Microbiology Flashcards
1.Comparison between primary and opportunistic systemic infections
2. Aetiologic agents of systemic mycoses
3. How does infection occur?
4. Are they dimorphic? Explain dimorphism
5. They are also known as?
6. How can they spread?
7. Are they transmissible from person to person? Stain??
8. Types of systemic mycoses: what part of the body does it affect?
Epidemiology
9. Aetiology? Transmission!?
10. Pathogenesis?
11. Clinical features: incubation period
12. Laboratory diagnosis
13. Treatment
- Primary systemic mycoses: they are geographically restricted, dimorphic, similar to TB, infection provides immunity, pyogenic/granulomatous host response, infection by inhalation.
Opportunistic infection: they are ubiquitous(found everywhere), yeast or mold not both, infection by various routes , no lasting immunity, host response varies, infection by various routes, - Histoplasmosis- histoplasma capsulatum duboiisi (Africans)
Coccidiodomycosis- coccidiodes immitis
Blastomycosis- blastomyces dermatitidis
Paracoccidiodomycosis- paracoccidiodes brasiliensis - Infection occurs by inhalation of spores(filamentous/mold form) from the environment. Within the lungs(body temp-37°C) the spores differentiate into yeast.
- They are thermally dimorphic except coccidiodomycosis(spontaneous conversion). They are mold(filamentous) in the environment at room temperature (25°C) and yeast at body tissue temperature(35-37°C).
- Also known as endemis mycoses
- Since infection in by inhalation, the primary site of infection is the pulmonary bed (which is why it is similar to TB) but can be disseminated into the reticuloendothelial system (bone marrow, spleen, liver, lungs) through hematogenous spread. Acute form may present as Pneumonia while chronic form presents as TB. They can disseminate to skin and bone if untreated.
- Not transmissible from person to person
- Histoplasmosis: it is a dimorphic organism that exists as mycelium at room temperature(25°C) and yeast at body tissue temperature(37°C). It affects the bone marrow, lungs, spleen, and liver. Can be sexually induced to give ascospores
Epidemiology: distributed world wide especially in warm humid environments. Incidence of H. Capsulatum is high in soils enriched with birds and bat droppings. Has a predilection for male(4:1) also occors more frequently in people who smoke and have COPD - Aetiologic agents are: histoplasma capsulatum var. duboiisi (Africans) and histoplasma capsulatum var. capsulatum(North and South America). Transmission is by inhalation of conidia(infective form small enough to reach the terminal bronchioles)
- Pathogenesis: it is thermally dimorphic and non-encapsulated. Infection occurs then the histoplasma microconidia are inhaled into the lungs, where they change into the yeast form. Neutrophils, macrophages, NK cells and lymphocytes are attracted in response to the infection. As in TB, macrophages assist in spreading the organism via lymphatics to the adjacent lymph nodes and hematogenous spread throughout the reticuloendothelial system. In disseminated infection, macrophages are engorged with yeast supporting the intracellular proliferation of the organism. The initial Inflammatory reaction becomes granulomatous where both caseating and non caseating granulomas are formed and fibrosis may follow.
- Incubation period: 1 week- few months. The disease may be local(pulmonary) or disseminated (reticuloendothelial system)
Acute pulmonary histoplasmosis: occurs in immunocompetent individuals due to inhalation of large inoculum. They give flu-like symptoms such as headache, fever, myalgia, non-productive cough.
Chronic pulmonary histoplasmosis: reactivation process; reactivation of dormant infection acquired a long time ago. Occurs more in men >50 years with COPD. They present as weight loss, night sweats, fever, cough and chest pain. In children, hepatosplenomegaly is the primary sign of infection while in adult it appears as pulmonary disease. There can be swelling(histoplasmoma) which enlarges, become calcified and obstrust airways. Fibrosis may distort airways causing bronchiectasis and emphysema. - Specimen and microscopic examination: spotum, urine, bone marrow aspirate, Csf, blood, cutaneous scraping, bronchoalveolar specimen.
