• Abosulte eosinophil count : 0.966 K/ul
( 0.04- 0.4 K/ul )
• TFT – Normal
• LFT – Normal
• ANA Screen : Negative
• HIV Emergency Screen : Negative
• HBsAg : Negative
• Anti HCV : Negative
• Peripheral Blood Smear : Normocytic
Normochromic blood picture with Eosinophilia
• WIDAL Test : Negative
• Blood C/S : No Growth
• Urine C/S : No Growth
CT CHEST WITH CONTRAST
CT CHEST WITH CONTRAST
• Varicoid & Cystic bronchiectatic changes
involving both upper lobes ( Left > Right ) ,
Right middle lobe, superior segment of both
lower lobes, proximal bronchi of basal
• Mucoid impaction in proximal lingular bronchi
• Gram Smear : negative
• AFB Smear : negative
• Fungal Smear : negative
• C/S : Pseudomonas
• AFB C/S : Awaited
• Fungal C/S : Awaited
• Cytology : No Atypical cells / Fungi
• SKIN TEST FOR ASPERGILLUS : POSITIVE
• Serum Aspergillus IgG : +
• Serum Aspergillus IgM : +
PROBABLE ALLERGIC BRONCHOPULMONARY
• Aspergillus may cause a broad spectrum of
disease in the human host, ranging from
hypersensitivity reactions to direct angioinvasion.
• Aspergillus primarily affects the lungs, causing 4
main syndromes, including
• Allergic Bronchopulmonary Aspergillosis (ABPA),
• Chronic Necrotizing Aspergillus Pneumonia or
Chronic Necrotizing Pulmonary Aspergillosis
• Invasive Aspergillosis
However, in patients who are severely
immunocompromised Aspergillus may
hematogenously disseminate beyond the lung
potentially causing :
• Abscesses in the myocardium, kidney, liver, spleen, soft
tissue, and bone
• Aspergillus is second to Candida species as a cause of
fungal endocarditis. Aspergillus -related endocarditis
and wound infections occur in the context of cardiac
• Allergic bronchopulmonary aspergillosis (ABPA) is caused
by a hypersensitivity reaction to the fungus and most
commonly occurs in those with asthma.
• Saprophytic aspergillosis, or aspergilloma, is the most
common form, which is noninvasive and involves
colonization of preexisting cavities.
• Chronic necrotizing aspergillosis, also called airway-invasive
or semi-invasive aspergillosis, is a chronic cavitary
pneumonic illness that often affects patients with
preexisting chronic lung disease.
• Angioinvasive aspergillosis affects immunocompromised
patients and is often fatal.
• ABPA is a hypersensitivity reaction to
A.fumigatus colonization of the tracheobronchial
tree and occurs in conjunction with asthma and
cystic fibrosis (CF).
• Allergic fungal sinusitis may also occur alone or
• Bronchocentric granulomatosis and
Malt worker's lung are 2 hypersensitivity lung
diseases that are caused by Aspergillus species,
but they are rare
Microscopic slide of lung tissue. This image
shows broad hyphae, which branch at acute
In ABPA, Branching finger-in-glove tubular opacities in the left
lower lobe due to mucus plugging of ectatic bronchi
Central Bronchiectasis in ABPA
DIAGNOSTIC CRITERIA FOR ABPA
ABPA WITH ASTHMA ( without CysticFibrosis )
• Immediate cutaneous reaction to Aspergillus
• Total serum Ig E > 1000 ng / ml
• Elevated serum specific Aspergillus IgE, IgG
• Serum precipitins to Aspergillus antigen
• Peripheral blood eosinophilia
• Transient or fixed pulmonary infiltrates
• Proximal bronchiectasis
When a patient with asthma does not have
bronchiectasis the following criteria are :
• high total serum IgE levels
• immediate cutaneous reaction to Aspergillus,
• elevated Aspergillus-specific IgE (or IgG) levels
• precipitating Aspergillus antibodies in serum
In other cases, particularly in the absence of
systemic corticosteroids :
• elevated blood eosinophil counts,
• marked increases in precipitating Aspergillus antibodies
• pulmonary infiltrate allow ABPA diagnosis
ABPA In Patients with Cystic Fibrosis
• Clinical deterioration (coughing, wheezing, increased
sputum production, exercise intolerance and decrease in
• Immediate hypersensitivity to A. fumigatus (positive
skin test or IgE response)
• Total serum IgE concentration >1000 kUI/l
• Precipitating antibodies to A. fumigatus
• Abnormal chest roentgenogram (infiltrate, plugs or
unexplained changes compared to previous chest X-ray).
