HIV/AIDS BY SYSTEM

HIV and the lung

Whats new?

Jamilah Meghji
C

Robert F Miller

Abstract
Respiratory disease remains a common cause of morbidity and mortality
in HIV-infected patients. The spectrum of disease is broad and includes
infection, malignancy, airway, parenchymal, pleural, and vascular pathology. The pattern of disease has changed markedly in populations where
combination antiretroviral therapy (cART) is available; the incidence of
many opportunistic infections and malignancies has fallen, although
rates remain higher than in the general population, and conditions such
as chronic obstructive pulmonary disease and lung cancer are increasing
as life expectancies rise. Controversies still remain over the timing of cART
in relation to the treatment of opportunistic infections such as tuberculosis, and the diagnosis and treatment of the immune reconstitution inflammatory syndrome (IRIS).

In populations with access to combination antiretroviral therapy (cART) there has been a marked reduction in the incidence
of many HIV-associated infectious and malignant pulmonary
diseases
Immune reconstitution inflammatory syndrome (IRIS) is more
widely recognized as a cause of paradoxical disease exacerbation on initiation of cART
Despite cART, bacterial pulmonary infections continue to be
more common in HIV-infected individuals than in the general
population
Non-infectious respiratory complications of HIV, such as chronic
obstructive airways disease and lung cancer, are increasingly
recognized in an ageing population

Bacterial infections
Upper respiratory tract infections, acute bronchitis and acute
sinusitis occur more commonly in HIV-infected patients than in
the general population. Symptomatic chronic sinusitis affects
more than 15% of HIV-infected individuals, particularly those
with CD4 counts less than 200/ml (normal count is 470e1450/ml).

Keywords AIDS; antiretroviral therapy; bacterial pneumonia; COPD; HIV

infection; pneumonia; pneumocystis pneumonia; prophylaxis

Introduction
Bronchiectasis: bronchiectasis is increasingly recognized among
HIV-infected adults. It is probably due to recurrent bacterial,
mycobacterial and P. jirovecii infections. Management is as for
adults bronchiectasis unassociated with cystic fibrosis. Among
those with vertically acquired HIV infection who survive to late
adolescence/early childhood (with or without cART), bronchiectasis probably occurs secondary to lymphocytic interstitial
pneumonitis or to obliterative bronchiolitis.

Despite the widespread use of combination antiretroviral therapy

(cART) respiratory disease remains a common cause of morbidity
and mortality among HIV-infected adults; most will experience at
least one significant respiratory illness during their lifetime
(Table 1). With cART the incidence of many opportunistic infections, including Pneumocystis jirovecii pneumonia (PCP),
cytomegalovirus disease and Mycobacterium avium complex, and
some malignancies, including Kaposis sarcoma, has fallen
significantly. cART has had less impact on the incidence of bacterial pneumonia, tuberculosis (TB) and non-Hodgkins lymphoma. As patients are living longer, non-malignant chronic lung
disease is increasingly encountered.1

Bacterial pneumonia: the incidence of community-acquired

bacterial pneumonia remains high in HIV-infected patients,
although reduced by cART. Injecting drug users, cigarette
smokers, and those with low CD4 counts are particularly at risk.
Presentation is similar to that in the HIV-uninfected population.
Commonly isolated pathogens are Streptococcus pneumoniae and
Haemophilus influenzae. Staphylococcus aureus and Gramnegative organisms such as Pseudomonas aeruginosa are seen
in advanced disease (CD4 <50/ml). Mycoplasma, Legionella and
Chlamydia species are uncommon causes. Bacteraemia is commoner in HIV-infected patients with bacterial pneumonia, irrespective of CD4 count.
The radiographic appearance depends on the underlying
pathogen; both bilateral infiltrates mimicking Pneumocystis
pneumonia and lobar consolidation are seen (Figure 1). Complications include parapneumonic effusion, empyema, intrapulmonary cavitation, and abscess formation. There is a high
relapse rate, despite appropriate treatment.
Empirical antibiotics similar to those required in HIV-negative
patients are used for treatment, according to local antibiotic
resistance patterns. Fluoroquinolones should be used with
caution if TB remains within the differential diagnosis.

