HIV and Opportunistic - Fungal Flashcards

1
Q

What is the most common fungal infection to get a hold of the immunocompromised?

A

Candida

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2
Q

Discuss the lab findings for Candida

A

Catalase Positive, so those with chronic granulomatous infection are at risk for infection

extracellular pathogen (on epithelial surfaces) that DOES NOT change the pH

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3
Q

When do we see candidiasis thrush in patients?

A

Candidal esophagitis- AIDS defining illness (CD4+ less than 100)

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4
Q

Other presentations of Cancida besides scraping white plaques?

A

Cutaneous: Kids& Diaper rash

IV drug user- Endocarditis and Tricuspid valve damage

Eyes - Retinitis

Bones: Vertebral osteomyelitis

mucosal - can wipe away, underlying red, painful

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5
Q

Two histology features for candida

A

KOH prep= hyphae, germ tubes

necrotic squamous epithelium w yeast overlying inflamed submucosa

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6
Q

Cold vs. warm candida and general structure we will look for

A

Cold temp = pseudohyphae = yeast form

Warm = germ tubes = mold form

Structure: Budding yeasts and pseudohyphae

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7
Q

Who is at risk besides AIDS patients for getting Candida?

A

Diabetes, Antibiotics (kill micro-flora in the gut, so Candida can take over), Birth Control

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8
Q

How do we treat Candida?

A

Azoles for minor infection like diaper rash

Amphotericin or Capsofungin (echinocandin) (if resistant to ampho) for severe disseminated infection in immunocompromised

oral/esophageal candidiasis = Nystatin

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9
Q

What count do we think of for PCP?

A

Less than 200

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10
Q

PCP symptoms in compromised vs normal health

A

Asymptomatic in healthy people.

Immune compromised = PCP Pneumonia (CD4+

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11
Q

Chest X ray for PCP

A

CXR: Ground glass appearance (diffuse interstitial infiltrates, bilateral, perihilar)

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12
Q

Discuss the lab findings of PCP

A

microscopy= trophozoites/cysts in sputum or bronchoalveolar Lavage.

Anemia with nonspecific increase in LDH.

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13
Q

Histology for PCP

A

Histo: methamine silver stain= Disc shaped yeast. Foamy exudate with “dented ball” alveolar damage. No inflammatory response.

Direct fluorescent antibody test (DFA) shows antibodies, sensitive, better than giemsa stains

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14
Q

PCP treatment

A

Bactrim (TMP/SMX, Trimethoprine and sulfamethaxazole), active sx and prophylaxis (CD435)

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15
Q

Leading cause of AIDS death?

A

Respiratory illness! Never forget PCP!

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16
Q

Discuss the structure of Cryptococcus Neoformans

A

HEAVILY encapsulated with repeating polysaccharide antigens (antiphagocytic), urease positive

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17
Q

Where do we get cryptococcus from? Discuss transmission and where it goes INSIDE OF YOU

A

CD4Lung –> Blood –> CNS

patho: Latency in macrophages of lung granulomas like TB, then acute infection in the lungs

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18
Q

Symptoms of cryptococcus infection

A

Lungs- Cough, dyspnea, pneumonia

CNS: common* fungal meningitis (spread via CSF): visible exudate unlike viral, AMS, diplopia, ataxia/palsy, Sz, meningismus, CN palsies, acute memory loss

Const: Fever, Headache, malaise
other: skin lesions, eye, prostate

19
Q

Discuss lab stuff for cryptococcus

A

Sensitivity: culture>antigen>microscopy

  • Blood Culture can grow c. neoformans
  • (+) cryptococcal antigen test:( CRAG) = latex agglutination= cryptococcal polysaccharide antigen: done on blood/ CSF* (most sensitive)
  • direct microscopy of any body fluid
20
Q

Discuss the histology for crypto

A

histo: india ink stain= large clear capsules around budding yeast (cryptococcal halos), background is dark
meningeal tissue shows fibrosis, expanded virchow-robin space with organism aggregates, no reactive gliosis, reactive CT can lead to obstruction and hydrocephalus,

other stains: red mucicarmine or silver methanamine

21
Q

Discuss imaging for crypto

A

Imaging: Soap bubble lesions in gray matter, basilar meningitis

22
Q

Discuss treatment and prognosis for crypto

A

Tx: Amphotericin B and flucytosine followed by maintenance with fluconazole (which we also use if there is only mild disease)
repeated LP’s to decrease ICP

prognosis: severe, death >60%

23
Q

Discuss the structure and transmission of coccidiomycosis

A

Trans: Inhalation of spore dust - widespread fevers with earthquakes and dust clouds.