The recommendation is that
• Cystic fibrosis patients should be screened for ABPA from 6
years of age, once a year / in response to ABPA.
• Onset can be in childhood but is more common in
• Most of the patients have other allergic
manifestations like rhinitis, conjunctivitis & atopic
• The ABPA onset occurs at the time of, or more
frequently after, asthma onset and is usually
associated with the transformation of mild
asthma into corticosteroid-dependent asthma
with some symptoms
symptoms like …..
• fever (body temperatures reaching 38.5C),
• Presence of sputum plugs and purulent
• coughing or
• chest pain
Clinically in to 5 stages
STAGE CLINICAL FEATURES BIOLOGY RADIOLOGY
I : ACUTE FEVER, COUGH, ELEVATED SERUM PULMONARY
CHEST PAIN, IgE levels + / - INFILTRATES IN
HEMOPTYSIS, PERIPHERAL BLOOD UPPER / MIDDLE
SPUTUM + EOSINOPHILIA LOBES
II : REMISSION ASYMPTOMATIC / NORMAL / NO INFILTRATES ( IN
STABLE ASTHMA ELEVATED TOTAL IgE ABSENCE OF
levels SYS.STEROIDS > 6m)
III : EXACERBATION SYMPTOMS ELEVATED SERUM PULMONARY
MIMICKING ACUTE IgE levels + / - INFILTRATES IN
STAGE OR PERIPHERAL BLOOD UPPER / MIDDLE
ASYMPTOMATIC EOSINOPHILIA LOBES
IV : CORTICO – PERSISTANT SEVERE NORMAL / WITH / WITHOUT
DEPENDENT ASTHMA ELEVATED TOTAL IgE PUL. INFILTRATES
V : FIBROSIS CYANOSIS & NORMAL / CAVITATORY
( end stage ) SEVERE DYSPNOEA ELEVATED TOTAL IgE LESIONS,
• Inadequately controlled asthma
• Pulmonary tuberculosis in high prevalent
• Bacterial, viral, fungal pneumonia
• Eosinophilic pneumonia,
• Bronchocentric granulomatosis
• Churg-Strauss syndrome
• Hypersensitivity pneumonitis
• Early detection and prompt treatment of ABPA
exacerbations, so as to prevent or minimize
• Manage associated asthma or irreversible
obstructive and restrictive lung disease
• Exclude others having ABPA in family, and
• To identify potential environmental source of
• Corticosteroids remain the early treatment
options and are cornerstone of treatment.
• Aggressive treatment of early stages, may halt
progression to stage of fibrosis.
• The recommended dose is Prednisolone 0.5
mg/kg/day for the first 2 weeks,
• Followed by a progressive decrease in dose
over the next 6–8 weeks
• Long-term systemic corticosteroid therapy is
• If the patient has no new exacerbation within
6 months, he is judged to be in remission
• Stage IV patients have severe asthma, which is
corticosteroid-dependent. In these cases, the minimal
dose required to stabilize the patient must be
• The extent of the bronchial destruction in Stage V
patients makes the prognosis poor.
• In addition, these patients suffer from recurrent
infections (the majority of which involve
Pseudomonas) and respiratory insufficiency with
limited exercise tolerance.
• Treatment with corticosteroids is generally proposed,
but is poorly efficient.
