Mycoses 2 Flashcards
Mycoses Aspergillus species : Aspergillus fumigatus bacteria:
Aspergillus fumigatus bacteria: found in wide range of environments (ubiquitous).
Ubiquitous. Locations: Soil, decaying vegetation, stored grain, water storage tanks, air conditioning, bedding, computer fans and disinfectants. . Survives well through range of temperatures up to 75 C. Over 100 species: fumigatus most pathogenic. More pigmented candida=more virulent strain. Species A. flavus common cause of hospital infections.
Mycoses Aspergillus - Transmission
Transmission: light-weight small pores : easily airborne into lower respiratory tract. Antibodies in serum of healthy as spores breathed in (antibodies non-diagnostic). Clinical Pathology: In resp tract conidia (spores) exposed to immune response as they produce hyphae and further colonise location. Macrophages destroy spores whilst neutrophils kill hyphae. Neutrophils: long term fungi suppression, macrophages: early line of defence.
Mycoses Aspergillus: Four key pathologies
Pathologies: Allergic bronchopulmonary aspergillosis ABPA (asthma), Chronic pulmonary aspergillosis (CPA), Aspergilloma (Fungal ball), Invasive Aspergillosis
Allergic bronchopulmonary aspergillosis (ABPA)
- Immediate hyper sensitive allergic reation to fungal spore antigens. Proteolytic enzymes released by hyphae increase the immune response as spores germinate causes an asthma attack. complication of CF, sinusits, atopic asthma
Allergic bronchopulmonary aspergillosis (ABPA) - Treatment / Detection
- Hyper immune response to A. fumigatus detected through blood or skin test.
- Treatment : corticosteroids to suppress immune response to fungus. Constant presence of spores in the air represent constant change of attacks reoccurring. Severe attacks: antifungals to reduce inflammatory load.
Chronic pulmonary aspergillosis (CPA)
Aka Subacute invasive pulomary aspergillosis (SIPA) and chronic necrotizing pulmonary aspergilliosis (CNPA). not common
Chronic pulmonary aspergillosis (CPA) - Symptoms/ Clinical Presentation
Pneumonia, often in mildly immunocompromised ( alcoholism, thoracic surgery, other illness) or underlying/ previous pulmonary condition (TB or previous treatment for lung cancer). Damage forms cavities, damaging lung tissues causing pneumonia non-responsive to antibiotics. Weakened immune system still functions and maintains the infection in the lungs unless more severe immunosuppression occurs. Cavities can become the site of aspergilloma and greater immunosuppression = more serious consequences. . Symptoms: Fever, night sweats, weight loss, shortness of breath, haemoptysis (coughing up of blood)
Immunosuppression and alcohol consumption
- Alcohol + immunosupression: Typically linked to impact of material entering the airways and contaminating a sterile part of the body by inhaling/ choking on vomit
Diagnosis of CPA
- Diagnosis: Chest X-rays show one or more lung cavities or similar damage. Symptoms lasting more than 3 months: weight loss, fatigue, cough, and breathlessness. coughing blood ( haemoptysis): immediate investigation. Blood test or tissue fluid test positive for Aspergillus species. Growth on culture or evidence via bronchoscopy.
Treatment of CPA
Treatment: begin with agent e.g itraconazole, then altered depending on success therapy. Surgery available but high risk due to extensive network of blood vessels present in the lungs
Aspergilloma Pathology/ Clinical presentation
Pathology: Colonises pre-exisitng cavities left by TB, CF (10-15% of patients with similar conditions). Cavity: out of reach of immune system. Invade, settle, form mass of hyphae. Dead tissue and mucus.
Rarely disrupts blood supply in the lungs. Slight bleeding but very rarely fatal. Can occur in other locations in immuno-compromised patients(rare).
Aspergilloma Symptoms
Often no symptoms.
Aspergilloma Treatment
manage the previous condition well; no cavities. If severe bleeding then surgery.
Invasive Aspergillosis (IA) - Causation
exposure in immuno-compromised individuals: low neutrophil counts or otherwise weakended immune system. Most serious condition. Onset 1-2 weeks then death. Incidence of IA increased 14 x in 10-20 years due to HIV/AIDS
Invasive aspergillosis (IA) - Risk Factors
Transplants (Bone marrow esp), Chemotherapy(leukaemia esp), most frequent fungal infection in AIDS patients.
