheters

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2
Q

Cystitis clinical presentation

A 
Pelvis pressure (women)
Fullness in rectum (men)
Lower abd discomfort
Frequent, burning, painful urination
Low-grade fever (sometimes)
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3
Q

Acute pyelonephritis clinical presentation

A
  • Upper back + flank pain
    High fever
    Shaking, chills, nausea
    Vomiting
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4
Q

Complicated UTI

A

Predisposing anatomic, fxn’l, or metabolic abnormalities -> requires more aggressive evaluation and follow-up

Causative bacteria: E. coli, (S. saprophyticus?), K. pneumoniae, Proteus mirabilis, Enterococcus, Pseudomonas aeruginosa

Tx: antibiotics based on sensitivity testing (urine culture)

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5
Q

Uncomplicated UTI causative organisms

A

Anyone who is young and healthy: no specific pre-disposing factors or structural abnormalities

E. coli most common. Virulence factors:
Adhesins - (Pili, Type I fimbriae, etc)
Hemolysin A - lyses cells → cytokine release → inflam)
Siderophores
Ig proteases
Ureases (P. mirabilis)
Factors promoting colonization

Others: P. mirabilis, S. saprophyticus, K. pneumoniae

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6
Q

UTI dx and tx

A

Clean catch urine specimen (unspun, midstream): Pus + bacteria, WBC, RBC

  • Culture and sensitivity (not often done, but best to know abx sensitivity)
  • No simple test to distinguish UUTIs and LUTIs

Leukocyte esterase test
Presence of nitrates -> nitrites
UTI symptoms + leukocytes = adequate to d/x

UTI symptoms + pus but can’t isolate organisms → Mycoplasma or Chlamydia

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7
Q

HIV virus class

A 
Retrovirus (Lentivirus)-slow viruses assoc w/ neurologic & immunosuppressive disease. Class VI RNA virus: s/s +, RT
2 copies (+) RNA noninfectious. RT → d/s provirus → integrates into host genome → mRNA → structural + NS proteins

4 accessory genes (vif, vpr, vpu, nef)
2 regulatory genes (virus-host interactions)
~1500 interactions between HIV-1 and human proteins

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8
Q

HIV characteristics

A

Host derived viral membrane. More orfs than simple retrovirus. 9 orfs -> 15 proteins
All Retroviruses encode:
Gag - grp spec Ag (core, capsid proteins)
Poly - enzs for transcription: RT, protease, integrase
Env - glycoproteins (gp120, gp41), spike proteins that stick out of envelope

Virus/host interactions:
2 regulatory genes:
tat-modulates gene expression
rev-nuclear/cyto shuttling
4 accessory genes
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9
Q

HIV life cycle

A

Binds/fusion-CD4+ T cell receptor/coreceptor
RT: ss RNA → ds DNA
Integrase-ds DNA enters host cell’s nucleus (hides) = provirus
Transcription-get signal to become active host RNA poly ds DNA → mRNA → protein, vRNA
Assembly-HIV protease cuts HIV proteins into smaller proteins (gag, gag-poly)
VIRUS=protein + vRNA
Budding-takes pt of cell’s outer envelope
Binds to CD4 receptors via glycoproteins

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10
Q

HIV pathogenesis

A

Tropism for CD4 T cells. Macrophage lineage cells. Enters via infected macrophages (reservoir). Dendritic cells-accumulate the virus particles on their surfaces but don’t internalize them (vehicles-carry virus to LN where they infect CD4 cells)
Chemokine receptors-CCR-5
AIDS due to ↓ CD4 T cells
Long period of clinically silent but dynamic virus replication/diversification
High host cell turnover
CPEs: HIV encephalopathy-virus spread → cell to cell syncytia seen in brain. Circulatory Ab’s have no effect
Immune evasion - Ag variation, carb masking target epitope, conform change by viral env to mask neutralization targets, ↓ reg of host HLA
viral latency in resting T cells + APC’s

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11
Q

HIV dx and tx

A

• Ab/Ag testing (usually w/ in a few wks of infxn), ELISA / Western Blot
• HIV testing: easier, more accessible, less invasive (e.g., oral fluid, urine, and finger-stick blood)
– in addition to serum specimens collected by venipuncture
• Rapid HIV testing - same day results
• Commercially available home sample collection devices (not FDA approved)

