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Multisystem Path > HIV and Opportunistic - Bacteria and Viral > Flashcards

HIV and Opportunistic - Bacteria and Viral Flashcards

1
Q

Discuss the structure of HIV

A

ssRNA+ retrovirus with RT (BUT it is diploid, so it has two copies of this ssRNA. Either one can be used!)

Enveloped (gp41 and gp120 from gp160), gag gene = p24 = capsule for RNA)

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2
Q

Discuss the course of HIV

A

Course: Initially infects macrophages. Then affects Helper T Cells, causing prodrome infection (cervical lymphadenopathy, fever, gets better on its own). Then latent period for up to ten years. Then steep drop below 200 = AIDS (or AIDS defining illness present, such as diffuse large B Cell lymphoma)

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3
Q

How do we screen a fetus for HIV if mom has HIV?

A

Remember mom passes down antibodies. If mom has HIV, baby will have positive ELISA and western blot. To check if baby has HIV, you need to do PCR of the virus itself.

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4
Q

There is a ton of treatment options for HIV, and having not gone through them yet, perhaps this is oversimplified.

But per sketchy micro, what drugs do we keep in mind for HIV treatment/maintenance?

A

1) NRTIs (pose as nucleotide, halt elongation during viral replication) (Zidovudine, used in pregnant patients)
2) NNRTIs (Does not incorporate but stops reverse transcriptase like NRTIs)
3) protease inhibitors (cleave proteins needed by virus to replicate)
4) Maraviroc - CCR5 inhibitor to stop initial infectivity of CD4 and macrophages.

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5
Q

What histology do we see with HSV? (Not HIV)

A

Histo: vesicle w necrotic epithelium & viral cytopathic effect (Multinucleation, Margination of chromatin, Molding of nuclei), cowdry bodies (pink intranuclear inclusions) in cells = “owl eye nuclei” appearance

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6
Q

HSV symptoms can be on the skin, in the brain, or disseminated. What symptoms can we see? (Long card, the idea is to recognize these when you see them, not regurgitate them all)

A

SEM disease (Localized to skin, eyes, and mucosal)-Vesicular lesions on an erythematous base, Keratoconjunctivitis, cataracts, chorioretinitis, Ulcerative lesions in mouth/palate/tongue (gingivostomatitis)

CNS disease: Seizure, lethargy, acute encephalitis (targets temporal lobe in brain. Latent in trigeminal nerve))

Disseminated disease: Multiple organ involvement (CNS, skin, eye, mouth, lung, liver, adrenal glands), appear septic (fever/hypothermia, apnea, irritability, lethargy, respiratory distress), Hepatitis, ascites, direct hyperbilirubinemia, neutropenia, disseminated intravascular coagulation, pneumonia, hemorrhagic pneumonitis, necrotizing enterocolitis, meningoencephalitis, skin vesicles

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7
Q

Treatment for HSV?

A

Acyclovir or Valcyclovir

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8
Q

Discuss the course of CMV

A

Latent in B and T cells and macrophages, woken up by immunosuppression

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9
Q

Discuss eye issues we see with CMV

A

Retinitis: flashing lights, blurred vision, visual field loss, full thickness necrosis= yellow/white “pizza pie” retinopathy, hemorrhages

immune recovery uveitis- Reconstitution syndrome: Vitreous inflammation, macular edema with inactive or regressed CMV. Only in immune recovery patients

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10
Q

Discuss GI issues we see with CMV

A

intestinal: ulcerated haustra (colitis) and esophagus (esophagitis) *linear/deep vs multiple/shallow in HSV

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11
Q

Discuss congenital issues we see with CMV

A

Congenital- Most common fetal viral infection, blueberry muffin rash, hepatosplenomegaly, jaundice, sensorineural deafness, intracranial calcifications in ventricles/parenchyma, seizures (85-90% are asymptomatic), hydrops fetalis in the 2nd trimester

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12
Q

What is the key histological finding for CMV?

A

Owl-eye inclusions

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13
Q

Who is at risk for getting CMV?

A

risk: AIDS patients with CD4

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14
Q

Discuss the treatment for CMV?

A
  • Gancyclovir, Foscarnet (Used with UL-97 mutation which makes the patient resistant to Gancyclovir)
  • Foscarnet can cause renal impairment, hypocalcemia, anemia
  • Valganciclovir over gancyclovir due to oral use and reduced side effects
  • Cidofovir - Can damage tubes = proteinuria
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15
Q

What does CMV often look similar to in the clinic?

A

Can present similarly to mono, do MonoSpot to distinguish

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16
Q

Structure of Varicella Zoster Virus

A

Enveloped virus, dsDNA virus

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17
Q

What does chicken pox look like and how do we treat it? Can adults get this?

A

Chicken pox (children): fever, headache, “dew drops on a rose petal” rash.

Adult (esp. in immunocompromised) chicken pox can lead to pneumonia and encephalitis.

