When do you typically see oral thrush in an HIV patient?
CD4 < 500 increases risk for opportunistic candidiasis
When do you typically see cryptococcus pneumonia or meningoencephalitis in an HIV patient?
CD4 < 100 increases risk for opportunistic cryptococcus
When do you typically see pneumocystosis in an HIV patient?
CD4 < 200
Which HIV infections are yeasts and which are molds? When do you typically see these arise?
Yeasts = candida, cryptococcus and pneumocystis. Molds = aspergillus, zygomycosis (mucor). You typically see yeasts arise when CD4 count is low because CD8 T-cells are crucial in eliminating them. You tend to see molds when Th17 response is low because PMNs are essential in getting rid of them.
Candida species resistant to antifungals
C. krusei, C. glabrata and C. lusitaniae show resistance to amphotericin B and fluconazole. C. glabrata and C. krusei are the ones you worry about the most because they are resistant to oral azoles.
What do all candida organisms produce?
Blastoconida (yeast buds)
What do all candida organisms besides C. glabrata produce?
Pseudohyphae (septum at branching points from repeated budding) and true hyphae (no septum at branch points and pores in septae for nutrient transmission)
What are the only candida species that produce germ tubes (no septum separating tube from yeast cells) and terminal thick-walled chlamydoconida?
C. albicans and C. dublinensis. This is significant because if germ tubes come up, then you know you can treat them with an azole.
Where in the body is candida normally found? How does it typically become pathogenic?
GI, GU and skin. Exogenous pathogenicity comes from parenteral nutrition or spread from another person to a person who is immunocompromised. Endogenous causes include bowel surgery with spread into peritoneum, movement from the skin into a central line
3 presentations of candidiasis in healthy individuals?
Oral thrush, vaginitis and diaper rash (dark and moist areas). Note that oral candida can also present in immuncompromised + those taking inhaled steroids that are not efficiently inhaled.
2 additional presentations of candidiasis in immunocompromised individuals
Esophagitis and disseminated (check retina!, heart, bones, joints, brain, liver and spleen can also be affected). Note that liver candidiasis after chemo does not typically present with symptoms until chemo is stopped and WBC gets back up.
Common cause of urinary tract candidiasis?
Common cause of intra-abdominal candidiasis?
Bowel perforation and pancreatitis
Common cause of liver and spleen candidiasis?
Candidiasis that requires a medical/surgical approach
Tx for candidiasis
Topical, oral or IV fluconazole, amphotericin B or echinocandins depending on the organs involved and species of Candida.
What organism does india ink stain help you to visualize?
Cryptococcus. It has a polysaccharide capsule
How do patients with HIV contract cryptococcus and get meningoencephalitis?
Inhalation of aerosolized C. neoformans -> Blood -> CNS. Note that in HIV patients the infection is typically reactivated from previous latency in macrophage granulomas because of low cell-mediated immunity. Note that pigeon droppings are commonly contaminated with c. neoformans and c. gatii are found in tropical eucalyptus trees.
Most common presentations of cryptococcus? How do they differ in HIV patients?
#1) Meningitis (headache, fever, neck stiffness) #2) Pneumonia. HIV patients have more CNS and extra-pulmonary involvement, fewer CNS inflammatory cells and higher rate of + blood culture/India Ink stain.
Best tests for cryptococcal infection
Culture > Antigen detection > Microscopy w/India ink. Antigen detection is the most common/easy way to dx.
Tx for mild and severe cryptococcosis
Mild = fluconazole. Severe = amphotericin B or 5FC.
Most common opportunistic infection in AIDS patients? What other population should receive prophylaxis for this infection?
Pneumocystis jirovecii. It also occurs in patients taking chronic oral steroids and they should be on prophylactic TMP-SMX.
What do you give patients with pneumocystis in addition to anti-fungals/anti-biotics?
Steroids are given to prevent an inflammatory response to the dying pneumocystis.
How do you diagnose pneumocystis?
Silver stain or Giemsa stain + bronchoscopy.
What is this?
Aspergillus, the mold. Note how they grow with straight walls, septations and acute angle branching.
Risk factors for aspergillus pneumonia
#1) Neutropenia #2) Phagocyte defects #3) Defects in cell-mediated pneumonia. Note that chemotherapy blocks rapidly dividing cells and neutrophils drop off right away, making them at risk for aspergillus.
Presentations of aspergillus infections
Allergic Bronchopulmonary Aspergillosus (like asthma from IgE hypersensitivity). Aspergilloma is a fungus ball that grows in a pre-existing cavity. Chronic necrotizing aspergillosis (erosion into pre-existing cavity). Invasive aspergillosis (life threatening in transplant patients that are neutropenic).
A patient presents with neutropenia and pneumonia. What must you think of to save them?
Aspergillosus. Once the hyphae grow they can get into the blood and 50% of patients die. Dx them with non-contract chest CT to show the fungus ball, (CXR won’t show it) + bronchoalveolar lavage to show branching hyphae.
Differentiating ABPA form asthma
Bronchiectasis, airway scarring and aspergillus-specific IgE antibody
Tx for aspergillosus
Invasive: voriconazole or amphotericin B if needed. Aspergilloma: surgical resection + azole. ABPA: corticosteroids + azole