Need to monitor CD4+T cell #’s and viral load (to monitor t/x + tells you how rapid disease progression). • Therapy usually initiated when CD4+ cells < 350 cells/μl. Regimen individualized - protease inhibitor. 2 nuceloside RT inhibitors

GOAL - get HIV RNA level below assay detection limits• Undetected does not equal Uninfected!
– < 400 copies/ml considered undetectable
**HIV disclosure ruling clarified by top court: People with low-level HIV and condoms needn’t disclose infection

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12
Q

Misc. HIV tree

A

Origin of HIV-1: contaminated oral polio, smallpox vaccine contam, butchering of animals

• HIV-2 probably from sooty mangabey
• HIV-1 probably from chimpanzees
• Spread:
– Locally: Migration from rural areas to cities; commercial sex trade
– Regionally: Along highways
– Worldwide: Air travel, then locally once introduced
– Also transfusions, blood products, injection equipment

• Has given rise to a number of lineages
• Continuing to evolve (e.g., recombinants
of different HIV-1 subtypes)
Evolution: “bushy” family tree - many variants/recombinants co-exist in diff populations (subtype B-N. America, Europe)

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13
Q

Normal UG microflora

A

Urethra - Lactobacilli, Streptococci, coagulase-negative Staphylococci

Vagina - newborn girls -> colonized w/Lactobacilli, vaginal flora becomes more diverse afterwards. Lactobacilli most prominent during reproductive years

Before and after reproductive years, more diverse organisms

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14
Q

Lactobacilli

A

Gram positive, non-spore forming. Facultative or strict anaerobes, produce lactic acid and peroxidase (inhibit growth of other microbes)

Normally found in UGT, mouth, intestines, stomach. Rarely cause UTIs -> do not grow well in urine

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15
Q

Asymptomatic bacteriuria

A

Relatively common. Seen in pregnant patients at term, HTN pts, and DM pts. Anatomic obstruction increases incidence. Nearly all pts w/indwelling catheter w/open drainage for 48+ hrs

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16
Q

Complications of long-term urinary catheterization

A
  • Obstruction -> bacterial glycocalyx
  • Formation of encrustations and infxn stones consisting of urea, other complex substances
  • Local infxns (urethritis, periurethral abscess, epididymitis, and prostatitis)
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17
Q

Most common bacterial cause of UTIs

A

UPEC (uropathogenic E.coli) - normal flora of GIT. ~85% of community- acquired, ~50% of hospital acquired UTIs

Pathogens: distinguished by acquired genes (iron acquisition, siderophores) -> virulence-distinct UPEC-associated biosynthesis

Key virulence features:
Type I - cystitis
P pili (attachment) - pyelonephritis
a- hemolysin, siderophore, PAIs

Serotypes: O (75% 6 of 200), K (capsular), F (fimbrial)

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18
Q

Host defenses in lumen of bladder

A

– Antimicrobial peptides
– Competition with iron-sequestering proteins
– Tamm-Horsfall Protein
• key urinary anti-adherence factor that prevents type 1 fimbriated E. coli from binding to the urothelial receptors

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19
Q

Non-E. coli UTIs

A

15% community, 50% nosocomial

  • S. saprophyticus - young sexually active girls, asymptomatic, summer time. Uropathogenicity d/t novel cell wall-anchored adhesin, redundant uro-adaptive transport system, urease
  • Proteus mirabilis - proteases, hemolysins, biofilm, urease (urine smells like ammonia, toxic to kidneys) (alkaline -> urine struvite cystals). Agar shows concentric circles -> ability to MOVE, SWARMING. Alternates between short vegetative state and longer HIGHLY flagellated state
  • Klebsiella pneumoniae
  • Mycoplasma and Ureaplasma
  • Candida
  • Chlamydia
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20
Q

Other UTI clinical outcomes

A

Prostatitis -> E. coli. Most serious but least common (chronic more common) (older men) reflux of urine into prostate ducts.

Epidiymitis - bacteria enters from prostate via ejac duct. Predisposing factors include prostatitis, indwelling urinary catheters, urologic surgery

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21
Q

Anal-oral

A
  • Giardlia lamblia - protozoan
  • Amoeba sp. - protozoan
  • Shigella sp, E. coli - true bacteria
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22
Q

Vaginal discharge

A

Vaginitis - Trichomoniasis, Candidiasis
Cervicitis - G+C

Unusual vaginal discharge, itching, dysuria, dyspareunia

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23
Q

Urethral discharge

A

G+C

Urethral discharge, dysuria, freq urination

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24
Q

Genital ulcer

A

Syphilis, chancroid, genital herpes

Genital sore

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25
Q

Lower abdominal pain

A

G+C, mixed anaerobes

Lower abdominal pain, dyspareunia, vaginal discharge, temperature >38C.