IA statistics
IA responsible for 30% of fungal infections in patients dying of cancer.
- Found in 19-26% of all heart-lung double transplants
- Up to 10% of liver, heart, lung or kidney transplants
- Makes up between 25-40% chronic granulomatous disease
- IA is now the most frequent fungal infection in AIDS patients (overtaking Candidiasis)
IA Types dependant on location
1) Pulmonary lungs 86% mortality
2)Tracheobronchitis (bronchial mucosa and cartilage) 70%-100%
3) Acute rhiosinusitus( sinuses) 66% mortality
4) Disseminated (brain, heart, kidneys, eyes, skin etc)
Disseminated: Starts with pneumonia then.
Heart: endocarditis, Bone: osteomyletis, Auditory canal: otomycosis
Cutaneous : skin either due to wound when immunocompromised or end result of disseminated
Blood brain barrier: meningitis 99% mortality
IA diagnosis
Positive ID is culture/microscope in sputum, antigens in serum and CT scan. ELISA and PCR being developed but a very common organism so need to be located in aseptic places.
IA Treatments
Usually cannot wait for confirmation of diagnosis so if neutropenic or weakened immune system for 12-15 days and symptoms don’t reduce with antibiotics: use antifungals. Limited use of Amphotericin B first line drug for 34% success rate. No treatment= fatal infection. After 2 weeks: only 54 % respond to treatment. Sometimes debridement ( removeal of dead or infected tissue from wound) used.
Stop neutropenia or other immunosuppression stops: aspergilliosis stops.
Histoplasmosis
Caused by Histoplasma capsulatum. Thrives in acidic conditions. Excrement of birds and bats. bats can contract and spread. Birds cant contract but bats can. Thermally dimorphic: temperature alters their form: transform to yeast at 37 C. 500k infected Worldwide (half in the U.S). 50-200k develop symptoms. 1500-4000 need hospital treatment. 80-90% of immunocompetent infected asymptomatic or have self limiting flu symptoms.
Histoplasmosis Disease pathology
Pathology: Fragments of mycelia and conidia are breathed in via aerosols: engulfed via Phagocytic macrophages, turn to pathogenic yeast. Yeast resist phagocytic killing active T cells contain infection. If none then transported by circulating macrophages round the body. Or latent: wait for immune status to drop and re-erupt as active disease
Granulomas
Histoplasmosis Disease Syptoms in the immuno-compromised
Serious clinical symptoms largely in immuno-compromised 1.Acute pulmonary. 2.Chronic pulmonary. 3.Progressive disseminated
Histoplasmosis: Acute pulmonary complication clinical presentations
Develops 3-14 days after exposure. Fever headache, chills . Large innoculum (lots of spores): severe complications:5-10% of patients: enlarged lymph nodes causing local obstructions e.g Superior vena cava (carries deoxygenated blood back to heart from upper body) ., may have extensive areas of pulmonary system involved . Pneumonitis (inflammation of lung tissue) fluid accumulates: oxygen exchange hampered
Histoplasmosis: Acute pulmonary complication symptoms
Symptoms: headache, visual distortion, tinnitus and altered consciousness. Other obstructions include compressing pulmonary airway, and trachea (cough heart pain, SOB, Haemoptysis)
Histoplasmosis: Chronic Pulmonary
Occurs due to underlying lung disease. Develop cavities, can occur at same time as other infections (TB, other mycoses)
Histoplasmosis: Chronic Pulmonary symptoms
Cough, fever and SOB. Untreated leads to respiratory failure and cardiac failure
Histoplasmosis: Progressive disseminated
0.05% cases of infected immuno-competent (often due to huge dose overwhelming immune system).Infection spreads beyond lungs. If untreated: progresses, death in weeks. Involves multiple organs leading to varied pathology: hepatosplenomegaly, lymphadenopathy, bone marrow involvement, oral or gastrointestinal ulcerations. Bone marrow leads to: anaemia, leukopenia, thrombocytopenia
Diagnosis: Clinical evaluation, imaging studies ( xray/ CT scan), blood culturesm serological tests, tissue biopsy, PCR: detect histoplasma DNA.
Histoplasmosis: Progressive disseminated Symtpoms/ Clinical presentations
Adrenal glands enlarge Addison’s disease (failure of adrenal glands)
UTI penile and bladder ulcers and inflammation of prostate
CNS (5-20% of patients) meningitis and cerobritis
Signs include lesions on mouth and gums
