MICROBIOLOGY - FUNGI, PARASITES Flashcards
How can fungi be classified
Yeasts, molds, dimorphic fungi
Fungi cell wall components and which is most abundant
1 specific cell membrane component unique to fungi and targeted by medication
Glucan (60% and most abundant being beta-(1,3-) glucan), chitin (10%), 30% protein
ergosterol
How do yeasts reproduce
Budding (spore forming)
Candida epidemiology and the disease it causes? Name some risk factors (5)
Candida: commensals on skin, GI tract, female reproductive tract
Candidiasis
Risk factors: Immunocompromised, Broad spectrum antibiotics, transplants, steroids, ICU, IV
Candidiasis in immunocompetent and immunocompromised hosts?
Immunocompetent: vaginal thrush
Immunocompromised: symptoms more refractory (do not respond to treatment), oral thrush, systemic candidiasis eg in liver/spleen
Candidiasis diagnostic methods?
Culture using Sabouraud agar, Gram stain (gram +ve), detection of antigen (Beta-d-glucan antigen) in serum
Treatment method for candidiasis?
Polyenes: Nystatin if topical (forms complex with ergosterol in cell membrane), amphotericin B when systemic infection
Azoles: eg Fluconazole to inhibit ergosterol synthesis
Echinocandins eg micafungin to inhibit cell wall synthesis
Name 1 nucleoside analogue used to treat fungal infection
5-flucytosine
Cryptococcus neoformans morphology under stain? What risk factors for C. neoformans?
Besides stain how can it be identified
WIth halo because of capsule when stained under India ink
Immunocompromised patients
Cultured or checked for capsular polysaccharide antigen
Mould morphology?
multicellular, long filaments, reproduce by spores
Aspergillus method of identification and disease? Risk factor?
Systemic infection, identified by galactomannan antigen, nucleic acid, culture
Risk factor: Immunocompromised (eg HIV/neutropenia/organ transplants/immunosuppressants/
Dermatophyte species? What disease do dermatophytes cause
Trichophyton, Epidermophyton, Microsporum
Disease: tinea - aka ringworm (tinea pedis, tinea capitum, tinea unguium)
Dimorphic fungi - name 1 example and its morphology at 37c and 25c
How can it be detected
Risk factors?
Symptoms?
Talaromyces marneffei - 37c yeast, 25c mold (mold has diffusible red pigment) on agar
Detected by patient antibodies
Immunocompromised patients
Multiple skin lesions with papules with central necrotic umbilication
Fungi that cannot be cultured?
Pneumocystis jirovecii
Define: Parasitism, parasite, host
Parasitism: any reciprocal association in which a species depends
upon another for its existence
parasite: the organism that derives all benefit from dependence upon another organism
host: the organism that harbors the parasite
How can parasites be typified (in relation to host)
Level of dependence, time, physical relationship
Level of dependence: obligate (fully dependent) or facultative
time: temporary or permanent
physical relationship: endoparasite or ectoparasite
Define definitive and intermediate host
Definitive host: Houses the parasite in active form
Intermediate host: houses intermediate form of parasite
How to diagnose parasitic infection?
1)Demonstration of parasites in appropriate clinical specimens by direct microscopic examination, staining, or tissue sections.
- Serology: detection of antigens or antibodies in blood or other body fluids.
- Culture of parasites (extremely uncommon): applicable only to a small number of parasites, mainly protozoa.
- Nucleic acid amplification (eg PCR)
How to prevent parasite infection
Elimination: 1) of parasites in reservoir 2) of parasite vectors
Avoid exposure to parasite/vector
Chemoprophylaxis (eg antimalarial)
Vaccines (eg 2 vaccines available against malaria)
Classify parasites based on physical relationship with hosts?
Endoparasites: Protozoa or helminth (trematode, cestode, nematode)
ectoparasite: arthropods
Protozoa - how many cells? Classified into which 2 groups? For lumen dwelling further classify
GIVE EXAMPLES FOR ALL GROUPS
Unicellular
Lumen-dwelling or blood and tissue dwelling (extraluminal)
Lumen-dwelling:
in GI tract (eg Entamoeba histolytica) - Causes amoebic colitis/dysentery and amoebic liver abscess
in Genital tract: Trichomonas vaginalis (STI), Giardia lamblia
Extraluminal (blood/tissue): Toxoplasma gondii, Plasmodium
Nematode morphology and classification? For each group give an example and properties of that example
Round worms
Classified into:
Intestinal nematodes, eg: Strongyloides stercoralis (asymptomatic in immunocompetent host, can lead to hyperinfection in immunocompromised host) (IF RUSH JUST REMEMBER THIS)
Blood and tissue nematodes, eg: Angiostrongylus cantonensis (associated with raw or undercooked snails/slugs/freshwater shrimp/land crabs - assoc. with meningitis)
Wuchereria bancrofti, Brugia malayi: Lymphatic filariasis
Enterobius vermicularis: perianal pruritusxz
Trematode morphology? What hosts do they all need?
1 example of: Liver, Lung, Intestinal and Blood fluke, and what is it associated with
Flukes, leaf-shaped flatworms, freshwater snails
Clonorchis sinensis the liver fluke - associated with intake of undercooked freshwater fish, carcinogen associated with CHOLANGIOCARCINOMA
Lung fluke: Paragonimus, associated with eosinophilic pneumonia
Intestinal fluke; Fasciolopsis buski
Blood fluke: Schistostoma spp.