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26
Q

Scrotal pain and swelling

A

G+C

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27
Q

Inguinal bubo

A

LGV, chancroid

Painful enlarged inguinal lymph nodes, fluctuation, abscesses or fistulae

28
Q

Neonatal conjunctivitis

A

G+C

Swollen eyelids, cannot open eyes, edema of the eyelids, purulent discharge

29
Q

Anaerobic Gram negs and GYN infxns

A

Mixture of anaerobes can lead to female GT infxns, including Prevotella bivia, Prevotella disiens, Bacteriodes fragilis

30
Q

Gonorrhea epidemiology

A

Occurs only in humans. Very rare fomite transmission. Major reservoir is asymptomatically infected individual. Infxn increases likelihood of HIV infxn

Men (~95% have sx’s) - restricted to urethra, purulent urethral discharge, dysuria
Women - site of infxn is cervix -> vaginal discharge, dysuria, and abdominal pain

Disseminated infxn can occur (highest in females)

31
Q

Neisseria gonorrhea

A

Gram positive diplococci. Oxidase positive. Outer surface w/multiple Ags.

Attachment to columnar epithelium of distal urethra or cervix.

  • Pili - Ag variation by DNA rearrangement
  • Opa
  • Por protein (porin protein, prevents fusion to phagolysosomes in neutrophils)
  • Lipooligosaccharide - induces TNF- a in some cells
  • Iron-binding proteins

Multiply in situ to huge numbers, found in genital secretions of both men and women. Urethral or uterine contractions may lead to ascending infxn. Bloodstream can be seeded (most common in pts w/complement defects)

32
Q

Gonorrhea dx

A
  • Suggestive - exudate + knowingly having sex w/someone who has gonorrhea
  • Presumptive - one of 1-3
  • Definitive - 2 and 3
  1. Microscopic exam of smears for intracellular Gram neg diplococci (can be extracellular in males)
  2. Non-culture lab test - PCR, etc
  3. Isolation on approp media for confirmation
    - 24 hrs: Thayer Martin (VCN agar, chocolate II agar w/vancomycin, colistin, nystatin)
    - Oxidase + colonies
33
Q

Chlamydia trachomatis

A

No peptidoglycan. Has inner and outer mems and LPS. Gain entry through abrasions/lacerations

3 biovars (biological variants):

  • Trachoma (A, B, Ba, C)
  • Conjunctivitis, infant pneumonia, urogenital dz (D-K)
  • Lymphogranuloma venereum (LGV1, -2, -3)

Infxn usually occurs w/o sx’s. Sx’s are nonspec: vaginal discharge, burning w/urination. With sx’s of cervicitis, C. trachomatis should be suspected IN ABSENCE of clue cells, yeasts, and trichomonads

Women w/untx’ed dz -> infertility, ectopic preg, chronic pelvic pain. Complications in men are uncommon (but include epididymitis and urethritis)

34
Q

Chlamydia pathogenesis

A

• Receptors for EBs: restricted to certain epithelial cells
– Mucous membranes of the urethra
– Endocervix, endometrium, fallopian tubes – anorectum
– Respiratory tract and conjunctivae

NOTE: Infection does not confer long-lasting immunity

35
Q

Chlamydia dx, ctrl/tx

A

• CDC - annual Chlamydia screening for all sexually active women under age of 26
→ intracellular parasites, swabs rather than exudate must be submitted for analysis. Do nuclear acid amplification test

Most cases undx’ed as people don’t go for screening. As of Jan 2000, CDC says all 50 states and DC -> must report chlamydia cases

Tx w/abx. Screening and txt can reduce PID by over 50%. Reduce/tx chlamydia in males to reduce impact

36
Q

Syphilis

A

Treponema pallidum. Increasing rate in US from 2000-2007. Highly infectious transmission via contact w/1ary or 2ndary lesions. Genital, ulcerative dz that is easily curable in early P&S stages