Structure: Cocci forms spherules filled with endospores inside lungs in the warm body, mold form in the cold

These spherules are larger than RBCs

location: SW US, california valley

24
Q

Discuss the symptoms of coccidio

A

sx: chronic pneumonia, lung granulomas, meninges, valley fever (rash,joint pain, fever, cough), erythema nodosum on shins in healthy people due to exaggerated immune response

25
Q

Discuss the histology of coccidio

A

histo: Cx which takes a while, KOH prep, IgM titers, eosinophilia

26
Q

Discuss the imaging for coccidio

A

Imaging: Radiography shows either nothing or cavities or nodules

27
Q

Discuss the treatment for coccidio

A

Tx: Azole drugs (ketoconazole) for lung infections.

Amphotericin B in systemic infection

28
Q

Discuss the treatment for histoplasmosis

A

Structure: Smaller than RBCs. Dimorphic: Cold/Soil = Mold form, Body/heat = yeast form

29
Q

Discuss transmission of histoplasmosis

A

Trans: Bird/Bat droppings (recently in a cave) or chicken coops, transmit via respiratory spores being ingested by macrophages

30
Q

Histology for Histoplasmosis

A

Histo: Macrophages with intracellular ovoid bodies often in coin lesion produced by granulomatous inflammatory process, KOH prep, Rapid Histoplasma blood or urine antigen test

31
Q

Where do we find histoplasmosis

A

Location: Midwestern and Central U.S. along the Mississippi and Ohio River valleys

32
Q

What happens to a person with histoplasmosis?

A

Sx:Pneumonia if granulomas present, Chronic pulmonary issues if granulomas calcify and fibrose

Can mimic TB!

Erythema nodosum on shins due to exaggerated immune response

Immune Compromised - Disseminated = hepatosplenomegaly with calcifications due to targeting macrophages

33
Q

Treatment for Histoplasmosis

A

Tx: Local/mild = Fluconazole, Ketoconazole. Systemic = Amphotericin B (lots of side effects)

34
Q

What dos this Aspergillus thing look like and what do our labs show us?

A

Structure: Hyphae at acute angles with septations (tree like). Make conidiaphores with fruiting bodies that bud off and are inhaled

Lab: Catalase positive

Diagnose: Serum galactomannan for early screening

35
Q

Symptoms of Aspergillus (4 main pathways. Don’t kill me, yes this card is long but it’s basic explanations. You’ll be fiiiiiiiiiiiiiiiiiiiiiiiiiine)

A

Sx: spectrum based on immune response

1) Allergic bronchopulmonary aspergillosis= allergic sinusitis (Type 1 hypersensitivity rxn= elevated IgE; wheezing, fever, recurrent asthma, pulmonary infiltrates)
2) Aspergilloma- solid balls of fungus in lower lungs (especially in pre-existing fibrocavitary lung disease, TB and cancers)
3) angioinvasive aspergillosis- immunocompromised, (invades blood vessels and disseminates) which presents with hemoptysis
4) invasive aspergillosis- systemic involvement ( kidney failure, endocarditis, ring enhancing lesions in brain on CT, necrosis of nose)

36
Q

What toxin do we see with Aspergillus

A

toxin: aflatoxin - Very carcinogenic especially for hepatic carcinoma in aspergillus flavus

37
Q

Histology for Aspergillus

A

histo: fungal septa hyphae branch at 45*

38
Q

What do we associate with Aspergillus?

A

a/w: peanut crops and wheat crops, african liver cancer, neutropenic patients

39
Q

Treatment for Aspergillus

A

Tx: Less serious use Voriconazole, systemic use amphotericin. Aspergilloma = surgical resection. ABPA = corticosteroids with antifungals (itraconazole)

40
Q

Structure of mucormycosis

A

Structure: broad, nonseptated hyphae (ribbon like), right angle (90 degrees) branching unlike Aspergillus (45 degrees)

41
Q

Discuss the transmission of Mucormycosis and who is at risk

A

Risk: Diabetics and immunocompromised. Found in bread (rhizopus)

Transmission: Spore inhalation, proliferate in blood vessel wall where there is high glucose and ketones (think DKA). Breaks through the cribriform plate to get to the brain

42
Q

Symptoms we see with mucormycosis

A

Sx: Rhinocerebromucormycoses (black eschar around nose and eyes = very bad prognosis = extensive necrosis)

disseminated disease (basal ganglia, cutaneous tissue, kidney, respiratory tract, etc.)

43
Q

Treatment of Mucormycosis

A

Tx: surgical debridement, liposomal amphotericin B (usually doesn’t matter, prognosis dismal - 67%), posaconazole