Infection
HIV directly impairs innate and adaptive immune responses
leaving the respiratory tract vulnerable to infection. Treatment
with cART does not fully restore immune function.2

Jamilah Meghji MBBS MRCP MPH is a Specialist Trainee in Respiratory

Medicine in the North West Thames Region, London, UK. Her research
interest lies in respiratory epidemiology. Competing interests: none
declared.
Robert F Miller MBBS FRCP is Reader in Clinical Infection at University
College London Medical School, University College London, London,
and Honorary Professor at the London School of Hygiene and Tropical
Medicine, UK. His research interests relate to the effects of HIV on
innate immunity and the respiratory complications of HIV infection,
particularly Pneumocystis jirovecii pneumonia and tuberculosis.
Competing interests: none declared.

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Radiology of bacterial pneumonia in HIV

HIV-associated respiratory disease

Infectious disease
C
Bacterial
 Acute bronchitis
 Acute and chronic sinusitis
 Bronchiectasis
 Bacterial pneumoniab
C
Fungal
 Pneumocystis jirovecii pneumonia (PCP)a
 Cryptococcus neoformans
 Histoplasma capsulatum
C
Viral
 Influenza A
C
Mycobacterial
 Mycobacterium tuberculosisa
 Atypical mycobacteria
Malignant disease
C
Kaposis sarcomaa
C
Lymphomaa
C
Lung cancer

Non-malignant disease
Fixed obstructive airways disease
C
Interstitial lung disease
 Non-specific interstitial pneumonitis
 Lymphoid interstitial pneumonitis
 Sarcoidosis
C
Pulmonary arterial hypertension
C
Pneumothorax
C
Reactions to HIV therapy
 Immune reconstitution inflammatory syndrome
C

a
b

AIDS-defining illness.
AIDS-defining illness if recurrent episode within 1 year.

Table 1

Fungal infections
Pneumocystis pneumonia: P. jirovecii (previously known as
Pneumocystis carinii) is the cause of Pneumocystis pneumonia
(PCP). In the post-cART era, PCP is seen mainly among those
presenting with a new diagnosis of HIV, and those not receiving
cART and/or prophylaxis due to poor adherence or limited
access to treatment.
The clinical presentation is sub-acute with several days to weeks
of non-productive cough and progressive exertional dyspnoea,
with or without fever. Chest auscultation may be normal or reveals
end-inspiratory crackles. Cyanosis may be detected in severe
(hypoxaemic) disease. The most common chest radiograph finding
is of bilateral perihilar infiltrates (Figure 2).
Atypical findings, such as upper zone infiltrates, hilar/mediastinal lymphadenopathy, lobar consolidation, and nodules, are
seen in up to 20%. A normal chest radiograph occurs in 10%,
particularly in those with early presentations, and does not
exclude the diagnosis, but the absence of ground-glass change on
CT makes PCP unlikely.
The gold standard for diagnosis is bronchoalveolar lavage
(BAL) with or without transbronchial biopsy. Sputum induction

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b
(a) Chest radiograph showing diffuse, bilateral infiltrates
mimicking Pneumocystis jirovecii pneumonia. The cause was
Streptococcus pneumoniae . (b) Chest radiograph showing lobar
consolidation. The cause was Staphylococcus aureus.
Figure 1

is an alternative. It is not possible to culture the organism, so it

must be seen on microscopy or identified by polymerase chain
reaction analysis. A negative BAL has a high negative predictive
value. Concurrent bacterial pneumonia, TB and Kaposis sarcoma are common.3
Poor prognostic factors identified at presentation, or soon after,
include older age, previous PCP, anaemia, hypoalbuminaemia,
high serum bilirubin or C-reactive protein, hypoxaemia, co-existent