Often in men who have sex w/men. Same w/chlamydia, HIV

37
Q

Syphilis: primary stage

A

Primary: HARD, PAINLESS but sensitive chancres 9-90 days post-infection (pi). Chancres have thin, grayish crust -> crater w/viscous fluid containing living T. pallidum cells. Often get multiple lesions
– Disappears w/in 1 week after proper txt
– Disappears spontaneously w/o txt after 4-12 wks
– 75% of all untreated cases resolve here and do not progress past this stage
– Easy, definitive diagnosis by Darkfield Microscopy: exudate from lesion is HIGHLY SENSITIVE. Serological testing

38
Q

Syphilis: secondary stage

A

• Secondary: generalized maculopapular rash + multiple symptoms indicative of systemic infection
– flulike syndrome, 2-8 weeks after ulcer
– rarely concurrent with chancre. CONDYLOMATA LATA (acuminatum is HPV)
– 80% of 2° infxns show maculopapular rash (rash may extend over face, PALMS and SOLES)
– lesions are “swarming” with the organism
- inflam rxn is similar to but less than that of primary chancre

39
Q

Syphilis: tertiary stage

A

• Tertiary: (15-20 yrs pi)
– diffuse chronic inflammation
– neurosyphilis (damage to CNS including progressive dementia, meningitis, hallucinations, etc.)
– cardiovascular effects such as aortic aneurysm
– “Gummatous” - A hypersensitive granulomatous reaction - Can be destructive to viscera or mucocutaneous areas

40
Q

Congenital syphilis

A

• T. pallidum can cross uterine + placental membranes → systemic infxn in developing fetus
• Most cases → spontaneous, septic abortion
• Occasionally live birth takes place; infants
are actively infected with the organism. S/s: saddle nose, Hutchinson’s teeth, stromal haze d/t late-staged congen syphilitic interstitial keratitis (IK)
• Teratogenic effects usually seen

41
Q

Treponema pallidum: characteristics

A
  • Thin, tightly coiled spirochetes w/pointed straight ends
  • 3 flagella @ each end: MOTILE
  • Replication slow – no in vitro culture
  • Obligate human pathogen
  • Unusual outer membrane (no LPS, no porins)
42
Q

Treponema pallidum: pathogenesis

A

• Tissue destruction and lesions → patient’s
immune response to infection
• Outer membrane proteins promote adherence
• Hyaluronidase may facilitate perivascular infiltration: “spreading factor”
• Coating of fibronectin may protect against phagocytosis

43
Q

Syphilis stage pathogenesis

A
  • 1ary – enters subepithelial tissues via skin breach
  • Slow rep, bc fastidious
  • Endarteritis and granulomas
  • Lesion heals but bacteria disseminate via lymph nodes and blood stream (latency poorly understood)
  • 2ndary – evasion of the immune system poorly understood
  • Inflammatory response may be responsible for some symptoms
  • 3ary – diffuse chronic inflammation, damage to CNS
44
Q

Syphilis: Prevention, Control and Treatment

A

• STI prevention
• CDC recommends sexually active men having sex with men be tested annually. More often if they are IVDAs or if they have sex with multiple anonymous partners
• Pregnant women should be screened at first prenatal visit
• Penicillin (generally used for all stages, is only treatment for neurosyphilis)

45
Q

Chancroid

A

• Obligate human pathogen Haemophilus ducreyi
• Predominant in the tropics (commonly in Africa, Asia and Latin America
• Sporadic in North America

• Soft chancre or chancroid
• Painful genital ulcer (5-10 days
incubation period)
• spontaneously rupturing buboes occur in approximately 25% of cases

46
Q

Haemophilus ducreyi

A

• Fastidious
• Gram – anaerobic rods (sometimes called
“coccobacilli”)
• Pleomorphic
• Related to H. influenzae
• Apparent extracellular pathogen that resists phagocytosis
• Virulence factors include:
– an outer membrane serum resistance protein
– two toxins: cytolethal distending toxin (CDT) and hemolysin, both of which contribute to tissue destruction

• Ag detection, serology and genetic amplification methods: reported for H. ducreyi, but are not easily available
• Culture: primary method available to most laboratories
– special media necessary for direct bedside inoculation is often not available
• Accuracy of clinical diagnosis for chancroid ranges from 30% to 80%

