The case described was initially treated empirically for community acquired bacterial pneumonia and PCP. Table 20.1 outlines common HIV associated pulmonary infections. In the absence of confirmatory tests, a diagnosis of PCP was most likely based on the clinical presentation and chest radiographic appearance in this at risk patient. PCP is nowadays most commonly seen in newly diagnosed HIV infected patients with advanced disease or HIV infected individuals not taking PCP prophylaxis or HAART. In the case described the patient had recently been diagnosed with advanced disease (CD4 count 30 cells/mm3) and was not taking PCP prophylaxis or HAART. PCP typically presents when the CD4 count falls below 200 cells/mm3 and is one of the most common opportunistic infections precipitating admission to the HDU and ICU for respiratory support.410-13 The risk of a first episode of infection below a CD4 count of 200 cells/mm3 (in patients not taking PCP prophylaxis or HAART) is estimated to be 18% at 12 months in asymptomatic individuals, rising to 44% in those with early symptomatic disease such as oral candidiasis as in the case described.14 PCP prophylaxis with co-trimoxazole is recommended when the CD4 count falls to 200 cells/mm3 or below. Patients with HIV infection on HAART with a CD4 count consistently improved to >200 cells/ mm3 have had PCP primary and secondary prophylaxis stopped without significant risk of subsequent PCP15-20
Methods of diagnosis range from sputum induction to open lung biopsy. The diagnostic test of choice is fibreoptic bronchoscopy with lavage, providing the patient can tolerate the procedure. Transbronchial biopsy is useful but is occasionally complicated by haemorrhage and pneumothorax. Sputum induction with nebulised saline has a lower diagnostic sensitivity and should be carried out in a negative pressure facility. Patients unable to tolerate bronchoscopy should be treated empirically, based on clinical judgement and expert advice, as was the case here. The case discussed was treated with high dose co-trimoxazole
Table 20.1 HIV associated pulmonary infections
Streptococcus pneumoniae* Haemophilus influenzae* Staphylococcus aureus* Klebsiella pneumoniae* Pseudomons aeruginosa* Nocardia asteroides Rochalimaea henselae
Bacterial pneumonia occurs more frequently in HIV positive patients at all CD4 counts than HIV negative controls. The risk increases as the CD4 count falls below 200 cells/mm3 and in intravenous drug users5
M tuberculosis** M avium intracellulare M kansasii
HIV positive individuals are at increased risk of infection with M tuberculosis, whatever the CD4 count, and should be offered an HIV test.7 Extrapulmonary tuberculosis tends to occur at CD4 counts <150 cells/mm3. M avium intracellular and M kansasii both occur late in the course of HIV infection when the CD4 count falls below 50-100 cells/mm3
Pneumocystis cariniif Cryptococcus neoformans*1 Candida albicans Aspergillus spp Penicillium marneffei Histoplasma capsulatum Coccidiodes immitis Blastomyces dermatitidis
Pulmonary infections with Candida and Aspergillus are relatively rare. Endemic mycoses caused by Histoplasma capsulatum, Coccidiodes immitis and Blastomyces dermatitidis occur in patients who live in North America
Toxoplasma gondii, Cryptosporidium spp Microsporidium spp Leishmania spp Strongyloides stercoralis
Respiratory syncytial virus
Common respiratory viral infections occur comparably in HIV infected and non-infected people. CMV is frequently isolated in BAL, but its role in causing disease is not clear. The presence of CMV in BAL is associated with a worse prognosis in PCP9
*The common causes of bacterial pneumonia are shown.5 6 One third of the pneumonias are bacteraemic. Bacteraemia is more common in pneumococcal pneumonia. Pseudomonal pneumonia is associated with a lower CD4 count than with pneumococcal pneumonia.6
**Multidrug-resistant (MDR) tuberculosis (resistant to isoniazid and rifampicin) is becoming an increasing problem among HIV positive individuals in North America. Antituberculous treatment requires careful monitoring for drug interactions and toxicity, especially if the patient is on HAART. Interactions such as those between the rifamycins and protease inhibitors or non-nucleoside reverse transcriptase inhibitors can lead to lower efficacy or increased toxicity of the anti-retroviral regimen.4
***Cryptococcal infection presents either as a primary lung infection or as part of a disseminated infection with cryptococcaemia, pneumonia, meningitis, and cutaneous disease.8
f Pneumocystis organisms from different host species have different DNA sequences. It has recently been suggested that the organism that causes human Pneumo Cysitis Pneumonia (PCP) should be named Pneumocystis jiroveci Frenkel 1999. Pneumocystis carinni should now be used to describe the rat derived infection (Stringer JR, Beard CB, Miller RF, Wakefield AE. A new name (Pneumocystis jiroveci] for Pneumocystis from humans. Emerging Infect Dis 2002;8:891-6.)
and adjuvant high dose steroids, which is the most effective first line treatment for severe PCP. Table 20.2 describes first and second line treatment for PCP in mild to moderate and severe disease. Second line treatment should be used for patients intolerant of or who have not responded to co-trimoxazole. The optimal dose of steroid and preferred second line treatment has yet to be determined.
The deterioration on day 9 was probably secondary to hospital acquired pneumonia and the patient was started on appropriate antibiotic treatment for this. He was also started on intravenous gancyclovir. The role of CMV infection during PCP is controversial and difficult to evaluate. Studies carried out before the introduction of adjuvant corticosteroid treatment in severe PCP concluded that CMV co-infection did not influence the outcome of PCP22 23 A more recent study showed that culture of CMV in the lavage of patients receiving adjuvant cortico-steroid treatment was, independently of CD4 count, associated with a 2.7-fold increased risk of death.9 Based on these findings, it has been proposed that survival rates for patients with severe PCP might be improved with anti-CMV therapy. The use of corticosteroids has also been related to the subsequent development of CMV retinitis and colitis in HIV infected patients.24 Furthermore, in vitro studies have shown increased CMV replication in corticosteroid treated macrophages.25 The mechanisms by which CMV shortens survival of patients on corticosteroid treatment are unknown. Further studies are needed to establish which patients receiving adjuvant corticosteroid therapy for severe PCP would benefit from treatment with foscarnet or gancyclovir.
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