• Several antifungal agents (e.g. amphotericin B,
ketoconazole,clotrimazole, nystatin and
natamycin) have been proposed as treatments
• However, no significant beneficial effects were
observed when these drug treatments were
tested and in several cases these agents were
responsible for severe adverse effects.
• In contrast, the new orally administered
antifungal agent, Itraconazole, appears to be
an effective adjunctive therapy for ABPA.
• Preliminary retrospective clinical study comparing
the outcome of a 1-year itraconazole treatment
with that of 2-year therapy with the normal
treatment of corticosteroids alone was done.
• The number of exacerbations was lower for the
itraconazole treated group than for the group
treated with corticosteroids alone.
• Corticosteroid daily requirements decreased from
22 to 6.5 mg/day, although the dose required
differed substantially between patients.
• A fungal ball (mycetoma) that develops in a
preexisting cavity in the lung parenchyma.
• Underlying causes of the cavitary disease may
include treated tuberculosis or other
necrotizing infection, sarcoidosis, CF, and
• The ball of fungus may move within the cavity
but does not invade the cavity wall
• It may cause hemoptysis.
• The development of a mycetoma produces a tumour-like
opacity on X-ray,
• But can usually be distinguished from a peripheral
bronchial carcinoma by the presence of a crescent of air
between the fungal ball and the upper wall of the cavity.
• HRCT provides greater clarity and often demonstrates the
presence of multiple mycetomas.
• Serum precipitins to A. fumigatus can be demonstrated in
virtually all patients.
• Sputum microscopy typically demonstrates scanty hyphal
fragments, and is usually positive on culture.
• Less than 50% of patients exhibit skin hypersensitivity to
extracts of A. fumigatus
• Treatment is often disappointing.
• Selected patients with good respiratory
reserve may benefit from surgery, particularly
those who experience massive haemoptysis.
• Surgical resection may be accompanied by
significant morbidity and mortality.
• Bronchial artery embolisation provides a
palliative approach to haemoptysis.
• Specific antifungal therapy is of no value
• A subacute process usually found in patients
with some degree of immunosuppression,
most commonly that associated with
underlying lung disease, alcoholism, or long-
term corticosteroid therapy.
• As it is uncommon, CNPA often remains
unrecognized for weeks or months and can
cause a progressive cavitary pulmonary
resources, visit eMedicine's Lung and Airway Center and Asthma Center. Also, see eMedicine's patient education articles Asthma, Allergy
Chronic, cavitating, upper lobe consolidation in patient with long-standing fibrosing
alveolitis; this finding is consistent with chronic necrotizing aspergillosis. Aspergillus
fumigatus was cultured from the sputum and percutaneous aspiration samples
• A rapidly progressive, often fatal infection that occurs
in patients who are severely immunosuppressed,
including those who are profoundly neutropenic, those
who have received bone marrow or solid organ
transplants, and patients with advanced AIDS1 or
chronic granulomatous disease.
• This infectious process is characterized by invasion of
• Result in multifocal infiltrates, which are often wedge-
shaped, pleural-based, and cavitary.
• Dissemination to other organs, particularly the central
nervous system, may occur.
Section of a blood vessel. This image
shows branching fungal hyphae that
invade the vessel wall.
• Invasive pulmonary aspergillosis should be
suspected in any patient thought to have
severe suppurative pneumonia that has not
responded to antibiotic
• Diagnosis can be established by the
demonstration of abundant fungal elements in
stained smears of sputum.
• Serum precipitins can be demonstrated in
some, but not all, patients.
• Invasive aspergillosis carries a high mortality rate but if the
diagnosis is established at an early stage, antifungal therapy can be
• Amphotericin 0.25-1 mg/kg daily by slow intravenous infusion over
6 hours should be given in combination with flucytosine 150-200
mg/kg daily by mouth or by intravenous infusion, in four divided
• The combination of flucytosine and amphotericin prevents
resistance to flucytosine developing and allows a smaller daily dose
of amphotericin to be used.
• Liposomal amphotericin is recommended when toxicity precludes
the use of conventional amphotericin.
• Itraconazole has also been used successfully in the treatment of