Module 5 Path Continued: Fungi Flashcards Preview

Pathology Pre-Midterm > Module 5 Path Continued: Fungi > Flashcards

Flashcards in Module 5 Path Continued: Fungi Deck (40):
1

Candida Albicans (moniliasis) is normal flora of what parts of the body?

Mouth, vagina, oral cavity, esophagus

2

what type of individuals typically get candida albicans?

Immunocompromised patients
Babies
elderly
Diabetics

3

In babies where do they typically get candida albicans infections?

Diaper rash so the skin

4

In the vagina, what is the presenation for a patient with candida albicans?

cheesy white vaginal discharge with puritis
additionally females on broad spectrum antibiotics are at risk for yeast infections

5

Candida can invade the blood and go where?

lung, liver, heart and brain and you get abscesses in these four organs

6

when you scrape the pseudomembrane -like off and look under the microscope what do you stain it with and what do you see?

PAS, Silver Stain and Mucicarmime
Budding yeast with pseudohyphae (Chinese letter appearance)

7

What cells do you see in candida albicans?

PMNs + lymphocytes + monocytes + giant cells (mixture of acute and chronic always for fungi)

8

What scenarios is candida albicans considered opportunistic ?

Diabetic patients, immunocompromised and patients on broad spectrum antibiotics

9

Pneumocystis Jiroveci is considered an opportunistic infections in what kind of patients?

Immunocompromised patients with a CD4 count less then 200 (AIDS patients)

10

How does a patient present with P. Jiroveci infection?

low grade Fever, SOB, dry cough (because the cotton candy exudate that is in the alveolar space is too thick to be coughed up), interstitial pneumonia, inflammation and thickening of alveolar wall with sparse mononuclear infiltrate

11

What cells are present in P. Jiroveci infection?

PMNs + lymphocytes + monocytes + giant cells (again mixture of acute and chronic for all fungal infections)

12

What is the best investigation for P. Jiroveci?

Bronchoalveolar lavage (this is how you get the actual sputum from the patient)
and then silver stain the sputum and therefore fungus stains black and has a black cup shaped cyst

13

What is located in the alveolar space for P. Jiroveci?

Cotton candy exudate without cells ( just proteins and fibrin)

14

The alveolar wall over time in P. Jiroveci what happens?

Cells (PMNs and lymphocytes and macrophages) overtime the alveolar wall becomes super thick

15

What is the most common cause of death in P. Jiroveci?

Resp Failure due to V/Q mismatch
(ventilation is messed up because exudate is a diffusion barrier, no O2 in and no CO2 out)
so patient O2 levels in blood goes down (hypoxia) and CO2 levels goes up (hypercapnia) and pH in blood goes down (because of resp acidosis)

16

What is the mode of infection in Aspergillus?

Inhalation of aspergillus (mycelial form)

17

There are three types of Aspergillus, each card will go through the type. 1 -->

1. Aspergilloma: fungal ball --> colonize pre existing cavity from TB or a lung abscess or Wegener's Granulomatosis
the slide shows the fungal ball. this can happen in immunocompetent ppl

18

2nd type of Aspergillus...

2. Allergic Bronchopulmonary Aspergillosis: type I (IgE from asthma) and type III (IgG and forms antigens to make immune complexes) hypersensitivity
This is seen in immunocompetent patients with bronchial asthma (IgE) -- inhale --- colonzies ----- causes wheezing, SOB, productive cough, fever ---- exacerbation of asthma

19

3rd type of Aspergillus...

3. Disseminated Aspergillosis: Immunocompromised patients get this one
Angio-Invasive ---- attacks the blood vessels and therefore you get thrombosis in the lumen and you get fibrinoid necrosis in the media of the vessel wall and coagulative necrosis of the actual organ

20

What is fibrinoid necrosis?

Media in small or medium vessels gets its oxygen supply from the lumen but if you get endothelial damage and then thrombus in the lumen the media is going to become ischemic and therefore you get fibrinoid necrosis
(media is basically starving for oxygen)

21

What do you stain Aspergillus with?