Histology: detects fungus in tissue using fungal stains(GMS and PAS) ovoid bodies on histology
Culture: culture for at least 2 days using sabourand dextrise agar(SDA) at 25°C and 37°C. Dimorphic convertion
Serology: complement Fixation are used
PCR - Treatment: Supportive therapy for acute pulmonary histoplasmosis
Itraconazole for mild to moderate infection
Amphotericin B is used in disseminated histoplasmosis
Itraconazole is used a maintenance therapy in AIDS patient.
Coccidiodomycosis
1.Epidemiology
2. Aetiology
3.Pathogenesis
4.Clinical presentation
5.Diagnosis
6. Treatment
Coccidiodomycosis
1. They are found in USA, Mexico and central America
2. Caused by coccidiodes posadosii and coccidiodes immitis. They are transmitted by inhalation of arthroconidia(arthrospores)
3. They are dimorphic fungi which grows as mycelium in the environment and spherules in lungs of humans. Infection occurs when the arthroconidia is inhaled. It invades the lungs and differentiate to form spherules containing endospores. Nodules are formed containing clumps of spherules which burst causing symptoms. Granuloma formation occurs in chronic infection.
Disseminated disease is rare and they can be disseminated into skin, CNS, bone and joints
4. 60% are asymptomatic, about 25% suffer flu-like symptoms. After 1-2 weeks, about 15% develop hypersensitive reactions which presents as rash, erythema nodusum and erythema multiform
4. +Specimen and microscopic investigations
+ serology: spherulin and coccidiodin
Histology
5. Fluconazole, voriconazole, amphotericin B
Superficial fungal infections
1. Definition and types
2. Introduction /aetiology
3. Epidemiology
4. Pathogenesis/
5. Clinical features
6. Diagnosis
7. Treatment
- Superficial fungal infections are infections that arise from pathogens restricted to the stratum corneum with little or no tissue reactions
Types:
+Pityriasis Vesicolor
+Black Piedra
+White Piedra
+Tinea Nigra - Pityriasis Versicolor
Introduction: it is a chronic superficial fungal infection caused by lipophilic yeast-Malassezia spp. The most common species are Malassezia globosa, furfur, sympodialis. They are also associated with other skin infections such as seborrheic dermatitis and folliculitis. - Epidemiology: occurs worldwide but mostly in the tropical region in warm humid environment. It affects mostly young adults because their sebaceous glands are active and they sweat heavily. There is genetic predilection. Also seen in cushing’s disease
- Pathogenesis: it is an Opportunistic infection that occurs when it converts from saprophytic yeats to parasitic mycelium in situations such as immunosuppression, cushing’s disease. The fungus release azelaic acid which is a decarboxylic acid (produced by oxidation of unsaturated fatty acids). It inhibits tyrosinase which results in hypo-pigmentation. It has a predilection for sebaceous glands, the fungi uses lipids as nutrients
- Clinical features:
+hypo-pigmentation or hyper-pigmentation macules which is found in upper back, chest, arms/thighs and abdomen.
+Fungemia
+Folliculitis less commonly
+ pruritus and family history in 20% of cases
+non contagious and leaves no permanent scarring or pigmentary changes - Diagnosis: direct microscopy using KOH shows spores with mycelium(spaghetti with meatballs)
Examination using wood’s lamp
Histology: detected using H&E, PAS, methanamine silver stain - Treatment:
+topical anti fungal such as ketoconazole, econazole, miconazole, clotrimazole
+selenium sulfide; can be used as lotions and shampoos
+ oral azoles for recurrence
+UV therapy to induce maturation of melanosomes and accelerate pigmentation
Recurrence is common
Black and white piedra
1. Introduction
2. Aetiology
3. Clinical features
4. Diagnosis
5. Treatment
Black piedra
1. Introduction: it is a fungal infection of the hair shaft. It is common in tropics and affects man and monkeys. Affects all ages but common in young adults. It less commonly affects the public hair, moustache, and beards
2. It is caused by piedraia hortae
3. +Presence of gritty nodules which is noticed by metallic sound while brushing hair. It usually affects the hair scalp