47
Q

Bacterial vaginosis/vaginitis

A
  • Normal balance of bacteria in vagina is disrupted - replaced by certain overgrowth
  • Most women report no signs / symptoms, but can increase HIV transmission
  • Examining the vaginal discharge under the microscope can help distinguish BV from Candidiasis and Trichomonas
  • A sign of BV: unusual vaginal cell called a clue cell
  • Women with BV (polymicrobial) have fewer than normal vaginal lactobacilli. Polymicrobial → difficult to treat
  • Vaginal pH > 4.5 → can be suggestive of BV
48
Q

Candidca albicans characteristics

A 
• Oval, yeastlike forms
• Primary site of colonization is GI tract 
• Normal microflora. Commensuals: 
– vagina
– urethra
– skin, under the nails

• ~75% of women → at least one genital “yeast infxnn” in lifetime (people w/ weakened immune systems, more frequent and severe)
• Rarely,men also experience genital Candidiasis
• Other risk conditions for female genital Candidiasis:
– Pregnancy
– Diabetes mellitus
– Use of broad-spectrum abx and/or corticosteroid medications

49
Q

Trichomoniasis epidemiology

A

• Common curable STD in young, sexually active women
• Vagina: most common infxn site in women
- Urethra: most common site in men
• Sexual intercourse transmission; fomite transmission possible
• Sx’s more common in women (most asymptomatic)

50
Q

Trichomonas vaginalis

A

Parasite with 4 flagella and short undulating membrane → motility

S/s: Vaginal pH > 4.5 → suggestive of trichomoniasis
- “Strawberry” cervix, cervix “blowing bubbles” = frothy discharge, tenderness, burning, dyspareunia

51
Q

HHV-1 and -2: Epidemiology

A
  • Most genital herpes: HHV-2
  • HHV-1 and -2 transmitted by close and/or sexual contact through mucosal membranes, breaks in the skin
  • HHV-1 and -2 can be found in viral ulcers
  • Viruses typically released from ulcers, but also released between outbreaks from skin
52
Q

HHV-1 and -2: Clinical Presentation

A

• Most individuals: no/minimal sx’s from HHV-1 or -2 infection
• Primary symptom: 1+ blisters on/around genitals or rectum (can have itching and vaginal discharge)
• Fever blisters,cold sores :blisters break → tender ulcers (take 2-4 weeks to heal the 1st occurrence)
• Subsequent outbreaks - weeks or months after the 1st, decreasing over time
• 1st outbreak more severe

53
Q

HHV-1 and -2: Pathogenesis

A

• HHV-1 and -2 can initially infect and replicate in mucoepithelial cells – lytic (most cells: Cowdry type A inclusion bodies, syncytia → go from cell to cell)
– persistent (lymphocytes and macrophages)
– latent infections (neurons)

• Virus blocks effects of interferon, prevents CD8 T-cell recognition of infected cells, escapes Ab neutralization and clearance by “hiding” during
latent infection

Dx - visual inspection of outbreak, test sample from ulcer. Between outbreaks: blood test to detect Abs to HHV-1 or -2 infection (results are not always definitive)

54
Q

Human Papillomavirus (HPV): Epidemiology

A

• Lifetime cumulative risk of acquiring HPV in sexually active persons = 80%. Cutaneous and mucosal
– 16, 18 -> 70% all cervical cancers (from countries reporting)

55
Q

HPV: Clinical Presentation, Anogenital Warts

A
  • HPV infections are often asx’s (both low- and high-risk)
  • May take wks, mos, yrs for sx’s to appear
  • Untreated, genital warts (low-risk HPV infections) may regress or increase in size and/or #
    • HPV 6 and 11 responsible for >90% of anogenital warts
    • HPV poses greater risk in contracting cancer than smoking or alcohol
    • HPV 16 - in the tumors of 72% of cancer patients
56
Q

Cervical Intraepithelial Neoplasia (CIN)

A

– CIN 1: Mild dysplasia; includes condyloma
– CIN 2: Moderate dysplasia
– CIN 3: Severe dysplasia; includes CIS

CIN can clear without treatment

57
Q

HPV dx

A
  • Genital warts → dx by visual inspection

* Cervical cell changes: 1) routine Pap tests, 2) HPV testing / typing

58
Q

HPV: Prevention, Control and Treatment (Screening Guidelines, US)