Cestode - morphology? Which 2 groups? Examples for each group?
Segmented adults - Taenia solium/saginata
Intestinal cestode (adult stage) - Taenia solium (ingesting larvae)
Tissue cestode - (larval stage) - Taenia solium (cysticercosis) - ingesting eggs of Taenia solium
Ectoparasite examples?
Some vectors of parasites?
Fleas, scabies mite, maggots of flies
Mosquitoes, tsetse flies, fleas, lice, sandflies, blackflies, triatomine bugs
5 main plasmodium species and their distribution? Which is most fatal? Which 2 species cause majority of human malaria cases?
Most fatal: P. falciparum
P. falciparum: tropics
P. malariae: sporadic
P. vivax: global
P. ovale: West Africa, some South Pacific islands, also found in other parts of the world sporadically.
P. knowlesi: Southeast Asia, esp Malaysia/Malaysian Borneo, simian malaria that sometimes causes human infection
P. vivax and P. falciparum cause most malaria cases
Malaria transmission methods? Its vector?
Vector: FEMALE Anopheles mosquito
Blood transfusion and organ transplantation
Contaminated needles/medical instruments and medications
Vertical transmission: mother to unborn infant before or after delivery
Plasmodium life cycle? In general
Infection
Pre-erythrocytic cycle
Erythrocytic cycle
Transmission to Anopheles
For P. vivax and ovale ONLY: Secondary schizogony in hepatocytes
Each step in depth?
A) Infection:
1) Anopheles mosquito injects sporozoites into human bloodstream, 2) Sporozoites reach the hepatocytes within 30 min
B) Pre-erythrocytic cycle:
1）sporozoites infect hepatocytes,
2）asexually reproduce to produce merozoites within a schizont,
3）schizont ruptures to release more merozoites
4） merozoites released invade circulating RBC
C) Erythrocytic cycle:
merozoites infect RBC, then:
1) Schizogony (make schizonts) - asexually reproduce to form more merozoites in schizont, schizont ruptures, releases merozoites to continue infecting
OR
2) Gametogony (make gametocytes) - formation of gametocytes (male is microgametocyte, female is macrogametocyte) within RBC, gametocytes taken up when female Anopheles mosquito takes a blood meal
D) Transmission by Anopheles:
1) Gametocytes mature, sexual reproduction to form zygote and oocyst
2) Sporogony: Sporozoite formation in oocyst, oocyst ruptures to release sporozoites, sporozoites migrate to salivary gland of mosquito
B chronogically)
Secondary schizogony (Vivax and ovale ONLY)
Hypnozoite formation:
Vivax and Ovale may stay in hepatocytes - sporozoite form hypnozoite, persists for many years (so can have 2nd infection)
Pathogenesis of malaria? the 5 stages?
3 + 2: 3 related to RBC, 2 inflammatory
1) Increased RBC destruction as:
RBCs lose deformability,
become infected by parasites (especially P. falciparum),
spleen becomes enlarged (splenomegaly) because of immune reaction to destroy more RBCs
2) Infected RBC cytoadherence to endothelium in P. falciparum infection - microvascular obstruction (think something like a clot)
3) RBC lysis - iron depletion, anemia, hemoglobinuria (blackwater fever - free hemoglobin excreted in urine, so urine becomes coca-cola colored)
4) Nephrotic syndrome - immune complexes deposit in kidneys during chronic P. malariae infection
5) Cytokine production during infection
4 symptoms of malaria?
JUST KNOW THE BASICS FOR TIME!
fevers, chills, nausea
severe then end organ damage eg brain/lung/kidney
1) Paroxysms - Chills, rigor in the first 1-2 hours, then spiking fever in subsequent hours, then sweating and defervescence (body temperature decreases rapidly) - patients do not follow typical fever patterns
Fever patterns for malaria:
Vivax, Ovale, Falciparum: 48-hour cycle
Malariae: 72-hour cycle
Knowlesi: 24-hour cycle
2) Severe malaria - falciparum infection mostly, vivax occasionally
- end organ damage, eg cerebral malaria, severe anemia, renal failure, circulatory shock, hypoglycaemia
3) Relapse - recurrence of symptoms after COMPLETE initial clearing of parasitaemia due to reinvasion of bloodstream by hypnozoite (P. vivax and P. ovale)
4) Recrudescence: recurrence of symptoms because of incomplete clearing to very low levels of parasitaemia (but not fully cleared)
Malaria diagnosis?
1) take history (travel location, prophylaxis, fever patterns but not useful clinically, blood/blood product transfusion etc)
2) Take specimens - peripheral blood anticoagulated with EDTA
3) Make thick and thin blood films with Giemsa, Wright or Field’s stains (1 single negative blood test DOES NOT rule out malaria)
4) Antigen testing or PCR
Principles of malaria treatment? List some examples of medications as well
Suppressive therapy - chemoprophylaxis to prevent development of clinical syndromes, destroy asexual erythrocytic stages
Clinical cure: eliminate asexual erythrocytic forms during acute attack
Medication: Blood schizonticides, eg: Artemisinin based combination therapy (ACT), chloroquine, mefloquine, atovaquone-proguanil (many older drugs limited utility bc of drug resistance)
Radical cure: kill gametocytes and hypnozoites
Medication: tissue schizonticide, eg primaquine