+breakage of hair
4. Direct microscopy of hair shaft nodules using 10-15% KOH
Culture: grows slowly on SDA
Histology
5. Topical antifungal agents, oral terbinafine, shaving/cutting off hair.
White piedra
1. It mostly affects the public hair, moustache, beards, axillary hair, eye brows and eye lashes. It is found in soil, air, water and vegetative matter
2. It is caused by trichosporon species
3. +Breakage of hair
+ larger, softer and yellowish nodules on hair. Lightly pigmented and loosely attached to the hair follicles
4. +Direct microscopy of hair shaft nodules using 10-15% KOH
+fungal culture, histology and molecular identification
5. Treatment: +topical anti- fungal agent
+2% selenium sulphide
Tinea nigra
1. Introduction
2. Epidemiology
3. Aetiology
4. Pathogenesis
5. Clinical features
6. Diagnosis
7. Treatment/ prevention
- They are uncommon superficial fungal infections that causes brown to black painless patched on the palms or soles
- They occur world wide. The female to male ratio is 3:1. Hyperhidrosis is a risk factor.
- Caused by dermatiaceous fungi called hortaea exophialla werneckii.
It is a saprophytic fungi found in soil, humus and humid compost. - Organism is inoculated from contaminated source to skin by trauma. The organism gets nutrients from decomposed lipids and requires low PH and high salinity provided by the skin.
- It is asymptomatic, incubation period is 2-7 weeks.
+ presents as brown to black painless macules on palms, soles, neck or chest.
+ may be single or multiple with clear demarcating borders between affected and in-affected skin
+ no erythema, no inoculation - +Skin scraping from edge of lesion for direct microscopy using 20%KOH
+ culture: 25°C on SDA
+ histology - Selenium sulphide, topical anti- fungal e.g ketoconazole, repeated application of ketolytics
Prevention: wear gloves, avoidance of contact in potentially infected material in high risk region.
SUBCUTANEOUS MYCOSES
+Identify agents of subcutaneous mycoses
+risk factor for occurrence
+management strategies
OPPORTUNISTIC MYCOSES
+ Introduction
+ Causative agents
+ introduction, risk factors, pathogenesis, clinical findings, diagnosis and treatment of the causative agents.
+ introduction: opportunistic mycosis are mycotic agents that thrive on the body’s low immunity to cause a disease state. it may be endogenous or exogenous or reactivation.
+candidiasis, aspergilloisis, cryptococcus, zygomycosis, pneumocystosis jirovecii, penicillum marneffi
+candidiasis: pseudo-hyphae normal flora found on the skin, mucous membrane and GIT. commonest fungal disease overgrows in colonized state or invasion in non-colonized due to invasion or breech of the skin and mucous membrane.
+cryptococcus: phylum-Basidiomycota. true yeast. it’s prominent feature is mucopolysaccharide capsule. infection is by inhalation of basidospores. causes self-limiting pneumonia in immunocompetent individuals and in immunosupressed, the yeast cell multiply and disseminate to various organs such as the brain,
eye, kidney, skin, bone, adrenals, prostate. uses India ink for microscopy.
+Aspergillosis: infection is initiated by inhalation of conidia. in immunocompetent individuals, the alveolar macrophage are able to engulf and kill the conidia. but in immunocompromised host, macrophages are unable to contain the inoculum, it swells and invade pre-existing cavities.
+zygomycosis: glomeromycota. risk factor-DKA. infection is initiated by inhalation of spores in immunocompromised individuals, there is impaired phagocytosis by macrophages and polymorphonuclear cells. neutrophils dysfunction and accumulation of acids and sugars results in relentless growth of organisms. rhinocerebral mucormycosis affects the sinuses causing thrombosis, necrosis and infarction.