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common and include rash, headache, nausea and diarrhoea,

fever, leukopenia and thrombocytopenia, hepatitis, and hyperkalaemia. Up to one-third of patients will not complete treatment
due to drug toxicity, and less than 10% will fail treatment
(defined as deterioration after a minimum of 5 days of therapy).
Alternative treatment options for those failing to respond to or
intolerant of co-trimoxazole include clindamycin (450e600 mg
orally or IV 6-hourly) with primaquine (15 mg orally daily), or
dapsone (10 mg orally daily) with trimethoprim (20 mg/kg orally
daily), or atovaquone (750 mg orally 12-hourly) in mild-tomoderate disease; and clindamycin with primaquine (doses as
above) or pentamidine (4 mg/kg IV daily) in severe disease.
Adjuvant glucocorticoids decrease the risk of respiratory failure
and mortality in severe PCP and should be started within 72
hours, if admission PO2 is 9.3 kPa or lower, or Aea O2 is over 4.7
kPa (breathing room air). Prednisolone 40 mg 12-hourly for
5 days, then 40 mg daily on days 6e10 and 20 mg daily on days
11e21, is the preferred regimen. All patients treated with cotrimoxazole, dapsone, and primaquine should be screened for
glucose-6-phosphate dehydrogenase deficiency.
It is recommended that patients begin cART before completing
treatment for the episode of PCP. There is limited evidence for
starting cART among HIV patients with opportunistic infections
who are critically unwell and admitted to the ICU. In this context,
some clinicians advocate delaying treatment until the patient has
left the ICU, and is showing signs of recovery.
Indications for prophylaxis of PCP are listed in Table 2. Cotrimoxazole is the treatment of first choice, and also protects
against several bacterial infections and toxoplasmosis. Alternative prophylaxis regimens include nebulized pentamidine, once
per month via a jet nebulizer (once per fortnight if CD4 <50/ml),
dapsone with pyrimethamine, and atovaquone.7
Prophylaxis can be discontinued if the CD4 count rises to above
200/ml with an undetectable plasma HIV-RNA for more than
3 months on cART, although there is some evidence that discontinuing at a CD4 count of over 100/ml is safe if viraemia is fully
suppressed. If the CD4 count falls later, recommencement of prophylaxis should be considered.7

Radiology of Pneumocystis pneumonia

Figure 2 (a): Chest radiograph showing diffuse bilateral infiltrates in

Pneumocystis jirovecii pneumonia. (b) Thoracic CT of Pneumocystis jirovecii pneumonia showing bilateral patchy ground-glass infiltrates.

Other fungal infections: Cryptococcus neoformans causes pulmonary infection when the CD4 count is below 200/ml. This can

pulmonary Kaposis sarcoma, and the presence of medical comorbidity, such as pregnancy. Subsequent to admission, development of pneumothorax, need for admission to the intensive
care unit (ICU), and need for mechanical ventilation are all associated with a poor outcome.4 The severity of PCP is clinically
stratified by the degree of hypoxaemia when breathing room
air, into mild (PaO2 >11.0 kPa, SaO2 >96%), moderate (PaO2
8.0e11.0 kPa, SaO2 91e96%) and severe (PaO2 <8.0, SaO2 <91%).
This grading system is used to guide treatment.
Empirical treatment pending diagnosis is used in those with
typical imaging, CD4 counts less than 200/ml, or clinical stigmata
of immunocompromise (e.g. oral hairy cell leukoplakia, cutaneous Kaposis sarcoma). High-dose co-trimoxazole (sulphamethoxazole 100 mg/kg/day with trimethoprim 20 mg/kg/day, in
two to four divided doses) is the treatment of first choice.5,6 It is
given orally in mild disease or intravenously (IV) in moderate-tosevere disease, and continued for 21 days. Adverse effects are

