Mycology and Parasitology Flashcards
Definition of mycology
Study of medically important fungi
Types of fungi
Moulds:
- further divided into dermatophytes
- Multicellular
Yeasts
- unicellular
Dermatophyte moulds infections
Scalp
- Tinea captis
- commonest infection in paeds population
- transfer via infected combs, towels
Nail
- tinea unguium
- increase with age
Feet
- Tinea pedis
Face (males)
- Tinea barbae
Trunk, legs arms
- Tinea corporis
Fingernail and toenails
- Tinea ungium
Groin
- Tinea cruris
Laboratory confirmation of a dermatophyte infection
Microscopy
- Interpretation of slides requires experience
- In most cases, cannot tell what type of fungus is causing the infection
Molecular detection
- Sensitive but more expensive than conventional methods
Culture
- Permits species identification
- majority identified by 7-10 days
Treatment for dermatophytes
- Terbinafine – inhibits squalene epoxidase resulting in accumulation of squalene & the reduction of ergosterol in fungal cells = altered cell wall function & synthesis
- Griseofulvin - binds to fungal microtubules altering mitosis & deposition of fungal cell walls
- Itraconazole - inhibits the fungal-mediated synthesis of ergosterol via its ability to inhibit cytochrome P450
Non dermatophyte moulds
- Aspergiullus species
- Macroaceas noulds
Aspergillus mode of infection
Inhalation
Aspergiullus species and where they are found
- Found in soil, plants, air
- 200 species, only 20 cause disease
- Most disease caused by Aspergillus fumigatus and Aspergillus flavus
Clinical manifestations of aspergillus infection
Immunocompromised
- Widespread growth of fungus in lungs, sinuses and dissemination to other organs & CNS
- Fever, failure to respond to broad spectum antibiotics, low grade chest pain
- CT scans reveal lung lesions, small nodules (halo sign
Immunocompromsed
- allergic sinusitis
Mucoraceous moulds species and where found?
- Found in soil, on foods, air-borne
- Affect mostly immunocompromised patients
- Examples include Rhizopus, Absidia
Clinical manifestations of mucroaceous moulds
- lung and nasal sinuses
- inoculation of broken skin
- fever, facial swelling, headache, nasal discharge, black lesions on roof of mouth,, black pus from eye
- often lethal
Treatment of moulds other than dermatophytes
- Amphotericin B (Ambisome) – binds to ergosterol to impair cell wall function by inducing pores causing ion leakage.
- Itraconazole, Voriconazole, Posaconazole - inhibits the fungal-mediated synthesis of ergosterol via cytochrome P450 inhibition.
- Caspofungin – inhibits β(1,3)-D-Glucan synthase thereby disrupting cell wall synthesis
Types of pathogenic yeasts
- Candida species
- Crytpococcus species
Yeast infection clinical features
- part of normal flora
- Colonisation in warmth and moist
- Thrush
- Candida albicans
- skin infections
- Malazzia species
Invasive candida infection features
- fourth most common bloodstream infection
- occurs in high risk patients
- affects:
- kidneys (80%)
- heart (prosthetic valves)
- gastrointestinal tract
- lungs
Invasive cryptococcus infections
- Pigeon droppings
- Cryptoccocus neoformans var neoformans
- Gum trees/ tropical regions
- Cryptoccocus neoformans var gattii in
- Acquired via inhalation of spores
- commonly presents as menigitis.
- also, productive cough, chest pain, weight loss, fever
Laboratory identification of yeasts
Cultruing on chromogenic agar
- Some yeasts have very similar colour
- Can observe if more than one yeast is present
Maldi-tof
- specific pattern
- mass spec
- 20 seconds
Treatment of superficial candida infections
- Fluconazole, itraconazole – both inhibit the fungal cytochrome P450 enzyme thus inhibiting ergosterol formation
- Nystatin, Clotrimazole– binds to ergosterol forming ion pores which lead to leakage
Treatment of invasive candida infections
- Amphotericin B (Ambisome) – binds to ergosterol to impair cell wall function.
- *Fluconazole
- Caspofungin – inhibits cell wall synthesis
- *Flucytosine – alters protein & DNA synthesis – resistance is common
Types of parasites
Protozoa
- Sporozoa - toxoplasma gondii
Helminths
- trematodes - Shicstomatosis
Schistosomaiasis species
Helminth - trematode
5 species infect humans (S species)
Schisosome life cycle
- infected person pees in the water
- eggs make contact with fresh water
- miracicila hatches
- finds snail host
- cercaria forms
- penetrate skin
- becomes itchy
- go to liver and mature into schistomoluae
- matures with female and releases eggs
Inital symptoms of schistomatosis
- often asymptomatic
- within 24 hours rash develops on skin
Chronic schistomiasis (late phase) affects
neurological
- eggs lodge in the CNS/brain -epilepsy
Gential
- females get ulcerative lesions of vagina, vulca, cervix (inferitility)
hepatic
- internal bleeding, usually sudden, massive and fatal
Intestinal
- inflammation of the large bowel and rectum, diarrhoea
Urinary
- ulceration of bladder, blood in urine, calcification of bladder resulting in kidney failure, bladder cancer
Diagnosis of schistomatosis
1) Serology to detect egg antigens
2) Microscopy screening of stools & urine
Treatment of Schistomatosis
- Praziquantel (alters parasite membrane permeability) – paralyses the worm
- •No side effects
- No effect on immature worms or eggs
- Effective for all species
Toxoplasmosis species and life cycle
- Oocysts are shed in cat stools
- Intermediate hosts include birds, rodents, cattle - become infected after ingesting contaminated soil & water.
- Oocysts transform into tachyzoites –> bradyzoite cysts in neural and muscle tissue
Humans become infected with toxoplasmosis by?
- eating undercooked meat of animals
- consuming food or water contaminated with cat stools
- blood trasnfusions
Clinical features of toxoplasmosis
tissue cysts in skin, heart, brain, eyes
Diagnosis of toxoplasmosis
Serology using ELISAs (IgG and IgM detection)
Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR
Treatment of toxoplasmosis
Pyrimethamine