A
  • 3 advisory groups in US agreed upon screening guidelines: American Cancer Society, ACObGyn and US Preventative Services Task Force (2012)
  • Women 21 – 29: Pap test every 3 years
  • Women 30 and 65: both Pap test and HPV test every 5 years (preferred), OR Pap test alone every 3 years

• HPV Vaccine – Gardasil®
– Active against 16, 18, 6, 11
– FDA approved in US for girls & boys ages 9-26 (Cervarix ® targets only HPV 16 and 18)
• Visible genital warts removal by patient- applied medications, or by a health care provider
• Cervical cancer and other HPV-related cancers - most treatable when diagnosed and treated early

59
Q

Link between various STIs and HIV/AIDS

A
  • Presence of HIV increases severity of some STIs and their resistance to treatment
  • Presence of STIs in genital tract stimulate the body’s immune system to increase the number of WBCs (both targets + sources of HIV)
  • Genital inflam
60
Q

HIV - Pathogenesis

A

• AIDS-defining opportunistic infections and tumors occur when CD4+ T cell numbers fall below a level that can sustain immunity
• Pathogenic infection: systemic activation of immune responses followed by destruction of lymphoid follicle integrity
• HIV enters the body in infected macrophages
• Dendritic cells
– Accumulate the virus particles on their surfaces, but do not usually internalize them
– carry virus to lymph nodes resulting in efficient infection of CD4+ T cells
• Present in most compartments in the body (with varying concentrations)
**HSC‐based HIV reservoir might well be permanent, no matter how small in size

• Mechanisms of immune evasion:
– antigenic variation
– carbohydrate masking
of target epitopes
– conformational changes
by viral envelope to mask neutralization targets
– downregulation of host HLA
– viral latency in resting T cells and antigen- presenting cells
61
Q

HIV - CPEs

A

HIV encephalopathy
Cells appear to be the result of syncytial fusion of HIV-infected macrophages and microglia
Virus spread → cell to cell; immune circulatory antibodies cannot have an effect
Syncytia often seen in the brain

62
Q

HIV preg dx

A

• For ~8 years → universal testing of pregnant women
– patient notification
– elimination of requirements for extensive pretest counseling
– explicit written consent for HIV testing
• Adoption of policies → increased prenatal screening, 95% decline in perinatally acquired AIDS cases

63
Q

Course of HIV Progression

A 
• Typical progression – 80%, 7-10 yrs
• Rapid progression
– 5-10%, within 2 yrs
• Non-progression
– 10-15%, no disease ~7-10+ yrs
– CD4 count stays high, viral load not detectable (no medications)

• Window period
– Negative HIV test (primary infection to sero- conversion)
– Viral load very high, ↑ high transmission risk
• Acute retroviral syndrome
– Symptoms can have a huge range – WIDE DIFFERENTIAL DIAGNOSIS
• Opportunistic infections
– GOAL is to prevent these from occurring – Greatly increase chance of death

64
Q

Mycobacterium avium complex (MAC)

A

• Mycobacterium avium complex (MAC)
– Advanced HIV infection and a CD4 lymphocyte count < 50 increases chances of
developing a systemic infection
• Weakly Gram +, strongly acid-fast aerobic rods
• Disease: host response to infection
– asymptomatic
colonization, chronic localized pulmonary disease, solitary nodule
– disseminated disease (particularly in patients w/ AIDS)
– Night sweats, weight loss, abdominal pain, fatigue, diarrhea and anemia

(1) pulmonary MAC: immunocompetent hosts (2) disseminated MAC: individuals w/ advanced AIDS
(3) MAC lymphadenitis in children

65
Q

Bartonella henselae

A

(Gram – rod)
– Bacillary angiomatosis: vascular proliferative disease in immunocompromised patients
– Infection primarily involves skin, lymph nodes, or liver and spleen
– Subacute endocarditis
– Cat-scratch disease: chronic regional lymphadenopathy assoc. w/ cat scratch

66
Q

Progressive multifocal leukoencephalopathy (PML)

A

– Serious brain infection caused by the human polyomavirus JC virus
• speech problems
• weakness on one side of the body • loss of vision in one eye
• numbness in one arm or leg
– PML usually occurs only when the immune system has been severely damaged (AIDS)
Irregular areas of granularity in white matter, which bear some resemblance to the plaques ofdemyelination with multiple sclerosis

Term 3/4 Flash Cards (7 decks)

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