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Indications for prophylaxis of Pneumocystis

pneumonia (PCP) in adult HIV patients
Primary prophylaxis
C
CD4 <200/ml
C
CD4 <14% total lymphocyte count
C
Unexplained fever (>3 weeks duration)
C
History of oropharyngeal Candida
C
History of another AIDS-defining illness (e.g. Kaposis sarcoma)
C
Consider starting prophylaxis if CD4 count is 200e250/ml but
frequent monitoring is not possible
Secondary prophylaxis
C
After an episode of PCP
Table 2

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be isolated, or occur as part of disseminated disease with meningitis, with or without cryptococcaemia. Chest radiographic
changes include diffuse bilateral infiltrates mimicking PCP, focal
infiltrates, nodules, mass lesions, cavities, pleural effusions, and
lymphadenopathy. Diagnosis is made by identifying of C. neoformans in sputum or BAL. Treatment for disseminated disease is
with amphotericin/flucytosine followed by fluconazole, or with
fluconazole alone in isolated pneumonia.
Histoplasma capsulatum and Coccidioides immitis are
endemic in parts of Africa and The Americas. Both present with
disseminated disease in persons with CD4 counts below 200/ml,
but can cause focal pneumonia in those with CD4 counts greater
than 200/ml. Presentation is often non-specific with fever and
weight loss. Diagnosis requires culture of sputum, BAL fluid, or
transbronchial biopsy for both organisms. Serum (1e3)-b-Dglucan may be elevated in histoplasmosis, but is non-specific.
Treatment requires a prolonged course of antifungal medication
until a sustained improvement in CD4 count and HIV-RNA level
has been achieved.8

Active TB: more than two-thirds of cases of active TB in HIVinfected patients present with pulmonary disease. Extrapulmonary disease is common in patients with CD4 counts
below 150/ml and may involve lymph nodes, bone marrow, liver
and pericardium.
In patients with early HIV disease and maintained CD4
counts, the clinical picture of pulmonary TB is similar to adult
post-primary disease. Symptoms include chronic cough, dyspnoea, haemoptysis, chest pain, fever, sweats, and weight loss.
Chest radiographs may show apical change and cavitation.
Sputum and BAL are often smear and culture positive. In more
advanced disease with low CD4 counts, the presentation is often
atypical and symptoms less specific. Chest radiographs may be
normal but tend to represent primary disease with mediastinal
and hilar lymphadenopathy, miliary patterns, and pleural effusions. Cavitation is less likely, due to a lower grade immune
response to the organism, and sputum and BAL are often smear
negative but culture positive.
As in HIV-negative groups, culture remains the gold standard
for diagnosing active disease. Molecular diagnostic tests can be
used on respiratory samples and provide results within hours.
Although increasingly sensitive, they cannot be used to exclude
the diagnosis if negative. They not only enable rapid identification
of M. tuberculosis versus atypical mycobacteria, but also identify
mutations in the rpoB, inhA and katG genes associated with drug
resistance. The role of IGRA in the diagnosis of active tuberculosis
in HIV-infected persons remains uncertain.
While awaiting species identification, all acid- and alcohol-fast
bacilli, regardless of CD4 count, should be treated empirically as
M. tuberculosis, with standard TB treatment (2 months of rifampicin, isoniazid, ethambutol and pyrazinamide, followed by a
further 4 months of isoniazid and rifampicin). Daily treatment is
preferred over intermittent treatment because of concerns about
development of drug resistance patients with a high mycobacterial
burden. Some authorities advocate extending the continuation
phase to seven months in patients with cavitating pulmonary
disease and where sputum remains smear positive at 2 months. In
central nervous system disease, treatment is for 12 months.
Adverse events, drug reactions and mortality are more frequent
compared with non-HIV-infected individuals. Following treatment, secondary prophylaxis of TB is not given in UK; its role in
areas with high rates of re-infection remains unclear.
Multidrug-resistant and extensively drug-resistant tuberculosis have been epidemiologically associated with HIV infection.
This is probably due to rapid development of active tuberculosis
in HIV co-infected persons exposed to drug-resistant cases, rather
than any predilection to infection with drug-resistant strains.

