Mycoses 2

Question 1

Mycoses Aspergillus species : Aspergillus fumigatus bacteria:

Answer 1

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.

Question 2

Mycoses Aspergillus - Transmission

Answer 2

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.

Question 3

Mycoses Aspergillus: Four key pathologies

Answer 3

Pathologies: Allergic bronchopulmonary aspergillosis ABPA (asthma), Chronic pulmonary aspergillosis (CPA), Aspergilloma (Fungal ball), Invasive Aspergillosis

Question 4

Allergic bronchopulmonary aspergillosis (ABPA)

Answer 4

• 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

Question 5

Allergic bronchopulmonary aspergillosis (ABPA) - Treatment / Detection

Answer 5

• 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.

Question 6

Chronic pulmonary aspergillosis (CPA)

Answer 6

Aka Subacute invasive pulomary aspergillosis (SIPA) and chronic necrotizing pulmonary aspergilliosis (CNPA). not common

Question 7

Chronic pulmonary aspergillosis (CPA) - Symptoms/ Clinical Presentation

Answer 7

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)

Question 8

Immunosuppression and alcohol consumption

Answer 8

• Alcohol + immunosupression: Typically linked to impact of material entering the airways and contaminating a sterile part of the body by inhaling/ choking on vomit

Question 9

Diagnosis of CPA

Answer 9

• 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.

Question 10

Treatment of CPA

Answer 10

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

Question 11

Aspergilloma Pathology/ Clinical presentation

Answer 11

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).

Question 12

Aspergilloma Symptoms

Answer 12

Often no symptoms.

Question 13

Aspergilloma Treatment

Answer 13

manage the previous condition well; no cavities. If severe bleeding then surgery.

Question 14

Invasive Aspergillosis (IA) - Causation

Answer 14

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

Question 15

Invasive aspergillosis (IA) - Risk Factors

Answer 15

Transplants (Bone marrow esp), Chemotherapy(leukaemia esp), most frequent fungal infection in AIDS patients.

Question 16

IA statistics

Answer 16

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)

Question 17

IA Types dependant on location

Answer 17

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

Question 18

IA diagnosis

Answer 18

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.

Question 19

IA Treatments

Answer 19

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.

Question 20

Histoplasmosis

Answer 20

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.

Question 21

Histoplasmosis Disease pathology

Answer 21

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

Question 22

Histoplasmosis Disease Syptoms in the immuno-compromised

Answer 22

Serious clinical symptoms largely in immuno-compromised 1.Acute pulmonary. 2.Chronic pulmonary. 3.Progressive disseminated

Question 23

Histoplasmosis: Acute pulmonary complication clinical presentations

Answer 23

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

Question 24

Histoplasmosis: Acute pulmonary complication symptoms

Answer 24

Symptoms: headache, visual distortion, tinnitus and altered consciousness. Other obstructions include compressing pulmonary airway, and trachea (cough heart pain, SOB, Haemoptysis)

Question 25

Histoplasmosis: Chronic Pulmonary

Answer 25

Occurs due to underlying lung disease. Develop cavities, can occur at same time as other infections (TB, other mycoses)

Question 26

Histoplasmosis: Chronic Pulmonary symptoms

Answer 26

Cough, fever and SOB. Untreated leads to respiratory failure and cardiac failure

Question 27

Histoplasmosis: Progressive disseminated

Answer 27

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.

Question 28

Histoplasmosis: Progressive disseminated Symtpoms/ Clinical presentations

Answer 28

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