Well this is fungal so either silver stain, PAS or mucicarmine

22

What does Aspergillus look like on histology?

Slender, septate hyphae that branch at acute angles

23

What is a complication of Apergillus?

Meningitis

24

What are the three Zygomycetes for mucormycosis?

Mucor, Rhizopus and Absidia

25

Mucormycosis affects what types of individuals?

Diabetes who get DKA ( pH is low enough and favors growth of organism)
Opportunistic fungi in immunocompromised patients

26

What is the pathogenesis for mucormycosis?

Inhalation of spores ----- tropism for endothelial cells of blood vessels ---- angio invasive ---- disseminated ---- endothelial damage ---- thrombosis ----- ischemia ---- hypoxia ----- coagulative necrosis

27

Explain the coagulative necrosis for mucormycosis for the brain

Ischemia ----- hypoxia ----- coagulative necrosis (So this again will be the first 12-24 hours) ---- red infarct
Once you see a hole in the brain then this is 48 hours and therefore this is liquefactive necrosis
Remember that gliosis is 2 weeks later and you are going to see astrocytes

28

What is the most commonly affected part of mucormycosis?

Cerebral hemispheres (Thats why they call it rhino (because it goes through the sinuses) cerebral mucormycosis)
In the picture in lab it shows the cerebellum affected but that is not the most common spot

29

What other areas besides the brain can mucormycosis affect?

GI ( red infarct --coagulative necrosis --- splenic flexures (watershed of GI)
Lungs
Sinuses

30

What are the signs of mucormycosis?

Sero-sangrenous nasal discharge (Aka bloody discharge), fever, pain, and headache and rhino-facial-palatal necrosis

31

What is the best investigation for mucormycosis?

Biopsy with PAS or silver stain
in the lab histology picture your looking at the blood vessel wall and again this type of necrosis would be fibrinoid necrosis

32

What will you see on histological stain of mucormycosis?

Broad organisms with non septate hyphae branching at right angles

33

Cryptococcus neoformans (Torulosis), what is the etiology and susceptible population?

-etiology - inhalation of soil with pigeon droppings

-Opportunistic infection in immunocompromised AIDS patients with CD4 less then 100

34

Quick recap on AIDS, CD4 and infection

AIDS patient CD4 less then 50 = CMV retinitis
AIDS patient CD4 less then 200 = P. Jiroveci
AIDS patient CD4 less then 100 = crytococcal infection

35

What is the pathogenesis for Crytococcus neoformans?

Spores in pigeon droppings --- inhalation ----- granulomas with giant cells
spores can go into the lungs and brain
if disseminated then meningitis

36

In crytococcus Neoformans, if this fungus becomes disseminated it can lead to meningitis, what are the symptoms?

NO FEVER OR NECK STIFFNESS
headache, increased intracranial pressure, projectile vomiting ( caused by the increased intracranial pressure) and photophobia and blurred vision
symptoms are super vague because these are immunocompromised patients

37

What would you see in the CSF of a patient with crytococcus neoformans?

MIXED (very minimal though because again these patients are immunocompromised so its hard for them to mount a response)
glucose goes down
protein will be elevated (highly)

38

What are the best investigation for crytococcus neoformans?

1. Most accurate is latex agglutination looking for the antibodies
2. CSF -- india ink stains polysaccharide of crytococcus --- organism appears as clear halo --- negative staining

39

On autopsy, what do you find in a patient with crytococcus neoformans?

Use either a silver stain, PAS or mucicarmine (stains organism red in perivascular space or virchow robbin space)..directly stains the organism so this is not a negative stain
The brain will have cystic spaces called soap bubble lesions

40

What are the three dimorphic fungi?

1. Coccoides Immitis -- thick walled and non budding spherules (largest pathogenic fungus, southwestern and western US and Valley fever )
2. Blastomyces Dermatidis: round (broad based budding and endemic area overlaps with histoplasma)
3. Histoplasma capsulatum