Viral infections
Influenza A: there is no evidence that influenza A is more
common in HIV-infected persons, but those with lower CD4
counts may experience more severe disease and infection may be
complicated by secondary bacterial pneumonia. Patients with
both seasonal and H1N1 influenza present with coryzal symptoms, myalgia, fever and headache. As for the general population, treatment with neuraminidase inhibitors should be given
if influenza A is suspected or confirmed, and is most effective
if started within 48 hours of symptom onset. Diagnosis is
confirmed when viral antigen or RNA is detected in a nasopharyngeal aspirate or nasal swab. HIV-infected patients may
continue to excrete influenza A in respiratory secretions for
prolonged periods, despite clinical recovery.
Mycobacterial infections
Mycobacterium tuberculosis: TB occurs between 20 and 40 times
more frequently in HIV-infected persons, can occur at any stage
of HIV, is an AIDS-defining illness regardless of CD4 count, and is
a notifiable disease in the USA, the UK and most European
countries. Worldwide about 15% of new TB cases occur in HIVinfected persons, and TB is the cause of about 25% of all adult
HIV-related deaths.
Latent TB infection (LTBI): the annual risk of progression from
latent to active disease is high in HIV-positive individuals,
estimated at 10% per annum, and is greater with lower CD4
counts. Long-term treatment with cART significantly decreases
this risk, but does not restore it to that of an HIV-negative
person. Acutely, cART may increase the risk of TB, so-called
unmasking disease. HIV-positive individuals who have a high
risk of latent TB due to their country of origin, and a high risk
of reactivation of disease due to a low CD4 count or limited
time on cART, should therefore be screened and treated for
LTBI. Interferon-g release assays (IGRA) are more specific than
the tuberculin skin test for screening for LTBI, and retain
sensitivity at low CD4 counts. Chemoprophylaxis regimens
include isoniazid for 6 months, and rifampicin with isoniazid
for 3 months.

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Timing of cART in patients being treated for TB: cART should be

started in all HIV-infected patients treated for active TB. cART
reduces short- and long-term mortality in co-infected persons.9 TB
treatment should be initiated first, with cART shortly after e the
interval allowed between introduction of these regimens varies,
and is determined largely by the patients immune status (i.e. the
lower the CD4 count the sooner cART is started). Problems
encountered when treating TB and starting cART include high pill
burden, and hence poor adherence, overlapping toxicities (e.g.
peripheral neuropathy), drugedrug interactions (e.g. rifampicin
and protease inhibitors) and immune reconstitution inflammatory

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syndrome (IRIS). Early initiation of cART has been shown to have

a survival benefit for patients with low CD4 counts, whereas in
those with higher CD4 counts the risk of HIV disease progression is
lower and the survival benefit of early cART less certain, such that
HIV treatment can be delayed.10e12 Current UK guidelines are
listed in Table 3. The timing of cART in TB meningitis remains
controversial.13

protection than polysaccharide. Clinical efficacy and humoral

responses are likely to be impaired in those with CD4 counts
below 200/ml. Haemophilus influenzae b vaccine is not indicated.

Atypical mycobacteria: non-tuberculous mycobacterial infection

is rare among HIV-infected patients. M. avium complex (M. avium
or Mycobacterium intracellulare) is the most common form and
causes disseminated disease or localized lymphadenitis, particularly among those with CD4 counts below 50/ml. It is diagnosed by
blood or tissue culture. Mycobacterium kansasii presents with
disseminated or pulmonary disease. The latter may be indistinguishable from M. tuberculosis on imaging, thus diagnosis relies
on culture and speciation.