Blastomycosis and paracoccidomycosis
+aetiologic agents
+pathogenesis
+Clinical features and investigations
+Blastomyces dermatidis, dimorphic convertion
+inhalation of conidia which convert to yeast in the lungs. Macrophages and cell mediated immune response are activated leading to the formation or non-castrating granuloma. Organism may disseminate into other organs such as the skin, bones/joints, prostate and testes, rarely CNS
+ fever headache, cough, ulcers, osteomyelitis, cavities on chest Xray
+microscopy, culture, serology
Paracoccidomycosis
+paracoccidiodes brasiliensis
+ inhalation of conidia which invades the lungs. They remain dormant for long period and become activated when patient is immunocompromised leading to chronic pulmonary disease and dissemination
Hemoflagellate
+introduction
+classification-etiology, classification, pathogenesis, life cycle, diagnosis and treatment
+They are parasitic flagellates found in the blood stream of man and animals. They are eukaryotes(nucleus and nuclear membrane). Reproduce by binary fission and movement is with flagella
+classification: trypomastigote, amastigote, promastigote, epimastigote
Amastigote are found in tissues, muscles, CNS and within the macrophages while trypomastigote are found in the lymphatics, blood and Csf. Epimatigote are found in arthropods vector while promasgigote are found in early infection
+trypanosomes: African trypanosomiasis and American trypanosomiasis
Causative organism: trypanosoma brucie gambiense(west Africa) and trypanosoma brucie rhodesiense(East Africa)
Vector: tsetse fly(G. Fuscipes, palpalis, pallidipes, mortisans)
Pathogenesis: African trypanosomiasis
Enterobacteriaceae
+Gram negative or positive
+where are they found
+list members
+Properties
+classification
+E. coli: properties, biochemical reaction, virulence properties, pathotypes.
SPIROCHETES
+list the species
+properties
+ causative agents of syphilis
+how does treponema replicate
+stages of syphilis
+transmission of syphilis
+endemic treponema
+investigations
+specific and non-specific tests
+treatment
+Causative agents of relapsing fever
+clinical features of relapsing fever
+diagnosis
+treatment and prevention
+causative agent of Lyme disease
+characteristic feature
+diagnosis and treatment
+spirochetes of the mouth
+clinical features
+causative agent of leptospirosis
+investigations and treatment
+ treponema, borrelia and leptospiral
+
+syphilis is caused by treponema pallidum
+by transverse fission
+primary, secondary, latent and tertiary stages
+it is transmitted sexuallly, vertical transmission and IV drug users
+treponema endemicum, T. Pertenue and T. Caratuem
+culture - testicular tissue of rabbit, *microscopy of primary chancre, dark field microscopy, direct fluorescent antibody
AMOEBIC INFECTION
+ causes of amoebiasis
+two morphological appearance of a protozoa
+epidemiology
+two main syndromes of amoebiasis
+mode of transmission
+pathophysiology
+determinant of E. histolytica virulence; host and pathogen factors
+differences between amoebic dysentery and bacillary dysentery
+list amoebic infections
+list extra intestinal manifestations
+most common extra intestinal manifestation; it is common in which gender and age group, reasons??
+diagnosis
+treatment
+differentials
ANAEROBIC BACTERIA
+reasons why they are anaerobic
+examples of gram negative bacilli and cocci anaerobes
+examples of gram positive bacilli (spore forming and non-spore forming) and cocci
+samples of anaerobic infections
+blood cultures of anaerobes
+lab techniques
+treatment
GENITAL FLAGELLATES
+ classification of parasites
+describe flagellates ad group them with examples
+species of trichomonas
+trichomonas is transmitted by?
+gender and age predilection
+ what stage does it exist in
+pathophysiology of T. vaginalis
+ T. Vaginslis replicates by??
+host factors ad organism factor
+incubation period
+clinical features i men and women
+ specimen, investigations ad diagnosis
+treatment
INTESTINAL FALAGELLATE
+Giardia lamblia affects which age group more?
+which genotype infect humans?
+excystation and encystation occurs where
+features as a prokaryotes
+clinical disease is called?
+incubation period? They cysts has a special feature during excystation
+acute stage and differentials
+toxin they produce
+chronic stage and differentials
+treatment
+ causative agent of balantidiosis
+ clinical features and risk factors
+differentials
+diagnosis and treatment
