Viral Skin Infections and Mycoses Flashcards Preview

Microbio (12.5) > Viral Skin Infections and Mycoses > Flashcards

Flashcards in Viral Skin Infections and Mycoses Deck (29):

Structure and nuclear makeup of Herpes

Herpes is icosahedral and is a linear double stranded DNA


Discuss the general pathogenesis of Herpes

These guys infect mucosal epithelial cells and replicate in the nucleus.

The viral particles bud through nuclear membranes and into the membranes of exocytic vesicles during egress from host cells


Discuss the three types of herpes viruses

alpha - HSV1,2, and VZV - These guys have a short replication cycle and stay latent in sensory ganglia and neurons

Beta - HHV6,7 and CMV - longer replication cycle and the infected cells become larger. This guy hides in monocytes/macrophages, lymphocytes and endothelial cells

Gamma - HHV-8 and EBV - Infect both epithelial cells and lymphocytes, are lymphoproliferative and cause cell transformation


Discuss the clinical features we observe in HSV

With the primary infection of HSV, it is accompanied by systemic symptoms such as fever and malaise. With reactivation, we get prodromal symptoms like pain, numbness, itching and a tingling sensation.

Acute infection is where we get the direct destruction of tissues or induction of immunopathologic response.


What is worse with HSV, primary or secondary infection

Primary because you don't have any immunity yet.

The patient with primary will have many lesions orally called gingivostomatitis all around the mouth, but on recurrent HSV-1, they just get a cold sore.


HSV-2 is associated with:

Genital bumps


What anti-herpes treatment do we have?

Herpes Thymidine Kinases like acyclovir and ganciclovir. The viral Thymidine kinase activates this DNA chain terminator and incorporates it into the viral DNA, causing a termination of replication


Acyclovir vs. Ganciclovir

Acyclovir - For HSV - Activated by viral TK and terminates as previously discussed

Ganciclovir - For CMV - Viral protein kinase analogue of TK activates it.


What does Foscarnet do?

It is a pyrophosphate analog that binds directly to the RNA pyrophosphate binding sites or to DNA polymerases.

Unlike ganciclovir and acyclovir, it does not need to be activated by anything.

We use it primarily for CMV


Discuss the general structure and physical attributes of fungi

- Eukaryotic
- Cell wall has chitins and glucans
- Fungal membrane contains ergosterol, which is not in humans
- No endotoxins


Three possible structures of fungi

Unicellular Yeast
Filamentous multicellular mold
Dimorphic (either)


How do yeast reproduce?

Budding and binary fission


How is mold organized?

In compartments within hyphae that grow outwards. The compartments have different organelles in them with pores between the compartments


What is the function of Sabouraud's agar?

For growing fungus. It inhibits bacterial growth with a low pH along with chloramphenicol and cycloheximide


What do azoles do?

Inhibit ergosterol synthesis


What do polyenes do?

Bind ergosterol and make pores in the wall


What do echinocandins do?

Inhibit synthesis of B-glucan and block cell wall


Side effects of fungal medications

Azoles - Can cause visual disturbances but are generally well tolerated

Polyenes - Renal toxicity, HA, chills

Echinocandins - GI side effects and flushing


What can our endothelial cells use to detect fungus?

Dectin-1 is a pattern recognition molecule for B-glucan



What do we mean by superficial mycoses?

These guys colonize the keratinized outer layer of skin, hair, and nails, and cause a scant immune response. They are typically nondestructive and are just a cosmetic concern


Discuss Pityriasis Versicolor, a superficial mycosis, and how we can see it

Pityriasis versicolor - caused by the Malassezia furfur yeast and causes hypo or hyperpigmented macules on the chest, neck, and back.

We diagnose this with direct visualization of short infrequently branched pseudohyphae in either 10% KOH or a PAS stain


Treating pityriasis versicolor

Topical therapy is needed as it rarely self cures. Azoles work just fine.


Discuss in general cutaneous mycoses and what tends to cause them

Most are caused by dermatophytic fungi (dermatophytes) that break down keratin, invade skin, hair, and nails, and invade the outermost layer of the epidermis (stratum corneum)

The most well known subgroup in this is Tinea, ring worm


Discuss in general subcutaneous mycoses and name the three subtypes

All are rare, and are introduced following trauma. They cause infection into the dermis, subcutaneous tissue, and bone, and rarely spread into distant organs.

Sporotrichosis, Chromoblastomycosis, and eumycotic mycetoma are all examples


Discuss the progression of sporotrichosis and what we see under the microscope

There is a primary lesion at the site of inoculation. The nodule grows, ulcerates, and in 2-3 weeks there are secondary lesions along lymphatics that progress proximally

Under the scope we see what is called the "Splendore-Hoeppli Phenomenon," an eosinophilic granulomatous structure with a starburst pattern. You may also see oval conidia in clusters at tips of slender branches


How do we treat sporotrichosis

Several weeks of itraconazole


What is chromomycosis?

A chronic local fungal infection of the skin that causes warty and/or nodular outgrowths.

We see this mostly in the tropics, and it causes a granulomatous infection.


How do we treat Chromomycosis? The same way we treat Sporotrichosis?

No, its very difficult to treat. and we can't do surgery either

We use local heat or cryotherapy to help shrink the lesion and hit it with loads of itraconazole.


What is eumycotic mycetoma

True fungal mycetomas that are deep subcutaneous fungal infections. We get aggregates of hyphae with granulomas and draining pus and granules.

It is caused by soil organisms entering wounds and we note black colored granules on excisions