Influenza: all HIV-infected patients should be given the annual

intramuscular influenza vaccination. The live attenuated intranasal vaccine should be avoided.

Tuberculosis: BCG is a live vaccine, and its efficacy in HIVinfected patients is unknown. Given the risk of disseminated
disease it is not recommended in HIV-infected persons.

Malignant disease
Pulmonary Kaposis sarcoma
Kaposis sarcoma (KS) is the most common HIV-associated
malignancy. General aspects are discussed elsewhere (see AIDSrelated malignant disease on pages 430e434 of this issue). Pulmonary involvement with KS is almost always accompanied by
cutaneous or lymphadenopathic KS, and palatal disease strongly
predicts the presence of pulmonary disease. Presentation is with
progressive dyspnoea and non-specific cough; haemoptysis is
uncommon. Pulmonary KS may affect the airways, parenchyma,
pleura, or intra-thoracic lymph nodes. Radiological abnormalities
include nodular or interstitial infiltrates, pleural effusion (up to
40%), and mediastinal/hilar lymphadenopathy (w25%). Diagnosis is confirmed on bronchoscopy where multiple, red or purple,
flat or raised endotracheal or endobronchial lesions may be seen in
up to 50% (Figure 3). Biopsy has a low yield and is rarely performed. Pleural biopsy or cytology is rarely diagnostic. cART may
induce remission of lesions. Chemotherapy is given for symptomatic or extensive parenchymal disease at presentation, or disease that progresses despite cART. Kaposis sarcoma-associated
pleural effusions are difficult to treat, medical pleurodesis is
seldom successful, and repeat thoracocentesis is often required.

Immune reconstitution inflammatory syndrome (IRIS): when

cART is introduced after treatment for an opportunistic infection
is started, a paradoxical deterioration of symptoms known as IRIS
(see Immune response to HIV and vaccination on pages 425e429
of this issue) may be seen, often after initial improvement.14
IRIS may present as a respiratory syndrome with new or worsening lymphadenopathy, pleural/pericardial effusions, or worsening clinical or radiographic, features of the underlying
opportunistic infection. In the context of TB, two patterns of IRIS
are encountered. First, a paradoxical type, similar to paradoxical
reactions seen in the non-HIV-infected population, but often more
pronounced; in this form of IRIS, patients develop new clinical
manifestations (e.g. new lymphadenopathy) a median of 2e3
weeks after starting cART. Second, patients with latent asymptomatic TB infection may experience unmasking IRIS, with
development of highly inflammatory active TB a median of 3e6
weeks after commencing cART.
Should IRIS develop, the aim should be to continue both
treatment of the initial infection, and cART, unless IRIS is severe
or life-threatening (e.g mediastinal or intracerebral disease
causing mass-effect). Treatment of IRIS is often symptomatic, but
in patients with worsening intracerebral or mediastinal disease
systemic corticosteroids should be used.15

Lymphoma
High-grade non-Hodgkins B cell lymphoma is the most common
intra-thoracic lymphoma. Hodgkins lymphoma also occurs with
increased frequency among HIV-infected individuals. Lung parenchyma, pleura (effusion or mass), and mediastinal/hilar
lymph nodes may be involved. Extra-thoracic disease is usually
evident at diagnosis. Outcome from chemotherapy is better if
cART is also given.

Preventing respiratory infections

Bacteria: immunization with pneumococcal vaccine is recommended at diagnosis of HIV (irrespective of CD4 count) and
5-yearly thereafter. Conjugate vaccines may offer better

Lung cancer
Lung cancer is the most common non-AIDS-defining cancer
among HIV-infected persons in the developed world.16 The
incidence is higher among the HIV-infected than the general
population, an effect only partially explained by tobacco smoking. In the cART era the incidence appears to be increasing.17
Clinical presentation is often with extensive local or metastatic
disease with a poor prognosis, which is not improved by starting
cART.