Tx w/ acyclovir. Prevent with live attenuated vaccine.

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18
Q

Discuss the course of Shingles and who it normally affects

A

Virus lies latent in dorsal root ganglion.

Reactivated during stress or immunocompromised state.

Travel to skin via sensory nerves and produce rash in dermatone distribution (usually L/T spine).

If rash crosses midline it is considered disseminated dz, which typically occurs in old and immunocompromised host.

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19
Q

Discuss the atypical presentations of shingles (so not the dermatomal distribution of rashes)

A

Postherpetic neuralgia can occur: pain in dermatone distribution w/o rash.

Herpes Zoster Opthalmicus: vision loss possible if V1 affected

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20
Q

Discuss vaccines and treatment for Varicella Zoster

A

Shingles vaccine: adults >60 and HIV pts with CD4 >200.

Tx: Famciclovir or valacyclovir

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21
Q

VZV is a TORCH infection. What congenital manifestations may be present

A

limb hypoplasia, cutaneous dermatomal scarring, blindness

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22
Q

What is the pathophys of JC Virus?

A

JC virus destroys oligodendrocytes= demyelination (happens everywhere = multifocal, leuko = white matter)

course: rapidly progressive (death in a few months): visual loss, weakness, dementia

Reactivates due to immunocompromised, CD4 count

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23
Q

Imaging of JC Virus?

A

Imaging: Non-enhancing multifocal brain lesions in white matter

24
Q

Structure of JC Virus?

A

Structure: DsDNA virus, circular, naked virus no envelope

25
Q

When do we see BK virus?

A

BK virus (same family as JC Virus) Damages the kidney causing nephropathy and hemorrhagic cystitis typically s/p bone marrow or kidney transplant

26
Q

EBV is what type of DNA/RNA virus?

A

dsDNA

27
Q

EBV causes something really gross in your mouth. Talk about it, and then throw up.

A

Hairy leukoplakia in (HIV)

  • Usually appears on lateral border of the tongue
  • Gross: confluent, fluffy (“hairy”) white patches that can’t be scraped off (not candida)
  • Histo: hyperparakeratosis, acanthosis, balloon cells
28
Q

Mono, the kissing disease, is caused by EBV. What symptoms do we see with it and what do we confuse it with?

A

Sx: Tender lymphadenopathy with occasional generalized lymphadenopathy and tonsillar exudate, fever, pharyngitis, splenomegaly

Mono often asymptomatic in kids, unlike strep pharyngitis

Often mistaken for a strep throat pharyngitis, treated with PCN or ampicillin/amoxicillin. If this is Mono, you will see a maculopapular rash (not an allergic rxn, unknown mechanism)

29
Q

What histo will we see with EBV caused mono?

A

Reactive CD8 T cells (Downey cells on blood smear) - Large with folded nucleus - These can also be NK cells, and because of all of the cell production, we can see splenomegaly and rarely, hepatomegaly

30
Q

Where do we find the EBV?

A

Targets B Lymphocytes (remains latent here) after binding to CD21 (complement receptor) with its envelope glycoprotein

31
Q

What cancers are related to EBV?

A
  • B Cell lymphoma
  • Nasopharyngeal carcinoma in asians
  • Hairy leukoplakia in HIV patients
32
Q

What is the monospot test?

A

The test relies on the agglutination of the horse RBCs by heterophile antibodies in patient’s serum (heterophile means it reacts with proteins across species lines).

One drop of the patient’s serum to be tested is mixed on an opal glass slide. Then ten micro liters of the horse red cell suspension are then added and mixed with each drop of adsorbed serum

Agglutination = positive

33
Q

What type of bacteria is mycobacterium and where does it exist?

A

intracellular (vesicular), obligate aerobe.

Infects and proliferates in macrophages

34
Q

Discuss the virulence factors of Mycobacterium tuberculosis

A

Cord factor: protects the bacteria by making granulomas by increasing TNF-a and other cytokines. Activates macrophages which make the granuloma. Now bacteria is protected.

Sulfatides allow TB to survive in macrophages by preventing phagosome and lysosome from fusing.

35
Q

What is this Ghon Complex we see with TB

A

Healed lung forms Ghon complex; Caseating granulomas in middle or lower lobe of lung + Focally fibrosed/calcified hilar lymph nodes

36
Q

When do we see reactivation of TB and what does it look like?

A

Reactivation: TNF-a downregulated. Common in old age, AIDS, immunocompromised

Affects upper lobes of lung

Sx: Cough, night sweats and hemoptysis, cachexia

Additional Sxs:

  • Pott disease (axial involvement): multiple vertebrae, bone demineralization and soft tissue pain and swelling
  • CNS: Meningitis, tuberculoma (cavitary lesion in the brain)
37
Q

How dowe treat TB?

A

Tx: Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE) (9 month treatment, holy cow!)

