Pneumocystis jirovecii is a fungus that causes infection specific to humans [3]. The great majority occur in immunocompromised subjects and

are associated with respiratory symptoms [4]. Current evidence suggests that PCP arises by re-infection from an exogenous source [5]. Evidence for nosocomial transmission exists but is limited [5]. Before the advent of preventative Smad tumor therapy and HAART, PCP occurred in up to 80% of HIV-seropositive individuals with AIDS [6]. In the UK this has declined considerably. Almost 90% of cases occur in HIV-seropositive persons with CD4 T-cell counts <200 cells/μL (or a CD4 T-cell percentage <14%). Other predictive factors for PCP in subjects not receiving effective HAART, include non-adherence to prophylaxis, oral candidiasis, oral hairy leukoplakia, unintentional weight loss, recurrent bacterial pneumonia, previous PCP and a high plasma HIV load [6–12]. The typical presentation of PCP is with exertional dyspnoea, which progresses selleck products over several weeks, malaise and a dry cough. An inability to take a deep breath and fever are often apparent [13]. Rarer presentations include a more rapid onset, haemoptysis and pleuritic chest pain. Purulent sputum production suggests bacterial infection – although this can

be present as a co-pathogen in around one-sixth of cases [14]. Physical examination reveals tachypnoea, normal breath sounds or, less frequently, end-inspiratory crackles. Wheezing and signs of focal consolidation or pleural effusion are less common presentations [13]. Spontaneous or infection-associated learn more pneumothorax in an HIV-seropositive individual should prompt exclusion of PCP [15]. Radiological findings in the chest include perihilar haze, interstitial infiltrates (characteristically

sparing the apices and costo-phrenic angles), pneumatocoeles and pneumothoraces. Upper lobe infiltrates alone have been reported to occur in individuals who are receiving inhaled pentamidine prophylaxis. A normal chest radiograph has been reported to occur in up to 39% of patients and should, therefore, not distract from pursuing the diagnosis of PCP if clinically suspected [16,17]. There are no clinical features specific to PCP. Radiology and nuclear medicine tests are not particularly sensitive or specific [18,19]. Other opportunistic infections may mimic the typical radiological features of PCP [20,21]. Demonstration of a fall in oxygenation between rest and exercise has been validated as a reasonably specific test for PCP in cases with a normal or near-normal chest radiograph who have no previous history of PCP [22], but is not reliable enough to make a diagnosis without confirmatory microbiology.