Timing of cART in TB/HIV co-infection20

CD4 count (cells/ml)

Initiation of cART

<100
100e350

As soon as practicable
As soon as practicable
Can wait until 8/52, especially
if difficulties with drug interactions,
drug adherence, and drug toxicities
At physicians discretion

>350

Non-malignant disease
Airways disease
The prevalence of fixed airway obstruction and diffusion impairment is higher in the HIV-infected population.18 HIV-infected

Table 3

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Lymphocytic interstitial pneumonitis: lymphocytic interstitial

pneumonitis is more common in HIV-infected children, particularly those with perinatal infection, than in adults. Patients present with cough and dyspnoea. Chest examination is often
normal. Imaging shows diffuse reticulo-nodular infiltrates, or
may mimic PCP. Diagnosis is made by biopsy. Treatment with
cART is often effective.

Pulmonary Kaposi's sarcoma

Sarcoidosis: before the era of cART, sarcoidosis was rarely

described. In the era of cART it is increasingly recognized and is
thought to represent an immune reconstitution phenomenon.
Presentation is with cough and dyspnoea; the CD4 count is
usually greater than 200/ml. Imaging shows bilateral hilar
lymphadenopathy, with or without reticulo-nodular shadowing.
Symptoms may be self-limiting, but prednisolone may be
required.
Pulmonary arterial hypertension
Pulmonary arterial hypertension occurs more commonly among
HIV-infected patients than in the general population (estimated
prevalence 0.5%). Presentation, imaging, ECG, and echocardiographic findings are similar to those seen in the general population. Secondary causes of pulmonary arterial hypertension, for
example chronic thromboembolic disease, should be excluded.
Treatment is as for the general population; additionally, cART is
associated with improved haemodynamics and survival.

Pneumothorax
Pneumothorax occurs more commonly in HIV-infected persons
than in the general population. Risk factors include cigarette
smoking and nebulised pentamidine. PCP should be excluded in
any patient presenting with a pneumothorax.

Conclusions
Among HIV-infected populations with access to cART, the spectrum of HIV-associated lung disease has changed, such that PCP is
less commonly seen, but patients with undiagnosed/declared HIV
infection continue to present with respiratory symptoms, to both
primary care and to emergency departments. Among this population a wide differential diagnosis exists. Any adult presenting with
severe or atypical respiratory disease should be offered an HIV test,
irrespective of the presence/absence of stigmata of immune suppression, in keeping with UK British Association for Sexual Health
and HIV (BASHH)/British HIV Association (BHIVA) national
guidelines.
A

b
(a) Chest radiograph showing multiple, nodular infiltrates in a
patient with pulmonary Kaposis sarcoma. (b) Endobronchial
lesions of pulmonary Kaposis sarcoma.
Figure 3

cigarette smokers are twice as likely as smokers without HIV

infection to have chronic obstructive pulmonary disease (COPD).
Additional factors including substance misuse, recurrent opportunistic and bacterial infections and direct inflammatory effects of
HIV and cART may also contribute.19 Smoking cessation should be
encouraged.

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Practice points
C

441

Although the use of cART has decreased the rate of pulmonary

infection, it exceeds that of the general population. A high
index of suspicion must be maintained and investigations
including CT imaging and bronchoscopy with bronchoalveolar
lavage may be required
Concurrent use of cART is advised when treating opportunistic
respiratory infections
Patients should be monitored for the development of immune
reconstitution inflammatory syndrome, particularly if starting
CD4 count is low, the burden of initial infection is high, and the
CD4 count rapidly recovers
TB-HIV co-infection should be managed in a specialist centre e
concurrent use of cART and anti-tuberculosis medications can be
challenging
More attention must be paid to aspects of general lung health
such as smoking cessation in HIV-infected populations, as life
expectancies increase and chronic non-infectious conditions
such as chronic obstructive pulmonary disease (COPD) and
primary lung cancer become more common

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