38
Q

Discuss the histology of TB

A

AFB stain= acid-fast bacilli (stains the mycolic acid in cell wall with carbol fuchsin stain, appears red)

Takes 2-6 wks to grow on Lowenstein-Jensen agar
- epithelioid histiocytes, giant cells

Many white blood cells, majority are lymphocytes, with a paucity of mesothelial cells

39
Q

Discuss imaging for TB

A

Xray: fibronodular apical infiltrates, cavitation, pleural effusion

40
Q

How does Mycobacterium Avium Complex spread and who is at risk for it?

A

risk: CD4 less than 100

Mycobacteria enter by respiratory or ingestion (found in soil and water) → spread by blood and lymph→ taken up by mononuclear phagocytic cells throughout the body and reticuloendothelial organs like the liver, spleen and bone marrow

41
Q

Symptoms of MAC

A

Sx: Fever, chills, weight loss, diarrhea, night sweats, weight loss, abdominal pain, anemia, increased Alk Phos.

Hepatosplenomegaly and intra abdominal lymphadenopathy

42
Q

Discuss the labs of MAC

A

Lab: Isolator Tube (AFB blood culture)

- Increased Alk Phos

43
Q

How do we treat MAC?

A

Tx and prophylaxis: Clarithromycin. Alt: Azithromycin. 2nd drug = ethambutol. Prophylaxis: Macrolides like clarithromycin and azithromycin

44
Q

Discuss the structure of Nocardiosis

A

Structure - Gram positive branching rod, obligate aerobe, found primarily in soil but it does not form spores

45
Q

Discuss the staining characteristics for Nocardia?

A

Weakly acid fast due to Mycolic Acid in the cell wall.

Also, catalase positive and urease positive

Note that the catalase positive is important because those with chronic granulomatous disease are at risk for getting catalase positive infections

46
Q

Discuss the symptoms of Nocardia

A

Pulm: PNA with lung abscess formation (cavitary lesions) Note that it disseminates from this point, starting with CNS

CNS: Brain abscess formation

Skin: Cutaneous norcardiosis (indurated lesions)

47
Q

How do we treat Nocardia?

A

Sulfonamides

48
Q

Discuss the structure and related labs for Salmonella

A

Motile, enteric, H2S+ = black colonies on Hektoen agar (how to differentiate from Shigella spp. on agar–they’re H2S-), encapsulated, acid labile = easily degraded in the stomach so you need a lot in order to cause infection (thus lowering stomach acidity increases risk of infection)

49
Q

What symptoms do we see with Non-typhoidal Salmonella and how does it change in the immunocompromised?

A

Non-typhoidal (S. enteriditis)= Enterocolitis and septicemia

sx: n/v/d (inflammatory), fever, death in immunocompromised

50
Q

Where does non-typhoidal salmonella hide and what causes the symptoms we see because of it?

A

Chicken is main reservoir

Virulence factor: Type 3 secretion system that detects eukaryotic cells and stimulates growth around eukaryotic cells

51
Q

Discuss the symptoms we see of typhoidal salmonella

A

1 cause of osteomyelitis of those with Sickle Cell Disease

Typhoidal salmonellae (S. typhi) = Typhoid (enteric) Fever

sx: rose-colored macules on abdomen, fever, constipation to bloody diarrhea, can also present as pea soup diarrhea, delirium, hepatitis, cholecystitis, intestinal hemorrhage

52
Q

Where does typhoidal salmonella hide and how do we treat it?

A

Gall bladder is main reservoir

Tx: Fluoroquinolone, live attenuated vaccine

53
Q

What is the structure of Chlamydia Trachomatis? Life cycle changes?

A

Structure: Obligate intracellular (can’t generate its own ATP), poor gram staining, lack of muramic acid in the cell wall

Life cycle: Elementary bodies (outside of the cell, very infectious), Reticulate body (replicates by binary fission, A LOT)

54
Q

Lab values for Chlamydia Trachomatis

A

Lab: Inclusion bodies in macrophages (reticulate bodies, Giemsa stain +

55
Q

For Chlamydia Trachomatis, what do we see with the D-K serotypes?

A

STI (most commonly reported bacterial STI in the U.S.), watery discharge, urethritis, cervicitis, acute inclusion conjunctivitis, reactive arthritis, reiter’s syndrome- (can’t see can’t pee, can’t climb a tree)

Congenitally the child will get Pneumonia (Staccato cough) and go blind but later on, not immediate like with gonorrhea

56
Q

For Chlamydia Trachomatis, what do we see with the L1-L3 serotypes?

A 
lymphogranuloma venerum (infected lymph nodes), inguinal lymphadenopathy, painless skin lesion early on
Histo: multiple abscesses with central necrosis surrounded by palisading histiocytes
57
Q

For Chlamydia Trachomatis, what do we see with the A-C serotypes?

A

(Trachoma - leading cause of blindness worldwide), hand transfer to eye

Multisystem Path (11 decks)

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